Compounds > capecitabine
Page last updated: 2024-12-06

capecitabine

Description

Capecitabine is an oral fluoropyrimidine anticancer drug that is a prodrug of 5-fluorouracil (5-FU). It is metabolized to 5-FU in the liver, and then further metabolized to active metabolites that inhibit thymidylate synthase, an enzyme essential for DNA synthesis. This inhibition of DNA synthesis leads to cell death, specifically in rapidly dividing cancer cells. Capecitabine is used to treat a variety of cancers, including breast cancer, colorectal cancer, and stomach cancer. It is often used in combination with other chemotherapy drugs. Capecitabine is well-tolerated and has a favorable safety profile. Its oral administration allows for convenient dosing and improved patient compliance compared to intravenous 5-FU. It is widely studied for its effectiveness in combination therapies and its potential for improving treatment outcomes in various cancer types. Capecitabine is important as it offers an effective and well-tolerated treatment option for various cancers, particularly those where intravenous 5-FU is not suitable or tolerated. Its research focus includes investigating its efficacy in combination therapies, exploring its potential in targeted therapies, and studying its impact on patient quality of life.'

Capecitabine: A deoxycytidine derivative and fluorouracil PRODRUG that is used as an ANTINEOPLASTIC ANTIMETABOLITE in the treatment of COLON CANCER; BREAST CANCER and GASTRIC CANCER. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

capecitabine : A carbamate ester that is cytidine in which the hydrogen at position 5 is replaced by fluorine and in which the amino group attached to position 4 is converted into its N-(penyloxy)carbonyl derivative. Capecitabine is a antineoplastic agent used in the treatment of cancers. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID60953
CHEMBL ID1773
CHEBI ID31348
SCHEMBL ID8153
MeSH IDM0287377

Synonyms (130)

Synonym
HY-B0016
AB01274776-01
AB01274776-02
cytidine, 5'-deoxy-5-fluoro-n-[(pentyloxy)carbonyl]-
xeloda
r-340
ro-09-1978
rg-340
5'-deoxy-5-fluoro-n-((pentyloxy)carbonyl)cytidine
cytidine, 5'-deoxy-5-fluoro-n-((pentyloxy)carbonyl)-
capecitabine [usan]
carbamic acid, (1-(5-deoxy-beta-d-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-, pentyl ester
ro 09-1978
n(4)-pentyloxycarbonyl-5'-deoxy-5-fluorocytidine
ro 09-1978/000
c15h22fn3o6
capecitabine
(1-(5-deoxy-beta-d-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-carbamic acid pentyl ester
154361-50-9
DB01101
xeloda (tn)
capecitabine (jan/usp/inn)
D01223
pentyl [1-(5-deoxy-beta-d-ribofuranosyl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl]carbamate
CHEBI:31348 ,
pentyl 1-(5-deoxy-beta-d-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamate
5'-deoxy-5-fluoro-n-[(pentyloxy)carbonyl]cytidine
capecitabina
capecitabin
capecitabinum
pentyl n-[1-[(2r,3r,4s,5r)-3,4-dihydroxy-5-methyloxolan-2-yl]-5-fluoro-2-oxopyrimidin-4-yl]carbamate
captabin
capecitabine sun
capecytabine
capecitabine teva
ro-09-1978000
capecitabine accord
CHEMBL1773
capiibine
capecitabine medac
capecitibine
nsc-759853
ro-091978000
ecansya
6804dj8z9u ,
nsc 759853
unii-6804dj8z9u
caxeta
capecitabine [usan:usp:inn:ban]
hsdb 7656
xabine
dtxcid1026451
cas-154361-50-9
tox21_112198
dtxsid3046451 ,
BCP9000483
MLS004774137
AKOS015920130
R340 ,
BCPP000300
MLS003915642
smr002530052
capecitabine [who-dd]
capecitabine [usp-rs]
capecitabine [mi]
xeliri component capecitibine
capecitabine [jan]
carbamic acid, (1-(5-deoxy-.beta.-d-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-, pentyl ester
pentyl 1-(5-deoxy-.beta.-d-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamate
capecitabine [ep monograph]
capecitabine [hsdb]
capecitabine [mart.]
capecitabine [orange book]
capecitabine [vandf]
capecitabine [inn]
capecitabine [usp impurity]
capecitabine [ema epar]
capecitabine [usp monograph]
xelox component capecitabine
AM84502
CS-0768
S1156
ro-09-1978-000
gtpl6799
pentyl n-{1-[(2r,3r,4s,5r)-3,4-dihydroxy-5-methyloxolan-2-yl]-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl}carbamate
SCHEMBL8153
tox21_112198_1
NCGC00164569-02
BS-1000
J-700154
n4-pentyloxycarbonyl-5'-deoxy-5-fluorocytidine
5'-deoxy-5-fluoro-n4-(pentyloxycarbonyl)cytidine
Q-200788
pentyl (1-((2r,3r,4s,5r)-3,4-dihydroxy-5-methyltetrahydrofuran-2-yl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl)carbamate
AB01274776_04
EX-A835
SR-01000931255-3
sr-01000931255
capecitabine, analytical standard
capecitabine, united states pharmacopeia (usp) reference standard
capecitabine, >=98% (hplc)
capecitabine, pharmaceutical secondary standard; certified reference material
capecitabine, european pharmacopoeia (ep) reference standard
pentyl 1-((2r,3r,4s,5r)-3,4-dihydroxy-5-methyltetrahydrofuran-2-yl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-ylcarbamate
Q420207
3-(2-hydroxyethyl)thiazoliumbromide
BRD-K61192372-001-08-9
5-deoxy-5-fluoro-n4-[(pentyloxy)carbonyl]cytidine
cpecitabine
ro-9-1978
5-deoxy-5-fluoro-n-[(pentyloxy)carbonyl]cytidine
CCG-264841
NCGC00164569-05
capecitabine- bio-x
BC164277
Z1501480421
BP-58647
capecitabine 500mg
pentyl (1-(5-deoxy-beta-d-ribofuranosyl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl)carbamate
capecitabine tablets, 150 mg
capecitabine tablets, 500 mg
capecitabine (usp monograph)
capecitabine 150mg
capecitabine (ep monograph)
5'-deoxy-5-fluoro-n-((pentyloxy)carbonyl)-cytidine
capecitabine (usp-rs)
l01bc06
capecitabine (usp impurity)
capecitabine (mart.)
capecitabine (usan:usp:inn:ban)

Research Excerpts

Overview

Capecitabine is an orally administered prodrug that converts preferentially to 5-fluorouracil within tumors. It is commonly used as adjuvant chemotherapy in colorectal cancer patients. Cape citabine, which is a first-line treatment for patients with metastatic colon cancer was also evaluated.

ExcerptReferenceRelevance
"Capecitabine is a common drug in the therapy against metastatic breast cancer due to its manageable safety profile. "( Capecitabine induced fingerprint loss: Case report and review of the literature.
Cherem-Kibrit, M; Colmenero-Mercado, JO; Deneken-Hernandez, Z; Gutiérrez-Andrade, L; Rodríguez-Gutiérrez, G, 2022)		3.61
"Capecitabine is an orally administered prodrug that converts preferentially to 5-fluorouracil within tumors, resulting in enhanced concentrations of 5-fluorouracil in tumor tissue. "( Capecitabine-induced leukoencephalopathy in a patient with triple-negative breast cancer: A case report and review of the literature.
Abu-Shahin, FI; Brown, EN; Liu, L, 2022)		3.61
"Capecitabine is a prodrug that is enzymatically converted to its active form, fluorouracil (also called 5-fluorouracil), which is commonly used as adjuvant chemotherapy in colorectal cancer patients. "( Severe ileum bleeding following adjuvant capecitabine chemotherapy for locally advanced colon cancer: a case report and review of the literature.
Liu, S; Sun, Z; Wu, J; Zou, Y, 2021)		2.33
"Capecitabine is an oral 5-fluorouracil prodrug with antimetabolite activity commonly used in advanced colorectal and breast cancer. "( Capecitabine-associated enterocolitis: Narrative literature review of a rare adverse event and a case presentation.
Gomatou, G; Kanellis, G; Kotteas, EA; Lagou, S; Rapti, VE; Syrigos, NK; Trontzas, IP, 2023)		3.8
"Capecitabine is an anticancer drug related to 5-fluorouracil (5-FU) that is used to treat multiple cancers. "( Reversible Toxic Encephalopathy Involving the Cerebellum and Subcortical White Matter Attributed to Capecitabine.
Li, Y; Tang, X; Wu, X; Zhong, W, 2022)		2.38
"Capecitabine is a pre-metabolite of 5-fluorouracil and is used as a chemotherapeutic agent. "( Capecitabine-related neurotoxicity presenting with agraphia.
Bayram, E; Bicakci, S; Demir, T; Iscan, D; Tolay, R, 2023)		3.8
"Capecitabine, which is a first-line treatment for patients with metastatic colon cancer, was also evaluated in these models."( Artificial Diets Based on Selective Amino Acid Restriction versus Capecitabine in Mice with Metastatic Colon Cancer.
Burgos-Morón, E; Calderón-Montaño, JM; Díaz-Ortega, P; Guillén-Mancina, E; Jiménez-Alonso, JJ; Jiménez-González, V; López-Lázaro, M, 2022)		1.68
"Capecitabine is a widely-used antineoplastic drug, a prodrug to 5-fluorouracil which commonly induces gastrointestinal toxicity. "( Capecitabine-induced enterocolitis: a case report and pharmacogenetic profile.
Chen, J; Liu, J; Shao, T; Shou, L; Shu, Q; Zhang, Y, 2022)		3.61
"Capecitabine is a molecule of choice in the therapeutic arsenal of anticancer drugs used in Morocco for the treatment of breast cancer and colorectal cancer. "( Assessment of patients' knowledge of their treatment with capecitabine at the National Institute of Oncology in Rabat.
Bechar, H; Belahcen, MJ; Cherif Chefchaouni, A; Nouibi, C; Rahali, Y, 2023)		2.6
"Capecitabine is an oral treatment of choice for colorectal and breast cancer in Morocco. "( Assessment of patients' knowledge of their treatment with capecitabine at the National Institute of Oncology in Rabat.
Bechar, H; Belahcen, MJ; Cherif Chefchaouni, A; Nouibi, C; Rahali, Y, 2023)		2.6
"Capecitabine (Xeloda®) is a cytotoxic, antimetabolite chemotherapeutic agent. "( Capecitabine-induced oral mucosal hyperpigmentation associated with hand-foot syndrome - A literature review.
Nascimento, ADAD; Porto, DM; Vidal, AKL, )		3.02
"Capecitabine is an oral prodrug of 5-fluorouracil. "( Oral Capecitabine Exposures and Use of Uridine Triacetate: A 20-Year Retrospective Analysis.
Cantrell, FL; Friedman, NA; Galust, H; Hardin, J; Minns, A; Seltzer, JA, 2023)		2.87
"Capecitabine (CAP) is a classic antimetabolic drug and has shown potential antirejection effects after liver transplantation (LT) in clinical studies. "( Metronomic capecitabine inhibits liver transplant rejection in rats by triggering recipients' T cell ferroptosis.
Cao, L; Fan, SL; Kong, DJ; Li, JH; Liu, T; Ren, JS; Shen, ZY; Song, ZL; Wang, H; Wang, JX; Wang, ZL; Yang, RN; Yoshida, S; Zhang, S; Zheng, H, 2023)		2.74
"Capecitabine is a therapeutic option in endocrine resistant HR+/HER2- metastatic breast cancer."( Capecitabine efficacy after cycline-dependent-kinase 4/6 inhibitor plus endocrine therapy in metastatic hormone receptor-positive breast cancer.
Bender, L; Fischbach, C; Kalish, M; Petit, T; Pflumio, C; Pierard, L; Trensz, P, 2023)		3.07
"Capecitabine is a commonly used oral chemotherapeutic agent. "( Capecitabine-induced Gastrointestinal Injury Shows a Graft-Versus-Host Disease (GVHD)-like Pattern.
Cox, BK; Guindi, M; Hutchings, DA; Larson, BK; Ojukwu, K; Waters, KM, 2023)		3.8
"Capecitabine is an anticancer agent and is the oral prodrug of 5-fluorouracil (5-FU). "( Development of a UPLC-MS/MS Assay for the Quantitative Determination of Capecitabine, 5'-deoxy-5-fluorocytidine (5'-dFCR), 5'-deoxy-5-fluorouridine (5'-dFUR), 5'-fluorouracil (5-FU), and α-fluoro-β-alanine (FBAL).
Beijnen, JH; Cats, A; de Vries, N; Guchelaar, HJ; Knikman, JE; Rosing, H, 2023)		2.59
"Capecitabine is a prodrug that converts to 5-fluorouracil (5-FU) in three steps. "( A polymorphism in ABCA2 is associated with neutropenia induced by capecitabine in Japanese patients with colorectal cancer.
Fujita, KI; Ishida, H; Kubota, Y; Matsumoto, N; Murase, R; Shibata, Y; Shimada, K, 2023)		2.59
"Capecitabine is a prodrug used primarily as a chemotherapeutic agent. "( Eruptive palmoplantar lesions induced by capecitabine: report of a case evaluated with dermoscopy.
García-Lozano, JA; González-Ramírez, RA; Ocampo-Candiani, J, 2019)		2.22
"Capecitabine is an oral fluoropyrimidine used to treat solid tumours such as colorectal and breast cancer. "( Permanent lesion to the corticospinal tract after therapy with capecitabine.
Hanssen, H; Heldmann, M; Münte, TF; Wagner-Altendorf, TA, 2019)		2.2
"Capecitabine is a prodrug of 5-fluorouracil, employed as a monotherapy or combination chemotherapy agent for treatment of colorectal cancer. "( Development and Validation of HPLC and HPTLC Methods for Therapeutic Drug Monitoring of Capecitabine in Colorectal Cancer Patients.
Chikhale, RV; Tajne, MR; Thorat, SG, 2020)		2.22
"Capecitabine is an oral prodrug of the anticancer drug 5-fluorouracil (5-FU). "( Pharmacokinetics of Capecitabine and Four Metabolites in a Heterogeneous Population of Cancer Patients: A Comprehensive Analysis.
Beijnen, JH; Cats, A; de Vries, N; Deenen, MJ; Huitema, ADR; Jacobs, BAW; Joerger, M; Meulendijks, D; Rosing, H; Schellens, JHM, 2019)		2.28
"Capecitabine is a chemotherapeutic agent used for the treatment of patients with metastatic cancers. "( Stopped-flow chemiluminescence determination of the anticancer drug capecitabine: Application in pharmaceutical analysis and drug-delivery systems.
Karimian, H; Mokhtari, A; Niazi Saei, J, 2020)		2.24
"Capecitabine is an orally bioavailable prodrug of the chemotherapeutic agent, fluorouracil. "( Real-time comprehensive toxicology testing in the clinical management of accidental pediatric capecitabine ingestion.
Badea, A; Garcia, E; Gintjee, TJ; Goodnough, R; Li, K; Lynch, KL; Repplinger, D, 2020)		2.22
"Capecitabine is an oral prodrug of 5-fluorouracil with a relevant role in the treatment of breast cancer. "( 5-Fluorouracil degradation rate as a predictive biomarker of toxicity in breast cancer patients treated with capecitabine.
Botticelli, A; Cerbelli, B; Lionetto, L; Marchetti, P; Roberto, M; Scagnoli, S; Simmaco, M, 2020)		2.21
"Capecitabine is a widely used 5-fluorouracil oral prodrug. "( SNPs in the COX-2/PGES/EP signaling pathway are associated with risk of severe capecitabine-induced hand-foot syndrome.
He, S; Huang, C; Huang, L; Li, Q; Liao, X; Yu, Q; Yuan, X, 2020)		2.23
"Capecitabine is a prodrug of 5-fluorouracil (5-FU) used for the treatment of colorectal cancer, with a two-week course of administration. "( Assessment of pharmacokinetic variations of capecitabine after multiple administration in rats: a physiologically based pharmacokinetic model.
Ito, Y; Kobuchi, S; Sakaeda, T; Sakai, S, 2020)		2.26
"Capecitabine is an oral pre-pro-drug of the anti-cancer drug 5-fluorouracil (5-FU). "( Phase I pharmacological study of continuous chronomodulated capecitabine treatment.
Beijnen, JH; de Vries, N; Huitema, ADR; Jacobs, BAW; Marchetti, S; Nuijen, B; Pluim, D; Roosendaal, J; Rosing, H; Schellens, JHM; van Werkhoven, E, 2020)		2.24
"Capecitabine is a prodrug that undergoes metabolism in three steps to form an active 5-fluorouracil (5-FU). "( Variants of carboxylesterase 1 have no impact on capecitabine pharmacokinetics and toxicity in capecitabine plus oxaliplatin treated-colorectal cancer patients.
Ariizumi, H; Fujita, KI; Hirasawa, Y; Hisamatsu, A; Ikusue, T; Ishida, H; Ishiguro, T; Kobayashi, K; Kubota, Y; Matsumoto, N; Ohkuma, R; Sekido, M; Shimada, K; Toshima, H; Tsunoda, T, 2020)		2.26
"MMC/capecitabine is an effective replacement for 5FU as a radiosensitizer in other malignancies but has not been studied in bladder cancer."( Radiation with concurrent radiosensitizing capecitabine tablets and single-dose mitomycin-C for muscle-invasive bladder cancer: A convenient alternative to 5-fluorouracil.
Mertens, LS; Noordzij, A; Pos, F; Schaake, EE; Schuring, N; van de Kamp, MW; van der Heijden, MS; van Rhijn, BWG; Voskuilen, CS, 2020)		1.3
"Capecitabine is a prodrug that is metabolized to its active form, 5-fluorouracil (5-FU), in three enzymatic steps. "( Correlation Between the Metabolic Conversion of a Capecitabine Metabolite, 5'-Deoxy-5-fluorocytidine, and Creatinine Clearance.
Ando, Y; Fujita, KI; Hattori, N; Inaishi, T; Kikumori, T; Maeda, O; Matsumoto, N; Nakayama, G; Shimokata, T, )		1.83
"Capecitabine is a prodrug of 5-FU, and S-1 is an oral 5-FU derivative."( The successful treatment of 5-fluorouracil overdose caused by the combination of capecitabine and S-1 in an elderly patient.
Li, J; Wang, R; Zheng, L, 2021)		1.57
"Capecitabine is an extensively used oral prodrug of 5-fluorouracil in treatment of colon cancer and is known to cause hand-foot syndrome (HFS). "( Polymorphisms in TYMS for Prediction of Capecitabine-Induced Hand-Foot Syndrome in Chinese Patients with Colorectal Cancer.
Cao, LJ; Dong, SQ; He, YQ; Huang, JW; Jia, WH; Li, XZ; Wang, TM; Wu, ZY; Xue, WQ; Yang, DW; Zhang, JB; Zhang, PF; Zheng, XH, 2021)		2.33
"Capecitabine is an oral pro-drug of 5-fluorouracil. "( Population Pharmacokinetics of Intracellular 5-Fluorouridine 5'-Triphosphate and its Relationship with Hand-and-Foot Syndrome in Patients Treated with Capecitabine.
Beijnen, JH; Derissen, EJB; Dorlo, TPC; Huitema, ADR; Jacobs, BAW; Janssen, JM; Marchetti, S; Roosendaal, J, 2021)		2.26
"Capecitabine is an oral anticancer drug which can cause some adverse reactions and the great challenge for its use is to ensure the medication adherence. "( Adverse reactions and adherence to capecitabine: A prospective study in patients with gastrointestinal cancer.
Barbosa, CR; Cobaxo, TS; de Souza, RN; Dias, LP; Duarte, NC; Lima, CS; Lima, TM; Moriel, P; Pincinato, EC; Tavares, MG; Teixeira, JC; Visacri, MB, 2022)		2.44
"Capecitabine (Cape) is an oral prodrug of the antimetabolite 5-fluorouracil. "( Activity of Sorafenib Plus Capecitabine in Previously Treated Metastatic Colorectal Cancer.
Ali, A; Daily, KC; Dang, LH; George, TJ; Iqbal, A; Ivey, AM; Lee, JH; Ramnaraign, BH; Read, TE; Tan, SA; Terracina, KP; Wang, Y, 2021)		2.36
"Capecitabine is an oral prodrug of 5-fluorouracil and is widely used for colorectal cancer (CRC) treatment. "( A Physiologically Based Pharmacokinetic-Pharmacodynamic Model for Capecitabine in Colorectal Cancer Rats: Simulation of Antitumor Efficacy at Various Administration Schedules.
Ito, Y; Kobuchi, S; Sakaeda, T; Sakai, S, 2021)		2.3
"Capecitabine is an oral prodrug of 5-FU, with reported preferential activation in malignant cells that may also cause cardiotoxic reactions."( 5-Fluorouracil, capecitabine and vasospasm: a scoping review of pathogenesis, management options and future research considerations.
Boulmpou, A; Charalampidis, P; Giannakoulas, G; Papadopoulos, CE; Teperikidis, E; Tsavousoglou, C; Vassilikos, V, 2022)		1.79
"Capecitabine is an oral fluoropyrimidine carbamate analogue of 5-Fluorouracil (5-FU)."( Capecitabine induced Steven-Johnson syndrome: A rare case report.
Karthikeyan, K; Madhu, CS; Sameera, KV; Shaji, S; Swetha, MAC, 2022)		2.89
"Capecitabine is an antimetabolite antineoplastic agent widely used in the treatment gastrointestinal cancers. "( A case of palmar hypopigmentation induced by capecitabine in a gastrointestinal cancer patient.
Botsen, D; Bouche, O; Gossery, C; Gratiaux, J; Rezzag-Mahcene, C; Slimano, F; Visseaux, L, 2022)		2.42
"Capecitabine monotherapy is an oncologically safe regimen compared to oxaliplatin-added regimens in elderly patients with high-risk stage II/stage III colon cancer."( Comparison between oxaliplatin therapy and capecitabine monotherapy for high-risk stage II - III elderly patients with colon cancer.
An, MS; Baik, H; Kang, SH; Kim, KH; Lee, HS; Lee, SH; Oh, MK; Park, J; Seo, SH, 2022)		2.43
"Capecitabine is a 5-fluorouracil basedchemotherapeutic drug widely used in the treatmentof solid tumors, especially colorectal and breast. "( Capecitabine-induced lichenoid drug eruption: a case report.
Aouthmany, M; Gehlhausen, JR; Katona, TM; Strausburg, MB; Turner, MJ, 2017)		3.34
"Capecitabine is an effective therapy for metastatic breast cancer. "( Capecitabine in early breast cancer: A meta-analysis of randomised controlled trials.
Amir, E; Cescon, DW; Ethier, JL; Natori, A, 2017)		3.34
"Capecitabine is an oral fluoropyrimidine chemotherapeutic agent, which, after oral administration, is metabolized to its active cytotoxic compound: 5-fluorouracil (5-FU). "( Report of two cases of acute cardiac adverse events in patients with colorectal carcinoma receiving oral capecitabine.
Godwin, SA; Kosmas, C; Koulouris, E; Kyratlidis, K; Lampropoulos, S; Pavlidis, K; Roditis, P; Tzimou, M; Zafiris, A, 2017)		2.11
"Capecitabine is a prodrug of 5-flurouracil, employed as a broad spectrum chemotherapeutic agent. "( A rapid and simple HPTLC assay for therapeutic drug monitoring of capecitabine in colorectal cancer patients.
Chikhale, RV; Tajne, MR; Thorat, SG, 2018)		2.16
"Capecitabine (Xeloda) is an oral 5-FU prodrug of comparable pharmacodynamic activity, currently preferred in place of 5-FU infusion, its established counterpart in neoadjuvant CRT for rectal cancer."( Comparing pathological complete response rate using oral capecitabine versus infusional 5-fluorouracil with preoperative radiotherapy in rectal cancer treatment.
Evans, T; Jootun, N; Mak, J; Makin, G; Platell, C, 2018)		1.45
"Capecitabine is a fluoropyrimidine commonly used in the treatment of colorectal cancer which may cause central nervous system toxicity, namely cerebellar dysfunction."( Acute reversible toxic encephalopathy during capecitabine and oxaliplatin treatment.
Araújo, F; Baptista, MJ; Casa-Nova, M; Godinho, J; Mesquita, T; Passos Coelho, JL; Vale, J, 2019)		2.22
"Capecitabine (CAP) is a chemotherapeutic agent used to treat breast and gastrointestinal cancers. "( Reversible severe fatty liver induced by capecitabine: A case report.
He, Q; Jiang, Y; Li, S; Shi, C; Yang, X, 2017)		2.16
"Capecitabine is an oral fluoropyrimidine that generates 5FU preferentially at the tumor site by exploiting the higher activity of the enzyme thymidine phosphorylase in tumor tissue compared with healthy tissue."( A prospective randomized trial comparing capecitabine-based chemoradiotherapy with 5-FU-based chemoradiotherapy in neoadjuvant setting in locally advanced carcinoma rectum.
Gupta, M; Gupta, MK; Seam, RK; Singh, K, )		1.12
"Capecitabine is an oral prodrug of fluorouracil, which is a common agent used in the management of many solid tumor malignancies. "( Photosensitive lichenoid skin reaction to capecitabine.
Bennett, DD; Burkard, ME; Shah, RA, 2017)		2.16
"Capecitabine is an approved standard therapy for anthracycline- and taxane-pretreated locally advanced or metastatic breast cancer (BC). "( Randomised phase III trial of vinflunine plus capecitabine versus capecitabine alone in patients with advanced breast cancer previously treated with an anthracycline and resistant to taxane.
Aapro, M; Bondarenko, I; Campone, M; Krishnamurthy, S; Lebedeva, L; Martin, M; Roman, L; Sakaeva, D; Vedovato, JC, 2018)		2.18
"Capecitabine is a potentially important treatment option for patients with advanced HCC and may even represent a cure in certain cases."( Sustained complete response of advanced hepatocellular carcinoma with metronomic capecitabine: a report of three cases.
Abbati, F; Barbera, MA; Brandi, G; De Lorenzo, S; Frega, G; Garajovà, I; Garuti, F; Golfieri, R; Palloni, A; Pantaleo, MA; Saccoccio, G; Venturi, M, 2018)		2.15
"Capecitabine is a pro-drug of 5-fluorouracil (5-FU), and is an orally available chemotherapeutic used to treat colorectal cancer (CRC). "( Investigation into Enhancing Capecitabine Efficacy in Colorectal Cancer by Inhibiting Focal Adhesion Kinase Signaling.
Baek, JH; Jeong, KY; Kim, HM; Lee, H; Park, MH; Sim, JJ, 2018)		2.21
"Capecitabine is a prodrug and is selectively activated by tumor cells to its cytotoxic moiety, 5-fluorouracil, by thymidine phosphorylase, which is generally expressed at high levels in tumors. "( Capecitabine bioequivalence in healthy volunteers.
Bosio-Guimarães, RA; De Nucci, G; Galvinas, PAR; Machado Matos, M; Mendes, GD; Moreno, RA; Pastre, KIF; Schmidt Niederauer, AJ; Schramm, SG, 2018)		3.37
"Capecitabine is an oral chemotherapeutic agent used in colorectal cancer. "( Evaluation of the clinical impact of concomitant acid suppression therapy in colorectal cancer patients treated with capecitabine monotherapy.
Baran, A; Phillips, MA; Rhinehart, HE; Wade, N, 2019)		2.17
"Capecitabine is an oral prodrug analog of 5-fluorouracil, and recent studies have suggested that proton pump inhibitors (PPIs) may detrimentally affect capecitabine efficacy."( Effects of Proton Pump Inhibitors on FOLFOX and CapeOx Regimens in Colorectal Cancer.
Chambers, CR; Chu, MP; Dersch-Mills, D; Ghosh, S; Ha, V; Sawyer, MB; Wong, GG, 2019)		1.24
"Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) which is converted to 5FU by a series of reactions catalyzed by different enzymes, the last of the enzymes being thymidine phosphorylase (TP). "( Capecitabine for the treatment of pancreatic cancer.
Byrne, MM; Godara, A; Saif, MW; Siddiqui, NS, 2019)		3.4
"Capecitabine is a safe regimen in terms of oncologic outcomes compared with FL in older patients with stage II colon cancer."( Oncologic outcomes after adjuvant chemotherapy with capecitabine compared to 5-fluorouracil/leucovorin for geriatric stage II colon cancer: a retrospective cohort study.
Cho, S; Jeong, SY; Kim, MJ; Kwon, YH; Lee, KY; Park, JW; Park, KJ; Ryoo, SB, 2019)		2.21
"Capecitabine (CAP) is an FDA-approved and frequently used chemotherapeutic agent for the treatment of various cancers. "( Capecitabine-loaded nanoniosomes and evaluation of anticancer efficacy.
Azarpira, N; Heli, H; Karimian, K; Nazari-Vanani, R, 2019)		3.4
"Capecitabine is a chemotherapeutic agent, approved by the United States-Food and Drug Administration for the management of colonic, metastatic colonic, and metastatic breast carcinoma."( A case of capecitabine-induced dermatomyositis.
Kumar, S; Neema, S; Saraswat, N; Verma, R, )		1.26
"Capecitabine is a commonly used oral chemotherapy agent. "( Concomitant use of capecitabine and proton pump inhibitors - Is it safe?
Badry, N; Cheng, V; Hunter, N; Lemos, J; Lemos, M, 2019)		2.29
"Capecitabine is an oral antineoplastic agent, and phenytoin is an anticonvulsant drug with a narrow therapeutic index. "( Combination of capecitabine and phenytoin may cause phenytoin intoxication: a case report.
Ciftci, R; Ciftci, S; Karabulut, S; Tas, F, )		1.93
"Like capecitabine, tegafur is a metabolic precursor of fluorouracil."( Tegafur + gimeracil + oteracil. Just another fluorouracil precursor.
, 2013)		0.84
"Capecitabine (CAP) is a 5-FU pro-drug approved for the treatment of several cancers and it is used in combination with gemcitabine (GEM) in the treatment of patients with pancreatic adenocarcinoma (PDAC). "( Anti-tumour efficacy of capecitabine in a genetically engineered mouse model of pancreatic cancer.
Bapiro, TE; Bramhall, JL; Cook, N; Courtin, A; Jodrell, DI; Krippendorff, BF; Neesse, A; Richards, FM; Tuveson, DA, 2013)		2.14
"Capecitabine (CA) is an orally administered fluoropyrimidine carbamate which is preferentially converted to active 5-FU and is one of the agents used instead of FU in such cases."( Can capecitabine be used instead of concurrent bolus 5-FU in postoperative chemoradiotherapy for gastric adenocarcinoma?
Isikli, L; Yoney, A, 2013)		1.67
"Capecitabine is an orally administered prodrug that converts preferentially to 5-FU within tumors, resulting in enhanced concentrations of 5-FU in tumor tissue."( Capecitabine induces both cardiomyopathy and multifocal cerebral leukoencephalopathy.
Endo, A; Nakashima, R; Takahashi, N; Tanabe, K; Yoshida, Y, 2013)		2.55
"Capecitabine is an oral 5-fluorouracil (5-FU) pro-drug commonly used to treat colorectal carcinoma and other tumours. "( A candidate gene study of capecitabine-related toxicity in colorectal cancer identifies new toxicity variants at DPYD and a putative role for ENOSF1 rather than TYMS.
Carracedo, A; Castells, A; Castellvi-Bel, S; Domingo, E; Fernández-Rozadilla, C; Freeman-Mills, L; Gonzalez-Neira, A; Howarth, K; Johnstone, E; Jones, A; Julier, P; Kaur, K; Kerr, D; Kerr, R; Love, S; Martin, M; Pagnamenta, A; Palles, C; Pita, G; Rosmarin, D; Ruiz-Ponte, C; Scudder, C; Taylor, J; Tomlinson, I; Wang, H, 2015)		2.16
"Capecitabine is an oral fluoropyrimidine derivative which is frequently used alone or in combination regimens for the treatment of metastatic breast cancer. "( Lack of prognostic value of mean corpuscular volume with capecitabine therapy in metastatic breast cancer.
Berk, V; Bozkurt, O; Cetin, B; Duran, AO; Inanc, M; Kaplan, MA; Karaca, H; Ozaslan, E; Ozkan, M, 2014)		2.09
"Capecitabine is a tumor-activated oral fluoropyrimidine used in breast and colorectal cancer. "( Hypertriglyceridemia and hyperglycemia induced by capecitabine: a report of two cases and review of the literature.
Han, GH; Huang, JX, 2015)		2.11
"Capecitabine is a safe chemotherapeutic agent with moderate activity for first-line treatment of older metastatic colorectal cancer patients with limited performance status."( First-line mono-chemotherapy in frail elderly patients with metastatic colorectal cancer.
Alacacioglu, A; Barutca, S; Degirmenci, M; Dirican, A; Karabulut, B; Oktay, E; Uslu, R; Varol, U; Yildiz, I, 2014)		1.85
"Capecitabine is an oral prodrug to 5-fluorouracil and is commonly used in the treatment of advanced breast, colon and stomach cancer. "( Capecitabine induced colitis.
Grin, A; Grover, SC; Maggo, G, 2014)		3.29
"Capecitabine is an oral fluoropyrimidine that can effectively replace infusional 5-fluorouracil (5-FU) for treatment of colorectal, gastric and breast cancer. "( Incidence and relative risk of grade 3 and 4 diarrhoea in patients treated with capecitabine or 5-fluorouracil: a meta-analysis of published trials.
de Braud, F; Di Bartolomeo, M; Iacovelli, R; Maggi, C; Palazzo, A; Pietrantonio, F; Ricchini, F, 2014)		2.07
"Capecitabine is an important oral fluoropyrimidine anticancer drug. "( Rapid and simplified HPLC-UV method with on-line wavelengths switching for determination of capecitabine in human plasma.
Fitatiuk, J; Kaza, M; Pawiński, T; Piórkowska, E; Rudzki, PJ; Szlaska, I, 2014)		2.07
"Capecitabine is a reasonable alternative and cost-effective treatment option under current conditions for patients with stage III colorectal cancer."( Health-related quality of life and cost comparison of adjuvant capecitabine versus 5-fluorouracil/leucovorin in stage III colorectal cancer patients.
Chen, HC; Chen, HH; Chen, WT; Chou, YH; Fang, CY; Hsu, HH; Huang, CC; Lee, HC; Lin, BW; Lin, JK; Lin, PC; Tan, EC; Ting, WC; Yang, MC; Yeh, CH, 2015)		2.1
"Capecitabine is an established treatment alternative to intravenous 5-fluorouracil (5-FU) for patients with rectal cancer receiving chemoradiotherapy. "( Chemoradiotherapy with capecitabine for locally advanced anal carcinoma: an alternative treatment option.
Beijnen, JH; Cats, A; Dewit, L; Meulendijks, D; Schellens, JH; Tomasoa, NB; van Tinteren, H, 2014)		2.16
"Oral capecitabine is a prodrug of 5-fluorouracil that has been used into the management of multiple cancers because of the convenience of administration and efficacy at least comparable with 5-fluorouracil. "( Acute coronary artery thrombosis and vasospasm following capecitabine in conjunction with oxaliplatin treatment for cancer.
Cleator, S; Dzaye, O; Nihoyannopoulos, P, 2014)		1.16
"Capecitabine is a complex chemotherapeutic agent with many side effects that might affect patient adherence to treatment."( Adherence to capecitabine treatment and contributing factors among cancer patients in Malaysia.
Hassan, NB; Norazwany, Y; Norhayati, I; Norsa'adah, B; Roslan, MH; Wan Nazuha, WR; Zahrina, AK, 2014)		1.49
"Capecitabine (CAP) is an oral drug of choice for treatment of colorectal cancer. "( Trichotomous gastric retention of amorphous capecitabine: an attempt to overcome pharmacokinetic gap.
Chourasia, MK; Meher, JG; Pawar, VK; Singh, M; Singh, Y, 2015)		2.12
"Capecitabine is an orally administered chemotherapeutic agent that is metabolized at the tumor site to 5-fluorouracil and thought to be without significant cardiac toxicity. "( Capecitabine-Induced Takotsubo Cardiomyopathy: A Case Report and Literature Review.
Aly, A; Bin Abdulhak, AA; Moormeier, J; Qasem, A, )		3.02
"Capecitabine (Cape) is a prodrug that is metabolized into 5'-deoxy-5-fluorocytidine (DFCR), 5'-deoxy-5-fluorouridine (DFUR), and 5-fluorouracil (5-FU) after oral administration. "( Simultaneous determination of capecitabine and its three nucleoside metabolites in human plasma by high performance liquid chromatography-tandem mass spectrometry.
Chen, X; Dai, X; Deng, P; Ding, L; Ji, C; Zhong, D, 2015)		2.15
"Capecitabine is a potent and safe agent that can be used after anthracycline and taxane treatment in patients with metastatic breast cancer (MBC). "( Efficacy of capecitabine monotherapy as the first-line treatment of metastatic HER2-negative breast cancer.
Akin, S; Aksoy, S; Altundag, K; Ates, O; Babacan, T; Balakan, O; Buyukhatipoglu, H; Demirci, F; Efe, O; Esin, E; Hasirci, AS; Kertmen, N; Sarici, F; Sever, AR, )		1.95
"Capecitabine monotherapy is an effective and safe regimen for ER-positive, HER2-negative patients with MBC. "( Efficacy of capecitabine monotherapy as the first-line treatment of metastatic HER2-negative breast cancer.
Akin, S; Aksoy, S; Altundag, K; Ates, O; Babacan, T; Balakan, O; Buyukhatipoglu, H; Demirci, F; Efe, O; Esin, E; Hasirci, AS; Kertmen, N; Sarici, F; Sever, AR, )		1.95
"Capecitabine is a chemotherapeutic agent which is converted to fluorouracil by thymidine phosphorylase in human body. "( A first case report of diffuse acneiform eruption caused by capecitabine in a patient with small-cell neuroendocrine lung carcinoma.
Alatas, E; Celik, SY; Dogan, G; Kara, A; Tanriverdi, O, 2016)		2.12
"Capecitabine is a highly water soluble prodrug of 5-fluorouracil that is dosed by patient body surface area. "( Effects of gender on capecitabine toxicity in colorectal cancer.
Chambers, CR; Danilak, M; Ghosh, S; Ilich, AI; Kim, CA; Mulder, KE; Sawyer, MB; Spratlin, JL, 2016)		2.2
"Capecitabine is an orally administered fluoropyrimidine that may be used instead of 5-fluorouracil/leucovorin."( Phase I/II trial of capecitabine, oxaliplatin, and irinotecan in combination with bevacizumab in first line treatment of metastatic colorectal cancer.
Aljubran, A; Alzahrani, A; Bazarbashi, S; Mohieldin, A; Shoukri, M; Soudy, H, 2015)		1.46
"Capecitabine (Cap) is an often prescribed chemotherapeutic agent, successfully used to cure some patients from cancer or reduce tumor burden for palliative care. "( (19)F MRSI of capecitabine in the liver at 7 T using broadband transmit-receive antennas and dual-band RF pulses.
Andreychenko, A; Boer, VO; Klomp, DW; Koopman, M; Luijten, PR; Raaijmakers, AJ; Seevinck, PR; van Gorp, JS; Viergever, MA, 2015)		2.22
"Capecitabine is an active drug in metastatic breast cancer (BC). "( Epirubicin Plus Cyclophosphamide Followed by Docetaxel Versus Epirubicin Plus Docetaxel Followed by Capecitabine As Adjuvant Therapy for Node-Positive Early Breast Cancer: Results From the GEICAM/2003-10 Study.
Adrover, E; Andrés, R; Baena-Cañada, JM; Ballesteros, AI; Barnadas, A; Calvo, L; Carrasco, EM; Casas, M; de la Haba-Rodríguez, J; Del Barco Berron, S; del Carmen Cámara, M; González, S; Jara, C; Lluch, A; López-Vega, JM; Margelí Vila, M; Martín, M; Martínez de Dueñas, E; Martínez-Jáñez, N; Mendiola Fernández, C; Muñoz-Mateu, M; Plazaola, A; Ramos, M; Ribelles, N; Rodríguez, CA; Rodríguez-Lescure, Á; Ruiz Borrego, M; Ruiz Simón, A; Sánchez-Rovira, P; Santaballa, A, 2015)		2.08
"Capecitabine is an orally administered prodrug of 5-fluorouracil (5-FU) and was designed to specifically affect tumor cells more than normal tissues. "( Capecitabine for the treatment of gastric cancer.
Bang, YJ; Kim, TY; Oh, DY, 2015)		3.3
"Capecitabine is an oral antineoplastic agent classified as a pyrimidin analogue. "( Forbidden to Drive -  a New Chemotherapy Side Effect.
De Lima, AS; Rovere, RK, 2015)		1.86
"Capecitabine is an oral fluoropirimidine that has been shown to be equally effective to 5-FU in many solid tumors."( Phase II Study of Capecitabine in Substitution of 5-FU in the Chemoradiotherapy Regimen for Patients with Localized Squamous Cell Carcinoma of the Anal Canal.
Alex, AK; Bariani, G; Braghirolli, MI; Hoff, PM; Moniz, CM; Nahas, C; Oliveira, SC; Riechelmann, R, 2016)		1.49
"Capecitabine is an orally administered tumor-selective fluoropyrimidine that acts as a prodrug of 5-Fluorouracil and bevacizumab is an antivascular endothelial growth factor (anti-VEGF) antibody, both are used for the treatment of patients with colorectal cancer."( Drug Induced Lupus Erythematosus Due to Capecitabine and Bevacizumab Treatment Presenting with Prolonged Thrombocytopenia.
Akyol, L; Baldane, S; Eroglu, E; Gok, K; Ozaslan, E; Ozkan, M; Senel, S, )		1.12
"Capecitabine is an oral prodrug of 5-fluorouracil and is commonly used oral chemotherapeutic drugs for advanced gastric and colorectal cancer. "( Self-identification and management of hand-foot syndrome (HFS): effect of a structured teaching program on patients receiving capecitabine-based chemotherapy for colon cancer.
Achrekar, MS; Carvalho, MD; D'souza, A; Govindarajan, S; Gupta, S; Murugan, K; Ostwal, V, 2016)		2.08
"Capecitabine is an oral fluoropyrimidine, and administration of oxaliplatin does not necessarily require the insertion of a central venous access device (CVAD)."( Feasibility of Capecitabine and Oxaliplatin Combination Chemotherapy Without Central Venous Access Device in Patients With Stage III Colorectal Cancer.
André, T; Bonnet, I; Bouché, O; Boucher, E; Chibaudel, B; Dauba, J; Faroux, R; Garcia, ML; Guering-Meyer, V; Hug de Larauze, M; Lapeyre-Prost, A; Lièvre, A; Malka, D; Obled, S; Taieb, J; Ychou, M, 2016)		1.51
"Capecitabine is a chemotherapeutic agent used in the treatment of metastatic colon cancer and metastatic breast cancer. "( Capecitabine-induced coronary artery vasospasm in a patient who previously experienced a similar episode with fluorouracil therapy.
Aladağ, E; Karakulak, UN; Maharjan, N; Övünç, K, 2016)		3.32
"Capecitabine is an orally administered prodrug that is preferentially converted to FU in tumor cells in comparison to normal cells."( Capecitabine for treating head and neck cancer.
Iqbal, H; Pan, Q, 2016)		2.6
"Capecitabine is an oral cytotoxic chemotherapeutic commonly used across cancer subtypes. "( Association of Proton Pump Inhibitors and Capecitabine Efficacy in Advanced Gastroesophageal Cancer: Secondary Analysis of the TRIO-013/LOGiC Randomized Clinical Trial.
Afenjar, K; Bang, YJ; Chu, MP; Chua, N; Hecht, JR; Hiller, JP; Hoff, PM; Houe, V; Huang, YJ; Khan-Wasti, S; King, K; Koski, S; Mulder, K; Qin, S; Sawyer, MB; Scarfe, A; Slamon, D; Sobrero, A; Spratlin, J; Wainberg, ZA, 2017)		2.16
"Capecitabine monotherapy is a treatment option for selected patients with metastatic colorectal cancer (mCRC) and is administered to up to 17% of patients. "( Tolerability of Capecitabine Monotherapy in Metastatic Colorectal Cancer: A Real-World Study.
Coers, W; de Graaf, JC; de Groot, JW; Leicher, LW; Tascilar, M, 2017)		2.24
"Capecitabine is an orally-administered chemotherapeutic agent used in the treatment of colorectal, gastric and breast carcinoma. "( [Capecitabine-induced ventricular fibrillation].
de Valk, J; Germans, T; Schakenraad, D; Ten Oever, D; van Capelle, AV, )		2.48
"Capecitabine-induced VF is a rare occurrence. "( [Capecitabine-induced ventricular fibrillation].
de Valk, J; Germans, T; Schakenraad, D; Ten Oever, D; van Capelle, AV, )		2.48
"Capecitabine which is an oral tumor activated fluoropyrimidine carbamate is an established treatment alternative to infusional fluorouracil for patients with gastrointestinal cancers."( Capecitabine in locally advanced anal cancer, do we need randomised evidence?
Chong, LC; Healey, T; Michele, T; Price, TJ, 2017)		2.62
"Capecitabine is an orally bioavailable prodrug that is converted to 5-fluorouracil through several enzymatic steps, the last of which is mediated by thymidine phosphorylase (TP). "( Thymidine phosphorylase expression and benefit from capecitabine in patients with advanced breast cancer.
Andreetta, C; Damante, G; Di Loreto, C; Fasola, G; Minisini, A; Pandolfi, M; Pegolo, E; Piga, A; Pizzolitto, S; Puglisi, F; Puppin, C; Valent, F, 2009)		2.05
"Capecitabine is a chemotherapeutic prodrug that is metabolised to 5-fluorouracil. "( Coronary spasm induced by capecitabine mimicks ST elevation myocardial infarction.
Curzen, NP; Ferchow, L; Hobson, A; Scott, PA, 2008)		2.09
"Capecitabine is a novel fluoropyrimidine carbamate, which has a broader spectrum of antitumor activity than other fluoropyrimidines, such as 5-FU, DFUR, or UFT; it has proved effective over a wide dose range. "( Antiangiogenic effect of capecitabine combined with ginsenoside Rg3 on breast cancer in mice.
Kang, X; Wang, J; Yang, B; Yang, F; Zhang, Q, 2008)		2.09
"Capecitabine is an oral chemotherapeutic agent, already used in breast and colon cancer. "( A phase II study of capecitabine in the treatment of ovarian cancer resistant or refractory to platinum therapy: a multicentre Italian trial in ovarian cancer (MITO-6) trial.
Beneduce, G; Breda, E; Di Maio, M; Forestieri, V; Gallo, C; Gebbia, V; Greggi, S; Lauria, R; Losito, S; Morabito, A; Pignata, S; Pisano, C; Scalone, S; Scaltriti, L; Sorio, R; Zagonel, V, 2009)		2.12
"Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) chemotherapy and is licensed for the treatment of breast and gastrointestinal cancers. "( Encephalopathy secondary to capecitabine chemotherapy: a case report and discussion.
Kolluri, RB; Raouf, S; Tipples, K, 2009)		2.09
"Capecitabine (XELODA) is a chemotherapeutic agent used widely in the treatment of adjuvant/metastatic colon cancer and metastatic breast cancer. "( Palmar-plantar hyperpigmentation with capecitabine in adjuvant colon cancer.
Easaw, JC; Vickers, MM, 2008)		2.06
"Capecitabine is a prodrug of fluorouracil. "( Focal acral hyperpigmentation in a patient undergoing chemotherapy with capecitabine.
Alonso, V; Calduch, L; Jordá, E; Martín, JM; Pinazo, MI; Villalón, G, 2009)		2.03
"Capecitabine is an oral pro-drug of fluorouracil, which is a commonly used cytotoxic drug in the treatment of colorectal carcinoma. "( Capecitabine-induced pancreatitis.
Warmerdam, LV; Yucel, H, 2010)		3.25
"Capecitabine is an oral fluoropyrimidine that was designed to allow selective activation in tumour tissues, thus reducing toxicity. "( Capecitabine-induced cerebellar toxicity in a patient with metastatic colorectal cancer.
Ahmad, A; Gounaris, I, 2010)		3.25
"Capecitabine is an oral prodrug of 5-fluorouracil (5-FU), used in the treatment of metastatic colon and breast cancers; it is also under investigation for use in gastric cancers. "( Longitudinal melanonychia induced by capecitabine.
Hymes, SR; Paravar, T, 2009)		2.07
"Capecitabine is an oral fluoropyrimidine designed to mimic a continuous infusion of 5-FU, and its use can prevent the need for cumbersome intravenous catheters and hospitalization of patients."( ML17032 trial: capecitabine/cisplatin versus 5-fluorouracil/cisplatin as first-line therapy in advanced gastric cancer.
Kang, YK; Ryu, MH, 2009)		1.43
"Capecitabine is an orally administered fluoropyrimidine carbamate that is absorbed intact from the gastrointestinal tract and becomes metabolically activated to 5-FU within the tumor."( Evolution of capecitabine dosing in colorectal cancer.
Sun, W, 2010)		1.45
"Capecitabine is an anticancer agent, prodrug of 5 fluorouracil (5-FU) administered orally and with a narrow therapeutic index. "( [Severe toxicity following capecitabine administration because of dihydropyrimidine deshydrogenase (DPD) deficiency].
Bontemps, H; Coursier, S; Emptoz, J; Guillermet, A; Martelet, S; Villier, C, 2010)		2.1
"Capecitabine is an effective and well-tolerated drug in elderly patients with MBC including for 1st line treatment."( Moderate dose capecitabine in older patients with metastatic breast cancer: a standard option for first line treatment?
Ashley, S; Johnston, S; Kotsori, AA; Noble, JL; Smith, IE, 2010)		1.44
"Capecitabine is an established therapy for metastatic breast cancer. "( Study of low-dose capecitabine monotherapy for metastatic breast cancer.
Abe, C; Akagi, K; Masuda, N; Nakayama, T; Nishida, Y; Noguchi, S; Ogino, N; Sakamoto, J; Taguchi, T; Yoshidome, K; Yoshikawa, Y, 2010)		2.14
"Capecitabine is an oral fluoropyrimidine which is transformed to 5-Fluorouracil inside tumor cells, where it achieves high drug concentrations. "( Cancer chemotherapy and cardiovascular risks: is capecitabine-induced hypertriglyceridemia a rare adverse effect?
Emiliani, A; Losanno, T; Manna, G; Seminara, P, 2010)		2.06
"Capecitabine is an oral chemotherapeutic agent converted to 5 fluorouracil (5-FU). "( Capecitabine and sixth cranial nerve palsy.
Adilieje, C; Bhattacharya, A; Dasgupta, S; Sheikh, Mu; Smith, B, )		3.02
"Capecitabine seems to be an active, feasible and well-tolerated mode of palliative treatment for advanced HNC patients who have previously received PBT schedules."( Phase II study of capecitabine as palliative treatment for patients with recurrent and metastatic squamous head and neck cancer after previous platinum-based treatment.
Adansa, JC; Cruz, JJ; Gil-Arnaiz, I; Hitt, R; Irigoyen, A; Isla, D; Lambea, J; Lecumberri, MJ; Martinez-Trufero, J, 2010)		2.14
"Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. "( Safety of capecitabine: a review.
Marshall, JL; Mikhail, SE; Sun, JF, 2010)		2.21
"Capecitabine is an oral fluoropyrimidine that is shown to have similar efficacy to 5-fluorouracil (5-FU) when used both alone and in combination with oxaliplatin in the treatment of colorectal cancer (CRC). "( Differences in efficacy and safety between capecitabine and infusional 5-fluorouracil when combined with irinotecan for the treatment of metastatic colorectal cancer.
Aliberti, C; Chiriatti, A; Fiorentini, G; Licitra, S; Montagnani, F, 2010)		2.07
"Capecitabine is a prodrug of 5-fluorouracil, more easily administered by mouth; its transformation in 5-fluorouracil is performed in the liver."( Toxic encephalopathy in elderly patients during treatment with capecitabine: literature review and a case report.
Bagli, L; Drudi, F; Fantini, M; Gianni, L; Nicoletti, S; Possenti, C; Ravaioli, A; Sintini, M; Tamburini, E; Tassinari, D, 2011)		1.33
"Capecitabine is an oral prodrug of 5-fluorouracil (5-FU)."( Capecitabine for the treatment of advanced gastric cancer.
Eastwood, A; Norman, G; Peura, P; Rice, S; Sculpher, M; Soares, M; Suh, D; Wright, K, 2010)		2.52
"Capecitabine is an orally available fluoropyrimidine carbamate that selectively delivers fluorouracil (5-FU) to tissues expressing high levels of thymidine phosphorylase (TP) such as tumors. "( Capecitabine in breast cancer: the issue of cardiotoxicity during fluoropyrimidine treatment.
Albini, A; Bucci, EO; Cergnul, M; Gottardi, O; Molteni, LP; Noonan, DM; Paino, AM; Rampinelli, I; Scaglietti, U, )		3.02
"Capecitabine is an orally administered fluoropyrimidine carbamate which has been developed as a prodrug of 5-FU with the goal to improve its tolerability and intratumoral drug concentration. "( Update on capecitabine alone and in combination regimens in colorectal cancer patients.
Azzariti, A; Cinieri, S; Colucci, G; De Vita, F; Lorusso, V; Maiello, E; Millaku, A; Numico, G; Petriella, D; Pisconti, S; Russo, A; Santini, D; Silvestris, N; Tommasi, S, 2010)		2.21
"capecitabine is an oral fluoropyrimidine which had been developed as a pro-drug of fluorouracil (FU), and had shown improved tolerability and intratumor drug concentrations through its tumor-specific conversion to the active drug. "( Capecitabine chemotherapy for metastatic colorectal cancer. Chemical structure, combinations and efficacy.
Koukourakis, G; Koukourakis, M; Kouloulias, V; Zacharias, G, )		3.02
"Capecitabine is an attractive radiosensitizer. "( Toxicity and complications of preoperative chemoradiotherapy for locally advanced rectal cancer.
Cats, A; Gerhards, MF; Heuff, G; Marijnen, CA; Swellengrebel, HA; van Geloven, AA; van Tets, WF; Verheij, M; Verwaal, VJ; Vincent, A, 2011)		1.81
"Capecitabine is a member of the fluoropyrimidine family of chemotherapeutic agents that selectively delivers 5-fluorouracil (5-FU) to tumors. "( Ventricular fibrillation as a likely consequence of capecitabine-induced coronary vasospasm.
Rather, A; Shah, A; Shah, NR, 2012)		2.07
"Capecitabine is an antineoplastic agent, of which metabolites can cross blood-brain barrier in CNS via epithelial tissue."( Capecitabine-related intracranial hypotension syndrome mimicking dural metastasis in a breast cancer patient: case report and review of the literature.
Alas, A; Aydogdu, N; Cosar-Alas, R; Denizli, B; Karagol, H; Kocak, Z; Ozen, A; Saynak, M; Uzal, C; Uzunoglu, S, )		2.3
"Capecitabine is a treatment option for patients with TN tumours in advanced disease including 1st line and 2nd/3rd line."( Is capecitabine efficacious in triple negative metastatic breast cancer?
Ashley, S; Dolly, S; Johnston, S; Kotsori, AA; Parton, M; Shaunak, N; Sheri, A; Smith, IE; Walsh, G, 2010)		2.42
"Capecitabine is a widely accepted option in pre-treated metastatic breast cancer (MBC) patients. "( Capecitabine after anthracycline and taxane exposure in HER2-negative metastatic breast cancer patients: response, survival and prognostic factors.
Bertucci, F; Esterni, B; Extra, JM; Gilabert, M; Gonçalves, A; Jacquemier, J; Madroszyk, A; Tarpin, C; Viens, P, 2011)		3.25
"Capecitabine is an oral anticancer prodrug which is converted to 5-fluorouracil (5-FU) via 3 enzymatic steps, these being 5'-deoxy-5-fluorocytidine (5'-DFCR), 5'-deoxy-5-fluorouridine (5'-DFUR), and finally 5-FU by carboxylesterase (CES), cytidine deaminase (CDA), and thymidine phosphorylase (TP), respectively. "( Comparison of in vitro metabolic conversion of capecitabine to 5-FU in rats, mice, monkeys and humans--toxicological implications.
Ishigai, M; Nakano, K; Shindoh, H; Yoshida, T, 2011)		2.07
"Oral capecitabine is an effective alternative to bolus 5-FU/FA as adjuvant treatment of patients with stage III colon cancer with efficacy benefits maintained at 5 years and in older patients."( Capecitabine versus 5-fluorouracil/folinic acid as adjuvant therapy for stage III colon cancer: final results from the X-ACT trial with analysis by age and preliminary evidence of a pharmacodynamic marker of efficacy.
Cassidy, J; Díaz-Rubio, E; Gilberg, F; McKendrick, J; Scheithauer, W; Seitz, JF; Twelves, C; Van Hazel, G; Wong, A, 2012)		2.34
"Capecitabine (Xeloda) is a prodrug of 5-FU used in the clinical management of advanced breast cancer. "( Inhibition of EGFR phosphorylation in a panel of human breast cancer cells correlates with synergistic interactions between gefitinib and 5'-DFUR, the bioactive metabolite of Xeloda.
Ait-Tihyaty, M; Jean-Claude, BJ; Mihalcioiu, C; Rachid, Z, 2012)		1.82
"Capecitabine is a good first-line chemotherapy option for women with advanced breast cancer who are unsuited to more intensive regimens."( Capecitabine versus classical cyclophosphamide, methotrexate, and fluorouracil as first-line chemotherapy for advanced breast cancer.
Ackland, SP; Byrne, MJ; Coates, AS; Fitzharris, B; Fong, A; Forbes, JF; Francis, PA; Gainford, MC; Gebski, V; Grimison, PS; Harvey, VJ; Nowak, AK; Paksec, L; Simes, RJ; Sourjina, T; Stockler, MR; Van Hazel, G; Wilcken, NR; Zannino, D, 2011)		2.53
"Capecitabine is an oral fluoropyrimidine with single-agent activity in metastatic nasopharyngeal carcinoma (NPC). "( Phase II trial of capecitabine plus cisplatin as first-line therapy in patients with metastatic nasopharyngeal cancer.
Chua, DT; Hong, RL; Krishnan, G; Kurnianda, J; Ng, AW; Ng, WT; Seetalarom, K; Shotelersuk, K; Sze, WK; Wang, CH; Yang, MH; Yiu, HH, 2012)		2.16
"Capecitabine is an active agent in the treatment of breast cancer. "( Adjuvant capecitabine, docetaxel, cyclophosphamide, and epirubicin for early breast cancer: final analysis of the randomized FinXX trial.
Ahlgren, J; Asola, R; Auvinen, P; Bono, P; Helle, L; Huovinen, R; Joensuu, H; Jukkola-Vuorinen, A; Kataja, V; Kellokumpu-Lehtinen, PL; Kokko, R; Leinonen, M; Lindman, H; Nilsson, G; Nyandoto, P; Paija, O; Pajunen, M; Poikonen, P; Tanner, M; Villman, K, 2012)		2.24
"Capecitabine is an oral prodrug of 5-fluorouracil (5-FU) which is converted in tumor cells to 5-FU by the enzyme thymidine phosphorylase. "( Capecitabine induced cardiotoxicity: a case report and review of literature.
Hashmi, A; Shoaib, M; Tunio, MA, 2012)		3.26
"Capecitabine (Xeloda) is an orally administered precursor of 5'deoxy-5-fluorouridine, which is a preferentially activated to 5-fluorouracil in tumors. "( A retrospective observational study on the use of capecitabine in patients with severe renal impairment (GFR <30 mL/min) and end stage renal disease on hemodialysis.
Flombaum, C; Jhaveri, KD; Latcha, S; Shah, M, 2012)		2.07
"Capecitabine is an oral prodrug of flurouracil with broad activity against various malignancies. "( Cisplatin with capecitabine: tolerance and activity in a phase I/II study preferentially enrolling patients with gastric cancer.
Hochster, HS; Levinson, B; Muggia, F; Newman, E; Ryan, T; Wu, J, 2012)		2.17
"Capecitabine is an oral prodrug converted to 5-fluorouracil (5-FU)."( [Late-onset leukoencephalopathy induced by long-term chemotherapy with capecitabine and cyclophosphamide for liver metastasis from breast cancer].
Ishikawa, T; Tukamoto, Y; Yasaki, S; Yoshii, F; Yuasa, N, 2012)		1.33
"Capecitabine is a rationally designed oral prodrug that is converted into 5-FU by intracellular thymidine phosphorylase."( The role of capecitabine in locally advanced rectal cancer treatment: an update.
Cejas, P; Feliu, J; Fernández-Martos, C; Machancoses, AH; Moreno-García, V; Nogué, M, 2012)		1.48
"Capecitabine monotherapy is an effective maintenance treatment after response to capecitabine-based combination chemotherapy in MBC with a favorable safety profile."( Single-agent capecitabine maintenance therapy after response to capecitabine-based combination chemotherapy in patients with metastatic breast cancer.
Bian, L; Cao, Y; Huang, H; Jiang, Z; Song, S; Wang, T; Wu, S; Zhang, S, 2012)		1.47
"Capecitabine is a new oral chemotherapeutic agent that is considered highly specific for sensitive tumor cells. "( Capecitabine may induce coronary artery vasospasm.
Stefanadis, C; Synetos, A; Tsiamis, E, )		3.02
"Capecitabine seems to be an active and well-tolerated regimen, even in heavily pretreated, frail patients."( Efficacy and safety of capecitabine in heavily pretreated recurrent/metastatic head and neck squamous cell carcinoma.
Ceruse, P; Fayette, J; Girodet, D; Péron, J; Poupart, M; Ramade, A; Zrounba, P, 2012)		1.41
"Capecitabine is an orally available chemotherapeutic agent that is converted to 5-fluorouracil (5-FU) after absorbtion. "( Acute myocardial infarction after capecitabine treatment: not always vasospasm is responsible.
Celiker, E; Eren, M; Güvenç, TS; Ilhan, E; Ozcan, KS, 2012)		2.1
"As capecitabine is a high-dosed drug, this is highly favourable in view of the size and thus clinical feasibility of the final dosage form."( Slow dissolution behaviour of amorphous capecitabine.
Beijnen, JH; Meulenaar, J; Nuijen, B; Schellens, JH, 2013)		1.17
"Capecitabine is an orally administered pro-drug of 5-fluorouracil that confers superior disease-free survival and presumably has a more favourable side-effect profile. "( Hypertriglyceridaemia-induced pancreatitis: a contributory role of capecitabine?
Chan, AO; Chan, HY; Ng, CM; Shek, CC; Tiu, SC, 2012)		2.06
"Capecitabine (Xeloda) is a new orally administered fluoropyrimidine carbamate that was rationally designed to exert its effect by tumor-selective activation. "( Preoperative chemoradiation using oral capecitabine in locally advanced rectal cancer.
Cho, MJ; Kim, JS; Song, KS; Yoon, WH, 2002)		2.03
"Capecitabine (Xeloda; CAP) is a recently developed oral antineoplastic prodrug of 5-fluorouracil (5-FU) with enhanced tumor selectivity. "( Metabolism of capecitabine, an oral fluorouracil prodrug: (19)F NMR studies in animal models and human urine.
Desmoulin, F; Gilard, V; Malet-Martino, M; Martino, R, 2002)		2.12
"Capecitabine (Xeloda) is an effective agent in advanced breast cancer, with a recent phase III trial demonstrating significant advantages of capecitabine/docetaxel (Taxotere) over single-agent docetaxel in response rate, time to disease progression, and overall survival in anthracycline-pretreated patients."( Single-agent vs combination therapy in advanced breast cancer: potential roles of capecitabine.
Hudis, CA, 2002)		1.26
"Oral capecitabine is a useful chemotherapy for metastatic breast cancer, both as monotherapy and in combination with other cytotoxic drugs. "( Moving forward with capecitabine: a glimpse of the future.
Biganzoli, L; Martin, M; Twelves, C, 2002)		1.15
"Capecitabine is a prodrug of 5-fluorouracil that is approved for use in patients with metastatic breast carcinoma and colorectal carcinoma, and it offers the convenience of oral administration."( A Phase I study of 9-nitrocamptothecin given concurrently with capecitabine in patients with refractory, metastatic solid tumors.
Clark, JW; Fuchs, CS; Garcia-Carbonero, R; Michaelson, MD; Paul Eder, J; Ryan, DP; Supko, JG, 2003)		1.28
"Capecitabine is an orally administered prodrug of fluorouracil which is indicated in the US and Europe, in combination with docetaxel, for the treatment of patients with metastatic breast cancer failing anthracycline therapy, and as monotherapy for metastatic breast cancer resistant to paclitaxel and anthracycline therapy (US) or failing intensive chemotherapy (Europe). "( Capecitabine: a review of its pharmacology and therapeutic efficacy in the management of advanced breast cancer.
Goa, KL; Ibbotson, T; Wagstaff, AJ, 2003)		3.2
"Capecitabine (Xeloda) is an oral prodrug that is enzymatically converted to fluorouracil (5-FU) within cancer cells. "( Current status of capecitabine in the treatment of colorectal cancer.
Rothenberg, ML, 2002)		2.09
"Capecitabine is a novel fluoropyrimidine carbamate which is selectively activated after oral administration to 5-fluorouracil (5-FU) by a sequential triple enzyme pathway in liver and tumor cells. "( Capecitabine treatment results in increased mean corpuscular volume of red blood cells in patients with advanced solid malignancies.
Kornek, GV; Locker, GJ; Mader, RM; Pluschnig, U; Scheithauer, W; Steger, GG; Wenzel, C, 2003)		3.2
"Capecitabine is an oral prodrug of 5-fluorouracil (FU). "( Penetration of capecitabine and its metabolites into malignant and healthy tissues of patients with advanced breast cancer.
Brunner, M; Eichler, HG; Locker, G; Mader, RM; Mueller, M; Rizovski, B; Schrolnberger, C; Steger, GG; Wenzel, C, 2003)		2.11
"Capecitabine is an effective salvage regimen in patients with recurrent and metastatic NPC."( A phase II study of capecitabine in patients with recurrent and metastatic nasopharyngeal carcinoma pretreated with platinum-based chemotherapy.
Au, GK; Chua, DT; Sham, JS, 2003)		1.36
"Capecitabine is a selectively tumor-activated fluoropyrimidine carbamate that is converted to 5-fluorouracil by the sequential activity of these enzymes, the final of which is thymidine phosphorylase, which is overexpressed in many human cancers."( The evolving role of capecitabine in breast cancer.
O'Shaughnessy, JA, 2003)		1.36
"Capecitabine (Xeloda) is a novel, oral fluoropyrimidine carbamate rationally designed to generate 5-fluorouracil (5-FU) preferentially in tumor tissue via a three-step enzymatic cascade."( Pharmacokinetics of capecitabine (Xeloda) in Japanese and Caucasian patients with breast cancer.
Bridgewater, J; Grange, S; Kimura, M; Kuranami, M; Lucraft, H; McAleer, J; Monkhouse, J; Poole, C; Reigner, B; Saeki, T; Sasaki, Y; Schüller, J; Watanabe, T; Weidekamm, E; Yorulmaz, C, 2003)		2.09
"Capecitabine is a rationally designed fluoropyrimidine that can be given orally and uses the high concentration of thymidine phosphorylase within cancer cells to concentrate heavily within the tumor."( Practical considerations in the use of oral fluoropyrimidines.
Hoff, PM, 2003)		1.04
"Capecitabine is an orally available fluoropyrimidine and is finally converted to 5-FU selectively in tumor tissues. "( Augmentation of the antitumor activity of capecitabine by a tumor selective dihydropyrimidine dehydrogenase inhibitor, RO0094889.
Eda, H; Endo, M; Hattori, K; Ishikawa, T; Ishitsuka, H; Miwa, M; Miyazaki-Nose, T; Shimma, N; Tanimura, H; Ura, M; Yamada-Okabe, H, 2003)		2.03
"Capecitabine is a rationally designed oral, tumor-activated fluoropyrimidine carbamate with high activity in metastatic breast cancer. "( Multicenter phase II study of oral capecitabine (Xeloda(")) in patients with metastatic breast cancer relapsing after treatment with a taxane-containing therapy.
Jänicke, F; Jonat, W; Kaufmann, M; Kieback, DG; Kölbl, H; Kuhn, W; Lück, HJ; Mohrmann, S; Reichardt, P; Schindler, AE; Thuss-Patience, PC; Von Minckwitz, G, 2003)		2.04
"Capecitabine is an orally administered pro-drug of 5-fluorouracil (5-FU), designed to exploit tissue-specific differences in metabolic enzyme activities in order to enhance efficacy and safety."( Clinical pharmacokinetic/pharmacodynamic and physiologically based pharmacokinetic modeling in new drug development: the capecitabine experience.
Blesch, KS; Burger, HU; Gieschke, R; Reigner, BG; Steimer, JL; Tsukamoto, Y, 2003)		1.25
"Capecitabine is an oral 5-fluorouracil (5-FU) prodrug that is more convenient than using infusional 5-FU, appears to have a similar therapeutic profile, and can be combined with daily irradiation."( COX-2 inhibitors as radiation sensitizers for upper GI tract cancers: esophagus, stomach, and pancreas.
Rich, TA; Shepard, R, 2003)		1.04
"Capecitabine is an oral fluoropyrimidine used for cancer treatment. "( Capecitabine-related neurotoxicity presenting as trismus.
Couch, LS; Groteluschen, DL; Mulkerin, DL; Stewart, JA, 2003)		3.2
"Capecitabine (Xeloda) is an oral fluoropyrimidine that is preferentially activated at the tumoral level, exploiting the higher thymidine phosphorylase activity in tumoral tissue."( Phase I and pharmacokinetic study of the association of capecitabine-cisplatin in head and neck cancer patients.
Chamorey, E; Giroux, B; Guardiola, E; Magné, N; Milano, G; Mouri, Z; Otto, J; Pivot, X; Schneider, M; Thyss, A, 2003)		1.29
"Capecitabine is an antineoplastic agent that is currently the only effective treatment for patients with advanced or metastatic breast cancer in whom anthracycline or taxoid treatment has failed. "( Onycholysis with the appearance of a "sunset" secondary to capecitabine.
Maino, KL; Norwood, C; Stashower, ME, 2003)		2
"Oral capecitabine is a highly active, well-tolerated and convenient treatment for breast and colorectal cancer. "( A phase II trial of capecitabine (Xeloda) in recurrent ovarian cancer.
Kaye, SB; McMahon, L; Paul, J; Reed, N; Vasey, PA, 2003)		1.16
"Capecitabine is a suitable replacement for i.v."( Oral capecitabine vs intravenous 5-fluorouracil and leucovorin: integrated efficacy data and novel analyses from two large, randomised, phase III trials.
Bukowski, RM; Cunningham, D; Dufour, P; Graeven, U; Harper, P; Hoff, PM; Lokich, J; Madajewicz, S; Maroun, JA; Marshall, JL; Mitchell, EP; Perez-Manga, G; Rougier, P; Schilsky, RL; Schmiegel, W; Schoelmerich, J; Sobrero, A; Van Cutsem, E, 2004)		1.56
"Capecitabine is an efficacious and better-tolerated alternative treatment for the patients with advanced and recurrent colorectal cancer."( [First-line Xeloda (Capecitabine) treatment for advanced and recurrent colorectal cancer].
Feng, FY; Fu, Q; Guan, ZZ; Huang, JJ; Liu, DG; Ruan, QL; Shi, D; Sun, SR; Wei, YQ; Wu, G; Wu, WQ; Wu, XD; Xiong, HH; Yang, CY; Yu, BM; Yu, SY; Zhang, P; Zhao, Y; Zheng, S; Zhuang, W; Zou, LQ, 2004)		2.09
"Capecitabine is an oral fluoropyrimidine, which is converted to fluorouracil (5-FU) by exploiting the comparatively higher activity of thymidine phosphorylase (TP) in tumor tissue. "( [Phase I clinical trial evaluation of capecitabine in concurrent combination of radiotherapy in nasopharyngeal carcinoma].
Cao, KJ; Chen, QY; Deng, MQ; Guo, L; Hong, MH; Huang, PY; Jiang, Y; Luo, DH; Mai, HQ; Mo, HY; Qiu, F; Sun, R, 2004)		2.04
"Capecitabine is an oral fluoropyrimidine converted to fluourouracil (FU) preferentially in tumor tissue. "( Phase II study of capecitabine in patients with fluorouracil-resistant metastatic colorectal carcinoma.
Abbruzzese, JL; Carter, S; Hoff, PM; Lassere, Y; Pazdur, R; Polito, D; Samid, D, 2004)		2.1
"Capecitabine is an oral prodrug of 5-fluorouracil and has been studied for the treatment of colorectal cancer. "( Cost-benefit analysis of capecitabine versus 5-fluorouracil/leucovorin in the treatment of colorectal cancer in the Netherlands.
Brouwers, JR; Jansman, FG; Postma, MJ; van Hartskamp, D; Willemse, PH, 2004)		2.07
"capecitabine) are a convenient alternative but have to prove a comparable efficacy to infusional 5-FU."( [New therapy options in colorectal carcinoma].
Folprecht, G; Köhne, CH, 2004)		1.04
"Capecitabine is a novel oral chemotherapy agent designed to generate 5-fluorouracil (5-FU) preferentially in tumor tissue, and is the most effective therapy for anthracycline and taxane-resistant breast cancer. "( Effect of capecitabine on mean corpuscular volume in patients with metastatic breast cancer.
Hamilton, M; Karvellas, CJ; Mackey, JR; Sawyer, M, 2004)		2.17
"Capecitabine (Xeloda) is a novel, oral, selectively tumor-activated fluoropyrimidine with proven activity in the treatment of advanced colorectal cancer. "( A phase II trial of capecitabine in previously untreated patients with advanced and/or metastatic gastric cancer.
Cho, JY; Choi, SH; Chung, HC; Han, JY; Hong, YS; Kang, JH; Lee, KS; Lee, SI; Noh, SH; Park, JN; Song, SY, 2004)		2.09
"Capecitabine is a fluoropyrimidine carbamate capable of exploiting the high concentrations of thymidine phosphorylase in tumor tissue to achieve activation preferentially at the tumor site. "( Combination therapy with capecitabine and interferon alfa-2A in patients with advanced renal cell carcinoma: a phase II study.
Arak, A; Leppik, K; Padrik, P, )		1.88
"Capecitabine (CAP) is a pro-drug of 5-FU and peripheral neuropathy associated with CAP has not been reported."( Peripheral neuropathy associated with capecitabine.
Diasio, RB; McGee, PJ; Saif, MW; Wood, TE, 2004)		1.32
"Capecitabine is an oral prodrug of 5-fluorouracil that is indicated for the treatment of breast and colorectal cancers. "( Hydrolysis of capecitabine to 5'-deoxy-5-fluorocytidine by human carboxylesterases and inhibition by loperamide.
Bosron, WF; Davis, WI; Hurley, TD; Murry, DJ; Quinney, SK; Sanghani, SP; Sun, Z, 2005)		2.13
"Capecitabine is a highly active oral fluoropyrimidine that is an attractive alternative to 5-fluorouracil in colorectal cancer treatment. "( A phase I clinical and pharmacokinetic study of capecitabine (Xeloda) and irinotecan combination therapy (XELIRI) in patients with metastatic gastrointestinal tumours.
Bertheault-Cvitkovic, F; Bugat, R; Canal, P; Chatelut, E; Cornen, X; Delord, JP; Dieras, V; Guimbaud, R; Lochon, I; Lokiec, F; Mery-Mignard, D; Mouri, Z; Pierga, JY; Turpin, FL, 2005)		2.03
"Capecitabine is an oral prodrug that is converted to its only active metabolite, FU, by thymidine phosphorylase. "( Capecitabine: a review.
Lindley, C; Walko, CM, 2005)		3.21
"Capecitabine is a three-step prodrug that was rationally designed to be a more effective and safer alternative to its intermediate metabolite, 5'-deoxy-5-fluorouridine (5'-DFUR). "( Pharmacokinetic and pharmacodynamic comparison of fluoropyrimidine derivatives, capecitabine and 5'-deoxy-5-fluorouridine (5'-DFUR).
Ebi, H; Igarashi, T; Kawada, K; Minami, H; Saeki, T; Sasaki, Y; Sigeoka, Y; Ueda, R; Usubuchi, N, 2005)		2
"Capecitabine is an attractive radiosensitizer which can be tumor specific. "( Preoperative concurrent radiotherapy with capecitabine before total mesorectal excision in locally advanced rectal cancer.
Ahn, SD; Chang, HM; Choi, EK; Kim, HC; Kim, JC; Kim, JH; Kim, JS; Kim, TW; Lee, SW; Park, JH; Ryu, MH; Shin, SS; Yu, CS, 2005)		2.04
"Oral capecitabine is an effective alternative to intravenous fluorouracil plus leucovorin in the adjuvant treatment of colon cancer."( Capecitabine as adjuvant treatment for stage III colon cancer.
Abt, M; Burris, H; Carrato, A; Cassidy, J; Cervantes, A; Fagerberg, J; Georgoulias, V; Husseini, F; Jodrell, D; Koralewski, P; Kröning, H; Maroun, J; Marschner, N; McKendrick, J; Nowacki, MP; Pawlicki, M; Rosso, R; Scheithauer, W; Schüller, J; Seitz, JF; Stabuc, B; Tujakowski, J; Twelves, C; Van Hazel, G; Wong, A; Zaluski, J, 2005)		2.29
"Capecitabine is an oral prodrug to 5-fluorouracil (5-FU). "( Immunohistochemical expression of thymidylate synthase as predictor of response to capecitabine in patients with advanced colorectal adenocarcinoma.
Hoeffding, LD; Jakobsen, A; Lindebjerg, J; Nielsen, JN, 2005)		2
"Capecitabine is a relatively new oral fluoropyrimidine currently licensed for the treatment of colorectal and breast cancer."( 5-Fluorouracil can cross brain-blood barrier and cause encephalopathy: should we expect the same from capecitabine? A case report on capecitabine-induced central neurotoxicity progressing to coma.
Chua, YJ; Cunningham, D; Formica, V; Leary, A, 2006)		1.99
"Capecitabine is a new oral fluoropyrimidine derivative. "( [Pharmacokinetic comparison of capecitabine and 5'-deoxy-5-fluorouridine (doxifluridine; 5'-DFUR)].
Ebi, H; Minami, H, 2005)		2.06
"Capecitabine is an oral fluoropyrimidine carbamate activated sequentially in both liver and tumor tissues by carboxylesterases, cytidine deaminase, and thymidine phosphorylase. "( Validation of real-time reverse-transcription-polymerase chain reaction for quantification of capecitabine-metabolizing enzymes.
Guichard, SM; Jodrell, DI; Macpherson, JS, 2006)		2
"Capecitabine is an orally active prodrug of fluorouracil (FU) and is extensively used as an antineoplastic agent. "( Drug interaction between capecitabine and warfarin: a case report and review of the literature.
Akcali, Z; Basturk, B; Ozyilkan, O; Yildirim, Y, 2006)		2.08
"Capecitabine is an oral fluoropyrimidine which is converted to 5-fluorouracil primarily in tumor tissue, and has the advantages of ease-of-administration, acceptable toxicity and significant antineoplastic activity."( Capecitabine in the treatment of colorectal cancer.
Cassidy, J; O'Neill, VJ, 2005)		2.49
"Oral capecitabine (Xeloda) is an effective drug with favourable safety in adjuvant and metastatic colorectal cancer. "( Pharmacoeconomic analysis of adjuvant oral capecitabine vs intravenous 5-FU/LV in Dukes' C colon cancer: the X-ACT trial.
Beham, A; Bertetto, O; Bustová, I; Cassidy, J; Cowell, W; Coxon, F; Díaz-Rubio, E; Douillard, JY; Dufour, P; Figer, A; Fountzilas, G; Garrison, LP; Jelic, S; Johnston, PG; Lesniewski-Kmak, K; Malzyner, A; Maughan, TS; McKendrick, JJ; Patel, KK; Scheithauer, W; Twelves, C, 2006)		1.11
"Capecitabine is a new chemotherapeutic agent considered highly specific for sensitive tumour cells, which convert the drug to 5-fluorouracil. "( Coronary artery spasm induced by capecitabine.
Barone, C; Cassano, A; Crea, F; Lanza, GA; Pozzo, C; Sestito, A; Sgueglia, GA, 2006)		2.06
"Capecitabine is a novel, orally administered fluoropyrimidine carbamate that has been approved for adjuvant treatment in patients with Stage III colon cancer, first-line metastatic colorectal cancer, and metastatic breast cancer, both as a single agent (for patients who are resistant to paclitaxel and anthracyclines) and in combination with docetaxel (after failure on anthracycline-based therapy). "( Review of capecitabine as oral treatment of gastric, gastroesophageal, and esophageal cancers.
Ajani, J, 2006)		2.18
"Capecitabine is a recently developed oral prodrug that is converted into 5-fluorouracil by sequential enzymatic steps."( Dramatic regression of multiple brain metastases from breast cancer with Capecitabine: another arrow at the bow?
Carlini, P; Cognetti, F; Fabi, A; Felici, A; Ferretti, G; Mirri, A; Nuzzo, C; Papaldo, P; Vidiri, A, )		1.08
"Capecitabine is an oral prodrug of 5-fluorouracil used in the treatment of adenocarcinoma of the colon. "( Capecitabine-induced cerebellar toxicity.
Gill, S; Renouf, D, 2006)		3.22
"Capecitabine is a tumor-activated oral fluoropyrimidine with established antitumor activity in breast and colorectal cancer. "( Capecitabine-induced hypertriglyceridemia: a report of two cases.
Habeos, IG; Kalofonos, HP; Koutras, AK; Vagenakis, AG, )		3.02
"Capecitabine is an oral prodrug of 5-fluorouracil, which is converted to 5-fluorouracil by three sequential enzymatic reactions. "( Capecitabine in carcinoma of the pancreas.
Neoptolemos, JP; Smith, DB, 2006)		3.22
"Capecitabine is an oral fluoropyrimidine carbamate which is converted to 5-fluorouracil (5-FU) via 3 enzymatic step to 5'-deoxy-5-fluorocytidine (5'-DFCR), 5'-deoxy-5-fluorouridine (5'-DFUR), and finally 5-FU. "( Relationship between AUC of 5'-DFUR and toxicity of capecitabine, fluoropyrimidine carbamate analogs, and 5'-DFUR in monkeys, mice, and rats.
Horii, I; Kawashima, A; Kobayashi, K; Nakano, K; Shindoh, H; Shishido, N, 2006)		2.03
"Capecitabine is an important drug in the therapeutic armamentarium for metastatic breast cancer. "( The role of capecitabine in first-line treatment for patients with metastatic breast cancer.
Chan, A; Gelmon, K; Harbeck, N, 2006)		2.16
"Capecitabine (Xeloda) is a systemic prodrug of 5-fluorouracil (5-FU), which is administered in an oral formulation. "( Management of hand-foot syndrome induced by capecitabine.
Gressett, SM; Hardwicke, F; Stanford, BL, 2006)		2.04
"Capecitabine is a fluoropyrimidine carbamate that acts as a prodrug, mimics continuous infusion of 5-fluorouracil (5-FU), and has encouraging antitumor activity in women with metastatic breast cancer. "( Capecitabine/Cyclophosphamide/Methotrexate for patients with metastatic breast cancer: a dose-finding, feasibility, and efficacy study.
Fasolo, A; Gianni, L; Marchiano, A; Mariani, G; Moliterni, A; Petrelli, F; Valagussa, P; Zambetti, M, 2006)		3.22
"Capecitabine is a fluoropyrimidine carbamate with antineoplasmatic activity, recommended for the treatment of colorectal cancer. "( The effect of capecitabine on the healing of colonic anastomoses in rats.
Athanasiadou, ZS; Ballas, KD; Demertzidis, CI; Economou, LD; Konstantinidis, HD; Pissanidou, TT; Sakadamis, AK; Sioga, AC; Slavakis, AP, 2007)		2.14
"Capecitabine is an orally administered prodrug that is converted to fluorouracil and is of potential use in the treatment of this disease."( Phase II study of capecitabine single-agent therapy in patients with metastatic renal cell carcinoma.
Daliani, DD; Pagliaro, LC; Perez, CA; Tu, SM, )		1.19
"Capecitabine is an orally administered fluoropyrimidine that is converted to 5-fluorouracil by thymidine phosphorylase. "( Phase II trial of capecitabine and rHu-interferon-alpha-2a in patients with metastatic renal cell carcinoma, limited efficacy, and moderate toxicity.
Bukowski, RM; Dreicer, R; Elson, P; Hutson, TE; Mekhail, T; Olencki, T; Osterwalder, B; Segota, E; Wacker, B; Zhou, M, )		1.91
"Capecitabine is an orally active fluoropyrimidine that has been approved for first-line treatment of metastatic colorectal cancer when fluoropyrimidines alone are indicated. "( Palmar-plantar erythrodysesthesia associated with scrotal and penile involvement with capecitabine.
DeSimone, P; Sapp, CM, 2007)		2.01
"Capecitabine is a highly effective and well-tolerated treatment for metastatic breast cancer (MBC) and extends survival when combined with docetaxel. "( Dosage of capecitabine and cyclophosphamide combination therapy in patients with metastatic breast cancer.
Hamada, Y; Kuroki, S; Mitsuyama, S; Nishimura, R; Ohno, S; Tamura, K; Tanaka, M, )		1.98
"Capecitabine is an oral fluoropyrimidine that mimics the pharmaconkinetics of infusional 5-FU."( A case of capecitabine-induced coronary microspasm in a patient with rectal cancer.
Arbea, L; Coma-Canella, I; García-Foncillas, J; Martinez-Monge, R, 2007)		1.46
"Capecitabine is an oral prodrug of 5-fluorouracil. "( Capecitabine in the treatment of colorectal cancer.
Cassidy, J; Kelly, C, 2007)		3.23
"Capecitabine (Xeloda) is a fluoropyrimidine which is transformed to 5-fluorouracil (5-FU) at the tumor site. "( Capecitabine (Xeloda) as monotherapy in advanced breast and colorectal cancer: effectiveness and side-effects.
Deliconstantinos, G; Koutantos, J; Lazaki, H; Rigatos, SK; Stathopoulos, GP; Stathopoulos, J, )		3.02
"Capecitabine is a well tolerated treatment with low toxicity, rendering a partial response in 29.16% and 11.76% of patients with breast and colorectal cancer, respectively."( Capecitabine (Xeloda) as monotherapy in advanced breast and colorectal cancer: effectiveness and side-effects.
Deliconstantinos, G; Koutantos, J; Lazaki, H; Rigatos, SK; Stathopoulos, GP; Stathopoulos, J, )		3.02
"Capecitabine is a fluoropyrimidine-based drug that offers physicians a more convenient treatment for advanced colorectal cancer (CRC), with manageable toxicity and antitumor activity comparable to that of continuous-infusion therapies with 5-fluorouracil (5-FU). "( DPD is a molecular determinant of capecitabine efficacy in colorectal cancer.
Danenberg, KD; Danenberg, PV; Jakobsen, A; Kuramochi, H; Lindebjerg, J; Nielsen, JN; Shimizu, D; Vallböhmer, D; Yang, DY, 2007)		2.06
"Capecitabine is a tumor selective pro-drug of 5-fluorouracil, indicated for the therapy of colorectal cancer."( Histological evaluation of colonic anastomotic healing, during perioperative Capecitabine administration. Experimental study in rats.
Demertzidis, CI; Economou, LD; Konstantinidis, HD; Mpallas, KD; Pissanidou, TT; Sioga, AC, 2007)		1.29
"Capecitabine is an antineoplastic agent used for the treatment of patients with metastatic solid tumors (breast and colon). "( [Capecitabine-induced hyperpigmentation].
Galán-Gutiérrez, M; Jiménez-Puya, R; Moreno-Giménez, JC; Rodríguez-Bujaldón, AL; Vázquez-Bayo, C, 2007)		2.69
"Capecitabine is a chemotherapeutic drug for use in cancers. "( Topical henna for capecitabine induced hand-foot syndrome.
Guzin, G; Yucel, I, 2008)		2.12
"Capecitabine is a recently developed oral antineoplastic prodrug of 5-fluorouracil. "( Effects of capecitabine and vinorelbine on cell proliferation, metabolism and COX2 and p16 expression in breast cancer cell lines and solid tumour tissues.
Chow, LW; Loo, WT; Sasano, H, 2007)		2.17
"Capecitabine is an orally-active fluoropyrimidine, which is selectively metabolised to fluorouracil in tumour cells."( Capecitabine in advanced gastric cancer.
Chau, I; Cunningham, D; Okines, A, 2007)		2.5
"Capecitabine is an oral fluoropyrimidine that generates 5-FU preferentially within the tumor."( Capecitabine and radiotherapy as neoadjuvant treatment for rectal cancer.
Ben-Josef, E, 2007)		2.5
"Capecitabine is an orally administered precursor of 5'-deoxy-5-fluorouridine that was rationally designed to generate 5-fluorouracil (5-FU) preferentially in tumor tissue. "( Safety profile and activity of lower capecitabine dose in patients with metastatic breast cancer.
Alessandroni, P; Baldelli, AM; Casadei, V; Catalano, G; Catalano, V; Ceccolini, M; Fedeli, A; Fedeli, SL; Giordani, P; Rossi, D, 2007)		2.06
"Capecitabine (Xeloda) is an oral 5-fluorouracil pro-drug used in the treatment of two of the commonest cancers: breast and colorectal. "( Capecitabine-associated coronary vasospasm: a case report.
Papadopoulos, CA; Wilson, H, 2008)		3.23
"Capecitabine is a drug that requires the consecutive action of three enzymes: carboxylesterase 2 (CES 2), cytidine deaminase (CDD), and thymidine phosphorylase (TP) for transformation into 5-fluorouracil (5FU). "( A carboxylesterase 2 gene polymorphism as predictor of capecitabine on response and time to progression.
Alba, E; Carabantes, F; Dueñas, R; González, E; López-Siles, J; Márquez, A; Ribelles, N; Sánchez, A; Sánchez, MJ; Sánchez-Rovira, P; Sevilla, I, 2008)		2.04
"Capecitabine appears to be an acceptable alternative to continuous-infusion fluorouracil (FU)/leucovorin (LV) in combination therapy and offers an effective, but more convenient alternative to continuous infusion FU/LV in the first-line treatment of patients with mCRC."( XELOX followed by XELIRI or the reverse sequence in advanced colorectal cancer.
Argon, A; Aykan, NF; Basaran, M; Gumus, M; Guney, N; Saglam, S; Sakar, B; Tenekeci, AN; Ustaoglu, MA; Ustuner, Z, 2007)		1.78
"Capecitabine is an oral prodrug of 5-FU that has potential advantages compared with intravenous 5-FU, including ease of administration and potentially increased therapeutic effect."( The use of capecitabine in the combined-modality therapy for rectal cancer.
Liauw, SL; Minsky, BD, 2008)		1.46
"Capecitabine (Ro 09-1978) is a novel oral fluoropyrimidine carbamate that was rationally designed to generate 5-fluorouracil (5-FU) selectively in tumors. "( Effect of food on the pharmacokinetics of capecitabine and its metabolites following oral administration in cancer patients.
Allman, D; Banken, L; Cassidy, J; Dirix, L; Osterwalder, B; Reigner, B; Roos, B; Twelves, C; Utoh, M; Verweij, J; Weidekamm, E, 1998)		2.01
"Capecitabine is an orally administered fluoropyrimidine carbamate selectively activated to fluorouracil (5-FU) in tumors. "( Phase I and pharmacologic study of intermittent twice-daily oral therapy with capecitabine in patients with advanced and/or metastatic cancer.
Allman, D; Griffin, T; Kaye, S; Mackean, M; Osterwalder, B; Planting, A; Reigner, B; Schellens, J; Twelves, C; Verweij, J, 1998)		1.97
"Capecitabine is a tolerable oral outpatient therapy that shows promising clinical activity in a variety of cancers. "( Phase I and pharmacologic study of intermittent twice-daily oral therapy with capecitabine in patients with advanced and/or metastatic cancer.
Allman, D; Griffin, T; Kaye, S; Mackean, M; Osterwalder, B; Planting, A; Reigner, B; Schellens, J; Twelves, C; Verweij, J, 1998)		1.97
"Capecitabine (Xeloda) is a novel rationally designed fluoropyrimidine carbamate. "( A Phase I study of capecitabine in combination with oral leucovorin in patients with intractable solid tumors.
Allman, D; Bissett, D; Cassidy, J; Dirix, L; Griffin, T; Osterwalder, B; Reigner, B; Van Oosterom, AT, 1998)		2.07
"Capecitabine is a novel, oral, selectively tumor-activated fluoropyrimidine carbamate. "( Multicenter phase II study of capecitabine in paclitaxel-refractory metastatic breast cancer.
Blum, JL; Brown, CS; Burger, HU; Buzdar, AU; Griffin, T; Jones, SE; Kuter, I; LoRusso, PM; Osterwalder, B; Vogel, C, 1999)		2.03
"Capecitabine is an active drug in the treatment of paclitaxel-refractory metastatic breast cancer. "( Multicenter phase II study of capecitabine in paclitaxel-refractory metastatic breast cancer.
Blum, JL; Brown, CS; Burger, HU; Buzdar, AU; Griffin, T; Jones, SE; Kuter, I; LoRusso, PM; Osterwalder, B; Vogel, C, 1999)		2.03
"Capecitabine (Xeloda) is a rationally designed oral, tumor-selective fluoropyrimidine carbamate aimed at preferential conversion to 5-fluorouracil (5-FU) within the tumor. "( Effect of hepatic dysfunction due to liver metastases on the pharmacokinetics of capecitabine and its metabolites.
Banken, L; Cassidy, J; Glynne-Jones, R; Goggin, T; Reigner, B; Roos, B; Schüller, J; Twelves, C; Utoh, M; Weidekamm, E, 1999)		1.97
"Capecitabine is an orally administered fluoropyrimidine carbamate used for the treatment of paclitaxel- or anthracycline-refractory breast cancer. "( Capecitabine.
Dooley, M; Goa, KL, 1999)		3.19
"Capecitabine is a novel fluoropyrimidine carbamate, orally administered and rationally designed to undergo tumor-selective activation. "( [Capecitabine--a review of its antitumor activity and toxicity in clinical studies].
Maeda, Y; Sasaki, T, 2000)		2.66
"Capecitabine (Xeloda) is a new, orally administered, enzyme-activated fluoropyrimidine carbamate designed to generate high levels of fluorouracil (5-FU) in tumor cells. "( Pharmacology and clinical status of capecitabine.
Schilsky, RL, 2000)		2.02
"Capecitabine is a rationally derived prodrug of 5-fluorouracil which is based upon the known high concentration of the enzyme thymidine phosphorylase in many human tumors."( Capecitabine.
Budman, DR, 2000)		2.47
"Capecitabine is an oral fluoropyrimidine that mimics continuous infusion 5-fluorouracil and generates 5-fluorouracil preferentially at the tumor site. "( The role of capecitabine, an oral, enzymatically activated fluoropyrimidine, in the treatment of metastatic breast cancer.
Blum, JL, 2001)		2.13
"Capecitabine is an excellent treatment option for patients who require symptom palliation and who prefer oral medications."( Clinical status of capecitabine in the treatment of breast cancer.
Gradishar, WJ, 2001)		1.36
"Capecitabine is an orally administered fluoropyrimidine carbamate that is preferentially converted to 5-fluorouracil in tumors relative to normal tissue. "( 5-fluorouracil/leucovorin versus capecitabine in patients with stage III colon cancer.
Seitz, JF, 2001)		2.03
"Capecitabine is a novel oral fluoropyrimidine carbamate that is preferentially converted to the cytotoxic moiety fluorouracil (5-fluorouracil; 5-FU) in target tumour tissue through a series of 3 metabolic steps. "( Clinical pharmacokinetics of capecitabine.
Blesch, K; Reigner, B; Weidekamm, E, 2001)		2.04
"Capecitabine is an oral fluoropyrimidine that was developed in response to the clinical need for new therapeutic options offering improved efficacy, tolerability, and convenience for patients."( The evolution of fluoropyrimidine therapy: from intravenous to oral.
Cassidy, J; Hoff, PM; Schmoll, HJ, 2001)		1.03
"Capecitabine is a thymidine phosphorylase (TP)-activated oral fluoropyrimidine, rationally designed to generate 5-fluorouracil (5-FU) preferentially within tumors. "( Vision of the future: capecitabine.
Twelves, C, 2001)		2.07
"Capecitabine is an oral, tumor-targeted fluoropyrimidine carbamate with high activity in metastatic breast carcinoma and in paclitaxel-pretreated metastatic breast carcinoma."( Multicenter, Phase II study of capecitabine in taxane-pretreated metastatic breast carcinoma patients.
Blum, JL; Buzdar, A; Dieras, V; Horton, J; Lo Russo, PM; Osterwalder, B; Rutman, O, 2001)		2.04
"Capecitabine is an orally administered fluoropyrimidine which is selectively activated in tumour tissue to the active moiety fluorouracil and is cytotoxic through inhibition of DNA synthesis. "( Capecitabine: a review of its use in the treatment of advanced or metastatic colorectal cancer.
Goa, KL; McGavin, JK, 2001)		3.2
"Capecitabine is a novel fluoropyrimidine carbamate, orally administered and selectively activated to fluorouracil by a sequential triple-enzyme pathway in liver and tumor cells. "( Capecitabine in the treatment of metastatic renal cell carcinoma failing immunotherapy.
Kramer, G; Locker, GJ; Mader, R; Marberger, M; Rauchenwald, M; Schmidinger, M; Steger, GG; Wenzel, C; Zielinski, CC, 2002)		3.2
"Oral capecitabine is an active and well-tolerated agent when used alone as first-line therapy in patients who have relapsed after HDC-ASCS for MBC."( Use of capecitabine as first-line therapy in patients with metastatic breast cancer relapsing after high-dose chemotherapy and autologous stem cell support.
Ball, ED; Bashey, A; Corringham, S; Jones, V; Lancaster, D; Law, P; Silva-Gietzen, J; Sundaram, S, 2001)		1.22
"Capecitabine is a fluoropyrimidine carbamate that was rationally designed as an oral drug capable of mimicking continuous infusion 5-fluorouracil (5-FU) and delivering 5-FU preferentially to tumour tissue. "( Rational development of capecitabine.
Venturini, M, 2002)		2.06
"Capecitabine is a prodrug that is converted into the active compound 5-FU preferentially at the tumor site."( Capecitabine in breast cancer: current status.
Bontenbal, M; Smorenburg, CH; Verweij, J, 2001)		2.47
"Capecitabine (Xeloda) is an orally administered precursor of 5'-deoxy-5-fluorouridine (5'-DFUR), which is preferentially activated to 5-fluorouracil (5-FU) in tumors."( Effect of renal impairment on the pharmacokinetics and tolerability of capecitabine (Xeloda) in cancer patients.
Banken, L; Cassidy, J; Gardiner, J; Harper, P; Johnston, P; Monkhouse, J; Poole, C; Reigner, B; Twelves, C; Weidekamm, E, 2002)		1.27
"Capecitabine is a synthetic oral fluoropyrimidine carbamate that is sequentially activated in a three-step process, which results in the preferential production of 5-fluorouracil in tumours, rather than in the normal surrounding tissue. "( Capecitabine: fulfilling the promise of oral chemotherapy.
Hwang, JJ; Marshall, JL, 2002)		3.2
"Capecitabine is an oral fluoropyrimidine with considerable activity and minimal myelosuppression and alopecia. "( Phase I, dose-finding study of capecitabine in combination with docetaxel and epirubicin as first-line chemotherapy for advanced breast cancer.
Angiolini, C; Baldini, A; Bergaglio, M; Canavese, G; Del Mastro, L; Garrone, O; Lambiase, A; Merlano, M; Rosso, R; Tolino, G; Venturini, M, 2002)		2.04
"Capecitabine is a member of a new class of oral fluoropyrimidines. "( Capecitabine can induce acute coronary syndrome similar to 5-fluorouracil.
Andrasch, H; Beck, FJ; Frickhofen, N; Fuhr, HG; Jung, B; Sigmund, M, 2002)		3.2

Effects

Capecitabine has a favourable safety profile. Most frequent adverse events are hand-foot syndrome, stomatitis and diarrhoea. Can be given safely to patients with advanced age, hepatic and renal dysfunctions.

Capecitabine has been investigated in early breast cancer in several studies, but it was undefined that whether it could improve survival. It has been approved for breast cancer patients whose disease is paclitaxel-resistant, and either anthracycline and either oxaliplatin.

ExcerptReferenceRelevance
"Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions."( Safety of capecitabine: a review.
Marshall, JL; Mikhail, SE; Sun, JF, 2010)		1.48
"Capecitabine has a favourable safety profile, the most frequent adverse events being hand-foot syndrome, stomatitis and diarrhoea."( Development of and clinical experience with capecitabine (Xeloda) in the treatment of solid tumours.
Holland, M; Reichardt, P; Sternberg, CN, 2004)		1.31
"Capecitabine has been shown to be well tolerated with minimal side effects, but the incidence of leukoencephalopathy is rare with a risk of less than one percent."( Capecitabine-induced leukoencephalopathy in a patient with triple-negative breast cancer: A case report and review of the literature.
Abu-Shahin, FI; Brown, EN; Liu, L, 2022)		2.89
"Capecitabine has extensive utilization in the treatment of diverse solid tumors, and its efficacy has been substantiated. "( Role and efficacy of capecitabine in the anthracycline-free regimen in breast cancer patients: a systematic review and meta-analysis.
Cao, H; Chen, J; Deng, L; Li, Y; Wang, S; Wang, Y; Zhong, Y, 2023)		2.67
"Capecitabine use has markedly increased from approval in 2014 in Australia, now being used in more than 80% of patients."( Real-world outcomes for neoadjuvant capecitabine versus infusional 5-fluorouracil in the treatment of locally advanced rectal cancer.
Christie, M; Croxford, M; Faragher, I; Gibbs, P; Guerrieri, M; Jones, IT; Kosmider, S; Lee, M; Loft, M; Steel, M; Tie, J; Wong, HL; Wong, R, 2021)		1.62
"Capecitabine has been more recognized for its cardiotoxicity with an incidence that varies widely. "( Cardio-oncology: Capecitabine Can Sometimes be Heatbreaking Capecitabine-Induced Takotsubo Cardiomyopathy Case Report and Literature Review.
Abdelmaseih, R; Abdelmasih, R; Balaraman, R; Blanco, A; Desai, K; Patel, J; Pothen, J, 2021)		2.4
"Capecitabine has consistently demonstrated high efficacy and acceptable tolerability in salvage chemotherapy for advanced breast cancer. "( Clinical Value of Capecitabine-Based Combination Adjuvant Chemotherapy in Early Breast Cancer: A Meta-Analysis of Randomized Controlled Trials.
Chen, G; Dong, J; Guo, J; Guo, Z; Liu, M; Yao, G; Ye, C, 2017)		2.23
"Capecitabine has antitumor activity in hepatobiliary cancers."( Phase II Trial of Sorafenib in Combination with Capecitabine in Patients with Hepatocellular Carcinoma: INST 08-20.
Bansal, P; Fekrazad, HM; Lee, FC; Patt, Y; Rojas-Hernandez, C, 2017)		1.43
"Capecitabine has been studied as a radiosensitizer, and our study seeks to examine the association of concurrent capecitabine/radiation therapy (RT) on event-free- (EFS) and overall survival (OS) in women with breast cancer (BC) with residual disease after neoadjuvant chemotherapy (NAC)."( Concurrent use of capecitabine with radiation therapy and survival in breast cancer (BC) after neoadjuvant chemotherapy.
Catanese, B; Chin, C; Connolly, EP; Kalinsky, K; Lee, SM; Liu, YL; Zhan, S, 2018)		2.26
"Capecitabine has been reported to cause haemolysis either alone or combined with lapatinib, each time with a mechanism other than immunological."( Autoimmune haemolytic anaemia in a patient treated with capecitabine.
Awada, P; Cardoso, F; Georgala, A; Gil, T; Lebrun, F; Loizidou, A; Piccart, P; Sideris, S, )		1.1
"Capecitabine has been widely recognized in the nCRT for patients with LARC, and has the tendency to replace 5-FU."( [Advances in new chemotherapeutic drugs for preoperative chemoradiation of locally advanced rectal cancer].
Gao, Y; Liu, M; Xiao, L, 2014)		1.12
"Capecitabine has become a standard treatment option for metastatic breast cancer, as a single agent or in combination."( Breast cancer, DPYD mutations and capecitabine-related ileitis: description of two cases and a review of the literature.
Aftimos, PG; Errihani, H; Mokrim, M; Piccart-Gebhart, M, 2014)		1.4
"Capecitabine has demonstrated significant activity in metastatic breast and colorectal cancer. "( Increased mean corpuscular volume of red blood cells in patients treated with capecitabine for advanced breast and colon cancer.
Gervasi, E; Giovanardi, F; Pezzuolo, D; Prati, G; Scaltriti, L; Scarabelli, L, 2013)		2.06
"Capecitabine has previously been compared to 5-fluorouracil-either as a monotherapy or in combination with oxaliplatin, irinotecan, or biological drugs-and has been found to have comparable efficacy and safety profiles."( Should capecitabine replace 5-fluorouracil in the first-line treatment of metastatic colorectal cancer?
Aguado, C; Díaz-Rubio, E; García-Paredes, B; Sastre, J; Sotelo, MJ, 2014)		1.58
"Capecitabine has activity against several types of cancer. "( Oromandibular dystonia: a serious side effect of capecitabine.
Alsma, J; Boere, IA; Geijteman, EC; Mathijssen, RH; Schuit, SC; van Pelt-Sprangers, MJ, 2015)		2.11
"Capecitabine has been shown to be much less cardiotoxic compared to 5-FU, with only a handful of cases reporting cardiotoxicity with capecitabine."( Capecitabine-induced coronary artery vasospasm in a patient who previously experienced a similar episode with fluorouracil therapy.
Aladağ, E; Karakulak, UN; Maharjan, N; Övünç, K, 2016)		2.6
"Capecitabine has been commonly used in recurrent or metastatic nasopharyngeal carcinoma. "( Radiation recall after capecitabine in a patient with recurrent nasopharyngeal carcinoma: a case report.
Kwong, D; Lam, KO; Lee, V; Leung, TW, 2016)		2.19
"Capecitabine has been investigated in early breast cancer in several studies, but it was undefined that whether it could improve survival. "( Capecitabine in Combination with Standard (Neo)Adjuvant Regimens in Early Breast Cancer: Survival Outcome from a Meta-Analysis of Randomized Controlled Trials.
Li, XY; Lin, SL; Xu, QN; Zhang, ZC, 2016)		3.32
"Capecitabine has relatively mild side effects."( [Capecitabine-induced ventricular fibrillation].
de Valk, J; Germans, T; Schakenraad, D; Ten Oever, D; van Capelle, AV, )		1.76
"Capecitabine has proven efficacy in combination with docetaxel and is under evaluation in the neoadjuvant, adjuvant, and metastatic settings in combination with several oral and IV chemotherapeutic and biologic agents."( Capecitabine-based combination therapy for breast cancer: implications for nurses.
Frye, DK, 2009)		3.24
"Capecitabine has been developed as a prodrug of FU, with the goal of improving tolerability and intratumor drug concentration through tumor-specific conversion to the active drug. "( The role of capecitabine in the management of tumors of the digestive system.
Gennatas, C; Gennatas, S; Michalaki, V, 2009)		2.17
"Capecitabine has another pharmacologic advantage over intravenous 5-FU as it is preferentially activated by 5-FU in tumor tissue, which has higher activity of thymidine phosphorylase than normal tissue, resulting in selective accumulation of 5-FU within tumor tissue."( ML17032 trial: capecitabine/cisplatin versus 5-fluorouracil/cisplatin as first-line therapy in advanced gastric cancer.
Kang, YK; Ryu, MH, 2009)		1.43
"Capecitabine has shown similar efficacy to 5-fluorouracil (5-FU); a regimen containing 2 weeks of capecitabine/oxaliplatin (CapOx) has demonstrated noninferiority to infusional 5-FU/oxaliplatin/leucovorin (FOLFOX) for the treatment of metastatic colorectal cancer (mCRC). "( A phase II study of oxaliplatin, 5-fluorouracil, leucovorin, and high-dose capecitabine in patients with metastatic colorectal cancer.
Eickhoff, JC; Holen, KD; Jumonville, A; Loconte, NK; Lubner, SJ; Mulkerin, DL; Schelman, W; Seo, S; Thomas, JP, 2010)		2.03
"Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions."( Safety of capecitabine: a review.
Marshall, JL; Mikhail, SE; Sun, JF, 2010)		1.48
"Oral capecitabine (CAP) has shown significant benefits in early stage breast cancer (BC). "( Clinical study of adjuvant capecitabine monotherapy in Chinese elderly patients (aged 55-70) with stage IIa breast cancer.
Hu, W; Li, L; Sheng, Y; Shi, J; Su, D; Wang, CK, 2010)		1.17
"Capecitabine has clinical activity in MRCC patients who have non-clear cell histology and a good or intermediate prognosis. "( Phase II, multicenter, uncontrolled trial of single-agent capecitabine in patients with non-clear cell metastatic renal cell carcinoma.
Demidov, L; Galchenko, V; Kharkevich, G; Naidzionak, U; Petenko, N; Sinelnikov, I; Tsimafeyeu, I, 2012)		2.07
"Capecitabine has antitumor activity in metastatic breast cancer (MBC); however, its optimal dose and schedule remain unclear. "( Phase 2 trial of a novel capecitabine dosing schedule in combination with bevacizumab for patients with metastatic breast cancer.
Feigin, K; Gajria, D; Geneus, S; Hudis, CA; Norton, L; Patil, S; Tan, LK; Theodoulou, M; Traina, TA, 2011)		2.12
"Capecitabine has substantial antitumor activity in the first-line treatment of patients with MBC in prospective, randomized, phase II/III clinical trials as monotherapy and in combination with biologic and novel agents."( Capecitabine monotherapy: review of studies in first-line HER-2-negative metastatic breast cancer.
Dalivoust, P; Debled, M; Harbeck, N; Kaufmann, M; O'Shaughnessy, JA; Robert, NJ; Siedentopf, F, 2012)		2.54
"Capecitabine(Xeloda®)has been a global standard drug for the treatment of colon cancer since large randomized controlled trials demonstrated its efficacy and safety in treating patients suffering from the disease. "( [Oral capecitabine as postoperative adjuvant chemotherapy in stage III colon cancer patients].
Fukuda, M; Hanada, K; Hata, H; Ikai, I; Kubo, K; Moriyama, S; Murakami, T; Ogiso, S; Okazaki, S; Okuchi, Y; Otani, T; Sakata, S; Setoguchi, Y; Tanaka, M; Tani, M; Une, Y; Yamaguchi, T; Yamato, T; Yasui, H, 2012)		2.3
"Capecitabine has also been combined with irinotecan."( The role of capecitabine in locally advanced rectal cancer treatment: an update.
Cejas, P; Feliu, J; Fernández-Martos, C; Machancoses, AH; Moreno-García, V; Nogué, M, 2012)		1.48
"Capecitabine has shown significant antitumor activity against anthracycline/taxane refractory breast cancer and advanced colorectal carcinoma. "( Capecitabine-induced hypertriglyceridemia and hyperglycemia: two cases.
Afsar, CU; Dilli, MŞ; Duman, BB; Erçolak, V; Gunaldı, M; Haksöyler, V; Paydas, S; Tetiker, T, 2012)		3.26
"Capecitabine has been reported to trigger mid-apical Takotsubo syndrome (TS)."( Capecitabine caused cardiogenic shock through induction of global Takotsubo syndrome.
Henareh, L; Törnerud, M; Tornvall, P; Y-Hassan, S, )		2.3
"Capecitabine has proven effective as a chemotherapy for metastatic breast cancer. "( Clinical efficacy of including capecitabine in neoadjuvant chemotherapy for breast cancer: a systematic review and meta-analysis of randomized controlled trials.
Jiang, Y; Li, Q; Liu, J; Wei, W; Yang, H, 2013)		2.12
"Capecitabine has been developed as an orally administered tumor selective fluoropyrimidine for use in the treatment of breast and colorectal cancer. "( Population pharmacokinetic analysis of the major metabolites of capecitabine.
Blesch, KS; Gieschke, R; Reigner, B; Steimer, JL, 2002)		2
"Capecitabine has shown promising activity in all tumor types sensitive to 5-FU and is therefore investigated in many clinical trials."( Capecitabine treatment results in increased mean corpuscular volume of red blood cells in patients with advanced solid malignancies.
Kornek, GV; Locker, GJ; Mader, RM; Pluschnig, U; Scheithauer, W; Steger, GG; Wenzel, C, 2003)		2.48
"Capecitabine has been evaluated as a single agent in women with advanced breast cancer where it offers an overall response rate of 20-30%."( Role of capecitabine (Xeloda) in breast cancer.
Gradishar, WJ; Kaklamani, VG, 2003)		1.47
"Capecitabine has demonstrated equivalent efficacy with 5-FU and has been approved as first line treatment."( Treatment of colorectal cancer metastasis: the role of chemotherapy.
Ajani, JA; Xiong, HQ, )		0.85
"Capecitabine has not been tested against thyroid cancers, and it is not known to what extent thyroid cancers express TP, TS or DPD."( Enzyme expression profiles suggest the novel tumor-activated fluoropyrimidine carbamate capecitabine (Xeloda) might be effective against papillary thyroid cancers of children and young adults.
Bauer, A; Francis, GL; Helms, A; Patel, A; Pluim, T; Tuttle, RM, 2004)		1.27
"Capecitabine has demonstrated high efficacy as first-line treatment for metastatic colorectal cancer (MCRC). "( XELOX (capecitabine plus oxaliplatin): active first-line therapy for patients with metastatic colorectal cancer.
Brunet, R; Butts, C; Cassidy, J; Conroy, T; Debraud, F; Díaz-Rubio, E; Figer, A; Grossmann, J; Sawada, N; Schöffski, P; Sobrero, A; Tabernero, J; Twelves, C; Van Cutsem, E, 2004)		2.22
"Capecitabine has the potential to replace FU/LV in combination with oxaliplatin for MCRC."( XELOX (capecitabine plus oxaliplatin): active first-line therapy for patients with metastatic colorectal cancer.
Brunet, R; Butts, C; Cassidy, J; Conroy, T; Debraud, F; Díaz-Rubio, E; Figer, A; Grossmann, J; Sawada, N; Schöffski, P; Sobrero, A; Tabernero, J; Twelves, C; Van Cutsem, E, 2004)		1.5
"Capecitabine has a favourable safety profile, the most frequent adverse events being hand-foot syndrome, stomatitis and diarrhoea."( Development of and clinical experience with capecitabine (Xeloda) in the treatment of solid tumours.
Holland, M; Reichardt, P; Sternberg, CN, 2004)		1.31
"Capecitabine has advantages of oral administration and favorable toxicity profiles."( Capecitabine monotherapy in patients with anthracycline- and taxane-pretreated metastatic breast cancer.
Im, YH; Jung, CW; Kang, WK; Kim, K; Lee, J; Lee, KE; Lee, MH; Lee, SH; Lee, SI; Nam, E; Park, J; Park, JO; Park, K; Park, SH; Park, YS; Yoon, SS, 2004)		2.49
"Capecitabine has also shown promising activity and good tolerability in combination with radiotherapy in rectal cancer."( Oral capecitabine: bridging the Atlantic divide in colon cancer treatment.
Tejpar, S; Van Cutsem, E; Verslype, C, 2005)		1.56
"Capecitabine has shown varying degrees of efficacy with acceptable tolerability in numerous cancers including prostate, renal cell, ovarian, and pancreatic, with the largest amount of evidence in metastatic breast and colorectal cancer."( Capecitabine: a review.
Lindley, C; Walko, CM, 2005)		2.49
"Capecitabine has significantly less serious toxicity than 5-FU when used alone or in combination with other cytotoxic agents."( Capecitabine: effective oral fluoropyrimidine chemotherapy.
Coutsouvelis, J; McKendrick, J, 2005)		2.49
"Capecitabine has limited activity as a single agent in prostate cancer, but appears to modulate tumour biology. "( Phase II study of oral capecitabine in patients with hormone-refractory prostate cancer.
Bolunwu, N; Chan, S; Kendall, A; Pandha, H; Plunkett, T; Somaiah, N; Spicer, J, 2005)		2.08
"Capecitabine has been shown to have single-agent activity in advanced carcinoma of the pancreas and to improve response rates and survival when administered in combination with gemcitabine compared with gemcitabine alone."( Capecitabine in carcinoma of the pancreas.
Neoptolemos, JP; Smith, DB, 2006)		2.5
"Capecitabine has proven efficacy in metastatic breast cancer, extending survival in combination with docetaxel and offering a favorable safety profile, including minimal myelosuppression and alopecia, as a single agent. "( Capecitabine: expanding options for the treatment of patients with early or locally advanced breast cancer.
Wardley, A, 2006)		3.22
"Capecitabine also has the added benefits of convenient oral administration and lower cost."( Effects of capecitabine and vinorelbine on cell proliferation, metabolism and COX2 and p16 expression in breast cancer cell lines and solid tumour tissues.
Chow, LW; Loo, WT; Sasano, H, 2007)		1.45
"Capecitabine has shown efficacy in treatment of metastatic pancreatic cancer. "( Long-term survival on capecitabine in two gemcitabine refractory pancreatic cancer patients. Is there a pharmacogenetic explanation?
Diasio, R; Johnson, M; Kang, SP; Ledbetter, L; Saif, MW; Steg, A, 2007)		2.1
"Capecitabine has the potential to replace 5-FU/LV as the optimal combination partner for oxaliplatin at a higher cost."( Capecitabine plus oxaliplatin for the treatment of colorectal cancer.
Carrato, A; Gallego-Plazas, J; Guillén-Ponce, C, 2008)		2.51
"Capecitabine has single agent activity in NPC and severe hand-foot syndrome predicts favorable outcome. "( Capecitabine monotherapy for recurrent and metastatic nasopharyngeal cancer.
Au, GK; Chua, D; Sham, JS; Wei, WI, 2008)		3.23
"Oral capecitabine (Cap) has shown promising activity in first-line chemotherapy trials in PC patients."( Oral capecitabine in gemcitabine-pretreated patients with advanced pancreatic cancer.
Boeck, S; Bruns, CJ; Golf, A; Haas, M; Heinemann, V; Issels, RD; Laessig, D; Moosmann, N; Schulz, C; Wilkowski, R, 2007)		1.31
"Capecitabine has demonstrated high efficacy as first-line treatment for metastatic colorectal cancer (mCRC). "( XELOX followed by XELIRI or the reverse sequence in advanced colorectal cancer.
Argon, A; Aykan, NF; Basaran, M; Gumus, M; Guney, N; Saglam, S; Sakar, B; Tenekeci, AN; Ustaoglu, MA; Ustuner, Z, 2007)		1.78
"Capecitabine has been approved for breast cancer patients whose disease is paclitaxel-resistant, and either anthracycline-resistant or for whom further anthracycline use is not indicated."( Oral 5-FU analogues in the treatment of breast cancer.
Bunnell, CA; Winer, EP, 1998)		1.02
"Capecitabine has additional characteristics not found with 5-FU, such as potent antimetastatic and anticachectic actions in mouse tumor models."( [Discovery and development of novel anticancer drug capecitabine].
Horii, I; Ishitsuka, H; Shimma, N, 1999)		1.28
"Capecitabine has additional characteristics not found with 5-FU, such as potent antimetastatic and anticachectic actions in mouse tumor models."( Capecitabine: preclinical pharmacology studies.
Ishitsuka, H, 2000)		2.47
"Capecitabine has the potential to replace bolus or continuous infusion 5-FU as the standard treatment for rectal cancer and offers a potentially enhanced therapeutic ratio."( Improving chemoradiotherapy in rectal cancer.
Debus, J; Glynne-Jones, R, 2001)		1.03
"Capecitabine has potential as monotherapy in these tumor types, or as a combination partner for other cytotoxic agents with different mechanisms of action and little overlap of key toxicities."( Vision of the future: capecitabine.
Twelves, C, 2001)		1.35
"Capecitabine has demonstrated high activity in preclinical xenograft models for a wide range of human solid tumours, including those resistant to 5-FU."( Rational development of capecitabine.
Venturini, M, 2002)		1.34

Actions

Capecitabine can cause severe hypersensitivity reactions which can be dangerous and life-threatening. It may inhibit the growth and metastasis of HCC.

ExcerptReferenceRelevance
"Capecitabine can cause severe hypersensitivity reactions which can be dangerous and life-threatening. "( Capecitabine induced Steven-Johnson syndrome: A rare case report.
Karthikeyan, K; Madhu, CS; Sameera, KV; Shaji, S; Swetha, MAC, 2022)		3.61
"Capecitabine may inhibit the growth and metastasis of HCC."( [The expression of platelet-derived endothelial cell growth factor in liver cancer].
Fan, J; Tang, Z; Zhou, J, 2000)		1.03

Treatment

Capecitabine is an oral treatment of choice for colorectal and breast cancer in Morocco. Treatment may be associated with a decrease in the incidence of SCCs in SOTRs.

ExcerptReferenceRelevance
"The capecitabine treatment was terminated, and methylprednisolone treatment was administered and plasmapheresis procedure was carried out. "( Capecitabine-related neurotoxicity presenting with agraphia.
Bayram, E; Bicakci, S; Demir, T; Iscan, D; Tolay, R, 2023)		2.91
"Capecitabine is an oral treatment of choice for colorectal and breast cancer in Morocco. "( Assessment of patients' knowledge of their treatment with capecitabine at the National Institute of Oncology in Rabat.
Bechar, H; Belahcen, MJ; Cherif Chefchaouni, A; Nouibi, C; Rahali, Y, 2023)		2.6
"Capecitabine treatment may be associated with a decrease in the incidence of SCCs in SOTRs. "( Evaluation of the Use of Capecitabine for the Treatment and Prevention of Actinic Keratoses, Squamous Cell Carcinoma, and Basal Cell Carcinoma: A Systematic Review.
Kim, J; Nijhawan, RI; Schauder, DM, 2020)		2.3
"More capecitabine-treated patients received post-operative oxaliplatin (44.2% vs 6.3%, P < 0.01)."( Real-world outcomes for neoadjuvant capecitabine versus infusional 5-fluorouracil in the treatment of locally advanced rectal cancer.
Christie, M; Croxford, M; Faragher, I; Gibbs, P; Guerrieri, M; Jones, IT; Kosmider, S; Lee, M; Loft, M; Steel, M; Tie, J; Wong, HL; Wong, R, 2021)		1.35
"Capecitabine treatment was added in several different ways across studies."( Capecitabine for hormone receptor-positive versus hormone receptor-negative breast cancer.
Banks, PD; Bulsara, MK; Hoon, SN; Lau, PK; Redfern, AD; White, AM, 2021)		2.79
"Capecitabine+Bmab treatment was also administered for 11 courses due to an adverse event of peripheral neuropathy."( [A case of cecum colon cancer with lymph node metastasis successfully treated with XELOX plus bevacizumab].
Aoki, J; Goto, M; Honjo, K; Ichikawa, R; Ishiyama, S; Ito, S; Kawai, M; Kojima, Y; Komiyama, H; Kure, K; Mizukoshi, K; Okazawa, Y; Okubo, H; Ro, H; Sakamoto, K; Sugimoto, K; Takahashi, M; Takehara, K; Tomiki, Y; Yaginuma, Y, 2014)		1.12
"A capecitabine treatment was initiated for 38 patients with advanced breast or colorectal cancer. "( Adherence to oral anticancer chemotherapy: What influences patients' over or non-adherence? Analysis of the OCTO study through quantitative-qualitative methods.
Bourmaud, A; Chauvin, F; Colomban, O; Freyer, G; Girard, P; Guitton, J; Hamant, C; Henin, E; Ranchon, F; Regnier, V; Rioufol, C; Tinquaut, F; Tod, M; Trillet-Lenoir, V; You, B, 2015)		1.14
"Capecitabine treatment significantly increased the intratumoral VEGF level compared with the control group; however, the combination with bevacizumab neutralized the VEGF."( Continuous administration of bevacizumab plus capecitabine, even after acquired resistance to bevacizumab, restored anti-angiogenic and antitumor effect in a human colorectal cancer xenograft model.
Harada, S; Iwai, T; Kurasawa, M; Sugimoto, M; Yamamoto, K; Yorozu, K, 2016)		1.41
"Capecitabine treatment was associated with less nausea, vomiting, and constipation and with better appetite than standard treatment (P ≤ .004), but worse hand-foot syndrome and diarrhea (P < .005)."( Quality of life of older patients with early-stage breast cancer receiving adjuvant chemotherapy: a companion study to cancer and leukemia group B 49907.
Archer, L; Bennett, S; Casey, R; Cohen, HJ; Hudis, C; Kimmick, G; Kornblith, AB; Lan, L; Muss, HB; Partridge, A; Winer, E, 2011)		1.09
"Capecitabine is a treatment option for patients with TN tumours in advanced disease including 1st line and 2nd/3rd line."( Is capecitabine efficacious in triple negative metastatic breast cancer?
Ashley, S; Dolly, S; Johnston, S; Kotsori, AA; Parton, M; Shaunak, N; Sheri, A; Smith, IE; Walsh, G, 2010)		2.42
"Capecitabine treatment was discontinued."( [Ileitis following capecitabine use].
Bouma, G; Imholz, AL, 2011)		1.42
"Capecitabine treatment resulted in a 70% decrease in blood cell counts of WT animals, with only a marginal effect in UPase(-/-) mice."( Differential expression of uridine phosphorylase in tumors contributes to an improved fluoropyrimidine therapeutic activity.
Cao, D; Flynn, S; Gach, M; Kim, B; McCabe, J; Pizzorno, G; Wan, L; Yan, R; Ziemba, A, 2011)		1.09
"As capecitabine/docetaxel treatment confers a median 3-month survival benefit compared with docetaxel monotherapy, the projected survival gain in these patients was 136 life-years."( Population-based pharmacoeconomic model for adopting capecitabine/docetaxel combination treatment for anthracycline-pretreated metastatic breast cancer.
Ilersich, AL; Verma, S, 2003)		1.08
"When capecitabine-treated breast cancer patients develop macrocytosis in the absence of anemia, investigations of other causes of macrocytosis are not warranted."( Effect of capecitabine on mean corpuscular volume in patients with metastatic breast cancer.
Hamilton, M; Karvellas, CJ; Mackey, JR; Sawyer, M, 2004)		1.18
"Capecitabine treatment was discontinued due to disease progression, and triglyceride levels decreased to 154 mg/dL after 11 weeks."( Capecitabine-induced severe hypertriglyceridemia: report of two cases.
Babaoglu, MO; Guler, N; Kurt, M; Shorbagi, A; Yasar, U, 2006)		2.5
"Capecitabine treatment of advanced colorectal carcinoma, when compared to 5FU, results in superior response rates (26.6% versus 17.9%, p=0.013), equivalent times to progression and survival, and improved safety, including less stomatitis and myelosuppression."( The role of capecitabine in the treatment of colorectal cancer in the elderly.
Monfardini, S; Pasetto, LM, )		1.23
"Capecitabine/trastuzumab treatment achieved objective responses in 12 patients (45%), including complete response in four patients (15%) and partial response in eight patients (30%). "( Phase II study of capecitabine plus trastuzumab in human epidermal growth factor receptor 2 overexpressing metastatic breast cancer pretreated with anthracyclines or taxanes.
Bangemann, N; Fuchs, I; Gonsch, T; Hindenburg, HJ; Hinke, A; Klare, P; Kleine-Tebbe, A; Lakner, V; Schaller, G; Weber, J, 2007)		2.12
"Capecitabine as third-line treatment showed a favourable toxicity profile, but exhibited low activity in patients with advanced renal cell carcinoma after failing immunotherapy."( Capecitabine as third-line treatment in patients with metastatic renal cell carcinoma after failing immunotherapy.
Barbanti, G; de Rubertis, G; Francini, E; Francini, G; Manganelli, A; Marsili, S; Paolelli, L; Pascucci, A; Petrioli, R; Salvestrini, F; Sciandivasci, A, 2007)		2.5
"Capecitabine treatment in comparison to 5-FU/LV in advanced colorectal carcinoma resulted in superior response rates (26.6% versus 17.9%, P=0.013) and improved safety including less stomatitis and myelosuppression."( Capecitabine (Xeloda) improves medical resource use compared with 5-fluorouracil plus leucovorin in a phase III trial conducted in patients with advanced colorectal carcinoma.
Barker, C; Boyer, M; Cassidy, J; Findlay, M; Hieke, K; Jamieson, C; Osterwalder, B; Twelves, C; Weitzel, C, 2001)		2.47
"Treatment with capecitabine did not significantly increase the mean antioxidant concentration."( Influence of Sorafenib, Sunitinib and Capecitabine on the Antioxidant Status of the Skin.
Fuss, H; Jung, S; Lademann, J, 2018)		1.09
"Treatment with capecitabine is characterized by an increased risk of severe diarrhoea, mainly in patients affected by CRC and treated with polichemotherapy. "( Incidence and relative risk of grade 3 and 4 diarrhoea in patients treated with capecitabine or 5-fluorouracil: a meta-analysis of published trials.
de Braud, F; Di Bartolomeo, M; Iacovelli, R; Maggi, C; Palazzo, A; Pietrantonio, F; Ricchini, F, 2014)		0.98
"Treatment with capecitabine had been replaced with weekly bolus 5FU-LV, without further cardiotoxicity."( Capecitabine cardiotoxicity--case reports and literature review.
Babic, D; Filipovic, I; Manojlovic, N; Radoje, D; Stojanovic, S, )		1.91
"Treatment was capecitabine 1700 mg/m2 (850 mg/m2 orally twice a day on days 1-14 for 3 weeks), irinotecan 200 mg/m2 intravenously (I.V.) on day 1 every 3 weeks, and weekly cetuximab (initially 400 mg/m2 I.V."( Results of a phase II trial of cetuximab plus capecitabine/irinotecan as first-line therapy for patients with advanced and/or metastatic colorectal cancer.
Asmar, L; Berger, M; Boehm, KA; Cartwright, T; Cohn, A; Hyman, W; Kuefler, P; Nugent, JE; Richards, D; Ruxer, RL; Vukelja, S, 2008)		0.95
"Treatment with capecitabine chemotherapy was associated with a significantly prolonged progression-free survival (WMD = 1.24; 95% CI, 0.04-2.44; P = 0.04), whereas overall survival was not statistically significant (WMD [random] = 0.29; P = 0.75). "( Capecitabine-based chemotherapy for metastatic colorectal cancer.
Fan, J; Ling, W; Ma, Y; Wang, H, 2011)		2.16
"Treatment with capecitabine was well tolerated with grade 2 hand-and-foot syndrome and mild nausea being the only side effects."( Capecitabine as salvage therapy for a breast cancer patient with extensive liver metastases and associated impairment of liver function.
Kornek, GV; Scheithauer, W; Schüll, B, 2003)		2.1
"Treatment with capecitabine lead to clinical amelioration."( Paraneoplastic neurological syndromes and breast cancer. Regression of paraneoplastic neurological sensorimotor neuropathy in a patient with metastatic breast cancer treated with capecitabine: a case study and mini-review of the literature.
Bergonzi, P; Fasola, G; Minisini, AM; Pauletto, G, 2007)		0.87
"Treatment with capecitabine and erlotinib in gemcitabine-refractory patients was associated with an overall objective radiologic response rate of 10% and a median survival duration of 6.5 months. "( Capecitabine plus erlotinib in gemcitabine-refractory advanced pancreatic cancer.
Blaszkowsky, LS; Clark, JW; Enzinger, PC; Fuchs, CS; Kulke, MH; Kwak, EL; Lawrence, C; Meyerhardt, JA; Muzikansky, A; Ryan, DP; Zhu, AX, 2007)		2.14
"Treatment with capecitabine resulted in clinically significant beneficial effects on tumor-related symptoms and yielded objective response activity in patients with metastatic or locally advanced pancreatic cancer. "( Phase II study of oral capecitabine in patients with advanced or metastatic pancreatic cancer.
Cartwright, TH; Chen, YM; Cohn, A; Cox, JV; Schulz, JJ; Szatrowski, TP; Varkey, JA, 2002)		0.98

Toxicity

Hand-foot syndrome (HFS) is the only clinical adverse event occurring more often during capecitabine treatment. The cape citabine-related adverse events included leukopenia, anemia, and thrombocytopenia. Screening of patients for DPYD mutations prior to treatment using new pharmacogenetic testing methods.

ExcerptReferenceRelevance
" Some studies have been proven it to be safe for outpatient treatment and to have significant antitumor activity in colorectal and breast cancer patients."( [Capecitabine--a review of its antitumor activity and toxicity in clinical studies].
Maeda, Y; Sasaki, T, 2000)		1.22
" In this case report the authors describe an unusually and reversible cardiac side effect which occurs to 39-year-old patient treated with capecitabine 2000 mg/m2/day for advanced gastric cancer."( Acute cardiotoxicity during capecitabine treatment: a case report.
Bertolini, A; Flumanò, M; Fusco, O; Muffatti, A; Pontiggia, G; Scarinci, A; Scopelliti, M, )		0.63
" All patients in the capecitabine group received a starting dose of 1250 mg/m2 twice daily and the majority (66%) did not require dose modification for adverse events."( First-line oral capecitabine therapy in metastatic colorectal cancer: a favorable safety profile compared with intravenous 5-fluorouracil/leucovorin.
Bajetta, E; Boyer, M; Bugat, R; Burger, U; Cassidy, J; Garin, A; Graeven, U; Hoff, P; Maroun, J; Marshall, J; McKendric, J; Osterwalder, B; Pérez-Manga, G; Rosso, R; Rougier, P; Schilsky, RL; Twelves, C; Van Cutsem, E, 2002)		0.98
" Analysis of data from two large phase III trials demonstrates that efficacy is not compromised in patients requiring a dose reduction for adverse events."( First-line oral capecitabine therapy in metastatic colorectal cancer: a favorable safety profile compared with intravenous 5-fluorouracil/leucovorin.
Bajetta, E; Boyer, M; Bugat, R; Burger, U; Cassidy, J; Garin, A; Graeven, U; Hoff, P; Maroun, J; Marshall, J; McKendric, J; Osterwalder, B; Pérez-Manga, G; Rosso, R; Rougier, P; Schilsky, RL; Twelves, C; Van Cutsem, E, 2002)		0.66
" A patient who had previously received adjuvant 5-fluorouracil without neurotoxicity had a severe adverse reaction when later given capecitabine in the metastatic setting."( Capecitabine-related neurotoxicity presenting as trismus.
Couch, LS; Groteluschen, DL; Mulkerin, DL; Stewart, JA, 2003)		1.97
" Hand-foot syndrome (HFS) is the only clinical adverse event occurring more often during capecitabine treatment."( Management of adverse events and other practical considerations in patients receiving capecitabine (Xeloda).
Grothey, A; Marsé, H; Valverde, S; Van Cutsem, E, 2004)		0.77
" The most frequent toxic effects were grade 3/4 diarrhea (arm A: 34%, B: 19%), grade 3/4 neutropenia (A: 5%, B: 19%) and grade 2/3 alopecia (A: 26%, B: 65%)."( A randomized phase II trial of capecitabine and two different schedules of irinotecan in first-line treatment of metastatic colorectal cancer: efficacy, quality-of-life and toxicity.
Bernhard, J; Borner, MM; Brauchli, P; Dietrich, D; Herrmann, R; Honegger, H; Koeberle, D; Lanz, D; Popescu, R; Rauch, D; Roth, AD; Saletti, P; Wernli, M, 2005)		0.61
" Due to the occurrence of two toxic deaths, capecitabine 1,000 mg/m(2) twice daily was given to the subsequent 43 patients."( Safety and efficacy of two different doses of capecitabine in the treatment of advanced breast cancer in older women.
Bajetta, E; Buzzoni, R; Catena, L; Celio, L; Della Torre, S; Gattinoni, L; Longarini, R; Mariani, L; Procopio, G; Ricotta, R; Zilembo, N, 2005)		0.85
"This study shows that capecitabine is safe and effective in the elderly breast cancer patient."( Safety and efficacy of two different doses of capecitabine in the treatment of advanced breast cancer in older women.
Bajetta, E; Buzzoni, R; Catena, L; Celio, L; Della Torre, S; Gattinoni, L; Longarini, R; Mariani, L; Procopio, G; Ricotta, R; Zilembo, N, 2005)		0.9
" Grade 3/4 toxic effects at dose levels A, B and C, respectively, included palmar-plantar erythrodysesthesia (33%, 63%, 20%), diarrhea (13%, 12%, 3%), stomatitis (8%, 0%, 3%), and nausea/vomiting (4%, 6%, 5%)."( Lower dose capecitabine has a more favorable therapeutic index in metastatic breast cancer: retrospective analysis of patients treated at M. D. Anderson Cancer Center and a review of capecitabine toxicity in the literature.
Gauthier, AM; Hennessy, BT; Hortobagyi, G; Michaud, LB; Valero, V, 2005)		0.72
"This retrospective analysis supports a starting dose of 2000 mg/m2/day because of its superior therapeutic index; however, patients may still have toxic effects and individualization of dosing is necessary."( Lower dose capecitabine has a more favorable therapeutic index in metastatic breast cancer: retrospective analysis of patients treated at M. D. Anderson Cancer Center and a review of capecitabine toxicity in the literature.
Gauthier, AM; Hennessy, BT; Hortobagyi, G; Michaud, LB; Valero, V, 2005)		0.72
" Capecitabine/oxaliplatin (XelOx) is a safe and active combination for the first-line treatment of metastatic CRC."( Capecitabine/oxaliplatin, a safe and active first-line regimen for older patients with metastatic colorectal cancer: post hoc analysis of a large phase II study.
Braud, Fd; Brunet, R; Butts, CA; Cassidy, J; Conroy, T; Diaz-Rubio, E; Figer, A; Grossmann, J; Schoffski, P; Sobrero, AF; Tabernero, JM; Twelves, CJ; Van Cutsem, EJ, 2005)		2.68
" The overall incidence of adverse events (including grade 3/4), dose reductions, and withdrawals because of adverse events were similar in both groups."( Capecitabine/oxaliplatin, a safe and active first-line regimen for older patients with metastatic colorectal cancer: post hoc analysis of a large phase II study.
Braud, Fd; Brunet, R; Butts, CA; Cassidy, J; Conroy, T; Diaz-Rubio, E; Figer, A; Grossmann, J; Schoffski, P; Sobrero, AF; Tabernero, JM; Twelves, CJ; Van Cutsem, EJ, 2005)		1.77
" All myelosuppressive adverse events and the majority of non-hematological adverse events were typical and characteristic of the individual concomitant cytotoxic agents."( Safety and efficacy of trastuzumab every 3 weeks combined with cytotoxic chemotherapy in patients with HER2-positive recurrent breast cancer: findings from a case series.
Alexopoulos, A; Ardavanis, A; Karamouzis, M; Orfanos, G; Rigatos, G; Scorilas, A; Tryfonopoulos, D, 2005)		0.33
" For both breast and colon cancer, capecitabine alone or in combination with other cytotoxics is safe and effective."( Capecitabine use in geriatric oncology: an analysis of current safety, efficacy, and quality of life data.
Ershler, WB, 2006)		2.05
" Grade 2/3 treatment-related adverse events were diarrhoea (34%), fatigue (27%), stomatitis (15%) and hand-foot syndrome (22%)."( A phase II study of fixed-dose capecitabine and assessment of predictors of toxicity in patients with advanced/metastatic colorectal cancer.
Beale, P; Clarke, SJ; Horvath, L; Ong, S; Rivory, L; Sharma, R, 2006)		0.62
" Capecitabine was less toxic in monkeys than oral 5'-DFUR according to dose (mmol/kg) and 5'-DFUR AUC."( Relationship between AUC of 5'-DFUR and toxicity of capecitabine, fluoropyrimidine carbamate analogs, and 5'-DFUR in monkeys, mice, and rats.
Horii, I; Kawashima, A; Kobayashi, K; Nakano, K; Shindoh, H; Shishido, N, 2006)		1.49
" Most treatment-related adverse events (AEs) occurred at similar rates in both treatment arms."( Phase III trial of capecitabine plus oxaliplatin as adjuvant therapy for stage III colon cancer: a planned safety analysis in 1,864 patients.
Cartwright, T; de Braud, F; Figer, A; Haller, DG; Hill, M; Lim, R; Maroun, J; McKendrick, J; Nowacki, MP; Park, YS; Price, T; Schmoll, HJ; Sirzén, F; Soler-Gonzalez, G; Tabernero, J; Topham, C; Van Cutsem, E, 2007)		0.67
" We conducted a study to identify a safe dose and potential drug-drug interactions of this combination."( Pharmacokinetic and safety study of weekly irinotecan and oral capecitabine in patients with advanced solid cancers.
Baker, S; Bulgaru, A; Camacho, F; Chaudhary, I; Desai, K; Einstein, M; Goel, S; Goldberg, G; Gollamudi, R; Karri, S; Kaubisch, A; Mani, S, 2007)		0.58
" The combination of irinotecan and capecitabine is safe and well tolerated at 100/2000, and warrants further evaluation in ovarian and breast cancer."( Pharmacokinetic and safety study of weekly irinotecan and oral capecitabine in patients with advanced solid cancers.
Baker, S; Bulgaru, A; Camacho, F; Chaudhary, I; Desai, K; Einstein, M; Goel, S; Goldberg, G; Gollamudi, R; Karri, S; Kaubisch, A; Mani, S, 2007)		0.86
"The present study supports the toxic effect of 5-FU on the myocardium, which is largely schedule-dependent, whereas a low but finite risk of such toxicity has been observed with oral capecitabine."( Cardiotoxicity of fluoropyrimidines in different schedules of administration: a prospective study.
Kallistratos, MS; Karabelis, A; Kopterides, P; Kosmas, C; Mylonakis, N; Skopelitis, H; Syrios, J; Tsavaris, N, 2008)		0.54
" Common adverse effects were hand-foot syndrome, liver dysfunction, and bone marrow suppression."( Efficacy and safety of trastuzumab plus capecitabine in heavily pretreated patients with HER2-positive metastatic breast cancer.
Hatake, K; Ito, Y; Iwase, T; Osako, T; Takahashi, S; Tokudome, N, 2008)		0.61
"Chemoradiotherapy of the last phase II study with intermittent capecitabine (1500 mg/m(2)/day, delivered on days 1-14 and 22-35) and irinotecan (4 x 60 mg/m(2)) concurrently to radiotherapy is a safe treatment with low toxicity and high efficacy."( Intensified irinotecan-based neoadjuvant chemoradiotherapy in rectal cancer: four consecutive designed studies to minimize acute toxicity and to optimize efficacy measured by pathologic complete response.
Fietkau, R; Foitzik, T; Klar, E; Klautke, G; Küchenmeister, U; Ludwig, K; Prall, F; Semrau, S, 2007)		0.58
"Treatment with the combination of (177)Lu-octreotate and capecitabine was feasible and safe considering acute and subacute side effects."( Report on short-term side effects of treatments with 177Lu-octreotate in combination with capecitabine in seven patients with gastroenteropancreatic neuroendocrine tumours.
de Herder, WW; Kam, BL; Krenning, EP; Kwekkeboom, DJ; van Aken, MO; van Essen, M, 2008)		0.81
" Knowledge of this toxicity can aid clinicians to choose the optimal and least toxic regimen suitable for an individual patient."( Cardiac toxicity: old and new issues in anti-cancer drugs.
Barriuso, J; Belda, C; Brunello, A; Casado, E; Chiappori, A; de Castro, J; Feliu, J; González-Barón, M; Sereno, M, 2008)		0.35
"The addition of cetuximab to capecitabine, oxaliplatin and bevacizumab in the first-line treatment of ACC appears to be safe and feasible."( A randomised phase III study on capecitabine, oxaliplatin and bevacizumab with or without cetuximab in first-line advanced colorectal cancer, the CAIRO2 study of the Dutch Colorectal Cancer Group (DCCG). An interim analysis of toxicity.
Antonini, NF; Cats, A; Creemers, GJ; Erdkamp, FL; Koopman, M; Mol, L; Punt, CJ; Rodenburg, CJ; Schrama, JG; Tol, J; Vos, AH, 2008)		0.92
" Although patients can take the drug orally in the convenience of their own home, the key to successful management of capecitabine is the clinician's awareness of its severe, but low in incidence, adverse effects, and the patients' education, emphasizing compliance with the treatment plan, prevention and timely recognition of its toxicities."( Capecitabine: an overview of the side effects and their management.
Katirtzoglou, NA; Saif, MW; Syrigos, KN, 2008)		2
" The most frequent adverse event was asthenia, which was grade 3 in two patients."( A phase I study of the safety and pharmacokinetics of the combination of pertuzumab (rhuMab 2C4) and capecitabine in patients with advanced solid tumors.
Albanell, J; Beech, J; Brewster, M; Gascon, P; Jones, ET; Mellado, B; Montagut, C; Pronk, L; Saunders, MP; Valle, JW; Zugmaier, G, 2008)		0.56
" Common adverse events were diarrhea, rash, dry skin, asthenia, nausea, anorexia."( Efficacy and safety of erlotinib in patients with locally advanced or metastatic breast cancer.
Cobleigh, MA; Dickler, MN; Klein, PM; Miller, KD; Winer, EP, 2009)		0.35
" Many drugs have been used for the treatment of this disease, but there is little information about how predictive factors can be used to aid treatment response and anticipate toxic effects related to anticancer treatment in colorectal cancer."( Predictive factors for chemotherapy-related toxic effects in patients with colorectal cancer.
Pantano, F; Santini, D; Schiavon, G; Tonini, G; Vincenzi, B, 2008)		0.35
"After 40 of the planned 74 patients had been randomly assigned, real-time adverse event monitoring led to early trial closure because of excess sequence-specific toxicity."( Severe sequence-specific toxicity when capecitabine is given after Fluorouracil and leucovorin.
Anthoney, DA; Bradley, C; Brown, JM; Brown, S; Crawford, SM; Hennig, IM; Jackson, DP; Melcher, AM; Naik, JD; Seymour, MT; Szubert, A, 2008)		0.62
" Incidence of grade 3/4 treatment-related adverse events during the first 12 weeks of treatment were 59%, 36%, and 67% for mFOLFOX6, bFOL, and CapeOx, respectively, (TREE-1) and 59%, 51%, and 56% for the corresponding treatments plus bevacizumab (TREE-2; primary end point)."( Safety and efficacy of oxaliplatin and fluoropyrimidine regimens with or without bevacizumab as first-line treatment of metastatic colorectal cancer: results of the TREE Study.
Abubakr, Y; Childs, BH; Cohn, AL; Fehrenbacher, L; Hainsworth, JD; Hart, LL; Hedrick, E; Hochster, HS; Ramanathan, RK; Saif, MW; Schwartzberg, L; Wong, L, 2008)		0.35
" The most common side effect is myelosuppression."( Gemcitabine-induced pulmonary toxicity during adjuvant therapy in a patient with pancreatic cancer.
Cornfeld, D; Lansigan, F; Saif, MW; Shaib, W; Syrigos, K, 2008)		0.35
" Cardiotoxicity is a relatively uncommon side effect of 5-fluorouracil and capecitabine."( Cardiotoxicity of 5-fluorouracil and capecitabine in a pancreatic cancer patient with a novel mutation in the dihydropyrimidine dehydrogenase gene.
Harold, L; Rajebi, MR; Saif, MW; Shahrokni, A, 2009)		0.86
" Genetic variations such as polymorphic abnormality of DPYD are potential causative factors for a significant portion of serious adverse reactions to 5-fluorouracil-based therapy."( Cardiotoxicity of 5-fluorouracil and capecitabine in a pancreatic cancer patient with a novel mutation in the dihydropyrimidine dehydrogenase gene.
Harold, L; Rajebi, MR; Saif, MW; Shahrokni, A, 2009)		0.63
" Major adverse events were neutropenia, nausea, diarrhea, hand/foot syndrome, and neurotoxicity."( Efficacy and safety of capecitabine and oxaliplatin combination as second-line treatment in advanced colorectal cancer.
Hatzopoulos, A; Heras, P; Karagiannis, S; Kritikos, K; Kritikos, N; Mitsibounas, D; Xourafas, V, )		0.44
" Serious/grade 3-5 adverse events of interest for bevacizumab included bleeding (3%), gastrointestinal perforation (2%), arterial thromboembolism (1%), hypertension (5."( Safety and efficacy of first-line bevacizumab with FOLFOX, XELOX, FOLFIRI and fluoropyrimidines in metastatic colorectal cancer: the BEAT study.
Berry, S; Bridgewater, J; Canon, JL; Cunningham, D; DiBartolomeo, M; Georgoulias, V; Kretzschmar, A; Mazier, MA; Michael, M; Peeters, M; Rivera, F; Van Cutsem, E, 2009)		0.35
"In this large pooled analysis, we found MMC, when capped at a cumulative dose of 36 mg/m(2), to be safe and tolerable in combination with capecitabine or irinotecan with no reportable cases of TTP/HUS."( Capped-dose mitomycin C: a pooled safety analysis from three prospective clinical trials.
Arce-Lara, C; Bekaii-Saab, T; Cataland, S; Kraut, E; Ntukidem, N; Otterson, GA, 2010)		0.56
"1236G>A), which was observed five- out of eight-times in patients with severe adverse effects."( Dihydropyrimidine dehydrogenase gene variation and severe 5-fluorouracil toxicity: a haplotype assessment.
Aebi, S; Amstutz, U; Farese, S; Largiadèr, CR, 2009)		0.35
" The most common adverse events were leukopenia (73."( [Efficacy and safety of combination of irinotecan and capecitabine in patients with metastatic colorectal cancer after failure of chemotherapy with oxaliplatin].
Bai, CM; Chen, SC; Cheng, YJ; Jia, N; Shao, YJ; Zhou, JF, 2009)		0.6
" Hand-foot syndrome (HFS) is a relatively common side effect of cytotoxic chemotherapy."( Toxicity and efficacy of 5-fluorouracil and capecitabine in a patient with TYMS gene polymorphism: A challenge or a dilemma?
Rajebi, MR; Saif, MW; Shahrokni, A, 2009)		0.61
" Cardiotoxicity causing angina, arrhythmia and infarction are serious adverse events associated with these agents."( [Cardiotoxicity induced by 5-fluorouracil or capecitabine].
Baeksgaard, L; Jensen, SA; Petersen, LN; Reiter, L; Sørensen, JB, 2010)		0.62
" The most frequently observed adverse events reported with AZD6244 were acneiform dermatitis, diarrhoea, asthenia and peripheral oedema, compared with hand-foot syndrome, diarrhoea, nausea and abdominal pain with capecitabine."( A Phase II, open-label, randomised study to assess the efficacy and safety of the MEK1/2 inhibitor AZD6244 (ARRY-142886) versus capecitabine monotherapy in patients with colorectal cancer who have failed one or two prior chemotherapeutic regimens.
Adenis, A; Bennouna, J; Boer, K; Douillard, JY; Escudero, P; Kim, TY; Lang, I; Morris, CD; Pover, GM; Valladares-Ayerbes, M, 2011)		0.76
" Main adverse events grades 2/3/4 were (n): leukocytopenia 3/2/2, anemia 13/4/0, thrombocytopenia 3/1/0, nausea/vomiting 2/1/0, diarrhea 5/1/0, hand-foot-skin reaction 7/0/0."( Efficacy and safety of capecitabine in combination with docetaxel and mitomycin C in patients with pre-treated pancreatic, gallbladder, and bile duct carcinoma.
Ernst, T; Hochhaus, A; Hofheinz, RD; Hofmann, WK; Kripp, M; Kruth, J; Lukan, N; Merx, K; Nissen, J, 2010)		0.67
" 3-year disease-free survival (DFS) and adverse events as end points were compared between the two groups."( [Efficacy and toxicity analysis of XELOX and FOLFOX4 regimens as adjuvant chemotherapy for stage III colorectal cancer].
Fang, F; Li, DC; Lu, GC, 2010)		0.36
" There was no significant difference for 3-year DFS and all grades adverse events between the two groups."( [Efficacy and toxicity analysis of XELOX and FOLFOX4 regimens as adjuvant chemotherapy for stage III colorectal cancer].
Fang, F; Li, DC; Lu, GC, 2010)		0.36
" The main adverse effects associated with the treatment included leucopenia, nausea/vomiting and peripheral neuritis."( [Short-term therapeutic effect and safety of endostar combined with XELIRI regimen in the treatment of advanced colorectal cancer].
Liao, WJ; Luo, RC; Shen, P; Shi, M; Wu, Wy, 2010)		0.36
"Endostar combined with XELIRI is effective and safe as the second-line treatment for advanced colorectal cancer, and further clinical investigation is warranted."( [Short-term therapeutic effect and safety of endostar combined with XELIRI regimen in the treatment of advanced colorectal cancer].
Liao, WJ; Luo, RC; Shen, P; Shi, M; Wu, Wy, 2010)		0.36
" In our experience, capecitabine-induced hypertriglyceridemia does not seem to be a rare adverse effect as it is observed in 10% of treated patients."( Cancer chemotherapy and cardiovascular risks: is capecitabine-induced hypertriglyceridemia a rare adverse effect?
Emiliani, A; Losanno, T; Manna, G; Seminara, P, 2010)		0.94
"(177)Lu-octreotate is a safe and well-tolerated therapy for patients who have previously been treated with (111)In-pentetreotide and can be safely combined with radiosensitising chemotherapy."( 177Lu-octreotate, alone or with radiosensitising chemotherapy, is safe in neuroendocrine tumour patients previously treated with high-activity 111In-octreotide.
Hicks, RJ; Hubble, D; Johnson, V; Kong, G; Michael, M; Ramdave, S, 2010)		0.36
" We stress the fact that while vasospasm is a well-recognized side-effect of this class of chemotherapeutic agent, broader cardiotoxicity is commonly seen and an increased awareness of the range of toxicity is necessary if repeat toxicity is to be avoided."( Cardiotoxicity with 5-fluorouracil and capecitabine: more than just vasospastic angina.
Pavlakis, N; Stewart, T; Ward, M, 2010)		0.63
" The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand-foot syndrome."( Safety of capecitabine: a review.
Marshall, JL; Mikhail, SE; Sun, JF, 2010)		1.02
"Capecitabine at a dose of 2000 mg/m(2) is active and safe as first-line treatment of patients with metastatic breast cancer."( First-line therapy with moderate dose capecitabine in metastatic breast cancer is safe and active: results of the MONICA trial.
Bauer, W; Costa, SD; Distelrath, A; Gerber, B; Hagen, V; Kaufmann, M; Kleine-Tebbe, A; Loibl, S; Maass, N; Mehta, K; Ruckhaeberle, E; Schneeweiss, A; Schrader, I; Sütterlin, MW; Tomé, O; von Minckwitz, G; Wiest, W, 2010)		2.07
"Although the 2009 edition of the Guidelines for Colorectal Cancer Therapy recommend capecitabine as a standard postoperative adjuvant chemotherapy for colorectal cancer therapy, a characteristic adverse event, hand-foot syndrome, develops at a high incidence, and appropriate management is necessary to continue therapy."( [Adverse events in patients treated with capecitabine as adjuvant chemotherapy after surgery for colorectal cancer--countermeasures against hand-foot syndrome].
Chiba, M; Fujimoto, H; Igawa, A; Iizawa, H; Ikeda, E; Inoue, K; Ishiyama, K; Kobayashi, Y; Matsuda, M; Mori, N; Saito, T; Sato, T; Sugawara, M; Suto, T; Suzuki, Y; Watanabe, T; Yabuki, H, 2010)		0.85
" The adverse events related to bevacizumab were grade 2 hypertension in 3 patients (27."( [Efficacy and safety of bevacizumab plus capecitabine for metastatic colorectal cancer].
Ai, B; Ding, L; Li, L; Wu, JY; Wu, XN; Zhao, YB; Zhou, MZ, 2010)		0.63
" The adverse drug reactions are well tolerated."( [Efficacy and safety of bevacizumab plus capecitabine for metastatic colorectal cancer].
Ai, B; Ding, L; Li, L; Wu, JY; Wu, XN; Zhao, YB; Zhou, MZ, 2010)		0.63
" Although these are considered safe drugs, a growing body of literature reports adverse cardiac effects."( Capecitabine in breast cancer: the issue of cardiotoxicity during fluoropyrimidine treatment.
Albini, A; Bucci, EO; Cergnul, M; Gottardi, O; Molteni, LP; Noonan, DM; Paino, AM; Rampinelli, I; Scaglietti, U, )		1.57
"Peripheral sensory neurotoxicity is a frequent and potentially debilitating side effect of oxaliplatin treatment."( The effect of prophylactic calcium and magnesium infusions on the incidence of neurotoxicity and clinical outcome of oxaliplatin-based systemic treatment in advanced colorectal cancer patients.
Imholz, AL; Knijn, N; Koopman, M; Mol, L; Punt, CJ; Teerenstra, S; Tol, J; Valster, FA; Vincent, AD; Werter, MJ, 2011)		0.37
" Most frequent drug-related adverse events were hand-foot skin reaction (HFSR, 89%), diarrhea (71%), and fatigue (69%)."( Safety and pharmacokinetics of sorafenib combined with capecitabine in patients with advanced solid tumors: results of a phase 1 trial.
Awada, A; Besse-Hammer, T; Brendel, E; Delesen, H; Gil, T; Hendlisz, A; Joosten, MC; Lathia, CD; Loembé, BA; Piccart-Ghebart, M; Van Hamme, J; Whenham, N, 2011)		0.62
"This study suggests that metabolic profiles can delineate subpopulations susceptible to adverse events and have a potential role in the assessment of treatment viability for cancer patients prior to commencing chemotherapy."( Pharmacometabonomic profiling as a predictor of toxicity in patients with inoperable colorectal cancer treated with capecitabine.
Backshall, A; Clarke, SJ; Keun, HC; Sharma, R, 2011)		0.58
" Vinorelbine in combination with capecitabine is an effective and safe schedule for patients with MBC especially after pretreatment with anthracycline/ taxane-based regimens."( Safety and efficacy of oral vinorelbine and capecitabine combination for metastatic breast cancer.
Adua, D; Basile, ML; De Sanctis, R; Del Signore, E; Di Seri, M; Gori, B; Grassi, P; Longo, F; Quadrini, S; Stumbo, L, 2011)		0.91
" Gastrointestinal adverse events (nausea, vomiting and diarrhea) were commonly observed in both treatment groups."( A phase II open-label randomized study to assess the efficacy and safety of selumetinib (AZD6244 [ARRY-142886]) versus capecitabine in patients with advanced or metastatic pancreatic cancer who have failed first-line gemcitabine therapy.
Bodoky, G; Ciuleanu, TE; La Stella, PJ; Pover, G; Spigel, DR; Tebbutt, NC; Timcheva, C, 2012)		0.59
"Hand-foot syndrome is a highly unpleasant adverse reaction caused by treatment protocols containing capecitabine (an orally administered drug), docetaxel, liposomal doxorubicin infusions or continuously infused 5-fluorouracil."( [Main treatment and preventive measures for hand-foot syndrome, a dermatologic side effect of cancer therapy].
Bartal, A; Liszkay, G; Mátrai, Z; Szûcs, A, 2011)		0.59
" Grade 3-4 adverse events were uncommon; haematologic toxicity was infrequent (5%) and consistently mild."( Efficacy and safety of low-dose metronomic chemotherapy with capecitabine in heavily pretreated patients with metastatic breast cancer.
Calvani, N; Cinefra, M; Cinieri, S; Fedele, P; Marino, A; Mazzoni, E; Nacci, A; Orlando, L; Rizzo, P; Schiavone, P; Sponziello, F, 2012)		0.62
" However, many toxic effects are evaluated on a categorical scale."( Dose adaptation of capecitabine based on individual prediction of limiting toxicity grade: evaluation by clinical trial simulation.
Freyer, G; Girard, P; Hénin, E; Paule, I; Tod, M; You, B, 2012)		0.71
" Randomized studies and retrospective analyses have shown that, in patients who received capecitabine monotherapy, or in combination with docetaxel, dose modification of capecitabine is effective in the management of adverse events without compromising efficacy."( Dose-adjusting capecitabine minimizes adverse effects while maintaining efficacy: a retrospective review of capecitabine for metastatic breast cancer.
Blum, JL; Hennessy, BT; Leonard, R; O'Shaughnessy, J, 2011)		0.94
" We identified relevant trial evidence and pooled the results on both efficacy and adverse events."( Capecitabine for the treatment for advanced gastric cancer: efficacy, safety and ethnicity.
Ma, Y; Tang, L; Wang, HX; Xu, YC; Zhang, FC, 2012)		1.82
" Adverse effects ≥ grade 2 were observed in 32% of the patients and adverse effects ≥ grade 3 in 15%."( Safety and outcome of chemoradiotherapy in elderly patients with rectal cancer: results from two French tertiary centres.
Bensadoun, RJ; Hamidou, H; Michel, P; Paillot, B; Roullet, B; Silvain, C; Tougeron, D; Tourani, JM, 2012)		0.38
"In selected elderly patients, chemoradiotherapy is well-tolerated, without any significant increase in adverse events, and the results are similar to those recorded in younger patients."( Safety and outcome of chemoradiotherapy in elderly patients with rectal cancer: results from two French tertiary centres.
Bensadoun, RJ; Hamidou, H; Michel, P; Paillot, B; Roullet, B; Silvain, C; Tougeron, D; Tourani, JM, 2012)		0.38
"The safety profiles of oral fluoropyrimidines were compared with 5-fluorouracil (5-FU) using adverse event reports (AERs) submitted to the Adverse Event Reporting System, AERS, of the US Food and Drug Administration (FDA)."( Adverse event profiles of 5-fluorouracil and capecitabine: data mining of the public version of the FDA Adverse Event Reporting System, AERS, and reproducibility of clinical observations.
Brown, JB; Kadoyama, K; Miki, I; Okuno, Y; Sakaeda, T; Tamura, T, 2012)		0.64
", drug-associated adverse events, including the proportional reporting ratio, the reporting odds ratio, the information component given by a Bayesian confidence propagation neural network, and the empirical Bayes geometric mean."( Adverse event profiles of 5-fluorouracil and capecitabine: data mining of the public version of the FDA Adverse Event Reporting System, AERS, and reproducibility of clinical observations.
Brown, JB; Kadoyama, K; Miki, I; Okuno, Y; Sakaeda, T; Tamura, T, 2012)		0.64
" The regimens demonstrated similar frequencies of all-grade and serious adverse events (SAEs), but different safety profiles."( Safety results from a phase III study (TURANDOT trial by CECOG) of first-line bevacizumab in combination with capecitabine or paclitaxel for HER-2-negative locally recurrent or metastatic breast cancer.
Beslija, S; Brodowicz, T; Greil, R; Inbar, MJ; Kahán, Z; Kaufman, B; Lang, I; Messinger, D; Steger, GG; Stemmer, SM; Zielinski, C; Zvirbule, Z, 2012)		0.59
"Skin toxicity is a frequent adverse event of epidermal growth factor receptor (EGFR) targeting agents."( Prognostic value of cetuximab-related skin toxicity in metastatic colorectal cancer patients and its correlation with parameters of the epidermal growth factor receptor signal transduction pathway: results from a randomized trial of the GERMAN AIO CRC Stu
Giessen, C; Heinemann, V; Jung, A; Kapaun, C; Kirchner, T; Laubender, RP; Modest, DP; Moosmann, N; Neumann, J; Stintzing, S; Wollenberg, A, 2013)		0.39
" Muscle biopsy findings were consistent with a toxic myopathy with necrotizing features and vacuolar changes; COX-negative fibers were also present."( Nerve, muscle and heart acute toxicity following oxaliplatin and capecitabine treatment.
Alì, G; Calabrese, R; Lenzi, P; Moretti, P; Orsucci, D; Petrozzi, L; Pizzanelli, C; Ricci, G; Siciliano, G, 2012)		0.62
" Grade three or worse adverse events were mainly hand-foot syndrome (11%), and there were no grade four adverse events."( Prospective efficacy and safety study of neoadjuvant gemcitabine with capecitabine combination chemotherapy for borderline-resectable or unresectable locally advanced pancreatic adenocarcinoma.
Han, DJ; Kim, JH; Kim, MH; Kim, SC; Kim, TW; Lee, JL; Lee, SK; Lee, SS; Park, DH; Park, JH; Seo, DW; Shin, SH, 2012)		0.61
" We sought to measure persistence with CMF, adherence to oral cyclophosphamide, and the association of these with toxic effects."( Persistence, adherence, and toxicity with oral CMF in older women with early-stage breast cancer (Adherence Companion Study 60104 for CALGB 49907).
Archer, LE; Cohen, HJ; Hudis, CA; Muss, HB; Partridge, AH; Pitcher, BN; Ruddy, KJ; Winer, EP, 2012)		0.38
"Self-reported adherence to cyclophosphamide was high, but persistence was lower, which may be attributable to toxic effects."( Persistence, adherence, and toxicity with oral CMF in older women with early-stage breast cancer (Adherence Companion Study 60104 for CALGB 49907).
Archer, LE; Cohen, HJ; Hudis, CA; Muss, HB; Partridge, AH; Pitcher, BN; Ruddy, KJ; Winer, EP, 2012)		0.38
" Adverse events were generally mild; the most common grade 3/4 events were neutropenia, anemia, anorexia, and nausea."( Efficacy and safety of capecitabine plus cisplatin in Japanese patients with advanced or metastatic gastric cancer: subset analyses of the AVAGAST study and the ToGA study.
Abe, T; Baba, E; Boku, N; Chin, K; Doi, T; Hamamoto, Y; Koizumi, W; Komatsu, Y; Miyata, Y; Nishina, T; Ohtsu, A; Omuro, Y; Saji, S; Sato, A; Satoh, T; Sawaki, A; Takiuchi, H; Tamura, T; Yamada, Y; Yamaguchi, K, 2013)		0.7
"Antimetabolites may cause severe toxicity and even toxic death in cancer patients."( Relationship between antimetabolite toxicity and pharmacogenetics in Turkish cancer patients.
Akbulut, H; Demirkazik, A; Dincol, D; Dogan, M; Icli, F; Karabulut, HG; Tukun, A; Utkan, G; Yalcin, B, 2012)		0.38
" Mucositis and dermatitis occurred in all groups, together with ALT elevation in the methotrexate group and 2 toxic deaths were encountered."( Relationship between antimetabolite toxicity and pharmacogenetics in Turkish cancer patients.
Akbulut, H; Demirkazik, A; Dincol, D; Dogan, M; Icli, F; Karabulut, HG; Tukun, A; Utkan, G; Yalcin, B, 2012)		0.38
" The response and adverse events rates and their exact confidence intervals (CIs) were calculated."( Efficacy and safety of capecitabine in heavily pretreated recurrent/metastatic head and neck squamous cell carcinoma.
Ceruse, P; Fayette, J; Girodet, D; Péron, J; Poupart, M; Ramade, A; Zrounba, P, 2012)		0.69
"The efficacy and adverse effects of capecitabine-based chemotherapy versus other regimens reported in previous trials were discordant."( Efficacy and toxicity of capecitabine-based chemotherapy in patients with metastatic or advanced breast cancer: results from ten randomized trials.
Meng, L; Wang, Y; Wei, JF; Yang, H, 2012)		0.96
" Most common adverse events (AE) were any grade nausea (58%), hand-foot syndrome (44%), diarrhea (33%), fatigue (33%), vomiting (31%), and asthenia (31%)."( Dasatinib plus capecitabine for advanced breast cancer: safety and efficacy in phase I study CA180004.
Atzori, F; Cortes, J; Geese, WJ; Gradishar, WJ; Rybicki, A; Somlo, G; Specht, JM; Strauss, LC; Sy, O; Vahdat, LT, 2013)		0.74
" All patients were genotyped for MTHFR 1298A>C and 677C>T polymorphisms and analysed in both cohorts separately for the association between the MTHFR genotype and incidence of grade 3-4 overall toxicity and specific adverse events, as well as efficacy parameters."( MTHFR polymorphisms and capecitabine-induced toxicity in patients with metastatic colorectal cancer.
Gelderblom, H; Guchelaar, HJ; Punt, CJ; van Huis-Tanja, LH, 2013)		0.7
" The most commonly reported adverse events in the FOLFOX6 cohorts included decreased appetite, neutropenia, diarrhea, peripheral neuropathy, and vomiting."( An open-label study of the safety and tolerability of pazopanib in combination with FOLFOX6 or CapeOx in patients with colorectal cancer.
Adams, LM; Botbyl, J; Brady, J; Chau, I; Corrie, P; Digumarti, R; Laubscher, KH; Mallath, M; Midgley, RS, 2013)		0.39
" Rates of grade 3 adverse events were neutropenia (n = 4, 10."( Efficacy and toxicity of Trastuzumab and Paclitaxel plus Capecitabine in the first-line treatment of HER2-positive metastatic breast cancer.
Benekli, M; Berk, V; Buyukberber, S; Coskun, U; Demirci, U; Ozkan, M; Sevinc, A; Tonyali, O; Ucgul, E; Uncu, D; Yildiz, R, 2013)		0.64
" Grade 3/4 diarrhea as predominant toxic effect occurred in 22% of patients with CapOx-bevacizumab and in 16% with mCapIri-bevacizumab."( Capecitabine/irinotecan or capecitabine/oxaliplatin in combination with bevacizumab is effective and safe as first-line therapy for metastatic colorectal cancer: a randomized phase II study of the AIO colorectal study group.
Arnold, D; Dietrich, G; Freier, W; Geißler, M; Graeven, U; Hegewisch-Becker, S; Hinke, A; Kubicka, S; Pohl, M; Reinacher-Schick, A; Schmiegel, W; Schmoll, HJ; Tannapfel, A, 2013)		1.83
"Both, CapOx-bevacizumab and mCapIri-bevacizumab, show promising activity and an excellent toxic effect profile."( Capecitabine/irinotecan or capecitabine/oxaliplatin in combination with bevacizumab is effective and safe as first-line therapy for metastatic colorectal cancer: a randomized phase II study of the AIO colorectal study group.
Arnold, D; Dietrich, G; Freier, W; Geißler, M; Graeven, U; Hegewisch-Becker, S; Hinke, A; Kubicka, S; Pohl, M; Reinacher-Schick, A; Schmiegel, W; Schmoll, HJ; Tannapfel, A, 2013)		1.83
"3-40 mg/kg) resulted in no dose-limiting toxicities (DLTs); adverse events (AEs) included fatigue, hypotension, abdominal pain, dyspnea, and nausea."( Safety, pharmacokinetics, and pharmacodynamics of the DR5 antibody LBY135 alone and in combination with capecitabine in patients with advanced solid tumors.
Bilic, S; Burris, HA; de Vries, EG; Gietema, JA; Goldbrunner, M; Infante, JR; Oldenhuis, CN; Parker, K; Scott, JW; Sharma, S; Yang, L, 2014)		0.62
" Screening of patients for DPYD mutations prior to administration of 5-FU/capecitabine using new pharmacogenetic testing methods, may help for identify those patients who are at greatest risk for adverse effects, allowing a more individualized approach to their chemotherapy management."( Dihydropyrimidine dehydrogenase gene (DPYD) polymorphism among Caucasian and non-Caucasian patients with 5-FU- and capecitabine-related toxicity using full sequencing of DPYD.
Saif, MW, )		0.57
" The majority of drug-related adverse events were mild to moderate (grade 1 or 2); the most common adverse events reported were palmar-plantar erythrodysesthesia syndrome (76 %), diarrhea (67 %) and stomatitis (41 %)."( Efficacy, safety, pharmacokinetics and biomarker findings in patients with HER2-positive advanced or metastatic breast cancer treated with lapatinib in combination with capecitabine: results from 51 Japanese patients treated in a clinical study.
Ellis, CE; Fujii, H; Gagnon, RC; Iwata, H; Katsura, K; Masuda, N; Mukai, H; Nakamura, S; Nishimura, Y, 2015)		0.61
" The most common adverse effect was Grade 1 hand-foot syndrome, which was seen in 75% of patients."( Neo-adjuvant capecitabine chemotherapy in women with newly diagnosed locally advanced breast cancer in a resource-poor setting (Nigeria): efficacy and safety in a phase II feasibility study.
Abidoye, O; Adelusola, K; Adetiloye, AV; Agbakwuru, AE; Akinkuolie, AA; Arowolo, OA; Babalola, CP; Durosinmi, MA; Falusi, AG; Fleming, G; Im, HK; Kayode, AA; Lawal, OO; Njiaju, UO; Obajimi, M; Oduntan, H; Ogundiran, TO; Olopade, OC; Olopade, OI; Oluwasola, A, )		0.5
"The purpose of this study was to investigate the association between single nucleotide polymorphism (SNP) of CCND1 A870G and acute adverse events (AEs) in postoperative rectal cancer patients who received capecitabine-based postoperative chemoradiotherapy (CRT)."( [Impact of CCND1 A870G polymorphism on acute adverse events in postoperative rectal cancer patients treated with adjuvant concurrent chemoradiotherapy].
DU, ZL; Huang, Y; Jin, J; Li, YX; Lin, DX; Qiao, Y; Ren, H; Tan, W; Yu, DK, 2013)		0.58
"Cardiac toxicity an uncommon but serious side-effect of some fluoropyrimides."( Final results of Australasian Gastrointestinal Trials Group ARCTIC study: an audit of raltitrexed for patients with cardiac toxicity induced by fluoropyrimidines.
Ferry, D; Fournier, M; Gebski, V; Gordon, S; Karapetis, CS; Price, TJ; Ransom, D; Simes, RJ; Tebbutt, N; Wilson, K; Yip, D, 2014)		0.4
" Raltitrexed, alone or in combination with oxaliplatin or irinotecan, provides a safe option in terms of cardiac toxicity for such patients."( Final results of Australasian Gastrointestinal Trials Group ARCTIC study: an audit of raltitrexed for patients with cardiac toxicity induced by fluoropyrimidines.
Ferry, D; Fournier, M; Gebski, V; Gordon, S; Karapetis, CS; Price, TJ; Ransom, D; Simes, RJ; Tebbutt, N; Wilson, K; Yip, D, 2014)		0.4
" The clinical efficacy and bevacizumab-related adverse reactions were observed."( [Efficacy and safety of bevacizumab (BEV) plus chemotherapeutic agents in the treatment of metastatic colorectal cancer, mCRC].
Chen, Y; Cui, YH; Guo, X; Liu, TS; Yu, YY; Zhou, YH; Zhuang, RY, 2013)		0.39
" In the ixabepilone plus capecitabine arm, grade 3/4 hematologic adverse events (AEs) were similar in both subgroups except leukopenia and febrile neutropenia, which had a higher incidence in patients aged ≥ 65 years."( Efficacy and safety of ixabepilone plus capecitabine in elderly patients with anthracycline- and taxane-pretreated metastatic breast cancer.
Baselga, J; Bosserman, L; Gómez, H; Li, RK; Mukhopadhyay, P; Sparano, JA; Vahdat, LT; Valero, V; Vrdoljak, E, 2013)		0.96
" Grades 3-4 adverse events were uncommon; hematologic toxicity was infrequent (5%) and consistently mild in the phase of maintenance treatment."( Efficacy and safety of capecitabine as maintenance treatment after first-line chemotherapy using oxaliplatin and capecitabine in advanced gastric adenocarcinoma patients: a prospective observation.
Bai, L; Jin, Y; Li, YH; Luo, HY; Qiu, MZ; Ren, C; Wang, DS; Wang, FH; Wang, ZQ; Wei, XL; Xu, RH; Yang, DJ; Zhang, DS; Zhou, YX, 2014)		0.71
" Genetic biomarkers have been used to predict these adverse events, but their utility is uncertain."( Genetic markers of toxicity from capecitabine and other fluorouracil-based regimens: investigation in the QUASAR2 study, systematic review, and meta-analysis.
Afzal, S; Boige, V; Braun, M; Church, D; Domingo, E; Enghusen, H; Etienne-Grimaldi, MC; Garcia-Foncillas, J; Garmo, H; Glimelius, B; Gonzalez-Neira, A; Green, E; Gusella, M; Jensen, SA; Johnstone, E; Jones, A; Julier, P; Kerr, D; Kleibl, Z; Lacas, B; Laurent-Puig, P; Lecomte, T; Love, S; Martin, M; Martinez-Balibrea, E; McLeod, H; Midgley, R; Milano, G; Morel, A; Nicholson, G; Palles, C; Pignon, JP; Ribelles, N; Rosmarin, D; Sargent, D; Schwab, M; Scudder, C; Seymour, M; Sharma, R; Thompson, L; Tomlinson, I; Wadelius, M; Wang, H; Zanger, UM, 2014)		0.68
" The proportion reporting at least one adverse event (any grade) with C, G, V, and E was 45%, 65%, 75%, and 63%."( A comparison of toxicity and health care resource use between eribulin, capecitabine, gemcitabine, and vinorelbine in patients with metastatic breast cancer treated in a community oncology setting.
Beegle, N; Blau, S; Cox, D; Dranitsaris, G; Faria, C; Kalberer, T, 2015)		0.65
"5 grams (the permissible safe dose is 4 grams) due to the viral infection."( [Hepatotoxicity of acetaminophen in a patient treated with capecitabine due to breast cancer].
Drzymała, M; Golon, K; Karczmarek-Borowska, B, 2014)		0.65
" The most common drug-related adverse events were diarrhea (88%) and palmar-plantar erythrodysesthesia syndrome (48%)."( Safety and efficacy of neratinib in combination with capecitabine in patients with metastatic human epidermal growth factor receptor 2-positive breast cancer.
Baselga, J; Cortés, J; Garcia-Saenz, JA; Germa, C; Harb, W; Kiger, C; Kim, SB; Martin, M; Moroose, R; Pluard, T; Saura, C; Wang, K; Xu, B, 2014)		0.65
" Source data verification of adverse events was performed by two independent observers."( Safety, efficacy, and long-term follow-up evaluation of perioperative epirubicin, Cisplatin, and capecitabine chemotherapy in esophageal resection for adenocarcinoma.
Boonstra, JJ; Borel Rinkes, IH; Lolkema, MP; Los, M; Ruurda, JP; Schipper, ME; Siersema, PD; Ubink, I; van der Horst, S; van der Sluis, PC; van Hillegersberg, R; Voest, EE; Wiezer, MJ, 2015)		0.63
" Grades 3 and 4 nonhematologic adverse events of preoperative chemotherapy mainly consisted of thromboembolic events (16."( Safety, efficacy, and long-term follow-up evaluation of perioperative epirubicin, Cisplatin, and capecitabine chemotherapy in esophageal resection for adenocarcinoma.
Boonstra, JJ; Borel Rinkes, IH; Lolkema, MP; Los, M; Ruurda, JP; Schipper, ME; Siersema, PD; Ubink, I; van der Horst, S; van der Sluis, PC; van Hillegersberg, R; Voest, EE; Wiezer, MJ, 2015)		0.63
"For patients with adenocarcinoma of the esophagus or GEJ, six cycles of ECC-based perioperative chemotherapy is associated with a relatively high number of adverse events."( Safety, efficacy, and long-term follow-up evaluation of perioperative epirubicin, Cisplatin, and capecitabine chemotherapy in esophageal resection for adenocarcinoma.
Boonstra, JJ; Borel Rinkes, IH; Lolkema, MP; Los, M; Ruurda, JP; Schipper, ME; Siersema, PD; Ubink, I; van der Horst, S; van der Sluis, PC; van Hillegersberg, R; Voest, EE; Wiezer, MJ, 2015)		0.63
"To investigate the association between polymorphisms of DNA repair genes and xenobiotic with acute adverse effects in locally advanced rectal cancer patients treated with neoadjuvant radiochemotherapy."( Potential Role of Single Nucleotide Polymorphisms of XRCC1, XRCC3, and RAD51 in Predicting Acute Toxicity in Rectal Cancer Patients Treated With Preoperative Radiochemotherapy.
Agolli, L; Borro, M; Bracci, S; De Sanctis, V; Di Nardo, F; Enrici, RM; Falco, T; Gentile, G; Maglio, M; Minniti, G; Nicosia, L; Osti, MF; Simmaco, M; Valeriani, M, 2017)		0.46
" Currently, there is insufficient evidence to recommend an optimal approach for safe and effective alternative treatment for patients who experience 5-fluorouracil-induced cardiac adverse events."( Paradoxical effect of capecitabine in 5-fluorouracil-induced cardiotoxicity: A case vignette and literature review.
Mahipal, A; Markey, KR; Saneeymehri, SS, 2016)		0.75
" The objective of this study was to estimate the costs of managing treatment-related grade ≥ 3 adverse events (AEs) that occurred in ≥ 2% of patients and grade 2 AEs that occurred in ≥ 5% of patients taking T-DM1 compared with patients taking CAP + LAP based on the EMILIA trial, from the perspective of Canadian public payers."( Safety Profile and Costs of Related Adverse Events of Trastuzumab Emtansine for the Treatment of HER2-Positive Locally Advanced or Metastatic Breast Cancer Compared to Capecitabine Plus Lapatinib from the Perspective of the Canadian Health-Care System.
Moser, A; Piwko, C; Pollex, E; Prady, C; Yunger, S, 2015)		0.61
" A deficiency in it is associated with the occurrence of adverse events following fluoropyrimidine-based therapies."( Toxicity Associated with Capecitabine in Patients Suffering from Dihydropyrimidine Dehydrogenase Deficiency.
Alés-Díaz, I; Benavides-Orgaz, M; Bermejo-Pérez, MJ; Durán-Ogalla, G; Galeote-Miguel, AM; Rodelo-Haad, LE, 2014)		0.71
" There was no statistically significant difference in the rates of grade 3-4 adverse events (EOX 79."( Comparison of efficacy and safety of first-line palliative chemotherapy with EOX and mDCF regimens in patients with locally advanced inoperable or metastatic HER2-negative gastric or gastroesophageal junction adenocarcinoma: a randomized phase 3 trial.
Budzynski, A; Fijorek, K; Konopka, K; Krzemieniecki, K; Lazar, A; Matlok, M; Ochenduszko, S; Pedziwiatr, M; Puskulluoglu, M; Sinczak-Kuta, A; Urbanczyk, K, 2015)		0.42
" Outcomes were progression-free survival (PFS), overall survival (OS), overall response rate (ORR) and grades 3-4 drug-related adverse events."( Efficacy and safety of capecitabine-based first-line chemotherapy in advanced or metastatic breast cancer: a meta-analysis of randomised controlled trials.
Feng, X; Gao, S; Huang, L; Liu, G; Pei, G; Yin, W, 2015)		0.73
" Thirty-one patients (37 %) experienced grade 3/4 adverse events, the most common being hand-foot syndrome (9."( The efficacy and safety of capecitabine plus bevacizumab combination as first-line treatment in elderly metastatic colorectal cancer patients.
Aliustaoglu, M; Aydin, D; Ercelep, O; Gumus, M; Isik, D; Isik, S; Mert, AG; Odabas, H; Oven Ustaalioglu, BB; Oyman, A; Ozcelik, M; Surmeli, H; Yuksel, S, 2016)		0.73
" Unfortunately, it does not come without a cost, as the drug may have adverse effects - largely diarrhea, but also hand -foot syndrome and loss of fingerprints in extreme cases."( Forbidden to Drive -  a New Chemotherapy Side Effect.
De Lima, AS; Rovere, RK, 2015)		0.42
" Secondary endpoints were overall survival (OS) and major adverse events were monitored."( Efficacy and safety of capecitabine as maintenance therapy after capecitabine-based combination chemotherapy for patients with advanced esophagogastric junction adenocarcinoma.
Bao, LB; Hua, ZL; Lu, B; Qu, CP; Sun, Z; Wang, X, 2015)		0.73
" The capecitabine-related adverse events included leukopenia, anemia, and thrombocytopenia, hand-foot syndrome, nausea/vomiting, neuropathy, and liver dysfunction."( Efficacy and safety of capecitabine as maintenance therapy after capecitabine-based combination chemotherapy for patients with advanced esophagogastric junction adenocarcinoma.
Bao, LB; Hua, ZL; Lu, B; Qu, CP; Sun, Z; Wang, X, 2015)		1.24
"Our finding shows that single-agent capecitabine maintenance therapy was effective, well-tolerated and safe after first-line capecitabine-based combination chemotherapy in patients with advanced EGJ adenocarcinoma."( Efficacy and safety of capecitabine as maintenance therapy after capecitabine-based combination chemotherapy for patients with advanced esophagogastric junction adenocarcinoma.
Bao, LB; Hua, ZL; Lu, B; Qu, CP; Sun, Z; Wang, X, 2015)		1
" In terms of adverse events, the serious adverse events of grade 3 or higher seen among all patients were neutropenia in four patients, thrombocytopenia in one patient, and peripheral sensory neuropathy in seven patients."( Efficacy and Safety of Capecitabine and Oxaliplatin (CapOX) as an Adjuvant Therapy in Japanese for Stage II/III Colon Cancer in a Group at High Risk of Recurrence in Retrospective Study.
Handa, N; Minakata, K; Osawa, H, 2014)		0.71
" The most serious adverse event was leucopenia in one patient."( [Clinical efficacy and safety of trastuzumab plus capecitabine as first-line therapy for HER-2 positive metastatic breast cancer].
Bian, L; Jiang, Z; Li, W; Song, S; Wang, T; Zhang, H; Zhang, S; Zhou, J, 2015)		0.67
"Trastuzumab plus capecitabine is an effective and safe regimen as first-line treatment for HER-2-positive metastatic breast cancer patients whose cancer is resistant to treatment with anthracyclines and taxanes."( [Clinical efficacy and safety of trastuzumab plus capecitabine as first-line therapy for HER-2 positive metastatic breast cancer].
Bian, L; Jiang, Z; Li, W; Song, S; Wang, T; Zhang, H; Zhang, S; Zhou, J, 2015)		1.01
"Among 1463 patients included, 231 patients (16%) experienced early severe toxicity, 132 patients (9%) were hospitalised for toxicity, and 146 patients (10%) discontinued treatment for toxicity; in total, 321 patients (22%) experienced any early toxicity-related adverse outcome."( Renal function, body surface area, and age are associated with risk of early-onset fluoropyrimidine-associated toxicity in patients treated with capecitabine-based anticancer regimens in daily clinical care.
Beijnen, JH; Cats, A; Deenen, MJ; Huitema, ADR; Meulendijks, D; Schellens, JHM; van Hasselt, JGC; van Tinteren, H, 2016)		0.63
" In respect of adverse events, both the rates of hematological and non-hematological toxicities were low and similar between the two groups (P>0."( [Comparison of the efficacy and safety of capecitabine or tegafur, gimeracil and oteracil potassium capsules combined with oxaliplatin chemotherapy regimens in the treatment of advanced gastric cancer].
Hui, H; Sun, S; Wan, Y; Wang, X; Wu, J, 2016)		0.7
" In all, the most frequently reported adverse events were G1/2 gastrointestinal toxicity (68."( [Efficacy and toxicity of vinorelbine (NVB)-based regimens in patients with metastatic triple negative breast cancer (mTNBC) pretreated with anthracyclines and taxanes].
Cai, R; Du, F; Fan, Y; Li, Q; Luo, Y; Ma, F; Wang, J; Xu, B; Yuan, P; Zhang, P, 2015)		0.42
" Conclusions HT with daily IGRT is efficacious and safe in the treatment of anal canal cancer patients, and is considered in our department standard of care in this clinical setting."( Efficacy and safety of helical tomotherapy with daily image guidance in anal canal cancer patients.
Bouchaab, H; Bourhis, J; De Bari, B; Hanhloser, D; Jumeau, R; Matzinger, O; Mirimanoff, RO; Ozsahin, EM; Troussier, I; Vallet, V; Wagner, AD, 2016)		0.43
" This infusion rate is safe for use in routine practice."( Faster FOLFOX: Oxaliplatin Can Be Safely Infused at a Rate of 1 mg/m2/min.
Cercek, A; Kemeny, NE; Park, V; Reidy-Lagunes, D; Saltz, LB; Segal, NH; Stadler, ZK; Varghese, A; Yaeger, R, 2016)		0.43
" Commenced 15 years ago, PRRT is now becoming established as first- and second-line therapy for gastroentero pancreatic neuroendocrine tumors (GEPNETs), and early treatment minimizes myelotoxicity, which is the most significant potential adverse event following PRRT."( Myelotoxicity of Peptide Receptor Radionuclide Therapy of Neuroendocrine Tumors: A Decade of Experience.
Kesavan, M; Turner, JH, 2016)		0.43
" Despite the good tolerability, treatment-related adverse events still occur following metronomic protocols."( The TYMS-TSER polymorphism is associated with toxicity of low-dose capecitabine in patients with advanced gastrointestinal cancer.
Barucca, V; Botticelli, A; D'Antonio, C; Falcone, R; Gentile, G; Lionetto, L; Marchetti, P; Mazzuca, F; Medda, E; Milano, A; Onesti, CE; Roberto, M; Romiti, A; Simmaco, M, 2016)		0.67
" Uridine triacetate delivers high concentrations of uridine, which competes with toxic 5-FU metabolites."( Emergency use of uridine triacetate for the prevention and treatment of life-threatening 5-fluorouracil and capecitabine toxicity.
Bamat, MK; Cartwright, TH; El-Rayes, BF; Fakih, MG; King, TR; Ma, WW; Posey, JA; Saif, MW; von Borstel, RW, 2017)		0.67
" Adverse reactions in patients receiving uridine triacetate included vomiting (8."( Emergency use of uridine triacetate for the prevention and treatment of life-threatening 5-fluorouracil and capecitabine toxicity.
Bamat, MK; Cartwright, TH; El-Rayes, BF; Fakih, MG; King, TR; Ma, WW; Posey, JA; Saif, MW; von Borstel, RW, 2017)		0.67
"In these studies, uridine triacetate was a safe and effective lifesaving antidote for capecitabine and 5-FU overexposure, and it facilitated the rapid resumption of chemotherapy."( Emergency use of uridine triacetate for the prevention and treatment of life-threatening 5-fluorouracil and capecitabine toxicity.
Bamat, MK; Cartwright, TH; El-Rayes, BF; Fakih, MG; King, TR; Ma, WW; Posey, JA; Saif, MW; von Borstel, RW, 2017)		0.89
" Grade 1-2 adverse events occurred in 45."( Efficacy and safety of vinorelbine-capecitabine oral metronomic combination in elderly metastatic breast cancer patients: VICTOR-1 study.
Bidoli, P; Capici, S; Cazzaniga, ME; Cicchiello, F; Cortinovis, D; Digiacomo, N; Porcu, L; Riva, F; Torri, V, 2017)		0.73
" The primary endpoint was the incidence of selected grade 3-5 adverse events (AE) including: febrile neutropenia, infection, sensory/motor neuropathy, and mucositis."( SAKK 24/09: safety and tolerability of bevacizumab plus paclitaxel vs. bevacizumab plus metronomic cyclophosphamide and capecitabine as first-line therapy in patients with HER2-negative advanced stage breast cancer - a multicenter, randomized phase III tr
Anchisi, S; Bärtschi, D; Bernhard, J; Bigler, M; Borner, M; Cathomas, R; Hasler-Strub, U; Küng, M; Matter-Walstra, K; Müller, A; Na, KJ; Rauch, D; Rochlitz, C; Rordorf, T; Ruhstaller, T; Trojan, A; Vetter, M; von Moos, R; Wicki, A; Winterhalder, R; Zaman, K, 2016)		0.64
" A lethal toxicity in two DPD patients suggests that fluoropyrimidines combined with other therapies such as radiotherapy might be particularly toxic for DPD deficient patients."( Severe fluoropyrimidine toxicity due to novel and rare DPYD missense mutations, deletion and genomic amplification affecting DPD activity and mRNA splicing.
Dezentjé, V; Dobritzsch, D; Hennekam, RC; Hertz, JM; Jansen, RL; Knegt, LC; Los, M; Maurer, D; Meijer, J; Meinsma, R; van Huis-Tanja, LH; van Kampen, RJ; van Kuilenburg, AB; Zoetekouw, L, 2017)		0.46
" Adding bevacizumab to a CAPOX regimen in patients undergoing a resection for their CLM is safe and showed higher QoL scores compared with CAPOX alone."( Randomized Phase III Study to Assess Efficacy and Safety of Adjuvant CAPOX with or without Bevacizumab in Patients after Resection of Colorectal Liver Metastases: HEPATICA study.
Bergman, AM; Borel Rinkes, IH; Dalesio, O; Schouten, SB; Snoeren, N; Tollenaar, RA; van der Sijp, J; van Hillegersberg, R; van Werkhoven, E; Verheul, HM; Voest, EE, 2017)		0.46
" The most frequently reported grade 2 treatment-related adverse events were leukopenia and hand and foot syndrome."( Safety and efficacy study of metronomic vinorelbine, cyclophosphamide plus capecitabine in metastatic breast cancer: A phase II trial.
Cancello, G; Cardillo, A; Colleoni, M; Esposito, A; Goldhirsch, A; Iorfida, M; Lai, A; Maisonneuve, P; Mazza, M; Montagna, E; Munzone, E; Palazzo, A; Sciandivasci, A, 2017)		0.69
"An important concern with the anticancer drug capecitabine (Cp), an oral prodrug of 5-fluorouracil, are dose-limiting adverse effects, in particular hand-foot syndrome (HFS) and diarrhea."( Novel Genetic Variants in Carboxylesterase 1 Predict Severe Early-Onset Capecitabine-Related Toxicity.
Aebi, S; Amstutz, U; Hamzic, S; Joerger, M; Kummer, D; Largiader, CR; Milesi, S; Mueller, D, 2017)		0.95
" The data collected were: demographic variables (age, gender), diagnostic (breast cancer, colorectal cancer, gastric cancer, off-label), adherence (tablet count, Morisky test,Sackett test), safety (assessment of adverse events, clinical evaluation by the oncologist) and quality of life (performance status, SF-12 test)."( Adherence and safety study in patients on treatment with capecitabine.
Crespo-Diz, C; Fernández-Ribeiro, F; Olivera-Fernández, R, 2017)		0.7
" Adverse events: skin toxicity (33."( Adherence and safety study in patients on treatment with capecitabine.
Crespo-Diz, C; Fernández-Ribeiro, F; Olivera-Fernández, R, 2017)		0.7
"The frequency of capecitabine-related cardiotoxicity has been reported to be low but includes serious adverse events."( Incidence of capecitabine-related cardiotoxicity in different treatment schedules of metastatic colorectal cancer: A retrospective analysis of the CAIRO studies of the Dutch Colorectal Cancer Group.
Kok, WE; Koopman, M; Kwakman, JJ; Mol, L; Punt, CJ; Simkens, LH, 2017)		1.16
"Predicting individual risk of chemotherapy-induced severe adverse reaction is a critical issue when selecting the best treatment for cancer patients."( Identification of new SNPs associated with severe toxicity to capecitabine.
Blanco, C; García, MI; García-Alfonso, P; García-González, X; Grávalos, C; Iglesias, I; Longo, F; López-Fernández, LA; Martínez, V; Pachón, V; Pellicer, M; Robles, L; Sanjurjo, M, 2017)		0.7
" Cardiotoxicity is a recognized side effect of 5-FU, a closely related fluorinated pyrimidine antagonist."( Report of two cases of acute cardiac adverse events in patients with colorectal carcinoma receiving oral capecitabine.
Godwin, SA; Kosmas, C; Koulouris, E; Kyratlidis, K; Lampropoulos, S; Pavlidis, K; Roditis, P; Tzimou, M; Zafiris, A, 2017)		0.67
" During dose escalation, grade 2 dose-limiting toxic effects occurred in two patients; no grade 3-4 dose-limiting toxic effects were noted."( Safety and tolerability of veliparib combined with capecitabine plus radiotherapy in patients with locally advanced rectal cancer: a phase 1b study.
Czito, BG; DeLuca, A; Deming, DA; Dudley, MW; He, L; Holen, KD; Jameson, GS; Komarnitsky, P; Michael, M; Mittapalli, RK; Mulcahy, MF; Munasinghe, W; Ngan, SY; Vaghefi, H; Zalcberg, JR, 2017)		0.71
" Common grade 3 or higher adverse events included neutropenia (1 in XP, 3 in SP, and 2 in SOX), decreased appetite (1 in SP), and hypertension (2 in XP)."( Safety, pharmacokinetic, and clinical activity profiles of ramucirumab in combination with three platinum/fluoropyrimidine doublets in Japanese patients with chemotherapy-naïve metastatic gastric/gastroesophageal junction cancer.
Gritli, I; Inoue, K; Kadowaki, S; Muro, K; Nishina, T; Ozeki, A; Piao, Y; Sakai, D; Shitara, K; Yoshikawa, R, 2018)		0.48
"Exomes from eight capecitabine-treated patients with severe adverse reactions (grade >2), among a population of 319, were sequenced (Ion Proton)."( Use of exome sequencing to determine the full profile of genetic variants in the fluoropyrimidine pathway in colorectal cancer patients affected by severe toxicity.
Blanco, C; García, MI; García-Alfonso, P; García-González, X; Grávalos, C; Iglesias, I; Longo, F; López-Fernández, LA; Martínez, J; Martínez, V; Pachón, V; Pellicer, M; Robles, L; Rueda, D; Salvador, S; Sanjurjo, M, 2017)		0.79
" We calculated the incidence of "any-grade" and "severe" toxicity for haematological and non-haematological adverse events of each group."( A systematic review of the safety profile of the different combinations of fluoropyrimidines and oxaliplatin in the treatment of colorectal cancer patients.
Baratelli, C; Brizzi, MP; Di Maio, M; Scagliotti, GV; Sonetto, C; Tampellini, M; Zichi, C, 2018)		0.48
" Secondary endpoints were the incidence of adverse events (AEs) and the completion rate of study therapy."( Safety of mFOLFOX6/XELOX as adjuvant chemotherapy after curative resection of stage III colon cancer: phase II clinical study (The FACOS study).
Ishibashi, K; Ishida, H; Kato, H; Kato, R; Koda, K; Kosugi, C; Mori, M; Narushima, K; Oya, M; Shuto, K; Tanaka, S; Yoshimatsu, K, 2018)		0.48
"The aim of this study was to investigate the associations between single nucleotide polymorphisms (SNPs) in the seed regions of microRNAs and acute adverse events (AEs) and survival in patients with rectal cancer receiving postoperative chemoradiation therapy."( Associations of Genetic Variations in MicroRNA Seed Regions With Acute Adverse Events and Survival in Patients With Rectal Cancer Receiving Postoperative Chemoradiation Therapy.
Feng, T; Feng, Y; Huang, Y; Jin, J; Li, H; Li, Y; Lin, D; Liu, Y; Qiao, Y; Ren, H; Song, Y; Tan, W; Wang, S; Wang, W; Yang, J; Zhang, M, 2018)		0.48
"We report the case of a 61-year-old man who experienced severe adverse effects of capecitabine because of dihydropyrimidine dehydrogenase (DPD) deficiency."( [Dihydropyrimidine dehydrogenase deficiency causes severe adverse effects of capecitabine].
Andou, A; Bamba, H; Imai, T; Inoue, H; Komai, Y; Nakamura, T; Sato, Y; Shintani, S; Tanabe, H, )		0.59
" This review summarizes the current state of knowledge of FIC with special regard to proposed pathogenetic models (coronary vasospasm, endothelium and cardiomyocytes damage, toxic metabolites, dihydropyrimidine dehydrogenase deficiency); risk and predictive factors; efficacy and usefulness in detection of laboratory markers, electrocardiographic changes and cardiac imaging; and specific treatment, including a novel agent, uridine triacetate."( Fluoropyrimidine-induced cardiotoxicity.
Aglietta, M; Bonzano, A; Cagnazzo, C; Depetris, I; Filippi, R; Leone, F; Marino, D, 2018)		0.48
"The results of the present multicenter study have shown that if selected on clinical factors, nCRT with capecitabine is safe and well tolerated in elderly patients."( Tolerability, Safety, and Outcomes of Neoadjuvant Chemoradiotherapy With Capecitabine for Patients Aged ≥ 70 Years With Locally Advanced Rectal Cancer.
Bloemendal, H; Intven, M; Jacobs, L; Los, M; Siersema, PD; Smits, AB; Ten Bokkel Huinink, D; van der Vlies, E; van Lelyveld, N; Weusten, BLAM, 2018)		0.93
" The nurse found that the treatment was safe and acceptable in all cases."( Safety and feasibility of home-based chemotherapy.
Christiansen, AB; Larsen, FO; Nelausen, KM; Nielsen, DL; Rishøj, A, 2018)		0.48
"Our study demonstrates that home-based chemotherapy is feasible and safe and that it might be a valuable alternative to treatment at an outpatient clinic."( Safety and feasibility of home-based chemotherapy.
Christiansen, AB; Larsen, FO; Nelausen, KM; Nielsen, DL; Rishøj, A, 2018)		0.48
" Adverse events were reported during the treatment and up to 28 days of follow-up."( Cardiotoxicity of 5-fluorouracil and capecitabine in Chinese patients: a prospective study.
Chen, G; Dong, C; Li, W; Peng, J; Qiu, M; Wang, C; Wang, F; Wu, Q; Yu, H; Yuan, Y; Zhang, J; Zhang, M; Zhao, Q; Zhou, W; Zhu, B, 2018)		0.75
"The purpose of this study was to evaluate the adverse drug reactions (ADRs) and serious adverse events associated with capecitabine use in Korean patients by analyzing data from a comprehensive national database of adverse events."( Analysis of data on capecitabine-related adverse drug reactions from the Korean adverse event reporting system database.
Park, JY, 2018)		1.01
"Data from all reports concerning capecitabine (Anatomical Therapeutic Chemical code: L01BC06) generated between January 2011 and December 2014 were collected from the Korean Adverse Event Reporting System database (KAERS)."( Analysis of data on capecitabine-related adverse drug reactions from the Korean adverse event reporting system database.
Park, JY, 2018)		1.09
"6%) were classified as serious adverse events."( Analysis of data on capecitabine-related adverse drug reactions from the Korean adverse event reporting system database.
Park, JY, 2018)		0.8
" Associations of serious fluoropyrimidine adverse effects have focused on inherited deficiency of the catabolic enzyme, dihydropyrimidine dehydrogenase."( Preliminary Evidence for Enhanced Thymine Absorption: A Putative New Phenotype Associated With Fluoropyrimidine Toxicity in Cancer Patients.
Charles, BG; Cowley, D; Duley, JA; George, R; Harris, M; Helsby, N; Ni, M; Norris, RL; Shannon, C; Sheffield, L; van Kuilenburg, ABP, 2018)		0.48
" Adverse events were as expected."( Safety and Feasibility of Integrating Yttrium-90 Radioembolization With Capecitabine-Temozolomide for Grade 2 Liver-Dominant Metastatic Neuroendocrine Tumors.
Cengel, KA; Damjanov, N; Metz, DC; Soulen, MC; Teitelbaum, UR; van Houten, D, 2018)		0.71
"CapTemY90 is feasible and safe for grade 2 NETs."( Safety and Feasibility of Integrating Yttrium-90 Radioembolization With Capecitabine-Temozolomide for Grade 2 Liver-Dominant Metastatic Neuroendocrine Tumors.
Cengel, KA; Damjanov, N; Metz, DC; Soulen, MC; Teitelbaum, UR; van Houten, D, 2018)		0.71
"CAPTEM is effective and relatively safe for treating patients with advanced NENs."( Safety and efficacy of combining capecitabine and temozolomide (CAPTEM) to treat advanced neuroendocrine neoplasms: A meta-analysis.
Fu, W; Li, W; Lu, L; Lu, Y; Lv, W; Wang, J; Zhao, Z, 2018)		0.76
" Cardiotoxic adverse events (AEs) such as angina, ischemia, arrhythmias, and cardiomyopathy associated with 5-fluorouracil (5-FU) and capecitabine (CAPE) have been sparingly described in studies, primarily through case reports."( Fluoropyrimidine Cardiotoxicity: Time for a Contemporaneous Appraisal.
Brell, JM; Carver, JR; Denlinger, CS; Dimond, EP; Kircher, SM; Ky, B; O'Neill, A; Upshaw, JN; Wagner, LI, 2019)		0.72
" All studies collected cardiovascular AEs using the Common Terminology Criteria for Adverse Events version available at the time of the study."( Fluoropyrimidine Cardiotoxicity: Time for a Contemporaneous Appraisal.
Brell, JM; Carver, JR; Denlinger, CS; Dimond, EP; Kircher, SM; Ky, B; O'Neill, A; Upshaw, JN; Wagner, LI, 2019)		0.51
" Overall, grade 3 adverse events, such as leukopenia and neutropenia, were observed in two of three patients (66."( Safety of intraperitoneal paclitaxel combined with conventional chemotherapy for colorectal cancer with peritoneal carcinomatosis: a phase I trial.
Emoto, S; Hata, K; Hiyoshi, M; Ishihara, S; Ishimaru, K; Kaneko, M; Kawai, K; Muro, K; Murono, K; Nagata, H; Nishikawa, T; Nozawa, H; Otani, K; Sasaki, K; Shuno, Y; Tanaka, T, 2019)		0.51
"The adverse events of mFOLFOX6-bevacizumab or CapeOX-bevacizumab in combination with ip PTX were considered similar to those described in previous studies of oxaliplatin-based treatment alone."( Safety of intraperitoneal paclitaxel combined with conventional chemotherapy for colorectal cancer with peritoneal carcinomatosis: a phase I trial.
Emoto, S; Hata, K; Hiyoshi, M; Ishihara, S; Ishimaru, K; Kaneko, M; Kawai, K; Muro, K; Murono, K; Nagata, H; Nishikawa, T; Nozawa, H; Otani, K; Sasaki, K; Shuno, Y; Tanaka, T, 2019)		0.51
" FLOX did not cause any cardiovascular adverse events in any of the 10 patients."( Bolus 5-fluorouracil (5-FU) In Combination With Oxaliplatin Is Safe and Well Tolerated in Patients Who Experienced Coronary Vasospasm With Infusional 5-FU or Capecitabine.
Chakrabarti, S; Eiring, R; Finnes, H; Grothey, A; Halfdanarson, T; Hartgers, M; Lobo, R; Mitchell, J; Okano, A; Sara, J, 2019)		0.71
"Bolus 5-FU in combination with oxaliplatin is safe in patients who have experienced coronary vasospasm with infusional 5-FU or capecitabine."( Bolus 5-fluorouracil (5-FU) In Combination With Oxaliplatin Is Safe and Well Tolerated in Patients Who Experienced Coronary Vasospasm With Infusional 5-FU or Capecitabine.
Chakrabarti, S; Eiring, R; Finnes, H; Grothey, A; Halfdanarson, T; Hartgers, M; Lobo, R; Mitchell, J; Okano, A; Sara, J, 2019)		0.92
" S-1 monotherapy was relatively effective and safe in the treatment of advanced breast cancer in elderly patients."( Clinical efficacy and safety of S-1 monotherapy in the treatment of advanced breast cancer in elderly patients.
Cui, S; Sun, Y; Ye, M; You, D; Zhao, Q, 2018)		0.48
" No statistical differences were observed in treatment-related adverse events, hospital admissions, or further treatment lines between age groups."( Second-line treatment efficacy and toxicity in older vs. non-older patients with advanced gastric cancer: A multicentre real-world study.
Antonuzzo, L; Aprile, G; Avallone, A; Bordonaro, R; Cinieri, S; Di Donato, S; Fanotto, V; Fornaro, L; Gerratana, L; Giampieri, R; Leone, F; Melisi, D; Nichetti, F; Pellegrino, A; Rimassa, L; Rosati, G; Santini, D; Scartozzi, M; Silvestris, N; Stragliotto, S; Tomasello, G; Vasile, E, 2019)		0.51
" Incidence of adverse events was similar between age groups."( Second-line treatment efficacy and toxicity in older vs. non-older patients with advanced gastric cancer: A multicentre real-world study.
Antonuzzo, L; Aprile, G; Avallone, A; Bordonaro, R; Cinieri, S; Di Donato, S; Fanotto, V; Fornaro, L; Gerratana, L; Giampieri, R; Leone, F; Melisi, D; Nichetti, F; Pellegrino, A; Rimassa, L; Rosati, G; Santini, D; Scartozzi, M; Silvestris, N; Stragliotto, S; Tomasello, G; Vasile, E, 2019)		0.51
" Most frequent (>10%) grade 3/4 treatment-related adverse events were neutropenia (14."( Safety and efficacy of nivolumab in combination with S-1/capecitabine plus oxaliplatin in patients with previously untreated, unresectable, advanced, or recurrent gastric/gastroesophageal junction cancer: interim results of a randomized, phase II trial (A
Azuma, M; Boku, N; Chen, LT; Cho, H; Chung, HC; Fumita, S; Hara, H; Kang, WK; Kang, YK; Kato, K; Komatsu, Y; Lee, KW; Minashi, K; Ryu, MH; Tsuda, M; Yamaguchi, K, 2019)		0.76
" Grade 3 treatment-related adverse events (AE) occurred in 12 (42."( Safety, Efficacy, and Biomarker Analysis of Pyrotinib in Combination with Capecitabine in HER2-Positive Metastatic Breast Cancer Patients: A Phase I Clinical Trial.
Cai, R; Chen, S; Fan, Y; Guan, X; Lan, B; Li, Q; Luo, Y; Ma, F; Wang, J; Xing, P; Xu, B; Yi, Z; Yuan, P; Zhang, P; Zhang, Y; Zhong, D; Zhu, X; Zou, J, 2019)		0.74
"CAPTEM treatment can be an effective and safe treatment even after prolonged administration for patients with NENs of various sites and Ki67 labeling index, associated with significant favorable responses and PFS."( Activity and Safety of Standard and Prolonged Capecitabine/Temozolomide Administration in Patients with Advanced Neuroendocrine Neoplasms.
Alexandraki, KI; Angelousi, A; Chatzellis, E; Daskalakis, K; Gross, D; Grozinsky-Glasberg, S; Kaltsas, G; Kos-Kudła, B; Koumarianou, A; Maimon, O; Meirovitz, A; Tsoli, M; Wachuła, E, 2019)		0.77
"Cardiotoxicity is an important side effect in patients receiving chemotherapy and the application of anthracycline drugs for gastric cancer treatment is uncommon."( Incidence of and risk factors for cardiotoxicity after fluorouracil-based chemotherapy in locally advanced or metastatic gastric cancer patients.
Bai, Y; Gao, L; Jin, X; Wu, S, 2019)		0.51
"9%) in arm B experienced grade 3/4 adverse events related to bevacizumab; the most frequent were 2 anastomotic fistulas (both in arm A) and abscesses (1 in arm A and 2 in arm B)."( Efficacy and Safety of Two Neoadjuvant Strategies With Bevacizumab in MRI-Defined Locally Advanced T3 Resectable Rectal Cancer: Final Results of a Randomized, Noncomparative Phase 2 INOVA Study.
Adenis, A; André, T; Azria, D; Bachet, JB; Balosso, J; Ben Abdelghani, M; Borg, C; Boudghène, F; Conroy, T; Coudert, M; François, Y; Ghiringhelli, F; Ionescu-Goga, M; Lakkis, Z; Mantion, G; Mornex, F; Quero, L; Rio, E; Roullet, B; Spaëth, D; Tanang, A; Vendrely, V, 2019)		0.51
" Odds ratio and hazard ratio of available outcomes including objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS), overall survival (OS), and adverse events (AEs) were pooled for analysis."( Comparison of efficacy and safety of S-1 and capecitabine in patients with metastatic colorectal carcinoma: A systematic review and meta-analysis.
Chen, J; Wang, J; Xu, T, 2019)		0.77
"To analyze adverse reactions in patients with nonmetastatic colorectal cancer due to treatment with either innovative  or generic capecitabine and/or to the chemotherapeutic regimen  employed, to the capecitabine alone, or in combination with oxaliplatin  (XELOX)."( Capecitabine safety profile, innovative and generic adjuvant formulation of nonmetastatic colorectal cancer.
Barreda-Hernández, D; Fernández-Carballido, AM; Sánchez-Gundín, J; Torres-Suárez, AI, 2019)		2.16
" Concerning the capecitabine drug  administered, no statistically significant differences were found in  the studied adverse reactions."( Capecitabine safety profile, innovative and generic adjuvant formulation of nonmetastatic colorectal cancer.
Barreda-Hernández, D; Fernández-Carballido, AM; Sánchez-Gundín, J; Torres-Suárez, AI, 2019)		2.3
"Hand-foot syndrome (HFS) is the main side effect of capecitabine and affects the compression zones of the body such as the palms and soles, causing numbness, paresthesias, skin swelling or erythema, scaling, chapping, hard nodule-like blisters, and severe pain."( Loss of Fingerprints as a Side Effect of Capecitabine Therapy: Case Report and Literature Review.
Ban, L; Cui, X; Wang, D; Zhang, B; Zhang, X; Zhao, J, 2020)		1.07
" To spare patients from the toxic effects, without comprising the required efficacy, we evaluated the safety and efficacy of a modified XELOX (mXELOX) adjuvant chemotherapy regimen with 6 cycles of oxaliplatin and a full cycle of capecitabine."( Safety and efficacy of a modified XELOX adjuvant regimen for patients with operated stage III colon cancer: a Chinese single-center experience.
Li, W; Lin, J; Lu, Z; Pan, Z; Peng, J; Tang, J; Wen, Y; Wu, X; Zhang, R, 2019)		0.7
" Cases (n = 9) and noncases (n = 23) of severe (grade ≥ 3) gastrointestinal toxicity were defined based on Common Terminology Criteria for Adverse Events."( A case-control study to assess the ability of the thymine challenge test to predict patients with severe to life threatening fluoropyrimidine-induced gastrointestinal toxicity.
Barlow, P; Bonnet, C; Brenman, E; Burns, KE; Duley, J; Findlay, M; Helsby, NA; Jeong, SH; Porter, D; Sharples, K, 2020)		0.56
"Adjuvant capecitabine and oxaliplatin (CAPOX) is a standard treatment for resected colon cancer; however, in patients with moderate renal impairment, the incidence of CAPOX-related adverse events (AEs) and the rate of early discontinuation are higher than in patients with no or mild renal impairment."( Clinical impact of baseline renal function on safety and early discontinuation of adjuvant capecitabine plus oxaliplatin in elderly patients with resected colon cancer: a multicenter post-marketing surveillance study.
Imamura, CK; Matsumoto, S; Shimizu, A; Yamagiwa, C; Yamazaki, K; Yoshino, T, 2020)		1.2
" The secondary endpoints were chronic cumulative neurotoxicity (EORTC QLQ-CIPN20), time to grade 2 neurotoxicity (NCI-CTCAE or the oxaliplatin-specific neuropathy scale), acute neurotoxicity (analog scale), rates of dose reduction or withdrawal due to OIPN, 3-year disease-free survival (DFS) and adverse events."( Phase III randomized, placebo-controlled, double-blind study of monosialotetrahexosylganglioside for the prevention of oxaliplatin-induced peripheral neurotoxicity in stage II/III colorectal cancer.
Chen, G; Deng, YH; Ding, PR; Fan, WH; Feng, F; Jin, Y; Li, YH; Liang, HL; Lu, ZH; Peng, JW; Ren, C; Shi, SM; Wang, DS; Wang, F; Wang, FH; Wang, W; Wang, ZQ; Xie, CB; Xu, RH; Zhang, JW, 2020)		0.56
"During escalation, four dose-limiting toxicities were observed among 24 patients: skin rash (1) and failure to deliver 100% of Xelox because of treatment-associated grade III-IV adverse events (AEs) (3: diarrhoea and vomiting; vomiting; fatigue)."( Dual Erb B Inhibition in Oesophago-gastric Cancer (DEBIOC): A phase I dose escalating safety study and randomised dose expansion of AZD8931 in combination with oxaliplatin and capecitabine chemotherapy in patients with oesophagogastric adenocarcinoma.
Anthoney, DA; Collins, L; Eatock, M; Elhussein, L; Falk, S; Goff, M; Lord, SR; Love, S; Middleton, MR; Moschandreas, J; Thomas, A; Turkington, RC; Virdee, PS, 2020)		0.75
"SEMS followed by neoadjuvant chemotherapy prior to elective surgery appears to be safe and well tolerated in patients with obstructing left-sided colon cancer."( Efficacy and safety of self-expanding metallic stent placement followed by neoadjuvant chemotherapy and scheduled surgery for treatment of obstructing left-sided colonic cancer.
Han, JG; Wang, YB; Wang, ZJ; Wei, GH; Yi, BQ; Zeng, WG; Zhai, ZW; Zhao, BC, 2020)		0.56
" Neuropathy severity was assessed after eight courses of chemotherapy based on National Cancer Institute Common Terminology for Adverse Events (NCI-CTCAE) criteria neuropathy grading scale and also sensory and motor electrophysiological assessment was performed by a neurologist."( Protective effect of N-acetylcysteine on oxaliplatin-induced neurotoxicity in patients with colorectal and gastric cancers: A randomized, double blind, placebo-controlled, clinical trial.
Allahyari, A; Barri, A; Bondad, N; Boostani, R; Elyasi, S, 2020)		0.56
"10 ng/mL/106 cells/min) increased the risk of G3-4 adverse events (OR = 10."( 5-Fluorouracil degradation rate as a predictive biomarker of toxicity in breast cancer patients treated with capecitabine.
Botticelli, A; Cerbelli, B; Lionetto, L; Marchetti, P; Roberto, M; Scagnoli, S; Simmaco, M, 2020)		0.77
"Capecitabine-RT appears to be safe in the adjuvant treatment of breast cancer with comparable toxicity to RT alone."( Combining Adjuvant Radiotherapy With Capecitabine in Chemotherapy-resistant Breast Cancer: Feasibility, Safety, and Toxicity.
Abramson, VG; Ayala-Peacock, DN; Chakravarthy, AB; Mayer, IA; Rexer, BN; Sherry, AD, 2020)		2.27
"A few days after starting the first cycle of treatment with capecitabine, a 50-year-old female with metastatic breast cancer experienced serious adverse events consisting of severe hematological, gastrointestinal and neurological toxicity."( Posterior reversible encephalopathy syndrome: A rare neurotoxicity after capecitabine.
Amadori, E; Barone, D; Bartolini, G; Frassineti, GL; Monti, M; Ruscelli, S, 2020)		1.03
" Outcomes included objective response rate (ORR); 6-, 12-, and 18-month progression-free survival (PFS); 1-, 2-, and 3-year overall survival (OS); and adverse events."( The efficacy and safety of capecitabine-based versus S-1-based chemotherapy for metastatic or recurrent gastric cancer: a systematic review and meta-analysis of clinical randomized trials.
Feng, J; Feng, Z; He, X; Hou, X; Yan, P; Yang, K, 2020)		0.86
"001) in the S-1-based chemotherapy, and there was no statistically significant difference for other adverse events."( A meta-analysis of efficacy and safety of S-1 monotherapy or combination therapy as first-line treatment in metastatic colorectal cancer.
Cheng, GL; Dai, WP; Liu, XL; Wang, MM; Wang, Z; Ye, CY; Zang, YS; Zhang, GM; Zhou, WL, 2020)		0.56
" Data of overall survival (OS), progression-free survival (PFS), 1-year survival rate, objective response rate (ORR), disease control rate (DCR) and adverse events were extracted and meta-analyzed."( Efficacy and safety of gemcitabine plus capecitabine in the treatment of advanced or metastatic pancreatic cancer: a systematic review and meta-analysis.
Li, PC; Lin, GH; Wang, BC; Xiao, BY, 2020)		0.83
" The capecitabine MTD was identified as 700 mg/m2 in 11 patients with mBC and 6 patients with LA/mGC evaluable for dose-limiting toxic effects."( Efficacy and Safety of Trastuzumab Emtansine Plus Capecitabine vs Trastuzumab Emtansine Alone in Patients With Previously Treated ERBB2 (HER2)-Positive Metastatic Breast Cancer: A Phase 1 and Randomized Phase 2 Trial.
Allegrini, G; Aout, M; Cortés, J; De Laurentiis, M; Diéras, V; Gelmon, K; Irahara, N; Lohrisch, C; Lorenzen, S; Montemurro, F; Oravcová, E; Perez-Garcia, JM; Ricci, F; Riera-Knorrenschild, J; Sakaeva, D; Serpanchy, R; Šufliarský, J; Thuss-Patience, P; Vidal, M; Wohlfarth, C, 2020)		1.33
" The combination group reported more AEs, but with no unexpected toxic effects."( Efficacy and Safety of Trastuzumab Emtansine Plus Capecitabine vs Trastuzumab Emtansine Alone in Patients With Previously Treated ERBB2 (HER2)-Positive Metastatic Breast Cancer: A Phase 1 and Randomized Phase 2 Trial.
Allegrini, G; Aout, M; Cortés, J; De Laurentiis, M; Diéras, V; Gelmon, K; Irahara, N; Lohrisch, C; Lorenzen, S; Montemurro, F; Oravcová, E; Perez-Garcia, JM; Ricci, F; Riera-Knorrenschild, J; Sakaeva, D; Serpanchy, R; Šufliarský, J; Thuss-Patience, P; Vidal, M; Wohlfarth, C, 2020)		0.81
" No toxic death was observed."( Safety and Efficacy of Gemcitabine, Docetaxel, Capecitabine, Cisplatin as Second-line Therapy for Advanced Pancreatic Cancer After FOLFIRINOX.
Bengrine, L; Fumet, JD; Ghiringhelli, F; Granconato, L; Hennequin, A; Palmier, R; Vincent, J, 2020)		0.82
" A latent class analysis defined the unobserved latent constructs that can be predicted as symptom clusters, considering the intensity of four types of adverse events (AEs)."( Impact of adjuvant therapy toxicity on quality of life and emotional symptoms in patients with colon cancer: a latent class analysis.
Cacho Lavin, D; Calderón, C; Carmona-Bayonas, A; Gomez, D; Jimenez-Fonseca, P; Martinez Cabañez, R; Muñoz, MM, 2021)		0.62
" Progression-free survival (PFS), overall survival (OS), overall response rate (ORR), and grades 3-4 drug-related adverse events were the outcomes assessed."( Efficacy and Safety of Capecitabine Alone or in Combination in Advanced Metastatic Breast Cancer Patients Previously Treated with Anthracycline and Taxane: A Systematic Review and Meta-Analysis.
Abdi, A; Alsaloumi, L; Basgut, B; Shawagfeh, S, 2020)		0.87
" On the other hand, the incidence of non-hematological adverse events such as hand-foot syndrome and diarrhea was lower in capecitabine combination compared to capecitabine monotherapy."( Efficacy and Safety of Capecitabine Alone or in Combination in Advanced Metastatic Breast Cancer Patients Previously Treated with Anthracycline and Taxane: A Systematic Review and Meta-Analysis.
Abdi, A; Alsaloumi, L; Basgut, B; Shawagfeh, S, 2020)		1.08
" Non-hematological adverse effects such as hand-foot syndrome were fewer with a combination regimen."( Efficacy and Safety of Capecitabine Alone or in Combination in Advanced Metastatic Breast Cancer Patients Previously Treated with Anthracycline and Taxane: A Systematic Review and Meta-Analysis.
Abdi, A; Alsaloumi, L; Basgut, B; Shawagfeh, S, 2020)		0.87
" Although several biomarkers predicted different toxic effects, they cannot be considered as risk factors for severe toxicity."( Effect of DPYD, MTHFR, ABCB1, XRCC1, ERCC1 and GSTP1 on chemotherapy related toxicity in colorectal carcinoma.
Cañadas-Garre, M; Carrasco-Campos, MI; Pérez-Ramírez, C; Puerta-García, E; Segura-Pérez, A; Urbano-Pérez, D, 2020)		0.56
" We retrospectively investigated the tolerability and adverse events of ACT for rectal cancer in patients with diverting ileostomy."( Tolerability and Adverse Events of Adjuvant Chemotherapy for Rectal Cancer in Patients With Diverting Ileostomy.
Fukuda, R; Machida, E; Maemoto, R; Miyakura, Y; Rikiyama, T; Sakio, R; Suzuki, K; Takahashi, J; Tsujinaka, S, )		0.13
"Peripheral neurotoxicity (PN) is a frequent side effect of oxaliplatin treatment, and also is its dose-limiting toxicity."( Prevention of oxaliplatin-related neurotoxicity by ω-3 PUFAs: A double-blind randomized study of patients receiving oxaliplatin combined with capecitabine for colon cancer.
Chen, H; Lu, Y; Xu, C; Xu, L; Yao, Q; Yao, W; Zhang, L; Zhang, R; Zhang, X, 2020)		0.76
" Given regional differences in treatment practices and rates of adverse events (AEs), we investigated the impact of pretreatment DPYD genotyping on AEs in a Canadian context."( Impact of pretreatment dihydropyrimidine dehydrogenase genotype-guided fluoropyrimidine dosing on chemotherapy associated adverse events.
Choi, YH; Keller, D; Kim, RB; Legan, RM; Lenehan, J; Mailloux, J; Medwid, S; Nevison, S; Panuganty, V; Povitz, BL; Sarma, S; Schwarz, UI; Siebring, V; Teft, WA; Welch, S; Wigle, TJ; Winquist, E, 2021)		0.62
" The incidence of any adverse effects (45% vs."( Safety and Efficacy of 7 Days on/7 Days off Versus 14 Days on/7 Days off Schedules of Capecitabine in Patients with Metastatic Colorectal Cancer: A Retrospective Review.
Akce, M; Alese, O; Bryson, E; Davis, C; Draper, A; El-Rayes, B; Goyal, S; Hall, K; Patel, U; Sakach, E; Shaib, W; Szabo, S; Watson, M; Wu, C, 2021)		0.84
" Adverse events, costs, healthcare resource utilization, and cost impact for noncompletion were investigated."( Suboptimal Completion Rates, Adverse Events, Costs, Resource Utilization, and Cost Impact of Noncompletion in Oral Adjuvant Capecitabine-Based Chemotherapy in Patients With Early-Stage Colon Cancer.
Chu, E; Frohlich, MM; Wang, X, 2021)		0.83
" The nonchemotherapy costs are significantly higher in noncompleters than completers, highlighting the financial burden of managing adverse events and preexisting comorbidities, which may lead to early discontinuation of therapy."( Suboptimal Completion Rates, Adverse Events, Costs, Resource Utilization, and Cost Impact of Noncompletion in Oral Adjuvant Capecitabine-Based Chemotherapy in Patients With Early-Stage Colon Cancer.
Chu, E; Frohlich, MM; Wang, X, 2021)		0.83
" The most frequent adverse event in the neratinib arm was diarrhea, which was manageable with prophylactic treatment with loperamide."( The Clinical Efficacy and Safety of Neratinib in Combination with Capecitabine for the Treatment of Adult Patients with Advanced or Metastatic HER2-Positive Breast Cancer.
Chilà, G; Galizia, D; Geuna, E; Guarini, V; Montemurro, F, 2021)		0.86
"Our study revealed that there was no adverse pathologic or oncological outcome with the concurrent use of PPIs along with Cape-NACRT in the treatment of LARC."( Concomitant Use of Proton Pump Inhibitors With Capecitabine Based Neoadjuvant Chemoradiotherapy for Locally Advanced Rectal Cancer: Is it Safe?
Abraham, AG; Ghosh, S; Joseph, K; Mahfouz, M; Menon, A; Mulder, K; Nijjar, T; Paulson, K; Roa, W; Severin, D; Tankel, K; Thachuthara, JJ; Usmani, N; Warkentin, H, 2021)		0.88
" The efficacy, toxic and side effects, and quality of life of the two groups were observed."( Cisplatin combined with capecitabine-induced chemotherapy for local nasopharyngeal carcinoma can improve the quality of life and reduce toxic and side effects.
Gao, Y; Liu, Y; Liu, Z, 2021)		0.93
" The toxic and side effects of group B were lower than that of group A (p<0."( Cisplatin combined with capecitabine-induced chemotherapy for local nasopharyngeal carcinoma can improve the quality of life and reduce toxic and side effects.
Gao, Y; Liu, Y; Liu, Z, 2021)		0.93
"Cisplatin combined with capecitabine-induced chemotherapy for local NPC can improve the quality of life and reduce the toxic and side effects."( Cisplatin combined with capecitabine-induced chemotherapy for local nasopharyngeal carcinoma can improve the quality of life and reduce toxic and side effects.
Gao, Y; Liu, Y; Liu, Z, 2021)		1.24
" These individuals are then at considerably increased risk of severe to life-threatening adverse events."( Testing for dihydropyrimidine dehydrogenase deficiency in New Zealand to improve the safe use of 5-fluorouracil and capecitabine in cancer patients.
Burns, K; Findlay, M; Helsby, N; Porter, D; Strother, M, 2021)		0.83
"Cardiotoxicity is a severe side effect for colorectal cancer (CRC) patients undergoing fluoropyrimidine-based chemotherapy."( Using Machine Learning Approaches to Predict Short-Term Risk of Cardiotoxicity Among Patients with Colorectal Cancer After Starting Fluoropyrimidine-Based Chemotherapy.
Chen, L; Chou, C; Li, C; Ngorsuraches, S; Qian, J, 2022)		0.72
" It presents with a generally good toxicity profile and most of the adverse events can be managed effectively."( Capecitabine-associated enterocolitis: Narrative literature review of a rare adverse event and a case presentation.
Gomatou, G; Kanellis, G; Kotteas, EA; Lagou, S; Rapti, VE; Syrigos, NK; Trontzas, IP, 2023)		2.35
" From the clinical course, we suspected that the severe adverse effects were caused due to a deficiency of DPD."( [A Case of Colon Cancer with Suspected DPD Deficiency Causing Severe Adverse Effects following Adjuvant Chemotherapy with Capecitabine].
Aoki, H; Araki, H; Arata, T; Katsuda, K; Kimura, Y; Minagi, H; Nagahisa, S; Ogawa, T; Tanakaya, K; Taniguchi, F; Watanabe, M, 2021)		0.83
" The efficacy and adverse effects of maintenance treatment were compared between the two groups."( Efficacy and safety analysis of bevacizumab combined with capecitabine in the maintenance treatment of RAS-mutant metastatic colorectal cancer.
Cha, Y; Huang, W; Tian, Y; Xiong, H; Yuan, X; Zhang, H, 2022)		0.97
" Both groups tolerated the toxic side effects."( Efficacy and safety analysis of bevacizumab combined with capecitabine in the maintenance treatment of RAS-mutant metastatic colorectal cancer.
Cha, Y; Huang, W; Tian, Y; Xiong, H; Yuan, X; Zhang, H, 2022)		0.97
"To evaluate the efficacy and safety of bevacizumab combined with chemotherapy in the treatment of advanced colorectal cancer and the effect on its adverse reactions, 100 patients with advanced colorectal cancer admitted to our hospital from March 2019 to March 2021 were identified as study subjects and were randomly divided into a control group and an experimental group, with 50 cases in each group."( Efficacy and safety of bevacizumab combined with chemotherapy in the treatment of advanced colorectal cancer and the effect on its adverse reactions.
Liu, Y; Su, X; Sun, L; Wang, X; Wang, Z; Yang, Y; Zhou, W, 2022)		0.72
" Other S-1-related adverse events were limited to grade 1-2."( Long-Term Safety Data on S-1 Administered After Previous Intolerance to Capecitabine-Containing Systemic Treatment for Metastatic Colorectal Cancer.
Kwakman, JJM; Mol, L; Punt, CJA, 2022)		0.95
"Chemotherapy-induced adverse effects (CIAEs) remain a challenging problem due to their high incidences and negative impacts on treatment in Chinese colorectal cancer (CRC) patients."( Milk and Egg Are Risk Factors for Adverse Effects of Capecitabine-Based Chemotherapy in Chinese Colorectal Cancer Patients.
Chen, J; Chen, X; Gao, Q; Li, M; Li, W; Lin, Z; Liu, X; Wei, H; Xing, J; Xu, J; Yao, H; Ye, Z; Zhai, J; Zhang, J; Zhang, R, )		0.38
"Switching to S-1-based therapy is safe and feasible after development of cardiotoxicity on 5-FU- or capecitabine-based therapy and allows patients to continue their pivotal fluoropyrimidine-based treatment."( Continuation of fluoropyrimidine treatment with S-1 after cardiotoxicity on capecitabine- or 5-fluorouracil-based therapy in patients with solid tumours: a multicentre retrospective observational cohort study.
Ålgars, A; Bärlund, M; Flygare, P; Frödin, JE; Glimelius, B; Hagman, H; Halonen, P; Heervä, E; Kallio, R; Kinos, S; Kwakman, JJM; Liposits, G; McDermott, R; O'Reilly, M; Osterlund, P; Pfeiffer, P; Punt, CJA; Ristamäki, R; Röckert, R; Salminen, T; Shah, CH; Sorbye, H; Soveri, LM; Teske, AJ; van Werkhoven, E, 2022)		1.17
" The adverse events were also analyzed."( Safety and efficacy of irinotecan, oxaliplatin, and capecitabine (XELOXIRI) regimen with or without targeted drugs in patients with metastatic colorectal cancer: a retrospective cohort study.
Gao, L; Liu, X; Ma, X; Ou, K; Wang, Q; Yang, L; Zhang, H, 2022)		0.97
" The incidence of any grade of adverse events (AEs) was 96."( Safety and efficacy of irinotecan, oxaliplatin, and capecitabine (XELOXIRI) regimen with or without targeted drugs in patients with metastatic colorectal cancer: a retrospective cohort study.
Gao, L; Liu, X; Ma, X; Ou, K; Wang, Q; Yang, L; Zhang, H, 2022)		0.97
"Capecitabine-related neurotoxicity is an uncommon cause of toxic encephalopathy, with a predilection for females."( Capecitabine related neurotoxicity: Clinical and radiologic features.
Gao, JL; Ong, CS; Tan, YJ, 2022)		3.61
" Finally, the safety of adjuvant chemotherapy was evaluated based on the incidence of grade 1-4 adverse events."( Efficacy and safety of adjuvant chemotherapy in T1N0M0 intrahepatic cholangiocarcinoma after radical resection.
Li, XH; Lin, XJ; Zhao, CY; Zhou, EL, 2022)		0.72
" In terms of safety, the incidence of grade 3 or 4 adverse reactions was < 18."( Efficacy and safety of adjuvant chemotherapy in T1N0M0 intrahepatic cholangiocarcinoma after radical resection.
Li, XH; Lin, XJ; Zhao, CY; Zhou, EL, 2022)		0.72
"Generic oxaliplatin is widely used in colorectal cancer chemotherapy; however, studies on the adverse events of generic drugs are limited."( [A Study of the Safety of Chemotherapy with Generic Oxaliplatin for the Treatment of Colorectal Cancer].
Fujita, Y; Fujiyama, J; Fukunaga, T; Tada, H; Tani, N; Watanabe, N, 2023)		0.91
"There were no statistically significant differences between generic and brand-name oxaliplatin in the frequency of adverse events."( [A Study of the Safety of Chemotherapy with Generic Oxaliplatin for the Treatment of Colorectal Cancer].
Fujita, Y; Fujiyama, J; Fukunaga, T; Tada, H; Tani, N; Watanabe, N, 2023)		0.91
" Approximately 56% (14 patients) had at least one Adverse Event (AE) of any grade."( Efficacy and safety of anlotinib-based chemotherapy for locally advanced or metastatic anaplastic thyroid carcinoma.
Liu, J; Pan, X; Tang, W; Wang, J; Wang, S; Ye, T; Zheng, X, 2023)		0.91
"Anlotinib-based chemotherapy as first-line therapy is a safe and effective intervention for the treatment of LA/M ATC patients."( Efficacy and safety of anlotinib-based chemotherapy for locally advanced or metastatic anaplastic thyroid carcinoma.
Liu, J; Pan, X; Tang, W; Wang, J; Wang, S; Ye, T; Zheng, X, 2023)		0.91
" Treatment-related adverse events (TRAEs) occurred more frequently in group A vs."( A Phase 3 Randomized Clinical Trial to Compare Efficacy and Safety between Combination Therapy and Monotherapy in Elderly Patients with Advanced Gastric Cancer (KCSG ST13-10).
Choi, IS; Han, HS; Kim, JW; Kim, KH; Kim, MJ; Ko, YH; Koh, SA; Koo, DH; Lee, KW; Lee, SS; Nam, BH; Park, JH; Ryu, MH; Sohn, BS; Zang, DY, 2023)		0.91
" Sixty-four patients (41%) treated with INCT-CRT and 57 CRT-CNCT patients (34%) experienced a grade 3+ adverse event (P = ."( Compliance and Toxicity of Total Neoadjuvant Therapy for Rectal Cancer: A Secondary Analysis of the OPRA Trial.
Garcia-Aguilar, J; Kim, JK; Lin, ST; Omer, DM; Qin, LX; Saltz, LB; Thompson, HM; Valdivieso, SC; Verheij, FS; Wu, AJ; Yuval, JB, 2024)		1.44
" No difference in adverse events was observed between groups."( Compliance and Toxicity of Total Neoadjuvant Therapy for Rectal Cancer: A Secondary Analysis of the OPRA Trial.
Garcia-Aguilar, J; Kim, JK; Lin, ST; Omer, DM; Qin, LX; Saltz, LB; Thompson, HM; Valdivieso, SC; Verheij, FS; Wu, AJ; Yuval, JB, 2024)		1.44
" The most frequent treatment-related adverse events included hand-foot syndrome, diarrhea, vomiting and nausea."( Safety and efficacy study of oral metronomic capecitabine combined with pyrotinib in HER2-positive metastatic breast cancer: A phase II trial.
Fan, Y; He, M; Lan, B; Li, Q; Liu, J; Luo, Y; Ma, F; Mo, H; Wang, J; Wang, Z; Xu, B; Yuan, P; Zhang, P, 2023)		1.17
" Adverse events, disease-free survival (DFS), and overall survival (OS) were observed."( Clinical efficacy and safety of adjuvant immunotherapy (Tislelizumab) plus chemotherapy vs. adjuvant chemotherapy alone in lymph node-positive patients with gastric cancer after D2 radical resection: a prospective, 2-arm, phase II study.
Shi, JW; Wu, S; Zhou, Y, 2023)		0.91
" The majority of adverse events in both groups were grade 1-2, with only hypothyroidism showing a significant difference (p=0."( Clinical efficacy and safety of adjuvant immunotherapy (Tislelizumab) plus chemotherapy vs. adjuvant chemotherapy alone in lymph node-positive patients with gastric cancer after D2 radical resection: a prospective, 2-arm, phase II study.
Shi, JW; Wu, S; Zhou, Y, 2023)		0.91
" Moreover, patients were able to tolerate the accompanying adverse effects, which were deemed safe."( Clinical efficacy and safety of adjuvant immunotherapy (Tislelizumab) plus chemotherapy vs. adjuvant chemotherapy alone in lymph node-positive patients with gastric cancer after D2 radical resection: a prospective, 2-arm, phase II study.
Shi, JW; Wu, S; Zhou, Y, 2023)		0.91

Pharmacokinetics

The study was to determine the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of the combination of weekly oxaliplatin x 4, weekly irinotecan x 4 and capecitabine.

ExcerptReferenceRelevance
" Intake of food prior to the administration of capecitabine resulted in pharmacokinetic changes of all compounds involved."( Effect of food on the pharmacokinetics of capecitabine and its metabolites following oral administration in cancer patients.
Allman, D; Banken, L; Cassidy, J; Dirix, L; Osterwalder, B; Reigner, B; Roos, B; Twelves, C; Utoh, M; Verweij, J; Weidekamm, E, 1998)		0.82
" Unexpectedly, moderate increases in the Cmax and AUC0-infinity values obtained for capecitabine and 5'-deoxy-5-fluorocytidine were observed when Maalox was given together with capecitabine."( Influence of the antacid Maalox on the pharmacokinetics of capecitabine in cancer patients.
Banken, L; Cassidy, J; Clive, S; Goggin, T; Jodrell, D; Mulligan, T; Reigner, B; Roos, B; Schulz, R; Utoh, M; Weidekamm, E, 1999)		0.77
" In summary, mild to moderate hepatic dysfunction had no clinically significant influence on the pharmacokinetic parameters of capecitabine and its metabolites."( Effect of hepatic dysfunction due to liver metastases on the pharmacokinetics of capecitabine and its metabolites.
Banken, L; Cassidy, J; Glynne-Jones, R; Goggin, T; Reigner, B; Roos, B; Schüller, J; Twelves, C; Utoh, M; Weidekamm, E, 1999)		0.74
"Based on the primary pharmacokinetic parameter, AUC(0-infinity) of 5'-DFUR, equivalence was concluded for the two formulations, since the 90% confidence interval of the estimate of formulation B relative to formulation A of 97% to 107% was within the acceptance region 80% to 125%."( Bioequivalence of two tablet formulations of capecitabine and exploration of age, gender, body surface area, and creatinine clearance as factors influencing systemic exposure in cancer patients.
Banken, L; Bush, E; Cameron, D; Cassidy, J; Goggin, T; Jodrell, D; Jones, D; O'Byrne, K; Reigner, B; Roos, B; Steward, W; Twelves, C; Weidekamm, E, 1999)		0.56
"An excretion balance and pharmacokinetic study was conducted in cancer patients with solid tumors who received a single oral dose of capecitabine of 2000 mg including 50 microCi of 14C-radiolabelled capecitabine."( A human capecitabine excretion balance and pharmacokinetic study after administration of a single oral dose of 14C-labelled drug.
Aherne, W; Beale, PJ; Bush, E; Crompton, T; Jones, D; Judson, IR; Reigner, B; Trigo, JM, 1999)		0.94
"To evaluate the feasibility of administering the oral fluoropyrimidine capecitabine in combination with paclitaxel, to characterize the principal toxicities of the combination, to recommend doses for subsequent disease-directed studies, and to determine whether significant pharmacokinetic interactions occur between these agents when combined."( Phase I and pharmacokinetic study of the oral fluoropyrimidine capecitabine in combination with paclitaxel in patients with advanced solid malignancies.
Burger, HU; Burris, HA; Drengler, RL; Eckhardt, SG; Griffin, T; Kraynak, M; Moczygemba, J; Reigner, B; Rodrigues, G; Rowinsky, EK; Villalona-Calero, MA; Von Hoff, DD; Weiss, GR, 1999)		0.78
" Pharmacokinetic studies indicated that capecitabine and paclitaxel did not affect the pharmacokinetic behavior of each other."( Phase I and pharmacokinetic study of the oral fluoropyrimidine capecitabine in combination with paclitaxel in patients with advanced solid malignancies.
Burger, HU; Burris, HA; Drengler, RL; Eckhardt, SG; Griffin, T; Kraynak, M; Moczygemba, J; Reigner, B; Rodrigues, G; Rowinsky, EK; Villalona-Calero, MA; Von Hoff, DD; Weiss, GR, 1999)		0.81
" Favorable preclinical mechanistic interactions between capecitabine and paclitaxel, as well as an acceptable toxicity profile without clinically relevant pharmacokinetic interactions, support the performance of disease-directed evaluations of this combination."( Phase I and pharmacokinetic study of the oral fluoropyrimidine capecitabine in combination with paclitaxel in patients with advanced solid malignancies.
Burger, HU; Burris, HA; Drengler, RL; Eckhardt, SG; Griffin, T; Kraynak, M; Moczygemba, J; Reigner, B; Rodrigues, G; Rowinsky, EK; Villalona-Calero, MA; Von Hoff, DD; Weiss, GR, 1999)		0.79
" This phase I study was performed to determine the maximum tolerated dose (MTD) and side-effects of the combination, and to establish whether there is any pharmacokinetic interaction between the two compounds."( A phase I and pharmacokinetic study of the combination of capecitabine and docetaxel in patients with advanced solid tumours.
Gordon, RJ; Osterwalder, B; Planting, AS; Pronk, LC; Reigner, B; Sparreboom, A; Twelves, C; Vasey, P; Verweij, J, 2000)		0.55
" After oral administration of 1250 mg/m2, capecitabine is rapidly and extensively absorbed from the gastrointestinal tract [with a time to reach peak concentration (tmax) of 2 hours and peak plasma drug concentration (Cmax) of 3 to 4 mg/L] and has a relatively short elimination half-life (t(1/2)) [0."( Clinical pharmacokinetics of capecitabine.
Blesch, K; Reigner, B; Weidekamm, E, 2001)		0.87
"The enzyme kinetic parameters for each of the four enzymes involved in the activation of capecitabine to 5-FU and its elimination were measured experimentally in vitro to construct a physiologically based pharmacokinetic model."( A physiologically based pharmacokinetic analysis of capecitabine, a triple prodrug of 5-FU, in humans: the mechanism for tumor-selective accumulation of 5-FU.
Horii, I; Ishitsuka, H; Kato, Y; Kusuhara, H; Sugiyama, Y; Tsukamoto, Y; Ura, M, 2001)		0.78
" A physiologically based pharmacokinetic (PBPK) model integrating the activation process of capecitabine to 5-FU and 5-FU elimination was constructed to describe the concentration/time profiles of capecitabine and its three metabolites, including 5-FU, in blood and organs."( Investigation of 5-FU disposition after oral administration of capecitabine, a triple-prodrug of 5-FU, using a physiologically based pharmacokinetic model in a human cancer xenograft model: comparison of the simulated 5-FU exposures in the tumour tissue b
Horii, I; Ishikawa, T; Ishitsuka, H; Kato, Y; Sugiyama, Y; Tsukamoto, Y; Ura, M, 2001)		0.77
" Pharmacokinetic parameters of capecitabine and its metabolites (5'-deoxy-5-fluorouridine, 5-fluorouracil and alpha-fluoro-beta-alanine) were similar to those reported by other authors."( Phase I trial of capecitabine in combination with interferon alpha in patients with metastatic renal cancer: toxicity and pharmacokinetics.
Budd, GT; Bukowski, R; Chang, DZ; Ganapathi, R; Olencki, T; Osterwalder, B; Peereboom, D, 2001)		0.94
"The primary pharmacokinetic parameter with respect to the effect of renal dysfunction was systemic exposure to 5'-DFUR, 5-FU and FBAL determined on study day 14."( Effect of renal impairment on the pharmacokinetics and tolerability of capecitabine (Xeloda) in cancer patients.
Banken, L; Cassidy, J; Gardiner, J; Harper, P; Johnston, P; Monkhouse, J; Poole, C; Reigner, B; Twelves, C; Weidekamm, E, 2002)		0.55
" Additional data from the clinical safety database and pharmacokinetic results from the present study support the recommendation that patients with moderate renal impairment should be treated with 75% of the recommended standard starting dose to achieve systemic exposure comparable to that in patients with normal renal function."( Effect of renal impairment on the pharmacokinetics and tolerability of capecitabine (Xeloda) in cancer patients.
Banken, L; Cassidy, J; Gardiner, J; Harper, P; Johnston, P; Monkhouse, J; Poole, C; Reigner, B; Twelves, C; Weidekamm, E, 2002)		0.55
" Therefore, a multi-response population pharmacokinetic (PK) model for the description of plasma concentrations of 5'-DFUR, 5-FU and FBAL following oral administration of capecitabine was developed using NONMEM."( Population pharmacokinetic analysis of the major metabolites of capecitabine.
Blesch, KS; Gieschke, R; Reigner, B; Steimer, JL, 2002)		0.75
" Systemic exposure based on plasma concentrations of capecitabine and its metabolites was determined using individual parameter estimates derived from a population pharmacokinetic model constructed for this purpose in NONMEM."( Population pharmacokinetics and concentration-effect relationships of capecitabine metabolites in colorectal cancer patients.
Blesch, KS; Burger, HU; Gieschke, R; Reigner, B; Steimer, JL, 2003)		0.8
" The primary pharmacokinetic parameter was AUC(0-infinity ) of 5'-deoxy-5-fluorouridine (5'-DFUR) on day 14."( Pharmacokinetics of capecitabine (Xeloda) in Japanese and Caucasian patients with breast cancer.
Bridgewater, J; Grange, S; Kimura, M; Kuranami, M; Lucraft, H; McAleer, J; Monkhouse, J; Poole, C; Reigner, B; Saeki, T; Sasaki, Y; Schüller, J; Watanabe, T; Weidekamm, E; Yorulmaz, C, 2003)		0.64
" However, these types of studies generally do not answer important questions about variability in specific factors that predict pharmacokinetic and pharmacodynamic (PKPD) activity, in turn affecting safety and efficacy."( Clinical pharmacokinetic/pharmacodynamic and physiologically based pharmacokinetic modeling in new drug development: the capecitabine experience.
Blesch, KS; Burger, HU; Gieschke, R; Reigner, BG; Steimer, JL; Tsukamoto, Y, 2003)		0.53
" Pharmacokinetic investigations concerned plasma measurement of unchanged capecitabine, 5'-deoxy-5-fluorocytidine, 5'-doxifluridine and 5-FU using an optimized high performance liquid chromatography method, and cisplatin measurement in plasma using a limited sampling procedure."( Phase I and pharmacokinetic study of the association of capecitabine-cisplatin in head and neck cancer patients.
Chamorey, E; Giroux, B; Guardiola, E; Magné, N; Milano, G; Mouri, Z; Otto, J; Pivot, X; Schneider, M; Thyss, A, 2003)		0.8
" This study assessed the tolerance to Ro 09-4889 treatment, and related pharmacokinetic and pharmacodynamic data such as inhibition of DPD activity in peripheral blood mononuclear cells (PBMCs) and plasma uracil levels."( Single ascending dose tolerability, pharmacokinetic-pharmacodynamic study of dihydropyrimidine dehydrogenase inhibitor Ro 09-4889.
Banken, L; Bellibas, SE; Brivet, B; Bush, ED; Chamorey, E; Kircher, C; Milano, G; Nave, S; Patel, I; Renée, N, 2004)		0.32
"The main purpose of the present review article was to shed light on the different 5-fluorouracil (5-FU) prodrugs by underlining their respective pharmacological features in terms of metabolic activation, dihydropyrimidine dehydrogenase inhibition, pharmacokinetic profile and biomodulation ability."( Comparative pharmacology of oral fluoropyrimidines: a focus on pharmacokinetics, pharmacodynamics and pharmacomodulation.
Ferrero, JM; François, E; Milano, G, 2004)		0.32
" Pharmacokinetic analysis showed that there was no interaction between oral irinotecan and capecitabine, and that body-surface area was not significantly contributing to the observed pharmacokinetic variability."( Phase I and pharmacokinetic study of oral irinotecan given once daily for 5 days every 3 weeks in combination with capecitabine in patients with solid tumors.
Assadourian, S; deJonge, MJ; Dumez, H; Eskens, FA; Sanderink, GJ; Selleslach, J; Semiond, D; Soepenberg, O; Sparreboom, A; ter Steeg, J; van Oosterom, AT; Verweij, J, 2005)		0.76
" The current study, undertaken in 27 patients with gastrointestinal tumours, aimed to assess the toxicity and potential for significant pharmacokinetic interactions of a combination regimen incorporating capecitabine with 3-weekly irinotecan (XELIRI)."( A phase I clinical and pharmacokinetic study of capecitabine (Xeloda) and irinotecan combination therapy (XELIRI) in patients with metastatic gastrointestinal tumours.
Bertheault-Cvitkovic, F; Bugat, R; Canal, P; Chatelut, E; Cornen, X; Delord, JP; Dieras, V; Guimbaud, R; Lochon, I; Lokiec, F; Mery-Mignard, D; Mouri, Z; Pierga, JY; Turpin, FL, 2005)		0.77
" However, this is typically impossible due to pharmacokinetic constraints."( The mathematical modelling of adjuvant chemotherapy scheduling: incorporating the effects of protocol rest phases and pharmacokinetics.
Gaffney, EA, 2005)		0.33
" Following treatment with 5'-DFUR, the median AUC and Cmax of 5'-DFUR tended to be higher in patients with a partial response (3."( Pharmacokinetic and pharmacodynamic comparison of fluoropyrimidine derivatives, capecitabine and 5'-deoxy-5-fluorouridine (5'-DFUR).
Ebi, H; Igarashi, T; Kawada, K; Minami, H; Saeki, T; Sasaki, Y; Sigeoka, Y; Ueda, R; Usubuchi, N, 2005)		0.56
" In conclusion, the LC-MS method developed is simple, highly selective and sensitive and permits pharmacodynamic studies of TS inhibitors in several species."( Rapid quantitation of plasma 2'-deoxyuridine by high-performance liquid chromatography/atmospheric pressure chemical ionization mass spectrometry and its application to pharmacodynamic studies in cancer patients.
Clarke, SJ; Li, KM; Rivory, LP, 2005)		0.33
" In addition, we aimed to explore the pharmacokinetic parameters of irinotecan and capecitabine when used in different sequences of administration, with irinotecan infusion either prior to or after the first intake of capecitabine."( A phase I/II and pharmacokinetic study of irinotecan in combination with capecitabine as first-line therapy for advanced colorectal cancer.
Bakker, JM; Falk, S; Groenewegen, G; Kerr, DJ; Maughan, T; Nortier, JW; Punt, CJ; Rea, DW; Richel, DJ; Semiond, D; Smit, JM; Steven, N; Ten Bokkel Huinink, WW, 2005)		0.79
" Pharmacokinetic analysis was performed in patients treated at the recommended dose in two cohorts of patients in which the sequence of the first administration of each drug was reversed."( A phase I/II and pharmacokinetic study of irinotecan in combination with capecitabine as first-line therapy for advanced colorectal cancer.
Bakker, JM; Falk, S; Groenewegen, G; Kerr, DJ; Maughan, T; Nortier, JW; Punt, CJ; Rea, DW; Richel, DJ; Semiond, D; Smit, JM; Steven, N; Ten Bokkel Huinink, WW, 2005)		0.56
" The pharmacokinetic data suggest that the sequence of administration does not impact significantly on the metabolism of the two drugs."( A phase I/II and pharmacokinetic study of irinotecan in combination with capecitabine as first-line therapy for advanced colorectal cancer.
Bakker, JM; Falk, S; Groenewegen, G; Kerr, DJ; Maughan, T; Nortier, JW; Punt, CJ; Rea, DW; Richel, DJ; Semiond, D; Smit, JM; Steven, N; Ten Bokkel Huinink, WW, 2005)		0.56
"During capecitabine treatment, the area under the plasma concentration time curve from 0 to infinity (AUC(0-infinity)) of S-warfarin increased by 57% (90% CI, 32% to 88%) with a 51% prolongation of the elimination half-life (t(1/2); 90% CI, 32% to 74%)."( Significant effect of capecitabine on the pharmacokinetics and pharmacodynamics of warfarin in patients with cancer.
Abt, M; Camidge, R; Cassidy, J; Grange, S; Jodrell, D; Reigner, B; Weidekamm, E, 2005)		1.1
"There is a significant pharmacokinetic interaction between capecitabine and S-warfarin, resulting in exaggerated anticoagulant activity."( Significant effect of capecitabine on the pharmacokinetics and pharmacodynamics of warfarin in patients with cancer.
Abt, M; Camidge, R; Cassidy, J; Grange, S; Jodrell, D; Reigner, B; Weidekamm, E, 2005)		0.89
" Both CPT-11 and CCB need to be activated by human carboxyl esterases, therefore a probable pharmacokinetic drug interaction was checked."( Pharmacokinetics and metabolism of irinotecan combined with capecitabine in patients with advanced colorectal cancer.
Czejka, M; Hauer, K; Ostermann, E; Schueller, J, )		0.37
"Forty patients and 75 pharmacokinetic time-courses were available for analysis."( Pharmacokinetic modelling of 5-FU production from capecitabine--a population study in 40 adult patients with metastatic cancer.
Lokiec, F; Rezaí, K; Urien, S, 2005)		0.58
"A phase I study was performed to determine the maximal tolerated dose, recommended doses (RDs), safety and efficacy of oral vinorelbine when combined with capecitabine in an all-oral chemotherapy regimen in patients with metastatic breast cancer (MBC), with pharmacokinetic blood sampling to investigate potential drug-drug interactions."( Dose-finding and pharmacokinetic study of an all-oral combination regimen of oral vinorelbine and capecitabine for patients with metastatic breast cancer.
Adamoli, L; Blanchot, G; Catania, C; Goldhirsch, A; Imadalou, K; Longerey, B; Munzone, E; Nolè, F; Sanna, G, 2006)		0.75
" Results from the pharmacokinetic study demonstrated the absence of mutual pharmacokinetic interactions when both drugs were co-administered."( Dose-finding and pharmacokinetic study of an all-oral combination regimen of oral vinorelbine and capecitabine for patients with metastatic breast cancer.
Adamoli, L; Blanchot, G; Catania, C; Goldhirsch, A; Imadalou, K; Longerey, B; Munzone, E; Nolè, F; Sanna, G, 2006)		0.55
" Due to these pharmacokinetic merits, capecitabine can be given at a higher dose, and therefore is expected to yield higher antitumor activity, than doxifluridine."( [Pharmacokinetic comparison of capecitabine and 5'-deoxy-5-fluorouridine (doxifluridine; 5'-DFUR)].
Ebi, H; Minami, H, 2005)		0.89
"The Hollow Fibre Assay (HFA) is usually applied as an early in vivo model for anti-cancer drug screening, but is potentially an excellent model for short-term in vivo pharmacodynamic studies."( The Hollow Fibre Assay as a model for in vivo pharmacodynamics of fluoropyrimidines in colon cancer cells.
Peters, GJ; Prins, HJ; Temmink, OH; van Gelderop, E, 2007)		0.34
" Additional patients were treated at the OTR dose level to further evaluate safety and for pharmacokinetic analyses."( Phase I and pharmacokinetic study of lapatinib in combination with capecitabine in patients with advanced solid malignancies.
Arya, N; Chu, QS; Curtright, J; de Bono, J; Fleming, RA; Ho, PT; Koch, KM; Pandite, L; Rowinsky, EK; Schwartz, G; Smith, DA; Versola, MJ, 2007)		0.58
"Lapatinib and capecitabine administered on a 3-week schedule were well tolerated, and no pharmacokinetic interaction was observed."( Phase I and pharmacokinetic study of lapatinib in combination with capecitabine in patients with advanced solid malignancies.
Arya, N; Chu, QS; Curtright, J; de Bono, J; Fleming, RA; Ho, PT; Koch, KM; Pandite, L; Rowinsky, EK; Schwartz, G; Smith, DA; Versola, MJ, 2007)		0.94
" Although a traditional toxicity-based maximum tolerated dose was not achieved, the highest dosing cohort represented a biologically relevant dose of enzastaurin, on the basis of preclinical data and correlative pharmacodynamic biomarker assays of protein kinase Cbeta inhibition in peripheral blood mononucleocytes, in combination with a standard dose of capecitabine."( A phase I safety, tolerability, and pharmacokinetic study of enzastaurin combined with capecitabine in patients with advanced solid tumors.
Baldwin, J; Basche, M; Britten, CD; Camidge, DR; Darstein, C; Finn, RS; Gail Eckhardt, S; Gore, L; Holden, SN; Leong, S; Musib, L; O'Bryant, CL; Thornton, D, 2008)		0.74
" Combination treatment did not affect pharmacokinetic parameters of capecitabine, epirubicin or their metabolites."( Dose-finding phase I and pharmacokinetic study of capecitabine (Xeloda) in combination with epirubicin and cyclophosphamide (CEX) in patients with inoperable or metastatic breast cancer.
Hozumi, Y; Ito, Y; Iwata, H; Kobayashi, T; Morita, S; Ohno, S; Saji, S; Sakamoto, J; Toi, M, 2007)		0.83
"Population pharmacokinetic (PK) (or pharmacodynamic (PD)) modelling aims to analyse the variability of drug kinetics (or dynamics) between numerous subjects belonging to a population."( Independent-model diagnostics for a priori identification and interpretation of outliers from a full pharmacokinetic database: correspondence analysis, Mahalanobis distance and Andrews curves.
Bruguerolle, B; Semmar, N; Simon, N; Urien, S, 2008)		0.35
"To determine the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of the combination of weekly oxaliplatin x 4, weekly irinotecan x 4 and capecitabine Monday through Friday for 4 weeks of every 6 week cycle in patients with solid tumors; to determine the pharmacokinetic profile of these agents in this combination; to observe patients for clinical anti-tumor response."( Phase I clinical and pharmacokinetic study of oxaliplatin, irinotecan and capecitabine.
Brell, JM; Cooney, MM; Dowlati, A; Egorin, MJ; Gibbons, J; Hoppel, CL; Ingalls, ST; Ivy, SP; Krishnamurthi, SS; Li, X; Overmoyer, BA; Remick, SC; Schluchter, MD; Weaver, KC; Zuhowski, EG, 2009)		0.78
" Pharmacokinetic analysis was performed on plasma samples collected at the first cycle of treatment."( A dose finding and pharmacokinetic study of capecitabine in combination with oxaliplatin and irinotecan in metastatic colorectal cancer.
Antonuzzo, A; Bocci, G; Bursi, S; Chiara, S; Del Tacca, M; Di Paolo, A; Falcone, A; Fornaro, L; Loupakis, F; Masi, G; Pfanner, E; Vasile, E, 2009)		0.61
" Large interpatient variability in the pharmacokinetic parameters of investigated drugs was observed."( A dose finding and pharmacokinetic study of capecitabine in combination with oxaliplatin and irinotecan in metastatic colorectal cancer.
Antonuzzo, A; Bocci, G; Bursi, S; Chiara, S; Del Tacca, M; Di Paolo, A; Falcone, A; Fornaro, L; Loupakis, F; Masi, G; Pfanner, E; Vasile, E, 2009)		0.61
" Although drug treatment did not alter tumor delivery pharmacokinetic variables (K1 and permeability product surface area) or blood flow, tumor FLT retention variables increased with drug treatment in all but one patient."( Altered tissue 3'-deoxy-3'-[18F]fluorothymidine pharmacokinetics in human breast cancer following capecitabine treatment detected by positron emission tomography.
Aboagye, EO; Al-Nahhas, A; Contractor, KB; Coombes, RC; Kenny, LM; Palmieri, C; Shousha, S; Stebbing, J, 2009)		0.57
" Based on the overall toxicity profile and pharmacokinetic parameters, the recommended phase 2 doses were therefore sorafenib 400 mg bid and capecitabine 850 mg/m(2) bid, as scheduled above."( Safety and pharmacokinetics of sorafenib combined with capecitabine in patients with advanced solid tumors: results of a phase 1 trial.
Awada, A; Besse-Hammer, T; Brendel, E; Delesen, H; Gil, T; Hendlisz, A; Joosten, MC; Lathia, CD; Loembé, BA; Piccart-Ghebart, M; Van Hamme, J; Whenham, N, 2011)		0.82
" There was no pharmacokinetic interaction between everolimus and capecitabine."( Phase I and pharmacokinetic study of capecitabine and the oral mTOR inhibitor everolimus in patients with advanced solid malignancies.
Beijnen, JH; Deenen, MJ; Klümpen, HJ; Richel, DJ; Schellens, JH; Sparidans, RW; Weterman, MJ; Wilmink, JW, 2012)		0.89
"The mechanism, preclinical testing, and clinical activity of perifosine in CRC and MM are discussed, with supportive pharmacokinetic information presented."( Perifosine , an oral, anti-cancer agent and inhibitor of the Akt pathway: mechanistic actions, pharmacodynamics, pharmacokinetics, and clinical activity.
Anderson, KC; Eng, C; Hideshima, T; Kolesar, J; Richardson, PG, 2012)		0.38
"To evaluate the maximum tolerated dose (MTD) and pharmacokinetic profile of a chronomodulated, dose-intensified regimen of capecitabine in combination with oxaliplatin (XELOX) in metastatic colorectal cancer (mCRC)."( Phase I pharmacokinetic study of chronomodulated dose-intensified combination of capecitabine and oxaliplatin (XELOX) in metastatic colorectal cancer.
Chen, X; Choo, SP; Chowbay, B; Farid, M; Koo, WH; Ong, SY; Ramasamy, S; Tan, SH; Toh, HC, 2012)		0.81
" However, toxicity and large interpatient pharmacokinetic variability occur despite body surface area (BSA)-dosing."( Fixed-dose capecitabine is feasible: results from a pharmacokinetic and pharmacogenetic study in metastatic breast cancer.
Armstrong, DK; Connolly, RM; Davidson, NE; Fetting, JH; Garrett-Mayer, E; Hoskins, JM; Jeter, SC; McLeod, HL; Rudek, MA; Stearns, V; Watkins, SP; Wolff, AC; Wright, LA; Zhao, M, 2013)		0.78
" Patients with the lowest Cmin had a shorter OS and the highest PD rate, but a distinct correlation was not observed for tumor response."( Population pharmacokinetics and exposure-response analyses of trastuzumab in patients with advanced gastric or gastroesophageal junction cancer.
Cosson, VF; Lehle, M; Lum, BL; Ng, VW, 2014)		0.4
" The population pharmacokinetic analysis was based on a four-compartment model describing the sequence of capecitabine and three of its metabolites."( Pharmacokinetics and exposure-effect relationships of capecitabine in elderly patients with breast or colorectal cancer.
Daher Abdi, Z; Lavau-Denes, S; Leobon, S; Marquet, P; Martin, J; Prémaud, A; Rousseau, A; Sauvage, FL; Tubiana-Mathieu, N; Urien, S, 2014)		0.86
" Pharmacokinetic (PK) studies were undertaken on day 1 of treatment."( A phase I and pharmacokinetic study of capecitabine in combination with radiotherapy in patients with localised inoperable pancreatic cancer.
Crellin, A; Evans, TR; Harden, S; James, A; Lumsden, GR; McDonald, AC; Morrison, R; Paul, J; Roxburgh, P; Sweeting, L, 2014)		0.67
" Predicted Cp [median and 90% prediction interval] was simulated using the population pharmacokinetic model established for other cancers (PPK model) and compared to observed Cp."( Lower exposure and faster clearance of bevacizumab in gastric cancer and the impact of patient variables: analysis of individual data from AVAGAST phase III trial.
Allison, DE; Han, K; Jin, J; Lowe, J; Maia, M; Sersch, MA, 2014)		0.4
"Nine patients treated with CCB and BVZ for advanced colorectal cancer entered this pharmacokinetic study."( Clinical pharmacokinetics of capecitabine and its metabolites in combination with the monoclonal antibody bevacizumab.
Buchner, P; Czejka, M; Farkouh, A; Georgopoulos, A; Gruenberger, B; Scheithauer, W; Schueller, J, 2014)		0.69
" After repeated cycles of BVZ no significant pharmacokinetic interaction was observed."( Clinical pharmacokinetics of capecitabine and its metabolites in combination with the monoclonal antibody bevacizumab.
Buchner, P; Czejka, M; Farkouh, A; Georgopoulos, A; Gruenberger, B; Scheithauer, W; Schueller, J, 2014)		0.69
"From the pharmacokinetic point of view and in agreement with numerous clinical study data, co-administration of BVZ with CCB appears to be safe and efficient."( Clinical pharmacokinetics of capecitabine and its metabolites in combination with the monoclonal antibody bevacizumab.
Buchner, P; Czejka, M; Farkouh, A; Georgopoulos, A; Gruenberger, B; Scheithauer, W; Schueller, J, 2014)		0.69
" But its short plasma half-life limits clinical utility and the usually prescribed dosing regimen results in significant periods of therapeutically irrelevant concentration."( Trichotomous gastric retention of amorphous capecitabine: an attempt to overcome pharmacokinetic gap.
Chourasia, MK; Meher, JG; Pawar, VK; Singh, M; Singh, Y, 2015)		0.68
"7) h mg/l], elimination half-life [t 1/2 21 (SD 7) vs."( Influence of metastatic disease on the usefulness of uracil pharmacokinetics as a screening tool for DPD activity in colorectal cancer patients.
Gelderblom, H; Guchelaar, HJ; Maring, JG; Opdam, F; van Kuilenburg, AB; van Staveren, MC, 2015)		0.42
" Pharmacokinetic parameters were estimated using non-compartmental analysis."( Exploring the intracellular pharmacokinetics of the 5-fluorouracil nucleotides during capecitabine treatment.
Beijnen, JH; Derissen, EJ; Huitema, AD; Jacobs, BA; Rosing, H; Schellens, JH, 2016)		0.66
" We sought to develop a pharmacokinetic model of the interaction between phenytoin and capecitabine."( Pharmacokinetic model analysis of interaction between phenytoin and capecitabine.
Fukui, E; Hori, S; Ikenishi, M; Kawahara, K; Matsuyama, K; Miki, A; Miyazaki, S; Nakatsuka, E; Ohtori, T; Sakurai, M; Satoh, H; Sawada, Y; Ueda, M; Ueda, R, 2016)		0.89
" Non-compartment pharmacokinetic parameters have been calculated by Phoenix WinNonlin."( Assessment of Pharmacokinetic Interaction Between Capecitabine and Cetuximab in Metastatic Colorectal Cancer Patients.
Buchner, P; Czejka, M; Dittrich, C; Geiler, H; Greil, R; Kitzmueller, M; Lichtneckert, M; Rachar, V, 2016)		0.69
"No clinically relevant impact of CTX on CCB pharmacokinetic parameters and metabolic conversion could be detected in both arms after statistical evaluation (ANOVA)."( Assessment of Pharmacokinetic Interaction Between Capecitabine and Cetuximab in Metastatic Colorectal Cancer Patients.
Buchner, P; Czejka, M; Dittrich, C; Geiler, H; Greil, R; Kitzmueller, M; Lichtneckert, M; Rachar, V, 2016)		0.69
"From the pharmacokinetic point of view, co-administration of CTX to CCB seems to be safe."( Assessment of Pharmacokinetic Interaction Between Capecitabine and Cetuximab in Metastatic Colorectal Cancer Patients.
Buchner, P; Czejka, M; Dittrich, C; Geiler, H; Greil, R; Kitzmueller, M; Lichtneckert, M; Rachar, V, 2016)		0.69
" The aim of this study was to evaluate the potential pharmacokinetic (PK)-based drug-drug interaction (DDI) between rilotumumab and epirubicin (E), cisplatin(C) and capecitabine (X)."( Assessment of pharmacokinetic interaction between rilotumumab and epirubicin, cisplatin and capecitabine (ECX) in a Phase 3 study in gastric cancer.
Doshi, S; Hoang, T; Kasichayanula, S; Kuchimanchi, M; Zhang, Y; Zhu, M, 2017)		0.87
" Additionally, a physiologically based pharmacokinetic (PBPK) model was created to assess such variations in silico."( Monitoring of erlotinib in pancreatic cancer patients during long-time administration and comparison to a physiologically based pharmacokinetic model.
Buchner, P; Czejka, M; Dittrich, C; Gruber, A; Kirchbaumer Baroian, N; Kitzmueller, M; Sahmanovic Hrgovcic, A, 2018)		0.48
"The cornerstone of this investigation is to determine the pharmacokinetic and histopathological behavior of solid lipid nanoparticles of capecitabine (CB-SLNs) in 1,2-dimethylhydrazine (DMH) induced colon cancer."( Capecitabine lipid nanoparticles for anti-colon cancer activity in 1,2-dimethylhydrazine-induced colon cancer: preparation, cytotoxic, pharmacokinetic, and pathological evaluation.
Dudhipala, N; Puchchakayala, G, 2018)		2.13
" Concretely, the aims of this research were to build a joint population pharmacokinetic model for capecitabine and three of its metabolites (5-DFUR, 5-FU and 5-FUH2) and to determine optimal sampling times for therapeutic drug monitoring."( Mining Small Routine Clinical Data: A Population Pharmacokinetic Model and Optimal Sampling Times of Capecitabine and its Metabolites.
Aldaz, A; Bueno, L; Insausti, A; Oyaga-Iriarte, E; Sayar, O, 2019)		0.95
" The population pharmacokinetic model was built as a multicompartmental model using NONMEM and was internally validated by visual predictive check."( Mining Small Routine Clinical Data: A Population Pharmacokinetic Model and Optimal Sampling Times of Capecitabine and its Metabolites.
Aldaz, A; Bueno, L; Insausti, A; Oyaga-Iriarte, E; Sayar, O, 2019)		0.73
"This study investigated the time course and magnitude of the pharmacokinetic interaction between capecitabine and the cytochrome P450 (CYP) 2C9 substrate celecoxib, with implications for coadministration of fluoropyrimidines with CYP2C9 substrates such as warfarin."( Prolonged Pharmacokinetic Interaction Between Capecitabine and a CYP2C9 Substrate, Celecoxib.
House, LK; Janisch, LA; Karrison, TG; Ramírez, J; Ratain, MJ; Salgia, R; Sharma, MR; Turcich, M, 2019)		0.99
" The primary aim of this study was to develop a pharmacokinetic model for capecitabine and its metabolites, 5'-deoxy-5-fluorocytidine (dFCR), 5'-deoxy-5-fluorouridine (dFUR), 5-FU, and fluoro-β-alanine (FBAL) using data from a heterogeneous population of cancer patients (n = 237) who participated in seven clinical studies."( Pharmacokinetics of Capecitabine and Four Metabolites in a Heterogeneous Population of Cancer Patients: A Comprehensive Analysis.
Beijnen, JH; Cats, A; de Vries, N; Deenen, MJ; Huitema, ADR; Jacobs, BAW; Joerger, M; Meulendijks, D; Rosing, H; Schellens, JHM, 2019)		1.07
" A physiologically based pharmacokinetic (PBPK) model was developed using in vitro results."( Assessment of pharmacokinetic variations of capecitabine after multiple administration in rats: a physiologically based pharmacokinetic model.
Ito, Y; Kobuchi, S; Sakaeda, T; Sakai, S, 2020)		0.82
" This prospective pharmacokinetic study evaluated cytidine deaminase (CDA) activity, the second drug-metabolizing enzyme that generates 5'-deoxy-5-fluorouridine (5'-DFUR) from 5'-deoxy-5-fluorocytidine (5'-DFCR), as well as creatinine clearance (CLcr)."( Correlation Between the Metabolic Conversion of a Capecitabine Metabolite, 5'-Deoxy-5-fluorocytidine, and Creatinine Clearance.
Ando, Y; Fujita, KI; Hattori, N; Inaishi, T; Kikumori, T; Maeda, O; Matsumoto, N; Nakayama, G; Shimokata, T, )		0.38
" Therefore, the previously identified increased toxicity and shorter survival in patients with a low SMM, could not be explained by changes in pharmacokinetic characteristics of capecitabine and metabolites."( Worse capecitabine treatment outcome in patients with a low skeletal muscle mass is not explained by altered pharmacokinetics.
Beijnen, JH; Dorlo, TPC; Huitema, ADR; Jacobs, BAW; Kurk, SA; May, AM; Molenaar-Kuijsten, L; Steeghs, N, 2021)		1.29
" To this end, an approach using a population pharmacokinetic (PPK)/pharmacodynamic (PD) model incorporating autoinduction was planned; however, the utility of this approach in the dose justification has not been reported."( A semimechanistic population pharmacokinetic and pharmacodynamic model incorporating autoinduction for the dose justification of TAS-114.
Araki, H; Ieiri, I; Matsuoka, K; Takahashi, K; Takenaka, T; Yamashita, F; Yoshisue, K, 2022)		0.72
" Pharmacokinetic parameters were calculated using non-compartmental methods."( Pharmacokinetic and bioequivalence study of two capecitabine tablets in Chinese patients with breast, colorectal or gastric cancer under fed condition: A multicentric, randomized, open-label, single-dose, two-period, two-way crossover clinical trial.
Gao, S; Luo, S; Ma, H; Sun, H; Yuan, Z; Zhan, X; Zhang, L; Zhang, Y; Zhao, N, 2023)		1.17
" A previous study indicated that pharmacokinetic profile of capecitabine was different depending on dosing time in rat."( Diurnal Changes in Capecitabine Clock-Controlled Metabolism Enzymes Are Responsible for Its Pharmacokinetics in Male Mice.
Akyel, YK; Gazioglu, I; Gul, S; Kavakli, IH; Lévi, F; Okyar, A; Ozturk Civelek, D; Ozturk Seyhan, N; Pala Kara, Z, 2023)		1.48
" We aimed to establish physiologically based pharmacokinetic (PBPK) models of capecitabine-metabolites and 5-FU-metabolites to describe their pharmacokinetics in tumor and plasma of cancer patients with liver impairment."( Physiologically Based Pharmacokinetic Modeling for Prediction of 5-FU Pharmacokinetics in Cancer Patients with Hepatic Impairment After 5-FU and Capecitabine Administration.
Hu, H; Wang, Y; Yu, L; Zeng, S, 2023)		1.34

Compound-Compound Interactions

Irinotecan in combination with capecitabine is a well tolerated regimen. No dose-limiting toxicities were noted at all bortezomib dose levels when administered with full dose cape citabine and oxaliplatin.

ExcerptReferenceRelevance
" Preclinical studies indicated an enhancement of the therapeutic index when capecitabine was combined with leucovorin."( A Phase I study of capecitabine in combination with oral leucovorin in patients with intractable solid tumors.
Allman, D; Bissett, D; Cassidy, J; Dirix, L; Griffin, T; Osterwalder, B; Reigner, B; Van Oosterom, AT, 1998)		0.86
"To evaluate the feasibility of administering the oral fluoropyrimidine capecitabine in combination with paclitaxel, to characterize the principal toxicities of the combination, to recommend doses for subsequent disease-directed studies, and to determine whether significant pharmacokinetic interactions occur between these agents when combined."( Phase I and pharmacokinetic study of the oral fluoropyrimidine capecitabine in combination with paclitaxel in patients with advanced solid malignancies.
Burger, HU; Burris, HA; Drengler, RL; Eckhardt, SG; Griffin, T; Kraynak, M; Moczygemba, J; Reigner, B; Rodrigues, G; Rowinsky, EK; Villalona-Calero, MA; Von Hoff, DD; Weiss, GR, 1999)		0.78
"The purpose of this study was to evaluate the dose-limiting toxicity (DLT) and maximum tolerated dose of capecitabine when used in combination with epirubicin and cisplatin (ECC) in patients with oesophageal or gastric adenocarcinoma."( A phase I and pharmacokinetic study of capecitabine in combination with epirubicin and cisplatin in patients with inoperable oesophago-gastric adenocarcinoma.
Blackie, R; Evans, TR; Fullarton, GM; McDonald, AC; McInnes, A; Morrison, R; Paul, J; Pentheroudakis, G; Raby, N; Soukop, M, 2002)		0.8
"A dose of 1000 mg/m(2) bd of capecitabine is recommended for use on an intermittent schedule in combination with these doses and schedule of epirubicin and cisplatin."( A phase I and pharmacokinetic study of capecitabine in combination with epirubicin and cisplatin in patients with inoperable oesophago-gastric adenocarcinoma.
Blackie, R; Evans, TR; Fullarton, GM; McDonald, AC; McInnes, A; Morrison, R; Paul, J; Pentheroudakis, G; Raby, N; Soukop, M, 2002)		0.88
"The aim of this phase I study was to determine the maximum-tolerated dose (MTD) and the dose-limiting toxicities (DLTs) of an intermittent weekly capecitabine regimen in combination with oxaliplatin."( Intermittent weekly high-dose capecitabine in combination with oxaliplatin: a phase I/II study in first-line treatment of patients with advanced colorectal cancer.
Huber, H; Kornek, GV; Längle, F; Raderer, M; Scheithauer, W; Schmid, K; Schüll, B, 2002)		0.8
"In the phase I part of the study, 21 patients were enrolled, and a total of 222 courses were administered through four dose levels of capecitabine combined with oxaliplatin 85 mg/m(2)."( Intermittent weekly high-dose capecitabine in combination with oxaliplatin: a phase I/II study in first-line treatment of patients with advanced colorectal cancer.
Huber, H; Kornek, GV; Längle, F; Raderer, M; Scheithauer, W; Schmid, K; Schüll, B, 2002)		0.81
" On the basis of the toxicological profile of the combination regimen shown in the present study, oxaliplatin 85 mg/m(2) as a 2-h intravenous infusion every 2 weeks administered in combination with capecitabine 3500 mg/m(2)/day x7 in two divided doses is recommended for further evaluations."( Intermittent weekly high-dose capecitabine in combination with oxaliplatin: a phase I/II study in first-line treatment of patients with advanced colorectal cancer.
Huber, H; Kornek, GV; Längle, F; Raderer, M; Scheithauer, W; Schmid, K; Schüll, B, 2002)		0.79
"The objective of this study was to evaluate the activity and safety of oral capecitabine in combination with docetaxel and epirubicin (TEX) as first-line treatment for patients with locally advanced/metastatic breast carcinoma."( Capecitabine in combination with docetaxel and epirubicin in patients with previously untreated, advanced breast carcinoma.
Bighin, C; Colozza, MA; Contu, A; Del Mastro, L; Durando, A; Garrone, O; Genta, F; Lambiase, A; Stevani, I; Venturini, M, 2003)		1.99
" The main objective of this study was to determine the maximum tolerated dose (MTD) of capecitabine when given in combination with fixed doses of epirubicin and cyclophosphamide (100 and 600 mg/m(2) day 1 every (q) 3 weeks) as primary treatment for large operable or locally advanced/inflammatory breast cancer without distant metastasis."( An EORTC phase I study of capecitabine (Xeloda) in combination with fixed doses of cyclophosphamide and epirubicin (cex) as primary treatment for large operable or locally advanced/inflammatory breast cancer.
Atalay, G; Biganzoli, L; Bonnefoi, H; Cufer, T; Mauriac, L; Piccart, M; Schaefer, P, 2003)		0.84
" The use of irinotecan together with raltitrexed is also being investigated, as is its combination with oxaliplatin."( Irinotecan in metastatic colorectal cancer: dose intensification and combination with new agents, including biological response modifiers.
Ducreux, M; Köhne, CH; Schwartz, GK; Vanhoefer, U, 2003)		0.32
" The MTD of capecitabine in combination with vinorelbine at 25 mg/m2 dosage on days 1 and 8 of a 3-week schedule is 2000 mg/m2/day for 14 consecutive days."( A phase I study of capecitabine in combination with vinorelbine in advanced breast cancer.
Crucitta, E; De Lena, M; Guida, M; Latorre, A; Lorusso, V; Misino, A; Silvestris, N, 2003)		1.03
"We studied the safety and clinical activity of exisulind in combination with capecitabine in 35 patients with metastatic breast cancer (MBC)."( Phase I and II study of exisulind in combination with capecitabine in patients with metastatic breast cancer.
Arun, B; Booser, D; Esteva, FJ; Gibbs, A; Hortobagyi, GN; Murray, JL; Nealy, KM; Pusztai, L; Rivera, E; Smith, TL; Symmans, WF; Thompson, WJ; Valero, V; Whitehead, C; Zhen, JH, 2003)		0.8
"Exisulind (125 mg orally bid) in combination with capecitabine is well tolerated and the combination has anticancer activity similar to that of capecitabine alone in heavily pretreated patients with MBC."( Phase I and II study of exisulind in combination with capecitabine in patients with metastatic breast cancer.
Arun, B; Booser, D; Esteva, FJ; Gibbs, A; Hortobagyi, GN; Murray, JL; Nealy, KM; Pusztai, L; Rivera, E; Smith, TL; Symmans, WF; Thompson, WJ; Valero, V; Whitehead, C; Zhen, JH, 2003)		0.82
"This prospective trial aimed to evaluate the therapeutic effects and systemic toxicities of capecitabine monotherapy and capecitabine treatment combined with biological response modifiers in patients with metastatic renal cell carcinoma."( Capecitabine monotherapy and in combination with immunotherapy in the treatment of metastatic renal cell carcinoma.
Bartsch, R; Hussian, D; Kramer, G; Lintner, C; Locker, GJ; Mader, R; Marberger, M; Pluschnig, U; Rauchenwald, M; Steger, GG; Wenzel, C; Zielinski, CC, 2003)		1.98
"The aim of the current randomized Phase II study was to investigate the efficacy and safety of capecitabine combined with irinotecan as first-line treatment in metastatic colorectal carcinoma (CRC)."( Randomized multicenter Phase II trial of two different schedules of irinotecan combined with capecitabine as first-line treatment in metastatic colorectal carcinoma.
Artale, S; Bajetta, E; Beretta, E; Biasco, G; Bonaglia, L; Bonetti, A; Buzzoni, R; Carreca, I; Cassata, A; Cortinovis, D; Di Bartolomeo, M; Ferrario, E; Frustaci, S; Iannelli, A; Lambiase, A; Mariani, L; Marini, G; Pinotti, G, 2004)		0.76
" The aim was to investigate the therapeutic efficacy and tolerance of mitomycin C (MMC) in combination with gemcitabine (GEM) or capecitabine (CAPE) in previously untreated patients with advanced biliary tract cancer."( Mitomycin C in combination with capecitabine or biweekly high-dose gemcitabine in patients with advanced biliary tract cancer: a randomised phase II trial.
Depisch, D; Gruenberger, T; Karall, K; Kornek, GV; Laengle, F; Lang, F; Penz, M; Scheithauer, W; Schuell, B, 2004)		0.81
"A total of 51 patients were entered in this study and randomly allocated to treatment with MMC 8 mg/m2 on day 1 in combination with GEM 2000 mg/m2 on days 1 and 15 every 4 weeks, or MMC 8 mg/m2 on day 1 plus CAPE 2000 mg/m2/day on days 1-14, every 4 weeks."( Mitomycin C in combination with capecitabine or biweekly high-dose gemcitabine in patients with advanced biliary tract cancer: a randomised phase II trial.
Depisch, D; Gruenberger, T; Karall, K; Kornek, GV; Laengle, F; Lang, F; Penz, M; Scheithauer, W; Schuell, B, 2004)		0.61
"A phase I clinical trial was started in order to determine the recommended doses of capecitabine and epirubicin, when administered in combination with a fixed dose of cyclophosphamide (600 mg/m(2) day 1 q3 weeks) in patients with inoperable or recurrent breast cancer."( Application of a continual reassessment method to a phase I clinical trial of capecitabine in combination with cyclophosphamide and epirubicin (CEX) for inoperable or recurrent breast cancer.
Hozumi, Y; Ito, Y; Iwata, H; Kobayashi, T; Morita, S; Ohno, S; Sakamoto, J; Toi, M, 2004)		0.78
" Because the toxicity profile of weekly docetaxel differs from the standard 21-day docetaxel schedule, we performed a phase I/II trial to test the efficacy and safety of weekly docetaxel in combination with capecitabine given for 14 days every 21 days."( Final results of a phase II clinical trial of weekly docetaxel in combination with capecitabine in anthracycline-pretreated metastatic breast cancer.
Au, HJ; Bodnar, DM; Joy, AA; Koski, SL; Mackey, JR; Scarfe, AG; Smith, SW; Smylie, MG; Soulieres, D; Tonkin, KS, 2004)		0.74
"To evaluate the clinical efficacy of capecitabine combined with transcatheter arterial chemoembolization (TACE) for advanced liver cancer."( [Capecitabine combined with TACE for advanced liver cancer].
Chen, AJ; Hu, MD; Li, L; Li, XY; Ran, JH; Sun, F; Tang, JH, 2004)		1.51
"Capecitabine combined with TACE is safe and effective for advanced liver cancer."( [Capecitabine combined with TACE for advanced liver cancer].
Chen, AJ; Hu, MD; Li, L; Li, XY; Ran, JH; Sun, F; Tang, JH, 2004)		2.68
"5-Fluorouracil (5-FU) and capecitabine alone and in combination with irinotecan/oxaliplatin are clinically active in the treatment of colorectal and other solid tumors."( Synergistic antitumor activity of capecitabine in combination with irinotecan.
Cao, S; Durrani, FA; Rustum, YM, 2005)		0.91
"To assess the maximum tolerated dose, dose-limiting toxicity, pharmacokinetics, and preliminary antitumor activity of oral irinotecan given in combination with capecitabine to patients with advanced, refractory solid tumors."( Phase I and pharmacokinetic study of oral irinotecan given once daily for 5 days every 3 weeks in combination with capecitabine in patients with solid tumors.
Assadourian, S; deJonge, MJ; Dumez, H; Eskens, FA; Sanderink, GJ; Selleslach, J; Semiond, D; Soepenberg, O; Sparreboom, A; ter Steeg, J; van Oosterom, AT; Verweij, J, 2005)		0.74
" With irinotecan 60 mg/m2/d and capecitabine 2 x 800 mg/m2/d, grade 3 delayed diarrhea in combination with grade 2 nausea (despite maximal antiemetic support) and grade 3 anorexia and colitis, were the first-cycle dose-limiting toxicities in two of six patients, respectively."( Phase I and pharmacokinetic study of oral irinotecan given once daily for 5 days every 3 weeks in combination with capecitabine in patients with solid tumors.
Assadourian, S; deJonge, MJ; Dumez, H; Eskens, FA; Sanderink, GJ; Selleslach, J; Semiond, D; Soepenberg, O; Sparreboom, A; ter Steeg, J; van Oosterom, AT; Verweij, J, 2005)		0.82
"To establish the feasibility and efficacy of capecitabine in combination with weekly irinotecan (CAPIRI) with concurrent pelvic radiotherapy (RT) in patients with locally advanced rectal cancer."( Phase I trial of capecitabine and weekly irinotecan in combination with radiotherapy for neoadjuvant therapy of rectal cancer.
Gnad, U; Hehlmann, R; Hochhaus, A; Hofheinz, RD; Kraus-Tiefenbacher, U; Müldner, A; Post, S; von Gerstenberg-Helldorf, B; Wenz, F; Willeke, F, 2005)		0.93
"Capecitabine in combination with docetaxel given every 3 weeks has shown a high degree of activity in a number of tumor types, but at the expense of significant toxicity."( Phase I study of weekly (day 1 and 8) docetaxel in combination with capecitabine in patients with advanced solid malignancies.
Belani, CP; Chatta, GS; Egorin, MJ; Fakih, M; Friedland, DM; Jacobs, SA; Jung, LL; Potter, DM; Ramalingam, S; Ramanathan, RK; Shin, DM; Strychor, S; Tutchko, S; Zamboni, WC, 2005)		2.01
"To explore the efficacy and safety of CPT-11 combined with fluoropyrimidine in treatment for advanced or metastatic colorectal carcinoma."( [Irinotecan combined with fluoropyrimidine in treatment for advanced/metastatic colorectal carcinoma].
Wu, WQ; Yu, BM, 2005)		0.33
" CPT-11 combined with capecitabine are not only more effective, but also its occurrence of side effect is lowered, and are especially high effective for lung metastasis."( [Irinotecan combined with fluoropyrimidine in treatment for advanced/metastatic colorectal carcinoma].
Wu, WQ; Yu, BM, 2005)		0.64
"The aim of this study was to determine in patients with previously untreated advanced colorectal cancer the maximum tolerated dose (MTD) and safety profile of irinotecan in combination with capecitabine, to identify a recommended dose and to determine the response rate and time to disease progression."( A phase I/II and pharmacokinetic study of irinotecan in combination with capecitabine as first-line therapy for advanced colorectal cancer.
Bakker, JM; Falk, S; Groenewegen, G; Kerr, DJ; Maughan, T; Nortier, JW; Punt, CJ; Rea, DW; Richel, DJ; Semiond, D; Smit, JM; Steven, N; Ten Bokkel Huinink, WW, 2005)		0.75
"Irinotecan (CPT-11) in combination with 5-fluorouracil/folinic acid is used successfully for first-line treatment of metastatic colorectal cancer."( Pharmacokinetics and metabolism of irinotecan combined with capecitabine in patients with advanced colorectal cancer.
Czejka, M; Hauer, K; Ostermann, E; Schueller, J, )		0.37
"Trastuzumab has been repeatedly shown to result in significant clinical benefits and was subsequently accepted as the treatment of choice for HER2-positive advanced breast cancer - particularly as first-line treatment in combination with taxanes and as monotherapy in the second-line or third-line setting."( Safety and efficacy of trastuzumab every 3 weeks combined with cytotoxic chemotherapy in patients with HER2-positive recurrent breast cancer: findings from a case series.
Alexopoulos, A; Ardavanis, A; Karamouzis, M; Orfanos, G; Rigatos, G; Scorilas, A; Tryfonopoulos, D, 2005)		0.33
" trastuzumab (8 mg/kg followed by 6 mg/kg) every 3 weeks in combination with chemotherapeutic agents administered in 3-weekly courses (docetaxel, vinorelbine and capecitabine) in 31 patients with HER2-positive recurrent locoregional and/or metastatic breast cancer."( Safety and efficacy of trastuzumab every 3 weeks combined with cytotoxic chemotherapy in patients with HER2-positive recurrent breast cancer: findings from a case series.
Alexopoulos, A; Ardavanis, A; Karamouzis, M; Orfanos, G; Rigatos, G; Scorilas, A; Tryfonopoulos, D, 2005)		0.52
"The aim of the study was to evaluate tolerance and efficacy of preoperative treatment with capecitabine in combination with radiation therapy (RT) in patients with locally advanced, resectable, rectal cancer."( Capecitabine in combination with preoperative radiation therapy in locally advanced, resectable, rectal cancer: a multicentric phase II study.
Beretta, GD; Chiara, S; Corvò, R; De Paoli, A; Del Prete, S; Friso, ML; Frustaci, S; Innocente, R; Luppi, G; Mantello, G; Pasetto, L; Rosso, R; Santantonio, M; Sarti, E, 2006)		2
"The efficacy of oxaliplatin combined with capecitabine (XELOX) as second-line therapy in patients with advanced colorectal cancer (ACRC) resistant to irinotecan is not well established."( Short-time infusion of oxaliplatin in combination with capecitabine (XELOX30) as second-line therapy in patients with advanced colorectal cancer after failure to irinotecan and 5-fluorouracil.
Baltesgard, L; Ehrsson, H; Fokstuen, T; Glimelius, B; Mortensen, JP; Pfeiffer, P; Qvortrup, C; Starkhammar, H; Sørbye, H; Tveit, KM; Wallin, I; Øgreid, D, 2006)		0.85
" Bevacizumab is currently approved for the first-line treatment of metastatic CRC and is currently being tested in combination with standard therapies for a range of indications."( Bevacizumab combined with standard fluoropyrimidine-based chemotherapy regimens to treat colorectal cancer.
Hurwitz, H; Kabbinavar, F, 2005)		0.33
" Erlotinib in combination with capecitabine was not associated with significantly increased toxicity compared with single-agent therapy."( Antitumor activity of erlotinib in combination with capecitabine in human tumor xenograft models.
Ouchi, KF; Sekiguchi, F; Tanaka, Y; Yanagisawa, M, 2006)		0.87
" The findings of this study support clinical evaluation of erlotinib, both as a single agent and in combination with capecitabine, for the treatment of CRC and breast cancer."( Antitumor activity of erlotinib in combination with capecitabine in human tumor xenograft models.
Ouchi, KF; Sekiguchi, F; Tanaka, Y; Yanagisawa, M, 2006)		0.79
", twice daily in combination with oxaliplatin 50 mg/m2/week and RT 50."( A Phase I study of weekly intravenous oxaliplatin in combination with oral daily capecitabine and radiation therapy in the neoadjuvant treatment of rectal adenocarcinoma.
Fakih, MG; Lawrence, DD; Pendyala, L; Rajput, A; Rustum, YM; Smith, JL; Toth, K; Yang, GY, 2006)		0.56
" The observed antitumor activity warrants further evaluation of this combination as an alternative to or in combination with whole-brain radiation therapy for the treatment of multiple brain metastases."( Phase I study of capecitabine in combination with temozolomide in the treatment of patients with brain metastases from breast carcinoma.
Arun, B; Broglio, K; Buchholz, T; Francis, D; Groves, M; Hortobagyi, GN; Meyers, C; Rivera, E; Valero, V; Yin, G, 2006)		0.67
"We sought to evaluate the efficacy and safety data of a combination regimen using weekly irinotecan in combination with capecitabine and concurrent radiotherapy (CapIri-RT) as neoadjuvant treatment in rectal cancer in a phase-II trial."( A phase II study of capecitabine and irinotecan in combination with concurrent pelvic radiotherapy (CapIri-RT) as neoadjuvant treatment of locally advanced rectal cancer.
Grobholz, R; Hochhaus, A; Hofheinz, RD; Horisberger, K; Kähler, G; Kraus-Tiefenbacher, U; Leitner, A; Post, S; Wenz, F; Willeke, F; Willer, A, 2007)		0.87
" Following a pivotal trial demonstrating that capecitabine confers increased survival when used in combination with docetaxel, it is being investigated intensively in combined regimens using other standard chemotherapeutic agents, as well as with novel molecularly targeted therapies."( Capecitabine in combination with novel targeted agents in the management of metastatic breast cancer: underlying rationale and results of clinical trials.
Tripathy, D, 2007)		2.04
"The levels of both VEGF and PDGF-BB were measured in three time points, in the serum of 32 rectal carcinoma patients receiving daily reduced-dose/continuous capecitabine in combination with preoperative pelvic irradiation."( Daily low-dose/continuous capecitabine combined with neo-adjuvant irradiation reduces VEGF and PDGF-BB levels in rectal carcinoma patients.
Be'ery, E; Fenig, E; Koren, C; Lavi, I; Loven, D; Shaked, Y; Sulkes, A; Yerushalmi, R, 2008)		0.84
" Capecitabine was given at a dose of 900 mg m(-2) for 5 days per week combined with 45 Gy of radiotherapy in 25 doses."( Preoperative radiotherapy combined with 5 days per week capecitabine chemotherapy in locally advanced rectal cancer.
Byrne, P; Cooper, R; Craven, I; Crellin, A; Melcher, A; Sebag-Montefiore, D, 2007)		1.5
" In conclusion, capecitabine can safely be combined with docetaxel (40 mg m(-2)) and mitomycin C (4 mg m(-2))."( Capecitabine in combination with docetaxel and mitomycin C in patients with pre-treated tumours: results of an extended phase-I trial.
Ernst, T; Gnad-Vogt, U; Hochhaus, A; Hofheinz, RD; Kripp, M; Lukan, N; Merx, K; Schultheis, B, 2007)		2.13
" Although a traditional toxicity-based maximum tolerated dose was not achieved, the highest dosing cohort represented a biologically relevant dose of enzastaurin, on the basis of preclinical data and correlative pharmacodynamic biomarker assays of protein kinase Cbeta inhibition in peripheral blood mononucleocytes, in combination with a standard dose of capecitabine."( A phase I safety, tolerability, and pharmacokinetic study of enzastaurin combined with capecitabine in patients with advanced solid tumors.
Baldwin, J; Basche, M; Britten, CD; Camidge, DR; Darstein, C; Finn, RS; Gail Eckhardt, S; Gore, L; Holden, SN; Leong, S; Musib, L; O'Bryant, CL; Thornton, D, 2008)		0.74
"CEX represents a well-tolerated regimen, and RD for Japanese patients was determined to be capecitabine 900 mg/m(2) twice daily in combination with epirubicin 90 mg/m(2) and cyclophosphamide 600 mg/m(2) using the CRM."( Dose-finding phase I and pharmacokinetic study of capecitabine (Xeloda) in combination with epirubicin and cyclophosphamide (CEX) in patients with inoperable or metastatic breast cancer.
Hozumi, Y; Ito, Y; Iwata, H; Kobayashi, T; Morita, S; Ohno, S; Saji, S; Sakamoto, J; Toi, M, 2007)		0.81
" We therefore started a randomised, controlled clinical trial to compare this combination with (177)Lu-octreotate as single agent with regard to anti-tumour effects and side effects."( Report on short-term side effects of treatments with 177Lu-octreotate in combination with capecitabine in seven patients with gastroenteropancreatic neuroendocrine tumours.
de Herder, WW; Kam, BL; Krenning, EP; Kwekkeboom, DJ; van Aken, MO; van Essen, M, 2008)		0.57
"Oxaliplatin combined with 5-FU/leucovorin or capecitabine was generally well tolerated in elderly patients."( Oxaliplatin in combination with 5-fluorouracil/leucovorin or capecitabine in elderly patients with metastatic colorectal cancer.
Arkenau, HT; Englisch-Fritz, C; Freier, W; Graeven, U; Greil, R; Grothey, A; Hinke, A; Kretzschmar, A; Kubicka, S; Porschen, R; Schmiegel, W; Schmoll, HJ; Seufferlein, T, 2008)		0.85
"Oxaliplatin in combination with capecitabine prolongs survival in patients with metastatic colorectal cancer (mCRC)."( Chronomodulated capecitabine in combination with short-time oxaliplatin: a Nordic phase II study of second-line therapy in patients with metastatic colorectal cancer after failure to irinotecan and 5-flourouracil.
Balteskard, L; Berglund, A; Fokstuen, T; Ogreid, D; Pfeiffer, P; Ploen, J; Qvortrup, C; Starkhammar, H; Sørbye, H; Tveit, K; Yilmaz, M, 2008)		0.98
"A phase II trial was initiated to analyze the activity of continuously administered pioglitazone and rofecoxib combined with low-dose chemotherapy (capecitabine or temozolomide) in patients with high-grade gliomas (glioblastoma or anaplastic glioma)."( Low-dose chemotherapy in combination with COX-2 inhibitors and PPAR-gamma agonists in recurrent high-grade gliomas - a phase II study.
Baumgart, U; Bogdahn, U; Hau, P; Hirschmann, B; Kunz-Schughart, L; Muhleisen, H; Reichle, A; Ruemmele, P; Steinbrecher, A; Weimann, E, 2007)		0.54
" No dose-limiting toxicities were noted at all bortezomib dose levels when administered with full dose capecitabine and oxaliplatin."( Phase I study of capecitabine and oxaliplatin in combination with the proteasome inhibitor bortezomib in patients with advanced solid tumors.
Beard, M; Cohen, SJ; Engstrom, PF; Langer, CJ; Lewis, NL; McLaughlin, S; Meropol, NJ; Weiner, LM, 2008)		0.9
"Weekly bortezomib can be safely combined with full doses of capecitabine and oxaliplatin."( Phase I study of capecitabine and oxaliplatin in combination with the proteasome inhibitor bortezomib in patients with advanced solid tumors.
Beard, M; Cohen, SJ; Engstrom, PF; Langer, CJ; Lewis, NL; McLaughlin, S; Meropol, NJ; Weiner, LM, 2008)		0.93
"This dose escalation study was designed to determine the recommended dose of the multi-targeted cell cycle inhibitor indisulam in combination with capecitabine in patients with solid tumours and to evaluate the pharmacokinetics of the combination."( A dose-escalation study of indisulam in combination with capecitabine (Xeloda) in patients with solid tumours.
Beijnen, JH; Diéras, V; Girre, V; Huitema, AD; King, A; Milano, G; Richmond, E; Schellens, JH; Siegel-Lakhai, WS; Tibben, MM; Wanders, J; Zandvliet, AS, 2008)		0.79
"A Phase I study was conducted to determine the maximal tolerated dose and the dose-limiting toxicity (DLT) of oxaliplatin (OXA) combined with capecitabine and radiotherapy as adjuvant treatment in patients with operable rectal cancer."( Phase I study of oxaliplatin in combination with capecitabine and radiotherapy as postoperative treatment for stage II and III rectal cancer.
Fang, H; Jin, J; Li, YX; Liu, YP; Wang, JW; Wang, K; Wang, WH; Yu, ZH; Zhou, AP; Zhou, ZX, 2008)		0.8
"OXA combined with a fixed dose of capecitabine at 625 mg/m(2) twice daily by mouth plus radiotherapy in the adjuvant setting was tolerable and clinically feasible."( Phase I study of oxaliplatin in combination with capecitabine and radiotherapy as postoperative treatment for stage II and III rectal cancer.
Fang, H; Jin, J; Li, YX; Liu, YP; Wang, JW; Wang, K; Wang, WH; Yu, ZH; Zhou, AP; Zhou, ZX, 2008)		0.88
"To describe the considerations leading to marketing approval of ixabepilone in combination with capecitabine and as monotherapy for the treatment of advanced breast cancer that is refractory to other chemotherapies."( Ixabepilone in combination with capecitabine and as monotherapy for treatment of advanced breast cancer refractory to previous chemotherapies.
Aziz, R; Booth, B; Bullock, J; Dagher, R; Harapanhalli, R; Jiang, X; Justice, R; Kaminskas, E; Kasliwal, R; Lechleider, RJ; Leighton, J; Pazdur, R; Pope, S; Sridhara, R, 2008)		0.85
"On October 16, 2007, the Food and Drug Administration approved ixabepilone for injection in combination with capecitabine or as monotherapy for the treatment of patients with advanced breast cancer who have experienced disease progression on previous chemotherapies."( Ixabepilone in combination with capecitabine and as monotherapy for treatment of advanced breast cancer refractory to previous chemotherapies.
Aziz, R; Booth, B; Bullock, J; Dagher, R; Harapanhalli, R; Jiang, X; Justice, R; Kaminskas, E; Kasliwal, R; Lechleider, RJ; Leighton, J; Pazdur, R; Pope, S; Sridhara, R, 2008)		0.84
"Our results show that the regimen of gemcitabine combined with capecitabine is effective and well tolerated in patients with unresectable relapsed or metastatic carcinoma of the biliary tract."( [Gemcitabine combined with capecitabine in the treatment for 41 patients with relapsed or metastatic biliary tract carcinoma].
Chen, X; Chen, ZS; Li, J; Ouyang, XN; Xie, FW; Yu, ZY, 2008)		0.88
"To determine the maximum tolerated dose (MTD), characterize the principal toxicities, and assess the pharmacokinetics of EKB-569, an oral selective irreversible inhibitor of the epidermal growth factor receptor tyrosine kinase, in combination with capecitabine in patients with advanced colorectal cancer."( A phase I study of EKB-569 in combination with capecitabine in patients with advanced colorectal cancer.
Abbas, R; Boni, J; Bukowski, R; Croghan, G; Donehower, R; Erlichman, C; Hidalgo, M; Jimeno, A; Laheru, D; Martins, P; Messersmith, W; Pelley, R; Rudek, M; Zacharchuk, C, 2008)		0.78
"In advanced colorectal cancer, 50 mg EKB-569 daily can be safely combined with 1,000 mg/m(2) capecitabine twice a day."( A phase I study of EKB-569 in combination with capecitabine in patients with advanced colorectal cancer.
Abbas, R; Boni, J; Bukowski, R; Croghan, G; Donehower, R; Erlichman, C; Hidalgo, M; Jimeno, A; Laheru, D; Martins, P; Messersmith, W; Pelley, R; Rudek, M; Zacharchuk, C, 2008)		0.82
"Treatment with metronomic capecitabine and cyclophosphamide in combination with bevacizumab was effective in advanced breast cancer and was minimally toxic."( Metronomic cyclophosphamide and capecitabine combined with bevacizumab in advanced breast cancer.
Bagnardi, V; Bertolini, F; Campagnoli, E; Colleoni, M; Dellapasqua, S; Goldhirsch, A; Mancuso, P; Pietri, E; Rocca, A; Scarano, E; Shaked, Y; Torrisi, R, 2008)		0.93
" The aim of this study was to determine the maximum tolerated dose of capecitabine, in substitution of 5-fluorouracil, combined with oxaliplatin and irinotecan and to evaluate the pharmacokinetics of the drugs."( A dose finding and pharmacokinetic study of capecitabine in combination with oxaliplatin and irinotecan in metastatic colorectal cancer.
Antonuzzo, A; Bocci, G; Bursi, S; Chiara, S; Del Tacca, M; Di Paolo, A; Falcone, A; Fornaro, L; Loupakis, F; Masi, G; Pfanner, E; Vasile, E, 2009)		0.85
" Food and Drug Administration approved lapatinib (Tykerb tablets; GlaxoSmithKline, Philadelphia), an oral, small molecule, dual tyrosine kinase inhibitor of ErbB-2 and ErbB-1, for use in combination with capecitabine for the treatment of patients with human epidermal growth factor receptor (HER)-2-overexpressing metastatic breast cancer who had received prior therapy including an anthracycline, a taxane, and trastuzumab."( FDA drug approval summary: lapatinib in combination with capecitabine for previously treated metastatic breast cancer that overexpresses HER-2.
Cohen, MH; Ibrahim, A; Johnson, J; Justice, R; Ko, CW; Pazdur, R; Ryan, Q; Sridhara, R, 2008)		0.78
"This study assessed radiotherapy combined with capecitabine and oxaliplatin in patients with primary, inextirpable colorectal adenocarcinoma."( Multicentre phase II trial of capecitabine and oxaliplatin in combination with radiotherapy for unresectable colorectal cancer: the CORGI-L Study.
Anderson, H; Berglund, K; Byström, P; Ekelund, M; Fernebro, E; Glimelius, B; Gunnlaugsson, A; Holm, T; Johnsson, A; Kjellén, E; Påhlman, L, 2009)		0.9
"4 Gy), combined with capecitabine 825 mg/m(2) bid every radiotherapy day and oxaliplatin 60 mg/m(2) once weekly."( Multicentre phase II trial of capecitabine and oxaliplatin in combination with radiotherapy for unresectable colorectal cancer: the CORGI-L Study.
Anderson, H; Berglund, K; Byström, P; Ekelund, M; Fernebro, E; Glimelius, B; Gunnlaugsson, A; Holm, T; Johnsson, A; Kjellén, E; Påhlman, L, 2009)		0.96
"To evaluate the safety and efficacy of preoperative radiotherapy (RT) in combination with cetuximab, capecitabine, and irinotecan in patients with locally advanced rectal cancer."( Cetuximab in combination with capecitabine, irinotecan, and radiotherapy for patients with locally advanced rectal cancer: results of a Phase II MARGIT trial.
Barreto-Miranda, M; Dinter, D; Erben, P; Hochhaus, A; Hofheinz, RD; Horisberger, K; Kähler, G; Kienle, P; Mai, S; Post, S; Ströbel, P; Treschl, A; Wenz, F; Willeke, F; Woernle, C, 2009)		0.86
"Patients with rectal cancer (clinical stage T3/4 or N+) were scheduled to receive cetuximab (400 mg/m(2) Day 1, 250 mg/m(2) Days 8, 15, 22, 29) in combination with weekly irinotecan 40 mg/m(2) and capecitabine 500 mg/m(2) twice daily (Days 1-38)."( Cetuximab in combination with capecitabine, irinotecan, and radiotherapy for patients with locally advanced rectal cancer: results of a Phase II MARGIT trial.
Barreto-Miranda, M; Dinter, D; Erben, P; Hochhaus, A; Hofheinz, RD; Horisberger, K; Kähler, G; Kienle, P; Mai, S; Post, S; Ströbel, P; Treschl, A; Wenz, F; Willeke, F; Woernle, C, 2009)		0.83
"Capecitabine combined with fractionated cisplatin is highly effective and well tolerated as a first-line treatment for advanced gastric cancer, with comparable results to 5-Fu plus cisplatin combination therapy."( [Capecitabine combined with cisplatin as first-line therapy in Chinese patients with advanced gastric carcinoma-a phase II clinical study].
Bai, YX; Chen, L; Chen, S; Cheng, Y; Hu, B; Jia, TZ; Jin, ML; Li, J; Liang, J; Shen, L; Shu, YQ; Wan, DS; Wang, BC; Wen, ZZ; Yin, HR; Yu, JR; Zhang, HG; Zhou, Y, 2008)		2.7
" The primary end-point was to establish the maximum tolerable dose (MTD) of capecitabine when combined with (188)Re-HEDP."( (188)Re-HEDP combined with capecitabine in hormone-refractory prostate cancer patients with bone metastases: a phase I safety and toxicity study.
Bosma, TB; Lam, MG; van Rijk, PP; Zonnenberg, BA, 2009)		0.88
"Capecitabine may be safely used in combination with (188)Re-HEDP in a dose of 2,500 mg/m(2) per day and 37 MBq/kg, respectively."( (188)Re-HEDP combined with capecitabine in hormone-refractory prostate cancer patients with bone metastases: a phase I safety and toxicity study.
Bosma, TB; Lam, MG; van Rijk, PP; Zonnenberg, BA, 2009)		2.09
"To understand the mechanisms of the effects of combination treatments, we established animal models showing antitumor activity of bevacizumab as a monotherapy and in combination with capecitabine or capecitabine and oxaliplatin and measured thymidine phosphorylase (TP) and vascular endothelial growth factor (VEGF) levels."( Antitumor activity of bevacizumab in combination with capecitabine and oxaliplatin in human colorectal cancer xenograft models.
Fujimoto-Ouchi, K; Mori, K; Yamashita, Y; Yanagisawa, M; Yorozu, K, 2009)		0.79
" This study was to investigate the efficacy and safety of oxaliplatin in combination with capecitabine as first-line chemotherapy for AGC patients."( [Oxaliplatin combined with capecitabine as first-line chemotherapy for patients with advanced gastric cancer].
Dong, NN; Liu, ZF; Wang, MY; Zhang, Q, 2009)		0.87
"To determine the efficacy and tolerability of capecitabine combined with oxaliplatin (CAPOX) or irinotecan (CAPIRI) as first-line treatment in patients with advanced/metastatic colorectal cancer aged > or =70 years."( Capecitabine in combination with oxaliplatin or irinotecan in elderly patients with advanced colorectal cancer: results of a randomized phase II study.
Bordonaro, R; Caputo, G; Cordio, S; Manzione, L; Novello, G; Reggiardo, G; Rosati, G, 2010)		2.06
"Administration of heated oxaliplatin in combination with capecitabine is feasible and well tolerated without additional toxicity."( Heated (37 degrees C) oxaliplatin infusion in combination with capecitabine for metastatic colorectal carcinoma: can it reduce neuropathy?
Cathomas, R; Köberle, D; Mayer, G; Mey, U; Räss, A; Ruhstaller, T; von Moos, R, 2010)		0.85
"We evaluated the efficacy and safety of cetuximab in combination with XELOX [XELoda® (capecitabine) and OXaliplatin] in advanced gastric cancer (AGC) patients."( A prospective phase II study of cetuximab in combination with XELOX (capecitabine and oxaliplatin) in patients with metastatic and/or recurrent advanced gastric cancer.
Chang, HM; Kang, HJ; Kang, YK; Kim, C; Kim, TW; Lee, JL; Lim, HY; Park, YS; Ryoo, BY; Ryu, MH, 2011)		0.83
"Cetuximab in combination with XELOX chemotherapy was active and safe as first-line treatment of metastatic and/or recurrent AGC patients."( A prospective phase II study of cetuximab in combination with XELOX (capecitabine and oxaliplatin) in patients with metastatic and/or recurrent advanced gastric cancer.
Chang, HM; Kang, HJ; Kang, YK; Kim, C; Kim, TW; Lee, JL; Lim, HY; Park, YS; Ryoo, BY; Ryu, MH, 2011)		0.6
"The purpose of this article is to report the first case of markedly increased anticoagulant activity of warfarin when used in combination with doxifluridine, given as a replacement for capecitabine."( Increased anticoagulant activity of warfarin used in combination with doxifluridine.
Genda, T; Hori, S; Miki, A; Nakajima, M; Satoh, H; Sawada, Y; Suehira, M, 2010)		0.55
"This phase I/II study was conducted to assess the maximal tolerated dose (MTD) and the dose-limiting toxicities (DLTs) of gefitinib in combination with capecitabine in patients with advanced colorectal cancer (aCRC)."( Gefitinib in combination with capecitabine as second-line therapy in patients with advanced colorectal cancer (aCRC): a phase I/II study of the Arbeitsgemeinschaft Internistische Onkologie (AIO).
Frieling, T; Graeven, U; Hegewisch-Becker, S; Lehnert, L; Reinacher-Schick, A; Schmiegel, W; Trarbach, T; Vanhoefer, U, 2010)		0.85
"After failure of a 1st-line therapy, patients with aCRC received escalating doses of gefitinib once daily in combination with capecitabine twice daily: dose level (DL) 1: gefitinib 250 mg and capecitabine 1,000 mg/m(2), DL 2: gefitinib 250 mg and capecitabine 1,250 mg/m(2), DL 3: gefitinib 500 mg and capecitabine 850 mg/m(2)."( Gefitinib in combination with capecitabine as second-line therapy in patients with advanced colorectal cancer (aCRC): a phase I/II study of the Arbeitsgemeinschaft Internistische Onkologie (AIO).
Frieling, T; Graeven, U; Hegewisch-Becker, S; Lehnert, L; Reinacher-Schick, A; Schmiegel, W; Trarbach, T; Vanhoefer, U, 2010)		0.86
" Treatment consisted of capecitabine (2,000 mg/m(2) days 1-14) in combination with docetaxel (40 mg/m(2) day 1) and mitomycin C (4 mg/m(2) day 1)."( Efficacy and safety of capecitabine in combination with docetaxel and mitomycin C in patients with pre-treated pancreatic, gallbladder, and bile duct carcinoma.
Ernst, T; Hochhaus, A; Hofheinz, RD; Hofmann, WK; Kripp, M; Kruth, J; Lukan, N; Merx, K; Nissen, J, 2010)		0.98
"We studied the safety and tolerability of telatinib, an orally available, small-molecule tyrosine kinase inhibitor of the vascular endothelial growth factor receptor (VEGFR-2/VEGFR-3), platelet-derived growth factor receptor beta, and c-Kit in combination with capecitabine and irinotecan."( Phase I evaluation of telatinib, a vascular endothelial growth factor receptor tyrosine kinase inhibitor, in combination with irinotecan and capecitabine in patients with advanced solid tumors.
Brendel, E; Laferriere, N; Langenberg, MH; Mergui-Roelvink, M; Roodhart, JM; Schellens, JH; van der Sar, J; Verheul, HM; Voest, EE; Witteveen, PO, 2010)		0.74
"Continuous administration of 900 mg telatinib twice daily can be safely combined with irinotecan (180 mg/m(2)) and capecitabine (1,000 mg/m(2) twice daily, day 1-14) and is the recommended schedule for further phase II studies."( Phase I evaluation of telatinib, a vascular endothelial growth factor receptor tyrosine kinase inhibitor, in combination with irinotecan and capecitabine in patients with advanced solid tumors.
Brendel, E; Laferriere, N; Langenberg, MH; Mergui-Roelvink, M; Roodhart, JM; Schellens, JH; van der Sar, J; Verheul, HM; Voest, EE; Witteveen, PO, 2010)		0.77
"To evaluate the short-term efficacy and toxicity of endostar in combination with XELIRI as the second-line treatment for advanced colorectal cancer."( [Short-term therapeutic effect and safety of endostar combined with XELIRI regimen in the treatment of advanced colorectal cancer].
Liao, WJ; Luo, RC; Shen, P; Shi, M; Wu, Wy, 2010)		0.36
"Endostar combined with XELIRI is effective and safe as the second-line treatment for advanced colorectal cancer, and further clinical investigation is warranted."( [Short-term therapeutic effect and safety of endostar combined with XELIRI regimen in the treatment of advanced colorectal cancer].
Liao, WJ; Luo, RC; Shen, P; Shi, M; Wu, Wy, 2010)		0.36
"4 Gy), combined with capecitabine 750-675 mg/m(2) bid every radiotherapy day and oxaliplatin 40-30 mg/m(2) once weekly)."( Multicentre phase I-II trial of capecitabine and oxaliplatin in combination with radiotherapy for unresectable pancreatic and biliary tract cancer: The CORGI-U study.
Anderson, H; Glimelius, B; Gunnlaugsson, A; Johnsson, A; Lind, P, 2010)		0.96
"XELOX-RT (30 mg/m(2) oxaliplatin/675 mg/m(2) capecitabine in combination with 50."( Multicentre phase I-II trial of capecitabine and oxaliplatin in combination with radiotherapy for unresectable pancreatic and biliary tract cancer: The CORGI-U study.
Anderson, H; Glimelius, B; Gunnlaugsson, A; Johnsson, A; Lind, P, 2010)		0.9
"Trastuzumab, a monoclonal antibody against human epidermal growth factor receptor 2 (HER2; also known as ERBB2), was investigated in combination with chemotherapy for first-line treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer."( Trastuzumab in combination with chemotherapy versus chemotherapy alone for treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer (ToGA): a phase 3, open-label, randomised controlled trial.
Aprile, G; Bang, YJ; Chung, HC; Feyereislova, A; Hill, J; Kang, YK; Kulikov, E; Lehle, M; Lordick, F; Ohtsu, A; Omuro, Y; Rüschoff, J; Satoh, T; Sawaki, A; Shen, L; Van Cutsem, E, 2010)		0.36
" Participants were randomly assigned in a 1:1 ratio to receive a chemotherapy regimen consisting of capecitabine plus cisplatin or fluorouracil plus cisplatin given every 3 weeks for six cycles or chemotherapy in combination with intravenous trastuzumab."( Trastuzumab in combination with chemotherapy versus chemotherapy alone for treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer (ToGA): a phase 3, open-label, randomised controlled trial.
Aprile, G; Bang, YJ; Chung, HC; Feyereislova, A; Hill, J; Kang, YK; Kulikov, E; Lehle, M; Lordick, F; Ohtsu, A; Omuro, Y; Rüschoff, J; Satoh, T; Sawaki, A; Shen, L; Van Cutsem, E, 2010)		0.58
"Trastuzumab in combination with chemotherapy can be considered as a new standard option for patients with HER2-positive advanced gastric or gastro-oesophageal junction cancer."( Trastuzumab in combination with chemotherapy versus chemotherapy alone for treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer (ToGA): a phase 3, open-label, randomised controlled trial.
Aprile, G; Bang, YJ; Chung, HC; Feyereislova, A; Hill, J; Kang, YK; Kulikov, E; Lehle, M; Lordick, F; Ohtsu, A; Omuro, Y; Rüschoff, J; Satoh, T; Sawaki, A; Shen, L; Van Cutsem, E, 2010)		0.36
"8 or 45 μg/m(2) in combination with capecitabine-oxaliplatin (XELOX)."( Two doses of NGR-hTNF in combination with capecitabine plus oxaliplatin in colorectal cancer patients failing standard therapies.
Andretta, V; Bennicelli, E; Bordignon, C; Caprioni, F; Comandini, D; Fornarini, G; Guglielmi, A; Lambiase, A; Mammoliti, S; Mazzola, G; Pessino, A; Sciallero, S; Sobrero, AF, 2011)		0.91
"Both NGR-hTNF doses were safely combined with XELOX in pretreated CRC patients."( Two doses of NGR-hTNF in combination with capecitabine plus oxaliplatin in colorectal cancer patients failing standard therapies.
Andretta, V; Bennicelli, E; Bordignon, C; Caprioni, F; Comandini, D; Fornarini, G; Guglielmi, A; Lambiase, A; Mammoliti, S; Mazzola, G; Pessino, A; Sciallero, S; Sobrero, AF, 2011)		0.63
"Capecitabine is an oral fluoropyrimidine that is shown to have similar efficacy to 5-fluorouracil (5-FU) when used both alone and in combination with oxaliplatin in the treatment of colorectal cancer (CRC)."( Differences in efficacy and safety between capecitabine and infusional 5-fluorouracil when combined with irinotecan for the treatment of metastatic colorectal cancer.
Aliberti, C; Chiriatti, A; Fiorentini, G; Licitra, S; Montagnani, F, 2010)		2.07
" Hazard ratios for progression and death were combined with an inverse variance method based on logarithmic conversion."( Differences in efficacy and safety between capecitabine and infusional 5-fluorouracil when combined with irinotecan for the treatment of metastatic colorectal cancer.
Aliberti, C; Chiriatti, A; Fiorentini, G; Licitra, S; Montagnani, F, 2010)		0.62
" This study aims to achieve an improved disease free survival for patients after resection or resection combined with RFA of colorectal liver metastases by adding the angiogenesis inhibitor bevacizumab to an adjuvant regimen of CAPOX."( A randomized two arm phase III study in patients post radical resection of liver metastases of colorectal cancer to investigate bevacizumab in combination with capecitabine plus oxaliplatin (CAPOX) vs CAPOX alone as adjuvant treatment.
Bergman, AM; Dalesio, O; Rinkes, IH; Schouten, SB; Snoeren, N; Tollenaar, RA; van der Sijp, JR; van Hillegersberg, R; Verheul, HM; Voest, EE, 2010)		0.56
" Patients will be randomized after resection or resection combined with RFA to receive CAPOX and Bevacizumab or CAPOX alone."( A randomized two arm phase III study in patients post radical resection of liver metastases of colorectal cancer to investigate bevacizumab in combination with capecitabine plus oxaliplatin (CAPOX) vs CAPOX alone as adjuvant treatment.
Bergman, AM; Dalesio, O; Rinkes, IH; Schouten, SB; Snoeren, N; Tollenaar, RA; van der Sijp, JR; van Hillegersberg, R; Verheul, HM; Voest, EE, 2010)		0.56
"The HEPATICA study is designed to demonstrate a disease free survival benefit by adding bevacizumab to an adjuvant regime of CAPOX in patients with colorectal liver metastases undergoing a radical resection or resection in combination with RFA."( A randomized two arm phase III study in patients post radical resection of liver metastases of colorectal cancer to investigate bevacizumab in combination with capecitabine plus oxaliplatin (CAPOX) vs CAPOX alone as adjuvant treatment.
Bergman, AM; Dalesio, O; Rinkes, IH; Schouten, SB; Snoeren, N; Tollenaar, RA; van der Sijp, JR; van Hillegersberg, R; Verheul, HM; Voest, EE, 2010)		0.56
" The aim of this study was to evaluate the efficacy and safety of this regimen in combination with bevacizumab (BV), as first-line treatment for mCRC."( Bevacizumab in combination with biweekly capecitabine and irinotecan, as first-line treatment for patients with metastatic colorectal cancer.
Alvarez-Suarez, S; García-Alfonso, P; Jerez-Gilarranz, Y; Khosravi, P; Martin, M; Muñoz-Martin, AJ; Riesco-Martinez, M, 2010)		0.63
"Bevacizumab combined with biweekly XELIRI is a highly active first-line regimen for mCRC treatment, showing encouraging PFS, ORR and OS with a good tolerability."( Bevacizumab in combination with biweekly capecitabine and irinotecan, as first-line treatment for patients with metastatic colorectal cancer.
Alvarez-Suarez, S; García-Alfonso, P; Jerez-Gilarranz, Y; Khosravi, P; Martin, M; Muñoz-Martin, AJ; Riesco-Martinez, M, 2010)		0.63
"To evaluate the efficacy and safety of weekly or 3-week docetaxel in combination with capecitabine."( [A pilot study of weekly versus 3-week docetaxel in combination with capecitabine in patients with anthracycline-pretreated metastatic breast cancer].
Bai, YX; Cheng, Y; Jiang, ZF; Jiao, SC; Li, X; Liu, DQ; Liu, JW; Liu, WC; Ren, J; Sun, Q; Tang, LL; Wang, HQ; Wang, Y; Wang, YS; Wei, Y; Xiao, JX; Xie, XD; Zhang, SH, 2010)		0.82
" The aim of this study was to evaluate the activity and safety of capecitabine combined with weekly docetaxel for the treatment of anthracycline-resistant metastatic breast cancer (MBC) in older Chinese patients."( Capecitabine combined with weekly docetaxel in Chinese patients > 65 years with anthracycline-resistant metastatic breast cancer.
Hao, XS; Hou, Y; Li, LF; Liu, XM; Qian, ZZ; Qiu, LH; Wang, HQ; Xie, CH; Zhang, HL; Zhou, SY, 2010)		2.04
" Efficacy and tolerability compare favourably with previously reported trials evaluating higher capecitabine doses in combination with 3-weekly or weekly docetaxel."( Capecitabine combined with weekly docetaxel in Chinese patients > 65 years with anthracycline-resistant metastatic breast cancer.
Hao, XS; Hou, Y; Li, LF; Liu, XM; Qian, ZZ; Qiu, LH; Wang, HQ; Xie, CH; Zhang, HL; Zhou, SY, 2010)		2.02
"We conducted a Phase I clinical trial to evaluate the safety, tolerability, and pharmacokinetics (PK) of CKD-732 [6-O-(4-dimethylaminoethoxy) cinnamoyl fumagillol hemioxalate] in combination with capecitabine and oxaliplatin (XELOX) in nine metastatic colorectal cancer patients who had progressed on irinotecan-based chemotherapy."( A Phase Ib pharmacokinetic study of the anti-angiogenic agent CKD-732 used in combination with capecitabine and oxaliplatin (XELOX) in metastatic colorectal cancer patients who progressed on irinotecan-based chemotherapy.
Ahn, JB; Chung, HC; Hong, YS; Kim, C; Kim, DH; Kim, HR; Kim, TW; Lee, YJ; Park, KS; Rha, SY; Roh, JK; Shin, SJ, 2012)		0.79
" The maximum tolerated dose was 10 mg/m(2)/d, and the clinically recommended dose was 5 mg/m(2)/d for CKD-732 in combination with XELOX."( A Phase Ib pharmacokinetic study of the anti-angiogenic agent CKD-732 used in combination with capecitabine and oxaliplatin (XELOX) in metastatic colorectal cancer patients who progressed on irinotecan-based chemotherapy.
Ahn, JB; Chung, HC; Hong, YS; Kim, C; Kim, DH; Kim, HR; Kim, TW; Lee, YJ; Park, KS; Rha, SY; Roh, JK; Shin, SJ, 2012)		0.6
"The Phase II recommended dose of CKD-732 was determined to be 5 mg/m(2)/d, and this dose was safely combined with a conventional dose of capecitabine and oxaliplatin in this patient population."( A Phase Ib pharmacokinetic study of the anti-angiogenic agent CKD-732 used in combination with capecitabine and oxaliplatin (XELOX) in metastatic colorectal cancer patients who progressed on irinotecan-based chemotherapy.
Ahn, JB; Chung, HC; Hong, YS; Kim, C; Kim, DH; Kim, HR; Kim, TW; Lee, YJ; Park, KS; Rha, SY; Roh, JK; Shin, SJ, 2012)		0.8
"Interstitial lung disease in patients with colorectal cancer during chemotherapy combined with bevacizumab is rare."( Interstitial lung disease during chemotherapy combined with oxaliplatin and/or bevacizumab in advanced colorectal cancer patients.
Furushima, K; Ishihara, T; Katou, Y; Tanai, C; Tanaka, Y; Usui, K, 2011)		0.37
" Pharmacokinetic analysis showed no apparent drug-drug interaction."( A multicentre dose-escalating study of cabazitaxel (XRP6258) in combination with capecitabine in patients with metastatic breast cancer progressing after anthracycline and taxane treatment: a phase I/II study.
Awada, A; Besse, T; Campone, M; Dubin, F; Machiels, JP; Magherini, E; Pivot, X; Semiond, D; Villanueva, C, 2011)		0.6
"Cabazitaxel combined with capecitabine is active, has a safety profile consistent with a taxane plus capecitabine combination and warrants further investigation in patients with MBC."( A multicentre dose-escalating study of cabazitaxel (XRP6258) in combination with capecitabine in patients with metastatic breast cancer progressing after anthracycline and taxane treatment: a phase I/II study.
Awada, A; Besse, T; Campone, M; Dubin, F; Machiels, JP; Magherini, E; Pivot, X; Semiond, D; Villanueva, C, 2011)		0.9
"To evaluate the efficacy and treatment-related toxicity of accelerated hyperfractionation field-involved re-irradiation combined with concurrent capecitabine chemotherapy for locally recurrent and irresectable rectal cancer (LRIRC)."( Accelerated hyperfractionation field-involved re-irradiation combined with concurrent capecitabine chemotherapy for locally recurrent and irresectable rectal cancer.
Dai, Y; Li, L; Shao, ZY; Sun, DS; Yu, JM; Zhang, JD, 2012)		0.8
"Three-dimensional conformal accelerated hyperfractionation field-involved re-irradiation combined with concurrent capecitabine chemotherapy might be an effective and well-tolerated regimen for patients with LRIRC."( Accelerated hyperfractionation field-involved re-irradiation combined with concurrent capecitabine chemotherapy for locally recurrent and irresectable rectal cancer.
Dai, Y; Li, L; Shao, ZY; Sun, DS; Yu, JM; Zhang, JD, 2012)		0.81
"Capecitabine administered for 7 days followed by a 7-day rest in combination with bevacizumab had modest efficacy and an acceptable toxicity profile in patients with MBC."( Phase 2 trial of a novel capecitabine dosing schedule in combination with bevacizumab for patients with metastatic breast cancer.
Feigin, K; Gajria, D; Geneus, S; Hudis, CA; Norton, L; Patil, S; Tan, LK; Theodoulou, M; Traina, TA, 2011)		2.12
"Vandetanib at doses of 100 mg and 300 mg daily in combination with capecitabine and oxaliplatin was well tolerated."( A phase I trial of vandetanib combined with capecitabine, oxaliplatin and bevacizumab for the first-line treatment of metastatic colorectal cancer.
Cabebe, EC; Fisher, GA; Sikic, BI, 2012)		0.88
"To confirm the efficacy and toxicity of Erlotinib in combination with Gemcitabine and Capecitabine when used as a first-line therapy in metastatic/recurrent pancreatic cancer (PC)."( A phase II trial of erlotinib in combination with gemcitabine and capecitabine in previously untreated metastatic/recurrent pancreatic cancer: combined analysis with translational research.
Bang, YJ; Kang, HJ; Kim, BS; Kim, JS; Lee, KH; Lee, KW; Oh, DY; Park, YS; Ryoo, HM; Sohn, CH; Song, HS; Zang, DY, 2012)		0.84
"0 mg/kg q2w, concomitantly with a combination of capecitabine and oxaliplatin (XELOX) and FOLFOX-4 (oxaliplatin in combination with infusional 5-FU/LV), respectively, in patients with metastatic colorectal cancer (mCRC)."( A multicenter, randomized, open-label study to assess the steady-state pharmacokinetics of bevacizumab given with either XELOX or FOLFOX-4 in patients with metastatic colorectal cancer.
Abt, M; Burns, I; Chen, E; Goldstein, D; Major, P; McKendrick, J; Rittweger, K; Robinson, B; Zhi, J, 2011)		0.62
" BV in combination with XELOX and FOLFOX-4 was generally well tolerated with no unexpected safety signals and no deaths."( A multicenter, randomized, open-label study to assess the steady-state pharmacokinetics of bevacizumab given with either XELOX or FOLFOX-4 in patients with metastatic colorectal cancer.
Abt, M; Burns, I; Chen, E; Goldstein, D; Major, P; McKendrick, J; Rittweger, K; Robinson, B; Zhi, J, 2011)		0.37
"This phase I study was conducted primarily to determine the maximum tolerated dose (MTD) of tesetaxel, a novel, orally active, semisynthetic microtubule inhibitor of the taxane class, administered with oral capecitabine to patients with advanced solid tumors."( Tesetaxel, a new oral taxane, in combination with capecitabine: a phase I, dose-escalation study in patients with advanced solid tumors.
Beeram, M; Patnaik, A; Saif, MW; Sarantopoulos, J; Takimoto, C; Tolcher, AW, 2011)		0.81
" These data further support the continued clinical development of tesetaxel both as a single agent and in combination with other active cancer therapeutics."( Tesetaxel, a new oral taxane, in combination with capecitabine: a phase I, dose-escalation study in patients with advanced solid tumors.
Beeram, M; Patnaik, A; Saif, MW; Sarantopoulos, J; Takimoto, C; Tolcher, AW, 2011)		0.62
" The drug combination elevated the plasma level of PHT in a patient on chemotherapy with capecitabine for colorectal cancer."( [A case of toxicity caused by drug interaction between capecitabine and phenytoin in patient with colorectal cancer].
Fukui, E; Kawahara, K; Sakurai, M; Ueda, R; Yamada, R, 2011)		0.84
"To observe and compare the response rate and toxicity of irinotecan or oxaliplatin combined with capecitabine in the treatment of advanced gastric cancer."( [Comparison between the effects of irinotecan or oxaliplatin combined with capecitabine in the treatment of advanced gastric cancer].
Chen, DY; Qi, Q; Zhao, WY, 2011)		0.82
"The therapeutic effects of irinotecan or oxaliplatin combined with capecitabine in the treatment of advanced gastric cancer are good and comparable, and their toxicities are tolerable."( [Comparison between the effects of irinotecan or oxaliplatin combined with capecitabine in the treatment of advanced gastric cancer].
Chen, DY; Qi, Q; Zhao, WY, 2011)		0.84
"This phase II study is performed to evaluate the efficacy and safety of capecitabine combined with preoperative radiotherapy (RT) in Chinese patients with locally advanced rectal cancer (LARC)."( Preoperative radiotherapy combined with capecitabine chemotherapy in Chinese patients with locally advanced rectal cancer.
Deng, J; Jin, J; Li, X; Lu, W; Meng, H; Wang, F; Xu, X; Xue, Z; Zhang, H; Zhou, G, 2011)		0.87
"The primary objective of this Phase I study was to assess the safety and tolerability of the vascular endothelial growth factor signalling inhibitor cediranib in combination with cisplatin plus an oral fluoropyrimidine, in Japanese patients with previously untreated advanced gastric cancer."( Phase I study of cediranib in combination with cisplatin plus fluoropyrimidine (S-1 or capecitabine) in Japanese patients with previously untreated advanced gastric cancer.
Boku, N; Brown, KH; Hayashi, H; Muro, K; Nakajima, TE; Satoh, T; Shi, X; Shimada, Y; Takahari, D; Taku, K; Yamada, Y, 2012)		0.6
"Patients received continuous, once-daily oral doses of cediranib 20 mg in combination with either cisplatin (60 mg/m(2) iv day 1) plus S-1 (40-60 mg bid, days 1-21) every 5 weeks for a maximum of eight cycles [Arm A]; or cisplatin (80 mg/m(2) iv, day 1) plus capecitabine (1,000 mg/m(2) bid, days 1-14) every 3 weeks for a maximum of six cycles [Arm B]."( Phase I study of cediranib in combination with cisplatin plus fluoropyrimidine (S-1 or capecitabine) in Japanese patients with previously untreated advanced gastric cancer.
Boku, N; Brown, KH; Hayashi, H; Muro, K; Nakajima, TE; Satoh, T; Shi, X; Shimada, Y; Takahari, D; Taku, K; Yamada, Y, 2012)		0.78
"Cediranib 20 mg/day in combination with cisplatin and S-1 or capecitabine was tolerable, with no new toxicities identified, and showed preliminary evidence of antitumour activity."( Phase I study of cediranib in combination with cisplatin plus fluoropyrimidine (S-1 or capecitabine) in Japanese patients with previously untreated advanced gastric cancer.
Boku, N; Brown, KH; Hayashi, H; Muro, K; Nakajima, TE; Satoh, T; Shi, X; Shimada, Y; Takahari, D; Taku, K; Yamada, Y, 2012)		0.84
"To evaluate the activity and tolerance of gemcitabine in combination with docetaxel and capecitabine in previously untreated patients with advanced pancreatic cancer."( Docetaxel plus gemcitabine in combination with capecitabine as treatment for inoperable pancreatic cancer: a phase II study.
Amarantidis, K; Chamalidou, E; Chelis, L; Chiotis, A; Courcoutsakis, N; Dimopoulos, P; Kakolyris, S; Prassopoulos, P; Tentes, A; Xenidis, N, 2012)		0.86
" Capecitabine dose was 2500 mg/m(2)/day on days 1-7 (n = 11) and was increased to 3000 mg/m(2)/day (n = 29) in combination with oxaliplatin (85 mg/m(2)) and bevacizumab (5 mg/kg)."( A phase I/II study of capecitabine given on a week on/week off schedule combined with bevacizumab and oxaliplatin for patients with untreated advanced colorectal cancer.
Balaban, EP; Crandall, TL; Kane, P; Lembersky, BC; Pinkerton, RA; Potter, DM; Rajasenan, KK; Ramanathan, RK; Schmotzer, A; Sehgal, R; Zeh, H, 2011)		1.59
"The first US experience of capecitabine to our knowledge (3000 mg/m(2) on days 1-7) in combination with oxaliplatin/bevacizumab in mCRC does not appear to have advantages compared with current standard first-line mCRC treatment regimens."( A phase I/II study of capecitabine given on a week on/week off schedule combined with bevacizumab and oxaliplatin for patients with untreated advanced colorectal cancer.
Balaban, EP; Crandall, TL; Kane, P; Lembersky, BC; Pinkerton, RA; Potter, DM; Rajasenan, KK; Ramanathan, RK; Schmotzer, A; Sehgal, R; Zeh, H, 2011)		0.98
" The conventional schedule of capecitabine limits full dosing in combination with other agents due to toxicity."( Phase II trial of a novel capecitabine dosing schedule in combination with lapatinib for the treatment of patients with HER2-positive metastatic breast cancer.
Chen, C; D'Andrea, G; Drullinsky, P; Feigin, K; Gajria, D; Gonzalez, J; Hudis, CA; Lake, D; Norton, L; Patil, S; Theodoulou, M; Traina, TA, 2012)		0.97
" In patients with human epidermal growth factor receptor type 2 (HER2)-negative metastatic breast cancer, bevacizumab is indicated as first-line therapy in combination with paclitaxel, or in combination with capecitabine when treatment with other chemotherapy options, including taxanes or anthracyclines, is not considered appropriate."( Bevacizumab: a review of its use in combination with paclitaxel or capecitabine as first-line therapy for HER2-negative metastatic breast cancer.
Croom, KF; Dhillon, S, 2011)		0.79
"A phase I study was performed to determine the maximal tolerated dose (MTD), recommended dose (RD), safety and efficacy of vinflunine when combined with capecitabine in patients with metastatic breast cancer (MBC) previously treated with anthracyclines and taxanes, with pharmacokinetic blood sampling to test potential drug-drug interactions."( A phase I study of vinflunine in combination with capecitabine in patients with metastatic breast cancer previously treated with anthracyclines and taxanes.
Bonneterre, J; Bourbouloux, E; Campone, M; Fumoleau, P; Isambert, N; Milano, G; Roché, H, 2012)		0.83
" The risk of clinical significant drug-drug interaction was considered weak."( A phase I study of vinflunine in combination with capecitabine in patients with metastatic breast cancer previously treated with anthracyclines and taxanes.
Bonneterre, J; Bourbouloux, E; Campone, M; Fumoleau, P; Isambert, N; Milano, G; Roché, H, 2012)		0.63
"To evaluate the pharmacokinetics (PK) of capecitabine and cisplatin, administered in combination with or without trastuzumab, in Japanese patients with HER2-positive advanced gastric cancer (AGC)."( Pharmacokinetic analysis of capecitabine and cisplatin in combination with trastuzumab in Japanese patients with advanced HER2-positive gastric cancer.
Boku, N; Hamamoto, Y; Ohtsu, A; Omuro, Y; Sasaki, Y; Satoh, T; Tamura, T, 2012)		0.94
"We performed a prospective phase II trial to investigate the safety and efficacy of radiotherapy combined with capecitabine in patients suffering from a recurrence of a squamous cell carcinoma of the head and neck (SCCHN) within a previously irradiated field."( Re-irradiation combined with capecitabine in locally recurrent squamous cell carcinoma of the head and neck. A prospective phase II trial.
Kornek, G; Lemaire, C; Radonjic, D; Selzer, E; Vormittag, L, 2012)		0.88
"A total of 31 evaluable patients with recurrent SCCHN received re-irradiation with a total dose of 50 Gy (25 fractions over 5 weeks) up to a maximum of 60 Gy combined with 900 mg/m(2)/day capecitabine given on the days of radiotherapy."( Re-irradiation combined with capecitabine in locally recurrent squamous cell carcinoma of the head and neck. A prospective phase II trial.
Kornek, G; Lemaire, C; Radonjic, D; Selzer, E; Vormittag, L, 2012)		0.86
"Capecitabine combined with re-irradiation is a well-tolerated treatment in patients with recurrent SCCHN."( Re-irradiation combined with capecitabine in locally recurrent squamous cell carcinoma of the head and neck. A prospective phase II trial.
Kornek, G; Lemaire, C; Radonjic, D; Selzer, E; Vormittag, L, 2012)		2.11
"To evaluate the efficacy of late accelerated hyperfractionated conformal radiotherapy (LACF) combined with capecitabine on esophageal carcinoma."( [Efficacy of late accelerated hyperfractionated conformal radiotherapy combined with capecitabine for esophageal carcinoma].
Feng, XZ; Han, JQ; Sheng, W, 2011)		0.81
"3 Gy per fraction to a total dose about 64 - 69 Gy, and LCAF + C group (late accelerated hyperfractionated radiotherapy combined with capecitabine), in which patients were treated as the same as the LCAF group, except that they were treated with capecitabine (1."( [Efficacy of late accelerated hyperfractionated conformal radiotherapy combined with capecitabine for esophageal carcinoma].
Feng, XZ; Han, JQ; Sheng, W, 2011)		0.8
"Capecitabine, as an effective chemosensitizater combined with late accelerate hyperfractionated radiotherapy can improve the short-term results of treatment of esophageal cancer."( [Efficacy of late accelerated hyperfractionated conformal radiotherapy combined with capecitabine for esophageal carcinoma].
Feng, XZ; Han, JQ; Sheng, W, 2011)		2.04
"We conducted a multiinstitutional phase II study of capecitabine in combination with vinorelbine and trastuzumab in patients eligible to receive first- or second-line treatment for human epidermal growth factor receptor type 2 (HER2)-positive (HER2(+)) metastatic breast cancer (MBC)."( Phase II interventional study (N0337) of capecitabine in combination with vinorelbine and trastuzumab for first- or second-line treatment of HER2-positive metastatic breast cancer: a north central cancer treatment group trial.
Allred, JB; Bernath, AM; Fishkin, PA; Fitch, TR; Flynn, P; Perez, EA; Salim, M; Stella, PJ; Tan, WW; Wiesenfeld, M, 2012)		0.9
"We report the first results from a phase II, open-label study designed to evaluate the efficacy and safety of bevacizumab in combination with trastuzumab and capecitabine as first-line therapy for human epidermal growth factor receptor (HER)-2-positive locally recurrent (LR) or metastatic breast cancer (MBC)."( Phase II study of bevacizumab in combination with trastuzumab and capecitabine as first-line treatment for HER-2-positive locally recurrent or metastatic breast cancer.
Gligorov, J; Lichinitser, M; Lluch, A; Makhson, A; Martín, M; Mitchell, L; Scotto, N; Semiglazov, V; Tjulandin, S, 2012)		0.81
"The aim of this study was to determine the safety and efficacy of metronomic chemotherapy combined with targeted drugs in patients with metastatic breast cancer (MBC)."( Metronomic chemotherapy combined with bevacizumab and erlotinib in patients with metastatic HER2-negative breast cancer: clinical and biological activity.
Bagnardi, V; Bertolini, F; Calleri, A; Cancello, G; Colleoni, M; Dellapasqua, S; Goldhirsch, A; Intra, M; Luini, A; Montagna, E; Pastrello, D; Perri, G; Rampinelli, C; Veronesi, P; Viale, G, 2012)		0.38
"The object of this study was to evaluate the safety and efficacy of metronomic chemotherapy in combination with bevacizumab and erlotinib in patients with HER2-negative (HER2(-)) metastatic breast cancer (MBC) and poor hormone receptor expression."( Metronomic chemotherapy combined with bevacizumab and erlotinib in patients with metastatic HER2-negative breast cancer: clinical and biological activity.
Bagnardi, V; Bertolini, F; Calleri, A; Cancello, G; Colleoni, M; Dellapasqua, S; Goldhirsch, A; Intra, M; Luini, A; Montagna, E; Pastrello, D; Perri, G; Rampinelli, C; Veronesi, P; Viale, G, 2012)		0.38
"Treatment with metronomic chemotherapy in combination with bevacizumab and erlotinib was effective in HER2(-), estrogen receptor (ER)- and progesterone receptor (PR)-poor advanced breast cancer."( Metronomic chemotherapy combined with bevacizumab and erlotinib in patients with metastatic HER2-negative breast cancer: clinical and biological activity.
Bagnardi, V; Bertolini, F; Calleri, A; Cancello, G; Colleoni, M; Dellapasqua, S; Goldhirsch, A; Intra, M; Luini, A; Montagna, E; Pastrello, D; Perri, G; Rampinelli, C; Veronesi, P; Viale, G, 2012)		0.38
" In this study, patient-derived tumor tissue (PDTT) xenograft models of primary colon carcinoma and lymphatic and hepatic metastases were established for assessment of the antitumor activity of FP3 in combination with capecitabine."( Antitumor effects of FP3 in combination with capecitabine on PDTT xenograft models of primary colon carcinoma and related lymphatic and hepatic metastases.
Cao, F; Han, N; He, K; Jin, K; Lan, H; Li, G; Teng, L; Xie, B; Xu, Z, 2012)		0.82
"The aim was to evaluate activity and toxicity of hepatic arterial infusion of oxaliplatin in combination with capecitabine in patients with metastatic breast cancer with liver metastases and limited extrahepatic disease."( Intrahepatic and systemic therapy with oxaliplatin combined with capecitabine in patients with hepatic metastases from breast cancer.
Bergenfeldt, M; Hermann, KL; Jensen, BK; Jensen, BV; Nelausen, KM; Nielsen, DL; Nørgaard, H; Pfeiffer, P; Vestermark, LW, 2012)		0.83
"Sixteen consecutive patients received capecitabine 13 00mg/m(2) daily combined with oxaliplatin 85 mg/m(2) every two weeks."( Intrahepatic and systemic therapy with oxaliplatin combined with capecitabine in patients with hepatic metastases from breast cancer.
Bergenfeldt, M; Hermann, KL; Jensen, BK; Jensen, BV; Nelausen, KM; Nielsen, DL; Nørgaard, H; Pfeiffer, P; Vestermark, LW, 2012)		0.89
" The results suggest that capecitabine may be useful in combination with standard fluorouracil-based regimens in patients with advanced and/or metastatic gastric cancer with favourable safety profile."( Incidence of hand-foot syndrome with capecitabine in combination with chemotherapy as first-line treatment in patients with advanced and/or metastatic gastric cancer suitable for treatment with a fluoropyrimidine-based regimen.
Aparicio, J; Dueñas, R; Falcó, E; Gómez-Martin, C; Irigoyen, A; Lacasta, A; Llorente, B; López, RL; Muñoz, ML; Pérez, B; Reboredo, M; Regueiro, P; Safont, MJ; Sánchez, A; Sanchez-Viñes, E; Serrano, R, 2012)		0.95
" This prospective phase II study evaluated the activity and toxicity of a modified regimen with lower doses of docetaxel and cisplatin combined with oral capecitabine instead of fluorouracil for patients with advanced gastric cancer."( Modified docetaxel-cisplatin in combination with capecitabine as first-line treatment in metastatic gastric cancer. a phase II study.
Dimitroulis, D; Felekouras, E; Griniatsos, J; Karatzas, T; Karavokyros, J; Kontzoglou, K; Mantas, D; Nikiteas, N; Polyzos, A; Polyzos, K; Syrigos, K; Tsavaris, N; Vafiadis, I, 2012)		0.83
" This phase I study investigated the safety, tolerability, pharmacokinetics and antitumour activity of axitinib combined with chemotherapy."( Phase I study of axitinib combined with paclitaxel, docetaxel or capecitabine in patients with advanced solid tumours.
Chen, Y; Cohen, RB; Herbst, RS; Kim, S; Kozloff, MF; Martin, LP; Olszanski, AJ; Rado, T; Rosbrook, B; Samuel, TA; Starr, A; Tarazi, J; Tortorici, M, 2012)		0.62
"Axitinib combined with paclitaxel or capecitabine was well tolerated; no additive increase in toxicities was observed."( Phase I study of axitinib combined with paclitaxel, docetaxel or capecitabine in patients with advanced solid tumours.
Chen, Y; Cohen, RB; Herbst, RS; Kim, S; Kozloff, MF; Martin, LP; Olszanski, AJ; Rado, T; Rosbrook, B; Samuel, TA; Starr, A; Tarazi, J; Tortorici, M, 2012)		0.89
"Oxaliplatin (OX), in combination with fluoropyrimidine (5-fluorouracil or Capecitabine, FU)-based regimens and radiation, has been expected to both enhance primary tumour shrinkage and reduce micrometastases at distant sites in the neoadjuvant chemoradiotherapy (CRT) for locally advanced rectal cancer (LARC)."( Short term results of neoadjuvant chemoradiotherapy with fluoropyrimidine alone or in combination with oxaliplatin in locally advanced rectal cancer: a meta analysis.
An, X; Cai, PQ; Ding, PR; Fang, YJ; Gao, YH; Goodman, K; Kong, LH; Lin, JZ; Lin, X; Pan, ZZ; Wan, DS; Wang, FH, 2013)		0.62
" (177)Lu-octreotate, in combination with capecitabine and temozolomide, is well tolerated in patients with advanced low-grade NETs, and shows substantial tumor control rates."( Phase I-II study of radiopeptide 177Lu-octreotate in combination with capecitabine and temozolomide in advanced low-grade neuroendocrine tumors.
Claringbold, PG; Price, RA; Turner, JH, 2012)		0.88
"We evaluated AMG 386, an investigational peptibody that neutralizes the interaction between angiopoietins-1 and -2 and the Tie2 receptor, combined with cisplatin/capecitabine (CX) as first-line treatment for metastatic gastro-oesophageal cancer."( Phase II randomized, double-blind, placebo-controlled study of AMG 386 (trebananib) in combination with cisplatin and capecitabine in patients with metastatic gastro-oesophageal cancer.
Adewoye, AH; Bampton, CL; Bass, MB; Bodoky, G; Eatock, MM; Nanayakkara, N; Strickland, AH; Sun, YN; Swieboda-Sadlej, A; Tebbutt, NC; Valladares-Ayerbes, M; Van Cutsem, E; Zhong, ZD, 2013)		0.79
"With better access to metastases and certain large or inoperable tumours, we applied two treatment sessions of combined therapy of whole-body hyperthermia and hyperthermic intraperitoneal chemo-perfusion in the treatment group, while patients in the control group were treated with oxaliplatin combined with 5-fluorouracil chemotherapy or Xeloda."( Whole-body hyperthermia combined with hyperthermic intraperitoneal chemotherapy for the treatment of stage IV advanced gastric cancer.
Chen, X; Dai, C; Zhao, C, 2012)		0.38
"These results suggest that whole-body hyperthermia combined with hyperthermic intraperitoneal chemotherapy is an effective treatment for patients with advanced gastric malignancies."( Whole-body hyperthermia combined with hyperthermic intraperitoneal chemotherapy for the treatment of stage IV advanced gastric cancer.
Chen, X; Dai, C; Zhao, C, 2012)		0.38
"This prospective observational study assessed the efficacy of bevacizumab in combination with chemotherapy as preoperative treatment to downsize tumours for radical resection in patients with unresectable metastatic colorectal cancer (mCRC)."( Preoperative treatment with bevacizumab in combination with chemotherapy in patients with unresectable metastatic colorectal carcinoma.
Albiol, M; Alsina, M; Codina-Barreras, A; Figueras, J; Guardeño, R; Hernandez-Yagüe, X; Lopez-Ben, S; Queralt, B; Soriano, J, 2013)		0.39
" Preoperative treatment consisted of bevacizumab (5 mg/kg) combined with oxaliplatin- or irinotecan-based chemotherapy, which was followed by surgery in patients showing clinical benefit."( Preoperative treatment with bevacizumab in combination with chemotherapy in patients with unresectable metastatic colorectal carcinoma.
Albiol, M; Alsina, M; Codina-Barreras, A; Figueras, J; Guardeño, R; Hernandez-Yagüe, X; Lopez-Ben, S; Queralt, B; Soriano, J, 2013)		0.39
"To evaluate the efficacy and tolerability of capecitabine combined with thalidomide in patients with advanced pancreatic cancer (APC) who have previously received gemcitabine-based therapy."( Phase II trial of capecitabine combined with thalidomide in second-line treatment of advanced pancreatic cancer.
Liu, QY; Niu, ZX; Shi, SB; Tang, XY; Wang, M, )		0.72
"Capecitabine combined with thalidomide is a well-tolerated second-line regimen, in patients with APC refractory to gemcitabine."( Phase II trial of capecitabine combined with thalidomide in second-line treatment of advanced pancreatic cancer.
Liu, QY; Niu, ZX; Shi, SB; Tang, XY; Wang, M, )		1.91
"The aim of this phase I trial was to define the maximum tolerated dose (MTD), the dose-limiting toxicity (DLT) and the recommended dose of erlotinib combined with capecitabine and gemcitabine in the treatment of advanced pancreatic cancer (APC)."( Phase I trial of gemcitabine combined with capecitabine and erlotinib in advanced pancreatic cancer: a clinical and pharmacological study.
Bennouna, J; Chamorey, E; Douillard, JY; Etienne-Grimaldi, MC; Follana, P; Francois, E; Mari, V; Michel, C; Milano, G; Renée, N; Senellart, H, 2012)		0.84
"To observe efficacy and side effects, as well as the impact on quality of life, of Kanglaite® (Coix Seed Oil) injections combined with chemotherapy in the treatment of advanced gastric cancer patiensts."( Clinical safety and efficacy of Kanglaite® (Coix Seed Oil) injection combined with chemotherapy in treating patients with gastric cancer.
Cao, J; Huang, XE; Liu, J; Lu, YY; Wu, XY; Xiang, J; Xu, X; Ye, LH; Zhan, YP, 2012)		0.38
"A consecutive cohort of 60 patients were divided into two groups:the experimental group receiving Kanglaite® Injection combined with chemotherapy and the control group with chemotherapy alone."( Clinical safety and efficacy of Kanglaite® (Coix Seed Oil) injection combined with chemotherapy in treating patients with gastric cancer.
Cao, J; Huang, XE; Liu, J; Lu, YY; Wu, XY; Xiang, J; Xu, X; Ye, LH; Zhan, YP, 2012)		0.38
" Patients were treated with cetuximab combined with either CAPIRI or CAPOX."( Early tumor shrinkage in patients with metastatic colorectal cancer receiving first-line treatment with cetuximab combined with either CAPIRI or CAPOX: an analysis of the German AIO KRK 0104 trial.
Giessen, C; Haas, M; Heinemann, V; Laubender, RP; Mansmann, U; Modest, DP; Schulz, C; Stintzing, S, 2013)		0.39
"To investigate the efficacy and safety of chemotherapy combined with intraperitoneal perfusion of cytokine-induced killer (CIK) cells for advanced gastric cancer patients with ascites."( [A pilot study of chemotherapy combined with intraperitoneal perfusion of cytokine-induced killer cells for advanced gastric cancer patients with ascites].
Chen, Y; Feng, Y; Li, Q; Liu, TS; Wang, ZM; Zhuang, RY, 2013)		0.39
" According to personal choice, patients were divided into 2 groups: XELOX chemotherapy alone (Capecitabine and Oxaliplatin) was applied in 22 patients (chemotherapy group) and XELOX combined with intraperitoneal perfusion of CIK cells in 20 patients (combination group)."( [A pilot study of chemotherapy combined with intraperitoneal perfusion of cytokine-induced killer cells for advanced gastric cancer patients with ascites].
Chen, Y; Feng, Y; Li, Q; Liu, TS; Wang, ZM; Zhuang, RY, 2013)		0.61
"Pazopanib combined with FOLFOX6 or reduced CapeOx was adequately tolerated in this patient population."( An open-label study of the safety and tolerability of pazopanib in combination with FOLFOX6 or CapeOx in patients with colorectal cancer.
Adams, LM; Botbyl, J; Brady, J; Chau, I; Corrie, P; Digumarti, R; Laubscher, KH; Mallath, M; Midgley, RS, 2013)		0.39
"The results from a phase III trial conducted outside of Japan demonstrated a significant improvement in time to progression (TTP) when lapatinib was combined with capecitabine compared with capecitabine alone in patients with HER2-positive advanced or metastatic breast cancer."( Efficacy, safety, pharmacokinetics and biomarker findings in patients with HER2-positive advanced or metastatic breast cancer treated with lapatinib in combination with capecitabine: results from 51 Japanese patients treated in a clinical study.
Ellis, CE; Fujii, H; Gagnon, RC; Iwata, H; Katsura, K; Masuda, N; Mukai, H; Nakamura, S; Nishimura, Y, 2015)		0.81
"Lapatinib in combination with capecitabine was well tolerated in the 51 patients enrolled in this study."( Efficacy, safety, pharmacokinetics and biomarker findings in patients with HER2-positive advanced or metastatic breast cancer treated with lapatinib in combination with capecitabine: results from 51 Japanese patients treated in a clinical study.
Ellis, CE; Fujii, H; Gagnon, RC; Iwata, H; Katsura, K; Masuda, N; Mukai, H; Nakamura, S; Nishimura, Y, 2015)		0.9
"Lapatinib in combination with capecitabine in Japanese HER2-positive breast cancer patients was well tolerated."( Efficacy, safety, pharmacokinetics and biomarker findings in patients with HER2-positive advanced or metastatic breast cancer treated with lapatinib in combination with capecitabine: results from 51 Japanese patients treated in a clinical study.
Ellis, CE; Fujii, H; Gagnon, RC; Iwata, H; Katsura, K; Masuda, N; Mukai, H; Nakamura, S; Nishimura, Y, 2015)		0.9
"A phase I trial of first-line vorinostat, an orally bio-available histone deacetylase inhibitor, in combination with capecitabine plus cisplatin (XP) was performed to assess recommend phase II trial dose in patients with advanced gastric cancer."( Phase I and pharmacodynamic study of vorinostat combined with capecitabine and cisplatin as first-line chemotherapy in advanced gastric cancer.
Kang, YK; Kim, SY; Koo, DH; Lee, CW; Maeng, J; Na, YS; Park, I; Ryoo, BY; Ryu, MH; Yoo, C, 2014)		0.85
" A multicenter phase II study was conducted to evaluate the efficacy and toxicity of capecitabine combined with nedaplatin for these patients."( Multicenter phase II study of capecitabine combined with nedaplatin for recurrent and metastatic nasopharyngeal carcinoma patients after failure of cisplatin-based chemotherapy.
Chen, ZB; Liao, H; Lin, Z; Ou, XQ; Peng, PJ; Peng, YL; Wang, SY; Zhang, HY, 2013)		0.9
"Capecitabine combined with nedaplatin offers a satisfactory clinical activity and an acceptable safety profile for recurrent and metastatic nasopharyngeal carcinoma patients after failure of cisplatin-based chemotherapy."( Multicenter phase II study of capecitabine combined with nedaplatin for recurrent and metastatic nasopharyngeal carcinoma patients after failure of cisplatin-based chemotherapy.
Chen, ZB; Liao, H; Lin, Z; Ou, XQ; Peng, PJ; Peng, YL; Wang, SY; Zhang, HY, 2013)		2.12
" Here we report the first phase 2 study of erlotinib in combination with adjuvant chemoradiation and chemotherapy for resected PDAC."( Phase 2 study of erlotinib combined with adjuvant chemoradiation and chemotherapy in patients with resectable pancreatic cancer.
Blackford, AL; Cameron, JL; Choti, MA; De Jesus-Acosta, A; Donehower, RC; Edil, BH; Ellsworth, S; Fan, KY; Hacker-Prietz, A; Herman, JM; Hidalgo, M; Hruban, RH; Laheru, DA; Le, DT; Pawlik, TM; Schulick, RD; Wild, AT; Wolfgang, CL; Wood, LD; Zheng, L, 2013)		0.39
"Erlotinib can be safely administered with adjuvant IMRT-based CRT and chemotherapy."( Phase 2 study of erlotinib combined with adjuvant chemoradiation and chemotherapy in patients with resectable pancreatic cancer.
Blackford, AL; Cameron, JL; Choti, MA; De Jesus-Acosta, A; Donehower, RC; Edil, BH; Ellsworth, S; Fan, KY; Hacker-Prietz, A; Herman, JM; Hidalgo, M; Hruban, RH; Laheru, DA; Le, DT; Pawlik, TM; Schulick, RD; Wild, AT; Wolfgang, CL; Wood, LD; Zheng, L, 2013)		0.39
" Patients are stratified by hormone-receptor status, geographic region, and prior metastatic chemotherapy status and randomized (1:1) to capecitabine (1000 mg/m2 orally twice daily (BID), days 1 to 14 of 21) in combination with sorafenib (orally BID, days 1 to 21, total dose 600 mg/day) or matching placebo."( A phase 3 tRial comparing capecitabinE in combination with SorafenIb or pLacebo for treatment of locally advanced or metastatIc HER2-Negative breast CancEr (the RESILIENCE study): study protocol for a randomized controlled trial.
Baselga, J; Costa, F; Gomez, H; Gradishar, WJ; Hudis, CA; Petrenciuc, O; Rapoport, B; Roche, H; Schwartzberg, LS; Shan, M, 2013)		0.89
"To evaluate the efficacy and safety of trastuzumab in combination with chemotherapy versus chemotherapy alone in the first-line treatment of HER-2-positive advanced gastric or gastro-oesophageal junction cancer."( [Trastuzumab in combination with chemotherapy versus chemotherapy alone for first-line treatment of HER2-positive advanced gastric or gastroesophageal junction cancer: a Phase III, multi-center, randomized controlled trial, Chinese subreport].
Feng, FY; Guan, ZZ; Jiao, SC; Jin, YN; Li, J; Pan, LX; Qin, SK; Shen, L; Tao, M; Wang, JJ; Wang, LW; Wang, YJ; Xu, JM; Yu, SY; Zheng, LZ, 2013)		0.39
" Patients were randomly assigned in a 1:1 ratio to receive a chemotherapy regimen consisting of capecitabine or 5-FU plus cisplatin or chemotherapy in combination with intravenous trastuzumab."( [Trastuzumab in combination with chemotherapy versus chemotherapy alone for first-line treatment of HER2-positive advanced gastric or gastroesophageal junction cancer: a Phase III, multi-center, randomized controlled trial, Chinese subreport].
Feng, FY; Guan, ZZ; Jiao, SC; Jin, YN; Li, J; Pan, LX; Qin, SK; Shen, L; Tao, M; Wang, JJ; Wang, LW; Wang, YJ; Xu, JM; Yu, SY; Zheng, LZ, 2013)		0.61
" Trastuzumab in combination with chemotherapy can be considered as a new option for patients with HER-2-positive advanced gastric or gastro-oesophageal junction cancer."( [Trastuzumab in combination with chemotherapy versus chemotherapy alone for first-line treatment of HER2-positive advanced gastric or gastroesophageal junction cancer: a Phase III, multi-center, randomized controlled trial, Chinese subreport].
Feng, FY; Guan, ZZ; Jiao, SC; Jin, YN; Li, J; Pan, LX; Qin, SK; Shen, L; Tao, M; Wang, JJ; Wang, LW; Wang, YJ; Xu, JM; Yu, SY; Zheng, LZ, 2013)		0.39
"To evaluate the inhibitory effect and its mechanism of celecoxib combined with capecitabine on the growth of implanted H22 hepatoma in mice."( [Inhibitory effects of celecoxib combined with capecitabine on H22 hepatoma mice and its mechanism].
Guo, HQ; Liu, YY; Yang, SJ; Yao, SN; Yao, ZH; Yuan, YD; Zhao, Y, 2013)		0.87
"The RP2D of dasatinib is 70 mg daily in combination with CapeOx/bevacizumab."( Phase I study of dasatinib in combination with capecitabine, oxaliplatin and bevacizumab followed by an expanded cohort in previously untreated metastatic colorectal cancer.
Arrowood, C; Blobe, GC; Brady, JC; Cohn, A; Haley, S; Hsu, SD; Hurwitz, HI; McCall, S; Meadows, KL; Morse, MA; Nixon, AB; Pang, H; Rushing, C; Starodub, A; Strickler, JH; Uronis, HE; Zafar, SY, 2014)		0.66
"We evaluated the safety and efficacy of biweekly capecitabine in combination with oxaliplatin in previously untreated patients with locally advanced or metastatic gastric cancer."( A multicenter phase II study of biweekly capecitabine in combination with oxaliplatin as first-line chemotherapy in patients with locally advanced or metastatic gastric cancer.
Bai, LY; Chao, Y; Chen, JS; Hsieh, JS; Li, CP; Su, WC; Su, YC; Tai, CJ; Wu, CC; Yeh, HT; Yeh, KH, 2014)		0.92
"To determine the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of capecitabine combined with postoperative radiotherapy for gastric cancer."( Phase I study of postoperative radiotherapy combined with capecitabine for gastric cancer.
Fang, H; Jin, J; Li, YX; Liu, XF; Liu, YP; Ren, H; Song, YW; Wang, SL; Wang, WH; Wang, X; Yu, ZH, 2014)		0.87
" Liver transplant patients receive a large number of medications and adverse drug reactions, and drug-drug interactions must be closely monitored."( Liver injury possibly related to drug interaction after liver transplant: a case report.
Jiang, WT; Liu, YH; Pan, C; Thian, Y; Zhu, LQ, 2014)		0.4
"Close monitoring and prompt discontinuation of the drugs with high volume of distribution and metabolized through the liver are necessary to avoid drug-drug interaction in liver transplant patients."( Liver injury possibly related to drug interaction after liver transplant: a case report.
Jiang, WT; Liu, YH; Pan, C; Thian, Y; Zhu, LQ, 2014)		0.4
"This study aimed to determine the recommended dose of capecitabine combined with peginterferon α-2a (Phase I) and evaluate its safety and efficacy for sorafenib-refractory advanced hepatocellular carcinoma (Phase II)."( A phase I/II trial of capecitabine combined with peginterferon α-2a in Patients with sorafenib-refractory advanced hepatocellular carcinoma.
Chiba, T; Kanai, F; Kanogawa, N; Motoyama, T; Ogasawara, S; Ooka, Y; Suzuki, E; Tawada, A; Yokosuka, AO, 2014)		0.97
"Capecitabine at 2000 mg/(m(2)∙day) combined with peginterferon α-2a (90 μg/week) exhibited moderate, albeit manageable, toxicity and was declared as the recommended phase II dose."( A phase I/II trial of capecitabine combined with peginterferon α-2a in Patients with sorafenib-refractory advanced hepatocellular carcinoma.
Chiba, T; Kanai, F; Kanogawa, N; Motoyama, T; Ogasawara, S; Ooka, Y; Suzuki, E; Tawada, A; Yokosuka, AO, 2014)		2.16
"A dose escalation study of biweekly irinotecan (CPT-11) combined with capecitabine was performed to determine the maximum tolerated dose (MTD) and recommended dose (RD) for metastatic breast cancer (MBC) previously treated with anthracyclines and taxanes."( A phase I study of capecitabine combined with CPT-11 in metastatic breast cancer pretreated with anthracyclines and taxanes.
Inaba, T; Ishida, K; Kashiwaba, M; Kawagishi, R; Komatsu, H; Matsui, Y; Sugai, T; Uesugi, N; Wakabayashi, G, 2014)		0.96
" We aimed to assess the safety, efficacy, biomarkers, and pharmacokinetics of rilotumumab combined with epirubicin, cisplatin, and capecitabine (ECX) in patients with advanced gastric or oesophagogastric junction cancer."( Rilotumumab in combination with epirubicin, cisplatin, and capecitabine as first-line treatment for gastric or oesophagogastric junction adenocarcinoma: an open-label, dose de-escalation phase 1b study and a double-blind, randomised phase 2 study.
Anderson, A; Davidenko, I; Deptala, A; Donehower, RC; Dubey, S; Harrison, M; Iveson, T; Jiang, Y; Lakshmaiah, K; Loh, E; Nirni, S; Oliner, KS; Tang, R; Thomas, A; Tjulandin, S; Zhu, M, 2014)		0.85
"This was a prospective single-centre, phase I study to document the maximum tolerated dose (MTD), dose-limiting toxicity (DLT), and the recommended phase II dose for future study of capecitabine in combination with radioembolization."( Phase I study of capecitabine combined with radioembolization using yttrium-90 resin microspheres (SIR-Spheres) in patients with advanced cancer.
Astsaturov, I; Ball, DS; Cade, DN; Cohen, SJ; Dickens, A; Konski, AA; Marlow, C; Meropol, NJ; Meyer, JE; Putnam, S; Yu, JQ, 2014)		0.93
"To evaluate the efficacy and safety of autologous cytokine-induced killer (CIK) cell t combined with XELOX regimen in treatment of senile advanced gastric cancer."( [Clinical study of autologous cytokine-induced killer cells combined with XELOX regimen in the treatment of senile advanced gastric cancer].
Bai, B; Cui, Y; Kuang, S; Wen, Y, 2014)		0.4
"Forty-six cases of senile advanced gastric cancer patients with a mean age of 70 years were prospectively divided into two groups according to individual acceptance of CIK cells: 25 patients receiving autologous CIK cell treatment combined with XELOX regimen (trial group) and 21 patients receiving simple chemotherapy (control group)."( [Clinical study of autologous cytokine-induced killer cells combined with XELOX regimen in the treatment of senile advanced gastric cancer].
Bai, B; Cui, Y; Kuang, S; Wen, Y, 2014)		0.4
"Autologous CIK cells combined with XELOX regimen can increase immune function, improve clinical efficacy, decrease adverse reaction and prolong OS for senile patients with advanced gastric cancers."( [Clinical study of autologous cytokine-induced killer cells combined with XELOX regimen in the treatment of senile advanced gastric cancer].
Bai, B; Cui, Y; Kuang, S; Wen, Y, 2014)		0.4
"Neratinib in combination with capecitabine had a manageable toxicity profile and showed promising antitumor activity in patients with HER2-positive metastatic breast cancer pretreated with trastuzumab and lapatinib."( Safety and efficacy of neratinib in combination with capecitabine in patients with metastatic human epidermal growth factor receptor 2-positive breast cancer.
Baselga, J; Cortés, J; Garcia-Saenz, JA; Germa, C; Harb, W; Kiger, C; Kim, SB; Martin, M; Moroose, R; Pluard, T; Saura, C; Wang, K; Xu, B, 2014)		0.94
"Docetaxel and cisplatin in combination with fluorouracil (DCF) regimen is accepted to be one of the standard regimens in the treatment of advanced gastric cancer."( Modified docetaxel and cisplatin in combination with capecitabine (DCX) as a first-line treatment in HER2-negative advanced gastric cancer.
Bilici, A; Demir, N; Dikilitas, M; Oven Ustaalioglu, BB; Selcukbiricik, F; Yildiz, O, 2014)		0.65
" Patients received docetaxel 60 mg/m2 plus cisplatin 60 mg/m2 (day 1) combined with capecitabine 1650 mg/m2 (days 1-14) every 3 weeks."( Modified docetaxel and cisplatin in combination with capecitabine (DCX) as a first-line treatment in HER2-negative advanced gastric cancer.
Bilici, A; Demir, N; Dikilitas, M; Oven Ustaalioglu, BB; Selcukbiricik, F; Yildiz, O, 2014)		0.88
"Bevacizumab (Bev) combined with chemotherapy significantly improves progression-free survival (PFS) but not overall survival (OS) in patients with human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer (MBC)."( The efficacy and safety of bevacizumab combined with chemotherapy in treatment of HER2-negative metastatic breast cancer: a meta-analysis based on published phase III trials.
Chen, F; Chen, Y; Cheng, B; Fang, Y; Qu, X; Wang, Z; Xiong, B, 2015)		0.42
"These preliminary results indicate that nimotuzumab can be safely combined with radiotherapy plus concurrent capecitabine."( Prospective phase II trial of nimotuzumab in combination with radiotherapy and concurrent capecitabine in locally advanced rectal cancer.
Fan, YT; Feng, HY; Jin, T; Ju, HX; Li, DC; Liu, LY; Liu, Y; Luo, JL; Zhou, N; Zhu, Y; Zhu, YP, 2015)		0.85
"Background This Phase 1b study aimed to determine the recommended Phase 2 dose of LY2334737, an oral pro-drug of gemcitabine, in combination with capecitabine, an oral pro-drug of 5-fluorouracil, in patients with advanced solid tumors."( Phase 1b study of the oral gemcitabine 'Pro-drug' LY2334737 in combination with capecitabine in patients with advanced solid tumors.
Adjei, AA; Bendell, J; Benhadji, KA; Callies, S; Dy, GK; Fetterly, G; Infante, JR; Ma, WW, 2015)		0.84
"Trastuzumab has been approved for use in combination with fluoropyrimidine plus cisplatin for the treatment of human epidermal growth factor receptor 2 (HER2)-positive advanced gastric cancer (AGC)."( Multicenter phase II study of trastuzumab in combination with capecitabine and oxaliplatin for advanced gastric cancer.
Chung, IJ; Han, HS; Kang, SY; Kang, YK; Kim, JG; Lee, KH; Park, SR; Park, YS; Ryoo, BY; Ryu, MH; Song, EK; Yoo, C, 2015)		0.66
"This phase I trial evaluated the question of whether the standard starting dose of axitinib could be administered in combination with therapeutic doses of cisplatin/capecitabine in patients with previously untreated advanced gastric cancer, and assessed overall safety, pharmacokinetics, and preliminary antitumor activity of this combination."( Phase I Study of Axitinib in Combination with Cisplatin and Capecitabine in Patients with Previously Untreated Advanced Gastric Cancer.
Bang, YJ; Chen, Y; Doi, T; Lee, KW; Oh, DY; Park, SR; Shirao, K; Valota, O; Yang, L, 2015)		0.85
" Therefore, we aimed to assess the clinical effect of XELOX neoadjuvant chemotherapy on AGC when combined with laparoscopic surgery."( Treatment of locally advanced gastric cancer with the XELOX program of neoadjuvantchemotherapy combined with laparoscopic surgery: the experience in China.
Huang, CM; Li, P; Lin, JX; Lu, J; Wang, JB; Xie, JW; Zheng, CH, 2014)		0.4
" Oxaliplatin in combination with intravenous 5-FU plus leucovorin (LV; modified [m]FOLFOX6) or capecitabine (XELOX) improves tolerability compared with 5-FU/cisplatin regimen."( Efficacy and safety of trastuzumab in combination with oxaliplatin and fluorouracil-based chemotherapy for patients with HER2-positive metastatic gastric and gastro-oesophageal junction adenocarcinoma patients: a retrospective study.
André, T; Bachet, JB; Chibaudel, B; Cohen, R; de Gramont, A; Hentic, O; Louvet, C; Samalin, E; Soularue, É; Tournigand, C; Zaanan, A, 2015)		0.64
"The primary objective of this study was to determine the activity and safety of 3-weekly oxaliplatin combined with gemcitabine and oral capecitabine in the first-line treatment of advanced biliary tract cancer."( Three-weekly oxaliplatin combined with gemcitabine and capecitabine in the first-line treatment of patients with advanced biliary tract cancer.
Fiaschi, AI; Francini, E; Laera, L; Marrelli, D; Petrioli, R; Roviello, F; Roviello, G, 2015)		0.87
" In this study, we compared the survival outcomes of mCRC patients treated with bevacizumab in combination with either modified 5-FU/FA/oxaliplatin (mFOL- FOX6) or capecitabine/oxaliplatin (XELOX)."( Comparison of first-line bevacizumab in combination with mFOLFOX6 or XELOX in metastatic colorectal cancer.
Akyol, M; Alacacioglu, A; Cokmert, S; Demir, L; Dirican, A; Kucukzeybek, Y; Oktay Tarhan, M; Varol, U; Vedat Bayoglu, I; Yildiz, I; Yildiz, Y, )		0.33
"Our results show that XELOX is a safe and effective alternative to mFOLFOX6 when combined with bevacizumab as first-line treatment for mCRC patients."( Comparison of first-line bevacizumab in combination with mFOLFOX6 or XELOX in metastatic colorectal cancer.
Akyol, M; Alacacioglu, A; Cokmert, S; Demir, L; Dirican, A; Kucukzeybek, Y; Oktay Tarhan, M; Varol, U; Vedat Bayoglu, I; Yildiz, I; Yildiz, Y, )		0.13
" The remission rate, control rate and time to disease progression were compared among patients receiving cetuximab combined with different chemotherapy regimens in different periods."( [Clinical efficacy observation of cetuximab combined with chemotherapy in the treatment of metastatic colorectal carcinoma].
Bai, L; Han, C; Jiao, S; Li, J; Su, D; Wang, Y; Zhang, T, 2015)		0.42
"Cetuximab in combination with oxaliplatin-based chemotherapy is recommended as the first-line application in the treatment of metastatic colorectal carcinoma patients, because it is helpful to improve the rate of disease control."( [Clinical efficacy observation of cetuximab combined with chemotherapy in the treatment of metastatic colorectal carcinoma].
Bai, L; Han, C; Jiao, S; Li, J; Su, D; Wang, Y; Zhang, T, 2015)		0.42
"4 mg/m(2) intravenously on days 1 and 8 of each cycle) combined with capecitabine (900 mg/m(2) orally twice daily on days 1-14 of each cycle [standard schedule] or 1500 mg orally twice daily using a 7-days on/7-days off schedule [weekly schedule])."( Phase II, Multicenter, Single-Arm, Feasibility Study of Eribulin Combined With Capecitabine for Adjuvant Treatment in Estrogen Receptor-Positive, Early-Stage Breast Cancer.
Berrak, E; Hoffman, AD; Jones, VE; McIntyre, K; O'Shaughnessy, J; Smith, JW; Song, JX; Vukelja, S, 2016)		0.9
" Recently, a phase II trial demonstrated that capecitabine and oxaliplatin (XELOX) combined with bevacizumab XELOX plus bevacizumab was effective and well tolerated by elderly patients with mCRC who reside in Western countries."( Capecitabine and oxaliplatin combined with bevacizumab are feasible for treating selected Japanese patients at least 75 years of age with metastatic colorectal cancer.
Fukunaga, M; Hasegawa, J; Hata, T; Ishibashi, K; Kanda, M; Kobayashi, M; Matsuoka, M; Mishima, H; Miyake, Y; Munemoto, Y; Nagase, M; Oba, K; Otsuji, T; Sakamoto, J; Takagane, A, 2015)		2.12
"5 mg/kg of intravenous bevacizumab and 130 mg/m(2) of oxaliplatin on day 1 of each cycle combined with 2000 mg/m(2) of oral capecitabine per day on days 1-14 of each cycle."( Capecitabine and oxaliplatin combined with bevacizumab are feasible for treating selected Japanese patients at least 75 years of age with metastatic colorectal cancer.
Fukunaga, M; Hasegawa, J; Hata, T; Ishibashi, K; Kanda, M; Kobayashi, M; Matsuoka, M; Mishima, H; Miyake, Y; Munemoto, Y; Nagase, M; Oba, K; Otsuji, T; Sakamoto, J; Takagane, A, 2015)		2.07
"XELOX combined with bevacizumab was well tolerated by selected Japanese patients aged ≥ 75 years with mCRC patients, and controlled clinical trials are now required to determine the survival benefit."( Capecitabine and oxaliplatin combined with bevacizumab are feasible for treating selected Japanese patients at least 75 years of age with metastatic colorectal cancer.
Fukunaga, M; Hasegawa, J; Hata, T; Ishibashi, K; Kanda, M; Kobayashi, M; Matsuoka, M; Mishima, H; Miyake, Y; Munemoto, Y; Nagase, M; Oba, K; Otsuji, T; Sakamoto, J; Takagane, A, 2015)		1.86
" Herein, we critically discuss the current data on the efficacy and safety profile of bevacizumab in combination with fluoropyrimidine-based chemotherapy for first-line and maintenance treatment of metastatic CRC and briefly comment on existing controversies and future perspectives."( Bevacizumab in combination with fluoropyrimidine-irinotecan- or fluoropyrimidine-oxaliplatin-based chemotherapy for first-line and maintenance treatment of metastatic colorectal cancer.
Grapsa, D; Saif, MW; Syrigos, K, 2015)		0.42
" In this context, alternatives to the lapatinib (L) and capecitabine (C) regimen, evaluating L combined with other cytotoxic drugs, are warranted."( A Phase II Randomized Study of Lapatinib Combined With Capecitabine, Vinorelbine, or Gemcitabine in Patients With HER2-Positive Metastatic Breast Cancer With Progression After a Taxane (Latin American Cooperative Oncology Group 0801 Study).
Barrios, CH; Bines, J; Blajman, C; Capó, A; Fanelli, M; Fein, L; Gómez, HL; Ismael, G; Lerzo, G; Mano, M; Martínez-Mesa, J; Neciosup, S; Nerón, Y; Pinczowski, H; Sampaio, C; Santi, PX; Tosello, C; Varela, MS; Werutsky, G; Zarba, JJ, 2016)		0.93
"In the present phase II, multicenter study, patients with HER2(+) MBC with progression after taxane were randomized between L, 1250 mg, combined with C, 2000 mg/m(2) on days 1 to 14 (LC), vinorelbine (V), 25 mg/m(2) on days 1 and 8 (LV), or gemcitabine (G), 1000 mg/m(2) on days 1 and 8 (LG), every 21 days."( A Phase II Randomized Study of Lapatinib Combined With Capecitabine, Vinorelbine, or Gemcitabine in Patients With HER2-Positive Metastatic Breast Cancer With Progression After a Taxane (Latin American Cooperative Oncology Group 0801 Study).
Barrios, CH; Bines, J; Blajman, C; Capó, A; Fanelli, M; Fein, L; Gómez, HL; Ismael, G; Lerzo, G; Mano, M; Martínez-Mesa, J; Neciosup, S; Nerón, Y; Pinczowski, H; Sampaio, C; Santi, PX; Tosello, C; Varela, MS; Werutsky, G; Zarba, JJ, 2016)		0.68
"To investigate the efficacy of bevacizumab and trastuzumab combined with docetaxel, oxaliplatin, and capecitabine (B-DOCT) as first-line treatment of advanced human epidermal growth factor receptor 2 (HER2)-positive gastric cancer (GC)."( Trastuzumab and bevacizumab combined with docetaxel, oxaliplatin and capecitabine as first-line treatment of advanced HER2-positive gastric cancer: a multicenter phase II study.
Beeker, A; Beerepoot, LV; Beijnen, JH; Boers, JE; Boot, H; Cats, A; de Groot, JW; de Jong, RS; Goey, SH; Kuiper, M; Los, M; Meulendijks, D; Polee, MB; Portielje, JE; Schellens, JH; Sikorska, K; Tesselaar, ME; Vanhoutvin, SA, 2016)		0.88
" This phase I study evaluated the safety profile of vandetanib in combination with standard doses of gemcitabine and capecitabine in order to determine the maximum tolerated dose (MTD)."( Phase I trial of vandetanib in combination with gemcitabine and capecitabine in patients with advanced solid tumors with an expanded cohort in pancreatic and biliary cancers.
Bradshaw-Pierce, EL; Eckhardt, SG; Eppers, S; Freas, E; Kane, MA; Kessler, ER; Leong, S; Lieu, CH; Messersmith, WA; Nallapreddy, S; O'byrant, CL; Pitts, TM; Spratlin, J; Weekes, C, 2016)		0.88
"To observe the efficacy and safety of chemotherapy regimens oxaliplatin combined with capecitabine (CAPOX) or oxaliplatin combined with tegafur, gimeracil and oteracil potassium capsules (S-1)(SOX), and to investigate the value of expression of thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) proteins in tumor tissue for predicting the efficacy of CAPOX and SOX regimens in advanced gastric cancer patients."( [Comparison of the efficacy and safety of capecitabine or tegafur, gimeracil and oteracil potassium capsules combined with oxaliplatin chemotherapy regimens in the treatment of advanced gastric cancer].
Hui, H; Sun, S; Wan, Y; Wang, X; Wu, J, 2016)		0.92
" The expression levels of TP and DPD in tumor tissue can be used as a predictive factor for the efficacy of capecitabine or tegafur, gimeracil and oteracil potassium capsules combined with oxaliplatin regimens."( [Comparison of the efficacy and safety of capecitabine or tegafur, gimeracil and oteracil potassium capsules combined with oxaliplatin chemotherapy regimens in the treatment of advanced gastric cancer].
Hui, H; Sun, S; Wan, Y; Wang, X; Wu, J, 2016)		0.91
"The current study was a multicenter, single-arm, phase 2 study performed to investigate the feasibility and efficacy of bevacizumab combined with docetaxel, oxaliplatin, and capecitabine (B-DOC) in patients with advanced human epidermal growth factor receptor 2 (HER2)-negative, previously untreated, gastric or gastroesophageal adenocarcinoma."( Bevacizumab combined with docetaxel, oxaliplatin, and capecitabine, followed by maintenance with capecitabine and bevacizumab, as first-line treatment of patients with advanced HER2-negative gastric cancer: A multicenter phase 2 study.
Beeker, A; Beerepoot, LV; Beijnen, JH; Boers, JE; Cats, A; de Groot, JW; de Jong, RS; Goey, SH; Grootscholten, C; Kuiper, M; Los, M; Meulendijks, D; Pluim, D; Polee, MB; Portielje, JE; Schellens, JH; Sikorska, K; Tesselaar, ME; Vanhoutvin, SA, 2016)		0.88
"5 mg/kg, docetaxel at a dose of 50 mg/m(2) , and oxaliplatin at a dose of 100 mg/m(2) (all on day 1) combined with capecitabine at a dose of 850 mg/m(2) twice daily (days 1-14) every 3 weeks followed by maintenance with capecitabine and bevacizumab in patients with disease control."( Bevacizumab combined with docetaxel, oxaliplatin, and capecitabine, followed by maintenance with capecitabine and bevacizumab, as first-line treatment of patients with advanced HER2-negative gastric cancer: A multicenter phase 2 study.
Beeker, A; Beerepoot, LV; Beijnen, JH; Boers, JE; Cats, A; de Groot, JW; de Jong, RS; Goey, SH; Grootscholten, C; Kuiper, M; Los, M; Meulendijks, D; Pluim, D; Polee, MB; Portielje, JE; Schellens, JH; Sikorska, K; Tesselaar, ME; Vanhoutvin, SA, 2016)		0.89
"Vorinostat, a histone deacetylase (HDAC) inhibitor, was investigated in combination with capecitabine plus cisplatin (XP) as a first-line chemotherapy for patients with unresectable or metastatic gastric cancer (GC)."( Vorinostat in combination with capecitabine plus cisplatin as a first-line chemotherapy for patients with metastatic or unresectable gastric cancer: phase II study and biomarker analysis.
Kang, YK; Lee, CW; Na, YS; Ryoo, BY; Ryu, MH; Yoo, C, 2016)		0.94
"To compare the short-term efficacy and treatment-related adverse reaction between preoperative three dimensional conformal radiotherapy (3D-CRT) and volumetric modulated arc therapy (VMAT) concurrently combined with chemotherapy in the treatment of locally advanced rectal carcinoma (LARC)."( [Short-term efficacy comparison between preoperative three dimensional conformal radiotherapy and volumetric modulated arc therapy concurrently combined with chemotherapy in the treatment of locally advanced rectal carcinoma].
Gao, Y; Liu, M; Xiao, L; Xiao, W; Yu, X; Zeng, Z; Zhang, R; Zhu, Y, 2016)		0.43
" The primary aim of this phase II study was to evaluate the efficacy and safety of utidelone as a monotherapy or in combination with capecitabine in metastatic breast cancer patients previously treated with and resistant to anthracyclines and taxanes."( Phase II trial of utidelone as monotherapy or in combination with capecitabine in heavily pretreated metastatic breast cancer patients.
Di, L; Li, W; Liu, W; Qiu, R; Tang, L; Tian, F; Tong, Z; Wang, Y; Xu, B; Yang, J; Zhang, P, 2016)		0.88
"In two open-label, noncomparative clinical studies, patients with metastatic breast cancer who previously received anthracycline- and/or taxane-containing regimens were given (1) 25 to 35 mg/m(2)/day intravenously infused utidelone, once daily for 5 days, in combination with 14 days of 2000 mg/m(2) capecitabine, divided in two equal daily oral doses or (2) 40 mg/m(2)/day intravenously infused utidelone, once daily for 5 days."( Phase II trial of utidelone as monotherapy or in combination with capecitabine in heavily pretreated metastatic breast cancer patients.
Di, L; Li, W; Liu, W; Qiu, R; Tang, L; Tian, F; Tong, Z; Wang, Y; Xu, B; Yang, J; Zhang, P, 2016)		0.85
"We report a case of human epidermal growth factor receptor(HER)2 positive stage IV advanced gastric cancer successfully treated with chemotherapy combined with trastuzumab."( [A Case of HER2-Positive Stage IV Advanced Gastric Cancer Treated with Chemotherapy Combined with Trastuzumab].
Chin, M; Hagiwara, M; Hashizume, E; Honma, S; Horii, S; Takahashi, H; Takahashi, R; Takaya, K, 2016)		0.43
"Advantages of neoadjuvant chemotherapy combined with monoclonal antibodies for treating patients with resectable colorectal cancer liver metastasis (CLM) have not been established."( The COMET Open-label Phase II Study of Neoadjuvant FOLFOX or XELOX Treatment Combined with Molecular Targeting Monoclonal Antibodies in Patients with Resectable Liver Metastasis of Colorectal Cancer.
Deguchi, T; Inagaki, H; Ishigure, K; Kanda, M; Kataoka, M; Kondo, A; Kondo, K; Matsui, T; Matsuoka, H; Oba, K; Sakamoto, J; Sato, M; Sato, Y; Shibata, Y; Takahashi, T; Takano, N; Tanaka, C; Tanaka, H, 2017)		0.46
"Neoadjuvant therapy using FOLFOX/XELOX combined with monoclonal antibodies did not improve PFS, although it was administered safely and had less adverse effects after liver resection."( The COMET Open-label Phase II Study of Neoadjuvant FOLFOX or XELOX Treatment Combined with Molecular Targeting Monoclonal Antibodies in Patients with Resectable Liver Metastasis of Colorectal Cancer.
Deguchi, T; Inagaki, H; Ishigure, K; Kanda, M; Kataoka, M; Kondo, A; Kondo, K; Matsui, T; Matsuoka, H; Oba, K; Sakamoto, J; Sato, M; Sato, Y; Shibata, Y; Takahashi, T; Takano, N; Tanaka, C; Tanaka, H, 2017)		0.46
" The present systematic review and meta-analysis evaluated the efficacy and safety data of bevacizumab combined with first-line fluoropyrimidine monochemotherapy for these complex patients."( Efficacy and Safety of Bevacizumab Combined With Fluoropyrimidine Monotherapy for Unfit or Older Patients With Metastatic Colorectal Cancer: A Systematic Review and Meta-Analysis.
Antonuzzo, L; Aprile, G; Barni, S; Maiello, E; Masi, G; Petrelli, F; Pinto, C; Porcu, L; Scartozzi, M; Torri, V, 2017)		0.46
" This open-label, randomized phase II study evaluated their efficacy and safety in combination with capecitabine (CAP) in patients with previously treated unresectable, locally advanced or metastatic breast cancer."( Randomized Phase II Study of Ramucirumab or Icrucumab in Combination with Capecitabine in Patients with Previously Treated Locally Advanced or Metastatic Breast Cancer.
Dalal, RP; Gao, L; Garcia, AA; Gradishar, W; Joy, AA; Kauh, J; Khatcheressian, J; Layman, R; Miller, K; Rodriguez, G; Salkeni, MA; Sparano, J; Tang, S; Vahdat, LT; Ward, P; Yardley, DA, 2017)		0.9
" We aimed to establish the maximum tolerated dose and establish the recommended phase 2 dose of veliparib combined with neoadjuvant capecitabine and radiotherapy."( Safety and tolerability of veliparib combined with capecitabine plus radiotherapy in patients with locally advanced rectal cancer: a phase 1b study.
Czito, BG; DeLuca, A; Deming, DA; Dudley, MW; He, L; Holen, KD; Jameson, GS; Komarnitsky, P; Michael, M; Mittapalli, RK; Mulcahy, MF; Munasinghe, W; Ngan, SY; Vaghefi, H; Zalcberg, JR, 2017)		0.91
"Our results demonstrated that thalidomide combined with capecitabine was mildly effective and safe for treating elderly patients with advanced GC."( Thalidomide combined with chemotherapy in treating elderly patients with advanced gastric cancer.
Chu, Y; Li, Y; Song, R; Xu, F, 2018)		0.73
"We evaluated the safety, tolerability, pharmacokinetics, and tumor response of ramucirumab in combination with one of three platinum/fluoropyrimidine regimens in Japanese patients with chemotherapy-naïve metastatic gastric/gastroesophageal junction cancer."( Safety, pharmacokinetic, and clinical activity profiles of ramucirumab in combination with three platinum/fluoropyrimidine doublets in Japanese patients with chemotherapy-naïve metastatic gastric/gastroesophageal junction cancer.
Gritli, I; Inoue, K; Kadowaki, S; Muro, K; Nishina, T; Ozeki, A; Piao, Y; Sakai, D; Shitara, K; Yoshikawa, R, 2018)		0.48
"Ramucirumab 8 mg/kg on days 1 and 8 every 3 weeks in combination with XP, SP, or SOX was generally well tolerated and demonstrated preliminary anti-tumor activity in chemotherapy-naïve Japanese metastatic gastric/gastroesophageal junction cancer patients."( Safety, pharmacokinetic, and clinical activity profiles of ramucirumab in combination with three platinum/fluoropyrimidine doublets in Japanese patients with chemotherapy-naïve metastatic gastric/gastroesophageal junction cancer.
Gritli, I; Inoue, K; Kadowaki, S; Muro, K; Nishina, T; Ozeki, A; Piao, Y; Sakai, D; Shitara, K; Yoshikawa, R, 2018)		0.48
"In general, bavituximab was safe and well tolerated in combination with radiation therapy and capecitabine in the treatment of rectal adenocarcinoma."( A Phase I Clinical Trial of the Phosphatidylserine-targeting Antibody Bavituximab in Combination With Radiation Therapy and Capecitabine in the Preoperative Treatment of Rectal Adenocarcinoma.
Abdelnaby, A; Anandam, J; Arriaga, Y; Balch, G; Beg, MS; Dong, Y; Karri, S; Meyer, J; Raja, G; Syed, S; Verma, U, 2018)		0.91
"Bavituximab is safe in combination with capecitabine and radiation therapy at the doses selected for the study."( A Phase I Clinical Trial of the Phosphatidylserine-targeting Antibody Bavituximab in Combination With Radiation Therapy and Capecitabine in the Preoperative Treatment of Rectal Adenocarcinoma.
Abdelnaby, A; Anandam, J; Arriaga, Y; Balch, G; Beg, MS; Dong, Y; Karri, S; Meyer, J; Raja, G; Syed, S; Verma, U, 2018)		0.96
"Preoperative radiotherapy (RT) in combination with fluoropyrimidine-based chemotherapy (CT) is the standard of care in patients with locally advanced, T3-T4 N0-2, rectal cancer (LARC)."( Preoperative intensity-modulated radiotherapy with a simultaneous integrated boost combined with Capecitabine in locally advanced rectal cancer: short-term results of a multicentric study.
Aristei, C; Chiloiro, G; De Paoli, A; Gambacorta, MA; Lupattelli, M; Macchia, G; Matrone, F; Navarria, F; Nicosia, L; Osti, M; Palazzari, E; Valentini, V, 2017)		0.67
"To evaluate the safety (including adverse events and dose-limiting toxicities [DLTs]), tolerability, pharmacokinetics and antitumor activity of the investigational MET inhibitor rilotumumab alone in patients with advanced solid tumors (Part 1) or in combination with cisplatin plus capecitabine (CX) in patients with MET-positive advanced gastric or gastroesophageal junction cancer (Part 2)."( A Phase 1/1b tolerability study of rilotumumab alone or in combination with cisplatin and capecitabine in Japanese patients with gastric cancer.
Ang, A; Doi, T; Jung, AS; Komatsu, Y; Muro, K; Nakajima, TE; Nishina, T; Tang, R; Yamaguchi, K; Yang, H; Yasui, H; Zhang, Y, 2017)		0.85
"In combination with CX, rilotumumab appeared tolerable and showed antitumor activity in Japanese patients with MET-positive gastric/gastroesophageal junction cancer."( A Phase 1/1b tolerability study of rilotumumab alone or in combination with cisplatin and capecitabine in Japanese patients with gastric cancer.
Ang, A; Doi, T; Jung, AS; Komatsu, Y; Muro, K; Nakajima, TE; Nishina, T; Tang, R; Yamaguchi, K; Yang, H; Yasui, H; Zhang, Y, 2017)		0.68
" Further study of the combination is not unreasonable, with expanded pharmacokinetics and sequencing analysis to better elucidate potential drug-drug interactions and more accurate predictive biomarkers of response."( A Phase I Trial of the PI3K Inhibitor Buparlisib Combined With Capecitabine in Patients With Metastatic Breast Cancer.
Anders, CK; Carey, LA; Dees, EC; Hu, Z; Kornblum, ZA; Marcom, PK; McRee, AJ; Moore, DT; Perou, CM; Phipps, R; Reeder-Hayes, K; Weck, KE; Zamboni, WC, 2018)		0.72
"The optimal Chinese herbal injections (CHIs) combined with XELOX regimen for patients with gastric cancer remains elusive."( Which are the best Chinese herbal injections combined with XELOX regimen for gastric cancer?: A PRISMA-compliant network meta-analysis.
Duan, X; Liu, S; Wang, K; Wu, J; Zhang, B; Zhang, D, 2018)		0.48
" Standard pair-wise and Bayesian NMAs were performed to compare the efficacy and safety of different CHIs combined with the XELOX regimen via Stata 13."( Which are the best Chinese herbal injections combined with XELOX regimen for gastric cancer?: A PRISMA-compliant network meta-analysis.
Duan, X; Liu, S; Wang, K; Wu, J; Zhang, B; Zhang, D, 2018)		0.48
" Nevertheless, CHIs combined with XELOX regimen did not confer higher better clinical effectiveness rate over receiving XELOX regimen alone, with nonstatistically significant between-group differences."( Which are the best Chinese herbal injections combined with XELOX regimen for gastric cancer?: A PRISMA-compliant network meta-analysis.
Duan, X; Liu, S; Wang, K; Wu, J; Zhang, B; Zhang, D, 2018)		0.48
"As the available evidence suggested that CHIs combined with XELOX regimen could provide treatment benefits for patients with gastric cancer."( Which are the best Chinese herbal injections combined with XELOX regimen for gastric cancer?: A PRISMA-compliant network meta-analysis.
Duan, X; Liu, S; Wang, K; Wu, J; Zhang, B; Zhang, D, 2018)		0.48
" The present study aimed to evaluate the safety and efficacy of neoadjuvant oxaliplatin and capecitabine (XELOX) combined with bevacizumab plus radiotherapy for locally advanced rectal cancer."( Neoadjuvant oxaliplatin and capecitabine combined with bevacizumab plus radiotherapy for locally advanced rectal cancer: results of a single-institute phase II study.
Chang, H; Chen, G; Ding, PR; Gao, YH; Lu, ZH; Pan, ZZ; Wan, DS; Wang, QX; Wu, XJ; Xiao, WW; Yu, X; Zeng, ZF, 2018)		1
" We compared tolerability and efficacy of the two different chemotherapy regimens; 5-FU/leucovorin (LV) versus cisplatin with capecitabine (XP) combined with radiotherapy (RT) in the adjuvant therapy of the lymph node positive locally advanced gastric cancer."( Capecitabine-cisplatin versus 5-fluorouracil/leucovorin in combination with radiotherapy for adjuvant therapy of lymph node positive locally advanced gastric cancer.
Bilici, A; Erkol, B; Figen, M; Surmelioglu, A; Tilki, M; Ustaalioglu, BBO; Uyar, S, 2018)		2.13
" Group 2 (n = 58) received 5-FU/LV combined with RT postoperatively."( Capecitabine-cisplatin versus 5-fluorouracil/leucovorin in combination with radiotherapy for adjuvant therapy of lymph node positive locally advanced gastric cancer.
Bilici, A; Erkol, B; Figen, M; Surmelioglu, A; Tilki, M; Ustaalioglu, BBO; Uyar, S, 2018)		1.92
"This study was designed to determine the safety and clinical efficacy of metronomic chemotherapy combined with aromatase inhibitors (AIs) for hormone receptor (HR)-positive advanced breast cancer (ABC) patients who cannot tolerate conventional-dose chemotherapy."( Metronomic capecitabine combined with aromatase inhibitors for new chemoendocrine treatment of advanced breast cancer: a phase II clinical trial.
Ivanova, D; Jia, XQ; Lei, L; Li, JW; Liu, GY; Zuo, WJ, 2019)		0.9
"Metronomic oral capecitabine combined with AIs showed good efficacy, minimal toxicities, and good tolerance in HR-positive patients with ABC."( Metronomic capecitabine combined with aromatase inhibitors for new chemoendocrine treatment of advanced breast cancer: a phase II clinical trial.
Ivanova, D; Jia, XQ; Lei, L; Li, JW; Liu, GY; Zuo, WJ, 2019)		1.25
" In this phase I study, we evaluated the safety of ip PTX combined with 5-fluorouracil, folinic acid, oxaliplatin, and bevacizumab (mFOLFOX6-bevacizumab) or capecitabine, oxaliplatin, and bevacizumab (CapeOX-bevacizumab) for colorectal cancer with peritoneal metastasis."( Safety of intraperitoneal paclitaxel combined with conventional chemotherapy for colorectal cancer with peritoneal carcinomatosis: a phase I trial.
Emoto, S; Hata, K; Hiyoshi, M; Ishihara, S; Ishimaru, K; Kaneko, M; Kawai, K; Muro, K; Murono, K; Nagata, H; Nishikawa, T; Nozawa, H; Otani, K; Sasaki, K; Shuno, Y; Tanaka, T, 2019)		0.71
"The adverse events of mFOLFOX6-bevacizumab or CapeOX-bevacizumab in combination with ip PTX were considered similar to those described in previous studies of oxaliplatin-based treatment alone."( Safety of intraperitoneal paclitaxel combined with conventional chemotherapy for colorectal cancer with peritoneal carcinomatosis: a phase I trial.
Emoto, S; Hata, K; Hiyoshi, M; Ishihara, S; Ishimaru, K; Kaneko, M; Kawai, K; Muro, K; Murono, K; Nagata, H; Nishikawa, T; Nozawa, H; Otani, K; Sasaki, K; Shuno, Y; Tanaka, T, 2019)		0.51
"Bolus 5-FU in combination with oxaliplatin is safe in patients who have experienced coronary vasospasm with infusional 5-FU or capecitabine."( Bolus 5-fluorouracil (5-FU) In Combination With Oxaliplatin Is Safe and Well Tolerated in Patients Who Experienced Coronary Vasospasm With Infusional 5-FU or Capecitabine.
Chakrabarti, S; Eiring, R; Finnes, H; Grothey, A; Halfdanarson, T; Hartgers, M; Lobo, R; Mitchell, J; Okano, A; Sara, J, 2019)		0.92
" In part 1 (phase II) of ATTRACTION-4, the safety and efficacy of nivolumab combined with S-1 plus oxaliplatin (SOX) or capecitabine plus oxaliplatin (CapeOX) as first-line therapy for unresectable advanced or recurrent human epidermal growth factor receptor 2 (HER2)-negative G/GEJ cancer were evaluated."( Safety and efficacy of nivolumab in combination with S-1/capecitabine plus oxaliplatin in patients with previously untreated, unresectable, advanced, or recurrent gastric/gastroesophageal junction cancer: interim results of a randomized, phase II trial (A
Azuma, M; Boku, N; Chen, LT; Cho, H; Chung, HC; Fumita, S; Hara, H; Kang, WK; Kang, YK; Kato, K; Komatsu, Y; Lee, KW; Minashi, K; Ryu, MH; Tsuda, M; Yamaguchi, K, 2019)		0.97
"Nivolumab combined with SOX/CapeOX was well tolerated and demonstrated encouraging efficacy for unresectable advanced or recurrent HER2-negative G/GEJ cancer."( Safety and efficacy of nivolumab in combination with S-1/capecitabine plus oxaliplatin in patients with previously untreated, unresectable, advanced, or recurrent gastric/gastroesophageal junction cancer: interim results of a randomized, phase II trial (A
Azuma, M; Boku, N; Chen, LT; Cho, H; Chung, HC; Fumita, S; Hara, H; Kang, WK; Kang, YK; Kato, K; Komatsu, Y; Lee, KW; Minashi, K; Ryu, MH; Tsuda, M; Yamaguchi, K, 2019)		0.76
" Radical surgery combined with adjuvant chemotherapy (AC) serves as the mainstream therapeutic scheme for most CRC patients."( Alterations in intestinal microbiota of colorectal cancer patients receiving radical surgery combined with adjuvant CapeOx therapy.
Gao, R; He, J; Huang, L; Kong, C; Li, H; Qin, H; Yan, X; You, J, 2019)		0.51
"This phase I study assessed the safety, tolerability, MTD, pharmacokinetics, antitumor activity, and predictive biomarkers of pyrotinib, an irreversible pan-ErbB inhibitor, in combination with capecitabine in patients with HER2-positive metastatic breast cancer (MBC)."( Safety, Efficacy, and Biomarker Analysis of Pyrotinib in Combination with Capecitabine in HER2-Positive Metastatic Breast Cancer Patients: A Phase I Clinical Trial.
Cai, R; Chen, S; Fan, Y; Guan, X; Lan, B; Li, Q; Luo, Y; Ma, F; Wang, J; Xing, P; Xu, B; Yi, Z; Yuan, P; Zhang, P; Zhang, Y; Zhong, D; Zhu, X; Zou, J, 2019)		0.93
"In a population largely naïve to HER2-targeted therapy, pyrotinib in combination with capecitabine was well-tolerated and demonstrates promising antitumor activity in patients with HER2-positive MBC."( Safety, Efficacy, and Biomarker Analysis of Pyrotinib in Combination with Capecitabine in HER2-Positive Metastatic Breast Cancer Patients: A Phase I Clinical Trial.
Cai, R; Chen, S; Fan, Y; Guan, X; Lan, B; Li, Q; Luo, Y; Ma, F; Wang, J; Xing, P; Xu, B; Yi, Z; Yuan, P; Zhang, P; Zhang, Y; Zhong, D; Zhu, X; Zou, J, 2019)		0.97
"To evaluate the efficacy and safety of celecoxib combined with chemotherapy in the treatment of metastatic or postoperative recurrent gastric cancer."( A comprehensive evaluation of clinical efficacy and safety of celecoxib in combination with chemotherapy in metastatic or postoperative recurrent gastric cancer patients: A preliminary, three-center, clinical trial study.
Chen, Z; Guan, Q; Guo, Q; Li, Q; Liu, M; Wang, J; Wang, Y; Ye, Y; Zhou, Y, 2019)		0.51
" In the experimental group (n = 100), patients were treated with celecoxib combined with chemotherapy, and chemotherapy alone was used in the control group."( A comprehensive evaluation of clinical efficacy and safety of celecoxib in combination with chemotherapy in metastatic or postoperative recurrent gastric cancer patients: A preliminary, three-center, clinical trial study.
Chen, Z; Guan, Q; Guo, Q; Li, Q; Liu, M; Wang, J; Wang, Y; Ye, Y; Zhou, Y, 2019)		0.51
"Celecoxib combined with chemotherapy offers more clinical benefits for COX-2 positive advanced gastric cancer patients."( A comprehensive evaluation of clinical efficacy and safety of celecoxib in combination with chemotherapy in metastatic or postoperative recurrent gastric cancer patients: A preliminary, three-center, clinical trial study.
Chen, Z; Guan, Q; Guo, Q; Li, Q; Liu, M; Wang, J; Wang, Y; Ye, Y; Zhou, Y, 2019)		0.51
" We assessed the efficacy and tolerability of pyrotinib versus lapatinib, both in combination with capecitabine, in women with human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer in an open-label, multicenter, randomized phase II study."( Pyrotinib or Lapatinib Combined With Capecitabine in HER2-Positive Metastatic Breast Cancer With Prior Taxanes, Anthracyclines, and/or Trastuzumab: A Randomized, Phase II Study.
Feng, J; Hu, X; Jiang, Z; Li, H; Li, W; Liu, Y; Ma, F; Ouyang, Q; Tong, Z; Wang, S; Xu, B; Yu, S; Zhu, X; Zou, J, 2019)		1
"gov, NCT01506167) that recruited patients with metastatic colorectal cancer scheduled to receive bevacizumab in combination with first-line chemotherapy as part of routine clinical practice."( ACORN: Observational Study of Bevacizumab in Combination With First-Line Chemotherapy for Treatment of Metastatic Colorectal Cancer in the UK.
Baijal, S; Chau, I; Cunningham, D; Ellis, R; Harrison, M; Khakoo, S; Ograbek, A; Pedley, I; Raouf, S; Ross, P; Steward, W; Tahir, S, 2019)		0.51
"In the current report we present the case of a patient experiencing a life-threatening drug-drug interaction involving the concurrent administration of capecitabine and brivudine."( A life-threatening drug-drug interaction between capecitabine and brivudine in a patient with metastatic breast cancer.
Antoniadou, V; Diamantopoulos, P; Gogas, H; Halioti, A; Mantzourani, M; Papaxoinis, G; Tsifi, A, )		0.58
" Single-HER2-targeted agent (trastuzumab) combined with taxane-based doublets (taxane+carboplatin/capecitabine/doxorubicin/bevacizumab) showed no further benefit than trastuzumab+a taxane."( A network meta-analysis on the efficacy of HER2-targeted agents in combination with taxane-containing regimens for treatment of HER2-positive metastatic breast cancer.
Ding, T; Dong, L; Gu, XS; Li, JB; Ma, C; Xie, BJ; Zhu, LN; Zhu, ZN, 2020)		0.78
"This study aimed to evaluate the clinical outcomes, toxicity, and prognostic factors of SBRT combined with gemcitabine plus capecitabine (GEM-CAP) in treating locally advanced pancreatic cancer (LAPC)."( Clinical outcomes and prognostic factors of stereotactic body radiation therapy combined with gemcitabine plus capecitabine for locally advanced unresectable pancreatic cancer.
Huang, GC; Ji, XQ; Jiang, CC; Li, AM; Li, B; Shen, ZT; Yuan, X; Zhou, H; Zhu, XX, 2020)		0.98
"A total of 56 patients with LAPC treated with SBRT combined with GEM-CAP were reviewed from October 2010 to October 2016."( Clinical outcomes and prognostic factors of stereotactic body radiation therapy combined with gemcitabine plus capecitabine for locally advanced unresectable pancreatic cancer.
Huang, GC; Ji, XQ; Jiang, CC; Li, AM; Li, B; Shen, ZT; Yuan, X; Zhou, H; Zhu, XX, 2020)		0.77
"AZD8931 (20 mg, 40 mg or 60 mg bd) was given with Xelox (oxaliplatin + capecitabine) for eight 21-day cycles, continuously or with intermittent schedule (4 days on/3 off every week; 14 days on/7 off, per cycle) in a rolling-six design."( Dual Erb B Inhibition in Oesophago-gastric Cancer (DEBIOC): A phase I dose escalating safety study and randomised dose expansion of AZD8931 in combination with oxaliplatin and capecitabine chemotherapy in patients with oesophagogastric adenocarcinoma.
Anthoney, DA; Collins, L; Eatock, M; Elhussein, L; Falk, S; Goff, M; Lord, SR; Love, S; Middleton, MR; Moschandreas, J; Thomas, A; Turkington, RC; Virdee, PS, 2020)		0.98
"In 2011, we demonstrated that bevacizumab in combination with capecitabine as first-line treatment is effective in elderly patients with metastatic colorectal cancer (mCRC)."( Predictors of outcome in elderly patients with metastatic colorectal cancer: the final results of a prospective phase II study of bevacizumab in combination with capecitabine as first-line treatment.
Eterović, D; Katić, A; Omrčen, T; Tomić, S; Vrdoljak, E, 2020)		0.99
"Temozolomide (TEM) has been reported to be active alone or in combination with capecitabine (CAP) in patients with neuroendocrine neoplasms (NENs)."( Temozolomide alone or in combination with capecitabine in patients with advanced neuroendocrine neoplasms: an Italian multicenter real-world analysis.
Antonuzzo, L; Barberis, M; Campana, D; Faviana, P; Fazio, N; Fumagalli, C; Gelsomino, F; Maisonneuve, P; Marconcini, R; Messerini, L; Puliafito, I; Rossi, G; Spada, F, 2021)		1.11
"Patients received oral TEM alone or in combination with CAP."( Temozolomide alone or in combination with capecitabine in patients with advanced neuroendocrine neoplasms: an Italian multicenter real-world analysis.
Antonuzzo, L; Barberis, M; Campana, D; Faviana, P; Fazio, N; Fumagalli, C; Gelsomino, F; Maisonneuve, P; Marconcini, R; Messerini, L; Puliafito, I; Rossi, G; Spada, F, 2021)		0.89
" We assessed the effect of ω-3 PUFAs on the neurotoxicity in colon cancer patients treated by oxaliplatin combined with capecitabine."( Prevention of oxaliplatin-related neurotoxicity by ω-3 PUFAs: A double-blind randomized study of patients receiving oxaliplatin combined with capecitabine for colon cancer.
Chen, H; Lu, Y; Xu, C; Xu, L; Yao, Q; Yao, W; Zhang, L; Zhang, R; Zhang, X, 2020)		0.97
" We performed this retrospective study to evaluate the efficacy and safety of apatinib combined with S-1/capecitabine as the oral maintenance therapy for these patients."( Oral maintenance therapy using apatinib combined with S-1/capecitabine for esophageal squamous cell carcinoma with residual disease after definitive chemoradiotherapy.
Bai, K; Chen, B; Chi, D; Guo, S; Hu, Y; Li, Q; Ma, H; Zhu, Y, 2021)		1.08
" Patients were treated with apatinib combined with S-1 /capecitabine after dCRT."( Oral maintenance therapy using apatinib combined with S-1/capecitabine for esophageal squamous cell carcinoma with residual disease after definitive chemoradiotherapy.
Bai, K; Chen, B; Chi, D; Guo, S; Hu, Y; Li, Q; Ma, H; Zhu, Y, 2021)		1.11
"This phase III study aimed to evaluate the efficacy, safety, and immunogenicity of HLX04 compared with reference bevacizumab in combination with XELOX or mFOLFOX6 as first-line treatment for recurrent/metastatic colorectal cancer (CRC)."( Efficacy, Safety, and Immunogenicity of HLX04 Versus Reference Bevacizumab in Combination with XELOX or mFOLFOX6 as First-Line Treatment for Metastatic Colorectal Cancer: Results of a Randomized, Double-Blind Phase III Study.
Bai, Y; Chen, K; Cheng, Y; Deng, Y; Kang, W; Li, J; Li, W; Li, Y; Qian, X; Qin, S; Shu, Y; Sun, G; Yin, X; Zhang, J; Zhang, L; Zhong, H, 2021)		0.62
"5 mg/kg every 3 weeks when combined with XELOX; 5 mg/kg every 2 weeks when combined with mFOLFOX6)."( Efficacy, Safety, and Immunogenicity of HLX04 Versus Reference Bevacizumab in Combination with XELOX or mFOLFOX6 as First-Line Treatment for Metastatic Colorectal Cancer: Results of a Randomized, Double-Blind Phase III Study.
Bai, Y; Chen, K; Cheng, Y; Deng, Y; Kang, W; Li, J; Li, W; Li, Y; Qian, X; Qin, S; Shu, Y; Sun, G; Yin, X; Zhang, J; Zhang, L; Zhong, H, 2021)		0.62
"The purpose of this study was to investigate the efficacy and safety of maintenance therapy of capecitabine metronomic chemotherapy combined with autologous cytokine-induced killer (CIK) cell immunotherapy in patients with recurrent metastatic triple-negative breast cancer (mTNBC)."( Capecitabine metronomic chemotherapy combined with autologous CIK cell immunotherapy in the treatment of recurrent and metastatic triple-negative breast cancer.
Chen, S; Jiao, Y; Sun, H; Yan, Z; Yang, Y, )		1.79
" Among, 55 were treated with maintenance therapy of capecitabine metronomic chemotherapy combined with autologous CIK cell immunotherapy (DC-CIK group), while the rest 55 were treated with simple metronomic chemotherapy (control group)."( Capecitabine metronomic chemotherapy combined with autologous CIK cell immunotherapy in the treatment of recurrent and metastatic triple-negative breast cancer.
Chen, S; Jiao, Y; Sun, H; Yan, Z; Yang, Y, )		1.82
"The maintenance therapy of capecitabine metronomic chemotherapy combined with DC-CIK cell immunotherapy is effective in the treatment of recurrent mTNBC, with tolerable adverse reactions."( Capecitabine metronomic chemotherapy combined with autologous CIK cell immunotherapy in the treatment of recurrent and metastatic triple-negative breast cancer.
Chen, S; Jiao, Y; Sun, H; Yan, Z; Yang, Y, )		1.87
"The purpose of this study was to investigate the efficacy and safety of transcatheter arterial chemoembolization (TACE) combined with capecitabine and cetuximab in the treatment of colorectal cancer with liver metastasis."( Efficacy of transcatheter arterial chemoembolization combined with capecitabine and cetuximab in the treatment of colorectal cancer with liver metastasis.
Jia, J; Meng, H; Qian, W; Yun, X; Zhou, A, )		0.57
"The colorectal cancer patients with liver metastasis were divided into two groups, namely, Capecitabine group (receiving TACE combined with capecitabine and cetuximab, n=70) and Control group (undergoing TACE combined with cetuximab, n=70)."( Efficacy of transcatheter arterial chemoembolization combined with capecitabine and cetuximab in the treatment of colorectal cancer with liver metastasis.
Jia, J; Meng, H; Qian, W; Yun, X; Zhou, A, )		0.59
"The short-term efficacy of TACE combined with capecitabine and cetuximab in treating colorectal cancer with liver metastasis is superior to that of TACE combined with cetuximab."( Efficacy of transcatheter arterial chemoembolization combined with capecitabine and cetuximab in the treatment of colorectal cancer with liver metastasis.
Jia, J; Meng, H; Qian, W; Yun, X; Zhou, A, )		0.63
"This study was designed to probe into the effect of cisplatin combined with capecitabine on nasopharyngeal carcinoma (NPC)."( Cisplatin combined with capecitabine-induced chemotherapy for local nasopharyngeal carcinoma can improve the quality of life and reduce toxic and side effects.
Gao, Y; Liu, Y; Liu, Z, 2021)		1.16
"Cisplatin combined with capecitabine-induced chemotherapy for local NPC can improve the quality of life and reduce the toxic and side effects."( Cisplatin combined with capecitabine-induced chemotherapy for local nasopharyngeal carcinoma can improve the quality of life and reduce toxic and side effects.
Gao, Y; Liu, Y; Liu, Z, 2021)		1.24
"The aim of the study was to investigate the effect of hyperthermic intraperitoneal perfusion chemotherapy (HIPEC) combined with radical surgery and capecitabine on stage III gallbladder cancer."( Effect of Hyperthermic Intraperitoneal Perfusion Chemotherapy Combined with Radical Surgery and Capecitabine on Stage III Gallbladder Cancer.
Jiang, B; Liu, S; Peng, C; Song, Y; Xia, G; Yi, W; Yu, Z; Zhang, Z; Zhong, Z, 2021)		1.04
" Depending on the treatment approach, the patients were divided into the control group (radical surgery and capecitabine) and the HIPEC group (hyperthermic intraperitoneal perfusion chemotherapy combined with radical surgery and capecitabine)."( Effect of Hyperthermic Intraperitoneal Perfusion Chemotherapy Combined with Radical Surgery and Capecitabine on Stage III Gallbladder Cancer.
Jiang, B; Liu, S; Peng, C; Song, Y; Xia, G; Yi, W; Yu, Z; Zhang, Z; Zhong, Z, 2021)		1.05
"HIPEC combined with radical surgery and capecitabine for stage III gallbladder cancer can effectively prolong survival time without increasing surgery-related complications."( Effect of Hyperthermic Intraperitoneal Perfusion Chemotherapy Combined with Radical Surgery and Capecitabine on Stage III Gallbladder Cancer.
Jiang, B; Liu, S; Peng, C; Song, Y; Xia, G; Yi, W; Yu, Z; Zhang, Z; Zhong, Z, 2021)		1.11
" Recent reports suggested that TMZ combined with capecitabine (CAPTEM) can be effective for the treatment of aggressive pituitary tumors."( Efficacy of temozolomide combined with capecitabine (CAPTEM) on refractory prolactinomas as assessed using an ex vivo 3D spheroid assay.
Fukuoka, H; Inoshita, N; Ishida, A; Ogawa, W; Shichi, H; Yamada, S, 2022)		1.24
" We aimed to investigate the differences in efficacy and safety between bevacizumab combined with capecitabine maintenance therapy and capecitabine monotherapy for RAS-mutant mCRC （as defined by mutations in KRAS and NRAS exons 2-4）controlled by bevacizumab plus FOLFIRI chemotherapy for at least 12 weeks."( Efficacy and safety analysis of bevacizumab combined with capecitabine in the maintenance treatment of RAS-mutant metastatic colorectal cancer.
Cha, Y; Huang, W; Tian, Y; Xiong, H; Yuan, X; Zhang, H, 2022)		1.18
" All patients were first treated with bevacizumab combined with FOLFIRI for at least 12 weeks of induction therapy."( Efficacy and safety analysis of bevacizumab combined with capecitabine in the maintenance treatment of RAS-mutant metastatic colorectal cancer.
Cha, Y; Huang, W; Tian, Y; Xiong, H; Yuan, X; Zhang, H, 2022)		0.97
"Bevacizumab combined with capecitabine was well tolerated and contributed to a longer PFS time than capecitabine alone, and it is worthy of popularization in clinical practice."( Efficacy and safety analysis of bevacizumab combined with capecitabine in the maintenance treatment of RAS-mutant metastatic colorectal cancer.
Cha, Y; Huang, W; Tian, Y; Xiong, H; Yuan, X; Zhang, H, 2022)		1.27
"To evaluate the efficacy and safety of bevacizumab combined with chemotherapy in the treatment of advanced colorectal cancer and the effect on its adverse reactions, 100 patients with advanced colorectal cancer admitted to our hospital from March 2019 to March 2021 were identified as study subjects and were randomly divided into a control group and an experimental group, with 50 cases in each group."( Efficacy and safety of bevacizumab combined with chemotherapy in the treatment of advanced colorectal cancer and the effect on its adverse reactions.
Liu, Y; Su, X; Sun, L; Wang, X; Wang, Z; Yang, Y; Zhou, W, 2022)		0.72
"Capecitabine and oxaliplatin in combination with pembrolizumab is tolerable and a potentially effective treatment for refractory advanced BTC."( A Phase II Study of Pembrolizumab in Combination with Capecitabine and Oxaliplatin with Molecular Profiling in Patients with Advanced Biliary Tract Carcinoma.
Budhu, A; Duffy, AG; Figg, WD; Greten, TF; Kleiner, DE; Ma, L; Mabry, D; Monge, C; Pehrsson, EC; Redd, B; Steinberg, SM; Tandon, M; Wang, S; Wei Wang, X; Wood, BJ; Xie, C, 2022)		2.41
"For patients with locally advanced (T3-4/N +) rectal cancer (LARC), the standard treatment is neoadjuvant chemoradiotherapy combined with total mesorectal resection, which greatly decreases local recurrence but does not improve overall survival."( Short-course radiotherapy combined with CAPOX and Toripalimab for the total neoadjuvant therapy of locally advanced rectal cancer: a randomized, prospective, multicentre, double-arm, phase II trial (TORCH).
Cai, S; Shen, L; Wan, J; Wang, J; Wang, Y; Wu, R; Xia, F; Xu, Y; Zhang, H; Zhang, Z, 2022)		0.72
"TORCH is a randomized, prospective, multicentre, double-arm, phase II trial of short-course radiotherapy (SCRT) combined with chemotherapy and immunotherapy in LARC."( Short-course radiotherapy combined with CAPOX and Toripalimab for the total neoadjuvant therapy of locally advanced rectal cancer: a randomized, prospective, multicentre, double-arm, phase II trial (TORCH).
Cai, S; Shen, L; Wan, J; Wang, J; Wang, Y; Wu, R; Xia, F; Xu, Y; Zhang, H; Zhang, Z, 2022)		0.72
"TORCH will investigate whether SCRT combined with chemotherapy and Toripalimab can achieve better complete response rates, good tolerance and prognosis in LARC patients."( Short-course radiotherapy combined with CAPOX and Toripalimab for the total neoadjuvant therapy of locally advanced rectal cancer: a randomized, prospective, multicentre, double-arm, phase II trial (TORCH).
Cai, S; Shen, L; Wan, J; Wang, J; Wang, Y; Wu, R; Xia, F; Xu, Y; Zhang, H; Zhang, Z, 2022)		0.72
" Recently, the addition of immunotherapy to preoperative CRT has been reported to be useful in LARC patients with mismatch-repair-deficiency and high levels of microsatellite instability (MSI-H), but there are no reports showing the therapeutic effect of nivolumab in combination with TNT."( Locally advanced rectal cancer receiving total neoadjuvant therapy combined with nivolumab: a case report and literature review.
Doki, Y; Eguchi, H; Hata, T; Miyoshi, N; Mizushima, T; Mori, R; Ogino, T; Sekido, Y; Takahashi, H; Uemura, M, 2022)		0.72
"To evaluate the efficacy and safety of sintilimab combined with apatinib plus capecitabine in the treatment of unresectable hepatocellular carcinoma (HCC) to provide a more effective first-line treatment for patients with advanced HCC."( Sintilimab combined with apatinib plus capecitabine in the treatment of unresectable hepatocellular carcinoma: A prospective, open-label, single-arm, phase II clinical study.
Bao, D; Chen, Z; Hu, J; Ji, J; Li, D; Li, X; Liu, S; Pang, Y; Qian, Y; Shi, M; Wang, H; Xu, L; Xu, X; Yi, C; Zhang, X; Zhou, Y, 2022)		1.22
"Sintilimab combined with apatinib plus capecitabine has good safety and anti-tumor activity as a first-line treatment for unresectable HCC."( Sintilimab combined with apatinib plus capecitabine in the treatment of unresectable hepatocellular carcinoma: A prospective, open-label, single-arm, phase II clinical study.
Bao, D; Chen, Z; Hu, J; Ji, J; Li, D; Li, X; Liu, S; Pang, Y; Qian, Y; Shi, M; Wang, H; Xu, L; Xu, X; Yi, C; Zhang, X; Zhou, Y, 2022)		1.26
" Previous reports of the HER2CLIMB trial have demonstrated that tucatinib in combination with trastuzumab and capecitabine provides survival and intracranial benefits for patients with ERBB2-positive MBC and BMs."( Tucatinib vs Placebo, Both in Combination With Trastuzumab and Capecitabine, for Previously Treated ERBB2 (HER2)-Positive Metastatic Breast Cancer in Patients With Brain Metastases: Updated Exploratory Analysis of the HER2CLIMB Randomized Clinical Trial.
Abramson, V; Anders, C; Bachelot, T; Bedard, PL; Borges, V; Cameron, D; Carey, LA; Chien, AJ; Curigliano, G; DiGiovanna, MP; Feng, W; Gelmon, K; Hortobagyi, G; Hurvitz, SA; Krop, I; Lin, NU; Loi, S; Loibl, S; Mueller, V; Murthy, RK; Oliveira, M; Paplomata, E; Pegram, M; Ramos, J; Slamon, D; Winer, E; Zelnak, A, 2023)		1.36
"To describe overall survival (OS) and intracranial outcomes from tucatinib in combination with trastuzumab and capecitabine in patients with ERBB2-positive MBC and BMs with an additional 15."( Tucatinib vs Placebo, Both in Combination With Trastuzumab and Capecitabine, for Previously Treated ERBB2 (HER2)-Positive Metastatic Breast Cancer in Patients With Brain Metastases: Updated Exploratory Analysis of the HER2CLIMB Randomized Clinical Trial.
Abramson, V; Anders, C; Bachelot, T; Bedard, PL; Borges, V; Cameron, D; Carey, LA; Chien, AJ; Curigliano, G; DiGiovanna, MP; Feng, W; Gelmon, K; Hortobagyi, G; Hurvitz, SA; Krop, I; Lin, NU; Loi, S; Loibl, S; Mueller, V; Murthy, RK; Oliveira, M; Paplomata, E; Pegram, M; Ramos, J; Slamon, D; Winer, E; Zelnak, A, 2023)		1.36
"HER2CLIMB is an international, multicenter, randomized, double-blind, placebo-controlled clinical trial evaluating tucatinib in combination with trastuzumab and capecitabine."( Tucatinib vs Placebo, Both in Combination With Trastuzumab and Capecitabine, for Previously Treated ERBB2 (HER2)-Positive Metastatic Breast Cancer in Patients With Brain Metastases: Updated Exploratory Analysis of the HER2CLIMB Randomized Clinical Trial.
Abramson, V; Anders, C; Bachelot, T; Bedard, PL; Borges, V; Cameron, D; Carey, LA; Chien, AJ; Curigliano, G; DiGiovanna, MP; Feng, W; Gelmon, K; Hortobagyi, G; Hurvitz, SA; Krop, I; Lin, NU; Loi, S; Loibl, S; Mueller, V; Murthy, RK; Oliveira, M; Paplomata, E; Pegram, M; Ramos, J; Slamon, D; Winer, E; Zelnak, A, 2023)		1.35
"Patients were randomized 2:1 to receive tucatinib (300 mg orally twice daily) or placebo (orally twice daily), both in combination with trastuzumab (6 mg/kg intravenously or subcutaneously every 3 weeks with an initial loading dose of 8 mg/kg) and capecitabine (1000 mg/m2 orally twice daily on days 1-14 of each 3-week cycle)."( Tucatinib vs Placebo, Both in Combination With Trastuzumab and Capecitabine, for Previously Treated ERBB2 (HER2)-Positive Metastatic Breast Cancer in Patients With Brain Metastases: Updated Exploratory Analysis of the HER2CLIMB Randomized Clinical Trial.
Abramson, V; Anders, C; Bachelot, T; Bedard, PL; Borges, V; Cameron, D; Carey, LA; Chien, AJ; Curigliano, G; DiGiovanna, MP; Feng, W; Gelmon, K; Hortobagyi, G; Hurvitz, SA; Krop, I; Lin, NU; Loi, S; Loibl, S; Mueller, V; Murthy, RK; Oliveira, M; Paplomata, E; Pegram, M; Ramos, J; Slamon, D; Winer, E; Zelnak, A, 2023)		1.33
"This subgroup analysis found that tucatinib in combination with trastuzumab and capecitabine improved OS while reducing the risk of developing new brain lesions, further supporting the importance of this treatment option for patients with ERBB2-positive MBC, including those with BMs."( Tucatinib vs Placebo, Both in Combination With Trastuzumab and Capecitabine, for Previously Treated ERBB2 (HER2)-Positive Metastatic Breast Cancer in Patients With Brain Metastases: Updated Exploratory Analysis of the HER2CLIMB Randomized Clinical Trial.
Abramson, V; Anders, C; Bachelot, T; Bedard, PL; Borges, V; Cameron, D; Carey, LA; Chien, AJ; Curigliano, G; DiGiovanna, MP; Feng, W; Gelmon, K; Hortobagyi, G; Hurvitz, SA; Krop, I; Lin, NU; Loi, S; Loibl, S; Mueller, V; Murthy, RK; Oliveira, M; Paplomata, E; Pegram, M; Ramos, J; Slamon, D; Winer, E; Zelnak, A, 2023)		1.38

Bioavailability

Capecitabine is an orally bioavailable prodrug that is converted to 5-fluorouracil through several enzymatic steps, the last of which is mediated by thymidine phosphorylase (TP) In adults, cape citabine has a bioavailability of approximately 100% with a Cmax of 3.

ExcerptReferenceRelevance
" The absolute bioavailability of 5'-deoxy-5-fluorouridine was estimated as 42% in patients with normal hepatic function and 62% in patients with impaired hepatic function."( Effect of hepatic dysfunction due to liver metastases on the pharmacokinetics of capecitabine and its metabolites.
Banken, L; Cassidy, J; Glynne-Jones, R; Goggin, T; Reigner, B; Roos, B; Schüller, J; Twelves, C; Utoh, M; Weidekamm, E, 1999)		0.53
"The bioavailability of 5'-DFUR in the systemic circulation was practically identical after administration of the two tablet formulations."( Bioequivalence of two tablet formulations of capecitabine and exploration of age, gender, body surface area, and creatinine clearance as factors influencing systemic exposure in cancer patients.
Banken, L; Bush, E; Cameron, D; Cassidy, J; Goggin, T; Jodrell, D; Jones, D; O'Byrne, K; Reigner, B; Roos, B; Steward, W; Twelves, C; Weidekamm, E, 1999)		0.56
" Among large numbers of the derivatives, capecitabine was selected based on its susceptibility to hepatic carboxylesterase, oral bioavailability in monkeys and efficacy in a human cancer xenograft."( [Discovery and development of novel anticancer drug capecitabine].
Horii, I; Ishitsuka, H; Shimma, N, 1999)		0.82
" However, marked intra- and interpatient variability, combined with nonlinear elimination kinetics and erratic oral bioavailability are relative limitations to further development of 5-FU."( The use of thymidylate synthase inhibitors in the treatment of advanced colorectal cancer: current status.
Papamichael, D, 1999)		0.3
" Numerous active 5-FU schedules are in clinical use, but erratic oral bioavailability has historically mandated intravenous administration."( Oral therapy for colorectal cancer: how to choose.
Damjanov, N; Meropol, NJ, 2000)		0.31
" The unpredictable and low oral bioavailability of 5FU initially discouraged this form of treatment."( The oral fluorinated pyrimidines.
de Bono, JS; Twelves, CJ, 2001)		0.31
" Bioavailability after oral administration is close to 100%."( Capecitabine: a review of its pharmacology and therapeutic efficacy in the management of advanced breast cancer.
Goa, KL; Ibbotson, T; Wagstaff, AJ, 2003)		1.76
"Capecitabine is an orally bioavailable prodrug that is converted to 5-fluorouracil through several enzymatic steps, the last of which is mediated by thymidine phosphorylase (TP)."( Thymidine phosphorylase expression and benefit from capecitabine in patients with advanced breast cancer.
Andreetta, C; Damante, G; Di Loreto, C; Fasola, G; Minisini, A; Pandolfi, M; Pegolo, E; Piga, A; Pizzolitto, S; Puglisi, F; Puppin, C; Valent, F, 2009)		2.05
" Given the oral bioavailability of capecitabine as well as in-vitro and in-vivo findings showing higher expression of thymidine phosphorylase in tumor cells and xenografts compared with normal tissue, capecitabine is an evolving candidate in the management of colorectal cancer with antimetabolite-based therapy."( Evolution of 5-fluorouracil-based chemoradiation in the management of rectal cancer.
Patel, PA, 2011)		0.65
" We also observed bioavailability of ursolic acid in the serum and tissue of animals."( Ursolic acid inhibits growth and metastasis of human colorectal cancer in an orthotopic nude mouse model by targeting multiple cell signaling pathways: chemosensitization with capecitabine.
Aggarwal, BB; Baladandayuthapani, V; Deorukhkar, A; Diagaradjane, P; Guha, S; Kannappan, R; Krishnan, S; Prasad, S; Reuter, S; Sung, B; Wei, C; Yadav, VR, 2012)		0.57
" It is combined with gimeracil in order to increase its bioavailability and with oteracil to try to reduce its gastrointestinal toxicity."( Tegafur + gimeracil + oteracil. Just another fluorouracil precursor.
, 2013)		0.39
"The absorption rate constant was found lower in the oldest patient group (≥75 years) compared with the youngest group, and the constant rate elimination of the 5-fluorouracil metabolite was found decreased over time (i."( Pharmacokinetics and exposure-effect relationships of capecitabine in elderly patients with breast or colorectal cancer.
Daher Abdi, Z; Lavau-Denes, S; Leobon, S; Marquet, P; Martin, J; Prémaud, A; Rousseau, A; Sauvage, FL; Tubiana-Mathieu, N; Urien, S, 2014)		0.65
" Because the oral bioavailability of 5-FU is unpredictable and highly variable, 5-FU is commonly administered intravenously."( Role of ABC transporters in fluoropyrimidine-based chemotherapy response.
Magdy, T; Nies, AT; Schwab, M; Zanger, UM, 2015)		0.42
" Average bioavailability was assessed by ANOVA."( Pharmacokinetics and pharmacogenetics of capecitabine and its metabolites following replicate administration of two 500 mg tablet formulations.
Baken, BC; Erlinghagen, V; Fuhr, U; Kubeš, V; Novotný, V; Peroutka, R; Queckenberg, C; Van Os, SH; Wargenau, M, 2015)		0.68
"7-folds enhancement in the oral bioavailability and in aberrant crypt foci number, apoptotic index comparison with suspension formulation."( Capecitabine lipid nanoparticles for anti-colon cancer activity in 1,2-dimethylhydrazine-induced colon cancer: preparation, cytotoxic, pharmacokinetic, and pathological evaluation.
Dudhipala, N; Puchchakayala, G, 2018)		1.92
" The POSS/MCM-41 codoped MIPs present favourable sustained release property in vitro and in vivo, displaying a high relative bioavailability of 173."( A polyhedral oligomeric silsesquioxane/molecular sieve codoped molecularly imprinted polymer for gastroretentive drug-controlled release in vivo.
Huang, YP; Liu, ZS; Wang, X; Yang, FF; Zhang, LP, 2018)		0.48
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019)		0.51
"Capecitabine is an orally bioavailable prodrug of the chemotherapeutic agent, fluorouracil."( Real-time comprehensive toxicology testing in the clinical management of accidental pediatric capecitabine ingestion.
Badea, A; Garcia, E; Gintjee, TJ; Goodnough, R; Li, K; Lynch, KL; Repplinger, D, 2020)		2.22
" Inappropriate or concomitant use of drugs can often lead to changes in the bioavailability of various compounds, resulting in pharmacokinetic alterations."( Controversial link between proton pump inhibitors and anticancer agents: review of the literature.
Meriggi, F, 2022)		0.72
" The bioavailability of Cap-loaded nanoparticles was found to be two fold increased than the pure drug, and also, it exhibited significantly more cytotoxic to tumor cells as compared to pure drug as confirmed by MTT assay."( QbD enabled optimization of solvent shifting method for fabrication of PLGA-based nanoparticles for promising delivery of Capecitabine for antitumor activity.
Jena, GK; Panigrahi, KC; Parhi, R; Patra, CN; Patra, P; Sruti, J, 2022)		0.93
"CAP, PGZ, and combination treatment nano-formulations were prepared by triblock (TB) (PCL-PEG-PCL) biodegradable copolymers to enhance drugs' bioavailability as anti-cancer agents."( Combination chemotherapy against colorectal cancer cells: Co-delivery of capecitabine and pioglitazone hydrochloride by polycaprolactone-polyethylene glycol carriers.
Fathi-Azarbayjani, A; Kheradmand, F; Pouya, FD; Rasmi, Y; Salehi, R, 2023)		1.14

Dosage Studied

Capecitabine is replacing continuous infusion fluorouracil as the backbone of combination chemotherapy in advanced gastric cancer patients. Data are limited with regard to adverse events and dosing practices associated with cape citabine monotherapy in real-world situations.

ExcerptRelevanceReference
"The suggested phase II dose on a continuous 42-day dosing schedule is 1,331 mg/m2/d."( Preliminary studies of a novel oral fluoropyrimidine carbamate: capecitabine.
Behr, J; Berghorn, E; Budman, DR; Creaven, PJ; Gordon, RJ; Griffin, T; Lichtman, SM; Meropol, NJ; Osterwalder, B; Reigner, B, 1998)		0.54
" All patients required a warfarin dosage reduction (range 18-74%, mean 44%)."( Warfarin-5-FU interaction--a consecutive case series.
Berlin, JD; Freeberg, BL; Johnson, CL; Kolesar, JM; Schiller, JH, 1999)		0.3
" Phase I trials have examined several schedules with the divided oral daily x 14 schedule every 3 weeks as the preferred phase II and phase III dosing method."( Capecitabine.
Budman, DR, 2000)		1.75
" Three different dosing regimens were investigated in phase I studies: continuous monotherapy, intermittent monotherapy, and intermittent therapy supplemented with leucovorin."( 5-fluorouracil/leucovorin versus capecitabine in patients with stage III colon cancer.
Seitz, JF, 2001)		0.59
" The combination showed better antitumor efficacy than the monotherapy of either agent in either dosing regimen."( Schedule dependency of antitumor activity in combination therapy with capecitabine/5'-deoxy-5-fluorouridine and docetaxel in breast cancer models.
Fujimoto-Ouchi, K; Tanaka, Y; Tominaga, T, 2001)		0.54
" Capecitabine in therapeutic dosage regimens generally has acceptable tolerability."( Capecitabine: a review of its use in the treatment of advanced or metastatic colorectal cancer.
Goa, KL; McGavin, JK, 2001)		2.66
" Phase I studies have determined the maximum tolerated dose (MTD) of capecitabine and identified a number of dosage regimens, which were subsequently evaluated in a randomised, phase II study as first-line treatment for metastatic colorectal cancer."( Rational development of capecitabine.
Venturini, M, 2002)		0.86
" An intermittent dosing schedule of capecitabine twice daily at a dose of 2510 mg/m2/day on days 1-14 in a 3-week cycle appeared to be feasible and resulted in a high dose intensity."( Capecitabine in breast cancer: current status.
Bontenbal, M; Smorenburg, CH; Verweij, J, 2001)		2.03
" Patients received capecitabine orally at the standard dosing regimen (1250 mg/m(2) capecitabine twice daily for 2 weeks followed by a 1-week rest period)."( Effect of renal impairment on the pharmacokinetics and tolerability of capecitabine (Xeloda) in cancer patients.
Banken, L; Cassidy, J; Gardiner, J; Harper, P; Johnston, P; Monkhouse, J; Poole, C; Reigner, B; Twelves, C; Weidekamm, E, 2002)		0.88
" Thus, a dosage of 825 mg/m(2) bid is the recommended dose level for further evaluation."( Phase I trial evaluating the concurrent combination of radiotherapy and capecitabine in rectal cancer.
Dunst, J; Frings, S; Hinke, A; Kölling-Schlebusch, K; Reese, T; Sutter, T; Zühlke, H, 2002)		0.55
" Three of 7 (43%) patients treated with irinotecan 300 mg/m(2) and capecitabine 2,300 mg/d had course 1 dose-limiting toxicity (DLT) defining maximum tolerated dosage (MTD)."( Phase I clinical trial of irinotecan with oral capecitabine in patients with gastrointestinal and other solid malignancies.
Baker, C; Chun, HG; Fehn, K; Goel, S; Hoffman, A; Hopkins, U; Jhawer, M; Landau, L; Makower, D; Mani, S; Rajdev, L; Wadler, S, 2002)		0.81
" The safety of capecitabine and optimal dosing schedules have been explored in phase I/II studies, resulting in the evaluation of the intermittent schedule (1250 mg/m2 twice daily for 14 days, every 3 weeks) in most subsequent clinical trials."( Capecitabine (Xeloda): from the laboratory to the patient's home.
Pentheroudakis, G; Twelves, C, 2002)		2.11
" Phase I/II studies exploring toxicity and the appropriate dosing resulted in the evaluation of the intermittent schedule (2510 mg/m2/day for 14 days every 3 weeks) in subsequent trials."( The rational development of capecitabine from the laboratory to the clinic.
Pentheroudakis, G; Twelves, C, )		0.43
" The present results have no clinical implications for the use of capecitabine and argue against the value of therapeutic drug monitoring for dosage adjustment."( Population pharmacokinetics and concentration-effect relationships of capecitabine metabolites in colorectal cancer patients.
Blesch, KS; Burger, HU; Gieschke, R; Reigner, B; Steimer, JL, 2003)		0.79
" Vinorelbine was administered at a fixed dosage of 25 mg/m2 on days 1 and 8 every 3 weeks."( A phase I study of capecitabine in combination with vinorelbine in advanced breast cancer.
Crucitta, E; De Lena, M; Guida, M; Latorre, A; Lorusso, V; Misino, A; Silvestris, N, 2003)		0.65
" She had been receiving capecitabine 2000 mg/m2/day; however, when the dosage was increased to 2500 mg/m2/day (the maximum dosage approved by the Food and Drug Administration) she experienced abdominal pain and cramping."( Capecitabine-induced pancreatitis.
Jones, KL; Valero, V, 2003)		2.07
" HFS, also known as erythrodysesthesia, manifests as acral erythema with swelling and dysesthesia of the palms and plantar aspects of the feet, and, in the absence of dosage reduction or stoppage of the drug, progresses to moist desquamation and ulceration with serious infections and loss of function."( Serious hand-and-foot syndrome in black patients treated with capecitabine: report of 3 cases and review of the literature.
Hitti, IF; Narasimhan, P; Narasimhan, S; Rachita, M, 2004)		0.56
" Also, food effect was assessed separately in a group dosed with 20 mg of the compound."( Single ascending dose tolerability, pharmacokinetic-pharmacodynamic study of dihydropyrimidine dehydrogenase inhibitor Ro 09-4889.
Banken, L; Bellibas, SE; Brivet, B; Bush, ED; Chamorey, E; Kircher, C; Milano, G; Nave, S; Patel, I; Renée, N, 2004)		0.32
" Fluorouracil (FU) chemoradiotherapy has demonstrated success in several organ sites with multiple dosing schedules that now guide the selection of oral analogs of FU to provide new chemoradiotherapy options."( Four decades of continuing innovation with fluorouracil: current and future approaches to fluorouracil chemoradiation therapy.
Mosley, ST; Rich, TA; Shepard, RC, 2004)		0.32
" During the last four decades, optimal dosing schedules have produced a therapeutic gain."( Four decades of continuing innovation with fluorouracil: current and future approaches to fluorouracil chemoradiation therapy.
Mosley, ST; Rich, TA; Shepard, RC, 2004)		0.32
" No DLT was observed at the dosage group of 500 mg/m(2) and 750 mg/m(2)."( [Phase I study of capecitabine with concurrent radiotherapy in early-stage nasopharyngeal carcinoma].
Guo, L; Guo, X; Hong, MH; Li, FY; Li, Q; Lin, HX; Luo, DH; Qiu, F, 2004)		0.66
" In addition, studies show that dosing flexibility with capecitabine/docetaxel allows management of side effects without compromising efficacy."( Optimizing the management of HER2-negative metastatic breast cancer with capecitabine (Xeloda).
Leonard, R; Miles, D; Reichardt, P; Twelves, C, 2004)		0.8
"Fifty-four patients were treated according to three different dosing schemes in which the capecitabine dose was fixed and the CI-994 dose was escalated."( A phase I study of the oral combination of CI-994, a putative histone deacetylase inhibitor, and capecitabine.
Janisch, L; Kimmel, KA; Kindler, HL; Macek, TA; Olson, SC; Ratain, MJ; Schilsky, RL; Undevia, SD; Vogelzang, NJ, 2004)		0.76
"The purpose of this article is to review the available information on capecitabine with respect to clinical pharmacology, mechanism of action, pharmacokinetic and pharmacodynamic properties, clinical efficacy for breast and colorectal cancer adverse-effect profile, documented drug interactions, dosage and administration, and future directions of ongoing research."( Capecitabine: a review.
Lindley, C; Walko, CM, 2005)		2
" The predominant route of elimination is renal, and dosage reduction of 75% is recommended in patients with creatinine clearance (CrCl) of 30 to 50 mL/min."( Capecitabine: a review.
Lindley, C; Walko, CM, 2005)		1.77
"In a phase II IRB approved trial, capecitabine was given at a dosage of 2000 mg/m2/day orally in a divided dose daily for 14 days followed by a 7-day rest period."( Phase II trial of capecitabine in recurrent squamous cell carcinoma of the cervix.
Atkinson, EN; Bodurka, DC; Brown, J; Jenkins, AD; Johnston, T; Levenback, C; Ramondetta, LM; Sun, C; Wolf, JK, 2005)		0.94
"This retrospective analysis supports a starting dose of 2000 mg/m2/day because of its superior therapeutic index; however, patients may still have toxic effects and individualization of dosing is necessary."( Lower dose capecitabine has a more favorable therapeutic index in metastatic breast cancer: retrospective analysis of patients treated at M. D. Anderson Cancer Center and a review of capecitabine toxicity in the literature.
Gauthier, AM; Hennessy, BT; Hortobagyi, G; Michaud, LB; Valero, V, 2005)		0.72
" Untoward side-effects were moderate, reversible and, therefore, did not require dosage to be corrected or cut down."( [Gemcitabine plus cisplatin therapy in breast cancer refractory to anthracyclines, docetaxel and capecitabine].
Filatova, LV; Gershanovich, ML; Semiglazova, TIu, 2005)		0.55
" A flat dosing scheme of both drugs was used to facilitate development of the oral regimen, and because neither drug's clearance is associated with body surface area (BSA), pharmacokinetic and pharmacogenetic endpoints were explored."( Combination vinorelbine and capecitabine for metastatic breast cancer using a non-body surface area dosing scheme.
Baker, LH; Griffith, KA; Hayes, DF; Rae, JM; Schott, AF; Sterns, V, 2006)		0.63
"A non-BSA based dosing scheme of capecitabine and vinorelbine is safe and efficacious."( Combination vinorelbine and capecitabine for metastatic breast cancer using a non-body surface area dosing scheme.
Baker, LH; Griffith, KA; Hayes, DF; Rae, JM; Schott, AF; Sterns, V, 2006)		0.91
" Only BILT significantly influenced the pharmacokinetics but this effect was not considered as relevant for dosing adjustment."( Pharmacokinetic modelling of 5-FU production from capecitabine--a population study in 40 adult patients with metastatic cancer.
Lokiec, F; Rezaí, K; Urien, S, 2005)		0.58
"This article describes a woman with metastatic upper gastrointestinal cancer who developed thoracic myelopathy unexpectedly after standard dosage and fractionation radiotherapy."( Myelopathy after radiation therapy and chemotherapy with capecitabine and gemcitabine.
Barstis, JL; Black, AC, 2005)		0.57
" The second patient was a 59-year-old man with metastatic colorectal carcinoma who was placed on capecitabine treatment at a dosage of 2500 mg/m2/day in 2 divided doses for 2 weeks followed by a one week rest period."( Capecitabine-induced severe hypertriglyceridemia: report of two cases.
Babaoglu, MO; Guler, N; Kurt, M; Shorbagi, A; Yasar, U, 2006)		1.99
" Twelve were on an average warfarin dosage of 19."( A retrospective study of coagulation abnormalities in patients receiving concomitant capecitabine and warfarin.
Diasio, R; Ledbetter, L; Saif, MW; Shah, HR, 2006)		0.56
"To evaluate the effects of the novel protein kinase C (PKC) inhibitor enzastaurin on intracellular phosphoprotein signaling using flow cytometry and to use this approach to measure enzastaurin effects on surrogate target cells taken from cancer patients that were orally dosed with this agent."( Development and validation of a drug activity biomarker that shows target inhibition in cancer patients receiving enzastaurin, a novel protein kinase C-beta inhibitor.
Basche, M; Britten, CD; Carducci, M; Cook, CA; Eckhardt, SG; Green, LJ; Herbst, RS; Jaken, S; Marder, P; Musib, LC; Ray, C; Thornton, D, 2006)		0.33
" Temozolomide and capecitabine were administered concomitantly to 4 sequential cohorts at different dosing levels on Days 1-5 and Days 8-12, with cycles repeated every 21 days until disease progression."( Phase I study of capecitabine in combination with temozolomide in the treatment of patients with brain metastases from breast carcinoma.
Arun, B; Broglio, K; Buchholz, T; Francis, D; Groves, M; Hortobagyi, GN; Meyers, C; Rivera, E; Valero, V; Yin, G, 2006)		1.01
" One such treatment, capecitabine, offers patients the benefit of oral dosing and permits at-home self-management."( Capecitabine: a new adjuvant option for colorectal cancer.
Berg, DT, 2006)		2.1
"Capecitabine/docetaxel dosing flexibility allows management of side-effects without compromising efficacy."( Detailed analysis of a randomized phase III trial: can the tolerability of capecitabine plus docetaxel be improved without compromising its survival advantage?
Barak-Wigler, N; Bexon, AS; Chan-Navarro, CA; Gorbounova, V; Harker, WG; Leonard, R; Maraninchi, D; McKendrick, JJ; O'Shaughnessy, J; Twelves, C; Vukelja, S, 2006)		2.01
" The clinical utility of capecitabine in the management of breast cancer is supported by its convenient oral dosing schedule and favorable safety profile, as well as its excellent clinical activity in primary and metastatic breast cancer."( The role of capecitabine in first-line treatment for patients with metastatic breast cancer.
Chan, A; Gelmon, K; Harbeck, N, 2006)		1.02
"Twenty patients with rectal cancer (clinical Stage uT3-T4 or N+) received a standard dosing regimen of cetuximab (400 mg/m(2) on Day 1 and 250 mg/m(2) on Days 8, 15, 22, and 29) and escalating doses of irinotecan and capecitabine according to phase I methods: dose level I, irinotecan 40 mg/m(2) on Days 1, 8, 15, 22, and 29 and capecitabine 800 mg/m(2) on Days 1-38; dose level II, irinotecan 40 mg/m(2) and capecitabine 1000 mg/m(2); and dose level III, irinotecan 50 mg/m(2) and capecitabine 1000 mg/m(2)."( Phase I trial of cetuximab in combination with capecitabine, weekly irinotecan, and radiotherapy as neoadjuvant therapy for rectal cancer.
Dinter, D; Grobholz, R; Heeger, S; Hochhaus, A; Hofheinz, RD; Horisberger, K; Kähler, G; Kraus-Tiefenbacher, U; Post, S; Wenz, F; Willeke, F; Woernle, C, 2006)		0.78
" doses of tipifarnib, without a dose-response relationship."( A phase I safety, pharmacological and biological study of the farnesyl protein transferase inhibitor, tipifarnib and capecitabine in advanced solid tumors.
Cohen, RB; Eckhardt, SG; Gore, L; Gustafson, D; Holden, SN; Mikule, C; Morrow, M; O'Bryant, CL; Palmer, PA; Persky, M; Pierson, AS; Zhang, S, 2006)		0.54
" The dosage should be reduced or therapeutic regimen changed."( [Unilateral acral necrosis as a minor form of hand-foot syndrome. Patient with unilateral acral necrosis secondary to capecitabine therapy for metastatic breast cancer].
Ockenfels, HM; Saborowski, A; Sauter, C, 2007)		0.55
" In April 2004, she had a recurrence manifesting itself as bone metastasis, partly because of poor compliance with the hospital-visit and dosing schedules."( [A patient with advanced recurrent breast cancer who firmly resisted hair loss and was then treated by combination therapy with high-dose toremifene and capecitabine].
Akahane, T; Chiba, T; Hashimoto, Y; Yano, H, 2007)		0.54
" Two sequential schema were used: Arm A fixed the dose of irinotecan at 100 mg/m(2) and escalated capecitabine in cohorts, and arm B fixed the dose of capecitabine at 750 mg/m(2) PO BID and escalated the dosage of irinotecan."( A Phase I dose-finding study using an innovative sequential biweekly schedule of irinotecan followed 24 hours later by capecitabine.
Allen, SL; Budman, DR; Fricano, M; Gonzales, A; Hirawat, S; Kolitz, J; Lichtman, SM; Villani, G, )		0.56
" Repetitive dosing was feasible with prolonged disease stabilization in 8 patients."( A Phase I dose-finding study using an innovative sequential biweekly schedule of irinotecan followed 24 hours later by capecitabine.
Allen, SL; Budman, DR; Fricano, M; Gonzales, A; Hirawat, S; Kolitz, J; Lichtman, SM; Villani, G, )		0.34
" Capecitabine was administered orally twice daily at a dosage of 2500 mg/m(2) for 14 days, followed by 7 days of rest."( Capecitabine as third-line treatment in patients with metastatic renal cell carcinoma after failing immunotherapy.
Barbanti, G; de Rubertis, G; Francini, E; Francini, G; Manganelli, A; Marsili, S; Paolelli, L; Pascucci, A; Petrioli, R; Salvestrini, F; Sciandivasci, A, 2007)		2.69
" HFS manifests as acral erythema, with swelling and dysesthesia of the palms and plantar aspects of the feet, which in the absence of dosage reduction or drug cessation, progresses to moist desquamation and ulceration, resulting in serious infections and loss of function."( Hand-foot syndrome with scleroderma-like change induced by the oral capecitabine: a case report.
Hwang, SJ; Kim, BS; Kim, HJ; Kim, YJ; Lee, SD; Nam, SH, 2007)		0.58
" In the man, the capecitabine dosage was reduced and metoprolol was prescribed, while in the woman the capecitabine was stopped."( [Myocardial ischaemia as a result of treatment with capecitabine].
Liem, AH; Planting, AS; van Halteren, HK, 2007)		0.93
" Dosing of S-1 is different between Western and Asian populations due to differences in metabolism by CYP2A6."( Medical treatment for advanced gastroesophageal adenocarcinoma.
Ajani, JA; Cen, P, 2007)		0.34
" In view of the convenience and flexibility of patients in adjusting dosage when encountering toxicities, capecitabine is replacing continuous infusion fluorouracil as the backbone of combination chemotherapy in advanced gastric cancer patients."( Capecitabine in advanced gastric cancer.
Chau, I; Cunningham, D; Okines, A, 2007)		2
" Although a traditional toxicity-based maximum tolerated dose was not achieved, the highest dosing cohort represented a biologically relevant dose of enzastaurin, on the basis of preclinical data and correlative pharmacodynamic biomarker assays of protein kinase Cbeta inhibition in peripheral blood mononucleocytes, in combination with a standard dose of capecitabine."( A phase I safety, tolerability, and pharmacokinetic study of enzastaurin combined with capecitabine in patients with advanced solid tumors.
Baldwin, J; Basche, M; Britten, CD; Camidge, DR; Darstein, C; Finn, RS; Gail Eckhardt, S; Gore, L; Holden, SN; Leong, S; Musib, L; O'Bryant, CL; Thornton, D, 2008)		0.74
" This study suggests that continuous oral capecitabine at a fixed daily dose of 2000 mg is well tolerated, and that it allows for the simplification and ease of dosing in elderly patients with metastatic colorectal and gastric cancer."( Continuous oral capecitabine at fixed dose in patients older than 75 years with metastatic colorectal and gastric cancer: a study of the Multidisciplinary Oncology Group on Gastrointestinal Tumors.
Battistelli, S; Civitelli, S; Fiaschi, AI; Francini, E; Francini, G; Lorenzi, M; Marsili, S; Pascucci, A; Petrioli, R; Roviello, F; Tanzini, G, 2008)		0.96
"Continuous dosing of the combination of capecitabine and celecoxib was well tolerated, produced antiangiogenic effects, and has antitumor activity."( Metronomic antiangiogenic therapy with capecitabine and celecoxib in advanced tumor patients--results of a phase II study.
Arends, J; Drevs, J; Frost, A; Häring, B; Hennig, J; Medinger, M; Mross, K; Steinbild, S; Strecker, R; Unger, C, 2007)		0.88
" Three treatment cohorts were assessed, using different dosing regimens."( Erlotinib in combination with capecitabine and docetaxel in patients with metastatic breast cancer: a dose-escalation study.
Baselga, J; De Rosa, F; Fettner, S; Jones, R; Rakhit, A; Trigo, JM; Twelves, C; Wright, T, 2008)		0.63
" The drug enables chronic dosing that mimics continuous infusion of 5-FU."( Safety profile and activity of lower capecitabine dose in patients with metastatic breast cancer.
Alessandroni, P; Baldelli, AM; Casadei, V; Catalano, G; Catalano, V; Ceccolini, M; Fedeli, A; Fedeli, SL; Giordani, P; Rossi, D, 2007)		0.61
" Each course consisted of capecitabine at a dosage of 1,800 mg/body/day for 2 weeks and docetaxel at a dosage of 60 mg/body (day 8 only) followed by withdrawal for 1 week."( [A case of triple negative recurrent breast cancer successfully treated with capecitabine+docetaxel combination chemotherapy].
Hachisuka, Y; Hatano, H; Johira, H; Kamei, Y; Kawata, N; Kimura, M; Miyata, N; Ohmori, K; Umeoka, T; Uomoto, M; Watanabe, R; Yunoki, S, 2008)		0.87
"As predicted by mathematical modeling, capecitabine dosing for 7 days followed by a 7-day rest is well tolerated."( Phase I study of a novel capecitabine schedule based on the Norton-Simon mathematical model in patients with metastatic breast cancer.
Dugan, U; Edwards, C; Feigin, K; Hudis, C; Norton, L; Patil, S; Tan, KL; Theodoulou, M; Traina, TA, 2008)		0.92
" OXA was administered at a dosage of 40 (n = 6), 50 (n = 3),60 (n = 3), 70 (n = 3), or 80 mg/m(2) (n = 6) once a week for 2 weeks (first cycle) followed by a second cycle after a 7-day break."( Phase I study of oxaliplatin in combination with capecitabine and radiotherapy as postoperative treatment for stage II and III rectal cancer.
Fang, H; Jin, J; Li, YX; Liu, YP; Wang, JW; Wang, K; Wang, WH; Yu, ZH; Zhou, AP; Zhou, ZX, 2008)		0.6
" As a result, the patient's QOL is hindered and led to a reduction of the dosage or discontinuation of the treatment depending on the grade of adverse event."( [Management of hand-foot syndrome in patient treated with capecitabine].
Anami, S; Fujii, C; Fujino, M; Fujita, M; Furukawa, H; Inoue, M; Kamigaki, S; Nakayama, T; Tatsuta, M; Yasui, Y, 2008)		0.59
" The capecitabine dosage was started at 2000 mg daily for 14 days during the first cycle and increased to 2500 and 3000 mg daily during the second and the third cycles, respectively."( Capecitabine-associated cerebellar ataxia.
Kaufman, DA; Lam, MS; Russin, MP, 2008)		2.3
" Capecitabine was given at an oral dosage of 825 mg/m(2)bid on each day of the radiotherapy period with the first daily dose applied 2 h before irradiation, followed by surgery 6 weeks later."( Neoadjuvant capecitabine combined with standard radiotherapy in patients with locally advanced rectal cancer: mature results of a phase II trial.
Budach, W; Debus, J; Dunst, J; Hinke, A; Hoelscher, T; Mose, S; Reese, T; Roedel, C; Rudat, V; Wulf, J; Zuehlke, H, 2008)		1.64
" Recent analyses show that capecitabine/docetaxel dosing flexibility for managing side effects does not compromise efficacy, and define this combination regimen as an important treatment option for its efficacy, tolerability and cost-effectiveness."( Capecitabine and docetaxel combination for the treatment of breast cancer.
Leonard, RC; Morishita, M, 2008)		2.09
"Modifying the capecitabine dosing schedule from 14 days on, 7 days off (14/7) to 7 days on, 7 days off (7/7) may enable higher doses and improved antitumor efficacy in colorectal cancer xenografts."( In vivo activity of novel capecitabine regimens alone and with bevacizumab and oxaliplatin in colorectal cancer xenograft models.
Dugan, U; Heimbrook, D; Higgins, B; Kohles, J; Kolinsky, K; Packman, K; Shen, BQ; Zhang, YE; Zioncheck, TF, 2009)		1.01
" The purpose of this article is to review the available information on capecitabine with respect to clinical efficacy for tumors of the digestive tract, adverse-effect profile, documented drug interactions, dosage and administration, and future directions of ongoing research."( The role of capecitabine in the management of tumors of the digestive system.
Gennatas, C; Gennatas, S; Michalaki, V, 2009)		0.96
" Additionally, no dosage decrease was required, and only 4 cycles were withheld for 1 week because of neutropenia."( Efficacy and safety of capecitabine and oxaliplatin combination as second-line treatment in advanced colorectal cancer.
Hatzopoulos, A; Heras, P; Karagiannis, S; Kritikos, K; Kritikos, N; Mitsibounas, D; Xourafas, V, )		0.44
" When sirolimus was added to this regimen at a dosage to achieve a serum level of at least 10 ng/dL at the time of the gemcitabine and docetaxel infusion, their tumors regressed."( Sirolimus can reverse resistance to gemcitabine, capecitabine and docetaxel combination therapy in pancreatic cancer.
Sherman, WH, 2009)		0.61
" Scheduled dosing of 5-FU was changed from infusion to a bolus type."( Bolus 5-Fluorouracil as an alternative modality to infusion 5-Fluorouracil in a patient with rectal cancer and capecitabine-induced cardiotoxicity.
Lee, V; Saif, MW; Shaib, W, )		0.34
" Starting chemotherapy dosage (dose level: 0) was capecitabine 550 mg/m bid, day 1 to 5 every week through out x-ray therapy, irinotecan 30 mg/ m IV on days 1, 8, 22, 29 (no treatment on day 15 and day 36), and celecoxib 400 mg PO bid from day 1 till the last day of radiation."( A phase I study of capecitabine, irinotecan, celecoxib, and radiation as neoadjuvant therapy of patients with locally advanced rectal cancer.
Alqaisi, M; Bernal, P; Bush, D; Byrd, J; Garberoglio, C; Hussein, F; Malik, I, 2010)		0.94
"Recommended dosage for future trials is capecitabine 625 mg/m bid, irinotecan 35 mg/m, and celecoxib 400 mg orally bid in combination with pelvic radiation."( A phase I study of capecitabine, irinotecan, celecoxib, and radiation as neoadjuvant therapy of patients with locally advanced rectal cancer.
Alqaisi, M; Bernal, P; Bush, D; Byrd, J; Garberoglio, C; Hussein, F; Malik, I, 2010)		0.96
" Therefore, the MTD was defined at 1500mg/m(2) of capecitabine in this dosing schedule with PHY906."( Phase I study of the botanical formulation PHY906 with capecitabine in advanced pancreatic and other gastrointestinal malignancies.
Cheng, YC; Elligers, K; Grant, N; Jiang, ZL; Lamb, L; Lansigan, F; Liu, SH; Mezes, M; Ruta, S; Saif, MW, 2010)		0.86
" The most (even if not fully) effective strategy was reducing capecitabine dosage together with nitrates, calcium-channel blockers and trimetazidine therapy."( Capecitabine cardiac toxicity presenting as effort angina: a case report.
Crivellari, D; Lestuzzi, C; Meneguzzo, N; Rigo, F; Viel, E, 2010)		2.04
" However, dosing has been the subject of considerable debate, and there is evidence that dosing differs among clinical practices in Europe, Asia, and North America."( Evolution of capecitabine dosing in colorectal cancer.
Sun, W, 2010)		0.73
" Since the concomitant use of warfarin and the oral fluoropyrimidines was unavoidable in this case, the warfarin dosage was adjusted to keep INR within goal range (1."( Increased anticoagulant activity of warfarin used in combination with doxifluridine.
Genda, T; Hori, S; Miki, A; Nakajima, M; Satoh, H; Sawada, Y; Suehira, M, 2010)		0.36
"To keep INR within goal range, the maintenance dosage of warfarin was reduced during the treatment with doxifluridine as well as capecitabine."( Increased anticoagulant activity of warfarin used in combination with doxifluridine.
Genda, T; Hori, S; Miki, A; Nakajima, M; Satoh, H; Sawada, Y; Suehira, M, 2010)		0.57
"In the United States, poor patient tolerability of the standard capecitabine dosing regimen (1250 mg/m2 twice daily on days 1-14 administered every 21 days) limits the established benefit of the agent."( Evolution of capecitabine dosing in breast cancer.
Naughton, M, 2010)		0.97
" In this article, we focus on capecitabine dosing in advanced breast cancer, review the available data and discuss the implications of this evidence on best treatment practice both for chemotherapy alone and for chemotherapy when combined with biological agents."( Optimising the dose of capecitabine in metastatic breast cancer: confused, clarified or confirmed?
Gralow, J; Martin, M; Zielinski, C, 2010)		0.96
" Adherence was calculated as the number of doses taken divided by doses expected, taking into account toxicity-related dosing changes."( Adherence and persistence with oral adjuvant chemotherapy in older women with early-stage breast cancer in CALGB 49907: adherence companion study 60104.
Archer, L; Berry, D; Gralow, J; Grenier, D; Hudis, C; Kastrissios, H; Kornblith, AB; Muss, H; Partridge, AH; Perez, E; Wang, X; Winer, E; Wolff, AC, 2010)		0.36
" As the drug is orally administered, capecitabine permits greater convenience and flexibility in dosing by eliminating the need for continuous infusion and its potential complications."( Dosing considerations for capecitabine-irinotecan regimens in the treatment of metastatic and/or locally advanced colorectal cancer.
Boehm, KA; Cartwright, T; McCollum, D, 2010)		0.93
"Following significant hematotoxicity, dosing was modified to gemcitabine 1000 mg/m (Days 1, 8), capecitabine 1000 mg twice daily (Days 1-14), and bevacizumab 15 mg/kg (Day 1) on a 21-day cycle with evaluation every 3 cycles."( A phase II trial of gemcitabine, capecitabine, and bevacizumab in metastatic renal carcinoma.
Chung, EK; Hahn, OM; Karrison, T; Kasza, K; Manchen, E; Posadas, EM; Stadler, WM, 2011)		0.87
"we demonstrated that the application of Norton-Simon modeling to the design and analysis of preclinical data predicts an improved capecitabine dosing schedule in xenograft models."( Optimizing chemotherapy dose and schedule by Norton-Simon mathematical modeling.
Dugan, U; Higgins, B; Hudis, CA; Kolinsky, K; Norton, L; Theodoulou, M; Traina, TA, 2010)		0.57
" Such variability, which may lead to treatment failure or toxicity, could need drug concentration measurement to individualize dosing regimen."( An APCI LC-MS/MS method for routine determination of capecitabine and its metabolites in human plasma.
Bérard, M; Demarchi, M; Kantelip, JP; Montange, D; Muret, P; Piédoux, S; Royer, B, 2010)		0.61
"2 Gy/f, 2 f/d plus concurrent capecitabine at an oral dosage of 825 mg/m2 bid on each day of radiotherapy period."( [Efficacy observation of accelerated hyperfractionation recourse radiotherapy plus concurrent capecitabine in the treatment of locoregional recurrent rectal cancer].
Dai, Y; Shao, ZY; Yu, JM; Zhang, JD, 2010)		0.87
" Secondary endpoints include evaluating response rate, safety profile and whether or not VN dosage escalation was required."( Phase I study of oral vinorelbine and capecitabine in patients with metastatic breast cancer.
Anton, A; Bermejo, B; Casado, A; Gayo, J; Lao, J; Lluch, A; Martin, M; Muñoz, M; Paules, AB; Provencio, M, 2010)		0.63
" Although some patients may benefit from the treatment, other dosing regimens and novel taxanes such as Nab-paclitaxel should be explored in this setting."( Docetaxel second-line therapy in patients with advanced pancreatic cancer: a retrospective study.
Kaley, K; Penney, R; Saif, MW; Syrigos, K, 2010)		0.36
" We also explore different dosing and schedules of capecitabine administration."( Safety of capecitabine: a review.
Marshall, JL; Mikhail, SE; Sun, JF, 2010)		1.01
"This study was conducted to determine the optimal dosage of the docetaxel-capecitabine-cisplatin (DXP) regimen and to evaluate its efficacy and safety in patients with advanced gastric cancer."( Phase I/II study of a combination of docetaxel, capecitabine, and cisplatin (DXP) as first-line chemotherapy in patients with advanced gastric cancer.
Chang, HM; Kang, YK; Kim, BS; Kim, TW; Oh, ST; Ryu, MH; Yoo, C; Yook, JH, 2011)		0.86
"5, or 50 mg) was administered orally once daily on three dosing schedules: 4 weeks on treatment, 2 weeks off treatment (Schedule 4/2); 2 weeks on treatment, 1 week off treatment (Schedule 2/1); and continuous daily dosing (CDD schedule)."( A phase I study of sunitinib plus capecitabine in patients with advanced solid tumors.
Bello, A; Burris, HA; Chao, R; Chiorean, EG; Jones, S; Lee, FC; Liau, KF; Royce, M; Sweeney, CJ; Tye, L; Verschraegen, CF, 2010)		0.64
"asparagine-glycine-arginine-human tumour necrosis factor (NGR-hTNF), an agent selectively damaging the tumour vasculature, showed a biphasic dose-response curve in preclinical models."( Two doses of NGR-hTNF in combination with capecitabine plus oxaliplatin in colorectal cancer patients failing standard therapies.
Andretta, V; Bennicelli, E; Bordignon, C; Caprioni, F; Comandini, D; Fornarini, G; Guglielmi, A; Lambiase, A; Mammoliti, S; Mazzola, G; Pessino, A; Sciallero, S; Sobrero, AF, 2011)		0.63
"The combination of sorafenib plus gemcitabine and capecitabine is tolerable, but requires attenuation of sorafenib and capecitabine dosing because of the overlapping toxicity of hand-foot syndrome."( A phase I trial of sorafenib plus gemcitabine and capecitabine for patients with advanced renal cell carcinoma: New York Cancer Consortium Trial NCI 6981.
Jeske, S; Kung, S; Lehrer, D; Matulich, D; Mazumdar, M; Milowsky, MI; Nanus, DM; Selzer, J; Sung, M; Tagawa, ST; Wright, JJ, 2011)		0.88
" Dose modification including dose reduction and dosing schedule modification may be utilized to manage toxicities, but this must be based on careful hematologic, neurologic, and liver function monitoring."( Optimizing ixabepilone treatment schedules in patients with advanced or metastatic breast cancer.
Egerton, N, 2010)		0.36
" Peripheral neuropathy with ixabepilone was generally reversible and was effectively managed by dosage reduction in most patients."( Ixabepilone plus capecitabine for breast cancer patients with an early metastatic relapse after adjuvant chemotherapy: two clinical trials.
Fornier, M, 2010)		0.7
" In those patients who required a warfarin dosage reduction, the dose was reduced by 38% and 41% in the 5-fluorouracil and capecitabine groups, respectively."( Comparison of the 5-fluorouracil-warfarin and capecitabine-warfarin drug interactions.
Dowell, JE; Martin, R; Shah, SR; Ussery, SM, 2010)		0.83
" The review aims to provide an evidence-based update of clinical trials investigating the clinical efficacy, adverse-event profile, dosage and administration of this drug, alone or in combination with conventional chemotherapeutics and/or new target-oriented drugs, in the management of colorectal cancer patients."( Update on capecitabine alone and in combination regimens in colorectal cancer patients.
Azzariti, A; Cinieri, S; Colucci, G; De Vita, F; Lorusso, V; Maiello, E; Millaku, A; Numico, G; Petriella, D; Pisconti, S; Russo, A; Santini, D; Silvestris, N; Tommasi, S, 2010)		0.76
"This dosing schedule of FDR gemcitabine plus capecitabine is active in patients with advanced pancreatobiliary cancers."( Optimizing the administration of fixed-dose rate gemcitabine plus capecitabine using an alternating-week schedule: a dose finding and early efficacy study in advanced pancreatic and biliary carcinomas.
Bergsland, EK; Coakley, FV; Dito, E; Espinoza, AM; Hanover, CS; Jones, KA; Kelley, RK; Ko, AH; Ong, A; Tempero, MA; Venook, AP, 2012)		0.88
" This case suggests that when capecitabine and PHT are coadministered, PHT levels should be monitored frequently, and that PHT dosage should be adjusted accordingly if it cannot be replaced by an alternative anticonvulsant."( [A case of toxicity caused by drug interaction between capecitabine and phenytoin in patient with colorectal cancer].
Fukui, E; Kawahara, K; Sakurai, M; Ueda, R; Yamada, R, 2011)		0.91
" The main factors affecting the quality of EBEs were the values of parameters governing the dose-response relationship and the within-subject distribution of categories."( Empirical Bayes estimation of random effects of a mixed-effects proportional odds Markov model for ordinal data.
Girard, P; Paule, I; Tod, M, 2011)		0.37
" Taken together, this non-clinical study shows that lapatinib and capecitabine modulate each other's molecular determinants of response and that concomitant dosing seems to be the optimal way to combine these drugs."( Positive interaction between lapatinib and capecitabine in human breast cancer models: study of molecular determinants.
Chefrour, M; Ciccolini, J; Denden, A; Fischel, JL; Formento, P; Giacometti, S; Iliadis, A; Milano, G; Renée, N, 2012)		0.88
" Cohort C explored an alternate schedule of 7-day on/7-day off flat dose capecitabine 1,000 mg BID with continuous dosing of sorafenib 400 mg BID."( A drug interaction study evaluating the pharmacokinetics and toxicity of sorafenib in combination with capecitabine.
Bendell, JC; Burris, HA; Greco, FA; Hainsworth, JD; Infante, JR; Jones, SF; Lane, CM; Spigel, DR; Yardley, DA, 2012)		0.83
" The rate of grade 3 HFSR is concerning and limits the feasibility of prolonged dosing of sorafenib with capecitabine 1,000 mg/m(2) on the 21-day schedule."( A drug interaction study evaluating the pharmacokinetics and toxicity of sorafenib in combination with capecitabine.
Bendell, JC; Burris, HA; Greco, FA; Hainsworth, JD; Infante, JR; Jones, SF; Lane, CM; Spigel, DR; Yardley, DA, 2012)		0.81
" The starting dosage of capecitabine was 2000 mg/m(2)/day (days 1-14, every 3 weeks)."( Adjuvant capecitabine chemotherapy using a tailored-dose strategy in elderly patients with colon cancer.
Bang, SM; Chang, HJ; Kang, SB; Kim, DW; Kim, JH; Kim, YJ; Lee, JS; Lee, KW, 2012)		1.1
" Dose escalation to 2500 mg/m(2)/day was possible in 56 patients, and this dosage was maintained in 24 patients until the completion of chemotherapy (eight cycles)."( Adjuvant capecitabine chemotherapy using a tailored-dose strategy in elderly patients with colon cancer.
Bang, SM; Chang, HJ; Kang, SB; Kim, DW; Kim, JH; Kim, YJ; Lee, JS; Lee, KW, 2012)		0.8
" The toxicity profile of this regimen is consistent with the standard every-3-week dosing schedule."( A phase II study of oxaliplatin, dose-intense capecitabine, and high-dose bevacizumab in the treatment of metastatic colorectal cancer.
Bendell, JC; Blobe, GC; Fernando, NH; Honeycutt, W; Hurwitz, HI; Morse, MA; Pang, H; Wong, NS, 2011)		0.63
"Oral administration of cyclophosphamide (CTX) and capecitabine may have a greater potential for treatment of metastatic breast cancer (MBC) due to anti-angiogenesis resulting from the metronomic dosage and upregulation of thymidine phosphorylase by CTX."( An all-oral combination of metronomic cyclophosphamide plus capecitabine in patients with anthracycline- and taxane-pretreated metastatic breast cancer: a phase II study.
Hong, X; Hu, X; Leaw, S; Lu, J; Shao, Z; Wang, J; Wang, Z, 2012)		0.87
"Our group applied mathematical modeling to capecitabine dosing and predicted 7 days of treatment followed by 7 days of rest (7-7) would improve efficacy and minimize toxicity."( Phase II trial of a novel capecitabine dosing schedule in combination with lapatinib for the treatment of patients with HER2-positive metastatic breast cancer.
Chen, C; D'Andrea, G; Drullinsky, P; Feigin, K; Gajria, D; Gonzalez, J; Hudis, CA; Lake, D; Norton, L; Patil, S; Theodoulou, M; Traina, TA, 2012)		0.94
" Weekday capecitabine dosing with weekly paclitaxel may improve tolerability without a detrimental effect on efficacy, and merits further evaluation in patients suited to combination chemotherapy."( A GINECO randomized phase II trial of two capecitabine and weekly paclitaxel schedules in metastatic breast cancer.
Alexandre, J; Bachelot, T; Bourgeois, H; de Rauglaudre, G; Hardy-Bessard, AC; Jaubert, D; Largillier, R; Lortholary, A; Paraiso, D, 2012)		1.06
" In MM, Phase I/II clinical trials have established the optimal dosing schedule for perifosine and bortezomib in combination, and demonstrated that perifosine can sensitize to, or overcome resistance to, bortezomib, associated with prolonged responses and a favorable side effect profile."( Perifosine , an oral, anti-cancer agent and inhibitor of the Akt pathway: mechanistic actions, pharmacodynamics, pharmacokinetics, and clinical activity.
Anderson, KC; Eng, C; Hideshima, T; Kolesar, J; Richardson, PG, 2012)		0.38
" Our findings suggest that it is necessary to manage drug dosage for Japanese patients while considering their renal function, and to actively monitor for any side effects."( [Side effect analyses in consideration of renal functions for capecitabine-administered patients].
Iwai, M; Kimura, M; Yasuda, T; Yoshimura, T, 2012)		0.62
" This dosing regimen warrants further study in the first-line setting for patients with less aggressive MBC who are not candidates for combination therapy."( Capecitabine in elderly patients with metastatic breast cancer.
Basile, ML; Bianco, V; De Filippis, L; De Sanctis, R; Del Signore, E; Di Seri, M; Gori, B; Lapadula, V; Longo, F; Quadrini, S; Restuccia, R; Speranza, I; Stumbo, L, )		1.57
" Another option is to use desensitization protocols that induce a temporary state of tolerance by gradually administering small quantities of the antineoplastic drug until the therapeutic dosage is reached."( Effectiveness of oxaliplatin desensitization protocols.
Aguilella-Vizcaíno, MJ; Calleja-Hernández, MÁ; Cortés-Funes Castro, H; Cortijo-Cascajares, S; García-Escobar, I; Herreros-de-Tejada, A; Nacle-López, I, 2013)		0.39
"Five patients with primary colorectal adenocarcinoma or anal squamous cell carcinoma were started on a 2-weeks-on, 1-week-off capecitabine dosing regimen in addition to other chemotherapeutic agents and/or radiation."( Capecitabine-induced chest pain relieved by diltiazem.
Ambrosy, AP; Fisher, GA; Kunz, PL; Witteles, RM, 2012)		2.03
" The lack of direct comparison PFS and treatment dosage modification data were the main limitations."( Budget impact analysis of the use of oral and intravenous anti-cancer drugs for the treatment of HER2-positive metastatic breast cancer.
Benjamin, L; Buthion, V; Farah, B; Iskedjian, M; Rioufol, C; Vidal-Trécan, G, 2013)		0.39
" Treatment was well tolerated in all dosage groups."( Phase I-II study of radiopeptide 177Lu-octreotate in combination with capecitabine and temozolomide in advanced low-grade neuroendocrine tumors.
Claringbold, PG; Price, RA; Turner, JH, 2012)		0.61
" This highly reproducible dissolution behaviour can be applied in the development of a sustained release dosage form as substantially less sustained release excipient is required in order to attain the desired release profile."( Slow dissolution behaviour of amorphous capecitabine.
Beijnen, JH; Meulenaar, J; Nuijen, B; Schellens, JH, 2013)		0.66
"XELOX is a promising regimen for anthracycline-pretreated metastatic breast cancer although careful patient selection is indicated and alternate dosing schedules should be explored to minimize neurologic morbidity."( Capecitabine and oxaliplatin in combination as first- or second-line therapy for metastatic breast cancer: a Wisconsin Oncology Network trial.
Champeny, TL; Chang, JE; Hansen, RM; Kim, K; Meadows, S; Njiaju, UO; Powers, K; Stewart, JA; Tevaarwerk, AJ; Traynor, AM; Van Ummersen, L, 2013)		1.83
" Once developed, the symptoms significantly impair quality of life(QOL), leading to a reduction in the dosage or discontinuation of the treatment."( [Assessment of hand-foot syndrome in cancer outpatients undergoing chemotherapy].
Amamori, K; Shigematsu, T; Shirai, M; Sunda, K; Takeda, K; Yamagiwa, K; Yamanda, T, 2012)		0.38
" The cost of drug acquisition was calculated based on dosage data and the mean number of treatment cycles from the pivotal studies NO16966 and NO16967."( Pharmaco-economic analysis of direct medical costs of metastatic colorectal cancer therapy with XELOX or modified FOLFOX-6 regimens: implications for health-care utilization in Australia.
Gibbs, P; Hack, SP; Kerr, A; Price, T; Stokes, L; Todd, C; Tran, G, 2013)		0.39
" This regimen was based on our studies with carcinoid cell lines that showed synergistic cytotoxicity with sequence-specific dosing of 5-fluorouracil preceding temozolomide (TMZ)."( Capecitabine and temozolomide (CAPTEM) for metastatic, well-differentiated neuroendocrine cancers: The Pancreas Center at Columbia University experience.
Allendorf, J; Chabot, JA; Dinnen, RD; Fine, RL; Gulati, AP; Krantz, BA; Lee, JA; Mao, Y; Moss, RA; Mowatt, KB; Schreibman, S; Schrope, B; Sherman, WH; Stevens, PD; Tsushima, DA, 2013)		1.83
" The optimum dosing combination of these two agents has yet to be determined however, and in many patients it is likely that greater overall survival will be achieved by using them in successive lines rather than in combination."( New oxaliplatin-based combinations in the treatment of colorectal cancer.
Cassidy, J; Hochster, H, 2003)		0.32
" We hypothesized that a fixed-dose schedule would simplify dosing and provide an effective and safe alternative to BSA-based dosing."( Fixed-dose capecitabine is feasible: results from a pharmacokinetic and pharmacogenetic study in metastatic breast cancer.
Armstrong, DK; Connolly, RM; Davidson, NE; Fetting, JH; Garrett-Mayer, E; Hoskins, JM; Jeter, SC; McLeod, HL; Rudek, MA; Stearns, V; Watkins, SP; Wolff, AC; Wright, LA; Zhao, M, 2013)		0.78
"Irinotecan dosing based on UGT1A1*28 and *6 is feasible, and higher doses of irinotecan can be safely administered in patients with 0 or 1 DA, compared to those with 2 DA."( A UGT1A1*28 and *6 genotype-directed phase I dose-escalation trial of irinotecan with fixed-dose capecitabine in Korean patients with metastatic colorectal cancer.
Bae, KS; Chang, HM; Hong, YS; Kang, YK; Kim, HS; Kim, KP; Kim, TW; Lee, JL; Lee, JS; Shin, JG; Sym, SJ, 2013)		0.61
" This dosing algorithm was designed to mitigate dermatologic and other toxicity, in addition to detailed guidelines for prophylactic and symptomatic treatment."( A phase 3 tRial comparing capecitabinE in combination with SorafenIb or pLacebo for treatment of locally advanced or metastatIc HER2-Negative breast CancEr (the RESILIENCE study): study protocol for a randomized controlled trial.
Baselga, J; Costa, F; Gomez, H; Gradishar, WJ; Hudis, CA; Petrenciuc, O; Rapoport, B; Roche, H; Schwartzberg, LS; Shan, M, 2013)		0.69
" We summarize evidence from the published literature supporting this association and provide dosing recommendations for fluoropyrimidines based on DPYD genotype (updates at http://www."( Clinical Pharmacogenetics Implementation Consortium guidelines for dihydropyrimidine dehydrogenase genotype and fluoropyrimidine dosing.
Caudle, KE; Diasio, RB; Klein, TE; McLeod, HL; Schwab, M; Swen, JJ; Thorn, CF, 2013)		0.39
"UGT1A1 genotype affects the dose and pharmacokinetics of the CAPIRINOX regimen and UGT1A1 genotype-guided dosing of CAPIRINOX is ongoing in a phase II study of small bowel cancer (NCT00433550)."( UGT1A1 genotype-guided phase I study of irinotecan, oxaliplatin, and capecitabine.
Ames, MM; Erlichman, C; Goetz, MP; Goldberg, RM; Grothey, AA; Kuffel, MA; Mandrekar, SJ; McGovern, RM; McKean, HA; McWilliams, R; Reid, JM; Safgren, SL; Tan, AD, 2013)		0.62
" However, bi-weekly dosing might offer a better dose intensity, with better tolerability and response rates."( Bi-weekly paclitaxel and capecitabine as a second- or third-line treatment for advanced breast cancer: a pilot study.
Kautio, AL; Kellokumpu-Lehtinen, PL; Lehtinen, I; Tanner, M; Tuunanen, T, 2013)		0.69
"Bi-weekly dosing of paclitaxel and capecitabine seems to yield promising responses in advanced breast cancer, with an acceptable adverse-event profile."( Bi-weekly paclitaxel and capecitabine as a second- or third-line treatment for advanced breast cancer: a pilot study.
Kautio, AL; Kellokumpu-Lehtinen, PL; Lehtinen, I; Tanner, M; Tuunanen, T, 2013)		0.97
"An oral extended-release (ER) formulation of capecitabine was developed for twice daily dosing, theoretically providing a continuous exposure to capecitabine, thus avoiding the undesirable in-between dosing gap inherent to the dosing schedule of the marketed capecitabine immediate-release formulation (Xeloda(®))."( Development of an extended-release formulation of capecitabine making use of in vitro-in vivo correlation modelling.
Beijnen, JH; Huitema, AD; Keizer, RJ; Meulenaar, J; Nuijen, B; Schellens, JH, 2014)		0.92
"A primary challenge in identifying replicable pharmacogenomic markers from clinical genomewide association study (GWAS) trials in oncology is the difficulty in performing a second large clinical trial with the same drugs and dosage regimen."( Identification of genetic variants associated with capecitabine-induced hand-foot syndrome through integration of patient and cell line genomic analyses.
Alba, E; Alonso, R; de la Torre-Montero, JC; Dolan, ME; González-Neira, A; Lopez-Fernandez, LA; Martín, M; Pita, G; Wheeler, HE, 2014)		0.65
"Capecitabine-based chemo-radiotherapy, using a twice daily dosing schedule of 825 mg/m² given 7 days per week concurrently with 50."( A phase I and pharmacokinetic study of capecitabine in combination with radiotherapy in patients with localised inoperable pancreatic cancer.
Crellin, A; Evans, TR; Harden, S; James, A; Lumsden, GR; McDonald, AC; Morrison, R; Paul, J; Roxburgh, P; Sweeting, L, 2014)		2.11
"To determine if a low fixed dosing strategy of capecitabine would produce comparable clinical activity with less adverse toxicities compared to published data with higher doses in the setting of metastatic breast cancer (mBC)."( A retrospective study evaluating a fixed low dose capecitabine monotherapy in women with HER-2 negative metastatic breast cancer.
Ahn, E; Ambros, T; Aruna, M; Kronish, L; Mahtani, RL; Montero, AJ; Vogel, CL; Zaravinos, J; Zeichner, SB, 2014)		0.91
"To review the pharmacology, pharmacokinetics, efficacy, adverse effects, drug-drug interactions, dosage and administration, and formulary considerations for ado-trastuzumab emtansine."( Ado-trastuzumab emtansine: a HER2-positive targeted antibody-drug conjugate.
Auten, JJ; Cicci, TA; Corrigan, PA; Lowe, DK, 2014)		0.4
" But its short plasma half-life limits clinical utility and the usually prescribed dosing regimen results in significant periods of therapeutically irrelevant concentration."( Trichotomous gastric retention of amorphous capecitabine: an attempt to overcome pharmacokinetic gap.
Chourasia, MK; Meher, JG; Pawar, VK; Singh, M; Singh, Y, 2015)		0.68
" Our own data as well as data from the literature was used to calculate those R levels revealing that the formation of 5'-DFUR - the immediate precursor of 5-fluorouracil - was not affected by concomitant medication within the dosing range investigated."( A simple method for comparing enzymatic capecitabine activation in various mono- and combination chemotherapies.
Baroian, N; Buchner, P; Czejka, M; Dittrich, C; Sahmanovic, A; Schreiber, V, 2015)		0.68
" It was designed to answer five research questions relating to safety, dosage and administration, and discontinuation from capecitabine-based adjuvant therapy."( Observational study of adjuvant therapy with capecitabine in colon cancer.
Guggenberger, D; Hansen, R; Jacobs, G; Kröning, H; Schardt, C; Schmidt, P; Steffens, CC; Tschechne, B; Valdix, AR; Wohlfarth, T, 2015)		0.88
" No difference in other treatment toxicity was observed between the two groups, and patients exhibited high compliance in dosing administration."( Double-blind, placebo-controlled, randomized phase II study of TJ-14 (Hangeshashinto) for infusional fluorinated-pyrimidine-based colorectal cancer chemotherapy-induced oral mucositis.
Aoyama, T; Kataoka, M; Kono, T; Matsuda, C; Mishima, H; Morita, S; Munemoto, Y; Nagata, N; Oshiro, M; Sakamoto, J, 2015)		0.42
"Capecitabine is a highly water soluble prodrug of 5-fluorouracil that is dosed by patient body surface area."( Effects of gender on capecitabine toxicity in colorectal cancer.
Chambers, CR; Danilak, M; Ghosh, S; Ilich, AI; Kim, CA; Mulder, KE; Sawyer, MB; Spratlin, JL, 2016)		2.2
" Dosing and toxicity information were gathered and dose-limiting toxicity incidence (defined as a composite endpoint of dose delay, dose reduction, or discontinuation of therapy) was compared between males and females using the chi-square test."( Effects of gender on capecitabine toxicity in colorectal cancer.
Chambers, CR; Danilak, M; Ghosh, S; Ilich, AI; Kim, CA; Mulder, KE; Sawyer, MB; Spratlin, JL, 2016)		0.75
"Female colorectal cancer patients experience a higher dose-limiting toxicity incidence than male patients when given adjuvant capecitabine dosed according to body surface area."( Effects of gender on capecitabine toxicity in colorectal cancer.
Chambers, CR; Danilak, M; Ghosh, S; Ilich, AI; Kim, CA; Mulder, KE; Sawyer, MB; Spratlin, JL, 2016)		0.96
"9%) for eribulin than for capecitabine using the standard dosing schedule."( Phase II, Multicenter, Single-Arm, Feasibility Study of Eribulin Combined With Capecitabine for Adjuvant Treatment in Estrogen Receptor-Positive, Early-Stage Breast Cancer.
Berrak, E; Hoffman, AD; Jones, VE; McIntyre, K; O'Shaughnessy, J; Smith, JW; Song, JX; Vukelja, S, 2016)		0.96
"Eribulin plus capecitabine with standard or weekly dosing schedules is feasible in patients with early-stage, HER2-negative, ER-positive breast cancer."( Phase II, Multicenter, Single-Arm, Feasibility Study of Eribulin Combined With Capecitabine for Adjuvant Treatment in Estrogen Receptor-Positive, Early-Stage Breast Cancer.
Berrak, E; Hoffman, AD; Jones, VE; McIntyre, K; O'Shaughnessy, J; Smith, JW; Song, JX; Vukelja, S, 2016)		1.02
" However, hand-foot syndrome (HFS) has high incidence, and once developed, the symptoms significantly impair quality of life (QOL), leading to a reduction in the dosage or discontinuation of the treatment."( Self-identification and management of hand-foot syndrome (HFS): effect of a structured teaching program on patients receiving capecitabine-based chemotherapy for colon cancer.
Achrekar, MS; Carvalho, MD; D'souza, A; Govindarajan, S; Gupta, S; Murugan, K; Ostwal, V, 2016)		0.64
" We demonstrated that histone deacetylase inhibitors (HDACi), including low anticonvulsant dosage of VPA, induced the dose- and time-dependent up-regulation of TP transcript and protein expression in breast cancer cells, but not in the non-tumorigenic breast MCF-10A cell line."( Valproic acid potentiates the anticancer activity of capecitabine in vitro and in vivo in breast cancer models via induction of thymidine phosphorylase expression.
Bruzzese, F; Budillon, A; D'Angelo, G; Di Gennaro, E; Franco, R; Leone, A; Roca, MS; Russo, D; Scogliamiglio, G; Terranova-Barberio, M; Vitagliano, C; Zotti, AI, 2016)		0.68
" The treatment allowed dosing adjustments of methotrexate and capecitabine for pretreatment renal function."( Effect of Pretreatment Renal Function on Treatment and Clinical Outcomes in the Adjuvant Treatment of Older Women With Breast Cancer: Alliance A171201, an Ancillary Study of CALGB/CTSU 49907.
Cirrincione, CT; Cohen, HJ; Gralow, J; Hurria, A; Jatoi, A; Lichtman, SM; Magrinat, G; Morganstern, DE; Muss, HB; Theodoulou, M; Wolff, AC, 2016)		0.67
"Excluding from clinical trials patients with renal insufficiency but good performance status on the basis of concern of excessive hematologic toxicity or poor outcomes may not be justified with appropriate dosing modifications."( Effect of Pretreatment Renal Function on Treatment and Clinical Outcomes in the Adjuvant Treatment of Older Women With Breast Cancer: Alliance A171201, an Ancillary Study of CALGB/CTSU 49907.
Cirrincione, CT; Cohen, HJ; Gralow, J; Hurria, A; Jatoi, A; Lichtman, SM; Magrinat, G; Morganstern, DE; Muss, HB; Theodoulou, M; Wolff, AC, 2016)		0.43
" Consecutive therapy such as onset of the side effect or an injection method change, dosage weight loss is difficult though chemotherapies is performed for the recurrence metastasis breast cancer case of the older patient."( [A Case of an Older Patient with Metastatic Breast Cancer Effectively Treated with Capecitabine, with Achievement of cCR].
Amano, S; Enomoto, K; Ono, Y; Sakurai, K, 2015)		0.64
" The areas of debate and development include the dosing and timing of MMC delivery, the role of cisplatin chemotherapy as an alternative to MMC, the replacement of the standard 96-h infusion of 5FU with oral capecitabine, the use of targeted chemotherapy agents, and the duration and dose of RT."( Advances in the Management of Anal Cancer.
Goodman, KA; Julie, DR, 2016)		0.62
"Capecitabine 1000 mg/m(2) bid × 14 days every 21 days (14/21) has been reported to have similar efficacy but more favorable toxicity profile than the approved dosage of 1250 mg/m(2)."( A comparison of toxicity profiles between the lower and standard dose capecitabine in breast cancer: a systematic review and meta-analysis.
Muss, HB; Nishijima, TF; Suzuki, M, 2016)		2.11
" The median cumulative dosage capecitabine was lower for patients treated with CAPOX (163,744 mg/m(2), interquartile range [IQR] 83,397-202,858 mg/m(2)) than for patients treated with CapMono (189,195 mg/m(2), IQR 111,667-228,125 mg/m(2), P = 0."( Intensity of adjuvant chemotherapy regimens and grade III-V toxicities among elderly stage III colon cancer patients.
Creemers, GJ; Janssen-Heijnen, ML; Lemmens, VE; Maas, HA; Pruijt, JF; Razenberg, LG; van Erning, FN, 2016)		0.72
"CAPOX is associated with significantly more grade III-V toxicities than CapMono, which had a pronounced impact on the cumulative dosage received and completion of all planned cycles."( Intensity of adjuvant chemotherapy regimens and grade III-V toxicities among elderly stage III colon cancer patients.
Creemers, GJ; Janssen-Heijnen, ML; Lemmens, VE; Maas, HA; Pruijt, JF; Razenberg, LG; van Erning, FN, 2016)		0.43
" The prothrombin time international normalized ratio divided by current warfarin dosage (PT-INR/dose) was measured over time to evaluate warfarin titer in each patient."( Impact of capecitabine and S-1 on anticoagulant activity of warfarin in patients with gastrointestinal cancer.
Doki, Y; Haraguchi, N; Hata, T; Kudo, T; Mizushima, T; Mori, M; Nishimura, J; Sakai, D; Satoh, T; Takahashi, H; Yamamoto, H, 2016)		0.84
" To prevent phenytoin intoxication, phenytoin dosage must be adjusted."( Pharmacokinetic model analysis of interaction between phenytoin and capecitabine.
Fukui, E; Hori, S; Ikenishi, M; Kawahara, K; Matsuyama, K; Miki, A; Miyazaki, S; Nakatsuka, E; Ohtori, T; Sakurai, M; Satoh, H; Sawada, Y; Ueda, M; Ueda, R, 2016)		0.67
" This model and these parameters allow us to predict the appropriate phenytoin dosage schedule when capecitabine is administered concomitantly."( Pharmacokinetic model analysis of interaction between phenytoin and capecitabine.
Fukui, E; Hori, S; Ikenishi, M; Kawahara, K; Matsuyama, K; Miki, A; Miyazaki, S; Nakatsuka, E; Ohtori, T; Sakurai, M; Satoh, H; Sawada, Y; Ueda, M; Ueda, R, 2016)		0.89
"This newly-developed model accurately describes changes in phenytoin concentration during concomitant capecitabine chemotherapy, and it may be clinically useful for predicting appropriate phenytoin dosage adjustments for maintaining serum phenytoin levels within the therapeutic range."( Pharmacokinetic model analysis of interaction between phenytoin and capecitabine.
Fukui, E; Hori, S; Ikenishi, M; Kawahara, K; Matsuyama, K; Miki, A; Miyazaki, S; Nakatsuka, E; Ohtori, T; Sakurai, M; Satoh, H; Sawada, Y; Ueda, M; Ueda, R, 2016)		0.88
"Current evidence suggests that a triweekly schedule of ixabepilone is more effective than weekly dosing in improving ORR."( Systematic review of ixabepilone for treating metastatic breast cancer.
Li, J; Ren, J; Sun, W, 2017)		0.46
" Life-threatening 5-FU overdoses occur because of infusion pump errors, dosage miscalculations, and accidental or suicidal ingestion of capecitabine."( Emergency use of uridine triacetate for the prevention and treatment of life-threatening 5-fluorouracil and capecitabine toxicity.
Bamat, MK; Cartwright, TH; El-Rayes, BF; Fakih, MG; King, TR; Ma, WW; Posey, JA; Saif, MW; von Borstel, RW, 2017)		0.87
" Data are limited with regard to adverse events and dosing practices associated with capecitabine monotherapy in real-world situations."( Tolerability of Capecitabine Monotherapy in Metastatic Colorectal Cancer: A Real-World Study.
Coers, W; de Graaf, JC; de Groot, JW; Leicher, LW; Tascilar, M, 2017)		1.03
" Dosing of capecitabine can range from 1000 mg orally daily for 4 weeks on and 1 week off to a continuous dosing schedule of 1500 mg orally daily."( Potential role of metronomic chemotherapy in the treatment of esophageal and gastroesophageal cancer.
Banavali, S; Chougule, A; Joshi, A; Noronha, V; Patil, VM; Prabhash, K, 2017)		0.84
" Potential correlation between treatment modalities (regimen, dosage and route of administration of L-OHP, and injection timing for dexamethasone administration) and HSRs was assessed."( Comparison between hypersensitivity reactions to cycles of modified FOLFOX6 and XELOX therapies in patients with colorectal cancer.
Ando, Y; Hayashi, T; Ikeda, Y; Ito, K; Kawada, K; Kumazawa, S; Maeda, K; Matsuoka, H; Murai, S; Ohta, H; Shiouchi, H; Yamada, S; Yasuda, K, 2017)		0.46
" The authors performed a phase 2 cooperative group study (North Central Cancer Treatment Group N0543, Alliance) using genotype-dosed capecitabine, irinotecan, and oxaliplatin (gCAPIRINOX), with dosing assigned based on UDP glucuronosyltransferase family 1 member A1 (UGT1A1) genotype to test: 1) whether the addition of irinotecan would improve outcomes; and 2) whether UGT1A1 genotype-based dosing could optimize tolerability."( North Central Cancer Treatment Group N0543 (Alliance): A phase 2 trial of pharmacogenetic-based dosing of irinotecan, oxaliplatin, and capecitabine as first-line therapy for patients with advanced small bowel adenocarcinoma.
Ames, MM; Foster, NR; Goetz, MP; Hobday, TJ; Horvath, LE; Jatoi, A; Mahoney, MR; McWilliams, RR; Meyers, JP; Murray, JA; Schneider, DJ; Smyrk, TC, 2017)		0.86
"Previously untreated patients with advanced small bowel adenocarcinoma received irinotecan (day 1), oxaliplatin (day 1), and capecitabine (days 2-15) in a 21-day cycle and were dosed with gCAPIRINOX according to UGT1A1*28 genotypes (6/6, 6/7, and 7/7)."( North Central Cancer Treatment Group N0543 (Alliance): A phase 2 trial of pharmacogenetic-based dosing of irinotecan, oxaliplatin, and capecitabine as first-line therapy for patients with advanced small bowel adenocarcinoma.
Ames, MM; Foster, NR; Goetz, MP; Hobday, TJ; Horvath, LE; Jatoi, A; Mahoney, MR; McWilliams, RR; Meyers, JP; Murray, JA; Schneider, DJ; Smyrk, TC, 2017)		0.86
"UGT1A1 genotype-directed dosing (gCAPIRINOX) appears to be feasible with favorable rates of hematologic toxicity compared with prior 3-drug studies in unselected patients."( North Central Cancer Treatment Group N0543 (Alliance): A phase 2 trial of pharmacogenetic-based dosing of irinotecan, oxaliplatin, and capecitabine as first-line therapy for patients with advanced small bowel adenocarcinoma.
Ames, MM; Foster, NR; Goetz, MP; Hobday, TJ; Horvath, LE; Jatoi, A; Mahoney, MR; McWilliams, RR; Meyers, JP; Murray, JA; Schneider, DJ; Smyrk, TC, 2017)		0.66
"Our experience with capecitabine shows that dosing adjustments can be warranted for chemotherapy in cancer patients, requiring monitoring of renal function."( Serial renography for evaluation of the impact of capecitabine therapy on renal function: A case report.
Huo, Z; Liu, Y; Ren, J; Wang, X; Yang, G, 2017)		1.03
"Fewer than half of patients correctly identified the safety and dosing objectives."( Informed Consent and Decision Making Among Participants in Novel-Design Phase I Oncology Trials.
Dees, EC; Henderson, GE; Reeder-Hayes, KE; Roberts, MC, 2017)		0.46
"Novel phase I oncology trial designs may attract patients with less constrained treatment options, but the inclusion of targeted drugs and combinations including standard chemotherapies is likely to complicate understanding of safety and dosing objectives and likelihood of personal benefit for purposes of informed consent."( Informed Consent and Decision Making Among Participants in Novel-Design Phase I Oncology Trials.
Dees, EC; Henderson, GE; Reeder-Hayes, KE; Roberts, MC, 2017)		0.46
"She received treatment with CAP that was administered orally at a dosage of 1500mg twice daily intermittently (2weeks on/1 week off)."( Reversible severe fatty liver induced by capecitabine: A case report.
He, Q; Jiang, Y; Li, S; Shi, C; Yang, X, 2017)		0.72
"The measure of body surface area (BSA) is a standard for planning optimal dosing in oncology."( Computer tomography-based body surface area evaluation for drug dosage: Quantitative radiology versus anthropomorphic evaluation.
Beaumont, H; Dittlot, C; Falewee, MN; Hebert, C; Iannessi, A, 2018)		0.48
" Dosing and completion of prescribed chemotherapy were assessed on the subset of patients who received all therapy at MSK."( Adoption of Total Neoadjuvant Therapy for Locally Advanced Rectal Cancer.
Cercek, A; Crane, CH; Garcia-Aguilar, J; Gollub, MJ; Gonen, M; Guillem, JG; Nash, GM; Paty, PB; Reidy, DL; Roxburgh, CSD; Saltz, LB; Segal, NH; Seier, K; Shia, J; Smith, JJ; Stadler, ZK; Strombom, P; Temple, LKF; Vakiani, E; Varghese, A; Weiser, MR; Wu, AJ; Yaeger, R, 2018)		0.48
" In vitro cytotoxicity against HT-29 cells revealed significant reduction of the cell growth when treated with optimized formulation indicating IPN microbeads as effective dosage form for treating colon cancer."( Development of biopolymers based interpenetrating polymeric network of capecitabine: A drug delivery vehicle to extend the release of the model drug.
Adena, SKR; Mishra, B; Upadhyay, M; Vardhan, H; Yadav, SK, 2018)		0.71
" Patient characteristics must be considered when determining the capecitabine dosage and risk of ADRs, and nursing intervention is critical for preventing exacerbation of these ADRs."( Analysis of data on capecitabine-related adverse drug reactions from the Korean adverse event reporting system database.
Park, JY, 2018)		1.04
" Adherence was assessed in all patients by self-completed questionnaires on disease, pill-count and pharmacological dosage of FBAL (metabolite of capecitabine); and in half of the cohort by electronic medication event monitoring systems (MEMS™) recording the opening times of the device."( Over-adherence to capecitabine: a potential safety issue in breast and colorectal cancer patients.
Bourmaud, A; Chauvin, F; Colomban, O; Freyer, G; Girard, P; Guitton, J; Henin, E; Le Saux, O; Maraval-Gaget, R; Ranchon, F; Regnier, V; Rioufol, C; Schwiertz, V; Tod, M; Trillet-Lenoir, V; You, B, 2018)		1.01
" Close analysis of MEMS™ data revealed unexpected medication patterns, such as patients taking extra days of medication beyond planned cycle, patients taking extra doses per day and patients missing a day of dosing and "compensating" by taking extra the following day (N = 7, 18%)."( Over-adherence to capecitabine: a potential safety issue in breast and colorectal cancer patients.
Bourmaud, A; Chauvin, F; Colomban, O; Freyer, G; Girard, P; Guitton, J; Henin, E; Le Saux, O; Maraval-Gaget, R; Ranchon, F; Regnier, V; Rioufol, C; Schwiertz, V; Tod, M; Trillet-Lenoir, V; You, B, 2018)		0.81
" Since fluoropyrimidines are among the most commonly used anticancer agents, these findings suggest that implementation of DPYD genotype-guided individualised dosing should be a new standard of care."( DPYD genotype-guided dose individualisation of fluoropyrimidine therapy in patients with cancer: a prospective safety analysis.
Baars, A; Beijnen, JH; Cats, A; Creemers, GJ; de Man, FM; Dezentjé, VO; Droogendijk, HJ; Frederix, GWJ; Gelderblom, H; Guchelaar, HJ; Hamberg, P; Henricks, LM; Imholz, ALT; Jansen, RLH; Jeurissen, FJF; Kienhuis, E; Koopman, M; Lunenburg, CATC; Mandigers, CMPW; Mathijssen, RHJ; Meulendijks, D; Nieboer, P; Portielje, JEA; Rosing, H; Schellens, JHM; Swen, JJ; Ten Tije, AJ; van de Poel, MHW; van Kuilenburg, ABP; van Schaik, RHN; Werkhoven, EV, 2018)		0.48
" The current use of FPDs includes multiple dosing regimens, oral or intravenous delivery, and administration with additional cardiotoxic therapies."( Fluoropyrimidine Cardiotoxicity: Time for a Contemporaneous Appraisal.
Brell, JM; Carver, JR; Denlinger, CS; Dimond, EP; Kircher, SM; Ky, B; O'Neill, A; Upshaw, JN; Wagner, LI, 2019)		0.51
" Severe (grade ≥III) toxicity in DPYD variant allele carriers receiving upfront FP dose reductions according to pharmacogenetic dosing guidelines and DPYD variant allele carriers not receiving FP dose reductions was compared with DPYD wild-type patients receiving standard dose of FPs in CRT."( Standard fluoropyrimidine dosages in chemoradiation therapy result in an increased risk of severe toxicity in DPYD variant allele carriers.
Cecchin, E; Dreussi, E; Fiocco, M; Gelderblom, H; Guchelaar, HJ; Henricks, LM; Lunenburg, CATC; Meulendijks, D; Peters, FP; Schellens, JHM; Swen, JJ; Toffoli, G, 2018)		0.48
" Our study is the first to show that DPYD*2A genotype-guided dosing appears to have no negative effect on effectiveness of fluoropyrimidine-based chemotherapy, while resulting in significantly improved patient safety."( Effectiveness and safety of reduced-dose fluoropyrimidine therapy in patients carrying the DPYD*2A variant: A matched pair analysis.
Beijnen, JH; Cats, A; de Boer, A; Deenen, MJ; Henricks, LM; Meulendijks, D; Schellens, JHM; van Merendonk, LN, 2019)		0.51
" We implemented a protocol for tolerance-guided capecitabine dosing in DPYD variant carriers and aimed to explore its effect on toxicity of treatment."( Tolerance-based capecitabine dose escalation after DPYD genotype-guided dosing in heterozygote DPYD variant carriers: a single-center observational study.
Bakema, R; Brinkman, I; Kleinjan, JP; van Rooijen, JM; van Zanden, JJ, 2019)		1.12
" Outcome was evaluated by clinical chart review and dosing characteristics from the hospital pharmacy."( Tolerance-based capecitabine dose escalation after DPYD genotype-guided dosing in heterozygote DPYD variant carriers: a single-center observational study.
Bakema, R; Brinkman, I; Kleinjan, JP; van Rooijen, JM; van Zanden, JJ, 2019)		0.86
" The dosing used in this trial is described in the qualifying statements, while it should be noted that the dose of capecitabine may also be determined by institutional and regional practices."( Adjuvant Therapy for Resected Biliary Tract Cancer: ASCO Clinical Practice Guideline.
Bachini, M; Bekaii-Saab, T; Crane, C; Edeline, J; El-Khoueiry, A; Feng, M; Katz, MHG; Kennedy, EB; Maithel, SK; Primrose, J; Shroff, RT; Soares, HP; Valle, J, 2019)		0.72
" Deterministic, probabilistic sensitivity analyses and a scenario analysis examined parameter uncertainty and accounted for drug wastage in dosage and cost calculations."( A cost-effectiveness analysis of trastuzumab-containing treatment sequences for HER-2 positive metastatic breast cancer patients in Taiwan.
Ali, AA; Alqhtani, H; Balkrishnan, R; de Lima Lopes, G; Diaby, V; Ko, Y; Palacio, S; van Boemmel-Wegmann, S; Wang, CY, 2020)		0.56
" Those patients with mCRC who respond well after 16-18 weeks of standard doublet chemotherapy as induction may be enrolled into this study, and randomly assigned to the capecitabine metronomic group or standard dosage group."( A study of capecitabine metronomic chemotherapy is non-inferior to conventional chemotherapy as maintenance strategy in responders after induction therapy in metastatic colorectal cancer.
Jiang, J; Ma, T; Shi, M; Wu, J; Xi, W; Yang, C; Zhang, J; Zhou, C; Zhu, Z, 2020)		1.14
" Given the known sex differences in fluoropyrimidine pharmacokinetics, sex-specific dosing of fluoropyrimidines warrants further investigation."( Sex and Adverse Events of Adjuvant Chemotherapy in Colon Cancer: An Analysis of 34 640 Patients in the ACCENT Database.
Alberts, SR; Allegra, CJ; Andre, T; Blanke, CD; de Gramont, A; Dixon, JG; Francini, E; George, TJ; Goldberg, RM; Grothey, A; Haller, DG; Kerr, R; Marsoni, S; O'Connell, MJ; Saltz, LB; Seitz, JF; Shi, Q; Taieb, J; Twelves, C; VanCutsem, E; Wagner, AD; Wolmark, N; Yothers, G, 2021)		0.62
" Furthermore, a simulation study of the probability of HFS severity over time was performed in which the standard dosing regimen and dose adjustments according to HFS severity were investigated."( Evaluation of patient-reported severity of hand-foot syndrome under capecitabine using a Markov modeling approach.
Jaehde, U; Ko, YD; Krolop, L; Ringsdorf, S; Schmulenson, E; Simons, S, 2020)		0.79
" Thus, a modeling framework for patient-reported outcomes was created which may assist in the optimization of dosage regimens and adjustment strategies aiming at minimizing symptom burden during anti-cancer drug therapy."( Evaluation of patient-reported severity of hand-foot syndrome under capecitabine using a Markov modeling approach.
Jaehde, U; Ko, YD; Krolop, L; Ringsdorf, S; Schmulenson, E; Simons, S, 2020)		0.79
" The first 2 quinacrine dosing levels were well tolerated."( First-in-Human Phase 1b Trial of Quinacrine Plus Capecitabine in Patients With Refractory Metastatic Colorectal Cancer.
Astaturov, I; Cohen, SJ; Cooper, HS; Denlinger, CS; Dotan, E; El-Deiry, WS; Gallant, JN; Harvey, HA; Korzekwa, K; Kunkel, M; Lim, B; Ross, EA; Ruth, K; Sivik, J; Vijayvergia, N; Wang, EW; White, K; Winer, A; Zhou, L, 2021)		0.88
" Historically, dosing of these drugs has been based on body surface area."( Overcoming barriers to implementing precision dosing with 5-fluorouracil and capecitabine.
Galettis, P; Martin, JH; Schneider, JJ, 2021)		0.85
"The main advantage of targeted genotyping is the existence of prospectively validated genotype-based dosing guidelines."( Joint Belgian recommendation on screening for DPD-deficiency in patients treated with 5-FU, capecitabine (and tegafur).
Bm Claes, K; Borbath, I; Casneuf, V; Demey, W; Geboes, KP; Haufroid, V; Van den Eynde, M; Verheezen, Y; Verstraete, AG, 2022)		0.94
" However, knowledge of its antitumor efficacy after modification of the dosing schedule is insufficient."( A Physiologically Based Pharmacokinetic-Pharmacodynamic Model for Capecitabine in Colorectal Cancer Rats: Simulation of Antitumor Efficacy at Various Administration Schedules.
Ito, Y; Kobuchi, S; Sakaeda, T; Sakai, S, 2021)		0.86
" After capecitabine regimen modification, a 1-week postponement of capecitabine administration was more efficacious than a reduction in the dosage to 80%."( A Physiologically Based Pharmacokinetic-Pharmacodynamic Model for Capecitabine in Colorectal Cancer Rats: Simulation of Antitumor Efficacy at Various Administration Schedules.
Ito, Y; Kobuchi, S; Sakaeda, T; Sakai, S, 2021)		1.31
"Consensus guidelines exist for genotype-guided fluoropyrimidine dosing based on variation in the gene dihydropyrimidine dehydrogenase (DPYD)."( Impact of pretreatment dihydropyrimidine dehydrogenase genotype-guided fluoropyrimidine dosing on chemotherapy associated adverse events.
Choi, YH; Keller, D; Kim, RB; Legan, RM; Lenehan, J; Mailloux, J; Medwid, S; Nevison, S; Panuganty, V; Povitz, BL; Sarma, S; Schwarz, UI; Siebring, V; Teft, WA; Welch, S; Wigle, TJ; Winquist, E, 2021)		0.62
" The primary objective was to determine the tolerability of the respective dosing schedules, defined according to frequency of dose reductions and treatment delays."( Safety and Efficacy of 7 Days on/7 Days off Versus 14 Days on/7 Days off Schedules of Capecitabine in Patients with Metastatic Colorectal Cancer: A Retrospective Review.
Akce, M; Alese, O; Bryson, E; Davis, C; Draper, A; El-Rayes, B; Goyal, S; Hall, K; Patel, U; Sakach, E; Shaib, W; Szabo, S; Watson, M; Wu, C, 2021)		0.84
"The GO2 randomized clinical trial sought to optimize chemotherapy dosing in older and/or frail patients with advanced gastroesophageal cancer, and explored baseline geriatric assessment (GA) as a tool for treatment decision-making."( Efficacy of Reduced-Intensity Chemotherapy With Oxaliplatin and Capecitabine on Quality of Life and Cancer Control Among Older and Frail Patients With Advanced Gastroesophageal Cancer: The GO2 Phase 3 Randomized Clinical Trial.
Allmark, C; Cairns, DA; Chatterjee, A; Crossley, A; Cummins, S; Dent, J; Falk, S; Garcia, A; Grabsch, HI; Grumett, S; Guptal, K; Hall, PS; Handforth, C; Howard, H; Kamposioras, KV; Katona, E; Khan, M; Lord, S; Maisey, N; Mano, J; Marshall, H; Nicoll, J; Ow, PL; Petty, R; Roy, R; Ruddock, S; Seymour, MT; Stokes, Z; Swinson, D; Tillett, T; Velikova, G; Waddell, T; Wadsley, J; Waters, JS, 2021)		0.86
" Further approaches taken to improve the efficacy of 5-FU chemotherapy regimens have focused on optimising the route and dosing schedules and regulating folate metabolism."( Metastatic colorectal cancer: Advances in the folate-fluoropyrimidine chemotherapy backbone.
de Gramont, A; Glimelius, B; Marshall, J; Stintzing, S; Yoshino, T, 2021)		0.62
" All patients received a radiation dosage of 25 × 2 Gy during a period of five weeks with either concomitant capecitabine administered on radiation days or continuously during radiotherapy."( Relation between body composition and severe diarrhea in patients treated with preoperative chemoradiation with capecitabine for rectal cancer: a single-centre cohort study.
Hartman, W; Nuyttens, JJME; Oomen-de Hoop, E; Rothbarth, J; van Meerten, E; van Rees, JM; van Vugt, JLA; Verhoef, C, 2021)		1.04
" Severe myelotoxicity is rare; the risk of grade 4 cytopenias is significantly increased in women, and therefore sex-based dosing should be considered."( Efficacy and Toxicity Analysis of Capecitabine and Temozolomide in Neuroendocrine Neoplasms.
Al-Toubah, T; Haider, M; Pelle, E; Strosberg, JR; Valone, T, 2021)		0.9
" Doctors should be aware of the sex difference in the incidence of early DLTs, adjust the CAPOX dosage and provide supportive care for female CRC patients."( Women are predisposed to early dose-limiting toxicities during adjuvant CAPOX for colorectal cancer.
Abe, S; Anzai, H; Emoto, S; Ishihara, S; Kawai, K; Kishikawa, J; Murono, K; Nagai, Y; Nozawa, H; Ozawa, T; Sasaki, K; Sonoda, H; Yokoyama, Y, 2021)		0.62
" Hand-foot syndrome is a frequent side effect caused by this drug, with dosage adjustment recommended with progression of symptoms."( Capecitabine induced fingerprint loss: Case report and review of the literature.
Cherem-Kibrit, M; Colmenero-Mercado, JO; Deneken-Hernandez, Z; Gutiérrez-Andrade, L; Rodríguez-Gutiérrez, G, 2022)		2.16
"Development of dosage form comprising of Capecitabine loaded carbon nanotubes for its targeted delivery to the colon."( Colon targeted dosage form of Capecitabine using folic acid anchored modified carbon nanotube:
Bhinge, SD; Bhutkar, MA; Gavade, AS; Jadhav, NR; Randive, DS; Shejawal, KP, 2021)		1.18
" Although consensus guidelines for genotype-guided dosing of 5-FU and capecitabine have existed for a number of years, the implementation of this type of personalised medicine has not been widely adopted."( Testing for dihydropyrimidine dehydrogenase deficiency in New Zealand to improve the safe use of 5-fluorouracil and capecitabine in cancer patients.
Burns, K; Findlay, M; Helsby, N; Porter, D; Strother, M, 2021)		1.06
" Uncertainty remains regarding optimal dosing practice."( Treating patients with dihydropyrimidine dehydrogenase (DPD) deficiency with fluoropyrimidine chemotherapy since the onset of routine prospective testing-The experience of a large oncology center in the United Kingdom.
Essapen, S; Howlett, S; Wang, L, 2022)		0.72
"2%) US medical oncologists, of whom 98% strongly or somewhat agree that patients with dihydropyrimidine dehydrogenase (DPD) deficiency have increased toxicity risk and 96% would modify FP dosing for a patient with known DPD deficiency."( Survey of US Medical Oncologists' Practices and Beliefs Regarding
Henry, NL; Hertz, DL; Koo, K; Pasternak, AL; Sahai, V, 2022)		0.72
" The objective of this systematic review/meta-analysis was to evaluate treatment outcomes between Pharmacogenetics Guided Dosing (PGD) versus non-PGD and within PGD (DPYD variant allele carriers versus wild type)."( A systematic review and meta-analysis of toxicity and treatment outcomes with pharmacogenetic-guided dosing compared to standard of care BSA-based fluoropyrimidine dosing.
Alexander, M; Brennan, A; Glewis, S; Khabib, MNH; Lazarakis, S; Lingaratnam, S; Martin, J; Michael, M; Tie, J, 2022)		0.72
" Studies investigating optimal dosing for celecoxib and urea cream are recommended."( Prophylactic strategies for hand-foot syndrome/skin reaction associated with systemic cancer treatment: a meta-analysis of randomized controlled trials.
Franco, PIG; Li, RK; Pandy, JGP, 2022)		0.72
" Tolerance was good and 5-FU dosing was next shifted to 25% reduction, then further shifted to normal dosing at the 5th course, with still no sign for drug-related toxicities."( Renal impairment and DPD testing: Watch out for false-positive results!
Carriat, L; Ciccolini, J; Quaranta, S; Rony, M; Solas, C, 2022)		0.72
" Currently, genotype-guided fluoropyrimidine dosing is recommended for four DPYD single nucleotide variants (SNVs)."( Fluoropyrimidine-associated toxicity and DPYD variants c.85T>C, c.496A>G, and c.1236G>A: impact of haplotype.
Kim, RB; Medwid, S; Wigle, TJ, 2023)		0.91
"Dihydropyrimidine dehydrogenase (DPYD) genotype is closely associated with fluoropyrimidine (FP)-induced toxicities in Caucasian population and European Medicines Agency now recommends DPYD genotype-based FP dosing strategy."( Poor association between dihydropyrimidine dehydrogenase (DPYD) genotype and fluoropyrimidine-induced toxicity in an Asian population.
Eto, T; Hasegawa, J; Kanai, M; Kato, T; Kawaguchi, T; Kotaka, M; Manaka, D; Matsuda, F; Matsui, T; Matsumoto, S; Mizushima, T; Mori, M; Munemoto, Y; Ohtsu, A; Saji, S; Sakamoto, J; Shinozaki, K; Takagane, A; Touyama, T; Yoshino, T, 2023)		0.91
" In this review, we survey the evidence-based pharmacogenetics and therapeutic recommendations regarding DPYD (the gene encoding DPD) genotyping and DPD phenotyping to prevent toxicity and optimize dosing adaptation before FP administration."( Current diagnostic and clinical issues of screening for dihydropyrimidine dehydrogenase deficiency.
Barin-Le Guellec, C; Boige, V; Chouchana, L; Ciccolini, J; Etienne-Grimaldi, MC; Loriot, MA; Narjoz, C; Pallet, N; Taieb, J; Thomas, F; Zaanan, A, 2023)		0.91
" A previous study indicated that pharmacokinetic profile of capecitabine was different depending on dosing time in rat."( Diurnal Changes in Capecitabine Clock-Controlled Metabolism Enzymes Are Responsible for Its Pharmacokinetics in Male Mice.
Akyel, YK; Gazioglu, I; Gul, S; Kavakli, IH; Lévi, F; Okyar, A; Ozturk Civelek, D; Ozturk Seyhan, N; Pala Kara, Z, 2023)		1.48
"8% of DPYD variant carriers died due to FP-TOX compared to 0% in the group receiving DPYD genotype-guided dosing of FP."( Implementation and clinical benefit of DPYD genotyping in a Danish cancer population.
Bergmann, TK; Damkier, P; Ewertz, M; Feddersen, S; Fruekilde, PBN; Holm, HS; Paulsen, NH; Pfeiffer, P; Qvortrup, C, 2023)		0.91
" After the experimental phase, an algorithm will be developed to determine the dose adjustment needed to reduce the risk of treatment toxicity according to CDA genotype, developing a clinical guide for capecitabine dosing according to genetic variants in DPYD and CDA."( Genetic variants and enzyme activity in citidin deaminase: Relationship with capecitabine toxicity and recommendation for dose adjustment.
Barrera-Ramírez, JA; Castro-Sánchez, P; Corno-Caparrós, A; Pitaluga-Poveda, L; Prieto-Castelló, MJ; Talens-Bolós, MA, )		0.55
"Continuous dosing of ipatasertib with chemotherapy was safe and well-tolerated."( Phase I Trial of Ipatasertib Plus Carboplatin, Carboplatin/Paclitaxel, or Capecitabine and Atezolizumab in Metastatic Triple-Negative Breast Cancer.
Bozoghlanian, M; Cui, Y; Frankel, PH; Martinez, N; Murga, M; Patel, N; Ruel, C; Schmolze, D; Stewart, D; Tang, A; Tumyan, L; Vora, L; Waisman, J; Yost, SE; Yuan, Y, 2023)		1.14
" After the experimental phase, an algorithm will be developed to determine the dose adjustment needed to reduce the risk of treatment toxicity according to CDA genotype, developing a Clinical Guide for capecitabine dosing according to genetic variants in DPYD and CDA."( [Translated article] Genetic variants and enzyme activity in citidin deaminase: Relationship with capecitabine toxicity and recommendation for dose adjustment.
Barrera-Ramírez, JA; Castro-Sánchez, P; Corno-Caparrós, A; Pitaluga-Poveda, L; Prieto-Castelló, MJ; Talens-Bolós, MA, )		0.54
"PBPK model prediction suggests no dosage adaption of capecitabine or 5-FU is required for cancer patients with hepatic impairment but it would be reduced when the toxic reaction is observed."( Physiologically Based Pharmacokinetic Modeling for Prediction of 5-FU Pharmacokinetics in Cancer Patients with Hepatic Impairment After 5-FU and Capecitabine Administration.
Hu, H; Wang, Y; Yu, L; Zeng, S, 2023)		1.36
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (3)

RoleDescription
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
prodrugA compound that, on administration, must undergo chemical conversion by metabolic processes before becoming the pharmacologically active drug for which it is a prodrug.
antimetaboliteA substance which is structurally similar to a metabolite but which competes with it or replaces it, and so prevents or reduces its normal utilization.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (3)

ClassDescription
carbamate esterAny ester of carbamic acid or its N-substituted derivatives.
organofluorine compoundAn organofluorine compound is a compound containing at least one carbon-fluorine bond.
cytidines
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Pathways (3)

PathwayProteinsCompounds
Capecitabine Action Pathway58
Capecitabine Metabolism Pathway58
Fluoropyrimidine activity015

Protein Targets (4)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
RAR-related orphan receptor gammaMus musculus (house mouse)Potency11.88320.006038.004119,952.5996AID1159521
TDP1 proteinHomo sapiens (human)Potency23.71500.000811.382244.6684AID686978
estrogen nuclear receptor alphaHomo sapiens (human)Potency9.52050.000229.305416,493.5996AID743075
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Other Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (16)

Processvia Protein(s)Taxonomy
cholesterol biosynthetic processLiver carboxylesterase 1Homo sapiens (human)
cholesterol metabolic processLiver carboxylesterase 1Homo sapiens (human)
response to toxic substanceLiver carboxylesterase 1Homo sapiens (human)
positive regulation of cholesterol effluxLiver carboxylesterase 1Homo sapiens (human)
negative regulation of cholesterol storageLiver carboxylesterase 1Homo sapiens (human)
epithelial cell differentiationLiver carboxylesterase 1Homo sapiens (human)
cholesterol homeostasisLiver carboxylesterase 1Homo sapiens (human)
reverse cholesterol transportLiver carboxylesterase 1Homo sapiens (human)
medium-chain fatty acid metabolic processLiver carboxylesterase 1Homo sapiens (human)
regulation of bile acid biosynthetic processLiver carboxylesterase 1Homo sapiens (human)
cellular response to cholesterolLiver carboxylesterase 1Homo sapiens (human)
cellular response to low-density lipoprotein particle stimulusLiver carboxylesterase 1Homo sapiens (human)
cholesterol ester hydrolysis involved in cholesterol transportLiver carboxylesterase 1Homo sapiens (human)
positive regulation of cholesterol metabolic processLiver carboxylesterase 1Homo sapiens (human)
regulation of bile acid secretionLiver carboxylesterase 1Homo sapiens (human)
lipid catabolic processLiver carboxylesterase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (4)

Processvia Protein(s)Taxonomy
sterol esterase activityLiver carboxylesterase 1Homo sapiens (human)
methylumbelliferyl-acetate deacetylase activityLiver carboxylesterase 1Homo sapiens (human)
carboxylesterase activityLiver carboxylesterase 1Homo sapiens (human)
carboxylic ester hydrolase activityLiver carboxylesterase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (5)

Processvia Protein(s)Taxonomy
cytoplasmLiver carboxylesterase 1Homo sapiens (human)
endoplasmic reticulumLiver carboxylesterase 1Homo sapiens (human)
endoplasmic reticulum lumenLiver carboxylesterase 1Homo sapiens (human)
lipid dropletLiver carboxylesterase 1Homo sapiens (human)
cytosolLiver carboxylesterase 1Homo sapiens (human)
lipid dropletLiver carboxylesterase 1Homo sapiens (human)
endoplasmic reticulumLiver carboxylesterase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (146)

Assay IDTitleYearJournalArticle
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1887761Antitumor activity against human HGC-27 cells xenografted in BALB/c mouse assessed as tumor growth inhibition at 150 mg/kg, po bid administered for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID1887764Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as lymphocyte level at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID102676Antitumor activity in human lung carcinoma2003Bioorganic & medicinal chemistry letters, Mar-10, Volume: 13, Issue:5
Design and synthesis of the tumor-activated prodrug of dihydropyrimidine dehydrogenase (DPD) inhibitor, RO0094889 for combination therapy with capecitabine.
AID116602Percent increase in life span of L1210 leukemic BDF1 mice when compound (0.0032 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID1887765Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as monocyte level at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID116762In vivo mean survival time of L1210 leukemic BDF1 mice when compound(0.67 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID116613Percent increase in life span of L1210 leukemic BDF1 mice when compound(0.40 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID1887773Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as platelet distribution width at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID667637Mutagenic activity in Salmonella typhimurium TA1535 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667631Mutagenic activity in Salmonella typhimurium TA98 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID116616Percent increase in life span of L1210 leukemic BDF1 mice when compound(2 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID667630Mutagenic activity in Salmonella typhimurium TA1537 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667771Mutagenic activity in Salmonella typhimurium TA1537 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID116614Percent increase in life span of L1210 leukemic BDF1 mice when compound(0.67 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID468443Inhibition of human FAAH at 1 uM2009Bioorganic & medicinal chemistry letters, Dec-01, Volume: 19, Issue:23
Mining biologically-active molecules for inhibitors of fatty acid amide hydrolase (FAAH): identification of phenmedipham and amperozide as FAAH inhibitors.
AID1887767Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as RBC level at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID116603Percent increase in life span of L1210 leukemic BDF1 mice when compound (0.016 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID667784Antitumor activity against mouse L1210 cells xenografted in BDF-1 mouse assessed as increase in mean survival time at 1.5 mmol/kg, po qd for 2 weeks2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1887771Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as platelet level at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID477295Octanol-water partition coefficient, log P of the compound2010European journal of medicinal chemistry, Apr, Volume: 45, Issue:4
QSPR modeling of octanol/water partition coefficient of antineoplastic agents by balance of correlations.
AID667632Mutagenic activity in Salmonella typhimurium TA98 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID231334Ratio of tumor and plasma 5-FU concentration in HT-3 (human cervical cancer) xenograft mice2003Bioorganic & medicinal chemistry letters, Mar-10, Volume: 13, Issue:5
Design and synthesis of the tumor-activated prodrug of dihydropyrimidine dehydrogenase (DPD) inhibitor, RO0094889 for combination therapy with capecitabine.
AID116611Percent increase in life span of L1210 leukemic BDF1 mice when compound(0.080 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID456232Activity at human recombinant CES1 expressed in baculovirus-infected Spodoptera frugiperda Sf21 cells assessed as substrate hydrolysis by fluorescence assay2010Bioorganic & medicinal chemistry, Jan-01, Volume: 18, Issue:1
In silico prediction of human carboxylesterase-1 (hCES1) metabolism combining docking analyses and MD simulations.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1518390Antitumor activity against human HCT116 cells xenografted in nude BALB/c mouse assessed as tumor growth inhibition at 540 mg/kg, po administered once daily for 4 weeks measured post-last dose relative to control2019European journal of medicinal chemistry, Dec-15, Volume: 184Discovery of 3-(((9H-purin-6-yl)amino)methyl)-4,6-dimethylpyridin-2(1H)-one derivatives as novel tubulin polymerization inhibitors for treatment of cancer.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID127784Tumour concentration of 5-FU in HT-3 (human cervical cancer) xenograft mice at 135 mg/kg oral dose2003Bioorganic & medicinal chemistry letters, Mar-10, Volume: 13, Issue:5
Design and synthesis of the tumor-activated prodrug of dihydropyrimidine dehydrogenase (DPD) inhibitor, RO0094889 for combination therapy with capecitabine.
AID116758In vivo mean survival time of L1210 leukemic BDF1 mice when compound(0.016 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID116761In vivo mean survival time of L1210 leukemic BDF1 mice when compound(0.40 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID667628Mutagenic activity in Salmonella typhimurium TA1535 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID1887769Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as mean corpuscular volume at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID667773Mutagenic activity in Salmonella typhimurium TA98 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1887766Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as granulocyte level at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID116764In vivo mean survival time of L1210 leukemic BDF1 mice when compound(2 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID1887768Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as hematocrit level at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID127781Plasma concentration of 5-FU in HT-3 (human cervical cancer) xenograft mice at 135 mg/kg oral dose2003Bioorganic & medicinal chemistry letters, Mar-10, Volume: 13, Issue:5
Design and synthesis of the tumor-activated prodrug of dihydropyrimidine dehydrogenase (DPD) inhibitor, RO0094889 for combination therapy with capecitabine.
AID667775Mutagenic activity in Salmonella typhimurium TA100 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID48318Susceptibility to carboxylesterase in human liver at a concentration 2.5 mM2003Bioorganic & medicinal chemistry letters, Mar-10, Volume: 13, Issue:5
Design and synthesis of the tumor-activated prodrug of dihydropyrimidine dehydrogenase (DPD) inhibitor, RO0094889 for combination therapy with capecitabine.
AID667779Mutagenic activity in Salmonella typhimurium TA102 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID667635Mutagenic activity in Salmonella typhimurium TA102 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID116757In vivo mean survival time of L1210 leukemic BDF1 mice when compound (0.0032 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID1827443Antiproliferative activity against human HCT-116 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2022ACS medicinal chemistry letters, Mar-10, Volume: 13, Issue:3
Rational Design of an Orally Active Anticancer Fluoropyrimidine, Pencitabine, a Hybrid of Capecitabine and Gemcitabine.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID116763In vivo mean survival time of L1210 leukemic BDF1 mice when compound(1.5 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID667774Mutagenic activity in Salmonella typhimurium TA98 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID667782Antitumor activity against mouse L1210 cells xenografted in BDF-1 mouse assessed as increase in mean survival time at 0.16 mmol/kg, po administered 5 days in a week for 2 weeks2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667629Mutagenic activity in Salmonella typhimurium TA1537 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667625Cytotoxicity against human MCF7 cells after 3 days MTT assay2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID353088Cytotoxicity against human RKOp27 cells by MTT assay2009Bioorganic & medicinal chemistry letters, May-01, Volume: 19, Issue:9
Synthesis of potent antitumor and antiviral benzofuran derivatives.
AID487906Cytotoxicity against human RKOp27 cells after 3 days by MTT assay2010European journal of medicinal chemistry, Jun, Volume: 45, Issue:6
Novel benzimidazole-pyrimidine conjugates as potent antitumor agents.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID667783Antitumor activity against mouse L1210 cells xenografted in BDF-1 mouse assessed as increase in mean survival time at 0.080 mmol/kg, po administered 5 days in a week for 2 weeks2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID667776Mutagenic activity in Salmonella typhimurium TA100 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667636Mutagenic activity in Salmonella typhimurium TA1535 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID116615Percent increase in life span of L1210 leukemic BDF1 mice when compound(1.5 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1887763Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as WBC level at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID48317Susceptibility to carboxylesterase in human intestine at a concentration 2.5 mM2003Bioorganic & medicinal chemistry letters, Mar-10, Volume: 13, Issue:5
Design and synthesis of the tumor-activated prodrug of dihydropyrimidine dehydrogenase (DPD) inhibitor, RO0094889 for combination therapy with capecitabine.
AID667778Mutagenic activity in Salmonella typhimurium TA102 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667623Cytotoxicity against human NCI-H69 cells after 3 days MTT assay2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667777Mutagenic activity in Salmonella typhimurium TA102 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667627Mutagenic activity in Salmonella typhimurium TA1535 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1887770Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as red blood cell distribution width at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID667624Cytotoxicity against human PZ-HPV-7 cells after 3 days MTT assay2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID226595Relative susceptibility to human carboxylesterase in liver and intestine (L/I ratio)2003Bioorganic & medicinal chemistry letters, Mar-10, Volume: 13, Issue:5
Design and synthesis of the tumor-activated prodrug of dihydropyrimidine dehydrogenase (DPD) inhibitor, RO0094889 for combination therapy with capecitabine.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID116612Percent increase in life span of L1210 leukemic BDF1 mice when compound(0.13 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID116759In vivo mean survival time of L1210 leukemic BDF1 mice when compound(0.080 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID667772Mutagenic activity in Salmonella typhimurium TA1537 at 0.312 to 5 mg/plate measured after incubation of upside down for 48 hrs in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667634Mutagenic activity in Salmonella typhimurium TA100 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in absence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667633Mutagenic activity in Salmonella typhimurium TA100 at 0.312 to 5 mg/plate preincubated for 20 mins before addition in presence of liver S9 mixture2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID667626Cytotoxicity against human HeLa cells after 3 days MTT assay2012European journal of medicinal chemistry, Aug, Volume: 54Synthesis and biological activity evaluation of cytidine-5'-deoxy-5-fluoro-N-[(alkoxy/aryloxy)] carbonyl-cyclic 2',3'-carbonates.
AID1887772Toxicity in BALB/c mouse xenografted with human HGC-27 cells assessed as mean platelet volume at 150 mg/kg, po bid for 19 days2022European journal of medicinal chemistry, Jan-05, Volume: 227Design, synthesis and biological evaluation of novel o-aminobenzamide derivatives as potential anti-gastric cancer agents in vitro and in vivo.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1827444Antiproliferative activity against human KG-1 cells assessed as reduction in cell viability incubated for 72 hrs by MTT assay2022ACS medicinal chemistry letters, Mar-10, Volume: 13, Issue:3
Rational Design of an Orally Active Anticancer Fluoropyrimidine, Pencitabine, a Hybrid of Capecitabine and Gemcitabine.
AID116760In vivo mean survival time of L1210 leukemic BDF1 mice when compound(0.13 nmol/kg/day) was administered perorally2002Bioorganic & medicinal chemistry letters, Feb-11, Volume: 12, Issue:3
Synthesis and biological activity of the new 5-fluorocytosine derivatives, 5'-deoxy-N-alkyloxycarbonyl-5-fluorocytosine-5'-carboxylic acid.
AID1518393Antitumor activity against human HCT116 cells xenografted in nude BALB/c mouse assessed as reduction in tumor weight at 540 mg/kg, po administered once daily for 4 weeks measured every 3 days during compound dosing2019European journal of medicinal chemistry, Dec-15, Volume: 184Discovery of 3-(((9H-purin-6-yl)amino)methyl)-4,6-dimethylpyridin-2(1H)-one derivatives as novel tubulin polymerization inhibitors for treatment of cancer.
AID1713163Antitumor activity against mouse H22 cells transplanted in Kunming mouse assessed as tumor growth inhibition at 100 mg/kg/day, po administered 5 days per week for 2 weeks2016European journal of medicinal chemistry, Oct-04, Volume: 121Discovery of BC-01, a novel mutual prodrug (hybrid drug) of ubenimex and fluorouracil as anticancer agent.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346022Human thymidylate synthetase (Nucleoside synthesis and metabolism)2005Clinical cancer research : an official journal of the American Association for Cancer Research, Feb-01, Volume: 11, Issue:3
UGT1A7 and UGT1A9 polymorphisms predict response and toxicity in colorectal cancer patients treated with capecitabine/irinotecan.
AID1346022Human thymidylate synthetase (Nucleoside synthesis and metabolism)1999The oncologist, , Volume: 4, Issue:6
The use of thymidylate synthase inhibitors in the treatment of advanced colorectal cancer: current status.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (5,045)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's48 (0.95)18.2507
2000's1414 (28.03)29.6817
2010's2758 (54.67)24.3611
2020's825 (16.35)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 93.24

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index93.24 (24.57)
Research Supply Index8.86 (2.92)
Research Growth Index6.09 (4.65)
Search Engine Demand Index171.00 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (93.24)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials1,719 (32.32%)5.53%
Reviews731 (13.75%)6.00%
Case Studies833 (15.66%)4.05%
Observational67 (1.26%)0.25%
Other1,968 (37.01%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (1679)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Study of Sintilimab vs Standard Therapy in Participants With Mismatch Repair Deficient (dMMR) or Microsatellite Instability-High (MSI-H) Stage III Colorectal Cancer [NCT05236972]Phase 3323 participants (Anticipated)Interventional2022-01-01Recruiting
Phase Ⅱ Study of Compare Apatinib Plus Capecitabine Versus Capecitabine in Maintenance Therapy for Patients With Advanced Triple-negative Breast Cancer [NCT03775928]Phase 280 participants (Anticipated)Interventional2018-12-18Recruiting
Effect of Intravenous Pump of Recombinant Human Endostatin Combined With XELOX Chemotherapy, and a Potential Prognostic Biomarkers in Patient With Advanced Colorectal Cancer [NCT03577392]Phase 2/Phase 3120 participants (Anticipated)Interventional2018-07-01Recruiting
Randomized Phase II Study of S-1 (SOX) or Capecitabine (XELOX) in Combination With Oxaliplatin in Patients With Recurrent or Metastatic Gastric Cancer [NCT00985556]Phase 2130 participants (Anticipated)Interventional2009-01-31Recruiting
A Randomized Open-Label, Phase II Study of Lapatinib-capecitabine or Lapatinib-vinorelbine or Lapatinib/Gemcitabine in Subjects With Her2/Neu Amplified Metastatic Breast Cancer Patients Progression After Taxanes Treatment [NCT01050322]Phase 2142 participants (Actual)Interventional2009-11-30Completed
A Phase I Clinical Trial of Hepatic Arterial Infusion of Oxaliplatin, Oral Capecitabine, With or Without Systemic Bevacizumab for Patients With Advanced Cancer Metastatic to the Liver [NCT01213238]Phase 1116 participants (Anticipated)Interventional2010-09-30Completed
Randomized Trial of Preoperative Radiotherapy With an Integrated Simultaneous Boost Compared to Chemoradiotherapy for T3-4 Rectal Cancer [NCT01224392]Phase 3156 participants (Anticipated)Interventional2010-01-31Completed
A Multicentre, Open-label Phase II Study of Irinotecan, Capecitabine(Xeloda), and Oxaliplatin (IXO) as First Line Treatment in Patients With Metastatic Gastric or Gastroesophageal (GEJ) Adenocarcinoma. [NCT01129310]Phase 247 participants (Actual)Interventional2010-07-31Completed
Anticancer Drug-induced Cardiac Adverse Events in Metastatic Colorectal Cancer: Insights From the French County Calvados Registry [NCT03923036]2,000 participants (Anticipated)Observational2019-04-30Not yet recruiting
A Comparative, Multicenter, Open-Label, Randomized, Phase 2 Study of the Safety and Antitumor Activity of Oral Eniluracil + 5 Fluorouracil + Leucovorin Versus Capecitabine Monotherapy in Subjects With Metastatic Breast Cancer [NCT01231802]Phase 2140 participants (Anticipated)Interventional2011-04-30Recruiting
A Phase III Open Label, Randomized Two-Parallel-Arm Multicenter Study of E7389 Versus Capecitabine in Patients With Locally Advanced or Metastatic Breast Cancer Previously Treated With Anthracyclines and Taxanes [NCT00337103]Phase 31,276 participants (Actual)Interventional2006-09-20Completed
Capecitabine as Radiosensitising Agent in Neoadjuvant Treatment of Locally Advanced Resectable Rectal Cancer [NCT01152710]Phase 257 participants (Actual)Interventional2004-06-30Completed
Phase II Study of Fixed Dose Rate Gemcitabine Plus Capecitabine in Locally Advanced Pancreatic Cancer [NCT01268384]Phase 243 participants (Actual)Interventional2006-04-30Completed
Phase II Clinical Study of Bevacizumab in Combination With Capecitabine as First-line Treatment in Elderly Patients With Metastatic Breast Cancer [NCT01195298]Phase 288 participants (Anticipated)Interventional2010-05-31Recruiting
An Open Label, Randomized, Multi-center, Phase II/III Trial of High Intensity Versus Low Intensity Neoadjuvant Chemoradiotherapy With Intensity-modified Radiation Therapy (IMRT) in Local Advanced Rectal Cancer [NCT01064999]Phase 2/Phase 3240 participants (Anticipated)Interventional2010-03-31Recruiting
A Phase II Trial of Gemcitabine (NSC-613327) and Capecitabine (NSC-712807) in Patients With Unresectable or Metastatic Gallbladder or Cholangiocarcinoma [NCT00033540]Phase 257 participants (Actual)Interventional2003-09-30Completed
"A Multicenter Phase II Study of Capecitabine and Docetaxel for Previously Treated Pancreatic Cancer Patients CapTere" [NCT00290693]Phase 245 participants (Actual)Interventional2004-07-31Completed
A Phase III Clinical Trial Comparing Oxaliplatin, Capecitabine and Hepatic Arterial Infusion of Floxuridine to Oxaliplatin and Capecitabine in Patients With Resected or Ablated Liver Metastases From Colorectal Cancer [NCT00268463]Phase 322 participants (Actual)Interventional2006-01-31Terminated(stopped due to The study was terminated due to low accrual.)
A Phase Ib, Open Label, Dose Escalation Study of the Safety and Pharmacology of GDC-0980 in Combination With a Fluoropyrimidine, Oxaliplatin, and Bevacizumab in Patients With Advanced Solid Tumors [NCT01332604]Phase 141 participants (Actual)Interventional2011-07-31Completed
Phase II Trial of Circulating Tumor DNA Monitoring During Adjuvant Capecitabine in Patients With Triple-negative Breast Cancer and Residual Disease Following Standard Neoadjuvant Chemotherapy [NCT04768426]Phase 225 participants (Anticipated)Interventional2021-02-03Recruiting
Capecitabine or Observation for Patients With pT1N+M0 or pT2-3N0M0 Gastric Adenocarcinoma Undergoing R0 Resection (CAPOGA): A Large Multicenter Phase III Randomized Controlled Trial [NCT03817268]Phase 3768 participants (Anticipated)Interventional2019-01-16Recruiting
A Phase II Trial Using a Combination of Oxaliplatin, Capecitabine, and Celecoxib With Concurrent Radiation for Patients With Newly Diagnosed Resectable Rectal Cancer [NCT00250835]Phase 238 participants (Actual)Interventional2005-04-30Terminated(stopped due to Low accrual)
A Multicenter Trial Investigating the Duration of Adjuvant Therapy(3 vs. 6 Months) With the FOLFOX 4 or XELOX Regimen for Patients With High Risk Stage II or Stage III Colon Cancer [NCT01308086]Phase 32,000 participants (Actual)Interventional2010-10-31Active, not recruiting
A Randomized, Phase III Study Comparing TAC (Docetaxel, Doxorubicin, Cyclophosphamide) With TCX ( Docetaxel, Cyclophosphamide, Capecitabine) as Adjuvant Treatment for Node-Positive Her2-Negative Breast Cancer [NCT01354522]Phase 3400 participants (Anticipated)Interventional2011-05-31Recruiting
A Phase II Study of Oral Xeloda (Capecitabine) in Combination With Intravenous Irinotecan for Patients With Locally Advanced and/or Metastatic Colorectal Cancer [NCT00022698]Phase 267 participants (Actual)Interventional2001-05-31Completed
A Phase II Clinical Study of PD-1 Inhibitors Combined With Fruquintinib and Chemotherapy in First-line Treatment of HER2-negative Advanced G/GEJ Cancer [NCT06158919]58 participants (Anticipated)Interventional2023-11-20Recruiting
A Randomized Phase II Study of Perioperative Atezolizumab +/- Chemotherapy in Resectable MSI-H/dMMR Gastric and Gastroesophageal Junction (GEJ) Cancer [NCT05836584]Phase 2240 participants (Anticipated)Interventional2024-06-08Recruiting
An Open-Label, Multi-Drug, Multi-Centre, Phase II Study to Evaluate the Efficacy, Safety, Tolerability, Pharmacokinetics, and Immunogenicity of Novel Combinations in Participants With Locally Advanced Unresectable or Metastatic Gastric or Gastroesophageal [NCT05702229]Phase 2240 participants (Anticipated)Interventional2023-01-16Recruiting
A Phase II-R and a Phase III Trial Evaluating Both Erlotinib (Ph II-R) and Chemoradiation (Ph III) as Adjuvant Treatment for Patients With Resected Head of Pancreas Adenocarcinoma [NCT01013649]Phase 2/Phase 3545 participants (Anticipated)Interventional2009-11-17Active, not recruiting
Phase II Study of the Combination of Cetuximab, Capecitabine, and Oxaliplatin With Out Without Bevacizumab as Initial Therapy for Metastatic Colorectal Cancer [NCT00321100]Phase 223 participants (Actual)Interventional2006-04-12Terminated(stopped due to Enrollment closed 10/15/2008 based on data about KRAS.)
Efficacy and Safety of Alternating Systemic and Hepatic Artery Infusion Therapy Versus Systemic Chemotherapy Alone As Adjuvant Treatment After Resection of Liver Metastases From Colorectal Cancer: A Randomized, Parallel-Group, Open-Labelled, Active-Contro [NCT02529774]Phase 2/Phase 3432 participants (Anticipated)Interventional2015-09-30Not yet recruiting
Phase III Study of Adjuvant Capecitabine Metronomic Chemotherapy in Triple-negative Operable Breast Cancer [NCT01112826]Phase 3443 participants (Actual)Interventional2010-04-23Completed
Phase II Clinical Trial of Neoadjuvant Weekly Doxorubicin, Polyglutamate Paclitaxel, Capecitabine and Metronomic Chemotherapy in Breast Cancer [NCT01227408]Phase 20 participants (Actual)Interventional2009-02-28Withdrawn(stopped due to Sponsor withdrew due to funding issues)
Pyrotinib Combined With Capecitabine Metronomic Therapy in HER2-postitive Advanced Breast Cancer: Single Arm, Single Center, Phase II Clinical Trial. [NCT03923166]Phase 235 participants (Anticipated)Interventional2019-04-19Recruiting
Phase II Trial to Evaluate the Addition of Nivolumab to Neoadjuvant Chemoradiation With FOLFOX for Locally Advanced Rectal Cancer [NCT03921684]Phase 229 participants (Anticipated)Interventional2019-04-30Recruiting
A Multicenter, Randomised, Open-label Phase II Study to Evaluate the Clinical Benefit of a Post-operative Treatment Associating Radiotherapy + Nivolumab + Ipilimumab Versus Radiotherapy + Capecitabine for Triple Negative Breast Cancer Patients With Residu [NCT03818685]Phase 295 participants (Actual)Interventional2019-07-02Active, not recruiting
A Phase II Trial to Evaluate the Efficacy and Safety of Bevacizumab in Combination With Capecitabine (Xeloda) in Frail Patients With Untreated Metastatic Colorectal Cancer [NCT00203411]Phase 245 participants (Actual)Interventional2006-03-31Completed
Randomized, Open, Multicenter Phase III Study With Capecitabine Plus Bevacizumab Versus Capecitabine Plus Irinotecan Plus Bevacizumab as First-line Therapy in Patients With Metastatic Colorectal Cancer [NCT01249638]Phase 3516 participants (Anticipated)Interventional2010-12-31Recruiting
Neoadjuvant Immunotherapy in Rectal Cancer: A Pilot Study Examining the Safety and Feasibility of PD-1 Blockade in the Treatment of dMMR or MSI-H Rectal Cancer [NCT04357587]Phase 110 participants (Anticipated)Interventional2020-08-06Recruiting
A Phase III Study of Comparing the Maintenance Treatment of Apatinib, Capecitabine and Observation After First-line Therapy in Advanced Gastric Cancer [NCT03889626]Phase 3242 participants (Anticipated)Interventional2019-03-22Not yet recruiting
Oxaliplatin Pharmacokinetics With and Without Ca2+/MG2+ Infusion in Colorectal Cancer Patients [NCT01157052]Phase 115 participants (Anticipated)Interventional2015-01-31Not yet recruiting
Randomised Phase II Study of the Combination of Oral Vinorelbine With Capecitabine Versus Gemcitabine in Combination With Paclitaxel Versus Gemcitabine in Combination With Docetaxel as First Line Chemotherapy in Patients With Metastatic Breast Cancer [NCT03887130]Phase 2152 participants (Actual)Interventional2006-03-31Completed
A Phase I Study of Nab-paclitaxel (Abraxane), Gemcitabine, and Capecitabine (Xeloda) (AGX) in Patients With Previously Untreated, Metastatic Pancreatic Adenocarcinoma [NCT01161186]Phase 115 participants (Actual)Interventional2010-07-31Completed
A Randomized Phase II Study of Chemotherapy ± Metformin in Metastatic Pancreatic Cancer [NCT01167738]Phase 260 participants (Actual)Interventional2010-07-31Terminated(stopped due to concern of detrimental effect)
Multinational, Multicenter, Phase 2 Study of Tesetaxel Plus a Reduced Dose of Capecitabine in Patients With HER2 Negative, Hormone Receptor Positive, Locally Advanced or Metastatic Breast Cancer Who Have Not Previously Received a Taxane [NCT03858972]Phase 2152 participants (Actual)Interventional2019-02-05Terminated(stopped due to The Sponsor has discontinued the development of tesetaxel)
A Single-arm Phase II Downsizing Study of Irinotecan, Capecitabine and Oxaliplatin (IXO) and Bevacizumab as First-line Treatment to Assess Conversion to Resectability of Liver-only Metastases in Colorectal Cancer Patients With Initially Unresectable Metas [NCT01293942]Phase 20 participants (Actual)Interventional2011-03-31Withdrawn
Phase II Study of the Combination of Bevacizumab Plus Somatostatin Analogue and Metronomic Capecitabine in Patients With Advanced Inoperable Well-Differentiated Neuroendocrine Tumors [NCT01203306]Phase 242 participants (Anticipated)Interventional2006-01-31Recruiting
A Phase II Study of Capecitabine and Pseudomonas Aeruginosa Combination in the Salvage Treatment of Metastatic Breast Cancer [NCT01380808]Phase 2100 participants (Actual)Interventional2011-05-31Completed
A Phase 1 and Pharmacologic Study of MM-111 in Combination With Multiple Treatment Regimens in Patients With Advanced HER2 Positive Solid Tumors [NCT01304784]Phase 1100 participants (Anticipated)Interventional2011-01-31Completed
An Open-label, Phase 1/2, Dose-escalation and Expansion Study of SBT6050 Combined With Other HER2-directed Therapies in Subjects With Pretreated Unresectable Locally Advanced and/or Metastatic HER2-expressing or HER2-amplified Cancers [NCT05091528]Phase 1/Phase 22 participants (Actual)Interventional2022-02-08Terminated(stopped due to Sponsor decision based on strategic re-alignment)
A Single-arm, Open-label, Multicenter Phase 2 Study to Evaluate XELOX + Tislelizumab in Combination With Doxorubicin Hydrochloride Liposome Injection （XELOX+PD-1+PLD）as Neoadjuvant Therapy for Resectable Gastric Cancer [NCT05536102]Phase 238 participants (Anticipated)Interventional2022-09-05Recruiting
Adjuvant Capecitabine Metronomic Chemotherapy Plus Endocrine Therapy for HR-positive, HER2-negative, Primary Breast Cancer: a Multicenter, Randomized, Double-blind Phase III Clinical Trial [NCT05063136]Phase 31,979 participants (Anticipated)Interventional2021-09-28Recruiting
A Phase I-II Trial of Capecitabine (Xeloda), Oxaliplatin and Irinotecan in Combination With Bevacizumab in 1st Line Treatment of Metastatic Colorectal Cancer [NCT01311050]46 participants (Anticipated)Observational2009-01-31Recruiting
The Influence of Micrometastases on Prognosis and Survival in Stage I-II Colon Cancer Patients: The EnRoute+ Study [NCT01097265]Phase 2/Phase 31,500 participants (Anticipated)Interventional2010-07-31Recruiting
A Phase II Study Examining the Feasibility of Long Term and Low Dose Oral Capecitabine (Xeloda®) in Newly Diagnosed Head and Neck Squamous Cell Carcinoma (HNSCC) After Surgery, Radiation and/or Chemotherapy [NCT00258310]Phase 235 participants (Actual)Interventional2003-12-31Completed
A Phase I/II Trial of RAD001/Capecitabine in Refractory Gastric Cancer [NCT01099527]Phase 1/Phase 259 participants (Actual)Interventional2009-10-31Completed
OXEL: A Pilot Study of Immune Checkpoint or Capecitabine or Combination Therapy as Adjuvant Therapy for Triple Negative Breast Cancer With Residual Disease Following Neoadjuvant Chemotherapy [NCT03487666]Phase 245 participants (Actual)Interventional2018-05-21Active, not recruiting
Single-arm, Open-label, Single-center Phase II Clinical Study of Cadonilimab Combined With CapeOX Regimen in Perioperative Treatment of Resectable Locally Advanced Gastric Cancer [NCT05974059]Phase 220 participants (Anticipated)Interventional2023-08-01Not yet recruiting
A Phase III, Randomized, Open-label Study to Evaluate Capecitabine Plus Pembrolizumab vs Pembrolizumab Alone as Post-operative Therapy for Triple Negative Breast Cancer With Residual Disease After Neoadjuvant Chemo-immunotherapy [NCT05973864]Phase 3418 participants (Anticipated)Interventional2024-01-31Not yet recruiting
A Phase II, Randomized, Open Label, Parallel-group Study of Atezolizumab With or Without Tiragolumab Following Neoadjuvant Chemoradiotherapy in Patients With Locally Advanced Rectal Cancer [NCT05009069]Phase 258 participants (Actual)Interventional2022-03-18Active, not recruiting
Prospective Safety Study of Sintilimab Combined With XELOX Plus Bevacizumab for Preoperative Neoadjuvant Therapy of CRLM Patients With pMMR/MSS Status [NCT04940546]Phase 1/Phase 236 participants (Actual)Interventional2021-06-16Active, not recruiting
A Pilot Trial of Pre-Operative Chemoradiotherapy Using Capecitabine (Xelodaâ), External Beam Radiation and Cetuximab (Erbitux®) Followed by Definitive Surgery in Patients With Localized (Non-Metastatic) Rectal Cancer [NCT01310985]15 participants (Actual)Observational2008-03-31Completed
Phase II Clinical Study of PD1 Antibody (SHR-1210) Combined With Trastuzumab, Oxaliplatin and Capecitabine for Neoadjuvant Therapy of Gastric Adenocarcinoma/Gastroesophageal Junction Adenocarcinoma [NCT03950271]Phase 225 participants (Anticipated)Interventional2020-01-21Recruiting
Neoadjuvant Chemotherapy and Biological Treatment for Patients With Locally Advanced Colon Cancer [NCT01108107]Phase 276 participants (Actual)Interventional2010-04-30Completed
Effectiveness of First Line Treatment With Lapatinib and ECF/X in Histologically Proven Adenocarcinoma of the Stomach or the Esophagogastric Junction, Metastatic or Not Amenable to Curative Surgery According to HER2 and EGFR Status: a Randomized Phase II [NCT01123473]Phase 229 participants (Actual)Interventional2010-12-31Terminated(stopped due to company withdrew interest)
Safety and Tolerability of Bevacizumab Plus Paclitaxel vs. Bevacizumab Plus Metronomic Cyclophosphamide and Capecitabine as First-Line Therapy in Patients With HER2-Negative Metastatic or Locally Recurrent Breast Cancer - A Multicenter, Randomized Phase I [NCT01131195]Phase 3139 participants (Actual)Interventional2010-07-19Completed
Sensitivity Detection and Drug Resistance Mechanism of Breast Cancer Therapeutic Drugs Based on Organ-like Culture [NCT03925233]300 participants (Anticipated)Observational2019-01-02Enrolling by invitation
A Phase II Study of Pazopanib in Combination With Capecitabine and Oxaliplatin (CAPEOX) in Patients With Advanced Gastric Cancer [NCT01130805]Phase 266 participants (Actual)Interventional2010-12-31Completed
A Phase 3, Open-Label, Randomized Study to Compare Adjuvant Chemotherapy of Docetaxel/Capecitabine/Oxaliplatin Versus Capecitabine/Oxaliplatin in Advanced Gastric Cancer Patients at Stage IIIB and IV (M0) (Based on AJCC Ed. 6) Who Received Radical Resecti [NCT01935778]Phase 3286 participants (Anticipated)Interventional2013-10-02Recruiting
Bevacizumab Plus Capecitabin vs S-1 as Maintenance Treatment Following First-line Chemotherapy in the Patients With Advanced Colorectal Adenocarcinoma. A Phase 3 Randomised Controlled Trial [NCT03708536]Phase 30 participants (Actual)Interventional2018-11-30Withdrawn(stopped due to There are no fund to support)
PHASE II STUDY Evaluating the Toxicity and Activity of the Combination Lapatinib + Capecitabine in Elderly Patients Aged 70 and Over With Metastatic Breast Cancer Over Expressing HER2 [NCT01262469]Phase 24 participants (Actual)Interventional2009-12-31Completed
Multi Gene Detection Tool Based Recurrence Score-guiding Chemotherapy in Non-pathologic Complete Response HR Positive and HER2 Negative Breast Cancer After Neoadjuvant Treatment [NCT03638648]Phase 280 participants (Anticipated)Interventional2019-11-01Not yet recruiting
Molecularly Informed Integrated Immunotherapy Combining Innate High-affinity Natural Killer (haNK) Cell Therapy w/ Adenoviral & Yeast-based Vaccines to Induce T-cell Responses in Subjects w/ Advanced, Unresectable & Untransplantable HCC [NCT03563170]Phase 1/Phase 20 participants (Actual)Interventional2018-05-25Withdrawn(stopped due to Enrollment not initiated)
An Open-Label, Multicenter, Randomized, Phase Ib/II Study of E7050 in Combination With Cisplatin and Capecitabine Versus Cisplatin and Capecitabine Alone in Patients With Advanced or Metastatic Solid Tumors and Previously Untreated Gastric Cancer [NCT01355302]Phase 1/Phase 27 participants (Actual)Interventional2011-11-30Terminated(stopped due to Sites not recruiting)
REDEL Trial: Reduced Elective Nodal Dose for Anal Cancer Toxicity Mitigation [NCT05902533]Phase 2/Phase 333 participants (Anticipated)Interventional2023-08-14Recruiting
An Investigational Randomized Study on Epirubicin Plus Cyclophospamide (EC) or Cyclophosphamide Plus Methotrexat Plus 5-fluorouracil (CMF) Versus Nab-paclitaxel Plus Capecitabine as Adjuvant Chemotherapy for Elderly Non Frail Patients With an Increased Ri [NCT01204437]Phase 2/Phase 3400 participants (Actual)Interventional2009-03-31Completed
A Two Stage Multicenter Phase II Trial of Concurrent Induction Chemoimmunotherapy With Epirubicine, Oxaliplatin, Capecitabine and Panitumumab in KRAs Wild-type, Resectable Type II Gastric Adenocarcinoma [NCT01351038]Phase 243 participants (Anticipated)InterventionalTerminated(stopped due to REAL trial showed a significant difference in OS for reduced EOX and standard EOX)
Irinotecan Gastro-resistant Tablet. An Open Label Phase I, Dose Escalating Study Evaluating Safety, Tolerability and Pharmacokinetics of Oral Administration of Irinotecan in Adult Patients With Solid Tumors [NCT03295084]Phase 139 participants (Actual)Interventional2015-07-15Completed
Phase 3, Randomized Study to Evaluate the Efficacy and Safety of Lenvatinib (E7080/MK-7902) Plus Pembrolizumab (MK-3475) Plus Chemotherapy Compared With Standard of Care Therapy as First-line Intervention in Participants With Advanced/Metastatic Gastroeso [NCT04662710]Phase 3890 participants (Anticipated)Interventional2020-12-30Active, not recruiting
Phase II Study of Docetaxel and Capecitabine in Advanced Squamous Cell Carcinoma of the Head and Neck [NCT02524275]Phase 214 participants (Actual)Interventional2015-03-30Terminated(stopped due to low enrollment)
A Phase I Study of Tesetaxel Administered in Combination With Capecitabine to Subjects With Solid Tumors [NCT01315431]Phase 19 participants (Anticipated)Interventional2011-03-31Active, not recruiting
An Open Label Study to Assess the Resection Rate of Liver Metastases Following Neoadjuvant Therapy With Avastin in Combination With Oxaliplatin and Capecitabine (XELOX) in Patients With Metastatic Colorectal Cancer With Unresectable Liver Metastasis [NCT00700570]Phase 245 participants (Actual)Interventional2008-08-31Completed
An Open-label Randomized Phase II Study of Panitumumab Plus Oral Capecitabine and Infusional Oxaliplatin (XELOX) or XELOX Alone for Second-line Treatment of Patients With Metastatic Colorectal Cancer (VOXEL-Study) [NCT00950820]Phase 29 participants (Actual)Interventional2009-09-30Terminated(stopped due to Recruitment rate to low; changed environment made protocol in its current state obsolete)
NANT Ovarian Cancer Vaccine: Combination Immunotherapy in Subjects With Epithelial Ovarian Cancer Who Have Progressed on or After Standard-of-care (SoC) Therapy [NCT03197584]Phase 1/Phase 20 participants (Actual)Interventional2017-12-31Withdrawn(stopped due to Trial not initiated)
NANT Triple Negative Breast Cancer (TNBC) Vaccine: Combination Immunotherapy in Subjects With TNBC Who Have Progressed on or After Anthracycline-based Chemotherapy [NCT03175666]Phase 1/Phase 20 participants (Actual)Interventional2017-12-31Withdrawn(stopped due to Trial not initiated)
NANT Non-small Cell Lung Cancer (NSCLC) Vaccine: Combination Immunotherapy in Subjects With NSCLC Who Have Progressed After Treatment With Programmed Cell Death Protein 1 (PD-1)/Programmed Death-ligand 1 (PD-L1) Inhibitors [NCT03169738]Phase 1/Phase 20 participants (Actual)Interventional2018-02-28Withdrawn(stopped due to Trial not initiated)
Image-Guided Radiation Therapy (IGRT) Associated With Concurrent Capecitabine and Oxaliplatin in the Treatment of Locally Advanced or Inoperable Hepatocellular Carcinoma (HCC): A Phase I Study [NCT02403544]Phase 130 participants (Anticipated)Interventional2013-09-30Recruiting
NANT Merkel Cell Carcinoma (MCC) Vaccine: Combination Immunotherapy in Subjects With MCC Who Have Progressed on or After Anti-programmed Death-ligand 1 (PD-L1) Therapy [NCT03167164]Phase 1/Phase 20 participants (Actual)Interventional2017-12-31Withdrawn(stopped due to Trial not initiated)
A Multicenter, Double-Blind, Randomized, Placebo-Controlled Study of Varlitinib Plus Capecitabine Versus Placebo Plus Capecitabine in Patients With Advanced or Metastatic Biliary Tract Cancer as Second Line Systemic Therapy [NCT03093870]Phase 2/Phase 3151 participants (Actual)Interventional2017-07-04Completed
A Phase II Study of Capecitabine Plus Oxaliplatin in Combination With Pre-operative Pelvic Radiotherapy in Rectal Cancer [NCT02694718]Phase 260 participants (Actual)Interventional2005-03-31Completed
A Phase II Study of Perioperative Disitamab Vedotin Plus Toripalimab and XELOX Versus Disitamab Vedotin Plus Toripalimab Versus XELOX in Subjects With HER2-expressing Locally Advanced Gastric or Gastroesophageal Junction Adenocarcinoma. [NCT06155383]Phase 290 participants (Anticipated)Interventional2023-11-27Recruiting
A Phase III Randomized Controlled Trial to Compare BL-B01D1 With Physician's Choice of Chemotherapy (Last Line) in Patients With Recurrent or Metastatic Nasopharyngeal Carcinoma (NPC) Previously Treated With PD-1/PD-L1 Monoclonal Antibody and at Least Two [NCT06118333]Phase 3368 participants (Anticipated)Interventional2023-12-04Recruiting
A Phase 3, Randomized, Multi-center, Open-Label Study of DB-1303 Versus Investigator's Choice Chemotherapy in Human Epidermal Growth Factor Receptor 2 (HER2)-Low, Hormone Receptor Positive (HR+) Metastatic Breast Cancer Patients Whose Disease Has Progress [NCT06018337]Phase 3532 participants (Anticipated)Interventional2024-01-31Not yet recruiting
A Randomized, Open-Label, Multicenter Phase 3 Trial of Domvanalimab, Zimberelimab, and Chemotherapy Versus Nivolumab and Chemotherapy in Participants With Previously Untreated Locally Advanced Unresectable or Metastatic Gastric, Gastroesophageal Junction, [NCT05568095]Phase 3970 participants (Anticipated)Interventional2022-11-21Recruiting
An Open-label, Single Arm Study to Evaluate the Efficacy and Safety of Trastuzumab in Combination With Capecitabine and Oxaliplatin (XELOX) as a First-line Chemotherapy for Inoperable, Locally Advanced or Recurrent and/or Metastatic Gastric Cancer [NCT01364493]Phase 251 participants (Actual)Interventional2011-05-31Completed
A Phase I Study of Pyrotinib In Combination With Capecitabine In Patients With HER2 Positive Metastatic Breast Cancer [NCT02361112]Phase 138 participants (Anticipated)Interventional2014-08-31Completed
An Adaptive, Open-Label, Randomized Phase 2 Study of Abemaciclib as a Monotherapy and in Combination With Other Agents Versus Choice of Standard of Care (Gemcitabine or Capecitabine) in Patients With Previously Treated Metastatic Pancreatic Ductal Adenoca [NCT02981342]Phase 2106 participants (Actual)Interventional2017-01-12Completed
mFOLFOXIRI Compared to mFOLFOX6 or CapeOx as Adjuvant Chemotherapy for Stage IIIB or Stage IIIC Colorectal Cancer: A Randomized Controlled Clinical Research [NCT05200299]Phase 2100 participants (Anticipated)Interventional2022-02-01Recruiting
Phase II Study of Pembrolizumab and Capecitabine for Advanced Triple Negative and Hormone-Refractory Breast Cancer [NCT03044730]Phase 230 participants (Actual)Interventional2017-05-25Active, not recruiting
Capecitabine Combined With Lenvatinib and Tislelizumab as Adjuvant Treatment After Resection in Patients With Biliary Tract Cancer: A Single-arm, Phase II Study [NCT05254847]Phase 275 participants (Anticipated)Interventional2021-12-30Recruiting
Phase Ib/II Study of Intra-Arterial Liver Isolation Chemotherapy in Patients With Hepatic Metastases From Colorectal Cancer [NCT04701281]Phase 1/Phase 295 participants (Anticipated)Interventional2019-06-20Recruiting
InterAACT - An International Multicentre Open Label Randomised Phase II Advanced Anal Cancer Trial Comparing Cisplatin Plus 5-Fluorouracil Versus Carboplatin Plus Weekly Paclitaxel in Patients With Inoperable Locally Recurrent or Metastatic Disease [NCT02560298]Phase 291 participants (Actual)Interventional2016-08-23Active, not recruiting
A Phase II Clinical Study of Trastuzumab in Combination With Capecitabine and Cisplatin (XP) in Patients With Tissue HER2-negative But Serum HER2-positive Advanced Gastric Cancer: XP+Samfenet [NCT04309578]Phase 228 participants (Anticipated)Interventional2020-03-12Recruiting
A Multicenter, Phase I/II Study of Every Other Week Capecitabine Dosing With Bevacizumab for the Treatment of Metastatic Breast Cancer Based Upon the Norton-Simon Mathematical Model [NCT00468585]Phase 1/Phase 262 participants (Actual)Interventional2005-06-30Completed
A Phase I, Open-Label, Dose-Seeking Study of AZD2171 Given Daily Orally in Combination With Standard Chemotherapy Regimens (CT) in Patients With Advanced Incurable Non-Small Cell Lung Cancer (NSCLC) or Colorectal Cancer or Other Tumor Types Suitable for T [NCT00107250]Phase 150 participants (Actual)Interventional2005-01-21Completed
Perioperative Chemotherapy Prior To and After Reoperation for Incidental Gallbladder Cancer - An International, Randomized Phase III Trial [NCT03579758]Phase 30 participants (Actual)Interventional2019-04-03Withdrawn(stopped due to This trial will open as an NCTN trial.)
SHR-1210，a Novel Anti-pd-1 Antibody, in Combination With BP102,a Biosimilar of Bevacizumab, and XELOX, (Oxaliplatin Plus Capecitabine) in Patient With Metastatic Colorectal Cancer: a Single-arm, Open Label, Multi-center, Phase II Study [NCT03645876]Phase 212 participants (Actual)Interventional2018-11-08Terminated(stopped due to The study was terminated early due to company decision)
A Phase IIb Randomized Study to Evaluate the Efficacy of Gemcitabine-erlotinib Versus Gemcitabine-erlotinib-capecitabine in Patients With Metastatic Pancreatic Cancer [NCT01303029]Phase 2120 participants (Actual)Interventional2011-02-28Completed
A Randomized Phase 2 Study in Patients With Triple-negative Androgen Receptor Positive Locally Recurrent (Unresectable) or Metastatic Breast Cancer Treated With Darolutamide or Capecitabine [NCT03383679]Phase 294 participants (Actual)Interventional2018-03-14Completed
A Phase II Study of Ziv-aflibercept in Combination With Capecitabine/Oxaliplatin (XELOX) Chemotherapy in the Front-Line Treatment of Patients With Metastatic Colorectal Cancer [NCT02079220]Phase 20 participants (Actual)Interventional2014-03-31Withdrawn(stopped due to Funding for the study was withdrawn, no participants were ever recruited.)
Fruquintinib Plus Camrelizumab and Capecitabine as Salvage Therapy After Progression on FOLFOXIRI-based First-line Treatment in Patients With Unresectable/Metastatic Colorectal Cancer: a Prospective Phase II Study [NCT06148402]Phase 230 participants (Anticipated)Interventional2024-01-31Recruiting
Anlotinib Plus Chemotherapy as First-line Therapy for Gastrointestinal Tumor Patients With Unresectable Liver Metastasis: A Multi-cohort, Multi-center Clinical Trial (ALTER-G-001) [NCT05262335]Phase 2116 participants (Anticipated)Interventional2021-12-01Recruiting
Metabolic and Molecular Response Evaluation for the Individualization of Therapy in Adenocarcinomas of the Gastroesophageal Junction [NCT02287129]Phase 275 participants (Actual)Interventional2014-12-05Completed
A Phase I-II Study of Tesetaxel Plus Capecitabine and Cisplatin in Subjects With Advanced Gastric Cancer [NCT01348009]Phase 1/Phase 263 participants (Anticipated)Interventional2011-05-31Recruiting
QUILT-3.088 NANT Pancreatic Cancer Vaccine: Phase II Randomized Trial of the NANT Pancreatic Cancer Vaccine vs. Standard-of-Care as First- Line Treatment for Patients With Metastatic Pancreatic Cancer [NCT03563144]Phase 20 participants (Actual)Interventional2018-08-31Withdrawn(stopped due to Trial not initiated)
A Randomized, Multicenter, Open-label Phase III Study to Evaluate the Efficacy and Safety of Adding Metronomic Chemotherapy of Capecitabine to Standard Adjuvant Therapy for Patients With High Risk HER2-positive Primary Breast Cancer [NCT03561740]Phase 3794 participants (Anticipated)Interventional2018-07-25Recruiting
Anrotinib in Combination With Capecitabine in the Single-arm, Open Phase II Treatment of Relapsed or Metastatic Triple-negative Breast Cancer Clinical Research [NCT05089643]Phase 235 participants (Anticipated)Interventional2019-04-11Recruiting
Phase II Study of Docetaxel, Oxaliplatin, Capecitabine With Bevacizumab and Trastuzumab in Case of Human Epidermal Growth Factor Receptor 2 (HER2)-Positivity in Patients With Locally Advanced or Metastatic Gastric Cancer or Adenocarcinoma of the Gastro-oe [NCT01359397]Phase 20 participants Interventional2011-03-31Active, not recruiting
A Phase Ib/II Study of PEP503 (Radioenhancer) With Radiotherapy, in Combination With Concurrent Chemotherapy for Patients With Locally Advanced or Unresectable Rectal Cancer [NCT02465593]Phase 1/Phase 232 participants (Actual)Interventional2015-06-30Terminated
Phase II Neoadjuvant Trial of Capecitabine, Cyclophosphamide and Epirubicin for Patients With Axillary Lymph Node Positive Stage II-III Operable Breast Cancer [NCT02115152]Phase 2100 participants (Anticipated)Interventional2014-06-30Not yet recruiting
Phase III Study of Adjuvant Capecitabine vs Observation Alone in Curatively Resected Stage IB (by AJCC 6th Edition) Gastric Cancer(KCSG ST14-05) [NCT01917552]Phase 3870 participants (Anticipated)Interventional2013-08-19Recruiting
A Randomized, Active-Controlled, Partially Blinded, Biomarker Select, Phase III Clinical Trial of Pembrolizumab as Monotherapy and in Combination With Cisplatin+5-Fluorouracil Versus Placebo+Cisplatin+5-Fluorouracil as First-Line Treatment in Subjects Wit [NCT02494583]Phase 3763 participants (Actual)Interventional2015-07-31Completed
The Management of Metastatic Neck Nodes in N2/3 Hypopharyngeal Squamous Cell Carcinoma: A Multi-center Randomized Controlled Prospective Study [NCT05494190]111 participants (Anticipated)Interventional2022-11-01Recruiting
A Combination of Sorafenib, Capecitabine and Oxaliplatin (SECOX) as Neoadjuvant Therapy in Patients With Locally Advanced Hepatocellular Carcinoma: A Phase II Study [NCT03578874]Phase 215 participants (Actual)Interventional2016-06-20Completed
Prospective Study on the Efficacy and Safety of 2 Week or 3 Week Xelox Regimen for Adjuvant Chemotherapy in Colorectal Patients After Surgery [NCT03564912]Phase 1/Phase 2160 participants (Actual)Interventional2018-08-12Completed
Non-OpeRative MANagement of Rectal Cancer Patients Who Had Clinical Complete Response After Pre-operative Chemo-raDiotherapY [NCT04696757]Early Phase 115 participants (Anticipated)Interventional2018-02-01Recruiting
Maintenance Capecitabine Plus Best Supportive Care Versus Best Supportive Care for Metastatic Nasopharyngeal Carcinoma: a Multicenter, Randomised, Phase 3 Study. [NCT02460419]Phase 3104 participants (Actual)Interventional2015-04-30Completed
A Randomized, Multi-center Phase III Trial of Adjuvant Chemotherapy With Gemcitabine and Capecitabine Compared to Capecitabine Alone in Curatively Resected Biliary Tract Cancer [NCT04401709]Phase 3490 participants (Anticipated)Interventional2021-04-01Recruiting
A Multicenter Prospective Phase III Clinical Trial of Neoadjuvant CapOx in Patients With Intermediate Risk CRM-negative Middle Rectal Cancer [NCT04134897]Phase 3316 participants (Anticipated)Interventional2019-10-14Enrolling by invitation
Pilot Trial of KD018 With Neo-Adjuvant Concurrent Chemo-Radiation Therapy in Patients With Locally Advanced Rectal Cancer [NCT02178644]Phase 129 participants (Actual)Interventional2014-07-31Completed
Study Assessing the Effects of Chemotherapy in Advanced Esophagogastric Adenocarcinoma - Carboplatin, Docetaxel and Capecitabine (CTX) or Epirubicin, Oxaliplatin and Capecitabine: a Randomised Phase 2 Trial. [NCT02177552]Phase 298 participants (Anticipated)Interventional2014-06-30Active, not recruiting
Randomized Phase II-III Trial of Peri- or Post-Operative Chemotherapy in Resectable Pancreatic Adenocarcinoma [NCT01150630]Phase 298 participants (Actual)Interventional2010-05-31Completed
A Phase 1 Study of RO4929097 (NSC749225) in Combination With Capecitabine in Refractory Solid Tumors [NCT01158274]Phase 130 participants (Actual)Interventional2010-06-30Completed
A Randomized, Open, Multi-center Phase IIb/III Clinical Study to Assess the Efficacy and Safety of Surufatinib Compared to Capecitabine in Advanced or Metastatic Biliary Tract Carcinoma (BTC) Patients [NCT03873532]Phase 2/Phase 3298 participants (Anticipated)Interventional2018-07-10Recruiting
A Single Arm, Open-label Trial Assessing the Effect of Capecitabine (Xeloda® ) on Progression-free Survival Rate at Four Months in Breast Cancer Patients With CNS Progression After Whole Brain Radiotherapy [NCT01077726]Phase 23 participants (Actual)Interventional2010-01-31Completed
Preoperative Chemoradiotherapy With Capecitabine With or Without Temozolomide in Patients With Locally Advanced Rectal Cancer; A Prospective Randomised Phase 2 Study Stratified by MGMT (O6-methylguanine DNA Methyltransferase) Status [NCT03156036]Phase 264 participants (Actual)Interventional2017-11-30Completed
A Phase II Trial Evaluating Weekly Docetaxel and Capecitabine in Patients With Metastatic or Advanced, Locally, Recurrent Head and Neck Cancer [NCT00148122]Phase 240 participants (Actual)Interventional2002-11-30Completed
Phase II Study of Capecitabine in Metastatic Non-clear Cell Renal Cell Carcinoma Patients [NCT01182142]Phase 251 participants (Anticipated)Interventional2007-09-30Completed
A Randomized Phase II Study of Capecitabine and Cisplatin (XP) +/- Sorafenib (Nexavar®) in Patients With Advanced Gastric Cancer [NCT01187212]Phase 2195 participants (Actual)Interventional2010-08-31Completed
Dose Determination of Taxotere®, Eloxatin® and Xeloda® (TEX)in Combination With Herceptin® as First-line Treatment for Patients With HER2 Positive Non-resectable Oesophagus, Cardia or Gastric Cancer (ECV) [NCT01295086]27 participants (Actual)Interventional2011-03-31Completed
Clinical Trial on Combination Chemotherapy Treatments in Patients With Colorectal Cancer Stage II and III Among Chinese Population [NCT01196260]Phase 2/Phase 38,000 participants (Anticipated)Interventional2004-01-31Recruiting
A Randomized, Multicenter, Open-Label, Phase 3 Study Comparing the Efficacy and Safety of SHR-1210 Plus Capecitabine and Oxaliplatin Sequenced by Apatinib With or Without SHR-1210 Versus Capecitabine and Oxaliplatin in Subjects With Previously Untreated A [NCT03813784]Phase 3887 participants (Actual)Interventional2019-03-07Active, not recruiting
A Randomized, Controlled, Open-label, Multicenter, Phase III Trial of Anus-preservation in Low Rectal Adenocarcinoma Based on MMR/MSI Status(APRAM) [NCT05669092]Phase 3174 participants (Anticipated)Interventional2022-11-01Recruiting
A Phase 1b, Open-Label, Dose-Escalating Trial of Tivozanib (AV-951) in Combination With Capecitabine (Xeloda®) in Subjects With Advanced Solid Tumors [NCT01306630]Phase 124 participants (Anticipated)Interventional2010-11-30Completed
A Phase Ⅱ Study of an All-Oral Combination of Low-dose Etoposide/Capecitabine in Patients With Metastatic Breast Cancer Previously Treated With Anthracyclines and/or Taxanes [NCT01589159]Phase 254 participants (Actual)Interventional2013-01-31Completed
Phase II Study of Irinotecan Plus Capecitabine as the First-line or Second-line Treatment for Advanced Colorectal Cancer Patients [NCT01322152]Phase 252 participants (Actual)Interventional2011-03-31Completed
Anti-Angiogenesis Treatment After Preoperative Chemotherapy: A Pilot Study in Women With Operable Breast Cancer [NCT00121134]164 participants (Actual)Interventional2005-06-30Completed
A Phase I/ II, Non-randomized, Feasibility/ Safety and Efficacy Study of the Combination of Everolimus, Cetuximab and Capecitabine in Patients With Metastatic Pancreatic Cancer [NCT01077986]Phase 1/Phase 235 participants (Actual)Interventional2009-08-31Completed
"An Open-Label Randomized Phase III Study of Intermittent Oral Capecitabine in Combination With Intravenous Oxaliplatin (Q3W) (XELOX) Versus Bolus and Continuous Infusion Fluorouracil/ Intravenous Leucovorin With Intravenous Oxaliplatin (Q2W) (FOLFOX4) as [NCT00069108]Phase 3627 participants (Actual)Interventional2003-07-31Completed
A Phase I/II, Non-randomized, Multi-center, Dose-escalating, Two-stage Efficacy and Feasibility Study of the Combination of Everolimus and Capecitabine in Patients With Advanced Malignancies [NCT01079702]Phase 1/Phase 235 participants (Anticipated)Interventional2008-04-30Recruiting
A Phase 2 Study of GTI-2040 (NSC 722929) in Combination With Capecitabine in Metastatic Breast Cancer [NCT00068588]Phase 224 participants (Actual)Interventional2003-10-31Completed
A Phase III Trial of Novel Epothilone BMS-247550 Plus Capecitabine Versus Capecitabine Alone in Patients With Advanced Breast Cancer Previously Treated With or Resistant to an Anthracycline and Who Are Taxane Resistant [NCT00080301]Phase 3752 participants (Actual)Interventional2003-09-30Completed
The Efficacy and Safety of Maintenance Therapy With Treprilimumab Combined With Capecitabine/Placebo for Recurrent and Metastatic Nasopharyngeal Carcinoma:Randomized, Double-blind, Placebo-controlled, Multicenter Phase III Clinical Study [NCT05869227]Phase 3166 participants (Anticipated)Interventional2023-04-28Recruiting
A Phase Ib/II Study of Regorafenib and Nivolumab Plus Chemotherapy in Patients With Unresectable Advanced/Recurrent Gastric/Gastroesophageal Junction/Esophageal Adenocarcinoma [NCT05394740]Phase 1/Phase 230 participants (Actual)Interventional2022-06-06Active, not recruiting
Toripalimab Combined With Neoadjuvant Chemoradiotherapy as First-line Treatment for Locally Advanced，High-Risk，MSS Rectal Cancer [NCT05877573]53 participants (Anticipated)Interventional2023-07-01Recruiting
A Phase II Trial of Escalated Dose Proton Radiotherapy With Elective Nodal Irradiation and Concomitant Chemotherapy for Patients With Unresectable, Borderline Resectable or Medically Inoperable Pancreatic Adenocarcinoma [NCT02598349]Phase 260 participants (Anticipated)Interventional2016-04-30Recruiting
A Phase I, Dose Escalation Trial of Endoluminal High Dose Rate Brachytherapy With Concurrent Chemotherapy for Rectal or Anal Cancer in Patients With Recurrent Disease or Undergoing Non-Operative Management [NCT02199236]Phase 115 participants (Actual)Interventional2014-07-31Active, not recruiting
Adjuvant Chemotherapy In Elderly With Colon Cancer Stage III - Geriatric Assessment and Prognostic Gene Signatures [NCT02978612]Phase 2170 participants (Anticipated)Interventional2016-06-30Active, not recruiting
MRI Simulation-guided Boost in Short-course Preoperative Radiotherapy (SCPRT) Followed by Consolidation Chemotherapy Versus Long Course Chemoradiation for Unresectable Rectal Cancer [NCT03714490]Phase 2200 participants (Anticipated)Interventional2018-10-23Recruiting
A Randomised, Double-blind, Phase III Study to Compare the Efficacy and Safety of Cediranib (AZD2171, RECENTIN™) When Added to 5 Fluorouracil, Leucovorin and Oxaliplatin (FOLFOX) or Capecitabine and Oxaliplatin (XELOX) With the Efficacy and Safety of Plac [NCT00399035]Phase 31,254 participants (Actual)Interventional2006-11-30Completed
A Phase 2 Study of Pembrolizumab, a Monoclonal Antibody Against PD-1, in Combination With Capecitabine and Oxaliplatin (CAPOX) in Subjects With Advanced Biliary Tract Carcinoma (BTC) [NCT03111732]Phase 211 participants (Actual)Interventional2017-06-14Completed
Multicenter, Open Label, Phase II Clinical Study of Gemcitabine, Capecitabine and Avastin in Pancreatic Cancer [NCT00100815]Phase 250 participants (Actual)Interventional2004-08-31Completed
A Prospective, Multicenter and Registry-based Cohort Study of Pyrotinib Plus Capecitabine for Adjuvant Treatment of HER2 Positive Early-stage Breast Cancer [NCT06035016]300 participants (Anticipated)Observational2023-06-01Recruiting
Phase II Study of Chemo-Radiation-Induced Abscopal Effect in Metastatic Breast Cancer and in Other Metastatic Sites of Solid Tumors [NCT02474186]Phase 241 participants (Actual)Interventional2003-04-30Completed
Metformin in Association to Chemoradiotherapy for the Neoadjuvant Treatment of Locally Advanced Rectal Cancer: a Randomized, Placebo-controlled Phase II Study [NCT02473094]Phase 23 participants (Actual)Interventional2015-07-31Terminated(stopped due to Slow Accrual)
A Randomized, Controlled Phase Ⅲ Study of Paclitaxel Polymeric Micelles for Injection Versus Physician's Choice(TPC) in Human Epidermal Growth Factor Receptor 2-negative (HER2-) Metastatic Breast Cancer (MBC) Subjects Who Have Failed at Least Two Previous [NCT06143553]Phase 3168 participants (Anticipated)Interventional2023-10-30Recruiting
Chemotherapy Combined With High-dose Radiotherapy for Low Rectal Cancer Using Magnetic Resonance Guided Radiotherapy Linear Accelerator：A Prospective Phase 2 Trial [NCT05338866]58 participants (Anticipated)Observational2022-01-01Enrolling by invitation
Risk-Adapted Therapy for HIV-Associated Anal Cancer [NCT04929028]Phase 253 participants (Anticipated)Interventional2022-08-09Recruiting
No Operation After Short Course Equivalent Dose (Ht) Radiation Therapy Followed By Consolidation Chemotherapy In Locally Advanced Rectal Cancer: The Prospective, Single Arm NOAHS-ARC Trial [NCT04864067]Phase 273 participants (Anticipated)Interventional2021-06-09Recruiting
A Randomised,Multi-Center Study of Docetaxol Plus Capecitabine or Cisplatin in Anthracycline-Pretreated Patients With Advanced Breast Cancer [NCT00717951]Phase 2120 participants (Actual)Interventional2008-05-31Active, not recruiting
"A Randomized Phase III Trial of Trastuzumab + ALpelisib +/- Fulvestrant Versus Trastuzumab + Chemotherapy in Patients With PIK3CA Mutated Previously Treated HER2+ Advanced BrEasT Cancer. ALPHABET Study." [NCT05063786]Phase 3300 participants (Anticipated)Interventional2021-09-14Recruiting
A Pilot and Phase II Study to Assess the Safety, Tolerability and Efficacy of Pembrolizumab Plus Chemotherapy in Metastatic Triple Negative Breast Cancer Patients [NCT02734290]Phase 1/Phase 229 participants (Actual)Interventional2016-02-23Active, not recruiting
Phase 1/2 Study of Valproic Acid and Short-course Radiotherapy Plus Capecitabine as preoperatIve Treatment in Low-moderate Risk Rectal Cancer [NCT01898104]Phase 1/Phase 2152 participants (Anticipated)Interventional2012-05-31Recruiting
A Phase II, Single-center, Open-label, Single-arm Study of Induction Chemotherapy Combined With Immunotherapy for Locally Advanced Hypopharyngeal Carcinoma [NCT04156698]Phase 251 participants (Anticipated)Interventional2020-05-21Active, not recruiting
Single-arm Phase II Clinical Study of Short-course Radiotherapy Combined With Neoadjuvant Chemotherapy and PD-1 Inhibitor in the Treatment of Locally Advanced Gastric Adenocarcinoma [NCT05563012]Phase 229 participants (Anticipated)Interventional2022-09-26Recruiting
A Randomized Phase II Trial of Standard of Care Alone or in Combination With Ad-CEA Vaccine and Avelumab in Patients With Previously Untreated Metastatic or Unresectable Colorectal Cancer [NCT03050814]Phase 230 participants (Actual)Interventional2017-04-05Terminated(stopped due to Terminated after an unplanned interim efficacy analysis.)
Henan Cancer Hospital, Affiliated Cancer Hospital of Zhengzhou University. [NCT05207735]Phase 273 participants (Anticipated)Interventional2022-01-31Not yet recruiting
A Randomized Single Center Controlled Study of Perioperative Chemotherapy of Oxaliplatin Combined With Capecitabine (XELOX) Versus XELOX as Post-operative Chemotherapy in Advanced Gastric Adenocarcinoma With D2 Dissection [NCT01665274]Phase 215 participants (Actual)Interventional2013-09-30Terminated(stopped due to we are working on a larger similar multicenter cinical trials as a participant.so in order to avoid conflicts of interest, we have to suspended this project.)
An Open-label, Randomised, Non-comparative Phase 2 Study Evaluating S 95005 (TAS-102) Plus Bevacizumab and Capecitabine Plus Bevacizumab in Patients With Previously Untreated Metastatic COlorectal Cancer Who Are Non-eligible for Intensive Therapy (TASCO1 [NCT02743221]Phase 2154 participants (Actual)Interventional2016-04-29Completed
A Phase 2A, Single Arm, Multicentre, Study of Varlitinib Plus Capecitabine in Chinese Patients With Advanced or Metastatic Biliary Tract Cancer Who Progressed on at Least 1 Line of Systemic Therapy [NCT03231176]Phase 262 participants (Actual)Interventional2017-12-19Completed
Phase II Study of Capecitabine, Oxaliplatin and Cetuximab Given Throughout Multi-Modal Therapy for Locally Advanced Rectal Adenocarcinoma [NCT00353457]Phase 26 participants (Actual)Interventional2006-02-28Terminated(stopped due to new studies were finding that Erbitux was not beneficial)
Evaluate Effectiveness and Security of Capecitabine or Endocrinotherapy as a Maintenance Therapy Regimen After 2nd-line or Over 2nd-line Therapy With Capecitabine Combine Regimen in Hormone Receptor Positive and HER2 Negative Metastatic Breast Cancer [NCT03204734]Phase 2132 participants (Anticipated)Interventional2016-01-01Recruiting
A Phase Ib/II Study of Nivolumab Plus Chemotherapy in Patients With Advanced Cancer (NivoPlus) [NCT02423954]Phase 1/Phase 233 participants (Actual)Interventional2015-04-30Terminated(stopped due to Investigator no longer at site to enroll patients or write up data)
A Phase 3 Randomized Controlled Study of Metronomic Capecitabine Combined With Aromatase Inhibitor Versus Aromatase Inhibitor Alone for First Line Treatment in Hormone Receptor-positive, Her2-negative Metastatic Breast Cancer [NCT02767661]Phase 3240 participants (Anticipated)Interventional2017-07-19Active, not recruiting
PAXG Out in the Country [NCT04480268]Phase 4175 participants (Anticipated)Interventional2020-07-08Recruiting
NANT Non-Hodgkin Lymphoma (NHL) Vaccine: Combination Immunotherapy in Subjects With Relapsed CD20-positive NHL [NCT03169790]Phase 1/Phase 20 participants (Actual)Interventional2017-12-31Withdrawn(stopped due to Trial not initiated)
Letrozole Plus Low-Dose Metronomic Capecitabine Versus EC-T (Epirubicin/Cyclophosphamide Followed by Docetaxel) as Neoadjuvant Therapy for ER+/HER2-negative Breast Cancer [NCT03507465]Phase 2/Phase 3290 participants (Anticipated)Interventional2017-11-29Recruiting
Randomised, Multicenter Phase II Study in Patients With High Risk Breast Cancer With Capecitabine Versus Vinorelbine With Pathologic Residual Tumors After Preoperative Chemotherapy Secondary ID [NCT03703427]Phase 2200 participants (Anticipated)Interventional2018-11-30Not yet recruiting
A Phase IB Study FOLFIRINOX and NIS793 in Patients With Pancreatic Cancer [NCT05417386]Phase 150 participants (Anticipated)Interventional2022-08-09Recruiting
Randomised, Multicenter Phase II Study in Patients With HER-2 Positive Breast Cancer With Capecitabine Versus Observation With Pathologic Residual Tumors After Preoperative Chemotherapy [NCT03684863]Phase 2200 participants (Anticipated)Interventional2018-10-31Not yet recruiting
A Phase II Study of AK112 With or Without AK117 for Patients With Metastatic Colorectal Cancer [NCT05382442]Phase 2114 participants (Anticipated)Interventional2022-07-27Recruiting
Totally Neoadjuvant FOLFOXIRI Chemotherapy Followed by Short-course Radiation and XELOX Chemotherapy in Patients With Locally Advanced Rectal Cancer：an Open-label, Single-arm, Multicenter Phase II Study. [NCT03484221]Phase 230 participants (Anticipated)Interventional2018-04-01Recruiting
A Phase I Dose-Escalation Trial of Biweekly Intraperitoneal Oxaliplatin With Systemic Capecitabine and Bevacizumab Following Cytoreduction in Patients With Peritoneal Carcinomatosis From Appendiceal or Colorectal Cancer [NCT01061515]Phase 121 participants (Actual)Interventional2011-05-10Active, not recruiting
Postoperation Maintenance Therapy for Resectable Liver Metastases of Colorectal Cancer Guided by ctDNA: a Multicenter, Randomized, Controlled, Phase III Clinical Trial. [NCT05797077]Phase 3346 participants (Anticipated)Interventional2023-02-20Recruiting
Rectal Preserving Treatment for Early Rectal Cancer. A Multi-centred Randomised Trial of Radical Surgery Versus Adjuvant Chemoradiotherapy After Local Excision for Early Rectal Cancers [NCT02371304]Phase 3302 participants (Anticipated)Interventional2015-10-31Recruiting
Sun Yat-sen University Cancer Center [NCT02362958]Phase 2159 participants (Actual)Interventional2015-01-09Completed
A Phase 2, Multi-Cohort Study to Investigate the Safety, Pharmacokinetics and Preliminary Antitumor Activity of the Anti-PD-1 Monoclonal Antibody BGB A317 in Combination With Chemotherapy as First-Line Treatment in Adults With Inoperable, Locally Advanced [NCT03469557]Phase 230 participants (Actual)Interventional2017-07-18Completed
Estudo Randomizado de Fase II Com Capecitabina Versus 5-Fluorouracil/Leucovorin em Bolus Associados à Radioterapia no Tratamento Neoadjuvante de câncer de Reto Localmente avançado: INCAGI004. [NCT03428529]Phase 2/Phase 363 participants (Actual)Interventional2011-01-12Completed
A Phase II Evaluation of Five Fractions of Radiotherapy Followed by Full Dose FOLFOX Chemotherapy as Preoperative Treatment for Rectal Cancer [NCT01060007]Phase 280 participants (Actual)Interventional2009-11-30Completed
The Efficacy of Induction Chemotherapy With Cisplatin and Capecitabine Followed by Concurrent Chemoradiotherapy for Locally Advanced Nasopharyngeal Carcinoma [NCT03427359]Phase 265 participants (Actual)Interventional2015-01-22Completed
Prospective Randomized Controlled Study of the Maintenance Regimen and Revised Regimen for Advanced Breast Cancer Survivors After First-line Salvage Therapy [NCT03423849]Phase 2/Phase 3200 participants (Anticipated)Interventional2018-02-08Not yet recruiting
An Open Label Continuation Study of TRC105 Therapy for Patients Who Have Completed a Prior TRC105 Trial and Are Judged by the Investigator to Have the Potential to Benefit From Continued TRC105 Therapy [NCT02354612]0 participants Expanded AccessNo longer available
QUILT-3.090: NANT Squamous Cell Carcinoma (SCC) Vaccine: Molecularly Informed Integrated Immunotherapy Combining (haNK) Cell Therapy With Adenoviral and Yeast-based Vaccines to Induce T-cell Responses in Subjects With SCC Who Have Progressed on or After P [NCT03387111]Phase 1/Phase 265 participants (Anticipated)Interventional2018-01-13Active, not recruiting
A Phase IB/II Clinical Study to Assess the Efficacy and Safety of QLS31905 in Combination With Chemotherapy as First-line Treatment in Patients With Claudin 18.2 (CLDN18.2) Positive Advanced Malignant Solid Tumors [NCT06041035]Phase 1/Phase 2115 participants (Anticipated)Interventional2023-10-31Not yet recruiting
A Prospective Phase II Trial of Immunotherapy Combined With Short-course Radiotherapy in Early Low Rectal Cancer [NCT05555888]Phase 234 participants (Anticipated)Interventional2022-12-12Recruiting
Multicenter, Single-arm, Open-label Phase II Clinical Study of Tislelizumab Combined With Chemotherapy (CAPOX) in the Perioperative Treatment of MSI-H/dMMR Stage II or III Colorectal Cancer [NCT05841134]Phase 225 participants (Anticipated)Interventional2023-06-01Not yet recruiting
A Study of Adjuvant Chemoradiation and Biomarkers of Response in High-risk Breast Cancer [NCT05288777]Phase 2/Phase 345 participants (Anticipated)Interventional2022-07-11Recruiting
A Multi-Center, Open Label Phase 1/2 Study of CYT-0851 in Patients With Relapsed/Refractory B-Cell Malignancies and Advanced Solid Tumors [NCT03997968]Phase 1/Phase 2170 participants (Anticipated)Interventional2019-10-09Active, not recruiting
An International, Multi-Center, Open-Label, Randomized, Phase III Trial of Sacituzumab Govitecan Versus Treatment of Physician Choice in Patients With Metastatic Triple-Negative Breast Cancer Who Received at Least Two Prior Treatments [NCT02574455]Phase 3529 participants (Actual)Interventional2017-11-07Completed
A Randomized Phase III Study Of Low-Docetaxel Oxaliplatin, Capecitabine (Low-Tox) Vs Epirubicin, Oxaliplatin And Capecitabine (Eox) In Patients With Locally Advanced Unresectable Or Metastatic Gastric Cancer [NCT02076594]Phase 3171 participants (Actual)Interventional2013-01-31Terminated(stopped due to The interim analysis performed on 09 November 2018, showed the failure to achieve the primary objective of effectiveness of the experimental treatment.)
A Randomized, Multicenter, Open Label Study of MM-302 Plus Trastuzumab vs. Chemotherapy of Physician's Choice Plus Trastuzumab in Anthracycline Naive Patients With Locally Advanced/Metastatic HER2-Positive Breast Cancer [NCT02213744]Phase 2/Phase 3113 participants (Actual)Interventional2014-07-31Terminated(stopped due to Felt not to show benefit over control per DMC and confirmed via futility analysis)
Randomized Prospective Multicentric Study: Radio-chemotherapy and Liver Transplantation Versus Liver Resection to Treat Respectable Hilar Cholangiocarcinoma [NCT02232932]60 participants (Anticipated)Interventional2014-03-31Active, not recruiting
MRI Guided Adaptive Radiation for Locally Advanced Rectal Adenocarcinoma to Enhance Complete Response [NCT05108428]Early Phase 120 participants (Actual)Interventional2021-12-23Active, not recruiting
A Phase 3 Randomized, Open-label Study to Evaluate the Efficacy and Safety of Olaparib Alone or in Combination With Bevacizumab Compared to Bevacizumab With a Fluoropyrimidine in Participants With Unresectable or Metastatic Colorectal Cancer Who Have Not [NCT04456699]Phase 3335 participants (Actual)Interventional2020-08-19Completed
Phase II Study Of Preoperative Chemoradiotherapy Plus Avelumab In Patients With Locally Advanced Rectal Cancer [NCT03854799]Phase 2101 participants (Actual)Interventional2019-04-01Completed
A Multi-centre, Open-label, Randomized Clinical Trial Comparing the Efficacy and Safety of the Antibody-drug Conjugate SYD985 to Physician's Choice in Patients With HER2-positive Unresectable Locally Advanced or Metastatic Breast Cancer [NCT03262935]Phase 3437 participants (Actual)Interventional2017-12-15Completed
Three Drugs in Advanced Gastric Cancer Neoadjuvant Chemotherapy for Stage Ⅲ Multicenter, Open, Randomized, Controlled Clinical Study [NCT02555358]Phase 2300 participants (Actual)Interventional2014-11-30Completed
A Phase III Randomized Study to Assess the Efficacy and Safety of Perifosine Plus Capecitabine Versus Placebo Plus Capecitabine in Patients With Refractory Advanced Colorectal Cancer [NCT01097018]Phase 3468 participants (Actual)Interventional2010-04-30Completed
PERIOPERATIVE TREATMENT WITH COI-B (CAPECITABINE, OXALIPLATIN, IRINOTECAN AND BEVACIZUMAB) OF HIGH RISK OR BORDERLINE RESECTABLE COLORECTAL CANCER LIVER METASTASES [NCT02086656]Phase 246 participants (Actual)Interventional2013-06-30Completed
A Prospective Phase II Trial of Short-course Radiotherapy Based Total Neoadjuvant Therapy Combined With PD-1 Inhibitor for Locally Advanced Rectal Cancer (TORCH） [NCT04518280]Phase 2130 participants (Anticipated)Interventional2021-05-01Recruiting
A Phase II, Open, Randomised Study to Assess the Efficacy and Safety of AZD6244 vs. Capecitabine (Xeloda®) in Patients With Advanced or Metastatic Pancreatic Cancer, Who Have Failed First Line Gemcitabine Therapy [NCT00372944]Phase 270 participants (Actual)Interventional2006-08-31Completed
Prospective Randomized Clinical Trial for no Inferiority With Preoperative Chemoradiotherapy and Transanal Endoscopic Microsurgery (TEM) Versus Total Mesorectal Excision in T2-T3s N0, M0 Rectal Cancer [NCT01308190]Phase 3173 participants (Actual)Interventional2010-08-31Completed
An Investigator Sponsored Phase I Trial of Selinexor Combined With Standard Capecitabine Based Chemoradiation as a Neoadjuvant Treatment in Locally Advanced Rectal Cancer [NCT02137356]Phase 128 participants (Anticipated)Interventional2014-12-31Recruiting
Camrelizumab Combined With Concurrent Radiotherapy and Chemotherapy for Treatment of Patients With Local Recurrence of Esophageal Cancer [NCT04390945]Phase 262 participants (Anticipated)Interventional2021-12-01Recruiting
An Open, Randomized Phase III Study of Famitinib With Camrelizumab Plus Treatment of Physician's Choice (TPC) Versus Camrelizumab Plus TPC in The First-line Treatment of Immunomodulatory Locally Advanced or Metastatic Triple-negative Breast Cancer [NCT05760378]Phase 3223 participants (Anticipated)Interventional2023-03-17Recruiting
LUME-Colon 2: An Open-label Randomized Phase II Study to Assess the Efficacy and Safety of Nintedanib Alone or in Combination With Capecitabine for Patients With Refractory Metastatic Colorectal Cancer [NCT02780700]Phase 21 participants (Actual)Interventional2016-07-05Terminated(stopped due to Substance discontinued)
To Observe the Pathological Remission Rate and Safety of FOLFOXIRI for Neoadjuvant Treatment of High-risk Locally Advanced Colorectal Cancer With a Single-arm, Open, Prospective Phase II Exploratory Clinical Study [NCT05018182]Phase 269 participants (Anticipated)Interventional2021-08-02Recruiting
Apatinib Combined Capecitabine Versus Capecitabine Alone for Adjuvant Therapy in Patients After Biliary Carcinoma Surgery: a Prospective Randomized Controlled Study [NCT03609489]Phase 240 participants (Anticipated)Interventional2018-09-10Not yet recruiting
Dose-escalation, Phase I Multicentric Trial, Evaluating the Combination of Ribociclib and Capecitabine in Locally Advanced or Metastatic Breast Cancer HER2 Negative in Patients Previously Treated With Anthracyclines and Taxanes [NCT02754011]Phase 118 participants (Actual)Interventional2017-02-02Completed
Magnetic Resonance-Guided High Intensity Focused Ultrasound for Recurrent Rectal Cancer - A Pilot Study [NCT02528175]6 participants (Actual)Interventional2015-04-30Completed
A Phase II Trial of Capecitabine and Irinotecan With or Without Amifostine in Neoadjuvant Chemoradiotherapy in Locally Advanced Rectal Cancer [NCT03702985]Phase 2160 participants (Anticipated)Interventional2018-05-28Recruiting
A Prospective Randomized Controlled Clinical Trial of Capecitabine Treatment in Patients With Locally Advanced Squamous Cell Carcinoma of the Head and Neck After Radiotherapy: Phase II Study [NCT03678649]Phase 2180 participants (Anticipated)Interventional2018-09-10Recruiting
Phase 1/2 Study of Gemcitabine/Taxotere/Xeloda (GTX) in Combination With Cisplatin and Irinotecan in Subjects With Metastatic Pancreatic Cancer [NCT02324543]Phase 1/Phase 247 participants (Actual)Interventional2015-02-28Completed
An Open-label, Phase II Study Evaluating the Efficacy and Safety of Trastuzumab Combined With Oral Chemotherapy in Patients With HER-2 Positive Stage I Breast Cancer [NCT04922008]Phase 2356 participants (Anticipated)Interventional2021-07-01Not yet recruiting
Fluoropyrimidine Tailored-dose Based on Uracil Concentration in Patients Treated for Digestive Carcinomas: Evaluation of Clinical Practice [NCT04918264]334 participants (Actual)Observational2020-11-02Completed
Tucatinib, Trastuzumab and Capecitabine With Brain and/or Spinal Radiotherapy (XRT) in Patients With HER2+ Metastatic Breast Cancer and Leptomeningeal Disease: A Multi-centre Phase II, Single Arm Feasibility Study [NCT06016387]Phase 230 participants (Anticipated)Interventional2023-10-05Not yet recruiting
Efficacy and Safety of Inetetamab Plus Pyrotiniband and Capecitabine in HER2-positive Metastatic Breast Cancer Patients With or Without Brain Metastasis [NCT06015100]40 participants (Anticipated)Interventional2021-02-20Active, not recruiting
A Phase 3, Randomized, Double-blind Clinical Study of Pembrolizumab (MK-3475) Plus Chemotherapy Versus Placebo Plus Chemotherapy as First-line Treatment in Participants With HER2 Negative, Previously Untreated, Unresectable or Metastatic Gastric Orgastroe [NCT04859582]Phase 30 participants (Actual)Interventional2018-11-08Withdrawn(stopped due to Withdrawn due to protocol amendment)
A Single Arm, Multicenter Phase II Clinical Study of TQB2450 (PD-L1 Inhibitor) Plus Anlotinib Combined With Oxaliplatin, Capecitabine in the First-line Treatment of Advanced Gastric Cancer (GC) or Adenocarcinoma of Esophagogastric Junction (AEG) [NCT04891900]25 participants (Anticipated)Interventional2021-05-31Not yet recruiting
Randomized Open-label Trial of Dose Dense, Fixed Dose Capecitabine Compared to Standard Dose Capecitabine in Metastatic Breast Cancer and Advanced/Metastatic Gastrointestinal Cancers. [NCT02595320]Phase 2200 participants (Actual)Interventional2015-10-05Active, not recruiting
An Open-Label, Randomized Phase II Study of Herceptin (Trastuzumab), Taxotere (Docetaxel), and Xeloda (Capecitabine) in Combination, Versus Herceptin (Trastuzumab) Plus Taxotere (Docetaxel), in Patients With Advanced and/or Metastatic Breast Cancers That [NCT02748213]Phase 2225 participants (Actual)Interventional2002-02-28Completed
A Phase Ib/II, Open-Label, Multicenter, Randomized Umbrella Study Evaluating the Efficacy and Safety of Multiple Treatment Combinations in Patients With Gastric or Gastroesophageal Junction Carcinoma (MORPHEUS C-Gastric and Gastroesophageal Junction Carci [NCT05251948]Phase 1/Phase 2255 participants (Anticipated)Interventional2022-03-01Active, not recruiting
A Study of RC48-ADC Combine With Toripalimab and Chemotherapy or RC48-ADC Combine With Toripalimab and Herceptin as First-line Treatment in Local Advanced or Metastatic Gastric Cancer With the HER2 Expression [NCT05980481]Phase 2/Phase 360 participants (Anticipated)Interventional2023-08-04Recruiting
A Prospective, Multicenter, Open, Randomized Controlled Phase II Clinical Study Evaluating Recombinant Oncolytic HSV2（OH2）Therapeutic Injecta(Vero Cell) for Human Use(rHSV2hGM-CSF) in Combination With Capecitabine for First-line Maintenance Therapy in Adv [NCT05648006]Phase 260 participants (Anticipated)Interventional2023-10-17Recruiting
Short-course Radiotherapy Versus Chemoradiotherapy, Followed by Consolidation Chemotherapy, and Selective Organ Preservation for MRI-defined Intermediate and High-risk Rectal Cancer Patients [NCT04246684]Phase 3702 participants (Anticipated)Interventional2020-10-15Active, not recruiting
Serial Measurements of Molecular and Architectural Responses to Therapy (SMMART) Trial: PRIME [NCT03878524]Phase 12 participants (Actual)Interventional2020-04-01Active, not recruiting
A Multi-Center, Double-Blind, Randomized, Phase III Study of CS1001 in Combination With CAPOX Chemotherapy Compared to Placebo in Combination With CAPOX Chemotherapy in Subjects With Unresectable Locally Advanced or Metastatic GC or GEJ Adenocarcinoma [NCT03802591]Phase 3479 participants (Actual)Interventional2019-03-28Completed
First-line Combination of Capecitabine and Oxaliplatin + Bevacizumab in Elderly Patients With Metastatic Colorectal Cancer [NCT03451370]121 participants (Anticipated)Observational [Patient Registry]2017-11-01Active, not recruiting
MR Guided Phase II Radiotherapy Dose Escalation in Unresectable Non-metastatic Pancreatic Cancer [NCT01972919]Phase 223 participants (Actual)Interventional2015-12-10Active, not recruiting
Preoperative Radiochemotherapy With IMRT - Simultaneous Integrated Boost in Locally Advanced Rectal Cancer - BISER [NCT02268006]Phase 250 participants (Anticipated)Interventional2014-01-31Recruiting
Evaluation of Polychemotherapy With XELOXIRI-3 in Elderly or Frail Patients With Advanced Pancreatic Adenocarcinoma (ALIX) [NCT03974854]Phase 290 participants (Anticipated)Interventional2019-07-08Recruiting
A Randomized Phase 2/3 Multi-Center Study of SM-88 in Subjects With Pancreatic Cancer Whose Disease Has Progressed or Recurred [NCT03512756]Phase 2/Phase 3132 participants (Actual)Interventional2018-03-27Completed
A Multicenter, Double-Blind, 3-Arm, Phase 1b/2 Study in Subjects With Unresectable Locally Advanced or Metastatic Gastric or Esophagogastric Junction Adenocarcinoma to Evaluate the Safety and Efficacy of First-line Treatment With Epirubicin, Cisplatin, an [NCT00719550]Phase 1/Phase 2130 participants (Actual)Interventional2009-02-28Completed
A Phase 2, Single Arm Study of Varlitinib Plus Capecitabine in Patients With Advanced or Metastatic Biliary Tract Cancer as First-line Systemic Therapy [NCT03129074]Phase 20 participants (Actual)Interventional2018-05-31Withdrawn(stopped due to sponsor decision)
Phase II Study of Recombinant Anti-tumor and Anti-Virus Protein for Injection Plus Capatabine in Treating Patients With Metastatic Colorectal Cancer After Failure of Standard Treatment [NCT02068131]Phase 230 participants (Anticipated)Interventional2014-02-28Recruiting
A Randomized, Open-label, Parallel Controlled, Multi-center Phase III Study of TQB2450 Injection Combined With Anlotinib Hydrochloride Capsule Versus Chemotherapy as Second-line Treatment in Subjects With Advanced Biliary Cancer [NCT04809142]Phase 3392 participants (Anticipated)Interventional2021-02-04Recruiting
A Randomized, Double Blind, Multi-Center, Phase 2 Study to Estimate the Efficacy and Evaluate the Safety and Tolerability of Cisplatin & Capecitabine (CX) in Combination With AMG 386 or Placebo in Subjects With Metastatic Gastric, Gastroesophageal Junctio [NCT00583674]Phase 2171 participants (Actual)Interventional2007-12-31Completed
A Phase Ib, Multicenter, Open-label, Dose-escalation and Dose-expansion Study of the Safety, Tolerability and Pharmacokinetics of HB002.1T in Combination With Chemotherapy in Patients With Advanced Solid Tumors. [NCT04802980]Phase 172 participants (Anticipated)Interventional2020-04-28Recruiting
Phase Ib/II Study of Capecitabine 7/7 Schedule With Neratinib in Patients With Metastatic HER2-Positive Breast Cancer [NCT03377387]Phase 1/Phase 234 participants (Actual)Interventional2017-12-13Active, not recruiting
A Phase II Study of Capecitabine (Xeloda)/Oxaliplatin (Eloxatin) With Concomitant Radiotherapy (XRT), XELOX/RT in Squamous Cell Carcinoma of the Anal Canal [NCT00093379]Phase 220 participants (Actual)Interventional2004-04-30Completed
XELOX for 4 Months Versus 6 Months as Adjuvant Chemotherapy in Gastric Cancer After D2 Resection (LOMAC) [NCT03399110]Phase 31,032 participants (Anticipated)Interventional2017-12-01Recruiting
The Effect of Monosialotetrahexosylganglioside (GM1) in Prevention of Oxaliplatin Induced Neurotoxicity in Colorectal Cancer Patients Who Received Oxaliplatin-based Adjuvant Chemotherapy: A Multi-center, Randomized, Placebo-controlled Trial [NCT02251977]Phase 3196 participants (Actual)Interventional2014-09-30Completed
A Randomized Controlled Trial of CAPEOX vs Observation in Early-stage Colorectal Cancer Patients With Positive MRD After Curative Surgery [NCT05699746]Phase 338 participants (Anticipated)Interventional2023-03-31Not yet recruiting
Phase III Clinical Trials of UTD1 Injection Plus Capecitabine Versus Capecitabine Alone in Patients With Advanced and Metastatic Breast Cancer [NCT02253459]Phase 3405 participants (Actual)Interventional2014-08-31Completed
Effect of Low Dose Metronomic Chemotherapy in Metastatic Breast Cancer - a Two Step Study With a Retrospective Analyses Followed by a Translational Phase II Study [NCT04350021]40 participants (Anticipated)Observational2019-03-01Recruiting
A Non-Interventional Trial of Xeloda in Metastatic Colorectal Cancer, Adjuvant Colon Cancer, Advanced Gastric Cancer and Breast Cancer [NCT01664494]563 participants (Actual)Observational2010-04-30Completed
Utidelone Plus Capecitabine Versus Taxane Plus Capecitabine in HER2-negative Locally Advanced or Metastatic Breast Cancer : A Phase III, Open-label, Randomized Controlled Trial [NCT05172518]Phase 3512 participants (Anticipated)Interventional2022-03-01Not yet recruiting
NANT Pancreatic Cancer Vaccine: Molecularly Informed Integrated Immunotherapy Combining Innate High-affinity Natural Killer (haNK) Cell Therapy With Adenoviral and Yeast-based Vaccines to Induce T-cell Responses in Subjects With Pancreatic Cancer Who Have [NCT03387098]Phase 1/Phase 2173 participants (Anticipated)Interventional2018-01-02Active, not recruiting
Phase II Study of TGFβ Type I Receptor Inhibitor LY2157299 With Neoadjuvant Chemoradiation in Patients With Locally Advanced Rectal Adenocarcinoma [NCT02688712]Phase 250 participants (Anticipated)Interventional2016-03-24Active, not recruiting
An International, Multicenter, Phase II, Randomized, Parallel-arm Trial Investigating the Role of Two Different Metronomic Chemotherapy Regimens in Locally Advanced or Metastatic Triple Negative Breast Cancer Patients (TNBC) as Maintenance Therapy After F [NCT03358004]Phase 24 participants (Actual)Interventional2017-06-14Terminated(stopped due to Low accrual rate)
Nedaplatin Versus Cisplatin and Capecitabine Versus Fluorouracil in Induction Chemotherapy Plus Concurrent Chemoradiotherapy for Locoregionally Advanced NPC： a Phase 3, Multicentre, Non-inferiority, Randomised Factorial Trial [NCT03503136]Phase 3632 participants (Anticipated)Interventional2018-06-30Not yet recruiting
GRECCAR 8 : Impact on Survival of the Primary Tumor Resection in Rectal Cancer With Unresectable Synchronous Metastasis a Randomized Multicenter Study [NCT02314182]Phase 35 participants (Actual)Interventional2014-11-20Completed
A Randomized Phase III Study to Investigate the Efficacy and Safety of Docetaxel + Capecitabine vs. Vinorelbine + Capecitabine Followed by Capecitabine Alone as 1st Therapy on Locally Advanced and Metastatic Breast Cancer Patients. [NCT01126138]Phase 3200 participants (Anticipated)Interventional2010-07-31Recruiting
An Open Label Randomized Controlled Phase II Trial of Panitumumab in Combination With Epirubicin, Cisplatin and Capecitabine (ECX) Versus ECX Alone in Subjects With Locally Advanced Gastric Cancer or Cancer of the Gastroesophageal Junction. [NCT01234324]Phase 2171 participants (Actual)Interventional2010-10-31Completed
A Phase II Trial of Chemoradiotherapy and Local Excision for uT2uN0 Rectal Cancer [NCT00114231]Phase 290 participants (Actual)Interventional2006-05-31Completed
Lapatinib Versus Lapatinib With Capecitabine as Second-line Treatment in Her2-Overexpressing Metastatic Gastro-Esophageal Cancer: A Randomized Phase II Trial [NCT01145404]Phase 276 participants (Anticipated)Interventional2010-06-30Terminated(stopped due to Changes of SoC for third line therapy resulting in poor recruitment)
Toxicity OF Fluoropyrimidines: A Comparative Study of the Cardiotoxicity of capEcitabine and tEysuno [NCT01845337]Phase 259 participants (Actual)Interventional2014-02-05Completed
A Phase III Study of Novel Epothilone (Ixabepilone) Plus Capecitabine Versus Capecitabine Alone in Patients With Advanced Breast Cancer Previously Treated With an Anthracycline and a Taxane [NCT00082433]Phase 31,221 participants (Actual)Interventional2003-11-30Completed
"A 2x2 Factorial Randomized Phase III Study of Intermittent Oral Capecitabine in Combination With Intravenous Oxaliplatin (Q3W) (XELOX) With/Without Intravenous Bevacizumab (Q3W) Versus Bolus and Continuous Infusion Fluorouracil/Intravenous Leucovorin Wit [NCT00069095]Phase 32,035 participants (Actual)Interventional2003-07-31Completed
Capecitabine and Bevacizumab With Radiotherapy After 3-6 Months Chemotherapy for Patients With Oligometastatic Colorectal Cancer (OLGA Trial) [NCT01759238]Phase 21 participants (Actual)Interventional2013-05-31Terminated(stopped due to unexpectedly slow recruitment)
Metronomic Poly-chemotherapy for Metastatic Colorectal Cancer at Progression Following Established Treatments: Clinical and Laboratory Research [NCT02280694]Phase 245 participants (Actual)Interventional2015-01-31Completed
Induction Chemotherapy Combined With Neoadjuvant Immunotherapy for MSS Colon Cancer: a Prospective Single-center Multi-arm Open-label Randomized Phase II Study [NCT05914389]Phase 2100 participants (Anticipated)Interventional2023-08-31Recruiting
A Phase 3, Randomized, Double-blind, Placebo-controlled Study Evaluating Combination of TST001, Nivolumab and Chemotherapy as First-Line Treatment in Subjects With Claudin18.2 Positive Locally Advanced or Metastatic Gastric or Gastroesophageal Junction (G [NCT06093425]Phase 3950 participants (Anticipated)Interventional2023-10-31Not yet recruiting
RIBBON-LA-01: Single-arm, Open-label, Phase 2 Trial of Tislelizumab and Metronomic Capecitabine as Maintenance Therapy in High-risk Locoregionally-advanced Nasopharyngeal Carcinoma [NCT06093061]Phase 269 participants (Anticipated)Interventional2023-12-31Not yet recruiting
BRE-08: A Phase II Study of an All-Oral Adjuvant Chemotherapy Regimen of Cyclophosphamide, Methotrexate, and Capecitabine (CMC) for Early-Stage Breast Cancer [NCT06085742]Phase 225 participants (Anticipated)Interventional2023-10-31Recruiting
A Randomized, Controlled, Open-label, Multi-center Phase III Clinical Trial of SKB264 for Injection Versus Investigator Selected Regimens in Patients With Unresectable Locally Advanced, Recurrent or Metastatic Triple-negative Breast Cancer Who Have Failed [NCT05347134]Phase 3254 participants (Anticipated)Interventional2022-06-10Active, not recruiting
Serial Measurements of Molecular and Architectural Responses to Therapy (SMMART) Trial: Adaptive Clinical Treatment (ACT) [NCT05238831]Early Phase 125 participants (Anticipated)Interventional2023-12-01Not yet recruiting
A Phase II Trial of HKI-272 (Neratinib), Neratinib and Capecitabine, and Ado-Trastuzumab Emtansine for Patients With Human Epidermal Growth Factor Receptor 2 (HER2)-Positive Breast Cancer and Brain Metastases [NCT01494662]Phase 2140 participants (Actual)Interventional2012-02-29Active, not recruiting
Phase II Study of Neoadjuvant Chemotherapy With Nab-paclitaxel Plus Cisplatin and Capecitabine for Locally Advanced Thoracic Esophageal Squamous Cell Carcinoma [NCT04390958]Phase 270 participants (Anticipated)Interventional2020-05-15Recruiting
Neoadjuvant Tislelizumab With Oxaliplatin and Capecitabine in Microsatellite Stable, Locally Advanced Colon Cancer: A Prospective, Single-arm, Single-center, Exploratory Phase II Clinical Study [NCT06124378]Phase 260 participants (Anticipated)Interventional2023-11-13Recruiting
A Phase II Circulating Tumor DNA Enriched, Genomically Directed Post-neoadjuvant Trial for Patients With Residual Triple Negative Breast Cancer (PERSEVERE) [NCT04849364]Phase 2197 participants (Anticipated)Interventional2021-08-24Recruiting
A Phase II, Randomized Study of Atezolizumab (Anti-PD-L1 Antibody) and Trastuzumab in Combination With Capecitabine and Oxaliplatin (Xelox) in Patients With HER2 Positive Locally Advanced Resectable Gastric Cancer of Adenocarcinoma of Gastroesophageal Jun [NCT04661150]Phase 241 participants (Actual)Interventional2021-03-12Active, not recruiting
Personalised, Rational, Efficacy-driven Cancer Drug Dosing Via an Artificial Intelligence SystEm - CURATE.AI (PRECISE CURATE.AI Trial) [NCT04522284]Phase 1/Phase 220 participants (Anticipated)Interventional2020-08-20Recruiting
A GCIG Intergroup Multicenter Phase III Trial of Open Label Carboplatin and Paclitaxel +/- NCI-Supplied Agent: Bevacizumab (NSC #704865) Compared With Oxaliplatin and Capecitabine +/- Bevacizumab as First Line Chemotherapy in Patients With Mucinous Epithe [NCT01081262]Phase 350 participants (Actual)Interventional2010-10-12Active, not recruiting
A Phase II Pilot Study to Evaluate the Efficacy and Safety of Neoadjuvant Chemoradiotherapy With Capecitabine, Panitumumab and External Beam Radiation, in Patients With Localized, Non-Metastatic Pancreatic Adenocarcinoma [NCT01130701]Phase 20 participants (Actual)Interventional2010-05-31Withdrawn(stopped due to Study never went beyond FDA application for an IND #. FDAA required institutional DSMC which this institution then lacked.)
Pattern and Clinical Implication of Lymph Node Metastasis From Gastric Cancer Which Was Resected by Radical Surgery With Extended Lymphadenectomy [NCT02298010]899 participants (Actual)Observational2016-01-31Completed
A Phase I Study of ABT-888 in Combination With Oxaliplatin and Capecitabine in Advanced Solid Tumors [NCT01233505]Phase 116 participants (Actual)Interventional2010-10-31Terminated
Combinational Therapy of Capecitabine, Lapatinib and Vinorelbine for the Treatment of Patients With her2/Neu Positive, Relapsed or Metastatic Breast Carcinoma Following Treatment Failure With Trastuzumab [NCT01238029]Phase 112 participants (Actual)Interventional2010-10-31Terminated(stopped due to new methods of treatment, no more patients appilicable for study)
Safety, Feasibility and Cost-effectiveness of Genotype-directed Individualized Dosing of Fluoropyrimidines [NCT02324452]1,103 participants (Actual)Interventional2015-03-31Completed
An Open-Label Study of AMG 386 in Combination With Either Paclitaxel and Trastuzumab or Capecitabine and Lapatinib in Subjects With HER2-positive Locally Recurrent or Metastatic Breast Cancer [NCT00807859]Phase 165 participants (Actual)Interventional2009-03-09Completed
Phase-1 Study of Escalated-dose Pelvic Radiation Therapy Using Intensity-Modulated Radiotherapy (IMRT) With Simultaneous Integrated Boost (SIB), in Combination With Xeloda, for Initially Metastatic, Low and Middle Rectal Cancer [NCT03634202]9 participants (Actual)Interventional2015-05-05Terminated(stopped due to the study was stopped for lack of inclusion)
Window of Opportunity Study With Neoadjuvant Pembrolizumab in Colorectal Cancer [NCT03984578]Phase 250 participants (Anticipated)Interventional2019-06-12Recruiting
Neoadjuvant Chemotherapy With Xeloda in Combination With Paclitaxel in Gastric Cancer With Liver Metastasis [NCT01167049]Phase 260 participants (Anticipated)Interventional2009-08-31Recruiting
An Open-Label Randomized Phase III Study Comparing Xeloda (Capecitabine) With IV Bolus 5-Fluorouracil in Combination With Low-Dose Leucovorin as Adjuvant Chemotherapy in Patients Who Underwent Surgery for Dukes C Colon Cancer [NCT00009737]Phase 31,987 participants (Actual)Interventional1998-11-30Completed
A Phase 3 Asian Study of Sacituzumab Govitecan (IMMU-132) Versus Treatment of Physician's Choice (TPC) in Subjects With Hormonal Receptor-positive (HR+)/Human Epidermal Growth Factor Receptor 2 Negative (HER2-) Metastatic Breast Cancer (MBC) Who Have Fail [NCT04639986]Phase 3331 participants (Actual)Interventional2020-11-23Active, not recruiting
Phase II Clinical Study of Capecitabine in Combination With Mitomycin C as First-Line Treatment in Patients With Metastatic Breast Cancer [NCT01196455]Phase 239 participants (Anticipated)Interventional2006-03-31Recruiting
Randomized Phase II Trial of Combination Chemotherapy With Panitumumab or Bevacizumab for Patients With Inoperable Cholangiocarcinoma Without KRAS Mutations [NCT01206049]Phase 288 participants (Actual)Interventional2010-09-30Completed
A Phase I Study of Induction AMG 479 and Gemcitabine, Followed by AMG 479, Capecitabine, and 3D-Conformal Radiation Therapy (3D-CRT) With Subsequent Maintenance Therapy for Locally Advanced Pancreatic Cancer [NCT01298401]Phase 18 participants (Actual)Interventional2012-02-29Completed
A Phase II Randomized Trial of Telatinib in Combination With Capecitabine/Oxaliplatin Versus Capecitabine/Oxaliplatin as First-Line Therapy in Patients With HER2-negative Advanced Adenocarcinoma of the Stomach or Gastroesophageal Junction [NCT03817411]Phase 290 participants (Anticipated)Interventional2019-01-25Recruiting
MoTriColor: Phase I/II Study With Galunisertib (LY2157299) Combined With Capecitabine in Patients With Advanced Chemotherapy Resistant Colorectal Cancer and an Activated TGF-beta Signature [NCT03470350]Phase 1/Phase 20 participants (Actual)Interventional2018-08-24Withdrawn(stopped due to No study drug available. Same concept with new study drug will be explored in M19TGA study)
Perioperative Versus Preoperative Chemotherapy With Surgery in Patients With Locoregional Squamous Carcinoma of Esophagus [NCT01225523]Phase 1350 participants (Actual)Interventional1997-01-31Completed
A Pilot and Phase II Study of Altered Chemotherapy Sequencing During Neoadjuvant Therapy for Patients With Stage II or III Rectal Adenocarcinoma [NCT01302613]Phase 1/Phase 20 participants (Actual)Interventional2011-03-31Withdrawn(stopped due to Drug shortage)
[NCT01229813]Phase 3233 participants (Actual)Interventional2010-10-31Completed
A Prospective Evaluation of Capecitabine and Metabolite Pharmacokinetics in Elderly Breast and Colorectal Cancer Patients and Their Association With Toxicity and Molecular Markers of Enzyme Activity and Aging [NCT03465202]Phase 4100 participants (Anticipated)Interventional2016-05-31Not yet recruiting
Organ Preservation for Patients With Locally Advanced Rectal Adenocarcinoma: Evaluating the Efficacy of Short Course Radiation Therapy Followed by FOLFOX or CapeOX [NCT04703101]Phase 125 participants (Anticipated)Interventional2021-02-11Recruiting
Adjuvant Chemotherapy With Gemcitabine and Capecitabine Compared to Capecitabine for Biliary Tract Cancer After Curative Resection [NCT03779035]Phase 3460 participants (Anticipated)Interventional2018-12-15Recruiting
Perioperative CapeOX Chemotherapy Versus Postoperative Chemotherapy for Locally Advanced Resectable Colon Cancer: An Open Label Randomized Controlled Phase III Trial [NCT03125980]Phase 31,370 participants (Anticipated)Interventional2017-05-31Recruiting
Randomised Phase III Trial of Chemoradiotherapy With or Without Paclitaxel in Patients With Squamous-cell Anal Cancer [NCT02526953]Phase 3314 participants (Anticipated)Interventional2016-01-31Enrolling by invitation
[NCT00710736]Phase 129 participants (Actual)Interventional2008-06-30Completed
A Randomized Phase II Trial of Capecitabine and Temozolomide (CAPTEM) or FOLFIRI as SEcond-line Therapy in NEuroendocrine CArcinomas and Exploratory Analysis of Predictive Role of Positron Emission Tomography (PET) Imaging and Biological Markers [NCT03387592]Phase 2112 participants (Anticipated)Interventional2017-03-06Recruiting
Pilot / Phase III Randomized Trial Comparing Standard Systemic Therapy to Cytoreduction + Hyperthermic Intraperitoneal Mitomycin C + Standard Systemic Therapy in Patients With Limited Peritoneal Dissemination of Colon Adenocarcinoma [NCT01167725]Phase 3340 participants (Anticipated)Interventional2010-08-31Active, not recruiting
Phase II Study of IMRT Radiotherapy Concurrent Chemothrerapy for Anal Cancer [NCT03381352]Phase 227 participants (Anticipated)Interventional2015-12-02Recruiting
Phase 1 Trail to Observe Safety and Efficacy of Metronomic Capecitabine Plus PD-L1 Antibody Camrelizumab as Third-line Regimen to Treat HER2 Negative Advanced Gastric Cancer Patients [NCT04508686]Phase 120 participants (Anticipated)Interventional2020-08-01Recruiting
A Phase II Prospective Trial of mXELOXIRI Reintroduction for the Unresectable Metastatic Colorectal Cancer [NCT04508452]Phase 291 participants (Anticipated)Interventional2020-05-18Recruiting
A Pilot Study of the Combination of Entinostat With Capecitabine in High Risk Breast Cancer After Neo-adjuvant Therapy [NCT03473639]Phase 113 participants (Actual)Interventional2019-01-29Completed
Phase Ⅱ Clinical Study of RALOX or CAPOX Combined With Bevacizumab in the First-line Treatment of Advanced Colorectal Cancer [NCT03813641]Phase 2100 participants (Anticipated)Interventional2019-01-28Recruiting
Randomized Phase 2 Trial Of Two Chemotherapy Regimens Plus Or Minus Bevacizumab In Patients With Well Differentiated Pancreatic Neuroendocrine Tumors [NCT03351296]Phase 2140 participants (Anticipated)Interventional2018-06-26Recruiting
Targeting Myeloid Derived Suppressor Cells in Recurrent Glioblastoma: Phase 0/1 Trial of Low Dose Capecitabine + Bevacizumab in Patients With Recurrent Glioblastoma [NCT02669173]Phase 112 participants (Actual)Interventional2016-10-11Active, not recruiting
A Pilot Study in Gastric Cancer of Assignment to Postoperative Chemoradiation or Chemotherapy Based Upon Surgical Lymph Node Assessment After Preoperative Chemotherapy, With Gene Assay as Correlate of Biologic Response [NCT03515941]Early Phase 16 participants (Actual)Interventional2018-06-22Terminated(stopped due to The PI has decided to close the study due to the outdated study design.)
NANT Pancreatic Cancer Vaccine: Molecularly Informed Integrated Immunotherapy Combining Innate High-affinity Natural Killer (haNK) Cell Therapy With Adaptive T-cell Therapy (Adenovirus, Yeast, Fusion Protein Vaccine) in Subjects With Pancreatic Cancer Who [NCT03329248]Phase 1/Phase 280 participants (Anticipated)Interventional2017-11-06Active, not recruiting
An Open-label, Randomized, Phase II Clinical Trial Comparing the Efficacy and Safety of Intraperitoneal and System Chemotherapy Versus XELOX as First-line Chemotherapy for Metastatic Colorectal Cancer [NCT03792269]Phase 2100 participants (Anticipated)Interventional2016-01-01Recruiting
A Multinational, Multicenter, Randomized, Phase 3 Study of Tesetaxel Plus a Reduced Dose of Capecitabine Versus Capecitabine Alone in Patients With HER2 Negative, HR Positive, Locally Advanced or Metastatic Breast Cancer Previously Treated With a Taxane [NCT03326674]Phase 3685 participants (Actual)Interventional2017-12-21Terminated(stopped due to The Sponsor has discontinued the development of tesetaxel)
A Phase II Study of Sequential Capecitabine Plus Oxaliplatin (XELOX) Followed by Docetaxel Plus Capecitabine (TX) in Patients With Unresectable Gastric [NCT01331928]Phase 251 participants (Anticipated)Interventional2011-01-31Recruiting
Phase II Trial of Accelerated Fraction Radiotherapy With Concomitant Capecitabine as Neoadjuvant Therapy of Resectable and Borderline Resectable Pancreas Cancer [NCT01333332]Phase 235 participants (Anticipated)Interventional2010-08-31Recruiting
Precise Targeted Therapy for Refractory HER2 Positive Advanced Breast Cancer Based on Genome Signature and Drug Sensitivity of PDO Model [NCT05429684]Phase 3120 participants (Anticipated)Interventional2021-01-01Recruiting
Sacituzumab Govitecan in Combination With Capecitabine for Advanced Gastrointestinal Cancers After Progression on Standard Therapy [NCT06065371]Phase 120 participants (Anticipated)Interventional2024-02-29Not yet recruiting
A Single-arm, Open-label，Phase Ib Clinical Study of ZKAB001 Combined With Capecitabine in Adjuvant Therapy for Patients With Biliary Tract Cancer After Radical Resection [NCT04608786]Phase 110 participants (Anticipated)Interventional2021-02-01Enrolling by invitation
Phase I/II Trial of Motesanib in Combination With Ixabepilone and Capecitabine in Women With Locally Recurrent or Metastatic Breast Cancer [NCT01349088]Phase 1/Phase 20 participants (Actual)Interventional2013-12-31Withdrawn
A Phase II Study Induction Chemotherapy, Neoadjuvant Chemoradiotherapy, Surgical Resection and Adjuvant Chemotherapy for Patients With Locally Advanced, Resectable Pancreatic Adenocarcinoma [NCT00609336]Phase 235 participants (Actual)Interventional2008-01-31Completed
Adjuvant Chemotherapy Versus Observation in Stage II Colon Cancer Patients With High-Risk Factors and High-Immunoscore® [NCT04303429]Phase 3962 participants (Anticipated)Interventional2020-08-31Not yet recruiting
A Phase I Study, With Expanded Cohort, of Biweekly Fixed-dose Rate Gemcitabine Plus Capecitabine in Patients With Advanced Pancreatic and Biliary Carcinomas [NCT00626158]Phase 145 participants (Actual)Interventional2008-02-29Completed
PD1 Antibody Toripalimab and Chemoradiotherapy for dMMR/MSI-H Locally Advanced Colorectal Cancer [NCT04301557]Phase 225 participants (Anticipated)Interventional2020-07-31Recruiting
Effect of PD-1 Antibody (SHR-1210) Combined With Capecitabine Treatment After Resection of Intrahepatic Cholangiocarcinoma With High Risk of Recurrence : a Phase 2 Study. [NCT04295317]Phase 265 participants (Anticipated)Interventional2020-08-01Recruiting
Liposomal iRInotecan, Carboplatin or oXaliplatin in the First Line Treatment of Esophagogastric Cancer: a Randomized Phase 2 Study [NCT03764553]Phase 2310 participants (Anticipated)Interventional2019-05-01Recruiting
A Multicenter Phase II Clinical Study of Bevacizumab Combined With Biweekly XELOX/XELIRI Alternative First-line Treatment for Unresectable Advanced Colorectal Cancer [NCT04324476]Phase 250 participants (Anticipated)Interventional2019-09-01Recruiting
A Multicenter Randomized Phase III Study to Compare the Combination Trastuzumab and Capecitabine, With or Without Pertuzumab, in Patients With HER2-Positive Metastatic Breast Cancer That Have Progressed After One Line of Trastuzumab-Based Therapy in the M [NCT01026142]Phase 3452 participants (Actual)Interventional2010-01-26Completed
A Prospective, Multi-cohort, Single-center Phase II Clinical Study of Chemoradiotherapy Sequential Fluzoparib in Pan-solid Tumors [NCT06055166]Phase 2120 participants (Anticipated)Interventional2023-11-01Not yet recruiting
A Randomized Trial Comparing Early Local Chemoradiation Therapy +/- Surgery Versus Systemic Therapy for Patients With Esophageal or Gastric Cancer With Oligometastases [NCT03161522]Phase 2100 participants (Anticipated)Interventional2018-02-19Recruiting
A Phase II, Randomised, Multi-Centre Study Evaluating Lapatinib in Combination With Vinorelbine or Capecitabine in Women With ErbB2 Overexpressing Metastatic Breast Cancer [NCT01013740]Phase 2112 participants (Actual)Interventional2009-11-25Completed
JCOG1801: A Phase III Randomized Controlled Trial Comparing Surgery Plus Adjuvant Chemotherapy With Preoperative Chemoradiotherapy Followed by Surgery Plus Adjuvant Chemotherapy for Locally Recurrent Rectal Cancer (RC-SURVIVE Study) [NCT04288999]Phase 3110 participants (Anticipated)Interventional2019-10-01Recruiting
Phase II Study of Bevacizumab Combined With Capecitabine and Oxaliplatin (CAPOX) in Patients With Advanced Adenocarcinoma of the Small Bowel or Ampulla of Vater [NCT01208103]Phase 230 participants (Actual)Interventional2011-05-06Completed
Phase I/II Study of Azacitidine and CAPOX (Capecitabine + Oxaliplatin) in Metastatic Colorectal Cancer Patients Enriched for Hypermethylation of CpG Promoter Islands [NCT01193517]Phase 1/Phase 226 participants (Actual)Interventional2010-08-31Completed
A Multicenter Phase II Study of Gemcitabine, Capecitabine and Bevacizumab for Locally Advanced or Metastatic Adenocarcinoma of the Gall Bladder or Biliary Ducts. [NCT01007552]Phase 250 participants (Actual)Interventional2009-12-31Completed
Phase II, Multicenter, Open-label, Non-randomized Study of Neoadjuvant Chemotherapy With Selective Radiotherapy Use in Patients With Intermediate-Risk Cancer of the Rectum Defined by Magnetic Resonance Imaging [NCT00909987]Phase 246 participants (Actual)Interventional2009-03-31Completed
Phase I Dose Escalation Trial of External Beam Radiation and Cyberknife Radiosurgery Boost With Concurrent Capecitabine for Hilar Cholangiocarcinoma (Klatskin Tumor) [NCT00630890]Phase 111 participants (Actual)Interventional2007-10-31Terminated(stopped due to investigator left UCSF and study was closed prematurely in 2008. No results to report.)
Phase II Study of a Novel Capecitabine Dosing Schedule in Combination With Lapatinib, Based on the Norton-Simon Mathematical Method in Patients With HER2 Overexpressed/Amplified, Trastuzumab (Herceptin) -Refractory, Metastatic Breast Cancer [NCT00721630]Phase 224 participants (Actual)Interventional2008-07-31Completed
Effect of Second-line Irinotecan and Capecitabine Versus Irinotecan Alone in Advanced Biliary Tract Cancer Patients Progressed After First-line Gemcitabine and Cisplatin: A Randomized Controlled Study [NCT02558959]Phase 264 participants (Actual)Interventional2015-09-01Completed
A Phase II Trial of Neoadjuvant Chemoradiation (CRT) and Pembrolizumab in Patients With Rectal Cancer: Hoosier Cancer Research Network GI15-213 [NCT02586610]Phase 20 participants (Actual)Interventional2016-10-31Withdrawn(stopped due to Dr. Rahma decided to run the study through a different group)
Phase III Study of Neoadjuvant Chemotherapy With Capecitabine and Oxaliplatin Versus Chemoradiation for Locally Advanced Rectal Cancer Patients [NCT02288195]Phase 3663 participants (Actual)Interventional2014-08-13Active, not recruiting
A Randomized, Open-Label, Multiple-center, Phase II Study to Evaluate the Efficacy and Safety of Margetuximab Plus Chemotherapy vs Trastuzumab Plus Chemotherapy in the Treatment of Chinese Patients With HER2+ Metastatic Breast Cancer Who Have Received Pri [NCT04262804]Phase 2123 participants (Actual)Interventional2020-01-13Active, not recruiting
A Double-Blind, Randomized, Phase 2 Trial of Capecitabine Plus Enzastaurin Versus Capecitabine Plus Placebo in Patients With Metastatic or Recurrent Breast Cancer Previously Treated With an Anthracycline and a Taxane [NCT00437294]Phase 286 participants (Actual)Interventional2007-03-31Terminated(stopped due to Lack of efficacy)
A Randomized, Phase II Study of Concurrent Radiotherapy and Oxaliplatin, Capecitabine With or Without Cetuximab in Rectal Cancer Tumor Stratified by KRAS Mutation Status. [NCT00795301]Phase 274 participants Interventional2008-07-31Active, not recruiting
A Randomized Study of the Effect of Maintenance Therapy With Bevacizumab + Capecitabine Versus Bevacizumab Alone on Progression-free Survival in Patients With HER2-negative Metastatic Breast Cancer That Has Not Progressed During First-line Docetaxel Plus [NCT00929240]Phase 3287 participants (Actual)Interventional2009-07-31Completed
Maintenance and Reinduction Chemotherapy With Avastin in Metastatic Colon Cancer: The MARTHA (SICOG 0803) Trial [NCT00797485]Phase 3672 participants (Anticipated)Interventional2008-07-31Recruiting
Second Line ERIbulin Followed by CApecitabine or the Reverse Sequence in HER2-negative Metastatic Breast Cancer (MBC) Patients: a Randomized Phase II Study - ERICA Trial [NCT05833919]Phase 2122 participants (Actual)Interventional2018-07-30Active, not recruiting
Neoadjuvant Chemotherapy Versus Standard Treatment in Patients With Locally Advanced Colon Cancer [NCT01918527]Phase 3250 participants (Actual)Interventional2013-09-30Active, not recruiting
Phase II Study of Pyrotinib in Combination With Capecitabine in Patients With Trastuzumab-resistant HER2-positive Advanced Breast Cancer [NCT04001621]Phase 2100 participants (Anticipated)Interventional2019-06-26Active, not recruiting
Total Neoadjuvant Induction and Consolidation CapeOX Plus Neoadjuvant Intensity Modulated Radiotherapy With Concurrent Capecitabine for MRI Defined High-risk Rectal Cancer [NCT02864849]Phase 281 participants (Actual)Interventional2016-08-31Completed
Camrelizumab Combined With Apatinib 、XELOX 、RFA in the Treatment of Liver Metastases of Colorectal Cancer: One-arm Exploratory Clinical Study [NCT04202978]Phase 1/Phase 223 participants (Anticipated)Interventional2020-03-01Recruiting
Phase Ib Study To Evaluate The Safety Of Combining IGF-1R Antagonist R1507 With Multiple Standard Chemotherapy Drug Treatments In Patients With Advanced Malignancies [NCT00811993]Phase 1104 participants (Actual)Interventional2009-02-28Terminated
Randomized Trial of Concurrent Cisplatin Chemoradiotherapy Plus Capecitabine Adjuvant Chemotherapy vs Concurrent Cisplatin Chemoradiotherapy Alone for Patients With Local Advanced Nasopharyngeal Carcinoma at High Risk of Distant Metastasis [NCT02973386]Phase 3278 participants (Anticipated)Interventional2017-01-31Recruiting
Phase II Study of Pembrolizumab Plus Capecitabine and Bevacizumab in Microsatellite Stable Metastatic Colorectal Cancer [NCT03396926]Phase 244 participants (Actual)Interventional2018-04-18Active, not recruiting
A Phase II Study of Capecitabine, Oxaliplatin and Selenomethionine and Radiation Therapy in Patients With Stage II and III Rectal Adenocarcinoma [NCT00625183]Phase 25 participants (Actual)Interventional2008-03-31Terminated(stopped due to Withdrawn due to poor/low accrual)
Multicenter, Open-label, Randomized Phase III to Evaluate Efficacy of Maintenance Treatment With Capecitabine Following Standard Adjuvant Chemotherapy in Operable Triple Negative Breast Cancer Patients [NCT00130533]Phase 3876 participants (Actual)Interventional2006-01-31Completed
REAL 3 : A Randomised Open-labelled Multicentre Trial of the Efficacy of Epirubicin, Oxaliplatin and Capecitabine (EOX) With or Without Panitumumab in Previously Untreated Advanced Oesophago-gastric Cancer [NCT00824785]Phase 3574 participants (Actual)Interventional2008-05-31Terminated(stopped due to Lack of efficacy)
Envafolimab Combined With XELOX in Neoadjuvant Therapy for Locally Advanced Colon Cancer，A Prospective, Single Arm, Single Center ǁ Phase Clinical Trial [NCT05335460]Phase 236 participants (Anticipated)Interventional2022-05-31Not yet recruiting
Randomized Phase II Study Assessing the Efficacy and Safety of 2 Therapeutic Strategies Combining Bevacizumab With Chemotherapy: De-escalation Versus Escalation in Patients With Non-pretreated Unresectable Metastatic Colorectal Cancer [NCT02842580]Phase 220 participants (Actual)Interventional2016-09-30Terminated(stopped due to Inclusion rythm too slow.)
Oxaliplatin Plus Gemcitabine Versus Capecitabine Alone as Adjuvant Treatment in the Prevention of Recurrence of Intrahepatic Cholangiocarcinoma [NCT02548195]Phase 3286 participants (Anticipated)Interventional2015-07-31Recruiting
A Phase II Study of Endostar (Recombinant Human Endostatin ®) With Cisplatin and Capecitabine (Xeloda) as 1st Line Treatment in the Advanced Gastric Cancer [NCT00842491]Phase 245 participants (Actual)Interventional2008-11-30Completed
A Single-Center, Phase II Trial of Sunitinib and Capecitabine in First Line Treatment of Patients With Metastatic Colorectal Cancer [NCT00961571]Phase 250 participants (Actual)Interventional2009-08-31Terminated(stopped due to Unanticipated side effects and futility)
A Pharmacokinetic Study of Capecitabine in Patients Undergoing Peri-operative Chemotherapy and a Total Gastrectomy for Adenocarcinoma of the Stomach [NCT00871273]Phase 413 participants (Actual)Interventional2009-11-30Terminated(stopped due to 1. Slow recruitment; 2. Change to clinical environment reducing the pool of potentially eligible patients; 3. Availability of data from another similar study)
Maintenance Tislelizumab Combined With Capecitabine to Treat Metastatic Colorectal Cancer With No Evidence of Disease [NCT05360277]Phase 252 participants (Anticipated)Interventional2023-08-22Recruiting
A Phase 1b/2 Dose Escalation and Expansion Study of Tucatinib in Combination With Trastuzumab and Oxaliplatin-based Chemotherapy or Pembrolizumab-containing Combinations for HER2+ Gastrointestinal Cancers [NCT04430738]Phase 1/Phase 2120 participants (Anticipated)Interventional2020-09-15Recruiting
A Phase II Study of Intraperitoneal and Intravenous Paclitaxel Chemotherapy With Oral Capecitabine for Gastric Adenocarcinoma With Peritoneal Carcinomatosis [NCT04034251]Phase 212 participants (Actual)Interventional2020-06-09Active, not recruiting
A Phase III Study of Gemcitabine Plus Capecitabine (GEMCAP) Versus Gemcitabine Alone in Advanced Biliary Cancer [NCT00658593]Phase 319 participants (Actual)Interventional2008-10-10Terminated(stopped due to due to poor accrual)
An Open-Label, Multicenter Study of IBI308 in Subjects With Selected Advanced Solid Tumors [NCT02937116]Phase 1233 participants (Actual)Interventional2016-10-19Completed
A Phase I and Pharmacokinetics Study of Docetaxel in Combination With Capecitabine and Cisplatin in Solid Tumors [NCT00084734]Phase 161 participants (Actual)Interventional2002-05-31Completed
A Study to Characterize and Evaluate Biomarkers of Chemotherapy in Patients With Metastatic Colorectal Cancer In The First-line Setting [NCT03532711]264 participants (Actual)Observational2012-01-01Completed
SRT Versus WBRT Combined With Pyrrotinib and Capecitabine in the Treatment of HER2-positive Advanced Breast Cancer Patients With Brain Metastases: A Randomized Controlled, Prospective Clinical Study [NCT05042791]Phase 2362 participants (Anticipated)Interventional2022-03-01Recruiting
X-TRAP: Phase I/II Study of Capecitabine Plus Aflibercept in Metastatic Colorectal Cancer [NCT01661972]Phase 1/Phase 263 participants (Actual)Interventional2012-08-31Completed
A Randomized Phase II Study of S-1 Versus Capecitabine as First-Line Chemotherapy in the Elderly and/or Poor Performance Status Patients With Recurrent or Metastatic Gastric Cancer [NCT00580359]Phase 296 participants (Anticipated)Interventional2007-05-31Recruiting
Phase IV Multi-Institutional Randomized Trial of Capecitabine Plus Oxaliplatin With Herceptin in Patients With Potentially Resectable HER-2 Positive Gastric Cancer With Liver Metastasis [NCT02380131]Phase 460 participants (Anticipated)Interventional2013-02-28Recruiting
Preoperative Short-course Radiation Followed by Envafolimab Plus CAPEOX for MSS Locally Advanced Rectal Adenocarcinoma (PRECAM): An Open Label, Prospective, Single Arm Clinical Trial [NCT05216653]Phase 232 participants (Actual)Interventional2022-04-07Active, not recruiting
NANT Pancreatic Cancer Vaccine: Combination Immunotherapy in Subjects With Pancreatic Cancer Who Have Progressed on or After Standard-of-care Therapy [NCT03136406]Phase 1/Phase 23 participants (Actual)Interventional2017-08-14Active, not recruiting
Watch and Wait Strategy in Patients With Locally Advanced Rectal Cancer After Neoadjuvant Chemoradiotherapy: A Multi-centre, Adaptive-design, Phase II Prospective Cohort Study [NCT04443543]Phase 2222 participants (Anticipated)Interventional2020-06-22Not yet recruiting
A Randomized, Open-label Phase III Trial to Evaluate the Efficacy and Safety of Pertuzumab Retreatment in Previously Pertuzumab, Trastuzuamb and Chemotherapy Treated Her2-Positive Metastatic Advanced Breast Cancer [NCT02514681]Phase 3370 participants (Anticipated)Interventional2015-08-01Active, not recruiting
The Comparison of XELOX and EOX in the First-line Treatment of Advanced Gastric Cancer: An Open-label, Multi-center, Prospective and Randomised Study [NCT02395640]Phase 3438 participants (Anticipated)Interventional2015-03-31Completed
Camrelizumab Plus Pyrotinib Plus Chemotherapy in Human Epidermal Growth Factor Receptor 2 Positive (HER2+) Advanced Gastric or Gastroesophageal Junction (GEJ) Adenocarcinoma [NCT05111444]Phase 265 participants (Anticipated)Interventional2021-12-31Not yet recruiting
Evaluation of Pathological Response in Patient With Resectable Gastric Cancer and Perioperative Chemotherapy FLOT Versus XELOX; Phase 2 [NCT04937738]Phase 2284 participants (Anticipated)Interventional2021-07-21Active, not recruiting
A Phase 2, International, Multicenter, Open-labeled, Randomized Trial of PAlbociclib and Fulvestrant vs. Standard Oral Capecitabine In Patients With Hormone Receptor (HR)+ / HER2- Advanced Breast Cancer and Documented Endocrine Resistance [NCT03322215]Phase 242 participants (Actual)Interventional2017-10-24Active, not recruiting
Phase II Clinical Study of the Maintenance Therapy of Capecitabine Afer the XELOX in Treatment of Advanced Gastric Cancer [NCT02038621]Phase 2224 participants (Anticipated)Interventional2014-01-31Not yet recruiting
Phase III Study of Palbociclib in Combination With Exemestane or Fulvestrant vs. Chemotherapy (Capecitabine) in Hormonal Receptor Positive/HER2 Negative Metastatic Breast Cancer Patients With Resistance to Aromatase Inhibitors [NCT02028507]Phase 3693 participants (Actual)Interventional2014-03-13Completed
Randomized Phase III Trial of 5-FU Based Maintenance Therapy With or Without Panitumumab in Patients With RAS Wild Type Metastatic Colorectal Cancer After Induction With FOLFOX + Panitumumab [NCT03300609]Phase 34 participants (Actual)Interventional2018-02-27Terminated(stopped due to Insufficient Accrual)
Tislelizumab Combined With XELOX as Neoadjuvant Therapy for G/GEJ Adenocarcinoma: A Single-center, Single-arm, Phase Ⅱ Study [NCT05507658]Phase 230 participants (Anticipated)Interventional2022-07-18Recruiting
A Multicenter Open-label Randomized Controlled Prospective Phase II Study Evaluating the Efficacy of Selective Internal Radiation Therapy (Yttrium-90 Glass Microspheres) Combined With Capecitabine in the Neoadjuvant Setting of Operable Intrahepatic CHOlan [NCT05265208]Phase 262 participants (Anticipated)Interventional2022-02-04Suspended(stopped due to 1st level of sequential inclusion reached)
Randomized Phase 2 Study of Valproic Acid in Combination With Bevacizumab and Oxaliplatin/Fluoropyrimidine Regimens in Patients With Ras-mutated Metastatic Colorectal Cancer [NCT04310176]Phase 2200 participants (Anticipated)Interventional2019-05-24Recruiting
A Phase Ib/II Clinical Study of BBI503 in Combination With Selected Anti-Cancer Therapeutics in Adult Patients With Advanced Cancer [NCT02483247]Phase 1165 participants (Actual)Interventional2015-09-30Completed
Comparison of Efficacy and Tolerance Between Combination Therapy and Monotherapy as a First Line Chemotherapy in Elderly Patient With Advanced Gastric Cancer; Multicenter Randomized Phase 3 Study [NCT02114359]Phase 3111 participants (Actual)Interventional2014-02-28Completed
NEOadjuvant Chemotherapy Only Compared With Standard Treatment for Locally Advanced Rectal Cancer: a Randomized Phase II Trial [NCT03280407]Phase 2124 participants (Anticipated)Interventional2017-03-01Recruiting
Randomized Controlled Trial of S-1 Maintenance Therapy in Metastatic Esophagogastric Cancer [NCT02128243]Phase 2242 participants (Actual)Interventional2014-09-30Completed
A Prospective, Open-lable, Multicenter, Randomized, Controlled Phase II Clinical Trial to Evaluate the Efficacy of Irinotecan Versus Oxaliplatin in the First-line Treatment of Refractory Metastatic Colorectal Cancer [NCT03567629]Phase 2130 participants (Anticipated)Interventional2018-05-29Active, not recruiting
A Phase III Trial of XELOX (Xeloda/Oxaliplatin) Followed by Xeloda Maintenance Versus Best Supportive Care (BSC) in Metastatic Colorectal Cancer [NCT02060669]Phase 310 participants (Actual)Interventional2010-06-20Terminated(stopped due to others)
[NCT02071043]Phase 248 participants (Actual)Interventional2008-11-30Completed
TISLELIZUMAB in Combination With Anlotinib and Chemotherapy(XELOX) as First-Line Treatment in Adults With Inoperable, Advanced or Metastatic Gastric, or Gastroesophageal Junction Carcinoma [NCT04963088]Phase 1/Phase 266 participants (Anticipated)Interventional2021-03-06Recruiting
A Rollover Protocol to Allow Continued Access to Tivozanib (AV 951) for Subjects Enrolled in Other Tivozanib Protocols [NCT01369433]225 participants (Actual)Interventional2010-06-30Terminated(stopped due to Lack of new studies contributing subjects to this study)
Phase II Study of First-line Capecitabine Plus Oxaliplatin Plus Aflibercept for 6 Cycles Followed by Capecitabine Plus Aflibercept as Maintenance Therapy in Patients With Metastatic Colorectal Cancer: DROP and GO Trial [NCT02085005]Phase 20 participants (Actual)Interventional2014-03-31Withdrawn
Efficacy of Postoperative Adjuvant Chemotherapy for Stage II Colon Cancer With High Risk Factors(EPAC1) [NCT03199989]Phase 31,254 participants (Anticipated)Interventional2017-06-01Recruiting
QUILT-3.048: NANT Urothelial Cancer Vaccine: Combination Immunotherapy in Subjects With Urothelial Cancer Who Have Progressed on or After Chemotherapy and Anti-programmed Cell Death Protein 1 (PD-1)/Programmed Death-ligand 1 (PD-L1) Therapy [NCT03197571]Phase 1/Phase 20 participants (Actual)Interventional2017-12-31Withdrawn(stopped due to Trial not initiated)
Trastuzumab Plus XELOX for HER2-positive Stage III Gastric Cancer After D2 Gastrectomy：Prospective Observational Study. [NCT02250209]Phase 240 participants (Anticipated)Interventional2014-07-31Recruiting
A Phase II Trial of AK104 Combined With Neoadjuvant Chemoradiotherapy in Proficient Mismatch Repair/Microsatellite Stable Locally Advanced Rectal Cancer [NCT05980689]Phase 233 participants (Anticipated)Interventional2023-10-24Recruiting
Total Neoadjuvant trEatment to Increase the Clinical Complete reSponse Rate for diStal Locally Advanced Rectal Cancer (TESS) [NCT03840239]Phase 298 participants (Anticipated)Interventional2018-12-25Active, not recruiting
Optimisation of Response for Organ Preservation in Rectal Cancer : Neoadjuvant Chemotherapy and Radiochemotherapy vs. Radiochemotherapy [NCT02514278]Phase 3218 participants (Actual)Interventional2016-01-28Active, not recruiting
A Phase I Clinical Trial of Capecitabine and SIR-Spheres® Y-90-Radioembolization in Patients With Advanced Intrahepatic Cholangiocarcinoma [NCT03117855]Phase 10 participants (Actual)Interventional2016-12-31Withdrawn(stopped due to Company no longer interested in supporting this trial)
A Randomized, Multicenter, Controlled Study of XELOX (Oxaliplatin With Capecitabine) Combined With Apatinib Versus XELOX as Post-operative Chemotherapy in Locally Advanced Gastric Signet Ring Carcinoma With D2 Dissection. [NCT03355612]Phase 3456 participants (Anticipated)Interventional2017-12-20Not yet recruiting
Phase I/II Study of Stereotactic Radiosurgery With Concurrent Administration of DNA Damage Response (DDR) Inhibitor (OLAparib) Followed by Adjuvant Combination of DuRvalumab (MEDI4736) and Physician's Choice Systemic Therapy in Subjects With BreAst Cancer [NCT04711824]Phase 1/Phase 241 participants (Anticipated)Interventional2022-03-09Recruiting
Concurrent Xeloda and Radiotherapy for Bone Metastases [NCT00192777]Phase 220 participants (Anticipated)Interventional2004-11-30Recruiting
Phase I/II Study With Galunisertib Combined With Capecitabine in Patients With Advanced Chemotherapy Resistant Colorectal Cancer With Peritoneal Metastases [NCT05700656]Phase 1/Phase 231 participants (Anticipated)Interventional2023-04-30Not yet recruiting
Precision Treatment of Luminal Advanced Breast Cancer Based on Molecular Subtyping [NCT04355858]Phase 2319 participants (Anticipated)Interventional2020-05-01Recruiting
A Single-center Prospective Single-arm Study of the Efficacy of Carrelizumab (PD-1) Combined With Chemotherapy in Neoadjuvant Treatment of Locally Advanced Gastric Cancer and Its Effect on Tumor Immune Microenvironment [NCT05545436]Phase 234 participants (Anticipated)Interventional2022-09-20Recruiting
CAPEcitabine eXtension of Adjuvant Therapy for Pancreatic Adenocarcinoma: (CAPE-X) [NCT06110598]Phase 286 participants (Anticipated)Interventional2024-01-31Not yet recruiting
A Phase lb/ll, Open Label, Single Arm Study to Assess Efficacy and Safety of Alpelisib and Capecitabine in Patients With PIK3CA Mutant Metastatic Colorectal Cancer Who Failed Two Prior Standard Chemotherapies [NCT04753203]Phase 1/Phase 265 participants (Anticipated)Interventional2021-02-28Active, not recruiting
A Phase lb/ll, Multicenter, Open Label, Single Arm Study to Assess the Safety and Efficacy of the Anti-VEGFR2 Monoclonal Antibody Olinvacimab and the Capecitabine in Patients With mCRC Who Failed Two Prior Chemotherapies [NCT04751955]Phase 1/Phase 20 participants (Actual)Interventional2022-01-01Withdrawn(stopped due to This clinical trial was not finally approved by the Korea FDA.)
a Phase II, Open-label, Single Arm Study of Sintilimab (an Anti-PD-1 Inhibitor) Combined With Apatinib and Capecitabine in Advanced Hepatocellular Carcinoma [NCT04411706]Phase 246 participants (Anticipated)Interventional2020-06-21Recruiting
Pd1 Antibody Sintilimab ± Chemoradiotherapy for Locally Advanced Rectal Cancer [NCT04304209]Phase 2195 participants (Anticipated)Interventional2019-10-28Active, not recruiting
A Multicenter Randomized Phase Ⅲ Clinical Trial of Gemcitabine in Combination With Capecitabine Versus Gemcitabine Plus Carboplatin as First-line Treatment in Triple-negative Recurrent or Metastatic Breast Cancer [NCT02207335]Phase 3120 participants (Anticipated)Interventional2013-12-31Recruiting
A Phase II/III, Randomized, Open-label, Multi-center Study to Evaluate the Efficacy and Safety of QL1706 in Combination With Bevacizumab and/or Chemotherapy Versus Sintilimab in Combination With Bevacizumab as First-line Treatment in Patients With Advance [NCT05976568]Phase 2/Phase 3668 participants (Anticipated)Interventional2023-09-01Not yet recruiting
An Open-label Study of Xeloda Plus Taxotere on Treatment Response in Patients With HER2-neu-negative, and the Addition of Herceptin for HER2-neu-positive Breast Cancer [NCT00127933]Phase 4157 participants (Actual)Interventional2005-08-31Completed
Integrating Gene Signatures to Guide HR+MBC Therapy in a Diverse Cohort (INSIGHT) [NCT05693766]Phase 264 participants (Anticipated)Interventional2023-09-11Recruiting
A Phase I Trial of Capecitabine in Combination With Cemiplimab in Patients With Hormone Receptor Positive Metastatic Breast Cancer [NCT05064085]Phase 113 participants (Actual)Interventional2021-10-12Active, not recruiting
A Randomized, Double-blind, Multicenter, Phase III Study Comparing the Efficacy and Safety of AK104 Plus Oxaliplatin and Capecitabine (XELOX) Versus Placebo Plus XELOX as First-line Treatment for Locally Advanced Unresectable or G/GEJ Adenocarcinoma [NCT05008783]Phase 3588 participants (Anticipated)Interventional2021-09-17Recruiting
A Double-Blind, Randomized Phase 2b Study of Sorafenib Compared to Placebo When Administered in Combination With Chemotherapy for Patients With Locally Advanced or MBC That Has Progressed During or After Bevacizumab Therapy [NCT00493636]Phase 2160 participants (Actual)Interventional2007-06-30Completed
An Open-Label Phase II Trial of Neratinib Plus Capecitabine in Subjects With HER2-Negative Metastatic Breast Cancer With Brain Metastases and Abnormally Active HER2 Signaling [NCT04965064]Phase 222 participants (Anticipated)Interventional2022-09-23Recruiting
A Phase II Trial of Postoperative Chemotherapy and Chemo-radiotherapy for Resected Adenocarcinoma of the Stomach and Gastro-esophageal Junction [NCT00718913]Phase 240 participants (Actual)Interventional2008-04-30Completed
Efficacy and Safety of Neoadjuvant Chemoradiotherapy Combined With PD-1 Inhibitor and Thymalfasin in pMMR/MSS Locally Advanced Middle and Low Rectal Cancer: An Open, Multi-center, Prospective, Single-arm Phase II Clinical Study [NCT06056804]Phase 220 participants (Anticipated)Interventional2023-12-01Not yet recruiting
Systemic Therapy Combined With Thoracic Concurrent Chemoradiotherapy Versus Systemic Therapy Alone in Stage IVB Esophageal Squamous Cell Carcinoma: A Prospective Randomized Phase II Study [NCT05512520]Phase 2126 participants (Anticipated)Interventional2022-09-20Recruiting
A Randomized, Multicenter, Phase 3 Study of Zanidatamab in Combination With Chemotherapy With or Without Tislelizumab in Subjects With HER2-positive Unresectable Locally Advanced or Metastatic Gastroesophageal Adenocarcinoma (GEA) [NCT05152147]Phase 3714 participants (Anticipated)Interventional2021-12-02Recruiting
A Phase III Study of Consolidative Radiotherapy in Patients With Oligometastatic HER2 Negative Esophageal and Gastric Adenocarcinoma (EGA) [NCT04248452]Phase 3314 participants (Anticipated)Interventional2020-05-26Recruiting
A Randomized Phase II Study of Temozolomide or Temozolomide and Capecitabine in Patients With Advanced Pancreatic Neuroendocrine Tumors [NCT01824875]Phase 2144 participants (Actual)Interventional2013-08-08Active, not recruiting
An Open Label Study to Evaluate the Safety of Xeloda as Adjuvant Monotherapy in Patients Who Have Undergone Surgery for Colon Cancer, Dukes Stage C. [NCT00502671]Phase 4228 participants (Actual)Interventional2007-07-31Completed
Randomized Controlled Trial Comparing Conventional and Fast Track Multi-Discipline Treatment Interventions for Colorectal Cancer [NCT01080547]Phase 3374 participants (Actual)Interventional2010-03-31Completed
A Pilot Safety And Feasibility Study Of Concurrent Capecitabine (Xeloda) And External Beam Irradiation In The Adjuvant Treatment Of High Risk Early Stage Breast Cancer. [NCT00562718]Phase 250 participants (Actual)Interventional2004-09-30Completed
An Open-label, Phase II Study of Capecitabine Plus Gemcitabine in Patients With Locally Advanced or Metastatic Pancreatic Cancer [NCT02565641]Phase 263 participants (Actual)Interventional2003-03-31Completed
A Multicenter Phase II Study of the Capecitabine, Oxaliplatin and Bevacizumab as First-line Treatment in Elderly Patients With Metastatic Colorectal Cancer [NCT01024504]Phase 246 participants (Anticipated)Interventional2006-03-31Completed
Phase I/II of Neoadjuvant Accelerated Short Course Radiation Therapy With Proton Beam and Capecitabine for Resectable Pancreatic Cancer [NCT00438256]Phase 1/Phase 250 participants (Actual)Interventional2007-12-31Completed
Open Label, Phase II Study of Capecitabine (Xeloda®) as Fluoropyrimidine of Choice in Combination With Chemotherapy in Patients With Advanced and/or Metastatic Gastric Cancer Suitable for Treatment With a Fluoropyrimidine-Based Regimen [NCT00454636]Phase 2158 participants (Actual)Interventional2007-03-31Completed
A Phase 1 Study Of Sunitinib Malate In Combination With Cisplatin/Capecitabine Or Oxaliplatin/Capecitabine In Patients With Advanced Gastric Cancer [NCT00555620]Phase 176 participants (Actual)Interventional2008-05-31Completed
A Single Arm, Open-label Study to Evaluate the Efficacy on Tumor Response and the Safety of Bevacizumab and Trastuzumab Combination and Sequential Capecitabine in Patients With HER2 +Ive Locally Recurrent or Metastatic Breast Cancer After Early Relapse to [NCT00964704]Phase 20 participants (Actual)Interventional2011-03-31Withdrawn(stopped due to No patients have been recruited therefore study has been cancelled)
Randomized Phase II-III Trial of Post-operative Treatment of Pancreatic Adenocarcinoma: Gemcitabine Versus PEFG Followed by Radiochemotherapy With Concomitant Continuous Infusion of 5-fluorouracil [NCT00960284]Phase 2/Phase 3102 participants (Actual)Interventional2003-06-30Completed
A Phase II Study of Lapatinib and Capecitabine in the Treatment of Metastatic Pancreatic Cancer. [NCT00962312]Phase 29 participants (Actual)Interventional2009-01-31Completed
Phase I Trial of Chemoradiation With Capecitabine and Vorinostat in Pancreatic Cancer. [NCT00983268]Phase 121 participants (Actual)Interventional2009-10-31Completed
A Phase II Randomized Study of the Combination of Ribociclib Plus Goserelin Acetate With Hormonal Therapy Versus Physician Choice Chemotherapy in Premenopausal or Perimenopausal Patients With Hormone Receptor-positive/ HER2-negative Inoperable Locally Adv [NCT03839823]Phase 2223 participants (Actual)Interventional2019-02-25Completed
A Phase 3, Multicenter, Randomized, Open-label, Active-controlled Study of Trastuzumab Deruxtecan (DS-8201a), an Anti-HER2-antibody Drug Conjugate, Versus Treatment of Investigator's Choice for HER2-positive, Unresectable and/or Metastatic Breast Cancer S [NCT03523585]Phase 3608 participants (Actual)Interventional2018-08-01Active, not recruiting
A Study Using Photon/Proton Beam Radiation Therapy and Chemotherapy for Unresectable Carcinoma of the Pancreas [NCT00685763]13 participants (Actual)Interventional2008-03-31Completed
A Phase IIa Trial of Sorafenib With Capecitabine and Oxaliplatin in Patients With Locally Advanced or Metastatic Hepatocellular Carcinoma [NCT00752063]Phase 252 participants (Anticipated)Interventional2007-09-30Recruiting
Phase II Study of Oxaliplatin, Capecitabine, and Cetuximab in Advanced Hepatocellular Carcinoma [NCT00483405]Phase 233 participants (Actual)Interventional2006-10-31Completed
Phase II Safety and Efficacy Study of Capecitabine, Gemcitabine, and Bevacizumab in Combination for Patients With Metastatic or Unresectable Sarcomatoid Renal Cell Carcinoma [NCT00496587]Phase 234 participants (Actual)Interventional2007-07-31Completed
A Phase II Study for Short Preoperative Chemoradiotherapy Utilizing Intensity Modulated Radiation Therapy (IMRT) in Combination With Capecitabine in Patients With Resectable Rectal Carcinoma [NCT00973778]Phase 262 participants (Anticipated)Interventional2009-07-31Recruiting
An Open-Label Phase 1b Study of the Safety and Tolerability of Veliparib in Combination With Capecitabine and Radiation in Subjects With Locally Advanced Rectal Cancer (LARC) [NCT01589419]Phase 132 participants (Actual)Interventional2012-06-30Completed
A Randomized, Open-label Study of the Effect of Different Dosing Regimens of Xeloda® in Combination With Taxotere® on Disease Progression in Patients With Locally Advanced and/or Metastatic Breast Cancer [NCT00077857]Phase 2470 participants (Actual)Interventional2003-07-31Completed
Phase 2 Study of Adjuvant Chemotherapy With Docetaxel, Capecitabine and Cisplatin in Patients With Advanced Gastric Cancer [NCT00976976]Phase 246 participants (Actual)Interventional2007-05-31Completed
"An Open-Label Randomized Phase III Study of Intermittent Oral Capecitabine in Combination With Intravenous Oxaliplatin (Q3W) (XELOX) Versus Fluorouracil/Leucovorin as Adjuvant Therapy for Patients Who Have Undergone Surgery for Colon Carcinoma, AJCC/UICC [NCT00069121]Phase 31,886 participants (Actual)Interventional2003-04-18Completed
A Phase II Study of Capecitabine, Oxaliplatin and Bevacizumab for Metastatic or Unresectable Neuroendocrine Tumors [NCT00398320]Phase 240 participants (Actual)Interventional2006-11-30Completed
Evaluation of Differing Taxanes/Taxane Combinations on the Outcome of Patients With Operable Breast Cancer [NCT00050167]Phase 1603 participants (Actual)Interventional2002-11-30Completed
A Phase I Dose Finding Study of RAD001 in Combination With Capecitabine and Oxaliplatin (XELOX) in Patients With Advanced Gastric Cancer [NCT01049620]Phase 140 participants (Actual)Interventional2010-02-28Completed
Phase II Clinical Trial of Capecitabine and Oxaliplatin Plus Bevacizumab as Neoadjuvant Treatment for Patients With Previously Untreated Unresectable Liver-only Metastases From Colorectal Cancer [NCT01022541]Phase 247 participants (Actual)Interventional2006-06-30Completed
A Randomized Phase II Study of Docetaxel in Combination With Oxaliplatin With or Without 5-FU or Capecitabine in Metastatic or Locally Recurrent Gastric Cancer Previously Untreated With Chemotherapy for Advanced Disease [NCT00382720]Phase 2275 participants (Actual)Interventional2006-09-30Completed
Phase I Study of Dasatinib (BMS-354825) and Capecitabine for Advanced Breast Cancer [NCT00452673]Phase 152 participants (Actual)Interventional2007-06-30Completed
Neoadjuvant Radiotherapy and Capecitabine With or Without Panitumumab in Patients With Advanced, K-ras Unmutated Rectal Cancer. A Randomized Multicenter Phase II Trial [NCT00814619]Phase 268 participants (Actual)Interventional2008-11-30Completed
An Open-label, Multicenter, Phase II Clinical Study to Evaluate the Efficacy and Safety of HLX07 (Recombinant Humanized Anti-EGFR Monoclonal Antibody Injection) + HLX10 (Recombinant Humanized Anti-PD-1 Monoclonal Antibody Injection) + Chemotherapy or HLX0 [NCT05246982]Phase 240 participants (Anticipated)Interventional2022-03-23Recruiting
Study EGF107671 - a Phase II Study of Lapatinib Plus Topotecan or Lapatinib Plus Capecitabine in the Treatment of Recurrent Brain Metastases From ErbB2-Positive Breast Cancer Following Cranial Radiotherapy [NCT00437073]Phase 222 participants (Actual)Interventional2007-05-31Terminated(stopped due to Lapatinib-topotecan arm enrollment closed early per protocol amendment 2. Then enrollment into remaining arm terminated due to operational issues.)
A Multi-Center Randomized Phase II Study of Induction Chemotherapy Followed by Gemcitabine or Capecitabine Based Chemoradiotherapy for Locally Advanced Non-Metastatic Pancreatic Cancer [NCT01032057]Phase 2114 participants (Actual)Interventional2009-07-31Completed
A Phase II Trial of Capecitabine Rapidly Disintegrating Tablets and Concomitant Radiation Therapy in Children With Newly Diagnosed Brainstem Gliomas [NCT01118377]Phase 245 participants (Actual)Interventional2007-05-31Completed
A Phase 1 Dose-Finding Study Of The Anti-Angiogenesis Agent, AG-013736, In Combinations Of Paclitaxel/Carboplatin, Weekly Paclitaxel, Docetaxel, Capecitabine, Gemcitabine/Cisplatin and Pemetrexed/Cisplatin In Patients With Advanced Solid Tumors [NCT00454649]Phase 1102 participants (Actual)Interventional2005-12-31Completed
A Pilot Trial of Sequential Primary (Neoadjuvant) Combination Chemotherapy With Docetaxel/Capecitabine (TX) and Doxorubicin/Cyclophosphamide (AC) in Primary Breast Cancer With Evaluation of Chemotherapy Effects on Gene Expression [NCT00005908]Phase 230 participants (Actual)Interventional2000-06-30Completed
A Phase I/IIa Clinical Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Preliminary Efficacy of TST001 - Claudin18.2 Monoclonal Antibody in the Treatment of Locally Advanced or Metastatic Solid Tumors [NCT04495296]Phase 1/Phase 2320 participants (Anticipated)Interventional2020-08-13Recruiting
An Efficacy and Safety Study of mXELIRI Versus. FOLFIRI + Bevacizumab Therapy as First-line Chemotherapy in Metastatic Colorectal Cancer [NCT04247984]Phase 2264 participants (Actual)Interventional2018-05-01Completed
A Single Center, Randomized, Double-Blind, Placebo-Controlled Phase 2 Study of Gemcitabine (GEM) and Capecitabine (CAP) With or Without T-ChOS as Adjuvant Therapy in Patients With Surgically Resected Pancreatic Cancer. [NCT02767752]Phase 221 participants (Actual)Interventional2016-11-30Terminated(stopped due to Poor accrual and change of SOC (FOLFIRINOX in adjuvant setting))
A Phase 2,Randomized, Evaluate Efficacy and Safety of Capecitabine Plus Pyrotinib Versus Capecitabine Plus Trastuzumab and Pertuzumab in the First-line Treatment of HER2-positive Metastatic Breast Cancer [NCT04246502]Phase 2200 participants (Anticipated)Interventional2020-01-31Not yet recruiting
A Double-Blind, Randomized, Multicenter, Phase III Study of Bevacizumab in Combination With Capecitabine and Cisplatin Versus Placebo in Combination With Capecitabine and Cisplatin, as First-Line Therapy in Patients With Advanced Gastric Cancer. [NCT00887822]Phase 3202 participants (Actual)Interventional2009-03-31Completed
Phase I Study of Capecitabine in Combination With SIR-Spheres in Patients With Advanced Cancer [NCT00604409]Phase 134 participants (Actual)Interventional2006-04-30Completed
A Multicenter Prospective Phase III Clinical Trial of Neoadjuvant CapOx Chemotherapy in Patients With Intermediate Risk Middle and Upper Rectal Cancer [NCT04103697]Phase 3560 participants (Anticipated)Interventional2019-08-01Enrolling by invitation
SCOPE2 - A Randomised Phase II/III Trial to Study Radiotherapy Dose Escalation in Patients With Oesophageal Cancer Treated With Definitive Chemo-radiation With an Embedded Phase II Trial for Patients With a Poor Early Response Using Positron Emission Tomo [NCT02741856]Phase 2/Phase 3584 participants (Anticipated)Interventional2016-11-04Recruiting
An Exploratory Study of Conversion Therapy With Sintilimab Plus CAPOX in Patients With Unresectable Locally Advanced or Limited Metastatic Adenocarcinoma of the Stomach or Esophagogastric Junction [NCT04263870]Phase 236 participants (Anticipated)Interventional2020-03-31Not yet recruiting
Feasibility of Switching Fluoropyrimidine Due to Cardiotoxicity in Patients With Solid Tumors: A Retrospective, International and Non-interventional Study [NCT04260269]200 participants (Anticipated)Observational2018-06-01Enrolling by invitation
An Open Label Study to Evaluate the Safety and Effect on Disease Progression of Triple Combination Treatment With Erlotinib (Tarceva), Bevacizumab (Avastin), and Capecitabine (Xeloda) in Patients With Locally Advanced and/or Metastatic Pancreatic Cancer ( [NCT00925769]Phase 132 participants (Actual)Interventional2009-01-31Completed
[NCT02798510]Phase 3140 participants (Anticipated)Interventional2016-04-30Recruiting
Association of Survival With Maintenance Therapy in Patients With Metastatic Breast Cancer After First-line Chemotherapy [NCT04258163]760 participants (Actual)Observational2019-01-01Completed
Adjuvant Gemcitabine and Capecitabine Chemotherapy in Resected Pancreatic Cancer Following Neoadjuvant Chemotherapy [NCT05415917]Phase 275 participants (Anticipated)Interventional2022-07-29Recruiting
BALLAD BELGIUM: A Trial to Evaluate the Potential Benefit of Adjuvant Chemotherapy for Small Bowel Adenocarcinoma [NCT04257461]Phase 330 participants (Anticipated)Interventional2020-02-20Recruiting
Single Arm, Open, Multicenter Phase II Clinical Study of Radical Radiotherapy and Chemotherapy Combined With Maintenance Chemotherapy in the Treatment of Stage N3 NPC [NCT04220528]Phase 2129 participants (Anticipated)Interventional2019-12-01Recruiting
A Randomized, Open-label, Multi-center Phase IV Study Evaluating Palbociclib Plus Endocrine Treatment Versus a Chemotherapy-based Treatment Strategy in Patients With Hormone Receptor Positive / HER2 Negative Breast Cancer in a Real World Setting (GBG 93 - [NCT03355157]Phase 4150 participants (Anticipated)Interventional2018-03-01Recruiting
Randomised Phase II Trial of Sorafenib, Capecitabine and Oxaliplatin (SECOX) Versus Single Agent Sorafenib in Patients With Advanced Hepatocellular Carcinoma [NCT02716766]Phase 246 participants (Actual)Interventional2016-03-31Completed
A Randomized, Double-blind, Multi-center Phase Ⅲ Clinical Study to Evaluate the Recombinant Anti-HER2 Humanized Monoclonal Antibody or Placebo in Combination With Capecitabine for the Treatment of HER-2-positive Advanced Breast Cancer [NCT04164615]Phase 3336 participants (Anticipated)Interventional2016-11-24Recruiting
Metronomic Capecitabine With or Without Tislelizuamb (PD-1 Antibody) as Adjuvant Therapy in High-risk Non-metastatic Nasopharyngeal Carcinoma: a Multicentre, Open-label, Randomised Phase 3 Trial [NCT05342792]Phase 3556 participants (Anticipated)Interventional2022-04-17Recruiting
A Multicenter, Open-label, Phase I Dose-escalation and Dose-expansion Study of Mitoxantrone Hydrochloride Liposome Injection Combination Therapy in Chinese Patients With Advanced Solid Tumors [NCT05344742]Phase 1116 participants (Anticipated)Interventional2022-04-30Not yet recruiting
A Multicenter, Open-label, Phase Ib/II Study of AK104, a PD-1/CTLA-4 Bispecific Antibody, in Subjects With Advanced Solid Tumors or AK104 in Combination With Oxaliplatin and Capecitabine As First-line Therapy in Subjects With Advanced Unresectable or Meta [NCT03852251]Phase 1/Phase 2338 participants (Actual)Interventional2019-01-18Active, not recruiting
A Phase I Clinical Trial to Investigate the Maximum Tolerated Dose and Pharmacokinetics of Liposomal Paclitaxel With/Without Capecitabine in Chinese Cancer Patients With Advanced Gastric Carcinoma. [NCT00639522]Phase 118 participants (Anticipated)Interventional2008-05-31Recruiting
Analysis of the Effectiveness of Neoadjuvant Chemotherapy in the Treatment of Colon Cancer Locally Advanced [NCT04188158]Phase 2238 participants (Anticipated)Interventional2017-03-10Recruiting
A Phase II Study of Hyperthermic Intraperitoneal Chemotherapy (HIPEC) in the Treatment of Locally Advanced Colorectal Cancer During Radical Colorectal Resection [NCT02830139]Phase 2100 participants (Actual)Interventional2016-07-31Completed
Phase I Study of Intermittent High-Dose Lapatinib in Tandem With Capecitabine for HER2 Overexpressed/Amplified Metastatic Breast Cancer With Central Nervous System (CNS) Metastases [NCT02650752]Phase 111 participants (Actual)Interventional2016-01-06Completed
A Single-arm, Open-label, Multicenter Phase II Clinical Study of Fruquintinib Combined With Sintilimab and XELOX in the First-line Treatment of Advanced Metastatic Gastric or Gastroesophageal Junction Adenocarcinoma [NCT06094868]Phase 245 participants (Anticipated)Interventional2023-10-31Not yet recruiting
Atorvastatin in Triple-Negative Breast Cancer (TNBC) Patients Who Did Not Achieve a Pathologic Complete Response (pCR) After Receiving Neoadjuvant Chemotherapy, a Multicenter Pilot Study [NCT03872388]Phase 26 participants (Actual)Interventional2019-01-14Completed
GUided Treatment Based on Mini-PDX in metastaTIc refractOry Triple Negative Breast Cancer(GUMPTION)：a Prospective Randomized Controlled Single Center Clinical Trial [NCT04745975]Phase 2100 participants (Anticipated)Interventional2021-02-01Recruiting
A Phase I, Open-label, Non-randomized Study, to Assess the Safety and Tolerability of Cediranib (AZD2171) in Combination With Cisplatin Plus a Fluoropyrimidine (Capecitabine or S-1) in Japanese Patients With Previously Untreated Locally Advanced or Metast [NCT00960349]Phase 114 participants (Actual)Interventional2009-08-31Completed
Accelerated Growth of Synchronous Colorectal Liver Metastases: Effects of Neo-adjuvant Therapy [NCT00659022]Phase 260 participants (Anticipated)Interventional2008-07-31Recruiting
Phase I Study Of Oxaliplatin, Gemcitabine And Capecitabine In Advanced Gastrointestinal Malignancies And Other Solid Tumors [NCT00660426]Phase 130 participants (Actual)Interventional2005-03-31Completed
Randomized Three Arm Phase III Trial on Induction Treatment With a Fluoropyrimidine-, Oxaliplatin- and Bevacizumab-based Chemotherapy for 24 Weeks Followed by Maintenance Treatment With a Fluoropyrimidine and Bevacizumab vs. Bevacizumab Alone vs. no Maint [NCT00973609]Phase 3853 participants (Actual)Interventional2009-08-31Completed
Phase Ib/II Study of Regorafenib and XELOX Combination as 2nd Line Treatment in Metastatic Colorectal Cancer Patients [NCT04008511]Phase 1/Phase 254 participants (Anticipated)Interventional2019-07-31Not yet recruiting
A Neo-Adjuvant Study of Sequential Epirubicin and Docetaxel in Combination With Capecitabine in Patients With Locally Advanced Breast Cancer [NCT00645866]Phase 247 participants (Anticipated)Interventional2003-04-30Completed
Single-arm, Prospective, Open-label, Exploratory Study of Pyrotinib Combined With Capecitabine for Metastatic HER-2 Positive Colorectal Cancer Patients After at Least Second-line Standard Treatment [NCT04227041]Phase 1/Phase 234 participants (Anticipated)Interventional2020-01-10Not yet recruiting
Study on Skin Microbiota of Hand Foot Syndrome [NCT04132713]50 participants (Anticipated)Observational2019-09-10Recruiting
CA225103: A Phase II Study of a Combination of Cetuximab and Capecitabine in Patients With Metastatic Colorectal Cancer After Progression on Previous Fluoropyrimidine Containing Therapy [NCT00538291]Phase 213 participants (Actual)Interventional2005-08-31Terminated(stopped due to Study was terminated early due to lack of efficacy.)
Randomized Phase II/III Study of Second-line Endocrine Treatment Followed by Capecitabine Versus Capecitabine Followed by Endocrine Treatment in Patients With Metastatic Estrogen Receptor Positive Breast Cancer [NCT00684216]Phase 2/Phase 310 participants (Actual)Interventional2008-04-30Terminated(stopped due to acrual too slow)
Randomized, Phase III-b, Multi-centre, Open-label, Parallel Study of Enoxaparin (Low Molecular Weight Heparin) Given Concomitantly With Chemotherapy vs Chemotherapy Alone in Patients With Inoperable Gastric and Gastro-oesophageal Cancer [NCT00718354]Phase 3740 participants (Actual)Interventional2008-07-31Completed
A Phase I/II Study of Lapatinib in Combination With Oxaliplatin and Capecitabine in Subjects With Advanced or Metastatic Colorectal Cancer [NCT00536809]Phase 112 participants (Actual)Interventional2007-09-26Completed
A Pharmacokinetic Study of Adjuvant Capecitabine in Patients Who Have Undergone Proximal Pancreatico-duodenectomy for Resection of Pancreatic Adenocarcinoma [NCT00854477]Phase 413 participants (Actual)Interventional2009-11-30Completed
An Open Non-randomized Multicenter Phase II Trial to Evaluate the Efficacy and Safety of Tarceva in Combination With Capecitabine in Patients With Advanced Pancreatic Cancer [NCT00873353]Phase 232 participants (Actual)Interventional2008-03-31Completed
Phase II Study of Irinotecan, Capecitabine and Bevacizumab in Metastatic Colorectal Cancer Patients [NCT00875771]Phase 280 participants (Actual)Interventional2009-04-30Completed
A Phase II Study of Capecitabine Plus Concomitant Radiotion Therapy Followed by Durvalumab (MEDI4736) as Preoperative Treatment in Rectal Cancer. [NCT04083365]Phase 2100 participants (Anticipated)Interventional2020-01-01Recruiting
A Randomized, Open-label, Phase 3 Study of Adjuvant Sacituzumab Govitecan and Pembrolizumab Versus Treatment of Physician's Choice in Patients With Triple Negative Breast Cancer Who Have Residual Invasive Disease After Surgery and Neoadjuvant Therapy [NCT05633654]Phase 31,514 participants (Anticipated)Interventional2022-12-12Recruiting
A Multicenter, Open-label, Phase 2 Basket Study of MK-7684A, a Co-formation of Vibostolimab (MK-7684) With Pembrolizumab (MK-3475), With or Without Other Anticancer Therapies in Participants With Selected Solid Tumors [NCT05007106]Phase 2610 participants (Anticipated)Interventional2021-09-16Recruiting
A Phase II, Single-Arm Study to Explore the Efficacy and Safety of Atezolizumab Plus Tiragolumab and Chemotherapy in 1st Line HER2 Negative Unresectable, Recurrent or Metastatic Gastric Cancer or Adenocarcinoma of Gastroesophageal Junction (GEJ) [NCT04933227]Phase 229 participants (Actual)Interventional2021-08-06Active, not recruiting
A Phase III, Randomized, Double-Blind, Clinical Trial of Pembrolizumab (MK-3475) Plus Chemotherapy (XP or FP) Versus Placebo Plus Chemotherapy (XP or FP) as Neoadjuvant/Adjuvant Treatment for Subjects With Gastric and Gastroesophageal Junction (GEJ) Adeno [NCT04882241]Phase 3120 participants (Anticipated)Interventional2020-07-29Active, not recruiting
Regorafenib in Combination With Metronomic Cyclophosphamide, Capecitabine, and Low-dose Aspirin in Metastatic Colorectal Cancer Carcinoma An Open-label Phase II [NCT04534218]Phase 249 participants (Actual)Interventional2020-10-16Completed
A Phase 2, Randomized, Open-label Three-arm Clinical Study to Evaluate the Safety and Efficacy of Lenvatinib (E7080/MK-7902) in Combination With Pembrolizumab (MK-3475) Versus Standard of Care Chemotherapy and Lenvatinib Monotherapy in Participants With R [NCT04428151]Phase 2400 participants (Anticipated)Interventional2020-08-06Recruiting
An Umbrella Trial Based on Molecular Pathway for Patients With Unresectable Locally Advanced or Metastatic Triple Negative Breast Cancer (FUTURE SUPER) [NCT04395989]Phase 2139 participants (Actual)Interventional2020-07-28Active, not recruiting
A Phase 3, Global, Multi-Center, Double-Blind, Randomized, Efficacy Study of Zolbetuximab (IMAB362) Plus CAPOX Compared With Placebo Plus CAPOX as First-line Treatment of Subjects With Claudin (CLDN) 18.2-Positive, HER2-Negative, Locally Advanced Unresect [NCT03653507]Phase 3507 participants (Actual)Interventional2018-11-28Active, not recruiting
A Phase Ib/II, Open-Label, Multicenter, Randomized Umbrella Study Evaluating The Efficacy And Safety Of Multiple Treatment Combinations In Patients With Metastatic Breast Cancer (Morpheus-panBC) [NCT03424005]Phase 1/Phase 2242 participants (Anticipated)Interventional2018-04-02Recruiting
Chemotherapy Intensification in Patients With High Lactate Dehydrogenase Values and Soluble Syndecan-1 Levels [NCT03117972]Phase 2177 participants (Anticipated)Interventional2017-08-04Active, not recruiting
A Phase II, Two-arm, Non-comparative, Multicentre Study of Tucatinib (ONT-380), Pembrolizumab and Trastuzumab in Patients With Pre-treated Advanced HER2-positive Breast Cancer [NCT04789096]Phase 250 participants (Anticipated)Interventional2023-03-07Recruiting
A Randomized, Open-label, Multicenter Phase 3 Study of SKB264 Versus Treatment of Physician's Choice (TPC) in Patients With Unresectable Locally Advanced, Recurrent or Metastatic HR+/HER2- Breast Cancer Who Had Failed at Least One Line of Chemotherapy [NCT06081959]Phase 3376 participants (Anticipated)Interventional2023-11-30Not yet recruiting
A Phase 1b/2 Multicenter, Open-label, Dose-escalation and Dose-expansion Study to Evaluate the Safety, Tolerability, Pharmacokinetics, Immunogenicity, and Antitumor Activity of Trastuzumab Deruxtecan (T-DXd) Monotherapy and Combinations in Adult Participa [NCT04379596]Phase 2357 participants (Anticipated)Interventional2020-06-03Recruiting
A Phase Ib, Dose Escalation Study of Lithium When Added to Standard Chemotherapy of Oxaliplatin and Capecitabine in Patients With Advanced Oesophago-Gastric or Colorectal Cancer [NCT03153280]Phase 12 participants (Actual)Interventional2022-01-13Active, not recruiting
A Phase III Study Evaluating Two Neoadjuvant Treatments Radiochemotherapy (5 Weeks - 50Gy+Capecitabine) and Radiotherapy (1week - 25Gy) in Patient Over 75 With Locally Advanced Rectal Carcinoma [NCT02551237]Phase 3103 participants (Actual)Interventional2016-01-07Completed
A Phase III, Randomized, Double-Blind, Clinical Trial of Pembrolizumab (MK-3475) Plus Chemotherapy (XP or FP) Versus Placebo Plus Chemotherapy (XP or FP) as Neoadjuvant/Adjuvant Treatment for Subjects With Gastric and Gastroesophageal Junction (GEJ) Adeno [NCT03221426]Phase 31,007 participants (Actual)Interventional2017-10-09Active, not recruiting
A Phase II Trial of Gemcitabine, Capecitabine, and Bevacizumab in Metastatic Renal Cell Carcinoma [NCT00523640]Phase 230 participants (Actual)Interventional2005-03-31Terminated(stopped due to Too slow accrual)
NANT Colorectal Cancer (CRC) Vaccine: A Phase 1b/2 Trial of the NANT CRC Vaccine vs Regorafenib in Subjects With Metastatic CRC Who Have Been Previously Treated With Standard-of-Care Therapy [NCT03563157]Phase 1/Phase 2332 participants (Anticipated)Interventional2018-05-25Active, not recruiting
A Phase I/II Study of Induction Conatumumab and Gemcitabine, Followed by Conatumumab, Capecitabine and 3-D Conformal Radiation Therapy (3D-CRT) With Subsequent Maintenance Therapy for Locally Advanced Pancreatic Cancer [NCT01017822]Phase 1/Phase 20 participants (Actual)InterventionalWithdrawn(stopped due to This study was withdrawn due to study agent availability.)
An Open-Label Multicenter Study Administering Lapatinib and Capecitabine (Xeloda) in Women With Advanced or Metastatic Breast Cancer [NCT00508274]Phase 352 participants (Actual)Interventional2007-07-18Terminated(stopped due to Primary analysis was completed in 2015 and data collection post 1-Jul-2019 was not reportable due to local regulations in China.)
Multicentric Pilot Study of Dihydropyrimidine Dehydrogenase (DPD) Deficiency for Predicting Capecitabine Toxicity in Breast Cancer Patients [NCT00953537]303 participants (Actual)Interventional2009-01-31Completed
Phase III Randomized, Multi Center Study Of Sunitinib Malate (SU 011248) Or Capecitabine In Subjects With Advanced Breast Cancer Who Failed Both A Taxane And An Anthracycline Chemotherapy Regimen Or Failed With A Taxane And For Whom Further Anthracycline [NCT00373113]Phase 3482 participants (Actual)Interventional2006-11-30Terminated(stopped due to See termination reason in detailed description.)
A Phase II Study to Evaluate the Efficacy and Safety of Neoadjuvant Radiation in Combination With Capecitabine & Paniumumab With and Without Irinotecan in Patients With Localized Rectal Cancer [NCT00967655]Phase 254 participants (Anticipated)Interventional2009-07-31Recruiting
A Multicenter Phase II Clinical Trial Assessing the Efficacy of the Combination of Lapatinib and Capecitabine in Patients With Non Pretreated Brain Metastasis From HER2 Positive Breast Cancer [NCT00967031]Phase 245 participants (Actual)Interventional2009-04-30Completed
EXCITE: Erbitux, Xeloda, Campto, Irradiation Then Excision for Locally Advanced Rectal Cancer (North West Clinical Oncology Group-04 on Behalf of the NCRI Rectal Cancer Subgroup) [NCT00972881]Phase 1/Phase 282 participants (Actual)Interventional2009-04-30Completed
A Randomized Phase 2 Study of ARQ 197 Versus Investigator's Choice of Second-Line Chemotherapy in Patients With Locally Advanced or Metastatic Gastric Cancer Who Have Progressive Neoplastic Disease Following Treatment With One Prior Chemotherapy Regimen [NCT01070290]Phase 20 participants (Actual)InterventionalWithdrawn
A Phase II Study of Cetuximab Plus Biweekly Capecitabine and Oxaliplatin (C-CO2) in the Treatment of Patients With KRAS Wild Type Metastatic Colorectal Cancer [NCT00444678]Phase 236 participants (Actual)Interventional2004-06-01Completed
Prospective, Randomized, Controlled, Multicenter, Phase III Study of Apatinib Plus Concurrent Neoadjuvant Chemoradiotherapy for Siewert II ，III of Locally Advanced HER-2 Negative Adenocarcinoma at Gastroesophageal Junction [NCT03986385]Phase 3180 participants (Anticipated)Interventional2019-06-01Recruiting
A Randomized, Multi-Center Phase III Trial Of Irinotecan In Combination With Three Different Methods Of Administration Of Fluoropyrimidine: Infusional 5-FU (FOLFIRI), Modified-Bolus 5-FU (Day 1 & 8), And Oral Capecitabine (Day 1-14); With Celecoxib Versus [NCT00101686]Phase 3547 participants (Actual)Interventional2003-02-28Completed
UPCC 04219 Phase 2 Study of Capecitabine-Temozolomide(CapTem) With Yttrium-90 Radioembolization in the Treatment of Patients With Unresectable Metastatic Grade 2 Neuroendocrine Tumors [NCT04339036]Phase 250 participants (Anticipated)Interventional2021-10-07Recruiting
Adjuvant Chemotherapy With Gemcitabine and Cisplatin Compared to Standard of Care After Curative Intent Resection of Cholangiocarcinoma and Muscle Invasive Gall Bladder Carcinoma (ACTICCA-1 Trial) [NCT02170090]Phase 3789 participants (Actual)Interventional2014-04-30Active, not recruiting
A Phase I/II Clinical Trial of Combination of Irinotecan, Xeloda and Oxaliplatin (IXO) Regimen With Avastin (Bevacizumab) in Patients With Metastatic Colorectal Cancer [NCT00819754]Phase 1/Phase 223 participants (Actual)Interventional2003-11-30Terminated
A Prospective, Open, Comparative Multicentre Phase II Study for the Evaluation of Irinotecan and Capecitabine Versus Cisplatin and Capecitabine in Advanced Gastric Adenocarcinoma or Gastric-Oesophagal Junction [NCT00675194]Phase 2120 participants (Anticipated)Interventional2003-10-31Completed
Phase II Study for Inoperable Non-Metastatic Pancreatic Cancer (Stage IVA) With Neoadjuvant Gemzar, Taxotere and Xeloda (GTX), and Radiation With Gemzar [NCT00869258]Phase 232 participants (Actual)Interventional2005-06-30Completed
An Open-Label Randomized International Multi-Center Phase III Study of Capecitabine (Xeloda) in Combination With Cisplatin Versus FU/Cisplatin in Patients With Advanced and/or Metastatic Gastric Cancer [NCT02563054]Phase 3316 participants (Actual)Interventional2003-04-30Completed
A Phase I Study of Capecitabine In Patients With Solid Tumors [NCT00697502]Phase 123 participants (Actual)Interventional2007-05-31Completed
A Pilot Phase II Study of Triplet Chemotherapy Regimen in Neoadjuvant Chemotherapy of Patients With Resectable Colorectal Cancer [NCT02688023]Phase 250 participants (Anticipated)Interventional2014-03-31Recruiting
A Randomised, Open-label Phase III Study to Assess Efficacy and Safety of Bevacizumab in Combination With Capecitabine as First-line Treatment for Elderly Patients With Metastatic Colorectal Cancer [NCT00484939]Phase 3280 participants (Actual)Interventional2007-07-31Completed
A Phase II Study of Adjuvant Gemcitabine/Capecitabine and Bevacizumab for Patients Treated Neoadjuvantly Chemotherapy for Early Stage Breast Cancer With High Risk for Relapse [NCT00462865]Phase 218 participants (Actual)Interventional2007-11-30Terminated(stopped due to DSMB determined toxicity of regimen more than originally thought. Slow accrual.)
A Perspective Study of the Predictive Value of microRNA in Patients With HER2 Positive Advanced Stage Breast Cancer Who Were Treated With Herceptin [NCT02656589]300 participants (Anticipated)Observational2015-06-30Recruiting
A Phase Ⅱ Trial Program Exploring The Integration Of Novel HER2-targeted Tyrosine Kinase Inhibitor Pyrotinib and CDK4/6 Inhibitor SHR6390 Into Current Chemotherapy/Endocrine Therapy Regimes For Prior Trastuzumab-treated Advanced HER2-positive Breast Cance [NCT04095390]Phase 260 participants (Anticipated)Interventional2019-09-30Recruiting
Gemcitabine, Oxaliplatin and Capecitabine (GEMOXEL) for Patients With Advanced Pancreatic Adenocarcinoma (APC): A Phase I/II Study [NCT00744640]Phase 1/Phase 246 participants (Actual)Interventional2005-10-31Completed
A Prospective Study to Evaluate Alterations in Molecular Biomarkers in HER2 Neu Positive Metastatic Breast Cancer Together With Assessment of Trastuzumab Use Beyond Progression After Initial Response to Trastuzumab-taxane Based Treatment [NCT00885755]Phase 233 participants (Actual)Interventional2009-08-13Completed
Preoperative Combined RadioChemo-MolecularTargetTherapy of the Locally Advanced Rectum Carcinoma (cT3NxM0) - a Phase II Pilot Study With Preoperative Application of Capecitabine, Bevacizumab and Radiotherapy (RTx) [NCT00671645]Phase 28 participants (Actual)Interventional2008-07-31Terminated(stopped due to reaching of step 1 (recruitment of 8 patients) per protocol -> risk assessment -> termination because of occurance of toxicity Grade 3 and 4)
A Phase 1 Study Of Axitinib In Combination With Cisplatin And Capecitabine In Patients With Advanced Gastric Cancer [NCT00842244]Phase 122 participants (Actual)Interventional2009-04-30Completed
An Open Label Study of the Effect of Xeloda and Radiotherapy on Pathological Response Rate in Patients With Locally Advanced Rectal Cancer [NCT00796718]Phase 262 participants (Actual)Interventional2008-10-31Completed
A Multicenter, Randomized Clinical Trail Evaluate Effectiveness and Security of Capecitabine or Endocrinotherapy as a Maintenance Therapy Regimen After the 1st-line Chemotherapy With Capecitabine Combine Regimen in Hormone Receptor Positive and HER2 Negat [NCT02597868]132 participants (Anticipated)Interventional2013-01-31Recruiting
A Phase 2 Open-label, Single Arm Study of MK-7119 in Combination With Trastuzumab and Capecitabine in Participants With Previously Treated Locally Advanced Unresectable or Metastatic HER2+ Breast Carcinoma [NCT04721977]Phase 266 participants (Actual)Interventional2021-04-08Active, not recruiting
A Multi-Center Phase II Trial of Capecitabine (Xeloda) in Combination With Cisplatin as First Line Chemotherapy in Patients With Metastatic Nasopharyngeal Carcinoma [NCT02608073]Phase 245 participants (Actual)Interventional2004-11-30Completed
Phase II Study of Lapatinib and Capecitabine in 2nd Line Treatment of Locally Advanced/Metastatic Pancreatic Cancer [NCT00881621]Phase 217 participants (Actual)Interventional2009-08-31Terminated(stopped due to slow enrollment)
A Phase 2 Study of the Efficacy and Safety of Apricoxib in Combination With Lapatinib and Capecitabine in the Treatment of Patients With HER2/Neu+ Breast Cancer Who Have Failed Trastuzumab and Chemotherapy Including a Taxane [NCT00657137]Phase 212 participants (Actual)Interventional2008-04-30Terminated(stopped due to Slow accrual)
Effects of S-1 and Capecitabine in Combination With Oxaliplatin on the Coronary Artery Blood Flow in Patients Metastatic Gastrointestinal Tract Adenocarcinoma: a Randomized Phase II Study [NCT02216149]Phase 220 participants (Actual)Interventional2015-01-31Terminated(stopped due to Slow accrual)
A Randomized Phase II Study of Bevacizumab, Capecitabine and Radiation Therapy With or Without Oxaliplatin in the Preoperative Treatment of Locally Advanced Rectal Cancer [NCT00828672]Phase 284 participants (Actual)Interventional2009-06-30Completed
A Randomized Phase III Trial of Capecitabine With or Without Irinotecan Driven by UGT1A1 in Neoadjuvant Chemoradiation of Locally Advanced Rectal Cancer [NCT02605265]Phase 3360 participants (Anticipated)Interventional2015-10-31Recruiting
Adjuvant Nab-paclitaxel Plus S-1 Versus Capecitabine Plus Oxaliplatin for Patients With Stage III Gastric Cancer After D2 Gastrectomy : a Randomised，Open-label, Phase III Study [NCT04135781]Phase 3616 participants (Anticipated)Interventional2020-03-01Recruiting
Induction and Consolidation Chemotherapy in Locally Advanced Rectal Cancer Patients With Circumferential Resection Margin Involvement: a Multicenter Prospective Randomized Phase III Clinical Trial [NCT04135313]Phase 3540 participants (Anticipated)Interventional2019-10-20Enrolling by invitation
Quadruplet 1st Line Treatment of CAPOXIRI Plus Bevacizumab Versus FOLFOXIRI Plus Bevacizumab for mCRC, Multicenter Randomised Phase II Study (QUATTRO-II) [NCT04097444]Phase 2112 participants (Anticipated)Interventional2019-10-11Recruiting
Capecitabine and Oxaliplatin in Patients With Advanced or Metastatic Pancreatic Adenocarcinoma [NCT00585078]Phase 240 participants (Actual)Interventional2004-05-31Completed
Two Cycles Versus Four Cycles of Capecitabine Combined Oxaliplatin Concurrent Radiotherapy as First-line Therapy for Chinese Locally Advanced Esophageal Squamous Cell Carcinomas, an Open Randomised Phase III Cilinical Trial [NCT02604615]Phase 360 participants (Anticipated)Interventional2014-10-31Recruiting
A Phase 1/2, Open-Label Study Of Neratinib (HKI-272) In Combination With Capecitabine In Subjects With Solid Tumors And ErbB-2 Positive Metastatic Or Locally Advanced Breast Cancer [NCT00741260]Phase 1/Phase 2105 participants (Actual)Interventional2008-12-09Completed
[NCT02603159]Phase 3200 participants (Anticipated)Interventional2014-10-31Recruiting
The CapSul Trial: A Phase II Study of Sunitinib and Capecitabine for the Treatment of Unresectable or Metastatic Hepatocellular Carcinoma (HCC) [NCT00787787]Phase 241 participants (Actual)Interventional2008-09-30Terminated
A Randomized, Phase 3 Study Of Sunitinib In Combination With Capecitabine Compared With Capecitabine In Patients With Previously Treated Breast Cancer [NCT00435409]Phase 3442 participants (Actual)Interventional2007-02-28Completed
Phase 1b Study of Indibulin in Combination With Capecitabine in Advanced Solid Tumors [NCT00726687]Phase 1/Phase 27 participants (Actual)Interventional2008-06-30Active, not recruiting
Effects of a Pneumatic Compression Device in Post-Chemoradiation Head and Neck Cancer Population [NCT05512767]0 participants (Actual)Interventional2022-12-01Withdrawn(stopped due to PI retired and study not moving forward)
An Open-label Study of the Safety, Tolerability, and Response Rate of Xeloda in Treatment-naïve Patients With Metastatic Colorectal Cancer [NCT02567331]Phase 428 participants (Actual)Interventional2004-10-31Completed
A Randomized, Multicenter, Phase III Open-label Study of the Efficacy and Safety of Trastuzumab MCC-DM1 vs. Capecitabine + Lapatinib in Patients With HER2-Positive Locally Advanced or Metastatic Breast Cancer Who Have Received Prior Trastuzumab-Based Ther [NCT00829166]Phase 3991 participants (Actual)Interventional2009-02-28Completed
A Phase II Study of Pre-operative Chemotherapy Plus Bevacizumab With Early Salvage Therapy Based on PET Assessment of Response in Patients With Locally Advanced But Resectable Gastric and GEJ Adenocarcinoma [NCT00737438]Phase 222 participants (Actual)Interventional2008-08-31Completed
A Phase II Randomized Study of Palbociclib in Combination With Exemestane Plus GnRH Versus Capecitabine in Premenopausal Women With Hormone Receptor-Positive Metastatic Breast Cancer [NCT02592746]Phase 2182 participants (Anticipated)Interventional2016-06-30Active, not recruiting
A Randomized Phase II Trial of Capecitabine Plus Cisplatin (XP) Versus Capecitabine Plus Paclitaxel (XT) as a First-line Treatment for Advanced or Recurrent Esophageal Squamous Cell Carcinoma [NCT00816634]Phase 294 participants (Anticipated)Interventional2008-10-31Recruiting
A Phase II Study of Erlotinib in Combination With Capecitabine as First-line Treatment in Elderly Patients With Stage IIIB/IV Adenocarcinoma Non-small Cell Lung Cancer (NSCLC) [NCT00816868]Phase 262 participants (Actual)Interventional2009-01-31Completed
A Phase 2 Study of the Efficacy and Safety of Irinotecan (Campto®) in Combination With Capecitabine (Xeloda®) as First-Line Chemotherapy in Asian Subjects With Inoperable Hepatocellular Carcinoma [NCT00635323]Phase 273 participants (Anticipated)Interventional2002-11-30Completed
Maintenance Treatment With Capecitabine Plus Cetuximab After First-line 5-Fluorouracil-based Chemotherapy Plus Cetuximab for Patients With RAS Wild-type Metastatic Colorectal Cancer: a Single Arm, Open-label, Multi-center Clinical Trial [NCT02717923]Phase 250 participants (Anticipated)Interventional2014-01-31Recruiting
Preoperative Chemoradiotherapy and Postoperative Chemotherapy With Capecitabine and Oxaplatin vs.Capecitabine Alone in Locally Advanced Rectal Cancer (PETACC-6) [NCT00766155]Phase 31,094 participants (Actual)Interventional2008-08-31Completed
Phase II Study of a Biochemically Synergistic Regimen for Metastatic Pancreatic Cancer (Stage IVB) With Gemzar, Taxotere and Xeloda (GTX) [NCT00996333]Phase 246 participants (Actual)Interventional2003-06-30Completed
Multi-omics Model Predicts Efficacy of Preoperative Neoadjuvant Chemoradiotherapy Combined PD-1 Antibody Therapy for Locally Advanced Rectal Cancer [NCT05368051]30 participants (Anticipated)Observational2021-10-01Recruiting
A Two-arm Phase II Randomised Trial of Intermittent Chemotherapy Plus Continuous Cetuximab and of Intermittent Chemotherapy Plus Intermittent Cetuximab in First Line Treatment of Patients With K-ras-normal (Wild-type) Metastatic Colorectal Cancer [NCT00640081]Phase 2169 participants (Actual)Interventional2007-07-31Completed
XERAD: Open-Label, Phase II, Randomized, Comparative, Multicentre Trial of Concurrent Whole Brain Radiation Therapy (WBRT) and Capecitabine (Xeloda®) Followed by Maintenance Capecitabine Compared With Standard WBRT in Breast Cancer Patients With Newly Dia [NCT00977379]Phase 224 participants (Actual)Interventional2009-08-31Terminated(stopped due to Due to an insufficient number of participants enrolled.)
A Phase II Study Of Sunitinib Malate In Combination With Capecitabine In Patients With Advanced Or Metastatic Breast Cancer [NCT00662025]Phase 263 participants (Actual)Interventional2008-04-30Completed
A Phase I/IB Study of Ipatasertib in Combination With Carboplatin, Carboplatin/Paclitaxel, or Capecitabine/Atezolizumab in Patients With Metastatic Triple Negative Breast Cancer [NCT03853707]Phase 1/Phase 228 participants (Actual)Interventional2019-03-04Active, not recruiting
A Randomized, Open-label Study Comparing the Effect of 3 Chemotherapy Regimens Containing Avastin on Time to Disease Progression in Patients With Metastatic Colorectal Cancer [NCT01131078]Phase 2306 participants (Actual)Interventional2005-06-30Completed
A Phase III Study of Surgery in Combination With Neoadjuvant Chemotherapy of Oxaliplatin Plus Capecitabine in Colorectal Cancer With Respectable Liver Metastasis [NCT00630045]Phase 3392 participants (Anticipated)Interventional2008-01-31Recruiting
Phase 1b/II Trial of Checkpoint Inhibitor (Pembrolizumab an Anti PD-1 Antibody) Plus Standard IMRT in HPV Induced Stage III/IV Carcinoma of Anus [NCT04046133]Phase 150 participants (Anticipated)Interventional2020-10-19Recruiting
Phase I Study to Evaluate the Safety and Tolerability of ASLAN001 in Combination With Cisplatin and 5-Fluorouracil or Cisplatin and Capecitabine [NCT02648425]Phase 131 participants (Actual)Interventional2014-08-05Completed
A Phase I/Ib, Multicenter, Open-label, Dose-Escalation, Safety, Pharmacodynamic and Pharmacokinetic Study of GZ17-6.02 Monotherapy and in Combination With Capecitabine, Given Orally on a Daily Schedule in Patients With Advanced Solid Tumors or Lymphoma [NCT03775525]Phase 1127 participants (Anticipated)Interventional2019-03-01Active, not recruiting
Preoperative Radiotherapy With Capecitabine and Bevacizumab in Locally Advanced Rectal Cancer: CRAB Phase II Study [NCT00842686]Phase 260 participants (Anticipated)Interventional2009-01-31Active, not recruiting
Pilot Feasibility Trial of Preoperative Capecitabine, Oxaliplatin, Cetuximab and Radiation Therapy for Locally Advanced Esophageal Adenocarcinoma [NCT00430027]8 participants (Actual)Interventional2006-11-30Terminated(stopped due to This study was terminated due slow accrual.)
An Open-Label Phase II Study of Capecitabine in Combination With Pegylated Interferon Alfa-2a in Patients With Advanced Hepatocellular Carcinoma [NCT02576964]Phase 216 participants (Actual)Interventional2005-01-31Completed
Selective Treatment With Magnetic Resonance Image Guided Pelvic Adaptive Radiation Therapy Combined With Total Neoadjuvant ChemoTherapy for the Conservative Management of Locally Advanced Rectal Cancer [NCT05412082]Phase 125 participants (Anticipated)Interventional2022-10-05Recruiting
Randomized Phase 3 Study on the Optimization of Bevacizumab With mFOLFOX/mOXXEL in the Treatment of Patients With Metastatic Colorectal Cancer [NCT01718873]Phase 3230 participants (Actual)Interventional2012-05-31Completed
A Phase I/II Study Evaluating the Combination of Weekly Docetaxel and Cisplatin Together With Capecitabine and Bevacizumab in Patients With Advanced Gastric Cancer [NCT00845884]Phase 1/Phase 249 participants (Anticipated)Interventional2009-02-28Not yet recruiting
A Phase I Study of Capecitabine, Oxaliplatin, Bevacizumab, and RAD001 (XELOX-A-Ev) for Subjects With Advanced Solid Tumors [NCT00849550]Phase 132 participants (Actual)Interventional2009-07-31Completed
Alternating Treatment With Fruquintinib and Bevacizumab Plus Capecitabine Versus Bevacizumab Plus Capecitabine as Maintenance Therapy Following First-line Treatment for Metastatic Colorectal Cancer: A Multi-center, Parallel-group, Phase II Study. [NCT05659290]Phase 240 participants (Anticipated)Interventional2023-01-31Recruiting
A Phase II Study of Irinotecan, Capecitabine and Avastin in Patients With Metastatic Colorectal Cancer, Who Have Progressed After 1ST Line Therapy With Folfox/Avastin. [NCT00717990]Phase 215 participants (Actual)Interventional2008-04-30Terminated(stopped due to Poor Accrual)
Phase II Study of Adjusted-dose Docetaxel-oxaliplatin-capecitabine in Patients With Advanced Gastric Adenocarcinoma and Intermediate General Status. [NCT00733616]Phase 244 participants (Actual)Interventional2008-11-30Completed
Concurrent Capecitabine and Radiotherapy in the Adjuvant Treatment of Resistant Breast Cancer: A Prospective Feasibility Trial [NCT03958721]Phase 120 participants (Actual)Interventional2019-07-18Completed
A Randomized, Controlled, Multi-center Phase II Clinical Study to Evaluate the Efficacy and Safety of Recombinant Humanized Anti-HER2 Monoclonal Antibody-MMAE Conjugate for Injection in the Treatment of HER2-positive Locally Advanced or Metastatic Breast [NCT03500380]Phase 2/Phase 3301 participants (Anticipated)Interventional2018-04-24Active, not recruiting
A Randomized Phase 2 Study of SCH 727965 in Subjects With Advanced Breast and Non Small Cell Lung (NSCLC) Cancers [NCT00732810]Phase 297 participants (Actual)Interventional2008-07-31Completed
An Open-Label, Multicenter, Randomized, Phase II Study to Evaluate the Efficacy and Safety of Two Combination Dose Regimens: Capecitabine + Epirubicin + Cyclophosphamide (CEX) Versus 5-FU + Epirubicin + Cyclophosphamide (FEC 100) as Neoadjuvant Therapy in [NCT02846428]Phase 2182 participants (Actual)Interventional2004-03-31Completed
A Prospective, Multicenter, Single-armed, Phase II Study Evaluating Efficacy and Safety of Neoadjuvant Sintilimab in Combination With Capecitabine and Oxaliplatin (XELOX) in Patients With Resectable Locally Advanced Gastric or Gastroesophageal Adenocarcin [NCT04065282]Phase 236 participants (Anticipated)Interventional2019-08-06Recruiting
A Phase I Study of Capecitabine, Oxaliplatin, Bevacizumab, and Dasatinib for Patients With Advanced Solid Tumors With Expanded Cohort of Patients With Previously Untreated Metastatic Colorectal Cancer. [NCT00920868]Phase 122 participants (Actual)Interventional2009-05-31Completed
A Randomized Phase III Study of SOX vs. COX in Patients With Advanced Colorectal Cancer [NCT00677443]Phase 3344 participants (Actual)Interventional2008-06-30Completed
A Phase II, Single-center, Dynamic Observational Study With PET of 68Ga-HER2-affibody in Anti-HER2 Treatment [NCT04769050]50 participants (Anticipated)Observational2021-02-18Recruiting
Phase 2 Study of Comparison Between XELOX (Capecitabine and Oxaliplatin) and Docetaxel, Oxaliplatin and S1 Regimen as Neoadjuvant Chemotherapy for Patients With Locally Advanced Gastric Cancer [NCT02623153]Phase 2200 participants (Anticipated)Interventional2016-01-31Not yet recruiting
Phase II Trial of Neoadjuvant Docetaxel ± Metronomic Capecitabine/CTX Followed by FEC in Women With Operable Triple Negative Breast Cancer [NCT02897050]Phase 2170 participants (Anticipated)Interventional2016-09-30Suspended
A Randomized, Multicenter, Parallel,Phase III Open-label Study of the Efficacy and Safety of Hemay022 + AI in Patients With ER+/HER2+ Advanced or Metastatic Breast Cancer Who Have Received Prior Trastuzumab-Based Therapy [NCT05122494]Phase 3339 participants (Anticipated)Interventional2022-01-19Recruiting
A Prospective, Observational, Multicenter Study on Biomarkers for Predicting the Efficacy and Toxicities of Neoadjuvant Chemoradiotherapy for Locally Advanced Rectal Cancer Based on Tissue and Plasma Exosome RNA [NCT04227886]250 participants (Anticipated)Observational2019-12-01Recruiting
177Lutethium - Peptide Receptor Radionuclide Therapy (Lu-PRRT) Plus Capecitabine Versus Lu-PRRT in FDG Positive, Gastro-entero-pancreatic Neuroendocrine Tumors: a Randomized Phase II Study. [NCT02736448]Phase 235 participants (Actual)Interventional2016-05-31Active, not recruiting
A Randomized, Multicenter Phase III Trial to Assess the Efficacy and Safety of Bevacizumab and Capecitabine as Maintenance Treatment, After Initial Combination Treatment With Capecitabine, Oxaliplatin and Bevacizumab in Patients With Metastatic Colorectal [NCT00623805]Phase 3123 participants (Actual)Interventional2008-03-31Completed
A Phase 1 Study of TKI 258 in Combination With Xeloda and Oxaliplatin in Upfront Treatment of Advanced Colorectal and Gastric Cancer With a Dose Expansion Cohort in Advanced Gastric Cancer [NCT02720926]Phase 13 participants (Actual)Interventional2011-09-30Terminated(stopped due to Unafavourable toxicity profile)
A Randomized Phase II Study of Combination Chemotherapy With Epirubicin , Cisplatin and Capecitabine (ECX) or Cisplatin and Capecitabine (CX) in Advanced Gastric Cancer [NCT00743964]Phase 291 participants (Actual)Interventional2008-04-30Completed
Capecitabine in Combination With Aromatase Inhibitor Versus Aromatase Inhibitors, in Hormonal Receptor Positive Recurrent or Metastatic Breast Cancer Patients, Randomized Controlled Study (CONCEPT Trial) [NCT04012918]Phase 2124 participants (Anticipated)Interventional2018-08-30Recruiting
FOxTROT - Fluoropyrimidine, Oxaliplatin and Targeted Receptor Pre-Operative Therapy: a Controlled Trial in High-Risk Operable Colon Cancer [NCT00647530]Phase 2/Phase 31,053 participants (Actual)Interventional2008-05-15Active, not recruiting
A Phase I Study Of Vinorelbine Oral Plus Capecitabine Combination In Patients With Metastatic Breast Cancer [NCT00706069]Phase 140 participants (Anticipated)Interventional2008-06-30Completed
A Phase III Study Comparing Adjuvant Chemotherapy Consisting of Capecitabine/Oxaliplatin Versus Surgery Alone in Patients With Stage II (T1N2, T2N1, T3N0), IIIa (T2N2, T3N1, T4N0) and IIIb (T3N2) Gastric Adenocarcinoma [NCT02560974]Phase 31,035 participants (Actual)Interventional2006-06-30Completed
A Phase II Study of Gemzar, Taxotere, and Xeloda (GTX) for Adjuvant Pancreatic Cancer [NCT00882310]Phase 237 participants (Actual)Interventional2006-09-30Completed
A Phase II Study of Oxaliplatin, Capecitabine, Cetuximab and Radiation in Pre-Operative Therapy of Rectal Cancer [NCT00686166]Phase 283 participants (Actual)Interventional2009-02-28Completed
A Single Arm Open-label, Phase II Study of Bevacizumab in Combination With Trastuzumab and Capecitabine as First-line Treatment of Patients With HER2-positive Locally Recurrent or Metastatic Breast Cancer [NCT00811135]Phase 288 participants (Actual)Interventional2008-12-31Completed
Dose Escalating Study of Yttrium 90 Microspheres (TheraSphere) With Capecitabine (Xeloda) for Intrahepatic Cholangiocarcinoma or Metastatic Disease to the Liver [NCT00858429]Phase 118 participants (Actual)Interventional2009-04-01Completed
A Phase I Study of a Combination of High Selenium Brassica Juncea With Irinotecan and Capecitabine [NCT00547547]Phase 122 participants (Actual)Interventional2006-04-30Completed
A Phase I Study of Gemcitabine, Capecitabine and ZD6474 (ZACTIMA) in Patients With Advanced Solid Tumors With an Expanded Cohort of Patients With Biliary or Pancreatic Malignancies. [NCT00551096]Phase 123 participants (Actual)Interventional2007-10-31Completed
Capecitabine as Adjuvant Chemotherapy to Prevent Recurrence of Hepatocellular Carcinoma After Curative Resection: a Randomized Controlled Trial [NCT00561522]Phase 2/Phase 3290 participants (Anticipated)Interventional2007-11-30Active, not recruiting
Total Neoadjuvant Therapy Versus Standard Therapy of Locally Advanced Rectal Cancer With High Risk Factors for Failure [NCT04679597]161 participants (Actual)Observational2016-01-01Completed
A Phase 3, Multicenter, Randomized, Double-Blind, Placebo Controlled Study of Rilotumumab (AMG 102) With Cisplatin and Capecitabine (CX) as First-line Therapy in Advanced MET-Positive Gastric or Gastroesophageal Junction Adenocarcinoma [NCT02137343]Phase 334 participants (Actual)Interventional2014-07-31Terminated(stopped due to All Amgen sponsored AMG102 clinical studies were terminated following a pre-planned Data Monitoring Committee safety review of study 20070622.)
Capecitabine-based Chemoradiotherapy in Combination With the IL-1 Receptor Antagonist Anakinra for Rectal Cancer Patients. A Phase I Trial of the German Rectal Cancer Study Group [NCT04942626]Phase 112 participants (Actual)Interventional2021-08-20Active, not recruiting
A Phase 3, Multicenter, Randomized, Double-Blind, Placebo Controlled Study of Rilotumumab (AMG102) With Epirubicin, Cisplatin, and Capecitabine (ECX) as First-line Therapy in Advanced MET-Positive Gastric or Gastroesophageal Junction Adenocarcinoma [NCT01697072]Phase 3609 participants (Actual)Interventional2012-10-31Terminated(stopped due to All Amgen sponsored AMG102 clinical studies were terminated following a pre-planned Data Monitoring Committee safety review of study 20070622.)
Phase I Study of Epigenetic Priming Using Azacitidine With Neoadjuvant Chemotherapy in Patients With Resectable Esophageal Cancer [NCT01386346]Phase 112 participants (Actual)Interventional2011-06-30Completed
A Phase I Study of the mTOR Inhibitor Temsirolimus Plus Capecitabine in Patients With Advanced Malignancies [NCT01050985]Phase 147 participants (Actual)Interventional2010-07-31Completed
A Double-blind, Randomised, Multicenter, Phase III Study of Bevacizumab in Combination With Capecitabine and Cisplatin Versus Placebo in Combination With Capecitabine and Cisplatin, as First-line Therapy in Patients With Advanced Gastric Cancer [NCT00548548]Phase 3774 participants (Actual)Interventional2007-09-30Completed
Phase Ⅱ Trial of Fixed Dose Rate Gemcitabine and Cisplatin Chemotherapy Followed by Chemoradiation With Capecitabine in Patients With Locally Advanced Pancreatic Cancer [NCT01396668]Phase 235 participants (Anticipated)Interventional2004-12-31Completed
IXTEND: A Randomized Phase 2 Study to Evaluate the Combination of Ixabepilone Plus Capecitabine or Capecitabine Plus Docetaxel in the Treatment of Metastatic Breast Cancer [NCT00546364]Phase 262 participants (Actual)Interventional2008-02-29Terminated(stopped due to Slow Accrual)
A Randomized, Open, Parallel-controlled, Multicenter Phase III Trial of SHR-A1811 Versus Investigator Chemotherapy in HER2-low Expressing Recurrent/Metastatic Breast Cancer [NCT05814354]Phase 3530 participants (Anticipated)Interventional2023-06-30Recruiting
A Phase II Study of Immunotherapy With Durvalumab and Tremelimumab in Combination With Capecitabine or Without Capecitabine in Adjuvant Situation for Biliary Tract Cancer [NCT05239169]Phase 240 participants (Anticipated)Interventional2022-05-23Recruiting
Correlation of Genomic Variation in Enzymes Responsible for Metabolism of Capecitabine With Drug Metabolism Using a Limited Pharmacokinetic Sampling Plan [NCT00960544]Phase 20 participants (Actual)Interventional2019-01-31Withdrawn(stopped due to Principal Investigator departed from institution)
PEXG (Cisplatin, Epirubicin, Capecitabine, Gemcitabine) Versus PDXG (Cisplatin, Docetaxel, Capecitabine, Gemcitabine) in Locally Advanced or Metastatic Pancreatic Adenocarcinoma: A Randomized Phase II Trial [NCT00966706]Phase 2105 participants (Actual)Interventional2005-06-30Completed
A Single Arm，Multicenter，Open-label Study of Dalpiciclib Plus Letrozole and Capecitabine of First-line Treatment With High-risk HR- Positive /HER-2 Negative Advanced Breast Cancer [NCT05469750]Phase 248 participants (Anticipated)Interventional2022-08-10Not yet recruiting
Multicenter, Open Lable Phase II Study to Evaluate the Safety and Efficacy of a Perioperative Chemotherapy With Docetaxel, Cisplatin and Capecitabine in Patients With Gastric Adenocarcinoma, Adenocarcinoma of the Gastro-esophageal Junction or the Distal E [NCT00865982]Phase 250 participants (Anticipated)Interventional2008-09-30Active, not recruiting
A Randomized Phase 2 Study to Evaluate Safety and Efficacy of the Combination of SHR-1210 With Capecitabine + Oxaliplatin or Apatinib as First-line Treatment in Patients With Advanced Gastric or Gastroesophageal Junction Adenocarcinoma [NCT03472365]Phase 267 participants (Actual)Interventional2018-04-02Completed
Short-course Radiotherapy Combined With CAPOX and Pd-1 Inhibitor for Locally Advanced Colon Cancer: a Randomized, Prospective, Multicentre, Phase II Trial (TORCH-C) [NCT05732493]Phase 2120 participants (Anticipated)Interventional2023-03-01Not yet recruiting
Capecitabine and Bevacizumab ± Vinorelbine as 1st Line Treatment in HER-2 Negative Metastatic or Locally Advanced Inoperable Breast Cancer Patients [NCT00868634]Phase 3600 participants (Actual)Interventional2009-02-28Completed
A Phase I/II Study of Gemcitabine, Nab-paclitaxel, Capecitabine, Cisplatin, and Irinotecan (GAX-CI) in Combination in Metastatic Pancreatic Cancer [NCT03535727]Phase 1/Phase 286 participants (Anticipated)Interventional2018-06-21Recruiting
Neoadjuvant Radiotherapy Combined With Capecitabine and Sorafenib in Patients With Advanced, K-ras Mutated Rectal Cancer. A Multicenter Phase I/IIa Trial. [NCT00869570]Phase 1/Phase 254 participants (Actual)Interventional2009-03-31Completed
Phase II Trial of Capecitabine (Xeloda) and Lapatinib (Tykerb) as First-line Therapy in Patients With HER2/Neu-Overexpressing Advanced or Metastatic Breast Cancer [NCT00496366]Phase 211 participants (Actual)Interventional2007-07-23Terminated
A Randomized Two-armed Open Study on the Adjuvant Therapy in Patients With R0/R1 Resected Pancreatic Carcinoma With Gemcitabine Plus Capecitabine (Arm GC) vs. Gemcitabine Plus Cisplatin With Regional Hyperthermia (Arm GPH) [NCT01077427]Phase 3336 participants (Anticipated)Interventional2012-03-31Recruiting
Neoadjuvant Chemoradiation Therapy With Oxaliplatin and Capecitabine for Patients With Surgically Resectable Gastric Cancer: A Pilot Phase II Trial With Molecular Correlates [NCT00335959]Phase 27 participants (Actual)Interventional2006-05-31Terminated(stopped due to Closed due to slow accrual)
Phase I Clinical Study of Liposomal Paclitaxel Plus Capecitabine in Chinese Patients With Advanced Gastric Carcinoma [NCT00881816]Phase 115 participants (Anticipated)Interventional2009-04-30Active, not recruiting
A Phase I Study of the Hsp90 Inhibitor AUY922 Plus Capecitabine for the Treatment of Patients With Advanced Solid Tumors [NCT01226732]Phase 123 participants (Actual)Interventional2010-11-30Completed
An Open Labelled, Multicenter-phase II Study of Chiauranib Combine With Capecitabine in Advanced Triple-negative Breast Cancer Failed to Prior Anthracyclines and Taxanes Therapy [NCT05336721]Phase 238 participants (Anticipated)Interventional2021-11-05Recruiting
Phase 1/2 Evaluation of Adenoviral p53 (Ad-p53) in Combination With Capecitabine (Xeloda) or Anti-PD-1 in Patients With Unresectable Liver Metastases of Colorectal Carcinoma(CRC) and Other Solid Tumors, Recurrent Head and Neck Squamous Cell Carcinoma (HNS [NCT02842125]Phase 1/Phase 24 participants (Actual)Interventional2018-11-20Terminated(stopped due to Arm C rolled into parallel study; Arms A and B halted for greater efficacy in Arm C)
Phase II Study of Capecitabine and Temozolomide for Progressive, Differentiated, Metastatic Neuroendocrine Cancers [NCT00869050]Phase 241 participants (Actual)Interventional2005-08-31Completed
A Phase II Study of XELOX and Toripalimab in the Neoadjuvant Treatment of Stage II/III Gastric or GE Junction Adenocarcinoma [NCT04119622]Phase 230 participants (Anticipated)Interventional2019-10-08Recruiting
Combined Biological Treatment and Chemotherapy for Patients With Inoperable Cholangiocarcinoma [NCT00779454]Phase 272 participants (Actual)Interventional2008-09-30Completed
A Phase I/II Study of Capecitabine/Oxaliplatin (XELOX) in Combination With Bevacizumab and Imatinib as First-line Treatment of Patients With Stage IV Colorectal Cancer [NCT00784446]Phase 1/Phase 251 participants (Actual)Interventional2008-04-30Completed
A Phase II Study of Preoperative Capecitabine and Concomitant Radiation in Women With Advanced Inflammatory or Non-Inflammatory Breast Cancer [NCT00916578]Phase 233 participants (Actual)Interventional2009-06-05Completed
A Prospective Phase I Study of Radiation Therapy and Concurrent Capecitabine and Oxaliplatin Chemotherapy in the Treatment of Locally Advanced Pancreas Adenocarcinoma [NCT00707278]Phase 113 participants (Actual)Interventional2005-09-30Completed
Short Course Oncology Therapy - A Study of Adjuvant Chemotherapy in Colorectal Cancer [NCT00749450]Phase 36,088 participants (Actual)Interventional2008-03-31Completed
Clinical Study to Assess Entry of Chemotherapeutic Agents Into Brain Metastases in Women With Breast Cancer [NCT00795678]10 participants (Actual)Observational2008-09-30Completed
A Randomized, Multicentre, Open-Label, Phase III Study of Lapatinib Plus Capecitabine Versus Trastuzumab Plus Capecitabine in Patients With Anthracycline- or Taxane-Exposed ErbB2-Positive Metastatic Breast Cancer [NCT00820222]Phase 3540 participants (Actual)Interventional2009-04-14Completed
A Parallel Phase II Study With Irinotecan/Cetuximab (Until PD) Followed by XELOX/Cetuximab (Until PD) vs the Reverse Sequence in Metastatic CRC With Previous Benefit on Irinotecan/Bevacizumab Based Therapy [NCT00755534]Phase 268 participants (Actual)Interventional2008-11-30Terminated(stopped due to Due to poor accrual)
A Phase II Study of Weekly Docetaxel and Capecitabine for Persistent or Recurrent Platinum Resistant Epithelial Carcinoma of the Ovary, Fallopian Tube or Peritoneum [NCT00354601]Phase 22 participants (Actual)Interventional2006-01-31Terminated(stopped due to funding withdrawn)
A Phase I, Multi-arm, Dose Escalation Study of Brivanib Alaninate Combined With Several Chemotherapy Regimens in Subjects With Solid Tumors [NCT00798252]Phase 1111 participants (Actual)Interventional2009-03-31Completed
A Phase Ib/II Study of SHR-A1811 Combinations in Patients With Advanced/Metastatic HER2+ Gastric /Gastroesophageal Junction Adenocarcinoma [NCT05671822]Phase 2156 participants (Anticipated)Interventional2023-03-14Recruiting
A Phase 2 Study to Evaluate the Efficacy and Safety of an Adjuvant Therapeutic Cancer Vaccine (AST-301, pNGVL3-hICD) in Patients With HER2 Low Breast Cancer (Cornerstone-001) [NCT05163223]Phase 2146 participants (Anticipated)Interventional2022-02-28Recruiting
Randomized Multicenter Phase III Study in Patients With Locally Advanced Adenocarcinoma of the Pancreas: Gemcitabine With or Without Chemoradiotherapy and With or Without Erlotinib. Intergroup Study [NCT00634725]Phase 3820 participants (Anticipated)Interventional2008-02-29Completed
Circulating Tumour DNA Based Decision for Adjuvant Treatment in Colon Cancer Stage II Evaluation (CIRCULATE) AIO-KRK-0217 [NCT04089631]Phase 34,812 participants (Anticipated)Interventional2020-06-26Recruiting
Preoperative Chemoradiation With VMAT-SIB in Rectal Cancer: a Phase II Study. [NCT02745639]Phase 218 participants (Actual)Interventional2010-02-28Completed
Professor, Ege University Faculty of Dentistry [NCT02744703]10 participants (Actual)Interventional2013-04-30Completed
Randomized, Controlled, Multicenter Phase III Clinical Study Evaluating the Efficacy and Safety of RC48-ADC for the Treatment of Locally Advanced or Metastatic Breast Cancer With Low Expression of HER2 [NCT04400695]Phase 3366 participants (Anticipated)Interventional2020-09-29Recruiting
A Phase 2 Trial of Capecitabine Concomitantly With Whole Brain Radiotherapy(WBRT) Followed by Capecitabine and Sunitinib for Central Nervous System, (CNS) Metastases in Breast Cancer [NCT00570908]Phase 212 participants (Actual)Interventional2009-02-28Terminated(stopped due to Due to poor accrual this study is being closed to accrual)
Phase 1/1b Study Investigating Safety, Tolerability, PK and Antitumor Activity of Anti-TIGIT Monoclonal Antibody BGB-A1217 in Combination With Anti-PD-1 Monoclonal Antibody Tislelizumab in Patients With Advanced Solid Tumors [NCT04047862]Phase 1542 participants (Anticipated)Interventional2019-08-26Recruiting
Phase II Study of Preoperative Radiation With Concurrent Capecitabine, Oxaliplatin and Bevacizumab Followed by Surgery and Postoperative 5-FU, Leucovorin, Oxaliplatin (FOLFOX) and Bevacizumab in Patients With Locally Advanced Rectal Cancer [NCT00321685]Phase 257 participants (Actual)Interventional2006-07-25Completed
A Phase I Trial of Capecitabine Rapidly Disintegrating Tablets and Concomitant Radiation Therapy in Children With Newly Diagnosed Brainstem Gliomas and High Grade Gliomas [NCT00532948]Phase 124 participants (Actual)Interventional2007-05-31Completed
A Phase II Trial of Combination Irinotecan and Capecitabine as Second-Line Treatment for Patients With Locally Advanced/Metastatic Biliary Tract Cancers Who Progressed or Intolerant to Front-Line Gemcitabine and Platinum Combination [NCT02720601]Phase 20 participants (Actual)Interventional2015-11-30Withdrawn(stopped due to Study was never submitted to the IRB & never opened. PI is leaving institution.)
An Open-Label, Multicenter Phase Ib Study of The Safety and Efficacy of Atezolizumab (Anti-PD-L1 Antibody) Administered in Combination With Bevacizumab and/or Other Treatments in Patients With Solid Tumors [NCT02715531]Phase 1243 participants (Actual)Interventional2016-04-06Completed
Evaluation on the Tolerance and Preliminary Efficacy of Sintilimab (IBI308) Combined With Bevacizumab, Oxaliplatin and Capecitabine Regimen for Ras Gene Mutant and Microsatellite Stable Unresectable Metastatic Colorectal Cancer [NCT04194359]Phase 225 participants (Anticipated)Interventional2021-02-04Active, not recruiting
A Non Randomized Phase II Trial to Assess Efficacy and Safety of Bevacizumab, Capecitabine and Oxaliplatin as First Line Treatment for Elderly Patients With Metastatic Colorectal Adenocarcinoma, Suitable for Polychemotherapy Treatment [NCT01067053]Phase 269 participants (Anticipated)Interventional2009-11-30Active, not recruiting
Antiangiogenic Treatment Strategy With Metronomic Chemotherapy Regimen Combined With a Cox-2 Inhibitor and a Bisphosphonate for Patients With Metastatic Breast Cancer [NCT01067989]Phase 222 participants (Actual)Interventional2010-03-31Terminated(stopped due to No satisfactory acrual)
A Phase II Trial of Adjuvant Capecitabine/Gemcitabine Chemotherapy Followed By Concurrent Capecitabine and Radiotherapy in Extrahepatic Cholangiocarcinoma (EHCC) [NCT00789958]Phase 2105 participants (Actual)Interventional2008-12-31Completed
A Randomised Phase II/III Trial of Peri-Operative Chemotherapy With or Without Bevacizumab in Operable Oesophagogastric Adenocarcinoma and A Feasibility Study Evaluating Lapatinib in HER-2 Positive Oesophagogastric Adenocarcinomas and (in Selected Centres [NCT00450203]Phase 2/Phase 31,103 participants (Anticipated)Interventional2007-10-31Recruiting
BACCI: A Phase II Randomized, Double-Blind, Placebo-Controlled Study of Capecitabine Bevacizumab Plus Atezolizumab Versus Capecitabine Bevacizumab Plus Placebo in Patients With Refractory Metastatic Colorectal Cancer [NCT02873195]Phase 2133 participants (Actual)Interventional2017-07-07Active, not recruiting
A Phase 2 Randomized Open-Label Study of Neratinib Versus Lapatinib Plus Capecitabine For The Treatment Of ErbB-2 Positive Locally Advanced Or Metastatic Breast Cancer [NCT00777101]Phase 2233 participants (Actual)Interventional2009-02-04Completed
Randomized Trial of Standard Dose Versus High Dose of Radiotherapy in Rectal Preservation With Chemo-radiotherapy to Patients With Early Low and Mid Rectal Cancer: The Watchful Waiting 3 Trial (WW3) [NCT04095299]Phase 2111 participants (Anticipated)Interventional2020-01-20Recruiting
A Phase 2 Open-Label Study Evaluating the Efficacy and Safety of Telatinib in Combination With Chemotherapy as First-Line Therapy in Subjects With Advanced Gastric Cancer [NCT00952497]Phase 248 participants (Actual)Interventional2009-06-30Completed
A Randomized Phase III Study of Metronomic vs. Intermittent Capecitabine Maintenance Therapy Following First-line Capecitabine and Docetaxel Therapy in HER2-negative Metastatic Breast Cancer [NCT01917279]Phase 3280 participants (Anticipated)Interventional2013-10-31Recruiting
Hypofractionated Radiotherapy Combined With Chemotherapy and Toripalimab for Locally Recurrent Rectal Cancer: a Single-arm, Two-cohort, Phase II Trial (TORCH-R) [NCT05628038]Phase 293 participants (Anticipated)Interventional2022-08-18Recruiting
A Phase 1b Multicentre, Open-label, Modular, Dose-finding and Dose-expansion Study to Explore the Safety, Tolerability, Pharmacokinetics and Anti-tumour Activity of Trastuzumab Deruxtecan (T-DXd) in Combination With Other Anti-cancer Agents in Patients Wi [NCT04556773]Phase 1139 participants (Actual)Interventional2020-12-17Active, not recruiting
A Phase III Open-label, Multicenter Trial of Maintenance Therapy With Avelumab (MSB0010718C) Versus Continuation of First-line Chemotherapy in Subjects With Unresectable, Locally Advanced or Metastatic, Adenocarcinoma of the Stomach, or of the Gastro-esop [NCT02625610]Phase 3499 participants (Actual)Interventional2015-12-24Completed
A Phase 1 Dose Escalation Safety Study Combining the ATR Inhibitor M6620 With Chemoradiotherapy in Oesophageal Cancer & Other Solid Cancers Using Time to Event Continual Reassessment Method [NCT03641547]Phase 136 participants (Actual)Interventional2018-12-04Completed
Maintenance Chemotherapy for Metastatic Colorectal Carcinoma [NCT02043821]80 participants (Anticipated)InterventionalNot yet recruiting
A Phase III Trial of Vinflunine Plus Capecitabine Versus Capecitabine Alone in Patients With Advanced Breast Cancer Previously Treated With or Resistant to an Anthracycline and Who Are Taxane Resistant. [NCT01095003]Phase 3770 participants (Actual)Interventional2009-05-31Completed
A Phase II Trial of Xeloda, Every Three Week Taxol and Herceptin in Metastatic Breast Cancer [NCT00006108]Phase 1/Phase 20 participants Interventional1999-08-31Completed
A Phase I Study Of Cyclophoshamide And Epirubicin In Combination With Capecitabine (XELODA) (CEX) As Primary Treatment Of Locally Advanced/Inflammatory Or Large Operable Breast Cancer [NCT00008034]Phase 115 participants (Actual)Interventional2000-02-29Completed
A Phase II Trial of Preoperative Capecitabine Plus Irinotecan Followed by Combined Modality Capecitabine and Radiation for Locally Advanced Rectal Cancer: Hoosier Oncology Group GI03-53 [NCT00216086]Phase 222 participants (Actual)Interventional2005-05-31Terminated(stopped due to Funding withdrawn)
A Phase 1, Multicenter, Dose-Escalation Study to Investigate the Safety and Tolerability of ADH-1 in Combination With 1) Carboplatin or 2) Docetaxel or 3) Capecitabine in Subjects With N-Cadherin Positive, Advanced Solid Tumors (Adherex Protocol Number AH [NCT00390676]Phase 10 participants Interventional2006-11-30Completed
A Phase II Study of Total Neoadjuvant Therapy for Locally Advanced Rectal Cancer [NCT02942563]Phase 2100 participants (Anticipated)Interventional2016-11-01Recruiting
A Pilot Study of Cytoxan, Epirubicin, and Capecitabine in Women With Stage I/II/IIIA Breast Cancer [NCT00146588]55 participants (Actual)Interventional2002-04-30Completed
A Phase II Evaluation of Preoperative Chemoradiotherapy Utilizing Intensity Modulated Radiation Therapy (IMRT) in Combination With Capecitabine and Oxaliplatin for Patients With Locally Advanced Rectal Cancer [NCT00613080]Phase 279 participants (Actual)Interventional2008-04-30Completed
"A Translational Randomized Phase III Study Exploring the Effect of the Addition of Capecitabine to Carboplatine Based Chemotherapy in Early Triple Negative Breast Cancer" [NCT04335669]Phase 3920 participants (Anticipated)Interventional2019-12-20Recruiting
Phase II Study of Irinotecan Plus Capecitabine in Patients With Antracycline and Taxane Pretreated Metastatic Breast Cancer [NCT00532714]Phase 236 participants (Actual)Interventional2006-08-31Completed
A Phase I Trial of Vandetanib Combined With Capecitabine, Oxaliplatin and Bevacizumab for the First-Line Treatment of Metastatic Colorectal Cancer [NCT00532909]Phase 113 participants (Actual)Interventional2006-07-31Completed
Pharmacokinetic Study of Capecitabine in Elderly Cancer Patient (≥75 Years) [NCT00812864]Phase 420 participants (Actual)Interventional2009-01-31Completed
Docetaxel and Carboplatin Followed by a Dose-Ranging Study of Oral Capecitabine, Weekly Docetaxel, and Concomitant External Beam Radiotherapy for the Treatment of Patients With Stage II-III Carcinoma of the Esophagus and Gastro-Esophageal Junction [NCT00153881]Phase 144 participants (Actual)Interventional2000-02-29Completed
Phase 1b Multiple Ascending Dose Study of BMS-833923 (XL139) Administered in Combination With Cisplatin and Capecitabine as First-Line Therapy in Patients With Inoperable, Metastatic Gastric, Gastroesophageal, or Esophageal Adenocarcinomas [NCT00909402]Phase 139 participants (Actual)Interventional2009-11-30Completed
A Three-Arm Randomised Controlled Trial Comparing Either Continuous Chemotherapy Plus Cetuximab or Intermittent Chemotherapy With Standard Continuous Palliative Combination Chemotherapy With Oxaliplatin and a Fluoropyrimidine in First Line Treatment of Me [NCT00182715]Phase 32,421 participants (Anticipated)Interventional2005-03-31Active, not recruiting
A Phase I/II Study on the Treatment With Taxotere in Combination With Xeloda in Patients With Metastatic Oesophageal Cancer or Cancer in the Cardia Region [NCT00821912]Phase 1/Phase 293 participants (Actual)Interventional2006-03-31Active, not recruiting
Pilot Study to Determine Therapeutic Response of Oral Capecitabine (Xeloda) in Recurrent High Grade Gliomas (HGGs) by Establishing the Radiographic Response Rate Using Modified Macdonald Criteria [NCT00717197]Phase 230 participants (Actual)Interventional2008-07-31Completed
A Single Arm, Open-label Phase II Study to Evaluate the Efficacy and Safety of Capecitabine Plus Oxaliplatin (XELOX) in the Peri-operative Treatment of Patients With Potentially Resectable Liver Metastasis From Colorectal Cancer [NCT00997685]Phase 2110 participants (Anticipated)Interventional2009-11-30Not yet recruiting
A Phase I/II, Multi-Center, Open-Label, Dose-Escalation, Safety and Efficacy Study of PHY906 Plus Capecitabine in Patients With Advanced Pancreatic Carcinoma [NCT00411762]Phase 1/Phase 225 participants (Actual)Interventional2006-12-31Completed
The Third Phase of Immunotherapy and Concurrent Chemoradiotherapy in Patients With Esophageal Cancer Recurrence Was Compared With the Clinical Comparison [NCT04404491]Phase 3240 participants (Anticipated)Interventional2020-06-01Not yet recruiting
A Randomized Phase III Trial of Neoadjuvant Therapy in Patients With Palpable and Operable Breast Cancer Evaluating the Effect on Pathologic Complete Response (pCR) of Adding Capecitabine or Gemcitabine to Docetaxel When Administered Before AC With or Wit [NCT00408408]Phase 31,206 participants (Actual)Interventional2006-11-30Active, not recruiting
Randomized Phase II Trial of Sequential Docetaxel Followed by Capecitabine Versus Concomitant, Dose-Dense Docetaxel/Capecitabine as in Induction Therapy for Early Stage Breast Cancer [NCT00209092]Phase 251 participants (Actual)Interventional2006-08-31Completed
An Intergroup Randomized Phase II Study of Bevacizumab (NSC 704865) or Cetuximab (NSC 714692) in Combination With Gemcitabine and in Combination With Chemoradiation (Capecitabine and Radiation) in Patients With Completely-Resected Pancreatic Carcinoma [NCT00305877]Phase 2137 participants (Actual)Interventional2006-02-28Completed
Phase II Randomized Study to Compare Capecitabine + Bevacizumab Concomitantly With Radiotherapy Versus Capecitabine Concomitantly With Radiotherapy, as Neoadjuvant Treatment for Patients With Localized and Resectable Rectal Cancer [NCT01043484]Phase 290 participants (Actual)Interventional2009-12-31Completed
A Randomised Fase I/II Trial With Irinotecan, Cetuximab and Everolimus (ICE)Compared to Capecitabine and Oxaliplatin (CapOx) for Patients With Gemcitabin Resistant Pancreatic Cancer [NCT01042028]Phase 1/Phase 239 participants (Actual)Interventional2010-01-31Terminated(stopped due to Emergence of FOLFIRINOX and slow recruitment)
A Multicenter Trial for Microarray Analysis of Colon Cancer Outcome-A (MACCO-A) [NCT00127036]Phase 265 participants (Actual)Interventional2003-10-31Terminated(stopped due to drug now on market)
An Open-label Study to Assess the Pharmacokinetic Interaction Between Xeloda and Oxaliplatin in Patients With Metastatic Colorectal Cancer. [NCT00353262]Phase 136 participants (Actual)Interventional2005-07-31Completed
A Phase I Study of Perifosine + Capecitabine for Patients With Advanced Colon Cancer [NCT01048580]Phase 110 participants (Actual)Interventional2009-10-31Completed
A Real-world Observational Study of Fruquintinib in Combination With Irinotecan and Capecitabine for the Second-line Treatment of Patients With Advanced Colorectal Cancer [NCT06169202]50 participants (Anticipated)Observational2023-06-01Recruiting
A Phase III, Open-label, Randomised Study of Neoadjuvant Datopotamab Deruxtecan (Dato-DXd) Plus Durvalumab Followed by Adjuvant Durvalumab With or Without Chemotherapy Versus Neoadjuvant Pembrolizumab Plus Chemotherapy Followed by Adjuvant Pembrolizumab W [NCT06112379]Phase 31,728 participants (Anticipated)Interventional2023-11-14Recruiting
Dose-finding Phase 1 Trial: Evaluating Safety and Biomarkers Using DK210 (EGFR) for Inoperable Locally Advanced and/or Metastatic EGFR+ Tumors With Progressive Disease Failing Systemic Therapy [NCT05704985]Phase 160 participants (Anticipated)Interventional2023-04-03Recruiting
Phase I Trial of ZW25 in Patients With Locally Advanced (Unresectable) and/or Metastatic HER2-expressing Cancers [NCT02892123]Phase 1279 participants (Actual)Interventional2016-09-30Active, not recruiting
A Phase I/II Study of Vorinostat (Zolinza®) in Combination With Capecitabine (X) and Cisplatin (P) for 1st Line Treatment of Metastatic or Recurrent Gastric Cancer [NCT01045538]Phase 1/Phase 245 participants (Actual)Interventional2010-02-28Completed
A Phase 1-2 Trial of Cetuximab in Combination With Oxaliplatin, Capecitabine, and Radiation Therapy Followed by Surgical Resection for Locally-Advanced Rectal Cancer [NCT00226941]Phase 1/Phase 223 participants (Actual)Interventional2004-06-30Terminated(stopped due to The response rate observed in the phase 1 portion of the study did not merit further evaluation in phase 2 portion of the study.)
Phase I-II Study of Capecitabine and Oxaliplatin in Combination With Radiotherapy in Patients With Unresectable Gastro-Intestinal Cancer [NCT01016639]Phase 1/Phase 2106 participants (Actual)Interventional2003-06-30Completed
A Phase II Study to Evaluate the Efficacy, Safety, and Genomic Markers of Response of Capecitabine as NeoAdjuvant Therapy in Women With Newly Diagnosed Locally Advanced Breast Cancer [NCT00347438]Phase 218 participants (Actual)Interventional2006-09-30Terminated(stopped due to a result of slow accrual)
Phase II Study: Neoadjuvant Gemcitabine, Docetaxel and Capecitabine Followed by Neoadjuvant Radiation Therapy With Gemcitabine and Capecitabine in the Treatment of Stage II and III Pancreatic Adenocarcinoma [NCT01065870]Phase 2/Phase 364 participants (Anticipated)Interventional2009-12-31Recruiting
Phase I Trial of Oral Capecitabine Combined With 131I-huA33 in Patients With Metastatic Colorectal Cancer [NCT00291486]Phase 119 participants (Actual)Interventional2003-10-31Completed
A Feasibility Study for Individualized Treatment of Patients With Advanced Pancreatic Cancer [NCT00276744]Phase 2249 participants (Actual)Interventional2005-10-31Terminated(stopped due to Because there was no longer an active laboratory component to this study.)
Phase II Study of Capecitabine in Combination With Vinorelbine and Trastuzumab for the First- or Second-LineTreatment of HER2+ Metastatic Breast Cancer [NCT00093808]Phase 247 participants (Actual)Interventional2004-08-31Completed
A Multi Phase II Clinical Trials Evaluating the Association of Bevacizumab With Weekly Paclitaxel and Capecitabine in First Line Treatment for Patients With Triple Negative Metastatic or Locally Advanced Cancer [NCT01069796]Phase 264 participants (Actual)Interventional2010-04-30Terminated(stopped due to The number of inclusion was reached normally)
Phase II Clinical Trial: Capecitabine Maintenance Therapy in Colorectal Cancer Patients With Stage IIIC and R0-R1 Resected Stage IV [NCT01880658]Phase 2100 participants (Anticipated)Interventional2013-06-30Recruiting
A Phase II Study of OSI-774 (Tarceva) in Combination With Capecitabine in Previously Treated Patients With Metastatic Pancreatic Cancer [NCT00125021]Phase 232 participants (Actual)Interventional2003-10-31Completed
Safety and Efficacy Evaluation of Capecitabine, Cisplatin, and Herzuma Combination Chemotherapy for the First Line Treatment of Advanced Gastric or Gastroesophageal Junction Adenocarcinoma Patients. [NCT03588533]Phase 250 participants (Anticipated)Interventional2018-06-10Recruiting
Pre-operative Radiotherapy/ Oxaliplatin/ Capecitabine Treatment For Unresectable Locally-advanced Rectal Cancer (PROCTFUL) [NCT00263029]Phase 218 participants (Actual)Interventional2002-06-30Completed
S1 Versus Capecitabine in the First Line Treatment of Metastatic Colorectal Cancer Patients, the SALTO Randomised Phase III Study of the Dutch Colorectal Cancer Group. A Safety Evaluation of Oral Fluoropyrimidines [NCT01918852]Phase 3161 participants (Actual)Interventional2013-12-31Completed
8 Continuous vs 8 Intermittent Cycles in First and Second Line Treatment of Patients With HER2/Neu Negative, Incurable, Metastatic or Unresectable Locally Advanced Breast Cancer. [NCT01935492]Phase 3420 participants (Actual)Interventional2010-11-30Completed
First- Line Treatment With Durvalumab Plus XELOX Chemotherapy in Patients With Advanced Gastrointestinal Neuroendocrine Carcinoma: A Prospective Single-arm Phase II Study [NCT06070740]Phase 222 participants (Anticipated)Interventional2023-11-01Recruiting
A Multicenter Phase II Study to Determine the Efficacy of Capecitabine as First Line Monochemotherapy in Patients With HER2 Negative, Medium-risk, Metastatic Breast Cancer [NCT00196820]Phase 2200 participants (Anticipated)Interventional2005-07-31Completed
Ibandronate With or Without Capecitabine in Elderly Patients With Early Breast Cancer [NCT00196859]Phase 31,500 participants (Anticipated)Interventional2004-06-30Completed
A Phase II Trial of Thalidomide and Capecitabine in Metastatic Renal Cell Carcinoma [NCT00226980]Phase 230 participants (Anticipated)Interventional2002-10-31Completed
A Randomized, Controlled, Open-Label, Multicenter, Phase 2 Study of Nimotuzumab Plus Docetaxel and Capecitabine Versus Docetaxel and Capecitabine as First-Line Treatment in Patients With Recurrent/Metastatic Triple Negative Breast Cancer [NCT01939054]Phase 290 participants (Anticipated)Interventional2013-09-30Recruiting
A Phase II Study of Oxaliplatin, 5-fluorouracil, and Leucovorin in Combination With Oral Capecitabine in Patients With Metastatic Colorectal Cancer [NCT00205322]Phase 245 participants (Actual)Interventional2004-04-30Completed
Randomized Phase II Trial of Capecitabine Plus Oral Vinorelbine Day 1 and 8 vs Metronomic Capecitabine Plus Oral Vinorelbine as Treatment of Metastatic Breast Cancer. [NCT01941771]Phase 2110 participants (Actual)Interventional2012-06-30Completed
A Phase II Study of Substitution of 5-FU (Fluorouracil) by Capecitabine in Scheme of Chemo-radiotherapy in Patients With Squamous Cell Carcinoma of the Anal Canal. [NCT01941966]Phase 251 participants (Anticipated)Interventional2010-11-30Completed
A Phase III, Randomized Study of Adjuvant Chemotherapy for Patients With Rectal Adenocarcinoma Who Achieved Suboptimal Response After Neoadjuvant Chemo-radiotherapy. [NCT01941979]Phase 3309 participants (Anticipated)Interventional2011-09-30Recruiting
Phase I Study to Assess the Optimal Dose for Pazopanib in Combination With Capecitabine in Patients With HER2-negative, Metastatic Breast Cancer (PazoX) [NCT01498458]Phase 19 participants (Actual)Interventional2010-10-31Completed
A Phase I Trial of Capecitabine or Continuous Infusion 5-Fluorouracil in Combination With Weekly Irinotecan and Cisplatin in Patients With Advanced Solid Tumor Malignancies [NCT00215501]Phase 154 participants (Actual)Interventional2001-11-30Completed
A Multicentre, Randomized Study of Trastuzumab Combined With Chemotherapy or Endocrine Therapy as the First Line Treatment for Patients With Metastatic Luminal B2 Breast Cancer Subtype [NCT01950182]Phase 3392 participants (Actual)Interventional2013-09-16Completed
A Phase I Dose Escalation Study to Assess the Maximum Tolerated Dose and Feasibility of Combining Oral Capecitabine (Xeloda) and Conformal Radiotherapy (CRT) for Patients With Unresectable Hepatocellular Carcinoma, Multiple Hepatic Metastases or Cholangio [NCT00216437]Phase 130 participants (Anticipated)Interventional2004-12-31Terminated(stopped due to lack of accrual)
An Open-label, Multicenter Phase II Study of QL1706 Monotherapy or in Combination With Bevacizumab and XELOX as First-line Treatment of Unresectable Advanced or Metastatic CRC [NCT05799820]Phase 260 participants (Anticipated)Interventional2022-09-29Recruiting
A Randomized Phase II Trial of Preoperative Chemoradiation (Preop CRT) Followed by CapOx (Capecitabine Plus Oxaliplatin) Versus Preop CRT Alone for Locally Advanced Rectal Cancer (LARC) [NCT01952951]Phase 2110 participants (Actual)Interventional2014-06-30Active, not recruiting
A Phase 3, Multi-Center, Double-Blind, Randomized, Efficacy and Safety Study of M108 Monoclonal Antibody Plus CAPOX Versus Placebo Plus CAPOX as First-line Treatment for Claudin (CLDN) 18.2-Positive, HER2-Negative, PD-L1 CPS<5, Locally Advanced Unresectab [NCT06177041]Phase 3486 participants (Anticipated)Interventional2023-12-18Not yet recruiting
A Phase III, Randomized, Double-Blind, Placebo-Controlled, Multicenter, Global Study of Rilvegostomig in Combination With Chemotherapy as Adjuvant Treatment After Resection of Biliary Tract Cancer With Curative Intent (ARTEMIDE-Biliary01) [NCT06109779]Phase 3750 participants (Anticipated)Interventional2023-12-04Recruiting
Phase IV Multi-Institutional Randomized Trial of Capecitabine Plus Oxaliplatin With Bevacizumab in Patients With Potentially Resectable Gastric Cancer With Liver Metastasis [NCT01962376]Phase 460 participants (Anticipated)Interventional2013-02-28Recruiting
Phase II Trial of Exploring the Predictive Factors of Docetaxol Plus Capecitabine(TX) Regimen and Oxaliplatin Plus Capecitabine (XELOX) Regimen in the First Line Treatment of Patients With Metastatic Gastric Cancer (MGC) [NCT01963702]Phase 2120 participants (Anticipated)Interventional2012-08-31Recruiting
A Phase 3 Open-label, Randomised Study of Datopotamab Deruxtecan (DatoDXd) With or Without Durvalumab Versus Investigator's Choice of Therapy in Patients With Stage I-III Triple-negative Breast Cancer Who Have Residual Invasive Disease in the Breast and/o [NCT05629585]Phase 31,075 participants (Anticipated)Interventional2022-11-28Recruiting
A Phase 1, Open-label, Multicenter Study of BMS-986360/CC-90001 Alone and in Combination With Chemotherapy or Nivolumab in Advanced Solid Tumors [NCT05625412]Phase 1220 participants (Anticipated)Interventional2022-12-09Recruiting
A Prospective, Multi-Center, Randomized Control Phase 2 Trial of Optimizing Platinum-Based Chemotherapy Based on ERCC1 Expression as First-Line Treatment in Patients With Locally Advanced or Metastatic Gastric Cancer [NCT01967875]Phase 227 participants (Actual)Interventional2013-07-31Terminated(stopped due to slow enrollment)
Phase 2 Study of Two Consequent Chemotherapy Regimens as Induction Preoperative Therapy for Patients With Locally Advanced Triple Negative Breast Cancer [NCT01969032]Phase 241 participants (Actual)Interventional2011-08-31Completed
A Pilot Study of Teng-Long-Bu-Zhong-Tang Based Herbal Therapy in Combination With Chemotherapy in Patients With Metastatic Colorectal Cancer [NCT01975454]Phase 1/Phase 262 participants (Actual)Interventional2012-04-30Completed
Andrographolides With or Without Capecitabine for Elderly Patients With Locally Advanced or Recurrent or Metastasis Inoperable Colorectal Cancer: a Randomized, Open-label Trial. [NCT01993472]Phase 2308 participants (Anticipated)Interventional2013-11-30Terminated(stopped due to low accrual rate)
A Multinational, Randomized, Phase III Study of XELIRI With/Without Bevacizumab Versus FOLFIRI With/Without Bevacizumab As Second-line Therapy in Patients With Metastatic Colorectal Cancer [NCT01996306]Phase 3650 participants (Actual)Interventional2013-12-02Completed
Gene Expression Analysis of Patients With Metastatic Colorectal Cancer Receiving Oxaliplatin Based Chemotherapy [NCT00250029]30 participants (Actual)Interventional2004-04-30Completed
Modified Folinic Acid-Fluorouracil-Oxaliplatin (FOLFOX) Followed by Capecitabine as First-line Chemotherapy for Elderly or Frail Patients With Metastatic or Recurrent Gastric Cancer [NCT02002195]47 participants (Anticipated)Observational2013-11-30Recruiting
Phase II Study of Trastuzumab in Combination With Chemotherapy (Docetaxel Plus Capecitabine) For First Line Treatment of Her2-Positive Advanced Gastric or Gastro-Esophageal Junction Cancer [NCT02004769]Phase 267 participants (Actual)Interventional2013-11-30Completed
Phase II Study of Capecitabine and Weekly Docetaxel Followed by Capecitabine Maintenance for Patients With Metastatic Breast Carcinoma [NCT00225056]Phase 243 participants Interventional2003-10-31Terminated(stopped due to Terminated due to lack of accrual)
XELOX and Bevacizumab in Combination With Tislelizumab for First-Line Treatment of Patients With MSS/pMMR RAS-mutated Metastatic Colorectal Cancer (mCRC): A Single-arm, Phase II Study. [NCT05970302]Phase 252 participants (Anticipated)Interventional2023-07-07Recruiting
Total Neoadjuvant Therapy With Split-course Hypofraction Radiotherapy Combined With CAPOX and Envafolimab Followed by Local Excision for Locally Advanced Very Low Rectal Cancer: an Open-label, Single-arm, Multi-center, Phase II Trial [NCT05969847]Phase 272 participants (Anticipated)Interventional2023-08-15Not yet recruiting
An Open-Label, Multi-center Phase Ⅰb/Ⅱ Study of SHR-A1811 Combined With Capecitabine in Treatment of Unresectable or Metastatic Breast Cancer With Low HER2 Expression. [NCT05845138]Phase 1/Phase 2116 participants (Anticipated)Interventional2023-07-25Recruiting
A Phase 1 Clinical Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Efficacy of ZN-A-1041 Enteric Capsules as a Single Agent or in Combination in Patients With HER2-Positive Advanced Solid Tumors [NCT04487236]Phase 184 participants (Anticipated)Interventional2020-10-15Recruiting
Perioperative Chemotherapy Plus PD-1 Antibody Compared With Perioperative Chemotherapy in the Locally Advanced Gastric Cancer: a Open-label, Phase 2 Randomised Controlled Trial [NCT04250948]Phase 2108 participants (Actual)Interventional2019-10-12Active, not recruiting
Phase III Clinical Study of PD-1 Monoclonal Antibody-activated Autologous Peripheral Blood T-lymphocyte (PD1-T) Combined With XELOX and Bevacizumab in the First-line Treatment of Recurrent and Metastatic Colorectal Cancer [NCT03950154]Phase 3198 participants (Anticipated)Interventional2019-06-01Recruiting
MetronomIc CApecitabine and DOcetaxel as Second-line Chemotherapy for Advanced Gastric Cancer Patients Previously Treated With Fluoropyrimidine and Platinum Agents MiCADO Study [NCT02007148]Phase 251 participants (Anticipated)Interventional2013-11-30Recruiting
A Randomized Phase III Post-operative Trial of Platinum Based Chemotherapy vs. Capecitabine in Patients With Residual Triple-Negative Basal-Like Breast Cancer Following Neoadjuvant Chemotherapy [NCT02445391]Phase 3415 participants (Actual)Interventional2015-10-20Active, not recruiting
Efficacy and Safety of Neoadjuvant Chemo-chemoradio-chemo Sequential Therapy in Locally Advanced Mid/Low Rectal Cancer: a Phase II Trial [NCT02022852]Phase 280 participants (Anticipated)Interventional2013-07-31Recruiting
A Multi-centre Randomised Study of Induction Chemotherapy Followed by Capecitabine (+/-Nelfinavir) With High or Standard Dose Radiotherapy for Locally Advanced Non-metastatic Pancreatic Cancer [NCT02024009]Phase 1/Phase 2289 participants (Anticipated)Interventional2016-03-31Recruiting
A Phase 1b, Open-label Study to Assess the Safety and Tolerability of Tucatinib (ONT-380) Combined With Capecitabine and Trastuzumab, Alone and in Combination in HER2+ Metastatic Breast Cancer [NCT02025192]Phase 160 participants (Actual)Interventional2013-12-31Completed
A Phase III, Multicenter, Open-label, Randomized Study to Assess the Efficacy and Safety of Cetuximab Plus Capecitabine Versus Cetuximab as Maintenance Treatment Following First-line Induction Treatment With FOLFOX and Cetuximab in Chinese Patients With R [NCT04262635]Phase 380 participants (Actual)Interventional2021-09-24Active, not recruiting
A Phase 1, Open-Label, Non-randomized, Dose-Escalating Safety, Tolerability, and Pharmacokinetic Study of TAS-114 in Combination With Capecitabine in Patients With Advanced Solid Tumors [NCT02025803]Phase 160 participants (Anticipated)Interventional2012-11-30Completed
Maintenance Treatment With Capecitabine Versus Observation After First Line Chemotherapy in Patients With Metastatic Colorectal Cancer: a Randomized Phase II Study [NCT02027363]Phase 2245 participants (Anticipated)Interventional2010-01-31Active, not recruiting
Evaluation of Response to Two Schedules of Capecitabine in Patients With Metastatic Breast Cancer [NCT02028494]350 participants (Anticipated)Interventional2013-08-31Recruiting
A Prospective Exploratory Clinical Study of Metronomic Capecitabine as Adjuvant Therapy in Locoregionally Advanced Hypopharyngeal Carcinoma [NCT05940441]74 participants (Anticipated)Observational [Patient Registry]2023-07-01Recruiting
A Phase I Study of Oxaliplatin in Combination With Capecitabine in Metastatic/Recurrent Solid Tumors [NCT00005839]Phase 10 participants Interventional2000-08-31Completed
Randomised Phase III Study Evaluating Adjuvant Chemotherapy After Resection of Stage III Colonic Adenocarcinoma in Patients of 70 and Over Intergroup Trial: Ffcd, Gercor, Gerico, Unicancer-gi [NCT02355379]Phase 3774 participants (Anticipated)Interventional2015-01-31Recruiting
Phase I Study of Oxaliplatin (NSC# 266046), Irinotecan, and Capecitabine in Patients With Solid Tumors [NCT00006465]Phase 122 participants (Actual)Interventional2000-12-31Completed
Organoid-Guided Functional Precision Therapy Versus Treatment of Physician's Choice in Previously Treated HER2-negative Advanced Breast Cancer: A Phase II, Multicenter, Open-label, Randomized Controlled Trial [NCT06102824]Phase 2252 participants (Anticipated)Interventional2024-01-20Recruiting
A Phase I/II Study of CDX-1140, a CD40 Agonist, in Combination With Capecitabine and Oxaliplatin (CAPOX) and Keytruda in Subjects With Biliary Tract Carcinoma (BTC) [NCT05849480]Phase 1/Phase 260 participants (Anticipated)Interventional2024-01-03Not yet recruiting
Exploiting Circulating Tumour DNA to Intensify the Postoperative Treatment of Stage III and High-risk Stage II Resected Colon Cancer Patients With Adjuvant FOLFOXIRI and/or Post-adjuvant Trifluridine/Tipiracil [NCT05062889]Phase 2477 participants (Anticipated)Interventional2023-05-17Recruiting
A Randomized, Double-blind, Placebo-controlled, Phase 3 Study of Pembrolizumab Plus Chemotherapy Versus Placebo Plus Chemotherapy for the Treatment of Chemotherapy-Candidate Hormone Receptor-Positive, Human Epidermal Growth Factor Receptor 2-Negative (HR+ [NCT04895358]Phase 3800 participants (Anticipated)Interventional2021-06-18Recruiting
Cetuximab (Erbitux®), Capecitabine and Radiotherapy in Neoadjuvant Treatment of Patients With Locally Advanced Resectable Rectal Cancer: A Phase II Pilot Study [NCT00689702]Phase 243 participants (Actual)Interventional2007-02-28Active, not recruiting
Phase II Study of the Combination of Bevacizumab (rhuMab VEGF) and Oxaliplatin Plus Capecitabine (XELOX) in Patients With Advanced Colorectal Cancer [NCT01159171]Phase 250 participants (Actual)Interventional2006-01-31Completed
Priming the Tumour MicroEnvironment for Effective Treatment With Immunotherapy in Locally Advanced Rectal Cancer A Phase II Trial of Durvalumab (MEDI 4736) in Combination With Extended Neoadjuvant Regimens in Rectal Cancer [NCT04621370]Phase 248 participants (Anticipated)Interventional2020-12-07Not yet recruiting
Phase I Study of Combination of Capecitabine and Erlotinib Concurrent With Radiotherapy in Patients With Non-Operable Locally Advanced Pancreatic Cancer [NCT00565487]Phase 115 participants (Actual)Interventional2007-12-31Completed
Phase II Study on Combination of Capecitabine and Oxaliplatin in Patients With Relapsed or Refractory Gastric Cancer [NCT00568529]Phase 230 participants (Anticipated)Interventional2007-10-31Suspended(stopped due to There are not enough patients enrolled.)
An Open-label Study of the Effect of First-line Treatment With Avastin+Xelox, Followed by Avastin+Tarceva, on Progression-free Survival in Patients With Metastatic Colorectal Cancer [NCT01135498]Phase 290 participants (Actual)Interventional2006-11-30Completed
Phase I Multicenter, Open-label, Clinical and Pharmacokinetic Study of Lurbinectedin (PM01183) in Combination With Capecitabine in Patients With Unresectable Metastatic Breast Cancer (MBC), Pancreatic Cancer (PC) or Metastatic Colorectal Cancer (CRC) [NCT02210364]Phase 181 participants (Actual)Interventional2013-04-30Completed
Phase II Study of Capecitabine in Combination With Oxaliplatin and Radiotherapy for Esophageal and Gastroesophageal Junction Cancer [NCT00470184]Phase 241 participants (Actual)Interventional2006-11-30Completed
Phase II Study of an All-Oral Combination of Capecitabine (X) and Cyclophosphamide (C) in Patients With Anthracycline- and Taxane-Pretreated Metastatic Breast Cancer [NCT00589901]Phase 260 participants (Anticipated)Interventional2006-08-31Recruiting
Phase II Study of Capecitabine and Interferon-Alpha in Metastatic Renal Cell Carcinoma Patients With Failure on Interleukin-2 Based Regimens [NCT00591188]Phase 249 participants (Anticipated)Interventional2006-12-31Completed
Neoadjuvant Complete Hormonal Blockade Followed by Neoadjuvant Chemotherapy for Resectable Hormone Receptor Positive, HER-2/Neu Negative Breast Cancer, A Phase II Study [NCT00194792]Phase 228 participants (Actual)Interventional2005-08-31Terminated
Clinical Evaluation of Lapatinib Administered With Capecitabine in Japanese Patients With ErbB2 Overexpressing Advanced or Metastatic Breast Cancer [NCT00477464]Phase 251 participants (Actual)Interventional2007-06-30Completed
An Open-label, Multi-centre Study of Lapatinib in Combinationwith Chemotherapy in Patients With ErbB2 Overexpressing Breastcancer After Trastuzumab Failure in the Neoadjuvant or Adjuvantsetting. [NCT00479856]Phase 29 participants (Actual)Interventional2007-11-30Terminated(stopped due to Study was terminated due to difficulty in identifying eligible subjects)
A Randomized Controlled Clinical Trial to Investigate the Effect of Neoadjuvant Chemotherapy for the Treatment of Resectable Locally Advanced Colon Cancer [NCT02882269]Phase 2/Phase 3400 participants (Anticipated)Interventional2016-12-31Not yet recruiting
A Phase 2 Study of Capecitabine or 5-FU With Pegylated Interferon Alpha-2b in Unresectable/Metastatic Cutaneous Squamous Cell Carcinoma [NCT02218164]Phase 28 participants (Actual)Interventional2014-08-12Completed
Randomized Phase II Trial of Preoperative Chemoradiation With or Without Induction Chemotherapy In Patients With Locally Advanced Or Borderlinely Resectable Rectal Cancer With Resectable Synchronous Liver Metastases [NCT01643070]Phase 238 participants (Anticipated)Interventional2010-01-31Active, not recruiting
Study Evaluating Vinorelbine Plus Capecitabine in the Treatment of Luminal B Breast Cancer Patients After Neoadjuvant Chemotherapy [NCT04307147]Phase 3316 participants (Anticipated)Interventional2018-07-03Recruiting
A Phase 1, Open-Label Study Of Neratinib (HKI-272) In Combination With Capecitabine In Japanese Subject With Solid Tumors [NCT01128842]Phase 17 participants (Actual)Interventional2010-04-30Completed
Pharmacogenetics and Therapeutic Drug Monitoring for the Optimization of Fluoropyrimidine Treatment in Patients With Advanced Colorectal Cancer [NCT01641458]Phase 437 participants (Actual)Interventional2012-10-31Completed
Preoperative ChemoRadiation And FOLFOXIRI To Escalate Complete Response for Rectal Cancer (CRAFTER) [NCT05358704]Phase 238 participants (Anticipated)Interventional2022-05-13Recruiting
A Phase 3, Multicenter, Randomized, Open-Label, Active-Controlled Trial Of JSKN003 Versus Treatment Of Physician'S Choice For HER2-low, Unresectable and/or Metastatic Breast Cancer Subjects [NCT06079983]Phase 3400 participants (Anticipated)Interventional2023-12-01Not yet recruiting
Neoadjuvant Chemoradiotherapy Versus Neoadjuvant Chemotherapy For Unresectable Locally Advanced Colon Cancer: An Open, Multi-centered, Randomize Controlled Phase 3 Trial. [NCT03970694]Phase 349 participants (Actual)Interventional2019-05-11Terminated(stopped due to Significant differences in conversion rate as well as R0 resection rate between the two groups.)
A Phase I/II Study Exploring the Safety and Activity of Trifluridine/Tipiracil in Combination With Capecitabine and Bevacizumab in Metastatic Colorectal Cancer Patients [NCT04564898]Phase 1/Phase 248 participants (Anticipated)Interventional2022-01-25Recruiting
A Phase 3, Randomized, Double-blind Clinical Study of Pembrolizumab (MK-3475) Plus Chemotherapy Versus Placebo Plus Chemotherapy as First-line Treatment in Participants With HER2 Negative, Previously Untreated, Unresectable or Metastatic Gastric Orgastroe [NCT03675737]Phase 31,579 participants (Actual)Interventional2018-11-08Active, not recruiting
A Phase II Clinical Trial Platform of Sensitization Utilizing Total Neoadjuvant Therapy (TNT) in Rectal Cancer [NCT02921256]Phase 2363 participants (Actual)Interventional2017-01-11Completed
A Phase III Study for ErbB2 Positive Advanced or Metastatic Gastric, Esophageal, or Gastroesophageal Junction Adenocarcinoma Treated With Capecitabine Plus Oxaliplatin With or Without Lapatinib [NCT00680901]Phase 3545 participants (Actual)Interventional2008-06-04Active, not recruiting
AN OPEN-LABEL, MULTICENTER, RANDOMIZED PHASE 3 STUDY OF FIRST-LINE ENCORAFENIB PLUS CETUXIMAB WITH OR WITHOUT CHEMOTHERAPY VERSUS STANDARD OF CARE THERAPY WITH A SAFETY LEAD-IN OF ENCORAFENIB AND CETUXIMAB PLUS CHEMOTHERAPY IN PARTICIPANTS WITH METASTATIC [NCT04607421]Phase 3815 participants (Anticipated)Interventional2020-12-21Recruiting
A Randomized, Phase II Study of Tesetaxel Once Every 3 Weeks Versus Tesetaxel Once Weekly for 3 Weeks Versus Capecitabine Twice Daily for 14 Days as First-line Therapy for Subjects With Locally Advanced or Metastatic Breast Cancer [NCT01609127]Phase 2213 participants (Anticipated)Interventional2012-05-31Recruiting
Phase II Randomized Study of Maintenance Treatment With Bevacizumab or Bevacizumab Plus Metronomic Chemotherapy After First-line Induction FOLFOXIRI Plus Bevacizumab for Metastatic Colorectal Cancer Patients [NCT02271464]Phase 2232 participants (Actual)Interventional2012-03-31Completed
A Phase II Study of Capecitabine and Bevacizumab in Elderly Patients With Metastatic Colorectal Cancer [NCT00107315]Phase 216 participants (Actual)Interventional2004-07-31Terminated(stopped due to Terminated due to low accrual)
Phase II Trial of Simple Oral Therapy (Continuous Oral Cyclophosphamide and Capecitabine) in Patients With Metastatic Breast Cancer [NCT00107276]Phase 2112 participants (Actual)Interventional2005-08-31Completed
A Randomised Phase II Study Comparing Capecitabine Plus Streptozocin With or Without Cisplatin Chemotherapy as Treatment for Unresectable or Metastatic Neuroendocrine Tumors [NCT00602082]Phase 284 participants (Anticipated)Interventional2005-08-31Completed
A Phase 1b/2, Multicenter, Open-Label, Dose-Escalation and Confirmation Study of Eribulin in Combination With Capecitabine [NCT01323530]Phase 1/Phase 276 participants (Actual)Interventional2010-01-26Completed
A Single-arm Open-label Phase II Study: Treatment Beyond Progression by Adding Bevacizumab to XELOX or FOLFOX Chemotherapy in Patients With Metastatic Colorectal Cancer and Disease Progression Under First-line FOLFIRI + Bevacizumab Combination [NCT01077739]Phase 275 participants (Actual)Interventional2009-07-31Completed
Randomized Phase II Study of NaliCap (Irinotecan Liposome/Capecitabine) Compared to NAPOLI (Irinotecan Liposome/5-fluorouracil/Leucovorin) in Gemcitabine-pretreated Advanced Pancreatic Cancer [NCT04371224]Phase 2200 participants (Anticipated)Interventional2020-06-23Recruiting
A Randomized Phase II Study of the Efficacy and Safety of Hypofractionated Stereotactic Radiotherapy and 5FU or Capecitabine With and Without Zometa in Patients With Locally Advanced Pancreatic Adenocarcinoma [NCT03073785]Phase 244 participants (Anticipated)Interventional2016-09-16Recruiting
TPC vs PF as Induction Chemotherapy Combined With CCRT for Stage IVa-b Nasopharyngeal Carcinoma, a Prospective,Parallel, Randomized, Open Labeled, Multicenter Phase III Clinical Trial [NCT02940925]Phase 3241 participants (Actual)Interventional2016-10-20Completed
Phase III, Multicenter, Ramdomised, Open-label, Study to Evaluate the Safety and Efficacy of Combination Therapy With XELOX vs. Oxaliplatin and 5-FU CI as First Line Treatment in Advanced or Metastatic Colorectal Cancer [NCT00202774]Phase 3348 participants (Actual)Interventional2002-04-30Completed
Phase II Study of Oxaliplatin, Capecitabine and Endostar as First Line Treatment for Patients With Advanced Colorectal Cancer [NCT00853684]Phase 244 participants (Anticipated)Interventional2009-02-28Recruiting
Phase IB Study to Evaluate the Safety of Selinexor (KPT-330) in Combination With Multiple Standard Chemotherapy or Immunotherapy Agents in Patients With Advanced Malignancies [NCT02419495]Phase 1221 participants (Actual)Interventional2015-06-26Active, not recruiting
Phase I Study of Gemcitabine, Capecitabine, and Erlotinib Together in Advanced Pancreatic Cancers [NCT00885066]Phase 130 participants (Actual)Interventional2008-05-31Completed
Pharmacogenomic and Pharmacokinetic Safety and Cost-saving Analysis in Patients Treated With Fluoropyrimidines [NCT00838370]Phase 122 participants (Actual)Interventional2007-05-31Completed
NGR005: Pilot Study of NGR-hTNF Administered at Low and High Doses in Combination With a Standard Oxaliplatin Based Regimen in Patients With Metastatic Colorectal Cancer [NCT00675012]Phase 224 participants (Actual)Interventional2007-12-31Completed
Phase I/IB Multi-center Study of Irreversible EGFR/HER2 Tyrosine Kinase Inhibitor Afatinib (BIBW 2992) in Combination With Capecitabine for Advanced Solid Tumors and Pancretico-Biliary Cancers [NCT02451553]Phase 141 participants (Actual)Interventional2015-11-05Completed
Phase II Study of the Gemzar, Taxotere and Xeloda Regimen (GTX) for Inoperable or Metastatic Adenocarcinoma of the Biliary System [NCT00868998]Phase 24 participants (Actual)Interventional2005-08-31Terminated(stopped due to Poor patient accrual)
A Phase I Pharmacokinetic and Safety Study of Sorafenib + Capecitabine in Advanced Solid Tumors [NCT00613145]Phase 132 participants (Actual)Interventional2008-02-29Completed
Clinical Study of Nab-paclitaxel Plus Carboplatin Versus Nab-paclitaxel Plus Capecitabine in the Treatment of Advanced Triple-negative Breast Cancer [NCT04159142]Phase 2414 participants (Anticipated)Interventional2019-11-20Recruiting
A Phase II Study of Capecitabine and Oxaliplatin With Radiation for Esophageal and Gastroesophageal Junction Adenocarcinoma [NCT00711412]Phase 244 participants (Actual)Interventional2006-05-31Completed
An Exploratory, Phase II Trial to Determine the Association of Lapatinib Induced Fluoropyrimidine Gene Changes With Efficacy Parameters of Lapatinib and Capecitabine in First Line Gastric Cancer [NCT00526669]Phase 268 participants (Actual)Interventional2008-03-31Completed
A Phase II Study of Capecitabine in Combination With Irinotecan and Oxaliplatin (Eloxatin) in Adult Patients With Advanced Colorectal Cancer [NCT00215982]Phase 224 participants (Actual)Interventional2004-12-31Completed
A Randomized Multicenter Phase III Study Comparing Paclitaxel Plus Capecitabine With Capecitabine Maintenance Treatment or Cisplatin Plus Capecitabine in Metastatic Adenocarcinoma of the Stomach or Esophagogastric Junction [NCT01015339]Phase 3320 participants (Anticipated)Interventional2009-11-30Recruiting
A Randomized Phase II Study of Oxaliplatin and S-1 (OS) Versus Oxaliplatin and Capecitabine (XELOX) in Patients With Advanced or Recurrent Colorectal Cancer [NCT00677144]Phase 288 participants (Actual)Interventional2008-04-30Completed
Clinical Study of Mitoxantrone Hydrochloride Liposome Injection Combined With Capecitabine in Patients With HER-2 Negative Advanced Breast Cancer [NCT06156761]24 participants (Anticipated)Interventional2023-11-28Not yet recruiting
Novel Targeting of the Microenvironment to Decrease Metastatic Recurrence of High-Risk TNBC: A Randomized Phase II Study of Tetrathiomolybdate (TM) Plus Capecitabine in Patients With Breast Cancer at High Risk of Recurrence [NCT06134375]Phase 1/Phase 2204 participants (Anticipated)Interventional2024-03-31Not yet recruiting
A Phase Ib, Open-Label, Multicenter Dose-Expansion Study Evaluating the Safety, Pharmacokinetics, and Activity of RO7496353 in Combination With a Checkpoint Inhibitor With or Without Standard-of-Care Chemotherapy in Patients With Locally Advanced or Metas [NCT05867121]Phase 1120 participants (Anticipated)Interventional2023-10-02Recruiting
A Phase 1b/2, Randomized, Open-Label Study Investigating the Efficacy and Safety of LBL-007 Plus Tislelizumab in Combination With Bevacizumab Plus Fluoropyrimidine Versus Bevacizumab Plus Fluoropyrimidine as Maintenance Therapy in Patients With Unresectab [NCT05609370]Phase 1/Phase 2226 participants (Anticipated)Interventional2023-01-29Recruiting
Metastatic Triple-Negative Taxane-Resistant Breast Cancer: Investigating the Role of Bexarotene in Inducing Susceptibility to Chemotherapy by Differentiating Cancer Cells From a Mesenchymal-Like to an Epithelial-Like Phenotype [NCT04664829]Phase 112 participants (Anticipated)Interventional2020-10-01Recruiting
Single Arm, Open, Multicenter Phase II Clinical Study of Sufficient Chemotherapy Combine With Maintenance Chemotherapy in the Treatment of Oligometastatic Nasopharyngeal Carcinoma [NCT04319471]Phase 270 participants (Anticipated)Interventional2020-06-01Not yet recruiting
Randomized Phase II Trial of Extended Neoadjuvant Therapy for Locally Advanced Adenocarcinoma of the Esophagus, Gastroesophageal Junction, and Gastric Cardia [NCT00938470]Phase 273 participants (Actual)Interventional2010-01-31Completed
Phase II Trial Assessing the Impact on the Activity of Daily Living of an Oral Chemotherapy by Capecitabine Associated With an Intravenous Chemotherapy by Oxaliplatin as First Line Treatment of Metastatic Colorectal Adenocarcinoma of Patients Aged Over 70 [NCT00104689]Phase 260 participants (Anticipated)Interventional2003-06-30Completed
Phase 1/2 Study of Anti-PD-L1 in Combination With Chemo(Radio)Therapy for Oesophageal Cancer [NCT02735239]Phase 1/Phase 273 participants (Actual)Interventional2016-06-24Completed
Single-agent Capecitabine as Metronomic Chemotherapy in Locoregionally Advanced Head and Neck Squamous Cell Carcinoma (CMHN)：A Phase III, Multicentre, Randomised Controlled Trial [NCT05044117]Phase 3220 participants (Anticipated)Interventional2021-10-18Recruiting
Phase I Trial of Preoperative Radiotherapy With Concurrent Bevacizumab, Erlotinib and Capecitabine for Locally Advanced Pancreatic Cancer [NCT00614653]Phase 117 participants (Actual)Interventional2008-01-31Completed
A Clinical Study Evaluating the Efficacy and Safety of BAT8001 Injection for the Treatment of HER2-positive Advanced Breast Cancer - A Multicenter, Randomized, Open-label, Positive-controlled, Superiority Phase III Clinical Trial in China [NCT04185649]Phase 3410 participants (Anticipated)Interventional2018-07-01Active, not recruiting
Neoadjuvant Chemoradiotherapy Combined With Tislelizumab in the Treatment of Locally Advanced Rectal Cancer--Randomized, Open, Multicenter Clinical Study [NCT05479240]Phase 294 participants (Anticipated)Interventional2023-09-01Not yet recruiting
A Phase II Open-label Randomized Study of a Fixed-dose Combination of Capecitabine and Cyclophosphamide Administered at Different Doses/Regimens With Metronomic Schedule in Patients With Metastatic Breast Cancer [NCT02664103]Phase 22 participants (Actual)Interventional2016-01-23Completed
A Randomized, Phase II Study Comparing Single X (Xeloda/Capetabine) With Placebo as Postoperative Adjuvant Treatment for Elder Breast Cancer [NCT02838238]Phase 2300 participants (Anticipated)Interventional2014-01-31Recruiting
The Effect of Preoperative Docetaxel, Cisplatin and Capecitabine on Serum RUNX3 Hypermethylation Status in Patients With Gastric and Lower Oesophagus Adenocarcinoma. [NCT00674167]Phase 221 participants (Actual)Interventional2007-05-31Active, not recruiting
A Phase 1 Safety And Pharmacokinetic Study Of SU011248 And Capecitabine In Patients With Advanced Solid Tumors [NCT00618124]Phase 177 participants (Actual)Interventional2005-05-31Completed
A Phase II Study to Assess the Effectiveness and Safety of Oral Vinorelbine or Capecitabine Combined With Trastuzumab as Adjuvant Treatment for Patients With Lymph Node Negative, HER-2 Positive and Small Tumor Size Breast Cancer (ORCHID) [NCT04296162]Phase 2178 participants (Anticipated)Interventional2019-03-01Recruiting
Safety and Efficacy of Induction and Individualized Neoadjuvant Chemotherapy Based on Oxaliplatin Combined With Fluorouracil for MRF-negative, Moderate-risk and Initially Resectable Middle and Low Rectal Cancer [NCT04296240]Phase 2119 participants (Anticipated)Interventional2019-03-01Recruiting
Randomized Multicenter Phase II Study of Sequential Versus Simultaneous Use of Vinorelbine and Capecitabine as First Line Chemotherapy for Patients With Metastatic Breast Cancer [NCT00629148]Phase 260 participants (Actual)Interventional2007-08-31Completed
Phase Ⅲ Randomized Trial of Cisplatin Plus Docetaxel Versus Cetuximab, Cisplatin, and Docetaxel Induction Chemotherapy Followed by Concurrent Chemoradiation in Previously Untreated Patients Metastatic Nasopharyngeal Carcinoma [NCT02633176]Phase 3120 participants (Anticipated)Interventional2015-01-31Recruiting
A Phase Ib/II, Open Label, Multi-center Study Evaluating the Safety and Efficacy of BKM120 in Combination With Trastuzumab in Patients With Relapsing HER2 Overexpressing Breast Cancer Who Have Previously Failed Trastuzumab [NCT01132664]Phase 1/Phase 272 participants (Actual)Interventional2010-05-31Terminated(stopped due to Due to the rare patient population and challenges to enroll patients.)
mXELOXIRI Combined With Molecular Targeted Drug as First-line Therapy in Patients With Initially Unresectable Metastatic Colorectal Cancer: A Phase II, Single-arm, Prospective Clinical Study [NCT04160416]Phase 248 participants (Anticipated)Interventional2019-07-01Recruiting
A Phase II Study of Concurrent Chemo-radiotherapy With Capecitabine for Unresectable Locally Advanced Pancreatic Carcinoma [NCT00658840]Phase 255 participants (Anticipated)Interventional2006-06-30Recruiting
Effect of Concurrent Capecitabine-based Long-term Radiotherapy Followed by 4 Cycles XELOX Pre- a Delayed TME Compared With 6 Cycles XELOX post-a Regular Timing TME in Patients With High Risk Rectal Cancer: a Multi-centers, Randomized, Open-Label Trial [NCT03038256]Phase 2244 participants (Anticipated)Interventional2018-01-31Recruiting
A Multicenter, Open-label, Treatment Protocol of Tucatinib in Combination With Capecitabine and Trastuzumab in Patients With Previously Treated Unresectable Locally Advanced or Metastatic HER2+ Breast Carcinoma [NCT04220203]0 participants Expanded AccessApproved for marketing
A Phase III Randomized, Double Blind, Placebo-controlled Trial Comparing Capecitabine Plus Sorafenib Versus Capecitabine Plus Placebo in the Treatment of Locally Advanced or Metastatic HER2-Negative Breast Cancer [NCT01234337]Phase 3537 participants (Actual)Interventional2011-02-21Completed
A Phase 1/2, Open-Label Study Of Bosutinib Administered In Combination With Capecitabine In Subjects With Solid Tumor And ErbB2 Negative Locally Advanced Or Metastatic Breast Cancer [NCT00959946]Phase 1/Phase 232 participants (Actual)Interventional2009-09-30Terminated
A Phase 2, Single Arm, Multi-center, Open-Label Trial to Evaluate the Safety and Efficacy of Treatment With Tumor Treating Fields (TTFields) and Chemotherapy as First-Line Treatment for Subjects With Unresectable Gastroesophageal Junction (GEJ) Adenocarci [NCT04281576]28 participants (Anticipated)Interventional2019-12-19Recruiting
A Randomized, Open Label Study Comparing the Efficacy of Topical Corticosteroids or Bepantol in the Prophylaxis of Hand-foot Syndrome in Patients Receiving Oral Xeloda for Treatment of Metastatic Breast Cancer or Colorectal Cancer. [NCT00661102]Phase 3598 participants (Actual)Interventional2008-12-31Completed
Biweekly Docetaxel (Taxotere®)in Combination With Capecitabine (Xeloda®)as First-Line Treatment in Patients With Advanced Gastric Cancer [NCT00669370]Phase 250 participants (Anticipated)Interventional2006-06-30Recruiting
A Phase II Trial of Capecitabine, Oxaliplatin and Trastuzumab (CAPOX-T) in Patients With HER-2 Positive Metastatic Breast Cancer: Hoosier Oncology Group BRE03-61 [NCT00216073]Phase 211 participants (Actual)Interventional2004-03-31Terminated(stopped due to Lack of patient accrual)
An Open-label Study to Assess the Effect of Combination Treatment With Avastin and Xeloda, Plus Pre-operative Standard Radiotherapy, on Response Rate in Patients With Locally Advanced Rectal Cancer. [NCT01227707]Phase 243 participants (Actual)Interventional2005-11-30Completed
MoTriColor: Phase I/II Study With LY3200882 Combined With Capecitabine in Patients With Advanced Chemotherapy Resistant Colorectal Cancer and an Activated TGF-beta Signature [NCT04031872]Phase 1/Phase 231 participants (Anticipated)Interventional2020-02-29Not yet recruiting
Tailored Operative or Non-operative Management for MRI Defined Low-risk Rectal Cancer Following Neoadjuvant Intensity Modulated Radiotherapy With Concurrent Capecitabine Plus Consolidation CapeOX. [NCT02860234]68 participants (Actual)Observational2016-08-31Completed
A Phase 1 Study of Veliparib (ABT-888) in Combination With Capecitabine and Temozolomide in Advanced Well-Differentiated Neuroendocrine Tumors [NCT02831179]Phase 10 participants (Actual)Interventional2017-12-31Withdrawn(stopped due to Loss of funding support)
A Prospective, Randomized, Open-label, Multicenter, Parallel Design, Phase III Study to Assess the Efficacy and Safety of GV1001 Concurrent With Gemcitabine/Capecitabine Versus Gemcitabine/Capecitabine Alone in Treating Locally Advanced and Metastatic Pan [NCT02854072]Phase 3148 participants (Anticipated)Interventional2015-11-30Recruiting
A Study to Evaluate Vinorelbine Plus Capecitabine Combined With Trastuzumab as the Adjuvant Treatment of HER2 Positive Patients Following Neoadjuvant Chemotherapy [NCT04302441]Phase 2550 participants (Anticipated)Interventional2016-11-10Recruiting
Phase III Multicenter Study of the Effects on Quality of Life of Three-weekly Versus Weekly First-line Chemotherapy for Metastatic or Locally Advanced Breast Cancer [NCT00540800]Phase 3139 participants (Actual)Interventional2004-02-29Completed
Phase II Multicenter Study of the Impact of the Therapeutic Sequence of Radiochemotherapy (50 Gy + Capecitabine + Oxaliplatin + Cetuximab) Followed by Total Mesorectal Excision Surgery Then Post-surgery Chemotherapy (FOLFOX 4 + Cetuximab) in Synchronous L [NCT00541112]Phase 219 participants (Actual)Interventional2007-10-29Terminated(stopped due to Toxicity and lack of efficacy)
Phase I/II Trial of Preoperative Radiotherapy With Concurrent Bevacizumab, Erlotinib and Capecitabine for Locally Advanced Rectal Cancer [NCT00543842]Phase 119 participants (Actual)Interventional2007-12-31Completed
Phase Ib Study of MEK162 in Combination With Capecitabine in Gemcitabine-pretreated Advanced Biliary Tract Cancer [NCT02773459]Phase 1/Phase 231 participants (Actual)Interventional2016-04-30Completed
A Phase II Study of Neoadjuvant FOLFOXIRI Followed by Concurrent Capecitabine and Radiotherapy for High Risk Rectal Cancer [NCT01941641]Phase 240 participants (Anticipated)Interventional2013-10-09Active, not recruiting
Intra-hepatic Chemotherapy With Oxaliplatin Every Second Week in Combination With Systemic Capecitabine in Patient With Non-resectable Liver Metastases From Breast Cancer. A Phase II Trial [NCT01387373]Phase 214 participants (Actual)Interventional2010-04-30Completed
A Phase II Study of Trastuzumab in Combination With Capecitabine and Oxaliplatin (XELOX) in Patients With Advanced Gastric Cancer [NCT01396707]Phase 255 participants (Actual)Interventional2011-06-30Completed
Precise Treatment for BLIS Subtype of Triple-negative Breast Cancer in the First-line Treatment of Locally Advanced or Metastatic Breast Cancer [NCT05806060]Phase 3192 participants (Anticipated)Interventional2023-04-25Recruiting
Induction Gemcitabine/Capecitabine Followed by SBRT in Pancreatic Adenocarcinoma A Prospective Evaluation in Patients With Locally Advanced Pancreas Cancer [NCT01360593]Phase 235 participants (Actual)Interventional2011-07-25Completed
Phase II Study to Evaluate Efficacy and Safety of Capecitabine/Cisplatin Combination Therapy in Gastric Cancer Patients Who Relapsed After S-1 Adjuvant Chemotherapy (XParTS) [NCT01412294]Phase 240 participants (Anticipated)Interventional2011-07-31Active, not recruiting
A Randomized, Open-Label, Phase III Study of RPR109881 IV Every 3 Weeks Versus Capecitabine (Xeloda) Tablets Twice Daily for 2 Weeks in 3-Week Cycles in Patients With Metastatic Breast Cancer Progressing After Taxanes and Anthracycline Therapy [NCT00081796]Phase 3438 participants (Actual)Interventional2004-04-30Completed
AX (Doxorubicin, Capecitabine) Versus AC (Doxorubicin, Cyclophosphamide) as Adjuvant Treatment for Node-Negative Breast Cancer [NCT01415336]Phase 2/Phase 3300 participants (Anticipated)Interventional2010-03-31Recruiting
INST: Phase I-II Study of Carboplatin, Vinorelbine and Capecitabine in Patients With Metastatic Breast Cancer [NCT00277069]Phase 1/Phase 233 participants (Actual)Interventional2000-05-31Completed
An Open Label Study of First Line Chemotherapy With Xeloda in Combination With Cisplatin on Treatment Response in Patients With Metastatic Nasopharyngeal Cancer [NCT00439426]Phase 225 participants (Actual)Interventional2007-04-30Completed
A Phase I Study of GTI-2040 in Combination With Oxaliplatin and Capecitabine in Patients With Advanced Metastatic Solid Tumors [NCT00084643]Phase 120 participants (Actual)Interventional2004-05-31Completed
Weekly Vinorelbine and Oral Capecitabine as Treatment for Stage IV Breast Cancer: A Phase II Trial With Molecular Correlates [NCT00194727]Phase 240 participants (Actual)Interventional2002-05-31Completed
A Phase I/II Study of Capecitabine (XELODA®, Roche) Plus Oxaliplatin (Eloxatin®, Sanofi) Plus ZD 1893 (IRESSA®) in the Treatment of Metastatic Colorectal Cancer [NCT00087334]Phase 1/Phase 210 participants (Actual)Interventional2004-01-31Terminated(stopped due to Withdrawn due to poor/low accrual)
S0225: Phase II Study of Adjuvant Low-Dose Capecitabine After Salvage Surgery in Patients With Locally Recurrent or Persistent Squamous Cell Carcinoma of the Head and Neck [NCT00095641]Phase 20 participants (Actual)InterventionalWithdrawn(stopped due to no longer studying this disease site)
Genomic and Proteomic Analysis of Docetaxel and Capecitabine as Primary Chemotherapy for Stage II-III Breast Cancer [NCT00198237]Phase 240 participants Interventional2003-03-31Completed
A Randomized, Open-label Study of the Effect of First-line Herceptin in Combination With a Fluoropyrimidine and Cisplatin Versus Chemotherapy Alone on Overall Survival in Patients With HER2-positive Advanced Gastric Cancer [NCT01041404]Phase 3584 participants (Actual)Interventional2005-09-30Completed
Phase IV Clinical Study of Safety and Tolerability of Oral Xeloda (Capecitabine) in Adjuvant Treatment of Resected Cancer of the Colon [NCT02581423]Phase 463 participants (Actual)Interventional2005-08-31Completed
Pilot Trial of Capecitabine and Radiation Therapy With Pre and Post Combination Chemotherapy in Advanced Pancreatic Cancer [NCT00176735]0 participants Interventional2001-12-31Terminated
Effect and Safety of Adjuvant Huaier Granule Versus Standard Chemotherapy Regimens in Resectable Stage II-III Gastric Cancer Patients: a Prospective, Multi-center, and Observational Study [NCT05498766]828 participants (Anticipated)Observational2023-10-12Recruiting
A Phase III, Randomized, Double-Blind, Placebo Controlled, Multi-Center, International Study of Durvalumab Given Concurrently With Definitive Chemoradiation Therapy in Patients With Locally Advanced, Unresectable Esophageal Squamous Cell Carcinoma (KUNLUN [NCT04550260]Phase 3640 participants (Actual)Interventional2020-10-19Active, not recruiting
Randomized Trial to Evaluate the Therapeutic Gain by Changing the Chemoradiotherapy From Concurrent-adjuvant to Induction-concurrent Sequence, and the Radiotherapy From Conventional to Accelerated Fractionation for Advanced Nasopharyngeal Carcinoma [NCT00577057]798 participants (Anticipated)Interventional2006-09-30Not yet recruiting
INtegratioN of Trastuzumab, With or Without Pertuzumab, Into periOperatiVe chemotherApy of HER-2 posiTIve stOmach caNcer: the INNOVATION-TRIAL [NCT02205047]Phase 2171 participants (Anticipated)Interventional2015-07-15Active, not recruiting
A Phase II Multicenter Randomized Trial Evaluating 3-year Disease Free Survival in Patients With Locally Advanced Rectal Cancer Treated With Chemoradiation Plus Induction or Consolidation Chemotherapy and Total Mesorectal Excision or Non-operative Managem [NCT02008656]Phase 2358 participants (Actual)Interventional2013-11-30Active, not recruiting
A Phase I Pilot Study of the Oral mTOR Inhibitor RAD001 in Combination With Capecitabine for Metastatic Breast Cancer [NCT00473005]Phase 118 participants (Actual)Interventional2007-08-31Terminated(stopped due to Principal Investigator (Dr. Guardino) left Stanford)
Phase I/II Study of Xeloda and Gleevec in Patients With Advanced Solid Tumors [NCT00183833]Phase 140 participants (Actual)Interventional2002-12-31Completed
Evaluation of Primary Chemotherapy With Docetaxel Plus Capecitabine in Selected Patients With Newly Diagnosed Localized or Locally Advanced Prostate Cancer [NCT00151047]Phase 215 participants (Actual)Interventional2003-03-31Completed
Adjuvant Pyrotinib and Capecitabine For HER2 Positive Micro Invasive Breast Cancer [NCT05861271]Phase 21,008 participants (Anticipated)Interventional2023-07-01Not yet recruiting
A Randomized Crossover Trial Comparing Oral Capecitabine and Intravenous Fluorouracil + Folinic Acid (Nordic FU/FA Regimen) for Patient Preference in Colorectal Cancer [NCT00212589]Phase 360 participants Interventional2002-12-31Completed
A Phase II Trial Assessing the Efficacy and Toxicity of Capecitabine and Oxaliplatin in the Treatment of Colorectal Cancer. [NCT00220116]Phase 2172 participants (Actual)Interventional2002-08-31Completed
[NCT00189683]Phase 30 participants InterventionalRecruiting
Nivolumab and CapeOX in Patients With FGFR2/PD-L1-positive Metastatic Gastric Adenocarcinoma: a Single-arm, Phase 2 Study [NCT05859477]Phase 223 participants (Anticipated)Interventional2022-06-05Recruiting
Implementation of a Therapeutic Educational Program Applicated to Adherence of Patients Treated by Capecitabine Alone or in Combination With Lapatinib [NCT01847599]65 participants (Actual)Interventional2011-09-06Terminated(stopped due to interim analysis : discontinuation for efficacy of the intervention)
Phase III Study of Docetaxel in Combination With Gemcitabine Versus Docetaxel in Combination With Capecitabine in Patients With Locally Advanced or Metastatic Breast Cancer [NCT00191438]Phase 3300 participants Interventional2002-10-31Completed
A Phase II Study of OSI-774 (Tarceva) in Combination With Oxaliplatin and Capecitabine in Previously Treated Patients With Stage IV Colorectal Cancer [NCT00123851]Phase 232 participants Interventional2003-03-31Completed
Phase II Study of Preoperative IMRT Combined With Capecitabine and Bevacizumab in Locally Advanced Rectal Cancer [NCT01871363]Phase 235 participants (Anticipated)Interventional2012-10-31Recruiting
A Phase 1b/2, Dose-escalation, Randomized, Multicenter Study of Maintenance Ivaltinostat Plus Capecitabine or Capecitabine in Patients With Metastatic Pancreatic Adenocarcinoma Whose Disease Has Not Progressed on FOLFIRINOX [NCT05249101]Phase 1/Phase 270 participants (Anticipated)Interventional2022-08-15Recruiting
Multi-agent Low Dose Chemotherapy (Gemcitabine, Nab-paclitaxel, Capecitabine, Cisplatin, Irinotecan) Followed by Maintenance Olaparib and Pembrolizumab in Untreated Metastatic Pancreatic Ductal Adenocarcinoma. [NCT04753879]Phase 238 participants (Anticipated)Interventional2021-09-29Recruiting
Study of Trastuzumab Combined With Capecitabine on HER2-positive Metastatic Breast Cancer Patients Pretreated With Trastuzumab and Taxanes or HER2- Positive Breast Cancer Patients Relapsed From (Neo)Adjuvant Therapy of Trastuzumab and Taxanes [NCT01290718]Phase 24 participants (Actual)Interventional2011-12-31Terminated(stopped due to Slow recruitment)
The Combination of Neoadjuvant Short-course Radiotherapy and Immunotherapy in Locally Advanced Rectal Cancer：A Open-label Single-arm Phase II Trial. [NCT04663763]Phase 240 participants (Anticipated)Interventional2020-12-01Not yet recruiting
Phase II Study Evaluating the Association of Bevacizumab and Chemotherapy of the Type Modified FOLFIRI 3 in Patients With Metastatic Colorectal Adenocarcinoma [NCT00544011]Phase 247 participants (Anticipated)Interventional2007-04-30Recruiting
A Phase II Trial of Lapatinib and Capectiabine for Patients With Refractory Advanced Colorectal Adenocarcinoma (LAP109859) [NCT00574171]Phase 229 participants (Actual)Interventional2007-09-30Completed
A Drug-drug Interaction Study of Capecitabine and Celecoxib in Patients With Advanced Solid Malignancies [NCT01705106]Phase 121 participants (Actual)Interventional2012-08-29Terminated(stopped due to The study was terminated early due to slow accrual.)
A Muti-center, Open-label, Randomized, Phase III Study of Camrelizumab Plus Treatment of Physician Choice Versus Treatment of Physician Choice for Metastatic Triple-Negative Breast Cancer Who Received at Least Two Prior Systemic Chemotherapy Regimens for [NCT05134194]Phase 3104 participants (Anticipated)Interventional2021-11-30Not yet recruiting
A Randomized, Open-label Study of the Effect of Adjuvant Therapy With Adriamycin Plus Cytoxan Followed by Taxotere or Taxotere Plus Xeloda on Overall Survival in Female Patients With High-risk Breast Cancer [NCT00089479]Phase 32,611 participants (Actual)Interventional2002-08-31Completed
Efficacy and Safety Evaluation of Sintilimab or Placebo in Combination With XELOX as First Line Treatment in Patients With Gastric Cancer [NCT03745170]Phase 3650 participants (Actual)Interventional2018-12-19Completed
A Phase II Study of Combination Chemotherapy With Bevacizumab, Capecitabine and Oxaliplatin in Patients With Previously Untreated Metastatic or Recurrent Colorectal Cancer [NCT00378066]Phase 249 participants (Actual)Interventional2006-08-31Completed
A Randomized, Phase III, Multicenter Clinical Trial Comparing Capecitabine Plus Oxaliplatin (XELOX) and Capecitabine (X) as First-line Chemotherapy in Elderly Patients With Advanced Gastric Cancer [NCT01470742]Phase 30 participants (Actual)Interventional2010-09-30Withdrawn(stopped due to We stop because of problems such as insurance.)
A Phase II Study of Gemcitabine and Capecitabine for Treatment Resistant, Metastatic Colorectal Cancer [NCT01472770]Phase 249 participants (Actual)Interventional2011-10-31Completed
Phase I/IIB Study of Induction Chemotherapy With XELOX, Followed by Radiation Therapy and Dose Escalation of RAD001 in Patients With Esophageal Cancer [NCT01490749]Phase 117 participants (Actual)Interventional2012-02-29Completed
A Phase I/IIa Study Combining Curcumin (Curcumin C3-Complex, Sabinsa) With Standard Care FOLFOX Chemotherapy in Patients With Inoperable Colorectal Cancer. [NCT01490996]Phase 1/Phase 241 participants (Actual)Interventional2012-02-29Completed
Phase II Study of Neoadjuvant Accelerated Short Course Radiation Therapy With Proton or Photon RT Plus Capecitabine and Hydroxychloroquine for Resectable Pancreatic Cancer [NCT01494155]Phase 250 participants (Actual)Interventional2011-12-31Active, not recruiting
Single Agent Chemotherapy With Weekly Docetaxel vs Combination Chemotherapy in Second-line Treatment of Advanced Non Small Cell Lung Cancer [NCT00345059]Phase 384 participants (Actual)Interventional2005-05-31Terminated(stopped due to slow accrual)
A Randomized Phase III Study of Irinotecan Plus 5-fluorouracil Plus Leucovorin and Bevacizumab (FOLFIRI+Avastin) Versus Irinotecan Plus Capecitabine and Bevacizumab (XELIRI+Avastin) as 1st Line Treatment of Locally Advanced or Metastatic Colorectal Cancer [NCT00469443]Phase 3330 participants (Anticipated)Interventional2006-12-31Completed
A Open Label Study of the Effect of First-line Therapy With Xeloda in Combination With Oxaliplatin on Overall Response Rate in Patients With Locally Advanced and/or Metastatic Gastric Cancer [NCT00436241]Phase 245 participants (Actual)Interventional2007-03-31Completed
Maintenance Treatment With Capecitabine and Bevacizumab Versus Observation After Induction Treatment With Chemotherapy and Bevacizumab as First-line Treatment in Patients With Advanced Colorectal Carcinoma [NCT00442637]Phase 3635 participants (Anticipated)Interventional2007-01-31Active, not recruiting
A Multicenter Randomized Phase III Study of Gemcitabine Plus Herceptin Combination Versus the Capecitabine Plus Herceptin Combination in Pretreated Patients With HER-2 Positive Metastatic Breast Cancer [NCT00440622]Phase 390 participants (Actual)Interventional2003-04-30Terminated(stopped due to Due to poor accrual)
A Phase I/II Study to Determine the Safety and Efficacy of Second-Line Treatment With XELOX Plus Gemcitabine in Irinotecan Pre-Treated Advanced Colorectal Cancer Patients [NCT00496704]Phase 1/Phase 256 participants (Anticipated)Interventional2007-01-31Recruiting
Capecitabine Metronomic Chemotherapy Versus Conventional Chemotherapy as Maintenance Treatment in Metastatic Colorectal Cancer [NCT02893540]Phase 2/Phase 3250 participants (Anticipated)Interventional2016-09-30Recruiting
An Open-label Study of the Effect of Intermittent Xeloda in Combination With Irinotecan on Treatment Response in Patients With Advanced and/or Metastatic Colorectal Cancer [NCT00048139]Phase 252 participants (Actual)Interventional2001-10-31Completed
A Randomized Phase II-III Trial Evaluating the Efficacy of Capecitabine and Vinorelbine in Anthracycline and Taxane Pre-Treated Metastatic Breast Cancer [NCT00049660]Phase 2/Phase 347 participants (Actual)Interventional2002-09-30Terminated(stopped due to low accrual)
A Phase I Study of Capecitabine, Cisplatin and Imatinib in Patients With Unresectable or Metastatic Gastric Cancer. [NCT00601510]Phase 138 participants (Actual)Interventional2007-11-30Completed
Intra-hepatic Chemotherapy With Oxaliplatin Every Second Week in Combination With Systemic Gemcitabine and Capecitabine in Combination With Cetuximab in Patient With Non-resectable Liver Metastases From Cholangiocarcinoma. A Phase II Trial. [NCT01247337]Phase 256 participants (Actual)Interventional2011-02-02Completed
A Phase I Trial of GemCap-T, Capecitabine in Combination With Gemcitabine and Erlotinib (Tarceva®) in Patients With Advanced Pancreatic Adenocarcinoma [NCT00480584]Phase 120 participants (Actual)Interventional2007-04-30Completed
Phase II Study of Comparing Toripalimab Combined With GP Regimen Chemotherapy Versus GP Regimen Chemotherapy for Primary Metastatic Nasopharyngeal Carcinoma [NCT04517214]Phase 2126 participants (Anticipated)Interventional2020-11-01Recruiting
A Phase Ⅱ Trials of Sintilimab as Consolidation Therapy After Radical Concurrent Chemoradiotherapy in Locally Advanced Unresectable ESCC [NCT04514835]Phase 244 participants (Anticipated)Interventional2021-12-01Not yet recruiting
A Phase I Trial of Epirubicin, Carboplatin and Capecitabine in Adult Cancer Patients [NCT00486356]Phase 146 participants (Actual)Interventional2004-10-31Completed
Phase 1 Trail to Observe Safety and Efficacy of Metronomic Capecitabine Plus Camrelizumab as Second-line Regimen to Treat Head and Neck Cancer or Esophageal Squamous Cancer Patients [NCT04510818]Phase 120 participants (Anticipated)Interventional2020-08-01Recruiting
A Phase II Study of Pre-Operative Concurrent Chemoradiotherapy With Cetuximab, Irinotecan, and Capecitabine in Resectable Rectal Cancer [NCT00506844]Phase 240 participants (Actual)Interventional2006-05-31Active, not recruiting
Phase II Clinical Trial, Non-Randomized, Multicentre, on the Combination of Gemcitabine, Capecitabine and Sorafenib (Bay 43-9006) in Treatment of Patients With Unresectable and/or Metastatic Renal Cell Carcinoma (RCC) [NCT00496301]Phase 240 participants (Anticipated)Interventional2006-11-30Completed
A Phase 3, Open-label, Randomised Study of Datopotamab Deruxtecan (Dato-DXd) Versus Investigator's Choice of Chemotherapy in Patients Who Are Not Candidates for PD-1/PD-L1 Inhibitor Therapy in First-line Locally Recurrent Inoperable or Metastatic Triple-n [NCT05374512]Phase 3600 participants (Anticipated)Interventional2022-05-16Recruiting
An Open Label, Multicentre, Long-Term Extension Study of Tislelizumab- Containing Treatment and/or Pamiparib-Containing Treatment in Patients With Advanced Malignancies [NCT04164199]Phase 3300 participants (Anticipated)Interventional2019-12-19Enrolling by invitation
Phase II/III Study of Circulating Tumor DNA as a Predictive Biomarker in Adjuvant Chemotherapy in Patients With Stage IIA Colon Cancer (COBRA) [NCT04068103]Phase 2/Phase 31,408 participants (Anticipated)Interventional2019-12-16Recruiting
Safety and Efficacy of Pembrolizumab Combined With CAPOX Plus Bevacizumab as Neoadjuvant Treatment of pMMR/MSS Locally Advanced Colorectal Cancer Patients：a Single-arm, Phase II, Prospective Study [NCT05585814]Phase 212 participants (Anticipated)Interventional2022-10-31Not yet recruiting
A Phase II, Open, Randomized Study to Assess the Efficacy and Safety of AZD6244 vs Capecitabine (Xeloda) in Patients With Colorectal Cancer Who Have Failed One or Two Prior Chemotherapeutic Regimens. [NCT00514761]Phase 264 participants (Anticipated)Interventional2006-09-30Completed
Phase II Trial of Bexarotene (Targretin) Capsules With Tretinoin and Chemotherapy in Patients With Advanced Non-small-cell Lung Cancer [NCT00514293]Phase 239 participants (Anticipated)Interventional2007-01-31Recruiting
A Randomised Phase II/III Multi-Centre Clinical Trial of Definitive Chemotherapy, With or Without Cetuximab, in Carcinoma of the Oesophagus [NCT00509561]Phase 2/Phase 3259 participants (Actual)Interventional2008-02-29Active, not recruiting
A Phase 1b/2 Multicenter Study to Investigate the Safety, Efficacy and Proof of Concept (POC) of Nivolumab Monotherapy as a Sequential Therapy Following Preoperative Chemoradiotherapy Patients With Locally Advanced Resectable Rectal Cancer [NCT02948348]Phase 1/Phase 290 participants (Anticipated)Interventional2016-10-31Recruiting
A Pilot Study of Bevacizumab Based Peri-Operative Therapy for Operable Pancreatic Adenocarcinoma [NCT00524069]0 participants (Actual)Interventional2007-01-31Withdrawn(stopped due to Withdrawn due to no accrual)
S1 Plus Docetaxel Versus Capecitabine Plus Docetaxel First-line Treatment in Patients With Advanced Breast Cancer: a Phase 2, Prospective,Multicenter, Randomised Study [NCT02947061]Phase 2300 participants (Anticipated)Interventional2015-04-30Recruiting
"A Randomized, Multicenter, Open-label, Phase III Study to Compare the Efficacy and Safety of ONO-4538 in Combination With Ipilimumab, Fluoropyrimidine-based and Platinum-based Chemotherapy (Hereinafter Referred to as Chemotherapy) Versus Chemotherapy in [NCT05144854]Phase 3626 participants (Actual)Interventional2021-11-05Active, not recruiting
Phase II Trial of CAPOX, Bevacizumab and Trastuzumab for Patients With HER2-Positive Metastatic Esophagogastric Cancer [NCT01191697]Phase 237 participants (Actual)Interventional2011-02-28Active, not recruiting
A Phase I Trial of Lenvatinib (Multi-kinase Inhibitor) and Capecitabine (Anti-metabolite) in Patients With Advanced Malignancies [NCT02915172]Phase 10 participants (Actual)Interventional2016-12-31Withdrawn
A Single -Centers, Randomized, Open-label, Controlled Phase Ⅱ Clinical Trial of Short-course Radiotherapy Followed by Tislelizumab + CapeOX in the Treatment for Locally Advanced Rectal Cancer [NCT05086627]Phase 2100 participants (Anticipated)Interventional2022-10-15Recruiting
Phase II Study of Neo-adjuvant Chemoradiotherapy Using Infusional Gemcitabine Followed by Surgery for Locally Advanced (T3 and T4 or Node Positive) Rectal Adenocarcinoma [NCT02919878]Phase 225 participants (Anticipated)Interventional2014-12-31Recruiting
Clinical Efficacy of Trastuzumab in Combination With Capecitabine and Oxaliplatin for the Treatment of HER2-positive Advanced Gastric Cancer: A Multicenter, Phase II Study [NCT05997524]Phase 260 participants (Actual)Interventional2021-03-01Completed
Phase I Study of Dovitinib (TKI258) in Combination With Gemcitabine and Capecitabine in Advanced Solid Tumors, Pancreatic Cancer and Biliary Cancers [NCT01497392]Phase 126 participants (Actual)Interventional2012-03-29Completed
A Multicenter, Double-blind, Randomized Study in Patients With Gastric Cancer Undergoing Postoperative Adjuvant Chemotherapy [NCT03006705]Phase 3800 participants (Actual)Interventional2017-01-31Completed
A Phase 1, First-in-Human Study Evaluating the Safety, Tolerability, and Pharmacokinetics of CPI-100 Via Intravenous Infusion in Patients With Advanced Solid Tumors [NCT03781362]Phase 136 participants (Actual)Interventional2018-12-21Completed
An Open-Label, Multicenter, Randomized Phase 2 Study Evaluating the Safety and Efficacy of Ramucirumab (IMC-1121B) Drug Product or Icrucumab (IMC-18F1) in Combination With Capecitabine or Capecitabine Monotherapy, in Unresectable, Locally Advanced or Meta [NCT01234402]Phase 2153 participants (Actual)Interventional2011-03-31Completed
A Phase I/II Trial of the PD-L1 Inhibitor, Durvalumab Plus CV301 in Combination With Maintenance Chemotherapy for Patients With Metastatic Colorectal or Pancreatic Adenocarcinoma [NCT03376659]Phase 1/Phase 28 participants (Actual)Interventional2018-08-08Terminated(stopped due to Study closed due to lack of enrollment.)
Chemoradiation OR Brachytherapy for RECTal Cancer [NCT02017704]Phase 29 participants (Actual)Interventional2014-06-12Completed
Fulvestrant or Capecitabine Combined With Pyrotinib in HR-positive and HER2-Positive Metastatic Breast Cancer: A Multicenter, Randomized, Phase III Study [NCT04646759]Phase 3516 participants (Anticipated)Interventional2020-10-14Recruiting
A Phase II Single-arm Clinical Trial of Inetetamab Combined With Pyrotinib and Chemotherapy in the Treatment of HER2 Positive Metastatic Breast Cancer [NCT04681911]Phase 271 participants (Anticipated)Interventional2020-09-09Recruiting
Phase 4 Study to Characterize and Evaluate Markers of Chemoresistance in Patients With Metastatic Colorectal Cancer [NCT00559676]Phase 4200 participants (Anticipated)Interventional2005-03-31Completed
Phase II Trial of Vinfluinine and Capecitabine in Previously Treated Metastatic Breast Cancer [NCT00450515]Phase 20 participants (Actual)Interventional2007-03-31Withdrawn(stopped due to Study was dropped prior to opening.)
Randomized Trial to Evaluate Therapeutic Gain by Changing Chemoradiotherapy From Concurrent-adjuvant to Induction-concurrent Sequence, and Radiotherapy From Conventional to Accelerated Fractionation for Advanced Nasopharyngeal Carcinoma [NCT00379262]Phase 3803 participants (Actual)Interventional2006-09-30Completed
Randomized Phase II Trial Of Neoadjuvant Combined Modality Therapy For Locally Advanced Rectal Cancer [NCT00081289]Phase 2146 participants (Actual)Interventional2004-03-31Completed
A Phase II Trial of Oxaliplatin and Capecitabine in the Treatment of Patients With Relapsed/Refractory Carcinoma of Unknown Primary Site [NCT00193609]Phase 248 participants (Actual)Interventional2004-09-30Completed
A Phase 1b Study Evaluating Momelotinib Combined With Capecitabine and Oxaliplatin in Subjects With Relapsed/Refractory Metastatic Pancreatic Ductal Adenocarcinoma [NCT02244489]Phase 116 participants (Actual)Interventional2014-11-05Terminated
Safety and Efficacy of Sintilimab in Combination With Albumin-Paclitaxel/Oxaliplatin/Capecitabine and Radiotherapy Followed by D2 Surgical Resection in Patients With Advanced Gastric Cancer With Retroperitoneal Lymph Node Metastasis: A Multiple Center Sin [NCT05002686]Phase 2/Phase 360 participants (Anticipated)Interventional2021-08-07Recruiting
A Phase 1b/2 Open-Label Study With Randomization in Phase 2 of IMU-131 HER2/Neu Peptide Vaccine Plus Standard of Care Chemotherapy in Patients With HER2/Neu Overexpressing Metastatic or Advanced Adenocarcinoma of the Stomach or Gastroesophageal Junction [NCT02795988]Phase 1/Phase 236 participants (Actual)Interventional2017-08-30Active, not recruiting
Preoperative Chemoradiation With Capecitabine and Cetuximab Within a Multidisciplinary Therapeutic Approach in Patients With Operable T3-T4 Rectal Cancer: a Phase II Study [NCT00297128]Phase 231 participants (Actual)Interventional2005-10-31Completed
Phase II Randomized Trial of Neoadjuvant Chemotherapeutic Treatment (XELOX) Followed by Chemoradiotherapy (XELOX/RT) and Surgery Versus Chemoradiotherapy Followed by Surgery and Chemotherapy in Patients With High Risk Rectal Cancer [NCT00421824]Phase 2108 participants (Actual)Interventional2006-05-31Completed
A Phase III Study of Chemotherapy With or Without Algenpantucel-L (HyperAcute®-Pancreas) Immunotherapy in Subjects With Borderline Resectable or Locally Advanced Unresectable Pancreatic Cancer [NCT01836432]Phase 3302 participants (Actual)Interventional2013-05-31Terminated(stopped due to Company decision)
A Phase II Study of Neoadjuvant Chemotherapy With Docetaxel, Capecitabine, Cisplatin, and Bevacizumab in Patients With Unresectable Advanced Gastric Cancer [NCT01471470]Phase 231 participants (Actual)Interventional2010-07-31Completed
A Phase Ib/Randomized Phase II Study of BEZ235 and Trastuzumab Versus Lapatinib and Capecitabine in Patients With HER2-positive Locally Advanced or Metastatic Breast Cancer Who Failed Prior to Trastuzumab [NCT01471847]Phase 15 participants (Actual)Interventional2012-02-29Completed
Genotype-driven Phase I Study of Irinotecan Administered in Neoadjuvant Chemoradiotherapy in Patients With Stage II/III Rectal Cancer [NCT01474187]Phase 160 participants (Anticipated)Interventional2011-11-30Recruiting
A Randomized Phase II Trial of Capecitabine Plus Cisplatin (XP) Versus Capecitabine Plus Genexol (XG) as a First-line Treatment for Advanced or Recurrent Esophageal Squamous Cell Carcinoma [NCT01474642]Phase 264 participants (Actual)Interventional2008-09-30Completed
Irinotecan Combined With Infusional 5-FU/Folinic Acid or Capecitabine and the Role of Celecoxib in Patients With Metastatic Colorectal Cancer [NCT00064181]Phase 386 participants (Actual)Interventional2003-05-31Completed
Phase I Trial With Weekly Docetaxel, Capecitabine and Carboplatin as Induction Chemotherapy Followed by Concomitant Capecitabine and Radiotherapy in Patients With Locally Advanced Esophageal Cancer [NCT00238147]Phase 118 participants (Anticipated)Interventional2004-09-30Completed
A Phase I/II, Multicentre Clinical Study Of ZD1839 (Iressa™) In Combination With Capecitabine (Xeloda™) In Subjects With Advanced Colorectal Carcinoma After Failure Of First-Line Chemotherapy [NCT00242788]Phase 1/Phase 240 participants Interventional2004-02-29Completed
A Randomized Phase II-study to Evaluate the Safety and Efficacy of Capecitabine Plus Irinotecan Plus Cetuximab Compared to Capecitabine Plus Oxaliplatin Plus Cetuximab in First-line Treatment of Patients With Metastatic Colorectal Cancer. [NCT00254137]Phase 292 participants Interventional2004-09-30Completed
Randomized Phase II Trial of Sequential Docetaxel Followed by Capecitabine Versus Concomitant Docetaxel/Capecitabine as in Induction Therapy for Early Stage Breast Cancer [NCT00415285]Phase 2100 participants Interventional2006-12-31Recruiting
A Multi-Institutional Phase II Trial Of Neoadjuvant Capecitabine (XELODA) And Oxaliplatin (ELOXATIN) For Resectable Colorectal Metastases In The Liver [NCT00070265]Phase 280 participants (Actual)Interventional2003-08-31Terminated(stopped due to Administratively complete.)
A Phase II Study of Celecoxib/Oxaliplatin/Capecitabine Combination Chemotherapy for Unresectable,Recurrent, or Metastatic Gastric/Gastroesophageal Junction Carcinoma [NCT00256321]Phase 24 participants (Actual)Interventional2004-10-31Terminated(stopped due to Closed due to poor accrual)
Phase II Study of Celecoxib, Capecitabine, and Irinotecan in Patients With Metastatic Colorectal Cancer [NCT00258232]Phase 20 participants Interventional2002-01-31Completed
A Prospective, Randomized, Open, Multi-center Phase III Clinical Study Comparing Efficacy and Safety of Sequential T-FEC and TX-XEC as Post-operative Adjuvant Chemotherapy Options for the Treatment of Triple-negative Breast Cancer [NCT01642771]Phase 3636 participants (Anticipated)Interventional2012-06-30Active, not recruiting
A Phase I And Pharmacogenetic Study Of CPT-11, Oxaliplatin, And Capecitabine In Patients With Solid Tumors [NCT00074321]Phase 184 participants (Actual)Interventional2003-11-30Completed
A Phase I Study of Oral Capecitabine in Combination With Weekly IV Carboplatin/Paclitaxel and Radiation Therapy for Patients [NCT00281788]Phase 113 participants (Actual)Interventional2003-09-30Completed
A Phase II Trial of Capecitabine in Combination With the Farnesyltransferase Inhibitor, R115777 (Tipifarnib, Zarnestra) in Patients With Metastatic Breast Cancer [NCT00077363]Phase 270 participants (Actual)Interventional2004-05-31Completed
A Phase III, Randomized, Open-label, Multicenter Study Comparing GW572016 and Capecitabine (XELODA) Versus Capecitabine in Women With Refractory Advanced or Metastatic Breast Cancer [NCT00078572]Phase 3408 participants (Actual)Interventional2004-03-31Completed
A Phase I/II Study of Weekly Intravenous Oxaliplatin in Combination With Oral Daily Capecitabine and Radiation Therapy in the Neoadjuvant Treatment of Rectal Cancer [NCT00086931]Phase 1/Phase 237 participants (Actual)Interventional2003-09-30Completed
A Phase II Trial Of Celecoxib (Celebrex) And Capecitabine (Xeloda) Combined With Pelvic Irradiation As Neoadjuvant Treatment Of Stage II or III Adenocarcinoma Of The Rectum [NCT00081224]Phase 23 participants (Actual)Interventional2004-12-31Terminated
A Phase I/II Study of Aroplatin and Capecitabine in Subjects With Unresectable Local Recurrence or Distant Metastases of Colorectal Cancer Refractory to 5-FU/Leucovorin and Irinotecan [NCT00081536]Phase 1/Phase 2105 participants InterventionalActive, not recruiting
Randomized Study of Second-Line Therapy Comprising Irinotecan With or Without Capecitabine in Patients Aged At Least 75 Years With Colorectal Cancer [NCT00303745]Phase 278 participants (Anticipated)Interventional2006-06-30Active, not recruiting
[NCT00083525]Phase 133 participants (Anticipated)Interventional2004-05-31Completed
A Randomized Phase III Study Comparing Epirubicin, Docetaxel and Capecitabine + G-CSF to Epirubicin and Docetaxel + G-CSF as Neoadjuvant Treatment for Early HER-2 Negative Breast Cancer and Comparing Epirubicin, Docetaxel and Capecitabine + G-CSF ± Trastu [NCT00309556]Phase 3536 participants (Actual)Interventional2005-02-28Completed
Phase II Trial Of Docetaxel With Capecitabine And Bevacizumab As First-Line Chemotherapy For Patients With Metastatic Breast Cancer [NCT00088998]Phase 246 participants (Actual)Interventional2004-12-31Completed
Combined Treatment With Capecitabine and Immunotherapy Versus Immunotherapy Alone in Advanced Renal Cell Carcinoma: a Prospective, Randomized, Multi-center phaseIII-Trial [NCT00311467]Phase 3172 participants (Actual)Interventional2004-03-31Terminated(stopped due to no patient recruitment)
Dose-Dense and Dose-Intense Alternating Irinotecan/Capecitabine and Oxaliplatin/Capecitabine: Phase I in Solid Tumors and Phase II With Bevacizumab a First-Line Therapy of Advanced Colorectal Cancer [NCT00296062]Phase 112 participants (Actual)Interventional2006-03-31Terminated(stopped due to Trial did not move to Phase II portion due to poor tolerance of treatment)
Levels of Circulating Tumor DNA as a Predictive Marker for Early Switch in Treatment for Patients With Metastatic (Stage IV) Breast Cancer: A Phase 2 Randomized, Open-Label Study [NCT05826964]Phase 2500 participants (Anticipated)Interventional2023-06-12Recruiting
Pembrolizumab in Combination With Xelox Bevacizumab in Patients With Microsatellite Stable Mestatic Colorectal Cancer and a High Immune Infiltrate : a Proof of Concept Study [NCT04262687]Phase 255 participants (Anticipated)Interventional2021-04-06Recruiting
A Phase II Study of Induction PD-1 Blockade in Subjects With Locally Advanced Mismatch Repair Deficient Solid Tumors [NCT04165772]Phase 2200 participants (Anticipated)Interventional2019-12-11Recruiting
Phase I Trial of Gemcitabine and Capecitabine (Xeloda) in Patients With Advanced Pancreatic Carcinoma [NCT00316420]Phase 120 participants (Actual)Interventional2003-12-31Completed
Phase 1 Study of the Oral Platinum Agent Satraplatin in Combination With Capecitabine for the Treatment of Patients With Advanced Solid Malignancies [NCT00329329]Phase 124 participants (Actual)Interventional2006-05-31Terminated(stopped due to Sponsor decided to discontinue study drug development)
Phase III Randomized Controlled Trial of Adjuvant Capecitabine/Cisplatin Chemotherapy and Chemoradiation Therapy for Gastric Adenocarcinoma [NCT00323830]Phase 3458 participants (Actual)Interventional2004-10-31Completed
Phase I/II Study of Tolerance and Pharmacokinetics With Capecitabine Given 5 Days Out of 7 in Metastatic Breast Cancer [NCT00324610]Phase 1/Phase 246 participants Interventional2006-03-31Recruiting
Phase 2 Clinical Trial of Bi-weekly Dosing of Irofulven Plus Capecitabine in Patients With Anaplastic or Locally Advanced/Metastatic Differentiated Thyroid Cancer [NCT00124527]Phase 235 participants Interventional2005-03-31Completed
Three-Arm Randomized Phase II Clinical Study of Irofulven/Prednisone, Irofulven/Capecitabine/Prednisone or Mitoxantrone/Prednisone in Docetaxel-Pretreated Hormone-Refractory Prostate Cancer Patients [NCT00124566]Phase 2135 participants (Actual)Interventional2004-06-30Completed
[NCT00087620]Phase 40 participants Interventional2004-09-30Terminated
An Open-Label, Multi-Center Phase II Clinical Study to Evaluate the Efficacy and Safety of MRG003 in Patients With Recurrent Metastatic Nasopharyngeal Carcinoma [NCT05126719]Phase 2238 participants (Anticipated)Interventional2021-08-04Recruiting
A Phase I, Dose-Escalating, Safety Study of an Intravenously Administered Pegylated Liposomal Mitomycin-C Lipid-based Prodrug (PL-MLP, PROMITIL) in Cancer Patients With Solid Tumors. [NCT01705002]Phase 188 participants (Actual)Interventional2012-10-31Completed
Single-agent Capecitabine as Adjuvant Chemotherapy in Locoregionally Advanced Nasopharyngeal Carcinoma: A Phase 3, Multicentre, Randomised Controlled Trial (CAN) [NCT02958111]Phase 3406 participants (Actual)Interventional2017-01-31Active, not recruiting
A Phase 2 Study of GTX-SRS: Neoadjuvant Gemcitabine, Docetaxel, and Capecitabine in Combination With Stereotactic Radiosurgery for Borderline Resectable Pancreatic Cancer [NCT00833859]Phase 22 participants (Actual)Interventional2009-03-31Terminated(stopped due to Abandoned - Lack of funding after only 2 patients enrolled)
A Phase II Study to Determine the Efficacy and Safety of Panitumumab in Combination With Chemoradiotherapy for Unresectable or Locally Recurrent Adenocarcinoma of the Rectum With or Without Metastatic Disease [NCT00346099]Phase 20 participants (Actual)Interventional2006-06-30Withdrawn(stopped due to Protocol closed based on new (and as yet unpublished) information from a phase II clinical trial.)
A Multicenter Randomized Comparative Study of Docetaxel Plus Epirubicin Versus Docetaxel Plus Capecitabine Combinations as First Line Treatment of Metastatic Breast Cancer [NCT00429871]Phase 3272 participants (Actual)Interventional2002-05-31Completed
Neo-AEGIS (NEOadjuvant Trial in Adenocarcinoma of the oEsophagus and oesophagoGastric Junction International Study): Randomised Clinical Trial of Neoadjuvant and Adjuvant Chemotherapy (Modified MAGIC or FLOT Regimen) vs. Neoadjuvant Chemoradiation (CROSS [NCT01726452]Phase 3377 participants (Actual)Interventional2013-01-24Completed
Phase II Study of Capecitabine and Oxaliplatin (XELOX) in Patients With Locally Advanced, Incurable, Salivary Gland Cancers [NCT00101075]Phase 29 participants (Actual)Interventional2004-10-31Terminated(stopped due to Slow Accrual)
Multicenter Phase IV.II Trial, for the Administration of Capecitabine Simultaneous to Radiotherapy for Local Relapse Breast Cancer Patients With Negative Her2 Tumours [NCT00434941]Phase 21 participants (Actual)Interventional2007-09-30Terminated(stopped due to Due to the slow rate of recruitment the study was stopped.)
A Randomized, Controlled Phase II Study to Compare Capecitabine Combined With Dacarbazine(CAPDTIC) Versus Capecitabine Combined Temozolomide(CAPTEM) in Advanced and Metastatic Gastrointestinal Pancreatic and Esophageal Neuroendocrine Tumor [NCT03279601]Phase 2148 participants (Anticipated)Interventional2017-09-01Recruiting
Phase II Study of Trastuzumab (Herceptin) and Capecitabine (Xeloda) in Women With Taxanes and Anthracyclines Refractory Metastatic Breast Cancer and HER2 Over-Expression [NCT00107393]Phase 275 participants (Anticipated)Interventional2003-06-30Completed
Randomized Phase III Trial With Capecitabine/Erlotinib Followed of Gemcitabine Versus Gemcitabine/Erlotinib Followed of Capecitabine in Patients With Advanced Pancreatic Cancer [NCT00440167]Phase 3280 participants (Anticipated)Interventional2006-06-30Active, not recruiting
Phase I Trial of Induction Paraplatin® and Xeloda® Followed by Concurrent Paraplatin and Xeloda With Intensity Modulated Radiotherapy for Locally Advanced Squamous Cell Carcinoma of the Head and Neck [NCT00114153]Phase 148 participants (Anticipated)Interventional2003-06-30Completed
A Phase III Randomized Study of Primary Chemotherapy With Adriamycin/Cyclophosphamide(AC) vs Taxotere/Xeloda(TX) for Stage II and III Breast Cancer [NCT00352378]Phase 3209 participants (Actual)Interventional2002-06-30Completed
A Randomized Phase III Study Comparing Docetaxel Followed by Cyclophosphamide, Epirubicin and 5-FU to Docetaxel With Capecitabine Followed by Cyclophosphamide, Epirubicin and Capecitabine as Adjuvant Treatment for Early Breast Cancer [NCT00114816]Phase 31,500 participants (Anticipated)Interventional2004-01-31Completed
A Phase I/II Study to Evaluate the Efficacy and Toxicity of Imatinib Mesylate in Combination With Dacarbazine and Capecitabine in Medullary Thyroid Carcinoma [NCT00354523]Phase 1/Phase 221 participants (Actual)Interventional2004-12-31Terminated(stopped due to Study closed following Phase I portion, insufficient activity to continue to Phase II.)
A Phase II Study of Bevacizumab With Concurrent Capecitabine and Radiation Followed by Maintenance Gemcitabine and Bevacizumab For Locally Advanced Pancreatic Cancer [NCT00114179]Phase 282 participants (Actual)Interventional2005-01-31Completed
Treatment of Relapsed or Metastatic Head and Neck Carcinomas With Oxaliplatin and Capecitabine [NCT00448552]Phase 230 participants (Anticipated)Interventional2004-02-29Completed
Parallel Phase I Study of Ixabepilone Plus Lapatinib and Ixabepilone Plus Lapatinib Plus Capecitabine in Subjects With HER2 Positive Locally Advanced or Metastatic Breast Cancer [NCT00634088]Phase 113 participants (Actual)Interventional2008-06-30Terminated(stopped due to Slow Accrual)
Phase II Trial of OSI-774 (Erlotinib, Tarceva™,) and Capecitabine for Patients With Previously Untreated Metastatic Colorectal Cancer [NCT00459901]Phase 213 participants (Actual)Interventional2004-06-30Terminated(stopped due to Study halted by drug manufacturer)
A Phase I, Open-Label, Dose-Escalation Study of the Safety and Tolerability of Ispinesib in Combination With Capecitabine on an Every 21-Day Schedule in Subjects With Advanced Solid Tumors [NCT00119171]Phase 130 participants Interventional2004-11-30Completed
A Phase I Study of Suberoylanilide Hydroxamic Acid (SAHA) in Combination With Capecitabine in Patients With Solid Tumors [NCT00121277]Phase 128 participants (Actual)Interventional2005-09-30Completed
A Prospective Single-arm Phase Ⅱ Study of Toripalimab Plus Neoadjuvant Chemotherapy Combined With Chemoradiotherapy for Locally Advanced Unresectable Esophageal Squamous Cell Carcinoma [NCT04844385]Phase 283 participants (Anticipated)Interventional2021-02-20Recruiting
A Phase 2 Study of Preoperative Radiation Therapy and Capecitabine (an Oral Fluoropyrimidine Carbamate) in Locally Advanced Rectal Cancer [NCT00122291]Phase 266 participants (Anticipated)Interventional2002-01-31Active, not recruiting
An Open Label Study of the Effect of First Line Treatment With Bevacizumab in Combination With Capecitabine and Oxaliplatin on Progression-free Survival in Patients With Metastatic Cancer of the Colon and Rectum [NCT01399190]68 participants (Actual)Observational2011-07-31Completed
A Phase I/II Trial of Proton Therapy With Concurrent Capecitabine for Locally Advanced and Recurrent Rectal Cancer [NCT00503932]Phase 1/Phase 20 participants (Actual)Interventional2007-07-31Withdrawn(stopped due to No participant enrollment.)
Phase II Study of Docetaxel and Capecitabine as 1st Line Therapy for Patients With Locally Advanced or Metastatic Gastric Cancer [NCT00142038]Phase 280 participants Interventional2004-03-31Completed
A Pilot Trial of Germline Polymorphisms as Predictors of Response to Gemcitabine, Docetaxel, and Capecitabine (GTX) in Metastatic or Unresectable Pancreatic Cancer. [NCT00159471]1 participants (Actual)Interventional2005-02-28Terminated(stopped due to Insufficient Accrual)
Docetaxel by 1 Hour Infusion Followed by 24 Hour Infusion of Cisplatin Plus Capecitabine as Neoadjuvant Chemotherapy for Locally Advanced Breast Cancer [NCT00155259]Phase 247 participants (Actual)Interventional2004-10-31Completed
A Phase Ⅱ Study of Pre-Operative Concurrent Chemoradiotherapy With Capecitabine Plus Irinotecan in Resectable Rectal Cancer. [NCT00506623]Phase 248 participants (Actual)Interventional2004-07-31Active, not recruiting
Evaluation of Thymidine Phosphorylase and Other Predictive/Prognostic Factors in Primary Breast Cancer Treated With Docetaxel and Capecitabine (DC) [NCT00156312]25 participants (Anticipated)Interventional2003-07-31Completed
Adjuvant Chemotherapy With Oxaliplatin and Capecitabine Versus Follow-up After Resection of Colorectal Liver Metastases- Randomized Phase III Study [NCT00156975]Phase 3384 participants Interventional2004-11-30Active, not recruiting
A Randomized, Open-label, Phase 3 Study of Sacituzumab Govitecan Versus Treatment of Physician's Choice in Patients With Hormone Receptor-Positive (HR+)/Human Epidermal Growth Factor Receptor 2 Negative (HER2-) (HER2 IHC0 or HER2-low [IHC 1+, IHC 2+/ISH-] [NCT05840211]Phase 3654 participants (Anticipated)Interventional2023-05-08Recruiting
Phase I Trial of ZEN003694 (ZEN-3694) in Combination With Capecitabine in Patients With Solid Tumors [NCT05803382]Phase 130 participants (Anticipated)Interventional2023-11-08Recruiting
A Phase Ib Trial of Preoperative Short-Course Chemoradiotherapy Followed by Chemotherapy for Resectable Gastric Adenocarcinoma [NCT04523818]Phase 125 participants (Actual)Interventional2020-08-11Active, not recruiting
Phase II Study of Neoadjuvant Gemcitabine/Oxaliplatin and Cetuximab Followed by Surgery or Concurrent External Beam Radiation With Capecitabine for Patients With Locally Advanced Unresectable Nonmetastatic Pancreatic Cancer [NCT00408564]Phase 239 participants (Actual)Interventional2006-01-31Completed
Combination of 6-Thioguanine, Capecitabine, Celecoxib and Temozolomide or CCNU for Recurrent Anaplastic Glioma and Glioblastoma Multiforme [NCT00504660]Phase 275 participants (Actual)Interventional2003-09-30Completed
A Phase ll Study of Oxaliplatin, Capecitabine, and Bevacizumab in the Treatment of Metastatic Esophagogastric Adenocarcinomas [NCT00447330]Phase 260 participants (Actual)Interventional2007-02-28Completed
Phase II Randomized Trial of Adjuvant XELOX Chemotherapy and XELOX With Concurrent Capecitabine and Radiotherapy for Gastric Adenocarcinoma With D2 Dissection [NCT01711242]Phase 2208 participants (Actual)Interventional2012-01-31Completed
A Phase II Study to Explore the Neoadjuvant Treatment of Serplulimab Combined With CAPEOX + Celecoxib in the Treatment of Locally Advanced Rectal Cancer [NCT05731726]Phase 250 participants (Anticipated)Interventional2023-02-22Recruiting
A Randomized, Open, Multicenter Phase III Clinical Trial of Combination of Sintilimab Injection (IBI308) and XELOX+Bevacizumab Compared With XELOX+Bevacizumab as 1st Line Therapy of RAS-Mutant Metastatic Colorectal Cancer [NCT05171660]Phase 3436 participants (Anticipated)Interventional2022-02-08Recruiting
A Phase 3, Randomized, Multicenter, Open-Label Study to Compare the Efficacy and Safety of Anti-HER2 Therapy Plus Fulvestrant or Capecitabine in First-line Treatment of Women With HR+, HER2+, Non-visceral Metastases, Stage IV Breast Cancer [NCT04337658]Phase 3493 participants (Anticipated)Interventional2020-07-01Not yet recruiting
Prognostic Value of Neutrophil-to-lymphocyte Ratio (NLR) on Rectal Cancer Patients Who Received Capecitabine and Concurrent Intensity Modulated Radiotherapy (IMRT) [NCT03015168]117 participants (Actual)Observational2012-01-31Completed
Multicentric Single Arm Phase II Study Evaluating the Efficacy of Association of Tucatinib, Capecitabine and Intra-CSF Trastuzumab in HER2 Amplified Breast Cancer Patients With Leptomeningeal Metastases [NCT05800275]Phase 230 participants (Anticipated)Interventional2023-11-30Not yet recruiting
Master Protocol for Metastatic Hormone-Resistant Prostatic Carcinoma - Phase II Trials - Protocol 5: Capecitabine [NCT00006023]Phase 20 participants Interventional2000-03-31Completed
The First-line Therapy With the Combination of Anlotinib, Penpulimab and Capecitabine in Recurrent/Metastatic Nasopharyngeal Carcinoma: a Single-arm, Open-label, Phase II Trial [NCT05807880]Phase 2110 participants (Anticipated)Interventional2023-10-01Not yet recruiting
A Multicenter Randomized Phase III Trial of Neo-adjuvant Chemotherapy Followed by Surgery and Chemotherapy or by Surgery and Chemoradiotherapy in Resectable Gastric Cancer (CRITICS Study) [NCT00407186]Phase 3788 participants (Actual)Interventional2007-01-11Active, not recruiting
Phase II Trial of Preoperative Radiation Therapy With Capecitabine in Rectal Cancer (UMCC 0046) [NCT00176787]Phase 230 participants Interventional2000-10-31Terminated(stopped due to recruitment goals met)
A Phase Ib/II Study of First Line Pembrolizumab in Combination With Trastuzumab, Capecitabine, and Cisplatin in HER2 Positive Gastric Cancer [NCT02901301]Phase 1/Phase 241 participants (Actual)Interventional2017-02-06Active, not recruiting
A Phase III Study to Evaluate the 3-year Disease-free Survival in Patients With Locally Advanced Colon Cancer Receiving Either Perioperative or Postoperative Chemotherapy With FOLFOX or CAPOX Regimens [NCT02572141]Phase 3738 participants (Anticipated)Interventional2015-01-01Active, not recruiting
Weekly Taxol® Plus Xeloda® Versus Taxotere® Every Three Weeks Plus Xeloda® in the Treatment of Metastatic Breast Cancer A Phase II/III Study [NCT00201435]Phase 2/Phase 3224 participants (Anticipated)Interventional2005-03-31Completed
A Single-arm, Single-center, Prospective Phase I/II Study of Fuquinitinib Combined With Capecitabine First-line Maintenance in the Treatment of Metastatic Colorectal Cancer [NCT06115733]56 participants (Anticipated)Interventional2023-12-28Not yet recruiting
Letrozole With or Without Metronomic Capecitabine in First Line Treatment of Patients With ER-positive HER2 Negative Advanced Breast Cancer: A Randomized Phase II Study. [NCT04571437]Phase 2204 participants (Anticipated)Interventional2020-03-01Recruiting
A Phase II Trial of Capecitabine and Oxaliplatin (CAPOX) in Patients With Metastatic Breast Cancer: Hoosier Oncology Group BRE03-60 [NCT00216021]Phase 225 participants (Actual)Interventional2004-03-31Completed
A Single Arm Phase II Trial of Docetaxel and Capecitabine for the First Line Treatment of Recurrent/Metastatic Squamous Cell Carcinoma of the Head and Neck (SCCHN): Hoosier Oncology Group HN02-40 [NCT00216138]Phase 219 participants (Actual)Interventional2004-03-31Terminated(stopped due to Interim analysis results did not meet criteria for second stage of trial)
Effect of Capecitabine on the Pharmacokinetics of BMS-247550 on the Pharmacokinetics of Capecitabine and Its Metabolites in Patients With Advanced Malignancies [NCT00207129]Phase 125 participants Interventional2004-10-31Completed
A Phase II Trial of Capecitabine and Oxaliplatin in Metastatic Breast Cancer [NCT00204776]Phase 237 participants (Anticipated)Interventional2005-03-31Completed
A Phase 1b Study of Venetoclax and Capecitabine In Subjects With Hormone Receptor-Positive, HER2-Negative Locally Advanced or Metastatic Breast Cancer Who Experienced Disease Progression During or After CDK4/6 Inhibitor Therapy [NCT04274933]Phase 14 participants (Actual)Interventional2020-05-21Terminated(stopped due to Company Decision)
XELOX III. Capecitabine (Xeloda) in Combination With Oxaliplatin (Eloxatin) as First-line Treatment of Patients With Advanced or Metastatic Colorectal Cancer. A Randomized Phase II Study [NCT00212615]Phase 2/Phase 3116 participants (Actual)Interventional2004-02-29Completed
Pre-operative Epirubicin, Capecitabine (Xeloda) and Cisplatin in Patients With Newly Diagnosed Localised Oesophageal Adenocarcinoma [NCT00220103]Phase 280 participants (Anticipated)Interventional2002-11-30Completed
An Open-label, Multi-center Study to Evaluate the Disease Free Survival Rate of a Perioperative Combination of Capecitabine (Xeloda), Trastuzumab (Herceptin) and Oxaliplatin (XELOX- Trastuzumab) in Patients With Resectable Gastric or Gastro-esophageal Jun [NCT01130337]Phase 236 participants (Actual)Interventional2010-07-31Completed
Rationale and Design of a Prospective, Multicenter Phase Ⅱ Clinical Trial of Safety and Efficacy Evaluation of Long Course Neoadjuvant Chemoradiotherapy Plus Tislelizumab Followed by TME for LARC. [NCT04911517]Phase 250 participants (Anticipated)Interventional2021-06-01Recruiting
A Multicenter Randomized Phase III Study of Combination Treatment With Vinorelbine and Gemcitabine Versus Capecitabine Monotherapy in Metastatic Breast Cancer Patients Following Treatment Failure With the Combination of a Taxane and an Anthracycline [NCT00431106]Phase 3144 participants (Anticipated)Interventional2002-04-30Completed
Phase I/II Study of R340 (Capecitabine), L-OHP (Oxaliplatin) and R435 (Bevacizumab) in Advanced and/or Metastatic Colorectal Cancer [NCT00345761]Phase 1/Phase 264 participants (Actual)Interventional2006-02-28Completed
Phase II Trial of Capecitabine for the Treatment of Unresectable/ Metastatic or Advanced Hepatocellular Carcinoma(HCC) [NCT00464295]Phase 215 participants (Actual)Interventional2006-08-31Completed
[NCT00477711]Phase 241 participants (Actual)Interventional2007-03-31Completed
Randomised, Multicenter Phase II Study in Patients With Metastatic Breast Cancer With Gemcitabine Plus Vinorelbine Versus Gemcitabine Plus Cisplatin Versus Gemcitabine Plus Capecitabine [NCT00480597]Phase 2141 participants (Actual)Interventional2002-10-31Completed
A Randomized Phase III Study of Oxaliplatin (Eloxatin) and Capecitabine on Top of Sorafenib Versus Sorafenib Alone as First-line Palliative Treatment in Advanced Hepatocellular Carcinoma Patients [NCT01245582]Phase 30 participants (Actual)Interventional2011-07-31Withdrawn
An Open Label Phase 1B Dose-Finding Study of TRC105 in Combination With Capecitabine for Progressive or Recurrent Metastatic Breast Cancer [NCT01326481]Phase 1/Phase 219 participants (Actual)Interventional2011-06-30Completed
A Prospective Randomised Open Label Trial of Oxaliplatin/Fluoropyrimidine Versus Oxaliplatin/Fluoropyrimidine Plus Cetuximab Pre and Post Operatively in Patients With Resectable Colorectal Liver Metastasis Requiring Chemotherapy [NCT00482222]Phase 3340 participants (Anticipated)Interventional2007-02-28Recruiting
A Phase II Study of Bevacizumab, Irinotecan and Capecitabine in Patients With Previously Untreated Metastatic Colorectal Cancer [NCT00483834]Phase 250 participants (Actual)Interventional2006-12-31Completed
A Randomized, Multicenter, Open-Label, Phase 3 Study of Nivolumab Plus Ipilimumab or Nivolumab in Combination With Oxaliplatin Plus Fluoropyrimidine Versus Oxaliplatin Plus Fluoropyrimidine in Subjects With Previously Untreated Advanced or Metastatic Gast [NCT02872116]Phase 32,031 participants (Actual)Interventional2016-10-12Active, not recruiting
A Four Part, Phase I Dose-Escalation Study of the Combinations of Concurrent BKM120 and Capecitabine, or Concurrent BYL719 and Capecitabine, or Concurrent BKM120 and Capecitabine and Trastuzumab, or Concurrent BKM120 and Capecitabine and Lapatinib in Pati [NCT01300962]Phase 147 participants (Actual)Interventional2011-08-31Completed
Phase II Trial of Docetaxel, Oxaliplatin and Capecitabine (TEX) in Advanced or Metastatic Gastric Cancer [NCT00511446]Phase 256 participants (Actual)Interventional2007-08-31Completed
Phase II Study of Irinotecan in Combination With Capecitabine in Previously Untreated Patients With Metastatic Colorectal Cancer [NCT00506168]Phase 237 participants (Actual)Interventional2001-11-30Terminated(stopped due to The study drugs are not covered anymore by insurance.)
A Single-arm, Multicenter, Open-labeled Clinical Study of UTD1 Combined With Capecitabine in Metastatic HER2-negative Breast Cancer Patients With Brain Metastases [NCT05535413]Phase 1/Phase 230 participants (Anticipated)Interventional2022-08-01Recruiting
A Multicenter Phase II Study of Neoadjuvant Docetaxel, Cisplatin and Capecitabine and Protocolized Surgery in Resectable Gastric Cancer [NCT01517009]Phase 250 participants (Anticipated)Interventional2008-06-30Completed
Perioperative Tegafur Gimeracil Oteracil Potassium Capsule Plus Oxaliplatin Versus Capecitabine Plus Oxaliplatin in Patients With Localized Advanced Gastric Cancer [NCT01516944]Phase 2/Phase 3749 participants (Actual)Interventional2012-02-29Completed
Preoperative, Proton- Radiotherapy Combined With Chemotherapy for Borderline Resectable Pancreatic Cancer [NCT04894643]10 participants (Anticipated)Interventional2020-09-14Recruiting
Radiotherapy Combined With Recombinant Human Endostatin and Capecitabine for Patients With Nasopharyngeal Carcinoma Resistant to Induction Chemotherapy [NCT05514275]Phase 241 participants (Anticipated)Interventional2022-08-01Recruiting
Total Neoadjuvant NALIRIFOX Plus Ablative Dose Radiation Therapy for Borderline Resectable and Locally Advanced Pancreatic Adenocarcinoma [NCT05851924]Phase 260 participants (Anticipated)Interventional2023-05-12Recruiting
A Phase Ia/Ib Open-Label, Dose-Escalation Study of the Safety and Pharmacokinetics of Tiragolumab as a Single Agent and in Combination With Atezolizumab and/or Other Anti-Cancer Therapies in Patients With Locally Advanced or Metastatic Tumors [NCT02794571]Phase 1518 participants (Actual)Interventional2016-05-23Active, not recruiting
Combined Chemotherapy and Tislelizumab With Preoperative Split-course Hypofraction Radiotherapy for Locally Advanced Rectal Cancer:Study Protocol of a Prospective, Single-arm Phase II Trial [NCT05176964]50 participants (Anticipated)Observational2021-12-31Recruiting
Pyrotinib Plus Capecitabine in Patients With Brain Metastases From HER2-positive Metastatic Breast Cancer : a Single-arm, Open-label, Ahead Study [NCT03691051]Phase 278 participants (Actual)Interventional2018-11-20Active, not recruiting
A Phase I-II Study of Systemic Capecitabine, Cisplatin and Intraperitoneal Docetaxel (XPID) in Patients With Advanced Stomach Cancer With Peritoneal Seeding [NCT01525771]Phase 1/Phase 237 participants (Actual)Interventional2011-02-28Completed
A Randomized Phase II Trial of Second Line Therapy in Advanced Biliary Tract Cancer: Capecitabine or Capecitabine Plus Mitomycin C [NCT01530503]Phase 252 participants (Actual)Interventional2011-11-30Completed
A Randomized, Multicenter, Controlled Phase III Study to Compare Perioperative Chemotherapy of Oxaliplatin Combined With S-1(SOX) Versus SOX or Oxaliplatin With Capecitabine (XELOX) as Post-operative Chemotherapy in Locally Advanced Gastric Adenocarcinoma [NCT01534546]Phase 31,094 participants (Actual)Interventional2012-03-31Active, not recruiting
Trapianto di Fegato Per Colangiocarcinoma (CCA) Ilare in Associazione a Radio e Chemioterapia Neoadiuvante [NCT01549795]33 participants (Anticipated)Interventional2012-01-31Recruiting
A Phase II Trial Evaluating a Modified Regimen of Oxaliplatin and Capecitabine in First-Line Treatment of Metastatic Colorectal Adenocarcinoma [NCT01552967]Phase 230 participants (Anticipated)Interventional2012-03-31Recruiting
Phase I Trial of Ganetespib, Capecitabine, and Radiation in Rectal Cancer [NCT01554969]Phase 116 participants (Actual)Interventional2012-05-31Completed
Phase II Evaluation Of Capecitabine In Recurrent Platinum-Sensitive Ovarian Or Primary Peritoneal Cancer [NCT00006812]Phase 20 participants Interventional2001-03-31Terminated
Capecitabine (Xeloda) in Malignant Mesothelioma: A Phase II Study [NCT00004183]Phase 227 participants (Actual)Interventional2000-11-30Completed
Phase 2 Study of Temozolomide Plus Capecitabine in Patients With Grade 3 and Low Ki-67 Gastroenteropancreatic Neuroendocrine Tumors [NCT03079440]Phase 231 participants (Actual)Interventional2017-05-15Completed
A Phase II Trial of Neoadjuvant Capecitabine, Oxaliplatin, and Bevacizumab for Resectable Colorectal Metastases in the Liver [NCT00118105]Phase 20 participants (Actual)Interventional2006-11-30Withdrawn(stopped due to Budget Constraints)
Phase I Study of Capecitabine (Xeloda) and Radiation Therapy in Patients With Locally Advanced Cervical and Pelvic Malignancies [NCT00118300]Phase 10 participants (Actual)Interventional2005-04-30Withdrawn(stopped due to Competing studies)
Carcinoma Unknown Primary: Treatment With Gemcitabine, Docetaxel and Capecitabine (GTX) an Evaluation and Treatment Study of The Cancer Institute of New Jersey Oncology Group [NCT00119314]Phase 20 participants (Actual)Interventional2004-07-31Withdrawn(stopped due to slow accrual)
A Phase II Study of Oxaliplatin, Capecitabine, and Bevacizumab in the Treatment of Elderly Patients With Metastatic Colorectal Cancer [NCT00120172]Phase 240 participants (Anticipated)Interventional2005-05-31Terminated(stopped due to positive results from a larger study with same regimen was released.)
A Phase I Study of Oral Fluoropyrimidine Capecitabine (Xeloda Roche) Combined With Intravenous Cisplatin in Patients With Advanced Cancer of the Digestive System [NCT00010023]Phase 10 participants Interventional2000-08-31Completed
Phase I/II Trial of Capecitabine With Weekly Paclitaxel for Advanced Breast Cancer [NCT00031876]Phase 1/Phase 234 participants (Actual)Interventional2000-05-31Completed
Tailored Treatment of Metastatic Colorectal Cancer Based on Genetic Markers [NCT00396487]Phase 31 participants (Actual)Interventional2006-11-30Terminated(stopped due to Only one patient included as per Feb. 4, 2008.)
Phase I-II Study to Evaluate Safety, Efficacy and Pharmacokinetic Interactions Between Capecitabine (XELODA) and Exisulind (APTOSYN) in Patients With Metastatic Breast Cancer [NCT00037609]Phase 1/Phase 235 participants (Actual)Interventional2001-01-31Completed
A Limited Access Phase II Trial Of Capecitabine In Advanced, Persistent Or Recurrent Squamous Cell Carcinoma Of The Cervix [NCT00016926]Phase 20 participants Interventional2001-04-30Completed
A Phase II Evaluation Of Capecitabine (NSC #712807) In The Treatment Of Persistent Or Recurrent Non-Squamous Cell Carcinoma Of The Cervix [NCT00039442]Phase 221 participants (Actual)Interventional2002-04-29Completed
Phase 1b Study of Ramucirumab in Combination With Fluoropyrimidines and Platinum-Based Agents in Japanese Patients With Metastatic Gastric/Gastroesophageal Junction Adenocarcinoma [NCT02359058]Phase 118 participants (Actual)Interventional2015-02-28Completed
A Phase I Trial of Concurrent RHUMAB VEGF (BEVACIZUMAB) and Capecitabine-based Chemoradiation for Patients With Locally Advanced Pancreatic Cancer [NCT00047710]Phase 148 participants (Actual)Interventional2002-09-30Completed
A Phase I Dose Escalation Study With Oral LY317615 in Combination With Capecitabine in Advanced Cancer Patients [NCT00052273]Phase 116 participants (Actual)Interventional2002-12-31Completed
A Phase II Study Of Docetaxel And Capecitabine In Patients With Measurable Metastatic Adenocarcinoma Of The Stomach And Gastroesophageal Junction [NCT00054457]Phase 246 participants (Actual)Interventional2003-09-30Completed
A Phase II Study of IV Gemcitabine and Oral Capecitabine in Patients With Advanced Renal Cell Cancer [NCT00058318]Phase 243 participants (Actual)Interventional2004-12-31Completed
A Clinical Trial Comparing Preoperative Radiation Therapy And Capecitabine With or Without Oxaliplatin With Preoperative Radiation Therapy And Continuous Intravenous Infusion Of 5-Fluorouracil With or Without Oxaliplatin In The Treatment Of Patients With [NCT00058474]Phase 31,608 participants (Actual)Interventional2004-07-31Active, not recruiting
A Single Center, Open-labeled, Single Arm Phase II Study of Fruquintinib Combined With Capecitabine as First-line Treatment for Advanced Metastatic Colorectal Cancer Unsuitable for Intravenous Chemotherapy [NCT04866108]Phase 249 participants (Anticipated)Interventional2021-12-08Recruiting
Drug Treatment for Bowel Cancer: Making the Best Choices When a Milder Treatment is Needed [NCT00070213]Phase 3460 participants (Actual)Interventional2003-09-30Completed
Phase Ib/II Neoadjuvant Trial of the Farnesyltransferase Inhibitor, R115777 With Docetaxel and Capecitabine for Patients With Stage IIIA or IIIB Breast Cancer [NCT00070252]Phase 1/Phase 253 participants (Actual)Interventional2003-09-30Completed
Phase II Study Of Radiotherapy And Capecitabine As Pre-Operative Treatment In Patients With Colorectal Cancer [NCT00075556]Phase 20 participants Interventional2002-01-31Active, not recruiting
Adjuvant PD-1 Antibody（Tislelizumab） in Combination With Capecitabine for Patients With Cholangiocarcinoma at High-Risk of Postoperative Recurrence [NCT04782804]Phase 1/Phase 230 participants (Anticipated)Interventional2021-01-01Recruiting
A Phase I/II Study of Botanical PHY906 Plus Capecitabine for Advanced Unresectable Hepatocellular Carcinoma [NCT00076609]Phase 1/Phase 231 participants Interventional2003-10-31Completed
A Phase I Study Of The Combination Of Oral DJ-927 And Capecitabine In Patients With Advanced Solid Tumors [NCT00077077]Phase 10 participants Interventional2004-02-29Completed
Phase II Study of Capecitabine, Oxaliplatin, Bevacizumab and Radiation Therapy in Biliary Tract and Gallbladder Cancer [NCT00142480]Phase 28 participants (Actual)Interventional2004-12-31Completed
Randomized Phase 2 Study of Capecitabine vs Gemcistabine Plus Cisplatin in Patients With Resected Extrahepatic Cholangiocarcinoma With Regional Lymph Node Metastasis [NCT03079427]Phase 2101 participants (Actual)Interventional2017-05-15Completed
Single Arm and Phase II Clinical Trial of a Sandwich Regimen as XELOX Regimen and Capecitabine Alternate Administration Combined With Preoperative Intensity Modulated Radiation Therapy for pMMR Locally Advanced Rectal Cancer [NCT05228431]Phase 2121 participants (Anticipated)Interventional2022-12-01Not yet recruiting
ESTUDIO FASE II DE BEVACIZUMAB EN COMBINACIÓN CON CAPECITABINA Y RADIOTERAPIA COMO TRATAMIENTO PREOPERATORIO EN PACIENTES CON CÁNCER RECTAL LOCALMENTE AVANZADO RESECABLE [NCT00847119]Phase 243 participants (Actual)Interventional2007-09-30Completed
A Phase II Trial of Evaluating Circulating Endothelial Cell as A Surrogate Marker for Monitoring Treatment Efficacy of Docetaxel Plus Capecitabine With Bevacizumab as First Line Treatment for Patients With Locally Recurrent and Metastatic Breast Cancer [NCT00845910]Phase 222 participants (Actual)Interventional2009-05-31Terminated(stopped due to To be confirmed)
Pilot Study of Oxaliplatin in Combination With Capecitabine in Adult Cancer Patients [NCT00019773]Phase 10 participants Interventional1999-07-31Completed
Efficacy and Safety of Short-course Radiotherapy Sequential Penpulimab in Combination With CAPEOX in the Neoadjuvant Treatment of Microsatellite Stable Locally Advanced Rectal Cancer: a Single-centre, Single-arm, Phase 2 Study [NCT05576480]Phase 255 participants (Anticipated)Interventional2022-10-31Not yet recruiting
Randomized Phase III Study Post Radical Resection of Liver Metastasis of Colorectal Cancer: Bevacizumab in Combination With XELOX as Adjuvant Chemotherapy vs XELOX Alone [NCT00394992]Phase 379 participants (Actual)Interventional2006-12-31Terminated(stopped due to Data from the C08 study and Avant study)
A Pilot Trial Of Two Different Doses Of Capecitabine (XELODA) In Patients With Advanced And/Or Metastatic Breast Cancer [NCT00026442]Phase 20 participants Interventional2001-11-30Active, not recruiting
A Multi-center, II Phase，Randomized Controlled Clinical Study of Capecitabine Metronomic Chemotherapy After Gemcitabine Plus Capecitabine Standard Adjuvant Therapy for Stage II/III Pancreatic Cancer [NCT03959150]Phase 2/Phase 3231 participants (Anticipated)Interventional2020-01-05Recruiting
Gemcitabine Plus Capecitabine Versus Gemcitabine Alone In Advanced Pancreatic Cancer. A Randomized Phase III Trial [NCT00030732]Phase 3319 participants (Actual)Interventional2001-06-30Completed
A Phase III Multicenter Randomized Clinical Trial Comparing Gemcitabine Alone Or In Combination With Capecitabine For The Treatment Of Patients With Advanced Pancreatic Cancer [NCT00032175]Phase 3508 participants (Anticipated)Interventional2002-04-30Completed
iMmunoscore Associated Decision GuIdance for adjuvaNt Chemotherapy and Physical Exercise in Stage III Colon Cancer (iMAGINE): a Prospective, Randomized, Open-label, Multicenter, Phase III Clinical Trial [NCT04488159]Phase 31,638 participants (Anticipated)Interventional2023-12-01Not yet recruiting
Phase II Trial PD-L1/PD-1 Blockade Avelumab (MSB0010718C) With Chemoradiotherapy for Locally Advanced Resectable Rectal Cancer [NCT03299660]Phase 237 participants (Actual)Interventional2018-04-30Completed
Phase II Trial of Pembrolizumab in Combination With Trastuzumab, Fluoropyrimidine, and Platinum Chemotherapy in First Line Stage IV HER2-positive Metastatic Esophagogastric (EG) Cancer [NCT02954536]Phase 237 participants (Actual)Interventional2016-11-03Completed
A Phase I Trial of ZD1839 With Capecitabine in Patients With Advanced Solid Tumors (Formerly a Phase I Trial of ZD1839 With Capecitabine and Celecoxib) [NCT00039390]Phase 141 participants (Actual)Interventional2002-04-30Completed
A Phase I/II Trial of Epirubicin, Carboplatin & Capecitabine in Adult Cancer Patients [NCT00021047]Phase 1/Phase 20 participants Interventional2001-07-31Completed
Protocol For Assessment Of Capecitabine For Advanced Colorectal Cancer In Patients Aged 70 Years And Older (And In A Cohort Of Patients Younger Than 60 Years) [NCT00049335]Phase 229 participants (Actual)Interventional2003-02-28Completed
Combination Capecitabine (Xeloda) and ABI-007 (Abraxane, Nanoparticle Albumin-Bound Paclitaxel) Chemotherapy as Neoadjuvant Treatment of Locally Advanced, Operable Breast Cancer [NCT00397761]Phase 2/Phase 30 participants (Actual)Interventional2006-07-31Withdrawn
A Phase II Trial Evaluating Multiple Metastasectomy Combined With Hepatic Artery Infusion Of Floxuridine (FUDR) And Dexamethasone (DXM), Alternating With Systemic Oxaliplatin (OXAL) And Capecitabine (CAPCIT) For Colorectal Carcinoma Metastatic To The Live [NCT00026234]Phase 275 participants (Actual)Interventional2002-02-28Completed
Phase II Randomized Study of First-Line Therapy Comprising Bevacizumab and Irinotecan Hydrochloride, Leucovorin Calcium, and Fluorouracil (FOLFIRI) Versus Bevacizumab and Irinotecan Hydrochloride and Capecitabine (XELIRI) in Patients With Unresectable Met [NCT00423696]Phase 2145 participants (Actual)Interventional2006-03-23Completed
A Phase III Trial of Modified FOLFOX6 Versus CAPOX, With Bevacizumab (NSC-704865) or Placebo, as First-Line Therapy in Patients With Previously Untreated Advanced Colorectal Cancer [NCT00070122]Phase 32,200 participants (Actual)Interventional2004-04-30Terminated(stopped due to Administratively complete.)
A Phase II Feasibility Translational Research Trial of Induction Chemotherapy Followed by Concomitant Chemoradiation in Patients With Clinical T4 Rectal Cancer [NCT00070434]Phase 20 participants (Actual)Interventional2004-08-31Withdrawn(stopped due to poor accrual)
A Phase III Study Comparing Adjuvant Chemotherapy Consisting of Capecitabine/Oxaliplatin vs Surgery Alone in Patients With Stage II (T1N2, T2N1, T3N0), IIIa (T2N2, T3N1, T4NO), and IIIb (T3N2) Gastric Adenocarcinoma [NCT00411229]Phase 31,035 participants (Actual)Interventional2006-06-30Completed
Cetuximab Added to Capecitabine, Oxaliplatin and Bevacizumab in Patients With Previously Untreated Advanced Colorectal Carcinoma, a Randomised Phase III Study [NCT00208546]Phase 3750 participants (Actual)Interventional2005-06-30Completed
A Phase II Study of Oxaliplatin and Capecitabine in Patients With Measurable Metastatic Adenocarcinoma of the Esophagus, Gastroesophageal Junction, and Gastric Cardia [NCT00040859]Phase 248 participants (Actual)Interventional2002-09-30Completed
A Pilot Study of Taxotere (Docetaxel) Combined With Xeloda (Capecitabine) in the Treatment of Metastatic Breast Cancer [NCT00214864]Phase 218 participants (Actual)Interventional2002-12-31Completed
An Open Label, Phase II Study of Capecitabine (Xeloda) Plus Conformal Radiotherapy for Patients With Locally Advanced, Non-Metastatic Rectosigmoid Carcinoma [NCT00216424]Phase 440 participants (Anticipated)Interventional2005-02-28Terminated(stopped due to lack of accrual)
Oxaliplatin, Irinotecan, and Capecitabine as a Combination Regimen for First-Line Treatment of Advanced or Metastatic Colorectal Cancer [NCT00217711]Phase 1/Phase 223 participants (Actual)Interventional2005-05-31Completed
A Phase II Study of Oxaliplatin (Eloxatin) Capecitabine (Xeloda) and Pre-operative Radiotherapy for Patients With Locally Advanced and Inoperable Rectal Cancer. [NCT00220051]Phase 2109 participants (Actual)Interventional2001-11-30Completed
Neoadjuvant Epirubicin, Cisplatin and Capecitabine (Xeloda) [ECX] Followed by Definitive Chemoradiation With or Without Surgery for Patients With Newly Diagnosed Localized Squamous Cell Carcinoma of the Oesophagus [NCT00220129]Phase 216 participants (Actual)Interventional2002-11-30Completed
A Phase II Trial Evaluating Irinotecan and Capecitabine in Patients With Relapsed/Refractory Upper Gastrointestinal Tumours [NCT00220168]Phase 433 participants (Actual)Interventional2003-01-31Completed
A Phase II Study Of Capecitabine Plus Gemcitabine For Metastatic Renal Cell Carcinoma [NCT00042965]Phase 260 participants (Actual)Interventional2002-10-31Completed
Capecitabine And Gemcitabine In Patients With Advanced Or Metastatic Biliary Tract Cancer, A Multicenter Phase II Trial [NCT00073905]Phase 244 participants (Actual)Interventional2003-04-30Completed
A Phase I Study of Oxaliplatin, 5-Fluorouracil, and Leucovorin in Combination With Oral Capecitabine in Patients With Advanced Malignancy [NCT00043121]Phase 150 participants (Actual)Interventional2002-06-30Completed
Randomized Controlled Trial Comparing Dendritic Cells Co-cultured With Cytokine-induced Killer Cells Immunotherapy Combined With Capecitabine Versus Capecitabine Monotherapy in Advanced Breast Cancer [NCT02491697]Phase 2400 participants (Anticipated)Interventional2016-02-29Active, not recruiting
A Randomized, Multi-center, Open-label, Phase III Trial of Fulvestrant Versus Capecitabine as Maintenance Therapy After First-line Chemotherapy in Patients With Hormone Receptor Positive, Human Epidermal Growth Factor Receptor-2 Negative Metastatic Breast [NCT04263298]Phase 3210 participants (Anticipated)Interventional2018-05-01Recruiting
Phase II Study With Capecitabine as Monotherapy in the Treatment of Platinum Resistant or Refractory Ovarian Cancer. [NCT00403429]Phase 236 participants (Actual)Interventional2006-03-31Completed
Randomized Trial to Assess the Benefit of Adding Trastuzumab to Capecitabine and Vinorelbine as Second Line for HER2positive Breast Cancer Patients With Locally Advanced or Metastatic Disease, Previously Treated With Trastuzumab and Taxanes [NCT00130507]Phase 214 participants (Actual)Interventional2005-11-04Terminated(stopped due to A new alternative treatment caused the decrease in the rhythm of recruitment.)
Combined Phase I/II Study of Epirubicin (Pharmorubicin®), Carboplatin (Paraplatin®) and Capecitabine (Xeloda®) (ECC) in the Treatment of Unresectable Locally Advanced or Metastatic Gastric/Gastroesophageal Junction Cancer With Pharmacogenetic Correlates [NCT00130936]Phase 1/Phase 250 participants (Anticipated)Interventional2005-10-31Terminated
A Phase II Trial Evaluating the Combination of Carboplatin, Gemcitabine, and Capecitabine in Patients With Carcinoma of Unknown Primary Site [NCT00148135]Phase 20 participants Interventional2001-05-31Terminated(stopped due to recruitment goals met)
A Phase II Study of Preoperative Capecitabine in Women With Operable Breast Cancer [NCT00148720]Phase 280 participants (Anticipated)Interventional2004-09-30Terminated(stopped due to Slow accrual)
A Multicenter Randomized Phase III Study to Compare Capecitabine Alone or in Combination With Trastuzumab in Patients With HER2 Positive Metastatic Breast Cancer and Progression After Previous Treatment With Trastuzumab [NCT00148876]Phase 3482 participants (Anticipated)Interventional2003-09-30Completed
A Randomized, Open-Label Trial Comparing Treatment With Either Pegylated Liposomal Doxorubicin or Capecitabine as First Line Chemotherapy for Metastatic Breast Cancer in Women 60 Years and Older [NCT00082095]Phase 362 participants (Actual)Interventional2004-04-30Terminated(stopped due to The study was terminated due to poor recruitment (after enrolling 62 of planned 300 patients in 20 months)
A Phase I Study of BMS-247550 in Combination With Capecitabine in Patients With Metastatic Breast Cancer Previously Treated With a Taxane and an Anthracycline [NCT00049244]Phase 10 participants Interventional2002-09-30Active, not recruiting
Phase I Study of Irinotecan Followed by Capecitabine in Patients With Advanced Breast Carcinoma [NCT00083148]Phase 112 participants (Actual)Interventional2002-11-30Completed
A Phase I Study of Oral Navelbine and Capecitabine in the Treatment of Metastatic Breast Cancer [NCT00153907]Phase 140 participants (Actual)Interventional2002-03-31Completed
Impact of Early FDG-PET Directed Intervention on Preoperative Therapy for Locally Advanced Gastric Cancer: A Random Assignment Phase II Study [NCT02485834]Phase 25 participants (Actual)Interventional2015-08-31Terminated(stopped due to Poor accrual)
Phase II Study of Capecitabine and Gemcitabine in Patients With Metastatic Colorectal Cancer [NCT00159445]Phase 253 participants (Anticipated)Interventional2004-03-31Completed
A Phase II Trial of Capecitabine and Thalidomide in Previously Treated Metastatic Colorectal Carcinoma [NCT00165217]Phase 237 participants Interventional2001-11-30Completed
Phase I Study of a Novel Schedule of Capecitabine and Docetaxel in Patients With Advanced Solid Tumors [NCT00169000]Phase 112 participants (Actual)Interventional2003-01-31Completed
Phase 2 Study of Weekly Oxaliplatin and Capecitabine (XELOX) in Combination With Preoperative Radiotherapy in Patients With MRI Defined Locally Advanced Rectal Cancer [NCT00174616]Phase 287 participants (Actual)Interventional2003-07-31Completed
Multicenter, Randomized Controlled Trial Designed to Evaluate the Efficacy and Safety of Adjuvant Hyperthermic Intraperitoneal Chemotherapy (HIPEC) With Raltitrexed or Oxaliplatin Versus no HIPEC in Locally Advanced Colorectal Cancer (APEC Study) [NCT02965248]Phase 3147 participants (Anticipated)Interventional2016-11-30Recruiting
Phase II Study of Oxaliplatin and Xeloda and Cetuximab as First Line Treatment for Metastatic or Unresectable Gastric or Gastroesophageal Junction Cancer [NCT00183898]Phase 275 participants (Actual)Interventional2004-12-28Active, not recruiting
Efficacy of Neoadjuvant XELOX/AVASTIN Therapy for Nonresectable Colorectal Liver Metastases With Secondary Hepatic Resection/Radiofrequency [NCT00408772]Phase 20 participants (Actual)Interventional2007-06-30Withdrawn(stopped due to Lack of accrual)
Phase II Study of Thalidomide in Combination With Capecitabine in Patients With Metastatic Breast Cancer [NCT00193102]Phase 240 participants (Anticipated)Interventional2001-04-30Terminated
An Open-label Study of the Effect of Continuous Xeloda Therapy in Combination With Irinotecan on Treatment Response in Patients With Advanced and/or Metastatic Colorectal Cancer [NCT00048126]Phase 257 participants (Actual)Interventional2001-07-31Completed
MAVERICC (Marker Evaluation for Avastin Research in CRC): A Randomized Phase II Study of Bevacizumab+mFOLFOX6 Vs. Bevacizumab+FOLFIRI With Biomarker Stratification in Patients With Previously Untreated Metastatic Colorectal Cancer [NCT01374425]Phase 2376 participants (Actual)Interventional2011-08-31Completed
Phase I Study of Preoperative Intensity Modulated Radiation Therapy (IMRT) With Incorporated Boost and Oral Capecitabine in Locally Advanced Rectal Cancer [NCT00084591]Phase 10 participants Interventional2003-12-31Completed
A Phase II Study of Gemcitabine in Combination With Capecitabine in Advanced Cholangiocarcinoma [NCT00084942]Phase 20 participants Interventional2002-10-31Completed
A Randomized, Prospective Study Comparing Three Regimens Of Eloxatin ™ Plus Fluoropyrimidine For Evaluation Of Safety And Tolerability In First Line Treatment Of Patients With Advanced Colorectal Cancer (Tree Study) [NCT00062426]Phase 30 participants Interventional2003-05-31Completed
Interleukin-2, Interferon Alpha,Capecitabine and Vinblastin for Treatment of Metastatic Renal Cell Carcinoma: A Multicenter Study [NCT00226798]Phase 245 participants Interventional2003-12-31Recruiting
A Phase II Study Of Capecitabine In Previously Treated, Recurrent And/Or Metastatic Nasopharyngeal Carcinoma [NCT00095901]Phase 23 participants (Actual)Interventional2004-06-30Completed
Phase II Trial of Capecitabine (Xeloda®) and Pegylated Interferon Alfa-2A(Pegasys®) for Recurrent or Progressive Brain Metastasis From Breast Carcinoma [NCT00227656]Phase 22 participants (Actual)Interventional2005-09-30Terminated(stopped due to Study slow to accrue.)
Capecitabine and Oxaliplatin Alone or in Combination With Cetuximab as First-Line Treatment for Metastatic EGFR-Positive Colorectal Cancer, A Randomized Multicenter Phase II Trial [NCT00227734]Phase 274 participants (Actual)Interventional2004-06-30Completed
A Dose Escalating (Phase I) Study Looking at the Biomodulation of Capecitabine by Docetaxel and Gemcitabine in Patients With Advanced Pancreas Cancer [NCT00320749]Phase 121 participants (Actual)Interventional2005-12-31Completed
A Phase 1, Open-Label Dose Escalation First-in-Human Study to Evaluate the Tolerability, Safety, Maximum Tolerated Dose, Preliminary Clinical Activity and Pharmacokinetics of AM0010 in Patients With Advanced Solid Tumors [NCT02009449]Phase 1350 participants (Actual)Interventional2013-11-15Active, not recruiting
Induction Cetuximab (IM-C225), Gemcitabine and Oxaliplatin, Followed by Radiotherapy With Concurrent Capecitabine, and Cetuximab, Followed by Maintenance Cetuximab and Gemcitabine for Patients With Locally Advanced Pancreatic Cancer [NCT00338039]Phase 269 participants (Actual)Interventional2005-09-30Completed
A Phase II Study of Capecitabine and Oxaliplatin (XELOX) in Adenocarcinoma of the Small Bowel and Ampulla of Vater [NCT00354887]Phase 231 participants (Actual)Interventional2004-11-30Completed
A Phase II Study of Neo-adjuvant Chemotherapy in Locally Advanced Gastric Cancer [NCT00414271]Phase 218 participants (Actual)Interventional2006-01-31Completed
A Phase II Clinical Trial of Bevacizumab Beginning Concurrently With a Sequential Regimen of Doxorubicin and Cyclophosphamide Followed by Docetaxel and Capecitabine as Neoadjuvant Therapy Followed by Postoperative Bevacizumab Alone for Women With Locally [NCT00365417]Phase 245 participants (Actual)Interventional2006-08-31Completed
A Randomized Phase 2 Study of Ruxolitinib Efficacy and Safety in Combination With Capecitabine for Subjects With Recurrent or Treatment Refractory Metastatic Pancreatic Cancer (The RECAP Trial) [NCT01423604]Phase 2136 participants (Actual)Interventional2011-07-31Completed
Carrilizumab Combined With Bevacizumab Plus Capecitabine in a Second-line Prospective, One-arm Exploratory Study of Relapsed Metastatic Squamous Cell Carcinoma of Head and Neck [NCT05965154]Phase 222 participants (Anticipated)Interventional2023-08-01Not yet recruiting
A Phase I/II Clinical Trial to Evaluate the Safety Tolerance and Initial Efficacy of Q-1802 Combined With Standard Treatment in Patients With Gastrointestinal Tumors [NCT05964543]Phase 1/Phase 272 participants (Anticipated)Interventional2023-06-21Recruiting
A Multicenter, Open-label, Phase II Pan-Tumor Study in Patients Who Have Participated in Trials to Investigate Efficacy and Safety of ONO-4538 as Monotherapy or in Combination With Other Therapies and Are Continuing ONO-4538 Treatment (ONO-4538-98) [NCT04566380]Phase 259 participants (Anticipated)Interventional2020-09-10Recruiting
Combination of Metronomic Capecitabine With Camrelizumab for Treatment of Refractory Solid Tumor (McCrest) Trial: Hepatobiliary, Pancreatic and Other Gastrointestinal Carcinoma (Non-stomach, Non-esophagi) (Cohort 3) [NCT04932187]Phase 120 participants (Anticipated)Interventional2021-08-01Recruiting
The ADAPTA Study: ADjuvant chemotherAPy After Curative Intent resecTion of Ampullary Cancer. A Pan-European Prospective Multicenter Double Single Arm Cohort Study. [NCT06068023]400 participants (Anticipated)Observational2023-07-01Recruiting
SHR-1701 in Combination With Radiotherapy and Chemotherapy as Perioperative Treatment for Resectable Locally Advanced Rectal Cancer, an Open Label, Single-arm, Multicenter Phase II Trial [NCT05300269]Phase 273 participants (Anticipated)Interventional2022-07-05Recruiting
A Phase 1 Study of IPdR in Combination With Capecitabine and Radiotherapy in Rectal Cancer [NCT04406857]Phase 11 participants (Actual)Interventional2021-03-17Terminated(stopped due to Inadequate accrual rate)
Phase II Trial of Metronomic Capecitabine and Cyclophosphamide With Lapatinib and Trastuzumab in Patients With HER2 Positive Metastatic Breast Cancer Who Have Progressed on a Previous Trastuzumab-Based Regimen [NCT01873833]Phase 210 participants (Actual)Interventional2013-07-29Terminated(stopped due to Insufficient accrual)
A Phase I/II Study of Panitumumab, Capecitabine and Oxaliplatin Chemotherapy With External Beam Radiation Therapy for the Treatment of Resectable, Locally Advanced/Unresectable or Metastatic Esophageal Cancer [NCT00578071]Phase 1/Phase 229 participants (Actual)Interventional2007-12-31Completed
Phase II Study of Capecitabine and Cisplatin in Anthracycline and Taxanes-pretreated Metastatic Triple Negative Breast Cancer Patients [NCT01928680]Phase 233 participants (Actual)Interventional2012-11-30Active, not recruiting
A Phase 1b-2 Study of Mitomycin-c/ Capecitabine ChemoRadiotherapy Combined With Nivolumab Monotherapy or Ipilumimab and Nivolumab, as Bladder Sparing Curative Treatment for Muscle Invasive Bladder Cancer: the CRIMI Study [NCT03844256]Phase 1/Phase 250 participants (Anticipated)Interventional2019-01-07Recruiting
Open-label, Randomized, Controlled, Multicenter Phase III Study Investigating Cetuximab in Combination With Capecitabine (Xeloda, X) and Cisplatin (P) Versus XP Alone as First-line Treatment for Subjects With Advanced Gastric Adenocarcinoma Including Aden [NCT00678535]Phase 3904 participants (Actual)Interventional2008-06-30Completed
A Randomized Phase II Study De-Intensified ChemoRadiation for Early-Stage Anal Squamous Cell Carcinoma (DECREASE) [NCT04166318]Phase 2252 participants (Anticipated)Interventional2020-01-02Recruiting
Intra-arterial Hepatic Bevacizumab and Systemic Chemotherapy in Hepatic Metastases of Metastatic Colorectal Cancer: a Phase II Multicentric Study With Patients in Progression After First Line Systemic Chemotherapy [NCT01677884]Phase 210 participants (Actual)Interventional2012-11-30Completed
Phase II Trial Of Imatinib Mesylate (Gleevec®) (NSC-716051) In Combination With Capecitabine (Xeloda®) (NSC-712807) In Metastatic Breast Cancer [NCT00087152]Phase 227 participants (Actual)Interventional2004-06-30Completed
Phase II Study of Panitumumab, Chemotherapy, and External Beam Radiation in Patients With Locally Advanced Pancreatic Cancer [NCT00601627]Phase 252 participants (Actual)Interventional2009-06-30Completed
A Phase III, Randomized, Multicenter Study of PD-1 Antibody Combined With mXELIRI Versus mXELIRI in the Second-line Treatment of Metastatic Esophageal Squamous Cell Carcinoma [NCT05737563]Phase 3380 participants (Anticipated)Interventional2023-02-17Recruiting
A Phase I Study of LBH589 in Combination With Capecitabine ± Lapatinib [NCT00632489]Phase 120 participants (Actual)Interventional2008-05-31Completed
Randomized Phase III Trial of mFOLFOX7 or XELOX Plus Bevacizumab Versus 5-Fluorouracil/Leucovorin or Capecitabine Plus Bevacizumab as First-line Treatment in Elderly Patients With Metastatic Colorectal Cancer [NCT01279681]Phase 332 participants (Actual)Interventional2011-01-31Terminated(stopped due to Slow accrual)
CHEMORADIOTHERAPY FOR RECTAL CANCER IN THE DISTAL RECTUM FOLLOWED BY ORGANSPARING TRANSANAL ENDOSCOPIC MICROSURGERY: CARTS Study CApecitabine, Radiotherapy and Tem Surgery. A PHASE II, FEASIBILITY TRIAL [NCT01273051]Phase 255 participants (Actual)Interventional2010-11-30Completed
Phase I/II Study Combining Tosedostat With Capecitabine in Patients With Metastatic Pancreatic Adenocarcinoma [NCT02352831]Phase 1/Phase 216 participants (Actual)Interventional2015-08-31Terminated(stopped due to Insufficient funding and drug supply from manufacturer)
An Open-label,Phase II Study Evaluating the Efficacy and Safety of Trastuzumab Combined With Oral Chemotherapy or Endocrine Therapy in Patients With HER-2 Positive Stage I Breast Cancer [NCT04383275]Phase 2356 participants (Anticipated)Interventional2020-05-15Not yet recruiting
A Randomized Phase-II Study of Patients With Locally Advanced Gastric of Gastro-Esophageal Adenocarcinoma Treated With Induction Irinotecan/Cisplatin, Potentially Curative Surgery With or Without Adjuvant Intraperitoneal Floxuridine, Followed by Prolonged [NCT00848783]Phase 28 participants (Actual)Interventional2008-05-31Terminated(stopped due to Due to slow accrual)
A Phase I/II Study of Irinotecan, Oxaliplatin, Capecitabine (XELOXIRI) and Bevacizumab as a First-line Therapy for Patients With Metastatic Colorectal Cancer [NCT04380103]Phase 1/Phase 2106 participants (Anticipated)Interventional2020-04-26Recruiting
Early Blocking Strategy for Metachronous Liver Metastasis of Colorectal Cancer Based on Pre-hepatic CTC Detection [NCT05720559]Phase 2100 participants (Anticipated)Interventional2023-03-01Not yet recruiting
A Phase II Study of Capecitabine and Lapatinib in Squamous Cell Carcinoma of the Head and Neck [NCT01044433]Phase 244 participants (Actual)Interventional2009-10-31Completed
Modified Short-Course Radiation Combined With CAPOX and Tislelizumab for MSS Locally Advanced of Middle and Low Rectal Cancer (mRCAT): An Open-label, Single-arm, Prospective Multicenter Clinical Trial [NCT05972655]Phase 232 participants (Anticipated)Interventional2023-08-02Recruiting
Pilot Study Evaluating Pharmacokinetic Parameters of Capecitabine Dosing in Patients With Advanced Cancer and Elevated Body Mass Index [NCT01828554]8 participants (Actual)Interventional2013-06-30Completed
Multi-target Radiotherapy Combined With PD-1 Monoclonal Antibody and Capecitabine Maintenance Therapy Treating Oligometastatic Nasopharyngeal Carcinoma: a Single-arm, Multicenter, Prospective, Open-label Phase II Clinical Trial [NCT05290194]Phase 228 participants (Anticipated)Interventional2022-03-28Recruiting
Phase II, Multi-Center, Open-Label, Prospective Study of Capecitabine and Cetuximab as First-Line Therapy in Patients With Metastatic Wild Type KRAS Colorectal Cancer Who Are Considered Nonoptimal Candidates or Are Intolerant to a First-Line Oxaliplatin/I [NCT00954876]Phase 20 participants (Actual)Interventional2009-08-31Withdrawn(stopped due to Study halted prematurely, prior to enrollment of first participant)
Surufatinib and Sintilimab in Combination With Capecitabine in Patients With Previously Treated Metastatic Adenocarcinoma of Small Intestine or Appendix Carcinoma : a Single-arm, a Single-center , Phase 2 Trial [NCT05472948]Phase 236 participants (Anticipated)Interventional2023-02-01Recruiting
Evaluating Trifluridine/Tipiracil Based Chemoradiation in Locally Advanced Rectal Cancer - The Phase I/II TARC Trial [NCT04177602]Phase 1/Phase 210 participants (Actual)Interventional2019-11-04Terminated(stopped due to Due to the amended therapy strategies for rectal cancer recently, it was decided not to transfer the study to the phase II part, as superiority over standard chemoradiation and transfer to a new therapy standard are increasingly unlikely.)
Maximal Ablative Irradiation Because of Encasement (MAIBE) for Patients With Potentially Resectable Locally Advanced Pancreatic Cancer [NCT03523312]Phase 247 participants (Actual)Interventional2018-04-30Active, not recruiting
Antiangiogenic Therapy or Chemotherapy Combined With PD-1 Inhibitor Versus Standard Chemotherapy for PD-1 Inhibitor Refractory R/M NPC [NCT05549466]Phase 284 participants (Anticipated)Interventional2022-10-08Recruiting
Capecitabine Metronomic Chemotherapy Combined With Aromatase Inhibitors in Postmenopausal Hormone-receptor-positive Breast Cancer [NCT01924078]Phase 2100 participants (Anticipated)Interventional2010-10-31Recruiting
Three-arm Phase III Trial Comparing Radiotherapy With Different Chemotherapy Regimens for Esophageal Cancer [NCT02025036]Phase 3249 participants (Actual)Interventional2014-10-31Active, not recruiting
Phase II Multi-Institutional Randomized Trial of Capecitabine Plus Oxaliplatin With Concurrent Radiotherapy in Patients With Potentially Resectable Adenocarcinoma of Gastroesophageal Cancer [NCT01962246]Phase 2/Phase 3169 participants (Actual)Interventional2012-02-29Completed
Randomized Phase III Trial Comparing in a Preoperative Schedule the Result of Two Concurrent Chemoradiation Schemes (45 Gy + Capecitabine vs 50 Gy + Capecitabine - Oxaliplatin) on the Rate of Sterilization of the Operative Specimen in Resectable Rectal Ca [NCT00227747]Phase 3598 participants (Anticipated)Interventional2005-11-08Completed
Randomized Trial of Gemcitabine Plus Docetaxel vs. Docetaxel Plus Capecitabine in Metastatic Breast Cancer in 1st and 2nd [NCT00191152]Phase 3475 participants (Actual)Interventional2002-02-28Completed
Phase II Study of the A-ICOX Regimen Consisting of Bevacizumab (Avastinâ), Intermittent Dose Capecitabine (Xelodaâ) and Oxaliplatin (Eloxatinâ) in Patients With Untreated Advanced Colorectal Cancer [NCT00177307]Phase 240 participants (Actual)Interventional2005-01-31Completed
A Phase I-II Dose Finding and Early Efficacy Study of Combination Therapy With Erlotinib (Tarceva), Gemcitabine, Bevacizumab (Avastin), and Capecitabine in Advanced Pancreatic Cancer [NCT00260364]Phase 1/Phase 244 participants (Actual)Interventional2005-11-30Completed
Predicting Response and Toxicity in Patients Receiving Chemotherapy for Breast Cancer: A Multicenter Genomic, Proteomic and Pharmacogenomic Correlative Study: Hoosier Oncology Group COE-01 [NCT00235235]80 participants (Actual)Observational2005-09-30Terminated(stopped due to Funding terminated)
Randomized Phase II Trial of Capecitabine and Lapatinib With or Without IMC-A12 in Patients With HER2 Positive Breast Cancer Previously Treated With Trastuzumab and an Anthracycline and/or a Taxane [NCT00684983]Phase 264 participants (Actual)Interventional2008-07-30Completed
An Open-Label Phase 2 Study to Characterize Colon Pathology in Patients With HER2 Amplified Breast Cancer Treated With Neratinib [NCT04366713]Phase 26 participants (Actual)Interventional2020-06-30Completed
Camrelizumab Combined With Apatinib and Capecitabine for Patients With Advanced Unresectable Biliary Tract Cancer: a Phase 2, Single-arm, Prospective Study. [NCT04720131]Phase 239 participants (Anticipated)Interventional2021-02-01Not yet recruiting
Phase I Study Of Capecitabine in Combination With Cisplatin and Irinotecan in Patients With Advanced Malignancies. [NCT00249977]Phase 121 participants (Actual)Interventional2003-04-30Completed
Pilot Study of Sorafenib and Bi-weekly Capecitabine in Patients With Advanced Breast and Gastrointestinal Tumors [NCT01640665]Phase 124 participants (Actual)Interventional2012-07-31Completed
Phase II Study of First-Line Capecitabine and Cetuximab for Treatment of Metastatic Colorectal Cancer in Elderly Patients and/or Those With Multiple Comorbidities Unable to Receive Chemotherapy Doublets [NCT00251186]Phase 218 participants Interventional2006-04-30Terminated(stopped due to Funding unavailable)
"Phase II Study of PET Guided Neoadjuvant Chemotherapy (NAC) and Oncotype Guided Hormonal Therapy of Breast Cancer" [NCT01641406]Phase 260 participants (Anticipated)Interventional2011-03-31Recruiting
A Phase I Study of AZD6244 in Combination With Capecitabine and Radiotherapy in Locally Advanced Adenocarcinoma of the Rectum [NCT01134601]Phase 11 participants (Actual)Interventional2010-05-24Terminated(stopped due to As per Cancer Therapy Evaluation Program (CTEP), this protocol has only enrolled one participant and it is unlikely that the study will be able to be completed successfully. CTEP slated the protocol to be administratively closed.)
A Phase I Dose Escalation Study of Imatinib Mesylate (Gleevec/STI571) Plus Capecitabine (Xeloda) in Advanced Solid Tumor Malignancies [NCT00253565]Phase 125 participants (Actual)Interventional2003-08-31Completed
A Phase II Trial of Capecitabine and Docetaxel in the Treatment of Advanced and Recurrent Cervical Cancer [NCT00257348]Phase 25 participants (Actual)Interventional2004-03-31Completed
Phase II Trial of Capecitabine (Xeloda) and Weekly Docetaxel (Taxotere) in Metastatic Androgen Independent Prostate Carcinoma [NCT00258284]Phase 230 participants (Actual)Interventional2003-08-31Completed
Adjuvant Capecitabine in Elderly Patients With Breast Cancer: a Phase II Study [NCT00263705]Phase 243 participants (Actual)Interventional2003-01-31Completed
Phase II Trial of CT-2103 (Xyotax™) With Capecitabine as First-Line Chemotherapy for Patients With Metastatic Breast Cancer [NCT00265733]Phase 248 participants (Actual)Interventional2006-02-28Completed
Phase I Study of Oxaliplatin (Eloxatin) and Capecitabine (Xeloda) and Concurrent Radiation Therapy (XELOX-RT) in Non-Small Cell Lung Cancer [NCT00268151]Phase 124 participants Interventional2005-02-28Terminated(stopped due to Study was terminated due to lack of funding.)
Preoperative Combined Radiochemotherapy for Patients With Newly Diagnosed, Primary Operable and Locally Advanced Rectal Carcinoma (cT3, Nx, M0) of the Lower and Middle Rectum [NCT00297141]Phase 260 participants (Actual)Interventional2004-10-31Completed
A Multicenter Randomized Phase II Study Evaluating Tolerance and Efficacy of Capecitabine 5/7 Days With Weekly Paclitaxel Versus the Recommended Treatment Plan of Weekly Paclitaxel-capecitabine, in Patients With Metastatic Breast Cancer. [NCT00270491]Phase 2130 participants (Anticipated)Interventional2005-12-31Completed
A Randomized Multicenter Pivotal Study of CDX-011 (CR011-vcMMAE)in Patients With Metastatic, gpNMB Over-Expressing, Triple Negative Breast Cancer (The METRIC Study) [NCT01997333]Phase 2327 participants (Actual)Interventional2013-11-30Completed
A Randomised Study of Sequential Versus Combination Chemotherapy in Patients With Previously Untreated Advanced Colorectal Carcinoma [NCT00312000]Phase 3820 participants (Actual)Interventional2003-01-31Completed
A Randomized Phase III Study Exploring the Efficacy of Capecitabine Given Concomitantly or in Sequence to EC-Doc With or Without Trastuzumab as Neoadjuvant Treatment of Primary Breast Cancer [NCT00288002]Phase 31,500 participants (Anticipated)Interventional2005-01-31Completed
A Phase Ib/II Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Preliminary Efficacy of JS015 Combination Therapy in Patients With Advanced Solid Tumors [NCT06139211]Phase 1/Phase 2186 participants (Anticipated)Interventional2023-11-30Not yet recruiting
A Phase Ib Study of Varlitinib in Japanese Subjects With Advanced or Metastatic Solid Tumours [NCT03082053]Phase 124 participants (Actual)Interventional2017-01-31Completed
Preoperative FOLFOX Versus Postoperative Risk-adapted Chemotherapy in Patients With Locally Advanced Rectal Cancer and Low Risk for Local Failure: A Randomized Phase III Trial of the German Rectal Cancer Study Group [NCT04495088]Phase 3818 participants (Anticipated)Interventional2020-09-30Recruiting
A STUDY TO OBSERVE PATIENTS CHARACTERISTICS, TREATMENT PATTERNS AND OUTCOMES IN PATIENTS WITH NEWLY DIAGNOSED BREAST CANCER IN LATIN AMERICA [NCT04158258]2,907 participants (Actual)Observational2020-02-21Active, not recruiting
Phase 3 Study of Sacituzumab Govitecan (IMMU-132) Versus Treatment of Physician's Choice (TPC) in Subjects With Hormonal Receptor-Positive (HR+) Human Epidermal Growth Factor Receptor 2 (HER2) Negative Metastatic Breast Cancer (MBC) Who Have Failed at Lea [NCT03901339]Phase 3543 participants (Actual)Interventional2019-05-08Completed
An Open-label, Randomised, Phase III Study cOmparing trifLuridine/Tipiracil (S 95005) in Combination With Bevacizumab to Capecitabine in Combination With Bevacizumab in firST-line Treatment of Patients With metastatIC Colorectal Cancer Who Are Not candida [NCT03869892]Phase 3856 participants (Actual)Interventional2019-03-21Active, not recruiting
Thymidylate Synthase (TS) Genotype-Directed Phase II Trial of Oral Capecitabine for 2-Line Treatment of Advanced Pancreatic Cancer [NCT00303927]Phase 265 participants (Anticipated)Interventional2005-12-31Completed
The MAX Study: A Randomised Phase II/III Study to Evaluate the Role of Mitomycin C, Avastin and Xeloda in Patients With Untreated Metastatic Colorectal Cancer [NCT00294359]Phase 2/Phase 3333 participants (Anticipated)Interventional2005-06-30Completed
Trial of Accelerated Adjuvant Chemotherapy With Capecitabine in Early Breast Cancer (TACT2) [NCT00301925]Phase 34,400 participants (Anticipated)Interventional2005-12-16Active, not recruiting
A Phase II Study of Weekly Paclitaxel and Capecitabine in Patients With Metastatic or Recurrent Esophageal Cancer [NCT00453323]Phase 233 participants (Actual)Interventional2006-06-30Active, not recruiting
C-2424: Phase II Study of Celecoxib, Capecitabine, and Irinotecan in Patients With Metastatic Colorectal Cancer [NCT00230399]Phase 215 participants Interventional2003-06-30Completed
An Open-Label Expanded Access Study of Lapatinib and Capecitabine Therapy in Subjects With ErbB2 Overexpressing Locally Advanced or Metastatic Breast Cancer [NCT00338247]0 participants Expanded Access2006-07-31Approved for marketing
A Randomized, Open-label, Single Dose, Two-way Cross-Over Study to Investigate the Relative Bioavailability of Capecitabine in Rapid Disintegrating Tablets (RDT) Versus the Commercial Xeloda® Tablets Following Oral Administrations in Adult Patients With S [NCT01493336]Phase 137 participants (Actual)Interventional2012-05-31Completed
Phase II Single Arm Trial of Low Dose Capecitabine in Patients With Advanced Breast Cancer [NCT06105684]Phase 240 participants (Anticipated)Interventional2024-04-30Not yet recruiting
A Phase II, Multicentre, Open-label, Master Protocol to Evaluate the Efficacy and Safety of Datopotamab Deruxtecan (Dato-DXd) as Monotherapy and in Combination With Anticancer Agents in Patients With Advanced/Metastatic Solid Tumours [NCT05489211]Phase 2670 participants (Anticipated)Interventional2022-09-06Recruiting
5-Fluorouracil Versus Capecitabine as Perioperative Treatment for Locally Advanced Rectal Cancer. a Randomized Phase III Trial [NCT01500993]Phase 3401 participants (Actual)Interventional2002-03-31Completed
Phase III Multicenter Randomized Open-label Study of Irinotecan Plus Capecitabine Versus Capecitabine in Patients Previously Treated With Anthracycline and Taxane for HER2 Negative Metastatic Breast Cancer[PROCEED] [NCT01501669]Phase 3222 participants (Anticipated)Interventional2011-06-30Recruiting
Phase II Study to Assess the Efficacy and Safety of Trastuzumab in Combination With Xelox as First-line Treatment of Patients With Advanced or Metastatic Gastric Cancer or Gastro-esophageal Junction, (HER2)-Positive. [NCT01503983]Phase 245 participants (Actual)Interventional2011-08-31Completed
An Observational Study of Avastin® (Bevacizumab) in Combination With Chemotherapy for Treatment of First-line Metastatic Colorectal Adenocarcinoma [NCT01506167]719 participants (Actual)Observational2012-07-06Completed
A Phase II Randomized Controlled Trial of Adjuvant Chemotherapy for High Risk Gastric Cancer Patients (IIIb-IIIc) [NCT01618474]Phase 2100 participants (Anticipated)Interventional2012-05-31Enrolling by invitation
A Multicenter, Open Label, Randomized, Balanced, Two Treatment, Three Period, Three Sequence, Reference Replicate Crossover, Single Dose, Bioequivalence Fed Study of Capecitabine Tablets in Comparison With XELODA in Adult Cancer Patients [NCT03435666]Phase 145 participants (Anticipated)Interventional2018-05-31Not yet recruiting
A Randomized Phase II Multicenter, Open-Label Study Evaluating the Efficacy and Safety of IMAB362 in Combination With the EOX (Epirubicin, Oxaliplatin, Capecitabine) Regimen as First-Line Treatment of Patients With CLDN18.2-Positive Advanced Adenocarcinom [NCT01630083]Phase 2252 participants (Actual)Interventional2012-07-19Completed
Prospective Observational Study of Patients With Locally Advanced Gastric Cancer Treated With Perioperative Chemotherapy and Surgery [NCT01633203]61 participants (Actual)Observational2010-08-31Completed
A Phase I Study of the Phosphatidylserine-Targeting Antibody Bavituximab in Combination With Capecitabine and Radiation Therapy for the Treatment of Stage II and III Rectal Adenocarcinoma [NCT01634685]Phase 115 participants (Actual)Interventional2012-08-08Completed
Metronomic Capecitabine With Digoxin for Metastatic Breast Cancer Progressing After Anthracycline and Taxane Treatment [NCT01887288]Phase 216 participants (Actual)Interventional2013-04-30Terminated(stopped due to PI Leaving Site)
A Randomized Open Label Multicenter Phase 3 Trial Comparing S1 Generic With Capecitabine in Patients With Metastatic Breast Cancer. [NCT01655992]Phase 3386 participants (Anticipated)Interventional2012-01-31Terminated(stopped due to The sponsor decided to stop the study.)
Quinacrine-Capecitabine Combinatorial Therapy for Advanced Stage Colorectal Adenocarcinoma:A Phase I/II Investigator-Initiated Clinical Trial [NCT01844076]Phase 1/Phase 219 participants (Actual)Interventional2016-01-14Terminated(stopped due to The single Quinacrine manufacture facility in the US was shut down by the FDA)
Randomized Phase II Open-Label Controlled Study of EMD 72000 (Matuzumab), in Combination With the Chemotherapy Regimen ECX or the Chemotherapy Regimen ECX Alone as First-line Treatment in Subjects With Metastatic Esophago-Gastric Adenocarcinoma [NCT00215644]Phase 272 participants (Actual)Interventional2005-08-31Completed
Randomized Controlled Trials of Efficacy and Safety With Xeloda as Sequential Adjuvant Therapy After Chemotherapy of Anthracycline and/or Taxane in Breast Cancer of Triple Negative or HER-2 Positive or Axillary Lymph Node Metastasis ≥4 [NCT01662128]Phase 2/Phase 3600 participants (Anticipated)Interventional2012-06-30Recruiting
Metronomic Chemotherapy With Anti-angiogenic Effect as Maintenance Treatment for Metastatic Colorectal Carcinoma Following Response to FOLFIRI+Bevacizumab: Clinical and Laboratory Studies [NCT01668680]Phase 280 participants (Anticipated)Interventional2012-09-30Terminated(stopped due to No satisfactory acrual)
Randomized Phase II Trial of Continuous Versus Standard Capecitabine in Advanced Breast Cancer. [NCT00418028]Phase 2/Phase 3195 participants (Actual)Interventional2005-09-30Completed
A Multicentre Randomised Phase II Trial of Neo-adjuvant Chemotherapy Followed by Surgery vs. Neo-adjuvant Chemotherapy and Subsequent Chemoradiotherapy Followed by Surgery vs. Neo-adjuvant Chemoradiotherapy Followed by Surgery in Resectable Gastric Cancer [NCT02931890]Phase 2207 participants (Anticipated)Interventional2017-12-21Recruiting
A Single-arm, Open-label Clinical Study of Combined Therapy of Tisleizumab , Lenvatinib and XELOX Regimen (Oxaliplatin Combined With Capecitabine) in the First-line Treatment of Advanced and Unresectable Biliary Tract Tumors [NCT05291052]Phase 220 participants (Anticipated)Interventional2022-02-14Recruiting
A Randomized, Open-label, Multicenter Study Comparing Continuation of Original Targeted Therapy With Trastuzumab Combined With Pyrotinib and Capecitabine as Postoperative Adjuvant Therapy in Non-pCR Patients With HER2 Positive Early Breast Cancer [NCT05292742]Phase 2206 participants (Anticipated)Interventional2021-07-02Recruiting
Total Neoadjuvant Therapy for the Treatment of Gastroesophageal Junction (GEJ) and Gastric Cancers: A Pilot Trial [NCT05296005]Phase 120 participants (Anticipated)Interventional2022-05-31Not yet recruiting
A Single-arm, Multicenter, Phase II Study Evaluating the Efficacy and Safety of Preoperative Short-course Radiotherapy Followed by Sequential Chemotherapy and AK104 for Locally Advanced Rectal Cancer [NCT05794750]Phase 250 participants (Anticipated)Interventional2023-04-24Not yet recruiting
Defining the Molecular Profile of Breast Cancer in Uganda and Its Clinical Implications [NCT03518242]Phase 1100 participants (Actual)Interventional2018-06-06Completed
Phase II Individualized Therapies Selection Study for Patients With Metastatic Colorectal Carcinoma According to the Genomic Expression Profile in Tumor Samples. [NCT01703910]Phase 229 participants (Actual)Interventional2012-11-30Completed
A Randomised Phase II Trial of Epirubicin, Oxaliplatin and Capecitabine (EOX) Versus Docetaxel and Oxaliplatin (ElTax) in the Treatment of Advanced Gastro-oesophageal Cancer [NCT01710592]Phase 235 participants (Actual)Interventional2007-05-31Completed
Multi-institutional Phase I/II Study: Neoadjuvant Chemoradiation With 5-FU (or Capecitabine) and Oxaliplatin Combined With Deep Regional Hyperthermia in Locally Advanced or Recurrent Rectal Cancer [NCT01716949]Phase 1/Phase 259 participants (Anticipated)Interventional2012-09-30Recruiting
Cetuximab Monotherapy and Cetuximab Plus Capecitabine as First-line Treatment in Elderly Patients With KRAS- and BRAF Wild-type Metastatic Colorectal Cancer. A Multicenter Phase II Trial [NCT01718808]Phase 224 participants (Actual)Interventional2012-11-30Terminated(stopped due to FU for 3 years from randomization as initially planned is stopped as we do not expect any changes to the endpoints in the future after one year of FU.)
A Phase I-II Study of PAXG in Stage III-IV Pancreatic Adenocarcinoma [NCT01730222]Phase 1/Phase 2137 participants (Actual)Interventional2012-11-30Completed
Safety and Tolerability of Oxaliplatin-Capecitabine-Trastuzumab Combination and Chemoradiotherapy in Operated Patients With HER-2 Positive Gastric or Gastroesophageal Junction Adenocarcinoma: Phase II Study, TOXAG [ML25574] [NCT01748773]Phase 234 participants (Actual)Interventional2013-01-29Completed
Combination Followed by Maintenance Chemotherapy Versus CDK4/6 Inhibitor Combined With Endocrine Therapy for HR Low/HER2-negative Advanced Breast Cancer: a Prospective, Randomized, Open-label Phase Ⅱ Clinical Trial [NCT06176534]Phase 2240 participants (Anticipated)Interventional2023-12-20Not yet recruiting
A Phase III, Randomized, Double-blind Trial Comparing Trastuzumab Plus Chemotherapy and Pembrolizumab With Trastuzumab Plus Chemotherapy and Placebo as First-line Treatment in Participants With HER2 Positive Advanced Gastric or Gastroesophageal Junction A [NCT03615326]Phase 3732 participants (Anticipated)Interventional2018-10-05Active, not recruiting
Neoadjuvant CAPOXIRI Chemotherapy in the Treatment of Resectable, Borderline Resectable and Locally Advanced Pancreatic Adenocarcinoma Protocol [NCT01760252]Phase 217 participants (Actual)Interventional2011-12-31Terminated
Treatment Options in Human Epidermal Growth Factor Receptor 2 (HER2) Positive Metastatic Breast Cancer Patients [NCT01782651]1 participants (Actual)Observational2014-08-31Completed
Phase 1b/2 Single-arm Trial Evaluating the Combination of Lapatinib, Everolimus and Capecitabine for the Treatment of Patients With HER2-positive Metastatic Breast Cancer With CNS Progression After Trastuzumab [NCT01783756]Phase 1/Phase 29 participants (Actual)Interventional2013-06-26Completed
Pilot Safety and Blood Immune Cell Transcriptional Profiling Study of Anakinra Plus the Physician's Chemotherapy Choice in Metastatic Breast Cancer Patients [NCT01802970]Phase 110 participants (Actual)Interventional2012-12-31Completed
Phase I/II Study of CB-839 and Capecitabine in Patients With Advanced Solid Tumors and Fluoropyrimidine Resistant PIK3CA Mutant Colorectal Cancer [NCT02861300]Phase 1/Phase 253 participants (Anticipated)Interventional2016-09-12Active, not recruiting
A Dose-escalating, Multicenter, Single Arm, Open-Label Study of XRP9881 in Combination With Capecitabine (Xeloda), in Metastatic Breast Cancer Patients With Disease Progressing After Anthracycline and Taxane Therapy [NCT00327743]Phase 1/Phase 234 participants (Actual)Interventional2006-08-31Completed
[NCT01818973]Phase 245 participants (Anticipated)Interventional2013-03-31Recruiting
Neoadjuvant FOLFIRINOX and Chemoradiation Followed by Definitive Surgery and Postoperative Gemcitabine for Patients With Borderline Resectable Pancreatic Adenocarcinoma: An Intergroup Single-Arm Pilot Study [NCT01821612]Early Phase 123 participants (Actual)Interventional2013-05-31Completed
Phase II Study of Concomitant Intensity-modulated Radiotherapy Combined to Capecitabine, Mitomycin and Panitumumab in Patients With Stage II-IIIB Squamous-cell Carcinoma of the Anal Canal [NCT01843452]Phase 28 participants (Actual)Interventional2012-12-31Terminated(stopped due to Poor recruitment)
Modulation of Metabolic Index in Tailoring Treatment of Incurable Metastatic ColoRectal Cancer (CRC) Program 1. [NCT01843725]Phase 137 participants (Actual)Interventional2013-09-30Completed
A Randomised Phase II Study of Two Pre-operative Chemoradiotherapy Regimens (Oxaliplatin and Capecitabine Followed by Radiotherapy With Either Oxaliplatin and Capecitabine or Paclitaxel and Carboplatin) for Resectable Oesophageal Cancer [NCT01843829]Phase 285 participants (Anticipated)Interventional2013-10-31Recruiting
A Bioequivalence Study of Capecitabine Tablets in Patients of Locally Advanced or Metastatic Breast Cancer or Metastatic Colorectal Cancer [NCT01846650]Phase 136 participants (Actual)Interventional2012-12-31Completed
European Phase III Study Comparing a Radiation Dose Escalation Using 2 Different Approaches : External Beam Radiation Therapy Versus Endocavitary Radiation Therapy With Contact X-ray Brachytherapy 50 kiloVolts (kV) for Patients With Rectal Adenocarcinoma [NCT02505750]Phase 3236 participants (Anticipated)Interventional2015-06-24Active, not recruiting
A Prospective Randomized Controlled Trail to Evaluate Efficacy and Safety of Sequential Neo-adjuvant Chemotherapy Plus Surgery Followed by Capecitabine Versus Conventional Postoperative Adjuvant Chemotherapy [NCT03011060]Phase 31,588 participants (Anticipated)Interventional2016-12-31Recruiting
Planning Treatment for Oesophago-gastric Cancer: a Randomised Maintenance Therapy Trial [NCT02678182]Phase 2924 participants (Anticipated)Interventional2015-02-28Recruiting
A Phase II Trial of Margetuximab in Combination With Tucatinib and Capecitabine in Patients With HER2-Positive Metastatic Breast Cancer [NCT05227131]Phase 20 participants (Actual)Interventional2022-05-15Withdrawn(stopped due to Funder decided to not continue the study)
An Open, Single Arm, Multicenter, Exploratory Phase II Clinical Trial of Anlotinib Hydrochloride Capsules Combined With CAPEOX in RAS and BRAF Wild-type Patients With Metastatic Colorectal Carcinoma as 1st Therapy [NCT04080843]Phase 230 participants (Actual)Interventional2019-11-15Completed
Using PERS(PErsonalized Regimen Selection) Genetic Model Assistant Decision-making System of Neoadjuvant Chemotherapy for Breast Cancer Multicentric, Prospective, Randomized Controlled Phase III Clinical Study [NCT03006614]Phase 3320 participants (Anticipated)Interventional2016-04-30Recruiting
A Fixed-Sequence, Open-Label Study to Determine the Activity of SCH 717454 as Assessed by Positron Emission Tomography in Subjects With Relapsed or Recurrent Colorectal Cancer [NCT00551213]Phase 267 participants (Actual)Interventional2007-11-21Completed
A Phase II Randomized Trial Evaluating the Addition of High or Standard Intensity Radiation to Gemcitabine and Nab-paclitaxel for Locally Advanced Pancreatic Cancer [NCT01921751]Phase 220 participants (Actual)Interventional2013-08-31Terminated(stopped due to Trial would not be completed in a reasonable timeframe per CTEP guidelines)
A Prospective, Phase II Trial Using ctDNA to Initiate Post-operation Boost Therapy After Adjuvant Chemotherapy in TNBC (Artemis) [NCT04803539]Phase 2/Phase 3260 participants (Anticipated)Interventional2021-04-01Recruiting
A Randomized, Open-Label, Phase II Study to Evaluate the Efficacy and Safety of Sintilimab Plus Capecitabine Versus Capecitabine Alone as Adjuvant Therapy for Patients With Locoregionally Advanced Nasopharyngeal Carcinoma [NCT05201859]Phase 2150 participants (Anticipated)Interventional2022-03-29Recruiting
A Phase II Trial of Gemcitabine and Erlotinib (GE) Plus Proton-chemotherapy (PCT) and Capox for Locally Advanced Pancreatic Cancer (LAPC) [NCT01683422]9 participants (Actual)Interventional2013-01-02Terminated(stopped due to Updated chemotherapy regimens currently evaluated in clinical trials due to lack of progress in treating this condition; analysis continues in the realm of patterns of failure and increasing quality of life)
A Prospective, Phase II Trial Using Circulating Tumor DNA to Initiate Post-operation Boost Therapy After Neoadjuvant Chemotherapy in Triple-negative Breast Cancer [NCT04501523]Phase 2460 participants (Anticipated)Interventional2020-08-03Recruiting
Phase II Study of Levocetirizine in Combination With Capecitabine + Bevacizumab to Overcome Resistance to Anti-angiogenic Therapy in Patients With Refractory Colorectal Cancer [NCT01722162]Phase 247 participants (Actual)Interventional2013-04-30Completed
An Exploratory Study of Chemotherapy for Metastatic Colorectal Cancer Based Upon Thymidine Phosphorylase Expression, KRAS and BRAF Mutation Status, and ERCC1 Expression [NCT01280643]3 participants (Actual)Interventional2010-03-31Terminated(stopped due to Slow accrual)
Phase II Study of Gemcitabine/Taxotere/Xeloda (GTX) in Combination With Cisplatin in Subjects With Metastatic Pancreatic Cancer [NCT01459614]Phase 244 participants (Actual)Interventional2011-11-30Completed
A Randomized, Open Label Study of the Effect of First Line Treatment With Xeloda in Combination With Avastin and Either Short Course Irinotecan or Short Course Oxaliplatin on Progression-free Survival in Patients With Metastatic Colorectal Cancer [NCT00642603]Phase 241 participants (Actual)Interventional2008-05-31Terminated
A Multicenter Phase III Placebo-Controlled Trial of Celecoxib for Prevention of Capecitabine-Induced Palmar/Plantar (Hand/Foot) Syndrome in Patients With Metastatic Breast and Colorectal Cancer [NCT00305643]Phase 311 participants (Actual)Interventional2006-02-28Terminated(stopped due to Terminated due to low accrual. No data analyzed.)
The Effect of Traditional Chinese Treatment Combined Adjuvant Chemotherapy in IIIb and IIIc Gastric Cancer: A Randomized Controlled Trial [NCT03607656]Phase 2/Phase 3270 participants (Actual)Interventional2018-06-08Completed
An Open-Label Multicenter Phase 1b Study of E7046 in Combination With Radiotherapy/Chemoradiotherapy (RT/CRT) in Preoperative Treatment of Subjects With Rectum Cancer [NCT03152370]Phase 129 participants (Actual)Interventional2017-05-17Completed
Phase 1b/2 Study Investigating Safety, Tolerability, Pharmacokinetics and Preliminary Antitumor Activity of Anti-HER2 Bispecific Antibody ZW25 in Combination With Chemotherapy With/Without Tislelizumab in Patients With Advanced HER2-positive Breast Cancer [NCT04276493]Phase 1/Phase 271 participants (Actual)Interventional2020-03-26Active, not recruiting
Cytoreductive Surgery Combined With Hyperthermic Intraperitoneal Chemotherapy and Systemic Chemotherapy in Gastric Cancer With Regional Peritoneal Metastasis, a Multicenter and Single-arm Phase III Study [NCT03023436]Phase 3220 participants (Anticipated)Interventional2016-01-31Recruiting
Aromatase Inhibitors Plus Metronomic Capecitabine in Treatment of Patients With Recurrent or Metastatic Hormone Receptor Positive, HER2 Negative Breast Cancer [NCT04942899]Phase 270 participants (Anticipated)Interventional2023-08-30Not yet recruiting
A Randomized, Multicenter, Phase 3 Study to Evaluate the Efficacy and Safety of Sintilimab Combined With Ramucirumab as Compared to Chemotherapy for the First-line Treatment of Unresectable Locally Advanced or Metastatic Gastric or Gastroesophageal Juncti [NCT04675983]Phase 336 participants (Actual)Interventional2021-03-10Terminated(stopped due to Due to the company's development strategy adjustment, Innovent Biologics has decided not to continue this study after consultation with investigators)
Phase III Postneoadjuvant Study Evaluating Sacituzumab Govitecan, an Antibody Drug Conjugate in Primary HER2-negative Breast Cancer Patients With High Relapse Risk After Standard Neoadjuvant Treatment - SASCIA [NCT04595565]Phase 31,332 participants (Anticipated)Interventional2020-10-28Recruiting
Treatment With the Combination of Epirubicin and Paclitaxel Alone or Together With Capecitabine as First Line Treatment in Metastatic Breast Cancer. A Multicenter, Randomized Phase III Study [NCT01433614]Phase 3304 participants (Actual)Interventional2002-12-31Completed
Preoperative Induction Chemotherapy in Combination With Bevacizumab Followed by Combined Chemoradiotherapy in Locally Advanced Rectal Cancer With High Risk of Recurrence- Phase II Pilot Study With Preoperative Administration of Capecitabine (Xeloda), Oxal [NCT01434147]Phase 225 participants (Actual)Interventional2011-10-31Completed
A Phase I Trial of Capecitabine Rapidly Disintegrating Tablets and Concomitant Radiation Therapy in Children With Newly Diagnosed Brainstem Gliomas and High Grade Gliomas [NCT00357253]Phase 124 participants (Actual)Interventional2006-01-31Completed
MRI-Guided Adaptive Radiation Therapy for Organ Preservation in Rectal Cancer [NCT04808323]Phase 122 participants (Anticipated)Interventional2021-06-17Recruiting
A Randomized, Double-Blind, Placebo-Controlled, Phase 3 Clinical Study Comparing the Efficacy and Safety of Tislelizumab (BGB-A317) Plus Platinum and Fluoropyrimidine Versus Placebo Plus Platinum and Fluoropyrimidine as First-Line Treatment in Patients Wi [NCT03777657]Phase 3997 participants (Actual)Interventional2018-12-13Active, not recruiting
A Randomised Clinical Trial Evaluating Adjuvant Chemotherapy With Capecitabine Compared to Expectant Treatment Alone (Observation) Following Surgery for Biliary Tract Cancer [NCT00363584]Phase 3360 participants (Anticipated)Interventional2006-03-31Completed
A Randomized Multicenter Phase III Study:Taxanes or Platinum in Combination With Capecitabine Followed by Capecitabine Alone vs.Taxanes or Platinum Combined With Capecitabine in Advanced Adenocarcinoma of the Stomach or Esophagogastric Junction. [NCT01468389]Phase 3300 participants (Anticipated)Interventional2011-11-30Recruiting
Neoadjuvant Chemotherapy With PD-1 Inhibitors Combined With Simultaneous Integrated Boost Intensity-modulated Radiotherapy in the Treatment of Locally Advanced Rectal Cancer [NCT06017583]Phase 348 participants (Anticipated)Interventional2023-09-01Recruiting
A Phase I Dose Escalation Study of Capecitabine, Carboplatin and Weekly Paclitaxel and a Phase II Trial of the Same Combination in Patients With Adenocarcinoma of Unknown Primary [NCT00201734]Phase 1/Phase 257 participants (Actual)Interventional2005-06-30Terminated(stopped due to Due to lack of funding provided for Phase II portion of trial)
Rectal Artery Infusion Chemotherapy of Oxaliplatin Plus Capecitabine Combined With Anti-PD1 Antibody After Induction Chemotherapy for Microsatellite Stable Locally Advanced Rectal Cancer：a Prospective Single-arm Phase II Study [NCT05307198]Phase 238 participants (Anticipated)Interventional2022-05-11Recruiting
A Phase-3, Open-Label, Randomized Study of Dato-DXd Versus Investigator's Choice of Chemotherapy (ICC) in Participants With Inoperable or Metastatic HR-Positive, HER2-Negative Breast Cancer Who Have Been Treated With One or Two Prior Lines of Systemic Che [NCT05104866]Phase 3733 participants (Actual)Interventional2021-10-18Active, not recruiting
Risk-Stratified Adjuvant Therapy: ctDNA-Directed Post-Hepatectomy Chemotherapy for Patients With Resectable Colorectal Liver Metastases [NCT05062317]Phase 2120 participants (Anticipated)Interventional2022-04-26Recruiting
MINDACT (Microarray In Node-Negative and 1 to 3 Positive Lymph Node Disease May Avoid Chemotherapy): A Prospective, Randomized Study Comparing the 70-Gene Signature With the Common Clinical-Pathological Criteria in Selecting Patients for Adjuvant Chemothe [NCT00433589]Phase 36,600 participants (Anticipated)Interventional2007-02-28Completed
The Therapeutic and Prognostic Implications of Tumor Immune Microenvironment in The Neoadjuvant Immunotherapy Combined With Chemoradiotherapy for Rectal Cancer [NCT05507112]Phase 2100 participants (Anticipated)Interventional2022-09-20Not yet recruiting
A Phase II Study of Oxaliplatin and Capecitabine in Unresectable Metastatic Hepatocellular Cancer [NCT03026803]Phase 24 participants (Actual)Interventional2006-11-30Terminated(stopped due to Due to Sorafenib became first line treatment for HCC, the designed treatment became less competitive. The company Sanofi decided not to continue to support)
A Randomised Phase II/III Trial of Preoperative Chemoradiotherapy Versus Preoperative Chemotherapy for Resectable Gastric Cancer [NCT01924819]Phase 2/Phase 3574 participants (Actual)Interventional2009-09-30Active, not recruiting
Randomized Phase 2A/2B Study to Compare the Efficacy and Safety of ASLAN001 + Capecitabine to Lapatinib + Capecitabine in Patients With HER 2-Positive MBC That Has Failed on Prior Trastuzumab Therapy [NCT02338245]Phase 2200 participants (Anticipated)Interventional2014-12-29Completed
A Phase I/II Study of Nintedanib and Capecitabine in Refractory Metastatic Colorectal Cancer [NCT02393755]Phase 1/Phase 242 participants (Actual)Interventional2015-05-08Completed
A Phase II Trial of Immunotherapy Combined With Neoadjuvant Chemoradiotherapy in Microsatellite Instability-High Locally Advanced Rectal Cancer [NCT04411524]Phase 250 participants (Anticipated)Interventional2020-07-01Not yet recruiting
Ensayo Fase II de selección Individualizada Del Tratamiento de Quimioterapia en Pacientes Con Carcinoma de páncreas Avanzado en función de la determinación de Dianas terapéuticas en el Tejido Tumoral [NCT01454180]Phase 231 participants (Actual)Interventional2011-10-31Completed
Phase 1 Study of Apatinib and Capecitabine Combination to Maintain Treating Metastatic Colorectal Cancer [NCT03132025]Phase 240 participants (Anticipated)Interventional2017-04-30Not yet recruiting
Locally Advanced Breast Cancer: Individualized Treatment Based On Tumor Molecular Characteristics [NCT02297230]Phase 1/Phase 244 participants (Actual)Interventional2002-06-30Terminated(stopped due to PI Left Institution prior to reaching accrual goal and analyzing data.)
DETECT V / CHEVENDO A Multicenter, Randomized Phase III Study to Compare Chemo- Versus Endocrine Therapy in Combination With Dual HER2-targeted Therapy of Herceptin® (Trastuzumab) and Perjeta® (Pertuzumab) Plus Kisqali® (Ribociclib) in Patients With HER2 [NCT02344472]Phase 3270 participants (Anticipated)Interventional2015-09-30Recruiting
Concurrent Cisplatin Chemoradiation With or Without Capecitabine as Adjuvant Chemotherapy in Local Advanced High Risk Nasopharyngeal Carcinoma: Randomized Control Clinical Trial [NCT02143388]Phase 3180 participants (Actual)Interventional2014-03-31Completed
Phase II Study of Stereotactic Body Radiotherapy (SBRT) and Chemotherapy for Unresectable Cholangiocarcinoma Followed by Liver Transplantation [NCT01151761]Phase 22 participants (Actual)Interventional2011-01-31Terminated(stopped due to Poor accrual)
Randomized Phase III Study Comparing Preoperative Chemoradiotherapy Alone Versus Neoadjuvant Chemotherapy With Folfirinox Regimen Followed by Preoperative Chemoradiotherapy for Patients With Resectable Locally Advanced Rectal Cancer [NCT01804790]Phase 3461 participants (Actual)Interventional2012-01-31Active, not recruiting
A Feasibility Study to Discern the Tolerability of 5-FU/Gemcitabine Based Chemotherapy Concurrent With Upper Abdominal Radiation and the Utility of Aprepitant/5HT-3 Antagonist (EMEND) for the Prevention of ChemoRadiation-Induced Nausea and Vomiting (CRINV [NCT01534637]Phase 222 participants (Actual)Interventional2006-08-31Completed
A Phase II Trial of Oral Capecitabine in Patients With Recurrent Epithelial Ovarian, Fallopian Tube, or Primary Peritoneal Carcinoma [NCT00004012]Phase 20 participants Interventional1998-12-31Completed
Efficacy and Safety of Triweekly Cetuximab in Combination With Capecitabine as First-line Maintenance Treatment for KRAS/BRAF Wild-type Metastatic Colorectal Cancer [NCT05775900]Phase 1/Phase 224 participants (Anticipated)Interventional2023-02-01Recruiting
Randomized Controlled Study on Optimize Neoadjuvant Chemoradiotherapy for Locally Advanced Rectal Cancer [NCT02031939]Phase 3556 participants (Anticipated)Interventional2014-01-31Active, not recruiting
Pyrotinib Plus Capecitabine Versus Placebo Plus Capecitabine in Patients With HER2+ Metastatic Breast Cancer:a Randomised, Double-blind, Multicentre, Phase 3 Trial [NCT02973737]Phase 3279 participants (Actual)Interventional2016-07-20Active, not recruiting
The Efficacy and Safety of Postoperative Chemotherapy With Docetaxel Plus Oxaliplatin and Capecitabine Versus Oxaliplatin Plus Capecitabine for Postoperative Pathological Stage IIIB/IIIC Gastric Adenocarcinoma: a Randomised, Phase 3 Trial [NCT04351867]Phase 3196 participants (Anticipated)Interventional2020-09-30Not yet recruiting
An Open Labelled Phase III Adjuvant Trial of Disease-free Survival in Patients With Resected Pancreatic Ductal Adenocarcinoma Randomized to Allocation of Oxaliplatin- or Gemcitabine-based Chemotherapy by Standard Clinical Criteria or by a Transcriptomic T [NCT05314998]Phase 3394 participants (Anticipated)Interventional2023-07-01Not yet recruiting
A Randomized Phase II Trial of Sunitinib Plus Capecitabine Versus Capecitabine Alone (With the Potential for Crossover) for Elderly and/or Poor Performance Status Patients With Metastatic Adenocarcinoma of the Esophagus or Gastroesophageal Junction [NCT00891878]Phase 212 participants (Actual)Interventional2009-08-31Completed
Phase II Study of Oxaliplatin, Irinotecan, and Capecitabine in Advanced Gastric/Gastroesophageal Junction Carcinoma [NCT00084617]Phase 239 participants (Actual)Interventional2004-03-31Completed
"A Phase I/II STudy of Oxaliplatin, Oral Capecitabine and Sorafenib in Patients With Advanced Pancreatic and Biliary Carcinoma" [NCT00634751]Phase 1/Phase 248 participants (Actual)Interventional2008-02-29Completed
Phase 1 Study of Postoperative Capecitabine With Concurrent Radiation in Elderly With Stage II/III Rectal Cancer [NCT01268943]Phase 118 participants (Actual)Interventional2010-11-30Completed
A Phase II, Single-center, Randomized Study of Albumin-bound Paclitaxel Combination With Capecitabine Versus Capecitabine Monotherapy in Paclitaxel/Docetaxel-resistant Advanced Breast Cancer [NCT04780347]Phase 292 participants (Anticipated)Interventional2020-12-15Recruiting
Phase III Trial to Compare Epirubicin and Cyclophosphamide (EC) Followed by Docetaxel (T) to Epirubicin and Docetaxel (ET) Followed by Capecitabine (X) as Adjuvant Treatment, Node Positive Breast Cancer Patients [NCT00129935]Phase 31,384 participants (Actual)Interventional2004-02-29Completed
A Randomized Open-Label Phase 2b Study of Hepatic Infusions of Anti-CEA CAR-T Cells Alternating With Systemic Chemotherapy Versus Chemotherapy Alone In Patients With Liver Metastases Due To CEA-Expressing Pancreatic Adenocarcinoma [NCT04037241]Phase 2/Phase 30 participants (Actual)Interventional2021-11-01Withdrawn(stopped due to Sponsor terminated)
Phase II Open-Label Trial of Neoadjuvant Atezolizumab in Combination With CAPEOX for Resectable Non-Metastatic Proficient Mismatch Repair (PMMR) Colon Cancer [NCT05870800]Phase 230 participants (Anticipated)Interventional2023-09-01Not yet recruiting
Randomized Phase 2 Study of Valproic Acid combinEd With Simvastatin and Gemcitabine/Nab-paclitaxel-based Regimens in Untreated Metastatic Pancreatic Adenocarcinoma Patients (The VESPA Trial). [NCT05821556]Phase 2240 participants (Anticipated)Interventional2023-06-12Recruiting
A Phase 3, Multicenter, Randomized, Open-label, Active Controlled Trial of DS-8201a, an Anti-HER2-antibody Drug Conjugate (ADC), Versus Treatment of Physician's Choice for HER2-low, Unresectable and/or Metastatic Breast Cancer Subjects [NCT03734029]Phase 3557 participants (Actual)Interventional2018-12-27Active, not recruiting
Combining Abraxane With Capecitabine and Radiation Therapy for Consolidation of Treatment Following Induction Chemotherapy for Locally Advanced Pancreatic Cancer [NCT02394535]Phase 125 participants (Actual)Interventional2015-11-12Completed
A Multicenter, Prospective, Randomized Clinical Trial to Investigate the Combined Modality Therapy for Locally Advanced Mid/Low Rectal Cancer. [NCT03042000]1,200 participants (Anticipated)Interventional2017-02-28Not yet recruiting
A Randomized Phase II Study Evaluating Maintenance Therapy After First Line Induction Chemotherapy in Metastatic Cancer Pancreas [NCT05566743]Phase 240 participants (Anticipated)Interventional2022-09-11Recruiting
A Randomized, Double-blinded，Multicenter，Phase II Clinical Study of HLX22 (Recombinant Humanized Anti-HER2 Monoclonal Antibody Injection) in Combination With Trastuzumab and Chemotherapy (XELOX) Versus Placebo in Combination With Trastuzumab and Chemother [NCT04908813]Phase 2150 participants (Anticipated)Interventional2021-09-29Recruiting
A Study of Weekly Doxorubicin and Daily Oral Cyclophosphamide Plus G-CSF Followed by Weekly Paclitaxel as Neoadjuvant Therapy for Resectable, Hormone Receptor Negative or Hormone Receptor Positive, HER-2/Neu Positive Breast Cancer Followed by a Novel Regi [NCT00194779]Phase 250 participants (Actual)Interventional2003-10-31Completed
Clinico-pharmacological Study of Metronomic Capecitabine and Oxaliplatin Versus Classic XELOX in Egyptian Metastatic Colorectal Cancer [NCT04425564]Phase 270 participants (Actual)Interventional2016-01-01Completed
A Phase II Trial of Maintenance ADAPT Therapy With Capecitabine and Celecoxib in Patients With Metastatic Colorectal Cancer [NCT01729923]Phase 227 participants (Actual)Interventional2013-03-31Terminated(stopped due to Funding ended)
Phase II Study of Preoperative FOLFIRINOX Versus Gemcitabine/Nab-Paclitaxel in Patients With Resectable Pancreatic Cancer [NCT02243007]Phase 27 participants (Actual)Interventional2014-09-30Terminated(stopped due to Slow Accrual)
Randomized Multicenter Phase II Trial of Capecitabine Versus S-1 as First-line Treatment in Elderly Patients With Advanced or Recurrent Unresectable Gastric Cancer [NCT00278863]Phase 296 participants (Actual)Interventional2004-11-30Completed
Neoadjuvant Treatment With Regorafenib and Capecitabine Combined With Radiotherapy in Locally Advanced Rectal Cancer. A Multicenter Phase Ib Trial (RECAP) [NCT02910843]Phase 125 participants (Actual)Interventional2017-02-22Terminated(stopped due to due to structural financial deficit of SAKK)
Phase II Study of Oxaliplatin and Capecitabine in Advanced Head and Neck Malignancies [NCT00266279]Phase 217 participants (Actual)Interventional2005-04-30Completed
Preoperative Chemoradiation With Capecitabine Plus Temozolomide in Patients With Locally Advanced Resectable Rectal Cancer: Phase I Study [NCT01781403]Phase 122 participants (Actual)Interventional2013-05-10Completed
Possible Protective Effect of Celecoxib Against Capecitabine Induced Hand and Foot Syndrome in Patients With Colorectal Cancer [NCT05327751]Phase 344 participants (Anticipated)Interventional2022-04-01Recruiting
NANT Head and Neck Squamous Cell Carcinoma (HNSCC) Vaccine: Combination Immunotherapy in Subjects With HNSCC Who Have Progressed on or After Chemotherapy and Anti-programmed Cell Death Protein 1 (PD-1)/Programmed Death-ligand 1 (PD-L1) Therapy [NCT03169764]Phase 1/Phase 20 participants (Actual)Interventional2017-12-31Withdrawn(stopped due to Trial not initiated)
Phase II Study of Oxaliplatin, Capecitabine, Cetuximab, and Bevacizumab in the Treatment of Metastatic Colorectal Cancer [NCT00290615]Phase 230 participants (Actual)Interventional2006-01-31Completed
A Randomized, Open-label Study of the Effect of 2 Different Treatment Schedules of Xeloda With Eloxatin and Avastin on Progression-free Survival in Treatment-naïve Patients With Locally Advanced or Metastatic Colorectal Cancer [NCT00118755]Phase 2435 participants (Actual)Interventional2005-07-31Completed
Phase I,II Study of First Line Intraperitoneal Paclitaxel With Systemic Capecitabine and Oxaliplatin Combination Therapy in Patients With Advanced Gastric Cancer With Peritoneal Metastasis [NCT04943653]Phase 1/Phase 261 participants (Anticipated)Interventional2021-06-08Recruiting
Safety and Efficacy of Metronomic Vinorelbine in Combination With Toripalimab for Patients With HER2- Metastatic Breast Cancer [NCT04389073]Phase 2138 participants (Anticipated)Interventional2020-04-01Recruiting
An Open-Label, Multicenter, Rollover Study to Enable Continued Treatment Access for Subjects Previously Enrolled in Studies of Ruxolitinib [NCT02955940]Phase 210 participants (Actual)Interventional2016-11-30Active, not recruiting
A Phase II Trial of Immunotherapy Combined With Neoadjuvant Chemoradiotherapy in Microsatellite Stable Locally Advanced Rectal Cancer [NCT04411537]Phase 250 participants (Anticipated)Interventional2020-07-01Not yet recruiting
Phase I/II Study of Neoadjuvant Accelerated Short Course Radiation Therapy With Photons and Capecitabine for Resectable Pancreatic Cancer [NCT00889187]Phase 1/Phase 210 participants (Actual)Interventional2009-12-31Terminated(stopped due to Excess toxicity was identified intraoperatively)
A Prospective Phase I Clinical Trial of Carbon Ion Radiation Therapy for Locally Advanced, Unresectable Pancreatic Cancer [NCT03403049]Phase 114 participants (Actual)Interventional2016-04-01Completed
A Randomized, Multicenter, Phase III Open-Label Study of the Efficacy and Safety of Trastuzumab Emtansine Versus Lapatinib Plus Capecitabine in Chinese Patients With HER2-Positive Locally Advanced or Metastatic Breast Cancer Who Have Received Prior Trastu [NCT03084939]Phase 3351 participants (Actual)Interventional2017-04-24Completed
Using Genetic Polymorphisms of Drug Metabolism and Immunohistochemical Stain to Predict the Efficacy and Toxicity in Patients With Gastric Adenocarcinoma - A Phase II Study [NCT01558011]Phase 251 participants (Actual)Interventional2012-03-31Terminated(stopped due to The budget issues.)
An Open-label, Single-centre, Single-arm Phase II Study of Capecitabine Combined With Oxaliplatin and Irinotecan (Xeloxiri) as First-line Treatment in Patients With Advanced Unresectable Pancreatic Adenocarcinoma [NCT01558869]Phase 237 participants (Actual)Interventional2012-04-30Completed
Phase II Study of Hepatic Arterial Infusion With Oxaliplatin and Fluorouracil in Patients With Unresectable Biliary Tract Carcinomas [NCT01572324]Phase 237 participants (Actual)Interventional2012-03-31Completed
A Randomized, Double-blind Study of Capecitabine Plus Tesetaxel Versus Capecitabine Plus Placebo as Second-line Therapy in Subjects With Gastric Cancer [NCT01573468]Phase 2580 participants (Anticipated)Interventional2012-04-30Recruiting
A Randomized, Open-label, Multicenter, Two-arm, Phase III Study to Evaluate Efficacy and Quality of Life in Patients With Metastatic Hormone Receptor-positive HER2-negative Breast Cancer Receiving Ribociclib in Combination With Endocrine Therapy or Chemot [NCT03462251]Phase 341 participants (Actual)Interventional2018-05-24Completed
Integration of Cetuximab, in Combination With Local Radiotherapy, in Perioperative Chemotherapy of Resectable and Locally Advanced Gastric Cancer. A Pilot Phase Ib-trial [NCT01611506]Phase 1/Phase 21 participants (Actual)Interventional2012-02-29Terminated(stopped due to Outcome of EXPAND study (no benefit from adding cetuximab to the first-line chemotherapy in advanced gastric cancer in the overall patient population))
A Phase Ib/II Pilot Study of Pyrotinib Plus Capecitabine Combined With Brain Radiotherapy in HER2 Positive Breast Cancer Patients With Brain Metastases [NCT04582968]Phase 1/Phase 239 participants (Anticipated)Interventional2020-01-02Active, not recruiting
A Phase II Randomized Study of the Protection Effect of Chinese Herbal Compound Dendrobium Huoshanense Granules in NCRT for Patients With Locally Advanced Rectal Cancer [NCT04394598]Phase 2210 participants (Anticipated)Interventional2020-03-01Recruiting
A Randomized, Double-blind, Placebo-controlled Study of Capecitabine in the Treatment of Early-stage Breast Cancer With Low-hormone Receptor Expression and Residual Invasive Carcinoma After Neoadjuvant Chemotherapy [NCT03821454]50 participants (Anticipated)Interventional2019-02-01Not yet recruiting
A Randomized Trial of Adjuvant Chemotherapy With Standard Regimens, Cyclophosphamide, Methotrexate and Fluorouracil - (CMF) or Doxorubicin and Cyclophosphamide - (AC), Versus Capecitabine in Women 65 Years and Older With Node Positive or Node-Negative Bre [NCT00024102]Phase 3633 participants (Actual)Interventional2001-09-30Completed
A Phase I/II Trial of Preoperative Oxaliplatin, Docetaxel, and Capecitabine With Concurrent Radiation Therapy in Localized Carcinoma of the Esophagus or Gastroesophageal Junction [NCT00193128]Phase 1/Phase 259 participants (Actual)Interventional2004-04-30Completed
An Open-label Study of Xeloda Plus Avastin at Time of Disease Progression in Treatment-naïve Women With HER2-negative Metastatic Breast Cancer [NCT00121836]Phase 4109 participants (Actual)Interventional2005-06-30Completed
Neoadjuvant FOLFOXIRI Chemotherapy Versus CapeOX Chemotherapy for Local Advanced Rectal Cancer: An Open Label Randomized Controlled Phase III Trial [NCT05201430]Phase 3300 participants (Anticipated)Interventional2021-08-27Recruiting
A Phase II Study of Oxaliplatin and Capecitabine in Patients With Unresectable Cholangiocarcinoma, Including Carcinoma of the Gallbladder and Biliary Tract [NCT00338988]Phase 244 participants (Actual)Interventional2003-08-31Completed
A Clinical Study of the Efficacy and Safety of Chidamide in Combination With Camrelizumab and Carboplatin or Capecitabine in the Second and Third Line Treatment of Relapsed/Metastatic Triple-negative Breast Cancer [NCT05438706]Phase 270 participants (Anticipated)Interventional2022-07-10Not yet recruiting
Intra-hepatic Chemotherapy With Oxaliplatin Every Second Week in Combination With Systemic Capecitabine in Patient With Non-resectable Liver Metastases From Breast Cancer A Phase II Trial in Patients With Limited Extrahepatic Disease [NCT01387295]Phase 238 participants (Actual)Interventional2010-04-30Completed
Phase II Study of First Line Capecitabine Administered on Continuous Way Combined With Oxaliplatin and Bevacizumab Every Two Weeks in Metastatic Colorectal Cancer Patients. [NCT00345696]Phase 232 participants (Actual)Interventional2006-06-30Completed
Phase I-II Study of bi-Weekly Fixed Dose Rate Gemcitabine, Oxaliplatin and Capecitabine in Patients With Advanced Cholangiocarcinoma [NCT00350961]Phase 1/Phase 239 participants (Anticipated)Interventional2004-06-30Completed
A Phase II Study of Etoposide, Oxaliplatin and Capecitabine in Patients With Advanced HCC [NCT00351195]Phase 239 participants (Anticipated)Interventional2006-02-28Terminated(stopped due to Did not meet the criteria for continuation to second stage)
Chemotherapy or No Chemotherapy in Clear Margins After Neoadjuvant Chemoradiation in Locally Advanced Rectal Cancer. A Randomised Phase III Trial of Control Vs Capecitabine Plus Oxaliplatin [CHRONICLE] [NCT00427713]Phase 3800 participants (Anticipated)Interventional2004-11-30Completed
A Phase Ia-Ib Dose-escalation Study Evaluating Safety and Efficacy of Neoadjuvant Stereotactic Body Radiotherapy (SBRT) With Concomitant Capecitabine Chemotherapy for Resectable Carcinoma of Exocrine Pancreas. [NCT01918644]Phase 121 participants (Actual)Interventional2014-04-08Completed
A Phase II Study of Vorinostat and Capecitabine in Recurrent and/or Metastatic Squamous Cell Carcinoma of Head and Neck (SCCHN) and Nasopharyngeal Carcinoma (NPC) [NCT01267240]Phase 225 participants (Actual)Interventional2010-12-31Terminated(stopped due to Study treatment did not show clinical activity.)
A Novel Phase I/IIa Open Label Study of IMM 101 in Combination With Selected Standard of Care (SOC) Regimens in Patients With Metastatic Cancer or Unresectable Cancer at Study Entry [NCT03009058]Phase 1/Phase 22 participants (Actual)Interventional2017-05-24Terminated(stopped due to Commercial reasons)
A Phase III, Multicenter, Randomized, Open-Label, Parallel Controlled Study of SHR-A1811 Versus Pyrotinib in Combination With Capecitabine for HER2-Positive, Unresectable and/or Metastatic Breast Cancer Subjects Previously Treated With Trastuzumab and Tax [NCT05424835]Phase 3269 participants (Anticipated)Interventional2022-07-29Recruiting
A Multi-Centre Randomised Clinical Trial of Biomarker-Driven Maintenance Treatment for First-Line Metastatic Colorectal Cancer (MODUL) [NCT02291289]Phase 2609 participants (Actual)Interventional2015-04-17Completed
Multicenter Phase II Study of Preoperative Chemoradiotherapy With CApecitabine Plus Temozolomide in Patients With MGMT Silenced and Microsatellite Stable Locally Advanced RecTal Cancer: the CATARTIC Trial [NCT05136326]Phase 221 participants (Anticipated)Interventional2021-12-01Recruiting
Randomized Phase II Clinical Trial of Bevacizumab Combined With Capecitabine and Either Oxaliplatin or Irinotecan as First Line Treatment for Metastatic Colorectal Cancer [NCT00314353]Phase 27 participants (Actual)Interventional2006-03-31Terminated(stopped due to The study was closed early due to low enrollment and new information regarding the benefit of the study regimen.)
Phase I Study of Oral Capecitabine (Xeloda) as a Radiation Enhancer in Locally Unresectable, Residual, or Recurrent Colorectal Cancer Localized in the Pelvis [NCT00003704]Phase 151 participants (Actual)Interventional1999-04-30Completed
Phase I/II of Capecitabine and Vinorelbine in Elderly Patients (At Least 65 Years) With Metastatic Breast Cancer With or Without Bone Involvement [NCT00003902]Phase 1/Phase 2110 participants (Anticipated)Interventional1999-03-31Completed
A Multicentre Randomised Phase II Clinical Trial Comparing Oxaliplatin (Eloxatin), Capecitabine (Xeloda) and Pre-Operative Radiotherapy With or Without Cetuximab Followed by Total Mesorectal Excision for the Treatment of Patients With Magnetic Resonance I [NCT00383695]Phase 2164 participants (Anticipated)Interventional2005-09-30Active, not recruiting
A Phase II Clinical Trial of Pembrolizumab as Monotherapy and in Combination With Cisplatin+5-Fluorouracil in Subjects With Recurrent or Metastatic Gastric or Gastroesophageal Junction Adenocarcinoma (KEYNOTE-059) [NCT02335411]Phase 2318 participants (Actual)Interventional2015-02-03Completed
A Phase Ⅰb/Ⅱ Study of Fruquintinib Combined With Capecitabine in the First-line Maintenance Treatment of RAS/BRAF Wild-type Metastatic Colorectal Cancer [NCT05016869]Phase 1/Phase 248 participants (Anticipated)Interventional2022-04-12Recruiting
A Phase II Study to Assess Efficacy and Safety of Capecitabine and Irinotecan Plus Bevacizumab Followed by Capecitabine and Oxaliplatin Plus Bevacizumab or the Reverse Sequence in Patients With Metastatic Colorectal Cancer [NCT02119026]Phase 2120 participants (Actual)Interventional2011-02-28Completed
Open-label, Randomized, Controlled, Multicenter Phase II Trial Investigating 2 Sym004 Doses Versus Investigator's Choice (Best Supportive Care, Capecitabine, 5-FU) in Subjects With Metastatic Colorectal Cancer and Acquired Resistance to Anti-EGFR Monoclon [NCT02083653]Phase 2254 participants (Actual)Interventional2014-03-06Completed
Phase Ib/II Study of Neoadjuvant Chemoradiotherapy With CRLX-101 and Capecitabine for Locally Advanced Rectal Cancer [NCT02010567]Phase 1/Phase 232 participants (Actual)Interventional2013-12-31Terminated(stopped due to The study was halted prematurely at the funding partner's request.)
Pyrotinib Combined With Capecitabine and Bevacizumab for Patients With HER2 Positive Breast Cancer and Brain Metastases：a Single-arm,Prospective,Phase II Study [NCT06152822]Phase 230 participants (Anticipated)Interventional2023-11-30Recruiting
A Randomized, Open-label, Parallel Controlled, Multi-center Phase III Study of Anlotinib Hydrochloride Capsule Combined With Chemotherapy as First-line Treatment in Subjects With RAS/BRAF Wild Metastatic Colorectal Cancer [NCT04854668]Phase 3748 participants (Actual)Interventional2020-07-30Active, not recruiting
A Double-Blind, Placebo-Controlled, Randomized, Multicenter Phase III Study Evaluating the Efficacy and Safety of Pertuzumab in Combination With Trastuzumab and Chemotherapy in Patients With HER2-Positive Metastatic Gastroesophageal Junction and Gastric C [NCT01774786]Phase 3780 participants (Actual)Interventional2013-06-10Completed
Validation of a Radiation Response Signature in Borderline Resectable Pancreatic Cancer Patients Treated With Induction Chemotherapy Followed by Stereotactic Body Radiation Therapy (SBRT) [NCT01754623]Phase 29 participants (Actual)Interventional2013-02-28Terminated(stopped due to Lack of pre-treatment tissue to make the study plan feasible.)
Program for Assessment of Capecitabine (Xeloda) Plus Docetaxel First-line Therapies in HER2-negative Metastatic Breast Cancer (XEBRA Study) [NCT01777945]46 participants (Actual)Observational2012-12-31Completed
Phase I Study of the Combination of Trastuzumab Emtansine (T-DM1) and Capecitabine in HER2-Positive Metastatic Breast Cancer and HER2-Positive Locally Advanced/Metastatic Gastric Cancer Patients, Followed by a Randomized, Open-Label Phase II Study of Tras [NCT01702558]Phase 2182 participants (Actual)Interventional2012-12-03Terminated(stopped due to The sponsor decided to terminate study after 70% of participants had experienced a progression-free survival event.)
BrUOG 302:BYL719, Capecitabine and Radiation for Rectal Cancer: A Brown University Oncology Research Group Phase I Study [NCT02550743]Phase 17 participants (Actual)Interventional2016-06-03Terminated(stopped due to lack of accural)
A Prospective Study of Apatinib Plus Concurrent Neoadjuvant Chemoradiotherapy for Siewert II ，III of Locally Advanced HER-2 Negative Adenocarcinoma at Gastroesophageal Junction [NCT03349866]Phase 248 participants (Anticipated)Interventional2017-11-30Recruiting
Safety and Efficacy of Nivolumab Combined With CAPOX Plus Bevacizumab as Neoadjuvant Treatment of pMMR/MSS Colorectal Cancer Liver Metastases Patients：a Single-arm, Phase II, Prospective Study [NCT05588297]Phase 212 participants (Anticipated)Interventional2022-10-31Not yet recruiting
Efficacy and Safety of Fruquintinib Plus Capecitabine Versus Capecitabine as Maintenance Treatment for Metastatic Colorectal Cancer After First-line Chemotherapy: A Phase II, Randomized, Controlled Study [NCT05451719]Phase 2116 participants (Anticipated)Interventional2022-07-31Not yet recruiting
A Single-Arm, Open Label Study of Aflibercept as Maintenance Therapy Following Induction With Aflibercept in Combination With XELOX, as First-Line Treatment for Metastatic Colorectal Cancer Patient [NCT01955629]Phase 1/Phase 24 participants (Actual)Interventional2013-12-31Terminated(stopped due to The study enrollment was prematurely halted due to safety reasons.)
A Phase II Study of Bevacizumab With Docetaxel and Capecitabine in the Neoadjuvant Setting for Breast Cancer Patients [NCT02005549]Phase 218 participants (Actual)Interventional2006-02-28Completed
Phase 2 Study of ZW25 Plus First-line Combination Chemotherapy in HER2-Expressing Gastrointestinal (GI) Cancers, Including Gastroesophageal Adenocarcinoma (GEA), Biliary Tract Cancer (BTC), and Colorectal Cancer (CRC) [NCT03929666]Phase 2362 participants (Anticipated)Interventional2019-08-29Recruiting
A Prospective Phase II Trial of Molecular Profiling to Guide Neoadjuvant Therapy for Resectable and Borderline Resectable Adenocarcinoma of the Pancreas [NCT01726582]Phase 2229 participants (Actual)Interventional2011-11-30Completed
A Single Arm, Phase II Study of Pembrolizumab, Oxaliplatin, and Capecitabine in the First Line Treatment of Patients With Gastro-esophageal Cancer. [NCT03342937]Phase 241 participants (Actual)Interventional2018-01-11Completed
A Phase II Non-randomized Study to Assess the Safety and Efficacy of the Combination of Tucatinib and Trastuzumab and Capecitabine for Treatment of Leptomeningeal Metastases in HER2 Positive Breast Cancer [NCT03501979]Phase 217 participants (Actual)Interventional2019-02-20Active, not recruiting
Comparison of the Clinical Response of Total nEoadjuvant Treatment of Two Methods of Long-term or Short-term cHemoRadiotherapy Followed by Consolidation Chemotherapy in Patients With Locally Advanced rectAl Cancer (TEHRAN) , a Randomized Controlled Clinic [NCT05920928]114 participants (Anticipated)Interventional2023-09-23Not yet recruiting
A Phase II Study of Metronomic Oral Chemotherapy With Cyclophosphamide Plus Capecitabine and Vinorelbine in Metastatic Breast Cancer Patients [NCT04304352]Phase 2162 participants (Anticipated)Interventional2011-07-29Recruiting
A Phase 1 Trial of the Safety, Tolerability and Biological Effects of Intravenous Enadenotucirev, a Novel Oncolytic Virus, in Combination With Chemoradiotherapy in Locally Advanced Rectal Cancer [NCT03916510]Phase 113 participants (Actual)Interventional2019-07-01Completed
Phase III Study to Evaluate the Quality of Life in Elderly Patients With Metastatic Colorectal Cancer Receiving First-line Therapy Based on Simplified Geriatric Parameters. [NCT03828227]Phase 3188 participants (Anticipated)Interventional2019-06-07Recruiting
Sorafenib in Combination With Capecitabine for Patients With Measurable Hepatocellular Carcinoma [NCT01032850]Phase 215 participants (Actual)Interventional2009-09-30Terminated(stopped due to Low accrual rate)
Proactive Management of Endoperitoneal Spread in Colonic Cancer [NCT02974556]Phase 3140 participants (Anticipated)Interventional2024-03-01Not yet recruiting
A Multicenter, Open-Label, Randomized-Controlled Study of Abemaciclib, a CDK4 and 6 Inhibitor, in Combination With Fulvestrant Compared to Chemotherapy in Women With HR Positive, HER2 Negative Metastatic Breast Cancer With Visceral Metastases [NCT04031885]Phase 44 participants (Actual)Interventional2019-08-14Terminated(stopped due to Business decision based on the inability to enroll subjects into the trial)
A Multicenter Phase II Trial of Nimotuzumab in Combination With Chemoradiation in Patients With Locally Advanced Rectal Cancer [NCT01899118]Phase 250 participants (Anticipated)Interventional2013-04-30Recruiting
Phase I Clinical Study of Every Three Week Irinotecan With Oral Capecitabine Given Twice Daily for Two Weeks Out of Three in Patients With Gastrointestinal and Other Solid Malignancies [NCT00003867]Phase 130 participants (Actual)Interventional1999-03-31Completed
An Open-Label Combination Study of Capecitabine and Standard Paclitaxel Therapy as First or Second Line Therapy in Women With Metastatic Breast Carcinoma [NCT00005649]Phase 20 participants Interventional1998-07-31Completed
A Randomized Phase 3 Clinical Trial Investigating Optimal Duration of Oxaliplatin Administration in Postoperative XELOX (Oxaliplatin + Capecitabine) Adjuvant Chemotherapy for the Patients With Stage II/III Gastric Cancer [NCT04787354]Phase 3976 participants (Anticipated)Interventional2021-11-01Recruiting
Open-label, Randomized, Multicenter, Phase III Study, Comparing Standard Chemotherapy to Standard Combination of Endocrine Therapy With Abemaciclib as Initial Metastatic Treatment Among Patients With Visceral Metastasis of ER+ HER2-breast Cancer, High Bur [NCT04158362]Phase 3378 participants (Anticipated)Interventional2020-06-11Recruiting
A Phase II Study of Total Neoadjuvant Chmoradiation Treatment Plus SHR1210 for High-risk Locally Advanced Rectal Cancer and Biomarker Screening Base on Neoantigen [NCT04340401]Phase 225 participants (Anticipated)Interventional2020-05-25Recruiting
Phase I Study of Dose Escalation Using Image-guided Radiotherapy to Deliver a Stereotactic Radiosurgical Boost After Neoadjuvant Chemoradiotherapy in Patients With Locally Advanced Esophageal Cancer [NCT00368329]Phase 14 participants (Actual)Interventional2006-06-30Terminated(stopped due to low accrual)
Capecitabine ON Temozolomide Radionuclide Therapy Octreotate Lutetium-177 NeuroEndocrine Tumours Study [NCT02358356]Phase 275 participants (Actual)Interventional2015-11-30Completed
A Multicenter Study With an Open-label Phase Ib Part Followed by a Randomized, Placebo-controlled, Double-blind, Phase II Part to Evaluate Efficacy, Safety, Tolerability, and Pharmacokinetics of the DNA-PK Inhibitor Peposertib (M3814) in Combination With [NCT03770689]Phase 1/Phase 219 participants (Actual)Interventional2019-03-20Completed
A Prospective, Phase III, Controlled, Multicentre, Randomised Clinical Trial Comparing Combination Gemcitabine and Capecitabine Therapy With Concurrent and Sequential Chemoimmunotherapy Using a Telomerase Vaccine in Locally Advanced and Metastatic Pancrea [NCT00425360]Phase 31,110 participants (Anticipated)Interventional2006-09-30Completed
Efficacy and Safety of Supplement Adjuvant Capecitabine in Postoperative Hormone Receptor (HR)-Positive, Human Epidermal Growth Factor Receptor 2 (HER2)-Negative High-risk Breast Cancer Patients: a Multicenter, Single-arm Clinical Trial [NCT05212454]Phase 3400 participants (Anticipated)Interventional2023-03-15Recruiting
Anti-PD-1, Capecitabine, and Oxaliplatin for the First-line Treatment of dMMR Esophagogastric Cancer (AuspiCiOus-dMMR): a Proof-of-principle Study [NCT05177133]Phase 225 participants (Anticipated)Interventional2021-11-05Recruiting
P-RAD: A Randomized Study of Preoperative Chemotherapy, Pembrolizumab and No, Low or High Dose RADiation in Node-Positive, HER2-Negative Breast Cancer [NCT04443348]Phase 2120 participants (Anticipated)Interventional2020-12-16Recruiting
A Randomized, Open-Label Trial Comparing Treatment With Either Pegylated Liposomal Doxorubicin or Capecitabine as First Line Chemotherapy for Metastatic Breast Cancer (PELICAN Trial) [NCT00266799]Phase 3210 participants (Actual)Interventional2006-01-13Completed
Phase I Trial of OXIRI [Oxaliplatin (O), Xeloda (X) and Irinotecan (I)] Treatment in Patients With Advanced and/or Metastatic Pancreatic Adenocarcinoma [NCT02368860]Phase 133 participants (Actual)Interventional2013-09-17Completed
Phase II Study of Second Line Capecitabine Plus Oxaliplatin (XELOX) in Patients With Advanced Biliary Tract Carcinoma After Failure of Gemcitabine-based Chemotherapy [NCT02350686]Phase 267 participants (Anticipated)Interventional2015-05-14Recruiting
Biological-guided Metronomic Chemotherapy as Maintenance Strategy in Responders After Induction Therapy in Metastatic Colorectal Cancer [NCT03158610]Phase 2/Phase 320 participants (Actual)Interventional2018-01-29Terminated(stopped due to Difficult to enrollment patient)
A Phase 1b Dose-escalation Study of the Safety and Pharmacokinetics of Fixed-dose PCS6422 With Escalating Doses of Capecitabine Administered Orally to Patients With Advanced, Refractory Gastrointestinal Tract Tumors [NCT04861987]Phase 142 participants (Anticipated)Interventional2021-06-18Recruiting
Epstein-Barr Virus DNA to Systemic Therapy for Treatment Adaptation in High Risk Nasopharyngeal Carcinoma (EP-STAR Trial) A Phase II, Multi-center, Biomarker-guided, Umbrella Trial [NCT04072107]Phase 2110 participants (Anticipated)Interventional2020-06-01Active, not recruiting
Phase II Trial of Capecitabine in Combination With Fulvestrant for Postmenopausal Women With Hormone Receptor Positive Metastatic Breast Cancer [NCT00534417]Phase 241 participants (Actual)Interventional2007-10-31Completed
Phase II Study of Ramucirumab With Trastuzumab, Fluoropyrimidine, and Platinum in Patients With Metastatic HER2-Positive Gastroesophageal Junction and Gastric Cancer [NCT02726399]Phase 27 participants (Actual)Interventional2016-03-18Terminated(stopped due to Low accrual rate)
Investigation of the Value of ctDNA Analysis in the Diagnosis, Treatment, and Surveillance of Patients With Surgically Resectable Colorectal Cancer [NCT03038217]Phase 3300 participants (Anticipated)Interventional2017-02-28Not yet recruiting
Phase I Study to Evaluate the Safety and Tolerability of ASLAN001 in Combination With Oxaliplatin and Capecitabine or Oxaliplatin and 5-FU With Leucovorin [NCT02435927]Phase 160 participants (Anticipated)Interventional2014-08-31Active, not recruiting
A Study of Pyrotinib Plus Capecitabine Versus Lapatinib Plus Capecitabine in Patients With HER2+Metastatic Breast Cancer Who Have Prior Received Anthracyclin, Taxane or Trastuzumab [NCT02422199]Phase 1/Phase 2128 participants (Anticipated)Interventional2015-05-31Active, not recruiting
Open-label, Randomized, Multicenter, Phase II Trial to Compare Efficacy of CAPTEM Versus FOLFIRI as Second Line in Patients Progressed on or After First-line Oxaliplatin Chemo for Advanced, MGMT Methylated, RAS Mutated Colorectal Cancer [NCT02414009]Phase 282 participants (Actual)Interventional2014-09-30Completed
Capecitabine Plus Toripalimab Maintenance Therapy in Metastatic Nasopharyngeal Carcinoma After First-line Gemcitabine/Cisplatin Plus Toripalimab Treatment: a Single Arm, Open Label, Multicenter, Phase II Clinical Study [NCT05484375]Phase 240 participants (Anticipated)Interventional2022-09-30Not yet recruiting
NANT Melanoma Vaccine: Combination Immunotherapy in Subjects With Melanoma Who Have Progressed on or After Chemotherapy and Anti-programmed Cell Death Protein 1 (PD-1)/Programmed Death Ligand 1 (PD-L1) Therapy [NCT03167177]Phase 1/Phase 20 participants (Actual)Interventional2017-12-31Withdrawn(stopped due to Trial not initiated)
Combination of Docetaxel, Cisplatin, and Capecitabine (DCX) in the Treatment of Locally Advanced or Metastatic Nasopharyngeal Carcinoma: a Prospective, Phase 2 Study [NCT02360501]Phase 250 participants (Actual)Interventional2008-01-31Completed
Systemic Targeted Adaptive RadioTherapy of NeuroEndocrine Tumors. An Open-label, Multicenter, Randomized Phase III Trial Comparing Safety and Efficacy of Personalized Versus Non-personalized Radionuclide Therapy With 177Lu (Lutetium)-DOTATOC. [NCT05387603]Phase 3300 participants (Anticipated)Interventional2022-06-30Not yet recruiting
Phase II Study to Evaluate Postoperative Chemotherapy in High-Grade Appendiceal Adenocarcinoma With Peritoneal Carcinomatosis [NCT02420509]2 participants (Actual)Observational2015-08-27Terminated(stopped due to unable to accrue)
[NCT02415829]Phase 255 participants (Anticipated)Interventional2014-11-30Recruiting
XELOX Combined With Anlotinib and Penpulimab vs XELOX as Adjuvant Therapy in ctDNA Positive Gastric and Esophagogastric Junction Adenocarcinoma, a Randomized, Controlled, Multicenter Clinical Trial [NCT05494060]Phase 280 participants (Anticipated)Interventional2022-03-16Recruiting
NANT Colorectal Cancer (CRC) Vaccine: Combination Immunotherapy in Subjects With Recurrent or Metastatic CRC [NCT03169777]Phase 1/Phase 20 participants (Actual)Interventional2018-08-31Withdrawn(stopped due to Trial not initiated)
Apatinib Combined With Capecitabine Compared With Apatinib in the Treatment of Advanced Non-resectable Hepatocellular Carcinoma [NCT03114085]Phase 2170 participants (Anticipated)Interventional2017-05-20Not yet recruiting
Open, Multicenter, Phase Ic Clinical Study on the Pharmacokinetics and Drug Interactions of Utidelone Plus Capecitabine in Patients With Recurrent and Metastatic Breast Cancer [NCT05052437]Phase 116 participants (Actual)Interventional2020-10-15Completed
An Open-label, Single-centre, Single-arm Phase II Study of Triplet Combination of Capecitabine, Oxaliplatin and Irinotecan (Xeloxiri) as Salvage Therapy in Patients With Refractory Metastatic Colorectal Cancer [NCT03146377]Phase 232 participants (Actual)Interventional2014-04-30Completed
Combination of Nelmastobart and Capecitabine Therapy in Metastatic Colorectal Cancer With Resistance or Intolerance to Oxaliplatin and Irinotecan-based Chemotherapy - A Single Arm, Phase 1b/2, Multicenter Study [NCT05990543]Phase 1/Phase 259 participants (Anticipated)Interventional2023-08-30Not yet recruiting
Randomized Phase II Trial of Postoperative Adjuvant Capecitabine and Temozolomide Versus Observation in High-Risk Pancreatic Neuroendocrine Tumors [NCT05040360]Phase 2141 participants (Anticipated)Interventional2022-05-05Recruiting
Phase 2 Randomized, Double-Blinded, Controlled Study of Tucatinib vs Placebo in Combination With Capecitabine and Trastuzumab in Patients With Pretreated Unresectable Locally Advanced or Metastatic HER2+ Breast Carcinoma [NCT02614794]Phase 2612 participants (Actual)Interventional2016-01-28Completed
An Open-Label Multicenter Phase 1b Study of Tolinapant (ASTX660) in Combination With Radiotherapy/Chemoradiotherapy (RT/CRT) in Preoperative Treatment of Patients With Rectum Cancer (PRAAR 1: Preoperative Radiotherapy And ASTX660 in Rectum Cancer) [NCT05912075]Phase 178 participants (Anticipated)Interventional2023-07-01Not yet recruiting
Randomized Phase II Study of Cisplatin and Etoposide Versus Temozolomide and Capecitabine in Patients With Advanced G3 Non-small Cell Gastroenteropancreatic Neuroendocrine Carcinomas [NCT02595424]Phase 2126 participants (Anticipated)Interventional2016-04-06Recruiting
A Phase II, Multicenter, Single-Arm, Feasibility Study of Eribulin in Combination With Capecitabine for Adjuvant Treatment in Estrogen Receptor-Positive Early Stage Breast Cancer [NCT01439282]Phase 277 participants (Actual)Interventional2011-08-31Completed
A Multicenter, Randomized, Controlled Phase III Study of Chemotherapy With or Without PD-1 Inhibitors and Chemoradiotherapy as Adjuvant Regimen for D2/R0 Resected pN3 Gastric (G) or Gastroesophageal Junction (GEJ) Adenocarcinoma [NCT04997837]Phase 3433 participants (Anticipated)Interventional2021-07-21Recruiting
A Randomized Single Center Phase II Study Comparing XELOX With Capecitabine Maintenance or XELOX Treatment in Elderly Metastatic Adenocarcinoma of Stomach [NCT01798251]Phase 240 participants (Anticipated)Interventional2012-12-31Recruiting
An Open Label Study of the Effect of Adjuvant Treatment With Capecitabine in Combination With Oxaliplatin on Disease-Free Survival in Patients With Stage III Colon Cancer [NCT01442155]74 participants (Actual)Observational2011-10-31Completed
MASTERPLAN: A Randomised Phase II Study of MFOLFIRINOX And Stereotactic Radiotherapy (SBRT) for Pancreatic Cancer With High Risk and Locally Advanced Disease [NCT04089150]Phase 2120 participants (Anticipated)Interventional2019-10-01Recruiting
Phase II Study of Oxaliplatin, Capecitabine and Bevacizumab as First Line Treatment for Patients With Advanced Colorectal Cancer [NCT00159432]Phase 263 participants (Actual)Interventional2005-02-28Completed
A Phase 2 Study of Capecitabine, Temozolomide, and Bevacizumab for Metastatic or Unresectable Pancreatic Neuroendocrine Tumors [NCT01525082]Phase 220 participants (Actual)Interventional2012-12-31Completed
A Phase II Study of XELOX in Locally Advanced or Metastatic Gastric Cancer [NCT00354224]Phase 210 participants (Actual)Interventional2005-01-31Terminated(stopped due to due to low accrual)
A Phase Ib, Open-Label, Multicenter Study of the Safety and Pharmacokinetics of the Combination of RhuMab 2C4 (Omnitarg), a Recombinant Humanized Antibody to HER2, and Capecitabine (Xeloda) in Patients With Advanced Solid Tumors [NCT02494596]Phase 119 participants (Actual)Interventional2004-01-31Completed
Phase II Study of Preoperative FOLFIRINOX Followed by Accelerated Short Course Radiation Therapy for Borderline-Resectable Pancreatic Cancer [NCT01591733]Phase 248 participants (Actual)Interventional2012-05-31Active, not recruiting
An Open Label, randomIzed Controlled Prospective Multicenter Two Arm Phase IV Trial to Determine Patient Preference for Everolimus in Combination With Exemestane or Capecitabine in Combination With Bevacizumab for Advanced (Inoperable or Metastatic) HER2- [NCT02248571]Phase 485 participants (Actual)Interventional2014-08-31Completed
Maintenance Treatment With Capecitabine Plus Apatinib vs. Apatinib and Observation After First-line XELOX/SOX Chemotherapy for Patients With Advanced Gastric Cancer: a Multicenter, Randomized, Controlled Trial [NCT03598348]Phase 3288 participants (Anticipated)Interventional2018-01-16Recruiting
Program for Assessment of Capecitabine (Xeloda) Based First-line Therapies in Metastatic Colorectal Cancer (AXEL Study) [NCT01696695]882 participants (Actual)Observational2011-07-31Completed
Pharmacokinetic and Safety Comparison of Two Capecitabine Tablets in Patients With Colorectal or Breast Cancer Under Fed Conditions: a Multicenter, Randomized, Open-label, Three-period, and Reference-replicated Crossover Study [NCT04420871]Phase 148 participants (Actual)Interventional2018-12-10Completed
Metro-PD1: a Phase I/II Trial Evaluating Anti-PD1 (Nivolumab) in Combination With Metronomic Chemotherapy in Children and Teenagers With Refractory / Relapsing Solid Tumors [NCT03585465]Phase 1/Phase 2102 participants (Anticipated)Interventional2019-03-26Recruiting
A Phase I Study of Talimogene Laherparepvec (Talimogene Laherparepvec) With Neoadjuvant Chemotherapy and Radiation in Adenocarcinoma of the Rectum [NCT03300544]Phase 13 participants (Actual)Interventional2017-09-20Active, not recruiting
Tucidinostat Combined With Metronomic Capecitabine and Endocrine Therapy for Advanced HR-positive, HER2-negative Breast Cancer After CDK4/6 Inhibitor：a Prospective, Single-arm, Phase II Clinical Trial. [NCT05411380]Phase 273 participants (Anticipated)Interventional2022-10-03Recruiting
Tucidinostat and Metronomic Capecitabine for Metastatic Triple-negative Breast Cancer:a Multicenter,Open-label, Randomized Controlled, Phase II Clinical Trial [NCT05390476]Phase 2126 participants (Anticipated)Interventional2022-08-01Recruiting
Sorafenib Plus Capecitabine (SorCape) in Previously Treated Metastatic Colorectal Cancer [NCT01471353]Phase 243 participants (Actual)Interventional2011-11-30Completed
A Randomized, Three Arm Multinational Phase III Study to Investigate Bevacizumab (q3w or q2w) in Combination With Either Intermittent Capecitabine Plus Oxaliplatin (XELOX) (q3w) or Fluorouracil/Leucovorin With Oxaliplatin (FOLFOX-4) Versus FOLFOX-4 Regime [NCT00112918]Phase 33,451 participants (Actual)Interventional2004-12-31Completed
Phase II Trial Of Neoadjuvant Concurrent Capecitabine, RHUMAB VEGF (Avastin) And Radiotherapy In Patients Presenting With Locally Advanced Rectal Cancer [NCT00113230]Phase 225 participants (Actual)Interventional2005-02-28Completed
XELOX Combined With Cadonilimab Versus XELOX as Neoadjuvant Treatment for MRF-negative Locally Advanced, pMMR Rectal Cancer: a Randomised, Phase 2 Trial [NCT05815303]Phase 292 participants (Anticipated)Interventional2023-03-29Recruiting
A Phase II/III Randomized Clinical Trial of CisPlatin plUs Gemcitabine and Nabpaclitaxel (GAP) as pReoperative Chemotherapy Versus Immediate Resection in patIents With resecTable BiliarY Tract Cancers (BTC) at High Risk for Recurrence: PURITY Study [NCT06037980]Phase 2/Phase 3300 participants (Anticipated)Interventional2023-11-07Recruiting
NeoOPTIMIZE: An Open-Label, Phase II Trial to Assess the Efficacy of Adaptive Switching of FOLFIRINOX or Gemcitabine/Nab-Paclitaxel as a Neoadjuvant Strategy for Patients With Resectable and Borderline Resectable/Locally Advanced Unresectable Pancreatic C [NCT04539808]Phase 260 participants (Anticipated)Interventional2021-05-27Recruiting
A Multicenter, Open-Label, Non-Comparative, Three-Arm, Phase IIa Trial of Ipatasertib (GDC-0068) in Combination With Non-Taxane Chemotherapy Agents for Taxane-Pretreated Unresectable Locally Advanced or Metastatic TNBC Patients [NCT04464174]Phase 254 participants (Actual)Interventional2020-10-08Completed
A Randomised Study to Assess the Efficacy of Cetuximab Rechallenge in Patients With Metastatic Colorectal Cancer (RAS Wild-type) Responding to First-line Treatment With FOLFIRI Plus Cetuximab [NCT02934529]Phase 3673 participants (Actual)Interventional2015-03-31Active, not recruiting
ONO-4538 Phase II/III Study A Multicenter, Randomized Study in Patients With Unresectable Advanced or Recurrent Gastric Cancer [NCT02746796]Phase 2/Phase 3680 participants (Anticipated)Interventional2016-03-31Completed
A Phase Ib/II Clinical Study of BBI608 in Combination With Standard Chemotherapies in Adult Patients With Advanced Gastrointestinal Cancer [NCT02024607]Phase 1/Phase 2495 participants (Actual)Interventional2014-01-31Completed
A Phase II Clinical Study of BBI608 in Adult Patients With Advanced Colorectal Cancer [NCT01776307]Phase 2200 participants (Actual)Interventional2012-03-31Completed
Phase II Study of Fixed-Dose Capecitabine in Metastatic Breast Cancer [NCT00274768]Phase 226 participants (Actual)Interventional2004-04-30Completed
An Open-Label, Randomized, Multicenter Phase IIa Study Evaluating Pertuzumab in Combination With Trastuzumab and Chemotherapy in Patients With HER2-Positive Advanced Gastric Cancer [NCT01461057]Phase 230 participants (Actual)Interventional2011-12-06Completed
A Prospective Phase II Study of Cetuximab (Erbitux®) in Combination With XELOX [XELoda® (Capecitabine) and OXaliplatin] in Patients With Advanced Gastric Cancer [NCT00398398]Phase 244 participants (Actual)Interventional2006-11-30Completed
Phase II Study of Oxaliplatin, Capecitabine and Bevacizumab in the Treatment of Metastatic Colorectal Cancer [NCT00416494]Phase 250 participants (Actual)Interventional2003-09-30Completed
Randomized Control Study of Capecitabine vs. S-1 in Unresectable or Recurrent Breast Cancer Patients [NCT00438100]Phase 2142 participants (Actual)Interventional2008-04-30Completed
A Prospective, Randomized, Open-label, Phase II Study of QYHJ Granules Versus Xeloda in the Second-line Treatment of Patients With Metastatic Pancreatic Cancer [NCT01796782]Phase 260 participants (Anticipated)Interventional2013-01-31Active, not recruiting
A Phase I Study of Docetaxel, Capecitabine and Oxaliplatin (DXO) in Patients With Advanced Stomach Cancer [NCT00446290]Phase 122 participants (Actual)Interventional2006-03-31Completed
Study on Xeloda® to Document Its Use in Routine Practice in Patients With Metastatic or Advanced Breast Cancer [NCT01725386]274 participants (Actual)Observational2011-03-31Completed
Improving the Safety of Fluoropyrimidine-based Chemotherapy by Combined DPYD Genotype-guided and DPD Phenotype-guided Dose Individualization: The ALPE2U Study [NCT04194957]1,440 participants (Anticipated)Interventional2020-01-15Recruiting
Capecitabine and Temozolomide for Treatment of Recurrent Pituitary Adenomas [NCT03930771]Phase 21 participants (Actual)Interventional2019-05-21Terminated(stopped due to the study had a low accrual rate)
Phase 1 Trial of Tucatinib, Trastuzumab, and Capecitabine With Stereotactic Radiosurgery (SRS) in Patients With Brain Metastases From HER-2 Positive Breast Cancer [NCT05553522]Phase 140 participants (Anticipated)Interventional2023-09-18Recruiting
A Phase 2, Multicenter, Open-Label Study of DKN-01 in Combination With Tislelizumab ± Chemotherapy as First-Line or Second-Line Therapy in Adult Patients With Inoperable, Locally Advanced or Metastatic Gastric or Gastroesophageal Junction Adenocarcinoma ( [NCT04363801]Phase 2232 participants (Anticipated)Interventional2020-07-29Recruiting
Post-surgical Liquid Biopsy-guided Treatment of Stage III and High-risk Stage II Colon Cancer Patients: the PEGASUS Trial [NCT04259944]Phase 2140 participants (Anticipated)Interventional2020-06-16Active, not recruiting
NANT Triple Negative Breast Cancer (TNBC) Vaccine: Molecularly Informed Integrated Immunotherapy Combining Innate High-affinity Natural Killer (haNK) Cell Therapy With Adenoviral and Yeast-based Vaccines to Induce T-cell Responses in Subjects With TNBC Wh [NCT03387085]Phase 1/Phase 279 participants (Anticipated)Interventional2018-03-16Active, not recruiting
A Phase III Randomized Trial Investigating the Duration of Adjuvant Therapy(3 Versus 6 Months) With the Modified FOLFOX 6 or XELOX Regimens for Patients With Stage III Colon Cancer [NCT00958737]Phase 32,000 participants (Anticipated)Interventional2009-05-12Active, not recruiting
A Randomized Double Blinded Study of Curcumin With Pre-operative Capecitabine and Radiation Therapy Followed by Surgery for Rectal Cancer [NCT00745134]Phase 222 participants (Actual)Interventional2008-08-11Terminated(stopped due to The trial was stopped early because there was only one patient with pCR among the first 15 patients randomized to the curcumin arm.)
Phase Ib/II Study of GQ1001 and Pyrotinib in HER2 Positive Metastatic Breast Cancer Patients Who Had Failed Previous Anti-HER2 Treatment（GRACE） [NCT05575804]Phase 1/Phase 275 participants (Anticipated)Interventional2022-10-01Active, not recruiting
A Randomized Phase III 2-arm Trial of Paclitaxel Plus Bevacizumab vs. Capecitabine Plus Bevacizumab for the First-line Treatment of Human Epidermal Growth Factor Receptor 2 (HER2)-Negative Locally Recurrent or Metastatic Breast Cancer [NCT00600340]Phase 3564 participants (Actual)Interventional2008-04-30Completed
QUILT-3.080: Phase 1B/2 Trial Of The NANT Pancreatic Cancer Vaccine As Treatment For Subjects With Pancreatic Cancer Who Have Progressed on or After Standard-Of-Care Therapy [NCT03586869]Phase 1/Phase 2173 participants (Anticipated)Interventional2018-07-28Active, not recruiting
Detection and Enumeration of Circulating Tumor Cells in Rectal Cancer [NCT01671891]100 participants (Anticipated)Observational2012-02-29Recruiting
A Randomised, Open-label, Parallel Controlled, Multicentre, Phase 3 Clinical Trial of Pyrotinib Plus Capecitabine Versus Lapatinib Plus Capecitabine in Patients With HER2+ Metastatic Breast Cancer: [NCT03080805]Phase 3240 participants (Anticipated)Interventional2017-05-03Active, not recruiting
A Phase 1 Study of NBTXR3 Activated by Radiotherapy With Concurrent Chemotherapy for Adenocarcinoma of the Esophagus [NCT04615013]Phase 124 participants (Anticipated)Interventional2020-11-23Recruiting
A Phase 3, Randomized, Multi-center, Open-label Study of Trastuzumab Deruxtecan (T-DXd) Versus Investigator's Choice Chemotherapy in HER2-Low, Hormone Receptor Positive Breast Cancer Patients Whose Disease Has Progressed on Endocrine Therapy in the Metast [NCT04494425]Phase 3866 participants (Actual)Interventional2020-07-24Active, not recruiting
A Dose Finding Phase 1 of Sarilumab Plus Capecitabine in HER2/Neu-Negative Metastatic Breast Cancer and a Single-arm, Historically-controlled Phase 2 Study of Sarilumab Plus Capecitabine in Stage I-III Triple Negative Breast Cancer With High-Risk Residual [NCT04333706]Phase 1/Phase 265 participants (Anticipated)Interventional2023-11-03Recruiting
Study of the Impact of DPD Activity on the Efficacy of Capecitabine [NCT04198727]155 participants (Anticipated)Interventional2020-07-20Recruiting
Randomized, Phase II Trial to Evaluate the Efficacy and Safety of Atezolizumab Plus Capecitabine Adjuvant Therapy Compared to Capecitabine Monotherapy for TNBC With Residual Invasive Cancer After Neoadjuvant Chemotherapy. [NCT03756298]Phase 2284 participants (Actual)Interventional2019-01-15Active, not recruiting
A Single-arm, Open-label Study of Avastin Plus Xeloda on Objective Treatment Response in Patients With Advanced or Metastatic Liver Cancer Who Have Had no Previous Cytotoxic Chemotherapy [NCT02013830]Phase 245 participants (Actual)Interventional2005-05-31Completed
Randomized Phase II Trial of Chemotherapy of Physician's Choice Plus Trastuzumab Versus Chemotherapy of Physician's Choice Plus Trastuzumab Plus Pertuzumab In Women With Pretreated, HER2-Overexpressing Metastatic Breast Cancer (MBC) [NCT02229149]Phase 233 participants (Actual)Interventional2014-12-31Terminated(stopped due to per Sponsor request)
A Prospective, Randomised, Controlled, Open-label, Multicentre Study to Evaluate Efficacy, Safety and Patient-Reported Outcomes of Peptide Receptor Radionuclide Therapy (PRRT) With 177Lu-Edotreotide Compared to Best Standard of Care in Patients With Well- [NCT04919226]Phase 3202 participants (Anticipated)Interventional2021-12-21Recruiting
A Phase II, Randomized, Controlled Study to Assess the Efficacy and Safety of Fruquintinib Plus Capecitabine Versus Bevacizumab Plus Capecitabine as Maintenance Treatment Following First-line Chemotherapy for Metastatic Colorectal Cancer [NCT04733963]Phase 2112 participants (Anticipated)Interventional2021-03-01Recruiting
A Phase I-II Study of Capecitabine and Oxaliplatin in Chemotherapy-Naive and Thymidylate Synthase Inhibitor Pretreated Advanced or Metastatic Colorectal Cancer [NCT00004187]Phase 1/Phase 20 participants Interventional1999-06-30Completed
Open-Label, Multicenter, Phase II/III Study of Combination Therapy of D07001-Softgel Capsules and Xeloda/TS-1 in Subjects With Advanced Biliary Tract Cancer After Gemcitabine and Cisplatin-Based Treatment Failure [NCT05065957]Phase 2/Phase 3180 participants (Anticipated)Interventional2022-03-29Recruiting
Differential Gene Regulation During Neoadjuvant Therapy Trial of Epirubicin/Cyclophosphamide (EC) vs Docetaxel/Capecitabine (DX) Regimens in Patients With Large ER-positive and ER-negative Breast Cancers: A Randomized Phase II Trial. [NCT01869192]Phase 272 participants (Actual)Interventional2003-03-05Completed
A Multicentre, Randomized, Open-label, Controlled Phase Ш Clinical Study to Evaluate the Efficacy and Safety of DP303cversus Trastuzumab Combined With Vinorelbine/Capecitabine in of HER2-positive Advanced Breast Cancer [NCT05901935]Phase 3420 participants (Anticipated)Interventional2023-07-31Not yet recruiting
A Phase II Trial of Pharmacogenetic-Based Dosing of Irinotecan, Oxaliplatin, and Capecitabine as First-Line Therapy for Advanced Small Bowel Adenocarcinoma [NCT00433550]Phase 233 participants (Actual)Interventional2007-05-31Completed
A Phase I-II Study of Sorafenib (Nexavar®) in Combination With Capecitabine and Cisplatin (XP) in Patients With Advanced Gastric Cancer [NCT00565370]Phase 1/Phase 222 participants (Actual)Interventional2007-11-30Completed
A Phase I Study of Ixabepilone in Combination With Capecitabine in Japanese Patients With Metastatic Breast Cancer Previously Treated With an Anthracycline and a Taxane [NCT00568022]Phase 19 participants (Actual)Interventional2008-02-29Completed
A Phase II Study of Capecitabine, Carboplatin, and Bevacizumab for Metastatic or Unresectable Gastroesophageal Junction and Gastric Adenocarcinoma [NCT00780494]Phase 235 participants (Actual)Interventional2009-02-28Completed
Phase II Multicenter Single-arm Study of BKM120 Plus Capecitabine for Breast Cancer Patients With Brain Metastases [NCT02000882]Phase 210 participants (Actual)Interventional2014-05-29Completed
Phase I Study of Preoperative Concurrent Chemo-radiation With Capecitabine in Elderly Rectal Cancer Patients [NCT01584544]Phase 124 participants (Actual)Interventional2011-01-31Completed
Adjuvant Hyperthermic Intraperitoneal Chemotherapy in Patients With Colon Cancer at High Risk of Peritoneal Carcinomatosis [NCT02231086]Phase 3204 participants (Actual)Interventional2015-03-31Completed
A Phase I, Open-Label, Multicenter Study to Investigate the Safety, Tolerability, Pharmacokinetics and Anti-tumor Activity of DZD1516 in Combination With Trastuzumab and Capecitabine, or DZD1516 in Combination With T-DM1, in Patients With Metastatic HER2 [NCT04509596]Phase 123 participants (Actual)Interventional2020-09-21Active, not recruiting
Neoadjuvant Therapy and Biomarker Analysis of Stage II and III Breast Cancer With Docetaxel/Capecitabine and Celecoxib Followed by Doxorubicin/Cyclophosphamide and Celecoxib [NCT00665457]Phase 23 participants (Actual)Interventional2004-04-15Terminated(stopped due to study drug was removed from the market and low enrollment.)
Phase I Study of Imatinib, Gemcitabine and Capecitabine in Patients With Solid Tumors [NCT00483366]Phase 113 participants (Actual)Interventional2006-08-15Completed
A STUDY OF NERATINIB PLUS CAPECITABINE VERSUS LAPATINIB PLUS CAPECITABINE IN PATIENTS WITH HER2+ METASTATIC BREAST CANCER WHO HAVE RECEIVED TWO OR MORE PRIOR HER2-DIRECTED REGIMENS IN THE METASTATIC SETTING (NALA) [NCT01808573]Phase 3621 participants (Actual)Interventional2013-03-29Completed
A Doublelet Metronomic Chemotherapeutic Regimen With Oral Vinorelbine and Capecitabine in Advanced HER2-negative Breast Cancer Patients: A Monocentric Retrospective Study in China [NCT05747326]Phase 230 participants (Anticipated)Interventional2022-01-01Recruiting
Single-center, Multi-cohort Exploratory Phase Ib/II Clinical Study of First-line Treatment of Unresectable Locally Advanced/Advanced Adenocarcinoma of the Stomach or Gastroesophageal Junction Based on Different Genotypes [NCT05608785]Phase 1/Phase 245 participants (Anticipated)Interventional2023-01-01Not yet recruiting
A Randomized Phase II Trial of Metronomic Oral Vinorelbine Plus Cyclophosphamide and Capecitabine (VEX) Versus Weekly Paclitaxel as First-line or Second-line Treatment in Patients With ER-positive/HER2-negative Advanced or Metastatic Breast Cancer [NCT02954055]Phase 2140 participants (Actual)Interventional2017-09-13Active, not recruiting
A Randomized Open-Label, Multi-Center Pivotal Study of ANG1005 Compared With Physician's Best Choice in HER2-Negative Breast Cancer Patients With Newly Diagnosed Leptomeningeal Carcinomatosis and Previously Treated Brain Metastases (ANGLeD) [NCT03613181]Phase 3150 participants (Anticipated)Interventional2023-12-31Not yet recruiting
Capecitabine in Combination With Bendamustine in Women With Pretreated Locally Advanced or Metastatic Her2-negative Breast Cancer, a Phase II Trial [NCT01891227]Phase 240 participants (Actual)Interventional2013-08-09Completed
A Biologic Study of Global Gene Expression, NF-Kappa B and p53 in Adenocarcinoma of the Rectum. [NCT00280761]47 participants (Actual)Observational2003-12-31Completed
The Janus Rectal Cancer Trial: A Randomized Phase II Trial Testing The Efficacy of Triplet Versus Doublet Chemotherapy to Achieve Clinical Complete Response in Patients With Locally Advanced Rectal Cancer [NCT05610163]Phase 2312 participants (Anticipated)Interventional2022-12-08Recruiting
Phase II Randomized, Prospective Trial of Lutetium Lu 177 Dotatate PRRT Versus Capecitabine and Temozolomide in Well-Differentiated Pancreatic Neuroendocrine Tumors [NCT05247905]Phase 2198 participants (Anticipated)Interventional2022-03-16Recruiting
A Single Arm Study of Brain Metastasis in Patients With HER2-positive Breast Cancer Treated With Pyrrolidine Maleate and Capecitabine Combined With Brain Radiotherapy [NCT04767828]Phase 443 participants (Anticipated)Interventional2020-05-01Recruiting
A Phase I Clinical Trial to Determine the Maximum Tolerated Dose and to Assess the Safety of OratecanTM in Combination With Capecitabine in Patients With Advanced Solid Cancer [NCT01463982]Phase 121 participants (Actual)Interventional2010-12-31Completed
Total Neoadjuvant Therapy Followed by 'Watch and Wait' Approach or Organ Preservation for MRI Stratified Low-risk Rectal Cancer: a Multi-center, Prospective, Single-arm Phase II Trial. [NCT04405206]54 participants (Anticipated)Observational2020-05-25Recruiting
Randomized Phase 3 Study of Xelox(Capecitabine Plus Oxaliplatin) Followed by Maintenance Capecitabine or Observation in Patients With Advanced Gastric Adenocarcinoma [NCT02289547]Phase 3184 participants (Anticipated)Interventional2015-05-31Recruiting
A Single Arm，Multicenter，Real-world Observational Study of Pyrotinib Plus Trastuzumab After First-line TH (P) Treatment With HER-2 Positive Breast Cancer [NCT05255523]Phase 260 participants (Anticipated)Interventional2022-02-20Not yet recruiting
Low-dose Versus Standard-dose Capecitabine Adjuvant Chemotherapy for Chinese Elderly Patients With Stage II/III Colorectal Cancer: A Randomized, Phase 3 Non-inferiority Study [NCT02316535]Phase 3710 participants (Anticipated)Interventional2014-11-30Recruiting
A Phase Ib/II Study of AK104#PD-1 / CTLA-4 Bispecific Antibody# and AK117#Anti-CD47 Antibody# in Combination With or Without Chemotherapy in Advanced Malignant Tumors [NCT05235542]Phase 1/Phase 2130 participants (Anticipated)Interventional2022-07-12Recruiting
Feasibility Study of Adaptive Radiotherapy for the Treatment of Locally-Advanced Anal Squamous Cell Carcinoma [NCT05838391]20 participants (Anticipated)Interventional2023-05-18Recruiting
A Phase II Study of Preoperative Pembrolizumab for Mismatch-Repair Deficient and Epstein-Barr Virus Positive Gastric Cancer Followed by Chemotherapy and Chemoradiation With Pembrolizumab [NCT03257163]Phase 240 participants (Anticipated)Interventional2017-09-29Recruiting
A Two-arm, Open-label, Randomized Phase III Study of Pembrolizumab (MK-3475) Monotherapy Versus Standard Chemotherapy in Platinum Pre-treated, Recurrent or Metastatic Nasopharyngeal Cancer (NPC) (Keynote-122) [NCT02611960]Phase 3233 participants (Actual)Interventional2016-04-18Completed
A Randomized, Open Label Multi-Center Study Of Single Agent Larotaxel (XRP9881) Compared To Continuous Administration of 5-FU For The Treatment Of Patients With Advanced Pancreatic Cancer Previously Treated With A Gemcitabine-Containing Regimen [NCT00417209]Phase 3408 participants (Actual)Interventional2006-12-31Completed
A Randomized Placebo-Controlled Study of Perifosine in Combination With Single Agent Chemotherapy for Metastatic Cancer Patients [NCT00398879]Phase 2381 participants (Actual)Interventional2005-08-31Completed
An Open-label, Single Center, Phase I/II Clinical Trial to Assess the Maximum Tolerated Dose, Safety and Efficacy of BEY1107 in Combination With Capecitabine in Patients With Metastatic Colorectal Cancer Refractory or Intolerant to Standard of Care [NCT05093907]Phase 1/Phase 227 participants (Anticipated)Interventional2021-08-31Recruiting
A Randomized Open-Label Phase III Study of Single Agent Pembrolizumab Versus Single Agent Chemotherapy Per Physician's Choice for Metastatic Triple Negative Breast Cancer (mTNBC) - (KEYNOTE-119) [NCT02555657]Phase 3622 participants (Actual)Interventional2015-10-13Completed
A Prospective Randomized Controlled Trial to Compare Oxaliplatin Combined With S-1 (SOX) Versus Oxaliplatin With Capecitabine (XELOX) as Adjuvant Chemotherapy for Stage III Colorectal Cancer Patients [NCT03448549]Phase 31,191 participants (Anticipated)Interventional2018-01-01Recruiting
Adjuvant CAPECITABINE in High Risk PSEUDOMYXOMA PERITONEI Patients Treated With CYTOREDUCTIVE SURGERY (CRS) and HYPERTERMIC INTRAPERITONEAL CHEMOTHERAPY (HIPEC) [NCT05321329]Phase 228 participants (Anticipated)Interventional2018-12-03Recruiting
Neoadjuvant Capecitabine, Oxaliplatin, Docetaxel and Atezolizumab in Non-metastatic, Resectable Gastric and GE-junction Cancer: The PANDA Trial [NCT03448835]Phase 220 participants (Anticipated)Interventional2018-03-07Recruiting
Biomarkers and Clinical Outcomes in Localized Rectal Adenocarcinoma Treated With Neoadjuvant Therapy [NCT04418895]Phase 20 participants (Actual)Interventional2021-08-13Withdrawn(stopped due to lack of resources)
Phase I Study of Pre-operative Capecitabine and Lenvatinib With External Radiation Therapy in Locally Advanced Rectal Adenocarcinoma [NCT02935309]Phase 120 participants (Actual)Interventional2016-10-14Completed
Efficacy of Adjuvant Chemotherapy in Patients With Clinical Stage III Rectal Cancer Undergoing Neoadjuvant Chemoradiotherapy: A Pathology-oriented, Prospective, Multicenter, Randomized, Open-label, Parallel Group Clinical Trial [NCT03415763]Phase 3764 participants (Anticipated)Interventional2018-11-05Recruiting
A Prospective Study of Concurrent Neoadjuvant Chemoradiotherapy Plus Trastuzumab for Siewert II ，III of HER-2 Positive Adenocarcinoma at Gastroesophageal Junction [NCT03368131]Phase 248 participants (Actual)Interventional2017-12-01Active, not recruiting
Neoadjuvant Treatment of Breast Cancer - a Prospective Observational Study, PANnon ONCology (PANONC) Group Non-commercial Clinical Trial [NCT05131893]300 participants (Anticipated)Observational [Patient Registry]2022-03-31Not yet recruiting
DURVA+ : Evaluation of the Safety and Pharmacodynamics of Anti-PD-L1 Antibody Durvalumab in Combination With Chemotherapy in Patients With Advanced Solid Tumors [NCT03907475]Phase 2115 participants (Anticipated)Interventional2019-07-16Recruiting
A Randomized, Placebo-Controlled, Double-Blind Phase 3 Study to Evaluate the Efficacy and Safety of Tislelizumab (BGB-A317) in Combination With Chemotherapy as First-Line Treatment in Patients With Unresectable, Locally Advanced Recurrent or Metastatic Es [NCT03783442]Phase 3649 participants (Actual)Interventional2018-12-11Active, not recruiting
Phase I/II Study of Oral Capecitabine and Temozolomide (CAPTEM) for Newly Diagnosed Glioblastoma (GBM) [NCT03213002]Phase 1/Phase 267 participants (Anticipated)Interventional2017-06-13Recruiting
A Phase I/II Trial of BAY 43-9006 Plus Gemcitabine and Capecitabine in the Treatment of Patients With Advanced Renal Cell Carcinoma [NCT00121251]Phase 1/Phase 217 participants (Actual)Interventional2005-06-03Completed
Precision Treatment of Refractory Triple Negative Breast Cancer Based on Molecular Subtyping --FUSCC-TNBC- Umbrella Trial [NCT03805399]Phase 1/Phase 2140 participants (Anticipated)Interventional2018-10-18Recruiting
A Randomized, Double-Blind, Phase 3 Study of the JAK1/2 Inhibitor, Ruxolitinib or Placebo in Combination With Capecitabine in Subjects With Advanced or Metastatic Adenocarcinoma of the Pancreas Who Have Failed or Are Intolerant to First-Line Chemotherapy [NCT02117479]Phase 3321 participants (Actual)Interventional2014-03-31Terminated(stopped due to The study was terminated early based on the results of the planned interim analysis.)
A Randomized, Open Label, Multicenter Phase IIIb Study Comparing Two Trastuzumab Dosing Regimens, Each in Combination With Cisplatin/Capecitabine Chemotherapy, as First-Line Therapy in Patients With HER2-Positive Metastatic Gastric or Gastro-Esophageal Ju [NCT01450696]Phase 3296 participants (Actual)Interventional2011-12-31Terminated(stopped due to futility following planned interim analysis)
Randomized Phase II Trial of Single Agent MEK Inhibitor Trametinib (GSK1120212) Vs 5-Fluorouracil or Capecitabine in Refractory Advanced Biliary Cancer [NCT02042443]Phase 253 participants (Actual)Interventional2014-02-28Completed
A Randomized, Double-Blind, Phase 2 Study of Ruxolitinib or Placebo in Combination With Capecitabine in Subjects With Advanced or Metastatic HER2-Negative Breast Cancer [NCT02120417]Phase 2149 participants (Actual)Interventional2014-05-31Terminated(stopped due to The study was terminated as other related studies of ruxolitinib did not provide sufficient efficacy to warrant continuation.)
A Phase 2 Study of Capecitabine in Patients With Advanced or Recurrent Squamous Cell Carcinoma of the Skin [NCT01823679]Phase 22 participants (Actual)Interventional2013-03-31Terminated(stopped due to Low accrual)
Tocotrienol and Bevacizumab in Metastatic Colorectal Cancer. A Randomized Phase II Marker Trial [NCT04245865]Phase 274 participants (Anticipated)Interventional2020-06-26Recruiting
Phase II of Short Course Radiation Therapy Followed by Pre-operative Chemotherapy and Surgery in Primary High-risk Rectal Cancer [NCT03729687]Phase 2280 participants (Actual)Interventional2016-07-04Active, not recruiting
A Phase III, Randomised, Double-Blind, Placebo-Controlled, Multicentre Study Of The Efficacy And Safety Of Atezolizumab Plus Chemotherapy For Patients With Early Relapsing Recurrent (Inoperable Locally Advanced Or Metastatic) Triple-Negative Breast Cancer [NCT03371017]Phase 3572 participants (Anticipated)Interventional2018-01-11Active, not recruiting
PERSONALIZED MEDICINE GROUP / UCBG UC-0105/1304: SAFIR02_Breast - Evaluation of the Efficacy of High Throughput Genome Analysis as a Therapeutic Decision Tool for Patients With Metastatic Breast Cancer [NCT02299999]Phase 21,460 participants (Actual)Interventional2014-04-07Active, not recruiting
A Pilot Study of Molecular Profile-Directed Chemotherapy for Metastatic HER2(-) Esophagogastric Adenocarcinoma [NCT02358863]13 participants (Actual)Interventional2015-02-28Terminated(stopped due to Issues with recruitment.)
Randomized Trial of Primary Surgery Followed Selective Radiochemotherapy Versus Conventional Preoperative Radiochemotherapy for Locally Advanced Rectal Cancer With MRI Negative Circumferential Margin [NCT02121405]Phase 3350 participants (Anticipated)Interventional2015-10-31Suspended(stopped due to DSMB stopped this trial due to the difference of 3-year DFS's rate between two groups more than 5% at the interim analysis in July 2021.)
A Phase II Study of Weekly Docetaxel (Taxotere®) in Combination With Capecitabine (Xeloda) in Advanced Gastric and Gastro-Esophageal Adenocarcinomas. [NCT00177255]Phase 240 participants (Actual)Interventional2005-04-30Terminated(stopped due to Roche has withdrawn support)
A Phase II Study of Capecitabine and Docetaxel in Previously Untreated Advanced Non-Small Cell Lung Cancer Patients [NCT00201825]Phase 229 participants (Actual)Interventional2004-12-31Completed
A Randomized, Open-label, Positive-controlled, Multicenter Phase Ш Study Comparing Mitoxantrone Hydrochloride Liposome Injection Combined With Capecitabine Versus Capecitabine Monotherapy in Patients With Recurrent Metastatic Nasopharyngeal Carcinoma Who [NCT05717764]Phase 3500 participants (Anticipated)Interventional2023-02-28Not yet recruiting
A Randomized, Double-Blind, Placebo-Controlled Phase 3 Study of Capecitabine and Cisplatin With or Without Ramucirumab as First-line Therapy in Patients With Metastatic Gastric or Gastroesophageal Junction Adenocarcinoma (RAINFALL) [NCT02314117]Phase 3645 participants (Actual)Interventional2015-01-20Completed
A Phase II, Open-Label Study of Capecitabine Versus S-1 as Adjuvant Therapy in Patients With Biliary Tract Carcinoma After Surgical Resection [NCT04856761]160 participants (Anticipated)Observational2020-11-01Recruiting
A Three-arm, Randomized, Open Label, Phase II Study of Everolimus in Combination With Exemestane Versus Everolimus Alone Versus Capecitabine in the Treatment of Postmenopausal Women With Estrogen Receptor Positive, Locally Advanced, Recurrent, or Metastat [NCT01783444]Phase 2309 participants (Actual)Interventional2013-02-26Completed
Steam (Sequencing Triplet With Avastin and Maintenance): FOLFOXIRI/Bevacizumab Regimens (Concurrent and Sequential) vs. FOLFOX/Bevacizumab in First-Line Metastatic Colorectal Cancer [NCT01765582]Phase 2280 participants (Actual)Interventional2013-01-23Terminated
Nab-paclitaxel (Abraxane) Plus Gemcitabine in Subjects With Locally Advanced Pancreatic Cancer (LAPC): An International, Open-label, Multi-center, Phase 2 Study (LAPACT). [NCT02301143]Phase 2107 participants (Actual)Interventional2015-04-21Completed
A Randomised, Multicentre, Open Label, Phase II Study of Prophylactic Octreotide to Prevent or Reduce the Frequency and Severity of Diarrhoea in Subjects Receiving Lapatinib With Capecitabine for the Treatment of Metastatic Breast Cancer [NCT02294786]Phase 262 participants (Actual)Interventional2014-12-17Terminated
A Multicenter, Randomised, Phase III Study of Vinflunine Plus Capecitabine Versus Capecitabine Alone in Patients With Advanced Breast Cancer Previously [NCT01953003]Phase 3112 participants (Actual)Interventional2013-09-30Completed
An Australian Translational Study to Evaluate the Prognostic Role of Inflammatory Markers in Patients With Metastatic Colorectal Cancer Treated With Bevacizumab (Avastin™) [NCT01588990]Phase 4128 participants (Actual)Interventional2012-06-26Completed
A Randomized, Double-Blind, Phase 3 Study of the JAK 1/2 Inhibitor Ruxolitinib or Placebo in Combination With Capecitabine in Subjects With Advanced or Metastatic Adenocarcinoma of the Pancreas Who Have Failed or Are Intolerant to First-Line Chemotherapy [NCT02119663]Phase 386 participants (Actual)Interventional2014-06-30Terminated(stopped due to The safety committee found no safety issues but recommended halting the study based on a lack of efficacy in a similar trial. The sponsor terminated the trial.)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00005908 (4) [back to overview]Overall Clinical Response Rate
NCT00005908 (4) [back to overview]Complementary Deoxyribonucleic Acid (cDNA) Expression
NCT00005908 (4) [back to overview]Number of Participants With Adverse Events
NCT00005908 (4) [back to overview]Number of Participants, e.g. Responders and Non-responders With a Percent Change in Expression Patterns After Chemotherapy With Changes in Expression Patterns After Chemotherapy in Preclinical Models
NCT00009737 (6) [back to overview]Disease-free Survival
NCT00009737 (6) [back to overview]Number of Participants With Abnormalities for Blood Chemistry and Hematological Parameters
NCT00009737 (6) [back to overview]Mean Change From Baseline in Global Health Status at Week 25
NCT00009737 (6) [back to overview]Overall Survival
NCT00009737 (6) [back to overview]Relapse-Free Survival
NCT00009737 (6) [back to overview]Number of Participants With Any Adverse Events and Serious Adverse Events
NCT00022698 (9) [back to overview]Duration of Overall Complete Response
NCT00022698 (9) [back to overview]Duration of Overall Response
NCT00022698 (9) [back to overview]Overall Survival
NCT00022698 (9) [back to overview]Percentage of Participants With One-year Survival
NCT00022698 (9) [back to overview]Time to Disease Progression
NCT00022698 (9) [back to overview]Time To Objective Response
NCT00022698 (9) [back to overview]Time to Treatment Failure
NCT00022698 (9) [back to overview]Number of Participants With Any Adverse Events, Serious Adverse Events and Deaths
NCT00022698 (9) [back to overview]Tumor Response Rate Based on Tumor Measurement as Per Response Evaluation Criteria In Solid Tumors Version 1.0 (RECIST 1.0)
NCT00024102 (3) [back to overview]Relapse-free Survival Rates at 2.4 Years
NCT00024102 (3) [back to overview]Number of Participants With Grade 3, 4 or 5 Adverse Event at Least Possibly Related to Treatment.
NCT00024102 (3) [back to overview]Overall Survival Rate at 2.4 Years
NCT00033540 (5) [back to overview]Overall Survival
NCT00033540 (5) [back to overview]Accrual of Patients With This Disease Site
NCT00033540 (5) [back to overview]Median Survival Time for Participants With Relevant Biologic Markers
NCT00033540 (5) [back to overview]Number of Patients With Grade 3 Through 5 Adverse Events That Are Related to Study Drug
NCT00033540 (5) [back to overview]Response
NCT00050167 (1) [back to overview]Percentage of Participants With Reoccurrence
NCT00068588 (2) [back to overview]Maximum Tolerated Dose Determined by Dose-limiting Toxicities
NCT00068588 (2) [back to overview]Response Rate of a Combination of GTI-2040 and Capecitabine
NCT00069095 (22) [back to overview]PFS by General Approach, Participants With Curative Surgery Not Censored: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]Progression-free Survival (PFS) as Assessed by the Investigator According to Response Evaluation Criteria in Solid Tumors (RECIST) by General Approach (Participants With Curative Surgery Censored): Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]Time to Response as Assessed by the Investigator According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]Time to Response as Assessed by the Investigator According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]Time to Treatment Failure (TTF) as Assessed by the Investigator According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]Time to Treatment Failure as Assessed by the Investigator According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]Overall Survival: Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]Overall Survival: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]PFS (On-treatment Approach): Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]PFS (On-treatment Approach): Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]PFS as Assessed by the Independent Review Committee (IRC) (General Approach, Participants With Curative Surgery Censored) - Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]PFS as Assessed by the Investigator According to Response Evaluation Criteria in Solid Tumors (RECIST) by General Approach (Participants With Curative Surgery Censored) - Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]PFS as Assessed by the Independent Review Committee (IRC) (General Approach, Participants With Curative Surgery Censored) - Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]Duration of Overall Response as Assessed by the Investigator According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]Best Overall Response (BOR) as Assessed by the Investigator According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]Best Overall Response (BOR) as Assessed by the Investigator According to Response Evaluation Criteria in Solid Tumors (RECIST): Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]BOR as Assessed by the IRC According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]BOR as Assessed by the IRC According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]Duration of Complete Response as Assessed by the Investigator According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]Duration of Complete Response as Assessed by the Investigator According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone
NCT00069095 (22) [back to overview]PFS by General Approach, Participants With Curative Surgery Not Censored: Non-inferiority of XELOX Versus FOLFOX-4
NCT00069095 (22) [back to overview]Duration of Overall Response as Assessed by the Investigator According to RECIST: Superiority Analysis of Chemotherapy Plus Bevacizumab Versus Chemotherapy Alone
NCT00069108 (11) [back to overview]Best Overall Response, Investigators' Assessments
NCT00069108 (11) [back to overview]Best Overall Response, Independent Review Committee Assessment
NCT00069108 (11) [back to overview]Time To Treatment Failure
NCT00069108 (11) [back to overview]Progression Free Survival Based on Treatment Analysis- Per Population
NCT00069108 (11) [back to overview]Progression Free Survival Based on Treatment Analysis- Intent To Treat Population
NCT00069108 (11) [back to overview]Overall Survival
NCT00069108 (11) [back to overview]Duration Of Response
NCT00069108 (11) [back to overview]Progression Free Survival
NCT00069108 (11) [back to overview]Time To Response
NCT00069108 (11) [back to overview]Number of Participants With Marked Post-baseline Laboratory Abnormalities by Trial Treatment
NCT00069108 (11) [back to overview]Progression Free Survival Based on Independent Review Committee Assessment
NCT00069121 (7) [back to overview]Relapse-Free Survival (RFS) [Number of Events]
NCT00069121 (7) [back to overview]Overall Survival [Number of Events]
NCT00069121 (7) [back to overview]Number of Participants With at Least One Adverse Event by Most Severe Intensity
NCT00069121 (7) [back to overview]Disease-Free Survival (DFS) [Time to Event]
NCT00069121 (7) [back to overview]Disease-Free Survival (DFS) [Number of Events]
NCT00069121 (7) [back to overview]Relapse-Free Survival (RFS) [Time to Event]
NCT00069121 (7) [back to overview]Overall Survival [Time to Event]
NCT00077857 (7) [back to overview]Duration of Overall Response
NCT00077857 (7) [back to overview]Overall Survival
NCT00077857 (7) [back to overview]Percentage of Participants With Best Overall Response Being Complete Response (CR) or Partial Response (PR)
NCT00077857 (7) [back to overview]Time to Progression of Disease or Death
NCT00077857 (7) [back to overview]Time to Treatment Failure
NCT00077857 (7) [back to overview]Number of Participants With Adverse Events and Serious Adverse Events
NCT00077857 (7) [back to overview]Time to Overall Response
NCT00080301 (7) [back to overview]Symptom Assessment Score Changes From Baseline for Functional Assessment of Cancer Therapy-Breast Symptom Index (FBSI)
NCT00080301 (7) [back to overview]Time to Response Per IRRC
NCT00080301 (7) [back to overview]Progression-free Survival (PFS) Per Independent Radiology Review Committee (IRRC)
NCT00080301 (7) [back to overview]Overall Survival (OS)
NCT00080301 (7) [back to overview]Overall Response Rate (ORR) Per IRRC
NCT00080301 (7) [back to overview]Duration of Response Per IRRC
NCT00080301 (7) [back to overview]Treatment-related Safety Summary
NCT00081289 (18) [back to overview]Pathologic Complete Response Rate
NCT00081289 (18) [back to overview]Second Primary Rate at 4 Years
NCT00081289 (18) [back to overview]Survival Rate at 4 Years
NCT00081289 (18) [back to overview]Change From Baseline in QLQ-C30 Global Health Status Score at Two Years
NCT00081289 (18) [back to overview]Disease-free Survival Rate at 4 Years
NCT00081289 (18) [back to overview]Distant Failure Rate at 4 Years
NCT00081289 (18) [back to overview]Local-regional Failure Rate at 4 Years
NCT00081289 (18) [back to overview]Number of Participants With Grade 3+ Treatment-related Adverse Events
NCT00081289 (18) [back to overview]Change From Baseline in EORTC QLQ-CR38 Gastro-intestinal Symptom Score at Two Years
NCT00081289 (18) [back to overview]Change From Baseline in EORTC QLQ-CR38 Gastro-intestinal Symptom Score at Completion of Chemoradiation
NCT00081289 (18) [back to overview]Change From Baseline in EORTC QLQ-CR38 Defecation Symptom Score at Two Years
NCT00081289 (18) [back to overview]Change From Baseline in EORTC QLQ-CR38 Defecation Symptom Score at Post-operative Chemotherapy
NCT00081289 (18) [back to overview]Change From Baseline in EORTC QLQ-CR38 Defecation Symptom Score at Completion of Chemoradiation
NCT00081289 (18) [back to overview]Number of Participants With Grade 3+ Treatment-related Adverse Events Postoperatively
NCT00081289 (18) [back to overview]Number of Participants With Grade 3+ Treatment-related Adverse Events Preoperatively
NCT00081289 (18) [back to overview]Change From Baseline in EORTC QLQ-CR38 Gastro-intestinal Symptom Score at Completion of Post-operative Chemotherapy
NCT00081289 (18) [back to overview]Change From Baseline in QLQ-C30 Global Health Status Score at Completion of Chemoradiation
NCT00081289 (18) [back to overview]Change From Baseline in QLQ-C30 Global Health Status Score at Completion of Post-operative Chemotherapy
NCT00082433 (7) [back to overview]Symptom Assessment Score Changes From Baseline for Functional Assessment of Cancer Therapy-Breast Symptom Index (FBSI)
NCT00082433 (7) [back to overview]Treatment-Related Safety Summary
NCT00082433 (7) [back to overview]Time to Response
NCT00082433 (7) [back to overview]Response Rate (RR)
NCT00082433 (7) [back to overview]Progression-Free Survival (PFS)
NCT00082433 (7) [back to overview]Overall Survival (OS)
NCT00082433 (7) [back to overview]Duration of Response
NCT00084617 (3) [back to overview]Response Rates (RR) in Metastatic Gastric/GE Junction Tumors
NCT00084617 (3) [back to overview]Overall Survival
NCT00084617 (3) [back to overview]Complete Response (CR) and Partial Response (PR) Duration
NCT00087152 (3) [back to overview]Progression-free Survival at 6 Months
NCT00087152 (3) [back to overview]Number of Patients With Grade 3 Through 5 Adverse Events That Are Related to Study Drug
NCT00087152 (3) [back to overview]Confirmed Response Rate (Complete and Partial)
NCT00089479 (10) [back to overview]Overall Survival [Number of Events]
NCT00089479 (10) [back to overview]Disease Free Survival Including New Primary Breast Cancer as Event [Number of Events]
NCT00089479 (10) [back to overview]Disease Free Survival Including Any New Cancer as Event [Number of Events]
NCT00089479 (10) [back to overview]Breast Cancer Free Survival [Time to Event]
NCT00089479 (10) [back to overview]Breast Cancer Free Survival [Number of Events]
NCT00089479 (10) [back to overview]Disease Free Survival [Number of Events]
NCT00089479 (10) [back to overview]Overall Survival [Time to Event]
NCT00089479 (10) [back to overview]Disease Free Survival Including New Primary Breast Cancer as Event [Time to Event
NCT00089479 (10) [back to overview]Disease Free Survival [Time to Event]
NCT00089479 (10) [back to overview]Disease Free Survival Including Any New Cancer as Event [Time to Event]
NCT00093379 (3) [back to overview]Number of Participants With Complete Response at 2 Years
NCT00093379 (3) [back to overview]Number of Participants With 2-year Colostomy-Free Survival
NCT00093379 (3) [back to overview]2 Year Failure Free Survival
NCT00093808 (4) [back to overview]Overall Survival as Assessed by Time
NCT00093808 (4) [back to overview]Time to Progression (TTP)
NCT00093808 (4) [back to overview]Duration of Response as Measured by RECIST Criteria
NCT00093808 (4) [back to overview]Confirmed Response Rate
NCT00100815 (5) [back to overview]Percentage of Participants With Improved Quality of Life
NCT00100815 (5) [back to overview]Clinical Response
NCT00100815 (5) [back to overview]Overall Survival
NCT00100815 (5) [back to overview]Percentage of Participants With Grades 3-5 Treatment Related Toxicities
NCT00100815 (5) [back to overview]Progression-free Survival
NCT00101686 (14) [back to overview]Survival Time: Celecoxib and Placebo
NCT00101686 (14) [back to overview]1 Year Survival: FOLFIRI, mIFL and CapeIRI
NCT00101686 (14) [back to overview]Time to Progression: Bevacizumab With FOLFIRI, mIFL
NCT00101686 (14) [back to overview]Survival Time at Last Follow-Up Visit: Bevacizumab With FOLFIRI, mIFL
NCT00101686 (14) [back to overview]Overall Response: FOLFIRI, mIFL and CapeIRI
NCT00101686 (14) [back to overview]Overall Response: Celecoxib and Placebo
NCT00101686 (14) [back to overview]Overall Response: Bevacizumab With FOLFIRI, mIFL
NCT00101686 (14) [back to overview]Dose Reduction Due to Treatment Emergent Adverse Events
NCT00101686 (14) [back to overview]Time to Progression: FOLFIRI, mIFL and CapeIRI
NCT00101686 (14) [back to overview]Overall Relative Dose Intensity of Irinotecan
NCT00101686 (14) [back to overview]1 Year Survival: Bevacizumab With FOLFIRI, mIFL
NCT00101686 (14) [back to overview]Survival Time: FOLFIRI, mIFL and CapeIRI
NCT00101686 (14) [back to overview]Time to Progression : Celecoxib and Placebo
NCT00101686 (14) [back to overview]Time to Progression (TTP) at Primary Completion: FOLFIRI and mIFL
NCT00107276 (3) [back to overview]Progression-free Survival and Overall Survival
NCT00107276 (3) [back to overview]Response Rate (Complete and Partial, Confirmed and Unconfirmed)
NCT00107276 (3) [back to overview]Toxicity
NCT00112918 (6) [back to overview]Overall Survival in Stage III Cancer Patients - Time to Event
NCT00112918 (6) [back to overview]Overall Survival in Stage III Cancer Patients - Number of Events: Final Analysis
NCT00112918 (6) [back to overview]Overall Survival in Stage III Cancer Patients - Number of Events
NCT00112918 (6) [back to overview]Disease-free Survival in Stage III Cancer Patients - Number of Events
NCT00112918 (6) [back to overview]Overall Survival in Stage III Cancer Patients - Time to Event: Final Analysis
NCT00112918 (6) [back to overview]Disease-free Survival in Stage III Cancer Patients - Time to Event
NCT00113230 (1) [back to overview]Pathologic Local Tumor Response
NCT00114231 (5) [back to overview]Morbidity and Mortality Rate
NCT00114231 (5) [back to overview]Rate of Pathologic Complete Response of the Primary Tumor
NCT00114231 (5) [back to overview]R0 Resection Rate (Negative Margin Rate)
NCT00114231 (5) [back to overview]3-Year Disease-free Survival
NCT00114231 (5) [back to overview]Local Recurrence Rate
NCT00118755 (4) [back to overview]Duration of Overall Clinical Response (CR or PR)
NCT00118755 (4) [back to overview]Overall Survival
NCT00118755 (4) [back to overview]Progression-free Survival (PFS)
NCT00118755 (4) [back to overview]Best Overall Clinical Response
NCT00121134 (1) [back to overview]The Completion Rate of 1 Year of Bevacizumab Therapy for All Four Cohorts
NCT00121251 (3) [back to overview]Number of Participants Who Survived (Overall Survival)
NCT00121251 (3) [back to overview]Median Number of Months of Progression Free Survival (PFS)
NCT00121251 (3) [back to overview]Objective Response for BAY 43-9006 in Combination With Gemcitabine and Capecitabine Evaluated by the Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00121836 (4) [back to overview]Number of Subjects With Adverse Events
NCT00121836 (4) [back to overview]Number of Participants With Marked Laboratory Abnormalities
NCT00121836 (4) [back to overview]Overall Survival
NCT00121836 (4) [back to overview]Premature Withdrawal From Study Due to Adverse Events
NCT00127036 (1) [back to overview]Number of Participants With Serious Adverse Events (SAEs)
NCT00127933 (6) [back to overview]Participants With Disease-Free Survival
NCT00127933 (6) [back to overview]Percentage of Participants Assessed for Pathological Complete Response (pCR) Plus Near Complete (npCR) in Primary Breast Tumor at Time of Definitive Surgery
NCT00127933 (6) [back to overview]Percentage of Participants With Complete Pathological Response in the Primary Breast Tumor at the Time of Definitive Surgery
NCT00127933 (6) [back to overview]Percentage of Participants With Overall Clinical Response (Complete Response (CR) Plus Partial Response (PR))
NCT00127933 (6) [back to overview]Percentage of Participants With Local Recurrence
NCT00127933 (6) [back to overview]Participants With Overall Survival
NCT00129935 (4) [back to overview]Quality of Life Questionnaire: Time to Taking Off the Wig
NCT00129935 (4) [back to overview]Number of Participants With Overall Survival (OS) Event
NCT00129935 (4) [back to overview]The Number of Participants Who Experienced Adverse Events (AE)
NCT00129935 (4) [back to overview]Number of Participants With Disease-free Survival (DFS) Event
NCT00130533 (3) [back to overview]Disease Free Survival (DFS) Events
NCT00130533 (3) [back to overview]The Number of Participants Who Experienced Adverse Events (AE)
NCT00130533 (3) [back to overview]Overall Survival (OS) Event
NCT00148122 (3) [back to overview]Frequency of Grade III/IV Toxicities Experienced by Participants
NCT00148122 (3) [back to overview]Probability of Progression Free Survival
NCT00148122 (3) [back to overview]Overall Response Rate at 4 Months
NCT00159432 (2) [back to overview]Median Time for Progression Free Survival
NCT00159432 (2) [back to overview]Number of Participants With Grade 3 or Higher Toxicity
NCT00177255 (2) [back to overview]Overall Survival
NCT00177255 (2) [back to overview]Overall Response Rate
NCT00177307 (4) [back to overview]1-, 2-, and 3-year Overall Survival
NCT00177307 (4) [back to overview]Response Rate (RR)
NCT00177307 (4) [back to overview]Progression Free Survival (PFS)
NCT00177307 (4) [back to overview]Overall Survival
NCT00191152 (13) [back to overview]Summary of Changes in Karnofsky Performance Status (KPS) by Treatment (Crossover Treatment)
NCT00191152 (13) [back to overview]Best Overall Response (Crossover Treatment)
NCT00191152 (13) [back to overview]Time to Disease Progression (Crossover Treatment)
NCT00191152 (13) [back to overview]Progression-Free Survival (Initial Treatment)
NCT00191152 (13) [back to overview]Time to Disease Progression (Initial Treatment)
NCT00191152 (13) [back to overview]Progression-Free Survival (Crossover Treatment)
NCT00191152 (13) [back to overview]Summary of Changes in Karnofsky Performance Status (KPS) by Treatment (Initial Treatment)
NCT00191152 (13) [back to overview]Overall Survival
NCT00191152 (13) [back to overview]Summary of Changes in Rotterdam Symptom Checklist by Treatment (Crossover Treatment)
NCT00191152 (13) [back to overview]Duration of Response (Crossover Treatment)
NCT00191152 (13) [back to overview]Duration of Response (Initial Treatment)
NCT00191152 (13) [back to overview]Best Overall Response (Initial Treatment)
NCT00191152 (13) [back to overview]Summary of Changes in Rotterdam Symptom Checklist (RSCL) by Treatment (Initial Treatment)
NCT00193128 (3) [back to overview]Overall Survival (OS)
NCT00193128 (3) [back to overview]Disease-Free Survival (DFS)
NCT00193128 (3) [back to overview]Pathologic Complete Response Rate (PCRR), the Percentage of Patients Who Have No Evidence of Cancer in Their Surgical Specimen Following Surgery
NCT00193609 (2) [back to overview]Overall Survival
NCT00193609 (2) [back to overview]Progression Free Survival
NCT00194779 (6) [back to overview]Time to Progression
NCT00194779 (6) [back to overview]Combined Rate of Microscopic pCR and Macroscopic Pathologic Complete Response (mCR)
NCT00194779 (6) [back to overview]Relapse Rate in Patients With Operable Breast Cancer Treated With Neoadjuvant Chemotherapy for 12 Weeks Followed by Weekly Paclitaxel for 12 Weeks and Adjuvant Chemotherapy
NCT00194779 (6) [back to overview]Disease-free Survival
NCT00194779 (6) [back to overview]OS in Patients With Operable Breast Cancer Treated With Neoadjuvant Chemotherapy for 12 Weeks Followed Weekly Paclitaxel for 12 Weeks and Adjuvant Chemotherapy With XMN
NCT00194779 (6) [back to overview]Number and Percent of Patients Reporting Grade 2, 3, 4, or Fatal Toxicities of These Regimens, Need for Dose Reduction, or Treatment Interruption or Discontinuation
NCT00194792 (6) [back to overview]Overall Survival
NCT00194792 (6) [back to overview]Quantification of All Grade 2, 3, 4 Adverse Events or Fatal Toxicities
NCT00194792 (6) [back to overview]Number of Participants With Microscopic Pathologic Complete Response and Macroscopic Pathologic Complete Response
NCT00194792 (6) [back to overview]Number of Participants With Clinical Response
NCT00194792 (6) [back to overview]Disease-free Survival
NCT00194792 (6) [back to overview]Number of Participants With Dose Reduction, Treatment Interruption, or Treatment Discontinuation
NCT00201734 (6) [back to overview]Objective Response Rate (ORR) for the Phase II Portion of the Study. CR+PR Per RECIST v1.0 Criteria Using a Single Arm , Two Stage Minimax Design.
NCT00201734 (6) [back to overview]One Year Survival for Patients
NCT00201734 (6) [back to overview]Progression-Free Survival at 6 Months for Patients
NCT00201734 (6) [back to overview]Phase I: To Determine Side Effects
NCT00201734 (6) [back to overview]Maximum Tolerated Dose in Phase I Portion of Study
NCT00201734 (6) [back to overview]Time to Tumor Progression for Patients
NCT00201825 (3) [back to overview]Time to Tumor Progression
NCT00201825 (3) [back to overview]Determine Objective Response Rate
NCT00201825 (3) [back to overview]One Year Survival
NCT00203411 (4) [back to overview]Quality of Life of Patients
NCT00203411 (4) [back to overview]Response Rates
NCT00203411 (4) [back to overview]Time to Disease Progression
NCT00203411 (4) [back to overview]Number of Subjects Requiring Dose Modifications
NCT00209092 (2) [back to overview]Number of Participants With Complete Pathologic Response Rate to Pre-operative Treatment in Arm A (Docetaxel for 4 Cycles Followed by Capecitabine for 4 Cycles) or Arm B (Docetaxel + Capecitabine for 8 Cycles) in Patients With Early Stage Breast Cancer.
NCT00209092 (2) [back to overview]Long Term Follow up Data on Recurrence and Survival
NCT00215644 (5) [back to overview]Overall Survival (OS)
NCT00215644 (5) [back to overview]Duration of Objective Response Assessed by Independent Review Committee
NCT00215644 (5) [back to overview]Percentage of Participants With Objective Response Assessed by Independent Review Committee
NCT00215644 (5) [back to overview]Progression-Free Survival
NCT00215644 (5) [back to overview]Best Overall Change From Baseline in European Organization for Research and Treatment of Cancer Quality-of-Life Questionnaire-Core 30 (EORTC QLQ-C30) Global Health Status (GHS)/Quality of Life (QoL) Score
NCT00216086 (3) [back to overview]Pathological Complete Response (pCR) Rate
NCT00216086 (3) [back to overview]Local and Distant Disease Recurrence Rates
NCT00216086 (3) [back to overview]Disease-Free Survival
NCT00226941 (7) [back to overview]Survival at 5 Years
NCT00226941 (7) [back to overview]Overall Survival (OS)
NCT00226941 (7) [back to overview]Dose-limiting Toxicity (DLT) - Number of Participants Affected
NCT00226941 (7) [back to overview]Dose-limiting Toxicity (DLT) - Number of DLTs by Treatment Group
NCT00226941 (7) [back to overview]Pathologic Response Rate
NCT00226941 (7) [back to overview]Tumor Downstaging at Surgical Resection
NCT00226941 (7) [back to overview]Time-to-Progression (TTP)
NCT00250835 (6) [back to overview]Incidence of Sphincter-sparing Surgery
NCT00250835 (6) [back to overview]Pelvic Local Control Rate
NCT00250835 (6) [back to overview]Progression-free Survival (PFS)
NCT00250835 (6) [back to overview]Toxicity
NCT00250835 (6) [back to overview]Surgical Downstaging Rate
NCT00250835 (6) [back to overview]Pathologic Complete Response (PCR)
NCT00258310 (4) [back to overview]Recurrence-free Survival
NCT00258310 (4) [back to overview]Overall Survival
NCT00258310 (4) [back to overview]Compliance With Treatment .
NCT00258310 (4) [back to overview]Incidence of Second Primary Tumors
NCT00266279 (2) [back to overview]Qualitative and Quantitative Toxicity
NCT00266279 (2) [back to overview]Overall Response Rate
NCT00266799 (5) [back to overview]Overall Survival Time in the PLD and Capecitabine Treatment Groups
NCT00266799 (5) [back to overview]Number of Participants With an Overall Response (Complete Response [CR] + Partial Response [PR]) Between PLD and Capecitabine Treatment Groups
NCT00266799 (5) [back to overview]Quality of Life (QoL) Measured by QoL Questionnaire (European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30) + Subjective Significance Questionnaire (SSQ))
NCT00266799 (5) [back to overview]Time to Disease Progression (TTP) Using Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00266799 (5) [back to overview]Time to Treatment Failure in the PLD and the Capecitabine Treatment Groups
NCT00274768 (6) [back to overview]Adherence and Compliance to Oral Medication Using Electronic Monitoring
NCT00274768 (6) [back to overview]Clinical Benefit as Assessed by Lack of Progression for at Least 24 Weeks
NCT00274768 (6) [back to overview]Response Rate
NCT00274768 (6) [back to overview]Time to Treatment Failure
NCT00274768 (6) [back to overview]Pharmacokinetics of Capecitabine and Metabolites as Assessed by Maximum Plasma Concentration
NCT00274768 (6) [back to overview]Pharmacokinetics of Capecitabine and Metabolites as Assessed by Area Under the Curve (AUC)
NCT00276744 (1) [back to overview]6-month Overall Survival
NCT00278863 (2) [back to overview]Number of Patients With Adverse Events
NCT00278863 (2) [back to overview]Response Rate
NCT00290615 (4) [back to overview]Response Rate (Percentage of Participants With Partial or Complete Response)
NCT00290615 (4) [back to overview]Progression-free Survival
NCT00290615 (4) [back to overview]Overall Survival
NCT00290615 (4) [back to overview]Safety and Tolerability
NCT00290693 (5) [back to overview]Number of Study Participants Experiencing Toxicity After Receiving Protocol Therapy
NCT00290693 (5) [back to overview]Overall Surival (OS)
NCT00290693 (5) [back to overview]Progression-free Survival (PFS)
NCT00290693 (5) [back to overview]Rate of Participants Achieving a 50% or More Reduction in CA 19-9 Levels
NCT00290693 (5) [back to overview]Rate of Participants Achieving Complete Response or Partial Response to Therapy.
NCT00291486 (11) [back to overview]Impact of Capecitabine on 131I-huA33 Clearance (CL) as Measured by Initial and Therapy Dose Clearance (CL)
NCT00291486 (11) [back to overview]Mean Specific Absorbed Dose of 131I-huA33 for Normal Organs Calculated From the Initial Infusion
NCT00291486 (11) [back to overview]Pharmacokinetics (PK) of 131I-huA33 as Measured by Area Under the Serum Concentration Curve Extrapolated to Infinite Time (AUC)
NCT00291486 (11) [back to overview]Pharmacokinetics (PK) of 131I-huA33 as Measured by Clearance (CL)
NCT00291486 (11) [back to overview]Number of Patients With Dose-Limiting Toxicities (DLT)
NCT00291486 (11) [back to overview]Pharmacokinetics (PK) of 131I-huA33 as Measured by Maximum Serum Concentration (Cmax)
NCT00291486 (11) [back to overview]Pharmacokinetics (PK) of 131I-huA33 as Measured by T½α and T½β (Half Lives of the Initial and Terminal Phases of Disposition, Respectively)
NCT00291486 (11) [back to overview]Pharmacokinetics (PK) of 131I-huA33 as Measured by the Volume of the Central Compartment (V1)
NCT00291486 (11) [back to overview]Number of Patients With Human Anti-human Antibodies (HAHA) to 131I-huA33
NCT00291486 (11) [back to overview]Biodistribution of 131I-huA33 Measured by Whole Body Clearance and Normal Organ Clearance Reported as Mean Biological Half-life (T1/2 Biological) After Initial 131I-huA33 Infusion
NCT00291486 (11) [back to overview]Mean Total Tumor Dose of 131I-huA33
NCT00305877 (3) [back to overview]Two-year Overall Survival Rate
NCT00305877 (3) [back to overview]Two-year Disease-free Survival (DFS)
NCT00305877 (3) [back to overview]Proportion of Patients With Specific Protocol Defined Adverse Event at Conclusion of All Therapy
NCT00320749 (3) [back to overview]Common Toxicities
NCT00320749 (3) [back to overview]Maximum Tolerated Dose (MTD)
NCT00320749 (3) [back to overview]Therapeutic Response
NCT00321100 (3) [back to overview]Overall Survival
NCT00321100 (3) [back to overview]Objective Response Rate (ORR)
NCT00321100 (3) [back to overview]Time to Progression (TTP)
NCT00321685 (5) [back to overview]Resection Rate for T4 Rectal Cancers
NCT00321685 (5) [back to overview]Resection Rate for T3 Rectal Cancers
NCT00321685 (5) [back to overview]Pathologic Complete Response Rate
NCT00321685 (5) [back to overview]5-year Overall Survival Rate
NCT00321685 (5) [back to overview]5-year Recurrence-free Survival Rate
NCT00335959 (2) [back to overview]Number of Patients With Grade 3 Through 5 Adverse Events That Are Related to Study Drug
NCT00335959 (2) [back to overview]Pathologic Complete Response
NCT00337103 (14) [back to overview]Progression Free Survival (PFS)
NCT00337103 (14) [back to overview]Overall Survival (OS)
NCT00337103 (14) [back to overview]Objective Response Rate (ORR): Independent Review
NCT00337103 (14) [back to overview]Number of Participants With Treatment-emergent Markedly Abnormal Laboratory Parameter Values
NCT00337103 (14) [back to overview]Number of Participants With Consumption of Analgesics During the Study
NCT00337103 (14) [back to overview]Number of Participants Who Took at Least One Concomitant Medication
NCT00337103 (14) [back to overview]Duration of Response (DOR): Independent Review
NCT00337103 (14) [back to overview]Change From Baseline in Global Health Status/Quality of Life (QoL) Measured by European Organization for the Treatment of Cancer Quality of Life Core Questionnaire Scores Based on Core 30 Items (EORTC-QLQ-C30) at Week 6
NCT00337103 (14) [back to overview]Change From Baseline in Pain Intensity by Visual Analog Scale (VAS) Until 30 Days After the Last Dose of Study Drug
NCT00337103 (14) [back to overview]Change From Baseline in European Organization for the Treatment of Cancer Quality of Life Core Questionnaire Scores Based on Breast Cancer Specific 23 Items (EORTC-QLQ- BR 23) at Week 6
NCT00337103 (14) [back to overview]Plasma Concentrations of Eribulin Mesylate
NCT00337103 (14) [back to overview]Overall Survival Rate
NCT00337103 (14) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)
NCT00337103 (14) [back to overview]Duration of Eribulin Mesylate Exposure
NCT00338039 (2) [back to overview]Median Overall Survival
NCT00338039 (2) [back to overview]Overall Survival Rate
NCT00338988 (1) [back to overview]Number of Participants With Objective Response
NCT00347438 (4) [back to overview]Complete Clinical Response Rate (CCR)
NCT00347438 (4) [back to overview]Complete Pathologic Response Rate (cPR)
NCT00347438 (4) [back to overview]Partial Clinical Response Rate (PR)
NCT00347438 (4) [back to overview]Overall Clinical Response Rate (OCR)
NCT00353262 (14) [back to overview]Maximum Plasma Concentration (Cmax) of Capecitabine and Its Metabolites (5'-DFUR, 5'-DFCR, 5 FU, and FBAL)
NCT00353262 (14) [back to overview]Clearance of Total And Free Platinum
NCT00353262 (14) [back to overview]Marked Laboratory Abnormalities
NCT00353262 (14) [back to overview]Elimination Half-life Period (t1/2 Beta) of Capecitabine and Its Metabolites (5'-DFUR , 5'-DFCR, 5 FU, and FBAL)
NCT00353262 (14) [back to overview]Cmax of Total And Free Platinum
NCT00353262 (14) [back to overview]AUC (0-infinity) of Capecitabine and Its Metabolites (5'-DFCR, 5-FU, and FBAL)
NCT00353262 (14) [back to overview]AUC0-inf for Free Platinum
NCT00353262 (14) [back to overview]AUC0-infinity for Total Platinum
NCT00353262 (14) [back to overview]AUC0-last of Capecitabine and Its Metabolites (5'-DFUR, 5'-DFCR, 5 FU, and FBAL)
NCT00353262 (14) [back to overview]AUC0-last of Total And Free Platinum
NCT00353262 (14) [back to overview]Volume of Distribution at Steady State (VSS) of Total And Free Platinum
NCT00353262 (14) [back to overview]Number Of Participants With Adverse Events (AEs)
NCT00353262 (14) [back to overview]Area Under The Plasma Concentration-Time Curve From Zero To Infinity (AUC0-Inf) of 5'-Deoxy-5-fluorouridine 5'-(DFUR)
NCT00353262 (14) [back to overview]T1/2 Beta of Total And Free Platinum
NCT00354224 (1) [back to overview]Number of Adverse Events
NCT00354601 (1) [back to overview]Number of Participants With Grade 3 or Higher Toxicity
NCT00354887 (1) [back to overview]Number of Participants With Overall Response
NCT00365417 (8) [back to overview]Number of Patients With at Least One Surgical Complications (Wound Dehiscence, Infection, Seroma, or Hematoma).
NCT00365417 (8) [back to overview]Clinical Response Rate (cRR) of the Sequential Regimen
NCT00365417 (8) [back to overview]Cardiac Events
NCT00365417 (8) [back to overview]pCR in the Breast and Nodes
NCT00365417 (8) [back to overview]Progression-free Survival
NCT00365417 (8) [back to overview]Overall Survival
NCT00365417 (8) [back to overview]Pathologic Complete Response (pCR) in the Breast
NCT00365417 (8) [back to overview]Reported Adverse Events
NCT00373113 (5) [back to overview]Time to Tumor Progression (TTP)
NCT00373113 (5) [back to overview]Number of Participants With Overall Response (OR)
NCT00373113 (5) [back to overview]Overall Survival (OS)
NCT00373113 (5) [back to overview]Progression-Free Survival (PFS)
NCT00373113 (5) [back to overview]Duration of Response (DR)
NCT00382720 (3) [back to overview]Overall Survival (OS)
NCT00382720 (3) [back to overview]Time to Progression
NCT00382720 (3) [back to overview]Best Overall Response Rate (ORR)
NCT00398320 (5) [back to overview]12-month Progression Free Survival (PFS)
NCT00398320 (5) [back to overview]Overall Survival (OS)
NCT00398320 (5) [back to overview]Number of Patients Who Experienced Treatment-related Grade 3 or Higher Adverse Events by CTCAE Version 3.0
NCT00398320 (5) [back to overview]Biochemical Markers
NCT00398320 (5) [back to overview]Response Rates
NCT00398398 (4) [back to overview]Progression-free Survival
NCT00398398 (4) [back to overview]Toxicity Profile
NCT00398398 (4) [back to overview]Overall Survival
NCT00398398 (4) [back to overview]Overall Response Rate
NCT00399035 (7) [back to overview]Rate of Resection of Liver Metastases
NCT00399035 (7) [back to overview]Time to Wound Healing Complications
NCT00399035 (7) [back to overview]Overall Survival
NCT00399035 (7) [back to overview]Overall Response Rate
NCT00399035 (7) [back to overview]Progression-free Survival
NCT00399035 (7) [back to overview]Duration of Response
NCT00399035 (7) [back to overview]Best Percentage Change in Tumour Size
NCT00408408 (9) [back to overview]Toxicities Including Events Other Than Congestive Heart Failure, of Chemotherapy Alone, Bevacizumab With Chemotherapy, and Bevacizumab Alone
NCT00408408 (9) [back to overview]Clinical Complete Resonse: cCR as Assessed by Physical Exam at the Completion of the Sequential Chemotherapy Regimens
NCT00408408 (9) [back to overview]Clinical Complete Response (cCR) Following Docetaxel Alone, Docetaxel/Capecitabine, and Docetaxel/Gemcitabine Hydrochloride, With or Without Bevacizumab, as Assessed by Physical Exam at Completion of Therapy
NCT00408408 (9) [back to overview]Clinical Overall Response: cOR as Assessed by Physical Exam at the Completion of the Sequential Chemotherapy Regimens
NCT00408408 (9) [back to overview]Pathologic Complete Response (pCR) of the Primary Tumor in the Breast
NCT00408408 (9) [back to overview]pCR in the Breast and Nodes
NCT00408408 (9) [back to overview]Clinical Overall Response (cOR) Following Docetaxel Alone, Docetaxel/Capecitabine, and Docetaxel/Gemcitabine Hydrochloride, With or Without Bevacizumab, as Assessed by Physical Exam at the Completion of the Docetaxel-based Portion of Chemotherapy
NCT00408408 (9) [back to overview]Disease-free Survival (DFS)
NCT00408408 (9) [back to overview]Surgical Complication
NCT00408564 (4) [back to overview]Number of Participants With Grade 3-4 Adverse Events Reported
NCT00408564 (4) [back to overview]Response Rate
NCT00408564 (4) [back to overview]Progression-free Survival at 6 Months
NCT00408564 (4) [back to overview]Overall Survival
NCT00411762 (2) [back to overview]Median Overall Survival
NCT00411762 (2) [back to overview]Median Progression Free Survival
NCT00414271 (4) [back to overview]Feasibility and Safety of Pre-operative Chemotherapy in Locally Advanced Gastric Cancer as Assessed by Number of Participants Who Experienced Adverse Events Grade 3 or Higher as Defined by CTCAE.
NCT00414271 (4) [back to overview]Overall Survival
NCT00414271 (4) [back to overview]Progression-free Survival as Measured by Number of Participants Without Disease Progression.
NCT00414271 (4) [back to overview]Number of Participants With Pathological Response
NCT00416494 (5) [back to overview]Time to Progression
NCT00416494 (5) [back to overview]Safety and Tolerability
NCT00416494 (5) [back to overview]Overall Survival
NCT00416494 (5) [back to overview]Disease Free Survival
NCT00416494 (5) [back to overview]Response Rate (Percentage of Participants With Partial or Complete Response)
NCT00418028 (7) [back to overview]Response Rate
NCT00418028 (7) [back to overview]Response Duration
NCT00418028 (7) [back to overview]Progression Free Survival
NCT00418028 (7) [back to overview]Overall Survival
NCT00418028 (7) [back to overview]Time to Progression
NCT00418028 (7) [back to overview]Time to Treatment Failure
NCT00418028 (7) [back to overview]Clinical Benefit
NCT00433550 (5) [back to overview]Duration of Response
NCT00433550 (5) [back to overview]Confirmed Tumor Response Rate (Proportion of Participants With Complete Response)
NCT00433550 (5) [back to overview]Time to Treatment Failure
NCT00433550 (5) [back to overview]Progression Free Survival
NCT00433550 (5) [back to overview]Overall Survival
NCT00435409 (5) [back to overview]Overall Survival (OS)
NCT00435409 (5) [back to overview]Duration of Response (DR)
NCT00435409 (5) [back to overview]Percent Chance of Participant Survival
NCT00435409 (5) [back to overview]Percentage of Participants With Objective Response (OR)
NCT00435409 (5) [back to overview]Progression Free Survival (PFS)
NCT00437073 (2) [back to overview]Number of Participants With the Indicated Central Nervous System (CNS) Objective Response (OR)
NCT00437073 (2) [back to overview]Number of Participants With the Indicated CNS Responses
NCT00437294 (8) [back to overview]Pharmacokinetics: Area Under the Concentration Versus Time Curve During One Dosing Interval at Steady State
NCT00437294 (8) [back to overview]Pharmacology Toxicity and Adverse Events (AEs)
NCT00437294 (8) [back to overview]Duration of Response (DOR)
NCT00437294 (8) [back to overview]Pharmacokinetics: Maximum Observed Concentration (Cmax) of Capecitabine
NCT00437294 (8) [back to overview]Overall Survival (OS)
NCT00437294 (8) [back to overview]Percentage of Participants With Complete Response (CR) or Partial Response (PR) (Objective Response Rate)
NCT00437294 (8) [back to overview]Progression Free Survival (PFS)
NCT00437294 (8) [back to overview]Pharmacokinetics: Area Under the Concentration Curve Versus Time From Time 0 to Last Quantifiable Value (AUC0-tlast) of Capecitabine
NCT00438100 (1) [back to overview]Progression Free Survival
NCT00438256 (7) [back to overview]Median Progression Free Survival
NCT00438256 (7) [back to overview]30-Day Post Operative Mortality
NCT00438256 (7) [back to overview]Number of Participants With Dose Limiting Toxicities in the 5 Radiation Sessions in One Week Arm
NCT00438256 (7) [back to overview]Number of Participants With a Pathological Complete Response
NCT00438256 (7) [back to overview]Number of Participants With Grade 3 or Greater Toxicity in Phase II
NCT00438256 (7) [back to overview]Number of Participants With Surgical Morbidity
NCT00438256 (7) [back to overview]Number of Participants With Treatment Related Serious Adverse Events
NCT00444678 (4) [back to overview]Toxicity Rates
NCT00444678 (4) [back to overview]Time to Progression
NCT00444678 (4) [back to overview]Survival
NCT00444678 (4) [back to overview]Response Rate for the Combination Treatment
NCT00446290 (1) [back to overview]Number of Participants With DLTs
NCT00447330 (4) [back to overview]Median Progression-Free Survival (PFS)
NCT00447330 (4) [back to overview]Response Rate
NCT00447330 (4) [back to overview]To Assess the Safety and Tolerability of the Combination of Bevacizumab, Oxaliplatin and Capecitabine in Patients With Previously Untreated Metastatic Esophagogastric Adenocarcinoma
NCT00447330 (4) [back to overview]Median Survival
NCT00452673 (6) [back to overview]Objective Response Rate (ORR) and Disease Control Rate - Efficacy Evaluable Population
NCT00452673 (6) [back to overview]Number of Participants With Dose Limiting Toxicities Per Dose Level - Safety Population
NCT00452673 (6) [back to overview]Number of Participants On-study With Grade 3 - 4 Chemistry Laboratory Values in Those Participants With a Baseline Laboratory Value of Grade 0 - Safety Population
NCT00452673 (6) [back to overview]Number of Participants With Overall Response to Tumor - Efficacy Evaluable Population
NCT00452673 (6) [back to overview]Number of Participants With Deaths, Serious Adverse Events, Adverse Events, Adverse Events Leading to Discontinuation and Treatment-related Adverse Events - Safety Population
NCT00452673 (6) [back to overview]Number of Participants On-Study With Grade 3 - 4 Hematology Laboratory Test Values in Those Participants With a Baseline Laboratory Value of Grade 0 - Safety Population
NCT00454636 (6) [back to overview]Time to Response
NCT00454636 (6) [back to overview]Progression-Free Survival (PFS)
NCT00454636 (6) [back to overview]Percentage of Participants With Grade 3 Hand-Foot Syndrome (HFS)
NCT00454636 (6) [back to overview]Overall Survival (OS)
NCT00454636 (6) [back to overview]Duration of Response
NCT00454636 (6) [back to overview]Overall Response Rate (ORR)
NCT00454649 (34) [back to overview]Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Carboplatin
NCT00454649 (34) [back to overview]Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Docetaxel
NCT00454649 (34) [back to overview]Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Gemcitabine
NCT00454649 (34) [back to overview]Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Paclitaxel
NCT00454649 (34) [back to overview]Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Pemetrexed
NCT00454649 (34) [back to overview]Area Under the Curve From Time Zero to Time 24 Hours [AUC (0-24)] for Axitinib (AG-013736)
NCT00454649 (34) [back to overview]Area Under the Curve From Time Zero to Time 24 Hours [AUC (0-24)] for Capecitabine
NCT00454649 (34) [back to overview]Area Under the Curve From Time Zero to Time 8 Hours [AUC (0-8)] for Cisplatin
NCT00454649 (34) [back to overview]Maximum Observed Plasma Concentration (Cmax) for Axitinib (AG-013736)
NCT00454649 (34) [back to overview]Maximum Observed Plasma Concentration (Cmax) for Capecitabine
NCT00454649 (34) [back to overview]Maximum Observed Plasma Concentration (Cmax) for Carboplatin
NCT00454649 (34) [back to overview]Maximum Observed Plasma Concentration (Cmax) for Cisplatin
NCT00454649 (34) [back to overview]Maximum Observed Plasma Concentration (Cmax) for Docetaxel
NCT00454649 (34) [back to overview]Maximum Observed Plasma Concentration (Cmax) for Gemcitabine
NCT00454649 (34) [back to overview]Maximum Observed Plasma Concentration (Cmax) for Paclitaxel
NCT00454649 (34) [back to overview]Maximum Observed Plasma Concentration (Cmax) for Pemetrexed
NCT00454649 (34) [back to overview]Maximum Tolerated Dose (MTD) of Axitinib (AG-013736) in Combination With Chemotherapy
NCT00454649 (34) [back to overview]Percentage of Participants With Objective Response
NCT00454649 (34) [back to overview]Plasma Clearance (CL) for Carboplatin
NCT00454649 (34) [back to overview]Plasma Clearance (CL) for Cisplatin
NCT00454649 (34) [back to overview]Plasma Clearance (CL) for Docetaxel
NCT00454649 (34) [back to overview]Plasma Clearance (CL) for Gemcitabine
NCT00454649 (34) [back to overview]Plasma Decay Half Life (t1/2) for Paclitaxel
NCT00454649 (34) [back to overview]Plasma Decay Half Life (t1/2) for Pemetrexed
NCT00454649 (34) [back to overview]Plasma Clearance (CL) for Pemetrexed
NCT00454649 (34) [back to overview]Plasma Decay Half Life (t1/2) for Axitinib (AG-013736)
NCT00454649 (34) [back to overview]Plasma Decay Half Life (t1/2) for Capecitabine
NCT00454649 (34) [back to overview]Plasma Decay Half Life (t1/2) for Carboplatin
NCT00454649 (34) [back to overview]Plasma Decay Half Life (t1/2) for Cisplatin
NCT00454649 (34) [back to overview]Plasma Decay Half Life (t1/2) for Docetaxel
NCT00454649 (34) [back to overview]Plasma Decay Half Life (t1/2) for Gemcitabine
NCT00454649 (34) [back to overview]Apparent Oral Clearance (CL/F) for Axitinib (AG-013736)
NCT00454649 (34) [back to overview]Apparent Oral Clearance (CL/F) for Capecitabine
NCT00454649 (34) [back to overview]Plasma Clearance (CL) for Paclitaxel
NCT00462865 (2) [back to overview]Number of Participants With Recurrent Disease
NCT00462865 (2) [back to overview]Toxicity Related to Treatment
NCT00468585 (1) [back to overview]Overall Objective Response
NCT00470184 (4) [back to overview]Overall Response Rate (Complete and Partial Response) as Measured by RECIST Criteria After Course 1
NCT00470184 (4) [back to overview]Quality of Life Improved Rate
NCT00470184 (4) [back to overview]Complete Response
NCT00470184 (4) [back to overview]Median Time to Progression
NCT00477464 (20) [back to overview]Trough Concentration of Lapatinib
NCT00477464 (20) [back to overview]6-Month Progression-free Survival (Independent Reviewer-assessed)
NCT00477464 (20) [back to overview]Area Under the Plasma Concentration-time Curve From Zero to 24 Hours AUC0-24 of Lapatinib
NCT00477464 (20) [back to overview]Area Under the Plasma Concentration-time Curve Within the Dosing Interval AUC0-tau of Lapatinib
NCT00477464 (20) [back to overview]Clinical Benefit Response (Independent Reviewer-assessed)
NCT00477464 (20) [back to overview]Duration of Response (Independent Reviewer-assessed)
NCT00477464 (20) [back to overview]Maximum Plasma Concentration (Cmax) of Lapatinib
NCT00477464 (20) [back to overview]Objective Response (Independent Reviewer-assessed)
NCT00477464 (20) [back to overview]Overall Survival (Independent Reviewer-assessed)
NCT00477464 (20) [back to overview]Progression-free Survival (PFS) (Independent Reviewer-assessed)
NCT00477464 (20) [back to overview]Terminal Elimination Half-life (t1/2) of Lapatinib
NCT00477464 (20) [back to overview]Time to Maximum Plasma Concentration (Tmax) of Lapatinib
NCT00477464 (20) [back to overview]Time to Progression (Independent Reviewer-assessed)
NCT00477464 (20) [back to overview]Time to Response (Independent Reviewer-assessed)
NCT00477464 (20) [back to overview]Area Under the Plasma Concentration-time Curve From Zero to 12 Hours (AUC0-12) of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)
NCT00477464 (20) [back to overview]AUC0-tau of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)
NCT00477464 (20) [back to overview]Cmax of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)
NCT00477464 (20) [back to overview]t1/2 of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)
NCT00477464 (20) [back to overview]Tmax of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)
NCT00477464 (20) [back to overview]Trough Concentration of Capecitabine, 5-FU, and FBAL
NCT00479856 (1) [back to overview]Overall Tumor Response
NCT00483405 (4) [back to overview]Time to Progression
NCT00483405 (4) [back to overview]Disease Response Rate
NCT00483405 (4) [back to overview]Number of Subjects Experiencing Adverse Events
NCT00483405 (4) [back to overview]Overall Survival
NCT00484939 (8) [back to overview]Duration of Follow-up
NCT00484939 (8) [back to overview]Duration of Response
NCT00484939 (8) [back to overview]Time to Response
NCT00484939 (8) [back to overview]Progression-free Survival
NCT00484939 (8) [back to overview]Percentage of Participants Requiring Additional Treatment for Malignancy
NCT00484939 (8) [back to overview]Overall Survival
NCT00484939 (8) [back to overview]Best Overall Response (BOR)
NCT00484939 (8) [back to overview]Eastern Cooperative Oncology Group (ECOG) Performance Status
NCT00493636 (5) [back to overview]Progression Free Survival
NCT00493636 (5) [back to overview]Overall Survival
NCT00493636 (5) [back to overview]Overall Response Rate
NCT00493636 (5) [back to overview]Duration of Overall Response
NCT00493636 (5) [back to overview]Time to Progression
NCT00496366 (2) [back to overview]-Determine the Clinical Benefit Rate (Complete Response, Partial Response, or Stable Disease for at Least 6 Months) of Capecitabine and Lapatinib. -Determine Time to Disease Progression After Treatment With Capecitabine and Lapatinib. -Evaluate Overall
NCT00496366 (2) [back to overview]Determine the Response Rate (as Determined by RECIST Criteria) of Capecitabine and Lapatinib as First-line Therapy in Patients With Advanced or Metastatic Breast Cancer That Overexpress HER2.
NCT00496587 (3) [back to overview]Time to Treatment Failure (TTF)
NCT00496587 (3) [back to overview]Objective Response Rate (ORR)
NCT00496587 (3) [back to overview]Progression Free Survival (PFS)
NCT00502671 (2) [back to overview]Percentage of Participants With an Adverse Event (AE), Serious AE, or Death Due to an AE
NCT00502671 (2) [back to overview]Percentage of Participants With Early Withdrawal or Discontinuation Due to an AE
NCT00504660 (2) [back to overview]6 Month Progression-free Survival for Participants With Glioblastoma
NCT00504660 (2) [back to overview]12 Month-progression-free Survival for Participants With Anaplastic Tumors
NCT00508274 (7) [back to overview]Number of Participants With Central Nervous System (CNS) as First Site of Relapse
NCT00508274 (7) [back to overview]All Collected Deaths
NCT00508274 (7) [back to overview]Time to Response (TTR)
NCT00508274 (7) [back to overview]Six Months Progression-Free Survival
NCT00508274 (7) [back to overview]Progression-Free Survival (PFS)
NCT00508274 (7) [back to overview]Duration of Response (DOR)
NCT00508274 (7) [back to overview]Clinical Benefit Rate (CBR)
NCT00523640 (3) [back to overview]Progression-free Survival
NCT00523640 (3) [back to overview]Overall Survival
NCT00523640 (3) [back to overview]Objective Response Rate
NCT00526669 (26) [back to overview]PFS
NCT00526669 (26) [back to overview]Response Rate (Measured as the Percentage of Participants With Response [Complete Response or Partial Response])
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Creatinine at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Potassium at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as Any Grade Increase [AGI], Increase to Grade 3 [ItoG3], and Increase to Grade 4 [ItoG4]) in Toxicity Grades for Albumin at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Lymphocytes at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Magnesium at the Indicated Time Points
NCT00526669 (26) [back to overview]Duration of Response
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Platelet Count at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Sodium at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Total Bilirubin at the Indicated Time Points
NCT00526669 (26) [back to overview]Time to Progression (All Deaths Are Treated as Competing Risk)
NCT00526669 (26) [back to overview]Time to Progression (All Deaths Due to Non-PD Are Treated as Competing Risk)
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Total Neutrophils at the Indicated Time Points
NCT00526669 (26) [back to overview]Overall Survival (OS)
NCT00526669 (26) [back to overview]Time to Response
NCT00526669 (26) [back to overview]Change From Start of Run-in Period in Biomarker Expression Levels at Day 0
NCT00526669 (26) [back to overview]Number of Participants in the Indicated Categories for Best Overall Response (BOR)
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4 ) in Toxicity Grades for Alanine Aminotransferase (ALT) at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Alkaline Phosphatase (ALP) at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Aspartate Aminotransferase (AST) at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Calcium at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Glucose at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Hemoglobin at the Indicated Time Points
NCT00526669 (26) [back to overview]Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for White Blood Cell (WBC) Count at the Indicated Time Points
NCT00526669 (26) [back to overview]Percentage of Participants (Par.) With 5-month Progression-free Survival (PFS)
NCT00532948 (8) [back to overview]Number of Participants With Baseline Shift From Normal to Low or High in Blood Chemistry Parameters
NCT00532948 (8) [back to overview]Number of Participants With Baseline Shift From Normal to Low or High in Hematology Parameters
NCT00532948 (8) [back to overview]The Area Under the Plasma Concentration-time Curve From Time of Dosing to the Last Measurable Concentration (AUClast) of Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR, 5-FU and FBAL)
NCT00532948 (8) [back to overview]Time to Maximum Plasma Concentration (Tmax) of Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR, 5-FU and FBAL)
NCT00532948 (8) [back to overview]Dose Limiting Toxicities (DLTs)
NCT00532948 (8) [back to overview]Maximum Tolerated Dose (MTD) of Capecitabine.
NCT00532948 (8) [back to overview]Number of Participants With Adverse Events (AE)
NCT00532948 (8) [back to overview]Maximum Observed Plasma Concentration (Cmax) of Capecitabine and Its Metabolites (5'-Deoxy-5-Fluorocytidine [5'-DFCR], 5'-Deoxy-5-Fluorouridine [5'-DFUR], 5-Fluorouracil [5-FU] and Alpha-fluoro-beta-alanine [FBAL])
NCT00534417 (9) [back to overview]Patients Experiencing Severe Symptom Burden (Physical Symptoms)
NCT00534417 (9) [back to overview]Patients Experiencing Severe Symptom Burden (Psychiatric Symptoms)
NCT00534417 (9) [back to overview]Patients Experiencing Severe Symptom Burden (Physical Functioning)
NCT00534417 (9) [back to overview]Best Overall Response
NCT00534417 (9) [back to overview]Time to Progression (TTP)
NCT00534417 (9) [back to overview]Clinical Benefit Rate
NCT00534417 (9) [back to overview]Progression-free Survival (PFS)
NCT00534417 (9) [back to overview]Overall Survival (OS)
NCT00534417 (9) [back to overview]Overall Response Rate
NCT00536809 (1) [back to overview]Overall Response in Phase II
NCT00538291 (1) [back to overview]Response Rate
NCT00546364 (8) [back to overview]Median Number of Treatment Cycles
NCT00546364 (8) [back to overview]Percentage of Nontriple-negative (NTN) Participants With Best Response to Treatment of Complete or Partial Per Cohort
NCT00546364 (8) [back to overview]Percentage of Participants With Best Response to Treatment of Complete or Partial
NCT00546364 (8) [back to overview]Percentage of Triple-negative (TN) Participants With Best Response to Treatment of Complete or Partial
NCT00546364 (8) [back to overview]Number of Participants With Abnormalities in Hematology Laboratory Results by Worst Common Terminology Criteria (CTC) Grade
NCT00546364 (8) [back to overview]Number of Participants With Best Tumor Response as Assessed With Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00546364 (8) [back to overview]Number of Participants With Death, Adverse Events (AEs), Drug-related AEs, Serious AEs (SAEs), Drug-related SAEs, AEs Leading to Discontinuation (AEDs), Drug-related AEDs, and Drug-related Peripheral Neuropathy
NCT00546364 (8) [back to overview]Number of Participants With Abnormalities in Serum Chemistry Laboratory Results
NCT00548548 (8) [back to overview]Overall Survival
NCT00548548 (8) [back to overview]Participants With Adverse Events
NCT00548548 (8) [back to overview]Progression-free Survival
NCT00548548 (8) [back to overview]Progression-free Survival During First-line Therapy
NCT00548548 (8) [back to overview]Participants With Disease Control
NCT00548548 (8) [back to overview]Duration of Response
NCT00548548 (8) [back to overview]Time to Disease Progression
NCT00548548 (8) [back to overview]Participants With a Best Overall Response of Complete or Partial Response
NCT00551213 (6) [back to overview]Number of Participants Who Experienced One or More Adverse Events (AEs)
NCT00551213 (6) [back to overview]Number of Participants Who Discontinued Study Drug Due to an AE
NCT00551213 (6) [back to overview]Best Overall Tumor Response Per Central Review
NCT00551213 (6) [back to overview]Change From Baseline in Tumor Growth Rate
NCT00551213 (6) [back to overview]Best Overall Tumor Response Per Investigator Review
NCT00551213 (6) [back to overview]Number of Participants With a >20% Decrease in Positron Emission Tomography (PET)-Assessed Tumor Glucose Metabolism: Fluorodeoxyglucose (FDG) Standardized Uptake Value (SUV) in the Target Lesion
NCT00555620 (30) [back to overview]Progression-Free Survival (PFS)
NCT00555620 (30) [back to overview]Percentage of Participants With Objective Response
NCT00555620 (30) [back to overview]Number of Participants With First-cycle Dose Limiting Toxicities (DLTs)
NCT00555620 (30) [back to overview]Duration of Response (DR)
NCT00555620 (30) [back to overview]Tmax for CAP
NCT00555620 (30) [back to overview]Tmax for 5'DFUR
NCT00555620 (30) [back to overview]Tmax for 5'DFCR
NCT00555620 (30) [back to overview]Tmax for 5-FU
NCT00555620 (30) [back to overview]Time to Reach Maximum Observed Plasma Concentration (Tmax) for SU, SU012662, and Total Drug (SU + SU012662)
NCT00555620 (30) [back to overview]Minimum Observed Plasma Trough Concentration (Cmin) of SU, SU012662, and Total Drug (SU + SU012662)
NCT00555620 (30) [back to overview]t1/2 for CAP
NCT00555620 (30) [back to overview]t1/2 for 5'DFUR
NCT00555620 (30) [back to overview]Cmax of 5'-Deoxy-5-fluorouridine (Metabolite of CAP, 5'DFUR)
NCT00555620 (30) [back to overview]Cmax of 5'-Deoxy-5-fluorocytidine (Metabolite of CAP, 5'DFCR)
NCT00555620 (30) [back to overview]Cmax of 5-fluorouracil (Metabolite of CAP, 5-FU)
NCT00555620 (30) [back to overview]AUClast for 5'DFUR
NCT00555620 (30) [back to overview]Cmin of 5-FU
NCT00555620 (30) [back to overview]Cmin of 5'DFCR
NCT00555620 (30) [back to overview]Cmin of 5'DFUR
NCT00555620 (30) [back to overview]Cmin of CAP
NCT00555620 (30) [back to overview]t1/2 for 5-FU
NCT00555620 (30) [back to overview]t1/2 for 5'DFCR
NCT00555620 (30) [back to overview]Cmax of CAP
NCT00555620 (30) [back to overview]Area Under the Curve From Time Zero to Last Quantifiable Concentration (AUClast) for CAP
NCT00555620 (30) [back to overview]Maximum Observed Plasma Concentration (Cmax) of SU, SU012662 (Metabolite of SU), and Total Drug (SU + SU012662)
NCT00555620 (30) [back to overview]AUClast for 5'DFCR
NCT00555620 (30) [back to overview]AUClast for 5-FU
NCT00555620 (30) [back to overview]Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0 - ∞)]: CAP, 5'DFCR, 5'DFUR, and 5-FU
NCT00555620 (30) [back to overview]Area Under the Curve From Time Zero to 12 Hours [AUC (12)] for CAP, 5'DFCR, 5'DFUR, and 5-FU
NCT00555620 (30) [back to overview]Area Under the Curve From Time 0 to 24 Hours Postdose (AUC [0-24]) for SU, SU012662, and Total Drug (SU + SU012662)
NCT00562718 (3) [back to overview]Recurrence
NCT00562718 (3) [back to overview]Cosmesis
NCT00562718 (3) [back to overview]Overall Safety
NCT00565370 (5) [back to overview]Overall Survival
NCT00565370 (5) [back to overview]Number of Participants Who Experienced Dose Limiting Toxicities (DLTs)
NCT00565370 (5) [back to overview]Progression-free Survival
NCT00565370 (5) [back to overview]Response Rate
NCT00565370 (5) [back to overview]Toxicity Profile (According to National Cancer Institute Common Terminology Criteria for Adverse Event Version 3.0)
NCT00568022 (9) [back to overview]Mean Ixabepilone Terminal Elimination Half Life (T 1/2) in One Dosing Interval
NCT00568022 (9) [back to overview]Mean Ixabepilone Volume of Distribution at Steady State (Vss) in One Dosing Interval
NCT00568022 (9) [back to overview]Mean Ixabepilone Area Under the Concentration Curve (AUC INF) in One Dosing Interval
NCT00568022 (9) [back to overview]Mean Ixabepilone Maximum Plasma Concentration (Cmax) in One Dosing Interval
NCT00568022 (9) [back to overview]Mean Ixabepilone Total Body Clearance (CLT) in One Dosing Interval
NCT00568022 (9) [back to overview]Participants Experiencing Dose Limiting Toxicity (DLT)
NCT00568022 (9) [back to overview]Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT00568022 (9) [back to overview]Participant Tumor Response at Study Endpoint
NCT00568022 (9) [back to overview]Participants Achieving the Maximum Tolerated Dose (MTD) and Recommended Phase 2 Dose (RP2D)
NCT00570908 (1) [back to overview]Progression Free Survival
NCT00574171 (1) [back to overview]Response Rate of Lapatinib/Capecitabine.
NCT00578071 (4) [back to overview]Number of Participants With Dose-limiting Toxicities (DLTs)
NCT00578071 (4) [back to overview]Overall Survival Rates for the Patients Studied on This Protocol.
NCT00578071 (4) [back to overview]Panitumumab Maximum Tolerated Dose in Milligrams (mg)
NCT00578071 (4) [back to overview]Pathological Complete Response Rates Associated With This Regimen.
NCT00585078 (4) [back to overview]Response Rate
NCT00585078 (4) [back to overview]Overall Survival
NCT00585078 (4) [back to overview]Progression-Free Survival
NCT00585078 (4) [back to overview]Best Response
NCT00600340 (15) [back to overview]Unconfirmed Objective Response Rate and Disease Control Rate (ITT Population)
NCT00600340 (15) [back to overview]Observation Time (ITT Population)
NCT00600340 (15) [back to overview]Duration of Response (PP Population)
NCT00600340 (15) [back to overview]Duration of Response (ITT Population)
NCT00600340 (15) [back to overview]Overall Survival (PP Population)
NCT00600340 (15) [back to overview]Progression Free Survival (ITT Population)
NCT00600340 (15) [back to overview]Progression Free Survival (PP Population)
NCT00600340 (15) [back to overview]Time to Treatment Failure (ITT Population)
NCT00600340 (15) [back to overview]Overall Survival (ITT Population)
NCT00600340 (15) [back to overview]Time to Treatment Failure (PP Population)
NCT00600340 (15) [back to overview]Objective Response Rate and Disease Control Rate (ITT Population)
NCT00600340 (15) [back to overview]Time to Response (ITT Population)
NCT00600340 (15) [back to overview]Unconfirmed Objective Response Rate and Disease Control Rate (PP Population)
NCT00600340 (15) [back to overview]Time to Response (PP Population)
NCT00600340 (15) [back to overview]Objective Response Rate and Disease Control Rate (PP Population)
NCT00601627 (5) [back to overview]One Year Survival Rate
NCT00601627 (5) [back to overview]Time to Treatment Failure
NCT00601627 (5) [back to overview]Confirmed Response Rate
NCT00601627 (5) [back to overview]Overall Survival
NCT00601627 (5) [back to overview]Progression Free Survival (PFS)
NCT00609336 (7) [back to overview]Pathologic Response Rate (Complete, Near-complete, Partial) to Neoadjuvant Chemotherapy and Chemoradiotherapy
NCT00609336 (7) [back to overview]Percent of Patients Surviving at 5 Years
NCT00609336 (7) [back to overview]Frequency and Severity of Toxicities Associated With This Treatment Regimen as Assessed by NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.0
NCT00609336 (7) [back to overview]Percent of Patients Surviving at Annual Intervals
NCT00609336 (7) [back to overview]Surgical Completion Rate and Complication Rate
NCT00609336 (7) [back to overview]Median Overall Survival of Patients With Adenocarcinoma of the Pancreas
NCT00609336 (7) [back to overview]Median Recurrence Free Survival Following Pancreaticoduodenectomy
NCT00613080 (9) [back to overview]Disease-free Survival: 4-year Rate
NCT00613080 (9) [back to overview]The Percentage of Patients Experiencing Treatment-related Gastrointestinal Adverse Events ≥ Grade 2 Per National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) v. 3.0, Occurring Preoperatively
NCT00613080 (9) [back to overview]Number of Patients in Protocol Adherence Categories for Intensity-modulated Radiotherapy (IMRT) Planning
NCT00613080 (9) [back to overview]Percentage of Patients With Grade 3 or Higher Treatment-related Adverse Events as Assessed by the Common Terminology Criteria for Adverse Events (CTCAE) v3.0
NCT00613080 (9) [back to overview]Overall Survival: 4-year Rate
NCT00613080 (9) [back to overview]Number of Patients With Pathologic Complete Response
NCT00613080 (9) [back to overview]Number of Patients Who Underwent Abdominoperineal Resection
NCT00613080 (9) [back to overview]Local-regional Failure: 4-year Rate
NCT00613080 (9) [back to overview]Distant Failure: 4-year Rate
NCT00623805 (5) [back to overview]Percentage of Participants With Metastatic Lesions Previously Considered Inoperable Who Became Operable and Underwent Surgery
NCT00623805 (5) [back to overview]Time Until a Complete Response or a Partial Response
NCT00623805 (5) [back to overview]Progression-free Survival
NCT00623805 (5) [back to overview]Percentage of Participants With a Complete Response or a Partial Response
NCT00623805 (5) [back to overview]Overall Survival
NCT00625183 (1) [back to overview]Safety and Tolerability as Assessed by NCI CTCAE Version 3.0
NCT00632489 (2) [back to overview]To Determine the Maximum Tolerated Doses (MTD) and Dose-limiting Toxicities (DLT) of LBH589 in Combination With Capecitabine When Administered to Patients With Refractory and Advanced Tumor Types That Are Sensitive to 5-fluorouracil
NCT00632489 (2) [back to overview]To Determine the Maximum Tolerated Doses (MTD) and Dose-limiting Toxicities (DLT) of LBH589 in Combination With Capecitabine When Administered to Patients With Refractory and Advanced Tumor Types That Are Sensitive to 5-fluorouracil
NCT00634088 (10) [back to overview]Number of Participants With Abnormalities in Hematology Laboratory Results by Worst CTC Grade
NCT00634088 (10) [back to overview]Area Under the Concentration-time Curve From 0 to Infinity (AUC[INF]) and AUC From 0 to Last Quantifiable Concentration (AUC[O-T] of Ixabepilone
NCT00634088 (10) [back to overview]Volume of Distribution at Steady State of Ixabepilone
NCT00634088 (10) [back to overview]Time to Peak Concentration of Ixabepilone
NCT00634088 (10) [back to overview]Number of Participants With DLT
NCT00634088 (10) [back to overview]Terminal Half-life of Ixabepilone
NCT00634088 (10) [back to overview]Maximum Concentration of Ixabepilone
NCT00634088 (10) [back to overview]Overall Tumor Response By Number of Participants
NCT00634088 (10) [back to overview]Number of Participants With Death, Serious Adverse Events (SAEs), Adverse Events (AEs) Leading to Discontinuation, Treatment-related AEs, Treatment-related AEs (Grade 3 or 4), Peripheral Neuropathy (PN), PN (Grade 3 or 4)
NCT00634088 (10) [back to overview]Number of Participants With Abnormalities in Serum Chemistry Laboratory Results by Worst CTC Grade
NCT00634751 (3) [back to overview]Overall Survival
NCT00634751 (3) [back to overview]Progression-free Survival (PFS)
NCT00634751 (3) [back to overview]Overall Response Rate
NCT00662025 (17) [back to overview]Time to Objective Tumor Response (TTR)
NCT00662025 (17) [back to overview]AUC(0-24) for Sunitinib, SU012662, and Total Drug (Sunitinib+SU012662)
NCT00662025 (17) [back to overview]Time to Tumor Progression (TTP)
NCT00662025 (17) [back to overview]Tmax for Sunitinib, SU012662, and Total Drug (Sunitinib+SU012662)
NCT00662025 (17) [back to overview]Trough Plasma Concentration (Ctrough) for Sunitinib, SU012662, and Total Drug (Sunitinib+SU012662)
NCT00662025 (17) [back to overview]Cmax for Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR and 5-FU)
NCT00662025 (17) [back to overview]Overall Survival (OS)
NCT00662025 (17) [back to overview]AUC(0-inf) for Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR and 5-FU)
NCT00662025 (17) [back to overview]Progression-Free Survival (PFS)
NCT00662025 (17) [back to overview]Duration of Objective Tumor Response (DR)
NCT00662025 (17) [back to overview]t1/2 for Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR and 5-FU)
NCT00662025 (17) [back to overview]Number of Subjects With CBR Based on Investigator's Assessment
NCT00662025 (17) [back to overview]Tmax for Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR and 5-FU)
NCT00662025 (17) [back to overview]Number of Participants With Objective Response Based on Investigator's Assessment
NCT00662025 (17) [back to overview]Number of Participants With Objective Response Based on Data Review Committee's Assessment
NCT00662025 (17) [back to overview]Number of Participants With Clinical Benefit Response (CBR) Based on Data Review Committee's Assessment
NCT00662025 (17) [back to overview]Cmax for Sunitinib, SU012662, and Total Drug (Sunitinib+SU012662)
NCT00665457 (1) [back to overview]Number of Participants With Grade 4 Adverse Events
NCT00678535 (6) [back to overview]Quality of Life (QoL) Assessed by European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ-C30)
NCT00678535 (6) [back to overview]Quality of Life (QoL) Assessed by EuroQol 5Dimensions (EQ-5D) Questionnaire
NCT00678535 (6) [back to overview]Safety - Number of Participants With Adverse Events (AEs)
NCT00678535 (6) [back to overview]Progression-free Survival (PFS) Time: Independent Review Committee (IRC) Assessments
NCT00678535 (6) [back to overview]Overall Survival (OS)
NCT00678535 (6) [back to overview]Best Overall Response (BOR) Rate: Independent Review Committee (IRC) Assessments
NCT00680901 (15) [back to overview]Number of Participants With Any Non-serious Adverse Event (AE: Occurring in >=5% Participants in Any Treatment Arm) or Any Serious Adverse Event (SAE)
NCT00680901 (15) [back to overview]Number of Participants With Adverse Events of the Indicated Severity, Per the National Cancer Institute (NCI) Common Terminology Criteria in Adverse Events (CTCAE)
NCT00680901 (15) [back to overview]Number of Participants With a Worst-case on Therapy Grade 3 or Grade 4 for the Indicated Hematology Parameters
NCT00680901 (15) [back to overview]Overall Survival
NCT00680901 (15) [back to overview]Number of Participants With a Worst-case on Therapy Grade 3 or Grade 4 for the Indicated Clinical Chemistry Parameters
NCT00680901 (15) [back to overview]Mean Change in Scores on the Questionnaire EuroQoL-5 Dimensions (EQ-5D) From Baseline to Week 36
NCT00680901 (15) [back to overview]Mean Change in Scores on the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life (QOL) Questionnaire Core 30 (QLQ-C30) From Baseline to Week 36
NCT00680901 (15) [back to overview]Mean Change in Scores on the EORTC Quality of Life (QOL) Questionnaire of Stomach 22 (QLQ-STO22) From Baseline to Week 36
NCT00680901 (15) [back to overview]Mean Change in Scores on the EORTC Quality of Life (QOL) Questionnaire of Stomach 22 (QLQ-STO22) From Baseline to Week 36
NCT00680901 (15) [back to overview]Time to Response (TTR)
NCT00680901 (15) [back to overview]Progression Free Survival (PFS)
NCT00680901 (15) [back to overview]Overall Survival in All Randomized Participants
NCT00680901 (15) [back to overview]Duration of Response (DOR)
NCT00680901 (15) [back to overview]Number of Participants With a Response of Confirmed Complete Response (CR) or Confirmed Partial Response (PR)
NCT00680901 (15) [back to overview]Number of Participants With Clinical Benefit (CB)
NCT00684983 (6) [back to overview]Overall Survival
NCT00684983 (6) [back to overview]Adverse Event Profile of Capecitabine and Lapatinib With and Without IMC-A12 (Using NCI CTCAE v3.0)
NCT00684983 (6) [back to overview]Confirmed Tumor Response, Defined as Either a Complete Response (CR) or Partial Response (PR) Noted as the Objective Status on 2 Consecutive Evaluations at Least 6 Weeks Apart, Assessed by Response Evaluation Criteria for Solid Tumors (RECIST)
NCT00684983 (6) [back to overview]Duration of Response
NCT00684983 (6) [back to overview]Progression-free Survival (PFS)
NCT00684983 (6) [back to overview]Time to Treatment Failure
NCT00685763 (1) [back to overview]Cumulative Incidence of grade3+ Bowel Perforation, Grade 3+ Bleeding (Ocurring Withing 1 Years) and grade4+ Nonhematologic Acute Adverse Events (Limited to Within 90 Days of Treatment Start)
NCT00686166 (3) [back to overview]3-year Disease-free Survival
NCT00686166 (3) [back to overview]Pathologic Complete Response Rate
NCT00686166 (3) [back to overview]Number of Patients With Grade 3 Through Grade 5 Adverse Events That Are Related to This Regimen.
NCT00700570 (5) [back to overview]Percentage of Participants With Disease Progression
NCT00700570 (5) [back to overview]Time to Disease Progression
NCT00700570 (5) [back to overview]Percentage of Participants by Best Overall Tumor Response According to RECIST Version 1.1
NCT00700570 (5) [back to overview]Percentage of Participants With a Best Overall Tumor Response of Complete Response (CR) or PR According to RECIST Version 1.1
NCT00700570 (5) [back to overview]Percentage of Participants With Conversion From Unresectable to Resectable Liver Metastases
NCT00711412 (7) [back to overview]Toxicity Profile
NCT00711412 (7) [back to overview]Time to Progression
NCT00711412 (7) [back to overview]Recurrence Rate
NCT00711412 (7) [back to overview]Determine Pathologic Complete Response
NCT00711412 (7) [back to overview]Clinical Response Rate
NCT00711412 (7) [back to overview]Overall Survival
NCT00711412 (7) [back to overview]Determine Progressive Free Survival
NCT00717197 (1) [back to overview]Percentage of Participants With Progression-free Survival.
NCT00721630 (1) [back to overview]Number of Participants With Toxicities Associated With Capecitabine and Lapatinib
NCT00737438 (1) [back to overview]Overall Response Will be Characterized by the Patient's FDG-PET Scan
NCT00741260 (6) [back to overview]Maximum Tolerated Dose (MTD) of Neratinib
NCT00741260 (6) [back to overview]Maximum Tolerated Dose (MTD) of Capecitabine
NCT00741260 (6) [back to overview]Duration of Response
NCT00741260 (6) [back to overview]Overall Response Rate
NCT00741260 (6) [back to overview]Clinical Benefit Rate
NCT00741260 (6) [back to overview]Number of Participants With Dose Limiting Toxicities
NCT00745134 (7) [back to overview]Tumor Regression Grade
NCT00745134 (7) [back to overview]Progression Free Survival (PFS)
NCT00745134 (7) [back to overview]Overall Survival (OS)
NCT00745134 (7) [back to overview]Number of Participants With Tumor Downstaging
NCT00745134 (7) [back to overview]Number of Participants With Pathologic Complete Response (pCR) Rate
NCT00745134 (7) [back to overview]Change in Curcumin Level in Tumor Tissue
NCT00745134 (7) [back to overview]Change in Curcumin Level in Serum
NCT00777101 (7) [back to overview]Frequency of CNS Metastases (Frequency)
NCT00777101 (7) [back to overview]Time to CNS Metastases
NCT00777101 (7) [back to overview]Clinical Benefit Rate
NCT00777101 (7) [back to overview]Duration of Response
NCT00777101 (7) [back to overview]Progression Free Survival
NCT00777101 (7) [back to overview]Overall Survival (OS)
NCT00777101 (7) [back to overview]Objective Response Rate (ORR).
NCT00780494 (4) [back to overview]Adverse Events ≥ Grade 3 and Related to Bevacizumab
NCT00780494 (4) [back to overview]Progression-Free Survival (PFS)
NCT00780494 (4) [back to overview]Objective (Overall) Therapeutic Response
NCT00780494 (4) [back to overview]Overall Survival (OS)
NCT00787787 (2) [back to overview]Median Overall Survival
NCT00787787 (2) [back to overview]Median Progression-free Survival
NCT00789958 (7) [back to overview]2-year Stratum-specific Disease-free Survival
NCT00789958 (7) [back to overview]2-year Stratum-specific Local Relapse Rate
NCT00789958 (7) [back to overview]Stratum-specific (R0 and R1) 2-year Overall Survival
NCT00789958 (7) [back to overview]Number of Patients With Grade 3 Through Grade 5 Adverse Events That Are Related to Study Drug
NCT00789958 (7) [back to overview]2-year Disease-free Survival in All Patients
NCT00789958 (7) [back to overview]2-year Overall Local Relapse Rate
NCT00789958 (7) [back to overview]2-year Overall Survival for All Patients
NCT00796718 (4) [back to overview]Percentage of Participants With Response to Treatment Assessed 4-6 Weeks After the Completion of Radiochemotherapy (Complete Response, Partial Remission or No Response to the Treatment)
NCT00796718 (4) [back to overview]Percentage of Participants With Adverse Events
NCT00796718 (4) [back to overview]Percentage of Participants With Response to the Treatment Assessed 1 Month After Surgery (Complete Response, Partial Remission or No Response to the Treatment)
NCT00796718 (4) [back to overview]Percentage of Participants With Pathological Complete Response
NCT00811135 (9) [back to overview]Progression Free Survival (PFS)
NCT00811135 (9) [back to overview]Number of Participants With Response
NCT00811135 (9) [back to overview]Number of Participants With Time to Progression (TTP)
NCT00811135 (9) [back to overview]Overall Survival (OS)
NCT00811135 (9) [back to overview]Percentage of Participants With a Best Overall Response (BOR) of Confirmed Complete Response (CR) or Partial Response (PR)
NCT00811135 (9) [back to overview]Duration of Response (DR)
NCT00811135 (9) [back to overview]Time to Progression (TTP)
NCT00811135 (9) [back to overview]Number of Participants With Disease Progression or Death
NCT00811135 (9) [back to overview]Number of Participants With Overall Survival (OS)
NCT00820222 (9) [back to overview]Number of Participants With CNS Progression at Any Time
NCT00820222 (9) [back to overview]Number of Participants With the Indicated Grade 3 or Grade 4 Adverse Events (AEs) Occurring in >=2% of Participants in Either Treatment Arm
NCT00820222 (9) [back to overview]Overall Survival
NCT00820222 (9) [back to overview]Progression Free Survival (PFS), as Assessed by the Investigator
NCT00820222 (9) [back to overview]Number of Participants With Overall Response (OR), as Assessed by the Investigator
NCT00820222 (9) [back to overview]Duration of Response
NCT00820222 (9) [back to overview]Number of Participants With Central Nervous System (CNS) Metastases (as Assessed by Independent Review) as the Site of First Relapse
NCT00820222 (9) [back to overview]Time to First CNS Progression, Defined as the Time From Randomization Until the Date of Documented CNS Progression as the First Site of Relapse
NCT00820222 (9) [back to overview]Number of Participants With Clinical Benefit (CB)
NCT00828672 (7) [back to overview]Death Rates and Overall Survival
NCT00828672 (7) [back to overview]Number of Participants With Histopathologic R0 and Negative CRM Resection
NCT00828672 (7) [back to overview]Number of Participants With Pathologic Complete Response at Surgery. Number of Participants With Good or Little Pathological Tumour Regression at Surgery.
NCT00828672 (7) [back to overview]Pathologic Response at Surgery. Overview of Complete Pathologic Responses, Good and Little Tumour Regression Rates at Surgery.
NCT00828672 (7) [back to overview]Recurrence Rates and Disease Free Survival
NCT00828672 (7) [back to overview]Types and Numbers of Adverse Events - General Overview
NCT00828672 (7) [back to overview]Clinical Response Rate
NCT00829166 (17) [back to overview]PFS as Assessed by the Investigator
NCT00829166 (17) [back to overview]Time to Treatment Failure
NCT00829166 (17) [back to overview]Duration of Objective Response (DOR) as Assessed by an IRC
NCT00829166 (17) [back to overview]Overall Survival: Final Analysis
NCT00829166 (17) [back to overview]Overall Survival: Second Interim Analysis (Co-primary Endpoint)
NCT00829166 (17) [back to overview]Percentage of Participants Who Died: Final Analysis
NCT00829166 (17) [back to overview]Percentage of Participants Who Died: Second Interim Analysis
NCT00829166 (17) [back to overview]Percentage of Participants Who Were Alive at Year 1
NCT00829166 (17) [back to overview]Percentage of Participants Who Were Alive at Year 2
NCT00829166 (17) [back to overview]Percentage of Participants With Clinical Benefit as Assessed by an IRC
NCT00829166 (17) [back to overview]Progression-free Survival (PFS) as Assessed by an IRC (Co-primary Endpoint)
NCT00829166 (17) [back to overview]Percentage of Participants With Objective Response (OR) as Assessed by an IRC
NCT00829166 (17) [back to overview]Percentage of Participants With PD or Death as Assessed by an Independent Review Committee (IRC)
NCT00829166 (17) [back to overview]Time to Symptom Progression
NCT00829166 (17) [back to overview]Percentage of Participants With PD or Death as Assessed by the Investigator
NCT00829166 (17) [back to overview]Percentage of Participants With Symptom Progression
NCT00829166 (17) [back to overview]Percentage of Participants With Treatment Failure
NCT00842244 (15) [back to overview]Volume of Distribution (Vz) for Cisplatin
NCT00842244 (15) [back to overview]Duration of Response (DR)
NCT00842244 (15) [back to overview]Time to Reach Maximum Observed Plasma Concentration (Tmax) for Axitinib, Capecitabine, Capecitabine's Metabolites and Cisplatin
NCT00842244 (15) [back to overview]Plasma Decay Half-Life (t1/2) for Axitinib, Capecitabine, Capecitabine's Metabolites and Cisplatin
NCT00842244 (15) [back to overview]Maximum Observed Plasma Concentration (Cmax) for Axitinib, Capecitabine, Capecitabine's Metabolites and Cisplatin
NCT00842244 (15) [back to overview]Clearance (CL) for Cisplatin
NCT00842244 (15) [back to overview]Area Under the Curve From Time Zero to Last Quantifiable Concentration (AUClast) for Capecitabine, Capecitabine's Metabolites and Cisplatin
NCT00842244 (15) [back to overview]Area Under the Curve From Time Zero to 24 Hours [AUC (0-24)] for Axitinib
NCT00842244 (15) [back to overview]Area Under the Curve From Time Zero Extrapolated to Infinite Time [AUC (0 - ∞)] for Axitinib, Capecitabine, Capecitabine's Metabolites and Cisplatin
NCT00842244 (15) [back to overview]Apparent Volume of Distribution (Vz/F) for Axitinib, Capecitabine and Capecitabine's Metabolites
NCT00842244 (15) [back to overview]Apparent Oral Clearance (CL/F) for Axitinib, Capecitabine and Capecitabine's Metabolites
NCT00842244 (15) [back to overview]Progression-Free Survival (PFS)
NCT00842244 (15) [back to overview]Percentage of Participants With Objective Response (OR)
NCT00842244 (15) [back to overview]Maximum Tolerated Dose (MTD) of Axitinib (AG-013736) in Combination With Cisplatin and Capecitabine
NCT00842244 (15) [back to overview]Number of Participants With Cycle 1 Dose-limiting Toxicities (DLTs)
NCT00848783 (1) [back to overview]Number of Patients With One-year Recurrence-free Survival
NCT00869050 (2) [back to overview]Number of Participants With Partial Response (PR)
NCT00869050 (2) [back to overview]Number of Participants With Complete Response (CR)
NCT00881621 (4) [back to overview]Overall Survival
NCT00881621 (4) [back to overview]Clinical Benefit Response
NCT00881621 (4) [back to overview]Adverse Events
NCT00881621 (4) [back to overview]Progression Free Survival
NCT00885755 (14) [back to overview]Overall Survival in ITT Population
NCT00885755 (14) [back to overview]Overall Survival in Per Protocol Population
NCT00885755 (14) [back to overview]Part I: TTP in Intent to Treat (ITT) Population
NCT00885755 (14) [back to overview]Part II: PFS in ITT Population
NCT00885755 (14) [back to overview]Part II: TTP in Intent to Treat (ITT) Population
NCT00885755 (14) [back to overview]Part I and II: Percentage of Participants With a Best Overall Response of CR or PR in ITT Population
NCT00885755 (14) [back to overview]Part I: Percentage of Participants With a Best Overall Response (BOR) of Complete Response (CR), Partial Response (PR), Stable Disease (SD) or Progrerssive Disease (PD) by Biomarker
NCT00885755 (14) [back to overview]Part I and II: Percentage of Participants With a Response by Best Overall Response by CR, PR, SD or PD in ITT Population
NCT00885755 (14) [back to overview]Part I: Time to Progression (TTP) by Biomarker
NCT00885755 (14) [back to overview]Part II: Percentage of Participants With a Best Overall Response of CR, PR, SD or PD by Biomarker
NCT00885755 (14) [back to overview]Part II: Progression Free Survival (PFS) by Biomarker
NCT00885755 (14) [back to overview]Part II: TTP by Biomarker
NCT00885755 (14) [back to overview]Part I: Progression Free Survival (PFS) by Biomarker
NCT00885755 (14) [back to overview]Part I: PFS in ITT Population
NCT00887822 (13) [back to overview]Time to Progression
NCT00887822 (13) [back to overview]Change From Cycle 1 in European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Core 36 (QLQ-C30) Scale Over Time
NCT00887822 (13) [back to overview]Change From Cycle 1 in EORTC QLQ-STO22 Scale Over Time
NCT00887822 (13) [back to overview]Progression-Free Survival (PFS)
NCT00887822 (13) [back to overview]PFS During First-line Therapy
NCT00887822 (13) [back to overview]Percentage of Participants With Progression-Free Survival (PFS) Events (Disease Progression/Death)
NCT00887822 (13) [back to overview]Percentage of Participants With PFS Events (Disease Progression/Death) During First-line Therapy
NCT00887822 (13) [back to overview]Percentage of Participants With Event (Death)
NCT00887822 (13) [back to overview]Percentage of Participants With Disease Progression
NCT00887822 (13) [back to overview]Percentage of Participants With Disease Control During First-Line Therapy
NCT00887822 (13) [back to overview]Percentage of Participants With Best Overall Response as Assessed by RECIST During First-Line Therapy
NCT00887822 (13) [back to overview]Overall Survival
NCT00887822 (13) [back to overview]Duration of Response During First-Line Therapy
NCT00889187 (2) [back to overview]Dose Limiting Toxicity (DLT) [Phase I]
NCT00889187 (2) [back to overview]Neoadjuvant Short-Course Photon Radiation Therapy Maximum Tolerated Dose (MTD) [Phase I]
NCT00891878 (6) [back to overview]Response Rate (Complete Response or Partial Response)
NCT00891878 (6) [back to overview]Time to Treatment Failure
NCT00891878 (6) [back to overview]Comparison of Progression-free Survival
NCT00891878 (6) [back to overview]Duration of Response
NCT00891878 (6) [back to overview]Overall Survival
NCT00891878 (6) [back to overview]Time to Disease Progression
NCT00916578 (1) [back to overview]Response Rate of Patients Who Receive Pre-operative or Palliative Concurrent Radiation w/ Capecitabine to the Breast & at Risk or Involved Regional Lymph Nodes Basins.
NCT00925769 (10) [back to overview]Part 1: Last Quantifiable Drug Concentration (Clast) of Erlotinib and Its Metabolite OSI-420 (CP373420), Capecitabine and Its Metabolites (5'-DFCR and 5'-DFUR)
NCT00925769 (10) [back to overview]Part 1: Maximum Serum Concentration (Cmax) of Erlotinib and Its Metabolite OSI-420 (CP373420), Capecitabine and Its Metabolites (5'-Deoxy-5-Fluorocytidine [5'-DFCR] and 5'-Deoxy-5-Fluorouridine [5'-DFUR])
NCT00925769 (10) [back to overview]Part 1: Time to Reach Cmax (Tmax) of Erlotinib and Its Metabolite OSI-420 (CP373420), Capecitabine and Its Metabolites (5'-DFCR and 5'-DFUR)
NCT00925769 (10) [back to overview]Part 1: MTD of Erlotinib
NCT00925769 (10) [back to overview]Part 1: Maximum Tolerated Dose (MTD) of Capecitabine
NCT00925769 (10) [back to overview]Part 1: MTD of Bevacizumab
NCT00925769 (10) [back to overview]Part 1: PRD of Bevacizumab for Part 2
NCT00925769 (10) [back to overview]Part 1: PRD of Erlotinib for Part 2
NCT00925769 (10) [back to overview]Part 1: Preliminary Recommended Dose (PRD) of Capecitabine for Part 2
NCT00925769 (10) [back to overview]Part 1: Area Under the Plasma Concentration-Time Curve From Time 0 to the Time of the Last Measurable Concentration (AUClast) of Erlotinib and Its Metabolite OSI-420 (CP373420), Capecitabine and Its Metabolites (5'-DFCR and 5'-DFUR)
NCT00929240 (12) [back to overview]Percentage Of Participants With PD or Death Due to PD (Maintenance Phase Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Time To Progression (Maintenance Phase Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Quality of Life Assessed As Change From Baseline in Global Health Status Using The European Organization for Research and Treatment of Cancer Quality of Life Questionnaire - 30 (EORTC QLQ - C30) (Maintenance Phase Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Percentage of Participants Expected to Be Alive After 1 and 2 Years on Treatment (Maintenance Phase Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Overall Survival (Maintenance Phase Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Percentage of Participants Who Died (Maintenance Phase Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Percentage of Participants With Best Overall Confirmed Objective Response of CR or PR Per RECIST 1.0 (Maintenance Phase Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Percentage of Participants With Clinical Benefit (CR, PR and SD) Per RECIST 1.0 (Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Percentage of Participants With Clinical Benefit (CR, PR and SD) Per RECIST 1.0 (Initial Treatment Phase)
NCT00929240 (12) [back to overview]Percentage of Participants With Disease Progression or Death (Maintenance Phase Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Progression Free Survival (Maintenance Phase Data Cutoff October 4, 2013)
NCT00929240 (12) [back to overview]Percentage of Participants With Best Overall Confirmed Objective Response of CR or PR Per RECIST 1.0 (Initial Treatment Phase)
NCT00938470 (5) [back to overview]Overall Survival
NCT00938470 (5) [back to overview]Percentage of Participants With Overall Clinical Tumor Response (CR or PR)
NCT00938470 (5) [back to overview]Number of Participants Who Experienced a Maximum Grade of 3 or Above Adverse Event
NCT00938470 (5) [back to overview]Percentage of Participants With Pathologic Complete Response (PCR)
NCT00938470 (5) [back to overview]Disease-free Survival
NCT00959946 (3) [back to overview]Percentage of Participants With Treatment-Emergent Adverse Events (AEs) or Serious Adverse Events (SAEs) - Part 1
NCT00959946 (3) [back to overview]Best Overall Response - Part 1
NCT00959946 (3) [back to overview]Maximum Tolerated Dose (MTD) - Part 1
NCT00961571 (1) [back to overview]Progression-free Survival
NCT00977379 (14) [back to overview]Percentage of Participants With Objective CNS Response at 4 Weeks After Completion of WBRT, Assessed by Investigator According to MRI
NCT00977379 (14) [back to overview]Time to CNS Progression, Assessed by Investigator According to MRI
NCT00977379 (14) [back to overview]Percentage of Participants With Objective Extra-cranial Disease Response at 4 Weeks After Completion of WBRT, Assessed by Investigator According to CT
NCT00977379 (14) [back to overview]Time to Extra-cranial Disease Progression, Assessed by Investigator According to CT
NCT00977379 (14) [back to overview]Time to Progression, Assessed by Investigator According to MRI and CT
NCT00977379 (14) [back to overview]Absolute Change From Baseline in Mini Mental State (MMS) Total Score
NCT00977379 (14) [back to overview]Duration of CNS Response, Assessed by Investigator According to MRI
NCT00977379 (14) [back to overview]Overall Survival (OS)
NCT00977379 (14) [back to overview]Percentage of Participants With Best Objective Central Nervous System (CNS) Response, Assessed by Centralized Independent Expert According to Magnetic Resonance Imaging (MRI) - Intent-to-Treat (ITT) Population
NCT00977379 (14) [back to overview]Percentage of Participants With Best Objective CNS Response, Assessed by Centralized Independent Expert According to MRI - Per-Protocol (PP) Population
NCT00977379 (14) [back to overview]Percentage of Participants With Best Objective CNS Response, Assessed by Investigator According to MRI
NCT00977379 (14) [back to overview]Percentage of Participants With Best Objective Extra-cranial Disease Response, Assessed by Investigator According to Computed Tomography (CT)
NCT00977379 (14) [back to overview]Percentage of Participants With Clinical Benefit, Assessed by Investigator According to MRI
NCT00977379 (14) [back to overview]Percentage of Participants With Objective CNS Response at 4 Weeks After Completion of WBRT, Assessed by Centralized Independent Expert According to MRI
NCT01007552 (6) [back to overview]Assess Overall Survival (OS)
NCT01007552 (6) [back to overview]Circulating Tumor Cells (CTC) Will be Assessed at Baseline, Day 22 and Day 43
NCT01007552 (6) [back to overview]Assess the Change in the Quality of Life Among Patients Using the FACT-Hep (Version 4) for Hepatobiliary Cancers.
NCT01007552 (6) [back to overview]The Primary Objective of This Study is to Assess Progression Free Survival (PFS) With Proposed Therapy for Patients With Locally Advanced or Metastatic Gallbladder and Biliary Cancers.
NCT01007552 (6) [back to overview]Estimate the Proportion of Patients With Clinical Response
NCT01007552 (6) [back to overview]Assess the Toxicity of the Regimen.
NCT01013740 (7) [back to overview]Duration of Response (DOR) in the Randomized Phase
NCT01013740 (7) [back to overview]Number of Participants With Clinical Benefit (CB) in the Randomized Phase
NCT01013740 (7) [back to overview]Number of Participants With Overall Response (OR), as Assessed by the Investigator in the Randomized Phase
NCT01013740 (7) [back to overview]Overall Survival (OS)
NCT01013740 (7) [back to overview]Progression Free Survival (PFS) in the Randomized Phase
NCT01013740 (7) [back to overview]Time to Response in the Randomized Phase
NCT01013740 (7) [back to overview]Number of Participants With Grade 4 and Grade 5 Adverse Events (AE)
NCT01026142 (9) [back to overview]Time to Progression (TTP) Based Upon Independent Review Facility (IRF) Assessment
NCT01026142 (9) [back to overview]Progression Free Survival (Independent Assessment)
NCT01026142 (9) [back to overview]Overall Survival (OS) Rate Based on a 2-year Truncated Analysis
NCT01026142 (9) [back to overview]Overall Objective Response Rate (ORR)
NCT01026142 (9) [back to overview]Clinical Benefit Rate (CBR)
NCT01026142 (9) [back to overview]Duration of Objective Response
NCT01026142 (9) [back to overview]Investigator Assessment Progression-Free Survival (PFS)
NCT01026142 (9) [back to overview]Time to Treatment Failure (TTF) Based Upon Independent Review Facility (IRF) Assessment
NCT01026142 (9) [back to overview]Overall Survival (OS)
NCT01032850 (4) [back to overview]Number of Participants Experiencing Adverse Events
NCT01032850 (4) [back to overview]Disease Control Rate of Response (DCR)
NCT01032850 (4) [back to overview]Progression Free Survival (PFS)
NCT01032850 (4) [back to overview]Overall Survival (OS)
NCT01041404 (19) [back to overview]Pain Intensity Scores as Assessed By Visual Analog Scale (VAS)
NCT01041404 (19) [back to overview]Trastuzumab Minimum Serum Concentration (Cmin)
NCT01041404 (19) [back to overview]Percentage of Participants With Change From Baseline in Body Weight by Percentage Change in Weight
NCT01041404 (19) [back to overview]Duration of Response - Percentage of Participants With an Event
NCT01041404 (19) [back to overview]Overall Survival - Time to Event
NCT01041404 (19) [back to overview]Body Weight (Kilograms [kg]) at BL
NCT01041404 (19) [back to overview]Steady State Trastuzumab Area Under the Concentration (AUC)
NCT01041404 (19) [back to overview]Percentage of Participants With a Change in Analgesic Medication During the Study
NCT01041404 (19) [back to overview]Time to Progression - Time to Event
NCT01041404 (19) [back to overview]European Organisation For the Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Core 30 (QLQ C-30) Questionnaire Scores
NCT01041404 (19) [back to overview]EORTC Quality of Life Questionnaire-Stomach Cancer Specific (QLQ STO22) Questionnaire Scores
NCT01041404 (19) [back to overview]Progression-Free Survival - Time to Event
NCT01041404 (19) [back to overview]Trastuzumab Maximum Serum Concentration (Cmax)
NCT01041404 (19) [back to overview]Time to Progression (TTP) - Percentage of Participants With an Event
NCT01041404 (19) [back to overview]Progression-Free Survival (PFS) - Percentage of Participants With an Event
NCT01041404 (19) [back to overview]Duration of Response
NCT01041404 (19) [back to overview]Percentage of Participants With Confirmed Complete Response (CR) or Partial Response (PR) Determined by Response Evaluation Criteria in Solid Tumors (RECIST)
NCT01041404 (19) [back to overview]Percentage of Participants With Clinical Benefit
NCT01041404 (19) [back to overview]Overall Survival (OS) - Percentage of Participants With an Event
NCT01044433 (5) [back to overview]Number of Participants With Adverse Events and Serious Adverse Events
NCT01044433 (5) [back to overview]Disease Control Rate
NCT01044433 (5) [back to overview]Overall Survival
NCT01044433 (5) [back to overview]Response Rate
NCT01044433 (5) [back to overview]Progression-free Survival
NCT01060007 (9) [back to overview]Rate of Locoregional Control
NCT01060007 (9) [back to overview]Preoperative Gastrointestinal Morbidity
NCT01060007 (9) [back to overview]Rate of Overall Control
NCT01060007 (9) [back to overview]Determine Quality of Anorectal Function
NCT01060007 (9) [back to overview]Incidence of Any Late Grade 3 or Higher Morbidity
NCT01060007 (9) [back to overview]Local Control
NCT01060007 (9) [back to overview]Rate of T Stage Downstaging
NCT01060007 (9) [back to overview]Incidence of Post Chemoradiotherapy Grade 3 or Higher Morbidity
NCT01060007 (9) [back to overview]Freedom From Disease Relapse
NCT01077739 (4) [back to overview]Percentage of Participants With an Overall Response of Complete Response (CR) or Partial Response (PR)
NCT01077739 (4) [back to overview]PFS From the Start of First-Line Therapy
NCT01077739 (4) [back to overview]Progression-Free Survival (PFS) From the Start of Treatment Beyond Progression
NCT01077739 (4) [back to overview]Geometric Mean Values of Pro-Angiogenic Cytokine Concentrations at Baseline and Prior to Progression
NCT01081262 (10) [back to overview]Patient Reported Quality of Life
NCT01081262 (10) [back to overview]Patient Reported Quality of Life
NCT01081262 (10) [back to overview]Patient Reported Quality of Life
NCT01081262 (10) [back to overview]Patient Reported Neurotoxicity
NCT01081262 (10) [back to overview]Patient Reported Neurotoxicity
NCT01081262 (10) [back to overview]Participants With Grade 1 or Higher Non-serious Adverse Effects Assessed by CTCAE Version 4.0
NCT01081262 (10) [back to overview]Progression-free Survival
NCT01081262 (10) [back to overview]Objective Tumor Response
NCT01081262 (10) [back to overview]Patient Reported Neurotoxicity
NCT01081262 (10) [back to overview]Overall Survival
NCT01095003 (5) [back to overview]Duration of Response
NCT01095003 (5) [back to overview]Overall Survival
NCT01095003 (5) [back to overview]Progression Free Survival
NCT01095003 (5) [back to overview]Overall Response Rate (ORR)
NCT01095003 (5) [back to overview]Disease Control Rate
NCT01118377 (3) [back to overview]Progression-free Survival
NCT01118377 (3) [back to overview]Percentage of Participants With a Tumor Response
NCT01118377 (3) [back to overview]Overall Survival
NCT01128842 (6) [back to overview]Tolerated Dose
NCT01128842 (6) [back to overview]Progression Free Survival
NCT01128842 (6) [back to overview]Objective Response Rate
NCT01128842 (6) [back to overview]Maximum Plasma Concentration of Neratinib in Combination With Capecitabine
NCT01128842 (6) [back to overview]Dose Limiting Toxicity (DLT) - Percentage of Participants With DLT Events
NCT01128842 (6) [back to overview]Area Under the Curve (AUC) of Neratinib in Combination With Capecitabine
NCT01130337 (4) [back to overview]Percentage of Participants With Pathological Complete Response (pCR)
NCT01130337 (4) [back to overview]Percentage of Participants With Objective Response
NCT01130337 (4) [back to overview]Percentage of Participants With Disease-free Survival (DFS) at Month 18
NCT01130337 (4) [back to overview]Percentage of Participants With Complete Tumor Resection (R0)
NCT01131078 (17) [back to overview]Time to Progression (TTP)
NCT01131078 (17) [back to overview]Time to Treatment Failure
NCT01131078 (17) [back to overview]Duration of Overall Complete Response
NCT01131078 (17) [back to overview]Duration of Overall Response
NCT01131078 (17) [back to overview]Duration of Stable Disease (SD)
NCT01131078 (17) [back to overview]Overall Survival
NCT01131078 (17) [back to overview]Percentage of Participants Who Died
NCT01131078 (17) [back to overview]Percentage of Participants With a Best Overall Response of CR or PR
NCT01131078 (17) [back to overview]Percentage of Participants With Disease Progression or Death
NCT01131078 (17) [back to overview]Time to Progression Excluding Deaths Not Related to Underlying Cancer
NCT01131078 (17) [back to overview]Percentage of Participants With Progression Excluding Deaths
NCT01131078 (17) [back to overview]Percentage of Participants With Progression Excluding Deaths Not Related to Underlying Cancer
NCT01131078 (17) [back to overview]Percentage of Participants With Progressive Disease Within 12 Weeks From Start of Treatment
NCT01131078 (17) [back to overview]Percentage of Participants With Stable Disease
NCT01131078 (17) [back to overview]Time to Progression Excluding Deaths
NCT01131078 (17) [back to overview]Percentage of Participants by Best Overall Response
NCT01131078 (17) [back to overview]Percentage of Participants With Treatment Failure
NCT01132664 (5) [back to overview]Progression Free Survival (PFS) - Based on Investigator Review Using Kaplan Meier - Phase l & ll
NCT01132664 (5) [back to overview]Overall Response Rate (ORR) - Phase ll
NCT01132664 (5) [back to overview]Clinical Benefit Rate (CBR) - Phase l & ll
NCT01132664 (5) [back to overview]Disease Control Rate (DCR) Based on Investigator Assessment- Phase l & ll
NCT01132664 (5) [back to overview]Dose Limiting Toxicity (DLT) - Phase l Only
NCT01134601 (1) [back to overview]Here is the Number of Participants With Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0).
NCT01135498 (6) [back to overview]Percentage of Participants Achieving Disease Control (CR, PR, or No Change [NC])
NCT01135498 (6) [back to overview]Percentage of Participants Achieving Objective Response (Complete Response [CR] or Partial Response [PR])
NCT01135498 (6) [back to overview]Percentage of Participants Who Died
NCT01135498 (6) [back to overview]Percentage of Participants With Disease Progression or Death
NCT01135498 (6) [back to overview]Progression-Free Survival
NCT01135498 (6) [back to overview]Overall Survival (OS)
NCT01151761 (8) [back to overview]Freedom From Local Progression at 12 Months
NCT01151761 (8) [back to overview]Liver Transplant Conversion Rate
NCT01151761 (8) [back to overview]Median Time to Overall Survival
NCT01151761 (8) [back to overview]Liver Transplant Rate
NCT01151761 (8) [back to overview]Overall Survival at 12 Months
NCT01151761 (8) [back to overview]Pathologic Complete Response Rate
NCT01151761 (8) [back to overview]Progression-free Survival at 12 Months
NCT01151761 (8) [back to overview]Serum CA 19-9 Levels
NCT01159171 (12) [back to overview]Duration of Response
NCT01159171 (12) [back to overview]Duration of Response - Percentage of Participants With an Event by 24 Months
NCT01159171 (12) [back to overview]Duration of Stable Disease
NCT01159171 (12) [back to overview]Duration of Stable Disease - Percentage of Participants With an Event by 24 Months
NCT01159171 (12) [back to overview]Overall Survival
NCT01159171 (12) [back to overview]Overall Survival (OS) - Percentage of Participants With an Event by 24 Months
NCT01159171 (12) [back to overview]Percentage of Participants With Objective Response (OR)
NCT01159171 (12) [back to overview]Time to Progression
NCT01159171 (12) [back to overview]Time to Progression (TTP) - Percentage of Participants With an Event by 24 Months
NCT01159171 (12) [back to overview]Time to Treatment Failure
NCT01159171 (12) [back to overview]Time to Treatment Failure (TTF) - Percentage of Participants With an Event by 24 Months
NCT01159171 (12) [back to overview]Percentage of Participants by Best Overall Response
NCT01191697 (4) [back to overview]Median Duration of Response (DOR)
NCT01191697 (4) [back to overview]Median Progression Free Survival (PFS)
NCT01191697 (4) [back to overview]Median Overall Survival
NCT01191697 (4) [back to overview]Objective Response Rate (ORR)
NCT01193517 (2) [back to overview]Maximum Tolerated Dose (MTD) of Azacitidine, and Capecitabine and Oxaliplatin (CAPOX)
NCT01193517 (2) [back to overview]Response Rate of Azacitidine, and Capecitabine and Oxaliplatin (CAPOX)
NCT01208103 (5) [back to overview]Number of Participants With Adverse Events
NCT01208103 (5) [back to overview]Number of Participants With Progression-free Survival (PFS) at Six Months
NCT01208103 (5) [back to overview]To Determine the Overall Survival (OS) for CAPOX and Bevacizumab
NCT01208103 (5) [back to overview]To Determine the Response Rate (RR) for CAPOX and Bevacizumab
NCT01208103 (5) [back to overview]To Determine the Overall PFS for CAPOX and Bevacizumab
NCT01226732 (3) [back to overview]Preliminary Efficacy Assessment: Response Rate (RR)
NCT01226732 (3) [back to overview]Drug Related Toxicities
NCT01226732 (3) [back to overview]Dose Determination
NCT01227707 (13) [back to overview]Overall Survival (OS) - Percentage of Participants With an Event
NCT01227707 (13) [back to overview]Percentage of Participants With an Overall Response of CR at the End of Neoadjuvant Treatment
NCT01227707 (13) [back to overview]Percentage of Participants Undergoing Sphincter-Saving Surgery by Type of Procedure
NCT01227707 (13) [back to overview]Percentage of Participants With Pathological Complete Response (pCR)
NCT01227707 (13) [back to overview]Percentage of Participants by Primary Tumor (T), Regional Lymph Nodes (N), and Distant Metastasis (M) Clinical Stage at Baseline and at the End of Neo-Adjuvant Treatment (NAT)
NCT01227707 (13) [back to overview]DFS - Time to Event
NCT01227707 (13) [back to overview]Disease-Free Survival (DFS) - Percentage of Participants With an Event
NCT01227707 (13) [back to overview]TTP - Time to Event
NCT01227707 (13) [back to overview]Percentage of Participants With New Lesions at the Primary Tumor Site at the End of Neoadjuvant Treatment
NCT01227707 (13) [back to overview]Time to Disease Progression (TTP) - Percentage of Participants With an Event
NCT01227707 (13) [back to overview]Percentage of Participants With Relapse During Follow-Up
NCT01227707 (13) [back to overview]Percentage of Participants With Complete Response (CR) at the End of Neoadjuvant Treatment
NCT01227707 (13) [back to overview]OS - Time to Event
NCT01234337 (12) [back to overview]Maximum Observed Drug Concentration (Cmax) of Capecitabine and 5-fluorouracil
NCT01234337 (12) [back to overview]Number of Participants With Treatment-emergent Grade 3 and 4 Laboratory Abnormalities
NCT01234337 (12) [back to overview]Patient Reported Outcomes: Euroqol-5 Dimensions (EQ-5D) - Visual Analogue Scale (VAS) Score
NCT01234337 (12) [back to overview]Patient Reported Outcomes: Euroqol-5 Dimensions (EQ-5D) - Index Score
NCT01234337 (12) [back to overview]Objective Response Rate (ORR) by Central Review
NCT01234337 (12) [back to overview]Area Under Curve From Time Zero to Last Quantifiable Concentration (AUC[0-tlast]) of Capecitabine and 5-fluorouracil
NCT01234337 (12) [back to overview]Time to Progression (TTP) by Central Review
NCT01234337 (12) [back to overview]Duration of Response (DOR) by Central Reader
NCT01234337 (12) [back to overview]Overall Survival (OS)
NCT01234337 (12) [back to overview]Progression-free Survival (PFS) Assessed by the Independent Review Panel According to Response Evaluation Criteria for Solid Tumors (RECIST) 1.1
NCT01234337 (12) [back to overview]Disease Control Rate (DCR) by Central Review
NCT01234337 (12) [back to overview]Patient Reported Outcomes: Functional Assessment of Cancer Therapy-Breast Symptom Index (8 Item) (FBSI-8)
NCT01234402 (13) [back to overview]Overall Survival (OS)
NCT01234402 (13) [back to overview]Number of Participants With Serious Adverse Events (SAEs)
NCT01234402 (13) [back to overview]Area Under the Concentration Versus Time Curve From Time Zero to Infinity of Ramucirumab or Icrucumab
NCT01234402 (13) [back to overview]Number of Participants With Anti-Ramucirumab and Anti-Icrucumab Antibodies
NCT01234402 (13) [back to overview]Minimum Concentration (Cmin) Ramucirumab Drug Product (DP) or Icrucumab
NCT01234402 (13) [back to overview]Volume of Distribution at Steady State (Vss) of Ramucirumab or Icrucumab
NCT01234402 (13) [back to overview]Number of Participants With Adverse Events (AEs)
NCT01234402 (13) [back to overview]Duration of Response
NCT01234402 (13) [back to overview]Clearance (Cl) of Ramucirumab or Icrucumab
NCT01234402 (13) [back to overview]Maximum Concentration (Cmax) Ramucirumab Drug Product (DP) or Icrucumab
NCT01234402 (13) [back to overview]Progression-Free Survival (PFS)
NCT01234402 (13) [back to overview]Terminal Half-life (t½) of Ramucirumab or Icrucumab
NCT01234402 (13) [back to overview]Percentage of Participants With Objective Response Rate (ORR)
NCT01267240 (3) [back to overview]Survival
NCT01267240 (3) [back to overview]Progression-free Survival
NCT01267240 (3) [back to overview]Response Rate According to Response Evaluation Criteria in Solid Tumors
NCT01268943 (1) [back to overview]Dose Related Toxicity
NCT01279681 (4) [back to overview]Number of Participants With Grade 3 Adverse Events At Least Possibly Related to Treatment
NCT01279681 (4) [back to overview]Overall Survival
NCT01279681 (4) [back to overview]Progression-Free Survival
NCT01279681 (4) [back to overview]Response Rate, Defined as the Percentage of Patients in Each Arm Who Have an Objective Status of Complete Response or Partial Response, Confirmed by a Second Assessment Measured at Least 6 Weeks From the Initial Assessment
NCT01323530 (10) [back to overview]Phase 2: Clinical Benefit Rate (CBR)
NCT01323530 (10) [back to overview]Phase 2: Stable Disease (SD) Rate
NCT01323530 (10) [back to overview]Phase 2: Duration of Response (DOR)
NCT01323530 (10) [back to overview]Phase 2: Disease Control Rate (DCR)
NCT01323530 (10) [back to overview]Phase 2: Objective Response Rate (ORR)
NCT01323530 (10) [back to overview]Phase 2: Progression-free Survival (PFS)
NCT01323530 (10) [back to overview]Phase 2: Time to Response
NCT01323530 (10) [back to overview]Phase 2: Duration of Stable Disease (SD)
NCT01323530 (10) [back to overview]Phase 1b and Phase 2: Percentage of Participants With Non-CR/Non-PD
NCT01323530 (10) [back to overview]Phase 1b: Number of Participants With Dose-limiting Toxicities (DLTs) as Per National Cancer Institute Common Terminology Criteria for Adverse Events Version 3.0 (NCI CTCAE v3.0)
NCT01326481 (1) [back to overview]TRC105 Steady State Pharmacokinetic Trough Concentration at the RP2D
NCT01355302 (4) [back to overview]Number of Participants With a Treatment-Emergent Adverse Event (TEAE)
NCT01355302 (4) [back to overview]Area Under The Concentration-Time Curve (AUC) From 0 to 24 Hours of Golvatinib
NCT01355302 (4) [back to overview]Maximum Concentration (Cmax) of Golvatinib
NCT01355302 (4) [back to overview]Time to Maximum Concentration (Tmax) of Golvatinib
NCT01360593 (9) [back to overview]Objective Response Rate (ORR) (Surgery After Chemotherapy and SBRT)
NCT01360593 (9) [back to overview]Acute Toxicities Associated With SBRT
NCT01360593 (9) [back to overview]Objective Response Rate (ORR) (Neoadjuvant Chemotherapy)
NCT01360593 (9) [back to overview]Overall Survival (OS)
NCT01360593 (9) [back to overview]The Functional Assessment of Cancer Therapy - General (FACT-G)
NCT01360593 (9) [back to overview]Number of Participants Able to Undergo a Margin-negative Resection After Neoadjuvant Therapy
NCT01360593 (9) [back to overview]Local Progression-free Survival (LPFS)
NCT01360593 (9) [back to overview]Late Toxicities Associated With SBRT
NCT01360593 (9) [back to overview]Time to Progression (TTP)
NCT01369433 (1) [back to overview]Number of Subjects With Adverse Events (AEs) and Serious AEs
NCT01374425 (37) [back to overview]PFS According to RECIST Version 1.1 in Participants With High ERCC-1 and Low VEGF-A Levels
NCT01374425 (37) [back to overview]PFS According to RECIST Version 1.1 in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]PFS According to RECIST Version 1.1 in Participants With High Vascular Endothelial Growth Factor (VEGF)-A Levels Versus Participants With Low VEGF-A Levels
NCT01374425 (37) [back to overview]PFS According to RECIST Version 1.1 in Participants With Low ERCC-1 and High VEGF-A Levels
NCT01374425 (37) [back to overview]PFS According to RECIST Version 1.1 in Participants With Low ERCC-1 and Low VEGF-A Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Objective Response According to RECIST Version 1.1
NCT01374425 (37) [back to overview]PFS According to RECIST Version 1.1 in Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Disease Control According to RECIST Version 1.1 in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels
NCT01374425 (37) [back to overview]OS in Participants With High ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Liver Metastasis Resection
NCT01374425 (37) [back to overview]Percentage of Participants With Liver Metastasis Resection in Participants With High ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Liver Metastasis Resection in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Liver Metastasis Resection in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Liver Metastasis Resection in Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]OS in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]Progression-Free Survival (PFS) According to Response Evaluation Criteria in Solid Tumors (RECIST) Version 1.1
NCT01374425 (37) [back to overview]PFS According to RECIST Version 1.1 in Participants With Wild-Type V-Ki-ras2 Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) Versus Participants With Mutant KRAS
NCT01374425 (37) [back to overview]PFS According to RECIST Version 1.1 in Participants With High ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Complete Liver Metastasis Resection
NCT01374425 (37) [back to overview]Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With High ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Complete Liver Metastasis Resection in Participants With High ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Complete Liver Metastasis Resection in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]Overall Survival (OS)
NCT01374425 (37) [back to overview]Percentage of Participants With Complete Liver Metastasis Resection in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Complete Liver Metastasis Resection in Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Disease Control According to RECIST Version 1.1
NCT01374425 (37) [back to overview]Percentage of Participants With Disease Control According to RECIST Version 1.1 in Participants With High ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Disease Control According to RECIST Version 1.1 in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]OS in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With Wild-Type KRAS Versus Participants With Mutant KRAS
NCT01374425 (37) [back to overview]PFS According to RECIST Version 1.1 in Participants With High ERCC-1 and High VEGF-A Levels
NCT01374425 (37) [back to overview]OS in Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels
NCT01374425 (37) [back to overview]Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With Low ERCC-1 Levels
NCT01374425 (37) [back to overview]OS in Participants With Wild-Type KRAS Versus Participants With Mutant KRAS
NCT01374425 (37) [back to overview]Percentage of Participants With Disease Control According to RECIST Version 1.1 in Participants With Low ERCC-1 Levels
NCT01387295 (4) [back to overview]Adverse Events
NCT01387295 (4) [back to overview]Number of Patients Suitable for Local Therapy (Radiofrequency)
NCT01387295 (4) [back to overview]PFS
NCT01387295 (4) [back to overview]Survival
NCT01399190 (3) [back to overview]Percentage of Participants With Adverse Events
NCT01399190 (3) [back to overview]Response Rate (Tumor Assessments According to RECIST)
NCT01399190 (3) [back to overview]Progression-free Survival
NCT01423604 (5) [back to overview]Summary of Clinical Benefit
NCT01423604 (5) [back to overview]Durable Response Rate
NCT01423604 (5) [back to overview]Overall Survival
NCT01423604 (5) [back to overview]Progression-Free Survival (PFS)
NCT01423604 (5) [back to overview]Objective Response Rate
NCT01439282 (3) [back to overview]Use of Cold Cap for Alopecia
NCT01439282 (3) [back to overview]Percentage of Participants Who Achieved the Target Relative Dose Intensity (RDI) of 85%
NCT01439282 (3) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)
NCT01442155 (2) [back to overview]Disease-Free Survival (Time to Event)
NCT01442155 (2) [back to overview]Safety: Percentage of Participants With Adverse Events
NCT01450696 (9) [back to overview]Percentage of Participants Who Died - Per Protocol Set (PPS)
NCT01450696 (9) [back to overview]Percentage of Participants With Disease Progression or Death - PPS
NCT01450696 (9) [back to overview]Percentage of Participants Who Died - FAS
NCT01450696 (9) [back to overview]Trastuzumab Cmin on Day 21 of Cycles 1 to 11 - FAS
NCT01450696 (9) [back to overview]Trastuzumab Serum Concentration on Day 1 of Cycle 1 - FAS
NCT01450696 (9) [back to overview]Overall Survival - PPS
NCT01450696 (9) [back to overview]Overall Survival - FAS
NCT01450696 (9) [back to overview]Progression-Free Survival - PPS
NCT01450696 (9) [back to overview]Percentage of Participants With Objective Response - PPS
NCT01459614 (5) [back to overview]Number of Patients Experiencing a Grade 3 or Above Treatment-related Toxicity
NCT01459614 (5) [back to overview]Disease Control Rate (DCR)
NCT01459614 (5) [back to overview]Percentage of Participants Without Disease Progression (Progression-Free Survival) at 6 Months
NCT01459614 (5) [back to overview]Progression-free Survival (PFS)
NCT01459614 (5) [back to overview]Overall Survival (OS)
NCT01461057 (2) [back to overview]Percentage of Participants With Day 43 Serum Pertuzumab Trough Concentrations (Cmin) Greater Than or Equal to (>=) 20 Microgram Per Milliliter (mcg/mL)
NCT01461057 (2) [back to overview]Number of Participants With Adverse Events (AEs)
NCT01463982 (2) [back to overview]Objective Response Rate (ORR), Response Rate (RR) and Disease Control Rate (DCR)
NCT01463982 (2) [back to overview]Dose Limiting Toxicity Assessment and Maximum Tolerated Dose Determination
NCT01471353 (4) [back to overview]Response Rate
NCT01471353 (4) [back to overview]Sorafenib Activity
NCT01471353 (4) [back to overview]Toxicity (Percentage of Subjects That Experienced an Adverse Event)
NCT01471353 (4) [back to overview]Overall Survival
NCT01498458 (6) [back to overview]Hematological Toxicity of the Combination of Pazopanib and Capecitabine
NCT01498458 (6) [back to overview]Clinical Benefit Rate (CBR)
NCT01498458 (6) [back to overview]Dose-limiting Toxicity (DLT)
NCT01498458 (6) [back to overview]Other Toxicity of the Combination of Pazopanib and Capecitabine
NCT01498458 (6) [back to overview]Maximum Tolerable Dose (MTD) of Pazopanib
NCT01498458 (6) [back to overview]Objective Response Rate (ORR)
NCT01525082 (6) [back to overview]Treatment-related Toxicity
NCT01525082 (6) [back to overview]Overall Survival (OS)
NCT01525082 (6) [back to overview]O6-methylguanine DNA Methyltransferase (MGMT) Status by Immunohistochemistry (IHC)
NCT01525082 (6) [back to overview]Radiographic Response (RR)
NCT01525082 (6) [back to overview]Progression-free Survival (PFS)
NCT01525082 (6) [back to overview]O6-methylguanine DNA Methyltransferase (MGMT) by Promoter Methylation
NCT01534637 (3) [back to overview]Impact of Aprepitant/5HT-3 Antagonist Therapy on the Patient Quality of Life as Measured by the Number of Patients Using Anti Nausea Drugs
NCT01534637 (3) [back to overview]Number of Patients With Gastrointestinal Toxicities (Grade 3 and 4 Nausea and Vomiting) Associated With Delivering Fluorouracil/Gemcitabine Hydrochloride-based Chemotherapy With Upper Abdominal Radiation
NCT01534637 (3) [back to overview]Impact of Aprepitant/5HT-3 Antagonist Therapy on the Patient Quality of Life as Measured by the Number of Patients Taking Anti Nausea Drugs
NCT01584544 (1) [back to overview]Number of Participants Experienced Dose Limited Toxicity
NCT01588990 (22) [back to overview]Time to Failure of Strategy (TFS): Overall
NCT01588990 (22) [back to overview]AQoL-8D Global Utility Score: Phase B
NCT01588990 (22) [back to overview]European Quality of Life 5-Dimension (EuroQol-5D) Utility Score: Phase A
NCT01588990 (22) [back to overview]EuroQol-5D Utility Score: Phase B
NCT01588990 (22) [back to overview]FACT-C Score: Phase B
NCT01588990 (22) [back to overview]Functional Assessment of Cancer Therapy-Colorectal (FACT-C) Score: Phase A
NCT01588990 (22) [back to overview]Percentage of Participants With Confirmed Complete or Partial Response as Assessed by the Investigator Based on Routine Clinical Practice: Overall
NCT01588990 (22) [back to overview]Percentage of Participants With Confirmed Complete or Partial Response as Assessed by the Investigator Based on Routine Clinical Practice: Phase A
NCT01588990 (22) [back to overview]Percentage of Participants With Confirmed Complete or Partial Response as Assessed by the Investigator Based on Routine Clinical Practice: Phase B
NCT01588990 (22) [back to overview]Survival Beyond First Disease Progression: Overall
NCT01588990 (22) [back to overview]PFS Until Second Disease Progression as Assessed by the Investigator Based on Routine Clinical Practice: Phase B
NCT01588990 (22) [back to overview]PFS Until First Disease Progression as Assessed by the Investigator Based on Routine Clinical Practice: Phase A
NCT01588990 (22) [back to overview]Assessment of Quality of Life - Eight Dimensions (AQoL-8D) Global Utility Score: Phase A
NCT01588990 (22) [back to overview]Association Between Longitudinal NLR (Longitudinal NLR ≤5 Versus NLR >5) and OS as Assessed by Hazard Ratio
NCT01588990 (22) [back to overview]Association Between Longitudinal NLR (Longitudinal NLR ≤5 Versus NLR >5) and PFS as Assessed by Hazard Ratio
NCT01588990 (22) [back to overview]Association Between Neutrophil to Lymphocyte Ratio (NLR) [NLR ≤5 Versus NLR >5] and Progression-Free Survival (PFS) as Assessed by Hazard Ratio
NCT01588990 (22) [back to overview]Association Between NLR (NLR ≤5 Versus NLR >5) and OS as Assessed by Hazard Ratio
NCT01588990 (22) [back to overview]Association Between NLR Normalization (First NLR Post-Baseline ≤5 Versus NLR >5) and PFS as Assessed by Hazard Ratio
NCT01588990 (22) [back to overview]Duration of Disease Control (DDC) as Assessed by the Investigator Based on Routine Clinical Practice: Overall
NCT01588990 (22) [back to overview]OS: Phase B
NCT01588990 (22) [back to overview]Overall Survival (OS) From the Start of Treatment to Study Completion: Overall
NCT01588990 (22) [back to overview]Percentage of Participants Who Underwent Liver Resection: Overall
NCT01591733 (7) [back to overview]Preoperative Toxicity of Grade 3 or Worse Related to FOLFIRINOX and Chemoradiation
NCT01591733 (7) [back to overview]Median Progression-Free Survival
NCT01591733 (7) [back to overview]The Proportion of Participants With Surgery Related Adverse Events
NCT01591733 (7) [back to overview]Rate of R0 Resection
NCT01591733 (7) [back to overview]30 Day Post-operative Mortality Rate
NCT01591733 (7) [back to overview]Median Overall Survival
NCT01591733 (7) [back to overview]Local Control Rates
NCT01661972 (5) [back to overview]Response Rate
NCT01661972 (5) [back to overview]Recommended Phase II Dose (RPTD) for the Capecitabine and Aflibercept Doublet Combination
NCT01661972 (5) [back to overview]Number of Dose-Limiting Toxicities (Phase 1)
NCT01661972 (5) [back to overview]Median Progression Free Survival (PFS)
NCT01661972 (5) [back to overview]Median Survival
NCT01664494 (2) [back to overview]Number of Participants With Routine Clinical Use of Capecitabine as Per the Line of Treatment
NCT01664494 (2) [back to overview]Median Dose of Capecitabine
NCT01683422 (1) [back to overview]One-year Survival Rate
NCT01696695 (7) [back to overview]Mean Duration of Capecitabine Therapy
NCT01696695 (7) [back to overview]Percentage of Participants With Dose Modification of Capecitabine
NCT01696695 (7) [back to overview]Percentage of Participants With Overall Response as Assessed by Investigator Using RECIST v1.1
NCT01696695 (7) [back to overview]PFS by Therapeutic Regimens
NCT01696695 (7) [back to overview]Percentage of Participants Who Underwent Metastasectomy
NCT01696695 (7) [back to overview]Percentage of Participants With Clinical Benefit as Assessed Using RECIST v1.1
NCT01696695 (7) [back to overview]Median Progression-free Survival (PFS)
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): AUC(0-inf) of 5-Fluorouracil (Metabolite of Capecitabine)
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): AUC(0-inf) of Capecitabine
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): Cmax of 5-Fluorouracil (Metabolite of Capecitabine)
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): Cmax of Capecitabine
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): MTD of Capecitabine When Combined With Trastuzumab Emtansine (2.4 mg/kg QW)
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): Percentage of Participants With BOR as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): t1/2 of 5-Fluorouracil (Metabolite of Capecitabine)
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): Percentage of Participants With DLTs
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): Serum Concentration of Trastuzumab
NCT01702558 (34) [back to overview]Phase 1 (mBC): Cmax of 5-Fluorouracil (Metabolite of Capecitabine)
NCT01702558 (34) [back to overview]Phase 1 (mBC): AUC(0-inf) of 5-Fluorouracil (Metabolite of Capecitabine)
NCT01702558 (34) [back to overview]Phase 1 (mBC): Percentage of Participants With BOR as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 1 (mBC): Area Under the Plasma Concentration-Time Curve From Time Zero to Infinity (AUC[0-inf]) of Capecitabine
NCT01702558 (34) [back to overview]Phase 1 (mBC): Maximum Tolerated Dose (MTD) of Capecitabine When Combined With Trastuzumab Emtansine (3.6 mg/kg Every 3 Weeks)
NCT01702558 (34) [back to overview]Phase 1 (mBC): Maximum Observed Plasma Concentration (Cmax) of Capecitabine
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): Serum Concentration of Trastuzumab Emtansine
NCT01702558 (34) [back to overview]Phase 1 (LA/mGC): t1/2 of Capecitabine
NCT01702558 (34) [back to overview]Phase 1 (mBC): Serum Concentration of Trastuzumab Emtansine
NCT01702558 (34) [back to overview]Phase 1 (mBC): Serum Concentration of Trastuzumab
NCT01702558 (34) [back to overview]Phase 2 (mBC): Time to Treatment Failure (TTF) as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 2 (mBC): Time to Response (TTR) as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 2 (mBC): Time to Progression (TTP) as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 2 (mBC): Progression-Free Survival (PFS) as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 2 (mBC): Percentage of Participants With Treatment Failure as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 2 (mBC): Percentage of Participants With PD as Assessed by the Investigator According to RECIST v1.1 or Death From Any Cause
NCT01702558 (34) [back to overview]Phase 2 (mBC): Percentage of Participants With PD as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 2 (mBC): Percentage of Participants With Clinical Benefit as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 2 (mBC): Percentage of Participants With Best Overall Response (BOR) as Assessed by the Investigator According to Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST v1.1)
NCT01702558 (34) [back to overview]Phase 2 (mBC): Percentage of Participants Who Died of Any Cause
NCT01702558 (34) [back to overview]Phase 2 (mBC): Overall Survival (OS)
NCT01702558 (34) [back to overview]Phase 2 (mBC): Duration of Response (DoR) as Assessed by the Investigator According to RECIST v1.1
NCT01702558 (34) [back to overview]Phase 1 (mBC): t1/2 of 5-Fluorouracil (Metabolite of Capecitabine)
NCT01702558 (34) [back to overview]Phase 1 (mBC): Plasma Terminal Half-Life (t1/2) of Capecitabine
NCT01702558 (34) [back to overview]Phase 1 (mBC): Percentage of Participants With Dose-Limiting Toxicities (DLTs)
NCT01718873 (5) [back to overview]Toxic Effects
NCT01718873 (5) [back to overview]Disease Control Rate
NCT01718873 (5) [back to overview]Objective Response Rate
NCT01718873 (5) [back to overview]Progression-free Survival (PFS)
NCT01718873 (5) [back to overview]Overall Survival
NCT01722162 (3) [back to overview]Incidence and Severity of Adverse Events as Measured by Number of Participants Who Experience Grade 3 and Higher Adverse Events
NCT01722162 (3) [back to overview]Progression Free Survival (Arm B)
NCT01722162 (3) [back to overview]Progression Free Survival (Arm A)
NCT01725386 (6) [back to overview]Mean Survival Time
NCT01725386 (6) [back to overview]Percentage of Participants Receiving Concomitant Medications During the Study
NCT01725386 (6) [back to overview]Percentage of Participants With Adverse Events
NCT01725386 (6) [back to overview]Percentage of Participants by Histopathology Grade Diagnosis Assessed at Baseline
NCT01725386 (6) [back to overview]Percentage of Participants With Relevant Medical History Assessed at Baseline
NCT01725386 (6) [back to overview]Percent of Participants With Capecitabine as a First Line, Second Line, or Third Line Therapy
NCT01726582 (4) [back to overview]Progression-free Survival
NCT01726582 (4) [back to overview]Use of Biomarkers to Determine Course of Treatment
NCT01726582 (4) [back to overview]Overall Survival in Months
NCT01726582 (4) [back to overview]Number of Subjects Completing Therapy Including Surgical Resection.
NCT01729923 (5) [back to overview]Rate of CR, Assessed According to CEA and CA 19-9 Measurements and Response Evaluation Criteria in Solid Tumors (RECIST) 1.1
NCT01729923 (5) [back to overview]Overall Survival
NCT01729923 (5) [back to overview]Best Overall Response Rate Among All Patients Who Had RECIST Measurements at Baseline and at Least One Subsequent Occasion and Did Not Have Surgery or Radiation Therapy
NCT01729923 (5) [back to overview]Best Overall Response Rate Among All Patients Who Had RECIST Measurements at Baseline and at Least One Subsequent Occasion
NCT01729923 (5) [back to overview]Relapse Free Survival in Patients Achieving CR
NCT01754623 (2) [back to overview]Margin-negative (R0) Resection Rate
NCT01754623 (2) [back to overview]Overall Survival (OS) Rate
NCT01765582 (7) [back to overview]Time to PFS2
NCT01765582 (7) [back to overview]Proportion of Participants Considered by the Investigator to be Unresectable on Study Enrollment Who Subsequently Underwent Attempted Curative Resections of Metastases
NCT01765582 (7) [back to overview]Progression-Free Survival During First-Line Therapy (PFS1)
NCT01765582 (7) [back to overview]Percentage of Participants With Overall Response During First-Line Therapy (ORR1)
NCT01765582 (7) [back to overview]Percentage of Participants With Adverse Events
NCT01765582 (7) [back to overview]Overall Survival (OS)
NCT01765582 (7) [back to overview]Proportion of Participants Who Underwent Liver Metastases Resections
NCT01774786 (14) [back to overview]Change From Baseline in EORTC QLQ-Gastric Cancer Module (EORTC QLQ-STO22) Score
NCT01774786 (14) [back to overview]Percentage of Participants With Clinical Benefit, as Determined by the Investigator According to RECIST v1.1 Criteria
NCT01774786 (14) [back to overview]Minimum Serum Concentration (Cmin) of Pertuzumab
NCT01774786 (14) [back to overview]Maximum Serum Concentration (Cmax) of Pertuzumab
NCT01774786 (14) [back to overview]Change From Baseline in European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Core 30 (QLQ-C30) Score
NCT01774786 (14) [back to overview]Cmax of Trastuzumab
NCT01774786 (14) [back to overview]Cmin of Trastuzumab
NCT01774786 (14) [back to overview]Duration of Objective Response, as Determined by Investigator According to RECIST v1.1 Criteria
NCT01774786 (14) [back to overview]Final Analysis of the Percentage of Participants With Overall Objective Response, as Determined by the Investigator According to RECIST v1.1 Criteria
NCT01774786 (14) [back to overview]Progression-Free Survival, as Determined by the Investigator According to Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST v1.1) Criteria
NCT01774786 (14) [back to overview]Primary Analysis of the Percentage of Participants With Overall Objective Response, as Determined by the Investigator According to RECIST v1.1 Criteria
NCT01774786 (14) [back to overview]Overview of Safety: Number of Participants With at Least One Adverse Event, Severity Determined According to National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE), Version 4.03
NCT01774786 (14) [back to overview]Overall Survival
NCT01774786 (14) [back to overview]Number of Participants With Symptomatic or Asymptomatic Left Ventricular Systolic Dysfunction (LVSD)
NCT01776307 (14) [back to overview]Progression Free Survival
NCT01776307 (14) [back to overview]Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 480mg, Twice Daily, on Day 21 of the First Study Cycle
NCT01776307 (14) [back to overview]Disease Control Rate
NCT01776307 (14) [back to overview]Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 500mg, Twice Daily, on Day 5 of the First Study Cycle
NCT01776307 (14) [back to overview]Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 500mg, Twice Daily, on Day 21 of the First Study Cycle
NCT01776307 (14) [back to overview]Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 480mg, Twice Daily, on Day 5 of the First Study Cycle
NCT01776307 (14) [back to overview]Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 240mg, Twice Daily, on Day 21 of the First Study Cycle
NCT01776307 (14) [back to overview]Number of Patients With Adverse Events and Serious Adverse Events
NCT01776307 (14) [back to overview]Overall Survival
NCT01776307 (14) [back to overview]Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 500mg, Twice Daily, on Day 5 of the First Study Cycle
NCT01776307 (14) [back to overview]Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 500mg, Twice Daily, on Day 21 of the First Study Cycle
NCT01776307 (14) [back to overview]Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 480mg, Twice Daily, on Day 5 of the First Study Cycle
NCT01776307 (14) [back to overview]Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 480mg, Twice Daily, on Day 21 of the First Study Cycle
NCT01776307 (14) [back to overview]Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 240mg, Twice Daily, on Day 21 of the First Study Cycle
NCT01777945 (7) [back to overview]Time to Treatment Failure
NCT01777945 (7) [back to overview]Progression-free Survival (PFS)
NCT01777945 (7) [back to overview]Number of Participants With Adverse Events
NCT01777945 (7) [back to overview]Overall Response Rate
NCT01777945 (7) [back to overview]Clinical Benefit Rate
NCT01777945 (7) [back to overview]Duration of Treatment With Xeloda
NCT01777945 (7) [back to overview]Percentage of Capecitabine Dose Modifications
NCT01781403 (4) [back to overview]Toxicity(Adeverse Event)
NCT01781403 (4) [back to overview]Maximum Tolerated Dose (MTD)
NCT01781403 (4) [back to overview]Pathological Complete Response
NCT01781403 (4) [back to overview]Recommended Dose (RD)
NCT01783444 (9) [back to overview]Mean Change in Treatment Satisfaction Questionnaire for Medication (TSQM) Between Week 3 and 12
NCT01783444 (9) [back to overview]Progression Free Survival (PFS) - Everolimus Plus Exemestane Versus Capecitabine Alone
NCT01783444 (9) [back to overview]Progression Free Survival (PFS) - Everolimus Plus Exemestane Versus Everolimus Alone
NCT01783444 (9) [back to overview]All Collected Deaths
NCT01783444 (9) [back to overview]Time to 10% Definitive Deterioration in the Global Health Status / Quality of Life
NCT01783444 (9) [back to overview]Time to Eastern Cooperative Oncology Group (ECOG) Performance Deterioration
NCT01783444 (9) [back to overview]Overall Survival (OS)
NCT01783444 (9) [back to overview]Clinical Benefit Rate (CBR)
NCT01783444 (9) [back to overview]Overall Response Rate (ORR)
NCT01808573 (7) [back to overview]Duration of Response (DOR) - Central Assessment (Population That Had a Response With Measurable Disease at Screening)
NCT01808573 (7) [back to overview]Percentage of Participants With Treatment-Emergent Adverse Events (Adverse Events and Serious Adverse Events)
NCT01808573 (7) [back to overview]Overall Survival
NCT01808573 (7) [back to overview]Centrally Assessed Progression Free Survival
NCT01808573 (7) [back to overview]Objective Response Rate (ORR) - Central Assessment (ITT Population With Measurable Disease at Screening)
NCT01808573 (7) [back to overview]Clinical Benefit Rate (CBR) - Central Assessment (ITT Population With Measurable Disease at Screening)
NCT01808573 (7) [back to overview]Intervention for Symptomatic Metastatic Central Nervous System Disease
NCT01823679 (5) [back to overview]Progression-free Survival (PFS) at 2 Years
NCT01823679 (5) [back to overview]Progression-free Survival (PFS) at 1 Year
NCT01823679 (5) [back to overview]Overall Survival (OS) at 2 Years
NCT01823679 (5) [back to overview]Objective Response Rate (ORR)
NCT01823679 (5) [back to overview]Overall Survival (OS) at 1 Year
NCT01824875 (3) [back to overview]Proportion of Patients With Response
NCT01824875 (3) [back to overview]Overall Survival
NCT01824875 (3) [back to overview]Progression-free Survival
NCT01828554 (4) [back to overview]Response Rate
NCT01828554 (4) [back to overview]Progression Free Survival
NCT01828554 (4) [back to overview]Cmax During Cycle 1
NCT01828554 (4) [back to overview]Area Under the Curve (AUC) on Cycle 1 Day 1 and Cycle 1 Day 9
NCT01844076 (3) [back to overview]Phase II - Rate of Response
NCT01844076 (3) [back to overview]Phase I - Number of Participants Who Experienced Dose Limiting Toxicities and Adverse Reactions
NCT01844076 (3) [back to overview]Phase II - Time to Progression (TTP)
NCT01869192 (2) [back to overview]Overall Response Rate
NCT01869192 (2) [back to overview]Pathological Response
NCT01873833 (5) [back to overview]Number of Participants With Any Adverse Events as a Measure of Safety and Tolerability
NCT01873833 (5) [back to overview]Clinical Benefit Rate (CBR)
NCT01873833 (5) [back to overview]Overall Response Rate (ORR)
NCT01873833 (5) [back to overview]Overall Survival (OS)
NCT01873833 (5) [back to overview]Progression Free Survival (PFS)
NCT01921751 (2) [back to overview]Overall Survival
NCT01921751 (2) [back to overview]Patterns of Failure (Local and Metastatic Failure)
NCT01928680 (1) [back to overview]Overall Response Rate
NCT01955629 (2) [back to overview]Part 1: Number of Participants With Tumor Responses (Complete Response [CR], Partial Response [PR], Stable Disease [SD] or Progressive Disease [PD])
NCT01955629 (2) [back to overview]Part 1: Number of Participants With Dose Limiting Toxicities (DLTs)
NCT01997333 (6) [back to overview]Overall Survival
NCT01997333 (6) [back to overview]Duration of Response
NCT01997333 (6) [back to overview]Objective Response Rate (ORR)
NCT01997333 (6) [back to overview]Progression Free Survival (PFS)
NCT01997333 (6) [back to overview]Adverse Events (AE)
NCT01997333 (6) [back to overview]Pharmacokinetics (PK)
NCT02000882 (5) [back to overview]Median Time to Progression
NCT02000882 (5) [back to overview]Objective Response Rate (ORR)
NCT02000882 (5) [back to overview]Median Overall Survival
NCT02000882 (5) [back to overview]Number of Treatment-related Serious AEs
NCT02000882 (5) [back to overview]Clinical Benefit Rate (CBR)
NCT02005549 (3) [back to overview]Percentage of Participants With pCR, Clinical Complete Response (CR), or Clinical Partial Response (PR)
NCT02005549 (3) [back to overview]Percentage of Participants With Pathological Complete Response (pCR)
NCT02005549 (3) [back to overview]Percentage of Participants Undergoing Breast-Conserving Surgery
NCT02010567 (7) [back to overview]Pathological Complete Response (pCR) Rate
NCT02010567 (7) [back to overview]Number of Participants With Grade 3 or Higher, Treatment-related Toxicities
NCT02010567 (7) [back to overview]Overall Survival (OS) Based on Pathological Complete Response (pCR).
NCT02010567 (7) [back to overview]Disease-free Survival (DFS) Rate Based on Pathological Complete Response (pCR).
NCT02010567 (7) [back to overview]Disease-free Survival (DFS) Rate
NCT02010567 (7) [back to overview]Maximum Tolerated Dose (MTD) of CRLX101 When Added to Standard Neoadjuvant Chemoradiotherapy Consisting of Capecitabine + Radiotherapy in Locally Advanced Rectal Cancer
NCT02010567 (7) [back to overview]Overall Survival (OS) Rate
NCT02013830 (8) [back to overview]Overall Survival - Percentage of Participants Event Free at 12 Months
NCT02013830 (8) [back to overview]Time to Disease Progression - Percentage of Participants With an Event
NCT02013830 (8) [back to overview]Time to Disease Progression - Percentage of Participants Progression-free at 12 Months
NCT02013830 (8) [back to overview]Time to Disease Progression
NCT02013830 (8) [back to overview]Percentage of Participants With Objective Response (OR)
NCT02013830 (8) [back to overview]Percentage of Participants With Disease Control
NCT02013830 (8) [back to overview]Overall Survival - Percentage of Participants With an Event
NCT02013830 (8) [back to overview]Overall Survival
NCT02017704 (4) [back to overview]Change in EORTC QLQ-C30 Global Health Status Score
NCT02017704 (4) [back to overview]Number of Participants With Grade 3 or Higher Adverse Events
NCT02017704 (4) [back to overview]Change in EORTC QLQ-C30 Global Health Status Score
NCT02017704 (4) [back to overview]Number of Patients With Pathologic Complete Response
NCT02024607 (6) [back to overview]Overall Survival of Patients With FOLFIRI/XELIRI-refractory Metastatic Colorectal Cancer
NCT02024607 (6) [back to overview]Number of Participants With Adverse Events and Serious Adverse Events
NCT02024607 (6) [back to overview]Disease Control Rate of Patients With FOLFIRI/XELIRI-refractory Metastatic Colorectal Cancer
NCT02024607 (6) [back to overview]Disease Control Rate
NCT02024607 (6) [back to overview]The Objective Response Rate of Napabucasin Administered in Combination in FOLFIRI in Patients With FOLFIRI/XELIRI-refractory Metastatic Colorectal Cancer
NCT02024607 (6) [back to overview]Progression Free Survival of Patients With FOLFIRI/XELIRI-refractory Metastatic Colorectal Cancer
NCT02042443 (4) [back to overview]Objective Response Rate
NCT02042443 (4) [back to overview]Progression-free Survival
NCT02042443 (4) [back to overview]Overall Survival
NCT02042443 (4) [back to overview]Number of Patients With Grade 3 Through Grade 5 Adverse Events That Are Related to Study Drug
NCT02083653 (13) [back to overview]Overall Survival (OS) Time for Patients in Europe + United States With Triple-Negative mCRC (EU+US TNmCRC)
NCT02083653 (13) [back to overview]Occurrence and Nature of Adverse Events (AEs), as Assessed by the Common Terminology Criteria for AEs (Version 4.03) (CTCAE v4.03).
NCT02083653 (13) [back to overview]Pharmacokinetic (PK) Parameters: Sym004 Concentrations
NCT02083653 (13) [back to overview]Pharmacokinetic (PK) Parameters: Time of Maximum Plasma Concentration (Tmax)
NCT02083653 (13) [back to overview]Quality of Life Assessed by FACT-EGFRI-18 for Skin Rash
NCT02083653 (13) [back to overview]Quality of Life Assessed by the EORTC QLQ-C30 (Version 3)
NCT02083653 (13) [back to overview]Quality of Life Assessed by EORTC QLQ-CR29
NCT02083653 (13) [back to overview]Host Immune Response: Number of Subjects With Anti-drug Antibodies (ADAs) to Sym004 Over Time
NCT02083653 (13) [back to overview]Overall Survival (OS) Time
NCT02083653 (13) [back to overview]Overall Survival (OS) Time for Patients in Europe + United States With Double-Negative mCRC (EU+US DNmCRC)
NCT02083653 (13) [back to overview]Progression Free Survival (PFS) Time
NCT02083653 (13) [back to overview]Relative Dose Intensity of Sym004
NCT02083653 (13) [back to overview]Time to Treatment Failure (TTF)
NCT02117479 (6) [back to overview]Progression-free Survival (PFS)
NCT02117479 (6) [back to overview]Objective Response Rate (ORR)
NCT02117479 (6) [back to overview]Overall Survival (OS)
NCT02117479 (6) [back to overview]Percentage of Participants Achieving Progression Free Survival (PFS)
NCT02117479 (6) [back to overview]Participants With Treatment-Emergent Adverse Events (TEAEs)
NCT02117479 (6) [back to overview]Duration of Response
NCT02119026 (9) [back to overview]Tumour Assessments (Based on RECIST Criteria) in 2nd-line
NCT02119026 (9) [back to overview]Tumour Assessments (Based on RECIST Criteria) in 1st-line
NCT02119026 (9) [back to overview]Time to Response
NCT02119026 (9) [back to overview]Second Line PFS
NCT02119026 (9) [back to overview]Overall Survival of XELIRI Plus Bevacizumab and XELOX Plus Bevacizumab
NCT02119026 (9) [back to overview]Overall Response Rate (Number of Participants With Response)
NCT02119026 (9) [back to overview]First Line Progression Free Survival (PFS)
NCT02119026 (9) [back to overview]Efficacy Duration of Disease Control by Tumor Assessment (CT/MRI/Clinical Examination)
NCT02119026 (9) [back to overview]Duration of Response
NCT02119663 (6) [back to overview]Objective Response Rate (ORR)
NCT02119663 (6) [back to overview]Progression Free Survival (PFS)
NCT02119663 (6) [back to overview]Duration of Response
NCT02119663 (6) [back to overview]Participants With Treatment-Emergent Adverse Events (TEAEs)
NCT02119663 (6) [back to overview]Percentage of Participants Achieving Progression Free Survival (PFS)
NCT02119663 (6) [back to overview]Overall Survival (OS)
NCT02120417 (6) [back to overview]Median Survival
NCT02120417 (6) [back to overview]Percentage of Participants Achieving Clinical Benefit Rate
NCT02120417 (6) [back to overview]Percentage of Participants Achieving Overall Survival
NCT02120417 (6) [back to overview]Percentage of Participants Achieving Objective Response Rate
NCT02120417 (6) [back to overview]Progression-free Survival (PFS)
NCT02120417 (6) [back to overview]Duration of Response (DOR)
NCT02218164 (4) [back to overview]Overall Survival (OS)
NCT02218164 (4) [back to overview]Occurence of Treatment Related Serious Adverse Events (SAEs)
NCT02218164 (4) [back to overview]Objective Response Rate (ORR)
NCT02218164 (4) [back to overview]Progression Free Survival (PFS)
NCT02231086 (2) [back to overview]Peritoneal Recurrence Free Survival at 18 Months
NCT02231086 (2) [back to overview]Treatment Related Toxicity of Adjuvant HIPEC
NCT02243007 (8) [back to overview]Survival Rate at 18 Month
NCT02243007 (8) [back to overview]Number of Participants With Serious and Non-Serious Adverse Events
NCT02243007 (8) [back to overview]Rate of Pathologic Downstaging
NCT02243007 (8) [back to overview]30-day Post-operative Mortality Rate
NCT02243007 (8) [back to overview]Correlation of Biomarkers With PFS
NCT02243007 (8) [back to overview]Local Control Rate
NCT02243007 (8) [back to overview]Pathologic Complete Response Rate (pCR).
NCT02243007 (8) [back to overview]Surgical Morbidity Rate
NCT02291289 (6) [back to overview]Percentage of Participants With Improvement and/or Stayed the Same on the Eastern Cooperative Oncology Group Performance Status (ECOG PS) Score
NCT02291289 (6) [back to overview]Progression-Free Survival (PFS)
NCT02291289 (6) [back to overview]Overall Response
NCT02291289 (6) [back to overview]Duration of Response
NCT02291289 (6) [back to overview]Disease Control Rate (DCR)
NCT02291289 (6) [back to overview]Time to Treatment Response
NCT02294786 (17) [back to overview]Proportion of Subjects Experiencing Diarrhoea of Grade 2 and Above (up to 24 Weeks)
NCT02294786 (17) [back to overview]Number of Lapatinib and Capecitabine Tablets Dispensed and Returned
NCT02294786 (17) [back to overview]Time to the First Subject Reported Change in Frequency and/or Consistency of Bowel Movements From Baseline as Recorded in the DMD
NCT02294786 (17) [back to overview]Proportion of Subjects Taking Anti-diarrhoeal Medication as Recorded in the DMD
NCT02294786 (17) [back to overview]Proportion of Subjects Taking Anti-diarrhoeal Medication
NCT02294786 (17) [back to overview]Proportion of Subjects Reporting Stopping Completely or Missing Doses of Anti-cancer Tablets Due to Diarrhoea as Recorded in the DMD
NCT02294786 (17) [back to overview]Proportion of Subjects Reporting Changes in Bowel Movements From Baseline (Frequency and/or Consistency) as Recorded in the Diarrhoea Management Diary (DMD)
NCT02294786 (17) [back to overview]Proportion of Subjects Making Dietary Changes Due to Diarrhoea as Recorded in the DMD
NCT02294786 (17) [back to overview]Time to Onset of the First Episode of Diarrhoea of Any Grade of Severity
NCT02294786 (17) [back to overview]Proportion of Subjects Experiencing Diarrhoea of Grade 3 and Above (up to 24 Weeks)
NCT02294786 (17) [back to overview]Proportion of Subjects Experiencing Diarrhoea of Any Grade of Severity (up to 24 Weeks)
NCT02294786 (17) [back to overview]Proportion of Subjects Contacting Other Non-hospital Healthcare Professionals to Discuss Diarrhoea as Recorded in the DMD
NCT02294786 (17) [back to overview]Duration of Diarrhoea of Any Grade of Severity
NCT02294786 (17) [back to overview]Clinical Benefit Response (up to 24 Weeks)
NCT02294786 (17) [back to overview]Proportion of Subjects Requiring Treatment Withdrawal in Lapatinib and Capecitabine
NCT02294786 (17) [back to overview]Proportion of Subjects Requiring Dose Reduction in Lapatinib and Capecitabine
NCT02294786 (17) [back to overview]Proportion of Subjects Requiring Dose Delay in Lapatinib and Capecitabine
NCT02301143 (11) [back to overview]Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire For Pancreatic Cancer (EORTC-QLQ PAN26): Satisfaction With Health Care Scale
NCT02301143 (11) [back to overview]Disease Control Rate (DCR): Percentage of Participants With Complete (CR) or Partial Response (PR), or Stable Disease (SD) for ≥ 16 Weeks According to RECIST Version 1.1
NCT02301143 (11) [back to overview]Kaplan-Meier Estimate of Progression-Free Survival (PFS)
NCT02301143 (11) [back to overview]Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire For Pancreatic Cancer (EORTC-QLQ PAN26): Six Summary Scales
NCT02301143 (11) [back to overview]Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire For Pancreatic Cancer (EORTC-QLQ PAN26): 10 Individual Item Scores
NCT02301143 (11) [back to overview]Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30): Symptom Scales and Single Symptom Items
NCT02301143 (11) [back to overview]Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30): Global Health Status and 5 Functioning Scales
NCT02301143 (11) [back to overview]Overall Response Rate (ORR): Percentage of Participants With Complete (CR) or Partial Response (PR) According to RECIST Version 1.1
NCT02301143 (11) [back to overview]Kaplan-Meier Estimates for Time to Treatment Failure (TTF)
NCT02301143 (11) [back to overview]Kaplan-Meier Estimates for Overall Survival (OS)
NCT02301143 (11) [back to overview]Participants With Treatment Emergent Adverse Events (TEAEs)
NCT02314117 (13) [back to overview]Time to Progression (TTP)
NCT02314117 (13) [back to overview]Time to Deterioration in Eastern Cooperative Oncology Group (ECOG) Performance Status (PS)
NCT02314117 (13) [back to overview]PK: Minimum Concentration (Cmin) of Ramucirumab
NCT02314117 (13) [back to overview]Pharmacokinetics (PK): Maximum Observed Drug Concentration (Cmax) of Ramucirumab
NCT02314117 (13) [back to overview]Number of Participants With Anti-Ramucirumab Antibodies
NCT02314117 (13) [back to overview]Time to Deterioration in Quality of Life (QoL) on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-Core 30 (EORTC QLQ-C30) - Global Health Status/ QoL Scale
NCT02314117 (13) [back to overview]Progression-free Survival (PFS)
NCT02314117 (13) [back to overview]Change in Health Status on the EuroQol 5-Dimensions 5-Level Instrument (EQ-5D- 5L)
NCT02314117 (13) [back to overview]Duration of Response (DoR)
NCT02314117 (13) [back to overview]Percentage of Participants With Complete Response (CR), Partial Response (PR) or Stable Disease (SD) (Disease Control Rate [DCR])
NCT02314117 (13) [back to overview]Overall Survival (OS)
NCT02314117 (13) [back to overview]Percentage of Participants With Complete Response (CR) or Partial Response (PR) (Objective Response Rate [ORR])
NCT02314117 (13) [back to overview]Progression- Free Survival 2 (PFS2)
NCT02324543 (10) [back to overview]Progression-free Survival (PFS) Using RECIST 1.1 Criteria
NCT02324543 (10) [back to overview]Response Rate (RR) Using RECIST 1.1 Criteria
NCT02324543 (10) [back to overview]Maximum Tolerated Dose (MTD) of Gemcitabine
NCT02324543 (10) [back to overview]Disease Control Rate (DCR) Using RECIST 1.1 Criteria
NCT02324543 (10) [back to overview]Maximum Tolerated Dose (MTD) of Capecitabine
NCT02324543 (10) [back to overview]Overall Survival (OS) Rate at 9 Months
NCT02324543 (10) [back to overview]Maximum Tolerated Dose (MTD) of Docetaxel
NCT02324543 (10) [back to overview]Maximum Tolerated Dose (MTD) of Cisplatin
NCT02324543 (10) [back to overview]Maximum Tolerated Dose (MTD) of Irinotecan
NCT02324543 (10) [back to overview]Overall Survival (OS)
NCT02335411 (14) [back to overview]Overall Survival (OS) For All Participants
NCT02335411 (14) [back to overview]Progression-Free Survival For PD-L1 Positive Participants
NCT02335411 (14) [back to overview]Progression-Free Survival (PFS) For All Participants
NCT02335411 (14) [back to overview]Overall Survival For PD-L1 Positive Participants
NCT02335411 (14) [back to overview]Objective Response Rate For PD-L1 Positive Participants in Cohorts 1 and 3
NCT02335411 (14) [back to overview]Number of Participants Discontinuing Study Drug Due to AEs
NCT02335411 (14) [back to overview]Disease Control Rate (DCR) For All Participants
NCT02335411 (14) [back to overview]Number of Participants Experiencing Adverse Events (AEs)
NCT02335411 (14) [back to overview]Disease Control Rate For PD-L1 Positive Participants
NCT02335411 (14) [back to overview]Duration of Response (DOR) For All Participants
NCT02335411 (14) [back to overview]Duration of Response For PD-L1 Positive Participants
NCT02335411 (14) [back to overview]Objective Response Rate (ORR) For All Participants in Cohort 2
NCT02335411 (14) [back to overview]Objective Response Rate (ORR) For All Participants in Cohorts 1 and 3
NCT02335411 (14) [back to overview]Objective Response Rate For PD-L1 Positive Participants in Cohort 2
NCT02352831 (7) [back to overview]Overall Response Rate (ORR)
NCT02352831 (7) [back to overview]Number of Participants With a CA19-9 Response
NCT02352831 (7) [back to overview]Phase I Only: Recommended Phase II Dose of Tosedostat
NCT02352831 (7) [back to overview]Time-to-progression (TTP)
NCT02352831 (7) [back to overview]Overall Survival Rate (OS)
NCT02352831 (7) [back to overview]Phase I Only: Number of Participants Who Experience Dose-limiting Toxicities (DLTs)
NCT02352831 (7) [back to overview]Progression-free Survival (PFS) Rate
NCT02358863 (1) [back to overview]The Number of Patients With Tumor Size Reduction (Objective Response Rate)
NCT02359058 (5) [back to overview]Number of Participants With One or More Serious Adverse Event(s) (SAEs) Considered by the Investigator to be Related to Study Drug Administration
NCT02359058 (5) [back to overview]Percentage of Participants With Complete Response (CR) or Partial Response (PR) (Objective Response Rate)
NCT02359058 (5) [back to overview]Pharmacokinetics (PK): Maximum Serum Concentration (Cmax) of Ramucirumab
NCT02359058 (5) [back to overview]Number of Participants With Treatment Emergent Anti-Ramucirumab Antibodies (TE-ADA)
NCT02359058 (5) [back to overview]Pharmacokinetics (PK): Minimum Serum Concentration (Cmin) of Ramucirumab
NCT02393755 (5) [back to overview]Median PFS (Phase II)
NCT02393755 (5) [back to overview]Median OS (Phase II)
NCT02393755 (5) [back to overview]To Examine the DLT
NCT02393755 (5) [back to overview]Progression Free Survival (PFS) Rate, Defined as the Proportion of Patients Who Survive Without Disease Progression Via the RECIST Version 1.1 (Phase II)
NCT02393755 (5) [back to overview]Objective Response Rate
NCT02445391 (6) [back to overview]3-year Overall Survival (OS) Rate in Basal-Subtype Patients
NCT02445391 (6) [back to overview]Health-related Quality of Life (HRQL) at 6-month Assessment
NCT02445391 (6) [back to overview]Health-related Quality of Life (HRQL) at 15-month Assessment
NCT02445391 (6) [back to overview]Proportion of Basal Subtype
NCT02445391 (6) [back to overview]3-year Recurrence-Free Survival (RFS) Rate in Basal-Subtype Patients
NCT02445391 (6) [back to overview]3-year Invasive Disease-Free Survival (IDFS) Rate in Basal-Subtype Patients
NCT02485834 (5) [back to overview]Progression-free Survival
NCT02485834 (5) [back to overview]Overall Survival
NCT02485834 (5) [back to overview]Number of Patients Had Pathologic Complete Response
NCT02485834 (5) [back to overview]Number of Patients Achieved R0 Resection During Surgery
NCT02485834 (5) [back to overview]Number of Participants Who Reported Grade 3 or Higher Adverse Events
NCT02494583 (16) [back to overview]Pembro Mono vs SOC: PFS Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)
NCT02494583 (16) [back to overview]Pembro Mono vs SOC: OS in Participants With PD-L1 CPS ≥10
NCT02494583 (16) [back to overview]Pembro Combo vs SOC: Objective Response Rate (ORR) Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)
NCT02494583 (16) [back to overview]Pembro Mono vs SOC: OS in Participants With PD-L1 CPS ≥1 (All Participants)
NCT02494583 (16) [back to overview]Pembro Mono vs SOC: ORR Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)
NCT02494583 (16) [back to overview]Pembro Mono vs SOC: DOR Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)
NCT02494583 (16) [back to overview]Pembro Mono vs SOC: Change From Baseline to Week 18 in the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Core 30 (QLQ-C30) Global Health Status/Quality of Life (Items 29 and 30) Combined Score
NCT02494583 (16) [back to overview]Pembro Combo vs. SOC: Change From Baseline to Week 18 in EORTC QLQ-STO22 Pain Symptom Subscale Score
NCT02494583 (16) [back to overview]Pembro Combo vs SOC: Progression Free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) by Blinded Independent Central Review (BICR) in Participants With PD-L1 CPS ≥1 (All Participants)
NCT02494583 (16) [back to overview]Pembro Combo vs SOC: Overall Survival (OS) in Participants With PD-L1 CPS ≥1 (All Participants)
NCT02494583 (16) [back to overview]Number of Participants Discontinuing Study Treatment Due to an AE
NCT02494583 (16) [back to overview]Pembro Combo vs SOC: OS in Participants With PD-L1 CPS ≥10
NCT02494583 (16) [back to overview]Number of Participants Experiencing an Adverse Event (AE)
NCT02494583 (16) [back to overview]Pembro Combo vs SOC: Change From Baseline to Week 18 in the EORTC QLQ-C30 Global Health Status/Quality of Life (Items 29 and 30) Combined Score
NCT02494583 (16) [back to overview]Pembro Combo vs SOC: Duration of Response (DOR) Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)
NCT02494583 (16) [back to overview]Pembro Mono vs. SOC: Change From Baseline to Week 18 in EORTC QLQ-Module for Gastric Cancer (STO22) Pain Symptom Subscale Score
NCT02494596 (12) [back to overview]Maximum Plasma Concentration of Capecitabine and it's Metabolites When Given Alone and in Combination With Pertuzumab
NCT02494596 (12) [back to overview]Plasma Half-Life of Capecitabine and it's Metabolites When Given Alone and in Combination With Pertuzumab
NCT02494596 (12) [back to overview]Time to Maximum Plasma Concentration of Capecitabine and it's Metabolites When Given Alone and in Combination With Pertuzumab
NCT02494596 (12) [back to overview]AUC From Time Zero to Infinity (AUC 0-infinity) of Pertuzumab
NCT02494596 (12) [back to overview]Apparent Total Clearance of Pertuzumab
NCT02494596 (12) [back to overview]Apparent Volume of Distribution of Pertuzumab
NCT02494596 (12) [back to overview]Area Under the Concentration Curve From Time Zero to Last Measurement (AUC 0-last) of Pertuzumab
NCT02494596 (12) [back to overview]Maximum Plasma Concentration (Cmax) of Pertuzumab
NCT02494596 (12) [back to overview]Maximum Tolerated Dose (MTD) of the Combination of Pertuzumab and Capecitabine
NCT02494596 (12) [back to overview]Percentage of Participants With DLTs
NCT02494596 (12) [back to overview]Plasma Half-Life (t1/2) of Pertuzumab
NCT02494596 (12) [back to overview]Time to Maximum Plasma Concentration (Tmax) of Pertuzumab
NCT02524275 (3) [back to overview]Overall Response Rate of Complete or Partial Response
NCT02524275 (3) [back to overview]Progression-free Survival
NCT02524275 (3) [back to overview]Survival
NCT02550743 (2) [back to overview]Pathologic Complete Response for Patients With Rectal Cancer
NCT02550743 (2) [back to overview]Maximum Tolerated Dose of BYL719
NCT02555657 (17) [back to overview]Overall Survival in Participants With Programmed Cell Death Ligand 1 (PD-L1) With Combined Positive Score (CPS) ≥10
NCT02555657 (17) [back to overview]Overall Survival in Participants With PD-L1 CPS ≥1
NCT02555657 (17) [back to overview]Number of Participants Who Experienced One or More Adverse Events
NCT02555657 (17) [back to overview]Progression-Free Survival Per RECIST 1.1 in Participants With PD-L1 CPS ≥10
NCT02555657 (17) [back to overview]Progression-Free Survival Per RECIST 1.1 in Participants With PD-L1 CPS ≥1
NCT02555657 (17) [back to overview]Progression-Free Survival Per RECIST 1.1 in All Participants
NCT02555657 (17) [back to overview]Disease Control Rate Per RECIST 1.1 in All Participants
NCT02555657 (17) [back to overview]Duration of Response Per RECIST 1.1 in All Participants Who Had a Confirmed Response
NCT02555657 (17) [back to overview]Disease Control Rate Per RECIST 1.1 in Participants With PD-L1 CPS ≥1
NCT02555657 (17) [back to overview]Duration of Response Per RECIST 1.1 in Participants With PD-L1 CPS ≥1 Who Had a Confirmed Response
NCT02555657 (17) [back to overview]Disease Control Rate Per RECIST 1.1 in Participants With PD-L1 CPS ≥10
NCT02555657 (17) [back to overview]Duration of Response Per RECIST 1.1 in Participants With PD-L1 CPS ≥10 Who Had a Confirmed Response
NCT02555657 (17) [back to overview]Number of Participants Who Discontinued Study Treatment Due to an Adverse Event
NCT02555657 (17) [back to overview]Overall Response Rate Per RECIST 1.1 in All Participants
NCT02555657 (17) [back to overview]Overall Response Rate Per RECIST 1.1 in Participants With PD-L1 CPS ≥1
NCT02555657 (17) [back to overview]Overall Response Rate Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) in Participants With PD-L1 CPS ≥10
NCT02555657 (17) [back to overview]Overall Survival in All Participants
NCT02574455 (14) [back to overview]Time to Objective Response by the Investigator Assessment in BM-ve Population
NCT02574455 (14) [back to overview]Overall Survival (OS) in ITT Population
NCT02574455 (14) [back to overview]Time to Progression (TTP) by IRC Assessment in BM-ve Population
NCT02574455 (14) [back to overview]Change From Baseline in European Organization for Research and Treatment of Cancer Quality-of-Life Questionnaire Core 30 (EORTC QLQ-C30) Score
NCT02574455 (14) [back to overview]Time to Progression (TTP) by Investigator Assessment in BM-ve Population
NCT02574455 (14) [back to overview]Duration of Response (DOR) by IRC and Investigator Assessment in BM-ve Population
NCT02574455 (14) [back to overview]Clinical Benefit Rate (CBR) by IRC and Investigator Assessment in BM-ve Population
NCT02574455 (14) [back to overview]Overall Survival (OS) in BM-ve Population
NCT02574455 (14) [back to overview]Time to Objective Response by the IRC Assessment in BM-ve Population
NCT02574455 (14) [back to overview]Progression-Free Survival (PFS) by Independent Review Committee (IRC) Assessment in Brain Metastasis Negative (BM-ve) Population
NCT02574455 (14) [back to overview]Progression-Free Survival (PFS) by IRC Assessment in the ITT Population
NCT02574455 (14) [back to overview]Percentage of Participants Experiencing the Worst Laboratory Abnormalities Grade 3 or 4 Post-Baseline
NCT02574455 (14) [back to overview]Percentage of Participants Experiencing Any Treatment Emergent Adverse Events (TEAEs), Serious Adverse Events (SAEs), and TEAEs Leading to Discontinuation of Study Drug
NCT02574455 (14) [back to overview]Objective Response Rate (ORR) by IRC and Investigator Assessment in BM-ve Population
NCT02611960 (10) [back to overview]Progression-free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1)
NCT02611960 (10) [back to overview]Percentage of Participants With PFS (PFS Rate) at 6 Months
NCT02611960 (10) [back to overview]Percentage of Participants With PFS (PFS Rate) at 12 Months
NCT02611960 (10) [back to overview]Percentage of Participants Who Experience One or More Adverse Events (AEs)
NCT02611960 (10) [back to overview]Percentage of Participants Who Discontinue Study Treatment Due to an AE
NCT02611960 (10) [back to overview]Percentage of Participants Surviving (OS Rate) at 24 Months
NCT02611960 (10) [back to overview]Percentage of Participants Surviving (OS Rate) at 12 Months
NCT02611960 (10) [back to overview]Overall Survival (OS)
NCT02611960 (10) [back to overview]Duration of Response (DOR) Per RECIST 1.1
NCT02611960 (10) [back to overview]Objective Response Rate (ORR) Per RECIST 1.1
NCT02614794 (19) [back to overview]Progression-free Survival (PFS) Per RECIST 1.1 as Determined by Blinded Independent Central Review (BICR)
NCT02614794 (19) [back to overview]Frequency of Dose Modifications
NCT02614794 (19) [back to overview]Frequency of Dose Modifications at Time of Final Analysis
NCT02614794 (19) [back to overview]Incidence of Adverse Events (AEs) at Time of Final Analysis
NCT02614794 (19) [back to overview]Incidence of Adverse Events (AEs) at Time of Primary Analysis
NCT02614794 (19) [back to overview]Incidence of Health Resources Utilization
NCT02614794 (19) [back to overview]Pharmacokinetic Measure: ONT-993
NCT02614794 (19) [back to overview]Pharmacokinetic Measure: Ctrough of Tucatinib
NCT02614794 (19) [back to overview]CBR Per RECIST 1.1 as Determined by Investigator Assessment
NCT02614794 (19) [back to overview]Clinical Benefit Rate (CBR) as Determined by BICR Per RECIST 1.1
NCT02614794 (19) [back to overview]Confirmed Objective Response Rate (ORR) Per RECIST 1.1 as Determined by BICR
NCT02614794 (19) [back to overview]Duration of Response (DOR) Per RECIST 1.1 as Determined by BICR
NCT02614794 (19) [back to overview]ORR Per RECIST 1.1 as Determined by Investigator Assessment
NCT02614794 (19) [back to overview]Overall Survival (OS) at Time of Final Analysis
NCT02614794 (19) [back to overview]Overall Survival (OS) at Time of Primary Analysis
NCT02614794 (19) [back to overview]PFS in Patients With Brain Metastases at Baseline Using RECIST 1.1 as Determined by BICR
NCT02614794 (19) [back to overview]PFS Per RECIST 1.1 as Determined by Investigator Assessment at Time of Final Analysis
NCT02614794 (19) [back to overview]PFS Per RECIST 1.1 as Determined by Investigator Assessment at Time of Primary Analysis
NCT02614794 (19) [back to overview]DOR Per RECIST 1.1 as Determined by Investigator Assessment
NCT02625610 (12) [back to overview]Progression Free Survival (PFS) by Independent Review Committee (IRC)
NCT02625610 (12) [back to overview]Maintenance Phase: Number of Participants With Treatment-Emergent Adverse Events (TEAEs) and Serious TEAEs According to National Cancer Institute-Common Terminology Criteria for Adverse Events Version 4.03 (NCI-CTCAE v4.03)
NCT02625610 (12) [back to overview]Maintenance Phase: Number of Participants With Potentially Clinically Significant Electrocardiogram (ECG) Abnormalities
NCT02625610 (12) [back to overview]Maintenance Phase: Number of Participants With Potentially Clinically Significant Abnormalities in Vital Signs
NCT02625610 (12) [back to overview]Maintenance Phase: Number of Participants With Grade Change From Baseline to Worst On-Treatment Grade 4 Hematology Values
NCT02625610 (12) [back to overview]Change From Baseline in European Quality of Life 5-dimensions Health Outcome Questionnaire Through Visual Analogue Scale up to Safety Follow-up (Up to 152.3 Weeks)
NCT02625610 (12) [back to overview]Maintenance Phase: Number of Participants With Shift in Eastern Cooperative Oncology Group (ECOG) Performance Status Score to 1 or Higher Than 1
NCT02625610 (12) [back to overview]Objective Response Rate (ORR) by Investigator Assessment
NCT02625610 (12) [back to overview]Overall Survival (OS)
NCT02625610 (12) [back to overview]Change From Baseline in European Organization for the Research and Treatment of Cancer Quality of Life (EORTC QLQ-C30) Global Health Status Scale Score up to Safety Follow-up (Up to 152.3 Weeks)
NCT02625610 (12) [back to overview]Change From Baseline in European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire-Stomach Cancer Specific (EORTC QLQ-STO22 ) Questionnaire Scores up to Safety Follow-up (Up to 152.3 Weeks)
NCT02625610 (12) [back to overview]Change From Baseline in European Quality of Life 5-dimensions (EQ-5D-5L) Health Outcome Questionnaire Through Composite Index Score up to Safety Follow-up (Up to 152.3 Weeks)
NCT02694718 (7) [back to overview]Percentage of Participants With Downstaging of Primary Tumor and/or Lymph Nodes
NCT02694718 (7) [back to overview]Number of Participants With Any Adverse Events and Serious Adverse Events
NCT02694718 (7) [back to overview]Percentage of Participants With Pathological Complete Tumor Response
NCT02694718 (7) [back to overview]Percentage of Participants With Pathological Incomplete Tumor Response
NCT02694718 (7) [back to overview]Percentage of Participants With Resection (R0) in Participants With T4 Rectal Cancer
NCT02694718 (7) [back to overview]Percentage of Participants With Sphincter-preservation
NCT02694718 (7) [back to overview]Number of Participants With Marked Laboratory Abnormalities
NCT02743221 (5) [back to overview]Disease Control Rate (DCR)
NCT02743221 (5) [back to overview]Overall Survival (OS)
NCT02743221 (5) [back to overview]Overall Response Rate (ORR)
NCT02743221 (5) [back to overview]Progression Free Survival (PFS)
NCT02743221 (5) [back to overview]Duration of Response (DR)
NCT02748213 (6) [back to overview]Percentage of Participants With a Best Overall Response of Complete Response (CR) or Partial Response (PR) According to Response Evaluation Criteria in Solid Tumors (RECIST)
NCT02748213 (6) [back to overview]Percentage of Participants With Death or Disease Progression According to RECIST
NCT02748213 (6) [back to overview]Progression-Free Survival (PFS) According to RECIST
NCT02748213 (6) [back to overview]Duration of Response (DOR) According to RECIST
NCT02748213 (6) [back to overview]Overall Survival (OS)
NCT02748213 (6) [back to overview]Percentage of Participants Who Died
NCT02780700 (5) [back to overview]Disease Control (DC)
NCT02780700 (5) [back to overview]Objective Response Rate (ORR)
NCT02780700 (5) [back to overview]Overall Survival (OS)
NCT02780700 (5) [back to overview]Percentage of Patients With Grade 3 or Worse Adverse Events
NCT02780700 (5) [back to overview]Progression Free Survival (PFS)
NCT02872116 (7) [back to overview]PFS in Participants Treated With Nivolumab Plus Ipilimumab vs Chemotherapy
NCT02872116 (7) [back to overview]PFS in Participants Treated With Nivolumab Plus Chemotherapy vs Chemotherapy
NCT02872116 (7) [back to overview]OS in Participants Treated With Nivolumab Plus Ipilimumab vs Chemotherapy
NCT02872116 (7) [back to overview]OS in Participants Treated With Nivolumab Plus Chemotherapy vs Chemotherapy
NCT02872116 (7) [back to overview]Objective Response Rate
NCT02872116 (7) [back to overview]Progression Free Survival (PFS) in Participants Treated With Nivolumab Plus Chemotherapy vs Chemotherapy With PD-L1 CPS ≥ 5
NCT02872116 (7) [back to overview]Overall Survival (OS) in Participants Treated With Nivolumab Plus Chemotherapy vs Chemotherapy With PD-L1 CPS ≥ 5
NCT02873195 (4) [back to overview]Progression Free Survival (PFS)
NCT02873195 (4) [back to overview]The Number of Participants Who Experienced at Least One Grade 3 or Higher Adverse Event Deemed at Least Possibly Related to Treatment (Toxicity)
NCT02873195 (4) [back to overview]Objective Response Rate
NCT02873195 (4) [back to overview]Overall Survival (OS)
NCT02921256 (3) [back to overview]Rate of Sphincter Preservation
NCT02921256 (3) [back to overview]Neoadjuvant Rectal Cancer (NAR) Score
NCT02921256 (3) [back to overview]Rate of Pathologic Complete Response (Nodes and Tumor) ypT0 and ypN0
NCT02937116 (13) [back to overview]TTR According to RECIST 1.1 as Assessed by Investigator
NCT02937116 (13) [back to overview]Volume of Distribution of IBI308 in Plasma After Single Dose Administration
NCT02937116 (13) [back to overview]Time to Maximum Concentration (Tmax) of Sintilimab in Solid Tumor Participants
NCT02937116 (13) [back to overview]OS for Participants
NCT02937116 (13) [back to overview]Area Under the Concentration-time Curve From Zero Time (Predose) to the Time of the Last Measurable Concentration (AUC0-t)
NCT02937116 (13) [back to overview]Clearance of IBI308 in Plasma After Single Dose Administration
NCT02937116 (13) [back to overview]DOR According to RECIST 1.1 as Assessed by Investigator
NCT02937116 (13) [back to overview]Maximum Concentration (Cmax) of Sintilimab in Solid Tumor Participants
NCT02937116 (13) [back to overview]Number of All Study Participants Who Demonstrate a Tumor Response
NCT02937116 (13) [back to overview]Number of Participants Experiencing Dose-limiting Toxicities (DLTs)
NCT02937116 (13) [back to overview]Objective Response Rate (ORR) According to RECIST 1.1 as Assessed by Independent Review Committee by Investigator
NCT02937116 (13) [back to overview]PFS According to RECIST 1.1 as Assessed by Investigator
NCT02937116 (13) [back to overview]The Half-life (t1/2) of IBI308 in Plasma After Single Dose Administration
NCT02954536 (1) [back to overview]Percentage of Participants With Progression Free Survival
NCT02981342 (11) [back to overview]Stage 1: Disease Control Rate (DCR): Percentage of Participants With a Best Overall Response of Complete Response (CR), Partial Response (PR) or Stable Disease (SD)
NCT02981342 (11) [back to overview]Stage 2: Clinical Benefit Rate (CBR): Percentage of Participants With Best Overall Response of CR, PR, or SD With Duration of SD for at Least 6 Months
NCT02981342 (11) [back to overview]Stage 2: Change From Baseline in Carbohydrate Antigen 19.9 (CA 19-9) Level
NCT02981342 (11) [back to overview]Stage 1: PK: Steady State Trough Pre Dose Concentration of LY3023414
NCT02981342 (11) [back to overview]Stage 1: Pharmacokinetics (PK): Mean Steady State Exposure of Abemaciclib and Its Metabolites (LSN2839567 (M2), LSN3106726 (M20))
NCT02981342 (11) [back to overview]Stage 2: Change From Baseline in Pain and Symptom Burden Assessment on the Modified Brief Pain Inventory-Short Form (mBPI-sf)
NCT02981342 (11) [back to overview]Stage 2: Progression Free Survival (PFS)
NCT02981342 (11) [back to overview]Stage 2: Change From Baseline in Symptom Burden on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30 (EORTC QLQ-C30)
NCT02981342 (11) [back to overview]Stage 1: Objective Response Rate (ORR): Percentage of Participants With a Best Overall Response (BOR) of CR or PR
NCT02981342 (11) [back to overview]Stage 1: PK: Mean Single Dose Concentration of LY3023414 at 2h Post-dose
NCT02981342 (11) [back to overview]Stage 2: Overall Survival (OS)
NCT03026803 (1) [back to overview]Response Rate
NCT03044730 (6) [back to overview]1-year Progression Free Survival (PFS) Rate
NCT03044730 (6) [back to overview]Objective Response Rate (ORR)
NCT03044730 (6) [back to overview]Objective Response Rate (ORR)
NCT03044730 (6) [back to overview]Median PFS (Median Progression-Free Survival)
NCT03044730 (6) [back to overview]Median PFS (Median Progression-Free Survival)
NCT03044730 (6) [back to overview]Clinical Benefit Rate (CBR)
NCT03050814 (3) [back to overview]Number of Participants That Are Hospitalized Because of Adverse Events Attributed to Disease Progression
NCT03050814 (3) [back to overview]Number of Participants With Serious and Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v5.0)
NCT03050814 (3) [back to overview]Progression Free Survival Between the Standard of Care (SOC) Arm A, and Standard of Care (SOC) Arm B + lead-in
NCT03093870 (10) [back to overview]Number of Participants With Clinically Significant Change in Vital Signs and Physical Examinations - Part 1
NCT03093870 (10) [back to overview]Progression-free Survival (PFS) - Part 1
NCT03093870 (10) [back to overview]Number of Participants With ECG Parameters of Interest - Safety Lead-In
NCT03093870 (10) [back to overview]Number of Participants With Clinically Significant Laboratory Tests - Part 1
NCT03093870 (10) [back to overview]Overall Survival (OS) - Part 1
NCT03093870 (10) [back to overview]Number of Participants With Clinically Significant Laboratory Tests- Safety Lead-in
NCT03093870 (10) [back to overview]Duration of Response (DoR) - Part 1
NCT03093870 (10) [back to overview]Number of Participants With Clinically Significant Change in Vital Signs and Physical Examinations - Safety Lead-In
NCT03093870 (10) [back to overview]Number of Participants With ECG Parameters of Interest - Part 1
NCT03093870 (10) [back to overview]Tumor Size - Part 1
NCT03111732 (7) [back to overview]Number Participants With Grade 1-4 Adverse Events Unrelated, Unlikely, Possibly, Probably and Definitely Related to Oxaliplatin
NCT03111732 (7) [back to overview]Number of Participants With Grade 1-4 Adverse Events Unrelated, Unlikely, Possibly, and Probably Related to Capecitabine
NCT03111732 (7) [back to overview]Number of Participants Obtaining a Complete Response (CR) and Partial Response (PR)
NCT03111732 (7) [back to overview]Overall Survival
NCT03111732 (7) [back to overview]Number of Participants With Serious and Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0)
NCT03111732 (7) [back to overview]Progression Free Survival (PFS)
NCT03111732 (7) [back to overview]Number Participants With Grade 1-4 Adverse Events Unrelated, Unlikely, Possibly, Probably and Definitely Related to Pembrolizumab
NCT03262935 (6) [back to overview]Investigator Assessed Progression Free Survival
NCT03262935 (6) [back to overview]Objective Response Rate
NCT03262935 (6) [back to overview]Overall Survival
NCT03262935 (6) [back to overview]Patient Reported Outcomes for Health Related Quality of Life
NCT03262935 (6) [back to overview]Patient Reported Outcomes for Health Related Quality of Life
NCT03262935 (6) [back to overview]Progression Free Survival
NCT03376659 (3) [back to overview]Progression Free Survival (PFS)
NCT03376659 (3) [back to overview]Progression Free Survival Rate (PFS) Pancreatic Cancer
NCT03376659 (3) [back to overview]Progression Free Survival Rate (PFS) Colorectal Cancer
NCT03501979 (1) [back to overview]Length of Subject Survival After Starting Study Treatment
NCT03515941 (2) [back to overview]Median Time to Recurrence
NCT03515941 (2) [back to overview]Number of Participants Who Complete the Recommended Therapy From Each Arm
NCT03523585 (5) [back to overview]Percentage of Participants With Objective Response Rate (ORR) in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine
NCT03523585 (5) [back to overview]Duration of Response (DoR) Based on BICR in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine
NCT03523585 (5) [back to overview]Overall Survival (OS) in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine
NCT03523585 (5) [back to overview]Progression-Free Survival (PFS) Based on Blinded Independent Central Review (BICR) in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine
NCT03523585 (5) [back to overview]Progression-Free Survival (PFS) Based on Investigator Assessment in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine
NCT03675737 (14) [back to overview]Objective Response Rate (ORR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥1
NCT03675737 (14) [back to overview]Objective Response Rate (ORR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥10
NCT03675737 (14) [back to overview]Overall Survival (OS) in All Participants
NCT03675737 (14) [back to overview]Overall Survival (OS) In Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥10
NCT03675737 (14) [back to overview]Progression Free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in All Participants
NCT03675737 (14) [back to overview]Progression Free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥1
NCT03675737 (14) [back to overview]Progression Free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥10
NCT03675737 (14) [back to overview]Duration of Response (DOR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in All Participants
NCT03675737 (14) [back to overview]Duration of Response (DOR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥1
NCT03675737 (14) [back to overview]Overall Survival (OS) In Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥1
NCT03675737 (14) [back to overview]Number of Participants Who Discontinued Study Treatment Due To an Adverse Event (AE)
NCT03675737 (14) [back to overview]Number of Participants Who Experienced an Adverse Event (AE)
NCT03675737 (14) [back to overview]Objective Response Rate (ORR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in All Participants
NCT03675737 (14) [back to overview]Duration of Response (DOR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥10
NCT03734029 (12) [back to overview]Best Overall Response and Confirmed Objective Response Rate (ORR) in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer
NCT03734029 (12) [back to overview]Duration of Response in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer
NCT03734029 (12) [back to overview]Duration of Response in Participants With HER2-low Breast Cancer (All Patients)
NCT03734029 (12) [back to overview]Best Overall Response and Confirmed Objective Response Rate (ORR) in Participants With HER2-low Breast Cancer (All Patients)
NCT03734029 (12) [back to overview]Progression-free Survival Based on Investigator Assessment in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer
NCT03734029 (12) [back to overview]Overall Survival (OS) in All Patients
NCT03734029 (12) [back to overview]Number of Overall Survival Events (Deaths)
NCT03734029 (12) [back to overview]All-Cause Mortality
NCT03734029 (12) [back to overview]Overall Survival (OS) in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer
NCT03734029 (12) [back to overview]Progression-free Survival (PFS) Based on Blinded Independent Central Review (BICR) in Participants With HER2-low Breast Cancer (All Patients) Regardless of Hormone Receptor Status
NCT03734029 (12) [back to overview]Progression-free Survival (PFS) Based on Blinded Independent Central Review (BICR) in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer
NCT03734029 (12) [back to overview]Progression-free Survival Based on Investigator Assessment in Participants With HER2-low Breast Cancer (All Patients)
NCT03770689 (20) [back to overview]Number of Participants With Abnormalities [Grade Greater Than or Equals to (>=) 3] in Laboratory Test Values
NCT03770689 (20) [back to overview]Number of Participants Who Experienced Dose Limiting Toxicity (DLT) Confirmed by Safety Monitoring Committee (SMC)
NCT03770689 (20) [back to overview]Apparent Volume of Distribution (Vz/f) of Peposertib
NCT03770689 (20) [back to overview]Neoadjuvant Rectal (NAR) Score
NCT03770689 (20) [back to overview]Apparent Volume of Distribution (Vz/f) of Peposertib
NCT03770689 (20) [back to overview]Disease-free Survival
NCT03770689 (20) [back to overview]Area Under the Plasma Concentration-time Curve From Time Zero to Last Sampling Time (Tlast) (AUC0-t) of Peposertib
NCT03770689 (20) [back to overview]Maximum Observed Plasma Concentration (Cmax) of Peposertib
NCT03770689 (20) [back to overview]Number of Participants Wtih Treatment Emergent Adverse Events (TEAEs) and Treatment-Related TEAEs According to National Cancer Institute Common Terminology Criteria of Adverse Events (NCI-CTCAE) Version 5.0
NCT03770689 (20) [back to overview]Time to Reach Maximum Plasma Concentration (Tmax) of Peposertib
NCT03770689 (20) [back to overview]Time From Surgery to Distant Metastasis
NCT03770689 (20) [back to overview]Apparent Terminal Half-life (t1/2) of Peposertib
NCT03770689 (20) [back to overview]Apparent Terminal Half-life (t1/2) of Peposertib
NCT03770689 (20) [back to overview]Total Body Clearance Following Oral Administration (CL/f) of Peposertib
NCT03770689 (20) [back to overview]Time From Surgery to Local Recurrence
NCT03770689 (20) [back to overview]Percentage of Participants With Pathological Complete Response (pCR)
NCT03770689 (20) [back to overview]Percentage of Participants With Composite Pathological Complete Response (pCR)/ Clinical Complete Response (cCR)
NCT03770689 (20) [back to overview]Percentage of Participants With Clinical Complete Response (cCR)
NCT03770689 (20) [back to overview]Number of Participants With Markedly Abnormal Vital Sign Measurements
NCT03770689 (20) [back to overview]Number of Participants With Clinically Significant Abnormalities in Electrocardiogram (ECG) Findings
NCT03783442 (1) [back to overview]Overall Survival (OS)
NCT03853707 (4) [back to overview]Overall Survival (OS)
NCT03853707 (4) [back to overview]Overall Response
NCT03853707 (4) [back to overview]Progression-free Survival (PFS)
NCT03853707 (4) [back to overview]Clinical Benefit Rate
NCT03930771 (4) [back to overview]Safety, as Measured by the Number of Subjects With at Least One AE
NCT03930771 (4) [back to overview]Effect of the CAP and TMZ Combination on Pituitary Function, Measured by Changes in Pituitary Hormone Secretion in Patients
NCT03930771 (4) [back to overview]Tolerability of the TMZ and Capecitabine Combination, as Measured by Number of Participants With a Dose-limiting Toxicity
NCT03930771 (4) [back to overview]Number of Subjects With Radiographic Response, as Defined by the RECIST Criteria.
NCT04031885 (1) [back to overview]Objective Response Rate (ORR): Percentage of Participants Who Achieve Complete Response (CR) or Partial Response (PR)
NCT04034251 (8) [back to overview]Number of Grades 3-5 Serious and/or Non-serious Adverse Events Related to the Research Interventions
NCT04034251 (8) [back to overview]Progression Free Survival (PFS) in Participants With Peritoneal Metastases From Gastric Cancer After Repeated Intraperitoneal Chemotherapeutic Infusion (IPC) and Systemic Paclitaxel Administration With Concomitant Capecitabine Therapy
NCT04034251 (8) [back to overview]Overall Survival (OS)
NCT04034251 (8) [back to overview]Number of Participants With Serious and/or Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0)
NCT04034251 (8) [back to overview]Number of Participants With Intra-peritoneal Progression Free Survival (iPFS)
NCT04034251 (8) [back to overview]Number of Participants With Distant Extra-peritoneal Disease-free Survival
NCT04034251 (8) [back to overview]Intra-peritoneal Progression Free Survival (iPFS) Reported With an 95% Confidence Interval
NCT04034251 (8) [back to overview]Intra-peritoneal Progression Free Survival (iPFS) Reported With an 80% Confidence Interval
NCT04366713 (2) [back to overview]Incidence and Severity of Diarrhea
NCT04366713 (2) [back to overview]Changes in Colon Pathology
NCT05091528 (4) [back to overview]Proportion of Participants With Dose Limiting Toxicities
NCT05091528 (4) [back to overview]Number of Participants With an Objective Response Rate
NCT05091528 (4) [back to overview]Number of Participants With Laboratory Abnormalities
NCT05091528 (4) [back to overview]Number of Participants With Treatment-emergent Adverse Events

Overall Clinical Response Rate

Overall response rate is defined as the percentage of participants with a CR (complete disappearance of all target lesions), PR (a 30% decrease in the sum of the longest diameter of target lesions) determined by clinical measurements per the Response Evaluation Criteria in Solid Tumors (RECIST) and/or a complete pathologic response (disappearance of all invasive tumor pathologically or presence of ductal carcinoma in situ) per the Chevallier criteria. For details about the RECIST or Chevallier criteria see the protocol link module. (NCT00005908)
Timeframe: 6 years

InterventionPercentage of participants (Number)
Complete ResponsePartial ResponseComplete pathologic response
Dose A & B-Cohort 1 & 2-Arm 1& 2-Docetaxel & Capecitabine315910

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Complementary Deoxyribonucleic Acid (cDNA) Expression

Patients were classified as responders or non-responders based on change in tumor size by clinical exam and pathologic response.For instance, patients with a pathological complete response, micro-invasive disease at surgery, or clinical complete response after four cycles of treatment were considered responders. Changes in gene expression associated with treatment was assessed before/after chemotherapy. All gene expression summary intensities below 50 were thresholded to the value of 50 and genes showing variability significantly smaller than the median gene variability were screened out. (NCT00005908)
Timeframe: 6 years

,
InterventionParticipants (Number)
RespondersNon-responders
Dose A-Cohort 1-Arm 1-Docetaxel & Capecitabine82
Dose B-Cohort 2-Arm 2 Reduced Dose-Docetaxel & Capecitabine713

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Number of Participants With Adverse Events

Here is the number of participants with adverse events. For the detailed list of adverse events see the adverse event module. (NCT00005908)
Timeframe: 6 years

InterventionParticipants (Number)
Dose A-Cohort 1-Arm 1-Docetaxel & Capecitabine9
Dose B-Cohort 2-Arm 2 Reduced Dose-Docetaxel & Capecitabine20

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Number of Participants, e.g. Responders and Non-responders With a Percent Change in Expression Patterns After Chemotherapy With Changes in Expression Patterns After Chemotherapy in Preclinical Models

Patients were classified as responders or non-responders based on change in tumor size by clinical exam and pathologic response.For instance, patients with a pathological complete response, micro-invasive disease at surgery, or clinical complete response after four cycles of treatment were considered responders. Changes in gene expression associated with treatment was assessed before/after chemotherapy. All gene expression summary intensities below 50 were thresholded to the value of 50 and genes showing variability significantly smaller than the median gene variability were screened out. (NCT00005908)
Timeframe: 6 years

InterventionParticipants (Number)
RespondersNon-responders
Dose A & B-Cohort 1 & 2-Arm 1 & 2-Docetaxel & Capecitabine813

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Disease-free Survival

Participants with disease-free survival were reported. Disease-free survival was assessed as the number of days between randomization and the first time at which relapse, a new occurrence of colon cancer, or death was recorded, or the last time at which a participant was known to be disease free (censoring time). (NCT00009737)
Timeframe: Approximately 3 years

InterventionParticipants (Number)
Capecitabine656
5-Fluorouracil + Leucovorin603

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Number of Participants With Abnormalities for Blood Chemistry and Hematological Parameters

Laboratory abnormalities were categorized according to the National Cancer Institute of Canada Common Toxicity Criteria (NCIC - CTC) grading system (May 1991 revised) as Grade 1 (mild), Grade 2 (moderate), Grade 3 (severe) and Grade 4 (life- threatening). Participants with abnormalities in hemoglobin, granulocytes, lymphocytes, neutrophils, neutrophils/granulocytes, platelets, white blood cell, potassium, serum creatinine, sodium, total bilirubin, alanine transaminase, aspartate aminotransferase, alkaline phosphatase, calcium (hyper), and calcium (hypo) with Grades 1-4 were presented. (NCT00009737)
Timeframe: Up to Week 25

,
InterventionParticipants (Number)
Alanine transaminaseAspartate aminotransferaseAlkaline PhosphataseCalcium (Hyper)Calcium (Hypo)GranulocytesHemoglobinLymphocytesNeutrophilsNeutrophils/GranulocytesPlateletsPotassiumSerum CreatinineSodiumTotal BilirubinWhite blood cell
5-Fluorouracil + Leucovorin3332882896811243650744596612160156138184185409
Capecitabine3273003346715020691778308316182209157189501220

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Mean Change From Baseline in Global Health Status at Week 25

Global health status was assessed as a sub scale of European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30. It was scored on a scale of 0-100; where higher score indicates better quality of life. Wherever the scores for the participants were not available, the last value carried forward (LVCF) were used. (NCT00009737)
Timeframe: Baseline (Days -7 to 1) and at Week 25

InterventionScore on a scale (Mean)
Capecitabine2.1
5-Fluorouracil + Leucovorin2.6

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Overall Survival

Participants with overall survival were reported. Overall survival was assessed as the number of days between randomization and death or the last time at which a participant was known to be alive (censoring time). (NCT00009737)
Timeframe: Approximately 3 years

InterventionParticipants (Number)
Capecitabine804
5-Fluorouracil + Leucovorin756

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Relapse-Free Survival

Participants with relapse-free survival were reported. Relapse-free survival was assessed as the number of days between randomization and the first time at which relapse, a new occurrence of colon cancer, or death was recorded, or the last time at which a participants was known to be disease free (censoring time), excluding deaths that were not related to treatment or to disease progression. (NCT00009737)
Timeframe: Approximately 3 years

InterventionParticipants (Number)
Capecitabine677
5-Fluorouracil + Leucovorin621

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Number of Participants With Any Adverse Events and Serious Adverse Events

An Adverse Event (AE) is defined as any untoward medical occurrence in a participant or clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered to be related to the medicinal product. An Serious Adverse Events (SAEs) is any untoward medical occurrence that, at any dose, results in death, is life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, or results in a congenital anomaly/birth defect. (NCT00009737)
Timeframe: Up to Week 29

,
InterventionParticipants (Number)
All adverse eventsSerious adverse events
5-Fluorouracil + Leucovorin885182
Capecitabine910181

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Duration of Overall Complete Response

The duration of overall complete response was assessed from the time that measurement criteria were met for complete response until the first date that recurrent or progressive disease was objectively documented. Participants without observed progressive disease after an objective complete response were censored at the date of the last tumor assessment. (NCT00022698)
Timeframe: Approximately 43 Months

Interventionmonths (Number)
Cohort 1, Initial Regimen: (Capecitabine + Irinotecan)12.45
Cohort 2, Amended Regimen: (Capecitabine + Irinotecan)12.68

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Duration of Overall Response

Duration of overall response was assessed from the time that measurement criteria were first met for CR/PR (whichever is first recorded) until the first date that recurrent or progressive disease was documented. It was analyzed for responders only. Participants without observed progressive disease after an objective response were censored at the date of the last tumor assessment. (NCT00022698)
Timeframe: Approximately 43 Months

Interventionmonths (Median)
Cohort 1, Initial Regimen: (Capecitabine + Irinotecan)7.0
Cohort 2, Amended Regimen: (Capecitabine + Irinotecan)7.7

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Overall Survival

Overall Survival is defined as the time from start of treatment to the date of death. Participants who did not die were censored at the last date the participant was known to be alive. (NCT00022698)
Timeframe: Approximately 43 Months

Interventionmonths (Median)
Cohort 1, Initial Regimen: (Capecitabine + Irinotecan)22.9
Cohort 2, Amended Regimen: (Capecitabine + Irinotecan)20.5

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Percentage of Participants With One-year Survival

Survival was measured as the time from start of treatment to the date of death or till one year whichever occurred first. (NCT00022698)
Timeframe: Up to Month 12

Interventionpercentage of participants (Number)
Cohort 1, Initial Regimen: (Capecitabine + Irinotecan)67
Cohort 2, Amended Regimen: (Capecitabine + Irinotecan)71

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Time to Disease Progression

Time to disease progression was assessed as the time from start of treatment to the time the participant was first recorded as having disease progression or died due to causes other than disease progression. If a participant never progressed while being followed, he/she was censored at the date of the last tumor assessment or the date of the last dose if no post-baseline tumor measurement was available. (NCT00022698)
Timeframe: Approximately 43 Months

Interventionmonths (Median)
Cohort 1, Initial Regimen: (Capecitabine + Irinotecan)6.1
Cohort 2, Amended Regimen: (Capecitabine + Irinotecan)7.6

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Time To Objective Response

The time to objective response is defined as the time from start of treatment to the date of first objective response. Participants who never responded during study were censored at the last tumor assessment or the date of last dose, whichever was later, or at the date of death if occurring prior to response. (NCT00022698)
Timeframe: Approximately 43 Months

Interventionmonths (Median)
Cohort 1, Initial Regimen: (Capecitabine + Irinotecan)5.5
Cohort 2, Amended Regimen: (Capecitabine + Irinotecan)4.3

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Time to Treatment Failure

Time to treatment failure was assessed as the time from start of treatment to the time the participant was withdrawn due to any of the reasons such as adverse events, progressive disease, insufficient therapeutic response, death, failure to return, or refused treatment, did not cooperate or withdrew consent. (NCT00022698)
Timeframe: Approximately 43 Months

Interventionmonths (Median)
Cohort 1, Initial Regimen: (Capecitabine + Irinotecan)5.8
Cohort 2, Amended Regimen: (Capecitabine + Irinotecan)7.3

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Number of Participants With Any Adverse Events, Serious Adverse Events and Deaths

An adverse event (AEs) is any untoward medical occurrence in a participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with the treatment. An adverse event can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding, for example), symptom, or disease temporally associated with the use of a pharmaceutical product, whether or not considered related to the pharmaceutical product. Preexisting conditions which worsen during a study are also considered as adverse events. A serious adverse event is defined as any event which was fatal (resulted in death), life-threatening (with immediate risk of death), resulted in a new or prolongation of a current hospitalization, resulted in persistent or significant disability or incapacity, was a congenital anomaly or birth defect, considered medically significant by the investigator, required intervention to prevent one or more of the outcomes listed above. (NCT00022698)
Timeframe: Approximately 43 Months

,,
InterventionNumber of participants (Number)
Any AEsSAEsDeaths During StudyDeaths During Follow-up
Cohort 1, Initial Regimen: (Capecitabine + Irinotecan)1510013
Cohort 2, Amended Regimen: (Capecitabine + Irinotecan)5225323
Total Participants (Cohort 1 + Cohort 2)6735336

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Tumor Response Rate Based on Tumor Measurement as Per Response Evaluation Criteria In Solid Tumors Version 1.0 (RECIST 1.0)

Objective Response Rate (ORR) is defined as the percentage of participants with complete response (CR) or partial response (PR) according to response evaluation criteria in solid tumors (RECIST 1.0). CR is defined as the disappearance of all target and non-target lesions and normalization of tumor marker level. PR is defined as a greater than or equal to (>/=) 30% decrease in the sum of the longest diameter (LD) of the target lesions, taking as reference the baseline sum of LD. Participants who did not have a post-baseline tumor measurement were considered non-responders in the assessment of ORR. (NCT00022698)
Timeframe: Approximately 43 Months

,
Interventionpercentage of participants (Number)
CRPR
Cohort 1, Initial Regimen:(Capecitabine + Irinotecan)740
Cohort 2, Amended Regimen: (Capecitabine + Irinotecan)242

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Relapse-free Survival Rates at 2.4 Years

"Percentage of participants who were alive and relapse-free at time of analysis were counted as Alive without relapse at 2.4 years. Participants who had a first local recurrence, first distant metastasis or death from any cause were counted as relapse, first occurrence. These rates were estimated using the Kaplan Meier method" (NCT00024102)
Timeframe: randomization until date of first event, or date last known to be event free if no event was reported (up to 5 years)

,
Interventionpercentage of participants (Number)
Relapse, first occurrenceAlive without relapse
Capecitabine2080
Standard Chemotherapy1189

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Overall Survival Rate at 2.4 Years

Percentage of patients who were alive at 2.4 years. This rate was estimated using the Kaplan Meier method. (NCT00024102)
Timeframe: Time from registration to death (up to 15 years)

Interventionpercentage of participants (Number)
Standard Chemotherapy93
Capecitabine88

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Overall Survival

Measured from time of registration to death, or last contact date (NCT00033540)
Timeframe: All patients will be followed until death or three years after registration, whichever is first.

Interventionmonths (Median)
Capecitabine + Gemcitabine7

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Accrual of Patients With This Disease Site

Only eligible patients who received treatment were evaluable for response and survival outcomes. (NCT00033540)
Timeframe: 1-20 months

Interventionparticipants (Number)
EligibleEligible and Analyzable
Capecitabine + Gemcitabine5452

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Median Survival Time for Participants With Relevant Biologic Markers

To evaluate in a preliminary fashion relevant prognostic markers in gallbladder and cholangiocarcinoma which may have prognostic implications as predictors of survival. Overall survival measured from time of registration to death, or last contact date. (NCT00033540)
Timeframe: All patients will be followed until death or three years after registration, whichever is first.

Interventionmonths (Median)
TS 3' +/+ (N=14)TS 3' +/- (N=6)TS 3' -/- (N=2)TS 5' Low functional significance (N=16)TS 5' Intermediate functional significance (N=16)MTHFR C677T - C/C (N=11)MTHFR C677T - C/T (N=11)MTHFR A1298C - A/A (N=11)MTHFR A1298C - A/C (N=8)MTHFR A1298C - C/C (N=3)RRMI G/A - G/G (N=9)RRMI G/A - G/A (N=10)RRMI G/A - A/A (N=3)CDA A79C - A/A (N=8)CDA A79C - A/C (N=12)CDA A79C - C/C (N=1)
Capecitabine + Gemcitabine779976774979547NA

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Response

Complete Response (CR) is complete disappearance of all measurable and non-measurable disease. No new lesions, no disease related symptoms. Normalization of markers and other abnormal lab values. Partial Response (PR) is greater than or equal to 30% decrease under baseline of the sum of longest diameters of all target measurable lesions. No unequivocal progression of non-measurable disease. No new lesions. Confirmation of CR or PR means a repeat scan at least 4 weeks apart documented before progression or symptomatic deterioration. Progression is 20% increase in sum of longest diameters of target measurable lesions over smallest sum observed and/or unequivocal progression of non-measurable disease and/or appearance of new lesion/site or death due to disease without prior documentation of progression and without symptomatic deterioration. Symptomatic deterioration is global deterioration of health status requiring discontinuation of treatment without objective evidence of progression. (NCT00033540)
Timeframe: Patients assessed at least every six weeks while on protocol treatment

Interventionparticipants (Number)
Confirmed Partial ResponseUnconfirmed Partial ResponseStable DiseaseProgressionSymptomatic DeteriorationEarly DeathInadequate Assessment
Capecitabine + Gemcitabine761215318

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Percentage of Participants With Reoccurrence

Percentage of participants where number with local recurrence, distant metastasis, or death of any cause at 50 months is divided by total number of participants and used as primary efficacy end point to compare paclitaxel to combination docetaxel and capecitabine in breast cancer treatment for preventing recurrence (return of cancer). (NCT00050167)
Timeframe: Median of 50 months

Interventionparticipants (Log Mean)
Weekly Paclitaxel (WP)90.7
Docetaxel and Capecitabine (DX)87.5

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Maximum Tolerated Dose Determined by Dose-limiting Toxicities

1st 3 pts will be treated on arm 2. If 0/3 DLTs observed, the dose will be escalated to arm 3. If 1/3 DLTs onserved on arm 2, 3 more pts will be treated on arm 2. If no additional DLTs are observed on arm 2, the dose will be escalated to arm 3. If at most 1/6 DLTs observed on arm 3, arm 3 will be considered the MTD. If more than 1/6 DLTs observed on arm 3, the dose will be de-escalated to arm 2. If at most 1/6 DLTs observed on arm 2, arm 2 will be considered the MTD. If more than 1/6 pts on arm 2 experience a DLT, the dose will be de-escalated to arm 1. The remaining pts will be treated on arm 1 as the MTD, unless more than 1/6 DLTs, in which case the study will stop. DLT is defined as any grade III or IV non-hematologic toxicity (incl. diarrhea w adequate antidiarrheal treatment & hydration & nausea/vomiting w maximal antiemetic prophylaxis, as per protocol) or grade IV hematologic toxicity. DLT will be based on the 1st course of treatment according to the revised NCI CTC v 2.0 (NCT00068588)
Timeframe: 21 days

InterventionPatients experiencing DLT (Number)
Arm 20
Arm 30

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Response Rate of a Combination of GTI-2040 and Capecitabine

Following the dose escalation step, additional patients will be accrued at the MTD and evaluated for disease response using RECIST v1.0 criteria. Patients with confirmed complete or partial response are considered to have responded favorably to treatment.The sample size and early stopping for futility was governed by a two stage Optimum design suggested by Simon. It was assumed that a true response rate less than 25% would not warrant further study of this agent. It was also assumed that a response rate of 45% would be considered promising. In the first stage (following the dose escalation step), 15 evaluable patients were treated. Four or fewer observed responses, would stop accrual, while 5 or more observed would continue accrual for an additional 12 patients during the second stage of the study. Ten or more responses out of 27 patients will be considered evidence warranting further study of the regimen providing toxicity and survival also appear favorable. (NCT00068588)
Timeframe: Up to 6 years

Interventionpercentage of patients responding (Number)
Arm 320

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PFS by General Approach, Participants With Curative Surgery Not Censored: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

PFS is defined as the time from randomization to disease progression (PD) or death due to any cause. Participants who underwent curative surgery after experiencing a sufficient shrinkage of their tumor were not censored at the date of surgery, but any relapse, new occurrence of colorectal cancer, or death was considered as an event. Superiority analysis that followed the general approach took into account all tumor assessments obtained during the primary study treatment phase, the post-study treatment phase and those obtained during the follow-up phase. Superiority of the BV-containing arms was compared with the chemotherapy alone arms. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4+P/XELOX+P245.0
FOLFOX-4+BV/XELOX+BV287.0

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Progression-free Survival (PFS) as Assessed by the Investigator According to Response Evaluation Criteria in Solid Tumors (RECIST) by General Approach (Participants With Curative Surgery Censored): Non-inferiority of XELOX Versus FOLFOX-4

PFS was defined as the time from randomization to progressive disease or death. Participants with neither disease progression nor death were censored at the last date of the last tumor assessment that confirmed that their disease had not progressed. Participants with no tumor assessments after baseline who were alive at the time of clinical cutoff were censored at the date of randomization. Participants who underwent surgical resection with curative intent without prior progression were censored at the date of surgery. PFS was based on tumor assessments made by the investigators according to the RECIST criteria. Non-inferiority analysis that followed the general approach took into account all tumor assessments obtained during the primary study treatment phase, the post-study treatment phase and those obtained during the follow-up phase. Non-inferiority of the XELOX-containing arms compared with the FOLFOX-4- containing arms was investigated. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV259
XELOX/XELOX+P/XELOX+BV241

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Time to Response as Assessed by the Investigator According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4

For participants whose BOR was CR or PR, time to response was measured as the time from randomization to the first time when the measurement criteria for CR or PR (whichever status was recorded first) was met. It was based on tumor assessments made by the investigators according to the RECIST criteria. Results were reported as the number of participants achieving a response in 8 time categories from Week 1 to Week 54. Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: Week 1 to Week 54

,
InterventionParticipants (Number)
Week 1-6Week 7-12Week 13-18Week 19-24Week 25-30Week 31-36Week 37-42Week 49-54
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV671901552514732
XELOX/XELOX+P/XELOX+BV931911103813310

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Time to Response as Assessed by the Investigator According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

For participants whose BOR was CR or PR, time to response was measured as the time from randomization to the first time when the measurement criteria for CR or PR (whichever status was recorded first) was met. It was based on tumor assessments made by the investigators according to the RECIST criteria. Results were reported as the number of participants achieving a response in 8 time categories from Week 1 to Week 54. Superiority of the BV-containing arms was compared with the chemotherapy alone arms. (NCT00069095)
Timeframe: Week 1 to Week 54

,
InterventionParticipants (Number)
Week 1-6Week 7-12Week 13-18Week 19-24Week 25-30Week 31-36Week 37-42Week 49-54
FOLFOX-4+P/XELOX+P58146105267210
XELOX/XELOX+P/XELOX+BV48138872912821

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Time to Treatment Failure (TTF) as Assessed by the Investigator According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4

Time to treatment failure was defined as the time from the date of randomization to the date of discontinuation of the primary study treatment phase due to adverse event/intercurrent illness, insufficient therapeutic response, death, failure to return, refusing treatment/being unwilling to cooperate, or withdrawing consent; discontinuation of the post study treatment phase due to adverse event, progressive disease, death, participant refusal/administrative reasons, or withdrawing consent; documented disease progression; or death due to any cause, whichever occurred first. The general approach took into account all tumor assessments obtained during the primary study treatment phase, the post-study treatment phase and those obtained during the follow-up phase.The on-treatment approach included only tumor assessments and deaths that occurred no later than 28 days after the last confirmed intake of any study medication in the primary study treatment phase only. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

,
Interventiondays (Median)
General ApproachOn-treatment Approach
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV191.0190.0
XELOX/XELOX+P/XELOX+BV179.0176.0

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Time to Treatment Failure as Assessed by the Investigator According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

Time to treatment failure was defined as the time from the date of randomization to the date of discontinuation of the primary study treatment phase due to adverse event/intercurrent illness, insufficient therapeutic response, death, failure to return, refusing treatment/being unwilling to cooperate, or withdrawing consent; discontinuation of the post study treatment phase due to adverse event, progressive disease, death, participant refusal/administrative reasons, or withdrawing consent; documented disease progression; or death due to any cause, whichever occurred first. The general approach included all tumor assessments or deaths that occurred during the primary study treatment phase, the post-study treatment phase, or the follow-up phase. The on-treatment approach included only tumor assessments and deaths that occurred no later than 28 days after the last confirmed intake of any study medication in the primary study treatment phase only. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

,
Interventiondays (Median)
General ApproachOn-treatment Approach
FOLFOX-4+BV/XELOX+BV209.0208.0
FOLFOX-4+P/XELOX+P183.0182.0

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Overall Survival: Non-inferiority of XELOX Versus FOLFOX-4

Overall survival was defined as the time from the date of randomization to the date of death. Participants who were not reported to have died at the time of the clinical cut-off date for the analysis were censored using the date they were last known to be alive. Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV549.0
XELOX/XELOX+P/XELOX+BV577.0

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Overall Survival: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

Overall survival was defined as the time from the date of randomization to the date of death. Participants who were not reported to have died at the time of the clinical cut-off date for the analysis were censored using the date they were last known to be alive. Superiority of the BV-containing arms was compared with the chemotherapy alone arms. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4+P/XELOX+P574.0
FOLFOX-4+BV/XELOX+BV551.0

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PFS (On-treatment Approach): Non-inferiority of XELOX Versus FOLFOX-4

PFS is defined as the time from randomization to disease progression (PD) or death due to any cause. The on-treatment analysis included only tumor assessments and death events that occurred no later than 28 days after the last confirmed intake of any study medication in the primary study treatment phase. Participants who did not have an event during this interval were censored at the date of the last tumor assessment within this time window, or on day 1 if no tumor assessment was available after baseline. Participants who underwent surgical resection with curative intent without prior progression within 28 days after the last confirmed intake of any study medication in the primary study treatment phase were censored at the date of surgery. The on-treatment approach excluded the possible impact of other treatments that might have been started before disease progression. Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV268.0
XELOX/XELOX+P/XELOX+BV234.0

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PFS (On-treatment Approach): Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

PFS is defined as the time from randomization to disease progression (PD) or death due to any cause. The on-treatment analysis included only tumor assessments and death events that occurred no later than 28 days after the last confirmed intake of any study medication in the primary study treatment phase. Participants who did not have an event during this interval were censored at the date of the last tumor assessment within this time window, or on day 1 if no tumor assessment was available after baseline. Participants who underwent surgical resection with curative intent without prior progression within 28 days after the last confirmed intake of any study medication in the primary study treatment phase were censored at the date of surgery. The on-treatment approach excluded the possible impact of other treatments that might have been started before disease progression. Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4+P/XELOX+P241.0
FOLFOX-4+BV/XELOX+BV316.0

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PFS as Assessed by the Independent Review Committee (IRC) (General Approach, Participants With Curative Surgery Censored) - Non-inferiority of XELOX Versus FOLFOX-4

PFS is defined as the time from randomization to disease progression (PD) or death due to any cause. Participants with neither disease progression nor death were censored at the last date of the last tumor assessment that confirmed that their disease had not progressed. Participants who underwent surgical resection with curative intent without prior progression were censored at the date of surgery. PFS was analyzed on the basis of the tumor response assessments made by the IRC. Non-inferiority analysis that followed the general approach took into account all tumor assessments obtained during the primary study treatment phase, the post-study treatment phase and those obtained during the follow-up phase. Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV304.0
XELOX/XELOX+P/XELOX+BV261.0

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PFS as Assessed by the Investigator According to Response Evaluation Criteria in Solid Tumors (RECIST) by General Approach (Participants With Curative Surgery Censored) - Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

PFS was defined as the time from randomization to progressive disease or death. Participants with neither disease progression nor death were censored at the last date of the last tumor assessment that confirmed that their disease had not progressed. Participants with no tumor assessments after baseline who were alive at the time of clinical cutoff were censored at the date of randomization. Participants who underwent surgical resection with curative intent without prior progression were censored at the date of surgery. PFS was based on tumor assessments made by the investigators according to the RECIST criteria. Superiority analysis that followed the general approach took into account all tumor assessments obtained during the primary study treatment phase, the post-study treatment phase and those obtained during the follow-up phase. Superiority of the BV-containing arms was compared with the chemotherapy alone arms. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4+P/XELOX+P244.0
FOLFOX-4+BV/XELOX+BV285.0

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PFS as Assessed by the Independent Review Committee (IRC) (General Approach, Participants With Curative Surgery Censored) - Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

PFS is defined as the time from randomization to disease progression (PD) or death due to any cause. Participants with neither disease progression nor death were censored at the last date of the last tumor assessment that confirmed that their disease had not progressed. Participants who underwent surgical resection with curative intent without prior progression were censored at the date of surgery. PFS was analyzed on the basis of the tumor response assessments made by the IRC. Superiority analysis that followed the general approach took into account all tumor assessments obtained during the primary study treatment phase, the post-study treatment phase and those obtained during the follow-up phase. Superiority of the bevacizumab-containing arms was compared with the placebo-containing arms. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4+P/XELOX+P259.0
FOLFOX-4+BV/XELOX+BV335.0

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Duration of Overall Response as Assessed by the Investigator According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4

Duration of overall response was measured from the time that measurement criteria were first met for CR or PR (whichever status was recorded first) until the first date when progressive disease or death was documented. It was based on tumor assessments made by the investigators according to the RECIST criteria. Participants who neither progressed nor died were censored at the date of the last tumor assessment. Participants undergoing surgical resection with curative intent were censored at the date of surgery. Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV239.0
XELOX/XELOX+P/XELOX+BV226.0

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Best Overall Response (BOR) as Assessed by the Investigator According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

According to the RECIST criteria, BOR in an individual participant was defined as the best response recorded from the start of the treatment until disease progression or recurrence. Only tumor assessments as assessed by the investigator and made up to and including 28 days after last intake of study medication in the primary study treatment phase not later than date of first curative surgery were included in these analyses. Responders were defined as the percentage of participants with a confirmed best overall response of complete response (CR) or partial response (PR). Superiority of the BV-containing arms was compared with the chemotherapy alone arms. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

InterventionPercentage of responders (Number)
FOLFOX-4+P/XELOX+P49.2
FOLFOX-4+BV/XELOX+BV46.5

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Best Overall Response (BOR) as Assessed by the Investigator According to Response Evaluation Criteria in Solid Tumors (RECIST): Non-inferiority of XELOX Versus FOLFOX-4

According to the RECIST criteria, BOR in an individual participant was defined as the best response recorded from the start of the treatment until disease progression or recurrence. Only tumor assessments as assessed by the investigator and made up to and including 28 days after last intake of study medication in the primary study treatment phase not later than date of first curative surgery were included in these analyses. Responders were defined as the percentage of participants with a confirmed best overall response of complete response (CR) or partial response (PR). Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

InterventionPercentage of responders (Number)
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV49.4
XELOX/XELOX+P/XELOX+BV46.4

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BOR as Assessed by the IRC According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4

According to the RECIST criteria, the BOR in an individual participant was the best response recorded from the start of the treatment until disease progression/recurrence (taking the smallest measurements recorded since the baseline assessment as a reference for PD). The BOR as assessed by the IRC was determined based on tumor assessments that were made up to and including 28 days after last intake of study medication in the primary study treatment phase. Responders were defined as the percentage of participants with a complete response (CR) or partial response (PR). Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

InterventionPercentage of responders (Number)
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV38.6
XELOX/XELOX+P/XELOX+BV37.1

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BOR as Assessed by the IRC According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

According to the RECIST criteria, the BOR in an individual participant was the best response recorded from the start of the treatment until disease progression/recurrence (taking the smallest measurements recorded since the baseline assessment as a reference for PD). The BOR as assessed by the IRC was determined based on tumor assessments that were made up to and including 28 days after last intake of study medication in the primary study treatment phase. Responders were defined as the percentage of participants with a complete response (CR) or partial response (PR). Superiority of the BV-containing arms was compared with the chemotherapy alone arms. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

InterventionPercentage of responders (Number)
FOLFOX-4+P/XELOX+P37.5
FOLFOX-4+BV/XELOX+BV37.5

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Duration of Complete Response as Assessed by the Investigator According to RECIST: Non-inferiority of XELOX Versus FOLFOX-4

For complete responders, the duration of complete response was measured from the time measurement criteria were first met for complete response until the date that progressive disease (or death) was documented. Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV347.0
XELOX/XELOX+P/XELOX+BV589.0

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Duration of Complete Response as Assessed by the Investigator According to RECIST: Superiority of Chemotherapy Plus BV Over Chemotherapy Alone

For complete responders, the duration of complete response was measured from the time measurement criteria were first met for complete response until the date that progressive disease (or death) was documented. Superiority of the BV-containing arms was compared with the chemotherapy alone arms. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4+P/XELOX+P403.0
FOLFOX-4+BV/XELOX+BV386.0

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PFS by General Approach, Participants With Curative Surgery Not Censored: Non-inferiority of XELOX Versus FOLFOX-4

PFS is defined as the time from randomization to disease progression (PD) or death due to any cause. Participants who underwent curative surgery after experiencing a sufficient shrinkage of their tumor were not censored at the date of surgery, but any relapse, new occurrence of colorectal cancer, or death was considered as an event. Non-inferiority analysis that followed the general approach took into account all tumor assessments obtained during the primary study treatment phase, the post-study treatment phase and those obtained during the follow-up phase. Non-inferiority of the XELOX-containing arms was compared with the FOLFOX-4-containing arms. (NCT00069095)
Timeframe: Baseline until disease progression or death, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4/FOLFOX-4+P/FOLFOX-4+BV260.0
XELOX/XELOX+P/XELOX+BV244.0

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Duration of Overall Response as Assessed by the Investigator According to RECIST: Superiority Analysis of Chemotherapy Plus Bevacizumab Versus Chemotherapy Alone

Duration of overall response was measured from the time that measurement criteria were first met for CR or PR (whichever status was recorded first) until the first date when progressive disease or death was documented. It was based on tumor assessments made by the investigators according to the RECIST criteria. Participants who neither progressed nor died were censored at the date of the last tumor assessment. Participants undergoing surgical resection with curative intent were censored at the date of surgery. Superiority of the BV-containing arms was compared with the chemotherapy alone arms. (NCT00069095)
Timeframe: From baseline until disease progression/recurrence, approximately 2 years 6 months

Interventiondays (Median)
FOLFOX-4+P/XELOX+P225.0
FOLFOX-4+BV/XELOX+BV257.0

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Best Overall Response, Investigators' Assessments

Best overall response is best response recorded from start of treatment until disease progression/recurrence where responses include complete response (CR), partial response (PR), or stable disease (SD). CR was defined as disappearance of all TLs, non-TLs along with normalization of tumor marker level. PR is at least 30% decrease in sum of the LD of TLs, taking as reference baseline sum LD. SD is defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking reference of smallest sum LD since treatment started. It was dependent on achievement of measurement and confirmation criteria. BOR .i.e. CR or PR was confirmed by repeat assessments performed within 4 weeks. For SD, follow-up assessments had to meet the SD criteria at least once after study entry within 6 to 8 weeks. (NCT00069108)
Timeframe: Up to 3 years

,
Interventionparticipants (Number)
Investigator Assessed, RespondersInvestigator assessed-CRInvestigator assessed-PR
FOLFOX-455253
XELOX63063

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Best Overall Response, Independent Review Committee Assessment

Best overall response is best response recorded from start of treatment until disease progression/recurrence where responses include CR, PR, or SD. CR was defined as disappearance of all TLs, non-TLs along with normalization of tumor marker level. PR is at least 30% decrease in sum of the LD of TLs, taking as reference baseline sum LD. SD defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking reference of smallest sum LD since treatment started. It was dependent on achievement of measurement and confirmation criteria. BOR .i.e. CR or PR was confirmed by repeat assessments performed within 4 weeks, for SD, follow-up assessments had to meet the SD criteria at least once after study entry within 6 to 8 weeks. This PFS evaluation was based on Independent Review Committee Assessment. (NCT00069108)
Timeframe: Up to 3 years

,
Interventionparticipants (Number)
IRC Assessed, RespondersIRC assessed-CRIRC assessed-PR
FOLFOX-439039
XELOX48048

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Time To Treatment Failure

Time to treatment failure was defined as the time from the date of randomization to the first occurrence of adverse event (AE), insufficient therapeutic response, death, failure to return, or refusing treatment/being uncooperative/withdrawing consent. (NCT00069108)
Timeframe: Up to 3 years

Interventiondays (Median)
XELOX125
FOLFOX-4121.5

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Progression Free Survival Based on Treatment Analysis- Per Population

Progression free survival (PFS) is defined as the time from the date of randomization to the day of documented disease progression or death from any cause. It was based on tumor assessments made according to the RECIST version 1.0, wherein PD was defined as at least a 20% increase in the sum of the LD of the TLs, taking as reference the smallest sum LD recorded since the treatment started or appearance of one or more new lesions or unequivocal progression of existing non-TLs. Participants with neither disease progression nor death were censored at the last date of the last tumor assessment confirming that they had not progressed. Participants with no tumor assessments after baseline but who were still alive at the time of the clinical cut-off were censored at date of randomization (NCT00069108)
Timeframe: Up to 3 years

Interventiondays (Median)
XELOX153
FOLFOX-4164

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Progression Free Survival Based on Treatment Analysis- Intent To Treat Population

Progression free survival (PFS) is defined as the time from date of randomization to day of documented disease progression or death from any cause. It was based on tumor assessments made according to the RECIST version 1.0, wherein PD was defined as at least a 20% increase in the sum of LD of the TLs, taking as reference the smallest sum LD recorded since the treatment started or appearance of one or more new lesions or unequivocal progression of existing non-TLs. Participants with neither disease progression nor death were censored at the last date of the last tumor assessment confirming that they had not progressed. Participants with no tumor assessments after baseline but who were still alive at the time of the clinical cut-off were censored at date of randomization. PFS was analyzed using an on-treatment approach included only disease progression and death that occurred no later than 28 days after the last confirmed intake of study medication in the primary study treatment phase. (NCT00069108)
Timeframe: Up to 3 years

Interventiondays (Median)
XELOX145
FOLFOX-4152

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Overall Survival

Overall survival was measured as the time from the date of randomization to the date of death. Participant who were not reported to have died at the time of the analysis were censored using the date they were last known to be alive. (NCT00069108)
Timeframe: Up to 3 years

Interventiondays (Median)
XELOX363
FOLFOX-4382

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Duration Of Response

Duration of response (DOR) is defined as the time when CR or PR was first met up to first date that PD or death is documented. CR is defined as disappearance of all TLs and non TLs, PR is defined as at least 30% decrease in the sum of the LD of TLs, taking as reference the baseline sum LD. PD was defined as at least a 20% increase in the sum of the LD of the TLs, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions for the TLs or the appearance of one or more new lesions and/or unequivocal progression of existing non-TLs. (NCT00069108)
Timeframe: Up to 3 years

Interventiondays (Median)
XELOX169
FOLFOX-4190

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Progression Free Survival

Progression free survival (PFS) is defined as the time from the date of randomization to the day of documented disease progression or death from any cause. It was based on tumor assessments made according to the Response Evaluation Criteria In Solid Tumors (RECIST) version 1.0, wherein progressive disease (PD) was defined as at least a 20% increase in the sum of the longest diameter (LD) of the target lesions (TLs), taking as reference the smallest sum LD recorded since the treatment started or appearance of one or more new lesions or unequivocal progression of existing non-target lesions. Participants with neither disease progression nor death were censored at the last date of the last tumor assessment confirming that they had not progressed. Participants with no tumor assessments after baseline but who were still alive at the time of the clinical cut-off were censored at date of randomization (NCT00069108)
Timeframe: Up to 3 years

Interventiondays (Median)
XELOX154
FOLFOX-4168

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Time To Response

Time to response (TOR) (best response of CR or PR) was measured as the time from randomization to the first date on which the measurement criteria for CR or PR (whichever status was recorded first) were met. CR for TLs was defined as disappearance of all TLs and for non-TLs as disappearance of all non-TLs and normalization of tumor marker level. PR was defined as at least 30% decrease in the sum of the LD of TLs, taking as reference the baseline sum LD. (NCT00069108)
Timeframe: Up to 3 years

,
Interventionparticipants (Number)
Week 1-6Week 7-12Week 13-18Week 19-24
FOLFOX-41123183
XELOX1326222

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Number of Participants With Marked Post-baseline Laboratory Abnormalities by Trial Treatment

Laboratory abnormalities were defined as those values that were outside the Roche defined reference range and showed a clinically relevant change from baseline. All laboratory parameters were categorized according to the National Cancer Center Common Toxicity Criteria (NCI-CTCAE) grading system. Incidence of Grade 1 to 4 laboratory abnormalities are presented in the table below. (NCT00069108)
Timeframe: Up to 3 years

,
Interventionparticipants (Number)
Serum Glutamic-Pyruvic Transaminase (SGPT)Serum Glutamic Oxaloacetic Transaminase (SGOT)Alkaline PhosphataseCalcium (hyper)Calcium (hypo )Glucose (hyper)Glucose (hypo)GranulocytesHaemoglobinNeutrophilsNeutrophils/GranulocytesPlateletsPotassium (hyper)Potassium (hypo)Serum AlbuminSerum CreatinineSodium (hyper)Sodium (hypo)Total BilirubinWhite blood cell (WBC)
FOLFOX-411017420197020796240199202212269213832217395205
XELOX901931847682011212161131141681768116181464107124

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Progression Free Survival Based on Independent Review Committee Assessment

Progression free survival (PFS) is defined as the time from the date of randomization to the day of documented disease progression or death from any cause. It was based on tumor assessments made according to the RECIST version 1.0, wherein PD was defined as at least a 20% increase in the sum of the LD of the TLs, taking as reference the smallest sum LD recorded since the treatment started or appearance of one or more new lesions or unequivocal progression of existing non-TLs. Participants with neither disease progression nor death were censored at the last date of the last tumor assessment confirming that they had not progressed. Participants with no tumor assessments after baseline but who were still alive at the time of the clinical cut-off were censored at date of randomization. This PFS evaluation was based on Independent Review Committee Assessment. (NCT00069108)
Timeframe: Up to 3 years

Interventiondays (Median)
XELOX168
FOLFOX-4162

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Relapse-Free Survival (RFS) [Number of Events]

A relapse-free survival (RFS) event included recurrence of the original colon cancer, development of a new colon or rectal cancer, and deaths related to any of the following: treatment, recurrence of the original colon cancer, or development of a new colon or rectal cancer. Participants who had not had any such event at the time of data analysis were censored at the last date they were known to be event-free. Participants whose cause of death was unrelated to treatment or disease recurrence were censored at the time of the last tumor assessment. (NCT00069121)
Timeframe: Time from randomization date to date of first RFS event/date last known to be event-free. Median observation time for RFS was 74 months (range: 0-95 months).

,
InterventionParticipants (Count of Participants)
Patients With EventPatients Without Events
5-FU/LV356586
XELOX290654

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Overall Survival [Number of Events]

Overall survival was measured as the time from randomization to the date of death, irrespective of the cause of death. Participants who were not reported as having died at the time of the analysis were censored using the date they were last known to be alive. (NCT00069121)
Timeframe: Time from randomization date to date of death/date last known to be alive. Median observation time was 83 months (range: 0-95 months).

,
InterventionParticipants (Count of Participants)
Patients With EventPatients Without Events
5-FU/LV286656
XELOX242702

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Number of Participants With at Least One Adverse Event by Most Severe Intensity

"The intensity of all adverse events (AEs) was categorized according to the National Cancer Institute Common Toxicity Criteria for Adverse Events (NCI CTCAE) (version 3.0) grading system. If an AE had occurred which was not contained in the NCI-CTC, a four-point scale (mild, moderate, severe, life-threatening) was used. The terms severe and serious are not synonymous and are independently assessed for each AE. Only the most severe intensity was counted for multiple occurrences of an AE in one individual. See the AEs results table for details." (NCT00069121)
Timeframe: From time of very first drug intake to 28 days after very last drug intake (median [full range] duration of study treatment per arm: 5-FU/LV MAYO CLINIC: 145 [4-208] days; 5-FU/LV ROSWELL PARK: 204 [1-239] days; XELOX: 163 [1-275] days).

,,
InterventionParticipants (Count of Participants)
Mild AEsModerate AEsSevere AEsLife-Threatening
5-FU/LV MAYO CLINIC55749329983
5-FU/LV ROSWELL PARK25621714621
XELOX85579254863

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Disease-Free Survival (DFS) [Time to Event]

Determination of an event was based on tumor assessments and survival follow-up assessments. A disease-free survival (DFS) event was defined as any recurrence of the original colon cancer or appearance of a new colon or rectal cancer (proven by cytology or histology, when possible) or death due to any cause, whichever was earliest. Participants who had not had any such event at the time of data analysis were censored at the last date they were known to be event-free. Participants with no tumor assessments after baseline were censored at Day 1. An isolated event of increased CEA, or unexplained clinical deterioration were not considered to be evidence of relapse without support of other objective measurements. The date of relapse was defined as the date of the definitive assessment by objective measurements. The median was estimated by the Kaplan-Meier method. The full range values include censored observations. (NCT00069121)
Timeframe: Time from randomization date to date of first DFS event/date last known to be event-free. Median observation time for DFS was 74 months (range: 0-95 months).

Interventionmonths (Median)
5-FU/LVNA
XELOX88.6

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Disease-Free Survival (DFS) [Number of Events]

Determination of an event was based on tumor assessments and survival follow-up assessments. A disease-free survival (DFS) event was defined as any recurrence of the original colon cancer or appearance of a new colon or rectal cancer (proven by cytology or histology, when possible) or death due to any cause, whichever was earliest. Participants who had not had any such event at the time of data analysis were censored at the last date they were known to be event-free. Participants with no tumor assessments after baseline were censored at Day 1. An isolated event of increased CEA, or unexplained clinical deterioration were not considered to be evidence of relapse without support of other objective measurements. The date of relapse was defined as the date of the definitive assessment by objective measurements. (NCT00069121)
Timeframe: Time from randomization date to date of first DFS event/date last known to be event-free. Median observation time for DFS was 74 months (range: 0-95 months).

,
InterventionParticipants (Count of Participants)
Patients with EventPatients without Events
5-FU/LV379563
XELOX320624

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Relapse-Free Survival (RFS) [Time to Event]

A relapse-free survival (RFS) event included recurrence of the original colon cancer, development of a new colon or rectal cancer, and deaths related to any of the following: treatment, recurrence of the original colon cancer, or development of a new colon or rectal cancer. Participants who had not had any such event at the time of data analysis were censored at the last date they were known to be event-free. Participants whose cause of death was unrelated to treatment or disease recurrence were censored at the time of the last tumor assessment. The median was estimated by the Kaplan-Meier method. The full range values include censored observations. (NCT00069121)
Timeframe: Time from randomization date to date of first RFS event/date last known to be event-free. Median observation time for RFS was 74 months (range: 0-95 months).

Interventionmonths (Median)
5-FU/LVNA
XELOX88.6

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Overall Survival [Time to Event]

Overall survival was measured as the time from randomization to the date of death, irrespective of the cause of death. Participants who were not reported as having died at the time of the analysis were censored using the date they were last known to be alive. The median was estimated by the Kaplan-Meier method. The full range values include censored observations. (NCT00069121)
Timeframe: Time from randomization date to date of death/date last known to be alive. Median observation time was 83 months (range: 0-95 months).

Interventionmonths (Median)
5-FU/LVNA
XELOXNA

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Duration of Overall Response

Duration of overall response was measured from the time that measurement criteria were first met for Complete Response or Partial Response until the first date that progressive disease or death was documented. (NCT00077857)
Timeframe: Until PD or death. Median duration of response was approximately 7 months.

InterventionMonths (Median)
1250 mg/m^2 Capecitabine + Docetaxel6.9
825 mg/m^2 Capecitabine + Docetaxel6.9

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Overall Survival

Overall Survival was measured as the time from the date of randomization to the date of death. (NCT00077857)
Timeframe: Throughout the study. Median observation time was approximately 16 months.

InterventionMonths (Median)
1250 mg/m^2 Capecitabine + Docetaxel16.4
825 mg/m^2 Capecitabine + Docetaxel15.1

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Percentage of Participants With Best Overall Response Being Complete Response (CR) or Partial Response (PR)

According to Response Evaluation Criteria in Solid Tumors (RECIST) criteria: CR is defined as the disappearance of all target lesions and PR is defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the nadir sum LD. (NCT00077857)
Timeframe: Until Progressive Disease (PD) or end of primary study treatment (up to 16 cycles) plus 28 days.

InterventionPercentage of participants (Number)
1250 mg/m^2 Capecitabine + Docetaxel45.1
825 mg/m^2 Capecitabine + Docetaxel37.4

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Time to Progression of Disease or Death

Progression Free Survival was defined as the time from the date of randomization to the day of documented disease progression or death due to any cause. (NCT00077857)
Timeframe: Event driven (after 350 events). Median observation time was approximately 16 months.

InterventionMonths (Median)
1250 mg/m^2 Capecitabine + Docetaxel7.9
825 mg/m^2 Capecitabine + Docetaxel5.8

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Time to Treatment Failure

"The time to treatment failure was the time from the date of randomization to the first occurrence of any of the following events:~adverse events~insufficient therapeutic response (disease progression)~death~failure to return~refusing treatment/being unwilling to cooperate~withdrawing consent." (NCT00077857)
Timeframe: Until premature withdrawal or end of primary study treatment (up to 16 cycles).

InterventionMonths (Median)
1250 mg/m^2 Capecitabine + Docetaxel5.1
825 mg/m^2 Capecitabine + Docetaxel4.6

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Number of Participants With Adverse Events and Serious Adverse Events

"An adverse event was considered any unfavorable and unintended sign, symptom, or disease associated with the use of the study drug, whether or not considered related to the study drug. Preexisting conditions that worsened during the study were reported as adverse events.~A serious adverse event is any experience that suggests a significant hazard, contraindication, side effect or precaution that: results in death, is Life-Threatening, required in-patient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or is medically significant.~Additional information about Adverse Events can be found in the Adverse Event Section." (NCT00077857)
Timeframe: First study drug intake until last study drug intake plus 28 days

,
InterventionParticipants (Number)
Adverse EventsSerious Adverse Events
1250 mg/m^2 Capecitabine + Docetaxel20641
825 mg/m^2 Capecitabine + Docetaxel23453

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Time to Overall Response

For patients with Best Overall Response being Complete Response (CR) or Partial Response (PR), time to response was measured as the time from randomization to the first time when the measurement criteria for CR or PR were met. The percentage of participants with overall response within the given time ranges in each of the categories: Weeks 1-6, 7-12, 13-18, 19-24, 25-30, 31-36, and 43-48 are reported. (NCT00077857)
Timeframe: Until PD or end of primary study treatment (up to 16 cycles) plus 28 days.

,
InterventionPercentage of participants (Number)
Week 1-6Week 7-12Week 13-18Week 19-24Week 25-30Week 31-36Week 43-48
1250 mg/m^2 Capecitabine + Docetaxel2548207330
825 mg/m^2 Capecitabine + Docetaxel3030177121

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Symptom Assessment Score Changes From Baseline for Functional Assessment of Cancer Therapy-Breast Symptom Index (FBSI)

Quality of life, as measured by the FBSI, an 8-item, participant-reported instrument to measure symptoms. Each item has 5 possible responses ranging from 0 (not at all) to 4 (very much). The scoring was conducted according to the Functional Assessment of Chronic Illness Therapy manual, Version 4; higher scores reflect fewer symptoms. (NCT00080301)
Timeframe: Baseline and prior to each 21-day cycle of treatment, and at first posttreatment follow-up assessment.

,
Interventionunits on a scale (Mean)
Week 3 (n=282; n=273)Week 6 (n=227; n=214)Week 9 (n=194; n=184)Week 12 (n=173; n=158)Week 15 (n=148; n=145)Week 18 (n=122; n=121)Week 21 (n=116; n=101)Week 24 (n=95; n=82)
Capecitabine0.31.11.81.41.71.71.12.3
Ixabepilone + Capecitabine-0.4-0.2-0.6-1.3-0.7-1.0-0.7-0.8

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Time to Response Per IRRC

Time to response was summarized using descriptive statistics and was defined as the time from first dose of study treatment until measurement criteria were first met for Partial Response or Complete Response. (NCT00080301)
Timeframe: based on assessments every 6 weeks while on treatment until documented disease progression/unacceptable toxicity

Interventionweeks (Median)
Ixabepilone + Capecitabine11.7
Capecitabine12.0

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Progression-free Survival (PFS) Per Independent Radiology Review Committee (IRRC)

PFS defined as the time in months from randomization to date of progression. Patients who died without a reported prior progression were considered to have progressed on date of death; those who didn't progress or die were censored on date of last tumor assessment. Median PFS time with 95% CI estimated using the Kaplan Meier product limit method. (NCT00080301)
Timeframe: based on assessments every 6 weeks while on treatment until documented disease progression/unacceptable toxicity

InterventionMonths (Median)
Ixabepilone + Capecitabine5.85
Capecitabine4.17

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Overall Survival (OS)

OS was defined as the time from randomization to death. Participants who did not die at the time of the analysis were censored at the latest follow-up date. Median OS with 95% CI was estimated using the Kaplan Meier product limit method. (NCT00080301)
Timeframe: from date of randomization until death

InterventionMonths (Median)
Ixabepilone + Capecitabine12.9
Capecitabine11.1

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Overall Response Rate (ORR) Per IRRC

"Participants with best response of Complete or Partial according to Response Evaluation Criteria in Solid Tumors (RECIST) a 4-item scale wherein complete response=disappearance of all target lesions and partial response=30% decrease in the sum of the longest diameter of target lesions" (NCT00080301)
Timeframe: based on assessments every 6 weeks while on treatment until documented disease progression/unacceptable toxicity

Interventionpercent (Mean)
Ixabepilone + Capecitabine34.7
Capecitabine14.3

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Duration of Response Per IRRC

"Computed for all patients with a best response of Partial or Complete per RECIST (a 4-item scale as described in previous outcome measure), calculated from the time when these criteria were first met until the first date of documented progression or death." (NCT00080301)
Timeframe: based on assessments every 6 weeks while on treatment until documented disease progression/unacceptable toxicity

Interventionmonths (Median)
Ixabepilone + Capecitabine6.4
Capecitabine5.6

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Pathologic Complete Response Rate

"A pathologic complete response (pCR) was defined as no evidence of residual cancer histologically; disease progression or death before surgery was considered less than pCR (even without surgical specimen). All cases were reviewed by the study's surgical oncology co-chair for the determination of pCR.~Each arm was first analyzed alone. If the arm had 9 or more pCRs in 48 evaluable pts, then the null hypothesis (H0) of 10% pCR rate would be rejected in favor of the alternative hypothesis of 25%, providing 90% power with a two-sided 10% type I error rate. If both arms reject H0, then statistical selection theory would be used to choose the arm for further study in a phase III trial. If only one arm has acceptable pCR rate, then that arm would be pursued in a phase III trial." (NCT00081289)
Timeframe: After protocol surgery, approximately 10-16 weeks from randomization based on surgery occurring 4-8 weeks after chemoradiation

Interventionpercentage of participants (Number)
Neoadjuvant Chemoradiation With Irinotecan10.4
Neoadjuvant Chemoradiation With Oxaliplatin20.8

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Second Primary Rate at 4 Years

Time to second primary is defined as time from randomization to date of the appearance of a second primary cancer, last known follow-up (censored), or death without second primary (competing risk). Second primary rates are estimated by the cumulative incidence method. (NCT00081289)
Timeframe: From randomization to four years

Interventionpercentage of participants (Number)
Neoadjuvant Chemoradiation With Irinotecan2
Neoadjuvant Chemoradiation With Oxaliplatin6

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Survival Rate at 4 Years

Survival time is defined as time from registration/randomization to the date of death from any cause or last known follow-up (censored). Survival rates are estimated by the Kaplan-Meier method. (NCT00081289)
Timeframe: From randomization to four years

Interventionpercentage of participants (Number)
Neoadjuvant Chemoradiation With Irinotecan85
Neoadjuvant Chemoradiation With Oxaliplatin75

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Change From Baseline in QLQ-C30 Global Health Status Score at Two Years

"Global Health Status is calculated from two questions on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-C30. The question responses range from 1 very poor to 7 excellent such that a higher response indicates better quality of life (QOL). The mean of these responses is linearly transformed to a range of 0 (worst) to 100 (best). Change from baseline is calculated as the time point value - baseline value and a decrease from baseline indicates decline in quality of life. A negative number indicates improvement in symptoms." (NCT00081289)
Timeframe: Baseline and two years

Interventionscore on a scale (Mean)
Neoadjuvant Chemoradiation With Irinotecan-6.8
Neoadjuvant Chemoradiation With Oxaliplatin-1.3

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Disease-free Survival Rate at 4 Years

Disease-free survival time is defined as time from randomization to date of local-regional failure, the appearance of distant metastases, the appearance of a second primary failure, or date of death from any cause/ Disease-free survival rates are estimated by the Kaplan-Meier method. Patients last known to be alive without failure are censored at the date of last contact. (NCT00081289)
Timeframe: From randomization to four years

Interventionpercentage of participants (Number)
Neoadjuvant Chemoradiation With Irinotecan68
Neoadjuvant Chemoradiation With Oxaliplatin62

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Distant Failure Rate at 4 Years

Time to distant failure is defined as time from randomization to date of the appearance of distant metastases, last known follow-up (censored), or death without distant failure (competing risk). Distant failure rates are estimated by the cumulative incidence method. (NCT00081289)
Timeframe: From randomization to four years

Interventionpercentage of participants (Number)
Neoadjuvant Chemoradiation With Irinotecan24
Neoadjuvant Chemoradiation With Oxaliplatin30

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Local-regional Failure Rate at 4 Years

Local-regional failure is defined as any of the following: no clinical complete response (cCR) in the primary site and/or nodes at any time after treatment completion (persistence), recurrence and/or progression in the primary site and/or nodes after cCR, and nonprotocol surgery to the primary site after cCR. Time to local-regional failure is defined as time from randomization to date of failure, last known follow-up (censored), or death without local-regional failure (competing risk). Local-regional failure rates are estimated by the cumulative incidence method. (NCT00081289)
Timeframe: From randomization to four years

Interventionpercentage of participants (Number)
Neoadjuvant Chemoradiation With Irinotecan16
Neoadjuvant Chemoradiation With Oxaliplatin18

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Change From Baseline in EORTC QLQ-CR38 Gastro-intestinal Symptom Score at Two Years

The gastro-intestinal (GI) symptom score is calculated from five symptom questions on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-CR38. The question responses range from 1 (not at all) to 4 (very much) such that a higher response indicates worse symptoms. The mean of these responses is linearly transformed to a range of 0 (best) to 100 (worst). Change from baseline is calculated as the time point value - baseline value and a decrease from baseline indicates improvement in symptoms. A negative number indicates improvement in symptoms. (NCT00081289)
Timeframe: Baseline and two years

Interventionscore on a scale (Mean)
Neoadjuvant Chemoradiation With Irinotecan0.4
Neoadjuvant Chemoradiation With Oxaliplatin6.7

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Change From Baseline in EORTC QLQ-CR38 Gastro-intestinal Symptom Score at Completion of Chemoradiation

The gastro-intestinal (GI) symptom score is calculated from five symptom questions on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-CR38. The question responses range from 1 (not at all) to 4 (very much) such that a higher response indicates worse symptoms. The mean of these responses is linearly transformed to a range of 0 (best) to 100 (worst). Change from baseline is calculated as the time point value - baseline value and a decrease from baseline indicates improvement in symptoms. A negative number indicates improvement in symptoms. (NCT00081289)
Timeframe: Baseline and completion of chemoradiation approximately 6-8 weeks from randomization

Interventionscore on a scale (Mean)
Neoadjuvant Chemoradiation With Irinotecan5.9
Neoadjuvant Chemoradiation With Oxaliplatin20.3

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Change From Baseline in EORTC QLQ-CR38 Defecation Symptom Score at Two Years

"The defecation symptom score is calculated from seven symptom questions on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-CR38. The question responses range from 1 not at all to 4 very much such that a higher response indicates worse symptoms. The mean of these responses is linearly transformed to a range of 0 (best) to 100 (worst). Change from baseline is calculated as the time point value - baseline value and a decrease from baseline indicates improvement in symptoms. A negative number indicates improvement in symptoms." (NCT00081289)
Timeframe: Baseline and two years

Interventionscore on a scale (Mean)
Neoadjuvant Chemoradiation With Irinotecan0.4
Neoadjuvant Chemoradiation With Oxaliplatin-1.6

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Change From Baseline in EORTC QLQ-CR38 Defecation Symptom Score at Post-operative Chemotherapy

"The defecation symptom score is calculated from seven symptom questions on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-CR38. The question responses range from 1 not at all to 4 very much such that a higher response indicates worse symptoms. The mean of these responses is linearly transformed to a range of 0 (best) to 100 (worst). Change from baseline is calculated as the time point value - baseline value and a decrease from baseline indicates improvement in symptoms. A negative number indicates improvement in symptoms." (NCT00081289)
Timeframe: Baseline and completion of post-operative chemotherapy, approximately 32 to 40 weeks from randomization based on 18 weeks of post-operative chemotherapy

Interventionscore on a scale (Mean)
Neoadjuvant Chemoradiation With Irinotecan-1.6
Neoadjuvant Chemoradiation With Oxaliplatin14.6

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Change From Baseline in EORTC QLQ-CR38 Defecation Symptom Score at Completion of Chemoradiation

"The defecation symptom score is calculated from seven symptom questions on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-CR38. The question responses range from 1 not at all to 4 very much such that a higher response indicates worse symptoms. The mean of these responses is linearly transformed to a range of 0 (best) to 100 (worst). Change from baseline is calculated as the time point value - baseline value and a decrease from baseline indicates improvement in symptoms. A negative number indicates improvement in symptoms." (NCT00081289)
Timeframe: Baseline and completion of chemoradiation, approximately 6-8 weeks from randomization

Interventionscore on a scale (Mean)
Neoadjuvant Chemoradiation With Irinotecan4.8
Neoadjuvant Chemoradiation With Oxaliplatin8.8

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Change From Baseline in EORTC QLQ-CR38 Gastro-intestinal Symptom Score at Completion of Post-operative Chemotherapy

The gastro-intestinal (GI) symptom score is calculated from five symptom questions on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-CR38. The question responses range from 1 (not at all) to 4 (very much) such that a higher response indicates worse symptoms. The mean of these responses is linearly transformed to a range of 0 (best) to 100 (worst). Change from baseline is calculated as the time point value - baseline value and a decrease from baseline indicates improvement in symptoms. A negative number indicates improvement in symptoms. (NCT00081289)
Timeframe: Baseline and completion of post-operative chemotherapy approximately 32 to 40 weeks from randomization based on 18 weeks of post-operative chemotherapy

Interventionscore on a scale (Mean)
Neoadjuvant Chemoradiation With Irinotecan-1.5
Neoadjuvant Chemoradiation With Oxaliplatin3.9

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Change From Baseline in QLQ-C30 Global Health Status Score at Completion of Chemoradiation

"Global Health Status is calculated from two questions on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-C30. The question responses range from 1 very poor to 7 excellent such that a higher response indicates better quality of life (QOL). The mean of these responses is linearly transformed to a range of 0 (worst) to 100 (best). Change from baseline is calculated as the time point value - baseline value and a decrease from baseline indicates decline in quality of life. A positive number indicates improvement in QOL." (NCT00081289)
Timeframe: Baseline and completion of chemoradiation, approximately 6-8 weeks from randomization

Interventionscore on a scale (Mean)
Neoadjuvant Chemoradiation With Irinotecan-10.3
Neoadjuvant Chemoradiation With Oxaliplatin-12.2

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Change From Baseline in QLQ-C30 Global Health Status Score at Completion of Post-operative Chemotherapy

"Global Health Status is calculated from two questions on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-C30. The question responses range from 1 very poor to 7 excellent such that a higher response indicates better quality of life (QOL). The mean of these responses is linearly transformed to a range of 0 (worst) to 100 (best). Change from baseline is calculated as the time point value - baseline value and a decrease from baseline indicates decline in quality of life. A positive number indicates improvement in QOL." (NCT00081289)
Timeframe: Baseline and completion of post-operative chemotherapy approximately 32 to 40 weeks from randomization based on 18 weeks of post-operative chemotherapy

Interventionscore on a scale (Mean)
Neoadjuvant Chemoradiation With Irinotecan-12.5
Neoadjuvant Chemoradiation With Oxaliplatin-7.1

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Symptom Assessment Score Changes From Baseline for Functional Assessment of Cancer Therapy-Breast Symptom Index (FBSI)

Quality of life, as measured by the FBSI, an 8-item, participant-reported instrument to measure symptoms. Each item has 5 possible responses ranging from 0 (not at all) to 4 (very much). The scoring was conducted according to the Functional Assessment of Chronic Illness Therapy manual, Version 4; higher scores reflect fewer symptoms. (NCT00082433)
Timeframe: Baseline and prior to each 21-day cycle of treatment, and at first posttreatment follow-up assessment

,
Interventionunits on a scale (Mean)
Week 3 (n=440; n=429)Week 6 (n=379; n=353)Week 9 (n=330; n=283)Week 12 (n=283; n=250)Week 15 (n=255; n=240)Week 18 (n=205; n=202)Week 21 (n=166; n=185)Week 24 (n=149; n=141)
Capecitabine0.00.50.71.11.51.21.71.1
Ixabepilone + Capecitabine-0.5-0.9-1.5-1.4-1.9-1.3-1.4-1.4

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Time to Response

"Time to response was defined as the time from the first dose of study therapy until measurement criteria were first met for partial or complete (whichever status was recorded first) per RECIST criteria (a 4-item scale described in the previous outcome measure)." (NCT00082433)
Timeframe: every 6 weeks (± 3 days) from randomization while on treatment until documented progression

Interventionweeks (Median)
Ixabepilone + Capecitabine6.6
Capecitabine6.6

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Response Rate (RR)

"RR=number of patients in that group whose best response is partial(30% decrease in the sum of the longest diameter of target lesions) or complete (disappearance of all target lesions), according to the 4-item Response Evaluation Criteria in Solid Tumors (RECIST), divided by the total number of response-evaluable participants" (NCT00082433)
Timeframe: every 6 weeks (± 3 days) from randomization while on treatment until documented progression

Interventionpercentage of participants (Mean)
Ixabepilone + Capecitabine43.3
Capecitabine28.8

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Progression-Free Survival (PFS)

PFS was defined for each patient as the time in months from randomization to the date of progression. Patients who died without a reported prior progression were considered to have progressed on their date of death. Patients who did not progress or die were censored on the date of their last tumor assessment. (NCT00082433)
Timeframe: every 6 weeks (± 3 days) from randomization while on treatment until documented progression

Interventionmonths (Median)
Ixabepilone + Capecitabine6.24
Capecitabine4.40

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Overall Survival (OS)

Overall survival was defined as the time in months from randomization until the date of death. For those patients who had not died, survival duration was censored at the last date the patient was known to be alive. Median OS with 95% CI estimated using the Kaplan-Meier Product Limit Method. (NCT00082433)
Timeframe: from date of randomization until death

Interventionmonths (Median)
Ixabepilone + Capecitabine16.39
Capecitabine15.64

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Duration of Response

"Measured from the time RECIST criteria (described in previous outcome measure) were first met for complete or partial response until first date of documented disease progression or death. Patients who neither relapsed nor died were censored on the date of last tumor assessment. Median w/ 95% CI estimated using Kaplan Meier Product Limit Method." (NCT00082433)
Timeframe: every 6 weeks (± 3 days) from randomization while on treatment until documented progression

InterventionMonths (Median)
Ixabepilone + Capecitabine6.1
Capecitabine6.3

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Response Rates (RR) in Metastatic Gastric/GE Junction Tumors

Response is defined as the number of patients with a CR (Complete Response) or PR (Partial Response) per Response Evaluation Criteria in Solid Tumor (RECIST criteria). Possible evaluations include: CR: Disappearance of all target lesions. PR: At least a 30% decrease in the size of target lesions. Progressive Disease (PD): At least a 20% increase in the size of the target lesions or appearance of one or more new lesions. Stable Disease (SD): Neither sufficient shrinkage or increase of target lesions. (NCT00084617)
Timeframe: at 12 weeks (after 2 cycles of treatment)

Interventionparticipants (Number)
Complete Response (CR)Partial Response (PR)Progressive Disease (PD)Stable Disease (SD)
Treatment (Oxaliplatin, Irinotecan, Capecitabine)29316

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Overall Survival

Length of time patients survived after treatment (NCT00084617)
Timeframe: at 40 months from study activation

Interventionmonths (Median)
Treatment (Oxaliplatin, Irinotecan, Capecitabine)8.98

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Complete Response (CR) and Partial Response (PR) Duration

The duration of overall response is measured from the time measurement criteria are met for CR or PR (whichever is first recorded) until the first date that recurrent or progressive disease is objectively documented (taking as reference for progressive disease the smallest measurements recorded since the treatment started). (NCT00084617)
Timeframe: at 40 months from study activation

Interventionmonths (Median)
Treatment (Oxaliplatin, Irinotecan, Capecitabine)5.95

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Progression-free Survival at 6 Months

Percentage of participants progression-free at 6 months. Progression-free survival (PFS) measured from date of registration to first observation of progressive disease (per RECIST criteria (V1.0)), death due to any cause, or symptomatic deterioration. Kaplan-Meier was used to estimate progression-free survival (PFS) at six months. (NCT00087152)
Timeframe: Six months

Interventionpercentage of participants (Number)
Imatinib Mesylate & Capecitabine16

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Confirmed Response Rate (Complete and Partial)

Number of participants with confirmed complete or partial response. Confirmed response (complete and partial) per Response Evaluation Criteria in Solid Tumors (RECIST) Criteria (V1.0). Complete Response (CR) is complete disappearance of all measurable and non-measurable disease; no new lesions; no disease related symptoms; and normalization of markers and other abnormal lab values. Partial response (PR) applies only to patients with at least one measurable lesion. PR is greater than or equal to 30% decrease under baseline of the sum of longest diameter of all target measurable lesions; no unequivocal progression of non-measurable disease and no new lesions. Confirmed response is two or more objective statuses a minimum of four weeks apart documented before progression or symptomatic deterioration. (NCT00087152)
Timeframe: 12 weeks

Interventionparticipants (Number)
Imatinib Mesylate & Capecitabine2

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Overall Survival [Number of Events]

Number of patients who died/were alive. (NCT00089479)
Timeframe: Time from the date of randomization to the date of death, or date last known to be alive. Patients were followed for an average of 5 years.

,
Interventionparticipants (Number)
Patients with eventPatients without events
AC Then T1081196
AC Then XT751232

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Disease Free Survival Including New Primary Breast Cancer as Event [Number of Events]

Number of patients with/without recurrence of breast cancer, new primary breast cancer, or death due to any cause. (NCT00089479)
Timeframe: Time from the date of randomization until the date of first event, or date last known to be event free if no event was reported. Patients were followed for an average of 5 years.

,
Interventionparticipants (Number)
Patients with eventPatients without events
AC Then T1691135
AC Then XT1541153

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Disease Free Survival Including Any New Cancer as Event [Number of Events]

Number of patients with/without recurrence of breast cancer, any new cancer, or death due to any cause. (NCT00089479)
Timeframe: Time from the date of randomization until the date of first event, or date last known to be event free if no event was reported. Patients were followed for an average of 5 years.

,
Interventionparticipants (Number)
Patients with eventPatients without events
AC Then T2001104
AC Then XT1771130

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Breast Cancer Free Survival [Time to Event]

Breast cancer-free survival was measured as time from the date of randomization to the date of recurrence of breast cancer, new primary breast cancer, or death related to the chemotherapy administered or due to breast cancer. Patients without event at the time of the analysis were censored using the date they were last known to be recurrent disease free. (NCT00089479)
Timeframe: Time from the date of randomization to death, or date last known to be event free if no event was reported. Patients were followed for an average of 5 years.

Interventionmonths (Median)
AC Then TNA
AC Then XTNA

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Breast Cancer Free Survival [Number of Events]

Number of patients with/without recurrence of breast cancer, new primary breast cancer, or death related to the chemotherapy administered or due to breast cancer. (NCT00089479)
Timeframe: Time from the date of randomization to event, or date last known to be event free if no event was reported. Patients were followed for an average of 5 years .

,
Interventionparticipants (Number)
Patients with eventPatients without events
AC Then T1581146
AC Then XT1441163

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Disease Free Survival [Number of Events]

Number of patients with/without recurrence of breast cancer, or death due to any cause. (NCT00089479)
Timeframe: Time from the date of randomization until the date of first event, or date last known to be event free if no event was reported. Patients were followed for an average of 5 years.

,
Interventionparticipants (Number)
Patients with eventPatients without events
AC Then T1641140
AC Then XT1401167

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Overall Survival [Time to Event]

Overall survival was measured as the time from the date of randomization to the date of death. Patients still alive at the time of the analysis were censored using the date they were last known to be alive. (NCT00089479)
Timeframe: Time from the date of randomization to the date of death, or date last known to be alive. Patients were followed for an average of 5 years.

Interventionmonths (Median)
AC Then TNA
AC Then XTNA

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Disease Free Survival Including New Primary Breast Cancer as Event [Time to Event

Time from the date of randomization until the date of first event (recurrence of breast cancer, new primary breast cancer, or death due to any cause). Patients without event at the time of the analysis were censored using the date they were last known to be recurrent disease free. (NCT00089479)
Timeframe: Time from the date of randomization until the date of first event, or date last known to be event free if no event was reported. Patients were followed for an average of 5 years.

Interventionmonths (Median)
AC Then TNA
AC Then XTNA

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Disease Free Survival [Time to Event]

Disease free survival was measured as the time from the date of randomization until the date of first event (recurrence of breast cancer, or death due to any cause). Patients without event at the time of the analysis were censored using the date they were last known to be recurrent disease free. (NCT00089479)
Timeframe: Time from the date of randomization until the date of first event, or date last known to be event free if no event was reported. Patients were followed for an average of 5 years.

Interventionmonths (Median)
AC Then TNA
AC Then XTNA

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Disease Free Survival Including Any New Cancer as Event [Time to Event]

Time from the date of randomization until the date of first event (recurrence of breast cancer, any new cancer, or death due to any cause). Patients without event at the time of the analysis were censored using the date they were last known to be recurrent disease free. (NCT00089479)
Timeframe: Time from the date of randomization until the date of first event, or date last known to be event free if no event was reported. Patients were followed for an average of 5 years.

Interventionmonths (Median)
AC Then TNA
AC Then XTNA

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Number of Participants With Complete Response at 2 Years

Response determined by computed tomography (CT)/magnetic resonance imaging (MRI), digital rectal examination, and proctoscopy, and a biopsy performed for clinical suspicion of residual or progressive disease. Response Evaluation Criteria in Solid Tumors (RECIST) where evaluation of target lesions Complete Response (CR): Disappearance of all target lesions; Partial Response (PR): At least a 30% decrease in sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD; Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions; Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT00093379)
Timeframe: 2 Years

Interventionparticipants (Number)
Capecitabine + Oxaliplatin + XRT16

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Number of Participants With 2-year Colostomy-Free Survival

Colostomy-free survival reported as number of participants who did not develop local recurrence or require salvage resection with colostomy. (NCT00093379)
Timeframe: 2 Years with median study follow up of 19 months

Interventionparticipants (Number)
Capecitabine + Oxaliplatin + XRT20

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2 Year Failure Free Survival

Treatment failure defined as: Biopsy proven residual disease identified 12 -14 weeks after the conclusion of chemoradiation therapy, Treatment-related mortality or Disease recurrence. (NCT00093379)
Timeframe: 2 years

Interventionparticipants (Number)
Capecitabine + Oxaliplatin + XRT20

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Overall Survival as Assessed by Time

Overall survival: The overall survival or survival time is defined as the time from registration to death due to any cause. The distribution of overall survival will be estimated using the method of Kaplan-Meier method. (NCT00093808)
Timeframe: Up to 5 years

Interventionmonths (Median)
Capecitabine + Vinorelbine + Trastuzumab28.5

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Time to Progression (TTP)

Time to progression is defined as the time from registration to disease progression. Patients who died without documentation of progression will be considered to have progressed on the date of their death. If a patient starts treatment and fails to return for any evaluations, that patient will be censored for progression of disease at day one post-registration. Otherwise, for patients that do not progress, censoring will occur at the last follow up date. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as at least a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions or unequivocal progression of existing non-target lesions. (NCT00093808)
Timeframe: Up to 5 years

Interventionmonths (Median)
Capecitabine + Vinorelbine + Trastuzumab11.3

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Duration of Response as Measured by RECIST Criteria

Duration of response is defined for all eligible patients who have achieved an objective response as the date at which the patient's objective status is first noted to be either a Complete Response (CR) or Partial Response (PR) to the date progression is documented. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions. (NCT00093808)
Timeframe: Up to 5 years

Interventionmonths (Median)
Capecitabine + Vinorelbine + Trastuzumab13.2

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Confirmed Response Rate

A confirmed tumor response is defined to be either a Complete Response (CR) or Partial Response (PR) noted as the objective status on 2 consecutive evaluations at least 6 weeks apart. All patients meeting the eligibility criteria who have signed a consent form and initiated study medication will be evaluable for response. The proportion of confirmed tumor responses will be estimated by the number of tumor regressions that meet the RECIST criteria for a confirmed CR or PR divided by the total number of evaluable patients. A 95% confidence interval for the true confirmed response rate will be calculated using the properties of the binomial distribution. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00093808)
Timeframe: Up to 5 years

Interventionproportion of patients (Number)
Capecitabine + Vinorelbine + Trastuzumab0.67

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Percentage of Participants With Improved Quality of Life

Quality of Life was assessed using EORTC QLQ-PAN26. All measures range in score from 1 to 4 as lower scores indicate better outcomes. The improved Quality of Life is defined as a greater than 5% decrease in 2 consecutive scores compared with the baseline score. (NCT00100815)
Timeframe: assessed at baseline then weekly for 3 weeks

Interventionpercentage of participants (Number)
GEMCITABINE, CAPECITABINE and AVASTIN56.0

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Clinical Response

Response was evaluated using the international criteria proposed by the Response Evaluation Criteria in Solid Tumors (RECIST) Committee [JNCI 92(3):205-216, 2000]. Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), At least a 30% decrease in the sum of the longest diameter of target lesions, taking as reference the baseline sum longest diameter; Overall Response (OR) = CR + PR. (NCT00100815)
Timeframe: Pre-treatment and every 6 weeks from treatment.

Interventionpercentage of participants (Number)
GEMCITABINE, CAPECITABINE and AVASTIN22.0

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Overall Survival

(NCT00100815)
Timeframe: every 2-4 months for 1 year and then every 6 months for 5 years

Interventionmonths (Median)
GEMCITABINE, CAPECITABINE and AVASTIN9.8

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Progression-free Survival

Progressive Disease is defined using the international criteria proposed by the Response Evaluation Criteria in Solid Tumors (RECIST) Committee [JNCI 92(3):205-216, 2000], as at least a 20% increase in the sum of the longest diameter of target lesions, taking as reference the smallest sum longest diameter recorded since the treatment started or the appearance of one or more new lesions, or appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. (NCT00100815)
Timeframe: every 2-4 months for 1 year and then every 6 months for 5 years

Interventionmonths (Median)
GEMCITABINE, CAPECITABINE and AVASTIN5.7

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Survival Time: Celecoxib and Placebo

Survival time defined as time from date of randomization to date of death. In the absence of confirmation of death, survival time was censored to last date the subject known to be alive. (NCT00101686)
Timeframe: assessed at least every week during treatment and at least every 3 months during follow-up

Interventionmonths (Median)
Celecoxib21.06
Placebo18.83

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1 Year Survival: FOLFIRI, mIFL and CapeIRI

Number of patients alive or dead at 1 year. In the absence of confirmation of death, survival time was censored to last date the subject known to be alive. (NCT00101686)
Timeframe: 1 year from date of randomization

,,
Interventionparticipants (Number)
Alive at 1 yearDead at 1 yearCensored
CapeIRI894610
FOLFIRI101349
mIFL86478

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Time to Progression: Bevacizumab With FOLFIRI, mIFL

Time to disease progression is defined as the number of months from date of randomization to the date of first documentation of disease progression (PD). (NCT00101686)
Timeframe: every 6 weeks until disease progression

Interventionmonths (Median)
Bevacizumab + FOLFIRI11.17
Bevacizumab + mIFL8.31

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Survival Time at Last Follow-Up Visit: Bevacizumab With FOLFIRI, mIFL

Survival time defined as time from date of randomization to date of death. In the absence of confirmation of death, survival time was censored to last date the subject known to be alive. Zero subjects analyzed indicates median could not be analyzed based on number of subjects who died. (NCT00101686)
Timeframe: Last Follow-Up Visit

Interventionmonths (Median)
Bevacizumab + FOLFIRI27.99
Bevacizumab + mIRI19.22

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Overall Response: FOLFIRI, mIFL and CapeIRI

A subject will be considered achieving an overall response if the subject has a sustained Complete Response (CR) or Partial Response (PR) for at least 4 weeks, confirmed by tumor assessments. (CR: Disappearance of all target lesions. PR: greater than or equal to 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the Pre-treatment sum LD. ) (NCT00101686)
Timeframe: every 6 weeks during chemotherapy until disease progression

Interventionparticipants (Number)
FOLFIRI68
mIFL61
CapeIRI56

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Overall Response: Celecoxib and Placebo

A subject will be considered achieving an overall response if the subject has a sustained CR or PR for at least 4 weeks, confirmed by tumor assessments. (Complete Response (CR): Disappearance of all target lesions. Partial Response (PR): ≥ 30% decrease in the sum of the LD of target lesions, taking as reference the Pre-treatment sum LD. ) (NCT00101686)
Timeframe: every 6 weeks during chemotherapy until disease progression

Interventionparticipants (Number)
Celecoxib84
Placebo101

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Overall Response: Bevacizumab With FOLFIRI, mIFL

A subject will be considered achieving an overall response if the subject has a sustained CR or PR for at least 4 weeks, confirmed by tumor assessments. (Complete Response (CR): Disappearance of all target lesions. Partial Response (PR): ≥ 30% decrease in the sum of the LD of target lesions, taking as reference the Pre-treatment sum LD. ) (NCT00101686)
Timeframe: every 6 weeks during chemotherapy until disease progression

Interventionparticipants (Number)
Bevacizumab + FOLFIRI33
Bevacizumab + mIFL32

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Dose Reduction Due to Treatment Emergent Adverse Events

Number of subjects that had at least one Treatment-Emergent Adverse Event (TEAE) that led to a dose reduction. TEAE includes all reported Adverse Events that occurred within 30 days of last study medication. (NCT00101686)
Timeframe: Day 1; Day 8; and at end of every 3 treatment cycles for FOLFIRI; end of every 2 cycles for mIRI

Interventionparticipants (Number)
FOLFIRI18
mIFL14
CapeIRI39
Bevacizumab + FOLFIRI6
Bevacizumab + mIRI8

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Time to Progression: FOLFIRI, mIFL and CapeIRI

Time to disease progression is defined as the number of months from date of randomization to the date of first documentation of disease progression (PD). (NCT00101686)
Timeframe: every 6 weeks until disease progression

Interventionmonths (Median)
FOLFIRI7.62
mIFL5.98
CapeIRI5.82

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Overall Relative Dose Intensity of Irinotecan

Relative dose intensity for a cycle was calculated as the percentage of the actual dose intensity of the cycle divided by the planned dose intensity of the cycle. Overall relative dose intensity was calculated as the average relative dose intensities over all cycles. (Dose intensity for each cycle was calculated as the actual dose level of the study medication received in that cycle divided by the number of weeks in the cycle.) (NCT00101686)
Timeframe: End of treatment cycle

Interventionpercent dose intensity (Mean)
FOLFIRI93.9
mIFL94.5
CapeIRI93.8
Bevacizumab + FOLFIRI93.3
Bevacizumab + mIRI95.5

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1 Year Survival: Bevacizumab With FOLFIRI, mIFL

Number of patients alive or dead at 1 year. In the absence of confirmation of death, survival time was censored to last date the subject known to be alive. (NCT00101686)
Timeframe: 1 year from date of randomization

,
Interventionparticipants (Number)
Alive at 1 yearDead at 1 yearCensored
Bevacizumab + FOLFIRI4575
Bevacizumab + mIRI33225

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Survival Time: FOLFIRI, mIFL and CapeIRI

Survival time defined as time from date of randomization to date of death. In the absence of confirmation of death, survival time was censored to last date the subject known to be alive. (NCT00101686)
Timeframe: assessed at least every week during treatment and at least every 3 months during follow-up

Interventionmonths (Median)
FOLFIRI23.06
mIFL17.64
CapeIRI18.92

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Time to Progression : Celecoxib and Placebo

Time to disease progression is defined as the number of months from date of randomization to the date of first documentation of disease progression (PD). (NCT00101686)
Timeframe: every 6 weeks until disease progression

Interventionmonths (Median)
Celecoxib6.64
Placebo6.70

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Time to Progression (TTP) at Primary Completion: FOLFIRI and mIFL

Time to disease progression is defined as the number of months from date of randomization to the date of first documentation of disease progression (PD). (NCT00101686)
Timeframe: every 6 weeks until disease progression

Interventionmonths (Median)
FOLFIRI8.18
mIFL6.01

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Progression-free Survival and Overall Survival

"Progression-Free Survival: From date of registration to time of first documentation of progression or symptomatic deterioration, or death due to any cause. Patients last known to be alive and progression-free are censored at last date of contact.~Overall Survival: From date of registration to date of death due to any cause. Patients last known to be alive are censored at last date of contact.~Progression is 20% increase in sum of longest diameters of target measurable lesions over smallest sum observed and/or unequivocal progression of non-measurable disease and/or appearance of new lesion/site or death due to disease without prior documentation of progression and without symptomatic deterioration. Symptomatic deterioration is global deterioration of health status requiring discontinuation of treatment without objective evidence of progression." (NCT00107276)
Timeframe: two years

Interventionmonths (Median)
PFSOS
Cyclophosphamide and Capecitabine5.918.8

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Response Rate (Complete and Partial, Confirmed and Unconfirmed)

Complete Response (CR) is complete disappearance of all measurable and non-measurable disease. No new lesions, no disease related symptoms. Normalization of markers and other abnormal lab values. Partial Response (PR) is greater than or equal to 30% decrease under baseline of the sum of longest diameters of all target measurable lesions. No unequivocal progression of non-measurable disease. No new lesions. Confirmation of CR or PR means a repeat scan at least 4 weeks apart documented before progression or symptomatic deterioration. Progression is 20% increase in sum of longest diameters of target measurable lesions over smallest sum observed and/or unequivocal progression of non-measurable disease and/or appearance of new lesion/site or death due to disease without prior documentation of progression and without symptomatic deterioration. Symptomatic deterioration is global deterioration of health status requiring discontinuation of treatment without objective evidence of progression. (NCT00107276)
Timeframe: Patients assessed at least every six weeks while on protocol treatment

Interventionparticipants (Number)
Cyclophosphamide and Capecitabine29

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Toxicity

Number of patients for whom Grade 3 or higher toxicity observed during treatment. Only adverse events that are possibly, probably or definitely related to study drug are reported. (NCT00107276)
Timeframe: Patients assessed after each 21-day cycle for 8 cycles (24 weeks of treatment)

InterventionParticipants (Number)
ALT, SGPT (serum glutamic pyruvic transaminase)Alkaline phosphataseDehydrationDiarrheaDyspnea (shortness of breath)Fatigue (asthenia, lethargy, malaise)Febrile neutropeniaHemoglobinLeukocytes (total WBC)LymphopeniaMood alteration - depressionNauseaNeuroendocrine: ADH secretion abnormalityNeutrophils/granulocytes (ANC/AGC)PlateletsPotassium, serum-low (hypokalemia)Pruritus/itchingRash/desquamationRash: hand-foot skin reactionSodium, serum-low (hyponatremia)Thrombosis/thrombus/embolismWeight loss
Cyclophosphamide and Capecitabine112212111513111711117121

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Overall Survival in Stage III Cancer Patients - Time to Event

Overall survival was defined as the time between date of randomization and date of death due to any cause. Patients not reported as having died at the time of the analysis were censored at the date they were last known to be alive. (NCT00112918)
Timeframe: From first patient randomized until the clinical data cut-off date of 30 June 2010 (36 months after the last patient randomized).

Interventionmonths (Median)
FOLFOX4NA
FOLFOX4 + BvNA
XELOX+BvNA

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Overall Survival in Stage III Cancer Patients - Number of Events: Final Analysis

An overall survival event was death due to any cause. (NCT00112918)
Timeframe: From first patient randomized until the final data cut-off date of 30 June 2012 (5 years after the last patient randomized).

,,
Interventionparticipants (Number)
Patients with eventsPatients without events
FOLFOX4161794
FOLFOX4 + Bv202758
XELOX+Bv182770

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Overall Survival in Stage III Cancer Patients - Number of Events

An overall survival event was death due to any cause. (NCT00112918)
Timeframe: From first patient randomized until the clinical data cut-off date of 30 June 2010 (36 months after the last patient randomized).

,,
Interventionparticipants (Number)
Patients with eventsPatients without events
FOLFOX4115840
FOLFOX4 + Bv151809
XELOX+Bv145807

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Disease-free Survival in Stage III Cancer Patients - Number of Events

A disease-free survival (DFS) event was composed of a recurrence, a new occurrence of colorectal cancer or death due to any cause. Recurrence and new occurrence of colorectal cancer were based on tumor assessments made by the investigator. Triggering events for DFS are reported; a patient can have both recurrence and a new occurrence of colon cancer. (NCT00112918)
Timeframe: From first patient randomized until the data cut-off date of 30 June 2010 (36 months after the last patient randomized).

,,
Interventionparticipants (Number)
Patients with a DFS eventRecurrenceNew OccurrenceDeathPatients without events
FOLFOX4237219317718
FOLFOX4 + Bv280253821680
XELOX+Bv253223625699

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Overall Survival in Stage III Cancer Patients - Time to Event: Final Analysis

Overall survival was defined as the time between date of randomization and date of death due to any cause. Patients not reported as having died at the time of the clinical cut-off date (30 June 2012) were censored at the date they were last known to be alive. (NCT00112918)
Timeframe: From first patient randomized until the final data cut-off date of 30 June 2012 (5 years after the last patient randomized).

Interventionmonths (Median)
FOLFOX4NA
FOLFOX4 + BvNA
XELOX+BvNA

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Disease-free Survival in Stage III Cancer Patients - Time to Event

Disease-free survival (DFS) was defined as the time from the date of randomization to the time of a recurrence, a new occurrence of colorectal cancer or death due to any cause, whichever occurred first. Patients without an event were censored at the last date the patient was known to be disease-free. Recurrence and new occurrence of colorectal cancer were based on tumor assessments made by the investigator. Patients with no tumor assessments after baseline but still alive at the time of the clinical cut-off were censored at day 1. (NCT00112918)
Timeframe: From first patient randomized until the data cut-off date of 30 June 2010 (36 months after the last patient randomized).

Interventionmonths (Median)
FOLFOX4NA
FOLFOX4 + BvNA
XELOX+BvNA

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Pathologic Local Tumor Response

At follow-up evaluation after completion of neoadjuvant and surgical therapy, resected primary tumor classified based on routine pathology staining in the following manner: Pathologic Complete Response (no evidence of residual cancer); Microscopic Residual (no grossly detected disease, but evidence of microscopic residual disease); and Gross Residual Disease. (NCT00113230)
Timeframe: Baseline to approximately 5 Months (Following 28 days of treatment, chemotherapy and surgical resection of tumor)

InterventionParticipants (Number)
Pathological Complete ResponseMicroscopic Residual (<10% viable tumor cells)Gross Residual Disease
Avastin8611

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Morbidity and Mortality Rate

Morbidity and mortality after neoadjuvant cheoradiotherapy and local excision. (NCT00114231)
Timeframe: Up to 30 days

Interventionpercentage of patients (Number)
MortalityMorbidity
Treatment (Capecitabine, Oxaliplatin, Radiotherapy, Surgery)610

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Rate of Pathologic Complete Response of the Primary Tumor

The rate (percentage) of patients with pathologic complete response (pCR) is reported below. Pathologic response will be determined by comparing tumor width and stage in the surgical specimen with the same parameters as determined by pre-CRT ERUS: PATHOLOGIC COMPLETE RESPONSE (pCR): no residual tumor. (NCT00114231)
Timeframe: Up to 5 years

Interventionpercentage of patients (Number)
Treatment (Capecitabine, Oxaliplatin, Radiotherapy, Surgery)44

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R0 Resection Rate (Negative Margin Rate)

The rate (percentage) of patients with negative resection margins after undergoing local excision is reported below. (NCT00114231)
Timeframe: At time of surgery

Interventionpercentage of patients (Number)
Treatment (Capecitabine, Oxaliplatin, Radiotherapy, Surgery)98.7

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3-Year Disease-free Survival

The primary endpoint was 3-year disease-free survival (DFS). Evidence of local recurrence, distant metastasis, or death from any cause within 3 years counted as events in the time-to-event Kaplan-Meier analysis of disease-free survival. (NCT00114231)
Timeframe: Up to 3 years

Interventionpercentage of patients (Number)
Treatment (Capecitabine, Oxaliplatin, Radiotherapy, Surgery)88.2

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Local Recurrence Rate

The local recurrence rate (percentage) is defined as the percentage of patients who had local recurrence as initial sites of failure at the end of follow-up. (NCT00114231)
Timeframe: Up to 5 years

Interventionpercentage of patients (Number)
Treatment (Capecitabine, Oxaliplatin, Radiotherapy, Surgery)4

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Duration of Overall Clinical Response (CR or PR)

Among tumor responders (i.e., patients with overall best response of CR or PR), duration of overall response was measured from the time criteria were first met for CR or PR (whichever status was recorded first) to the date of either recurrent/progressive disease was objectively documented or death from any cause. (NCT00118755)
Timeframe: Time to Disease Progression or Death (through follow-up phase): Approximate Median of 302 days

InterventionDays to event (Median)
XELOX Q3W + Bevacizumab281
XELOX Q2W + Bevacizumab316

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Overall Survival

Overall survival was defined as the time from the date of randomization to the date of death, for any cause. (NCT00118755)
Timeframe: Time to death (through follow-up phase): Approximate Median of 718 days

InterventionDays (Median)
XELOX Q3W + Bevacizumab852
XELOX Q2W + Bevacizumab662

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Progression-free Survival (PFS)

Progression-free survival was defined as the time from the date of randomization to the first occurrence of having documented disease progression or death due to any cause, whichever comes first. Progression was based on tumor assessments made by the investigators according to Response Evaluation Criteria in Solid Tumors (RECIST). (NCT00118755)
Timeframe: Time to disease progression or death (through follow-up phase)

InterventionDays (Median)
XELOX Q3W + Bevacizumab287
XELOX Q2W + Bevacizumab273

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Best Overall Clinical Response

"Overall response rate was assessed according to RECIST (the best response recorded from the time of randomization to the first CR or PR. The patient's overall best response was complete response (CR), partial response (PR) (CR and PR considered responders), stable disease (SD), or progressive disease (PD). To be assigned a status of complete response (CR) or partial response (PR), changes in tumor measurements were confirmed by repeat assessments performed no less than 4 weeks after the criteria for response were first met." (NCT00118755)
Timeframe: Through follow-up phase: Approximate Median of 318 days

,
InterventionPatients (Number)
Nonresponders (without CR or PR)Responders (with CR or PR)Complete Response (CR)Partial Response (PR)
XELOX Q2W + Bevacizumab16751348
XELOX Q3W + Bevacizumab14572270

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The Completion Rate of 1 Year of Bevacizumab Therapy for All Four Cohorts

(NCT00121134)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Group A- Bevacizumab Alone60
Group B-Bevacizumab+Cyclophosphamide+Methotrexate58
Group C-Bevacizumab + Capcitabine(18 Wks)49
Group D-bevacizumab + Capecitibine (24wks)76

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Number of Participants Who Survived (Overall Survival)

Overall survival (OS) is defined as the time from start of treatment to death from any cause. (NCT00121251)
Timeframe: Up to 9 years

InterventionParticipants (Count of Participants)
Sorafenib + Gemcitabine + Capecitabine6

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Median Number of Months of Progression Free Survival (PFS)

PFS will be measured from the time of the patient's initial best response (PR or CR) until documented progression. (NCT00121251)
Timeframe: From the time of the patient's initial best response (PR or CR) until documented progression, assessed up to 9 years

InterventionMonths (Median)
Sorafenib + Gemcitabine + Capecitabine5

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Objective Response for BAY 43-9006 in Combination With Gemcitabine and Capecitabine Evaluated by the Response Evaluation Criteria in Solid Tumors (RECIST)

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Objective Response (OR) = CR + PR (NCT00121251)
Timeframe: Up to 9 years

InterventionParticipants (Count of Participants)
Sorafenib + Gemcitabine + Capecitabine5

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Number of Subjects With Adverse Events

"The secondary outcome measure was to evaluate the safety profile, including a summary of adverse events (AEs) assessed by the National Cancer Institute Common Terminology Criteria for Adverse Events version 3.0.~Intensity of AEs were graded according to NCI CTCAE version 3.0 on a 5-point scale: Grade 1=Mild Discomfort, Grade 2=Moderate, Grade 3=Severe, Grade 4=Life Threatening/Disabling and Grade 5=Death. An SAE was defined as any experience that suggested a significant hazard,contraindication, side effect, or precaution." (NCT00121836)
Timeframe: Throughout study

,
InterventionParticipants (Number)
At least 1 adverse event (AE)At least 1 treatment-related AEAt least 1 Grade 3 or 4 AEAt least 1 serious adverse event (SAE)At least 1 AE causing withdrawal
Capecitabine+Bevacizumab (Bev); Paclitaxel or Vinorelbine +Bev108104823937
First Study Treatment Phase Only5451412225

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Number of Participants With Marked Laboratory Abnormalities

The secondary outcome measure was to evaluate the safety profile, including a summary of marked laboratory abnormalities in >= 5% of patients. n=number of participants with the laboratory measure,Number=number of participants with the abnormality. Laboratory values were flagged as Low(L) or High(H) if they were below the lower limit or above the upper limit of Roche standard reference range, respectively. Marked laboratory abnormalities (flagged as HH and LL) were defined as those values that were outside the Roche marked reference range and showed a clinically relevant change from baseline. (NCT00121836)
Timeframe: until progressive disease or for up to 3 years

InterventionParticipants (Number)
Hematocrit (fraction) (n=104); Abnormality: LowHemoglobin (g/L) (n=104); Abnormality: LowPlatelets (10^9/L) (n=104); Abnormality: LowRed blood cells (10¹²/L) (n=104); Abnormality: LowWhite blood cells (10^9/L)(n=104); Abnormality:LowNeutrophils (10^9/L) (n=92); Abnormality: HighNeutrophils (10^9/L) (n=92); Abnormality: LowProthrombin time (ratio) (n=36); Abnormality: HighAspartate transaminase(U/L)(n=104)Abnormality:HighAlanine transaminase(U/L)(n=104);Abnormality: HighAlkaline phosphatase(U/L)(n=104);Abnormality: HighDirect bilirubin (umol/L) (n=78);Abnormality: HighAlbumin (g/L) (n=104); Abnormality: LowTotal protein (g/L) (n=104); Abnormality: LowChloride (mmol/L) (n=104); Abnormality: LowCalcium (mmol/L) (n=104); Abnormality: LowUric acid (umol/L) (n=94); Abnormality: High
Capecitabine+Bevacizumab (Bev); Paclitaxel or Vinorelbine +Bev1618915231425319101141385105

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Overall Survival

Overall survival was defined as the time from date of first treatment dose (Day 1) to date of death, across the study phases regardless of the cause of death (NCT00121836)
Timeframe: approximately 505 days (Median Time to Death)

InterventionDays (Median)
Capecitabine+Bevacizumab (Bev); Paclitaxel or Vinorelbine +Bev505

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Premature Withdrawal From Study Due to Adverse Events

The secondary outcome measure was to evaluate the safety profile, including a summary of premature withdrawals due to adverse events occurring in more than 1 patient in either study group, by system organ class. (NCT00121836)
Timeframe: Throughout study

,
InterventionParticipants (Number)
All system organ classesGeneral disorders, administration site conditionsMusculoskeletal and connective tissue disordersRespiratory, thoracic and mediastinal disordersRenal and urinary disorders
Capecitabine+Bevacizumab (Bev); Paclitaxel or Vinorelbine +Bev254222
First Study Treatment Phase Only377652

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Number of Participants With Serious Adverse Events (SAEs)

Review of Serious Adverse Events (SAEs) To assess the toxicity associated with Arms A and B. Response rates and toxicity rates for each arm were to be estimated and exact (using Casella's method) 95% confidence intervals for those proportions computed. With the anticipated 75 patients in each arm, these estimated proportions would have standard errors not exceeding 7%. (NCT00127036)
Timeframe: 30 Days After End of Treatment - Average of 6 Months

Interventionparticipants (Number)
XELOX + Bevacizumab9
XELIRI + Bevacizumab11

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Participants With Disease-Free Survival

Disease-free survival was defined as the time from date of surgery to date of first evidence of cancer recurrence in the breast (ie, local or distant recurrence or contra lateral disease) or death from any cause, whichever came first. Patients who were alive or withdrawn from the study and had no evidence of disease recurrence and for whom there was CRF evidence that evaluations had been made were censored at the date of the last clinical follow-up assessment when the patient was known to be disease free. (NCT00127933)
Timeframe: 30 - 1102 days

Interventionparticipants (Number)
HER2-Neu Negative92
HER2-Neu Positive25

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Percentage of Participants Assessed for Pathological Complete Response (pCR) Plus Near Complete (npCR) in Primary Breast Tumor at Time of Definitive Surgery

Pathological complete response was defined as the absence of histological evidence of invasive breast cancer cells in the tissue specimen removed from the breast after 4 cycles of preoperative treatment. Near pCR (npCR) was defined as the presence of invasive tumor cells with a size of 5 mm or less in aggregate in the tissue specimen removed from the breast after 4 cycles of preoperative treatment. Only pathological assessments occurring prior to the first date of adjuvant treatment were included in the analysis of pCR rate. (NCT00127933)
Timeframe: at the time of definitive surgery; after four 3-week cycles (3-4 months)

Interventionpercentage of participants (Number)
HER2-Neu Negative15.8
HER2-Neu Positive50.0

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Percentage of Participants With Complete Pathological Response in the Primary Breast Tumor at the Time of Definitive Surgery

Pathological complete response was defined as the absence of histological evidence of invasive breast cancer cells in the tissue specimen removed from the breast after 4 cycles of preoperative treatment. (NCT00127933)
Timeframe: at the time of definitive surgery; after four 3-week cycles (3-4 months)

Interventionpercentage of participants (Number)
HER2-Neu Negative9.9
HER2-Neu Positive35.7

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Percentage of Participants With Overall Clinical Response (Complete Response (CR) Plus Partial Response (PR))

The best overall response in an individual patient, according to RECIST, during preoperative treatment was the best response recorded from the start of study treatment until disease progression/recurrence (taking as reference for PD the smallest measurements recorded since the baseline assessment) or completion of preoperative treatment. Patients with CR or PR were considered responders. Patients with no tumor assessment after the start of study treatment were considered nonresponders. (NCT00127933)
Timeframe: post 2 and 4, 3-week cycles of treatment

Interventionpercentage of participants (Number)
HER2-Neu Negative23.8
HER2-Neu Positive23.5

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Percentage of Participants With Local Recurrence

Local recurrence was defined as evidence of recurrent carcinoma in the same breast where it was diagnosed initially before preoperative treatment. (NCT00127933)
Timeframe: 30 - 1102 days

Interventionpercentage of participants (Number)
HER2-Neu Negative3.1
HER2-Neu Positive3.7

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Participants With Overall Survival

Overall survival was defined as the time from date of start of study treatment to the date of death, regardless of the cause of death. Patients who were alive at the time of the analysis were censored at the date of the last follow-up assessment. Patients without follow-up assessment were censored at the day of the last dose. Patients with no post-baseline information were censored at the start of study treatment. (NCT00127933)
Timeframe: 22 - 1191 days

Interventionparticipants (Number)
HER2-Neu Negative118
HER2-Neu Positive32

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Quality of Life Questionnaire: Time to Taking Off the Wig

"Time to taking off the wig was assessed by a specific Hair Toxicity Questionnaire were patients answered when they stop to use the wig.~The questionnaire was evaluated up to two years after the end of chemotherapy." (NCT00129935)
Timeframe: Up to 30 months

InterventionMonths (Median)
Arm A: EC-T8.35
Arm B: ET-X6.03

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Number of Participants With Overall Survival (OS) Event

A participant was considered to have had a OS event if patient died from any cause. (NCT00129935)
Timeframe: Up to 5 years

InterventionParticipants (Count of Participants)
Arm A: EC-T70
Arm B: ET-X83

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The Number of Participants Who Experienced Adverse Events (AE)

Safety was assessed by standard clinical and laboratory tests, and were evaluated using NCI-CTC criteria v2.0 (NCT00129935)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
Arm A: EC-T665
Arm B: ET-X699

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Number of Participants With Disease-free Survival (DFS) Event

A participant was considered to have had a DFS event if there was evidence of local, regional or metastatic recurrence, second primary cancer (with the exception of carcinoma of squamous cells or basal cells of the skin, cervical carcinoma in situ or lobular or ductal carcinoma in situ of the breast) or death for any reason. (NCT00129935)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
Arm A: EC-T127
Arm B: ET-X170

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Disease Free Survival (DFS) Events

DFS was measured from the date of randomization assignment in the intent to treat (ITT) population to loco-regional or distant recurrence, second primary malignancy or death date, whichever occurred first. (NCT00130533)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
Xeloda (Capecitabine)105
Observation120

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The Number of Participants Who Experienced Adverse Events (AE)

Safety will be assessed by standard clinical and laboratory tests (haematology, serum chemistry). AE grade were defined by the NCI CTCAE (National Cancer Institute Common Terminology Criteria for Adverse Events). (NCT00130533)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
Xeloda (Capecitabine)416
Observation271

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Overall Survival (OS) Event

OS event is defined as the death from any cause. (NCT00130533)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
Xeloda (Capecitabine)71
Observation73

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Frequency of Grade III/IV Toxicities Experienced by Participants

The frequency of grade 3 and grade 4 adverse events experienced by all treated participants. (NCT00148122)
Timeframe: 30 days post treatment

Interventionparticipants (Number)
Grade 3 and 4 LymphopeniaGrade 3 and 4 Infection w/o NeutropeniaGrade 3 and 4 FatigueGrade 3 and 4 LeukocytesGrade 3 and 4 StomatitisGrade 3 and 4 NeutrophilsGrade 3 and 4 DiarrheaGrade 3 and 4 Hand-Foot Skin ReactionGrade 3 and 4 HemoglobinGrade 3 and 4 PlateletsGrade 3 and 4 Allergic ReactionGrade 3 and 4 AnorexiaGrade 3 and 4 Cardiac-IschemiaGrade 3 and 4 DysphagiaGrade 3 and 4 DyspneaGrade 3 and 4 Abnormal ENT ExaminationGrade 3 and 4 Edema LimbsGrade 3 and 4 Febrile NeutropeniaGrade 3 and 4 Hand-Foot SyndromeGrade 3 and 4 HyperglycemiaGrade 3 and 4 HyponatremiaGrade 3 and 4 Infection with Unknown ANCGrade 3 and 4 Infection, LungGrade 3 and 4 MelenaGrade 3 and 4 Mental Status ChangesGrade 3 and 4 MucositisGrade 3 and 4 NauseaGrade 3 and 4 Oral PainGrade 3 and 4 Pain, ExtremityGrade 3 and 4 Pharyngolaryngeal PainGrade 3 and 4 AST ElevationGrade 3 and 4 Vomiting
Arm 185444322221111111111111111111111

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Probability of Progression Free Survival

The estimated 1 year progression free survival. Progression was defined, using RECIST (Response Evaluation Criteria In Solid Tumors Criteria), as a 20% increase in the sum of the longest diameter of target lesions, the development of any new lesion, or the significant clinical deterioration related to the progression of patient's disease. The probability of progression-free survival was presented in a Kaplan-Meier curve to illustrate the distribution of progression time. The median time to progression was determined with a 95% CI (Confidence Interval). (NCT00148122)
Timeframe: 1 year post treatment

Interventionpercentage of patients (Number)
Arm 125

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Overall Response Rate at 4 Months

Disease was assessed by radiologic imaging and RECIST (Response Evaluation Criteria in Solid Tumors) was used to determine response: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00148122)
Timeframe: 4 months

Interventionpercentage of participants (Number)
Arm 116

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Median Time for Progression Free Survival

Progression-free survival was measured from the start of treatment until the time the subject is first recorded as having disease progression (progression = 20% increase in sum of longest diameters of target measurable lesions over smallest sum observed or baseline, progression of non-measurable disease in the opinion of treating physician, appearance of new lesion/site, death due to disease), or death due to any cause. If a subject has not progressed or died, progression-free survival was censored at the time of last follow-up or the start of another treatment, whichever came first. (NCT00159432)
Timeframe: Up to 6 years

InterventionMonths (Median)
Oxaliplatin Followed by Bevacizumab, With Capecitabine15.8

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Number of Participants With Grade 3 or Higher Toxicity

Summary of grade 3 (per CTCAE v3.0) or higher toxicities which generally is described as a severe adverse reaction or symptom. (NCT00159432)
Timeframe: Baseline, every 2 weeks of each cycle, and at end of treatment, up to 18 months.

InterventionParticipants (Number)
Oxaliplatin Followed by Bevacizumab, With Capecitabine51

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Overall Survival

The time interval between the date on which a patient first received protocol treatment and the documented date of death. (NCT00177255)
Timeframe: 2 years

InterventionMonths (Median)
Docetaxel + Capecitabine10.7

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Overall Response Rate

The number of responders (complete responders + partial responders) divided by the number of evaluable patients. (NCT00177255)
Timeframe: Every 2 cycles (6 weeks)

Interventionpercentage of participants (Number)
Docetaxel + Capecitabine28.2

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1-, 2-, and 3-year Overall Survival

Probability of being alive at 1-, 2-, and 3-years from start of protocol therapy (NCT00177307)
Timeframe: Up to 40 months

Interventionpercent chance (Number)
1 year-overall survival2 year-overall survival3 year-overall survival
Oxaliplatin, Capecitabine, and Bevacizumab623624

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Response Rate (RR)

Percentage of partial responses (PR) + complete responses (CR). (NCT00177307)
Timeframe: Up to 27 months

Interventionpercentage of participants (Number)
Oxaliplatin, Capecitabine, and Bevacizumab38

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Progression Free Survival (PFS)

time from start of protocol therapy until objective tumor progression or death (NCT00177307)
Timeframe: Up to 27 Months

InterventionMonths (Median)
Oxaliplatin, Capecitabine, and Bevacizumab8.6

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Overall Survival

time from start of protocol therapy until death from any cause (NCT00177307)
Timeframe: Up to 40 months

InterventionMonths (Median)
Oxaliplatin, Capecitabine, and Bevacizumab17.2

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Summary of Changes in Karnofsky Performance Status (KPS) by Treatment (Crossover Treatment)

KPS ranges from 0 to 100, subdivided into three categories: incapacitated (0-40), self-care (50-70), and normal activity (80-100). (NCT00191152)
Timeframe: First day of crossover treatment until end of crossover treatment at trial discontinuation (up to 82 moths)

,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Capecitabine89.09-0.30
Gemcitabine87.94-1.27

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Best Overall Response (Crossover Treatment)

Best overall response was the best response recorded from the start of treatment until disease progression/recurrence (taking as reference for progressive disease the smallest measurements recorded since the treatment started). Response assessed using RECIST criteria. Complete Response=disappearance of all target lesions; Partial Response=30% decrease in sum of longest diameter of target lesions; Progressive Disease=20% increase in sum of longest diameter of target lesions; Stable Disease=small changes that did not meet above criteria. (NCT00191152)
Timeframe: Best response from start of treatment until disease progression/recurrence (up to 82 months)

,
Interventionparticipants (Number)
Complete Response (confirmed)Partial Response (confirmed)Stable DiseaseProgressive DiseaseUnknown
Capecitabine110193413
Gemcitabine16203618

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Time to Disease Progression (Crossover Treatment)

For crossover treatment, time to disease progression (TTDP) was defined as the number of months between the first dose date of crossover treatment and the date of disease progression or the date of death due to disease under study, whichever came first. TTDP for crossover treatment only applied to those participants who crossed over from initial treatment to crossover treatment. TTDP censored at earliest of: 1)date of death not due to disease; or 2)date of last contact for participants alive without disease progression; or 3)start date of other anti-tumor therapy due to progression. (NCT00191152)
Timeframe: Date of first dose of crossover treatment to date of first-documented disease progression after receiving first crossover treatment or date of death due to study disease, whichever came first (up to 82 months)

Interventionmonths (Median)
Capecitabine4.51
Gemcitabine2.34

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Progression-Free Survival (Initial Treatment)

For initial treatment, progression-free survival (PFS) was defined as the number of months between the date of randomization and the date of first documented disease progression or the date of death due to any cause, whichever came first. Time to PFS was censored at the earliest of: 1) date of last contact for participants alive without disease progression; or 2) start date of other anti-tumor therapy for progression; or 3) first dose date of crossover treatment. (NCT00191152)
Timeframe: Date of randomization until the date of first documented progression or date of death from any cause, whichever came first (up to 82 months)

Interventionmonths (Median)
Gemcitabine Plus Docetaxel9.01
Docetaxel Plus Capecitabine8.88

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Time to Disease Progression (Initial Treatment)

Time to disease progression (TTDP) at initial treatment was defined as the number of months between date of randomization and the date of first documented disease progression or the date of death due to disease under study, whichever came first. TTDP censored at earliest of: 1) date of death not due to disease; or 2) date of last contact for participants alive without disease progression; or 3) start date of other anti-tumor therapy; or 4) first dose date of crossover treatment. (NCT00191152)
Timeframe: Randomization date to the earliest date of first documented disease progression date or the date of death if the participant died due to study disease (up to 82 months)

Interventionmonths (Median)
Gemcitabine Plus Docetaxel9.28
Docetaxel Plus Capecitabine8.88

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Progression-Free Survival (Crossover Treatment)

For crossover treatment, progression-free survival (PFS) was defined as the number of months between first dose date of crossover treatment and date of documented disease progression or date of death due to any cause, whichever came first. PFS for crossover treatment only applied to those participants who crossed over from initial treatment to crossover treatment. PFS was censored at the earliest of: 1) date of last contact for participants alive without disease progression; or 2) start date of other anti-tumor therapy for participants with documented disease progression. (NCT00191152)
Timeframe: First dose date of crossover treatment to date of first-documented progression after receiving crossover treatment or date of death due to any cause, whichever came first (up to 82 months)

Interventionmonths (Median)
Capecitabine4.51
Gemcitabine2.34

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Summary of Changes in Karnofsky Performance Status (KPS) by Treatment (Initial Treatment)

KPS ranges from 0 to 100, subdivided into three categories: incapacitated (0-40), self-care (50-70), and normal activity (80-100). (NCT00191152)
Timeframe: Baseline until crossover treatment began (up to 82 months)

,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Docetaxel Plus Capecitabine90.09-3.27
Gemcitabine Plus Docetaxel90.85-3.30

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Overall Survival

Overall survival time was defined as the number of months between the date of randomization and the date of death due to any cause. The overall survival time was censored at the date of last contact for participants who were still alive. (NCT00191152)
Timeframe: Date of randomization to date of death from any cause (up to 82 months)

Interventionmonths (Median)
Gemcitabine Plus Docetaxel22.99
Docetaxel Plus Capecitabine23.29

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Summary of Changes in Rotterdam Symptom Checklist by Treatment (Crossover Treatment)

RSCL includes 4 scales to assess quality of life (QOL) endpoints: 1) a 23-item physical distress level with scale score ranges from 23 to 92 [low score represents better QOL] 2)a 7-item psychological distress level with scale score ranges from 7 to 28[low score represents better QOL] 3)8-item activity level with scale score ranges from 8 to 32 [high score represents better QOL]; 1-item overall valuation of life with score range from 1 to 7 [low score represents better QOL]. (NCT00191152)
Timeframe: First day of crossover treatment until end of crossover treatment at trial discontinuation (up to 82 months)

,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Capecitabine75.00-2.78
Gemcitabine76.39-0.69

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Duration of Response (Crossover Treatment)

At crossover treatment, duration of response was measured from the time criteria were met for complete response (CR) or partial response (PR), until first date that recurrent or progressive disease was objectively documented or date of death due to any cause, whichever came first. This definition only applied to those who crossed over & achieved CR or PR in crossover treatment. Duration of response censored at earliest of: 1) date of last contact for those alive without disease progression; or 2) start date of other anti-tumor therapy for documented disease progression. (NCT00191152)
Timeframe: Date of CR or PR until first date of recurrent or progressive disease after receiving crossover treatment was objectively documented or date of date due to any cause, whichever came first (up to 82 months)

Interventionmonths (Median)
Capecitabine25.89
Gemcitabine42.50

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Duration of Response (Initial Treatment)

Among tumor responders, duration of tumor response was measured from the date of response (complete response [CR] or partial response [PR] until the first date of documented progression or death from any cause. Duration of response was censored at the earliest of: 1) date of last contact for participants alive without disease progression (DP); or 2) start date of other anti-tumor therapy for DP; or 3) dose date of crossover treatment. (NCT00191152)
Timeframe: Date of response (CR or PR) until the first date of documented progression or death from any cause (up to 82 months)

Interventionmonths (Median)
Gemcitabine Plus Docetaxel9.11
Docetaxel Plus Capecitabine10.39

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Best Overall Response (Initial Treatment)

Best overall response was the best response recorded from the start of the treatment until disease progression/recurrence (taking as reference for progressive disease the smallest measurements recorded since the treatment started). Response was assessed using Response Evaluation Criteria In Solid Tumors (RECIST) criteria. Complete Response=disappearance of all target lesions; Partial Response=30% decrease in sum of longest diameter of target lesions; Progressive Disease=20% increase in sum of longest diameter of target lesions; Stable Disease=small changes that did not meet above criteria. (NCT00191152)
Timeframe: Best response from start of treatment until disease progression/recurrence (up to 82 months)

,
Interventionparticipants (Number)
Complete Response (confirmed)Partial Response (confirmed)Stable DiseaseProgressive DiseaseUnknown
Docetaxel Plus Capecitabine679902734
Gemcitabine Plus Docetaxel671963234

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Summary of Changes in Rotterdam Symptom Checklist (RSCL) by Treatment (Initial Treatment)

RSCL includes 4 scales to assess quality of life (QOL) endpoints: 1) a 23-item physical distress level with scale score ranges from 23 to 92 [low score represents better QOL] 2)a 7-item psychological distress level with scale score ranges from 7 to 28[low score represents better QOL] 3)8-item activity level with scale score ranges from 8 to 32 [high score represents better QOL]; 1-item overall valuation of life with score range from 1 to 7 [low score represents better QOL]. (NCT00191152)
Timeframe: Baseline until crossover treatment began (up to 82 months)

,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Docetaxel Plus Capecitabine72.32-2.68
Gemcitabine Plus Docetaxel68.092.42

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Overall Survival (OS)

Length of time, in months, that patients were alive from their first date of protocol treatment until death. (NCT00193128)
Timeframe: 36 months

Interventionmonths (Median)
Oxaliplatin/Docetaxel/Capecitabine/Radiation (Cohort 2)24.1

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Disease-Free Survival (DFS)

Defined as the interval between the start date of treatment and the date of occurrence of progressive disease or death from any cause. (NCT00193128)
Timeframe: 18 months

Interventionmonths (Median)
Oxaliplatin/Docetaxel/Capecitabine/Radiation (Cohort 2)16.3

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Pathologic Complete Response Rate (PCRR), the Percentage of Patients Who Have No Evidence of Cancer in Their Surgical Specimen Following Surgery

The absence of any residual tumor cells in a histologic evaluation of a tumor specimen following surgery is defined as a complete pathologic response (NCT00193128)
Timeframe: 18 months

InterventionParticipants (Count of Participants)
Oxaliplatin/Docetaxel/Capecitabine/Radiation (Cohort 2)24

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Overall Survival

Length of time, in months, that patients were alive from their first date of protocol treatment until death. (NCT00193609)
Timeframe: 18 months

Interventionmonths (Median)
Intervention9.7

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Progression Free Survival

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00193609)
Timeframe: 18 months

Interventionmonths (Median)
Intervention3.7

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Time to Progression

Median time to progression free survival. (NCT00194779)
Timeframe: Up to 5 years

Interventionmonths (Median)
Treatment (Neoadjuvant Therapy, Adjuvant Therapy)NA

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Combined Rate of Microscopic pCR and Macroscopic Pathologic Complete Response (mCR)

"Microscopic pCR: No evidence of microscopic invasive tumor at the primary site or in the regional lymph nodes at the time of definitive surgical resection. mCR: The examining pathologist cannot identify gross residual tumor mass in the surgical specimen. This differs from a pCR where the specimen must also be negative for invasive tumor by microscopy. For this study, we are using a definition of mCR that will make the trial more translatable to other institutions. For this study, mCR will be defined as no focus of invasive cancer >= 1 cm.~Count of participants with either a pCR or mCR." (NCT00194779)
Timeframe: Up to 16 weeks

InterventionParticipants (Count of Participants)
Treatment (Neoadjuvant Therapy, Adjuvant Therapy)29

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Relapse Rate in Patients With Operable Breast Cancer Treated With Neoadjuvant Chemotherapy for 12 Weeks Followed by Weekly Paclitaxel for 12 Weeks and Adjuvant Chemotherapy

Count of patients that relapsed. (NCT00194779)
Timeframe: Up to 8 years

InterventionParticipants (Count of Participants)
Treatment (Neoadjuvant Therapy, Adjuvant Therapy)7

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Disease-free Survival

Kaplan-Meier estimate of disease-free survival, assessed at 1, 2, and 5 years. (NCT00194779)
Timeframe: 1, 2, and 5 years

Interventiondisease-free survival probability (Number)
1 year2 years5 years
Treatment (Neoadjuvant Therapy, Adjuvant Therapy).97.90.84

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OS in Patients With Operable Breast Cancer Treated With Neoadjuvant Chemotherapy for 12 Weeks Followed Weekly Paclitaxel for 12 Weeks and Adjuvant Chemotherapy With XMN

Kaplan-Meier estimate of overall survival, assessed at 1, 2, and 5 years. (NCT00194779)
Timeframe: 1, 2, and 5 years

Interventionsurvival probability (Number)
1 year2 years5 years
Treatment (Neoadjuvant Therapy, Adjuvant Therapy)1.94.90

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Number and Percent of Patients Reporting Grade 2, 3, 4, or Fatal Toxicities of These Regimens, Need for Dose Reduction, or Treatment Interruption or Discontinuation

(NCT00194779)
Timeframe: From the initiation of study treatments to 30 days after the end of neoadjuvant treatment or adjuvant treatment if received

InterventionParticipants (Count of Participants)
Treatment (Neoadjuvant Therapy, Adjuvant Therapy)32

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Overall Survival

From the start of protocol therapy until the date of death from any cause or the last date the patient was known to be alive. Kaplan-Meier estimate assessed at 5 years. (NCT00194792)
Timeframe: Up to 5 years

Interventionsurvival probability (Number)
Treatment (Hormone Therapy and Chemotherapy)0.88

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Quantification of All Grade 2, 3, 4 Adverse Events or Fatal Toxicities

Count of all incidences of grade 2, 3, 4 adverse events and fatal toxicities (NCT00194792)
Timeframe: Monthly during neoadjuvant treatment and then 6 months following treatment (including surgery)

Interventionevents (Number)
Grade 2Grade 3Grade 4Fatal toxicity
Treatment (Hormone Therapy and Chemotherapy)801200

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Number of Participants With Microscopic Pathologic Complete Response and Macroscopic Pathologic Complete Response

Defined as no evidence of microscopic invasive tumor at the primary site or in the regional lymph nodes at the time of definitive surgical resection and the examining pathologist cannot identify gross residual tumor mass in the surgical specimen. (NCT00194792)
Timeframe: From date of treatment start to surgery

InterventionParticipants (Count of Participants)
Treatment (Hormone Therapy and Chemotherapy)0

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Number of Participants With Clinical Response

Defined as a > 50% decrease in sum of the products of the perpendicular diameters of bidimensionally measurable disease. (NCT00194792)
Timeframe: 1 month

InterventionParticipants (Count of Participants)
Treatment (Hormone Therapy and Chemotherapy)19

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Disease-free Survival

Kaplan-Meier estimate assessed at 5 years (NCT00194792)
Timeframe: Up to 5 years

Interventiondisease free survival probability (Number)
Treatment (Hormone Therapy and Chemotherapy)0.76

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Number of Participants With Dose Reduction, Treatment Interruption, or Treatment Discontinuation

Count of patients with dose reduction, treatment interruption, or treatment discontinuation. (NCT00194792)
Timeframe: During adjuvant and neoadjuvant chemotherapy

InterventionParticipants (Count of Participants)
Adjuvant therapyNeoadjuvant therapy
Treatment (Hormone Therapy and Chemotherapy)111

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Objective Response Rate (ORR) for the Phase II Portion of the Study. CR+PR Per RECIST v1.0 Criteria Using a Single Arm , Two Stage Minimax Design.

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00201734)
Timeframe: Every 3 weeks, for up to 24 weeks

Interventionpercent of patients (Number)
Phase I21
Phase II32

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One Year Survival for Patients

For patients enrolled on the Phase II portion of the trial the One-year survival was measured as the percentage of patients alive 1 year after their treatment in the trial. (NCT00201734)
Timeframe: Up to 1 year

Interventionpercent of patients (Number)
Phase II44

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Progression-Free Survival at 6 Months for Patients

For patients enrolled on the Phase II portion of the trial Progression Free Survival (PFS) was measured from the percentage of patients that were still alive, without evidence of disease progression for 6 months following the initiation of treatment. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00201734)
Timeframe: up to 6 years

Interventionpercent of patients (Number)
Phase II38

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Phase I: To Determine Side Effects

The common clinically significant grade 3 and 4 toxicities graded using the National Cancer Institutes Common Toxicity Criteria version 3.0 (NCT00201734)
Timeframe: Every 3 weeks, for up to 24 weeks

,
Interventionpercent of patients (Number)
NeutropeniaThrombocytopeniaFatigue
Phase I867276
Phase II727284

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Maximum Tolerated Dose in Phase I Portion of Study

Determine the maximum tolerated dose of the triplet combination of capecitabine that can be administered in combination with weekly paclitaxel and every four weeks carboplatin. (NCT00201734)
Timeframe: Every 3 weeks, for up to 24 weeks

Interventionmg/m2 (Number)
Phase I Patients750

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Time to Tumor Progression for Patients

For patients enrolled on the Phase II portion of the trial the time to progression was measured as the time from when the patient started treatment to the time the patient is first recorded as having disease progression or the date of death if the patient dies due to causes other than disease progression. (NCT00201734)
Timeframe: Up to 6 years

Interventionmonths (Median)
Phase II5.5

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Time to Tumor Progression

(NCT00201825)
Timeframe: Every 35 days

Interventionmonths (Median)
Docetaxel and Capecitabine3.3

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Determine Objective Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00201825)
Timeframe: Every 35 days

Interventionpatients (Number)
Complete response (CR)Partial response (PR)Stable DiseaseDisease ProgressionOverall response (CR + PR)
Docetaxel and Capecitabine051495

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One Year Survival

(NCT00201825)
Timeframe: one year

Interventionmonths (Median)
Docetaxel and Capecitabine10.5

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Quality of Life of Patients

"Functional Assessment of Cancer Therapy-Colorectal (FACT-C) Trial Outcome Index (TOI) - a questionnaire assessing quality of life concerns pertinent to colorectal cancer patients. Questions address Physical, Emotional and Functional Well-Being. Scale: Not at all (0), A little bit (1), Somewhat (2), Quite a bit (3), and very much (4). Higher numbers indicate a better state of well being. Scale 0 -136. Higher numbers indicating a better state of well-being.~The Overall scores for the FACT-C Composite scale range between 0-100 with higher scores indicating a better state of well being.~The EQ VAS= Euro Quality of Life 5 Dimension Self Reported Healthstate. It records the respondent's self-rated health on a vertical, visual analogue scale where the endpoints are labeled 0 'Best imaginable health state' and 100 'Worst imaginable health state'." (NCT00203411)
Timeframe: Baseline, Cycle 2, and End of Study

Interventionscore on a scale (Mean)
Baseline FACT-C Trial outcome index (TOI)Cycle 2 FACT-C TOIEnd of Study FACT-C TOIBaseline FACT-C CompositeCycle 2 FACT-C CompositeEnd of Study FACT-CompositeBaseline EQ-5D VASCycle 2 EQ-5D VASEnd of Study EQ-5D VAS
Bevacizumab Plus Capecitabine62.8566.3162.0999.87105.3898.6161.7668.5966.54

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Response Rates

Evaluation of target lesions Complete Response (CR): Disappearance of all target lesions Partial Response (PR): At least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions (NCT00203411)
Timeframe: every 21 days up to 12 months

Interventionparticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressionNot Evaluable
Bevacizumab Plus Capecitabine2141694

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Time to Disease Progression

Progression Free Survival (PFS)- the interval from the date of enrollment to the first documented date of disease progression, death due to cancer, or the last date of a definitive assessment (not an unknown assessment) at which the patient is known to be progression-free. If there is an unknown assessment, then (a) if the next subsequent definitive assessment is complete response (CR), partial response (PR), or stable disease (SD), the patient is considered to be progression-free at the date of the subsequent definitive assessment and PFS is calculated as above; (b) if the next subsequent definitive assessment is progressive disease (PD), the patient is considered to be a failure at the time of the (earliest) assessment of unknown preceding the documented disease progression (i.e. PFS is back-dated to the date of the unknown assessment) and (c) if there is no subsequent definitive assessment, PFS for the patient is considered to be a censored observation at the date (NCT00203411)
Timeframe: 12 months

Interventionmonths (Median)
Bevacizumab Plus Capecitabine6.87

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Number of Subjects Requiring Dose Modifications

Number of Subjects that required Bevacizumab or Capecitabine dose modifications, delay, reduction or discontinuation due to adverse reactions. (NCT00203411)
Timeframe: 3 months

Interventionparticipants (Number)
Delay in Bevacizumab DoseDiscontinuation of BevacizumabDelay in Capec itabineDoseReduction of Capecitabine DoseDiscontinuation of Capecitabine
Bevacizumab Plus Capecitabine151481316

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Number of Participants With Complete Pathologic Response Rate to Pre-operative Treatment in Arm A (Docetaxel for 4 Cycles Followed by Capecitabine for 4 Cycles) or Arm B (Docetaxel + Capecitabine for 8 Cycles) in Patients With Early Stage Breast Cancer.

"Pathologic complete response (pCR): Absence of invasive breast cancer in the breast.~Overall Clinical Response=Complete response(CR-complete disappearance of all measurable malignant disease)+partial response(PR-reduction by at least 30%)~Stable disease (SD): No decrease or <25% increase in the sum of the products of the longest perpendicular diameters of all measurable lesions.~Progressive disease (PD): A 20% or greater increase in a single lesion, OR reappearance of any lesion which has disappeared, OR clear worsening of any evaluable disease OR appearance of any new lesion/site." (NCT00209092)
Timeframe: 1 year

,
Interventionparticipants (Number)
Pathologic Complete Response-Overall populationOverall Clinical ResponseStable diseaseProgressive Disease
Arm A:Sequential Therapy21537
Arm B:Concurrent Therapy32312

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Long Term Follow up Data on Recurrence and Survival

Number of Patients remained alive and relapse free (NCT00209092)
Timeframe: 2 years

Interventionparticipants (Number)
Arm A:Sequential Therapy19
Arm B:Concurrent Therapy21

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Overall Survival (OS)

OS was defined as the duration from randomization to death (due to any cause). OS was estimated using Kaplan-Meier analysis. (NCT00215644)
Timeframe: Baseline until death due to any cause (up to approximately 3 years)

Interventionmonths (Median)
Epirubicin, Cisplatin, Capecitabine (ECX)+Matuzumab9.4
ECX Only12.2

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Duration of Objective Response Assessed by Independent Review Committee

Objective response was defined as having a CR or a PR. Response assessment was performed using modified WHO criteria. CR: disappearance of all index and non-index lesions, without appearance of any new lesion. PR: >50% decrease from baseline in sum of product of diameters of index lesions, without appearance of any new lesion. Duration of objective response was defined as time from first appearance of CR or PR to time of PD (PD: >25% increase in one or more lesions, or appearance new lesions) or death. Duration of objective response was to be assessed using Kaplan-Meier analysis. (NCT00215644)
Timeframe: From first documented objective response to PD or death due to any cause (up to approximately 3 years)

Interventionmonths (Median)
Epirubicin, Cisplatin, Capecitabine (ECX)+MatuzumabNA
ECX OnlyNA

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Percentage of Participants With Objective Response Assessed by Independent Review Committee

Objective response was defined as having a complete response (CR) or a partial response (PR). Response assessment was performed using modified World Health Organization (WHO) criteria. CR: disappearance of all index and non-index lesions, without appearance of any new lesion. PR: greater than (>) 50 percent (%) decrease from baseline in sum of product of diameters of index lesions, without appearance of any new lesion. (NCT00215644)
Timeframe: Baseline up to PD or death due to any cause (up to approximately 3 years)

Interventionpercentage of participants (Number)
Epirubicin, Cisplatin, Capecitabine (ECX)+Matuzumab31
ECX Only58

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Progression-Free Survival

PFS was defined as the time from randomization to the first documentation of PD or to death due to any cause, whichever occurred first. PD: >25% increase in one or more lesions, or appearance new lesions. PFS was estimated using Kaplan-Meier analysis. (NCT00215644)
Timeframe: Baseline up to PD or death due to any cause (up to approximately 3 years)

Interventionmonths (Median)
Epirubicin, Cisplatin, Capecitabine (ECX)+Matuzumab4.8
ECX Only7.1

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Best Overall Change From Baseline in European Organization for Research and Treatment of Cancer Quality-of-Life Questionnaire-Core 30 (EORTC QLQ-C30) Global Health Status (GHS)/Quality of Life (QoL) Score

EORTC QLQ-C30 included GHS/QoL, functional scales (physical, role, cognitive, emotional, social), symptom scales (fatigue, pain, nausea/vomiting), and single items (dyspnea, appetite loss, insomnia, constipation, diarrhea, financial difficulties). Most questions from EORTC QLQ-C30 were a 4-point scale (1/Not at All to 4/Very Much), except Items 29-30, which comprise GHS scale and were a 7-point scale (1/Very Poor to 7/Excellent). For this instrument, GHS/QOL was linearly transformed and ranged 0-100, where lower scores indicate poorer functioning (e.g., worsening) and higher scores indicate better functioning (e.g., improvement). EORTC QLQ-C30 GHS/QoL score at baseline and best overall change from baseline (throughout study) are reported. (NCT00215644)
Timeframe: Baseline (Day 1), Post Baseline (Up to 3 Years)

,
Interventionunits on a scale (Mean)
BaselinePost-Baseline
ECX Only67.9-10.0
Epirubicin, Cisplatin, Capecitabine (ECX)+Matuzumab53.30.0

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Pathological Complete Response (pCR) Rate

"· To determine the pathological response rate of preoperative chemotherapy with capecitabine and irinotecan followed by combined modality chemoradiation with capecitabine in patients with locally advanced rectal cancer.~Pathological response was defined in the protocol as the proportion of complete (pCR) and non-complete pathological response (pNCR) among all evaluable patients." (NCT00216086)
Timeframe: 36 months

Interventionpercentage of patients (Number)
pCRpNCR
Single Group Assignment3356

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Local and Distant Disease Recurrence Rates

To determine the rates of local and distant disease recurrence after treatment. (NCT00216086)
Timeframe: 36 months

Interventionpercentage of particpants (Number)
metastatic disease recurrencelocally recurrence
Single Group Assignment220

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Disease-Free Survival

The three year rate of Disease-Free Survival (NCT00216086)
Timeframe: 36 months

Interventionpercentage (Number)
Single Group Assignment75.5

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Survival at 5 Years

Survival at 5 years was assessed as the number of participants alive 5 years after starting treatment. (NCT00226941)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
Group 1 - Cetuximab + Capecitabine-800 + XRT + Oxaliplatin-1005
Group 2 - Cetuximab + Capecitabine-700 + XRT + Oxaliplatin-854
Group A - Cetuximab + Capecitabine-800 + XRT3
Group B - Cetuximab + Capecitabine-800 + XRT3

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Overall Survival (OS)

Overall Survival (OS) was assessed as the mean survival from the date of entry on study though 72 months. (NCT00226941)
Timeframe: 72 months

Interventionmonths (Mean)
Group 1 - Cetuximab + Capecitabine-800 + XRT + Oxaliplatin-10059.7
Group 2 - Cetuximab + Capecitabine-700 + XRT + Oxaliplatin-8557.0
Group A - Cetuximab + Capecitabine-800 + XRT54.4
Group B - Cetuximab + Capecitabine-1000 + XRT53.7

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Dose-limiting Toxicity (DLT) - Number of Participants Affected

Dose-limiting Toxicity (DLT) is the measure used to establish overall Maximum-tolerated dose (MTD) of cetuximab + capecitabine + radiotherapy +/- oxaliplatin. MTD is defined as the highest dose level for which participants have a < 30% incidence of dose-limiting toxicity (DLT). The outcome is expressed as the number of participants experiencing a DLT. (NCT00226941)
Timeframe: 10 weeks

InterventionParticipants (Count of Participants)
Group 1 - Cetuximab + Capecitabine-800 + XRT + Oxaliplatin-1004
Group 2 - Cetuximab + Capecitabine-700 + XRT + Oxaliplatin-852
Group A - Cetuximab + Capecitabine-800 + XRT0
Group B - Cetuximab + Capecitabine-1000 + XRT0

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Dose-limiting Toxicity (DLT) - Number of DLTs by Treatment Group

Dose-limiting Toxicity (DLT) is the measure used to establish overall Maximum-tolerated dose (MTD) of cetuximab + capecitabine + radiotherapy +/- oxaliplatin. MTD is defined as the highest dose level for which participants have a < 30% incidence of dose-limiting toxicity (DLT). The outcome is expressed as the number of DLTs by treatment group. (NCT00226941)
Timeframe: 10 weeks

InterventionDLTs (Number)
Group 1 - Cetuximab + Capecitabine-800 + XRT + Oxaliplatin-10010
Group 2 - Cetuximab + Capecitabine-700 + XRT + Oxaliplatin-852
Group A - Cetuximab + Capecitabine-800 + XRT0
Group B - Cetuximab + Capecitabine-1000 + XRT0

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Pathologic Response Rate

After treatment with capecitabine, cetuximab, radiotherapy, and oxaliplatin, the pathologic response rate was assessed based on the excised tumor taken at the time of surgical resection. Pathologic response rate was determined as the number and proportion of participants who experienced either downstaging of their disease, or complete response (CR, no detectable disease). A participant will be considered to have downstaging of the tumor as a result of the neoadjuvant therapy when the primary tumor (T) stage by pathology isless than the T stage by clinical (endoscopic) evaluation, or when the regional lymph node (N) tumor stage by pathology is less than the N stage by clinical (endoscopic) evaluation. (NCT00226941)
Timeframe: 12 to 14 weeks after radiotherapy

InterventionParticipants (Count of Participants)
Group 1 - Cetuximab + Capecitabine-800 + XRT + Oxaliplatin-1004
Group 2 - Cetuximab + Capecitabine-700 + XRT + Oxaliplatin-855
Group A - Cetuximab + Capecitabine-800 + XRT3
Group B - Cetuximab + Capecitabine-1000 + XRT5

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Tumor Downstaging at Surgical Resection

Downstaging means a reduction from the stage of disease observed at baseline to the stage of disease after treatment with cetuximab, radiotherapy, oxaliplatin, and capecitabine, as determined at the time of surgical removal of the tumor. Downstaging may be observed as improvements in tumor staging at the primary site of the tumor; in nearby (regional) lymph nodes; or in metastatic disease beyond the regional lymph nodes. This outcome specifically does not include participants that achieved a complete response, nor those that experienced no response or disease progression. (NCT00226941)
Timeframe: 12 to 14 weeks after radiotherapy

InterventionParticipants (Count of Participants)
Group 1 - Cetuximab + Capecitabine-800 + XRT + Oxaliplatin-1004
Group 2 - Cetuximab + Capecitabine-700 + XRT + Oxaliplatin-855
Group A - Cetuximab + Capecitabine-800 + XRT3
Group B - Cetuximab + Capecitabine-1000 + XRT5

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Time-to-Progression (TTP)

Time-to-progression was assessed as the time from the date of surgical resection to the appearance of either local disease recurrence or distant metastases by any modality (eg, clinical exam, endoscopy, radiographic imaging). All relapses were to be confirmed by biopsy and pathology review. (NCT00226941)
Timeframe: 5 years

Interventionyears (Median)
Group 1 - Cetuximab + Capecitabine-800 + XRT + Oxaliplatin-1001.4
Group A - Cetuximab + Capecitabine-800 + XRT3.0
Group B - Cetuximab + Capecitabine-1000 + XRT3.9

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Incidence of Sphincter-sparing Surgery

Incidence of sphincter-saving surgery is defined as the proportion of subjects who do not have permanent colostomy at the final follow-up out of all evaluable patients. (NCT00250835)
Timeframe: At surgery (up to 6 weeks after end of treatment)

Interventionpercentage of evaluable participants (Number)
Chemotherapy, Celecoxib, and Radiation56

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Pelvic Local Control Rate

Pelvic local control rate is defined as the proportion of subjects who have no evidence of pelvic recurrence (by standard clinical assessment, including CT scan and clinical examination) at the final follow-up evaluation, out of all evaluable patients (NCT00250835)
Timeframe: Up to 3 years after surgery

Interventionpercentage of evaluable participants (Number)
Chemotherapy, Celecoxib, and Radiation6

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Progression-free Survival (PFS)

"The Response Evaluation Criteria In Solid Tumors (RECIST) guidelines (Version 1.0) will be used to determine tumor response and progression. Progressive disease (PD) for target lesions: >= 20% increase in the sum of diameters of the target lesions taking as reference the smallest sum on study, and an absolute increase of at least 5 mm. The appearance of one or more new lesions is also considered . PD for non-target lesions is defined as unequivocal appearance of one or more new malignant lesions or unequivocal progression of existing non-target lesions. Time to progression will be measured from the time of surgery or clinically documented down staging if surgery for whatever reason is not carried in the subject until there is evidence of PD.~Progression-free survival is reported as the percentage of patients who have not experienced progression of disease at three years post-surgery" (NCT00250835)
Timeframe: 3 years after surgery

Interventionpercentage of evaluable participants (Number)
Chemotherapy, Celecoxib, and Radiation84

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Toxicity

"All toxicities encountered during the study will be evaluated according to the grading system (0-5) NCI CTCAE (Common Terminology Criteria for Adverse Events) version 3.0.~Toxicity will be reported as the proportion of subjects experiencing Grades 3,4, and 5 adverse events (AEs) out of all evaluable patients" (NCT00250835)
Timeframe: Up to 3 years

Interventionpercentage of participants (Number)
Grade 3 and 4 diarrheaGrade 3 and 4 abnormal liver function testsGrade 3 and 4 abdominal painDeath (from severe infection)
Chemotherapy, Celecoxib, and Radiation9966

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Surgical Downstaging Rate

Downstaging rate after neoadjuvant treatment with combination oxaliplatin, capecitabine, celecoxib and concurrent radiation is defined as the proportion of patients whose pathological stage (stage at surgery) is different from their clinical stage (stage at baseline) (NCT00250835)
Timeframe: At surgery (up to 6 weeks after treatment)

Interventionpercentage of evaluable participants (Number)
Chemotherapy, Celecoxib, and Radiation75

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Pathologic Complete Response (PCR)

The pathologic complete response (PCR) rate will be calculated as the proportion of patients who achieve complete response out of all evaluable patients. PCR is defined as the total absence of residual tumor cells by microscopic examination of the resected surgical specimen, including all of the sampled lymph nodes. (NCT00250835)
Timeframe: At surgery (up to 6 weeks after end of treatment)

Interventionpercentage of evaluable participants (Number)
Chemotherapy, Celecoxib, and Radiation31

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Recurrence-free Survival

Time to recurrence or death (NCT00258310)
Timeframe: Within 3 years of end of study.

Interventionmonths (Median)
CapecitabineNA

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Overall Survival

Estimated time from study entry to death from any cause (NCT00258310)
Timeframe: Within 3 years of end of study

Interventionmonths (Median)
CapecitabineNA

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Compliance With Treatment .

Compliance is defined as taking at least 80% of the prescribed dose for one year. (NCT00258310)
Timeframe: within 365 days

Interventionpercentage of participants (Number)
Capecitabine74

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Incidence of Second Primary Tumors

(NCT00258310)
Timeframe: Within 3 years of end of study

InterventionParticipants (Count of Participants)
Capecitabine3

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Qualitative and Quantitative Toxicity

Number of patients that developed common side effect of diarrhea. (NCT00266279)
Timeframe: At study enrollment, Every two 28 day treatment cycles, and at end of treatment due to disease progression

Interventionparticipants (Number)
Treatment With Study Drugs2

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Overall Response Rate

"Among the 15 patients treated, 2 (13%) achieved partial response (PR), and 5 (33%) achieved stable disease (SD), for a Overall Response Rate (ORR) of 46% measured by RECIST criteria.~Partial Response (PR): At least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD.~Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started.~Overall Response Rate (ORR)=PR+CR." (NCT00266279)
Timeframe: Every two 28 day treatment cycles until subject no longer on treatment due to disease progression

InterventionParticipants (Number)
Partial ResponseStable Disease
Treatment With Study Drugs25

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Overall Survival Time in the PLD and Capecitabine Treatment Groups

Survival time was defined as duration time from onset of treatment with the study drug until death. (NCT00266799)
Timeframe: From Day 1 (Cycle 1) until Death

InterventionMonths (Median)
Pegylated Liposomal Doxorubicin (PLD)23.31
Capecitabine26.79

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Number of Participants With an Overall Response (Complete Response [CR] + Partial Response [PR]) Between PLD and Capecitabine Treatment Groups

Overall responses by investigator assessment/RECIST criteria of participant responses; CR=disappearance of target/nontarget lesions + PR=30% decrease in longest diameter sum (noting baseline sum) of target lesions. RECIST used changes in the largest diameter of target/non-target lesions. Target lesions were up to a maximum of 5 per organ & >20 mm by clinical imaging (>=10 mm with spiral CT scan). Non-target lesions were all other lesions. Evaluation of progress was repeated every 3 months (+/-7 days) post first date of lesion measurements, in detection absence until the participant´s death. (NCT00266799)
Timeframe: From Day 1 (Cycle 1) until First Evidence/Diagnosis of Progressive Disease or Death

,
InterventionParticipants (Number)
By Investigator Assessment - CRBy Investigator Assessment - PRBy Investigator Assessment Overall ResponseBy RECIST Criteria - CRBy RECIST Criteria - PRBy RECIST Criteria Overall Response
Capecitabine0121201111
Pegylated Liposomal Doxorubicin (PLD)156189

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Quality of Life (QoL) Measured by QoL Questionnaire (European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30) + Subjective Significance Questionnaire (SSQ))

QoL questionnaire was an EORTC QLQ-C30 & SSQ integration. Scores on the SSQ scale ranged from 1 (very much worse) - 7 (very much better). SSQ consisted of 4 items which corresponded to core domains in the 30 Item EORTC QLQ-C30, such as improvement/deterioration in physical functioning, emotional functioning, social functioning, global QoL. Percentages were based on number of participants at each cycle & rounded to the nearest whole number. Early Withdrawal Questionnaires were obtained in 7-14 days of study drug final dose. (NCT00266799)
Timeframe: From Screening to Day 1 of every Treatment Cycle up to 12 Cycles

,
InterventionPercentage of Participants (Number)
Screening - Very Much WorseScreening - Moderately WorseScreening - A Little WorseScreening - About the SameScreening - A Little BetterScreening - Moderately BetterScreening - Very Much BetterCycle 1 - Very Much WorseCycle 1 - Moderately WorseCycle 1 - A Little WorseCycle 1 - About the SameCycle 1 - A Little BetterCycle 1 - Moderately BetterCycle 1 - Very Much BetterCycle 2 - Very Much WorseCycle 2 - Moderately WorseCycle 2 - A Little WorseCycle 2 - About the SameCycle 2 - A Little BetterCycle 2 - Moderately BetterCycle 2 - Very Much BetterCycle 3 - Very Much WorseCycle 3 - Moderately WorseCycle 3 - A Little WorseCycle 3 - About the SameCycle 3 - A Little BetterCycle 3 - Moderately BetterCycle 3 - Very Much BetterCycle 4 - Very Much WorseCycle 4 - Moderately WorseCycle 4 - A Little WorseCycle 4 - About the SameCycle 4 - A Little BetterCycle 4 - Moderately BetterCycle 4 - Very Much BetterCycle 5 - Very Much WorseCycle 5 - Moderately WorseCycle 5 - A Little WorseCycle 5 - About the SameCycle 5 - A Little BetterCycle 5 - Moderately BetterCycle 5 - Very Much BetterCycle 6 - Very Much WorseCycle 6 - Moderately WorseCycle 6 - A Little WorseCycle 6 - About the SameCycle 6 - A Little BetterCycle 6 - Moderately BetterCycle 6 - Very Much BetterCycle 7 - Very Much WorseCycle 7 - Moderately WorseCycle 7 - A Little WorseCycle 7 - About the SameCycle 7 - A Little BetterCycle 7 - Moderately BetterCycle 7 - Very Much BetterCycle 8 - Very Much WorseCycle 8 - Moderately WorseCycle 8 - A Little WorseCycle 8 - About the SameCycle 8 - A Little BetterCycle 8 - Moderately BetterCycle 8 - Very Much BetterCycle 9 - Very Much WorseCycle 9 - Moderately WorseCycle 9 - A Little WorseCycle 9 - About the SameCycle 9 - A Little BetterCycle 9 - Moderately BetterCycle 9 - Very Much BetterCycle 10 - Very Much WorseCycle 10 - Moderately WorseCycle 10 - A Little WorseCycle 10 - About the SameCycle 10 - A Little BetterCycle 10 - Moderately BetterCycle 10 - Very Much BetterCycle 11 - Very Much WorseCycle 11 - Moderately WorseCycle 11 - A Little WorseCycle 11 - About the SameCycle 11 - A Little BetterCycle 11 - Moderately BetterCycle 11 - Very Much BetterCycle 12 - Very Much WorseCycle 12 - Moderately WorseCycle 12 - A Little WorseCycle 12 - About the SameCycle 12 - A Little BetterCycle 12 - Moderately BetterCycle 12 - Very Much Better
Capecitabine1414244100799965250118155095331323481020612225524002196214203611601433332342616636166166003215510374813501348091339139174813501384
Pegylated Liposomal Doxorubicin (PLD)48126742201022635003925519114131358840411264792050214019105579581452041752131300131757904602550666081767800011067111100011781100

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Time to Disease Progression (TTP) Using Response Evaluation Criteria in Solid Tumors (RECIST)

TTP was defined as the time from onset of treatment with study drug until first evidence/diagnosis of progressive disease or - in the absence of any diagnosis of progressive disease - until the participant´s death. Diagnosis of progressive disease was done according to RECIST (Version 1.0) and/or investigator assessment based on RECIST. RECIST criteria used changes in the largest diameter of target/non-target lesions. Target (measurable) lesions were up to a maximum of 5 per organ & >20 mm by clinical imaging (>=10 mm with spiral CT scan). Non-target lesions were all other lesions. (NCT00266799)
Timeframe: From Day 1 (Cycle 1) until First Evidence/Diagnosis of Progressive Disease or Death

,
InterventionMonths (Median)
By Investigator Assessment (ITT)By RECIST Criteria (ITT)By Investigator Assessment (TTP N = 63, N = 59)By RECIST Criteria (TTP N = 63, N = 59)
Capecitabine6.057.105.886.05
Pegylated Liposomal Doxorubicin (PLD)6.026.585.856.02

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Time to Treatment Failure in the PLD and the Capecitabine Treatment Groups

Time to treatment failure was defined as the duration of time from the date of the first administration of the study drug to the date of discontinuation of the study drug for any reason. (NCT00266799)
Timeframe: From Day 1 (Cycle 1) until End of Treatment

InterventionMonths (Median)
Pegylated Liposomal Doxorubicin (PLD)4.60
Capecitabine3.68

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Adherence and Compliance to Oral Medication Using Electronic Monitoring

This was assessed by number of participants who did not miss any doses of Capecitabine during treatment using the Medication Event Monitoring System (MEMS). (NCT00274768)
Timeframe: 3-week cycles of treatment up to 16 cycles

InterventionParticipants (Count of Participants)
Capecitabine13

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Clinical Benefit as Assessed by Lack of Progression for at Least 24 Weeks

The overall clinical benefit rate as assessed by number of participants with lack of progression for at least 24 weeks. (NCT00274768)
Timeframe: 3-week cycles of treatment up to 16 cycles

InterventionParticipants (Count of Participants)
Capecitabine4

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Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by CT/MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00274768)
Timeframe: Participants were followed to progression, evaluated every 12 weeks

Interventionparticipants (Number)
Capecitabine21

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Time to Treatment Failure

Time to treatment failure in weeks (NCT00274768)
Timeframe: 3-week cycles of treatment up to 16 cycles

Interventionweeks (Median)
Capecitabine12

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Pharmacokinetics of Capecitabine and Metabolites as Assessed by Maximum Plasma Concentration

Pharmacokinetics of Capecitabine and metabolites [5-fluoro-5'-deoxycytidine (5'-DFCR), 5-fluoro-5'-dexoxyuridine (5'-DFUR), and 5-fluorouracil (FU)] assessed using maximum plasma concentration (Cmax) in ng/mL. (NCT00274768)
Timeframe: 0.25, 0.5, 1, 2, 3, 4, 5, 6 and 8 hours

Interventionng/mL (Mean)
Capecitabine5'-DFCR5'-DFUR5-FU
Capecitabine932463534597753

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Pharmacokinetics of Capecitabine and Metabolites as Assessed by Area Under the Curve (AUC)

Pharmacokinetics of Capecitabine and metabolites [5-fluoro-5'-deoxycytidine (5'-DFCR), 5-fluoro-5'-dexoxyuridine (5'-DFUR), and 5-FU] assessed using AUC in ng*h/mL. (NCT00274768)
Timeframe: 0.25, 0.5, 1, 2, 3, 4, 5, 6 and 8 hours

Interventionng*h/mL (Mean)
Capecitabine5'-DFCR5'-DFUR5-FU
Capecitabine72551134466531230

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6-month Overall Survival

Percentage of patients survived at 6 months for patients whose tumors were xenografted and treated in the mouse when treated with the most active agent identified in that model (NCT00276744)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Arm 153

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Number of Patients With Adverse Events

Per National Cancer Institute Common Toxicity Criteria Version 2.0, up to 2 years (NCT00278863)
Timeframe: Up to 2 years

Interventionparticipants (Number)
S-1 for 2 Week on/1 Week Off42
Capecitabine 2 Weeks on/1 Week Off44

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Response Rate

"Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR; Progressive disease (PD), >20% increase in the sum of the longest diameter of target lesions; Stable Disease (SD), Insufficient change to qualify for PR or PD~Response rate is defined as the proportion of patients who showed OR." (NCT00278863)
Timeframe: Up to 2 years

Interventionpercentage of participants (Number)
S-1 for 2 Week on/1 Week Off28.9
Capecitabine 2 Weeks on/1 Week Off26.1

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Response Rate (Percentage of Participants With Partial or Complete Response)

"Restaging scans occurred every 9 weeks from time of study drug initiation until disease progression.~Disease assessment was performed and recorded according to the Response Evaluation Criteria in Solid Tumors (RECIST v.1.0) Guidelines.~The definitions were:~Complete response (CR)- Disappearance of all target lesions Partial response (PD)- At least a 30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD Stable disease (SD)- Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started Progressive disease (PD) - At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions" (NCT00290615)
Timeframe: After all subjects were evaluated for restaging which occured every 9 weeks from drug initiation until disease progression, assesed up to 24 months.

Interventionpercentage of participants with response (Number)
Capecitabine, Oxaliplatin, Bevacizumab, Cetuximab43

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Progression-free Survival

"Disease assessment was performed and recorded according to the Response Evaluation Criteria in Solid Tumors (RECIST v.1.0) Guidelines.~Progressive disease is defined as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions.~This is the average number of months participants survived without showing progressive disease." (NCT00290615)
Timeframe: From time of treatment until documented progression or death from any cause, whichever came first, assesed up to 60 months.

Interventionmonths (Median)
Capecitabine, Oxaliplatin, Bevacizumab, Cetuximab10.3

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Overall Survival

Average months of survival of participants after receiving study drug. (NCT00290615)
Timeframe: From time of treatment until death from any cause, assesed up to 60 months.

Interventionmonths (Median)
Capecitabine, Oxaliplatin, Bevacizumab, Cetuximab18.8

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Safety and Tolerability

Number of participants with adverse events (NCT00290615)
Timeframe: After all participants went off study drug regimine.

Interventionparticipants with adverse event (Number)
Capecitabine, Oxaliplatin, Bevacizumab, Cetuximab30

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Number of Study Participants Experiencing Toxicity After Receiving Protocol Therapy

Number of study participants experiencing toxicity (serious adverse events or adverse events). Study participants assessed for this outcome measure must have received at least one dose of protocol therapy. Toxicity assessed according to Common Terminology Criteria for Adverse Events v3.0 (CTCAE). (NCT00290693)
Timeframe: Up to 1 year

Interventionparticipants (Number)
CapTere (Capecitabine + Docetaxel)38

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Overall Surival (OS)

Overall survival is measured from the time from date of initial protocol therapy to date of death. In the absence of confirmation of death, survival time will be censored to last date of follow-up. (NCT00290693)
Timeframe: Up to 1 year

Interventionmonths (Median)
CapTere (Capecitabine + Docetaxel)5.3

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Progression-free Survival (PFS)

Progression-free survival (PFS) is measured the time from the start of protocol therapy to disease progression or death from any cause. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT00290693)
Timeframe: Up to 1 year

Interventionmonths (Median)
CapTere (Capecitabine + Docetaxel)3.7

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Rate of Participants Achieving a 50% or More Reduction in CA 19-9 Levels

Rate of participants achieving a 50% or more reduction in CA 19-9 levels after receiving protocol therapy. Baseline CA-19-9 will be compared to the lowest recorded value on patients receiving therapy on protocol. A 50% drop in CA 19-9 in patients with baseline levels above 100 U/ml will be recorded as a CA 19-9 response if the > 50% drop can be confirmed with at least one more CA 19-9 level thereafter with > 50% drop compared to baseline. (NCT00290693)
Timeframe: Up to 1 year

Interventionpercentage of participants (Number)
CapTere (Capecitabine + Docetaxel)35.48

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Rate of Participants Achieving Complete Response or Partial Response to Therapy.

Rate of participants achieving complete response (CR) or partial response (PR) to Captere therapy according to RECIST criteria v 1.0. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions. (NCT00290693)
Timeframe: Up to 1 year

Interventionparticipants (Number)
Partial Response (PR) >= 2 cyclesStable Disease (SD), >= 2 cyclesComplete Response (CR), >= 2 cycles
CapTere (Capecitabine + Docetaxel)6250

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Impact of Capecitabine on 131I-huA33 Clearance (CL) as Measured by Initial and Therapy Dose Clearance (CL)

"Blood samples for pharmacokinetics (PK) were drawn in week 0 immediately pre-initial 131I-huA33 infusion; then 5 minutes, 60 minutes and 2 hours post-initial 131I-huA33 infusion, Day 1, Day 2 or Day 3, Day 4 or Day 5. In week 1, PK samples were collected immediately pre-therapy 131I-huA33 infusion, 5 minutes, 24 ± 2 hours and approximately 7 days post-therapy 13II-huA33 infusion, then weekly until 4 weeks post therapy.~Pharmacokinetic calculations were performed on serum 131I-huA33 data using a curve fitting Program (WinNonLin version 5.2; Pharsight Co., Mountain View, CA)." (NCT00291486)
Timeframe: 5 weeks

,,
Interventionml/hr (Mean)
Initial dose CLTherapy dose CL
Cohort 5; 1250 mg/m2/Day Capecitabine34.6535.53
Cohorts 1 and 2; 1500 mg/m2/Day Capecitabine34.8826.88
Cohorts 3 and 4; 1000 mg/m2/Day Capecitabine40.5439.41

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Mean Specific Absorbed Dose of 131I-huA33 for Normal Organs Calculated From the Initial Infusion

"Gamma camera imaging with anterior and posterior whole body scans using conjugate view methodology were performed on four occasions (1-4 hours, Day 1, Day 2 or 3, and Day 4 or 5) following completion of the intravenous initial infusion.~Dosimetric analysis was performed on the series of gamma camera whole-body planar images acquired in all patients following the first infusion.~Organ radioactivity content was estimated from the geometric mean of anterior and posterior regions of interest counts. The counts for each organ were corrected for background using regions of interest drawn adjacent to each organ where whole body thickness was comparable." (NCT00291486)
Timeframe: 1 week

InterventioncGy/MBq (Mean)
LiverSpleenKidneyLungRed Marrow
Cohorts 1-50.120.180.140.090.056

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Pharmacokinetics (PK) of 131I-huA33 as Measured by Area Under the Serum Concentration Curve Extrapolated to Infinite Time (AUC)

"Blood samples for pharmacokinetics (PK) were drawn in week 0 immediately pre-initial 131I-huA33 infusion; then 5 minutes, 60 minutes and 2 hours post-initial 131I-huA33 infusion, Day 1, Day 2 or Day 3, Day 4 or Day 5. In week 1, PK samples were collected immediately pre-therapy 131I-huA33 infusion, 5 minutes, 24 ± 2 hours and approximately 7 days post-therapy 131I-huA33 infusion, then weekly until 4 weeks post therapy.~Pharmacokinetic calculations were performed on serum 131I-huA33 data using a curve fitting Program (WinNonLin version 5.2; Pharsight Co., Mountain View, CA)." (NCT00291486)
Timeframe: 5 weeks

Interventionmcg.hr/mL (Mean)
AUC after initial 131I-huA33 infusionAUC after therapy 131I-huA33 infusion
Cohorts 1-5130.43592.46

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Pharmacokinetics (PK) of 131I-huA33 as Measured by Clearance (CL)

"Blood samples for pharmacokinetics (PK) were drawn in week 0 immediately pre-initial 131I-huA33 infusion; then 5 minutes, 60 minutes and 2 hours post-initial 131I-huA33 infusion, Day 1, Day 2 or Day 3, Day 4 or Day 5. In week 1, PK samples were collected immediately pre-therapy 131I-huA33 infusion, 5 minutes, 24 ± 2 hours and approximately 7 days post-therapy 13II-huA33 infusion, then weekly until 4 weeks post therapy.~Pharmacokinetic calculations were performed on serum 131I-huA33 data using a curve fitting Program (WinNonLin version 5.2; Pharsight Co., Mountain View, CA)." (NCT00291486)
Timeframe: 5 weeks

InterventionmL/hr (Mean)
CL after initial 131I-huA33 infusionCL after therapy 131I-huA33 infusion
Cohorts 1-536.7232.60

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Number of Patients With Dose-Limiting Toxicities (DLT)

"Adverse events were graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE v3.0). DLT was defined as any of the following related events:~Any grade 2 or greater allergic reaction related to huA33. Any grade ≥ 3 non-haematological toxicity related to 131I-huA33 or capecitabine.~These toxicities included palmar plantar erythema, but skin rash thought to be related to huA33 protein was not a DLT as previous studies have shown no relation of this toxicity to dose of huA33 or radioiodine dose.~Capecitabine cardiotoxicity grade ≥ 3 - including vasospasm, acute coronary syndrome and arrhythmia, necessitated the cessation of study drug in the affected patient but were not considered DLT as these are recognized as idiosyncratic in nature and not known to be related to capecitabine dose.~Any grade ≥ 4 neutropenia ≥ 7 days in duration or any thrombocytopenia with a platelet count < 10 x 10^9/L." (NCT00291486)
Timeframe: 7 weeks

InterventionParticipants (Count of Participants)
Cohort 10
Cohort 22
Cohort 30
Cohort 40
Cohort 50

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Pharmacokinetics (PK) of 131I-huA33 as Measured by Maximum Serum Concentration (Cmax)

"Blood samples for pharmacokinetics (PK) were drawn in week 0 immediately pre-initial 131I-huA33 infusion; then 5 minutes, 60 minutes and 2 hours post-initial 131I-huA33 infusion, Day 1, Day 2 or Day 3, Day 4 or Day 5. In week 1, PK samples were collected immediately pre-therapy 131I-huA33 infusion, 5 minutes, 24 ± 2 hours and approximately 7 days post-therapy 131I-huA33 infusion, then weekly until 4 weeks post therapy.~Pharmacokinetic calculations were performed on serum 131I-huA33 data using a curve fitting Program (WinNonLin version 5.2; Pharsight Co., Mountain View, CA)." (NCT00291486)
Timeframe: 5 weeks

Interventionmcg/mL (Mean)
Cmax after initial 131I-huA33 infusionCmax after therapy 131I-huA33 infusion
Cohorts 1-51.535.52

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Pharmacokinetics (PK) of 131I-huA33 as Measured by T½α and T½β (Half Lives of the Initial and Terminal Phases of Disposition, Respectively)

"Blood samples for pharmacokinetics (PK) were drawn in week 0 immediately pre-initial 131I-huA33 infusion; then 5 minutes, 60 minutes and 2 hours post-initial 131I-huA33 infusion, Day 1, Day 2 or Day 3, Day 4 or Day 5. In week 1, PK samples were collected immediately pre-therapy 131I-huA33 infusion, 5 minutes, 24 ± 2 hours and approximately 7 days post-therapy 131I-huA33 infusion, then weekly until 4 weeks post therapy.~Pharmacokinetic calculations were performed on serum 131I-huA33 data using a curve fitting Program (WinNonLin version 5.2; Pharsight Co., Mountain View, CA)." (NCT00291486)
Timeframe: 5 weeks

Interventionhours (Mean)
T½α after initial 131I-huA33 infusionT½α after therapy 131I-huA33 infusionT½β after initial 131I-huA33 infusionT½β after therapy 131I-huA33 infusion
Cohorts 1-515.7828.63100.24152.60

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Pharmacokinetics (PK) of 131I-huA33 as Measured by the Volume of the Central Compartment (V1)

"Blood samples for pharmacokinetics (PK) were drawn in week 0 immediately pre-initial 131I-huA33 infusion; then 5 minutes, 60 minutes and 2 hours post-initial 131I-huA33 infusion, Day 1, Day 2 or Day 3, Day 4 or Day 5. In week 1, PK samples were collected immediately pre-therapy 131I-huA33 infusion, 5 minutes, 24 ± 2 hours and approximately 7 days post-therapy 131I-huA33 infusion, then weekly until 4 weeks post therapy.~Pharmacokinetic calculations were performed on serum 131I-huA33 data using a curve fitting Program (WinNonLin version 5.2; Pharsight Co., Mountain View, CA)." (NCT00291486)
Timeframe: 5 weeks

InterventionmL (Mean)
V1 after initial 131I-huA33 infusionV1 after therapy 131I-huA33 infusion
Cohorts 1-53204.263363.69

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Number of Patients With Human Anti-human Antibodies (HAHA) to 131I-huA33

Serum samples for human anti-human antibody (HAHA) assessment were collected prior to each 131I-huA33 infusion, at weekly intervals during weeks 0-7, then alternate weeks until the end-of-study visit. Measurement of immune responses to huA33 in patients serum was performed using a BIAcore 2000 biosensor (Biacore AB, Uppsala, Sweden). (NCT00291486)
Timeframe: 13 weeks

InterventionParticipants (Count of Participants)
Pre-treatment72460703Pre-treatment72460704Pre-treatment72460705Pre-treatment72460706Pre-treatment72460702Week 172460703Week 172460704Week 172460705Week 172460706Week 172460702Week 272460703Week 272460704Week 272460705Week 272460706Week 272460702Week 372460703Week 372460704Week 372460705Week 372460706Week 372460702Week 472460703Week 472460704Week 472460702Week 472460705Week 472460706Week 572460703Week 572460704Week 572460705Week 572460702Week 572460706Week 672460703Week 672460704Week 672460706Week 672460702Week 672460705Week 872460702Week 872460703Week 872460704Week 872460705Week 872460706Week 10-1172460703Week 10-1172460704Week 10-1172460705Week 10-1172460706Week 10-1172460702Week 12-1372460703Week 12-1372460704Week 12-1372460705Week 12-1372460706Week 12-1372460702
Negative HAHAPositive HAHA
Cohort 20
Cohort 40
Cohort 50
Cohort 26
Cohort 33
Cohort 43
Cohort 54
Cohort 41
Cohort 32
Cohort 42
Cohort 30
Cohort 52
Cohort 51
Cohort 13
Cohort 10
Cohort 24
Cohort 23
Cohort 31
Cohort 53
Cohort 12

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Biodistribution of 131I-huA33 Measured by Whole Body Clearance and Normal Organ Clearance Reported as Mean Biological Half-life (T1/2 Biological) After Initial 131I-huA33 Infusion

T1/2 biological is the clearance of the isotope from the whole body. Following the initial 131I-huA33 infusion, gamma camera scans were acquired over a 1 week period (1-4 hours, Day 1, Day 2 or 3, and Day 4 or 5). Whole body clearance, or biological half time, T1/2 biological, was calculated from the whole body anterior and posterior planar images. A region of interest (ROI) was calculated to encompass the whole body, and for each ROI at each time point, the mean counts per pixel per minute was normalised to imaging time point Day 1. (NCT00291486)
Timeframe: 1 week

Interventionhours (Mean)
Whole Body Clearance (T1/2 biologic)Normal Organ Clearance in the Liver (T1/2 biological - liver)Normal Organ Clearance in the kidney (T1/2 biological - kidney)
Cohorts 1-5219.5662.29104.89

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Mean Total Tumor Dose of 131I-huA33

"Gamma camera imaging were performed on four occasions (1-4 hours, Day 1, Day 2 or 3, and Day 4 or 5) following completion of the initial infusion and 7+2 days post-therapy infusion in week 2, and again in week 3 or 4 and week 5 following the therapy infusion.~Dosimetry analysis was performed on the series of gamma camera whole-body planar images.~Tumor radioactivity content after the initial infusion was estimated from the geometric mean of anterior and posterior regions of interest counts. The counts for each organ were corrected for background using regions of interest drawn adjacent to each tumor. Resultant counts were converted to activity using a camera sensitivity factor calculated from a gamma camera standard of known activity which was scanned at the same time." (NCT00291486)
Timeframe: 5 weeks

InterventionGy (Mean)
All Patients13.83
Cohorts 2 and 3; 30 mCi 131I-huA3313.15
Cohorts 4 and 5: 40 mCi 131I-huA3314.89

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Two-year Overall Survival Rate

Overall survival (OS) is defined as the time from randomization to death from any cause, or censored at last known date of survival. (NCT00305877)
Timeframe: Assessed every 3 months for 2 years

InterventionProportion of patients (Number)
Arm A (Cetuximab, Gemcitabine, Capecitabine, Radiation)0.38
Arm B (Bevacizumab, Gemcitabine, Capecitabine, Radiation)0.37

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Two-year Disease-free Survival (DFS)

Disease-free survival (DFS) is defined as the time from randomization to the first treatment failure (recurrence or death before recurrence). (NCT00305877)
Timeframe: Assessed every 3 months for 2 years, and every 6 months after completion of treatment for 2 years, then annually for 3 years

InterventionProportion of patients (Number)
Arm A (Cetuximab, Gemcitabine, Capecitabine, Radiation)0.17
Arm B (Bevacizumab, Gemcitabine, Capecitabine, Radiation)0.23

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Proportion of Patients With Specific Protocol Defined Adverse Event at Conclusion of All Therapy

"Specific toxicities to be monitored pursuant to the primary endpoint include:~Any grade 5 toxicities~Grade 4 dyspnea, neutropenic fever, allergic reaction, rash, wound dehiscence, wound infection, hypertension~Grade 3 or higher arterial thromboembolic phenomena, bleeding, phlebitis/deep vein thrombosis (DVT)/pulmonary embolism (PE), hemorrhage, ileus, bowel perforation, diarrhea, and mucositis~ECOG performance status decline by 2 or greater for >24 hours~Weight loss >10%" (NCT00305877)
Timeframe: Every 2 weeks while on treatment and for 30 days after the end of treatment

InterventionProportion of patients (Number)
Arm A (Cetuximab, Gemcitabine, Capecitabine, Radiation)0.30
Arm B (Bevacizumab, Gemcitabine, Capecitabine, Radiation)0.25

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Common Toxicities

The NCI Common Terminology Criteria for Adverse Events version 3.0 was used for adverse event reporting and toxicity grading. (NCT00320749)
Timeframe: Weekly up to 24 weeks

Interventionpercent of patients (Number)
leukopenianeutropeniafatigue
Capecitabine, Docetaxel, Gemcitabine292925

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Maximum Tolerated Dose (MTD)

MTD will be the dose at which 1 or fewer patients (≤ 1/6) experiences a DLT during the first or second cycle with the next higher dose having at least 2/3 or 2/6 patients experiencing Dose Limiting Toxicities (DLT). (NCT00320749)
Timeframe: Weekly up to 24 weeks

Interventionmg/m^2 (Number)
docetaxelgemcitabinecapecitabine
Capecitabine, Docetaxel, Gemcitabine36750625

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Therapeutic Response

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00320749)
Timeframe: every 8 weeks, up to 24 weeks

Interventionpercent of patients (Number)
Partial ResponseComplete ResponseStable Disease
Capecitabine, Docetaxel, Gemcitabine11072

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Overall Survival

Follow-up for survival to be done at 3 month intervals for 2 years, then 6 month intervals for up to 5 years from study registration (NCT00321100)
Timeframe: From dose of first study drug to last timepoint known to be alive (median follow-up for all patients was 25.9 months)

Interventionmonths (Median)
Cetuximab, Oxaliplatin, Capecitabine, Bevacizumab18
Cetuximab, Oxaliplatin, Capecitabine42.5

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Objective Response Rate (ORR)

"Objective response rate calculated by the proportion of overall response: CR+PR. Patients were categorized by one of the following (1-4 per RECISTv1.0 criteria on CT, MRI, x-ray; 4-9 considered failure to respond/disease progression):~complete response (CR): Disappearance of all lesions~partial response (PR): >=30% decrease in the sum of the longest diameter of target lesions (SoL); from baseline SoL~stable disease (SD): Neither PR, PD, or CR~progressive disease (PD): >=20% increase in the SoL; from smallest SoL. Or appearance of new lesion~early death from malignant disease~early death from toxicity~early death from other cause~9) unknown (not assessable, insufficient data)" (NCT00321100)
Timeframe: every 6-9 weeks; from date of first study drug dose until off treatment date (median of 8 cycles; range <1-19)

,
InterventionParticipants (Count of Participants)
Overall responseComplete responsePartial responseStable disease
Cetuximab, Oxaliplatin, Capecitabine8173
Cetuximab, Oxaliplatin, Capecitabine, Bevacizumab4137

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Time to Progression (TTP)

"Per Response Evaluation Criteria In Solid Tumors (RECISTv1.0) assessed by CT, MRI, x-ray scan:~Complete response (CR): Disappearance of all lesions Partial response (PR): >=30% decrease in the sum of the longest diameter of target lesions (SoL); from baseline SoL Stable disease (SD): Neither PR, PD, or CR Progressive disease (PD): >=20% increase in the SoL; from smallest SoL. Or appearance of new lesion" (NCT00321100)
Timeframe: every 6-9 weeks; from dose of first study drug to event

Interventionmonths (Median)
Cetuximab, Oxaliplatin, Capecitabine, Bevacizumab8.7
Cetuximab, Oxaliplatin, Capecitabine14.4

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Resection Rate for T4 Rectal Cancers

Resection rate is defined as number of patients with T4 rectal cancer who underwent curative surgical resection among all eligible and treated patients with T4 rectal cancers (NCT00321685)
Timeframe: Assessed at surgery time

Interventionpercentage of participants (Number)
Arm I75

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Resection Rate for T3 Rectal Cancers

Resection rate is defined as number of patients with T3 rectal cancer who underwent curative surgical resection among all eligible and treated patients with T3 rectal cancers (NCT00321685)
Timeframe: Assessed at surgery time

Interventionpercentage of participants (Number)
Arm I92

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Pathologic Complete Response Rate

Pathologic complete response to preoperative therapy was determined at the time of surgical resection. Pathologic complete response (pCR) is defined as no evidence of invasive cells on pathologic examination of the primary rectal cancer (or tissue from the area where the tumor had been if there is a complete clinical response). Pathologic complete response rate is calculated as number of patients achieving pathologic complete response divided by all eligible and treated patients (NCT00321685)
Timeframe: Assessed at surgery time

Interventionpercentage of participants (Number)
Arm I17

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5-year Overall Survival Rate

Overall survival is defined as time from registration to death from any cause. 5-year overall survival rate is estimated using Kaplan-Meier method. (NCT00321685)
Timeframe: survival follow-up began after post-operative chemotherapy, assessed every 3 months for patients 3-5 years from registration, every 6 months for patients 5-10 years from registration and every 12 months for patients 10 years from registration

Interventionpercentage of participants (Number)
Arm I80

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5-year Recurrence-free Survival Rate

Recurrence free survival is defined as time from surgery to disease recurrence or death without recurrence (whichever occurred first) among resected patients. 5-year recurrence-free survival rate is estimated using Kaplan-Meier method, with 90% confidence interval calculated using Greenwood's formula. (NCT00321685)
Timeframe: recurrence follow-up began after post-operative chemotherapy, assessed every 3 months for patients 3-5 years from registration, every 6 months for patients 5-10 years from registration and every 12 months for patients 10 years from registration

Interventionpercentage of participants (Number)
Arm I81

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Pathologic Complete Response

Pathologic complete response rates (pCR) of primary gastric adenocarcinoma when treated with oxaliplatin and capecitabine followed by capecitabine and radiation pre-operatively. On review of the resected gastric specimen and accompanying lymph nodes, pCR is no cancer recognized by the pathologist. Margins are free of tumor. (NCT00335959)
Timeframe: 17-19 weeks

Interventionparticipants (Number)
Unconfirmed Complete ResponseUnconfirmed Partial ResponseStable/No ResponseIncreasing DiseaseAssessment Inadequate
Chemotherapy, Chemoradiation, Surgery12211

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Progression Free Survival (PFS)

PFS was defined as the time (in days) from the date of randomization to the date of the first sign of disease progression based on Response Evaluation Criteria In Solid Tumors (RECIST) version 1.1 (v 1.1) or date of death, regardless of cause. Disease progression was measured by computed tomography (CT) and magnetic resonance imaging (MRI) performed on lesions targeted at baseline for tumor assessment. Disease progression (as assessed by independent review of the imaging scans) per RECIST v 1.1 was defined as at least a 20% increase in the sum of the diameters of the target lesions (taking as reference the smallest sum on study, including the baseline sum if that is the smallest), and an absolute increase of at least 5 millimeter (mm). Note that the appearance of one or more new lesions was also considered as disease progression. (NCT00337103)
Timeframe: From date of randomization to the date of disease progression or death (whichever occurred first), assessed up to data cutoff date of 12 Mar 2012 or up to approximately 6 years

InterventionDays (Median)
Eribulin Mesylate 1.4 mg/m^2126
Capecitabine 2.5 g/m^2/Day129

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Overall Survival (OS)

OS was measured from the date of randomization until the date of death from any cause, or the last date the participant was known to be alive. Participants who were lost to follow-up or who were alive at the date of data cutoff were censored. The censoring rules for OS were as follows: 1) if the participant was still alive at data cutoff, the date of data cutoff was considered the end date, and 2) if the participant was lost to follow-up before data cutoff, the date they were last known to be alive was considered the end date. Participants who survived past the end of the study were counted as in the full study period. If death occurred after data cutoff, the end date was to be censored at the time of data cutoff. (NCT00337103)
Timeframe: From date of randomization until date of death from any cause, assessed up to data cutoff date of 12 Mar 2012, or up to approximately 6 years

Interventiondays (Median)
Eribulin Mesylate 1.4 mg/m^2484
Capecitabine 2.5 g/m^2/Day440

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Objective Response Rate (ORR): Independent Review

ORR was defined as the percentage of participants with a best overall response of complete response (CR) or partial response (PR) based on Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 (v 1.1). CR is defined as disappearance of all target legions and non-target lesions. All pathological lymph nodes (whether target and non-target), must have reduction in their short axis to less than 10 mm. PR is defined as at least 30% decrease in the sum of the long diameter LD (hereafter referred to as sum of LD) of all target lesions, as compared with Baseline summed LD. (NCT00337103)
Timeframe: From date of randomization until date of first documentation of CR or PR, assessed up to data cutoff date of 12 Mar 2012 or up to approximately 6 years

Interventionpercentage of participants (Number)
Eribulin Mesylate 1.4 mg/m^211.0
Capecitabine 2.5 g/m^2/Day11.5

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Number of Participants With Treatment-emergent Markedly Abnormal Laboratory Parameter Values

(NCT00337103)
Timeframe: First dose of study drug (Baseline) up to 30 days after last dose of study drug (up to approximately 6 years 3 months)

InterventionParticipants (Count of Participants)
Eribulin Mesylate 1.4 mg/m^2362
Capecitabine 2.5 g/m^2/Day224

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Number of Participants With Consumption of Analgesics During the Study

Participants took analgesics as concomitant pain medications which are defined as pain medications that (1) started before the first dose of study drug and were continuing at the time of the first dose of study drug, or (2) started on/after the day of the first dose of study drug up to 30 days after the last dose of study drug medication (NCT00337103)
Timeframe: First dose of study drug (Baseline) up to 30 days after last dose of study drug (up to approximately 6 years 3 months)

InterventionParticipants (Count of Participants)
Eribulin Mesylate 1.4 mg/m^2222
Capecitabine 2.5 g/m^2/Day196

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Number of Participants Who Took at Least One Concomitant Medication

Concomitant medications included medications that either (1) started before the first dose of study drug and were continuing at the time of the first dose of study drug, or (2) started on or after the first dose of study drug up to 30 days after the last dose of study drug. (NCT00337103)
Timeframe: First dose of study drug (Baseline) up to 30 days after last dose of study drug (up to approximately 6 years 3 months)

InterventionParticipants (Count of Participants)
Eribulin Mesylate 1.4 mg/m^2496
Capecitabine 2.5 g/m^2/Day483

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Duration of Response (DOR): Independent Review

DOR was defined as the time from first documented CR or PR until disease progression or death from any cause for those participants with a confirmed PR or CR measured by RECIST v1.1. CR defined as disappearance of all target and non-target lesions. All pathological lymph nodes(whether target and non-target), must have reduction in their short axis to less than 10 mm. PR defined as at least 30% decrease in the sum of the long diameter LD (hereafter referred to as sum of LD) of all target lesions, as compared with Baseline summed LD. (NCT00337103)
Timeframe: From first documented CR or PR until date of recurrent or progressive disease or death, assessed up to data cutoff of date of 12 Mar 2012 or up to approximately 6 years

Interventiondays (Median)
Eribulin Mesylate 1.4 mg/m^2198
Capecitabine 2.5 g/m^2/Day330

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Change From Baseline in Global Health Status/Quality of Life (QoL) Measured by European Organization for the Treatment of Cancer Quality of Life Core Questionnaire Scores Based on Core 30 Items (EORTC-QLQ-C30) at Week 6

EORTC-QLQ-C30:cancer-specific instrument with 30 questions to assess the participant QoL. First 28 questions used to evaluate 5 functional scales (physical, role, cognitive, emotional, social), 3 symptom scales (fatigue, nausea and vomiting, pain) and other single items(dyspnoea, appetite loss, insomnia, constipation, diarrhea, financial difficulties). Each of these 28 questions assessed on 4-point scale(1=not at all, 2=a little, 3=quite a bit, 4=very much); functional scales: higher score=better level of functioning; symptom scale: higher score=more severe symptoms; for single items: higher score= more severe problem. Last 2 questions used to evaluate global health status (GHS)/QoL. Each question was assessed on 7-point scale (1=very poor to 7=excellent). Scores averaged, transformed to 0-100 scale; higher score=better quality of life/better level of functioning. (NCT00337103)
Timeframe: Baseline and Week 6

Interventionunits on a scale (Mean)
Eribulin Mesylate 1.4 mg/m^20.1
Capecitabine 2.5 g/m^2/Day1.7

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Change From Baseline in Pain Intensity by Visual Analog Scale (VAS) Until 30 Days After the Last Dose of Study Drug

"Pain intensity was measured by marking a single vertical line that crosses a 1-100 mm unmarked VAS scale. The left-end of the visual analog scale was labelled least possible pain and the right-end of the visual analog scale was labelled worst possible pain. The pain rating ranged from 0 to 100, with a higher score indicating more pain. A negative change score indicated improvement." (NCT00337103)
Timeframe: First dose of study drug (Baseline) up to 30 days after last dose of study drug (up to approximately 6 years 3 months)

Interventionunits on a scale (Mean)
Eribulin Mesylate 1.4 mg/m^2-3.7
Capecitabine 2.5 g/m^2/Day0.4

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Change From Baseline in European Organization for the Treatment of Cancer Quality of Life Core Questionnaire Scores Based on Breast Cancer Specific 23 Items (EORTC-QLQ- BR 23) at Week 6

EORTC-QLQ-BR23:disease-specific module for breast cancer developed as a supplement for the EORTC-QLQ-C30 to assess quality of life of participants with breast cancer. The scores from 23 items of QLQ-BR23 included functional scales (body image, sexual functioning, sexual enjoyment, future perspective), symptom scales (systemic therapy side effects, breast symptoms, arm symptoms, upset by hair loss). Each item was rated on a scale of 1 to 4 to record level of intensity (1= not at all, 2= a little, 3= quite a bit, 4= very much) within each scales. Scores averaged and transformed to 0-100 scale. High score indicated high/better level of functioning/healthy functioning. Negative change from Baseline indicated deterioration in QOL and positive change from Baseline indicated an improvement in QOL. (NCT00337103)
Timeframe: Baseline and Week 6

,
Interventionunits on a scale (Mean)
Body ImageSexual functioningSexual enjoymentFuture perspectiveSystemic therapy side effectsBreast SymptomsArm SymptomsUpset by hair loss
Capecitabine 2.5 g/m^2/Day4.8-0.13.110.0-1.2-3.6-3.4-10.1
Eribulin Mesylate 1.4 mg/m^20.71.20.87.74.5-3.4-4.2-4.4

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Plasma Concentrations of Eribulin Mesylate

(NCT00337103)
Timeframe: Cycle 1 Day 1: 5-10 minutes(min), 15-30 min, 30-60 min, 60-90 min, 2-4 hours(hrs), 4-8 hrs, 10-24 hrs, 48-72 hrs, 72-96 hrs, 96-120 hrs after the start of infusion of Eribulin mesylate (Duration of each cycle is 21 days)

Interventionnanogram per milliliter (ng/mL) (Mean)
5-10 minutes15-30 minutes30-60 minutes60-90 minutes2-4 hours4-8 hours10-24 hours48-72 hours72-96 hours96-120 hours
Eribulin Mesylate 1.4 mg/m^2415.8152.695.552.720.710.05.83.72.47.6

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Overall Survival Rate

One-, two-, and three- year's survival rates were defined as the percentage of participants who were alive at one, two, and three years respectively, and estimated using the Kaplan-Meier method and Greenwood Formula. (NCT00337103)
Timeframe: From the date of randomization to Year 1, 2 and 3

,
Interventionpercentage of participants (Number)
At 1-yearAt 2-yearsAt 3-years
Capecitabine 2.5 g/m^2/Day0.5800.2980.145
Eribulin Mesylate 1.4 mg/m^20.6440.3280.178

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Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)

TEAEs included both SAEs as well as non-SAEs. (NCT00337103)
Timeframe: First dose of study drug (Baseline) up to 30 days after last dose of study drug (up to approximately 6 years 3 months)

,
InterventionParticipants (Count of Participants)
TEAEsSAEs
Capecitabine 2.5 g/m^2/Day494115
Eribulin Mesylate 1.4 mg/m^251295

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Duration of Eribulin Mesylate Exposure

Data have been reported per primary analysis completion stage and final analysis completion stage. After primary analysis completion (at cutoff date of 12 March 2012), only 10 participants were still receiving study treatment. (NCT00337103)
Timeframe: Up to approximately 6 years for primary analysis completion stage, Up to approximately 6 years 2 months for final analysis completion stage

,
Interventiondays (Median)
At primary analysis completion stageAt final analysis completion stage
Capecitabine 2.5 g/m^2/Day119.01506.0
Eribulin Mesylate 1.4 mg/m^2125.01743.0

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Median Overall Survival

Median survival is defined as the time of initiation of the first dose of chemotherapy to the date of death. (NCT00338039)
Timeframe: Baseline to disease progression or death, up to 4 years

InterventionMonths (Median)
Chemotherapy + Chemoradation19.2

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Overall Survival Rate

1-year, 2-year, and 4-year actuarial overall survival (OS) rates defined as number of participants out of total participants alive at 1, 2 or 4 years post baseline treatment. (NCT00338039)
Timeframe: 1 to 4 years

Interventionpercentage of participants (Number)
1-year OS Rate2-year OS Rate4-year OS Rate
Chemotherapy + Chemoradation66.025.0211.3

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Number of Participants With Objective Response

Objective Response = Complete Response + Partial Response. Response evaluated using modification of new international criteria proposed by RECIST [changes in only largest diameter (unidimensional measurement) of tumor lesions used in the RECIST criteria]. Complete Response (CR): Disappearance of all target lesions; Partial Response (PR): At least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. (NCT00338988)
Timeframe: Baseline with restaging every 3 cycles (cycle=21 days)

Interventionparticipants (Number)
Capecitabine + Oxaliplatin1

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Complete Clinical Response Rate (CCR)

Complete Clinical Response (CCR) was defined as complete disappearance of all measurable malignant disease, and no new malignant lesion, disease-related symptoms, or evidence of evaluable disease. (NCT00347438)
Timeframe: After the first three cycles of therapy, an average of 9 weeks

Interventionpercentage of participants (Number)
Capecitabine0

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Complete Pathologic Response Rate (cPR)

Complete Pathologic Response rate (cPR) was defined as the absence of invasive breast cancer in the breast (mastectomy or lumpectomy) specimen at the time of definitive surgery. (NCT00347438)
Timeframe: After the first three cycles of therapy, an average of 9 weeks

Interventionpercentage of participants (Number)
Capecitabine0

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Partial Clinical Response Rate (PR)

Partial Clinical Response (PR) was defined as reduction by at least 50% of the sum of the products of the longest perpendicular diameters of all measurable lesions. (NCT00347438)
Timeframe: After the first three cycles of therapy, an average of 9 weeks

Interventionparticipants (Number)
Capecitabine5

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Overall Clinical Response Rate (OCR)

Overall clinical response rate (OCR) was defined as a proportion of patients with a best response of Complete Clinical Response (CCR) or Partial Clinical Response (PCR). CCR was defined as complete disappearance of all measurable malignant disease, and no new malignant lesion, disease-related symptoms, or evidence of evaluable disease. PCR was defined as reduction by at least 50% of the sum of the products of the longest perpendicular diameters of all measurable lesions. (NCT00347438)
Timeframe: After the first three cycles of therapy, an average of 9 weeks

Interventionpercentage of participants (Number)
Capecitabine31.3

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Maximum Plasma Concentration (Cmax) of Capecitabine and Its Metabolites (5'-DFUR, 5'-DFCR, 5 FU, and FBAL)

Cmax is defined as maximum observed analyte concentration of capecitabine and its metabolites (5'-DFUR, 5'-DFCR, 5 FU, and FBAL) (NCT00353262)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, and 12 hours post the dose

Interventionng/mL (Geometric Mean)
5'-DFUR, Cycle 1, Day 15'-DFUR , Cycle 2, Day 15'-DFUR , Cycle 3, Day 1Capecitabine, Cycle 1, Day 1Capecitabine, Cycle 2, Day 1Capecitabine, Cycle 3, Day 15' DFCR, Cycle 1, Day 15' DFCR, Cycle 2, Day 15' DFCR , Cycle 3, Day 15-FU, Cycle 1 , Day 15-FU, Cycle 2, Day 15-FU, Cycle 3, Day 1FBAL, Cycle 1, Day 1FBAL, Cycle 2, Day 1FBAL, Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab884765455693493040654167390234073747292216168397036273292

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Clearance of Total And Free Platinum

CL is a calculation of the rate at which a drug is removed from the body via renal, hepatic and other clearance pathways, expressed as volume (milliliters) per unit of time (hour). (NCT00353262)
Timeframe: Pre-dose, and 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24, 48 and 72 hours from the beginning of the two hour oxaliplatin infusion on Days 2 to 5 of Cycle 1, and Days 1 to 4 for Cycle 2 and 3

InterventionmL/Hr (Geometric Mean)
Total Platinum: Cycle 1, Day 2Total Platinum: Cycle 2, Day 1Total Platinum: Cycle 3, Day 1Free Platinum: Cycle 1, Day 2Free Platinum: Cycle 2, Day 1Free Platinum: Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab160313311198221832117621823

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Marked Laboratory Abnormalities

Number of participants with marked laboratory abnormalities (hematology, coagulation, liver function, renal function, protein, electrolytes, miscellaneous). (NCT00353262)
Timeframe: Up to 28 days after last chemotherapy administration

InterventionParticipants (Number)
Hematocrit - highHematocrit - lowHemoglobin - lowPlatelets - highPlatelets - lowRBC - lowWBC - highWBC - lowNeutrophils - highNeutrophils - lowPT (INR) - highASAT (SGOT) - highLDH - highALAT (SGPT) - highAlk. Phos. - highDir. Bilirubin - highTotal Bilirubin - highCreatinine - highAlbumin - lowPotassium - lowSodium - lowCalcium - lowGlucose Fasting - high
Capecitabine+ Oxaliplatin+ Bevacizumab256191217132627632042214

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Elimination Half-life Period (t1/2 Beta) of Capecitabine and Its Metabolites (5'-DFUR , 5'-DFCR, 5 FU, and FBAL)

t1/2 Beta is the time measured for the plasma concentration to decrease by 1 half to its original concentration of capecitabine and its metabolites (5'-DFUR , 5'-DFCR, 5 FU, and FBAL) (NCT00353262)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, and 12 hours post the dose

Interventionhour (Geometric Mean)
5' DFUR; Cycle 1, Day 15' DFUR, Cycle 2 , Day 15' DFUR, Cycle 3, Day 1Capecitabine, Cycle 1, Day 1Capecitabine, Cycle 2, Day 1Capecitabine, Cycle 3, Day 15'-DFCR, Cycle 1, Day 15'-DFCR, Cycle 2 , Day 15'-DFCR, Cycle 3, Day 15-FU, Cycle 1, Day 15-FU, Cycle 2, Day 15-FU, Cycle 3, Day 1FBAL, Cycle 1, Day 1FBAL, Cycle 2, Day 1FBAL, Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab0.650.640.750.370.510.560.710.750.790.610.670.712.772.682.64

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Cmax of Total And Free Platinum

Cmax is defined as maximum observed analyte concentration of Total And Free Platinum. (NCT00353262)
Timeframe: Pre-dose, and 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24, 48 and 72 hours from the beginning of the two hour oxaliplatin infusion on Days 2 to 5 of Cycle 1, and Days 1 to 4 for Cycle 2 and 3.

Interventionng/mL (Geometric Mean)
Total Platinum: Cycle 1, Day 2Total Platinum: Cycle 2, Day 1Total Platinum: Cycle 3, Day 1Free Platinum: Cycle 1, Day 2Free Platinum: Cycle 2, Day 1Free Platinum: Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab365237413706181818401813

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AUC (0-infinity) of Capecitabine and Its Metabolites (5'-DFCR, 5-FU, and FBAL)

AUC0-infinity represents the area under the concentration-time curve of the analytes (5'-DFCR, 5-FU, and FBAL) in plasma over the time interval from 0 extrapolated to infinity. After oral administration, capecitabine is first metabolized in the liver to 5'-deoxy-5-fluorocytidine (5'-DFCR), which is then converted to 5'-DFUR, and then catalytically activated to 5-FU. (NCT00353262)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, and 12 hours post the dose

Interventionng/mL*hr (Geometric Mean)
Capcetabine , Cycle 1, Day 1Capcetabine , Cycle 2, Day 1Capcetabine , Cycle 3, Day 15'-DFCR , Cycle 1, Day 15'-DFCR , Cycle 2, Day 15'-DFCR, Cylce 3, Day 15-FU , Cycle 1, Day 15-FU , Cycle 2, Day 15-FU , Cycle 3, Day 1FBAL , Cycle 1, Day 1FBAL , Cycle 2, Day 1FBAL , Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab521752996130763064097989437355343179041741317356

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AUC0-inf for Free Platinum

AUC0-infinity represents the area under the concentration-time curve of the analyte (free platinum) in plasma over the time interval from 0 extrapolated to infinity. AUC0-inf for free platinum was calculated for each participant from the concentration-data obtained on Days 2 to 5 of Cycle 1, and Days 1 to 4 for Cycle 2 and 3. Free platinum is not bound to plasma proteins and is considered to be the most clinically significant measure of pharmacological and toxicological activity. (NCT00353262)
Timeframe: Predose , 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24, 48 and 72 hours from the beginning of the 2 hour oxaliplatin infusion on Days 2 to 5 of Cycle 1, and Days 1 to 4 for Cycle 2 and 3.

Interventionng/mL * hr (Geometric Mean)
Cycle 1, Day 2Cycle 2 , Day 1Cycle 3, Day 1.
Capecitabine+ Oxaliplatin+ Bevacizumab100691053710225

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AUC0-infinity for Total Platinum

AUC0-infinity represents the area under the concentration-time curve of the analyte (total platinum) in plasma over the time interval from 0 extrapolated to infinity. (NCT00353262)
Timeframe: Pre-dose, and 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24, 48 and 72 hours from the beginning of the two hour oxaliplatin infusion on Days 2 to 5 of Cycle 1, and Days 1 to 4 for Cycle 2 and 3

Interventionng/mL* hr (Geometric Mean)
Cycle 1, Day 2Cycle 2, Day 1Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab139329167610186268

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AUC0-last of Capecitabine and Its Metabolites (5'-DFUR, 5'-DFCR, 5 FU, and FBAL)

Area under the plasma concentration-time curve from time zero to the time of the last measurable plasma concentration time point of capecitabine and its metabolites (5'-DFUR, 5'-DFCR, 5 FU, and FBAL). (NCT00353262)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, and 12 hours post the dose

Interventionng/mL*hr (Geometric Mean)
5' DFUR , Cycle 1, Day 15' DFUR, Cycle 2 , Day 15' DFUR, Cycle 3, Day 1Capecitabine, Cycle 1, Day 1Capecitabine, Cycle 2, Day 1Capecitabine, Cycle 3, Day 15'-DFCR, Cycle 1, Day 15'-DFCR, Cycle 2 , Day 15'-DFCR, Cycle 3, Day 15-FU, Cycle 1, Day 15-FU, Cycle 2, Day 15-FU, Cycle 3, Day 1FBAL, Cycle 1, Day 1FBAL, Cycle 2, Day 1FBAL, Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab135031205711618520152736093615063787909433350336167731599214947

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AUC0-last of Total And Free Platinum

Area under the plasma concentration-time curve from time zero to the time of the last measurable plasma concentration time point of Total And Free Platinum. (NCT00353262)
Timeframe: pre-dose, and 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24, 48 and 72 hours from the beginning of the two hour oxaliplatin infusion on Days 2 to 5 of Cycle 1, and Days 1 to 4 for Cycle 2 and 3.

Interventionng/mL* hr (Geometric Mean)
Total Platinum: Cycle 1, Day 2Total Platinum: Cycle 2, Day 1Total Platinum: Cycle 3, Day 1Free Platinum: Cycle 1, Day 2Free Platinum: Cycle 2, Day 1Free Platinum: Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab854069708397011939998189604

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Volume of Distribution at Steady State (VSS) of Total And Free Platinum

VSS is defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired blood concentration of a drug. Steady state volume of distribution (Vss) is the apparent volume of distribution at steady-state. (NCT00353262)
Timeframe: Pre-dose, and 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24, 48 and 72 hours

InterventionmL (Geometric Mean)
Total Platinum: Cycle 1, Day 2Total Platinum: Cycle 2, Day 1Total Platinum: Cycle 3, Day 1Free Platinum: Cycle 1, Day 2Free Platinum: Cycle 2, Day 1Free Platinum: Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab109007105097112141387158389193401040

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Number Of Participants With Adverse Events (AEs)

An adverse event is defined as any untoward medical occurrence in a participant or clinical investigation participant administered a pharmaceutical product. This includes any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. Pre-existing conditions which worsened during the study were also to be reported as AEs. (NCT00353262)
Timeframe: Approximately 3 Years (up to 28 days after the last intake of study medication)

InterventionParticipants (Number)
Any AEAny SAE
Capecitabine+ Oxaliplatin+ Bevacizumab3616

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Area Under The Plasma Concentration-Time Curve From Zero To Infinity (AUC0-Inf) of 5'-Deoxy-5-fluorouridine 5'-(DFUR)

AUC0-infinity represents the area under the concentration-time curve of the analyte (5'-DFUR) in plasma over the time interval from 0 extrapolated to infinity. The analyte 5'-DFUR, the direct precursor of 5-fluorouracil (5-FU), is considered to be the most important metabolite of capecitabine in plasma. The unit of measure was nanograms per millilitre per hour (ng/mL * hr). (NCT00353262)
Timeframe: Pre-dose, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, and 12 hours post the dose.

Interventionng/mL*hr (Geometric Mean)
Cycle 1, Day 1Cycle 2, Day 1Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab136051217711817

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T1/2 Beta of Total And Free Platinum

T1/2 beta is the time measured for the plasma concentration to decrease by 1 half to its original concentration of total and free platinum. (NCT00353262)
Timeframe: Pre-dose, and 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24, 48 and 72 hours from the beginning of the two hour oxaliplatin infusion on Days 2 to 5 of Cycle 1, and Days 1 to 4 for Cycle 2 and 3

Interventionhour (Geometric Mean)
Total Platinum: Cycle 1, Day 2Total Platinum: Cycle 2, Day 1Total Platinum: Cycle 3, Day 1Free Platinum: Cycle 1, Day 2Free Platinum: Cycle 2, Day 1Free Platinum: Cycle 3, Day 1
Capecitabine+ Oxaliplatin+ Bevacizumab48.7055.7367.2817.6418.4118.47

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Number of Adverse Events

(NCT00354224)
Timeframe: From the start of study treatment through study completion for up to about 18 weeks

InterventionSerious Adverse Events (Number)
Oxaliplatin + Capecitabine4

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Number of Participants With Grade 3 or Higher Toxicity

summary of grade 3 (per Common Toxicity Criteria) or higher toxicities which generally is described as a severe adverse reaction or symptom. (NCT00354601)
Timeframe: Days 1, 8, 15, 21 of each course and treatment end (28 days after last dose or start of new therapy)

Interventionparticipants (Number)
Docetaxel and Capecitabine1

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Number of Participants With Overall Response

Overall response rate defined as Complete Response (CR), disappearance of all target lesions; or Partial Response (PR), at least a 30% decrease in sum of longest diameter (LD) of target lesions, taking as reference the baseline sum LD, assessed by Response Evaluation Criteria in Solid Tumors (RECIST) Committee [JNCI 92(3):205-216, 2000]. In addition to a baseline scan, confirmatory scans for those deemed to have achieved a PR or CR. (NCT00354887)
Timeframe: Every 9 weeks from treatment initiation and confirmatory images 6 weeks or more after initial responses

Interventionparticipants (Number)
Participants with CRParticipants with PR
Oxaliplatin + Capecitabine312

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Number of Patients With at Least One Surgical Complications (Wound Dehiscence, Infection, Seroma, or Hematoma).

Number of patients with at least one surgical complications (wound dehiscence, infection, seroma, or hematoma) (NCT00365417)
Timeframe: Two (2) years

Interventionparticipants (Number)
Chemo Plus Bevacizumab24

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Clinical Response Rate (cRR) of the Sequential Regimen

Clinical tumor measurements were required before study entry & before cycle 5 of chemotherapy (between AC & TX). Final tumor measurements were obtained 4-5 weeks after the last dose of chemotherapy. Clinical tumor assessments by physical examination were recommended before each chemotherapy cycle. The criteria proposed by the Response Evaluation Criteria in Solid Tumors Committee(RECIST) were used to define clinical response status. CR was defined as the disappearance of all lesions with no evidence of PD. PR was defined as at least 30% decrease in the sum of the longest diameter of target lesions, using as reference the baseline sum longest diameter and/or the persistence of greater than or equal to 1 nontarget lesion without worsening of any other clinical manifestations of disease. PD was defined as at least a 20% increase in the sum of the longest diameter of target lesions, the appearance of new lesions, or unequivocal progression of existing lesions. (NCT00365417)
Timeframe: Approximately 6 months

Interventionpercentage of patients (Number)
Chemo Plus Bevacizumab77.27

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Cardiac Events

Events: Congestive Heart Failure; Cardiac Death (NCT00365417)
Timeframe: Assessments throughout; up to 18 months following study entry

Interventioncardiac events (Number)
Chemo Plus Bevacizumab0

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pCR in the Breast and Nodes

Measured by no histologic evidence of invasive tumor cells in the surgical breast specimen, axillary nodes, or sentinel nodes (NCT00365417)
Timeframe: Approximately 7 months

Interventionparticipants (Number)
pCR in the breast and nodesNo pCR in the breast and nodesNo data available
Neoadjuvant Study Treatment4383

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Progression-free Survival

Percentage of patients free from disease progression. Progression is determined using international criteria proposed by the Response Evaluation Criteria in Solid Tumors (RECIST) Committee. At least a 20% increase in the sum of the longest diameter of the target lesions. Other manifestations of progressive disease would also be classified as disease progression, eg., appearance of one or more new lesions in the breast, regional lymph nodes or distant sites, unequivocal progression of existing non-target lesions, and appearance of inflammatory carcinoma on clinical exam. (NCT00365417)
Timeframe: 2 years

Interventionpercentage of patients (Number)
Chemo Plus Bevacizumab57.69

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Overall Survival

Percentage of patients alive. (NCT00365417)
Timeframe: 2 years

Interventionpercentage of patients (Number)
Chemo Plus Bevacizumab74.52

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Pathologic Complete Response (pCR) in the Breast

Measured by no histologic evidence of invasive tumor cells in the surgical breast specimen (NCT00365417)
Timeframe: Approximately 7 months

Interventionparticipants (Number)
pCR in the breastNo pCR in the breastNo data available
Neoadjuvant Study Treatment4383

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Reported Adverse Events

Number of Adverse Events (NCT00365417)
Timeframe: Approximately 14 months

Interventionevents (Number)
Neoadjuvant Study Treatment566

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Time to Tumor Progression (TTP)

Time from randomization to first documentation of objective tumor progression. (NCT00373113)
Timeframe: From time of randomization to every 6 weeks thereafter through 22 months

InterventionMonths (Median)
Sunitinib2.8
Capecitabine4.2

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Number of Participants With Overall Response (OR)

OR was defined as the number of participants with confirmed complete response (CR) or partial response (PR) according to Response Evaluation Criteria in Solid Tumors (RECIST, Version 1.0) for at least 4 weeks, confirmed by repeat tumor assessments. CR was defined as the disappearance of all target lesions. PR was defined as a greater than or equal to (>=) 30% decrease in the sum of the longest dimensions of the target lesions taking as a reference the baseline sum longest dimensions. (NCT00373113)
Timeframe: From time of randomization to every 6 weeks thereafter through 22 months

InterventionParticipants (Number)
Sunitinib27
Capecitabine40

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Overall Survival (OS)

Average time from randomization to first documentation of death due to any cause. (NCT00373113)
Timeframe: From time of randomization until death

InterventionMonths (Median)
Sunitinib15.3
Capecitabine16.9

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Progression-Free Survival (PFS)

Time from the date of randomization to the date of the first documentation of objective tumor progression or death due to any cause, whichever occured first. (NCT00373113)
Timeframe: From time of randomization to every 6 weeks thereafter through 22 months or until death

InterventionMonths (Median)
Sunitinib2.8
Capecitabine4.2

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Duration of Response (DR)

Time from the first documentation of OR (CR or PR) that was subsequently confirmed to the first documentation of tumor progression or death due to any cause. CR was defined as disappearance of all target lesions. PR was defined as a >= 30% decrease in sum of longest dimensions of target lesions taking as a reference baseline sum longest dimensions. (NCT00373113)
Timeframe: From time of randomization to every 6 weeks thereafter through 22 months or death

InterventionMonths (Median)
Sunitinib6.9
Capecitabine9.3

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Overall Survival (OS)

The number of months measured from the date of randomization to the date of death due to any cause. (NCT00382720)
Timeframe: up to a maximum of 36 months

Interventionmonths (Median)
(TE) Taxotere and Eloxatin8.97
(TEF) Taxotere, Eloxatin and 5-fluorouracil14.59
(TEX) Taxotere, Eloxatin and Xeloda11.30

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Time to Progression

"The number of months measured from the day of randomization to the first tumor progression according to World Health Organization (WHO) criteria evaluation of cancer response, or death from any cause.~WHO Criteria for Progressive Disease: ≥ 25% increase in the size of at least one bidimensionally or unidimensionally measurable lesion." (NCT00382720)
Timeframe: every 8 weeks up to a maximum of 36 months

InterventionMonths (Median)
(TE) Taxotere and Eloxatin4.50
(TEF) Taxotere, Eloxatin and 5-fluorouracil7.66
(TEX) Taxotere, Eloxatin and Xeloda5.55

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Best Overall Response Rate (ORR)

"Percentage of partial and complete responses, according to WHO criteria:~Complete Response: Disappearance of all known disease, determined by 2 observations not less than 4 weeks apart.~Partial Response: Decrease by at least 50% of the diameters of all measurable lesions, determined by 2 observations not less than 4 weeks apart." (NCT00382720)
Timeframe: every 8 weeks up to a maximum of 36 months

Interventionpercentage of participants (Number)
(TE) Taxotere and Eloxatin23.1
(TEF) Taxotere, Eloxatin and 5-fluorouracil46.6
(TEX) Taxotere, Eloxatin and Xeloda25.6

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12-month Progression Free Survival (PFS)

Percentage of participants with 12-month progression-free survival (PFS) was assessed. PFS is defined as the time from enrollment until documented disease progression or death (whichever occurred first). RECIST criteria (version 1). Complete response (CR) defined as disappearance of all target lesions. Partial Response (PR) defined as ≥ 30% decrease of SLD. Progressive disease (PD) defined as ≥ 20% increase in Sum Longest Diameters (SLD). Stable Disease (SD) defined as being between 20% increase and < 30% decrease in SLD. (NCT00398320)
Timeframe: PFS assessed every 3 months through 12 months

Interventionpercentage of participants w/ 12 mo PFS (Number)
Capecitabine / Oxaliplatin / Bevacizumab64.7

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Overall Survival (OS)

OS is defined as time from enrollment until death from any cause. (NCT00398320)
Timeframe: Continuous

Interventionmonths (Median)
Capecitabine / Oxaliplatin / Bevacizumab42.2

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Biochemical Markers

(NCT00398320)
Timeframe: Assessed every 3 weeks while on treatment

Interventionparticipants (Number)
25 to 49% reduction in 1 or more hormones≥ 50% reduction in 1 or more hormones
Capecitabine / Oxaliplatin / Bevacizumab612

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Response Rates

Response rate is defined as percent of patients with complete response (CR) and partial response (PR) as their best response as defined by RECIST criteria (version 1). Complete response (CR) is defined as disappearance of all target lesions. Partial Response (PR) is defined as ≥ 30 decrease in the sum of longest diameters of target lesions (SLD). Overall response (OR) = CR + PR. (NCT00398320)
Timeframe: Response rates by RECIST criteria assessed every 3 months while on treatment

Interventionpercentage of participants (Number)
Capecitabine / Oxaliplatin / Bevacizumab17.5

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Progression-free Survival

(NCT00398398)
Timeframe: 1 year

Interventionmonths (Median)
Xelox Plus Cetuximab6.5

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Toxicity Profile

Number of patients who experienced toxicity from study treatment to evaluate the safety and tolerability of XELOX plus Cetuximab (NCT00398398)
Timeframe: 1 years

Interventionparticipants (Number)
Xelox Plus Cetuximab44

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Overall Survival

(NCT00398398)
Timeframe: 1 year

Interventionmonths (Median)
Xelox Plus Cetuximab11.8

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Overall Response Rate

Tumor response was evaluated every two cycles by CT scans and other indicated methods, and the patients with complete or partial response required a confirmatory response evaluation at least 4 weeks later. Patients without confirmatory evaluation were not regarded as responders. (NCT00398398)
Timeframe: 6 months

Interventionparticipants (Number)
Xelox Plus Cetuximab23

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Rate of Resection of Liver Metastases

Number of patients undergoing liver resection, based on patients with liver disease at baseline (NCT00399035)
Timeframe: Post-randomisation until end of study

InterventionParticipants (Number)
Cediranib 20 mg21
Placebo17

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Time to Wound Healing Complications

Number of days from post-randomisation surgery until wound healing complications (NCT00399035)
Timeframe: Post-randomisation until end of study

InterventionDays (Median)
Cediranib 20 mg18
Placebo18

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Overall Survival

Number of months from randomisation to the date of death from any cause (NCT00399035)
Timeframe: Baseline through to date of death upto and including data cut off date of 21/03/10

InterventionMonths (Median)
Cediranib 20 mg19.7
Placebo18.9

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Overall Response Rate

Objective tumour response(defined as a confirmed response of CR or PR).The definition for a confirmed response was met when an initial RECIST response of PR/CR was confirmed at the next scheduled visit as a PR/CR according to an evaluable assessment.Intervening assessments of non-evaluable or stable disease were allowable as long as the initial RECIST response was confirmed.RECIST criteria defined as follows: Target lesions Complete Response(CR)Disappearance of all target lesions Partial Response (PR).At least a 30% decrease in the sum of LD of target lesions taking as reference the baseline sum LD. Progressive Disease (PD) At least a 20% increase in the sum of LD of target lesions taking as references the smallest sum LD recorded (either at baseline or at previous assessment since treatment began).Stable Disease (SD) Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD.Non-target lesions Complete Response (CR) Disappearance of all non-target lesi (NCT00399035)
Timeframe: Baseline through to date of death upto and including data cut off date of 21/03/10

InterventionParticipants (Number)
Cediranib 20 mg254
Placebo178

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Progression-free Survival

RECIST criteria defined as follows: Target lesions Complete Response (CR) Disappearance of all target lesions Partial Response (PR) At least a 30% decrease in the sum of LD of target lesions taking as reference the baseline sum LD.Progressive Disease (PD) At least a 20% increase in the sum of LD of target lesions taking as references the smallest sum LD recorded (either at baseline or at previous assessment since treatment began).Stable Disease (SD) Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. Non-target lesions Complete Response (CR) Disappearance of all non-target lesions Non-Complete Response (non-CR/Non- Progression [non-PD]) Persistence of one or more non-target lesion or/and maintenance of tumour marker level above the normal limits. Progression (PD) Unequivocal progression of existing nontarget lesions. (NCT00399035)
Timeframe: RECIST assessed at baseline every 6 weeks through to week 24 and 12 week thereafter through to progression or data cut off date of 21/03/10 whichever was earliest.

InterventionMonths (Median)
Cediranib 20 mg8.6
Placebo8.2

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Duration of Response

Based on RECIST measurements taken throughout the study and best objective tumour response at the defined analysis cut-off point. Measured from the time the criteria for CR/PR are first met (whichever is recorded first) until the patient progresses or dies. (NCT00399035)
Timeframe: Treatment period from initial response up until data cut-off date of 21/03/10

InterventionMonths (Median)
Cediranib 20 mg8.5
Placebo6.9

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Best Percentage Change in Tumour Size

Maximum percentage reduction or minimum percentage increase in tumour size where size is the sum of the longest diameters of the target lesions (NCT00399035)
Timeframe: Baseline through to date of death upto and including data cut off date of 21/03/10

InterventionPercentage [change in tumour size (mm) ] (Mean)
Cediranib 20 mg-42.49
Placebo-40.61

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Toxicities Including Events Other Than Congestive Heart Failure, of Chemotherapy Alone, Bevacizumab With Chemotherapy, and Bevacizumab Alone

The number of patients who experienced Grade 1 or above Adverse Events. Referring to the Adverse Events tables for specifics. (NCT00408408)
Timeframe: 24 months after study entry

Interventionparticipants (Number)
Arm 1A: Docetaxel Then AC180
Arm 1B Docetaxel + Bev Then AC + Bev157
Arm 2A: Docetaxel + Capecitabine Then AC172
Arm 2B: Docetaxel + Cape + Bev Then AC + Bev185
Arm 3A: Docetaxel + Gem Then AC158
Arm 3B: Docetaxel + Gem + Bev Then AC + Bev185

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Clinical Complete Resonse: cCR as Assessed by Physical Exam at the Completion of the Sequential Chemotherapy Regimens

The percentage of patients assessed by physical exam as Clinical Complete Response according to RECIST. (NCT00408408)
Timeframe: Three to four weeks after the last chemotherapy dose, on average at 6 or 13 months

Interventionpercentage of patients (Number)
Arm 1A: Docetaxel Then AC52.3
Arm 1B Docetaxel + Bev Then AC + Bev64.6
Arm 2A: Docetaxel + Capecitabine Then AC51.3
Arm 2B: Docetaxel + Cape + Bev Then AC + Bev59.1
Arm 3A: Docetaxel + Gem Then AC52.6
Arm 3B: Docetaxel + Gem + Bev Then AC + Bev60

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Clinical Complete Response (cCR) Following Docetaxel Alone, Docetaxel/Capecitabine, and Docetaxel/Gemcitabine Hydrochloride, With or Without Bevacizumab, as Assessed by Physical Exam at Completion of Therapy

Percentages of patients assessed as Clinical Complete Response or Clinical Partial Response according to RECIST. (NCT00408408)
Timeframe: Assessed at cycle 5 of chemotherapy, on average at 15 weeks

Interventionpercentage of patients (Number)
Arm 1A: Docetaxel Then AC30
Arm 1B Docetaxel + Bev Then AC + Bev43.3
Arm 2A: Docetaxel + Capecitabine Then AC29.8
Arm 2B: Docetaxel + Cape + Bev Then AC + Bev34.5
Arm 3A: Docetaxel + Gem Then AC37.9
Arm 3B: Docetaxel + Gem + Bev Then AC + Bev42

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Clinical Overall Response: cOR as Assessed by Physical Exam at the Completion of the Sequential Chemotherapy Regimens

The percentage of patients assessed by physical exam as Clinical Complete Response or Clinical Partial Response according to RECIST. (NCT00408408)
Timeframe: Three to four weeks after the last chemotherapy dose on average 6 or 13 months

Interventionpercentage of patients (Number)
Arm 1A: Docetaxel Then AC79.9
Arm 1B Docetaxel + Bev Then AC + Bev87.7
Arm 2A: Docetaxel + Capecitabine Then AC75.4
Arm 2B: Docetaxel + Cape + Bev Then AC + Bev90.7
Arm 3A: Docetaxel + Gem Then AC83.3
Arm 3B: Docetaxel + Gem + Bev Then AC + Bev80.5

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Pathologic Complete Response (pCR) of the Primary Tumor in the Breast

Percentage of patients absent of histologic evidence of invasive tumor cells in the surgical breast specimen. (NCT00408408)
Timeframe: Time of surgery, on average 6 or 13 months

Interventionpercentage of patients (Number)
Arm 1A: Docetaxel Then AC33.7
Arm 1B Docetaxel + Bev Then AC + Bev31.6
Arm 2A: Docetaxel + Capecitabine Then AC23.5
Arm 2B: Docetaxel + Cape + Bev Then AC + Bev36.1
Arm 3A: Docetaxel + Gem Then AC27.6
Arm 3B: Docetaxel + Gem + Bev Then AC + Bev35.8

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pCR in the Breast and Nodes

Percentage of patients absent of histologic evidence of invasive tumor cells in the surgical breast specimen and axillary lymph nodes. (NCT00408408)
Timeframe: Time of surgery, on average 6 or 13 months

Interventionpercentage of patients (Number)
Arm 1A: Docetaxel Then AC27.3
Arm 1B Docetaxel + Bev Then AC + Bev24.4
Arm 2A: Docetaxel + Capecitabine Then AC18.7
Arm 2B: Docetaxel + Cape + Bev Then AC + Bev27.4
Arm 3A: Docetaxel + Gem Then AC22.9
Arm 3B: Docetaxel + Gem + Bev Then AC + Bev30.3

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Clinical Overall Response (cOR) Following Docetaxel Alone, Docetaxel/Capecitabine, and Docetaxel/Gemcitabine Hydrochloride, With or Without Bevacizumab, as Assessed by Physical Exam at the Completion of the Docetaxel-based Portion of Chemotherapy

Percentages of patients assessed as Clinical Complete Response or Clinical Partial Response according to RECIST. (NCT00408408)
Timeframe: Assessed at cycle 5 of chemotherapy, on average at 15 weeks

Interventionpercentage of patients (Number)
Arm 1A: Docetaxel Then AC77
Arm 1B Docetaxel + Bev Then AC + Bev87.6
Arm 2A: Docetaxel + Capecitabine Then AC73.7
Arm 2B: Docetaxel + Cape + Bev Then AC + Bev84
Arm 3A: Docetaxel + Gem Then AC82.6
Arm 3B: Docetaxel + Gem + Bev Then AC + Bev88

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Disease-free Survival (DFS)

Percentage of patients free from local recurrence following mastectomy, local recurrence in the ipsilateral breast following lumpectomy, regional recurrence, distant recurrence, contralateral breast cancer, second primary cancer after 5 years. (NCT00408408)
Timeframe: Measured through 5 years after study enrollment

Interventionpercentage of patients (Number)
Arm 1A: Docetaxel Then AC73.4
Arm 1B Docetaxel + Bev Then AC + Bev72.2
Arm 2A: Docetaxel + Capecitabine Then AC68.5
Arm 2B: Docetaxel + Cape + Bev Then AC + Bev77.1
Arm 3A: Docetaxel + Gem Then AC72.9
Arm 3B: Docetaxel + Gem + Bev Then AC + Bev74.8

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Surgical Complication

Number of patients with Grade 4 or above surgery-related toxicities (NCT00408408)
Timeframe: 24 months after study entry

Interventionparticipants (Number)
Arm 1A: Docetaxel Then AC1
Arm 1B Docetaxel + Bev Then AC + Bev1
Arm 2A: Docetaxel + Capecitabine Then AC0
Arm 2B: Docetaxel + Cape + Bev Then AC + Bev1
Arm 3A: Docetaxel + Gem Then AC0
Arm 3B: Docetaxel + Gem + Bev Then AC + Bev1

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Number of Participants With Grade 3-4 Adverse Events Reported

(NCT00408564)
Timeframe: from start of study treatment until end of study visit, about 30 weeks

Interventionparticipants (Number)
Gemcitabine,Oxaliplatin and Cetuximab9

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Response Rate

defined as the total number of subjects whose best response is PR or CR. (NCT00408564)
Timeframe: up to 46 weeks after the start of study treatment

InterventionParticipants (Count of Participants)
Gemcitabine,Oxaliplatin and Cetuximab5

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Progression-free Survival at 6 Months

(NCT00408564)
Timeframe: up to 46 weeks after the start of study treatment

Interventionpercentage of participants (Number)
Gemcitabine,Oxaliplatin and Cetuximab82

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Overall Survival

(NCT00408564)
Timeframe: up to 46 weeks after the start of study treatment

Interventionpercentage of participants (Number)
Gemcitabine,Oxaliplatin and Cetuximab49

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Median Overall Survival

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00411762)
Timeframe: Up to 100 weeks

Interventionweeks (Median)
PHY906 Administration21.6

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Median Progression Free Survival

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00411762)
Timeframe: Up to 100 weeks

Interventionweeks (Median)
PHY906 Administration10.1

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Feasibility and Safety of Pre-operative Chemotherapy in Locally Advanced Gastric Cancer as Assessed by Number of Participants Who Experienced Adverse Events Grade 3 or Higher as Defined by CTCAE.

Number of participants who experience Grade 3/4 neutropenia, Grade 3 nausea or Grade 3 diarrhea. (NCT00414271)
Timeframe: up to 5 years

InterventionParticipants (Count of Participants)
Grade 3/4 neutropeniaGrade 3 nauseaGrade 3 diarrhea
Open Label, Single Arm1012

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Overall Survival

Median number of months participants alive at the time of observation. Calculated using Kaplan-Meier method. (NCT00414271)
Timeframe: up to 8 years

Interventionmonths (Median)
Open Label, Single Arm17.1

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Progression-free Survival as Measured by Number of Participants Without Disease Progression.

(NCT00414271)
Timeframe: up to 5 years

InterventionParticipants (Count of Participants)
Open Label, Single Arm3

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Number of Participants With Pathological Response

Number of participants who completed neoadjuvant chemotherapy and underwent repeat CT and endoscopic ultrasound (EUS) with pathological complete response (pCR), partial response in the primary tumor, stable disease or progressive disease as defined by EUS criteria. (NCT00414271)
Timeframe: up to 5 years

InterventionParticipants (Count of Participants)
pathological complete response (pCR)partial responsestable diseaseprogressive disease
Open Label, Single Arm0483

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Time to Progression

"Disease assessment was performed and recorded according to the Response Evaluation Criteria in Solid Tumors (RECIST v.1.0) Guidelines.~Progressive disease is defined as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions." (NCT00416494)
Timeframe: From time of treatment until documented progression, assesed up to 60 months.

Interventionmonths (Median)
Initial Cohort10.1
Second Cohort10.4

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Safety and Tolerability

Number of participants with adverse events (NCT00416494)
Timeframe: After all participants went off study drug regimine.

Interventionparticipants with adverse event (Number)
Initial Cohort19
Second Cohort29

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Overall Survival

Average months of survival of participants after receiving study drug. (NCT00416494)
Timeframe: From time of treatment until death from any cause, assesed up to 60 months.

Interventionmonths (Median)
Initial Cohort19.6
Second Cohort24.8

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Disease Free Survival

"Disease assessment was performed and recorded according to the Response Evaluation Criteria in Solid Tumors (RECIST v.1.0) Guidelines.~Progressive disease is defined as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions." (NCT00416494)
Timeframe: From time of treatment until documented progression or death from any cause, whichever came first, assesed up to 60 months.

Interventionmonths (Median)
Initial Cohort10.1
Second Cohort10.4

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Response Rate (Percentage of Participants With Partial or Complete Response)

"Restaging scans occurred every 9 weeks from time of study drug initiation until disease progression.~Disease assessment was performed and recorded according to the Response Evaluation Criteria in Solid Tumors (RECIST v.1.0) Guidelines.~The definitions were:~Complete response (CR)- Disappearance of all target lesions Partial response (PD)- At least a 30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD Stable disease (SD)- Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started Progressive disease (PD) - At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions" (NCT00416494)
Timeframe: After all subjects were evaluated for restaging which occured every 9 weeks from drug initiation until disease progression, assesed up to 24 months.

Interventionpercentage of participants with response (Number)
Initial Cohort63
Second Cohort42

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Response Rate

Response was evaluated using the Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), every 3 cycles of chemotherapy (each cycle lasts 3 weeks) and at the end of treatment (at 21 weeks from the start of treatment). (NCT00418028)
Timeframe: Through the study treatment, an average of 5 months.

InterventionParticipants (Count of Participants)
Arm A (Cint)30
Arm B (Ccont)31

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Response Duration

"Response duration is computed for all patients with Partial Response or Complete Response, during the treatment period, as the time from the moment the Partial or Complete Response is reported to the date the patient Progresses or Dies, whichever happens first.~A patient is censored if she does not progress or die. In these cases Response duration is computed as the time from the moment the Partial or Complete Response is reported to the last contact date." (NCT00418028)
Timeframe: Time from the moment the Partial or Complete Response is reported to the date the patient Progresses or Dies, whichever happens first, assessed up to 72 weeks.

InterventionMonths (Median)
Arm A (Cint)10.07
Arm B (Ccont)7.20

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Progression Free Survival

Progression Free Survival is defined as the time (in months) from the moment the patient starts the study treatment to the date of progressive disease. That is, a patient has an event is she progresses or dies for any reason. (NCT00418028)
Timeframe: Time (in months) from the moment the patient starts the study treatment to the date of progressive disease assessed up to 84 months.

InterventionMonths (Median)
Arm A (Cint)8.52
Arm B (Ccont)6.84

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Overall Survival

An event is defined as death. A patient is censored if she does not die. The censoring date is last contact date. (NCT00418028)
Timeframe: Time to survival is the number of months from the study treatment start date to the date of death, assessed up to 100 months.

InterventionMonths (Median)
Arm A (Cint)27.34
Arm B (Ccont)24.11

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Time to Progression

Time to Progression (TTP) is defined as the time (in months) from the moment the patient starts the study treatment to the date of progressive disease. That is, a patient has an event is she progresses or dies due to progressive disease. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0). (NCT00418028)
Timeframe: After 1 year from the treatment start day.

Interventionmonths (Median)
Arm A (Cint)8.68
Arm B (Ccont)6.84

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Time to Treatment Failure

"Time to treatment failure (TTF) is defined as the time (in months) from the moment the patient starts the study treatment to the end of treatment date (due to death, progressive disease, adverse events, patient's decision or investigator criteria.~If a patient did not end the treatment, it is censored. The censoring date is the date of the last dose received." (NCT00418028)
Timeframe: Time (in months) from the moment the patient starts the study treatment to the end of treatment date (due to death, progressive disease, adverse events, patient's decision or investigator criteria, assessed up to 72 months.

InterventionMonths (Median)
Arm A (Cint)5.41
Arm B (Ccont)5.87

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Clinical Benefit

"A patient experiences a Clinical Benefit if the following is satisfied:~Criterion: The patient has Complete response, Partial Response or Stable Disease and it continues during more than 3 months." (NCT00418028)
Timeframe: "Months from CR,PR or SD (the first one) until Progression date, new treatment or last contact date."

InterventionParticipants (Count of Participants)
Arm A (Cint)56
Arm B (Ccont)56

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Duration of Response

Duration of response is defined for all evaluable patients who have achieved an objective response as the date at which the patient's objective status is first noted to be either a CR or PR to the date progression is documented. Duration of response will be analyzed using Kaplan-Meier methods. (NCT00433550)
Timeframe: Up to 2 years

Interventionmonths (Median)
All Patients (6/6, 6/7, 7/7 UGT1A1 Genotype)9.0

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Confirmed Tumor Response Rate (Proportion of Participants With Complete Response)

Evaluated using RECIST version 1.0. Confirmed tumor response rate was defined as achieving partial response (PR) or complete response (CR) in two consecutive assessments at least 6 weeks apart. CR is complete disappearance of all target lesions and PR is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. The confirmed response rate is reported as the number of participants with confirmed responses divided by the number of evaluated participants. (NCT00433550)
Timeframe: 36 weeks

Interventionproportion of patients (Number)
All Patients (6/6, 6/7, 7/7 UGT1A1 Genotype).38

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Time to Treatment Failure

Time to treatment failure is defined to be the time from the date of registration to the date at which the patient is removed from treatment due to progression, toxicity, or refusal. If the patient is considered to have had a major treatment violation or is taken off study as a non-protocol failure, the patient will be censored on the date they are removed from treatment. Time to treatment failure will be analyzed using Kaplan-Meier methods. (NCT00433550)
Timeframe: Up to 2 years

Interventionmonths (Median)
All Patients (6/6, 6/7, 7/7 UGT1A1 Genotype)6.7

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Progression Free Survival

Time to disease progression is defined as the time from registration to the earlier of documentation of disease progression or death. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. The distribution of time to progression will be estimated using Kaplan-Meier methodology. (NCT00433550)
Timeframe: Up to 2 years

Interventionmonths (Median)
All Patients (6/6, 6/7, 7/7 UGT1A1 Genotype)8.9

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Overall Survival

Overall survival will be defined as the time from registration to death. Patients lost to follow-up for this endpoint will be censored at the date of last contact (i.e., last known alive). The distribution of overall survival will be estimated using Kaplan-Meier methodology. (NCT00433550)
Timeframe: Up to 2 years

Interventionmonths (Median)
All Patients (6/6, 6/7, 7/7 UGT1A1 Genotype)13.4

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Overall Survival (OS)

Time from the date of randomization to the date of death due to any cause. OS (in months) calculated as (date of death minus randomization date plus 1) divided by 30.4. For patients lacking survival data beyond the date of their last follow-up, the OS time was censored on the last date they were known to be alive. Patients lacking survival data beyond randomization had their OS times censored at randomization. (NCT00435409)
Timeframe: Baseline until death or up to 3 years from first dose

Interventionmonths (Median)
Sunitinib + Capecitabine16.5
Capecitabine17.2

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Duration of Response (DR)

Time from the first documentation of objective tumor response (CR or PR) that was subsequently confirmed to the first documentation of disease progression (PD) or to death due to any cause, whichever occurred first. If tumor progression data included more than 1 date, the first date was used. DR (in months) was calculated as [the date response ended (date of PD or death) minus first CR or PR date that was subsequently confirmed plus 1)] divided by 30.4. (NCT00435409)
Timeframe: Baseline until response or disease progression (up to 3 years from first dose)

,
Interventionmonths (Median)
Independent radiology assessmentInvestigator's assessment
Capecitabine8.87.6
Sunitinib + Capecitabine9.05.7

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Percent Chance of Participant Survival

Probability of survival 2 years and 3 years after the first dose of study treatment. (NCT00435409)
Timeframe: Year 1, Year 2, Year 3

,
Interventionprobability of survival (Number)
Year 1Year 2Year 3
Capecitabine0.6540.3730.174
Sunitinib + Capecitabine0.6350.3680.150

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Percentage of Participants With Objective Response (OR)

Proportion of participants with confirmed complete response (CR) or partial response (PR) according to the Response Evaluation Criteria in Solid Tumors (RECIST); CR: disappearance of all target lesions, PR: greater than or equal to (>=) 30 percent (%) decrease in the sum of the longest dimensions (SLD) of the target lesions taking as a reference the baseline SLD. Confirmed responses = persist on repeat imaging study at least 4 weeks after initial documentation of response. Designation of best response of stable disease (SD) required the criteria to be met at least 5 weeks after randomization. (NCT00435409)
Timeframe: Baseline until response or disease progression (up to 3 years from first dose)

,
Interventionpercentage of participants (Number)
Independent radiology assessmentInvestigator's assessment
Capecitabine16.320.4
Sunitinib + Capecitabine18.625.3

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Progression Free Survival (PFS)

Defined as the time from the date of randomization to the date of the first documentation of objective tumor progression or death due to any cause, whichever occurs first. If tumor progression data include more than 1 date, the first date will be used. PFS (in months) will be calculated as (first event date minus randomization date plus 1) divided by 30.4. (NCT00435409)
Timeframe: Baseline until disease progression (up to 3 years from first dose)

,
Interventionmonths (Median)
Independent radiology assessmentInvestigator's assessment
Capecitabine5.95.5
Sunitinib + Capecitabine5.55.4

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Number of Participants With the Indicated Central Nervous System (CNS) Objective Response (OR)

CNS OR is defined as the number of participants with either a complete response (CR) or partial response (PR) as assessed by volumetric analysis of brain magnetic resonance imaging (MRI) and Response Evaluation Criteria In Solid Tumors (RECIST). CR: complete resolution of all evaluable and non-evaluable brain metastases; PR: =>50% reduction in the volumetric sum of all evaluable brain metastases compared to baseline. (NCT00437073)
Timeframe: From the start of treatment until disease progression, death, or discontinuation from the study, up to a maximum of Week 88

Interventionparticipants (Number)
Lapatinib Plus Capecitabine5
Lapatinib Plus Topotecan0

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Number of Participants With the Indicated CNS Responses

"CNS responses were assessed by volumetric (V) analysis of brain MRI and RECIST. CR: complete resolution of all evaluable and non-evaluable brain metastases (BMs). PR: =>50% reduction in the V sum of all evaluable BMs compared to baseline. A response of Other was used for participants who discontinued the study prior to the first efficacy assessment. Stable Disease (SD): disease that does not meet CR, PR, or CNS progression criteria. Progressive disease (PD): a requirement for a new steroid or an increasing steroid dose for the treatment of worsening neurological signs/symptoms due to BMs." (NCT00437073)
Timeframe: From the start of treatment until disease progression, death, or discontinuation from the study, up to a maximum of Week 88

,
Interventionparticipants (Number)
Complete responsePartial responseStable DiseaseProgressive DiseaseUnknownOther
Lapatinib Plus Capecitabine056200
Lapatinib Plus Topotecan003132

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Pharmacokinetics: Area Under the Concentration Versus Time Curve During One Dosing Interval at Steady State

Area Under the Concentration versus time curve during 1 dosing interval at steady state (AUCτ,ss) for Cycle 2 Day 1 for Enzastaurin, its metabolite LY326020 and total analytes (enzastaurin + LY326020). AUCτ,ss was calculated using concentration versus time data by post hoc estimation of enzastaurin, its metabolite LY326020, and total analytes (enzastaurin + LY326020). (NCT00437294)
Timeframe: From pre-dose to 24 hours post-dose on Day 1 of Cycle 2

Interventionnanomoles*hour per liter (nmol*hr/L) (Geometric Mean)
EnzastaurinEnzastaurin Metabolite LY326020Total Analytes (enzastaurin + LY326020)
Capecitabine + Enzastaurin9000040700137000

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Pharmacology Toxicity and Adverse Events (AEs)

Data presented are the number of participants who experienced serious AEs, AEs, death due to progressive disease (PD), death due to AEs while on treatment and death during the 30-day post-treatment. A summary of SAEs and other non-serious AEs, regardless of causality, is located in the Reported Adverse Events module. (NCT00437294)
Timeframe: Baseline to study completion [Cycle 19 (21 days/cycle) and 30-day safety follow-up]

,
InterventionParticipants (Count of Participants)
Serious AEsOther non-serious AEsDeaths Due to PDDeaths Due to AEsDeaths in 30-day follow-up
Capecitabine + Enzastaurin12381346
Capecitabine + Placebo12401221

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Duration of Response (DOR)

The DOR was defined as the time from first objective status assessment of complete response (CR) or partial response (PR) to the first time of progression or death as a result of any cause. According to the Response Evaluation Criteria in Solid Tumors (RECIST V1.0) criteria, CR was the disappearance of all tumor lesions. PR was at least a 30% decrease in the sum of the longest diameter (LD) of target lesions or complete disappearance of target lesions, with persistence (but not worsening) of 1 or more non-target lesions, with occurrence of no new lesions. For participants not known to have died as of the data cut-off date and who did not have progressive disease, DOR was censored at the date of last visit with adequate assessment. For participants who received subsequent anticancer therapy (after discontinuation from the study treatment) prior to disease progression or death, DOR was censored at the date of last visit with adequate assessment. (NCT00437294)
Timeframe: Randomization to last visit (up to 9.66 months)

Interventionmonths (Median)
Capecitabine + Enzastaurin4.27
Capecitabine + Placebo3.47

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Pharmacokinetics: Maximum Observed Concentration (Cmax) of Capecitabine

Cmax for Capecitabine, 5'-deoxy-5-fluorouridine (5'-DFUR) and its metabolites 5-fluorouracil (5-FU) was calculated from the plasma concentration-time data for each analyte for Day 1 of Cycle 2. (NCT00437294)
Timeframe: From pre-dose to 6 hours post-dose on Day 1 of Cycle 2

,
Interventionmicrograms/milliliter(ug/mL) (Geometric Mean)
Capecitabine5-DFUR5-FU
Capecitabine + Enzastaurin4.426.090.374
Capecitabine + Placebo2.756.050.206

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Overall Survival (OS)

OS was defined as the time in months from the date of study enrollment to the date of death from any cause. For participants not known to have died as of the cut-off date, OS was censored at the last contact date. (NCT00437294)
Timeframe: Randomization to date of death from any cause up to 20.83 months

Interventionmonths (Median)
Capecitabine + Enzastaurin9.86
Capecitabine + Placebo14.88

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Percentage of Participants With Complete Response (CR) or Partial Response (PR) (Objective Response Rate)

Response rate was defined as percent of participants with objective response [CR or PR] over randomized and treated participants using the Response Evaluation Criteria in Solid Tumors (RECIST v1.0) Guidelines. CR was defined as the disappearance of all tumor lesions. PR was defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions taking as reference the baseline sum of LDs or complete disappearance of target lesions, with persistence (but not worsening) of one or more non-target lesions. No new lesions may have appeared. (NCT00437294)
Timeframe: Randomization to last visit (up to 9.66 months)

Interventionpercentage of participants (Number)
Capecitabine + Enzastaurin11.9
Capecitabine + Placebo11.6

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Progression Free Survival (PFS)

PFS was defined as the time from randomization to the first observation of disease progression or death due to any cause. For participants not known to have died as of the data cut-off date and who did not have progressive disease, PFS was censored at the date of last visit with adequate assessment. For participants who received subsequent anticancer therapy (after discontinuation from the study treatment) prior to disease progression or death, PFS was censored at the date of last visit with adequate assessment prior to the initiation of post-discontinuation anticancer therapy. (NCT00437294)
Timeframe: Randomization to measured progressive disease or death up to 14 months

Interventionmonths (Median)
Capecitabine + Enzastaurin2.79
Capecitabine + Placebo4.27

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Pharmacokinetics: Area Under the Concentration Curve Versus Time From Time 0 to Last Quantifiable Value (AUC0-tlast) of Capecitabine

AUC0-tlast for Capecitabine, 5'-deoxy-5-fluorouridine (5'-DFUR) and 5-fluorouracil (5-FU) was calculated from the plasma concentration-time data for each analyte for Cycle 2, Day 1. (NCT00437294)
Timeframe: Pre-dose to 6 hours post-dose on Day 1 of Cycle 2

,
Interventionmicrograms*hour/milliliter (ug*hr/mL) (Geometric Mean)
Capecitabine5'-deoxy-5-fluorouridine (5'-DFUR)5-fluorouracil (5-FU)
Capecitabine + Enzastaurin6.0911.60.683
Capecitabine + Placebo4.1811.00.358

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Progression Free Survival

(NCT00438100)
Timeframe: The follow up period will be two years after the last dose has been administered.

Interventionyears (Median)
Capecitabine Arm1.2
S-1 Arm1.3

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Median Progression Free Survival

"The median amount of time from the start of treatment until death or disease progression, whichever occurs first.~Progressive Disease (PD): A 20% or greater increase in the sum of Longest Diameter (LD) of all target lesions, taking as reference the smallest sum LD recorded since baseline." (NCT00438256)
Timeframe: from the start of treatment until death or progression, median duration of 10.4 months

InterventionMonths (Median)
Proton Beam Radiation/ Capecitabine10.4

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30-Day Post Operative Mortality

The number of participants that died within 30 days of undergoing a pancreaticoduodenectomy. (NCT00438256)
Timeframe: 30 days after the time of surgery (Surgery is 28-42 days after start of treatment)

InterventionParticipants (Count of Participants)
Proton Beam Radiation/ Capecitabine0

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Number of Participants With Dose Limiting Toxicities in the 5 Radiation Sessions in One Week Arm

"The number of participants that experienced a dose limiting toxicity in the arm where radiation was administered over 5 consecutive for a total dose of 25 Gray Equivalents (GyE) (Group 4). Participants were monitored for potential Dose Limiting Toxicities (DLT) for three weeks after the start of radiation. DLTs included:~Any grade 3 non-hematologic or hematologic toxicity requiring a greater than 7 day interruption in therapy (excluding alopecia and nausea/vomiting not controlled by optimal supportive care or~Any grade 4 non-hematologic toxicity or~Any grade 4 neutropenia or thrombocytopenia as defined by Common Terminology Criteria for Adverse Events (CTCAE v3.0)" (NCT00438256)
Timeframe: 3 Weeks

InterventionParticipants (Count of Participants)
Proton Beam Radiation/ Capecitabine0

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Number of Participants With a Pathological Complete Response

All patients that received surgery underwent a full pathological review of their pancreaticoduodenectomy specimen according to the American Joint Committee on Cancer (AJCC) Staging Classification, 6th. Initial gross evaluation and identification of resection margins was performed jointly by the surgeon and the pathologist. Pathological complete response will be defined as the absence of any viable tumor cells within the pathologic specimen. (NCT00438256)
Timeframe: at the time of surgery (28-42 days after start of treatment)

InterventionParticipants (Count of Participants)
Proton Beam Radiation/ Capecitabine0

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Number of Participants With Grade 3 or Greater Toxicity in Phase II

Adverse events were assessed using Common Terminology Criteria for Adverse Events (CTCAE 3). The regimen was considered to be tolerated if less than 20% of participants experienced a grade 3 or greater toxicity. (NCT00438256)
Timeframe: 30 days after the end of treatment, up to approximately 6 months total

InterventionParticipants (Count of Participants)
Phase II: Proton Beam Radiation/ Capecitabine2

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Number of Participants With Surgical Morbidity

Number of participants with pancreatic or any other anastomotic leakage within 30 days of surgery (NCT00438256)
Timeframe: 30 days post surgery (surgery was 28-42 days after the start of treatment)

InterventionParticipants (Count of Participants)
Proton Beam Radiation/ Capecitabine0

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Toxicity Rates

# of subjects who experienced >= grade 1 adverse event that is positively related to treatment. (NCT00444678)
Timeframe: 1 year since the first treatment and every year after for up to 10 years

InterventionParticipants (Count of Participants)
Cetuximab, Capecitabine and Oxaliplatin36

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Time to Progression

Time to Treatment Failure (progression or death) will be defined as the time from the first day of treatment until the date Progressive Disease (PD) or death is first reported. Subjects who die without a reported prior progression will be considered to have progressed on the day of their death. Subjects who did not progress will be censored at the day of their last tumor assessment. (NCT00444678)
Timeframe: 6 months since the start of treatment and every 3 months after treatment for up to 10 years

InterventionDays (Median)
Cetuximab, Capecitabine and Oxaliplatin275

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Survival

Survival will be defined as the number of days from the first day of therapy to the date of death. If the subject is lost to follow-up, survival will be censored on the last date the subject was known to be alive. (NCT00444678)
Timeframe: 6 months since the start of treatment and every 3 months after treatment for up to 10 years

InterventionDays (Median)
Cetuximab, Capecitabine and Oxaliplatin417

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Response Rate for the Combination Treatment

The tumor response rate (RR) will be defined as the total number of subjects whose best response is partial response (PR) or complete response (CR) during the first six months of treatment, divided by the number of subjects. (NCT00444678)
Timeframe: 6 months since the start of treatment

InterventionParticipants (Count of Participants)
Cetuximab, Capecitabine and Oxaliplatin21

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Number of Participants With DLTs

Dose limiting toxicity (DLTs) was determined during the Wrst two cycles of treat- ment. The definitions of DLTs were as follows: (1) grade 4 neutropenia lasting for more than 5 days, or grade 3/4 neu- tropenia with fever; (2) grade 4 thrombocytopenia; (3) any other grade 3 non-hematological toxicity (excluding alope- cia); or (4) treatment delay of more than 2 weeks following the time of planned treatment. Maximal tolerated dose was defined as that the DLTs were observed in two or more patients from a cohort of two to six patients (NCT00446290)
Timeframe: 2 years

Interventionparticipants (Number)
DXO Arm3

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Median Progression-Free Survival (PFS)

Time in months from the start of study treatment to the date of first progression (PD) according to the RECIST criteria, or death due to any cause. PER RECIST, a PD is indicated when there is at least a 20% increase in the sum of the longest diameters from target lesions relative to the smallest sum recorded since treatment is initiated. Median PFS was estimated using a Kaplan-Meier curve, and is the time at which 50% of patients remain alive without disease progression. (NCT00447330)
Timeframe: 5 years from study start date

Interventionsurvival time in months (Median)
1- Capecitabine (Xeloda), Oxaliplatin and Bevacizumab (Avastin6.97

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Response Rate

The proportion of patients for whom the best overall response is complete response (CR) or partial response (PR). A CR occurs when all lesions disappear; whereas, a PR is indicated when there is at least a 30% decrease in the sum of the longest diameters (LD) of the target lesion. A PD (progressive disese) occurs when there is at least a 20% increase in the sum of the LD relative to the smallest sum LD recorded since treatment is initiated. Disease is considered stable if there is no response and no PD. All patients were assigned a best response for inclusion in this calculation in accordance with the protocol. (NCT00447330)
Timeframe: Every 9 weeks for up to 1 year

Interventionpercentage of participants (Number)
1 - Capecitabine (Xeloda), Oxaliplatin and Bevacizumab (Avasti41.7

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To Assess the Safety and Tolerability of the Combination of Bevacizumab, Oxaliplatin and Capecitabine in Patients With Previously Untreated Metastatic Esophagogastric Adenocarcinoma

Number of subjects who experienced an adverse event (NCT00447330)
Timeframe: Every 21 days

Interventionparticipants (Number)
1 - Capecitabine (Xeloda), Oxaliplatin and Bevacizumab (Avasti56

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Median Survival

Time in months from the start of study treatment to date of death due to any cause. Median survival was estimated using a Kaplan-Meier curve and is the time point at which 50% of patients remain alive. (NCT00447330)
Timeframe: 5 years after study start date

Interventionsurvival time in months (Median)
1 - Capecitabine (Xeloda), Oxaliplatin and Bevacizumab (Avasti10.51

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Objective Response Rate (ORR) and Disease Control Rate - Efficacy Evaluable Population

Objective response rate was the percentage of participants, (n/N; number with objective response per Number evaluated) whose best response is either a Complete Response (CR) or a Partial Response (PR). Disease control rate was defined as percentage (n/N) of participants with stable disease greater than (>) 6 months, PR, or CR. Efficacy Evaluable Population: All participants with at least one measurable lesion at baseline, who received at least one dose of combination study drug and have at least one on-study tumor assessment or stopped study treatment prior to first assessment, were evaluated. Those who stop treatment prior to tumor assessment for reasons unrelated to disease or drug were excluded. (NCT00452673)
Timeframe: Day 1 up to 30 days post last dose

,,,
Interventionpercentage of participants (Number)
Objective Response RateDisease control rate
100 mg Dasatinib + 1000 mg/m^2Capecitabine24.056.00
50 mg Dasatinib + 825 mg/m^2Capecitabine50.075.0
70 mg Dasatinib + 1000 mg/m^2Capecitabine040.0
70 mg Dasatinib + 825 mg/m^2Capecitabine16.6733.33

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Number of Participants With Dose Limiting Toxicities Per Dose Level - Safety Population

Safety was assessed from first dose of study drug through at least 30 days after the last dose, until resolution of drug-related toxicity or when toxicity was deemed irreversible, whichever was longer. An adverse event (AE) was considered a dose limiting toxicity (DLT) if it occurred in the first 21 days and was at least possibly related to study drugs and were: Clinically-evident toxicity of Grade >= 3, or of Grade 2 which required interruption of treatment for >= 7 days (consecutive or non-consecutive); non-hematologic abnormal laboratory value of Grade >= 3, or hematologic toxicity of Grade 4, which persisted 7 days; any grade toxicity which in the judgment of the investigator required a dose reduction or removal from further study therapy. (NCT00452673)
Timeframe: Day 1 to 30 days post last dose

Interventionparticipants (Number)
50 mg Dasatinib + 825 mg/m^2Capecitabine1
70 mg Dasatinib + 825 mg/m^2Capecitabine1
70 mg Dasatinib + 1000 mg/m^2Capecitabine1
100 mg Dasatinib + 1000 mg/m^2Capecitabine2

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Number of Participants On-study With Grade 3 - 4 Chemistry Laboratory Values in Those Participants With a Baseline Laboratory Value of Grade 0 - Safety Population

CTC, Version 3 used to assess parameters. (ULN)=upper limit of normal: (ALT)= alanine transaminase; (AST)=aspartate aminotransferase; (ALP)=alkaline phosphatase. ALT Grade (Gr)1:>ULN to 2.5*ULN; Gr 2: >2.5 to 5.0*ULN; Gr 3: >5.0 to 20.0*ULN; Gr 4: >20.0*ULN. AST Gr 1: >ULN to 2.5*ULN; Gr 2: >2.5 to 5.0*ULN; Gr 3: >5.0 to 20.0*ULN; Gr 4: >20.0*ULN. Total bilirubin Gr 1: >ULN to 1.5*ULN; Gr 2: >1.5 to 3.0*ULN; Gr 3: >3.0 to 10.0*ULN; Gr 4: >10.0*ULN. ALP (U/L) Gr1:>ULN to 2.5*ULN, Gr2:>2.5 to 5.0*ULN, Gr3:>5.0 to 20.0*ULN, Gr4:>20.0*ULN. Albumin (low) Gr 1:NCT00452673)
Timeframe: Day 1 to 30 days post last dose

,,,
Interventionparticipants (Number)
Alkaline Phosphatase (N=4, 6, 5, 21)Alanine Aminotransferase (N=6, 9, 6, 25)Aspartate Aminotransferase (N=4, 8, 6, 25)Total Bilirubin (N=6, 9, 6, 29)
100 mg Dasatinib + 1000 mg/m^2Capecitabine0210
50 mg Dasatinib + 825 mg/m^2Capecitabine0000
70 mg Dasatinib + 1000 mg/m^2Capecitabine0000
70 mg Dasatinib + 825 mg/m^2Capecitabine0000

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Number of Participants With Overall Response to Tumor - Efficacy Evaluable Population

Complete Response (CR): disappearance of all target and non-target lesions, with confirmation at >=4 weeks interval; Partial Response (PR): >= 30% decrease in sum of longest diameter (LDs) of target lesions, taking as reference the baseline sum LD, with confirmation at >= 4 weeks interval. Progressive Disease (PD): Appearance of new lesion(s), or >=20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since treatment start, or unequivocal progression of existing non-target lesions. Stable disease was defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, without unequivocal progression of non-target lesions, after >=6 weeks on study. Radiological tumor assessment by computed tomography (CT) or magnetic resonance imaging (MRI) occurred every 6 weeks. For those patients who were on treatment > 24 weeks, the tumor assessment occurred every 9 weeks. (NCT00452673)
Timeframe: Day 1 to 30 days post last dose

,,,
Interventionparticipants (Number)
Complete ResponseUnconfirmed partial responsePartial ResponseStable DiseaseProgressive DiseaseClinical ProgressionDiscontinuation due to study drug toxicity
100 mg Dasatinib + 1000 mg/m^2Capecitabine03611311
50 mg Dasatinib + 825 mg/m^2Capecitabine0120100
70 mg Dasatinib + 1000 mg/m^2Capecitabine0102200
70 mg Dasatinib + 825 mg/m^2Capecitabine0111210

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Number of Participants With Deaths, Serious Adverse Events, Adverse Events, Adverse Events Leading to Discontinuation and Treatment-related Adverse Events - Safety Population

Adverse events (AEs) were evaluated according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) Version 3.0. AE=any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that may not have a causal relationship with treatment. Serious AE (SAE)=a medical event that at any dose results in death, persistent or significant disability/incapacity, or drug dependency/abuse; is life-threatening, an important medical event, or a congenital anomaly/birth defect; or requires or prolongs hospitalization. Treatment-related=having certain, probable, possible, or missing relationship to study drug. Grade (Gr) 1=Mild, Gr 2=Moderate, Gr 3=Severe, Gr 4=Life-threatening or disabling, Gr 5=Death. (NCT00452673)
Timeframe: Day 1 up to 30 days post last dose

,,,
Interventionparticipants (Number)
Deaths within 30 days of last doseDeaths reported beyond 30 days post last doseParticipants with SAEsParticipants with Grade 3 - 4 SAEsParticipants with AEsAEs leading to discontinuation of therapyParticipants with study drug-related AEs
100 mg Dasatinib + 1000 mg/m^2Capecitabine04131130428
50 mg Dasatinib + 825 mg/m^2Capecitabine0022727
70 mg Dasatinib + 1000 mg/m^2Capecitabine0044646
70 mg Dasatinib + 825 mg/m^2Capecitabine0021939

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Number of Participants On-Study With Grade 3 - 4 Hematology Laboratory Test Values in Those Participants With a Baseline Laboratory Value of Grade 0 - Safety Population

National Cancer Institute Common terminology criteria (CTC), Version 3 used to assess parameters. Lower limit of normal (LLN). CTC criteria: Absolute neutrophil count (ANC). Leukocytes (White blood cells) Grade (Gr) 1:NCT00452673)
Timeframe: Day 1 up to 30 days post last dose

,,,
Interventionparticipants (Number)
Leukocytes ( N=7, 9, 5, 29)ANC (N=6, 9, 6, 30)Platelet Count (N=7, 9, 6, 30)Hemoglobin (N=7, 6, 4, 18)
100 mg Dasatinib + 1000 mg/m^2Capecitabine1313
50 mg Dasatinib + 825 mg/m^2Capecitabine0000
70 mg Dasatinib + 1000 mg/m^2Capecitabine0000
70 mg Dasatinib + 825 mg/m^2Capecitabine0000

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Time to Response

Time to Response was defined as the date of start of treatment until the first date of complete response (CR) or a partial response (PR), based on Response Evaluation Criteria in Solid Tumors (RECIST) v.1.0 criteria. CR was defined as the disappearance of all target lesions; for non-target lesions, disappearance of lesions and normal tumor marker levels. PR was defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, using the baseline sum LD as reference. (NCT00454636)
Timeframe: Approximately 3.25 years

Interventiondays (Mean)
Cisplatin / Capecitabine132.92
Epirubicin / Cisplatin / Capecitabine126.64
Epirubicin / Oxaliplatin / Capecitabine123.50
Docetaxel / Cisplatin / Capecitabine138.16

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Progression-Free Survival (PFS)

PFS was defined as the time from the start of treatment to the first documentation of disease progression or death for any cause. Disease progression was based on Response Evaluation Criteria in Solid Tumors (RECIST) v.1.0 criteria and was defined as at least a 20% increase in the sum of LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT00454636)
Timeframe: Approximately 3.25 years

Interventionmonths (Median)
Cisplatin / Capecitabine4.43
Epirubicin / Cisplatin / Capecitabine5.17
Epirubicin / Oxaliplatin / Capecitabine7.07
Docetaxel / Cisplatin / Capecitabine7.87

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Percentage of Participants With Grade 3 Hand-Foot Syndrome (HFS)

(NCT00454636)
Timeframe: Approximately 3.25 years

Interventionpercentage of participants (Number)
Cisplatin / Capecitabine2.4
Epirubicin / Cisplatin / Capecitabine6.3
Epirubicin / Oxaliplatin / Capecitabine3.7
Docetaxel / Cisplatin / Capecitabine5.2

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Overall Survival (OS)

OS was defined as the time elapsing from the date of the start of treatment until death, or last known follow-up. (NCT00454636)
Timeframe: Approximately 3.25 years

Interventionmonths (Median)
Cisplatin / Capecitabine10.23
Epirubicin / Cisplatin / Capecitabine8.87
Epirubicin / Oxaliplatin / Capecitabine13.87
Docetaxel / Cisplatin / Capecitabine12.43

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Duration of Response

Duration of Response was defined as the time of complete response (CR) or partial response (PR) until the first date of recurrent or progressive disease, based on Response Evaluation Criteria in Solid Tumors (RECIST) v.1.0 criteria. CR was defined as the disappearance of all target lesions; for non-target lesions, disappearance of lesions and normal tumor marker levels. PR was defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, using the baseline sum LD as reference. Progressive disease was defined as at least a 20% increase in the sum of LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT00454636)
Timeframe: Approximately 3.25 years

Interventiondays (Mean)
Cisplatin / Capecitabine308.92
Epirubicin / Cisplatin / Capecitabine154.09
Epirubicin / Oxaliplatin / Capecitabine203.06
Docetaxel / Cisplatin / Capecitabine205.52

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Overall Response Rate (ORR)

ORR was defined as the percentage of participants achieving either a complete response (CR) or a partial response (PR), based on Response Evaluation Criteria in Solid Tumors (RECIST) v.1.0 criteria. CR was defined as the disappearance of all target lesions; for non-target lesions, disappearance of lesions and normal tumor marker levels. PR was defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, using the baseline sum LD as reference. (NCT00454636)
Timeframe: Approximately 3.25 years

Interventionpercentage of participants (Number)
Cisplatin / Capecitabine43.3
Epirubicin / Cisplatin / Capecitabine40.7
Epirubicin / Oxaliplatin / Capecitabine69.6
Docetaxel / Cisplatin / Capecitabine59.6

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Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Carboplatin

AUC (0-∞) = Area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) to extrapolated infinite time (0-∞). It is obtained from AUC (0-t) plus AUC (t-∞). (NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 5 hr after start of infusion on Day 1 of Cycle 2 for cohort 1-3

Interventionng*hr/mL (Mean)
Axitinib + Paclitaxel + Carboplatin (Combined Cohort 1, 2, 3)55580.26

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Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Docetaxel

AUC (0-∞) = Area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) to extrapolated infinite time (0-∞). It is obtained from AUC (0-t) plus AUC (t-∞). (NCT00454649)
Timeframe: 0 (pre-dose), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 5

Interventionng*hr/mL (Mean)
Axitinib + Docetaxel (Cohort 5)3478.49

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Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Gemcitabine

AUC (0-∞) = Area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) to extrapolated infinite time (0-∞). It is obtained from AUC (0-t) plus AUC (t-∞). (NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 0.75, 1, 1.25, 1.5, 2, 3, 4 hr after start of infusion on Day 1 of Cycle 2 for cohort 8

Interventionng*hr/mL (Mean)
Axitinib + Gemcitabine + Cisplatin (Cohort 8)10991.16

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Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Paclitaxel

AUC (0-∞) = Area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) to extrapolated infinite time (0-∞). It is obtained from AUC (0-t) plus AUC (t-∞). (NCT00454649)
Timeframe: 0 (pre-dose), 1, 2, 3, 3.25, 3.5, 4, 5, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 1-3; 0 (pre-dose), 0.5, 1, 2, 3, 4, 5, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 4

Interventionng*hr/mL (Mean)
Axitinib + Paclitaxel (Cohort 4)5683.55
Axitinib + Paclitaxel + Carboplatin (Combined Cohort 1, 2, 3)19959.91

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Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0-∞)] for Pemetrexed

AUC (0-∞) = Area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) to extrapolated infinite time (0-∞). It is obtained from AUC (0-t) plus AUC (t-∞). (NCT00454649)
Timeframe: 0 (pre-dose), 10 minutes (end of infusion), 0.5, 1, 1.5, 2, 4, 6, 8 hr after end of infusion on Day 1 of Cycle 2 for cohort 9

Interventionng*hr/mL (Mean)
Axitinib + Pemetrexed + Cisplatin (Cohort 9)133032.97

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Area Under the Curve From Time Zero to Time 24 Hours [AUC (0-24)] for Axitinib (AG-013736)

AUC (0-24) = Area under the plasma concentration versus time curve from time zero (pre-dose) to time 24 hours (0-24). (NCT00454649)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hr post-dose on Day -1 for cohort 1, 2, 3, 5 and 8; on Day 22 of Cycle 1 for cohort 4; on Day 18 of Cycle 1 for cohorts 6 and 7; 0 (pre-dose), 1.2, 2.2, 3.2, 4.2, 6.2, 8.2 hr post-dose on Day -1 for cohort 9

Interventionnanogram*hour/milliliter (ng*hr/mL) (Mean)
Axitinib + Paclitaxel + Carboplatin (Cohort 1)61.58
Axitinib + Paclitaxel + Carboplatin (Cohort 2)242.41
Axitinib + Paclitaxel + Carboplatin (Cohort 3)475.18
Axitinib + Paclitaxel (Cohort 4)154.43
Axitinib + Docetaxel (Cohort 5)780.99
Axitinib + Capecitabine (Cohort 6)365.95
Axitinib + Capecitabine (Cohort 7)449.99
Axitinib + Gemcitabine + Cisplatin (Cohort 8)416.30
Axitinib + Pemetrexed + Cisplatin (Cohort 9)420.64

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Area Under the Curve From Time Zero to Time 24 Hours [AUC (0-24)] for Capecitabine

AUC (0-24) = Area under the plasma concentration versus time curve from time zero (pre-dose) to time 24 hours (0-24). (NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hr post-dose on Day 1 of Cycle 2 for cohort 6 and 7

Interventionng*hr/mL (Mean)
Axitinib + Capecitabine (Cohort 6)20534.52
Axitinib + Capecitabine (Cohort 7)22163.88

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Area Under the Curve From Time Zero to Time 8 Hours [AUC (0-8)] for Cisplatin

AUC (0-8) = Area under the plasma concentration versus time curve from time zero (pre-dose) to time 8 hours (0-8). (NCT00454649)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 3, 5, 7 hr after start of infusion on Day 1 of Cycle 2 for cohort 8 and 9

Interventionng*hr/mL (Mean)
Axitinib + Gemcitabine + Cisplatin (Cohort 8)2932.43
Axitinib + Pemetrexed + Cisplatin (Cohort 9)2703.92

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Maximum Observed Plasma Concentration (Cmax) for Axitinib (AG-013736)

(NCT00454649)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hr post-dose on Day -1 for cohort 1, 2, 3, 5 and 8; on Day 22 of Cycle 1 for cohort 4; on Day 18 of Cycle 1 for cohorts 6 and 7; 0 (pre-dose), 1.2, 2.2, 3.2, 4.2, 6.2, 8.2 hr post-dose on Day -1 for cohort 9

Interventionng/mL (Mean)
Axitinib + Paclitaxel + Carboplatin (Cohort 1)5.97
Axitinib + Paclitaxel + Carboplatin (Cohort 2)23.36
Axitinib + Paclitaxel + Carboplatin (Cohort 3)42.58
Axitinib + Paclitaxel (Cohort 4)44.58
Axitinib + Docetaxel (Cohort 5)67.96
Axitinib + Capecitabine (Cohort 6)37.51
Axitinib + Capecitabine (Cohort 7)43.97
Axitinib + Gemcitabine + Cisplatin (Cohort 8)40.97
Axitinib + Pemetrexed + Cisplatin (Cohort 9)31.53

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Maximum Observed Plasma Concentration (Cmax) for Capecitabine

(NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hr post-dose on Day 1 of Cycle 2 for cohort 6 and 7

Interventionng/mL (Mean)
Axitinib + Capecitabine (Cohort 6)10808.00
Axitinib + Capecitabine (Cohort 7)10588.38

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Maximum Observed Plasma Concentration (Cmax) for Carboplatin

(NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 5 hr after start of infusion on Day 1 of Cycle 2 for cohort 1-3

Interventionng/mL (Mean)
Axitinib + Paclitaxel + Carboplatin (Combined Cohort 1, 2, 3)23383.33

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Maximum Observed Plasma Concentration (Cmax) for Cisplatin

(NCT00454649)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 3, 5, 7 hr after start of infusion on Day 1 of Cycle 2 for cohort 8 and 9

Interventionng/mL (Mean)
Axitinib + Gemcitabine + Cisplatin (Cohort 8)1680.54
Axitinib + Pemetrexed + Cisplatin (Cohort 9)1176.00

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Maximum Observed Plasma Concentration (Cmax) for Docetaxel

(NCT00454649)
Timeframe: 0 (pre-dose), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 5

Interventionng/mL (Mean)
Axitinib + Docetaxel (Cohort 5)3130.00

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Maximum Observed Plasma Concentration (Cmax) for Gemcitabine

(NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 0.75, 1, 1.25, 1.5, 2, 3, 4 hr after start of infusion on Day 1 of Cycle 2 for cohort 8

Interventionng/mL (Mean)
Axitinib + Gemcitabine + Cisplatin (Cohort 8)20635.29

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Maximum Observed Plasma Concentration (Cmax) for Paclitaxel

(NCT00454649)
Timeframe: 0 (pre-dose), 1, 2, 3, 3.25, 3.5, 4, 5, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 1-3; 0 (pre-dose), 0.5, 1, 2, 3, 4, 5, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 4

Interventionng/mL (Mean)
Axitinib + Paclitaxel (Cohort 4)3698.33
Axitinib + Paclitaxel + Carboplatin (Combined Cohort 1, 2, 3)6105.00

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Maximum Observed Plasma Concentration (Cmax) for Pemetrexed

(NCT00454649)
Timeframe: 0 (pre-dose), 10 minutes (end of infusion), 0.5, 1, 1.5, 2, 4, 6, 8 hr after end of infusion on Day 1 of Cycle 2 for cohort 9

Interventionng/mL (Mean)
Axitinib + Pemetrexed + Cisplatin (Cohort 9)83925.00

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Maximum Tolerated Dose (MTD) of Axitinib (AG-013736) in Combination With Chemotherapy

MTD defined as the dose level at which more than 1 out of 6 participants experienced a dose limiting toxicity (DLT). DLT included grade (Gr) 4 neutropenia or thrombocytopenia, greater than or equal to (>=) Gr 3 nonhematological toxicities or >=0.5 teaspoon/day hemoptysis or >=2 gram /24 hours proteinuria or inability to resume background chemotherapy or axitinib (AG-013736) dosing within 14 days of stopping due to treatment related toxicity. (NCT00454649)
Timeframe: Baseline to withdrawal from study or Day 21 of Cycle 1 [all cohorts except cohort 4 (Day 28 of Cycle 1)]

Interventionmg BID (Number)
Axitinib + Paclitaxel + Carboplatin (Cohort 1)5
Axitinib + Paclitaxel + Carboplatin (Cohort 2)5
Axitinib + Paclitaxel + Carboplatin (Cohort 3)5
Axitinib + Paclitaxel (Cohort 4)5
Axitinib + Docetaxel (Cohort 5)NA
Axitinib + Capecitabine (Cohort 6)5
Axitinib + Capecitabine (Cohort 7)5
Axitinib + Gemcitabine + Cisplatin (Cohort 8)5
Axitinib + Pemetrexed + Cisplatin (Cohort 9)5

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Percentage of Participants With Objective Response

Percentage of participants with objective response based assessment of confirmed complete response (CR) or confirmed partial response (PR) according to Response Evaluation Criteria in Solid Tumors (RECIST) 1.0. Confirmed response are those that persist on repeat imaging study at least 4 weeks after initial documentation of response. CR are defined as the disappearance of all lesions (target and/or non target). PR are those with at least 30% decrease in the sum of the longest dimensions of the target lesions taking as a reference the baseline sum longest dimensions. (NCT00454649)
Timeframe: Baseline and thereafter every 2 cycles up to disease progression or discontinuation from study or up to 155 weeks

InterventionPercentage of Participants (Number)
Axitinib + Paclitaxel + Carboplatin (Cohort 1)100.0
Axitinib + Paclitaxel + Carboplatin (Cohort 2)0
Axitinib + Paclitaxel + Carboplatin (Cohort 3)35.0
Axitinib + Paclitaxel (Cohort 4)66.7
Axitinib + Docetaxel (Cohort 5)50.0
Axitinib + Capecitabine (Cohort 6)11.1
Axitinib + Capecitabine (Cohort 7)11.8
Axitinib + Gemcitabine + Cisplatin (Cohort 8)23.8
Axitinib + Pemetrexed + Cisplatin (Cohort 9)0

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Plasma Clearance (CL) for Carboplatin

Clearance of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Drug clearance is a quantitative measure of the rate at which a drug substance is removed from the plasma. (NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 5 hr after start of infusion on Day 1 of Cycle 2 for cohort 1-3

InterventionL/hr (Mean)
Axitinib + Paclitaxel + Carboplatin (Combined Cohort 1, 2, 3)12.57

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Plasma Clearance (CL) for Cisplatin

Clearance of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Drug clearance is a quantitative measure of the rate at which a drug substance is removed from the plasma. (NCT00454649)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 3, 5, 7 hr after start of infusion on Day 1 of Cycle 2 for cohort 8 and 9

InterventionL/hr (Mean)
Axitinib + Gemcitabine + Cisplatin (Cohort 8)46.31
Axitinib + Pemetrexed + Cisplatin (Cohort 9)46.80

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Plasma Clearance (CL) for Docetaxel

Clearance of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Drug clearance is a quantitative measure of the rate at which a drug substance is removed from the plasma. (NCT00454649)
Timeframe: 0 (pre-dose), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 5

InterventionL/hr (Mean)
Axitinib + Docetaxel (Cohort 5)42.96

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Plasma Clearance (CL) for Gemcitabine

Clearance of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Drug clearance is a quantitative measure of the rate at which a drug substance is removed from the plasma. (NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 0.75, 1, 1.25, 1.5, 2, 3, 4 hr after start of infusion on Day 1 of Cycle 2 for cohort 8

InterventionL/hr (Mean)
Axitinib + Gemcitabine + Cisplatin (Cohort 8)224.36

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Plasma Decay Half Life (t1/2) for Paclitaxel

t1/2 is the time measured for the plasma concentration to decrease by one half. (NCT00454649)
Timeframe: 0 (pre-dose), 1, 2, 3, 3.25, 3.5, 4, 5, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 1-3; 0 (pre-dose), 0.5, 1, 2, 3, 4, 5, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 4

Interventionhr (Mean)
Axitinib + Paclitaxel (Cohort 4)12.51
Axitinib + Paclitaxel + Carboplatin (Combined Cohort 1, 2, 3)8.36

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Plasma Decay Half Life (t1/2) for Pemetrexed

t1/2 is the time measured for the plasma concentration to decrease by one half. (NCT00454649)
Timeframe: 0 (pre-dose), 10 minutes (end of infusion), 0.5, 1, 1.5, 2, 4, 6, 8 hr after end of infusion on Day 1 of Cycle 2 for cohort 9

Interventionhr (Mean)
Axitinib + Pemetrexed + Cisplatin (Cohort 9)2.77

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Plasma Clearance (CL) for Pemetrexed

Clearance of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Drug clearance is a quantitative measure of the rate at which a drug substance is removed from the plasma. (NCT00454649)
Timeframe: 0 (pre-dose), 10 minutes (end of infusion), 0.5, 1, 1.5, 2, 4, 6, 8 hr after end of infusion on Day 1 of Cycle 2 for cohort 9

InterventionL/hr (Mean)
Axitinib + Pemetrexed + Cisplatin (Cohort 9)7.26

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Plasma Decay Half Life (t1/2) for Axitinib (AG-013736)

t1/2 is the time measured for the plasma concentration to decrease by one half. (NCT00454649)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hr post-dose on Day -1 for cohort 1, 2, 3, 5 and 8; on Day 22 of Cycle 1 for cohort 4; on Day 18 of Cycle 1 for cohorts 6 and 7; 0 (pre-dose), 1.2, 2.2, 3.2, 4.2, 6.2, 8.2 hr post-dose on Day -1 for cohort 9

Interventionhr (Mean)
Axitinib + Paclitaxel + Carboplatin (Cohort 1)2.75
Axitinib + Paclitaxel + Carboplatin (Cohort 2)2.90
Axitinib + Paclitaxel + Carboplatin (Cohort 3)2.80
Axitinib + Paclitaxel (Cohort 4)1.45
Axitinib + Docetaxel (Cohort 5)4.07
Axitinib + Capecitabine (Cohort 6)3.85
Axitinib + Capecitabine (Cohort 7)3.64
Axitinib + Gemcitabine + Cisplatin (Cohort 8)2.68
Axitinib + Pemetrexed + Cisplatin (Cohort 9)5.02

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Plasma Decay Half Life (t1/2) for Capecitabine

t1/2 is the time measured for the plasma concentration to decrease by one half. (NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hr post-dose on Day 1 of Cycle 2 for cohort 6 and 7

Interventionhr (Mean)
Axitinib + Capecitabine (Cohort 6)0.85
Axitinib + Capecitabine (Cohort 7)1.44

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Plasma Decay Half Life (t1/2) for Carboplatin

t1/2 is the time measured for the plasma concentration to decrease by one half. (NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 5 hr after start of infusion on Day 1 of Cycle 2 for cohort 1-3

Interventionhr (Mean)
Axitinib + Paclitaxel + Carboplatin (Combined Cohort 1, 2, 3)2.62

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Plasma Decay Half Life (t1/2) for Cisplatin

t1/2 is the time measured for the plasma concentration to decrease by one half. (NCT00454649)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 3, 5, 7 hr after start of infusion on Day 1 of Cycle 2 for cohort 8 and 9

Interventionhr (Mean)
Axitinib + Gemcitabine + Cisplatin (Cohort 8)2.61
Axitinib + Pemetrexed + Cisplatin (Cohort 9)3.91

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Plasma Decay Half Life (t1/2) for Docetaxel

t1/2 is the time measured for the plasma concentration to decrease by one half. (NCT00454649)
Timeframe: 0 (pre-dose), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 5

Interventionhr (Mean)
Axitinib + Docetaxel (Cohort 5)11.49

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Plasma Decay Half Life (t1/2) for Gemcitabine

t1/2 is the time measured for the plasma concentration to decrease by one half. (NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 0.75, 1, 1.25, 1.5, 2, 3, 4 hr after start of infusion on Day 1 of Cycle 2 for cohort 8

Interventionhr (Mean)
Axitinib + Gemcitabine + Cisplatin (Cohort 8)0.29

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Apparent Oral Clearance (CL/F) for Axitinib (AG-013736)

Clearance (CL) of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes and F is the absolute oral bioavailability. Apparent oral clearance(CL/F) is obtained following oral administration. (NCT00454649)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hr post-dose on Day -1 for cohort 1, 2, 3, 5 and 8; on Day 22 of Cycle 1 for cohort 4; on Day 18 of Cycle 1 for cohorts 6 and 7; 0 (pre-dose), 1.2, 2.2, 3.2, 4.2, 6.2, 8.2 hr post-dose on Day -1 for cohort 9

InterventionLiter/hour (L/hr) (Mean)
Axitinib + Paclitaxel + Carboplatin (Cohort 1)49.39
Axitinib + Paclitaxel + Carboplatin (Cohort 2)40.72
Axitinib + Paclitaxel + Carboplatin (Cohort 3)29.73
Axitinib + Paclitaxel (Cohort 4)65.69
Axitinib + Docetaxel (Cohort 5)14.35
Axitinib + Capecitabine (Cohort 6)26.64
Axitinib + Capecitabine (Cohort 7)83.46
Axitinib + Gemcitabine + Cisplatin (Cohort 8)50.05
Axitinib + Pemetrexed + Cisplatin (Cohort 9)25.10

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Apparent Oral Clearance (CL/F) for Capecitabine

Clearance (CL) of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes and F is the absolute oral bioavailability. Apparent oral clearance(CL/F) is obtained following oral administration. (NCT00454649)
Timeframe: 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hr post-dose on Day 1 of Cycle 2 for cohort 6 and 7

InterventionLiter/hr (Mean)
Axitinib + Capecitabine (Cohort 6)209.05
Axitinib + Capecitabine (Cohort 7)314.12

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Plasma Clearance (CL) for Paclitaxel

Clearance of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Drug clearance is a quantitative measure of the rate at which a drug substance is removed from the plasma. (NCT00454649)
Timeframe: 0 (pre-dose), 1, 2, 3, 3.25, 3.5, 4, 5, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 1-3; 0 (pre-dose), 0.5, 1, 2, 3, 4, 5, 6, 8, 24, 30 hr after start of infusion on Day 1 of Cycle 2 for cohort 4

InterventionL/hr (Mean)
Axitinib + Paclitaxel (Cohort 4)30.48
Axitinib + Paclitaxel + Carboplatin (Combined Cohort 1, 2, 3)21.61

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Number of Participants With Recurrent Disease

(NCT00462865)
Timeframe: 6 months and again at the end of the study (1 year)

InterventionParticipants (Count of Participants)
Gemcitabine, Capectiabine, Avastin4

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Overall Objective Response

This is defined as the percentage of patients who achieve either an objective complete or partial target lesion response that is confirmed based on the RECIST criteria. (NCT00468585)
Timeframe: 2 years

,,,
Interventionparticipants (Number)
Partial Response (PR)Stable Disease (SD)Progression of Disease (POD)
Group 0021
Group 1012
Group 282215
Group 3032

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Overall Response Rate (Complete and Partial Response) as Measured by RECIST Criteria After Course 1

(NCT00470184)
Timeframe: 5.5 weeks

Interventionpercentage of patients (Number)
COR (Capecitabine in Combination w/Oxaliplatin & Radiotherapy58.33

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Quality of Life Improved Rate

(NCT00470184)
Timeframe: 5.5 weeks

Interventionpercentage of patients (Number)
COR (Capecitabine in Combination w/Oxaliplatin & Radiotherapy66.67

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Complete Response

(NCT00470184)
Timeframe: 5.5 weeks

Interventionpercentage of patients (Number)
COR(Capecitabine in Combination w/Oxaliplatin and Radiotherapy27.78

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Median Time to Progression

(NCT00470184)
Timeframe: 5.5 weeks

Interventionmonths (Number)
COR (Capecitabine in Combination w/Oxaliplatin & RadiotherapyNA

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Trough Concentration of Lapatinib

PK samples were collected at pre-dose on Day 14 and Day 21 (minus 2 days). Trough concentration is defined as the minimum serum concentration at steady state after a repeated dose of lapatinib. (NCT00477464)
Timeframe: Week 2

Interventionng/ml (Mean)
Week 2, n=42Week 3, n=41
Lapatinib 1250 mg and Capecitabine 2000 mg/m^21065.5581243.540

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6-Month Progression-free Survival (Independent Reviewer-assessed)

6-Month progression-free survival is defined as the percentage of participants surviving without progressive disease at 6 months (24 weeks) after the start of treatment. Progressive disease is defined as at least a 20% increase in the sum of the longest diameter of target lesions. (NCT00477464)
Timeframe: Baseline and then every 6 weeks until Month 6 (Week 24)

Interventionpercentage of participants (Number)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^268.2

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Area Under the Plasma Concentration-time Curve From Zero to 24 Hours AUC0-24 of Lapatinib

PK samples were collected at pre-dose, and at 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, 10, 12, and 24 hr (plus or minus 30 minutes) after dosing. AUC is defined as the area under the concentration-time curve from 0 to 24 hour after dosing (AUC 0-24). AUC is a measure of exposure. (NCT00477464)
Timeframe: Week 2

Interventionhr*ng/ml (Geometric Mean)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^248063.990

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Area Under the Plasma Concentration-time Curve Within the Dosing Interval AUC0-tau of Lapatinib

PK samples were collected at pre-dose, and at 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, 10, 12, and 24 hr (plus or minus 30 minutes) after dosing. AUC is defined as the area under the concentration-time curve from 0 to last quantifiable concentration (AUC 0-tau). AUC is a measure of exposure. (NCT00477464)
Timeframe: Week 2

Interventionhr*ng/ml (Geometric Mean)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^248153.776

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Clinical Benefit Response (Independent Reviewer-assessed)

"CBR is defined as the percentage of participants receiving at least one dose of study medication who achieved a best overall response classified as a complete or partial (confirmed) tumor response or stable disease for at least 6 months (24 weeks). A complete response is defined as the disappearance of all target or non-target lesions, partial response and disease progression as at least a 30% decrease and at least a 20% increase, respectively, in the sum of the longest diameter of target lesions, and stable disease as neither partial response nor disease progression." (NCT00477464)
Timeframe: Baseline, every 6 weeks until Week 24 and then every 12 weeks until disease progression (up to Week 119)

Interventionpercentage of participants (Number)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^259

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Duration of Response (Independent Reviewer-assessed)

For the subset of participants who showed a complete or partial response, duration of response is defined as the time from the first documented evidence of partial or complete tumor response until the first documented sign of disease progression or death due to breast cancer, if sooner. (NCT00477464)
Timeframe: Baseline, every 6 weeks until Week 24 and then every 12 weeks until disease progression or death (up to Week 119)

Interventionweeks (Median)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^242.7

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Maximum Plasma Concentration (Cmax) of Lapatinib

Pharmacokinetic (PK) samples were collected at pre-dose, and at 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, 10, 12, and 24 hours (hr) (plus or minus 30 minutes) after dosing. Cmax is defined as the maximum concentration of lapatinib. (NCT00477464)
Timeframe: Week 2

Interventionnanograms/milliliter (ng/ml) (Geometric Mean)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^23520.872

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Objective Response (Independent Reviewer-assessed)

Objective response is defined as the percentage of participants achieving a best overall response classified as a complete or partial (confirmed) tumor response. Complete response is defined as the disappearance of all target or non-target lesions, and partial response is defined as at least a 30% decrease in the sum of the longest diameter of target lesions. (NCT00477464)
Timeframe: Baseline every 6 weeks until Week 24 and then every 12 weeks until disease progression or death (up to Week 119)

Interventionpercentage of participants (Number)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^224

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Overall Survival (Independent Reviewer-assessed)

Overall survival is defined as the time from the start of treatment until death regardless of cause. For participants who did not die, time to death was censored at the time of last confirmation of survival. (NCT00477464)
Timeframe: Baseline and then followed every 4 weeks until death (up to Week 157.9) while on treatment. After treatment termination, followed every 12 weeks until death (up to Week 157.9)

Interventionweeks (Median)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^278.6

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Progression-free Survival (PFS) (Independent Reviewer-assessed)

PFS is defined as the interval between the start of treatment and the earliest date of disease progression or death of any cause, if sooner. (NCT00477464)
Timeframe: Baseline, every 6 weeks until Week 24 and then every 12 weeks until disease progression or death (up to Week 119)

Interventionweeks (Median)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^236.0

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Terminal Elimination Half-life (t1/2) of Lapatinib

Terminal elimination half-life is defined as the duration until observation of half of the maximum concentration. PK samples were collected at pre-dose, and at 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, 10, 12, and 24 hr (plus or minus 30 minutes) after dosing. (NCT00477464)
Timeframe: Week 2

Interventionhr (Geometric Mean)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^211.948

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Time to Maximum Plasma Concentration (Tmax) of Lapatinib

PK samples were collected at pre-dose, and at 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, 10, 12, and 24 hr (plus or minus 30 minutes) after dosing. Tmax is defined as the time to peak concentration from initiation of lapatinib dosing. (NCT00477464)
Timeframe: Week 2

Interventionhr (Geometric Mean)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^24.727

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Time to Progression (Independent Reviewer-assessed)

Time to progression is defined as the interval between the start of treatment and the earliest date of disease progression or death due to breast cancer, if sooner. Time to progression was calculated by using the Kaplan Meier estimate. (NCT00477464)
Timeframe: Baseline, every 6 weeks until Week 24 and then every 12 weeks until disease progression or death due to breast cancer (up to Week 119)

Interventionweeks (Median)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^236.0

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Time to Response (Independent Reviewer-assessed)

Time to response is defined as the time from the start of treatment until the first documented evidence of complete response or partial response. (NCT00477464)
Timeframe: Baseline, every 6 weeks until Week 24 and then every 12 weeks until disease progression or death (up to Week 119)

Interventionweeks (Median)
Lapatinib 1250 mg and Capecitabine 2000 mg/m^26.9

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Area Under the Plasma Concentration-time Curve From Zero to 12 Hours (AUC0-12) of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)

PK samples were collected at pre-dose, and at 0.5 (plus or minus 5 minutes), 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, and 10 hr (plus or minus 30 minutes) after dosing. AUC is defined as the area under the concentration-time curve from 0 to 12 hours after dosing (AUC 0-12). 5-FU and FBAL were evaluated because of the following reasons: (1) capecitabine is an orally administered fluoropyrimidine carbamate selectively activated to fluorouracil (5-FU) in tumors; (2) FBAL is an inactive major metabolite of capecitabine, and metabolites of capecitabine are excreted mainly in urine. (NCT00477464)
Timeframe: Week 2

Interventionhr*ng/ml (Geometric Mean)
Capecitabine5-FUFBAL
Lapatinib 1250 mg and Capecitabine 2000 mg/m^23999.383544.31830478.416

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AUC0-tau of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)

PK samples were collected at pre-dose, and at 0.5 (plus or minus 5 minutes), 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, and 10 hr (plus or minus 30 minutes) after dosing. AUC is defined as the area under the concentration-time curve from 0 to last quantifiable concentration (AUC 0-tau). 5-FU and FBAL were evaluated because of the following reasons: (1) capecitabine is an orally administered fluoropyrimidine carbamate selectively activated to fluorouracil (5-FU) in tumors; (2) FBAL is an inactive major metabolite of capecitabine, and metabolites of capecitabine are excreted mainly in urine. (NCT00477464)
Timeframe: Week 2

Interventionhr*ng/ml (Geometric Mean)
Capecitabine5-FUFBAL
Lapatinib 1250 mg and Capecitabine 2000 mg/m^23997.313514.67029035.744

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Cmax of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)

PK samples were collected at pre-dose, and at 0.5 (plus or minus 5 minutes), 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, and 10 hr (plus or minus 30 minutes) after dosing. Cmax is defined as the maximum concentration of drug. 5-FU and FBAL were evaluated because of the following reasons: (1) capecitabine is an orally administered fluoropyrimidine carbamate selectively activated to fluorouracil (5-FU) in tumors; (2) FBAL is an inactive major metabolite of capecitabine, and metabolites of capecitabine are excreted mainly in urine. (NCT00477464)
Timeframe: Week 2

Interventionng/ml (Geometric Mean)
Capecitabine5-FUFBAL
Lapatinib 1250 mg and Capecitabine 2000 mg/m^22698.033282.9675771.578

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t1/2 of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)

Terminal elimination half-life is defined as the duration until observation of half of the maximum concentration. PK samples were collected at pre-dose, and at 0.5 (plus or minus 5 minutes), 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, and 10 hr (plus or minus 30 minutes) after dosing. 5-FU and FBAL were evaluated because of the following reasons: (1) capecitabine is an orally administered fluoropyrimidine carbamate selectively activated to fluorouracil (5-FU) in tumors; (2) FBAL is an inactive major metabolite of capecitabine, and metabolites of capecitabine are excreted mainly in urine. (NCT00477464)
Timeframe: Week 2

Interventionhr (Geometric Mean)
Capecitabine5-FUFBAL
Lapatinib 1250 mg and Capecitabine 2000 mg/m^20.8650.8382.437

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Tmax of Capecitabine, 5'-Fluorouracil (5-FU), and Alpha-fluoro-beta-alanine (FBAL)

PK samples were collected at pre-dose, and at 0.5 (plus or minus 5 minutes), 1, 2, 3, 4 (plus or minus 15 minutes), 6, 8, and 10 hr (plus or minus 30 minutes) after dosing. Tmax is defined as the time to peak concentration from initiation of dosing. 5-FU and FBAL were evaluated because of the following reasons: (1) capecitabine is an orally administered fluoropyrimidine carbamate selectively activated to fluorouracil (5-FU) in tumors; (2) FBAL is an inactive major metabolite of capecitabine, and metabolites of capecitabine are excreted mainly in urine. (NCT00477464)
Timeframe: Week 2

Interventionhr (Geometric Mean)
Capecitabine5-FUFBAL
Lapatinib 1250 mg and Capecitabine 2000 mg/m^21.3051.3052.899

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Trough Concentration of Capecitabine, 5-FU, and FBAL

PK samples were collected at pre-dose on Day 14 (minus 2 days). Trough concentration is defined as the minimum serum concentration at steady state after a repeated dose. 5-FU and FBAL were evaluated because of the following reasons: (1) capecitabine is an orally administered fluoropyrimidine carbamate selectively activated to fluorouracil (5-FU) in tumors; (2) FBAL is an inactive major metabolite of capecitabine, and metabolites of capecitabine are excreted mainly in urine. (NCT00477464)
Timeframe: Week 2

Interventionng/ml (Mean)
Capecitabine5-FUFBAL
Lapatinib 1250 mg and Capecitabine 2000 mg/m^2NANA668.73

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Overall Tumor Response

Overall tumor response is defined as the percentage of participants with a confirmed complete or partial tumor response per Response Evaluation Criteria in Solid Tumors (RECIST). Complete response (CR) is defined as the disappearance of all target lesions. CR could only be declared if all target and non-target lesions had disappeared. Partial response (PR) is defined as a decrease of 30% or greater in the sum of the longest diameter of target lesions. (NCT00479856)
Timeframe: from start of treatment and every 6 weeks (wks) until Wk 12, then every 12 wks thereafter through the end of treatment (~95 wks; dependent on when participant discontinued study therapy due to disease progression, death, adverse event, of other reason)

Interventionpercentage of participants (Number)
Lapatinib + Chemotherapy33.3

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Time to Progression

Time to progression will be calculated from the time of enrollment until confirmed disease progression. Defined by RECIST (Response Evaluation Criteria in Solid Tumors), Progressive Disease (PD) - at least a 20% increase in the sum of the longest diameter of target lesions, taking as reference the smallest sum longest diameter recorded since the treatment started or the appearance of one or more new lesions. (NCT00483405)
Timeframe: Median 23 month follow-up

Interventionmonths (Median)
Single Arm Trial4.5

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Disease Response Rate

"Radiographic response will be measured every six weeks while subject is on treatment. Response will be measured using RECIST criteria.~Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions." (NCT00483405)
Timeframe: 42 days (2 cycles)

Interventionpercentage of participants with response (Number)
Single Arm Trial12.5

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Number of Subjects Experiencing Adverse Events

Adverse events will be assessed using CTCAE criteria. (NCT00483405)
Timeframe: every 3 weeks of treatment with an average of 15 weeks on treatment

InterventionParticipants (Count of Participants)
Single Arm Trial29

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Overall Survival

Overall survival will be calculated from time of enrollment to death or last contact date. (NCT00483405)
Timeframe: Median 23 month follow-up

Interventionmonths (Median)
Single Arm Trial4.4

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Duration of Follow-up

Duration of follow-up is defined as the time in days from randomization until disease progression or death, or time to censoring for overall survival. (NCT00484939)
Timeframe: Baseline to the end of the study (up to 5 years 8 months)

InterventionDays (Mean)
Bevacizumab + Capecitabine540.5
Capecitabine479.2

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Duration of Response

Duration of response was defined as the time in months from the first confirmed complete response (CR) or partial response (PR) until disease progression or death from any cause, whichever occurred first. CR was defined as the disappearance of all target (TL) and non-target lesions (non-TL). PR was defined as ≥ 30% decrease in the sum of the longest diameter (SLD) of TLs, taking as reference the baseline SLD, or the persistence of 1 or more non-TLs. (NCT00484939)
Timeframe: Baseline to the end of the study (up to 5 years 8 months)

InterventionMonths (Median)
Bevacizumab + Capecitabine9.7
Capecitabine9.4

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Time to Response

Time to response was defined as the time in months from the date of first study treatment to the date of the first documentation of complete response (CR) or partial response (PR), whichever occurred first. CR was defined as the disappearance of all target (TL) and non-target lesions (non-TL). PR was defined as ≥ 30% decrease in the sum of the longest diameter (SLD) of TLs, taking as reference the baseline SLD, or the persistence of 1 or more non-TLs. Participants who did not have a confirmed response were censored at the date of the last evaluable tumor assessment, or if that was unavailable, at the date of the first dose of study medication. (NCT00484939)
Timeframe: Baseline to the end of the study (up to 5 years 8 months)

InterventionMonths (Median)
Bevacizumab + CapecitabineNA
CapecitabineNA

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Progression-free Survival

Progression-free survival was defined as the time in months from the date of randomization to the date of disease progression or death from any cause, whichever occurred first. All measurable lesions (maximum of 5 per organ and 10 in total, those with the longest diameter and suitability for accurate repeated measurements) were identified as target lesions (TL). A sum of the longest diameter for all TLs was calculated and reported as the baseline sum longest diameter (SLD). All other lesions were identified as non-TLs and recorded at baseline. PD was defined as ≥ 20% increase in the sum of the longest diameter of TLs, taking as reference the smallest SLD recorded since treatment started, the unequivocal progression of existing non-TLs, or the appearance of 1 or more new lesions. (NCT00484939)
Timeframe: Baseline to the end of the study (up to 5 years 8 months)

InterventionMonths (Median)
Bevacizumab + Capecitabine9.1
Capecitabine5.1

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Percentage of Participants Requiring Additional Treatment for Malignancy

Reported is the percentage of participants requiring additional treatment for malignancy in the survival follow-up period. (NCT00484939)
Timeframe: Baseline to the end of the study (up to 5 years 8 months)

InterventionPercentage of participants (Number)
Bevacizumab + Capecitabine50.7
Capecitabine49.3

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Overall Survival

Overall survival was defined as the time in months from randomization to death from any cause. (NCT00484939)
Timeframe: Baseline to the end of the study (up to 5 years 8 months)

InterventionMonths (Median)
Bevacizumab + Capecitabine20.7
Capecitabine17.0

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Best Overall Response (BOR)

BOR was defined as the best response (complete response [CR], partial response [PR], stable disease [SD], progressive disease [PD], not evaluable [NE], or not assessed [NA]) recorded from the start of study treatment until disease progression (PD) or death. CR was defined as the disappearance of all target (TL) and non-target lesions (non-TL). PR was defined as ≥ 30% decrease in the sum of the longest diameter (SLD) of TLs, taking as reference the baseline SLD, or the persistence of 1 or more non-TLs. For TLs, SD was defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SLD since treatment started. For non-TLs, SD was defined as the persistence of 1 or more lesions. PD was defined as ≥ 20% increase in the sum of the longest diameter of TLs, taking as reference the smallest SLD recorded since treatment started, the unequivocal progression of existing non-TLs, or the appearance of 1 or more new lesions. (NCT00484939)
Timeframe: Baseline to the end of the study (up to 5 years 8 months)

,
InterventionPercentage of participants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressive DiseaseNot assessed
Bevacizumab + Capecitabine2.917.154.310.015.7
Capecitabine1.48.648.621.420.0

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Eastern Cooperative Oncology Group (ECOG) Performance Status

The ECOG performance status is a scale used to quantify cancer patients' general well-being and activities of daily life. The scale ranges from 0 to 5, with 0 denoting perfect health and 5 indicating death. The 6 categories are 0=Asymptomatic (Fully active, able to carry on all predisease activities without restriction), 1=Symptomatic but completely ambulatory (Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature), 2=Symptomatic, < 50% in bed during the day (Ambulatory and capable of all self-care but unable to carry out any work activities. Up and about more than 50% of waking hours), 3=Symptomatic, > 50% in bed, but not bedbound (Capable of only limited self-care, confined to bed or chair 50% or more of waking hours), 4=Bedbound (Completely disabled. Cannot carry on any self-care. Totally confined to bed or chair), 5=Death. Reported is the percentage of participants in each of the 6 ECOG performance status categories. (NCT00484939)
Timeframe: Baseline to the Safety Follow-up which occurred 28 days after the last dose of treatment (up to 5 years 8 months).

,
InterventionPercentage of participants (Number)
Week 7 ECOG = 0 (n=117,110)Week 7 ECOG = 1Week 7 ECOG = 2Week 7 ECOG = 3Week 7 ECOG = 4Week 7 ECOG = 5Week 16 ECOG = 0 (n=88,77)Week 16 ECOG = 1Week 16 ECOG = 2Week 16 ECOG = 3Week 16 ECOG = 4Week 16 ECOG = 5Week 25 ECOG = 0 (n=66,42)Week 25 ECOG = 1Week 25 ECOG = 2Week 25 ECOG = 3Week 25 ECOG = 4Week 25 ECOG = 5Week 34 ECOG = 0 (n=48,24)Week 34 ECOG = 1Week 34 ECOG = 2Week 34 ECOG = 3Week 34 ECOG = 4Week 34 ECOG = 5Safety Follow-up ECOG = 0 (n=89,82)Safety Follow-up ECOG = 1Safety Follow-up ECOG = 2Safety Follow-up ECOG = 3Safety Follow-up ECOG = 4Safety Follow-up ECOG = 5
Bevacizumab + Capecitabine50.447.01.70.90.00.050.045.53.41.10.00.043.948.56.11.50.00.039.658.30.02.10.00.033.747.212.46.70.00.0
Capecitabine34.558.25.51.80.00.036.451.911.70.00.00.045.245.29.50.00.00.033.358.38.30.00.00.032.945.114.64.91.21.2

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Progression Free Survival

(NCT00493636)
Timeframe: From the date of randomization to date of first documented disease progression (i.e., the date on which a radiologic procedure or clinical evaluation was performed) or the date of death due to any cause, if before progression, assessed up to 39 months.

InterventionDays (Median)
A (Sorafenib + Gemcitabine or Capecitabine)103
B (Placebo + Gemcitabine or Capecitabine)81

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Overall Survival

(NCT00493636)
Timeframe: From the date of randomization to date of death due to any cause, assessed up to 56 months.

InterventionDays (Median)
A (Sorafenib + Gemcitabine or Capecitabine)407
B (Placebo + Gemcitabine or Capecitabine)348

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Overall Response Rate

Overall response rate was defined as the proportion of participants experiencing complete response (CR) and partial response (PR) as best overall response. Response was evaluated via changes from baseline in radiological tumor measurements using RECIST version 1.0 guidelines, where complete response (CR) is the disappearance of all target lesions; partial response (PR) is >=30% decrease in the sum of the longest diameter (LD) of target lesions; Stable Disease (SD) is neither sufficient shrinkage in sum of LD of target lesions to be PR nor increase of >=20%; Progressive Disease (PD) is the increase in existing lesions or new lesions. (NCT00493636)
Timeframe: The overall tumor burden at baseline will be compared with subsequent measurements up to the date of first documented disease progression or the date of death due to any cause, if before progression, assessed up to 39 months.

Interventionpercentage of participants (Number)
A (Sorafenib + Gemcitabine or Capecitabine)19.8
B (Placebo + Gemcitabine or Capecitabine)12.7

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Duration of Overall Response

Duration of overall response was calculated as the time (days) from first documentation of CR or PR (whichever status is recorded first) until the first date that recurrent or progressive disease (PD) or death is objectively documented. Response was evaluated via changes from baseline in radiological tumor measurements using RECIST version 1.0 guidelines, where complete response (CR) is the disappearance of all target lesions; partial response (PR) is >=30% decrease in the sum of the longest diameter (LD) of target lesions; Stable Disease (SD) is neither sufficient shrinkage in sum of LD of target lesions to be PR nor increase of >=20%; Progressive Disease (PD) is the increase in existing lesions or new lesions. (NCT00493636)
Timeframe: Period measured from the first documentation of complete or partial response (whichever status is recorded first) until the first date that recurrent or progressive disease or death is objectively documented.

InterventionDays (Median)
A (Sorafenib + Gemcitabine or Capecitabine)94
B (Placebo + Gemcitabine or Capecitabine)147

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Time to Progression

(NCT00493636)
Timeframe: Calculated as the time (days) from date of randomization to date of first observed disease progression (radiological or clinical, whichever is earlier), assessed up to 39 months.

InterventionDays (Median)
A (Sorafenib + Gemcitabine or Capecitabine)111
B (Placebo + Gemcitabine or Capecitabine)82

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-Determine the Clinical Benefit Rate (Complete Response, Partial Response, or Stable Disease for at Least 6 Months) of Capecitabine and Lapatinib. -Determine Time to Disease Progression After Treatment With Capecitabine and Lapatinib. -Evaluate Overall

(NCT00496366)
Timeframe: 2 years

Intervention ()
Capecitabine (Xeloda) + Lapatinib (Tykerb)0

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Determine the Response Rate (as Determined by RECIST Criteria) of Capecitabine and Lapatinib as First-line Therapy in Patients With Advanced or Metastatic Breast Cancer That Overexpress HER2.

(NCT00496366)
Timeframe: 2 years

Intervention ()
Capecitabine (Xeloda) + Lapatinib (Tykerb)0

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Time to Treatment Failure (TTF)

Time to treatment failure, TTF, with failure defined as death or disease progression where progression is defined per RECIST criteria as an increase in disease of 20% or more in the sum of longest tumor diameters compared to baseline. (NCT00496587)
Timeframe: 12 months or until progression of disease

InterventionMonths (Median)
Capecitabine + Gemcitabine + Bevacizumab4.2

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Objective Response Rate (ORR)

Objective response defined as Complete Response + Partial Response, with response recorded from the start of treatment until disease progression/recurrence (taking as reference for progressive disease the smallest measurements recorded since the treatment started). Complete Response: The disappearance of all target lesions. Partial Response: >30% decrease in the sum of the longest diameter of target lesions, reference baseline sum longest diameter. Progressive Disease: At least a 20% increase in the sum of the longest diameter of target lesions, taking as reference the smallest sum longest diameter recorded since the treatment started, or the appearance of one or more new lesions. Stable Disease: Neither sufficient shrinkage to qualify for partial response nor sufficient increase to qualify for progressive disease, reference smallest sum longest diameter since the treatment started. (NCT00496587)
Timeframe: 12 months or until progression of disease

Interventionpercentage of participants (Number)
Capecitabine + Gemcitabine + Bevacizumab20

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Progression Free Survival (PFS)

Event or disease-free survival given as progression free survival (PFS) which was defined as the length of time after primary treatment that the participant survives without disease progression. Evaluation of response will follow the Response Evaluation Criteria in Solid Tumors (RECIST) where progression is defined per RECIST criteria as an increase in disease of 20% or more in the sum of longest tumor diameters compared to baseline. (NCT00496587)
Timeframe: 12 months or until progression of disease

InterventionMonths (Median)
Capecitabine + Gemcitabine + Bevacizumab5.5

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Percentage of Participants With an Adverse Event (AE), Serious AE, or Death Due to an AE

The postmarketing safety profile of capecitabine was evaluated by collection of AEs, clinical laboratory data, vital signs, and other findings from physical examination. Abnormalities in these findings were captured as AEs, defined as any untoward medical occurrence in a study participant regardless of the suspected cause. Serious AEs were those which, at any dose, met one or more of the following criteria: resulted in fatality, were life-threatening, necessitated new or prolonged existing hospitalization, produced persistent or significant disability, resulted in congenital anomaly or birth defect, were considered medically significant, or required intervention to prevent any of the aforementioned outcomes. Those specific serious AEs which resulted in fatality were also reported separately. The percentage of participants with an AE, serious AE, or AE resulting in death was calculated as [number of participants with event divided by number analyzed] multiplied by 100. (NCT00502671)
Timeframe: Up to 25 weeks (from Baseline to the end of safety follow-up)

Interventionpercentage of participants (Number)
Any AESerious AEDeath due to an AE
Capecitabine56.16.10.4

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Percentage of Participants With Early Withdrawal or Discontinuation Due to an AE

The postmarketing safety profile of capecitabine was evaluated by collection of AEs, clinical laboratory data, vital signs, and other findings from physical examination. Abnormalities in these findings were captured as AEs, defined as any untoward medical occurrence in a study participant regardless of the suspected cause. The percentage of participants with early withdrawal or treatment discontinuation due to an AE was calculated as [number of participants with event divided by number analyzed] multiplied by 100. (NCT00502671)
Timeframe: Up to 25 weeks (from Baseline to the end of safety follow-up)

Interventionpercentage of participants (Number)
Early withdrawal due to an AEDiscontinuation due to an AE
Capecitabine8.310.1

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6 Month Progression-free Survival for Participants With Glioblastoma

Progression-free Survival (PFS) at 6 months measured as percentage of participants that are alive and progression-free at 6 months (glioblastoma multiforme). A combination of neurological examination and MRI brain scan used to define overall response or progression. (NCT00504660)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Participants With Glioblastoma Multiforme14

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12 Month-progression-free Survival for Participants With Anaplastic Tumors

Progression-free Survival (PFS) at 12 months measured as percentage of participants that are alive and progression-free at 12 months (anaplastic tumors). A combination of neurological examination and MRI brain scan used to define overall response or progression. (NCT00504660)
Timeframe: 12 months

Interventionpercentage of participants (Number)
Participants With Recurrent Anaplastic Glioma44

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Number of Participants With Central Nervous System (CNS) as First Site of Relapse

Number of participants who had Central Nervous System metastasis as the first site of relapse. CT, Magnetic Resonance Imaging, etc. were used for the assessment. (NCT00508274)
Timeframe: Baseline; every 6 weeks for the first 36 weeks and then every 12 weeks until disease progression. The maximum time participants were followed was 90 months

Interventionparticipants (Number)
Participants with any site of relapseParticipants with CNS disease as first site of relapse
Lapatinib + Capecitabine172

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All Collected Deaths

On treatment deaths were collected from the start of treatment up to 30 days after study drug discontinuation, for a maximum duration of 4276 days (treatment duration ranged from 13 - 4246 days) for Lapatinib and 3384 days (treatment duration ranged form 8 - 3354 days) for Capecitabine. Total deaths was collected from study start to study end (LPLV). (NCT00508274)
Timeframe: up to 4276 days for Lapatinib/up to 3384 days for Capecitabine (on-treatment), approx. 12 years (all collected deaths)

InterventionParticipants (Count of Participants)
Total DeathsOn-treatment Deaths
Lapatinib + Capecitabine112

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Time to Response (TTR)

Time to response is defined as the time from first dose date until first documentation of disease response. TTR only applied to participants for whom best overall response was complete response (CR), partial response (PR) or stable disease (SD). Participants who had not had a partial response, complete response or stable disease at the cut-off date for this endpoint analysis were censored for time to response. (NCT00508274)
Timeframe: Baseline; every 6 weeks for the first 36 weeks and then every 12 weeks until disease progression. The maximum time participants were followed was approx. 14.78 months

InterventionMonths (Median)
Lapatinib + Capecitabine4.07

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Six Months Progression-Free Survival

Six Months Progression-Free Survival is defined as the percentage of surviving participants who are progression-free longer than six months (greather than 180 days) after the first start date of study treatment. (NCT00508274)
Timeframe: at Baseline and every 6 weeks for the first 36 weeks and then every 12 weeks until disease progression. The maximum time participants were followed up to 90.38 months, with 6 months PFS reported.

InterventionPercentage of participants (Number)
Lapatinib + Capecitabine53.55

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Progression-Free Survival (PFS)

PFS is defined as the time from first dose date until the date of disease progression or death due to any reason, whichever occurs first. (NCT00508274)
Timeframe: Baseline; every 6 weeks for the first 36 weeks and then every 12 weeks until disease progression. The maximum time participants were followed was 90.38 months.

InterventionMonths (Median)
Lapatinib + Capecitabine6.34

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Duration of Response (DOR)

Duration of response (complete response, partial response or stable disease) is defined as the time of first documentation of disease response until the date of disease progression or death due to breast cancer, whichever occurs first. DOR only applied to participants for whom best overall response was complete response (CR), partial response (PR) or stable disease (SD). Participants who had not had a partial response, complete response or stable disease at the cut-off date for this endpoint analysis were censored for duration of response. (NCT00508274)
Timeframe: Baseline; every 6 weeks for the first 36 weeks and then every 12 weeks until disease progression. The maximum time participants were followed was 88.80 months.

InterventionMonths (Median)
Lapatinib + Capecitabine8.18

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Clinical Benefit Rate (CBR)

"CBR is defined by the percentage of participants achieving either a confirmed tumor response of complete response (CR) or partial response (PR) or stable disease (SD) for at least 24 weeks. Response Criteria in Solid Tumors (RECIST) is a system for measuring tumor shrinkage or progression in terms of the longest dimensions of the tumor on imaging scans such as computerized tomography (CT). A partial response requires a decrease of 30% or more, complete response requires all target lesions disappear, Progression requires an increase of at least 20%, and Stable disease falls in between these two. All responses have a repeat assessment to confirm the response." (NCT00508274)
Timeframe: Baseline; every 6 weeks for the first 36 weeks and then every 12 weeks until disease progression. The maximum time participants were followed was approx. 90 months

InterventionPercentage of participants (Number)
Lapatinib + Capecitabine57.7

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Progression-free Survival

Progression is defined as a measurable increase in the sum of longest diameters of all target lesions, or unequivocable progression of non-target lesions, or the appearance of new lesions, since baseline (NCT00523640)
Timeframe: 60 months

Interventionmonths (Median)
Combination of Gemcitabine, Capecitabine, and Bevacizumab5.3

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Overall Survival

Time from enrollment until death from any cause. (NCT00523640)
Timeframe: 60 months

Interventionmonths (Median)
Combination of Gemcitabine, Capecitabine, and Bevacizumab9.8

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Objective Response Rate

Per RECIST Criteria (V1.0) using standard cross-sectional CT scanning: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Response (R)= CR + PR. (NCT00523640)
Timeframe: 12 weeks

Interventionproportion (Number)
Combination of Gemcitabine, Capecitabine, and Bevacizumab0.24

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PFS

PFS is defined as the time from the initial treatment until the first observation of disease progression or death due to any cause. The date of documented disease progression was defined as the earliest date of radiographic disease assessment progression or symptomatic progression, whichever came first. For participants who did not die/progress, survival was censored at the time of the last assessment (or contact). (NCT00526669)
Timeframe: From Baseline (Day 0) until disease progression or death due to any cause (up to approximately 85 weeks)

Interventionweeks (Median)
Lapatinib + Capecitabine14.3

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Response Rate (Measured as the Percentage of Participants With Response [Complete Response or Partial Response])

Response is defined as documented evidence of complete response (CR) or partial response (PR). The investigator evaluated response based on Response Evaluation Criteria in Solid Tumors (RECIST) criteria. Complete response is defined as the disappearance of all target lesions (TLs) and non-TLs and the appearance of no new lesions (NLs). Partial response for TLs is defined as >= a 30% decrease in the sum of the longest diameter (LD) of TLs, taking as a reference the Baseline sum LD. For non-TLs it is defined as the persistence of 1 or more non-TL and no new TLs or non-TLs. (NCT00526669)
Timeframe: From Baseline (Day 0) until disease progression or death due to any cause evaluated every 6 or 12 weeks (up to approximately 85 weeks)

Interventionpercentage of participants (Number)
Lapatinib + Capecitabine17.9

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Creatinine at the Indicated Time Points

Blood samples were collected for the evaluation of creatinine. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For creatinine: G 1 (>ULN to 1.5x ULN), mild; G 2 (>1.5 to 3.0x ULN), moderate; G 3 (>3.0 to 6.0x ULN), severe; G 4 (>6.0x ULN), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=54Week 2, AGI; n=56Week 3, AGI; n=61Week 6, AGI; n=47Week 9, AGI; n=40Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=14Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84 AGI; n=1WD/study conclusion, AGI; n=50Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=54Week 2, ItoG3; n=56Week 3, ItoG3; n=61Week 6, ItoG3; n=47Week 9, ItoG3; n=40Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=14Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=50Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=54Week 2, ItoG4; n=56Week 3, ItoG4; n=61Week 6, ItoG4; n=47Week 9, ItoG4; n=40Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=14Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=50Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine211101020000100000003600000000000000000000000000000000000000000000

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Potassium at the Indicated Time Points

Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For potassium (high and low [per blood samples], respectively): G 1 (>ULN to 5.5 millimoles per liter [mmol/L]; 5.5 to 6.0 mmol/L; value not available), moderate; G 3 (>6.0 to 7.0 mmol/L; <3.0 to 2.5 mmol/L), severe; G 4 (>7.0 mmol/L; <2.5 mmol/L), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=54Week 2, AGI; n=54Week 3, AGI; n=59Week 6, AGI; n=46Week 9, AGI; n=41Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=13Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1WD/study conclusion, AGI; n=48Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=54Week 2, ItoG3; n=54Week 3, ItoG3; n=59Week 6, ItoG3; n=46Week 9, ItoG3; n=41Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=13Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=48Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=54Week 2, ItoG4; n=54Week 3, ItoG4; n=59Week 6, ItoG4; n=46Week 9, ItoG4; n=41Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=13Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=48Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine9353441210200000000072510100000000000000000250000100000000000000001

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Number of Participants With Change From Baseline (Measured as Any Grade Increase [AGI], Increase to Grade 3 [ItoG3], and Increase to Grade 4 [ItoG4]) in Toxicity Grades for Albumin at the Indicated Time Points

Toxicity was measured in grades (AE severity) per National Cancer Institute Common Toxicity Criteria for Adverse Event (NCI CTCAE) version (v) 3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For albumin (per blood samples): G 1 (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=54Week 2, AGI; n=57Week 3, AGI; n=61Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=14Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1Withdrawal /study conclusion, AGI; n=50Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=54Week 2, ItoG3; n=57Week 3, ItoG3; n=61Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=14Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=50Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=54Week 2, ItoG4; n=57Week 3, ItoG4; n=61Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=14Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=50Worst-case on-therapy ItoG4; n=65
Lapatinib + Capecitabine1091042431110000010000112900000000000000000000000000000000000000000000

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Lymphocytes at the Indicated Time Points

Blood samples were collected for the evaluation of lymphocytes. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For lymphocytes: G 1, mild; G 2, moderate; G 3, severe; G 4, life threatening/disabling; G 5, death related to AE; ranges were provided by local laboratories. Change from Baseline was measured as any grade increase (AGI), increase to G 3 (ItoG3), and increase to G 4 (ItoG4). Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=14Week 2, AGI; n=16Week 3, AGI; n=16Week 6, AGI; n=12Week 9, AGI; n=11Week 12, AGI; n=7Week 15, AGI; n=6Week 18, AGI; n=5Week 21, AGI; n=4Week 24, AGI; n=3Week 30, AGI; n=2Week 36, AGI; n=1Week 42, AGI; n=0Week 48, AGI; n=0Week 54, AGI; n=0Week 60, AGI; n=0Week 66, AGI; n=0Week 72, AGI; n=0Week 78, AGI; n=0Week 84, AGI; n=0Withdrawal/study conclusion, AGI; n=10Worst-case on-therapy, AGI; n=16Week 1, ItoG3; n=14Week 2, ItoG3; n=16Week 3, ItoG3; n=16Week 6, ItoG3; n=12Week 9, ItoG3; n=11Week 12, ItoG3; n=7Week 15, ItoG3; n=6Week 18, ItoG3; n=5Week 21, ItoG3; n=4Week 24, ItoG3; n=3Week 30, ItoG3; n=2Week 36, ItoG3; n=1Week 42, ItoG3; n=0Week 48, ItoG3; n=0Week 54, ItoG3; n=0Week 60, ItoG3; n=0Week 66, ItoG3; n=0Week 72, ItoG3; n=0Week 78, ItoG3; n=0Week 84, ItoG3; n=0Withdrawal/study conclusion, ItoG3; n=10Worst-case on-therapy, ItoG3; n=16Week 1, ItoG4; n=14Week 2, ItoG4; n=16Week 3, ItoG4; n=16Week 6, ItoG4; n=12Week 9, ItoG4; n=11Week 12, ItoG4; n=7Week 15, ItoG4; n=6Week 18, ItoG4; n=5Week 21, ItoG4; n=4Week 24, ItoG4; n=3Week 30, ItoG4; n=2Week 36, ItoG4; n=1Week 42, ItoG4; n=0Week 48, ItoG4; n=0Week 54, ItoG4; n=0Week 60, ItoG4; n=0Week 66, ItoG4; n=0Week 72, ItoG4; n=0Week 78, ItoG4; n=0Week 84, ItoG4; n=0Withdrawal/study conclusion, ItoG4; n=10Worst-case on-therapy, ItoG4; n=16
Overall Study Arm000000002000000000001300000000000000000000000000000000000000000000

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Magnesium at the Indicated Time Points

Blood samples were collected for magnesium evaluation. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For magnesium (high and low, respectively): G 1 (>ULN to 3.0 mg/dL; 3.0 to 8.0 mg/dL; <0.9 to 0.7 mg/dL), severe; G 4 (>8.0 mg/dL; <0.7 mg/dL), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=33Week 2, AGI; n=33Week 3, AGI; n=44Week 6, AGI; n=37Week 9, AGI; n=36Week 12, AGI; n=27Week 15, AGI; n=18Week 18, AGI; n=16Week 21, AGI; n=11Week 24, AGI; n=9Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=2Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1WD/study conclusion, AGI; n=35Worst-case on-therapy, AGI; n=59Week 1, ItoG3; n=33Week 2, ItoG3; n=33Week 3, ItoG3; n=44Week 6, ItoG3; n=37Week 9, ItoG3; n=36Week 12, ItoG3; n=27Week 15, ItoG3; n=18Week 18, ItoG3; n=16Week 21, ItoG3; n=11Week 24, ItoG3; n=9Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=2Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=35Worst-case on-therapy, ItoG3; n=59Week 1, ItoG4; n=33Week 2, ItoG4; n=33Week 3, ItoG4; n=44Week 6, ItoG4; n=37Week 9, ItoG4; n=36Week 12, ItoG4; n=27Week 15, ItoG4; n=18Week 18, ItoG4; n=16Week 21, ItoG4; n=11Week 24, ItoG4; n=9Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=2Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=35Worst-case on-therapy, ItoG4; n=59
Lapatinib + Capecitabine1634101100000000000061700010000000000000000120000000000000000000000

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Duration of Response

Duration of response is defined as the time from the first documented evidence of tumor response (CR or PR) until the first documented sign of disease progression or death due to any cause, whichever came first. (NCT00526669)
Timeframe: From date of first documented evidence of response until the date of first documented sign of disease progression or death due to any cause (up to approximately 78 weeks)

Interventionweeks (Median)
Lapatinib + Capecitabine18.4

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Platelet Count at the Indicated Time Points

Blood samples were collected for the evaluation of platelet count. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For platelet count: G 1 (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=62Week 2, AGI; n=64Week 3, AGI; n=62Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=30Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=13Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1Withdrawal/study conclusion, AGI; n=51Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=62Week 2, ItoG3; n=64Week 3, ItoG3; n=62Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=30Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=13Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1Withdrawal/study conclusion, ItoG3; n=51Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=62Week 2, ItoG4; n=64Week 3, ItoG4; n=62Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=30Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=13Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1Withdrawal/study conclusion, ItoG4; n=51Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine1202322010200000000041000000000000000000000010000000000000000000000

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Sodium at the Indicated Time Points

Blood samples were collected for sodium evaluation. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of each AE severity. For sodium (high and low, respectively): G 1 (>ULN to 150 mmol/L; 150 to 155 mmol/L; value not available), moderate; G 3 (>155 to 160 mmol/L; <130 to 120 mmol/L), severe; G 4 (>160 mmol/L; <120 mmol/L), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=54Week 2, AGI; n=53Week 3, AGI; n=59Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=13Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1WD/study conclusion, AGI; n=48Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=54Week 2, ItoG3; n=53Week 3, ItoG3; n=59Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=13Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=48Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=54Week 2, ItoG4; n=53Week 3, ItoG4; n=59Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=13Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=48Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine97574131012000000000102801001000001000000000241000000000000000000001

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Total Bilirubin at the Indicated Time Points

Blood samples were collected for the evaluation of total bilirubin. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For total bilirubin: G 1 (>ULN to 1.5x ULN), mild; G 2 (>1.5 to 3.0x ULN), moderate; G 3 (>3.0 to 10.0x ULN), severe; G 4 (>10.0x ULN), life threatening/disabling; G 5 (value not available), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=54Week 2, AGI; n=57Week 3, AGI; n=61Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=14Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1WD/study conclusion, AGI; n=50Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=54Week 2, ItoG3; n=57Week 3, ItoG3; n=61Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=14Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3I; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=50Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=54Week 2, ItoG4; n=57Week 3, ItoG4; n=61Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=14Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=50Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine0212833233411100010141300000000000000000000110000000000000000000000

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Time to Progression (All Deaths Are Treated as Competing Risk)

Time to progression is defined as the time from the initial treatment (first dose) until the first documented radiological symptomatic sign of disease progression. Time to progression data are presented as cumulative incidence estimate, which is defined as the time from the initial treatment until crude hazard probability of the occurrence of a particular event is reached to a particular point. All factors that hinder the observation of the event are defined as competing risks. (NCT00526669)
Timeframe: From Baseline (Day 0) until disease progression or death due to any cause (up to approximately 85 weeks)

Interventionweeks (Median)
Lapatinib + Capecitabine18.9

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Time to Progression (All Deaths Due to Non-PD Are Treated as Competing Risk)

Time to progression is defined as the time from the initial treatment (first dose) until the first documented radiological symptomatic sign of disease progression. Time to progression data are presented as cumulative incidence estimate, which is defined as the time from the initial treatment until crude hazard probability of occurrence of a particular event is reached to a particular point. All factors that hinder the observation of the event are defined as competing risks. (NCT00526669)
Timeframe: From Baseline (Day 0) until disease progression or death due to any cause (up to approximately 85 weeks)

Interventionweeks (Median)
Lapatinib + Capecitabine14.3

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Total Neutrophils at the Indicated Time Points

Blood samples were collected for the evaluation of total neutrophils. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For neutrophils: G 1 (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=15Week 2, AGI; n=17Week 3, AGI; n=17Week 6, AGI; n=12Week 9, AGI; n=11Week 12, AGI; n=7Week 15, AGI; n=6Week 18, AGI; n=5Week 21, AGI; n=4Week 24, AGI; n=3Week 30, AGI; n=2Week 36, AGI; n=1Week 42, AGI; n=0Week 48, AGI; n=0Week 54, AGI; n=0Week 60, AGI; n=0Week 66, AGI; n=0Week 72, AGI; n=0Week 78, AGI; n=0Week 84, AGI; n=0Withdrawal/study conclusion,, AGI; n=12Worst-case on-therapy, AGI; n=17Week 1, ItoG3; n=15Week 2, ItoG3; n=17Week 3, ItoG3; n=17Week 6, ItoG3; n=12Week 9, ItoG3; n=11Week 12, ItoG3; n=7Week 15, ItoG3; n=6Week 18, ItoG3; n=5Week 21, ItoG3; n=4Week 24, ItoG3; n=3Week 30, ItoG3; n=2Week 36, ItoG3; n=1Week 42, ItoG3; n=0Week 48, ItoG3; n=0Week 54, ItoG3; n=0Week 60, ItoG3; n=0Week 66, ItoG3; n=0Week 72, ItoG3; n=0Week 78, ItoG3; n=0Week 84, ItoG3; n=0Withdrawal/study conclusion, ItoG3; n=12Worst-case on-therapy, ItoG3; n=17Week 1, ItoG4; n=15Week 2, ItoG4; n=17Week 3, ItoG4; n=17Week 6, ItoG4; n=12Week 9, ItoG4; n=11Week 12, ItoG4; n=7Week 15, ItoG4; n=6Week 18, ItoG4; n=5Week 21, ItoG4; n=4Week 24, ItoG4; n=3Week 30, ItoG4; n=2Week 36, ItoG4; n=1Week 42, ItoG4; n=0Week 48, ItoG4; n=0Week 54, ItoG4; n=0Week 60, ItoG4; n=0Week 66, ItoG4; n=0Week 72, ItoG4; n=0Week 78, ItoG4; n=0Week 84, ItoG4; n=0Withdrawal/study conclusion, ItoG4; n=12Worst-case on-therapy, ItoG4; n=17
Lapatinib + Capecitabine011111112000000000001300000000000000000000000000000000000000000000

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Overall Survival (OS)

Overall survival is defined as the time from the initial treatment until death due to any cause. A death occurring during the study is defined as a death occurring during treatment or within 30 days of the last administration of study medication. (NCT00526669)
Timeframe: From Baseline (Day 0) until death due to any cause evaluated at approximately 12 months (up to approximately 100 weeks)

Interventionweeks (Median)
Lapatinib + Capecitabine27.6

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Time to Response

Time to response is defined as the time from the initial treatment until the first documented evidence of CR (disappearance of all TLs and non-TLs and the appearance of no new lesions) or PR (>= a 30% decrease in the sum of the longest diameter of TLs, taking as reference the Baseline sum longest diameter) (whichever status was recorded first). Time to response data are presented as cumulative incidence estimate, which is defined as the time from the initial treatment until crude hazard probability of the occurrence of a particular event is reached to a particular point. (NCT00526669)
Timeframe: Baseline (Day 0) until first documented evidence of response (up to approximately 60 weeks)

Interventionweeks (Median)
Lapatinib + CapecitabineNA

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Change From Start of Run-in Period in Biomarker Expression Levels at Day 0

Participants were analyzed for intratumoral expression levels of genes involved in the 5-fluorouracil (FU) pathway and lapatinib-targeted genes. Change in biomarker expression levels was calculated as the levels measured after the lapatinib Run-in Period (Baseline) of the study minus the levels measured at the start of monotherapy (Day -7). EGFR, epidermal growth factor receptor; HER, human epidermal growth factor receptor. Data are presented as ratios of the normalized gene expression of the target gene to that of beta actin. (NCT00526669)
Timeframe: evaluated at baseline and after 7 days of study treatment

Interventionratio (Median)
Thymidylate synthase (TS), n=34Deoxypyridinoline (DPD), n=26EGFR/HER1, n=32HER2, n=28HER3, n=33
Lapatinib0.380.120.150.010.87

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Number of Participants in the Indicated Categories for Best Overall Response (BOR)

Best overall response was evaluated by the investigator based on RECIST criteria: CR; PR; Stable Disease (SD), defined as no sufficient shrinkage to qualify for PR, no sufficient increase to qualify for progressive disease (PD), taking as reference the smallest sum LD since the treatment started; PD, defined as at least a 20% increase in the sum of the LD of target lesions, taking as a reference the smallest sum LD recorded since the treatment started or the appearance of >= 1 new lesions; Unknown, defined as participants who do not have CR, PR, SD, or PD. (NCT00526669)
Timeframe: From Baseline (Day 0) until disease progression or death due to any cause (up to approximately 85 weeks)

Interventionparticipants (Number)
CRPRSDPDUnknown
Lapatinib + Capecitabine01231168

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4 ) in Toxicity Grades for Alanine Aminotransferase (ALT) at the Indicated Time Points

Blood samples were collected for the evaluation of ALT. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For ALT: G 1 (>ULN to 2.5x ULN), mild; G 2 (>2.5 to 5.0x ULN), moderate; G 3 (>5.0 to 20.0x ULN), severe; G 4 (>20.0x ULN), life threatening/disabling; G 5 (value not available), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=54Week 2, AGI; n=57Week 3, AGI; n=61Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=14Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1WD/study conclusion, AGI; n=50Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=54Week 2, ItoG3; n=57Week 3, ItoG3; n=61Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=14Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3I; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=50Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=54Week 2, ItoG4; n=57Week 3, ItoG4; n=61Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=14Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=50Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine1023222000000000000001000000000000000000000110000000000000000000000

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Alkaline Phosphatase (ALP) at the Indicated Time Points

Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For ALP: G 1 (upper limit of normal [ULN] to 2.5x ULN), mild; G 2 (>2.5 to 5.0x ULN), moderate; G 3 (>5.0 to 20.0x ULN), severe; G 4 (>20.0x ULN), life threatening/disabling; G 5 (value not available), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=54Week 2, AGI; n=57Week 3, AGI; n=61Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=14Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=2Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1WD/study conclusion, AGI; n=49Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=54Week 2, ItoG3; n=57Week 3, ItoG3; n=61Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=14Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=2Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=49Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=54Week 2, ItoG4; n=57Week 3, ItoG4; n=61Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=14Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=2Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=49Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine6585252344311121111182100000000100000000000120000000000000000000000

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Aspartate Aminotransferase (AST) at the Indicated Time Points

Blood samples were collected for the evaluation of AST. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For AST: G 1 (>ULN to 2.5x ULN), mild; G 2 (>2.5 to 5.0x ULN), moderate; G 3 (>5.0 to 20.0x ULN), severe; G 4 (>20.0x ULN), life threatening/disabling; G 5 (value not available), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=54Week 2, AGI; n=57Week 3, AGI; n=61Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=14Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1WD/study conclusion, AGI; n=50Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=54Week 2, ItoG3; n=57Week 3, ItoG3; n=61Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=14Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3I; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=50Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=54Week 2, ItoG4; n=57Week 3, ItoG4; n=61Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=14Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=50Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine1336324110200000000171600000000000000000000110000000000000000000000

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Calcium at the Indicated Time Points

Blood samples were collected for calcium evaluation. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For calcium (low and high, respectively): G 1 (ULN to 11.5x ULN), mild; G 2 (<8.0 to 7.0 mg/dL; >11.5 to 12.5 ULN), moderate; G 3 (<7.0 to 6.0 mg/dL; >12.5 to 13.5 mg/dL), severe; G 4 (<6 mg/dL; >13.5 mg/dL), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=55Week 2, AGI; n=56Week 3, AGI; n=60Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=14Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=2Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1WD/study conclusion, AGI; n=49Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=55Week 2, ItoG3; n=56Week 3, ItoG3; n=60Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=14Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=2Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=49Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=55Week 2, ItoG4; n=56Week 3, ItoG4; n=60Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=14Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=2Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=49Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine74533212011010120001122300000000000000000000000000000000000000000000

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Glucose at the Indicated Time Points

Blood samples were collected for the evaluation of glucose. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For glucose (high and low, respectively): G 1 (>ULN to 160 mg/dL; 160 to 250 mg/dL; <55 to 40 mg/dL), moderate; G 3 (>250 to 500 mg/dL; <40 to 30 mg/dL), severe; G 4 (>500 mg/dL; <30 mg/dL), life threatening/disabling; G 5 (death), death related to AE. Worst-case on-therapy reflects the most severe change at any time point measured post treatment. (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=54Week 2, AGI; n=57Week 3, AGI; n=61Week 6, AGI; n=47Week 9, AGI; n=40Week 12, AGI; n=31Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=14Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1WD/study conclusion, AGI; n=49Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=54Week 2, ItoG3; n=57Week 3, ItoG3; n=61Week 6, ItoG3; n=47Week 9, ItoG3; n=40Week 12, ItoG3; n=31Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=14Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1WD/study conclusion, ItoG3; n=49Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=54Week 2, ItoG4; n=57Week 3, ItoG4; n=61Week 6, ItoG4; n=47Week 9, ItoG4; n=40Week 12, ItoG4; n=31Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=14Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1WD/study conclusion, ItoG4; n=49Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine13101076431120100100000153200000000000000000000110000000000000000000000

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for Hemoglobin at the Indicated Time Points

Blood samples were collected for the evaluation of hemoglobin. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For hemoglobin: G 1 (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=62Week 2, AGI; n=64Week 3, AGI; n=62Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=30Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=13Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1Withdrawal/study conclusion, AGI; n=51Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=62Week 2, ItoG3; n=64Week 3, ItoG3; n=62Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=30Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=13Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1Withdrawal/study conclusion, ItoG3; n=51Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=62Week 2, ItoG4; n=64Week 3, ItoG4; n=62Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=30Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=13Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1Withdrawal/study conclusion, ItoG4; n=51Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine101612107652433000000000163300010010000000000000590000010000000000000001

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Number of Participants With Change From Baseline (Measured as AGI, ItoG3, and ItoG4) in Toxicity Grades for White Blood Cell (WBC) Count at the Indicated Time Points

Blood samples were collected for the evaluation of WBC count. Toxicity was measured in grades (AE severity) per NCI CTCAE, v3.0, displaying Grades (G) 1-5 with unique clinical descriptions of the severity of each AE. For WBCs: G 1 (NCT00526669)
Timeframe: Baseline (Day 0); Weeks 1, 2, 3, 6, 9, 12, 15, 18, 21, 24, 30, 36, 42, 48, 54, 60, 66, 72, 78, and 84; withdrawal (WD)/study conclusion (up to approximately 87 weeks); and worst-case on-therapy

Interventionparticipants (Number)
Week 1, AGI; n=62Week 2, AGI; n=64Week 3, AGI; n=62Week 6, AGI; n=47Week 9, AGI; n=41Week 12, AGI; n=30Week 15, AGI; n=22Week 18, AGI; n=17Week 21, AGI; n=13Week 24, AGI; n=11Week 30, AGI; n=9Week 36, AGI; n=5Week 42, AGI; n=4Week 48, AGI; n=3Week 54, AGI; n=3Week 60, AGI; n=2Week 66, AGI; n=1Week 72, AGI; n=1Week 78, AGI; n=1Week 84, AGI; n=1Withdrawal/study conclusion, AGI; n=51Worst-case on-therapy, AGI; n=65Week 1, ItoG3; n=62Week 2, ItoG3; n=64Week 3, ItoG3; n=62Week 6, ItoG3; n=47Week 9, ItoG3; n=41Week 12, ItoG3; n=30Week 15, ItoG3; n=22Week 18, ItoG3; n=17Week 21, ItoG3; n=13Week 24, ItoG3; n=11Week 30, ItoG3; n=9Week 36, ItoG3; n=5Week 42, ItoG3; n=4Week 48, ItoG3; n=3Week 54, ItoG3; n=3Week 60, ItoG3; n=2Week 66, ItoG3; n=1Week 72, ItoG3; n=1Week 78, ItoG3; n=1Week 84, ItoG3; n=1Withdrawal/study conclusion, ItoG3; n=51Worst-case on-therapy, ItoG3; n=65Week 1, ItoG4; n=62Week 2, ItoG4; n=64Week 3, ItoG4; n=62Week 6, ItoG4; n=47Week 9, ItoG4; n=41Week 12, ItoG4; n=30Week 15, ItoG4; n=22Week 18, ItoG4; n=17Week 21, ItoG4; n=13Week 24, ItoG4; n=11Week 30, ItoG4; n=9Week 36, ItoG4; n=5Week 42, ItoG4; n=4Week 48, ItoG4; n=3Week 54, ItoG4; n=3Week 60, ItoG4; n=2Week 66, ItoG4; n=1Week 72, ItoG4; n=1Week 78, ItoG4; n=1Week 84, ItoG4; n=1Withdrawal/study conclusion, ItoG4; n=51Worst-case on-therapy, ItoG4; n=65
Lapatinib + Capecitabine5965374331322110000021700000100000000000000010000000000000000000000

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Percentage of Participants (Par.) With 5-month Progression-free Survival (PFS)

5-month (mo.) PFS was defined as the percentage of par. who were alive/progression free for 5 months from the time of initial treatment. PFS is defined as the time from the initial treatment until the first observation of disease progression (DP)/death due to any cause; the percentage of par. whose follow-up ended or was ongoing was reported. DP is defined as symptomatic progression or the appearance of >=1 NL and/or unequivocal progression of existing non-TLs, and a >=20% increase in the sum of the LD of TLs, taking as a reference the smallest sum LD recorded since treatment started. (NCT00526669)
Timeframe: From initial treatment up to 24 weeks (next available assessment after the 5-month assessment for progressive disease)

Interventionpercentage of participants (Number)
Lapatinib + Capecitabine29

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Number of Participants With Baseline Shift From Normal to Low or High in Blood Chemistry Parameters

For blood chemistry, the parameters assessed were: Sodium, potassium, calcium, magnesium, chloride, bicarbonate, total protein, albumin, alkaline phosphatase, alanine transaminase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), Lactate dehydrogenase (LDH), total bilirubin, direct bilirubin, indirect bilirubin, creatinine (serum creatinine or creatinine clearance), glucose. (NCT00532948)
Timeframe: Up to 06 years

,,
InterventionParticipants (Number)
Lactic dehydrogenase, normal to low, n=0,0,0Lactic dehydrogenase, normal to high, n=0,0,0Indirect bilirubin, normal to low, n=1,1,1Indirect bilirubin, normal to high, n=1,1,1BUN, normal to low, n=3,1,5BUN, normal to high, n=3,1,5Alkaline phosphatase, normal to low, n=1,1,4Alkaline phosphatase, normal to high, n=1,1,4Direct blirubin, normal to low, n=2,1,1Direct bilirubin, normal to high, n=2,1,1Total bilirubin, normal to low, n=4,2,6Total bilirubin, normal to high, n=4,2,6Fasting glucose, normal to low, n=1,0,4Fasting glucose, normal to high, n=1,0,4Protein, normal to low, n=1,0,2Protein, normal to high, n=1,0,2Serum albumin, normal to low, n=3,1,5Serum albumin, normal to high, n=3,1,5Serum creatinine, normal to low, n=4,2,6Serum creatinine, normal to high, n=4,2,6ASAT (SGOT), normal to low, n=1,0,4ASAT (SGOT), normal to high, n=1,0,4ALAT (SGPT), normal to low, n=4,2,6ALAT (SGPT), normal to high, n=4,2,6Calcium, normal to low, n=3, 1,5Calcium, normal to high, n=3,1,5Phosphate, normal to low, n=3,1,5Phosphate, normal to high, n=3,1,5Potassium, normal to low, n=3, 1,5Potassium, normal to high, n=3,1,5Sodium, normal to low, n=3,1,5Sodium, normal to high, n=3,1,5Magnesium, normal to low, n=3,1,5Magnesium, normal to high, n=3,1,5Chloride, normal to low, n=3,1,5Chloride, normal to high, n=3,1,5Bicarbonate, normal to low, n=3,0,5Bicarbonate, normal to high, n=3,0,5
Capecitabine 500 mg/m^200000000000000102000000210102010010000
Capecitabine 650 mg/m^200010100000000000000000210000110010100
Capecitabine 850 mg/m^200002110000000101002020401110030001103

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Number of Participants With Baseline Shift From Normal to Low or High in Hematology Parameters

For hematology, the parameters assessed were: Hemoglobin, hematocrit, platelet count, RBC, WBC, lymphocytes, monocytes,granulocytes (blasts), neutrophils(segs, bands),eosinophils and basophils. (NCT00532948)
Timeframe: Up to 06 years

,,
InterventionParticipants (Number)
Haematocrit, normal to low, n=3,1,5Haematocrit, normal to high, n=3,1,5Hemoglobin, normal to low, n=4,2,6Hemoglobin, normal to high, n=4,2,6White blood cell, normal to low, n=3,1,5White blood cell, normal to high, n=3,1,5Platelets, normal to low, n=4,2,6Platelets, normal to high, n=4,2,6Red blood cells, normal to low, n=3,1,3Red blood cells, normal to high, n=3,1,3Neutrophils (segmented), normal to low , n=3,0,5Neutrophils (segmented), normal to high, n=3,0,5Basophils (relative), normal to low, n=0,1,2Basophils (relative), normal to high, n=0,1,2Lymphocytes (relative), normal to low, n=3,1,5Lymphocytes (relative), normal to high, n=3,1,5Monocytes (relative), normal to low, n=3,1,4Monocytes (relative), normal to high, n=3,1,4Eosinophils (relative), normal to low, n=1,1,3Eosinophils (relative), normal to high, n=1,1,3
Capecitabine 500 mg/m^220000100200000000100
Capecitabine 650 mg/m^210000110010001000010
Capecitabine 850 mg/m^240200101100002000300

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The Area Under the Plasma Concentration-time Curve From Time of Dosing to the Last Measurable Concentration (AUClast) of Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR, 5-FU and FBAL)

AUC last concentration of capecitabine and its metabolites. Participants who consented to participating in the PK studies were randomized to either sampling series A or Series B. The collection time points included 2 different series, Series A (Baseline [pre-dose], 10 mins, 30 mins, 1, 2.5, 6, 8 and 10 hours after dosing) and Series B (Baseline [pre-dose], 15 minutes, 45 minutes, 1.5, 4, 8 and 10 hours after dosing). (NCT00532948)
Timeframe: Day 1 and Day 14

,,
Interventionh*ng/mL (Mean)
Capecitabine, Day 1, n= 2, 4, 3Capecitabine, Day 14, n=2,2,25'-DFCR, Day 1, n=2,4,35'-DFCR, Day 14, n=2,2,25'-DFUR, Day 1, n=2,4,35'-DFUR, Day 14, n=2,2,25-FU Day 1, n=2,4,35-FU Day 14, n=2,2,2FBAL, Day 1, n=2,4,3FBAL, Day 14, n=2,2,2
Capecitabine 500 mg/m^233702890525043004790424081.618159905720
Capecitabine 650 mg/m^2516096605140925043008010114253811010700
Capecitabine 850 mg/m^23470567041806520665010500271499701010400

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Time to Maximum Plasma Concentration (Tmax) of Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR, 5-FU and FBAL)

Tmax is the corresponding time at which Cmax occurs of capecitabine and its metabolites.Participants who consented to participating in the PK studies were randomized to either sampling series A or Series B. The collection time points included 2 different series, Series A (Baseline [pre-dose], 10 mins, 30 mins, 1, 2.5, 6, 8 and 10 hours after dosing) and Series B (Baseline [pre-dose], 15 minutes, 45 minutes, 1.5, 4, 8 and 10 hours after dosing). (NCT00532948)
Timeframe: Day 1 and Day 14

,,
InterventionHour (Median)
Capecitabine, Day 1, n= 2, 4, 3Capecitabine, Day 14, n=2,2,25'-DFCR, Day 1, n=2,4,35'-DFCR, Day 14, n=2,2,25'-DFUR, Day 1, n=2,4,35'-DFUR, Day 14, n=2,2,25-FU, Day 1, n=2,4,35-FU, Day 14, n=2,2,2FBAL, Day 1, n=2,4,3FBAL, Day 14, n=2,2,2
Capecitabine 500 mg/m^20.581.331.01.4911.511.52.531.74
Capecitabine 650 mg/m^20.630.820.751.180.90.820.750.831.52.2
Capecitabine 850 mg/m^20.850.611.550.611.50.611.511.552.03

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Dose Limiting Toxicities (DLTs)

DLT was defined as any of the following events occurring during the 11 week dose-finding period: any event that leads to interruption of planned radiation for 5 consecutive days or 10 days total; Grade 4 neutropenia or thrombocytopenia; Grade 3 thrombocytopenia that required a platelet transfusion on 2 or more occasions; any Grade 3 or 4 non-hematologic toxicity (with the exception of grade 3 nausea or vomiting of less than 5 days duration, Grade 3 transaminases that returned to baseline value within 7 days of study drug interruption and that did not recur upon re-challenge with study drug, and/or Grade 3 fever or infection of <5 days duration); Grade 2 non-hematologic toxicities that persisted for >7 days and required treatment interruption, or any other capecitabine-related adverse events that required need for dose reduction or permanent cessation of therapy, interruption of study drug for >7 days or recurred on re-challenge with capecitabine rapidly disintegrating tablets (RDTs). (NCT00532948)
Timeframe: Upto 11 weeks

InterventionParticipants (Number)
Capecitabine 500 mg/m^20
Capecitabine 650 mg/m^23
Capecitabine 850 mg/m^23

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Maximum Tolerated Dose (MTD) of Capecitabine.

The MTD was the dose level at which six evaluable patients had been treated and at most one patient experienced a dose limiting toxicity (DLT) and the next highest dose level was too toxic. Dose escalation occurred if 0 out of 3 or at most 1 out of 6 patients experienced DLT while being treated at a dose level; otherwise the dose was declared unsafe and thus above the MTD. (NCT00532948)
Timeframe: Upto 11 weeks.

Interventionmilligrams (Number)
Capecitabine (Overall)650

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Number of Participants With Adverse Events (AE)

An AE is an unfavourable and unintended sign (including an abnormal laboratory finding, for example), symptom, or disease temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. Toxicity was monitored and graded according to the Cancer Therapy Evaluation Program Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. Adverse events that were not included in the CTCAEv3.0 were reported and graded under the other AE within the appropriate category. (NCT00532948)
Timeframe: Up to 06 years

InterventionParticipants (Number)
Capecitabine 500 mg/m^23
Capecitabine 650 mg/m^212
Capecitabine 850 mg/m^26

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Maximum Observed Plasma Concentration (Cmax) of Capecitabine and Its Metabolites (5'-Deoxy-5-Fluorocytidine [5'-DFCR], 5'-Deoxy-5-Fluorouridine [5'-DFUR], 5-Fluorouracil [5-FU] and Alpha-fluoro-beta-alanine [FBAL])

The maximum observed plasma concentration of capecitabine and its metabolites. Participants who consented to participating in the PK studies were randomized to either sampling series A or Series B. The collection time points included 2 different series, Series A (Baseline [pre-dose], 10 mins, 30 mins, 1, 2.5, 6, 8 and 10 hours after dosing) and Series B (Baseline [pre-dose], 15 minutes, 45 minutes, 1.5, 4, 8 and 10 hours after dosing). (NCT00532948)
Timeframe: Day 1 and Day 14

,,
Interventionng/mL (Mean)
Capecitabine, Day 1, n= 2, 4, 3Capecitabine, Day 14, n=2,2,25'-DFCR, Day 1, n=2,4,35'-DFCR, Day 14, n=2,2,25'-DFUR, Day 1, n=2,4,35'-DFUR, Day 14, n=2,2,2FBAL, Day 1, n=2,4,3FBAL, Day 14, n=2,2,2
Capecitabine 500 mg/m^214402100205029801910330013501770
Capecitabine 650 mg/m^230805440219035002640312017402430
Capecitabine 850 mg/m^218903710218032003770502020502140

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Patients Experiencing Severe Symptom Burden (Physical Symptoms)

The subject rates each question about physical symptoms on a scale of 0 through 10, where 0 is not bad and 10 is as bad as possible. Severe symptoms are indicated by a response > or = to 7 on an item. (NCT00534417)
Timeframe: The questionnaire was administered on day 1 of every cycle (approximately every 4 weeks) during study treatment.

Interventionpercentage of participants (Number)
Hives/WeltsSinus problemsSwellingFatigueWeight lossChange in tasteDifficulty hearingReduced sexual enjoyment, interest, or performanceDry eyesTearingTrouble seeingConstipationDecrease in appetiteDiarrheaHeartburnIncrease in appetiteProblem with urinationVaginal drynessBruisingNew lump/massBreast tendernessDry skinHair lossItchingNails changeJoint painMuscle achesWeakness of body partsBurning sensation in hands or feetDaytime sleepinessDizziness/lightheadednessMemory lossNumbness/tinglingTrouble thinkingHeadachePainCoughingShortness of breathWheezing
Capecitabine and Fulvestrant3.33.310.026.710.06.73.310.010.010.016.720.06.73.36.73.33.33.33.36.73.313.33.313.310.026.726.710.010.010.03.36.713.310.06.726.713.36.76.7

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Patients Experiencing Severe Symptom Burden (Psychiatric Symptoms)

The subject rates each question about psychiatric symptoms on a scale of 0 through 10, where 0 is not bad and 10 is as bad as possible. Severe symptoms are indicated by a response > or = to 7 on an item. (NCT00534417)
Timeframe: The questionnaire was administered on day 1 of every cycle (approximately every 4 weeks) during study treatment.

Interventionpercentage of participants (Number)
Crying/feeling like cryingFeeling helplessFeeling hopelessFeeling I would be better off deadLost interest in peopleLost interest in pleasurable activitiesNervous, tense, anxiousSad/depressedWorry
Capecitabine and Fulvestrant10.36.910.33.43.410.313.810.310.3

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Patients Experiencing Severe Symptom Burden (Physical Functioning)

The subject rates each question about physical functioning on a scale of 0 through 10, where 0 is not bad and 10 is as bad as possible. Severe symptoms are indicated by a response > or = to 7 on an item. (NCT00534417)
Timeframe: The questionnaire was administered on day 1 of every cycle (approximately every 4 weeks) during study treatment.

Interventionpercentage of participants (Number)
Attend paid job (N=27)Attend social activityBathe or dress selfCook for selfDriving (N=27)Function normallyHard work or activity (N=27)Household workLight work or activityRun (N=27)Run errandsSit upStay out of bedWalk
Capecitabine and Fulvestrant37.07.110.710.725.914.333.321.410.733.317.910.77.117.9

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Best Overall Response

Best overall response is defined as the best response across all time points. Response was evaluated via changes from baseline in radiological tumor measurements performed after every two treatment cycles and at the end of treatment or time of progression. Response was evaluated using RECIST version 1.0 guidelines, where complete response (CR) is the disappearance of all target lesions; partial response (PR) is >=30% decrease in the sum of the longest diameter (LD) of target lesions; Stable Disease (SD) is neither sufficient shrinkage in sum of LD of target lesions to be PR nor increase of >=20%; Progressive Disease (PD) is the increase in existing lesions or new lesions. (NCT00534417)
Timeframe: Response to treatment was assessed after every 8 weeks of treatment

Interventionparticipants (Number)
Complete response (CR)Partial response (PR)Stable disease (SD)Progressive disease (PD)
Capecitabine and Fulvestrant28283

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Time to Progression (TTP)

Time to progression is defined as the time from treatment start until objective tumor progression. Progression is defined per Response Evaluation Criteria in Solid Tumors (RECIST)v1.0 guidelines as a measurable increase in the smallest diameter of any target lesion, progression of existing non-target lesions, or the appearance of 1 or more new lesions. The median time to progression is the parameter used to describe TTP. (NCT00534417)
Timeframe: TTP was measured from day 1 of treatment until time of progression (assessed every 8 weeks), up to 29 months.

InterventionMonths (Median)
Capecitabine and Fulvestrant26.94

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Clinical Benefit Rate

Clinical benefit rate was defined as the percentage of participants experiencing stable disease (SD) of at least 24 weeks plus complete response (CR) and partial response (PR). Response was evaluated via changes from baseline in radiological tumor measurements performed after every two treatment cycles and at the end of treatment or time of progression. Response was evaluated using RECIST version 1.0 guidelines, where CR is the disappearance of all target lesions; PR is >=30% decrease in the sum of the longest diameter(LD) of target lesions; SD is neither sufficient shrinkage in sum of longest diameter of target lesions to be PR nor increase of >=20%. (NCT00534417)
Timeframe: Response to treatment was assessed after every 8 weeks of treatment

Interventionpercentage of participants (Number)
Capecitabine and Fulvestrant58.5

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Progression-free Survival (PFS)

Disease progression was determined through radiology imaging measurements and by clinical or symptomatic progression during or after treatment. Progression is defined per RECIST v1.0 guidelines as a measurable increase in the smallest diameter of any target lesion, progression of existing non-target lesions, or the appearance of 1 or more new lesions. (NCT00534417)
Timeframe: PFS was measured from day 1 of treatment until time of progression (assessed every 8 weeks) or death, whichever came first, up to 32.5 months.

InterventionMonths (Median)
Capecitabine and Fulvestrant14.98

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Overall Survival (OS)

Overall survival is defined as the time from treatment start until death from any cause. The median overall survival time is used to measure OS. (NCT00534417)
Timeframe: OS was measured from day 1 of treatment until time of death from any cause, up to 32.5 months.

InterventionMonths (Median)
Capecitabine and Fulvestrant28.65

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Overall Response Rate

Overall response rate was defined as the percentage of participants experiencing complete response (CR) and partial response (PR). Response was evaluated via changes from baseline in radiological tumor measurements performed after every two treatment cycles and at the end of treatment or time of progression. Response was evaluated using RECIST version 1.0 guidelines, where complete response (CR) is the disappearance of all target lesions; partial response (PR) is >=30% decrease in the sum of the longest diameter (LD) of target lesions; Stable Disease (SD) is neither sufficient shrinkage in sum of LD of target lesions to be PR nor increase of >=20%; Progressive Disease (PD) is the increase in existing lesions or new lesions. (NCT00534417)
Timeframe: Response to treatment was assessed after every 8 weeks of treatment

Interventionpercentage of participants (Number)
Capecitabine and Fulvestrant24.4

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Overall Response in Phase II

The overall response is defined as the number of participants whose tumor response was classified as a complete response (CR; disappearance of all target lesions) or partial response (PR; 30% decrease in the sum of the longest diameter of target lesions) per Response Evaluation Criteria in Solid Tumors. Response was measured for participants in Phase II only. To determine response, radiographic images were taken at baseline, 8 weeks, and every 8 weeks thereafter until the participant withdrew from the study. (NCT00536809)
Timeframe: Baseline to response (up to 135 days)

Interventionparticipants (Number)
Lap. 1000 mg/Oxaliplatin 130 mg/m^2/Capecitabine 1500 mg/m^22

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Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by spiral CT scan: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00538291)
Timeframe: Assessment after every 2 cycles of treatment, up to 1 year.

Interventionnumber of responding participants (Number)
Arm 11

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Median Number of Treatment Cycles

The first dosing date is defined as the date of the first dose of chemotherapy or capecitabine, whichever was administered first. Cycles are defined as the time from Day 1 of the cycle until the day before the next cycle. The last cycle per participant is the 21-day period following Day 1 of that cycle. (NCT00546364)
Timeframe: Day 1 to end of Cycle 18, maximum (54 weeks)

InterventionTreatment cycles (Median)
Ixabepilone, 40 mg/m^2 + Capecitabine, 1000 mg/m^23.0
Ixabepilone, 32 mg/m^2 + Capecitabine, 1000 mg/m^24.5
Docetaxel, 75 mg/m^2 + Capecitabine, 1000 mg/m^26.0

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Percentage of Nontriple-negative (NTN) Participants With Best Response to Treatment of Complete or Partial Per Cohort

The tumor response rate is defined as the total number of participants whose best response is CR or PR, divided by the number of randomized participants. Participants not evaluable for response are considered to be nonresponders. NTN participants are who are not TN participants (TN participants are those with tumors that do not express estrogen or progesterone receptors and that do not overexpress HER2) and who received ixabepilone plus capecitabine or docetaxel plus capecitabine. (NCT00546364)
Timeframe: Baseline to 6 weeks (end of Cycle 2)

InterventionPercentage of NTN Participants (Number)
Ixabepilone, 40 mg/m^2 + Capecitabine, 1000 mg/m^233
Ixabepilone, 32 mg/m^2 + Capecitabine, 1000 mg/m^254
Docetaxel, 75 mg/m^2 + Capecitabine, 1000 mg/m^242

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Percentage of Participants With Best Response to Treatment of Complete or Partial

The tumor response rate is defined as the number of participants with a best tumor response of CR or PR (as assessed by the investigator according to RECIST criteria), divided by the number of participants randomized in that arm. (NCT00546364)
Timeframe: Baseline to 6 weeks (end of Cycle 2)

InterventionPercentage of patients (Number)
Ixabepilone, 40 mg/m^2 + Capecitabine, 1000 mg/m^235
Ixabepilone, 32 mg/m^2 + Capecitabine, 1000 mg/m^241
Docetaxel, 75 mg/m^2 + Capecitabine, 1000 mg/m^230

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Percentage of Triple-negative (TN) Participants With Best Response to Treatment of Complete or Partial

The tumor response rate is defined as the total number of participants whose best response is CR or PR, divided by the number of randomized participants. Participants not evaluable for response are considered to be nonresponders. TN participants are those with tumors that do not express estrogen or progesterone receptors and that do not over express human epidermal growth factor receptor 2 (HER2). (NCT00546364)
Timeframe: Baseline to 6 weeks (end of Cycle 2)

InterventionPercentage of TN Participants (Number)
Ixabepilone, 40 mg/m^2 + Capecitabine, 1000 mg/m^238
Ixabepilone, 32 mg/m^2 + Capecitabine, 1000 mg/m^222
Docetaxel, 75 mg/m^2 + Capecitabine, 1000 mg/m^213

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Number of Participants With Abnormalities in Hematology Laboratory Results by Worst Common Terminology Criteria (CTC) Grade

CTC Grade 1=Mild; asymptomatic or mild symptoms; clinical or diagnostic observations only; intervention not indicated. Grade 2=Moderate; minimal, local or noninvasive intervention indicated. Grade 3=Severe or medically significant but not immediately life-threatening; hospitalization or prolongation of hospitalization indicated; disabling. Grade 4=Life-threatening consequences; urgent intervention indicated. (NCT00546364)
Timeframe: Baseline in Cycle 1 (21 days) and then prior to start of each 21-day cycle

,,
InterventionParticipants (Number)
Neutropenia (Grades 1-4)Neutropenia (Grade 3 or 4)Leukopenia (Grades 1-4)Leukopenia (Grade 3 or 4)Thrombocytopenia (Grades 1-4)Thrombocytopenia (Grade 3 or 4)Anemia (Grades 1-4)Anemia (Grade 3 or 4)
Docetaxel, 75 mg/m^2 + Capecitabine, 1000 mg/m^21715171270170
Ixabepilone, 32 mg/m^2 + Capecitabine, 1000 mg/m^21510199111211
Ixabepilone, 40 mg/m^2 + Capecitabine, 1000 mg/m^2181220990180

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Number of Participants With Best Tumor Response as Assessed With Response Evaluation Criteria in Solid Tumors (RECIST)

RECIST definitions: Complete reponse (CR)=disappearance of all nontarget lesions; partial response (PR)=at least 30% reduction in the sum of the longest diameter (LD) of all target lesions in reference to the baseline sum LD; stable disease (SD)=neither PR nor progressive disease (PD) criteria were met; PD=at least 20% increase in the sum of the LD of all target lesions, taking as reference the smallest sum LD recorded at or following baseline. Tumor status assessed by investigator. (NCT00546364)
Timeframe: Baseline to 6 weeks (end of Cycle 2)

,,
InterventionParticipants (Number)
Complete response (CR)Partial response (PR)Stable disease (SD)Progressive disease (PD)Discontinued before first tumor assessmentNo tumor assessment due to other reasonsUnable to determine
Docetaxel, 75 mg/m^2 + Capecitabine, 1000 mg/m^20639110
Ixabepilone, 32 mg/m^2 + Capecitabine, 1000 mg/m^21839001
Ixabepilone, 40 mg/m^2 + Capecitabine, 1000 mg/m^21664300

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Number of Participants With Abnormalities in Serum Chemistry Laboratory Results

ULN=Upper limit of normal among all laboratory ranges. Alanine aminotransferase (ALT) Grade 1:>ULN to 2.5*ULN; Grade 2: >2.5 to 5.0*ULN; Grade 3: >5.0 to 20.0*ULN; Grade 4: >20.0*ULN. Aspartate aminotransferase (AST) Grade 1: >ULN to 2.5*ULN; Grade 2: >2.5 to 5.0*ULN; Grade 3: >5.0 to 20.0*ULN; Grade 4: >20.0*ULN. Total bilirubin Grade 1: >ULN to 1.5*ULN; Grade 2: >1.5 to 3.0*ULN; Grade 3: >3.0 to 10.0*ULN; Grade 4: >10.0*ULN. Creatine Grade 1: >ULN to 1.5*ULN; Grade 2: 1.5 to 3.0*ULN; Grade 3: >3.0 to 6.0*ULN; Grade 4: >6.0*ULN. (NCT00546364)
Timeframe: Baseline in Cycle 1 (21 days) and then prior to start of each 21-day cycle

,,
InterventionParticipants (Number)
ALT, high (Grades 1-4)ALT, high (Grade 3 or 4)AST, high (Grades 1-4)AST, high (Grade 3 or 4)Total bilirubin, high (Grades 1-4)Total bilirubin, high (Grade 3 or 4)Creatinine, high (Grades 1-4)Creatinine, high (Grade 3 or 4)
Docetaxel, 75 mg/m^2 + Capecitabine, 1000 mg/m^250500020
Ixabepilone, 32 mg/m^2 + Capecitabine, 1000 mg/m^230501010
Ixabepilone, 40 mg/m^2 + Capecitabine, 1000 mg/m^240700010

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Overall Survival

The primary efficacy endpoint for this study was overall survival (time to death), defined as the time between randomization and the date of death irrespective of the cause of death. Patients for whom no death was captured on the clinical database were censored at the most recent date they were known to be alive. Median survival was estimated by the Kaplan-Meier method. (NCT00548548)
Timeframe: From randomization until death, up to 26 months

Interventionmonths (Median)
Bevacizumab12.1
Placebo10.1

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Participants With Adverse Events

The intensity of Adverse Events (AEs) was graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE), Version 3.0 on a five-point scale from Grade 1 (Mild) to Grade 5 (Death). A serious AE (SAE) was defined as any event that is fatal, life-threatening, requires in-patient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect, is medically significant or requires intervention to prevent one or other of the outcomes listed above. (NCT00548548)
Timeframe: From randomization until 3 months after last dose (up to 26 months)

,
Interventionparticipants (Number)
Any Adverse eventSerious AEGrade 3/4/5 AEGrade 5 AEDeaths not due to Progression
Bevacizumab3801342931831
Placebo3771372942529

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Progression-free Survival

Progression-free survival (PFS) is defined as the time between randomization and the date of first documented disease progression or death, whichever occurs first. Patients who neither progressed nor died at the time of study completion or who were lost to follow-up were censored at the date of the last tumor assessment or last follow up for progression of disease. Median PFS was estimated using the Kaplan-Meier method. (NCT00548548)
Timeframe: From randomization until disease progression or death, up to 26 months.

Interventionmonths (Median)
Bevacizumab6.7
Placebo5.3

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Progression-free Survival During First-line Therapy

Progression-free survival (PFS) during first-line therapy is defined as the time between randomization and the date of first documented disease progression or death, whichever occurs first and only if it occurs no later than 28 days after last confirmed intake of any study medication and only if it occurs before the start of non-study antineoplastic treatment. Participants who did not progress or die in this interval or were lost to follow-up were censored at the date of the last tumor assessment within this time window. Median PFS was estimated using the Kaplan-Meier method. (NCT00548548)
Timeframe: From randomization until 28-days after the last study treatment was administered, up to 26 months.

Interventionmonths (Median)
Bevacizumab6.9
Placebo5.4

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Participants With Disease Control

Disease control for participants with measurable disease was defined as a complete response (CR), partial response (PR) or stable disease (SD) for 6 weeks or longer, as determined by the RECIST criteria. For participants without measurable disease, disease control was defined as no disease progression for ≥ 6 weeks. (NCT00548548)
Timeframe: From randomization until the end of study, up to 26 months.

,
Interventionparticipants (Number)
Participants with Disease ControlParticipants without Disease Control
Bevacizumab30087
Placebo271116

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Duration of Response

Duration of response during first line therapy is defined as the time from when response (CR or PR) was first documented to first documented disease progression or death (whichever occurs first) during first line therapy. This was only be calculated for participants who achieved a best overall response of CR or PR. Participants who did not progress or die after they had a confirmed response were censored at the date of their last tumor measurement or last follow up for progression of disease during first line therapy. Median duration of response was estimated using the Kaplan-Meier method. (NCT00548548)
Timeframe: From randomization to the end of study, up to 26 months

Interventionmonths (Median)
Bevacizumab7.1
Placebo5.8

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Time to Disease Progression

Time to progression is defined as the time from randomization to the first occurrence of progressive disease (PD). PD was assessed according to the Response Evaluation Criteria in Solid Tumors (RECIST) criteria and defined as at least a 20% increase in the sum of the longest diameter of target lesions, or appearance of ≥1 new lesions and/or unequivocal progression of existing non-target lesions. Patients with no PD at study completion (including those who died before PD) were censored at the date of the last tumor assessment. Median time to PD was estimated using the Kaplan-Meier method. (NCT00548548)
Timeframe: From randomization until disease progression; assessed every 6 weeks for the first year and every 12 weeks thereafter, up to 26 months.

Interventionmonths (Median)
Bevacizumab7.0
Placebo5.6

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Participants With a Best Overall Response of Complete or Partial Response

Best overall response during first-line therapy is defined as the occurrence of either a confirmed complete (CR) or a partial (PR) best overall response, as determined by the RECIST criteria. CR is defined as the disappearance of all target and non-target lesions and PR is defined as at least a 30% decrease in the sum of the longest diameter of target lesions and no new or progression of non-target lesions, or the disappearance of all target lesions and persistence of one or more non-target lesion(s). (NCT00548548)
Timeframe: From randomization until the end of study, up to 26 months.

,
Interventionparticipants (Number)
RespondersNon-responders
Bevacizumab143168
Placebo111186

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Number of Participants Who Experienced One or More Adverse Events (AEs)

An AE is any untoward medical occurrence in a participant administered study drug which does not necessarily have a causal relationship with the study drug. AEs may include the onset of new illness and the exacerbation of pre-existing conditions. (NCT00551213)
Timeframe: Up to 30 days after last dose of study drug (Up to approximately 22 weeks)

InterventionParticipants (Number)
Robatumumab→Robatumumab49
Chemotherapy→Robatumumab15

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Number of Participants Who Discontinued Study Drug Due to an AE

An AE is any untoward medical occurrence in a participant administered study drug which does not necessarily have a causal relationship with the study drug. AEs may include the onset of new illness and the exacerbation of pre-existing conditions. (NCT00551213)
Timeframe: Up to last dose of study drug (Up to approximately 18 weeks)

InterventionParticipants (Number)
Robatumumab→Robatumumab6
Chemotherapy→Robatumumab3

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Best Overall Tumor Response Per Central Review

Tumor response was assessed by CT or MRI scan using RECIST v1.0 criteria at Screening, at every 8 weeks of robatumumab treatment during Period 2 and at post study. A sum of the LD for all target lesions was calculated and reported as the baseline sum LD. Overall tumor responses were defined as: Complete Response (CR) - Disappearance of all target lesions; Partial Response (PR) - At least a 30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD; Progressive Disease (PD) - At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions; or Stable Disease (SD) - Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT00551213)
Timeframe: Up to 30 days after last dose of study drug (Up to approximately 22 weeks)

,
InterventionParticipants (Number)
Partial ResponseStable DiseaseProgressive DiseaseNo post-Baseline assessment
Chemotherapy→Robatumumab0591
Robatumumab→Robatumumab010318

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Change From Baseline in Tumor Growth Rate

Tumor growth rate was assessed by CT or MRI scans using RECIST criteria at Screening, at every 8 weeks of robatumumab treatment and at post study. For Pre Baseline 1, tumor growth rate=(sum of longest diameter of target lesions at Baseline - the most recent prior to Baseline)/duration between Baseline and Pre Baseline. For all other cycles, tumor growth rate=(sum of longest diameter of target lesions at a cycle - Baseline)/ duration between Baseline and the cycle. The cycles presented below are relative to the first dose of robatumumab in Period 1. (NCT00551213)
Timeframe: Baseline and up to approximately 22 weeks

Interventionmm/day (Mean)
Pre Baseline 1 (n=46)Cycle 1 (n=24)Cycle 2 (n=25)Cycle 5 (n=25)Cycle 9 (n=7)
Robatumumab→Robatumumab0.490.070.410.530.19

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Best Overall Tumor Response Per Investigator Review

Tumor response was assessed by computed tomography (CT) or magnetic resonance imaging (MRI) scans using RECIST v 1.0 criteria at Screening, at every 8 weeks of robatumumab treatment during Period 2 and at post study. A sum of the longest diameter (LD) for all target lesions was calculated and reported as the baseline sum LD. Overall tumor responses were defined as: Complete Response (CR) - Disappearance of all target lesions; Partial Response (PR) - At least a 30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD; Progressive Disease (PD) - At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions; or Stable Disease (SD) - Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT00551213)
Timeframe: Up to 30 days after last dose of study drug (Up to approximately 22 weeks)

,
InterventionParticipants (Number)
Partial ResponseStable DiseaseProgressive DiseaseNo post-Baseline assessment
Chemotherapy→Robatumumab0762
Robatumumab→Robatumumab110335

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Number of Participants With a >20% Decrease in Positron Emission Tomography (PET)-Assessed Tumor Glucose Metabolism: Fluorodeoxyglucose (FDG) Standardized Uptake Value (SUV) in the Target Lesion

FDG-PET was used in this study to detect the biological activity of modulation of the target within the tumor. Response Evaluation Criteria in Solid Tumors (RECIST) version 1.0 was used to select the target lesion. All measurable lesions up to a maximum of 5 lesions per organ and 10 lesions in total, representative of all involved organs were identified as target lesions and recorded and measured at Baseline. The changes in SUVmax were calculated using the formula: (endpoint SUVmax - baseline SUVmax)/baseline SUVmax as a percentage. If multiple lesions had been measured at a visit, percentages calculated for all target lesions were averaged to find the decrease during the treatment period per participant. FDG SUVmax responder was defined as participants with >20% decrease in SUVmax after the first cycle of robatumumab in Period 2. (NCT00551213)
Timeframe: After the first robatumumab dose in Period 2 (Up to approximately 4 weeks after first robatumumab dose in Period 1)

InterventionParticipants (Number)
Robatumumab→Robatumumab7

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Progression-Free Survival (PFS)

PFS defined as time from the first dose of study treatment to the first documentation of objective tumor progression or to death due to any cause, whichever occurs first. (NCT00555620)
Timeframe: Baseline up to Month 15

Interventionmonths (Median)
SU 37.5 mg, CIS 60 mg/m^2, CAP 1600 mg/m^23.2
SU 37.5 mg, CIS 60 mg/m^2, CAP 2000 mg/m^26.6
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^26.4
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^28.0
SU 37.5 mg, OXA 110 mg/m^2, CAP 2000 mg/m^22.8
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^25.5

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Percentage of Participants With Objective Response

Percentage of participants with an objective response-based assessment of confirmed complete response (CR) or confirmed partial response (PR) according to Response Evaluation Criteria in Solid Tumors (RECIST). CR defined as the disappearance of all target lesions. PR defined as ≥30 percent (%) decrease in the sum of the longest dimensions of the target lesions taking as a reference the baseline sum longest dimensions. (NCT00555620)
Timeframe: Baseline, Day 21 of every even-numbered cycle up to 15 months

Interventionpercentage of participants (Number)
SU 37.5 mg, CIS 60 mg/m^2, CAP 1600 mg/m^216.7
SU 37.5 mg, CIS 60 mg/m^2, CAP 2000 mg/m^242.9
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^246.7
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^243.5
SU 37.5 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^245.5

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Number of Participants With First-cycle Dose Limiting Toxicities (DLTs)

Any DLT event in Cycle 1: Grade (GR) 3/4 nausea, vomiting, or diarrhea despite anti-emetics, anti-diarrheals; GR 3 nonhematological toxicity for greater than or equal to (≥)7 days (except alopecia, skin or hair discoloration, hyperamylasemia, or hyperlipasemia without other clinical evidence of pancreatitis and asymptomatic hyperuricemia); GR 4 nonhematological toxicity; GR 4 neutropenia ≥7 days or thrombocytopenia; GR ≥3 febrile neutropenia or neutropenic infection; GR 3 thrombocytopenia ≥7 days; any treatment-related toxicity having >3 consecutive CAP or SU missed doses per cycle; delayed toxicity recovery >14 days. (NCT00555620)
Timeframe: Baseline up to Day 21

Interventionparticipants (Number)
SU 37.5 mg, CIS 60 mg/m^2, CAP 1600 mg/m^21
SU 37.5 mg, CIS 60 mg/m^2, CAP 2000 mg/m^20
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^23
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^22
SU 37.5 mg, OXA 110 mg/m^2, CAP 2000 mg/m^22
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20

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Duration of Response (DR)

DR defined as time from start of first documented objective tumor response (CR or PR) to first documented objective tumor progression or death due to any cause, whichever occurs first. (NCT00555620)
Timeframe: Baseline up to Month 15

Interventionmonths (Median)
SU 37.5 mg, CIS 60 mg/m^2, CAP 1600 mg/m^214.1
SU 37.5 mg, CIS 60 mg/m^2, CAP 2000 mg/m^26.3
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^210.5
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^25.9
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^26.3

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Tmax for CAP

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionhr (Median)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^24.30.3
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.50.4
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^22.02.0

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Tmax for 5'DFUR

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionhr (Median)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^24.50.4
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.80.5
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^22.03.0

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Tmax for 5'DFCR

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionhr (Median)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^24.30.4
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.60.5
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^22.03.0

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Tmax for 5-FU

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionhr (Median)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^24.50.4
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.60.5
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^22.03.0

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Time to Reach Maximum Observed Plasma Concentration (Tmax) for SU, SU012662, and Total Drug (SU + SU012662)

(NCT00555620)
Timeframe: Day 14 of Cycle 1 (predose and 2, 4, 6, 8, 10, and 24 hours postdose)

,,
Interventionhour (hr) (Median)
Tmax SU011248Tmax SU012662Tmax total drug (SU011248+SU012662)
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^24.09.04.0
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^28.06.06.0
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^28.08.08.0

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Minimum Observed Plasma Trough Concentration (Cmin) of SU, SU012662, and Total Drug (SU + SU012662)

(NCT00555620)
Timeframe: Day 14 of Cycle 1 (predose and 2, 4, 6, 8, 10, and 24 hours postdose)

,,
Interventionng/mL (Mean)
Cmin SU011248Cmin SU012662Cmin total drug (SU011248+SU012662)
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^229.011.941.6
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^230.211.141.8
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^249.218.768.5

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t1/2 for CAP

Plasma decay half-life is the time measured for the plasma concentration to decrease by one half. (NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionhr (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^20.30.4
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.40.4
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^20.30.5

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t1/2 for 5'DFUR

Plasma decay half-life is the time measured for the plasma concentration to decrease by one half. (NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionhr (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^20.70.6
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.70.7
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^21.01.0

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Cmax of 5'-Deoxy-5-fluorouridine (Metabolite of CAP, 5'DFUR)

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^240106259
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^2716610082
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^228912074

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Cmax of 5'-Deoxy-5-fluorocytidine (Metabolite of CAP, 5'DFCR)

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^248005500
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^280178036
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^233522267

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Cmax of 5-fluorouracil (Metabolite of CAP, 5-FU)

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^2176552
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^2495866
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^2165153

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AUClast for 5'DFUR

Area under the plasma concentration time-curve from zero to the last measured concentration (AUClast) (NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose) and Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours)

,,
Interventionng*hr/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^288558500
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^2895110017
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^256584829

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Cmin of 5-FU

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^20.00.0
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.80.0
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^20.00.0

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Cmin of 5'DFCR

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^211.150.5
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^255.600.00
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^213.00.00

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Cmin of 5'DFUR

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^20.033.5
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^234.40.0
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^22.40.0

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Cmin of CAP

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^224.832.0
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.00.0
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^20.00.0

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t1/2 for 5-FU

Plasma decay half-life is the time measured for the plasma concentration to decrease by one half. (NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionhr (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^20.80.6
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.60.6
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^21.21.1

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t1/2 for 5'DFCR

Plasma decay half-life is the time measured for the plasma concentration to decrease by one half. (NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionhr (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^20.70.7
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^20.80.8
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^21.01.1

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Cmax of CAP

(NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose); Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^2700020491
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^21168116276
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^220511989

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Area Under the Curve From Time Zero to Last Quantifiable Concentration (AUClast) for CAP

Area under the plasma concentration time-curve from zero to the last measured concentration (AUClast) (NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose) and Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours)

,,
Interventionng*hr/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^2755513532
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^273738213
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^228993157

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Maximum Observed Plasma Concentration (Cmax) of SU, SU012662 (Metabolite of SU), and Total Drug (SU + SU012662)

(NCT00555620)
Timeframe: Day 14 of Cycle 1 (predose and 2, 4, 6, 8, 10, and 24 hours postdose)

,,
Interventionnanograms per milliliter (ng/mL) (Mean)
Cmax SU011248Cmax SU012662Cmax total drug (SU011248+SU012662)
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^240.114.053.9
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^246.516.662.4
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^269.723.793.0

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AUClast for 5'DFCR

Area under the plasma concentration time-curve from zero to the last measured concentration (AUClast) (NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose) and Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours)

,,
Interventionng*hr/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^2128158614
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^2112299776
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^280286464

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AUClast for 5-FU

Area under the plasma concentration time-curve from zero to the last measured concentration (AUClast) (NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose) and Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours)

,,
Interventionng*hr/mL (Mean)
Cycle 1, Day 1Cycle 1, Day 14
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^2355688
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^2506854
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^2291350

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Area Under the Curve From Time Zero to Extrapolated Infinite Time [AUC (0 - ∞)]: CAP, 5'DFCR, 5'DFUR, and 5-FU

AUC (0 - ∞) = Area under the plasma concentration versus time curve (AUC) from time zero (predose) to extrapolated infinite time (0 - ∞). It is obtained from AUC (0 - t) plus AUC (t - ∞). (NCT00555620)
Timeframe: Day 1 of Cycle 1 (0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng*hr/mL (Mean)
CAP (n = 1, 4, 10)5'DFCR (n = 1, 7, 10)5'DFUR (n = 1, 6, 10)5-FU (n = 1, 5, 9)
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^2748092007770386
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^28069114679099489
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^2282888535703285

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Area Under the Curve From Time Zero to 12 Hours [AUC (12)] for CAP, 5'DFCR, 5'DFUR, and 5-FU

AUC (12) = Area under the plasma concentration versus time curve from time zero (predose) to the extrapolated time 12 hours postdose. It is obtained from AUC (0 - last) plus AUC (last - 12) (NCT00555620)
Timeframe: Day 14 of Cycle 1 (predose and 0.25, 0.5, 1, 2, 3, 4, 8, and 10 hours postdose)

,,
Interventionng*hr/mL (Mean)
CAP (n = 1, 4, 9)5'DFCR (n = 1, 7, 10)5'DFUR (n = 1, 6, 10)5-FU (n = 1, 5, 10)
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^22543515522155221299
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^288651009110291842
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^2266370874822353

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Area Under the Curve From Time 0 to 24 Hours Postdose (AUC [0-24]) for SU, SU012662, and Total Drug (SU + SU012662)

Area under the plasma concentration-time curve from time 0 to 24 hours postdose (0-24), also considered the AUC between doses at steady state. (NCT00555620)
Timeframe: Day 14 of Cycle 1 (predose and 2, 4, 6, 8, 10, and 24 hours postdose)

,,
Interventionnanogram hours per milliliter (ng*hr/mL) (Mean)
AUC (0-24) SU011248AUC (0-24) SU012662AUC (0-24) total drug (SU011248+SU012662)
SU 25 mg, CIS 80 mg/m^2, CAP 2000 mg/m^28443211163
SU 25 mg, OXA 110 mg/m^2, CAP 2000 mg/m^29023271230
SU 37.5 mg, OXA 110 mg/m^2, CAP 1600 mg/m^214205241944

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Recurrence

This population has aggressive disease with a high rate of recurrence and death within 1 year of completing radiation therapy (NCT00562718)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Surgery and Chemotherapy14

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Cosmesis

(NCT00562718)
Timeframe: 1 year

Interventionparticipants (Number)
Surgery and Chemotherapy22

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Overall Safety

Primarily Grade 1 and 2 toxicities attributable to capecitabine (NCT00562718)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Surgery and Chemotherapy12.6

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Overall Survival

(NCT00565370)
Timeframe: 28 months

InterventionMonths (Median)
XP Plus Sorafenib14.7

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Number of Participants Who Experienced Dose Limiting Toxicities (DLTs)

Number of Participants who Experienced Dose Limiting Toxicities (DLTs) (NCT00565370)
Timeframe: 28weeks

Interventionparticipants (Number)
XP Plus Sorafenib3

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Progression-free Survival

(NCT00565370)
Timeframe: 1 year

InterventionMonths (Median)
XP Plus Sorafenib10.0

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Response Rate

"Tumor response was assessed every two cycles by RECIST(v1.0) using the same imaging techniques and methods used at baseline.~Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR., or similar definition that is accurate and appropriate" (NCT00565370)
Timeframe: 6 months

Interventionpercentage of participants (Number)
XP Plus Sorafenib62.8

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Toxicity Profile (According to National Cancer Institute Common Terminology Criteria for Adverse Event Version 3.0)

Number of patients who experienced toxicity from study treatment to evaluate the safety and tolerability of Capecitabine and cisplatin plus sorafenib (NCT00565370)
Timeframe: 28weeks

Interventionparticipants (Number)
XP Plus Sorafenib21

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Mean Ixabepilone Terminal Elimination Half Life (T 1/2) in One Dosing Interval

T 1/2 = terminal elimination half life as determined from participant serum samples in one dosing interval. (NCT00568022)
Timeframe: During Cycle 1 at specified timepoints (Day 1 to Day 8).

InterventionHours (Mean)
Ixabepilone 32 mg/m^2 + Capecitabine 1650 mg/m^2/Day41.77
Ixabepilone 40 mg/m^2 + Capecitabine 1650 mg/m^2/Day44.17
Ixabepilone 40 mg/m^2 + Capecitabine 2000 mg/m^2/Day54.27

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Mean Ixabepilone Volume of Distribution at Steady State (Vss) in One Dosing Interval

Vss = volume of distribution at steady state determined from participant serum samples from one dosing interval. (NCT00568022)
Timeframe: During Cycle 1 at specified timepoints (Day 1 to Day 8).

InterventionLiters (Mean)
Ixabepilone 32 mg/m^2 + Capecitabine 1650 mg/m^2/Day1910.13
Ixabepilone 40 mg/m^2 + Capecitabine 1650 mg/m^2/Day1498.46
Ixabepilone 40 mg/m^2 + Capecitabine 2000 mg/m^2/Day2055.55

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Mean Ixabepilone Area Under the Concentration Curve (AUC INF) in One Dosing Interval

AUC = the average area under the concentration curve (AUC [INF]) of ixabepilone as determined from participant serum samples in one dosing interval over 24 hours. (NCT00568022)
Timeframe: During Cycle 1 at specified timepoints (Day 1 to Day 8).

Interventionng·h/mL (Geometric Mean)
Ixabepilone 32 mg/m^2 + Capecitabine 1650 mg/m^2/Day1260.71
Ixabepilone 40 mg/m^2 + Capecitabine 1650 mg/m^2/Day1676.46
Ixabepilone 40 mg/m^2 + Capecitabine 2000 mg/m^2/Day1417.78

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Mean Ixabepilone Maximum Plasma Concentration (Cmax) in One Dosing Interval

Cmax = maximum observed plasma concentration of ixabepilone as determined from participant serum samples in one dosing interval. (NCT00568022)
Timeframe: During Cycle 1 at specified timepoints (Day 1 to Day 8).

Interventionng/mL (Geometric Mean)
Ixabepilone 32 mg/m^2 + Capecitabine 1650 mg/m^2/Day164.01
Ixabepilone 40 mg/m^2 + Capecitabine 1650 mg/m^2/Day219.44
Ixabepilone 40 mg/m^2 + Capecitabine 2000 mg/m^2/Day192.13

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Mean Ixabepilone Total Body Clearance (CLT) in One Dosing Interval

CLT = total body clearance as determined from participant serum samples in one dosing interval. (NCT00568022)
Timeframe: During Cycle 1 at specified timepoints (Day 1 to Day 8).

InterventionL/h (Mean)
Ixabepilone 32 mg/m^2 + Capecitabine 1650 mg/m^2/Day41.52
Ixabepilone 40 mg/m^2 + Capecitabine 1650 mg/m^2/Day37.21
Ixabepilone 40 mg/m^2 + Capecitabine 2000 mg/m^2/Day42.79

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Participants Experiencing Dose Limiting Toxicity (DLT)

DLT was defined as any ixabepilone and/or capecitabine related events requiring study discontinuation during the first two treatment cycles. (NCT00568022)
Timeframe: From initiation of drug through last day of Cycle 2 (Day 42)

InterventionParticipants (Number)
Ixabepilone 32 mg/m^2 + Capecitabine 1650 mg/m^2/Day0
Ixabepilone 40 mg/m^2 + Capecitabine 1650 mg/m^2/Day0
Ixabepilone 40 mg/m^2 + Capecitabine 2000 mg/m^2/Day0

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Adverse Events (AEs) and Serious Adverse Events (SAEs)

AE = any new untoward medical occurrence/worsening of a pre-existing medical condition which does not necessarily have a causal relationship with this treatment. SAE = any untoward medical occurrence that at any dose: results in death, is life-threatening, requires inpatient hospitalization or causes prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect, results in development of drug dependency or drug abuse, is an important medical event. Treatment-related=Possible, Probable, or Certain relationship to drug (NCT00568022)
Timeframe: Baseline to Day 42, continuously

,,
InterventionParticipants (Number)
AEsRelated AEsDiscontinued Due to AEsSAEsRelated SAEsDiscontinued Due to SAEsDeaths
Ixabepilone 32 mg/m^2 + Capecitabine 1650 mg/m^2/Day3300000
Ixabepilone 40 mg/m^2 + Capecitabine 1650 mg/m^2/Day3301100
Ixabepilone 40 mg/m^2 + Capecitabine 2000 mg/m^2/Day3301100

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Participant Tumor Response at Study Endpoint

Tumor response was assessed using the Response Evaluation Criteria in Solid Tumors (RECIST) in which complete response (CR) = disappearance of all target lesions; partial response (PR) = 30% decrease in the sum of the longest diameter of target lesions; progressive disease (PD) = 20% increase in the sum of the longest diameter of target lesions; and stable disease (SD) = small changes that do not meet above criteria. (NCT00568022)
Timeframe: At baseline and after every 42 days (every 2 21-day cycles) after baseline

,,
InterventionParticipants (Number)
CRPRPDSD
Ixabepilone 32 mg/m^2 + Capecitabine 1650 mg/m^2/Day0111
Ixabepilone 40 mg/m^2 + Capecitabine 1650 mg/m^2/Day0111
Ixabepilone 40 mg/m^2 + Capecitabine 2000 mg/m^2/Day1200

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Progression Free Survival

Progression free survival is defined as form initiation of WBRT with capecitabine to the time of first documented progression at any site (CNS or non-CNS site) or death due to any cause, where progression is defined stringently by progression in either CNS or extra-CNS metastases. (NCT00570908)
Timeframe: 2 years

Interventionmonths (Median)
WBRT + Capecitabine + Sunitinib4.7

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Response Rate of Lapatinib/Capecitabine.

(NCT00574171)
Timeframe: duration of study; on average 1 year

Interventionparticipants (Number)
PDSD
Lapatinib/Capecitabine41

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Number of Participants With Dose-limiting Toxicities (DLTs)

(NCT00578071)
Timeframe: Within 30 days of the last day of radiation

Interventionparticipants (Number)
Chemoradiation2

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Overall Survival Rates for the Patients Studied on This Protocol.

Number of patients alive one year after completing study protocol treatment. (NCT00578071)
Timeframe: One year

Interventionparticipants (Number)
Arm 1 Chemoradiation18

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Panitumumab Maximum Tolerated Dose in Milligrams (mg)

(NCT00578071)
Timeframe: 60 days

Interventionmg (Number)
Chemoradiation3.6

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Pathological Complete Response Rates Associated With This Regimen.

Absence of residual viable tumor cells at the time of surgical resection of the esophagus performed 7-9 weeks following completion of chemoradiotherapy. (NCT00578071)
Timeframe: 90 days

Interventionpercentage of participants (Number)
Arm 1 Chemoradiation40

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Response Rate

Response rate (RR) is defined as the proportion of participants achieving partial response (PR) or complete response (CR) based on RECIST 1.0 criteria on treatment. Per RECIST 1.0 for target lesions, CR is complete disappearance of all target lesions and PR is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. To be assigned a status of CR or PR, changes in tumor measurements must be confirmed by repeat assessments performed no fewer than 4 weeks after the response criteria are first met. PR or better overall response assumes at a minimum incomplete response/stable disease (SD) for the evaluation of non-target lesions and absence of new lesions. (NCT00585078)
Timeframe: Response was assessed by computed tomography (CT) or magnetic resonance imaging (MRI) every two cycles (42 days ±2 days) on treatment. Participants received a median (range) of 2 cycles (1-12) of CAPOX.

Interventionproportion of participants (Number)
CAPOX.125

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Overall Survival

Overall survival is defined as the time from study entry to death or date last known alive and estimated using Kaplan-Meier (KM) methods. (NCT00585078)
Timeframe: Participants were followed long-term for survival every 3 months from the end of treatment until death or lost to follow-up. Median survival follow-up was 10.8 months (95% CI: 7.1-37.7) in this study cohort.

Interventionmonths (Median)
CAPOX7.4

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Progression-Free Survival

Progression-free survival based on the Kaplan-Meier method is defined as the duration of time from study entry to documented disease progression (PD) requiring removal from treatment or death. Per RECIST 1.0 criteria: progressive disease (PD) is at least a 20% increase in the sum of longest diameter (LD) of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. PD for the evaluation of non-target lesions is the appearance of one or more new lesions and/or unequivocal progression of non-target lesions. (NCT00585078)
Timeframe: Disease evaluations occurred every two cycles (42 days ±2 days) on treatment. In this study cohort, participants were followed for progression up to 38 months.

Interventionmonths (Median)
CAPOX3.8

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Best Response

Best response on treatment was based on RECIST 1.0 criteria: Complete Response (CR) is complete disappearance of all target lesions; Partial Response (PR) is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. Both require confirmation no fewer than 4 weeks apart. CR/PR assumes at a minimum incomplete response/stable disease (SD) for the evaluation of non-target lesions and absence of new lesions. Progressive disease (PD) is at least a 20% increase in the sum of longest diameter of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. PD for the evaluation of non-target lesions is the appearance of one or more new lesions and/or unequivocal progression of non-target lesions. Stable disease is defined as any condition not meeting above criteria. (NCT00585078)
Timeframe: Response was assessed by computed tomography (CT) or magnetic resonance imaging (MRI) every two cycles (42 days ±2 days) on treatment. Participants received a median (range) of 2 cycles (1-12) of CAPOX.

Interventionparticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressive Disease
CAPOX03138

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Unconfirmed Objective Response Rate and Disease Control Rate (ITT Population)

Objective response rate (ORR) is defined as the proportion of patients with complete response or partial response. Disease control rate (DCR) is defined as the proportion of patients with complete response, partial response and stable disease. The best overall response according to the RECIST criteria is the best response recorded from the start of the treatment until disease progression/recurrence or within 28 days of last intake of study medication in the Study Treatment Phase. Complete and partial response in this summary did not require a confirmation by a second tumor assessment. (NCT00600340)
Timeframe: Up to disease progression or up to 28 days after last intake of study medication, assessed up to approximately 5 years.

,
InterventionParticipants (Count of Participants)
Objective responseDisease control
Bevacizumab Plus Capecitabine105214
Bevacizumab Plus Paclitaxel163252

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Observation Time (ITT Population)

Median observation time estimated with reverse Kaplan-Meier methods. Observation time (in months) is defined as time from randomization to the day the patient was last confirmed to be alive. In case of patient deaths the time was censored at the day of death. (NCT00600340)
Timeframe: Up to approximately 6 years

Interventionmonths (Median)
Bevacizumab Plus Paclitaxel54.3
Bevacizumab Plus Capecitabine55.7

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Duration of Response (PP Population)

Duration of response (DR) was defined as time from date of first occurrence of any response (complete response (CR) or partial response (PR)) until the occurrence of progression of disease or death. Patients with response who neither progressed nor died were censored at the date of their last tumor assessment. Median DR, associated stratified Hazard Ratio (HR). (NCT00600340)
Timeframe: Time from first occurrence of CR or PR until disease progression, death or study closure, whichever occurred first, assessed up to 3.4 years after occurrence of response.

Interventionmonths (Median)
Bevacizumab Plus Paclitaxel11.2
Bevacizumab Plus Capecitabine10.3

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Duration of Response (ITT Population)

Duration of response (DR) was defined as time from date of first occurrence of any response (complete response (CR) or partial response (PR)) until the occurrence of progression of disease or death. Patients with response who neither progressed nor died were censored at the date of their last tumor assessment. Median DR, associated stratified Hazard Ratio (HR). (NCT00600340)
Timeframe: Time from first occurrence of CR or PR until disease progression, death or study closure, whichever occurred first, assessed up to 3.4 years after occurrence of response.

Interventionmonths (Median)
Bevacizumab Plus Paclitaxel11.2
Bevacizumab Plus Capecitabine10.3

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Overall Survival (PP Population)

Overall survival (OS) defined as time from randomization to date of death from any cause. Patients without recorded death were censored at the date the patient was last known to be alive. OS was analyzed at two looks, one interim look and the final analysis. Due to group sequential testing, the overall significance level alpha = 0.025 was spent on both looks according to Lan-DeMets spending method with O'Brien-Fleming-type boundaries. Alpha spent at Interim after 47% of information was 0.0010. Alpha spent at final analysis after 99% of information was 0.0250. (NCT00600340)
Timeframe: Time from the date of randomization to the date of death or date last known to be alive, assessed up to approximately 6 years

Interventionmonths (Median)
Bevacizumab Plus Paclitaxel30.2
Bevacizumab Plus Capecitabine26.1

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Progression Free Survival (ITT Population)

Progression Free Survival (PFS) is defined as time from randomization to date of documented progression or date of death due to any cause, whichever occurred first. Patients without recorded progression or death were censored at the last date they were known to have not progressed. Patients who were randomized and had no post-baseline tumor assessment were censored on the day of randomization. Median PFS, associated stratified Hazard Ratio (HR). (NCT00600340)
Timeframe: Time from the date of randomization to disease progression, death or censoring (whichever occurred first), assessed up to approximately 5 years.

Interventionmonths (Median)
Bevacizumab Plus Paclitaxel10.9
Bevacizumab Plus Capecitabine8.1

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Progression Free Survival (PP Population)

Progression Free Survival (PFS) is defined as time from randomization to date of documented progression or date of death due to any cause, whichever occurred first. Patients without recorded progression or death were censored at the last date they were known to have not progressed. Patients who were randomized and had no post-baseline tumor assessment were censored on the day of randomization. Median PFS, associated stratified Hazard Ratio (HR). (NCT00600340)
Timeframe: Time from the date of randomization to disease progression, death or censoring (whichever occurred first), assessed up to approximately 5 years.

Interventionmonths (Median)
Bevacizumab Plus Paclitaxel10.9
Bevacizumab Plus Capecitabine8.2

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Time to Treatment Failure (ITT Population)

Time to treatment failure (TTF) was defined as time from first drug intake to progression, death or withdrawal from study treatment, whichever occurred first. Patients without an event were censored at the date of the last tumor assessment or last treatment administration, whichever occurred last. Median TTF, associated stratified Hazard Ratio (HR). (NCT00600340)
Timeframe: From first drug intake to progression, death or withdrawal from study treatment or study closure (whichever occurred first), assessed up to approximately 4.5 years

Interventionmonths (Median)
Bevacizumab Plus Paclitaxel8.4
Bevacizumab Plus Capecitabine7.2

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Overall Survival (ITT Population)

Overall survival (OS) defined as time from randomization to date of death from any cause. Patients without recorded death were censored at the date the patient was last known to be alive. OS was analyzed at two looks, one interim look and the final analysis. Due to group sequential testing, the overall significance level alpha = 0.025 was spent on both looks according to Lan-DeMets spending method with O'Brien-Fleming-type boundaries. Alpha spent at Interim after 50% of information was 0.0014. Alpha spent at final analysis after 99% of information was 0.0250. (NCT00600340)
Timeframe: Time from the date of randomization to the date of death or date last known to be alive, assessed up to approximately 6 years

Interventionmonths (Median)
Bevacizumab Plus Paclitaxel29.5
Bevacizumab Plus Capecitabine26.0

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Time to Treatment Failure (PP Population)

Time to treatment failure (TTF) was defined as time from first drug intake to progression, death or withdrawal from study treatment, whichever occurred first. Patients without an event were censored at the date of the last tumor assessment or last treatment administration, whichever occurred last. Median TTF, associated stratified Hazard Ratio (HR). (NCT00600340)
Timeframe: From first drug intake to progression, death or withdrawal from study treatment or study closure (whichever occurred first), assessed up to approximately 4.5 years

Interventionmonths (Median)
Bevacizumab Plus Paclitaxel8.3
Bevacizumab Plus Capecitabine7.3

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Objective Response Rate and Disease Control Rate (ITT Population)

Objective response rate (ORR) is defined as the proportion of patients with complete response or partial response. Disease control rate (DCR) is defined as the proportion of patients with complete response, partial response and stable disease. The best overall response according to the RECIST criteria is the best response recorded from the start of the treatment until disease progression/recurrence or within 28 days of last intake of study medication in the Study Treatment Phase (NCT00600340)
Timeframe: Up to disease progression or up to 28 days after last intake of study medication, assessed up to approximately 5 years.

,
InterventionParticipants (Count of Participants)
Objective responseDisease control
Bevacizumab Plus Capecitabine76214
Bevacizumab Plus Paclitaxel125252

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Time to Response (ITT Population)

Time to response (TR) was defined as time from randomization until occurrence of response (complete response (CR) or partial response (PR)) according to RECIST criteria. Patients without response were censored after the longest time to response observed in any patient. Median TR, associated stratified Hazard Ratio (HR). Since the median TR was not observed, the number of subjects with a response at given timepoints were reported. (NCT00600340)
Timeframe: Time from randomization until occurrence of response, assessed up 1.7 years

,
InterventionParticipants (Count of Participants)
Month 3Month 6Month 9Month 12Month 15
Bevacizumab Plus Capecitabine5769747575
Bevacizumab Plus Paclitaxel83111121123123

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Unconfirmed Objective Response Rate and Disease Control Rate (PP Population)

Objective response rate (ORR) is defined as the proportion of patients with complete response or partial response. Disease control rate (DCR) is defined as the proportion of patients with complete response, partial response and stable disease. The best overall response according to the RECIST criteria is the best response recorded from the start of the treatment until disease progression/recurrence or within 28 days of last intake of study medication in the Study Treatment Phase. Complete and partial response in this summary did not require a confirmation by a second tumor assessment (NCT00600340)
Timeframe: Up to disease progression or up to 28 days after last intake of study medication, assessed up to approximately 5 years.

,
InterventionParticipants (Count of Participants)
Objective responseDisease control
Bevacizumab Plus Capecitabine100204
Bevacizumab Plus Paclitaxel157238

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Time to Response (PP Population)

Time to response (TR) was defined as time from randomization until occurrence of response (complete response (CR) or partial response (PR)) according to RECIST criteria. Patients without response were censored after the longest time to response observed in any patient. Median TR, associated stratified Hazard Ratio (HR). Since the median TR was not observed, the number of subjects with a response at given timepoints were reported. (NCT00600340)
Timeframe: Time from randomization until occurrence of response, assessed up 1.7 years

,
InterventionParticipants (Count of Participants)
Month 3Month 6Month 9Month 12Month 15
Bevacizumab Plus Capecitabine5668727373
Bevacizumab Plus Paclitaxel81108118119119

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Objective Response Rate and Disease Control Rate (PP Population)

Objective response rate (ORR) is defined as the proportion of patients with complete response or partial response. Disease control rate (DCR) is defined as the proportion of patients with complete response, partial response and stable disease. The best overall response according to the RECIST criteria is the best response recorded from the start of the treatment until disease progression/recurrence or within 28 days of last intake of study medication in the Study Treatment Phase (NCT00600340)
Timeframe: Up to disease progression or up to 28 days after last intake of study medication, assessed up to approximately 5 years.

,
InterventionParticipants (Count of Participants)
Objective responseDisease control
Bevacizumab Plus Capecitabine74204
Bevacizumab Plus Paclitaxel121238

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One Year Survival Rate

The proportion of successes will be estimated by the number of successes divided by the total number of evaluable patients. Confidence intervals for the true success proportion will be calculated according to the exact binomial method. (NCT00601627)
Timeframe: Baseline to 12 months

Interventionproportion of patients (Number)
Panitumumab0.502

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Time to Treatment Failure

Time to treatment failure is defined to be the time from the date of registration to the date at which the patient is removed from treatment due to progression, adverse events, or refusal. The distribution of survival time will be estimated using the method of Kaplan-Meier. (NCT00601627)
Timeframe: baseline to 2 years

Interventionmonths (Median)
Panitumumab2.71

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Confirmed Response Rate

"A confirmed tumor response is defined to be a complete response (CR) or partial response (PR) noted as the objective status on 2 consecutive evaluations at least 4 weeks apart according to the Response Evaluation Criteria In Solid Tumors (RECIST) version 1.1.~A complete response is defined as the disappearance of all target and non-target lesions.~A partial response is defined as at least a 30% decrease in the sum of the longest diameter (LD) of the target lesion from baseline.~Confirmed tumor response will be evaluated using the first 6 cycles of treatment." (NCT00601627)
Timeframe: baseline to 2 years

Interventionrate of confirmed response (Number)
Panitumumab0.059

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Overall Survival

Survival time is defined as the time from registration to death due to any cause. The distribution of survival time will be estimated using the method of Kaplan-Meier (NCT00601627)
Timeframe: baseline to 2 years

Interventionmonths (Median)
Panitumumab12.1

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Progression Free Survival (PFS)

Progression Free Survival is defined as the time from registration to the earliest documented evidence of disease progression. (NCT00601627)
Timeframe: baseline to 2 years

Interventionmonths (Median)
Panitumumab7.4

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Pathologic Response Rate (Complete, Near-complete, Partial) to Neoadjuvant Chemotherapy and Chemoradiotherapy

The resected pancreaticoduodenectomy specimen and accompanying lymph nodes will be staged according to American Joint Committee on Cancer 6th Edition incorporating the prefix y to indicate a specimen status-post neoadjuvant treatment (ypTNM). Cancer 2012;118:1382-90 (NCT00609336)
Timeframe: Up to 7 years

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Radiation, Pancreaticoduodenectomy)20

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Percent of Patients Surviving at 5 Years

Kaplan-Meier estimate of overall survival at 5 years (NCT00609336)
Timeframe: Up to 5 years

Interventionpercentage of eligible pts alive (Number)
Treatment (Chemotherapy, Radiation, Pancreaticoduodenectomy)31.6

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Frequency and Severity of Toxicities Associated With This Treatment Regimen as Assessed by NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.0

(NCT00609336)
Timeframe: Up to 26 weeks after surgery (the end of adjuvant chemotherapy)

Interventionoccurrence of toxicities (Number)
Any Grade 2 CTCAE toxicityAny Grade 3 CTCAE toxicityAny Grade 4 CTCAE toxicity
Treatment (Chemotherapy, Radiation, Pancreaticoduodenectomy)2112114

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Percent of Patients Surviving at Annual Intervals

(NCT00609336)
Timeframe: 5 years

Interventionpercentage of participants (Number)
Year 1Year 2Year 3Year 4Year 5
Treatment (Chemotherapy, Radiation, Pancreaticoduodenectomy)8162453731

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Surgical Completion Rate and Complication Rate

(NCT00609336)
Timeframe: Up to 6 weeks following the completion of chemoradiotherapy

InterventionParticipants (Count of Participants)
Completion rateComplication rate
Treatment (Chemotherapy, Radiation, Pancreaticoduodenectomy)222

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Median Overall Survival of Patients With Adenocarcinoma of the Pancreas

Time at which Kaplan-Meier estimate of overall survival drops below 50% (NCT00609336)
Timeframe: 5 years

Interventionmonths (Median)
Treatment (Chemotherapy, Radiation, Pancreaticoduodenectomy)31.6

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Median Recurrence Free Survival Following Pancreaticoduodenectomy

The appearance of radiographic findings consistent with recurrent tumor at the local resection site or at a distant location is considered a radiographic recurrence. (NCT00609336)
Timeframe: From the date of pancreaticoduodenectomy to date of first observation of radiographic recurrence or death due to any cause, assessed up to 7 years

Interventionmonths (Median)
Treatment (Chemotherapy, Radiation, Pancreaticoduodenectomy)31.3

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Disease-free Survival: 4-year Rate

Disease is defined as local-regional failure or distant failure. Distant failure is defined as the appearance of peritoneal seeding or distant metastases. Local-regional failure is defined as: (1) any recurrence or surgery to the primary site after a complete response (CR) / any recurrence after a nodal CR - reported at surgery or reported after the end of protocol treatment; or (2) persistence [failure at one day post study entry], absence of primary/nodal CR after protocol treatment was completed and patient lived at least 90 days from the end of treatment. Disease-free survival time is defined as time from registration to the date of disease, death, or last known follow-up (censored). Disease-free survival rates are estimated using the Kaplan-Meier method. (NCT00613080)
Timeframe: From registration to four years

Interventionpercentage of participants (Number)
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy60.6

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Number of Patients in Protocol Adherence Categories for Intensity-modulated Radiotherapy (IMRT) Planning

Real-time quality assurance was performed remotely by the study chair or the radiation oncology co-chair prior to initiation of treatment for the first 40 cases. The final cases enrolled were reviewed within 3 months after accrual was completed. Review included evaluation of clinical target volume (CTV) and planning target volume (PTV), Organs at Risk (OARs), and treatment plan dosimetry. (NCT00613080)
Timeframe: Pretreatment

InterventionParticipants (Count of Participants)
Tumor volume: Contouring score72417637Organs at risk: Contouring score72417637Tumor volume: Dose volume analysis score72417637Organs at risk: Dose volume analysis score72417637
Unacceptable variationPer ProtocolAcceptable variation
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy58
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy5
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy62
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy6
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy0
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy59
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy8
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy1
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy48
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy17
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy3

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Overall Survival: 4-year Rate

Overall survival time is defined as time from registration to the date of death from any cause. Overall survival rates are estimated by the Kaplan-Meier method. Patients last known to be alive are censored at the date of last contact. (NCT00613080)
Timeframe: From registration to four years

Interventionpercentage of participants (Number)
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy82.9

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Number of Patients With Pathologic Complete Response

Pathologic complete response is defined as no evidence of residual cancer histologically in the resection specimen. (NCT00613080)
Timeframe: At the time of surgery, which is 4-8 weeks after radiation therapy, approximately 9-13 weeks from treatment start.

InterventionParticipants (Count of Participants)
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy10

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Number of Patients Who Underwent Abdominoperineal Resection

All patients were to undergo surgery 4 to 8 weeks following the completion of radiation therapy. The choice of procedure (abdominoperineal resection (APR), low anterior resection (LAR), or LAR/coloanal anastomosis) was at the discretion of the surgeon. If more than 28 patients received abdominoperineal resection, this would result in a conclusion of an excessive number of abdominoperineal resections. (NCT00613080)
Timeframe: Surgery occurred 4 to 8 weeks following the completion of radiation therapy, approximately 9-13 weeks from start of treatment.

InterventionParticipants (Count of Participants)
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy14

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Local-regional Failure: 4-year Rate

Local failure is defined as: (1) any recurrence or surgery to the primary site after a complete response (CR) reported at surgery or reported after the end of protocol treatment; or (2) persistence [failure at one day post study entry], absence of CR after protocol treatment was completed and patient lived at least 90 days from the end of treatment. Regional failure is defined as: (1) any recurrence after a nodal CR reported at surgery or reported after the end of protocol treatment; or (2) persistence, absence of nodal CR after protocol treatment was completed and patient lived at least 90 days from the end of treatment. Local-regional failure time is defined as time from registration to local or regional failure, last known follow-up (censored), or death (competing risk). Local-regional failure rates are estimated by the cumulative incidence method. (NCT00613080)
Timeframe: From registration to four years

Interventionpercentage of participants (Number)
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy7.4

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Distant Failure: 4-year Rate

Distant failure is defined as the appearance of peritoneal seeding or distant metastases. Time to distant failure is defined as time from registration to the date of distant failure, last known follow-up (censored), or death (competing risk). Distant failure rates are estimated by the cumulative incidence method. (NCT00613080)
Timeframe: From registration to four years

Interventionpercentage of participants (Number)
IMRT + Chemotherapy , Resection, Postoperative Chemotherapy29.7

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Percentage of Participants With Metastatic Lesions Previously Considered Inoperable Who Became Operable and Underwent Surgery

(NCT00623805)
Timeframe: Baseline to the end of the study (up to 4 years, 2 months)

InterventionPercentage of participants (Number)
Bevacizumab+Capecitabine+Oxaliplatin58.1
Bevacizumab(B)+Capecitabine(C)+Oxaliplatin Followed by B+C54.1

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Time Until a Complete Response or a Partial Response

Time until a complete response or a partial response was defined as the time from the first administration of study drug until the first complete response or partial response. (NCT00623805)
Timeframe: Baseline to Month 13

InterventionMonths (Mean)
Bevacizumab+Capecitabine+Oxaliplatin3.5
Bevacizumab(B)+Capecitabine(C)+Oxaliplatin Followed by B+C2.9

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Progression-free Survival

Progression-free survival was defined as the time from the first administration of study drug to the first documented disease progression or death, whichever occurs first. Progressive disease was defined as at least a 20% increase in the sum of the longest diameter of target lesions, taking as reference the smallest sum longest diameter recorded since treatment started or the unequivocal progression of existing non-target lesions. All measurable lesions up to a maximum of 5 lesions per organ and 10 lesions in total, representative of all involved organs, should be identified as target lesions at Baseline. Target lesions should be selected on the basis of their size (lesions with the longest diameter) and their suitability for accurate repeated measurements (either by imaging techniques or clinically). A sum of the longest diameter for all target lesions will be calculated and reported as the Baseline sum longest diameter. (NCT00623805)
Timeframe: Baseline to the end of the study (up to 4 years, 2 months)

InterventionMonths (Mean)
Bevacizumab+Capecitabine+Oxaliplatin9.0
Bevacizumab(B)+Capecitabine(C)+Oxaliplatin Followed by B+C12.6

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Percentage of Participants With a Complete Response or a Partial Response

A complete response was defined as the disappearance of all target lesions. A partial response was defined as at least a 30% decrease in the sum of the longest diameter of target lesions taking as reference the Baseline sum longest diameter. All measurable lesions up to a maximum of 5 lesions per organ and 10 lesions in total, representative of all involved organs, should be identified as target lesions at Baseline. All other lesions (or sites of disease) should be identified as non-target lesions. Target lesions should be selected on the basis of their size (lesions with the longest diameter) and their suitability for accurate repeated measurements (either by imaging techniques or clinically). A sum of the longest diameter for all target lesions will be calculated and reported as the Baseline sum longest diameter. (NCT00623805)
Timeframe: Baseline to the end of the study (up to 4 years, 2 months)

InterventionPercentage of participants (Number)
Bevacizumab+Capecitabine+Oxaliplatin53.2
Bevacizumab(B)+Capecitabine(C)+Oxaliplatin Followed by B+C59.0

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Overall Survival

Overall survival was defined as the time from the first administration of study drug to death. (NCT00623805)
Timeframe: Baseline to the end of the study (up to 4 years, 2 months)

InterventionMonths (Mean)
Bevacizumab+Capecitabine+Oxaliplatin21.0
Bevacizumab(B)+Capecitabine(C)+Oxaliplatin Followed by B+C25.4

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Safety and Tolerability as Assessed by NCI CTCAE Version 3.0

Number of participants with any adverse event as assessed by NCI CTCAE version 3.0. (NCT00625183)
Timeframe: Adverse events were queried for and collected every cycle for the duration of treatment.

InterventionParticipants (Count of Participants)
Capecitabine, Oxaliplatin, Selenomethionine, Radiation Therapy5

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To Determine the Maximum Tolerated Doses (MTD) and Dose-limiting Toxicities (DLT) of LBH589 in Combination With Capecitabine When Administered to Patients With Refractory and Advanced Tumor Types That Are Sensitive to 5-fluorouracil

MTD for Panobinostat, twice weekly (NCT00632489)
Timeframe: 18 months

Interventionmg (Number)
LBH589 With Capecitabine30

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To Determine the Maximum Tolerated Doses (MTD) and Dose-limiting Toxicities (DLT) of LBH589 in Combination With Capecitabine When Administered to Patients With Refractory and Advanced Tumor Types That Are Sensitive to 5-fluorouracil

MTD for Capecitabine, BID (NCT00632489)
Timeframe: 18 months

Interventionmg/m2 (Number)
LBH589 With Capecitabine100

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Number of Participants With Abnormalities in Hematology Laboratory Results by Worst CTC Grade

CTC, Version 3.0 used to assess parameters. ULN=upper level of normal among all laboratory ranges. WBC (c/L): Grade (Gr)1:NCT00634088)
Timeframe: Baseline and weekly from Days 1 to 21 (Cycle 1)

,,
InterventionParticipants (Number)
White blood cell count (WBC) (Grade 1)WBC (Grade 2)WBC (Grade 3)WBC (Grade 4)Absolute neutrophil count (ANC) (Grade 1)ANC (Grade 2)ANC (Grade 3)ANC (Grade 4)Platelet count (Grade 1)Platelet count (Grade 2)Platelet count (Grade 3)Platelet count (Grade 4)Hemoglobin (Grade 1)Hemoglobin (Grade 2)Hemoglobin (Grade 3)Hemoglobin (Grade 4)
Ixabepilone, 32 mg/m^2 + Lapatinib, 1000 mg/d1121012210003300
Ixabepilone, 32 mg/m^2 + Lapatinib, 1250 mg/d0030001210003000
Ixabepilone, 40 mg/m^2 + Lapatinib, 1250 mg/d1000000020006400

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Area Under the Concentration-time Curve From 0 to Infinity (AUC[INF]) and AUC From 0 to Last Quantifiable Concentration (AUC[O-T] of Ixabepilone

(NCT00634088)
Timeframe: Day 1 of 21-day cycle

,,
Interventionng*h/mL (Geometric Mean)
AUC(INF)AUC(O-T)
Ixabepilone, 32 mg/m^2 + Lapatinib, 1000 mg/d2212.91851.8
Ixabepilone, 32 mg/m^2 + Lapatinib, 1250 mg/d2427.02082.0
Ixabepilone, 40 mg/m^2 + Lapatinib, 1250 mg/d1610.71284.2

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Volume of Distribution at Steady State of Ixabepilone

(NCT00634088)
Timeframe: Day 1 of 21-day cycle

InterventionLiters (Mean)
Ixabepilone, 32 mg/m^2 + Lapatinib, 1000 mg/d1484.3
Ixabepilone, 32 mg/m^2 + Lapatinib, 1250 mg/d1780.8
Ixabepilone, 40 mg/m^2 + Lapatinib, 1250 mg/d1915.8

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Time to Peak Concentration of Ixabepilone

(NCT00634088)
Timeframe: Day 1 of 21-day cycle

InterventionHours (Median)
Ixabepilone, 32 mg/m^2 + Lapatinib, 1000 mg/d3.0
Ixabepilone, 32 mg/m^2 + Lapatinib, 1250 mg/d3.0
Ixabepilone, 40 mg/m^2 + Lapatinib, 1250 mg/d2.9

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Number of Participants With DLT

DLT=Any of the following events, attributable to study drug and occurring within 21 days after ixabepilone administration: Grade 3 or 4 nausea, vomiting, or diarrhea despite the use of adequate medical intervention; other Grade 3 or greater nonhematologic toxicity requiring removal from study drug; recovery from study drug-related toxicity that delayed scheduled retreatment for longer than 3 weeks; Grade 4 neutropenia for 5 or more consecutive days or Grade 3 or 4 neutropenia of any duration with sepsis or fever; thrombocytopenia or bleeding requiring platelet transfusion. (NCT00634088)
Timeframe: Baseline to Day 21, continuously

InterventionParticipants (Number)
Ixabepilone, 32 mg/m^2 + Lapatinib, 1000 mg/d1
Ixabepilone, 32 mg/m^2 + Lapatinib, 1250 mg/d0
Ixabepilone, 40 mg/m^2 + Lapatinib, 1250 mg/d0

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Terminal Half-life of Ixabepilone

(NCT00634088)
Timeframe: Day 1 of 21-day cycle

InterventionHours (Mean)
Ixabepilone, 32 mg/m^2 + Lapatinib, 1000 mg/d51.6
Ixabepilone, 32 mg/m^2 + Lapatinib, 1250 mg/d63.1
Ixabepilone, 40 mg/m^2 + Lapatinib, 1250 mg/d33.1

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Maximum Concentration of Ixabepilone

(NCT00634088)
Timeframe: Day 1 of 21-day cycle

Interventionng/mL (Geometric Mean)
Ixabepilone, 32 mg/m^2 + Lapatinib, 1000 mg/d200.6
Ixabepilone, 32 mg/m^2 + Lapatinib, 1250 mg/d109.2
Ixabepilone, 40 mg/m^2 + Lapatinib, 1250 mg/d133.4

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Overall Tumor Response By Number of Participants

Target lesion criteria: Complete Response(CR)=Disappearance of all clinical and radiologic evidence of target lesions; Partial Response (PR)=A 30% or greater decrease in the sum of longest diameter(LD) of all lesions in reference to the baseline sum LD. Stable Disease (SD)=Insufficient increase to qualify for Progressive Disease (PD) and insufficient shrinkage to qualify for PR; PD=A 20% or greater increase in the sum of LD of all target lesions, taking as reference the smallest sum LD recorded at or following baseline. (NCT00634088)
Timeframe: Baseline and Day 21 (21-day cycle)

,,
InterventionParticipants (Number)
CRPRSDPD
Ixabepilone, 32 mg/m^2 + Lapatinib, 1000 mg/d3030
Ixabepilone, 32 mg/m^2 + Lapatinib, 1250 mg/d2010
Ixabepilone, 40 mg/m^2 + Lapatinib, 1250 mg/d0010

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Number of Participants With Abnormalities in Serum Chemistry Laboratory Results by Worst CTC Grade

CTC, Version 3.0 used to assess parameters. ULN=upper level of normal among all laboratory ranges. ALT(U/L) Gr 1:>ULN-2.5*ULN,Gr 2:>2.5-5.0*ULN,Gr 3:>5.0-20.0*ULN,Gr 4:>20.0* ULN; AST(U/L) Gr 1:>ULN-2.5* ULN,Gr 2:>2.5-5.0*ULN,Gr 3:>5.0-20.0*ULN,Gr 4:>20.0* ULN; ALP(U/L)Gr 1:>ULN-2.5*ULN, Gr 2:>2.5-5.0*ULN, Gr 3:>5.0-20.0*ULN, Gr 4:>20.0*ULN; Creatinine (mg/dL): Gr 1:>ULN-1.5*ULN, Gr 2:>1.5-3.0*ULN, Gr 3:>3.0-6.0*ULN, Gr 4:>6.0*ULN; Total bilirubin (mg/dL): Gr 1:>ULN-1.5*ULN, Gr 2:>1.5-3.0*ULN, Gr 3:>3.0-10.0*ULN, Gr 4:>10.0*ULN (NCT00634088)
Timeframe: At baseline and within 72 hours of Day 1 of 21-day cycle

,,
InterventionParticipants (Number)
Alanine aminotransferase (ALT) (Grade 1)ALT (Grade 2)ALT (Grade 3)ALT (Grade 4)Aspartate aminotransferase (AST) (Grade 1)AST (Grade 2)AST (Grade 3)AST (Grade 4)Alkaline phosphatase (ALP) (Grade 1)ALP (Grade 2)ALP (Grade 3)ALP (Grade 4)Creatinine (Grade 1)Creatinine (Grade 2)Creatinine (Grade 3)Creatinine (Grade 4)Total bilirubin (Grade 1)Total bilirubin (Grade 2)Total bilirubin (Grade 3)Total bilirubin (Grade 4)
Ixabepilone, 32 mg/m^2 + Lapatinib, 1000 mg/d10001000300000000000
Ixabepilone, 32 mg/m^2 + Lapatinib, 1250 mg/d00000000000000000000
Ixabepilone, 40 mg/m^2 + Lapatinib, 1250 mg/d00000000000000000000

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Overall Survival

Overall survival, defined as number of days from the day of first study drug administration to the day the patient dies, summarized using point estimates of the median time to progression, and associated 95% confidence intervals (NCT00634751)
Timeframe: Up to 18 months

InterventionMonths (Median)
Phase II: Pancreatic Cancer8.1

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Progression-free Survival (PFS)

Time to progression, defined as number of days from day of first study drug administration to the day the patient experiences an event of disease progression or death; summarized using point estimates of the median time to progression and associated 95% confidence intervals for each stratum separately. (NCT00634751)
Timeframe: Up to 18 months

InterventionMonths (Median)
Phase II: Pancreatic Cancer6.0

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Overall Response Rate

Response rate of participant to treatment (NCT00634751)
Timeframe: Up to 18 months

,,,
Interventionparticipants (Number)
Partial ResponseStable DiseaseProgressive Disease
Phase I: 200mg Sorafenib+2DOC151
Phase I: 400mg Sorafenib BID+2DOC120
Phase II: Biliary Tract Cancer151
Phase II: Pancreatic Cancer3116

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Time to Objective Tumor Response (TTR)

Based on Data Review Committee's Assessment. TTR is defined as the time from the start of study treatment to first documentation of objective tumor response (confirmed CR or PR). CR is defined as disappearance of all target and non-target lesions. PR is defined as ≥30% decrease in sum of the LDs of the target lesions taking as reference the baseline sum LD according to RECIST. Confirmed responses are those that persist on repeat evaluation ≥4 weeks after initial documentation of response. (NCT00662025)
Timeframe: Day 1 of Cycle 2, every 6 weeks after Cycle 2, and at the end of Cycle 8. Up to 28 days after the last administration of the study drug.

Interventionmonths (Median)
SUNITINIB+CAPECITABINE1.4

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AUC(0-24) for Sunitinib, SU012662, and Total Drug (Sunitinib+SU012662)

"SU012662 is a metabolite of sunitinib. AUC(0-24) means an area under the plasma concentration time curve from time zero to 24 hours post-dose.~The AUC(0-24) for total drug (sunitinib+SU012662) was calculated as the mean of the AUC(0-24) of total drug from individual participant." (NCT00662025)
Timeframe: Days 14 and 15 of Cycle 1

Interventionnanogram∙hour/milliliter (Mean)
SunitinibSU012662Total drug (Sunitinib+SU012662)
SUNITINIB+CAPECITABINE18867042590

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Time to Tumor Progression (TTP)

Based on Data Review Committee's Assessment. TTP is defined as the time from the start of study treatment to first documentation of objective tumor progression. (NCT00662025)
Timeframe: Day 1 of Cycle 2, every 6 weeks after Cycle 2, and at the end of Cycle 8. Up to 28 days after the last administration of the study drug.

Interventionmonths (Median)
SUNITINIB+CAPECITABINE5.3

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Tmax for Sunitinib, SU012662, and Total Drug (Sunitinib+SU012662)

"SU012662 is a metabolite of sunitinib. Tmax means a time to first occurrence of maximum observed plasma concentration (Cmax).~The Tmax for total drug (sunitinib+SU012662) was calculated as the median of the Tmax of total drug from individual participant." (NCT00662025)
Timeframe: Days 14 and 15 of Cycle 1

Interventionhours (Median)
SunitinibSU012662Total Drug (Sunitinib+SU012662)
SUNITINIB+CAPECITABINE1036

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Trough Plasma Concentration (Ctrough) for Sunitinib, SU012662, and Total Drug (Sunitinib+SU012662)

"SU012662 is a metabolite of sunitinib. Trough plasma concentration (Ctrough) means the concentration prior to study drug administration.~The Ctrough for total drug (sunitinib+SU012662) was calculated as the mean of the Ctrough of total drug from individual participant." (NCT00662025)
Timeframe: Days 14 and 15 of Cycle 1

Interventionnanogram/milliliter (Mean)
SunitinibSU012662Total Drug (Sunitinib+SU012662)
SUNITINIB+CAPECITABINE68.730.899.5

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Cmax for Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR and 5-FU)

Cmax means a maximum observed plasma concentration. 5'-DFCR = 5'-deoxy-5-fluorocytidine, 5'-DFUR = 5'-deoxy-5-fluorouridine, 5-FU = 5-fluorouracil (NCT00662025)
Timeframe: Day 14 of Cycle 1

Interventionnanogram/milliliter (Mean)
Capecitabine (n=4)5'-DFCR (n=4)5'-DFUR (n=4)5-FU (n=4)
SUNITINIB+CAPECITABINE377357586885387

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Overall Survival (OS)

OS is defined as the time from the start of study treatment to death due to any cause. OS data is censored on the last day they were known to be alive in the absence of confirmation of death. (NCT00662025)
Timeframe: A survival survey was conducted at least every 6 months after the completion of study treatment or withdrawal from the study.

Interventionmonths (Median)
SUNITINIB+CAPECITABINE20.0

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AUC(0-inf) for Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR and 5-FU)

"AUC(0-inf) means an area under the plasma concentration time curve from time zero to Infinity.~5'-DFCR = 5'-deoxy-5-fluorocytidine, 5'-DFUR = 5'-deoxy-5-fluorouridine, 5-FU = 5-fluorouracil" (NCT00662025)
Timeframe: Day 14 of Cycle 1

Interventionnanogram∙hour/milliliter (Mean)
Capecitabine (n=3)5'-DFCR (n=4)5'-DFUR (n=3)5-FU (n=3)
SUNITINIB+CAPECITABINE55051317712236635

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Progression-Free Survival (PFS)

Based on Data Review Committee's Assessment. PFS is defined as the time from the start of study treatment to first documentation of objective tumor progression, or to death on study due to any cause, whichever occurred first. (NCT00662025)
Timeframe: Day 1 of Cycle 2, every 6 weeks after Cycle 2, and at the end of Cycle 8. Up to 28 days after the last administration of the study drug.

Interventionmonths (Median)
SUNITINIB+CAPECITABINE5.3

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Duration of Objective Tumor Response (DR)

Based on Data Review Committee's Assessment. DR is defined as the time from the first documentation of objective tumor response (confirmed CR or PR) to the first documentation of disease progression or to death due to cancer, whichever occurred first. CR is defined as disappearance of all target and non-target lesions. PR is defined as ≥30% decrease in sum of the LDs of the target lesions taking as reference the baseline sum LD according to RECIST. Confirmed responses are those that persist on repeat evaluation ≥4 weeks after initial documentation of response. (NCT00662025)
Timeframe: Day 1 of Cycle 2, every 6 weeks after Cycle 2, and at the end of Cycle 8. Up to 28 days after the last administration of the study drug.

Interventionmonths (Median)
SUNITINIB+CAPECITABINE4.1

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t1/2 for Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR and 5-FU)

t1/2 means a terminal phase half-life. 5'-DFCR = 5'-deoxy-5-fluorocytidine, 5'-DFUR = 5'-deoxy-5-fluorouridine, 5-FU = 5-fluorouracil (NCT00662025)
Timeframe: Day 14 of Cycle 1

Interventionhours (Mean)
Capecitabine (n=3)5'-DFCR (n=4)5'-DFUR (n=3)5-FU (n=3)
SUNITINIB+CAPECITABINE0.801.010.730.77

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Number of Subjects With CBR Based on Investigator's Assessment

Number of participants with confirmed CR, PR or SD for at least 24 weeks on study according to RECIST. CR is defined as disappearance of all target and non-target lesions. PR is defined as ≥30% decrease in sum of the LDs of the target lesions taking as a reference the baseline sum LD according to RECIST. SD is defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease taking as reference smallest sum of LDs since treatment started. (NCT00662025)
Timeframe: Day 1 of Cycle 2, every 6 weeks after Cycle 2, and at the end of study.

Interventionparticipants (Number)
Total Number of Participatnts with CBRComplete Response (CR)Partial Response (PR)Stable Disease (SD) >= 168 days
SUNITINIB+CAPECITABINE3301716

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Tmax for Capecitabine and Its Metabolites (5'-DFCR, 5'-DFUR and 5-FU)

"Tmax means a time to first occurrence of maximum observed plasma concentration (Cmax).~5'-DFCR = 5'-deoxy-5-fluorocytidine, 5'-DFUR = 5'-deoxy-5-fluorouridine, 5-FU = 5-fluorouracil" (NCT00662025)
Timeframe: Day 14 of Cycle 1

Interventionhours (Median)
Capecitabine (n=4)5'-DFCR (n=4)5'-DFUR (n=4)5-FU (n=4)
SUNITINIB+CAPECITABINE0.7511.51.5

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Number of Participants With Objective Response Based on Investigator's Assessment

Number of participants with objective response based on assessment of confirmed CR or confirmed PR according to RECIST. CR is defined as disappearance of all target and non-target lesions. PR is defined as ≥30% decrease in sum of the LDs of the target lesions taking as reference the baseline sum LD according to RECIST. Confirmed responses are those that persist on repeat evaluation ≥4 weeks after initial documentation of response. (NCT00662025)
Timeframe: Day 1 of Cycle 2, every 6 weeks after Cycle 2, and at the end of study.

Interventionparticipants (Number)
Total Number of Participants with CR+PRComplete Response (CR)Partial Response (PR)
SUNITINIB+CAPECITABINE17017

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Number of Participants With Objective Response Based on Data Review Committee's Assessment

Number of participants with objective response based on assessment of confirmed complete response (CR) or confirmed partial response (PR) according to Response Evaluation Criteria in Solid Tumors version 1.0 (RECIST). CR is defined as disappearance of all target and non-target lesions. PR is defined as ≥30% decrease in sum of the longest dimensions (LDs) of the target lesions taking as reference the baseline sum LD according to RECIST. Confirmed responses are those that persist on repeat evaluation ≥4 weeks after initial documentation of response. (NCT00662025)
Timeframe: Day 1 of Cycle 2, every 6 weeks after Cycle 2, and at the end of Cycle 8.

Interventionparticipants (Number)
Total Number of Participants with CR+PRComplete Response (CR)Partial Response (PR)
SUNITINIB+CAPECITABINE19019

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Number of Participants With Clinical Benefit Response (CBR) Based on Data Review Committee's Assessment

Number of participants with confirmed CR, PR or stable disease (SD) for at least 24 weeks on study according to RECIST. CR is defined as disappearance of all target and non-target lesions. PR is defined as ≥30% decrease in sum of the LDs of the target lesions taking as a reference the baseline sum LD according to RECIST. SD is defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease taking as reference smallest sum of LDs since treatment started. (NCT00662025)
Timeframe: Day 1 of Cycle 2, every 6 weeks after Cycle 2, and at the end of Cycle 8.

Interventionparticipants (Number)
Total Number of Participants with CBRComplete Response (CR)Partial Response (PR)Stable Disease (SD) >= 168 days
SUNITINIB+CAPECITABINE3201913

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Cmax for Sunitinib, SU012662, and Total Drug (Sunitinib+SU012662)

"SU012662 is a metabolite of sunitinib. Cmax means a maximum observed plasma concentration.~The Cmax for total drug (sunitinib+SU012662) was calculated as the mean of the Cmax of total drug from individual participant." (NCT00662025)
Timeframe: Days 14 and 15 of Cycle 1

Interventionnanogram/milliliter (Mean)
SunitinibSU012662Total Drug (Sunitinib+SU012662)
SUNITINIB+CAPECITABINE87.733.9119

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Number of Participants With Grade 4 Adverse Events

Grading of adverse events was determine by the principal investigator according to NCI common toxicity criteria (CTC version 3.0). Safety analysis is based on any participant experiencing a grade 4 AE. (NCT00665457)
Timeframe: every 3 weeks X 4, then every 2 weeks X4

InterventionParticipants (Count of Participants)
Celecoxib1

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Quality of Life (QoL) Assessed by European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ-C30)

Mean global health status and social functioning scores (EORTC QLQ-C30) against time for each treatment group. Scores were derived from mutually exclusive sets of items, with scale scores ranging from 0 to 100 after a linear transformation. Higher scores indicate a better QoL. (NCT00678535)
Timeframe: Baseline, Week 6, 12, 18, 24, 30, 36, 42, 48, 54 and 60, reported between day of first participant randomized, that is, 30 Jun 2008 until cut-off date (31 Mar 2012)

,
Interventionunits on a scale (Mean)
Global health status: BaselineGlobal health status: Week 6Global health status: Week 12Global health status: Week 18Global health status: Week 24Global health status: Week 30Global health status: Week 36Global health status: Week 42Global health status: Week 48Global health status: Week 54Global health status: Week 60Social functioning status: BaselineSocial functioning status: Week 6Social functioning status: Week 12Social functioning status: Week 18Social functioning status: Week 24Social functioning status: Week 30Social functioning status: Week 36Social functioning status: Week 42Social functioning status at Week 48Social functioning status: Week 54Social functioning status: Week 60
Capecitabine Plus Cisplatin57.1961.8063.3561.8363.6164.1157.7262.6466.6766.6761.8176.5275.7075.6575.5178.2676.6773.5878.1678.0080.5668.06
Cetuximab Plus Capecitabine Plus Cisplatin57.4959.0060.1760.4562.4663.6565.0659.2963.3960.6362.5074.3668.9471.4871.2274.2078.5176.2868.5780.3674.7178.33

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Quality of Life (QoL) Assessed by EuroQol 5Dimensions (EQ-5D) Questionnaire

EQ-5D questionnaire is a measure of health status that provides a simple descriptive profile and a single index value. The EQ-5D defines health in terms of mobility, self-care, usual activities, pain/discomfort and anxiety/depression. The 5 single items are combined to obtain a single index score that is health utility index (HUI) score reflecting subject's preferences for different health states. The lowest possible score is -0.59 and the highest is 1.00, higher scores on the EQ-5D represent a better QoL. (NCT00678535)
Timeframe: Baseline, Week 6, 12, 18, 24, 30, 36, 42, 48, 54 and 60, reported between day of first participant randomized, that is, 30 Jun 2008 until cut-off date (31 Mar 2012)

,
Interventionunits on a scale (Mean)
BaselineWeek 6Week 12Week 18Week 24Week 30Week 36Week 42Week 48Week 54Week 60
Capecitabine Plus Cisplatin0.7490.7690.7750.7550.7610.7900.7110.6890.7700.7300.742
Cetuximab Plus Capecitabine Plus Cisplatin0.7430.7390.7520.7420.7330.7370.7100.7220.7190.7330.760

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Safety - Number of Participants With Adverse Events (AEs)

An Adverse Event (AE) is defined as any untoward medical occurrence in the form of signs, symptoms, abnormal laboratory findings, or diseases that emerges or worsens relative to Baseline during a clinical study with an investigational medicinal product (IMP), regardless of causal relationship and even if no IMP has been administered. (NCT00678535)
Timeframe: Time from first dose up to Day 30 after last dose of study treatment, reported between day of first participant randomized, that is, 30 Jun 2008 until cut-off date (31 Mar 2012)

Interventionparticipants (Number)
Cetuximab Plus Capecitabine Plus Cisplatin446
Capecitabine Plus Cisplatin432

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Progression-free Survival (PFS) Time: Independent Review Committee (IRC) Assessments

The PFS time is defined as the duration from randomization to either first observation of progressive disease (PD) or occurrence of death due to any cause within 60 days of the last tumor assessment or randomization. Participants without event are censored on the date of last tumor assessment. (NCT00678535)
Timeframe: Time from randomization to disease progression, death or last tumor assessment, reported between day of first participant randomized, that is, 30 Jun 2008 until cut-off date (31 Mar 2012)

Interventionmonths (Median)
Cetuximab Plus Capecitabine Plus Cisplatin4.4
Capecitabine Plus Cisplatin5.6

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Overall Survival (OS)

The OS time is defined as the time from randomization to death or last day known to be alive. Participants without event are censored at the last date known to be alive or at the clinical cut-off date, whatever is earlier. (NCT00678535)
Timeframe: Time from randomization to death or last day known to be alive, reported between day of first participant randomized, that is, 30 Jun 2008 until cut-off date, (31 Mar 2012)

Interventionmonths (Median)
Cetuximab Plus Capecitabine Plus Cisplatin9.4
Capecitabine Plus Cisplatin10.7

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Best Overall Response (BOR) Rate: Independent Review Committee (IRC) Assessments

The BOR rate is defined as the percentage of participants having achieved complete response (CR) or partial response (PR) as the best overall response, based on radiological assessments (based on response evaluation criteria in solid tumors [RECIST] Version 1.0) from the IRC. (NCT00678535)
Timeframe: Every 6 weeks until progression, reported between day of first participant randomized, that is, 30 Jun 2008 until cut-off date, (31 Mar 2012)

Interventionpercentage of participants (Number)
Cetuximab Plus Capecitabine Plus Cisplatin29.9
Capecitabine Plus Cisplatin29.2

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Number of Participants With Any Non-serious Adverse Event (AE: Occurring in >=5% Participants in Any Treatment Arm) or Any Serious Adverse Event (SAE)

An AE is defined as any untoward medical occurrence in a participant or clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a medicinal product. An SAE is defined as any untoward medical occurrence that, at any dose, results in death, is life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, is a congenital anomaly/birth defect, or is an event of possible drug-induced liver injury. Refer to the general Adverse AE/SAE module for a complete list of AEs and SAEs. (NCT00680901)
Timeframe: From the first dose of study medication until 30 days after the last dose (average of 229 days)

,
InterventionParticipants (Number)
Non-serious AEsSAEs
CapeOx + Lapatinib24572
CapeOx + Placebo21652

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Number of Participants With Adverse Events of the Indicated Severity, Per the National Cancer Institute (NCI) Common Terminology Criteria in Adverse Events (CTCAE)

An AE is defined as any untoward medical occurrence in a participant or clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a medicinal product. An SAE is defined as any untoward medical occurrence that, at any dose, results in death, is life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, is a congenital anomaly/birth defect, or is an event of possible drug-induced liver injury. AE/SAE severity was graded according to NCI CTCAE, version 3.0: Grade (G) 1, mild; G2, moderate; G3, severe; G4, life threatening; G5, death related to toxicity. (NCT00680901)
Timeframe: From the first dose of study medication until 30 days after the last dose (average of 229 days)

,
InterventionParticipants (Number)
Grade 1Grade 2Grade 3Grade 4Grade 5
CapeOx + Lapatinib4488911715
CapeOx + Placebo577669259

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Number of Participants With a Worst-case on Therapy Grade 3 or Grade 4 for the Indicated Hematology Parameters

Data are summarized by NCI CTCAE, version 3.0 toxicity grades. Data are reported as the number of participants who had a Grade 3 (G3) or Grade 4 (G4) toxicity for indicated hematology parameters: G3 indicates a severe toxicity, and G4 indicates a life-threatening toxicity. Hematology parameter included: Hemoglobin (Hemo), Total Neutrophils (TN) Absolute, Platelet Count (PC), and White Blood Cell (WBC) Count. (NCT00680901)
Timeframe: From Baseline (Day 1) until 28 days after the last dose (average of 239 days)

,
InterventionParticipants (Number)
Hemo, G3, n=261, 263Hemo, G4, n=261, 263TN Absolute, G3, n=240, 248TN Absolute, G4, n=240, 248PC, G3, n=261, 261PC, G4, n=261, 261WBC Count, G3, n=261, 262WBC Count, G4, n=261, 262
CapeOx + Lapatinib269226215121
CapeOx + Placebo19827229241

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Overall Survival

Overall Survival is defined as the time from randomization until death due to any cause. Participants who had not died were censored at the follow-up visit as either follow-up ended or follow-up ongoing. (NCT00680901)
Timeframe: From randomization until death due to any cause (average of 51 weeks)

Interventionmonths (Median)
CapeOx + Lapatinib12.2
CapeOx + Placebo10.5

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Number of Participants With a Worst-case on Therapy Grade 3 or Grade 4 for the Indicated Clinical Chemistry Parameters

Data are summarized by NCI CTCAE, version 3.0 toxicity grades. Data are reported as the number of participants who had a Grade 3 (G3) or Grade 4 (G4) toxicity for the indicated clinical chemistry parameters: G3 indicates a severe toxicity, and G4 indicates a life-threatening toxicity. Clinical chemistry parameters included: Albumin, Alkaline Phosphatase (AP), Alanine Amino Transferase (ALT), Aspartate Amino Transeferase (AST), Total Bilirubin (TB), Calcium (Hypercalcemia and Hypocalcemia), Creatine Kinase (CK), Creatinine, Glucose (Hyperglycemia [high] and Hypoglycemia [low]), Potassium (Hyperkalemia [high] and Hypokalemia [low]), Magnesium (Hypermagnesemia [high] and Hypomagnesemia [low]), and Sodium (Hypernatremia [high] and Hyponatremia [low]). (NCT00680901)
Timeframe: From Baseline (Day 1) until 28 days after the last dose (average of 239 days)

,
InterventionParticipants (Number)
Albumin, G3, n=257, 258Albumin, G4, n=257, 258AP, G3, n=260, 260AP, G4, n=260, 260ALT, G3, n=260, 262ALT, G4, n=260, 262AST, G3, n=260, 262AST, G4, n=260, 262TB, G3, n=260, 261TB, G4, n=260, 261Calcium (Hypercalcemia), G3, n=256, 262Calcium (Hypercalcemia), G4, n=256, 262Calcium (Hypocalcemia), G3, n=256, 262Calcium (Hypocalcemia), G4, n=256, 262CK, G3, n=1, 3CK, G4, n=1, 3Creatinine, G3, n=260, 262Creatinine, G4, n=260, 262Glucose (Hyperglycemia), G3, n=259, 262Glucose (Hyperglycemia), G4, n=259, 262Glucose (Hypoglycemia), G3, n=259, 262Glucose (Hypoglycemia), G4, n=259, 262Potassium (Hyperkalemia), G3, n=259, 261Potassium (Hyperkalemia), G4, n=259, 261Potassium (Hypokalemia), G3, n=259, 261Potassium (Hypokalemia), G4, n=259, 261Magnesium (Hypermagnesemia), G3, n=254, 256Magnesium (Hypermagnesemia), G4, n=254, 256Magnesium (Hypomagnesemia), G3, n=254, 256Magnesium (Hypomagnesemia), G4, n=254, 256Sodium (Hypernatremia), G3, n=259, 261Sodium (Hypernatremia), G4, n=259, 261Sodium (Hyponatremia), G3, n=259, 261Sodium (Hyponatremia), G4, n=259, 261
CapeOx + Lapatinib305020206200300020611021213501012192
CapeOx + Placebo4012040603500400010801210111500020164

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Mean Change in Scores on the Questionnaire EuroQoL-5 Dimensions (EQ-5D) From Baseline to Week 36

The EQ-5D is a generic preference-based HROOL self administered tool comprising of a 5-dimensional health status measure (5D utility measure) and a visual analog rating scale feeling thermometer (T.). 5D utility measures mobility, self-care, usual activities, pain/discomfort, and anxiety/depression. T. assesses participant's current health state. Each 5D utility question was responded to on a 3-point scale, indicating the level of impairment (1=no problem; 2=some or moderate problem(s); 3=unable, or extreme problems). The index utility values corresponding to the 243 health states were defined by the EuroQol classification and calculated based on country-specific regression coefficients. In the UK-based value set, the possible EQ-5D index utility values range from -0.594 to 1. The T. value ranges from 0 to 100. EQ-5D utility index score 0=death, 1=perfect health, -0.594 = worse than death. The T. score: 100=best imaginable health state, 0=worse imaginable health state. (NCT00680901)
Timeframe: From Baseline (Day1) to Week 36

,
InterventionScores on a scale (Mean)
Utility Index, n=50, 19Thermometer, n=50, 20
CapeOx + Lapatinib0.15.5
CapeOx + Placebo-0.12.6

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Mean Change in Scores on the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life (QOL) Questionnaire Core 30 (QLQ-C30) From Baseline to Week 36

"The QLQ-C30, a self administered tool used to assess HROL, consists of 30 items that assesses 15 domains consisting of 5 functional scales (s.) (physical, role, emotional, cognitive, social) and nine symptom s. or single items (fatigue, nausea and vomiting, pain, dyspnea, insomnia, appetite loss, constipation, diarrhea, financial difficulties) and a global health status or QOL s.. For the functional s. and symptom s. or single items, participants assessed using a 4-point s. (1=not at all; 2=a little; 3=quite a bit; 4=very much), whereas global health status or QOL was assessed using a 7-item Likert s., ranging from poor to excellent. All s. and single-item scores ranged from 0 to 100. For the functional scores, a higher score indicated a better HRQOL, i.e. 0=worst HRQOL, 100=best HRQOL; for the symptom s. or single items , a higher score indicated a high level of symptoms and problems, i.e. 0=no symptoms, 100=most severe symptoms." (NCT00680901)
Timeframe: From Baseline (Day1) to Week 36

,
InterventionScores on a scale (Mean)
Global health status/quality of life, n= 49, 19Physical functioning, n=50, 19Role functioning, n=50, 19Emotional functioning, n=50, 19Cognitive functioning, n=50, 19Social functioning, n=50, 19Fatigue symptom scale, n=50, 19Nausea and vomiting symptom scale, n=50, 19Pain symptom scale, n=50, 19Dyspnea symptom scale, n=50, 18Insomnia symptom scale, n=50, 19Appetite loss symptom scale, n=50, 19Constipation symptom scale, n=49, 19Diarrhea symptom scale, n=50, 19
CapeOx + Lapatinib6.60.64.74.1-0.26.7-6.0-4.7-6.70.7-4.0-8.0-6.86.0
CapeOx + Placebo1.8-4.4-1.80.4-5.3-4.42.36.10.05.6-1.8-5.30.01.8

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Mean Change in Scores on the EORTC Quality of Life (QOL) Questionnaire of Stomach 22 (QLQ-STO22) From Baseline to Week 36

The EORTC QLQ-STO22, the Gastric module of QLQ-C30, is a self administered tool use to assess HROOL of patients with gastric cancer. It consists of 22 items consisting of nine symptom scales or single items (dysphagia, pain, reflux, eating restrictions, anxiety, dry mouth, taste, body image, hair loss) that were developed for participants with gastric cancer. For the symptom scales or single items, participants assessed using a 4-point scale (1=not at all; 2=a little; 3=quite a bit; 4=very much). All scales and single-item scores ranged from 0 to 100. For the symptom scales or single items, a higher score indicated a high level of symptoms and problems, i.e. 0=no symptoms, 100=most severe symptoms. (NCT00680901)
Timeframe: From Baseline (Day1) to Week 36

InterventionScores on a scale (Mean)
Dysphagia symptom scale, n=48, 15Pain symptom scale, n=26, 15Reflux symptom scale, n=48, 16Eating restrictions symptom scale, n=48, 16Anxiety symptom scale, n=48, 16Dry mouth symptom scale, n=46, 16Taste symptom scale, n=48, 16Body image symptom scale, n=48, 16Hair loss symptom scale, n=2, 0
CapeOx + Lapatinib-6.7-12.6-8.3-7.8-16.7-8.0-3.5-10.4-16.7

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Mean Change in Scores on the EORTC Quality of Life (QOL) Questionnaire of Stomach 22 (QLQ-STO22) From Baseline to Week 36

The EORTC QLQ-STO22, the Gastric module of QLQ-C30, is a self administered tool use to assess HROOL of patients with gastric cancer. It consists of 22 items consisting of nine symptom scales or single items (dysphagia, pain, reflux, eating restrictions, anxiety, dry mouth, taste, body image, hair loss) that were developed for participants with gastric cancer. For the symptom scales or single items, participants assessed using a 4-point scale (1=not at all; 2=a little; 3=quite a bit; 4=very much). All scales and single-item scores ranged from 0 to 100. For the symptom scales or single items, a higher score indicated a high level of symptoms and problems, i.e. 0=no symptoms, 100=most severe symptoms. (NCT00680901)
Timeframe: From Baseline (Day1) to Week 36

InterventionScores on a scale (Mean)
Dysphagia symptom scale, n=48, 15Pain symptom scale, n=26, 15Reflux symptom scale, n=48, 16Eating restrictions symptom scale, n=48, 16Anxiety symptom scale, n=48, 16Dry mouth symptom scale, n=46, 16Taste symptom scale, n=48, 16Body image symptom scale, n=48, 16
CapeOx + Placebo1.4-4.04.20.3-7.38.34.2-2.1

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Time to Response (TTR)

TTR is defined as the time from randomization until the date of the first documented evidence of CR (the disappearance if all target and non-target lesions) or PR (at least a 30% decrease in the sum of the LD of target lesions, taking a reference the Baseline sum LD) as assessed by the investigator. (NCT00680901)
Timeframe: From Baseline (Day 1) until the first documented evidence of confirmed CR or PR (average of 9 weeks)

InterventionMonths (Median)
CapeOx + Lapatinib1.4
CapeOx + Placebo1.4

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Progression Free Survival (PFS)

PFS is defined as the interval between the date of randomization and the earliest date of disease progression (PD) or death due to any cause. Per Response Evaluation Criteria in Solid Tumors (RECIST) version 1.0, PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as a reference, the smallest sum of diameters recorded since the treatment started or the appearance of >= 1 new lesion. Participants who did not have a radiological assessed PD but had symptomatic PD were also counted. Participants who had neither progressed nor died were censored at the follow-up visit as either follow-up ended or follow-up ongoing. Participants who received non-study anti-cancer therapies before disease progression were treated as censored. (NCT00680901)
Timeframe: From randomization until the earliest date of disease progression or death due to any cause (average of 30 weeks)

Interventionmonths (Median)
CapeOx + Lapatinib6.0
CapeOx + Placebo5.4

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Overall Survival in All Randomized Participants

Overall Survival is defined as the time from randomization until death due to any cause. Participants who had not died were censored at the follow-up visit as either follow-up ended or follow-up ongoing. (NCT00680901)
Timeframe: From randomization until death due to any cause (average of 51 weeks)

Interventionmonths (Median)
CapeOx + Lapatinib11.9
CapeOx + Placebo10.4

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Duration of Response (DOR)

DOR is defined as the time from the first documented evidence of a CR (the disappearance of all target and non-target lesions) or PR (at least a 30% decrease in the sum of the LD of target lesions, taking as a reference the Baseline sum LD) until the first documented sign of PD or death due to any cause. Per RECIST, PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as a reference, the smallest sum of diameters recorded since the treatment started or the appearance of >=1 new lesion. Participants who had neither progressed nor died were censored at the follow-up visit as either follow-up ended or follow-up ongoing. Participants who received non-study anti-cancer therapies before disease progression were treated as censored. (NCT00680901)
Timeframe: From the time of the first documented evidence of a confirmed CR or PR until the earliest date of disease progression or death due to any cause (average of 36 weeks)

InterventionMonths (Median)
CapeOx + Lapatinib7.3
CapeOx + Placebo5.6

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Number of Participants With a Response of Confirmed Complete Response (CR) or Confirmed Partial Response (PR)

A participant was defined as a responder if he/she achieved either a CR (the disappearance of all target and non-target lesions) or a PR (at least a 30% decrease in the sum of the longest diameters [LD] of target lesions, taking as a reference the Baseline sum LD) as assessed by the investigator (confirmed by radiographic imaging within 4 weeks from initial observations). (NCT00680901)
Timeframe: From randomization until the date of the first documented response of CR or PR (average of 9 weeks)

InterventionParticipants (Number)
CapeOx + Lapatinib131
CapeOx + Placebo93

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Number of Participants With Clinical Benefit (CB)

CB is defined as evidence of a CR (disappearance of all target and non-target lesions) or PR (at least a 30% decrease in the sum of the LD of target lesions, taking as a reference the Baseline sum LD) at any time or stable disease (SD, neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started) as assessed by the investigator. (NCT00680901)
Timeframe: From randomization until disease progression (PD) or death due to any cause (average of 30 weeks)

InterventionParticipants (Number)
CapeOx + Lapatinib199
CapeOx + Placebo188

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Overall Survival

Median Survival time (months) (NCT00684983)
Timeframe: From randomization to death due to any cause, up to 5 years

InterventionMonths (Median)
Arm A16.8
Arm B14.7

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Adverse Event Profile of Capecitabine and Lapatinib With and Without IMC-A12 (Using NCI CTCAE v3.0)

"All eligible patients that have initiated treatment will be considered evaluable for assessing adverse event rate(s) according to CTCAE v3.0 within each treatment arm. The maximum grade for each type of adverse event will be recorded for each patient, and frequency tables will be reviewed to determine patterns. Additionally, the relationship of the adverse event(s) to the study treatment will be taken into consideration.~4/19 (21.05%) 14/45 (31.11%)" (NCT00684983)
Timeframe: Baseline to 30 days past end of treatment

Interventionpercentage of patients with AEs (Number)
Arm I (Lapatinib Ditosylate, Capecitabine)21
Arm II (Cixutumumab, Lapatinib Ditosylate, Capecitabine)31

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Confirmed Tumor Response, Defined as Either a Complete Response (CR) or Partial Response (PR) Noted as the Objective Status on 2 Consecutive Evaluations at Least 6 Weeks Apart, Assessed by Response Evaluation Criteria for Solid Tumors (RECIST)

(NCT00684983)
Timeframe: Up to 5 years

Intervention% of evaluable participants (Number)
Arm A43.8
Arm B29

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Duration of Response

Distribution estimated by the Kaplan-Meier (1958) method for each treatment arm. (NCT00684983)
Timeframe: Up to 5 years

InterventionMonths (Median)
Arm A4.8
Arm B6.9

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Progression-free Survival (PFS)

Analysis of the primary endpoint, PFS, will be performed using Cox regression with treatment group as a single covariate. (NCT00684983)
Timeframe: From randomization to the earliest date of documentation of disease progression, up to 5 years

InterventionMedian survival and CI in months (Median)
Arm A6.0
Arm B4.9

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Time to Treatment Failure

Distribution estimated by the Kaplan-Meier (1958) method for each treatment arm. (NCT00684983)
Timeframe: From the date of randomization to the date at which the patient is removed from treatment due to progression, adverse events, or refusal, up to 5 years

InterventionMonths (Median)
Arm A4.6
Arm B4.4

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Cumulative Incidence of grade3+ Bowel Perforation, Grade 3+ Bleeding (Ocurring Withing 1 Years) and grade4+ Nonhematologic Acute Adverse Events (Limited to Within 90 Days of Treatment Start)

(NCT00685763)
Timeframe: 1 year following the completion of radiation therapy

Interventionparticipants (Number)
Proton Radiation and Chemotherapy0

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3-year Disease-free Survival

From date of registration to date of first documentation of progression or symptomatic deterioration, or death due to any cause. Patients last known to be alive and progression free are censored at date of last contact. (NCT00686166)
Timeframe: 3 years

Interventionpercentage of participants (Number)
Chemo + Chemo and Radiation + Surgery68

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Pathologic Complete Response Rate

Pathologic response is evaluated after the patient has had surgery, and is based on local pathology review of the resected surgical specimen, according to the following: a) Pathologic complete response (pCR): on review of the resected rectal specimen and accompanying lymph nodes, no cancer is recognized by the pathologist; b) Microscopic cancer: gross tumor is not seen by the pathologist but tumor remains in the microscopic analysis of any part of the entire specimen; c) no response: gross cancer is found on pathologic examination of the resected rectal cancer and draining lymph nodes. (NCT00686166)
Timeframe: 15-20 weeks from registration

Interventionpercentage of participants (Number)
Chemo + Chemo and Radiation + Surgery25

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Percentage of Participants With Disease Progression

Objective tumor response was assessed using RECIST version 1.1. Disease progression was defined as a ≥20 percent (%) increase in the sum of longest diameters of target lesions, taking as reference the smallest sum obtained at previous tumor assessment, or the appearance of any new lesions. The percentage of participants with disease progression was calculated as [number of participants meeting the above criteria divided by the number analyzed] multiplied by 100. (NCT00700570)
Timeframe: Up to approximately 3 years (at Baseline, end of Cycle 5, time of surgery, and within 4 weeks of end of treatment [EOT])

Interventionpercentage of participants (Number)
Resected52.6
Unresected46.2

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Time to Disease Progression

Objective tumor response was assessed using RECIST version 1.1. Disease progression was defined as a ≥20% increase in the sum of longest diameters of target lesions, taking as reference the smallest sum obtained at previous tumor assessment, or the appearance of any new lesions. Time to disease progression was defined as the time from first dose to time of disease progression. Participants without progression were censored at the time of last tumor assessment. Time to disease progression was estimated using Kaplan-Meier analysis and expressed in months. (NCT00700570)
Timeframe: Up to approximately 3 years (at Baseline, end of Cycle 5, time of surgery, and within 4 weeks of EOT)

Interventionmonths (Median)
Resected10.1
Unresected8.7

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Percentage of Participants by Best Overall Tumor Response According to RECIST Version 1.1

Objective tumor response was assessed using RECIST version 1.1. CR was defined as the disappearance of all target lesions, and PR was defined as a ≥30% decrease in the sum of longest diameters compared to Baseline. Response was to be confirmed at a minimum of 4 weeks after the first documented response. Stable disease (SD) was defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, as well as no new target lesions. Disease progression or PD was defined as a ≥20% increase in the sum of longest diameters of target lesions, taking as reference the smallest sum obtained at previous tumor assessment, or the appearance of any new lesions. Non-evaluability for tumor assessment was also documented when applicable. The percentage of participants with each level of response was calculated as [number of participants meeting the respective criteria divided by the number analyzed] multiplied by 100. (NCT00700570)
Timeframe: Up to approximately 3 years (at Baseline, end of Cycle 5, time of surgery, within 4 weeks of EOT, and at least 4 weeks after initial response)

,
Interventionpercentage of participants (Number)
CRPRSDPDNon-evaluable
Resected36.810.5052.60
Unresected034.615.446.23.8

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Percentage of Participants With a Best Overall Tumor Response of Complete Response (CR) or PR According to RECIST Version 1.1

Objective tumor response was assessed using RECIST version 1.1. CR was defined as the disappearance of all target lesions, and PR was defined as a ≥30% decrease in the sum of longest diameters compared to Baseline. Response was confirmed at a minimum of 4 weeks after the first documented response. The percentage of participants with confirmed CR or PR was calculated as [number of participants meeting the respective criteria divided by the number analyzed] multiplied by 100. (NCT00700570)
Timeframe: Up to approximately 3 years (at Baseline, end of Cycle 5, time of surgery, within 4 weeks of EOT, and at least 4 weeks after initial response)

Interventionpercentage of participants (Number)
Resected47.4
Unresected34.6

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Percentage of Participants With Conversion From Unresectable to Resectable Liver Metastases

Participants were assessed via microscopic and macroscopic examination for tumor resectability after completion of 5 cycles of neoadjuvant treatment. Unresectable participants exhibited any of the following criteria: greater than or equal to (≥) 4 liver metastases; location and/or distribution of metastatic disease within the liver considered unsuitable for resection with clear margins; liver involvement precluding resection, in the setting of adequate parenchymal volume for otherwise viable liver function in the immediate postoperative period; and inability to maintain adequate circulation for viable liver function. Participants who had not met any of the above criteria at the end of 5 cycles underwent surgical resection. The percentage of participants with conversion from initially unresectable to resectable liver metastases was calculated as [number of participants eligible for surgical resection divided by the number analyzed] multiplied by 100. (NCT00700570)
Timeframe: After 5 cycles of neoadjuvant treatment (10 weeks)

Interventionpercentage of participants (Number)
All Participants42.2

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Toxicity Profile

"Toxicity will be assessed at the beginning of every cycle during chemotherapy for a total of 4 cycles (1 cycle =21 days) and then 30 days post last dose of chemotherapy. All toxicities will be graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events version 3.0 (CTCAE 3.0)~In general adverse events (AEs) will be graded according to the following:~Grade 1 Mild AE Grade 2 Moderate AE Grade 3 Severe AE Grade 4 Life-threatening or disabling AE Grade 5 Death related to AE~Only incidents of AEs determined to be related to chemotherapy are recorded here." (NCT00711412)
Timeframe: During chemotherapy treatment and up to 30 days post-last dose of chemotherapy.

Interventionparticipants (Number)
ThrombocytopeniaAnemialymphopeniaLeukopeniaNeutropeniaThrombosisNauseaDiarrheaDysphagiaVomitingConstipatationAbdominal painStomatitisEsophgitis
Induction and Combination Treatment201716158518151587664

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Time to Progression

Time to Progression will be measured as time from the first day of therapy until death, disease progression or last contact. (NCT00711412)
Timeframe: From start of first treatment until time of first documentation of progression of disease or death, whichever comes first, until the study closes, up to a maximum of 6 years and 7 months.

InterventionParticipants (Count of Participants)
Induction, Combination and Surgery28

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Recurrence Rate

Recurrence rate will be defined as disease recurrence, progressive disease or death. Patients will be followed for disease recurrence or death until the end of the study. (NCT00711412)
Timeframe: From the time of start of treatment until first documentation of disease recurrence, progression or death, whichever comes first until the end of the study, a maximum of 6 years and 7 months.

InterventionParticipants (Count of Participants)
Induction and Combination Treatment23

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Determine Pathologic Complete Response

"Pathologic response will be assessed semiquantitatively irrespective of lymph node status based on the estimated percentage of residual carcinoma in relation total carcinoma area, including amount of radiotherapy-induced tissue injury, in mural histologic sections.~Pathologic response will be defined as:~P0: 0% residual cancer P1: 1% to 50% residual cancer P2: more than 50% residual cancer" (NCT00711412)
Timeframe: At time of surgery

InterventionParticipants (Count of Participants)
Induction, Combination and Surgery9

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Clinical Response Rate

"Clinical response Rate will be expressed as the proportion of patients demonstrating a complete and/or partial response based on all evaluable patients treated.Clinical response will be evaluated according to Response Evaluation Criteria In Solid Tumors 1.0 (RECIST) .~Complete Response (CR) is defined as the disappearance of all target lesions Partial Response (PR) is defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions,taking as reference the baseline sum LD" (NCT00711412)
Timeframe: four to six weeks following completion of 4 cycles (1 cycle = 21days) of chemotherapy treatment and prior to surgery

InterventionParticipants (Count of Participants)
Induction and Combination Treatment28

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Overall Survival

(NCT00711412)
Timeframe: From the start of treatment and then every 3 months until death or a maximum of 24 months.

Interventionpercentage of patients alive (Number)
3 months6 months12 months24 months
Induction and Combination Treatment93.0283.7266.8158.51

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Determine Progressive Free Survival

(NCT00711412)
Timeframe: After cycles 2, and 4 (pre-surgery) 30 days after surgery and then every 3 months until first documentation of progressive disease, death and up to a maximum of 24 months.

Interventionpercentage of patents progression free (Number)
3 months6 months12 months24 months
Induction and Combination Treatment86.0567.4462.6251.83

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Percentage of Participants With Progression-free Survival.

Gadolinium-contrasted MRIs were used to assess radiographic response every 2 cycles (~6 weeks). Tumor progression was defined by increasing tumor size, new areas of tumor, or unequivocal neurologic deterioration. (NCT00717197)
Timeframe: From date of first dose of study drug until month 6.

Interventionpercentage of participants with PFS6 (Number)
Capecitabine21.7

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Number of Participants With Toxicities Associated With Capecitabine and Lapatinib

Toxicities evaluated according to NCI CTC v.3 (NCT00721630)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Capecitabine + Lapatinib23

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Overall Response Will be Characterized by the Patient's FDG-PET Scan

A good early FDG Response is a reduction in FDG uptake on the week 3 PET scan of > or = to 35% from baseline. An FDG PET non-responder will be defined as having a decrease of < 35% on the week 3 PET scan compared with baseline. (NCT00737438)
Timeframe: 2 years

Interventionparticipants (Number)
Metabolic ResponderNon-Metabolic Responder
All Patients119

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Maximum Tolerated Dose (MTD) of Neratinib

MTD reflects the highest dose of neratinib plus capeciteabine that did not cause a selected Grade 3 toxicity in >= 2 participants, which is any of 1) Grade 3 or 4 non-hematologic toxicity (Grade 3 asthenia was not considered a DLT unless lasting >3 days, 2) Grade 3 diarrhea lasting >2 days on optimal medical therapy or associated with fever or dehydration. 3) Grade 4 neutropenia lasting ≥ 3 days or Grade 4 febrile neutropenia, 4) Grade 4 thrombocytopenia lasting ≥3 days or associated with bleeding or requiring platelet transfusion, 5) Delayed recovery [to ≥ National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) Grade 1 or baseline] from one of the above listed toxicities that were related to neratinib and/or capecitabine that delayed the initiation of the next dose by more than 3 weeks. (NCT00741260)
Timeframe: From first dose date to day 21.

Interventionmg (Number)
Neratinib in Combination With Capecitabine240

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Maximum Tolerated Dose (MTD) of Capecitabine

MTD reflects the highest dose of capecitabine in combination with neratinib that did not cause a selected Grade 3 toxicity in >= 2 participants, which is any of 1) Grade 3 or 4 non-hematologic toxicity (Grade 3 asthenia was not considered a DLT unless lasting >3 days, 2) Grade 3 diarrhea lasting >2 days on optimal medical therapy or associated with fever or dehydration. 3) Grade 4 neutropenia lasting ≥ 3 days or Grade 4 febrile neutropenia, 4) Grade 4 thrombocytopenia lasting ≥3 days or associated with bleeding or requiring platelet transfusion, 5) Delayed recovery [to ≥ National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) Grade 1 or baseline] from one of the above listed toxicities that were related to neratinib and/or capecitabine that delayed the initiation of the next dose by more than 3 weeks. (NCT00741260)
Timeframe: From first dose date to day 21.

Interventionmg/m^2 (Number)
Capecitabine in Combination With Neratinib1500

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Duration of Response

Duration of response was measured from the time at which response criteria were met for complete response (CR) or partial response (PR) (whichever status was recorded first) until the first date of recurrence or progressive disease (PD) or death per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) v1.0: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions. (NCT00741260)
Timeframe: From start date of response to first PD/death, up to three years.

Interventionweeks (Median)
Prior Lapatinib Subjects48.3
Lapatinib Naive Subjects P146.3
Lapatinib Naive Subjects Part 2 + Part 146.3

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Overall Response Rate

Number of Subjects with Complete or Partial Response per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) v.1.0: Complete Response (CR), disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; and Non-PD for non-target lesions, and no new lesions. (NCT00741260)
Timeframe: From first dose date to progression or last tumor assessment, up to three years.

Interventionpercentage of participants (Number)
Prior Lapatinib Subjects57.1
Lapatinib Naive Subjects P163.9
Lapatinib Naive Subjects Part 2 + Part 163.5

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Clinical Benefit Rate

The percentage of subjects with Complete Response, Partial Response, or Stable Disease at least 24 weeks per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) v1.0: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study. (NCT00741260)
Timeframe: From first dose date to progression or last tumor assessment, up to three years.

Interventionpercentage of participants (Number)
Prior Lapatinib Subjects71.4
Lapatinib Naive Subjects P172.1
Lapatinib Naive Subjects Part 2 + Part 173.0

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Number of Participants With Dose Limiting Toxicities

Number of participants reporting Adverse Events Causing Dose Limiting Toxicities (DLT). (NCT00741260)
Timeframe: From first dose date to day 21

InterventionParticipants (Count of Participants)
N160 + C15000
N160 + C20002
N200 + C20002
N240 + C15000
N240 + C20002
N + C MTD - No Prior Lap0
N + C MTD - Prior Lap0

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Tumor Regression Grade

tumor regression grade (1= pCR, 2= near pCR, 3= partial response, 4= no response, 5=progression). (NCT00745134)
Timeframe: Baseline to 11.5 weeks

,
InterventionParticipants (Count of Participants)
Grade 1Grade 2Grade 3Grade 4Grade 5
Arm I (Curcumin)12480
Arm II (Placebo)21120

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Progression Free Survival (PFS)

PFS was calculated from start of CRT to date of disease progression or death, censored at last endoscopy/imaging evaluation. (NCT00745134)
Timeframe: 5 years

Interventionpercentage of participants (Number)
Arm I (Curcumin)66.7
Arm II (Placebo)71.4

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Overall Survival (OS)

OS was calculated from start of CRT to date of death, censored at last follow-up. Estimated with the Kaplan-Meier method. (NCT00745134)
Timeframe: 5 years

Interventionpercentage of participants (Number)
Arm I (Curcumin)85.7
Arm II (Placebo)85.7

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Number of Participants With Tumor Downstaging

Tumor downstaging (DS) is defined as a decrease in the T stage of the primary tumor by at least 1. (NCT00745134)
Timeframe: Baseline to 11.5 weeks

InterventionParticipants (Count of Participants)
Arm I (Curcumin)7
Arm II (Placebo)4

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Number of Participants With Pathologic Complete Response (pCR) Rate

Compared the rate of pCR between treatment arms with Fisher's exact test. (NCT00745134)
Timeframe: At time of surgery

InterventionParticipants (Count of Participants)
Arm I (Curcumin)1
Arm II (Placebo)2

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Change in Curcumin Level in Tumor Tissue

A logistic regression model with pCR as the dependent variable will be used to assess the association between pCR and NF-kB activity and treatment. (NCT00745134)
Timeframe: Baseline to 11.5 weeks

Interventionng/mg tissue (Median)
Arm I (Curcumin)33.7
Arm II (Placebo)0.0

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Change in Curcumin Level in Serum

"Plasma levels were assessed pre and post curcumin/placebo administration. During week 2 (after at least 5 fractions of radiation therapy) of chemoradiation therapy:~Optional endoscopic biopsy~Optional blood collection for pharmacology (1 hour before and 1 hour after intake of curcumin or placebo)" (NCT00745134)
Timeframe: assessed 1 hr pre/post curcumin administration on one of the days during week 2 of radiation therapy (fractions 6-10)

Interventionng/mL (Median)
Serum curcumin concentrations before curcumin/placebo administration.Serum curcumin concentrations after curcumin/placebo administration.
Arm I (Curcumin)3.043.32

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Frequency of CNS Metastases (Frequency)

The percent of patients with symptomatic or progressive CNS lesions was the proportion of subjects who had PD considering CNS lesions only, according to RECIST criteria. (NCT00777101)
Timeframe: From randomization date to first CNS symptom or lesions

Interventionpercentage of participants (Number)
Neratinib9.4
Lapatinib+Capecitabine12.9

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Time to CNS Metastases

Time to symptomatic or progressive Central nervous system (CNS) lesions. Time to symptomatic or progressive CNS lesions was the time from the date of randomization until the date of progressive disease (PD) considering CNS lesions only (ie, appearance of newly diagnosed CNS lesions or progressive CNS lesions). (NCT00777101)
Timeframe: From randomization date to first CNS symptom or lesions

Interventionmonths (Median)
Neratinib19.68
Lapatinib+CapecitabineNA

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Clinical Benefit Rate

"Clinical benefit rate (CR, PR, or SD = 24 weeks) for women For ErbB2 Positive Advanced Breast Cancer. Clinical benefit rate was the percentage of subjects who achieved overall tumor response per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) v1.0: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study.~Clinical Benefit (CB) = CR + PR + SD >= 24 weeks." (NCT00777101)
Timeframe: From randomization date to progression or last tumor assessment, assessed up to 69 months

Interventionpercentage of participants (Median)
Neratinib44.4
Lapatinib+Capecitabine63.8

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Duration of Response

Duration of response was measured from the time at which response criteria were met for complete response (CR) or partial response (PR) (whichever status was recorded first) until the first date of recurrence or progressive disease (PD) or death. For subjects without death or progression, censorship was at the last valid tumor assessment per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) v1.0: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions. (NCT00777101)
Timeframe: From start date of response to first PD, assessed up to 69 months after the first subject was randomized.

Interventionmonths (Median)
Neratinib12.48
Lapatinib+Capecitabine7.98

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Progression Free Survival

Progression Free Survival, Measured in Months, for Subjects Randomized. Investigator assessment. The time interval from the date of randomization until the earliest date of progression per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) or death due to any cause. For subjects without death or progression, censorship was at the last valid tumor assessment. (NCT00777101)
Timeframe: From randomization date to progression or death, assessed up to 69 months

Interventionmonths (Median)
Neratinib4.53
Lapatinib+Capecitabine6.83

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Overall Survival (OS)

Overall Survival (OS) was defined as the time from randomization to death due to any cause. Subjects last known to be alive were censored at the last date of last contact or the data cutoff employed for the analysis, whichever was earlier. (NCT00777101)
Timeframe: From randomization date to death, assessed up to 69 months

Interventionmonths (Median)
Neratinib19.74
Lapatinib+Capecitabine23.62

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Objective Response Rate (ORR).

Objective Response Rate, investigator assessment. The ORR was defined as the percentage of participants demonstrating a confirmed objective response, either Complete Response (CR) or Partial Response (PR) during the study per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) v.1.0: Complete Response (CR), disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; and Non-PD for non-target lesions, and no new lesions. (NCT00777101)
Timeframe: From randomization date to progression or last tumor assessment, assessed up to 69 months

Interventionpercentage of participants (Number)
Neratinib29.1
Lapatinib+Capecitabine40.5

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Progression-Free Survival (PFS)

"Tumor progression was assessed according to the Response Evaluation Criteria in Solid Tumors Criteria (RECIST v1.1), presented below.~Complete Response (CR) = Disappearance of all target lesions~Partial Response (PR) = ≥ 30% decrease in the sum of the longest diameter of target lesions~Objective Response (OR) = CR + PR~Progressive disease (PD) = 20% increase in the sum of the longest diameter of target lesions, and/or the appearance of one or more new lesion(s)~Stable disease (SD) = Small changes that do not meet any of the above criteria.~Progression-Free Survival is assessed as the number of evaluable participants who were alive without disease progression at 1 year. Participants without out assessment at 12 months will not be included." (NCT00780494)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Bevacizumab+ Carboplatin +Capecitabine9

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Objective (Overall) Therapeutic Response

"Tumor response was assessed per the Response Evaluation Criteria in Solid Tumors Criteria (RECIST v1.1) for target lesions, and assessed by physical measurement; magnetic resonance imaging (MRI); computed tomography (CT), positron emission tomography (PET)-CT; and/or X-rays/radiologic scan. Response was determined based on the criteria below.~Complete Response (CR) = Disappearance of all target lesions~Partial Response (PR) = ≥ 30% decrease in the sum of the longest diameter of target lesions~Objective Response (OR) = CR + PR~Progressive disease (PD) = 20% increase in the sum of the longest diameter of target lesions, and/or the appearance of one or more new lesion(s)~Stable disease (SD) = Small changes that do not meet any of the above criteria The outcome is provided as the number of participants who achieved each of the defined responses, with objective (overall) response defined as the sum of CR and PR. The outcome is reported as values without dispersion." (NCT00780494)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Partial ResponseComplete Response (CR)Objective Response (OR) = CR + PRStable DiseaseProgressive Disease
Bevacizumab+ Carboplatin +Capecitabine1801865

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Overall Survival (OS)

Overall survival (OS) will be assessed from time from the date of enrollment to the date of death due to any cause or the last date the patient was known to be alive (censored observation) at the date of data cutoff for the final analysis. The outcome is presented as the median survival in days with standard deviation. (NCT00780494)
Timeframe: 7.5 years

InterventionDays (Median)
Bevacizumab+ Carboplatin +Capecitabine458

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Median Overall Survival

Survival estimated by Kaplan-Meier method (NCT00787787)
Timeframe: From start of treatment until death from any cause, assessed up to 3 years

Interventiondays (Median)
Treatment (Sunitinib Malate and Capecitabine)282

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Median Progression-free Survival

Analyzed using the Kaplan-Meier method. Progression was defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0). Progressive disease (PD) indicates at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT00787787)
Timeframe: From the start of treatment to time of progression or death from any cause, assessed up to 3 years

Interventiondays (Median)
Treatment (Sunitinib Malate and Capecitabine)203

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2-year Stratum-specific Disease-free Survival

Disease-free survival is calculated from date of registration to date of first documentation of relapse or death due to any cause. Patients last known to be alive are censored at date of last contact. (NCT00789958)
Timeframe: Up to 2 years from registration

Interventionpercentage of participants (Number)
Patients With Negative Margins of Resection (R0)54
Patients w/Microscopically Positive Margin of Resection (R1)48

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2-year Stratum-specific Local Relapse Rate

Local relapse is any evidence of new disease within the primary tumor bed or the regional (retroperitoneal, celiac, and portal vein nodes) lymphatics (these areas are to be encompassed within the radiation fields). (NCT00789958)
Timeframe: Up to 2 years from registration

Interventionpercentage of participants (Number)
Patients With Negative Margins of Resection (R0)9
Patients w/Microscopically Positive Margin of Resection (R1)16

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Stratum-specific (R0 and R1) 2-year Overall Survival

Time to death is calculated from date of registration to date of death due to any cause. Patients last known to be alive are censored at date of last contact. (NCT00789958)
Timeframe: Up to 2 years from registration

Interventionpercentage of participants (Number)
Patients With Negative Margins of Resection (R0)67
Patients w/Microscopically Positive Margin of Resection (R1)60

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2-year Disease-free Survival in All Patients

Disease-free survival is calculated from date of registration to date of first documentation of relapse or death due to any cause. Patients last known to be alive are censored at date of last contact. (NCT00789958)
Timeframe: Up to 2 years from registration

Interventionpercentage of participants (Number)
Adjuvant Chemotherapy + Chemoradiotherapy52

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2-year Overall Local Relapse Rate

Local relapse is any evidence of new disease within the primary tumor bed or the regional (retroperitoneal, celiac, and portal vein nodes) lymphatics (these areas are to be encompassed within the radiation fields). (NCT00789958)
Timeframe: Up to 2 years from registration

Interventionpercentage of participants (Number)
Adjuvant Chemotherapy + Chemoradiotherapy11

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2-year Overall Survival for All Patients

Time to death is calculated from date of registration to date of death due to any cause. Patients last known to be alive are censored at date of last contact. (NCT00789958)
Timeframe: Up to 2 years from registration

Interventionpercentage of participants (Number)
Adjuvant Chemotherapy + Chemoradiotherapy65

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Percentage of Participants With Response to Treatment Assessed 4-6 Weeks After the Completion of Radiochemotherapy (Complete Response, Partial Remission or No Response to the Treatment)

Complete response was defined as the disappearance of all target and non-target lesions. Partial remission was defined as ≥ 30% decrease in the sum of the longest diameter (SLD) of target lesions, taking as reference the baseline SLD, or the persistence of 1 or more non-target lesions. No response to treatment was defined as neither sufficient shrinkage to qualify for partial remission nor sufficient increase to qualify for progressive disease, compared to the baseline SLD. (NCT00796718)
Timeframe: Up to 11 weeks (assessed 4-6 weeks after the completion of radiochemotherapy)

Interventionpercentage of participants (Number)
Complete ResponsePartial RemissionNo Response
Capecitabine212.277.6

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Percentage of Participants With Adverse Events

An adverse event was defined as any untoward medical occurrence in a participant administered the investigational product which does not necessarily have a causal relationship with this treatment. (NCT00796718)
Timeframe: Up to 15 weeks

Interventionpercentage of participants (Number)
Capecitabine91.9

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Percentage of Participants With Response to the Treatment Assessed 1 Month After Surgery (Complete Response, Partial Remission or No Response to the Treatment)

Complete response was defined as the disappearance of all target and non-target lesions. Partial remission was defined as ≥ 30% decrease in the sum of the longest diameter (SLD) of target lesions, taking as reference the baseline SLD, or the persistence of 1 or more non-target lesions. No response to treatment was defined as neither sufficient shrinkage to qualify for partial remission nor sufficient increase to qualify for progressive disease, compared to the baseline SLD. (NCT00796718)
Timeframe: Up to 15 weeks (assessed 1 month after surgery)

Interventionpercentage of participants (Number)
Complete ResponsePartial RemissionNo Response
Capecitabine561014

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Percentage of Participants With Pathological Complete Response

Pathological complete response was defined as the absence of viable tumor cells in the tumor specimen, including regional lymph nodes determined with standard histological procedures. (NCT00796718)
Timeframe: Up to 11 weeks (assessed at the time of post-treatment surgery)

Interventionpercentage of participants (Number)
Capecitabine16

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Progression Free Survival (PFS)

PFS was defined as the time from enrollment to time of first documented disease progression or death due to any cause, whichever occurred first. Progression: at least a 20% increase in the sum of LD of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. PFS was estimated using Kaplan-Meier methods. (NCT00811135)
Timeframe: Screening until disease progression (assessed at screening, every 6 weeks up to Week 36, thereafter every 9 weeks during treatment period, and then every 3 months during follow-up, up to approximately 4 years)

Interventionmonths (Median)
Trastuzumab + Bevacizumab + Capecitabine14.2

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Number of Participants With Response

Participants who had CR or PR were considered as responders. CR: disappearance of all target and non-target lesions and normalization of tumor marker level; PR: at least a 30% decrease in the sum of the LD of target lesions taking as reference the baseline sum LD. (NCT00811135)
Timeframe: Screening until disease progression (assessed at screening, every 6 weeks up to Week 36, thereafter every 9 weeks during treatment period, and then every 3 months during follow-up, up to approximately 4 years)

Interventionparticipants (Number)
Trastuzumab + Bevacizumab + Capecitabine66

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Number of Participants With Time to Progression (TTP)

TTP was defined as the time from enrollment to first documented disease progression (at least a 20% increase in the sum of LD of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions). TTP was estimated using Kaplan-Meier methods. (NCT00811135)
Timeframe: Screening until disease progression (assessed at screening, every 6 weeks up to Week 36, thereafter every 9 weeks during treatment period, and then every 3 months during follow-up, up to approximately 4 years)

Interventionparticipants (Number)
Trastuzumab + Bevacizumab + Capecitabine62

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Overall Survival (OS)

OS was defined as the time from enrollment to death from any cause where enrollment was defined as successfully passed screening visit, enrolled in the study and received first dose of study treatment. OS was estimated using Kaplan-Meier methods. (NCT00811135)
Timeframe: Screening until death (assessed at screening, every 6 weeks up to Week 36, thereafter every 9 weeks during treatment period, and then every 3 months during follow-up, up to approximately 4 years)

Interventionmonths (Median)
Trastuzumab + Bevacizumab + Capecitabine31.8

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Percentage of Participants With a Best Overall Response (BOR) of Confirmed Complete Response (CR) or Partial Response (PR)

Tumor response was assessed using the Response Evaluation Criteria in Solid Tumors (RECIST), Version 1.0. BOR was defined as the best response recorded for a participant from the start of treatment until disease progression/recurrence. Percentage of participants with a BOR of confirmed CR or PR (responders) was reported. CR: disappearance of all target and non-target lesions and normalization of tumor marker level; PR: at least a 30 percent (%) decrease in the sum of the longest diameter (LD) of target lesions taking as reference the baseline sum LD. Confirmed responses were those which were confirmed by a repeat assessment, performed 4 weeks after the criteria for response first met. (NCT00811135)
Timeframe: Screening until disease progression (assessed at screening, every 6 weeks up to Week 36, thereafter every 9 weeks during treatment period, and then every 3 months during follow-up, up to approximately 4 years)

Interventionpercentage of participants (Number)
Trastuzumab + Bevacizumab + Capecitabine75.0

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Duration of Response (DR)

DR was defined as the time from the first recorded response (CR/PR) to the date of first documented progression or death. CR: disappearance of all target lesions and non-target lesions and normalization of tumor marker level. PR: at least a 30% decrease in the sum of the LD of target lesions taking as reference the baseline sum LD. Progression: at least a 20% increase in the sum of LD of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. DR was estimated using Kaplan-Meier methods. (NCT00811135)
Timeframe: Screening until disease progression (assessed at screening, every 6 weeks up to Week 36, thereafter every 9 weeks during treatment period, and then every 3 months during follow-up, up to approximately 4 years)

Interventionmonths (Median)
Trastuzumab + Bevacizumab + Capecitabine12.7

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Time to Progression (TTP)

TTP was defined as the time from enrollment to first documented disease progression (at least a 20% increase in the sum of LD of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions). (NCT00811135)
Timeframe: Screening until disease progression (assessed at screening, every 6 weeks up to Week 36, thereafter every 9 weeks during treatment period, and then every 3 months during follow-up, up to approximately 4 years)

Interventionmonths (Median)
Trastuzumab + Bevacizumab + Capecitabine14.5

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Number of Participants With Disease Progression or Death

Disease progression was defined as at least a 20% increase in the sum of LD of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. (NCT00811135)
Timeframe: Screening until disease progression (assessed at screening, every 6 weeks up to Week 36, thereafter every 9 weeks during treatment period, and then every 3 months during follow-up, up to approximately 4 years)

Interventionparticipants (Number)
Trastuzumab + Bevacizumab + Capecitabine70

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Number of Participants With Overall Survival (OS)

OS was defined as the time from enrollment to death from any cause where enrollment was defined as successfully passed screening visit, enrolled in the study and received first dose of study treatment. (NCT00811135)
Timeframe: Screening until death (assessed at screening, every 6 weeks up to Week 36, thereafter every 9 weeks during treatment period, and then every 3 months during follow-up, up to approximately 4 years)

Interventionparticipants (Number)
Trastuzumab + Bevacizumab + Capecitabine40

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Number of Participants With CNS Progression at Any Time

CNS progression was documented by a brain scan and was indicated by the investigator on the follow-up electronic Case Report Form. CNS relapse is defined as the appearance of >=1 enhancing lesion measuring >=6 mm on T1W MRI without CNS symptoms that were considered to be unequivocal based on all relevant radiological features (e.g., associated T2W signal abnormality); the appearance of any enhancing lesion on T1W MRI with CNS symptoms; unequivocal finding of leptomeningeal disease, with or without symptoms; and unequivocal finding of multifocal intraparenchymal lesions with or without symptoms. In the event of the appearance of a <6 mm lesions(s) without CNS lesions, or equivocal findings potentially suggesting leptomeningeal disease, these findings were followed with a subsequent scan within 6 weeks. If unequivocal progression was determined with the subsequent scan and/or CNS symptoms occurred, then CNS relapse crieria were met. (NCT00820222)
Timeframe: From the time of randomization until death due to any cause (average of 10 months). Cut-off 11-Jun-2012

Interventionparticipants (Number)
Lapatinib Plus Capecitabine17
Trastuzumab Plus Capecitabine15

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Number of Participants With the Indicated Grade 3 or Grade 4 Adverse Events (AEs) Occurring in >=2% of Participants in Either Treatment Arm

An AE is defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which does not necessarily have a causal relationship with this treatment. The Investigator assessed whether the AE was related to study drug. AEs were graded using the Common Toxicity Criteria from the Cancer Therapy Evaluation Program, Division of Cancer Therapy, National Cancer Institute. Grades: 0=No AE or within normal limits; 1=Mild AE; 2=Moderate AE; 3=Severe and undesirable AE; 4=Life-threatening or disabling AE; 5=Death related to AE. (NCT00820222)
Timeframe: From the first dose of study medication until 30 days after the last dose of study treatment (average of 10 months).

,
InterventionParticipants (Count of Participants)
Palmar-plantar erythrodysaesthesia syndromeDiarrhoeaAspartate aminotransferase increasedNeutropeniaAstheniaFatigueAlanine aminotransferase increasedHypokalaemia
Lapatinib Plus Capecitabine29191199743
Trastuzumab Plus Capecitabine452241864611

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Overall Survival

Overall survival is defined as the time from randomization until death due to any cause or to the date of censor. In the absence of confirmation of death, survival time was to be censored at the time of the last investigator contact. (NCT00820222)
Timeframe: From randomization until death due to any cause (average of 10 months). Cut-off 11-Jun-2012

Interventionmonths (Median)
Lapatinib Plus Capecitabine22.7
Trastuzumab Plus Capecitabine27.3

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Progression Free Survival (PFS), as Assessed by the Investigator

PFS is defined as the interval between the date of randomization and the earliest date of progressive disease (PD), or death due to any cause. PD is defined as at least a 20% increase in the sum of the longest diameter (LD) of target lesions, compared with the smallest sum LD recorded since the treatment started, or the appearance of 1 or more new lesions based on investigator assessment of both CNS and non-CNS for response. (NCT00820222)
Timeframe: From randomization until disease progression, death, or discontinuation from the study (average of 10 months). Cut-off 11-Jun-2012

Interventionmonths (Median)
Lapatinib Plus Capecitabine6.60
Trastuzumab Plus Capecitabine8.05

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Number of Participants With Overall Response (OR), as Assessed by the Investigator

OR is defined as the number of participants with either a confirmed complete response (CR; disappearance of all target lesions) or partial response (PR: at least a 30% decrease in the sum of the LD of the target lesions, compared with the baseline sum LD). CR and PR were assessed per Response Evaluation Criteria in Solid Tumors (RECIST). To be assigned a status of PR or CR, a confirmatory disease assessment was to be performed 28 days (4 weeks) or greater after the criteria for response were first met. In addition, a bone scan must have been obtained to rule out the presence of new bone lesions or progression of existing bone lesions, even if the participant had no bone lesions present at Baseline. If a bone scan was performed at the time of initial response or near the time of response, the bone scan did not need to be repeated. (NCT00820222)
Timeframe: From randomization until disease progression, death, or discontinuation from the study (average of 10 months). Cut-off 11-Jun-2012

,
InterventionParticipants (Count of Participants)
CRPROverall Response (CR+PR)
Lapatinib Plus Capecitabine86573
Trastuzumab Plus Capecitabine127385

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Duration of Response

Duration of response is defined as the time from the first documented evidence of CR (disappearance of all target lesions) or PR (at least a 30% decrease in the sum of the LD of the target lesions, compared with the baseline sum LD) until the first documented sign of PD (at least a 20% increase in the sum of the LD of target lesions, compared with the smallest sum LD recorded since the treatment started, or the appearance of 1 or more new lesions) or death due to breast cancer. In the absence of confirmation of death, survival time was to be censored at the time of the last investigator contact. (NCT00820222)
Timeframe: From the time of the first documented confirmed complete or partial response until disease progression or death, if sooner (average of 10 months). Cut-off 11-Jun-2012

Interventionmonths (Median)
Lapatinib Plus Capecitabine6.2
Trastuzumab Plus Capecitabine8.4

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Number of Participants With Central Nervous System (CNS) Metastases (as Assessed by Independent Review) as the Site of First Relapse

CNS relapse is defined as the appearance of >=1 enhancing lesion measuring >=6 millimeters (mm) on T1Weighted (T1W) Magnetic Resonance Imaging (MRI) without CNS symptoms that were considered to be unequivocal based on all relevant radiological features (e.g., associated T2W signal abnormality); the appearance of any enhancing lesion on T1W MRI with CNS symptoms; unequivocal finding of leptomeningeal disease (defined as the dissemination of cancer throughout the spinal fluid), with or without symptoms; and unequivocal finding of multifocal intraparenchymal lesions with or without symptoms. In the event of the appearance of a <6 mm lesions(s) without CNS lesions, or equivocal findings potentially suggesting leptomeningeal disease, these findings were followed with a subsequent scan within 6 weeks. If unequivocal progression was determined with the subsequent scan and/or CNS symptoms occurred, then CNS relapse crieria were met. (NCT00820222)
Timeframe: From randomization until disease progression, death, or discontinuation from the study (average of 10 months). Cut-off 11-Jun-2012

Interventionparticipants (Number)
Lapatinib Plus Capecitabine8
Trastuzumab Plus Capecitabine12

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Time to First CNS Progression, Defined as the Time From Randomization Until the Date of Documented CNS Progression as the First Site of Relapse

CNS relapse is defined as the appearance of >=1 enhancing lesion measuring >=6 mm on T1W MRI without CNS symptoms that were considered to be unequivocal based on all relevant radiological features (e.g., associated T2W signal abnormality); the appearance of any enhancing lesion on T1W MRI with CNS symptoms; unequivocal finding of leptomeningeal disease (defined as the dissemination of cancer throughout the spinal fluid), with or without symptoms; and unequivocal finding of multifocal intraparenchymal lesions with or without symptoms. In the event of the appearance of a <6 mm lesions(s) without CNS lesions, or equivocal findings potentially suggesting leptomeningeal disease, these findings were followed with a subsequent scan within 6 weeks. If unequivocal progression was determined with the subsequent scan and/or CNS symptoms occurred, then CNS relapse crieria were met. (NCT00820222)
Timeframe: From randomization until the date of documented CNS progression (average of 10 months). Cut-off 11-Jun-2012

Interventionmonths (Mean)
Lapatinib Plus Capecitabine8.2
Trastuzumab Plus Capecitabine6.7

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Number of Participants With Clinical Benefit (CB)

CB is defined as the number of participants with evidence of confirmed CR (disappearance of all target lesions) or PR (at least a 30% decrease in the sum of the LD of the target lesions, compared with the baseline sum LD) at any time or stable disease (SD, neither sufficient shrinkage to qualify for a PR nor sufficient increase to qualify for PD [defined as at least a 20% increase in the sum of the LD of target lesions, compared with the smallest sum LD recorded since the treatment started, or the appearance of 1 or more new lesions] based on investigator assessment), for at least 24 weeks. (NCT00820222)
Timeframe: From randomization until disease progression, death, or discontinuation from the study (average of 10 months). Cut-off 11-Jun-2012

,
InterventionParticipants (Count of Participants)
CRPRSD >= 24 weeksClinical Benefit (CR + PR + SD >= 24 weeks)
Lapatinib Plus Capecitabine86539112
Trastuzumab Plus Capecitabine127333118

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Death Rates and Overall Survival

Counts and proportions of patients deceased (post-study). (NCT00828672)
Timeframe: up to 5 years

,
InterventionParticipants (Count of Participants)
Deceased (Dec 2017)Alive (Dec 2017)Lost to FU
AX (ARM 2)7340
AXE (ARM 1)6361

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Number of Participants With Histopathologic R0 and Negative CRM Resection

Histopathologic R0 resection rate was defined as margins histologically negative for tumour involvement after resection. The circumferential resection margin (CRM) is considered to be involved if microscopic tumour is present <1mm from or at the inked circumferential or radial resection margin. Data on quality of mesorectal excision were expected but not collected consistently. (NCT00828672)
Timeframe: 4 months

,
InterventionParticipants (Count of Participants)
Negative resection marginsPositive resection margins
AX (ARM 2)372
AXE (ARM 1)401

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Number of Participants With Pathologic Complete Response at Surgery. Number of Participants With Good or Little Pathological Tumour Regression at Surgery.

Dworak tumour regression grades (TRG) were used to assess pathologic response: TRG0=no regression. TRG1=dominant tumor mass with obvious fibrosis and/or vasculopathy; TRG2=dominant fibrotic changes with few tumour cells or groups; TRG3=very few (difficult to find microscopically) tumour cells in fibrotic tissue with or without mucus substance. TRG4=no intact viable tumour cells, only fibrotic mass or presence of mucin lakes without associated malignant cells (total tumour regression). Pathologic assessments of tumour response post chemoradiotherapy as provided by investigators (read by local pathologists on operative specimens) were reviewed centrally for all pts for whom surgical materials were available (centrally reviewed set). The diagnosis of independent central reviewers primed. Pathologic complete response rates (TRG4) are reported (%). Good (TRG3 and TRG4 together) and little (TRG 0,1 and 2) tumour regression rates are summarized. For these 2 last rows, % add to 100. (NCT00828672)
Timeframe: 4 months

,
InterventionParticipants (Count of Participants)
Complete response, no tumour left Dworak TRG=4Good tumour regression TRG=3-4No or little tumour regression Dworak TRG=0-1-2
AX (ARM 2)4929
AXE (ARM 1)141724

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Pathologic Response at Surgery. Overview of Complete Pathologic Responses, Good and Little Tumour Regression Rates at Surgery.

Dworak tumour regression grades (TRG) were used to assess pathologic response: TRG0=no regression. TRG1=dominant tumor mass with obvious fibrosis and/or vasculopathy; TRG2=dominant fibrotic changes with few tumour cells or groups; TRG3=very few (difficult to find microscopically) tumour cells in fibrotic tissue with or without mucus substance. TRG4=no intact viable tumour cells, only fibrotic mass or presence of mucin lakes without associated malignant cells (total tumour regression). Pathologic assessments of tumour response post chemoradiotherapy as provided by investigators (read by local pathologists on operative specimens) were reviewed centrally for all pts for whom surgical materials were available (centrally reviewed set). The diagnosis of independent central reviewers primed. Pathologic complete response rates (TRG4) are reported (%). Good (TRG3 and TRG4 together) and little (TRG 0,1 and 2) tumour regression rates are summarized. For these 2 last rows, % add to 100. (NCT00828672)
Timeframe: 4 months

,
Interventionpercentage of cases (Number)
Pathological complete response (Dworak TRG=4) %Good tumour regression (Dworak TRG=3-4) %Little tumour regression (Dworak TRG=0-1-2) %
AX (ARM 2)112476
AXE (ARM 1)344159

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Recurrence Rates and Disease Free Survival

Counts and proportions of patients experiencing recurrence of disease (local and distant). (NCT00828672)
Timeframe: up to 5 years

,
InterventionParticipants (Count of Participants)
Recurred Dec 2017Not recurred Dec 2017Lost to FU
AX (ARM 2)9320
AXE (ARM 1)9331

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Types and Numbers of Adverse Events - General Overview

Adverse events graded as per NCI CTCAE (US National Cancer Institute Common Terminology Criteria for Adverse Events) version 3.0. All Serious Adverse Events occurrences are reported and counts are summarized here; all Adverse Events (all grades) related and not related to study treatment are reported and summarized here; all severe laboratory events (hematology and biochemistry Gr 3 and higher) are reported and summarized here; all severe postoperative complications (Gr 3 and higher) occurred within the first month post surgery are reported and summarized here. See section Adverse events for details. (NCT00828672)
Timeframe: continuous up to 1 year

,
Interventioncounts of events (Number)
Serious adverse eventsAll adverse eventsSevere lab eventsPost operative complications at 1 month
AX (ARM 2)12426169
AXE (ARM 1)225642714

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Clinical Response Rate

"Baseline tumour measurements were performed within 4 weeks prior to treatment start (RECIST). The same methods of assessment (CT and/or MRI) were used for each measurable lesion at baseline and during follow-up.~Complete Response (CR) is disappearance of all clinical and radiological evidence of tumour (both target and non-target lesions).~Partial Response (PR) is at least a 30% decrease in the sum of LD of target lesions, taking as reference the baseline sum of tumour longest diameters (LD).~Stable Disease (SD) is steady state of disease. Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD.~Progressive Disease (PD) is at least a 20% increase in the sum of LD of measured lesions taking as references the smallest sum LD recorded since the treatment started. Appearance of new lesions constitutes PD. In exceptional circumstances, unequivocal progression of non-target lesions was considered evidence of PD." (NCT00828672)
Timeframe: 3 months

,
InterventionParticipants (Count of Participants)
CRPRSDPDNA
AX (ARM 2)5171315
AXE (ARM 1)324907

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PFS as Assessed by the Investigator

Tumor response was assessed by the investigator according to modified RECIST. All measurable lesions up to a maximum of 5 per organ and 10 in total were identified as TLs and recorded at baseline. A sum of the longest diameter for all TLs was calculated as baseline SLD. PD for TLs was defined as >/=20% increase in the SLD, taking as reference the smallest SLD recorded since treatment started or the appearance of 1 or more new lesions. PD for non-TLs was defined as appearance of 1 or more new lesions and/or unequivocal progression of existing non-TLs. PFS was defined as the time from randomization to first documented PD by Investigator or death from any cause (whichever occurred earlier). The median duration of PFS was estimated using Kaplan-Meier method. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

InterventionMonths (Median)
Trastuzumab Emtansine9.4
Lapatinib + Capecitabine5.8

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Time to Treatment Failure

"Time to treatment failure was defined as the time from randomization to discontinuation of treatment for any reason, including PD (per investigator review), treatment toxicity, or death from any cause. For Lapatinib + Capecitabine arm, a participant was considered as treatment failure only if both drugs were discontinued with treatment failure date as the later of the 2 discontinuation dates. For TLs, PD was defined as >/=20% increase in the SLD, taking as reference the smallest SLD recorded since treatment started or the appearance of 1 or more new lesions. For non-TLs, PD was defined as appearance of 1 or more new lesions and/or unequivocal progression of existing non-TLs. The median time to treatment failure was estimated using Kaplan-Meier method. The 95% CI was computed using the method of Brookmeyer and Crowley." (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

InterventionMonths (Median)
Trastuzumab Emtansine7.9
Lapatinib + Capecitabine5.8

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Duration of Objective Response (DOR) as Assessed by an IRC

Tumor response was assessed by an IRC according to modified RECIST. DOR was defined as the time from first documented OR to first documented PD or death from any cause, whichever occurred earlier. OR was defined as a CR or PR determined on 2 consecutive tumor assessments at least 4 weeks apart. For TLs, CR was defined as the disappearance of all TLs; PR was defined as >/=30% decrease in the SLD of TLs, taking as reference the baseline SLD; and PD was defined as >/=20% increase in the SLD, taking as reference the smallest SLD recorded since treatment started or the appearance of 1 or more new lesions. For non-TLs, CR was defined as the disappearance of all non-TLs; PR was defined as the persistence of 1 or more non-TLs; and PD was defined as appearance of 1 or more new lesions and/or unequivocal progression of existing non-TLs. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

InterventionMonths (Median)
Trastuzumab Emtansine12.6
Lapatinib + Capecitabine6.5

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Overall Survival: Final Analysis

OS was defined as the time from the date of randomization to the date of death from any cause. The median duration of OS was estimated using Kaplan-Meier method. The 95% CI was computed using the method of Brookmeyer and Crowley. The results reported are from the final analysis. The final analysis is descriptive. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 31 Dec 2014 (up to 5 years, 11 months)

InterventionMonths (Median)
Trastuzumab Emtansine29.9
Lapatinib + Capecitabine25.9

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Overall Survival: Second Interim Analysis (Co-primary Endpoint)

OS was defined as the time from the date of randomization to the date of death from any cause. The median duration of OS was estimated using Kaplan-Meier method. The 95% CI was computed using the method of Brookmeyer and Crowley. The results are reported from second interim analysis, which deemed to be the confirmatory. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 31 Jul 2012 (up to 3 years, 5 months)

InterventionMonths (Median)
Trastuzumab Emtansine30.9
Lapatinib + Capecitabine25.1

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Percentage of Participants Who Died: Final Analysis

The percentage of participants who died from any cause was reported. The results reported are from the final analysis. The final analysis is descriptive. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 31 Dec 2014 (up to 5 years, 11 months)

Interventionpercentage of participants (Number)
Trastuzumab Emtansine61.2
Lapatinib + Capecitabine67.1

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Percentage of Participants Who Died: Second Interim Analysis

The percentage of participants who died from any cause was reported. The results are reported from second interim analysis, which deemed to be the confirmatory. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 31 Jul 2012 (up to 3 years, 5 months)

Interventionpercentage of participants (Number)
Trastuzumab Emtansine30.1
Lapatinib + Capecitabine36.7

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Percentage of Participants Who Were Alive at Year 1

1 year survival was defined as the percentage of participants alive 1 year after starting treatment. The results reported are from the final analysis. (NCT00829166)
Timeframe: Year 1

Interventionpercentage of participants (Number)
Trastuzumab Emtansine85.3
Lapatinib + Capecitabine78.9

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Percentage of Participants Who Were Alive at Year 2

2 year survival was defined as the percentage of participants alive 2 years after starting treatment. The results reported are from the final analysis. (NCT00829166)
Timeframe: Year 2

Interventionpercentage of participants (Number)
Trastuzumab Emtansine59.6
Lapatinib + Capecitabine52.4

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Percentage of Participants With Clinical Benefit as Assessed by an IRC

Tumor response was assessed by an IRC according to modified RECIST. Participants were considered as experienced clinical benefit if they had an OR or maintained stable disease (SD) for at least 6 months from randomization. OR: CR or PR determined on 2 consecutive tumor assessments >/=4 weeks apart. For TLs, CR: disappearance of all TLs; PR: >/=30% decrease in the SLD of TLs, taking as reference the baseline SLD; PD: >/=20% increase in the SLD, taking as reference the smallest SLD recorded since treatment started or appearance of 1 or more new lesions; and SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. For non-TLs, CR: disappearance of all non-TLs; PR/SD: persistence of 1 or more non-TLs; and PD: appearance of 1 or more new lesions and/or unequivocal progression of existing non-TLs. Participants without a post-baseline tumor assessment were considered non-responders. The 95% CI was computed using Blyth-Still Casella exact CI method. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

Interventionpercentage of participants (Number)
Trastuzumab Emtansine58.2
Lapatinib + Capecitabine44.2

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Progression-free Survival (PFS) as Assessed by an IRC (Co-primary Endpoint)

Tumor response was assessed by an IRC according to modified RECIST. All measurable lesions up to a maximum of 5 per organ and 10 in total were identified as TLs (on the basis of their size and their suitability for accurate repeated measurements either by imaging or clinically) and recorded at baseline. A sum of the longest diameter for all TLs was calculated as baseline SLD. All other lesions were identified as non-TLs and recorded at baseline. PD for TLs: >/= 20% increase in the SLD, taking as reference the smallest SLD recorded since treatment started or appearance of 1 or more new lesions. PD for non-TLs: appearance of 1 or more new lesions and/or unequivocal progression of existing non-TLs. PFS: time from randomization to first documented PD by IRC or death from any cause (whichever occurred earlier). The median duration of PFS was estimated using Kaplan-Meier method. The 95% confidence interval (CI) was computed using the method of Brookmeyer and Crowley. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

InterventionMonths (Median)
Trastuzumab Emtansine9.6
Lapatinib + Capecitabine6.4

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Percentage of Participants With Objective Response (OR) as Assessed by an IRC

Tumor response was assessed by an IRC according to modified RECIST. OR was defined as the percentage of participants with a complete response (CR) or partial response (PR). All measurable lesions up to a maximum of 5 per organ and 10 in total were identified as TLs and recorded at baseline. A sum of the longest diameter for all TLs was calculated as baseline SLD. For TLs, a CR was defined as the disappearance of all TLs and a PR was defined as >/= 30% decrease in the SLD of TLs, taking as reference the baseline SLD. For non-TLs, a CR was defined as the disappearance of all non-TLs and a PR was defined as the persistence of 1 or more non-TLs. Confirmation of response at a consecutive tumor assessment at least 4 weeks apart was required. Participants without a post-baseline tumor assessment were considered non-responders. The percentage of participants with CR or PR by IRC was reported. The 95% CI was computed using Blyth-Still Casella exact CI method. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

Interventionpercentage of participants (Number)
Trastuzumab Emtansine43.6
Lapatinib + Capecitabine30.8

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Percentage of Participants With PD or Death as Assessed by an Independent Review Committee (IRC)

PD was assessed by an IRC using modified Response Evaluation Criteria in Solid Tumors (RECIST). All measurable lesions up to a maximum of 5 per organ and 10 in total were identified as target lesions (TLs) and recorded at baseline. TLs should be selected on the basis of their size (those with the longest diameter) and their suitability for accurate repeated measurements either by imaging or clinically. A sum of the longest diameter for all TLs was calculated as baseline sum longest diameter (SLD). All other lesions (or sites of disease) should be identified as non-TLs and recorded at baseline. PD for TLs was defined as greater than or equal to (>/=) 20 percent (%) increase in SLD, taking as reference smallest SLD recorded since treatment started or appearance of 1 or more new lesions. PD for non-TLs was defined as appearance of 1 or more new lesions and/or unequivocal progression of existing non-TLs. Percentage of Participants with PD by IRC or death from any cause was reported. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

Interventionpercentage of participants (Number)
Trastuzumab Emtansine53.5
Lapatinib + Capecitabine61.3

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Time to Symptom Progression

"Time to symptom progression was defined as the time from randomization to the first documentation of a >/= 5-point decrease from baseline in the scoring of responses as measured by the FACT-B questionnaire with the TOI-PFB subscale. The FACT-B TOI-PFB subscale contained 24 items from 3 subsections of the FACT-B questionnaire: Physical well-being, functional well-being, and additional concerns for breast cancer participants (BCS). All items in the questionnaire were rated by the participant on a 5-point scale ranging from 0 (not at all) to 4 (very much). The total score ranged from 0 to 96 with higher score indicating better perceived quality of life. The median time to symptom progression was estimated using Kaplan-Meier method. The 95% CI was computed using the method of Brookmeyer and Crowley." (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

InterventionMonths (Median)
Trastuzumab Emtansine7.1
Lapatinib + Capecitabine4.6

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Percentage of Participants With PD or Death as Assessed by the Investigator

PD was assessed by the investigator using modified RECIST. All measurable lesions up to a maximum of 5 per organ and 10 in total were identified as TLs and recorded at baseline. A sum of the longest diameter for all TLs was calculated as baseline SLD. PD for TLs was defined as >/=20% increase in the SLD, taking as reference the smallest SLD recorded since treatment started or the appearance of 1 or more new lesions. PD for non-TLs was defined as appearance of 1 or more new lesions and/or unequivocal progression of existing non-TLs. The percentage of participants who died or experienced PD by Investigator was reported. (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

Interventionpercentage of participants (Number)
Trastuzumab Emtansine58.0
Lapatinib + Capecitabine67.5

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Percentage of Participants With Symptom Progression

"Symptom progression was defined as the documentation of a >/= 5-point decrease from baseline in the scoring of responses as measured by the Functional Assessment of Cancer Therapy-for participants with Breast Cancer (FACT-B) questionnaire with the Trial Outcomes Index-Physical/Functional/Breast (TOI-PFB) subscale. The FACT-B TOI-PFB subscale contained 24 items from 3 subsections of the FACT-B questionnaire: Physical well-being, functional well-being, and additional concerns for breast cancer participants (breast cancer subscale [BCS]). All items in the questionnaire were rated by the participant on a 5-point scale ranging from 0 (not at all) to 4 (very much). The total score ranged from 0 to 96 with higher score indicating better perceived quality of life. The percentage of participants with symptom progression was reported." (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

Interventionpercentage of participants (Number)
Trastuzumab Emtansine54.7
Lapatinib + Capecitabine57.8

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Percentage of Participants With Treatment Failure

"Treatment failure was defined as discontinuation of treatment for any reason, including PD (per investigator review), treatment toxicity, or death from any cause. For Lapatinib + Capecitabine arm, a participant was considered as treatment failure only if both drugs were discontinued. For TLs, PD was defined as >/=20% increase in the SLD, taking as reference the smallest SLD recorded since treatment started or the appearance of 1 or more new lesions. For non-TLs, PD was defined as appearance of 1 or more new lesions and/or unequivocal progression of existing non-TLs. Percentage of participants with treatment failure was reported." (NCT00829166)
Timeframe: From the date of randomization through the data cut-off date of 14 Jan 2012 (up to 2 years, 11 months)

Interventionpercentage of participants (Number)
Trastuzumab Emtansine63.2
Lapatinib + Capecitabine74.8

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Volume of Distribution (Vz) for Cisplatin

Volume of distribution is defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired blood concentration of a drug. Clearance for cisplatin (assessed by estimating total platinum in plasma ultrafiltrate) in presence of steady-state axitinib was evaluated on Cycle 1 Day 1 and in absence of axitinib (cisplatin alone) on Cycle 2 Day 1. (NCT00842244)
Timeframe: 0 (pre-dose), 0.5, 1, 2, 3, 4, 6, 8 hrs post-cisplatin infusion start on C1D1, C2D1

InterventionLiter (Geometric Mean)
Cisplatin aloneCisplatin in presence of axitinib
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)55.3570.32

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Duration of Response (DR)

Time in months from the first documentation of objective tumor response to objective tumor progression or death due to any cause. Duration of tumor response was calculated as (the date of the first documentation of objective tumor progression or death minus the date of the first CR or PR that was subsequently confirmed plus 1) divided by 30.4. DR was calculated for the subgroup of participants with a confirmed objective tumor response. CR = disappearance of all target lesions. PR = at least 30% decrease in sum of the longest dimensions of target lesions taking the baseline sum of the longest dimensions as a reference. (NCT00842244)
Timeframe: Baseline up to disease progression or withdrawal, assessed on Day 21 of every other cycle starting from Cycle 2 up to Day 784

Interventionmonths (Median)
Axitinib + Capecitabine + Cisplatin9.07

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Time to Reach Maximum Observed Plasma Concentration (Tmax) for Axitinib, Capecitabine, Capecitabine's Metabolites and Cisplatin

Tmax for axitinib in absence of chemotherapy (axitinib alone) was evaluated on Cycle 1 Day -1 and in combination with chemotherapy on Cycle 1 Day 1. Tmax for cisplatin (assessed by estimating total platinum in plasma ultrafiltrate), capecitabine and capecitabine's metabolites (5-FU, 5-DFUR and 5-DFC) in presence of steady-state axitinib were evaluated on Cycle 1 Day 1 and in absence of axitinib (cisplatin/capecitabine alone) on Cycle 2 Day 1. (NCT00842244)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hrs post-axitinib dose on C1D-1, C1D1; 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hrs post-capecitabine dose C1D1, C2D1; 0 (pre-dose), 0.5, 1, 2, 3, 4, 6, 8 hrs post-cisplatin infusion start C1D1, C2D1

Interventionhrs (Median)
Axitinib alone (n = 10)Axitinib in combination with chemotherapy (n = 10)Capecitabine alone (n = 8)Capecitabine in presence of axitinib (n = 8)5-FU alone (n = 8)5-FU in presence of axitinib (n = 8)5-DFUR alone (n = 8)5-DFUR in presence of axitinib (n = 8)5-DFC alone (n = 8)5-DFC in presence of axitinib (n = 8)Cisplatin alone (n = 8)Cisplatin in presence of axitinib (n = 8)
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)3.984.002.453.122.502.622.502.622.503.092.001.02

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Plasma Decay Half-Life (t1/2) for Axitinib, Capecitabine, Capecitabine's Metabolites and Cisplatin

Plasma decay half-life is the time measured for the plasma concentration to decrease by one half. Plasma decay half life for axitinib in absence of chemotherapy (axitinib alone) was evaluated on Cycle 1 Day -1 and in combination with chemotherapy on Cycle 1 Day 1. Plasma decay half life for cisplatin (assessed by estimating total platinum in plasma ultrafiltrate), capecitabine and capecitabine's metabolites (5-FU, 5-DFUR and 5-DFC) in presence of steady-state axitinib were evaluated on Cycle 1 Day 1 and in absence of axitinib (cisplatin/capecitabine alone) on Cycle 2 Day 1. (NCT00842244)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hrs post-axitinib dose on C1D-1, C1D1; 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hrs post-capecitabine dose C1D1, C2D1; 0 (pre-dose), 0.5, 1, 2, 3, 4, 6, 8 hrs post-cisplatin infusion start C1D1, C2D1

Interventionhrs (Mean)
Axitinib alone (n = 9)Axitinib in combination with chemotherapy (n = 9)Capecitabine alone (n = 6)Capecitabine in presence of axitinib (n = 6)5-FU alone (n = 3)5-FU in presence of axitinib (n = 3)5-DFUR alone (n = 4)5-DFUR in presence of axitinib (n = 4)5-DFC alone (n = 5)5-DFC in presence of axitinib (n = 5)Cisplatin alone (n = 7)Cisplatin in presence of axitinib (n = 7)
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)5.763.500.710.891.111.050.960.770.980.781.251.61

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Maximum Observed Plasma Concentration (Cmax) for Axitinib, Capecitabine, Capecitabine's Metabolites and Cisplatin

Cmax for axitinib in absence of chemotherapy (axitinib alone) was evaluated on Cycle 1 Day -1 and in combination with chemotherapy on Cycle 1 Day 1. Cmax for cisplatin (assessed by estimating total platinum in plasma ultrafiltrate), capecitabine and capecitabine's metabolites (5-fluorouracil [5-FU], 5-deoxy-5-fluorouridine [5-DFUR] and 5-deoxy-5-fluorocytidine [5-DFC]) in presence of steady-state axitinib were evaluated on Cycle 1 Day 1 and in absence of axitinib (cisplatin/capecitabine alone) on Cycle 2 Day 1. Results for axitinib were normalized to axitinib 5 mg dose, results for capecitabine and its metabolites (5-FU, 5-DFUR and 5-DFC) were normalized to Cycle 1 Day 1 capecitabine dose and results for cisplatin were normalized to Cycle 1 Day 1 cisplatin dose. (NCT00842244)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hrs post-axitinib dose on Cycle 1 (C1) Day -1 (D-1), C1D1; 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hrs post-capecitabine dose C1D1, C2D1; 0 (pre-dose), 0.5, 1, 2, 3, 4, 6, 8 hrs post-cisplatin infusion start C1D1, C2D1

Interventionnanogram/milliliter (ng/mL) (Geometric Mean)
Axitinib alone (n = 10)Axitinib in combination with chemotherapy (n = 10)Capecitabine alone (n = 8)Capecitabine in presence of axitinib (n = 8)5-FU alone (n = 8)5-FU in presence of axitinib (n = 8)5-DFUR alone (n = 8)5-DFUR in presence of axitinib (n = 8)5-DFC alone (n = 8)5-DFC in presence of axitinib (n = 8)Cisplatin alone (n = 8)Cisplatin in presence of axitinib (n = 8)
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)16.1124.335255.622274.80220.4990.975791.813017.275891.293227.571665.271865.07

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Clearance (CL) for Cisplatin

Drug clearance is a quantitative measure of the rate at which a drug substance is removed from the blood. It is defined as the volume of blood from which drug can be completely removed per unit of time. Clearance for cisplatin (assessed by estimating total platinum in plasma ultrafiltrate) in presence of steady-state axitinib was evaluated on Cycle 1 Day 1 and in absence of axitinib (cisplatin alone) on Cycle 2 Day 1. (NCT00842244)
Timeframe: 0 (pre-dose), 0.5, 1, 2, 3, 4, 6, 8 hrs post-cisplatin infusion start on C1D1, C2D1

InterventionLiter/hr (Geometric Mean)
Cisplatin aloneCisplatin in presence of axitinib
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)30.9432.50

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Area Under the Curve From Time Zero to Last Quantifiable Concentration (AUClast) for Capecitabine, Capecitabine's Metabolites and Cisplatin

Area under the plasma concentration time-curve from zero to the last measurable concentration (AUClast). AUClast for cisplatin (assessed by estimating total platinum in plasma ultrafiltrate), capecitabine and capecitabine's metabolites (5-FU, 5-DFUR, 5-DFC) in presence of steady-state axitinib were evaluated on Cycle 1 Day 1 and in absence of axitinib (cisplatin/capecitabine alone) on Cycle 2 Day 1. Results for capecitabine and its metabolites (5-FU, 5-DFUR and 5-DFC) were normalized to Cycle 1 Day 1 capecitabine dose and results for cisplatin were normalized to Cycle 1 Day 1 cisplatin dose. (NCT00842244)
Timeframe: 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hrs post-capecitabine dose C1D1, C2D1; 0 (pre-dose), 0.5, 1, 2, 3, 4, 6, 8 hrs post-cisplatin infusion start C1D1, C2D1

Interventionnanogram*hour/milliliter (ng*hr/mL) (Geometric Mean)
Capecitabine aloneCapecitabine in presence of axitinib5-FU alone5-FU in presence of axitinib5-DFUR alone5-DFUR in presence of axitinib5-DFC alone5-DFC in presence of axitinibCisplatin aloneCisplatin in presence of axitinib
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)7109.594194.97332.37176.819996.556683.3310820.147983.143814.933951.57

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Area Under the Curve From Time Zero to 24 Hours [AUC (0-24)] for Axitinib

AUC (0-24) = Area under the plasma concentration versus time curve from time zero (pre-dose) to 24 hours. AUC (0-24) for axitinib in absence of chemotherapy (axitinib alone) was evaluated on Cycle 1 Day -1 and in combination with chemotherapy on Cycle 1 Day 1. Results for axitinib were normalized to axitinib 5 mg dose. (NCT00842244)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hrs post-axitinib dose on C1D-1, C1D1

Interventionng*hr/mL (Geometric Mean)
Axitinib aloneAxitinib in combination with chemotherapy
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)206.20265.89

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Area Under the Curve From Time Zero Extrapolated to Infinite Time [AUC (0 - ∞)] for Axitinib, Capecitabine, Capecitabine's Metabolites and Cisplatin

AUC (0 - ∞) = Area under the plasma concentration versus time curve (AUC) from time zero (pre-dose) extrapolated to infinite time (0 - ∞). It is obtained from AUC (0 - t) plus AUC (t - ∞). AUC (0 - ∞) for axitinib in absence of chemotherapy (axitinib alone) was evaluated on Cycle 1 Day -1 and in combination with chemotherapy on Cycle 1 Day 1. AUC (0 - ∞) for cisplatin (assessed by estimating total platinum in plasma ultrafiltrate), capecitabine and capecitabine's metabolites (5-FU, 5-DFUR and 5-DFC) in presence of steady-state axitinib were evaluated on Cycle 1 Day 1 and in absence of axitinib (cisplatin/capecitabine alone) on Cycle 2 Day 1. Results for axitinib were normalized to axitinib 5 mg dose, results for capecitabine and its metabolites (5-FU, 5-DFUR and 5-DFC) were normalized to Cycle 1 Day 1 capecitabine dose and results for cisplatin were normalized to Cycle 1 Day 1 cisplatin dose. (NCT00842244)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hrs post-axitinib dose on C1D-1, C1D1; 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hrs post-capecitabine dose C1D1, C2D1; 0 (pre-dose), 0.5, 1, 2, 3, 4, 6, 8 hrs post-cisplatin infusion start C1D1, C2D1

Interventionng*hr/mL (Geometric Mean)
Axitinib alone (n = 9)Axitinib in combination with chemotherapy (n = 9)Capecitabine alone (n = 6)Capecitabine in presence of axitinib (n = 6)5-FU alone (n = 3)5-FU in presence of axitinib (n = 3)5-DFUR alone (n = 4)5-DFUR in presence of axitinib (n = 4)5-DFC alone (n = 5)5-DFC in presence of axitinib (n = 5)Cisplatin alone (n = 7)Cisplatin in presence of axitinib (n = 7)
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)147.04156.007140.624213.72337.85261.959568.706966.0711587.977787.393979.073990.34

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Apparent Volume of Distribution (Vz/F) for Axitinib, Capecitabine and Capecitabine's Metabolites

Volume of distribution is defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired blood concentration of a drug. Vz/F is influenced by the fraction absorbed. Vz/F for axitinib in absence of chemotherapy (axitinib alone) was evaluated on Cycle 1 Day -1 and in combination with chemotherapy on Cycle 1 Day 1. Vz/F for capecitabine in presence of steady-state axitinib was evaluated on Cycle 1 Day 1 and in absence of axitinib (capecitabine alone) on Cycle 2 Day 1. (NCT00842244)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hrs post-axitinib dose on C1D-1, C1D1; 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hrs post-capecitabine dose on C1D1, C2D1

InterventionLiter (Geometric Mean)
Axitinib alone (n = 9)Axitinib in combination with chemotherapy (n = 9)Capecitabine alone (n = 6)Capecitabine in presence of axitinib (n = 6)
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)344.87171.83190.94425.00

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Apparent Oral Clearance (CL/F) for Axitinib, Capecitabine and Capecitabine's Metabolites

Clearance (CL) of a drug is a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Clearance obtained after oral dose (apparent oral clearance) is influenced by the fraction of the dose absorbed (F). Clearance is defined as the volume of blood from which drug can be completely removed per unit of time. CL/F for axitinib in absence of chemotherapy (axitinib alone) was evaluated on Cycle 1 Day -1 and in combination with chemotherapy on Cycle 1 Day 1. CL/F for capecitabine in presence of steady-state axitinib was evaluated on Cycle 1 Day 1 and in absence of axitinib (capecitabine alone) on Cycle 2 Day 1. (NCT00842244)
Timeframe: 0 (pre-dose), 1, 2, 3, 4, 6, 8 hrs post-axitinib dose on C1D-1, C1D1; 0 (pre-dose), 0.25, 0.5, 1, 2, 3, 4, 6, 8 hrs post-capecitabine dose on C1D1, C2D1

InterventionLiter/hr (Geometric Mean)
Axitinib alone (n = 9)Axitinib in combination with chemotherapy (n = 9)Capecitabine alone (n = 6)Capecitabine in presence of axitinib (n = 6)
Axitinib + Capecitabine + Cisplatin (PK Expansion Cohort)48.5537.69217.60368.47

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Progression-Free Survival (PFS)

"Time in months from start of study treatment to first documentation of objective tumor progression or death due to any cause. PFS was calculated as (first event date minus the date of first dose of study medication plus 1) divided by 30.4. Tumor progression was determined from oncologic assessment data (where data meet the criteria for progressive disease [PD]), or from adverse event (AE) data (where the outcome was Death). PD was a>=20% increase in sum of the longest dimensions of target lesions taking as a reference the smallest sum of the longest dimensions recorded since the treatment started, or the appearance of 1 or more new lesions." (NCT00842244)
Timeframe: Baseline up to disease progression or withdrawal, assessed on Day 21 of every other cycle starting from Cycle 2 up to Day 784

Interventionmonths (Median)
Axitinib + Capecitabine + Cisplatin3.75

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Percentage of Participants With Objective Response (OR)

Number of participants with objective response based assessment of confirmed complete response (CR) or confirmed partial response (PR) according to Response Evaluation Criteria in Solid Tumors (RECIST). Confirmed response are those that persist on repeat imaging study at least 4 weeks after initial documentation of response. CR are those with disappearance of all target lesions. PR are those with at least 30 percent (%) decrease in sum of the longest dimensions of target lesions taking the baseline sum of the longest dimensions as a reference. (NCT00842244)
Timeframe: Baseline up to disease progression or withdrawal, assessed on Day 21 of every other cycle starting from Cycle 2 up to Day 784

Interventionpercentage of participants (Number)
Axitinib + Capecitabine + Cisplatin36.36

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Maximum Tolerated Dose (MTD) of Axitinib (AG-013736) in Combination With Cisplatin and Capecitabine

MTD = highest dose at which no more than 30 percent (%) of 12 participants experience DLT during Cycle 1. DLT = GR2 proteinuria; GR3 NHT (excluding alopecia and those that can be controlled with appropriate treatment)for >=7 days, GR3 thrombocytopenia with active bleeding; GR >=3 febrile NP/NP infection; GR 3 or 4 nausea, vomiting or diarrhea despite anti-emetics, anti-diarrheals; GR4 NHT, thrombocytopenia, NP for >=7 days; >= 1/2 teaspoon per day hemoptysis; any treatment-related toxicity with >3 consecutive days of capecitabine or 5 consecutive days of axitinib missed doses per cycle; delayed toxicity recovery >14 days. (NCT00842244)
Timeframe: Baseline up to Day 21 of Cycle 1

Interventionmg (Number)
Axitinib + Capecitabine + Cisplatin (MTD Determination)5

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Number of Participants With Cycle 1 Dose-limiting Toxicities (DLTs)

DLT = Grade (GR) 2 proteinuria; GR3 nonhematological toxicity (NHT) (excluding alopecia and those that can be controlled with appropriate treatment) for greater than or equal to (>=)7 days, GR3 thrombocytopenia with active bleeding; GR >=3 febrile neutropenia (NP) or NP infection; GR 3 or 4 nausea, vomiting or diarrhea despite anti-emetics, anti-diarrheals; GR4 NHT, thrombocytopenia, NP for >=7 days; >= 1/2 teaspoon per day hemoptysis; any treatment related toxicity with >3 consecutive days of capecitabine or 5 consecutive days of axitinib missed doses per cycle; delayed toxicity recovery >14 days. (NCT00842244)
Timeframe: Baseline up to Day 21 of Cycle 1

Interventionparticipants (Number)
Axitinib + Capecitabine + Cisplatin (MTD Determination)3

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Number of Patients With One-year Recurrence-free Survival

This is defined as the patients who did not have recurrence of cancer at 1 year since the start of induction chemotherapy. (NCT00848783)
Timeframe: 1 year

Interventionparticipants (Number)
A-with IP Floxuridine3
B-Without IP Floxuridine2

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Number of Participants With Partial Response (PR)

PR according to Response Evaluation Criteria in Solid Tumors (RECIST) criteria, which is defined as a reduction of ≥ 30% in the sum of the longest diameter for all target lesions lasting > 4 weeks, during which no new lesions may appear, when compared with with pretreatment measurements. (NCT00869050)
Timeframe: 12 months

Interventionparticipants (Number)
Capecitabine and Temozolomide9

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Number of Participants With Complete Response (CR)

CR according to Response Evaluation Criteria in Solid Tumors (RECIST) criteria, which is defined as disappearance of all target lesions (primary and metastases), signs, symptoms, and biochemical changes related to the tumor for >4 weeks, during which no new lesions may appear and no existing lesion may enlarge. (NCT00869050)
Timeframe: 12 months

Interventionparticipants (Number)
Capecitabine and Temozolomide3

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Overall Survival

Time of study entry to time of death (NCT00881621)
Timeframe: 24 months

Interventionmonths (Median)
Lapatinib and Capecitabine5.2

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Clinical Benefit Response

"number of participants who had stable disease or partial response or complete response per Response Evaluation Criteria In Solid Tumors.~Complete Response: Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~Partial Response: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters.~Progressive Disease: At least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm.~Stable Disease: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study." (NCT00881621)
Timeframe: 3 months

Interventionparticipants (Number)
Lapatinib and Capecitabine6

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Adverse Events

Grade 3 or 4 toxicities (NCT00881621)
Timeframe: 2 years

Interventionparticipants (Number)
Lapatinib and Capecitabine3

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Progression Free Survival

Time of study entry to cancer progression. (NCT00881621)
Timeframe: 24 months

Interventionmonths (Median)
Lapatinib and Capecitabine2.6

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Overall Survival in ITT Population

Overall survival was calculated in months from the day of screening until death. (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until death (up to 46 months)

Interventionmonths (Median)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)NA

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Overall Survival in Per Protocol Population

Overall survival was calculated in months from the day of screening until death. (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until death (up to 46 months)

Interventionmonths (Median)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)36.40

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Part I: TTP in Intent to Treat (ITT) Population

TTP was determined as the time in months from the date of screening until first progression. In participants with measurable disease, progression was defined according to RECIST (SLD increased by at least 20% from the smallest value on study [including baseline, if that is the smallest]). In participants with non-measurable disease, progression was defined as the presence of new lesions or unequivocal progression during treatment. (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

Interventionmonths (Median)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)22.21
Group B: Trastuzumab+Taxane/ Capecitabine <6 Weeks1.22

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Part II: PFS in ITT Population

PFS was calculated from first study medication in Part II to date of progression or death. In participants with measurable disease progression was defined according to RECIST (SLD increased by at least 20% from the smallest value on study [including baseline, if that is the smallest]). In participants with non-measurable disease, progression was defined as the presence of new lesions or unequivocal progression during treatment. (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

Interventionmonths (Median)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)5.65
Group B: Trastuzumab+Taxane/ Capecitabine <6 Weeks13.83

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Part II: TTP in Intent to Treat (ITT) Population

TTP was calculated from first study medication in Part II to date of progression. In participants with measurable disease progression was defined according to RECIST(SLD increased by at least 20% from the smallest value on study [including baseline, if that is the smallest]). In participants with non-measurable disease, progression was defined as the presence of new lesions or unequivocal progression during treatment. (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 Cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

Interventionmonths (Median)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)5.65
Group B: Trastuzumab+Taxane/ Capecitabine <6 Weeks13.83

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Part I and II: Percentage of Participants With a Best Overall Response of CR or PR in ITT Population

Best Overall response was defined according to RECIST. CR: disappearance of all target lesions and all pathological lymph nodes below 10 mm. PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. PD: At least a 20% increase in the sum of diameters of target lesions, and the sum must also demonstrate an absolute increase of at least 5 mm or persistence of non-target lesions. (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 Cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

Interventionpercentage of participants (Number)
Part I: Responders (n=20)Part I: Non-Responders (n=20)Part I: Missing (n=20)Part II: Responders (n=9)Part II: Non-Responders (n=9)Part II: Missing (n=9)
Group A: Trastuzumab+Taxane /Capcetabine (6 Weeks)75.020.05.011.188.90.0

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Part I: Percentage of Participants With a Best Overall Response (BOR) of Complete Response (CR), Partial Response (PR), Stable Disease (SD) or Progrerssive Disease (PD) by Biomarker

BOR was defined according to the Response Evaluation Criteria In Solid Tumors (RECIST). CR: disappearance of all target lesions and all pathological lymph nodes below 10 mm. PR: At least a 30% decrease in the sum of diameters of target lesions. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. PD: At least a 20% increase in the sum of diameters of target lesions, and the sum must also demonstrate an absolute increase of at least 5 mm or persistence of non-target lesions. The relationship between best response and the following biomarkers was investigated: p95 HER2 (+ve/-ve), IGF1R, c-MET, PTEN, HER2 (median/≥median), PI3K catalytic subunit (WT/M), and FC gamma receptors IIIa, IIa and IIb (phenotypes FF, VF, VV, HH, HR, RR and II, IT and TT respectively). The correlation between the biomarker variables and percentage of participants with best response were investigated using a univariate regression analysis. (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 weeks

Interventionpercentage of participants (Number)
p95 HER2 +ve CR (n=5)p95 HER2 +ve PR (n=5)p95 HER2 +ve SD (n=5)p95 HER2 +ve PD (n=5)p95 HER2 -ve CR (n=12)p95 HER2 -ve PR (n=12)p95 HER2 -ve SD (n=12)p95 HER2 -ve PD (n=12)IGF1R < median CR (n=9)IGF1R < median PR (n=9)IGF1R < median SD (n=9)IGF1R < median PD (n=9)IGF1R ≥median CR (n=9)IGF1R ≥median PR (n=9,0)IGF1R ≥median SD (n=9)IGF1R ≥median PD (n=9)c-MET c-METt c-MET c-MET c-MET ≥median CR (n=11)c-MET ≥median PR (n=11)c-MET ≥median SD (n=11)c-MET ≥median PD (n=11)PTEN PTEN PTEN PTEN PTEN ≥median CR (n=12)PTEN ≥median PR (n=12)PTEN ≥median SD (n=12)PTEN ≥median PD (n=12)HER2 HER2 HER2 HER2 HER2 ≥median CR (n=10)HER2 ≥median PR (n=10)HER2 ≥median SD (n=10)HER2 ≥median PD (n=10)PI3K Amino Acids WT CR (n=11)PI3K Amino Acids WT PR (n=11,0)PI3K Amino Acids WT SD (n=11)PI3K Amino Acids WT PD (n=11)PI3K Amino Acids M CR (n=7)PI3K Amino Acids M PR (n=7,0)PI3K Amino Acids M SD (n=7)PI3K Amino Acids M PD (n=7)FC Gamma Receptor IIIa F176V FF CR (n=6)FC Gamma Receptor IIIa F176V FF PR (n=6)FC Gamma Receptor IIIa F176V FF SD (n=6)FC Gamma Receptor IIIa F176V FF PD (n=6)FC Gamma Receptor IIIa F176V VF CR (n=4)FC Gamma Receptor IIIa F176V VF PR (n=4)FC Gamma Receptor IIIa F176V VF SD (n=4)FC Gamma Receptor IIIa F176V VF PD (n=4)FC Gamma Receptor IIIa F176V VV CR (n=2)FC Gamma Receptor IIIa F176V VV PR (n=2)FC Gamma Receptor IIIa F176V VV SD (n=2)FC Gamma Receptor IIIa F176V VV PD (n=2)FC Gamma Receptor IIa R166H HH CR (n=3)FC Gamma Receptor IIa R166H HH PR (n=3)FC Gamma Receptor IIa R166H HH SD (n=3)FC Gamma Receptor IIa R166H HH PD (n=3)FC Gamma Receptor IIa R166H HR CR (n=5)FC Gamma Receptor IIa R166H HR PR (n=5)FC Gamma Receptor IIa R166H HR SD (n=5)FC Gamma Receptor IIa R166H HR PD (n=5)FC Gamma Receptor IIa R166H RR CR (n=5)FC Gamma Receptor IIa R166H RR PR (n=5)FC Gamma Receptor IIa R166H SD RR (n=5)FC Gamma Receptor IIa R166H RR PD (n=5)FC Gamma Receptor IIb I232T II CR (n=8)FC Gamma Receptor IIb I232T II PR (n=8)FC Gamma Receptor IIb I232T II SD (n=8)FC Gamma Receptor IIb I232T II PD (n=8)FC Gamma Receptor IIb I232T IT CR (n=1)FC Gamma Receptor IIb I232T IT PR (n=1)FC Gamma Receptor IIb I232T IT SD (n=1)FC Gamma Receptor IIb I232T IT PD (n=1)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)0.025.050.025.00.091.78.30.00.062.537.50.00.088.90.011.10.083.30.016.70.070.030.00.00.083.316.70.00.072.718.29.10.075.012.512.50.077.822.20.00.090.00.010.00.057.142.90.016.750.016.716.70.066.733.30.00.0100.00.00.033.366.70.00.00.025.050.025.00.080.020.00.012.550.037.50.00.0100.00.00.0

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Part I and II: Percentage of Participants With a Response by Best Overall Response by CR, PR, SD or PD in ITT Population

Best Overall response was defined according to RECIST. CR: disappearance of all target lesions and all pathological lymph nodes below 10 mm. PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. PD: At least a 20% increase in the sum of diameters of target lesions, and the sum must also demonstrate an absolute increase of at least 5 mm or persistence of non-target lesions. (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

Interventionpercentage of participants (Number)
Part I: CR (n=20)Part I: PR (n=20)Part I: SD (n=20)Part I: PD (n=20)Part I: Missing (n=20)Part II: CR (n=9)Part II: PR (n=9)Part II: SD (n=9)Part II: PD (n=9)Part II: Missing (n=9)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)5.070.015.05.05.00.011.166.722.20.0

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Part I: Time to Progression (TTP) by Biomarker

Progression was defined as an increase by at least 20% from the smallest value in the SLD of lesions.TTP was determined as the time in months from the date of screening until first progression.The relationship between PFS and the following biomarker variables was investigated in each of study Part 1 and 2: p95 HER2 +ve and -ve population, IGF1R NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 Cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 weeks

,
Interventionmonths (Median)
p95 +ve (n=9,0)p95 -ve (n=15,1)IGF1R IGF1R ≥median (n=14,1)c-MET c-MET ≥median (n=15,0)PTEN PTEN ≥median (n=14,1)HER2 HER2 ≥median (n=14,0)PI3K Amino Acids WT (n=17,1)PI3K Amino Acids M (n=9,00)FC Gamma Receptor IIIa F176V FF (n=9,0)FC Gamma Receptor IIIa F176V VF (n=5,1)FC Gamma Receptor IIIa F176V VV (n=4,0)FC Gamma Receptor IIa R166H HH (n=3,0)FC Gamma Receptor IIa R166H HR (n=8,1)FC Gamma Receptor IIa R166H RR (n=8,0)FC Gamma Receptor IIb I232T II (n=12,1)FC Gamma Receptor IIb I232T IT (n=1,0)FC Gamma Receptor IIb I232T TT (n=1,0)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)NA13.96311.33522.40731.17922.20922.20913.963NA22.20913.96322.40713.96311.33522.407NA22.20913.96313.963NANA
Group B: Trastuzumab+Taxane/ Capecitabine <6 WeeksNA1.216NA1.2161.216NANA1.2161.216NA1.216NANA1.216NANA1.216NA1.216NANA

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Part II: Percentage of Participants With a Best Overall Response of CR, PR, SD or PD by Biomarker

Best Overall response was defined according to RECIST. CR: disappearance of all target lesions and all pathological lymph nodes below 10 mm.PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. PD: At least a 20% increase in the sum of diameters of target lesions, and the sum must also demonstrate an absolute increase of at least 5 mm or persistence of non-target lesions. The relationship between best response and the following biomarkers was investigated: p95 HER2 (+ve/-ve), IGF1R, c-MET, PTEN, HER2 (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

Interventionpercentage of participants (Number)
p95 HER2 +ve CR (n=2)p95 HER2 +ve PR (n=2)p95 HER2 +ve SD (n=2)p95 HER2 +ve PD (n=2)p95 HER2 -ve CR (n=4)p95 HER2 -ve PR (n=4)p95 HER2 -ve SD (n=4)p95 HER2 -ve PD (n=4)IGF1R IGF1R IGF1R IGF1R IGF1R ≥median CR (n=3)IGF1R ≥median PR (n=3)IGF1R ≥median SD (n=3)IGF1R ≥median PD (n=3)c-MET c-MET c-MET c-MET c-MET ≥median CR (n=4)c-MET ≥median PR (n=4)c-MET ≥median SD (n=4)c-MET ≥median PD (n=4)PTEN PTEN PTEN PTEN PTEN ≥median CR (n=2)PTEN ≥median PR (n=2)PTEN ≥median SD (n=2)PTEN ≥median PD (n=2)HER2 HER2 HER2 HER2 HER2 ≥median CR (n=4)HER2 ≥median PR (n=4)HER2 ≥median SD (n=4)HER2 ≥median PD (n=4)PI3K Amino Acids WT CR (n=7)PI3K Amino Acids WT PR (n=7)PI3K Amino Acids WT SD (n=7)PI3K Amino Acids WT PD (n=7)PI3K Amino Acids M CR (n=2)PI3K Amino Acids M PR (n=2)PI3K Amino Acids M SD (n=2)PI3K Amino Acids M PD (n=2)FC Gamma Receptor IIIa F176V FF CR (n=3)FC Gamma Receptor IIIa F176V FF PR (n=3)FC Gamma Receptor IIIa F176V FF SD (n=3)FC Gamma Receptor IIIa F176V FF PD (n=3)FC Gamma Receptor IIIa F176V VF CR (n=1)FC Gamma Receptor IIIa F176V VF PR (n=1)FC Gamma Receptor IIIa F176V VF SD (n=1)FC Gamma Receptor IIIa F176V VF PD (n=1)FC Gamma Receptor IIIa F176V VV CR (n=1)FC Gamma Receptor IIIa F176V VV PR (n=1)FC Gamma Receptor IIIa F176V VV SD (n=1)FC Gamma Receptor IIIa F176V VV PD (n=1)FC Gamma Receptor IIa R166H HH CR (n=0)FC Gamma Receptor IIa R166H HH PR (n=0)FC Gamma Receptor IIa R166H HH SD (n=0)FC Gamma Receptor IIa R166H HH PD (n=0)FC Gamma Receptor IIa R166H HR CR (n=5)FC Gamma Receptor IIa R166H HR PR (n=4)FC Gamma Receptor IIa R166H HR SD (n=4)FC Gamma Receptor IIa R166H HR PD (n=4)FC Gamma Receptor IIa R166H RR CR (n=4)FC Gamma Receptor IIa R166H RR PR (n=2)FC Gamma Receptor IIa R166H RR SD (n=2)FC Gamma Receptor IIa R166H RR PD (n=2)FC Gamma Receptor IIb I232T II CR (n=4)FC Gamma Receptor IIb I232T II PR (n=4)FC Gamma Receptor IIb I232T II SD (n=4)FC Gamma Receptor IIb I232T II PD (n=4)FC Gamma Receptor IIb I232T IT CR (N=0)FC Gamma Receptor IIb I232T IT PR (n=0)FC Gamma Receptor IIb I232T IT SD (n=0)FC Gamma Receptor IIb I232T IT PD (n=0)FC Gamma Receptor IIb I232T TT CR (n=4)FC Gamma Receptor IIb I232T TT PR (n=4)FC Gamma Receptor IIb I232T TT SD (n=4)FC Gamma Receptor IIb I232T TT PD (n=4)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)0.00.0100.00.00.00.050.050.00.00.066.733.30.00.066.733.30.00.0100.00.00.00.050.050.00.00.075.025.00.00.050.050.00.00.0100.00.00.00.050.050.00.014.371.414.30.00.050.050.00.00.066.733.30.00.0100.00.00.0100.00.00.0NANANANA0.025.050.025.00.00.0100.00.00.00.075.025.0NANANANA0.00.075.025.0

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Part II: Progression Free Survival (PFS) by Biomarker

PFS was calculated from first study medication in Part II to date of progression or death.The relationship between PFS and the following biomarker variables was investigated in each of study Part 1 and 2: p95HER2 +ve and -ve population, IGF1R NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

,
Interventionmonths (Median)
p95 +ve (n=2,0)p95 -ve (n=5,1)IGF1R IGF1R ≥median (n=4,1)c-METc-MET≥median (n=4,0)PTEN PTEN ≥median (n=3,1)HER2 HER2 ≥median (n=5,0)PI3K Amino Acids WT (n=10,1)PI3K Amino Acids M (n=2,0)FC Gamma Receptor IIIa F176V FF (n=4,0)FC Gamma Receptor IIIa F176V VF (n=2,1)FC Gamma Receptor IIIa F176V VV (n=2,0)FC Gamma Receptor IIa R166H HH (n=1,0)FC Gamma Receptor IIa R166H HR (n=5,1)FC Gamma Receptor IIa R166H RR (n=3,0)FC Gamma Receptor IIb I232T II (n=7,1)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)8.1483.4508.1154.0744.6985.0434.6983.4508.1483.4505.6514.4854.32013.832NA3.4508.1155.6515.651
Group B: Trastuzumab+Taxane/ Capecitabine <6 WeeksNA13.832NA13.83213.832NANA13.83213.832NA13.832NANA13.832NANA13.832NA13.832

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Part II: TTP by Biomarker

TTP was calculated from first study medication in Part II to date of progression. The relationship between TTP and the following biomarker variables was investigated in each of study Part 1 and 2: p95 HER2 +ve and -ve population, IGF1R NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

,
Interventionmonths (Median)
p95 HER2 +ve (n=2,0)p95 HER2 -ve (n=5,1)IGF1R IGF1R ≥median (n=4,1)c-MET c-MET ≥median (n=4,0)PTEN PTEN ≥median (n=3,1)HER2 HER2 ≥median (n=5,0)PI3K Amino Acids WT (n=10,1)PI3K Amino Acids M (n=2,0)FC Gamma Receptor IIIa F176V FF (n=4,0)FC Gamma Receptor IIIa F176V VF (n=2,1)FC Gamma Receptor IIIa F176V VV (n=2,0)FC Gamma Receptor IIa R166H HH (n=1,0)FC Gamma Receptor IIa R166H HR (n=5,1)FC Gamma Receptor IIa R166H RR (n=3,0)FC Gamma Receptor IIb I232T II (n=7,1)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)8.1483.4508.1154.0744.6985.0434.6983.4508.1483.4505.6514.4854.320NANA3.4508.1155.6515.651
Group B: Trastuzumab+Taxane/ Capecitabine <6 WeeksNA13.832NA13.83213.832NANA13.83213.832NA13.832NANA13.832NANA13.832NA13.832

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Part I: Progression Free Survival (PFS) by Biomarker

Progression was defined as an increase by at least 20 percent (%) from the smallest value in the Sum of Longest Diameter (SLD) of lesions. Biomarkers investigated: p95 human epidermal growth factor receptor 2 (p95HER2) positive (+ve) and negative (-ve) , insulin growth factor-1 receptor (IGF1R) less than (<) median and greater than or equal to (≥) median membrane H score, c-MET NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 Cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

,
Interventionmonths (Median)
p95 HER2 +ve (n=9,0)p95 HER2 -ve (n=15,1)IGF1R IGF1R ≥median (n=14,1)c-MET c-MET ≥median (n=15,0)PTEN PTEN ≥median (n=14,1)HER2 HER2 ≥median (n=14,0)PI3K Amino Acids WT (n=17,1)PI3K Amino Acids M (n=9,0)FC Gamma Receptor IIIa F176V FF (n=9,0)FC Gamma Receptor IIIa F176V VF (n=5,1)FC Gamma Receptor IIIa F176V VV (n=4,0)FC Gamma Receptor IIa R166H HH (n=3,0)FC Gamma Receptor IIa R166H HR (n=8,1)FC Gamma Receptor IIa R166H RR (n=8,0)FC Gamma Receptor IIb I232T II (n=12,1)FC Gamma Receptor IIb I232T IT (n=1,0)FC Gamma Receptor IIb I232T TT (n=1,0)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)NA13.96312.64922.20918.59513.73322.20913.96313.73322.20913.84822.40710.61211.33522.407NA22.20913.96311.335NANA
Group B: Trastuzumab+Taxane/ Capecitabine <6 WeeksNA1.216NA1.2161.216NANA1.2161.216NA1.216NANA1.216NANA1.216NA1.216NANA

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Part I: PFS in ITT Population

PFS was determined as the time in months from the date of screening until first progression. In participants with measurable disease, progression was defined according to RECIST (SLD increased by at least 20% from the smallest value on study [including baseline, if that is the smallest]).. In participants with non-measurable disease, progression was defined as the presence of new lesions or unequivocal progression during treatment. (NCT00885755)
Timeframe: End of first 2 Cycles (Weeks 3 and 6), every 3 cycles for 18 weeks, then every 4 cycles until progression, unacceptable toxicity or participant decision to cease treatment up to 46 months

Interventionmonths (Median)
Group A: Trastuzumab+Taxane /Capecitabine (6 Weeks)18.60
Group B: Trastuzumab+Taxane/ Capecitabine <6 Weeks1.22

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Time to Progression

Time to progression was defined as the time between randomization and the first occurrence of disease progression. Progression of disease was defined as at least 20% increase in the sum of longest diameters of target lesions compared to the smallest sum of longest diameters on-study and absolute increase of at least 5 mm, progression of existing non-target lesions, or presence of new lesions. Time to progression was estimated using Kaplan Meier method. Reported data included censored observations. Participants who had not progressed at the time of study completion (including participants who had died before disease progression) or who were lost to follow-up were censored at the date of the last tumor assessment or last follow-up for progression of disease. Participants for whom no post-baseline tumor assessments were available were censored at day of randomization. (NCT00887822)
Timeframe: From randomization until disease progression or death (up to 26 months)

Interventionmonths (Median)
Bevacizumab, Capecitabine and Cisplatin6.5
Placebo, Capecitabine and Cisplatin7.0

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Change From Cycle 1 in European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Core 36 (QLQ-C30) Scale Over Time

EORTC QLQ-C30 included global health status (GHS)/quality of life (QOL), functional scales (physical, role, cognitive, emotional, and social), symptom scales (fatigue, pain, nausea/vomiting), and single items (dyspnea, appetite loss, insomnia, constipation, diarrhea, and financial difficulties). Most questions used a 4-point scale (1 'Not at All' to 4 'Very Much'); 2 questions used a 7-point scale (1 'Very Poor' to 7 'Excellent'). Scores were averaged and transformed to 0-100 scale; a higher score for Global Qol/functional scales=better level of QoL/functioning, or a higher score for symptom scale=greater degree of symptoms. (NCT00887822)
Timeframe: From Cycle 1 until disease progression (up to 26 months)

,
Interventionscores on scale (Mean)
GHS/QOLPhysical FuntioningRole FunctioningEmotional FunctioningCognitive FunctioningSocial FunctioningFatigueNausea and VomitingPainDyspnoeaInsomniaAppetite LossConstipationDiarrhoeaFinancial Difficulties
Bevacizumab, Capecitabine and Cisplatin1.24-0.89-0.65-0.22-0.51-0.27-0.36-0.82-0.55-0.10-0.57-0.65-0.14-0.290.31
Placebo, Capecitabine and Cisplatin0.73-0.99-0.370.19-0.410.08-0.27-0.55-0.22-0.070.26-1.17-0.020.000.04

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Change From Cycle 1 in EORTC QLQ-STO22 Scale Over Time

The EORTC QLQ-STO22 is a gastric cancer quality of life questionnaire. There are 22 questions which comprise 5 scales (dysphagia, pain, reflux symptom, dietary restrictions, and anxiety) and 4 single items (dry mouth, hair loss, taste, body image). Most questions used 4-point scale (1 'Not at all' to 4 'Very much'; 1 question was a yes or no answer). A linear transformation was used to standardize all scores and single-items to a scale of 0 to 100; higher score=better level of functioning or greater degree of symptoms. (NCT00887822)
Timeframe: From Cycle 1 until disease progression (up to 26 months)

,
Interventionscores on scale (Mean)
DysphagiaPainReflux SymptomsEating RestrictionsAnxietyDry MouthTasteBody ImageHair Loss
Bevacizumab, Capecitabine and Cisplatin-0.31-0.97-0.27-0.30-0.17-0.19-0.440.27-0.35
Placebo, Capecitabine and Cisplatin-0.05-0.52-0.43-0.36-0.730.68-0.660.13-0.61

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Progression-Free Survival (PFS)

PFS was defined as the time between randomization and the date of first documented disease progression or death, whichever occurred first, according to RECIST. Progression of disease was defined as at least 20% increase in the sum of longest diameters of target lesions compared to the smallest sum of longest diameters on-study and absolute increase of at least 5 mm, progression of existing non-target lesions, or presence of new lesions. PFS was estimated using Kaplan Meier method. Reported data included censored observations. Participants who had neither progressed nor died at the time of study completion or who were lost to follow-up were censored at the date of the last tumor assessment or last follow-up for progression of disease. Participants for whom no post-baseline tumor assessments were available were censored at day of randomization. (NCT00887822)
Timeframe: From randomization until disease progression or death (up to 26 months)

Interventionmonths (Median)
Bevacizumab, Capecitabine and Cisplatin6.3
Placebo, Capecitabine and Cisplatin6.0

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PFS During First-line Therapy

PFS during first-line therapy was defined as time between randomization and date of first documented disease progression or death, whichever occurred first and only if it occurred no later than 28 days after last intake of any study medication and only if it occurred before start of non-study antineoplastic treatment, according to RECIST. Progression of disease was defined as at least 20% increase in sum of longest diameters of target lesions compared to smallest sum of longest diameters on-study & absolute increase of at least 5 mm, progression of existing non-target lesions, or presence of new lesions. PFS was estimated using Kaplan Meier method. Reported data included censored observations. Participants who neither progressed nor died in this interval, or who were lost to follow-up were censored at date of last tumor assessment/last follow-up within this time window. Participants for whom no post-baseline tumor assessments were available were censored at day of randomization. (NCT00887822)
Timeframe: From randomization until disease progression or death (up to 26 months)

Interventionmonths (Median)
Bevacizumab, Capecitabine and Cisplatin6.3
Placebo, Capecitabine and Cisplatin6.1

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Percentage of Participants With Progression-Free Survival (PFS) Events (Disease Progression/Death)

Progression of disease was defined as at least 20 percent (%) increase in the sum of longest diameters of target lesions compared to the smallest sum of longest diameters on-study and absolute increase of at least 5 millimeters (mm), progression of existing non-target lesions, or presence of new lesions. PFS was defined as the time between randomization and the date of first documented disease progression or death, whichever occurred first, according to Response Evaluation Criteria In Solid Tumors (RECIST). (NCT00887822)
Timeframe: From randomization until disease progression or death (up to 26 months)

Interventionpercentage of participants (Number)
Bevacizumab, Capecitabine and Cisplatin81.0
Placebo, Capecitabine and Cisplatin81.4

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Percentage of Participants With PFS Events (Disease Progression/Death) During First-line Therapy

Progression of disease was defined as at least 20% increase in the sum of longest diameters of target lesions compared to the smallest sum of longest diameters on-study and absolute increase of at least 5 mm, progression of existing non-target lesions, or presence of new lesions. PFS during first-line therapy was defined as the time between randomization and the date of first documented disease progression or death, whichever occurred first and only if it occurred no later than 28 days after last confirmed intake of any study medication and before the start of non-study antineoplastic treatment, according to RECIST. (NCT00887822)
Timeframe: From randomization until disease progression or death (up to 26 months)

Interventionpercentage of participants (Number)
Bevacizumab, Capecitabine and Cisplatin51.0
Placebo, Capecitabine and Cisplatin59.8

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Percentage of Participants With Event (Death)

Percentage of participants who died due to any cause was reported. As planned, ad hoc analysis was done for overall survival up to clinical cut-off date of 12 January 2012 (34 months), subsequent to the protocol-defined clinical cut-off date of 13 May 2011 (26 months). Overall survival was defined as the time between randomization and the date of death due to any cause. (NCT00887822)
Timeframe: From randomization until death (up to 34 months)

Interventionpercentage of participants (Number)
Bevacizumab, Capecitabine and Cisplatin77.0
Placebo, Capecitabine and Cisplatin75.5

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Percentage of Participants With Disease Progression

Progression of disease was defined as at least 20% increase in the sum of longest diameters of target lesions compared to the smallest sum of longest diameters on-study and absolute increase of at least 5 mm, progression of existing non-target lesions, or presence of new lesions. (NCT00887822)
Timeframe: From randomization until disease progression or death (up to 26 months)

Interventionpercentage of participants (Number)
Bevacizumab, Capecitabine and Cisplatin56.0
Placebo, Capecitabine and Cisplatin53.9

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Percentage of Participants With Disease Control During First-Line Therapy

Disease control was defined as stable disease(SD) for 6 weeks or longer, CR plus PR as assessed by RECIST criteria for participants with measurable disease.CR:disappearance of all TLs & normalization of tumor markers. Pathological lymph nodes must have short axis measures<10 mm. PR:at least 30% decrease in sum of measures(longest diameter for tumor lesions and short axis measure for nodes)of TLs, taking as reference baseline sum of longest diameters.SD:neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for disease progression taking as reference smallest sum of longest diameters on study. For participants without measurable disease, clinical benefit rate was defined as no clinical disease progression for >/=6 weeks. Disease progression was defined as at least 20% increase in sum of diameters of TLs compared to smallest sum of diameters on-study and absolute increase of at least 5 mm, progression of existing non-target lesions, or presence of new lesions. (NCT00887822)
Timeframe: From randomization until disease progression or death (up to 26 months)

Interventionpercentage of participants (Number)
Bevacizumab, Capecitabine and Cisplatin73.0
Placebo, Capecitabine and Cisplatin72.5

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Percentage of Participants With Best Overall Response as Assessed by RECIST During First-Line Therapy

Best overall response during first-line therapy was defined as the occurrence of either a confirmed complete (CR) or a partial response (PR), as assessed by the RECIST criteria. CR: disappearance of all target and non-target lesions (TLs) and normalization of tumor markers. Pathological lymph nodes must have short axis measures less than (<) 10 mm. PR: at least a 30 % decrease in the sum of measures (longest diameter for tumor lesions and short axis measure for nodes) of TLs, taking as reference the baseline sum of longest diameters. (NCT00887822)
Timeframe: From randomization until disease progression or death (up to 26 months)

Interventionpercentage of participants (Number)
Bevacizumab, Capecitabine and Cisplatin40.7
Placebo, Capecitabine and Cisplatin33.7

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Overall Survival

Overall survival was defined as the time between randomization and the date of death due to any cause. Overall survival was estimated using Kaplan Meier method. Reported data included censored observations. Participants for whom no death was captured on the clinical database were censored at the most recent date they were known to be alive. As planned, ad hoc analysis was done for overall survival up to clinical clinical cut-off date of 12 January 2012 (34 months), subsequent to the protocol-defined clinical cut-off date of 13 May 2011 (26 months). (NCT00887822)
Timeframe: From randomization until death (up to 34 months)

Interventionmonths (Median)
Bevacizumab, Capecitabine and Cisplatin10.5
Placebo, Capecitabine and Cisplatin11.4

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Duration of Response During First-Line Therapy

Duration of response during first-line therapy was defined as the time from when response (CR or PR) was first documented to first documented disease progression or death (whichever occurs first) during first-line therapy. CR: disappearance of all target and non-TLs and normalization of tumor markers. Pathological lymph nodes must have short axis measures <10 mm. PR: at least a 30 % decrease in the sum of measures (longest diameter for tumor lesions and short axis measure for nodes) of TLs, taking as reference the baseline sum of longest diameters. Duration of response was estimated using Kaplan Meier method. Reported data included censored observations. Participants who did not progress or die after they had had a confirmed response were censored at the date of their last tumor measurement or last follow-up for progression of disease during first line therapy. (NCT00887822)
Timeframe: From randomization until disease progression or death (up to 26 months)

Interventionmonths (Median)
Bevacizumab, Capecitabine and Cisplatin7.2
Placebo, Capecitabine and Cisplatin5.8

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Dose Limiting Toxicity (DLT) [Phase I]

DLT occurring within 3 weeks of the start of chemoradiation therapy was defined as: Grade 3 non-hematologic or hematologic toxicity requiring interruption of >7 days (d) of chemo or >3d chemoradiation; Grade 4 non-hematologic; Grade 4 neutropenia or thrombocytopenia; Treatment-related death; Delays in surgery >3 weeks due to treatment-related toxicity. A 30% increase in any surgical complication rate beyond those previously established rates (readmission rate: 16%; pancreatic fistula/intra-abdominal abscess/infection rate: 27%, major intra-abdominal bleeding requiring return to OR: 1.6%, delayed gastric emptying: 4.4%, and superficial wound infection rate: 8%) was also considered a DLT. (NCT00889187)
Timeframe: within 3 weeks of the start of chemoradiation therapy

Interventionpatients with DLT (Number)
Phase 1 Cohort 1: Photon Rad (30 Gy/12 Days)+Capecitabine0
Phase I Cohort 2: Photon Rad (25 Gy/11 Days)+Capecitabine0
Phase I Cohort 3: Photon Rad (25 Gy/5 Days)+Capecitabine0

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Neoadjuvant Short-Course Photon Radiation Therapy Maximum Tolerated Dose (MTD) [Phase I]

Neoadjuvant short-course photon radiation therapy MTD in combination with capecitabine 825 mg/m2 orally BID for ten consecutive weekdays, beginning on the morning of the first day of radiation therapy is determined by the number of patients who experience a dose limiting toxicity (DLT). See subsequent primary outcome measure for the DLT definition. The MTD is defined as the highest dose at which fewer than one-third of patients experience a DLT. If none of 3 initial patients or only 1 of 6 patients have a DLT on dose level 3 then 6 additional patients are treated at this dose. If during this expansion, the rate of DLT exceeds 30% then the next lower dose level is declared the MTD. If no DLTs are observed, the MTD is not reached. (NCT00889187)
Timeframe: within 3 weeks of the start of chemoradiation therapy

InterventionGy per fraction (Number)
All Phase I: Photon Rad+CapecitabineNA

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Response Rate (Complete Response or Partial Response)

A confirmed tumor response is defined to be a CR or PR noted as the objective status on 2 consecutive evaluations ≥4 weeks apart. Confirmed tumor response will be evaluated using the first 6 cycles of treatment. All patients meeting the eligibility criteria who have signed a consent form and have begun treatment will be evaluable for response. The confirmed response rates between the 2 arms will be compared using a Chi-Square or Fisher's Exact test. Complete Response (CR): Disappearance of all target lesions. Partial Response (PR): At least a 30% decrease in the sum of the LD of target lesions taking as reference the baseline sum LD. (NCT00891878)
Timeframe: Up to 3 years

Interventionpercentage of patients (Number)
Arm A (Capecitabine)0
Arm B (Capecitabine+Sunitinib Malate)33

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Time to Treatment Failure

Time to treatment failure is defined to be the time from the date of randomization to the date at which the patient is removed from treatment due to progression, adverse events, or refusal. (NCT00891878)
Timeframe: Up to 3 years

Interventionmonths (Median)
Arm A (Capecitabine)1.63
Arm B (Capecitabine+Sunitinib Malate)2.53

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Comparison of Progression-free Survival

The primary analysis will be a comparison of Arm A to Arm B using a one-sided log-rank test between the 2 Kaplan-Meier curves. All patients meeting the eligibility criteria, who started treatment will be considered evaluable for the primary endpoint. If a patient is still alive 3 years after registration, no further follow-up is required. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00891878)
Timeframe: Up to 3 years

InterventionMonths (Median)
Arm A (Capecitabine)6.1
Arm B (Capecitabine+Sunitinib Malate)2.4

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Duration of Response

Duration of response is defined for all evaluable patients who have achieved an objective response as the date at which the patient's earliest best objective status is first noted to be either a CR or PR to the earliest date progression is documented. (NCT00891878)
Timeframe: Up to 3 years

Interventionmonths (Median)
Arm B (Capecitabine+Sunitinib Malate)4.75

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Overall Survival

Overall survival is defined as the time from randomization to death due to any cause. The distribution of overall survival will be estimated using the method of Kaplan-Meier. (NCT00891878)
Timeframe: Up to 3 years

InterventionMonths (Median)
Arm A (Capecitabine)6.2
Arm B (Capecitabine+Sunitinib Malate)5.9

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Time to Disease Progression

Time to disease progression is defined as the time from randomization to the earliest date documentation of disease progression occurs. If a patient dies without a documentation of disease progression, the patient will be considered to have had tumor progression at the time of their death unless there is sufficient documented evidence to conclude no progression occurred prior to death. The distribution of time-to-progression will be estimated using the method of Kaplan-Meier. (NCT00891878)
Timeframe: Up to 3 years

Interventionmonths (Median)
Arm A (Capecitabine)7.56
Arm B (Capecitabine+Sunitinib Malate)2.46

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Response Rate of Patients Who Receive Pre-operative or Palliative Concurrent Radiation w/ Capecitabine to the Breast & at Risk or Involved Regional Lymph Nodes Basins.

The response by RECIST was assessed after 45 Gy of radiation for patients with breast cancer treated with concurrent capecitabine and radiation therapy. (NCT00916578)
Timeframe: Participants were monitored from 2009 to 2012.

Interventionparticipants (Number)
Single Arm Institution, Open Label, Phase II26

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Part 1: Last Quantifiable Drug Concentration (Clast) of Erlotinib and Its Metabolite OSI-420 (CP373420), Capecitabine and Its Metabolites (5'-DFCR and 5'-DFUR)

(NCT00925769)
Timeframe: CAP: 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 5, 6 hours (h) of every 2-week cycle (until Week 259) ERL: 2, 3 4, 5, 6, 7, 8, 10, 24, 28, 48, 52, 72, 76, 96, 100, 120, 124, 144, 148, 168 and 172 h of every 2-week cycle (until Week 259)

,,,,,
Interventionµg/mL (Mean)
Erlotinib (n=6,6,6,6,3,3)OSI-420 (n=6,6,6,6,3,3)Capecitabine (n=6,6,6,6,3,3)5'-DFCR (n=5,5,6,6,3,3)5'-DFUR (n=4,5,6,6,3,3)
ERL+BEV+CAP Dose Level-10.370.040.050.232.54
ERL+BEV+CAP Dose Level-20.310.020.20.081.03
ERL+BEV+CAP Dose Level-30.230.010.170.640.77
ERL+BEV+CAP Dose Level-40.390.040.060.750.58
ERL+BEV+CAP Dose Level-50.230.010.290.990.14
ERL+BEV+CAP Dose Level-60.520.040.170.30.14

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Part 1: Maximum Serum Concentration (Cmax) of Erlotinib and Its Metabolite OSI-420 (CP373420), Capecitabine and Its Metabolites (5'-Deoxy-5-Fluorocytidine [5'-DFCR] and 5'-Deoxy-5-Fluorouridine [5'-DFUR])

(NCT00925769)
Timeframe: CAP: 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 5, 6 hours (h) of every 2-week cycle (until Week 259) ERL: 2, 3 4, 5, 6, 7, 8, 10, 24, 28, 48, 52, 72, 76, 96, 100, 120, 124, 144, 148, 168 and 172 h of every 2-week cycle (until Week 259)

,,,,,
Interventionmicrograms per milliliter (µg/mL) (Mean)
Erlotinib (n=6,6,6,6,3,3)OSI-420 (n=6,6,6,6,3,3)Capecitabine (n=6,6,6,6,3,3)5'-DFCR (n=5,5,6,6,3,3)5'-DFUR (n=4,5,6,6,3,3)
ERL+BEV+CAP Dose Level-11.500.091.693.57.9
ERL+BEV+CAP Dose Level-20.950.051.134.287.3
ERL+BEV+CAP Dose Level-30.680.044.8911.466.17
ERL+BEV+CAP Dose Level-40.930.065.486.267.24
ERL+BEV+CAP Dose Level-50.580.039.475.443.28
ERL+BEV+CAP Dose Level-61.690.109.94.155.1

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Part 1: Time to Reach Cmax (Tmax) of Erlotinib and Its Metabolite OSI-420 (CP373420), Capecitabine and Its Metabolites (5'-DFCR and 5'-DFUR)

(NCT00925769)
Timeframe: CAP: 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 5, 6 hours (h) of every 2-week cycle (until Week 259) ERL: 2, 3 4, 5, 6, 7, 8, 10, 24, 28, 48, 52, 72, 76, 96, 100, 120, 124, 144, 148, 168 and 172 h of every 2-week cycle (until Week 259)

,,,,,
Interventionhours (h) (Median)
Erlotinib (n=6,6,6,6,3,3)OSI-420 (n=6,6,6,6,3,3)Capecitabine (n=6,6,6,6,3,3)5'-DFCR (n=5,5,6,6,3,3)5'-DFUR (n=4,5,6,6,3,3)
ERL+BEV+CAP Dose Level-12.503.000.50.51
ERL+BEV+CAP Dose Level-22.002.00111.5
ERL+BEV+CAP Dose Level-32.002.001.51.51.5
ERL+BEV+CAP Dose Level-43.007.000.7511.5
ERL+BEV+CAP Dose Level-55.006.00111
ERL+BEV+CAP Dose Level-62.004.000.51.51.5

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Part 1: MTD of Erlotinib

MTD for each of the medications was defined as the lowest dose studied which resulted in DLT in at least 33% of participants of the same quality category. DLT was defined as >= G3 or G4 toxicity; >= G3 non-hematological toxicities directly related to study treatment (other than untreated nausea/vomiting, alopecia, G3/G4 bilirubinemia for less than 7 days due to edema of the ductus choledochus and anemia); G4 thrombocytopenia, neutropenia lasting >= 7 days or G3 thrombocytopenia with complications, requiring transfusions, febrile neutropenia; stopping of oral CAP and/or ERL intake for >= 7 days, and/or cancellation of one or more BEV infusion(s) due to AEs. (NCT00925769)
Timeframe: Up to Week 6 (Cycle 1-3)

Interventionmg/day (Number)
Triple Combination (Bevacizumab/Erlotinib/Capecitabine)NA

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Part 1: Maximum Tolerated Dose (MTD) of Capecitabine

MTD for each of the medications was defined as the lowest dose studied which resulted in dose limiting toxicity (DLT) in at least 33 percent (%) of participants of the same quality category. DLT was defined as any greater than or equal to (>=) Grade (G) 3 or G4 toxicity; >= G3 non-hematological toxicities directly related to study treatment (other than untreated nausea/vomiting, alopecia, G3/G4 bilirubinemia for less than 7 days due to edema of the ductus choledochus and anemia); G4 thrombocytopenia, neutropenia lasting >= 7 days or G3 thrombocytopenia with complications, requiring transfusions, febrile neutropenia; stopping of oral CAP and/or ERL intake for >= 7 days, and/or cancellation of one or more BEV infusion(s) due to adverse events (AEs). (NCT00925769)
Timeframe: Up to Week 6 (Cycle 1-3)

Interventionmg/m^2 BID (Number)
Triple Combination (Bevacizumab/Erlotinib/Capecitabine)900

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Part 1: MTD of Bevacizumab

MTD for each of the medications was defined as the lowest dose studied which resulted in DLT in at least 33% of participants of the same quality category. DLT was defined as >= G3 or G4 toxicity; >= G3 non-hematological toxicities directly related to study treatment (other than untreated nausea/vomiting, alopecia, G3/G4 bilirubinemia for less than 7 days due to edema of the ductus choledochus and anemia); G4 thrombocytopenia, neutropenia lasting >= 7 days or G3 thrombocytopenia with complications, requiring transfusions, febrile neutropenia; stopping of oral CAP and/or ERL intake for >= 7 days, and/or cancellation of one or more BEV infusion(s) due to AEs. (NCT00925769)
Timeframe: Up to Week 6 (Cycle 1-3)

Interventionmg/kg once every 2 weeks (Q2W) (Number)
Triple Combination (Bevacizumab/Erlotinib/Capecitabine)NA

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Part 1: PRD of Bevacizumab for Part 2

Once the MTD was reached then the preceding lower dose level was used as PRD. MTD for each of the medications was defined as the lowest dose studied which resulted in DLT in at least 33% of participants of the same quality category. DLT was defined as >= G3 or G4 toxicity; >= G3 non-hematological toxicities directly related to study treatment (other than untreated nausea/vomiting, alopecia, G3/G4 bilirubinemia for less than 7 days due to edema of the ductus choledochus and anemia); G4 thrombocytopenia, neutropenia lasting >= 7 days or G3 thrombocytopenia with complications, requiring transfusions, febrile neutropenia; stopping of oral CAP and/or ERL intake for >= 7 days, and/or cancellation of one or more BEV infusion(s) due to AEs. If MTD was not defined for a drug treatment then the maximum planned dose of that particular drug was considered as PRD for Part 2. (NCT00925769)
Timeframe: Up to Week 6 (Cycle 1-3)

Interventionmg/kg Q2W (Number)
Triple Combination (Bevacizumab/Erlotinib/Capecitabine)10

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Part 1: PRD of Erlotinib for Part 2

Once the MTD was reached then the preceding lower dose level was used as PRD. MTD for each of the medications was defined as the lowest dose studied which resulted in DLT in at least 33% of participants of the same quality category. DLT was defined as >= G3 or G4 toxicity; >= G3 non-hematological toxicities directly related to study treatment (other than untreated nausea/vomiting, alopecia, G3/G4 bilirubinemia for less than 7 days due to edema of the ductus choledochus and anemia); G4 thrombocytopenia, neutropenia lasting >= 7 days or G3 thrombocytopenia with complications, requiring transfusions, febrile neutropenia; stopping of oral CAP and/or ERL intake for >= 7 days, and/or cancellation of one or more BEV infusion(s) due to AEs. If MTD was not defined for a drug treatment then the maximum planned dose of that particular drug was considered as PRD for Part 2. (NCT00925769)
Timeframe: Up to Week 6 (Cycle 1-3)

Interventionmg/day (Number)
Triple Combination (Bevacizumab/Erlotinib/Capecitabine)150

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Part 1: Area Under the Plasma Concentration-Time Curve From Time 0 to the Time of the Last Measurable Concentration (AUClast) of Erlotinib and Its Metabolite OSI-420 (CP373420), Capecitabine and Its Metabolites (5'-DFCR and 5'-DFUR)

(NCT00925769)
Timeframe: CAP: 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 5, 6 hours (h) of every 2-week cycle (until Week 259) ERL: 2, 3 4, 5, 6, 7, 8, 10, 24, 28, 48, 52, 72, 76, 96, 100, 120, 124, 144, 148, 168 and 172 h of every 2-week cycle (until Week 259)

,,,,,
Interventionh*µg/mL (Mean)
Erlotinib (n=6,6,6,6,3,3)OSI-420 (n=6,6,6,6,3,3)Capecitabine (n=6,6,6,6,3,3)5'-DFCR (n=5,5,6,6,3,3)5'-DFUR (n=4,5,6,6,3,3)
ERL+BEV+CAP Dose Level-115.811.151.433.9715.42
ERL+BEV+CAP Dose Level-211.060.481.637.0113.58
ERL+BEV+CAP Dose Level-39.150.415.8820.279.76
ERL+BEV+CAP Dose Level-413.070.995.289.3510.86
ERL+BEV+CAP Dose Level-58.540.3613.6312.635.17
ERL+BEV+CAP Dose Level-619.881.429.748.068.53

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Percentage Of Participants With PD or Death Due to PD (Maintenance Phase Data Cutoff October 4, 2013)

PD was defined per RECIST 1.0 as 20% increase in the sum of the longest diameter of target lesions. (NCT00929240)
Timeframe: Randomization, at the end of every third cycle (every 9 weeks) until the end of maintenance phase and every 3 months until disease progression or death until data cutoff on October 4, 2013

Interventionpercentage of participants (Number)
Maintenance Phase: Bevacizumab88.3
Maintenance Phase: Bevacizumab + Capecitabine74.7

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Time To Progression (Maintenance Phase Data Cutoff October 4, 2013)

Time to Progression was defined as the time from randomization to the first documented disease progression (using investigator assessments of disease progression by RECIST 1.0). PD was defined as 20% increase in the sum of the longest diameter of target lesions. (NCT00929240)
Timeframe: Randomization, at the end of every third cycle (every 9 weeks) until the end of maintenance phase and every 3 months until disease progression or death until data cutoff on October 4, 2013

Interventionmonths (Median)
Maintenance Phase: Bevacizumab4.3
Maintenance Phase: Bevacizumab + Capecitabine11.9

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Quality of Life Assessed As Change From Baseline in Global Health Status Using The European Organization for Research and Treatment of Cancer Quality of Life Questionnaire - 30 (EORTC QLQ - C30) (Maintenance Phase Data Cutoff October 4, 2013)

The EORTC QLQ-C30 incorporates 9 multi-item scales: 5 functional scales (physical, role, cognitive, emotional, and social); 9 symptom scales (fatigue, pain, nausea and vomiting, dyspnoea, insomnia, appetite loss, constipation, diarrhea and financial difficulties); and a global health and quality-of-life scale. Most questions used 4 point scale (1 'Not at all' to 4 'Very much'; 2 questions used 7-point scale (1 'very poor' to 7 'Excellent'). Scores were averaged and transformed to 0-100 scale; higher score=better level of functioning or greater degree of symptoms. The change in global health status was determined to be the difference in values at baseline and each specific visit. The term ''baseline'' refers to the time of randomization to the maintenance phase. (NCT00929240)
Timeframe: Baseline, Randomization and Cycles 3, 6, 9 and 12

,
Interventionunits on a scale (Mean)
Randomization (n= 83, 86)Cycle 3 (n= 44, 52)Cycle 6 (n= 26, 54)Cycle 9 (n= 18, 37)Cycle 12 (n= 12, 31)
Maintenance Phase: Bevacizumab-3.510.764.178.800.69
Maintenance Phase: Bevacizumab + Capecitabine-4.46-3.21-5.40-1.800.00

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Percentage of Participants Expected to Be Alive After 1 and 2 Years on Treatment (Maintenance Phase Data Cutoff October 4, 2013)

Probability of being alive after 1 and 2 years on treatment with 95% CIs was calculated using Kaplan Meier approach with LOGLOG transformation. (NCT00929240)
Timeframe: Years 1 and 2

,
Interventionpercentage of participants (Number)
1 Year2 Years
Maintenance Phase: Bevacizumab71.649.4
Maintenance Phase: Bevacizumab + Capecitabine90.469.0

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Overall Survival (Maintenance Phase Data Cutoff October 4, 2013)

Duration of Overall Survival (OS) was defined as the time from randomization to death of any cause. The OS data for participants for whom no death was captured in the clinical database were censored at the last time they were known to be alive. Kaplan Meier estimation was used to determine OS. (NCT00929240)
Timeframe: Randomization, at the end of every third cycle (every 9 weeks) until the end of maintenance phase and every 3 months until disease progression or death until data cutoff on October 4, 2013, up to 4 years

Interventionmonths (Median)
Maintenance Phase: Bevacizumab23.7
Maintenance Phase: Bevacizumab + Capecitabine39.0

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Percentage of Participants Who Died (Maintenance Phase Data Cutoff October 4, 2013)

(NCT00929240)
Timeframe: Randomization, at the end of every third cycle (every 9 weeks) until the end of maintenance phase and every 3 months until disease progression or death until data cutoff on October 4, 2013, up to 4 years

Interventionpercentage of participants (Number)
Maintenance Phase: Bevacizumab56.4
Maintenance Phase: Bevacizumab + Capecitabine36.3

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Percentage of Participants With Best Overall Confirmed Objective Response of CR or PR Per RECIST 1.0 (Maintenance Phase Data Cutoff October 4, 2013)

Objective Response was determined by the investigator using modified RECIST criteria, Version 1.0. An objective response was a complete or partial overall confirmed response as determined by investigators. CR was defined as complete disappearance of all target and non-target lesions and no new lesions. PR was defined as greater than or equal to (≥) 30 % decrease in the sum of appropriate diameters of all target measurable lesions, no progress in the non-measurable disease, and no new lesions. Progressive disease (PD) was defined as 20% increase in the sum of the longest diameter of target lesions and SD was defined as small changes that do not meet above criteria. Pearson-Clopper one-sample method was used for Confidence intervals (CIs). (NCT00929240)
Timeframe: Randomization, at the end of every third cycle (every 9 weeks) until the end of maintenance phase and every 3 months until disease progression or death until data cutoff on October 4, 2013, up to 4 years

Interventionpercentage of participants (Number)
Maintenance Phase: Bevacizumab76.6
Maintenance Phase: Bevacizumab + Capecitabine85.7

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Percentage of Participants With Clinical Benefit (CR, PR and SD) Per RECIST 1.0 (Data Cutoff October 4, 2013)

CR was defined as complete disappearance of all target and non-target lesions and no new lesions. PR was defined as ≥ 30 % decrease in the sum of appropriate diameters of all target measurable lesions, no progress in the non-measurable disease, and no new lesions. SD was defined as small changes that do not meet above criteria. (NCT00929240)
Timeframe: Randomization, at the end of every third cycle (every 9 weeks) until the end of maintenance phase and every 3 months until disease progression or death until data cutoff on October 4, 2013, up to 4 years

Interventionpercentage of participants (Number)
Maintenance Phase: Bevacizumab97.9
Maintenance Phase: Bevacizumab + Capecitabine98.9

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Percentage of Participants With Clinical Benefit (CR, PR and SD) Per RECIST 1.0 (Initial Treatment Phase)

CR was defined as complete disappearance of all target and non-target lesions and no new lesions. PR was defined as ≥30% decrease in the sum of appropriate diameters of all target measurable lesions, no progress in the non-measurable disease, and no new lesions. SD was defined as small changes that do not meet above criteria. (NCT00929240)
Timeframe: Screening and at the end of every third cycle until randomization for an average of 18 weeks

Interventionpercentage of participants (Number)
Initial Treatment Phase: Bevacizumab + Docetaxel56.9

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Percentage of Participants With Disease Progression or Death (Maintenance Phase Data Cutoff October 4, 2013)

Progression Free Survival (PFS) was defined as the time from first study drug dosing (during the maintenance treatment phase) to the first documented disease progression or death, whichever occurred first. Progression was based on tumor assessment made by the investigators according to the Response Evaluation Criteria In Solid Tumors (RECIST). Progressive Disease (PD) was defined as a 20 percent (%) or greater increase in the sum of the Longest Diameter (LD) of the target lesions taking as reference the smallest sum LD recorded or appearance of new lesions. (NCT00929240)
Timeframe: Randomization, at the end of every third cycle (every 9 weeks) until the end of maintenance phase and every 3 months until disease progression or death until data cutoff on October 4, 2013, up to 4 years

Interventionpercentage of participants (Number)
Maintenance Phase: Bevacizumab88.3
Maintenance Phase: Bevacizumab + Capecitabine75.8

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Progression Free Survival (Maintenance Phase Data Cutoff October 4, 2013)

PFS was defined as the time from first study drug dosing to the first documented disease progression or death, whichever occurred first.Time to progression was defined as the time from randomization to the first documented disease progression defined per RECIST 1.0 criteria. Participants without an event at data cut-off or who were withdrawn from the study without documented progression were censored at the date of the last tumor assessment when the participant was known to be progression free. Participants who took other non-protocol anti-cancer drugs while being on study medication, and who were still event free were censored on the date of first dose of the anti-cancer drug. Participants without post-randomization tumor assessments but alive were censored at the time of randomization. Participants without post-randomization assessments, who died after randomization were considered to have the PFS event at date of death. Kaplan-Meier estimation was used for median time to PFS (NCT00929240)
Timeframe: Randomization, at the end of every third cycle (every 9 weeks) until the end of maintenance phase and every 3 months until disease progression or death until data cutoff on October 4, 2013, up to 4 years

Interventionmonths (Median)
Maintenance Phase: Bevacizumab4.3
Maintenance Phase: Bevacizumab + Capecitabine11.9

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Percentage of Participants With Best Overall Confirmed Objective Response of CR or PR Per RECIST 1.0 (Initial Treatment Phase)

Objective Response was determined by the investigator using RECIST criteria, Version 1.0. An objective response was a complete or partial overall confirmed response as determined by investigators. CR was defined as complete disappearance of all target and non-target lesions and no new lesions. PR was defined as ≥ 30% decrease in the sum of appropriate diameters of all target measurable lesions, no progress in the non-measurable disease, and no new lesions. Pearson-Clopper one-sample method was used for CI. (NCT00929240)
Timeframe: Screening and at the end of every third cycle until randomization for an average of 18 weeks

Interventionpercentage of participants (Number)
Initial Treatment Phase: Bevacizumab + Docetaxel8.8

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Overall Survival

Overall survival was defined as the time from randomization to the time of death from any cause. Overall survival was censored at the date of last follow-up visit for patients who are still alive or loss of follow-up. (NCT00938470)
Timeframe: Up to 2 years

Interventionmonths (Median)
Arm I (DOC, 5FU/O/RT, Surgery)NA
Arm II (5FU/O/RT, Surgery)18.8

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Percentage of Participants With Overall Clinical Tumor Response (CR or PR)

Overall clinical tumor response rate was defined as the percentage of evaluable participants who achieved either complete response (CR) or partial response (PR) noted on the objective status from pre-surgical staging (for arm II) or either from pre-RT or pre-surgical staging (for arm I).> CR was defined as disappearance of all non-target lesion (TL) and normalization of tumor biomarker level, all lymph nodes (LN) must be non-pathological in size (<1 cm short axis); or disappearance of all TL and normalization of tumor biomarkers, any pathological LN (whether target or non-target) must have reduction in short axis to <1 cm; or >=30% decrease in the sum of the diameters of TL taking as reference the baseline sum of the diameters. (NCT00938470)
Timeframe: Up to 2 years

Interventionpercentage of participants (Number)
Arm I (DOC, 5FU/O/RT, Surgery)32.1
Arm II (5FU/O/RT, Surgery)33.3

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Number of Participants Who Experienced a Maximum Grade of 3 or Above Adverse Event

Adverse events were assessed using National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. (NCT00938470)
Timeframe: Up to 2 years

,
InterventionParticipants (Count of Participants)
Grade 3=SevereGrade 4=Life threateningGrade 5=Death
Arm I (DOC, 5FU/O/RT, Surgery)10104
Arm II (5FU/O/RT, Surgery)1274

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Percentage of Participants With Pathologic Complete Response (PCR)

Pathologic complete response was defined as no gross or microscopic tumor identified with the surgical specimen. All lymph nodes should be free of tumor to document a PCR. If no gross tumor is visible, section around the area of inflammation (nodularity) should be made every 2-3 cm and specimens examined. (NCT00938470)
Timeframe: Up to 2 years

Interventionpercentage of participants (Number)
Arm I (DOC, 5FU/O/RT, Surgery)28.6
Arm II (5FU/O/RT, Surgery)40.7

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Disease-free Survival

Disease-free survival was defined as the time from randomization to the date of recurrent or death, whichever comes first. (NCT00938470)
Timeframe: Up to 2 years

Interventionmonths (Median)
Arm I (DOC, 5FU/O/RT, Surgery)31.2
Arm II (5FU/O/RT, Surgery)17.0

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Percentage of Participants With Treatment-Emergent Adverse Events (AEs) or Serious Adverse Events (SAEs) - Part 1

An AE was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. An SAE was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. Treatment-emergent are events between first dose of study drug and up to 28 days after last dose that were absent before treatment or that worsened relative to pretreatment state. (NCT00959946)
Timeframe: Part 1 Baseline up to 28 days after last dose of study treatment

,,,,,,,
InterventionPercentage of Participants (Number)
AEsSAEs
Bosutinib 200 mg + Capecitabine 1000 mg/m^2 (Part 1)100.050.0
Bosutinib 200 mg + Capecitabine 625 mg/m^2 (Part 1)100.00.0
Bosutinib 200 mg + Capecitabine 750 mg/m^2 (Part 1)100.050.0
Bosutinib 300 mg + Capecitabine 1000 mg/m^2 (Part 1)100.033.3
Bosutinib 300 mg + Capecitabine 625 mg/m^2 (Part 1)100.040.0
Bosutinib 300 mg + Capecitabine 750 mg/m^2 (Part 1)100.00.0
Bosutinib 400 mg + Capecitabine 1000 mg/m^2 (Part 1)100.050.0
Bosutinib 400 mg + Capecitabine 750 mg/m^2 (Part 1)100.00.0

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Best Overall Response - Part 1

Best overall response based on investigator's disease status assessment. CR: disappearance of all lesions. PR: at least 30% decrease in sum of LDs of target lesions taking as reference baseline sum LDs. Progressive disease (PD): at least 20% increase in sum of LD of target lesions taking as a reference smallest sum of the recorded LDs since treatment start, or the appearance of 1 or more new lesions. Stable disease (SD): neither sufficient shrinkage for PR nor sufficient increase for PD taking as reference smallest sum of LD since treatment started. (NCT00959946)
Timeframe: Part 1 Baseline, every 6 weeks up to 6 months

,,,,,,,
InterventionParticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressive DiseaseIndeterminate
Bosutinib 200 mg + Capecitabine 1000 mg/m^2 (Part 1)00220
Bosutinib 200 mg + Capecitabine 625 mg/m^2 (Part 1)00010
Bosutinib 200 mg + Capecitabine 750 mg/m^2 (Part 1)00130
Bosutinib 300 mg + Capecitabine 1000 mg/m^2 (Part 1)00621
Bosutinib 300 mg + Capecitabine 625 mg/m^2 (Part 1)00050
Bosutinib 300 mg + Capecitabine 750 mg/m^2 (Part 1)02110
Bosutinib 400 mg + Capecitabine 1000 mg/m^2 (Part 1)00100
Bosutinib 400 mg + Capecitabine 750 mg/m^2 (Part 1)00110

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Maximum Tolerated Dose (MTD) - Part 1

The MTD contour is defined as the dose combinations that achieve a toxicity rate (dose-limiting toxicity [DLT] rate) of less than (<) 1/3. The observed toxicity rates for all the reporting groups (to which at least 1 cohort of participants was allocated) was estimated by calculating the proportion of DLTs observed in the first 21 days of treatment at those reporting groups. DLT includes grade (Gr) 3/4 nausea, vomiting, diarrhea, or asthenia more than 3 days, Gr 4 hematologic toxicities, delayed study treatment administration due to dose toxicities by more than 3 weeks. Pre-defined criterion for MTD: if a higher dose level of capecitabine existed such that the same dose level of bosutinib had a DLT rate of <1/3, no MTD was recommended for that capecitabine dose and if even the lowest dose of bosutinib achieved a toxicity rate of greater than (>) 1/3, no MTD was recommended for that capecitabine dose level. (NCT00959946)
Timeframe: Part 1 Baseline up to Day 21

Interventionmg (Number)
Bosutinib + Capecitabine 625 mg/m^2NA
Bosutinib + Capecitabine 750 mg/m^2NA
Bosutinib + Capecitabine 1000 mg/m^2300

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Progression-free Survival

Progression-free survival (PFS) will be measured as the number of months between each patient's enrollment and his/her date of progression or date of death. (NCT00961571)
Timeframe: 36 months

Interventionmonths (Median)
Sunitinib and Cepecitabine18.35

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Percentage of Participants With Objective CNS Response at 4 Weeks After Completion of WBRT, Assessed by Investigator According to MRI

Objective CNS response was defined as having CR or PR for CNS metastasis, assessed by contrast-enhanced MRI using RECIST. CR: disappearance of all CNS lesions. PR: >/=30 % decrease in sum of LD of CNS lesions taking as reference the baseline sum LD. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first up to 4 weeks after completion of WBRT (up to approximately 7 weeks)"

Interventionpercentage of participants (Number)
WBRT Followed by Standard of Care41.7
WBRT+Capecitabine Followed by Capecitabine Maintenance27.3

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Time to CNS Progression, Assessed by Investigator According to MRI

Time to CNS progression was defined as the time from start of study treatment to first documentation of PD or death due to CNS metastasis. PD was assessed by contrast-enhanced MRI according to RECIST. PD: a 20% or greater increase in the sum of the LD of CNS lesions taking as reference the smallest sum LD recorded since the treatment started or appearance of one or more CNS lesions and/or unequivocal progression of existing CNS lesions. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first (up to approximately 1 year 5.5 months overall)"

Interventionmonths (Median)
WBRT Followed by Standard of Care3.8
WBRT+Capecitabine Followed by Capecitabine Maintenance3.4

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Percentage of Participants With Objective Extra-cranial Disease Response at 4 Weeks After Completion of WBRT, Assessed by Investigator According to CT

Objective extra-cranial response was defined as having CR or PR for extra-cranial lesions, assessed by CT using RECIST. CR: disappearance of all extra-cranial lesions. PR: >/=30 % decrease in sum of LD of extra-cranial lesions taking as reference the baseline sum LD. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first up to 4 weeks after completion of WBRT (up to approximately 7 weeks)"

Interventionpercentage of participants (Number)
WBRT Followed by Standard of Care0.0
WBRT+Capecitabine Followed by Capecitabine Maintenance9.1

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Time to Extra-cranial Disease Progression, Assessed by Investigator According to CT

Time to extra-cranial progression was defined as the time from start of study treatment to first documentation of PD or death due to extra-cranial lesions. PD was assessed by CT according to RECIST. PD: a 20% or greater increase in the sum of the LD of extra-cranial lesions taking as reference the smallest sum LD recorded since the treatment started or appearance of one or more extra-cranial lesions and/or unequivocal progression of existing extra-cranial lesions. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first (up to approximately 1 year 5.5 months overall)"

Interventionmonths (Median)
WBRT Followed by Standard of Care3.5
WBRT+Capecitabine Followed by Capecitabine Maintenance2.7

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Time to Progression, Assessed by Investigator According to MRI and CT

Time to progression was defined as the time from start of study treatment to first documentation of PD or death due to tumor (CNS or extra-cranial). PD was assessed by MRI or CT according to RECIST. PD: a 20% or greater increase in the sum of the LD of CNS or extra-cranial lesions taking as reference the smallest sum LD recorded since the treatment started or appearance of one or more CNS or extra-cranial lesions and/or unequivocal progression of existing CNS or extra-cranial lesions. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first (up to approximately 1 year 5.5 months overall)"

Interventionmonths (Median)
WBRT Followed by Standard of Care3.3
WBRT+Capecitabine Followed by Capecitabine Maintenance2.7

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Absolute Change From Baseline in Mini Mental State (MMS) Total Score

MMS was an 11-question measure that tested five areas of cognitive function: orientation, registration, attention and calculation, recall, and language. Four items were scored on a scale of 0 to 1; 1 item was scored on a scale of 0 to 2; 3 items were scored on a scale of 0 to 3; and 3 items were scored on a scale of 0 to 5. MMS total score was obtained by adding the scores of all individual items and ranged from 0 to 30, where higher scores indicate better cognitive state. (NCT00977379)
Timeframe: Baseline, Up to end of Treatment (up to 10.6 months overall)

Interventionunits on a scale (Mean)
WBRT Followed by Standard of Care-1.5
WBRT+Capecitabine Followed by Capecitabine Maintenance0.9

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Duration of CNS Response, Assessed by Investigator According to MRI

Duration of CNS response was defined as the time from first documented cranial CR or PR (whichever was recorded first) until the first date CNS recurrence or progression was documented as assessed by contrast-enhanced MRI according to RECIST criteria but without exam for response confirmation. CR: disappearance of all CNS lesions. PR: >/=30 % decrease in sum of LD of CNS lesions taking as reference the baseline sum LD. PD: a 20% or greater increase in the sum of the LD of CNS lesions taking as reference the smallest sum LD recorded since the treatment started or appearance of one or more CNS lesions and/or unequivocal progression of existing CNS lesions. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first (up to approximately 1 year 5.5 months overall)"

Interventionmonths (Median)
WBRT Followed by Standard of Care6.2
WBRT+Capecitabine Followed by Capecitabine Maintenance2.6

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Overall Survival (OS)

OS was defined as the time from the start of study treatment to date of death due to any cause. OS was assessed using Kaplan-Meier analysis. (NCT00977379)
Timeframe: Baseline until death (up to approximately 1 year 5.5 months overall)

Interventionmonths (Median)
WBRT Followed by Standard of Care9.8
WBRT+Capecitabine Followed by Capecitabine Maintenance4.6

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Percentage of Participants With Best Objective Central Nervous System (CNS) Response, Assessed by Centralized Independent Expert According to Magnetic Resonance Imaging (MRI) - Intent-to-Treat (ITT) Population

Best objective CNS response was defined as having complete response (CR) or partial response (PR) for CNS metastasis, assessed by contrast-enhanced MRI using response evaluation criteria in solid tumors (RECIST). CR: disappearance of all CNS lesions. PR: greater than or equal to (>/=) 30 percent (%) decrease in sum of longest diameters (LD) of CNS lesions taking as reference the baseline sum LD. (NCT00977379)
Timeframe: "Baseline until disease progression (PD), unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first (up to approximately 1 year 5.5 months overall)"

Interventionpercentage of participants (Number)
WBRT Followed by Standard of Care25.0
WBRT+Capecitabine Followed by Capecitabine Maintenance36.4

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Percentage of Participants With Best Objective CNS Response, Assessed by Centralized Independent Expert According to MRI - Per-Protocol (PP) Population

Best objective CNS response was defined as having CR or PR for CNS metastasis, assessed by contrast-enhanced MRI using RECIST. CR: disappearance of all CNS lesions. PR: >/=30% decrease in sum of LD of CNS lesions taking as reference the baseline sum LD. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first (up to approximately 1 year 5.5 months overall)"

Interventionpercentage of participants (Number)
WBRT Followed by Standard of Care20.0
WBRT+Capecitabine Followed by Capecitabine Maintenance33.3

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Percentage of Participants With Best Objective CNS Response, Assessed by Investigator According to MRI

Best objective CNS response was defined as having CR or PR for CNS metastasis, assessed by contrast-enhanced MRI using RECIST. CR: disappearance of all CNS lesions. PR: >/=30% decrease in sum of LD of CNS lesions taking as reference the baseline sum LD. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first (up to approximately 1 year 5.5 months overall)"

Interventionpercentage of participants (Number)
WBRT Followed by Standard of Care50.0
WBRT+Capecitabine Followed by Capecitabine Maintenance54.5

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Percentage of Participants With Best Objective Extra-cranial Disease Response, Assessed by Investigator According to Computed Tomography (CT)

Best objective extra-cranial response was defined as having CR or PR for extra-cranial lesions, assessed by CT using RECIST. CR: disappearance of all extra-cranial lesions. PR: >/=30 % decrease in sum of LD of extra-cranial lesions taking as reference the baseline sum LD. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first (up to approximately 1 year 5.5 months overall)"

Interventionpercentage of participants (Number)
WBRT Followed by Standard of Care0.0
WBRT+Capecitabine Followed by Capecitabine Maintenance9.1

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Percentage of Participants With Clinical Benefit, Assessed by Investigator According to MRI

Clinical benefit was defined as having CR, PR, or stable disease (SD), assessed by contrast-enhanced MRI using RECIST. CR: disappearance of all CNS lesions. PR: >/=30 % decrease in sum of LD of CNS lesions taking as reference the baseline sum LD. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD) taking as reference smallest sum LD since treatment started. PD: a 20% or greater increase in the sum of the LD of CNS lesions taking as reference the smallest sum LD recorded since the treatment started or appearance of one or more CNS lesions and/or unequivocal progression of existing CNS lesions. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first (up to approximately 1 year 5.5 months overall)"

Interventionpercentage of participants (Number)
WBRT Followed by Standard of Care83.3
WBRT+Capecitabine Followed by Capecitabine Maintenance72.7

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Percentage of Participants With Objective CNS Response at 4 Weeks After Completion of WBRT, Assessed by Centralized Independent Expert According to MRI

Objective CNS response was defined as having CR or PR for CNS metastasis, assessed by contrast-enhanced MRI using RECIST. CR: disappearance of all CNS lesions. PR: >/=30% decrease in sum of LD of CNS lesions taking as reference the baseline sum LD. (NCT00977379)
Timeframe: "Baseline until PD, unacceptable toxicity, withdrawal of consent, change of therapeutic strategy (for arm WBRT Followed by Standard of Care only), or death, whichever occurred first up to 4 weeks after completion of WBRT (up to approximately 7 weeks)"

Interventionpercentage of participants (Number)
WBRT Followed by Standard of Care25.0
WBRT+Capecitabine Followed by Capecitabine Maintenance36.4

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Assess Overall Survival (OS)

(NCT01007552)
Timeframe: From date of randomization until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 5 years

Interventionmonths (Mean)
Gemcitabine, Capecitabine and Bevacizumab10.2

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Circulating Tumor Cells (CTC) Will be Assessed at Baseline, Day 22 and Day 43

Mean number of CTCs in 7.5 ml of whole blood (NCT01007552)
Timeframe: baseline, day 22 and day 43

Interventioncells (Mean)
BaselineDay 22Day 43
Gemcitabine, Capecitabine and Bevacizumab2.31.00.8

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Assess the Change in the Quality of Life Among Patients Using the FACT-Hep (Version 4) for Hepatobiliary Cancers.

"We utilized the FACT-HEP TOTAL SCORE (version 4) quality-of-life scale, which is a 45 item scale ranging from 96-178. Higher scores of the reflect better quality of life.~For a Detailed description see:~Nancy Heffernan, David Cella, Kimberly Webster, Linda Odom, Mary Martone, Steven Passik, Marilyn Bookbinder, Yuman Fong, William Jarnagin, and Leslie Blumgart: Measuring Health-Related Quality of Life in Patients With Hepatobiliary Cancers: The Functional Assessment of Cancer Therapy-Hepatobiliary Questionnaire. Journal of Clinical Oncology, Vol 20, No 9 (May 1), 2002: pp 2229-2239.~No subscales were analyzed.~." (NCT01007552)
Timeframe: Baseline, Day 22 and Day 43

Interventionunits on a scale (Mean)
BaselineCycle 2Cycle 3
Gemcitabine, Capecitabine and Bevacizumab136.7135.6139.9

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The Primary Objective of This Study is to Assess Progression Free Survival (PFS) With Proposed Therapy for Patients With Locally Advanced or Metastatic Gallbladder and Biliary Cancers.

"Progression will be evaluated in this study using the international criteria proposed by the Response Evaluation Criteria in Solid Tumors (RECIST 1.0). Changes in only the largest diameter (unidimensional measurement) of the tumor lesions are used in the RECIST criteria. Note: Lesions are either measurable or non-measurable using the criteria provided below. The term evaluable in reference to measurability will not be used because it does not provide additional meaning or accuracy." (NCT01007552)
Timeframe: From date of randomization until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 5 years

Interventionmonths (Median)
Gemcitabine, Capecitabine and Bevacizumab8.1

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Estimate the Proportion of Patients With Clinical Response

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01007552)
Timeframe: From date of randomization until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 5 years

Interventionpercentage of participants (Number)
Gemcitabine, Capecitabine and Bevacizumab24

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Assess the Toxicity of the Regimen.

Number of patients with Serious Adverse Events. Please refer to the adverse event reporting for more detail. (NCT01007552)
Timeframe: up to 5 years

Interventionparticipants (Number)
Gemcitabine, Capecitabine and Bevacizumab30

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Duration of Response (DOR) in the Randomized Phase

DOR is defined as the time from the first documented evidence of response (CR or PR) until the first documented sign of disease progression (a >=20% increase in the sum of the LD of TLs, taking as reference the smallest sum LD recorded since the treatment started or the appearance of >=1 new lesion) or death, if sooner. CR=the disappearance of all TLs. PR=a >=30% decrease in the sum of the LD of target lesions, taking as a reference the Baseline sum LD. (NCT01013740)
Timeframe: From the time of the first documented confirmed complete or partial response until disease progression or death, if sooner (average of 27 study weeks)

Interventionmonths (Median)
Lapatinib Plus Capecitabine10.8
Lapatinib Plus Vinorelbine6.7

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Number of Participants With Clinical Benefit (CB) in the Randomized Phase

CB is defined as the the number of participants achieving either a confirmed CR or PR or having stable disease (SD) for at least 24 weeks (i.e., approximately 6 months). CR=the disappearance of all TLs. PR=a >=30% decrease in the sum of the LD of TLs, taking as a reference the Baseline sum LD. SD is defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD=at least a 20% increase in the sum of the LD of target lesions, taking as a reference the smallest sum LD recorded since the treatment started or the appearance of >=1 new lesion). Participants with unknown or missing responses were treated as non-responders. (NCT01013740)
Timeframe: From randomization until disease progression, death, or discontinuation from the study (average of 27 study weeks)

Interventionparticipants (Number)
Lapatinib Plus Capecitabine18
Lapatinib Plus Vinorelbine29

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Number of Participants With Overall Response (OR), as Assessed by the Investigator in the Randomized Phase

OR is defined as the number of participants achieving either a confirmed complete response (CR: the disappearance of all target lesions [TLs]) or partial response (PR: a >=30% decrease in the sum of the longest diameter [LD] of the TLs, taking as reference the baseline sum LD) as assessed by the investigator as the best OR. (NCT01013740)
Timeframe: From randomization until disease progression, death, or discontinuation from the study (average of 27 study weeks)

Interventionparticipants (Number)
Lapatinib Plus Capecitabine13
Lapatinib Plus Vinorelbine15

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Overall Survival (OS)

OS is defined as the time from randomization to the date of death due to any cause. Participants who had not died were censored at the date of the last adequate tumor assessment at the time of the cut-off. (NCT01013740)
Timeframe: From the date of randomization until death (average of 55 study weeks)

Interventionmonths (Median)
Lapatinib Plus Capecitabine19.4
Lapatinib Plus Vinorelbine24.3

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Progression Free Survival (PFS) in the Randomized Phase

PFS is defined as the time from randomization until the earliest date of disease progression (PD) or death due to any cause, if sooner. PD is defined as at least a 20 % increase in the sum of the longest diameter (LD) of target lesions, taking as a reference the smallest sum LD recorded since the treatment started or the appearance of >=1 new lesion. (NCT01013740)
Timeframe: From randomization until disease progression, death, or discontinuation from the study (average of 27 study weeks)

Interventionmonths (Median)
Lapatinib Plus Capecitabine6.2
Lapatinib Plus Vinorelbine6.2

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Time to Response in the Randomized Phase

Time to response is defined as the time from randomization until the first documented evidence of CR (the disappearance of all TLs) or PR (a >=30% decrease in the sum of the LD of the TLs, taking as a reference the basline sum LD) (whichever status is recorded first). When tumor response was confirmed at a repeat assessment, the time to response was taken to be the first time that the response was observed. (NCT01013740)
Timeframe: From randomization until the time of the first documented confirmed CR or PR (average of 27 study weeks)

Interventionweeks (Median)
Lapatinib Plus Capecitabine9.3
Lapatinib Plus Vinorelbine9.4

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Number of Participants With Grade 4 and Grade 5 Adverse Events (AE)

An AE is defined as any untoward medical occurrence in a patient or clinical investigation subject, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. AEs were graded using the Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. Grades: 0 = no AE or within normal limits; 1 = mild AE; 2 = moderate AE; 3 = severe and undesirable AE; 4 = life-threatening or disabling AE; 5 = death related to AE. (NCT01013740)
Timeframe: From randomization until disease progression, death, or discontinuation from the study (average of 55 study weeks)

,
Interventionparticipants (Number)
Helicobacter gastritis, Grade 4Neutropenia, Grade 4Leukopenia, Grade 4Febrile neutropenia, Grade 4Mucosal inflammation, Grade 4Pulmonary embolism, Grade 4Intestinal obstruction, Grade 5
Lapatinib Plus Capecitabine1000000
Lapatinib Plus Vinorelbine0911111

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Time to Progression (TTP) Based Upon Independent Review Facility (IRF) Assessment

Time to Progression (TTP) was defined as time between randomization and the first occurrence of progressive disease (PD), based on IRF assessment. (NCT01026142)
Timeframe: Tumor assessments every 9 weeks from randomization until Week 27, then every 12 weeks thereafter, until IRF-determined PD, initiation of alternative anticancer medication, or death (up to 5.5 years).

InterventionWeeks (Median)
A: Capecitabine + Trastuzumab39.0
B: Capecitabine + Trastuzumab + Pertuzumab50.6

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Progression Free Survival (Independent Assessment)

Progression Free Survival (PFS) was defined as the time from randomization to first documented disease progression (PD), as determined by an Independent Review Facility (IRF) using Response Evaluation Criteria in Solid Tumors (RECIST) version 1.0, or death from any cause, whichever occurred first. PD was defined as at least a 20% increase in the sum of the longest diameter (LD) of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions; or the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. IRF review of tumor assessment ceased after the primary PFS analysis. The primary endpoint was analyzed after approximately 337 IRF-assessed PFS events were observed. (NCT01026142)
Timeframe: Tumor assessments every 9 weeks from randomization until Week 27, then every 12 weeks thereafter, until IRF-determined PD, initiation of alternative anticancer medication, or death (up to 5.5 years).

Interventionmonths (Median)
A: Capecitabine + Trastuzumab9.0
B: Capecitabine + Trastuzumab + Pertuzumab11.1

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Overall Survival (OS) Rate Based on a 2-year Truncated Analysis

The Overall Survival (OS) 2-year truncated analysis is the Kaplan-Meier estimate of the percentage of participants who were surviving at 2 years. OS is defined as the time from the date of randomization to the date of death from any cause, with censoring of all events and follow-up beyond the end of the second year. (NCT01026142)
Timeframe: From randomization until death from any cause (up to 2 years)

InterventionPercentage of participants (Number)
A: Capecitabine + Trastuzumab55.0
B: Capecitabine + Trastuzumab + Pertuzumab74.9

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Overall Objective Response Rate (ORR)

Overall Objective Response Rate is based upon investigator and IRF assessments. Objective Response Rate (ORR) was defined as the percentage of participants with a confirmed complete response (CR) or partial response (PR) among those who had measurable disease at baseline. CR was defined as the disappearance of all target lesions. PR was defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. (NCT01026142)
Timeframe: Tumor assessments every 9 weeks from randomization until Week 27, then every 12 weeks thereafter, until IRF-determined PD, initiation of alternative anticancer medication, or death (up to 5.5 years).

,
InterventionPercentage of participants (Number)
Complete Response (CR) - IRF AssessmentPartial Response (PR) - IRF assessmentComplete Response (CR) - Investigator AssessedPartial Response (PR) - Investigator Assessed
A: Capecitabine + Trastuzumab032.91.236.0
B: Capecitabine + Trastuzumab + Pertuzumab1.838.76.738.0

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Clinical Benefit Rate (CBR)

Clinical Benefit Rate is based upon Independent Review Facility (IRF) assessments; defined as the percentage of participants a complete response (CR), partial response (PR), or stable disease for at least 8 cycles or 6 months. (NCT01026142)
Timeframe: Tumor assessments every 9 weeks from randomization until Week 27, then every 12 weeks thereafter, until IRF-determined PD, initiation of alternative anticancer medication, or death (up to 5.5 years).

InterventionPercentage of participants (Number)
A: Capecitabine + Trastuzumab54.0
B: Capecitabine + Trastuzumab + Pertuzumab63.6

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Duration of Objective Response

Duration of Objective Response was defined for the subpopulation of responders as time from first Independent Review Facility (IRF)-assessed complete response (CR) or partial response (PR) to subsequent first documented, IRF-confirmed evidence of disease progression. Only participants with an objective response were included in the analysis of duration of objective response. (NCT01026142)
Timeframe: Tumor assessments every 9 weeks from randomization until Week 27, then every 12 weeks thereafter, until IRF-determined PD, initiation of alternative anticancer medication, or death (up to 5.5 years).

InterventionWeeks (Median)
A: Capecitabine + Trastuzumab30.0
B: Capecitabine + Trastuzumab + Pertuzumab51.6

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Investigator Assessment Progression-Free Survival (PFS)

Investigator Assessment Progression-Free Survival (PFS) was defined as the time from randomization to the first documented progressive disease, as determined by the investigator using Response Evaluation Criteria in Solid Tumors (RECIST) v1.0, or death from any cause, whichever occurred first. PD is defined as at least a 20% increase in the sum of the longest diameter (LD) of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions; or the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. (NCT01026142)
Timeframe: Tumor assessments every 9 weeks from randomization until Week 27, then every 12 weeks thereafter, until IRF-determined PD, initiation of alternative anticancer medication, or death (up to 7.5 years).

InterventionMonths (Median)
A: Capecitabine + Trastuzumab9.0
B: Capecitabine + Trastuzumab + Pertuzumab11.8

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Time to Treatment Failure (TTF) Based Upon Independent Review Facility (IRF) Assessment

Time to Treatment Failure (TTF) was defined as time between randomization and date of disease progression based on independent review, death, or withdrawal of treatment due to adverse events, withdrawn informed consent, refusal of treatment/failure to cooperate, or failure to return, whichever occurred first. (NCT01026142)
Timeframe: Tumor assessments every 9 weeks from randomization until Week 27, then every 12 weeks thereafter, until IRF-determined PD, initiation of alternative anticancer medication, or death (up to 5.5 years).

InterventionWeeks (Median)
A: Capecitabine + Trastuzumab39.0
B: Capecitabine + Trastuzumab + Pertuzumab50.9

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Overall Survival (OS)

Overall Survival (OS) was defined as the time from the date of randomization to the date of death from any cause. The results of the final OS analysis are presented here. Participants who were alive or lost to follow-up at the time of the analysis were censored at the last known alive date. Participants with no postbaseline information were censored at the time of randomization plus 1 day. Prior to the final data analysis cut-off, it was ensured that all participants who were in survival follow-up had been contacted as recently as possible within the last 3 months to confirm current survival status. (NCT01026142)
Timeframe: From randomization until death from any cause (up to 7.5 years).

InterventionMonths (Median)
A: Capecitabine + Trastuzumab28.1
B: Capecitabine + Trastuzumab + Pertuzumab37.2

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Number of Participants Experiencing Adverse Events

The primary objective of the study is to evaluate safety and tolerability of the study treatment regimen. The analyses will be descriptive and no formal hypotheses testing will be performed. Toxicities (i.e. Adverse Events) are evaluated prior to each treatment and during any clinical visit. (NCT01032850)
Timeframe: 6 months

Interventionparticipants (Number)
ThrombocytopeniaNeutropeniaLow phosphate levelsLow magnesium levelsLow calcium levelsLow sodium levelsHigh bilirubin levelsElevated aspartate aminotransferaseHand and foot syndromeMucositisAlopecia (Hair loss)Skin rashDeep vein thrombosisTreatment related deaths
Arm 1: Sorafenib & Capecitabine91322132311130

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Disease Control Rate of Response (DCR)

Tumor response is evaluated according to Response Evaluation Criteria in Solid Tumors (RECIST) (version 1.0). Target lesions are assessed by computerized tomography (CT) or magnetic resonance imaging (MRI:) Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), neither sufficient decrease in the sum of the longest diameter of target lesions to qualify for PR nor sufficient increase in the sum of the longest diameter of target lesions to qualify for Progressive Disease; Progressive Disease (PD), 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. Disease control rate (DCR) is the sum of the percentages of patients achieving complete and partial responses and stable disease (NCT01032850)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Complete Response (CR)Partial Response (PR)Stable Disease (SD)Disease Control Rate of Response (DCR)
Arm 1: Sorafenib & Capecitabine886177

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Progression Free Survival (PFS)

The time from treatment initiation to disease progression or death by any cause. Progression is evaluated according to Response Evaluation Criteria in Solid Tumors (RECIST) (version 1.0). Target lesions are assessed by computerized tomography (CT) or magnetic resonance imaging (MRI:) Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), neither sufficient decrease in the sum of the longest diameter of target lesions to qualify for PR nor sufficient increase in the sum of the longest diameter of target lesions to qualify for Progressive Disease; Progressive Disease (PD), 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT01032850)
Timeframe: 5 years

Interventionmonths (Median)
Arm 1: Sorafenib & Capecitabine4.15

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Overall Survival (OS)

The time from treatment initiation to death by any cause (NCT01032850)
Timeframe: 5 years

InterventionMonths (Median)
Arm 1: Sorafenib & Capecitabine12.7

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Pain Intensity Scores as Assessed By Visual Analog Scale (VAS)

"The participant assessed their pain on a 0 to 100 millimeter (mm) horizontal VAS. The left-hand extreme of the line equals 0 mm, and is described as no pain and the right-hand extreme equals 100 mm as unbearable pain. A negative change indicated improvement." (NCT01041404)
Timeframe: BL, Days 1, 22, 43, 64, 85, 106, 127, and every 21 days until disease progression of the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

,
Interventionmm (Mean)
BL (n=275,284)Week 4 (n=234,249)Week 7 (n=181,219)Week 10 (n=174, 202)Week 13 (n=152,181)Week 16 (n=121,165)Week 19 (n=114,142)Week 22 (n=79,141)Week 25 (n=64,124)Week 28 (n=47,111)Week 31 (n=45,95)Week 34 (n=37,86)Week 37 (n=29,64)Week 40 (n=24,54)Week 43 (n=12,43)Week 46 (n=14,41)Week 49 (n=10,36)Week 52 (n=8,30)Week 55 (n=6,24)Week 58 (n=6,20)Week 61 (n=4,17)Week 64 (n=3,20)Week 67 (n=4,17)Week 70 (n=3,13)Week 73 (n=3,10)Week 76 (n=3,8)Week 79 (n=3,9)Week 82 (n=2,6)Week 85 (n=2,6)Week 88 (n=2,6)Week 91 (n=2,4)Week 94 (n=2,6)Week 97 (n=1,5)Week 100 (n=1,4)Week 103 (n=1,4)Week 106 (n=1,4)Week 109 (n=1,4)Week 112 (n=1,5)Week 115 (n=1,4)Week 118 (n=1,5)Week 121 (n=1,5)Week 124 (n=1,4)Week 127 (n=1,3)Week 130 (n=0,3)Week 133 (n=1,3)Week 136 (n=0,2)Week 139 (n=0,2)Week 142 (n=0,2)Week 145 (n=0,1)Final visit/withdrawal (n=157,161)
Fluoropyrimidine/Cisplatin (FP)21.114.611.114.511.314.015.413.312.78.68.79.415.516.412.616.17.25.82.34.75.32.01.51.31.01.71.00.01.00.50.50.50.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA23.8
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)17.913.313.812.912.212.812.015.111.012.312.510.710.98.87.27.46.56.93.33.87.26.88.91.316.512.95.94.86.35.77.55.80.20.36.57.87.34.25.83.83.24.56.35.75.06.08.07.515.021.9

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Trastuzumab Minimum Serum Concentration (Cmin)

Median Cmin (measured as milligrams per liter [mg/L]) calculated for all treated participants using the nominal dosage schedule administered as an IV infusion. (NCT01041404)
Timeframe: Predose and end of infusion on Days 1, 8, 15, and 64, and predose on Days 22 and 106

Interventionmg/L (Median)
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)23.0

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Percentage of Participants With Change From Baseline in Body Weight by Percentage Change in Weight

Change in body weight was categorized as an increase of greater than (>)5 percent (%), no change (plus or minus [±]5%), decrease of >5-10%, or a decrease of >10% from BL to the end of study. Time windows were applied in order to assign visits to weight measurements, and the lowest post-screening value recorded was used for the analysis. The percentage change in weight from screening was summarized over time. (NCT01041404)
Timeframe: BL, Days 1, 22, 43, 64, 85, 106, 127, and every 21 days until disease progression of the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

,
Interventionpercentage of participants (Number)
Increase >5%No change (±5%)Decrease >5-10%Decrease >10%
Fluoropyrimidine/Cisplatin (FP)1.551.628.218.7
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)1.150.527.221.2

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Duration of Response - Percentage of Participants With an Event

Duration of response was defined for responders as the time from the date on which the CR or PR was first recorded to the date on which PD is first noted. Participants were censored on the date of death, the date of last tumor measurement, the last date in study drug log, or the date of last follow-up. (NCT01041404)
Timeframe: BL, Days 43, 85, and 127, and every 21 days thereafter until disease progression or the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionpercentage of participants (Number)
Fluoropyrimidine/Cisplatin (FP)80.0
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)71.9

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Overall Survival - Time to Event

The median time, in months, from the date of randomization to the date of an OS event. Participants were censored at the last date tumor measurement, the last date in the study drug log, or the date of last follow-up. (NCT01041404)
Timeframe: BL, Days 1, 8, 15, 22, 43, 64, 85, 106, 127, and every 21 days until the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionmonths (Median)
Fluoropyrimidine/Cisplatin (FP)11.1
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)13.8

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Body Weight (Kilograms [kg]) at BL

(NCT01041404)
Timeframe: BL

Interventionkg (Median)
Fluoropyrimidine/Cisplatin (FP)60
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)61

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Steady State Trastuzumab Area Under the Concentration (AUC)

Individual steady state predicted exposure, as assessed by median AUC (measured as mg multiplied by [*] day per liter [L]) calculated for all treated participants using the nominal dosage schedule administered as an IV infusion. Individual steady state AUC was calculated using all available PK samples from all timepoints. (NCT01041404)
Timeframe: Predose and end of infusion on Days 1, 8, 15, and 64, and predose on Days 22 and 106

Interventionmg*day/L (Median)
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)1030

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Percentage of Participants With a Change in Analgesic Medication During the Study

Analgesic medications were recorded throughout the study until disease progression. (NCT01041404)
Timeframe: BL, Days 1, 22, 43, 64, 85, 106, 127, and every 21 days until disease progression of the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

,
Interventionpercentage of participants (Number)
Taking any analgesic medicationDiscontinued at least 1 medicationDecreased dose of at least 1 medicationNo change in any medicationIncreased dose or added at least 1 medication
Fluoropyrimidine/Cisplatin (FP)29.05.90.35.517.2
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)29.31.70.37.120.1

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Time to Progression - Time to Event

The median time, in months, from the date of randomized to the date of a TTP event. Participants were censored at the last date of tumor assessment, the last date in the study drug log, or the last date of follow-up. (NCT01041404)
Timeframe: BL, Days 43, 85, and 127, and every 21 days thereafter until disease progression or the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionmonths (Median)
Fluoropyrimidine/Cisplatin (FP)5.6
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)7.1

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European Organisation For the Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Core 30 (QLQ C-30) Questionnaire Scores

EORTC QLQ-C30: included functional scales (physical, role, cognitive, emotional, and social), global health status, symptom scales (fatigue, pain, nausea/vomiting) and single items (dyspnoea, appetite loss, insomnia, constipation/diarrhea and financial difficulties). Most questions used 4 point scale (1 'Not at all' to 4 'Very much'; 2 questions used 7-point scale (1 'very poor' to 7 'Excellent'). Scores averaged, transformed to 0-100 scale; higher score equals (=) better level of functioning or greater degree of symptoms. (NCT01041404)
Timeframe: BL, Days 1, 22, 43, 64, 85, 106, 127, and every 21 days until disease progression of the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

,
Interventionscores on a scale (Mean)
Global Health Status: BL (n=274,287)Global Health Status: Week 4 (n=235,249)Global Health Status: Week 7 (n=180,220)Global Health Status: Week 10 (n=176,202)Global Health Status: Week 13 (n=152,182)Global Health Status: Week 16 (n=121,165)Global Health Status: Week 19 (n=114,143)Global Health Status: Week 22 (n=78,143)Global Health Status: Week 25 (n=64,124)Global Health Status: Week 28 (n=47,111)Global Health Status: Week 31 (n=45,95)Global Health Status: Week 34 (n=36,87)Global Health Status: Week 37 (n=29,64)Global Health Status: Week 40 (n=23,55)Global Health Status: Week 43 (n=12,43)Global Health Status: Week 46 (n=13,42)Global Health Status: Week 49 (n=9,36)Global Health Status: Week 52 (n=7,29)Global Health Status: Week 55 (n=5,24)Global Health Status: Week 58 (n=5,21)Global Health Status: Week 61 (n=4,17)Global Health Status: Week 64 (n=3,20)Global Health Status: Week 67 (n=4,17)Global Health Status: Week 70 (n=3,14)Global Health Status: Week 73 (n=3,12)Global Health Status: Week 76 (n=3,8)Global Health Status: Week 79 (n=3,9)Global Health Status: Week 82 (n=2,5)Global Health Status: Week 85 (n=2,6)Global Health Status: Week 88 (n=2,6)Global Health Status: Week 91 (n=2,4)Global Health Status: Week 94 (n=2,6)Global Health Status: Week 97 (n=1,5)Global Health Status: Week 100 (n=1,4)Global Health Status: Week 103 (n=1,3)Global Health Status: Week 106 (n=1,4)Global Health Status: Week 109 (n=1,4)Global Health Status: Week 112 (n=1,5)Global Health Status: Week 115 (n=1,4)Global Health Status: Week 118 (n=1,5)Global Health Status: Week 121 (n=1,5)Global Health Status: Week 124 (n=1,5)Global Health Status: Week 127 (n=1,3)Global Health Status: Week 130 (n=0,3)Global Health Status: Week 133 (n=1,3)Global Health Status: Week 136 (n=0,2)Global Health Status: Week 139 (n=0,2)Global Health Status: Week 142 (n=0,2)Global Health Status: Week 145 (n=0,1)Global Health Status: Final Visit (n=158,160)Physical Functioning: BL (n=276,287)Physical Functioning: Week 4 (n=235,250)Physical Functioning: Week 7 (n=181,220)Physical Functioning: Week 10 (n=174,201)Physical Functioning: Week 13 (n=151,183)Physical Functioning: Week 16 (n=121,165)Physical Functioning: Week 19 (n=114,143)Physical Functioning: Week 22 (n=79,143)Physical Functioning: Week 25 (n=64,124)Physical Functioning: Week 28 (n=47,110)Physical Functioning: Week 31 (n=45,95)Physical Functioning: Week 34 (n=37,87)Physical Functioning: Week 37 (n=29,64)Physical Functioning: Week 40 (n=24,55)Physical Functioning: Week 43 (n=12,43)Physical Functioning: Week 46 (n=14,42)Physical Functioning: Week 49 (n=10,36)Physical Functioning: Week 52 (n=8,30)Physical Functioning: Week 55 (n=6,24)Physical Functioning: Week 58 (n=6,21)Physical Functioning: Week 61 (n=4,17)Physical Functioning: Week 64 (n=3,20)Physical Functioning: Week 67 (n=4,17)Physical Functioning: Week 70 (n=3,14)Physical Functioning: Week 73 (n=3,12)Physical Functioning: Week 76 (n=3,8)Physical Functioning: Week 79 (n=3,9)Physical Functioning: Week 82 (n=2,6)Physical Functioning: Week 85 (n=2,6)Physical Functioning: Week 88 (n=2,6)Physical Functioning: Week 91 (n=2,4)Physical Functioning: Week 94 (n=2,6)Physical Functioning: Week 97 (n=1,5)Physical Functioning: Week 100 (n=1,4)Physical Functioning: Week 103 (n=1,4)Physical Functioning: Week 106 (n=1,4)Physical Functioning: Week 109 (n=1,4)Physical Functioning: Week 112 (n=1,5)Physical Functioning: Week 115 (n=1,4)Physical Functioning: Week 118 (n=1,5)Physical Functioning: Week 121 (n=1,5)Physical Functioning: Week 124 (n=1,5)Physical Functioning: Week 127 (n=1,3)Physical Functioning: Week 130 (n=0,3)Physical Functioning: Week 133 (n=1,3)Physical Functioning: Week 136 (n=0,2)Physical Functioning: Week 139 (n=0,2)Physical Functioning: Week 142 (n=0,2)Physical Functioning: Week 145 (n=0,1)Physical Functioning: Final Visit (n=158,161)Role Functioning: BL (n=276,287)Role Functioning: Week 4 (n=234,250)Role Functioning: Week 7 (n=181,220)Role Functioning: Week 10 (n=176,202)Role Functioning: Week 13 (n=152,182)Role Functioning: Week 16 (n=121,165)Role Functioning: Week 19 (n=114,143)Role Functioning: Week 22 (n=79,142)Role Functioning: Week 25 (n=64,124)Role Functioning: Week 28 (n=47,110)Role Functioning: Week 31 (n=45,95)Role Functioning: Week 34 (n=37,87)Role Functioning: Week 37 (n=29,64)Role Functioning: Week 40 (n=24,55)Role Functioning: Week 43 (n=12,43)Role Functioning: Week 46 (n=14,42)Role Functioning: Week 49 (n=10,36)Role Functioning: Week 52 (n=8,30)Role Functioning: Week 55 (n=6,24)Role Functioning: Week 58 (n=6,21)Role Functioning: Week 61 (n=4,17)Role Functioning: Week 64 (n=3,20)Role Functioning: Week 67 (n=4,17)Role Functioning: Week 70 (n=3,14)Role Functioning: Week 73 (n=3,12)Role Functioning: Week 76 (n=3,8)Role Functioning: Week 79 (n=3,9)Role Functioning: Week 82 (n=2,6)Role Functioning: Week 85 (n=2,6)Role Functioning: Week 88 (n=2,6)Role Functioning: Week 91 (n=2,4)Role Functioning: Week 94 (n=2,6)Role Functioning: Week 97 (n=1,5)Role Functioning: Week 100 (n=1,4)Role Functioning: Week 103 (n=1,4)Role Functioning: Week 106 (n=1,4)Role Functioning: Week 109 (n=1,4)Role Functioning: Week 112 (n=1,5)Role Functioning: Week 115 (n=1,4)Role Functioning: Week 118 (n=1,5)Role Functioning: Week 121 (n=1,5)Role Functioning: Week 124 (n=1,5)Role Functioning: Week 127 (n=1,3)Role Functioning: Week 130 (n=0,3)Role Functioning: Week 133 (n=1,3)Role Functioning: Week 136 (n=0,2)Role Functioning: Week 139 (n=0,2)Role Functioning: Week 142 (n=0,2)Role Functioning: Week 145 (n=0,1)Role Functioning: Final Visit (n=158,161)Emotional Functioning: BL (n=276,287)Emotional Functioning: Week 4 (n=235,250)Emotional Functioning: Week 7 (n=180,220)Emotional Functioning: Week 10 (n=176,202)Emotional Functioning: Week 13 (n=152,183)Emotional Functioning: Week 16 (n=121,165)Emotional Functioning: Week 19 (n=114,143)Emotional Functioning: Week 22 (n=79,143)Emotional Functioning: Week 25 (n=64,124)Emotional Functioning: Week 28 (n=47,111)Emotional Functioning: Week 31 (n=45,95)Emotional Functioning: Week 34 (n=37,87)Emotional Functioning: Week 37 (n=29,64)Emotional Functioning: Week 40 (n=24,55)Emotional Functioning: Week 43 (n=12,43)Emotional Functioning: Week 46 (n=14,42)Emotional Functioning: Week 49 (n=10,36)Emotional Functioning: Week 52 (n=8,29)Emotional Functioning: Week 55 (n=6,24)Emotional Functioning: Week 58 (n=6,21)Emotional Functioning: Week 61 (n=4,17)Emotional Functioning: Week 64 (n=3,20)Emotional Functioning: Week 67 (n=4,17)Emotional Functioning: Week 70 (n=3,14)Emotional Functioning: Week 73 (n=3,12)Emotional Functioning: Week 76 (n=3,8)Emotional Functioning: Week 79 (n=3,9)Emotional Functioning: Week 82 (n=2,6)Emotional Functioning: Week 85 (n=2,6)Emotional Functioning: Week 88 (n=2,6)Emotional Functioning: Week 91 (n=2,4)Emotional Functioning: Week 94 (n=2,6)Emotional Functioning: Week 97 (n=1,5)Emotional Functioning: Week 100 (n=1,4)Emotional Functioning: Week 103 (n=1,4)Emotional Functioning: Week 106 (n=1,4)Emotional Functioning: Week 109 (n=1,4)Emotional Functioning: Week 112 (n=1,5)Emotional Functioning: Week 115 (n=1,4)Emotional Functioning: Week 118 (n=1,5)Emotional Functioning: Week 121 (n=1,5)Emotional Functioning: Week 124 (n=1,5)Emotional Functioning: Week 127 (n=1,3)Emotional Functioning: Week 130 (n=0,3)Emotional Functioning: Week 133 (n=1,3)Emotional Functioning: Week 136 (n=0,2)Emotional Functioning: Week 139 (n=0,2)Emotional Functioning: Week 142 (n=0,2)Emotional Functioning: Week 145 (n=0,1)Emotional Functioning: Final Visit (n=158,161)Cognitive Functioning: BL (n=276,287)Cognitive Functioning: Week 4 (n=235,250)Cognitive Functioning: Week 7 (n=180,220)Cognitive Functioning: Week 10 (n=176,202)Cognitive Functioning: Week 13 (n=152,183)Cognitive Functioning: Week 16 (n=121,165)Cognitive Functioning: Week 19 (n=114,143)Cognitive Functioning: Week 22 (n=79,143)Cognitive Functioning: Week 25 (n=64,124)Cognitive Functioning: Week 28 (n=47,111)Cognitive Functioning: Week 31 (n=45,95)Cognitive Functioning: Week 34 (n=37,87)Cognitive Functioning: Week 37 (n=29,64)Cognitive Functioning: Week 40 (n=24,55)Cognitive Functioning: Week 43 (n=12,43)Cognitive Functioning: Week 46 (n=14,42)Cognitive Functioning: Week 49 (n=10,36)Cognitive Functioning: Week 52 (n=8,29)Cognitive Functioning: Week 55 (n=6,24)Cognitive Functioning: Week 58 (n=6,21)Cognitive Functioning: Week 61 (n=4,17)Cognitive Functioning: Week 64 (n=3,20)Cognitive Functioning: Week 67 (n=4,17)Cognitive Functioning: Week 70 (n=3,14)Cognitive Functioning: Week 73 (n=3,12)Cognitive Functioning: Week 76 (n=3,8)Cognitive Functioning: Week 79 (n=3,9)Cognitive Functioning: Week 82 (n=2,6)Cognitive Functioning: Week 85 (n=2,6)Cognitive Functioning: Week 88 (n=2,6)Cognitive Functioning: Week 91 (n=2,4)Cognitive Functioning: Week 94 (n=2,6)Cognitive Functioning: Week 97 (n=1,5)Cognitive Functioning: Week 100 (n=1,4)Cognitive Functioning: Week 103 (n=1,4)Cognitive Functioning: Week 106 (n=1,4)Cognitive Functioning: Week 109 (n=1,4)Cognitive Functioning: Week 112 (n=1,5)Cognitive Functioning: Week 115 (n=1,4)Cognitive Functioning: Week 118 (n=1,5)Cognitive Functioning: Week 121 (n=1,5)Cognitive Functioning: Week 124 (n=1,5)Cognitive Functioning: Week 127 (n=1,3)Cognitive Functioning: Week 130 (n=0,3)Cognitive Functioning: Week 133 (n=1,3)Cognitive Functioning: Week 136 (n=0,2)Cognitive Functioning: Week 139 (n=0,2)Cognitive Functioning: Week 142 (n=0,2)Cognitive Functioning: Week 145 (n=0,1)Cognitive Functioning: Final Visit (n=158,161)Social Functioning: BL (n=276,286)Social Functioning: Week 4 (n=235,250)Social Functioning: Week 7 (n=179,220)Social Functioning: Week 10 (n=176,202)Social Functioning: Week 13 (n=152,183)Social Functioning: Week 16 (n=180,165)Social Functioning: Week 19 (n=114,143)Social Functioning: Week 22 (n=79,143)Social Functioning: Week 25 (n=64,124)Social Functioning: Week 28 (n=47,111)Social Functioning: Week 31 (n=45,95)Social Functioning: Week 34 (n=37,87)Social Functioning: Week 37 (n=29,64)Social Functioning: Week 40 (n=24,55)Social Functioning: Week 43 (n=12,43)Social Functioning: Week 46 (n=14,42)Social Functioning: Week 49 (n=10,36)Social Functioning: Week 52 (n=8,29)Social Functioning: Week 55 (n=6,24)Social Functioning: Week 58 (n=6,21)Social Functioning: Week 61 (n=4,17)Social Functioning: Week 64 (n=3,20)Social Functioning: Week 67 (n=4,17)Social Functioning: Week 70 (n=3,14)Social Functioning: Week 73 (n=3,12)Social Functioning: Week 76 (n=3,8)Social Functioning: Week 79 (n=3,9)Social Functioning: Wek 82 (n=2,6)Social Functioning: Week 85 (n=2,6)Social Functioning: Week 88 (n=2,6)Social Functioning: Week 91 (n=2,4)Social Functioning: Week 94 (n=2,6)Social Functioning: Week 97 (n=1,5)Social Functioning: Week 100 (n=1,4)Social Functioning: Week 103 (n=1,4)Social Functioning: Week 106 (n=1,4)Social Functioning: Week 109 (n=1,4)Social Functioning: Week 112 (n=1,5)Social Functioning: Week 115 (n=1,4)Social Functioning: Week 118 (n=1,5)Social Functioning: Week 121 (n=1,5)Social Functioning: Week 124 (n=1,5)Social Functioning: Week 127 (n=1,3)Social Functioning: Week 130 (n=0,3)Social Functioning: Week 133 (n=1,3)Social Functioning: Week 136 (n=0,2)Social Functioning: Week 139 (n=0,2)Social Functioning: Week 142 (n=0,2)Social Functioning: Week 145 (n=0,1)Social Functioning: Final Visit (n=158,161)Fatigue: BL (n=276,287)Fatigue: Week 4 (n=235,250)Fatigue: Week 7 (n=181,220)Fatigue: Week 10 (n=176,201)Fatigue: Week 13 (n=152,183)Fatigue: Week 16 (n=121,165)Fatigue: Week 19 (n=114,143)Fatigue: Week 22 (n=79,143)Fatigue: Week 25 (n=64,124)Fatigue: Week 28 (n=47,110)Fatigue: Week 31 (n=45,95)Fatigue: Week 34 (n=37,87)Fatigue: Week 37 (n=29,64)Fatigue: Week 40 (n=24,55)Fatigue: Week 43 (n=12,43)Fatigue: Week 46 (n=14,42)Fatigue: Week 49 (n=10,36)Fatigue: Week 52 (n=8,30)Fatigue: Week 55 (n=6,24)Fatigue: Week 58 (n=6,21)Fatigue: Week 61 (n=4,17)Fatigue: Week 64 (n=3,20)Fatigue: Week 67 (n=4,17)Fatigue: Week 70 (n=3,14)Fatigue: Week 73 (n=3,12)Fatigue: Week 76 (n=3,8)Fatigue: Week 79 (n=3,9)Fatigue: Week 82 (n=2,6)Fatigue: Week 85 (n=2,6)Fatigue: Week 88 (n=2,6)Fatigue: Week 91 (n=2,4)Fatigue: Week 94 (n=2,6)Fatigue: Week 97 (n=1,5)Fatigue: Week 100 (n=1,4)Fatigue: Week 103 (n=1,4)Fatigue: Week 106 (n=1,4)Fatigue: Week 109 (n=1,4)Fatigue: Week 112 (n=1,5)Fatigue: Week 115 (n=1,4)Fatigue: Week 118 (n=1,5)Fatigue: Week 121 (n=1,5)Fatigue: Week 124 (n=1,5)Fatigue: Week 127 (n=1,3)Fatigue: Week 130 (n=0,3)Fatigue: Week 133 (n=1,3)Fatigue: Week 136 (n=0,2)Fatigue: Week 139 (n=0,2)Fatigue: Week 142 (n=0,2)Fatigue: Week 145 (n=0,1)Fatigue: Final Visit (n=158,160)Nausea & Vomiting: BL (n=276,287)Nausea & Vomiting: Week 4 (n=235,250)Nausea & Vomiting: Week 7 (n=181,220)Nausea & Vomiting: Week 10 (n=176,201)Nausea & Vomiting: Week 13 (n=121,183)Nausea & Vomiting: Week 16 (n=121,165)Nausea & Vomiting: Week 19 (n=114,143)Nausea & Vomiting: Week 22 (n=79,143)Nausea & Vomiting: Week 25 (n=64,124)Nausea & Vomiting: Week 28 (n=47,110)Nausea & Vomiting: Week 31 (n=45,95)Nausea & Vomiting: Week 34 (n=37,87)Nausea & Vomiting: Week 37 (n=29,64)Nausea & Vomiting: Week 40 (n=24,55)Nausea & Vomiting: Week 43 (n=12,43)Nausea & Vomiting: Week 46 (n=14,42)Nausea & Vomiting: Week 49 (n=10,36)Nausea & Vomiting: Week 52 (n=8,30)Nausea & Vomiting: Week 55 (n=6,24)Nausea & Vomiting: Week 58 (n=6,21)Nausea & Vomiting: Week 61 (n=4,17)Nausea & Vomiting: Week 64 (n=3,20)Nausea & Vomiting: Week 67 (n=4,17)Nausea & Vomiting: Week 70 (n=3,14)Nausea & Vomiting: Week 73 (n=3,12)Nausea & Vomiting: Week 76 (n=3,8)Nausea & Vomiting: Week 79 (n=3,9)Nausea & Vomiting: Week 82 (n=2,6)Nausea & Vomiting: Week 85 (n=2,6)Nausea & Vomiting: Week 88 (n=2,6)Nausea & Vomiting: Week 91 (n=2,4)Nausea & Vomiting: Week 94 (n=2,6)Nausea & Vomiting: Week 97 (n=1,5)Nausea & Vomiting: Week 100 (n=1,4)Nausea & Vomiting: Week 103 (n=1,4)Nausea & Vomiting: Week 106 (n=1,4)Nausea & Vomiting: Week 109 (n=1,4)Nausea & Vomiting: Week 112 (n=1,5)Nausea & Vomiting: Week 115 (n=1,4)Nausea & Vomiting: Week 118 (n=1,5)Nausea & Vomiting: Week 121 (n=1,5)Nausea & Vomiting: Week 124 (n=1,5)Nausea & Vomiting: Week 127 (n=1,3)Nausea & Vomiting: Week 130 (n=0,3)Nausea & Vomiting: Week 133 (n=1,3)Nausea & Vomiting: Week 136 (n=0,2)Nausea & Vomiting: Week 139 (n=0,2)Nausea & Vomiting: Week 142 (n=0,2)Nausea & Vomiting: Week 145 (n=0,1)Nausea & Vomiting: Final Visit (n=158,161)Pain: BL (n=276,287)Pain: Week 4 (n=235,250)Pain: Week 7 (n=181,220)Pain: Week 10 (n=176,202)Pain: Week 13 (n=152,183)Pain: Week 16 (n=121,165)Pain: Week 19 (n=114,143)Pain: Week 22 (n=79,143)Pain: Week 25 (n=64,124)Pain: Week 28 (n=47,111)Pain: Week 31 (n=45,95)Pain: Week 34 (n=37,87)Pain: Week 37 (n=29,64)Pain: Week 40 (n=24,55)Pain: Week 43 (n=12,43)Pain: Week 46 (n=14,42)Pain: Week 49 (n=10,36)Pain: Week 52 (n=8,30)Pain: Week 55 (n=6,24)Pain: Week 58 (n=6,21)Pain: Week 61 (n=4,17)Pain: Week 64 (n=3,20)Pain: Week 67 (n=4,17)Pain: Week 70 (n=3,14)Pain: Week 73 (n=3,12)Pain: Week 76 (n=3,8)Pain: Week 79 (n=3,9)Pain: Week 82 (n=2,6)Pain: Week 85 (n=2,6)Pain: Week 88 (n=2,6)Pain: Week 91 (n=2,4)Pain: Week 94 (n=2,6)Pain: Week 97 (n=1,5)Pain: Week 100 (n=1,4)Pain: Week 103 (n=1,4)Pain: Week 106 (n=1,4)Pain: Week 109 (n=1,4)Pain: Week 112 (n=1,5)Pain: Week 115 (n=1,4)Pain: Week 118 (n=1,5)Pain: Week 121 (n=1,5)Pain: Week 124 (n=1,5)Pain: Week 127 (n=1,3)Pain: Week 130 (n=0,3)Pain: Week 133 (n=1,3)Pain: Week 136 (n=0,2)Pain: Week 139 (n=0,2)Pain: Week 142 (n=0,2)Pain: Week 145 (n=0,1)Pain: Final Visit (n=158,161)Dyspnoea: BL (n=274,281)Dyspnoea: Week 4 (n=232,249)Dyspnoea: Week 7 (n=181,217)Dyspnoea: Week 10 (n=176,198)Dyspnoea: Week 13 (n=151,182)Dyspnoea: Week 16 (n=121,165)Dyspnoea: Week 19 (n=113,143)Dyspnoea: Week 22 (n=79,143)Dyspnoea: Week 25 (n=63,124)Dyspnoea: Week 28 (n=47,110)Dyspnoea: Week 31 (n=45,95)Dyspnoea: Week 34 (n=36,87)Dyspnoea: Week 37 (n=29,64)Dyspnoea: Week 40 (n=24,55)Dyspnoea: Week 43 (n=12,43)Dyspnoea: Week 46 (n=14,42)Dyspnoea: Week 49 (n=10,36)Dyspnoea: Week 52 (n=8,30)Dyspnoea: Week 55 (n=6,24)Dyspnoea: Week 58 (n=6,21)Dyspnoea: Week 61 (n=4,17)Dyspnoea: Week 64 (n=3,20)Dyspnoea: Week 67 (n=4,17)Dyspnoea: Week 70 (n=3,14)Dyspnoea: Week 73 (n=3,12)Dyspnoea: Week 76 (n=3,8)Dyspnoea: Week 79 (n=3,9)Dyspnoea: Week 82 (n=2,6)Dyspnoea: Week 85 (n=180,6)Dyspnoea: Week 88 (n=2,6)Dyspnoea: Week 91 (n=2,4)Dyspnoea: Week 94 (n=2,6)Dyspnoea: Week 97 (n=1,5)Dyspnoea: Week 100 (n=1,4)Dyspnoea: Week 103 (n=1,4)Dyspnoea: Week 106 (n=1,4)Dyspnoea: Week 109 (n=1,4)Dyspnoea: Week 112 (n=1,5)Dyspnoea: Week 115 (n=1,4)Dyspnoea: Week 118 (n=1,5)Dyspnoea: Week 121 (n=1,5)Dyspnoea: Week 124 (n=1,5)Dyspnoea: Week 127 (n=1,3)Dyspnoea: Week 130 (n=0,3)Dyspnoea: Week 133 (n=1,3)Dyspnoea: Week 136 (n=0,2)Dyspnoea: Week 139 (n=0,2)Dyspnoea: Week 142 (n=0,2)Dyspnoea: Week 145 (n=0,1)Dyspnoea: Final Visit (n=157,160)Insomnia: BL (n=276,285)Insomnia: Week 4 (n=234,248)Insomnia: Week 7 (n=181,219)Insomnia: Week 10 (n=175,200)Insomnia: Week 13 (n=152,183)Insomnia: Week 16 (n=120,164)Insomnia: Week 19 (n=113,143)Insomnia: Week 22 (n=79,143)Insomnia: Week 25 (n=64,124)Insomnia: Week 28 (n=47,110)Insomnia: Week 31 (n=45,94)Insomnia: Week 34 (n=37,87)Insomnia: Week 37 (n=29,63)Insomnia: Week 40 (n=24,55)Insomnia: Week 43 (n=12,43)Insomnia: Week 46 (n=13,42)Insomnia: Week 49 (n=10,36)Insomnia: Week 52 (n=8,30)Insomnia: Week 55 (n=6,24)Insomnia: Week 58 (n=6,21)Insomnia: Week 61 (n=4,17)Insomnia: Week 64 (n=3,20)Insomnia: Week 67 (n=4,17)Insomnia: Week 70 (n=3,14)Insomnia: Week 73 (n=3,12)Insomnia: Week 76 (n=3,8)Insomnia: Week 79 (n=3,9)Insomnia: Week 82 (n=2,6)Insomnia: Week 85 (n=2,6)Insomnia: Week 88 (n=2,6)Insomnia: Week 91 (n=2,4)Insomnia: Week 94 (n=2,6)Insomnia: Week 97 (n=1,5)Insomnia: Week 100 (n=1,4)Insomnia: Week 103 (n=1,4)Insomnia: Week 106 (n=1,4)Insomnia: Week 109 (n=1,4)Insomnia: Week 112 (n=1,5)Insomnia: Week 115 (n=1,4)Insomnia: Week 118 (n=1,5)Insomnia: Week 121 (n=1,5)Insomnia: Week 124 (n=1,5)Insomnia: Week 127 (n=1,3)Insomnia: Week 130 (n=0,3)Insomnia: Week 133 (n=1,3)Insomnia: Week 136 (n=0,2)Insomnia: Week 139 (n=0,2)Insomnia: Week 142 (n=0,2)Insomnia: Week 145 (n=0,1)Insomnia: Final Visit (n=157,160)Appetite Loss: BL (n=275,286)Appetite Loss: Week 4 (n=235,250)Appetite Loss: Week 7 (n=180,216)Appetite Loss: Week 10 (n=176,201)Appetite Loss: Week 13 (n=151,183)Appetite Loss: Week 16 (n=121,165)Appetite Loss: Week 19 (n=114,141)Appetite Loss: Week 22 (n=79,143)Appetite Loss: Week 25 (n=64,124)Appetite Loss: Week 28 (n=47,109)Appetite Loss: Week 31 (n=45,95)Appetite Loss: Week 34 (n=37,87)Appetite Loss: Week 37 (n=29,64)Appetite Loss: Week 40 (n=24,55)Appetite Loss: Week 43 (n=12,43)Appetite Loss: Week 46 (n=14,42)Appetite Loss: Week 49 (n=9,36)Appetite Loss: Week 52 (n=8,30)Appetite Loss: Week 55 (n=6,24)Appetite Loss: Week 58 (n=6,21)Appetite Loss: Week 61 (n=4,17)Appetite Loss: Week 64 (n=3,20)Appetite Loss: Week 67 (n=4,17)Appetite Loss: Week 70 (n=3,14)Appetite Loss: Week 73 (n=3,12)Appetite Loss: Week 76 (n=3,8)Appetite Loss: Week 79 (n=3,9)Appetite Loss: Week 82 (n=2,6)Appetite Loss: Week 85 (n=2,6)Appetite Loss: Week 88 (n=2,6)Appetite Loss: Week 91 (n=2,4)Appetite Loss: Week 94 (n=2,6)Appetite Loss: Week 97 (n=1,5)Appetite Loss: Week 100 (n=1,4)Appetite Loss: Week 103 (n=1,4)Appetite Loss: Week 106 (n=1,4)Appetite Loss: Week 109 (n=1,4)Appetite Loss: Week 112 (n=1,5)Appetite Loss: Week 115 (n=1,4)Appetite Loss: Week 118 (n=1,5)Appetite Loss: Week 121 (n=1,5)Appetite Loss: Week 124 (n=1,5)Appetite Loss: Week 127 (n=1,3)Appetite Loss: Week 130 (n=0,3)Appetite Loss: Week 133 (n=1,3)Appetite Loss: Week 136 (n=0,2)Appetite Loss: Week 139 (n=0,2)Appetite Loss: Week 142 (n=0,2)Appetite Loss: Week 145 (n=0,1)Appetite Loss: Week Final Visit (n=156,161)Constipation: BL (n=276,285)Constipation: Week 4 (n=235,247)Constipation: Week 7 (n=179,220)Constipation: Week 10 (n=175,203)Constipation: Week 13 (n=152,183)Constipation: Week 16 (n=121,165)Constipation: Week 19 (n=114,143)Constipation: Week 22 (n=78,143)Constipation: Week 25 (n=64,124)Constipation: Week 28 (n=47,111)Constipation: Week 31 (n=45,95)Constipation: Week 34 (n=37,86)Constipation: Week 37 (n=29,64)Constipation: Week 40 (n=24,55)Constipation: Week 43 (n=12,43)Constipation: Week 46 (n=14,42)Constipation: Week 49 (n=10,36)Constipation: Week 52 (n=8,29)Constipation: Week 55 (n=6,24)Constipation: Week 58 (n=6,21)Constipation: Week 61 (n=4,17)Constipation: Week 64 (n=3,20)Constipation: Week 67 (n=4,17)Constipation: Week 70 (n=3,14)Constipation: Week 73 (n=3,12)Constipation: Week 76 (n=3,8)Constipation: Week 79 (n=3,9)Constipation: Week 82 (n=2,6)Constipation: Week 85 (n=2,6)Constipation: Week 88 (n=2,6)Constipation: Week 91 (n=2,4)Constipation: Week 94 (n=2,6)Constipation: Week 97 (n=1,5)Constipation: Week 100 (n=1,4)Constipation: Week 103 (n=1,4)Constipation: Week 106 (n=1,4)Constipation: Week 109 (n=1,4)Constipation: Week 112 (n=1,5)Constipation: Week 115 (n=1,4)Constipation: Week 118 (n=1,5)Constipation: Week 121 (n=1,5)Constipation: Week 124 (n=1,5)Constipation: Week 127 (n=1,3)Constipation: Week 130 (n=0,3)Constipation: Week 133 (n=1,3)Constipation: Week 136 (n=0,2)Constipation: Week 139 (n=0,2)Constipation: Week 142 (n=0,2)Constipation: Week 145 (n=0,1)Constipation: Final Visit (n=158,160)Diarrhoea: BL (n=276,283)Diarrhoea: Week 4 (n=234,246)Diarrhoea: Week 7 (n=180,220)Diarrhoea: Week 10 (n=174,202)Diarrhoea: Week 13 (n=152,183)Diarrhoea: Week 16 (n=120,165)Diarrhoea: Week 19 (n=114,143)Diarrhoea: Week 22 (n=78,143)Diarrhoea: Week 25 (n=64,124)Diarrhoea: Week 28 (n=47,111)Diarrhoea: Week 31 (n=45,95)Diarrhoea: Week 34 (n=37,87)Diarrhoea: Week 37 (n=29,64)Diarrhoea: Week 40 (n=24,55)Diarrhoea: Week 43 (n=12,42)Diarrhoea: Week 46 (n=14,42)Diarrhoea: Week 49 (n=10,36)Diarrhoea: Week 52 (n=8,29)Diarrhoea: Week 55 (n=6,24)Diarrhoea: Week 58 (n=6,21)Diarrhoea: Week 61 (n=4,17)Diarrhoea: Week 64 (n=3,20)Diarrhoea: Week 67 (n=4,17)Diarrhoea: Week 70 (n=3,14)Diarrhoea: Week 73 (n=3,12)Diarrhoea: Week 76 (n=3,8)Diarrhoea: Week 79 (n=3,9)Diarrhoea: Week 82 (n=2,6)Diarrhoea: Week 85 (n=2,6)Diarrhoea: Week 88 (n=2,6)Diarrhoea: Week 91 (n=2,4)Diarrhoea: Week 94 (n=2,6)Diarrhoea: Week 97 (n=1,5)Diarrhoea: Week 100 (n=1,4)Diarrhoea: Week 103 (n=1,4)Diarrhoea: Week 106 (n=1,4)Diarrhoea: Week 109 (n=1,4)Diarrhoea: Week 112 (n=1,5)Diarrhoea: Week 115 (n=1,4)Diarrhoea: Week 118 (n=1,5)Diarrhoea: Week 121 (n=1,5)Diarrhoea: Week 124 (n=1,5)Diarrhoea: Week 127 (n=1,3)Diarrhoea: Week 130 (n=0,3)Diarrhoea: Week 133 (n=1,3)Diarrhoea: Week 136 (n=0,2)Diarrhoea: Week 139 (n=0,2)Diarrhoea: Week 142 (n=0,2)Diarrhoea: Week 145 (n=0,1)Diarrhoea: Final Visit (n=157,160)Financial Difficulties: BL (n=274,286)Financial Difficulties: Week 4 (n=234,249)Financial Difficulties: Week 7 (n=178,220)Financial Difficulties: Week 10 (n=175,202)Financial Difficulties: Week 13 (n=151,181)Financial Difficulties: Week 16 (n=120,165)Financial Difficulties: Week 19 (n=113,143)Financial Difficulties: Week 22 (n=78,142)Financial Difficulties: Week 25 (n=63,124)Financial Difficulties: Week 28 (n=45,111)Financial Difficulties: Week 31 (n=45,94)Financial Difficulties: Week 34 (n=36,87)Financial Difficulties: Week 37 (n=29,64)Financial Difficulties: Week 40 (n=24,55)Financial Difficulties: Week 43 (n=12,43)Financial Difficulties: Week 46 (n=14,42)Financial Difficulties: Week 49 (n=10,35)Financial Difficulties: Week 52 (n=8,29)Financial Difficulties: Week 55 (n=6,24)Financial Difficulties: Week 58 (n=6,21)Financial Difficulties: Week 61 (n=4,17)Financial Difficulties: Week 64 (n=3,20)Financial Difficulties: Week 67 (n=4,17)Financial Difficulties: Week 70 (n=3,14)Financial Difficulties: Week 73 (n=3,12)Financial Difficulties: Week 76 (n=3,8)Financial Difficulties: Week 79 (n=3,9)Financial Difficulties: Week 82 (n=2,6)Financial Difficulties: Week 85 (n=2,6)Financial Difficulties: Week 88 (n=2,6)Financial Difficulties: Week 91 (n=2,4)Financial Difficulties: Week 94 (n=2,6)Financial Difficulties: Week 97 (n=1,5)Financial Difficulties: Week 100 (n=1,4)Financial Difficulties: Week 103 (n=1,4)Financial Difficulties: Week 106 (n=1,4)Financial Difficulties: Week 109 (n=1,4)Financial Difficulties: Week 112 (n=1,5)Financial Difficulties: Week 115 (n=1,4)Financial Difficulties: Week 118 (n=1,5)Financial Difficulties: Week 121 (n=1,5)Financial Difficulties: Week 124 (n=1,5)Financial Difficulties: Week 127 (n=1,3)Financial Difficulties: Week 130 (n=0,3)Financial Difficulties: Week 133 (n=1,3)Financial Difficulties: Week 136 (n=0,2)Financial Difficulties: Week 139 (n=0,2)Financial Difficulties: Week 142 (n=0,2)Financial Difficulties: Week 145 (n=0,1)Financial Difficulties: Final Visit (n=158,160)
Fluoropyrimidine/Cisplatin (FP)55.361.060.962.363.860.861.065.168.072.069.670.866.162.072.975.068.572.676.776.779.277.875.077.880.677.877.883.383.383.383.383.383.383.383.383.383.383.383.383.383.383.383.3NA83.3NANANANA53.278.976.079.378.280.279.878.880.785.886.285.686.385.784.485.687.688.788.385.686.791.795.693.397.897.895.695.693.3100.0100.0100.0100.0100.0100.0100.0100.0100.093.3100.0100.0100.0100.0100.0NA100.0NANANANA72.173.267.470.970.273.472.071.174.781.380.582.283.381.679.980.682.181.785.480.677.883.383.383.388.988.983.383.391.7100.091.791.7100.083.383.3100.0100.0100.083.3100.0100.083.383.3100.0NA100.0NANANANA63.575.480.581.382.982.683.182.285.988.286.085.788.583.983.681.982.188.386.576.485.695.810095.897.294.4100.097.295.895.8100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0NA100.0NANANANA75.186.986.085.785.688.282.884.285.985.986.587.088.388.583.388.989.385.091.794.491.791.7100.091.7100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0NA100.0NANANANA79.572.472.173.174.572.772.774.479.383.383.081.584.785.185.487.586.985.087.586.188.991.794.495.894.4100.094.494.4100.091.791.7100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0100.0NA100.0NANANANA68.136.337.134.435.332.933.033.130.022.224.122.022.821.823.619.420.619.416.718.516.78.37.413.911.17.47.47.40.05.60.00.00.011.10.00.011.10.00.00.00.00.00.00.0NA0.0NANANANA40.415.016.616.916.412.814.214.210.38.63.53.74.52.94.22.81.23.32.10.00.00.00.00.00.00.05.60.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA14.924.917.814.513.412.013.614.215.010.78.212.212.211.518.816.713.113.36.32.88.30.05.60.00.05.65.65.60.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA27.412.412.112.714.611.315.415.313.912.79.210.410.210.39.719.411.96.712.55.65.616.70.08.30.00.011.10.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA20.027.222.121.919.814.715.317.114.815.19.910.49.08.013.913.97.710.012.516.711.18.30.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA21.935.231.527.226.724.724.526.919.012.014.211.111.712.613.95.64.83.70.00.05.68.30.08.30.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA35.322.920.619.019.216.714.613.512.07.37.810.45.411.58.38.34.83.34.25.611.18.30.00.00.00.00.00.016.716.70.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA19.010.99.18.710.56.68.17.36.07.35.75.95.45.76.98.34.810.08.311.111.116.711.116.711.111.122.211.10.00.00.016.716.70.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA10.027.323.623.621.522.523.120.619.716.417.015.610.213.822.216.716.716.78.316.711.116.711.116.711.111.111.111.116.716.716.716.716.70.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA26.6
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)54.960.960.561.963.661.963.864.967.868.570.072.070.670.673.673.876.671.373.873.872.570.072.568.568.167.769.460.079.273.679.279.278.385.475.077.177.175.072.975.075.081.772.272.272.266.766.766.766.753.179.679.579.380.280.580.781.583.684.883.785.485.185.888.289.991.992.089.293.191.491.091.093.392.991.190.092.690.095.695.698.397.897.396.796.798.395.097.393.396.094.796.093.393.395.693.393.393.3100.073.873.976.173.374.375.174.675.879.782.479.781.182.281.582.186.886.588.084.488.289.787.387.590.286.980.681.381.580.691.794.491.7100.090.0100.0100.0100.095.893.383.386.790.090.088.988.988.983.383.383.3100.068.773.177.980.281.280.581.982.484.084.885.585.785.486.386.787.887.591.488.288.588.990.786.389.289.382.987.584.383.391.790.395.888.991.787.587.589.691.795.093.890.095.090.0100.088.991.795.895.895.8100.074.385.786.386.586.885.786.887.687.487.488.090.088.791.491.591.591.792.689.791.090.591.293.391.291.783.383.381.588.991.794.495.894.490.095.891.795.895.893.395.896.796.796.7100.088.994.4100.0100.0100.0100.080.072.074.175.176.776.377.579.580.180.280.278.980.781.882.784.186.984.782.285.487.390.285.885.386.980.681.385.280.688.988.991.791.790.095.8100.091.795.896.795.896.7100.096.783.394.4100.0100.0100.0100.0100.071.434.234.534.133.233.732.829.426.725.123.222.219.719.818.617.113.814.517.214.416.414.417.215.016.716.718.118.529.611.19.311.17.411.111.119.413.916.717.825.017.817.813.314.818.514.822.222.222.211.137.615.719.718.916.414.714.513.912.28.26.58.87.56.84.81.22.80.95.02.13.20.04.22.92.41.40.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.019.825.117.916.114.413.312.412.813.212.212.011.811.312.210.38.96.76.510.08.37.14.96.74.94.89.78.39.32.80.02.84.20.03.38.30.00.00.03.30.03.33.30.00.05.65.60.00.00.00.025.413.411.810.811.313.713.511.912.19.410.39.19.610.44.86.25.64.65.68.36.33.98.35.97.18.38.37.416.75.65.68.35.60.00.08.38.38.36.78.36.76.76.711.111.111.116.716.716.733.318.323.623.320.418.018.917.720.017.015.913.314.913.411.110.39.39.57.47.88.39.57.810.09.89.511.18.311.111.111.15.60.05.66.78.30.00.00.06.70.06.76.70.00.011.111.10.00.00.00.024.633.833.631.329.428.427.925.120.716.711.613.09.610.99.77.05.66.510.010.04.80.08.35.97.15.64.20.05.65.611.10.05.60.00.08.38.30.00.00.00.00.00.00.011.111.10.00.00.00.033.521.520.217.615.115.815.414.510.010.29.66.34.710.47.97.07.15.610.36.96.35.95.05.94.811.14.23.716.70.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.020.010.712.214.211.912.012.910.39.66.24.84.95.74.23.02.41.63.72.34.24.80.03.32.03.32.00.00.00.00.00.00.00.00.00.00.00.00.06.70.00.00.06.70.00.00.00.00.00.00.010.029.327.723.923.322.724.422.424.922.321.623.424.523.423.619.418.320.020.718.122.223.516.717.619.019.425.025.922.216.716.725.016.720.016.78.316.716.713.316.713.313.313.311.111.10.00.00.00.00.027.9

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EORTC Quality of Life Questionnaire-Stomach Cancer Specific (QLQ STO22) Questionnaire Scores

The QLQ-STO22 is a gastric cancer quality of life questionnaire. There are 22 questions concerning disease, treatment related symptoms, side effects, dysphagia, nutritional aspects, and questions about the emotional problems of gastric cancer (dysphagia, pain, reflux, eating restrictions, anxiety, dry mouth, body image, and hair loss). The questions are grouped into five scales and 4 single items which are related to the symptoms of the disease. Most questions used 4-point scale (1 'Not at all' to 4 'Very much'; 1 question was a yes or no answer). A linear transformation was used to standardize all scores and single-items to a scale of 0 to 100; higher score=better level of functioning or greater degree of symptoms. (NCT01041404)
Timeframe: BL, Days 1, 22, 43, 64, 85, 106, 127, and every 21 days until disease progression of the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

,
Interventionscores on a scale (Mean)
Dysphagia Scale: BL (n=276,287)Dysphagia Scale: Week 4 (n=234,250)Dysphagia Scale: Week 7 (n=181,220)Dysphagia Scale: Week 10 (n=176,203)Dysphagia Scale: Week 13 (n=152,183)Dysphagia Scale: Week 16 (n=120,165)Dysphagia Scale: Week 19 (n=114,143)Dysphagia Scale: Week 22 (n=79,143)Dysphagia Scale: Week 25 (n=64,124)Dysphagia Scale: Week 28 (n=47,111)Dysphagia Scale: Week 31 (n=45,95)Dysphagia Scale: Week 34 (n=37,87)Dysphagia Scale: Week 37 (n=29,64)Dysphagia Scale: Week 40 (n=24,55)Dysphagia Scale: Week 43 (n=12,43)Dysphagia Scale: Week 46 (n=14,42)Dysphagia Scale: Week 49 (n=10,36)Dysphagia Scale: Week 52 (n=8,30)Dysphagia Scale: Week 55 (n=6,24)Dysphagia Scale: Week 58 (n=6,21)Dysphagia Scale: Week 61 (n=4,17)Dysphagia Scale: Week 64 (n=3,20)Dysphagia Scale: Week 67 (n=4,16)Dysphagia Scale: Week 70 (n=3,14)Dysphagia Scale: Week 73 (n=3,12)Dysphagia Scale: Week 76 (n=3,8)Dysphagia Scale: Week 79 (n=3,9)Dysphagia Scale: Week 82 (n=2,6)Dysphagia Scale: Week 85 (n=2,6)Dysphagia Scale: Week 88 (n=2,6)Dysphagia Scale: Week 91 (n=2,4)Dysphagia Scale: Week 94 (n=2,6)Dysphagia Scale: Week 97 (n=1,5)Dysphagia Scale: Week 100 (n=1,4)Dysphagia Scale: Week 103 (n=1,4)Dysphagia Scale: Week 106 (n=1,4)Dysphagia Scale: Week 109 (n=1,4)Dysphagia Scale: Week 112 (n=1,5)Dysphagia Scale: Week 115 (n=1,4)Dysphagia Scale: Week 118 (n=1,5)Dysphagia Scale: Week 121 (n=1,5)Dysphagia Scale: Week 124 (n=1,5)Dysphagia Scale: Week 127 (n=1,3)Dysphagia Scale: Week 130 (n=0,3)Dysphagia Scale: Week 133 (n=1,3)Dysphagia Scale: Week 136 (n=0,2)Dysphagia Scale: Week 139 (n=0,2)Dysphagia Scale: Week 142 (n=0,2)Dysphagia Scale: Week 145 (n=0,1)Dysphagia Scale: Final Visit (n=157,159Pain Scale: BL (n=276,287)Pain Scale: Week 4 (n=234,250)Pain Scale: Week 7 (n=181,219)Pain Scale: Week 10 (n=176,203)Pain Scale: Week 13 (n=152,183)Pain Scale: Week 16 (n=120,165)Pain Scale: Week 19 (n=114,143)Pain Scale: Week 22 (n=79,143)Pain Scale: Week 25 (n=64,124)Pain Scale: Week 28 (n=47,111)Pain Scale: Week 31 (n=45,95)Pain Scale: Week 34 (n=37,87)Pain Scale: Week 37 (n=29,64)Pain Scale: Week 40 (n=24,55)Pain Scale: Week 43 (n=12,43)Pain Scale: Week 46 (n=14,42)Pain Scale: Week 49 (n=10,36)Pain Scale: Week 52 (n=8,30)Pain Scale: Week 55 (n=6,24)Pain Scale: Week 58 (n=6,21)Pain Scale: Week 61 (n=4,17)Pain Scale: Week 64 (n=3,20)Pain Scale: Week 67 (n=4,16)Pain Scale: Week 70 (n=3,14)Pain Scale: Week 73 (n=3,12)Pain Scale: Week 76 (n=3,8)Pain Scale: Week 79 (n=3,9)Pain Scale: Week 82 (n=2,6)Pain Scale: Week 85 (n=2,6)Pain Scale: Week 88 (n=2,6)Pain Scale: Week 91 (n=2,6)Pain Scale: Week 94 (n=2,6)Pain Scale: Week 97 (n=1,5)Pain Scale: Week 100 (n=1,4)Pain Scale: Week 103 (n=1,4)Pain Scale: Week 106 (n=1,4)Pain Scale: Week 109 (n=1,4)Pain Scale: Week 112 (n=1,5)Pain Scale: Week 115 (n=1,4)Pain Scale: Week 118 (n=1,5)Pain Scale: Week 121 (n=1,5)Pain Scale: Week 124 (n=1,5)Pain Scale: Week 127 (n=1,3)Pain Scale: Week 130 (n=0,3)Pain Scale: Week 133 (n=1,3)Pain Scale: Week 136 (n=0,2)Pain Scale: Week 139 (n=0,2)Pain Scale: Week 142 (n=0,2)Pain Scale: Week 145 (n=0,1)Pain Scale: Final Visit (n=157,160)Reflux Symptoms Scale: BL (n=275,287)Reflux Symptoms Scale: Week 4 (n=234,250)Reflux Symptoms Scale: Week 7 (n=180,220)Reflux Symptoms Scale: Week 10 (n=176,203)Reflux Symptoms Scale: Week 13 (n=152,182)Reflux Symptoms Scale: Week 16 (n=120,165)Reflux Symptoms Scale: Week 19 (n=114,165)Reflux Symptoms Scale: Week 22 (n=79,143)Reflux Symptoms Scale: Week 25 (n=64,124)Reflux Symptoms Scale: Week 28 (n=47,111)Reflux Symptoms Scale: Week 31 (n=45,95)Reflux Symptoms Scale: Week 34 (n=45,95)Reflux Symptoms Scale: Week 37 (n=29,64)Reflux Symptoms Scale: Week 40 (n=24,55)Reflux Symptoms Scale: Week 43 (n=12,42)Reflux Symptoms Scale: Week 46 (n=14,42)Reflux Symptoms Scale: Week 49 (n=10,36)Reflux Symptoms Scale: Week 52 (n=8,30)Reflux Symptoms Scale: Week 55 (n=6,24)Reflux Symptoms Scale: Week 58 (n=6,21)Reflux Symptoms Scale: Week 61 (n=4,17)Reflux Symptoms Scale: Week 64 (n=3,20)Reflux Symptoms Scale: Week 67 (n=4,16)Reflux Symptoms Scale: Week 70 (n=3,13)Reflux Symptoms Scale: Week 73 (n=3,12)Reflux Symptoms Scale: Week 76 (n=3,8)Reflux Symptoms Scale: Week 79 (n=3,9)Reflux Symptoms Scale: Week 82 (n=2,6)Reflux Symptoms Scale: Week 85 (n=2,6)Reflux Symptoms Scale: Week 88 (n=2,6)Reflux Symptoms Scale: Week 91 (n=2,4)Reflux Symptoms Scale: Week 94 (n=2,6)Reflux Symptoms Scale: Week 97 (n=1,5)Reflux Symptoms Scale: Week 100 (n=1,4)Reflux Symptoms Scale: Week 103 (n=1,4)Reflux Symptoms Scale: Week 106 (n=1,4)Reflux Symptoms Scale: Week 109 (n=1,4)Reflux Symptoms Scale: Week 112 (n=1,5)Reflux Symptoms Scale: Week 115 (n=1,4)Reflux Symptoms Scale: Week 118 (n=1,5)Reflux Symptoms Scale: Week 121 (n=1,5)Reflux Symptoms Scale: Week 124 (n=1,5)Reflux Symptoms Scale: Week 127 (n=1,3)Reflux Symptoms Scale: Week 130 (n=0,3)Reflux Symptoms Scale: Week 133 (n=1,3)Reflux Symptoms Scale: Week 136 (n=0,2)Reflux Symptoms Scale: Week 139 (n=0,2)Reflux Symptoms Scale: Week 142 (n=0,2)Reflux Symptoms Scale: Week 145 (n=0,1)Reflux Symptoms Scale: Final Visit (n=1,5)Eating Restrictions (ER) Scale: BL (n=276,287)ER Scale: Week 4 (n=234,250)ER Scale: Week 7 (n=181,220)ER Scale: Week 10 (n=176,203)ER Scale: Week 13 (n=152,183)ER Scale: Week 16 (n=120,165)ER Scale: Week 19 (n=114,143)ER Scale: Week 22 (n=79,143)ER Scale: Week 25 (n=64,124)ER Scale: Week 28 (n=47,111)ER Scale: Week 31 (n=45,95)ER Scale: Week 34 (n=37,87)ER Scale: Week 37 (n=29,64)ER Scale: Week 40 (n=24,55)ER Scale: Week 43 (n=12,43)ER Scale: Week 46 (n=14,42)ER Scale: Week 49 (n=10,36)ER Scale: Week 52 (n=8,30)ER Scale: Week 55 (n=6,24)ER Scale: Week 58 (n=6,21)ER Scale: Week 61 (n=4,17)ER Scale: Week 64 (n=3,20)ER Scale: Week 67 (n=4,16)ER Scale: Week 70 (n=3,14)ER Scale: Week 73 (n=3,12)ER Scale: Week 76 (n=3,8)ER Scale: Week 79 (n=3,9)ER Scale: Week 82 (n=2,6)ER Scale: Week 85 (n=2,6)ER Scale: Week 88 (n=2,6)ER Scale: Week 91 (n=2,4)ER Scale: Week 94 (n=2,6)ER Scale: Week 97 (n=1,5)ER Scale: Week 100 (n=1,4)ER Scale: Week 103 (n=1,4)ER Scale: Week 106 (n=1,4)ER Scale: Week 109 (n=1,4)ER Scale: Week 112 (n=1,5)ER Scale: Week 115 (n=1,4)ER Scale: Week 118 (n=1,5)ER Scale: Week 121 (n=1,5)ER Scale: Week 124 (n=1,5)ER Scale: Week 127 (n=1,3)ER Scale: Week 130 (n=0,3)ER Scale: Week 133 (n=1,3)ER Scale: Week 136 (n=0,2)ER Scale: Week 139 (n=0,2)ER Scale: Week 142 (n=0,2)ER Scale: Week 145 (n=0,1)ER Scale: Final Visit (n=157,160)Anxiety Scale: BL (n=276,287)Anxiety Scale: Week 4 (n=234,250)Anxiety Scale: Week 7 (n=181,220)Anxiety Scale: Week 10 (n=176,203)Anxiety Scale: Week 13 (n=152,183)Anxiety Scale: Week 16 (n=120,165)Anxiety Scale: Week 19 (n=114,143)Anxiety Scale: Week 22 (n=79,143)Anxiety Scale: Week 25 (n=64,124)Anxiety Scale: Week 28 (n=47,111)Anxiety Scale: Week 31 (n=45,95)Anxiety Scale: Week 34 (n=37,87)Anxiety Scale: Week 37 (n=29,64)Anxiety Scale: Week 40 (n=24,55)Anxiety Scale: Week 43 (n=12,43)Anxiety Scale: Week 46 (n=14,42)Anxiety Scale: Week 49 (n=14,42)Anxiety Scale: Week 52 (n=8,30)Anxiety Scale: Week 55 (n=6,24)Anxiety Scale: Week 58 (n=6,21)Anxiety Scale: Week 61 (n=4,17)Anxiety Scale: Week 64 (n=3,20)Anxiety Scale: Week 67 (n=4,16)Anxiety Scale: Week 70 (n=3,14)Anxiety Scale: Week 73 (n=3,12)Anxiety Scale: Week 76 (n=3,8)Anxiety Scale: Week 79 (n=3,9)Anxiety Scale: Week 82 (n=2,6)Anxiety Scale: Week 85 (n=2,6)Anxiety Scale: Week 88 (n=2,6)Anxiety Scale: Week 91 (n=2,4)Anxiety Scale: Week 94 (n=2,6)Anxiety Scale: Week 97 (n=1,5)Anxiety Scale: Week 100 (n=1,4)Anxiety Scale: Week 103 (n=1,4)Anxiety Scale: Week 106 (n=1,4)Anxiety Scale: Week 109 (n=1,4)Anxiety Scale: Week 112 (n=1,5)Anxiety Scale: Week 115 (n=1,4)Anxiety Scale: Week 118 (n=1,5)Anxiety Scale: Week 121 (n=1,5)Anxiety Scale: Week 124 (n=1,5)Anxiety Scale: Week 127 (n=1,3)Anxiety Scale: Week 130 (n=0,3)Anxiety Scale: Week 133 (n=1,3)Anxiety Scale: Week 136 (n=0,2)Anxiety Scale: Week 139 (n=0,2)Anxiety Scale: Week 142 (n=0,2)Anxiety Scale: Week 145 (n=0,2)Anxiety Scale: Final Visit (n=157,160)Dry Mouth: BL (n=274,287)Dry Mouth: Week 4 (n=232,249)Dry Mouth: Week 7 (n=180,219)Dry Mouth: Week 10 (n=176,203)Dry Mouth: Week 13 (n=152,183)Dry Mouth: Week 16 (n=120,165)Dry Mouth: Week 19 (n=113,143)Dry Mouth: Week 22 (n=79,143)Dry Mouth: Week 25 (n=64,124)Dry Mouth: Week 28 (n=47,111)Dry Mouth: Week 31 (n=45,95)Dry Mouth: Week 34 (n=37,87)Dry Mouth: Week 37 (n=29,64)Dry Mouth: Week 40 (n=23,55)Dry Mouth: Week 43 (n=12,43)Dry Mouth: Week 46 (n=14,42)Dry Mouth: Week 49 (n=10,36)Dry Mouth: Week 52 (n=8,30)Dry Mouth: Week 55 (n=6,24)Dry Mouth: Week 58 (n=6,21)Dry Mouth: Week 61 (n=4,17)Dry Mouth: Week 64 (n=3,20)Dry Mouth: Week 67 (n=4,16)Dry Mouth: Week 70 (n=3,14)Dry Mouth: Week 73 (n=3,12)Dry Mouth: Week 76 (n=3,8)Dry Mouth: Week 79 (n=3,9)Dry Mouth: Week 82 (n=2,6)Dry Mouth: Week 85 (n=2,6)Dry Mouth: Week 88 (n=2,6)Dry Mouth: Week 91 (n=2,4)Dry Mouth: Week 94 (n=2,6)Dry Mouth: Week 97 (n=1,5)Dry Mouth: Week 100 (n=1,4)Dry Mouth: Week 103 (n=1,4)Dry Mouth: Week 106 (n=1,4)Dry Mouth: Week 109 (n=1,4)Dry Mouth: Week 112 (n=1,5)Dry Mouth: Week 115 (n=1,4)Dry Mouth: Week 118 (n=1,5)Dry Mouth: Week 121 (n=1,5)Dry Mouth: Week 124 (n=1,5)Dry Mouth: Week 127 (n=1,3)Dry Mouth: Week 130 (n=0,3)Dry Mouth: Week 133 (n=1,3)Dry Mouth: Week 136 (n=0,2)Dry Mouth: Week 139 (n=0,2)Dry Mouth: Week 142 (n=0,2)Dry Mouth: Week 145 (n=0,1)Dry Mouth: Final Visit (n=157,157)Taste: BL (n=275,286)Taste: Week 4 (n=234,249)Taste: Week 7 (n=179,217)Taste: Week 10 (n=176,200)Taste: Week 13 (n=151,181)Taste: Week 16 (n=119,165)Taste: Week 19 (n=113,143)Taste: Week 22 (n=79,143)Taste: Week 25 (n=64,124)Taste: Week 28 (n=47,111)Taste: Week 31 (n=45,95)Taste: Week 34 (n=37,87)Taste: Week 37 (n=28,64)Taste: Week 40 (n=24,55)Taste: Week 43 (n=12,43)Taste: Week 46 (n=14,42)Taste: Week 49 (n=9,36)Taste: Week 52 (n=8,30)Taste: Week 55 (n=6,24)Taste: Week 58 (n=6,21)Taste: Week 61 (n=4,17)Taste: Week 64 (n=3,20)Taste: Week 67 (n=4,16)Taste: Week 70 (n=3,14)Taste: Week 73 (n=3,12)Taste: Week 76 (n=3,8)Taste: Week 79 (n=3,9)Taste: Week 82 (n=2,6)Taste: Week 85 (n=2, 6)Taste: Week 88 (n=2,6)Taste: Week 91 (n=2,4)Taste: Week 94 (n=2,6)Taste: Week 97 (n=1,5)Taste: Week 100 (n=1,4)Taste: Week 103 (n=1,4)Taste: Week 106 (n=1,4)Taste: Week 109 (n=1,4)Taste: Week 112 (n=1,5)Taste: Week 115 (n=1,4)Taste: Week 118 (n=1,5)Taste: Week 121 (n=1,5)Taste: Week 124 (n=1,5)Taste: Week 127 (n=1,3)Taste: Week 130 (n=0,3)Taste: Week 133 (n=1,3)Taste: Week 136 (n=0,2)Taste: Week 139 (n=0,2)Taste: Week 142 (n=0,2)Taste: Week 145 (n=0,1)Taste: Final Visit (n=157,158)Body Image: BL (n=272,286)Body Image: Week 4 (n=233,249)Body Image: Week 7 (n=180,219)Body Image: Week 10 (n=175,203)Body Image: Week 13 (n=152,182)Body Image: Week 16 (n=119,165)Body Image: Week 19 (n=114,140)Body Image: Week 22 (n=79,143)Body Image: Week 25 (n=64,124)Body Image: Week 28 (n=47,111)Body Image: Week 31 (n=45,95)Body Image: Week 34 (n=37,87)Body Image: Week 37 (n=29,64)Body Image: Week 40 (n=24,55)Body Image: Week 43 (n=12,43)Body Image: Week 46 (n=14,42)Body Image: Week 49 (n=10,36)Body Image: Week 52 (n=8,30)Body Image: Week 55 (n=6,24)Body Image: Week 58 (n=6,21)Body Image: Week 61 (n=4,17)Body Image: Week 64 (n=3,20)Body Image: Week 67 (n=4,16)Body Image: Week 70 (n=4,14)Body Image: Week 73 (n=3,12)Body Image: Week 76 (n=3,8)Body Image: Week 79 (n=3,9)Body Image: Week 82 (n=2,6)Body Image: Week 85 (n=2,6)Body Image: Week 88 (n=2,5)Body Image: Week 91 (n=2,4)Body Image: Week 94 (n=2,6)Body Image: Week 97 (n=1,5)Body Image: Week 100 (n=1,4)Body Image: Week 103 (n=1,4)Body Image: Week 106 (n=1,4)Body Image: Week 109 (n=1,4)Body Image: Week 112 (n=1,5)Body Image: Week 115 (n=1,4)Body Image: Week 118 (n=1,5)Body Image: Week 121 (n=1,5)Body Image: Week 124 (n=1,5)Body Image: Week 127 (n=1,3)Body Image: Week 130 (n=0,3)Body Image: Week 133 (n=1,3)Body Image: Week 136 (n=0,2)Body Image: Week 139 (n=0,2)Body Image: Week 142 (n=0,2)Body Image: Week 145 (n=0,1)Body Image: Final Visit (n=157,159)Hair Loss: BL (n=64,76)Hair Loss: Week 4 (n=68,71)Hair Loss: Week 7 (n=65,82)Hair Loss: Week 10 (n=75,78)Hair Loss: Week 13 (n=66,80)Hair Loss: Week 16 (n=53,72)Hair Loss: Week 19 (n=50,56)Hair Loss: Week 22 (n=38,54)Hair Loss: Week 25 (n=24,49)Hair Loss: Week 28 (n=20,39)Hair Loss: Week 31 (n=17,26)Hair Loss: Week 34 (n=13,24)Hair Loss: Week 37 (n=12,16)Hair Loss: Week 40 (n=11,13)Hair Loss: Week 43 (n=5,9)Hair Loss: Week 46 (n=5,13)Hair Loss: Week 49 (n=4,7)Hair Loss: Week 52 (n=3,4)Hair Loss: Week 55 (n=2,6)Hair Loss: Week 58 (n=2,3)Hair Loss: Week 61 (n=1,2)Hair Loss: Week 64 (n=1,4)Hair Loss: Week 67 (n=1,4)Hair Loss: Week 70 (n=1,2)Hair Loss: Week 73 (n=1,5)Hair Loss: Week 76 (n=1,3)Hair Loss: Week 79 (n=1,4)Hair Loss: Week 82 (n=1,1)Hair Loss: Week 85 (n=1,1)Hair Loss: Week 88 (n=1,2)Hair Loss: Week 91 (n=1,1)Hair Loss: Week 94 (n=1,2)Hair Loss: Week 97 (n=1,2)Hair Loss: Week 100 (n=1,2)Hair Loss: Week 103 (n=1,1)Hair Loss: Week 106 (n=1,1)Hair Loss: Week 109 (n=0,2)Hair Loss: Week 112 (n=1,3)Hair Loss: Week 115 (n=1,2)Hair Loss: Week 118 (n=1,3)Hair Loss: Week 121 (n=1,2)Hair Loss: Week 124 (n=1,2)Hair Loss: Week 127 (n=1,1)Hair Loss: Week 130 (n=0,1)Hair Loss: Week 133 (n=1,1)Hair Loss: Final Visit (n=61,60)
Fluoropyrimidine/Cisplatin (FP)18.711.810.98.58.810.29.510.06.96.66.43.95.43.74.62.44.41.40.03.72.80.02.80.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA15.429.721.619.417.016.017.019.215.811.311.212.612.213.814.913.015.511.79.49.75.64.22.84.22.80.05.62.80.04.28.30.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA24.718.314.812.812.612.812.011.39.05.66.67.47.26.17.97.44.82.22.85.60.02.83.72.83.70.03.70.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA15.327.420.618.817.516.017.820.815.511.613.913.410.612.513.59.710.911.75.28.39.74.20.08.32.85.62.85.64.24.24.28.30.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA23.847.542.040.638.235.732.935.831.725.227.429.123.127.229.630.626.220.023.631.520.48.35.611.13.77.40.011.111.111.111.111.15.60.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA41.524.524.024.623.523.223.922.419.016.110.612.69.912.68.711.19.516.712.55.611.18.30.08.30.00.00.00.00.016.70.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA24.017.220.720.121.819.920.424.519.010.912.18.16.38.38.35.64.87.44.211.111.18.311.18.30.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA25.330.932.630.730.128.929.130.728.722.423.425.218.923.020.827.821.416.716.716.711.18.30.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.0NANANANA31.015.120.125.121.822.228.323.320.213.926.715.77.78.312.16.726.70.011.116.716.70.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.0NA0.00.00.00.00.00.0NA0.023.0
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)16.612.512.810.69.09.18.87.86.85.36.87.57.36.55.22.92.24.43.73.20.73.32.83.24.62.82.53.71.91.90.01.92.22.80.00.00.00.00.02.20.00.00.00.00.00.05.65.60.017.027.021.820.117.516.215.916.315.114.414.014.612.513.811.89.710.19.58.64.56.35.49.68.36.59.75.27.46.95.65.62.15.68.36.38.36.34.210.04.28.310.08.38.311.113.912.58.38.30.026.816.916.015.413.512.914.410.610.69.79.610.19.310.99.39.06.66.58.16.55.32.63.96.34.37.91.43.75.60.00.00.00.00.00.00.02.80.00.00.04.40.06.77.40.00.00.00.00.00.018.323.921.119.017.417.015.115.513.612.911.312.510.99.59.57.06.08.19.35.26.05.48.310.46.59.05.25.62.84.24.24.24.26.76.36.34.24.23.34.26.75.01.70.08.35.60.04.20.00.022.848.243.839.338.237.537.134.932.829.226.928.427.828.226.325.123.325.927.428.221.725.523.918.827.028.727.833.325.924.114.822.222.231.116.722.219.416.722.219.420.015.617.822.218.518.516.711.116.70.040.923.923.326.925.021.123.420.516.312.110.811.29.69.47.36.24.86.510.08.314.311.86.78.311.913.920.811.15.60.05.60.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.023.617.924.824.025.325.223.822.619.615.914.713.09.67.87.97.07.94.67.84.24.80.01.74.20.02.80.00.05.60.05.60.05.66.70.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.020.331.931.727.928.428.228.125.022.422.620.119.318.018.219.415.515.913.916.716.715.913.718.314.616.727.837.525.916.711.16.716.716.713.38.38.316.78.36.716.76.76.76.6711.10.011.116.70.016.70.030.425.016.419.120.120.423.621.422.218.414.510.316.712.512.83.75.19.58.30.00.016.70.00.00.06.70.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.00.019.4

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Progression-Free Survival - Time to Event

The median time, in months, from the date of randomization to the date of a PFS event. Participants were censored at the last date of tumor measurement, the last date in the study drug log, or the date of last follow-up. (NCT01041404)
Timeframe: BL, Days 43, 85, and 127, and every 21 days thereafter until disease progression or the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionmonths (Median)
Fluoropyrimidine, Cisplatin5.5
Trastuzumab, Fluoropyrimidine, Cisplatin6.7

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Trastuzumab Maximum Serum Concentration (Cmax)

Median Cmax (measured as mg/L) calculated for all treated participants using the nominal dosage schedule administered as an IV infusion. (NCT01041404)
Timeframe: Predose and end of infusion on Days 1, 8, 15, and 64, and predose on Days 22 and 106

Interventionmg/L (Median)
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)128

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Time to Progression (TTP) - Percentage of Participants With an Event

TTP was defined as the time from the date of randomization and the date of the first occurrence of PD. Participants were censored at the last date of tumor assessment, the last date in the study drug log, or the last date of follow-up. (NCT01041404)
Timeframe: BL, Days 43, 85, and 127, and every 21 days thereafter until disease progression or the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionpercentage of participants (Number)
Fluoropyrimidine/Cisplatin (FP)74.1
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)70.7

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Progression-Free Survival (PFS) - Percentage of Participants With an Event

PFS was defined as the time from the date of randomization to the date of the first documentation of progressive disease (PD) or date of death, whichever occurs first. For target lesions (TL), PD was defined as at least a 20 percent (%) increase in the sum of the longest diameter (SLD) of TLs, taking as a reference the smallest SLD recorded since the treatment started, or the appearance of one or more lesions. For non-target lesions (NTL), PD was defined as an unequivocal progression of existing NTLs. Participants were censored at the last date of tumor measurement, the last date in the study drug log, or the date of last follow-up. (NCT01041404)
Timeframe: BL, Days 43, 85, and 127, and every 21 days thereafter until disease progression or the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionpercentage of participants (Number)
Fluoropyrimidine/Cisplatin (FP)81.0
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)76.9

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Duration of Response

The median time, in months, of the duration of response. Participants were censored at the date of death, the date of last tumor measurement, the last date in study drug log, or the date of last follow-up. (NCT01041404)
Timeframe: BL, Days 43, 85, and 127, and every 21 days thereafter until disease progression or the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionmonths (Median)
Fluoropyrimidine/Cisplatin (FP)4.8
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)6.9

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Percentage of Participants With Confirmed Complete Response (CR) or Partial Response (PR) Determined by Response Evaluation Criteria in Solid Tumors (RECIST)

For TLs, a CR was defined as the disappearance of all TLs and a PR was defined as at least a 30% decrease in the SLD of the TLs, taking as a reference the baseline SLD. For NTLs, a CR was defined as the disappearance of all NTLs and normalization of tumor marker levels. (NCT01041404)
Timeframe: BL, Days 43, 85, and 127, and every 21 days thereafter until disease progression or the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionpercentage of participants (Number)
Fluoropyrimidine/Cisplatin (FP)34.5
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)47.3

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Percentage of Participants With Clinical Benefit

Clinical benefit was defined as stable disease (SD), CR, or PR for 6 weeks or longer as determined by RECIST. For TLs, SD was defined as neither sufficient shrinkage to qualify for PR, nor sufficient increase to qualify for PD, taking as a reference the smallest SLD recorded since treatment had started. For NTLs, SD was defined as a persistence of one or more NTLs and/or maintenance of tumor marker levels above the normal limits. (NCT01041404)
Timeframe: BL, Days 43, 85, and 127, and every 21 days thereafter until disease progression or the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionpercentage of participants (Number)
Fluoropyrimidine/Cisplatin (FP)69.3
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)78.9

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Overall Survival (OS) - Percentage of Participants With an Event

OS was defined as the time from the date of randomization to the date of death due to any cause. Participants were censored at the last date of tumor measurement, the last date in the study drug log, or the date of last follow-up. (NCT01041404)
Timeframe: Baseline (BL), Days 1, 8, 15, 22, 43, 64, 85, 106, 127, and every 21 days until the end of study, 1 year after the cut-off date for the 2nd interim efficacy analysis

Interventionpercentage of participants (Number)
Fluoropyrimidine/Cisplatin (FP)62.8
Trastuzumab + Fluoropyrimidine/Cisplatin (FP + H)56.8

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Number of Participants With Adverse Events and Serious Adverse Events

ADVERSE EVENTS (AE) AND SERIOUS ADVERSE EVENTS (SAE) Adverse Events (AEs) will use the descriptions and grading scales found in the NCI CTCAE v3.0 (NCT01044433)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
DiarrheaRashPainFatigueInfectionNauseaMucositisVomitingConstipationHand-foot syndromeCoughAcute kidney injuryDry skinAnorexiaDehydrationEdema of limbHeartburnHyponatremiaNeuropathyNeutropeniaFebrile
Arm I313126231919141310876665555521

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Disease Control Rate

(NCT01044433)
Timeframe: 5 years

Interventionpercentage (Number)
Arm I68

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Overall Survival

(NCT01044433)
Timeframe: 5 years

InterventionMonths (Mean)
Lapatinib Ditosylate and Capecitabine10.7

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Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01044433)
Timeframe: 5 years

Interventionpercentage (Number)
Arm I25

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Progression-free Survival

(NCT01044433)
Timeframe: 5 years

Interventionmonths (Number)
Arm I4.2

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Rate of Locoregional Control

(NCT01060007)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Neoadjuvant Radiation Followed by FOLFOX96

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Preoperative Gastrointestinal Morbidity

As measured by participants who experience grade 3 or higher gastrointestinal morbidity (NCT01060007)
Timeframe: Mean number of weeks before surgery 17.3 (SD +/- 2.9 weeks)

Interventionparticipants (Number)
Neoadjuvant Radiation Followed by FOLFOX7

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Rate of Overall Control

(NCT01060007)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Neoadjuvant Radiation Followed by FOLFOX89

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Determine Quality of Anorectal Function

"Anorectal function was measured by the participant's response to the FACT-C questionnaire question I have control of my bowels. The answers ranged from 0=not at all to 4=very much." (NCT01060007)
Timeframe: Up to 1 year

,,
InterventionParticipants (Count of Participants)
0 = not at all1 = a little bit2 = somewhat3 = quite a bit4 = very much
1 Year Post-treatment241375
Pre-surgery4482122
Pre-treatment73221426

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Incidence of Any Late Grade 3 or Higher Morbidity

(NCT01060007)
Timeframe: Preoperative (mean time from start of radiation to surgery 17.3 weeks (SD +/- 2.9 weeks)

Interventionparticipants (Number)
Non-hematologic toxicitiesHematologic toxicities
Neoadjuvant Radiation Followed by FOLFOX1621

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Local Control

"Kaplan-Meier projections~Local control = control of primary tumor" (NCT01060007)
Timeframe: 30 months

Interventionpercentage of participants (Number)
Neoadjuvant Radiation Followed by FOLFOX95

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Rate of T Stage Downstaging

T stage downstaging is defined as clinical pretreatment American Joint Committee on Cancer T stage (cT) being greater than pathologic T stage at surgery (ypT). (NCT01060007)
Timeframe: Mean number of weeks before surgery 17.3 (SD +/- 2.9 weeks)

Interventionpercentage of participants (Number)
Neoadjuvant Radiation Followed by FOLFOX71

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Incidence of Post Chemoradiotherapy Grade 3 or Higher Morbidity

(NCT01060007)
Timeframe: 1 year (completion of all treatment)

Interventionparticipants (Number)
Neoadjuvant Radiation Followed by FOLFOX21

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Freedom From Disease Relapse

Kaplan-Meier projections. (NCT01060007)
Timeframe: 30 months

Interventionpercentage of participants (Number)
Neoadjuvant Radiation Followed by FOLFOX87

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Percentage of Participants With an Overall Response of Complete Response (CR) or Partial Response (PR)

"Percentage of participants with an overall response of CR or PR according to RECIST criteria.~CR was defined as complete disappearance of all target lesions and non-target disease, with the exception of nodal disease. All nodes, both target and non-target, must have decreased to normal (short axis less than [<]10 millimeters [mm]). No new lesions. PR was defined as greater than or equal to (≥)30 percent (%) decrease under baseline of the sum of diameters of all target lesions. The short axis was used in the sum for target nodes, while the longest diameter was used in the sum for all other target lesions. No unequivocal progression of non-target disease. No new lesions." (NCT01077739)
Timeframe: Baseline, every 9 weeks until disease progression, at end of treatment or withdrawal, for up to 24 months

Interventionpercentage of participants (Number)
Bevacizumab + Oxaliplatin + Capecitabine27.3
Bevacizumab + FOLFOX6.4

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PFS From the Start of First-Line Therapy

PFS from the start of first-line therapy was defined as the interval between the start of first-line therapy and the date at which second disease progression (after the start of beyond progression therapy) was documented. Progression of disease was evaluated using RECIST version 1.1 and abdominal/pelvic CT or MRI scanning. The same method of assessment and the same technique were to be used to evaluate each lesion throughout the entire study. If more than one method was used, data from the most accurate method according to RECIST were recorded. Median PFS was estimated using the Kaplan-Meier method. (NCT01077739)
Timeframe: Baseline, every 9 weeks until disease progression, at end of treatment or withdrawal, for up to 24 months

Interventionmonths (Median)
Bevacizumab + Oxaliplatin + Capecitabine17.8
Bevacizumab + FOLFOX18.0

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Progression-Free Survival (PFS) From the Start of Treatment Beyond Progression

PFS from the start of treatment beyond progression was defined as the interval between the start of beyond-progression therapy and the date at which disease progression was documented. Progression of disease was evaluated using Response Evaluation Criteria in Solid Tumors (RECIST) criteria version 1.1 and abdominal/pelvic computerized tomography (CT) or magnetic resonance imaging (MRI) scanning as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. The same method of assessment and the same technique were to be used to evaluate each lesion throughout the entire study. If more than one method was used, data from the most accurate method according to RECIST were recorded. Median PFS was estimated using the Kaplan-Meier method. (NCT01077739)
Timeframe: Baseline, every 9 weeks until disease progression, at end of treatment or withdrawal, for up to 24 months

Interventionmonths (Median)
Bevacizumab + Oxaliplatin + Capecitabine6.3
Bevacizumab + FOLFOX5.1

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Geometric Mean Values of Pro-Angiogenic Cytokine Concentrations at Baseline and Prior to Progression

Pro-angiogenic cytokine concentrations of placental growth factor (PlGF), basic fibroblast growth factor (bFGF), and hepatocyte growth factor (HGF) in participant sera were measured and reported in units of picograms/milliliter (pg/mL). The geometric mean was calculated as exp10 (mean of log10 transformed concentration) and the standard deviation (SD) is SD of log10 transformed concentration. (NCT01077739)
Timeframe: Baseline, every 9 weeks until disease progression, at final visit or at withdrawal, for up to 24 months

,
Interventionpg/mL (Geometric Mean)
Baseline bFGF (n=13,23)bFGF, Prior to progression levels (n=12,18)Baseline HGF (n=13,23)HGF, Prior to progression levels (n=12,18)Baseline PIGF (n=13,23)PIGF, Prior to progression levels (n=12,18)
Bevacizumab + FOLFOX6.14.2186.0230.326.337.1
Bevacizumab + Oxaliplatin + Capecitabine6.83.6133.0187.329.834.7

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Patient Reported Quality of Life

Patient reported quality of life was measured with the Treatment Outcome Index of the Functional Assessment of Cancer Therapy for endometrial cancer (FACT-O TOI). The FACT-O TOI is a scale for assessing general QOL of ovarian cancer patients. It consists of three subscales: Physical Well Being (7 items), Functional Well Being (7 items), and Ovarian Cancer subscale (11 items). Each item in the FACT-O TOI was scored using a 5-point scale (0=not at all; 1=a little bit; 2=somewhat; 3=quite a bit; 4=very much). For the negative statements (or questions), reversal was performed prior to score calculation. According to the FACIT measurement system, a subscale score was the summation of the individual item scores if more than 50% of subscale items were answered. The FACT-O TOI score ranges 0-100 with a large score suggests better QOL (NCT01081262)
Timeframe: baseline (pre-treatment), pre cycle 4, post cycle 6, six months post-chemo, end of bevacizumab [BEV] (or 39 weeks after completion of chemotherapy in the non-BEV arms or in those who discontinue BEV), six months after BEV, and years 2, 3, 4, and 5

Interventionunits on a scale (Mean)
Baseline (pre-treatment)Pre-Cycle 4Post-Cycle 6End of Bevacizumab (BEV)Six Months after BEV2 Years after BEV
Arm II (Oxaliplatin and Capecitabine)62.372.973.553.353.056.0

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Patient Reported Quality of Life

Patient reported quality of life was measured with the Treatment Outcome Index of the Functional Assessment of Cancer Therapy for endometrial cancer (FACT-O TOI). The FACT-O TOI is a scale for assessing general QOL of ovarian cancer patients. It consists of three subscales: Physical Well Being (7 items), Functional Well Being (7 items), and Ovarian Cancer subscale (11 items). Each item in the FACT-O TOI was scored using a 5-point scale (0=not at all; 1=a little bit; 2=somewhat; 3=quite a bit; 4=very much). For the negative statements (or questions), reversal was performed prior to score calculation. According to the FACIT measurement system, a subscale score was the summation of the individual item scores if more than 50% of subscale items were answered. The FACT-O TOI score ranges 0-100 with a large score suggests better QOL (NCT01081262)
Timeframe: baseline (pre-treatment), pre cycle 4, post cycle 6, six months post-chemo, end of bevacizumab [BEV] (or 39 weeks after completion of chemotherapy in the non-BEV arms or in those who discontinue BEV), six months after BEV, and years 2, 3, 4, and 5

,
Interventionunits on a scale (Mean)
Baseline (pre-treatment)Pre-Cycle 4Post-Cycle 6Six Months Post-ChemoEnd of Bevacizumab (BEV)Six Months after BEV2 Years after BEV3 Years after BEV
Arm I (Carboplatin and Paclitaxel)62.657.565.274.168.954.071.776.4
Arm IV (Oxaliplatin, Capecitabine, Bevacizumab)75.476.071.868.749.970.577.076.0

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Patient Reported Quality of Life

Patient reported quality of life was measured with the Treatment Outcome Index of the Functional Assessment of Cancer Therapy for endometrial cancer (FACT-O TOI). The FACT-O TOI is a scale for assessing general QOL of ovarian cancer patients. It consists of three subscales: Physical Well Being (7 items), Functional Well Being (7 items), and Ovarian Cancer subscale (11 items). Each item in the FACT-O TOI was scored using a 5-point scale (0=not at all; 1=a little bit; 2=somewhat; 3=quite a bit; 4=very much). For the negative statements (or questions), reversal was performed prior to score calculation. According to the FACIT measurement system, a subscale score was the summation of the individual item scores if more than 50% of subscale items were answered. The FACT-O TOI score ranges 0-100 with a large score suggests better QOL (NCT01081262)
Timeframe: baseline (pre-treatment), pre cycle 4, post cycle 6, six months post-chemo, end of bevacizumab [BEV] (or 39 weeks after completion of chemotherapy in the non-BEV arms or in those who discontinue BEV), six months after BEV, and years 2, 3, 4, and 5

Interventionunits on a scale (Mean)
Baseline (pre-treatment)Pre-Cycle 4Post-Cycle 6Six Months Post-ChemoEnd of Bevacizumab (BEV)Six Months after BEV2 Years after BEV3 Years after BEV4 Years after BEV5 Years after BEV
Arm III (Carboplatin, Paclitaxel, Bevacizumab)68.768.768.380.373.087.576.380.571.578.0

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Patient Reported Neurotoxicity

Patient reported neurotoxicity symptoms as measured with the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - neurotoxicity subscale (short version) (FACT/GOG-Ntx subscale). The FACT/GOG-Ntx subscale contains 4 items. Each item was scored using a 5-point scale (0=not at all; 1=a little bit; 2=somewhat; 3=quite a bit; 4=very much). For the negative items, reversal was performed prior to score calculation. According to the FACIT measurement system, the Ntx score was the summation of the individual item scores if more than 50% of subscale items were answered. When unanswered items existed, a subscale score was prorated by multiplying the mean of the answered item scores by the number of items in the scale. The Ntx score ranges 0-16 with a large score suggests less neurotoxicity. (NCT01081262)
Timeframe: baseline (pre-treatment), pre cycle 4, post cycle 6, six months post-chemo, end of bevacizumab [BEV] (or 39 weeks after completion of chemotherapy in the non-BEV arms or in those who discontinue BEV), six months after BEV, and years 2, 3, 4, and 5

,
Interventionunits on a scale. (Mean)
Baseline (pre-treatment)Pre-cycle 4Post cycle 6Six months post chemoEnd of bevacizumab (BEV)Six months after BEV2 years after BEV3 years after BEV
Arm I (Carboplatin and Paclitaxel)16.07.36.55.016.010.08.014.0
Arm IV (Oxaliplatin, Capecitabine, Bevacizumab)16.05.78.010.711.77.016.016.0

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Patient Reported Neurotoxicity

Patient reported neurotoxicity symptoms as measured with the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - neurotoxicity subscale (short version) (FACT/GOG-Ntx subscale). The FACT/GOG-Ntx subscale contains 4 items. Each item was scored using a 5-point scale (0=not at all; 1=a little bit; 2=somewhat; 3=quite a bit; 4=very much). For the negative items, reversal was performed prior to score calculation. According to the FACIT measurement system, the Ntx score was the summation of the individual item scores if more than 50% of subscale items were answered. When unanswered items existed, a subscale score was prorated by multiplying the mean of the answered item scores by the number of items in the scale. The Ntx score ranges 0-16 with a large score suggests less neurotoxicity. (NCT01081262)
Timeframe: baseline (pre-treatment), pre cycle 4, post cycle 6, six months post-chemo, end of bevacizumab [BEV] (or 39 weeks after completion of chemotherapy in the non-BEV arms or in those who discontinue BEV), six months after BEV, and years 2, 3, 4, and 5

Interventionunits on a scale. (Mean)
Baseline (pre-treatment)Pre-cycle 4Post cycle 6End of bevacizumab (BEV)Six months after BEV2 years after BEV
Arm II (Oxaliplatin and Capecitabine)15.311.811.710.010.014.0

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Participants With Grade 1 or Higher Non-serious Adverse Effects Assessed by CTCAE Version 4.0

Grade 1 or higher non-serious adverse events were graded by CTC AE v 4. (NCT01081262)
Timeframe: Every cycle while on treatment, up to 5 years

,,,
InterventionParticipants (Count of Participants)
Abnormal lab valuesAllergic reactionAllergic rhinitisAlopeciaAnemiaBleedingCold-like symptomsConstipationDiarrheadyspneaEdema LimbsFatigueFeverHand/Foot SyndromeHeadacheHypertensionHypomagnesemiaInfectionLaryngeal SpasmLow LymphocytesLow MoodLow NeutrophilsLow plateletsLow white Blood CellsMucositisNausea/VomitingOral ProblemsOtherOther GI ProblemsPainPeripheral/Sensory NeuropathyPneumothoraxRaised CA19-9Raised Blood CountsRashStomatitisTaste AlterationUrinary ProblemsVaginal BleedingWeight GainWeight Loss
Arm I (Carboplatin and Paclitaxel)830111212352010313314011785183489110014031002
Arm II (Oxaliplatin and Capecitabine)10111713461110004800412535182466111012220113
Arm III (Carboplatin, Paclitaxel, Bevacizumab)100194377530820592302145419477780203111114
Arm IV (Oxaliplatin, Capecitabine, Bevacizumab)104156569800111741003001776399767100014022225

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Progression-free Survival

Progression is defined using Response Evaluation Criteria in Solid Tumors criteria (RECIST v1.0) as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT01081262)
Timeframe: Is measured from date of randomization until first indication of progression based on RECIST criteria or death from any cause, or if progression-free at last contact, the date of last disease assessment up to 10 years.

InterventionMonths (Median)
Arm I (Carboplatin and Paclitaxel)36.1
Arm II (Oxaliplatin and Capecitabine)7.4
Arm III (Carboplatin, Paclitaxel, Bevacizumab)15.4
Arm IV (Oxaliplatin, Capecitabine, Bevacizumab)23.3

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Objective Tumor Response

Complete and Partial Tumor Response by RECIST 1.1. Per Response Evaluation Criteria in Solid Tumors Criteria (RECIST v.1.1) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR),.>=30% decrease in the sum of the longest diameter of target lesions; Overall response (OR) = CR + PR (NCT01081262)
Timeframe: CT scan or MRI if used to follow lesion for measurable disease every other cycle for the first 6 months; then every 3 months x 2; then every 6 months thereafter until disease progression, and any other time clinically indicated, up to 5 years

InterventionPercentage of Participants (Number)
Arm I (Carboplatin and Paclitaxel)22
Arm II (Oxaliplatin and Capecitabine)27
Arm III (Carboplatin, Paclitaxel, Bevacizumab)43
Arm IV (Oxaliplatin, Capecitabine, Bevacizumab)40

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Patient Reported Neurotoxicity

Patient reported neurotoxicity symptoms as measured with the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group - neurotoxicity subscale (short version) (FACT/GOG-Ntx subscale). The FACT/GOG-Ntx subscale contains 4 items. Each item was scored using a 5-point scale (0=not at all; 1=a little bit; 2=somewhat; 3=quite a bit; 4=very much). For the negative items, reversal was performed prior to score calculation. According to the FACIT measurement system, the Ntx score was the summation of the individual item scores if more than 50% of subscale items were answered. When unanswered items existed, a subscale score was prorated by multiplying the mean of the answered item scores by the number of items in the scale. The Ntx score ranges 0-16 with a large score suggests less neurotoxicity. (NCT01081262)
Timeframe: baseline (pre-treatment), pre cycle 4, post cycle 6, six months post-chemo, end of bevacizumab [BEV] (or 39 weeks after completion of chemotherapy in the non-BEV arms or in those who discontinue BEV), six months after BEV, and years 2, 3, 4, and 5

Interventionunits on a scale. (Mean)
Baseline (pre-treatment)Pre-cycle 4Post cycle 6Six months post chemoEnd of bevacizumab (BEV)Six months after BEV2 years after BEV3 years after BEV4 years after BEV5 years after BEV
Arm III (Carboplatin, Paclitaxel, Bevacizumab)14.312.711.011.39.59.05.59.56.57.5

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Overall Survival

Overall survival is defined as the duration of time from study entry to time of death, or the date of last contact. (NCT01081262)
Timeframe: Up to five years

Interventionmonths (Median)
Arm I (Carboplatin and Paclitaxel)37.6
Arm II (Oxaliplatin and Capecitabine)27.8
Arm III (Carboplatin, Paclitaxel, Bevacizumab)27.7
Arm IV (Oxaliplatin, Capecitabine, Bevacizumab)55.7

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Duration of Response

Measured from the first time that measurement criteria were first met for objective response (documented CR or PR) until recurrence/progression or death whatever the cause. (NCT01095003)
Timeframe: Baseline up to 2 years 7 months

InterventionMonths (Median)
Vinflunine Plus Capecitabine57.3
Capecitabine Single-agent47.9

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Overall Survival

The overall survival (OS) was defined as the duration between the date of randomisation and the date of death from any cause. The OS analysis was performed in the ITT population and the eligible and per protocol populations once the required number of events (631 deaths) was observed Patients lost to follow-up, or without a known record of death at time of analysis had the OS censored at the date of last contact. (NCT01095003)
Timeframe: Baseline upto 3 years 10 months

InterventionMonths (Median)
Vinflunine Plus Capecitabine13.9
Capecitabine Single-agent11.7

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Progression Free Survival

"PFS is defined as time from date of randomization to date of the first documentation of objective tumor progression (according to the Independent Response Review Committee (IRC) and based on RECIST version 1.1) or death due to any cause.~The PFS was primarily analysed in the Intent-to-treat (ITT) population. Patients lost to follow-up, or without a known record of progression or death at time of analysis had the progression-free survival censored at the date of last tumour assessment or the date of last contact of a follow-up showing no progression, whichever occurs last." (NCT01095003)
Timeframe: Baseline up to 2 years 7 months

InterventionMonths (Median)
Vinflunine Plus Capecitabine5.6
Capecitabine Single-agent4.3

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Overall Response Rate (ORR)

ORR defined as documentation of complete or partial response that was subsequently confirmed to first documentation of disease progression or to death due to any cause, whichever occurred first. (NCT01095003)
Timeframe: Baseline upto 2 years 7 months

InterventionPercent (Number)
Vinflunine Plus Capecitabine22.9
Capecitabine Single-agent17.9

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Disease Control Rate

Disease control rate defined (DCR) as the sum of confirmed complete response, confirmed partial response and stabilisation rate. (NCT01095003)
Timeframe: Baseline up to 2 years 7 months

InterventionPercent (Number)
Vinflunine Plus Capecitabine57.3
Capecitabine Single-agent47.9

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Progression-free Survival

Progression-free survival was defined as the time from the initiation of treatment to the earliest date of failure (disease progression, death from any cause, or a second malignancy) or to the last assessment date for patients who did not fail. Disease progression was defined as progressive neurologic abnormalities or worsening neurologic status not explained by causes unrelated to tumor progression (eg, anticonvulsant or corticosteroid toxicity, electrolyte disturbances, sepsis, hyperglycemia, weaning of steroids, radiation necrosis, etc); or a greater than 25% increase in the bi-dimensional measurement of the tumor, as compared with the previous scan; or the appearance of a new lesion; or an increase in the doses of dexamethasone required to maintain stable neurologic status or imaging. (NCT01118377)
Timeframe: Baseline to the end of the study (up to 20 weeks)

InterventionMonths (Median)
Capecitabine + Radiation Therapy4.9

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Percentage of Participants With a Tumor Response

Tumor response was defined as either a complete response or a partial response prior to failure (disease progression, death from any cause, or a second malignancy). A complete response was defined as the complete disappearance on magnetic response imaging of all enhancing tumor and mass effect on a stable or decreasing dose of dexamethasone (or only receiving adrenal replacement doses) accompanied by a stable or improving neurologic examination that was maintained for at least 12 weeks. A partial response was defined as a greater than or equal to 50% reduction in tumor size by bi-dimensional measurement on a stable or decreasing dose of dexamethasone accompanied by a stable or improving neurologic examination that was maintained for at least 12 weeks. (NCT01118377)
Timeframe: Baseline to the end of the study (up to 20 weeks)

InterventionPercentage of participants (Number)
Capecitabine + Radiation Therapy2.3

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Overall Survival

Overall survival was defined as the time from the initiation of therapy to the date of death from any cause or to the date the patient was last known to be alive for surviving patients. (NCT01118377)
Timeframe: Baseline to the end of the study (up to 20 weeks)

InterventionMonths (Median)
Capecitabine + Radiation Therapy10.3

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Tolerated Dose

"Six subjects will be initially enrolled (neratinib 240 mg/day; capecitabine 1500 mg/m²/day on days 1 through 14). AEs and DLTs will be assessed from the first dose of investigational product through day 21. Based on the DLT rate in these first 6 subjects, dose tolerability will be confirmed as follows:~If ≤1 of the first 6 evaluable subjects experience a DLT by day 21, then this dose is considered tolerable, and enrollment will stop.~If ≥3 of the first 6 evaluable subjects experience a DLT by day 21, this dose is considered intolerable.~If 2 of the first 6 evaluable subjects experience a DLT by day 21, then an additional 4 subjects will be enrolled at the same dose level.~If a total of 10 subjects are enrolled, then the tolerability will be confirmed as follows:~If ≤3 of the total 10 subjects experience a DLT by day 21, then this dose will be considered tolerable.~If ≥4 of the total 10 subjects experience a DLT by day 21, then the dose will be considered intolerable." (NCT01128842)
Timeframe: From first dose date to day 21.

Interventionmg (Number)
Neratinib + Capecitabine240

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Progression Free Survival

Number of weeks between the date of the first dose of test article and the first date of disease recurrence or disease progression (PD), or death due to any cause, was documented, censored at the last evaluation, investigator assessment. Progression is defined using Response Evaluation Criteria in Solid Tumors Criteria (v1.0), as at least a 20% increase in the sum of the longest diameters (LD) of target lesions, taking as reference the nadir LD, meaning the smallest sum of the LDs recorded since the treatment started; or unequivocal progression of existing nontarget lesions; or the appearance of any new lesions. (NCT01128842)
Timeframe: From first dose date to PD or death, up to 41 weeks.

Interventionweeks (Median)
Neratinib + Capecitabine15.6

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Objective Response Rate

Percentage of participants with partial response (PR) or complete response (CR) per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) v.1.0: CR, disappearance of all target lesions; PR, >=30% decrease in the sum of the longest diameter of target lesions; and Non Progressive Disease (PD) for non-target lesions, and no new lesions. (NCT01128842)
Timeframe: From first dose date to progression or last tumor assessment, up to 41 weeks.

Interventionpercentage of participants (Number)
Neratinib + Capecitabine14.3

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Maximum Plasma Concentration of Neratinib in Combination With Capecitabine

Maximum plasma concentration (nanograms/milliliter) of Neratinib at day 14 following Administration of Neratinib 240 mg in combination with Capecitabine 1500 mg/m^2 per day to Japanese Subjects with Cancer. (NCT01128842)
Timeframe: Measured at 1, 2, 4, 6, 8 and 21-24 hours after dose on day 14.

Interventionng/mL (Mean)
Neratinib + Capecitabine61.9

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Dose Limiting Toxicity (DLT) - Percentage of Participants With DLT Events

DLT was defined as 1. Grade 3 or 4 non-hematologic toxicity (exceptions listed below as a.-c.), a. Grade 3 asthenia was NOT considered to be a DLT UNLESS it lasted >3 days. b. Grade 3 nausea or vomiting was NOT considered to be a DLT UNLESS the subject was already receiving optimal medical therapy. c. Grade 3 or 4 infection was NOT considered to be a DLT UNLESS it is associated with grade 3 or 4 neutropenia. 2. Grade 3 diarrhea that lasted >2 days while the subject was on optimal medical therapy or that was associated with fever (greater than or equal 38.0 ºC) or grade 3 dehydration. 3. Grade 4 neutropenia lasting ≥3 days or grade 4 febrile neutropenia. 4. Grade 4 thrombocytopenia lasting ≥3 days or complicated with bleeding or requiring platelet transfusion. 5. Delayed recovery (to National Cancer Institute [NCI] grade 1 or less, or baseline) from any of the toxicities listed above (items 1-4), that was related to study drug, and that delayed the next dose by more than 3 weeks. (NCT01128842)
Timeframe: From first dose date to day 21.

InterventionParticipants (Count of Participants)
Neratinib + Capecitabine1

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Area Under the Curve (AUC) of Neratinib in Combination With Capecitabine

AUC of Neratinib at day 14 following Administration of Neratinib 240 mg in combination with Capecitabine 1500 mg/m^2 per day to Japanese Subjects with Cancer. (NCT01128842)
Timeframe: At 1, 2, 4, 6, 8 and 21-24 hours after dose on day 14.

Interventionng*hr/mL (Mean)
Neratinib + Capecitabine1070

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Percentage of Participants With Pathological Complete Response (pCR)

pCR was defined as an absence of any invasive cancer cell of the primary tumor after the time of major neoadjuvant chemotherapy, with or without surgery. (NCT01130337)
Timeframe: Between Days 7 and 21 of the 3rd cycle of neoadjuvant treatment, thereafter, every 9 weeks during adjuvant treatment and then after adjuvant treatment every 3 months until Month 25

Interventionpercentage of participants (Number)
Capecitabine+Oxaliplatin+Trastuzumab8.33

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Percentage of Participants With Objective Response

An objective response was defined as either a complete response (CR) or a partial response (PR). Using the Response Evaluation Criteria in Solid Tumors (RECIST), CR was defined as the disappearance of all target lesions and all non-target lesions, normalization of tumor marker level, and no new lesions. PR was defined as the disappearance of all target lesions and persistence of greater than or equal to (≥) 1 non-target lesions and/or the maintenance of tumor marker level above the normal limits, or, at least a 30% decrease in the sum of the longest diameter of target lesions, and no new lesions or unequivocal progression of existing non-target lesions. (NCT01130337)
Timeframe: Between Days 7 and 21 of the 3rd cycle of neoadjuvant treatment, thereafter, every 9 weeks during adjuvant treatment and then after adjuvant treatment every 3 months until Month 25

Interventionpercentage of participants (Number)
Capecitabine+Oxaliplatin+Trastuzumab38.89

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Percentage of Participants With Disease-free Survival (DFS) at Month 18

DFS was the time elapsed from the time of surgery (for complete resection [R0] participants) until the date on which progression or death from any cause was documented (whichever occured first). Progression was defined as target lesions greater than (>) 20 percent (%) increase in the sum of the longest diameter (SLD) taking as reference the smallest SLD recorded since the treatment started (nadir) and minimum 5 millimeter (mm) increase over the nadir. When the sum becomes very small, increases within the measurement error (2-3 mm) can lead to a 20% increase. Participants who did not present progression and who had not died were censored on the last date on which it was known that there was no progression (last response assessment). (NCT01130337)
Timeframe: Month 18

Interventionpercentage of participants (Number)
Capecitabine+Oxaliplatin+Trastuzumab76.12

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Percentage of Participants With Complete Tumor Resection (R0)

R0 resection was defined as having performed a complete resection of the tumor with adequate tumor-free margins and regional lymph node extirpation. (NCT01130337)
Timeframe: Between Days 7 and 21 of the 3rd cycle of neoadjuvant treatment, thereafter, every 9 weeks during adjuvant treatment and then after adjuvant treatment every 3 months until Month 25

Interventionpercentage of participants (Number)
Capecitabine+Oxaliplatin+Trastuzumab90.32

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Time to Progression (TTP)

TTP is defined as the time from date of randomization until objective tumor progression or death due to any cause. It includes deaths and thus can be correlated to overall survival. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionmonths (Median)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)8.35
Bevacizumab + Capecitabine (1250 mg/m^2)8.15
Bevacizumab + Capecitabine (650 mg/m^2)7.27

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Time to Treatment Failure

Time to treatment failure is defined as a composite endpoint measuring time from date of randomization to discontinuation of treatment for any reason, including disease progression, death, treatment toxicity, insufficient therapeutic response, failure to return, refusing treatment, being unwilling to cooperate and withdrawing consent. Analysis was performed using Kaplan-Meier estimates. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionmonths (Median)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)6.67
Bevacizumab + Capecitabine (1250 mg/m^2)6.87
Bevacizumab + Capecitabine (650 mg/m^2)5.75

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Duration of Overall Complete Response

Duration of complete response was calculated as the time in months from the date of randomization to the date of first documentation of CR. Kaplan-Meier estimates were used for analysis. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years

Interventionmonths (Median)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)8.35
Bevacizumab + Capecitabine (1250 mg/m^2)6.05
Bevacizumab + Capecitabine (650 mg/m^2)12.89

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Duration of Overall Response

Duration of overall response included participants who achieved a CR or PR. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionmonths (Median)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)6.51
Bevacizumab + Capecitabine (1250 mg/m^2)6.61
Bevacizumab + Capecitabine (650 mg/m^2)9.12

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Duration of Stable Disease (SD)

Duration of SD was calculated as the number of months the participants remained in CR, PR or SD. Kaplan-Meier estimates were used for analysis. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionmonths (Median)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)8.81
Bevacizumab + Capecitabine (1250 mg/m^2)8.65
Bevacizumab + Capecitabine (650 mg/m^2)8.98

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Overall Survival

Overall survival is defined as the time from date of randomization until death from any cause; Kaplan-Meier estimates were used for analysis. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionmonths (Median)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)22.75
Bevacizumab + Capecitabine (1250 mg/m^2)19.76
Bevacizumab + Capecitabine (650 mg/m^2)18.02

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Percentage of Participants Who Died

Overall survival is defined as the time from date of randomization until death from any cause (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionpercentage of participants (Number)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)67.33
Bevacizumab + Capecitabine (1250 mg/m^2)71.57
Bevacizumab + Capecitabine (650 mg/m^2)73.79

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Percentage of Participants With a Best Overall Response of CR or PR

CR: Complete disappearance of all target lesions; PR: At least 30% decrease in the sum of the longest diameter of all target lesions taking as reference the baseline sum of all target lesions; (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionpercentage of participants (Number)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)52.0
Bevacizumab + Capecitabine (1250 mg/m^2)34.0
Bevacizumab + Capecitabine (650 mg/m^2)34.0

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Percentage of Participants With Disease Progression or Death

Disease progression was defined according to National Cancer Institute (NCI) guidelines and best clinical practices. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionpercentage of participants (Number)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)86.14
Bevacizumab + Capecitabine (1250 mg/m^2)90.20
Bevacizumab + Capecitabine (650 mg/m^2)88.35

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Percentage of Participants With Progression Excluding Deaths

The failure event was defined as tumor progression excluding deaths due to any reason. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionpercentage of participants (Number)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)71.29
Bevacizumab + Capecitabine (1250 mg/m^2)81.37
Bevacizumab + Capecitabine (650 mg/m^2)75.73

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Percentage of Participants With Progressive Disease Within 12 Weeks From Start of Treatment

Early progression was the proportion of participants with progressive disease within 12 weeks from the start of treatment. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and 12

Interventionpercentage of participants (Number)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)9.0
Bevacizumab + Capecitabine (1250 mg/m^2)13.0
Bevacizumab + Capecitabine (650 mg/m^2)18.0

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Percentage of Participants With Stable Disease

Stable disease rate was the proportion of participants who achieved CR, PR, or SD. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionpercentage of participants (Number)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)91.0
Bevacizumab + Capecitabine (1250 mg/m^2)86.0
Bevacizumab + Capecitabine (650 mg/m^2)80.0

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Time to Progression Excluding Deaths

The failure event was defined as tumor progression excluding deaths due to any reason. Kaplan-Meier estimates were used for analysis. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionmonths (Median)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)8.81
Bevacizumab + Capecitabine (1250 mg/m^2)8.48
Bevacizumab + Capecitabine (650 mg/m^2)7.40

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Percentage of Participants by Best Overall Response

Best overall response is defined as the best response recorded from the date of randomization until disease progression or recurrence. Complete response (CR): at least 2 determinations of CR at least 4 weeks apart before progression; Partial response (PR): at least 2 determinations of PR at least 4 weeks apart before progression; Stable disease (SD): at least one SD assessment; Progressive Disease (PD): Disease progression or death due to underlying cancer. CR: Complete disappearance of all target lesions; PR: At least 30% decrease in the sum of the longest diameter of all target lesions taking as reference the baseline sum of all target lesions; PD: At least 20% decrease in the sum of the longest diameter of all target lesions taking as reference the baseline sum of longest diameter of all target lesions or the appearance of one or more new lesions; SD: Neither sufficient shrinkage to qualify for CR or PR or increase in lesions; (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

,,
Interventionpercentage of participants (Number)
CRPRSDPD
Bevacizumab + Capecitabine (1250 mg/m^2)1.0932.6152.1714.13
Bevacizumab + Capecitabine (650 mg/m^2)5.3228.7245.7420.21
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)5.4946.1539.568.79

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Percentage of Participants With Treatment Failure

Treatment failure is defined as discontinuation of treatment for any reason, including disease progression, death, treatment toxicity, insufficient therapeutic response, failure to return, refusing treatment, being unwilling to cooperate and withdrawing consent. (NCT01131078)
Timeframe: Randomization, Weeks 3, 6 and 9, and every 3 months up to 5 years or Death

Interventionpercentage of participants (Number)
Bevacizumab + Irinotecan + Capecitabine (1000 mg/m^2)100.0
Bevacizumab + Capecitabine (1250 mg/m^2)99.02
Bevacizumab + Capecitabine (650 mg/m^2)99.03

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Progression Free Survival (PFS) - Based on Investigator Review Using Kaplan Meier - Phase l & ll

(NCT01132664)
Timeframe: 18 months

,,
InterventionMonths (Median)
Phase lPhase ll: PIK3CA wildtype (n =18)Phase ll: PIK3CA mutated (n =8)
Phase Ib - 100mg3.3NANA
Phase Ib - 50 mg1.7NANA
Phase II - 100mgNA1.71.8

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Overall Response Rate (ORR) - Phase ll

"Objective response rate (ORR) was defined as the rate of patients with best overall response (BOR) equal to complete response (CR) or partial response (PR) according to RECIST 1.0 from the Investigators review.~Per Response Evaluation Criteria In Solid Tumors (RECIST) version 1.0 assessed of the disease status by imaging (i.e. CT/MRI): Complete Response (CR) = Disappearance of all tumor lesions; Partial Response (PR)= >=30% shrinkage of lesions; Overall Response (OR) = patients with CR and PR." (NCT01132664)
Timeframe: 18 months

InterventionParticipants (Number)
Phase II - 100mg5

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Clinical Benefit Rate (CBR) - Phase l & ll

"CBR = patients with CR, PR or SD ≥ 24 weeks according to RECIST by the investigator.~Response Evaluation Criteria In Solid Tumors (RECIST) version 1.0 assessed the disease status by imaging (i.e. CT/MRI): CR = Disappearance of all tumor lesions; PR= >=30% shrinkage of lesions; SD = Neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for PD; PD = At least a 20% increase in the sum of the longest diameter of all measured target lesions, taking as reference the smallest sum of longest diameter of all target lesions recorded at or after baseline." (NCT01132664)
Timeframe: 18 months

,,
InterventionParticipants (Number)
Phase lPhase ll
Phase Ib - 100mg30
Phase Ib - 50 mg00
Phase II - 100mg07

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Disease Control Rate (DCR) Based on Investigator Assessment- Phase l & ll

"Disease control rate (DCR) = patients with complete response (CR), partial response (PR) or stable disease (SD) as per RECIST criteria.~Response Evaluation Criteria In Solid Tumors (RECIST) version 1.0 assessed the disease status by imaging (i.e. CT/MRI): CR = disappearance of all tumor lesions; PR = >=30% shrinkage of lesions; SD = Neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for progressive disease (PD); PD = At least a 20% increase in the sum of the longest diameter of all measured target lesions, taking as reference the smallest sum of longest diameter of all target lesions recorded at or after baseline." (NCT01132664)
Timeframe: 18 months

,,
InterventionParticipants (Number)
Phase lPhase ll
Phase Ib - 100mg70
Phase Ib - 50 mg10
Phase II - 100mg025

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Dose Limiting Toxicity (DLT) - Phase l Only

Determination of the maximum tolerated dose (MTD) in the dose escalation part of the study was based upon the estimation of the probability of DLT in Cycle 1 in patients of the dose-determining set. (NCT01132664)
Timeframe: cycle 1 - 28 days

,,,
InterventionParticipants (Number)
Primary system orgran class (SOC) PT - grade 1Primary SOC PT - grade 2Primary SOC PT (asthenia) - grade 3Primary SOC PT - grade 4Primary SOC PT - missingPrimary SOC PT (somatits/diarrhea) - grade 3
BM Cohort - 100mg000001
BM Cohort - 80mg000000
Phase Ib - 100mg001000
Phase Ib - 50 mg000000

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Here is the Number of Participants With Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0).

Here is the number of participants with non-serious adverse events assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0). A non-serious adverse event is any untoward medical occurrence. A serious adverse event is an adverse event or suspected adverse reaction that results in death, a life-threatening adverse drug experience, hospitalization, disruption of the ability to conduct normal life functions, congenital anomaly/birth defect or important medical events that jeopardize the patient or subject and may require medical or surgical intervention to prevent one of the previous outcomes mentioned. (NCT01134601)
Timeframe: Date treatment consent signed to date off study, and up to 30 days following the last dose of study drug, approximately 14 months and 26 days.

InterventionParticipants (Count of Participants)
Selumetinib (AZD6244): 50 mg & Capecitabine: 825 mg/m^21

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Percentage of Participants Achieving Disease Control (CR, PR, or No Change [NC])

Percent of participants with confirmed CR, PR, or NC. Per RECIST version (v)1.0: CR was defined as disappearance of all target and non-target lesions. PR was defined as ≥30% decrease in sum of longest diameters of target lesions taking as reference baseline sum longest diameters associated to non-progressive disease response for non-target lesions. NC was defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease taking as reference smallest sum of longest dimensions since treatment started associated to non-progressive disease response for non-target lesions. (NCT01135498)
Timeframe: From study start up to approximately 4 years

Interventionpercentage of participants (Number)
Bevacizumab+Oxaliplatin+Capecitabine/Bevacizumab+Erlotinib92.86

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Percentage of Participants Achieving Objective Response (Complete Response [CR] or Partial Response [PR])

Percentage of participants with objective response based assessment of CR or PR according to Response Evaluation Criteria in Solid Tumors (RECIST). CR was defined as complete disappearance of all target lesions and non-target disease, with the exception of nodal disease. All nodes, both target and non-target, must have decreased to normal (short axis less than [<]10 millimeters [mm]) and no new lesions. PR was defined as greater than or equal to (≥)30 percent (%) decrease under baseline of the sum of diameters of all target lesions. The short axis was used in the sum for target nodes, while the longest diameter was used in the sum for all other target lesions. No unequivocal progression of non-target disease. No new lesions. (NCT01135498)
Timeframe: From study start up to approximately 4 years

Interventionpercentage of participants (Number)
Bevacizumab+Oxaliplatin+Capecitabine/Bevacizumab+Erlotinib55.95

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Percentage of Participants Who Died

(NCT01135498)
Timeframe: From study start up to approximately 4 years

Interventionpercentage of participants (Number)
Bevacizumab+Oxaliplatin+Capecitabine/Bevacizumab+Erlotinib58.89

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Percentage of Participants With Disease Progression or Death

Disease progression was defined according to Response Evaluation Criteria in Solid Tumors (RECIST) as a 20 percent (%) increase in the sum of the longest diameter of target lesions, or a measureable increase in a non-target lesion, or the appearance of new lesions. (NCT01135498)
Timeframe: Start of study to approximately 4 years

Interventionpercentage of participants (Number)
Bevacizumab+Oxaliplatin+Capecitabine/Bevacizumab+Erlotinib61.1

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Progression-Free Survival

Progression-free survival was defined as the time from the date of informed consent until the date when the participant had progression of disease or died from disease progression. Participants who received surgical treatment after treatment ended were censored at the time of surgery. Participants who left the study for reasons other than progression of the disease were censored on the date on which they received a later antitumor therapy (with the same or different drugs, radiotherapy, or surgery). (NCT01135498)
Timeframe: From study start up to approximately 4 years

Interventionmonths (Median)
Bevacizumab+Oxaliplatin+Capecitabine/Bevacizumab+Erlotinib9.18

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Overall Survival (OS)

Overall survival was defined as the time from the date of informed consent to the date of death (regardless of the cause of death). There was no restriction; survival was calculated until the date of death, even if another line of treatment was received, or until the date censored (last contact with the participant even if drugs different from the study treatment schedule were received). For all participants, survival information was collected until the date of death, the last contact, or the last follow-up. (NCT01135498)
Timeframe: From study start up to approximately 4 years

Interventionmonths (Median)
Bevacizumab+Oxaliplatin+Capecitabine/Bevacizumab+Erlotinib25.79

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Freedom From Local Progression at 12 Months

the proportion of patients who experienced a local recurrence at 12 months with death as a competing risk (NCT01151761)
Timeframe: 12 months

Interventionpercentage of patients (Number)
SBRT and Chemo0

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Liver Transplant Conversion Rate

The ability to successfully perform liver transplant among patients who initially have tumor >3 cm (NCT01151761)
Timeframe: 12 months

Interventionparticipants (Number)
SBRT and Chemo0

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Median Time to Overall Survival

The time to overall survival is defined as the time to death from any cause. The median was determined via Kaplan Meier methodology. (NCT01151761)
Timeframe: 18 months

Interventionmonths (Median)
SBRT and Chemo8.5

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Liver Transplant Rate

The number of patients receiving liver transplant among patients who initially have tumors ≤3 cm (NCT01151761)
Timeframe: 12 months

Interventionparticipants (Number)
SBRT and Chemo0

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Overall Survival at 12 Months

the estimated probability for the percentage of participants with overall survival at 12 months. (NCT01151761)
Timeframe: 12 months

Interventionprobability (Number)
SBRT and Chemo0

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Pathologic Complete Response Rate

Pathologic complete response will be defined as no residual tumor cells seen on the explanted liver specimen. (NCT01151761)
Timeframe: 12 months

Interventionparticipants (Number)
SBRT and Chemo0

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Progression-free Survival at 12 Months

Progression free survival is defined to be the time to progression of disease or death. (NCT01151761)
Timeframe: 12 months

Interventionparticipants (Number)
SBRT and Chemo0

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Serum CA 19-9 Levels

Initial level of Cancer antigen 19-9 (NCT01151761)
Timeframe: 12 months

InterventionU/ml (Mean)
SBRT and Chemo3329.1

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Duration of Response

Duration of overall response (CR or PR) was calculated for participants of the ITT population whose best overall response was CR or PR based on RECIST criteria. Duration of overall response was defined as the time from the date of the first assessment of CR or PR status until the date of progression or death. Data for participants who were alive without any objectively documented disease progression at the end of the study were censored as of the date of last contact. Mean time to event was estimated using the Kaplan-Meier method. (NCT01159171)
Timeframe: Baseline, every 3 months to progression of disease or end of study (up to 24 months)

Interventionmonths (Mean)
Bevacizumab + Oxaliplatin + Capecitabine8.31

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Duration of Response - Percentage of Participants With an Event by 24 Months

Duration of overall response (CR or PR) was calculated only for participants of the ITT population whose best overall response was CR or PR based on RECIST criteria. Duration of overall response was defined as the time from the date of the first assessment of CR or PR status until the date of progression or death. Data for participants who were alive without any objectively documented disease progression at the end of the study were censored as of the date of last contact. (NCT01159171)
Timeframe: Baseline, every 3 months to progression of disease or end of study (up to 24 months)

Interventionpercentage of participants (Number)
Bevacizumab + Oxaliplatin + Capecitabine57.14

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Duration of Stable Disease

Duration of stable response (CR, PR, or SD) was calculated only for participants of the ITT population whose best overall response was CR, PR, or SD based on RECIST criteria. Duration of overall response was defined as the time from the date of the first assessment of CR, PR, or SD status until the date of progression or death. Data for participants who were alive without any objectively documented disease progression at the end of the study were censored as of the date of last contact. Mean time to event was estimated using the Kaplan-Meier method. (NCT01159171)
Timeframe: Baseline, every 3 months to progression of disease or end of study (up to 24 months)

Interventionmonths (Mean)
Bevacizumab + Oxaliplatin + Capecitabine10.09

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Duration of Stable Disease - Percentage of Participants With an Event by 24 Months

Duration of stable response (CR, PR, or stable disease [SD]) was calculated only for participants of the ITT population whose best overall response was CR, PR, or SD based on RECIST criteria. Duration of overall response was defined as the time from the date of the first assessment of CR, PR, or SD status until the date of progression or death. Data for participants who were alive without any objectively documented disease progression at the end of the study were censored as of the date of last contact. (NCT01159171)
Timeframe: Baseline, every 3 months to progression of disease or end of study (up to 24 months)

Interventionpercentage of participants (Number)
Bevacizumab + Oxaliplatin + Capecitabine52.50

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Overall Survival

OS was defined as the time in months from Day 1 until the date of death due to any cause. Data for participants who were alive at the end of the study were censored at the date of the last available follow-up visit. Mean OS was estimated using the Kaplan-Meier method. (NCT01159171)
Timeframe: Baseline, monthly to end of study (up to 24 months)

Interventionmonths (Mean)
Bevacizumab + Oxaliplatin + Capecitabine20.23

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Overall Survival (OS) - Percentage of Participants With an Event by 24 Months

OS was defined as the time in months from Day 1 until the date of death due to any cause. Data for participants who were alive at the end of the study were censored at the date of the last available follow-up visit. (NCT01159171)
Timeframe: Baseline, monthly to end of study (up to 24 months)

Interventionpercentage of participants (Number)
Bevacizumab + Oxaliplatin + Capecitabine89.90

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Percentage of Participants With Objective Response (OR)

Percentage of participants with OR was defined as the percentage of participants who achieved complete response (CR) or partial response (PR) according to Response Evaluation Criteria in Solid Tumors (RECIST). CR was defined as disappearance of all target lesions, non-target lesions, and normalization of tumor marker level. PR was defined as greater than or equal to (≥)30 percent (%) decrease under baseline of the sum of the longest diameter (LD) diameters of all target lesions. No unequivocal progression of non-target disease. No new lesions. Complete and partial responses must have been confirmed no less than 4 weeks after the criteria for response were first met. (NCT01159171)
Timeframe: Baseline, every 3 months to progression of disease or end of study (up to 24 months)

Interventionpercentage of participants (Number)
Bevacizumab + Oxaliplatin + Capecitabine42.86

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Time to Progression

TTP was defined as the time in months from Day 1 until the date of first documented progressive disease, or death due to any cause. Data for participants who were alive without disease progression at the end of study, or who were non-responder participants (without tumor assessment after baseline) were censored at Day 1. Mean TTP was estimated using the Kaplan-Meier method. (NCT01159171)
Timeframe: Baseline, monthly to end of study (up to 24 months)

Interventionmonths (Mean)
Bevacizumab + Oxaliplatin + Capecitabine9.61

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Time to Progression (TTP) - Percentage of Participants With an Event by 24 Months

TTP was defined as the time time in months from Day 1 until the date of first documented progressive disease, or death due to any cause. Data for participants who were alive without disease progression at the end of study, or who were non-responder participants (without tumor assessment after baseline) were censored at Day 1. (NCT01159171)
Timeframe: Baseline, monthly to end of study (up to 24 months)

Interventionpercentage of participants (Number)
Bevacizumab + Oxaliplatin + Capecitabine91.84

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Time to Treatment Failure

TTF was defined as the time in months from Day 1 until discontinuation of treatment for any reasons. These reasons included: death due to any cause, treatment toxicity (adverse event), insufficient therapeutic response (progression of disease), failure to return (lost to follow-up), refusing treatment (participant non-compliance), being unwilling to cooperate and withdrawing consent (participant withdrew consent). Mean TTF was estimated using the Kaplan-Meier method. (NCT01159171)
Timeframe: Baseline, monthly to end of study (up to 24 months)

Interventionmonths (Mean)
Bevacizumab + Oxaliplatin + Capecitabine7.44

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Time to Treatment Failure (TTF) - Percentage of Participants With an Event by 24 Months

TTF was defined as the time in months from Day 1 until discontinuation of treatment for any reasons. These reasons included: death due to any cause, treatment toxicity (adverse event), insufficient therapeutic response (progression of disease), failure to return (lost to follow-up), refusing treatment (participant non-compliance), being unwilling to cooperate and withdrawing consent (participant withdrew consent). (NCT01159171)
Timeframe: Baseline, every month to end of treatment (up to 24 months)

Interventionpercentage of participants (Number)
Bevacizumab + Oxaliplatin + Capecitabine81.63

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Percentage of Participants by Best Overall Response

Best response recorded from the start of treatment until disease progression. Based on assessment of CR, PR, stable disease (SD), or progressive disease (PD), according to RECIST. CR: disappearance of all target lesions, non-target lesions, and normalization of tumor marker level. PR: ≥30% decrease under baseline of the sum of the LD diameters of all target lesions. CR and PR persist on repeat imaging study at least 4 weeks after initial documentation. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. Reference is the smallest sum LD. PD: at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum longest diameter recorded or the appearance of one or more new lesions. (NCT01159171)
Timeframe: Baseline, every 3 months to progression of disease or end of study (up to 24 months)

Interventionpercentage of participants (Number)
CRPRSDPD
Bevacizumab + Oxaliplatin + Capecitabine4.0838.7838.788.16

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Median Duration of Response (DOR)

DOR is defined as the time from date of first documented confirmed objective response to date of first documented progressive disease (PD). Per RECIST 1.1 for target lesions: PD is at least a 20% increase in sum LD, taking as reference the smallest sum on study with at least 5 mm absolute increase. For non-target lesions, progression-free means no new lesions or unequivocal progression on existing non-target lesions or not evaluated. (NCT01191697)
Timeframe: 23.2 months (IQR: 11.0 - 46.9 months ).

Interventionmonths (Median)
Trastuzumab, Bevacizumab, Oxaliplatin and Capecitabine14.9

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Median Progression Free Survival (PFS)

PFS is defined as the duration of time from study entry to documented disease progression (PD) requiring removal from the study or death. Participants alive without PD were censored at the earliest of the date of the last disease evaluation or start of new anticancer therapy. Per RECIST 1.1 for target lesions: PD is at least a 20% increase in sum LD, taking as reference the smallest sum on study with at least 5 mm absolute increase. For non-target lesions, progression-free means no new lesions or unequivocal progression on existing non-target lesions or not evaluated. (NCT01191697)
Timeframe: Patients received a median of 19 cycles of therapy (Interquartile range (IQR): 8 - 34.5 cycles). Median duration of follow up of 23.2 months (IQR: 11.0 - 46.9 months ).

Interventionmonths (Median)
Trastuzumab, Bevacizumab, Oxaliplatin and Capecitabine14.0

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Median Overall Survival

Overall survival based on the Kaplan-Meier method is defined as the time from randomization to death. Participants alive are censored at the last date of contact (including lost-to-follow-up) or at the date of withdrawal of consent, if relevant. (NCT01191697)
Timeframe: 23.2 months (IQR: 11.0 - 46.9 months ).

Interventionmonths (Median)
Trastuzumab, Bevacizumab, Oxaliplatin and Capecitabine23.2

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Objective Response Rate (ORR)

ORR was defined as the percentage of participants achieving complete response (CR) or partial response (PR) on treatment based on RECIST 1.1 criteria. Per RECIST 1.1 for target lesions: CR is complete disappearance of all target lesions and PR is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. PR or better overall response assumes at a minimum incomplete response/stable disease (SD) for the evaluation of non-target lesions and absence of new lesions. (NCT01191697)
Timeframe: Patients received a median of 19 cycles of therapy (Interquartile range (IQR): 8 - 34.5 cycles). Median duration of follow-up of 23.2 months (IQR: 11.0 - 46.9 months ).

Interventionpercentage of patients (Number)
Trastuzumab, Bevacizumab, Oxaliplatin and Capecitabine81

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Maximum Tolerated Dose (MTD) of Azacitidine, and Capecitabine and Oxaliplatin (CAPOX)

Dose just below the one at which ≥ 1/3 of subjects experience a dose limiting toxicity (DLT) considered the MTD. (NCT01193517)
Timeframe: Up to 3 weeks from the first dose

Interventionmg/m^2 (Number)
AzacitidineOxaliplatinCapecitabine
Azacitidine+CAPOX (Capecitabine, Oxaliplatin)751101500

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Response Rate of Azacitidine, and Capecitabine and Oxaliplatin (CAPOX)

Per Response Evaluation Criteria in solid Tumors Criteria (RECISTv1.0) for target lesions and assessed by CT or MRI: Partial Response (PR), >= 30%decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), neither PD nor PR, the sum of the longest diameters no change or increase by <20% from baseline or from nadir (smallest sum on treatment); Progressive Disease (PD), the sum of the longest diameters increases by>= 20% from nadir (smallest sum on treatment). For non-target lesions assessed by CT or MRI: Stable Disease (SD), Persistence of >=1 non-target lesion; Progressive Disease (PD), Enlargement of non-target lesions and/or appearance of new lesions. (NCT01193517)
Timeframe: After 9 weeks (three, 21 day cycles)

,,
InterventionParticipants (Count of Participants)
NA (Early Progression)PD (Progression Disease)SD (Stable Disease)
Phase I: Highest Dose Level066
Phase I: Starting Dose111
Phase II0110

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Number of Participants With Adverse Events

Toxicity was graded according to the NCI Common terminology Criteria for Adverse Events (CTCAE) 4.0 except for neurosensory and skin toxicity. Neurosensory toxicity was graded according to the Neurologic Toxicity Scale for Oxaliplatin Dose Adjustments. (NCT01208103)
Timeframe: 39 months

Interventionparticipants (Number)
Bevacizumab + Capecitabine + Oxaliplatin30

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Number of Participants With Progression-free Survival (PFS) at Six Months

A Bayesian sequential monitoring design will be used. PFS will be estimated using the Kaplan-Meier method.The length of time interval in months from date of first treatment, during and after the treatment a participant lives without progression. (NCT01208103)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Bevacizumab + Capecitabine + Oxaliplatin68

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To Determine the Overall Survival (OS) for CAPOX and Bevacizumab

The length of time interval in months from date of first treatment until the date of death or lost follow-up (NCT01208103)
Timeframe: 39 months

Interventionmonths (Median)
Bevacizumab + Capecitabine + Oxaliplatin12.9

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To Determine the Response Rate (RR) for CAPOX and Bevacizumab

Complete response + Partial response using RECIST 1.1 (Response Evaluation Criteria in Solid Tumor) (NCT01208103)
Timeframe: 39 months

InterventionParticipants (Count of Participants)
Complete ResponsePartial ResponseStable DiseaseProgressive DiseaseUnevaluable
Bevacizumab + Capecitabine + Oxaliplatin1131051

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To Determine the Overall PFS for CAPOX and Bevacizumab

Time interval in months from date of first treatment until the date of first documented progression (NCT01208103)
Timeframe: 39 months

Interventionmonths (Median)
Bevacizumab + Capecitabine + Oxaliplatin8.7

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Preliminary Efficacy Assessment: Response Rate (RR)

Response Rate (RR) is defined as the total number of patients with Complete Response (CR) or Partial Response (PR) as defined in RECIST v2. CR is defined as the dissappearance of all target lesions, disappearance of all non-target lesions and normalization of tumor markers. PR is defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. (NCT01226732)
Timeframe: 18 months

Interventionparticipants (Number)
Dose Level 11
Dose Level 20
Dose Level 30
Dose Level 42
Dose Level 51
Dose Level 60

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Dose Determination

To determine the maximum tolerated dose (MTD) of AUY922 plus capecitabine in patients with advanced solid tumors. (NCT01226732)
Timeframe: 18 months

Interventionmg/m^2 (Number)
AUY922 doseCapecitabine dose
All Patients701250

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Overall Survival (OS) - Percentage of Participants With an Event

OS was defined as the time from the date of first day of treatment until death due to any cause or the last date the participant was known to be alive. (NCT01227707)
Timeframe: BL, within 6 weeks after the completion of neoadjuvant treatment, every 2 weeks for 1 year following surgery, every 3 months thereafter until death, up to 45 months

Interventionpercentage of participants (Number)
Bv+Capecitabine/Bv+Leucovorin+5-FU25.58

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Percentage of Participants With an Overall Response of CR at the End of Neoadjuvant Treatment

Percentage of participants with an overall response of CR was evaluated as the proportion of participants with CR for the target and non-target lesions plus absence of new lesions at the end of NAT according to RECIST. CR was defined as disappearance of all target lesions, all non-target lesions, and normalization of tumor marker levels. (NCT01227707)
Timeframe: BL and within 6 weeks after the completion of study treatment

Interventionpercentage of participants (Number)
Bv+Capecitabine/Bv+Leucovorin+5-FU9.30

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Percentage of Participants Undergoing Sphincter-Saving Surgery by Type of Procedure

(NCT01227707)
Timeframe: 6 to 8 weeks after completion of study treatment

Interventionpercentage of participants (Number)
Anterior resectionAbdomen-peritoneal amputation (Miles)OtherColostomy, temporary (n=32)Colostomy, definitive (n=32)No colostomy
Bv+Capecitabine/Bv+Leucovorin+5-FU70.022.53.047.5032.5020.0

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Percentage of Participants With Pathological Complete Response (pCR)

pCR was defined as the absence of viable tumor cells, as determined by standard histologic procedure, in the tumor specimen (including regional lymph nodes) obtained at surgery. In order to minimize evaluation bias, tumor specimens were analyzed by both a central and local pathologist. The number of participants with pathological tumor stage 0 (pT0) and regional lymph nodes stage 0 (pN0) at surgery was determined. pCR was defined as the number of participants with pT0 and pN0 at surgery divided by the total number of participants with pathological tumor stage data collected. (NCT01227707)
Timeframe: 6 to 8 weeks following completion of neoadjuvant treatment

Interventionpercentage of participants (Number)
Bv+Capecitabine/Bv+Leucovorin+5-FU10.00

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Percentage of Participants by Primary Tumor (T), Regional Lymph Nodes (N), and Distant Metastasis (M) Clinical Stage at Baseline and at the End of Neo-Adjuvant Treatment (NAT)

The frequencies of clinical tumor stage T (0, 1, 2, 3, 4, or X), regional lymph nodes stage N (0, 1, 2, 3, or 4), and distant metastasis clinical stage M (0, 1, or X) at baseline and at the end of NAT were assessed. The frequencies of pathological tumor stage T and regional lymph nodes stage N at surgery were evaluated. The clinical tumor and lymph node status was assessed by clinical examination, endosonography, and/or rectosigmoidoscopy, and pelvic and abdomen computerized tomography (CT) scan or magnetic resonance imaging (MRI). Response to treatment had to be assessed within 6 weeks after end of treatment by using the same techniques performed at baseline. (NCT01227707)
Timeframe: Baseline (BL) and end of neoadjuvant treatment (within 6 weeks after the completion of study treatment)

Interventionpercentage of participants (Number)
Baseline: T0, N0End of NAT: T0, N0Baseline: T1, N0End of NAT: T1, N0Baseline: T1, NXEnd of NAT: T1, NXBaseline: T2, N0End of NAT: T2, N0Baseline: T2, N1End of NAT: T2, N1Baseline: T2, NXEnd of NAT: T2, NXBaseline: T3, N0End of NAT: T3, N0Baseline: T3, N1End of NAT: T3, N1Baseline: T3, N2End of NAT: T3, N2Baseline: T3, NXEnd of NAT: T3, NXBaseline: T4, N0End of NAT: T4, N0Baseline: T4, N1End of NAT: T4, N1Baseline: T4, N2End of NAT: T4, N2Baseline: T4, N3End of NAT: T4, N3Baseline: TX, N0End of NAT: TX, N0Baseline: TX, N2End of NAT: TX, N2Baseline: M0End of NAT: M0Baseline: M1End of NAT: M1Baseline: MXEnd of NAT: MX
Bv+Capecitabine/Bv+Leucovorin+5-FU04.6504.6502.33018.609.309.3006.9832.5618.6046.519.3002.332.336.9804.652.3302.3302.33002.332.33097.6781.402.332.3309.30

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DFS - Time to Event

The time in months from date of start-of-treatment to the date of event defined as the first documented disease progression or death due to any cause. If a participant did not have an event, the time was censored at the date of last adequate tumor assessment. DFS was estimated using the Kaplan-Meier method. (NCT01227707)
Timeframe: BL, within 6 weeks after the completion of neoadjuvant treatment, every 2 weeks for 1 year following surgery, every 3 months thereafter until progression, up to 45 months

Interventionmonths (Mean)
Bv+Capecitabine/Bv+Leucovorin+5-FU27.43

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Disease-Free Survival (DFS) - Percentage of Participants With an Event

DFS was defined as the time from treatment start date to the date of first progression of disease or date of death due to any cause. (NCT01227707)
Timeframe: BL, within 6 weeks after the completion of neoadjuvant treatment, every 2 weeks for 1 year following surgery, every 3 months thereafter until progression, up to 45 months

Interventionpercentage of participants (Number)
Bv+Capecitabine/Bv+Leucovorin+5-FU30.23

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TTP - Time to Event

TTP was defined as the time from date of treatment start until first documented progression of disease or death due to underlying cancer. TTP was estimated using the Kaplan-Meier method. (NCT01227707)
Timeframe: BL, within 6 weeks after the completion of neoadjuvant treatment, every 2 weeks for 1 year following surgery, every 3 months thereafter until death, up to 45 months

Interventionmonths (Mean)
Bv+Capecitabine/Bv+Leucovorin+5-FU27.68

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Percentage of Participants With New Lesions at the Primary Tumor Site at the End of Neoadjuvant Treatment

The percentage of participants with new lesions located at the primary tumor site were evaluated at the end of NAT. (NCT01227707)
Timeframe: BL and within 6 weeks after the completion of study treatment

Interventionpercentage of participants (Number)
Bv+Capecitabine/Bv+Leucovorin+5-FU4.65

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Time to Disease Progression (TTP) - Percentage of Participants With an Event

TTP was defined as the time from date of treatment start until first documented progression of disease or death due to underlying cancer. (NCT01227707)
Timeframe: BL, within 6 weeks after the completion of neoadjuvant treatment, every 2 weeks for 1 year following surgery, every 3 months thereafter until death, up to 45 months

Interventionpercentage of participants (Number)
Bv+Capecitabine/Bv+Leucovorin+5-FU27.91

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Percentage of Participants With Relapse During Follow-Up

The percentage of participants with local and/or regional relapse during follow-up. New lesions located at rectum or at colon or at lymph node detected at the end of NAT were evaluated as local and/or regional relapse. (NCT01227707)
Timeframe: BL, within 6 weeks after the completion of neoadjuvant treatment, every 2 weeks for 1 year following surgery, every 3 months thereafter until progression, up to 45 months

Interventionpercentage of participants (Number)
No Relapse1 Relapse2 Relapses
Bv+Capecitabine/Bv+Leucovorin+5-FU84.217.897.89

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Percentage of Participants With Complete Response (CR) at the End of Neoadjuvant Treatment

Percentage of participants with CR was evaluated as the proportion of participants with complete response for the target and non-target lesions, separately, at the end of NAT according to the Response Evaluation Criteria in Solid Tumors (RECIST). CR was defined as disappearance of all target lesions or all non-target lesions and normalization of tumor marker levels. (NCT01227707)
Timeframe: BL and within 6 weeks after the completion of study treatment

Interventionpercentage of participants (Number)
CR of target lesion(s)CR of non-target lesion(s)
Bv+Capecitabine/Bv+Leucovorin+5-FU11.6318.60

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OS - Time to Event

OS was defined as the time from the date of first day of treatment until death due to any cause or the last date the participant was known to be alive. OS was estimated using the Kaplan-Meier method. (NCT01227707)
Timeframe: BL, within 6 weeks after the completion of neoadjuvant treatment, every 2 weeks for 1 year following surgery, every 3 months thereafter until death, up to 45 months

Interventionmonths (Mean)
Bv+Capecitabine/Bv+Leucovorin+5-FU32.14

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Maximum Observed Drug Concentration (Cmax) of Capecitabine and 5-fluorouracil

Maximum observed drug concentration, directly taken from analytical data. Geometric mean and percentage geometric coefficient of variation (%CV) were reported. In the listed categories below, 'N' signifies the number of evaluable participants for the drug administered. (NCT01234337)
Timeframe: Pre-dose and 0.5, 1, 2, and 4 hours after capecitabine dosing at Cycle 2, Day 14

,
Interventionmilligram per liter (Geometric Mean)
Capecitabine5-fluorouracil
Placebo + Capecitabine4.680.382
Sorafenib (Nexavar, BAY43-9006) + Capecitabine6.050.434

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Number of Participants With Treatment-emergent Grade 3 and 4 Laboratory Abnormalities

Hematological (anemia, hemoglobin, international normalized ratio [INR], lymphocyte, neutrophil, platelet, white blood cell [WBC]), biochemical (ALT [alanine aminotransferase], AST [aspartate aminotransferase], GGT [gamma-glutamyl-transferase], lipase, hypoalbuminemia, hypocalcemia, hyperglycemia, hyperuricemia) evaluations were done. Common terminology criteria for adverse events (CTCAE) version 4-Grade 3: Severe or medically significant; hospitalization or prolongation of hospitalization and CTCAE version 4-Grade 4: life-threatening consequences; urgent intervention were indicated. (NCT01234337)
Timeframe: From the start of study treatment up to 30 days after the last dose

,
InterventionParticipants (Number)
Anemia (grade 3)Hemoglobin increased (grade 3)INR increased (grade 3)Lymphocyte count decreased (grade 3)Neutrophil count decreased (grade 3)Platelet count decreased (grade 3)WBC decreased (grade 3)ALT increased (grade 3)AST increased (grade 3)Alkaline phosphatase increased (grade 3)Bilirubin increased (grade 3)GGT increased (grade 3)Lipase increased (grade 3)Serum amylase increased (grade 3)Hypoalbuminemia (grade 3)Hypocalcemia (grade 3)Hypokalemia (grade 3)Hyponatremia (grade 3)Hypophosphatemia (grade 3)Hyperglycemia (grade 3)Lymphocyte count decreased (grade 4)Neutrophil count decreased (grade 4)Platelet count decreased (grade 4)WBC decreased (grade 4)ALT increased (grade 4)GGT increased (grade 4)Lipase increased (grade 4)Hypokalemia (grade 4)Hyponatremia (grade 4)Hypophosphatemia (grade 4)Hyperuricemia (grade 4)
Placebo + Capecitabine7391719213551312112426117151027730214000
Sorafenib (Nexavar, BAY43-9006) + Capecitabine12092011615410129221984920947937123652455

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Patient Reported Outcomes: Euroqol-5 Dimensions (EQ-5D) - Visual Analogue Scale (VAS) Score

The EQ-5D was a generic QoL preference based instrument and has been validated in the cancer populations. VAS was generated from 0 (worst imaginable health state) to 100 (best imaginable health state). This VAS score was referred to as the EQ-5D self-reported health status score. The results on ANCOVA of time-adjusted AUC were reported. The time-adjusted AUC was calculated by dividing the AUC by duration (in days) over the period of interest, and reported as 'scores on a scale'. (NCT01234337)
Timeframe: Day 1 of Cycles 1, 3, 5, 7, 9, 11, 13, 16, 19, 22, 25, 28, and EOT (21 days after last dose of study drug)

InterventionScores on a scale (Least Squares Mean)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine67.532
Placebo + Capecitabine69.228

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Patient Reported Outcomes: Euroqol-5 Dimensions (EQ-5D) - Index Score

The EQ-5D was a generic Quality of life (QoL) based instrument validated in cancer populations. EQ-5D questionnaire contained a 5-item descriptive system of health states (mobility, self-care, usual activities, pain/discomfort, anxiety/depression) and visual analogue scale (VAS). A single HRQoL score ranging from -0.59 to 1 was generated from standard scoring algorithm developed by the EuroQoL was the EQ-5D index score, higher scores represent better health status. A change of at least 0.10 to 0.12 points was considered clinically meaningful. The results on the ANCOVA of time-adjusted AUC for the EQ-5D - Index Score were reported. The time-adjusted AUC was calculated by dividing the AUC by duration (in days) over the period of interest, and reported as 'scores on a scale'. (NCT01234337)
Timeframe: Day 1 of Cycles 1, 3, 5, 7, 9, 11, 13, 16, 19, 22, 25, 28, and EOT (21 days after last dose of study drug)

InterventionScores on a scale (Least Squares Mean)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine0.665
Placebo + Capecitabine0.69

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Objective Response Rate (ORR) by Central Review

ORR was defined as the best tumor response (Complete Response [CR] or Partial Response [PR]) observed during treatment or within 30 days after termination of study treatment, assessed according to the RECIST version 1.1. CR=all target lesions disappeared, and any pathological lymph node, whether target or non-target, had a reduction in short axis to <10 mm. If any residual lesion was present, cyto-histology was made available to unequivocally document benignity. PR=at least 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. ORR=CR+PR. CR and PR were confirmed by another scan at least 4 weeks later. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later or until disease radiological progression

InterventionPercentage (%) of participants (Number)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine13.5
Placebo + Capecitabine15.5

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Area Under Curve From Time Zero to Last Quantifiable Concentration (AUC[0-tlast]) of Capecitabine and 5-fluorouracil

AUC(0-tlast) is defined as AUC from time 0 to the last data point, calculated up by linear trapezoidal rule, down by logarithmic trapezoidal rule. Geometric mean and percentage geometric coefficient of variation (%CV) were reported. In the listed categories below, 'N' signifies the number of evaluable participants for the drug administered. (NCT01234337)
Timeframe: Pre-dose and 0.5, 1, 2, and 4 hours after capecitabine dosing at Cycle 2, Day 14

,
Interventionmilligram*hour per liter (Geometric Mean)
Capecitabine5-fluorouracil
Placebo + Capecitabine5.130.557
Sorafenib (Nexavar, BAY43-9006) + Capecitabine7.120.621

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Time to Progression (TTP) by Central Review

TTP was defined as the time from date of randomization to disease radiological progression by central review. Per RECIST version 1.1, progressive disease was determined when there was at least 20% increase in the sum of diameters of the target lesions, taking as a reference the smallest sum on study (this included the baseline sum if that was the smallest sum on trial). In addition to a relative increase of 20%, the sum had demonstrated an absolute increase of at least 5 mm. Appearance of new lesions and unequivocal progression of existing non-target lesions was also interpreted as progressive disease. Participants without progression or death at the time of analysis were censored at their last date of evaluable tumor evaluation. Median and other 95% confidence intervals (CIs) computed using Kaplan-Meier estimates. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later or until disease radiological progression

Interventiondays (Median)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine168
Placebo + Capecitabine165

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Duration of Response (DOR) by Central Reader

DOR was defined as the time from date of first response (CR or PR) to the date when PD is first documented, or to the date of death, whichever occurred first according to RECIST version 1.1. CR=all target lesions disappeared, and any pathological lymph node, whether target or non-target, had a reduction in short axis to <10 mm. If any residual lesion was present, cyto-histology was made available to unequivocally document benignity. PR=at least 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. Participants still having CR or PR and have not died at the time of analysis were censored at their last date of tumor evaluation. DOR defined for confirmed responders only (that is, CR or PR). 'NA' indicates that value could not be estimated due to censored data. Median and 95% CIs were computed using Kaplan-Meier estimates. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later or until disease radiological progression

Interventiondays (Median)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine313
Placebo + Capecitabine290

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Overall Survival (OS)

OS was defined as the time from date of randomization to death due to any cause. Participants still alive at the time of analysis were censored at their last known alive date. Median and other 95% CIs computed using Kaplan-Meier estimates. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later

Interventiondays (Median)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine575
Placebo + Capecitabine616

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Progression-free Survival (PFS) Assessed by the Independent Review Panel According to Response Evaluation Criteria for Solid Tumors (RECIST) 1.1

PFS was defined as the time from date of randomization to disease progression, radiological or death due to any cause, whichever occurs first. Per RECIST version 1.1, progressive disease was determined when there was at least 20% increase in the sum of diameters of the target lesions, taking as a reference the smallest sum on study (this included the baseline sum if that was the smallest sum on trial). In addition to a relative increase of 20%, the sum had demonstrated an absolute increase of at least 5 mm. Appearance of new lesions and unequivocal progression of existing non-target lesions was also interpreted as progressive disease. Participants without progression or death at the time of analysis were censored at their last date of evaluable tumor evaluation. Median and other 95% confidence intervals (CIs) computed using Kaplan-Meier estimates. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years or until disease radiological progression

Interventiondays (Median)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine166
Placebo + Capecitabine165

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Disease Control Rate (DCR) by Central Review

DCR was defined as the proportion of participants whose best response was CR, PR, stable disease (SD) or Non-CR/Non-PD. Per RECIST version 1.1, CR=all target lesions disappeared, any pathological lymph node, target/non-target, a reduction in short axis to <10 mm. PR=at least 30% decrease in the sum of diameters of target lesions taking as reference baseline sum diameters. PD=at least 20% increase in the sum of diameters of the target lesions, taking as a reference smallest sum on study. Appearance of new lesions and unequivocal progression of existing non-target lesions. SD=neither sufficient shrinkage qualified for PR nor sufficient increase qualified for PD, taking smallest sum of diameters as a reference. Non-CR/Non-PD=persistence of 1/more non-target lesion(s) and/or maintenance of tumor marker level above normal limits. DCR=CR+PR+SD or Non-CR/Non-PD. CR and PR confirmed by another scan at least 4 weeks later. SD and Non-CR/Non-PD documented at least 6 weeks after randomization. (NCT01234337)
Timeframe: From randomization of the first participant until approximately 3 years later or until disease radiological progression

Interventionpercentage (%) of participants (Number)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine60.5
Placebo + Capecitabine58.3

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Patient Reported Outcomes: Functional Assessment of Cancer Therapy-Breast Symptom Index (8 Item) (FBSI-8)

The FBSI-8 was an 8-item questionnaire. Participants responded to each item using a 5-point Likert-type scale ranging from 0 (not at all) to 4 (very much). A total scale score was calculated (range from 0 to 32), with higher scores indicating low symptomatology and reflecting a better Health-Related Quality of Life (HRQoL). The results on the analysis of covariance (ANCOVA) of time-adjusted area under curve (AUC) for the FBSI-8 score were reported. The time-adjusted AUC was calculated by dividing the AUC by duration (in days) over the period of interest, and reported as 'scores on a scale'. (NCT01234337)
Timeframe: Day 1 of Cycles 1, 3, 5, 7, 9, 11, 13, 16, 19, 22, 25, 28, 31, 34, 37, and end of treatment (EOT, 21 days after last dose of study drug)

InterventionScores on a scale (Least Squares Mean)
Sorafenib (Nexavar, BAY43-9006) + Capecitabine20.915
Placebo + Capecitabine21.356

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Overall Survival (OS)

Overall survival is defined as the time from the date of randomization to the date of death from any cause. If the participant is alive at the end of the follow-up period or is lost to follow-up, OS will be censored on the last date the participant is known to be alive. (NCT01234402)
Timeframe: From Date of Randomization until Death Due to Any Cause (Up To 160 weeks)

InterventionWeeks (Median)
Ramucirumab + Capecitabine67.4
Icrucumab + Capecitabine62.1
Capecitabine71.6

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Number of Participants With Serious Adverse Events (SAEs)

"SAE was defined as any untoward medical occurrence that at any dose:~Resulted in death; Was life-threatening; Required inpatient hospitalization or caused prolongation of existing hospitalization; Resulted in persistent or significant disability/incapacity; Was a congenital anomaly/birth defect; Required intervention to prevent permanent impairment/damage; Was an important medical event (defined as a medical event that may not have been immediately life-threatening or resulted in death or hospitalization but, based upon appropriate medical and scientific judgment, may jeopardize the participant or may require intervention to prevent one of the other serious outcomes listed in the definition above).~A summary of other nonserious AEs, and all SAE's, regardless of causality, is located in the Reported Adverse Events section." (NCT01234402)
Timeframe: Up To 160 Weeks

InterventionParticipants (Count of Participants)
Ramucirumab + Capecitabine20
Icrucumab + Capecitabine25
Capecitabine6

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Area Under the Concentration Versus Time Curve From Time Zero to Infinity of Ramucirumab or Icrucumab

Area Under the Concentration (AUC) Versus Time Curve From Time Zero to Infinity of Ramucirumab and Icrucumab. (NCT01234402)
Timeframe: Cycle 1: Pre-infusion, 1h, 48h, 72h, 168, 336h post infusion

Interventionmicrogram*hour/mL (Geometric Mean)
Ramucirumab + Capecitabine54400

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Number of Participants With Anti-Ramucirumab and Anti-Icrucumab Antibodies

(NCT01234402)
Timeframe: Cycle 1: Pre-infusion, 1h, 48h, 72h, 168, 336h post infusion

InterventionParticipants (Count of Participants)
Treatment emergent antibodyNeutralizing antibody
Ramucirumab + Capecitabine00

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Minimum Concentration (Cmin) Ramucirumab Drug Product (DP) or Icrucumab

Minimum Concentration (Cmin) Ramucirumab Drug Product (DP) or Icrucumab. (NCT01234402)
Timeframe: Cycle 2,4,6,8,0,12,14,16,18,22: Pre-infusion, 1h, 48h, 72h, 168, 336h post infusion

InterventionMicro gram per milliliter (Geometric Mean)
Cycle 2Cycle 4Cycle 6Cycle 8Cycle 10Cycle 12Cycle 14Cycle 16Cycle 18Cycle 22
Ramucirumab + Capecitabine23.780.644.765.866.874.362.550.550.555.0

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Volume of Distribution at Steady State (Vss) of Ramucirumab or Icrucumab

Volume of Distribution at Steady State (Vss) of Ramucirumab and Icrucumab. (NCT01234402)
Timeframe: Cycle 1: Pre-infusion, 1h, 48h, 72h, 168, 336h post infusion

InterventionLiters (Geometric Mean)
Ramucirumab + Capecitabine3.17

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Number of Participants With Adverse Events (AEs)

"Adverse event (AE) will be regarded as treatment-emergent if onset date occurs any time on or after the administration of the first dose of study treatment up to 30 days after the last dose of study treatment (or up to any time if related to study treatment); or it occurs prior to first dose date and worsens while on therapy or up to 30 days after the last dose of study treatment (or up to any time if related to study treatment).~A summary of other nonserious AEs, and all SAE's, regardless of causality, is located in the Reported Adverse Events section." (NCT01234402)
Timeframe: Up To 160 Weeks

InterventionParticipants (Count of Participants)
Ramucirumab + Capecitabine52
Icrucumab + Capecitabine49
Capecitabine48

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Duration of Response

Duration of response is measured from the time measurement criteria are first met for CR/PR (whichever is first recorded) until the first date that the criteria for progressive disease (PD) is met (taking as a reference for PD that smallest measurement recorded since the treatment started), or death, is objectively documented.CR was defined as the disappearance of all non-nodal target lesions, with the short axes of any target lymph nodes reduced to <10 mm. PR was defined as ≥30% decrease in the sum of the diameters of target lesions (including the short axes of any target lymph nodes), taking as reference the baseline sum diameter.PD defined as ≥20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). Sum must also have demonstrated an absolute increase of ≥5 mm, or the appearance of 1 or more new lesions was considered progression. (NCT01234402)
Timeframe: From Date of CR, PR until Disease Progression or Death Due to Any Cause (Up To 97 weeks)

Interventionweeks (Median)
Ramucirumab + Capecitabine43.1
Icrucumab + Capecitabine20.1
Capecitabine17.1

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Clearance (Cl) of Ramucirumab or Icrucumab

Clearance (Cl) of Ramucirumab and Icrucumab. (NCT01234402)
Timeframe: Cycle 1: Pre-infusion, 1h, 48h, 72h, 168, 336h post infusion

InterventionLiters per hour (Geometric Mean)
Ramucirumab + Capecitabine0.0141

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Maximum Concentration (Cmax) Ramucirumab Drug Product (DP) or Icrucumab

(NCT01234402)
Timeframe: Cycle 1: Pre-infusion, 1h, 48h, 72h, 168, 336h post infusion

InterventionMicrogram per milliliter (Geometric Mean)
Ramucirumab + Capecitabine308

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Progression-Free Survival (PFS)

PFS is defined as the time from the date of randomization until the date of objectively determined progression as defined by Response Evaluation Criteria in Solid Tumors (RECIST v1.1) or death from any cause, whichever is first. Disease progression is defined as ≥20% increase in the sum of diameters of target lesions, taking as reference smallest sum on study (included baseline sum if that was the smallest on study); sum must have demonstrated an absolute increase of ≥5 millimeter (mm) and the appearance of ≥1 new lesions was progression. Participants who did not progress, were lost to follow-up, or had missed 2 or more scheduled tumor assessments were censored at the day of their last adequate tumor assessment. (NCT01234402)
Timeframe: From Date of Randomization until Disease Progression or Death Due to Any Cause (Up To 97 weeks)

InterventionWeeks (Median)
Ramucirumab + Capecitabine22.1
Icrucumab + Capecitabine7.3
Capecitabine19.0

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Terminal Half-life (t½) of Ramucirumab or Icrucumab

Terminal half-life (t½) of Ramucirumab and Icrucumab. (NCT01234402)
Timeframe: Cycle 1: Pre-infusion, 1h, 48h, 72h, 168, 336h post infusion

InterventionDays (Geometric Mean)
Ramucirumab + Capecitabine6.80

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Percentage of Participants With Objective Response Rate (ORR)

The ORR is the number of all participants with Partial Response (PR) or Complete Response (CR) according to RECIST v1.1 from the start of the treatment until disease progression/recurrence. CR was defined as the disappearance of all non-nodal target lesions, with the short axes of any target lymph nodes reduced to <10 mm. PR was defined as ≥30% decrease in the sum of the diameters of target lesions (including the short axes of any target lymph nodes), taking as reference the baseline sum diameter. Disease progression is defined as ≥20% increase in the sum of diameters of target lesions, taking as reference smallest sum on study (included baseline sum if that was the smallest on study); sum must have demonstrated an absolute increase of ≥5 mm and the appearance of ≥1 new lesions was progression. (NCT01234402)
Timeframe: From Date of Randomization until Disease Progression/Recurrence (Up to 97 weeks)

InterventionPercentage of Participants (Number)
Ramucirumab + Capecitabine28.8
Icrucumab + Capecitabine20.4
Capecitabine34.7

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Survival

Overall survival is defined as the length of time from start of treatment to death from any cause. Estimated using the Kaplan-Meier method. (NCT01267240)
Timeframe: Up to 1 year

Interventionmonths (Median)
Arm I (Capecitabine, Vorinostat)10.8

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Progression-free Survival

"PFS is defined as the duration of time from start of treatment to time of progression, death, or completion of the 1-year follow-up, whichever occurs first.~Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as at least a 20% increase in the sum of the longest diameter of target lesions." (NCT01267240)
Timeframe: From time of treatment initiation to disease progression, death, or completion of the 1 year follow-up, whichever occurs first.

Interventionmonths (Median)
Arm I (Capecitabine, Vorinostat)2.3

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Response Rate According to Response Evaluation Criteria in Solid Tumors

Per Response Evaluation Criteria in Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by CT and MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters; Overall Response (OR) = CR + PR. (NCT01267240)
Timeframe: Up to 1 year

Interventionparticipants (Number)
Arm I (Capecitabine, Vorinostat)2

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Overall Survival

Overall survival was defined as the time (in months) from randomization to death. (NCT01279681)
Timeframe: Up to 5 years

Interventionmonths (Median)
Arm A [Fluoropyrimidine + Bevacizumab (BEV)]18.8
Arm B [Fluoropyrimidine/Oxaliplatin (OXAL) + BEV]15.4

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Progression-Free Survival

Progression was defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. Progression free survival was defined as the time (in months) from the date of randomization to the date of documented disease progression or death, whichever occurs first. Patients were followed until progression (and progression was declared) regardless of whether the patient was on the first line treatment or not. Patients who progress following a missed scan will have their date of progression back-dated to the date of missing scan. Patients without a progression who are still alive at the time of analysis will be censored at the date of last follow-up. (NCT01279681)
Timeframe: Up to 5 years

Interventionmonths (Median)
Arm A [Fluoropyrimidine + Bevacizumab (BEV)]6.7
Arm B [Fluoropyrimidine/Oxaliplatin (OXAL) + BEV]6.7

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Response Rate, Defined as the Percentage of Patients in Each Arm Who Have an Objective Status of Complete Response or Partial Response, Confirmed by a Second Assessment Measured at Least 6 Weeks From the Initial Assessment

"Response was defined using Response Evaluation Criteria In Solid Tumors (RECIST) criteria:~Complete Response (CR): disappearance of all target lesions;~Partial Response (PR) 30% decrease in sum of longest diameter of target lesions;~Progressive Disease (PD): 20% increase in sum of longest diameter of target lesions;~Stable Disease (SD): small changes that do not meet above criteria.~Response rate is reported as the percentage of participants who achieved Complete Response or Partial Response." (NCT01279681)
Timeframe: Up to 5 years

Interventionpercentage of participants (Number)
Arm A [Fluoropyrimidine + Bevacizumab (BEV)]47
Arm B [Fluoropyrimidine/Oxaliplatin (OXAL) + BEV]38

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Phase 2: Clinical Benefit Rate (CBR)

CBR was defined as the percentage of participants with a confirmed CR, PR, or SD of at least 6 months duration (durable SD) divided by the number of participants in the analysis set. CBR was determined by an investigator based on RECIST v1.1. CR: disappearance of all target lesions. All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis to <10 mm. PR: at least a 30% decrease in the sum of the longest diameter of target lesions, taking as reference the baseline sum of the longest diameter. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study. PD: at least a 20% increase in sum of diameters of target lesions, taking as reference the smallest sum on study (this includes baseline sum if that is the smallest on study). CBR was summarized using the Clopper-Pearson method. (NCT01323530)
Timeframe: From the first dose of study drug until PD or 30 days after the last dose of study treatment (up to approximately 3.75 years)

Interventionpercentage of participants (Number)
Phase 2: Eribulin Mesilate 1.4 mg/m^257.1

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Phase 2: Stable Disease (SD) Rate

SD rate was defined as the percentage of participants with a SD that lasted for a minimum of 5 weeks. SD rate was assessed based on RECIST version 1.1. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study. PR: at least a 30% decrease in sum of longest diameter of target lesions, taking as reference the baseline sum of longest diameter. PD: at least a 20% increase in sum of diameters of target lesions, taking as reference the smallest sum on study (this includes baseline sum if that is the smallest on study). (NCT01323530)
Timeframe: From the first dose of study drug until PD or up to 30 days after the last dose of study treatment (up to approximately 3.75 years)

Interventionpercentage of participants (Number)
Phase 2: Eribulin Mesilate 1.4 mg/m^238.1

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Phase 2: Duration of Response (DOR)

DOR: time from first documented evidence of CR or PR until first documented sign of PD or death. DOR was assessed based on RECIST v 1.1. CR: disappearance of all target lesions. All pathological lymph nodes (whether target/non-target) must have a reduction in their short axis to >10 mm. PR: at least a 30% decrease in sum of longest diameter of target lesions, taking as reference the baseline sum of longest diameter. PD: at least a 20% increase in sum of diameters of target lesions, taking as reference the smallest sum on study (this includes baseline sum if that is the smallest on study). DOR was summarized using the Kaplan-Meier method. (NCT01323530)
Timeframe: From date of the first CR or PR until the date of first documentation of PD or death or up to 30 days after the last dose of study treatment (up to approximately 3.75 years)

Interventiondays (Median)
Phase 2: Eribulin Mesilate 1.4 mg/m^2261.0

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Phase 2: Disease Control Rate (DCR)

DCR was defined as the percentage of participants with a confirmed CR, PR, or SD divided by the number of participants in the analysis set. DCR was assessed by an investigator based on RECIST v1.1. CR: disappearance of all target lesions. All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis to <10 mm. PR: at least a 30% decrease in the sum of the longest diameter of target lesions, taking as reference the baseline sum of the longest diameter. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study. PD: at least a 20% increase in sum of diameters of target lesions, taking as reference the smallest sum on study (this includes baseline sum if that is the smallest on study). DCR was summarized using the Clopper-Pearson method. (NCT01323530)
Timeframe: From the first dose of study drug until PD or 30 days after the last dose of study treatment (up to approximately 3.75 years)

Interventionpercentage of participants (Number)
Phase 2: Eribulin Mesilate 1.4 mg/m^281.0

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Phase 2: Objective Response Rate (ORR)

ORR was defined as the percentage of participants who had either a confirmed complete response (CR) or partial response (PR). ORR was assessed based on Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST v 1.1). CR was defined as disappearance of all target lesions. All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis to less than (<) 10 millimeter (mm). PR was defined as at least a 30 percent (%) decrease in the sum of the longest diameter of target lesions, taking as reference the baseline sum of the longest diameter. ORR was summarized using the Clopper-Pearson method. (NCT01323530)
Timeframe: From the first dose of study drug until PD or up to 30 days after the last dose of study treatment (up to approximately 3.75 years)

Interventionpercentage of participants (Number)
Phase 2: Eribulin Mesilate 1.4 mg/m^242.9

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Phase 2: Progression-free Survival (PFS)

PFS was defined as the time from the first dose date until PD or death due to any cause. PFS was determined by an investigator based on RECIST v1.1. PD: at least a 20% increase in sum of diameters of target lesions, taking as reference the smallest sum on study (this includes baseline sum if that is the smallest on study). PFS was summarized using the Kaplan-Meier method. (NCT01323530)
Timeframe: From the first dose of study drug until PD or death due to any cause or 30 days after the last dose of study treatment (up to approximately 3.75 years)

Interventiondays (Median)
Phase 2: Eribulin Mesilate 1.4 mg/m^2219.0

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Phase 2: Time to Response

Time to response (CR or PR) was defined as the time from the first dose until first documented evidence of CR or PR (whichever status was recorded first). Time to response was assessed based on RECIST v 1.1. CR was defined as disappearance of all target lesions. All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis to less than 10 mm. PR was defined as at least a 30% decrease in the sum of the longest diameter of target lesions, taking as reference the baseline sum of the longest diameter. Time to response was summarized using the Kaplan-Meier method. (NCT01323530)
Timeframe: From the first dose of study drug treatment start date until date of first documented evidence of CR or PR or up to 30 days after the last dose of study treatment (up to approximately 3.75 years)

Interventiondays (Median)
Phase 2: Eribulin Mesilate 1.4 mg/m^244.0

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Phase 2: Duration of Stable Disease (SD)

Duration of SD was measured from date of the first dose until progression. Duration of SD was assessed based on RECIST v1.1. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study. PR: at least a 30% decrease in sum of longest diameter of target lesions, taking as reference the baseline sum of longest diameter. PD: at least a 20% increase in sum of diameters of target lesions, taking as reference the smallest sum on study (this includes baseline sum if that is the smallest on study). Duration of SD was summarized using the Kaplan-Meier method. (NCT01323530)
Timeframe: From the first dose of study drug until PD or 30 days after the last dose of study treatment (up to approximately 3.75 years)

Interventiondays (Median)
Phase 2: Eribulin Mesilate 1.4 mg/m^2162.0

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Phase 1b and Phase 2: Percentage of Participants With Non-CR/Non-PD

Non-CR/Non-PD was for participants who had non-target disease only (minimum duration from randomization to Non-CR/Non-PD >=7 weeks) and assessed by investigator based on RECIST v1.1. Non-CR/Non-PD: persistence of one or more non-target lesions, maintenance of tumor marker level above the normal limits. (NCT01323530)
Timeframe: From the first dose of study drug until PD or up to 30 days after the last dose of study treatment (up to approximately 3.75 years)

Interventionpercentage of participants (Number)
Phase 1b (Schedule 1): Eribulin Mesilate (1.2 mg/m^2)0
Phase 1b (Schedule 1): Eribulin Mesilate (1.6 mg/m^2)0
Phase 1b (Schedule 1): Eribulin Mesilate (2.0 mg/m^2)0
Phase 1b (Schedule 2): Eribulin Mesilate (0.7 mg/m^2)0
Phase 1b (Schedule 2): Eribulin Mesilate (1.1 mg/m^2)16.7
Phase 1b (Schedule 2): Eribulin Mesilate (1.4 mg/m^2)0
Phase 2: Eribulin Mesilate 1.4 mg/m^20

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Phase 1b: Number of Participants With Dose-limiting Toxicities (DLTs) as Per National Cancer Institute Common Terminology Criteria for Adverse Events Version 3.0 (NCI CTCAE v3.0)

DLTs as per NCI CTCAE v3.0 were defined as:1) Neutropenia Grade 4 that lasted at least 7 days, 2) Neutropenia Grade 3 or 4 complicated by fever and/or infection (absolute neutrophil count [ANC] less than 1.0*10^9/liter [L], fever of at least 38.5 degree celsius [°C]), 3)Thrombocytopenia Grade 4, 4) Thrombocytopenia Grade 3 complicated by bleeding and/or requiring platelet or blood transfusion, 5) Non-hematological toxicity Grade 3 or higher (excluding Grade 3 nausea, and Grade 3 or 4 vomiting or diarrhea in participants who had not received optimal treatment with antiemetic and/or antidiarrheal medication; excluding laboratory abnormalities without clinical symptoms), 6) Delayed recovery from treatment-related toxicity resulting in dose delay greater than 14 days, 7) Failure to administer at least 75 percent (%) of planned study drugs during Cycle 1 as result of Grade 2 or higher treatment-related toxicity that constituted increase of at least 2 grades from baseline. (NCT01323530)
Timeframe: Cycle 1 (21 days)

InterventionParticipants (Count of Participants)
Phase 1b (Schedule 1): Eribulin Mesilate (1.2 mg/m^2)1
Phase 1b (Schedule 1): Eribulin Mesilate (1.6 mg/m^2)1
Phase 1b (Schedule 1): Eribulin Mesilate (2.0 mg/m^2)2
Phase 1b (Schedule 2): Eribulin Mesilate (0.7 mg/m^2)0
Phase 1b (Schedule 2): Eribulin Mesilate (1.1 mg/m^2)1
Phase 1b (Schedule 2): Eribulin Mesilate (1.4 mg/m^2)1

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TRC105 Steady State Pharmacokinetic Trough Concentration at the RP2D

Mean trough concentration for patients dosed at 10 mg/kg at cycle 2 day 1 (NCT01326481)
Timeframe: Cycle 2 day 1 (3 weeks)

Interventionng/mL (Mean)
Single66668.75

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Number of Participants With a Treatment-Emergent Adverse Event (TEAE)

Safety assessments consisted of monitoring and recording all adverse events (AEs) and serious AEs; regular monitoring of hematology, blood chemistry, and urine values; periodic measurement of vital signs and electrocardiograms (ECGs); and performance of physical examinations. A TEAE was defined as an adverse event (AE) that had an onset date, or a worsening in severity from Baseline (pretreatment), on or after the first dose of study drug up to 30 days after the date of last study treatment. (NCT01355302)
Timeframe: From date of first dose up to 30 days after the last dose of study treatment, up to approximately 1 year 1 month.

InterventionParticipants (Number)
Phase 1b: Golvatinib+Capecitabine+Cisplatin7

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Area Under The Concentration-Time Curve (AUC) From 0 to 24 Hours of Golvatinib

On days when pharmacokinetic (PK) samples were to be drawn, a predose blood sample was obtained prior to administration of golvatinib and capecitabine. After administration of study drugs, a second postdose blood sample was taken. The amount of golvatinib in the participant's blood was analyzed and the AUC was calculated. The AUC reflects the actual body exposure to drug after administration of a dose of the drug and is dependent on the rate of elimination of the drug from the body and the dose administered. Predose samples that were below the limit of quantitation (BLQ) or missing were assigned a numerical value of zero for the calculation of AUC. Any other BLQ concentrations were assigned a value of zero. Results were expressed in nanograms·hour/milliter (ng·h/mL). (NCT01355302)
Timeframe: Cycle 1 (Day -2); predose, 30 minutes, 1, 2, 3, 4, 8, 12 (if feasible), 24, and 48 hours after study treatment. Cycle 2 (Day 1); predose, 30 minutes, 1, 2, 3, 4, 8, 12 (if feasible), and 24 hours after study treatment.

Interventionng·h/mL (Median)
Cycle 1, Day -2Cycle 2, Day 1
Phase 1b: Golvatinib+Capecitabine+Cisplatin2340026300

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Maximum Concentration (Cmax) of Golvatinib

Blood samples were drawn to analyze the amount of golvatinib in the participant's serum. Maximum concentration refers to the maximum (or peak) serum concentration of study drug in the participant's system after administration of the study drug and prior to the administration of a second dose of the study drug. Results were expressed in nanograms/milliliter (ng/mL). (NCT01355302)
Timeframe: Cycle 1 (Day -2); predose, 30 minutes, 1, 2, 3, 4, 8, 12 (if feasible), 24, and 48 hours after study treatment. Cycle 2 (Day 1); predose, 30 minutes, 1, 2, 3, 4, 8, 12 (if feasible), and 24 hours after study treatment.

Interventionng/mL (Median)
Cycle 1, Day -2Cycle 2, Day 1
Phase 1b: Golvatinib+Capecitabine+Cisplatin16801620

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Time to Maximum Concentration (Tmax) of Golvatinib

Tmax was defined as the time at which Cmax was observed for golvatinib in combination with cisplatin and capecitabine. (NCT01355302)
Timeframe: Cycle 1 (Day -2); predose, 30 minutes, 1, 2, 3, 4, 8, 12 (if feasible), 24, and 48 hours after study treatment. Cycle 2 (Day 1); predose, 30 minutes, 1, 2, 3, 4, 8, 12 (if feasible), and 24 hours after study treatment.

InterventionHours (Median)
Cycle 1, Day -2Cycle 2, Day 1
Phase 1b: Golvatinib+Capecitabine+Cisplatin3.006.07

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Objective Response Rate (ORR) (Surgery After Chemotherapy and SBRT)

Percentage of participants with response per RECIST v1.0. Per RECIST v1.0: Complete Response (CR): the disappearance of a lesion; Near Complete Response (NCR): at least an 80% decrease in the longest diameter of a lesion, taking as reference the longest diameter recorded since the treatment started. Partial Response (PR): at least a 30% decrease in the longest diameter of a lesion, taking as reference the longest diameter recorded since the treatment started. (NCT01360593)
Timeframe: Up to 24 months

Interventionpercentage of participants (Number)
Gem + Xeloda + SBRT20.0

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Acute Toxicities Associated With SBRT

Percentage of patients that experience treatment-related toxicities as graded according to Common Terminology Criteria for Adverse Events (CTCAE v4), within 3 months after treatment, by grade. Patients were monitored for potential toxicity throughout treatment. (NCT01360593)
Timeframe: Up to 3 months following SBRT treatment

Interventionpercentage of participants (Number)
Grade 1Grade 2Grade 3Grade 4
Gem + Xeloda + SBRT88.2429.4114.712.94

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Objective Response Rate (ORR) (Neoadjuvant Chemotherapy)

Percentage of participants with response per RECIST v1.0. Per RECIST v1.0: Complete Response (CR): the disappearance of a lesion; Near Complete Response (NCR): at least an 80% decrease in the longest diameter of a lesion, taking as reference the longest diameter recorded since the treatment started. Partial Response (PR): at least a 30% decrease in the longest diameter of a lesion, taking as reference the longest diameter recorded since the treatment started. (NCT01360593)
Timeframe: Up to 24 months

Interventionpercentage of participants (Number)
Gem + Xeloda + SBRT28.13

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Overall Survival (OS)

The (median) length of time from enrollment to confirmed death from any cause. (NCT01360593)
Timeframe: Up to 32 months

Interventionmonths (Median)
Gem + Xeloda + SBRT18.82546

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The Functional Assessment of Cancer Therapy - General (FACT-G)

The Functional Assessment of Cancer Therapy - General (FACT-G) is a self-administered, 27-item questionnaire designed to measure four domains of HRQOL in cancer patients: Physical, social, emotional, and functional well-being. Quality of Life (QOL) evaluation will be administered prior to SBRT, after completion of SBRT, and at each follow-up. Scaling of items: Five-point scale for each questions from 0 (not at all) to 4 (very much); overall scoring 0-108. Higher scores indicated better quality of life. (NCT01360593)
Timeframe: Baseline; 2 - 4 weeks post chemotherapy; 4-6 weeks post SBRT; after surgery (up to 24 months)

Interventionscore on a scale (Median)
Baseline2-4 weeks after Chemo4-6 weeks after SBRTafter Surgery, up to 24 months
Gem + Xeloda + SBRT54.054.051.549.5

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Number of Participants Able to Undergo a Margin-negative Resection After Neoadjuvant Therapy

Number of patients that are able to undergo a margin-negative resection after neoadjuvant therapy. Surgical evaluation: pathology records reviewed by operating surgeon to determine margin status as negative (not close (1-2.5mm), microscopically positive, and/or grossly positive). (NCT01360593)
Timeframe: Up to 24 months

InterventionParticipants (Count of Participants)
Gem + Xeloda + SBRT11

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Local Progression-free Survival (LPFS)

LPFS is defined as the time from enrollment to first documentation of progressive disease (PD) in the target lesion. For patients that undergo surgical resection, local progression will be defined as disease recurrence detected on follow-up imaging (CT or FDG-PET/CT) that is located within the SBRT target volume. Death or development of distant disease is not regarded as an event. Per Response Evaluation Criteria in Solid Tumors (RECIST) v1.0, progressive disease is defined as at least a 25% increase in the longest diameter of a lesion, taking as reference the longest diameter recorded since the treatment started. (NCT01360593)
Timeframe: Up to 32 months

Interventionmonths (Median)
Gem + Xeloda + SBRT22.30801

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Late Toxicities Associated With SBRT

Percentage of patients that experience treatment-related toxicities as graded according to Common Terminology Criteria for Adverse Events (CTCAE v4), greater than 3 months after treatment, by grade. Patients were monitored for potential toxicity throughout treatment. (NCT01360593)
Timeframe: From 3 months following SBRT treatment up to 24 months

Interventionpercentage of participants (Number)
Gem + Xeloda + SBRT0

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Time to Progression (TTP)

The (median) length of time from enrollment to disease progression per Response Evaluation Criteria in Solid Tumors (v1.0). Per RECIST, Progressive Disease (PD) is defined at least a 25% increase in the longest diameter of a lesion, taking as reference the longest diameter recorded since the treatment started. For lesions without size response the maintenance of CA 19-9 level above the normal limits indicates disease progression. (NCT01360593)
Timeframe: Up to 5 years

Interventionmonths (Median)
Gem + Xeloda + SBRT16

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Number of Subjects With Adverse Events (AEs) and Serious AEs

Safety and tolerability will be assessed in accordance to the protocol of the parent study in which the subjects had participated, before enrolling in the AV-951-09-901 rollover study. (NCT01369433)
Timeframe: 24 Months

,
InterventionParticipants (Count of Participants)
AEsTreatment-related AEsAEs ≥Grade 3 toxicityAEs-study drug interruptionAEs-study drug dose reductionAEs-discontinuation of study drugAEs-deathSerious Adverse events (SAEs)SAEs ≥Grade 3 toxicitySerious treatment-related AEs
Combination Therapy1615126011550
Monotherapy17815911154133113443816

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PFS According to RECIST Version 1.1 in Participants With High ERCC-1 and Low VEGF-A Levels

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as ≥20% increase in sum of LD of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 mm. Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX6 (ERCC-1 High, VEGF-A Low)12.52
Bevacizumab + FOLFIRI (ERCC-1 High, VEGF-A Low)12.68

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PFS According to RECIST Version 1.1 in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as ≥20% increase in sum of LD of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 mm. Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 High)10.87
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 Low)11.56

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PFS According to RECIST Version 1.1 in Participants With High Vascular Endothelial Growth Factor (VEGF)-A Levels Versus Participants With Low VEGF-A Levels

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as ≥20% increase in sum of LD of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 mm. Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A High)10.02
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A Low)12.68

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PFS According to RECIST Version 1.1 in Participants With Low ERCC-1 and High VEGF-A Levels

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as ≥20% increase in sum of LD of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 mm. Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX6 (ERCC-1 Low, VEGF-A High)9.76
Bevacizumab + FOLFIRI (ERCC-1 Low, VEGF-A High)11.07

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PFS According to RECIST Version 1.1 in Participants With Low ERCC-1 and Low VEGF-A Levels

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as ≥20% increase in sum of LD of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 mm. Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX6 (ERCC-1 Low, VEGF-A Low)11.10
Bevacizumab + FOLFIRI (ERCC-1 Low, VEGF-A Low)14.32

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Percentage of Participants With Objective Response According to RECIST Version 1.1

Objective response was defined as complete response (CR) or partial response (PR) according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to less than (<) 10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. The percentage of participants with CR or PR was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX661.2
Bevacizumab + FOLFIRI65.4

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PFS According to RECIST Version 1.1 in Participants With Low ERCC-1 Levels

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as ≥20% increase in sum of LD of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 mm. Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX6 (ERCC-1 Low)10.97
Bevacizumab + FOLFIRI (ERCC-1 Low)12.68

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Percentage of Participants With Disease Control According to RECIST Version 1.1 in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels

Disease control was defined as CR, PR, or SD according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. SD was defined as neither sufficient shrinkage to quality for PR nor sufficient increase to qualify for disease progression (≥20% increase in sum of LD of target lesions plus absolute increase ≥5 mm) in reference to the smallest sum of LD on study. The percentage of participants with CR, PR, or SD was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A High)91.9
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A Low)93.0

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OS in Participants With High ERCC-1 Levels

Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. OS was defined as the time from randomization to death. The median duration of OS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX6 (ERCC-1 High)22.54
Bevacizumab + FOLFIRI (ERCC-1 High)26.51

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Percentage of Participants With Liver Metastasis Resection

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. R1 was defined as the presence of exposed tumor or histologically detected tumor cells at the line of transection, or <1 mm microscopic margins. In the case of use of radiofrequency ablation or cryotherapy, the resection was considered as R1. R2 was defined as macroscopic positive margins or incomplete resection at time of surgery. The percentage of participants with resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX614.9
Bevacizumab + FOLFIRI10.9

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Percentage of Participants With Liver Metastasis Resection in Participants With High ERCC-1 Levels

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. R1 was defined as the presence of exposed tumor or histologically detected tumor cells at the line of transection, or <1 mm microscopic margins. In the case of use of radiofrequency ablation or cryotherapy, the resection was considered as R1. R2 was defined as macroscopic positive margins or incomplete resection at time of surgery. The percentage of participants with resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX6 (ERCC-1 High)17.6
Bevacizumab + FOLFIRI (ERCC-1 High)6.7

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Percentage of Participants With Liver Metastasis Resection in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. R1 was defined as the presence of exposed tumor or histologically detected tumor cells at the line of transection, or <1 mm microscopic margins. In the case of use of radiofrequency ablation or cryotherapy, the resection was considered as R1. R2 was defined as macroscopic positive margins or incomplete resection at time of surgery. The percentage of participants with resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 High)4.6
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 Low)9.0

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Percentage of Participants With Liver Metastasis Resection in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. R1 was defined as the presence of exposed tumor or histologically detected tumor cells at the line of transection, or <1 mm microscopic margins. In the case of use of radiofrequency ablation or cryotherapy, the resection was considered as R1. R2 was defined as macroscopic positive margins or incomplete resection at time of surgery. The percentage of participants with resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A High)5.9
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A Low)9.2

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Percentage of Participants With Liver Metastasis Resection in Participants With Low ERCC-1 Levels

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. R1 was defined as the presence of exposed tumor or histologically detected tumor cells at the line of transection, or <1 mm microscopic margins. In the case of use of radiofrequency ablation or cryotherapy, the resection was considered as R1. R2 was defined as macroscopic positive margins or incomplete resection at time of surgery. The percentage of participants with resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX6 (ERCC-1 Low)10.5
Bevacizumab + FOLFIRI (ERCC-1 Low)7.5

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OS in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels

Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. OS was defined as the time from randomization to death. The median duration of OS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 High)23.23
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 Low)27.27

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Progression-Free Survival (PFS) According to Response Evaluation Criteria in Solid Tumors (RECIST) Version 1.1

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as greater than or equal to (≥) 20 percent (%) increase in sum of largest diameters (LD) of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 millimeters (mm). Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% confidence interval (CI) was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX610.09
Bevacizumab + FOLFIRI12.55

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PFS According to RECIST Version 1.1 in Participants With Wild-Type V-Ki-ras2 Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) Versus Participants With Mutant KRAS

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as ≥20% increase in sum of LD of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 mm. Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX/FOLFIRI (KRAS Wild-Type)12.45
Bevacizumab + mFOLFOX/FOLFIRI (KRAS Mutant)10.94

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PFS According to RECIST Version 1.1 in Participants With High ERCC-1 Levels

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as ≥20% increase in sum of LD of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 mm. Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX6 (ERCC-1 High)9.92
Bevacizumab + FOLFIRI (ERCC-1 High)11.17

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Percentage of Participants With Complete Liver Metastasis Resection

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. The percentage of participants with R0 resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX611.9
Bevacizumab + FOLFIRI5.5

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Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With High ERCC-1 Levels

Objective response was defined as CR or PR according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. The percentage of participants with CR or PR was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX6 (ERCC-1 High)56.3
Bevacizumab + FOLFIRI (ERCC-1 High)65.7

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Percentage of Participants With Complete Liver Metastasis Resection in Participants With High ERCC-1 Levels

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. The percentage of participants with R0 resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX6 (ERCC-1 High)17.6
Bevacizumab + FOLFIRI (ERCC-1 High)6.7

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Percentage of Participants With Complete Liver Metastasis Resection in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. The percentage of participants with R0 resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 High)4.6
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 Low)6.1

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Overall Survival (OS)

Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. OS was defined as the time from randomization to death. The median duration of OS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX623.85
Bevacizumab + FOLFIRI27.47

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Percentage of Participants With Complete Liver Metastasis Resection in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. The percentage of participants with R0 resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A High)3.2
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A Low)8.1

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Percentage of Participants With Complete Liver Metastasis Resection in Participants With Low ERCC-1 Levels

The timing of resective surgery was not defined in the protocol and was left at the discretion of the Investigator. Resection was classified as R0, R1, or R2 following surgery. R0 was defined as complete resection with clear margins ≥1 mm. The percentage of participants with R0 resection of liver or liver plus lymph node metastases was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: At time of resective surgery during study (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX6 (ERCC-1 Low)8.9
Bevacizumab + FOLFIRI (ERCC-1 Low)3.3

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Percentage of Participants With Disease Control According to RECIST Version 1.1

Disease control was defined as CR, PR, or stable disease (SD) according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. SD was defined as neither sufficient shrinkage to quality for PR nor sufficient increase to qualify for disease progression (≥20% increase in sum of LD of target lesions plus absolute increase ≥5 mm) in reference to the smallest sum of LD on study. The percentage of participants with CR, PR, or SD was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX693.1
Bevacizumab + FOLFIRI91.0

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Percentage of Participants With Disease Control According to RECIST Version 1.1 in Participants With High ERCC-1 Levels

Disease control was defined as CR, PR, or SD according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. SD was defined as neither sufficient shrinkage to quality for PR nor sufficient increase to qualify for disease progression (≥20% increase in sum of LD of target lesions plus absolute increase ≥5 mm) in reference to the smallest sum of LD on study. The percentage of participants with CR, PR, or SD was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX6 (ERCC-1 High)93.8
Bevacizumab + FOLFIRI (ERCC-1 High)85.1

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Percentage of Participants With Disease Control According to RECIST Version 1.1 in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels

Disease control was defined as CR, PR, or SD according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. SD was defined as neither sufficient shrinkage to quality for PR nor sufficient increase to qualify for disease progression (≥20% increase in sum of LD of target lesions plus absolute increase ≥5 mm) in reference to the smallest sum of LD on study. The percentage of participants with CR, PR, or SD was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 High)89.3
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 Low)93.9

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Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With High ERCC-1 Levels Versus Participants With Low ERCC-1 Levels

Objective response was defined as CR or PR according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. The percentage of participants with CR or PR was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 High)61.1
Bevacizumab + mFOLFOX/FOLFIRI (ERCC-1 Low)64.8

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OS in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels

Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. OS was defined as the time from randomization to death. The median duration of OS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A High)22.83
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A Low)27.93

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Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With Wild-Type KRAS Versus Participants With Mutant KRAS

Objective response was defined as CR or PR according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. The percentage of participants with CR or PR was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX/FOLFIRI (KRAS Wild-Type)66.3
Bevacizumab + mFOLFOX/FOLFIRI (KRAS Mutant)60.9

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PFS According to RECIST Version 1.1 in Participants With High ERCC-1 and High VEGF-A Levels

Tumor assessments were performed according to RECIST Version 1.1. Disease progression was defined as ≥20% increase in sum of LD of target lesions in reference to the smallest sum of LD on study, in addition to an absolute increase ≥5 mm. Disease progression was further defined as the last documented progression determined by the Investigator no later than 1 day before initiation of second-line therapy. Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. PFS was defined as the time from randomization to death or disease progression, whichever occurred first. The median duration of PFS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death or disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX6 (ERCC-1 High, VEGF-A High)8.80
Bevacizumab + FOLFIRI (ERCC-1 High, VEGF-A High)11.17

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OS in Participants With Low ERCC-1 Levels

Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. OS was defined as the time from randomization to death. The median duration of OS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX6 (ERCC-1 Low)25.53
Bevacizumab + FOLFIRI (ERCC-1 Low)27.93

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Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With High VEGF-A Levels Versus Participants With Low VEGF-A Levels

Objective response was defined as CR or PR according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. The percentage of participants with CR or PR was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A High)60.5
Bevacizumab + mFOLFOX/FOLFIRI (VEGF-A Low)66.5

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Percentage of Participants With Objective Response According to RECIST Version 1.1 in Participants With Low ERCC-1 Levels

Objective response was defined as CR or PR according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. The percentage of participants with CR or PR was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX6 (ERCC-1 Low)63.7
Bevacizumab + FOLFIRI (ERCC-1 Low)65.8

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OS in Participants With Wild-Type KRAS Versus Participants With Mutant KRAS

Death on study included death from any cause occurring no later than 3 months after the last component of study treatment. OS was defined as the time from randomization to death. The median duration of OS was estimated by Kaplan-Meier analysis and expressed in months. The 95% CI was computed using the method of Brookmeyer and Crowley. (NCT01374425)
Timeframe: From Baseline until death (maximum up to 45 months overall)

Interventionmonths (Median)
Bevacizumab + mFOLFOX/FOLFIRI (KRAS Wild-Type)28.75
Bevacizumab + mFOLFOX/FOLFIRI (KRAS Mutant)24.64

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Percentage of Participants With Disease Control According to RECIST Version 1.1 in Participants With Low ERCC-1 Levels

Disease control was defined as CR, PR, or SD according to RECIST Version 1.1. CR was defined as disappearance of all target lesions and short-axis reduction to <10 mm of any pathological lymph nodes. PR was defined as ≥30% decrease in sum of LD of target lesions in reference to sum of LD at Baseline. Confirmation of response at a consecutive assessment was not required. SD was defined as neither sufficient shrinkage to quality for PR nor sufficient increase to qualify for disease progression (≥20% increase in sum of LD of target lesions plus absolute increase ≥5 mm) in reference to the smallest sum of LD on study. The percentage of participants with CR, PR, or SD was reported. The 95% CI was computed using normal approximation to the binomial distribution. (NCT01374425)
Timeframe: From Baseline until disease progression; assessed every 6 weeks (maximum up to 45 months overall)

Interventionpercentage of participants (Number)
Bevacizumab + mFOLFOX6 (ERCC-1 Low)92.7
Bevacizumab + FOLFIRI (ERCC-1 Low)95.0

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Adverse Events

Number of participants with at least 1 AE related to study treatment - The details on which AEs occured are listed in the Adverse Event section below (NCT01387295)
Timeframe: from start of treatment to 28 days after last treatment, an average of 7 months

InterventionParticipants (Count of Participants)
Chemotherapy38

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Number of Patients Suitable for Local Therapy (Radiofrequency)

Total number of patients receiving RF treatment or surgical treatment (NCT01387295)
Timeframe: upon completion of treatment, an average of 7 months

InterventionParticipants (Count of Participants)
Chemotherapy2

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PFS

From start of therapy to progression or death of any cause. (NCT01387295)
Timeframe: up to 6 years

Interventionmonths (Median)
Chemotherapy12.8

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Survival

All patients in intent-to-treat population , calculated from start of treatment to death of any course (NCT01387295)
Timeframe: up to 7 years

Interventionmonths (Median)
Chemotherapy24.0

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Percentage of Participants With Adverse Events

An adverse event was defined as any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. (NCT01399190)
Timeframe: Up to approximately 30 months

Interventionpercentage of participants (Number)
Bevacizumab74.6

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Response Rate (Tumor Assessments According to RECIST)

Response to treatment (Response Rate) was defined as the percentage of participants with a complete remission (CR) or partial remission (PR), and was assessed by the investigators according to modified RECIST criteria. CR was defined as disappearance of all lesions. PR was defined as a decrease in sum of lesions size by more than 30%. Response Rate = CR +PR (NCT01399190)
Timeframe: Up to approximately 30 months

Interventionpercentage of participants (Number)
Response RateComplete remissionPartial remission
Bevacizumab48.46.741.7

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Progression-free Survival

Progression-free survival was defined as the interval between the day of first treatment and the first documentation of disease progression or death and was assessed by the investigators according to modified Response Evaluation Criteria in Solid Tumors (RECIST). Disease progression was defined as an increase in sum of lesions size by more than 20% or new lesions. (NCT01399190)
Timeframe: From randomization to progression or death during the study (up to approximately 30 months)

Interventionmonths (Median)
Bevacizumab7.000

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Summary of Clinical Benefit

"A subject was considered a clinical benefit responder if he/she met at least 1 of the following criteria:~Subject showed improvement in at least one of the following parameters on successive scheduled observations without worsening in the others: pain intensity, analgesic use, or performance status~Subject was stable or improved on the pain intensity, analgesic use, and performance status and had a ≥ 7% increase in body weight maintained for 2 consecutive reporting periods that was not because of fluid accumulation." (NCT01423604)
Timeframe: Measured every 4 weeks until death or PD, whichever was earlier (up to 8 months)

,
Interventionpercentage of participants (Number)
Subjects with clinical benefitPain intensity - ImprovedAnalgesic use - ImprovedKarnofsky performance status - ImprovedBody weight - Improved
Placebo1.61.60.00.00.0
Ruxolitinib12.510.94.73.13.1

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Durable Response Rate

Durable response was defined as subjects with a response of Partial response (PR) or better at 2 subsequent measurements that were at least 4 weeks apart. (NCT01423604)
Timeframe: Measured every 4 weeks until death or PD, whichever was earlier (up to 8 months)

Interventionpercentage of participants (Number)
Ruxolitinib7.8
Placebo0.0

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Overall Survival

Overall survival was measured as the length of time (in days) between the randomization date and the date of death. (NCT01423604)
Timeframe: Primary analysis includes study data from the start of the study (first dose for that subject) until the death of the subject (up to 8 months).

Interventiondays (Median)
Ruxolitinib136.5
Placebo129.5

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Progression-Free Survival (PFS)

Progression-free survival was defined as the length of time between the date of randomization and the earlier of death or progressive disease (PD), whichever was earlier, as assessed by RECIST. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT01423604)
Timeframe: Analysis includes study data from the start of the study (first dose for that subject) until death or PD, whichever was earlier up to 8 months.

Interventiondays (Median)
Ruxolitinib51.0
Placebo46.0

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Objective Response Rate

Objective response rate (ORR) was defined as the percentage of participants with either a confirmed complete response (CR) or partial response (PR) measured by the investigator per modified Response Evaluation Criteria in Solid Tumors (RECIST) version 1.0 criteria during the treatment period. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01423604)
Timeframe: Measured every 4 weeks for duration of study treatment (up to 8 months)

,
Interventionpercentage of participants (Number)
Overall responseComplete responsePartial response
Placebo1.60.01.6
Ruxolitinib7.81.66.3

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Use of Cold Cap for Alopecia

Alopecia (hair loss) is a potential side effect of some chemotherapy agents. Chemotherapeutic drugs are toxic and could potentially harm the hair follicles (wear hair grows from) resulting in the hair falling out. It can occur in small patches on various parts of the body or all over the body and is usually temporary when related to cancer treatment. Cold cap therapy is one form of therapy for alopecia involving hair loss from the scalp. Wearing a cap or head covering with cold packs before, during, or after chemotherapy may help prevent hair loss as the cold narrows the blood vessels in the skin on your head which may lead to less of the drug reaching the hair follicles. Alopecia was one of the most common adverse events (AEs) related to eribulin only. (NCT01439282)
Timeframe: On the day of study drug infusion treatments during Cycles 1 through 4

,
InterventionParticipants (Number)
Participants with alopeciaParticipants who used a cold capParticipants who did not use a cold cap
Cohort 1: Eribulin Mesylate Plus 900 mg/m^2 Capecitabine52349
Cohort 2: Eribulin Mesylate Plus 1500 mg Capecitabine909

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Percentage of Participants Who Achieved the Target Relative Dose Intensity (RDI) of 85%

Relative Dose Intensity (RDI) is defined as the amount of drug administered over a specific time and is expressed as the fraction of that recommended for standard of care. The RDI for each participant was calculated as follows: (1) based on each participant's body surface area (BSA), a total planned dose for both eribulin (Dep) and capecitabine (Dcp) calculated for a full 4-cycle regimen; (2) actual total dose of eribulin (Dea) and capecitabine (Dca) for the full 4-cycle regimen as collected on the case report form; (3) overall RDI = (Dea/Dep + Dca/Dcp)/2. For each individual participant, the regimen was considered feasible if that participant was able to achieve an RDI of at least 85% of the 4 cycles of eribulin plus capecitabine treatment. Missing doses due to any reason was counted as zero in the RDI calculation. (NCT01439282)
Timeframe: 21-Day Cycle 1 through 21-Day Cycle 4

InterventionPercentage of participants (Number)
Cohort 1: Eribulin Mesylate Plus 900 mg/m^2 Capecitabine77.6
Cohort 2: Eribulin Mesylate Plus 1500 mg Capecitabine90.0

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Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)

(NCT01439282)
Timeframe: Day 1 through 30 days after last dose of study drugs (approximately up to 3 years)

,
Interventionparticipants (Number)
TEAESAE
Cohort 1: Eribulin Mesylate Plus 900 mg/m^2 Capecitabine6714
Cohort 2: Eribulin Mesylate Plus 1500 mg Capecitabine101

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Disease-Free Survival (Time to Event)

Disease free survival was measured as the time from the date of randomization until the date of first event (recurrence of colon cancer, or death due to any cause). (NCT01442155)
Timeframe: Up to 3 years

Interventionmonths (Median)
Capecitabine + Oxaliplatin25

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Safety: Percentage of Participants With Adverse Events

An adverse event is any untoward medical occurrence in a participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with the treatment. An adverse event can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding, for example), symptom, or disease temporally associated with the use of a pharmaceutical product, whether or not considered related to the pharmaceutical product. Preexisting conditions which worsen during a study are also considered as adverse events. (NCT01442155)
Timeframe: Up to 3 years

Interventionpercentage of participants (Number)
Capecitabine + Oxaliplatin39.19

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Percentage of Participants Who Died - Per Protocol Set (PPS)

The percentage of participants who died as of the analysis data cutoff date of 13 February 2015 was reported among participants from the PPS. (NCT01450696)
Timeframe: From date of randomization until death or premature withdrawal (up to approximately 31 months or data cutoff date of 13 February 2015)

Interventionpercentage of participants (Number)
Capecitabine + Cisplatin + Herceptin (6 mg/kg)51.5
Capecitabine + Cisplatin + Herceptin (10 mg/kg)59.4

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Percentage of Participants With Disease Progression or Death - PPS

Disease progression was defined by Response Evaluation Criteria in Solid Tumors (RECIST) Version 1.1 as a ≥20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study including Baseline (nadir). In addition to the relative increase of 20%, the sum was also required to demonstrate an absolute increase of ≥5 millimeters (mm). The percentage of participants who died or experienced disease progression as of the analysis data cutoff date of 13 February 2015 was reported among participants from the PPS. (NCT01450696)
Timeframe: From date of randomization until first occurrence of disease progression or death; assessed every 6 weeks (up to approximately 31 months or data cutoff date of 13 February 2015)

Interventionpercentage of participants (Number)
Capecitabine + Cisplatin + Herceptin (6 mg/kg)75.8
Capecitabine + Cisplatin + Herceptin (10 mg/kg)81.3

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Percentage of Participants Who Died - FAS

The percentage of participants who died as of the analysis data cutoff date of 13 February 2015 was reported among participants from the FAS with available data. (NCT01450696)
Timeframe: From date of randomization until death or premature withdrawal (up to approximately 31 months or data cutoff date of 13 February 2015)

Interventionpercentage of participants (Number)
Capecitabine + Cisplatin + Herceptin (6 mg/kg)46.8
Capecitabine + Cisplatin + Herceptin (10 mg/kg)54.0

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Trastuzumab Cmin on Day 21 of Cycles 1 to 11 - FAS

Cmin samples were obtained in all participants randomized to receive Herceptin (FAS). The observed Cmin was recorded, averaged among all participants, and expressed in μg/mL. (NCT01450696)
Timeframe: Day 21 of Cycle 1, 2, 3, 4, 5, 7, 9, 11 (cycle length = 21 days)

,
Interventionμg/mL (Mean)
Cycle 1 (n=100,99)Cycle 2 (n=93,76)Cycle 3 (n=77,71)Cycle 4 (n=73,61)Cycle 5 (n=70,60)Cycle 7 (n=51,44)Cycle 9 (n=31,24)Cycle 11 (n=24,16)
Capecitabine + Cisplatin + Herceptin (10 mg/kg)18.135.340.747.649.358.161.068.4
Capecitabine + Cisplatin + Herceptin (6 mg/kg)17.119.223.225.926.731.433.732.5

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Trastuzumab Serum Concentration on Day 1 of Cycle 1 - FAS

Trastuzumab serum concentration samples were obtained in all participants randomized to receive Herceptin (FAS). The observed concentration values were recorded, averaged among all participants, and expressed in μg/mL. (NCT01450696)
Timeframe: Pre-dose (0 minutes) and within 15 minutes after end of 2-hour Herceptin infusion on Day 1 of Cycle 1 (cycle length = 21 days)

,
Interventionμg/mL (Mean)
Pre-dose (n=109,110)End of infusion (n=110,111)
Capecitabine + Cisplatin + Herceptin (10 mg/kg)0.0204137
Capecitabine + Cisplatin + Herceptin (6 mg/kg)0.168126

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Overall Survival - PPS

Overall survival was defined as the time from the date of randomization to the date of death from any cause. Overall survival was estimated among participants from the PPS using the Kaplan-Meier approach. The 95% CI for median was computed using the method of Brookmeyer and Crowley. (NCT01450696)
Timeframe: From date of randomization until death or premature withdrawal (up to approximately 31 months or data cutoff date of 13 February 2015)

Interventionmonths (Median)
Capecitabine + Cisplatin + Herceptin (6 mg/kg)10.809
Capecitabine + Cisplatin + Herceptin (10 mg/kg)9.363

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Overall Survival - FAS

Overall survival was defined as the time from the date of randomization to the date of death from any cause. Overall survival was estimated among participants from the FAS using the Kaplan-Meier approach. The 95 percent (%) confidence interval (CI) for median was computed using the method of Brookmeyer and Crowley. (NCT01450696)
Timeframe: From date of randomization until death or premature withdrawal (up to approximately 31 months or data cutoff date of 13 February 2015)

Interventionmonths (Median)
Capecitabine + Cisplatin + Herceptin (6 mg/kg)12.485
Capecitabine + Cisplatin + Herceptin (10 mg/kg)10.612

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Progression-Free Survival - PPS

Progression-free survival was defined as the time between the day of randomization and the date of first documentation of disease progression or date of death, whichever occurred first, measured following RECIST Version 1.1 criteria. Disease progression was defined as a ≥20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study including Baseline (nadir). In addition to the relative increase of 20%, the sum was also required to demonstrate an absolute increase of ≥5 mm. The 95% CI for median was computed using the method of Brookmeyer and Crowley. (NCT01450696)
Timeframe: From date of randomization until first occurrence of disease progression or death; assessed every 6 weeks (up to approximately 31 months or data cutoff date of 13 February 2015)

Interventionmonths (Median)
Capecitabine + Cisplatin + Herceptin (6 mg/kg)5.388
Capecitabine + Cisplatin + Herceptin (10 mg/kg)4.370

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Percentage of Participants With Objective Response - PPS

Objective response was defined as the occurrence of either a complete response (CR) or partial response (PR) as determined by RECIST Version 1.1 based on investigator assessment. CR was defined as disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) were required to have reduction in short axis to <10 mm. PR was defined as a ≥30% decrease in the sum of diameters of target lesions, taking as reference the Baseline sum diameters. The 95% CI was constructed using Blyth-Still-Casella method. (NCT01450696)
Timeframe: From date of randomization until first occurrence of disease progression or death; assessed every 6 weeks (up to approximately 31 months or data cutoff date of 13 February 2015)

Interventionpercentage of participants (Number)
Capecitabine + Cisplatin + Herceptin (6 mg/kg)57.6
Capecitabine + Cisplatin + Herceptin (10 mg/kg)50.0

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Disease Control Rate (DCR)

DCR is defined as the percentage of patients achieving a complete response (CR), partial response (PR), or stable disease (SD) based on the Response Evaluation Criteria in Solid Tumors (RECIST 1.1). CR = disappearance of all target lesions, PR is =>30% decrease in sum of diameters of target lesions, progressive disease (PD) is >20% increase in sum of diameters of target lesions, stable disease (SD) is <30% decrease or <20% increase in sum of diameters of target lesions. (NCT01459614)
Timeframe: Up to 22 months

InterventionPercentage of Participants (Number)
Primary Cohort (21 Day Cycle)89

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Percentage of Participants Without Disease Progression (Progression-Free Survival) at 6 Months

PFS is defined as the percentage of patients with disease progression (progressive disease [PD] or relapse from complete response [CR] as assessed using RECIST 1.1 criteria) or death due to any cause at 6 months. Per RECIST 1.1 criteria, CR = disappearance of all target lesions, Partial Response (PR) is =>30% decrease in sum of diameters of target lesions, Progressive Disease (PD) is >20% increase in sum of diameters of target lesions, Stable Disease (SD) is <30% decrease or <20% increase in sum of diameters of target lesions. Estimation based on the Kaplan-Meier curve. (NCT01459614)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Primary Cohort (21 Day Cycle)78.6
Expansion Cohort (28 Day Cycle)30

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Progression-free Survival (PFS)

PFS is defined as the the number of months from the date of first dose to disease progression (progressive disease [PD] or relapse from complete response [CR] as assessed using RECIST 1.1 criteria) or death due to any cause . Per RECIST 1.1 criteria, CR = disappearance of all target lesions, Partial Response (PR) is =>30% decrease in sum of diameters of target lesions, Progressive Disease (PD) is >20% increase in sum of diameters of target lesions, Stable Disease (SD) is <30% decrease or <20% increase in sum of diameters of target lesions. Estimation based on the Kaplan-Meier curve. (NCT01459614)
Timeframe: Up to 21 months

InterventionMonths (Median)
Primary Cohort (21 Day Cycle)8.4
Expansion Cohort (28 Day Cycle)4.1

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Overall Survival (OS)

OS (in months) will be measured from date of first dose until death (OS will be censored on the date the subject was last known to be alive for subjects without documentation of death at the time of analysis). Estimation based on the Kaplan-Meier curve. (NCT01459614)
Timeframe: Up to 28 months

InterventionMonths (Median)
Primary Cohort (21 Day Cycle)13.42

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Percentage of Participants With Day 43 Serum Pertuzumab Trough Concentrations (Cmin) Greater Than or Equal to (>=) 20 Microgram Per Milliliter (mcg/mL)

(NCT01461057)
Timeframe: Day 43

Interventionpercentage of participants (Number)
Pertuzumab 840/420 mg91.6
Pertuzumab 840/840 mg98.3

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Number of Participants With Adverse Events (AEs)

An adverse event (AE) was defined as any untoward medical occurrence in a participant administered the investigational product which does not necessarily have a causal relationship with this treatment. (NCT01461057)
Timeframe: From randomization of first participant to end of study (approximately 6 years)

Interventionparticipants (Number)
Pertuzumab 840/420 mg15
Pertuzumab 840/840 mg15

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Objective Response Rate (ORR), Response Rate (RR) and Disease Control Rate (DCR)

"by RECIST guideline Objective response rate = (Number of subjects with best overall response as confirmed CR or PR / Total number of subjects)*100.~Response rate = (Number of subjects with best overall response as CR or PR / Total number of subjects)*100.~Disease control rate = (Number of subjects with best overall response as confirmed CR or PR or SD / Total number of subjects)*100." (NCT01463982)
Timeframe: tumor response evaluation can continue to receive the study drug until PD confirmation

,,,
Interventionpercentage of participants (Number)
Objective Response rateResponse RateDisease Control Rate
Capecitabine 1000mg/㎡ + Oratecan 15mg/㎡33.333.350.0
Capecitabine 800mg/㎡ + Oratecan 10mg/㎡0.00.066.7
Capecitabine 800mg/㎡ + Oratecan 15mg/㎡0.00.042.9
Capecitabine 800mg/㎡ + Oratecan 20mg/㎡0.00.0100

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Dose Limiting Toxicity Assessment and Maximum Tolerated Dose Determination

If Dose Limiting Toxicity(DLT) was not observed in the third subject at a dose level from the first study drug dosing date (Day 1) to the end of Cycle 1(21 days), increase the dose to the next level and enroll subjects; enrollment up to Level 4 was allowed. (NCI-CTCAE version 3.0) (NCT01463982)
Timeframe: Cycle 1 (21 days)

Interventionpercentage of participants (Number)
Capecitabine 800mg/㎡ + Oratecan 10mg/㎡0.0
Capecitabine 800mg/㎡ + Oratecan 15mg/㎡0.0
Capecitabine 800mg/㎡ + Oratecan 20mg/㎡50.0
Capecitabine 1000mg/㎡ + Oratecan 15mg/㎡0.0

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Response Rate

This is the percentage of subjects that achieved either a complete response or a partial response per RECIST 1.1 criteria (NCT01471353)
Timeframe: 3 months

Interventionpercentage of participants (Number)
Sorafenib Plus Capecitabine (SorCape)2.38

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Sorafenib Activity

Determine activity of sorafenib plus capecitabine on progression free survival (PFS) in patients with advanced colorectal cancer. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT01471353)
Timeframe: 2 years

Interventiondays (Median)
Sorafenib Plus Capecitabine (SorCape)123

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Toxicity (Percentage of Subjects That Experienced an Adverse Event)

Evaluate acute toxicity of treatment. The toxicity assessments were graded by the NCI CTCAE (Clinical Trial Common Adverse Event) grading system - a global standard for assessments of clinical and laboratory toxicities. All toxicities are scored 1(mild) through 5 (death related to the event) based upon well-defined and reproducible definitions. (NCT01471353)
Timeframe: 12 months

Interventionpercentage of participants (Number)
Adverse Events - Any GradeAdverse Events - Grade 3Adverse Events - Grade 4
Sorafenib Plus Capecitabine (SorCape)100742

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Overall Survival

Evaluate overall survival after treatment. (NCT01471353)
Timeframe: 5 years

Interventiondays (Median)
Sorafenib Plus Capecitabine (SorCape)261

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Hematological Toxicity of the Combination of Pazopanib and Capecitabine

(NCT01498458)
Timeframe: 3 years

InterventionNumber of cycles (Number)
Anemia Grade 1 to 4Leucopenia Grade 1 to 4Number of Cycles
Pazopanib + Capecitabine8855132

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Clinical Benefit Rate (CBR)

To determine the clinical benefit rate (CBR) in patients with measurable disease. CBR consists of complete response , partial response, and stable disease lasting greater than 24 weeks. All patients are included when determining this rate. 2 patients were on study treatment for a long time.Hence the outcome rate of 25 percent ( 2 from 8 patients) (NCT01498458)
Timeframe: 3 years

Interventionpercentage of participants (Number)
Pazopanib Plus Capecitabine25

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Dose-limiting Toxicity (DLT)

(NCT01498458)
Timeframe: 3 years

Interventionparticipants (Number)
Pazopanib Plus Capecitabine5

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Other Toxicity of the Combination of Pazopanib and Capecitabine

(NCT01498458)
Timeframe: 3 years

Interventionparticipants (Number)
HepatotoxicityHypertensionPancreatectomyThrombocytopenia
Pazopanib Plus Capecitabine3111

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Maximum Tolerable Dose (MTD) of Pazopanib

The maximum tolerated dose (MTD) is defined as the highest dose level with DLT in no more than 1 out of 6 patients. A maximal tolerated dose (MTD) could not be established. (NCT01498458)
Timeframe: 3 years

Interventionmg (Number)
Pazopanib Plus CapecitabineNA

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Objective Response Rate (ORR)

To determine the objective response rate (ORR) in patients with measurable disease. ORR consists of complete response and partial response according to the RECIST criteria. Complete Response refers to the disappearance of all target lesions. Any pathological lymph nodes must have a reduction in short axis to less than 10 mm. Partial Response refers to an at least 30 percent decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. (NCT01498458)
Timeframe: 3 years

Interventionpercentage of participants (Number)
Pazopanib Plus Capecitabine0

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Overall Survival (OS)

"Time from the date of enrollment to the date of death due to any cause or the last date the patient was known to be alive (censored observation) at the date of data cutoff for the final analysis. The results will be reported as median in months~The length of overall survival (OS) of participants was assessed by Kaplan-Meier analysis. The outcome is given as the median in months with full range." (NCT01525082)
Timeframe: 82 mo

Interventionmonths (Median)
Bevacizumab + Capecitabine + Temozolomide49.8

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O6-methylguanine DNA Methyltransferase (MGMT) Status by Immunohistochemistry (IHC)

"O6-alkylguanine DNA alkyltransferase is a protein that in humans is encoded by the gene O6-methylguanine DNA methyltransferase (MGMT). Deficiency of the gene product, ie, the protein, is refereed to as MGMT deficiency, and is thought to be predictive of response to temozolomide and is more often associated with pancreatic NETs.~MGMT status in pre-treatment biopsy specimens was to be assessed by immuno-histochemistry (IHC), and associated to best clinical response. The outcome is reported by the the number of patients that were IHC-positive (MGMT detected) or IHC-negative (MGMT not detected), and by best clinical response [ie, complete response (CR), partial response (PR), stable disease (SD), or progressive disease (PD)]. The outcome is reported as a number without dispersion." (NCT01525082)
Timeframe: 18 months

Interventionparticipants (Number)
IHC-positive and CRIHC-positive and PRIHC-positive and SDIHC-positive and PDIHC-negative and CRIHC-negative and PRIHC-negative and SDIHC-negative and PD
Bevacizumab + Capecitabine + Temozolomide02210420

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Radiographic Response (RR)

"Tumor response to treatment with the combination of capecitabine & temozolomide plus bevacizumab in patients with metastatic or unresectable pancreatic neuroendocrine tumors was assessed per Response Evaluation Criteria in Solid Tumors Criteria (RECIST v1.1) for target lesions. Response is defined as:~Complete Response (CR) = Disappearance of all target lesions~Partial Response (PR) = ≥ 30% decrease in the sum of the longest diameter of target lesions~Overall Response (OR) = CR + PR~Progressive disease (PD) = 20% increase in the sum of the longest diameter of target lesions, and/or the appearance of one or more new lesion(s)~Stable disease (SD) = Small changes that do not meet any of the above criteria~The outcome is reported as the number of participants who between 3 and 18 months after treatment initiation achieve CR, PR, or clinical response (PR + CR), each a number without dispersion." (NCT01525082)
Timeframe: 18 months

InterventionParticipants (Count of Participants)
Overall response (OR)Complete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive disease (PD)
Bevacizumab + Capecitabine + Temozolomide90991

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Progression-free Survival (PFS)

Progression-free survival (PFS) means the length of time that participants survive without disease (tumor) progression, and was assessed using Kaplan-Meier analysis. The outcome is given as the mean in months with standard error of the mean. (NCT01525082)
Timeframe: 82 months

Interventionmonths (Mean)
Bevacizumab + Capecitabine + Temozolomide25.2

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O6-methylguanine DNA Methyltransferase (MGMT) by Promoter Methylation

"O6-alkylguanine DNA alkyltransferase is a protein that in humans is encoded by the gene O6-methylguanine DNA methyltransferase (MGMT). Deficiency of the gene product, ie, the protein, is refered to as MGMT deficiency, and is thought to be predictive of response to temozolomide and is more often associated with pancreatic NETs.~MGMT status in pre-treatment biopsy specimens was to be assessed by extent of genetic promoter methylation (an analysis of DNA), and correlated to subject survival.~MGMT status in pre-treatment biopsy specimens was to be assessed by promoter methylation assessment (PM), and associated to best clinical response. The outcome is reported by the the number of patients that were PM-positive (MGMT detected) or PM-negative (MGMT not detected), and by best clinical response [ie, complete response (CR), partial response (PR), stable disease (SD), or progressive disease (PD)]. The outcome is reported as a number without dispersion." (NCT01525082)
Timeframe: 18 months

Interventionparticipants (Number)
PM-positive and CRPM-positive and PRPM-positive and SDPM-positive and PDPM-negative and CRPM-negative and PRPM-negative and SDPM-negative and PD
Bevacizumab + Capecitabine + Temozolomide01000451

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Impact of Aprepitant/5HT-3 Antagonist Therapy on the Patient Quality of Life as Measured by the Number of Patients Using Anti Nausea Drugs

(NCT01534637)
Timeframe: Week 1

Interventionparticipants (Number)
Treatment (Antiemetic, Chemotherapy, and Radiation Therapy)6

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Number of Patients With Gastrointestinal Toxicities (Grade 3 and 4 Nausea and Vomiting) Associated With Delivering Fluorouracil/Gemcitabine Hydrochloride-based Chemotherapy With Upper Abdominal Radiation

Toxicity will be determined using the revised National Cancer Institute (NCI) Common Toxicity Criteria (CTC) version 3.0 for Toxicity and Adverse Event Reporting. Descriptive statistics (means, standard deviations, frequencies, etc.) will be presented for pretreatment patient characteristics. The rate of grade 3 and 4 nausea will be compared to the cut points during interim and final analyses. (NCT01534637)
Timeframe: Over 10 weeks

Interventionparticipants (Number)
Treatment (Antiemetic, Chemotherapy, and Radiation Therapy)3

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Impact of Aprepitant/5HT-3 Antagonist Therapy on the Patient Quality of Life as Measured by the Number of Patients Taking Anti Nausea Drugs

(NCT01534637)
Timeframe: Week 5

Interventionparticipants (Number)
Treatment (Antiemetic, Chemotherapy, and Radiation Therapy)5

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Number of Participants Experienced Dose Limited Toxicity

Dose related toxicity is defined as follows:1. luecopenia > grade 2; granular cell decrease > grade 2; anemia > grade 1; platelet > grade 1;SGPT/SGOT elevation > grade 1; ALP > grade 1; GGT > grade 1; Tbil > grade 1;renal function damag > grade 2;Non-gradular cell decreased fever > grade 1;nausea/vomiting > grade 1; fatigue > grade 2; weight loss > grade 2;gastritis > grade 2; dairrea > grade 2; abdominal pain > grade 2; upper gastrointestinal bleeding > grade 1;other toxic reaction > grade 2;KPS < 50 during the treatment (NCT01584544)
Timeframe: up to 7 weeks from start of the treatment

Interventionparticipants (Number)
1000mg0
1200mg1
1350mg1
1500mg0
1650mg1

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Time to Failure of Strategy (TFS): Overall

TFS was defined as time from the start of initial treatment to documentation of first disease progression without entering Phase B, or second disease progression having entered Phase B. Disease progression was determined according to standard practice based on radiological, biochemical (CEA) or clinical factors. Determination of disease progression was to be unequivocal and was defined as any of the following: an unequivocal and clinically meaningful increase in the size of known tumors, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, elevated CEA accompanied by other radiological or clinical evidence of progression, or symptomatic deterioration. Kaplan-Meier methodology was used to estimate TFS. (NCT01588990)
Timeframe: Baseline up to disease progression, death or end of study (up to 4 years)

Interventionmonths (Median)
Bevacizumab: Phase A and Phase B14.8

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AQoL-8D Global Utility Score: Phase B

AQoL-8D provides a global utility score and consists of 8 separately scored dimensions including Independent Living, Life Satisfaction, Mental Health, Coping, Relationships, Self Worth, Pain, and Senses. Each of the 8 scales is calculated based on the answers to 3 questions. Each question is given an answer dependent utility score (0 [worst] to 1 [best]) and then these scores are combined using a multiplicative model to get the normalized scale score value, each scale ranging between 0.0 (representing death) and 1.0 (representing full health). (NCT01588990)
Timeframe: Baseline, every 8-9 weeks thereafter, EOT (30 days after disease progression [up to 4 years]), survival follow-up 12-weekly visits (up to 4 years) [Detailed time points are presented in the category titles]

Interventionunits on a scale (Mean)
Phase B BaselinePhase B Visit 2 (up to 4 years)Phase B Visit 3 (up to 4 years)Phase B Visit 4 (up to 4 years)Phase B Visit 5 (up to 4 years)Phase B Visit 6 (up to 4 years)Phase B Visit 7 (up to 4 years)Phase B Visit 8 (up to 4 years)Phase B Visit 9 (up to 4 years)Phase B Visit 10 (up to 4 years)Phase B Visit 11 (up to 4 years)Phase B Visit 12 (up to 4 years)Phase B Visit 13 (up to 4 years)Phase B Visit 14 (up to 4 years)Phase B Visit 15 (up to 4 years)Phase B Visit 16 (up to 4 years)Phase B Visit 17 (up to 4 years)Phase B Visit 18 (up to 4 years)Phase B Visit 19 (up to 4 years)Phase B Visit 20 (up to 4 years)Phase B Visit 21 (up to 4 years)Phase B Visit 22 (up to 4 years)Phase B Visit 23 (up to 4 years)Phase B Visit 24 (up to 4 years)Phase B EOT Visit (up to 4 years)Survival Follow-Up 1 (up to 4 years)Survival Follow-Up 2 (up to 4 years)Survival Follow-Up 3 (up to 4 years)Survival Follow-Up 4 (up to 4 years)Survival Follow-Up 6 (up to 4 years)
Bevacizumab: Phase B0.7360.7730.8130.8780.8080.8090.8250.9100.8190.8560.7300.9600.9650.9580.9670.9420.9270.9310.8660.8870.9400.9190.9370.9500.7080.7880.7910.9890.9810.875

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European Quality of Life 5-Dimension (EuroQol-5D) Utility Score: Phase A

"EQ-5D is a standardized generic preference based health related quality of life instrument. It records how one's health is today and consists of a descriptive system. The descriptive system is comprised of 5 dimensions: mobility, self-care, usual activities, pain/discomfort, anxiety/depression. Each dimension on the EQ-5D involves a 3-point response scale which indicates the level of impairment (level 1 = no problem; level 2 = some or moderate problem[s] and level 3 = unable, or extreme problems). Level of problem reported in each EQ-5D dimension determines a unique health state which is converted into a weighted health state index by applying scores from EQ-5D preference weights elicited from general population samples. This generates a unique description of the subjects' health status, which is valued between 0 (representing death) and 1 (representing perfect health). Higher the score, the better the quality of life." (NCT01588990)
Timeframe: Baseline, every 8-9 weeks thereafter, end of treatment (EOT) (30 days after disease progression [up to 4 years]), survival follow-up 12-weekly visits (up to 4 years) [Detailed time points are presented in the category titles]

Interventionunits on a scale (Mean)
Phase A BaselinePhase A Visit 2 (Weeks 8-9)Phase A Visit 3 (Weeks 16-17)Phase A Visit 4 (Weeks 24-25)Phase A Visit 5 (Weeks 32-33)Phase A Visit 6 (Weeks 40-41)Phase A Visit 7 (Weeks 48-49)Phase A Visit 8 (Weeks 56-57)Phase A Visit 9 (Weeks 64-65)Phase A Visit 10 (Weeks 72-73)Phase A Visit 11 (Weeks 80-81)Phase A Visit 12 (Weeks 88-89)Phase A Visit 13 (Weeks 96-97)Phase A Visit 14 (Weeks 104-105)Phase A Visit 15 (Weeks 112-113)Phase A Visit 16 (Weeks 120-121)Phase A Visit 17 (Weeks 128-129)Phase A Visit 18 (Weeks 136-137)Phase A Visit 19 (Weeks 144-145)Phase A Visit 20 (Weeks 152-153)Phase A Visit 21 (Weeks 160-161)Phase A Visit 22 (Weeks 168-169)Phase A Visit 23 (Weeks 176-177)Phase A EOT Visit (up to 4 years)Survival Follow-Up 1 (up to 4 years)Survival Follow-Up 2 (up to 4 years)Survival Follow-Up 3 (up to 4 years)Survival Follow-Up 4 (up to 4 years)Survival Follow-Up 5 (up to 4 years)Survival Follow-Up 6 (up to 4 years)Survival Follow-Up 7 (up to 4 years)
Bevacizumab: Phase A0.8300.8570.8650.8530.8690.8920.8720.8810.8940.8430.8980.9150.8440.8990.8780.8990.8730.9090.9470.8520.9330.8130.9000.8170.7680.9010.8190.8431.0000.8350.816

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EuroQol-5D Utility Score: Phase B

"EQ-5D is a standardized generic preference based health related quality of life instrument. It records how one's health is today and consists of a descriptive system. The descriptive system is comprised of 5 dimensions: mobility, self-care, usual activities, pain/discomfort, anxiety/depression. Each dimension on the EQ-5D involves a 3-point response scale which indicates the level of impairment (level 1 = no problem; level 2 = some or moderate problem[s] and level 3 = unable, or extreme problems). Level of problem reported in each EQ-5D dimension determines a unique health state which is converted into a weighted health state index by applying scores from EQ-5D preference weights elicited from general population samples. This generates a unique description of the subjects' health status, which is valued between 0 (representing death) and 1 (representing perfect health). Higher the score, the better the quality of life." (NCT01588990)
Timeframe: Baseline, every 8-9 weeks thereafter, EOT (30 days after disease progression [up to 4 years]), survival follow-up 12-weekly visits (up to 4 years) [Detailed time points are presented in the category titles]

Interventionunits on a scale (Mean)
Phase B BaselinePhase B Visit 2 (up to 4 years)Phase B Visit 3 (up to 4 years)Phase B Visit 4 (up to 4 years)Phase B Visit 5 (up to 4 years)Phase B Visit 6 (up to 4 years)Phase B Visit 7 (up to 4 years)Phase B Visit 8 (up to 4 years)Phase B Visit 9 (up to 4 years)Phase B Visit 10 (up to 4 years)Phase B Visit 11 (up to 4 years)Phase B Visit 12 (up to 4 years)Phase B Visit 13 (up to 4 years)Phase B Visit 14 (up to 4 years)Phase B Visit 15 (up to 4 years)Phase B Visit 16 (up to 4 years)Phase B Visit 17 (up to 4 years)Phase B Visit 18 (up to 4 years)Phase B Visit 19 (up to 4 years)Phase B Visit 20 (up to 4 years)Phase B Visit 21 (up to 4 years)Phase B Visit 22 (up to 4 years)Phase B Visit 23 (up to 4 years)Phase B Visit 24 (up to 4 years)Phase B EOT Visit (up to 4 years)Survival Follow-Up 1 (up to 4 years)Survival Follow-Up 2 (up to 4 years)Survival Follow-Up 3 (up to 4 years)Survival Follow-Up 4 (up to 4 years)Survival Follow-Up 6 (up to 4 years)
Bevacizumab: Phase B0.8140.8590.8940.8970.8660.8370.8760.8740.9080.8110.8060.8441.0001.0000.8440.8330.8440.8330.8270.8160.8440.8440.8270.8440.8090.7400.7720.8270.8271.000

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FACT-C Score: Phase B

FACT-C is one part of the FACIT Measurement System, which comprehensively assesses the health-related QoL of cancer participants and participants with other chronic illnesses. It is composed of 27 items of the general version of the FACT-C as a general core QoL measure and has a disease-specific subscale containing 9 colorectal cancer-specific items. It consists of total 36 items, summarized to 5 subscales: physical well-being (7 items), functional well-being (7 items), social/family well-being (7 items); all 3 subscales range from 0 to 28, emotional well-being (6 items) range from 0 to 24, colorectal cancer subscale (9 items) range from 0 to 36; higher subscale score=better QoL. All single-item measures range from 0='Not at all' to 4='Very much'. Total possible score range: 0 to 144. High scale score represents a better QoL. (NCT01588990)
Timeframe: Baseline, every 8-9 weeks thereafter, EOT (30 days after disease progression [up to 4 years]), survival follow-up 12-weekly visits (up to 4 years) [Detailed time points are presented in the category titles]

Interventionunits on a scale (Mean)
Phase B BaselinePhase B Visit 2 (up to 4 years)Phase B Visit 3 (up to 4 years)Phase B Visit 4 (up to 4 years)Phase B Visit 5 (up to 4 years)Phase B Visit 6 (up to 4 years)Phase B Visit 7 (up to 4 years)Phase B Visit 8 (up to 4 years)Phase B Visit 9 (up to 4 years)Phase B Visit 10 (up to 4 years)Phase B Visit 11 (up to 4 years)Phase B Visit 12 (up to 4 years)Phase B Visit 13 (up to 4 years)Phase B Visit 14 (up to 4 years)Phase B Visit 15 (up to 4 years)Phase B Visit 16 (up to 4 years)Phase B Visit 17 (up to 4 years)Phase B Visit 18 (up to 4 years)Phase B Visit 19 (up to 4 years)Phase B Visit 20 (up to 4 years)Phase B Visit 21 (up to 4 years)Phase B Visit 22 (up to 4 years)Phase B Visit 23 (up to 4 years)Phase B Visit 24 (up to 4 years)Phase B EOT Visit (up to 4 years)Survival Follow-Up 1 (up to 4 years)Survival Follow-Up 2 (up to 4 years)Survival Follow-Up 3 (up to 4 years)Survival Follow-Up 4 (up to 4 years)Survival Follow-Up 6 (up to 4 years)
Bevacizumab: Phase B103.47108.71108.19114.89110.60111.28114.78120.39108.08110.50109.33125.00119.00117.00126.00123.00127.00126.00127.00126.00123.00124.00126.00130.00101.6798.72102.50126.33125.00124.67

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Functional Assessment of Cancer Therapy-Colorectal (FACT-C) Score: Phase A

FACT-C is one part of the Functional Assessment of Chronic Illness Therapy (FACIT) Measurement System, which comprehensively assesses the health-related QoL of cancer participants and participants with other chronic illnesses. It is composed of 27 items of the general version of the FACT-C as a general core QoL measure and has a disease-specific subscale containing 9 colorectal cancer-specific items. It consists of total 36 items, summarized to 5 subscales: physical well-being (7 items), functional well-being (7 items), social/family well-being (7 items); all 3 subscales range from 0 to 28, emotional well-being (6 items) range from 0 to 24, colorectal cancer subscale (9 items) range from 0 to 36; higher subscale score=better QoL. All single-item measures range from 0='Not at all' to 4='Very much'. Total possible score range: 0 to 144. High scale score represents a better QoL. (NCT01588990)
Timeframe: Baseline, every 8-9 weeks thereafter, EOT (30 days after disease progression [up to 4 years]), survival follow-up 12-weekly visits (up to 4 years) [Detailed time points are presented in the category titles]

Interventionunits on a scale (Mean)
Phase A BaselinePhase A Visit 2 (Weeks 8-9)Phase A Visit 3 (Weeks 16-17)Phase A Visit 4 (Weeks 24-25)Phase A Visit 5 (Weeks 32-33)Phase A Visit 6 (Weeks 40-41)Phase A Visit 7 (Weeks 48-49)Phase A Visit 8 (Weeks 56-57)Phase A Visit 9 (Weeks 64-65)Phase A Visit 10 (Weeks 72-73)Phase A Visit 11 (Weeks 80-81)Phase A Visit 12 (Weeks 88-89)Phase A Visit 13 (Weeks 96-97)Phase A Visit 14 (Weeks 104-105)Phase A Visit 15 (Weeks 112-113)Phase A Visit 16 (Weeks 120-121)Phase A Visit 17 (Weeks 128-129)Phase A Visit 18 (Weeks 136-137)Phase A Visit 19 (Weeks 144-145)Phase A Visit 20 (Weeks 152-153)Phase A Visit 21 (Weeks 160-161)Phase A Visit 22 (Weeks 168-169)Phase A Visit 23 (Weeks 176-177)Phase A EOT Visit (up to 4 years)Survival Follow-Up 1 (up to 4 years)Survival Follow-Up 2 (up to 4 years)Survival Follow-Up 3 (up to 4 years)Survival Follow-Up 4 (up to 4 years)Survival Follow-Up 5 (up to 4 years)Survival Follow-Up 6 (up to 4 years)Survival Follow-Up 7 (up to 4 years)
Bevacizumab: Phase A103.84103.33106.34109.66109.39111.30111.40113.51113.92115.11114.00115.99113.54112.36119.48116.38113.69112.94117.55115.86106.00112.00105.00103.94102.89104.00105.50109.00119.00103.61115.00

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Percentage of Participants With Confirmed Complete or Partial Response as Assessed by the Investigator Based on Routine Clinical Practice: Overall

Percentage of participants with best overall response of confirmed complete response or partial response based on the investigator assessment of the response as per routine clinical practice was reported. The confirmation of response must be no less than 4 weeks after initial assessment. (NCT01588990)
Timeframe: Baseline up to disease progression, death or end of study (up to 4 years)

Interventionpercentage of participants (Number)
Complete responsePartial response
Bevacizumab: Phase A and Phase B3.18.6

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Percentage of Participants With Confirmed Complete or Partial Response as Assessed by the Investigator Based on Routine Clinical Practice: Phase A

Percentage of participants with best overall response of confirmed complete response or partial response based on the investigator assessment of the response as per routine clinical practice was reported. The confirmation of response must be no less than 4 weeks after initial assessment. (NCT01588990)
Timeframe: Baseline up to disease progression, death or end of study (up to 4 years)

Interventionpercentage of participants (Number)
Complete responsePartial response
Bevacizumab: Phase A3.18.6

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Percentage of Participants With Confirmed Complete or Partial Response as Assessed by the Investigator Based on Routine Clinical Practice: Phase B

Percentage of participants with best overall response of confirmed complete response or partial response based on the investigator assessment of the response as per routine clinical practice was reported. The confirmation of response must be no less than 4 weeks after initial assessment. (NCT01588990)
Timeframe: From the start of Phase B treatment to disease progression, death or end of study (up to 4 years)

Interventionpercentage of participants (Number)
Complete responsePartial response
Bevacizumab: Phase B00

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Survival Beyond First Disease Progression: Overall

Survival beyond first progression was defined as the time from the date of first disease progression to death due to any cause. Disease progression was determined according to standard practice based on radiological, biochemical (CEA) or clinical factors. Determination of disease progression was to be unequivocal and was defined as any of the following: an unequivocal and clinically meaningful increase in the size of known tumors, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, elevated CEA accompanied by other radiological or clinical evidence of progression, or symptomatic deterioration. Kaplan-Meier methodology was used to estimate survival beyond first disease progression. (NCT01588990)
Timeframe: Baseline until death or end of study (up to 4 years)

Interventionmonths (Median)
Bevacizumab: Phase A and Phase B12.6

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PFS Until Second Disease Progression as Assessed by the Investigator Based on Routine Clinical Practice: Phase B

PFS in Phase B (PFS-B) was defined as the time from the start of Phase B treatment to documentation of second disease progression or death from any cause, whichever occurred first. Disease progression was determined according to standard practice based on radiological, biochemical (CEA) or clinical factors. Determination of disease progression was to be unequivocal and was defined as any of the following: an unequivocal and clinically meaningful increase in the size of known tumors, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, elevated CEA accompanied by other radiological or clinical evidence of progression, or symptomatic deterioration. Kaplan-Meier methodology was used to estimate PFS. (NCT01588990)
Timeframe: From the start of Phase B treatment to disease progression, death or end of study (up to 4 years)

Interventionmonths (Median)
Bevacizumab: Phase B6.7

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PFS Until First Disease Progression as Assessed by the Investigator Based on Routine Clinical Practice: Phase A

PFS until first progression was defined as the time from the start of initial treatment to documentation of first disease progression or death from any cause, whichever occurred first. Disease progression was determined according to standard practice based on radiological, biochemical (CEA) or clinical factors. Determination of disease progression was to be unequivocal and was defined as any of the following: an unequivocal and clinically meaningful increase in the size of known tumors, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, elevated CEA accompanied by other radiological or clinical evidence of progression, or symptomatic deterioration. Kaplan-Meier methodology was used to estimate PFS. (NCT01588990)
Timeframe: Baseline up to first disease progression, death or end of study (up to 4 years)

Interventionmonths (Median)
Bevacizumab: Phase A9.2

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Assessment of Quality of Life - Eight Dimensions (AQoL-8D) Global Utility Score: Phase A

AQoL-8D provides a global utility score and comprised of 35 questions from which 8 dimensions (Independent Living, Life Satisfaction, Mental Health, Coping, Relationships, Self Worth, Pain, and Senses) are derived. Each of the 8 scales is calculated based on the answers to 3 questions. Each question is given an answer dependent utility score (0 [worst] to 1 [best]) and then these scores are combined using a multiplicative model to get the normalized scale score value, each scale ranging between 0.0 (representing death) and 1.0 (representing full health). (NCT01588990)
Timeframe: Baseline, every 8-9 weeks thereafter, EOT (30 days after disease progression [up to 4 years]), survival follow-up 12-weekly visits (up to 4 years) [Detailed time points are presented in the category titles]

Interventionunits on a scale (Mean)
Phase A BaselinePhase A Visit 2 (Weeks 8-9)Phase A Visit 3 (Weeks 16-17)Phase A Visit 4 (Weeks 24-25)Phase A Visit 5 (Weeks 32-33)Phase A Visit 6 (Weeks 40-41)Phase A Visit 7 (Weeks 48-49)Phase A Visit 8 (Weeks 56-57)Phase A Visit 9 (Weeks 64-65)Phase A Visit 10 (Weeks 72-73)Phase A Visit 11 (Weeks 80-81)Phase A Visit 12 (Weeks 88-89)Phase A Visit 13 (Weeks 96-97)Phase A Visit 14 (Weeks 104-105)Phase A Visit 15 (Weeks 112-113)Phase A Visit 16 (Weeks 120-121)Phase A Visit 17 (Weeks 128-129)Phase A Visit 18 (Weeks 136-137)Phase A Visit 19 (Weeks 144-145)Phase A Visit 20 (Weeks 152-153)Phase A Visit 21 (Weeks 160-161)Phase A Visit 22 (Weeks 168-169)Phase A Visit 23 (Weeks 176-177)Phase A EOT Visit (up to 4 years)Survival Follow-Up 1 (up to 4 years)Survival Follow-Up 2 (up to 4 years)Survival Follow-Up 3 (up to 4 years)Survival Follow-Up 4 (up to 4 years)Survival Follow-Up 5 (up to 4 years)Survival Follow-Up 6 (up to 4 years)Survival Follow-Up 7 (up to 4 years)
Bevacizumab: Phase A0.7470.7600.7670.7960.8000.8310.8180.8510.8220.8270.8390.8560.8310.8150.8710.8690.8590.8800.9150.8640.8060.8110.7090.7390.7180.7920.6960.6200.8000.8100.874

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Association Between Longitudinal NLR (Longitudinal NLR ≤5 Versus NLR >5) and OS as Assessed by Hazard Ratio

NLR was calculated from the laboratory values as the ratio of Neutrophils to Lymphocytes. Longitudinal NLR was assessed by treating the NLR measurements taken over the time-course of treatment as a time-dependent covariate. OS was defined as the time from the start of initial treatment to the date of death, regardless of the cause of death. The association between longitudinal NLR (longitudinal NLR ≤5 vs NLR >5) and OS was reported as hazard ratio. (NCT01588990)
Timeframe: Baseline up to death or end of study (up to 4 years)

Interventionhazard ratio (Number)
Bevacizumab: Phase A and Phase B2.2

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Association Between Longitudinal NLR (Longitudinal NLR ≤5 Versus NLR >5) and PFS as Assessed by Hazard Ratio

NLR was calculated from the laboratory values as the ratio of Neutrophils to Lymphocytes. Longitudinal NLR was assessed by treating the NLR measurements taken over the time-course of treatment as a time-dependent covariate. PFS was defined as time from the start of initial treatment to documentation of first disease progression or death from any cause, whichever occurred first. Disease progression was determined according to standard practice based on radiological, biochemical (CEA) or clinical factors. Determination of disease progression was to be unequivocal and was defined as: an unequivocal and clinically meaningful increase in size of known tumors, appearance of one or more new lesions, death due to disease without prior objective documentation of progression, elevated CEA accompanied by other radiological or clinical evidence of progression, or symptomatic deterioration. The association between longitudinal NLR (longitudinal NLR ≤5 vs N>5) and PFS was reported as hazard ratio. (NCT01588990)
Timeframe: Baseline up to disease progression, death or end of study (up to 4 years)

Interventionhazard ratio (Number)
Bevacizumab: Phase A and Phase B1.3

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Association Between Neutrophil to Lymphocyte Ratio (NLR) [NLR ≤5 Versus NLR >5] and Progression-Free Survival (PFS) as Assessed by Hazard Ratio

NLR was calculated from the laboratory values as the ratio of Neutrophils to Lymphocytes. PFS was defined as the time from the start of initial treatment to documentation of first disease progression or death from any cause, whichever occurred first. Disease progression was determined according to standard practice based on radiological, biochemical (carcinoembryonic antigen [CEA]) or clinical factors. Determination of disease progression was to be unequivocal and was defined as any of the following: an unequivocal and clinically meaningful increase in the size of known tumors, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, elevated CEA accompanied by other radiological or clinical evidence of progression, or symptomatic deterioration. The association between NLR (NLR less than or equal to [≤] 5 vs greater than [>] 5) and PFS was reported as hazard ratio. (NCT01588990)
Timeframe: Baseline up to disease progression, death or end of study (up to 4 years)

Interventionhazard ratio (Number)
Bevacizumab: Phase A and Phase B1.4

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Association Between NLR (NLR ≤5 Versus NLR >5) and OS as Assessed by Hazard Ratio

NLR was calculated from the laboratory values as the ratio of Neutrophils to Lymphocytes. OS was defined as the time from the start of initial treatment to the date of death, regardless of the cause of death. The association between NLR (NLR ≤ 5 vs > 5) and OS was reported as hazard ratio. (NCT01588990)
Timeframe: Baseline up to disease progression, death or end of study (up to 4 years)

Interventionhazard ratio (Number)
Bevacizumab: Phase A and Phase B1.6

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Association Between NLR Normalization (First NLR Post-Baseline ≤5 Versus NLR >5) and PFS as Assessed by Hazard Ratio

NLR was calculated from laboratory values as ratio of Neutrophils to Lymphocytes. NLR normalization was assessed by adding first post-baseline measurement of NLR to the primary model. This is equivalent to testing whether first change in NLR is significantly associated with outcome. PFS was defined as time from start of initial treatment to documentation of first disease progression or death from any cause. Disease progression was determined according to standard practice based on radiological, biochemical (CEA) or clinical factors. Determination of disease progression was defined as: an unequivocal and clinically meaningful increase in size of known tumors, appearance of ≥1 new lesions, death due to disease without prior objective documentation of progression, elevated CEA accompanied by other radiological or clinical evidence of progression, or symptomatic deterioration.The association between NLR normalization (first NLR post-baseline ≤5 vs >5) and PFS was reported as hazard ratio. (NCT01588990)
Timeframe: Baseline up to disease progression, death or end of study (up to 4 years)

Interventionhazard ratio (Number)
Bevacizumab: Phase A and Phase B0.9

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Duration of Disease Control (DDC) as Assessed by the Investigator Based on Routine Clinical Practice: Overall

DDC was defined as PFS + PFS-B. In cases where a participant did not enter Phase B, then DDC was defined as PFS. PFS was defined as time from start of initial treatment to documentation of first disease progression or death from any cause, whichever occurred first. PFS-B was time from start of Phase B treatment to documentation of second disease progression or death from any cause, whichever occurred first. Disease progression was determined according to standard practice based on radiological, biochemical (CEA) or clinical factors. Determination of disease progression was to be unequivocal and was defined as any of the following: an unequivocal and clinically meaningful increase in the size of known tumors, appearance of one or more new lesions, death due to disease without prior objective documentation of progression, elevated CEA accompanied by other radiological or clinical evidence of progression, or symptomatic deterioration. Kaplan-Meier methodology was used to estimate DDC. (NCT01588990)
Timeframe: Baseline up to disease progression, death or end of study (up to 4 years)

Interventionmonths (Median)
Bevacizumab: Phase A and Phase B14.0

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OS: Phase B

Overall Survival in Phase B was defined as the time from the start of treatment in Phase B to death due to any cause. Kaplan-Meier methodology was used to estimate OS. (NCT01588990)
Timeframe: From the start of Phase B treatment death or end of study (up to 4 years)

Interventionmonths (Median)
Bevacizumab: Phase B14.9

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Overall Survival (OS) From the Start of Treatment to Study Completion: Overall

OS was defined as the time from the start of initial treatment to the date of death, regardless of the cause of death. Kaplan-Meier methodology was used to estimate OS. (NCT01588990)
Timeframe: Baseline until death or end of study (up to 4 years)

Interventionmonths (Median)
Bevacizumab: Phase A and Phase B25.0

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Percentage of Participants Who Underwent Liver Resection: Overall

The results include percentage of participants who underwent potentially curative liver resection. (NCT01588990)
Timeframe: Baseline up to disease progression, death or end of study (up to 4 years)

Interventionpercentage of participants (Number)
Bevacizumab: Phase A and Phase B1.6

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Median Progression-Free Survival

The median progression free survival as measured from the start of treatment until the time of disease progression or death, whichever occurs first. Disease status was evaluated using RECIST (Response Evaluation Criteria in Solid Tumors). Disease progression is defined as having at least a 20% increase in the sum of the longest diameter (LD) of target lesion, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT01591733)
Timeframe: From the start of treatment until death or disease progression, median duration of follow-up of 14.7 months

InterventionMonths (Median)
FOLFIRINOX + Radiation14.7

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Rate of R0 Resection

The rate of R0 resection of patients with borderline-resectable adenocarcinoma of the head of the pancreas, along with borderline-resectable and resectable adenocarcinoma of the body and tail of the pancreas. R0 resection means that following surgery, no cancer cells are seen microscopically at the resection margin. (NCT01591733)
Timeframe: Post-surgery (about 4 months post baseline)

InterventionParticipants (Count of Participants)
All Eligible - FOLFIRINOX + Radiation31
Resected Participants - FOLFIRINOX + Radiation31

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30 Day Post-operative Mortality Rate

The number of participants that died within 30 days after undergoing pancreaticoduodenectomy or distal pancreatectomy. (NCT01591733)
Timeframe: 30 days post surgery (about 6 months from baseline)

InterventionParticipants (Count of Participants)
FOLFIRINOX + Radiation0

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Median Overall Survival

Median overall survival, as measured from the start of treatment until the time of death. (NCT01591733)
Timeframe: From the start of treatment until the time of death, median duration of follow-up of 37.7 months

InterventionMonths (Median)
FOLFIRINOX + Radiation37.7

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Local Control Rates

The number of participants that achieved local control. Local control was evaluated using RECIST (Response Evaluation Criteria in Solid Tumors). Local Failure is defined as progression of the primary tumor, or to the reappearance of tumor at the primary site. (NCT01591733)
Timeframe: From the start of treatment until the end of treatment with FOLFIRINOX, or until disease progression (median duration of follow-up of approximately 14 months)

InterventionParticipants (Count of Participants)
FOLFIRINOX + Radiation32

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Response Rate

The percentage of patients for whom the best overall response is complete response (CR) or partial response (PR). A CR occurs when all lesions disappear; whereas, a PR is indicated when there is at least a 30% decrease in the sum of the longest diameters (LD) of the target lesion. A PD (progressive disease) occurs when there is at least a 20% increase in the sum of the LD relative to the smallest sum LD recorded since treatment is initiated. Disease is considered stable if there is no response and no PD. All patients were assigned a best response for inclusion in this calculation in accordance with the protocol. (NCT01661972)
Timeframe: approximately every 9 weeks and/or restaging, through study completion

Interventionpercentage of participants (Number)
Phase 22.22

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Number of Dose-Limiting Toxicities (Phase 1)

"Number of patients experiencing a dose-limiting toxicity in each cohort.~A dose-limiting toxicity is defined as Grade 4 neutropenia, thrombocytopenia or anemia or grade 3 neutropenia or thrombocytopenia lasting over 7 days Grade 3 thrombocytopenia associated with bleeding Febrile Neutropenia Nausea/Vomiting or Diarrhea ≥ grade 3 and lasting ≥ 4 days despite adequate supportive measures Grade ≥ 3 Bilirubin, ALT or AST > 7 days Other non-hematologic toxicity ≥ grade 3 excluding alopecia, anorexia, fatigue, hypertension, isolated lab abnormalities (not clinically significant) and/ rare, idiosyncratic reactions to any of the study drugs. Anorexia, fatigue and hypertension will be considered as DLT only if they reach grade 4 or are considered unmanageable Treatment delay of ≥ 14 days for cycle 2 due to unresolved toxicity Treatment-related death or clinically significant,treatment-related hospitalization" (NCT01661972)
Timeframe: 28 days

InterventionParticipants (Count of Participants)
Phase 1 Cohort 11
Phase 1 Cohort 22

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Median Progression Free Survival (PFS)

Time in months from the start of study treatment to the date of first progression (PD) according to the RECIST criteria, or death due to any cause. Per RECIST criteria, a PD is indicated when there is at least a 20% increase in the sum of the longest diameters from target lesions relative to the smallest sum recorded since treatment is initiated. Median PFS was estimated using a Kaplan-Meier curve, and is the time at which 50% of patients remain alive without disease progression. (NCT01661972)
Timeframe: approximately 5 months

InterventionMonths (Median)
Phase 23.91

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Median Survival

Time in months from the start of study treatment to date of death due to any cause. Median survival was estimated using a Kaplan-Meier curve and is the time point at which 50% of patients remain alive. (NCT01661972)
Timeframe: Subjects will be followed until death which is estimated to be on average 6 months - 1 year after coming off protocol therapy

Interventionmonths (Median)
Phase 27.43

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Number of Participants With Routine Clinical Use of Capecitabine as Per the Line of Treatment

Choice of line of treatment in adjuvant and advanced or metastatic cancer for capecitabine was observed. (NCT01664494)
Timeframe: Approximately 3 years; or up to disease progression, death or stop of capecitabine treatment, whichever occurred first

InterventionParticipants (Number)
Adjuvant therapyFirst line therapySecond line therapyThird line therapy
Capecitabine2201768978

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Median Dose of Capecitabine

Median dose of capecitabine for treatment of metastatic colorectal cancer, adjuvant colon cancer, advanced gastric cancer, or metastatic breast cancer in this study was presented. (NCT01664494)
Timeframe: Approximately 3 years; or up to disease progression, death or stop of capecitabine treatment, whichever occurred first

InterventionMilligrams (Median)
Month 7From Month 8 onwards
Capecitabine35003000

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One-year Survival Rate

Subjects will be followed after treatment completed to determine length of survival rate. The primary study objective was 1-year overall survival (OS, failure: death due to any cause). The Kaplan-Meier method was used to estimate the one-year OS. Secondary Objectives were the frequency of serious adverse events, disease control rate and progression-free survival. (NCT01683422)
Timeframe: One year after treatment completed.

Interventionpercentage of participants (Number)
Proton Radiation55.6

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Mean Duration of Capecitabine Therapy

(NCT01696695)
Timeframe: Baseline up to 1254 days

InterventionDays (Mean)
mCRC Participants188.8

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Percentage of Participants With Dose Modification of Capecitabine

(NCT01696695)
Timeframe: Baseline up to 1254 days

InterventionPercentage of participants (Number)
mCRC Participants85.6

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Percentage of Participants With Overall Response as Assessed by Investigator Using RECIST v1.1

Overall response is defined as a complete response (CR) or a partial response (PR) as determined by the Investigator using RECIST v1.1 on 2 consecutive occasions at least 6 weeks apart. Participants were evaluated for tumor response per RECIST v1.1 and assessed by computed tomography (CT) or magnetic resonance imaging (MRI):CR was defined as complete disappearance of all target lesions and non-target disease, with the exception of nodal disease. All nodes, both target and non-target, must decrease to normal (short axis less than (<) 10 mm). No new lesions.PR was defined as greater than or equal to (>=) 30% decrease under baseline of the sum of diameters of all target lesions. The short axis was used in the sum for target nodes, while the longest diameter was used in the sum for all other target lesions. No unequivocal progression of non-target disease. No new lesions. (NCT01696695)
Timeframe: Baseline until disease progression, death, unacceptable toxicity, or withdrawal of consent, whichever occurred first, evaluated up to Day 1254

InterventionPercentage of participants (Number)
mCRC Participants24.3

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PFS by Therapeutic Regimens

PFS was assessed using RECIST v1.1 and is defined as the time from the first dose of indicated treatment to PD or death, whichever occurred first. Participants who did not progress or died while being followed were censored on the date of the last visit. PD: at least 20% increase in the sum of diameters of target lesions compared to the smallest sum of diameters on-study and absolute increase of at least 5 mm; progression of existing non-target lesions; or presence of new lesions. Median PFS was estimated using Kaplan-Meier method. (NCT01696695)
Timeframe: Baseline until disease progression, death, unacceptable toxicity, or withdrawal of consent, whichever occurred first, evaluated up to Day 1254

InterventionDays (Median)
Capecitabine monotherapy (n=246)Capecitabine + bevacizumab (n=25)Capecitabine + irinotecan (n=106)Capecitabine + irinotecan + bevacizumab (n= 91)Capecitabine + oxaliplatin (n=173)Capecitabine + oxaliplatin + bevacizumab (n= 49)
mCRC Participants194391242392240392

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Percentage of Participants Who Underwent Metastasectomy

Metastasectomy is the surgical removal of metastases, which are secondary cancerous growths that have spread from cancer originating in another organ in the body. (NCT01696695)
Timeframe: Baseline up to 1254 days

InterventionPercentage of participants (Number)
mCRC Participants6.2

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Percentage of Participants With Clinical Benefit as Assessed Using RECIST v1.1

Clinical benefit was defined as having a confirmed CR, PR or stable disease (SD) for at least 24 weeks on study according to RECIST v1.1.CR: complete disappearance of all target lesions and non-target disease,with the exception of nodal disease.All nodes,both target and non-target, must decrease to normal (short axis <10 mm).No new lesions.PR: >=30% decrease under baseline of the sum of diameters of all target lesions.The short axis was used in the sum for target nodes,while the longest diameter was used in the sum for all other target lesions.No unequivocal progression of non-target disease.No new lesions.SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD,taking as reference the smallest sum diameters while on study.PD:at least 20% increase in the sum of diameters of target lesions compared to the smallest sum of diameters on-study and absolute increase of at least 5 mm, progression of existing non-target lesions,or presence of new lesions. (NCT01696695)
Timeframe: Baseline until disease progression, death, unacceptable toxicity, or withdrawal of consent, whichever occurred first, evaluated up to Day 1254

InterventionPercentage of participants (Number)
mCRC Participants82.9

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Median Progression-free Survival (PFS)

PFS was assessed using Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST v1.1) and is defined as the time from the first dose of indicated treatment to disease progression (PD) or death, whichever occurred first. Participants who did not progress or died while being followed were censored on the date of the last visit. Participants without post-baseline tumor assessments were conservatively censored on the date of first study medication, which is PFS was assigned a value of 1 day. PD: at least 20 percent (%) increase in the sum of diameters of target lesions compared to the smallest sum of diameters on-study and absolute increase of at least 5 millimeter (mm); progression of existing non-target lesions; or presence of new lesions. Median PFS was estimated using Kaplan-Meier method. (NCT01696695)
Timeframe: Baseline until disease progression, death, unacceptable toxicity, or withdrawal of consent, whichever occurred first, evaluated up to Day 1254

InterventionDays (Median)
mCRC Participants254

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Phase 1 (LA/mGC): AUC(0-inf) of 5-Fluorouracil (Metabolite of Capecitabine)

5-fluorouracil is a metabolite of capecitabine. AUC(0-inf) is the measure of total drug exposure and is dependent on the total amount of drug absorbed. AUC(0-inf) for 5-fluorouracil was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionh*ng/mL (Mean)
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape213

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Phase 1 (LA/mGC): AUC(0-inf) of Capecitabine

AUC(0-inf) is the measure of total drug exposure and is dependent on the total amount of drug absorbed. AUC(0-inf) for capecitabine was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionh*ng/mL (Mean)
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape5131

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Phase 1 (LA/mGC): Cmax of 5-Fluorouracil (Metabolite of Capecitabine)

5-fluorouracil is a metabolite of capecitabine. Cmax for 5-fluorouracil was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionng/mL (Mean)
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape137

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Phase 1 (LA/mGC): Cmax of Capecitabine

Cmax for capecitabine was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionng/mL (Mean)
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape4925

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Phase 1 (LA/mGC): MTD of Capecitabine When Combined With Trastuzumab Emtansine (2.4 mg/kg QW)

MTD was defined as the dose level for which the probability of DLT is equal to a protocol-specified target probability. A DLT was defined as any one of the following study treatment related toxicities: Uncomplicated Grade 4 thrombocytopenia that does not recover before Day 21; thrombocytopenia complicated with clinically significant bleeding requiring medical intervention; Grade 4 neutropenia lasting >7 consecutive days; febrile neutropenia with ANC <1000 cells/mm^3; Grade >/=3 diarrhea or Grade 3 hand-foot syndrome; any other Grade >/=3 toxicity prohibiting start of Cycle 2; Grade 2 toxicity requiring treatment interruption for >14 days; <14 full doses of capecitabine; Cycle 2 dose level <100%. (NCT01702558)
Timeframe: Continuously during 3 weeks

Interventionmg/m^2 (Number)
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape700

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Phase 1 (LA/mGC): Percentage of Participants With BOR as Assessed by the Investigator According to RECIST v1.1

Tumor response was assessed by the investigator according to RECIST v1.1. BOR in Phase 1 was defined as percentage of participants with a CR or PR. CR was defined as the disappearance of all TLs and non-TLs; SA reduction to <10 mm for nodal TLs/non-TLs; and no new lesions. PR was defined as >/=30% decrease in SoD of TLs, taking as reference the baseline SoD; no progression in non-TLs; and no new lesions. (NCT01702558)
Timeframe: Baseline until CR/PR, consent withdrawal, or study end whichever occurred first (up to approximately 1.5 years overall)

Interventionpercentage of participants (Number)
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape83.3

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Phase 1 (LA/mGC): t1/2 of 5-Fluorouracil (Metabolite of Capecitabine)

5-fluorouracil is a metabolite of capecitabine. Plasma terminal half-life is the time measured for the plasma drug concentration to decrease by one half during the elimination phase of the drug. t1/2 for 5-fluorouracil was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionhours (Mean)
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape0.83

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Phase 1 (LA/mGC): Percentage of Participants With DLTs

A DLT was defined as any one of the following study treatment related toxicities: Uncomplicated Grade 4 thrombocytopenia that does not recover before Day 21; thrombocytopenia complicated with clinically significant bleeding requiring medical intervention; Grade 4 neutropenia lasting >7 consecutive days; febrile neutropenia with ANC <1000 cells/mm^3; Grade >/=3 diarrhea or Grade 3 hand-foot syndrome; any other Grade >/=3 toxicity prohibiting start of Cycle 2; Grade 2 toxicity requiring treatment interruption for >14 days; <14 full doses of capecitabine; Cycle 2 dose level <100%. (NCT01702558)
Timeframe: Continuously during 3 weeks

Interventionpercentage of participants (Number)
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape0.0

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Phase 1 (LA/mGC): Serum Concentration of Trastuzumab

Trastuzumab was derived from trastuzumab emtansine. (NCT01702558)
Timeframe: Pre-trastuzumab emtansine dose (0 h) on Day 1 Cycle 2; 15-30 min after end of trastuzumab emtansine infusion (maximum infusion duration = 90 min) on Day 2 Cycle 1 and Day 1 Cycle 2 (cycle length=21 days)

Interventionmcg/mL (Mean)
Cycle 1, Post-doseCycle 2, Pre-doseCycle 2, Post-dose
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape33.118.557.6

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Phase 1 (mBC): Cmax of 5-Fluorouracil (Metabolite of Capecitabine)

5-fluorouracil is a metabolite of capecitabine. Cmax for 5-fluorouracil was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionng/mL (Mean)
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape148
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape143

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Phase 1 (mBC): AUC(0-inf) of 5-Fluorouracil (Metabolite of Capecitabine)

5-fluorouracil is a metabolite of capecitabine. AUC(0-inf) is the measure of total drug exposure and is dependent on the total amount of drug absorbed. AUC(0-inf) for 5-fluorouracil was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionh*ng/mL (Mean)
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape257
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape244

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Phase 1 (mBC): Percentage of Participants With BOR as Assessed by the Investigator According to RECIST v1.1

Tumor response was assessed by the investigator according to RECIST v1.1. BOR in Phase 1 was defined as percentage of participants with a CR or PR. CR was defined as the disappearance of all TLs and non-TLs; SA reduction to <10 mm for nodal TLs/non-TLs; and no new lesions. PR was defined as >/=30% decrease in SoD of TLs, taking as reference the baseline SoD; no progression in non-TLs; and no new lesions. (NCT01702558)
Timeframe: Baseline until CR/PR, consent withdrawal, or study end whichever occurred first (up to approximately 3.5 years overall)

Interventionpercentage of participants (Number)
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape83.3
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape100.0

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Phase 1 (mBC): Area Under the Plasma Concentration-Time Curve From Time Zero to Infinity (AUC[0-inf]) of Capecitabine

AUC(0-inf) is the measure of total drug exposure and is dependent on the total amount of drug absorbed. AUC(0-inf) for capecitabine was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionhours*nanograms per milliliter (h*ng/mL) (Mean)
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape3973
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape5440

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Phase 1 (mBC): Maximum Tolerated Dose (MTD) of Capecitabine When Combined With Trastuzumab Emtansine (3.6 mg/kg Every 3 Weeks)

MTD was defined as the dose level for which the probability of DLT is equal to a protocol-specified target probability. A DLT was defined as any one of the following study treatment related toxicities: Uncomplicated Grade 4 thrombocytopenia that does not recover before Day 21; thrombocytopenia complicated with clinically significant bleeding requiring medical intervention; Grade 4 neutropenia lasting >7 consecutive days; febrile neutropenia with ANC <1000 cells/mm^3; Grade >/=3 diarrhea or Grade 3 hand-foot syndrome (in absence of DPD deficiency only for DL 1); any other Grade >/=3 toxicity prohibiting start of Cycle 2; Grade 2 toxicity requiring treatment interruption for >14 days (>7 days for DL 1); for DL -1 only: <14 full doses of capecitabine; Cycle 2 dose level <100%. (NCT01702558)
Timeframe: Continuously during Cycle 1 (up to 3 weeks)

Interventionmg/m^2 (Number)
Phase 1 (mBC) Cohort 1: T-DM1 + Cape700

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Phase 1 (mBC): Maximum Observed Plasma Concentration (Cmax) of Capecitabine

Cmax for Capecitabine was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for percent coefficient of variation (CV%) and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionnanograms per milliliter (ng/mL) (Mean)
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape2990
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape5652

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Phase 1 (LA/mGC): Serum Concentration of Trastuzumab Emtansine

(NCT01702558)
Timeframe: Pre-trastuzumab emtansine dose (0 h) on Day 1 Cycle 2; 15-30 min after end of trastuzumab emtansine infusion (maximum infusion duration = 90 min) on Day 2 Cycle 1 and Day 1 Cycle 2 (cycle length=21 days)

Interventionmcg/mL (Mean)
Cycle 1, Post-doseCycle 2, Pre-doseCycle 2, Post-dose
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape30.110.146.4

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Phase 1 (LA/mGC): t1/2 of Capecitabine

Plasma terminal half-life is the time measured for the plasma drug concentration to decrease by one half during the elimination phase of the drug. t1/2 for capecitabine was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionhours (Mean)
Phase 1 (LA/mGC) Cohort 2 (DL -1): T-DM1 + Cape0.65

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Phase 1 (mBC): Serum Concentration of Trastuzumab Emtansine

(NCT01702558)
Timeframe: Pre-trastuzumab emtansine dose (0 hour [h]) on Day 1 Cycle 2; 15-30 minutes (min) after end of trastuzumab emtansine infusion (maximum infusion duration = 90 min) on Day 2 Cycle 1 and Day 1 Cycle 2 (cycle length=21 days)

,
Interventionmicrograms per milliliter (mcg/mL) (Mean)
Cycle 1, Post-doseCycle 2, Pre-doseCycle 2, Post-dose
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape78.62.178.5
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape81.31.1770.5

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Phase 1 (mBC): Serum Concentration of Trastuzumab

Trastuzumab was derived from trastuzumab emtansine. (NCT01702558)
Timeframe: Pre-trastuzumab emtansine dose (0 h) on Day 1 Cycle 2; 15-30 min after end of trastuzumab emtansine infusion (maximum infusion duration = 90 min) on Day 2 Cycle 1 and Day 1 Cycle 2 (cycle length=21 days)

,
Interventionmcg/mL (Mean)
Cycle 1, Post-doseCycle 2, Pre-doseCycle 2, Post-dose
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape92.914.094.7
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape89.111.874.8

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Phase 2 (mBC): Time to Treatment Failure (TTF) as Assessed by the Investigator According to RECIST v1.1

TTF was defined as the time (in months) from randomization until treatment failure (PD, death, withdrawal due to AE or laboratory abnormality, or refusal of treatment). PD as assessed by the investigator according to RECIST v1.1 was defined as >/=20% relative increase with >/=5 mm of absolute increase in the SoD, taking as reference the smallest SoD recorded since treatment started; 1 or more new lesion(s); and/or unequivocal progression of non-TLs. Participants who did not experience any of the above events while on study were censored on the date of their last tumor assessment. The median TTF and 90% CI was estimated using Kaplan-Meier method. (NCT01702558)
Timeframe: Baseline until treatment failure, consent withdrawal, or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionmonths (Median)
Phase 2 (mBC): T-DM1 + Cape9.86
Phase 2 (mBC): T-DM17.66

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Phase 2 (mBC): Time to Response (TTR) as Assessed by the Investigator According to RECIST v1.1

Tumor response was assessed by the investigator according to RECIST v1.1. TTR was defined as the time (in months) from randomization to first documentation of confirmed PR or CR (whichever occurred first). CR was defined as the disappearance of all TLs and non-TLs; SA reduction to <10 mm for nodal TLs/non-TLs; and no new lesions. PR was defined as >/=30% decrease in SoD of TLs, taking as reference the baseline SoD; no progression in non-TLs; and no new lesions. (NCT01702558)
Timeframe: Baseline until first documentation of confirmed PR or CR, whichever occurred first (up to approximately 2.5 years overall)

Interventionmonths (Median)
Phase 2 (mBC): T-DM1 + Cape2.10
Phase 2 (mBC): T-DM12.10

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Phase 2 (mBC): Time to Progression (TTP) as Assessed by the Investigator According to RECIST v1.1

Tumor response was assessed by the investigator according to RECIST v1.1. TTP was defined as the time (in months) from randomization to the first occurrence of PD. PD was defined as >/=20% relative increase with >/=5 mm of absolute increase in the SoD, taking as reference the smallest SoD recorded since treatment started; 1 or more new lesion(s); and/or unequivocal progression of non-TLs. Participants with no documented PD at the time of study end (including participants who died before PD) or who were lost to follow-up were censored on the date of the last tumor assessment. The median TTP and 90% CI was estimated using Kaplan-Meier method. (NCT01702558)
Timeframe: Baseline until PD, consent withdrawal, or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionmonths (Median)
Phase 2 (mBC): T-DM1 + Cape10.38
Phase 2 (mBC): T-DM110.32

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Phase 2 (mBC): Progression-Free Survival (PFS) as Assessed by the Investigator According to RECIST v1.1

Tumor response was assessed by the investigator according to RECIST v1.1. PFS was defined as the time (in months) from randomization until the first documented PD or death from any cause, whichever occurred first. PD was defined as >/=20% relative increase with >/=5 mm of absolute increase in the SoD, taking as reference the smallest SoD recorded since treatment started; 1 or more new lesion(s); and/or unequivocal progression of non-TLs. Participants with no PFS events were censored on the date of the last tumor assessment. Participants without post-baseline tumor assessment were censored at randomization plus 1 day. The median PFS and 90% CI was estimated using Kaplan-Meier method. (NCT01702558)
Timeframe: Baseline until PD, death from any cause, consent withdrawal, or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionmonths (Median)
Phase 2 (mBC): T-DM1 + Cape10.15
Phase 2 (mBC): T-DM19.82

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Phase 2 (mBC): Percentage of Participants With Treatment Failure as Assessed by the Investigator According to RECIST v1.1

Treatment failure was defined as occurrence of any of the following event while on treatment: PD, death, withdrawal due to adverse event (AE) or laboratory abnormality, or refusal of treatment. PD as assessed by the investigator according to RECIST v1.1 was defined as >/=20% relative increase with >/=5 mm of absolute increase in the SoD, taking as reference the smallest SoD recorded since treatment started; 1 or more new lesion(s); and/or unequivocal progression of non-TLs. (NCT01702558)
Timeframe: Baseline until treatment failure, consent withdrawal, or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionpercentage of participants (Number)
Phase 2 (mBC): T-DM1 + Cape77.8
Phase 2 (mBC): T-DM183.8

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Phase 2 (mBC): Percentage of Participants With PD as Assessed by the Investigator According to RECIST v1.1 or Death From Any Cause

Tumor response was assessed by the investigator according to RECIST v1.1. PD was defined as >/=20% relative increase with >/=5 mm of absolute increase in the SoD, taking as reference the smallest SoD recorded since treatment started; 1 or more new lesion(s); and/or unequivocal progression of non-TLs. (NCT01702558)
Timeframe: Baseline until PD, death from any cause, consent withdrawal, or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionpercentage of participants (Number)
Phase 2 (mBC): T-DM1 + Cape67.9
Phase 2 (mBC): T-DM173.8

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Phase 2 (mBC): Percentage of Participants With PD as Assessed by the Investigator According to RECIST v1.1

Tumor response was assessed by the investigator according to RECIST v1.1. PD was defined as >/=20% relative increase with >/=5 mm of absolute increase in the SoD, taking as reference the smallest SoD recorded since treatment started; 1 or more new lesion(s); and/or unequivocal progression of non-TLs. (NCT01702558)
Timeframe: Baseline until PD, consent withdrawal, or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionpercentage of participants (Number)
Phase 2 (mBC): T-DM1 + Cape64.2
Phase 2 (mBC): T-DM170.0

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Phase 2 (mBC): Percentage of Participants With Clinical Benefit as Assessed by the Investigator According to RECIST v1.1

The clinical benefit was defined as a confirmed response of CR, PR, or stable disease (SD) that lasted for at least 6 months. Tumor response was assessed by the investigator according to RECIST v1.1. CR: the disappearance of all TLs and non-TLs; SA reduction to <10 mm for nodal TLs/non-TLs; and no new lesions. PR: >/=30% decrease in SoD of TLs, taking as reference the baseline SoD; no progression in non-TLs; and no new lesions. PD: >/=20% relative increase with >/=5 mm of absolute increase in the SoD, taking as reference the smallest SoD recorded since treatment started; 1 or more new lesion(s); and/or unequivocal progression of non-TLs. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SoD on study. The 90% CI was computed using Clopper-Pearson approach. (NCT01702558)
Timeframe: Baseline until clinical benefit response, consent withdrawal, or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionpercentage of participants (Number)
Phase 2 (mBC): T-DM1 + Cape66.7
Phase 2 (mBC): T-DM162.5

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Phase 2 (mBC): Percentage of Participants With Best Overall Response (BOR) as Assessed by the Investigator According to Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST v1.1)

Tumor response was assessed by the investigator according to RECIST v1.1. BOR was defined as percentage of participants with a complete response (CR) or partial response (PR) that was confirmed by repeat assessments >/=4 weeks after initial documentation. CR was defined as the disappearance of all target lesions (TLs) and non-TLs; short axis (SA) reduction to <10 millimeters (mm) for nodal TLs/non-TLs; and no new lesions. PR was defined as >/=30% decrease in sum of diameters (SoD) of TLs, taking as reference the baseline SoD; no progression in non-TLs; and no new lesions. The 90% confidence Interval (CI) was computed using Clopper-Pearson approach. (NCT01702558)
Timeframe: Baseline until CR/PR, consent withdrawal, or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionpercentage of participants (Number)
Phase 2 (mBC): T-DM1 + Cape44.4
Phase 2 (mBC): T-DM136.3

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Phase 2 (mBC): Percentage of Participants Who Died of Any Cause

(NCT01702558)
Timeframe: Baseline until death or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionpercentage of participants (Number)
Phase 2 (mBC): T-DM1 + Cape22.2
Phase 2 (mBC): T-DM126.3

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Phase 2 (mBC): Overall Survival (OS)

OS was defined as the time (in months) from randomization until death from any cause. Participants who were alive at the time of data cut-off were censored on the date of the last follow-up assessment. Participants who were lost to follow-up were censored as having no event (alive) on the date of last contact. The median OS and 90% CI was estimated using Kaplan-Meier method, which use the patients at risk as denominator rather than the whole number of patients. (NCT01702558)
Timeframe: Baseline until death or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionmonths (Median)
Phase 2 (mBC): T-DM1 + CapeNA
Phase 2 (mBC): T-DM124.71

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Phase 2 (mBC): Duration of Response (DoR) as Assessed by the Investigator According to RECIST v1.1

Tumor response was assessed by the investigator according to RECIST v1.1. DoR was defined as the time (in months) from the date of first recorded PR/CR until the date of PD or death from any cause. CR: the disappearance of all TLs and non-TLs; SA reduction to <10 mm for nodal TLs/non-TLs; and no new lesions. PR: >/=30% decrease in SoD of TLs, taking as reference the baseline SoD; no progression in non-TLs; and no new lesions. PD: >/=20% relative increase with >/=5 mm of absolute increase in the SoD, taking as reference the smallest SoD recorded since treatment started; 1 or more new lesion(s); and/or unequivocal progression of non-TLs. Participants with no documented PD after CR/PR were censored at the time of last tumor assessment. Participants without post-baseline tumor assessment were censored at randomization plus 1 day. The median DOR and 90% CI were estimated using Kaplan-Meier method. (NCT01702558)
Timeframe: From the documentation of response until PD, death, consent withdrawal, or study end whichever occurred first (up to approximately 2.5 years overall)

Interventionmonths (Median)
Phase 2 (mBC): T-DM1 + Cape11.30
Phase 2 (mBC): T-DM112.22

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Phase 1 (mBC): t1/2 of 5-Fluorouracil (Metabolite of Capecitabine)

5-fluorouracil is a metabolite of capecitabine. Plasma terminal half-life is the time measured for the plasma drug concentration to decrease by one half during the elimination phase of the drug. t1/2 for 5-fluorouracil was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionhours (Mean)
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape0.63
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape0.64

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Phase 1 (mBC): Plasma Terminal Half-Life (t1/2) of Capecitabine

Plasma terminal half-life is the time measured for the plasma drug concentration to decrease by one half during the elimination phase of the drug. t1/2 for capecitabine was estimated from plasma concentration versus time data using non-compartmental methods of analysis. Reported dispersion values are for CV% and not for standard deviation. (NCT01702558)
Timeframe: Pre-capecitabine dose (0 h) and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h post-capecitabine dose on Day 1 Cycle 1

Interventionhours (Mean)
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape0.70
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape0.39

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Phase 1 (mBC): Percentage of Participants With Dose-Limiting Toxicities (DLTs)

A DLT was defined as any one of the following study treatment related toxicities: Uncomplicated Grade 4 thrombocytopenia that does not recover before Day 21; thrombocytopenia complicated with clinically significant bleeding requiring medical intervention; Grade 4 neutropenia lasting more than (>) 7 consecutive days; febrile neutropenia with absolute neutrophil count (ANC) less than (<) 1000 cells/millimeter cube (mm^3); Grade greater than or equal to (>/=) 3 diarrhea or Grade 3 hand-foot syndrome (in absence of dihydropyrimidine dehydrogenase [DPD] deficiency only for DL 1); any other Grade >/=3 toxicity prohibiting start of Cycle 2; Grade 2 toxicity requiring treatment interruption for >14 days (>7 days for DL 1); for DL -1 only: <14 full doses of capecitabine; Cycle 2 dose level <100 percent (%). (NCT01702558)
Timeframe: Continuously during Cycle 1 (up to 3 weeks)

Interventionpercentage of participants (Number)
Phase 1 (mBC) Cohort 1 (DL 1): T-DM1 + Cape33.3
Phase 1 (mBC) Cohort 1 (DL -1): T-DM1 + Cape0.0

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Toxic Effects

Toxic effects were scored according to the National Cancer Institute Common Toxicity Criteria for Adverse Events (CTCAE), version 4.0. For the National Cancer Institute Common Toxicity Criteria for Adverse Events (CTCAE), version 4.0 scale score range from 1 to 4. A high score, that is 3 and 4, represents a high level of toxicity, whereas the minimum values, that is 1 and 2, represents a mild/modest level of toxicity. (NCT01718873)
Timeframe: up to 4 weeks after the end of the treatment

InterventionParticipants (Count of Participants)
Bevacizumab Before Chemotherapy108
Bevacizumab With Chemotherapy113

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Disease Control Rate

Disease control rate was calculated by adding complete and partial responses and stable disease. (NCT01718873)
Timeframe: At weeks 12 and 24 from randomization and every 3 months thereafter, assessed up to 90 months

InterventionParticipants (Count of Participants)
Bevacizumab Before Chemotherapy107
Bevacizumab With Chemotherapy103

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Objective Response Rate

"Objective response rate (ORR), according to Response Evaluation Criteria in Solid Tumors (RECIST),version 1.1, was the primary end point and was defined as the number of complete plus partial responses divided by the number of enrolled patients.~Per RECIST v 1.1 for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR." (NCT01718873)
Timeframe: Objective response was assessed by computed tomographic scan or other appropriate imaging at weeks 12 and 24 from randomization, and every 3 months thereafter, assessed up to 90 months.

Interventionparticipants (Number)
Bevacizumab Before Chemotherapy65
Bevacizumab With Chemotherapy66

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Progression-free Survival (PFS)

"Progression-free survival was defined as the time from randomization to the date of progression or death, whichever occurred first. Patients without progression were censored on the date of the last follow-up visit.~Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions." (NCT01718873)
Timeframe: assessed up to 90 months

Interventionmonths (Median)
Bevacizumab Before Chemotherapy11.7
Bevacizumab With Chemotherapy10.5

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Overall Survival

Overall survival was defined as the time from randomization to the date of death. Patients alive at the time of the final analysis were censored on the date of the last follow-up information available. (NCT01718873)
Timeframe: assessed up to 90 months

Interventionmonths (Median)
Bevacizumab Before Chemotherapy29.8
Bevacizumab With Chemotherapy24.1

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Incidence and Severity of Adverse Events as Measured by Number of Participants Who Experience Grade 3 and Higher Adverse Events

NCI Common Terminology Criteria for Adverse Events (CTCAE) version 4.0 (NCT01722162)
Timeframe: Up to 6 months

,
Interventionparticipants (Number)
Small intestinal obstructionFatigueUrinary tract infectionBlood bilirubin increasedPeripheral motor neuropathyPeripheral sensory neuropathyDyspneaHypertensionThromboembolic eventAnemiaHeart failureColonic fistulaColonic perforationGram-negative bacilli infectionClostridium bloodstream infectionAlanine aminotransferase increasedAnorexiaBone painGeneralized muscle weaknessMuscle weakness lower limbsUrinary retentionRespiratory failure
Arm A: (Start Levocetirizine After Bevacizumab/Capecitabine)1112111110000000000000
Arm B: (Start Levocetirizine Before Bevacizumab/Capecitabine)0100002201111111111111

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Progression Free Survival (Arm B)

"Time from start of treatment to the time of progression or death, whichever occurs first~Progressive disease (target lesions): at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm.~Progressive disease (non-target lesions): appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. Unequivocal progression should not normally trump target lesion status. It must be representative of overall disease status change, not a single lesion increase." (NCT01722162)
Timeframe: Until progressive disease (PD) (up to 60 days)

Interventionproportion of patients with PFS (Number)
PFS Days = 29PFS Days = 33PFS Days = 44PFS Days = 50PFS Days = 54PFS Days = 60
Arm A: (Start Levocetirizine After Bevacizumab/Capecitabine)0.9460.8920.8380.6860.6310.576

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Progression Free Survival (Arm A)

"Time from start of treatment to the time of progression or death, whichever occurs first~Progressive disease (target lesions): at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm.~Progressive disease (non-target lesions): appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. Unequivocal progression should not normally trump target lesion status. It must be representative of overall disease status change, not a single lesion increase." (NCT01722162)
Timeframe: Until progressive disease (PD) (estimated to be 92 days)

Interventionproportion of patients with PFS (Number)
PFS Days = 29PFS Days = 36PFS Days = 43PFS Days = 46PFS Days = 50PFS Days = 92
Arm A: (Start Levocetirizine After Bevacizumab/Capecitabine)0.9460.8920.7390.6850.6300.575

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Mean Survival Time

(NCT01725386)
Timeframe: Up to approximately 4 years

InterventionMonths (Mean)
Monotherapy15.493
Combination Therapy15.417

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Percentage of Participants Receiving Concomitant Medications During the Study

Percentage of participants receiving concomitant medications during the study along with their prescribed monotherapy or combination therapy were reported. (NCT01725386)
Timeframe: Up to approximately 4 years

Interventionpercentage of participants (Number)
Monotherapy17.5
Combination Therapy23.8

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Percentage of Participants With Adverse Events

(NCT01725386)
Timeframe: Up to approximately 4 years

Interventionpercentage of participants (Number)
Monotherapy45.2
Combination Therapy66.7

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Percentage of Participants by Histopathology Grade Diagnosis Assessed at Baseline

To document the metastatic breast cancer participant profile, the percentage of participants with histopathology grade diagnosis of moderately differentiated, well differentiated, poorly differentiated/undifferentiated as assessed at baseline was summarized. (NCT01725386)
Timeframe: Day 1

,
Interventionpercentage of participants (Number)
Moderately DifferentiatedWell DifferentiatedPoorly Differentiated/Undifferentiated
Combination Therapy42.911.146.0
Monotherapy42.69.048.4

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Percentage of Participants With Relevant Medical History Assessed at Baseline

To document the metastatic breast cancer participant profile, the percentage of participants with relevant medical history as assessed at baseline was summarized. (NCT01725386)
Timeframe: Day 1

,
Interventionpercentage of participants (Number)
History of Other Types of CancerFamily History of Breast CancerHistory of Co-morbiditiesPremenopausal StatusPostmenopausal Status
Combination Therapy1.612.728.641.358.7
Monotherapy0.59.618.154.845.2

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Percent of Participants With Capecitabine as a First Line, Second Line, or Third Line Therapy

To document use of Capecitabine regimen in the management of participants with metastatic breast cancer, the choice of Capecitabine monotherapy versus combination therapy was summarized according to whether the selection was for the participant's first, second, or third line of treatment. (NCT01725386)
Timeframe: Up to approximately 4 years

,
Interventionpercentage of participants (Number)
First LineSecond LineThird Line
Combination Therapy55.641.33.1
Monotherapy10.671.817.6

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Progression-free Survival

This measure is the number of subjects not experiencing tumor progression at five years from initiating therapy. (NCT01726582)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
Milestones Related to Usual Therapy36

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Use of Biomarkers to Determine Course of Treatment

The number of subjects for whom a biomarker (i.e., molecular profile) was used to determine the course of treatment. (NCT01726582)
Timeframe: Initiation of therapy (approximately 4 to 12 weeks after screening) until surgery (approximately 10 to 20 weeks after screening)

InterventionParticipants (Count of Participants)
Milestones Related to Usual Therapy92

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Overall Survival in Months

This measure is the median time of survival (in months) at five years from the initiation of therapy. Results will be presented for two cohorts: subjects completing neoadjuvant therapy and surgical resection; and subjects completing neoadjuvant therapy but without surgical resection. (NCT01726582)
Timeframe: 5 years

InterventionMonths (Median)
Milestones Related to Therapy (Resected)45
Milestones Related to Therapy (Non-Resected)11

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Number of Subjects Completing Therapy Including Surgical Resection.

This outcome measure is the number of subjects completing therapy up to and including surgical resection. In this context, surgical excision of residual tumor is an option in the progression of usual care. Surgery was contraindicated for some participants. This measure is the number of subject who were eligible for and completed the surgical procedure. (NCT01726582)
Timeframe: At time of surgery (approximately 10 to 20 weeks after screening)

InterventionParticipants (Count of Participants)
Milestones Related to Usual Therapy107

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Rate of CR, Assessed According to CEA and CA 19-9 Measurements and Response Evaluation Criteria in Solid Tumors (RECIST) 1.1

Complete Response (CR): Disappearance of all non-target lesions and normalization of tumor marker level in response to ADAPT therapy. (NCT01729923)
Timeframe: 3 years

InterventionParticipants (Count of Participants)
Capecitabine and Celecoxib1

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Overall Survival

Estimated using the Kaplan-Meier method based on the ITT population starting from the time of induction chemotherapy initiation until death or last reported survival. (NCT01729923)
Timeframe: Until death or last reported survival, up to 5 years

Interventionmonths (Median)
Capecitabine and Celecoxib15

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Best Overall Response Rate Among All Patients Who Had RECIST Measurements at Baseline and at Least One Subsequent Occasion and Did Not Have Surgery or Radiation Therapy

RECIST 1.1 criteria will be used to measure changes in the size of a selected sentinel lesion for each patient. Computed tomographic images will be measured at baseline and at subsequent 9 week intervals. Changes will be measured as percentage of the baseline measure. Results will be reported as the largest negative change. For patients with no negative changes, results will be reported as the smallest positive change. (NCT01729923)
Timeframe: Serial measures at 9 week intervals up to 5 years

Interventionpercentage of baseline lesion size (Mean)
Capecitabine and Celecoxib11

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Best Overall Response Rate Among All Patients Who Had RECIST Measurements at Baseline and at Least One Subsequent Occasion

RECIST 1.1 criteria will be used to measure changes in the size of a selected sentinel lesion for each patient. Computed tomographic images will be measured at baseline and at subsequent 9 week intervals. Changes will be measured as percentage of the baseline measure. Results will be reported as the largest negative change. For patients with no negative changes, results will be reported as the smallest positive change. (NCT01729923)
Timeframe: Serial measures at 9 week intervals up to 5 years

Interventionpercentage of baseline lesion size (Mean)
Capecitabine and Celecoxib-17

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Relapse Free Survival in Patients Achieving CR

Relapse-free survival estimated using the Kaplan-Meier method based on the ITT population starting from the time of induction chemotherapy initiation. (NCT01729923)
Timeframe: Up to 5 years

Interventionmonths (Number)
Capecitabine and Celecoxib7

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Margin-negative (R0) Resection Rate

R0 rate for all participants with resection. Margin negative surgery (R0 resection) is an absolute part of the curative treatment of pancreatic cancer.The primary endpoint is correlation of a radio sensitivity index score derived from the microarray analysis and pathologic response on surgical specimens. Tumor regression Rating: R0 (Complete Response). R0 resections are scored as those resections in which the common bile duct margin, pancreatic resection margin, retroperitoneal margin are negative for tumor involvement. (NCT01754623)
Timeframe: Up to 3 years

Interventionpercentage of participants (Number)
Chemotherapy Followed by Radiation Treatment67

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Overall Survival (OS) Rate

OS at time of analysis, calculated from date of enrollment to date of death from any cause. (NCT01754623)
Timeframe: 12 months

Interventionpercentage of participants (Number)
All Participants -Chemotherapy Followed by Radiation Treatment33
Resection Group -Chemotherapy Followed by Radiation Treatment100

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Time to PFS2

Time to PFS2 was defined as time from randomization to the first occurrence of disease progression after reinduction of second-line therapy, as assessed by the Investigator using RECIST v1.1, or death from any cause, whichever occurs first. Disease progression was defined as sum of longest diameters increased by at least 20% from the smallest value on study. The sum of longest diameters must also demonstrate an absolute increase of at least 5mm. (NCT01765582)
Timeframe: Randomization up to disease progression during second-line therapy or death, whichever occurs first (up to approximately 3 years)

Interventionmonths (Median)
Arm A: Concurrent FOLFOXIRI + Bevacizumab18.76
Arm B: Sequential FOLFOXIRI + Bevacizumab13.17
Arm C: FOLFOX + Bevacizumab14.75
Arms A + B: Pooled FOLFOXIRI + Bevacizumab15.08

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Proportion of Participants Considered by the Investigator to be Unresectable on Study Enrollment Who Subsequently Underwent Attempted Curative Resections of Metastases

The proportion of participants considered by the investigator to be unresectable at study enrollment who subsequently underwent attempted curative resections of metastases was calculated as follows: number of participants considered by the investigator to be unresectable at study enrollment who subsequently underwent attempted curative resections of metastases divided by total number of participants in each arm. This outcome represents a measure of the rate of conversion from unresectable to resectable disease. (NCT01765582)
Timeframe: Randomization up to approximately 3 years

InterventionProportion of participants (Number)
Arm A: Concurrent FOLFOXIRI + Bevacizumab0.24
Arm B: Sequential FOLFOXIRI + Bevacizumab0.17
Arm C: FOLFOX + Bevacizumab0.14
Arms A + B: Pooled FOLFOXIRI + Bevacizumab0.21

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Progression-Free Survival During First-Line Therapy (PFS1)

PFS1 was defined as time from randomization to the first occurrence of disease progression during first-line therapy, as assessed by the Investigator using RECIST v1.1, or death from any cause, whichever occurs first. Disease progression was defined as sum of longest diameters increased by at least 20% from the smallest value on study. The sum of longest diameters must also demonstrate an absolute increase of at least 5 mm. (NCT01765582)
Timeframe: Randomization up to disease progression during first-line therapy or death, whichever occurs first (up to approximately 3 years)

Interventionmonths (Median)
Arm A: Concurrent FOLFOXIRI + Bevacizumab11.86
Arm B: Sequential FOLFOXIRI + Bevacizumab11.37
Arm C: FOLFOX + Bevacizumab9.46
Arms A + B: Pooled FOLFOXIRI + Bevacizumab11.70

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Percentage of Participants With Overall Response During First-Line Therapy (ORR1)

ORR1 was the percentage of participants with complete response (CR) or partial response (PR) during first-line therapy as assessed by investigator according to Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST v.1.1). CR was defined as disappearance of all extranodal target lesions and all pathological lymph nodes had to have decreased to <10 millimeter (mm) in short axis. PR was defined as at least a 30% decrease in the sum of longest diameters of target lesions, taking as reference the baseline sum diameters. ORR1 = CR + PR (NCT01765582)
Timeframe: Randomization up to disease progression during first-line therapy or death, whichever occurs first (up to approximately 3 years)

InterventionPercentage of participants (Number)
Arm A: Concurrent FOLFOXIRI + Bevacizumab72.0
Arm B: Sequential FOLFOXIRI + Bevacizumab72.8
Arm C: FOLFOX + Bevacizumab62.1
Arms A + B: Pooled FOLFOXIRI + Bevacizumab72.4

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Percentage of Participants With Adverse Events

An adverse event is any untoward medical occurrence in a subject administered a pharmaceutical product and which does not necessarily have to have a causal relationship with the treatment. An adverse event can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding, for example), symptom, or disease temporally associated with the use of a pharmaceutical product, whether or not considered related to the pharmaceutical product. Preexisting conditions which worsen during a study are also considered as adverse events. (NCT01765582)
Timeframe: Randomization up to approximately 3 years

InterventionPercentage of participants (Number)
Arm A: Concurrent FOLFOXIRI + Bevacizumab100
Arm B: Sequential FOLFOXIRI + Bevacizumab98.9
Arm C: FOLFOX + Bevacizumab100
Arms A + B: Pooled FOLFOXIRI + Bevacizumab99.4

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Overall Survival (OS)

OS was defined as the time from the date of randomization to the date of death from any cause. (NCT01765582)
Timeframe: Randomization until death due to any cause (up to approximately 3 years)

Interventionmonths (Median)
Arm A: Concurrent FOLFOXIRI + Bevacizumab33.97
Arm B: Sequential FOLFOXIRI + Bevacizumab28.32
Arm C: FOLFOX + Bevacizumab30.65
Arms A + B: Pooled FOLFOXIRI + Bevacizumab28.32

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Proportion of Participants Who Underwent Liver Metastases Resections

Reported here is the proportion of participants who underwent liver metastases resections calculated as follows: number of participants who underwent liver metastases resections divided by total number of participants in each arm. (NCT01765582)
Timeframe: Randomization up to approximately 3 years

InterventionProportion of participants (Number)
Arm A: Concurrent FOLFOXIRI + Bevacizumab0.17
Arm B: Sequential FOLFOXIRI + Bevacizumab0.10
Arm C: FOLFOX + Bevacizumab0.08
Arms A + B: Pooled FOLFOXIRI + Bevacizumab0.14

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Change From Baseline in EORTC QLQ-Gastric Cancer Module (EORTC QLQ-STO22) Score

The EORTC QLQ-STO22 is a gastric cancer quality of life questionnaire. There are 22 questions concerning disease, treatment related symptoms, side effects, dysphagia, nutritional aspects, and questions about the emotional problems of gastric cancer (dysphagia, pain, reflux, eating restrictions, anxiety, dry mouth, body image, and hair loss). The questions are grouped into five scales and 4 single items which are related to the symptoms of the disease. Most questions used 4-point scale (1 'Not at all' to 4 'Very much'; 1 question was a yes or no answer). A linear transformation was used to standardize all scores and single-items to a scale of 0 to 100; higher score=better level of functioning or greater degree of symptoms. A positive value means an increase, while a negative values means a decrease, in score at the indicated time-point relative to the score at baseline (Cycle 1, Day 1). (NCT01774786)
Timeframe: Day 1 of each 21-day treatment cycle up to 28 and 60-90 days (post-treatment [PT] monitoring visits 1 and 2, respectively) after Day 1 of last treatment cycle (up to approximately 3.5 years)

,
Interventionscore on a scale (Mean)
Anxiety: Cycle 1 (Baseline)Anxiety: Change at Cycle 2Anxiety: Change at Cycle 3Anxiety: Change at Cycle 4Anxiety: Change at Cycle 5Anxiety: Change at Cycle 6Anxiety: Change at Cycle 7Anxiety: Change at Cycle 8Anxiety: Change at Cycle 9Anxiety: Change at Cycle 10Anxiety: Change at Cycle 11Anxiety: Change at Cycle 12Anxiety: Change at Cycle 13Anxiety: Change at Cycle 14Anxiety: Change at Cycle 15Anxiety: Change at Cycle 16Anxiety: Change at Cycle 17Anxiety: Change at Cycle 18Anxiety: Change at Cycle 19Anxiety: Change at Cycle 20Anxiety: Change at Cycle 21Anxiety: Change at Cycle 22Anxiety: Change at Cycle 23Anxiety: Change at Cycle 24Anxiety: Change at Cycle 25Anxiety: Change at Cycle 26Anxiety: Change at Cycle 27Anxiety: Change at Cycle 28Anxiety: Change at PT Visit 1Anxiety: Change at PT Visit 2Body Image: Cycle 1 (Baseline)Body Image: Change at Cycle 2Body Image: Change at Cycle 3Body Image: Change at Cycle 4Body Image: Change at Cycle 5Body Image: Change at Cycle 6Body Image: Change at Cycle 7Body Image: Change at Cycle 8Body Image: Change at Cycle 9Body Image: Change at Cycle 10Body Image: Change at Cycle 11Body Image: Change at Cycle 12Body Image: Change at Cycle 13Body Image: Change at Cycle 14Body Image: Change at Cycle 15Body Image: Change at Cycle 16Body Image: Change at Cycle 17Body Image: Change at Cycle 18Body Image: Change at Cycle 19Body Image: Change at Cycle 20Body Image: Change at Cycle 21Body Image: Change at Cycle 22Body Image: Change at Cycle 23Body Image: Change at Cycle 24Body Image: Change at Cycle 25Body Image: Change at Cycle 26Body Image: Change at Cycle 27Body Image: Change at Cycle 28Body Image: Change at PT Visit 1Body Image: Change at PT Visit 2Dry Mouth: Cycle 1 (Baseline)Dry Mouth: Change at Cycle 2Dry Mouth: Change at Cycle 3Dry Mouth: Change at Cycle 4Dry Mouth: Change at Cycle 5Dry Mouth: Change at Cycle 6Dry Mouth: Change at Cycle 7Dry Mouth: Change at Cycle 8Dry Mouth: Change at Cycle 9Dry Mouth: Change at Cycle 10Dry Mouth: Change at Cycle 11Dry Mouth: Change at Cycle 12Dry Mouth: Change at Cycle 13Dry Mouth: Change at Cycle 14Dry Mouth: Change at Cycle 15Dry Mouth: Change at Cycle 16Dry Mouth: Change at Cycle 17Dry Mouth: Change at Cycle 18Dry Mouth: Change at Cycle 19Dry Mouth: Change at Cycle 20Dry Mouth: Change at Cycle 21Dry Mouth: Change at Cycle 22Dry Mouth: Change at Cycle 23Dry Mouth: Change at Cycle 24Dry Mouth: Change at Cycle 25Dry Mouth: Change at Cycle 26Dry Mouth: Change at Cycle 27Dry Mouth: Change at Cycle 28Dry Mouth: Change at PT Visit 1Dry Mouth: Change at PT Visit 2Dysphagia: Cycle 1 (Baseline)Dysphagia: Change at Cycle 2Dysphagia: Change at Cycle 3Dysphagia: Change at Cycle 4Dysphagia: Change at Cycle 5Dysphagia: Change at Cycle 6Dysphagia: Change at Cycle 7Dysphagia: Change at Cycle 8Dysphagia: Change at Cycle 9Dysphagia: Change at Cycle 10Dysphagia: Change at Cycle 11Dysphagia: Change at Cycle 12Dysphagia: Change at Cycle 13Dysphagia: Change at Cycle 14Dysphagia: Change at Cycle 15Dysphagia: Change at Cycle 16Dysphagia: Change at Cycle 17Dysphagia: Change at Cycle 18Dysphagia: Change at Cycle 19Dysphagia: Change at Cycle 20Dysphagia: Change at Cycle 21Dysphagia: Change at Cycle 22Dysphagia: Change at Cycle 23Dysphagia: Change at Cycle 24Dysphagia: Change at Cycle 25Dysphagia: Change at Cycle 26Dysphagia: Change at Cycle 27Dysphagia: Change at Cycle 28Dysphagia: Change at PT Visit 1Dysphagia: Change at PT Visit 2Eating Restrictions: Cycle 1 (Baseline)Eating Restrictions: Change at Cycle 2Eating Restrictions: Change at Cycle 3Eating Restrictions: Change at Cycle 4Eating Restrictions: Change at Cycle 5Eating Restrictions: Change at Cycle 6Eating Restrictions: Change at Cycle 7Eating Restrictions: Change at Cycle 8Eating Restrictions: Change at Cycle 9Eating Restrictions: Change at Cycle 10Eating Restrictions: Change at Cycle 11Eating Restrictions: Change at Cycle 12Eating Restrictions: Change at Cycle 13Eating Restrictions: Change at Cycle 14Eating Restrictions: Change at Cycle 15Eating Restrictions: Change at Cycle 16Eating Restrictions: Change at Cycle 17Eating Restrictions: Change at Cycle 18Eating Restrictions: Change at Cycle 19Eating Restrictions: Change at Cycle 20Eating Restrictions: Change at Cycle 21Eating Restrictions: Change at Cycle 22Eating Restrictions: Change at Cycle 23Eating Restrictions: Change at Cycle 24Eating Restrictions: Change at Cycle 25Eating Restrictions: Change at Cycle 26Eating Restrictions: Change at Cycle 27Eating Restrictions: Change at Cycle 28Eating Restrictions: Change at PT Visit 1Eating Restrictions: Change at PT Visit 2Hair Loss: Cycle 1 (Baseline)Hair Loss: Change at Cycle 2Hair Loss: Change at Cycle 3Hair Loss: Change at Cycle 4Hair Loss: Change at Cycle 5Hair Loss: Change at Cycle 6Hair Loss: Change at Cycle 7Hair Loss: Change at Cycle 8Hair Loss: Change at Cycle 9Hair Loss: Change at Cycle 10Hair Loss: Change at Cycle 11Hair Loss: Change at Cycle 12Hair Loss: Change at Cycle 13Hair Loss: Change at Cycle 14Hair Loss: Change at Cycle 15Hair Loss: Change at Cycle 16Hair Loss: Change at Cycle 17Hair Loss: Change at Cycle 18Hair Loss: Change at Cycle 19Hair Loss: Change at Cycle 20Hair Loss: Change at Cycle 21Hair Loss: Change at Cycle 22Hair Loss: Change at Cycle 23Hair Loss: Change at Cycle 24Hair Loss: Change at Cycle 25Hair Loss: Change at Cycle 26Hair Loss: Change at Cycle 27Hair Loss: Change at Cycle 28Hair Loss: Change at PT Visit 1Hair Loss: Change at PT Visit 2Pain: Cycle 1 (Baseline)Pain: Change at Cycle 2Pain: Change at Cycle 3Pain: Change at Cycle 4Pain: Change at Cycle 5Pain: Change at Cycle 6Pain: Change at Cycle 7Pain: Change at Cycle 8Pain: Change at Cycle 9Pain: Change at Cycle 10Pain: Change at Cycle 11Pain: Change at Cycle 12Pain: Change at Cycle 13Pain: Change at Cycle 14Pain: Change at Cycle 15Pain: Change at Cycle 16Pain: Change at Cycle 17Pain: Change at Cycle 18Pain: Change at Cycle 19Pain: Change at Cycle 20Pain: Change at Cycle 21Pain: Change at Cycle 22Pain: Change at Cycle 23Pain: Change at Cycle 24Pain: Change at Cycle 25Pain: Change at Cycle 26Pain: Change at Cycle 27Pain: Change at Cycle 28Pain: Change at PT Visit 1Pain: Change at PT Visit 2Reflux Symptoms: Cycle 1 (Baseline)Reflux Symptoms: Change at Cycle 2Reflux Symptoms: Change at Cycle 3Reflux Symptoms: Change at Cycle 4Reflux Symptoms: Change at Cycle 5Reflux Symptoms: Change at Cycle 6Reflux Symptoms: Change at Cycle 7Reflux Symptoms: Change at Cycle 8Reflux Symptoms: Change at Cycle 9Reflux Symptoms: Change at Cycle 10Reflux Symptoms: Change at Cycle 11Reflux Symptoms: Change at Cycle 12Reflux Symptoms: Change at Cycle 13Reflux Symptoms: Change at Cycle 14Reflux Symptoms: Change at Cycle 15Reflux Symptoms: Change at Cycle 16Reflux Symptoms: Change at Cycle 17Reflux Symptoms: Change at Cycle 18Reflux Symptoms: Change at Cycle 19Reflux Symptoms: Change at Cycle 20Reflux Symptoms: Change at Cycle 21Reflux Symptoms: Change at Cycle 22Reflux Symptoms: Change at Cycle 23Reflux Symptoms: Change at Cycle 24Reflux Symptoms: Change at Cycle 25Reflux Symptoms: Change at Cycle 26Reflux Symptoms: Change at Cycle 27Reflux Symptoms: Change at Cycle 28Reflux Symptoms: Change at PT Visit 1Reflux Symptoms: Change at PT Visit 2Taste: Cycle 1 (Baseline)Taste: Change at Cycle 2Taste: Change at Cycle 3Taste: Change at Cycle 4Taste: Change at Cycle 5Taste: Change at Cycle 6Taste: Change at Cycle 7Taste: Change at Cycle 8Taste: Change at Cycle 9Taste: Change at Cycle 10Taste: Change at Cycle 11Taste: Change at Cycle 12Taste: Change at Cycle 13Taste: Change at Cycle 14Taste: Change at Cycle 15Taste: Change at Cycle 16Taste: Change at Cycle 17Taste: Change at Cycle 18Taste: Change at Cycle 19Taste: Change at Cycle 20Taste: Change at Cycle 21Taste: Change at Cycle 22Taste: Change at Cycle 23Taste: Change at Cycle 24Taste: Change at Cycle 25Taste: Change at Cycle 26Taste: Change at Cycle 27Taste: Change at Cycle 28Taste: Change at PT Visit 1Taste: Change at PT Visit 2
Pertuzumab + Trastuzumab + Chemotherapy40.10-2.58-4.14-4.52-4.10-4.54-6.40-9.00-10.09-11.17-10.78-12.62-13.32-14.32-13.42-12.75-13.41-13.53-14.50-15.34-16.03-13.30-17.28-16.11-16.03-19.73-21.71-22.51-0.73-4.0423.531.331.484.202.860.75-0.56-1.74-3.58-5.07-4.62-5.31-4.73-5.43-3.08-1.74-2.70-2.64-2.81-3.971.69-1.49-5.82-0.56-3.21-4.760.78-4.272.482.3621.807.726.104.762.472.96-1.96-2.43-3.70-6.27-7.69-8.18-9.69-8.33-7.89-6.32-7.44-5.56-5.90-6.35-7.17-3.98-7.94-6.67-8.33-2.72-6.98-8.550.19-1.3516.29-2.27-3.39-2.94-3.22-4.20-4.83-5.96-6.17-6.03-6.25-7.06-6.93-8.01-6.45-4.41-5.36-4.90-4.40-2.51-3.80-3.65-4.23-5.00-5.98-5.67-5.68-8.260.44-2.8123.26-1.41-1.04-2.24-1.39-1.35-2.45-4.29-6.99-7.06-8.22-7.74-8.55-8.62-6.85-5.77-5.56-7.27-7.03-4.56-5.80-3.65-3.70-5.00-5.77-6.80-5.62-7.911.52-2.104.730.204.345.406.126.935.725.002.380.64-0.100.210.36-1.37-0.39-1.47-1.07-1.68-0.90-0.20-1.07-0.50-0.54-1.39-1.96-1.02-3.10-4.704.9815.8226.48-4.63-6.96-6.45-7.28-7.24-9.52-10.53-10.08-10.63-11.65-11.76-11.92-11.66-11.15-8.72-8.88-8.31-6.63-5.72-8.19-9.08-9.66-9.86-10.58-9.01-12.02-11.54-1.70-7.4916.68-0.13-0.52-0.98-1.92-2.90-4.18-4.96-5.02-6.12-6.44-4.82-6.42-5.39-5.00-3.07-3.35-2.94-2.43-1.85-1.83-3.81-5.11-4.07-5.56-4.99-7.75-7.120.880.5613.7912.0916.7218.4317.6117.9716.2511.649.227.934.965.274.080.493.085.514.803.593.135.566.339.458.997.783.214.084.653.4212.768.42
Placebo + Trastuzumab + Chemotherapy40.48-4.11-3.87-7.25-7.39-8.42-10.40-11.92-11.43-12.64-12.09-13.16-13.33-12.43-10.65-12.57-12.79-12.38-12.48-12.37-14.47-15.46-14.47-17.09-17.78-13.26-12.70-12.89-4.73-3.9823.681.203.881.151.062.780.290.00-0.69-3.25-1.53-2.66-2.73-4.62-2.43-1.19-2.28-5.71-5.21-5.38-8.18-10.87-8.53-11.11-11.43-6.45-7.14-4.003.426.3523.323.004.872.662.571.190.44-2.66-4.32-3.46-1.96-4.35-8.48-3.63-7.29-8.33-3.20-8.10-7.69-9.68-9.43-8.70-3.88-9.40-9.52-7.53-7.14-8.002.381.8914.15-0.53-2.15-1.08-1.83-2.25-1.97-3.29-3.86-4.61-2.83-4.19-3.54-4.95-2.14-3.70-3.20-3.33-3.59-3.76-2.10-4.83-3.88-3.70-2.22-2.87-4.37-3.562.833.2522.33-1.54-2.20-1.39-0.09-3.32-2.67-5.56-6.48-5.89-5.05-6.34-8.41-8.58-5.56-6.94-7.42-6.90-5.38-4.44-5.03-6.16-5.23-7.91-5.95-2.42-3.87-5.000.940.944.041.274.526.537.1810.079.267.386.464.222.541.962.291.831.581.420.23-0.710.51-1.61-1.57-3.26-1.191.71-0.95-0.54-0.60-1.334.5122.2226.47-5.86-5.86-7.48-6.89-7.22-6.62-8.16-8.98-8.59-8.01-7.19-9.24-9.82-8.51-10.52-9.93-11.19-10.38-10.35-7.55-9.42-8.53-8.76-8.10-9.41-9.23-7.33-2.99-0.0317.34-1.99-2.28-1.90-1.72-3.59-3.20-5.74-5.18-6.48-6.03-7.49-6.77-7.37-4.98-4.89-4.57-6.51-6.15-5.38-4.19-7.00-6.98-7.98-5.71-4.30-6.75-4.44-0.45-1.4716.226.619.9911.0711.8511.829.193.291.731.632.610.24-0.91-5.28-1.04-3.57-3.65-4.29-4.62-3.76-5.03-4.350.00-5.13-4.76-3.23-3.57-6.679.066.67

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Percentage of Participants With Clinical Benefit, as Determined by the Investigator According to RECIST v1.1 Criteria

The clinical benefit rate was defined as best response of complete response (CR) or partial response (PR) or stable disease (SD) for 6 weeks or longer, as determined by the investigator using RECIST v1.1. CR: disappearance of all target lesions. PR: at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum of diameters. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for disease progression, taking as reference the smallest sum diameters while on study. Measurable disease is defined as tumor lesions measured in at least one dimension (longest diameter in plane of measurement) with a minimum size of: 10 mm by CT or MRI scan; 10 mm caliper measurement by clinical examination; 20 mm by chest X-ray. For a malignant lymph node to be considered pathologically enlarged and measurable, it must be >/=15 mm in short axis when assessed by CT scan. The clinical benefit rate was not updated at the final analysis. (NCT01774786)
Timeframe: Baseline up to death or progressive disease, whichever occurred first (Median [full range] duration of follow-up in Pertuzumab vs. Placebo arms for Primary Analysis: 24.9 [0-41] months vs. 21.3 [0-39] months)

Interventionpercentage of participants (Number)
Pertuzumab + Trastuzumab + Chemotherapy84.6
Placebo + Trastuzumab + Chemotherapy81.3

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Minimum Serum Concentration (Cmin) of Pertuzumab

(NCT01774786)
Timeframe: Pre-dose (0-6 hours before infusion) on Day 1 of Cycles 1, 2, 3, 4, 6, and 8 (1 cycle = 21 days)

Interventionμg/mL (Mean)
Cycle 1Cycle 2Cycle 3Cycle 4Cycle 6Cycle 8
Pertuzumab + Trastuzumab + ChemotherapyNA42.474.090.4114142

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Maximum Serum Concentration (Cmax) of Pertuzumab

(NCT01774786)
Timeframe: Post-dose (0.5 hour after end of 30-60 minutes infusion) on Day 1 of Cycles 1, 2, 4, and 8 (1 cycle = 21 days)

Interventionmicrograms per milliliter (μg/mL) (Mean)
Cycle 1Cycle 2Cycle 4Cycle 8
Pertuzumab + Trastuzumab + Chemotherapy258288341371

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Change From Baseline in European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Core 30 (QLQ-C30) Score

The EORTC QLQ-C30 included global health status, functional scales (physical, role, emotional, cognitive, and social), symptom scales (fatigue, nausea/vomiting, and pain) and single items (dyspnoea, insomnia, appetite loss, constipation, diarrhea, and financial difficulties). Most questions used a 4-point scale (1 'Not at all' to 4 'Very much'; 2 questions used 7-point scale [1 'very poor' to 7 'Excellent']). Scores were averaged and transformed to 0 - 100 scale, whereby higher scores indicate greater functioning, greater quality of life, or a greater degree of symptoms, with changes of 5 - 10 points considered to be a minimally important difference to participants. A positive value means an increase, while a negative value means a decrease, in score at the indicated time-point relative to the score at baseline (Cycle 1, Day 1). (NCT01774786)
Timeframe: Day 1 of each 21-day treatment cycle up to 28 and 60-90 days (post-treatment [PT] monitoring visits 1 and 2, respectively) after Day 1 of last treatment cycle (up to approximately 3.5 years)

,
Interventionscore on a scale (Mean)
Appetite Loss: Cycle 1 (Baseline)Appetite Loss: Change at Cycle 2Appetite Loss: Change at Cycle 3Appetite Loss: Change at Cycle 4Appetite Loss: Change at Cycle 5Appetite Loss: Change at Cycle 6Appetite Loss: Change at Cycle 7Appetite Loss: Change at Cycle 8Appetite Loss: Change at Cycle 9Appetite Loss: Change at Cycle 10Appetite Loss: Change at Cycle 11Appetite Loss: Change at Cycle 12Appetite Loss: Change at Cycle 13Appetite Loss: Change at Cycle 14Appetite Loss: Change at Cycle 15Appetite Loss: Change at Cycle 16Appetite Loss: Change at Cycle 17Appetite Loss: Change at Cycle 18Appetite Loss: Change at Cycle 19Appetite Loss: Change at Cycle 20Appetite Loss: Change at Cycle 21Appetite Loss: Change at Cycle 22Appetite Loss: Change at Cycle 23Appetite Loss: Change at Cycle 24Appetite Loss: Change at Cycle 25Appetite Loss: Change at Cycle 26Appetite Loss: Change at Cycle 27Appetite Loss: Change at Cycle 28Appetite Loss: Change at PT Visit 1Appetite Loss: Change at PT Visit 2Cognitive Functional Scale: Cycle 1 (Baseline)Cognitive Functional Scale: Change at Cycle 2Cognitive Functional Scale: Change at Cycle 3Cognitive Functional Scale: Change at Cycle 4Cognitive Functional Scale: Change at Cycle 5Cognitive Functional Scale: Change at Cycle 6Cognitive Functional Scale: Change at Cycle 7Cognitive Functional Scale: Change at Cycle 8Cognitive Functional Scale: Change at Cycle 9Cognitive Functional Scale: Change at Cycle 10Cognitive Functional Scale: Change at Cycle 11Cognitive Functional Scale: Change at Cycle 12Cognitive Functional Scale: Change at Cycle 13Cognitive Functional Scale: Change at Cycle 14Cognitive Functional Scale: Change at Cycle 15Cognitive Functional Scale: Change at Cycle 16Cognitive Functional Scale: Change at Cycle 17Cognitive Functional Scale: Change at Cycle 18Cognitive Functional Scale: Change at Cycle 19Cognitive Functional Scale: Change at Cycle 20Cognitive Functional Scale: Change at Cycle 21Cognitive Functional Scale: Change at Cycle 22Cognitive Functional Scale: Change at Cycle 23Cognitive Functional Scale: Change at Cycle 24Cognitive Functional Scale: Change at Cycle 25Cognitive Functional Scale: Change at Cycle 26Cognitive Functional Scale: Change at Cycle 27Cognitive Functional Scale: Change at Cycle 28Cognitive Functional Scale: Change at PT Visit 1Cognitive Functional Scale: Change at PT Visit 2Constipation Symptom Scale: Cycle 1 (Baseline)Constipation Symptom Scale: Change at Cycle 2Constipation Symptom Scale: Change at Cycle 3Constipation Symptom Scale: Change at Cycle 4Constipation Symptom Scale: Change at Cycle 5Constipation Symptom Scale: Change at Cycle 6Constipation Symptom Scale: Change at Cycle 7Constipation Symptom Scale: Change at Cycle 8Constipation Symptom Scale: Change at Cycle 9Constipation Symptom Scale: Change at Cycle 10Constipation Symptom Scale: Change at Cycle 11Constipation Symptom Scale: Change at Cycle 12Constipation Symptom Scale: Change at Cycle 13Constipation Symptom Scale: Change at Cycle 14Constipation Symptom Scale: Change at Cycle 15Constipation Symptom Scale: Change at Cycle 16Constipation Symptom Scale: Change at Cycle 17Constipation Symptom Scale: Change at Cycle 18Constipation Symptom Scale: Change at Cycle 19Constipation Symptom Scale: Change at Cycle 20Constipation Symptom Scale: Change at Cycle 21Constipation Symptom Scale: Change at Cycle 22Constipation Symptom Scale: Change at Cycle 23Constipation Symptom Scale: Change at Cycle 24Constipation Symptom Scale: Change at Cycle 25Constipation Symptom Scale: Change at Cycle 26Constipation Symptom Scale: Change at Cycle 27Constipation Symptom Scale: Change at Cycle 28Constipation Symptom Scale: Change at PT Visit 1Constipation Symptom Scale: Change at PT Visit 2Diarrhea Symptom Scale: Cycle 1 (Baseline)Diarrhea Symptom Scale: Change at Cycle 2Diarrhea Symptom Scale: Change at Cycle 3Diarrhea Symptom Scale: Change at Cycle 4Diarrhea Symptom Scale: Change at Cycle 5Diarrhea Symptom Scale: Change at Cycle 6Diarrhea Symptom Scale: Change at Cycle 7Diarrhea Symptom Scale: Change at Cycle 8Diarrhea Symptom Scale: Change at Cycle 9Diarrhea Symptom Scale: Change at Cycle 10Diarrhea Symptom Scale: Change at Cycle 11Diarrhea Symptom Scale: Change at Cycle 12Diarrhea Symptom Scale: Change at Cycle 13Diarrhea Symptom Scale: Change at Cycle 14Diarrhea Symptom Scale: Change at Cycle 15Diarrhea Symptom Scale: Change at Cycle 16Diarrhea Symptom Scale: Change at Cycle 17Diarrhea Symptom Scale: Change at Cycle 18Diarrhea Symptom Scale: Change at Cycle 19Diarrhea Symptom Scale: Change at Cycle 20Diarrhea Symptom Scale: Change at Cycle 21Diarrhea Symptom Scale: Change at Cycle 22Diarrhea Symptom Scale: Change at Cycle 23Diarrhea Symptom Scale: Change at Cycle 24Diarrhea Symptom Scale: Change at Cycle 25Diarrhea Symptom Scale: Change at Cycle 26Diarrhea Symptom Scale: Change at Cycle 27Diarrhea Symptom Scale: Change at Cycle 28Diarrhea Symptom Scale: Change at PT Visit 1Diarrhea Symptom Scale: Change at PT Visit 2Dyspnoea Symptom Scale: Cycle 1 (Baseline)Dyspnoea Symptom Scale: Change at Cycle 2Dyspnoea Symptom Scale: Change at Cycle 3Dyspnoea Symptom Scale: Change at Cycle 4Dyspnoea Symptom Scale: Change at Cycle 5Dyspnoea Symptom Scale: Change at Cycle 6Dyspnoea Symptom Scale: Change at Cycle 7Dyspnoea Symptom Scale: Change at Cycle 8Dyspnoea Symptom Scale: Change at Cycle 9Dyspnoea Symptom Scale: Change at Cycle 10Dyspnoea Symptom Scale: Change at Cycle 11Dyspnoea Symptom Scale: Change at Cycle 12Dyspnoea Symptom Scale: Change at Cycle 13Dyspnoea Symptom Scale: Change at Cycle 14Dyspnoea Symptom Scale: Change at Cycle 15Dyspnoea Symptom Scale: Change at Cycle 16Dyspnoea Symptom Scale: Change at Cycle 17Dyspnoea Symptom Scale: Change at Cycle 18Dyspnoea Symptom Scale: Change at Cycle 19Dyspnoea Symptom Scale: Change at Cycle 20Dyspnoea Symptom Scale: Change at Cycle 21Dyspnoea Symptom Scale: Change at Cycle 22Dyspnoea Symptom Scale: Change at Cycle 23Dyspnoea Symptom Scale: Change at Cycle 24Dyspnoea Symptom Scale: Change at Cycle 25Dyspnoea Symptom Scale: Change at Cycle 26Dyspnoea Symptom Scale: Change at Cycle 27Dyspnoea Symptom Scale: Change at Cycle 28Dyspnoea Symptom Scale: Change at PT Visit 1Dyspnoea Symptom Scale: Change at PT Visit 2Emotional Functional Scale: Cycle 1 (Baseline)Emotional Functional Scale: Change at Cycle 2Emotional Functional Scale: Change at Cycle 3Emotional Functional Scale: Change at Cycle 4Emotional Functional Scale: Change at Cycle 5Emotional Functional Scale: Change at Cycle 6Emotional Functional Scale: Change at Cycle 7Emotional Functional Scale: Change at Cycle 8Emotional Functional Scale: Change at Cycle 9Emotional Functional Scale: Change at Cycle 10Emotional Functional Scale: Change at Cycle 11Emotional Functional Scale: Change at Cycle 12Emotional Functional Scale: Change at Cycle 13Emotional Functional Scale: Change at Cycle 14Emotional Functional Scale: Change at Cycle 15Emotional Functional Scale: Change at Cycle 16Emotional Functional Scale: Change at Cycle 17Emotional Functional Scale: Change at Cycle 18Emotional Functional Scale: Change at Cycle 19Emotional Functional Scale: Change at Cycle 20Emotional Functional Scale: Change at Cycle 21Emotional Functional Scale: Change at Cycle 22Emotional Functional Scale: Change at Cycle 23Emotional Functional Scale: Change at Cycle 24Emotional Functional Scale: Change at Cycle 25Emotional Functional Scale: Change at Cycle 26Emotional Functional Scale: Change at Cycle 27Emotional Functional Scale: Change at Cycle 28Emotional Functional Scale: Change at PT Visit 1Emotional Functional Scale: Change at PT Visit 2Fatigue Symptom Scale: Cycle 1 (Baseline)Fatigue Symptom Scale: Change at Cycle 2Fatigue Symptom Scale: Change at Cycle 3Fatigue Symptom Scale: Change at Cycle 4Fatigue Symptom Scale: Change at Cycle 5Fatigue Symptom Scale: Change at Cycle 6Fatigue Symptom Scale: Change at Cycle 7Fatigue Symptom Scale: Change at Cycle 8Fatigue Symptom Scale: Change at Cycle 9Fatigue Symptom Scale: Change at Cycle 10Fatigue Symptom Scale: Change at Cycle 11Fatigue Symptom Scale: Change at Cycle 12Fatigue Symptom Scale: Change at Cycle 13Fatigue Symptom Scale: Change at Cycle 14Fatigue Symptom Scale: Change at Cycle 15Fatigue Symptom Scale: Change at Cycle 16Fatigue Symptom Scale: Change at Cycle 17Fatigue Symptom Scale: Change at Cycle 18Fatigue Symptom Scale: Change at Cycle 19Fatigue Symptom Scale: Change at Cycle 20Fatigue Symptom Scale: Change at Cycle 21Fatigue Symptom Scale: Change at Cycle 22Fatigue Symptom Scale: Change at Cycle 23Fatigue Symptom Scale: Change at Cycle 24Fatigue Symptom Scale: Change at Cycle 25Fatigue Symptom Scale: Change at Cycle 26Fatigue Symptom Scale: Change at Cycle 27Fatigue Symptom Scale: Change at Cycle 28Fatigue Symptom Scale: Change at PT Visit 1Fatigue Symptom Scale: Change at PT Visit 2Financial Difficulties Scale: Cycle 1 (Baseline)Financial Difficulties Scale: Change at Cycle 2Financial Difficulties Scale: Change at Cycle 3Financial Difficulties Scale: Change at Cycle 4Financial Difficulties Scale: Change at Cycle 5Financial Difficulties Scale: Change at Cycle 6Financial Difficulties Scale: Change at Cycle 7Financial Difficulties Scale: Change at Cycle 8Financial Difficulties Scale: Change at Cycle 9Financial Difficulties Scale: Change at Cycle 10Financial Difficulties Scale: Change at Cycle 11Financial Difficulties Scale: Change at Cycle 12Financial Difficulties Scale: Change at Cycle 13Financial Difficulties Scale: Change at Cycle 14Financial Difficulties Scale: Change at Cycle 15Financial Difficulties Scale: Change at Cycle 16Financial Difficulties Scale: Change at Cycle 17Financial Difficulties Scale: Change at Cycle 18Financial Difficulties Scale: Change at Cycle 19Financial Difficulties Scale: Change at Cycle 20Financial Difficulties Scale: Change at Cycle 21Financial Difficulties Scale: Change at Cycle 22Financial Difficulties Scale: Change at Cycle 23Financial Difficulties Scale: Change at Cycle 24Financial Difficulties Scale: Change at Cycle 25Financial Difficulties Scale: Change at Cycle 26Financial Difficulties Scale: Change at Cycle 27Financial Difficulties Scale: Change at Cycle 28Financial Difficulties Scale: Change at PT Visit 1Financial Difficulties Scale: Change at PT Visit 2Nausea and Vomiting Scale: Cycle 1 (Baseline)Nausea And Vomiting Scale: Change at Cycle 2Nausea And Vomiting Scale: Change at Cycle 3Nausea And Vomiting Scale: Change at Cycle 4Nausea And Vomiting Scale: Change at Cycle 5Nausea And Vomiting Scale: Change at Cycle 6Nausea And Vomiting Scale: Change at Cycle 7Nausea And Vomiting Scale: Change at Cycle 8Nausea And Vomiting Scale: Change at Cycle 9Nausea And Vomiting Scale: Change at Cycle 10Nausea And Vomiting Scale: Change at Cycle 11Nausea And Vomiting Scale: Change at Cycle 12Nausea And Vomiting Scale: Change at Cycle 13Nausea And Vomiting Scale: Change at Cycle 14Nausea And Vomiting Scale: Change at Cycle 15Nausea And Vomiting Scale: Change at Cycle 16Nausea And Vomiting Scale: Change at Cycle 17Nausea And Vomiting Scale: Change at Cycle 18Nausea And Vomiting Scale: Change at Cycle 19Nausea And Vomiting Scale: Change at Cycle 20Nausea And Vomiting Scale: Change at Cycle 21Nausea And Vomiting Scale: Change at Cycle 22Nausea And Vomiting Scale: Change at Cycle 23Nausea And Vomiting Scale: Change at Cycle 24Nausea And Vomiting Scale: Change at Cycle 25Nausea And Vomiting Scale: Change at Cycle 26Nausea And Vomiting Scale: Change at Cycle 27Nausea And Vomiting Scale: Change at Cycle 28Nausea and Vomiting Scale: Change at PT Visit 1Nausea and Vomiting Scale: Change at PT Visit 2Pain Symptom Scale: Cycle 1 (Baseline)Pain Symptom Scale: Change at Cycle 2Pain Symptom Scale: Change at Cycle 3Pain Symptom Scale: Change at Cycle 4Pain Symptom Scale: Change at Cycle 5Pain Symptom Scale: Change at Cycle 6Pain Symptom Scale: Change at Cycle 7Pain Symptom Scale: Change at Cycle 8Pain Symptom Scale: Change at Cycle 9Pain Symptom Scale: Change at Cycle 10Pain Symptom Scale: Change at Cycle 11Pain Symptom Scale: Change at Cycle 12Pain Symptom Scale: Change at Cycle 13Pain Symptom Scale: Change at Cycle 14Pain Symptom Scale: Change at Cycle 15Pain Symptom Scale: Change at Cycle 16Pain Symptom Scale: Change at Cycle 17Pain Symptom Scale: Change at Cycle 18Pain Symptom Scale: Change at Cycle 19Pain Symptom Scale: Change at Cycle 20Pain Symptom Scale: Change at Cycle 21Pain Symptom Scale: Change at Cycle 22Pain Symptom Scale: Change at Cycle 23Pain Symptom Scale: Change at Cycle 24Pain Symptom Scale: Change at Cycle 25Pain Symptom Scale: Change at Cycle 26Pain Symptom Scale: Change at Cycle 27Pain Symptom Scale: Change at Cycle 28Pain Symptom Scale: Change at PT Visit 1Pain Symptom Scale: Change at PT Visit 2Physical Functional Scale: Cycle 1 (Baseline)Physical Functional Scale: Change at Cycle 2Physical Functional Scale: Change at Cycle 3Physical Functional Scale: Change at Cycle 4Physical Functional Scale: Change at Cycle 5Physical Functional Scale: Change at Cycle 6Physical Functional Scale: Change at Cycle 7Physical Functional Scale: Change at Cycle 8Physical Functional Scale: Change at Cycle 9Physical Functional Scale: Change at Cycle 10Physical Functional Scale: Change at Cycle 11Physical Functional Scale: Change at Cycle 12Physical Functional Scale: Change at Cycle 13Physical Functional Scale: Change at Cycle 14Physical Functional Scale: Change at Cycle 15Physical Functional Scale: Change at Cycle 16Physical Functional Scale: Change at Cycle 17Physical Functional Scale: Change at Cycle 18Physical Functional Scale: Change at Cycle 19Physical Functional Scale: Change at Cycle 20Physical Functional Scale: Change at Cycle 21Physical Functional Scale: Change at Cycle 22Physical Functional Scale: Change at Cycle 23Physical Functional Scale: Change at Cycle 24Physical Functional Scale: Change at Cycle 25Physical Functional Scale: Change at Cycle 26Physical Functional Scale: Change at Cycle 27Physical Functional Scale: Change at Cycle 28Physical Functional Scale: Change at PT Visit 1Physical Functional Scale: Change at PT Visit 2Global Health Status Scale: Cycle 1 (Baseline)Global Health Status Scale: Change at Cycle 2Global Health Status Scale: Change at Cycle 3Global Health Status Scale: Change at Cycle 4Global Health Status Scale: Change at Cycle 5Global Health Status Scale: Change at Cycle 6Global Health Status Scale: Change at Cycle 7Global Health Status Scale: Change at Cycle 8Global Health Status Scale: Change at Cycle 9Global Health Status Scale: Change at Cycle 10Global Health Status Scale: Change at Cycle 11Global Health Status Scale: Change at Cycle 12Global Health Status Scale: Change at Cycle 13Global Health Status Scale: Change at Cycle 14Global Health Status Scale: Change at Cycle 15Global Health Status Scale: Change at Cycle 16Global Health Status Scale: Change at Cycle 17Global Health Status Scale: Change at Cycle 18Global Health Status Scale: Change at Cycle 19Global Health Status Scale: Change at Cycle 20Global Health Status Scale: Change at Cycle 21Global Health Status Scale: Change at Cycle 22Global Health Status Scale: Change at Cycle 23Global Health Status Scale: Change at Cycle 24Global Health Status Scale: Change at Cycle 25Global Health Status Scale: Change at Cycle 26Global Health Status Scale: Change at Cycle 27Global Health Status Scale: Change at Cycle 28Global Health Status Scale: Change at PT Visit 1Global Health Status Scale: Change at PT Visit 2Role Functional Scale: Cycle 1 (Baseline)Role Functional Scale: Change at Cycle 2Role Functional Scale: Change at Cycle 3Role Functional Scale: Change at Cycle 4Role Functional Scale: Change at Cycle 5Role Functional Scale: Change at Cycle 6Role Functional Scale: Change at Cycle 7Role Functional Scale: Change at Cycle 8Role Functional Scale: Change at Cycle 9Role Functional Scale: Change at Cycle 10Role Functional Scale: Change at Cycle 11Role Functional Scale: Change at Cycle 12Role Functional Scale: Change at Cycle 13Role Functional Scale: Change at Cycle 14Role Functional Scale: Change at Cycle 15Role Functional Scale: Change at Cycle 16Role Functional Scale: Change at Cycle 17Role Functional Scale: Change at Cycle 18Role Functional Scale: Change at Cycle 19Role Functional Scale: Change at Cycle 20Role Functional Scale: Change at Cycle 21Role Functional Scale: Change at Cycle 22Role Functional Scale: Change at Cycle 23Role Functional Scale: Change at Cycle 24Role Functional Scale: Change at Cycle 25Role Functional Scale: Change at Cycle 26Role Functional Scale: Change at Cycle 27Role Functional Scale: Change at Cycle 28Role Functional Scale: Change at PT Visit 1Role Functional Scale: Change at PT Visit 2Social Functional Scale: Cycle 1 (Baseline)Social Functional Scale: Change at Cycle 2Social Functional Scale: Change at Cycle 3Social Functional Scale: Change at Cycle 4Social Functional Scale: Change at Cycle 5Social Functional Scale: Change at Cycle 6Social Functional Scale: Change at Cycle 7Social Functional Scale: Change at Cycle 8Social Functional Scale: Change at Cycle 9Social Functional Scale: Change at Cycle 10Social Functional Scale: Change at Cycle 11Social Functional Scale: Change at Cycle 12Social Functional Scale: Change at Cycle 13Social Functional Scale: Change at Cycle 14Social Functional Scale: Change at Cycle 15Social Functional Scale: Change at Cycle 16Social Functional Scale: Change at Cycle 17Social Functional Scale: Change at Cycle 18Social Functional Scale: Change at Cycle 19Social Functional Scale: Change at Cycle 20Social Functional Scale: Change at Cycle 21Social Functional Scale: Change at Cycle 22Social Functional Scale: Change at Cycle 23Social Functional Scale: Change at Cycle 24Social Functional Scale: Change at Cycle 25Social Functional Scale: Change at Cycle 26Social Functional Scale: Change at Cycle 27Social Functional Scale: Change at Cycle 28Social Functional Scale: Change at PT Visit 1Social Functional Scale: Change at PT Visit 2Insomnia Symptom Scale: Cycle 1 (Baseline)Insomnia Symptom Scale: Change at Cycle 2Insomnia Symptom Scale: Change at Cycle 3Insomnia Symptom Scale: Change at Cycle 4Insomnia Symptom Scale: Change at Cycle 5Insomnia Symptom Scale: Change at Cycle 6Insomnia Symptom Scale: Change at Cycle 7Insomnia Symptom Scale: Change at Cycle 8Insomnia Symptom Scale: Change at Cycle 9Insomnia Symptom Scale: Change at Cycle 10Insomnia Symptom Scale: Change at Cycle 11Insomnia Symptom Scale: Change at Cycle 12Insomnia Symptom Scale: Change at Cycle 13Insomnia Symptom Scale: Change at Cycle 14Insomnia Symptom Scale: Change at Cycle 15Insomnia Symptom Scale: Change at Cycle 16Insomnia Symptom Scale: Change at Cycle 17Insomnia Symptom Scale: Change at Cycle 18Insomnia Symptom Scale: Change at Cycle 19Insomnia Symptom Scale: Change at Cycle 20Insomnia Symptom Scale: Change at Cycle 21Insomnia Symptom Scale: Change at Cycle 22Insomnia Symptom Scale: Change at Cycle 23Insomnia Symptom Scale: Change at Cycle 24Insomnia Symptom Scale: Change at Cycle 25Insomnia Symptom Scale: Change at Cycle 26Insomnia Symptom Scale: Change at Cycle 27Insomnia Symptom Scale: Change at Cycle 28Insomnia Symptom Scale: Change at PT Visit 1Insomnia Symptom Scale: Change at PT Visit 2
Pertuzumab + Trastuzumab + Chemotherapy26.686.573.635.244.553.942.07-2.42-6.67-8.06-9.36-9.22-10.17-12.10-8.21-6.03-6.55-4.90-8.33-3.97-5.91-4.98-6.35-7.78-7.05-7.48-10.08-10.007.30-0.3387.95-1.90-0.83-2.04-3.04-5.10-4.34-3.15-2.22-3.32-2.83-3.35-1.79-1.98-1.15-2.73-2.53-2.78-1.04-2.18-2.11-4.73-2.38-2.78-5.45-2.38-3.88-3.75-9.13-8.4220.43-5.39-7.48-5.32-5.94-7.13-8.13-8.05-10.00-9.32-9.16-10.27-11.19-11.60-10.51-8.62-8.33-7.52-3.47-3.97-3.80-4.98-6.35-7.78-7.05-6.12-7.75-6.67-6.78-6.938.8715.1214.6414.1313.1714.8112.268.916.836.635.263.984.293.953.335.462.683.593.825.953.806.976.887.228.975.443.887.508.147.2612.07-0.50-0.311.232.583.200.00-0.14-1.12-0.54-2.16-2.53-1.43-1.98-2.84-1.45-1.82-0.98-1.74-1.191.27-1.99-1.591.110.640.000.781.676.973.3076.903.532.653.102.621.011.723.434.723.725.854.935.005.936.035.176.013.684.693.474.545.355.825.285.935.447.567.08-5.48-2.6431.963.131.412.773.874.372.36-0.19-2.38-3.41-4.35-3.14-4.57-6.75-5.47-3.54-4.27-4.14-5.32-5.56-3.94-1.49-5.82-1.67-4.70-4.99-6.98-6.3910.027.7026.67-0.900.310.891.751.111.111.151.110.900.39-1.05-0.95-1.73-1.81-3.16-3.87-2.29-0.351.191.272.49-0.531.113.212.72-3.10-1.671.701.9811.145.855.124.105.134.112.07-0.86-2.54-4.30-3.51-3.04-4.02-3.46-3.59-0.43-0.60-0.65-0.87-1.79-1.05-3.48-4.23-4.72-4.17-3.40-5.04-1.254.684.2923.92-6.80-9.89-10.26-8.86-8.95-10.95-9.97-9.29-9.41-10.33-10.27-10.28-10.49-11.15-9.91-7.59-8.82-8.16-6.94-9.92-7.71-10.85-10.00-9.94-10.54-11.24-10.421.13-1.4980.86-3.58-2.99-3.28-3.10-5.00-3.66-2.24-1.590.110.35-1.05-0.80-0.020.41-1.08-0.460.131.390.710.42-2.79-1.48-2.67-2.18-1.900.16-1.17-11.37-11.4959.771.811.561.391.170.681.833.064.394.805.783.113.515.974.263.122.933.023.255.125.383.794.034.243.597.277.544.49-7.24-2.7277.06-3.78-3.62-4.64-4.72-6.13-4.82-1.85-1.19-1.79-0.78-1.05-2.01-0.86-1.03-3.16-1.04-0.161.04-1.19-0.84-2.24-3.44-4.44-3.53-1.36-1.55-0.42-14.61-10.7377.96-3.45-4.62-2.59-5.54-5.72-2.69-1.720.56-0.810.580.520.831.981.79-0.72-0.45-0.982.261.591.271.246.085.831.603.745.816.25-9.13-5.4522.94-0.69-3.53-2.88-2.21-2.94-4.56-6.13-8.97-8.24-8.97-8.81-10.17-9.14-9.74-8.91-11.01-8.82-11.46-10.32-11.81-10.95-10.58-9.44-10.26-9.52-13.18-11.672.815.67
Placebo + Trastuzumab + Chemotherapy27.590.973.810.792.90-0.391.61-3.69-4.76-6.63-9.68-9.05-10.81-12.09-9.18-10.59-9.91-14.08-13.13-13.23-14.20-16.31-11.36-13.33-12.04-12.50-9.20-11.542.644.5588.22-1.81-3.17-2.99-4.59-3.84-4.31-3.30-4.59-3.11-3.44-2.52-3.60-2.29-2.38-2.55-1.130.470.000.790.62-0.711.141.25-0.93-1.56-1.150.00-9.16-11.2118.410.29-2.11-3.73-1.28-2.33-4.09-4.45-5.61-7.43-6.88-7.25-5.76-6.21-7.14-7.45-5.86-6.57-3.03-4.76-9.26-8.51-8.33-10.00-9.26-6.25-10.34-6.41-4.62-0.919.165.204.994.634.992.472.922.612.040.602.601.921.500.981.023.142.253.292.023.701.854.268.333.332.785.213.452.561.984.2412.650.29-0.321.811.390.390.590.930.171.00-1.29-0.71-1.20-2.612.721.180.90-2.350.51-1.06-0.620.711.52-1.67-3.701.043.453.856.779.3976.563.053.963.672.744.934.415.664.786.744.965.245.186.295.195.296.315.875.565.426.486.916.638.548.805.995.757.05-3.92-4.4732.272.323.191.583.052.620.97-1.18-2.01-3.08-3.44-4.60-4.50-6.54-4.99-6.93-3.45-8.92-9.01-6.53-7.41-10.64-9.60-12.50-12.35-11.46-5.36-4.705.259.7026.21-2.460.000.112.580.920.300.47-0.51-2.42-0.22-0.970.30-0.981.360.391.352.35-0.511.59-4.94-4.26-2.27-5.83-4.63-2.221.15-1.281.334.2411.924.085.063.565.152.592.49-0.77-2.98-2.81-3.66-3.45-3.60-5.72-3.91-2.55-3.15-3.52-4.04-3.97-6.48-8.16-6.44-7.92-7.41-9.38-7.47-6.414.132.7323.72-6.38-7.23-7.46-6.25-7.33-7.46-8.53-7.82-8.13-6.34-5.24-4.80-5.56-3.74-4.71-5.63-8.22-5.05-6.08-6.48-8.51-7.95-10.00-12.96-8.33-5.75-9.622.065.4582.05-3.01-3.92-3.50-4.62-3.84-3.79-1.56-0.75-0.270.270.890.271.70-0.95-0.08-0.810.751.310.850.251.420.613.004.81-1.88-3.68-2.82-7.51-11.8259.904.292.864.153.923.613.335.184.685.073.825.343.834.821.703.043.832.583.974.895.403.194.072.928.105.471.724.81-6.14-5.6879.33-2.82-4.55-5.99-7.41-6.03-5.34-2.38-2.470.90-2.690.24-2.40-1.31-3.23-2.35-3.380.23-0.250.790.001.061.142.084.630.52-4.02-3.85-9.49-15.4575.90-0.44-2.07-1.70-3.26-1.04-0.151.080.772.311.942.402.102.120.000.391.582.113.280.795.862.841.894.172.781.56-1.72-0.64-3.80-8.4825.41-0.39-3.48-3.62-2.66-5.58-4.82-6.45-6.12-4.42-5.81-6.43-5.11-7.84-5.10-4.31-5.41-8.45-7.58-5.29-4.94-7.80-6.06-7.50-8.33-4.17-4.60-1.28-1.323.03

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Cmax of Trastuzumab

(NCT01774786)
Timeframe: Post-dose (0.5 hour after end of 30-60 minutes infusion) on Day 1 of Cycles 1, 2, 4, and 8 (1 cycle = 21 days)

,
Interventionμg/mL (Mean)
Cycle 1Cycle 2Cycle 4Cycle 8
Pertuzumab + Trastuzumab + Chemotherapy142120127130
Placebo + Trastuzumab + Chemotherapy139120129147

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Cmin of Trastuzumab

(NCT01774786)
Timeframe: Pre-dose (0-6 hours before infusion) on Day 1 of Cycles 1, 2, 3, 4, 6, and 8 (1 cycle = 21 days)

,
Interventionμg/mL (Mean)
Cycle 1Cycle 2Cycle 3Cycle 4Cycle 6Cycle 8
Pertuzumab + Trastuzumab + ChemotherapyNA15.419.922.926.332.7
Placebo + Trastuzumab + ChemotherapyNA17.220.724.129.837.4

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Duration of Objective Response, as Determined by Investigator According to RECIST v1.1 Criteria

Duration of objective response is defined as the time from first occurrence of documented objective response to documented disease progression, as determined by the investigator using RECIST v1.1, or death from any cause. Objective response: PR or CR occurring on 2 consecutive occasions ≥4 weeks apart. PR: at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum of diameters. CR: disappearance of all target lesions. PD: at least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study, including baseline; an absolute increase of at least 5 mm in the sum of diameters of target lesions; the appearance of one or more new lesions. Measurable disease defined as tumor lesions with a minimum size of: 10 mm by CT or MRI scan; 10 mm caliper measurement by clinical examination; 20 mm by chest X-ray. For a malignant lymph node, it must be ≥15 mm in short axis when assessed by CT scan. (NCT01774786)
Timeframe: Baseline to death or progressive disease (PD), whichever occurred first (Median [full range] duration of follow-up in Pertuzumab vs. Placebo arms for Primary Analysis: 24.9 [0-41] vs. 21.3 [0-39] months; Final Analysis: 50.4 [0-70] vs. 47.4 [0-66] months)

,
Interventionmonths (Median)
Primary AnalysisFinal Analysis
Pertuzumab + Trastuzumab + Chemotherapy10.210.2
Placebo + Trastuzumab + Chemotherapy8.48.4

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Final Analysis of the Percentage of Participants With Overall Objective Response, as Determined by the Investigator According to RECIST v1.1 Criteria

The overall objective response rate was defined as the percentage of participants with partial response (PR) or complete response (CR) occurring on two consecutive occasions ≥4 weeks apart, as determined by the investigator using RECIST v1.1. Tumor assessments with computed tomography (CT) or magnetic resonance imaging (MRI) scans of the chest, abdomen, and pelvis were performed every 9 weeks. PR: at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum of diameters. CR: disappearance of all target lesions. Measurable disease is defined as tumor lesions measured in at least one dimension (longest diameter in plane of measurement) with a minimum size of: 10 mm by CT or MRI scan; 10 mm caliper measurement by clinical examination; 20 mm by chest X-ray. For a malignant lymph node to be considered pathologically enlarged and measurable, it must be greater than or equal to (≥) 15 mm in short axis when assessed by CT scan. (NCT01774786)
Timeframe: Baseline up to death or progressive disease, whichever occurred first (Median [full range] duration of follow-up in Pertuzumab vs. Placebo arms for Final Analysis: 50.4 [0-70] months vs. 47.4 [0-66] months)

,
InterventionPercentage of participants (Number)
Objective Response (CR + PR)Complete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive Disease (PD)Not Evaluable/Missing
Pertuzumab + Trastuzumab + Chemotherapy57.05.751.327.64.810.5
Placebo + Trastuzumab + Chemotherapy48.62.046.632.78.210.5

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Progression-Free Survival, as Determined by the Investigator According to Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST v1.1) Criteria

Progression-free survival (PFS) is defined as the time from randomization to the first occurrence of progressive disease (PD), as determined by the investigator using RECIST v1.1, or death from any cause, whichever occurred first. Tumor assessments with CT or MRI scans of the chest, abdomen, and pelvis were performed every 9 weeks. Participants without documented PD or death were censored at the tumor assessment date for which the participant was last known to be progression-free. Participants who did not have any post-baseline tumor assessment data were censored at the date of randomization plus 1 day. PD was defined as at least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study, including baseline; an absolute increase of at least 5 millimeters (mm) in the sum of diameters of target lesions; the appearance of one or more new lesions. (NCT01774786)
Timeframe: Baseline to death or progressive disease (PD), whichever occurred first (Median [full range] duration of follow-up in Pertuzumab vs. Placebo arms for Primary Analysis: 24.9 [0-41] vs. 21.3 [0-39] months; Final Analysis: 50.4 [0-70] vs. 47.4 [0-66] months)

,
Interventionmonths (Median)
Primary AnalysisFinal Analysis
Pertuzumab + Trastuzumab + Chemotherapy8.58.5
Placebo + Trastuzumab + Chemotherapy7.07.2

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Primary Analysis of the Percentage of Participants With Overall Objective Response, as Determined by the Investigator According to RECIST v1.1 Criteria

The overall objective response rate was defined as the percentage of participants with partial response (PR) or complete response (CR) occurring on two consecutive occasions ≥4 weeks apart, as determined by the investigator using RECIST v1.1. Tumor assessments with computed tomography (CT) or magnetic resonance imaging (MRI) scans of the chest, abdomen, and pelvis were performed every 9 weeks. PR: at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum of diameters. CR: disappearance of all target lesions. Measurable disease is defined as tumor lesions measured in at least one dimension (longest diameter in plane of measurement) with a minimum size of: 10 mm by CT or MRI scan; 10 mm caliper measurement by clinical examination; 20 mm by chest X-ray. For a malignant lymph node to be considered pathologically enlarged and measurable, it must be greater than or equal to (≥) 15 mm in short axis when assessed by CT scan. (NCT01774786)
Timeframe: Baseline up to death or progressive disease, whichever occurred first (Median [full range] duration of follow-up in Pertuzumab vs. Placebo arms for Primary Analysis: 24.9 [0-41] months vs. 21.3 [0-39] months)

,
InterventionPercentage of participants (Number)
Objective Response (CR + PR)Complete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive Disease (PD)Not Evaluable/Missing
Pertuzumab + Trastuzumab + Chemotherapy56.75.151.627.94.810.5
Placebo + Trastuzumab + Chemotherapy48.30.947.433.08.010.8

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Overview of Safety: Number of Participants With at Least One Adverse Event, Severity Determined According to National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE), Version 4.03

An adverse event (AE) is any untoward medical occurrence in a clinical investigation participant administered a pharmaceutical product, regardless of causal attribution. The investigator graded all AEs for severity per the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE), Version 4.03; if not listed, the AE was assessed as follows: Grade 1 = mild; Grade 2 = moderate; Grade 3 = severe; Grade 4 = life-threatening/disabling; Grade 5 = death. The investigator determined whether an AE was related to study drug and independently assessed severity and seriousness of each AE. (NCT01774786)
Timeframe: From Baseline until end of post-treatment follow-up (up to 70 months)

,
InterventionParticipants (Count of Participants)
Any Adverse Event (AE)AE with Fatal OutcomeSerious AEGrade 3-5 AEAE Leading to Pertuz/Pbo & Trastuz DiscontinuationAE Leading to Dose Interruption &/or Dose Delay
Pertuzumab + Trastuzumab + Chemotherapy3812717831048110
Placebo + Trastuzumab + Chemotherapy385311562884694

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Overall Survival

Overall survival (OS) was defined as the time from randomization to death from any cause. For participants who were still alive on the date of clinical data cut-off for the OS analysis, the last date when the participant was known to be alive on, or prior to the clinical cut-off date, was used to determine the censoring date. Participants who did not have any post-baseline data (e.g., dosing records, imaging dates, visit dates) were censored at the date of randomization plus 1 day. (NCT01774786)
Timeframe: From Baseline until death from any cause (Median [full range] duration of follow-up in Pertuzumab vs. Placebo arms for Primary Analysis: 24.4 [0-42] months vs. 25.0 [0-41] months; Final Analysis: 46.1 [0-70] months vs. 44.4 [0-68] months)

,
InterventionMonths (Median)
Primary AnalysisFinal Analysis
Pertuzumab + Trastuzumab + Chemotherapy17.518.1
Placebo + Trastuzumab + Chemotherapy14.214.2

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Number of Participants With Symptomatic or Asymptomatic Left Ventricular Systolic Dysfunction (LVSD)

The number and percentage of participants with symptomatic left ventricular systolic dysfunction (LVSD) and asymptomatic LVSD events (defined as a left ventricular ejection fraction [LVEF] ≥10% decrease from baseline to an absolute value <50%) at any time during the study was summarized by treatment arm. (NCT01774786)
Timeframe: From Baseline until end of post-treatment follow-up (up to 70 months)

,
InterventionParticipants (Count of Participants)
Symptomatic LVSDAsymptomatic LVSD
Pertuzumab + Trastuzumab + Chemotherapy320
Placebo + Trastuzumab + Chemotherapy118

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Progression Free Survival

The effect of napabucasin given in combination with cetuximab, panitumumab or capecitabine on Progression Free Survival (PFS) of patients with advanced colorectal cancer. (NCT01776307)
Timeframe: The time from the date of first treatment to the date of first documentation of disease progression or death due to any cause, up to 24 months

Interventionmonths (Median)
Napabucasin Plus Cetuximab1.87
Napabucasin Plus Panitumumab2.27
Napabucasin Plus Capecitabine1.94

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Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 480mg, Twice Daily, on Day 21 of the First Study Cycle

To determine the maximum concentration of napabucasin when given at 480mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 21 during the first study cycle

Interventionng/mL (Geometric Mean)
Napabucasin Plus Cetuximab627
Napabucasin Plus Panitumumab398

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Disease Control Rate

Assessment of Disease Control Rate, defined as the proportion of patients with a documented complete response, partial response and stable disease based on RECIST 1.1, in patients with advanced colorectal cancer given napabucasin in combination with cetuximab, panitumumab or capecitabine (NCT01776307)
Timeframe: From the date of first treatment, every 8 weeks, until the date of first documented objective disease progression, up to 24 months

InterventionPercentage of participants (Number)
Napabucasin Plus Cetuximab34.5
Napabucasin Plus Panitumumab36.6
Napabucasin Plus Capecitabine25.6

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Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 500mg, Twice Daily, on Day 5 of the First Study Cycle

To determine the maximum concentration of napabucasin when given at 500mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 5 during the first study cycle

Interventionng/mL (Geometric Mean)
Napabucasin Plus Panitumumab1020
Napabucasin Plus Capecitabine858

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Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 500mg, Twice Daily, on Day 21 of the First Study Cycle

To determine the maximum concentration of napabucasin when given at 500mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 21 during the first study cycle

Interventionng/mL (Geometric Mean)
Napabucasin Plus Panitumumab1060
Napabucasin Plus Capecitabine789

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Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 480mg, Twice Daily, on Day 5 of the First Study Cycle

To determine the maximum concentration of napabucasin when given at 480mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 5 during the first study cycle

Interventionng/mL (Geometric Mean)
Napabucasin Plus Cetuximab661
Napabucasin Plus Panitumumab468

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Determination of the Maximum Observed Concentration (Cmax) of Napabucasin When Administered 240mg, Twice Daily, on Day 21 of the First Study Cycle

To determine the maximum concentration of napabucasin when given at 240mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 21 during the first study cycle

Interventionng/mL (Geometric Mean)
Napabucasin Plus Cetuximab494

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Number of Patients With Adverse Events and Serious Adverse Events

Assessment of safety of napabucasin given in combination with cetuximab, panitumumab or capecitabine to patients with advanced colorectal cancer by reporting of adverse events and serious adverse events (NCT01776307)
Timeframe: The time from the date of first treatment, while the patient is taking napabucasin, and for 30 days after stopping therapy, an average of 4 months.

InterventionParticipants (Count of Participants)
Napabucasin Plus Cetuximab49
Napabucasin Plus Panitumumab75
Napabucasin Plus Capecitabine75

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Overall Survival

The effect of napabucasin given in combination with cetuximab, panitumumab or capecitabine on the Overall Survival of patients with advanced colorectal cancer (NCT01776307)
Timeframe: 4 weeks after the patient has been off study treatment, every 3 months thereafter until death, up to 60 months.

InterventionMonths (Median)
Napabucasin Plus Cetuximab7.79
Napabucasin Plus Panitumumab9.10
Napabucasin Plus Capecitabine6.34

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Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 500mg, Twice Daily, on Day 5 of the First Study Cycle

To determine the area under the plasma concentration vs. time curve of napabucasin when given at 500mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 5 during the first study cycle

Interventionh*ng/mL (Geometric Mean)
Napabucasin Plus Panitumumab5420
Napabucasin Plus Capecitabine5350

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Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 500mg, Twice Daily, on Day 21 of the First Study Cycle

To determine the area under the plasma concentration vs. time curve of napabucasin when given at 500mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 21 during the first study cycle

Interventionh*ng/mL (Geometric Mean)
Napabucasin Plus Panitumumab6290
Napabucasin Plus Capecitabine4720

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Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 480mg, Twice Daily, on Day 5 of the First Study Cycle

To determine the area under the plasma concentration vs. time curve of napabucasin when given at 480mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 5 during the first study cycle

Interventionh*ng/mL (Geometric Mean)
Napabucasin Plus Cetuximab3380
Napabucasin Plus Panitumumab2730

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Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 480mg, Twice Daily, on Day 21 of the First Study Cycle

To determine the area under the plasma concentration vs. time curve of napabucasin when given at 480mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 21 during the first study cycle

Interventionh*ng/mL (Geometric Mean)
Napabucasin Plus Cetuximab2930
Napabucasin Plus Panitumumab2630

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Area Under the Plasma Concentration vs. Time Curve (AUClast) of Napabucasin When Administered 240mg, Twice Daily, on Day 21 of the First Study Cycle

To determine the area under the plasma concentration vs. time curve of napabucasin when given at 240mg, twice daily, in combination with cetuximab, panitumumab, or capecitabine in patients with advanced colorectal cancer. (NCT01776307)
Timeframe: Blood samples drawn on day 21 during the first study cycle

Interventionh*ng/mL (Geometric Mean)
Napabucasin Plus Cetuximab2870

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Time to Treatment Failure

The time from enrollment to discontinuation of any drug of the treatment combination. (NCT01777945)
Timeframe: approximately 2 years

Interventionmonths (Mean)
Participants Receiving Capecitabine/Docetaxel4.64

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Progression-free Survival (PFS)

The time from enrollment until disease progression, assessed as the time to tumor progression, as evaluated by regular examinations per routine clinical practice, or death from any cause. (NCT01777945)
Timeframe: approximately 2 years

Interventionmonths (Median)
Participants Receiving Capecitabine/Docetaxel9.89

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Number of Participants With Adverse Events

(NCT01777945)
Timeframe: approximately 2 years

Interventionparticipants (Number)
Participants Receiving Capecitabine/Docetaxel33

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Overall Response Rate

The percentage of participants with complete or partial remission, based on evaluation of tumor responses assessed at regular examinations per routine clinical practice. (NCT01777945)
Timeframe: approximately 2 years

Interventionpercentage of participants (Number)
Participants Receiving Capecitabine/Docetaxel28.9

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Clinical Benefit Rate

The percentage of participants with an overall response (complete or partial remission) or with stable disease. (NCT01777945)
Timeframe: approximately 2 years

Interventionpercentage of participants (Number)
Participants Receiving Capecitabine/Docetaxel73.3

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Duration of Treatment With Xeloda

(NCT01777945)
Timeframe: approximately 2 years

Interventiontreatment cycle (Mean)
Participants Receiving Capecitabine/Docetaxel6.24

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Percentage of Capecitabine Dose Modifications

(NCT01777945)
Timeframe: approximately 2 years

Interventionpercentage of doses (Number)
Participants Receiving Capecitabine/Docetaxel44.4

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Toxicity(Adeverse Event)

"Toxicity will be monitored and recorded every week during study treatment (5 or 6 weeks) as following according to the NCI-CTCAE version 4.0~An interval history and physical examination with particular attention to drug-induced side effects along with documentation of the patient's weight and performance status will be performed on each visit.~CBC with differential count, blood chemistry including calcium, phosphorus, glucose, BUN, creatinine, total protein, albumin, AST, ALT, alkaline phosphatase, total bilirubin, and electrolyte will be performed before next planned treatment.~All relevant information regarding drug dosage, laboratory examinations, and treatment-related toxicities must be recorded before each treatment is given.~Summaries of the frequency and severity of adverse effects are based on the worst episodes recorded." (NCT01781403)
Timeframe: 5-6 weeks during study treatment

,,
Interventionevents (Number)
Any grade 1 adverse eventAny grade 2 adverse eventAny grade 3 adverse eventAny grade 4 adverse event
Dose Level 16210
Dose Level 28200
Dose Level 3/Recommended Dose601730

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Maximum Tolerated Dose (MTD)

The MTD is defined as the maximum dose level in the doses of temozolomide tested with capecitabine and radiation in which the incidence proportion of DLT exceeds 30%. (NCT01781403)
Timeframe: 5-6 weeks during study treatment

Interventionmg/m^2 (Number)
Dose Level 10
Dose Level 20
Dose Level 3/Recommended Dose0

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Pathological Complete Response

"Pathologic responses and stages were classified according to Dworak's classification and the 7th edition of the American Joint Committee on Cancer staging system, respectively.~The pathologic complete response (pCR) was defined as the total regression of the primary tumor regardless of regional lymph nodal status (ypT0), with residual fibrotic mass or acellular mucin pools only, thus without detectable tumor cells." (NCT01781403)
Timeframe: at the time of surgery (6-8 weeks after study treatment)

Interventionparticipants (Number)
Unmethylated MGMT1
Hypermethylated MGMT6

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Mean Change in Treatment Satisfaction Questionnaire for Medication (TSQM) Between Week 3 and 12

TSQM was used to measure the Patients' self-reported satisfaction or dissatisfaction with the study treatment. The differences in mean scale scores between weeks 3 and 12 comparing treatment satisfaction in the different treatment arms: everolimus + exemestane combination therapy versus everolimus monotherapy, and everolimus + exemestane combination therapy versus capecitabine monotherapy. The TSQM version 1.4 domain scores range from 0 to 100 with higher scores representing a higher satisfaction on that domain. (NCT01783444)
Timeframe: Week 3, Week 12

,,
InterventionUnit on a scale (Mean)
Side-effectsEffectivenessConvenienceGlobal satisfaction
Capecitabine 1250 mg/m2-2.61.20.52.3
Everolimus 10 mg-9.11.21.01.8
Everolimus 10 mg + Exemestane 25 mg-4.8-2.2-0.6-1.0

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Progression Free Survival (PFS) - Everolimus Plus Exemestane Versus Capecitabine Alone

Progression Free Survival (PFS) is defined as the time from date of randomization to the date of first radiologically documented progression or death due to any cause. If a patient did not have an event, PFS was censored at the date of the last adequate tumor assessment. PFS was compared between the everolimus + exemestane combination therapy with the everolimus monotherapy. (NCT01783444)
Timeframe: Date of randomization to the date of first documented tumor progression or death from any cause, whichever occurs first, reported between day of first patient randomized up to 39 months

InterventionMonths (Median)
Everolimus 10 mg + Exemestane 25 mg8.41
Capecitabine 1250 mg/m29.59

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Progression Free Survival (PFS) - Everolimus Plus Exemestane Versus Everolimus Alone

Progression Free Survival (PFS) is defined as the time from date of randomization to the date of first radiologically documented progression or death due to any cause. If a patient did not have an event, PFS was censored at the date of the last adequate tumor assessment. PFS was compared between the everolimus + exemestane combination therapy with the everolimus monotherapy. (NCT01783444)
Timeframe: Date of randomization to the date of first documented tumor progression or death from any cause, whichever occurs first, reported between day of first patient randomized up to 39 months

InterventionMonths (Median)
Everolimus 10 mg + Exemestane 25 mg8.41
Everolimus 10 mg6.77

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All Collected Deaths

"On treatment deaths were collected from FPFT up to 30 days after study drug discontinuation, for a maximum duration of 224 weeks (treatment duration ranged from 1.3 to 220.0 weeks).~Deaths post treatment survival follow up were collected after the on- treatment period, up to approximately 5 years. Patients who didn't die during the on-treatment period and had not stopped study participation at the time of data cut-off (end of study) were censored." (NCT01783444)
Timeframe: up to 224 weeks (on-treatment), up to approximately 5 years (study duration)

,,
InterventionParticipants (Count of Participants)
On-treatment deathsPost-treatment deathsAll deaths
Capecitabine 1250 mg/m225759
Everolimus 10 mg55560
Everolimus 10 mg + Exemestane 25 mg96271

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Time to 10% Definitive Deterioration in the Global Health Status / Quality of Life

The global health status/QoL scale score of the QLQ-C30 is identified as the primary PRO variable of interest. Physical Functioning (PF), Emotional Functioning (EF) and Social Functioning (SF) scale scores of the QLQ-C30. The time to definitive 10% deterioration is the number of days between the date of randomization and the date of the assessment at which definitive deterioration is seen. Definitive 10% (5-point) deterioration is defined as a decrease in score by at least 10% (5-points) compared to baseline, with no later increase above this threshold observed during the course of the study. (NCT01783444)
Timeframe: Baseline, every 6 weeks up to about 43 months

InterventionWeeks (Median)
Everolimus 10 mg + Exemestane 25 mg30.86
Everolimus 10 mg23.86
Capecitabine 1250 mg/m261.29

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Time to Eastern Cooperative Oncology Group (ECOG) Performance Deterioration

The Eastern Cooperative Oncology Group (ECOG) Performance Status is a scale used to assess physical health of subjects,ranging from 0 (most active) to 5 (least active). Definitive deterioration is defined as no improvement in the ECOG status following observation of the deterioration. (NCT01783444)
Timeframe: Baseline, every 6 weeks up to about 43 months

InterventionWeeks (Median)
Everolimus 10 mg + Exemestane 25 mg72.57
Everolimus 10 mg126.57
Capecitabine 1250 mg/m2120.00

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Overall Survival (OS)

Overall Survival (OS) is defined as the time from date of randomization to date of death due to any cause. If a patient was not known to have died by the date of analysis cut-off, OS was censored at the date of last known date patient alive. (NCT01783444)
Timeframe: Every 3 months following end of treatment visit, assessed for approximately 54 months

InterventionMonths (Median)
Everolimus 10 mg + Exemestane 25 mg23.06
Everolimus 10 mg29.27
Capecitabine 1250 mg/m225.56

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Clinical Benefit Rate (CBR)

Clinical Benefit Rate (CBR) is defined as the proportion of participants with a best overall response of complete response (CR) or partial response (PR) or stable disease (SD) or Non-CR/non-PD lasting more than 24 weeks based on local investigator's assessment according to RECIST 1.1. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR, Stable disease (SD), neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for PD; CBR = CR+PR+SD. Only descriptive statistics. (NCT01783444)
Timeframe: From the date of randomization until the date of the first documented disease progression or date of death from any cause whichever came first, assessed for approximately 43 months

InterventionPercentage of Participants (Number)
Everolimus 10 mg + Exemestane 25 mg59
Everolimus 10 mg43
Capecitabine 1250 mg/m253

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Overall Response Rate (ORR)

Overall Response Rate (ORR) as the proportion of patients whose best overall response is either complete response (CR) or partial response (PR) according to RECIST 1.1 This was assessed in the full patient population. Complete response is achieved when all lesions evaluated at baseline are absent at subsequent visit. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. Only descriptive statistics. (NCT01783444)
Timeframe: From the date of randomization until the date of the first documented disease progression or date of death from any cause whichever came first, assessed for approximately 43 months

InterventionPercentage of Participants (Number)
Everolimus 10 mg + Exemestane 25 mg21
Everolimus 10 mg12
Capecitabine 1250 mg/m223

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Duration of Response (DOR) - Central Assessment (Population That Had a Response With Measurable Disease at Screening)

"The Duration of Response (DOR) is for Central Assessment for the Population that Had a Response with Measurable Disease at Screening.~Duration of response is measured from the time at which measurement criteria are first met for CR or PR (whichever status is recorded first) until the first date of recurrence or progressive disease (PD) or death is objectively documented, taking as a reference for PD the smallest measurements recorded since enrollment, per RECIST v1.1. This value is censored at the last valid tumor assessment if PD or death has not been documented." (NCT01808573)
Timeframe: From start date of response after randomization to first PD, up to 33 months.The result is based on primary analysis data cut.

Interventionmonths (Median)
Neratinib Plus Capecitabine8.54
Lapatinib Plus Capecitabine5.55

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Percentage of Participants With Treatment-Emergent Adverse Events (Adverse Events and Serious Adverse Events)

Adverse Events to be measured are Treatment-Emergent and Serious AEs that occurred on or after first dose of investigational product and up to 28 days after the last dose (NCT01808573)
Timeframe: From first dose through last dose + 28 days, up to 41 months. The result is based on final data cut.

,
Interventionpercentage of participants (Number)
All Treatment-Emergent Adverse EventsSerious Treatment-Emergent Adverse Events
Lapatinib Plus Capecitabine99.429.9
Neratinib Plus Capecitabine99.734.0

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Overall Survival

Overall survival (OS) is defined as the time from randomization to death due to any cause, censored at the last date known alive on or prior to the data cutoff employed for the analysis, whichever was earlier. Here, the time to event was reported as the restricted mean survival time. The restricted mean survival time was defined as the area under the curve of the survival function up to 48 months. (NCT01808573)
Timeframe: From randomization date to death, assessed up to 59 months.The result is based on primary analysis data cut.

Interventionmonths (Mean)
Neratinib Plus Capecitabine24.0
Lapatinib Plus Capecitabine22.2

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Centrally Assessed Progression Free Survival

Progression Free Survival (PFS), Measured in Months, for Randomized Subjects of the Central Assessment. The time interval from the date of randomization until the first date on which recurrence, progression (per Response Evaluation Criteria in Solid Tumors Criteria (RECIST) v1.1), or death due to any cause, is documented. For subjects without recurrence, progression or death, it is censored at the last valid tumor assessment. Progression is defined using Response Evaluation Criteria in Solid Tumors Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. Here, the time to event was reported as the restricted mean survival time. The restricted mean survival time was defined as the area under the curve of the survival function up to 24 months. (NCT01808573)
Timeframe: From randomization date to recurrence, progression or death, assessed up to 38 months. The result is based on primary analysis data cut.

Interventionmonths (Mean)
Neratinib Plus Capecitabine8.8
Lapatinib Plus Capecitabine6.6

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Objective Response Rate (ORR) - Central Assessment (ITT Population With Measurable Disease at Screening)

Objective response rate is defined as the percentage of participants demonstrating an objective response during the study. Objective response includes confirmed complete responses (CR) and partial responses (PR) as defined in the RECIST criteria included in the study protocol. The ORR is for Central Assessment for subjects that had measurable disease at screening. Per Response Evaluation Criteria in Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01808573)
Timeframe: From randomization date to first confirmed Complete or Partial Response, whichever came earlier, up to 42 months.The result is based on primary analysis data cut.

Interventionpercentage of participants (Number)
Neratinib Plus Capecitabine32.8
Lapatinib Plus Capecitabine26.7

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Clinical Benefit Rate (CBR) - Central Assessment (ITT Population With Measurable Disease at Screening)

Clinical benefit rate is the percentage of participants who achieve overall tumor response (confirmed CR or PR) or stable disease (SD) lasting for at least 24 weeks from randomization. The CBR was for Central Assessment for subjects who had Measurable Disease at Screening. (NCT01808573)
Timeframe: From randomization date to either first confirmed CR or PR or Stable Disease, whichever came earlier, up to 42 months.The result is based on primary analysis data cut.

Interventionpercentage of participants (Number)
Neratinib Plus Capecitabine44.5
Lapatinib Plus Capecitabine35.6

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Intervention for Symptomatic Metastatic Central Nervous System Disease

Intervention for symptomatic metastatic central nervous system disease is defined as the time from randomization to the first start date of an intervention for symptomatic metastatic CNS disease. Subjects that do not have an intervention for symptomatic metastatic CNS and do not die will be censored at the last date known alive on or prior to the data cutoff. Deaths are treated as competing events. Percentage of participants with intervention for CNS, estimated by cumulative incidence methods. Cumulative incidence methods are the standard way to estimate incidence of an endpoint in the presence of competing risks and censoring. (NCT01808573)
Timeframe: From randomization date to first intervention for symptomatic metastatic CNS disease, assessed up to 59 months.The result is based on primary analysis data cut.

Interventionpercentage of participants (Number)
Neratinib Plus Capecitabine22.76
Lapatinib Plus Capecitabine29.19

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Progression-free Survival (PFS) at 2 Years

Proportion of participants with progression-free survival (PFS) at 2 years, as calculated based on Kaplan-Meier estimates. (NCT01823679)
Timeframe: 2 years

Interventionpercentage of participants (Number)
Capecitabine 1000 mg/m20

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Progression-free Survival (PFS) at 1 Year

Proportion of participants with progression-free survival (PFS) at 1 year, as calculated based on Kaplan-Meier estimates. (NCT01823679)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Capecitabine 1000 mg/m250

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Overall Survival (OS) at 2 Years

Proportion of participants with overall survival (OS) at 2 years, as calculated based on Kaplan-Meier estimates. (NCT01823679)
Timeframe: 2 years

Interventionpercentage of participants (Number)
Capecitabine 1000 mg/m20

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Objective Response Rate (ORR)

Response assessed by Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST v1.1) (NCT01823679)
Timeframe: 9 weeks (3 cycles)

Interventionpercentage of participants (Number)
Capecitabine 1000 mg/m²0

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Overall Survival (OS) at 1 Year

Proportion of participants with overall survival (OS) at 1 year, as calculated based on Kaplan-Meier estimates. (NCT01823679)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Capecitabine 1000 mg/m250

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Proportion of Patients With Response

"Response was evaluated using the revised Response Evaluation Criteria in Solid Tumors (RECIST) guideline (version 1.1) and defined as either complete response (CR) or partial response (PR).~CR is defined as disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 10 mm.~PR is defined as at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters." (NCT01824875)
Timeframe: Assessed every 3 months for 3 years and then every 6 months for years 3-5

Interventionproportion of participants (Number)
Arm A (Temozolomide)0.338
Arm B (Temozolomide and Capecitabine)0.397

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Overall Survival

Overall survival is defined as time from randomization to death or date last known alive. (NCT01824875)
Timeframe: Assessed every 3 months for 3 years and then every 6 months for years 3-5

Interventionmonths (Median)
Arm A (Temozolomide)53.8
Arm B (Temozolomide and Capecitabine)58.7

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Progression-free Survival

Progression-free survival (PFS) is defined as the time from randomization to progression or death without evidence of progression. Progression was evaluated using the revised Response Evaluation Criteria in Solid Tumors (RECIST) guideline (version 1.1) and defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. Kaplan-Meier method was used to estimate PFS. (NCT01824875)
Timeframe: Assessed every 3 months for 3 years and then every 6 months for years 3-5

Interventionmonths (Median)
Arm A (Temozolomide)15.1
Arm B (Temozolomide and Capecitabine)23.2

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Response Rate

Responses will be determined using RECIST v. 1.1 criteria and summarized in tabular format. The complete and partial response rates will be calculated and reported along with the corresponding 95% confidence intervals. (NCT01828554)
Timeframe: Up to 6 months

Interventionpercentage (Number)
Xeloda (Capecitabine)0

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Progression Free Survival

Progression-free survival will be analyzed using the Kaplan-Meier method. (NCT01828554)
Timeframe: Up to 6 months

Interventionmonths (Median)
Xeloda (Capecitabine)NA

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Cmax During Cycle 1

Cmax will be reported for Capecitabine dosed for Ideal Body Weight during the first cycle (days 1-7) and for Capecitabine dosed for Actual Body Weight for first cycle (days 9-15). [nonlinear mixed effects modeling approach] (NCT01828554)
Timeframe: Up to 15 days

InterventionCmax (ug/ml) (Mean)
Cycle 1 Day 1Cycle 1 Day 9
Xeloda (Capecitabine)2.442.71

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Area Under the Curve (AUC) on Cycle 1 Day 1 and Cycle 1 Day 9

AUC will be calculated for Capecitabine dosed for Ideal Body Weight during the first cycle (days 1-7) and for Capecitabine dosed for Actual Body Weight for first cycle (days 9-15). [nonlinear mixed effects modeling approach] (NCT01828554)
Timeframe: Up to 15 days

InterventionAUC (ug/ml)*h (Mean)
Cycle 1 Day 1Cycle 1 Day 9
Xeloda (Capecitabine)6.848.28

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Phase II - Rate of Response

Determine rate of response in patients receiving quinacrine in combination with capecitabine. Using Response Evaluation Criteria in Solid Tumors (RECIST) guideline (version 1.1) complete response (CR) is a disappearance of all target lesions, partial response (PR) is at least 30% decrease in the sum of diameters of target lesions, and overall response is the number of patients who experience a complete response or partial response. (NCT01844076)
Timeframe: 2-3 years

InterventionParticipants (Count of Participants)
Phase I Level -20
Phase I Level -10
Phase I Level 00
Phase II1

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Phase I - Number of Participants Who Experienced Dose Limiting Toxicities and Adverse Reactions

Establish the tolerability of both agents in combination when used at established clinical doses. The objective is to determine toxicities and adverse reactions of patients in each group with different dose levels to find the maximum tolerated dose (MTD). (NCT01844076)
Timeframe: One year

InterventionParticipants (Count of Participants)
Phase I Level -20
Phase I Level -10
Phase I Level 03

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Phase II - Time to Progression (TTP)

Determine time to progression from start of treatment in patients receiving quinacrine in combination with capecitabine. Using Response Evaluation Criteria in Solid Tumors (RECIST) guideline (version 1.1), progression is defined as a 20% increase in sum of target lesions, with at least a 5 mm absolute increase. (NCT01844076)
Timeframe: 2-3 years

Interventionmonths (Median)
Phase II2.12

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Overall Response Rate

To describe the overall response rate as measured by physical exam and MRI if indicated using the following definition: Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01869192)
Timeframe: Up to 8 months

InterventionParticipants (Count of Participants)
Arm A25
Arm B21

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Pathological Response

Pathological response (pCR or microscopic only primary) in both primary and nodes using the Miller-Payne criteria for pathologic response. (NCT01869192)
Timeframe: Up to 8 months

InterventionParticipants (Count of Participants)
Arm A2
Arm B8

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Number of Participants With Any Adverse Events as a Measure of Safety and Tolerability

Assessment based on CTCAE version 4.0 toxicity criteria. For the detailed list of adverse events see the adverse event module. (NCT01873833)
Timeframe: ****Time Frame: Adverse events were collected from first dose of study treatment up to 30 days after last dose of treatment, up to 63 months (number or treatment given ranged from 2 cycles to 85 cycles).

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Lapatinib Ditosylate, Trastuzumab)10

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Clinical Benefit Rate (CBR)

Participants with a best response of CR, PR, or stable disease (SD) sustained for ≥24 weeks, as assessed using RECIST v1.1. CR: Disappearance of all non-nodal target and non-target lesions, including target and non-target lymph nodes reduction to <10 mm in short axis. PR: >=30% decrease in sum of diameters of target lesions, compared to the sum at baseline. SD: Neither PR nor progression of disease (PD) criteria met. SD follow PR only when sum increases by less than 20% from the nadir, but previously seen 30% decrease from baseline no longer hold. PD: >=20% increase (>=5 mm absolute increase) in the sum of target lesion measurements, compared to the smallest sum on study (including baseline), or unequivocal progression of non-target lesions, evaluated as a whole, such that it is clear that treatment has failed and disease is progressing, regardless of the status of the target lesions. (NCT01873833)
Timeframe: From study entry until the date of the first documented disease progression of date of death whichever came first, assessed for approximately 351 weeks

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Lapatinib Ditosylate, Trastuzumab)7

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Overall Response Rate (ORR)

Overall response rate (ORR) is complete response (CR) + partial response (PR) recorded from study entry until disease progression based on RECIST v1.1 criteria. Per RECIST 1.1 for target lesions: CR is complete disappearance of all target lesions and PR is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. PR or better overall response assumes at a minimum incomplete response/stable disease (SD) for the evaluation of non-target lesions and absence of new lesions. (NCT01873833)
Timeframe: From study entry until disease progression/recurrence (maximum duration: 351 weeks)

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Lapatinib Ditosylate, Trastuzumab)4

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Overall Survival (OS)

OS is the duration from study entry to death. Participants last known to be alive are censored at date of last contact. (NCT01873833)
Timeframe: From study entry until death from any cause or date of last contact (up to 70 months)

InterventionMonths (Median)
Treatment (Chemotherapy, Lapatinib Ditosylate, Trastuzumab)29.6

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Progression Free Survival (PFS)

PFS was defined as duration of time from the first dose of study drug to the first documentation of Progressive Disease (PD) by investigator assessment using RECIST 1.1 or death on study due to any cause on or before the data cutoff date, whichever occurred first. PD: >=20% increase (>=5 mm absolute increase) in the sum of target lesion measurements, compared to the smallest sum on study (including baseline), or unequivocal progression of non-target lesions, evaluated as a whole, such that it is clear that treatment has failed and disease is progressing, regardless of the status of the target lesions. (NCT01873833)
Timeframe: From study entry to the date of first documented disease progression (assessed every 6 weeks) or death due to any cause, whichever came first, approximately 63 months.

Interventionmonths (Median)
Treatment (Chemotherapy, Lapatinib Ditosylate, Trastuzumab)13.7

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Overall Survival

Survival time is defined as time from randomization to date of death from any cause and was to be estimated by the Kaplan-Meier method. Given the limited follow-up due to early closure and termination of data collection, only the number of patients last reported to be alive at time of study termination is reported. (NCT01921751)
Timeframe: From randomization until last follow-up. Analysis was to occur after a total of 140 deaths were reported within the pairing of each radiation arm with the chemotherapy alone arm. Maximum follow-up at time of study termination was 8.3 months.

InterventionParticipants (Count of Participants)
Chemotherapy + High Intensity Radiation4
Chemotherapy + Low Intensity Radiation4
Chemotherapy5

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Patterns of Failure (Local and Metastatic Failure)

Local progression is defined as least a 20% increase in the sum of diameters of the primary, taking as reference the baseline sum. Given the inherent inaccuracy in determining size of a primary pancreatic carcinoma, in addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm and progression must be demonstrated on at least two sequential scans. Metastatic failure is defined as metastatic disease. Local and distant failure were to be estimated by the cumulative incidence method. Given the limited follow-up due to early closure and termination of data collection, only the number of patients with failure is reported. (NCT01921751)
Timeframe: From randomization until last follow-up. Maximum follow-up at time of study termination was 8.3 months.

,
InterventionParticipants (Count of Participants)
Local FailureMetastatic Failure
Chemotherapy + High Intensity Radiation00
Chemotherapy + Low Intensity Radiation01

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Overall Response Rate

(NCT01928680)
Timeframe: 6 months

Interventionpercentage of response (Number)
Cisplatin/Capecitabine63.6

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Part 1: Number of Participants With Tumor Responses (Complete Response [CR], Partial Response [PR], Stable Disease [SD] or Progressive Disease [PD])

Tumor assessment was performed by abdomino-pelvic computed tomography scan or magnetic resonance imaging (MRI) and chest X-ray or chest CT-scan to assess the disease status at baseline and then every 9 weeks during study treatment up to DP. Target lesions were evaluated using response evaluation criteria in solid tumors (RECIST) version 1.1, wherein CR = disappearance of all target lesions; PR = 30% decrease in the sum of the longest diameter (LD) of target lesions taking as reference the baseline sum LD; PD =20% increase in the sum of the LD of target lesions taking as reference the smallest sum in the study and SD = small changes that did not meet above criteria. (NCT01955629)
Timeframe: Baseline and every 9 weeks up to DP (up to 15 months).

InterventionParticipants (Number)
CRPRPDSD
Aflibercept + XELOX (Oxaliplatin and Capecitabine)0103

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Part 1: Number of Participants With Dose Limiting Toxicities (DLTs)

DLTs were assessed using the national cancer institute (NCI) common terminology criteria for adverse events (CTCAE) version 4.03. DLTs were defined as any of following AEs: grade 4 neutropenia lasting >7 consecutive days; febrile neutropenia or neutropenic infection; grade 4 thrombocytopenia; grade 3 thrombocytopenia associated with bleeding requiring transfusion; grade 4 non-hematological treatment related event; grade 3 nausea/vomiting or diarrhea lasting >/= 4 days despite corrective measures; grade 3 other non-hematological toxicities: anorexia, fatigue, hypertension only if G4 or not medically controlled and G3 peripheral sensory neuropathy that did not improve to G<2 at time of retreatment; urinary protein excretion of >3.5 gram per 24 hours that did not recover to <2.0 gram per 24 hours within 2 weeks; symptomatic arterial thromboembolic events including cerebrovascular accidents, myocardial infarction, transient ischemic attacks, new onset or worsening of pre-existing angina. (NCT01955629)
Timeframe: Cycle 1 (Up to 3 weeks)

InterventionParticipants (Number)
Aflibercept + XELOX (Oxaliplatin and Capecitabine)1

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Overall Survival

Overall Survival (OS) is defined as the number of months from randomization to the date of death due to any cause. (NCT01997333)
Timeframe: During treatment and 3 months from end of treatment through end of study or approximately up to 5 years.

Interventionmonths (Median)
Capecitabine8.7
CDX-0118.9

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Duration of Response

Duration of response (DOR) is the number of months from the time criteria are first met for either CR or PR, until the first date that PD is objectively documented. The analysis of DOR was determined retrospectively by the central independent review committee,blinded to treatment assignment and investigator assessments according to RECIST 1.1 criteria. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), Complete Response (CR) = Disappearance of all target lesions and non-target lesions, Partial Response (PR), >= 30% decrease in the sum of the longest diameter of target lesions with no progression in non-target lesions and no new lesions. (NCT01997333)
Timeframe: Evaluated every 6 - 9 weeks following treatment initiation

Interventionmonths (Median)
Capecitabine4.2
CDX-0112.8

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Objective Response Rate (ORR)

ORR is defined as the percentage of patients who achieve best overall response of complete or partial response. The analysis of ORR was based on ORR events determined retrospectively by the central independent review committee, blinded to treatment assignment and investigator assessments according to RECIST 1.1 criteria. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), Complete Response (CR) = Disappearance of all target lesions and non-target lesions, Partial Response (PR), >= 30% decrease in the sum of the longest diameter of target lesions with no progression in non-target lesions and no new lesions. (NCT01997333)
Timeframe: Evaluated every 6 - 9 weeks following treatment initiation

Interventionpercentage of participants (Median)
Capecitabine21
CDX-01126

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Progression Free Survival (PFS)

PFS is defined as the time from randomization to the earlier of disease progression or death due to any cause. Disease progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or progression in a non-target lesion, or the appearance of new lesions. The primary analysis of PFS was based on PFS events determined retrospectively by the central independent review committee, blinded to treatment assignment and investigator assessments according to RECIST 1.1 criteria. (NCT01997333)
Timeframe: Evaluated every 6 - 9 weeks following treatment initiation

Interventionmonths (Median)
Capecitabine2.8
CDX-0112.9

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Adverse Events (AE)

The percentage of patients experiencing one or more adverse events will be summarized by treatment arm, relationship to study drug, and severity. (NCT01997333)
Timeframe: Usually following at least 1 cycle of study treatment (1 dose of CDX-011 or capecitabine and until discontinuation of follow-up)

,
InterventionParticipants (Count of Participants)
Patients with at least 1 AEPatients with at least 1 treatment related AEPatients with Grade 1 treatment related AEPatients with Grade 2 treatment related AEPatients with Grade 3 treatment related AEPatients with Grade 4 treatment related AEPatients with Grade 5 treatment related AE
Capecitabine92847334480
CDX-011211204754114324

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Pharmacokinetics (PK)

Concentration of the antibody drug conjugate (ADC), total antibody (TA) and free MMAE will be determined. (NCT01997333)
Timeframe: Following 1 dose of CDX-011.

Interventionug/ml (Mean)
Cycle 1 post infusion ADC levelsCycle 1 post infusion TA levelsCycle 1 post infusion MMAE levels
CDX-01158.649.40.0015

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Median Time to Progression

To assess median time to progression (TTP) associated with BKM120 plus capecitabine. (NCT02000882)
Timeframe: until disease progression (assessed by RECIST 1.1), unacceptable toxicity, death, or discontinuation from study for any other reason, up to 2 years from date of patient registration

Interventionmonths (Median)
BKM120 Plus Capecitabine5.59

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Objective Response Rate (ORR)

"To assess ORR (CR + PR) associated with BKM120 plus capecitabine in the central nervous system based on local investigator assessment. Complete Response (CR): Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~Partial Response (PR): At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters." (NCT02000882)
Timeframe: until disease progression (assessed by RECIST 1.1), unacceptable toxicity, death, or discontinuation from study for any other reason, up to 2 years from date of patient registration

Interventionproportion of patients with ORR (Number)
BKM120 Plus Capecitabine0.0

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Median Overall Survival

To determine median overall survival (OS) associated with BKM120 plus capecitabine. (NCT02000882)
Timeframe: up to 2 years from date of patient registration

Interventionmonths (Median)
BKM120 Plus Capecitabine11.135

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Clinical Benefit Rate (CBR)

"CBR in the patients following WBRT or SRS or both will be the primary endpoint and is calculated as the total number of responders (CR or PR, assessed by RECIST 1.1) plus stable disease greater than or equal to 24 weeks (CR + PR + SD ≥ 24 weeks) divided by the total number of evaluable patients.~Complete Response (CR): Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~Partial Response (PR): At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters." (NCT02000882)
Timeframe: until disease progression (assessed by RECIST 1.1), unacceptable toxicity, death, or discontinuation from study for any other reason, up to 2 years from date of patient registration

Interventionproportion of patients with CBR (Number)
BKM120 Plus Capecitabine0.1

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Percentage of Participants With pCR, Clinical Complete Response (CR), or Clinical Partial Response (PR)

Percentage of participants with pCR plus the percentage of participants without pCR who achieved CR or PR as measured by the Response Evaluation Criteria in Solid Tumors (RECIST) criteria. CR was defined as complete disappearance of all target lesions and non-target disease, with the exception of nodal disease. All nodes, both target and non-target, must have decreased to normal (short axis less than [<] 10 millimeters [mm]). No new lesions. PR was defined as greater than or equal to (≥) 30 percent (%) decrease under baseline of the sum of diameters of all target lesions. The short axis was used in the sum for target nodes, while the longest diameter was used in the sum for all other target lesions. No unequivocal progression of non-target disease. No new lesions. (NCT02005549)
Timeframe: Baseline, 20-24 weeks (final surgery, performed 2 to 4 weeks after the last chemotherapy cycle [Week 18])

Interventionpercentage of participants (Number)
Bevacizumab+Docetaxel+Capecitabine72.22

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Percentage of Participants With Pathological Complete Response (pCR)

pCR was defined as the absence of signs for invasive tumor in the final surgical sample as judged by the local pathologist. Surgery was performed 2 to 4 weeks after the last chemotherapy cycle. (NCT02005549)
Timeframe: Baseline, 20-24 weeks (final surgery, performed 2 to 4 weeks after the last chemotherapy cycle [Week 18])

Interventionpercentage of participants (Number)
Bevacizumab+Docetaxel+Capecitabine22.22

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Percentage of Participants Undergoing Breast-Conserving Surgery

Percentage of participants undergoing a breast-conserving procedure versus a modified radical mastectomy at final surgery, performed 2 to 4 weeks after the last chemotherapy cycle (Week 18) (NCT02005549)
Timeframe: 20-24 weeks (final surgery, performed 2 to 4 weeks after the last chemotherapy cycle [Week 18])

Interventionpercentage of participants (Number)
Bevacizumab+Docetaxel+Capecitabine83

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Pathological Complete Response (pCR) Rate

Primary Objective Phase II: Pathological response will be made based on microscopic assessment of the surgical specimen at the primary treatment site. A pCR must include no gross or microscopic tumor identified anywhere within the surgical specimen. This must include:No evidence of malignant cells in the primary tumor specimen and No lymph nodes that contain tumor. (NCT02010567)
Timeframe: 12 weeks

Interventionpercentage of participants with pCR (Number)
All Participants19

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Overall Survival (OS) Based on Pathological Complete Response (pCR).

Phase II only - a comparison of OS for patients who achieve pCR and those who do not. OS is defined as the time from surgical resection until death reported as the count of participants still alive at the end of study follow-up. (NCT02010567)
Timeframe: an average of 2.6 years (full range 2.1 to 3.1 years)

InterventionParticipants (Count of Participants)
pathological complete response (pCR)Did not achieve pCR
Cohort A, Phase II, Dose Level 2211

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Disease-free Survival (DFS) Rate Based on Pathological Complete Response (pCR).

Phase II only - a comparison of DFS for patients who achieve pCR and those who do not. DFS will be defined as the time from surgical resection until disease recurrence or death as a result of any cause, reported as the count of participants still alive without recurrence at the end of study follow-up. (NCT02010567)
Timeframe: an average of 2.6 years (full range 2.1 to 3.1 years)

InterventionParticipants (Count of Participants)
pathological complete response (pCR)Did not achieve pCR
Cohort A, Phase II, Dose Level 228

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Disease-free Survival (DFS) Rate

Phase II only - DFS will be defined as the time from surgical resection until disease recurrence or death as a result of any cause, reported as the count of participants still alive without recurrence at the end of study follow-up. (NCT02010567)
Timeframe: An average of 2.6 years (full range 2.1 to 3.1 years)

InterventionParticipants (Count of Participants)
Cohort A, Phase II, Dose Level 210

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Maximum Tolerated Dose (MTD) of CRLX101 When Added to Standard Neoadjuvant Chemoradiotherapy Consisting of Capecitabine + Radiotherapy in Locally Advanced Rectal Cancer

The MTD is the highest dose of CRLX101 at which ≤1 out of 6 patients had a dose limiting toxicity (DLT) using CTCAE v4.0 toxicity criteria. DLTs include Grade (G) >3 neutropenia for ≥7 days; G 3 or 4 neutropenia with fever; G 4 anemia not related to cancer-associated bleeding; G 4 thrombocytopenia or G 3 with clinically significant bleeding; G ≥3 nausea or vomiting >48 hours despite anti-emetics; G 2 cystitis not resolved within 14 days; second G 2 cystitis; G 3 or 4 cystitis; diarrhea requiring dose reduction; Any other non-hematologic toxicity G ≥3 requiring a dose reduction (G ≥3 infusion-related reactions were not a DLT unless they recur despite slowing down the infusion); Other CRLX101 related treatment emergent adverse effect (TEAE) that requires patient withdrawal prior to completing all doses; Radiotherapy interruption due to TEAEs ≥5 days; or Dose interruption or reduction of capecitabine due to TEAE that results in <50% of the scheduled capecitabine dose for entire course (NCT02010567)
Timeframe: 12 weeks

Interventionmg/m^2 every other week (Number)
Dose Escalation Phase Ib15

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Overall Survival (OS) Rate

Phase II only - OS is defined as the time from surgical resection until death reported as the count of participants still alive at the end of study follow-up. (NCT02010567)
Timeframe: an average of 2.6 years (full range 2.1 to 3.1 years)

InterventionParticipants (Count of Participants)
Cohort A, Phase II, Dose Level 213

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Overall Survival - Percentage of Participants Event Free at 12 Months

Overall Survival was defined as the time in months from randomization to date of death due to any cause. Participants without an event were censored the last time they were known to be alive. (NCT02013830)
Timeframe: Day 1, Weeks 1-18, Weeks 24 and 30, then every 3 months until death.

Interventionpercentage of participants (Number)
Bevacizumab/Capecitabine27

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Time to Disease Progression - Percentage of Participants With an Event

Time to progression was measured from time of treatment commencement to time of disease progression, or the date of death. Participants who were not progressed at the time of study completion (including participants who died before progressive disease) or who were lost to follow-up were censored at the date of last tumor assessment. (NCT02013830)
Timeframe: Screening; Weeks 6, 12, 18, 24, and 30; Every 3 months through follow-up

Interventionpercentage of participants (Number)
Bevacizumab/Capecitabine77.8

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Time to Disease Progression - Percentage of Participants Progression-free at 12 Months

Time to progression was measured from time of treatment commencement to time of disease progression, or the date of death. Participants who were not progressed at the time of study completion (including participants who died before progressive disease) or who were lost to follow-up were censored at the date of last tumor assessment. (NCT02013830)
Timeframe: Day 1, Weeks 1-18, Weeks 24 and 30, then every 3 months until death.

Interventionpercentage of participants (Number)
Bevacizumab/Capecitabine24.0

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Time to Disease Progression

Time to progression was measured from time of treatment commencement to time of disease progression, or the date of death. Participants who were not progressed at the time of study completion (including participants who died before progressive disease) or who were lost to follow-up were censored at the date of their tumor assessment. (NCT02013830)
Timeframe: Screening; Weeks 6, 12, 18, 24, and 30; Every 3 months through follow-up

Interventionmonths (Median)
Bevacizumab/Capecitabine2.8

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Percentage of Participants With Objective Response (OR)

Percentage of participants with OR based on assessment of confirmed complete response (CR) or confirmed partial response (PR) according to Response Evaluation Criteria in Solid Tumors (RECIST). Confirmed responses were those that persisted on repeat imaging study at least 4 weeks after initial documentation of response. The best overall response achieved within the time from first drug administration to progressive disease or end of study was reported. CR was defined as complete disappearance of all target lesions and non-target disease, with the normalization of tumor marker levels. No new lesions. PR was defined as greater than or equal to (≥) 30 percent (%) decrease under baseline of the sum of diameters of all target lesions. The short axis was used in the sum for target lesions. Persistence of one or more non-target lesion(s) or/and maintenance of tumor marker levels above the normal limits. No new lesions. (NCT02013830)
Timeframe: Screening; Weeks 6, 12, 18, 24, and 30; Every 3 months through follow-up

Interventionpercentage of participants (Number)
Bevacizumab/Capecitabine9.1

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Percentage of Participants With Disease Control

The percentage of participants with disease control was based on assessment of confirmed CR, PR, or stable disease (SD) according to RECIST criteria. Confirmed responses were those that persisted on repeat imaging study at least 4 weeks after initial documentation of response. The best overall response achieved within the time from first drug administration to progressive disease or end of study was reported. CR was defined as complete disappearance of all target lesions and non-target disease, with the normalization of tumor marker levels. No new lesions. PR was defined as ≥ 30 % decrease under baseline of the sum of diameters of all target lesions. The short axis was used in the sum for target lesions. Persistence of one or more non-target lesion(s) or/and maintenance of tumor marker levels above the normal limits. No new lesions. SD was defined as not qualifying for PR or progressive disease. (NCT02013830)
Timeframe: Screening; Weeks 6, 12, 18, 24, and 30; Every 3 months through follow-up

Interventionpercentage of participants (Number)
Bevacizumab/Capecitabine52.3

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Overall Survival - Percentage of Participants With an Event

Overall Survival was defined as the time in months from randomization to date of death due to any cause. Participants without an event were censored the last time they were known to be alive. (NCT02013830)
Timeframe: Day 1, Weeks 1-18, Weeks 24 and 30, then every 3 months until death.

Interventionpercentage of participants (Number)
Bevacizumab/Capecitabine77.8

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Overall Survival

Overall Survival was defined as the time in months from randomization to date of death due to any cause. Participants without an event were censored the last time they were known to be alive. Median Overall Survival was estimated using the Kaplan-Meier method. (NCT02013830)
Timeframe: Day 1, Weeks 1-18, Weeks 24 and 30, then every 3 months until death.

Interventionmonths (Median)
Bevacizumab/Capecitabine5.9

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Change in EORTC QLQ-C30 Global Health Status Score

"Patients were given the EORTC QLQ-C30 at baseline, preop, postop, and at follow ups Y1-5. The forms were scored as per the manual available at EORTC. Raw scores are transformed to fall in a range of 0-100. Generally, higher scores on QoL scales represent higher levels of QoL.~The scores are reported as the mean of the Global Health Status/QoL scale score when more than 1 patient completed the form for a time point. If only 1 form was available for a time point, then the score for that form is reported." (NCT02017704)
Timeframe: baseline, preop, postop, and at follow ups Y1-5

Interventionscore on a scale (Mean)
baselinepre-oppost-opyear 1year 2year 3year 4year 5
Endo-HDR71.249.672.57366.377.39191.5

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Number of Participants With Grade 3 or Higher Adverse Events

"Number of participants with grade 3 or higher adverse events will be listed by relationship.~Grading is by CTCAE 4 guidelines.~Relationship, as determined by PI, is unrelated/unlikely/possible/probable/definite." (NCT02017704)
Timeframe: Up to 60 months

,
InterventionParticipants (Count of Participants)
Grade: 3; Relationship: probableGrade: 3; Relationship: possibleGrade 3; Relationship: Unlikely
Endo-HDR110
IMRT and Capecitabine111

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Change in EORTC QLQ-C30 Global Health Status Score

"Patients were given the EORTC QLQ-C30 at baseline, preop, postop, and at follow ups Y1-5. The forms were scored as per the manual available at EORTC. Raw scores are transformed to fall in a range of 0-100. Generally, higher scores on QoL scales represent higher levels of QoL.~The scores are reported as the mean of the Global Health Status/QoL scale score when more than 1 patient completed the form for a time point. If only 1 form was available for a time point, then the score for that form is reported." (NCT02017704)
Timeframe: baseline, preop, postop, and at follow ups Y1-5

Interventionscore on a scale (Mean)
baselinepre-oppost-opyear 2year 3year 4
IMRT and Capecitabine8333545066.583

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Number of Patients With Pathologic Complete Response

"Pathologic complete response rate is reported as the number of patients who achieve pathologic complete response after the treatment for each arm.~As per the NCCN guidelines, pathologic response is graded by the system recommended by the AJCC Cancer Staging Manual and CAP guidelines:~Complete response - no remaining viable cancer cells~Moderate response - only small clusters/single cancer cells remain~Minimal response - residual cancer remaining, but with predominant fibrosis~Poor response - minimal/no tumor kills, extensive residual cancer" (NCT02017704)
Timeframe: Up to 60 months

InterventionParticipants (Count of Participants)
IMRT and Capecitabine0
Endo-HDR2

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Overall Survival of Patients With FOLFIRI/XELIRI-refractory Metastatic Colorectal Cancer

The effect of napabucasin given in combination with FOLFIRI on Overall Survival (OS) of patients with FOLFIRI/XELIRI-refractory metastatic colorectal cancer. (NCT02024607)
Timeframe: 4 weeks after the patient has been off study treatment, every 3 months thereafter until death, the study closes, up to 36 months.

Interventionmonths (Median)
Napabucasin Plus FOLFIRI8.97

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Number of Participants With Adverse Events and Serious Adverse Events

Assessment of safety of napabucasin administered in combination with either FOLFOX6 with and without bevacizumab, or CAPOX, or FOLFIRI with and without bevacizumab, or regorafenib, or irinotecan in participants with advanced gastrointestinal malignancies by reporting of adverse events and serious adverse events (NCT02024607)
Timeframe: The time from the date of first treatment, while the patient is taking napabucasin, and for 30 days after stopping therapy, an average of 4 months.

InterventionParticipants (Count of Participants)
Napabucasin Plus FOLFOX6115
Napabucasin Plus FOLFOX6 Plus Bevacizumab41
Napabucasin Plus CAPOX87
Napabucasin Plus FOLFIRI156
Napabucasin Plus FOLFIRI Plus Bevacizumab40
Napabucasin Plus Regorafenib54
Napabucasin Plus Irinotecan2

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Disease Control Rate of Patients With FOLFIRI/XELIRI-refractory Metastatic Colorectal Cancer

To determine the disease control rate of napabucasin administered in combination with FOLFIRI in patients with FOLFIRI/XELIRI-refractory metastatic colorectal cancer. Percentage of participants with a documented complete response, partial response and stable disease based on RECIST 1.1. (NCT02024607)
Timeframe: From the date of first treatment, every 8 weeks, until the date of first documented objective disease progression, up to 24 months

Interventionpercentage of participants (Number)
Napabucasin Plus FOLFIRI56.9

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Disease Control Rate

To determine the anti-tumor activity (specifically the disease control rate) of napabucasin administered in combination with either FOLFOX6 with and without bevacizumab, or CAPOX, or FOLFIRI with and without bevacizumab, or regorafenib, or irinotecan. Percentage of participants with a documented complete response, partial response and stable disease based on RECIST 1.1. (NCT02024607)
Timeframe: From the date of first treatment, every 8 weeks, until the date of first documented objective disease progression, up to 24 months.

Interventionpercentage of participants (Number)
Napabucasin Plus FOLFOX654.7
Napabucasin Plus FOLFOX6 Plus Bevacizumab76.2
Napabucasin Plus CAPOX55.3
Napabucasin Plus FOLFIRI65.7
Napabucasin Plus FOLFIRI Plus Bevacizumab87.0
Napabucasin Plus Regorafenib34.4
Napabucasin Plus Irinotecan100

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The Objective Response Rate of Napabucasin Administered in Combination in FOLFIRI in Patients With FOLFIRI/XELIRI-refractory Metastatic Colorectal Cancer

Assessment of the objective response rate (ORR) of napabucasin administered in combination with FOLFIRI in patients with FOLFIRI/XELIRI-refractory metastatic colorectal cancer. The Objective Response Rate (ORR) is the proportion of participants with a complete response or partial response who have measurable disease at baseline imaging. (NCT02024607)
Timeframe: From the date of first treatment, every 8 weeks, until the date of first documented objective disease progression, up to 24 months

Interventionpercentage of participants (Number)
Napabucasin Plus FOLFIRI0

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Progression Free Survival of Patients With FOLFIRI/XELIRI-refractory Metastatic Colorectal Cancer

The effect of napabucasin given in combination with FOLFIRI on Progression Free Survival (PFS) of patients with FOLFIRI/XELIRI-refractory metastatic colorectal cancer. PFS of patients with FOLFIRI/XELIRI-refractory metastatic colorectal cancer. (NCT02024607)
Timeframe: The time from the date of first treatment to the date of first documentation of disease progression or death due to any cause, up to thirty six months

Interventionmonths (Number)
Napabucasin Plus FOLFIRI20.82

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Objective Response Rate

Confirmed response (CR) is two or more objective statuses of CR a minimum of four weeks apart documented before progression or symptomatic deterioration. Partial response (PR) is two or more objective statuses of PR or better a minimum of four weeks apart documented before progression or symptomatic deterioration. Unconfirmed CR is one objective status of CR documented before progression or symptomatic deterioration but not qualifying as CR or PR. Unconfirmed PR is one objective status of PR documented before progression or symptomatic deterioration but not qualifying as CR, PR or unconfirmed CR. (NCT02042443)
Timeframe: Up to 2 years from registration

,
InterventionParticipants (Count of Participants)
Partial ResponseUnconfirmed Partial ResponseStable/No ResponseIncreasing DiseaseSymptomatic Deterioration
Chemotherapy20981
Trametinib022191

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Progression-free Survival

From date of registration to date of first documentation of progression or symptomatic deterioration, or death due to any cause. Patients last known to be alive and progression free are censored at date of last contact. (NCT02042443)
Timeframe: Up to 2 years from registration

Interventionmonths (Median)
Trametinib1.3
Chemotherapy2.8

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Overall Survival

From date of registration to date of death due to any cause. Patients last known to be alive are censored at date of last contact. (NCT02042443)
Timeframe: Up to 2 years from registration

Interventionmonths (Median)
Trametinib4.3
Chemotherapy7.9

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Overall Survival (OS) Time for Patients in Europe + United States With Triple-Negative mCRC (EU+US TNmCRC)

"OS based on product-limit (Kaplan-Meier) estimates. Confidence intervals for the median are calculated according to Brookmeyer and Crowley.~This outcome measure is considered exploratory. Because of the unanticipated long OS in the control group, initial exploratory subgroup analyses identified that findings in patients enrolled in Russia differed when compared with patients enrolled in the ITT subpopulation and the EU+US subpopulation. For this reason, subjects in Russia were excluded from further exploratory subset analyses that evaluated the effects of genomic parameters known to impact patient responses to anti-EGFR monoclonal antibodies. Removal of the outlier Russian subpopulation of patients provided a patient population that was more homogeneous with respect to their prior treatment regimens, thereby facilitating further exploratory analyses. If a subject had not died, survival time was censored at the last date the subject was known to be alive." (NCT02083653)
Timeframe: From randomization until the date of death (assessed up to 32 months).

Interventionmonths (Median)
Arm A: Sym004 (12 mg/kg)10.6
Arm B: Sym004 (9/6 mg/kg)12.8
Arm C: Investigator's Choice7.3

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Occurrence and Nature of Adverse Events (AEs), as Assessed by the Common Terminology Criteria for AEs (Version 4.03) (CTCAE v4.03).

AEs were coded according to the Medical Dictionary for Regulatory Activities (MedDRA) classification. The incidence and type of AEs (i.e., serious AE [SAE], treatment-emergent AE [TEAE]) were summarized by dose cohort according to MedDRA system organ classes and preferred terms. An AE was considered as treatment-emergent if it occurred during or after the first IMP administration. An AE that occurred before the first IMP administration and worsened thereafter was also considered an AE. Worsening was reported as a new AE. (NCT02083653)
Timeframe: From Baseline up to 28 days after the last IMP administration.

,,
InterventionParticipants (Count of Participants)
At least one TEAEAt least one Serious TEAETEAE leading to dose reductionTEAE leading to interruption of trial treatmentTEAE leading to trial treatment withdrawalTEAE related to trial treatmentTEAE, Grade >=3Dermatologic toxicityInfusion-related reactionTEAE resulting in deathRelated Serious TEAERelated TEAE leading to dose reductionRelated TEAE leading to interruption of treatmentRelated TEAE leading to treatment withdrawalRelated TEAE, Grade >=3Related TEAE resulting in death
Arm A: Sym004 (12 mg/kg)8327295812816778274929539580
Arm B: Sym004 (9/6 mg/kg)842317475805378264617422410
Arm C: Investigator's Choice671281064625803267390

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Pharmacokinetic (PK) Parameters: Sym004 Concentrations

"The Sym004 serum concentration used for the PK evaluation was calculated as the sum of the serum concentrations of the 2 component monoclonal antibodies of Sym004 (futuximab and modotuximab).~Trough Concentration (Ctrough) is equivalent to the concentration collected at the pre-dose timepoint.~Maximum Concentration (Cmax) is equivalent to the concentration collected at the end of infusion (EOI) timepoint." (NCT02083653)
Timeframe: Weeks 3, 5, and 7 and at the End of Treatment visit, including a Week 1 and Week 2 subset.

,
Interventionug/mL (Mean)
Screening (Pre-dose)Week 1 Day 1 (Pre-dose)Week 1 Day 1 (EOI)Week 1 Day 1 (0.5 hours after EOI)Week 1 Day 1 (1 hour after EOI)Week 1 Day 1 (2 hours after EOI)Week 1 Day 1 (4 hours after EOI)Week 2 Day 1 (Pre-dose)Week 2 Day 1 (EOI)Week 3 Day 1 (Pre-dose)Week 3 Day 1 (EOI)Week 5 Day 1 (Pre-dose)Week 5 Day 1 (EOI)Week 7 Day 1 (Pre-dose)Week 7 Day 1 (EOI)End of Treatment
Arm A: Sym004 (12 mg/kg)0.500.50182.95214.98209.80197.31188.7545.37275.4292.66323.35125.73354.91128.30346.8364.55
Arm B: Sym004 (9/6 mg/kg)0.500.75174.44184.84189.24181.68171.6338.76145.9144.26170.1849.26168.9458.38163.1117.61

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Pharmacokinetic (PK) Parameters: Time of Maximum Plasma Concentration (Tmax)

Tmax was defined as the time the PK sample was taken at end of infusion (EOI) relative to the start time of infusion (i.e., time between the start of infusion and the time of the EOI sample). For presentation of individual PK parameters and calculation of mean parameters, half of the lower limit of quantitation (LLOQ) value was used for concentration values below the LLOQ. The Sym004 serum concentration used for the PK evaluation was calculated as the sum of the serum concentrations of the 2 component monoclonal antibodies of Sym004, futuximab and modotuximab. (NCT02083653)
Timeframe: Day 1 on Weeks 1-3 followed by Week 5 Day 1 and Week 7 Day 1.

,
Interventionhours (Mean)
Week 1 Day 1Week 2 Day 1Week 3 Day 1Week 5 Day 1Week 7 Day 1
Arm A: Sym004 (12 mg/kg)3.142.823.012.742.83
Arm B: Sym004 (9/6 mg/kg)2.792.332.342.062.06

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Quality of Life Assessed by FACT-EGFRI-18 for Skin Rash

"Scale: Functional Assessment of Cancer Therapy-Epidermal Growth Factor Receptor Inhibitor 18 (FACT-EGFRI-18).~The FACT-EGFRI-18 is an 18-question scale used to assess EGFR-inhibitor-treated cancer patients' quality of life relative to their experience of skin rash based on three (3) multi-item subscales. The subscales combined (i.e., Symptom Index) range in score from 0 to 72. A higher score represents a high level of symptomatology (problems).~High scores for all subscales represent a worse outcome:~The Physical subscale ranges in score from 0 to 28.~The Social/Emotional subscale ranges in score from 0 to 24.~The Functional subscale ranges in score from 0 to 20." (NCT02083653)
Timeframe: Assessed every 3 weeks (week 1 and week 4 reported)

,,
Interventionscore on a scale (Mean)
Physical (Week 1 Day 1)Physical (Week 4 Day 1)Social/Emotional (Week 1 Day 1)Social/Emotional (Week 4 Day 1)Functional (Week 1 Day 1)Functional (Week 4 Day 1)Symptom Index (Week 1 Day 1)Symptom Index (Week 4 Day 1)
Arm A: Sym004 (12 mg/kg)22.918.021.519.917.916.362.354.2
Arm B: Sym004 (9/6 mg/kg)23.119.721.520.318.317.062.957.0
Arm C: Investigator's Choice24.325.122.623.218.719.365.667.6

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Quality of Life Assessed by the EORTC QLQ-C30 (Version 3)

"Scale: European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (Version 3) [QLQ-C30, Version 3].~The QLQ-C30 is a 30-question scale used to assess cancer patients' quality of life based on 15 factors (e.g., global health status, physical functioning, role functioning, etc.). The scale is composed of both multi-item scales and single-item measures. All of the scales and single-item measures range in score from 0 to 100:~A high score for a functional scale represents a healthy level of functioning.~A high score for the global health status represents a high quality of life.~A high score for a symptom scale/item represents a high level of symptomatology (problems)." (NCT02083653)
Timeframe: Assessed every 6 weeks (week 1 and week 7 reported)

,,
Interventionscore on a scale (Mean)
Global Health Status (Week 1 Day 1)Global Health Status (Week 7 Day 1)Physical Functioning (Week 1 Day 1)Physical Functioning (Week 7 Day 1)Role Functioning (Week 1 Day 1)Role Functioning (Week 7 Day 1)Emotional Functioning (Week 1 Day 1)Emotional Functioning (Week 7 Day 1)Cognitive Functioning (Week 1 Day 1)Cognitive Functioning (Week 7 Day 1)Social Functioning (Week 1 Day 1)Social Functioning (Week 7 Day 1)Fatigue Symptoms (Week 1 Day 1)Fatigue Symptoms (Week 7 Day 1)Nausea & Vomiting Symptoms (Week 1 Day 1)Nausea & Vomiting Symptoms (Week 7 Day 1)Pain Symptoms (Week 1 Day 1)Pain Symptoms (Week 7 Day 1)Dyspnoea Symptoms (Week 1 Day 1)Dyspnoea Symptoms (Week 7 Day 1)Insomnia Symptoms (Week 1 Day 1)Insomnia Symptoms (Week 7 Day 1)Appetite Loss Symptoms (Week 1 Day 1)Appetite Loss Symptoms (Week 7 Day 1)Constipation Symptoms (Week 1 Day 1)Constipation Symptoms (Week 7 Day 1)Diarrhoea Symptoms (Week 1 Day 1)Diarrhoea Symptoms (Week 7 Day 1)Financial Difficulties (Week 1 Day 1)Financial Difficulties (Week 7 Day 1)
Arm A: Sym004 (12 mg/kg)55.557.476.482.175.081.176.674.887.488.178.277.935.326.37.95.627.212.715.910.429.327.422.316.915.011.512.58.819.719.4
Arm B: Sym004 (9/6 mg/kg)59.759.478.783.076.482.477.882.786.288.580.283.432.225.36.45.123.614.617.28.819.116.917.617.516.08.38.511.116.615.2
Arm C: Investigator's Choice55.859.777.776.772.572.873.275.387.587.075.472.734.733.27.88.427.824.116.415.721.716.622.223.011.411.115.911.023.319.3

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Quality of Life Assessed by EORTC QLQ-CR29

"Scale: European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire - Colorectal Cancer Module (QLQ-CR29).~The QLQ-CR29 is a 29-question scale used to assess colorectal cancer patients' quality of life based on 22 factors (e.g., body image, anxiety, weight, etc.). The scale is composed of both multi-item scales and single-item measures. All of the scales and single-item measures range in score from 0 to 100:~A high score for a functional scale/item represents an unhealthy level of functioning, with the exception of one (1) scale pertaining to sexual interest (separated by sex).~A high score for a symptom scale/item represents a high level of symptomatology (problems)." (NCT02083653)
Timeframe: Assessed every 6 weeks (week 1 and week 7 reported)

,,
Interventionscore on a scale (Mean)
Body Image (Week 1 Day 1)Body Image (Week 7 Day 1)Anxiety (Week 1 Day 1)Anxiety (Week 7 Day 1)Weight (Week 1 Day 1)Weight (Week 7 Day 1)Sexual Function (Men) (Week 1 Day 1)Sexual Function (Men) (Week 7 Day 1)Sexual Function (Women) (Week 1 Day 1)Sexual Function (Women) (Week 7 Day 1)Urinary Frequency (Week 1 Day 1)Urinary Frequency (Week 7 Day 1)Blood and Mucus (Week 1 Day 1)Blood and Mucus (Week 7 Day 1)Stool Frequency (Week 1 Day 1)Stool Frequency (Week 7 Day 1)Urinary Incontinence (Week 1 Day 1)Urinary Incontinence (Week 7 Day 1)Dysuria (Week 1 Day 1)Dysuria (Week 7 Day 1)Abdominal Pain (Week 1 Day 1)Abdominal Pain (Week 7 Day 1)Buttock Pain (Week 1 Day 1)Buttock Pain (Week 7 Day 1)Bloated Feeling (Week 1 Day 1)Bloated Feeling (Week 7 Day 1)Dry Mouth (Weel 1 Day 1)Dry Mouth (Weel 7 Day 1)Hair Loss (Week 1 Day 1)Hair Loss (Week 7 Day 1)Trouble with Taste (Week 1 Day 1)Trouble with Taste (Week 7 Day 1)Flatulence (Week 1 Day 1)Flatulence (Week 7 Day 1)Faecal Incontinence (Week 1 Day 1)Faecal Incontinence (Week 7 Day 1)Sore Skin (Week 1 Day 1)Sore Skin (Week 7 Day 1)Embarrassed by Bowel Movement (Week 1 Day 1)Embarrassed by Bowel Movement (Week 7 Day 1)Stoma Care Problem (Week 1 Day 1)Stoma Care Problem (Week 7 Day 1)Impotence (Week 1 Day 1)Impotence (Week 7 Day 1)Dyspareunia (Week 1 Day 1)Dyspareunia (Week 7 Day 1)
Arm A: Sym004 (12 mg/kg)76.276.450.057.179.586.631.733.216.516.634.428.24.12.615.513.48.27.04.03.218.810.411.64.420.413.325.126.817.17.020.018.518.312.48.92.59.611.68.57.516.69.946.940.412.114.3
Arm B: Sym004 (9/6 mg/kg)80.177.648.261.185.689.621.226.612.313.630.328.81.53.111.311.87.54.82.92.112.810.810.88.814.812.117.029.211.17.613.915.219.516.18.87.38.89.77.88.13.32.438.742.77.210.3
Arm C: Investigator's Choice75.878.243.050.978.388.023.534.910.111.032.618.52.02.314.113.17.41.93.00.923.016.69.97.421.712.922.113.814.64.615.112.923.112.47.13.16.04.213.910.46.68.349.550.711.013.3

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Host Immune Response: Number of Subjects With Anti-drug Antibodies (ADAs) to Sym004 Over Time

A validated double antigen bridging ELISA was used for screening, confirmation, and titration of patient samples for anti-Sym004 ADA. Using rabbit anti-Sym004 as an ADA control antibody, the lower limit of detection was 54 ng/mL in the absence of Sym004 and 500 ng/mL in the presence of Sym004 at 5 µg/mL The timepoints for ADA sampling were chosen by the original sponsor for this trial. After the trial was transferred to Symphogen A/S, it was determined that not all samples were necessary for analysis. This is why the collection time points specified in the Outcome Measure Time Frame do not match with the Outcome Measure Data Table. (NCT02083653)
Timeframe: Every two weeks (Days 15, 29, and 43) followed by every six weeks thereafter (Days 78, 120, 162, etc.) until the End of Treatment Visit

InterventionParticipants (Count of Participants)
Screening71950433Screening71950434Week 5 Day 171950434Week 5 Day 171950433Week 1271950433Week 1271950434Week 1371950433Week 1371950434Week 2471950433Week 2471950434End of Treatment Visit71950434End of Treatment Visit71950433
MissingNegativePositiveNot Reportable
Arm A: Sym004 (12 mg/kg)78
Arm B: Sym004 (9/6 mg/kg)81
Arm A: Sym004 (12 mg/kg)2
Arm B: Sym004 (9/6 mg/kg)3
Arm B: Sym004 (9/6 mg/kg)62
Arm A: Sym004 (12 mg/kg)24
Arm B: Sym004 (9/6 mg/kg)22
Arm B: Sym004 (9/6 mg/kg)35
Arm A: Sym004 (12 mg/kg)59
Arm B: Sym004 (9/6 mg/kg)49
Arm A: Sym004 (12 mg/kg)1
Arm B: Sym004 (9/6 mg/kg)1
Arm A: Sym004 (12 mg/kg)0
Arm A: Sym004 (12 mg/kg)82
Arm B: Sym004 (9/6 mg/kg)83
Arm A: Sym004 (12 mg/kg)83
Arm A: Sym004 (12 mg/kg)60
Arm B: Sym004 (9/6 mg/kg)55
Arm B: Sym004 (9/6 mg/kg)0
Arm A: Sym004 (12 mg/kg)23
Arm B: Sym004 (9/6 mg/kg)29

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Overall Survival (OS) Time

"OS based on product-limit (Kaplan-Meier) estimates. Confidence intervals for the median are calculated according to Brookmeyer and Crowley.~If a subject had not died, survival time was censored at the last date the subject was known to be alive." (NCT02083653)
Timeframe: From randomization until the date of death (assessed up to 32 months).

Interventionmonths (Median)
Arm A: Sym004 (12 mg/kg)7.9
Arm B: Sym004 (9/6 mg/kg)10.3
Arm C: Investigator's Choice9.6

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Overall Survival (OS) Time for Patients in Europe + United States With Double-Negative mCRC (EU+US DNmCRC)

"OS based on product-limit (Kaplan-Meier) estimates. Confidence intervals for the median are calculated according to Brookmeyer and Crowley.~This outcome measure is considered exploratory. Because of the unanticipated long OS in the control group, initial exploratory subgroup analyses identified that findings in patients enrolled in Russia differed when compared with patients enrolled in the ITT subpopulation and the EU+US subpopulation. For this reason, subjects in Russia were excluded from further exploratory subset analyses that evaluated the effects of genomic parameters known to impact patient responses to anti-EGFR monoclonal antibodies. Removal of the outlier Russian subpopulation of patients provided a patient population that was more homogeneous with respect to their prior treatment regimens, thereby facilitating further exploratory analyses. If a subject had not died, survival time was censored at the last date the subject was known to be alive." (NCT02083653)
Timeframe: From randomization until the date of death (assessed up to 32 months).

Interventionmonths (Median)
Arm A: Sym004 (12 mg/kg)8.9
Arm B: Sym004 (9/6 mg/kg)11.9
Arm C: Investigator's Choice8.4

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Progression Free Survival (PFS) Time

PFS based on product-limit (Kaplan-Meier) estimates. Confidence intervals for the median are calculated according to Brookmeyer and Crowley. Death will only be considered as an event if it occurs within 12 weeks after last tumor response assessment without progression. (NCT02083653)
Timeframe: From randomization until first event, where an event can be a progression (radiological confirmed or clinical progression) or death due to any cause (assessed up to 32 months).

Interventionmonths (Median)
Arm A: Sym004 (12 mg/kg)2.8
Arm B: Sym004 (9/6 mg/kg)2.7
Arm C: Investigator's Choice2.6

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Relative Dose Intensity of Sym004

"Treatment duration (weeks) is calculated as [(last dose date of Sym004 - first dose date of Sym004)+7] / 7 days.~Sym004 dose received (mg/kg) is calculated as (total dose administered (mg)/weight (kg)).~Dose Intensity is calculated as (cumulative Sym004 dose (mg/kg) / treatment duration (weeks)).~Relative Dose Intensity is calculated as (dose intensity / planned dose intensity at randomization)*100.~Percentages are based on the number of subjects in the safety analysis set." (NCT02083653)
Timeframe: From first dose of study drug until disease progression (assessed up to 32 months).

Interventionpercentage of relative dose intensity (Mean)
Arm A: Sym004 (12 mg/kg)80.49
Arm B: Sym004 (9/6 mg/kg)88.91

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Time to Treatment Failure (TTF)

TTF based on product-limit (Kaplan-Meier) estimates. Confidence intervals for the median are calculated according to Brookmeyer and Crowley. (NCT02083653)
Timeframe: From randomization until treatment discontinuation for any reason, including disease progression or death (assessed up to 32 months).

Interventionmonths (Median)
Arm A: Sym004 (12 mg/kg)2.1
Arm B: Sym004 (9/6 mg/kg)2.6
Arm C: Investigator's Choice1.6

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Progression-free Survival (PFS)

Progressive Disease (PD) is defined using Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions, unequivocal progression of non-target lesions, or the appearance of new lesions. (NCT02117479)
Timeframe: Randomization to disease progression, or death due to any cause if sooner; up to 6-months or to the data cutoff 11FEB2016.

Interventiondays (Median)
Ruxolitinib Plus Capecitabine43.0
Placebo Plus Capecitabine44.0

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Objective Response Rate (ORR)

Objective response rate determined by radiographic disease assessments per RECIST (v1.1), by investigator assessment and was defined as the percentage of participants with Complete Response (CR) or Partial Response (PR) by Response Evaluation Criteria in Solid Tumours (RECIST) at any post baseline visit. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) for target lesions and assessed by computed tomography (CT) and/or magnetic resonance imaging (MRI) : Complete Response (CR), Disappearance of all target and non-target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions with no worsening of non-target lesions and no new lesions; Overall Response (OR) = CR + PR. (NCT02117479)
Timeframe: Baseline through end of study; up to 6-months or to the data cutoff 11FEB2016.

,
Interventionpercentage of participants (Number)
Objective responseComplete responsePartial response
Placebo Plus Capecitabine1.901.9
Ruxolitinib Plus Capecitabine3.703.7

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Overall Survival (OS)

Overall survival is reported here based on the number of deaths from randomization up to 6-months or to the data cutoff 11FEB2016. (NCT02117479)
Timeframe: Randomization until death due to any cause; up to the data cutoff 11FEB2016.

,
InterventionParticipants (Count of Participants)
ObservedCensored
Placebo Plus Capecitabine12436
Ruxolitinib Plus Capecitabine11348

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Percentage of Participants Achieving Progression Free Survival (PFS)

PFS is defined as the time from randomization until the earliest date of disease progression determined by investigator assessment of objective radiographic disease assessments per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1, or death due to any cause if sooner. Progressive Disease (PD) is defined using Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions, unequivocal progression of non-target lesions, or the appearance of new lesions. (NCT02117479)
Timeframe: Randomization to disease progression, or death due to any cause if sooner; up to 6-months or to the data cutoff 11FEB2016.

,
Interventionpercentage of participants (Median)
Survival rate at 3 monthsSurvival rate at 6 monthsSurvival rate at 9 monthsSurvival rate at 12 months
Placebo Plus Capecitabine19.85.73.4NA
Ruxolitinib Plus Capecitabine18.96.12.52.5

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Participants With Treatment-Emergent Adverse Events (TEAEs)

A treatment-emergent AE was defined as an event occurring after exposure to at least 1 dose of study drug (ruxolitinib or placebo). A treatment-related AE was defined as an event with a definite, probable, or possible causality to study medication. A serious AE is an event resulting in death, hospitalization, persistent or significant disability/incapacity, or is life threatening, a congenital anomaly/birth defect or requires medical or surgical intervention to prevent 1 of the outcomes above. The intensity of an AE was graded according to the National Cancer Institute common terminology criteria for adverse events (NCI-CTCAE) version 4.03: Grade 1 (Mild); Grade 2 (Moderate); Grade 3 (Severe); Grade 4 (life-threatening). (NCT02117479)
Timeframe: Baseline through approximately 30 days post treatment discontinuation; up to 6-months or to the data cutoff 11FEB2016.

,
InterventionParticipants (Count of Participants)
Participants who had any TEAEsParticipants who had treatment-related TEAEsParticipants who had SAEsParticipants who had Grade 3 or higher TEAEsParticipants hospitalized because of a TEAEParticipants discontinued treatment due to TEAEParticipants with a dose modification due to TEAEParticipants on concomitant medication due to TEAEParticipants with procedure performed due to TEAEParticipants who had a fatal TEAE
Placebo Plus Capecitabine15259831137522481224615
Ruxolitinib Plus Capecitabine15273941128912681316020

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Duration of Response

Duration of overall response was defined as the time in months from Complete Response (CR) or Partial Response (PR) by Response Evaluation Criteria in Solid Tumours (RECIST v1.1) until the first date Progressive Disease (PD) was objectively documented or until the date of death. (NCT02117479)
Timeframe: Baseline through end of study; up to 6-months or to the data cutoff 11FEB2016.

Interventiondays (Median)
Ruxolitinib Plus CapecitabineNA
Placebo Plus CapecitabineNA

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Tumour Assessments (Based on RECIST Criteria) in 2nd-line

Best response in second line was based on the tumor assessments (based on RECIST criteria) for target lesions and assessed by CT scans, MRI scans, X-ray, bone scan and clinical examination: Complete Response (CR), disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter (sum LD) of target lesions; Progressive Disease (PD), >= 20% increase in the sum of the LD of target lesions; Stable Disease (SD), neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT02119026)
Timeframe: Baseline, every 8-9 weeks, 28d Safety follow-up

,
Interventionparticipants (Number)
Progressive Disease (PD)Stable Disease (SD)Partial Response (PR)Complete Response (CR)Not available (NA)
A: XELIRI + BEV Followed by XELOX + BEV711608
B: XELOX + BEV Followed by XELIRI + BEV813201

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Tumour Assessments (Based on RECIST Criteria) in 1st-line

Best response in first line was based on the tumor assessments (based on RECIST criteria) for target lesions and assessed by CT scans, MRI scans, X-ray, bone scan and clinical examination: Complete Response (CR), disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter (sum LD) of target lesions; Progressive Disease (PD), >= 20% increase in the sum of the LD of target lesions; Stable Disease (SD), neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT02119026)
Timeframe: Baseline, every 8-9 weeks, 28d Safety follow-up

,
Interventionparticipants (Number)
Progressive Disease (PD)Stable Disease (SD)Partial Response (PR)Complete Response (CR)
A: XELIRI + BEV Followed by XELOX + BEV421262
B: XELOX + BEV Followed by XELIRI + BEV123300

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Time to Response

Time to overall response was measured from the time of randomization until the day of documented complete response (CR) or partial response (PR) (whichever status is recorded first). Patients without response were censored at the date of the last tumor assessment, the date of death or the date of refusal. (NCT02119026)
Timeframe: at the day of documented complete or partial response or at 28 days safety follow-up in cases without PD

Interventiondays (Median)
A: XELIRI + BEV Followed by XELOX + BEV185.0
B: XELOX + BEV Followed by XELIRI + BEV178.0

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Second Line PFS

"The second line PFS was defined as the progression free survival interval during second line treatment. Patients without progression at the last tumor assessment date during their study participation were censored at this last tumor assessment date (exception: availability of validated information about a later onset of progression or a longer progression free interval - in such a case the date of the follow-up assessment was either defined as the onset of progression or replaced the last tumor assessment date). Missing onset of progression data because of refusal or because of death was replaced.~If several response evaluations for a patient showed progressive disease (PD), the time to PD was assessed by using the first of these measurements." (NCT02119026)
Timeframe: at progression of disease (PD) in second line therapy or at 28 days safety follow-up in cases without PD

Interventiondays (Median)
A: XELIRI + BEV Followed by XELOX + BEV129
B: XELOX + BEV Followed by XELIRI + BEV155

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Overall Survival of XELIRI Plus Bevacizumab and XELOX Plus Bevacizumab

Overall survival was measured as the time from the randomization date to the date of death. Patients without death date were censored at the date of the last tumor assessment (exception: availability of validated information about a later exitus date or a prolonged survival - in such a case the date of the follow-up assessment was either defined as the exitus date or replaced the last tumor assessment date) or the date of refusal. (NCT02119026)
Timeframe: date of death or date of last tumor assessment (28d safety f-u) in patients without death

Interventiondays (Median)
A: XELIRI + BEV Followed by XELOX + BEV593.0
B: XELOX + BEV Followed by XELIRI + BEV643

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Overall Response Rate (Number of Participants With Response)

The rate of overall response was measured as the response rate from randomization until the day of documented complete response (CR) or partial response (PR) (whichever status is recorded first). (NCT02119026)
Timeframe: at the day of documented complete or partial response or at 28 days safety follow-up in cases without PD

InterventionParticipants (Count of Participants)
A: XELIRI + BEV Followed by XELOX + BEV32
B: XELOX + BEV Followed by XELIRI + BEV36

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First Line Progression Free Survival (PFS)

The first line PFS was defined as the progression free survival interval during first line treatment. Patients without progression at the last tumor assessment date during their study participation were censored at this last tumor assessment date (exception: availability of validated information about a later onset of progression or a longer progression free interval - in such a case the date of the follow-up assessment was either defined as the onset of progression or replaced the last tumor assessment date). Missing onset of progression data because of refusal or because of death was replaced. If several response evaluations for a patient showed progressive disease (PD), the time to PD was assessed by using the first of these measurements. (NCT02119026)
Timeframe: at progression of disease (PD) in first line therapy or at 28 days safety follow-up in cases without PD

Interventiondays (Median)
A: XELIRI + BEV Followed by XELOX + BEV241
B: XELOX + BEV Followed by XELIRI + BEV280

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Efficacy Duration of Disease Control by Tumor Assessment (CT/MRI/Clinical Examination)

The primary variable was duration of disease control (DDC) and was defined as the sum of progression free survival intervals during first line and second line treatment (= time from the beginning of first line treatment until onset of progression during second line treatment). Patients without progression at the last tumor assessment date during their study participation were censored at this last tumor assessment date (exception: availability of validated information about a later onset of progression or a longer progression free interval - in such a case the date of the follow-up assessment was either defined as the onset of progression or replaced the last tumor assessment date). (NCT02119026)
Timeframe: screening, every 8 to 9 weeks until progression, at end of treatment (other than progression), every 3 months until progression, death or up to 24 months (whatever comes first)

Interventiondays (Median)
A: XELIRI + BEV Followed by XELOX + BEV373.00
B: XELOX + BEV Followed by XELIRI + BEV370.00

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Duration of Response

"Duration of overall response was measured from the time that measurement criteria are met for complete response (CR) or partial response (PR) (whichever status was recorded first) until the onset of progression. Patients without progression at the last tumor assessment date during their study participation were censored at this last tumor assessment date (exception: availability of validated information about a later onset of progression or a longer progression free interval - in such a case the date of the follow-up assessment was either defined as the onset of progression or replaced the last tumor assessment date).~Missing onset of progression data because of refusal or because of death was replaced.~If several response evaluations for a patient showed progressive disease (PD), the time to PD was assessed by using the first of these measurements." (NCT02119026)
Timeframe: at the day of documented complete or partial response or at 28 days safety follow-up in cases without PD

Interventiondays (Median)
A: XELIRI + BEV Followed by XELOX + BEV244.0
B: XELOX + BEV Followed by XELIRI + BEV315

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Objective Response Rate (ORR)

Objective response rate determined by radiographic disease assessments per Response Evaluation Criteria in Solid Tumours RECIST (v1.1), by investigator assessment and was defined as the percentage of participants with Complete Response (CR) or Partial Response (PR) by RECIST at any post baseline visit. Per RECIST for target lesions and assessed by computed tomography (CT) and/or magnetic resonance imaging (MRI): Complete Response (CR), Disappearance of all target and non-target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions with no worsening of non-target lesions and no new lesions; Overall Response (OR) = CR + PR. (NCT02119663)
Timeframe: Baseline through end of study; up to 6-months or to the data cutoff 11FEB2016.

,
Interventionpercentage of participants (Number)
Objective responseComplete responsePartial response
Placebo Plus Capecitabine2.30.02.3
Ruxolitinib Plus Capecitabine4.72.32.3

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Progression Free Survival (PFS)

PFS is defined as the time from randomization until the earliest date of disease progression determined by investigator assessment of objective radiographic disease assessments per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1, or death due to any cause if sooner. Progressive Disease (PD) is defined using Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions, unequivocal progression of non-target lesions, or the appearance of new lesions. (NCT02119663)
Timeframe: Randomization to disease progression, or death due to any cause if sooner; up to 6-months or to the data cutoff 11FEB2016.

Interventiondays (Median)
Ruxolitinib Plus Capecitabine48.0
Placebo Plus Capecitabine61.0

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Duration of Response

Duration of overall response was defined as the time in months from Complete Response (CR) or Partial Response (PR) by Response Evaluation Criteria in Solid Tumours (RECIST v1.1) until the first date Progressive Disease (PD) was objectively documented or until the date of death. Per RECIST for target lesions and assessed by computed tomography (CT) and/or magnetic resonance imaging (MRI): Complete Response (CR), Disappearance of all target and non-target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions with no worsening of non-target lesions and no new lesions; Overall Response (OR) = CR + PR. (NCT02119663)
Timeframe: Baseline through end of study; up to 6-months or to the data cutoff 11FEB2016.

Interventiondays (Median)
Ruxolitinib Plus CapecitabineNA
Placebo Plus CapecitabineNA

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Participants With Treatment-Emergent Adverse Events (TEAEs)

A treatment-emergent AE was defined as an event occurring after exposure to at least 1 dose of study drug (ruxolitinib or placebo). A treatment-related AE was defined as an event with a definite, probable, or possible causality to study medication. A serious AE is an event resulting in death, hospitalization, persistent or significant disability/incapacity, or is life threatening, a congenital anomaly/birth defect or requires medical or surgical intervention to prevent 1 of the outcomes above. The intensity of an AE was graded according to the National Cancer Institute common terminology criteria for adverse events (NCI-CTCAE) version 4.03: Grade 1 (Mild); Grade 2 (Moderate); Grade 3 (Severe); Grade 4 (life-threatening). (NCT02119663)
Timeframe: Baseline through approximately 30 days post treatment discontinuation; up to 6-months or to the data cutoff 11FEB2016.

,
InterventionParticipants (Count of Participants)
Participants who had any TEAEsParticipants who had treatment-related TEAEsParticipants who had SAEsParticipants who had Grade 3 or higher TEAEsParticipants hospitalized because of a TEAEParticipants discontinued treatment due to TEAEParticipants with a dose modification due to TEAEParticipants on concomitant medication due to TEAEParticipants with procedure performed due to TEAEParticipants who had a fatal TEAE
Placebo Plus Capecitabine402520311851435142
Ruxolitinib Plus Capecitabine412128312671736228

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Percentage of Participants Achieving Progression Free Survival (PFS)

PFS is defined as the time from randomization until the earliest date of disease progression determined by investigator assessment of objective radiographic disease assessments per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1, or death due to any cause if sooner. Progressive Disease (PD) is defined using Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions, unequivocal progression of non-target lesions, or the appearance of new lesions. (NCT02119663)
Timeframe: Randomization to disease progression, or death due to any cause if sooner; up to 6-months or to the data cutoff 11FEB2016.

,
Interventionpercentage of participants (Median)
Survival rate at 3 monthsSurvival rate at 6 months
Placebo Plus Capecitabine0.2970.204
Ruxolitinib Plus Capecitabine0.3370.131

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Overall Survival (OS)

Overall survival is reported here based on the number of deaths from randomization until the data cut-off. (NCT02119663)
Timeframe: Randomization until death due to any cause up to 6-months or to the data cutoff 11FEB2016.

,
InterventionParticipants (Count of Participants)
Observed deathsCensored deaths
Placebo Plus Capecitabine2320
Ruxolitinib Plus Capecitabine2914

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Median Survival

Survival was assessed by the time to death or censoring up until 08Feb2016. Participants with no observed death were treated as right-censored at their last date known to be alive. The survival time was analyzed using the Kaplan-Meier method. (NCT02120417)
Timeframe: Randomization until death due to any cause up to 19 months or the data cutoff 08FEB2016.

Interventionmonths (Median)
Treatment A - Capecitabine and Ruxolitinib11.2
Treatment B - Capecitabine and Placebo10.9

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Percentage of Participants Achieving Clinical Benefit Rate

Clinical benefit rate was defined as a complete response, partial response, or stable disease, determined by investigator assessment of objective radiographic disease assessments per RECIST (v1.1) that lasted for ≥ 6 months. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) for target lesions and assessed by computed tomography (CT) and/or magnetic resonance imaging (MRI) : Complete Response (CR), Disappearance of all target and non-target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions with no worsening of non-target lesions and no new lesions; Overall Response (OR) = CR + PR. (NCT02120417)
Timeframe: Randomization through end of study up to 19 months or the data cutoff 08FEB2016.

Interventionpercentage of participants (Number)
Treatment A - Capecitabine and Ruxolitinib13.2
Treatment B - Capecitabine and Placebo6.8

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Percentage of Participants Achieving Overall Survival

Overall survival was assessed by the time to death or censoring up until 08Feb2016. Participants with no observed death were treated as right-censored at their last date known to be alive. The survival time was analyzed using the Kaplan-Meier method. (NCT02120417)
Timeframe: Randomization until death due to any cause at month 3, 6, 9, 12 and 15 or the data cutoff 08FEB2016.

,
Interventionpercentage of participants (Number)
Month 3 Survival RateMonth 6 Survival RateMonth 9 Survival RateMonth 12 Survival RateMonth 15 Survival Rate
Treatment A - Capecitabine and Ruxolitinib0.8550.6740.5370.4350.319
Treatment B - Capecitabine and Placebo0.7500.6350.5460.4270.294

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Percentage of Participants Achieving Objective Response Rate

Objective response rate determined by radiographic disease assessments per RECIST (v1.1), by investigator assessment and was defined as the percentage of participants with Complete Response (CR) or Partial Response (PR) by Response Evaluation Criteria in Solid Tumours (RECIST) at any post baseline visit. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) for target lesions and assessed by computed tomography (CT) and/or magnetic resonance imaging (MRI) : Complete Response (CR), Disappearance of all target and non-target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions with no worsening of non-target lesions and no new lesions; Overall Response (OR) = CR + PR. (NCT02120417)
Timeframe: Randomization through end of study up to 19 months or the data cutoff 08FEB2016.

,
Interventionpercentage of participants (Number)
Complete Response ratePartial Response rate
Treatment A - Capecitabine and Ruxolitinib0.028.9
Treatment B - Capecitabine and Placebo0.013.7

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Progression-free Survival (PFS)

Progression-free survival was defined as the time from the randomization date to the earliest date of disease progression, as measured by investigator assessment of objective radiographic disease assessments per RECIST (v1.1), or death from any cause if earlier. Progression-free survival time distribution and median survival for each treatment group were analyzed using the Kaplan-Meier method. (NCT02120417)
Timeframe: Randomization to disease progression, or death due to any cause if sooner up to 19 months or the data cutoff 08FEB2016.

Interventionmonths (Median)
Treatment A - Capecitabine and Ruxolitinib4.5
Treatment B - Capecitabine and Placebo2.5

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Duration of Response (DOR)

The DOR was defined as the difference (in number of months) between the end of response and the start of response for participants who had at least 1 response measurement. The start of a response was the first visit where the participant achieved a partial response or better based on RECIST (v1.1) criteria. The end of response was the earlier of death or progressive disease based on RECIST (v1.1) criteria. The date of progressive disease was the date on which progression was first recorded. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) for target lesions and assessed by computed tomography (CT) and/or magnetic resonance imaging (MRI) : Complete Response (CR), Disappearance of all target and non-target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions with no worsening of non-target lesions and no new lesions; Overall Response (OR) = CR + PR. (NCT02120417)
Timeframe: Randomization through end of study up to 19 months or the data cutoff 08FEB2016.

Interventionmonths (Median)
Treatment A - Capecitabine and Ruxolitinib4.2
Treatment B - Capecitabine and Placebo4.4

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Overall Survival (OS)

OS: The time from registration to death or date of last contact. Participants with overall survival at 1 year. Kaplan-Meier estimator will be utilized. (NCT02218164)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Expired in less than a yearAlive at the end of the yearHad not completed survival follow-up at closeout
Capecitabine or 5-FU With Pegylated Interferon Alpha-2b422

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Objective Response Rate (ORR)

ORR: Stable Disease (SD); Partial Response (PR); Complete Response (CR). Response according to Response Evaluation Criteria in Solid Tumors (RECIST) v1.1. CR: disappearance of all target lesions; PR: At least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD; Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions; SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started. (NCT02218164)
Timeframe: 9 weeks per participant

InterventionParticipants (Count of Participants)
Stable DiseaseComplete ResponsePartial Response
Capecitabine or 5-FU With Pegylated Interferon Alpha-2b411

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Progression Free Survival (PFS)

PFS: Alive without RECIST progression. Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT02218164)
Timeframe: 1 year

Interventionmonths (Median)
Capecitabine or 5-FU With Pegylated Interferon Alpha-2b11.3

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Peritoneal Recurrence Free Survival at 18 Months

Peritoneal recurrence-free survival at 18 months determined by CT and CEA. If CEA was normal and CT did not show any signs of peritoneal metastase at 18 months, a diagnostic laparoscopy was performed in those patients who consented to this intervention. Complete peritoneal staging was performed during laparoscopy, and biopsies were taken from suspicious lesions. If no peritoneal lesions were seen or biopsies were negative, this indicated that the patient was free from peritoneal recurrence. (NCT02231086)
Timeframe: 18 months

Interventionparticipants (Number)
Standard Adjuvant Systemic Chemotherapy79
Adjuvant HIPEC (Open/Laparoscopic)80

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Survival Rate at 18 Month

Number of participants surviving after 18 months of study follow-up (NCT02243007)
Timeframe: 18 Month

InterventionParticipants (Count of Participants)
Folfirinox-ARM A2
Gemcitabine/Nab-Paclitaxel- Arm B3

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Number of Participants With Serious and Non-Serious Adverse Events

Number of Participants with Serious and Non-Serious Adverse Events from baseline to 28 days (NCT02243007)
Timeframe: Baseline, 28 Days

,
Interventionparticipants (Number)
Serious Adverse EventsOther Adverse Events
Folfirinox-ARM A04
Gemcitabine/Nab-Paclitaxel- Arm B23

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Rate of Pathologic Downstaging

The number of participants achieving a reduction in the pathological staging of the primary cancer. (NCT02243007)
Timeframe: 2 Years

Intervention ()
Folfirinox-ARM A0
Gemcitabine/Nab-Paclitaxel- Arm B0

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30-day Post-operative Mortality Rate

Number of patients who died following surgery. (NCT02243007)
Timeframe: 30 Days

Intervention ()
Folfirinox-ARM A0
Gemcitabine/Nab-Paclitaxel- Arm B0

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Correlation of Biomarkers With PFS

Analysis of the correlation between selected bio-markers and progression free survival. (NCT02243007)
Timeframe: 2 Years

Intervention ()
Folfirinox-ARM A0
Gemcitabine/Nab-Paclitaxel- Arm B0

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Local Control Rate

The number of participants achieving local control. The local control rate is defined as the number of participants achieving stable disease, partial response, or a complete response. (NCT02243007)
Timeframe: 2 Years

Intervention ()
Folfirinox-ARM A0
Gemcitabine/Nab-Paclitaxel- Arm B0

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Pathologic Complete Response Rate (pCR).

Number of patients achieving pathologic complete response at 18 months. Pathologic complete response is defined as the absence of residual invasive disease in the panaceas and in the regional lymph nodes. (NCT02243007)
Timeframe: 18 Months

Intervention ()
Folfirinox-ARM A0
Gemcitabine/Nab-Paclitaxel- Arm B0

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Surgical Morbidity Rate

Number of patients experiencing a specific surgery related morbidity (NCT02243007)
Timeframe: within 30 days of surgery

Intervention ()
Folfirinox-ARM A0
Gemcitabine/Nab-Paclitaxel- Arm B0

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Percentage of Participants With Improvement and/or Stayed the Same on the Eastern Cooperative Oncology Group Performance Status (ECOG PS) Score

(NCT02291289)
Timeframe: From baseline until end of study (up to 5 years)

,,,,,,,
Interventionpercentage of participants (Number)
ImprovedImproved or stayed the same
Cohort 1 (Maintenance Phase[MP]):5-FU/LV,Cetuximab,Vemurafenib10.075.0
Cohort 1 Control(MP):5-FU/LV or Capecitabin, Bevacizumab5.085.0
Cohort 2 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab5.482.5
Cohort 2(MP):5-FU/LV or Capecitabine,Bevacizumab,Atezolizumab10.476.7
Cohort 3 (MP): Capecitabine,Trastuzumab,Pertuzumab0100
Cohort 3 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab0100
Cohort 4 (MP): Cobimetinib,Atezolizumab7.763.1
Cohort 4 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab5.979.4

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Progression-Free Survival (PFS)

PFS is defined as the time from randomization to the first occurrence of disease progression according to RECIST v1.1, or death from any cause, whichever occurs first. Progressive disease (PD) for target lesion: At least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum of diameters on study (including baseline). In addition to the relative increase of 20%, the sum of diameters must also demonstrate an absolute increase of >/=5 mm. PD for non-target lesion: Unequivocal progression of existing non-target lesions. (NCT02291289)
Timeframe: From randomization until disease progression or death from any cause, up to 5 years

Interventionmonths (Median)
Cohort 1 (Maintenance Phase[MP]):5-FU/LV,Cetuximab,Vemurafenib9.99
Cohort 1 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab11.60
Cohort 2 (MP):5-FU/LV or Capecitabine,Bevacizumab,Atezolizumab7.13
Cohort 2 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab7.36
Cohort 3 (MP): Capecitabine,Trastuzumab,Pertuzumab4.44
Cohort 3 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab4.04
Cohort 4 (MP): Cobimetinib,Atezolizumab3.75
Cohort 4 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab7.79

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Overall Response

Calculated as the number of participants with a best overall response of CR or PR according to RECIST 1.1. CR: disappearance of all target lesions. PR: At least a 30% decrease in the sum of diameters of all target lesions, taking as reference the baseline sum of diameters, in the absence of CR. OR= CR + PR. (NCT02291289)
Timeframe: From randomization until disease progression, up to 5 years

InterventionParticipants (Count of Participants)
Cohort 1 (Maintenance Phase[MP]):5-FU/LV,Cetuximab,Vemurafenib20
Cohort 1 Control(MP): 5-FU/LV or Capecitabin, Bevacizumab5
Cohort 2 (MP):5-FU/LV or Capecitabine,Bevacizumab,Atezolizumab49
Cohort 2 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab22
Cohort 3 (MP): Capecitabine,Trastuzumab,Pertuzumab1
Cohort 3 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab0
Cohort 4 (MP): Cobimetinib,Atezolizumab7
Cohort 4 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab8

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Duration of Response

Defined as the time from the first assessment of CR or PR until disease progression or death from any cause, whichever occurs first. CR is defined as disappearance of all target lesions. PR is defined as at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum of diameters. (NCT02291289)
Timeframe: From first objective response until disease progression or death from any cause, up to 5 years

Interventionmonths (Median)
Cohort 1 (Maintenance Phase[MP]):5-FU/LV,Cetuximab,Vemurafenib11.50
Cohort 1 Control(MP):5-FU/LV or Capecitabin, Bevacizumab8.74
Cohort 2(MP):5-FU/LV or Capecitabine,Bevacizumab,Atezolizumab9.30
Cohort 2 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab7.59
Cohort 3 (MP): Capecitabine,Trastuzumab,Pertuzumab9.205
Cohort 3 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab0
Cohort 4 (MP): Cobimetinib,Atezolizumab7.11
Cohort 4 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab6.06

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Disease Control Rate (DCR)

DCR is defined as the percentage of participants with CR, PR, or stable disease (SD) at 16 weeks. Per RECIST v1.1, CR is defined as disappearance of all target lesions. PR is defined as at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum of diameters. SD is defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for disease progression, taking as reference the smallest sum on study. Disease progression is defined as at least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study including baseline, or the appearance of one or more new lesions. (NCT02291289)
Timeframe: From randomization until disease progression, up to 5 years

InterventionParticipants (Count of Participants)
Cohort 1 (Maintenance Phase[MP]):5-FU/LV,Cetuximab,Vemurafenib36
Cohort 1 Control(MP): 5-FU/LV or Capecitabin, Bevacizumab15
Cohort 2(MP):5-FU/LV or Capecitabine,Bevacizumab,Atezolizumab227
Cohort 2 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab111
Cohort 3 (MP): Capecitabine,Trastuzumab,Pertuzumab1
Cohort 3 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab0
Cohort 4 (MP): Cobimetinib,Atezolizumab44
Cohort 4 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab26

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Time to Treatment Response

Calculated as the time from randomization to the first Occurrence of a documented Objective Response (CR or PR) determined according to RECIST 1.1. CR is defined as disappearance of all target lesions. PR is defined as at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum of diameters. (NCT02291289)
Timeframe: From randomization until disease progression or death from any cause, up to 5 years

Interventionmonths (Median)
Cohort 1 (Maintenance Phase[MP]):5-FU/LV,Cetuximab,Vemurafenib3.943
Cohort 1 Control(MP):5-FU/LV or Capecitabin, Bevacizumab5.552
Cohort 2(MP):5-FU/LV or Capecitabine,Bevacizumab,Atezolizumab5.224
Cohort 2 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab4.616
Cohort 3 (MP): Capecitabine,Trastuzumab,Pertuzumab5.490
Cohort 3 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab0
Cohort 4 (MP): Cobimetinib,Atezolizumab3.745
Cohort 4 Control (MP): 5-FU/LV or Capecitabin, Bevacizumab2.530

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Proportion of Subjects Experiencing Diarrhoea of Grade 2 and Above (up to 24 Weeks)

Proportion of subjects experiencing at least one episode of diarrhoea with a severity of Grade 2 and above, as defined by the National Cancer Institute common terminology criteria for adverse events (NCI CTCAE) version 4.03, recorded as AEs in the Electronic case report form (eCRF) (NCT02294786)
Timeframe: Up to 24 weeks

,
InterventionParticipants (Count of Participants)
Cyclce 1-3 (up to 9 weeks)with impuationCyclce 1-8 (up to 24 weeks)without imputation
No Octreotide Treatment95
Octreotide Treatment76

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Number of Lapatinib and Capecitabine Tablets Dispensed and Returned

Number of Lapatinib and Capecitabine tablets dispensed and returned as recorded in the eCRF (NCT02294786)
Timeframe: Up to 24 weeks

,
Interventiontablets (Mean)
Number of Lapatinib tablets dispensedNumber of Lapatinib tablets returnedNumber of Capecitabine tablets dispensedNumber of Capecitabine tablets returned
No Octreotide Treatment1115.6403.31011.2210
Octreotide Treatment1197.5477.11022.6186.1

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Time to the First Subject Reported Change in Frequency and/or Consistency of Bowel Movements From Baseline as Recorded in the DMD

Event is defined as Subjects reporting change in frequency and/or consistency of bowel movements from baseline at least once in DMD. Subject are censored if there is no change in bowel movement frequency/consistency as compared to baseline. Median time and 95% confidence intervals were calculated using Kaplan-Meier estimates. (NCT02294786)
Timeframe: Up to 24 weeks

InterventionDays (Median)
Octreotide Treatment22.0
No Octreotide Treatment8.0

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Proportion of Subjects Taking Anti-diarrhoeal Medication as Recorded in the DMD

The proportion of subjects taking medication at least once as a result of diarrhoea are summarised (NCT02294786)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
Octreotide Treatment2
No Octreotide Treatment2

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Proportion of Subjects Taking Anti-diarrhoeal Medication

Proportion of subjects taking anti-diarrhoeal medication as recorded in the eCRF (NCT02294786)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
Octreotide Treatment7
No Octreotide Treatment11

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Proportion of Subjects Reporting Stopping Completely or Missing Doses of Anti-cancer Tablets Due to Diarrhoea as Recorded in the DMD

The proportion of subjects reducing or completely stopping the number of anti-cancer tablets to help with diarrhoea are summarised (NCT02294786)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
Octreotide Treatment2
No Octreotide Treatment3

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Proportion of Subjects Reporting Changes in Bowel Movements From Baseline (Frequency and/or Consistency) as Recorded in the Diarrhoea Management Diary (DMD)

All subjects completed the baseline DMD during the 3 days prior to randomisation, before any study-related treatment is administered. Subjects randomised to receive Octreotide completed a second baseline DMD before starting the first cycle of treatment with Lapatinib and Capecitabine. The baseline DMD comprised of 3 questions to record stool form and consistency. The DMD to be completed throughout the rest of the study comprised of 3 questions in the baseline DMD and a further 5 questions and 6 sub-questions to evaluate the consequences and management of diarrhoea. (NCT02294786)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
Octreotide Treatment23
No Octreotide Treatment29

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Proportion of Subjects Making Dietary Changes Due to Diarrhoea as Recorded in the DMD

The proportion of subjects making dietary changes to help with the diarrhoea are summarised (NCT02294786)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
Octreotide Treatment9
No Octreotide Treatment11

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Time to Onset of the First Episode of Diarrhoea of Any Grade of Severity

Time to onset of the first episode of diarrhoea of any grade of severity, recorded as an AE in the eCRF. Subject are censored if there was no event. Median time and 95% confidence intervals were calculated using Kaplan-Meier estimates. (NCT02294786)
Timeframe: Up to 24 weeks

InterventionDays (Median)
Octreotide TreatmentNA
No Octreotide Treatment170

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Proportion of Subjects Experiencing Diarrhoea of Grade 3 and Above (up to 24 Weeks)

Proportion of subjects experiencing diarrhoea with a severity of Grade 3 and above, as defined by the NCI CTCAE, version 4.03 and recorded as AEs in the eCRF (NCT02294786)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
Octreotide Treatment2
No Octreotide Treatment0

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Proportion of Subjects Experiencing Diarrhoea of Any Grade of Severity (up to 24 Weeks)

Proportion of subjects experiencing diarrhoea of any grade of severity as defined by the NCI CTCAE, version 4.03 and recorded as AEs in the eCRF (NCT02294786)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
Octreotide Treatment18
No Octreotide Treatment14

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Proportion of Subjects Contacting Other Non-hospital Healthcare Professionals to Discuss Diarrhoea as Recorded in the DMD

The proportion of subjects contacting a health care professional other than the hospital doctors/nurses to discuss diarrhoea are summarised (NCT02294786)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
Octreotide Treatment4
No Octreotide Treatment3

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Duration of Diarrhoea of Any Grade of Severity

Duration of diarrhoea of any grade of severity, recorded as AEs in the eCRF (NCT02294786)
Timeframe: Up to 24 weeks

Interventiondays (Mean)
Octreotide Treatment8.7
No Octreotide Treatment36.8

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Clinical Benefit Response (up to 24 Weeks)

"Clinical benefit response as measured in accordance with the Response Evaluation Criteria In Solid Tumours (RECIST) version 1.1. Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD.~Clinical Benefit Response rate (CBR) is defined as the percentage of subjects with a CR, PR or SD at week 24." (NCT02294786)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
Octreotide Treatment7
No Octreotide Treatment9

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Proportion of Subjects Requiring Treatment Withdrawal in Lapatinib and Capecitabine

Proportion of subjects requiring diarrhoea related Lapatinib and Capecitabine treatment withdrawal as recorded in the eCRF (NCT02294786)
Timeframe: Up to 24 weeks

,
InterventionParticipants (Count of Participants)
Requiring treatment withdrawal in LapatinibRequiring treatment withdrawal in Capecitabine
No Octreotide Treatment00
Octreotide Treatment00

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Proportion of Subjects Requiring Dose Reduction in Lapatinib and Capecitabine

Proportion of subjects requiring diarrhoea related Lapatinib and Capecitabine dose reduction as recorded in the eCRF (NCT02294786)
Timeframe: Up to 24 weeks

,
InterventionParticipants (Count of Participants)
Subjects requiring dose reduction in LapatinibSubjects requiring dose reduction in Capecitabine
No Octreotide Treatment02
Octreotide Treatment11

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Proportion of Subjects Requiring Dose Delay in Lapatinib and Capecitabine

Proportion of subjects requiring diarrhoea related Lapatinib and Capecitabine dose delay as recorded in the eCRF (NCT02294786)
Timeframe: Up to 24 weeks

,
InterventionParticipants (Count of Participants)
Subjects requiring dose delay in LapatinibSubjects requiring dose delay in Capecitabine
No Octreotide Treatment22
Octreotide Treatment22

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Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire For Pancreatic Cancer (EORTC-QLQ PAN26): Satisfaction With Health Care Scale

The EORTC pancreatic cancer module is a validated tool intended for patients at all disease stages undergoing surgical resection, palliative surgical intervention, endoscopic palliation or palliative chemotherapy. The module includes 26 questions, organized into 7 scales and 10 individual item scores. The summary scale for Satisfaction with Health Care is reported. All reported measures are transformed to a 0 to 100 scale. Scores of 0 = not satisfied, worst possible health state and 100 = extremely satisfied, best possible health state. The best score on treatment is the best score from all post-baseline visits and is compared to the baseline to get the following responder categories. Responder categories: - Improved: >=MID increase from baseline - Stable: no increase or decrease >MID - Worsened: >=MID decrease from baseline MID = half the baseline standard deviation (NCT02301143)
Timeframe: Baseline (Day -1), Day 1 of each cycle, for up to 19 cycles each cycle consisting of 28 days and the 28-day follow-up visit

InterventionParticipants (Count of Participants)
Satisfaction with Health Care Scale: ImprovedSatisfaction with Health Care Scale: StableSatisfaction with Health Care Scale: Worsened
Nab-Paclitaxel Plus Gemcitabine424013

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Disease Control Rate (DCR): Percentage of Participants With Complete (CR) or Partial Response (PR), or Stable Disease (SD) for ≥ 16 Weeks According to RECIST Version 1.1

"DCR was defined as the percentage of participants with a CR or PR or SD from of date of first treatment to 16 weeks. Tumor assessments after start of non-protocol-defined anticancer therapy were excluded.~RECIST 1.1 Definition:~CR: disappearance of all target and non-target lesions; any pathological lymph nodes (target or non-target) must have reduction in short axis to < 10 mm and no new lesions diagnosed.~PR: a >= 30% decrease in the sum of diameters of target lesions from baseline; no evidence of progression in any of the non-target lesions diagnosed at baseline; and no new lesions diagnosed.~SD: neither sufficient shrinkage to qualify for PR nor sufficient increase of lesions to qualify for PD.~The two-sided 90% binomial confidence intervals (CIs) were estimated by Wilson score method." (NCT02301143)
Timeframe: Day 1 of study treatment up to the end of investigator choice period plus 28 days; up to 76.9 weeks

Interventionpercentage of participants (Number)
Nab-Paclitaxel Plus Gemcitabine77.6

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Kaplan-Meier Estimate of Progression-Free Survival (PFS)

"Progression-free Survival (PFS) was defined as the time from the date of the first dose to the date of disease progression or death (by any cause), whichever is earlier. The analysis day was calculated from enrollment date for one participant who was not treated. Participants who have no disease progression or have not died were censored to last tumor assessment date with progression-free.~The definition for progressive disease (PD) was at least a 20% increase in the sum of diameters of target lesions from nadir; the sum must also demonstrate an absolute increase of >= 5 mm; the progression of a non-target lesion or the appearance of any new lesions is also considered progression.~Median and its 90% confidence interval of PFS were estimated using the method of Brookmeyer and Crowley." (NCT02301143)
Timeframe: Day 1 of study treatment up to 28.75 months (maximum time for the last tumor assessment)

Interventionmonths (Median)
Nab-Paclitaxel Plus Gemcitabine10.9

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Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire For Pancreatic Cancer (EORTC-QLQ PAN26): Six Summary Scales

The EORTC pancreatic cancer module is a validated tool intended for patients at all disease stages undergoing surgical resection, palliative surgical intervention, endoscopic palliation or palliative chemotherapy. The module includes 26 questions, organized into 7 scales and 10 individual item scores. All reported measures are transformed to a 0 to 100 scale. Six summary scales reported are: - Pancreatic Pain - Digestive Symptoms - Altered Bowel Habits - Hepatic Scale - Body Image - Sexuality Scores of 0 = optimal health state and 100 = worst possible health state. The best score on treatment is the best score from all post-baseline visits and is compared to the baseline. Responder categories: - Improved: >=MID decrease from baseline - Stable: no increase or decrease >MID - Worsened: >=MID increase from baseline MID = half the baseline standard deviation (NCT02301143)
Timeframe: Baseline (Day -1), Day 1 of each cycle, for up to 19 cycles each cycle consisting of 28 days and the 28-day follow-up visit

InterventionParticipants (Count of Participants)
Pancreatic Pain Scale: ImprovedPancreatic Pain Scale: StablePancreatic Pain Scale: WorsenedDigestive Symptom Scale: ImprovedDigestive Symptom Scale: StableDigestive Symptom Scale: WorsenedAltered Bowel Habits Scale: ImprovedAltered Bowel Habits Scale: StableAltered Bowel Habits Scale: WorsenedHepatic Scale: ImprovedHepatic Scale: StableHepatic Scale: WorsenedBody Image Scale: ImprovedBody Image Scale: StableBody Image Scale: WorsenedSexuality Scale: ImprovedSexuality Scale: StableSexuality Scale: Worsened
Nab-Paclitaxel Plus Gemcitabine6233049361028531425664225023315113

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Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire For Pancreatic Cancer (EORTC-QLQ PAN26): 10 Individual Item Scores

The EORTC pancreatic cancer module is a validated tool intended for patients at all disease stages undergoing surgical resection, palliative surgical intervention, endoscopic palliation or palliative chemotherapy. The module includes 26 questions, organized into 7 scales and 10 individual item scores. The 10 individual item scores are reported. All reported measures are transformed to a 0 to 100 scale. Scores of 0 = best possible health state and 100 = worst possible health state. The best score on treatment is the best score from all post-baseline visits and is compared to the baseline to get the following responder categories. Responder categories: - Improved: >=MID decrease from baseline - Stable: no increase or decrease >MID - Worsened: >=MID increase from baseline MID = half the baseline standard deviation (NCT02301143)
Timeframe: Baseline (Day -1), Day 1 of each cycle, for up to 19 cycles each cycle consisting of 28 days and the 28-day follow-up visit

InterventionParticipants (Count of Participants)
Abdominal Bloating: ImprovedAbdominal Bloating: StableAbdominal Bloating: WorsenedTaste Changes: ImprovedTaste Changes: StableTaste Changes: WorsenedIndigestion: ImprovedIndigestion: StableIndigestion: WorsenedFlatulence: ImprovedFlatulence: StableFlatulence: WorsenedWeight Loss: ImprovedWeight Loss: StableWeight Loss: WorsenedLimb Weakness: ImprovedLimb Weakness: StableLimb Weakness: WorsenedDry Mouth: ImprovedDry Mouth: StableDry Mouth: WorsenedTreatment Side-Effects: ImprovedTreatment Side-Effects: StableTreatment Side-Effects: WorsenedWorry About Future Health: ImprovedWorry About Future Health: StableWorry About Future Health: WorsenedLimits on Activity Planning: ImprovedLimits on Activity Planning: StableLimits on Activity Planning: Worsened
Nab-Paclitaxel Plus Gemcitabine5042320542141477473711365632255183745138483942458424211

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Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30): Symptom Scales and Single Symptom Items

The European Organization for Research and Treatment of Cancer Quality-of-Life questionnaire (EORTC QLQ-C30) is a validated health-related quality of life (HRQoL) measure. The EORTC QLQ-C30 is composed of both multi-item scales and single-item measures, including 5 functional scales, 3 symptom scales, 6 single symptom items, and 1 global health status / quality of life scale. No item occurs in more than one scale. All reported measures are transformed to a 0 to 100 scale. In the symptom scales and single symptom items, 0 = optimal health state and 100 = worst possible health state. The best score on treatment is the best score from all post-baseline visits and is compared to the baseline to get the following responder categories. Responder categories: - Improved: >=10 decrease from baseline - Stable: neither increase nor decrease >10 - Worsened: >=10 increase from baseline (NCT02301143)
Timeframe: Baseline (Day -1), Day 1 of each cycle, for up to 19 cycles each cycle consisting of 28 days and the 28-day follow-up visit

InterventionParticipants (Count of Participants)
Symptom Scale-Fatigue: ImprovedSymptom Scale-Fatigue: StableSymptom Scale-Fatigue: WorsenedScale-Nausea+Vomiting: ImprovedScale-Nausea+Vomiting: StableScale-Nausea+Vomiting: WorsenedSymptom Scale-Pain: ImprovedSymptom Scale-Pain: StableSymptom Scale-Pain: WorsenedSymptom - Dyspnoea: ImprovedSymptom - Dyspnoea: StableSymptom - Dyspnoea: WorsenedSymptom - Insomnia: ImprovedSymptom - Insomnia: StableSymptom - Insomnia: WorsenedSymptom - Appetite loss: ImprovedSymptom - Appetite loss: StableSymptom - Appetite loss: WorsenedSymptom - Constipation: ImprovedSymptom - Constipation: StableSymptom - Constipation: WorsenedSymptom - Diarrhoea: ImprovedSymptom - Diarrhoea: StableSymptom - Diarrhoea: WorsenedSymptom - Financial difficulties: ImprovedSymptom - Financial difficulties: stable:Symptom - Financial difficulties: Worsened
Nab-Paclitaxel Plus Gemcitabine4624252964262294127495335748398464541869817744

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Participant Counts in Response Categories Using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30): Global Health Status and 5 Functioning Scales

The European Organization for Research and Treatment of Cancer Quality-of-Life questionnaire (EORTC QLQ-C30) is a validated health-related quality of life (HRQoL) measure. The EORTC QLQ-C30 is composed of both multi-item scales and single-item measures, including 5 functional scales, 3 symptom scales, 6 single symptom items, and 1 global health status / quality of life scale. No item occurs in more than one scale. All reported measures are transformed to a 0 - 100 scale. In the Global Health Status and 5 functional scales, 0 = worst possible quality of life/health status and 100 = best possible quality of life/health status. The best score on treatment is the best score from all post-baseline visits and is compared to the baseline to get the following responder categories. Responder categories: - Improved: >=10 increase from baseline - Stable: neither increase nor decrease >10 - Worsened: >=10 decrease from baseline (NCT02301143)
Timeframe: Baseline (Day -1), Day 1 of each cycle, for up to 19 cycles each cycle consisting of 28 days and the 28-day follow-up visit

InterventionParticipants (Count of Participants)
Global Health Status: ImprovedGlobal Health Status: StableGlobal Health Status: WorsenedPhysical Functioning Scale: ImprovedPhysical Functioning Scale: StablePhysical Functioning Scale: WorsenedRole Functioning Scale: ImprovedRole Functioning Scale: StableRole Functioning Scale: WorsenedEmotional Functioning Scale: ImprovedEmotional Functioning Scale: StableEmotional Functioning Scale: WorsenedCognitive Functioning Scale: ImprovedCognitive Functioning Scale: StableCognitive Functioning Scale: WorsenedSocial Functioning Scale: ImprovedSocial Functioning Scale: StableSocial Functioning Scale: Worsened
Nab-Paclitaxel Plus Gemcitabine4334182066936461350405335111384314

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Overall Response Rate (ORR): Percentage of Participants With Complete (CR) or Partial Response (PR) According to RECIST Version 1.1

"ORR was defined as the percentage of participants that achieved a combined incidence of complete (CR) and partial response (PR) using RECIST 1.1 guidelines as assessed by the investigator. Assessments after new non-protocol-defined anticancer therapy are excluded. For participants who had resectable surgery in Investigator Choice period, assessments after surgical intervention are excluded.~RECIST 1.1 Definition:~CR: disappearance of all target and non-target lesions; any pathological lymph nodes (target or non-target) must have reduction in short axis to < 10 mm and no new lesions diagnosed.~PR: a >= 30% decrease in the sum of diameters of target lesions from baseline; no evidence of progression in any of the non-target lesions diagnosed at baseline; and no new lesions diagnosed.~The two-sided 90% binomial confidence intervals (CIs) were estimated by Wilson score method" (NCT02301143)
Timeframe: Day 1 of study treatment up to the end of investigator choice period plus 28 days; up to 76.9 weeks

Interventionpercentage of participants (Number)
Nab-Paclitaxel Plus Gemcitabine39.3

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Kaplan-Meier Estimates for Time to Treatment Failure (TTF)

"TTF was defined as the time after the first dose of study therapy to discontinuation of study therapy due to disease progression, death by any cause, or the start of a new non-protocol-defined anticancer therapy/surgery. If a participant does not progress, die or start a new non-protocol-defined anticancer therapy, the participant was censored on the last tumor assessment date.~Tumor evaluations of CT or MRI scans were assessed by the investigative sites and response determined according to Response Evaluation Criteria in Solid Tumors (RECIST) guidelines, version 1.1.~The definition for progressive disease (PD) was >= 20% increase in the sum of diameters of target lesions from nadir, and the sum showed an absolute increase of >= 5 mm; the progression of a non-target lesion or the appearance of any new lesions is also considered progression.~Median and its 90% confidence interval (CI) of TTF were estimated using the method of Brookmeyer and Crowley." (NCT02301143)
Timeframe: Day 1 of study treatment up to 28.75 months; (maximum time for the last tumor assessment)

Interventionmonths (Median)
Nab-Paclitaxel Plus Gemcitabine9.0

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Kaplan-Meier Estimates for Overall Survival (OS)

Overall survival was defined as the time from the date of first dose of study therapy to the date of death (by any cause). Participants who were alive at the end of study or clinical data cut were censored on the last known time that the participant was alive or the clinical cutoff date, whichever was earlier. Median and its 90% confidence interval of OS were estimated using the method of Brookmeyer and Crowley (NCT02301143)
Timeframe: Day 1 of study treatment up to 31.34 months (maximum time for survival follow-up)

Interventionmonths (Median)
Nab-Paclitaxel Plus Gemcitabine18.8

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Participants With Treatment Emergent Adverse Events (TEAEs)

"TEAEs are defined as any adverse event (AE) that begin or worsen on or after the start of study drug or procedure of the study period through the maximum duration of the period plus 28 days. The severity of AEs was graded based on National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE), Version 4.0 and the scale: Grade 1 = Mild Grade 2 = Moderate Grade 3 = Severe Grade 4 = Life threatening Grade 5 = Death. Relation to study drug was determined by the investigator. A treatment-related TEAE is defined as TEAE which was considered to be related to one or both of the study drugs and reported as 'Suspected' on the case report form. AEs with a missing relationship were treated as 'treatment-related' in data summaries. IP (investigational product) refers to nab-Paclitaxel and/or Gemcitabine. Related TEAE refers to relation to study drug (IP)." (NCT02301143)
Timeframe: Day 1 of study drug up to end of the study; up to 31.3 months

,
InterventionParticipants (Count of Participants)
>= 1 TEAE>=1 related TEAE>=1 TEAE of severity grade 3 or higher>=1 related TEAE of severity grade 3 or higher>=1 serious TEAE>= 1 related serious TEAE>=1 TEAE leading to discontinuation of IP>=1 related TEAE leading to discontinuation of IP>=1 TEAE leading to dose reduction of IP>=1 related TEAE leading to dose reduction of IP>=1 TEAE leading to interruption of IP>=1 related TEAE leading to interruption of IP>= TEAE leading to death>=1 related TEAE leading to death
Nab-Paclitaxel Plus Gemcitabine (Induction Period)1051028572381425156968664820
Nab-Paclitaxel Plus Gemcitabine (Overall)1051039075391428187271685020

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Time to Progression (TTP)

TTP was time from the date of randomization to the date of radiographic progression (according to RECIST v.1.1). If a participant died due to any reason without radiographic progression, TTP is censored at the last adequate tumor assessment. Target lesions: Progressive Disease (PD): At least a 20% increase in the sum of diameters of lesions vs the smallest sum on study (the sum must also demonstrate an absolute increase of at least 5 mm); or the appearance of new lesion(s). Non target lesions: PD: Unequivocal progression of existing lesions or the appearance of new lesion(s). (NCT02314117)
Timeframe: Randomization to Disease Progression (Up To 24 Months)

Interventionmonths (Median)
Ramucirumab + Cisplatin + Capecitabine6.77
Placebo + Cisplatin + Capecitabine5.78

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Time to Deterioration in Eastern Cooperative Oncology Group (ECOG) Performance Status (PS)

The time from the date of randomization to the first date observing ECOG PS ≥2 (that is, deterioration from baseline status of 0 or 1). Participants without PS deterioration were censored at their last documented assessments of 0 or 1. ECOG Performance Status: 2- Ambulatory and capable of all selfcare but unable to carry out any work activities. Up and about more than 50% of waking hours, 3 -Capable of only limited selfcare, confined to bed or chair more than 50% of waking hours, 4 -Completely disabled. Cannot carry on any selfcare.Totally confined to bed or chair,5- Dead. (NCT02314117)
Timeframe: Randomization to ECOG PS ≥2 (Up To 26 Months)

Interventionmonths (Median)
Ramucirumab + Cisplatin + CapecitabineNA
Placebo + Cisplatin + CapecitabineNA

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PK: Minimum Concentration (Cmin) of Ramucirumab

Pharmacokinetics (PK): Minimum Concentration (Cmin) of Ramucirumab (NCT02314117)
Timeframe: Cycle 1 Day 1: 1 hour (hr) end of infusion (EOI), Cycle 3 Day 1: 1hr EOI, Cycle 9 Day 1: 1 hr EOI

Interventionµg/mL (Geometric Mean)
Cycle 1, Day 8Cycle 2, Day 1Cycle 3, Day 1Cycle 5, Day 1Cycle 9, Day 1
Ramucirumab + Cisplatin + Capecitabine40.735.751.269.777.6

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Pharmacokinetics (PK): Maximum Observed Drug Concentration (Cmax) of Ramucirumab

Pharmacokinetics (PK): Pharmacokinetics (PK): Maximum Observed Drug Concentration (Cmax) of Ramucirumab (NCT02314117)
Timeframe: Cycle 1 Day 1: 1 hour (hr) end of infusion (EOI), Cycle 3 Day 1: 1hr EOI, Cycle 9 Day 1: 1 hr EOI

InterventionMicrogram/milliliter (µg/mL) (Geometric Mean)
Cycle 1, Day 1Cycle 3, Day 1Cycle 9, Day 1
Ramucirumab + Cisplatin + Capecitabine133173169

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Number of Participants With Anti-Ramucirumab Antibodies

Participants who developed treatment-emergent antibody responses to Ramucirumab postbaseline. (NCT02314117)
Timeframe: Predose Cycle 1 through 30 Days After Treatment Discontinuation (Up To 24 Months)

InterventionParticipants (Count of Participants)
Ramucirumab + Cisplatin + Capecitabine4
Placebo + Cisplatin + Capecitabine5

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Time to Deterioration in Quality of Life (QoL) on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-Core 30 (EORTC QLQ-C30) - Global Health Status/ QoL Scale

Time to sustained deterioration was defined as time from randomization to first worsening in QoL with no subsequent non-worsened assessment. Worsening in global health status/QoL was defined as a decrease of ≥10 points on a 100-point scale. If a participant did not report worsening, time to sustained deterioration was censored at date of last non-worsened assessment. (NCT02314117)
Timeframe: Randomization, First worsening in QoL (Up To 26 Months)

Interventionmonths (Median)
Ramucirumab + Cisplatin + Capecitabine9.00
Placebo + Cisplatin + Capecitabine9.46

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Progression-free Survival (PFS)

PFS time was measured from the date of randomization to the date of radiographic(rgr) documentation of progression(by RECIST v.1.1) or the date of death due to any cause, whichever was earlier.If a participant did not have a complete baseline tumor assessment,then the PFS time was censored at the randomization date.If a participant was not known to have died or have rgr documented progression as of the data cutoff date for the analysis, the PFS time was censored at the last adequate tumor assessment date. If death or progressive disease(PD) occurred after 2 or more consecutive missing rgr visits,censoring occurred at the date of the last rgr visit prior to the missed visits.If death or PD occurred after postdiscontinuation(pdis) systemic anticancer therapy,censoring occurred at the date of last rgr visit prior to the start of pdis systemic anticancer therapy. PD was defined according to RECIST v.1.1. (NCT02314117)
Timeframe: Randomization to Radiological Disease Progression or Death from Any Cause (Up to 26 Months)

Interventionmonths (Median)
Ramucirumab + Cisplatin + Capecitabine5.72
Placebo + Cisplatin + Capecitabine5.39

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Change in Health Status on the EuroQol 5-Dimensions 5-Level Instrument (EQ-5D- 5L)

The EQ-5D-5L is a standardized instrument for use as a measure of self-reported health status. Five dimensions of health status are each assessed with 5 response options and scored as a composite index which were anchored on a scale of 0 to 1 with a higher score representing better health status. Additionally, current health status was assessed on a visual analogue scale (VAS) ranging from 0 to 100 with a higher score representing better health status. (NCT02314117)
Timeframe: Randomization, 30 Days After Treatment Discontinuation (Up To 5 Months)

,
Interventionunits on a scale (Mean)
EQ-5D indexEQ-5D VAS
Placebo + Cisplatin + Capecitabine-0.0101.5
Ramucirumab + Cisplatin + Capecitabine-0.0080.8

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Duration of Response (DoR)

Participants achieved an objective response if they had a best overall response of CR or PR.Target lesions- CR:Disappearance of all lesions;any pathological lymph nodes must have reduction in short axis to <10 mm.PR: At least a 30% decrease in the sum of diameters of lesions vs the baseline sum.PD: At least a 20% increase in the sum of diameters of lesions vs the smallest sum on study(the sum must also demonstrate an absolute increase of at least 5 mm); or the appearance of new lesion(s).Non target lesions - CR: Disappearance of all lesions and normalization of tumour marker levels;all lymph nodes must be non-pathological in size. Non-CR/Non-PD:Persistence of lesion(s) and/or maintenance of abnormal tumor marker levels.PD:Unequivocal progression of existing lesions or the appearance of new lesion(s).If a participant was not known to have died or have radiographically documented PD as of the data inclusion cutoff date,DOR was censored at the date of the last adequate tumor assessment. (NCT02314117)
Timeframe: Date of Complete Response (CR) or Partial Response (PR) to Date of Objective Disease Progression or Death Due to Any Cause (Up To 26 Months)

Interventionmonths (Median)
Ramucirumab + Cisplatin + Capecitabine5.72
Placebo + Cisplatin + Capecitabine4.27

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Percentage of Participants With Complete Response (CR), Partial Response (PR) or Stable Disease (SD) (Disease Control Rate [DCR])

DCR was the percentage of participants with a best overall response of CR, PR, or SD as per Response using RECIST v1.1 criteria. Target lesions - CR: Disappearance of all lesions; any pathological lymph nodes must have reduction in short axis to <10 mm. PR: At least a 30% decrease in the sum of diameters of lesions vs the baseline sum. Progressive Disease (PD): At least a 20% increase in the sum of diameters of lesions vs the smallest sum on study (the sum must also demonstrate an absolute increase of at least 5 mm); or the appearance of new lesion(s). Stable Disease: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. Non target lesions - CR: Disappearance of all lesions and normalization of tumor marker levels; all lymph nodes must be non-pathological in size. Non-CR/Non-PD: Persistence of lesion(s) and/or maintenance of abnormal tumor marker levels. PD: Unequivocal progression of existing lesions or the appearance of new lesion(s). (NCT02314117)
Timeframe: Randomization to Disease Progression (Up To 26 Months)

Interventionpercentage of participants (Number)
Ramucirumab + Cisplatin + Capecitabine81.9
Placebo + Cisplatin + Capecitabine76.5

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Overall Survival (OS)

OS was time from the date of randomization to the date of death from any cause. If the participant was alive at the cutoff for analysis (or was lost to follow-up), OS data were censored for analysis on the last date the participant was known to be alive. (NCT02314117)
Timeframe: Randomization to Death from Any Cause (Up To 30 Months)

Interventionmonths (Median)
Ramucirumab + Cisplatin + Capecitabine11.17
Placebo + Cisplatin + Capecitabine10.74

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Percentage of Participants With Complete Response (CR) or Partial Response (PR) (Objective Response Rate [ORR])

Response was defined using Response Evaluation Criteria In Solid Tumors (RECIST v1.1).Target lesions - CR: Disappearance of all lesions; any pathological lymph nodes must have reduction in short axis to <10 mm. PR: At least a 30% decrease in the sum of diameters of lesions vs the baseline sum. PD: At least a 20% increase in the sum of diameters of lesions vs the smallest sum on study (the sum must also demonstrate an absolute increase of at least 5 mm); or the appearance of new lesion(s). Non target lesions - CR: Disappearance of all lesions and normalization of tumor marker levels; all lymph nodes must be non-pathological in size. Non-CR/Non-PD: Persistence of lesion(s) and/or maintenance of abnormal tumor marker levels. PD: Unequivocal progression of existing lesions or the appearance of new lesion(s).ORR calculated as:(sum of the number of participants with PRs and CRs) divided by (number of evaluable participants) multiplied by 100. (NCT02314117)
Timeframe: Randomization to Disease Progression (Up To 26 Months)

Interventionpercentage of participants (Number)
Ramucirumab + Cisplatin + Capecitabine41.1
Placebo + Cisplatin + Capecitabine36.4

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Progression- Free Survival 2 (PFS2)

PFS2 was defined as the time from the date of randomization to second disease progression (defined as objective radiological or symptomatic progression), or death of any cause, whichever occurs first. Participants alive and for whom a second disease progression has not been observed (including participants who did not receive any additional systemic anticancer treatments) were censored at the last time known to be alive and without second disease progression. The second progression refers to disease progression on or after additional systemic anticancer therapy, regardless if any earlier progression is observed or not(e.g. at the end of study treatment). It is assessed by investigator based on overall clinical evaluation, not limited to RECIST. (NCT02314117)
Timeframe: Randomization to Second Radiological or Symptomatic Disease Progression After the Start of Additional Systemic Anticancer Treatment or Death from Any Cause (Up To 26 Months)

Interventionmonths (Median)
Ramucirumab + Cisplatin + Capecitabine10.18
Placebo + Cisplatin + Capecitabine9.20

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Progression-free Survival (PFS) Using RECIST 1.1 Criteria

PFS is defined as the number of months from the date of first dose to disease progression (progressive disease [PD] or relapse from complete response [CR] as assessed using RECIST 1.1 criteria) or death due to any cause. Per RECIST 1.1 criteria, CR = disappearance of all target lesions, Partial Response (PR) is =>30% decrease in sum of diameters of target lesions, Progressive Disease (PD) is >20% increase in sum of diameters of target lesions, Stable Disease (SD) is <30% decrease or <20% increase in sum of diameters of target lesions. Estimation based on the Kaplan-Meier curve. (NCT02324543)
Timeframe: 5 years

InterventionMonths (Median)
Phase 28.34

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Response Rate (RR) Using RECIST 1.1 Criteria

RR is defined as the percentage of participants achieving a complete response (CR) or partial response (PR) based on the Response Evaluation Criteria in Solid Tumors (RECIST 1.1) at any time during the study. CR = disappearance of all target lesions, PR is =>30% decrease in sum of diameters of target lesions, progressive disease (PD) is >20% increase in sum of diameters of target lesions, stable disease (SD) is <30% decrease or <20% increase in sum of diameters of target lesions. (NCT02324543)
Timeframe: 43 months

Interventionpercentage of participants (Number)
Phase 257

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Maximum Tolerated Dose (MTD) of Gemcitabine

Dose escalation (phase I portion of the trial only) to determine the MTD in mg/m^2. (NCT02324543)
Timeframe: 28 days

Interventionmg/m^2 (Number)
Phase 1500

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Disease Control Rate (DCR) Using RECIST 1.1 Criteria

DCR is defined as the percentage of participants achieving a complete response (CR) or partial response (PR) and stable disease (SD) based on the Response Evaluation Criteria in Solid Tumors (RECIST 1.1) at any time during the study. CR = disappearance of all target lesions, PR is =>30% decrease in sum of diameters of target lesions, progressive disease (PD) is >20% increase in sum of diameters of target lesions, stable disease (SD) is <30% decrease or <20% increase in sum of diameters of target lesions. (NCT02324543)
Timeframe: 43 months

Interventionpercentage of participants (Number)
Phase 287

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Maximum Tolerated Dose (MTD) of Capecitabine

Dose escalation (phase I portion of the trial only) to determine the MTD in mg for twice daily (BID) use. (NCT02324543)
Timeframe: 28 days

Interventionmg (Number)
Phase 1500

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Overall Survival (OS) Rate at 9 Months

OS will be measured as the percentage of subjects alive at 9 months. (OS will be censored on the date the subject was last known to be alive for subjects without documentation of death at the time of analysis). Estimation based on the Kaplan-Meier curve. (Phase 2 data only) (NCT02324543)
Timeframe: 9 months

Interventionpercentage of participants (Number)
Phase 257

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Maximum Tolerated Dose (MTD) of Docetaxel

Dose escalation (phase I portion of the trial only) to determine the MTD in mg/m^2. (NCT02324543)
Timeframe: 28 days

Interventionmg/m^2 (Number)
Phase 120

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Maximum Tolerated Dose (MTD) of Cisplatin

Dose escalation (phase I portion of the trial only) to determine the MTD in mg/m^2. (NCT02324543)
Timeframe: 28 days

Interventionmg/m^2 (Number)
Phase 120

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Maximum Tolerated Dose (MTD) of Irinotecan

Dose escalation (phase I portion of the trial only) to determine the MTD in mg/m^2. (NCT02324543)
Timeframe: 28 days

Interventionmg/m^2 (Number)
Phase 120

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Overall Survival (OS)

OS will be measured (in months) from date of first dose until death or end of follow-up (OS will be censored on the date the subject was last known to be alive for subjects without documentation of death at the time of analysis). Estimation based on the Kaplan-Meier curve. (NCT02324543)
Timeframe: 5 years

InterventionMonths (Median)
Phase 211.02

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Overall Survival (OS) For All Participants

Overall Survival (OS) was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the final analysis were censored at the date of the last follow-up. The OS for all participants (regardless of PD-L1 tumor status) during first course pembrolizumab treatment per protocol, is presented. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionMonths (Median)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated5.5
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive13.8
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive20.7

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Progression-Free Survival For PD-L1 Positive Participants

PFS was defined as the time from randomization to the first documented disease progression, or death due to any cause, whichever occurred first. Per RECIST 1.1, progressive disease was defined as at least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. The appearance of one or more new lesions was also considered progression. The PFS for only PD-L1 positive participants during first course pembrolizumab treatment per protocol, is presented. Note: All participants in Cohort 3 had a PD-L1-positive tumor status. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionMonths (Median)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated2.1
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive6.5
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive2.9

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Progression-Free Survival (PFS) For All Participants

Progression-Free Survival (PFS) was defined as the time from randomization to the first documented disease progression, or death due to any cause, whichever occurred first. Per RECIST 1.1, progressive disease was defined as at least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. The appearance of one or more new lesions was also considered progression. The PFS for all participants (regardless of PD-L1 tumor status) during first course pembrolizumab treatment per protocol, is presented. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionMonths (Median)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated2.0
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive6.6
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive2.9

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Overall Survival For PD-L1 Positive Participants

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the final analysis were censored at the date of the last follow-up. The OS for only PD-L1 positive participants during first course pembrolizumab treatment per protocol, is presented. Note: All participants in Cohort 3 had a PD-L1-positive tumor status. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionMonths (Median)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated5.8
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive11.1
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive20.7

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Objective Response Rate For PD-L1 Positive Participants in Cohorts 1 and 3

The ORR was defined as the percentage of participants in the analysis population who had a CR or PR (CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of diameters of target lesions) per RECIST 1.1, as assessed by central radiology review. The percentage of all participants in Cohorts 1 and 3 with PD-L1+ tumor status who experienced a CR or PR during first course pembrolizumab treatment per protocol, is presented. Note: All participants in Cohort 3 had a PD-L1-positive tumor status. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionPercentage of Participants (Number)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated15.5
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive22.6

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Number of Participants Discontinuing Study Drug Due to AEs

An AE was defined as any untoward medical occurrence in a participant administered study drug and which does not necessarily have to have a causal relationship with the study drug. The number of participants who discontinued study drug due to an AE is presented. Per protocol, the number of participants who discontinued drug during first course pembrolizumab treatment is presented. (NCT02335411)
Timeframe: Up to approximately 52 months

InterventionParticipants (Count of Participants)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated18
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive4
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive0

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Disease Control Rate (DCR) For All Participants

Disease Control Rate (DCR) was defined as the percentage of participants in the analysis population who had a CR or a PR (CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of diameters of target lesions) or stable disease (SD); (SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease) for ≥6 months, (for Cohort 1 ≥2 months) as assessed by central radiology review. The percentage of all participants (regardless of PD-L1 tumor status) who had a CR or PR or SD during first course pembrolizumab treatment per protocol, is presented. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionPercentage of Participants (Number)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated27.0
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive80.0
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive32.3

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Number of Participants Experiencing Adverse Events (AEs)

An AE is defined as any untoward medical occurrence in a participant administered study drug and which does not necessarily have to have a causal relationship with the study drug. The number of participants who experienced at least one AE is presented. Per protocol, the number of participants who experienced at least one AE during first course pembrolizumab treatment is presented. (NCT02335411)
Timeframe: Up to approximately 65 months

InterventionParticipants (Count of Participants)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated248
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive25
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive31

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Disease Control Rate For PD-L1 Positive Participants

DCR was defined as the percentage of participants in the analysis population who had a CR or a PR (CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of diameters of target lesions) or stable disease (SD); (SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease) for ≥6 months, (for Cohort 1 ≥2 months) as assessed by central radiology review. The percentage of participants with PD-L1+ tumor status who experienced a CR or PR or SD during first course pembrolizumab treatment per protocol, is presented. Note: All participants in Cohort 3 had a PD-L1-positive tumor status. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionPercentage of Participants (Number)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated33.1
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive80.0
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive32.3

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Duration of Response (DOR) For All Participants

Duration of Response (DOR) was defined as the time from first documented evidence of CR or PR (CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of diameters of target lesions) per RECIST 1.1, based on central imaging vendor assessment, until disease progression (PD) or death, whichever occurred first. PD is defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions is also considered PD. Participants who had not progressed or died at the time of analysis were censored at the date of their last tumor assessment. The DOR for all participants (regardless of PD-L1 tumor status) during first course pembrolizumab treatment per protocol, is presented. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionMonths (Median)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated16.1
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive4.6
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive38.0

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Duration of Response For PD-L1 Positive Participants

DOR was defined as the time from first documented evidence of CR or PR (CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of diameters of target lesions) per RECIST 1.1, based on central imaging vendor assessment, until disease progression (PD) or death, whichever occurred first. PD is defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions is also considered PD. Participants who had not progressed or died at the time of analysis were censored at the date of their last tumor assessment. The DOR for only PD-L1 positive participants during first course pembrolizumab treatment per protocol, is presented. Note: All participants in Cohort 3 had a PD-L1-positive tumor status. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionMonths (Median)
Cohort 1: Pembrolizumab Monotherapy, Previously TreatedNA
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive4.6
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive38.0

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Objective Response Rate (ORR) For All Participants in Cohort 2

The Objective Response Rate (ORR) was defined as the percentage of participants in the analysis population who had a Complete Response (CR: Disappearance of all target lesions) or Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions) per Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST 1.1) as assessed by central radiology review. The percentage of all participants (regardless of PD-L1 tumor status) in Cohort 2 who had a CR or PR during first course pembrolizumab treatment per protocol, is presented. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionPercentage of Participants (Number)
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive60.0

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Objective Response Rate (ORR) For All Participants in Cohorts 1 and 3

The Objective Response Rate (ORR) was defined as the percentage of participants in the analysis population who had a Complete Response (CR: Disappearance of all target lesions) or Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions) per Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST 1.1) as assessed by central radiology review. The percentage of all participants (regardless of programmed death-ligand 1 [PD-L1] tumor status) in Cohorts 1 and 3 who had a CR or PR during first course pembrolizumab treatment per protocol, is presented. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionPercentage of Participants (Number)
Cohort 1: Pembrolizumab Monotherapy, Previously Treated11.6
Cohort 3: Pembrolizumab Monotherapy, Treatment Naive, PD-L1 Positive22.6

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Objective Response Rate For PD-L1 Positive Participants in Cohort 2

The ORR was defined as the percentage of participants in the analysis population who had a CR or PR (CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of diameters of target lesions) per RECIST 1.1, as assessed by central radiology review. The percentage of participants in Cohort 2 with PD-L1+ tumor status who experienced a CR or PR during first course pembrolizumab treatment per protocol, is presented. (NCT02335411)
Timeframe: Up to approximately 75 months

InterventionPercentage of Participants (Number)
Cohort 2: Pembrolizumab Combination Therapy, Treatment Naive73.3

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Overall Response Rate (ORR)

"ORR = Complete response + partial response~Target lesions~Complete Response (CR): Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~Partial Response (PR): At least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters.~Non target lesions *Complete Response (CR): Disappearance of all non-target lesions and normalization of tumor marker level. All lymph nodes must be non-pathological in size (<10 mm short axis)." (NCT02352831)
Timeframe: Up to 18 months

InterventionParticipants (Count of Participants)
Phase I (Tosedostat + Capecitabine)0
Phase II (Tosedostat + Capecitabine)0

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Number of Participants With a CA19-9 Response

"CA19-9 is a tumor marker that is used in the management of pancreatic cancer. Rising CA19-9 levels may mean the tumor is growing and decreasing CA19-9 levels may mean the tumor is shrinking or the amount of cancer in the body is decreasing~A CA19-9 response means that the tumor marker has decreased over baseline (before treatment started) levels" (NCT02352831)
Timeframe: Completion of treatment (median treatment length 81.50 days (28.00-346.00)

InterventionParticipants (Count of Participants)
Phase I (Tosedostat + Capecitabine)6
Phase II (Tosedostat + Capecitabine)10

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Time-to-progression (TTP)

"-Progressive disease (PD)~Target lesions: At least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. (Note: the appearance of one or more new lesions is also considered progressions).~Non target lesions: Appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. Unequivocal progression should not normally trump target lesion status. It must be representative of overall disease status change, not a single lesion increase" (NCT02352831)
Timeframe: Up to 24 months

Interventiondays (Median)
Phase I (Tosedostat + Capecitabine)210.50
Phase II (Tosedostat + Capecitabine)94.50

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Overall Survival Rate (OS)

(NCT02352831)
Timeframe: Up to 1 year from completion of treatment (median treatment length 81.50 days (28.00-346.00)

InterventionParticipants (Count of Participants)
Phase I (Tosedostat + Capecitabine)3
Phase II (Tosedostat + Capecitabine)2
Phase I and Phase II (Tosedostat + Capecitabine)5

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Phase I Only: Number of Participants Who Experience Dose-limiting Toxicities (DLTs)

"Possibly/probably/definitely related to study treatment in 1st cycle (cyc)~*Grade (Gr) 4 neutropenia >7 day, Febrile neutropenia of any duration with temperature ≥ 38.5 °C, Gr 4 anemia requires transfusion therapy on more than 2 occasions in 7 days, Gr 4 thrombocytopenia~Possibly/probably/definitely related gr. 3/4 non-hematologic toxicity that occurs 1st cyc with the following EXCEPTIONS:~Gr 3 nausea/vomiting/diarrhea/anorexia <72 hours that returns to Gr 1 prior to the start of cyc 2, Gr 3 hand-foot syndrome will only be considered a DLT for patients who have received 1 week of supportive care treatment with no improvement, Gr 3 fatigue that returns to Gr 1 prior to the start of cyc 2, Gr 3 flu-like symptoms <72 hours that returns to Gr 1 prior to start of cyc 2, Gr 3 arthralgia or myalgias <72 hours that return to Gr 1 prior to the start of cyc 2, Gr 3 potassium/phosphorus/magnesium that is asymptomatic or of non-clinical significance <72 hours, Gr 3 hypoalbuminemia" (NCT02352831)
Timeframe: Completion of cycle 1 of all participants in Phase I portion of study (approximately 14 months)

InterventionParticipants (Count of Participants)
Phase I (Tosedostat + Capecitabine)1

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Progression-free Survival (PFS) Rate

"PFS is defined as the duration of time from start of treatment to time of progression or death, whichever occurs first.~Progressive disease (PD)~Target lesions: At least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. (Note: the appearance of one or more new lesions is also considered progressions).~Non target lesions: Appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. Unequivocal progression should not normally trump target lesion status. It must be representative of overall disease status change, not a single lesion increase." (NCT02352831)
Timeframe: 3 months

InterventionParticipants (Count of Participants)
Phase I (Tosedostat + Capecitabine)3
Phase II (Tosedostat + Capecitabine)8
Phase I and Phase II Combined11

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The Number of Patients With Tumor Size Reduction (Objective Response Rate)

Objective response rate is the sum of partial responses plus complete responses and will be assessed per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by CT: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions. (NCT02358863)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Chemotherapy0

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Percentage of Participants With Complete Response (CR) or Partial Response (PR) (Objective Response Rate)

Objective response rate (ORR) was defined as the percentage of randomized participants achieving a best confirmed overall response of CR or PR using Response Evaluation Criteria in Solid Tumors (RECIST v1). CR was defined as the disappearance of all target and non-target lesions. PR was defined as at least a 30% decrease in the sum of the longest diameters (LD) of target lesions, taking as reference the baseline sum LD and no progression in non-target lesions. (NCT02359058)
Timeframe: First Dose to Date of Objective Progressive Disease or Death Due to Any Cause (Up To 22 Months)

InterventionPercentage of participants (Number)
Ramucirumab + Capecitabine + Cisplatin20
Ramucirumab + S-1 + Cisplatin100
Ramucirumab + S-1 + Oxaliplatin60
Total45.5

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Pharmacokinetics (PK): Maximum Serum Concentration (Cmax) of Ramucirumab

Maximum Serum Concentration (Cmax) of Ramucirumab. (NCT02359058)
Timeframe: Day 1, Day 8, Day 43, Day 50, Day 85 and Day 92: End of Infusion

,,
Interventionmicrogram per milliliter (μg/mL) (Geometric Mean)
Day 1Day 8Day 43Day 50Day 85Day 92
Ramucirumab + Capecitabine + Cisplatin149229205273NANA
Ramucirumab + S-1 + Cisplatin139200253249272289
Ramucirumab + S-1 + Oxaliplatin137211180207NANA

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Number of Participants With Treatment Emergent Anti-Ramucirumab Antibodies (TE-ADA)

Number of participants with positive treatment emergent anti-ramucirumab antibodies was summarized by treatment group. (NCT02359058)
Timeframe: First dose to study completion plus 30-day safety follow-up (Up To 22 Months)

InterventionParticipants (Count of Participants)
Ramucirumab + Capecitabine + Cisplatin0
Ramucirumab + S-1 + Cisplatin0
Ramucirumab + S-1 + Oxaliplatin0

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Pharmacokinetics (PK): Minimum Serum Concentration (Cmin) of Ramucirumab

Minimum Serum Concentration (Cmin) of Ramucirumab. (NCT02359058)
Timeframe: Day 8, Day 22, Day 29, Day 43, Day 50, Day 64, Day 71, Day 85, Day 92 and Day 106: Pre-Dose

,,
Interventionμg/mL (Geometric Mean)
Day 8Day 22Day 29Day 43Day 50Day 64Day 71Day 85Day 92Day 106
Ramucirumab + Capecitabine + Cisplatin43.840.984.660.891.747.771.155.597.668.6
Ramucirumab + S-1 + Cisplatin51.663.910587.691.385.4109102119118
Ramucirumab + S-1 + Oxaliplatin43.241.881.668.586.281.5124NANANA

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Median PFS (Phase II)

Progressive disease is defined as at least a 20% increase in the sum of diameters of target lesions (the sum must also demonstrate an absolute increase of at least 5 mm) or the appearance of new lesions. Estimates of median PFS will be obtained with corresponding 90% confidence intervals. (NCT02393755)
Timeframe: Up to 2 years

Interventionmonths (Median)
Treatment (Capecitabine, Nintedanib)3.4

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Median OS (Phase II)

Overall survival is defined as time from date of subject enrollment to the date of death due to any cause. Estimates of median OS will be obtained with corresponding 90% confidence intervals. (NCT02393755)
Timeframe: From the date of enrollment to the time of death, assessed up to 2 years

Interventionmonths (Median)
Treatment (Capecitabine, Nintedanib)8.9

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To Examine the DLT

"The recommended Phase II dose is of the Nintedanib and Capecitabine combination is defined as the dose level that causes dose limiting toxicities (DLTs) in ≤ 1 out of 6 patients at highest dose level below the maximally administered dose.~Capecitabine is fixed dose at 2000 mg/m2; while Nintedanib is evaluated at 150mg (dose level 1) and 200 mg (dose level 2)." (NCT02393755)
Timeframe: At least 21 days.

Interventionmg (Number)
Treatment (Capecitabine, Nintedanib)200

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Progression Free Survival (PFS) Rate, Defined as the Proportion of Patients Who Survive Without Disease Progression Via the RECIST Version 1.1 (Phase II)

"Progressive disease is defined as at least a 20% increase in the sum of diameters of target lesions (the sum must also demonstrate an absolute increase of at least 5 mm) or the appearance of new lesions.~Will be summarized using standard Kaplan-Meier methods." (NCT02393755)
Timeframe: At 18 weeks

Interventionpercentage of participants (Number)
Treatment (Capecitabine, Nintedanib)41.7

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Objective Response Rate

Overall Response is defined as Complete Response: Disappearance of all target lesions and any lymph nodes must have a reduction in short axis to < 10 mm; or Partial Response: At least a 30% decrease in the sum of diameters of target lesions; or Stable Disease: Neither sufficient shrinkage to qualify for partial response, nor sufficient increase to qualify for progressive disease. (NCT02393755)
Timeframe: After every 3 cycles (9 weeks) of therapy.

Interventionpercentage of participants (Number)
Treatment (Capecitabine, Nintedanib)58.3

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3-year Overall Survival (OS) Rate in Basal-Subtype Patients

OS was defined as time from randomization to death from any cause. Patient alive were censored at date of known alive. The 3-year OS rate was estimated using Kaplan-Meier method. (NCT02445391)
Timeframe: Assessed every 3 months within 2 years from randomization, every 6 months if 2-3 years

Interventionpercentage of participants (Number)
Arm B (Cisplatin or Carboplatin) (Enrolled While Arm C Was Open)57.8
Arm C (Capecitabine) (Open to Accrual 6/22/2016)66.2

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Proportion of Basal Subtype

Proportion of basal subtype was calculated as number of patients who had basal subtype disease divided by all triple-negative breast cancers who were randomized to arms B and C after 6/22/2016 and had intrinsic subtype results. (NCT02445391)
Timeframe: Assessed at registration to step 0 (baseline)

Interventionpercentage of participants (Number)
All Patients Concurrently Randomized to Arms B and C78

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3-year Recurrence-Free Survival (RFS) Rate in Basal-Subtype Patients

RFS was defined as time from randomization to local/regional recurrence, distant recurrence or death, whichever occurred first. Cases with incomplete follow up or without adequate disease evaluations were censored at the date last documented to be free of RFS events. 3-year RFS rate was estimated using Kaplan-Meier method. (NCT02445391)
Timeframe: No mandatory timeline, assessed at any time as a standard of care procedure or at the investigator's discretion; data reported every 3 months within 2 years from randomization, every 6 months if 2-3 years.

Interventionpercentage of participants (Number)
Arm B (Cisplatin or Carboplatin) (Enrolled While Arm C Was Open)46.2
Arm C (Capecitabine) (Open to Accrual 6/22/2016)49.3

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3-year Invasive Disease-Free Survival (IDFS) Rate in Basal-Subtype Patients

IDFS was defined to be time from randomization to the earliest of documented disease recurrence (local, regional and/or distant), invasive contralateral breast cancer, invasive any other second cancer, or death. Cases with incomplete follow up or without adequate disease evaluations were censored at the date last documented to be free of IDFS events. 3-year IDFS rate was estimated using Kaplan-Meier method. (NCT02445391)
Timeframe: No mandatory timeline, assessed at any time as a standard of care procedure or at the investigator's discretion; data reported every 3 months within 2 years from randomization, every 6 months if 2-3 years.

Interventionpercentage of participants (Number)
Arm B (Cisplatin or Carboplatin) (Enrolled While Arm C Was Open)42.0
Arm C (Capecitabine) (Open to Accrual 6/22/2016)49.4

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Progression-free Survival

Progression free survival (PFS) is defined as the time from the date of randomization to the date of disease progression or death resulting from any cause, whichever comes first. Progression is defined according to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. The median and 95% confidence intervals are estimated using the Kaplan-Meier estimator. (NCT02485834)
Timeframe: Up to 3 years

Interventionmonths (Median)
Randomized PatientsNA

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Overall Survival

Overall survival is defined as the time from date of randomization to death due to any cause. (NCT02485834)
Timeframe: Up to 3 years

Interventionmonths (Median)
Randomized PatientsNA

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Number of Patients Had Pathologic Complete Response

The number of patients had pathologic complete response (pCR). (pCR is defined as no gross or microscopic tumor identified with the surgical specimen. All lymph nodes should be free of tumor to document a PCR. If no gross tumor is visible, section around the area of inflammation (nodularity) should be made every 2-3 cm and specimens examined.) (NCT02485834)
Timeframe: Up to 3 years

InterventionParticipants (Count of Participants)
Randomized Patients4

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Number of Patients Achieved R0 Resection During Surgery

The number of patients achieved R0 resection during surgery (NCT02485834)
Timeframe: At time of surgery

InterventionParticipants (Count of Participants)
Randomized Patients3

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Number of Participants Who Reported Grade 3 or Higher Adverse Events

The number of patients who reported grade 3 or higher Adverse Events according to Common Terminology Criteria for Adverse Events version 4.0. (NCT02485834)
Timeframe: Up to 30 days after completion of protocol treatment

InterventionParticipants (Count of Participants)
Randomized Patients3

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Pembro Mono vs SOC: PFS Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)

"PFS was defined as the time from randomization to the first documented PD per RECIST 1.1 based on BICR, or death due to any cause, whichever occurred first. Per RECIST 1.1, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum had to demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD.~Per protocol, PFS in the pembro mono arm was compared to the SOC arm as a pre-specified secondary analysis of the ITT population. PFS is reported here for all participants in the pembro mono arm and SOC arm who were PD-L1 CPS ≥1 (all participants). Per protocol, PFS was compared separately between CPS ≥1 participants of the pembro combo arm and SOC arm and is presented earlier in the record." (NCT02494583)
Timeframe: Up to approximately 42 months

InterventionMonths (Median)
Pembrolizumab Monotherapy (Pembro Mono)2.0
Placebo + SOC Chemotherapy (SOC)6.4

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Pembro Mono vs SOC: OS in Participants With PD-L1 CPS ≥10

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the final analysis were censored at the date of the last follow-up. Per protocol, OS in the pembro mono arm was compared to the SOC arm as a pre-specified primary analysis of the ITT population. OS is reported here for all participants in the pembro mono arm and SOC arm who were PD-L1 CPS ≥10. Per protocol, OS was compared separately between CPS ≥10 participants of the pembro combo arm and SOC arm and is presented earlier in the record. (NCT02494583)
Timeframe: Up to approximately 42 months

InterventionMonths (Median)
Pembrolizumab Monotherapy (Pembro Mono)17.4
Placebo + SOC Chemotherapy (SOC)10.8

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Pembro Combo vs SOC: Objective Response Rate (ORR) Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)

ORR was defined as the percentage of participants in the analysis population who have a Complete Response (CR: disappearance of all target lesions) or a Partial Response (PR: ≥30% decrease in the sum of diameters of target lesions) per RECIST 1.1. based upon BICR. Per protocol, ORR in the pembro combo arm was compared to the SOC arm as a pre-specified secondary analysis of the ITT population. The percentage of participants who experienced CR or PR is reported here as the ORR for all participants in the pembro combo arm and SOC arm who were PD-L1 CPS ≥1 (all participants). Per protocol, ORR was compared separately between CPS ≥1 participants of the pembro mono arm and SOC arm and is presented later in the record. (NCT02494583)
Timeframe: Up to approximately 42 months

InterventionPercentage of Participants (Number)
Pembrolizumab + SOC Chemotherapy (Pembro Combo)48.6
Placebo + SOC Chemotherapy (SOC)37.2

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Pembro Mono vs SOC: OS in Participants With PD-L1 CPS ≥1 (All Participants)

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the final analysis were censored at the date of the last follow-up. Per protocol, OS in the pembro mono arm was compared to the SOC arm as a pre-specified primary analysis of the ITT population. OS is reported here for all participants in the pembro mono arm and SOC arm who were PD-L1 CPS ≥1 (all participants). Per protocol, OS was compared separately between CPS ≥1 participants of the pembro combo arm and SOC arm and is presented earlier in the record. (NCT02494583)
Timeframe: Up to approximately 42 months

InterventionMonths (Median)
Pembrolizumab Monotherapy (Pembro Mono)10.6
Placebo + SOC Chemotherapy (SOC)11.1

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Pembro Mono vs SOC: ORR Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)

ORR was defined as the percentage of participants in the analysis population who have a CR (disappearance of all target lesions) or PR (≥30% decrease in the sum of diameters of target lesions) per RECIST 1.1. based upon BICR. Per protocol, ORR in the pembro mono arm was compared to the SOC arm as a pre-specified secondary analysis of the ITT population. The percentage of participants who experienced CR or PR is reported here as the ORR for all participants in the pembro mono arm and SOC arm who were PD-L1 CPS ≥1 (all participants). Per protocol, ORR was compared separately between CPS ≥1 participants of the pembro combo arm and SOC arm and is presented earlier in the record. (NCT02494583)
Timeframe: Up to approximately 42 months

InterventionPercentage of Participants (Number)
Pembrolizumab Monotherapy (Pembro Mono)14.8
Placebo + SOC Chemotherapy (SOC)37.2

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Pembro Mono vs SOC: DOR Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)

For participants who demonstrated a confirmed CR (disappearance of all target lesions) or PR (≥30% decrease in the sum of diameters of target lesions) per RECIST 1.1 based upon BICR, DOR was defined as the time from first documented evidence of confirmed CR or PR until PD or death, whichever occurred first. DOR for participants who had not progressed or died at the time of analysis was censored at the date of their last tumor assessment. Per RECIST 1.1, PD was defined as at least a 20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum had to demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD. DOR is reported here for all participants in the pembro mono arm and SOC arm who were PD-L1 CPS ≥1 (all participants) and had CR or PR. Per protocol, DOR was compared separately between CPS ≥1 responders of the pembro combo arm and SOC arm and is presented earlier in the record. (NCT02494583)
Timeframe: Up to approximately 42 months

InterventionMonths (Median)
Pembrolizumab Monotherapy (Pembro Mono)NA
Placebo + SOC Chemotherapy (SOC)NA

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Pembro Mono vs SOC: Change From Baseline to Week 18 in the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Core 30 (QLQ-C30) Global Health Status/Quality of Life (Items 29 and 30) Combined Score

"The EORTC-QLQ-C30 is a 30-item questionnaire developed to assess the quality of life of cancer patients. Participant responses to the Global Health Status (GHS) question How would you rate your overall health during the past week? (Item 29) and the Quality of Life (QoL) question How would you rate your overall quality of life during the past week? (Item 30) were scored on a 7-point scale (1=Very Poor to 7=Excellent). Using linear transformation, raw scores were standardized so that scores ranged from 0 to 100, with a higher score indicating a better overall outcome. Per protocol, change from baseline to Week 18 in the GHS/QoL combined score was compared between all participants of the pembro mono arm and the SOC arm as a pre-specified secondary analysis. As specified by the protocol, change from baseline to Week 18 in the GHS/QoL combined score was compared separately between all participants of the pembro combo arm and SOC arm and is presented later in the record." (NCT02494583)
Timeframe: Baseline, Week 18

InterventionScore on a Scale (Least Squares Mean)
Pembrolizumab Monotherapy (Pembro Mono)-1.91
Placebo + SOC Chemotherapy (SOC)-1.75

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Pembro Combo vs. SOC: Change From Baseline to Week 18 in EORTC QLQ-STO22 Pain Symptom Subscale Score

EORTC-QLQ-STO22 is a 22-item questionnaire developed to assess QoL of gastric cancer participants. It consists of 5 multi-item subscales that assess dysphagia (3 items), dietary restriction (4 items), pain (4 items), upper gastro-esophageal symptoms (3 items), and emotional problems (3 items), and questions on dry mouth, taste, body image, and hair loss. Participant responses to the Pain symptom subscale (Items 34-37) were scored on a 4-point scale (1=Not at all to 4=Very much). Raw scores were standardized by linear transformation so that scores ranged from 0 to 100, with a higher score indicating more problems. Per protocol, change from baseline to Week 18 in the EORTC-QLQ-STO22 Pain score was compared between the pembro combo arm and the SOC arm as a pre-specified secondary analysis. As specified by the protocol, change from baseline to Week 18 in the EORTC-QLQ-STO22 Pain score was compared separately between the pembro mono arm and SOC arm and is presented earlier in the record. (NCT02494583)
Timeframe: Baseline, Week 18

InterventionScore on a Scale (Least Squares Mean)
Pembrolizumab + SOC Chemotherapy (Pembro Combo)-10.12
Placebo + SOC Chemotherapy (SOC)-3.56

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Pembro Combo vs SOC: Progression Free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) by Blinded Independent Central Review (BICR) in Participants With PD-L1 CPS ≥1 (All Participants)

"PFS was defined as the time from randomization to the first documented progressive disease (PD) per RECIST 1.1 based on BICR, or death due to any cause, whichever occurred first. Per RECIST 1.1, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum had to demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD.~Per protocol, PFS in the pembro combo arm was compared to the SOC arm as a pre-specified primary analysis of the Intent-To-Treat (ITT) population. PFS is reported here for all participants in the pembro combo arm and SOC arm who were PD-L1 CPS ≥1 (all participants). Per protocol, PFS was compared separately between CPS ≥1 participants of the pembro mono arm and SOC arm and is presented later in the record." (NCT02494583)
Timeframe: Up to approximately 36 months

InterventionMonths (Median)
Pembrolizumab + SOC Chemotherapy (Pembro Combo)6.9
Placebo + SOC Chemotherapy (SOC)6.4

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Pembro Combo vs SOC: Overall Survival (OS) in Participants With PD-L1 CPS ≥1 (All Participants)

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the final analysis were censored at the date of the last follow-up. Per protocol, OS in the pembro combo arm was compared to the SOC arm as a pre-specified primary analysis of the ITT population. OS is reported here for all participants in the pembro combo arm and SOC arm who were PD-L1 CPS ≥1 (all participants). Per protocol, OS was compared separately between CPS ≥1 participants of the pembro mono arm and SOC arm and is presented later in the record. (NCT02494583)
Timeframe: Up to approximately 42 months

InterventionMonths (Median)
Pembrolizumab + SOC Chemotherapy (Pembro Combo)12.5
Placebo + SOC Chemotherapy (SOC)11.1

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Number of Participants Discontinuing Study Treatment Due to an AE

An AE was defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which did not necessarily have a causal relationship with this treatment. An AE could therefore be any unfavourable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the medicinal product or protocol-specified procedure. Any worsening of a pre-existing condition that was temporally associated with the use of the Sponsor's product was also an adverse event. The number of participants who discontinued study treatment due to an AE was reported for each arm according to the treatment received. (NCT02494583)
Timeframe: Up to approximately 30 months

InterventionParticipants (Count of Participants)
Pembrolizumab Monotherapy (Pembro Mono)29
Pembrolizumab + SOC Chemotherapy (Pembro Combo)85
Placebo + SOC Chemotherapy (SOC)58

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Pembro Combo vs SOC: OS in Participants With PD-L1 CPS ≥10

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the final analysis were censored at the date of the last follow-up. Per protocol, OS in the pembro combo arm was compared to the SOC arm as a pre-specified primary analysis of the ITT population. OS is reported here for all participants in the pembro combo arm and SOC arm who were PD-L1 CPS ≥10. Per protocol, OS was compared separately between CPS ≥10 participants of the pembro mono arm and SOC arm and is presented later in the record. (NCT02494583)
Timeframe: Up to approximately 42 months

InterventionMonths (Median)
Pembrolizumab + SOC Chemotherapy (Pembro Combo)12.3
Placebo + SOC Chemotherapy (SOC)10.8

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Number of Participants Experiencing an Adverse Event (AE)

An AE was defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which did not necessarily have a causal relationship with this treatment. An AE could therefore be any unfavourable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the medicinal product or protocol-specified procedure. Any worsening of a pre-existing condition that was temporally associated with the use of the Sponsor's product was also an adverse event. The number of participants who experienced an AE was reported for each arm according to the treatment received. (NCT02494583)
Timeframe: Up to approximately 33 months

InterventionParticipants (Count of Participants)
Pembrolizumab Monotherapy (Pembro Mono)242
Pembrolizumab + SOC Chemotherapy (Pembro Combo)244
Placebo + SOC Chemotherapy (SOC)240

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Pembro Combo vs SOC: Change From Baseline to Week 18 in the EORTC QLQ-C30 Global Health Status/Quality of Life (Items 29 and 30) Combined Score

"The EORTC-QLQ-C30 is a 30-item questionnaire developed to assess the quality of life of cancer patients. Participant responses to the GHS question How would you rate your overall health during the past week? (Item 29) and the QoL question How would you rate your overall quality of life during the past week? (Item 30) were scored on a 7-point scale (1=Very Poor to 7=Excellent). Using linear transformation, raw scores were standardized so that scores ranged from 0 to 100, with a higher score indicating a better overall outcome. Per protocol, change from baseline to Week 18 in the GHS/QoL combined score was compared between all participants of the pembro combo arm and the SOC arm as a pre-specified secondary analysis. As specified by the protocol, change from baseline to Week 18 in the GHS/QoL combined score was compared separately between all participants of the pembro mono arm and SOC arm and is presented earlier in the record." (NCT02494583)
Timeframe: Baseline, Week 18

InterventionScore on a Scale (Least Squares Mean)
Pembrolizumab + SOC Chemotherapy (Pembro Combo)-0.09
Placebo + SOC Chemotherapy (SOC)-2.07

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Pembro Combo vs SOC: Duration of Response (DOR) Per RECIST 1.1 by BICR in Participants With PD-L1 CPS ≥1 (All Participants)

For participants who demonstrated a confirmed CR (disappearance of all target lesions) or PR (at least a 30% decrease in the sum of diameters of target lesions) per RECIST 1.1 based upon BICR, DOR was defined as the time from first documented evidence of confirmed CR or PR until PD or death, whichever occurred first. DOR for participants who had not progressed or died at the time of analysis was censored at the date of their last tumor assessment. Per RECIST 1.1, PD was defined as at least a 20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum had to demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD. DOR is reported here for all participants in the pembro combo arm and SOC arm who were PD-L1 CPS ≥1 (all participants) and had CR or PR. Per protocol, DOR was compared separately between CPS ≥1 responders of the pembro mono arm and SOC arm and is presented later in the record. (NCT02494583)
Timeframe: Up to approximately 42 months

InterventionMonths (Median)
Pembrolizumab + SOC Chemotherapy (Pembro Combo)NA
Placebo + SOC Chemotherapy (SOC)NA

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Pembro Mono vs. SOC: Change From Baseline to Week 18 in EORTC QLQ-Module for Gastric Cancer (STO22) Pain Symptom Subscale Score

EORTC-QLQ-STO22 is a 22-item questionnaire developed to assess QoL of gastric cancer participants. It consists of 5 multi-item subscales that assess dysphagia (3 items), dietary restriction (4 items), pain (4 items), upper gastro-esophageal symptoms (3 items), and emotional problems (3 items), and questions on dry mouth, taste, body image, and hair loss. Participant responses to the Pain symptom subscale (Items 34-37) were scored on a 4-point scale (1=Not at all to 4=Very much). Raw scores were standardized by linear transformation so that scores ranged from 0 to 100, with a higher score indicating more problems. Per protocol, change from baseline to Week 18 in the EORTC-QLQ-STO22 Pain score was compared between the pembro mono arm and the SOC arm as a pre-specified secondary analysis. As specified by the protocol, change from baseline to Week 18 in the EORTC-QLQ-STO22 Pain score was compared separately between the pembro combo arm and SOC arm and is presented later in the record. (NCT02494583)
Timeframe: Baseline, Week 18

InterventionScore on a Scale (Least Squares Mean)
Pembrolizumab Monotherapy (Pembro Mono)-1.14
Placebo + SOC Chemotherapy (SOC)-3.49

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Maximum Plasma Concentration of Capecitabine and it's Metabolites When Given Alone and in Combination With Pertuzumab

Capecitabine is an oral fluoropyrimidine carbamate that is preferentially converted to the cytotoxic moiety 5-FU in target tumour tissue through a series of 3 metabolic steps through the intermediate metabolites 5'-DFCR, 5'-DFUR, and FBAL. Cmax refers to the maximum (or peak) serum concentration that a drug achieves in a specified compartment or test area of the body after the drug has been administrated and prior to the administration of a second dose and is measures as nanograms per milliliter (ng/mL). (NCT02494596)
Timeframe: Day -7: Predose, 30 minutes, 1, 2, 3, 4, 5, 6 and 10 hours postdose; Cycle 1 Day 1: Predose, 0 and 30 minutes, 1, 2, 3, 4, 5, 6 and 10 hours Postdose

,,
Interventionng/mL (Mean)
Capecitabine Alone 5'-DFCRCapecitabine Alone 5'-DFURCapecitabine Alone 5-FUCapecitabine Alone CapecitabineCapecitabine Alone FBALCapecitabine + Pertuzumab 5'-DFCRCapecitabine + Pertuzumab 5'-DFURCapecitabine + Pertuzumab 5-FUCapecitabine + Pertuzumab CapecitabineCapecitabine + Pertuzumab FBAL
Capecitabine 1000 + Pertuzumab 105076877657355911239633917410318733673498
Capecitabine 1250 + Pertuzumab 1050864710311369754352906569868334547315136
Capecitabine 825 + Pertuzumab 105045085274201480232144909573621980603674

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Plasma Half-Life of Capecitabine and it's Metabolites When Given Alone and in Combination With Pertuzumab

Capecitabine is a novel oral fluoropyrimidine carbamate that is preferentially converted to the cytotoxic moiety fluorouracil (5-fluorouracil; 5-FU) in target tumour tissue through a series of 3 metabolic steps through the intermediate metabolites 5'-deoxy-5-fluorocytidine (5'-DFCR), 5'-deoxy-5-fluorouridine (5'-DFUR), and α-fluoro-β-alanine (FBAL). The biological half-life or terminal half-life is the time in days it takes for it to lose half of its pharmacologic activity. (NCT02494596)
Timeframe: Day -7: Predose, 30 minutes, 1, 2, 3, 4, 5, 6 and 10 hours postdose; Cycle 1 Day 1: Predose, 0 and 30 minutes, 1, 2, 3, 4, 5, 6 and 10 hours Postdose

,,
Interventionhours (Mean)
Capecitabine Alone 5'-DFCRCapecitabine Alone 5'-DFURCapecitabine Alone 5-FUCapecitabine Alone CapecitabineCapecitabine Alone FBALCapecitabine + Pertuzumab 5'-DFCRCapecitabine + Pertuzumab 5'-DFURCapecitabine + Pertuzumab 5-FUCapecitabine + Pertuzumab CapecitabineCapecitabine + Pertuzumab FBAL
Capecitabine 1000 + Pertuzumab 10500.820.760.640.402.690.760.730.670.622.58
Capecitabine 1250 + Pertuzumab 10500.820.660.700.363.080.750.790.800.542.81
Capecitabine 825 + Pertuzumab 10500.890.750.670.542.540.780.620.730.422.59

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Time to Maximum Plasma Concentration of Capecitabine and it's Metabolites When Given Alone and in Combination With Pertuzumab

Capecitabine is a novel oral fluoropyrimidine carbamate that is preferentially converted to the cytotoxic moiety fluorouracil (5-fluorouracil; 5-FU) in target tumour tissue through a series of 3 metabolic steps through the intermediate metabolites 5'-deoxy-5-fluorocytidine (5'-DFCR), 5'-deoxy-5-fluorouridine (5'-DFUR), and α-fluoro-β-alanine (FBAL). Tmax is defined as the time after administration of a drug when the maximum plasma concentration is reached; when the rate of absorption equals the rate of elimination. (NCT02494596)
Timeframe: Day -7: Predose, 30 minutes, 1, 2, 3, 4, 5, 6 and 10 hours postdose; Cycle 1 Day 1: Predose, 0 and 30 minutes, 1, 2, 3, 4, 5, 6 and 10 hours Postdose

,,
Interventionhours (Mean)
Capecitabine Alone 5'-DFCRCapecitabine Alone 5'-DFURCapecitabine Alone 5-FUCapecitabine Alone CapecitabineCapecitabine Alone FBALCapecitabine + Pertuzumab 5'-DFCRCapecitabine + Pertuzumab 5'-DFURCapecitabine + Pertuzumab 5-FUCapecitabine + Pertuzumab CapecitabineCapecitabine + Pertuzumab FBAL
Capecitabine 1000 + Pertuzumab 10500.820.760.640.42.691.422.01.841.173.16
Capecitabine 1250 + Pertuzumab 10501.051.051.050.772.211.861.861.931.152.50
Capecitabine 825 + Pertuzumab 10501.31.31.31.22.40.91.00.90.72.6

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AUC From Time Zero to Infinity (AUC 0-infinity) of Pertuzumab

The AUC0-infinity is calculated from time 0 (prior to administration of medication) to infinity (the time of complete elimination of the drug). The AUC is of particular use in estimating the bioavailability of drugs, by measuring the extent of absorption. AUC is measured as nanograms times days per milliliter (ng*day/mL). (NCT02494596)
Timeframe: Cycle 1: Days 2, 5, 8 and 15 Postdose; Cycle 2: Day 1 at drug administration, predose and 15 minutes postdose, and predose on Days 8, 15 and 22

Interventionng*day/mL (Mean)
Capecitabine + Pertuzumab4096501

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Apparent Total Clearance of Pertuzumab

Clearance (expressed as volume/time) describes the removal of drug from a volume of plasma in a given unit of time (drug loss from the body). It is measured as milliliters per day (mL/day). (NCT02494596)
Timeframe: Cycle 1: Days 2, 5, 8 and 15 Postdose; Cycle 2: Day 1 at drug administration, predose and 15 minutes postdose, and predose on Days 8, 15 and 22

InterventionmL/day (Mean)
Capecitabine + Pertuzumab283.0

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Apparent Volume of Distribution of Pertuzumab

The volume of distribution at steady state (Vss), also known as apparent volume of distribution, is a pharmacological, theoretical volume that the total amount of administered drug would have to occupy (if it were uniformly distributed), to provide the same concentration as it currently is in blood plasma. Vss was measured in mL (NCT02494596)
Timeframe: Cycle 1: Days 2, 5, 8 and 15 Postdose; Cycle 2: Day 1 at drug administration, predose and 15 minutes postdose, and predose on Days 8, 15 and 22

InterventionmL (Mean)
Capecitabine + Pertuzumab5202

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Area Under the Concentration Curve From Time Zero to Last Measurement (AUC 0-last) of Pertuzumab

The area under the plot of plasma concentration of drug against time after drug administration is defined as the area under the curve (AUC). The AUC0-last is calculated from time 0 (prior to administration of medication) to last measured data point. The AUC is of particular use in estimating the bioavailability of drugs, by measuring the extent of absorption. AUC was measured as ng*day/mL. (NCT02494596)
Timeframe: Cycle 1: Days 2, 5, 8 and 15 Postdose; Cycle 2: Day 1 at drug administration, predose and 15 minutes postdose, and predose on Days 8, 15 and 22

Interventionng*day/mL (Mean)
Capecitabine + Pertuzumab2742561

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Maximum Plasma Concentration (Cmax) of Pertuzumab

Cmax refers to the maximum (or peak) serum concentration that a drug achieves in a specified compartment or test area of the body after the drug has been administrated and prior to the administration of a second dose and was measured as nanograms per milliliter (ng/mL). (NCT02494596)
Timeframe: Cycle 1: Days 2, 5, 8 and 15 Postdose; Cycle 2: Day 1 at drug administration, predose and 15 minutes postdose, and predose on Days 8, 15 and 22

Interventionng/mL (Mean)
Capecitabine + Pertuzumab355111

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Maximum Tolerated Dose (MTD) of the Combination of Pertuzumab and Capecitabine

MTD was defined as the highest tolerated dose combination of capecitabine (825 mg, 1000 mg or 1250 mg) and pertuzumab, without causing Dose Limiting Toxicities (DLTs). DLTs were defined as follows: 1) Any non-hematological toxicity greater than or equal to (≥) Grade 3 according to Common Terminology Criteria for Adverse Events (CTCAE) version 3.0 except for fever, chills and flu-like symptoms, in spite of adequate toxicity management; 2) Grade 4 neutropenia lasting > 7 days; 3) Febrile neutropenia; 4) Thrombocytopenia Grade 4 or any thrombocytopenia requiring platelet transfusion; 5) Any subjectively intolerable toxicity felt by the investigator to be related to either one of the compounds. Participants who withdrew from the study without completing the first treatment cycle for reasons other than DLT were not considered evaluable for DLT. MTD was measured in mg/m^2. (NCT02494596)
Timeframe: Cycle 1 (3 Weeks)

Interventionmg/m^2 (Number)
Capecitabine + Pertuzumab1250

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Percentage of Participants With DLTs

DLTs were defined as follows: 1)Any non-hematological toxicity greater than or equal to (≥) Grade 3 according to Common Terminology Criteria for Adverse Events (CTCAE) version 3.0 except for fever, chills and flu-like symptoms, in spite of adequate toxicity management; 2) Grade 4 neutropenia lasting > 7 days; 3) Febrile neutropenia; 4) Thrombocytopenia Grade 4 or any thrombocytopenia requiring platelet transfusion; 5) Any subjectively intolerable toxicity felt by the investigator to be related to either one of the compounds. Participants who withdrew from the study without completing the first treatment cycle for reasons other than DLT were not considered evaluable for DLT. (NCT02494596)
Timeframe: Cycle 1 (3 Weeks)

Interventionpercentage of participants (Number)
Capecitabine 825 Plus (+) Pertuzumab 10500.0
Capecitabine 1000 + Pertuzumab 10500.0
Capecitabine 1250 + Pertuzumab 10500.0

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Plasma Half-Life (t1/2) of Pertuzumab

The biological half-life or terminal half-life of pertuzumab is the time in days it takes for it to lose half of its pharmacologic activity. t1/2 was measured in days. (NCT02494596)
Timeframe: Cycle 1: Days 2, 5, 8 and 15 Postdose; Cycle 2: Day 1 at drug administration, predose and 15 minutes postdose, and Predose on Days 8, 15 and 22

Interventiondays (Mean)
Capecitabine + Pertuzumab14.6

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Time to Maximum Plasma Concentration (Tmax) of Pertuzumab

Tmax is defined as the time after administration of a drug when the maximum plasma concentration is reached; when the rate of absorption equals the rate of elimination. Tmax was measured in days. (NCT02494596)
Timeframe: Cycle 1: Days 2, 5, 8 and 15 Postdose; Cycle 2: Day 1 at drug administration, predose and 15 minutes postdose, and predose on Days 8, 15 and 22

Interventiondays (Mean)
Capecitabine + Pertuzumab0.137

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Overall Response Rate of Complete or Partial Response

The response rates of complete or partial response rate as defined by the Response Evaluation Criteria for Solid Tumors at 15 weeks of a chemotherapy regimen involving docetaxel and capecitabine as front line therapy at 95% confidence interval. Complete Response (CR): the disappearance of all target lesions Partial Response (PR): at least a 30% decrease in the sum of the longest diameter of target lesions, taking as reference the baseline sum longest diameter (NCT02524275)
Timeframe: At 15 weeks

InterventionParticipants (Count of Participants)
Treatment (Docetaxel, Capecitabine)1

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Progression-free Survival

The Kaplan-Meier method will be used to estimate time to event distributions for progression-free survival. Progression-free survival will be defined as from the first date of therapy until the first notation of clinical progression, relapse or death from any cause. (NCT02524275)
Timeframe: First date of therapy until the first notation of clinical progression, relapse or death from any cause, assessed up to 5 years

Interventiondays (Median)
Treatment (Docetaxel, Capecitabine)211

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Survival

The Kaplan-Meier method will be used to estimate time to event distributions for survival. Survival will be defined as from the first date of therapy until the date of death from any cause. (NCT02524275)
Timeframe: First date of therapy until the date of death from any cause, assessed up to 5 years

Interventiondays (Median)
Treatment (Docetaxel, Capecitabine)264.5

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Pathologic Complete Response for Patients With Rectal Cancer

Pathologic complete response is defined as the lack of all signs of cancer in tissue samples removed during surgery or biopsy after treatment with radiation or chemotherapy. (NCT02550743)
Timeframe: Approximately 6-10 weeks post treatment

InterventionParticipants (Count of Participants)
Dose 10
Dose 20
Dose 30
Dose -10

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Maximum Tolerated Dose of BYL719

(NCT02550743)
Timeframe: approximately 6 weeks

Interventionmg (Number)
Maximum Tolerated Dose of BYL719NA

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Overall Survival in Participants With Programmed Cell Death Ligand 1 (PD-L1) With Combined Positive Score (CPS) ≥10

Overall survival (OS) was defined as the time from randomization to death due to any cause. (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionMonths (Median)
Pembrolizumab12.7
Chemotherapy11.6

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Overall Survival in Participants With PD-L1 CPS ≥1

Overall survival (OS) was defined as the time from randomization to death due to any cause. (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionMonths (Median)
Pembrolizumab10.7
Chemotherapy10.2

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Number of Participants Who Experienced One or More Adverse Events

An adverse event (AE) is any untoward medical occurrence in a study participant administered a pharmaceutical product that does not necessarily have to have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product, whether or not related to the medicinal product. (NCT02555657)
Timeframe: Up to approximately 60 months

InterventionParticipants (Count of Participants)
Pembrolizumab285
Chemotherapy281

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Progression-Free Survival Per RECIST 1.1 in Participants With PD-L1 CPS ≥10

Progression-Free Survival (PFS), based on BICR assessment per RECIST 1.1, was defined as the time from randomization to the first documented progressive disease (PD) or death due to any cause, whichever occurred first. Per RECIST 1.1, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD. (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionMonths (Median)
Pembrolizumab2.1
Chemotherapy3.4

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Progression-Free Survival Per RECIST 1.1 in Participants With PD-L1 CPS ≥1

Progression-Free Survival (PFS), based on BICR assessment per RECIST 1.1, was defined as the time from randomization to the first documented progressive disease (PD) or death due to any cause, whichever occurred first. Per RECIST 1.1, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD. (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionMonths (Median)
Pembrolizumab2.1
Chemotherapy3.1

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Progression-Free Survival Per RECIST 1.1 in All Participants

Progression-Free Survival (PFS), based on BICR assessment per RECIST 1.1, was defined as the time from randomization to the first documented progressive disease (PD) or death due to any cause, whichever occurred first. Per RECIST 1.1, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD. (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionMonths (Median)
Pembrolizumab2.1
Chemotherapy3.3

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Disease Control Rate Per RECIST 1.1 in All Participants

Disease Control Rate (DCR), based on BICR assessment per RECIST 1.1, was defined as the percentage of participants who had a Complete Response (CR: Disappearance of all target lesions) or Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions) or Stable Disease for at least 24 weeks (SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for Progressive Disease [PD: At least a 20% increase in the sum of diameters of target lesions and an absolute increase of at least 5 mm. The appearance of one or more new lesions was also considered PD.]) (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionPercentage of participants (Number)
Pembrolizumab12.2
Chemotherapy18.7

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Duration of Response Per RECIST 1.1 in All Participants Who Had a Confirmed Response

For participants who demonstrated a confirmed Complete Response (CR: disappearance of all target lesions) or Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions) per RECIST 1.1, Duration of Response (DOR) was defined as the time from first documented evidence of a CR or PR until progressive disease (PD) or death. DOR for participants who had not progressed or died at the time of analysis was to be censored at the date of their last tumor assessment. Per RECIST 1.1, PD was defined as at least a 20% increase in the sum of diameters of target lesions as well as an absolute increase of at least a 5 mm in the sum of diameters. The appearance of one or more new lesions was also considered PD. DOR assessments were based on BICR. (NCT02555657)
Timeframe: Up to approximately 36 months (from time of first documented evidence of CR or PR through Final Analysis database cutoff date of 11-April-2019)

InterventionMonths (Median)
Pembrolizumab12.2
ChemotherapyNA

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Disease Control Rate Per RECIST 1.1 in Participants With PD-L1 CPS ≥1

Disease Control Rate (DCR), based on BICR assessment per RECIST 1.1, was defined as the percentage of participants who had a Complete Response (CR: Disappearance of all target lesions) or Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions) or Stable Disease for at least 24 weeks (SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for Progressive Disease [PD: At least a 20% increase in the sum of diameters of target lesions and an absolute increase of at least 5 mm. The appearance of one or more new lesions was also considered PD.]) (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionPercentage of participants (Number)
Pembrolizumab14.3
Chemotherapy15.8

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Duration of Response Per RECIST 1.1 in Participants With PD-L1 CPS ≥1 Who Had a Confirmed Response

For participants with PD-L1 CPS ≥1 who demonstrated a confirmed Complete Response (CR: disappearance of all target lesions) or Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions) per RECIST 1.1, Duration of Response (DOR) was defined as the time from first documented evidence of a CR or PR until progressive disease (PD) or death. DOR for participants who had not progressed or died at the time of analysis was to be censored at the date of their last tumor assessment. Per RECIST 1.1, PD was defined as at least a 20% increase in the sum of diameters of target lesions as well as an absolute increase of at least a 5 mm in the sum of diameters. The appearance of one or more new lesions was also considered PD. DOR assessments were based on BICR. (NCT02555657)
Timeframe: Up to approximately 36 months (from time of first documented evidence of CR or PR through Final Analysis database cutoff date of 11-April-2019)

InterventionMonths (Median)
Pembrolizumab12.2
ChemotherapyNA

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Disease Control Rate Per RECIST 1.1 in Participants With PD-L1 CPS ≥10

Disease Control Rate (DCR), based on BICR assessment per RECIST 1.1, was defined as the percentage of participants who had a Complete Response (CR: Disappearance of all target lesions) or Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions) or Stable Disease for at least 24 weeks (SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for Progressive Disease [PD: At least a 20% increase in the sum of diameters of target lesions and an absolute increase of at least 5 mm. The appearance of one or more new lesions was also considered PD.]) (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionPercentage of participants (Number)
Pembrolizumab19.8
Chemotherapy17.3

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Duration of Response Per RECIST 1.1 in Participants With PD-L1 CPS ≥10 Who Had a Confirmed Response

For participants with PD-L1 CPS ≥10 who demonstrated a confirmed Complete Response (CR: disappearance of all target lesions) or Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions) per RECIST 1.1, Duration of Response (DOR) was defined as the time from first documented evidence of a CR or PR until progressive disease (PD) or death. DOR for participants who had not progressed or died at the time of analysis was to be censored at the date of their last tumor assessment. Per RECIST 1.1, PD was defined as at least a 20% increase in the sum of diameters of target lesions as well as an absolute increase of at least a 5 mm in the sum of diameters. The appearance of one or more new lesions was also considered PD. DOR assessments were based on BICR. (NCT02555657)
Timeframe: Up to approximately 36 months (from time of first documented evidence of CR or PR through Final Analysis database cutoff date of 11-April-2019)

InterventionMonths (Median)
PembrolizumabNA
Chemotherapy7.1

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Number of Participants Who Discontinued Study Treatment Due to an Adverse Event

An adverse event (AE) is any untoward medical occurrence in a study participant administered a pharmaceutical product that does not necessarily have to have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product, whether or not related to the medicinal product. (NCT02555657)
Timeframe: Up to approximately 60 months

InterventionParticipants (Count of Participants)
Pembrolizumab14
Chemotherapy16

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Overall Response Rate Per RECIST 1.1 in All Participants

Overall Response Rate (ORR), based on BICR assessment per RECIST 1.1, was defined as the percentage of participants who had a confirmed Complete Response (CR: Disappearance of all target lesions) or a Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions). (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionPercentage of participants (Number)
Pembrolizumab9.6
Chemotherapy10.6

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Overall Response Rate Per RECIST 1.1 in Participants With PD-L1 CPS ≥1

Overall Response Rate (ORR), based on BICR assessment per RECIST 1.1, was defined as the percentage of participants who had a confirmed Complete Response (CR: Disappearance of all target lesions) or a Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions). (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionPercentage of participants (Number)
Pembrolizumab12.3
Chemotherapy9.4

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Overall Response Rate Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) in Participants With PD-L1 CPS ≥10

Overall Response Rate (ORR), based on a Blinded Independent Central Review (BICR) assessment per RECIST 1.1, was defined as the percentage of participants who had a confirmed Complete Response (CR: Disappearance of all target lesions) or a Partial Response (PR: At least a 30% decrease in the sum of diameters of target lesions). (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionPercentage of participants (Number)
Pembrolizumab17.7
Chemotherapy9.2

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Overall Survival in All Participants

Overall survival (OS) was defined as the time from randomization to death due to any cause. (NCT02555657)
Timeframe: Up to approximately 36 months (through Final Analysis database cutoff date of 11-April-2019)

InterventionMonths (Median)
Pembrolizumab9.9
Chemotherapy10.8

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Time to Objective Response by the Investigator Assessment in BM-ve Population

Time to response was defined as the time from randomization to the first recorded objective response (ie, CR or PR). CR: Disappearance of all target and non-target lesions; and normalization of tumor marker levels initially above upper limits of normal; and no new lesions. PR: ≥30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD; and no new lesions. (NCT02574455)
Timeframe: From randomization to the first recorded objective response (assessed every 6 weeks for 9 months and then every 9 weeks thereafter until the occurrence of progression of disease; maximum exposure: 29.6 months)

Interventionmonths (Mean)
Sacituzumab Govitecan2.14
Treatment of Physician's Choice (TPC)2.72

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Overall Survival (OS) in ITT Population

Overall survival (OS) was defined as the time from the randomization to death from any cause. OS was estimated using Kaplan-Meier estimate. (NCT02574455)
Timeframe: From the randomization to death from any cause (maximum follow-up duration: 30.8 months)

Interventionmonths (Median)
Sacituzumab Govitecan11.8
Treatment of Physician's Choice (TPC)6.9

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Time to Progression (TTP) by IRC Assessment in BM-ve Population

Time to Progression (TTP) was defined as the time from the date of randomization to the date of the first evidence of disease progression as assessed using RECIST 1.1 criteria. The date of progression was date of the last observation or radiological assessment of target lesions that either showed a predefined increase (≥20%) in the sum of the target lesions or the appearance of new non-target lesions. Participants without progression were censored. (NCT02574455)
Timeframe: From randomization until disease progression (assessed every 6 weeks for 9 months and then every 9 weeks thereafter until the occurrence of progression of disease; maximum exposure: 29.6 months)

Interventionmonths (Median)
Sacituzumab Govitecan5.8
Treatment of Physician's Choice (TPC)2.1

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Change From Baseline in European Organization for Research and Treatment of Cancer Quality-of-Life Questionnaire Core 30 (EORTC QLQ-C30) Score

The EORTC QLQ-C30 is a questionnaire to assess quality of life (QoL), it is composed of 30 questions (items) resulting in 5 functional scales (physical functioning, role functioning, emotional functioning, cognitive functioning, social functioning), 1 global health status scale, 3 symptom scales (fatigue, nausea and vomiting, pain), and 6 single items (dyspnea, insomnia, loss of appetite, constipation, diarrhea, financial difficulties). All of the scales and single-item measures range in score from 0 to 100. Higher score for the functioning scales and global health status indicate a better quality of life; a positive change from baseline indicates improvement. Lower scores on the symptom and single-item scales indicate a better quality of life; a negative change from baseline indicates improvement. (NCT02574455)
Timeframe: Baseline; End of Treatment (EOT) (up to 29.6 months)

,
Interventionscore on a scale (Mean)
Global Health Status/QoL: BaselineGlobal Health Status/QoL: Change From Baseline at EOTPhysical Functioning: BaselinePhysical Functioning: Change From Baseline at EOTRole Functioning: BaselineRole Functioning: Change From Baseline at EOTEmotional Functioning: BaselineEmotional Functioning: Change From Baseline at EOTCognitive Functioning: BaselineCognitive Functioning: Change From Baseline at EOTSocial Functioning: BaselineSocial Functioning: Change From Baseline at EOTFatigue: BaselineFatigue: Change From Baseline at EOTNausea and Vomiting: BaselineNausea and Vomiting: Change From Baseline at EOTPain: BaselinePain: Change From Baseline at EOTDyspnoea: BaselineDyspnoea: Change From Baseline at EOTInsomnia: BaselineInsomnia: Change From Baseline at EOTAppetite Loss: BaselineAppetite Loss: Change From Baseline at EOTConstipation: BaselineConstipation: Change From Baseline at EOTDiarrhoea: BaselineDiarrhoea: Change From Baseline at EOTFinancial Difficulties: BaselineFinancial Difficulties: Change From Baseline at EOT
Sacituzumab Govitecan61.9-5.873.2-4.668.1-8.471.9-3.881.7-7.569.1-5.939.45.18.35.237.92.825.40.733.24.420.83.117.73.37.211.427.60.4
Treatment of Physician's Choice (TPC)56.4-9.471.2-13.565.1-18.868.9-3.579.5-6.169.6-10.342.114.010.37.342.56.825.05.935.6-4.325.810.019.07.06.53.622.41.1

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Time to Progression (TTP) by Investigator Assessment in BM-ve Population

Time to Progression (TTP) was defined as the time from the date of randomization to the date of the first evidence of disease progression as assessed using RECIST 1.1 criteria. The date of progression was date of the last observation or radiological assessment of target lesions that either showed a predefined increase (≥20%) in the sum of the target lesions or the appearance of new non-target lesions. Participants without progression were censored. (NCT02574455)
Timeframe: From randomization until disease progression (assessed every 6 weeks for 9 months and then every 9 weeks thereafter until the occurrence of progression of disease; maximum exposure: 29.6 months)

Interventionmonths (Median)
Sacituzumab Govitecan5.7
Treatment of Physician's Choice (TPC)1.8

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Duration of Response (DOR) by IRC and Investigator Assessment in BM-ve Population

DOR was defined as the number of days between the first date showing a documented response of CR or PR and the date of progression or death. CR: Disappearance of all target and non-target lesions; and normalization of tumor marker levels initially above upper limits of normal; and no new lesions. PR: ≥30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD; and no new lesions. The date of progression was date of the last observation or radiological assessment of target lesions that either showed a predefined increase (≥20%) in the sum of the target lesions or the appearance of new non-target lesions. (NCT02574455)
Timeframe: From the first date of documented response of CR or PR to the date of progression or death (assessed every 6 weeks for 9 months and then every 9 weeks thereafter until the occurrence of progression of disease; maximum exposure: 29.6 months)

,
Interventionmonths (Median)
IRC AssessmentInvestigator Assessment
Sacituzumab Govitecan6.36.9
Treatment of Physician's Choice (TPC)3.63.0

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Clinical Benefit Rate (CBR) by IRC and Investigator Assessment in BM-ve Population

CBR was defined as the percentage of participants with best response as either CR, PR, or stable disease (SD) with a duration of ≥6 months. CR: Disappearance of all target and non-target lesions; and normalization of tumor marker levels initially above upper limits of normal; and no new lesions. PR: ≥30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD; and no new lesions. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD), taking as reference the smallest sum LD since the treatment started; and Persistence of one or more non-target lesion(s) or/and maintenance of tumor marker level above the normal limits. PD: ≥20% increase in the sum of LD of target lesions, taking as reference the smallest sum LD recorded since treatment started or appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. (NCT02574455)
Timeframe: From randomization to the date of progression or death (assessed every 6 weeks for 9 months and then every 9 weeks thereafter until the occurrence of progression of disease; maximum exposure: 29.6 months)

,
Interventionpercentage of participants (Number)
IRC AssessmentInvestigator Assessment
Sacituzumab Govitecan44.745.5
Treatment of Physician's Choice (TPC)8.610.3

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Overall Survival (OS) in BM-ve Population

Overall survival (OS) was defined as the time from the randomization to death from any cause. OS was estimated using Kaplan-Meier estimate. (NCT02574455)
Timeframe: From the randomization to death from any cause (maximum follow-up duration: 30.8 months)

Interventionmonths (Median)
Sacituzumab Govitecan12.1
Treatment of Physician's Choice (TPC)6.7

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Time to Objective Response by the IRC Assessment in BM-ve Population

Time to response was defined as the time from randomization to the first recorded objective response (ie, CR or PR). CR: Disappearance of all target and non-target lesions; and normalization of tumor marker levels initially above upper limits of normal; and no new lesions. PR: ≥30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD; and no new lesions. (NCT02574455)
Timeframe: From randomization to the first recorded objective response (assessed every 6 weeks for 9 months and then every 9 weeks thereafter until the occurrence of progression of disease; maximum exposure: 29.6 months)

Interventionmonths (Mean)
Sacituzumab Govitecan2.67
Treatment of Physician's Choice (TPC)1.86

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Progression-Free Survival (PFS) by Independent Review Committee (IRC) Assessment in Brain Metastasis Negative (BM-ve) Population

PFS was defined as the time from randomization until objective tumor progression by Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 or death, whichever came first. The date of progression was date of the last observation or radiological assessment of target lesions that either showed a predefined increase (greater than or equal to [≥] 20%) in the sum of the target lesions or the appearance of new non-target lesions. PFS was estimated using Kaplan-Meier estimate. (NCT02574455)
Timeframe: From randomization until objective tumor progression or death (assessed every 6 weeks for 9 months and then every 9 weeks thereafter until the occurrence of progression of disease; maximum exposure: 29.6 months)

Interventionmonths (Median)
Sacituzumab Govitecan5.6
Treatment of Physician's Choice (TPC)1.7

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Progression-Free Survival (PFS) by IRC Assessment in the ITT Population

PFS was defined as the time from randomization until objective tumor progression by RECIST v1.1 or death, whichever came first. The date of progression was date of the last observation or radiological assessment of target lesions that either showed a predefined increase (≥20%) in the sum of the target lesions or the appearance of new non-target lesions. PFS was estimated using Kaplan-Meier estimate. (NCT02574455)
Timeframe: From randomization until objective tumor progression or death (assessed every 6 weeks for 9 months and then every 9 weeks thereafter until the occurrence of progression of disease; maximum exposure: 29.6 months)

Interventionmonths (Median)
Sacituzumab Govitecan4.8
Treatment of Physician's Choice (TPC)1.7

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Percentage of Participants Experiencing the Worst Laboratory Abnormalities Grade 3 or 4 Post-Baseline

Blood samples were collected for hematology, serum chemistry and the laboratory abnormalities were assessed. The most severe graded abnormality observed post-baseline for each graded test was counted for each participant. Safety as assessed by grading of laboratory values and AEs according to the National Cancer Institutes' Common Terminology Criteria for Adverse Events (NCI CTCAE) covering grades 0-5 (0=Normal, 1=Mild, 2=Moderate, 3=Severe, 4=Life-threatening, 5=Death). The percentage of participants with worst postbaseline grades 3 or 4 are reported. (NCT02574455)
Timeframe: First dose date up to last follow-up (maximum up to 30.8 months)

,
Interventionpercentage of participants (Number)
AnemiaLymphocyte Count DecreasedNeutrophil Count DecreasedPlatelet Count DecreasedWhite Blood Cell DecreasedAlanine Aminotransferase IncreasedAlkaline Phosphatase IncreasedAspartate Aminotransferase IncreasedBlood Bilirubin IncreasedCreatinine IncreasedHypercalcemiaHyperglycemiaHyperkalemiaHypermagnesemiaHypernatremiaHypoalbumenemiaHypocalcemiaHypoglycemiaHypokalemiaHypomagnesemiaHyponatremiaHypophosphatemia
Sacituzumab Govitecan8.933.348.81.241.11.23.13.51.90.403.10.80.400.81.60.44.30.83.98.1
Treatment of Physician's Choice (TPC)5.425.035.32.725.42.23.62.22.700.43.100.401.31.300.903.63.6

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Percentage of Participants Experiencing Any Treatment Emergent Adverse Events (TEAEs), Serious Adverse Events (SAEs), and TEAEs Leading to Discontinuation of Study Drug

"Treatment-emergent adverse events (TEAEs) were defined as any adverse events (AEs) that begin or worsen on or after the start of study drug through 30 days after the last dose of study drug. The severity was graded based on the National Cancer Institute's Common Terminology Criteria for Adverse Events Version 4.03. An AE that met one or more of the following outcomes was classified as serious:~Fatal~Life-threatening~Disabling/incapacitating~Results in hospitalization or prolongs a hospital stay~A congenital abnormality~Other important medical events may also be considered serious AEs if they may require medical or surgical intervention to prevent one of the outcomes listed above" (NCT02574455)
Timeframe: First dose date up to last follow-up (maximum up to 30.8 months)

,
Interventionpercentage of participants (Number)
Any TEAEsSAEsTEAEs Leading to Discontinuation of Study Drug
Sacituzumab Govitecan99.626.74.7
Treatment of Physician's Choice (TPC)97.828.65.4

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Objective Response Rate (ORR) by IRC and Investigator Assessment in BM-ve Population

ORR was defined as the percentage of participants who had the overall best response as either a confirmed complete response (CR) or partial response (PR) relative to the size of population under evaluation. CR: Disappearance of all target and non-target lesions; and normalization of tumor marker levels initially above upper limits of normal; and no new lesions. PR: ≥30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD; and no new lesions. (NCT02574455)
Timeframe: From randomization to the date of progression or death (assessed every 6 weeks for 9 months and then every 9 weeks thereafter until the occurrence of progression of disease; maximum exposure: 29.6 months)

,
Interventionpercentage of participants (Number)
ORR by IRC AssessmentORR by Investigator Assessment
Sacituzumab Govitecan34.933.2
Treatment of Physician's Choice (TPC)4.76.4

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Progression-free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1)

PFS was defined as the time from randomization to the first documented progressive disease (PD) per RECIST 1.1 based on blinded independent central review (BICR), or death due to any cause, whichever occurs earlier. Per RECIST 1.1, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum had to demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD. The sponsor allowed a maximum of 10 target lesions in total and 5 per organ on this study. PFS was reported for each treatment arm. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm, with a protocol-specified analysis data cut-off date of 30-Nov-2020. (NCT02611960)
Timeframe: Up to approximately 53 months (through analysis cut-off date of 30-Nov-2020)

InterventionMonths (Median)
Pembrolizumab4.1
Standard Treatment5.5

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Percentage of Participants With PFS (PFS Rate) at 6 Months

PFS was defined as the time from randomization to the first documented PD per RECIST 1.1 based on BICR, or death due to any cause, whichever occurs earlier. Per RECIST 1.1, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum had to demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD. The sponsor allowed a maximum of 10 target lesions in total and 5 per organ on this study. The percentage of participants with PFS (PFS rate) at 6 months is reported for each treatment arm based on the product-limit (Kaplan-Meier) method for censored data. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm, with a protocol-specified analysis data cut-off date of 30-Nov-2020. (NCT02611960)
Timeframe: 6 months

InterventionPercentage of Participants (Number)
Pembrolizumab36.3
Standard Treatment43.9

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Percentage of Participants With PFS (PFS Rate) at 12 Months

PFS was defined as the time from randomization to the first documented PD per RECIST 1.1 based on BICR, or death due to any cause, whichever occurs earlier. Per RECIST 1.1, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum had to demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD. The sponsor allowed a maximum of 10 target lesions in total and 5 per organ on this study. The percentage of participants with PFS (PFS rate) at 12 months is reported for each treatment arm based on the product-limit (Kaplan-Meier) method for censored data. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm, with a protocol-specified analysis data cut-off date of 30-Nov-2020. (NCT02611960)
Timeframe: 12 months

InterventionPercentage of Participants (Number)
Pembrolizumab18.7
Standard Treatment30.8

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Percentage of Participants Who Experience One or More Adverse Events (AEs)

An AE was defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which did not necessarily have to have a causal relationship with this treatment. An AE could therefore be any unfavourable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the medicinal product or protocol-specified procedure. Any worsening of a pre-existing condition that was temporally associated with the use of the Sponsor's product was also an AE. The percentage of participants that experienced at least one AE was reported for each treatment arm. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm. (NCT02611960)
Timeframe: Up to approximately 73 months

InterventionPercentage of Participants (Number)
Pembrolizumab97.4
Standard Treatment97.3

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Percentage of Participants Who Discontinue Study Treatment Due to an AE

An AE was defined as any untoward medical occurrence in a participant administered a pharmaceutical product and which did not necessarily have to have a causal relationship with this treatment. An AE could therefore be any unfavourable and unintended sign, symptom, or disease temporally associated with the use of a medicinal product or protocol-specified procedure, whether or not considered related to the medicinal product or protocol-specified procedure. Any worsening of a pre-existing condition that was temporally associated with the use of the Sponsor's product was also an AE. The percentage of participants that discontinued study treatment due to an AE was reported for each treatment arm. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm. (NCT02611960)
Timeframe: Up to approximately 72 months

InterventionPercentage of Participants (Number)
Pembrolizumab8.6
Standard Treatment15.2

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Percentage of Participants Surviving (OS Rate) at 24 Months

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the final analysis were censored at the date of the last known contact. The percentage of participants surviving (OS rate) at 24 months is reported for each treatment arm based on the product-limit (Kaplan-Meier) method for censored data. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm, with a protocol-specified analysis data cut-off date of 30-Nov-2020. (NCT02611960)
Timeframe: 24 months

InterventionPercentage of Participants (Number)
Pembrolizumab40.2
Standard Treatment32.2

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Percentage of Participants Surviving (OS Rate) at 12 Months

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the final analysis were censored at the date of the last known contact. The percentage of participants surviving (OS rate) at 12 months is reported for each treatment arm based on the product-limit (Kaplan-Meier) method for censored data. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm, with a protocol-specified analysis data cut-off date of 30-Nov-2020. (NCT02611960)
Timeframe: 12 months

InterventionPercentage of Participants (Number)
Pembrolizumab58.1
Standard Treatment57.4

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Overall Survival (OS)

Overall Survival was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the final analysis were censored at the date of the last known contact. OS was reported for each treatment arm. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm, with a protocol-specified analysis data cut-off date of 30-Nov-2020. (NCT02611960)
Timeframe: Up to approximately 53 months (through analysis cut-off date of 30-Nov-2020)

InterventionMonths (Median)
Pembrolizumab17.2
Standard Treatment15.3

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Duration of Response (DOR) Per RECIST 1.1

For participants who demonstrated a confirmed CR (disappearance of all target lesions) or PR (at least a 30% decrease in the sum of diameters of target lesions) per RECIST 1.1 as assessed by BICR, DOR was defined as the time from first documented evidence of confirmed CR or PR until PD or death due to any cause, whichever occurred first. DOR for participants who had not progressed or died at the time of analysis was censored at the date of their last tumor assessment. Per RECIST 1.1, PD was defined as at least a 20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum had to demonstrate an absolute increase of ≥5 mm. The appearance of one or more new lesions was also considered PD. DOR was reported for each treatment arm. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm, with a protocol-specified analysis data cut-off date of 30-Nov-2020. (NCT02611960)
Timeframe: Up to approximately 53 months (through analysis cut-off date of 30-Nov-2020)

InterventionMonths (Median)
Pembrolizumab12.0
Standard Treatment13.1

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Objective Response Rate (ORR) Per RECIST 1.1

ORR was defined as the percentage of participants in the analysis population who had a confirmed Complete Response (CR: disappearance of all target lesions) or a Partial Response (PR: ≥30% decrease in the sum of diameters of target lesions) per RECIST 1.1. based upon BICR. The sponsor allowed a maximum of 10 target lesions in total and 5 per organ on this study. ORR was reported for each treatment arm. Per protocol, analysis for this outcome measure was performed for the first pembrolizumab course and for the standard treatment arm, with a protocol-specified analysis data cut-off date of 30-Nov-2020. (NCT02611960)
Timeframe: Up to approximately 53 months (through analysis cut-off date of 30-Nov-2020)

InterventionPercentage of Participants (Number)
Pembrolizumab21.4
Standard Treatment23.3

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Progression-free Survival (PFS) Per RECIST 1.1 as Determined by Blinded Independent Central Review (BICR)

Defined as the time from the date of randomization to the date of documented disease progression. (NCT02614794)
Timeframe: 34.6 months

Interventionmonths (Median)
Tuc+Cap+Tra7.8
Pbo+Cap+Tra5.6

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Frequency of Dose Modifications

(NCT02614794)
Timeframe: 35.1 months

,
InterventionParticipants (Count of Participants)
TEAEs resulting in tuc/pbo dose modificationTEAEs resulting in tucatinib/placebo dose holdTEAEs resulting in tuc/pbo dose reductionTEAEs resulting capecitabine dose modificationTEAEs resulting in capecitabine dose holdTEAEs resulting in capecitabine dose reductionTEAEs resulting trastuzumab dose modificationTEAEs resulting in trastuzumab dose hold
Pbo+Cap+Tra818021122113773838
Tuc+Cap+Tra22021684313276243104104

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Frequency of Dose Modifications at Time of Final Analysis

(NCT02614794)
Timeframe: Up to 60.1 months

,
InterventionParticipants (Count of Participants)
TEAEs resulting in tuc/pbo dose modificationTEAEs resulting in tucatinib/placebo dose holdTEAEs resulting in tuc/pbo dose reductionTEAEs resulting capecitabine dose modificationTEAEs resulting in capecitabine dose holdTEAEs resulting in capecitabine dose reductionTEAEs resulting trastuzumab dose modificationTEAEs resulting in trastuzumab dose hold
Pbo+Cap+Tra858421125117794141
Tuc+Cap+Tra23723292322288251117117

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Incidence of Adverse Events (AEs) at Time of Final Analysis

As determined by assessment of AEs, clinical laboratory tests, and vital signs measurements. AEs were classified by system organ class (SOC) and preferred term using the Medical Dictionary for Regulatory Activities (MedDRA) Version 22.0 or higher; AE severities were classified using Version 4.03 of the (Common Terminology Criteria for Adverse Events) CTCAE criteria. (NCT02614794)
Timeframe: Up to 60.1 months

,
InterventionParticipants (Count of Participants)
Any treatment-emergent AE (TEAE)Any Grade 3 or higher TEAEAny treatment-emergent serious AETEAE leading to death
Pbo+Cap+Tra191101586
Tuc+Cap+Tra4012481238

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Incidence of Adverse Events (AEs) at Time of Primary Analysis

As determined by assessment of AEs, clinical laboratory tests, and vital signs measurements. AEs were classified by system organ class (SOC) and preferred term using the Medical Dictionary for Regulatory Activities (MedDRA) Version 22.0 or higher; AE severities were classified using Version 4.03 of the (Common Terminology Criteria for Adverse Events) CTCAE criteria. (NCT02614794)
Timeframe: 36.1 months

,
InterventionParticipants (Count of Participants)
Any treatment-emergent AE (TEAE)Any Grade 3 or higher TEAEAny treatment-emergent serious AETEAE leading to death
Pbo+Cap+Tra19196536
Tuc+Cap+Tra4012231048

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Incidence of Health Resources Utilization

Cumulative incidence of health resource utilization, including length of stay, hospitalizations, and ER visits using the EQ-5D-5L questionnaire. (NCT02614794)
Timeframe: 36.1 months

,
Interventionhospitalizations (Number)
Total number of hospitalizationsHospitalization for AEPlanned hospitalization (other than AE)Ambulatory SurgeryOther
Pbo+Cap+Tra7564605
Tuc+Cap+Tra1431241036

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Pharmacokinetic Measure: ONT-993

Individual plasma primary metabolite concentrations at each sampling time (NCT02614794)
Timeframe: 3.5 months

Interventionng/mL (Mean)
Cycle 2, Day 1 (Pre-dose)Cycle 3, Day 1 (Pre-dose)Cycle 3, Day 1 (Post-dose)Cycle 4, Day 1 (Pre-dose)Cycle 5, Day 1 (Pre-dose)Cycle 6, Day 1 (Pre-dose)
Tuc+Cap+Tra25.522.647.725.224.520.9

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Pharmacokinetic Measure: Ctrough of Tucatinib

Individual plasma tucatinib concentrations at each sampling time (NCT02614794)
Timeframe: 3.5 months

Interventionng/mL (Mean)
Cycle 2, Day 1 (Pre-dose)Cycle 3, Day 1 (Pre-dose)Cycle 3, Day 1 (Post-dose)Cycle 4, Day 1 (Pre-dose)Cycle 5, Day 1 (Pre-dose)Cycle 6, Day 1 (Pre-dose)
Tuc+Cap+Tra246.1227.6507.1253.2257.6247.8

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CBR Per RECIST 1.1 as Determined by Investigator Assessment

Clinical benefit was defined as achieving stable disease (SD) or non-CR/non-PD for at least 6 months or a best overall response of confirmed CR or confirmed PR. (NCT02614794)
Timeframe: 34.6 months

Interventionpercentage of participants (Number)
Tuc+Cap+Tra58.0
Pbo+Cap+Tra37.6

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Clinical Benefit Rate (CBR) as Determined by BICR Per RECIST 1.1

Clinical benefit was defined as achieving stable disease (SD) or non-complete response (CR)/non-progressive disease (PD) for at least 6 months or a best overall response of confirmed CR or confirmed partial response (PR). (NCT02614794)
Timeframe: 34.6 months

Interventionpercentage of participants (Number)
Tuc+Cap+Tra59.8
Pbo+Cap+Tra38.1

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Confirmed Objective Response Rate (ORR) Per RECIST 1.1 as Determined by BICR

Defined as achieving a best overall response of confirmed complete response (CR) or confirmed partial response (PR). (NCT02614794)
Timeframe: 34.6 months

Interventionpercentage of participants (Number)
Tuc+Cap+Tra40.7
Pbo+Cap+Tra23.4

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Duration of Response (DOR) Per RECIST 1.1 as Determined by BICR

Defined as the time from the first objective response to documented disease progression or death from any cause, whichever occurred first. (NCT02614794)
Timeframe: 24.6 months

Interventionmonths (Median)
Tuc+Cap+Tra8.3
Pbo+Cap+Tra6.3

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ORR Per RECIST 1.1 as Determined by Investigator Assessment

Defined as achieving a best overall response of confirmed CR or confirmed PR. (NCT02614794)
Timeframe: 34.6 months

Interventionpercentage of participants (Number)
Tuc+Cap+Tra41.4
Pbo+Cap+Tra23.0

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Overall Survival (OS) at Time of Final Analysis

Defined as time from randomization to death from any cause (NCT02614794)
Timeframe: Up to 60.1 months

Interventionmonths (Median)
Tuc+Cap+Tra24.7
Pbo+Cap+Tra19.2

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Overall Survival (OS) at Time of Primary Analysis

Defined as time from randomization to death from any cause (NCT02614794)
Timeframe: 35.9 months

Interventionmonths (Median)
Tuc+Cap+Tra21.9
Pbo+Cap+Tra17.4

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PFS in Patients With Brain Metastases at Baseline Using RECIST 1.1 as Determined by BICR

Defined as the time from the date of randomization to the date of documented disease progression. (NCT02614794)
Timeframe: 34.6 months

Interventionmonths (Median)
Tuc+Cap+Tra7.6
Pbo+Cap+Tra5.4

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PFS Per RECIST 1.1 as Determined by Investigator Assessment at Time of Final Analysis

Defined as the time from the date of randomization to the date of documented disease progression (NCT02614794)
Timeframe: Up to 58.0 months

Interventionmonths (Median)
Tuc+Cap+Tra7.6
Pbo+Cap+Tra4.9

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PFS Per RECIST 1.1 as Determined by Investigator Assessment at Time of Primary Analysis

Defined as the time from the date of randomization to the date of documented disease progression (NCT02614794)
Timeframe: 34.6 months

Interventionmonths (Median)
Tuc+Cap+Tra7.5
Pbo+Cap+Tra4.3

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DOR Per RECIST 1.1 as Determined by Investigator Assessment

Defined as the time from the first objective response to documented disease progression or death from any cause, whichever occurred first. (NCT02614794)
Timeframe: 33.2 months

Interventionmonths (Median)
Tuc+Cap+Tra7.0
Pbo+Cap+Tra6.9

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Progression Free Survival (PFS) by Independent Review Committee (IRC)

The PFS time was defined as the time from date of randomization until date of the first documentation of progressive disease (PD) or death due to any cause (whichever occurs first). PFS was assessed as per Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST v1.1) as per IRC. PD was defined as at least a 20 percent (%) increase in the sum of longest diameter (SLD), taking as reference the smallest SLD recorded from baseline or the appearance of 1 or more new lesions. PFS was measured using Kaplan-Meier (KM) estimates. (NCT02625610)
Timeframe: From randomization into maintenance phase up to 1276 days

Interventionmonths (Median)
Chemotherapy + Best Supportive Care (BSC)4.4
Avelumab3.2

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Maintenance Phase: Number of Participants With Treatment-Emergent Adverse Events (TEAEs) and Serious TEAEs According to National Cancer Institute-Common Terminology Criteria for Adverse Events Version 4.03 (NCI-CTCAE v4.03)

Adverse event (AE) was defined as any untoward medical occurrence in a participant, which does not necessarily have causal relationship with treatment. A serious AE was defined as an AE that resulted in any of the following outcomes: death; life threatening; persistent/significant disability/incapacity; initial or prolonged in participant hospitalization; congenital anomaly/birth defect or was otherwise considered medically important. The term TEAE is defined as AEs starting or worsening after the first intake of the study drug. TEAEs included both serious TEAEs and non-serious TEAEs. Number of participants with TEAEs and serious TEAEs were reported. (NCT02625610)
Timeframe: From randomization into maintenance phase up to 1276 days

,
InterventionParticipants (Count of Participants)
Any TEAEsAny Serious TEAE
Avelumab22389
Chemotherapy + Best Supportive Care (BSC)21475

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Maintenance Phase: Number of Participants With Potentially Clinically Significant Electrocardiogram (ECG) Abnormalities

ECG parameters included heart rate, pulse rate intervals, QRS interval, QT interval corrected based on Fridericia's formula (QTcF) intervals and QTcB intervals. Clinical significance was determined by the investigator. Number of participants with potentially clinically significant ECG abnormalities were reported. (NCT02625610)
Timeframe: From randomization into maintenance phase up to 1276 days

,
InterventionParticipants (Count of Participants)
Decreased heart rateIncreased heart rateIncreased Pulse Rate intervalIncreased QRS intervalQTcF interval greater than (>)450milisecond (ms)less than or equal to(<=)480msQTcF interval: > 480 ms <= 500 msQTcF interval: > 500 msQTcB Interval: > 450 msec <= 480 msecQTcB Interval: > 480 msec <= 500 msecQTcB Interval: > 500 msec
Avelumab12389311823
Chemotherapy + Best Supportive Care (BSC)02159231925

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Maintenance Phase: Number of Participants With Potentially Clinically Significant Abnormalities in Vital Signs

Vital signs assessment included Systolic blood pressure (SBP), Diastolic blood pressure (DBP) and Pulse Rate (PR). Number of Participants with any potentially clinically significant abnormalities in vital signs were reported. Clinical significance was determined by the investigator. (NCT02625610)
Timeframe: From randomization into maintenance phase up to 1276 days

,
InterventionParticipants (Count of Participants)
Increased in Systolic blood pressureDecreased in Systolic blood pressureIncreased in Diastolic blood pressureDecreased in Diastolic blood pressureIncreased in pulse rateDecreased in pulse rate
Avelumab626924264830
Chemotherapy + Best Supportive Care (BSC)574314214632

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Maintenance Phase: Number of Participants With Grade Change From Baseline to Worst On-Treatment Grade 4 Hematology Values

Blood samples were collected for the analysis of following hematology parameters: lymphocyte count, neutrophil count, white blood cells, platelet count, lipase, serum amylase, creatinine phosphokinase and creatinine. The hematology parameters were graded according to National Cancer Institute - Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 4.03. Grade 1: mild; Grade 2: moderate; Grade 3: severe or medically significant; Grade 4: life-threatening consequences. An increase is defined as an increase in CTCAE grade relative to Baseline grade. Data for worst-case (Grade 4) post Baseline is presented. Only those participants with increase to grade 4 have been presented. (NCT02625610)
Timeframe: From baseline up to 1276 days

,
InterventionParticipants (Count of Participants)
lymphocyte count decreasedneutrophil count decreasedwhite blood cells decreasedplatelet count decreasedlipase increasedserum amylase increasedcreatinine phosphokinase increasedcreatinine increased
Avelumab11008221
Chemotherapy + Best Supportive Care (BSC)06216300

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Change From Baseline in European Quality of Life 5-dimensions Health Outcome Questionnaire Through Visual Analogue Scale up to Safety Follow-up (Up to 152.3 Weeks)

EQ-5D-5L is comprised of the following 5 participant-reported dimensions: mobility, self-care, usual activities, pain/discomfort, and anxiety/depression. Each dimension has 5 levels: no problems, slight problems, moderate problems, severe problems, and extreme problems. The responses are used to derive overall score using a visual analog scale (VAS) that ranged from 0 to 100 millimeter (mm), where 0 is the worst health you can imagine and 100 is the best health you can imagine. (NCT02625610)
Timeframe: Baseline, Week 3/4, Week 7, Week 13, Week 19, Week 25, Week 31, Week 37, Week 43, Week 49, Week 55, Week 61, Week 67, End of Treatment ( EOT up to 148 weeks) and Safety Follow-up (Up to 152.3 Weeks)

,
InterventionMillimeter (Mean)
Week 3/4Week 7Week 13Week 19Week 25Week 31Week 37Week 43Week 49Week 55Week 61Week 67End Of TreatmentSafety Follow-Up
Avelumab0.6-2.1-0.7-0.1-1.41.40.93.22.13.43.54.9-10.3-9.6
Chemotherapy + Best Supportive Care (BSC)0.9-0.5-3.2-3.5-4.5-2.3-1.7-4.4-2.9-9.4-6.4-7.3-12.2-8.0

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Maintenance Phase: Number of Participants With Shift in Eastern Cooperative Oncology Group (ECOG) Performance Status Score to 1 or Higher Than 1

ECOG PS score is widely used by doctors and researchers to assess how a participants' disease is progressing, and is used to assess how the disease affects the daily living abilities of the participant, and determine appropriate treatment and prognosis. The score ranges from Grade 0 to Grade 5, where Grade 0 = Fully active, able to carry on all pre-disease performance without restriction, Grade 1 = Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature (like light house work, office work), Grade 2 = Ambulatory and capable of all self-care but unable to carry out any work activities, Grade 3 = Capable of only limited self-care, confined to bed or chair more than 50% of waking hours and Grade 4 = Completely disabled. Cannot carry on any self-care. Totally confined to bed or chair, Grade 5 = Death. Number of participants with shift in ECOG PS Score to 1 or Higher Than 1 were reported. (NCT02625610)
Timeframe: From randomization into maintenance phase up to 1276 days

InterventionParticipants (Count of Participants)
Chemotherapy + Best Supportive Care (BSC)140
Avelumab144

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Objective Response Rate (ORR) by Investigator Assessment

The ORR defined as the percentage of all randomized participants with a confirmed best overall response (BOR) of partial response (PR),or complete response (CR) according to RECIST v1.1 and as per Investigator assessment. CR: Disappearance of all evidence of target and non-target lesions. PR: At least 30 percent (%) reduction from baseline in sum of longest diameter (SLD) of all lesions. (NCT02625610)
Timeframe: From randomization into maintenance phase up to 1276 days

Interventionpercentage of participants (Number)
Chemotherapy + Best Supportive Care (BSC)14.4
Avelumab13.3

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Overall Survival (OS)

Overall Survival was defined as the time from randomization to the date of death due to any cause. For participants who were still alive at the time of data analysis or who were lost to follow-up, OS time was censored at the date of last contact. OS was measured using Kaplan-Meier (KM) estimates. (NCT02625610)
Timeframe: From randomization into maintenance phase up to 1276 days

Interventionmonths (Median)
Chemotherapy + Best Supportive Care (BSC)10.9
Avelumab10.4

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Change From Baseline in European Organization for the Research and Treatment of Cancer Quality of Life (EORTC QLQ-C30) Global Health Status Scale Score up to Safety Follow-up (Up to 152.3 Weeks)

European Organization for the Research and Treatment of Cancer Quality of Life (EORTC QLQ-C30) is a 30-question tool used to assess the overall quality of life (QoL) in cancer participants. It consisted of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, role, cognitive, emotional, social), and 9 symptom scales/items (Fatigue, nausea and vomiting, pain, dyspnoea, sleep disturbance, appetite loss, constipation, diarrhea, financial impact. The EORTC QLQ-C30 GHS/QoL score ranges from 0 to 100; High score indicates better GHS/QoL. Score 0 represents: very poor physical condition and QoL. Score 100 represents: excellent overall physical condition and QoL. (NCT02625610)
Timeframe: Baseline, Week 3/4, Week 7, Week 13, Week 19, Week 25, Week 31, Week 37, Week 43, Week 49, Week 55, Week 61, Week 67, End of Treatment ( EOT up to 148 weeks) and Safety Follow-up (Up to 152.3 Weeks)

,
Interventionunits on a scale (Mean)
Week 3/4Week 7Week 13Week 19Week 25Week 31Week 37Week 43Week 49Week 55Week 61Week 67End Of TreatmentSafety Follow-Up
Avelumab0.85-1.010.241.370.411.851.773.334.014.002.384.90-11.67-9.29
Chemotherapy + Best Supportive Care (BSC)1.30-1.44-2.50-5.85-4.43-3.09-1.39-1.191.520.00-5.000.00-11.54-7.51

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Change From Baseline in European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire-Stomach Cancer Specific (EORTC QLQ-STO22 ) Questionnaire Scores up to Safety Follow-up (Up to 152.3 Weeks)

European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire-Stomach Cancer Specific (EORTC QLQ-STO22 ) supplements the EORTC QLQ-C30 to assess symptoms and treatment-related side effects commonly reported in participants. There are 22 questions which comprise 5 scales (dysphagia, pain, reflux symptom, dietary restrictions, and anxiety) and 4 single items (dry mouth, hair loss, taste, body image). Most questions use 4-point scale (1 'Not at all' to 4 'Very much'; 1 question was a yes or no answer). A linear transformation was used to standardize all scores and single-items to a scale of 0 to 100; higher score=better level of functioning or greater degree of symptoms. (NCT02625610)
Timeframe: Baseline, Week 3/4, Week 7, Week 13, Week 19, Week 25, Week 31, Week 37, Week 43, Week 49, Week 55, Week 61, Week 67, End of Treatment ( EOT up to 148 weeks) and Safety Follow-up (Up to 152.3 Weeks)

,
Interventionunits on a scale (Mean)
Dysphagia: Week 3/4Dysphagia Week 7Dysphagia Week 13Dysphagia Week 19Dysphagia Week 25Dysphagia Week 31Dysphagia Week 37Dysphagia Week 43Dysphagia Week 49Dysphagia Week 55Dysphagia Week 61Dysphagia Week 67Dysphagia End Of TreatmentDysphagia Safety Follow-UpPain Week 3/4Pain Week 7Pain Week 13Pain Week 19Pain Week 25Pain Week 31Pain Week 37Pain Week 43Pain Week 49Pain Week 55Pain Week 61Pain Week 67Pain End Of TreatmentPain Safety Follow-UpReflux Week 3/4Reflux Week 7Reflux Week 13Reflux Week 19Reflux Week 25Reflux Week 31Reflux Week 37Reflux Week 43Reflux Week 49Reflux Week 55Reflux Week 61Reflux Week 67Reflux End of TreatmentReflux Safety Follow-upEating Restrictions Week 3/4Eating Restrictions Week 7Eating Restrictions Week 13Eating Restrictions Week 19Eating Restrictions Week 25Eating Restrictions Week 31Eating Restrictions Week 37Eating Restrictions Week 43Eating Restrictions Week 49Eating Restrictions Week 55Eating Restrictions Week 61Eating Restrictions Week 67Eating Restrictions EOTEating Restrictions Safety Follow-upAnxiety Week 3/4Anxiety Week 7Anxiety Week 13Anxiety Week 19Anxiety Week 25Anxiety Week 31Anxiety Week 37Anxiety Week 43Anxiety Week 49Anxiety Week 55Anxiety Week 61Anxiety Week 67Anxiety End of TreatmentAnxiety Safety Follow-Up
Avelumab0.601.340.651.521.694.39-0.67-2.591.230.891.061.318.217.25-0.042.600.16-0.51-1.550.97-1.26-1.94-0.62-1.00-1.59-0.499.4510.990.120.50-1.09-1.681.69-1.29-4.38-5.56-2.06-3.56-6.350.004.732.900.13-0.270.00-0.63-1.550.39-3.28-3.89-5.25-6.00-5.56-2.4510.0111.59-4.06-1.20-2.83-1.68-1.69-0.52-1.01-1.11-6.17-4.00-4.76-1.965.894.99
Chemotherapy + Best Supportive Care (BSC)0.762.841.60-0.58-1.390.82-7.19-4.76-3.030.000.00-1.857.279.391.512.532.963.22-1.564.01-4.901.791.520.003.330.009.258.221.040.310.991.750.69-2.06-6.54-3.171.012.226.677.413.431.560.730.981.02-2.34-2.08-2.47-8.82-4.760.763.330.001.398.277.04-0.28-1.30-0.86-1.56-2.784.12-3.92-3.970.002.22-4.449.264.585.48

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Change From Baseline in European Quality of Life 5-dimensions (EQ-5D-5L) Health Outcome Questionnaire Through Composite Index Score up to Safety Follow-up (Up to 152.3 Weeks)

EQ-5D-5L is comprised of the following 5 participant-reported dimensions: mobility, self-care, usual activities, pain/discomfort, and anxiety/depression. Each dimension has 5 levels: no problems, slight problems, moderate problems, severe problems, and extreme problems. The responses are used to derive overall composite health state index score, with scores ranging from -0.594 to 1. A higher score indicates better health state. (NCT02625610)
Timeframe: Baseline, Week 3/4, Week 7, Week 13, Week 19, Week 25, Week 31, Week 37, Week 43, Week 49, Week 55, Week 61, Week 67, End of Treatment ( EOT up to 148 weeks) and Safety Follow-up (Up to 152.3 Weeks)

,
InterventionUnits on Scale (Mean)
Week 3/4Week 7Week 13Week 19Week 25Week 31Week 37Week 43Week 49Week 55Week 61Week 67End Of TreatmentSafety Follow-Up
Avelumab0.004-0.009-0.017-0.0110.0140.0130.0130.0580.0260.0280.0310.039-0.138-0.099
Chemotherapy + Best Supportive Care (BSC)-0.002-0.032-0.053-0.039-0.049-0.023-0.035-0.046-0.100-0.164-0.091-0.076-0.125-0.062

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Percentage of Participants With Downstaging of Primary Tumor and/or Lymph Nodes

Downstaging of primary tumor (T) and/or lymph nodes (N) was defined as decrease by 1 point in T-value and/or N-value (comparing at screening and after treatment). It was assessed by colonoscopy, pathology, endosonography of rectum, chest X-ray, abdominopelvic Computed Tomography and Magnetic Resonance Imaging. Staging for tumor are: TX (primary tumor cannot be assessed), T0 (no evidence of primary tumor), Tis (carcinoma in situ), T1 (tumor invades submucosa), T2 (tumor invades muscularis propria), T3 (tumor invades through muscularis propria into subserosa/into non-peritonealized pericolic/perirectal tissues, T4 (tumor directly invades other organs or structures). Staging for lymph nodes are: NX (regional lymph nodes cannot be assessed), N0 (no regional lymph node metastasis), N1 (metastasis in 1 to 3 regional lymph nodes), N2 (metastasis in 4 or more regional lymph nodes). (NCT02694718)
Timeframe: From screening to Week 16

InterventionPercentage of participants (Number)
T stageN stageOverall
Capecitabine + Oxaliplatin474865

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Number of Participants With Any Adverse Events and Serious Adverse Events

An adverse event (AE) is defined as any untoward medical occurrence in participants or clinical investigation participants administered a pharmaceutical product and which did not necessarily have to have a causal relationship with this treatment. A serious adverse event (SAE) is any untoward medical occurrence that at any dose results in death, are life threatening, requires hospitalization or prolongation of hospitalization or results in disability/incapacity, and congenital anomaly/birth defect. (NCT02694718)
Timeframe: Up to Week 16

InterventionParticipants (Number)
Any AEsAny SAEs
Capecitabine + Oxaliplatin598

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Percentage of Participants With Pathological Complete Tumor Response

Pathological complete tumor response was defined as grade 3 or 4 in the histological grading of regression according to Dworak classification. Grade 0 is no regression; Grade 1 is dominant tumor mass with obvious fibrosis and/or vasculopathy; Grade 2 is dominantly fibrotic changes with few tumor cells or groups; Grade 3 is defined as very few (difficult to find microscopically) tumor cells in fibrotic tissue with or without mucous substance; Grade 4 is defined as no tumor cells, only fibrotic mass (total regression or response). (NCT02694718)
Timeframe: Up to Week 16

InterventionPercentage of participants (Number)
Capecitabine + Oxaliplatin23

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Percentage of Participants With Pathological Incomplete Tumor Response

Pathological incomplete tumor response was defined as grade 1 or 2 in the histological grading of regression according to Dworak grading of regression. Pathological incomplete tumor response rate, Grade 1: dominant tumor mass with obvious fibrosis and/or vasculopathy; Grade 2: dominantly fibrotic changes with few tumor cells or groups (easy to find) were assessed. (NCT02694718)
Timeframe: Up to Week 16

InterventionPercentage of participants (Number)
Capecitabine + Oxaliplatin72

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Percentage of Participants With Resection (R0) in Participants With T4 Rectal Cancer

R0 resection was defined as complete resection of the tumor with adequate tumor-free margins and regional lymph node extirpation as confirmed by pathology after pre-operative chemotherapy plus capecitabine + oxaliplatin therapy. (NCT02694718)
Timeframe: Up to Week 16

InterventionPercentage of participants (Number)
Capecitabine + Oxaliplatin100

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Percentage of Participants With Sphincter-preservation

Percentage of participants with sphincter-preservation is reported. (NCT02694718)
Timeframe: Up to Week 16

InterventionPercentage of participants (Number)
Capecitabine + Oxaliplatin84.48

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Number of Participants With Marked Laboratory Abnormalities

Number of participants with marked laboratory abnormalities is reported. (NCT02694718)
Timeframe: Up to Week 16

InterventionParticipants (Number)
HemoglobinHematocritErythrocytesLeucocytes totalNeutrophilsBasophilsEosinophilsMonocytesLymphocytesPlateletsASAT/SGOTALAT/SGPTSerum albuminTotal proteinSerum creatinineGlucoseSodiumPotassiumCalcium
Capecitabine + Oxaliplatin771689122421321032213222

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Disease Control Rate (DCR)

DCR was the proportion of patients with confirmed CR, PR or stable disease (SD) as best overall response. SD defined as neither sufficient decrease to qualify for PR nor sufficient increase to qualify for PD. (NCT02743221)
Timeframe: Baseline and every 8 weeks (maximum follow-up duration: 17.9 months)

InterventionParticipants (Count of Participants)
Trifluridine/Tipiracil + Bevacizumab66
Capecitabine + Bevacizumab59

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Overall Survival (OS)

The OS was defined as the time from the date of randomisation to the date of death. If death was not confirmed, or patient was alive at study cut-off date, survival time was censored at the date of last follow-up or at the study cut-off date, whichever was earlier. (NCT02743221)
Timeframe: Baseline up to death or study cut-off (maximum follow-up duration: 19.9 months)

Interventionmonths (Median)
Trifluridine/Tipiracil + Bevacizumab18.0
Capecitabine + Bevacizumab16.2

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Overall Response Rate (ORR)

As per RECIST v1.1, Complete Response (CR) was disappearance of all target lesions; Partial Response (PR) was at least 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. The ORR was the proportion of patients who presented CR or PR with confirmation at subsequent time point or at least 4 weeks later. (NCT02743221)
Timeframe: Baseline and every 8 weeks (maximum follow-up duration: 17.9 months)

InterventionParticipants (Count of Participants)
Trifluridine/Tipiracil + Bevacizumab26
Capecitabine + Bevacizumab23

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Progression Free Survival (PFS)

The progression free survival (PFS), defined as the time from the date of randomisation until the date of the investigator-assessed radiological disease progression or death due to any cause according to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. Progressive disease (PD) was defined at least a 20% increase in the sum of diameters of target lesions (taking as reference the smallest sum on study) and an absolute increase of at least 5 mm in the sum of lesions or the appearance of new lesions. (NCT02743221)
Timeframe: Baseline and every 8 weeks (maximum follow-up duration: 17.9 months)

Interventionmonths (Median)
Trifluridine/Tipiracil + Bevacizumab9.2
Capecitabine + Bevacizumab7.8

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Duration of Response (DR)

The DR was calculated among patients with CR or PR as the time (months) from the first documentation of response to the first documentation of objective tumor progression or death due to any cause, whichever occurred first. (NCT02743221)
Timeframe: Baseline and every 8 weeks (maximum follow-up duration: 16.6 months)

Interventionmonths (Median)
Trifluridine/Tipiracil + Bevacizumab7.9
Capecitabine + Bevacizumab9.9

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Percentage of Participants With a Best Overall Response of Complete Response (CR) or Partial Response (PR) According to Response Evaluation Criteria in Solid Tumors (RECIST)

Tumor response was assessed by RECIST during the study. CR was defined as disappearance of all target and non-target lesions and normalization of tumor marker levels. PR was defined as greater than or equal to (≥) 30 percent (%) decrease in sum of longest diameter (LD) of target lesions in reference to Baseline sum LD. Response was to be confirmed ≥4 weeks after the initial assessment of CR or PR. The percentage of participants with a best overall response for CR or PR was reported. The exact 95% confidence interval (CI) for one-sample binomial was determined using the Pearson-Clopper method. (NCT02748213)
Timeframe: Tumor assessments at Baseline, then every 6 weeks until Cycle 8 (cycle length of 21 days), then every 12 weeks until progressive disease and/or one year after enrollment; thereafter according to routine clinical practice (up to 66 months overall)

Interventionpercentage of participants (Number)
Herceptin + Taxotere + Xeloda70.5
Herceptin + Taxotere72.7

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Percentage of Participants With Death or Disease Progression According to RECIST

Tumor response was assessed by RECIST during the study. Disease progression or progressive disease (PD) was defined as ≥20% increase in sum LD in reference to the smallest on-treatment sum LD, or the appearance of new lesions. The percentage of participants who died or experienced PD was reported. (NCT02748213)
Timeframe: Tumor assessments at Baseline, then every 6 weeks until Cycle 8 (cycle length of 21 days), then every 12 weeks until progressive disease and/or one year after enrollment; thereafter according to routine clinical practice (up to 66 months overall)

Interventionpercentage of participants (Number)
Herceptin + Taxotere + Xeloda67.9
Herceptin + Taxotere77.3

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Progression-Free Survival (PFS) According to RECIST

Tumor response was assessed by RECIST during the study. Disease progression or PD was defined as ≥20% increase in sum LD in reference to the smallest on-treatment sum LD, or the appearance of new lesions. PFS was defined as the time from start of treatment to the first event of death or PD. Participants without event at the time of analysis were censored at the latest date of last tumor assessment or last date in drug log. The median duration of PFS and corresponding 95% CI were estimated by Kaplan-Meier analysis and expressed in months. (NCT02748213)
Timeframe: Tumor assessments at Baseline, then every 6 weeks until Cycle 8 (cycle length of 21 days), then every 12 weeks until progressive disease and/or one year after enrollment; thereafter according to routine clinical practice (up to 66 months overall)

Interventionmonths (Median)
Herceptin + Taxotere + Xeloda17.9
Herceptin + Taxotere12.8

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Duration of Response (DOR) According to RECIST

Tumor response was assessed by RECIST during the study. CR was defined as disappearance of all target and non-target lesions and normalization of tumor marker levels. PR was defined as ≥30% decrease in sum LD of target lesions in reference to Baseline sum LD. Response was to be confirmed ≥4 weeks after the initial assessment of CR or PR. DOR was defined as the time from first assessment of CR or PR until the first occurrence of documented PD, death, or withdrawal. The median DOR was reported and expressed in months. (NCT02748213)
Timeframe: Tumor assessments at Baseline, then every 6 weeks until Cycle 8 (cycle length of 21 days), then every 12 weeks until progressive disease and/or one year after enrollment; thereafter according to routine clinical practice (up to 66 months overall)

Interventionmonths (Median)
Herceptin + Taxotere + Xeloda15.9
Herceptin + Taxotere13.4

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Overall Survival (OS)

OS was defined as the time from start of treatment to date of death for any reason. Participants who were alive at the time of analysis were censored at the latest date of last tumor assessment, last drug intake, or last follow-up information. The median duration of OS and corresponding 95% CI were estimated by Kaplan-Meier analysis and expressed in months. (NCT02748213)
Timeframe: Continuously during treatment (up to 66 months) and at any time after treatment discontinuation until 18 months after last participant enrolled (up to 66 months overall)

Interventionmonths (Median)
Herceptin + Taxotere + Xeloda43.5
Herceptin + Taxotere47.3

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Percentage of Participants Who Died

The percentage of participants who died from any cause was reported. (NCT02748213)
Timeframe: Continuously during treatment (up to 66 months) and at any time after treatment discontinuation until 18 months after last participant enrolled (up to 66 months overall)

Interventionpercentage of participants (Number)
Herceptin + Taxotere + Xeloda35.7
Herceptin + Taxotere41.8

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Disease Control (DC)

"Disease control is defined as CR or PR or Stable disease (SD) per RECIST version 1.1.~Since only one patient was enrolled prior to termination of the trial, no data summarization or analysis was carried out." (NCT02780700)
Timeframe: Data collected up to cut-off date 09 Sep 2016, Up to 02 months

InterventionPercentage of participants (Number)
Nintedanib Plus CapecitabineNA

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Objective Response Rate (ORR)

"ORR is defined as complete response (CR) or partial response (PR) per Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1.~Since only one patient was enrolled prior to termination of the trial, no data summarization or analysis was carried out." (NCT02780700)
Timeframe: tumor response was to be assessed by imaging according to RECIST (version 1.1) every 6 weeks.

InterventionPercentage of participants (Number)
Nintedanib Plus CapecitabineNA

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Overall Survival (OS)

"Overall survival is defined as the time from randomization until death from any cause.~Since only one patient was enrolled prior to termination of the trial, no data summarization or analysis was carried out." (NCT02780700)
Timeframe: Data collected up to cut-off date 09 Sep 2016, Up to 02 months

Interventionmonths (Median)
Nintedanib Plus CapecitabineNA

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Percentage of Patients With Grade 3 or Worse Adverse Events

Percentage of patients with grade 3 or worse adverse events. (NCT02780700)
Timeframe: Data collected up to cut-off date 09 Sep 2016, Up to 02 months

InterventionPercentage of participants (Number)
Nintedanib Plus Capecitabine0

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Progression Free Survival (PFS)

"PFS is defined as the time from randomization until objective tumor progression or death.~Since only one patient was enrolled prior to termination of the trial, no data summarization or analysis was carried out." (NCT02780700)
Timeframe: Data collected up to cut-off date 09 Sep 2016, Up to 02 months

Interventionmonths (Median)
Nintedanib Plus CapecitabineNA

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PFS in Participants Treated With Nivolumab Plus Ipilimumab vs Chemotherapy

Progression Free Survival (PFS) is defined as the time from randomization to the date of the first documented PD or death due to any cause. PD is determined by blinded independent committee review (BICR) per RECIST1.1 criteria in participants treated with Nivolumab plus Ipilumab vs Chemotherapy with PD-L1 CPS ≥ 10, 5, 1 or all randomized participants. Progressive disease (PD) is defined as at least a 20% increase in the sum of diameters of target lesions, taking in reference the smallest sum on study that also demonstrated an absolute increase of at least 5 mm. CPS is defined as the number of PD-L1 staining cells (tumor cells, lymphocytes, macrophages) divided by the total number of viable tumor cells, multiplied by 100. (NCT02872116)
Timeframe: From randomization to the date of the first documented progressive disease (PD) per BICR or death due to any cause (up to approximately 9 months)

,
InterventionMonths (Median)
All randomized participantsPD-L1 CPS ≥ 1PD-L1 CPS ≥ 5PD-L1 CPS ≥ 10
Arm 2b: Chemotherapy (XELOX or FOLFOX)7.066.936.286.28
Arm 3: Nivolumab + Ipilimumab2.832.792.832.89

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PFS in Participants Treated With Nivolumab Plus Chemotherapy vs Chemotherapy

Progression free survival (PFS), defined as the time from randomization to the date of the first documented progressive disease (PD) or death due to any cause, in participants treated with Nivolumab plus Chemotherapy vs Chemotherapy by BICR per RECIST1.1 in participants with PD-L1 CPS ≥ 10, 1, or all randomized subjects. Progreessive disease (PD) is defined as at least a 20% increase in the sum of diameters of target lesions, taking in reference the smallest sum on study that also demonstrated an absolute increase of at least 5 mm. CPS is defined as the number of PD-L1 staining cells (tumor cells, lymphocytes, macrophages) divided by the total number of viable tumor cells, multiplied by 100. (NCT02872116)
Timeframe: From randomization to the date of the first documented progressive disease (PD) per BICR or death due to any cause (up to approximately 10 months)

,
InterventionMonths (Median)
All randomized participantsParticipants with CPS ≥ 1Participants with CPS ≥ 10
Arm 1: Nivolumab + Chemotherapy (XELOX or FOLFOX)7.667.498.31
Arm 2a: Chemotherapy (XELOX or FOLFOX)6.936.905.78

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OS in Participants Treated With Nivolumab Plus Ipilimumab vs Chemotherapy

Overall survival (OS), defined as the time from randomization to the time of death, in participants treated with Nivolumab plus Ipilimumab vs Chemotherapy with PD-L1 CPS (combined positive score) ≥ 1, 5, 10, and all randomized participants. CPS is defined as the number of PD-L1 staining cells (tumor cells, lymphocytes, macrophages) divided by the total number of viable tumor cells, multiplied by 100. (NCT02872116)
Timeframe: From the date of randomization up to the date of death, up to approximately 14 months

,
InterventionMonths (Median)
All randomized participantsParticipants with CPS ≥ 1Participants with CPS ≥ 5Participants with CPS ≥ 10
Arm 2b: Chemotherapy (XELOX or FOLFOX)11.8311.4711.6311.33
Arm 3: Nivolumab + Ipilimumab11.7311.7311.2411.63

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OS in Participants Treated With Nivolumab Plus Chemotherapy vs Chemotherapy

Overall survival (OS), defined as the time from randomization to the time of death, in participants treated with Nivolumab plus Chemotherapy vs Chemotherapy with PD-L1 CPS ≥ 1, 10, and all randomized participants. CPS is defined as the number of PD-L1 staining cells (tumor cells, lymphocytes, macrophages) divided by the total number of viable tumor cells, multiplied by 100. (NCT02872116)
Timeframe: From the date of randomization up to the date of death, up to approximately 17 months

,
InterventionMonths (Median)
All randomized participantsParticipants with CPS ≥ 1Participants with PD-L1 CPS ≥ 10
Arm 1: Nivolumab + Chemotherapy (XELOX or FOLFOX)13.8313.9615.01
Arm 2a: Chemotherapy (XELOX or FOLFOX)11.5611.3310.87

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Objective Response Rate

Objective response rate (ORR) as assessed by BICR in participants with PD-L1 CPS ≥ 10, 5, 1, or all randomized participants. ORR is a percentage of participants determined by the number of participants with a best overall response (BOR) of complete response (CR) or partial response (PR) divided by the number of measurable participants with target lesion at baseline. BOR is defined as the best response designation as determined by the BICR, recorded between the date of randomization and the date of objectively documented progression (per RECIST 1.1 as determined by the BICR) or the date of subsequent anti-cancer therapy, whichever occurs first. CR is defined as the disappearance of all target lesions. PR is define as at 30% decrease in the sum of diameters of target lesions. The 806 chemotherapy treated participants are split into two separate arms (Arm 2a and Arm 2b) to act as comparison groups to the other treatment arms. (NCT02872116)
Timeframe: From randomization to the date of objectively documented progression or the date of subsequent anti-cancer therapy, whichever occurs first (up to approximately 43 months)

,,,
InterventionPercentage of Participants (Number)
Participants with CPS ≥ 1Participants with CPS ≥ 5Participants with CPS ≥ 10All randomized participants
Arm 1: Nivolumab + Chemotherapy (XELOX or FOLFOX)59.559.858.346.9
Arm 2a: Chemotherapy (XELOX or FOLFOX)46.445.344.237.0
Arm 2b: Chemotherapy (XELOX or FOLFOX)37.337.735.934.9
Arm 3: Nivolumab + Ipilimumab21.723.124.320.8

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Progression Free Survival (PFS) in Participants Treated With Nivolumab Plus Chemotherapy vs Chemotherapy With PD-L1 CPS ≥ 5

Progression Free Survival (PFS) is defined as the time from randomization to the date of the first documented PD or death due to any cause. PD is determined by blinded independent committee review (BICR) per RECIST1.1 criteria in participants treated with Nivolumab plus Chemotherapy vs Chemotherapy with PD-L1 CPS ≥ 5. Progressive disease (PD) is defined as at least a 20% increase in the sum of diameters of target lesions, taking in reference the smallest sum on study that also demonstrated an absolute increase of at least 5 mm. CPS is defined as the number of PD-L1 staining cells (tumor cells, lymphocytes, macrophages) divided by the total number of viable tumor cells, multiplied by 100. (NCT02872116)
Timeframe: From randomization to the date of the first documented progressive disease (PD) per BICR or death due to any cause (up to approximately 10 months)

InterventionMonths (Median)
Arm 1: Nivolumab + Chemotherapy (XELOX or FOLFOX)7.69
Arm 2a: Chemotherapy (XELOX or FOLFOX)6.05

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Overall Survival (OS) in Participants Treated With Nivolumab Plus Chemotherapy vs Chemotherapy With PD-L1 CPS ≥ 5

Overall survival (OS), defined as the time from randomization to the time of death, in participants treated with Nivolumab plus Chemotherapy vs Chemotherapy with PD-L1 CPS (combined positive score) ≥ 5. CPS is defined as the number of PD-L1 staining cells (tumor cells, lymphocytes, macrophages) divided by the total number of viable tumor cells, multiplied by 100. (NCT02872116)
Timeframe: From the date of randomization up to the date of death, up to approximately 17 months

InterventionMonths (Median)
Arm 1: Nivolumab + Chemotherapy (XELOX or FOLFOX)14.39
Arm 2a: Chemotherapy (XELOX or FOLFOX)11.10

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Progression Free Survival (PFS)

Assessed by Response Evaluation Criteria in Solid Tumors (RECIST) version (v) 1.1. The primary comparisons will be superiority of the active treatment for PFS of atezolizumab versus placebo. PFS will be compared between treatment arms using the un-stratified log-rank test at one-sided level of 0.10 and the p-value will be used for decision making. The hazard ratio (HR) for PFS will be estimated using a Cox proportional hazards model and the 95% confidence interval (CI) for the HR will be provided. Kaplan-Meier methodology will be used to estimate the median PFS for each treatment arm, and Kaplan-Meier curves will be produced. Progression is defined as any new lesion or increase by ≥20% of previously involved sites from nadir based on RECIST criteria. (NCT02873195)
Timeframe: From randomization to first documentation of disease progression by RECIST v1.1, or death from any cause, assessed up to 20 months

Interventionmonths (Median)
Atezolizumab, Bevacizumab, Capecitabine4.37
Placebo, Bevacizumab, Capecitabine3.32

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Objective Response Rate

The objective response rate is defined as the percentage of participants who achieve a partial response or compete response as assessed (partial response [PR] or complete response [CR] per RECIST v1.1) during treatment with study therapy. Rates of response will be compared across arms using a fisher's exact test for proportion. Point estimates will be generated for objective response rates within each arm along with 95% binomial confidence intervals. Complete response (CR): Disappearance of all evidence of disease, Partial response (PR): Regression of measurable disease and no new sites (NCT02873195)
Timeframe: Up to 20 months

Interventionpercentage of participants (Number)
Atezolizumab, Bevacizumab, Capecitabine8.54
Placebo, Bevacizumab, Capecitabine4.35

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Overall Survival (OS)

The distribution of survival time will be estimated using the method of Kaplan-Meier. OS will be compared between treatment arms using the unstratified log-rank test. OS medians, survival rates and HR will be estimated along with 95% confidence intervals. (NCT02873195)
Timeframe: From randomization to death due to any cause, assessed up to 20 months

Interventionmonths (Median)
Atezolizumab, Bevacizumab, Capecitabine10.55
Placebo, Bevacizumab, Capecitabine10.61

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Rate of Sphincter Preservation

Sphincter preservation means that the surgical procedure used to remove the tumor did not disturb the sphincter muscle. Analyzed by a logistic regression model that controls for the stratification factors (cT-stage and cN-stage). Observed proportions along with confidence intervals will be presented by treatment. (NCT02921256)
Timeframe: Up to 3 years

Interventionpercentage of participants (Mean)
Arm Ia (mFOLFOX6, RT, Capecitabine)52.5
Arm II (mFOLFOX6, RT, Capecitabine, Veliparib)59.3
Arm Ib (mFOLFOX6, RT, Capecitabine, Pembrolizumab)71.0
Arm III (mFOLFOX6, RT, Capecitabine, Pembrolizumab)59.4

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Neoadjuvant Rectal Cancer (NAR) Score

A linear regression model that controls for the stratification factors (cT-stage and cN-stage) will be used. Mean NAR scores along with standard errors and confidence intervals will be reported by treatment. The NAR score ranges from zero to 100 with lower values corresponding to better prognosis. (NCT02921256)
Timeframe: Baseline to up to 3 years

Interventionscore on a scale (Mean)
Arm Ia (mFOLFOX6, RT, Capecitabine)12.6
Arm II (mFOLFOX6, RT, Capecitabine, Veliparib)13.7
Arm Ib (mFOLFOX6, RT, Capecitabine)14.1
Arm III (mFOLFOX6, RT, Capecitabine, Pembrolizumab)11.5

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Rate of Pathologic Complete Response (Nodes and Tumor) ypT0 and ypN0

Pathologic Complete Response means no remaining cancer detectable in the pathology sample. Analyzed by a logistic regression model that controls for the stratification factors (cT-stage and cN-stage). Observed proportions along with confidence intervals will be presented by treatment. (NCT02921256)
Timeframe: Up to 3 years

Interventionpercentage of participants (Mean)
Arm Ia (mFOLFOX6, RT, Capecitabine)21.6
Arm II (mFOLFOX6, RT, Capecitabine, Veliparib)33.8
Arm Ib (mFOLFOX6, RT, Capecitabine)29.4
Arm III (mFOLFOX6, RT, Capecitabine, Pembrolizumab)31.9

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TTR According to RECIST 1.1 as Assessed by Investigator

(NCT02937116)
Timeframe: Through out the study (up to 2 years)

InterventionDays (Median)
MEL: Sintilimab 200mg Q3W (Cohort A)63.0
Malignant Tumor or Neuroendocrine Tumor: Sintilimab 200mg Q3W (Cohort B)64.0
NSCLC: Sintilimab 200mg Q3W (Cohort C)63.0
nsNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort D)63.0
scNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort E)62.0
Gastric or Gastroesophageal Junction Adenocarcinoma: Sintilimab 200mg Q3W + Chemotherapy (Cohort F)63.0
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort G)62.0
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort H)62.0

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Volume of Distribution of IBI308 in Plasma After Single Dose Administration

(NCT02937116)
Timeframe: Cycle 1: pre-dose, post-dose at 0, 1, 6 hours, and Days 2, 3, 8, 15, and 22, and 29

InterventionL (Geometric Mean)
Solid Tumors: Sintilimab 1mg/kg Q2W (Part A1)5.02
Solid Tumors: Sintilimab 3mg/kg Q2W (Part A2)5.14
Solid Tumors: Sintilimab 10mg/kg Q2W (Part A3)5.95
Solid Tumors: Sintilimab 200mg/kg Q3W (Part A4)7.2

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Time to Maximum Concentration (Tmax) of Sintilimab in Solid Tumor Participants

(NCT02937116)
Timeframe: Cycle 1: pre-dose, post-dose at 0, 1, 6 hours, and Days 2, 3, 8, 15, and 22, and 29

Interventionhours (Median)
Solid Tumors: Sintilimab 1mg/kg Q2W (Part A1)1.05
Solid Tumors: Sintilimab 3mg/kg Q2W (Part A2)2.07
Solid Tumors: Sintilimab 10mg/kg Q2W (Part A3)2.27
Solid Tumors: Sintilimab 200mg/kg Q3W (Part A4)1.93

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OS for Participants

(NCT02937116)
Timeframe: Through out the study

InterventionDays (Median)
MEL: Sintilimab 200mg Q3W (Cohort A)518.0
Malignant Tumor or Neuroendocrine Tumor: Sintilimab 200mg Q3W (Cohort B)342.0
NSCLC: Sintilimab 200mg Q3W (Cohort C)431.0
nsNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort D)566.0
scNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort E)461.0
Gastric or Gastroesophageal Junction Adenocarcinoma: Sintilimab 200mg Q3W + Chemotherapy (Cohort F)NA
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort G)NA
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort H)NA

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Area Under the Concentration-time Curve From Zero Time (Predose) to the Time of the Last Measurable Concentration (AUC0-t)

(NCT02937116)
Timeframe: Cycle 1: pre-dose, post-dose at 0, 1, and 6 hours, and Days 2, 3, 8, 15, and 22, and 29

Interventionh*ug/ml (Geometric Mean)
Solid Tumors: Sintilimab 1mg/kg Q2W (Part A1)4800
Solid Tumors: Sintilimab 3mg/kg Q2W (Part A2)12300
Solid Tumors: Sintilimab 10mg/kg Q2W (Part A3)39800
Solid Tumors: Sintilimab 200mg/kg Q3W (Part A4)10800

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Clearance of IBI308 in Plasma After Single Dose Administration

(NCT02937116)
Timeframe: Cycle 1: pre-dose, post-dose at 0, 1, 6 hours, and Days 2, 3, 8, 15, and 22, and 29

Interventionml/h (Geometric Mean)
Solid Tumors: Sintilimab 1mg/kg Q2W (Part A1)8.53
Solid Tumors: Sintilimab 3mg/kg Q2W (Part A2)11.7
Solid Tumors: Sintilimab 10mg/kg Q2W (Part A3)13.7
Solid Tumors: Sintilimab 200mg/kg Q3W (Part A4)12.9

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DOR According to RECIST 1.1 as Assessed by Investigator

(NCT02937116)
Timeframe: Through out the study (up to 2 years)

InterventionDays (Median)
MEL: Sintilimab 200mg Q3W (Cohort A)NA
Malignant Tumor or Neuroendocrine Tumor: Sintilimab 200mg Q3W (Cohort B)NA
NSCLC: Sintilimab 200mg Q3W (Cohort C)368.0
nsNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort D)NA
scNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort E)170.5
Gastric or Gastroesophageal Junction Adenocarcinoma: Sintilimab 200mg Q3W + Chemotherapy (Cohort F)181.0
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort G)NA
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort H)NA

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Maximum Concentration (Cmax) of Sintilimab in Solid Tumor Participants

(NCT02937116)
Timeframe: Cycle 1: pre-dose, post-dose at 0, 1, 6 hours, and Days 2, 3, 8, 15, and 22, and 29

Interventionug/ml (Geometric Mean)
Solid Tumors: Sintilimab 1mg/kg Q2W (Part A1)21.9
Solid Tumors: Sintilimab 3mg/kg Q2W (Part A2)69.7
Solid Tumors: Sintilimab 10mg/kg Q2W (Part A3)220
Solid Tumors: Sintilimab 200mg/kg Q3W (Part A4)54.6

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Number of All Study Participants Who Demonstrate a Tumor Response

(NCT02937116)
Timeframe: Through out the study (up to 2 years)

InterventionParticipants (Number)
Solid Tumors: Sintilimab 1mg/kg Q2W (Part A1)0
Solid Tumors: Sintilimab 3mg/kg Q2W (Part A2)1
Solid Tumors: Sintilimab 10mg/kg Q2W (Part A3)0
Solid Tumors: Sintilimab 200mg/kg Q3W (Part A4)1
MEL: Sintilimab 200mg Q3W (Cohort A)1
Malignant Tumor or Neuroendocrine Tumor: Sintilimab 200mg Q3W (Cohort B)13
NSCLC: Sintilimab 200mg Q3W (Cohort C)5
nsNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort D)13
scNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort E)11
Gastric or Gastroesophageal Junction Adenocarcinoma: Sintilimab 200mg Q3W + Chemotherapy (Cohort F)17
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort G)3
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort H)1

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Number of Participants Experiencing Dose-limiting Toxicities (DLTs)

(NCT02937116)
Timeframe: Up to 28 days in Cycle 1

InterventionParticipants (Number)
Solid Tumors: Sintilimab 1mg/kg Q2W (Part A1)0
Solid Tumors: Sintilimab 3mg/kg Q2W (Part A2)0
Solid Tumors: Sintilimab 10mg/kg Q2W (Part A3)0
Solid Tumors: Sintilimab 200mg/kg Q3W (Part A4)0

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Objective Response Rate (ORR) According to RECIST 1.1 as Assessed by Independent Review Committee by Investigator

ORR was defined as the percentage of participants in the analysis population who had achieved BOR of CR or PR according to RECIST 1.1. (NCT02937116)
Timeframe: Through out the study (up to 2 years)

Interventionpercentage of participants (Number)
MEL: Sintilimab 200mg Q3W (Cohort A)4.5
Malignant Tumor or Neuroendocrine Tumor: Sintilimab 200mg Q3W (Cohort B)14.9
NSCLC: Sintilimab 200mg Q3W (Cohort C)13.5
nsNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort D)61.9
scNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort E)55.0
Gastric or Gastroesophageal Junction Adenocarcinoma: Sintilimab 200mg Q3W + Chemotherapy (Cohort F)85.0
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort G)42.9
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort H)14.3

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PFS According to RECIST 1.1 as Assessed by Investigator

(NCT02937116)
Timeframe: Through out the study (up to 2 years)

InterventionDays (Median)
MEL: Sintilimab 200mg Q3W (Cohort A)62.0
Malignant Tumor or Neuroendocrine Tumor: Sintilimab 200mg Q3W (Cohort B)66.0
NSCLC: Sintilimab 200mg Q3W (Cohort C)84.0
nsNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort D)377.0
scNSCLC: Sintilimab 200mg Q3W + Chemotherapy (Cohort E)194.0
Gastric or Gastroesophageal Junction Adenocarcinoma: Sintilimab 200mg Q3W + Chemotherapy (Cohort F)230.0
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort G)NA
Neuroendocrine Tumors: Sintilimab 200mg Q3W + Chemotherapy (Cohort H)NA

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The Half-life (t1/2) of IBI308 in Plasma After Single Dose Administration

(NCT02937116)
Timeframe: Cycle 1: pre-dose, post-dose at 0, 1, 6 hours, and Days 2, 3, 8, 15, and 22, and 29

InterventionDays (Geometric Mean)
Solid Tumors: Sintilimab 1mg/kg Q2W (Part A1)17
Solid Tumors: Sintilimab 3mg/kg Q2W (Part A2)12.7
Solid Tumors: Sintilimab 10mg/kg Q2W (Part A3)12.5
Solid Tumors: Sintilimab 200mg/kg Q3W (Part A4)16.1

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Percentage of Participants With Progression Free Survival

We will define progression of disease per RECIST 1.1 criteria (NCT02954536)
Timeframe: 6 months

Interventionpercentage of participants with PRS (Number)
Pembrolizumab, Trastuzumab,Capecitabine/Cisplatin70

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Stage 1: Disease Control Rate (DCR): Percentage of Participants With a Best Overall Response of Complete Response (CR), Partial Response (PR) or Stable Disease (SD)

Disease control rate (DCR) is the percentage of participants with a best overall response of CR, PR or SD as defined by RECIST v1.1. CR is defined as the disappearance of all target and non-target lesions and no appearance of new lesions. PR is defined as at least a 30% decrease in the sum of the longest diameter (LD) of target lesions (taking as reference the baseline sum LD), no progression of non-target lesions, and no appearance of new lesions. SD is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD) for target lesions, no progression of non-target lesions, and no appearance of new lesions. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, with reference being the smallest sum on study and an absolute increase of at least 5 mm, or unequivocal progression of non-target lesions, or 1 or more new lesions. (NCT02981342)
Timeframe: Baseline to Measured Progressive Disease or Start of New Anticancer Therapy (Up to 6 Months)

Interventionpercentage of Participants (Number)
200mg Abemaciclib15.2
150mg Abemaciclib + 150mg LY302341412.1
Gemcitabine or Capecitabine36.4

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Stage 2: Clinical Benefit Rate (CBR): Percentage of Participants With Best Overall Response of CR, PR, or SD With Duration of SD for at Least 6 Months

"Clinical benefit rate (CBR) is the percentage of participants with a BOR of CR or PR, or SD ≥6 months. CR is defined as the disappearance of all target and non-target lesions & no appearance of new lesions. PR is defined as at least a 30% decrease in the sum of the LD of target lesions (taking as reference the baseline sum LD), no progression of non-target lesions, and no appearance of new lesions. SD is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD for target lesions, no progression of non-target lesions, and no appearance of new lesions. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, with reference being the smallest sum on study and an absolute increase of at least 5 mm, or unequivocal progression of non-target lesions, or 1 or more new lesions.~No participants were enrolled to stage 2; however, results for stage 2 outcomes are reported from the data collected for participants enrolled to stage 1." (NCT02981342)
Timeframe: Baseline to Disease Progression or Start of New Anticancer Therapy (Up to 6 Months)

Interventionpercentage of participants (Number)
200mg Abemaciclib3
150mg Abemaciclib + 150mg LY30234140
Gemcitabine or Capecitabine3

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Stage 2: Change From Baseline in Carbohydrate Antigen 19.9 (CA 19-9) Level

No participants were enrolled to stage 2; however, results for stage 2 outcomes are reported from the data collected for participants enrolled to stage 1. (NCT02981342)
Timeframe: Baseline, 6 Months

InterventionU/mL (Mean)
200mg Abemaciclib4281.53
150mg Abemaciclib + 150mg LY30234143225.29
Gemcitabine or Capecitabine-501.17

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Stage 1: PK: Steady State Trough Pre Dose Concentration of LY3023414

Mean steady state exposure was reported by trough pre-dose plasma concentrations. (NCT02981342)
Timeframe: C2D1: 0h, C3D1: 0h, C4D1: 0h

Interventionng/mL (Geometric Mean)
150mg Abemaciclib + 150mg LY302341427.3

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Stage 1: Pharmacokinetics (PK): Mean Steady State Exposure of Abemaciclib and Its Metabolites (LSN2839567 (M2), LSN3106726 (M20))

Mean steady state exposure was reported as measured by maximum observed plasma concentration (Cmax). (NCT02981342)
Timeframe: Cycle(C)1 Day(D)14: 0 hour(h),0.5h,1h,2h,4h,6h,8h post dose

InterventionNanogram per Millilitre (ng/mL) (Geometric Mean)
AbemaciclibLSN2839567 (M2)LSN3106726 (M20)
150mg Abemaciclib + 150mg Galunisertib35685.1153

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Stage 2: Change From Baseline in Pain and Symptom Burden Assessment on the Modified Brief Pain Inventory-Short Form (mBPI-sf)

"mBPI-sf is an 11-item instrument used as a multiple-item measure of cancer pain intensity. In addition to pain intensity (4 items), the mBPI-sf is designed for participants to record the presence of pain in general, pain relief, and pain interference with function (general activity, mood, ability to walk, ability to perform normal work, relations with others, sleep, and enjoyment of life). Responses for the mBPI-sf items are captured through the use of 11-point numeric rating scales anchored at 0 (no pain or does not interfere) and ranged through 10 (pain as bad as you can imagine or completely interferes). The mBPI-sf recall period is 24 hours, and typical completion time for this instrument is less than 5 minutes.~No participants were enrolled to stage 2; however, results for stage 2 outcomes are reported from the data collected for participants enrolled to stage 1." (NCT02981342)
Timeframe: Baseline, 6 Months

,,
Interventionscore on a scale (Least Squares Mean)
Pain at its Worst in Last 24 hoursPain at its Least in Last 24 hoursPain on the AveragePain Right NowPain Interfered General ActivityPain Interfered with MoodPain Interfered Walking AbilityPain Interfered with Normal WorkPain Interfered with RelationsPain Interfered with SleepPain Interfered Enjoyment of LifeBPI Mean Pain Interference Score
150mg Abemaciclib + 150mg LY3023414-0.330.18-0.030.340.070.280.830.660.670.340.390.50
200mg Abemaciclib0.630.860.620.380.640.540.051.070.390.190.690.55
Gemcitabine or Capecitabine-0.020.39-0.07-0.380.220.600.190.190.26-0.56-0.130.05

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Stage 2: Progression Free Survival (PFS)

PFS was defined as the time from the date of randomization until first observation of objective progressive disease as defined by RECIST v1.1 or death from any cause, whichever comes first. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, with reference being the smallest sum on study and an absolute increase of at least 5 mm, or unequivocal progression of non-target lesions, or 1 or more new lesions. If a patient does not have a complete baseline disease assessment, then the PFS time will be censored at the randomization date, regardless of whether or not objectively determined disease progression or death has been observed for the patient; otherwise, if a patient is not known to have died or have objective progression as of the data inclusion cutoff date for the analysis, the PFS time will be censored at the last complete objective progression-free disease assessment date. (NCT02981342)
Timeframe: Baseline to Measured Progressive Disease or Death Due to Any Cause (Up to 6 Months)

InterventionMonths (Median)
200mg Abemaciclib1.68
150mg Abemaciclib + 150mg LY30234141.81
Gemcitabine or Capecitabine3.25

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Stage 2: Change From Baseline in Symptom Burden on the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30 (EORTC QLQ-C30)

"The EORTC QLQ-C30 self-reported general cancer instrument consists of 30 items covered by 1 of 3 dimensions:~Global health status/quality of life (2 items) with scores ranging from 1 (Very Poor) to 7 (Excellent).~Functional scales (15 total items addressing either physical, role, emotional, cognitive, or social functioning), each item scores ranging from 1 (not at all) to 4 (very much)~Symptom scales (13 total items addressing either fatigue, nausea/vomiting, pain, dyspnea, insomnia, appetite loss, constipation, diarrhea, or financial impact), each item scores ranging from 1 (not at all) to 4 (very much).~Raw scores are linearly converted to a 0-100 scale with higher scores reflecting higher levels of function/QOL or higher levels of symptom burden.~No participants were enrolled to stage 2; however, results for stage 2 outcomes are reported from the data collected for participants enrolled to stage 1." (NCT02981342)
Timeframe: Baseline, 6 Months

,,
Interventionunits on a scale (Least Squares Mean)
Global Health StatusFunctional Scales: Physical FunctioningFunctional Scales: Role FunctioningFunctional Scales: Emotional FunctioningFunctional Scales: Cognitive FunctioningFunctional Scale: Social FunctioningSymptom Scales: FatigueSymptom Scales: Nausea and VomitingSymptom Scales: PainSymptom Scale: DysopneaSymptom Scale: InsomniaSymptom Scale: Appetite LossSymptom Scale: ConstipationSymptom Scale: DiarrhoeaSymptom Scale: Financial difficulties
150mg Abemaciclib + 150mg LY3023414-4.82-11.65-18.05-0.63-8.39-17.0914.909.422.6811.191.8315.32-6.5126.282.45
200mg Abemaciclib-6.21-14.44-17.09-4.89-10.43-21.1214.137.989.790.35-5.1912.542.9615.713.96
Gemcitabine or Capecitabine-2.40-5.42-17.102.06-5.18-2.005.6411.885.43-4.51-6.719.5112.9320.51-3.30

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Stage 1: Objective Response Rate (ORR): Percentage of Participants With a Best Overall Response (BOR) of CR or PR

Objective response rate (ORR) is the percentage of participants with a BOR of CR or PR as defined by RECIST v1.1. CR is defined as the disappearance of all target and non-target lesions and no appearance of new lesions. PR is defined as at least a 30% decrease in the sum of the LD of target lesions (taking as reference the baseline sum LD), no progression of non-target lesions, and no appearance of new lesions. (NCT02981342)
Timeframe: Baseline to Measured Progressive Disease or Start of New Anti-Cancer Therapy (Up to 6 Months)

Interventionpercentage of Participants (Number)
200mg Abemaciclib3
150mg Abemaciclib + 150mg LY30234140
Gemcitabine or Capecitabine3

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Stage 1: PK: Mean Single Dose Concentration of LY3023414 at 2h Post-dose

Mean single dose exposure was reported by plasma concentrations collected approximately 2 hours post-dose. (NCT02981342)
Timeframe: C1D1: 2h Post dose

Interventionng/mL (Geometric Mean)
150mg Abemaciclib + 150mg LY3023414518

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Stage 2: Overall Survival (OS)

"OS duration is measured from the date of randomization to the date of death from any cause. for participants who is not known to have died as of the data-inclusion cutoff date, OS was censored at the last known alive date.~No participants were enrolled to stage 2; however, results for stage 2 outcomes are reported from the data collected for participants enrolled to stage 1." (NCT02981342)
Timeframe: Baseline to Death from Any Cause (Up to 10 Months)

InterventionMonths (Median)
200mg Abemaciclib2.71
150mg Abemaciclib + 150mg LY30234143.29
Gemcitabine or CapecitabineNA

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Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT03026803)
Timeframe: Up to 2 years

Interventionpercentage of participants (Number)
Oxaliplatin and Capecitabine0

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1-year Progression Free Survival (PFS) Rate

"To evaluate the 1-year progression free survival (PFS) rate per RECIST v. 1.1.~PFS is defined as the length of time during and after the treatment that a patient does not experience progression.~Progressive Disease (PD) as defined per RECIST 1.1 is at least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. (Note: the appearance of one or more new lesions is also considered progression).~PFS was analyzed using a Kaplan-Meier curve." (NCT03044730)
Timeframe: Up to 1 year after starting treatment

Interventionpercentage of participants (Number)
Treatment: Pembrolizumab + Capecitabine20.7

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Objective Response Rate (ORR)

"The ORR is the percentage of patients whose cancer shrinks or disappears after treatment. Objective response rate was calculated based on the number of patients who had a Complete Response (CR) or a Partial Response (PR). CR and PR were measured according to RECIST v. 1.1 guidelines:~Complete Response (CR): Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~Partial Response (PR): At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters." (NCT03044730)
Timeframe: Up to 9 Cycles (1 cycle = 21 days)

Interventionparticipants (Number)
Complete ResponsePartial Response
Treatment: Pembrolizumab + Capecitabine04

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Objective Response Rate (ORR)

"The ORR is the percentage of patients whose cancer shrinks or disappears after treatment. Objective response rate was calculated based on percentage of patients who had a Complete Response (CR) or a Partial Response (PR). CR and PR were measured according to RECIST v. 1.1 guidelines:~Complete Response (CR): Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~Partial Response (PR): At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters." (NCT03044730)
Timeframe: Up to 9 Cycles (1 cycle = 21 days)

Interventionpercentage of participants (Number)
Treatment: Pembrolizumab + Capecitabine14

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Median PFS (Median Progression-Free Survival)

"To evaluate the median Progression-Free Survival (PFS) for participants receiving pembrolizumab with capecitabine for the treatment of locally advanced or metastatic TNBC and hormone-refractory MBC. PFS is defined as the length of time during and after the treatment that a patient does not experience progression.~Progressive Disease (PD) as defined per RECIST 1.1 is at least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. (Note: the appearance of one or more new lesions is also considered progression).~PFS was analyzed using a Kaplan-Meier curve.~For PFS, assumptions were that the addition of pembrolizumab would increase PFS to 5 months compared to historical control of 3 months." (NCT03044730)
Timeframe: Approximately 20 months

Interventionmonths (Median)
Treatment: Pembrolizumab + Capecitabine4.13

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Median PFS (Median Progression-Free Survival)

"To evaluate the median Progression-Free Survival (PFS) for participants receiving pembrolizumab with capecitabine for the treatment of locally advanced or metastatic TNBC and hormone-refractory MBC. PFS is defined as the length of time during and after the treatment that a patient does not experience progression.~Progressive Disease (PD) as defined per RECIST 1.1 is at least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. (Note: the appearance of one or more new lesions is also considered progression).~PFS was analyzed using a Kaplan-Meier curve. For PFS, assumptions were that the addition of pembrolizumab would increase PFS to 5 months compared to historical control of 3 months." (NCT03044730)
Timeframe: Approximately 20 months

Interventionmonths (Median)
Treatment: Pembrolizumab + Capecitabine4.0

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Clinical Benefit Rate (CBR)

To evaluate the clinical benefit rate (CBR) per RECIST v. 1.1. CBR is the rate of participants with complete response (CR), partial response (PR) or stable disease (SD) > 6 months. PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD), taking as reference the smallest sum diameters while on study. PD: At least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. The appearance of one or more new lesions is also considered progression. CR: Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm. (NCT03044730)
Timeframe: Up to 14 cycles (1 cycle= 21 days)

Interventionpercentage of participants (Number)
Treatment: Pembrolizumab + Capecitabine28

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Number of Participants That Are Hospitalized Because of Adverse Events Attributed to Disease Progression

Participants hospitalized because of adverse events measured by the Common Terminology Criteria for Adverse Events (CTCAE) v5.0 attributed to disease progression. Progression was measured by the Response Evaluation Criteria in Solid Tumors (RECIST) and is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. The appearance of one or more new lesions is also considered progressions. (NCT03050814)
Timeframe: Up to 51.5 months

InterventionParticipants (Count of Participants)
Standard of Care (SOC) - Arm A4
Standard of Care (SOC) - Arm B + Lead in4

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Number of Participants With Serious and Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v5.0)

Here is the number of participants with serious and non-serious adverse events assessed by the Common Terminology Criteria for Adverse Events (CTCAE v5.0). A non-serious adverse event is any untoward medical occurrence. A serious adverse event is an adverse event or suspected adverse reaction that results in death, a life-threatening adverse drug experience, hospitalization, disruption of the ability to conduct normal life functions, congenital anomaly/birth defect or important medical events that jeopardize the patient or subject and may require medical or surgical intervention to prevent one of the previous outcomes mentioned. (NCT03050814)
Timeframe: Date treatment consent signed to date off study, approximately 33 months and 20 days for Arm A and 51 months and 7 days for Arm B.

InterventionParticipants (Count of Participants)
Standard of Care (SOC) - Arm A10
Standard of Care (SOC) - Arm B + Lead in16

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Progression Free Survival Between the Standard of Care (SOC) Arm A, and Standard of Care (SOC) Arm B + lead-in

Progression free survival is defined as the duration of time from start of treatment to time of progression or death, whichever occurs first. Progression was measured by the Response Evaluation Criteria in Solid Tumors (RECIST) and is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. The appearance of one or more new lesions is also considered progressions. (NCT03050814)
Timeframe: Up to 1.5 years

InterventionMonths (Median)
Standard of Care (SOC) - Arm A8.8
Standard of Care (SOC) - Arm B + Lead in10.1

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Number of Participants With Clinically Significant Change in Vital Signs and Physical Examinations - Part 1

Number of participants with clinically significant change in vital signs (blood pressure [diastolic and systolic], heart rate, respiratory rate, body temperature) and physical examination. (NCT03093870)
Timeframe: Subject screening visit to 28 days post last study drug administration

InterventionParticipants (Count of Participants)
Varlitinib and Capecitabine0
Placebo and Capecitabine0

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Progression-free Survival (PFS) - Part 1

Part 1: Progression-free survival (PFS) was defined as the time from randomization (or starting treatment for the Safety Lead-in) until the date of objective disease progression or death (by any cause in the absence of disease progression) regardless of whether the subject withdrew from randomized therapy or received another antitumor therapy prior to disease progression. Subjects who did not experience disease progression or died at the time of analysis were censored at the time of the latest date of assessment from their last evaluable RECIST assessment. However, if the patient progressed or died after ≥ 2 missed visits (12 weeks ± 5 days maximum), the subject was censored at the time of the latest evaluable RECIST assessment. The PFS time was based on the scan/assessment dates rather than visit dates. (NCT03093870)
Timeframe: Time from randomization until date of objective disease progression or death (by any cause in absence of disease progression) regardless of whether subject withdrew from randomized therapy or received another antitumor therapy prior to PD, up to 2 years.

InterventionMonths (Median)
Varlitinib and Capecitabine2.83
Placebo and Capecitabine2.79

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Number of Participants With ECG Parameters of Interest - Safety Lead-In

Number of participants with ECG parameters of interest: Max. on-treatment QTcF Value: >450 to 480 msec, max. on-treatment QTcF Value: >480 to 500 msec, max. on-treatment QTcF Value: >500 msec, max. on-treatment QTcB Value: >450 to 480 msec, max. on-treatment QTcB Value: >480 to 500 msec, max. on-treatment QTcB Value: >500 msec, max. QTcF CFB Value: >30 to 60 msec, max. QTcF CFB Value: >60 msec, max. QTcB CFB Value: >30 to 60 msec, max. QTcB CFB Value: >60 msec. (NCT03093870)
Timeframe: Subject screening visit to 28 days post last study drug administration

Interventionparticipants (Number)
Maximum on-treatment QTcF Value: >450 to 480 msecMaximum on-treatment QTcF Value: >480 to 500 msecMaximum on-treatment QTcF Value: >500 msecMaximum on-treatment QTcB Value: >450 to 480 msecMaximum on-treatment QTcB Value: >480 to 500 msecMaximum on-treatment QTcB Value: >500 msecMaximum QTcF CFB Value: >30 to 60 msecMaximum QTcF CFB Value: >60 msecMaximum QTcB CFB Value: >30 to 60 msecMaximum QTcB CFB Value: >60 msec
Varlitinib + Capecitabine80010208161

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Number of Participants With Clinically Significant Laboratory Tests - Part 1

Clinical laboratory tests (hematology, clinical chemistry, urinalysis) - Number of Participants with Clinically Significant Laboratory Tests. (NCT03093870)
Timeframe: Subject screening visit to 28 days post last study drug administration

InterventionParticipants (Count of Participants)
Varlitinib and Capecitabine0
Placebo and Capecitabine0

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Overall Survival (OS) - Part 1

Part 1: Overall survival (OS) was defined as the time from the date of randomization until death due to any cause. Any subject not known to have died at the time of the data cut-off was censored based on the last recorded date on which the subject was known to be alive. (NCT03093870)
Timeframe: Time from the date of randomization until death due to any cause, up to 2 years

InterventionMonths (Median)
Varlitinib and Capecitabine7.8
Placebo and Capecitabine7.5

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Number of Participants With Clinically Significant Laboratory Tests- Safety Lead-in

Clinical laboratory tests (hematology, clinical chemistry, urinalysis) - Number of Participants with Clinically Significant Laboratory Tests. (NCT03093870)
Timeframe: Subject screening visit to 28 days post last study drug administration

InterventionParticipants (Count of Participants)
Varlitinib + Capecitabine0

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Duration of Response (DoR) - Part 1

"Part 1: Duration of response (DoR) was defined as the time from the date of first documented response until the date of documented PD or death in the absence of disease progression. The end of the response should have coincided with the date of disease progression or death from any cause used for the PFS endpoint.~For Part 1, DoR was calculated based on data from the ICR of radiological data." (NCT03093870)
Timeframe: Time from the date of first documented response until the date of documented PD or death in the absence of disease progression, up to 2 years

InterventionDays (Median)
Varlitinib and Capecitabine158
Placebo and Capecitabine90

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Number of Participants With Clinically Significant Change in Vital Signs and Physical Examinations - Safety Lead-In

Number of participants with clinically significant change in vital signs (blood pressure [diastolic and systolic], heart rate, respiratory rate, body temperature) and physical examination. (NCT03093870)
Timeframe: Subject screening visit to 28 days post last study drug administration

InterventionParticipants (Count of Participants)
Varlitinib + Capecitabine0

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Number of Participants With ECG Parameters of Interest - Part 1

Number of participants with ECG parameters of interest: Max. on-treatment QTcF Value: <=450 msec, max. on-treatment QTcF Value: >450 to 480 msec, max. on-treatment QTcF Value: >480 to 500 msec, max. on-treatment QTcF Value: >500 msec, max. on-treatment QTcB Value: <=450 msec, max. on-treatment QTcB Value: >450 to 480 msec, max. on-treatment QTcB Value: >480 to 500 msec, max. on-treatment QTcB Value: >500 msec, max. QTcF CFB Value: <=30 msec, max. QTcF CFB Value: >30 to 60 msec, max. QTcF CFB Value: >60 msec, max. QTcB CFB Value: <=30 msec, max. QTcB CFB Value: >30 to 60 msec, max. QTcB CFB Value: >60 msec. (NCT03093870)
Timeframe: Subject screening visit to 28 days post last study drug administration

,
InterventionParticipants (Number)
Maximum on-treatment QTcF Value: <=450 msecMaximum on-treatment QTcF Value: >450 to 480 msecMaximum on-treatment QTcF Value: >480 to 500 msecMaximum on-treatment QTcF Value: >500 msecMaximum on-treatment QTcB Value: <=450 msecMaximum on-treatment QTcB Value: >450 to 480 msecMaximum on-treatment QTcB Value: >480 to 500 msecMaximum on-treatment QTcB Value: >500 msecMaximum QTcF CFB Value: <=30 msecMaximum QTcF CFB Value: >30 to 60 msecMaximum QTcF CFB Value: >60 msecMaximum QTcB CFB Value: <=30 msecMaximum QTcB CFB Value: >30 to 60 msecMaximum QTcB CFB Value: >60 msec
Placebo and Capecitabine5760040221057415471
Varlitinib and Capecitabine53100142210156705580

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Tumor Size - Part 1

Part 1: The percentage change from baseline in tumor size at Week 12 (%ΔTSWk12) was a secondary endpoint for Part 1 and was used to present waterfall plots of the target lesion data in the Evaluable for Response (EFR) Population (NCT03093870)
Timeframe: Week 12

InterventionPercentage change from Baseline (Mean)
Varlitinib and Capecitabine18.1
Placebo and Capecitabine22.6

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Number of Participants Obtaining a Complete Response (CR) and Partial Response (PR)

Number of participants obtaining CR and PR per the Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 criteria of all evaluable patients. CR is disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm. PR is at least a 30% decrease in the sum of the diameters of target lesions,taking as reference the baseline sum of diameters. (NCT03111732)
Timeframe: Every 9 Weeks, until disease progression or patient is taken off the trial, whichever comes first, approximately 36 weeks.

InterventionParticipants (Count of Participants)
Complete ResponsePartial Response
1/Arm 1 - Pembrolizumab Plus Oxaliplatin Plus Capecitabine03

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Overall Survival

Median amount of time subject survives after therapy. (NCT03111732)
Timeframe: Death, approximately 48 weeks after stopping therapy.

InterventionWeeks (Median)
1/Arm 1 - Pembrolizumab Plus Oxaliplatin Plus Capecitabine43

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Number of Participants With Serious and Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0)

Here is the number of participants with serious and non-serious adverse events assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0). A non-serious adverse event is any untoward medical occurrence. A serious adverse event is an adverse event or suspected adverse reaction that results in death, a life-threatening adverse drug experience, hospitalization, disruption of the ability to conduct normal life functions, congenital anomaly/birth defect or important medical events that jeopardize the patient or subject and may require medical or surgical intervention to prevent one of the previous outcomes mentioned. (NCT03111732)
Timeframe: Date treatment consent signed to date off study, approximately 38 months and 25 days.

InterventionParticipants (Count of Participants)
1/Arm 1 - Pembrolizumab Plus Oxaliplatin Plus Capecitabine11

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Progression Free Survival (PFS)

Median amount of time subject survives without disease progression for 5 months after treatment. Disease progression was assessed by the Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 and is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). The appearance of one or more new lesions is also considered progressions. (NCT03111732)
Timeframe: 5 Months

InterventionMonths (Median)
1/Arm 1 - Pembrolizumab Plus Oxaliplatin Plus Capecitabine4.54

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Investigator Assessed Progression Free Survival

Progression-free survival is defined as the time from the date of randomization to the date of first documented disease progression by investigator assessment according to RECIST v1.1 or death due to any cause, whichever occurred earlier. (NCT03262935)
Timeframe: baseline until primary analysis data cut-off date of 31March2021

Interventionmonths (Median)
(Vic-)Trastuzumab Duocarmazine6.9
Physician's Choice4.6

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Objective Response Rate

Objective Response Rate is defined as the proportion of patients with a centrally assessed best overall response of complete response or partial response according to RECIST v1.1. (NCT03262935)
Timeframe: baseline until primary analysis data cut-off date of 31March2021

Interventionpercentage of patients (Number)
(Vic-)Trastuzumab Duocarmazine27.8
Physician's Choice29.5

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Overall Survival

Overall survival is defined as the time from date of randomization to death due to any cause. (NCT03262935)
Timeframe: baseline until final Overall Survival analysis data cut-off date of 30June2022

Interventionmonths (Median)
(Vic-)Trastuzumab Duocarmazine21.0
Physician's Choice19.5

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Progression Free Survival

Progression-free survival is defined as the time from the date of randomization to the date of first documented disease progression by central assessment according to Response Evaluation Criteria In Solid Tumors (RECIST) v1.1 or death due to any cause, whichever occurred earlier. (NCT03262935)
Timeframe: baseline until primary analysis data cut-off date of 31March2021

Interventionmonths (Median)
(Vic-)Trastuzumab Duocarmazine7.0
Physician's Choice4.9

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Progression Free Survival (PFS)

To determine the progression free survival (NCT03376659)
Timeframe: 24 months

Interventionmonths (Median)
Phase I - Safety- Overall4.7

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Progression Free Survival Rate (PFS) Pancreatic Cancer

To determine the 4 month progression free survival rate (PFS4mos) of durvalumab plus CV301 in combination with maintenance capecitabine in patients with metastatic pancreatic cancer, whose disease is stable on, or responding to 1st line therapy for metastatic disease (NCT03376659)
Timeframe: 24 months

Interventionmonths (Median)
Phase I - Safety- Pancreatic Cancer4.5

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Progression Free Survival Rate (PFS) Colorectal Cancer

To determine the progression free survival rate (PFS) of durvalumab plus CV301 in combination with maintenance capecitabine and bevacizumab in patients with metastatic colorectal cancer, whose disease is stable on, or responding to 1st line therapy for metastatic disease (NCT03376659)
Timeframe: 24 months

Interventionmonths (Median)
Phase I - Safety- Colorectal Cancer7.4

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Length of Subject Survival After Starting Study Treatment

Number of participants alive. A Gehan-like trial design with an interim futility analysis will be used. (NCT03501979)
Timeframe: Through study completions, an average of 2 years

InterventionParticipants (Count of Participants)
Tucatinib + Trastuzumab + Capecitabine6

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Median Time to Recurrence

Disease recurrence will be defined as radiographic tumor evidence detected by surveillance imaging. Confirmation of recurrence by biopsy will be at the discretion of the treating physician. This study closed early on June 18, 2020. It was earlier than one planned because of the lack of accrual. (NCT03515941)
Timeframe: From the end of completion of assigned therapy, subjects undergo follow-up every 3 months for a total of 36 months(planned) after the date of surgery or until the study closure

Interventionmonths (Median)
Arm 1: Adjuvant ChemotherapyNA
Arm 2: Adjuvant ChemoradiationNA

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Percentage of Participants With Objective Response Rate (ORR) in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine

The Objective Response Rate (ORR) was defined as the percentage of participants who achieved a best overall response of confirmed Complete Response (CR) or Partial Response (PR), assessed by BICR and investigator assessment based on RECIST version 1.1. CR was defined as a disappearance of all target lesions and PR was defined as at least a 30% decrease in the sum of diameters of target lesions. Confirmed ORR based on BICR and Investigator Assessment is reported. (NCT03523585)
Timeframe: Baseline up to 46 months postdose

,
InterventionPercentage of Participants (Number)
BICRInvestigator Assessment
Trastuzumab Deruxtecan (T-DXd)69.774.1
Treatment of Investigator's/Physician's Choice (TPC)29.226.7

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Duration of Response (DoR) Based on BICR in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine

Duration of Response (DoR) was defined as the time from the date of the first documentation of objective response (complete response [CR] or partial response [PR]) to the date of the first objective documentation of progressive disease (PD) or death due to any cause. DoR in participants with confirmed CR/PR based on BICR and investigator assessment is reported. (NCT03523585)
Timeframe: Baseline up to 46 months postdose

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)19.6
Treatment of Investigator's/Physician's Choice (TPC)8.3

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Overall Survival (OS) in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine

Overall survival (OS) was defined as the time from the date of randomization to the date of death due to any cause. If there is no death reported for a subject before the data cutoff for OS analysis, OS will be censored at the last contact date at which the subject is known to be alive. (NCT03523585)
Timeframe: Baseline up to 46 months postdose

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)39.2
Treatment of Investigator's/Physician's Choice (TPC)26.5

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Progression-Free Survival (PFS) Based on Blinded Independent Central Review (BICR) in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine

Progression-free survival (PFS) by BICR was defined as the time from the date of randomization to the earlier of the dates of the first objective documentation of disease progression (as per RECIST v1.1) or death due to any cause. (NCT03523585)
Timeframe: Baseline up to 46 months postdose

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)17.8
Treatment of Investigator's/Physician's Choice (TPC)6.9

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Progression-Free Survival (PFS) Based on Investigator Assessment in Participants With HER2-positive, Unresectable and/or Metastatic Breast Cancer Participants Previously Treated With Trastuzumab Emtansine

Progression-free survival (PFS) by investigator assessment was defined as the time from the date of randomization to the earlier of the dates of the first objective documentation of disease progression (as per RECIST v1.1) or death due to any cause. (NCT03523585)
Timeframe: Up to 46 months

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)16.7
Treatment of Investigator's/Physician's Choice (TPC)5.5

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Objective Response Rate (ORR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥1

ORR was defined as the percentage of the participants who had a confirmed Complete Response (CR: disappearance of all target lesions) or Partial Response (PR: ≥30% decrease in the sum of diameters (SOD) of target lesions, taking as reference the baseline SOD) according to RECIST 1.1 as assessed by BICR. (NCT03675737)
Timeframe: Up to 49.5 months

InterventionPercentage of Participants (Number)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)52.1
Placebo + Chemotherapy (FP or CAPOX Regimen)42.6

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Objective Response Rate (ORR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥10

ORR was defined as the percentage of the participants who had a confirmed Complete Response (CR: disappearance of all target lesions) or Partial Response (PR: ≥30% decrease in the sum of diameters (SOD) of target lesions, taking as reference the baseline SOD) according to RECIST 1.1 as assessed by BICR. (NCT03675737)
Timeframe: Up to 49.5 months

InterventionPercentage of Participants (Number)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)60.6
Placebo + Chemotherapy (FP or CAPOX Regimen)43.0

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Overall Survival (OS) in All Participants

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the analysis were censored at the date of the last follow-up. OS was estimated using the product-limit (Kaplan-Meier) method for censored data. (NCT03675737)
Timeframe: Up to 45.9 months

InterventionMonths (Median)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)12.9
Placebo + Chemotherapy (FP or CAPOX Regimen)11.5

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Overall Survival (OS) In Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥10

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the analysis were censored at the date of the last follow-up. OS was estimated using the product-limit (Kaplan-Meier) method for censored data. (NCT03675737)
Timeframe: Up to 45.9 months

InterventionMonths (Median)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)15.7
Placebo + Chemotherapy (FP or CAPOX Regimen)11.8

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Progression Free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in All Participants

PFS was defined as the time from randomization to the first documented progressive disease (PD) or death due to any cause, whichever occurred first. Per RECIST 1.1 as assessed by BICR, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum must also have demonstrated an absolute increase of ≥5 mm. The appearance of ≥1 new lesions was also considered PD. PFS was estimated using the product-limit (Kaplan-Meier) method for censored data. (NCT03675737)
Timeframe: Up to 49.5 months

InterventionMonths (Median)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)6.9
Placebo + Chemotherapy (FP or CAPOX Regimen)5.6

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Progression Free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥1

PFS was defined as the time from randomization to the first documented progressive disease (PD) or death due to any cause, whichever occurred first. Per RECIST 1.1 as assessed by BICR, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum must also have demonstrated an absolute increase of ≥5 mm. The appearance of ≥1 new lesions was also considered PD. PFS was estimated using the product-limit (Kaplan-Meier) method for censored data. (NCT03675737)
Timeframe: Up to 49.5 months

InterventionMonths (Median)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)6.9
Placebo + Chemotherapy (FP or CAPOX Regimen)5.6

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Progression Free Survival (PFS) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥10

PFS was defined as the time from randomization to the first documented progressive disease (PD) or death due to any cause, whichever occurred first. Per RECIST 1.1 as assessed by BICR, PD was defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum must also have demonstrated an absolute increase of ≥5 mm. The appearance of ≥1 new lesions was also considered PD. PFS was estimated using the product-limit (Kaplan-Meier) method for censored data. (NCT03675737)
Timeframe: Up to 49.5 months

InterventionMonths (Median)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)8.1
Placebo + Chemotherapy (FP or CAPOX Regimen)5.6

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Duration of Response (DOR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in All Participants

DOR was defined as the time from first documented evidence of a confirmed Complete Response (CR) or Partial Response (PR) until progressive disease (PD) or death, whichever occurred first. Per RECIST 1.1 as assessed by BICR, CR was the disappearance of all target lesions and PR was ≥30% decrease in the sum of diameters (SOD) of target lesions, taking as reference the baseline SOD. PD was defined as ≥20% increase in the SOD of target lesions according to RECIST 1.1. In addition to the relative increase of 20%, the SOD must also have demonstrated an absolute increase of ≥5 mm. The appearance of ≥1 new lesions was also considered PD. DOR for participants who had not progressed or died at the time of analysis was censored at the date of the last tumor assessment. DOR was estimated using the product-limit (Kaplan-Meier) method for censored data. (NCT03675737)
Timeframe: Up to 49.5 months

InterventionMonths (Median)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)8.0
Placebo + Chemotherapy (FP or CAPOX Regimen)5.7

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Duration of Response (DOR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥1

DOR was defined as the time from first documented evidence of a confirmed Complete Response (CR) or Partial Response (PR) until progressive disease (PD) or death, whichever occurred first. Per RECIST 1.1 as assessed by BICR, CR was the disappearance of all target lesions and PR was ≥30% decrease in the sum of diameters (SOD) of target lesions, taking as reference the baseline SOD. PD was defined as ≥20% increase in the SOD of target lesions according to RECIST 1.1. In addition to the relative increase of 20%, the SOD must also have demonstrated an absolute increase of ≥5 mm. The appearance of ≥1 new lesions was also considered PD. DOR for participants who had not progressed or died at the time of analysis was censored at the date of the last tumor assessment. DOR was estimated using the product-limit (Kaplan-Meier) method for censored data. (NCT03675737)
Timeframe: Up to 49.5 months

InterventionMonths (Median)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)8.3
Placebo + Chemotherapy (FP or CAPOX Regimen)5.6

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Overall Survival (OS) In Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥1

OS was defined as the time from randomization to death due to any cause. Participants without documented death at the time of the analysis were censored at the date of the last follow-up. OS was estimated using the product-limit (Kaplan-Meier) method for censored data. (NCT03675737)
Timeframe: Up to 45.9 months

InterventionMonths (Median)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)13.0
Placebo + Chemotherapy (FP or CAPOX Regimen)11.4

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Number of Participants Who Discontinued Study Treatment Due To an Adverse Event (AE)

An AE was defined as any untoward medical occurrence in a clinical study participant, temporally associated with the use of study intervention, whether or not considered related to the study intervention. An AE could therefore have been any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a study intervention. The number of participants who discontinued study treatment due to an AE is presented. (NCT03675737)
Timeframe: Up to 33.7 months

InterventionParticipants (Count of Participants)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)257
Placebo + Chemotherapy (FP or CAPOX Regimen)204

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Number of Participants Who Experienced an Adverse Event (AE)

An AE was defined as any untoward medical occurrence, in a clinical study participant, temporally associated with the use of study intervention, whether or not considered related to the study intervention. An AE could therefore have been any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a study intervention. The number of participants with at least one AE is presented. (NCT03675737)
Timeframe: Up to 36.7 months

InterventionParticipants (Count of Participants)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)776
Placebo + Chemotherapy (FP or CAPOX Regimen)771

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Objective Response Rate (ORR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in All Participants

ORR was defined as the percentage of the participants who had a confirmed Complete Response (CR: disappearance of all target lesions) or Partial Response (PR: ≥30% decrease in the sum of diameters (SOD) of target lesions, taking as reference the baseline SOD) according to RECIST 1.1 as assessed by BICR. (NCT03675737)
Timeframe: Up to 49.5 months

InterventionPercentage of Participants (Number)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)51.3
Placebo + Chemotherapy (FP or CAPOX Regimen)42.0

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Duration of Response (DOR) Per Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1) Assessed by Blinded Independent Central Review (BICR) in Participants With Programmed Cell Death Ligand 1 (PD-L1) Combined Positive Score (CPS) ≥10

DOR was defined as the time from first documented evidence of a confirmed Complete Response (CR) or Partial Response (PR) until progressive disease (PD) or death, whichever occurred first. Per RECIST 1.1 as assessed by BICR, CR was the disappearance of all target lesions and PR was ≥30% decrease in the sum of diameters (SOD) of target lesions, taking as reference the baseline SOD. PD was defined as ≥20% increase in the SOD of target lesions according to RECIST 1.1. In addition to the relative increase of 20%, the SOD must also have demonstrated an absolute increase of ≥5 mm. The appearance of ≥1 new lesions was also considered PD. DOR for participants who had not progressed or died at the time of analysis was censored at the date of the last tumor assessment. DOR was estimated using the product-limit (Kaplan-Meier) method for censored data. (NCT03675737)
Timeframe: Up to 49.5 months

InterventionMonths (Median)
Pembrolizumab + Chemotherapy (FP or CAPOX Regimen)10.9
Placebo + Chemotherapy (FP or CAPOX Regimen)5.8

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Best Overall Response and Confirmed Objective Response Rate (ORR) in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer

Best overall response rate and confirmed objective response rate (ORR) were assessed by blinded independent central review (BICR) and investigator assessment. Complete response (CR) was defined as a disappearance of all target lesions, partial response (PR) was defined as at least a 30% decrease in the sum of diameters of target lesions, and stable disease (SD) was defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD; at least a 20% increase in the sum of diameters of target lesions. Confirmed ORR was defined as the number of participants with complete and partial responses and confirmed by a second assessment. (NCT03734029)
Timeframe: From screening and every 6 weeks up to withdrawal of subject consent, progressive disease (PD), or unacceptable toxicity, up to approximately 3 years

,
InterventionParticipants (Count of Participants)
BICR: Complete responseBICR: Partial responseBICR: Stable diseaseBICR: Progressive diseaseBICR: Not evaluableInvestigator: Complete responseInvestigator: Partial responseInvestigator: Stable diseaseInvestigator: Progressive diseaseInvestigator: Not evaluableBICR: Confirmed Objective response rateInvestigator: Confirmed Objective response rate
Physician's Choice1268134210308034192730
Trastuzumab Deruxtecan (T-DXd)12164115261451631242811175168

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Duration of Response in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer

Duration of Response (DoR) is defined as the date of the first documented objective response (complete response [CR] or partial response [PR]) to the first documented disease progression or death, whichever occurs first. DoR was based on blinded independent central review (BICR) and investigator assessment. Median was from Kaplan-Meier estimate. Confidence interval for median was computed using the Brookmeyer-Crowley method. (NCT03734029)
Timeframe: From the date of the first documented objective response (CR or PR) to the first documented disease progression or death, whichever occurs first, up to approximately 3 years

,
Interventionmonths (Median)
BICR: DoRInvestigator: DoR
Physician's Choice6.85.6
Trastuzumab Deruxtecan (T-DXd)10.78.3

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Duration of Response in Participants With HER2-low Breast Cancer (All Patients)

Duration of Response (DoR) is defined as the date of the first documented objective response (complete response [CR] or partial response [PR]) to the first documented disease progression or death, whichever occurs first. DoR was based on blinded independent central review (BICR) and investigator assessment. Median was from Kaplan-Meier estimate. Confidence interval for median was computed using the Brookmeyer-Crowley method. (NCT03734029)
Timeframe: From the date of the first documented objective response (CR or PR) to the first documented disease progression or death, whichever occurs first, up to approximately 3 years

,
Interventionmonths (Median)
BICR: DoRInvestigator: DoR
Physician's Choice6.85.6
Trastuzumab Deruxtecan (T-DXd)10.78.3

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Best Overall Response and Confirmed Objective Response Rate (ORR) in Participants With HER2-low Breast Cancer (All Patients)

Best overall response rate and confirmed objective response rate (ORR) were assessed by blinded independent central review (BICR) and investigator assessment. Complete response (CR) was defined as a disappearance of all target lesions, partial response (PR) was defined as at least a 30% decrease in the sum of diameters of target lesions, and stable disease (SD) was defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD; at least a 20% increase in the sum of diameters of target lesions. Confirmed ORR was defined as the number of participants with complete and partial responses and confirmed by a second assessment. (NCT03734029)
Timeframe: From screening and every 6 weeks up to withdrawal of subject consent, progressive disease (PD), or unacceptable toxicity, up to approximately 3 years

,
InterventionParticipants (Count of Participants)
BICR: Complete responseBICR: Partial responseBICR: Stable diseaseBICR: Progressive diseaseBICR: Not evaluableInvestigator: Complete responseInvestigator: Partial responseInvestigator: Stable diseaseInvestigator: Progressive diseaseInvestigator: Not evaluableBICR: Confirmed Objective response rateInvestigator: Confirmed Objective response rate
Physician's Choice2289141220319340203031
Trastuzumab Deruxtecan (T-DXd)13183129311761871353213195193

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Progression-free Survival Based on Investigator Assessment in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer

Progression-free survival (PFS), defined as at least a 20% increase in the sum of diameters of target lesions, was assessed from the date of randomization to the date of the first radiographic disease progression or death due to any cause, whichever came first. PFS was based on investigator assessment in the hormone receptor-positive cohort according to modified Response Evaluation Criteria in Solid Tumors (mRECIST) version 1.1. Median PFS was from Kaplan-Meier analysis. Confidence interval for median was computed using the Brookmeyer-Crowley method. (NCT03734029)
Timeframe: From the date of randomization to the earliest date of the first objective documentation of radiographic disease progression or death due to any cause, up to approximately 3 years

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)9.6
Physician's Choice4.2

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Overall Survival (OS) in All Patients

Overall survival (OS) was defined as the time from the date of randomization to the date of death due to any cause. If there was no death reported for a participant before the data cutoff for OS analysis, OS was censored at the last contact date at which the participant was known to be alive. (NCT03734029)
Timeframe: From the date of randomization up to the date of death due to any cause, up to approximately 3 years

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)23.4
Physician's Choice16.8

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Number of Overall Survival Events (Deaths)

(NCT03734029)
Timeframe: From the date of randomization up to the date of death due to any cause, up to approximately 3 years

Interventionevents (deaths) (Number)
Trastuzumab Deruxtecan (T-DXd)149
Physician's Choice90

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All-Cause Mortality

All-cause mortality is defined as all anticipated and unanticipated deaths due to any cause, with the number and frequency of such events by arm or comparison group of the clinical study. (NCT03734029)
Timeframe: From the date of randomization up to the date of death due to any cause, up to approximately 3 years

InterventionParticipants (Count of Participants)
Trastuzumab Deruxtecan (T-DXd)148
Physician's Choice88

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Overall Survival (OS) in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer

Overall survival (OS) was defined as the time from the date of randomization to the date of death due to any cause. If there was no death reported for a participant before the data cutoff for OS analysis, OS was censored at the last contact date at which the participant was known to be alive. (NCT03734029)
Timeframe: From the date of randomization up to the date of death due to any cause, up to approximately 3 years

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)23.9
Physician's Choice17.5

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Progression-free Survival (PFS) Based on Blinded Independent Central Review (BICR) in Participants With HER2-low Breast Cancer (All Patients) Regardless of Hormone Receptor Status

Progression-free survival (PFS), defined as at least a 20% increase in the sum of diameters of target lesions, was assessed from the date of randomization to the date of the first radiographic disease progression or death due to any cause, whichever came first. PFS was based on blinded independent central review (BICR) according to modified Response Evaluation Criteria in Solid Tumors (mRECIST) version 1.1. Median PFS was from Kaplan-Meier analysis. Confidence interval for median was computed using the Brookmeyer-Crowley method. (NCT03734029)
Timeframe: From the date of randomization to the earliest date of the first objective documentation of radiographic disease progression or death due to any cause, up to approximately 3 years

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)9.9
Physician's Choice5.1

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Progression-free Survival (PFS) Based on Blinded Independent Central Review (BICR) in the Hormone Receptor-Positive Cohort in Participants With HER2-low Breast Cancer

Progression-free survival (PFS), defined as at least a 20% increase in the sum of diameters of target lesions, was assessed from the date of randomization to the date of the first radiographic disease progression or death due to any cause, whichever came first. PFS was based on blinded independent central review (BICR) in the hormone receptor-positive cohort according to modified Response Evaluation Criteria in Solid Tumors (mRECIST) version 1.1. Median PFS was from Kaplan-Meier analysis. Confidence interval for median was computed using the Brookmeyer-Crowley method. (NCT03734029)
Timeframe: From the date of randomization to the earliest date of the first objective documentation of radiographic disease progression or death due to any cause, up to approximately 3 years

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)10.1
Physician's Choice5.4

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Progression-free Survival Based on Investigator Assessment in Participants With HER2-low Breast Cancer (All Patients)

Progression-free survival (PFS), defined as at least a 20% increase in the sum of diameters of target lesions, was assessed from the date of randomization to the date of the first radiographic disease progression or death due to any cause, whichever came first. PFS was based on investigator assessment according to modified Response Evaluation Criteria in Solid Tumors (mRECIST) version 1.1. Median PFS was from Kaplan-Meier analysis. Confidence interval for median was computed using the Brookmeyer-Crowley method. (NCT03734029)
Timeframe: From the date of randomization to the earliest date of the first objective documentation of radiographic disease progression or death due to any cause, up to approximately 3 years

Interventionmonths (Median)
Trastuzumab Deruxtecan (T-DXd)8.8
Physician's Choice4.2

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Number of Participants With Abnormalities [Grade Greater Than or Equals to (>=) 3] in Laboratory Test Values

The laboratory measurements included hematology and biochemistry values were graded with National Cancer Institute - Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 5.0 toxicity grades (where Grade 1 = mild, Grade 2 = moderate, Grade 3 = severe, Grade 4 = life threatening and Grade 5 = death). Number of participants with abnormalities Grade >= 3 in laboratory test values were reported. (NCT03770689)
Timeframe: Time from first study intervention up to long term safety follow-up period (Up to Month 35)

InterventionParticipants (Count of Participants)
Peposertib 50 mg + RT + Capecitabine:1
Peposertib 100 mg + RT + Capecitabine:6
Peposertib 150 mg + RT + Capecitabine:6
Peposertib 250 mg + RT + Capecitabine:6

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Number of Participants Who Experienced Dose Limiting Toxicity (DLT) Confirmed by Safety Monitoring Committee (SMC)

DLT is defined as any of following treatment emergent adverse events (TEAEs) considered possibly related to study treatment by Investigator and/or Sponsor up to completion of assigned chemoradiotherapy treatment. DLT were based on SMC: Adverse drug reaction that, in the opinion of SMC, is of potential clinical significance such that further dose escalation would expose participants to unacceptable risk; Any occurrence of drug-induced liver injury meeting the Hy's law criteria; Any Grade 3 toxicity excluding diarrhea, neutropenia lasting for ≤ 5 days, nausea & vomiting, Grade 3 thrombocytopenia without bleeding; Grade ≥ 4 AEs at least possibly related to study drug, irrespective of duration, excluding: Isolated Grade 4 lymphocytopenia without clinical symptoms; Neutropenia lasting for ≤ 5 days and not associated with fever; Any toxicity related to study drug that causes participant to receive > 80% of planned peposertib, capecitabine or RT dose. (NCT03770689)
Timeframe: Time from first study intervention up to 19 weeks (including 5.5 weeks of treatment and 13.5 weeks of short term safety follow-up period)

InterventionParticipants (Count of Participants)
Peposertib 50 mg + RT + Capecitabine:0
Peposertib 100 mg + RT + Capecitabine:1
Peposertib 150 mg + RT + Capecitabine:1
Peposertib 250 mg + RT + Capecitabine:3

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Apparent Volume of Distribution (Vz/f) of Peposertib

The apparent volume of distribution during the terminal phase following extravascular administration, based on the fraction of dose absorbed. Vz/f = Dose/(AUC0-inf multiplied by Lambda z) following single dose. Vz/f= Dose/(AUCtau*Lambda z) following multiple dose. One participant was assigned to receive peposertib 100 mg; however, this participant took peposertib 50 mg for FD 1 through FD 10 and then took peposertib 100 mg for remainder of study participation. PK results for this participant was summarized by actual dose received (50 mg) whereas non-PK results are summarized by planned dose (100 mg). (NCT03770689)
Timeframe: Pre-dose, 1, 2, 3, 4 and 6 hour post-dose on Fraction Day 1 and Fraction Day 9

,,
InterventionLiter (Geometric Mean)
Fraction Day 1Fraction Day 9
Peposertib 100 mg + RT + Capecitabine:256261
Peposertib 150 mg + RT + Capecitabine:274217
Peposertib 250 mg + RT + Capecitabine:245234

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Neoadjuvant Rectal (NAR) Score

"The NAR formula includes the clinical tumor (cT) stage, pathologic tumor (pT), and node (pN) stage according to the tumor, node, metastasis classification system for colorectal cancers. The NAR formula is as follows:~[5pN- 3 (cT- pT) + 12]2 / 9.61~NAR score ranges from 0 to 100, whereas a score close to 100 is indicative of a poorer prognosis." (NCT03770689)
Timeframe: At Week 15

Interventionscore on a scale (Mean)
Peposertib 100 mg + RT + Capecitabine:9.4
Peposertib 150 mg + RT + Capecitabine:13.8
Peposertib 250 mg + RT + Capecitabine:21.2

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Apparent Volume of Distribution (Vz/f) of Peposertib

The apparent volume of distribution during the terminal phase following extravascular administration, based on the fraction of dose absorbed. Vz/f = Dose/(AUC0-inf multiplied by Lambda z) following single dose. Vz/f= Dose/(AUCtau*Lambda z) following multiple dose. One participant was assigned to receive peposertib 100 mg; however, this participant took peposertib 50 mg for FD 1 through FD 10 and then took peposertib 100 mg for remainder of study participation. PK results for this participant was summarized by actual dose received (50 mg) whereas non-PK results are summarized by planned dose (100 mg). (NCT03770689)
Timeframe: Pre-dose, 1, 2, 3, 4 and 6 hour post-dose on Fraction Day 1 and Fraction Day 9

InterventionLiter (Geometric Mean)
Fraction Day 9
Peposertib 50 mg + RT + Capecitabine:NA

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Disease-free Survival

Disease-free Survival time, defined as the time from first treatment day to the date of the first documentation of objective progressive disease or death due to any cause, whichever occurs first. Median disease-free survival time was estimated according to Kaplan-Meier method. (NCT03770689)
Timeframe: Time from first study intervention up to approximately 35 months

InterventionMonths (Median)
Overall Participants21.2

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Area Under the Plasma Concentration-time Curve From Time Zero to Last Sampling Time (Tlast) (AUC0-t) of Peposertib

Area under the plasma concentration vs time curve from time zero to the last sampling time t at which the concentration was at or above the lower limit of quantification (LLQ). AUC0-t was to be calculated according to the mixed log-linear trapezoidal rule. (NCT03770689)
Timeframe: Pre-dose, 1, 2, 3, 4 and 6 hour post-dose on Fraction Day 1 and Fraction Day 9

,,,
Interventionhour*nanogram per milliliter (h*ng/mL) (Geometric Mean)
Fraction Day 1Fraction Day 9
Peposertib 100 mg + RT + Capecitabine:29503450
Peposertib 150 mg + RT + Capecitabine:40005540
Peposertib 250 mg + RT + Capecitabine:73009450
Peposertib 50 mg + RT + Capecitabine:NANA

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Maximum Observed Plasma Concentration (Cmax) of Peposertib

Cmax was obtained directly from the concentration versus time curve. One participant was assigned to receive peposertib 100 mg; however, this participant took peposertib 50 mg for FD 1 through FD 10 and then took peposertib 100 mg for remainder of study participation. PK results for this participant was summarized by actual dose received (50 mg) whereas non-PK results are summarized by planned dose (100 mg). (NCT03770689)
Timeframe: Pre-dose, 1, 2, 3, 4 and 6 hours post-dose on Fraction Day 1 and Fraction Day 9

,,,
Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
Fraction Day 1Fraction Day 9
Peposertib 100 mg + RT + Capecitabine:593653
Peposertib 150 mg + RT + Capecitabine:728792
Peposertib 250 mg + RT + Capecitabine:13501760
Peposertib 50 mg + RT + Capecitabine:NANA

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Time to Reach Maximum Plasma Concentration (Tmax) of Peposertib

Time to reach the maximum plasma concentration (Tmax) was obtained directly from the concentration versus time curve. (NCT03770689)
Timeframe: Pre-dose, 1, 2, 3, 4 and 6 hour post-dose on Fraction Day 1 and Fraction Day 9

,,,
Interventionhours (Median)
Fraction Day 1Fraction Day 9
Peposertib 100 mg + RT + Capecitabine:1.002.05
Peposertib 150 mg + RT + Capecitabine:2.332.09
Peposertib 250 mg + RT + Capecitabine:2.432.01
Peposertib 50 mg + RT + Capecitabine:NANA

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Time From Surgery to Distant Metastasis

Time from surgery to distant metastasis defined as time from day of surgery to the date of the first documentation of progression of disease, flagged as distant metastasis. Median time from surgery to distant metastasis was estimated according to Kaplan-Meier method. (NCT03770689)
Timeframe: Time from surgery up to 15 months

Interventionmonths (Median)
All ParticipantsNA

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Apparent Terminal Half-life (t1/2) of Peposertib

Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by lambda z. One participant was assigned to receive peposertib 100 mg; however, this participant took peposertib 50 mg for FD 1 through FD 10 and then took peposertib 100 mg for remainder of study participation. PK results for this participant was summarized by actual dose received (50 mg) whereas non-PK results are summarized by planned dose (100 mg). (NCT03770689)
Timeframe: Pre-dose, 1, 2, 3, 4 and 6 hour post-dose on Fraction Day 1 and Fraction Day 9

,,
Interventionhours (Geometric Mean)
Fraction Day 1Fraction Day 9
Peposertib 100 mg + RT + Capecitabine:5.606.28
Peposertib 150 mg + RT + Capecitabine:5.515.04
Peposertib 250 mg + RT + Capecitabine:5.146.12

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Apparent Terminal Half-life (t1/2) of Peposertib

Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by lambda z. One participant was assigned to receive peposertib 100 mg; however, this participant took peposertib 50 mg for FD 1 through FD 10 and then took peposertib 100 mg for remainder of study participation. PK results for this participant was summarized by actual dose received (50 mg) whereas non-PK results are summarized by planned dose (100 mg). (NCT03770689)
Timeframe: Pre-dose, 1, 2, 3, 4 and 6 hour post-dose on Fraction Day 1 and Fraction Day 9

Interventionhours (Geometric Mean)
Fraction Day 9
Peposertib 50 mg + RT + Capecitabine:NA

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Total Body Clearance Following Oral Administration (CL/f) of Peposertib

The apparent total body clearance of study intervention following extravascular administration on FD1, taking into account the fraction of dose absorbed. CL/f = Dose oral (p.o.)/AUC0-inf. The predicted AUC0-inf should be used. (NCT03770689)
Timeframe: Pre-dose, 1, 2, 3, 4 and 6 hour post-dose on Fraction Day 1

InterventionLiter per hour (Geometric Mean)
Peposertib 100 mg + RT + Capecitabine:31.7
Peposertib 150 mg + RT + Capecitabine:34.5
Peposertib 250 mg + RT + Capecitabine:33.0

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Time From Surgery to Local Recurrence

Time from surgery to local recurrence defined as time from day of surgery to the date of the first documentation of progression of disease, flagged as local recurrence. Median time from surgery to local recurrence was estimated according to Kaplan-Meier method. (NCT03770689)
Timeframe: Time from surgery up to 15 months

Interventionmonths (Median)
All ParticipantsNA

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Percentage of Participants With Pathological Complete Response (pCR)

pCR is defined as the absence of viable tumor cells in the primary tumor and lymph nodes. Participants are considered to have a pCR if they undergo surgery and no residual cancer is found on histological examination of the removed specimen. (NCT03770689)
Timeframe: At Week 15

Interventionpercentage of participants (Number)
Peposertib 50 mg + RT + Capecitabine:0.0
Peposertib 100 mg + RT + Capecitabine:0.0
Peposertib 150 mg + RT + Capecitabine:0.0
Peposertib 250 mg + RT + Capecitabine:0.0

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Percentage of Participants With Composite Pathological Complete Response (pCR)/ Clinical Complete Response (cCR)

pCR: It is defined as absence of viable tumor cells in the primary tumor and lymph nodes. Participants considered to have a pCR if they undergo surgery and no residual cancer is found on histological examination of removed specimen. cCR: Participants are considered to have a cCR if: 1) Absence of any residual tumor in primary site and draining lymph nodes on imaging with magnetic resonance imaging; 2) No visible lesion at endoscopy except a flat scar, telangiectasia, and/or whitening of mucosa; 3) Absence of any palpable tumor or irregularity on digital rectal examination (DRE) and endoscopic ultrasonography (EUS); 4) If a biopsy is taken, it must be negative. Participants are considered as responders to composite endpoint pCR/cCR if participant had surgery and had pCR; participant did not undergo surgery but had cCR. Number of participants with composite pathological complete response (pCR)/ clinical complete response (cCR) were reported. (NCT03770689)
Timeframe: At Week 15

Interventionpercentage of participants (Number)
Peposertib 50 mg + RT + Capecitabine:0.0
Peposertib 100 mg + RT + Capecitabine:16.7
Peposertib 150 mg + RT + Capecitabine:0.0
Peposertib 250 mg + RT + Capecitabine:0.0

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Percentage of Participants With Clinical Complete Response (cCR)

cCR: It is defined as participants considered to have a cCR if: 1) Absence of any residual tumor in the primary site and draining lymph nodes on imaging with magnetic resonance; 2) No visible lesion at endoscopy except a flat scar, telangiectasia, and/or whitening of the mucosa; 3) Absence of any palpable tumor or irregularity on digital rectal examination (DRE) and endoscopic ultrasonography (EUS); 4) If a biopsy is taken, it must be negative. (NCT03770689)
Timeframe: At Week 15

Interventionpercentage of participants (Number)
Peposertib 50 mg + RT + Capecitabine:0.0
Peposertib 100 mg + RT + Capecitabine:16.7
Peposertib 150 mg + RT + Capecitabine:16.7
Peposertib 250 mg + RT + Capecitabine:16.7

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Number of Participants With Markedly Abnormal Vital Sign Measurements

Vital sign assessments included assessments of heart rate, diastolic blood pressure, systolic blood pressure, respiratory rate and temperature. Number of participants with markedly abnormal vital sign measurements were reported. (NCT03770689)
Timeframe: Time from first study intervention up to long term safety follow-up period (Up to Month 35)

InterventionParticipants (Count of Participants)
Peposertib 50 mg + RT + Capecitabine:0
Peposertib 100 mg + RT + Capecitabine:0
Peposertib 150 mg + RT + Capecitabine:0
Peposertib 250 mg + RT + Capecitabine:0

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Number of Participants With Clinically Significant Abnormalities in Electrocardiogram (ECG) Findings

Electrocardiograms (ECG) was obtained after the participant has been in a semi-supine position for at least 5 min. ECG parameters included heart rate, PQ/PR duration, QRS and QT duration, QT Interval. Clinical significance was determined by the investigator. Number of participants with clinically significant abnormalities in 12-lead ECG were reported. (NCT03770689)
Timeframe: Time from first study intervention up to long term safety follow-up period (Up to Month 35)

InterventionParticipants (Count of Participants)
Peposertib 50 mg + RT + Capecitabine:0
Peposertib 100 mg + RT + Capecitabine:0
Peposertib 150 mg + RT + Capecitabine:0
Peposertib 250 mg + RT + Capecitabine:0

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Overall Survival (OS)

OS is defined as the time from the date of randomization until the date of death due to any cause (NCT03783442)
Timeframe: Up to approximately 3 years and 2 months (as of primary analysis data cut-off date of 28FEB2022)

InterventionMonths (Median)
Tislelizumab + Chemotherapy17.2
Placebo + Chemotherapy10.6

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Overall Survival (OS)

Estimated using the product-limit method of Kaplan and Meier. Failure defined as death from any cause. (NCT03853707)
Timeframe: Up to 36 months

InterventionMonths (Median)
Arm A (Ipatasertib, Carboplatin, Paclitaxel)11.2
Arm B (Ipatasertib and Carboplatin)17.0
Arm C (Ipatasertib, Capecitabine, Atezolizumab)NA

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Overall Response

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT03853707)
Timeframe: Up to 36 months

InterventionParticipants (Count of Participants)
Arm A (Ipatasertib, Carboplatin, Paclitaxel)7
Arm B (Ipatasertib and Carboplatin)2
Arm C (Ipatasertib, Capecitabine, Atezolizumab)3

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Progression-free Survival (PFS)

Estimated using the product-limit method of Kaplan and Meier. Failure defined as disease progression or death from any cause. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT03853707)
Timeframe: Up to 36 months

InterventionMonths (Median)
Arm A (Ipatasertib, Carboplatin, Paclitaxel)4.8
Arm B (Ipatasertib and Carboplatin)3.9
Arm C (Ipatasertib, Capecitabine, Atezolizumab)8.2

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Clinical Benefit Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial response (PR): At least a 30% decrease in the sum of diameters of all target lesions, taking as reference the baseline sum of diameters, in the absence of CR; Stable disease (SD): Neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD; Progressive disease (PD): At least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum of diameters on study (including baseline). Clinical Benefit Rate (CBR) = CR + PR + SD at 6 months. (NCT03853707)
Timeframe: Up to 6 months

Interventionpercentage of participants (Number)
Arm A (Ipatasertib, Carboplatin, Paclitaxel)20.0
Arm B (Ipatasertib and Carboplatin)41.7
Arm C (Ipatasertib, Capecitabine, Atezolizumab)50.0

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Safety, as Measured by the Number of Subjects With at Least One AE

(NCT03930771)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
All Patients1

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Effect of the CAP and TMZ Combination on Pituitary Function, Measured by Changes in Pituitary Hormone Secretion in Patients

Serum prolactin, IGF-1, ACTH, FSH, LH and TSH levels are used to assess changes in pituitary hormone function. These tests will only be repeated if found to be abnormal at baseline. (NCT03930771)
Timeframe: At baseline and every 8 weeks, up to 6 months

Interventionng/mL (Number)
BaselineCycle 3 Day 1Cycle 5 Day 1Cycle 6 Day 1End of TreatmentFollow-Up Week 6
All Patients134.786.969.469.880.177.0

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Tolerability of the TMZ and Capecitabine Combination, as Measured by Number of Participants With a Dose-limiting Toxicity

(NCT03930771)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
All Patients1

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Number of Subjects With Radiographic Response, as Defined by the RECIST Criteria.

"Evaluation of Target lesions:~Complete Response (CR):~Disappearance of all target lesions.~Partial Response (PR):~At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters.~Progressive Disease (PD):~At least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum onstudy (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. (Note: the appearance of one or more new lesions is also considered progression).~Stable Disease (SD):~Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study." (NCT03930771)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
All Patients0

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Objective Response Rate (ORR): Percentage of Participants Who Achieve Complete Response (CR) or Partial Response (PR)

ORR is defined as the number of participants who achieve a best overall response (BOR) of complete response (CR) or partial response (PR) divided by the total number of participants randomized to the corresponding treatment arm [intent-to-treat (ITT) population], based on investigator-assessed tumor responses.CR is defined as the disappearance of all target and non-target lesions and no appearance of new lesions. PR is defined as at least a 30% decrease in the sum of the longest diameters (LD) of target lesions (taking in reference the baseline sum LD), no progression of non-target lesions, and no appearance of new lesions. Confirmations of CR and PR are not required. (NCT04031885)
Timeframe: Randomization to Measured Progressive Disease (Up to 12 Months)

Interventionpercentage of participants (Number)
Abemaciclib + Fulvestrant0
Standard Chemotherapy0

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Progression Free Survival (PFS) in Participants With Peritoneal Metastases From Gastric Cancer After Repeated Intraperitoneal Chemotherapeutic Infusion (IPC) and Systemic Paclitaxel Administration With Concomitant Capecitabine Therapy

PFS is the amount of time a participant survives without progression of disease after treatment with peritoneal metastases from gastric cancer after repeated intraperitoneal chemotherapeutic infusion (IPC) and systemic paclitaxel administration with concomitant capecitabine therapy. Progression was measured by the Response Evaluation Criteria in Solid Tumors (RECIST) guideline (version 1.1). Progression is defined as an increase in peritoneal cancer index (PCI) score of greater than 4 points from baseline PCI, new ascites requiring repeat (more than 1) therapeutic paracentesis, malignant bowel obstruction, new intraperitoneal nodules or masses concerning for peritoneal metastasis, and decline in performance status not attributable to other medical causes. (NCT04034251)
Timeframe: From the first treatment to progression of disease, up to 2 years and 1 month

InterventionMonths (Median)
Paclitaxel Intraperitoneal 20mg & Intravenous 80mg Every 3Weeks & Capecitabine 825mg/m^2 Twice Daily4.2
Paclitaxel Intraperitoneal 60mg & Intravenous 80mg Every 3Weeks &Capecitabine 825mg/m^2 Twice Daily13.3

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Overall Survival (OS)

OS is the median amount of time a participant survives after treatment. (NCT04034251)
Timeframe: From first treatment until death, an average of 1.5 years

InterventionMonths (Median)
Paclitaxel Intraperitoneal 20mg & Intravenous 80mg Every 3Weeks & Capecitabine 825mg/m^2 Twice Daily10.6
Paclitaxel Intraperitoneal 60mg & Intravenous 80mg Every 3Weeks &Capecitabine 825mg/m^2 Twice Daily14.7

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Number of Participants With Serious and/or Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0)

Here is the number of participants with serious and/or non-serious adverse events assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0). A non-serious adverse event is any untoward medical occurrence. A serious adverse event is an adverse event or suspected adverse reaction that results in death, a life-threatening adverse drug experience, hospitalization, disruption of the ability to conduct normal life functions, congenital anomaly/birth defect or important medical events that jeopardize the patient or subject and may require medical or surgical intervention to prevent one of the previous outcomes mentioned. (NCT04034251)
Timeframe: Date treatment consent signed to date off study, 18 months and 8 days; and 25 months and 10 days for the first and second group, respectively.

InterventionParticipants (Count of Participants)
Paclitaxel Intraperitoneal 20mg & Intravenous 80mg Every 3Weeks & Capecitabine 825mg/m^2 Twice Daily4
Paclitaxel Intraperitoneal 60mg & Intravenous 80mg Every 3Weeks &Capecitabine 825mg/m^2 Twice Daily7

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Number of Participants With Intra-peritoneal Progression Free Survival (iPFS)

iPFS was determined based on identification of only intraperitoneal sites such as new, malignant ascites, peritoneal nodules, or ovarian metastases. Progression was measured by the Response Evaluation Criteria in Solid Tumors (RECIST) guideline (version 1.1). Progression is defined as an increase in peritoneal cancer index (PCI) score of greater than 4 points from baseline PCI. New ascites requiring repeat (more than 1) therapeutic paracentesis, malignant bowel obstruction, new intraperitoneal nodules or masses concerning for peritoneal metastasis, and decline in performance status not attributable to other medical causes. (NCT04034251)
Timeframe: At extra-peritoneal progression, an average of 1 year

InterventionParticipants (Count of Participants)
Paclitaxel Intraperitoneal 20mg & Intravenous 80mg Every 3Weeks & Capecitabine 825mg/m^2 Twice Daily1
Paclitaxel Intraperitoneal 60mg & Intravenous 80mg Every 3Weeks &Capecitabine 825mg/m^2 Twice Daily0

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Number of Participants With Distant Extra-peritoneal Disease-free Survival

dDFS was determined based on identification of only distant sites of disease progression, such as lungs or intra-parenchymal liver. Progression was measured by the Response Evaluation Criteria in Solid Tumors (RECIST) guideline (version 1.1). Progression is defined as an increase in peritoneal cancer index (PCI) score of greater than 4 points from baseline PCI. New ascites requiring repeat (more than 1) therapeutic paracentesis, malignant bowel obstruction, new intraperitoneal nodules or masses concerning for peritoneal metastasis, and decline in performance status not attributable to other medical causes. (NCT04034251)
Timeframe: From start of treatment to until time of extra-peritoneal progression, an average of 1 year

InterventionParticipants (Count of Participants)
Paclitaxel Intraperitoneal 20mg & Intravenous 80mg Every 3Weeks & Capecitabine 825mg/m^2 Twice Daily1
Paclitaxel Intraperitoneal 60mg & Intravenous 80mg Every 3Weeks &Capecitabine 825mg/m^2 Twice Daily0

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Intra-peritoneal Progression Free Survival (iPFS) Reported With an 95% Confidence Interval

Progression was measured by the Response Evaluation Criteria in Solid Tumors (RECIST) guideline (version 1.1). Progression is defined as an increase in peritoneal cancer index (PCI) score of greater than 4 points from baseline PCI. New ascites requiring repeat (more than 1) therapeutic paracentesis, malignant bowel obstruction, new intraperitoneal nodules or masses concerning for peritoneal metastasis, and decline in performance status not attributable to other medical causes. (NCT04034251)
Timeframe: From the first treatment to progression of disease, up to 2 years and 1 month

InterventionMonths (Median)
Paclitaxel Intraperitoneal 20mg & Intravenous 80mg Every 3Weeks & Capecitabine 825mg/m^2 Twice Daily4.2
Paclitaxel Intraperitoneal 60mg & Intravenous 80mg Every 3Weeks &Capecitabine 825mg/m^2 Twice Daily13.3

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Intra-peritoneal Progression Free Survival (iPFS) Reported With an 80% Confidence Interval

iPFS is the median amount of time a participant survives without intra-peritoneal disease progression reported with an 80% confidence interval. Progression was measured by the Response Evaluation Criteria in Solid Tumors (RECIST) guideline (version 1.1). Progression is defined as an increase in peritoneal cancer index (PCI) score of greater than 4 points from baseline PCI. New ascites requiring repeat (more than 1) therapeutic paracentesis, malignant bowel obstruction, new intraperitoneal nodules or masses concerning for peritoneal metastasis, and decline in performance status not attributable to other medical causes. (NCT04034251)
Timeframe: From the first treatment to progression of disease, up to 2 years and 1 month

InterventionMonths (Median)
Paclitaxel Intraperitoneal 20mg & Intravenous 80mg Every 3Weeks & Capecitabine 825mg/m^2 Twice Daily4.2
Paclitaxel Intraperitoneal 60mg & Intravenous 80mg Every 3Weeks &Capecitabine 825mg/m^2 Twice Daily13.3

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Incidence and Severity of Diarrhea

Incidence and severity of treatment emergent (TEAE) diarrhea will be summarized according to the NCI-CTCAE version 4.0 in the first cycle of neratinib treatment, which is from the time of the first colonoscopy to the second colonoscopy, or 28 days for subjects with only one colonoscopy. Incidence is defined as the number of patients experiencing diarrhea divided by the number of patients at risk. (NCT04366713)
Timeframe: From baseline to second colonoscopy, which is 88 days after start of neratinib treatment.

Interventionpercentage of participants (Number)
TEAE DiarrheaSerious Diarrhea
Safety800

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Changes in Colon Pathology

The primary endpoint is to describe the changes in colon pathology between the baseline colonoscopy and the second colonoscopy. (NCT04366713)
Timeframe: From baseline to second colonoscopy, which is 88 days after start of neratinib treatment.

Interventionparticipants (Number)
No Significant FindingsMild Changes
Neratinib Patients With 2 Colonoscopies22

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Proportion of Participants With Dose Limiting Toxicities

Severity of treatment-emergent adverse events as assessed by the NCI CTCAE Version 5.0. This outcome measure applies only to participants in the dose escalation cohorts. (NCT05091528)
Timeframe: 21 days

InterventionParticipants (Count of Participants)
SBT6050 + T-DXd (6.4 mg/kg)0
SBT6050 + Tucatinib + Trastuzumab0

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Number of Participants With an Objective Response Rate

Complete response and partial response as assessed by RECIST Version 1.1 Criteria. This outcome measure applies only to participants in the dose escalation cohorts. (NCT05091528)
Timeframe: 18 weeks

InterventionParticipants (Count of Participants)
SBT6050 + T-DXd (6.4 mg/kg)1
SBT6050 + Tucatinib + Trastuzumab0

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Number of Participants With Laboratory Abnormalities

Clinically significant treatment-emergent laboratory abnormalities as assessed by the NCI CTCAE Version 5.0. This outcome measure applies only to participants in the dose escalation cohorts. (NCT05091528)
Timeframe: 18 weeks

InterventionParticipants (Count of Participants)
SBT6050 + T-DXd (6.4 mg/kg)0
SBT6050 + Tucatinib + Trastuzumab0

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Number of Participants With Treatment-emergent Adverse Events

Severity of treatment-emergent adverse events as assessed by the NCI CTCAE Version 5.0. This outcome measure applies only to participants in the dose escalation cohorts. (NCT05091528)
Timeframe: 18 weeks

InterventionParticipants (Count of Participants)
SBT6050 + T-DXd (6.4 mg/kg)1
SBT6050 + Tucatinib + Trastuzumab1

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SubstanceRelationship StrengthStudiesTrialsClassesRoles
n-carbamoyl-beta-alanine
N-carbamoyl-beta-alanine: RN given refers to parent cpd. N-carbamoyl-beta-alanine : A beta-alanine derivative that is propionic acid bearing a ureido group at position 3.		2.0310beta-alanine derivativemetabolite;
mouse metabolite
gamma-aminobutyric acid
gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.. gamma-aminobutyric acid : A gamma-amino acid that is butanoic acid with the amino substituent located at C-4.		2.0510amino acid zwitterion;
gamma-amino acid;
monocarboxylic acid		human metabolite;
neurotransmitter;
Saccharomyces cerevisiae metabolite;
signalling molecule
aminolevulinic acid
Aminolevulinic Acid: A compound produced from succinyl-CoA and GLYCINE as an intermediate in heme synthesis. It is used as a PHOTOCHEMOTHERAPY for actinic KERATOSIS.. 5-aminolevulinic acid : The simplest delta-amino acid in which the hydrogens at the gamma position are replaced by an oxo group. It is metabolised to protoporphyrin IX, a photoactive compound which accumulates in the skin. Used (in the form of the hydrochloride salt)in combination with blue light illumination for the treatment of minimally to moderately thick actinic keratosis of the face or scalp.		2.52204-oxo monocarboxylic acid;
amino acid zwitterion;
delta-amino acid		antineoplastic agent;
dermatologic drug;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
photosensitizing agent;
plant metabolite;
prodrug;
Saccharomyces cerevisiae metabolite
acetic acid
Acetic Acid: Product of the oxidation of ethanol and of the destructive distillation of wood. It is used locally, occasionally internally, as a counterirritant and also as a reagent. (Stedman, 26th ed). acetic acid : A simple monocarboxylic acid containing two carbons.		2.0510monocarboxylic acidantimicrobial food preservative;
Daphnia magna metabolite;
food acidity regulator;
protic solvent
acetamide
acetimidic acid : A carboximidic acid that is acetic acid in which the carbonyl oxygen is replaced by an imino group.		2.0510acetamides;
carboximidic acid;
monocarboxylic acid amide;
N-acylammonia
adenine
[no description available]		2.05106-aminopurines;
purine nucleobase		Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
allantoin
[no description available]		2.0510imidazolidine-2,4-dione;
ureas		Escherichia coli metabolite;
human metabolite;
Saccharomyces cerevisiae metabolite;
vulnerary
ammonium hydroxide
azane : Saturated acyclic nitrogen hydrides having the general formula NnHn+2.		2.4110azane;
gas molecular entity;
mononuclear parent hydride		EC 3.5.1.4 (amidase) inhibitor;
metabolite;
mouse metabolite;
neurotoxin;
NMR chemical shift reference compound;
nucleophilic reagent;
refrigerant
quinacrine
Quinacrine: An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2.. quinacrine : A member of the class of acridines that is acridine substituted by a chloro group at position 6, a methoxy group at position 2 and a [5-(diethylamino)pentan-2-yl]nitrilo group at position 9.		8.9121acridines;
aromatic ether;
organochlorine compound;
tertiary amino compound		antimalarial;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor
beta-alanine
[no description available]		10.472amino acid zwitterion;
beta-amino acid		agonist;
fundamental metabolite;
human metabolite;
inhibitor;
neurotransmitter
betaine
glycine betaine : The amino acid betaine derived from glycine.		3.5920amino-acid betaine;
glycine derivative		fundamental metabolite
carbamates
[no description available]		2.9440amino-acid anion
carnitine
[no description available]		2.0510amino-acid betainehuman metabolite;
mouse metabolite
methane
Methane: The simplest saturated hydrocarbon. It is a colorless, flammable gas, slightly soluble in water. It is one of the chief constituents of natural gas and is formed in the decomposition of organic matter. (Grant & Hackh's Chemical Dictionary, 5th ed). methane : A one-carbon compound in which the carbon is attached by single bonds to four hydrogen atoms. It is a colourless, odourless, non-toxic but flammable gas (b.p. -161degreeC).		2.3110alkane;
gas molecular entity;
mononuclear parent hydride;
one-carbon compound		bacterial metabolite;
fossil fuel;
greenhouse gas
citric acid, anhydrous
Citric Acid: A key intermediate in metabolism. It is an acid compound found in citrus fruits. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability.. citric acid : A tricarboxylic acid that is propane-1,2,3-tricarboxylic acid bearing a hydroxy substituent at position 2. It is an important metabolite in the pathway of all aerobic organisms.		2.0510tricarboxylic acidantimicrobial agent;
chelator;
food acidity regulator;
fundamental metabolite
chlorine
chloride : A halide anion formed when chlorine picks up an electron to form an an anion.		2.1510halide anion;
monoatomic chlorine		cofactor;
Escherichia coli metabolite;
human metabolite
cuminaldehyde
cuminaldehyde : A member of the class of benzaldehydes that is benzaldehyde substituted by an isopropyl group at position 4. It is a component of essential oils from Cumin and exhibits insecticidal activities.		2.0510benzaldehydesinsecticide;
plant metabolite;
volatile oil component
salicylic acid
Scalp: The outer covering of the calvaria. It is composed of several layers: SKIN; subcutaneous connective tissue; the occipitofrontal muscle which includes the tendinous galea aponeurotica; loose connective tissue; and the pericranium (the PERIOSTEUM of the SKULL).		2.9940monohydroxybenzoic acidalgal metabolite;
antifungal agent;
antiinfective agent;
EC 1.11.1.11 (L-ascorbate peroxidase) inhibitor;
keratolytic drug;
plant hormone;
plant metabolite
4-methylumbelliferyl acetate
4-methylumbelliferyl acetate : An acetate ester consiting of umbelliferone carrying a 7-O-acetyl group.		2.0510acetate ester;
coumarins		plant metabolite
bupropion
Bupropion: A propiophenone-derived antidepressant and antismoking agent that inhibits the uptake of DOPAMINE.. bupropion : An aromatic ketone that is propiophenone carrying a tert-butylamino group at position 2 and a chloro substituent at position 3 on the phenyl ring.		3.8530aromatic ketone;
monochlorobenzenes;
secondary amino compound		antidepressant;
environmental contaminant;
xenobiotic
aminocaproic acid
Aminocaproic Acid: An antifibrinolytic agent that acts by inhibiting plasminogen activators which have fibrinolytic properties.. 6-aminohexanoic acid : An epsilon-amino acid comprising hexanoic acid carrying an amino substituent at position C-6. Used to control postoperative bleeding, and to treat overdose effects of the thrombolytic agents streptokinase and tissue plasminogen activator.		3.5920amino acid zwitterion;
epsilon-amino acid;
omega-amino fatty acid		antifibrinolytic drug;
hematologic agent;
metabolite
creatine
[no description available]		2.0510glycine derivative;
guanidines;
zwitterion		geroprotector;
human metabolite;
mouse metabolite;
neuroprotective agent;
nutraceutical
lactic acid
Lactic Acid: A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed). 2-hydroxypropanoic acid : A 2-hydroxy monocarboxylic acid that is propanoic acid in which one of the alpha-hydrogens is replaced by a hydroxy group.		6.32422-hydroxy monocarboxylic acidalgal metabolite;
Daphnia magna metabolite
dihydrouracil
hexahydropyrimidine-2,4-dione: structure in first source. 5,6-dihydrouracil : A pyrimidine obtained by formal addition of hydrogen across the 5,6-position of uracil.		4.9271pyrimidoneEscherichia coli metabolite;
human metabolite;
metabolite;
mouse metabolite
dimethyl sulfoxide
Dimethyl Sulfoxide: A highly polar organic liquid, that is used widely as a chemical solvent. Because of its ability to penetrate biological membranes, it is used as a vehicle for topical application of pharmaceuticals. It is also used to protect tissue during CRYOPRESERVATION. Dimethyl sulfoxide shows a range of pharmacological activity including analgesia and anti-inflammation.. dimethyl sulfoxide : A 2-carbon sulfoxide in which the sulfur atom has two methyl substituents.		2.0510sulfoxide;
volatile organic compound		alkylating agent;
antidote;
Escherichia coli metabolite;
geroprotector;
MRI contrast agent;
non-narcotic analgesic;
polar aprotic solvent;
radical scavenger
formaldehyde
paraform: polymerized formaldehyde; RN given refers to parent cpd; used in root canal therapy		2.0510aldehyde;
one-carbon compound		allergen;
carcinogenic agent;
disinfectant;
EC 3.5.1.4 (amidase) inhibitor;
environmental contaminant;
Escherichia coli metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
glycine
[no description available]		2.0510alpha-amino acid;
amino acid zwitterion;
proteinogenic amino acid;
serine family amino acid		EC 2.1.2.1 (glycine hydroxymethyltransferase) inhibitor;
fundamental metabolite;
hepatoprotective agent;
micronutrient;
neurotransmitter;
NMDA receptor agonist;
nutraceutical
glycerol
Moon: The natural satellite of the planet Earth. It includes the lunar cycles or phases, the lunar month, lunar landscapes, geography, and soil.		2.0510alditol;
triol		algal metabolite;
detergent;
Escherichia coli metabolite;
geroprotector;
human metabolite;
mouse metabolite;
osmolyte;
Saccharomyces cerevisiae metabolite;
solvent
dalteparin
Dalteparin: A low-molecular-weight fragment of heparin, prepared by nitrous acid depolymerization of porcine mucosal heparin. The mean molecular weight is 4000-6000 daltons. It is used therapeutically as an antithrombotic agent. (From Merck Index, 11th ed)		2.0610
hydrogen
Hydrogen: The first chemical element in the periodic table with atomic symbol H, and atomic number 1. Protium (atomic weight 1) is by far the most common hydrogen isotope. Hydrogen also exists as the stable isotope DEUTERIUM (atomic weight 2) and the radioactive isotope TRITIUM (atomic weight 3). Hydrogen forms into a diatomic molecule at room temperature and appears as a highly flammable colorless and odorless gas.. dihydrogen : An elemental molecule consisting of two hydrogens joined by a single bond.		3.5911elemental hydrogen;
elemental molecule;
gas molecular entity		antioxidant;
electron donor;
food packaging gas;
fuel;
human metabolite
hydroquinone
[no description available]		2.0510benzenediol;
hydroquinones		antioxidant;
carcinogenic agent;
cofactor;
Escherichia coli metabolite;
human xenobiotic metabolite;
mouse metabolite;
skin lightening agent
iodine
Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically.. diiodine : Molecule comprising two covalently bonded iodine atoms with overall zero charge..		2.1310diatomic iodinenutrient
itaconic acid
itaconic acid : A dicarboxylic acid that is methacrylic acid in which one of the methyl hydrogens is substituted by a carboxylic acid group.		7.610dicarboxylic acid;
dicarboxylic fatty acid;
olefinic compound		fungal metabolite;
human metabolite
methanol
Methanol: A colorless, flammable liquid used in the manufacture of FORMALDEHYDE and ACETIC ACID, in chemical synthesis, antifreeze, and as a solvent. Ingestion of methanol is toxic and may cause blindness.. primary alcohol : A primary alcohol is a compound in which a hydroxy group, -OH, is attached to a saturated carbon atom which has either three hydrogen atoms attached to it or only one other carbon atom and two hydrogen atoms attached to it.. methanol : The primary alcohol that is the simplest aliphatic alcohol, comprising a methyl and an alcohol group.		2.1510alkyl alcohol;
one-carbon compound;
primary alcohol;
volatile organic compound		amphiprotic solvent;
Escherichia coli metabolite;
fuel;
human metabolite;
mouse metabolite;
Mycoplasma genitalium metabolite
phytic acid
Phytic Acid: Complexing agent for removal of traces of heavy metal ions. It acts also as a hypocalcemic agent.. myo-inositol hexakisphosphate : A myo-inositol hexakisphosphate in which each hydroxy group of myo-inositol is monophosphorylated.		2.3110inositol phosphate
inositol
Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction.. inositol : Any cyclohexane-1,2,3,4,5,6-hexol.. 1D-chiro-inositol : Belonging to the inositol family of compounds, D-chiro-inositol (DCI) is an isomer of glucose. It is an important secondary messenger in insulin signal transduction.. muco-inositol : An inositol that is cyclohexane-1,2,3,4,5,6-hexol having a (1R,2R,3r,4R,5S,6r)-configuration.		7.5220cyclitol;
hexol
melatonin
[no description available]		7.0610acetamides;
tryptamines		anticonvulsant;
central nervous system depressant;
geroprotector;
hormone;
human metabolite;
immunological adjuvant;
mouse metabolite;
radical scavenger
niacinamide
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.		14.153919pyridine alkaloid;
pyridinecarboxamide;
vitamin B3		anti-inflammatory agent;
antioxidant;
cofactor;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor;
EC 3.5.1.98 (histone deacetylase) inhibitor;
Escherichia coli metabolite;
geroprotector;
human urinary metabolite;
metabolite;
mouse metabolite;
neuroprotective agent;
Saccharomyces cerevisiae metabolite;
Sir2 inhibitor
niacin
Niacin: A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.. vitamin B3 : Any member of a group of vitamers that belong to the chemical structural class called pyridines that exhibit biological activity against vitamin B3 deficiency. Vitamin B3 deficiency causes a condition known as pellagra whose symptoms include depression, dermatitis and diarrhea. The vitamers include nicotinic acid and nicotinamide (and their ionized and salt forms).. nicotinic acid : A pyridinemonocarboxylic acid that is pyridine in which the hydrogen at position 3 is replaced by a carboxy group.		3.5920pyridine alkaloid;
pyridinemonocarboxylic acid;
vitamin B3		antidote;
antilipemic drug;
EC 3.5.1.19 (nicotinamidase) inhibitor;
Escherichia coli metabolite;
human urinary metabolite;
metabolite;
mouse metabolite;
plant metabolite;
vasodilator agent
nitrites
Nitrites: Salts of nitrous acid or compounds containing the group NO2-. The inorganic nitrites of the type MNO2 (where M=metal) are all insoluble, except the alkali nitrites. The organic nitrites may be isomeric, but not identical with the corresponding nitro compounds. (Grant & Hackh's Chemical Dictionary, 5th ed)		2.0310monovalent inorganic anion;
nitrogen oxoanion;
reactive nitrogen species		human metabolite
orotic acid
Orotic Acid: An intermediate product in PYRIMIDINE synthesis which plays a role in chemical conversions between DIHYDROFOLATE and TETRAHYDROFOLATE.. orotic acid : A pyrimidinemonocarboxylic acid that is uracil bearing a carboxy substituent at position C-6.		2.4720pyrimidinemonocarboxylic acidEscherichia coli metabolite;
metabolite;
mouse metabolite
4-aminobenzoic acid
4-Aminobenzoic Acid: An aminobenzoic acid isomer that combines with pteridine and GLUTAMIC ACID to form FOLIC ACID. The fact that 4-aminobenzoic acid absorbs light throughout the UVB range has also resulted in its use as an ingredient in SUNSCREENS.. 4-ammoniobenzoate : A zwitterion obtained by transfer of a proton from the carboxy to the amino group of 4-aminobenzoic acid.. 4-aminobenzoic acid : An aminobenzoic acid in which the amino group is para to the carboxy group.		2.0510aminobenzoic acid;
aromatic amino-acid zwitterion		allergen;
Escherichia coli metabolite;
plant metabolite
phenol
[no description available]		2.0510phenolsantiseptic drug;
disinfectant;
human xenobiotic metabolite;
mouse metabolite
phenylacetic acid
phenylacetic acid : A monocarboxylic acid that is toluene in which one of the hydrogens of the methyl group has been replaced by a carboxy group.		2.0510benzenes;
monocarboxylic acid;
phenylacetic acids		allergen;
Aspergillus metabolite;
auxin;
EC 6.4.1.1 (pyruvate carboxylase) inhibitor;
Escherichia coli metabolite;
human metabolite;
plant growth retardant;
plant metabolite;
Saccharomyces cerevisiae metabolite;
toxin
phosphorylcholine
Phosphorylcholine: Calcium and magnesium salts used therapeutically in hepatobiliary dysfunction.. phosphocholine : The phosphate of choline; and the parent compound of the phosphocholine family.		4.7821phosphocholinesallergen;
epitope;
hapten;
human metabolite;
mouse metabolite
1-propanol
1-Propanol: A colorless liquid made by oxidation of aliphatic hydrocarbons that is used as a solvent and chemical intermediate.. propan-1-ol : The parent member of the class of propan-1-ols that is propane in which a hydrogen of one of the methyl groups is replaced by a hydroxy group.		2.0510propan-1-ols;
short-chain primary fatty alcohol		metabolite;
protic solvent
pyrazinamide
pyrazinecarboxamide : A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of pyrazinoic acid (pyrazine-2-carboxylic acid) with ammonia. A prodrug for pyrazinoic acid, pyrazinecarboxamide is used as part of multidrug regimens for the treatment of tuberculosis.		3.5920monocarboxylic acid amide;
N-acylammonia;
pyrazines		antitubercular agent;
prodrug
pyridoxal phosphate
Pyridoxal Phosphate: This is the active form of VITAMIN B 6 serving as a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid. During transamination of amino acids, pyridoxal phosphate is transiently converted into pyridoxamine phosphate (PYRIDOXAMINE).. pyridoxal 5'-phosphate : The monophosphate ester obtained by condensation of phosphoric acid with the primary hydroxy group of pyridoxal.		2.0510methylpyridines;
monohydroxypyridine;
pyridinecarbaldehyde;
vitamin B6 phosphate		coenzyme;
cofactor;
EC 2.7.7.7 (DNA-directed DNA polymerase) inhibitor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
pyridoxine
4,5-bis(hydroxymethyl)-2-methylpyridin-3-ol: structure in first source. vitamin B6 : Any member of the group of pyridines that exhibit biological activity against vitamin B6 deficiency. Vitamin B6 deficiency is associated with microcytic anemia, electroencephalographic abnormalities, dermatitis with cheilosis (scaling on the lips and cracks at the corners of the mouth) and glossitis (swollen tongue), depression and confusion, and weakened immune function. Vitamin B6 consists of the vitamers pyridoxine, pyridoxal, and pyridoxamine and their respective 5'-phosphate esters (and includes their corresponding ionized and salt forms).		12.081710hydroxymethylpyridine;
methylpyridines;
monohydroxypyridine;
vitamin B6		cofactor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
spermine
[no description available]		2.1510polyazaalkane;
tetramine		antioxidant;
fundamental metabolite;
immunosuppressive agent
thiamine
thiamine(1+) : A primary alcohol that is 1,3-thiazol-3-ium substituted by (4-amino-2-methylpyrimidin-5-yl)methyl, methyl and 2-hydroxyethyl groups at positions 3, 4 and 5, respectively.		3.5920primary alcohol;
vitamin B1		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
thymine
[no description available]		7.84102pyrimidine nucleobase;
pyrimidone		Escherichia coli metabolite;
human metabolite;
mouse metabolite
uracil
2,4-dihydroxypyrimidine: a urinary biomarker for bipolar disorder		14.31906pyrimidine nucleobase;
pyrimidone		allergen;
Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
prodrug;
Saccharomyces cerevisiae metabolite
urea
pseudourea: clinical use; structure. isourea : A carboximidic acid that is the imidic acid tautomer of urea, H2NC(=NH)OH, and its hydrocarbyl derivatives.		7.8564isourea;
monocarboxylic acid amide;
one-carbon compound		Daphnia magna metabolite;
Escherichia coli metabolite;
fertilizer;
flour treatment agent;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
vanillin
Vanilla: A plant genus of the family ORCHIDACEAE that is the source of the familiar flavoring used in foods and medicines (FLAVORING AGENTS).		2.0510benzaldehydes;
monomethoxybenzene;
phenols		anti-inflammatory agent;
anticonvulsant;
antioxidant;
flavouring agent;
plant metabolite
catechin
[no description available]		2.0510hydroxyflavan
menthol
Menthol: A monoterpene cyclohexanol produced from mint oils.		2.0510p-menthane monoterpenoid;
secondary alcohol		volatile oil component
1,2-dimethylhydrazine
1,2-Dimethylhydrazine: A DNA alkylating agent that has been shown to be a potent carcinogen and is widely used to induce colon tumors in experimental animals.. 1,2-dimethylhydrazine : A member of the class of hydrazines that is hydrazine in which one of the hydrogens attached to each nitrogen is replaced by a methyl group. A powerful DNA alkylating agent and carcinogen, it is used to induce colon cancer in laboratory rats and mice.		7.1710hydrazinesalkylating agent;
carcinogenic agent
phenytoin
[no description available]		5.39100imidazolidine-2,4-dioneanticonvulsant;
drug allergen;
sodium channel blocker;
teratogenic agent
acebutolol
Acebutolol: A cardioselective beta-1 adrenergic antagonist with little effect on the bronchial receptors. The drug has stabilizing and quinidine-like effects on cardiac rhythm, as well as weak inherent sympathomimetic action.. acebutolol : An ether that is the 2-acetyl-4-(butanoylamino)phenyl ether of the primary hydroxy group of 3-(propan-2-ylamino)propane-1,2-diol.		3.5920aromatic amide;
ethanolamines;
ether;
monocarboxylic acid amide;
propanolamine;
secondary amino compound		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
sympathomimetic agent
acetaminophen
Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.. paracetamol : A member of the class of phenols that is 4-aminophenol in which one of the hydrogens attached to the amino group has been replaced by an acetyl group.		8.8830acetamides;
phenols		antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
cyclooxygenase 3 inhibitor;
environmental contaminant;
ferroptosis inducer;
geroprotector;
hepatotoxic agent;
human blood serum metabolite;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
acetazolamide
Acetazolamide: One of the CARBONIC ANHYDRASE INHIBITORS that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337)		3.5920monocarboxylic acid amide;
sulfonamide;
thiadiazoles		anticonvulsant;
diuretic;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
acetohexamide
Acetohexamide: A sulfonylurea hypoglycemic agent that is metabolized in the liver to 1-hydrohexamide.. acetohexamide : An N-sulfonylurea that is urea in which a hydrogen attached to one of the nitrogens is replaced by a p-acetylphenylsulfonyl group, while a hydrogen attached to the other nitrogen is replaced by a cyclohexyl group.		2.0510acetophenones;
N-sulfonylurea		hypoglycemic agent;
insulin secretagogue
acetohydroxamic acid
acetohydroxamic acid: urease inhibitor. oxime : Compounds of structure R2C=NOH derived from condensation of aldehydes or ketones with hydroxylamine. Oximes from aldehydes may be called aldoximes; those from ketones may be called ketoximes.. N-hydroxyacetimidic acid : A carbohydroximic acid consisting of acetimidic acid having a hydroxy group attached to the imide nitrogen.. acetohydroxamic acid : A member of the class of acetohydroxamic acids that is acetamide in which one of the amino hydrogens has been replaced by a hydroxy group.		3.5920acetohydroxamic acids;
carbohydroximic acid		algal metabolite;
EC 3.5.1.5 (urease) inhibitor
ethacridine
Ethacridine: A topically applied anti-infective agent.		2.0110acridines
alaproclate
alaproclate: specific 5-hydroxytryptamine uptake inhibitors; RN given refers to (DL)-isomer		3.2310alpha-amino acid ester
albendazole
[no description available]		3.5920aryl sulfide;
benzimidazoles;
benzimidazolylcarbamate fungicide;
carbamate ester		anthelminthic drug;
microtubule-destabilising agent;
tubulin modulator
albuterol
Albuterol: A short-acting beta-2 adrenergic agonist that is primarily used as a bronchodilator agent to treat ASTHMA. Albuterol is prepared as a racemic mixture of R(-) and S(+) stereoisomers. The stereospecific preparation of R(-) isomer of albuterol is referred to as levalbuterol.. albuterol : A member of the class of phenylethanolamines that is 4-(2-amino-1-hydroxyethyl)-2-(hydroxymethyl)phenol having a tert-butyl group attached to the nirogen atom. It acts as a beta-adrenergic agonist used in the treatment of asthma and chronic obstructive pulmonary disease (COPD).		3.5920phenols;
phenylethanolamines;
secondary amino compound		beta-adrenergic agonist;
bronchodilator agent;
environmental contaminant;
xenobiotic
alendronate
alendronic acid : A 1,1-bis(phosphonic acid) that is methanebis(phosphonic acid) in which the two methylene hydrogens are replaced by hydroxy and 3-aminopropyl groups.		3.23101,1-bis(phosphonic acid);
primary amino compound		bone density conservation agent;
EC 2.5.1.1 (dimethylallyltranstransferase) inhibitor
alfuzosin
alfuzosin: structure given in first source		3.5920monocarboxylic acid amide;
quinazolines;
tetrahydrofuranol		alpha-adrenergic antagonist;
antihypertensive agent;
antineoplastic agent
alosetron
alosetron : A pyrido[4,3-b]indole compound having a 5-methyl-1H-imidazol-4-ylmethyl group at the 2-position.		3.2310imidazoles;
pyridoindole		antiemetic;
gastrointestinal drug;
serotonergic antagonist
alprazolam
Alprazolam: A triazolobenzodiazepine compound with antianxiety and sedative-hypnotic actions, that is efficacious in the treatment of PANIC DISORDERS, with or without AGORAPHOBIA, and in generalized ANXIETY DISORDERS. (From AMA Drug Evaluations Annual, 1994, p238). alprazolam : A member of the class of triazolobenzodiazepines that is 4H-[1,2,4]triazolo[4,3-a][1,4]benzodiazepine carrying methyl, phenyl and chloro substituents at positions 1, 6 and 8 respectively. Alprazolam is only found in individuals that have taken this drug.		3.2310organochlorine compound;
triazolobenzodiazepine		anticonvulsant;
anxiolytic drug;
GABA agonist;
muscle relaxant;
sedative;
xenobiotic
altretamine
Altretamine: A hexamethyl-2,4,6-triamine derivative of 1,3,5-triazine.		3.5920triamino-1,3,5-triazine
amantadine
amant: an antiviral compound consisting of an adamantane derivative chemically linked to a water-solube polyanioic matrix; structure in first source		3.5920adamantanes;
primary aliphatic amine		analgesic;
antiparkinson drug;
antiviral drug;
dopaminergic agent;
NMDA receptor antagonist;
non-narcotic analgesic
ambenonium
ambenonium : A symmetrical oxalamide-based bis-quaternary ammonium ion having ethyl and 2-chlorobenzyl groups attached to the nitrogens.		3.2310quaternary ammonium ionEC 3.1.1.8 (cholinesterase) inhibitor
ambroxol
Ambroxol: A metabolite of BROMHEXINE that stimulates mucociliary action and clears the air passages in the respiratory tract. It is usually administered as the hydrochloride.		2.0510aromatic amine
diatrizoic acid
Diatrizoate: A commonly used x-ray contrast medium. As DIATRIZOATE MEGLUMINE and as Diatrizoate sodium, it is used for gastrointestinal studies, angiography, and urography.. amidotrizoic acid : A member of the class of benzoic acids that is benzoic acid having iodo substituents at the 2-, 4- and 6-positions and acetamido substituents at the 3- and 5-positions. It is used, mainly as its N-methylglucamine and sodium salts, as an X-ray contrast medium in gastrointestinal studies, angiography, and urography.		3.2310acetamides;
benzoic acids;
organoiodine compound		environmental contaminant;
radioopaque medium;
xenobiotic
amifostine anhydrous
Amifostine: A phosphorothioate proposed as a radiation-protective agent. It causes splenic vasodilation and may block autonomic ganglia.. amifostine : An organic thiophosphate that is the S-phospho derivative of 2-[(3-aminopropyl)amino]ethanethiol. A prodrug for the free thiol, WR-1065, which is used as a cytoprotectant in cancer chemotherapy and radiotherapy.		4.9821diamine;
organic thiophosphate		antioxidant;
prodrug;
radiation protective agent
aminoglutethimide
Aminoglutethimide: An aromatase inhibitor that is used in the treatment of advanced BREAST CANCER.. aminoglutethimide : A dicarboximide that is a six-membered cyclic compound having ethyl and 4-aminophenyl substituents at the 3-position.		2.0510dicarboximide;
piperidones;
substituted aniline		adrenergic agent;
anticonvulsant;
antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor
pimagedine
pimagedine: diamine oxidase & nitric oxide synthase inhibitor; an advanced glycosylation end product inhibitor; used in the treatment of diabetic complications; structure. aminoguanidine : A one-carbon compound whose unique structure renders it capable of acting as a derivative of hydrazine, guanidine or formamide.		2.0510guanidines;
one-carbon compound		EC 1.14.13.39 (nitric oxide synthase) inhibitor;
EC 1.4.3.4 (monoamine oxidase) inhibitor
p-aminohippuric acid
p-Aminohippuric Acid: The glycine amide of 4-aminobenzoic acid. Its sodium salt is used as a diagnostic aid to measure effective renal plasma flow (ERPF) and excretory capacity.. p-aminohippurate : A hippurate that is the conjugate base of p-aminohippuric acid, arising from deprotonation of the carboxy group.. p-aminohippuric acid : An N-acylglycine that is the 4-amino derivative of hippuric acid; used as a diagnostic agent in the measurement of renal plasma flow.		3.2310N-acylglycineDaphnia magna metabolite
theophylline
[no description available]		3.5920dimethylxanthineadenosine receptor antagonist;
anti-asthmatic drug;
anti-inflammatory agent;
bronchodilator agent;
drug metabolite;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
fungal metabolite;
human blood serum metabolite;
immunomodulator;
muscle relaxant;
vasodilator agent
amiodarone
Amiodarone: An antianginal and class III antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting POTASSIUM CHANNELS and VOLTAGE-GATED SODIUM CHANNELS. There is a resulting decrease in heart rate and in vascular resistance.. amiodarone : A member of the class of 1-benzofurans that is 1-benzofuran substituted by a butyl group at position 2 and a 4-[2-(diethylamino)ethoxy]-3,5-diiodobenzoyl group at position 3. It is a cardiovascular drug used for the treatment of cardiac dysrhythmias.		3.59201-benzofurans;
aromatic ketone;
organoiodine compound;
tertiary amino compound		cardiovascular drug
amitriptyline
Amitriptyline: Tricyclic antidepressant with anticholinergic and sedative properties. It appears to prevent the re-uptake of norepinephrine and serotonin at nerve terminals, thus potentiating the action of these neurotransmitters. Amitriptyline also appears to antagonize cholinergic and alpha-1 adrenergic responses to bioactive amines.. amitriptyline : An organic tricyclic compound that is 10,11-dihydro-5H-dibenzo[a,d][7]annulene substituted by a 3-(dimethylamino)propylidene group at position 5.		3.5920carbotricyclic compound;
tertiary amine		adrenergic uptake inhibitor;
antidepressant;
environmental contaminant;
tropomyosin-related kinase B receptor agonist;
xenobiotic
amlodipine
Amlodipine: A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of ANGINA PECTORIS and HYPERTENSION.. amlodipine : A fully substituted dialkyl 1,4-dihydropyridine-3,5-dicarboxylate derivative, which is used for the treatment of hypertension, chronic stable angina and confirmed or suspected vasospastic angina.		3.5920dihydropyridine;
ethyl ester;
methyl ester;
monochlorobenzenes;
primary amino compound		antihypertensive agent;
calcium channel blocker;
vasodilator agent
amobarbital
Amobarbital: A barbiturate with hypnotic and sedative properties (but not antianxiety). Adverse effects are mainly a consequence of dose-related CNS depression and the risk of dependence with continued use is high. (From Martindale, The Extra Pharmacopoeia, 30th ed, p565). amobarbital : A member of the class of barbiturates that is pyrimidine-2,4,6(1H,3H,5H)-trione substituted by a 3-methylbutyl and an ethyl group at position 5. Amobarbital has been shown to exhibit sedative and hypnotic properties.		2.0510barbiturates
amoxapine
Amoxapine: The N-demethylated derivative of the antipsychotic agent LOXAPINE that works by blocking the reuptake of norepinephrine, serotonin, or both; it also blocks dopamine receptors. Amoxapine is used for the treatment of depression.. amoxapine : A dibenzooxazepine compound having a chloro substituent at the 2-position and a piperazin-1-yl group at the 11-position.		3.2310dibenzooxazepineadrenergic uptake inhibitor;
antidepressant;
dopaminergic antagonist;
geroprotector;
serotonin uptake inhibitor
amsacrine
Amsacrine: An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.. amsacrine : A sulfonamide that is N-phenylmethanesulfonamide substituted by a methoxy group at position 3 and an acridin-9-ylamino group at position 4. It exhibits antineoplastic activity.		2.4620acridines;
aromatic ether;
sulfonamide		antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
anastrozole
[no description available]		11.63100nitrile;
triazoles		antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor
anethole trithione
Anethole Trithione: Choleretic used to allay dry mouth and constipation due to tranquilizers.		2.0510methoxybenzenes
aniracetam
[no description available]		2.4620N-acylpyrrolidine;
pyrrolidin-2-ones
anthralin
Anthralin: An anthracene derivative that disrupts MITOCHONDRIA function and structure and is used for the treatment of DERMATOSES, especially PSORIASIS. It may cause FOLLICULITIS.. anthralin : An anthracene compound derived by the substitution of -OH groups for hydrogen at C-1 and C-8, and with an oxo group at C-9.		2.0510anthracenesantipsoriatic
antipyrine
Antipyrine: An analgesic and antipyretic that has been given by mouth and as ear drops. Antipyrine is often used in testing the effects of other drugs or diseases on drug-metabolizing enzymes in the liver. (From Martindale, The Extra Pharmacopoeia, 30th ed, p29). antipyrine : A pyrazolone derivative that is 1,2-dihydropyrazol-3-one substituted with methyl groups at N-1 and C-5 and with a phenyl group at N-2.		2.0510pyrazoloneantipyretic;
cyclooxygenase 3 inhibitor;
environmental contaminant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
apraclonidine
apraclonidine: relieves postoperative intraocular pressure following trabeculoplasty; RN given refers to parent cpd. apraclonidine : An imidazoline that is 2-amino 4,5-dihydro-1H-imidazoline in which one of the exocyclic amino hydrogens has been replaced by a 4-amino-2,6-dichlorophenyl group.		2.0110dichlorobenzene;
guanidines;
imidazolines		alpha-adrenergic agonist;
antiglaucoma drug;
beta-adrenergic agonist;
diagnostic agent;
ophthalmology drug
aspirin
Aspirin: The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5). acetylsalicylate : A benzoate that is the conjugate base of acetylsalicylic acid, arising from deprotonation of the carboxy group.. acetylsalicylic acid : A member of the class of benzoic acids that is salicylic acid in which the hydrogen that is attached to the phenolic hydroxy group has been replaced by an acetoxy group. A non-steroidal anti-inflammatory drug with cyclooxygenase inhibitor activity.		9.350benzoic acids;
phenyl acetates;
salicylates		anticoagulant;
antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
EC 1.1.1.188 (prostaglandin-F synthase) inhibitor;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
plant activator;
platelet aggregation inhibitor;
prostaglandin antagonist;
teratogenic agent
astemizole
Astemizole: Antihistamine drug now withdrawn from the market in many countries because of rare but potentially fatal side effects.. astemizole : A piperidine compound having a 2-(4-methoxyphenyl)ethyl group at the 1-position and an N-[(4-fluorobenzyl)benzimidazol-2-yl]amino group at the 4-position.		2.2510benzimidazoles;
piperidines		anti-allergic agent;
anticoronaviral agent;
H1-receptor antagonist
atenolol
Atenolol: A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.. atenolol : An ethanolamine compound having a (4-carbamoylmethylphenoxy)methyl group at the 1-position and an N-isopropyl substituent.		3.5920ethanolamines;
monocarboxylic acid amide;
propanolamine		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
environmental contaminant;
sympatholytic agent;
xenobiotic
azathioprine
Azathioprine: An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed). azathioprine : A thiopurine that is 6-mercaptopurine in which the mercapto hydrogen is replaced by a 1-methyl-4-nitroimidazol-5-yl group. It is a prodrug for mercaptopurine and is used as an immunosuppressant, prescribed for the treatment of inflammatory conditions and after organ transplantation and also for treatment of Crohn's didease and MS.		3.5920aryl sulfide;
C-nitro compound;
imidazoles;
thiopurine		antimetabolite;
antineoplastic agent;
carcinogenic agent;
DNA synthesis inhibitor;
hepatotoxic agent;
immunosuppressive agent;
prodrug
baclofen
[no description available]		3.5920amino acid zwitterion;
gamma-amino acid;
monocarboxylic acid;
monochlorobenzenes;
primary amino compound		central nervous system depressant;
GABA agonist;
muscle relaxant
barbital
5,5-diethylbarbituric acid : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by two ethyl groups. Formerly used as a hypnotic (sleeping aid).		2.0510barbituratesdrug allergen
bendazac
bendazac : A monocarboxylic acid that is glycolic acid in which the hydrogen attached to the 2-hydroxy group is replaced by a 1-benzyl-1H-indazol-3-yl group. Although it has anti-inflammatory, antinecrotic, choleretic and antilipidaemic properties and has been used for the treatment of various inflammatory skin disorders, its principal effect is to inhibit the denaturation of proteins. Its lysine salt is used in the management of cataracts.		3.5920indazoles;
monocarboxylic acid		non-steroidal anti-inflammatory drug;
radical scavenger
bendiocarb
bendiocarb: FICAM 80W contains 80% of the above chemical cpd as the active ingredient		2.0510benzodioxoles;
carbamate ester		agrochemical;
carbamate insecticide;
EC 3.1.1.7 (acetylcholinesterase) inhibitor
bendroflumethiazide
Bendroflumethiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. It has been used in the treatment of familial hyperkalemia, hypertension, edema, and urinary tract disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p810). bendroflumethiazide : A sulfonamide consisting of 7-sulfamoyl-3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide in which the hydrogen at position 6 is substituted by a trifluoromethyl group and that at position 3 is substituted by a benzyl group.		3.2310benzothiadiazine;
sulfonamide		antihypertensive agent;
diuretic
benzbromarone
Benzbromarone: Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout.. benzbromarone : 1-Benzofuran substituted at C-2 and C-3 by an ethyl group and a 3,5-dibromo-4-hydroxybenzoyl group respectively. An inhibitor of CYP2C9, it is used as an anti-gout medication.		3.59201-benzofurans;
aromatic ketone		uricosuric drug
betaxolol
[no description available]		3.2310propanolamineantihypertensive agent;
beta-adrenergic antagonist;
sympatholytic agent
bethanechol
Bethanechol: A slowly hydrolyzing muscarinic agonist with no nicotinic effects. Bethanechol is generally used to increase smooth muscle tone, as in the GI tract following abdominal surgery or in urinary retention in the absence of obstruction. It may cause hypotension, HEART RATE changes, and BRONCHIAL SPASM.. bethanechol : The carbamic acid ester of 2-methylcholine. A slowly hydrolysed muscarinic agonist with no nicotinic effects, it is used as its chloride salt to increase smooth muscle tone, as in the gastrointestinal tract following abdominal surgery, treatment of gastro-oesophageal reflux disease, and as an alternative to catheterisation in the treatment of non-obstructive urinary retention.		3.2310carbamate ester;
quaternary ammonium ion		muscarinic agonist
bicalutamide
bicalutamide: approved for treatment of advanced prostate cancer. N-[4-cyano-3-(trifluoromethyl)phenyl]-3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanamide : A member of the class of (trifluoromethyl)benzenes that is 4-amino-2-(trifluoromethyl)benzonitrile in which one of the amino hydrogens is substituted by a 3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanoyl group.. bicalutamide : A racemate comprising of equal amounts of (R)-bicalutamide and (S)-bicalutamide. It is an oral non-steroidal antiandrogen used in the treatment of prostate cancer and hirsutism.		4.1140(trifluoromethyl)benzenes;
monocarboxylic acid amide;
monofluorobenzenes;
nitrile;
sulfone;
tertiary alcohol
bay h 4502
bifonazole : A racemate comprising equimolar amounts of R- and S-bifonazole. It is a broad spectrum antifungal drug used for the treatment of fungal skin and nail infections.. 1-[biphenyl-4-yl(phenyl)methyl]imidazole : A member of the class of imidazoles carrying an alpha-(biphenyl-4-yl)benzyl substituent at position 1.		2.0510biphenyls;
imidazoles
biperiden
Biperiden: A muscarinic antagonist that has effects in both the central and peripheral nervous systems. It has been used in the treatment of arteriosclerotic, idiopathic, and postencephalitic parkinsonism. It has also been used to alleviate extrapyramidal symptoms induced by phenothiazine derivatives and reserpine.. biperiden : A member of the class of piperidines that is N-propylpiperidine in which the methyl hydrogens have been replaced by hydroxy, phenyl, and 5-norbornen-2-yl groups. A muscarinic antagonist affecting both the central and peripheral nervous systems, it is used in the treatment of all forms of Parkinson's disease.		3.2310piperidines;
tertiary alcohol;
tertiary amino compound		antidote to sarin poisoning;
antidyskinesia agent;
antiparkinson drug;
muscarinic antagonist;
parasympatholytic
bisacodyl
Bisacodyl: A diphenylmethane stimulant laxative used for the treatment of CONSTIPATION and for bowel evacuation. (From Martindale, The Extra Pharmacopoeia, 30th ed, p871)		3.2310diarylmethane
bisoprolol
Bisoprolol: A cardioselective beta-1 adrenergic blocker. It is effective in the management of HYPERTENSION and ANGINA PECTORIS.		3.8730secondary alcohol;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
sympatholytic agent
bromisovalum
Bromisovalum: A sedative and mild hypnotic with potentially toxic effects.. bromisoval : A racemate comprising equimolar amounts of (R)- and (S)-bromisoval. It was previously used for its hypnotic and sedative properties but the use of bromides is now deprecated due to the possibility of the toxic accumulation of bromine in the body.. 2-bromo-N-carbamoyl-3-methylbutanamide : An N-acylurea that is urea in which one of the hydrogens is replaced by a 2-bromo-3-methybutanoyl group.		2.0510N-acylurea;
organobromine compound
brotizolam
brotizolam: structure		2.0510organic molecular entity
bumetanide
[no description available]		3.5920amino acid;
benzoic acids;
sulfonamide		diuretic;
EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor
bupivacaine
Bupivacaine: A widely used local anesthetic agent.. 1-butyl-N-(2,6-dimethylphenyl)piperidine-2-carboxamide : A piperidinecarboxamide obtained by formal condensation of the carboxy group of N-butylpipecolic acid with the amino group of 2,6-dimethylaniline.. bupivacaine : A racemate composed of equimolar amounts of dextrobupivacaine and levobupivacaine. Used (in the form of its hydrochloride hydrate) as a local anaesthetic.		2.0510aromatic amide;
piperidinecarboxamide;
tertiary amino compound
buspirone
Buspirone: An anxiolytic agent and serotonin receptor agonist belonging to the azaspirodecanedione class of compounds. Its structure is unrelated to those of the BENZODIAZAPINES, but it has an efficacy comparable to DIAZEPAM.. buspirone : An azaspiro compound that is 8-azaspiro[4.5]decane-7,9-dione substituted at the nitrogen atom by a 4-(piperazin-1-yl)butyl group which in turn is substituted by a pyrimidin-2-yl group at the N(4) position.		3.8630azaspiro compound;
N-alkylpiperazine;
N-arylpiperazine;
organic heteropolycyclic compound;
piperidones;
pyrimidines		anxiolytic drug;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
sedative;
serotonergic agonist
busulfan
[no description available]		3.8630methanesulfonate esteralkylating agent;
antineoplastic agent;
carcinogenic agent;
insect sterilant;
teratogenic agent
secbutabarbital
secbutabarbital: Butabarbital (a synonym for Secbutabarbital) should be distinguished from Butobarbital		3.2310barbiturates
butalbital
butalbital: management of butalbital withdrawal can be simplified by using a phenobarbital-loading protocol; RN given refers to parent cpd. butalbital : A member of the class of barbiturates that is barbituric acid in which the hydrogens at position 5 are substituted by an allyl group and an isobutyl group. Frequently combined with other medicines, such as aspirin, paracetamol and codeine, it is used for treatment of pain and headache.		2.0510barbituratesanalgesic;
sedative
caffeine
[no description available]		3.5920purine alkaloid;
trimethylxanthine		adenosine A2A receptor antagonist;
adenosine receptor antagonist;
adjuvant;
central nervous system stimulant;
diuretic;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
environmental contaminant;
food additive;
fungal metabolite;
geroprotector;
human blood serum metabolite;
mouse metabolite;
mutagen;
plant metabolite;
psychotropic drug;
ryanodine receptor agonist;
xenobiotic
verapamil
Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent.. verapamil : A racemate comprising equimolar amounts of dexverapamil and (S)-verapamil. An L-type calcium channel blocker of the phenylalkylamine class, it is used (particularly as the hydrochloride salt) in the treatment of hypertension, angina pectoris and cardiac arrhythmia, and as a preventive medication for migraine.. 2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile : A tertiary amino compound that is 3,4-dimethoxyphenylethylamine in which the hydrogens attached to the nitrogen are replaced by a methyl group and a 4-cyano-4-(3,4-dimethoxyphenyl)-5-methylhexyl group.		3.5920aromatic ether;
nitrile;
polyether;
tertiary amino compound
camostat
camostat : A benzoate ester resulting from the formal condensation of the carboxy group of 4-guanidinobenzoic acid with the hydroxy group of 2-(dimethylamino)-2-oxoethyl (4-hydroxyphenyl)acetate. It is a potent inhibitor of the human transmembrane protease serine 2 (TMPRSS2) and its mesylate salt is currently under investigation for its effectiveness in COVID-19 patients.		2.0510benzoate ester;
carboxylic ester;
diester;
guanidines;
tertiary carboxamide		anti-inflammatory agent;
anticoronaviral agent;
antifibrinolytic drug;
antihypertensive agent;
antineoplastic agent;
antiviral agent;
serine protease inhibitor
camphor, (+-)-isomer
[no description available]		2.0510bornane monoterpenoid;
cyclic monoterpene ketone		plant metabolite
candesartan cilexetil
candesartan cilexetil: a prodrug which is metabolized to an active form candesartan to exert its biological effects		2.0510biphenyls
candesartan
candesartan: a nonpeptide angiotensin II receptor antagonist. candesartan : A benzimidazolecarboxylic acid that is 1H-benzimidazole-7-carboxylic acid substituted by an ethoxy group at position 2 and a ({2'-(1H-tetrazol-5-yl)[1,1'-biphenyl]-4-yl}methyl) group at position 1. It is a angiotensin receptor antagonist used for the treatment of hypertension.		3.2310benzimidazolecarboxylic acid;
biphenylyltetrazole		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
carbamazepine
Carbamazepine: A dibenzazepine that acts as a sodium channel blocker. It is used as an anticonvulsant for the treatment of grand mal and psychomotor or focal SEIZURES. It may also be used in the management of BIPOLAR DISORDER, and has analgesic properties.. carbamazepine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine carrying a carbamoyl substituent at the azepine nitrogen, used as an anticonvulsant.		4.7630dibenzoazepine;
ureas		analgesic;
anticonvulsant;
antimanic drug;
drug allergen;
EC 3.5.1.98 (histone deacetylase) inhibitor;
environmental contaminant;
glutamate transporter activator;
mitogen;
non-narcotic analgesic;
sodium channel blocker;
xenobiotic
carbinoxamine
carbinoxamine: Note: tradenames that start with Histex refer to more than one drug. carbinoxamine : An organochlorine compound that is 2-(4-chlorobenzyl)pyridine in which one of the benzylic hydrogens is substituted by 2-(dimethylamino)ethoxy group. It is an ethanolamine-type antihistamine, used as its maleate salt for treating hay fever, as well as mild cases of Parkinson's disease.		3.2310monochlorobenzenes;
pyridines;
tertiary amino compound		anti-allergic agent;
antiparkinson drug;
H1-receptor antagonist;
muscarinic antagonist
carbofuran
Carbofuran: A cholinesterase inhibitor that is used as a systemic insecticide, an acaricide, and nematocide. (From Merck Index, 11th ed)		2.05101-benzofurans;
carbamate ester		acaricide;
agrochemical;
avicide;
carbamate insecticide;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
nematicide
carisoprodol
Carisoprodol: A centrally acting skeletal muscle relaxant whose mechanism of action is not completely understood but may be related to its sedative actions. It is used as an adjunct in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1202). carisoprodol : A carbamate ester that is the mono-N-isopropyl derivative of meprobamate (which is a significant metabolite). Carisoprodol interrupts neuronal communication within the reticular formation and spinal cord, resulting in sedation and alteration in pain perception. It is used as a muscle relaxant in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm.		3.8630carbamate estermuscle relaxant
carmofur
[no description available]		2.0410organohalogen compound;
pyrimidines
carmustine
Carmustine: A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed). carmustine : A member of the class of N-nitrosoureas that is 1,3-bis(2-chloroethyl)urea in which one of the nitrogens is substituted by a nitroso group.		2.7730N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent
carprofen
carprofen: RN given refers to cpd without isomeric designation. carprofen : Propanoic acid in which one of the methylene hydrogens is substituted by a 6-chloro-9H-carbazol-2-yl group. A non-steroidal anti-inflammatory drug, it is no longer used in human medicine but is still used for treatment of arthritis in elderly dogs.		2.0510carbazoles;
organochlorine compound		EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug;
photosensitizing agent
carvedilol
[no description available]		3.5920carbazoles;
secondary alcohol;
secondary amino compound		alpha-adrenergic antagonist;
antihypertensive agent;
beta-adrenergic antagonist;
cardiovascular drug;
vasodilator agent
celecoxib
[no description available]		13.473214organofluorine compound;
pyrazoles;
sulfonamide;
toluenes		cyclooxygenase 2 inhibitor;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
cetirizine
Cetirizine: A potent second-generation histamine H1 antagonist that is effective in the treatment of allergic rhinitis, chronic urticaria, and pollen-induced asthma. Unlike many traditional antihistamines, it does not cause drowsiness or anticholinergic side effects.. cetirizine : A member of the class of piperazines that is piperazine in which the hydrogens attached to nitrogen are replaced by a (4-chlorophenyl)(phenyl)methyl and a 2-(carboxymethoxy)ethyl group respectively.		3.5920ether;
monocarboxylic acid;
monochlorobenzenes;
piperazines		anti-allergic agent;
environmental contaminant;
H1-receptor antagonist;
xenobiotic
chloral hydrate
[no description available]		2.0510aldehyde hydrate;
ethanediol;
organochlorine compound		general anaesthetic;
mouse metabolite;
sedative;
xenobiotic
chlorambucil
Chlorambucil: A nitrogen mustard alkylating agent used as antineoplastic for chronic lymphocytic leukemia, Hodgkin's disease, and others. Although it is less toxic than most other nitrogen mustards, it has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (Merck Index, 11th ed). chlorambucil : A monocarboxylic acid that is butanoic acid substituted at position 4 by a 4-[bis(2-chloroethyl)amino]phenyl group. A chemotherapy drug that can be used in combination with the antibody obinutuzumab for the treatment of chronic lymphocytic leukemia.		3.8630aromatic amine;
monocarboxylic acid;
nitrogen mustard;
organochlorine compound;
tertiary amino compound		alkylating agent;
antineoplastic agent;
carcinogenic agent;
drug allergen;
immunosuppressive agent
chlorcyclizine
chlorcyclizine: was heading 1964-94 (Prov 1964-73); CHLOROCYCLIZINE & HISTACHLORAZINE were see CHLORCYCLIZINE 1977-94; use PIPERAZINES to search CHLORCYCLIZINE 1966-94; histamine H1-blocker used both orally and topically in allergies and also for the prevention of motion sickness		3.2310diarylmethane
chlordiazepoxide
Chlordiazepoxide: An anxiolytic benzodiazepine derivative with anticonvulsant, sedative, and amnesic properties. It has also been used in the symptomatic treatment of alcohol withdrawal.. chlordiazepoxide : A benzodiazepine that is 3H-1,4-benzodiazepine 4-oxide substituted by a chloro group at position 7, a phenyl group at position 5 and a methylamino group at position 2.		3.5920benzodiazepine
chlormezanone
Chlormezanone: A non-benzodiazepine that is used in the management of anxiety. It has been suggested for use in the treatment of muscle spasm.. chlormezanone : A 1,3-thiazine that is 1,3-thiazinan-4-one S,S-dioxide in which a hydrogen at position 2 is substituted by a 4-chlorophenyl group and the hydrogen attached to the nitrogen is substituted by methyl. A non-benzodiazepine muscle relaxant, it was used in the management of anxiety and in the treatment of muscle spasms until being discontinued worldwide by its manufacturer in 1996, due to rare but serious cutaneous reactions.		3.59201,3-thiazine;
lactam;
monochlorobenzenes;
sulfone		antipsychotic agent;
anxiolytic drug;
muscle relaxant
chloroquine
Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.. chloroquine : An aminoquinoline that is quinoline which is substituted at position 4 by a [5-(diethylamino)pentan-2-yl]amino group at at position 7 by chlorine. It is used for the treatment of malaria, hepatic amoebiasis, lupus erythematosus, light-sensitive skin eruptions, and rheumatoid arthritis.		3.5920aminoquinoline;
organochlorine compound;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antimalarial;
antirheumatic drug;
autophagy inhibitor;
dermatologic drug
chlorothiazide
Chlorothiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p812). thiazide : Heterocyclic compound with sulfur and nitrogen in the ring.. chlorothiazide : 4H-1,2,4-benzothiadiazine 1,1-dioxide in which the hydrogen at position is substituted by chlorine and that at position 7 is substituted by a sulfonamide group. A diuretic, it is used for treatment of oedema and hypertension.		3.2310benzothiadiazineantihypertensive agent;
diuretic
chloroxylenol
chloroxylenol: topical antiseptic; RN given refers to parent cpd; structure. 4-chloro-3,5-dimethylphenol : A member of the class of phenols that is 3,5-xylenol which is substituted at position 4 by chlorine. It is bactericidal against most Gram-positive bacteria but less effective against Staphylococci and Gram-negative bacteria, and often inactive against Pseudomonas species. It is ineffective against bacterial spores.		2.0510monochlorobenzenes;
phenols		antiseptic drug;
disinfectant;
molluscicide
chlorpheniramine
Chlorpheniramine: A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than PROMETHAZINE.. chlorphenamine : A tertiary amino compound that is propylamine which is substituted at position 3 by a pyridin-2-yl group and a p-chlorophenyl group and in which the hydrogens attached to the nitrogen are replaced by methyl groups. A histamine H1 antagonist, it is used to relieve the symptoms of hay fever, rhinitis, urticaria, and asthma.		3.5920monochlorobenzenes;
pyridines;
tertiary amino compound		anti-allergic agent;
antidepressant;
antipruritic drug;
H1-receptor antagonist;
histamine antagonist;
serotonin uptake inhibitor
chlorpromazine
Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking DOPAMINE RECEPTORS. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup.. chlorpromazine : A substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropanamine moiety.		3.5920organochlorine compound;
phenothiazines;
tertiary amine		anticoronaviral agent;
antiemetic;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
phenothiazine antipsychotic drug
chlorpropamide
Chlorpropamide: A sulfonylurea hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277). chlorpropamide : An N-sulfonylurea that is urea in which a hydrogen attached to one of the nitrogens is substituted by 4-chlorobenzenesulfonyl group and a hydrogen attached to the other nitrogen is substituted by propyl group. Chlorpropamide is a hypoglycaemic agent used in the treatment of type 2 (non-insulin-dependent) diabetes mellitus not responding to dietary modification.		3.5920monochlorobenzenes;
N-sulfonylurea		hypoglycemic agent;
insulin secretagogue
chlorpropham
Chlorpropham: A carbamate that is used as an herbicide and as a plant growth regulator.. chlorpropham : A carbamate ester that is the isopropyl ester of 3-chlorophenylcarbamic acid.		2.0510benzenes;
carbamate ester;
monochlorobenzenes		herbicide;
plant growth retardant
chlorthalidone
Chlorthalidone: A benzenesulfonamide-phthalimidine that tautomerizes to a BENZOPHENONES form. It is considered a thiazide-like diuretic.		3.2310isoindoles;
monochlorobenzenes;
sulfonamide
chlorzoxazone
Chlorzoxazone: A centrally acting central muscle relaxant with sedative properties. It is claimed to inhibit muscle spasm by exerting an effect primarily at the level of the spinal cord and subcortical areas of the brain. (From Martindale, The Extra Pharmacopoea, 30th ed, p1202). chlorzoxazone : A member of the class of 1,3-benzoxazoles that is 1,3-benzoxazol-2-ol in which the hydrogen atom at position 5 is substituted by chlorine. A centrally acting muscle relaxant with sedative properties, it is used for the symptomatic treatment of painful muscle spasm.		3.86301,3-benzoxazoles;
heteroaryl hydroxy compound;
organochlorine compound		muscle relaxant;
sedative
ci 994
tacedinaline: oral cytostatic drug with impressive differential activity against leukemic cells & normal stem-cells. tacedinaline : A benzamide obtained by formal condensation of the carboxy group of 4-acetamidobenzoic acid with one of the amino groups of 1,2-phenylenediamine. An oral cytostatic drug with impressive differential activity against leukemic cells and normal stem-cells. Also used in combination therapy for selected tumors including non-smoll cell lung, pancreatic, breast, and colorectal cancers.		3.411acetamides;
benzamides;
substituted aniline		antineoplastic agent;
EC 3.5.1.98 (histone deacetylase) inhibitor
cilostazol
[no description available]		3.2310lactam;
tetrazoles		anticoagulant;
bronchodilator agent;
EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor;
fibrin modulating drug;
neuroprotective agent;
platelet aggregation inhibitor;
vasodilator agent
cimetidine
Cimetidine: A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.. cimetidine : A member of the class of guanidines that consists of guanidine carrying a methyl substituent at position 1, a cyano group at position 2 and a 2-{[(5-methyl-1H-imidazol-4-yl)methyl]sulfanyl}ethyl group at position 3. It is a H2-receptor antagonist that inhibits the production of acid in stomach.		3.5920aliphatic sulfide;
guanidines;
imidazoles;
nitrile		adjuvant;
analgesic;
anti-ulcer drug;
H2-receptor antagonist;
P450 inhibitor
cinoxacin
Cinoxacin: Synthetic antimicrobial related to OXOLINIC ACID and NALIDIXIC ACID and used in URINARY TRACT INFECTIONS.. cinoxacin : A member of the class of cinnolines that is 6,7-methylenedioxycinnolin-4(1H)-one bearing an ethyl group at position 1 and a carboxylic acid group at position 3. An analogue of oxolinic acid, it has similar antibacterial actions. It was formerly used for the treatment of urinary tract infections.		2.4620cinnolines;
oxacycle;
oxo carboxylic acid		antibacterial drug;
antiinfective agent
ciprofibrate
[no description available]		2.0510cyclopropanes;
monocarboxylic acid;
organochlorine compound		antilipemic drug
ciprofloxacin
Ciprofloxacin: A broad-spectrum antimicrobial carboxyfluoroquinoline.. ciprofloxacin : A quinolone that is quinolin-4(1H)-one bearing cyclopropyl, carboxylic acid, fluoro and piperazin-1-yl substituents at positions 1, 3, 6 and 7, respectively.		3.5920aminoquinoline;
cyclopropanes;
fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone;
zwitterion		antibacterial drug;
antiinfective agent;
antimicrobial agent;
DNA synthesis inhibitor;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
environmental contaminant;
topoisomerase IV inhibitor;
xenobiotic
cisapride
Cisapride: A substituted benzamide used for its prokinetic properties. It is used in the management of gastroesophageal reflux disease, functional dyspepsia, and other disorders associated with impaired gastrointestinal motility. (Martindale The Extra Pharmacopoeia, 31st ed). cisapride : The amide resulting from formal condensation of 4-amino-5-chloro-2-methoxybenzoic acid with cis-1-[3-(4-fluorophenoxy)propyl]-3-methoxypiperidin-4-amine. It has been used (as its monohydrate or as its tartrate) for the treatment of gastro-oesophageal reflux disease and for non-ulcer dyspepsia, but its propensity to cause cardiac arrhythmias resulted in its complete withdrawal from many countries, including the U.K., and restrictions on its use elsewhere.		2.0510benzamides
citalopram
Citalopram: A furancarbonitrile that is one of the serotonin uptake inhibitors used as an antidepressant. The drug is also effective in reducing ethanol uptake in alcoholics and is used in depressed patients who also suffer from TARDIVE DYSKINESIA in preference to tricyclic antidepressants, which aggravate dyskinesia.. citalopram : A racemate comprising equimolar amounts of (R)-citalopram and its enantiomer, escitalopram. It is used as an antidepressant, although only escitalopram is active.. 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile : A nitrile that is 1,3-dihydro-2-benzofuran-5-carbonitrile in which one of the hydrogens at position 1 is replaced by a p-fluorophenyl group, while the other is replaced by a 3-(dimethylamino)propyl group.		3.85302-benzofurans;
cyclic ether;
nitrile;
organofluorine compound;
tertiary amino compound
clioquinol
Clioquinol: A potentially neurotoxic 8-hydroxyquinoline derivative long used as a topical anti-infective, intestinal antiamebic, and vaginal trichomonacide. The oral preparation has been shown to cause subacute myelo-optic neuropathy and has been banned worldwide.. 5-chloro-7-iodoquinolin-8-ol : A monohydroxyquinoline that is quinolin-8-ol in which the hydrogens at positions 5 and 7 are replaced by chlorine and iodine, respectively. It has antibacterial and atifungal properties, and is used in creams for the treatment of skin infections. It has also been investigated as a chelator of copper and zinc ions for the possible treatment of Alzheimer's disease.		2.0510monohydroxyquinoline;
organochlorine compound;
organoiodine compound		antibacterial agent;
antifungal agent;
antimicrobial agent;
antineoplastic agent;
antiprotozoal drug;
chelator;
copper chelator
clobazam
Clobazam: A benzodiazepine derivative that is a long-acting GABA-A RECEPTOR agonist. It is used as an antiepileptic in the treatment of SEIZURES, including seizures associated with LENNOX-GASTAUT SYNDROME. It is also used as an anxiolytic, for the short-term treatment of acute ANXIETY.. clobazam : 7-Chloro-1H-1,5-benzodiazepine-2,4(3H,5H)-dione in which the hydrogen attached to the nitrogen at position 1 is substituted by a methyl group, whilst that attached to the other nitrogen is substituted by a phenyl group. It is used for the short-term management of acute anxiety and as an adjunct in the treatment of epilepsy in association with other antiepileptics.		2.05101,4-benzodiazepinone;
organochlorine compound		anticonvulsant;
anxiolytic drug;
GABA modulator
clofazimine
Clofazimine: A fat-soluble riminophenazine dye used for the treatment of leprosy. It has been used investigationally in combination with other antimycobacterial drugs to treat Mycobacterium avium infections in AIDS patients. Clofazimine also has a marked anti-inflammatory effect and is given to control the leprosy reaction, erythema nodosum leprosum. (From AMA Drug Evaluations Annual, 1993, p1619). clofazimine : 3-Isopropylimino-3,5-dihydro-phenazine in which the hydrogen at position 5 is substituted substituted by a 4-chlorophenyl group, and that at position 2 is substituted by a (4-chlorophenyl)amino group. A dark red crystalline solid, clofazimine is an antimycobacterial and is one of the main drugs used for the treatment of multi-bacillary leprosy. However, it can cause red/brown discolouration of the skin, so other treatments are often preferred in light-skinned patients.		2.0510monochlorobenzenes;
phenazines		dye;
leprostatic drug;
non-steroidal anti-inflammatory drug
clofibrate
angiokapsul: contains clofibrate & insoitolnicotinate		3.5920aromatic ether;
ethyl ester;
monochlorobenzenes		anticholesteremic drug;
antilipemic drug;
geroprotector;
PPARalpha agonist
clomiphene
[no description available]		3.5920tertiary amineestrogen antagonist;
estrogen receptor modulator
clomipramine
Clomipramine: A tricyclic antidepressant similar to IMIPRAMINE that selectively inhibits the uptake of serotonin in the brain. It is readily absorbed from the gastrointestinal tract and demethylated in the liver to form its primary active metabolite, desmethylclomipramine.. clomipramine : A dibenzoazepine that is 10,11-dihydro-5H-dibenzo[b,f]azepine which is substituted by chlorine at position 3 and in which the hydrogen attached to the nitrogen is replaced by a 3-(dimethylamino)propyl group. One of the more sedating tricyclic antidepressants, it is used as the hydrochloride salt for the treatment of depression as well as obsessive-compulsive disorder and phobias.		3.2310dibenzoazepineanticoronaviral agent;
antidepressant;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
serotonergic antagonist;
serotonergic drug;
serotonin uptake inhibitor
clonazepam
Clonazepam: An anticonvulsant used for several types of seizures, including myotonic or atonic seizures, photosensitive epilepsy, and absence seizures, although tolerance may develop. It is seldom effective in generalized tonic-clonic or partial seizures. The mechanism of action appears to involve the enhancement of GAMMA-AMINOBUTYRIC ACID receptor responses.. clonazepam : 1,3-Dihydro-2H-1,4-benzodiazepin-2-one in which the hydrogens at positions 5 and 7 are substituted by 2-chlorophenyl and nitro groups, respectively. It is used in the treatment of all types of epilepsy and seizures, as well as myoclonus and associated abnormal movements, and panic disorders. However, its use can be limited by the development of tolerance and by sedation.		3.23101,4-benzodiazepinone;
monochlorobenzenes		anticonvulsant;
anxiolytic drug;
GABA modulator
clonidine
Clonidine: An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.. clonidine (amino form) : A clonidine that is 4,5-dihydro-1H-imidazol-2-amine in which one of the amino hydrogens is replaced by a 2,6-dichlorophenyl group.		4.0640clonidine;
imidazoline
chlorazepate
clorazepic acid : A 1,4-benzodiazepinone in which the oxo group is at position 2, and which is substituted at positions 3, 5, and 7 by carboxy, phenyl and chloro groups, respectively.		3.23101,4-benzodiazepinoneanticonvulsant;
anxiolytic drug;
GABA modulator;
prodrug
clotiazepam
clotiazepam: was heading 1975-94 (see under AZEPINES 1978-90; was Y 6047 see under AZEPINES 1975-77); Y 6047 was see CLOTIAZEPAM 1978-94; use AZEPINES to search CLOTIAZEPAM 1975-94; thienodiazepine derivative with actions similar to those of benzodiazepines		2.0510organic molecular entity
clotrimazole
[no description available]		3.5920conazole antifungal drug;
imidazole antifungal drug;
imidazoles;
monochlorobenzenes		antiinfective agent;
environmental contaminant;
xenobiotic
cyclandelate
Cyclandelate: A direct-acting SMOOTH MUSCLE relaxant used to dilate BLOOD VESSELS.. cyclandelate : The ester obtained by formal condensation of mandelic acid and 3,3,5-tricyclohexanol. It is a direct-acting smooth muscle relaxant used to dilate blood vessels.		2.0510carboxylic ester;
secondary alcohol		vasodilator agent
cyclobenzaprine
cyclobenzaprine: RN given refers to parent cpd; Lisseril is synonymous for HCl; structure. cyclobenzaprine : 5-Methylidene-5H-dibenzo[a,d]cycloheptene in which one of the hydrogens of the methylidene group is substituted by a 2-(dimethylamino)ethyl group. A centrally acting skeletal muscle relaxant, it is used as its hydrochloride salt in the symptomatic treatment of painful muscle spasm.		3.2310carbotricyclic compoundantidepressant;
muscle relaxant;
tranquilizing drug
cyclofenil
Cyclofenil: A gonadal stimulant and inducer of ovulation. It is used in the treatment of infertility and amenorrhea, but is thought to be less effective than CLOMIPHENE.		3.2310organic molecular entity
cyproheptadine
Cyproheptadine: A serotonin antagonist and a histamine H1 blocker used as antipruritic, appetite stimulant, antiallergic, and for the post-gastrectomy dumping syndrome, etc.. cyproheptadine : The product resulting from the formal oxidative coupling of position 5 of 5H-dibenzo[a,d]cycloheptene with position 4 of 1-methylpiperidine resulting in the formation of a double bond between the two fragments. It is a sedating antihistamine with antimuscarinic and calcium-channel blocking actions. It is used (particularly as the hydrochloride sesquihydrate) for the relief of allergic conditions including rhinitis, conjunctivitis due to inhalant allergens and foods, urticaria and angioedema, and in pruritic skin disorders. Unlike other antihistamines, it is also a seratonin receptor antagonist, making it useful in conditions such as vascular headache and anorexia.		3.5920piperidines;
tertiary amine		anti-allergic agent;
antipruritic drug;
gastrointestinal drug;
H1-receptor antagonist;
serotonergic antagonist
danthron
danthron: structure. chrysazin : A dihydroxyanthraquinone that is anthracene-9,10-dione substituted by hydroxy groups at positions 1 and 8.		2.0510dihydroxyanthraquinoneapoptosis inducer;
plant metabolite
dapsone
[no description available]		3.5920substituted aniline;
sulfone		anti-inflammatory drug;
antiinfective agent;
antimalarial;
leprostatic drug
deferoxamine
Deferoxamine: Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the mesylate form.. desferrioxamine B : An acyclic desferrioxamine that is butanedioic acid in which one of the carboxy groups undergoes formal condensation with the primary amino group of N-(5-aminopentyl)-N-hydroxyacetamide and the second carboxy group undergoes formal condensation with the hydroxyamino group of N(1)-(5-aminopentyl)-N(1)-hydroxy-N(4)-[5-(hydroxyamino)pentyl]butanediamide. It is a siderophore native to Streptomyces pilosus biosynthesised by the DesABCD enzyme cluster as a high affinity Fe(III) chelator.		3.5920acyclic desferrioxaminebacterial metabolite;
ferroptosis inhibitor;
iron chelator;
siderophore
desipramine
Desipramine: A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.. desipramine : A dibenzoazepine consisting of 10,11-dihydro-5H-dibenzo[b,f]azepine substituted on nitrogen with a 3-(methylamino)propyl group.		3.2310dibenzoazepine;
secondary amino compound		adrenergic uptake inhibitor;
alpha-adrenergic antagonist;
antidepressant;
cholinergic antagonist;
drug allergen;
EC 3.1.4.12 (sphingomyelin phosphodiesterase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
H1-receptor antagonist;
serotonin uptake inhibitor
amphetamine
Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.. 1-phenylpropan-2-amine : A primary amine that is isopropylamine in which a hydrogen attached to one of the methyl groups has been replaced by a phenyl group.. amphetamine : A racemate comprising equimolar amounts of (R)-amphetamine (also known as levamphetamine or levoamphetamine) and (S)-amphetamine (also known as dexamfetamine or dextroamphetamine.		3.5920primary amine
eflornithine
Eflornithine: An inhibitor of ORNITHINE DECARBOXYLASE, the rate limiting enzyme of the polyamine biosynthetic pathway.. eflornithine : A fluoroamino acid that is ornithine substituted by a difluoromethyl group at position 2.		2.0510alpha-amino acid;
fluoroamino acid		trypanocidal drug
diazepam
Diazepam: A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.. diazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a methyl group at position 1 and a phenyl group at position 5.		3.59201,4-benzodiazepinone;
organochlorine compound		anticonvulsant;
anxiolytic drug;
environmental contaminant;
sedative;
xenobiotic
diazoxide
Diazoxide: A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.. diazoxide : A benzothiadiazine that is the S,S-dioxide of 2H-1,2,4-benzothiadiazine which is substituted at position 3 by a methyl group and at position 7 by chlorine. A peripheral vasodilator, it increases the concentration of glucose in the plasma and inhibits the secretion of insulin by the beta- cells of the pancreas. It is used orally in the management of intractable hypoglycaemia and intravenously in the management of hypertensive emergencies.		3.5920benzothiadiazine;
organochlorine compound;
sulfone		antihypertensive agent;
beta-adrenergic agonist;
bronchodilator agent;
cardiotonic drug;
diuretic;
K-ATP channel agonist;
sodium channel blocker;
sympathomimetic agent;
vasodilator agent
diclofenac
Diclofenac: A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.. diclofenac : A monocarboxylic acid consisting of phenylacetic acid having a (2,6-dichlorophenyl)amino group at the 2-position.		11.2231amino acid;
aromatic amine;
dichlorobenzene;
monocarboxylic acid;
secondary amino compound		antipyretic;
drug allergen;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
ddt
1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane: structure in first source		2.0510benzenoid aromatic compound;
chlorophenylethane;
monochlorobenzenes;
organochlorine insecticide		bridged diphenyl acaricide;
carcinogenic agent;
endocrine disruptor;
persistent organic pollutant
dichlorphenamide
Dichlorphenamide: A carbonic anhydrase inhibitor that is used in the treatment of glaucoma.. diclofenamide : A sulfonamide that is benzene-1,3-disulfonamide in which the hydrogens at positions 4 and 5 are substituted by chlorine. An oral carbonic anhydrase inhibitor, it partially suppresses the secretion (inflow) of aqueous humor in the eye and so reduces intraocular pressure. It is used for the treatment of glaucoma.		3.2310dichlorobenzene;
sulfonamide		antiglaucoma drug;
EC 4.2.1.1 (carbonic anhydrase) inhibitor;
ophthalmology drug
dicyclomine
Dicyclomine: A muscarinic antagonist used as an antispasmodic and in urinary incontinence. It has little effect on glandular secretion or the cardiovascular system. It does have some local anesthetic properties and is used in gastrointestinal, biliary, and urinary tract spasms.. dicyclomine : The ester resulting from the formal condensation of 1-cyclohexylcyclohexanecarboxylic acid with 2-(diethylamino)ethanol. An anticholinergic, it is used as the hydrochloride to treat or prevent spasm in the muscles of the gastrointestinal tract, particularly that associated with irritable bowel syndrome.		3.2310carboxylic ester;
tertiary amine		antispasmodic drug;
muscarinic antagonist;
parasympatholytic
pentetic acid
Pentetic Acid: An iron chelating agent with properties like EDETIC ACID. DTPA has also been used as a chelator for other metals, such as plutonium.		3.2310pentacarboxylic acidcopper chelator
diflunisal
Diflunisal: A salicylate derivative and anti-inflammatory analgesic with actions and side effects similar to those of ASPIRIN.. diflunisal : An organofluorine compound comprising salicylic acid having a 2,4-difluorophenyl group at the 5-position.		3.5920monohydroxybenzoic acid;
organofluorine compound		non-narcotic analgesic;
non-steroidal anti-inflammatory drug
dilazep
Dilazep: Coronary vasodilator with some antiarrhythmic activity.. dilazep : A member of the class of diazepanes that is 1,4-diazepane substituted by 3-[(3,4,5-trimethoxybenzoyl)oxy]propyl groups at positions 1 and 4. It is a potent adenosine uptake inhibitor that exhibits antiplatelet, antianginal and vasodilator properties.		2.0510benzoate ester;
diazepane;
diester;
methoxybenzenes		cardioprotective agent;
platelet aggregation inhibitor;
vasodilator agent
dimercaprol
Dimercaprol: An anti-gas warfare agent that is effective against Lewisite (dichloro(2-chlorovinyl)arsine) and formerly known as British Anti-Lewisite or BAL. It acts as a chelating agent and is used in the treatment of arsenic, gold, and other heavy metal poisoning.. dimercaprol : A dithiol that is propane-1,2-dithiol in which one of the methyl hydrogens is replaced by a hydroxy group. a chelating agent originally developed during World War II as an experimental antidote against the arsenic-based poison gas Lewisite, it has been used clinically since 1949 for the treatment of poisoning by arsenic, mercury and gold. It can also be used for treatment of poisoning by antimony, bismuth and possibly thallium, and (with sodium calcium edetate) in cases of acute leaad poisoning. Administration is by (painful) intramuscular injection of a suspension of dimercaprol in peanut oil, typically every 4 hours for 2-10 days depending on the toxicity. In the past, dimercaprol was also used for the treatment of Wilson's disease, a severely debilitating genetic disorder in which the body tends to retain copper, with resultant liver and brain injury.		3.2310dithiol;
primary alcohol		chelator
diphenhydramine
Diphenhydramine: A histamine H1 antagonist used as an antiemetic, antitussive, for dermatoses and pruritus, for hypersensitivity reactions, as a hypnotic, an antiparkinson, and as an ingredient in common cold preparations. It has some undesired antimuscarinic and sedative effects.. diphenhydramine : An ether that is the benzhydryl ether of 2-(dimethylamino)ethanol. It is a H1-receptor antagonist used as a antipruritic and antitussive drug.. antitussive : An agent that suppresses cough. Antitussives have a central or a peripheral action on the cough reflex, or a combination of both. Compare with expectorants, which are considered to increase the volume of secretions in the respiratory tract, so facilitating their removal by ciliary action and coughing, and mucolytics, which decrease the viscosity of mucus, facilitating its removal by ciliary action and expectoration.		3.5920ether;
tertiary amino compound		anti-allergic agent;
antidyskinesia agent;
antiemetic;
antiparkinson drug;
antipruritic drug;
antitussive;
H1-receptor antagonist;
local anaesthetic;
muscarinic antagonist;
oneirogen;
sedative
dipyridamole
Dipyridamole: A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752). dipyridamole : A pyrimidopyrimidine that is 2,2',2'',2'''-(pyrimido[5,4-d]pyrimidine-2,6-diyldinitrilo)tetraethanol substituted by piperidin-1-yl groups at positions 4 and 8 respectively. A vasodilator agent, it inhibits the formation of blood clots.		3.5920piperidines;
pyrimidopyrimidine;
tertiary amino compound;
tetrol		adenosine phosphodiesterase inhibitor;
EC 3.5.4.4 (adenosine deaminase) inhibitor;
platelet aggregation inhibitor;
vasodilator agent
disopyramide
Disopyramide: A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine. It also possesses some anticholinergic and local anesthetic properties.. disopyramide : A monocarboxylic acid amide that is butanamide substituted by a diisopropylamino group at position 4, a phenyl group at position 2 and a pyridin-2-yl group at position 2. It is used as a anti-arrhythmia drug.		3.5920monocarboxylic acid amide;
pyridines;
tertiary amino compound		anti-arrhythmia drug
disulfiram
[no description available]		3.5920organic disulfide;
organosulfur acaricide		angiogenesis inhibitor;
antineoplastic agent;
apoptosis inducer;
EC 1.2.1.3 [aldehyde dehydrogenase (NAD(+))] inhibitor;
EC 3.1.1.1 (carboxylesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
ferroptosis inducer;
fungicide;
NF-kappaB inhibitor
valproic acid
Valproic Acid: A fatty acid with anticonvulsant and anti-manic properties that is used in the treatment of EPILEPSY and BIPOLAR DISORDER. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of VOLTAGE-GATED SODIUM CHANNELS.. valproic acid : A branched-chain saturated fatty acid that comprises of a propyl substituent on a pentanoic acid stem.		6.7661branched-chain fatty acid;
branched-chain saturated fatty acid		anticonvulsant;
antimanic drug;
EC 3.5.1.98 (histone deacetylase) inhibitor;
GABA agent;
neuroprotective agent;
psychotropic drug;
teratogenic agent
donepezil
Donepezil: An indan and piperidine derivative that acts as a selective and reversible inhibitor of ACETYLCHOLINESTERASE. Donepezil is highly selective for the central nervous system and is used in the management of mild to moderate DEMENTIA in ALZHEIMER DISEASE.. donepezil : A racemate comprising equimolar amounts of (R)- and (S)-donepezil. A centrally acting reversible acetylcholinesterase inhibitor, its main therapeutic use is in the treatment of Alzheimer's disease where it is used to increase cortical acetylcholine.. 2-[(1-benzylpiperidin-4-yl)methyl]-5,6-dimethoxyindan-1-one : A member of the class of indanones that is 5,6-dimethoxyindan-1-one which is substituted at position 2 by an (N-benzylpiperidin-4-yl)methyl group.		3.2310aromatic ether;
indanones;
piperidines;
racemate		EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
nootropic agent
doxapram
Doxapram: A central respiratory stimulant with a brief duration of action. (From Martindale, The Extra Pharmocopoeia, 30th ed, p1225). doxapram : A member of the class of pyrrolidin-2-ones that is N-ethylpyrrolidin-2-one in which both of the hydrogens at the 3 position (adjacent to the carbonyl group) are substituted by phenyl groups, and one of the hydrogens at the 4 position is substituted by a 2-(morpholin-4-yl)ethyl group. A central and respiratory stimulant with a brief duration of action, it is used (generally as the hydrochloride or the hydrochloride hydrate) as a temporary treatment of acute respiratory failure, particularly when superimposed on chronic obstructive pulmonary disease, and of postoperative respiratory depression. It has also been used for treatment of postoperative shivering.		3.2310morpholines;
pyrrolidin-2-ones		central nervous system stimulant
doxazosin
Doxazosin: A prazosin-related compound that is a selective alpha-1-adrenergic blocker.. doxazosin : A member of the class of quinazolines that is quinazoline substituted by an amino group at position 4, methoxy groups at positions 6 and 7 and a piperazin-1-yl group at position 2 which in turn is substituted by a 2,3-dihydro-1,4-benzodioxin-2-ylcarbonyl group at position 4. An antihypertensive agent, it is used in the treatment of high blood pressure.		3.2310aromatic amine;
benzodioxine;
monocarboxylic acid amide;
N-acylpiperazine;
N-arylpiperazine;
quinazolines		alpha-adrenergic antagonist;
antihyperplasia drug;
antihypertensive agent;
antineoplastic agent;
vasodilator agent
doxepin
Doxepin: A dibenzoxepin tricyclic compound. It displays a range of pharmacological actions including maintaining adrenergic innervation. Its mechanism of action is not fully understood, but it appears to block reuptake of monoaminergic neurotransmitters into presynaptic terminals. It also possesses anticholinergic activity and modulates antagonism of histamine H(1)- and H(2)-receptors.. doxepin : A dibenzooxepine that is 6,11-dihydrodibenzo[b,e]oxepine substituted by a 3-(dimethylamino)propylidene group at position 11. It is used as an antidepressant drug.		3.5920dibenzooxepine;
tertiary amino compound		antidepressant
doxylamine
Doxylamine: Histamine H1 antagonist with pronounced sedative properties. It is used in allergies and as an antitussive, antiemetic, and hypnotic. Doxylamine has also been administered in veterinary applications and was formerly used in PARKINSONISM.		3.2310pyridines;
tertiary amine		anti-allergic agent;
antiemetic;
antitussive;
cholinergic antagonist;
H1-receptor antagonist;
histamine antagonist;
sedative
droperidol
Droperidol: A butyrophenone with general properties similar to those of HALOPERIDOL. It is used in conjunction with an opioid analgesic such as FENTANYL to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon. It is also used as a premedicant, as an antiemetic, and for the control of agitation in acute psychoses. (From Martindale, The Extra Pharmacopoeia, 29th ed, p593). droperidol : An organofluorine compound that is haloperidol in which the hydroxy group has been eliminated with the introduction of a double bond in the piperidine ring, and the 4-chlorophenyl group has been replaced by a benzimidazol-2-on-1-yl group. It is used in the management of chemotherapy-induced nausea and vomiting, and in conjunction with an opioid analgesic such as fentanyl to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon.		3.8630aromatic ketone;
benzimidazoles;
organofluorine compound		anaesthesia adjuvant;
antiemetic;
dopaminergic antagonist;
first generation antipsychotic
dyphylline
Dyphylline: A THEOPHYLLINE derivative with broncho- and vasodilator properties. It is used in the treatment of asthma, cardiac dyspnea, and bronchitis.. dyphylline : An oxopurine that is theophylline bearing a 2,3-dihydroxypropyl group at the 7 position. It has broncho- and vasodilator properties, and is used in the treatment of asthma, cardiac dyspnea, and bronchitis. It is also an ingredient in preparations that have been promoted for coughs.		3.2310oxopurine;
propane-1,2-diols		bronchodilator agent;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
muscle relaxant;
vasodilator agent
econazole
Econazole: An imidazole derivative that is commonly used as a topical antifungal agent.. econazole : A racemate composed of equimolar amounts of (R)- and (S)-econazole. Used (as its nitrate salt) to treat skin infections such as athlete's foot, jock itch, ringworm and other fungal skin infections.. 1-{2-(4-chlorobenzyloxy)-2-(2,4-dichlorophenyl)ethyl}imidazole : A member of the class of imidazoles that is 1-(2,4-dichlorophenyl)-2-(imidazol-1-yl)ethanol in which the hydroxyl hydrogen is replaced by a 4-chlorobenzyl group.		2.0510dichlorobenzene;
ether;
imidazoles;
monochlorobenzenes
edrophonium
Edrophonium: A rapid-onset, short-acting cholinesterase inhibitor used in cardiac arrhythmias and in the diagnosis of myasthenia gravis. It has also been used as an antidote to curare principles.. edrophonium : A quaternary ammonium ion that is N-ethyl-N,N-dimethylanilinium in which one of the meta positions is substituted by a hydroxy group. It is a reversible inhibitor of cholinesterase, with a rapid onset (30-60 seconds after injection) but a short duration of action (5-15 minutes). The chloride salt is used in myasthenia gravis both diagnostically and to distinguish between under- or over-treatment with other anticholinesterases. It has also been used for the reversal of neuromuscular blockade in anaesthesia, and for the management of poisoning due to tetrodotoxin, a neuromuscular blocking toxin found in puffer fish and other marine animals.		3.2310phenols;
quaternary ammonium ion		antidote;
diagnostic agent;
EC 3.1.1.8 (cholinesterase) inhibitor
emodin
Emodin: Purgative anthraquinone found in several plants, especially RHAMNUS PURSHIANA. It was formerly used as a laxative, but is now used mainly as a tool in toxicity studies.. emodin : A trihydroxyanthraquinone that is 9,10-anthraquinone which is substituted by hydroxy groups at positions 1, 3, and 8 and by a methyl group at position 6. It is present in the roots and barks of numerous plants (particularly rhubarb and buckthorn), moulds, and lichens. It is an active ingredient of various Chinese herbs.		7.0610trihydroxyanthraquinoneantineoplastic agent;
laxative;
plant metabolite;
tyrosine kinase inhibitor
enflurane
Enflurane: An extremely stable inhalation anesthetic that allows rapid adjustments of anesthesia depth with little change in pulse or respiratory rate.. enflurane : An ether in which the oxygen atom is connected to 2-chloro-1,1,2-trifluoroethyl and difluoromethyl groups.		2.0510ether;
organochlorine compound;
organofluorine compound		anaesthetic
enoxacin
Enoxacin: A broad-spectrum 6-fluoronaphthyridinone antibacterial agent that is structurally related to NALIDIXIC ACID.. enoxacin : A 1,8-naphthyridine derivative that is 1,4-dihydro-1,8-naphthyridine with an ethyl group at the 1 position, a carboxy group at the 3-position, an oxo sustituent at the 4-position, a fluoro substituent at the 5-position and a piperazin-1-yl group at the 7 position. An antibacterial, it is used in the treatment of urinary-tract infections and gonorrhoea.		2.05101,8-naphthyridine derivative;
amino acid;
fluoroquinolone antibiotic;
monocarboxylic acid;
N-arylpiperazine;
quinolone antibiotic		antibacterial drug;
DNA synthesis inhibitor
estazolam
Estazolam: A benzodiazepine with anticonvulsant, hypnotic, and muscle relaxant properties. It has been shown in some cases to be more potent than DIAZEPAM or NITRAZEPAM.. estazolam : A triazolo[4,3-a][1,4]benzodiazepine having a phenyl group at position 6 and a chloro substituent at position 8. A short-acting benzodiazepine with general properties similar to diazepam, it is given by mouth as a hypnotic in the short-term management of insomnia.		3.5920triazoles;
triazolobenzodiazepine		anticonvulsant;
anxiolytic drug;
GABA modulator
etazolate
Etazolate: A potent phosphodiesterase inhibitor proposed as an antipsychotic agent.. etazolate : A pyrazolopyridine that is 1H-pyrazolo[3,4-b]pyridine which is substituted at positions 1, 4, and 5 by ethyl, 2-isopropylidenehydrazino, and ethoxycarbonyl groups, respectively. A phosphodiesterase IV inhibitor with antidepressant and anxiolytic properties.		2.0510ethyl ester;
hydrazone;
pyrazolopyridine		alpha-secretase activator;
antidepressant;
antipsychotic agent;
anxiolytic drug;
GABA agent;
neuroprotective agent;
phosphodiesterase IV inhibitor
ethacrynic acid
Ethacrynic Acid: A compound that inhibits symport of sodium, potassium, and chloride primarily in the ascending limb of Henle, but also in the proximal and distal tubules. This pharmacological action results in excretion of these ions, increased urinary output, and reduction in extracellular fluid. This compound has been classified as a loop or high ceiling diuretic.. etacrynic acid : An aromatic ether that is phenoxyacetic acid in which the phenyl ring is substituted by chlorines at positions 2 and 3, and by a 2-methylidenebutanoyl group at position 4. It is a loop diuretic used to treat high blood pressure resulting from diseases such as congestive heart failure, liver failure, and kidney failure. It is also a glutathione S-transferase (EC 2.5.1.18) inhibitor.		3.5920aromatic ether;
aromatic ketone;
dichlorobenzene;
monocarboxylic acid		EC 2.5.1.18 (glutathione transferase) inhibitor;
ion transport inhibitor;
loop diuretic
ethosuximide
Ethosuximide: An anticonvulsant especially useful in the treatment of absence seizures unaccompanied by other types of seizures.. ethosuximide : A dicarboximide that is pyrrolidine-2,5-dione in which the hydrogens at position 3 are substituted by one methyl and one ethyl group. An antiepileptic, it is used in the treatment of absence seizures and may be used for myoclonic seizures, but is ineffective against tonic-clonic seizures.		3.2310dicarboximide;
pyrrolidinone		anticonvulsant;
geroprotector;
T-type calcium channel blocker
ethotoin
ethotoin: was heading 1966-94 (see under HYDANTOINS 1966-90); use HYDANTOINS to search ETHOTOIN 1966-94. ethotoin : An imidazolidine-2,4-dione that is hydantoin substituted by ethyl and phenyl at positions 3 and 5, respectively. An antiepileptic, it is less toxic than phenytoin but also less effective.		3.2310imidazolidine-2,4-dioneanticonvulsant
ethoxzolamide
Ethoxzolamide: A carbonic anhydrase inhibitor used as diuretic and in glaucoma. It may cause hypokalemia.. ethoxzolamide : A sulfonamide that is 1,3-benzothiazole-2-sulfonamide which is substituted by an ethoxy group at position 6. A carbonic anhydrase inhibitor, it has been used in the treatment of glaucoma, and as a diuretic.		2.0510aromatic ether;
benzothiazoles;
sulfonamide		antiglaucoma drug;
diuretic;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
etidronate
Etidronic Acid: A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover.. etidronic acid : A 1,1-bis(phosphonic acid) that is (ethane-1,1-diyl)bis(phosphonic acid) having a hydroxy substituent at the 1-position. It inhibits the formation, growth, and dissolution of hydroxyapatite crystals by chemisorption to calcium phosphate surfaces.		4.97211,1-bis(phosphonic acid)antineoplastic agent;
bone density conservation agent;
chelator
etodolac
Etodolac: A non-steroidal anti-inflammatory agent and cyclooxygenase-2 (COX-2) inhibitor with potent analgesic and anti-arthritic properties. It has been shown to be effective in the treatment of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; ANKYLOSING SPONDYLITIS; and in the alleviation of postoperative pain (PAIN, POSTOPERATIVE).. etodolac : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is substituted by a 1,8-diethyl-1,3,4,9-tetrahydropyrano[3,4-b]indol-1-yl moiety. A preferential inhibitor of cyclo-oxygenase 2 and non-steroidal anti-inflammatory, it is used for the treatment of rheumatoid arthritis and osteoarthritis, and for the alleviation of postoperative pain. Administered as the racemate, only the (S)-enantiomer is active.		3.5920monocarboxylic acid;
organic heterotricyclic compound		antipyretic;
cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
brl 42810
[no description available]		3.59202-aminopurines;
acetate ester		antiviral drug;
prodrug
felbamate
Felbamate: A PEGylated phenylcarbamate derivative that acts as an antagonist of NMDA RECEPTORS. It is used as an anticonvulsant, primarily for the treatment of SEIZURES in severe refractory EPILEPSY.. felbamate : The bis(carbamate ester) of 2-phenylpropane-1,3-diol. An anticonvulsant, it is used in the treatment of epilepsy.		3.5920carbamate esteranticonvulsant;
neuroprotective agent
felodipine
Felodipine: A dihydropyridine calcium antagonist with positive inotropic effects. It lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels.. felodipine : The mixed (methyl, ethyl) diester of 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylic acid. A calcium-channel blocker, it lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels. It is used in the management of hypertension and angina pectoris.		3.5920dichlorobenzene;
dihydropyridine;
ethyl ester;
methyl ester		anti-arrhythmia drug;
antihypertensive agent;
calcium channel blocker;
vasodilator agent
fenbendazole
Fenbendazole: Antinematodal benzimidazole used in veterinary medicine.. fenbendazole : A member of the class of benzimidazoles that is 1H-benzimidazole which is substituted at positons 2 and 5 by (methoxycarbonyl)amino and phenylsulfanediyl groups, respectively. A broad-spectrum anthelmintic, it is used, particularly in veterinary medicine, for the treatment of nematodal infections.		2.0510aryl sulfide;
benzimidazoles;
carbamate ester		antinematodal drug
fenofibrate
Pharmavit: a polyvitamin product, comprising vitamins A, D2, B1, B2, B6, C, E, nicotinamide, & calcium pantothene; may be a promising agent for application to human populations exposed to carcinogenic and genetic hazards of ionizing radiation; RN from CHEMLINE		4.9360aromatic ether;
chlorobenzophenone;
isopropyl ester;
monochlorobenzenes		antilipemic drug;
environmental contaminant;
geroprotector;
xenobiotic
fenoldopam
Fenoldopam: A dopamine D1 receptor agonist that is used as an antihypertensive agent. It lowers blood pressure through arteriolar vasodilation.		3.2310benzazepinealpha-adrenergic agonist;
antihypertensive agent;
dopamine agonist;
dopaminergic antagonist;
vasodilator agent
fenoprofen
Fenoprofen: A propionic acid derivative that is used as a non-steroidal anti-inflammatory agent.. fenoprofen : A monocarboxylic acid that is propanoic acid in which one of the hydrogens at position 2 is substituted by a 3-phenoxyphenyl group. A non-steroidal anti-inflammatory drug, the dihydrate form of the calcium salt is used for the management of mild to moderate pain and for the relief of pain and inflammation associated with disorders such as arthritis. It is pharmacologically similar to aspirin, but causes less gastrointestinal bleeding.		3.2310monocarboxylic acidantipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
fenspiride
fenspiride: was heading 1975-94 (see under SPIRO COMPOUNDS 1975-90); use SPIRO COMPOUNDS to search FENSPIRIDE 1975-94; bronchodilator agent used in asthma		2.0510azaspiro compound
fentanyl
Fentanyl: A potent narcotic analgesic, abuse of which leads to habituation or addiction. It is primarily a mu-opioid agonist. Fentanyl is also used as an adjunct to general anesthetics, and as an anesthetic for induction and maintenance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1078). fentanyl : A monocarboxylic acid amide resulting from the formal condensation of the aryl amino group of N-phenyl-1-(2-phenylethyl)piperidin-4-amine with propanoic acid.		2.0510anilide;
monocarboxylic acid amide;
piperidines		adjuvant;
anaesthesia adjuvant;
anaesthetic;
intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic
fexofenadine
fexofenadine: a second generation antihistamine; metabolite of the antihistaminic drug terfenadine; structure in first source; RN refers to HCl. fexofenadine : A piperidine-based anti-histamine compound.		3.2310piperidines;
tertiary amine		anti-allergic agent;
H1-receptor antagonist
fipexide
fipexide: regulates dopaminergic systems at macromolecular level		3.2310benzodioxoles
flavoxate
Flavoxate: A drug that has been used in various urinary syndromes and as an antispasmodic. Its therapeutic usefulness and its mechanism of action are not clear. It may have local anesthetic activity and direct relaxing effects on smooth muscle as well as some activity as a muscarinic antagonist.. flavoxate : A carboxylic ester resulting from the formal condensation of 3-methylflavone-8-carboxylic acid with 2-(1-piperidinyl)ethanol.		3.2310carboxylic ester;
flavones;
piperidines;
tertiary amino compound		antispasmodic drug;
muscarinic antagonist;
parasympatholytic
flecainide
Flecainide: A potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial ARRHYTHMIAS and TACHYCARDIAS.. flecainide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 2,5-bis(2,2,2-trifluoroethoxy)benzoic acid with the primary amino group of piperidin-2-ylmethylamine. An antiarrhythmic agent used (in the form of its acetate salt) to prevent and treat tachyarrhythmia (abnormal fast rhythm of the heart).		3.5920aromatic ether;
monocarboxylic acid amide;
organofluorine compound;
piperidines		anti-arrhythmia drug
fluconazole
Fluconazole: Triazole antifungal agent that is used to treat oropharyngeal CANDIDIASIS and cryptococcal MENINGITIS in AIDS.. fluconazole : A member of the class of triazoles that is propan-2-ol substituted at position 1 and 3 by 1H-1,2,4-triazol-1-yl groups and at position 2 by a 2,4-difluorophenyl group. It is an antifungal drug used for the treatment of mucosal candidiasis and for systemic infections including systemic candidiasis, coccidioidomycosis, and cryptococcosis.		3.5920conazole antifungal drug;
difluorobenzene;
tertiary alcohol;
triazole antifungal drug		environmental contaminant;
P450 inhibitor;
xenobiotic
flucytosine
Flucytosine: A fluorinated cytosine analog that is used as an antifungal agent.. flucytosine : An organofluorine compound that is cytosine that is substituted at position 5 by a fluorine. A prodrug for the antifungal 5-fluorouracil, it is used for the treatment of systemic fungal infections.		3.5920aminopyrimidine;
nucleoside analogue;
organofluorine compound;
pyrimidine antifungal drug;
pyrimidone		prodrug
flufenamic acid
Flufenamic Acid: An anthranilic acid derivative with analgesic, anti-inflammatory, and antipyretic properties. It is used in musculoskeletal and joint disorders and administered by mouth and topically. (From Martindale, The Extra Pharmacopoeia, 30th ed, p16). flufenamic acid : An aromatic amino acid consisting of anthranilic acid carrying an N-(trifluoromethyl)phenyl substituent. An analgesic and anti-inflammatory, it is used in rheumatic disorders.		2.0510aromatic amino acid;
organofluorine compound		antipyretic;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
fluphenazine
[no description available]		3.2310N-alkylpiperazine;
organofluorine compound;
phenothiazines		anticoronaviral agent;
dopaminergic antagonist;
phenothiazine antipsychotic drug
flumazenil
Flumazenil: A potent benzodiazepine receptor antagonist. Since it reverses the sedative and other actions of benzodiazepines, it has been suggested as an antidote to benzodiazepine overdoses.. flumazenil : An organic heterotricyclic compound that is 5,6-dihydro-4H-imidazo[1,5-a][1,4]benzodiazepine which is substituted at positions 3, 5, 6, and 8 by ethoxycarbonyl, methyl, oxo, and fluoro groups, respectively. It is used as an antidote to benzodiazepine overdose.		3.5920ethyl ester;
imidazobenzodiazepine;
organofluorine compound		antidote to benzodiazepine poisoning;
GABA antagonist
flunitrazepam
Flunitrazepam: A benzodiazepine with pharmacologic actions similar to those of DIAZEPAM that can cause ANTEROGRADE AMNESIA. Some reports indicate that it is used as a date rape drug and suggest that it may precipitate violent behavior. The United States Government has banned the importation of this drug.. flunitrazepam : A 1,4-benzodiazepinone that is nitrazepam substituted by a methyl group at position 1 and by a fluoro group at position 2'. It is a potent hypnotic, sedative, and amnestic drug used to treat chronic insomnia.		2.05101,4-benzodiazepinone;
C-nitro compound;
monofluorobenzenes		anxiolytic drug;
GABAA receptor agonist;
sedative
fluorescite
fluorescein (acid form) : A xanthene dye that is highly fluorescent and commonly used as a fluorescent tracer.		3.2310benzoic acids;
cyclic ketone;
hydroxy monocarboxylic acid;
organic heterotricyclic compound;
phenols;
xanthene dye		fluorescent dye;
radioopaque medium
fluorouracil
Fluorouracil: A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.. 5-fluorouracil : A nucleobase analogue that is uracil in which the hydrogen at position 5 is replaced by fluorine. It is an antineoplastic agent which acts as an antimetabolite - following conversion to the active deoxynucleotide, it inhibits DNA synthesis (by blocking the conversion of deoxyuridylic acid to thymidylic acid by the cellular enzyme thymidylate synthetase) and so slows tumour growth.		32.144,0121,525nucleobase analogue;
organofluorine compound		antimetabolite;
antineoplastic agent;
environmental contaminant;
immunosuppressive agent;
radiosensitizing agent;
xenobiotic
fluoxetine
Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.. fluoxetine : A racemate comprising equimolar amounts of (R)- and (S)-fluoxetine. A selective serotonin reuptake inhibitor (SSRI), it is used (generally as the hydrochloride salt) for the treatment of depression (and the depressive phase of bipolar disorder), bullimia nervosa, and obsessive-compulsive disorder.. N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]propan-1-amine : An aromatic ether consisting of 4-trifluoromethylphenol in which the hydrogen of the phenolic hydroxy group is replaced by a 3-(methylamino)-1-phenylpropyl group.		3.5920(trifluoromethyl)benzenes;
aromatic ether;
secondary amino compound
flurazepam
Flurazepam: A benzodiazepine derivative used mainly as a hypnotic.. flurazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a 2-(diethylamino)ethyl group, 2-fluorophenyl group and chloro group at positions 1, 5 and 7, respectively. It is a partial agonist of GABAA receptors and used for the treatment of insomnia.		3.23101,4-benzodiazepinone;
monofluorobenzenes;
organochlorine compound;
tertiary amino compound		anticonvulsant;
anxiolytic drug;
GABAA receptor agonist;
sedative
flurbiprofen
Flurbiprofen: An anti-inflammatory analgesic and antipyretic of the phenylalkynoic acid series. It has been shown to reduce bone resorption in periodontal disease by inhibiting CARBONIC ANHYDRASE.. flurbiprofen : A monocarboxylic acid that is a 2-fluoro-[1,1'-biphenyl-4-yl] moiety linked to C-2 of propionic acid. A non-steroidal anti-inflammatory, analgesic and antipyretic, it is used as a pre-operative anti-miotic as well as orally for arthritis or dental pain.		3.5920fluorobiphenyl;
monocarboxylic acid		antipyretic;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
flutamide
Flutamide: An antiandrogen with about the same potency as cyproterone in rodent and canine species.		3.5920(trifluoromethyl)benzenes;
monocarboxylic acid amide		androgen antagonist;
antineoplastic agent
fomepizole
Fomepizole: A pyrazole and competitive inhibitor of ALCOHOL DEHYDROGENASE that is used for the treatment of poisoning by ETHYLENE GLYCOL or METHANOL.. fomepizole : A member of the class of pyrazoles that is 1H-pyrazole substituted by a methyl group at position 4.		3.5920pyrazolesantidote;
EC 1.1.1.1 (alcohol dehydrogenase) inhibitor;
protective agent
foscarnet
Foscarnet: An antiviral agent used in the treatment of cytomegalovirus retinitis. Foscarnet also shows activity against human herpesviruses and HIV.. phosphonoformic acid : Phosphoric acid in which one of the hydroxy groups is replaced by a carboxylic acid group. It is used as the trisodium salt as an antiviral agent in the treatment of cytomegalovirus retinitis (CMV retinitis, an inflamation of the retina that can lead to blindness) and as an alternative to ganciclovir for AIDS patients who require concurrent antiretroviral therapy but are unable to tolerate ganciclovir due to haematological toxicity.		3.2310carboxylic acid;
one-carbon compound;
phosphonic acids		antiviral drug;
geroprotector;
HIV-1 reverse transcriptase inhibitor;
sodium-dependent Pi-transporter inhibitor
furosemide
Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.. furosemide : A chlorobenzoic acid that is 4-chlorobenzoic acid substituted by a (furan-2-ylmethyl)amino and a sulfamoyl group at position 2 and 5 respectively. It is a diuretic used in the treatment of congestive heart failure.		3.5920chlorobenzoic acid;
furans;
sulfonamide		environmental contaminant;
loop diuretic;
xenobiotic
gabapentin
Gabapentin: A cyclohexane-gamma-aminobutyric acid derivative that is used for the treatment of PARTIAL SEIZURES; NEURALGIA; and RESTLESS LEGS SYNDROME.. gabapentin : A gamma-amino acid that is cyclohexane substituted at position 1 by aminomethyl and carboxymethyl groups. Used for treatment of neuropathic pain and restless legs syndrome.		3.2310gamma-amino acidanticonvulsant;
calcium channel blocker;
environmental contaminant;
xenobiotic
gemfibrozil
[no description available]		3.5920aromatic etherantilipemic drug
glafenine
Glafenine: An anthranilic acid derivative with analgesic properties used for the relief of all types of pain.. glafenine : A carboxylic ester that is 2,3-dihydroxypropyl anthranilate in which the amino group is substituted by a 7-chloroquinolin-4-yl group. A non-steroidal anti-inflammatory drug, glafenine and its hydrochloride salt were used for the relief of all types of pain, but high incidence of anaphylactic reactions resulted in their withdrawal from the market.		3.8630aminoquinoline;
carboxylic ester;
glycol;
organochlorine compound;
secondary amino compound		inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
gliclazide
Gliclazide: An oral sulfonylurea hypoglycemic agent which stimulates insulin secretion.		2.0510N-sulfonylureahypoglycemic agent;
insulin secretagogue;
radical scavenger
glimepiride
glimepiride: structure given in first source		3.2310sulfonamide
glipizide
Glipizide: An oral hypoglycemic agent which is rapidly absorbed and completely metabolized.. glipizide : An N-sulfonylurea that is glyburide in which the (5-chloro-2-methoxybenzoyl group is replaced by a (5-methylpyrazin-2-yl)carbonyl group. An oral hypoglycemic agent, it is used in the treatment of type 2 diabetes mellitus.		3.5820aromatic amide;
monocarboxylic acid amide;
N-sulfonylurea;
pyrazines		EC 2.7.1.33 (pantothenate kinase) inhibitor;
hypoglycemic agent;
insulin secretagogue
glutethimide
Glutethimide: A hypnotic and sedative. Its use has been largely superseded by other drugs.		2.0510piperidines
glyburide
Glyburide: An antidiabetic sulfonylurea derivative with actions like those of chlorpropamide. glyburide : An N-sulfonylurea that is acetohexamide in which the acetyl group is replaced by a 2-(5-chloro-2-methoxybenzamido)ethyl group.		3.5920monochlorobenzenes;
N-sulfonylurea		anti-arrhythmia drug;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor;
hypoglycemic agent
2-cyclopentyl-2-hydroxy-2-phenylacetic acid (1,1-dimethyl-3-pyrrolidin-1-iumyl) ester
[no description available]		3.2310benzenes
gossypol
Gossypol: A dimeric sesquiterpene found in cottonseed (GOSSYPIUM). The (-) isomer is active as a male contraceptive (CONTRACEPTIVE AGENTS, MALE) whereas toxic symptoms are associated with the (+) isomer.		2.0510
granisetron
[no description available]		3.2310aromatic amide;
indazoles
guaiazulene
guaiazulene: structure		2.0510sesquiterpene
guaifenesin
Guaifenesin: An expectorant that also has some muscle relaxing action. It is used in many cough preparations.		3.2310methoxybenzenes
guanethidine
Guanethidine: An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.. guanethidine : A member of the class of guanidines in which one of the hydrogens of the amino group has been replaced by a 2-azocan-1-ylethyl group.. guanethidine sulfate : A organic sulfate salt composed of two molecules of guanethidine and one of sulfuric acid.		3.2310azocanes;
guanidines		adrenergic antagonist;
antihypertensive agent;
sympatholytic agent
guanfacine
Guanfacine: A centrally acting antihypertensive agent with specificity towards ADRENERGIC ALPHA-2 RECEPTORS.		3.2310acetamides
guanidine
Guanidine: A strong organic base existing primarily as guanidium ions at physiological pH. It is found in the urine as a normal product of protein metabolism. It is also used in laboratory research as a protein denaturant. (From Martindale, the Extra Pharmacopoeia, 30th ed and Merck Index, 12th ed) It is also used in the treatment of myasthenia and as a fluorescent probe in HPLC.. guanidine : An aminocarboxamidine, the parent compound of the guanidines.		3.2310carboxamidine;
guanidines;
one-carbon compound
fasudil
fasudil: intracellular calcium antagonist; structure in first source. fasudil : An isoquinoline substituted by a (1,4-diazepan-1-yl)sulfonyl group at position 5. It is a Rho-kinase inhibitor and its hydrochloride hydrate form is approved for the treatment of cerebral vasospasm and cerebral ischemia.		2.0510isoquinolines;
N-sulfonyldiazepane		antihypertensive agent;
calcium channel blocker;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
geroprotector;
neuroprotective agent;
nootropic agent;
vasodilator agent
haloperidol
Haloperidol: A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279). haloperidol : A compound composed of a central piperidine structure with hydroxy and p-chlorophenyl substituents at position 4 and an N-linked p-fluorobutyrophenone moiety.		3.5920aromatic ketone;
hydroxypiperidine;
monochlorobenzenes;
organofluorine compound;
tertiary alcohol		antidyskinesia agent;
antiemetic;
dopaminergic antagonist;
first generation antipsychotic;
serotonergic antagonist
halothane
[no description available]		2.0510haloalkane;
organobromine compound;
organochlorine compound;
organofluorine compound		inhalation anaesthetic
hexachlorophene
Hexachlorophene: A chlorinated bisphenol antiseptic with a bacteriostatic action against Gram-positive organisms, but much less effective against Gram-negative organisms. It is mainly used in soaps and creams and is an ingredient of various preparations used for skin disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p797). hexachlorophene : An organochlorine compound that is diphenylmethane in which each of the phenyl groups is substituted by chlorines at positions 2, 3, and 5, and by a hydroxy group at position 6. An antiseptic that is effective against Gram-positive organisms, it is used in soaps and creams for the treatment of various skin disorders. It is also used in agriculture as an acaricide and fungicide, but is not approved for such use within the European Union.		2.0510bridged diphenyl fungicide;
polyphenol;
trichlorobenzene		acaricide;
antibacterial agent;
antifungal agrochemical;
antiseptic drug
miltefosine
miltefosine: hexadecyl phosphocholine derivative of cisplatin; did not substantially activate HIV long terminal repeat; less toxic than cisplatin. miltefosine : A phospholipid that is the hexadecyl monoester of phosphocholine.		2.0510phosphocholines;
phospholipid		anti-inflammatory agent;
anticoronaviral agent;
antifungal agent;
antineoplastic agent;
antiprotozoal drug;
apoptosis inducer;
immunomodulator;
protein kinase inhibitor
hexestrol
[no description available]		2.0510stilbenoid
hexetidine
Hexetidine: A bactericidal and fungicidal antiseptic. It is used as a 0.1% mouthwash for local infections and oral hygiene. (From Martindale, The Extra Pharmacopoeia, 30th ed, p797)		2.0510organic heteromonocyclic compound;
organonitrogen heterocyclic compound
hexobarbital
Hexobarbital: A barbiturate that is effective as a hypnotic and sedative.. hexobarbital : A member of the class of barbiturates taht is barbituric acid substituted at N-1 by methyl and at C-5 by methyl and cyclohex-1-enyl groups.		2.0510barbiturates
hydralazine
Hydralazine: A direct-acting vasodilator that is used as an antihypertensive agent.. hydralazine : The 1-hydrazino derivative of phthalazine; a direct-acting vasodilator that is used as an antihypertensive agent.		3.5920azaarene;
hydrazines;
ortho-fused heteroarene;
phthalazines		antihypertensive agent;
vasodilator agent
hydrochlorothiazide
Hydrochlorothiazide: A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.. hydrochlorothiazide : A benzothiadiazine that is 3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide substituted by a chloro group at position 6 and a sulfonamide at 7. It is diuretic used for the treatment of hypertension and congestive heart failure.		3.5920benzothiadiazine;
organochlorine compound;
sulfonamide		antihypertensive agent;
diuretic;
environmental contaminant;
xenobiotic
hydroflumethiazide
Hydroflumethiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p822). hydroflumethiazide : A benzothiadiazine consisting of a 3,4-dihydro-HH-1,2,4-benzothiadiazine bicyclic system dioxygenated on sulfur and carrying trifluoromethyl and aminosulfonyl groups at positions 6 and 7 respectively. A diuretic with actions and uses similar to those of hydrochlorothiazide.		3.2310benzothiadiazine;
thiazide		antihypertensive agent;
diuretic
hydroxychloroquine
Hydroxychloroquine: A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970). hydroxychloroquine : An aminoquinoline that is chloroquine in which one of the N-ethyl groups is hydroxylated at position 2. An antimalarial with properties similar to chloroquine that acts against erythrocytic forms of malarial parasites, it is mainly used as the sulfate salt for the treatment of lupus erythematosus, rheumatoid arthritis, and light-sensitive skin eruptions.		3.2310aminoquinoline;
organochlorine compound;
primary alcohol;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antimalarial;
antirheumatic drug;
dermatologic drug
hydroxyurea
[no description available]		3.5920one-carbon compound;
ureas		antimetabolite;
antimitotic;
antineoplastic agent;
DNA synthesis inhibitor;
EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor;
genotoxin;
immunomodulator;
radical scavenger;
teratogenic agent
hydroxyzine
Hydroxyzine: A histamine H1 receptor antagonist that is effective in the treatment of chronic urticaria, dermatitis, and histamine-mediated pruritus. Unlike its major metabolite CETIRIZINE, it does cause drowsiness. It is also effective as an antiemetic, for relief of anxiety and tension, and as a sedative.. hydroxyzine : A N-alkylpiperazine that is piperzine in which the nitrogens atoms are substituted by 2-(2-hydroxyethoxy)ethyl and (4-chlorophenyl)(phenyl)methyl groups respectively.		3.5920hydroxyether;
monochlorobenzenes;
N-alkylpiperazine		anticoronaviral agent;
antipruritic drug;
anxiolytic drug;
dermatologic drug;
H1-receptor antagonist
ibudilast
[no description available]		2.0510pyrazolopyridine
ibuprofen
Midol: combination of cinnamedrine, phenacetin, aspirin & caffeine		3.5920monocarboxylic acidantipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
environmental contaminant;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
radical scavenger;
xenobiotic
phenelzine
Phenelzine: One of the MONOAMINE OXIDASE INHIBITORS used to treat DEPRESSION; PHOBIC DISORDERS; and PANIC.		3.5920primary amine
lidocaine
Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.. lidocaine : The monocarboxylic acid amide resulting from the formal condensation of N,N-diethylglycine with 2,6-dimethylaniline.		3.5920benzenes;
monocarboxylic acid amide;
tertiary amino compound		anti-arrhythmia drug;
drug allergen;
environmental contaminant;
local anaesthetic;
xenobiotic
alverine
alverine : A tertiary amine having one ethyl and two 3-phenylprop-1-yl groups attached to the nitrogen. An antispasmodic that acts directly on intestinal and uterine smooth muscle, it is used (particularly as the citrate salt) in the treatment of irritable bowel syndrome.		2.0510tertiary amineantispasmodic drug
idebenone
[no description available]		2.46201,4-benzoquinones;
primary alcohol		antioxidant;
ferroptosis inhibitor
ifosfamide
[no description available]		5.3970ifosfamidesalkylating agent;
antineoplastic agent;
environmental contaminant;
immunosuppressive agent;
xenobiotic
imipramine
Imipramine: The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group.. imipramine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine substituted by a 3-(dimethylamino)propyl group at the nitrogen atom.		3.5920dibenzoazepineadrenergic uptake inhibitor;
antidepressant;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
amrinone
Amrinone: A positive inotropic cardiotonic (CARDIOTONIC AGENTS) with vasodilator properties, phosphodiesterase 3 inhibitory activity, and the ability to stimulate calcium ion influx into the cardiac cell.. amrinone : A 3,4'-bipyridine substituted at positions 5 and 6 by an amino group and a keto function respectively. A pyridine phosphodiesterase 3 inhibitor, it is a drug that may improve the prognosis in patients with congestive heart failure.		3.5920bipyridinesEC 3.1.4.* (phosphoric diester hydrolase) inhibitor
indapamide
Indapamide: A benzamide-sulfonamide-indole derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.. indapamide : A sulfonamide formed by condensation of the carboxylic group of 4-chloro-3-sulfamoylbenzoic acid with the amino group of 2-methyl-2,3-dihydro-1H-indol-1-amine.		3.8430indoles;
organochlorine compound;
sulfonamide		antihypertensive agent;
diuretic
indomethacin
Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits CYCLOOXYGENASE, which is necessary for the formation of PROSTAGLANDINS and other AUTACOIDS. It also inhibits the motility of POLYMORPHONUCLEAR LEUKOCYTES.. indometacin : A member of the class of indole-3-acetic acids that is indole-3-acetic acid in which the indole ring is substituted at positions 1, 2 and 5 by p-chlorobenzoyl, methyl, and methoxy groups, respectively. A non-steroidal anti-inflammatory drug, it is used in the treatment of musculoskeletal and joint disorders including osteoarthritis, rheumatoid arthritis, gout, bursitis and tendinitis.		3.5920aromatic ether;
indole-3-acetic acids;
monochlorobenzenes;
N-acylindole		analgesic;
drug metabolite;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
gout suppressant;
non-steroidal anti-inflammatory drug;
xenobiotic metabolite;
xenobiotic
iohexol
Iohexol: An effective non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiographic procedures. Its low systemic toxicity is the combined result of low chemotoxicity and low osmolality.. iohexol : A benzenedicarboxamide compound having N-(2,3-dihydroxypropyl)carbamoyl groups at the 1- and 3-positions, iodo substituents at the 2-, 4- and 6-positions and an N-(2,3-dihydroxypropyl)acetamido group at the 5-position.		2.0510benzenedicarboxamide;
organoiodine compound		environmental contaminant;
radioopaque medium;
xenobiotic
iodipamide
Iodipamide: A water-soluble radiographic contrast media for cholecystography and intravenous cholangiography.. adipiodone : An organoiodine compound that is 3-amino-2,4,6-triiodobenzoic acid in which one of the amino hydrogens is substituted by a 6-(3-carboxy-2,4,6-triiodoanilino)-6-oxohexanoyl group. It is a water-soluble radiographic contrast media for cholecystography and intravenous cholangiography.		2.0510benzoic acids;
organoiodine compound;
secondary carboxamide		radioopaque medium
ioversol
[no description available]		3.2310amidobenzoic acid
iproniazid
[no description available]		3.5920carbohydrazide;
pyridines
avapro
Irbesartan: A spiro compound, biphenyl and tetrazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION, and in the treatment of kidney disease.. irbesartan : A biphenylyltetrazole that is an angiotensin II receptor antagonist used mainly for the treatment of hypertension.		3.5920azaspiro compound;
biphenylyltetrazole		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
isocarboxazid
Isocarboxazid: An MAO inhibitor that is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in the treatment of panic disorder and the phobic disorders. (From AMA, Drug Evaluations Annual, 1994, p311)		3.2310benzenes
isoflurane
Isoflurane: A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.		2.0510organofluorine compoundinhalation anaesthetic
isoniazid
Hydra: A genus of freshwater polyps in the family Hydridae, order Hydroida, class HYDROZOA. They are of special interest because of their complex organization and because their adult organization corresponds roughly to the gastrula of higher animals.. hydrazide : Compounds derived from oxoacids RkE(=O)l(OH)m (l =/= 0) by replacing -OH by -NRNR2 (R groups are commonly H). (IUPAC).		3.5920carbohydrazideantitubercular agent;
drug allergen
2-propanol
2-Propanol: An isomer of 1-PROPANOL. It is a colorless liquid having disinfectant properties. It is used in the manufacture of acetone and its derivatives and as a solvent. Topically, it is used as an antiseptic.. propan-2-ol : A secondary alcohol that is propane in which one of the hydrogens attached to the central carbon is substituted by a hydroxy group.		2.4620secondary alcohol;
secondary fatty alcohol		protic solvent
isoproterenol
Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.. isoprenaline : A secondary amino compound that is noradrenaline in which one of the hydrogens attached to the nitrogen is replaced by an isopropyl group. A sympathomimetic acting almost exclusively on beta-adrenergic receptors, it is used (mainly as the hydrochloride salt) as a bronghodilator and heart stimulant for the management of a variety of cardiac disorders.		3.5920catechols;
secondary alcohol;
secondary amino compound		beta-adrenergic agonist;
bronchodilator agent;
cardiotonic drug;
sympathomimetic agent
isoxsuprine
Isoxsuprine: A beta-adrenergic agonist that causes direct relaxation of uterine and vascular smooth muscle. Its vasodilating actions are greater on the arteries supplying skeletal muscle than on those supplying skin. It is used in the treatment of peripheral vascular disease and in premature labor.		3.5920alkylbenzene
isradipine
Isradipine: A potent antagonist of CALCIUM CHANNELS that is highly selective for VASCULAR SMOOTH MUSCLE. It is effective in the treatment of chronic stable angina pectoris, hypertension, and congestive cardiac failure.		3.5920benzoxadiazole;
dihydropyridine;
isopropyl ester;
methyl ester
itraconazole
[no description available]		3.5920piperazines
ketamine
Ketamine: A cyclohexanone derivative used for induction of anesthesia. Its mechanism of action is not well understood, but ketamine can block NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE) and may interact with sigma receptors.. ketamine : A member of the class of cyclohexanones in which one of the hydrogens at position 2 is substituted by a 2-chlorophenyl group, while the other is substituted by a methylamino group.		3.5920cyclohexanones;
monochlorobenzenes;
secondary amino compound		analgesic;
environmental contaminant;
intravenous anaesthetic;
neurotoxin;
NMDA receptor antagonist;
xenobiotic
ketanserin
Ketanserin: A selective serotonin receptor antagonist with weak adrenergic receptor blocking properties. The drug is effective in lowering blood pressure in essential hypertension. It also inhibits platelet aggregation. It is well tolerated and is particularly effective in older patients.. ketanserin : A member of the class of quinazolines that is quinazoline-2,4(1H,3H)-dione which is substituted at position 3 by a 2-[4-(p-fluorobenzoyl)piperidin-1-yl]ethyl group.		2.0510aromatic ketone;
organofluorine compound;
piperidines;
quinazolines		alpha-adrenergic antagonist;
antihypertensive agent;
cardiovascular drug;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
serotonergic antagonist
ketoconazole
1-acetyl-4-(4-{[2-(2,4-dichlorophenyl)-2-(1H-imidazol-1-ylmethyl)-1,3-dioxolan-4-yl]methoxy}phenyl)piperazine : A dioxolane that is 1,3-dioxolane which is substituted at positions 2, 2, and 4 by imidazol-1-ylmethyl, 2,4-dichlorophenyl, and [para-(4-acetylpiperazin-1-yl)phenoxy]methyl groups, respectively.		3.8530dichlorobenzene;
dioxolane;
ether;
imidazoles;
N-acylpiperazine;
N-arylpiperazine
ketoprofen
Ketoprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.. ketoprofen : An oxo monocarboxylic acid that consists of propionic acid substituted by a 3-benzoylphenyl group at position 2.		3.5920benzophenones;
oxo monocarboxylic acid		antipyretic;
drug allergen;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
non-steroidal anti-inflammatory drug;
xenobiotic
ketorolac
Ketorolac: A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed). ketorolac : A racemate comprising equimolar amounts of (R)-(+)- and (S)-(-)-5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid. While only the (S)-(-) enantiomer is a COX1 and COX2 inhibitor, the (R)-(+) enantiomer exhibits potent analgesic activity. A non-steroidal anti-inflammatory drug, ketorolac is mainly used (generally as the tromethamine salt) for its potent analgesic properties in the short-term management of post-operative pain, and in eye drops to relieve the ocular itching associated with seasonal allergic conjunctivitis. It was withdrawn from the market in many countries in 1993 following association with haemorrhage and renal failure.. 5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid : A member of the class of pyrrolizines that is 2,3-dihydro-1H-pyrrolizine which is substituted at positions 1 and 5 by carboxy and benzoyl groups, respectively.		3.2310amino acid;
aromatic ketone;
monocarboxylic acid;
pyrrolizines;
racemate		analgesic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
khellin
Khellin: A vasodilator that also has bronchodilatory action. It has been employed in the treatment of angina pectoris, in the treatment of asthma, and in conjunction with ultraviolet light A, has been tried in the treatment of vitiligo. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1024). khellin : A furanochrome in which the basic tricyclic skeleton is substituted at positions 4 and 9 with methoxy groups and at position 7 with a methyl group. A major constituent of the plant Ammi visnaga it is a herbal folk medicine used for various illnesses, its main effect being as a vasodilator.		2.0510furanochromone;
organic heterotricyclic compound;
oxacycle		anti-asthmatic agent;
bronchodilator agent;
cardiovascular drug;
vasodilator agent
labetalol
Labetalol: A salicylamide derivative that is a non-cardioselective blocker of BETA-ADRENERGIC RECEPTORS and ALPHA-1 ADRENERGIC RECEPTORS.. labetalol : A diastereoisomeric mixture of approximately equal amounts of all four possible stereoisomers ((R,S)-labetolol, (S,R)-labetolol, (S,S)-labetalol and (R,R)-labetalol). It is an adrenergic antagonist used to treat high blood pressure.. 2-hydroxy-5-{1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl}benzamide : A member of the class of benzamides that is benzamide substituted by a hydroxy group at position 2 and by a 1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl group at position 5.		3.5920benzamides;
benzenes;
phenols;
primary carboxamide;
salicylamides;
secondary alcohol;
secondary amino compound
lamotrigine
[no description available]		3.59201,2,4-triazines;
dichlorobenzene;
primary arylamine		anticonvulsant;
antidepressant;
antimanic drug;
calcium channel blocker;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
excitatory amino acid antagonist;
geroprotector;
non-narcotic analgesic;
xenobiotic
lansoprazole
Lansoprazole: A 2,2,2-trifluoroethoxypyridyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS. Lansoprazole is a racemic mixture of (R)- and (S)-isomers.		3.5920benzimidazoles;
pyridines;
sulfoxide		anti-ulcer drug;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor
beta-lapachone
beta-lapachone: antineoplastic inhibitor of reverse transcriptase, DNA topoisomerase, and DNA polymerase. beta-lapachone : A benzochromenone that is 3,4-dihydro-2H-benzo[h]chromene-5,6-dione substituted by geminal methyl groups at position 2. Isolated from Tabebuia avellanedae, it exhibits antineoplastic and anti-inflammatory activities.		2.4620benzochromenone;
orthoquinones		anti-inflammatory agent;
antineoplastic agent;
plant metabolite
leflunomide
Leflunomide: An isoxazole derivative that inhibits dihydroorotate dehydrogenase, the fourth enzyme in the pyrimidine biosynthetic pathway. It is used an immunosuppressive agent in the treatment of RHEUMATOID ARTHRITIS and PSORIATIC ARTHRITIS.. leflunomide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-methyl-1,2-oxazole-4-carboxylic acid with the anilino group of 4-(trifluoromethyl)aniline. The prodrug of teriflunomide.		4.2350(trifluoromethyl)benzenes;
isoxazoles;
monocarboxylic acid amide		antineoplastic agent;
antiparasitic agent;
EC 1.3.98.1 [dihydroorotate oxidase (fumarate)] inhibitor;
EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
hepatotoxic agent;
immunosuppressive agent;
non-steroidal anti-inflammatory drug;
prodrug;
pyrimidine synthesis inhibitor;
tyrosine kinase inhibitor
letrozole
[no description available]		8.94141nitrile;
triazoles		antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor
lofepramine
Lofepramine: A psychotropic IMIPRAMINE derivative that acts as a tricyclic antidepressant and possesses few anticholinergic properties. It is metabolized to DESIPRAMINE.		2.0510aromatic ketone;
dibenzoazepine;
monochlorobenzenes;
tertiary amino compound		antidepressant
lomefloxacin
lomefloxacin: structure given in first source. lomefloxacin : A fluoroquinolone antibiotic, used (generally as the hydrochloride salt) to treat bacterial infections including bronchitis and urinary tract infections. It is also used to prevent urinary tract infections prior to surgery.		3.2310fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antimicrobial agent;
antitubercular agent;
photosensitizing agent
lomustine
[no description available]		9.2750N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent
loperamide
Loperamide: One of the long-acting synthetic ANTIDIARRHEALS; it is not significantly absorbed from the gut, and has no effect on the adrenergic system or central nervous system, but may antagonize histamine and interfere with acetylcholine release locally.. loperamide : A synthetic piperidine derivative, effective against diarrhoea resulting from gastroenteritis or inflammatory bowel disease.		11.3841monocarboxylic acid amide;
monochlorobenzenes;
piperidines;
tertiary alcohol		anticoronaviral agent;
antidiarrhoeal drug;
mu-opioid receptor agonist
loratadine
Loratadine: A second-generation histamine H1 receptor antagonist used in the treatment of allergic rhinitis and urticaria. Unlike most classical antihistamines (HISTAMINE H1 ANTAGONISTS) it lacks central nervous system depressing effects such as drowsiness.. loratadine : A benzocycloheptapyridine that is 6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridine substituted by a chloro group at position 8 and a 1-(ethoxycarbonyl)piperidin-4-ylidene group at position 11. It is a H1-receptor antagonist commonly employed in the treatment of allergic disorders.		3.2310benzocycloheptapyridine;
ethyl ester;
N-acylpiperidine;
organochlorine compound;
tertiary carboxamide		anti-allergic agent;
cholinergic antagonist;
geroprotector;
H1-receptor antagonist
lorazepam
Lorazepam: A benzodiazepine used as an anti-anxiety agent with few side effects. It also has hypnotic, anticonvulsant, and considerable sedative properties and has been proposed as a preanesthetic agent.		3.2310benzodiazepine
losartan
Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.. losartan : A biphenylyltetrazole where a 1,1'-biphenyl group is attached at the 5-position and has an additional trisubstituted imidazol-1-ylmethyl group at the 4'-position		3.5920biphenylyltetrazole;
imidazoles		angiotensin receptor antagonist;
anti-arrhythmia drug;
antihypertensive agent;
endothelin receptor antagonist
loxapine
Loxapine: An antipsychotic agent used in SCHIZOPHRENIA.		3.2310dibenzooxazepineantipsychotic agent;
dopaminergic antagonist
malathion
Malathion: A wide spectrum aliphatic organophosphate insecticide widely used for both domestic and commercial agricultural purposes.. malathion : A racemate comprising equimolar amounts of (R) and (S)-malathion. It is a broad spectrum organophosphate proinsecticide used to control a wide range of pests including Coleoptera, Diptera, fruit flies, mosquitos and spider mites.. diethyl 2-[(dimethoxyphosphorothioyl)thio]succinate : A diester that is diethyl succinate in which position 2 is substituted by a (dimethoxyphosphorothioyl)thio group.		2.0510diester;
ethyl ester;
organic thiophosphate
diisopropyl 1,3-dithiol-2-ylidenemalonate
diisopropyl 1,3-dithiol-2-ylidenemalonate: structure in first source		2.0510isopropyl ester
maprotiline
Maprotiline: A bridged-ring tetracyclic antidepressant that is both mechanistically and functionally similar to the tricyclic antidepressants, including side effects associated with its use.		3.2310anthracenes
mazindol
Mazindol: Tricyclic anorexigenic agent unrelated to and less toxic than AMPHETAMINE, but with some similar side effects. It inhibits uptake of catecholamines and blocks the binding of cocaine to the dopamine uptake transporter.		2.0510organic molecular entity
mebendazole
Mebendazole: A benzimidazole that acts by interfering with CARBOHYDRATE METABOLISM and inhibiting polymerization of MICROTUBULES.. mebendazole : A carbamate ester that is methyl 1H-benzimidazol-2-ylcarbamate substituted by a benzoyl group at position 5.		3.5920aromatic ketone;
benzimidazoles;
carbamate ester		antinematodal drug;
microtubule-destabilising agent;
tubulin modulator
mecamylamine
Mecamylamine: A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool.		3.2310primary aliphatic amine
mechlorethamine
nitrogen mustard : Compounds having two beta-haloalkyl groups bound to a nitrogen atom, as in (X-CH2-CH2)2NR.		3.2310nitrogen mustard;
organochlorine compound		alkylating agent
meclizine
Meclizine: A histamine H1 antagonist used in the treatment of motion sickness, vertigo, and nausea during pregnancy and radiation sickness.		3.5920diarylmethane
meclofenamic acid
Meclofenamic Acid: A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.. meclofenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 2,6-dichloro-3-methylphenyl group. A non-steroidal anti-inflammatory drug, it is used as the sodium salt for the treatment of dysmenorrhoea (painful periods), osteoarthritis and rheumatoid arthritis.		3.2310aminobenzoic acid;
organochlorine compound;
secondary amino compound		analgesic;
anticonvulsant;
antineoplastic agent;
antipyretic;
antirheumatic drug;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug
meclofenoxate
Meclofenoxate: An ester of DIMETHYLAMINOETHANOL and para-chlorophenoxyacetic acid.		2.0510monocarboxylic acid
mefenamic acid
Mefenamic Acid: A non-steroidal anti-inflammatory agent with analgesic, anti-inflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase.. mefenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 2,3-dimethylphenyl group. Although classed as a non-steroidal anti-inflammatory drug, its anti-inflammatory properties are considered to be minor. It is used to relieve mild to moderate pain, including headaches, dental pain, osteoarthritis and rheumatoid arthritis.		3.5920aminobenzoic acid;
secondary amino compound		analgesic;
antipyretic;
antirheumatic drug;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
non-steroidal anti-inflammatory drug;
xenobiotic
memantine
[no description available]		3.2310adamantanes;
primary aliphatic amine		antidepressant;
antiparkinson drug;
dopaminergic agent;
neuroprotective agent;
NMDA receptor antagonist
vitamin k 3
Vitamin K 3: A synthetic naphthoquinone without the isoprenoid side chain and biological activity, but can be converted to active vitamin K2, menaquinone, after alkylation in vivo.		2.05101,4-naphthoquinones;
vitamin K		angiogenesis inhibitor;
antineoplastic agent;
EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor;
human urinary metabolite;
nutraceutical
mepenzolate
mepenzolic acid: anticholinergic, antispasmodic agent; RN given refers to parent cpd; structure		3.2310diarylmethane
meperidine
Meperidine: A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration.. pethidine : A piperidinecarboxylate ester that is piperidine which is substituted by a methyl group at position 1 and by phenyl and ethoxycarbonyl groups at position 4. It is an analgesic which is used for the treatment of moderate to severe pain, including postoperative pain and labour pain.		3.8630ethyl ester;
piperidinecarboxylate ester;
tertiary amino compound		antispasmodic drug;
kappa-opioid receptor agonist;
mu-opioid receptor agonist;
opioid analgesic
mephenytoin
Mephenytoin: An anticonvulsant effective in tonic-clonic epilepsy (EPILEPSY, TONIC-CLONIC). It may cause blood dyscrasias.. mephenytoin : An imidazolidine-2,4-dione (hydantoin) in which the imidazolidine nucleus carries a methyl group at N-3 and has ethyl and phenyl substituents at C-5. An anticonvulsant, it is no longer available in the USA or the UK but is still studied largely because of its interesting hydroxylation polymorphism.		3.5920imidazolidine-2,4-dioneanticonvulsant
mepivacaine
Mepivacaine: A local anesthetic that is chemically related to BUPIVACAINE but pharmacologically related to LIDOCAINE. It is indicated for infiltration, nerve block, and epidural anesthesia. Mepivacaine is effective topically only in large doses and therefore should not be used by this route. (From AMA Drug Evaluations, 1994, p168). mepivacaine : A piperidinecarboxamide in which N-methylpipecolic acid and 2,6-dimethylaniline have combined to form the amide bond. It is used as a local amide-type anaesthetic.		3.5920piperidinecarboxamidedrug allergen;
local anaesthetic
meprobamate
Meprobamate: A carbamate with hypnotic, sedative, and some muscle relaxant properties, although in therapeutic doses reduction of anxiety rather than a direct effect may be responsible for muscle relaxation. Meprobamate has been reported to have anticonvulsant actions against petit mal seizures, but not against grand mal seizures (which may be exacerbated). It is used in the treatment of ANXIETY DISORDERS, and also for the short-term management of INSOMNIA but has largely been superseded by the BENZODIAZEPINES. (From Martindale, The Extra Pharmacopoeia, 30th ed, p603)		3.8630organic molecular entity
mesalamine
Mesalamine: An anti-inflammatory agent, structurally related to the SALICYLATES, which is active in INFLAMMATORY BOWEL DISEASE. It is considered to be the active moiety of SULPHASALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed). mesalamine : A monohydroxybenzoic acid that is salicylic acid substituted by an amino group at the 5-position.		3.5920amino acid;
aromatic amine;
monocarboxylic acid;
monohydroxybenzoic acid;
phenols		non-steroidal anti-inflammatory drug
mesoridazine
Mesoridazine: A phenothiazine antipsychotic with effects similar to CHLORPROMAZINE.. mesoridazine : A phenothiazine substituted at position 2 (para to the S atom) by a methylsulfinyl group, and on the nitrogen by a 2-(1-methylpiperidin-2-yl)ethyl group.		3.2310phenothiazines;
sulfoxide;
tertiary amino compound		dopaminergic antagonist;
first generation antipsychotic
metaproterenol
Metaproterenol: A beta-2 adrenergic agonist used in the treatment of ASTHMA and BRONCHIAL SPASM.. orciprenaline : A racemate composed of equimolar amounts of (R)- and (S)-orciprenaline. Used (as its sulfate salt) to relax the airway muscles and improve breathing for patients suffering from asthma or bronchitis.. 5-[1-hydroxy-2-(isopropanylamino)ethyl]benzene-1,3-diol : A member of the class of resorcinols bearing an additional 1-hydroxy-2-(isopropanylamino)ethyl substituent at position 5 of resorcinol itself.		3.2310aralkylamino compound;
phenylethanolamines;
resorcinols;
secondary alcohol;
secondary amino compound
metformin
Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289). metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.		5.2731guanidinesenvironmental contaminant;
geroprotector;
hypoglycemic agent;
xenobiotic
methacrylic acid
methacrylic acid: RN given refers to parent cpd. methacrylic acid : An alpha,beta-unsaturated monocarboxylic acid that is acrylic acid in which the hydrogen at position 2 is substituted by a methyl group.		7.2510alpha,beta-unsaturated monocarboxylic acid
methadone
Methadone: A synthetic opioid that is used as the hydrochloride. It is an opioid analgesic that is primarily a mu-opioid agonist. It has actions and uses similar to those of MORPHINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1082-3). methadone : A racemate comprising equimolar amounts of dextromethadone and levomethadone. It is a opioid analgesic which is used as a painkiller and as a substitute for heroin in the treatment of heroin addiction.. 6-(dimethylamino)-4,4-diphenylheptan-3-one : A ketone that is heptan-3-one substituted by a dimethylamino group at position 6 and two phenyl groups at position 4.		3.5920benzenes;
diarylmethane;
ketone;
tertiary amino compound
methazolamide
Methazolamide: A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.		3.2310sulfonamide;
thiadiazoles
methocarbamol
Methocarbamol: A centrally acting muscle relaxant whose mode of action has not been established. It is used as an adjunct in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1206). methocarbamol : A racemate comprising equimolar amounts of (R)- and (S)-methocarbamol. A centrally acting skeletal muscle relaxant, it is used as an adjunct in the short-term symptomatic treatment of painful muscle spasm. The (R)-enantiomer is more active than the (S)-enantiomer.. 2-hydroxy-3-(2-methoxyphenoxy)propyl carbamate : A carbamate ester that is glycerol in which one of the primary alcohol groups has been converted to its 2-methoxyphenyl ether while the other has been converted to the corresponding carbamate ester.		3.2310aromatic ether;
carbamate ester;
secondary alcohol
methoxsalen
Methoxsalen: A naturally occurring furocoumarin compound found in several species of plants, including Psoralea corylifolia. It is a photoactive substance that forms DNA ADDUCTS in the presence of ultraviolet A irradiation.. methoxsalen : A member of the class of psoralens that is 7H-furo[3,2-g]chromen-7-one in which the 9 position is substituted by a methoxy group. It is a constituent of the fruits of Ammi majus. Like other psoralens, trioxsalen causes photosensitization of the skin. It is administered topically or orally in conjunction with UV-A for phototherapy treatment of vitiligo and severe psoriasis.		3.5920aromatic ether;
psoralens		antineoplastic agent;
cross-linking reagent;
dermatologic drug;
photosensitizing agent;
plant metabolite
methoxyflurane
Methoxyflurane: An inhalation anesthetic. Currently, methoxyflurane is rarely used for surgical, obstetric, or dental anesthesia. If so employed, it should be administered with NITROUS OXIDE to achieve a relatively light level of anesthesia, and a neuromuscular blocking agent given concurrently to obtain the desired degree of muscular relaxation. (From AMA Drug Evaluations Annual, 1994, p180). methoxyflurane : An ether in which the two groups attached to the central oxygen atom are methyl and 2,2-dichloro-1,1-difluoroethyl.		2.0510ether;
organochlorine compound;
organofluorine compound		hepatotoxic agent;
inhalation anaesthetic;
nephrotoxic agent;
non-narcotic analgesic
methyclothiazide
Methyclothiazide: A thiazide diuretic with properties similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p825)		3.2310benzothiadiazine
methyl salicylate
methyl salicylate: used in over-the-counter liniments, ointments, lotions for relief of musculoskeletal aches and pains; has hemolytic effect on human & sheep erythrocytes; RN given refers to parent cpd; structure in Merck Index, 9th ed, #5990. methyl salicylate : A benzoate ester that is the methyl ester of salicylic acid.		2.0510benzoate ester;
methyl ester;
salicylates		flavouring agent;
insect attractant;
metabolite
methylphenidate
Methylphenidate: A central nervous system stimulant used most commonly in the treatment of ATTENTION DEFICIT DISORDER in children and for NARCOLEPSY. Its mechanisms appear to be similar to those of DEXTROAMPHETAMINE. The d-isomer of this drug is referred to as DEXMETHYLPHENIDATE HYDROCHLORIDE.. methylphenidate : A racemate comprising equimolar amounts of the two threo isomers of methyl phenyl(piperidin-2-yl)acetate. A central stimulant and indirect-acting sympathomimetic, is used (generally as the hydrochloride salt) in the treatment of hyperactivity disorders in children and for the treatment of narcolepsy.. methyl phenyl(piperidin-2-yl)acetate : A amino acid ester that is methyl phenylacetate in which one of the hydrogens alpha to the carbonyl group is replaced by a piperidin-2-yl group.		3.5920beta-amino acid ester;
methyl ester;
piperidines
methyprylon
methyprylon: was heading 1973-94 (see under HYPNOTICS AND SEDATIVES 1963-72); use PIPERIDONES to search METHYPRYLON 1973-94		2.0510organic molecular entity
metoclopramide
Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic.. metoclopramide : A member of the class of benzamides resulting from the formal condensation of 4-amino-5-chloro-2-methoxybenzoic acid with the primary amino group of N,N-diethylethane-1,2-diamine.		3.5920benzamides;
monochlorobenzenes;
substituted aniline;
tertiary amino compound		antiemetic;
dopaminergic antagonist;
environmental contaminant;
gastrointestinal drug;
xenobiotic
metolazone
Metolazone: A quinazoline-sulfonamide derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.. metolazone : A quinazoline that consists of 1,2,3,4-tetrahydroquinazolin-4-one bearing additional methyl, 2-tolyl, sulfamyl and chloro substituents at positions 2, 3, 6 and 7 respectively. A quinazoline diuretic, with properties similar to thiazide diuretics.		3.2310organochlorine compound;
quinazolines;
sulfonamide		antihypertensive agent;
diuretic;
ion transport inhibitor
metoprolol
Metoprolol: A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.. metoprolol : A propanolamine that is 1-(propan-2-ylamino)propan-2-ol substituted by a 4-(2-methoxyethyl)phenoxy group at position 1.		3.5920aromatic ether;
propanolamine;
secondary alcohol;
secondary amino compound		antihypertensive agent;
beta-adrenergic antagonist;
environmental contaminant;
geroprotector;
xenobiotic
metronidazole
Metronidazole: A nitroimidazole used to treat AMEBIASIS; VAGINITIS; TRICHOMONAS INFECTIONS; GIARDIASIS; ANAEROBIC BACTERIA; and TREPONEMAL INFECTIONS.. metronidazole : A member of the class of imidazoles substituted at C-1, -2 and -5 with 2-hydroxyethyl, nitro and methyl groups respectively. It has activity against anaerobic bacteria and protozoa, and has a radiosensitising effect on hypoxic tumour cells. It may be given by mouth in tablets, or as the benzoate in an oral suspension. The hydrochloride salt can be used in intravenous infusions. Metronidazole is a prodrug and is selective for anaerobic bacteria due to their ability to intracellularly reduce the nitro group of metronidazole to give nitroso-containing intermediates. These can covalently bind to DNA, disrupting its helical structure, inducing DNA strand breaks and inhibiting bacterial nucleic acid synthesis, ultimately resulting in bacterial cell death.		6.0442C-nitro compound;
imidazoles;
primary alcohol		antiamoebic agent;
antibacterial drug;
antimicrobial agent;
antiparasitic agent;
antitrichomonal drug;
environmental contaminant;
prodrug;
radiosensitizing agent;
xenobiotic
metyrapone
Metyrapone: An inhibitor of the enzyme STEROID 11-BETA-MONOOXYGENASE. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of CUSHING SYNDROME.. metyrapone : An aromatic ketone that is 3,3-dimethylbutan-2-one in which the methyl groups at positions 1 and 4 are replaced by pyridin-3-yl groups. A steroid 11beta-monooxygenase (EC 1.14.15.4) inhibitor, it is used in the diagnosis of adrenal insufficiency.		3.5920aromatic ketoneantimetabolite;
diagnostic agent;
EC 1.14.15.4 (steroid 11beta-monooxygenase) inhibitor
mexiletine
Mexiletine: Antiarrhythmic agent pharmacologically similar to LIDOCAINE. It may have some anticonvulsant properties.. mexiletine : An aromatic ether which is 2,6-dimethylphenyl ether of 2-aminopropan-1-ol.		3.2310aromatic ether;
primary amino compound		anti-arrhythmia drug
mianserin
Mianserin: A tetracyclic compound with antidepressant effects. It may cause drowsiness and hematological problems. Its mechanism of therapeutic action is not well understood, although it apparently blocks alpha-adrenergic, histamine H1, and some types of serotonin receptors.. mianserin : A dibenzoazepine (specifically 1,2,3,4,10,14b-hexahydrodibenzo[c,f]pyrazino[1,2-a]azepine) methyl-substituted on N-2. Closely related to (and now mostly superseded by) the tetracyclic antidepressant mirtazapinean, it is an atypical antidepressant used in the treatment of depression throughout Europe and elsewhere.		2.0510dibenzoazepineadrenergic uptake inhibitor;
alpha-adrenergic antagonist;
antidepressant;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
geroprotector;
H1-receptor antagonist;
histamine agonist;
sedative;
serotonergic antagonist
miconazole
Miconazole: An imidazole antifungal agent that is used topically and by intravenous infusion.. 1-[2-(2,4-dichlorobenzyloxy)-2-(2,4-dichlorophenyl)ethyl]imidazole : A member of the class of imidazoles that is 1-(2,4-dichlorophenyl)-2-(imidazol-1-yl)ethanol in which the hydroxyl hydrogen is replaced by a 2,4-dichlorobenzyl group.. miconazole : A racemate composed of equimolar amounts of (R)- and (S)-miconazole. Used (as its nitrate salt) to treat skin infections such as athlete's foot, jock itch, ringworm and other fungal skin infections. It inhibits the synthesis of ergosterol, a critical component of fungal cell membranes.		2.0510dichlorobenzene;
ether;
imidazoles
midazolam
Midazolam: A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.. midazolam : An imidazobenzodiazepine that is 4H-imidazo[1,5-a][1,4]benzodiazepine which is substituted by a methyl, 2-fluorophenyl and chloro groups at positions 1, 6 and 8, respectively.		3.5920imidazobenzodiazepine;
monofluorobenzenes;
organochlorine compound		anticonvulsant;
antineoplastic agent;
anxiolytic drug;
apoptosis inducer;
central nervous system depressant;
GABAA receptor agonist;
general anaesthetic;
muscle relaxant;
sedative
midodrine
Midodrine: An ethanolamine derivative that is an adrenergic alpha-1 agonist. It is used as a vasoconstrictor agent in the treatment of HYPOTENSION.. midodrine : An aromatic ether that is 1,4-dimethoxybenzene which is substituted at position 2 by a 2-(glycylamino)-1-hydroxyethyl group. A direct-acting sympathomimetic with selective alpha-adrenergic agonist activity, it is used (generally as its hydrochloride salt) as a peripheral vasoconstrictor in the treatment of certain hypotensive states. The main active moiety is its major metabolite, deglymidodrine.		3.2310amino acid amide;
aromatic ether;
secondary alcohol		alpha-adrenergic agonist;
prodrug;
sympathomimetic agent;
vasoconstrictor agent
milrinone
[no description available]		3.2310bipyridines;
nitrile;
pyridone		cardiotonic drug;
EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor;
platelet aggregation inhibitor;
vasodilator agent
minoxidil
Minoxidil: A potent direct-acting peripheral vasodilator (VASODILATOR AGENTS) that reduces peripheral resistance and produces a fall in BLOOD PRESSURE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p371). minoxidil : A pyrimidine N-oxide that is pyrimidine-2,4-diamine 3-oxide substituted by a piperidin-1-yl group at position 6.		3.5920dialkylarylamine;
tertiary amino compound
mirtazapine
Mirtazapine: A piperazinoazepine tetracyclic compound that enhances the release of NOREPINEPHRINE and SEROTONIN through blockage of presynaptic ALPHA-2 ADRENERGIC RECEPTORS. It also blocks both 5-HT2 and 5-HT3 serotonin receptors and is a potent HISTAMINE H1 RECEPTOR antagonist. It is used for the treatment of depression, and may also be useful for the treatment of anxiety disorders.		3.5920benzazepine;
tetracyclic antidepressant		alpha-adrenergic antagonist;
anxiolytic drug;
H1-receptor antagonist;
histamine antagonist;
oneirogen;
serotonergic antagonist
mitotane
Mitotane: A derivative of the insecticide DICHLORODIPHENYLDICHLOROETHANE that specifically inhibits cells of the adrenal cortex and their production of hormones. It is used to treat adrenocortical tumors and causes CNS damage, but no bone marrow depression.		4.6240diarylmethane
mitoxantrone
Mitoxantrone: An anthracenedione-derived antineoplastic agent.. mitoxantrone : A dihydroxyanthraquinone that is 1,4-dihydroxy-9,10-anthraquinone which is substituted by 6-hydroxy-1,4-diazahexyl groups at positions 5 and 8.		4.0840dihydroxyanthraquinoneanalgesic;
antineoplastic agent
modafinil
Modafinil: A benzhydryl acetamide compound, central nervous system stimulant, and CYP3A4 inducing agent that is used in the treatment of NARCOLEPSY and SLEEP WAKE DISORDERS.. modafinil : A racemate comprising equimolar amounts of armodafinil and (S)-modafinil. A central nervous system stimulant, it is used for the treatment of sleeping disorders such as narcolepsy, obstructive sleep apnoea, and shift-work sleep disorder. The optical enantiomers of modafinil have similar pharmacological actions in animals.. 2-[(diphenylmethyl)sulfinyl]acetamide : A sulfoxide that is dimethylsulfoxide in which two hydrogens attached to one of the methyl groups are replaced by phenyl groups, while one hydrogen attached to the other methyl group is replaced by a carbamoyl (aminocarbonyl) group.		3.8630monocarboxylic acid amide;
sulfoxide
moxisylyte
Moxisylyte: An alpha-adrenergic blocking agent that is used in Raynaud's disease. It is also used locally in the eye to reverse the mydriasis caused by phenylephrine and other sympathomimetic agents. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1312)		3.5920monoterpenoid
entinostat
[no description available]		2.4110benzamides;
carbamate ester;
primary amino compound;
pyridines;
substituted aniline		antineoplastic agent;
apoptosis inducer;
EC 3.5.1.98 (histone deacetylase) inhibitor
myoseverin
myoseverin: a micotubule-binding molecule with cellular effects; structure in first source		2.2110
deet
N,N-diethyl-m-toluamide : A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of m-toluic acid with the nitrogen of diethylamine. First developed by the U.S. Army in 1946 for use by military personnel in insect-infested areas, it is the most widely used insect repellent worldwide.		2.0510benzamides;
monocarboxylic acid amide		environmental contaminant;
insect repellent;
xenobiotic
nabumetone
Nabumetone: A butanone non-steroidal anti-inflammatory drug and cyclooxygenase-2 (COX2) inhibitor that is used in the management of pain associated with OSTEOARTHRITIS and RHEUMATOID ARTHRITIS.. nabumetone : A methyl ketone that is 2-butanone in which one of the methyl hydrogens at position 4 is replaced by a 6-methoxy-2-naphthyl group. A prodrug that is converted to the active metabolite, 6-methoxy-2-naphthylacetic acid, following oral administration. It is shown to have a slightly lower risk of gastrointestinal side effects than most other non-steroidal anti-inflammatory drugs.		3.5920methoxynaphthalene;
methyl ketone		cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
prodrug
nadolol
[no description available]		3.2310tetralins
nalidixic acid
[no description available]		3.59201,8-naphthyridine derivative;
monocarboxylic acid;
quinolone antibiotic		antibacterial drug;
antimicrobial agent;
DNA synthesis inhibitor
naratriptan
naratriptan: structure given in first source		3.2310heteroarylpiperidine;
sulfonamide;
tryptamines		serotonergic agonist;
vasoconstrictor agent
nefazodone
nefazodone: may be useful as an opiate adjunct		3.5920aromatic ether;
monochlorobenzenes;
N-alkylpiperazine;
N-arylpiperazine;
triazoles		alpha-adrenergic antagonist;
analgesic;
antidepressant;
serotonergic antagonist;
serotonin uptake inhibitor
nevirapine
Nevirapine: A potent, non-nucleoside reverse transcriptase inhibitor used in combination with nucleoside analogues for treatment of HIV INFECTIONS and AIDS.. nevirapine : A dipyridodiazepine that is 5,11-dihydro-6H-dipyrido[3,2-b:2',3'-e][1,4]diazepine which is substituted by methyl, oxo, and cyclopropyl groups at positions 4, 6, and 11, respectively. A non-nucleoside reverse transcriptase inhibitor with activity against HIV-1, it is used in combination with other antiretrovirals for the treatment of HIV infection.		3.5920cyclopropanes;
dipyridodiazepine		antiviral drug;
HIV-1 reverse transcriptase inhibitor
nialamide
Nialamide: An MAO inhibitor that is used as an antidepressive agent.		3.5920organonitrogen compound;
organooxygen compound
nicardipine
Nicardipine: A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.. nicardipine : A racemate comprising equimolar amounts of (R)- and (S)-nicardipine. It is a calcium channel blocker which is used to treat hypertension.. 2-[benzyl(methyl)amino]ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine substituted by a methyl, {2-[benzyl(methyl)amino]ethoxy}carbonyl, 3-nitrophenyl, methoxycarbonyl and methyl groups at positions 2, 3, 4, 5 and 6, respectively.		3.2310benzenes;
C-nitro compound;
diester;
dihydropyridine;
methyl ester;
tertiary amino compound
niceritrol
Niceritrol: An ester of nicotinic acid that lowers cholesterol and triglycerides in total plasma and in the VLD- and LD-lipoprotein fractions.		2.0510organic molecular entity
nifedipine
Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.		3.5920C-nitro compound;
dihydropyridine;
methyl ester		calcium channel blocker;
human metabolite;
tocolytic agent;
vasodilator agent
niflumic acid
Niflumic Acid: An analgesic and anti-inflammatory agent used in the treatment of rheumatoid arthritis.		2.0510aromatic carboxylic acid;
pyridines
nilutamide
[no description available]		3.5920(trifluoromethyl)benzenes;
C-nitro compound;
imidazolidinone		androgen antagonist;
antineoplastic agent
nimesulide
nimesulide: structure. nimesulide : An aromatic ether having phenyl and 2-methylsulfonamido-5-nitrophenyl as the two aryl groups.		3.5920aromatic ether;
C-nitro compound;
sulfonamide		cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
nimodipine
Nimodipine: A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.. nimodipine : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a (2-methoxyethoxy)carbonyl group at position 3, a m-nitrophenyl group at position 4, and an isopropoxycarbonyl group at position 5. An L-type calcium channel blocker, it acts particularly on cerebral circulation, and is used both orally and intravenously for the prevention and treatment of subarachnoid hemorrhage from ruptured intracranial aneurysm.		3.59202-methoxyethyl ester;
C-nitro compound;
dicarboxylic acids and O-substituted derivatives;
diester;
dihydropyridine;
isopropyl ester		antihypertensive agent;
calcium channel blocker;
cardiovascular drug;
vasodilator agent
nisoldipine
Nisoldipine: A dihydropyridine calcium channel antagonist that acts as a potent arterial vasodilator and antihypertensive agent. It is also effective in patients with cardiac failure and angina.. nisoldipine : A racemate consisting of equimolar amounts of (R)- and (S)-nisoldipine. A calcium channel blocker, it is used in the treatment of hypertension and angina pectoris.. methyl 2-methylpropyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a methoxycarbonyl group at position 3, an o-nitrophenyl group at position 4, and an isobutoxycarbonyl group at position 5. The racemate, a calcium channel blocker, is used in the treatment of hypertension and angina pectoris.		3.5920C-nitro compound;
dicarboxylic acids and O-substituted derivatives;
diester;
dihydropyridine;
methyl ester
nitrazepam
Nitrazepam: A benzodiazepine derivative used as an anticonvulsant and hypnotic.. nitrazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one which is substituted at positions 5 and 7 by phenyl and nitro groups, respectively. It is used as a hypnotic for the short-term management of insomnia and for the treatment of epileptic spasms in infants (West's syndrome).		2.05101,4-benzodiazepinone;
C-nitro compound		anticonvulsant;
antispasmodic drug;
drug metabolite;
GABA modulator;
sedative
nitrendipine
Nitrendipine: A calcium channel blocker with marked vasodilator action. It is an effective antihypertensive agent and differs from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive.. nitrendipine : A dihydropyridine that is 1,4-dihydropyridine substituted by methyl groups at positions 2 and 6, a 3-nitrophenyl group at position 4, a ethoxycarbonyl group at position 3 and a methoxycarbonyl group at position 5. It is a calcium-channel blocker used in the treatment of hypertension.		2.0510C-nitro compound;
dicarboxylic acids and O-substituted derivatives;
diester;
dihydropyridine;
ethyl ester;
methyl ester		antihypertensive agent;
calcium channel blocker;
geroprotector;
vasodilator agent
nitroglycerin
Nitroglycerin: A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.. nitroglycerol : A nitrate ester that is glycerol in which nitro group(s) replace the hydrogen(s) attached to one or more of the hydroxy groups.. nitroglycerin : A nitroglycerol that is glycerol in which the hydrogen atoms of all three hydroxy groups are replaced by nitro groups. It acts as a prodrug, releasing nitric oxide to open blood vessels and so alleviate heart pain.		5.861nitroglycerolexplosive;
muscle relaxant;
nitric oxide donor;
prodrug;
tocolytic agent;
vasodilator agent;
xenobiotic
nizatidine
[no description available]		3.59201,3-thiazoles;
C-nitro compound;
carboxamidine;
organic sulfide;
tertiary amino compound		anti-ulcer drug;
cholinergic drug;
H2-receptor antagonist
nomifensine
Nomifensine: An isoquinoline derivative that prevents dopamine reuptake into synaptosomes. The maleate was formerly used in the treatment of depression. It was withdrawn worldwide in 1986 due to the risk of acute hemolytic anemia with intravascular hemolysis resulting from its use. In some cases, renal failure also developed. (From Martindale, The Extra Pharmacopoeia, 30th ed, p266). nomifensine : An N-methylated tetrahydroisoquinoline carrying phenyl and amino substituents at positions C-4 and C-8, respectively.		3.2310isoquinolinesdopamine uptake inhibitor
masoprocol
nordihydroguaretic acid: antioxidant compound found in the creosote bush (Larrea tridentata)		2.4620catechols;
lignan;
tetrol		antioxidant;
ferroptosis inhibitor;
geroprotector;
plant metabolite
norfloxacin
Norfloxacin: A synthetic fluoroquinolone (FLUOROQUINOLONES) with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin inhibits bacterial DNA GYRASE.. norfloxacin : A quinolinemonocarboxylic acid with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase.		3.5920fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antibacterial drug;
DNA synthesis inhibitor;
environmental contaminant;
xenobiotic
nortriptyline
Nortriptyline: A metabolite of AMITRIPTYLINE that is also used as an antidepressive agent. Nortriptyline is used in major depression, dysthymia, and atypical depressions.. nortriptyline : An organic tricyclic compound that is 10,11-dihydro-5H-dibenzo[a,d][7]annulene substituted by a 3-(methylamino)propylidene group at position 5. It is an active metabolite of amitriptyline.		3.5920organic tricyclic compound;
secondary amine		adrenergic uptake inhibitor;
analgesic;
antidepressant;
antineoplastic agent;
apoptosis inducer;
drug metabolite
ofloxacin
Ofloxacin: A synthetic fluoroquinolone antibacterial agent that inhibits the supercoiling activity of bacterial DNA GYRASE, halting DNA REPLICATION.. 9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid : An oxazinoquinoline that is 2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinolin-7-one substituted by methyl, carboxy, fluoro, and 4-methylpiperazin-1-yl groups at positions 3, 6, 9, and 10, respectively.. ofloxacin : A racemate comprising equimolar amounts of levofloxacin and dextrofloxacin. It is a synthetic fluoroquinolone antibacterial agent which inhibits the supercoiling activity of bacterial DNA gyrase, halting DNA replication.		3.23103-oxo monocarboxylic acid;
N-arylpiperazine;
N-methylpiperazine;
organofluorine compound;
oxazinoquinoline
omeprazole
Omeprazole: A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.. omeprazole : A racemate comprising equimolar amounts of (R)- and (S)-omeprazole.. 5-methoxy-2-{[(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl}-1H-benzimidazole : A member of the class of benzimidazoles that is 1H-benzimidazole which is substituted by a [4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl group at position 2 and a methoxy group at position 5.		8.9130aromatic ether;
benzimidazoles;
pyridines;
sulfoxide
ondansetron
Ondansetron: A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties.		5.541carbazoles
orphenadrine
Orphenadrine: A muscarinic antagonist used to treat drug-induced parkinsonism and to relieve pain from muscle spasm.. orphenadrine : A tertiary amino compound which is the phenyl-o-tolylmethyl ether of 2-(dimethylamino)ethanol.		3.5920ether;
tertiary amino compound		antidyskinesia agent;
antiparkinson drug;
H1-receptor antagonist;
muscarinic antagonist;
muscle relaxant;
NMDA receptor antagonist;
parasympatholytic
oxonic acid
Oxonic Acid: Antagonist of urate oxidase.		18.46128251,3,5-triazines;
monocarboxylic acid
oxamniquine
Oxamniquine: An anthelmintic with schistosomicidal activity against Schistosoma mansoni, but not against other Schistosoma spp. Oxamniquine causes worms to shift from the mesenteric veins to the liver where the male worms are retained; the female worms return to the mesentery, but can no longer release eggs. (From Martindale, The Extra Pharmacopoeia, 31st ed, p121). oxamniquine : A racemate comprising equimolar amounts of (R)- and (S)-oxamniquine. An anthelmintic, it is administered orally for the treatment of schistomiasis caused by Schistosoma mansoni (but not by other Schistosoma species); intramuscular administration is no longer used as it causes severe pain at the injection site.. {2-[(isopropylamino)methyl]-7-nitro-1,2,3,4-tetrahydroquinolin-6-yl}methanol : A member of the class of quinolines that is 1,2,3,4-tetrahydroquinoline which is substituted at positions 2, 6, and 7 by (isopropylamino)methyl, hydroxymethyl, and nitro groups, respectively.		2.0510aromatic primary alcohol;
C-nitro compound;
quinolines;
secondary amino compound
oxaprozin
Oxaprozin: An oxazole-propionic acid derivative, cyclooxygenase inhibitor, and non-steroidal anti-inflammatory drug that is used in the treatment of pain and inflammation associated with of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; and ARTHRITIS, JUVENILE.. oxaprozin : A monocarboxylic acid that is a propionic acid derivative having a 4,5-diphenyl-1,3-oxazol-2-yl substituent at position 3. It is non-steroidal anti-inflammatory drug commonly used to relieve the pain and inflammatory responses associated with osteoarthritis and rheumatoid arthritis.		3.59201,3-oxazoles;
monocarboxylic acid		analgesic;
non-steroidal anti-inflammatory drug
oxazepam
Oxazepam: A benzodiazepine used in the treatment of anxiety, alcohol withdrawal, and insomnia.. oxazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a hydroxy group at position 3 and phenyl group at position 5.		3.59201,4-benzodiazepinone;
organochlorine compound		anxiolytic drug;
environmental contaminant;
xenobiotic
oxethazaine
[no description available]		2.0510amino acid amide
oxibendazole
oxibendazole: structure		2.0510benzimidazoles;
carbamate ester
oxprenolol
Oxprenolol: A beta-adrenergic antagonist used in the treatment of hypertension, angina pectoris, arrhythmias, and anxiety.		2.0510aromatic ether
oxybenzone
oxybenzone : A hydroxybenzophenone that is benzophenone which is substituted at the 2- and 4-positions of one of the benzene rings by hydroxy and methoxy groups respectively.		2.0510hydroxybenzophenone;
monomethoxybenzene		dermatologic drug;
environmental contaminant;
protective agent;
ultraviolet filter;
xenobiotic
oxybutynin
oxybutynin: RN given refers to parent cpd. oxybutynin : A racemate comprising equimolar amounts of (R)-oxybutynin and esoxybutynin. An antispasmodic used for the treatment of overactive bladder.		3.2310acetylenic compound;
carboxylic ester;
racemate;
tertiary alcohol;
tertiary amino compound		antispasmodic drug;
calcium channel blocker;
local anaesthetic;
muscarinic antagonist;
muscle relaxant;
parasympatholytic
oxyphenbutazone
Oxyphenbutazone: A non-steroidal anti-inflammatory drug. Oxyphenbutazone eyedrops have been used abroad in the management of postoperative ocular inflammation, superficial eye injuries, and episcleritis. (From AMA, Drug Evaluations Annual, 1994, p2000) It had been used by mouth in rheumatic disorders such as ankylosing spondylitis, osteoarthritis, and rheumatoid arthritis but such use is no longer considered justified owing to the risk of severe hematological adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p27). oxyphenbutazone : A metabolite of phenylbutazone obtained by hydroxylation at position 4 of one of the phenyl rings. Commonly used (as its hydrate) to treat pain, swelling and stiffness associated with arthritis and gout, it was withdrawn from the market 1984 following association with blood dyscrasis and Stevens-Johnson syndrome.		2.0510phenols;
pyrazolidines		antimicrobial agent;
antineoplastic agent;
antipyretic;
drug metabolite;
gout suppressant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic metabolite
aminosalicylic acid
Aminosalicylic Acid: An antitubercular agent often administered in association with ISONIAZID. The sodium salt of the drug is better tolerated than the free acid.. 4-aminosalicylic acid : An aminobenzoic acid that is salicylic acid substituted by an amino group at position 4.		3.5920aminobenzoic acid;
phenols		antitubercular agent
pamidronate
[no description available]		3.2310phosphonoacetic acid
pantoprazole
Pantoprazole: 2-pyridinylmethylsulfinylbenzimidazole proton pump inhibitor that is used in the treatment of GASTROESOPHAGEAL REFLUX and PEPTIC ULCER.. pantoprazole : A member of the class of benzimidazoles that is 1H-benzimidazole substituted by a difluoromethoxy group at position 5 and a [(3,4-dimethoxypyridin-2-yl)methyl]sulfinyl group at position 2.		3.8830aromatic ether;
benzimidazoles;
organofluorine compound;
pyridines;
sulfoxide		anti-ulcer drug;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor;
environmental contaminant;
xenobiotic
papaverine
Papaverine: An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels.. papaverine : A benzylisoquinoline alkaloid that is isoquinoline substituted by methoxy groups at positions 6 and 7 and a 3,4-dimethoxybenzyl group at position 1. It has been isolated from Papaver somniferum.		3.2310benzylisoquinoline alkaloid;
dimethoxybenzene;
isoquinolines		antispasmodic drug;
vasodilator agent
pemoline
Pemoline: A central nervous system stimulant used in fatigue and depressive states and to treat hyperkinetic disorders in children.. pemoline : A member of the class of 1,3-oxazoles that is 1,3-oxazol-4(5H)-one which is substituted by an amino group at position 2 and by a phenyl group at position 5. A central nervous system stimulant, it was used to treat hyperactivity disorders in children, but withdrawn from use following reports of serious hepatotoxicity.		3.59201,3-oxazolescentral nervous system stimulant
pentamidine
Pentamidine: Antiprotozoal agent effective in trypanosomiasis, leishmaniasis, and some fungal infections; used in treatment of PNEUMOCYSTIS pneumonia in HIV-infected patients. It may cause diabetes mellitus, central nervous system damage, and other toxic effects.. pentamidine : A diether consisting of pentane-1,5-diol in which both hydroxyl hydrogens have been replaced by 4-amidinophenyl groups. A trypanocidal drug that is used for treatment of cutaneous leishmaniasis and Chagas disease.		3.2310aromatic ether;
carboxamidine;
diether		anti-inflammatory agent;
antifungal agent;
calmodulin antagonist;
chemokine receptor 5 antagonist;
EC 2.3.1.48 (histone acetyltransferase) inhibitor;
NMDA receptor antagonist;
S100 calcium-binding protein B inhibitor;
trypanocidal drug;
xenobiotic
pentobarbital
Pentobarbital: A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236). pentobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and sec-pentyl groups.		3.5920barbituratesGABAA receptor agonist
pentoxifylline
[no description available]		3.5920oxopurine
perazine
Perazine: A phenothiazine antipsychotic with actions and uses similar to those of CHLORPROMAZINE. Extrapyramidal symptoms may be more common than other side effects.. perazine : A phenothiazine derivative in which 10H-phenothiazinecarries a 3-(4-methylpiperazin-1-yl)propyl substituent at the N-10 position.		2.0510N-alkylpiperazine;
N-methylpiperazine;
phenothiazines		dopaminergic antagonist;
phenothiazine antipsychotic drug
perhexiline
Perhexiline: 2-(2,2-Dicyclohexylethyl)piperidine. Coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis.		3.2310piperidinescardiovascular drug
perphenazine
Perphenazine: An antipsychotic phenothiazine derivative with actions and uses similar to those of CHLORPROMAZINE.. perphenazine : A phenothiazine derivative in which the phenothiazine tricycle carries a chloro substituent at the 2-position and a 3-[4-(2-hydroxyethyl)piperazin-1-yl]propyl group at N-10.		3.5920N-(2-hydroxyethyl)piperazine;
N-alkylpiperazine;
organochlorine compound;
phenothiazines		antiemetic;
dopaminergic antagonist;
phenothiazine antipsychotic drug
phenacetin
Saridon: contains phenacetin, caffeine, propyphenazone & pyrithyldione		2.0510acetamides;
aromatic ether		cyclooxygenase 3 inhibitor;
non-narcotic analgesic;
peripheral nervous system drug
phenobarbital
Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.. phenobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and phenyl groups.		3.5920barbituratesanticonvulsant;
drug allergen;
excitatory amino acid antagonist;
sedative
phenolphthalein
Phenolphthalein: An acid-base indicator which is colorless in acid solution, but turns pink to red as the solution becomes alkaline. It is used medicinally as a cathartic.		2.0510phenols
phenoxybenzamine
Phenoxybenzamine: An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.		3.5920aromatic amine
phenprobamate
phenprobamate: structure		2.0510benzenes
phentermine
Phentermine: A central nervous system stimulant and sympathomimetic with actions and uses similar to those of DEXTROAMPHETAMINE. It has been used most frequently in the treatment of obesity.		3.2310primary amineadrenergic agent;
appetite depressant;
central nervous system drug;
central nervous system stimulant;
dopaminergic agent;
sympathomimetic agent
4-phenylbutyric acid
4-phenylbutyric acid: RN refers to the parent cpd. 4-phenylbutyric acid : A monocarboxylic acid the structure of which is that of butyric acid substituted with a phenyl group at C-4. It is a histone deacetylase inhibitor that displays anticancer activity. It inhibits cell proliferation, invasion and migration and induces apoptosis in glioma cells. It also inhibits protein isoprenylation, depletes plasma glutamine, increases production of foetal haemoglobin through transcriptional activation of the gamma-globin gene and affects hPPARgamma activation.		3.2310monocarboxylic acidantineoplastic agent;
apoptosis inducer;
EC 3.5.1.98 (histone deacetylase) inhibitor;
prodrug
phenylbutazone
Phenylbutazone: A butyl-diphenyl-pyrazolidinedione that has anti-inflammatory, antipyretic, and analgesic activities. It has been used in ANKYLOSING SPONDYLITIS; RHEUMATOID ARTHRITIS; and REACTIVE ARTHRITIS.. phenylbutazone : A member of the class of pyrazolidines that is 1,2-diphenylpyrazolidine-3,5-dione carrying a butyl group at the 4-position.		2.0510pyrazolidinesantirheumatic drug;
EC 1.1.1.184 [carbonyl reductase (NADPH)] inhibitor;
metabolite;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
peripheral nervous system drug
moxonidine
moxonidine: structure given in first source		2.0510organohalogen compound;
pyrimidines
pinacidil
Pinacidil: A guanidine that opens POTASSIUM CHANNELS producing direct peripheral vasodilatation of the ARTERIOLES. It reduces BLOOD PRESSURE and peripheral resistance and produces fluid retention. (Martindale The Extra Pharmacopoeia, 31st ed)		2.0510pyridines
pindolol
Pindolol: A moderately lipophilic beta blocker (ADRENERGIC BETA-ANTAGONISTS). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638). pindolol : A member of the class of indols which is the 2-hydroxy-3-(isopropylamino)propyl ether derivative of 1H-indol-4-ol.		3.2310indoles;
secondary amine		antiglaucoma drug;
antihypertensive agent;
beta-adrenergic antagonist;
serotonergic antagonist;
vasodilator agent
pioglitazone
Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.. pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.		7.1374aromatic ether;
pyridines;
thiazolidinediones		antidepressant;
cardioprotective agent;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
geroprotector;
hypoglycemic agent;
insulin-sensitizing drug;
PPARgamma agonist;
xenobiotic
pipemidic acid
Pipemidic Acid: Antimicrobial against Gram negative and some Gram positive bacteria. It is protein bound and concentrated in bile and urine and used for gastrointestinal, biliary, and urinary infections.. pipemidic acid : A pyridopyrimidine that is 5-oxo-5,8-dihydropyrido[2,3-d]pyrimidine-6-carboxylic acid substituted at position 2 by a piperazin-1-yl group and at position 8 by an ethyl group. A synthetic broad-spectrum antibacterial, it is used for treatment of gastrointestinal, biliary, and urinary infections.		2.0510amino acid;
monocarboxylic acid;
N-arylpiperazine;
pyridopyrimidine;
quinolone antibiotic		antibacterial drug;
DNA synthesis inhibitor
piperazine
[no description available]		2.0510azacycloalkane;
piperazines;
saturated organic heteromonocyclic parent		anthelminthic drug
pipobroman
Pipobroman: An antineoplastic agent that acts by alkylation.. pipobroman : An N-acylpiperazine that is piperazine in which each of the nitrogens has been acylated by a 3-bromopropionoyl group. An anti-cancer drug.		2.0510N-acylpiperazine;
organobromine compound;
tertiary carboxamide		alkylating agent;
antineoplastic agent
polythiazide
[no description available]		3.2310benzothiadiazine
duodote
duodote: consists of atropine and pralidoxime chloride; for treating those exposed to organophosphorus-containing nerve agents		3.2310pyridinium ionantidote to organophosphate poisoning;
antidote to sarin poisoning;
cholinergic drug;
cholinesterase reactivator
praziquantel
azinox: Russian drug		3.5920isoquinolines
prazosin
Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.. prazosin : A member of the class of piperazines that is piperazine substituted by a furan-2-ylcarbonyl group and a 4-amino-6,7-dimethoxyquinazolin-2-yl group at positions 1 and 4 respectively.		3.5920aromatic ether;
furans;
monocarboxylic acid amide;
piperazines;
quinazolines		alpha-adrenergic antagonist;
antihypertensive agent;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
primaquine
Primaquine: An aminoquinoline that is given by mouth to produce a radical cure and prevent relapse of vivax and ovale malarias following treatment with a blood schizontocide. It has also been used to prevent transmission of falciparum malaria by those returning to areas where there is a potential for re-introduction of malaria. Adverse effects include anemias and GI disturbances. (From Martindale, The Extra Pharmacopeia, 30th ed, p404). primaquine : An N-substituted diamine that is pentane-1,4-diamine substituted by a 6-methoxyquinolin-8-yl group at the N(4) position. It is a drug used in the treatment of malaria and Pneumocystis pneumonia.		3.5920aminoquinoline;
aromatic ether;
N-substituted diamine		antimalarial
primidone
Primidone: A barbiturate derivative that acts as a GABA modulator and anti-epileptic agent. It is partly metabolized to PHENOBARBITAL in the body and owes some of its actions to this metabolite.. primidone : A pyrimidone that is dihydropyrimidine-4,6(1H,5H)-dione substituted by an ethyl and a phenyl group at position 5. It is used as an anticonvulsant for treatment of various types of seizures.		3.5920pyrimidoneanticonvulsant;
environmental contaminant;
xenobiotic
probenecid
Probenecid: The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.. probenecid : A sulfonamide in which the nitrogen of 4-sulfamoylbenzoic acid is substituted with two propyl groups.		3.5920benzoic acids;
sulfonamide		uricosuric drug
probucol
Probucol: A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).. probucol : A dithioketal that is propane-2,2-dithiol in which the hydrogens attached to both sulfur atoms are replaced by 3,5-di-tert-butyl-4-hydroxyphenyl groups. An anticholesteremic drug with antioxidant and anti-inflammatory properties, it is used to treat high levels of cholesterol in blood.		2.0510dithioketal;
polyphenol		anti-inflammatory drug;
anticholesteremic drug;
antilipemic drug;
antioxidant;
cardiovascular drug
procainamide
Procainamide: A class Ia antiarrhythmic drug that is structurally-related to PROCAINE.. procainamide : A benzamide that is 4-aminobenzamide substituted on the amide N by a 2-(diethylamino)ethyl group. It is a pharmaceutical antiarrhythmic agent used for the medical treatment of cardiac arrhythmias.		3.5920benzamidesanti-arrhythmia drug;
platelet aggregation inhibitor;
sodium channel blocker
procarbazine
Procarbazine: An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease.. procarbazine : A benzamide obtained by formal condensation of the carboxy group of 4-[(2-methylhydrazino)methyl]benzoic acid with the amino group of isopropylamine. An antineoplastic chemotherapy drug used for treatment of Hodgkin's lymphoma. Metabolism yields azo-procarbazine and hydrogen peroxide, which results in the breaking of DNA strands.		4.640benzamides;
hydrazines		antineoplastic agent
prochlorperazine
Prochlorperazine: A phenothiazine antipsychotic used principally in the treatment of NAUSEA; VOMITING; and VERTIGO. It is more likely than CHLORPROMAZINE to cause EXTRAPYRAMIDAL DISORDERS. (From Martindale, The Extra Pharmacopoeia, 30th ed, p612). prochlorperazine : A member of the class of phenothiazines that is 10H-phenothiazine having a chloro substituent at the 2-position and a 3-(4-methylpiperazin-1-yl)propyl group at the N-10 position.		3.5920N-alkylpiperazine;
N-methylpiperazine;
organochlorine compound;
phenothiazines		alpha-adrenergic antagonist;
antiemetic;
cholinergic antagonist;
dopamine receptor D2 antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
first generation antipsychotic
procyclidine
Procyclidine: A muscarinic antagonist that crosses the blood-brain barrier and is used in the treatment of drug-induced extrapyramidal disorders and in parkinsonism.. procyclidine : A tertiary alcohol that consists of propan-1-ol substituted by a cyclohexyl and a phenyl group at position 1 and a pyrrolidin-1-yl group at position 3.		3.2310pyrrolidines;
tertiary alcohol		antidyskinesia agent;
antiparkinson drug;
muscarinic antagonist
promethazine
Promethazine: A phenothiazine derivative with histamine H1-blocking, antimuscarinic, and sedative properties. It is used as an antiallergic, in pruritus, for motion sickness and sedation, and also in animals.. promethazine : A tertiary amine that is a substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropan-2-amine moiety.		3.5920phenothiazines;
tertiary amine		anti-allergic agent;
anticoronaviral agent;
antiemetic;
antipruritic drug;
H1-receptor antagonist;
local anaesthetic;
sedative
propafenone
Propafenone: An antiarrhythmia agent that is particularly effective in ventricular arrhythmias. It also has weak beta-blocking activity.. propafenone : An aromatic ketone that is 3-(propylamino)propane-1,2-diol in which the hydrogen of the primary hydroxy group is replaced by a 2-(3-phenylpropanoyl)phenyl group. It is a class 1C antiarrhythmic drug with local anesthetic effects, and is used as the hydrochloride salt in the management of supraventricular and ventricular arrhythmias.		3.2310aromatic ketone;
secondary alcohol;
secondary amino compound		anti-arrhythmia drug
propantheline
Propantheline: A muscarinic antagonist used as an antispasmodic, in rhinitis, in urinary incontinence, and in the treatment of ulcers. At high doses it has nicotinic effects resulting in neuromuscular blocking.		3.2310xanthenes
propentofylline
[no description available]		2.0510oxopurine
propofol
Propofol: An intravenous anesthetic agent which has the advantage of a very rapid onset after infusion or bolus injection plus a very short recovery period of a couple of minutes. (From Smith and Reynard, Textbook of Pharmacology, 1992, 1st ed, p206). Propofol has been used as ANTICONVULSANTS and ANTIEMETICS.. propofol : A phenol resulting from the formal substitution of the hydrogen at the 2 position of 1,3-diisopropylbenzene by a hydroxy group.		3.5920phenolsanticonvulsant;
antiemetic;
intravenous anaesthetic;
radical scavenger;
sedative
propoxur
Propoxur: A carbamate insecticide.. propoxur : A carbamate ester that is phenyl methylcarbamate substituted at position 2 by a propan-2-yloxy group.		2.0510aromatic ether;
carbamate ester		acaricide;
agrochemical;
carbamate insecticide;
EC 3.1.1.7 (acetylcholinesterase) inhibitor
propranolol
Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.. propranolol : A propanolamine that is propan-2-ol substituted by a propan-2-ylamino group at position 1 and a naphthalen-1-yloxy group at position 3.		3.5920naphthalenes;
propanolamine;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
anxiolytic drug;
beta-adrenergic antagonist;
environmental contaminant;
human blood serum metabolite;
vasodilator agent;
xenobiotic
protriptyline
Protriptyline: Tricyclic antidepressant similar in action and side effects to IMIPRAMINE. It may produce excitation.		3.2310carbotricyclic compoundantidepressant
pyridinolcarbamate
Pyridinolcarbamate: A drug that has been given by mouth in the treatment of atherosclerosis and other vascular disorders, hyperlipidemias, and thrombo-embolic disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1408)		2.0510pyridines
pyridostigmine
[no description available]		3.2310pyridinium ion
pyrimethamine
Maloprim: contains above 2 cpds		3.5920aminopyrimidine;
monochlorobenzenes		antimalarial;
antiprotozoal drug;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor
sch 16134
quazepam: structure given in first source		3.2310benzodiazepine
quetiapine
[no description available]		3.2310dibenzothiazepine;
N-alkylpiperazine;
N-arylpiperazine		adrenergic antagonist;
dopaminergic antagonist;
histamine antagonist;
second generation antipsychotic;
serotonergic antagonist
rabeprazole
Rabeprazole: A 4-(3-methoxypropoxy)-3-methylpyridinyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.		10.3331benzimidazoles;
pyridines;
sulfoxide		anti-ulcer drug;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor
raloxifene
raloxifene : A member of the class of 1-benzothiophenes that is 1-benzothiophene in which the hydrogens at positions 2, 3, and 6 have been replaced by p-hydroxyphenyl, p-[2-(piperidin-1-yl)ethoxy]benzoyl, and hydroxy groups, respectively.		3.23101-benzothiophenes;
aromatic ketone;
N-oxyethylpiperidine;
phenols		bone density conservation agent;
estrogen antagonist;
estrogen receptor modulator
ranitidine
[no description available]		2.0510aralkylamine
opc 12759
rebamipide: structure in first source; RN refers to (+-)-isomer; inhibits gastric xanthine oxidase		2.0510secondary carboxamide
riluzole
Riluzole: A glutamate antagonist (RECEPTORS, GLUTAMATE) used as an anticonvulsant (ANTICONVULSANTS) and to prolong the survival of patients with AMYOTROPHIC LATERAL SCLEROSIS.		3.5920benzothiazoles
rimantadine
Rimantadine: An RNA synthesis inhibitor that is used as an antiviral agent in the prophylaxis and treatment of influenza.		3.2310alkylamine
risperidone
Risperidone: A selective blocker of DOPAMINE D2 RECEPTORS and SEROTONIN 5-HT2 RECEPTORS that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of SCHIZOPHRENIA.. risperidone : A member of the class of pyridopyrimidines that is 2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one carrying an additional 2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl group at position 2.		3.59201,2-benzoxazoles;
heteroarylpiperidine;
organofluorine compound;
pyridopyrimidine		alpha-adrenergic antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
H1-receptor antagonist;
psychotropic drug;
second generation antipsychotic;
serotonergic antagonist
rizatriptan
rizatriptan: structure given in first source; RN given refers to benzoate		3.2310tryptaminesanti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
rofecoxib
[no description available]		11.2275butenolide;
sulfone		analgesic;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
ropinirole
[no description available]		3.2310indolones;
tertiary amine		antidyskinesia agent;
antiparkinson drug;
central nervous system drug;
dopamine agonist
salicylamide
salamide: a major impurity of hydrochlorothiazide; structure in first source		2.0510phenols;
salicylamides		antirheumatic drug;
non-narcotic analgesic
salicylsalicylic acid
salicylsalicylic acid: structure. salsalate : A dimeric benzoate ester obtained by intermolecular condensation between the carboxy of one molecule of salicylic acid with the phenol group of a second. It is a prodrug for salycylic acid that is used for treatment of rheumatoid arthritis and osteoarthritis and also shows activity against type II diabetes.		3.5520benzoate ester;
benzoic acids;
phenols;
salicylates		antineoplastic agent;
antirheumatic drug;
EC 3.5.2.6 (beta-lactamase) inhibitor;
hypoglycemic agent;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
prodrug
sb 206553
SB 206553: a high-affinity 5-HT(2C/2B) antagonist; structure given in first source		2.0510pyrroloindole
secobarbital
Secobarbital: A barbiturate that is used as a sedative. Secobarbital is reported to have no anti-anxiety activity.. secobarbital : A member of the class of barbiturates that is barbituric acid in which the hydrogens at position 5 are substituted by prop-2-en-1-yl and pentan-2-yl groups.		3.2310barbituratesanaesthesia adjuvant;
GABA modulator;
sedative
semustine
Semustine: 4-Methyl derivative of LOMUSTINE; (CCNU). An antineoplastic agent which functions as an alkylating agent.. semustine : An organochlorine compound that is urea in which the two hydrogens on one of the amino groups are replaced by nitroso and 2-chloroethyl groups and one hydrogen from the other amino group is replaced by a 4-methylcyclohexyl group.		3.1510N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent;
carcinogenic agent
sevoflurane
Sevoflurane: A non-explosive inhalation anesthetic used in the induction and maintenance of general anesthesia. It does not cause respiratory irritation and may also prevent PLATELET AGGREGATION.. sevoflurane : An ether compound having fluoromethyl and 1,1,1,3,3,3-hexafluoroisopropyl as the two alkyl groups.		2.0510ether;
organofluorine compound		central nervous system depressant;
inhalation anaesthetic;
platelet aggregation inhibitor
sibutramine
sibutramine: serotonin and norepinephrine transporter inhibitor; Meridia is tradename for sibutramine hydrochloride		3.5920organochlorine compound;
tertiary amino compound		anti-obesity agent;
serotonin uptake inhibitor
sulfadiazine
Sulfadiazine: One of the short-acting SULFONAMIDES used in combination with PYRIMETHAMINE to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections.. sulfadiazine : A sulfonamide consisting of pyrimidine with a 4-aminobenzenesulfonamido group at the 2-position.. diazine : The parent structure of the diazines.		3.5920pyrimidines;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
antimicrobial agent;
antiprotozoal drug;
coccidiostat;
drug allergen;
EC 1.1.1.153 [sepiapterin reductase (L-erythro-7,8-dihydrobiopterin forming)] inhibitor;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor;
environmental contaminant;
xenobiotic
risedronic acid
Risedronic Acid: A pyridine and diphosphonic acid derivative that acts as a CALCIUM CHANNEL BLOCKER and inhibits BONE RESORPTION.		3.2310pyridines
sotalol
Sotalol: An adrenergic beta-antagonist that is used in the treatment of life-threatening arrhythmias.. sotalol : A sulfonamide that is N-phenylmethanesulfonamide in which the phenyl group is substituted at position 4 by a 1-hydroxy-2-(isopropylamino)ethyl group. It has both beta-adrenoreceptor blocking (Vaughan Williams Class II) and cardiac action potential duration prolongation (Vaughan Williams Class III) antiarrhythmic properties. It is used (usually as the hydrochloride salt) for the management of ventricular and supraventricular arrhythmias.		3.5920ethanolamines;
secondary alcohol;
secondary amino compound;
sulfonamide		anti-arrhythmia drug;
beta-adrenergic antagonist;
environmental contaminant;
xenobiotic
4-phenylbutyric acid, sodium salt
sodium phenylbutyrate : The organic sodium salt of 4-phenylbutyric acid. A prodrug for phenylacetate, it is used to treat urea cycle disorders.		2.0510organic sodium saltEC 3.5.1.98 (histone deacetylase) inhibitor;
geroprotector;
neuroprotective agent;
orphan drug;
prodrug
stearic acid
octadecanoic acid : A C18 straight-chain saturated fatty acid component of many animal and vegetable lipids. As well as in the diet, it is used in hardening soaps, softening plastics and in making cosmetics, candles and plastics.		2.110long-chain fatty acid;
saturated fatty acid;
straight-chain saturated fatty acid		algal metabolite;
Daphnia magna metabolite;
human metabolite;
plant metabolite
imatinib
[no description available]		3.5920aromatic amine;
benzamides;
N-methylpiperazine;
pyridines;
pyrimidines		antineoplastic agent;
apoptosis inducer;
tyrosine kinase inhibitor
streptonigrin
[no description available]		2.0510pyridines;
quinolone		antimicrobial agent;
antineoplastic agent
vorinostat
Vorinostat: A hydroxamic acid and anilide derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used in the treatment of CUTANEOUS T-CELL LYMPHOMA and SEZARY SYNDROME.. vorinostat : A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and hydroxylamine. A histone deacetylase inhibitor, it is marketed under the name Zolinza for the treatment of cutaneous T cell lymphoma (CTCL).		6.6482dicarboxylic acid diamide;
hydroxamic acid		antineoplastic agent;
apoptosis inducer;
EC 3.5.1.98 (histone deacetylase) inhibitor
succinylcholine
Succinylcholine: A quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.. succinylcholine : A quaternary ammonium ion that is the bis-choline ester of succinic acid.		3.2310quaternary ammonium ion;
succinate ester		drug allergen;
muscle relaxant;
neuromuscular agent
sulfadimethoxine
Sulfadimethoxine: A sulfanilamide that is used as an anti-infective agent.. sulfadimethoxine : A sulfonamide consisting of pyrimidine having methoxy substituents at the 2- and 6-positions and a 4-aminobenzenesulfonamido group at the 4-position.		2.0510aromatic ether;
pyrimidines;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
antimicrobial agent;
drug allergen;
environmental contaminant;
xenobiotic
sulfamerazine
[no description available]		2.0510pyrimidines;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
drug allergen
sulfameter
Sulfameter: Long acting sulfonamide used in leprosy, urinary, and respiratory tract infections.. sulfamethoxydiazine : A sulfonamide consisting of pyrimidine having a methoxy substituent at the 5-position and a 4-aminobenzenesulfonamido group at the 2-position.		2.0510pyrimidines;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
leprostatic drug;
renal agent
sulfamethazine
Sulfamethazine: A sulfanilamide anti-infective agent. It has a spectrum of antimicrobial action similar to other sulfonamides.. sulfamethazine : A sulfonamide consisting of pyrimidine with methyl substituents at the 4- and 6-positions and a 4-aminobenzenesulfonamido group at the 2-position.		2.0510pyrimidines;
sulfonamide antibiotic;
sulfonamide		antibacterial drug;
antiinfective agent;
antimicrobial agent;
carcinogenic agent;
drug allergen;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor;
environmental contaminant;
ligand;
xenobiotic
sulfamethizole
Sulfamethizole: A sulfathiazole antibacterial agent.. sulfamethizole : A sulfonamide consisting of a 1,3,4-thiadiazole nucleus with a methyl substituent at C-5 and a 4-aminobenzenesulfonamido group at C-2.		3.5920sulfonamide antibiotic;
sulfonamide;
thiadiazoles		antiinfective agent;
antimicrobial agent;
drug allergen;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor
sulfamethoxazole
Sulfamethoxazole: A bacteriostatic antibacterial agent that interferes with folic acid synthesis in susceptible bacteria. Its broad spectrum of activity has been limited by the development of resistance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p208). sulfamethoxazole : An isoxazole (1,2-oxazole) compound having a methyl substituent at the 5-position and a 4-aminobenzenesulfonamido group at the 3-position.		2.0510isoxazoles;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antibacterial agent;
antiinfective agent;
antimicrobial agent;
drug allergen;
EC 1.1.1.153 [sepiapterin reductase (L-erythro-7,8-dihydrobiopterin forming)] inhibitor;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor;
environmental contaminant;
epitope;
P450 inhibitor;
xenobiotic
sulfanilamide
[no description available]		2.0510substituted aniline;
sulfonamide antibiotic;
sulfonamide		antibacterial agent;
drug allergen;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
sulfaphenazole
Sulfaphenazole: A sulfonilamide anti-infective agent.. sulfaphenazole : A sulfonamide that is sulfanilamide in which the sulfonamide nitrogen is substituted by a 1-phenyl-1H-pyrazol-5-yl group. It is a selective inhibitor of cytochrome P450 (CYP) 2C9 isozyme, and antibacterial agent.		2.0510primary amino compound;
pyrazoles;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antibacterial drug;
EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor;
EC 1.14.13.67 (quinine 3-monooxygenase) inhibitor;
P450 inhibitor
sulfapyridine
Sulfapyridine: Antibacterial, potentially toxic, used to treat certain skin diseases.. sulfapyridine : A sulfonamide consisting of pyridine with a 4-aminobenzenesulfonamido group at the 2-position.		2.0510pyridines;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
dermatologic drug;
drug allergen;
environmental contaminant;
xenobiotic
sulfasalazine
Sulfasalazine: A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907). sulfasalazine : An azobenzene consisting of diphenyldiazene having a carboxy substituent at the 4-position, a hydroxy substituent at the 3-position and a 2-pyridylaminosulphonyl substituent at the 4'-position.		3.5920
sulfathiazole
Sulfathiazole: A sulfathiazole compound that is used as a short-acting anti-infective agent. It is no longer commonly used systemically due to its toxicity, but may still be applied topically in combination with other drugs for the treatment of vaginal and skin infections, and is still used in veterinary medicine.. sulfathiazole : A 1,3-thiazole compound having a 4-aminobenzenesulfonamido group at the 2-position.		3.23101,3-thiazoles;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
drug allergen;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor;
environmental contaminant;
xenobiotic
sulfinpyrazone
Sulfinpyrazone: A uricosuric drug that is used to reduce the serum urate levels in gout therapy. It lacks anti-inflammatory, analgesic, and diuretic properties.		2.0510pyrazolidines;
sulfoxide		uricosuric drug
2-(octylamino)-1-[4-(propan-2-ylthio)phenyl]-1-propanol
[no description available]		3.5920alkylbenzene
sulpiride
Sulpiride: A dopamine D2-receptor antagonist. It has been used therapeutically as an antidepressant, antipsychotic, and as a digestive aid. (From Merck Index, 11th ed). sulpiride : A member of the class of benzamides obtained from formal condensation between the carboxy group of 2-methoxy-5-sulfamoylbenzoic acid and the primary amino group of (1-ethylpyrrolidin-2-yl)methylamine.		2.0510benzamides;
N-alkylpyrrolidine;
sulfonamide		antidepressant;
antiemetic;
antipsychotic agent;
dopaminergic antagonist
sumatriptan
Sumatriptan: A serotonin agonist that acts selectively at 5HT1 receptors. It is used in the treatment of MIGRAINE DISORDERS.. sumatriptan : A sulfonamide that consists of N,N-dimethyltryptamine bearing an additional (N-methylsulfamoyl)methyl substituent at position 5. Selective agonist for a vascular 5-HT1 receptor subtype (probably a member of the 5-HT1D family). Used (in the form of its succinate salt) for the acute treatment of migraine with or without aura in adults.		3.2310sulfonamide;
tryptamines		serotonergic agonist;
vasoconstrictor agent
suprofen
Suprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It inhibits prostaglandin synthesis and has been proposed as an anti-arthritic.. suprofen : An aromatic ketone that is thiophene substituted at C-2 by a 4-(1-carboxyethyl)benzoyl group.		2.0510aromatic ketone;
monocarboxylic acid;
thiophenes		antirheumatic drug;
drug allergen;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
peripheral nervous system drug
suramin
Suramin: A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties.. suramin : A member of the class of phenylureas that is urea in which each of the amino groups has been substituted by a 3-({2-methyl-5-[(4,6,8-trisulfo-1-naphthyl)carbamoyl]phenyl}carbamoyl)phenyl group. An activator of both the rabbit skeletal muscle RyR1 and sheep cardiac RyR2 isoform ryanodine receptor channels, it has been used for the treatment of human African trypanosomiasis for over 100 years.		2.0510naphthalenesulfonic acid;
phenylureas;
secondary carboxamide		angiogenesis inhibitor;
antinematodal drug;
antineoplastic agent;
apoptosis inhibitor;
EC 2.7.11.13 (protein kinase C) inhibitor;
GABA antagonist;
GABA-gated chloride channel antagonist;
purinergic receptor P2 antagonist;
ryanodine receptor agonist;
trypanocidal drug
gatifloxacin
Gatifloxacin: A fluoroquinolone antibacterial agent and DNA TOPOISOMERASE II inhibitor that is used as an ophthalmic solution for the treatment of BACTERIAL CONJUNCTIVITIS.. gatifloxacin : A monocarboxylic acid that is 4-oxo-1,4-dihydroquinoline-3-carboxylic acid which is substituted on the nitrogen by a cyclopropyl group and at positions 6, 7, and 8 by fluoro, 3-methylpiperazin-1-yl, and methoxy groups, respectively. Gatifloxacin is an antibiotic of the fourth-generation fluoroquinolone family, that like other members of that family, inhibits the bacterial topoisomerase type-II enzymes.		2.4820N-arylpiperazine;
organofluorine compound;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antiinfective agent;
antimicrobial agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
tegafur
[no description available]		19.8920231organohalogen compound;
pyrimidines
temazepam
Temazepam: A benzodiazepine that acts as a GAMMA-AMINOBUTYRIC ACID modulator and anti-anxiety agent.		3.5920benzodiazepine
temozolomide
[no description available]		16.589413imidazotetrazine;
monocarboxylic acid amide;
triazene derivative		alkylating agent;
antineoplastic agent;
prodrug
terazosin
Terazosin: induces decreased blood pressure; used in the treatment of benign prostatic hyperplasia		3.2310furans;
piperazines;
primary amino compound;
quinazolines		alpha-adrenergic antagonist;
antihypertensive agent;
antineoplastic agent
terbutaline
Terbutaline: A selective beta-2 adrenergic agonist used as a bronchodilator and tocolytic.. terbutaline : A member of the class of phenylethanolamines that is catechol substituted at position 5 by a 2-(tert-butylamino)-1-hydroxyethyl group.		3.5920phenylethanolamines;
resorcinols		anti-asthmatic drug;
beta-adrenergic agonist;
bronchodilator agent;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
hypoglycemic agent;
sympathomimetic agent;
tocolytic agent
terfenadine
Terfenadine: A selective histamine H1-receptor antagonist devoid of central nervous system depressant activity. The drug was used for ALLERGY but withdrawn due to causing LONG QT SYNDROME.		2.0510diarylmethane
tetracaine
Tetracaine: A potent local anesthetic of the ester type used for surface and spinal anesthesia.. tetracaine : A benzoate ester in which 4-N-butylbenzoic acid and 2-(dimethylamino)ethanol have combined to form the ester bond; a local ester anaesthetic (ester caine) used for surface and spinal anaesthesia.		2.0510benzoate ester;
tertiary amino compound		local anaesthetic
thalidomide
Thalidomide: A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action.. thalidomide : A racemate comprising equimolar amounts of R- and S-thalidomide.. 2-(2,6-dioxopiperidin-3-yl)-1H-isoindole-1,3(2H)-dione : A dicarboximide that is isoindole-1,3(2H)-dione in which the hydrogen attached to the nitrogen is substituted by a 2,6-dioxopiperidin-3-yl group.		11.332410phthalimides;
piperidones
thiabendazole
Tresaderm: dermatologic soln containing dexamethasone, thiabendazole & neomycin sulfate		3.59201,3-thiazoles;
benzimidazole fungicide;
benzimidazoles		antifungal agrochemical;
antinematodal drug
thioridazine
Thioridazine: A phenothiazine antipsychotic used in the management of PHYCOSES, including SCHIZOPHRENIA.. thioridazine : A phenothiazine derivative having a methylsulfanyl subsitituent at the 2-position and a (1-methylpiperidin-2-yl)ethyl] group at the N-10 position.		3.5920phenothiazines;
piperidines		alpha-adrenergic antagonist;
dopaminergic antagonist;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
first generation antipsychotic;
H1-receptor antagonist;
serotonergic antagonist
thiotepa
Thiotepa: A very toxic alkylating antineoplastic agent also used as an insect sterilant. It causes skin, gastrointestinal, CNS, and bone marrow damage. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), thiotepa may reasonably be anticipated to be a carcinogen (Merck Index, 11th ed).		6.231aziridines
tiaprofenic acid
tiaprofenic acid: RN given refers to parent cpd; structure. tiaprofenic acid : An aromatic ketone that is thiophene substituted at C-2 by benzoyl and at C-4 by a 1-carboxyethyl group.		2.0510aromatic ketone;
monocarboxylic acid;
thiophenes		drug allergen;
non-steroidal anti-inflammatory drug
ticlopidine
Ticlopidine: An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.. ticlopidine : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group.		3.8530monochlorobenzenes;
thienopyridine		anticoagulant;
fibrin modulating drug;
hematologic agent;
P2Y12 receptor antagonist;
platelet aggregation inhibitor
tinidazole
Tinidazole: A nitroimidazole alkylating agent that is used as an antitrichomonal agent against TRICHOMONAS VAGINALIS; ENTAMOEBA HISTOLYTICA; and GIARDIA LAMBLIA infections. It also acts as an antibacterial agent for the treatment of BACTERIAL VAGINOSIS and anaerobic bacterial infections.. tinidazole : 1H-imidazole substituted at C-1 by a (2-ethylsulfonyl)ethyl group, at C-2 by a methyl group and at C-5 by a nitro group. It is used as an antiprotozoal, antibacterial agent.		3.2310imidazolesantiamoebic agent;
antibacterial drug;
antiparasitic agent;
antiprotozoal drug
tiopronin
Tiopronin: Sulfhydryl acylated derivative of GLYCINE.		3.5920N-acyl-amino acid
tizanidine
tizanidine: RN given refers to parent cpd; structure. tizanidine : 2,1,3-Benzothiadiazole substituted at C-4 by a Delta(1)-imidazolin-2-ylamino group and at C-4 by a chloro group. It is an agonist at alpha2-adrenergic receptor sites.		3.8630benzothiadiazole;
imidazoles		alpha-adrenergic agonist;
muscle relaxant
todralazine
Todralazine: An antihypertensive agent with both central and peripheral action; it has some central nervous system depressant effects.		2.0510phthalazines
tolazamide
Tolazamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE.. tolazamide : An N-sulfonylurea that is 1-tosylurea in which a hydrogen attached to the nitrogen at position 3 is replaced by an azepan-1-yl group. A hypoglycemic agent, it is used for the treatment of type 2 diabetes mellitus.		3.5920N-sulfonylureahypoglycemic agent;
potassium channel blocker
tolbutamide
Tolbutamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). tolbutamide : An N-sulfonylurea that consists of 1-butylurea having a tosyl group attached at the 3-position.		3.5920N-sulfonylureahuman metabolite;
hypoglycemic agent;
insulin secretagogue;
potassium channel blocker
tolmetin
Tolmetin: A non-steroidal anti-inflammatory agent (ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL) similar in mode of action to INDOMETHACIN.. tolmetin : A monocarboxylic acid that is (1-methylpyrrol-2-yl)acetic acid substituted at position 5 on the pyrrole ring by a 4-methylbenzoyl group. Used in the form of its sodium salt dihydrate as a nonselective nonsteroidal anti-inflammatory drug.		3.2310aromatic ketone;
monocarboxylic acid;
pyrroles		EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug
tolperisone
Tolperisone: A centrally acting muscle relaxant that has been used for the symptomatic treatment of spasticity and muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1211)		2.4620aromatic ketone
ultram
2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanol : A tertiary alcohol that is cyclohexanol substituted at positions 1 and 2 by 3-methoxyphenyl and dimethylaminomethyl groups respectively.		3.5920aromatic ether;
tertiary alcohol;
tertiary amino compound
tranexamic acid
Tranexamic Acid: Antifibrinolytic hemostatic used in severe hemorrhage.		4.4130amino acid
trazodone
Trazodone: A serotonin uptake inhibitor that is used as an antidepressive agent. It has been shown to be effective in patients with major depressive disorders and other subsets of depressive disorders. It is generally more useful in depressive disorders associated with insomnia and anxiety. This drug does not aggravate psychotic symptoms in patients with schizophrenia or schizoaffective disorders. (From AMA Drug Evaluations Annual, 1994, p309). trazodone : An N-arylpiperazine in which one nitrogen is substituted by a 3-chlorophenyl group, while the other is substituted by a 3-(3-oxo[1,2,4]triazolo[4,3-a]pyridin-2(3H)-yl)propyl group.		3.8630monochlorobenzenes;
N-alkylpiperazine;
N-arylpiperazine;
triazolopyridine		adrenergic antagonist;
antidepressant;
anxiolytic drug;
H1-receptor antagonist;
sedative;
serotonin uptake inhibitor
triamterene
Triamterene: A pteridinetriamine compound that inhibits SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS.. triamterene : Pteridine substituted at positions 2, 4 and 7 with amino groups and at position 6 with a phenyl group. A sodium channel blocker, it is used as a diuretic in the treatment of hypertension and oedema.		3.2310pteridinesdiuretic;
sodium channel blocker
triazolam
Triazolam: A short-acting benzodiazepine used in the treatment of insomnia. Some countries temporarily withdrew triazolam from the market because of concerns about adverse reactions, mostly psychological, associated with higher dose ranges. Its use at lower doses with appropriate care and labeling has been reaffirmed by the FDA and most other countries.		3.2310triazolobenzodiazepinesedative
triclosan
[no description available]		2.0510aromatic ether;
dichlorobenzene;
monochlorobenzenes;
phenols		antibacterial agent;
antimalarial;
drug allergen;
EC 1.3.1.9 [enoyl-[acyl-carrier-protein] reductase (NADH)] inhibitor;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
fungicide;
persistent organic pollutant;
xenobiotic
trifluoperazine
[no description available]		3.2310N-alkylpiperazine;
N-methylpiperazine;
organofluorine compound;
phenothiazines		antiemetic;
calmodulin antagonist;
dopaminergic antagonist;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
EC 5.3.3.5 (cholestenol Delta-isomerase) inhibitor;
phenothiazine antipsychotic drug
triflupromazine
Triflupromazine: A phenothiazine used as an antipsychotic agent and as an antiemetic.. triflupromazine : A member of the class of phenothiazines that is 10H-phenothiazine having a trifluoromethyl subsitituent at the 2-position and a 3-(dimethylamino)propyl group at the N-10 position.		2.0510organofluorine compound;
phenothiazines;
tertiary amine		anticoronaviral agent;
antiemetic;
dopaminergic antagonist;
first generation antipsychotic
trihexyphenidyl
Trihexyphenidyl: One of the centrally acting MUSCARINIC ANTAGONISTS used for treatment of PARKINSONIAN DISORDERS and drug-induced extrapyramidal movement disorders and as an antispasmodic.		3.2310amine
trimethadione
Trimethadione: An anticonvulsant effective in absence seizures, but generally reserved for refractory cases because of its toxicity. (From AMA Drug Evaluations Annual, 1994, p378). trimethadione : An oxazolidinone that is 1,3-oxazolidine-2,4-dione substituted by methyl groups at positions 3, 5 and 5. It is an antiepileptic agent.		3.5920oxazolidinoneanticonvulsant;
geroprotector
trimethobenzamide
trimethobenzamide: major descriptor (64-84); on-line search BENZAMIDES (64-84); Index Medicus search TRIMETHOBENZAMIDE (64-84); RN given refers to parent cpd. trimethobenzamide : The amide obtained by formal condensation of 3,4,5-trihydroxybenzoic acid with 4-[2-(N,N-dimethylamino)ethoxy]benzylamine. It is used to prevent nausea and vomitting in humans.		3.2310benzamides;
tertiary amino compound		antiemetic
trimethoprim
Trimethoprim: A pyrimidine inhibitor of dihydrofolate reductase, it is an antibacterial related to PYRIMETHAMINE. It is potentiated by SULFONAMIDES and the TRIMETHOPRIM, SULFAMETHOXAZOLE DRUG COMBINATION is the form most often used. It is sometimes used alone as an antimalarial. TRIMETHOPRIM RESISTANCE has been reported.. trimethoprim : An aminopyrimidine antibiotic whose structure consists of pyrimidine 2,4-diamine and 1,2,3-trimethoxybenzene moieties linked by a methylene bridge.		3.5920aminopyrimidine;
methoxybenzenes		antibacterial drug;
diuretic;
drug allergen;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
environmental contaminant;
xenobiotic
trimetrexate
Trimetrexate: A nonclassical folic acid inhibitor through its inhibition of the enzyme dihydrofolate reductase. It is being tested for efficacy as an antineoplastic agent and as an antiparasitic agent against PNEUMOCYSTIS PNEUMONIA in AIDS patients. Myelosuppression is its dose-limiting toxic effect.		10.7231
trimipramine
Trimipramine: Tricyclic antidepressant similar to IMIPRAMINE, but with more antihistaminic and sedative properties.. trimipramine : A dibenzoazepine that is 10,11-dihydro-5H-dibenzo[b,f]azepine substituted by a 3-(dimethylamino)-2-methylpropyl group at the nitrogen atom. It is used as an antidepressant.		3.2310dibenzoazepine;
tertiary amino compound		antidepressant;
environmental contaminant;
xenobiotic
troglitazone
Troglitazone: A chroman and thiazolidinedione derivative that acts as a PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS (PPAR) agonist. It was formerly used in the treatment of TYPE 2 DIABETES MELLITUS, but has been withdrawn due to hepatotoxicity.		3.5920chromanes;
thiazolidinone		anticoagulant;
anticonvulsant;
antineoplastic agent;
antioxidant;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
hypoglycemic agent;
platelet aggregation inhibitor;
vasodilator agent
tyramine
[no description available]		3.2310monoamine molecular messenger;
primary amino compound;
tyramines		EC 3.1.1.8 (cholinesterase) inhibitor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
neurotransmitter
delavirdine
Delavirdine: A potent, non-nucleoside reverse transcriptase inhibitor with activity specific for HIV-1.. delavirdine : The amide resulting from the formal condensation of 5-[(methylsulfonyl)amino]-1H-indole-2-carboxylic acid and 4-amino group of 1-[3-(isopropylamino)pyridin-2-yl]piperazine, delavirdine is a non-nucleoside reverse transcriptase inhibitor with activity specific for HIV-1. Viral resistance emerges rapidly when delavirdine is used alone, so it is therefore used (as the methanesulfonic acid salt) with other antiretrovirals for combination therapy of HIV infection.		3.5820aminopyridine;
indolecarboxamide;
N-acylpiperazine;
sulfonamide		antiviral drug;
HIV-1 reverse transcriptase inhibitor
venlafaxine
venlafaxine : A tertiary amino compound that is N,N-dimethylethanamine substituted at position 1 by a 1-hydroxycyclohexyl and 4-methoxyphenyl group.		3.5920cyclohexanols;
monomethoxybenzene;
tertiary alcohol;
tertiary amino compound		adrenergic uptake inhibitor;
analgesic;
antidepressant;
dopamine uptake inhibitor;
environmental contaminant;
serotonin uptake inhibitor;
xenobiotic
vesnarinone
[no description available]		2.0510organic molecular entity
vigabatrin
[no description available]		3.5920gamma-amino acidanticonvulsant;
EC 2.6.1.19 (4-aminobutyrate--2-oxoglutarate transaminase) inhibitor
ici 204,219
zafirlukast: a leukotriene D4 receptor antagonist		3.5920carbamate ester;
indoles;
N-sulfonylcarboxamide		anti-asthmatic agent;
leukotriene antagonist
zaleplon
zaleplon: an azabicyclo(4.3.0)nonane; a nonbenzodiazepine; one of the so-called of Z drugs (zopiclone, eszopiclone, zolpidem, and zaleplon) for which there is some correlation with tumors; a hypnotic with less marked effect on psychomotor functions compared to lorazepam. zaleplon : A pyrazolo[1,5-a]pyrimidine having a nitrile group at position 3 and a 3-(N-ethylacetamido)phenyl substituent at the 7-position.		3.2310nitrile;
pyrazolopyrimidine		anticonvulsant;
anxiolytic drug;
central nervous system depressant;
sedative
zolpidem
Zolpidem: An imidazopyridine derivative and short-acting GABA-A receptor agonist that is used for the treatment of INSOMNIA.. zolpidem : An imidazo[1,2-a]pyridine compound having a 4-tolyl group at the 2-position, an N,N-dimethylcarbamoylmethyl group at the 3-position and a methyl substituent at the 6-position.		3.5920imidazopyridinecentral nervous system depressant;
GABA agonist;
sedative
zonisamide
Zonisamide: A benzisoxazole and sulfonamide derivative that acts as a CALCIUM CHANNEL blocker. It is used primarily as an adjunctive antiepileptic agent for the treatment of PARTIAL SEIZURES, with or without secondary generalization.. zonisamide : A 1,2-benzoxazole compound having a sulfamoylmethyl substituent at the 3-position.		3.58201,2-benzoxazoles;
sulfonamide		anticonvulsant;
antioxidant;
central nervous system drug;
protective agent;
T-type calcium channel blocker
zopiclone
zopiclone: S(+)-enantiomer of racemic zopiclone; azabicyclo(4.3.0)nonane; a nonbenzodiazepine; one of the so-called of Z drugs (zopiclone, eszopiclone, zolpidem, and zaleplon) for which there is some correlation with tumors; was term of zopiclone 2004-2007. zopiclone : A pyrrolo[3,4-b]pyrazine compound having a 4-methylpiperazine-1-carboxyl group at the 5-position, a 5-chloropyridin-2-yl group at the 6-position and an oxo-substituent at the 7-position.		2.0510monochloropyridine;
pyrrolopyrazine		central nervous system depressant;
sedative
guanidine hydrochloride
[no description available]		2.0510one-carbon compound;
organic chloride salt		protein denaturant
hydrocortisone acetate
hydrocortisone acetate: RN given refers to cpd without isomeric designation		2.0510cortisol ester;
tertiary alpha-hydroxy ketone
cortisone acetate
Cortisone Acetate: The acetate ester of cortisone that is used mainly for replacement therapy in adrenocortical insufficiency and in the treatment of many allergic and inflammatory disorders.		3.5920corticosteroid hormone
mitomycin
Mitomycin: An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.. mitomycin : A family of aziridine-containing natural products isolated from Streptomyces caespitosus or Streptomyces lavendulae.		15.937029mitomycinalkylating agent;
antineoplastic agent
prednisolone
Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.. prednisolone : A glucocorticoid that is prednisone in which the oxo group at position 11 has been reduced to the corresponding beta-hydroxy group. It is a drug metabolite of prednisone.		4.14011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antineoplastic agent;
drug metabolite;
environmental contaminant;
immunosuppressive agent;
xenobiotic
estriol
hormonin: estrogen replacement; each tablet contains 600 ug micronized 17beta-estradiol, 270 ug estriol and 1.4 mg estrone. chlorapatite : A phosphate mineral with the formula Ca5(PO4)3Cl.		2.051016alpha-hydroxy steroid;
17beta-hydroxy steroid;
3-hydroxy steroid		estrogen;
human metabolite;
human xenobiotic metabolite;
mouse metabolite
reserpine
Reserpine: An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.. reserpine : An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria.		3.5920alkaloid ester;
methyl ester;
yohimban alkaloid		adrenergic uptake inhibitor;
antihypertensive agent;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
first generation antipsychotic;
plant metabolite;
xenobiotic
cephaloridine
Cephaloridine: A cephalosporin antibiotic.. cefaloridine : A cephalosporin compound having pyridinium-1-ylmethyl and 2-thienylacetamido side-groups. A first-generation semisynthetic derivative of cephalosporin C.		2.0510beta-lactam antibiotic allergen;
cephalosporin;
semisynthetic derivative		antibacterial drug
phentolamine
Phentolamine: A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.. phentolamine : A substituted aniline that is 3-aminophenol in which the hydrogens of the amino group are replaced by 4-methylphenyl and 4,5-dihydro-1H-imidazol-2-ylmethyl groups respectively. An alpha-adrenergic antagonist, it is used for the treatment of hypertension.		3.5920imidazoles;
phenols;
substituted aniline;
tertiary amino compound		alpha-adrenergic antagonist;
vasodilator agent
sorbitol
D-glucitol : The D-enantiomer of glucitol (also known as D-sorbitol).		3.5920glucitolcathartic;
Escherichia coli metabolite;
food humectant;
human metabolite;
laxative;
metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite;
sweetening agent
thymidine
[no description available]		7.4820pyrimidine 2'-deoxyribonucleosideEscherichia coli metabolite;
human metabolite;
metabolite;
mouse metabolite
floxuridine
Floxuridine: An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by slow, continuous, intra-arterial infusion, it is converted to floxuridine monophosphate. It has been used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.. floxuridine : A pyrimidine 2'-deoxyribonucleoside compound having 5-fluorouracil as the nucleobase; used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.		13.596310nucleoside analogue;
organofluorine compound;
pyrimidine 2'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
antiviral drug;
radiosensitizing agent
piperonyl butoxide
[no description available]		2.0510benzodioxolespesticide synergist
bromouracil
Bromouracil: 5-Bromo-2,4(1H,3H)-pyrimidinedione. Brominated derivative of uracil that acts as an antimetabolite, substituting for thymine in DNA. It is used mainly as an experimental mutagen, but its deoxyriboside (BROMODEOXYURIDINE) is used to treat neoplasms.. 5-bromouracil : A pyrimidine having keto groups at the 2- and 4-positions and a bromo group at the 5-position. Used mainly as an experimental mutagen.		2.0510nucleobase analogue;
pyrimidines		mutagen
3,3',5-triiodothyroacetic acid
tiratricol : A monocarboxylic acid that is (4-hydroxy-3,5-diiodophenyl)acetic acid in which the phenolic hydroxy group has been replaced by a 4-hydroxy-3-iodophenoxy group. It is a thyroid hormone analogue that has been used in the treatment of thyroid hormone resistance syndrome.		2.0510
histamine dihydrochloride
Ceplene: Tradename for histamine dihydrochloride.		2.0510
thyroxine
Thyroxine: The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.. thyroxine : An iodothyronine compound having iodo substituents at the 3-, 3'-, 5- and 5'-positions.		3.59202-halophenol;
iodophenol;
L-phenylalanine derivative;
non-proteinogenic L-alpha-amino acid;
thyroxine zwitterion;
thyroxine		antithyroid drug;
human metabolite;
mouse metabolite;
thyroid hormone
dextroamphetamine
Dextroamphetamine: The d-form of AMPHETAMINE. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic.. (S)-amphetamine : A 1-phenylpropan-2-amine that has S configuration.		3.59201-phenylpropan-2-amineadrenergic agent;
adrenergic uptake inhibitor;
dopamine uptake inhibitor;
dopaminergic agent;
neurotoxin;
sympathomimetic agent
carbachol
Carbachol: A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.		2.4720ammonium salt;
carbamate ester		cardiotonic drug;
miotic;
muscarinic agonist;
nicotinic acetylcholine receptor agonist;
non-narcotic analgesic
norethindrone acetate
norethisterone acetate : A 3-oxo Delta(4)-steroid that is norethisterone in which the hydroxy group has been converted to its acetate ester.		2.05103-oxo-Delta(4) steroid;
acetate ester;
terminal acetylenic compound		progestin;
synthetic oral contraceptive
spironolactone
Spironolactone: A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827). spironolactone : A steroid lactone that is 17alpha-pregn-4-ene-21,17-carbolactone substituted by an oxo group at position 3 and an alpha-acetylsulfanyl group at position 7.		3.59203-oxo-Delta(4) steroid;
oxaspiro compound;
steroid lactone;
thioester		aldosterone antagonist;
antihypertensive agent;
diuretic;
environmental contaminant;
xenobiotic
cyclobarbital
cyclobarbital: was heading 1977-94 (see under BARBITURATES 1977-90); CYCLOBARBITONE, HEXEMAL, & TETRAHYDROPHENOBARBITAL were see CYCLOBARBITAL 1977-94; use BARBITURATES to search CYCLOBARBITAL 1977-94; short to intermediate duration barbiturate used as hypnotic and sedative		2.0510barbiturates
allobarbital
allobarbital: was heading 1976-94 (see under BARBITURATES 1976-90); ALLOBARBITONE, DIALLYLBARBITAL, DIALLYLBARBITURIC ACID, & DIALLYLMAL were see ALLOBARBITAL 1976-94; use BARBITURATES to search ALLOBARBITAL 1976-94; a barbiturate derivative with effects of intermediate duration; at lower doses, it is used as a sedative; at higher doses, it displays hypnotic effects		2.0510barbiturates
penicillamine
Penicillamine: 3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease.. penicillamine : An alpha-amino acid having the structure of valine substituted at the beta position with a sulfanyl group.		3.5920non-proteinogenic alpha-amino acid;
penicillamine		antirheumatic drug;
chelator;
copper chelator;
drug allergen
trichlorfon
Trichlorfon: An organochlorophosphate cholinesterase inhibitor that is used as an insecticide for the control of flies and roaches. It is also used in anthelmintic compositions for animals. (From Merck, 11th ed). trichlorfon : A phosphonic ester that is dimethyl phosphonate in which the hydrogen atom attched to the phosphorous is substituted by a 2,2,2-trichloro-1-hydroxyethyl group.		2.0510organic phosphonate;
organochlorine compound;
phosphonic ester		agrochemical;
anthelminthic drug;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
insecticide
cysteine
[no description available]		3.2310cysteine zwitterion;
cysteine;
L-alpha-amino acid;
proteinogenic amino acid;
serine family amino acid		EC 4.3.1.3 (histidine ammonia-lyase) inhibitor;
flour treatment agent;
human metabolite
prednisone
Prednisone: A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.. prednisone : A synthetic glucocorticoid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. Prednisone is a prodrug that is converted by the liver into prednisolone (a beta-hydroxy group instead of the oxo group at position 11), which is the active drug and also a steroid.		9.275011-oxo steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antineoplastic agent;
immunosuppressive agent;
prodrug
estrone
Hydroxyestrones: Estrone derivatives substituted with one or more hydroxyl groups in any position. They are important metabolites of estrone and other estrogens.		3.592017-oxo steroid;
3-hydroxy steroid;
phenolic steroid;
phenols		antineoplastic agent;
bone density conservation agent;
estrogen;
human metabolite;
mouse metabolite
oxandrolone
Oxandrolone: A synthetic hormone with anabolic and androgenic properties.		3.592017beta-hydroxy steroid;
3-oxo steroid;
anabolic androgenic steroid;
oxa-steroid		anabolic agent;
androgen
dehydroepiandrosterone
Dehydroepiandrosterone: A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.. dehydroepiandrosterone : An androstanoid that is androst-5-ene substituted by a beta-hydroxy group at position 3 and an oxo group at position 17. It is a naturally occurring steroid hormone produced by the adrenal glands.		2.051017-oxo steroid;
3beta-hydroxy-Delta(5)-steroid;
androstanoid		androgen;
human metabolite;
mouse metabolite
nad
[no description available]		2.0510NADgeroprotector
penicillin g
Penicillin G: A penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It has also been used as an experimental convulsant because of its actions on GAMMA-AMINOBUTYRIC ACID mediated synaptic transmission.. benzylpenicillin : A penicillin in which the substituent at position 6 of the penam ring is a phenylacetamido group.		3.5920penicillin allergen;
penicillin		antibacterial drug;
drug allergen;
epitope
pilocarpine
Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.. (+)-pilocarpine : The (+)-enantiomer of pilocarpine.		3.5920pilocarpineantiglaucoma drug
triiodothyronine
Triiodothyronine: A T3 thyroid hormone normally synthesized and secreted by the thyroid gland in much smaller quantities than thyroxine (T4). Most T3 is derived from peripheral monodeiodination of T4 at the 5' position of the outer ring of the iodothyronine nucleus. The hormone finally delivered and used by the tissues is mainly T3.. 3,3',5-triiodo-L-thyronine : An iodothyronine compound having iodo substituents at the 3-, 3'- and 5-positions. Although some is produced in the thyroid, most of the 3,3',5-triiodo-L-thyronine in the body is generated by mono-deiodination of L-thyroxine in the peripheral tissues. Its metabolic activity is about 3 to 5 times that of L-thyroxine. The sodium salt is used in the treatment of hypothyroidism.		3.59202-halophenol;
amino acid zwitterion;
iodophenol;
iodothyronine		human metabolite;
mouse metabolite;
thyroid hormone
(4-(m-chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium chloride
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride: A drug that selectively activates certain subclasses of muscarinic receptors and also activates postganglionic nicotinic receptors. It is commonly used experimentally to distinguish muscarinic receptor subtypes.		2.0510
chloramphenicol
Amphenicol: Chloramphenicol and its derivatives.		3.5920C-nitro compound;
carboxamide;
diol;
organochlorine compound		antibacterial drug;
antimicrobial agent;
Escherichia coli metabolite;
geroprotector;
Mycoplasma genitalium metabolite;
protein synthesis inhibitor
glutamine
Glutamine: A non-essential amino acid present abundantly throughout the body and is involved in many metabolic processes. It is synthesized from GLUTAMIC ACID and AMMONIA. It is the principal carrier of NITROGEN in the body and is an important energy source for many cells.. L-glutamine : An optically active form of glutamine having L-configuration.. glutamine : An alpha-amino acid that consists of butyric acid bearing an amino substituent at position 2 and a carbamoyl substituent at position 4.		6.5851amino acid zwitterion;
glutamine family amino acid;
glutamine;
L-alpha-amino acid;
polar amino acid zwitterion;
proteinogenic amino acid		EC 1.14.13.39 (nitric oxide synthase) inhibitor;
Escherichia coli metabolite;
human metabolite;
metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
Saccharomyces cerevisiae metabolite
cetrimonium bromide
cetyltrimethylammonium bromide : The organic bromide salt that is the bromide salt of cetyltrimethylammonium; one of the components of the topical antiseptic cetrimide.		2.0510organic bromide salt;
quaternary ammonium salt		detergent;
surfactant
vincristine
[no description available]		3.8630acetate ester;
formamides;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
tertiary alcohol;
tertiary amino compound;
vinca alkaloid		antineoplastic agent;
drug;
microtubule-destabilising agent;
plant metabolite;
tubulin modulator
physostigmine
Physostigmine: A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.		3.8630carbamate ester;
indole alkaloid		antidote to curare poisoning;
EC 3.1.1.8 (cholinesterase) inhibitor;
miotic
sucrose
Saccharum: A plant genus of the family POACEAE widely cultivated in the tropics for the sweet cane that is processed into sugar.		2.0510glycosyl glycosidealgal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
osmolyte;
Saccharomyces cerevisiae metabolite;
sweetening agent
ethinyl estradiol
Ethinyl Estradiol: A semisynthetic alkylated ESTRADIOL with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally, and is often used as the estrogenic component in ORAL CONTRACEPTIVES.. 17alpha-ethynylestradiol : A 3-hydroxy steroid that is estradiol substituted by a ethynyl group at position 17. It is a xenoestrogen synthesized from estradiol and has been shown to exhibit high estrogenic potency on oral administration.		2.051017-hydroxy steroid;
3-hydroxy steroid;
terminal acetylenic compound		xenoestrogen
testosterone propionate
Testosterone Propionate: An ester of TESTOSTERONE with a propionate substitution at the 17-beta position.. androgen : A sex hormone that stimulates or controls the development and maintenance of masculine characteristics in vertebrates by binding to androgen receptors.		2.0510steroid ester
apomorphine
Apomorphine: A derivative of morphine that is a dopamine D2 agonist. It is a powerful emetic and has been used for that effect in acute poisoning. It has also been used in the diagnosis and treatment of parkinsonism, but its adverse effects limit its use.		3.5920aporphine alkaloidalpha-adrenergic drug;
antidyskinesia agent;
antiparkinson drug;
dopamine agonist;
emetic;
serotonergic drug
aminopyrine
Aminopyrine: A pyrazolone with analgesic, anti-inflammatory, and antipyretic properties but has risk of AGRANULOCYTOSIS. A breath test with 13C-labeled aminopyrine has been used as a non-invasive measure of CYTOCHROME P-450 metabolic activity in LIVER FUNCTION TESTS.. aminophenazone : A pyrazolone that is 1,2-dihydro-3H-pyrazol-3-one substituted by a dimethylamino group at position 4, methyl groups at positions 1 and 5 and a phenyl group at position 2. It exhibits analgesic, anti-inflammatory, and antipyretic properties.		2.0510pyrazolone;
tertiary amino compound		antipyretic;
environmental contaminant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
methyltestosterone
Methyltestosterone: A synthetic hormone used for androgen replacement therapy and as an hormonal antineoplastic agent (ANTINEOPLASTIC AGENTS, HORMONAL).. methyltestosterone : A 17beta-hydroxy steroid that is testosterone bearing a methyl group at the 17alpha position.		3.592017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
enone		anabolic agent;
androgen;
antineoplastic agent
tetrabenazine
9,10-dimethoxy-3-isobutyl-1,3,4,6,7,11b-hexahydro-2H-pyrido[2,1-a]isoquinolin-2-one : A benzoquinolizine that is 1,2,3,4,4a,9,10,10a-octahydrophenanthrene in which the carbon at position 10a is replaced by a nitrogen and which is substituted by an isobutyl group at position 2, an oxo group at position 3, and methoxy groups at positions 6 and 7.		3.5920benzoquinolizine;
cyclic ketone;
tertiary amino compound
cephalothin
Cephalothin: A cephalosporin antibiotic.. cefalotin : A semisynthetic, first-generation cephalosporin antibiotic with acetoxymethyl and (2-thienylacetyl)nitrilo moieties at positions 3 and 7, respectively, of the core structure. Administered parenterally during surgery and to treat a wide spectrum of blood infections.		2.0510azabicycloalkene;
beta-lactam antibiotic allergen;
carboxylic acid;
cephalosporin;
semisynthetic derivative;
thiophenes		antibacterial drug;
antimicrobial agent
uridine
[no description available]		6.42120uridinesdrug metabolite;
fundamental metabolite;
human metabolite
kanamycin a
Kanamycin: Antibiotic complex produced by Streptomyces kanamyceticus from Japanese soil. Comprises 3 components: kanamycin A, the major component, and kanamycins B and C, the minor components.. kanamycin : Kanamycin is a naturally occurring antibiotic complex from Streptomyces kanamyceticus that consists of several components: kanamycin A, the major component (also usually designated as kanamycin), and kanamycins B, C, D and X the minor components.		3.5920kanamycinsbacterial metabolite
bromodeoxyuridine
Bromodeoxyuridine: A nucleoside that substitutes for thymidine in DNA and thus acts as an antimetabolite. It causes breaks in chromosomes and has been proposed as an antiviral and antineoplastic agent. It has been given orphan drug status for use in the treatment of primary brain tumors.		3.8630pyrimidine 2'-deoxyribonucleosideantimetabolite;
antineoplastic agent
carbostyril
Quinolones: A group of derivatives of naphthyridine carboxylic acid, quinoline carboxylic acid, or NALIDIXIC ACID.. quinolin-2(1H)-one : A quinolone that is 1,2-dihydroquinoline substituted by an oxo group at position 2.		7.0553monohydroxyquinoline;
quinolone		bacterial xenobiotic metabolite
phenylephrine
Phenylephrine: An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.. phenylephrine : A member of the class of the class of phenylethanolamines that is (1R)-2-(methylamino)-1-phenylethan-1-ol carrying an additional hydroxy substituent at position 3 on the phenyl ring.		2.0510phenols;
phenylethanolamines;
secondary amino compound		alpha-adrenergic agonist;
cardiotonic drug;
mydriatic agent;
nasal decongestant;
protective agent;
sympathomimetic agent;
vasoconstrictor agent
levodopa
Levodopa: The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.. L-dopa : An optically active form of dopa having L-configuration. Used to treat the stiffness, tremors, spasms, and poor muscle control of Parkinson's disease		2.0510amino acid zwitterion;
dopa;
L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid		allelochemical;
antidyskinesia agent;
antiparkinson drug;
dopaminergic agent;
hapten;
human metabolite;
mouse metabolite;
neurotoxin;
plant growth retardant;
plant metabolite;
prodrug
edetic acid
Edetic Acid: A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.		3.2310ethylenediamine derivative;
polyamino carboxylic acid;
tetracarboxylic acid		anticoagulant;
antidote;
chelator;
copper chelator;
geroprotector
cysteamine
Cysteamine: A mercaptoethylamine compound that is endogenously derived from the COENZYME A degradative pathway. The fact that cysteamine is readily transported into LYSOSOMES where it reacts with CYSTINE to form cysteine-cysteamine disulfide and CYSTEINE has led to its use in CYSTINE DEPLETING AGENTS for the treatment of CYSTINOSIS.. cysteamine : An amine that consists of an ethane skeleton substituted with a thiol group at C-1 and an amino group at C-2.		3.2310amine;
thiol		geroprotector;
human metabolite;
mouse metabolite;
radiation protective agent
acetylcholine chloride
acetylcholine chloride : The chloride salt of acetylcholine, and a parasympatomimetic drug.		3.2310quaternary ammonium salt
mepazine
mepazine: major descriptor (66-85); on-line search PHENOTHIAZINES (66-85); Index Medicus search MEPAZINE (66-85); RN given refers to parent cpd. pacatal : A phenothiazine derivative in which 10H-phenothiazine has an N-methylpiperidin-4-ylmethyl substituent at the N-10 position.		3.2310phenothiazines
niridazole
Niridazole: An antischistosomal agent that has become obsolete.		2.05101,3-thiazoles;
C-nitro compound
cloxacillin
Cloxacillin: A semi-synthetic antibiotic that is a chlorinated derivative of OXACILLIN.. cloxacillin : A semisynthetic penicillin antibiotic carrying a 3-(2-chlorophenyl)-5-methylisoxazole-4-carboxamido group at position 6.		3.2310penicillin allergen;
penicillin;
semisynthetic derivative		antibacterial agent;
antibacterial drug
calcium acetate
calcium acetate: a principal compound used as phosphate binders in patients with chronic renal failure; used like sevelamer. calcium acetate : The calcium salt of acetic acid. It is used, commonly as a hydrate, to treat hyperphosphataemia (excess phosphate in the blood) in patients with kidney disease: the calcium ion combines with dietary phosphate to form (insoluble) calcium phosphate, which is excreted in the faeces.		3.2310calcium saltchelator
carbaryl
Carbaryl: A carbamate insecticide and parasiticide. It is a potent anticholinesterase agent belonging to the carbamate group of reversible cholinesterase inhibitors. It has a particularly low toxicity from dermal absorption and is used for control of head lice in some countries.. carbaryl : A carbamate ester obtained by the formal condensation of 1-naphthol with methylcarbamic acid.		2.0510carbamate ester;
naphthalenes		acaricide;
agrochemical;
carbamate insecticide;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
plant growth retardant
uridine triphosphate
Uridine Triphosphate: Uridine 5'-(tetrahydrogen triphosphate). A uracil nucleotide containing three phosphate groups esterified to the sugar moiety.		4.8532pyrimidine ribonucleoside 5'-triphosphate;
uridine 5'-phosphate		Escherichia coli metabolite;
mouse metabolite
lactose
Lactose: A disaccharide of GLUCOSE and GALACTOSE in human and cow milk. It is used in pharmacy for tablets, in medicine as a nutrient, and in industry.. lactose : A glycosylglucose disaccharide, found most notably in milk, that consists of D-galactose and D-glucose fragments bonded through a beta-1->4 glycosidic linkage. The glucose fragment can be in either the alpha- or beta-pyranose form, whereas the galactose fragment can only have the beta-pyranose form.. beta-lactose : The beta-anomer of lactose.		2.4520lactose
methionine
Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.. methionine : A sulfur-containing amino acid that is butyric acid bearing an amino substituent at position 2 and a methylthio substituent at position 4.		3.5920aspartate family amino acid;
L-alpha-amino acid;
methionine zwitterion;
methionine;
proteinogenic amino acid		antidote to paracetamol poisoning;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical
Mebutamate
[no description available]		2.0510organic molecular entity
colchicine
(S)-colchicine : A colchicine that has (S)-configuration. It is a secondary metabolite, has anti-inflammatory properties and is used to treat gout, crystal-induced joint inflammation, familial Mediterranean fever, and many other conditions.		3.5920alkaloid;
colchicine		anti-inflammatory agent;
gout suppressant;
mutagen
mebanazine
mebanazine: RN given refers to parent cpd without isomeric designation; structure		3.2310benzenes
oxacillin
Oxacillin: An antibiotic similar to FLUCLOXACILLIN used in resistant staphylococci infections.. oxacillin : A penicillin antibiotic carrying a 5-methyl-3-phenylisoxazole-4-carboxamide group at position 6beta.		3.2310penicillinantibacterial agent;
antibacterial drug
norethindrone
Norethindrone: A synthetic progestational hormone with actions similar to those of PROGESTERONE but functioning as a more potent inhibitor of ovulation. It has weak estrogenic and androgenic properties. The hormone has been used in treating amenorrhea, functional uterine bleeding, endometriosis, and for CONTRACEPTION.. norethisterone : A 17beta-hydroxy steroid that is testosterone in which the hydrogen at position 17 is replaced by an ethynyl group and in which the methyl group attached to position 10 is replaced by hydrogen.		2.051017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
terminal acetylenic compound;
tertiary alcohol		progestin;
synthetic oral contraceptive
norethynodrel
Norethynodrel: A synthetic progestational hormone with actions and uses similar to those of PROGESTERONE. It has been used in the treatment of functional uterine bleeding and ENDOMETRIOSIS. As a contraceptive (CONTRACEPTIVE AGENTS), it has usually been administered in combination with MESTRANOL.		2.0510oxo steroid
cycloserine
Cycloserine: Antibiotic substance produced by Streptomyces garyphalus.. D-cycloserine : A 4-amino-1,2-oxazolidin-3-one that has R configuration. It is an antibiotic produced by Streptomyces garyphalus or S. orchidaceus and is used as part of a multi-drug regimen for the treatment of tuberculosis when resistance to, or toxicity from, primary drugs has developed. An analogue of D-alanine, it interferes with bacterial cell wall synthesis in the cytoplasm by competitive inhibition of L-alanine racemase (which forms D-alanine from L-alanine) and D-alanine--D-alanine ligase (which incorporates D-alanine into the pentapeptide required for peptidoglycan formation and bacterial cell wall synthesis).		3.23104-amino-1,2-oxazolidin-3-one;
organonitrogen heterocyclic antibiotic;
organooxygen heterocyclic antibiotic;
zwitterion		antiinfective agent;
antimetabolite;
antitubercular agent;
metabolite;
NMDA receptor agonist
benziodarone
benziodarone: minor descriptor (75-89); on-line & INDEX MEDICUS search BENZOFURANS (68-89) & IODOBENZOATES (74)		3.5920aromatic ketone
ampicillin
Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic.. ampicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-phenylacetamido group.		3.5920beta-lactam antibiotic;
penicillin allergen;
penicillin		antibacterial drug
mannitol
[no description available]		3.5920mannitolallergen;
antiglaucoma drug;
compatible osmolytes;
Escherichia coli metabolite;
food anticaking agent;
food bulking agent;
food humectant;
food stabiliser;
food thickening agent;
hapten;
metabolite;
osmotic diuretic;
sweetening agent
cytarabine
[no description available]		7.5592beta-D-arabinoside;
monosaccharide derivative;
pyrimidine nucleoside		antimetabolite;
antineoplastic agent;
antiviral agent;
immunosuppressive agent
trifluridine
Trifluridine: An antiviral derivative of THYMIDINE used mainly in the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis due to HERPES SIMPLEX virus. (From Martindale, The Extra Pharmacopoeia, 30th ed, p557). trifluridine : A pyrimidine 2'-deoxyribonucleoside compound having 5-trifluoromethyluracil as the nucleobase. An antiviral drug used mainly in the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis.		12.8873nucleoside analogue;
organofluorine compound;
pyrimidine 2'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
antiviral drug;
EC 2.1.1.45 (thymidylate synthase) inhibitor
medroxyprogesterone acetate
[no description available]		7.743020-oxo steroid;
3-oxo-Delta(4) steroid;
acetate ester;
corticosteroid;
steroid ester		adjuvant;
androgen;
antineoplastic agent;
antioxidant;
female contraceptive drug;
inhibitor;
progestin;
synthetic oral contraceptive
mestranol
[no description available]		2.051017beta-hydroxy steroid;
aromatic ether;
terminal acetylenic compound		prodrug;
xenoestrogen
methaqualone
Methaqualone: A quinazoline derivative with hypnotic and sedative properties. It has been withdrawn from the market in many countries because of problems with abuse. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604). methaqualone : A member of the class of quinazolines that is quinazolin-4-one substituted at positions 2 and 3 by methyl and o-tolyl groups respectively. A depressant that increases the activity of the GABA receptors in the brain and nervous system, it is used as a sedative and hypnotic medication. It became popular as a recreational drug and club drug in the late 1960s and 1970s.		2.0510quinazolinesGABA agonist;
sedative
trypan blue
VisionBlue: A trypan blue ophthalmic solution.		2.0510
cordycepin
[no description available]		2.05103'-deoxyribonucleoside;
adenosines		antimetabolite;
nucleoside antibiotic
tryptophan
Tryptophan: An essential amino acid that is necessary for normal growth in infants and for NITROGEN balance in adults. It is a precursor of INDOLE ALKALOIDS in plants. It is a precursor of SEROTONIN (hence its use as an antidepressant and sleep aid). It can be a precursor to NIACIN, albeit inefficiently, in mammals.. tryptophan : An alpha-amino acid that is alanine bearing an indol-3-yl substituent at position 3.		2.0510erythrose 4-phosphate/phosphoenolpyruvate family amino acid;
L-alpha-amino acid zwitterion;
L-alpha-amino acid;
proteinogenic amino acid;
tryptophan zwitterion;
tryptophan		antidepressant;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
arginine
Arginine: An essential amino acid that is physiologically active in the L-form.. arginine : An alpha-amino acid that is glycine in which the alpha-is substituted by a 3-guanidinopropyl group.		4.1240arginine;
glutamine family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		biomarker;
Escherichia coli metabolite;
micronutrient;
mouse metabolite;
nutraceutical
acetonitrile
acetonitrile: RN given refers to unlabeled cpd. acetonitrile : A nitrile that is hydrogen cyanide in which the hydrogen has been replaced by a methyl group.		2.0510aliphatic nitrile;
volatile organic compound		EC 3.5.1.4 (amidase) inhibitor;
NMR chemical shift reference compound;
polar aprotic solvent
trichloroacetic acid
Trichloroacetic Acid: A strong acid used as a protein precipitant in clinical chemistry and also as a caustic for removing warts.. trichloroacetic acid : A monocarboxylic acid that is acetic acid in which all three methyl hydrogens are substituted by chlorine.		2.4620monocarboxylic acid;
organochlorine compound		carcinogenic agent;
metabolite;
mouse metabolite
perflutren
Definity: a fluorocarbon-filled ultrasonic contrast agent; Definity is tradename. octafluoropropane : A fluorocarbon that is propane in which all of the hydrogens have been replaced by fluorines.		3.2310fluoroalkane;
fluorocarbon
triamcinolone acetonide
Triamcinolone Acetonide: An esterified form of TRIAMCINOLONE. It is an anti-inflammatory glucocorticoid used topically in the treatment of various skin disorders. Intralesional, intramuscular, and intra-articular injections are also administered under certain conditions.. triamcinolone acetonide : A synthetic glucocorticoid that is the 16,17-acetonide of triamcinolone. Used to treat various skin infections.		2.051011beta-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
cyclic ketal;
fluorinated steroid;
glucocorticoid;
primary alpha-hydroxy ketone		anti-allergic agent;
anti-inflammatory drug
fluoxymesterone
Fluoxymesterone: An anabolic steroid that has been used in the treatment of male HYPOGONADISM, delayed puberty in males, and in the treatment of breast neoplasms in women.		3.231011beta-hydroxy steroid;
17beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
anabolic androgenic steroid;
fluorinated steroid		anabolic agent;
antineoplastic agent
allylpropymal
allylpropymal: RN given refers to parent cpd. aprobarbital : A member of the class of barbiturates that is pyrimidine-2,4,6(1H,3H,5H)-trione substituted by an isopropyl and a prop-1-en-3-yl group at position 5.		2.0510barbiturates
butobarbital
butobarbital: Butobarbital should be distinguished from Butabarbital (a synonym for Secbutabarbital)		2.0510barbiturates
methsuximide
methsuximide: anticonvulsant effective in petit mal & psychomotor epilepsy; has a number of unpleasant & toxic side effects; minor descriptor (75-86); on-line & INDEX MEDICUS search SUCCINIMIDES (75-86); RN given refers to parent cpd without isomeric designation		3.2310organic molecular entity
tromethamine
Tromethamine: An organic amine proton acceptor. It is used in the synthesis of surface-active agents and pharmaceuticals; as an emulsifying agent for cosmetic creams and lotions, mineral oil and paraffin wax emulsions, as a biological buffer, and used as an alkalizer. (From Merck, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p1424)		3.2310primary amino compound;
triol		buffer
trichloroethylene
Trichloroethylene: A highly volatile inhalation anesthetic used mainly in short surgical procedures where light anesthesia with good analgesia is required. It is also used as an industrial solvent. Prolonged exposure to high concentrations of the vapor can lead to cardiotoxicity and neurological impairment.. triol : A chemical compound containing three hydroxy groups.		2.0510chloroethenesinhalation anaesthetic;
mouse metabolite
acrylamide
[no description available]		7.610acrylamides;
N-acylammonia;
primary carboxamide		alkylating agent;
carcinogenic agent;
Maillard reaction product;
mutagen;
neurotoxin
acrylic acid
acrylic acid: RN given refers to parent cpd. acrylic acid : A alpha,beta-unsaturated monocarboxylic acid that is ethene substituted by a carboxy group.		2.0810alpha,beta-unsaturated monocarboxylic acidmetabolite
dichloroacetic acid
[no description available]		2.0810monocarboxylic acid;
organochlorine compound		astringent;
marine metabolite
dehydrocholic acid
Dehydrocholic Acid: A semisynthetic bile acid made from cholic acid. It is used as a cholagogue, hydrocholeretic, diuretic, and as a diagnostic aid.. 3,7,12-trioxo-5beta-cholanic acid : An oxo-5beta-cholanic acid in which three oxo substituents are located at positions 3, 7 and 12 on the cholanic acid skeleton.		2.051012-oxo steroid;
3-oxo-5beta-steroid;
7-oxo steroid;
oxo-5beta-cholanic acid		gastrointestinal drug
methylprednisolone
Methylprednisolone: A PREDNISOLONE derivative with similar anti-inflammatory action.. 6alpha-methylprednisolone : The 6alpha-stereoisomer of 6-methylprednisolone.		5.22316-methylprednisolone;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antiemetic;
environmental contaminant;
neuroprotective agent;
xenobiotic
lawsone
lawsone: a molluscacide from leaves of Lawsonia inermis L. topical sunscreening agent; structure; powdered leaves of Lawsonia inermis(Lythraceae) used as brown hair dye. lawsone : 1,4-Naphthoquinone carrying a hydroxy function at C-2. It is obtained from the leaves of Lawsonia inermis.		5.131
brompheniramine
Brompheniramine: Histamine H1 antagonist used in treatment of allergies, rhinitis, and urticaria.. brompheniramine : Pheniramine in which the hydrogen at position 4 of the phenyl substituent is substituted by bromine. A histamine H1 receptor antagonist, brompheniramine is used (commonly as its maleate salt) for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.		3.2310organobromine compound;
pyridines		anti-allergic agent;
H1-receptor antagonist
penicillin v
Penicillin V: A broad-spectrum penicillin antibiotic used orally in the treatment of mild to moderate infections by susceptible gram-positive organisms.. phenoxymethylpenicillin : A penicillin compound having a 6beta-(phenoxyacetyl)amino side-chain.		3.2310penicillin allergen;
penicillin
isosorbide dinitrate
Isosorbide Dinitrate: A vasodilator used in the treatment of ANGINA PECTORIS. Its actions are similar to NITROGLYCERIN but with a slower onset of action.		5.4741glucitol derivative;
nitrate ester		nitric oxide donor;
vasodilator agent
n-vinyl-2-pyrrolidinone
N-vinyl-2-pyrrolidinone: monomer of POVIDONE; structure given in first source		2.110pyrrolidin-2-ones
salicylaldehyde
o-hydroxybenzaldehyde: structure in first source		2.0510hydroxybenzaldehydenematicide;
plant metabolite
pseudoephedrine
Pseudoephedrine: A phenethylamine that is an isomer of EPHEDRINE which has less central nervous system effects and usage is mainly for respiratory tract decongestion.. pseudoephedrine : A member of the class of the class of phenylethanolamines that is (1S)-2-(methylamino)-1-phenylethan-1-ol in which the pro-S hydrogen at position 2 is replaced by a methyl group.		3.2310phenylethanolamines;
secondary alcohol;
secondary amino compound		anti-asthmatic drug;
bronchodilator agent;
central nervous system drug;
nasal decongestant;
plant metabolite;
sympathomimetic agent;
vasoconstrictor agent;
xenobiotic
diethylpropion
Diethylpropion: A appetite depressant considered to produce less central nervous system disturbance than most drugs in this therapeutic category. It is also considered to be among the safest for patients with hypertension. (From AMA Drug Evaluations Annual, 1994, p2290). diethylpropion : An aromatic ketone that is propiophenone in which one of the hydrogens alpha- to the carbonyl is substituted by a diethylamino group. A central stimulant and indirect-acting sympathomimetic, it is an appetite depressant and is used as the hydrochloride as an anoretic in the short term management of obesity.		3.2310aromatic ketone;
tertiary amine		appetite depressant
synephrine
[no description available]		2.0510ethanolamines;
phenethylamine alkaloid;
phenols		alpha-adrenergic agonist;
plant metabolite
benzoyl peroxide
Benzoyl Peroxide: A peroxide derivative that has been used topically for BURNS and as a dermatologic agent in the treatment of ACNE and POISON IVY DERMATITIS. It is used also as a bleach in the food industry.		2.0510carbonyl compound
2,4-dihydroxybenzaldehyde
2,4-dihydroxybenzaldehyde : A dihydroxybenzaldehyde that is resorcinol which has been substituted by a formyl group para to one of the hydroxy groups.		2.0510dihydroxybenzaldehyde
quinuclidines
Quinuclidines: A class of organic compounds which contain two rings that share a pair of bridgehead carbon atoms and contains an amine group.		3.4611quinuclidines;
saturated organic heterobicyclic parent
triclocarban
triclocarban: bacteriostat; antiseptic in soaps & other cleansing solns; germicide; structure. triclocarban : A member of the class of phenylureas that is urea substituted by a 4-chlorophenyl group and a 3,4-dichlorophenyl group at positions 1 and 3 respectively.		2.0510dichlorobenzene;
monochlorobenzenes;
phenylureas		antimicrobial agent;
antiseptic drug;
disinfectant;
environmental contaminant;
xenobiotic
benzonatate
benzonatate: structure in Merck Index, 9th ed, #1107. benzonatate : The ester obtained by formal condensation of 4-butylaminobenzoic acid with nonaethylene glycol monomethyl ether. Structurally related to procaine and benzocaine, it has an anaesthetic effect on the stretch sensors in the lungs, and is used as a non-narcotic cough suppressant.		3.2310benzoate ester;
secondary amino compound;
substituted aniline		anaesthetic;
antitussive
pyrroles
1H-pyrrole : A tautomer of pyrrole that has the double bonds at positions 2 and 4.. pyrrole : A five-membered monocyclic heteroarene comprising one NH and four CH units which forms the parent compound of the pyrrole group of compounds. Its five-membered ring structure has three tautomers. A 'closed class'.. azole : Any monocyclic heteroarene consisting of a five-membered ring containing nitrogen. Azoles can also contain one or more other non-carbon atoms, such as nitrogen, sulfur or oxygen.		12.452210pyrrole;
secondary amine
tetrahydrofuran
oxolane : A cyclic ether that is butane in which one hydrogen from each methyl group is substituted by an oxygen.		2.0510cyclic ether;
oxolanes;
saturated organic heteromonocyclic parent;
volatile organic compound		polar aprotic solvent
furan
furan : A monocyclic heteroarene with a structure consisting of a 5-membered ring containing four carbons and one oxygen, with formula C4H4O. It is a toxic, flammable, low-boiling (31degreeC) colourless liquid.		2.0510furans;
mancude organic heteromonocyclic parent;
monocyclic heteroarene		carcinogenic agent;
hepatotoxic agent;
Maillard reaction product
thiophenes
Thiophenes: A monocyclic heteroarene furan in which the oxygen atom is replaced by a sulfur.. thiophenes : Compounds containing at least one thiophene ring.		8.97260mancude organic heteromonocyclic parent;
monocyclic heteroarene;
thiophenes;
volatile organic compound		non-polar solvent
heptanal
heptanal : An n-alkanal resulting from the oxidation of the alcoholic hydroxy group of heptan-1-ol to the corresponding aldehyde. An endogenous aldehyde coming from membrane lipid oxidation, it is found in the blood of lung cancer patients and has been regarded as a potential biomarker of lung cancer.		2.0510medium-chain fatty aldehyde;
n-alkanal;
saturated fatty aldehyde		biomarker
carbitol
carbitol: used as lubricating oil & in braking fluid, structure. diethylene glycol monoethyl ether : A primary alcohol that is ethanol substituted by a 2-ethoxyethoxy group at position 2.		2.2110diether;
glycol ether;
hydroxypolyether;
primary alcohol		protic solvent
ergotamine
Ergotamine: A vasoconstrictor found in ergot of Central Europe. It is a serotonin agonist that has been used as an oxytocic agent and in the treatment of MIGRAINE DISORDERS.. ergotamine : A peptide ergot alkaloid that is dihydroergotamine in which a double bond replaces the single bond between positions 9 and 10.		2.0510peptide ergot alkaloidalpha-adrenergic agonist;
mycotoxin;
non-narcotic analgesic;
oxytocic;
serotonergic agonist;
vasoconstrictor agent
methylergonovine
Methylergonovine: A homolog of ERGONOVINE containing one more CH2 group. (Merck Index, 11th ed)		3.2310ergoline alkaloid
neostigmine bromide
neostigmine bromide : The bromide salt of neostigmine.		2.4620bromide salt
phenformin
Phenformin: A biguanide hypoglycemic agent with actions and uses similar to those of METFORMIN. Although it is generally considered to be associated with an unacceptably high incidence of lactic acidosis, often fatal, it is still available in some countries. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). phenformin : A member of the class of biguanides that is biguanide in which one of the terminal nitrogen atoms is substituted by a 2-phenylethyl group. It was used as an anti-diabetic drug but was later withdrawn from the market due to potential risk of lactic acidosis.		2.0510biguanidesantineoplastic agent;
geroprotector;
hypoglycemic agent
mephobarbital
Mephobarbital: A barbiturate that is metabolized to PHENOBARBITAL. It has been used for similar purposes, especially in EPILEPSY, but there is no evidence mephobarbital offers any advantage over PHENOBARBITAL.. mephobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at N-1 by a methyl group and at C-5 by ethyl and phenyl groups.		2.0510barbituratesanticonvulsant
diethylhexyl phthalate
Diethylhexyl Phthalate: An ester of phthalic acid. It appears as a light-colored, odorless liquid and is used as a plasticizer for many resins and elastomers.. bis(2-ethylhexyl) phthalate : A phthalate ester that is the bis(2-ethylhexyl) ester of benzene-1,2-dicarboxylic acid.		210diester;
phthalate ester		androstane receptor agonist;
apoptosis inhibitor;
plasticiser
hexachlorobenzene
Hexachlorobenzene: An agricultural fungicide and seed treatment agent.. hexachlorobenzene : A member of the class of chlorobenzenes that is benzene in which all of the hydrogens are replaced by chlorines. An agricultural fungicide introduced in the mid-1940s and formerly used as a seed treatment, its use has been banned since 1984 under the Stockholm Convention on Persistent Organic Pollutants.		2.0510aromatic fungicide;
chlorobenzenes		antifungal agrochemical;
carcinogenic agent;
persistent organic pollutant
trinitrotoluene
Trinitrotoluene: A 2,4,6-trinitrotoluene, which is an explosive chemical that can cause skin irritation and other toxic consequences.. 2,4,6-trinitrotoluene : A trinitrotoluene having the nitro groups at positions 2, 4 and 6.		2.0510trinitrotolueneexplosive
framycetin
Framycetin: A component of NEOMYCIN that is produced by Streptomyces fradiae. On hydrolysis it yields neamine and neobiosamine B. (From Merck Index, 11th ed). framycetin : A tetracyclic antibacterial agent derived from neomycin, being a glycoside ester of neamine and neobiosamine B.		2.0510aminoglycosideallergen;
antibacterial drug;
Escherichia coli metabolite
pyrazolanthrone
pyrazolanthrone: JNK (c-Jun N-terminal kinase) inhibitor; structure in first source. anthra[1,9-cd]pyrazol-6(2H)-one : A member of the class of anthrapyrazoles that is anthra[1,9-cd]pyrazole substituted at position 6 by an oxo group. An inhibitor of c-Jun N-terminal kinase.		2.0510anthrapyrazole;
aromatic ketone;
cyclic ketone		antineoplastic agent;
c-Jun N-terminal kinase inhibitor;
geroprotector
meglumine
Meglumine: 1-Deoxy-1-(methylamino)-D-glucitol. A derivative of sorbitol in which the hydroxyl group in position 1 is replaced by a methylamino group. Often used in conjunction with iodinated organic compounds as contrast medium.. N-methylglucamine : A hexosamine that is D-glucitol in which the hydroxy group at position 1 is substituted by the nitrogen of a methylamino group. A crystalline base, it is used in preparing salts of certain acids for use as diagnostic radiopaque media, while its antimonate is used as an antiprotozoal in the treatment of leishmaniasis.		2.0510hexosamine;
secondary amino compound
cinchophen
cinchophen: was heading 1963-94; ACIPHENOCHINOLIUM was see CHINOPHEN 1978-94; use QUINOLINES to search CINCHOPHEN 1966-94		3.5920quinolines
yohimbine
Yohimbine: A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.. yohimbine : An indole alkaloid with alpha2-adrenoceptor antagonist activity. It is produced by Corynanthe johimbe and Rauwolfia serpentina.		2.0510methyl 17-hydroxy-20xi-yohimban-16-carboxylatealpha-adrenergic antagonist;
dopamine receptor D2 antagonist;
serotonergic antagonist
nafcillin
Nafcillin: A semi-synthetic antibiotic related to penicillin.. nafcillin : A penicillin in which the substituent at position 6 of the penam ring is a (2-ethoxy-1-naphthoyl)amino group.		3.2310penicillin allergen;
penicillin		antibacterial drug
mequinol
mequinol: depigmenting agent; RN given refers to parent cpd		2.0510methoxybenzenes;
phenols		metabolite
methohexital
Methohexital: An intravenous anesthetic with a short duration of action that may be used for induction of anesthesia.. methohexital : A barbiturate, the structure of which is that of barbituric acid substituted at N-1 by a methyl group and at C-5 by allyl and 1-methylpent-2-ynyl groups.		3.2310acetylenic compound;
barbiturates		drug allergen;
intravenous anaesthetic
quinestrol
Quinestrol: The 3-cyclopentyl ether of ETHINYL ESTRADIOL. After gastrointestinal absorption, it is stored in ADIPOSE TISSUE, slowly released, and metabolized principally to the parent compound. It has been used in ESTROGEN REPLACEMENT THERAPY. (From AMA Drug Evaluations Annual, 1992, p1011)		2.051017-hydroxy steroid;
terminal acetylenic compound		xenoestrogen
dydrogesterone
[no description available]		2.051020-oxo steroid;
3-oxo-Delta(4) steroid		progestin
quinazolines
Quinazolines: A group of aromatic heterocyclic compounds that contain a bicyclic structure with two fused six-membered aromatic rings, a benzene ring and a pyrimidine ring.. quinazoline : A mancude organic heterobicyclic parent that is naphthalene in which the carbon atoms at positions 1 and 3 have been replaced by nitrogen atoms.. quinazolines : Any organic heterobicyclic compound based on a quinazoline skeleton and its substituted derivatives.		21.8527199azaarene;
mancude organic heterobicyclic parent;
ortho-fused heteroarene;
quinazolines
indazoles
Indazoles: A group of heterocyclic aromatic organic compounds consisting of the fusion of BENZENE and PYRAZOLES.		10.41106indazole
isoxazoles
Isoxazoles: Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.. isoxazole : A monocyclic heteroarene with a structure consisting of a 5-membered ring containing three carbon atoms and an oxygen and nitrogen atom adjacent to each other. It is the parent of the class of isoxazoles.. isoxazoles : Oxazoles in which the N and O atoms are adjacent.		4.131isoxazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
oxazoles
Oxazoles: Five-membered heterocyclic ring structures containing an oxygen in the 1-position and a nitrogen in the 3-position, in distinction from ISOXAZOLES where they are at the 1,2 positions.. 1,3-oxazole : A five-membered monocyclic heteroarene that is an analogue of cyclopentadiene with O in place of CH2 at position 1 and N in place of CH at position 3.. oxazole : An azole based on a five-membered heterocyclic aromatic skeleton containing one N and one O atom.		9.51941,3-oxazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
thiazoles
[no description available]		5.62321,3-thiazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
pyrimidine
pyrimidine : The parent compound of the pyrimidines; a diazine having the two nitrogens at the 1- and 3-positions.		12.4472diazine;
pyrimidines		Daphnia magna metabolite
pyrazines
Pyrazines: A heterocyclic aromatic organic compound with the chemical formula C4H4N2.. pyrazine : A diazine that is benzene in which the carbon atoms at positions 1 and 4 have been replaced by nitrogen atoms.		6.6952diazine;
pyrazines		Daphnia magna metabolite
calcium gluconate
[no description available]		3.4411calcium saltnutraceutical
ephedrine
Ephedrine: A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.. (-)-ephedrine : A phenethylamine alkaloid that is 2-phenylethanamine substituted by a methyl group at the amino nitrogen and a methyl and a hydroxy group at position 2 and 1 respectively.		3.5920phenethylamine alkaloid;
phenylethanolamines		bacterial metabolite;
environmental contaminant;
nasal decongestant;
plant metabolite;
sympathomimetic agent;
vasoconstrictor agent;
xenobiotic
chlormadinone acetate
Chlormadinone Acetate: An orally active synthetic progestational hormone used often in combinations as an oral contraceptive (CONTRACEPTIVES, ORAL).		2.0510corticosteroid hormone
2,3-dimercaptosuccinic acid
[no description available]		2.0510
evans blue
Evans Blue: An azo dye used in blood volume and cardiac output measurement by the dye dilution method. It is very soluble, strongly bound to plasma albumin, and disappears very slowly.. Evans blue : An organic sodium salt that is the tetrasodium salt of 6,6'-{(3,3'-dimethyl[1,1'-biphenyl]-4,4'-diyl)bis[diazene-2,1-diyl]}bis(4-amino-5-hydroxynaphthalene-1,3-disulfonate). It is sometimes used as a counterstain, especially in fluorescent methods to suppress background autofluorescence.		2.0510organic sodium saltfluorochrome;
histological dye;
sodium channel blocker;
teratogenic agent
testosterone enanthate
[no description available]		2.0510heptanoate ester;
sterol ester		androgen
aminophylline
Aminophylline: A drug combination that contains THEOPHYLLINE and ethylenediamine. It is more soluble in water than theophylline but has similar pharmacologic actions. It's most common use is in bronchial asthma, but it has been investigated for several other applications.. aminophylline : A mixture comprising of theophylline and ethylenediamine in a 2:1 ratio.		3.5920mixturebronchodilator agent;
cardiotonic drug
azacitidine
Azacitidine: A pyrimidine analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent.. 5-azacytidine : An N-glycosyl-1,3,5-triazine that is 4-amino-1,3,5-triazin-2(1H)-one substituted by a beta-D-ribofuranosyl residue via an N-glycosidic linkage. An antineoplastic agent, it is used in the treatment of myeloid leukaemia.		10.2731N-glycosyl-1,3,5-triazine;
nucleoside analogue		antineoplastic agent
phenyramidol
phenyramidol: considered as a drug that possibly causes hepatotoxicity		2.0510aminopyridine
nicarbazin
Nicarbazin: An equimolar complex of 4,4'-Dinitrocarbanilide and 2-Hydroxy-4,6-dimethylpyrimidine. A coccidiostat for poultry.		2.0510organic molecular entity
carbutamide
Carbutamide: A sulfonylurea antidiabetic agent with similar actions and uses to CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277)		2.0510benzenes;
sulfonamide
galantamine
Galantamine: A benzazepine derived from norbelladine. It is found in GALANTHUS and other AMARYLLIDACEAE. It is a cholinesterase inhibitor that has been used to reverse the muscular effects of GALLAMINE TRIETHIODIDE and TUBOCURARINE and has been studied as a treatment for ALZHEIMER DISEASE and other central nervous system disorders.. galanthamine : A benzazepine alkaloid isolated from certain species of daffodils.		3.2310benzazepine alkaloid fundamental parent;
benzazepine alkaloid;
organic heterotetracyclic compound;
tertiary amino compound		antidote to curare poisoning;
cholinergic drug;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
plant metabolite
nandrolone decanoate
Nandrolone Decanoate: Decanoic acid ester of nandrolone that is used as an anabolic agent to prevent or treat WASTING SYNDROME associated with severe chronic illness or HIV infection (HIV WASTING SYNDROME). It may also be used in the treatment of POSTMENOPAUSAL OSTEOPOROSIS.		3.5920steroid ester
bucladesine
[no description available]		2.05103',5'-cyclic purine nucleotide;
butanamides;
butyrate ester		agonist;
cardiotonic drug;
vasodilator agent
betamethasone
Betamethasone: A glucocorticoid given orally, parenterally, by local injection, by inhalation, or applied topically in the management of various disorders in which corticosteroids are indicated. Its lack of mineralocorticoid properties makes betamethasone particularly suitable for treating cerebral edema and congenital adrenal hyperplasia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p724)		2.462011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
fluorinated steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		anti-asthmatic agent;
anti-inflammatory drug;
immunosuppressive agent
perflubron
perflubron: potential anti-obesity compound; reduces food adsorption; 8-carbon perfluorocarbon radiopaque compound; an oral contrast agent for use with MRI to enhance delineation of the bowel distinguishing it from adjacent organs. perflubron : A haloalkane that is perfluorooctane in which a fluorine attached to one of the terminal carbons has been replaced by a bromine.		2.0510haloalkane;
organobromine compound;
perfluorinated compound		blood substitute;
radioopaque medium
fluorometholone
Fluorometholone: A glucocorticoid employed, usually as eye drops, in the treatment of allergic and inflammatory conditions of the eye. It has also been used topically in the treatment of various skin disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p732). fluorometholone : A member of the class of glucocorticoids that is Delta(1)-progesterone substituted at positions 11beta and 17 by hydroxy groups, at position 6alpha by a methyl group and at position 9 by a fluoro group. Used for the treatment of corticosteroid-responsive inflammation of the palpebral and bulbar conjunctiva, cornea and anterior segment of the globe.		2.111011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(1),Delta(4)-steroid;
fluorinated steroid;
glucocorticoid;
tertiary alpha-hydroxy ketone		anti-inflammatory drug
cyproterone acetate
[no description available]		2.051020-oxo steroid;
3-oxo-Delta(4) steroid;
acetate ester;
chlorinated steroid;
steroid ester		androgen antagonist;
geroprotector;
progestin
dextropropoxyphene
Dextropropoxyphene: A narcotic analgesic structurally related to METHADONE. Only the dextro-isomer has an analgesic effect; the levo-isomer appears to exert an antitussive effect.. propoxyphene : A racemate of the (1R,2R)- and (1S,2R)- diastereoisomers.. dextropropoxyphene : The (1S,2R)-(+)-diastereoisomer of propoxyphene.		3.59201-benzyl-3-(dimethylamino)-2-methyl-1-phenylpropyl propanoatemu-opioid receptor agonist;
opioid analgesic
glycyrrhetinic acid
[no description available]		2.0510cyclic terpene ketone;
hydroxy monocarboxylic acid;
pentacyclic triterpenoid		immunomodulator;
plant metabolite
chenodeoxycholic acid
Chenodeoxycholic Acid: A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones.. chenodeoxycholic acid : A dihydroxy-5beta-cholanic acid that is (5beta)-cholan-24-oic acid substituted by hydroxy groups at positions 3 and 7 respectively.. chenodeoxycholate : Conjugate base of chenodeoxycholic acid; major species at pH 7.3.		3.5920bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
dihydralazine
Dihydralazine: 1,4-Dihydrazinophthalazine. An antihypertensive agent with actions and uses similar to those of HYDRALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p354)		2.0510phthalazines
thymoquinone
thymoquinone: constituent of cedarwood; can cause dermatitis; structure. thymoquinone : A member of the class of 1,4-benzoquinones that is 1,4-bezoquinone in which the hydrogens at positions 2 and 5 are replaced by methyl and isopropyl groups, respectively. It is a natural compound isolated from Nigella sativa which has demonstrated promising chemotherapeutic activity.		7.6101,4-benzoquinonesadjuvant;
anti-inflammatory agent;
antidepressant;
antineoplastic agent;
antioxidant;
cardioprotective agent;
plant metabolite
phenylpropanolamine
Phenylpropanolamine: A sympathomimetic that acts mainly by causing release of NOREPINEPHRINE but also has direct agonist activity at some adrenergic receptors. It is most commonly used as a nasal vasoconstrictor and an appetite depressant.. phenylpropanolamine : An amphetamine in which the parent 1-phenylpropan-2-amine skeleton is substituted at position 1 with an hydroxy group. A decongestant and appetite suppressant, it is commonly used in prescription and over-the-counter cough and cold preparations.. (-)-norephedrine : An amphetamine that is propylbenzene substituted by a hydroxy group at position 1 and by an amino group at position 2 (the 1R,2S-stereoisomer). It is a plant alkaloid.		2.0510amphetamines;
phenethylamine alkaloid		plant metabolite
4-hydroxybutyric acid
4-hydroxybutyric acid: was an entry term to Sodium Oxybate (74-98). 4-hydroxybutyric acid : A 4-hydroxy monocarboxylic acid that is butyric acid in which one of the hydrogens at position 4 is replaced by a hydroxy group.		3.23104-hydroxy monocarboxylic acid;
hydroxybutyric acid		general anaesthetic;
GHB receptor agonist;
neurotoxin;
sedative
alpha-aminopyridine
alpha-aminopyridine: RN given refers to parent cpd; structure in Merck Index, 9th ed, #485. aminopyridine : Compounds containing a pyridine skeleton substituted by one or more amine groups.		5.0642
dihydroergotamine
Dihydroergotamine: A 9,10alpha-dihydro derivative of ERGOTAMINE. It is used as a vasoconstrictor, specifically for the therapy of MIGRAINE DISORDERS.. dihydroergotamine : Ergotamine in which a single bond replaces the double bond between positions 9 and 10. A semisynthetic ergot alkaloid with weaker oxytocic and vasoconstrictor properties than ergotamine, it is used (as the methanesulfonic or tartaric acid salts) for the treatment of migraine and orthostatic hypotension.		3.5920ergot alkaloid;
semisynthetic derivative		dopamine agonist;
non-narcotic analgesic;
serotonergic agonist;
sympatholytic agent;
vasoconstrictor agent
podophyllotoxin
Podophyllum: A genus of poisonous American herbs, family BERBERIDACEAE. The roots yield PODOPHYLLOTOXIN and other pharmacologically important agents. The plant was formerly used as a cholagogue and cathartic. It is different from the European mandrake, MANDRAGORA.		3.5920furonaphthodioxole;
lignan;
organic heterotetracyclic compound		antimitotic;
antineoplastic agent;
keratolytic drug;
microtubule-destabilising agent;
plant metabolite;
tubulin modulator
hesperidin
Hesperidin: A flavanone glycoside found in CITRUS fruit peels.. hesperidin : A disaccharide derivative that consists of hesperetin substituted by a 6-O-(alpha-L-rhamnopyranosyl)-beta-D-glucopyranosyl moiety at position 7 via a glycosidic linkage.		2.05103'-hydroxyflavanones;
4'-methoxyflavanones;
dihydroxyflavanone;
disaccharide derivative;
flavanone glycoside;
monomethoxyflavanone;
rutinoside		mutagen
medroxyprogesterone
[no description available]		3.231017alpha-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(4) steroid;
tertiary alpha-hydroxy ketone		contraceptive drug;
progestin;
synthetic oral contraceptive
dimenhydrinate
gravinol: has antioxidant and ant-inflammatory activities; structure in first source		3.2310diarylmethane
chlormethiazole
Chlormethiazole: A sedative and anticonvulsant often used in the treatment of alcohol withdrawal. Chlormethiazole has also been proposed as a neuroprotective agent. The mechanism of its therapeutic activity is not entirely clear, but it does potentiate GAMMA-AMINOBUTYRIC ACID receptors response and it may also affect glycine receptors.		2.0510thiazoles
diperodon
diperodon: RN given refers to parent cpd; structure given in first source		2.0510carbamate ester
methamphetamine
Methamphetamine: A central nervous system stimulant and sympathomimetic with actions and uses similar to DEXTROAMPHETAMINE. The smokable form is a drug of abuse and is referred to as crank, crystal, crystal meth, ice, and speed.. methamphetamine : A member of the class of amphetamines in which the amino group of (S)-amphetamine carries a methyl substituent.		3.5920amphetamines;
secondary amine		central nervous system stimulant;
environmental contaminant;
neurotoxin;
psychotropic drug;
xenobiotic
levocarnitine
(R)-carnitine : The (R)-enantiomer of carnitine.		3.2310carnitineantilipemic drug;
nootropic agent;
nutraceutical;
Saccharomyces cerevisiae metabolite;
water-soluble vitamin (role)
malondialdehyde
Malondialdehyde: The dialdehyde of malonic acid.. malonaldehyde : A dialdehyde that is propane substituted by two oxo groups at the terminal carbon atoms respectively. A biomarker of oxidative damage to lipids caused by smoking, it exists in vivo mainly in the enol form.		2.2110dialdehydebiomarker
sulfanilylurea
sulfanilylurea: antimicrobial agent; structure		3.2310benzenes;
sulfonamide
gentian violet
Gentian Violet: A dye that is a mixture of violet rosanilinis with antibacterial, antifungal, and anthelmintic properties.. crystal violet : An organic chloride salt that is the monochloride salt of crystal violet cation. It has been used in creams for the topical treatment of bacterial and fungal infections, being effective against some Gram-positive bacteria (notably Staphylococcus species) and some pathogenic fungi (including Candida species) but use declined following reports of animal carcinogenicity. It has also been used for dying wood, silk, and paper, as well as a histological stain.		2.0510organic chloride saltanthelminthic drug;
antibacterial agent;
antifungal agent;
antiseptic drug;
histological dye
hematoporphyrin
Hematoporphyrins: Iron-free derivatives of heme with 4 methyl groups, 2 hydroxyethyl groups and 2 propionic acid groups attached to the pyrrole rings. Some of these PHOTOSENSITIZING AGENTS are used in the PHOTOTHERAPY of malignant NEOPLASMS.. hematoporphyrin : A dicarboxylic acid that is protoporphyrin in which the vinyl groups at positions 7 and 12 are replaced by 1-hydroxyethyl groups.		2.0510
lactulose
[no description available]		3.5920glycosylfructosegastrointestinal drug;
laxative
megestrol acetate
[no description available]		2.442020-oxo steroid;
3-oxo-Delta(4) steroid;
acetate ester;
steroid ester		antineoplastic agent;
appetite enhancer;
contraceptive drug;
progestin;
synthetic oral contraceptive
pamabrom
[no description available]		3.2310
acetylcysteine
N-acetyl-L-cysteine : An N-acetyl-L-amino acid that is the N-acetylated derivative of the natural amino acid L-cysteine.		5.2931acetylcysteine;
L-cysteine derivative;
N-acetyl-L-amino acid		antidote to paracetamol poisoning;
antiinfective agent;
antioxidant;
antiviral drug;
ferroptosis inhibitor;
geroprotector;
human metabolite;
mucolytic;
radical scavenger;
vulnerary
erythromycin stearate
[no description available]		2.0510aminoglycoside
erythromycin
Erythromycin: A bacteriostatic antibiotic macrolide produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.. erythromycin : Any of several wide-spectrum macrolide antibiotics obtained from actinomycete Saccharopolyspora erythraea (formerly known as Streptomyces erythraeus).. erythromycin A : An erythromycin that consists of erythronolide A having 2,6-dideoxy-3-C-methyl-3-O-methyl-alpha-L-ribo-hexopyranosyl and 3,4,6-trideoxy-3-(dimethylamino)-beta-D-xylo-hexopyranosyl residues attahced at positions 4 and 6 respectively.		5.4841cyclic ketone;
erythromycin
levonorgestrel
Levonorgestrel: A synthetic progestational hormone with actions similar to those of PROGESTERONE and about twice as potent as its racemic or (+-)-isomer (NORGESTREL). It is used for contraception, control of menstrual disorders, and treatment of endometriosis.		3.231017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
terminal acetylenic compound		contraceptive drug;
female contraceptive drug;
progestin;
synthetic oral contraceptive
calcium lactate
[no description available]		2.1710
4-nitrophenyl acetate
[no description available]		2.0510C-nitro compound;
phenyl acetates
vinblastine
[no description available]		2.4620
alpha-fluoro-beta-alanine
alpha-fluoro-beta-alanine: metabolite of HCFU & 5-fluorouracil; structure in first source		10.2862organonitrogen compound;
organooxygen compound
diphenoxylate
Diphenoxylate: A MEPERIDINE congener used as an antidiarrheal, usually in combination with ATROPINE. At high doses, it acts like morphine. Its unesterified metabolite difenoxin has similar properties and is used similarly. It has little or no analgesic activity.. diphenoxylate : A piperidinecarboxylate ester that is the ethyl ester of difenoxin.		3.2310ethyl ester;
nitrile;
piperidinecarboxylate ester;
tertiary amine		antidiarrhoeal drug
deoxycytidine
[no description available]		31.783,5551,435pyrimidine 2'-deoxyribonucleosideEscherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
deoxyuridine
[no description available]		10.0952pyrimidine 2'-deoxyribonucleosideEscherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
estradiol valerate
[no description available]		2.0510steroid ester
ethambutol
Ethambutol: An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863). ethambutol : An ethylenediamine derivative that is ethane-1,2-diamine in which one hydrogen attached to each of the nitrogens is sutstituted by a 1-hydroxybutan-2-yl group (S,S-configuration). It is a bacteriostatic antimycobacterial drug, effective against Mycobacterium tuberculosis and some other mycobacteria. It is used (as the dihydrochloride salt) in combination with other antituberculous drugs in the treatment of pulmonary and extrapulmonary tuberculosis; resistant strains of M. tuberculosis are readily produced if ethambutol is used alone.		3.2310ethanolamines;
ethylenediamine derivative		antitubercular agent;
environmental contaminant;
xenobiotic
pyrovalerone
pyrovalerone: RN given refers to parent cpd; synonyms F 1983 & Centroton refer to HCl; structure		7.6344aromatic ketone
arsenic trioxide
Arsenic Trioxide: An inorganic compound with the chemical formula As2O3 that is used for the treatment of ACUTE PROMYELOCYTIC LEUKEMIA in patients who have relapsed from, or are resistant to, conventional drug therapy.		8.5420
vancomycin
Vancomycin: Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to RISTOCETIN that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear.. vancomycin : A complex glycopeptide from Streptomyces orientalis. It inhibits a specific step in the synthesis of the peptidoglycan layer in the Gram-positive bacteria Staphylococcus aureus and Clostridium difficile.		3.5920glycopeptideantibacterial drug;
antimicrobial agent;
bacterial metabolite
glycyrrhizic acid
glycyrrhizinic acid : A triterpenoid saponin that is the glucosiduronide derivative of 3beta-hydroxy-11-oxoolean-12-en-30-oic acid.		3.511enone;
glucosiduronic acid;
pentacyclic triterpenoid;
tricarboxylic acid;
triterpenoid saponin		EC 3.4.21.5 (thrombin) inhibitor;
plant metabolite
d-alpha tocopherol
Vitamin E: A generic descriptor for all TOCOPHEROLS and TOCOTRIENOLS that exhibit ALPHA-TOCOPHEROL activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of ISOPRENOIDS.. tocopherol : A collective name for a group of closely related lipids that contain a chroman-6-ol nucleus substituted at position 2 by a methyl group and by a saturated hydrocarbon chain consisting of three isoprenoid units. They are designated as alpha-, beta-, gamma-, and delta-tocopherol depending on the number and position of additional methyl substituents on the aromatic ring. Tocopherols occur in vegetable oils and vegetable oil products, almost exclusively with R,R,R configuration. Tocotrienols differ from tocopherols only in having three double bonds in the hydrocarbon chain.. vitamin E : Any member of a group of fat-soluble chromanols that exhibit biological activity against vitamin E deficiency. The vitamers in this class consists of a chroman-6-ol core which is substituted at position 2 by a methyl group and (also at position 2) either a saturated or a triply-unsaturated hydrocarbon chain consisting of three isoprenoid units. The major function of vitamin E is to act as a natural antioxidant by scavenging free radicals and molecular oxygen.. (R,R,R)-alpha-tocopherol : An alpha-tocopherol that has R,R,R configuration. The naturally occurring stereoisomer of alpha-tocopherol, it is found particularly in sunflower and olive oils.		6.4470alpha-tocopherolalgal metabolite;
antiatherogenic agent;
anticoagulant;
antioxidant;
antiviral agent;
EC 2.7.11.13 (protein kinase C) inhibitor;
immunomodulator;
micronutrient;
nutraceutical;
plant metabolite
ibufenac
ibufenac: used in the treatment of rheumatism; also possesses antipyretic properties; minor descriptor (75-84); on-line & Index Medicus search PHENYLACETATES (75-84); RN given refers to parent cpd. ibufenac : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by a 4-isobutylphenyl group. Although it was shown to be effective in treatment of rheumatoid arthritis, the clinical use of ibufenac was discontinued due to hepatotoxic side-effects.		3.2310monocarboxylic acidEC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
hepatotoxic agent;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
methyl tert-butyl ether
methyl tert-butyl ether: used to dissolve gallstones; gasoline additive. methyl tert-butyl ether : An ether having methyl and tert-butyl as the two alkyl components.		2.0510etherfuel additive;
metabolite;
non-polar solvent
metaxalone
[no description available]		3.5820aromatic ether
spectinomycin
Spectinomycin: An antibiotic produced by Streptomyces spectabilis. It is active against gram-negative bacteria and used for the treatment of GONORRHEA.. spectinomycin dihydrochloride : A hydrochloride obtained by combining spectinomycin with two molar equivalents of hydrochloric acid. An antibiotic that is active against gram-negative bacteria and used (as its pentahydrate) to treat gonorrhea.. spectinomycin : A pyranobenzodioxin and antibiotic that is active against gram-negative bacteria and used (as its dihydrochloride pentahydrate) to treat gonorrhea. It is produced by the bacterium Streptomyces spectabilis.		3.2310cyclic acetal;
cyclic hemiketal;
cyclic ketone;
pyranobenzodioxin;
secondary alcohol;
secondary amino compound		antibacterial drug;
antimicrobial agent;
bacterial metabolite
5-chlorouracil
5-chlorouracil : An organochlorine compound consisting of uracil having an chloro substituent at the 5-position.		2.0510organochlorine compound
dronabinol
Dronabinol: A psychoactive compound extracted from the resin of Cannabis sativa (marihuana, hashish). The isomer delta-9-tetrahydrocannabinol (THC) is considered the most active form, producing characteristic mood and perceptual changes associated with this compound.. Delta(9)-tetrahydrocannabinol : A diterpenoid that is 6a,7,8,10a-tetrahydro-6H-benzo[c]chromene substituted at position 1 by a hydroxy group, positions 6, 6 and 9 by methyl groups and at position 3 by a pentyl group. The principal psychoactive constituent of the cannabis plant, it is used for treatment of anorexia associated with AIDS as well as nausea and vomiting associated with cancer chemotherapy.		3.5920benzochromene;
diterpenoid;
phytocannabinoid;
polyketide		cannabinoid receptor agonist;
epitope;
hallucinogen;
metabolite;
non-narcotic analgesic
amiloride
Amiloride: A pyrazine compound inhibiting SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with DIURETICS to spare POTASSIUM loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705). amiloride : A member of the class of pyrazines resulting from the formal monoacylation of guanidine with the carboxy group of 3,5-diamino-6-chloropyrazine-2-carboxylic acid.		3.5920aromatic amine;
guanidines;
organochlorine compound;
pyrazines		diuretic;
sodium channel blocker
aminocarb
aminocarb: structure. aminocarb : A carbamate ester that is phenyl methylcarbamate substituted by a dimethylamino group at position 4 and a methyl group at position 3.		2.0510carbamate ester;
toluenes		acaricide;
agrochemical;
carbamate insecticide;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
molluscicide
methiocarb
Methiocarb: Insecticide, molluscacide, acaricide.. methiocarb : A carbamate ester obtained by the formal condensation of the phenolic group of 3,5-dimethyl-4-(methylsulfanyl)phenol with the carboxy group of methylcarbamic acid.		2.0510aryl sulfide;
carbamate ester;
methyl sulfide		acaricide;
agrochemical;
avicide;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
environmental contaminant;
insecticide;
molluscicide;
xenobiotic
pimozide
Pimozide: A diphenylbutylpiperidine that is effective as an antipsychotic agent and as an alternative to HALOPERIDOL for the suppression of vocal and motor tics in patients with Tourette syndrome. Although the precise mechanism of action is unknown, blockade of postsynaptic dopamine receptors has been postulated. (From AMA Drug Evaluations Annual, 1994, p403). pimozide : A member of the class of benzimidazoles that is 1,3-dihydro-2H-benzimidazol-2-one in which one of the nitrogens is substituted by a piperidin-4-yl group, which in turn is substituted on the nitrogen by a 4,4-bis(p-fluorophenyl)butyl group.		3.5920benzimidazoles;
heteroarylpiperidine;
organofluorine compound		antidyskinesia agent;
dopaminergic antagonist;
first generation antipsychotic;
H1-receptor antagonist;
serotonergic antagonist
perillaldehyde
perillaldehyde: from oil of Perillae herba; has neuropharmacological actions; RN given refers to cpd without isomeric designation; structure in Merck Index, 9th ed, #6956. perillyl aldehyde : An aldehyde that is cyclohex-1-ene-1-carbaldehyde substituted by a prop-1-en-2-yl group at position 4.		2.0510aldehyde;
olefinic compound		human metabolite;
mouse metabolite;
volatile oil component
dexbrompheniramine
dexbrompheniramine : The (pharmacologically active) (S)-(+)-enantiomer of brompheniramine. A histamine H1 receptor antagonist, it is used (commonly as its maleate salt) for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.		3.2310brompheniramineanti-allergic agent;
H1-receptor antagonist
sulfadoxine
Sulfadoxine: A long acting sulfonamide that is used, usually in combination with other drugs, for respiratory, urinary tract, and malarial infections.. sulfadoxine : A sulfonamide consisting of pyrimidine having methoxy substituents at the 5- and 6-positions and a 4-aminobenzenesulfonamido group at the 4-position. In combination with the antiprotozoal pyrimethamine (CHEBI:8673) it is used as an antimalarial.		2.0510pyrimidines;
sulfonamide		antibacterial drug;
antimalarial
acadesine
[no description available]		2.05101-ribosylimidazolecarboxamide;
aminoimidazole;
nucleoside analogue		antineoplastic agent;
platelet aggregation inhibitor
promecarb
promecarb: structure		2.0510alkylbenzene
stavudine
Stavudine: A dideoxynucleoside analog that inhibits reverse transcriptase and has in vitro activity against HIV.. stavudine : A nucleoside analogue obtained by formal dehydration across positions 2 and 3 of thymidine. An inhibitor of HIV-1 reverse transcriptase		3.5920dihydrofuran;
nucleoside analogue;
organic molecular entity		antimetabolite;
antiviral agent;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
doxifluridine
doxifluridine : A pyrimidine 5'-deoxyribonucleoside that is 5-fluorouridine in which the hydroxy group at the 5' position is replaced by a hydrogen. It is an oral prodrug of the antineoplastic agent 5-fluorouracil. Designed to circumvent the rapid degradation of 5-fluorouracil by dihydropyrimidine dehydrogenase in the gut wall, it is converted into 5-fluorouracil in the presence of pyrimidine nucleoside phosphorylase.		13.22619organofluorine compound;
pyrimidine 5'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
prodrug
dicloxacillin
Dicloxacillin: One of the PENICILLINS which is resistant to PENICILLINASE.. dicloxacillin : A penicillin that is 6-aminopenicillanic acid in which one of the amino hydrogens is replaced by a 3-(2,6-dichlorophenyl)-5-methyl-1,2-oxazol-4-yl]formyl group.		3.2310dichlorobenzene;
penicillin		antibacterial drug
mannose
mannopyranose : The pyranose form of mannose.		9.4111D-aldohexose;
D-mannose;
mannopyranose		metabolite
iproclozide
iproclozide: structure		2.0510aromatic ether
megestrol
Megestrol: A progestational hormone used most commonly as the acetate ester. As the acetate, it is more potent than progesterone both as a progestagen and as an ovulation inhibitor. It has also been used in the palliative treatment of breast cancer.. megestrol : A 3-oxo Delta(4)-steroid that is pregna-4,6-diene-3,20-dione substituted by a methyl group at position 6 and a hydroxy group at position 17.		8.572017alpha-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(4) steroid;
tertiary alpha-hydroxy ketone		antineoplastic agent;
appetite enhancer;
contraceptive drug;
progestin;
synthetic oral contraceptive
streptomycin
[no description available]		3.5920antibiotic antifungal drug;
antibiotic fungicide;
streptomycins		antibacterial drug;
antifungal agrochemical;
antimicrobial agent;
antimicrobial drug;
bacterial metabolite;
protein synthesis inhibitor
pn 401
uridine triacetate: A uridine prodrug that is used in the treatment of hereditary orotic aciduria.. uridine triacetate : An acetate ester that is uracil in which the three hydroxy hydrogens are replaced by acetate group. A prodrug for uridine, it is used for the treatment of hereditary orotic aciduria and for management of fluorouracil toxicity.		6.45120acetate ester;
uridines		neuroprotective agent;
orphan drug;
prodrug
cladribine
[no description available]		4.5840organochlorine compound;
purine 2'-deoxyribonucleoside		antineoplastic agent;
immunosuppressive agent
carbenicillin
Carbenicillin: Broad-spectrum semisynthetic penicillin derivative used parenterally. It is susceptible to gastric juice and penicillinase and may damage platelet function.. carbenicillin : A penicillin antibiotic having a 6beta-2-carboxy-2-phenylacetamido side-chain.		3.2310penicillin allergen;
penicillin		antibacterial drug
carbenicillin disodium
[no description available]		2.0510organic sodium salt
dehydroemetine
dehydroemetine: was MH 1991-94 (see under EMETINE 1976-90); use EMETINE to search DEHYDROEMETINE 1976-94; amebicide, derivative of emetine. dehydroemetine : A pyridoisoquinoline which was developed in response to the cardiovascular toxicity associated with emetine and results from the dehydrogenation of the heterotricylic ring of emetine. It is an antiprotozoal agent and displays antimalarial, antiamoebic, and antileishmanial properties.		2.0510aromatic ether;
isoquinolines;
pyridoisoquinoline		antileishmanial agent;
antimalarial;
antiprotozoal drug
benorilate
benorilate: was heading 1980-94 (see under SALICYLATES 1980-90); was BENORYLATE see under SALICYLATES 1975-79; BENORYLATE was see BENORILATE 1980-94; use SALICYLATES to search BENORILATE 1980-90 & BENORYLATE 1975-79; an ester of aspirin and paracetamol with analgesic, antipyretic, and anti-inflammatory activity used in the treatment of rheumatoid diseases; it has less severe side effects than aspirin		2.0510carbonyl compound
trimetazidine
Trimetazidine: A vasodilator used in angina of effort or ischemic heart disease.		2.0510aromatic amine
floxacillin
Floxacillin: Antibiotic analog of CLOXACILLIN.. flucloxacillin : A penicillin compound having a 6beta-[3-(2-chloro-6-fluorophenyl)-5-methyl-1,2-oxazole-4-carboxamido] side-chain.		2.0510penicillin allergen;
penicillin		antibacterial drug
clomacran
clomacran: RN given refers to parent cpd; structure		3.2310acridines
vidarabine
adenine arabinoside : A purine nucleoside in which adenine is attached to arabinofuranose via a beta-N(9)-glycosidic bond.		3.8330beta-D-arabinoside;
purine nucleoside		antineoplastic agent;
bacterial metabolite;
nucleoside antibiotic
iodinated glycerol
iodinated glycerol: secretolytic agent; RN given refers to cpd without iodine locant		4.3611dioxolane
methenamine hippurate
methenamine hippurate: both parts of molecule contribute to its antibacterial action		3.2310N-acylglycine
olsalazine
olsalazine: cpd with 2 salicylate molecules linked together by an azo bond. olsalazine : An azobenzene that consists of two molecules of 4-aminosalicylic acid joined by an azo linkage. A prodrug for mesalazine, an anti-inflammatory drug, it is used (as the disodium salt) in the treatment of inflammatory bowel disease.		3.2310azobenzenes;
dicarboxylic acid		non-steroidal anti-inflammatory drug;
prodrug
tiadenol
tiadenol: structure		2.0510aliphatic sulfide
lutetium
Lutetium: An element of the rare earth family of metals. It has the atomic symbol Lu, atomic number 71, and atomic weight 175.		3.2310d-block element atom;
lanthanoid atom
platinum
Platinum: A heavy, soft, whitish metal, resembling tin, with atomic number 78, atomic weight 195.084, symbol Pt. It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as alutiae.		8.0382elemental platinum;
nickel group element atom;
platinum group metal atom
rhenium
Rhenium: A metal, atomic number 75, atomic weight 186.207, symbol Re.		3.4311manganese group element atom
silver
Silver: An element with the atomic symbol Ag, atomic number 47, and atomic weight 107.87. It is a soft metal that is used medically in surgical instruments, dental prostheses, and alloys. Long-continued use of silver salts can lead to a form of poisoning known as ARGYRIA.		2.6320copper group element atom;
elemental silver		Escherichia coli metabolite
titanium
Titanium: A dark-gray, metallic element of widespread distribution but occurring in small amounts with atomic number, 22, atomic weight, 47.867 and symbol, Ti; specific gravity, 4.5; used for fixation of fractures.		3.1310titanium group element atom
gold
Gold: A yellow metallic element with the atomic symbol Au, atomic number 79, and atomic weight 197. It is used in jewelry, goldplating of other metals, as currency, and in dental restoration. Many of its clinical applications, such as ANTIRHEUMATIC AGENTS, are in the form of its salts.		7.0710copper group element atom;
elemental gold
yttrium
Yttrium: An element of the rare earth family of metals. It has the atomic symbol Y, atomic number 39, and atomic weight 88.91. In conjunction with other rare earths, yttrium is used as a phosphor in television receivers and is a component of the yttrium-aluminum garnet (YAG) lasers.		9.411d-block element atom;
rare earth metal atom;
scandium group element atom
zirconium
Zirconium: A rather rare metallic element with atomic number 40, atomic weight 91.224, and symbol Zr.		2.1110titanium group element atom
zalcitabine
Zalcitabine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy.. zalcitabine : A pyrimidine 2',3'-dideoxyribonucleoside compound having cytosine as the nucleobase.		2.0510pyrimidine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
HIV-1 reverse transcriptase inhibitor
magnesium sulfate
Magnesium Sulfate: A small colorless crystal used as an anticonvulsant, a cathartic, and an electrolyte replenisher in the treatment of pre-eclampsia and eclampsia. It causes direct inhibition of action potentials in myometrial muscle cells. Excitation and contraction are uncoupled, which decreases the frequency and force of contractions. (From AMA Drug Evaluations Annual, 1992, p1083). magnesium sulfate : A magnesium salt having sulfate as the counterion.		3.4411magnesium salt;
metal sulfate;
organic magnesium salt		anaesthetic;
analgesic;
anti-arrhythmia drug;
anticonvulsant;
calcium channel blocker;
cardiovascular drug;
fertilizer;
tocolytic agent
camptothecin
NSC 100880: carboxylate (opened lactone) form of camptothecin; RN refers to (S)-isomer; structure given in first source		23.43428166delta-lactone;
pyranoindolizinoquinoline;
quinoline alkaloid;
tertiary alcohol		antineoplastic agent;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
genotoxin;
plant metabolite
zinc sulfate
Zinc Sulfate: A compound given in the treatment of conditions associated with zinc deficiency such as acrodermatitis enteropathica. Externally, zinc sulfate is used as an astringent in lotions and eye drops. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995). zinc sulfate : A metal sulfate compound having zinc(2+) as the counterion.		2.0310metal sulfate;
zinc molecular entity		fertilizer
sodium thiosulfate
sodium thiosulfate: do not confuse synonym sodium hyposulfite with sodium hyposulfite, synonym for di-Na salt of dithionous acid. sodium thiosulfate : An inorganic sodium salt composed of sodium and thiosulfate ions in a 2:1 ratio.		3.2310inorganic sodium saltantidote to cyanide poisoning;
antifungal drug;
nephroprotective agent
fluorine
Fluorine: A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as fluoride (FLUORIDES) to prevent dental caries.		3.1450diatomic fluorine;
gas molecular entity		NMR chemical shift reference compound
propham
propham: minor descriptor (72-85); on-line & Index Medicus search HERBICIDES, CARBAMATE (72-85); RN given refers to parent cpd. propham : A carbamate ester that is the isopropyl ester of phenylcarbamic acid. It is a selective herbicide used for the control of annual grasses and some broad-leaf weeds and is also a growth regulator for control of sprouting in stored potatoes.		2.0510benzenes;
carbamate ester		herbicide;
plant growth retardant
phenmedipham
phenmedipham: minor descriptor (72-84); on-line search CARBAMATES (72-84); Index Medicus search HERBICIDES, CARBAMATE (75-84), CARBAMATES (72-75). phenmedipham : A carbamate ester that is (3-methylphenyl)carbamic acid in which the hydrogen of the hydroxy group has been replaced by a 3-[(methoxycarbonyl)amino]phenyl group.		2.0510carbamate esterenvironmental contaminant;
herbicide;
xenobiotic
stanozolol
Stanozolol: A synthetic steroid that has anabolic and androgenic properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1194). stanozolol : An organic heteropentacyclic compound resulting from the formal condensation of the 3-keto-aldehyde moiety of oxymetholone with hydrazine. Like oxymetholone, it is a synthetic anabolic steroid. It has both anabolic and androgenic properties, and has been used to treat hereditary angioedema and various vascular disorders. It has also been widely abused by professional athletes.		2.051017beta-hydroxy steroid;
anabolic androgenic steroid;
organic heteropentacyclic compound;
tertiary alcohol		anabolic agent;
androgen
clodronic acid
Clodronic Acid: A diphosphonate which affects calcium metabolism. It inhibits bone resorption and soft tissue calcification.. clodronic acid : An organochlorine compound that is methylene chloride in which both hydrogens are replaced by phosphonic acid groups. It inhibits bone resorption and soft tissue calcification, and is used (often as the disodium salt tetrahydrate) as an adjunct in the treatment of severe hypercalcaemia associated with malignancy, and in the management of osteolytic lesions and bone pain associated with skeletal metastases.		2.05101,1-bis(phosphonic acid);
one-carbon compound;
organochlorine compound		antineoplastic agent;
bone density conservation agent
xipamide
Xipamide: A sulfamoylbenzamide analog of CLOPAMIDE. It is diuretic and saluretic with antihypertensive activity. It is bound to PLASMA PROTEINS, thus has a delayed onset and prolonged action.		2.0510benzamides
selegiline
Selegiline: A selective, irreversible inhibitor of Type B monoamine oxidase that is used for the treatment of newly diagnosed patients with PARKINSON DISEASE, and for the treatment of depressive disorders. The compound without isomeric designation is Deprenyl.		3.5920selegiline;
terminal acetylenic compound		geroprotector
levamisole
Levamisole: An antihelminthic drug that has been tried experimentally in rheumatic disorders where it apparently restores the immune response by increasing macrophage chemotaxis and T-lymphocyte function. Paradoxically, this immune enhancement appears to be beneficial in rheumatoid arthritis where dermatitis, leukopenia, and thrombocytopenia, and nausea and vomiting have been reported as side effects. (From Smith and Reynard, Textbook of Pharmacology, 1991, p435-6). levamisole : A 6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazole that has S configuration. It is used (generally as the monohydrochloride salt) to treat parasitic worm infections in pigs, sheep and cattle and was formerly used in humans as an adjuvant to chemotherapy for the treatment of various cancers. It is also widely used as an adulterant to coccaine.		5.09506-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazoleantinematodal drug;
antirheumatic drug;
EC 3.1.3.1 (alkaline phosphatase) inhibitor;
immunological adjuvant;
immunomodulator
clemastine
Clemastine: A histamine H1 antagonist used as the hydrogen fumarate in hay fever, rhinitis, allergic skin conditions, and pruritus. It causes drowsiness.. clemastine : 2-[(2R)-1-Methylpyrrolidin-2-yl]ethanol in which the hydrogen of the hydroxy group is substituted by a 1-(4-chlorophenyl)-1-phenylethyl group (R configuration). An antihistamine with antimuscarinic and moderate sedative properties, it is used as its fumarate salt for the symptomatic relief of allergic conditions such as rhinitis, urticaria, conjunctivitis and in pruritic (severe itching) skin conditions.		3.2310monochlorobenzenes;
N-alkylpyrrolidine		anti-allergic agent;
antipruritic drug;
H1-receptor antagonist;
muscarinic antagonist
thiamphenicol
[no description available]		2.0510monocarboxylic acid amide;
sulfone		antimicrobial agent;
immunosuppressive agent
pizotyline
Pizotyline: Serotonin antagonist used against MIGRAINE DISORDERS and vascular headaches.. pizotifen : A benzocycloheptathiophene that is 9,10-dihydro-4H-benzo[4,5]cyclohepta[1,2-b]thiophene 4-ylidene)-1-methylpiperidine which is joined from the 4 position to the 4 position of an N-methylpiperidine moiety by a double bond. It is a sedating antihistamine, with strong serotonin antagonist and weak antimuscarinic activity. It is generally used as the malate salt for the treatment of migraine and the prevention of headache attacks during cluster periods.		2.0510benzocycloheptathiophenehistamine antagonist;
muscarinic antagonist;
serotonergic antagonist
cephalexin
Cephalexin: A semisynthetic cephalosporin antibiotic with antimicrobial activity similar to that of CEPHALORIDINE or CEPHALOTHIN, but somewhat less potent. It is effective against both gram-positive and gram-negative organisms.. cephalexin : A semisynthetic first-generation cephalosporin antibiotic having methyl and beta-(2R)-2-amino-2-phenylacetamido groups at the 3- and 7- of the cephem skeleton, respectively. It is effective against both Gram-negative and Gram-positive organisms, and is used for treatment of infections of the skin, respiratory tract and urinary tract.		3.2310beta-lactam antibiotic allergen;
cephalosporin;
semisynthetic derivative		antibacterial drug
isosorbide-5-mononitrate
isosorbide-5-mononitrate: for prevention of angina pectoris; structure given in first source; a Russian drug		9.1431glucitol derivative;
nitrate ester		nitric oxide donor;
vasodilator agent
ornidazole
Ornidazole: A nitroimidazole antiprotozoal agent used in ameba and trichomonas infections. It is partially plasma-bound and also has radiation-sensitizing action.. ornidazole : A C-nitro compound that is 5-nitroimidazole in which the hydrogens at positions 1 and 2 are replaced by 3-chloro-2-hydroxypropyl and methyl groups, respectively. It is used in the treatment of susceptible protozoal infections and for the treatment of anaerobic bacterial infections.		2.2110C-nitro compound;
imidazoles;
organochlorine compound;
secondary alcohol		antiamoebic agent;
antibacterial drug;
antiinfective agent;
antiprotozoal drug;
antitrichomonal drug;
epitope
danazol
Danazol: A synthetic steroid with antigonadotropic and anti-estrogenic activities that acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. Danazol has been used in the treatment of endometriosis and some benign breast disorders.		3.592017beta-hydroxy steroid;
terminal acetylenic compound		anti-estrogen;
estrogen antagonist;
geroprotector
metergoline
Metergoline: A dopamine agonist and serotonin antagonist. It has been used similarly to BROMOCRIPTINE as a dopamine agonist and also for MIGRAINE DISORDERS therapy.. metergoline : An ergoline alkaloid that is the N-benzyloxycarbonyl derivative of lysergamine. A 5-HT2 antagonist. Also 5-HT1 antagonist and 5-HT1D ligand. Has moderate affinity for 5-HT6 and high affinity for 5-HT7.		2.0510carbamate ester;
ergoline alkaloid		dopamine agonist;
geroprotector;
serotonergic antagonist
benomyl
[no description available]		2.0510aromatic amide;
benzimidazole fungicide;
benzimidazoles;
benzimidazolylcarbamate fungicide;
carbamate ester		acaricide;
anthelminthic drug;
antifungal agrochemical;
microtubule-destabilising agent;
tubulin modulator
fenclozic acid
fenclozic acid: an analgesic & antipyretic with anti-inflammatory properties; minor descriptor (75-86); on-line & INDEX MEDICUS search THIAZOLES (75-86); RN given refers to parent cpd		3.2310
laxagetten 4,4'-diacetoxydiphenylpyridylemethane
[no description available]		3.2310
oxadiazon
oxadiazon: manufactured by the Societe Rhone-poulenc, France; structure		2.0510aromatic ether
daunorubicin
Daunorubicin: A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.. anthracycline : Anthracyclines are polyketides that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.. daunorubicin : A natural product found in Actinomadura roseola.		3.8630aminoglycoside antibiotic;
anthracycline;
p-quinones;
tetracenequinones		antineoplastic agent;
bacterial metabolite
razoxane
Razoxane: An antimitotic agent with immunosuppressive properties.		2.0610N-alkylpiperazine
fludarabine phosphate
fludarabine phosphate: structure given in first source. fludarabine phosphate : A purine arabinonucleoside monophosphate having 2-fluoroadenine as the nucleobase. A prodrug, it is rapidly dephosphorylated to 2-fluoro-ara-A and then phosphorylated intracellularly by deoxycytidine kinase to the active triphosphate, 2-fluoro-ara-ATP. Once incorporated into DNA, 2-fluoro-ara-ATP functions as a DNA chain terminator. It is used for the treatment of adult patients with B-cell chronic lymphocytic leukemia (CLL) who have not responded to, or whose disease has progressed during, treatment with at least one standard alkylating-agent containing regimenas.		4.0720nucleoside analogue;
organofluorine compound;
purine arabinonucleoside monophosphate		antimetabolite;
antineoplastic agent;
antiviral agent;
DNA synthesis inhibitor;
immunosuppressive agent;
prodrug
alclofenac
alclofenac: was heading 1975-94 (was see under PHENYLACETATES 1975-90); use PHENYLACETATES to search ALCLOFENAC 1975-94; an anti-inflammatory agent used in the treatment of rheumatoid arthritis; acts also as an analgesic and an antipyretic. alclofenac : An aromatic ether in which the ether oxygen links an allyl group to the 4-position of (3-chlorophenyl)acetic acid.A non-steroidal anti-inflammatory drug, it was withdrawn from the UK market in 1979 due to concerns with its association with vasculitis and rash.		3.2310aromatic ether;
monocarboxylic acid;
monochlorobenzenes		drug allergen;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
carbimazole
Carbimazole: An imidazole antithyroid agent. Carbimazole is metabolized to METHIMAZOLE, which is responsible for the antithyroid activity.. carbimazole : A member of the class of imidazoles that is methimazole in which the nitrogen bearing a hydrogen is converted into its ethoxycarbonyl derivative. A prodrug for methimazol, carbimazole is used for the treatment of hyperthyroidism.		2.05101,3-dihydroimidazole-2-thiones;
carbamate ester		antithyroid drug;
prodrug
bromocriptine
Bromocriptine: A semisynthetic ergotamine alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion.		3.5920indole alkaloidantidyskinesia agent;
antiparkinson drug;
dopamine agonist;
hormone antagonist
phenyl acetate
phenyl acetate: The ester formed between phenol and acetic acid. Don't confuse with phenylacetic acid derivatives listed under PHENYLACETATES.. phenyl acetate : An acetate ester obtained by the formal condensation of phenol with acetic acid.		6.47130benzenes;
phenyl acetates
triamcinolone
Triamcinolone: A glucocorticoid given, as the free alcohol or in esterified form, orally, intramuscularly, by local injection, by inhalation, or applied topically in the management of various disorders in which corticosteroids are indicated. (From Martindale, The Extra Pharmacopoeia, 30th ed, p739). triamcinolone : A C21-steroid hormone that is 1,4-pregnadiene-3,20-dione carrying four hydroxy substituents at positions 11beta, 16alpha, 17alpha and 21 as well as a fluoro substituent at position 9. Used in the form of its 16,17-acetonide to treat various skin infections.		2.051011beta-hydroxy steroid;
16alpha-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid hormone;
fluorinated steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		anti-allergic agent;
anti-inflammatory drug
oxyphenisatin
[no description available]		3.5920indoles
tetrachloroethylene
Tetrachloroethylene: A chlorinated hydrocarbon used as an industrial solvent and cooling liquid in electrical transformers. It is a potential carcinogen.		2.0510chlorocarbon;
chloroethenes		nephrotoxic agent
fludrocortisone
Fludrocortisone: A synthetic mineralocorticoid with anti-inflammatory activity.		3.231011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid;
fluorinated steroid;
mineralocorticoid		adrenergic agent;
anti-inflammatory drug
ursodeoxycholic acid
Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.. ursodeoxycholic acid : A bile acid found in the bile of bears (Ursidae) as a conjugate with taurine. Used therapeutically, it prevents the synthesis and absorption of cholesterol and can lead to the dissolution of gallstones.. ursodeoxycholate : A bile acid anion that is the conjugate base of ursodeoxycholic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.		3.5920bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
butachlor
butachlor : An aromatic amide that is 2-choro-N-(2,6-diethylphenyl)acetamide in which the amide nitrogen has been replaced by a butoxymethyl group.		2.0510aromatic amide;
organochlorine compound;
tertiary carboxamide		environmental contaminant;
herbicide;
xenobiotic
transferrin
Transferrin: An iron-binding beta1-globulin that is synthesized in the LIVER and secreted into the blood. It plays a central role in the transport of IRON throughout the circulation. A variety of transferrin isoforms exist in humans, including some that are considered markers for specific disease states.		2.1510
rose bengal b disodium salt
[no description available]		2.0510
glutamic acid
Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.. glutamic acid : An alpha-amino acid that is glutaric acid bearing a single amino substituent at position 2.		2.0510glutamic acid;
glutamine family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		Escherichia coli metabolite;
ferroptosis inducer;
micronutrient;
mouse metabolite;
neurotransmitter;
nutraceutical
dexchlorpheniramine
dexchlorpheniramine: RN given refers to parent cpd(S)-isomer		3.2310chlorphenamine
alovudine
[no description available]		2.1310pyrimidine 2',3'-dideoxyribonucleoside
clometacin
clometacin: structure		3.2310N-acylindole
cefazolin
Cefazolin: A semisynthetic cephalosporin analog with broad-spectrum antibiotic action due to inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine.. cefazolin : A first-generation cephalosporin compound having [(5-methyl-1,3,4-thiadiazol-2-yl)sulfanyl]methyl and (1H-tetrazol-1-ylacetyl)amino side-groups at positions 3 and 7 respectively.		3.5920beta-lactam antibiotic allergen;
cephalosporin;
tetrazoles;
thiadiazoles		antibacterial drug
amoxicillin
Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to AMPICILLIN except that its resistance to gastric acid permits higher serum levels with oral administration.. amoxicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-(4-hydroxyphenyl)acetamido group.		3.5920penicillin allergen;
penicillin		antibacterial drug
timolol
(S)-timolol (anhydrous) : The (S)-(-) (more active) enantiomer of timolol. A beta-adrenergic antagonist, both the hemihydrate and the maleate salt are used in the mangement of glaucoma, hypertension, angina pectoris and myocardial infarction, and for the prevention of migraine.		8.930timololanti-arrhythmia drug;
antiglaucoma drug;
antihypertensive agent;
beta-adrenergic antagonist
nicergoline
Nicergoline: An ergot derivative that has been used as a cerebral vasodilator and in peripheral vascular disease. It may ameliorate cognitive deficits in CEREBROVASCULAR DISORDERS.		2.0510organic heterotetracyclic compound;
organonitrogen heterocyclic compound
oxcarbazepine
Oxcarbazepine: A carbamazepine derivative that acts as a voltage-gated sodium channel blocker. It is used for the treatment of PARTIAL SEIZURES with or without secondary generalization. It is also an inducer of CYTOCHROME P-450 CYP3A4.. oxcarbazepine : A dibenzoazepine derivative, having a carbamoyl group at the ring nitrogen, substituted with an oxo group at C-4 of the azepeine ring which is also hydrogenated at C-4 and C-5. It is a anticholinergic anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy.		3.5920cyclic ketone;
dibenzoazepine		anticonvulsant;
drug allergen
carbidopa
carbidopa (anhydrous) : 3-(3,4-Dihydroxyphenyl)propanoic acid in which the hydrogens alpha- to the carboxyl group are substituted by hydrazinyl and methyl groups (S-configuration). Carbidopa is a dopa decarboxylase inhibitor, so prevents conversion of levodopa to dopamine. It has no antiparkinson activity by itself, but is used (commonly as its hydrate) in the management of Parkinson's disease to reduce peripheral adverse effects of levodopa.		3.2310catechols;
hydrazines;
monocarboxylic acid		antiparkinson drug;
dopaminergic agent;
EC 4.1.1.28 (aromatic-L-amino-acid decarboxylase) inhibitor
toloxatone
toloxatone: oxazolidinone derivative; psychotropic drug; structure. toloxatone : A racemate consisting of equimolar amounts of (R)- and (S)-toloxatone. It is a reversible monoamine oxidase A inhibitor and antidepressant.. 5-(hydroxymethyl)-3-(3-methylphenyl)-1,3-oxazolidin-2-one : A member of the class of oxazolidinones that is 5-(hydroxymethyl)-1,3-oxazolidin-2-one substituted by a 3-methylphenyl group at position 3.		2.0510oxazolidinone;
primary alcohol;
toluenes
moricizine
Moricizine: An antiarrhythmia agent used primarily for ventricular rhythm disturbances.. moricizine : A phenothiazine substituted on the nitrogen by a 3-(morpholin-4-yl)propanoyl group, and at position 2 by an (ethoxycarbonyl)amino group.		3.2310carbamate ester;
morpholines;
phenothiazines		anti-arrhythmia drug
vidarabine phosphate
Vidarabine Phosphate: An adenosine monophosphate analog in which ribose is replaced by an arabinose moiety. It is the monophosphate ester of VIDARABINE with antiviral and possibly antineoplastic properties.		3.1210
amineptin
amineptin: used in treatment of neuroses with psychoasthenic, anxio-phobic & depressive manifestations; synonym S 1694 refers to HCl; structure. amineptine : A carbocyclic fatty acid that is 5-aminoheptanoic acid in which one of the hydrogens attached to the nitrogen is replaced by a 10,11-dihydro-5H-dibenzo[a,d][7]annulen-5-yl group. A tricyclic antidepressant, it was never approved in the US and was withdrawn from the French market in 1999 due to concerns over abuse, dependence and severe acne.		3.5920amino acid;
carbocyclic fatty acid;
carbotricyclic compound;
secondary amino compound		antidepressant;
dopamine uptake inhibitor
zidovudine
Zidovudine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.. zidovudine : A pyrimidine 2',3'-dideoxyribonucleoside compound having a 3'-azido substituent and thymine as the nucleobase.		3.5920azide;
pyrimidine 2',3'-dideoxyribonucleoside		antimetabolite;
antiviral drug;
HIV-1 reverse transcriptase inhibitor
pirprofen
pirprofen: anti-inflammatory agent used in therapy of rheumatoid arthritis; prostaglandin synthetase inhibitor; more potent than indomethacin; structure		3.5920pyrroline
tobramycin
Tobramycin: An aminoglycoside, broad-spectrum antibiotic produced by Streptomyces tenebrarius. It is effective against gram-negative bacteria, especially the PSEUDOMONAS species. It is a 10% component of the antibiotic complex, NEBRAMYCIN, produced by the same species.. tobramycin : A amino cyclitol glycoside that is kanamycin B lacking the 3-hydroxy substituent from the 2,6-diaminoglucose ring.		2.0510amino cyclitol glycosideantibacterial agent;
antimicrobial agent;
toxin
paclitaxel
Taxus: Genus of coniferous yew trees or shrubs, several species of which have medicinal uses. Notable is the Pacific yew, Taxus brevifolia, which is used to make the anti-neoplastic drug taxol (PACLITAXEL).		21.25234102taxane diterpenoid;
tetracyclic diterpenoid		antineoplastic agent;
human metabolite;
metabolite;
microtubule-stabilising agent
etoposide
[no description available]		7.93170beta-D-glucoside;
furonaphthodioxole;
organic heterotetracyclic compound		antineoplastic agent;
DNA synthesis inhibitor
dobutamine
Dobutamine: A catecholamine derivative with specificity for BETA-1 ADRENERGIC RECEPTORS. It is commonly used as a cardiotonic agent after CARDIAC SURGERY and during DOBUTAMINE STRESS ECHOCARDIOGRAPHY.. dobutamine : A catecholamine that is 4-(3-aminobutyl)phenol in which one of the hydrogens attached to the nitrogen is substituted by a 2-(3,4-dihydroxyphenyl)ethyl group. A beta1-adrenergic receptor agonist that has cardiac stimulant action without evoking vasoconstriction or tachycardia, it is used as the hydrochloride to increase the contractility of the heart in the management of acute heart failure.		3.5920catecholamine;
secondary amine		beta-adrenergic agonist;
cardiotonic drug;
sympathomimetic agent
penbutolol
Penbutolol: A nonselective beta-blocker used as an antihypertensive and an antianginal agent.		3.2310ethanolamines
ribavirin
Rebetron: Rebetron is tradename		3.59201-ribosyltriazole;
aromatic amide;
monocarboxylic acid amide;
primary carboxamide		anticoronaviral agent;
antiinfective agent;
antimetabolite;
antiviral agent;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
amikacin
Amikacin: A broad-spectrum antibiotic derived from KANAMYCIN. It is reno- and oto-toxic like the other aminoglycoside antibiotics.. amikacin : An amino cyclitol glycoside that is kanamycin A acylated at the N-1 position by a 4-amino-2-hydroxybutyryl group.		3.5920alpha-D-glucoside;
amino cyclitol glycoside;
aminoglycoside;
carboxamide		antibacterial drug;
antimicrobial agent;
nephrotoxin
cephradine
Cephradine: A semi-synthetic cephalosporin antibiotic.. cephradine : A first-generation cephalosporin antibiotic with a methyl substituent at position 3, and a (2R)-2-amino-2-cyclohexa-1,4-dien-1-ylacetamido substituent at position 7, of the cephem skeleton.		3.2310beta-lactam antibiotic allergen;
cephalosporin		antibacterial drug
ticrynafen
Ticrynafen: A novel diuretic with uricosuric action. It has been proposed as an antihypertensive agent.. tienilic acid : An aromatic ketone that is 2,3-dichlorophenoxyacetic acid in which the hydrogen at position 4 on the benzene ring is replaced by a thiophenecarbonyl group. A loop diuretic used to treat hypertension, it was withdrawn from the market in 1982 due to links with hepatitis.		3.5920aromatic ether;
aromatic ketone;
dichlorobenzene;
monocarboxylic acid;
thiophenes		antihypertensive agent;
hepatotoxic agent;
loop diuretic
methyldopa
Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.. alpha-methyl-L-dopa : A derivative of L-tyrosine having a methyl group at the alpha-position and an additional hydroxy group at the 3-position on the phenyl ring.		3.5920L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid		alpha-adrenergic agonist;
antihypertensive agent;
hapten;
peripheral nervous system drug;
sympatholytic agent
bezafibrate
[no description available]		2.4620aromatic ether;
monocarboxylic acid amide;
monocarboxylic acid;
monochlorobenzenes		antilipemic drug;
environmental contaminant;
geroprotector;
xenobiotic
sq-11725
Nadolol: A non-selective beta-adrenergic antagonist with a long half-life, used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension. Nadolol is also used for MIGRAINE DISORDERS and for tremor.. nadolol : Nadolol is a diastereoisomeric mixture consisting of equimolar amounts of the four possible 2,3-cis-isomers of 5-[3-(tert-butylamino)-2-hydroxypropoxy]-1,2,3,4-tetrahydronaphthalene-2,3-diol.		2.0510
diltiazem
Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.. diltiazem : A 5-[2-(dimethylamino)ethyl]-2-(4-methoxyphenyl)-4-oxo-2,3,4,5-tetrahydro-1,5-benzothiazepin-3-yl acetate in which both stereocentres have S configuration. A calcium-channel blocker and vasodilator, it is used as the hydrochloride in the management of angina pectoris and hypertension.		4.26505-[2-(dimethylamino)ethyl]-2-(4-methoxyphenyl)-4-oxo-2,3,4,5-tetrahydro-1,5-benzothiazepin-3-yl acetateantihypertensive agent;
calcium channel blocker;
vasodilator agent
vinclozolin
vinclozolin : A racemate comprising equimolar amounts of (R)- and (S)-vinclozolin. A fungicide used mainly on oilseed rape, vines, fruit and vegetables to control Botrytis, Sclerotinia and Monilia spp.. 3-(3,5-dichlorophenyl)-5-ethenyl-5-methyl-2,4-oxazolidinedione : A member of the class of oxazolidinones that is 5-ethenyl-5-methyl-2,4-oxazolidinedione in which the imide hydrogen is replaced by a 3,5-dichlorophenyl group.		2.0510dicarboximide;
dichlorobenzene;
olefinic compound;
oxazolidinone
vecuronium
vecuronium : A 5alpha-androstane compound having 3alpha-acetoxy-, 17beta-acetoxy-, 2beta-piperidino- and 16beta-N-methylpiperidinium substituents.		3.2310acetate ester;
androstane;
quaternary ammonium ion		drug allergen;
muscle relaxant;
neuromuscular agent;
nicotinic antagonist
benoxaprofen
benoxaprofen: RN given refers to parent cpd; structure. benoxaprofen : A monocarboxylic acid that is propionic acid substituted at position 2 by a 2-(4-chlorophenyl)-1,3-benzoxazol-5-yl group. It was used as a non-steroidal anti-inflammatory drug until 1982 when it was withdrawn from the market due to adverse side-effects including liver necrosis, photosensitivity, and carcinogenicity in animals.		3.59201,3-benzoxazoles;
monocarboxylic acid;
monochlorobenzenes		antipsoriatic;
antipyretic;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
hepatotoxic agent;
nephrotoxin;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
protein kinase C agonist
thidiazuron
[no description available]		2.0510ureas
permethrin
hemoglobin Atlanta-Coventry: Leu replaced by Pro at beta75 and Leu deleted at beta141		2.0510cyclopropanecarboxylate ester;
cyclopropanes		agrochemical;
ectoparasiticide;
pyrethroid ester acaricide;
pyrethroid ester insecticide;
scabicide
exifone
[no description available]		3.2310benzophenones
pirfenidone
pirfenidone : A pyridone that is 2-pyridone substituted at positions 1 and 5 by phenyl and methyl groups respectively. An anti-inflammatory drug used for the treatment of idiopathic pulmonary fibrosis.		2.0510pyridoneantipyretic;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
mefloquine
(-)-(11S,2'R)-erythro-mefloquine : An optically active form of [2,8-bis(trifluoromethyl)quinolin-4-yl]-(2-piperidyl)methanol having (-)-(11S,2'R)-erythro-configuration. An antimalarial agent, used in racemic form, which acts as a blood schizonticide; its mechanism of action is unknown.		3.2310[2,8-bis(trifluoromethyl)quinolin-4-yl]-(2-piperidyl)methanolantimalarial
oxfendazole
[no description available]		2.0510benzimidazoles;
carbamate ester;
sulfoxide		antinematodal drug
desogestrel
Desogestrel: A synthetic progestational hormone used often as the progestogenic component of combined oral contraceptive agents (ORAL CONTRACEPTIVES, COMBINED).		2.051017beta-hydroxy steroid;
terminal acetylenic compound		contraceptive drug;
progestin;
synthetic oral contraceptive
muzolimine
Muzolimine: A pyrazole diuretic with long duration and high capacity of action. It was proposed for kidney failure and hypertension but was withdrawn worldwide because of severe neurological effects.		2.0510dichlorobenzene
nitazoxanide
nitazoxanide: a 5-nitrothiazolyl derivative used for a broad range of intestinal parasitic infections including CRYPTOSPORIDIUM and GIARDIA; it is a redox-active nitrothiazolyl-salicylamide prodrug		3.2310benzamides;
carboxylic ester
sufentanil
Sufentanil: An opioid analgesic that is used as an adjunct in anesthesia, in balanced anesthesia, and as a primary anesthetic agent.. sufentanil : An anilide resulting from the formal condensation of the aryl amino group of 4-(methoxymethyl)-N-phenyl-1-[2-(2-thienyl)ethyl]piperidin-4-amine with propanoic acid.		3.2310anilide;
ether;
piperidines;
thiophenes		anaesthesia adjuvant;
intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic
acarbose
[no description available]		3.2310tetrasaccharide derivativeEC 3.2.1.1 (alpha-amylase) inhibitor;
EC 3.2.1.20 (alpha-glucosidase) inhibitor;
geroprotector;
hypoglycemic agent
torsemide
Torsemide: A pyridine and sulfonamide derivative that acts as a sodium-potassium chloride symporter inhibitor (loop diuretic). It is used for the treatment of EDEMA associated with CONGESTIVE HEART FAILURE; CHRONIC RENAL INSUFFICIENCY; and LIVER DISEASES. It is also used for the management of HYPERTENSION.. torasemide : An N-sulfonylurea obtained by formal condensation of [(3-methylphenyl)amino]pyridine-3-sulfonic acid with the free amino group of N-isopropylurea. It is a potent loop diuretic used for the treatment of hypertension and edema in patients with congestive heart failure.		3.2310aminopyridine;
N-sulfonylurea;
secondary amino compound		antihypertensive agent;
loop diuretic
epirubicin
Epirubicin: An anthracycline which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA.		19.88195108aminoglycoside;
anthracycline antibiotic;
anthracycline;
deoxy hexoside;
monosaccharide derivative;
p-quinones;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		antimicrobial agent;
antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
desflurane
Desflurane: A fluorinated ether that is used as a volatile anesthetic for maintenance of general anesthesia.		2.0510organofluorine compoundinhalation anaesthetic
idarubicin
Idarubicin: An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA.		10.6651anthracycline antibiotic;
deoxy hexoside;
monosaccharide derivative
eniluracil
eniluracil: structure in first source; inactivates dihydropyrimidine dehydrogenase		15.72261pyrimidone
nitrosobis(2-oxopropyl)amine
nitrosobis(2-oxopropyl)amine: structure. nitrosobis(2-oxopropyl)amine : A nitrosamine that is iminodiacetone that is substituted by a nitroso group at the N-atom. It induces pancreatic ductal adenocarcinomas in Syrian golden hamsters (other rodents are not susceptible).		2.4620ketone;
nitrosamine		carcinogenic agent
piperacillin
Piperacillin: Semisynthetic, broad-spectrum, AMPICILLIN derived ureidopenicillin antibiotic proposed for PSEUDOMONAS infections. It is also used in combination with other antibiotics.. piperacillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-[(4-ethyl-2,3-dioxopiperazin-1-yl)carboxamido]-2-phenylacetamido group.		3.5920penicillin allergen;
penicillin		antibacterial drug
paroxetine
Paroxetine: A serotonin uptake inhibitor that is effective in the treatment of depression.. paroxetine : A benzodioxole that consists of piperidine bearing 1,3-benzodioxol-5-yloxy)methyl and 4-fluorophenyl substituents at positions 3 and 4 respectively; the (3S,4R)-diastereomer. Highly potent and selective 5-HT uptake inhibitor that binds with high affinity to the serotonin transporter (Ki = 0.05 nM). Ki values are 1.1, 350 and 1100 nM for inhibition of [3H]-5-HT, [3H]-l-NA and [3H]-DA uptake respectively. Displays minimal affinity for alpha1-, alpha2- or beta-adrenoceptors, 5-HT2A, 5-HT1A, D2 or H1 receptors at concentrations below 1000 nM, however displays weak affinity for muscarinic ACh receptors (Ki = 42 nM). Antidepressant and anxiolytic in vivo.		3.5920aromatic ether;
benzodioxoles;
organofluorine compound;
piperidines		antidepressant;
anxiolytic drug;
hepatotoxic agent;
P450 inhibitor;
serotonin uptake inhibitor
captopril
Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.. captopril : A L-proline derivative in which L-proline is substituted on nitrogen with a (2S)-2-methyl-3-sulfanylpropanoyl group. It is used as an anti-hypertensive ACE inhibitor drug.		3.5920alkanethiol;
L-proline derivative;
N-acylpyrrolidine;
pyrrolidinemonocarboxylic acid		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
cefoperazone
Cefoperazone: Semisynthetic broad-spectrum cephalosporin with a tetrazolyl moiety that is resistant to beta-lactamase. It may be used to treat Pseudomonas infections.. cefoperazone : A semi-synthetic parenteral cephalosporin with a tetrazolyl moiety that confers beta-lactamase resistance.		3.5920cephalosporinantibacterial drug
foscarnet sodium
trisodium phosphonoformate : The trisodium salt of phosphonoformic acid. It is used as an antiviral agent in the treatment of cytomegalovirus retinitis (CMV retinitis, an inflamation of the retina that can lead to blindness) and as an alternative to ganciclovir for AIDS patients who require concurrent antiretroviral therapy but are unable to tolerate ganciclovir due to haematological toxicity.		2.0510one-carbon compound;
organic sodium salt		antiviral drug
atracurium
Atracurium: A non-depolarizing neuromuscular blocking agent with short duration of action. Its lack of significant cardiovascular effects and its lack of dependence on good kidney function for elimination provide clinical advantage over alternate non-depolarizing neuromuscular blocking agents.. atracurium : A diester compound consisting of pentane-1,5-diol with both hydroxyls bearing 3-[1-(3,4-dimethoxybenzyl)-6,7-dimethoxy-2-methyl-3,4-dihydroisoquinolinium-2(1H)-yl]propanoyl groups.		3.2310diester;
quaternary ammonium ion		muscle relaxant;
nicotinic antagonist
moxalactam
Moxalactam: Broad- spectrum beta-lactam antibiotic similar in structure to the CEPHALOSPORINS except for the substitution of an oxaazabicyclo moiety for the thiaazabicyclo moiety of certain CEPHALOSPORINS. It has been proposed especially for the meningitides because it passes the blood-brain barrier and for anaerobic infections.. moxalactam : A broad-spectrum oxacephem antibiotic in which the oxazine ring is substituted with a tetrazolylthiomethyl group and the azetidinone ring carries methoxy and 2-carboxy-2-(4-hydroxyphenyl)acetamido substituents.		2.0510cephalosporin;
oxacephem		antibacterial drug
nicorandil
Nicorandil: A derivative of the NIACINAMIDE that is structurally combined with an organic nitrate. It is a potassium-channel opener that causes vasodilatation of arterioles and large coronary arteries. Its nitrate-like properties produce venous vasodilation through stimulation of guanylate cyclase.. nicorandil : A pyrimidinecarboxamide that is nicotinamide in which one of the hydrogens attached to the carboxamide nitrogen is replaced by a 2-(nitrooxy)ethyl group. It has both nitrate-like and ATP-sensitive potassium channel activator properties, and is used for the prevention and treatment of angina pectoris.		2.0510nitrate ester;
pyridinecarboxamide		potassium channel opener;
vasodilator agent
pergolide
Pergolide: A long-acting dopamine agonist which has been used to treat PARKINSON DISEASE and HYPERPROLACTINEMIA but withdrawn from some markets due to potential for HEART VALVE DISEASES.. pergolide : A diamine that is ergoline in which the beta-hydrogen at position 8 is replaced by a (methylthio)methyl group and the hydrogen attached to the piperidine nitrogen (position 6) is replaced by a propyl group. A dopamine D2 receptor agonist which also has D1 and D2 agonist properties, it is used as the mesylate salt in the management of Parkinson's disease, although it was withdrawn from the U.S. and Canadian markets in 2007 due to an increased risk of cardiac valve dysfunction.		3.2310diamine;
methyl sulfide;
organic heterotetracyclic compound		antiparkinson drug;
dopamine agonist
cefadroxil anhydrous
Cefadroxil: Long-acting, broad-spectrum, water-soluble, CEPHALEXIN derivative.. cefadroxil : A cephalosporin bearing methyl and (2R)-2-amino-2-(4-hydroxyphenyl)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton.		3.5920cephalosporinantibacterial drug
encainide
Encainide: One of the ANTI-ARRHYTHMIA AGENTS, it blocks VOLTAGE-GATED SODIUM CHANNELS and slows conduction within the His-Purkinje system and MYOCARDIUM.. encainide : 4-Methoxy-N-phenylbenzamide in which the hydrogen at the 2 position of the phenyl group is substituted by a 2-(1-methylpiperidin-2-yl)ethyl group. A class Ic antiarrhythmic, the hydrochloride was used for the treatment of severe or life-threatening ventricular arrhythmias, but it was associated with increased death rates in patients who had asymptomatic heart rhythm abnormalities after a recent heart attack and was withdrawn from the market.		2.0510benzamides;
piperidines		anti-arrhythmia drug;
sodium channel blocker
talniflumate
talniflumate: an anti-inflammatory molecule for the treatment of cystic fibrosis, chronic obstructive pulmonary disease and asthma		2.0510benzofurans
fialuridine
[no description available]		3.2310
cefaclor anhydrous
Cefaclor: Semisynthetic, broad-spectrum antibiotic derivative of CEPHALEXIN.. cefaclor : A cephalosporin bearing chloro and (R)-2-amino-2-phenylacetamido groups at positions 3 and 7, respectively, of the cephem skeleton.		3.5920cephalosporinantibacterial drug;
drug allergen
alfentanil
Alfentanil: A short-acting opioid anesthetic and analgesic derivative of FENTANYL. It produces an early peak analgesic effect and fast recovery of consciousness. Alfentanil is effective as an anesthetic during surgery, for supplementation of analgesia during surgical procedures, and as an analgesic for critically ill patients.. alfentanil : A member of the class of piperidines that is piperidine having a 2-(4-ethyl-5-oxo-4,5-dihydro-1H-tetrazol-1-yl)ethyl group at the 1-position as well as N-phenylpropanamido- and methoxymethyl groups at the 4-position.		3.2310monocarboxylic acid amide;
piperidines		central nervous system depressant;
intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic;
peripheral nervous system drug
fenoxycarb
fenoxycarb: used against mosquitoes (Diptera:Culicidae); structure given in first source. fenoxycarb : A carbamate ester that is the O-ethyl carbamate of 2-(4-phenoxyphenoxy)ethylamine.		3.2350aromatic ether;
carbamate ester		environmental contaminant;
insecticide;
juvenile hormone mimic;
xenobiotic
miglustat
miglustat: a glucosylceramide synthase inhibitor. miglustat : A hydroxypiperidine that is deoxynojirimycin in which the amino hydrogen is replaced by a butyl group.		3.5920piperidines;
tertiary amino compound		anti-HIV agent;
EC 2.4.1.80 (ceramide glucosyltransferase) inhibitor
haloperidol decanoate
[no description available]		3.2310organic molecular entity
cefotetan
Cefotetan: A semisynthetic cephamycin antibiotic that is administered intravenously or intramuscularly. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative microorganisms.. cefotetan : A semi-synthetic second-generation cephamycin antibiotic with [(1-methyl-1H-tetrazol-5-yl)sulfanyl]methyl, methoxy and {[4-(2-amino-1-carboxy-2-oxoethylidene)-1,3-dithietan-2-yl]carbonyl}amino groups at the 3, 7alpha, and 7beta positions, respectively, of the cephem skeleton. It is resistant to a wide range of beta-lactamases and is active against a broad spectrum of aerobic and anaerobic Gram-positive and Gram-negative microorganisms.		3.5920
lovastatin
Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.. lovastatin : A fatty acid ester that is mevastatin carrying an additional methyl group on the carbobicyclic skeleton. It is used in as an anticholesteremic drug and has been found in fungal species such as Aspergillus terreus and Pleurotus ostreatus (oyster mushroom).		3.5920delta-lactone;
fatty acid ester;
hexahydronaphthalenes;
polyketide;
statin (naturally occurring)		anticholesteremic drug;
antineoplastic agent;
Aspergillus metabolite;
prodrug
flupirtine
flupirtine: RN given refers to parent cpd without isomeric designation		2.0510aminopyridine
tolrestat
tolrestat: RN & structure given in first source		3.2310naphthalenesEC 1.1.1.21 (aldehyde reductase) inhibitor
enoximone
Enoximone: A selective phosphodiesterase inhibitor with vasodilating and positive inotropic activity that does not cause changes in myocardial oxygen consumption. It is used in patients with CONGESTIVE HEART FAILURE.		2.0510aromatic ketone
piritrexim
piritrexim: RN given refers to parent cpd; structure given in first source		2.0510
simvastatin
Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.. simvastatin : A member of the class of hexahydronaphthalenes that is lovastatin in which the 2-methylbutyrate ester moiety has been replaced by a 2,2-dimethylbutyrate ester group. It is used as a cholesterol-lowering and anti-cardiovascular disease drug.		8.0974delta-lactone;
fatty acid ester;
hexahydronaphthalenes;
statin (semi-synthetic)		EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor;
EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor;
ferroptosis inducer;
geroprotector;
prodrug
remoxipride
Remoxipride: An antipsychotic agent that is specific for dopamine D2 receptors. It has been shown to be effective in the treatment of schizophrenia.		2.0510dimethoxybenzene
balsalazide
balsalazide: a mesalamine 5-aminosalicylate prodrug; 99% of ingested drug remains intact through the stomach and is delivered to and activated in the colon; used for inflammatory bowel disease, ulcerative colitis and radiation-induced proctosigmoiditis but avoided in patients with known hypersensitivity reaction to salicylates or mesalamine; structure in first source. balsalazide : A monohydroxybenzoic acid consisting of 5-aminosalicylic acid (mesalazine) linked to 4-aminobenzoyl-beta-alanine via an azo bond.		3.2310
pravastatin
Pravastatin: An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).. pravastatin : A carboxylic ester resulting from the formal condensation of (S)-2-methylbutyric acid with the hydroxy group adjacent to the ring junction of (3R,5R)-7-[(1S,2S,6S,8S,8aR)-6,8-dihydroxy-2-methyl-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]-3,5-dihydroxyheptanoic acid. Derived from microbial transformation of mevastatin, pravastatin is a reversible inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA). The sodium salt is used for lowering cholesterol and preventing cardiovascular disease. It is one of the lower potency statins, but has the advantage of fewer side effects compared with lovastatin and simvastatin.		5.68513-hydroxy carboxylic acid;
carbobicyclic compound;
carboxylic ester;
hydroxy monocarboxylic acid;
secondary alcohol;
statin (semi-synthetic)		anticholesteremic drug;
environmental contaminant;
metabolite;
xenobiotic
cabergoline
Cabergoline: An ergoline derivative and dopamine D2-agonist that inhibits PROLACTIN secretion. It is used in the management of HYPERPROLACTINEMIA, and to suppress lactation following childbirth for medical reasons. Cabergoline is also used in the management of PARKINSON DISEASE.. cabergoline : An N-acylurea that is (8R)-ergoline-8-carboxamide in which the hydrogen attached to the piperidine nitrogen (position 6) is substituted by an allyl group and the hydrogens attached to the carboxamide nitrogen are substituted by a 3-(dimethylamino)propyl group and an N-ethylcarbamoyl group. A dopamine D2 receptor agonist, cabergoline is used in the management of Parkinson's disease and of disorders associated with hyperprolactinaemia.		3.2310N-acylureaantineoplastic agent;
antiparkinson drug;
dopamine agonist
clomazone
clomazone: an herbicide. clomazone : An isoxazolidinone that is 1,2-oxazolidin-3-one substituted by a 2-chlorobenzyl group at position 2 and two methyl groups at position 4.		2.0510isoxazolidinone;
monochlorobenzenes		agrochemical;
carotenoid biosynthesis inhibitor;
environmental contaminant;
herbicide;
xenobiotic
atomoxetine hydrochloride
Atomoxetine Hydrochloride: A propylamine derivative and selective ADRENERGIC UPTAKE INHIBITOR that is used in the treatment of ATTENTION DEFICIT HYPERACTIVITY DISORDER.. atomoxetine hydrochloride : The hydrochloride salt of atomoxetine.		2.0510hydrochlorideadrenergic uptake inhibitor;
antidepressant
atomoxetine
atomoxetine : A secondary amino compound having methyl and 3-(2-methylphenoxy)-3-phenylpropan-1-yl substituents.		3.2310aromatic ether;
secondary amino compound;
toluenes		adrenergic uptake inhibitor;
antidepressant;
environmental contaminant;
xenobiotic
quinapril
Quinapril: A tetrahydroisoquinoline derivative and ANGIOTENSIN CONVERTING ENZYME inhibitor that is used in the treatment of HYPERTENSION and HEART FAILURE.. quinapril : A member of the class of isoquinolines that is (3S)-2-L-alanyl-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid in which the alpha-amino group of the alanyl residue has been substituted by a 1-ethoxycarbonyl-4-phenylbutan-2-yl group (the all-S isomer). A prodrug for quinaprilat (by hydrolysis of the ethyl ester to the corresponding carboxylic acid), it is used as an angiotensin-converting enzyme inhibitor (ACE inhibitor) used (generally as the hydrochloride salt) for the treatment of hypertension and congestive heart failure.		3.8630dicarboxylic acid monoester;
ethyl ester;
isoquinolines;
tertiary carboxamide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
alpidem
[no description available]		3.2310imidazoles
raloxifene hydrochloride
Raloxifene Hydrochloride: A second generation selective estrogen receptor modulator (SERM) used to prevent osteoporosis in postmenopausal women. It has estrogen agonist effects on bone and cholesterol metabolism but behaves as a complete estrogen antagonist on mammary gland and uterine tissue.. raloxifene hydrochloride : A hydrochloride salt resulting from the reaction of equimolar amounts of raloxifene and hydrogen chloride.		2.1310hydrochloridebone density conservation agent;
estrogen antagonist;
estrogen receptor modulator
gepirone
gepirone: RN given refers to parent cpd; structure given in first source		2.0510N-arylpiperazine
mifepristone
Mifepristone: A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.		3.59203-oxo-Delta(4) steroid;
acetylenic compound;
tertiary amino compound		abortifacient;
contraceptive drug;
hormone antagonist;
synthetic oral contraceptive
cilazapril, anhydrous
Cilazapril: One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors) used for hypertension. It is a prodrug that is hydrolyzed after absorption to its main metabolite cilazaprilat.. cilazapril : A pyridazinodiazepine resulting from the formal condensation of the carboxy group of cilazaprilat with ethanol. It is a drug used in the treatment of hypertension and heart failure.		2.0510dicarboxylic acid monoester;
ethyl ester;
pyridazinodiazepine		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
fosphenytoin
fosphenytoin: structure given in first & second source		3.2310imidazolidine-2,4-dione
ranolazine
Ranolazine: An acetanilide and piperazine derivative that functions as a SODIUM CHANNEL BLOCKER and prevents the release of enzymes during MYOCARDIAL ISCHEMIA. It is used in the treatment of ANGINA PECTORIS.. N-(2,6-dimethylphenyl)-2-{4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]piperazin-1-yl}acetamide : An aromatic amide obtained by formal condensation of the carboxy group of 2-{4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]piperazin-1-yl}acetic acid with the amino group of 2,6-dimethylaniline.. ranolazine : A racemate comprising equal amounts of (R)- and (S)-ranolazine. Used for treatment of chronic angina.		3.2310aromatic amide;
monocarboxylic acid amide;
monomethoxybenzene;
N-alkylpiperazine;
secondary alcohol
finasteride
Finasteride: An orally active 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE inhibitor. It is used as a surgical alternative for treatment of benign PROSTATIC HYPERPLASIA.. finasteride : An aza-steroid that is a synthetic drug for the treatment of benign prostatic hyperplasia.		3.23103-oxo steroid;
aza-steroid;
delta-lactam		androgen antagonist;
antihyperplasia drug;
EC 1.3.1.22 [3-oxo-5alpha-steroid 4-dehydrogenase (NADP(+))] inhibitor
esmolol
methyl 3-{4-[2-hydroxy-3-(propan-2-ylamino)propoxy]phenyl}propanoate : A methyl ester that is methyl 3-(4-hydroxyphenyl)propanoate in which the hydrogen attached to the phenolic hydroxy group is substituted by a 2-hydroxy-3-(isopropylamino)propyl group.. esmolol : A racemate comprising equimolar amounts of (R)- and (S)-esmolol. A cardioselective and short-acting beta1 receptor blocker with rapid onset but lacking intrinsic sympathomimetic and membrane-stabilising properties, it is used as the hydrochloride salt in the management of supraventricular arrhythmias, and for the control of hypertension and tachycardia during surgery. While the S enantiomer possesses all of the heart rate control, both enantiomers contribute to lowering blood pressure.		3.2310aromatic ether;
ethanolamines;
methyl ester;
secondary alcohol;
secondary amino compound
sertindole
sertindole : A phenylindole that is 1H-indole which is substituted on the nitrogen by a p-chlorophenyl group, at position 5 by chlorine, and at position 3 by a piperidin-4-yl group, which is itself substituted on the nitrogen by a 2-(2-oxoimidazolidin-1-yl)ethyl group.		2.0510heteroarylpiperidine;
imidazolidinone;
organochlorine compound;
organofluorine compound;
phenylindole		alpha-adrenergic antagonist;
H1-receptor antagonist;
second generation antipsychotic;
serotonergic antagonist
adefovir
adefovir: inhibitor of African swine fever virus. adefovir(1-) : A organophosphonate oxoanion obtained by removal of a proton from the phosphonate group of adefovir, a nucleoside reverse transcriptase inhibitor. It is the major microspecies at pH 7.3 (according to Marvin v 6.2.0.).. adefovir : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens has been replaced by a 2-(6-amino-9H-purin-9-yl)ethoxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(t-butoxycarbonyloxymethyl) ester (dipivoxil ester) prodrug is used to treat chronic hepatitis B viral infection.		3.23106-aminopurines;
ether;
phosphonic acids		antiviral drug;
DNA synthesis inhibitor;
drug metabolite;
HIV-1 reverse transcriptase inhibitor;
nephrotoxic agent
aromasil
[no description available]		9.839517-oxo steroid;
3-oxo-Delta(1),Delta(4)-steroid		antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor;
environmental contaminant;
xenobiotic
sparfloxacin
[no description available]		2.0510fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone
zileuton
[no description available]		3.59201-benzothiophenes;
ureas		anti-asthmatic drug;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
ferroptosis inhibitor;
leukotriene antagonist;
non-steroidal anti-inflammatory drug
clopidogrel
Clopidogrel: A ticlopidine analog and platelet purinergic P2Y receptor antagonist that inhibits adenosine diphosphate-mediated PLATELET AGGREGATION. It is used to prevent THROMBOEMBOLISM in patients with ARTERIAL OCCLUSIVE DISEASES; MYOCARDIAL INFARCTION; STROKE; or ATRIAL FIBRILLATION.. clopidogrel : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group, the methylene hydrogen of which is replaced by a methoxycarbonyl group (the S enantiomer). A P2Y12 receptor antagonist, it is used to inhibit blood clots and prevent heart attacks.		4.0840methyl ester;
monochlorobenzenes;
thienopyridine		anticoagulant;
P2Y12 receptor antagonist;
platelet aggregation inhibitor
cidofovir anhydrous
Cidofovir: An acyclic nucleoside phosphonate that acts as a competitive inhibitor of viral DNA polymerases. It is used in the treatment of RETINITIS caused by CYTOMEGALOVIRUS INFECTIONS and may also be useful for treating HERPESVIRUS INFECTIONS.. cidofovir anhydrous : Cytosine substituted at the 1 position by a 3-hydroxy-2-(phosphonomethoxy)propyl group (S configuration). A nucleoside analogue, it is an injectable antiviral used for the treatment of cytomegalovirus (CMV) retinitis in AIDS patients.		3.5920phosphonic acids;
pyrimidone		anti-HIV agent;
antineoplastic agent;
antiviral drug;
photosensitizing agent
tiagabine
Tiagabine: A nipecotic acid derivative that acts as a GABA uptake inhibitor and anticonvulsant agent. It is used in the treatment of EPILEPSY, for refractory PARTIAL SEIZURES.. tiagabine : A piperidinemonocarboxylic acid that is (R)-nipecotic acid in which the hydrogen attached to the nitrogen has been replaced by a 1,1-bis(3-methyl-2-thienyl)but-1-en-4-yl group. A GABA reuptake inhibitor, it is used (generally as the hydrochloride salt) for the treatment of epilepsy.		3.2310beta-amino acid;
piperidinemonocarboxylic acid;
tertiary amino compound;
thiophenes		anticonvulsant;
GABA reuptake inhibitor
topotecan
Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.. topotecan : A pyranoindolizinoquinoline used as an antineoplastic agent. It is a derivative of camptothecin and works by binding to the topoisomerase I-DNA complex and preventing religation of these 328 single strand breaks.		8.4592pyranoindolizinoquinolineantineoplastic agent;
EC 5.99.1.2 (DNA topoisomerase) inhibitor
bromfenac
bromfenac: bromfenac sodium is the active cpd; structure in first source. bromfenac : Amfenac in which the the hydrogen at the 4 position of the benzoyl group is substituted by bromine. It is used for the management of ocular pain and treatment of postoperative inflammation in patients who have undergone cataract extraction. It was withdrawn from the US market in 1998, following concerns over off-label abuse and hepatic failure.		3.5920aromatic amino acid;
benzophenones;
organobromine compound;
substituted aniline		non-narcotic analgesic;
non-steroidal anti-inflammatory drug
gemcitabine hydrochloride
[no description available]		2.4620hydrochloride;
organofluorine compound		anticoronaviral agent;
antimetabolite;
antineoplastic agent;
antiviral drug;
EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor;
immunosuppressive agent;
radiosensitizing agent
gemcitabine
gemcitabine : A 2'-deoxycytidine having geminal fluoro substituents in the 2'-position. An inhibitor of ribonucleotide reductase, gemcitabine is used in the treatment of various carcinomas, particularly non-small cell lung cancer, pancreatic cancer, bladder cancer and breast cancer.		22.73362145organofluorine compound;
pyrimidine 2'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
antiviral drug;
DNA synthesis inhibitor;
EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor;
environmental contaminant;
immunosuppressive agent;
photosensitizing agent;
prodrug;
radiosensitizing agent;
xenobiotic
ibutilide
ibutilide: RN & structure in first source; RN refers to the fumarate salt		3.2310benzenes;
organic amino compound
aripiprazole
Aripiprazole: A piperazine and quinolone derivative that is used primarily as an antipsychotic agent. It is a partial agonist of SEROTONIN RECEPTOR, 5-HT1A and DOPAMINE D2 RECEPTORS, where it also functions as a post-synaptic antagonist, and an antagonist of SEROTONIN RECEPTOR, 5-HT2A. It is used for the treatment of SCHIZOPHRENIA and BIPOLAR DISORDER, and as an adjunct therapy for the treatment of depression.. aripiprazole : An N-arylpiperazine that is piperazine substituted by a 4-[(2-oxo-1,2,3,4-tetrahydroquinolin-7-yl)oxy]butyl group at position 1 and by a 2,3-dichlorophenyl group at position 4. It is an antipsychotic drug used for the treatment of Schizophrenia, and other mood disorders.		3.2310aromatic ether;
delta-lactam;
dichlorobenzene;
N-alkylpiperazine;
N-arylpiperazine;
quinolone		drug metabolite;
H1-receptor antagonist;
second generation antipsychotic;
serotonergic agonist
remifentanil
Remifentanil: A piperidine-propionate derivative and opioid analgesic structurally related to FENTANYL. It functions as a short-acting MU OPIOID RECEPTOR agonist, and is used as an analgesic during induction or maintenance of general anesthesia, following surgery, during childbirth, and in mechanically ventilated patients under intensive care.. remifentanil : A piperidinecarboxylate ester that is methyl piperidine-4-carboxylate in which the hydrogen attached to the nitrogen is substituted by a 3-methoxy-3-oxopropyl group and the hydrogen at position 4 is substituted the nitrogen of N-propanoylaniline.		3.2310alpha-amino acid ester;
anilide;
monocarboxylic acid amide;
piperidinecarboxylate ester		intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic;
sedative
atorvastatin
[no description available]		3.8730aromatic amide;
dihydroxy monocarboxylic acid;
monofluorobenzenes;
pyrroles;
statin (synthetic)		environmental contaminant;
xenobiotic
lamivudine
[no description available]		3.5920monothioacetal;
nucleoside analogue;
oxacycle;
primary alcohol		allergen;
anti-HBV agent;
antiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor;
HIV-1 reverse transcriptase inhibitor;
prodrug
duloxetine
[no description available]		3.5920duloxetine
irinotecan
[no description available]		23.39419166carbamate ester;
delta-lactone;
N-acylpiperidine;
pyranoindolizinoquinoline;
ring assembly;
tertiary alcohol;
tertiary amino compound		antineoplastic agent;
apoptosis inducer;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
prodrug
valsartan
Valsartan: A tetrazole derivative and ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to treat HYPERTENSION.. valsartan : A monocarboxylic acid amide consisting of L-valine in which the amino hydrogens have been replaced by a pentanoyl and a [2'-(1H-tetrazol-5-yl)biphenyl]-4-yl]methyl group. It exhibits antihypertensive activity.		3.5920biphenylyltetrazole;
monocarboxylic acid amide;
monocarboxylic acid		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
atevirdine
atevirdine: inhibits replication of HIV-1; U 87201E is the methanesulfonate salt		2.0510
ibandronic acid
Ibandronic Acid: Aminobisphosphonate that is a potent inhibitor of BONE RESORPTION. It is used in the treatment of HYPERCALCEMIA associated with malignancy, for the prevention of fracture and bone complications in patients with breast cancer and bone metastases, and for the treatment and prevention of POSTMENOPAUSAL OSTEOPOROSIS.		6.4743
ziprasidone
ziprasidone: a benzisothiazoylpiperazine derivative; has combined dopamine and serotonin receptor antagonist activity; structurally related to tiospirone. ziprasidone : A piperazine compound having 1,2-benzothiazol-3-yl- and 2-(6-chloro-1,3-dihydro-2-oxindol-5-yl)ethyl substituents attached to the nitrogen atoms.		3.58201,2-benzisothiazole;
indolones;
organochlorine compound;
piperazines		antipsychotic agent;
dopaminergic antagonist;
histamine antagonist;
muscarinic antagonist;
psychotropic drug;
serotonergic antagonist
zolmitriptan
zolmitriptan: an antimigraine compound; a serotonin (5HT)-1D receptor agonist. zolmitriptan : A member of the class of tryptamines that is N,N-dimethyltryptamine in which the hydrogen at position 5 of the indole ring has been replaced by a [(4S)-2-oxo-1,3-oxazolidin-4-yl]methyl group. A serotonin 5-HT1 B and D receptor agonist, it is used for the treatment of migraine.		3.5820oxazolidinone;
tryptamines		anti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
adefovir dipivoxil
bis(pivaloyloxymethyl)-9-(2-phosphonylmethoxyethyl)adenine: structure given in first source. adefovir pivoxil : An organic phosphonate that is the dipivoxil ester of adefovir. A prodrug for adefovir, an HIV-1 reverse transcriptase inhibitor, adefovir pivoxil is used to treat chronic hepatitis B viral infection.		2.05106-aminopurines;
carbonate ester;
ether;
organic phosphonate		antiviral drug;
DNA synthesis inhibitor;
HIV-1 reverse transcriptase inhibitor;
nephrotoxic agent;
prodrug
emtricitabine
Emtricitabine: A deoxycytidine analog and REVERSE TRANSCRIPTASE INHIBITOR with antiviral activity against HIV-1 and HEPATITIS B viruses. It is used to treat HIV INFECTIONS.. emtricitabine : An organofluorine compound that is 5-fluorocytosine substituted at the 1 position by a 2-(hydroxymethyl)-1,3-oxathiolan-5-yl group (2R,5S configuration). It is used in combination therapy for the treatment of HIV-1 infection.		3.2310monothioacetal;
nucleoside analogue;
organofluorine compound;
pyrimidone		antiviral drug;
HIV-1 reverse transcriptase inhibitor
tasosartan
tasosartan: angiotensin II antagonist; structure given in first source		3.2310biphenyls
tiludronic acid
tiludronic acid: a bone resorption inhibitor; an antihypercalcemic agent; used in the tratment of Paget's disease; used in the treatment and prevention of osteoporosis; structure given in first source		3.2310organochlorine compound
tirofiban
Tirofiban: Tyrosine analog and PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX antagonist that inhibits PLATELET AGGREGATION and is used in the treatment of ACUTE CORONARY SYNDROME.. tirofiban : A member of the class of piperidines that is L-tyrosine in which a hydrogen attached to the amino group is replaced by a butylsulfonyl group and in which the hydrogen attached to the phenolic hydroxy group is replaced by a 4-(piperidin-4-yl)butyl group.		3.2310L-tyrosine derivative;
piperidines;
sulfonamide		anticoagulant;
fibrin modulating drug;
platelet glycoprotein-IIb/IIIa receptor antagonist
adenosine
quinquefolan B: isolated from roots of Panax quinquefolium L.; RN not in Chemline 10/87; RN from Toxlit		3.8930adenosines;
purines D-ribonucleoside		analgesic;
anti-arrhythmia drug;
fundamental metabolite;
human metabolite;
vasodilator agent
halofuginone
[no description available]		2.0510quinazolines
ortho-cept
ethinyl estradiol-desogestrel combination: Ethinyl Estradiol and Desogestrell given in fixed proportions; has proved to be an effective & well-tolerated oral contraceptive, which improves cycle control & has a beneficial effect on acne		2.0510
trovafloxacin
trovafloxacin: a trifluoronaphthyridone derivative of 7-(3-azabicyclo(3.1.0)hexyl)naphthyridone; has antineoplastic activity. trovafloxacin : A 1,8-naphthyridine derivative that is 4-oxo-1,4-dihydro-1,8-naphthyridine-3-carboxylic acid bearing additional 2,4-difluorophenyl, fluoro and 6-amino-3-azabicyclo[3.1.0]hex-3-yl substituents at positions 1, 6 and 7 respectively. A broad-spectrum antibiotic that was withdrawn from the market due to risk of liver failure.		3.2310
cefprozil
[no description available]		3.5920cephalosporin;
semisynthetic derivative		antibacterial drug
4-[1-[4-[2-(dimethylamino)ethoxy]phenyl]-2-phenylbut-1-enyl]phenol
[no description available]		2.0510stilbenoid
efavirenz
efavirenz: HIV-1 reverse transcriptase inhibitor. efavirenz : 1,4-Dihydro-2H-3,1-benzoxazin-2-one substituted at the 4 position by cyclopropylethynyl and trifluoromethyl groups (S configuration) and at the 6 position by chlorine. A non-nucleoside reverse transcriptase inhibitor with activity against HIV, it is used with other antiretrovirals for combination therapy of HIV infection.		3.5920acetylenic compound;
benzoxazine;
cyclopropanes;
organochlorine compound;
organofluorine compound		antiviral drug;
HIV-1 reverse transcriptase inhibitor
nelfinavir
Nelfinavir: A potent HIV protease inhibitor. It is used in combination with other antiviral drugs in the treatment of HIV in both adults and children.. nelfinavir : An aryl sulfide that is used (as its mesylate salt) for treatment of HIV and also exhibits some anticancer properties.		11.5951aryl sulfide;
benzamides;
organic heterobicyclic compound;
phenols;
secondary alcohol;
tertiary amino compound		antineoplastic agent;
HIV protease inhibitor
doxapram hydrochloride
[no description available]		2.0510hydrochloridecentral nervous system stimulant
fenofibric acid
fenofibric acid: RN given refers to parent cpd without isomeric designation; structure. fenofibric acid : A monocarboxylic acid that is 2-methylpropanoic acid substituted by a 4-(4-chlorobenzoyl)phenoxy group at position 2. It is a metabolite of the drug fenofibrate.		4.0920aromatic ketone;
chlorobenzophenone;
monocarboxylic acid		drug metabolite;
marine xenobiotic metabolite
ursolic acid
[no description available]		7.0710hydroxy monocarboxylic acid;
pentacyclic triterpenoid		geroprotector;
plant metabolite
1,5-anhydroglucitol
1,5-anhydroglucitol: structure. 1,5-anhydro-D-glucitol : An anhydro sugar of D-glucitol.		2.0510anhydro sugarhuman metabolite
betulinic acid
[no description available]		2.0510hydroxy monocarboxylic acid;
pentacyclic triterpenoid		anti-HIV agent;
anti-inflammatory agent;
antimalarial;
antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
plant metabolite
plerixafor
plerixafor: a bicyclam derivate, highly potent & selective inhibitor of HIV-1 & HIV-2. plerixafor : An azamacrocycle consisting of two cyclam rings connected by a 1,4-phenylenebis(methylene) linker. It is a CXCR4 chemokine receptor antagonist and a hematopoietic stem cell mobilizer. It is used in combination with grulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells to the perpheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin's lymphoma and multiple myeloma.		3.2310azacycloalkane;
azamacrocycle;
benzenes;
crown amine;
secondary amino compound;
tertiary amino compound		anti-HIV agent;
antineoplastic agent;
C-X-C chemokine receptor type 4 antagonist;
immunological adjuvant
amprenavir
[no description available]		3.5920carbamate ester;
sulfonamide;
tetrahydrofuryl ester		antiviral drug;
HIV protease inhibitor
oseltamivir
Oseltamivir: An acetamido cyclohexene that is a structural homolog of SIALIC ACID and inhibits NEURAMINIDASE.. oseltamivir : A cyclohexenecarboxylate ester that is the ethyl ester of oseltamivir acid. An antiviral prodrug (it is hydrolysed to the active free carboxylic acid in the liver), it is used to slow the spread of influenza.		3.5920acetamides;
amino acid ester;
cyclohexenecarboxylate ester;
primary amino compound		antiviral drug;
EC 3.2.1.18 (exo-alpha-sialidase) inhibitor;
environmental contaminant;
prodrug;
xenobiotic
o-(6)-methylguanine
O-(6)-methylguanine: structure. 6-O-methylguanine : A methylguanine in which the methyl group is positioned on the oxygen at position 6. Formed in DNA by alkylation of the oxygen atom of guanine, most often by N-nitroso compounds and sometimes due to methylation by other compounds such as endogenous S-adenosylmethionine, it base-pairs to thymine rather than cytidine, causing a G:C to A:T transition in DNA.. methylguanine : A 2-aminopurine that is guanine bearing a single methyl substituent.		3.9911methylguaninemutagen
glutathione disulfide
Glutathione Disulfide: A GLUTATHIONE dimer formed by a disulfide bond between the cysteine sulfhydryl side chains during the course of being oxidized.		2.0510glutathione derivative;
organic disulfide		Escherichia coli metabolite;
mouse metabolite
4-nitrobenzylthioinosine
4-nitrobenzylthioinosine: inhibitor of nucleoside transport; acts on ENT1		2.0110purine nucleoside
histamine phosphate
histamine phosphate : A phosphate salt that is the diphosphate salt of histamine.		3.2310phosphate salthistamine agonist
cephalosporin c
cephalosporin C: RN given refers to parent cpd; structure in Merck, 9th ed, #1937. cephalosporin C : A cephalosporin antibiotic carrying a 3-acetoxymethyl substituent and a 6-oxo-N(6)-L-lysino group at position 7.		2.2110cephalosporinfungal metabolite
tilbroquinol
[no description available]		3.2310organohalogen compound;
quinolines
bendamustine
[no description available]		3.5920benzimidazoles
erdosteine
[no description available]		2.0510N-acyl-amino acid
droxicam
droxicam: structure given in first source. droxicam : An organic heterotricyclic compound that is 2H,5H-[1,3]oxazino[5,6-c][1,2]benzothiazine-2,4(3H)-dione 6,6-dioxide substituted at positions 3 and 5 by pyridin-2-yl and methyl groups respectively. A prodrug of piroxicam, it is used for the relief of pain and inflammation in musculoskeletal disorders such as rheumatoid arthritis and osteoarthritis.		3.2310organic heterotricyclic compound;
pyridines		cyclooxygenase 1 inhibitor;
hepatotoxic agent;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
platelet aggregation inhibitor;
prodrug
trofosfamide
trofosfamide: cyclophosphamide analog; structure		2.0310ifosfamides
ebrotidine
ebrotidine: an H2-receptor antagonist and gastric mucosa protector		3.2310sulfonamide
mizolastine
[no description available]		2.0510benzimidazoles
emitefur
Emitefur: structure given in first source		4.6430
intoplicine
intoplicine: structure in first source		2.0510pyridoindole
repaglinide
[no description available]		3.2310piperidines
telmisartan
Telmisartan: A biphenyl compound and benzimidazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION.. telmisartan : A member of the class of benzimidazoles used widely in the treatment of hypertension.		3.5920benzimidazoles;
biphenyls;
carboxybiphenyl		angiotensin receptor antagonist;
antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
environmental contaminant;
xenobiotic
dexfenfluramine
Dexfenfluramine: The S-isomer of FENFLURAMINE. It is a serotonin agonist and is used as an anorectic. Unlike fenfluramine, it does not possess any catecholamine agonist activity.. (S)-fenfluramine : The S-enantiomer of fenfluramine. It stimulates the release of serotonin and selectively inhibits its reuptake, but unlike fenfluramine it does not possess catecholamine agonist activity. It was formerly given by mouth as the hydrochloride in the treatment of obesity, but, like fenfluramine, was withdrawn wolrdwide following reports of valvular heart defects.		2.0510fenfluramineappetite depressant;
serotonergic agonist;
serotonin uptake inhibitor
2-methoxyestradiol
2-methoxy-17beta-estradiol : A 17beta-hydroxy steroid, being 17beta-estradiol methoxylated at C-2.		2.051017beta-hydroxy steroid;
3-hydroxy steroid		angiogenesis modulating agent;
antimitotic;
antineoplastic agent;
human metabolite;
metabolite;
mouse metabolite
triazoles
Triazoles: Heterocyclic compounds containing a five-membered ring with two carbon atoms and three nitrogen atoms with the molecular formula C2H3N3.. triazoles : An azole in which the five-membered heterocyclic aromatic skeleton contains three N atoms and two C atoms.		7.311301,2,3-triazole
3-fluoropyruvate
3-fluoropyruvate: a substrate for E coli pyruvate dehydrogenase; structure; RN given refers to parent cpd. 3-fluoropyruvic acid : A pyruvic acid derivative having a 3-fluoro substituent.. 3-fluoropyruvate : The anion of 3-fluoropyruvic acid.		3.23102-oxo monocarboxylic acid;
organofluorine compound
medetomidine
Medetomidine: An agonist of RECEPTORS, ADRENERGIC ALPHA-2 that is used in veterinary medicine for its analgesic and sedative properties. It is the racemate of DEXMEDETOMIDINE.		2.0510imidazoles
fluorodeoxyglucose f18
Fluorodeoxyglucose F18: The compound is given by intravenous injection to do POSITRON-EMISSION TOMOGRAPHY for the assessment of cerebral and myocardial glucose metabolism in various physiological or pathological states including stroke and myocardial ischemia. It is also employed for the detection of malignant tumors including those of the brain, liver, and thyroid gland. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1162)		9.12862-deoxy-2-((18)F)fluoro-D-glucose;
2-deoxy-2-fluoro-aldehydo-D-glucose
sertraline
Sertraline: A selective serotonin uptake inhibitor that is used in the treatment of depression.. sertraline : A member of the class of tetralins that is tetralin which is substituted at positions 1 and 4 by a methylamino and a 3,4-dichlorophenyl group, respectively (the S,S diastereoisomer). A selective serotonin-reuptake inhibitor (SSRI), it is administered orally as the hydrochloride salt as an antidepressant for the treatment of depression, obsessive-compulsive disorder, panic disorder and post-traumatic stress disorder.		3.930dichlorobenzene;
secondary amino compound;
tetralins		antidepressant;
serotonin uptake inhibitor
picosulfate sodium
picosulfate sodium: contains two active ingredients, sodium picosulfate and magnesium citrate, which are both laxatives; structure		2.0510aryl sulfate;
pyridines
befuraline
befuraline: RN given refers to parent cpd; structure		2.0510
zoledronic acid
Zoledronic Acid: An imidobisphosphonate inhibitor of BONE RESORPTION that is used for the treatment of malignancy-related HYPERCALCEMIA; OSTEITIS DEFORMANS; and OSTEOPOROSIS.. zoledronic acid : An imidazole compound having a 2,2-bis(phosphono)-2-hydroxyethane-1-yl substituent at the 1-position.		3.58201,1-bis(phosphonic acid);
imidazoles		bone density conservation agent
dienogest
[no description available]		2.051017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
aliphatic nitrile;
steroid hormone		progesterone receptor agonist;
progestin;
synthetic oral contraceptive
5-nitrouracil
5-nitrouracil: prevents thymidine degradation. 5-nitrouracil : A C-nitro compound consisting of uracil having a nitro group at the 5-position.		7.2510C-nitro compound
5-fluoropyrimidine
[no description available]		5.470
5-iodouracil
5-iodouracil: RN given refers to parent cpd. 5-iodouracil : An organoiodine compound consisting of uracil having an iodo substituent at the 5-position.		2.0110organoiodine compoundantimetabolite
morphazinamide
morphazinamide: RN given refers to parent cpd; RN in Chemline for mono-HCL: 1473-73-0; structure in Merck Index		2.0510morpholines;
pyrazines;
secondary carboxamide
nefiracetam
[no description available]		2.0510organonitrogen compound;
organooxygen compound
acamprosate
Acamprosate: Structural analog of taurine that is used for the prevention of relapse in individuals with ALCOHOLISM.. acamprosate : An organosulfonic acid that is propane-1-sulfonic acid substituted by an acetylamino group at position 3.		3.2310acetamides;
organosulfonic acid		environmental contaminant;
neurotransmitter agent;
xenobiotic
isaxonine
isaxonine: promotes nerve growth		3.2310aminopyrimidine
nebivolol
2,2'-iminobis[1-(6-fluoro-3,4-dihydro-2H-chromen-2-yl)ethanol] : A member of the class of chromanes that is 2,2'-iminodiethanol in which one hydrogen attached to each hydroxy-bearing carbon is replaced by a 6-fluorochroman-2-yl group.		3.2310chromanes;
diol;
organofluorine compound;
secondary alcohol;
secondary amino compound
uk 68798
[no description available]		3.2310aromatic ether;
sulfonamide;
tertiary amino compound		anti-arrhythmia drug;
potassium channel blocker
hp 873
iloperidone: an atypical, negative symptom antipsychotic agent. iloperidone : A member of the class of piperidines that is the 4-acetyl-2-methoxyphenyl ether of 3-(piperidin-1-yl)propan-1-ol which is substituted at position 4 of the piperidine ring by a 6-fluoro-1,2-benzoxazol-3-yl group. A member of the group of second generation antipsychotics (also known as an atypical antipsychotics), it is used for the treatment of schizophrenia.		3.23101,2-benzoxazoles;
aromatic ether;
aromatic ketone;
methyl ketone;
monoamine;
organofluorine compound;
piperidines;
tertiary amino compound		dopaminergic antagonist;
second generation antipsychotic;
serotonergic antagonist
dexrazoxane
Dexrazoxane: The (+)-enantiomorph of razoxane.		3.5920razoxaneantineoplastic agent;
cardiovascular drug;
chelator;
immunosuppressive agent
fenoxypropazine
[no description available]		3.2310aromatic ether
voriconazole
Voriconazole: A triazole antifungal agent that specifically inhibits STEROL 14-ALPHA-DEMETHYLASE and CYTOCHROME P-450 CYP3A.. voriconazole : A triazole-based antifungal agent used for the treatment of esophageal candidiasis, invasive pulmonary aspergillosis, and serious fungal infections caused by Scedosporium apiospermum and Fusarium spp. It is an inhibitor of cytochrome P450 2C9 (CYP2C9) and CYP3A4.		3.5920conazole antifungal drug;
difluorobenzene;
pyrimidines;
tertiary alcohol;
triazole antifungal drug		P450 inhibitor
aceclofenac
[no description available]		3.2310amino acid;
carboxylic ester;
dichlorobenzene;
monocarboxylic acid;
secondary amino compound		EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
nitrefazole
[no description available]		3.2310imidazoles
cyclobutyrol
cyclobutyrol: RN given refers to parent cpd; structure. cyclobutyrol : A hydroxy monocarboxylic acid in which the hydroxy group is geminal to a 1-carboxypropyl group on a cyclohexane ring.		2.0510hydroxy monocarboxylic acidbile therapy drug
terlipressin
terlivaz: first FDA approved injection to improve kidney function in adults with hepatorenal syndrome (HRS) with rapid reduction in kidney function.		2.0510polypeptide
ubenimex
ubenimex: growth inhibitor		2.1310
isoflavone
[no description available]		2.0510isoflavones
clevudine
[no description available]		2.0510
9-aminocamptothecin
[no description available]		3.0910pyranoindolizinoquinoline
picropodophyllin
picropodophyllin: isolated from American May apple (Podophyllum); inhibits IGF-I autophosphorylation without interfering with tyrosine kinase activity. picropodophyllotoxin : An organic heterotetracyclic compound that has a furonaphthodioxole skeleton bearing 3,4,5-trimethoxyphenyl and hydroxy substituents.		3.2310furonaphthodioxole;
lignan;
organic heterotetracyclic compound		antineoplastic agent;
insulin-like growth factor receptor 1 antagonist;
plant metabolite;
tyrosine kinase inhibitor
tetrandrine
tetrandrine: a bisbenzylisoquinoline that exhibits antifibrogenic activity		2.0510bisbenzylisoquinoline alkaloid;
isoquinolines
3-deazaneplanocin
3-deazaneplanocin: S-adenosylhomocysteine hydrolase antagonist		2.1510
doripenem
Doripenem: A carbapenem derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of infections such as HOSPITAL-ACQUIRED PNEUMONIA, and complicated intra-abdominal or urinary-tract infections, including PYELONEPHRITIS.		3.2310carbapenems
amperozide
amperozide : A member of the class of ureas that is urea in which three of the four hydrogens are replaced by ethyl and 4-[4,4-bis(4-fluorophenyl)butyl]piperazin-1-yl groups. An atypical antipsychotic which was in clinical development for the treatment of schizophrenia and substance-related disorders. It is a potent 5-HT2A antagonist and used in veterinary medicine because of its sedative effect on pigs.		2.0510diarylmethane;
monofluorobenzenes;
N-alkylpiperazine;
secondary carboxamide;
ureas		anxiolytic drug;
dopamine uptake inhibitor;
geroprotector;
second generation antipsychotic;
serotonergic antagonist
atovaquone
Atovaquone: A hydroxynaphthoquinone that has antimicrobial activity and is being used in antimalarial protocols.. atovaquone : A naphthoquinone compound having a 4-(4-chlorophenyl)cyclohexyl group at the 2-position and a hydroxy substituent at the 3-position.		3.2310hydroxy-1,2-naphthoquinone
citronellal, (r)-isomer
(R)-(+)-citronellal : The (3R)-stereoisomer of 3,7-dimethyloct-6-enal (citronellal).		2.0510citronellal
4-nitrophenyl butyrate
p-nitrophenyl butyrate : A butyrate ester resulting from the formal condensation of the hydroxy group of 4-nitrophenol with the carboxy group of butyric acid.		2.0510butyrate ester;
C-nitro compound
rivastigmine
[no description available]		3.5520carbamate ester;
tertiary amino compound		cholinergic drug;
EC 3.1.1.8 (cholinesterase) inhibitor;
neuroprotective agent
frovatriptan
[no description available]		3.2310carbazoles
eletriptan
eletriptan: 5-HT(1B/1D) receptor agonist; structure in first source. eletriptan : An N-alkylpyrrolidine, that is N-methylpyrrolidine in which the pro-R hydrogen at position 2 is replaced by a {5-[2-(phenylsulfonyl)ethyl]-1H-indol-3-yl}methyl group.		3.2310indoles;
N-alkylpyrrolidine;
sulfone		non-steroidal anti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
rosiglitazone
[no description available]		3.5920aminopyridine;
thiazolidinediones		EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
insulin-sensitizing drug
5-cyanouracil
[no description available]		2.0110
bexarotene
[no description available]		3.5920benzoic acids;
naphthalenes;
retinoid		antineoplastic agent
clarithromycin
Clarithromycin: A semisynthetic macrolide antibiotic derived from ERYTHROMYCIN that is active against a variety of microorganisms. It can inhibit PROTEIN SYNTHESIS in BACTERIA by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation.. clarithromycin : The 6-O-methyl ether of erythromycin A, clarithromycin is a macrolide antibiotic used in the treatment of respiratory-tract, skin and soft-tissue infections. It is also used to eradicate Helicobacter pylori in the treatment of peptic ulcer disease. It prevents bacteria from growing by interfering with their protein synthesis.		3.5920macrolide antibioticantibacterial drug;
environmental contaminant;
protein synthesis inhibitor;
xenobiotic
nicotine
(S)-nicotine : A 3-(1-methylpyrrolidin-2-yl)pyridine in which the chiral centre has S-configuration. The naturally occurring and most active enantiomer of nicotine, isolated from Nicotiana tabacum.		2.05103-(1-methylpyrrolidin-2-yl)pyridineanxiolytic drug;
biomarker;
immunomodulator;
mitogen;
neurotoxin;
nicotinic acetylcholine receptor agonist;
peripheral nervous system drug;
phytogenic insecticide;
plant metabolite;
psychotropic drug;
teratogenic agent;
xenobiotic
moexipril
[no description available]		3.2310peptide
homocysteine
Homocysteine: A thiol-containing amino acid formed by a demethylation of METHIONINE.. homocysteine : A sulfur-containing amino acid consisting of a glycine core with a 2-mercaptoethyl side-chain.. L-homocysteine : A homocysteine that has L configuration.		4.3722amino acid zwitterion;
homocysteine;
serine family amino acid		fundamental metabolite;
mouse metabolite
sarsasapogenin
[no description available]		2.2510sapogenin
mci 9038
[no description available]		3.2310peptide
lopinavir
[no description available]		2.0510amphetamines;
dicarboxylic acid diamide		anticoronaviral agent;
antiviral drug;
HIV protease inhibitor
glucuronic acid
Glucuronic Acid: A sugar acid formed by the oxidation of the C-6 carbon of GLUCOSE. In addition to being a key intermediate metabolite of the uronic acid pathway, glucuronic acid also plays a role in the detoxification of certain drugs and toxins by conjugating with them to form GLUCURONIDES.. D-glucuronic acid : The D-enantiomer of glucuronic acid.. D-glucopyranuronic acid : A D-glucuronic acid in cyclic pyranose form.		3.0840D-glucuronic acidalgal metabolite
5-vinyluracil
5-vinyluracil: RN given refers to unlabeled parent cpd		2.0110
diosgenin
[no description available]		2.25103beta-sterol;
hexacyclic triterpenoid;
sapogenin;
spiroketal		antineoplastic agent;
antiviral agent;
apoptosis inducer;
metabolite
fulvestrant
Fulvestrant: An estradiol derivative and estrogen receptor antagonist that is used for the treatment of estrogen receptor-positive, locally advanced or metastatic breast cancer.. fulvestrant : A 3-hydroxy steroid that is 17beta-estradiol in which the 7alpha hydrogen has been replaced by a nonyl group in which one of the hydrogens of the terminal methyl has been replaced by a (4,4,5,5,5-pentafluoropentyl)sulfinyl group. An estrogen receptor antagonist, it is used in the treatment of breast cancer.		10.112417beta-hydroxy steroid;
3-hydroxy steroid;
organofluorine compound;
sulfoxide		antineoplastic agent;
estrogen antagonist;
estrogen receptor antagonist
uftoral
UFT(R) drug: a drug containing tegafur and uracil; a biochemical modulator of 5-fluorouracil; used for postoperative chemotherapy of colon cancer; reported to cause severe liver injury; do not confuse with 1-UFT protocol		6.85110
yttrium radioisotopes
Yttrium Radioisotopes: Unstable isotopes of yttrium that decay or disintegrate emitting radiation. Y atoms with atomic weights 82-88 and 90-96 are radioactive yttrium isotopes.		6.1961
vitamin b 6
Vitamin B 6: VITAMIN B 6 refers to several PICOLINES (especially PYRIDOXINE; PYRIDOXAL; & PYRIDOXAMINE) that are efficiently converted by the body to PYRIDOXAL PHOSPHATE which is a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, and aminolevulinic acid. During transamination of amino acids, pyridoxal phosphate is transiently converted into PYRIDOXAMINE phosphate. Although pyridoxine and Vitamin B 6 are still frequently used as synonyms, especially by medical researchers, this practice is erroneous and sometimes misleading (EE Snell; Ann NY Acad Sci, vol 585 pg 1, 1990). Most of vitamin B6 is eventually degraded to PYRIDOXIC ACID and excreted in the urine.		2.0510
sr141716
[no description available]		2.0510amidopiperidine;
carbohydrazide;
dichlorobenzene;
monochlorobenzenes;
pyrazoles		anti-obesity agent;
appetite depressant;
CB1 receptor antagonist
bosentan anhydrous
Bosentan: A sulfonamide and pyrimidine derivative that acts as a dual endothelin receptor antagonist used to manage PULMONARY HYPERTENSION and SYSTEMIC SCLEROSIS.		3.5920primary alcohol;
pyrimidines;
sulfonamide		antihypertensive agent;
endothelin receptor antagonist
selenomethionine
[no description available]		2.0510amino acid zwitterion;
selenomethionine		plant metabolite
perindopril
Perindopril: An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.. perindopril : An alpha-amino acid ester that is the ethyl ester of N-{(2S)-1-[(2S,3aS,7aS)-2-carboxyoctahydro-1H-indol-1-yl]-1-oxopropan-2-yl}-L-norvaline		3.5920alpha-amino acid ester;
dicarboxylic acid monoester;
ethyl ester;
organic heterobicyclic compound		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
fingolimod
fingolimod : An aminodiol that consists of propane-1,3-diol having amino and 2-(4-octylphenyl)ethyl substituents at the 2-position. It is a sphingosine 1-phosphate receptor modulator used for the treatment of relapsing-remitting multiple sclerosis. A prodrug, fingolimod is phosphorylated by sphingosine kinase to active metabolite fingolimod-phosphate, a structural analogue of sphingosine 1-phosphate.		2.0510aminodiol;
primary amino compound		antineoplastic agent;
CB1 receptor antagonist;
immunosuppressive agent;
prodrug;
sphingosine-1-phosphate receptor agonist
ecteinascidin 743
[no description available]		3.8521acetate ester;
azaspiro compound;
bridged compound;
hemiaminal;
isoquinoline alkaloid;
lactone;
organic heteropolycyclic compound;
organic sulfide;
oxaspiro compound;
polyphenol;
tertiary amino compound		alkylating agent;
angiogenesis modulating agent;
anti-inflammatory agent;
antineoplastic agent;
marine metabolite
tadalafil
[no description available]		3.2310benzodioxoles;
pyrazinopyridoindole		EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
paliperidone
3-{2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl}-9-hydroxy-2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one : A member of the class of pyridopyrimidines that is 9-hydroxy-2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one carrying an additional 2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl group at position 2.. paliperidone : A racemate comprising equimolar amounts of (R)- and (S)-paliperidone. Paliperidone is the primary active metabolite of the older antipsychotic risperidone and is used for treatment of schizophrenia.		3.23101,2-benzoxazoles;
heteroarylpiperidine;
organofluorine compound;
pyridopyrimidine;
secondary alcohol
nitisinone
[no description available]		3.5920(trifluoromethyl)benzenes;
C-nitro compound;
cyclohexanones;
mesotrione		EC 1.13.11.27 (4-hydroxyphenylpyruvate dioxygenase) inhibitor
marimastat
marimastat: a matrix metalloproteinase inhibitor active in patients with advanced carcinoma of the pancreas, prostate, or ovary. marimastat : A secondary carboxamide resulting from the foraml condensation of the carboxy group of (2R)-2-[(1S)-1-hydroxy-2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the alpha-amino group of N,3-dimethyl-L-valinamide.		3.5320hydroxamic acid;
secondary carboxamide		antineoplastic agent;
matrix metalloproteinase inhibitor
clofarabine
[no description available]		3.8630adenosines;
organofluorine compound		antimetabolite;
antineoplastic agent
pramipexole
Pramipexole: A benzothiazole derivative and dopamine agonist with antioxidant properties that is used in the treatment of PARKINSON DISEASE and RESTLESS LEGS SYNDROME.. pramipexole : A member of the class of benzothiazoles that is 4,5,6,7-tetrahydro-1,3-benzothiazole in which the hydrogens at the 2 and 6-pro-S-positions are substituted by amino and propylamino groups, respectively.		3.2310benzothiazoles;
diamine		antidyskinesia agent;
antiparkinson drug;
dopamine agonist;
radical scavenger
valdecoxib
[no description available]		3.2310isoxazoles;
sulfonamide		antipyretic;
antirheumatic drug;
cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
carglumic acid
carglumic acid: carglumic acid could be helpful in lowering plasma ammonia levels over 400 micromol/L more rapidly. carglumic acid : A urea that is the N-carbamoyl derivative of L-glutamic acid. An orphan drug used to treat a deficiency in the enzyme N-acetylglutamate synthase, which leads to acute hyperammonaemia.		2.1710N-acyl-L-glutamic acid;
ureas		carbamylphosphate synthetase I activator;
orphan drug
mitiglinide
mitiglinide: a rapid and short-acting hypoglycemic agent; acts on sulfonylurea receptor closing KATP channels; considered one of the glinides-an imprecise grouping; structure given in first source		2.0510benzenes;
monocarboxylic acid
5-fluorodihydrouracil
5-fluorodihydrouracil: metabolite of 5-fluorouracil; RN given refers to parent cpd		7.0510pyrimidone
imatinib mesylate
imatinib methanesulfonate : A methanesulfonate (mesylate) salt that is the monomesylate salt of imatinib. Used for treatment of chronic myelogenous leukemia and gastrointestinal stromal tumours.		9.91145methanesulfonate saltanticoronaviral agent;
antineoplastic agent;
apoptosis inducer;
tyrosine kinase inhibitor
almotriptan
almotriptan : An indole compound having a 2-(dimethylamino)ethyl group at the 3-position and a (pyrrolidin-1-ylsulfonyl)methyl group at the 5-position.		3.2310indoles;
sulfonamide;
tertiary amine		non-steroidal anti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
mk 0663
[no description available]		4.4122bipyridines;
organochlorine compound;
sulfone		cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
gefitinib
[no description available]		11.22236aromatic ether;
monochlorobenzenes;
monofluorobenzenes;
morpholines;
quinazolines;
secondary amino compound;
tertiary amino compound		antineoplastic agent;
epidermal growth factor receptor antagonist
n(6)-(3-iodobenzyl)-5'-n-methylcarboxamidoadenosine
N(6)-(3-iodobenzyl)-5'-N-methylcarboxamidoadenosine: structure given in first source; a selective A(3) adenosine receptor agonist. 3-iodobenzyl-5'-N-methylcarboxamidoadenosine : A derivative of adenosine in which the 5'-hydroxymethyl group is replaced by N-ethylcarboxamido and one of the hydrogens of the exocyclic amino function is substituted by a 3-iodobenzyl group.		2.0510adenosines;
monocarboxylic acid amide;
organoiodine compound		adenosine A3 receptor agonist
desloratadine
desloratadine: major metabolite of loratadine. desloratadine : Loratadine in which the ethoxycarbonyl group attached to the piperidine ring is replaced by hydrogen. The major metabolite of loratidine, desloratadine is an antihistamine which is used for the symptomatic relief of allergic conditions including rhinitis and chronic urticaria. It does not readily enter the central nervous system, so does not cause drowsiness.		3.2310benzocycloheptapyridineanti-allergic agent;
cholinergic antagonist;
drug metabolite;
H1-receptor antagonist
desvenlafaxine
O-desmethylvenlafaxine : A tertiary amino compound that is N,N-dimethylethanamine substituted at position 1 by a 1-hydroxycyclohexyl and 4-hydroxyphenyl group. It is a metabolite of the drug venlafaxine.		3.2310cyclohexanols;
phenols;
tertiary amino compound		antidepressant;
drug metabolite;
marine xenobiotic metabolite
methotrexate
[no description available]		14.354012dicarboxylic acid;
monocarboxylic acid amide;
pteridines		abortifacient;
antimetabolite;
antineoplastic agent;
antirheumatic drug;
dermatologic drug;
DNA synthesis inhibitor;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
immunosuppressive agent
tamsulosin
[no description available]		3.23105-(2-{[2-(2-ethoxyphenoxy)ethyl]amino}propyl)-2-methoxybenzenesulfonamidealpha-adrenergic antagonist;
antineoplastic agent
rufinamide
rufinamide: for treatment of Lennox-Gastaut syndrome; structure in first source		3.2310aromatic amide;
heteroarene
antiprimod
azaspirane: structure given in first source		2.0510
sulbactam
[no description available]		2.0510penicillanic acids
olmesartan medoxomil
Olmesartan Medoxomil: An ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to manage HYPERTENSION.		3.5920biphenyls
dexpanthenol
dexpanthenol: The alcohol of pantothenic acid		3.2310amino alcohol;
monocarboxylic acid amide		cholinergic drug;
provitamin
fosamprenavir
fosamprenavir: a prodrug of the protease inhibitor amprenavir. fosamprenavir : A sulfonamide with a structure based on that of sulfanilamide substituted on the sulfonamide nitrogen by a (2R,3S)-4-phenyl-2-(phosphonooxy)-3-({[(3S)-tetrahydrofuran-3-yloxy]carbonyl}amino)butyl group. It is a pro-drug of the HIV protease inhibitor and antiretroviral drug amprenavir.		3.2310sulfonamideprodrug
c 1311
C 1311: an imidazoacridinone; arrests cell-cycle progression in the G2 phase of L1210 cells; structure given in first source		2.0310
ilomastat
CS 610: matrix metalloproteinase inhibitor; structure in first source. ilomastat : An N-acyl-amino acid obtained by formal condensation of the carboxy group of (2R)-2-[2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the amino group of N-methyl-L-tryptophanamide. A cell permeable broad-spectrum matrix metalloproteinase (MMP) inhibitor		2.0510hydroxamic acid;
L-tryptophan derivative;
N-acyl-amino acid		anti-inflammatory agent;
antibacterial agent;
antineoplastic agent;
EC 3.4.24.24 (gelatinase A) inhibitor;
neuroprotective agent
febuxostat
Febuxostat: A thiazole derivative and inhibitor of XANTHINE OXIDASE that is used for the treatment of HYPERURICEMIA in patients with chronic GOUT.. febuxostat : A 1,3-thiazolemonocarboxylic acid that is 4-methyl-1,3-thiazole-5-carboxylic acid which is substituted by a 3-cyano-4-(2-methylpropoxy)phenyl group at position 2. It is an orally-active, potent, and selective xanthine oxidase inhibitor used for the treatment of chronic hyperuricaemia in patients with gout.		3.23101,3-thiazolemonocarboxylic acid;
aromatic ether;
nitrile		EC 1.17.3.2 (xanthine oxidase) inhibitor
escitalopram
Escitalopram: S-enantiomer of CITALOPRAM. Belongs to a class of drugs known as SELECTIVE SEROTONIN REUPTAKE INHIBITORS, used to treat depression and generalized anxiety disorder.. escitalopram : A 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile that has S-configuration at the chiral centre. It is the active enantiomer of citalopram.		3.23101-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrileantidepressant;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
10-propargyl-10-deazaaminopterin
10-propargyl-10-deazaaminopterin: structure in first source. pralatrexate : A pteridine that is the N-4-[1-(2,4-diaminopteridin-6-yl)pent-4-yn-2-yl]benzoyl derivative of L-glutamic acid. Used for treatment of Peripheral T-Cell Lymphoma, an aggressive form of non-Hodgkins lymphoma.		3.2310N-acyl-L-glutamic acid;
pteridines;
terminal acetylenic compound		antimetabolite;
antineoplastic agent;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor
docetaxel
[no description available]		2.4620hydrate;
secondary alpha-hydroxy ketone		antineoplastic agent
docetaxel anhydrous
Docetaxel: A semisynthetic analog of PACLITAXEL used in the treatment of locally advanced or metastatic BREAST NEOPLASMS and NON-SMALL CELL LUNG CANCER.. docetaxel anhydrous : A tetracyclic diterpenoid that is paclitaxel with the N-benzyloxycarbonyl group replaced by N-tert-butoxycarbonyl, and the acetoxy group at position 10 replaced by a hydroxy group.		22.59341175secondary alpha-hydroxy ketone;
tetracyclic diterpenoid		antimalarial;
antineoplastic agent;
photosensitizing agent
perifosine
[no description available]		9.7821ammonium betaine;
phospholipid		EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
irofulven
irofulven: structure in first source		9.3822cyclohexenones
atazanavir
atazanavir : A heavily substituted carbohydrazide that is an antiretroviral drug of the protease inhibitor (PI) class used to treat infection of human immunodeficiency virus (HIV).		3.5920carbohydrazideantiviral drug;
HIV protease inhibitor
lonafarnib
lonafarnib: inhibitor of farnesyl protein transferase. lonafarnib : A 4-{2-[4-(3,10-dibromo-8-chloro-6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridin-11-yl)piperidin-1-yl]-2-oxoethyl}piperidine-1-carboxamide that has R configuration. It is used as oral farnesyltransferase inhibitor.		3.11104-{2-[4-(3,10-dibromo-8-chloro-6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridin-11-yl)piperidin-1-yl]-2-oxoethyl}piperidine-1-carboxamideantineoplastic agent;
EC 2.5.1.58 (protein farnesyltransferase) inhibitor
5-vinyl-2'-deoxyuridine
5-vinyl-2'-deoxyuridine: structure		3.411
levofloxacin
Levofloxacin: The L-isomer of Ofloxacin.. levofloxacin : An optically active form of ofloxacin having (S)-configuration; an inhibitor of bacterial topoisomerase IV and DNA gyrase.		3.59209-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid;
fluoroquinolone antibiotic;
quinolone antibiotic		antibacterial drug;
DNA synthesis inhibitor;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
topoisomerase IV inhibitor
ezetimibe
Ezetimibe: An azetidine derivative and ANTICHOLESTEREMIC AGENT that inhibits intestinal STEROL absorption. It is used to reduce total CHOLESTEROL; LDL CHOLESTEROL, and APOLIPOPROTEINS B in the treatment of HYPERLIPIDEMIAS.. ezetimibe : A beta-lactam that is azetidin-2-one which is substituted at 1, 3, and 4 by p-fluorophenyl, 3-(p-fluorophenyl)-3-hydroxypropyl, and 4-hydroxyphenyl groups, respectively (the 3R,3'S,4S enantiomer).		3.5920azetidines;
beta-lactam;
organofluorine compound		anticholesteremic drug;
antilipemic drug;
antimetabolite
ertapenem
Ertapenem: A carbapenem derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of Gram-positive and Gram-negative bacterial infections including intra-abdominal infections, acute gynecological infections, complicated urinary tract infections, skin infections, and respiratory tract infections. It is also used to prevent infection in colorectal surgery.. ertapenem : Meropenem in which the one of the two methyl groups attached to the amide nitrogen is replaced by hydrogen while the other is replaced by a 3-carboxyphenyl group. The sodium salt is used for the treatment of moderate to severe susceptible infections including intra-abdominal and acute gynaecological infections, pneumonia, and infections of the skin and of the urinary tract.		3.2310carbapenemcarboxylic acid;
pyrrolidinecarboxamide		antibacterial drug
dx 8951
[no description available]		3.1310pyranoindolizinoquinoline
cox 189
lumiracoxib: a COX-2 inhibitor. lumiracoxib : An amino acid that is phenylacetic acid which is substituted at position 2 by the nitrogen of 2-chloro-6-fluoroaniline and at position 5 by a methyl group. A highly selective cyclooxygenase 2 inhibitor, it was briefly used for the treatment of osteoarthritis, but was withdrawn due to concersns of hepatotoxicity.		3.2310amino acid;
monocarboxylic acid;
organochlorine compound;
organofluorine compound;
secondary amino compound		cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
conivaptan
conivaptan : The amide resulting from the formal condensation of 4-[(biphenyl-2-ylcarbonyl)amino]benzoic acid with the benzazepine nitrogen of 2-methyl-1,4,5,6-tetrahydroimidazo[4,5-d][1]benzazepine. It is an antagonist for two of the three types of arginine vasopressin (AVP) receptors, V1a and V2. It is used as its hydrochloride salt for the treatment of hyponatraemia (low blood sodium levels) caused by syndrome of inappropriate antidiuretic hormone (SIADH).		3.2310benzazepineaquaretic;
vasopressin receptor antagonist
cariporide
cariporide: a selective sodium-hydrogen exchange subtype 1 inhibitor; structure in first source		2.0510
tezosentan
tezosentan: structure in first source		2.0510
vatalanib
[no description available]		4.3430monochlorobenzenes;
phthalazines;
pyridines;
secondary amino compound		angiogenesis inhibitor;
antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
vascular endothelial growth factor receptor antagonist
moxifloxacin
Moxifloxacin: A fluoroquinolone that acts as an inhibitor of DNA TOPOISOMERASE II and is used as a broad-spectrum antibacterial agent.. moxifloxacin : A quinolone that consists of 4-oxo-1,4-dihydroquinoline-3-carboxylic acid bearing a cyclopropyl substituent at position 1, a fluoro substitiuent at position 6, a (4aS,7aS)-octahydro-6H-pyrrolo[3,4-b]pyridin-6-yl group at position 7 and a methoxy substituent at position 8. A member of the fluoroquinolone class of antibacterial agents.		3.5920aromatic ether;
cyclopropanes;
fluoroquinolone antibiotic;
pyrrolidinopiperidine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antibacterial drug
pralnacasan
pralnacasan: NSAID, ICE inhibitor & metastasis inhibitor; RN & structure in first source		3.2310
clevidipine
clevidipine: a calcium channel blocker and antihypertensive agent; structure in first source		3.2310dihydropyridine
jtt 501
JTT 501: an insulin sensitizer; structure in first source		2.0510
solifenacin
[no description available]		3.2310isoquinolines
dexmethylphenidate
dexmethylphenidate : A methyl phenyl(piperidin-2-yl)acetate in which both stereocentres have R configuration. It is the active enantiomer in the racemic drug methylphenidate.		3.5920methyl phenyl(piperidin-2-yl)acetateadrenergic agent
naproxen
Naproxen: An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout.. naproxen : A methoxynaphthalene that is 2-methoxynaphthalene substituted by a carboxy ethyl group at position 6. Naproxen is a non-steroidal anti-inflammatory drug commonly used for the reduction of pain, fever, inflammation and stiffness caused by conditions such as osteoarthritis, kidney stones, rheumatoid arthritis, psoriatic arthritis, gout, ankylosing spondylitis, menstrual cramps, tendinitis, bursitis, and for the treatment of primary dysmenorrhea. It works by inhibiting both the COX-1 and COX-2 enzymes.		3.5920methoxynaphthalene;
monocarboxylic acid		antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
environmental contaminant;
gout suppressant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
cinacalcet
cinacalcet : A secondary amino compound that is (1R)-1-(naphthalen-1-yl)ethanamine in which one of the hydrogens attached to the nitrogen is substituted by a 3-[3-(trifluoromethyl)phenyl]propyl group.		3.2310(trifluoromethyl)benzenes;
naphthalenes;
secondary amino compound		calcimimetic;
P450 inhibitor
lubiprostone
[no description available]		3.2310
methyl 5-aminolevulinate
methyl 5-aminolevulinate: esterified form of aminolevulinic acid used as PHOTOCHEMOTHERAPY. methyl 5-aminolevulinate : The methyl ester of 5-aminolevulinic acid. A prodrug, it is metabolised to protoporphyrin IX, a photosensitizer, and is used in the photodynamic treatment of non-melanoma skin cancer (including basal cell carcinoma). Topical application (often as the hydrochloride salt) results in an accumulation of protoporphyrin IX in the skin lesions to which the cream has been applied. Subsequent illumination with red light results in the generation of toxic singlet oxygen that destroys cell membranes and thereby kills the tumour cells.		2.0510delta-amino acid esterantineoplastic agent;
dermatologic drug;
photosensitizing agent;
prodrug
telbivudine
[no description available]		3.2310pyrimidine 2'-deoxyribonucleosideantiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
tipifarnib
[no description available]		6.542imidazoles;
monochlorobenzenes;
primary amino compound;
quinolone		antineoplastic agent;
apoptosis inducer;
EC 2.5.1.58 (protein farnesyltransferase) inhibitor
cyc 202
seliciclib : 2,6-Diaminopurine carrying benzylamino, (2R)-1-hydroxybutan-2-yl and isopropyl substituents at C-6, C-2-N and N-9 respectively. It is an experimental drug candidate in the family of pharmacological cyclin-dependent kinase (CDK) inhibitors.		2.05102,6-diaminopurinesantiviral drug;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
paromomycin
Paromomycin: An aminoglycoside antibacterial and antiprotozoal agent produced by species of STREPTOMYCES.. paromomycin : An amino cyclitol glycoside that is the 1-O-(2-amino-2-deoxy-alpha-D-glucopyranoside) and the 3-O-(2,6-diamino-2,6-dideoxy-beta-L-idopyranosyl)-beta-D-ribofuranoside of 4,6-diamino-2,3-dihydroxycyclohexane (the 1R,2R,3S,4R,6S diastereoisomer). It is obtained from various Streptomyces species. A broad-spectrum antibiotic, it is used (generally as the sulfate salt) for the treatment of acute and chronic intestinal protozoal infections, but is not effective for extraintestinal protozoal infections. It is also used as a therapeutic against visceral leishmaniasis.		3.5920amino cyclitol glycoside;
aminoglycoside antibiotic		anthelminthic drug;
antibacterial drug;
antiparasitic agent;
antiprotozoal drug
anidulafungin
Anidulafungin: Echinocandin antifungal agent that is used in the treatment of CANDIDEMIA and CANDIDIASIS.. anidulafungin : A semisynthetic echinocandin anti-fungal drug. It is active against Aspergillus and Candida species and is used for the treatment of invasive candidiasis.		3.2310antibiotic antifungal drug;
azamacrocycle;
echinocandin;
heterodetic cyclic peptide;
semisynthetic derivative
avasimibe
[no description available]		2.0510monoterpenoid
17 alpha-hydroxyprogesterone caproate
17 alpha-Hydroxyprogesterone Caproate: Hydroxyprogesterone derivative that acts as a PROGESTIN and is used to reduce the risk of recurrent MISCARRIAGE and of PREMATURE BIRTH. It is also used in combination with ESTROGEN in the management of MENSTRUATION DISORDERS.		3.2310corticosteroid hormone
varenicline
Varenicline: A benzazepine derivative that functions as an ALPHA4-BETA2 NICOTINIC RECEPTOR partial agonist. It is used for SMOKING CESSATION.. varenicline : An organic heterotetracyclic compound that acts as a partial agonist for nicotinic cholinergic receptors and is used (in the form of its tartate salt) as an aid to giving up smoking.		3.2310
biotin
vitamin B7 : Any member of a group of vitamers that belong to the chemical structural class called biotins that exhibit biological activity against vitamin B7 deficiency. Vitamin B7 deficiency is very rare in individuals who take a normal balanced diet. Foods rich in biotin are egg yolk, liver, cereals, vegetables (spinach, mushrooms) and rice. Symptoms associated with vitamin B7 deficiency include thinning hair, scaly skin rashes around eyes, nose and mouth, and brittle nails. The vitamers include biotin and its ionized and salt forms.		2.0510biotins;
vitamin B7		coenzyme;
cofactor;
Escherichia coli metabolite;
fundamental metabolite;
human metabolite;
mouse metabolite;
nutraceutical;
prosthetic group;
Saccharomyces cerevisiae metabolite
fiduxosin
fiduxosin: fiduxosin (ABT-980) is the (3aR,9bR)-isomer; structure in first source		3.2310
atropine
tropan-3alpha-yl 3-hydroxy-2-phenylpropanoate : A tropane alkaloid that is (1R,5)-8-methyl-8-azabicyclo[3.2.1]octane substituted by a (3-hydroxy-2-phenylpropanoyl)oxy group at position 3.		3.5920
enzastaurin
[no description available]		5.5932indoles;
maleimides
erlotinib
[no description available]		3.5920aromatic ether;
quinazolines;
secondary amino compound;
terminal acetylenic compound		antineoplastic agent;
epidermal growth factor receptor antagonist;
protein kinase inhibitor
erlotinib hydrochloride
[no description available]		16.187029hydrochloride;
terminal acetylenic compound		antineoplastic agent;
protein kinase inhibitor
psyllium
Psyllium: Dried, ripe seeds of PLANTAGO PSYLLIUM; PLANTAGO INDICA; and PLANTAGO OVATA. Plantain seeds swell in water and are used as demulcents and bulk laxatives.		7.610very long-chain fatty acid
phenserine
phenserine: a carbamate analog of physostigmine; a long-acting inhibitor of cholinesterase		2.0510
etravirine
[no description available]		3.2310aminopyrimidine;
aromatic ether;
dinitrile;
organobromine compound		antiviral agent;
HIV-1 reverse transcriptase inhibitor
troleandomycin
Troleandomycin: A macrolide antibiotic that is similar to ERYTHROMYCIN.. troleandomycin : A semi-synthetic macrolide antibiotic obtained by acetylation of the three free hydroxy groups of oleandomycin. Troleandomycin is only found in individuals that have taken the drug.		2.0510acetate ester;
epoxide;
macrolide antibiotic;
monosaccharide derivative;
polyketide;
semisynthetic derivative		EC 1.14.13.97 (taurochenodeoxycholate 6alpha-hydroxylase) inhibitor;
xenobiotic
dronedarone
Dronedarone: A non-iodinated derivative of amiodarone that is used for the treatment of ARRHYTHMIA.. dronedarone : A member of the class of 1-benzofurans used for the treatment of cardiac arrhythmias.		3.23101-benzofurans;
aromatic ether;
aromatic ketone;
sulfonamide;
tertiary amino compound		anti-arrhythmia drug;
environmental contaminant;
xenobiotic
ramelteon
ramelteon: melatonin MT1/MT2 receptor agonist		3.2310indanes
lapatinib
[no description available]		20.2518267furans;
organochlorine compound;
organofluorine compound;
quinazolines		antineoplastic agent;
tyrosine kinase inhibitor
darunavir
Darunavir: An HIV PROTEASE INHIBITOR that is used in the treatment of AIDS and HIV INFECTIONS. Due to the emergence of ANTIVIRAL DRUG RESISTANCE when used alone, it is administered in combination with other ANTI-HIV AGENTS.. darunavir : An N,N-disubstituted benzenesulfonamide bearing an unsubstituted amino group at the 4-position, used for the treatment of HIV infection. A second-generation HIV protease inhibitor, darunavir was designed to form robust interactions with the protease enzyme from many strains of HIV, including those from treatment-experienced patients with multiple resistance mutations to other protease inhibitors.		3.2310carbamate ester;
furofuran;
sulfonamide		antiviral drug;
HIV protease inhibitor
deferasirox
Deferasirox: A triazole and benzoate derivative that acts as a selective iron chelator. It is used in the management of chronic IRON OVERLOAD due to blood transfusion or non-transfusion dependent THALASSEMIA.. deferasirox : A member of the class of triazoles, deferasirox is 1,2,4-triazole substituted by a 4-carboxyphenyl group at position 1 and by 2-hydroxyphenyl groups at positions 3 and 5. An orally active iron chelator, it is used to manage chronic iron overload in patients receiving long-term blood transfusions.		3.5920benzoic acids;
monocarboxylic acid;
phenols;
triazoles		iron chelator
tbc-11251
sitaxsentan: endothelin A receptor antagonist; structure in first source		3.5920benzodioxoles
tolvaptan
[no description available]		3.2310benzazepine;
benzenedicarboxamide		aquaretic;
vasopressin receptor antagonist
sorafenib
[no description available]		14.674521(trifluoromethyl)benzenes;
aromatic ether;
monochlorobenzenes;
phenylureas;
pyridinecarboxamide		angiogenesis inhibitor;
anticoronaviral agent;
antineoplastic agent;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
ferroptosis inducer;
tyrosine kinase inhibitor
lenalidomide
[no description available]		4.3930aromatic amine;
dicarboximide;
isoindoles;
piperidones		angiogenesis inhibitor;
antineoplastic agent;
immunomodulator
n-(3-chloro-7-indolyl)-1,4-benzenedisulphonamide
N-(3-chloro-7-indolyl)-1,4-benzenedisulphonamide: structure in first source. indisulam : A chloroindole that is 3-chloro-1H-indole substituted by a [(4-sulfamoylphenyl)sulfonyl]nitrilo group at position 7. It is a carbonic anhydrase inhibitor and a potential anti-cancer agent currently in clinical development.		3.8321chloroindole;
organochlorine compound;
sulfonamide		antineoplastic agent;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
regadenoson
[no description available]		3.2310purine nucleoside
lacosamide
Lacosamide: An acetamide derivative that acts as a blocker of VOLTAGE-GATED SODIUM CHANNELS. It is used as an anticonvulsant, for adjunctive or monotherapy, in the treatment of PARTIAL SEIZURES.		3.2310N-acyl-amino acid
sitosterol, (3beta)-isomer
Sobatum: tradename; active fraction of Solanum trilobatum; reduces side-effects of radiation-induced toxicity. sitosterol : A member of the class of phytosterols that is stigmast-5-ene substituted by a beta-hydroxy group at position 3.		2.05103beta-hydroxy-Delta(5)-steroid;
3beta-sterol;
C29-steroid;
phytosterols;
stigmastane sterol		anticholesteremic drug;
antioxidant;
mouse metabolite;
plant metabolite;
sterol methyltransferase inhibitor
vincaleukoblastine
[no description available]		3.2310acetate ester;
indole alkaloid fundamental parent;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
tertiary alcohol;
tertiary amino compound;
vinca alkaloid		antineoplastic agent;
immunosuppressive agent;
microtubule-destabilising agent;
plant metabolite
benzarone
benzarone: antihemorrhagic agent; structure		3.59201-benzofurans
estramustine
Estramustine: A nitrogen mustard linked to estradiol, usually as phosphate; used to treat prostatic neoplasms; also has radiation protective properties.. estramustine : A carbamate ester obtained by the formal condensation of the hydroxy group of 17beta-estradiol with the carboxy group of bis(2-chloroethyl)carbamic acid.		3.863017beta-hydroxy steroid;
carbamate ester;
organochlorine compound		alkylating agent;
antineoplastic agent;
radiation protective agent
calendula
Calendula: A plant genus of the family ASTERACEAE. Members contain CAROTENOIDS, essential oils (OILS, VOLATILE), flavonoids, mucilage, SAPONINS, and STEROLS. The plants are used both topically and internally. The common name of Marigold is also used for TAGETES.		2.0310
noscapine
Noscapine: A naturally occurring opium alkaloid that is a centrally acting antitussive agent.. (-)-noscapine : A benzylisoquinoline alkaloid that is 1,2,3,4-tetrahydroisoquinoline which is substituted by a 4,5-dimethoxy-3-oxo-1,3-dihydro-2-benzofuran-1-yl group at position 1, a methylenedioxy group at positions 6-7 and a methoxy group at position 8. Obtained from plants of the Papaveraceae family, it lacks significant painkilling properties and is primarily used for its antitussive (cough-suppressing) effects.		2.0510aromatic ether;
benzylisoquinoline alkaloid;
cyclic acetal;
isobenzofuranone;
organic heterobicyclic compound;
organic heterotricyclic compound;
tertiary amino compound		antineoplastic agent;
antitussive;
apoptosis inducer;
plant metabolite
homoharringtonine
Homoharringtonine: Semisynthetic derivative of harringtonine that acts as a protein synthesis inhibitor and induces APOPTOSIS in tumor cells. It is used in the treatment of MYELOID LEUKEMIA, CHRONIC.. omacetaxine mepesuccinate : A cephalotaxine-derived alkaloid ester obtained from Cephalotaxus harringtonia; used for the treatment of chronic or accelerated phase chronic myeloid leukaemia.		2.0510alkaloid ester;
enol ether;
organic heteropentacyclic compound;
tertiary alcohol		anticoronaviral agent;
antineoplastic agent;
apoptosis inducer;
protein synthesis inhibitor
6-fluorouracil
6-fluorouracil: structure given in first source		3.2710
2'-fluorothymidine
[no description available]		2.1310
o-(chloroacetylcarbamoyl)fumagillol
O-(Chloroacetylcarbamoyl)fumagillol: Semisynthetic analog of fumagillin (a cyclohexane-sesquiterpene antibiotic isolated from ASPERGILLUS FUMIGATUS) that inhibits angiogenesis.. O-(chloroacetylcarbamoyl)fumagillol : A carbamate ester that is fumagillol in which the hydroxy group has been converted to the corresponding N-(chloroacetyl)carbamate derivative.		2.0510carbamate ester;
organochlorine compound;
semisynthetic derivative;
sesquiterpenoid;
spiro-epoxide		angiogenesis inhibitor;
antineoplastic agent;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
methionine aminopeptidase 2 inhibitor;
retinoic acid receptor alpha antagonist
bortezomib
[no description available]		7.3272amino acid amide;
L-phenylalanine derivative;
pyrazines		antineoplastic agent;
antiprotozoal drug;
protease inhibitor;
proteasome inhibitor
ritonavir
Ritonavir: An HIV protease inhibitor that works by interfering with the reproductive cycle of HIV. It also inhibits CYTOCHROME P-450 CYP3A.. ritonavir : An L-valine derivative that is L-valinamide in which alpha-amino group has been acylated by a [(2-isopropyl-1,3-thiazol-4-yl)methyl]methylcarbamoyl group and in which a hydrogen of the carboxamide amino group has been replaced by a (2R,4S,5S)-4-hydroxy-1,6-diphenyl-5-{[(1,3-thiazol-5-ylmethoxy)carbonyl]amino}hexan-2-yl group. A CYP3A inhibitor and antiretroviral drug from the protease inhibitor class used to treat HIV infection and AIDS, it is often used as a fixed-dose combination with another protease inhibitor, lopinavir. Also used in combination with dasabuvir sodium hydrate, ombitasvir and paritaprevir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.		3.59201,3-thiazoles;
carbamate ester;
carboxamide;
L-valine derivative;
ureas		antiviral drug;
environmental contaminant;
HIV protease inhibitor;
xenobiotic
nexavar
[no description available]		2.0510organosulfonate salt
carboplatin
[no description available]		12.73612
n-acetylneuraminic acid
N-Acetylneuraminic Acid: An N-acyl derivative of neuraminic acid. N-acetylneuraminic acid occurs in many polysaccharides, glycoproteins, and glycolipids in animals and bacteria. (From Dorland, 28th ed, p1518). N-acetylneuraminic acid : An N-acylneuraminic acid where the N-acyl group is specified as acetyl.		2.610N-acetylneuraminic acidsantioxidant;
bacterial metabolite;
EC 3.2.1.18 (exo-alpha-sialidase) inhibitor;
human metabolite;
mouse metabolite
glucosamine
D-glucosamine : An amino sugar whose structure comprises D-glucose having an amino substituent at position 2.. 2-amino-2-deoxy-D-glucopyranose : A D-glucosamine whose structure comprises D-glucopyranose having an amino substituent at position 2.		2.0510D-glucosamineEscherichia coli metabolite;
geroprotector;
mouse metabolite
oxytocin
Oxytocin: A nonapeptide hormone released from the neurohypophysis (PITUITARY GLAND, POSTERIOR). It differs from VASOPRESSIN by two amino acids at residues 3 and 8. Oxytocin acts on SMOOTH MUSCLE CELLS, such as causing UTERINE CONTRACTIONS and MILK EJECTION.. oxytocin : A cyclic nonapeptide hormone with amino acid sequence CYIQNCPLG that also acts as a neurotransmitter in the brain; the principal uterine-contracting and milk-ejecting hormone of the posterior pituitary. Together with the neuropeptide vasopressin, it is believed to influence social cognition and behaviour.		3.2310heterodetic cyclic peptide;
peptide hormone		oxytocic;
vasodilator agent
theanine
theanine: RN given refers to (L)-isomer; precursor of ethylamine; found in green tea. N(5)-ethyl-L-glutamine : A N(5)-alkylglutamine where the alkyl group is ethyl. It has been isolated from green tea.		4.5622amino acid zwitterion;
N(5)-alkyl-L-glutamine		geroprotector;
neuroprotective agent;
plant metabolite
pentostatin
Pentostatin: A potent inhibitor of ADENOSINE DEAMINASE. The drug induces APOPTOSIS of LYMPHOCYTES, and is used in the treatment of many lymphoproliferative malignancies, particularly HAIRY CELL LEUKEMIA. It is also synergistic with some other antineoplastic agents and has immunosuppressive activity.. pentostatin : A member of the class of coformycins that is coformycin in which the hydroxy group at position 2' is replaced with a hydrogen. It is a drug used for the treatment of hairy cell leukaemia.		4.3930coformycinsantimetabolite;
antineoplastic agent;
Aspergillus metabolite;
bacterial metabolite;
EC 3.5.4.4 (adenosine deaminase) inhibitor
quinidine
Quinidine: An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.. quinidine : A cinchona alkaloid consisting of cinchonine with the hydrogen at the 6-position of the quinoline ring substituted by methoxy.		3.5920cinchona alkaloidalpha-adrenergic antagonist;
anti-arrhythmia drug;
antimalarial;
drug allergen;
EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor;
EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor;
muscarinic antagonist;
P450 inhibitor;
potassium channel blocker;
sodium channel blocker
meropenem
Meropenem: A thienamycin derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of bacterial infections, including infections in immunocompromised patients.. meropenem : A carbapenemcarboxylic acid in which the azetidine and pyrroline rings carry 1-hydroxymethyl and in which the azetidine and pyrroline rings carry 1-hydroxymethyl and 5-(dimethylcarbamoyl)pyrrolidin-3-ylthio substituents respectively.		3.5920alpha,beta-unsaturated monocarboxylic acid;
carbapenemcarboxylic acid;
organic sulfide;
pyrrolidinecarboxamide		antibacterial agent;
antibacterial drug;
drug allergen
griseofulvin
Griseofulvin: An antifungal agent used in the treatment of TINEA infections.. griseofulvin : An oxaspiro compound produced by Penicillium griseofulvum. It is used by mouth as an antifungal drug for infections involving the scalp, hair, nails and skin that do not respond to topical treatment.		3.59201-benzofurans;
antibiotic antifungal drug;
benzofuran antifungal drug;
organochlorine compound;
oxaspiro compound		antibacterial agent;
Penicillium metabolite
cefoxitin
Cefoxitin: A semisynthetic cephamycin antibiotic resistant to beta-lactamase.. cefoxitin : A semisynthetic cephamycin antibiotic which, in addition to the methoxy group at the 7alpha position, has 2-thienylacetamido and carbamoyloxymethyl side-groups. It is resistant to beta-lactamase.		3.2310beta-lactam antibiotic allergen;
cephalosporin;
cephamycin;
semisynthetic derivative		antibacterial drug
digitoxin
Digitoxin: A cardiac glycoside sometimes used in place of DIGOXIN. It has a longer half-life than digoxin; toxic effects, which are similar to those of digoxin, are longer lasting. (From Martindale, The Extra Pharmacopoeia, 30th ed, p665). digitoxin : A cardenolide glycoside in which the 3beta-hydroxy group of digitoxigenin carries a 2,6-dideoxy-beta-D-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-beta-D-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-beta-D-ribo-hexopyranosyl trisaccharide chain.		2.0510cardenolide glycosideEC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor
saquinavir
Saquinavir: An HIV protease inhibitor which acts as an analog of an HIV protease cleavage site. It is a highly specific inhibitor of HIV-1 and HIV-2 proteases, and also inhibits CYTOCHROME P-450 CYP3A.. saquinavir : An aspartic acid derivative obtained by formal condensation of the primary amino group of (2S,3R)-4-[(3S,4aS,8aS)-3-(tert-butylcarbamoyl)octahydroisoquinolin-2(1H)-yl]-3-hydroxy-1-phenylbutan-2-ylamine with the carboxy group of N(2)(-quinolin-2-ylcarbonyl)-L-asparagine. An inhibitor of HIV-1 protease.		3.5920L-asparagine derivative;
quinolines		antiviral drug;
HIV protease inhibitor
pancuronium
Pancuronium: A bis-quaternary steroid that is a competitive nicotinic antagonist. As a neuromuscular blocking agent it is more potent than CURARE but has less effect on the circulatory system and on histamine release.. pancuronium : A steroid ester in which a 5alpha-androstane skeleton is C-3alpha- and C-17beta-disubstituted with acetoxy groups and 2beta- and 16beta-disubstituted with 1-methylpiperidinium-1-yl groups. It is a non-depolarizing curare-mimetic muscle relaxant.		3.2310acetate ester;
steroid ester		cholinergic antagonist;
muscle relaxant;
nicotinic antagonist
abacavir
abacavir: a carbocyclic nucleoside with potent selective anti-HIV activity. abacavir : A 2,6-diaminopurine that is (1S)-cyclopent-2-en-1-ylmethanol in which the pro-R hydrogen at the 4-position is substituted by a 2-amino-6-(cyclopropylamino)-9H-purin-9-yl group. A nucleoside analogue reverse transcriptase inhibitor (NRTI) with antiretroviral activity against HIV, it is used (particularly as the sulfate) with other antiretrovirals in combination therapy of HIV infection.		3.23102,6-diaminopurinesantiviral drug;
drug allergen;
HIV-1 reverse transcriptase inhibitor
netilmicin
Netilmicin: Semisynthetic 1-N-ethyl derivative of SISOMYCIN, an aminoglycoside antibiotic with action similar to gentamicin, but less ear and kidney toxicity.		2.0510
trimethaphan camsylate
trimethaphan camsylate : The (S)-camphorsulfonate salt of trimethaphan.		2.0510
miglitol
[no description available]		3.2310piperidines
metyrosine
alpha-methyl-L-tyrosine : An L-tyrosine derivative that consists of L-tyrosine bearing an additional methyl substituent at position 2. An inhibitor of the enzyme tyrosine 3-monooxygenase, and consequently of the synthesis of catecholamines. It is used to control the symptoms of excessive sympathetic stimulation in patients with pheochromocytoma.		3.2310L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid		antihypertensive agent;
EC 1.14.16.2 (tyrosine 3-monooxygenase) inhibitor
erythromycin estolate
Erythromycin Estolate: A macrolide antibiotic, produced by Streptomyces erythreus. It is the lauryl sulfate salt of the propionic ester of erythromycin. This erythromycin salt acts primarily as a bacteriostatic agent. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.		2.0510aminoglycoside sulfate salt;
erythromycin derivative		enzyme inhibitor
linezolid
[no description available]		3.5820acetamides;
morpholines;
organofluorine compound;
oxazolidinone		antibacterial drug;
protein synthesis inhibitor
cyclopamine
[no description available]		2.0510piperidinesglioma-associated oncogene inhibitor
devazepide
Devazepide: A derivative of benzodiazepine that acts on the cholecystokinin A (CCKA) receptor to antagonize CCK-8's (SINCALIDE) physiological and behavioral effects, such as pancreatic stimulation and inhibition of feeding.. devazepide : An indolecarboxamide obtained by formal condensation of the carboxy group of indole-2-carboxylic acid with the exocyclic amino group of (3S)-3-amino-1-methyl-5-phenyl-1,3-dihydro-1,4-benzodiazepin-2-one. A cholecystokinin antagonist used for treatment of gastrointestinal disorders.		2.05101,4-benzodiazepinone;
indolecarboxamide		antineoplastic agent;
apoptosis inducer;
cholecystokinin antagonist;
gastrointestinal drug
clindamycin phosphate
[no description available]		3.2310
eplerenone
Eplerenone: A spironolactone derivative and selective ALDOSTERONE RECEPTOR antagonist that is used in the management of HYPERTENSION and CONGESTIVE HEART FAILURE, post-MYOCARDIAL INFARCTION.		3.23103-oxo-Delta(4) steroid;
epoxy steroid;
gamma-lactone;
methyl ester;
organic heteropentacyclic compound;
oxaspiro compound;
steroid acid ester		aldosterone antagonist;
antihypertensive agent
temocapril
[no description available]		2.0510dipeptide
tolterodine
[no description available]		3.5920tertiary amineantispasmodic drug;
muscarinic antagonist;
muscle relaxant
doxorubicin hydrochloride
[no description available]		2.0510anthracycline
erythromycin ethylsuccinate
Erythromycin Ethylsuccinate: A macrolide antibiotic, produced by Streptomyces erythreus. This compound is an ester of erythromycin base and succinic acid. It acts primarily as a bacteriostatic agent. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.. erythromycin ethylsuccinate : A erythromycin derivative that is erythromycin A in which the hydroxy group at position 3R is substituted by a (4-ethoxy-4-oxobutanoyl)oxy group. It is used for the treatment of a wide variety of bacterial infections.		2.0510cyclic ketone;
erythromycin derivative;
ethyl ester;
succinate ester
ao 128
AO 128: alpha-glucosidase inhibitor; structure given in first source		2.0510organic molecular entity
darifenacin
darifenacin : 2-[(3S)-1-Ethylpyrrolidin-3-yl]-2,2-diphenylacetamide in which one of the hydrogens at the 2-position of the ethyl group is substituted by a 2,3-dihydro-1-benzofuran-5-yl group. It is a selective antagonist for the M3 muscarinic acetylcholine receptor, which is primarily responsible for bladder muscle contractions, and is used as the hydrobromide salt in the management of urinary incontinence.		3.23101-benzofurans;
monocarboxylic acid amide;
pyrrolidines		antispasmodic drug;
muscarinic antagonist
betadex
beta-Cyclodextrins: Cyclic GLUCANS consisting of seven (7) glucopyranose units linked by 1,4-glycosidic bonds.		2.610cyclodextrin
acarbose
[no description available]		2.0510amino cyclitol;
glycoside
trichostatin a
trichostatin A: chelates zinc ion in the active site of histone deacetylases, resulting in preventing histone unpacking so DNA is less available for transcription; do not confuse with TRICHOSANTHIN which is a protein; found in STREPTOMYCES		2.0610antibiotic antifungal agent;
hydroxamic acid;
trichostatin		bacterial metabolite;
EC 3.5.1.98 (histone deacetylase) inhibitor;
geroprotector
tretinoin
Tretinoin: An important regulator of GENE EXPRESSION during growth and development, and in NEOPLASMS. Tretinoin, also known as retinoic acid and derived from maternal VITAMIN A, is essential for normal GROWTH; and EMBRYONIC DEVELOPMENT. An excess of tretinoin can be teratogenic. It is used in the treatment of PSORIASIS; ACNE VULGARIS; and several other SKIN DISEASES. It has also been approved for use in promyelocytic leukemia (LEUKEMIA, PROMYELOCYTIC, ACUTE).. retinoic acid : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraenoic acid substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).. all-trans-retinoic acid : A retinoic acid in which all four exocyclic double bonds have E- (trans-) geometry.		3.8930retinoic acid;
vitamin A		anti-inflammatory agent;
antineoplastic agent;
antioxidant;
AP-1 antagonist;
human metabolite;
keratolytic drug;
retinoic acid receptor agonist;
retinoid X receptor agonist;
signalling molecule
3-hydroxy-3-methylglutaryl-coenzyme a
3-hydroxy-3-methylglutaryl-coenzyme A: RN given refers to cpd without isomeric designation. 3-hydroxy-3-methylglutaryl-CoA : An alpha,omega dicarboxyacyl-CoA that results from the formal condensation of the thiol group of coenzyme A with one of the carboxy groups of 3-hydroxy-3-methylglutaric acid.. (3S)-3-hydroxy-3-methylglutaryl-CoA : A 3-hydroxy-3-methylglutaryl-CoA where the 3-hydroxy-3-methylglutaryl component has (S)-configuration.		4.4113-hydroxy-3-methylglutaryl-CoA;
3-hydroxy fatty acyl-CoA		human metabolite;
mouse metabolite
resveratrol
trans-resveratrol : A resveratrol in which the double bond has E configuration.		3.1910resveratrolantioxidant;
phytoalexin;
plant metabolite;
quorum sensing inhibitor;
radical scavenger
retinol
Vitamin A: Retinol and derivatives of retinol that play an essential role in metabolic functioning of the retina, the growth of and differentiation of epithelial tissue, the growth of bone, reproduction, and the immune response. Dietary vitamin A is derived from a variety of CAROTENOIDS found in plants. It is enriched in the liver, egg yolks, and the fat component of dairy products.. vitamin A : Any member of a group of fat-soluble retinoids produced via metabolism of provitamin A carotenoids that exhibit biological activity against vitamin A deficiency. Vitamin A is involved in immune function, vision, reproduction, and cellular communication.. all-trans-retinol : A retinol in which all four exocyclic double bonds have E- (trans-) geometry.. retinol : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraen-1-ol substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).		3.5920retinol;
vitamin A		human metabolite;
mouse metabolite;
plant metabolite
alpha-D-fructofuranose 1,6-bisphosphate
alpha-D-fructofuranose 1,6-bisphosphate : A D-fructofuranose 1,6-bisphosphate with an alpha-configuration at the anomeric position.		2.0510D-fructofuranose 1,6-bisphosphate
docosahexaenoate
efalex: a mixture of fish oil and primrose oil; used as a high-docosahexaenoic acid fatty acid supplement. docosahexaenoic acid : Any C22 polyunsaturated fatty acid containing six double bonds.. docosahexaenoate : A polyunsaturated fatty acid anion that is the conjugate base of docosahexaenoic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.. all-cis-docosa-4,7,10,13,16,19-hexaenoic acid : A docosahexaenoic acid having six cis-double bonds at positions 4, 7, 10, 13, 16 and 19.		2.0510docosahexaenoic acid;
omega-3 fatty acid		algal metabolite;
antineoplastic agent;
Daphnia tenebrosa metabolite;
human metabolite;
mouse metabolite;
nutraceutical
oleic acid
Oleic Acid: An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed). oleic acid : An octadec-9-enoic acid in which the double bond at C-9 has Z (cis) stereochemistry.		2.0510octadec-9-enoic acidantioxidant;
Daphnia galeata metabolite;
EC 3.1.1.1 (carboxylesterase) inhibitor;
Escherichia coli metabolite;
mouse metabolite;
plant metabolite;
solvent
tacrolimus
Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro.. tacrolimus (anhydrous) : A macrolide lactam containing a 23-membered lactone ring, originally isolated from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis.		3.5920macrolide lactambacterial metabolite;
immunosuppressive agent
cerivastatin
cerivastatin: cerivastatin is the ((E)-(+))-isomer; structure given in first source. cerivastatin : (3R,5S)-3,5-dihydroxyhept-6-enoic acid in which the (7E)-hydrogen is substituted by a 4-(4-fluorophenyl)-2,6-diisopropyl-5-(methoxymethyl)pyridin-3-yl group. Formerly used (as its sodium salt) to lower cholesterol and prevent cardiovascular disease, it was withdrawn from the market worldwide in 2001 following reports of a severe form of muscle toxicity.		2.0510dihydroxy monocarboxylic acid;
pyridines;
statin (synthetic)
rosuvastatin
rosuvastatin : A dihydroxy monocarboxylic acid that is (6E)-7-{4-(4-fluorophenyl)-2-[methyl(methylsulfonyl)amino]-6-(propan-2-yl)pyrimidin-5-yl} hept-6-enoic acid carrying two hydroxy substituents at positions 3 and 5 (the 3R,5S-diastereomer).		3.5920dihydroxy monocarboxylic acid;
monofluorobenzenes;
pyrimidines;
statin (synthetic);
sulfonamide		anti-inflammatory agent;
antilipemic drug;
cardioprotective agent;
CETP inhibitor;
environmental contaminant;
xenobiotic
cocaine
Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.. cocaine : A tropane alkaloid obtained from leaves of the South American shrub Erythroxylon coca.		2.4620benzoate ester;
methyl ester;
tertiary amino compound;
tropane alkaloid		adrenergic uptake inhibitor;
central nervous system stimulant;
dopamine uptake inhibitor;
environmental contaminant;
local anaesthetic;
mouse metabolite;
plant metabolite;
serotonin uptake inhibitor;
sodium channel blocker;
sympathomimetic agent;
vasoconstrictor agent;
xenobiotic
eicosapentaenoic acid
icosapentaenoic acid : Any straight-chain, C20 polyunsaturated fatty acid having five C=C double bonds.. all-cis-5,8,11,14,17-icosapentaenoic acid : An icosapentaenoic acid having five cis-double bonds at positions 5, 8, 11, 14 and 17.		2.0510icosapentaenoic acid;
omega-3 fatty acid		anticholesteremic drug;
antidepressant;
antineoplastic agent;
Daphnia galeata metabolite;
fungal metabolite;
micronutrient;
mouse metabolite;
nutraceutical
mycophenolic acid
Mycophenolic Acid: Compound derived from Penicillium stoloniferum and related species. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase (IMP DEHYDROGENASE). Mycophenolic acid exerts selective effects on the immune system in which it prevents the proliferation of T-CELLS, LYMPHOCYTES, and the formation of antibodies from B-CELLS. It may also inhibit recruitment of LEUKOCYTES to sites of INFLAMMATION.. mycophenolate : A monocarboxylic acid anion resulting from the removal of a proton from the carboxy group of mycophenolic acid.. mycophenolic acid : A member of the class of 2-benzofurans that is 2-benzofuran-1(3H)-one which is substituted at positions 4, 5, 6, and 7 by methyl, methoxy, (2E)-5-carboxy-3-methylpent-2-en-1-yl, and hydroxy groups, respectively. It is an antibiotic produced by Penicillium brevi-compactum, P. stoloniferum, P. echinulatum and related species. An immunosuppressant, it is widely used (partiularly as its sodium salt and as the 2-(morpholin-4-yl)ethyl ester prodrug, mycophenolate mofetil) to prevent tissue rejection following organ transplants and for the treatment of certain autoimmune diseases.		3.87302-benzofurans;
gamma-lactone;
monocarboxylic acid;
phenols		anticoronaviral agent;
antimicrobial agent;
antineoplastic agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
environmental contaminant;
immunosuppressive agent;
mycotoxin;
Penicillium metabolite;
xenobiotic
mupirocin
Mupirocin: A topically used antibiotic from a strain of Pseudomonas fluorescens. It has shown excellent activity against gram-positive staphylococci and streptococci. The antibiotic is used primarily for the treatment of primary and secondary skin disorders, nasal infections, and wound healing.. mupirocin : An alpha,beta-unsaturated ester resulting from the formal condensation of the alcoholic hydroxy group of 9-hydroxynonanoic acid with the carboxy group of (2E)-4-[(2S)-tetrahydro-2H-pyran-2-yl]-3-methylbut-2-enoic acid in which the tetrahydropyranyl ring is substituted at positions 3 and 4 by hydroxy groups and at position 5 by a {(2S,3S)-3-[(2S,3S)-3-hydroxybutan-2-yl]oxiran-2-yl}methyl group. Originally isolated from the Gram-negative bacterium Pseudomonas fluorescens, it is used as a topical antibiotic for the treatment of Gram-positive bacterial infections.		2.0310alpha,beta-unsaturated carboxylic ester;
epoxide;
monocarboxylic acid;
oxanes;
secondary alcohol;
triol		antibacterial drug;
bacterial metabolite;
protein synthesis inhibitor
clindamycin
Clindamycin: An antibacterial agent that is a semisynthetic analog of LINCOMYCIN.. clindamycin : A carbohydrate-containing antibiotic that is the semisynthetic derivative of lincomycin, a natural antibiotic.		3.5920
brivudine
brivudine: anti-herpes agent		8.8630
fosfomycin
Fosfomycin: An antibiotic produced by Streptomyces fradiae.. fosfomycin : A phosphonic acid having an (R,S)-1,2-epoxypropyl group attached to phosphorus.		3.5920epoxide;
phosphonic acids		antimicrobial agent;
EC 2.5.1.7 (UDP-N-acetylglucosamine 1-carboxyvinyltransferase) inhibitor
zithromax
Azithromycin: A semi-synthetic macrolide antibiotic structurally related to ERYTHROMYCIN. It has been used in the treatment of Mycobacterium avium intracellulare infections, toxoplasmosis, and cryptosporidiosis.. azithromycin : A macrolide antibiotic useful for the treatment of bacterial infections.		3.5920macrolide antibioticantibacterial drug;
environmental contaminant;
xenobiotic
drf 2725
ragaglitazar: a phenoxazine analogue of phenyl propanoic acid; Ragaglitazar is a coligand of PPARalpha and PPARgamma		2.0510
desoxyepothilone b
desoxyepothilone B: microtubule-targeted antitumor agent; lacking the epoxide of epothilone B; may be equiv to epothilone D. epothilone D : An epithilone that is epithilone C in which the hydrogen at position 13 of the oxacyclohexadec-13-ene-2,6-dione macrocycle has been replaced by a methyl group.		4.0520epothilonemicrotubule-stabilising agent
epothilone b
[no description available]		4.6830epothilone;
epoxide		antineoplastic agent;
apoptosis inducer;
microtubule-stabilising agent
diethylstilbestrol
Diethylstilbestrol: A synthetic nonsteroidal estrogen used in the treatment of menopausal and postmenopausal disorders. It was also used formerly as a growth promoter in animals. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), diethylstilbestrol has been listed as a known carcinogen. (Merck, 11th ed). diethylstilbestrol : An olefinic compound that is trans-hex-3-ene in which the hydrogens at positions 3 and 4 have been replaced by p-hydroxyphenyl groups.		2.0510olefinic compound;
polyphenol		antifungal agent;
antineoplastic agent;
autophagy inducer;
calcium channel blocker;
carcinogenic agent;
EC 1.1.1.146 (11beta-hydroxysteroid dehydrogenase) inhibitor;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor;
endocrine disruptor;
xenoestrogen
octreotide
[no description available]		3.2310
epothilone a
Epothilones: A group of 16-member MACROLIDES which stabilize MICROTUBULES in a manner similar to PACLITAXEL. They were originally found in the myxobacterium Sorangium cellulosum, now renamed to Polyangium (MYXOCOCCALES).		15.414418epothilone;
epoxide		antineoplastic agent;
metabolite;
microtubule-stabilising agent;
tubulin modulator
eptifibatide
[no description available]		3.2310homodetic cyclic peptide;
macrocycle;
organic disulfide		anticoagulant;
platelet aggregation inhibitor
alitretinoin
Alitretinoin: A retinoid that is used for the treatment of chronic hand ECZEMA unresponsive to topical CORTICOSTEROIDS. It is also used to treat cutaneous lesions associated with AIDS-related KAPOSI SARCOMA.		2.0510retinoic acidantineoplastic agent;
keratolytic drug;
metabolite;
retinoid X receptor agonist
decitabine
[no description available]		3.59202'-deoxyribonucleoside
teniposide
[no description available]		3.8630aromatic ether;
beta-D-glucoside;
cyclic acetal;
furonaphthodioxole;
gamma-lactone;
monosaccharide derivative;
phenols;
thiophenes		antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
valrubicin
[no description available]		2.0510anthracycline;
trifluoroacetamide
dactinomycin
Dactinomycin: A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)		3.5920actinomycinmutagen
tiazofurin
tiazofurin: RN given refers to (beta-D)-isomer; structure given in first source. tiazofurine : A C-glycosyl compound that is 1,3-thiazole-4-carboxamide in which the hydrogen at position 2 has been replaced by a beta-D-ribofuranosyl group. It is metabolised to thiazole-4-carboxamide adenine dinucleotide (TAD), a selective inhibitor of inosine monophosphate dehydrogenase (IMP dehydrogenase).		2.05101,3-thiazoles;
C-glycosyl compound;
monocarboxylic acid amide		antineoplastic agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
prodrug
melphalan
Melphalan: An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.. melphalan : A phenylalanine derivative comprising L-phenylalanine having [bis(2-chloroethyl)amino group at the 4-position on the phenyl ring.		3.8630L-phenylalanine derivative;
nitrogen mustard;
non-proteinogenic L-alpha-amino acid;
organochlorine compound		alkylating agent;
antineoplastic agent;
carcinogenic agent;
drug allergen;
immunosuppressive agent
tenofovir
tenofovir (anhydrous) : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens is replaced by a [(2R)-1-(6-amino-9H-purin-9-yl)propan-2-yl]oxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(isopropyloxycarbonyloxymethyl) ester (disoproxil ester) prodrug is used as the fumaric acid salt in combination therapy for the treatment of HIV infection.		3.5920nucleoside analogue;
phosphonic acids		antiviral drug;
drug metabolite;
HIV-1 reverse transcriptase inhibitor
posaconazole
[no description available]		3.2310aromatic ether;
conazole antifungal drug;
N-arylpiperazine;
organofluorine compound;
oxolanes;
triazole antifungal drug;
triazoles		trypanocidal drug
rubitecan
rubitecan: RN refers to (+-)-isomer; anti-HIV agent; DNA Topoisomerases, Type I inhibitor. rubitecan : A pyranoindolizinoquinoline that is camptothecin in which the hydrogen at position 9 has been replaced by a nitro group. It is a prodrug for 9-aminocamptothecin.		5.231C-nitro compound;
delta-lactone;
pyranoindolizinoquinoline;
semisynthetic derivative;
tertiary alcohol		antineoplastic agent;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
prodrug
micafungin
Micafungin: A cyclic lipo-hexapeptide echinocandin antifungal agent that is used for the treatment and prevention of CANDIDIASIS.. micafungin : A cyclic hexapeptide echinocandin antibiotic which exerts its effect by inhibiting the synthesis of 1,3-beta-D-glucan, an integral component of the fungal cell wall. It is used as the sodium salt for the treatment of invasive candidiasis, and of aspergillosis in patients who are intolerant of other therapy.		3.5920antibiotic antifungal drug;
echinocandin		antiinfective agent
riboflavin
vitamin B2 : Any member of a group of vitamers that belong to the chemical structural class called flavins that exhibit biological activity against vitamin B2 deficiency. Symptoms associated with vitamin B2 deficiency include glossitis, seborrhea, angular stomaitis, cheilosis and photophobia. The vitamers include riboflavin and its phosphate derivatives (and includes their salt, ionised and hydrate forms).		3.5920flavin;
vitamin B2		anti-inflammatory agent;
antioxidant;
cofactor;
Escherichia coli metabolite;
food colouring;
fundamental metabolite;
human urinary metabolite;
mouse metabolite;
photosensitizing agent;
plant metabolite
potassium permanganate
Potassium Permanganate: Permanganic acid (HMnO4), potassium salt. A highly oxidative, water-soluble compound with purple crystals, and a sweet taste. (From McGraw-Hill Dictionary of Scientific and Technical Information, 4th ed)		2.2510
sodium bicarbonate
Sodium Bicarbonate: A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.		4.1240one-carbon compound;
organic sodium salt		antacid;
food anticaking agent
sodium acetate, anhydrous
Sodium Acetate: The trihydrate sodium salt of acetic acid, which is used as a source of sodium ions in solutions for dialysis and as a systemic and urinary alkalizer, diuretic, and expectorant.		2.0510organic sodium saltNMR chemical shift reference compound
sodium benzoate
Sodium Benzoate: The sodium salt of BENZOIC ACID. It is used as an antifungal preservative in pharmaceutical preparations and foods. It may also be used as a test for liver function.. sodium benzoate : An organic sodium salt resulting from the replacement of the proton from the carboxy group of benzoic acid by a sodium ion.		2.0510organic sodium saltalgal metabolite;
antimicrobial food preservative;
drug allergen;
EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor;
EC 3.1.1.3 (triacylglycerol lipase) inhibitor;
human xenobiotic metabolite;
plant metabolite
arsenic trioxide
Tetraarsenic Oxide: A form of As2O3 that exists as As4O6 in the solid state. It dissociates to As2O3 upon heating to the vapor phase above 800 degrees Celsius.		3.2310arsenic oxideantineoplastic agent;
insecticide
dipyrone
Dipyrone: A drug that has analgesic, anti-inflammatory, and antipyretic properties. It is the sodium sulfonate of AMINOPYRINE.. metamizole sodium : An organic sodium salt of antipyrine substituted at C-4 by a methyl(sulfonatomethyl)amino group, commonly used as a powerful analgesic and antipyretic.		2.0510organic sodium saltanti-inflammatory agent;
antipyretic;
antirheumatic drug;
cyclooxygenase 3 inhibitor;
non-narcotic analgesic;
peripheral nervous system drug;
prodrug
ditiocarb sodium
[no description available]		2.0510organic molecular entity
bromochloroacetic acid
Keratins: A class of fibrous proteins or scleroproteins that represents the principal constituent of EPIDERMIS; HAIR; NAILS; horny tissues, and the organic matrix of tooth ENAMEL. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms a coiled-coil alpha helical structure consisting of TYPE I KERATIN and a TYPE II KERATIN, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. alpha-Keratins have been classified into at least 20 subtypes. In addition multiple isoforms of subtypes have been found which may be due to GENE DUPLICATION.. bromochloroacetic acid : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by bromine while a second is replaced by chlorine. A low-melting (27.5-31.5degreeC), hygroscopic crystalline solid, it can be formed during the disinfection (by chlorination) of water that contains bromide ions and organic matter, so can occur in drinking water as a byproduct of the disinfection process.		2.07102-bromocarboxylic acid;
monocarboxylic acid;
organochlorine compound
sr 90107
fondaparinux sodium : An organic sodium salt, being the decasodium salt of fondaparinux.		3.2310
carbenoxolone
[no description available]		2.0510
meglumine iodipamide
[no description available]		3.2310organoammonium saltradioopaque medium
glycosides
[no description available]		2.2510
isomethyleugenol
Methylation: Addition of methyl groups. In histo-chemistry methylation is used to esterify carboxyl groups and remove sulfate groups by treating tissue sections with hot methanol in the presence of hydrochloric acid. (From Stedman, 25th ed)		2.6620isomethyleugenol
citral
citral: Xref geranial: geraniol is also available; Xref neral: nerol is also available; vitamin A antagonist; oxygenated monoterpene; inhibits cytosolic dehydrogenases; structure. citral : An enal that consists of octa-2,6-dienal bearing methyl substituents at positions 3 and 7. A mixture of the two geometric isomers geranial and neral, it is the major constituent (75-85%) of oil of lemon grass, the volatile oil of Cymbopogon citratus, or of C. flexuosus. It also occurs in oils of verbena, lemon, and orange.		2.0510enal;
monoterpenoid;
polyprenal		plant metabolite;
volatile oil component
stilbenes
Stilbenes: Organic compounds that contain 1,2-diphenylethylene as a functional group.. trans-stilbene : The trans-isomer of stilbene.		3.1910stilbene
thyrotropin-releasing hormone
PR 546: no other info available 9/89. protirelin : A tripeptide composed of L-pyroglutamyl, L-histidyl and L-prolinamide residues joined in sequence.		3.2310peptide hormone;
tripeptide		human metabolite
discodermolide
[no description available]		2.0510diterpenoid
floxuridine
[no description available]		2.1310
cannabidiol
Cannabidiol: Compound isolated from Cannabis sativa extract.. cannabidiol : An cannabinoid that is cyclohexene which is substituted by a methyl group at position 1, a 2,6-dihydroxy-4-pentylphenyl group at position 3, and a prop-1-en-2-yl group at position 4.		2.0510olefinic compound;
phytocannabinoid;
resorcinols		antimicrobial agent;
plant metabolite
arginine vasopressin
Arginine Vasopressin: The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.. argipressin : The predominant form of mammalian vasopressin (antidiuretic hormone). It is a nonapeptide containing an arginine at residue 8 and two disulfide-linked cysteines at residues of 1 and 6.		3.2310vasopressincardiovascular drug;
hematologic agent;
mitogen
s 1033
[no description available]		3.2310(trifluoromethyl)benzenes;
imidazoles;
pyridines;
pyrimidines;
secondary amino compound;
secondary carboxamide		anticoronaviral agent;
antineoplastic agent;
tyrosine kinase inhibitor
leuprolide
Leuprolide: A potent synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE that regulates the synthesis and release of pituitary gonadotropins, LUTEINIZING HORMONE and FOLLICLE STIMULATING HORMONE.. leuprolide : An oligopeptide comprising pyroglutamyl, histidyl, tryptophyl, seryl, tyrosyl, D-leucyl, leucyl, arginyl, and N-ethylprolinamide residues joined in sequence. It is a synthetic nonapeptide analogue of gonadotropin-releasing hormone, and is used as a subcutaneous hydrogel implant (particularly as the acetate salt) for the treatment of prostate cancer and for the suppression of gonadal sex hormone production in children with central precocious puberty.		3.5420oligopeptideanti-estrogen;
antineoplastic agent;
gonadotropin releasing hormone agonist
fludarabine
[no description available]		3.8330purine nucleoside
propylthiouracil
Propylthiouracil: A thiourea antithyroid agent. Propythiouracil inhibits the synthesis of thyroxine and inhibits the peripheral conversion of throxine to tri-iodothyronine. It is used in the treatment of hyperthyroidism. (From Martindale, The Extra Pharmacopeoia, 30th ed, p534). 6-propyl-2-thiouracil : A pyrimidinethione consisting of uracil in which the 2-oxo group is substituted by a thio group and the hydrogen at position 6 is substituted by a propyl group.		3.5920pyrimidinethioneantidote to paracetamol poisoning;
antimetabolite;
antioxidant;
antithyroid drug;
carcinogenic agent;
EC 1.14.13.39 (nitric oxide synthase) inhibitor;
hormone antagonist
prothionamide
Prothionamide: Antitubercular agent similar in action and side effects to ETHIONAMIDE. It is used mostly in combination with other agents.		2.0510pyridines
sesquiterpenes
[no description available]		5.0333
etomidate
Etomidate: Imidazole derivative anesthetic and hypnotic with little effect on blood gases, ventilation, or the cardiovascular system. It has been proposed as an induction anesthetic.. etomidate : The ethyl ester of 1-[(1R)-1-phenylethyl]-1H-imidazole-5-carboxylic acid. It is an intravenous general anaesthetic with no analgesic activity.		3.5920ethyl ester;
imidazoles		intravenous anaesthetic;
sedative
mercaptopurine
Mercaptopurine: An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia.. purine-6-thiol : A thiol that is the tautomer of mercaptopurine.. mercaptopurine : A member of the class of purines that is 6,7-dihydro-1H-purine carrying a thione group at position 6. An adenine analogue, it is used in the treatment of acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML), Crohn's disease, and ulcerative colitis.		4.640aryl thiol;
purines;
thiocarbonyl compound		anticoronaviral agent;
antimetabolite;
antineoplastic agent
thioinosine
Thioinosine: Sulfhydryl analog of INOSINE that inhibits nucleoside transport across erythrocyte plasma membranes, and has immunosuppressive properties. It has been used similarly to MERCAPTOPURINE in the treatment of leukemia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p503)		2.0110
pyrantel
Pyrantel: A depolarizing neuromuscular-blocking agent, that causes persistent nicotinic activation resulting in spastic paralysis of susceptible nematodes. It is a drug of second-choice after benzimidazoles for treatment of ascariasis, hookworm, and pinworm infections, being effective after a single dose. (From Smith and Reynard, Textbook of Pharmacology, 1992, p920). pyrantel : A carboxamidine that is 1,4,5,6-tetrahydropyrimidine that is substituted at position 1 by a methyl group and at position 2 by an (E)-2-(2-thienyl)vinyl group. It is used, particularly as the embonate [4,4'-methylenebis(3-hydroxy-2-naphthoate)] salt, as an anthelmintic that is effective against intestinal nematodes including threadworms, roundworms and hookworms, and is included in the WHO 'Model List of Essential Medicines'.		3.23101,4,5,6-tetrahydropyrimidines;
carboxamidine;
thiophenes		antinematodal drug
2-amino-3-(4-chlorobenzoyl)-5,6,7,8-tetrahydrobenzothiophene
2-amino-3-(4-chlorobenzoyl)-5,6,7,8-tetrahydrobenzothiophene: an allosteric adenosine modulator		2.0510
thiothixene
[no description available]		3.2310N-methylpiperazineanticoronaviral agent
eszopiclone
Eszopiclone: A pyridine, pyrazine, and piperazine derivative that is used as a HYPNOTIC AND SEDATIVE in the treatment of INSOMNIA.. eszopiclone : The (5S)- (active) enantiomer of zopiclone. Unlike almost all other hypnotic sedatives, which are approved only for the relief of short-term (6-8 weeks) insomnia, eszopiclone is approved by the U.S. Food and Drug Administration for long-term use.		3.2310zopiclonecentral nervous system depressant;
sedative
curcumin
Curcumin: A yellow-orange dye obtained from tumeric, the powdered root of CURCUMA longa. It is used in the preparation of curcuma paper and the detection of boron. Curcumin appears to possess a spectrum of pharmacological properties, due primarily to its inhibitory effects on metabolic enzymes.. curcumin : A beta-diketone that is methane in which two of the hydrogens are substituted by feruloyl groups. A natural dyestuff found in the root of Curcuma longa.		4.5851aromatic ether;
beta-diketone;
diarylheptanoid;
enone;
polyphenol		anti-inflammatory agent;
antifungal agent;
antineoplastic agent;
biological pigment;
contraceptive drug;
dye;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
EC 1.1.1.21 (aldehyde reductase) inhibitor;
EC 1.1.1.25 (shikimate dehydrogenase) inhibitor;
EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor;
EC 1.8.1.9 (thioredoxin reductase) inhibitor;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor;
EC 3.5.1.98 (histone deacetylase) inhibitor;
flavouring agent;
food colouring;
geroprotector;
hepatoprotective agent;
immunomodulator;
iron chelator;
ligand;
lipoxygenase inhibitor;
metabolite;
neuroprotective agent;
nutraceutical;
radical scavenger
benztropine
Benztropine: A centrally active muscarinic antagonist that has been used in the symptomatic treatment of PARKINSON DISEASE. Benztropine also inhibits the uptake of dopamine.. benzatropine : Tropane in which a hydrogen at position 3 is substituted by a diphenylmethoxy group (endo-isomer). An acetylcholine receptor antagonist, it is used (particularly as its methanesulphonate salt) in the treatment of Parkinson's disease, and to reduce parkinsonism and akathisia side effects of antipsychotic treatments.		3.2310diarylmethane
methimazole
Methimazole: A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. This is done by interfering with the oxidation of iodide ion and iodotyrosyl groups through inhibition of the peroxidase enzyme.. methimazole : A member of the class of imidazoles that it imidazole-2-thione in which a methyl group replaces the hydrogen which is attached to a nitrogen.		3.59201,3-dihydroimidazole-2-thionesantithyroid drug
sulindac
Sulindac: A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.. sulindac : A monocarboxylic acid that is 1-benzylidene-1H-indene which is substituted at positions 2, 3, and 5 by methyl, carboxymethyl, and fluorine respectively, and in which the phenyl group of the benzylidene moiety is substituted at the para position by a methylsulfinyl group. It is a prodrug for the corresponding sulfide, a non-steroidal anti-inflammatory drug, used particularly in the treatment of acute and chronic inflammatory conditions.		5.2331monocarboxylic acid;
organofluorine compound;
sulfoxide		analgesic;
antineoplastic agent;
antipyretic;
apoptosis inducer;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
prodrug;
tocolytic agent
capsaicin
ALGRX-4975: an injectable capsaicin (TRPV1 receptor agonist) formulation for longlasting pain relief. capsaicinoid : A family of aromatic fatty amides produced as secondary metabolites by chilli peppers.		2.0510capsaicinoidnon-narcotic analgesic;
TRPV1 agonist;
voltage-gated sodium channel blocker
terbinafine
[no description available]		3.5920acetylenic compound;
allylamine antifungal drug;
enyne;
naphthalenes;
tertiary amine		EC 1.14.13.132 (squalene monooxygenase) inhibitor;
P450 inhibitor;
sterol biosynthesis inhibitor
thioguanine anhydrous
Thioguanine: An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.. tioguanine : A 2-aminopurine that is the 6-thiono derivative of 2-amino-1,9-dihydro-6H-purine. Incorporates into DNA and inhibits synthesis. Used in the treatment of leukaemia.		4.27502-aminopurinesanticoronaviral agent;
antimetabolite;
antineoplastic agent
tacrine hydrochloride
[no description available]		2.0510
sodium propionate
sodium propionate: was term of propionic acid (1986-2006). sodium propionate : An organic sodium salt comprising equal numbers of sodium and propionate ions.		2.0510organic sodium saltantifungal drug;
food preservative
potassium oxonate
potassium oxonate: used to induce hyperuricemia in mice		3.8521organic molecular entity
succimer
Succimer: A mercaptodicarboxylic acid used as an antidote to heavy metal poisoning because it forms strong chelates with them.. succimer : A sulfur-containing carboxylic acid that is succinic acid bearing two mercapto substituents at positions 2 and 3. A lead chelator used as an antedote to lead poisoning.		3.2310dicarboxylic acid;
dithiol;
sulfur-containing carboxylic acid		chelator
digoxin
Digoxin: A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666). digoxin : A cardenolide glycoside that is digitoxin beta-hydroxylated at C-12. A cardiac glycoside extracted from the foxglove plant, Digitalis lanata, it is used to control ventricular rate in atrial fibrillation and in the management of congestive heart failure with atrial fibrillation, but the margin between toxic and therapeutic doses is small.		3.5920cardenolide glycoside;
steroid saponin		anti-arrhythmia drug;
cardiotonic drug;
EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor;
epitope
streptozocin
[no description available]		3.8630
tamoxifen
[no description available]		7.41141stilbenoid;
tertiary amino compound		angiogenesis inhibitor;
antineoplastic agent;
bone density conservation agent;
EC 1.2.3.1 (aldehyde oxidase) inhibitor;
EC 2.7.11.13 (protein kinase C) inhibitor;
estrogen antagonist;
estrogen receptor antagonist;
estrogen receptor modulator
ethionamide
Ethionamide: A second-line antitubercular agent that inhibits mycolic acid synthesis.. ethionamide : A thiocarboxamide that is pyridine-4-carbothioamide substituted by an ethyl group at position 2. A prodrug that undergoes metabolic activation by conversion to the corresponding S-oxide.		3.5920pyridines;
thiocarboxamide		antilipemic drug;
antitubercular agent;
fatty acid synthesis inhibitor;
leprostatic drug;
prodrug
cancidas
[no description available]		3.2310
fusidic acid
Fusidic Acid: An antibiotic isolated from the fermentation broth of Fusidium coccineum. (From Merck Index, 11th ed). It acts by inhibiting translocation during protein synthesis.. fusidic acid : A steroid antibiotic that is isolated from the fermentation broth of Fusidium coccineum.		2.051011alpha-hydroxy steroid;
3alpha-hydroxy steroid;
alpha,beta-unsaturated monocarboxylic acid;
steroid acid;
steroid antibiotic;
sterol ester		EC 2.7.1.33 (pantothenate kinase) inhibitor;
Escherichia coli metabolite;
protein synthesis inhibitor
lincomycin
Lincomycin: An antibiotic produced by Streptomyces lincolnensis var. lincolnensis. It has been used in the treatment of staphylococcal, streptococcal, and Bacteroides fragilis infections.. lincomycin : A carbohydrate-containing antibiotic produced by the actinomyces Streptomyces lincolnensis.		3.2310carbohydrate-containing antibiotic;
L-proline derivative;
monocarboxylic acid amide;
pyrrolidinecarboxamide;
S-glycosyl compound		antimicrobial agent;
bacterial metabolite
estrone sulfate
estrone sulfate: sulfoconjugated estrone; RN given refers to parent cpd		2.051017-oxo steroid;
steroid sulfate		human metabolite;
mouse metabolite
ranitidine
Ranitidine: A non-imidazole blocker of those histamine receptors that mediate gastric secretion (H2 receptors). It is used to treat gastrointestinal ulcers.. ranitidine : A member of the class of furans used to treat peptic ulcer disease (PUD) and gastroesophageal reflux disease.		3.2310C-nitro compound;
furans;
organic sulfide;
tertiary amino compound		anti-ulcer drug;
drug allergen;
environmental contaminant;
H2-receptor antagonist;
xenobiotic
aplaviroc
aplaviroc: a spiro-diketo-piperazine; a potent noncompetitive allosteric antagonist of the CCR5 receptor with concomitantly potent antiviral effects for HIV-1; structure in first source		3.2310
hmr 3647
[no description available]		3.5920
maraviroc
[no description available]		3.2310tropane alkaloid
toremifene
Toremifene: A first generation selective estrogen receptor modulator (SERM). Like TAMOXIFEN, it is an estrogen agonist for bone tissue and cholesterol metabolism but is antagonistic on mammary and uterine tissue.		9.0740aromatic ether;
organochlorine compound;
tertiary amine		antineoplastic agent;
bone density conservation agent;
estrogen antagonist;
estrogen receptor modulator
telaprevir
[no description available]		2.4620cyclopentapyrrole;
cyclopropanes;
oligopeptide;
pyrazines		antiviral drug;
hepatitis C protease inhibitor;
peptidomimetic
nelarabine
nelarabine: prodrug of ara-G. nelarabine : A purine nucleoside in which O-methylguanine is attached to arabinofuranose via a beta-N(9)-glycosidic bond. Inhibits DNA synthesis and causes cell death; a prodrug of 9-beta-D-arabinofuranosylguanine (ara-G).		3.2310beta-D-arabinoside;
monosaccharide derivative;
purine nucleoside		antineoplastic agent;
DNA synthesis inhibitor;
prodrug
lithium
Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight [6.938; 6.997]. Salts of lithium are used in treating BIPOLAR DISORDER.		2.610alkali metal atom
thiophanate
thiophanate-methyl : A member of the class of thioureas that is the dimethyl ester of (1,2-phenylenedicarbamothioyl)biscarbamic acid. A fungicide effective against a broad spectrum of diseases in fruit, vegetables, turf and other crops including eyespot, scab, powdery mildew and grey mould.		2.0510benzimidazole precursor fungicide;
carbamate ester;
carbamate fungicide;
thioureas		antifungal agrochemical
dermatan sulfate
Dermatan Sulfate: A naturally occurring glycosaminoglycan found mostly in the skin and in connective tissue. It differs from CHONDROITIN SULFATE A (see CHONDROITIN SULFATES) by containing IDURONIC ACID in place of glucuronic acid, its epimer, at carbon atom 5. (from Merck, 12th ed). alpha-L-IdopA-(1->3)-beta-D-GalpNAc4S : An oligosaccharide sulfate that is 2-acetamido-2-deoxy-4-O-sulfo-beta-D-galactopyranose in which the hydroxy group at position 3 has been converted to the corresponding alpha-L-idopyranuronoside.. dermatan sulfate : Any of a group of glycosaminoglycans with repeating units consisting of variously sulfated beta1->4-linked L-iduronyl-(alpha1->3)-N-acetyl-D-galactosamine units.		3.2310amino disaccharide;
glycosylgalactose derivative;
iduronic acids;
oligosaccharide sulfate
droloxifene
[no description available]		2.0510stilbenoid
dolasetron
[no description available]		3.2310indolyl carboxylic acid
or 1259
[no description available]		2.0510hydrazone;
nitrile;
pyridazinone		anti-arrhythmia drug;
cardiotonic drug;
EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor;
vasodilator agent
gestodene
Gestodene: synthetic steroid with progestational activity; RN given refers to (17alpha)-isomer		2.0510steroidestrogen
orlistat
Orlistat: A lactone derivative of LEUCINE that acts as a pancreatic lipase inhibitor to limit the absorption of dietary fat; it is used in the management of obesity.. orlistat : A carboxylic ester resulting from the formal condensation of the carboxy group of N-formyl-L-leucine with the hydroxy group of (3S,4S)-3-hexyl-4-[(2S)-2-hydroxytridecyl]oxetan-2-one. A pancreatic lipase inhibitor, it is used as an anti-obesity drug.		3.5920beta-lactone;
carboxylic ester;
formamides;
L-leucine derivative		anti-obesity agent;
bacterial metabolite;
EC 2.3.1.85 (fatty acid synthase) inhibitor;
EC 3.1.1.3 (triacylglycerol lipase) inhibitor
idoxifene
idoxifene: structure given in first source		2.0510stilbenoid
quinine
[no description available]		3.2310cinchona alkaloidantimalarial;
muscle relaxant;
non-narcotic analgesic
cystine
[no description available]		4.5622
fospropofol
[no description available]		3.2310alkylbenzene
rasagiline
[no description available]		3.2310indanes;
secondary amine;
terminal acetylenic compound		EC 1.4.3.4 (monoamine oxidase) inhibitor;
neuroprotective agent
dasatinib
N-(2-chloro-6-methylphenyl)-2-((6-(4-(2-hydroxyethyl)piperazin-1-yl)-2-methylpyrimidin-4-yl)amino)-1,3-thiazole-5-carboxamide: a dasatinib prodrug; structure in first source. dasatinib (anhydrous) : An aminopyrimidine that is 2-methylpyrimidine which is substituted at position 4 by the primary amino group of 2-amino-1,3-thiazole-5-carboxylic acid and at position 6 by a 4-(2-hydroxyethyl)piperazin-1-yl group, and in which the carboxylic acid group has been formally condensed with 2-chloro-6-methylaniline to afford the corresponding amide. A multi-targeted kinase inhibitor, it is used, particularly as the monohydrate, for the treatment of chronic, accelerated, or myeloid or lymphoid blast phase chronic myeloid leukemia. Note that the name 'dasatinib' is used to refer to the monohydrate (USAN) as well as to anhydrous dasatinib (INN).		6.95421,3-thiazoles;
aminopyrimidine;
monocarboxylic acid amide;
N-(2-hydroxyethyl)piperazine;
N-arylpiperazine;
organochlorine compound;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antineoplastic agent;
tyrosine kinase inhibitor
zd 6474
CH 331: structure in first source		7.4442aromatic ether;
organobromine compound;
organofluorine compound;
piperidines;
quinazolines;
secondary amine		antineoplastic agent;
tyrosine kinase inhibitor
2-fluoro-2-deoxyglucose-6-phosphate
2-fluoro-2-deoxyglucose-6-phosphate: metabolite of 2-fluoro-2-deoxyglucose; RN given refers to D-Glu cpd; RN for parent cpd not avail 10/90		4.4111
ginsenosides
ginsenoside : Triterpenoid saponins with a dammarane-like skeleton originally isolated from ginseng (Panax) species. Use of the term has been extended to include semi-synthetic derivatives.		2.9610
silybin
[no description available]		2.0510
chloramine-t
chloramine-T: RN given refers to unlabeled parent cpd. chloramine T : An organic sodium salt derivative of toluene-4-sulfonamide with a chloro substituent in place of an amino hydrogen.		2.0510organic sodium saltallergen;
antifouling biocide;
disinfectant
sb 242084
6-chloro-5-methyl-1-((2-(2-methylpyrid-3-yloxy)pyrid-5-yl)carbamoyl)indoline: 5-HT(2C) receptor inverse agonist (antagonist); structure in first source		2.0510
naphthoquinones
Naphthoquinones: Naphthalene rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups.		5.131
sitagliptin
sitagliptin : A triazolopyrazine that exhibits hypoglycemic activity.		3.2310triazolopyrazine;
trifluorobenzene		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
environmental contaminant;
hypoglycemic agent;
serine proteinase inhibitor;
xenobiotic
flosequinan
[no description available]		2.0510quinolines
rhodamine 123
Rhodamine 123: A fluorescent probe with low toxicity which is a potent substrate for ATP BINDING CASSETTE TRANSPORTER, SUBFAMILY B, MEMBER 1 and the bacterial multidrug efflux transporter. It is used to assess mitochondrial bioenergetics in living cells and to measure the efflux activity of ATP BINDING CASSETTE TRANSPORTER, SUBFAMILY B, MEMBER 1 in both normal and malignant cells. (Leukemia 1997;11(7):1124-30). rhodamine 123(1+) : A cationic fluorescent dye derived from 9-phenylxanthene.		2.0610organic cation;
xanthene dye		fluorochrome
tolcapone
Tolcapone: A benzophenone and nitrophenol compound that acts as an inhibitor of CATECHOL O-METHYLTRANSFERASE, an enzyme involved in the metabolism of DOPAMINE and LEVODOPA. It is used in the treatment of PARKINSON DISEASE in patients for whom levodopa is ineffective or contraindicated.. tolcapone : Benzophenone substituted on one of the phenyl rings at C-3 and C-4 by hydroxy groups and at C-5 by a nitro group, and on the other phenyl ring by a methyl group at C-4. It is an inhibitor of catechol O-methyltransferase.		3.59202-nitrophenols;
benzophenones;
catechols		antiparkinson drug;
EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
quercetin
[no description available]		2.96307-hydroxyflavonol;
pentahydroxyflavone		antibacterial agent;
antineoplastic agent;
antioxidant;
Aurora kinase inhibitor;
chelator;
EC 1.10.99.2 [ribosyldihydronicotinamide dehydrogenase (quinone)] inhibitor;
geroprotector;
phytoestrogen;
plant metabolite;
protein kinase inhibitor;
radical scavenger
bilirubin
[no description available]		4.6732biladienes;
dicarboxylic acid		antioxidant;
human metabolite;
mouse metabolite
dinoprostone
prostaglandin E2 : Prostaglandin F2alpha in which the hydroxy group at position 9 has been oxidised to the corresponding ketone. Prostaglandin E2 is the most common and most biologically potent of mammalian prostaglandins.		2.0510prostaglandins Ehuman metabolite;
mouse metabolite;
oxytocic
dinoprost
Dinoprost: A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.. prostaglandin F2alpha : A prostaglandins Falpha that is prosta-5,13-dien-1-oic acid substituted by hydroxy groups at positions 9, 11 and 15. It is a naturally occurring prostaglandin used to induce labor.		2.0510monocarboxylic acid;
prostaglandins Falpha		human metabolite;
mouse metabolite
calcitriol
dihydroxy-vitamin D3: as a major in vitro metabolite of 1alpha,25-dihydroxyvitamin D3, produced in primary cultures of neonatal human keratinocytes		3.5920D3 vitamins;
hydroxycalciol;
triol		antineoplastic agent;
antipsoriatic;
bone density conservation agent;
calcium channel agonist;
calcium channel modulator;
hormone;
human metabolite;
immunomodulator;
metabolite;
mouse metabolite;
nutraceutical
beta carotene
beta Carotene: A carotenoid that is a precursor of VITAMIN A. Beta carotene is administered to reduce the severity of photosensitivity reactions in patients with erythropoietic protoporphyria (PORPHYRIA, ERYTHROPOIETIC).. provitamin A : A provitamin that can be converted into vitamin A by enzymes from animal tissues.		2.0510carotenoid beta-end derivative;
cyclic carotene		antioxidant;
biological pigment;
cofactor;
ferroptosis inhibitor;
human metabolite;
mouse metabolite;
plant metabolite;
provitamin A
alprostadil
[no description available]		2.0510prostaglandins Eanticoagulant;
human metabolite;
platelet aggregation inhibitor;
vasodilator agent
vitamin d 2
Ergocalciferols: Derivatives of ERGOSTEROL formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. They differ from CHOLECALCIFEROL in having a double bond between C22 and C23 and a methyl group at C24.. vitamin D2 : A vitamin D supplement and has been isolated from alfalfa.		3.2310hydroxy seco-steroid;
seco-ergostane;
vitamin D		bone density conservation agent;
nutraceutical;
plant metabolite;
rodenticide
cholecalciferol
Cholecalciferol: Derivative of 7-dehydroxycholesterol formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. It differs from ERGOCALCIFEROL in having a single bond between C22 and C23 and lacking a methyl group at C24.. calciol : A hydroxy seco-steroid that is (5Z,7E)-9,10-secocholesta-5,7,10(19)-triene in which the pro-S hydrogen at position 3 has been replaced by a hydroxy group. It is the inactive form of vitamin D3, being hydroxylated in the liver to calcidiol (25-hydroxyvitamin D3), which is then further hydroxylated in the kidney to give calcitriol (1,25-dihydroxyvitamin D3), the active hormone.		2.0510D3 vitamins;
hydroxy seco-steroid;
seco-cholestane;
secondary alcohol;
steroid hormone		geroprotector;
human metabolite
genistein
[no description available]		2.25107-hydroxyisoflavonesantineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
geroprotector;
human urinary metabolite;
phytoestrogen;
plant metabolite;
tyrosine kinase inhibitor
amphotericin b
Amphotericin B: Macrolide antifungal antibiotic produced by Streptomyces nodosus obtained from soil of the Orinoco river region of Venezuela.. amphotericin B : A macrolide antibiotic used to treat potentially life-threatening fungal infections.		3.5920antibiotic antifungal drug;
macrolide antibiotic;
polyene antibiotic		antiamoebic agent;
antiprotozoal drug;
bacterial metabolite
clavulanic acid
Clavulanic Acid: A beta-lactam antibiotic produced by the actinobacterium Streptomyces clavuligerus. It is a suicide inhibitor of bacterial beta-lactamase enzymes. Administered alone, it has only weak antibacterial activity against most organisms, but given in combination with other beta-lactam antibiotics it prevents antibiotic inactivation by microbial lactamase.. clavulanate : The conjugate base of clavulanic acid.. clavulanic acid : Antibiotic isolated from Streptomyces clavuligerus. It acts as a suicide inhibitor of bacterial beta-lactamase enzymes.		2.0510oxapenamantibacterial drug;
anxiolytic drug;
bacterial metabolite;
EC 3.5.2.6 (beta-lactamase) inhibitor
pulmicort
Budesonide: A glucocorticoid used in the management of ASTHMA, the treatment of various skin disorders, and allergic RHINITIS.. budesonide : A glucocorticoid steroid having a highly oxygenated pregna-1,4-diene structure. It is used mainly in the treatment of asthma and non-infectious rhinitis and for treatment and prevention of nasal polyposis.		3.93011beta-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
cyclic acetal;
glucocorticoid;
primary alpha-hydroxy ketone		anti-inflammatory drug;
bronchodilator agent;
drug allergen
oxymetholone
Oxymetholone: A synthetic hormone with anabolic and androgenic properties. It is used mainly in the treatment of anemias. According to the Fourth Annual Report on Carcinogens (NTP 85-002), this compound may reasonably be anticipated to be a carcinogen. (From Merck Index, 11th ed). oxymetholone : A 3-oxo-5alpha- steroid that is 4,5alpha-dihydrotestosterone which is substituted by a hydroxymethylidene group at position 2 and by a methyl group at the 17alpha position. A synthetic androgen, it was mainly used for the treatment of anaemias until being replaced by treatments with fewer side effects.		3.5920
eprosartan
eprosartan: angiotensin II receptor antagonist. eprosartan : A member of the class of imidazoles and thiophenes that is an angiotensin II receptor antagonist used for the treatment of high blood pressure.		3.2310dicarboxylic acid;
imidazoles;
thiophenes		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
montelukast
montelukast: a leukotriene D4 receptor antagonist		3.8330aliphatic sulfide;
monocarboxylic acid;
quinolines		anti-arrhythmia drug;
anti-asthmatic drug;
leukotriene antagonist
mivacurium
Mivacurium: An isoquinoline derivative that is used as a short-acting non-depolarizing agent.		3.2310isoquinolines
hemabate
carboprost tromethamine : The tromethamine salt of carboprost. It is used as an abortifacient agent that is effective in both the first and second trimesters of pregnancy.		3.2310
mycophenolate mofetil
mycophenolate mofetil : A carboxylic ester resulting from the formal condensation between the carboxylic acid group of mycophenolic acid and the hydroxy group of 2-(morpholin-4-yl)ethanol. In the liver, it is metabolised to mycophenolic acid, an immunosuppressant for which it is a prodrug. It is widely used to prevent tissue rejection following organ transplants as well as for the treatment of certain autoimmune diseases.		3.5920carboxylic ester;
ether;
gamma-lactone;
phenols;
tertiary amino compound		anticoronaviral agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
immunosuppressive agent;
prodrug
entacapone
entacapone: structure given in first source. entacapone : A monocarboxylic acid amide that is N,N-diethylprop-2-enamide in which the hydrogen at position 2 is substituted by a cyano group and the hydrogen at the 3E position is substituted by a 3,4-dihydroxy-5-nitrophenyl group.		3.59202-nitrophenols;
catechols;
monocarboxylic acid amide;
nitrile		antidyskinesia agent;
antiparkinson drug;
central nervous system drug;
EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
paricalcitol
[no description available]		3.2310hydroxy seco-steroid;
seco-cholestane		antiparathyroid drug
astaxanthine
astaxanthine: a keto form of carotene; pigment in flesh of Scottish salmon (Salmo salar) crustacoa-lobster (Homarus gammarus, flamingo feathers; structure; a carotenoid without vitamin A activity, has shown anti-oxidant and anti-inflammatory activities. astaxanthin : A carotenone that consists of beta,beta-carotene-4,4'-dione bearing two hydroxy substituents at positions 3 and 3' (the 3S,3'S diastereomer). A carotenoid pigment found mainly in animals (crustaceans, echinoderms) but also occurring in plants. It can occur free (as a red pigment), as an ester, or as a blue, brown or green chromoprotein.		2.0510carotenol;
carotenone		animal metabolite;
anticoagulant;
antioxidant;
food colouring;
plant metabolite
baicalein
[no description available]		7.610trihydroxyflavoneangiogenesis inhibitor;
anti-inflammatory agent;
antibacterial agent;
anticoronaviral agent;
antifungal agent;
antineoplastic agent;
antioxidant;
apoptosis inducer;
EC 1.13.11.31 (arachidonate 12-lipoxygenase) inhibitor;
EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor;
EC 4.1.1.17 (ornithine decarboxylase) inhibitor;
ferroptosis inhibitor;
geroprotector;
hormone antagonist;
plant metabolite;
prostaglandin antagonist;
radical scavenger
chrysin
chrysin : A dihydroxyflavone in which the two hydroxy groups are located at positions 5 and 7.		2.05107-hydroxyflavonol;
dihydroxyflavone		anti-inflammatory agent;
antineoplastic agent;
antioxidant;
EC 2.7.11.18 (myosin-light-chain kinase) inhibitor;
hepatoprotective agent;
plant metabolite
diosmin
[no description available]		2.0510dihydroxyflavanone;
disaccharide derivative;
glycosyloxyflavone;
monomethoxyflavone;
rutinoside		anti-inflammatory agent;
antioxidant
3-methylquercetin
isorhamnetin : A monomethoxyflavone that is quercetin in which the hydroxy group at position 3' is replaced by a methoxy group.		2.11107-hydroxyflavonol;
monomethoxyflavone;
tetrahydroxyflavone		anticoagulant;
EC 1.14.18.1 (tyrosinase) inhibitor;
metabolite
cynarine
cynarine: active principle of the artichoke; functions primarily as a cholagogue and choleretic and also as antilipemic agent		2.0510alkyl caffeate ester;
quinic acid		plant metabolite
maytansine
Maytansine: An ansa macrolide isolated from the MAYTENUS genus of East African shrubs.. maytansine : An organic heterotetracyclic compound and 19-membered macrocyclic lactam antibiotic originally isolated from the Ethiopian shrub Maytenus serrata but also found in other Maytenus species. It exhibits cytotoxicity against many tumour cell lines.		13.312512alpha-amino acid ester;
carbamate ester;
epoxide;
maytansinoid;
organic heterotetracyclic compound;
organochlorine compound		antimicrobial agent;
antimitotic;
antineoplastic agent;
plant metabolite;
tubulin modulator
sdz psc 833
valspodar: nonimmunosuppressive cyclosporin analog which is a potent multidrug resistance modifier; 7-10 fold more potent than cyclosporin A; a potent P glycoprotein inhibitor; MW 1215		2.0510homodetic cyclic peptide
coenzyme q10
coenzyme Q10: Ubiquinone ring with a chain of 10 isoprene units; redox equilibrium with ubiqunol serving in mitochondrial inner membrane to transfer electrons; presence during reconstitution of acetylcholine receptor into phospholipid vesicles yields vesicles active in catalyzing carbamylcholine-sensitive Na+ flux; coenzyme Q10 depletion has been noted with use of statins. coenzyme Q10 : A ubiquinone having a side chain of 10 isoprenoid units. In the naturally occurring isomer, all isoprenyl double bonds are in the E- configuration.		2.0510ubiquinonesantioxidant;
ferroptosis inhibitor;
human metabolite
tranilast
tranilast: antiallergic drug; potent inhibitor of homologous passive cutaneous anaphylaxis. tranilast : An amidobenzoic acid that is anthranilic acid in which one of the anilino hydrogens is replaced by a 3,4-dimethoxycinnamoyl group.		2.0510amidobenzoic acid;
cinnamamides;
dimethoxybenzene;
secondary carboxamide		anti-allergic agent;
anti-asthmatic drug;
antineoplastic agent;
aryl hydrocarbon receptor agonist;
calcium channel blocker;
hepatoprotective agent;
nephroprotective agent
7432 s
Ceftibuten: A cephalosporin antibacterial agent that is used in the treatment of infections, including urinary-tract and respiratory-tract infections.. ceftibuten : A third-generation cephalosporin antibiotic with a [(2Z)-2-(2-amino-1,3-thiazol-4-yl)-4-carboxybut-2-enoyl]amino substituent at the 7 position of the cephem skeleton. An orally-administered agent, ceftibuten is used as the dihydrate to treat urinary-tract and respiratory-tract infections.		3.2310cephalosporin;
dicarboxylic acid		antibacterial drug
etretinate
retinoid : Oxygenated derivatives of 3,7-dimethyl-1-(2,6,6-trimethylcyclohex-1-enyl)nona-1,3,5,7-tetraene and derivatives thereof.		2.0510enoate ester;
ethyl ester;
retinoid		keratolytic drug
isotretinoin
Isotretinoin: A topical dermatologic agent that is used in the treatment of ACNE VULGARIS and several other skin diseases. The drug has teratogenic and other adverse effects.. isotretinoin : A retinoic acid that is all-trans-retinoic acid in which the double bond which is alpha,beta- to the carboxy group is isomerised to Z configuration. A synthetic retinoid, it is used for the treatment of severe cases of acne and other skin diseases.		6.6963retinoic acidantineoplastic agent;
keratolytic drug;
teratogenic agent
misoprostol
Misoprostol: A synthetic analog of natural prostaglandin E1. It produces a dose-related inhibition of gastric acid and pepsin secretion, and enhances mucosal resistance to injury. It is an effective anti-ulcer agent and also has oxytocic properties.. misoprostol : A diastereoisomeric mixture composed of approximately equal amounts of a double racemate of four of the sixteen possible diastereoisomers of methyl (13E)-11,16-dihydroxy-16-methyl-9-oxoprost-13-en-1-oate that is racemic prostaglandin E1 which is lacking the hydroxy group at position 15, but which has an additional hydroxy group at position 16. It is a synthetic prostaglandin E1 analogue, used in the treatment of gastric and duodenal ulcers. A weak abortifacient, it is also used for cervical ripening prior to surgical termination of pregnancy. The (11R,16S)-diastereoisomer is the pharmacologically active form.		2.0510
epoprostenol
[no description available]		3.2310prostaglandins Imouse metabolite
indocyanine green
[no description available]		3.23101,1-diunsubstituted alkanesulfonate;
benzoindole;
cyanine dye
ozagrel
ozagrel: RN refers to (E)-isomer		2.0510cinnamic acids
triprolidine
Triprolidine: Histamine H1 antagonist used in allergic rhinitis; ASTHMA; and URTICARIA. It is a component of COUGH and COLD medicines. It may cause drowsiness.. triprolidine : An N-alkylpyrrolidine that is acrivastine in which the pyridine ring is lacking the propenoic acid substituent. It is a sedating antihistamine that is used (generally as the monohydrochloride monohydrate) for the relief of the symptoms of uticaria, rhinitis, and various pruritic skin disorders.		3.2310N-alkylpyrrolidine;
olefinic compound;
pyridines		H1-receptor antagonist
pitavastatin
pitavastatin : A dihydroxy monocarboxylic acid that is (6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]hept-6-enoic acid in which the two hydroxy groups are located at positions 3 and 5 (the 3R,5S-stereoisomer). Used as its calcium salt for treatment of hypercholesterolemia (elevated levels of cholesterol in the blood) on patients unable to sufficiently lower their cholesterol levels by diet and exercise.		3.5920cyclopropanes;
dihydroxy monocarboxylic acid;
monofluorobenzenes;
quinolines;
statin (synthetic)		antioxidant
ethamolin
monoethanolamine oleate: used for treatment of pyogenic granuloma		3.2310long-chain fatty acid
alatrofloxacin mesylate
[no description available]		3.5920
2-nonenal, (trans)-isomer
2-nonenal: RN given refers to cpd without isomeric designation. non-2-enal : An enal consisting of non-2-ene having an oxo group at the 1-position.. (E)-non-2-enal : A monounsaturated fatty aldehyde that is (2E)-non-2-ene which is carrying an oxo group at position 1.		2.0510enal;
medium-chain fatty aldehyde;
monounsaturated fatty aldehyde		plant metabolite
codeine
[no description available]		3.5920morphinane alkaloid;
organic heteropentacyclic compound		antitussive;
drug allergen;
environmental contaminant;
opioid analgesic;
opioid receptor agonist;
prodrug;
xenobiotic
cyclosporine
ramihyphin A: one of the metabolites produced by Fusarium sp. S-435; RN given refers to cpd with unknown MF		3.5920homodetic cyclic peptideanti-asthmatic drug;
anticoronaviral agent;
antifungal agent;
antirheumatic drug;
carcinogenic agent;
dermatologic drug;
EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
geroprotector;
immunosuppressive agent;
metabolite
natamycin
[no description available]		2.0510antibiotic antifungal drug;
dicarboxylic acid monoester;
epoxide;
macrolide antibiotic;
monosaccharide derivative;
polyene antibiotic		antifungal agrochemical;
antimicrobial food preservative;
apoptosis inducer;
bacterial metabolite;
ophthalmology drug
acitretin
Acitretin: An oral retinoid effective in the treatment of psoriasis. It is the major metabolite of ETRETINATE with the advantage of a much shorter half-life when compared with etretinate.. acitretin : A retinoid that consists of 3,7-dimethylnona-2,4,6,8-tetraenoic acid having a 4-methoxy-2,3,6-trimethylphenyl group attached at position 9.		3.8830acitretin;
alpha,beta-unsaturated monocarboxylic acid;
retinoid		keratolytic drug
dorzolamide
dorzolamide: topically effective ocular hypotensive carbonic anhydrase inhibitor; RN refers to mono-HCl (4S-trans)-isomer. dorzolamide : 5,6-Dihydro-4H-thieno[2,3-b]thiopyran-2-sulfonamide 7,7-dioxide in which hydrogens at the 4 and 6 positions are substituted by ethylamino and methyl groups, respectively (4S, trans-configuration). A carbonic anhydrase inhibitor, it is used as the hydrochloride in ophthalmic solutions to lower increased intraocular pressure in the treatment of open-angle glaucoma and ocular hypertension.		2.0110sulfonamide;
thiophenes		antiglaucoma drug;
antihypertensive agent;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
dothiepin
[no description available]		2.0510dothiepin
estropipate
estropipate: used therapeutically in menopausal patients		3.2310piperazinium salt;
steroid sulfate
granisetron
Granisetron: A serotonin receptor (5HT-3 selective) antagonist that has been used as an antiemetic for cancer chemotherapy patients.. granisetron : A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of 1-methyl-1H-indazole-3-carboxylic acid with the primary amino group of (3-endo)-9-methyl-9-azabicyclo[3.3.1]nonan-3-amine. A selective 5-HT3 receptor antagonist, it is used (generally as the monohydrochloride salt) to manage nausea and vomiting caused by cancer chemotherapy and radiotherapy, and to prevent and treat postoperative nausea and vomiting.		3.1410aromatic amide;
indazoles
hydromorphone
Hydromorphone: An opioid analgesic made from MORPHINE and used mainly as an analgesic. It has a shorter duration of action than morphine.. hydromorphone : A morphinane alkaloid that is a hydrogenated ketone derivative of morphine. A semi-synthetic drug, it is a centrally acting pain medication of the opioid class.		3.2310morphinane alkaloid;
organic heteropentacyclic compound		mu-opioid receptor agonist;
opioid analgesic
levetiracetam
Levetiracetam: A pyrrolidinone and acetamide derivative that is used primarily for the treatment of SEIZURES and some movement disorders, and as a nootropic agent.. levetiracetam : A pyrrolidinone and carboxamide that is N-methylpyrrolidin-2-one in which one of the methyl hydrogens is replaced by an aminocarbonyl group, while another is replaced by an ethyl group (the S enantiomer). An anticonvulsant, it is used for the treatment of epilepsy in both human and veterinary medicine.		3.5920pyrrolidin-2-onesanticonvulsant;
environmental contaminant;
xenobiotic
ly 163892
loracarbef: 1-carbacephem antibiotic; has a broad spectrum of antimicrobial activity; structure given in first source; carbacephems differ from cephalosporins in the substitution of a sulfur atom in the dihydrothiazine ring with a methylene group to form a tetrahydropyridine ring. loracarbef : A synthetic "carba" analogue of cefaclor, with carbon replacing sulfur at position 1. Used to treat a wide range of infections caused by both gram-positive and gram-negative bacteria.		3.2310carbacephem;
zwitterion		antibacterial drug;
antimicrobial agent
nabilone
nabilone: cannabinol deriv; RN given refers to cpd without isomeric designation; structure		3.2310
nalorphine
Nalorphine: A narcotic antagonist with some agonist properties. It is an antagonist at mu opioid receptors and an agonist at kappa opioid receptors. Given alone it produces a broad spectrum of unpleasant effects and it is considered to be clinically obsolete.		2.0510morphinane alkaloid
naloxone
Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.. naloxone : A synthetic morphinane alkaloid that is morphinone in which the enone double bond has been reduced to a single bond, the hydrogen at position 14 has been replaced by a hydroxy group, and the methyl group attached to the nitrogen has been replaced by an allyl group. A specific opioid antagonist, it is used (commonly as its hydrochloride salt) to reverse the effects of opioids, both following their use of opioids during surgery and in cases of known or suspected opioid overdose.		3.5920morphinane alkaloid;
organic heteropentacyclic compound;
tertiary alcohol		antidote to opioid poisoning;
central nervous system depressant;
mu-opioid receptor antagonist
oxycodone
Oxycodone: A semisynthetic derivative of CODEINE.. oxycodone : A semisynthetic opioid of formula C18H21NO4 that is derived from thebaine. It is a moderately potent opioid analgesic, generally used for relief of moderate to severe pain.		3.2310organic heteropentacyclic compound;
semisynthetic derivative		antitussive;
mu-opioid receptor agonist;
opioid analgesic
oxymorphone
Oxymorphone: An opioid analgesic with actions and uses similar to those of MORPHINE, apart from an absence of cough suppressant activity. It is used in the treatment of moderate to severe pain, including pain in obstetrics. It may also be used as an adjunct to anesthesia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1092)		3.5920morphinane alkaloid
vitamin k 1
Vitamin K 1: A family of phylloquinones that contains a ring of 2-methyl-1,4-naphthoquinone and an isoprenoid side chain. Members of this group of vitamin K 1 have only one double bond on the proximal isoprene unit. Rich sources of vitamin K 1 include green plants, algae, and photosynthetic bacteria. Vitamin K1 has antihemorrhagic and prothrombogenic activity.. phylloquinone : A member of the class of phylloquinones that consists of 1,4-naphthoquinone having methyl and phytyl groups at positions 2 and 3 respectively. The parent of the class of phylloquinones.		3.8630phylloquinones;
vitamin K		cofactor;
human metabolite;
plant metabolite
sirolimus
Sirolimus: A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to IMMUNOPHILINS. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties.. sirolimus : A macrolide lactam isolated from Streptomyces hygroscopicus consisting of a 29-membered ring containing 4 trans double bonds, three of which are conjugated. It is an antibiotic, immunosupressive and antineoplastic agent.		16.13188antibiotic antifungal drug;
cyclic acetal;
cyclic ketone;
ether;
macrolide lactam;
organic heterotricyclic compound;
secondary alcohol		antibacterial drug;
anticoronaviral agent;
antineoplastic agent;
bacterial metabolite;
geroprotector;
immunosuppressive agent;
mTOR inhibitor
topiramate
Topiramate: A sulfamate-substituted fructose analog that was originally identified as a hypoglycemic agent. It is used for the treatment of EPILEPSY and MIGRAINE DISORDERS, and may also promote weight loss.. topiramate : A hexose derivative that is 2,3:4,5-di-O-isopropylidene-beta-D-fructopyranose in which the hydroxy group has been converted to the corresponding sulfamate ester. It blocks voltage-dependent sodium channels and is used as an antiepileptic and for the prevention of migraine.		3.5920cyclic ketal;
ketohexose derivative;
sulfamate ester		anticonvulsant;
sodium channel blocker
trospium chloride
trospium chloride : An organic chloride salt of trospium. It is an antispasmodic drug used for the treatment of overactive bladder.		3.2310
alvocidib
alvocidib: structure given in first source. alvocidib : A synthetic dihydroxyflavone that is 5,7-dihydroxyflavone which is substituted by a 3-hydroxy-1-methylpiperidin-4-yl group at position 8 and by a chlorine at the 2' position (the (-)-3S,4R stereoisomer). A cyclin-dependent kinase 9 (CDK9) inhibitor, it has been studied for the treatment of acute myeloid leukaemia, arthritis and atherosclerotic plaque formation.		3.5320dihydroxyflavone;
hydroxypiperidine;
monochlorobenzenes;
tertiary amino compound		antineoplastic agent;
antirheumatic drug;
apoptosis inducer;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
seocalcitol
seocalcitol: structure given in first source		2.0510
fenretinide
Fenretinide: A synthetic retinoid that is used orally as a chemopreventive against prostate cancer and in women at risk of developing contralateral breast cancer. It is also effective as an antineoplastic agent.. 4-hydroxyphenyl retinamide : A retinoid obtained by formal condensation of the carboxy group of all-trans retinoic acid and the anilino group of 4-hydroxyaniline. Synthetic retinoid agonist. Antiproliferative, antioxidant and anticancer agent with a long half-life in vivo. Apoptotic effects appear to be mediated by a mechanism distinct from that of 'classical' retinoids.		2.0510monocarboxylic acid amide;
retinoid		antineoplastic agent;
antioxidant
geldanamycin
[no description available]		2.05101,4-benzoquinones;
ansamycin;
carbamate ester;
organic heterobicyclic compound		antimicrobial agent;
antineoplastic agent;
antiviral agent;
cysteine protease inhibitor;
Hsp90 inhibitor
morphine
Meconium: The thick green-to-black mucilaginous material found in the intestines of a full-term fetus. It consists of secretions of the INTESTINAL GLANDS; BILE PIGMENTS; FATTY ACIDS; AMNIOTIC FLUID; and intrauterine debris. It constitutes the first stools passed by a newborn.		3.5920morphinane alkaloid;
organic heteropentacyclic compound;
tertiary amino compound		anaesthetic;
drug allergen;
environmental contaminant;
geroprotector;
mu-opioid receptor agonist;
opioid analgesic;
plant metabolite;
vasodilator agent;
xenobiotic
demycarosylturimycin h
[no description available]		2.0510
benzphetamine
Benzphetamine: A sympathomimetic agent with properties similar to DEXTROAMPHETAMINE. It is used in the treatment of obesity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1222). benzphetamine : Dextroamphetamine in which the the hydrogens attached to the amino group are substituted by a methyl and a benzyl group. A sympathomimetic agent with properties similar to dextroamphetamine, it is used as its hydrochloride salt in the treatment of obesity.		3.2310amphetamines;
tertiary amine		adrenergic uptake inhibitor;
appetite depressant;
dopamine uptake inhibitor;
sympathomimetic agent
deamino arginine vasopressin
Deamino Arginine Vasopressin: A synthetic analog of the pituitary hormone, ARGININE VASOPRESSIN. Its action is mediated by the VASOPRESSIN receptor V2. It has prolonged antidiuretic activity, but little pressor effects. It also modulates levels of circulating FACTOR VIII and VON WILLEBRAND FACTOR.		3.2310heterodetic cyclic peptidediagnostic agent;
renal agent;
vasopressin receptor agonist
dexmedetomidine
[no description available]		3.2310medetomidinealpha-adrenergic agonist;
analgesic;
non-narcotic analgesic;
sedative
goserelin
Goserelin: A synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE. Goserelin is used in treatments of malignant NEOPLASMS of the prostate, uterine fibromas, and metastatic breast cancer.		3.8430organic molecular entity
iloprost
Iloprost: An eicosanoid, derived from the cyclooxygenase pathway of arachidonic acid metabolism. It is a stable and synthetic analog of EPOPROSTENOL, but with a longer half-life than the parent compound. Its actions are similar to prostacyclin. Iloprost produces vasodilation and inhibits platelet aggregation.. iloprost : A carbobicyclic compound that is prostaglandin I2 in which the endocyclic oxygen is replaced by a methylene group and in which the (1E,3S)-3-hydroxyoct-1-en-1-yl side chain is replaced by a (3R)-3-hydroxy-4-methyloct-1-en-6-yn-1-yl group. A synthetic analogue of prostacyclin, it is used as the trometamol salt (generally by intravenous infusion) for the treatment of peripheral vascular disease and pulmonary hypertension.		2.0510carbobicyclic compound;
monocarboxylic acid;
secondary alcohol		platelet aggregation inhibitor;
vasodilator agent
nalbuphine
Nalbuphine: A narcotic used as a pain medication. It appears to be an agonist at KAPPA RECEPTORS and an antagonist or partial agonist at MU RECEPTORS.		3.2310organic heteropentacyclic compoundmu-opioid receptor antagonist;
opioid analgesic
nateglinide
Nateglinide: A phenylalanine and cyclohexane derivative that acts as a hypoglycemic agent by stimulating the release of insulin from the pancreas. It is used in the treatment of TYPE 2 DIABETES.. nateglinide : An N-acyl-D-phenylalanine resulting from the formal condensation of the amino group of D-phenylalanine with the carboxy group of trans-4-isopropylcyclohexanecarboxylic acid. An orally-administered, rapidly-absorbed, short-acting insulinotropic agent, it is used for the treatment of type 2 diabetes mellitus.		3.2310phenylalanine derivative
vinorelbine
[no description available]		3.8630acetate ester;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
ring assembly;
vinca alkaloid		antineoplastic agent;
photosensitizing agent
silodosin
silodosin: an alpha(1a)-adrenoceptor-selective antagonist; structure given in first source		3.2310indolecarboxamide
furazolidone
[no description available]		2.0510
fluvoxamine
Fluvoxamine: A selective serotonin reuptake inhibitor that is used in the treatment of DEPRESSION and a variety of ANXIETY DISORDERS.. fluvoxamine : An oxime O-ether that is benzene substituted by a (1E)-N-(2-aminoethoxy)-5-methoxypentanimidoyl group at position 1 and a trifluoromethyl group at position 4. It is a selective serotonin reuptake inhibitor that is used for the treatment of obsessive-compulsive disorder.		3.5920(trifluoromethyl)benzenes;
5-methoxyvalerophenone O-(2-aminoethyl)oxime		antidepressant;
anxiolytic drug;
serotonin uptake inhibitor
bosutinib
4-((2,4-dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methyl-1-piperazinyl)propoxy)-3-quinolinecarbonitrile: a Src kinase inhibitor; structure in first source		9.411aminoquinoline;
aromatic ether;
dichlorobenzene;
N-methylpiperazine;
nitrile;
tertiary amino compound		antineoplastic agent;
tyrosine kinase inhibitor
semaxinib
semaxanib : An oxindole that is 3-methyleneoxindole in which one of the hydrogens of the methylene group is replaced by a 3,5-dimethylpyrrol-2-yl group.		2.0510olefinic compound;
oxindoles;
pyrroles		angiogenesis modulating agent;
antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
vascular endothelial growth factor receptor antagonist
orantinib
orantinib: an antiangiogenic agent. orantinib : An oxindole that is 3-methyleneoxindole in which one of the hydrogens of the methylene group is substituted by a 2-(2-carboxyethyl)-3,5-dimethylpyrrol-3-yl group. It is an ATP-competitive inhibitor of the tyrosine kinase activity of fibroblast growth factor receptor 1.		2.0510
su 11248
[no description available]		12.872310monocarboxylic acid amide;
pyrroles		angiogenesis inhibitor;
antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
immunomodulator;
neuroprotective agent;
vascular endothelial growth factor receptor antagonist
palbociclib
[no description available]		8.4195aminopyridine;
aromatic ketone;
cyclopentanes;
piperidines;
pyridopyrimidine;
secondary amino compound;
tertiary amino compound		antineoplastic agent;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
fosbretabulin
[no description available]		2.2110stilbenoid
lead
Lead: A soft, grayish metal with poisonous salts; atomic number 82, atomic weight 207.2, symbol Pb.		7.0210carbon group element atom;
elemental lead;
metal atom		neurotoxin
(6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid
(6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid : A dihydroxy monocarboxylic acid that is N-isopropylindole which is substituted at position 3 by a p-fluorophenyl group and at position 2 by a 6-carboxy-3,5-dihydroxyhex-1-en-1-yl group. It has four possible diastereoisomers.		3.5920dihydroxy monocarboxylic acid;
indoles;
organofluorine compound
molsidomine
[no description available]		2.0510ethyl ester;
morpholines;
oxadiazole;
zwitterion		antioxidant;
apoptosis inhibitor;
cardioprotective agent;
nitric oxide donor;
vasodilator agent
levorphanol
Levorphanol: A narcotic analgesic that may be habit-forming. It is nearly as effective orally as by injection.		3.2310morphinane alkaloid
arsenic
Arsenic: A shiny gray element with atomic symbol As, atomic number 33, and atomic weight 75. It occurs throughout the universe, mostly in the form of metallic arsenides. Most forms are toxic. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), arsenic and certain arsenic compounds have been listed as known carcinogens. (From Merck Index, 11th ed)		8.5420metalloid atom;
pnictogen		micronutrient
naltrexone
Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.. naltrexone : An organic heteropentacyclic compound that is naloxone substituted in which the allyl group attached to the nitrogen is replaced by a cyclopropylmethyl group. A mu-opioid receptor antagonist, it is used to treat alcohol dependence.		3.5920cyclopropanes;
morphinane-like compound;
organic heteropentacyclic compound		antidote to opioid poisoning;
central nervous system depressant;
environmental contaminant;
mu-opioid receptor antagonist;
xenobiotic
dextromethorphan
Dextromethorphan: Methyl analog of DEXTRORPHAN that shows high affinity binding to several regions of the brain, including the medullary cough center. This compound is an NMDA receptor antagonist (RECEPTORS, N-METHYL-D-ASPARTATE) and acts as a non-competitive channel blocker. It is one of the widely used ANTITUSSIVES, and is also used to study the involvement of glutamate receptors in neurotoxicity.. dextromethorphan : A 6-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthrene in which the sterocenters at positions 4a, 10 and 10a have S-configuration. It is a prodrug of dextrorphan and used as an antitussive drug for suppressing cough.		3.59206-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthreneantitussive;
environmental contaminant;
neurotoxin;
NMDA receptor antagonist;
oneirogen;
prodrug;
xenobiotic
butorphanol
Butorphanol: A synthetic morphinan analgesic with narcotic antagonist action. It is used in the management of severe pain.. butorphanol : Levorphanol in which a hydrogen at position 14 of the morphinan skeleton is substituted by hydroxy and one of the hydrogens of the N-methyl group is substituted by cyclopropyl. A semi-synthetic opioid agonist-antagonist analgesic, it is used as its (S,S)-tartaric acid salt for relief or moderate to severe pain.		3.2310morphinane alkaloidantitussive;
kappa-opioid receptor agonist;
mu-opioid receptor agonist;
opioid analgesic
cefixime
[no description available]		3.5920cephalosporinantibacterial drug;
drug allergen
delapril
delapril: RN refers to HCl; structure given in first source		2.0510peptide
lisinopril
Lisinopril: One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.		3.5920dipeptideEC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
benazepril
benazepril: structure given in first source. benazepril : A benzazepine that is benazeprilat in which the carboxy group of the 2-amino-4-phenylbutanoic acid moiety has been converted to the corresponding ethyl ester. It is used (generally as its hydrochloride salt) as a prodrug for the angiotensin-converting enzyme inhibitor benazeprilat in the treatment of hypertension and heart failure.		3.5920benzazepine;
dicarboxylic acid monoester;
ethyl ester;
lactam		EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
ramipril
Ramipril: A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.. ramipril : A dipeptide that is the prodrug for ramiprilat, the active metabolite obtained by hydrolysis of the ethyl ester group. An angiotensin-converting enzyme (ACE) inhibitor, used to treat high blood pressure and congestive heart failure.. quark : Quarks comprise one of two classes of the fundamental particles. Quarks possess fractional electric charges and are not observed in free state. The word "quark" first appears in James Joyce's Finnegans Wake and has been chosen by Murray Gell-Mann as a name for fundamental building blocks of particles.		3.5920azabicycloalkane;
cyclopentapyrrole;
dicarboxylic acid monoester;
dipeptide;
ethyl ester		bradykinin receptor B2 agonist;
cardioprotective agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
matrix metalloproteinase inhibitor;
prodrug
verteporfin
(2R,2(1)S)-8-ethenyl-2(1),2(2)-bis(methoxycarbonyl)-17-(3-methoxy-3-oxopropyl)-2,7,12,18-tetramethyl-2,2(1)-dihydrobenzo[b]porphyrin-13-propanoic acid : The 2(1),2(2),17-trimethyl ester of (2R,2(1)S)-2(1),2(2)-dicarboxy-8-ethenyl-2,7,12,18-tetramethyl-2,2(1)-dihydrobenzo[b]porphyrin-13,17-dipropanoic acid.		3.2310
indinavir sulfate
Indinavir: A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.		3.5920dicarboxylic acid diamide;
N-(2-hydroxyethyl)piperazine;
piperazinecarboxamide		HIV protease inhibitor
geldanamycin
[no description available]		7.2110
zimeldine
Zimeldine: One of the SEROTONIN UPTAKE INHIBITORS formerly used for depression but was withdrawn worldwide in September 1983 because of the risk of GUILLAIN-BARRE SYNDROME associated with its use. (From Martindale, The Extra Pharmacopoeia, 29th ed, p385)		3.2310styrenes
enalapril
Enalapril: An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.. enalapril : A dicarboxylic acid monoester that is ethyl 4-phenylbutanoate in which a hydrogen alpha to the carboxy group is substituted by the amino group of L-alanyl-L-proline (S-configuration).		3.5920dicarboxylic acid monoester;
dipeptide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
geroprotector;
prodrug
nitrofurazone
Nitrofurazone: A topical anti-infective agent effective against gram-negative and gram-positive bacteria. It is used for superficial WOUNDS AND INJURIES and skin infections. Nitrofurazone has also been administered orally in the treatment of TRYPANOSOMIASIS.. nitrofurazone : A semicarbazone resulting from the formal condensation of semicarbazide with 5-nitrofuraldehyde. A broad spectrum antibacterial drug, although with little activity against Pseudomonas species, it is used as a local application for burns, ulcers, wounds and skin infections.		2.0510
trientine hydrochloride
[no description available]		3.2310
n-methylscopolamine bromide
scopolamine methobromide : A quaternary ammonium salt resulting from the reaction of the amino group of scopolamine with methyl bromide.		3.2310
bleomycin
[no description available]		3.5920bleomycinantineoplastic agent;
metabolite
cysteine
Cysteine: A thiol-containing non-essential amino acid that is oxidized to form CYSTINE.. L-cysteinium : The L-enantiomer of cysteinium.. cysteine : A sulfur-containing amino acid that is propanoic acid with an amino group at position 2 and a sulfanyl group at position 3.		2.4110cysteiniumfundamental metabolite
heroin
Heroin: A narcotic analgesic that may be habit-forming. It is a controlled substance (opium derivative) listed in the U.S. Code of Federal Regulations, Title 21 Parts 329.1, 1308.11 (1987). Sale is forbidden in the United States by Federal statute. (Merck Index, 11th ed). heroin : A morphinane alkaloid that is morphine bearing two acetyl substituents on the O-3 and O-6 positions. As with other opioids, heroin is used as both an analgesic and a recreational drug. Frequent and regular administration is associated with tolerance and physical dependence, which may develop into addiction. Its use includes treatment for acute pain, such as in severe physical trauma, myocardial infarction, post-surgical pain, and chronic pain, including end-stage cancer and other terminal illnesses.		2.0510morphinane alkaloidmu-opioid receptor agonist;
opioid analgesic;
prodrug
enalaprilat anhydrous
Enalaprilat: The active metabolite of ENALAPRIL and one of the potent, intravenously administered, ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. It is an effective agent for the treatment of essential hypertension and has beneficial hemodynamic effects in heart failure. The drug produces renal vasodilation with an increase in sodium excretion.. enalaprilat dihydrate : The dihydrate form of enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor that is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is administered by intravenous injection.. enalaprilat (anhydrous) : Enalapril in which the ethyl ester group has been hydrolysed to the corresponding carboxylic acid. Enalaprilat is an angiotensin-converting enzyme (ACE) inhibitor and is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is given by intravenous injection, usually as the dihydrate.		3.5920dicarboxylic acid;
dipeptide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
6-o-monoacetylmorphine
6-O-monoacetylmorphine: RN given refers to parent cpd(5alpha,6alpha)-isomer		2.0510morphinane alkaloid
imidapril
imidapril: structure given in first source. imidapril : A member of the class of imidazolidines that is (4S)-1-methyl-2-oxoimidazolidine-4-carboxylic acid in which the hydrogen of the imidazolidine nitrogen has been substituted by (1S)-1-{[(2S)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino}ethyl group. It is the prodrug for imidaprilat, an ACE inhibitor used for the treatment of chronic heart failure.		2.4620dicarboxylic acid monoester;
dipeptide;
ethyl ester;
imidazolidines;
N-acylurea;
secondary amino compound		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
sulindac sulfone
sulindac sulfone: inhibits K-ras-dependent cyclooxygenase-2; sulfated analog of indomethacin;; CP248 is an antineoplastic agent that fosters microtubule depolymerization; structure in first source. sulindac sulfone : A sulfone metabolite of sulindac that inhibits cell growth by inducing apoptosis independently of cyclooxygenase inhibition. It inhibits the development and induces regression of premalignant adenomatous polyps. Lipoxygenase and Cox-2 inhibitor.		3.8221monocarboxylic acid;
organofluorine compound;
sulfone		apoptosis inducer;
cyclooxygenase 2 inhibitor;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor
ximelagatran
ximelagatran: prodrug (via hydroxylation) of melagatran & a direct thrombin inhibitor; liver toxicity concerns so AZD0837 being developed to replace this. ximelagatran : A member of the class of azetidines that is melagatran in which the carboxylic acid group has been converted to the corresponding ethyl ester and in which the amidine group has been converted into the corresponding amidoxime. A prodrug for melagatran, ximelagatran was the first orally available direct thrombin inhibitor to be brought to market as an anticoagulant, but was withdrawn in 2006 following reports of it causing liver damage.		3.5920amidoxime;
azetidines;
carboxamide;
ethyl ester;
hydroxylamines;
secondary amino compound;
secondary carboxamide;
tertiary carboxamide		anticoagulant;
EC 3.4.21.5 (thrombin) inhibitor;
prodrug;
serine protease inhibitor
cefuroxime
[no description available]		3.23103-(carbamoyloxymethyl)cephalosporin;
furans;
oxime O-ether		drug allergen
ceftriaxone
[no description available]		3.59201,2,4-triazines;
1,3-thiazoles;
cephalosporin;
oxime O-ether		antibacterial drug;
drug allergen;
EC 3.5.2.6 (beta-lactamase) inhibitor
cefepime
Cefepime: A fourth-generation cephalosporin antibacterial agent that is used in the treatment of infections, including those of the abdomen, urinary tract, respiratory tract, and skin. It is effective against PSEUDOMONAS AERUGINOSA and may also be used in the empiric treatment of FEBRILE NEUTROPENIA.. cefepime : A cephalosporin bearing (1-methylpyrrolidinium-1-yl)methyl and (2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton.		3.2310cephalosporin;
oxime O-ether		antibacterial drug
pafuramidine
pafuramidine: a prodrug of furamidine		3.2310
ceftazidime
[no description available]		3.2310cephalosporin;
oxime O-ether		antibacterial drug;
drug allergen;
EC 2.4.1.129 (peptidoglycan glycosyltransferase) inhibitor
trandolapril
trandolapril : A heterobicylic compound that is (2S,3aR,7aS)-1-[(2S)-2-aminopropanoyl]octahydro-1H-indole-2-carboxylic acid in which the hydrogen of the amino group is substituted by a (2R)-1-ethoxy-1-oxo-4-phenylbutan-2-yl group. It is a angiotensin-converting enzyme inhibitor and a prodrug used for the treatment of hypertension.		3.5920dicarboxylic acid monoester;
dipeptide;
ethyl ester;
organic heterobicyclic compound;
secondary amino compound;
tertiary carboxamide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
pregabalin
Pregabalin: A gamma-aminobutyric acid (GABA) derivative that functions as a CALCIUM CHANNEL BLOCKER and is used as an ANTICONVULSANT as well as an ANTI-ANXIETY AGENT. It is also used as an ANALGESIC in the treatment of NEUROPATHIC PAIN and FIBROMYALGIA.. pregabalin : A gamma-amino acid that is gamma-aminobutyric acid (GABA) carrying an isobutyl substitutent at the beta-position (the S-enantiomer). Binds with high affinity to the alpha2-delta site (an auxiliary subunit of voltage-gated calcium channels) in central nervous system tissues.		3.5920gamma-amino acidanticonvulsant;
calcium channel blocker
alvimopan anhydrous
alvimopan: mu opioid receptor antagonist; intended to treat constipation in patients taking opiates for pain		3.2310peptide
aliskiren
aliskiren: orally active nonpeptidic renin inhibitor. aliskiren : A monomethoxybenzene compound having a 3-methoxypropoxy group at the 2-position and a multi-substituted branched alkyl substituent at the 4-position.		3.2310monocarboxylic acid amide;
monomethoxybenzene		antihypertensive agent
guanabenz acetate
[no description available]		2.0510dichlorobenzenegeroprotector
famotidine
[no description available]		3.59201,3-thiazoles;
guanidines;
sulfonamide		anti-ulcer drug;
H2-receptor antagonist;
P450 inhibitor
cefotaxime
Cefotaxime: Semisynthetic broad-spectrum cephalosporin.. cefotaxime : A cephalosporin compound having acetoxymethyl and [2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups.		3.59201,3-thiazoles;
cephalosporin;
oxime O-ether		antibacterial drug;
drug allergen
aztreonam
[no description available]		3.5920beta-lactam antibiotic allergen;
monobactam		antibacterial drug;
drug allergen;
EC 2.4.1.129 (peptidoglycan glycosyltransferase) inhibitor
proguanil
Proguanil: A biguanide compound which metabolizes in the body to form cycloguanil, an anti-malaria agent.. proguanil : A biguanide compound which has isopropyl and p-chlorophenyl substituents on the terminal N atoms. A prophylactic antimalarial drug, it works by inhibiting the enzyme dihydrofolate reductase, which is involved in the reproduction of the malaria parasites Plasmodium falciparum and P. vivax within the red blood cells.		2.0510biguanides;
monochlorobenzenes		antimalarial;
antiprotozoal drug;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor
ma-1
tipiracil: inhibits thymidine phosphorylase. tipiracil : A member of the class of pyrimidones that is uracil substituted by chloro and (2-iminopyrrolidin-1-yl)methyl groups at positions 5 and 6 respectively. Used (as the hydrochloride salt) in combination with trifluridine, a nucleoside metabolic inhibitor, for treatment of advanced/relapsed unresectable colorectal cancer.		6.5243carboxamidine;
organochlorine compound;
pyrimidone;
pyrrolidines		antineoplastic agent;
EC 2.4.2.4 (thymidine phosphorylase) inhibitor
rifamycin sv
rifamycin SV: RN given refers to parent cpd; structure in Merck Index, 9th ed, #8009. rifamycin SV : A member of the class of rifamycins that exhibits antibiotic and antitubercular properties.		2.0510acetate ester;
cyclic ketal;
lactam;
macrocycle;
organic heterotetracyclic compound;
polyphenol;
rifamycins		antimicrobial agent;
antitubercular agent;
bacterial metabolite
radium
Radium: A radioactive element of the alkaline earth series of metals. It has the atomic symbol Ra and atomic number 88. Radium is the product of the disintegration of URANIUM and is present in pitchblende and all ores containing uranium. It is used clinically as a source of beta and gamma-rays in radiotherapy, particularly BRACHYTHERAPY.		8.6411alkaline earth metal atom
aluminum hydroxide, magnesium hydroxide, drug combination
aluminum hydroxide, magnesium hydroxide, simethicone drug combination: antacid contains aluminum hydroxide, magnesium hydroxide and simethicone; mylanta II contains aluminum/magnesium hydroxide mixture		3.3811
cefpodoxime
[no description available]		3.2310carboxylic acid;
cephalosporin		antibacterial drug
palonosetron
Palonosetron: Isoquinoline and quinuclidine derivative that acts as a 5-HT3 RECEPTOR antagonist. It is used in the prevention of nausea and vomiting induced by cytotoxic chemotherapy, and for the prevention of post-operative nausea and vomiting.. palonosetron : An organic heterotricyclic compound that is an antiemetic used (as its hydrochloride salt) in combination with netupitant (under the trade name Akynzeo) to treat nausea and vomiting in patients undergoing cancer chemotherapy.		4.9921azabicycloalkane;
delta-lactam;
organic heterotricyclic compound		antiemetic;
serotonergic antagonist
epoprostenol sodium
[no description available]		2.0510prostanoid
rifaximin
[no description available]		3.2310acetate ester;
cyclic ketal;
lactam;
macrocycle;
organic heterohexacyclic compound;
rifamycins;
semisynthetic derivative		antimicrobial agent;
gastrointestinal drug;
orphan drug
plastochromanol 8
plastochromanol 8: has antiproliferative activity against 3T3-L1 cells and anti-adipogenic activity; structure; plastochromanol 3 is gamma-tocotrienol		2.520
everolimus
[no description available]		12.342412cyclic acetal;
cyclic ketone;
ether;
macrolide lactam;
primary alcohol;
secondary alcohol		anticoronaviral agent;
antineoplastic agent;
geroprotector;
immunosuppressive agent;
mTOR inhibitor
ixabepilone
[no description available]		15.3444161,3-thiazoles;
beta-hydroxy ketone;
epoxide;
lactam;
macrocycle		antineoplastic agent;
microtubule-destabilising agent
ekb 569
EKB 569: an EGF receptor kinase inhibitor		3.4311aminoquinoline;
monocarboxylic acid amide;
monochlorobenzenes;
nitrile		protein kinase inhibitor
axitinib
[no description available]		11.5542aryl sulfide;
benzamides;
indazoles;
pyridines		antineoplastic agent;
tyrosine kinase inhibitor;
vascular endothelial growth factor receptor antagonist
azlocillin
Azlocillin: A semisynthetic ampicillin-derived acylureido penicillin.. azlocillin : A semisynthetic penicillin having a 6beta-{(2R)-2-[(2-oxoimidazolidine-1-carbonyl)amino]-2-phenylacetyl}amino side-group. It is an antibiotic used in treating infections caused by Pseudomonas aeruginosa, Escherichia coli and Haemophilus influenzae.		2.0510penicillin allergen;
penicillin;
semisynthetic derivative		antibacterial drug
ceftizoxime
[no description available]		3.2310cephalosporinantibacterial drug
1-methyl-d-lysergic acid butanolamide
[no description available]		3.2310ergot alkaloid;
monocarboxylic acid amide		serotonergic antagonist;
sympatholytic agent;
vasoconstrictor agent
beta-escin
[no description available]		3.511
dantrolene sodium
dantrolene sodium (anhydrous) : The anhydrous sodium salt of dantrolene.		2.0510
nitrofurantoin
Nitrofurantoin: A urinary anti-infective agent effective against most gram-positive and gram-negative organisms. Although sulfonamides and antibiotics are usually the agents of choice for urinary tract infections, nitrofurantoin is widely used for prophylaxis and long-term suppression.. nitrofurantoin : An imidazolidine-2,4-dione that is hydantoin substituted at position 1 by a [(5-nitro-2-furyl)methylene]amino group. An antibiotic that damages bacterial DNA.		3.5920imidazolidine-2,4-dione;
nitrofuran antibiotic;
organonitrogen heterocyclic antibiotic;
organooxygen heterocyclic antibiotic		antibacterial drug;
antiinfective agent;
hepatotoxic agent
nifurtimox
Nifurtimox: A nitrofuran thiazine that has been used against TRYPANOSOMIASIS.		2.0510nitrofuran antibiotic
peplomycin
Peplomycin: An antineoplastic agent derived from BLEOMYCIN.		2.0710glycopeptide
gadolinium dtpa
Gadolinium DTPA: A complex of gadolinium with a chelating agent, diethylenetriamine penta-acetic acid (DTPA see PENTETIC ACID), that is given to enhance the image in cranial and spinal MRIs. (From Martindale, The Extra Pharmacopoeia, 30th ed, p706)		2.3110gadolinium coordination entityMRI contrast agent
dantrolene
[no description available]		3.5820
roxithromycin
(E)-roxithromycin : A major geometrical isomer of roxithromycin.		2.0510roxithromycinenvironmental contaminant;
xenobiotic
cefdinir
[no description available]		3.2310cephalosporin;
ketoxime		antibacterial drug
etonogestrel
[no description available]		3.231017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
terminal acetylenic compound		contraceptive drug;
female contraceptive drug;
progestin
beraprost
beraprost: stable prostacyclin analog; structure given in first source. beraprost : An organic heterotricyclic compound that is (3aS,8bS)-2,3,3a,8b-tetrahydro-1H-benzo[b]cyclopenta[d]furan in which the hydrogens at positions 1R, 2R and 5 are replaced by (3S)-3-hydroxy-4-methyloct-1-en-6-yn-1-yl, hydroxy and 3-carboxypropyl groups, respectively. It is a prostaglandin receptor agonist which is approved to treat pulmonary arterial hypertension in Asia.		2.0510enyne;
monocarboxylic acid;
organic heterotricyclic compound;
secondary alcohol;
secondary allylic alcohol		anti-inflammatory agent;
antihypertensive agent;
platelet aggregation inhibitor;
prostaglandin receptor agonist;
vasodilator agent
lanreotide
[no description available]		2.0510
larotaxel
larotaxel: has antineoplastic activity		3.1510
temsirolimus
[no description available]		3.2310macrolide lactam
dutasteride
Dutasteride: A 5-ALPHA-REDUCTASE INHIBITOR that is reported to inhibit both type-1 and type2 isoforms of the enzyme and is used to treat BENIGN PROSTATIC HYPERPLASIA.. dutasteride : An aza-steroid that is inasteride in which the tert-butyl group is replaced by a 2,5-bis(trifluoromethyl)phenyl group. A synthetic 4-azasteroid, dutasteride is a selective inhibitor of both the type 1 and type 2 isoforms of steroid 5alpha-reductase, an intracellular enzyme that converts testosterone to 5alpha-dihydrotestosterone. Dutasteride is used for the treatment of symptomatic benign prostatic hyperplasia in men with an enlarged prostate gland.		3.2310(trifluoromethyl)benzenes;
aza-steroid;
delta-lactam		antihyperplasia drug;
EC 1.3.1.22 [3-oxo-5alpha-steroid 4-dehydrogenase (NADP(+))] inhibitor
bay 12-9566
Bay 12-9566: an angiogenesis inhibitor with matrix metalloproteinase inhibitory activity		3.1110biphenyls;
organochlorine compound
lu 208075
ambrisentan: an ET(A) receptor antagonist and antihypertensive agent; studied for use in pulmonary arterial hypertension		3.5920diarylmethane
bibx 1382bs
BIBX 1382BS: an ErbB receptor kinase inhibitor; no further information available 4/2001		3.2310substituted aniline
fesoterodine
fesoterodine: a muscarinic antagonist for treatment of overactive bladder		3.2310diarylmethane
tesetaxel
tesetaxel: structure in first source		9.3711
acetylcarnitine
O-acetyl-L-carnitine : An O-acyl-L-carnitine where the acyl group specified is acetyl. It facilitates movement of acetyl-CoA into the matrices of mammalian mitochondria during the oxidation of fatty acids.		2.0510O-acetylcarnitine;
saturated fatty acyl-L-carnitine		human metabolite;
Saccharomyces cerevisiae metabolite
taxane
taxane: produced by Taxomyces andreanae		16.055828diterpene;
terpenoid fundamental parent
chlorhexidine
Chlorhexidine: A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.. chlorhexidine : A bisbiguanide compound with a structure consisting of two (p-chlorophenyl)guanide units linked by a hexamethylene bridge.		2.0510biguanides;
monochlorobenzenes		antibacterial agent;
antiinfective agent
s 1743
Esomeprazole: The S-isomer of omeprazole.. esomeprazole : A 5-methoxy-2-{[(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl}-1H-benzimidazole that has S configuration at the sulfur atom. An inhibitor of gastric acid secretion, it is used (generally as its sodium or magnesium salt) for the treatment of gastro-oesophageal reflux disease, dyspepsia, peptic ulcer disease, and Zollinger-Ellison syndrome.		3.811magnesium saltanti-ulcer drug;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor
nifurtoinol
nifurtoinol : An imidazolidine-2,4-dione that is hydantoin substituted at position 1 by a [(5-nitro-2-furyl)methylene]amino group and at position 3 by a hydroxymethyl group.		2.0510hydrazone;
imidazolidine-2,4-dione;
nitrofuran antibiotic;
organonitrogen heterocyclic antibiotic		antibacterial drug;
antiinfective agent;
hepatotoxic agent
gemifloxacin
Gemifloxacin: A naphthyridine and fluoroquinolone derivative antibacterial agent and DNA TOPOISOMERASE II inhibitor that is used for the treatment of community-acquired pneumonia and acute bacterial infections associated with chronic bronchitis.. gemifloxacin : A 1,4-dihydro-1,8-naphthyridine with a carboxy group at the 3-position, an oxo sustituent at the 4-position, a fluoro substituent at the 5-position and a substituted pyrrolin-1-yl group at the 7-position.		3.23101,8-naphthyridine derivative;
fluoroquinolone antibiotic;
monocarboxylic acid;
quinolone antibiotic		antibacterial drug;
antimicrobial agent;
topoisomerase IV inhibitor
dexlansoprazole
Dexlansoprazole: The R-isomer of lansoprazole that is used to treat severe GASTROESOPHAGEAL REFLUX DISEASE.		3.2310benzimidazoles;
sulfoxide
fosinopril
[no description available]		3.5920
armodafinil
armodafinil : A 2-[(diphenylmethyl)sulfinyl]acetamide that has R configuration at the sulfur atom. Like its racemate, modafinil, it is used for the treatment of sleeping disorders such as narcolepsy, obstructive sleep apnoea, and shift-work sleep disorder. Peak concentration in the blood later occurs later following administration than with modafinil, so it is thought that armodafinil may be more effective than modafinil in treating people with excessive daytime sleepiness.		3.23102-[(diphenylmethyl)sulfinyl]acetamidecentral nervous system stimulant;
eugeroic
eflucimibe
eflucimibe: a powerful and systemic acylcoenzyme A: cholesterol acyltransferase inhibitor		2.0510
telatinib
[no description available]		8.4411
lenvatinib
lenvatinib : A member of the class of quinolines that is the carboxamide of 4-{3-chloro-4-[(cyclopropylcarbamoyl)amino]phenoxy}-7-methoxyquinoline-6-carboxylic acid. A multi-kinase inhibitor and orphan drug used (as its mesylate salt) for the treatment of various types of thyroid cancer that do not respond to radioiodine.		9.7211aromatic amide;
aromatic ether;
cyclopropanes;
monocarboxylic acid amide;
monochlorobenzenes;
phenylureas;
quinolines		antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
fibroblast growth factor receptor antagonist;
orphan drug;
vascular endothelial growth factor receptor antagonist
bms 310705
BMS 310705: a water-soluble analog of epothilone B		4.0520
sincalide
Sincalide: An octapeptide hormone present in the intestine and brain. When secreted from the gastric mucosa, it stimulates the release of bile from the gallbladder and digestive enzymes from the pancreas.		3.6220oligopeptide
tapentadol
Tapentadol: An opioid analgesic, MU OPIOID RECEPTOR agonist, and noradrenaline reuptake inhibitor that is used in the treatment of moderate to severe pain, and of pain associated with DIABETIC NEUROPATHIES.		3.2310alkylbenzene
etomoxir
[no description available]		2.0510aromatic ether
1-(2-deoxy-beta-ribofuranosyl)-5-iodo-2-pyrimidinone
ropidoxuridine: a prodrug of 5-iodo-2'-deoxyuridine and a radiosensitizing agent; RN given refers to erythro-(D)-isomer; structure given in first source		2.610
upamostat
[no description available]		3.4711
pentagastrin
Pentagastrin: A synthetic pentapeptide that has effects like gastrin when given parenterally. It stimulates the secretion of gastric acid, pepsin, and intrinsic factor, and has been used as a diagnostic aid.		3.5920organic molecular entity
cabazitaxel
cabazitaxel: an antineoplastic agent; structure in first source. cabazitaxel : A tetracyclic diterpenoid that is 10-deacetylbaccatin III having O-methyl groups attached at positions 7 and 10 as well as an O-(2R,3S)-3-[(tert-butoxycarbonyl)amino]-2-hydroxy-3-phenylpropanoyl group attached at position 13. Acts as a microtubule inhibitor, binds tubulin and promotes microtubule assembly and simultaneously inhibits disassembly.		9.3711tetracyclic diterpenoidantineoplastic agent;
microtubule-stabilising agent
mocetinostat
mocetinostat: undergoing phase II clinical trials for treatment of cancer. mocetinostat : A benzamide obtained by formal condensation of the carboxy group of 4-({[4-(pyridin-3-yl)pyrimidin-2-yl]amino}methyl)benzoic acid with one of the amino groups of benzene-1,2-diamine. It is an orally active and isotype-selective HDAC inhibitor which exhibits antitumour activity (IC50 = 0.15, 0.29, 1.66 and 0.59 muM for HDAC1, HDAC2, HDAC3 and HDAC11).		2.610aminopyrimidine;
benzamides;
pyridines;
secondary amino compound;
secondary carboxamide;
substituted aniline		antineoplastic agent;
apoptosis inducer;
autophagy inducer;
cardioprotective agent;
EC 3.5.1.98 (histone deacetylase) inhibitor;
hepatotoxic agent
cefditoren
cefditoren: structure given in first source; RN given refers to the (6R-(3(Z),6alpha,7beta(Z)))-isomer. cefditoren : A broad spectrum, third-generation cephalosporin antibiotic with (Z)-2-(4-methyl-1,3-thiazol-5-yl)ethenyl and (2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton. Generally administered as its orally absorbed pivaloyloxymethyl ester prodrug, it is used for the treatment of mild to moderate infections caused by susceptible strains of microorganisms in acute bacterial exacerbation of chronic bronchitis, community-acquired pneumonia, pharyngitis/tonsillitis, and uncomplicated skin and skin-structure infections.		3.2310carboxylic acid;
cephalosporin		antibacterial drug
gentamicin sulfate
[no description available]		2.0510
hki 272
[no description available]		11165nitrile;
quinolines		antineoplastic agent;
tyrosine kinase inhibitor
ginsenoside rg3
ginsenoside Rg3: from Red ginseng; inhibits lung metastasis of tumor cells; structure given in first source. (20S)-ginsenoside Rg3 : A ginsenoside found in Panax ginseng and Panax japonicus var. major that is dammarane which is substituted by hydroxy groups at the 3beta, 12beta and 20 pro-S positions, in which the hydroxy group at position 3 has been converted to the corresponding beta-D-glucopyranosyl-beta-D-glucopyranoside, and in which a double bond has been introduced at the 24-25 position.		7.9610ginsenoside;
glycoside;
tetracyclic triterpenoid		angiogenesis modulating agent;
antineoplastic agent;
apoptosis inducer;
plant metabolite
motexafin gadolinium
[no description available]		2.0710
rucaparib
AG14447: Poly(ADP-ribose) polymerase inhibitor; structure in first source		2.1710azepinoindole;
caprolactams;
organofluorine compound;
secondary amino compound		antineoplastic agent;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
cediranib
[no description available]		11.653aromatic ether
g(m1) ganglioside
G(M1) Ganglioside: A specific monosialoganglioside that accumulates abnormally within the nervous system due to a deficiency of GM1-b-galactosidase, resulting in GM1 gangliosidosis.. ganglioside GM1 : A sialotetraosylceramide consisting of a branched pentasaccharide made up from one sialyl residue, two galactose residues, one N-acetylgalactosamine residue and a glucose residue at the reducing end attached to N-stearoylsphingosine via a beta-linkage.		5.6732alpha-N-acetylneuraminosyl-(2->3)-[beta-D-galactosyl-(1->3)-N-acetyl-beta-D-galactosaminyl-(1->4)]-beta-D-galactosyl-(1->4)-beta-D-glucosyl-(1<->1')-N-acylsphingosine;
sialotetraosylceramide
5'-deoxy-5-fluorocytidine
5'-deoxy-5-fluorocytidine: structure in first source		7.14244N-glycosyl compound
pazopanib
pazopanib: a protein kinase inhibitor. pazopanib : A pyrimidine that is 5-(pyrimidin-2-yl}amino-2-methylbenzenesulfonamide substituted at position 4 by a (2,3-dimethylindazol-6-yl)(methyl)amino group. Used as its hydrochloride salt for treatment of kidney cancer.		9.2864aminopyrimidine;
indazoles;
sulfonamide		angiogenesis modulating agent;
antineoplastic agent;
tyrosine kinase inhibitor;
vascular endothelial growth factor receptor antagonist
azd 6244
AZD 6244: a MEK inhibitor		5.6232benzimidazoles;
bromobenzenes;
hydroxamic acid ester;
monochlorobenzenes;
organofluorine compound;
secondary amino compound		anticoronaviral agent;
antineoplastic agent;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
prasugrel hydrochloride
Prasugrel Hydrochloride: A piperazine derivative and PLATELET AGGREGATION INHIBITOR that is used to prevent THROMBOSIS in patients with ACUTE CORONARY SYNDROME; UNSTABLE ANGINA and MYOCARDIAL INFARCTION, as well as in those undergoing PERCUTANEOUS CORONARY INTERVENTIONS.. prasugrel hydrochloride : A racemate comprising equal amounts of (R)- and (S)-prasugrel hydrochloride. Used to prevent blood clots in people with acute coronary syndrome who are undergoing a procedure after a recent heart attack or stroke, and in people with certain disorders of the heart or blood vessels.		3.2310
5-fluorouridine 5'-triphosphate
[no description available]		9.8532
aee 788
AEE 788: structure in first source		3.14106-{4-[(4-ethylpiperazin-1-yl)methyl]phenyl}-N-(1-phenylethyl)-7H-pyrrolo[2,3-d]pyrimidin-4-amineangiogenesis inhibitor;
antineoplastic agent;
apoptosis inducer;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
epidermal growth factor receptor antagonist;
trypanocidal drug
vinflunine
vinflunine: inhibits tubulin assembly; structure in first source. vinflunine : An organic heteropentacyclic compound and an organic heterotetracyclic compound that is vinorelbine in which the tetrahydropyridine moiety of the heterotetracyclic part of the molecule has been redced to the corresponding piperidine, and in which the ethyl group attached to this ring has been replaced by a 1,1-difluoroethyl group.		7.6452acetate ester;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
semisynthetic derivative;
vinca alkaloid		antineoplastic agent
baci-im
[no description available]		3.5920homodetic cyclic peptide;
polypeptide;
zwitterion		antibacterial agent;
antimicrobial agent
lactulose
Lactulose: A synthetic disaccharide used in the treatment of constipation and hepatic encephalopathy. It has also been used in the diagnosis of gastrointestinal disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p887). lactulose : A synthetic galactosylfructose disaccharide used in the treatment of constipation and hepatic encephalopathy.		2.2510
regorafenib
[no description available]		12.171(trifluoromethyl)benzenes;
aromatic ether;
monochlorobenzenes;
monofluorobenzenes;
phenylureas;
pyridinecarboxamide		antineoplastic agent;
hepatotoxic agent;
tyrosine kinase inhibitor
bms 477118
[no description available]		3.2310adamantanes;
azabicycloalkane;
monocarboxylic acid amide;
nitrile;
tertiary alcohol		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
hypoglycemic agent
nystatin a1
Nystatin: Macrolide antifungal antibiotic complex produced by Streptomyces noursei, S. aureus, and other Streptomyces species. The biologically active components of the complex are nystatin A1, A2, and A3.. nystatin : A heterogeneous mixture of polyene compounds produced by cultures of Streptomyces noursei. It mainly consists of three biologically active components designated nystatin A1, nystatin A2, and nystatin A3. It is used to treat oral and dermal fungal infections.. nystatin A1 : A polyene macrolide antibiotic; part of the nystatin complex produced by several Streptomyces species. It is an antifungal antibiotic used for the treatment of topical fungal infections caused by a broad spectrum of fungal pathogens comprising yeast-like and filamentous species.		3.2310nystatins
pirarubicin
[no description available]		8.511anthracycline
er-086526
eribulin: a halichondrin B derivative that suppresses microtubule growth and acts as an antimitotic agent; structure in first source. eribulin : A fully synthetic macrocyclic ketone analogue of marine sponge natural products. Inhibits growth phase of microtubules via tubulin-based antimitotic mechanism, which leads to G2/M cell-cycle block, disruption of mitotic spindles, and, ultimately, apoptotic cell death after prolonged mitotic blockage		12.352915cyclic ketal;
cyclic ketone;
macrocycle;
polycyclic ether;
polyether;
primary amino compound		antineoplastic agent;
microtubule-destabilising agent
psn 632408
PSN 632408: a GPR119 agonist; structure in first source		2.0510
ridaforolimus
[no description available]		8.8521macrolide lactam
milnacipran
[no description available]		3.2310acetamides
vindesine
[no description available]		2.0510
ly2334737
LY2334737: an orally available prodrug of gemcitabine for treatment of patients with advanced solid tumors		8.511
trametinib
[no description available]		8.6411acetamides;
aromatic amine;
cyclopropanes;
organofluorine compound;
organoiodine compound;
pyridopyrimidine;
ring assembly		anticoronaviral agent;
antineoplastic agent;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
geroprotector
veliparib
[no description available]		9.4511benzimidazolesEC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
indocyanine green
Indocyanine Green: A tricarbocyanine dye that is used diagnostically in liver function tests and to determine blood volume and cardiac output.		2.21101,1-diunsubstituted alkanesulfonate;
benzoindole;
cyanine dye
scopolamine hydrobromide
[no description available]		3.2310
pf 03491390
[no description available]		2.0510
arabinofuranosyluracil
Arabinofuranosyluracil: A pyrimidine nucleoside formed in the body by the deamination of CYTARABINE.		2.1310
tetrahydrouridine
Tetrahydrouridine: An inhibitor of nucleotide metabolism.		2.4520
jaw
[no description available]		2.1110indolecarboxamide
amodiaquine hydrochloride
[no description available]		2.0510
bivalirudin
bivalirudin: designed to bind to the alpha-thrombin catalytic site and anion-binding exosite for fibrin(ogen) recognition. bivalirudin : A synthetic peptide of 20 amino acids, comprising D-Phe, Pro, Arg, Pro, Gly, Gly, Gly, Gly, Asn, Gly, Asp, Phe, Glu, Glu, Ile, Pro, Glu, Glu, Tyr, and Leu in sequence. A congener of hirudin (a naturally occurring drug found in the saliva of the medicinal leech), it a specific and reversible inhibitor of thrombin, and is used as an anticoagulant.		3.2310polypeptideanticoagulant;
EC 3.4.21.5 (thrombin) inhibitor
tannins
gallotannin : A class of hydrolysable tannins obtained by condensation of the carboxy group of gallic acid (and its polymeric derivatives) with the hydroxy groups of a monosaccharide (most commonly glucose).		2.0510tannin
enfuvirtide
Enfuvirtide: A synthetic 36-amino acid peptide that corresponds to the heptad repeat sequence of HIV-1 gp41. It blocks HIV cell fusion and viral entry and is used with other anti-retrovirals for combination therapy of HIV INFECTIONS and AIDS.. enfuvirtide : A synthetic 36-amino acid peptide consisting of N-acetyltyrosyl, threonyl, seryl, leucyl, isoleucyl, histidyl, seryl, leucyl, isoleucyl, alpha-glutamyl, alpha-glutamyl, seryl, glutaminyl, asparaginyl, glutaminyl, glutaminyl, alpha-glutamyl, lysyl, asparaginyl, alpha-glutamyl, alpha-glutamyl, alpha-glutamyl, leucyl, leucyl, alpha-glutamyl, leucyl, alpha-aspartyl, lysyl, tryptophyl, alanyl, seryl, leucyl, tryptophyl, asparaginyl, tryptophyl, and phenylalaninamide residues joined in sequence. An HIV fusion inhibitor, it was the first of a novel class of antiretroviral drugs used in combination therapy for the treatment of HIV-1 infection. It interferes with entry of HIV into cells by binding to the gp41 sub-unit of the viral envelope glycoprotein, so inhibiting fusion of viral and cellular membranes.		3.2310
ganirelix
[no description available]		3.2310polypeptide
abarelix
abarelix: RN & structure in first source. abarelix : A polypeptide compound composed of ten natural and non-natural amino acid resiudes in a linear sequence.		3.1210polypeptideantineoplastic agent;
hormone antagonist
gastrins
Gastrins: A family of gastrointestinal peptide hormones that excite the secretion of GASTRIC JUICE. They may also occur in the central nervous system where they are presumed to be neurotransmitters.		3.1110
glucagon
Glucagon: A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511). glucagon : A 29-amino acid peptide hormone consisting of His, Ser, Gln, Gly, Thr, Phe, Thr, Ser, Asp, Tyr, Ser, Lys, Tyr, Leu, Asp, Ser, Arg, Arg, Ala, Gln, Asp, Phe, Val, Gln, Trp, Leu, Met, Asn and Thr residues joined in sequence.		2.1510peptide hormone
teriparatide
[no description available]		3.2310polypeptide
salmon calcitonin
[no description available]		3.2310heterodetic cyclic peptide;
peptide hormone;
polypeptide		bone density conservation agent;
metabolite
oligonucleotides
[no description available]		3.1910
ly-146032
[no description available]		3.2310heterodetic cyclic peptide;
lipopeptide antibiotic;
lipopeptide;
macrocycle;
macrolide		antibacterial drug;
bacterial metabolite;
calcium-dependent antibiotics
glucagon-like peptide 1
Glucagon-Like Peptide 1: A peptide of 36 or 37 amino acids that is derived from PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. GLP-1(1-37 or 1-36) is further N-terminally truncated resulting in GLP-1(7-37) or GLP-1-(7-36) which can be amidated. These GLP-1 peptides are known to enhance glucose-dependent INSULIN release, suppress GLUCAGON release and gastric emptying, lower BLOOD GLUCOSE, and reduce food intake.		2.1510
acetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ilys-prolyl-alaninamide
acetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ILys-prolyl-alaninamide: FE-200486 is the acetate salt		3.2310polypeptide
exenatide
[no description available]		3.2310
cellulose
DEAE-Cellulose: Cellulose derivative used in chromatography, as ion-exchange material, and for various industrial applications.		2.2510glycoside
phosphatidylcholines
Phosphatidylcholines: Derivatives of PHOSPHATIDIC ACIDS in which the phosphoric acid is bound in ester linkage to a CHOLINE moiety.		3.06101,2-diacyl-sn-glycero-3-phosphocholine
buparlisib
NVP-BKM120: a pan class I PI3 kinase inhibitor with antineoplastic activity; structure in first source		9.832aminopyridine;
aminopyrimidine;
morpholines;
organofluorine compound		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
chitosan
[no description available]		4.6670
mesna
Mesna: A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from ANTINEOPLASTIC AGENTS, such as IFOSFAMIDE or CYCLOPHOSPHAMIDE.		3.5920organosulfonic acid
cerivastatin sodium
cerivastatin sodium : The sodium salt of cerivastatin. Formerly used to lower cholesterol and prevent cardiovascular disease, it was withdrawn from the market worldwide in 2001 following reports of a severe form of muscle toxicity.		2.0510organic sodium salt;
statin (synthetic)
sodium lactate
Sodium Lactate: The sodium salt of racemic or inactive lactic acid. It is a hygroscopic agent used intravenously as a systemic and urinary alkalizer.. sodium lactate : An organic sodium salt having lactate as the counterion.		3.2310lactate salt;
organic sodium salt		food acidity regulator;
food preservative
monensin
[no description available]		2.0510
sodium iothalamate
[no description available]		3.2310
oxacillin sodium
[no description available]		2.0510organic sodium salt
sodium diatrizoate
histopaque: used for separating mononuclear & other cells. sodium amidotrizoate : The sodium salt of a benzoic acid having iodo substituents at the 2-, 4- and 6-positions and acetamido substituents at the 3- and 5-positions. It is used, often as a mixture with the meglumine salt, as an X-ray contrast medium in gastrointestinal studies, angiography, and urography.		2.0510organic sodium salt;
organoiodine compound		radioopaque medium
ro13-9904
Ceftriaxone: A broad-spectrum cephalosporin antibiotic and cefotaxime derivative with a very long half-life and high penetrability to meninges, eyes and inner ears.. ceftriaxone : A third-generation cephalosporin compound having 2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetylamino and [(2-methyl-5,6-dioxo-1,2,5,6-tetrahydro-1,2,4-triazin-3-yl)sulfanyl]methyl side-groups.		2.0110
olaparib
[no description available]		11.3243cyclopropanes;
monofluorobenzenes;
N-acylpiperazine;
phthalazines		antineoplastic agent;
apoptosis inducer;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
s-adenosylmethionine
(R)-S-adenosyl-L-methionine : An S-adenosyl-L-methionine that has R-configuration.. S-adenosyl-L-methionine zwitterion : A zwitterionic tautomer of S-adenosyl-L-methionine arising from shift of the proton from the carboxy group to the amino group.. (R)-S-adenosyl-L-methionine zwitterion : An S-adenosyl-L-methionine zwitterion that has R-configuration; major species at pH 7.3.. (S)-S-adenosyl-L-methionine zwitterion : An S-adenosyl-L-methionine zwitterion that has S-configuration; major species at pH 7.3.. S-adenosyl-L-methionine : A sulfonium compound that is the S-adenosyl derivative of L-methionine. It is an intermediate in the metabolic pathway of methionine.		2.0710organic cation;
sulfonium compound		coenzyme;
cofactor;
human metabolite;
micronutrient;
Mycoplasma genitalium metabolite;
nutraceutical;
Saccharomyces cerevisiae metabolite
lde225
sonidegib: specific Smoothened/Smo antagonist. sonidegib : A member of the classo of biphenyls that is the amide obtained by formal condensation of the carboxy group of 2-methyl-4'-(trifluoromethoxy)[1,1'-biphenyl]-3-carboxylic acid with the amino group of 6-(2,6-dimethylmorpholin-4-yl)pyridin-3-amine. Used (as its phosphate salt) for treatment of locally advanced basal cell carcinoma.		3.2310aminopyridine;
aromatic ether;
benzamides;
biphenyls;
morpholines;
organofluorine compound;
tertiary amino compound		antineoplastic agent;
Hedgehog signaling pathway inhibitor;
SMO receptor antagonist
gdc 0449
HhAntag691: inhibits the hedgehog pathway and ABC transporters; has antineoplastic activity		3.2310benzamides;
monochlorobenzenes;
pyridines;
sulfone		antineoplastic agent;
Hedgehog signaling pathway inhibitor;
SMO receptor antagonist;
teratogenic agent
gdc-0068
ipatasertib: an Akt kinase inhibitor; structure in first source		3.9911N-arylpiperazine
mk-1775
adavosertib: a Wee1 kinase inhibitor; structure in first source		2.0510piperazines
niraparib
niraparib: structure in first source. niraparib : A 2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamide that has S-configuration. It is a potent inhibitor of PARP1 and PARP2 (IC50 of 3.8 and 2.1 nM, respectively) and approved as a first-line maintenance treatment for women with advanced ovarian cancer after responding to platinum-based chemotherapy.		2.17102-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamideantineoplastic agent;
apoptosis inducer;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor;
radiosensitizing agent
cardiovascular agents
Cardiovascular Agents: Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.		4.4920
cetrorelix
cetrorelix: LHRH antagonist. cetrorelix : A synthetic ten-membered oligopeptide comprising N-acetyl-3-(naphthalen-2-yl)-D-alanyl, 4-chloro-D-phenylalanyl, 3-(pyridin-3-yl)-D-alanyl, L-seryl, L-tyrosyl, N(5)-carbamoyl-D-ornithyl, L-leucyl, L-arginyl, L-prolyl, and D-alaninamide residues coupled in sequence. A gonadotrophin-releasing hormone (GnRH) antagonist, it is used for treatment of infertility and of hormone-sensitive cancers of the prostate and breast.		3.2310oligopeptideantineoplastic agent;
GnRH antagonist
incb-018424
[no description available]		7.3444nitrile;
pyrazoles;
pyrrolopyrimidine		antineoplastic agent;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
mannans
[no description available]		2.5920
plx4032
[no description available]		2.4920aromatic ketone;
difluorobenzene;
monochlorobenzenes;
pyrrolopyridine;
sulfonamide		antineoplastic agent;
B-Raf inhibitor
piperidines
Piperidines: A family of hexahydropyridines.		8.662
interleukin-8
Interleukin-8: A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.		2.4110
ribociclib
ribociclib: inhibits both CDK4 and CDK6		2.4110
apatinib
apatinib: reverses multidrug resistance by inhibiting the efflux function of multiple ATP-binding cassette transporters; structure in first source		6.0942
dinaciclib
[no description available]		9.411pyrazolopyrimidine
gsk525762a
molibresib: mimicks acetylated histones; structure in first source		2.1510benzodiazepine
ly2940680
[no description available]		3.2310
methylcellulose
Methylcellulose: Methylester of cellulose. Methylcellulose is used as an emulsifying and suspending agent in cosmetics, pharmaceutics and the chemical industry. It is used therapeutically as a bulk laxative.		2.0810
ascorbic acid
Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.. L-ascorbic acid : The L-enantiomer of ascorbic acid and conjugate acid of L-ascorbate.. L-ascorbate : The L-enantiomer of ascorbate and conjugate base of L-ascorbic acid, arising from selective deprotonation of the 3-hydroxy group. Required for a range of essential metabolic reactions in all animals and plants.. vitamin C : Any member of a group of vitamers that belong to the chemical structural class called butenolides that exhibit biological activity against vitamin C deficiency in animals. The vitamers include L-ascorbic acid and its salt, ionized and oxidized forms.		3.5920ascorbic acid;
vitamin C		coenzyme;
cofactor;
flour treatment agent;
food antioxidant;
food colour retention agent;
geroprotector;
plant metabolite;
skin lightening agent
raltegravir
[no description available]		3.23101,2,4-oxadiazole;
dicarboxylic acid amide;
hydroxypyrimidine;
monofluorobenzenes;
pyrimidone;
secondary carboxamide		antiviral drug;
HIV-1 integrase inhibitor
novobiocin
Novobiocin: An antibiotic compound derived from Streptomyces niveus. It has a chemical structure similar to coumarin. Novobiocin binds to DNA gyrase, and blocks adenosine triphosphatase (ATPase) activity. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p189). novobiocin : A coumarin-derived antibiotic obtained from Streptomyces niveus.		2.0510carbamate ester;
ether;
hexoside;
hydroxycoumarin;
monocarboxylic acid amide;
monosaccharide derivative;
phenols		antibacterial agent;
antimicrobial agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
Escherichia coli metabolite;
hepatoprotective agent
tetracycline
Tetracycline: A naphthacene antibiotic that inhibits AMINO ACYL TRNA binding during protein synthesis.. tetracycline : A broad-spectrum polyketide antibiotic produced by the Streptomyces genus of actinobacteria.		3.5920
chlortetracycline
Chlortetracycline: A TETRACYCLINE with a 7-chloro substitution.. chlortetracycline : A member of the class of tetracyclines with formula C22H23ClN2O8 isolated from Streptomyces aureofaciens.		2.0510
oxytetracycline, anhydrous
Oxytetracycline: A TETRACYCLINE analog isolated from the actinomycete STREPTOMYCES RIMOSUS and used in a wide variety of clinical conditions.. oxytetracycline : A tetracycline used for treatment of infections caused by a variety of Gram positive and Gram negative microorganisms including Mycoplasma pneumoniae, Pasteurella pestis, Escherichia coli, Haemophilus influenzae (respiratory infections), and Diplococcus pneumoniae.		3.5920
minocycline
Minocycline: A TETRACYCLINE analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant STAPHYLOCOCCUS infections.. minocycline : A tetracycline analogue having a dimethylamino group at position 7 and lacking the methyl and hydroxy groups at position 5.		3.5920
salicylates
Salicylates: The salts or esters of salicylic acids, or salicylate esters of an organic acid. Some of these have analgesic, antipyretic, and anti-inflammatory activities by inhibiting prostaglandin synthesis.. hydroxybenzoate : Any benzoate derivative carrying a single carboxylate group and at least one hydroxy substituent.. salicylates : Any salt or ester arising from reaction of the carboxy group of salicylic acid, or any ester resulting from the condensation of the phenolic hydroxy group of salicylic acid with an organic acid.. salicylate : A monohydroxybenzoate that is the conjugate base of salicylic acid.		2.0110monohydroxybenzoateplant metabolite
dicumarol
Dicumarol: An oral anticoagulant that interferes with the metabolism of vitamin K. It is also used in biochemical experiments as an inhibitor of reductases.		2.0510hydroxycoumarinanticoagulant;
EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor;
Hsp90 inhibitor;
vitamin K antagonist
piroxicam
[no description available]		3.5920benzothiazine;
monocarboxylic acid amide;
pyridines		analgesic;
antirheumatic drug;
cyclooxygenase 1 inhibitor;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug
acenocoumarol
Acenocoumarol: A coumarin that is used as an anticoagulant. Its actions and uses are similar to those of WARFARIN. (From Martindale, The Extra Pharmacopoeia, 30th ed, p233). acenocoumarol : A hydroxycoumarin that is warfarin in which the hydrogen at position 4 of the phenyl substituent is replaced by a nitro group.		7.4720C-nitro compound;
hydroxycoumarin;
methyl ketone		anticoagulant;
EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor
mobic
Meloxicam: A benzothiazine and thiazole derivative that acts as a NSAID and cyclooxygenase-2 (COX-2) inhibitor. It is used in the treatment of RHEUMATOID ARTHRITIS; OSTEOARTHRITIS; and ANKYLOSING SPONDYLITIS.. meloxicam : A benzothiazine that is piroxicam in which the pyridin-2-yl group is replaced by a 5-methyl-1,3-thiazol-2-yl group. A non-steroidal anti-inflammatory drug and selective inhibitor of COX-2, it is used particularly for the management of rheumatoid arthritis.		3.59201,3-thiazoles;
benzothiazine;
monocarboxylic acid amide		analgesic;
antirheumatic drug;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
mobiflex
tenoxicam : A thienothiazine-derived monocarboxylic acid amide obtained by formal condensation of the carboxy group of 4-hydroxy-2-methylthieno[2,3-e][1,2]thiazine-3-carboxylic acid 1,1-dioxide with the amino group of 2-aminopyridine. Used for the treatment of pain and inflammation in osteoarthritis and rheumatoid arthritis. It is also indicated for short term treatment of acute musculoskeletal disorders including strains, sprains and other soft-tissue injuries.		2.0510heteroaryl hydroxy compound;
monocarboxylic acid amide;
pyridines;
thienothiazine		antipyretic;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
warfarin
Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.. warfarin : A racemate comprising equal amounts of (R)- and (S)-warfarin. Extensively used as both an anticoagulant drug and as a pesticide against rats and mice.. 4-hydroxy-3-(3-oxo-1-phenylbutyl)-1-benzopyran-2-one : A member of the class of coumarins that is 4-hydroxycoumarin which is substituted at position 3 by a 1-phenyl-3-oxo-1-butyl group.		9.16211benzenes;
hydroxycoumarin;
methyl ketone
gimeracil
gimeracil: a biochemical and pharmacological modulator of 5-FU		12.5492organic molecular entity
demeclocycline
Demeclocycline: A TETRACYCLINE analog having a 7-chloro and a 6-methyl. Because it is excreted more slowly than tetracycline, it maintains effective blood levels for longer periods of time.. demeclocycline : Tetracycline which lacks the methyl substituent at position 7 and in which the hydrogen para- to the phenolic hydroxy group is substituted by chlorine. Like tetracycline, it is an antibiotic, but being excreted more slowly, effective blood levels are maintained for longer. It is used (mainly as the hydrochloride) for the treatment of Lyme disease, acne and bronchitis, as well as for hyponatraemia (low blood sodium concentration) due to the syndrome of inappropriate antidiuretic hormone (SIADH) where fluid restriction alone has been ineffective.		3.2310
phenprocoumon
Phenprocoumon: Coumarin derivative that acts as a long acting oral anticoagulant.. phenprocoumon : A hydroxycoumarin that is 4-hydroxycoumarin which is substituted at position 3 by a 1-phenylpropyl group.		2.0510hydroxycoumarinanticoagulant;
EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor
tipranavir
tipranavir: inhibits HIV-1 protease. tipranavir : A pyridine-2-sulfonamide substituted at C-5 by a trifluoromethyl group and at the sulfonamide nitrogen by a dihydropyrone-containing m-tolyl substituent. It is an HIV-1 protease inhibitor.		3.2310sulfonamideantiviral drug;
HIV protease inhibitor
rolitetracycline
Rolitetracycline: A pyrrolidinylmethyl TETRACYCLINE.. rolitetracycline : A derivative of tetracycline in which the amide function is substituted with a pyrrolidinomethyl group.		2.0510
tigecycline
[no description available]		3.2310
lornoxicam
lornoxicam : A thienothiazine-derived monocarboxylic acid amide obtained by formal condensation of the carboxy group of 6-chloro-4-hydroxy-2-methylthieno[2,3-e][1,2]thiazine-3-carboxylic acid 1,1-dioxide with the amino group of 2-aminopyridine. Used for the treatment of pain, primarily resulting from inflammatory diseases of the joints, osteoarthritis, surgery, sciatica and other inflammations.		2.0510heteroaryl hydroxy compound;
monocarboxylic acid amide;
organochlorine compound;
pyridines;
thienothiazine		antipyretic;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
s 1 (combination)
S 1 (combination): consists of tegafur, 5-chloro-2,4-dihydroxyuridine & potassium oxonate; an inhibitor of fluorouracil(5-FU) degradation; prolongs the blood 5-FU level as well as increases selective toxicity to tumor; used for the treatment of colon cancer		18.2912123
epidermal growth factor
Epidermal Growth Factor: A 6-kDa polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. Epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and EPITHELIAL CELLS. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form.		4.0740
transforming growth factor beta
Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.		3.9821
ajmaline
[no description available]		2.0510
etirinotecan pegol
[no description available]		9.4111
imetelstat
[no description available]		3.1910
cyclin d1
Cyclin D1: Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.		5.6461
ckd732
CKD732: angiogenesis inhibitor		8.4611
fertinex
[no description available]		3.2310
vitamin b 12
Vitamin B 12: A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.		3.411
oblimersen
oblimersen: targets the Bcl-2 oncogene good efficacy with low toxicity tumour regressions		3.1210
transforming growth factor alpha
Transforming Growth Factor alpha: An EPIDERMAL GROWTH FACTOR related protein that is found in a variety of tissues including EPITHELIUM, and maternal DECIDUA. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form which binds to the EGF RECEPTOR.		6.9442
cyclosporine
Cyclosporine: A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).		2.4420
orabase
Orabase: used in therapy of oral mucosal ulcers		2.1510
nedaplatin
nedaplatin: structure given in first source		9.7921
lutetium lu 177 dotatate
177Lu-DOTA-octreotate: an somatostatin receptor agonist		6.0371
trabedersen
Trabedersen: TGF-beta2 inhibitor antisense therapeutic for tumor treatment		2.0710
exudates
Malaysia: A parliamentary democracy with a constitutional monarch in southeast Asia, consisting of 11 states (West Malaysia) on the Malay Peninsula and two states (East Malaysia) on the island of BORNEO. It is also called the Federation of Malaysia. Its capital is Kuala Lumpur. Before 1963 it was the Union of Malaya. It reorganized in 1948 as the Federation of Malaya, becoming independent from British Malaya in 1957 and becoming Malaysia in 1963 as a federation of Malaya, Sabah, Sarawak, and Singapore (which seceded in 1965). The form Malay- probably derives from the Tamil malay, mountain, with reference to its geography. (From Webster's New Geographical Dictionary, 1988, p715 & Room, Brewer's Dictionary of Names, 1992, p329)		2.830
entecavir
entecavir (anhydrous) : Guanine substituted at the 9 position by a 4-hydroxy-3-(hydroxymethyl)-2-methylidenecyclopentyl group. A synthetic analogue of 2'-deoxyguanosine, it is a nucleoside reverse transcriptase inhibitor with selective antiviral activity against hepatitis B virus. Entecavir is phosphorylated intracellularly to the active triphosphate form, which competes with deoxyguanosine triphosphate, the natural substrate of hepatitis B virus reverse transcriptase, inhibiting every stage of the enzyme's activity, although it has no activity against HIV. It is used for the treatment of chronic hepatitis B.		3.59202-aminopurines;
oxopurine;
primary alcohol;
secondary alcohol		antiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
acyclovir
Acyclovir: A GUANOSINE analog that acts as an antimetabolite. Viruses are especially susceptible. Used especially against herpes.. acyclovir : An oxopurine that is guanine substituted by a (2-hydroxyethoxy)methyl substituent at position 9. Used in the treatment of viral infections.		3.9302-aminopurines;
oxopurine		antimetabolite;
antiviral drug
levoleucovorin
Levoleucovorin: A folate analog consisting of the pharmacologically active isomer of LEUCOVORIN.. (6S)-5-formyltetrahydrofolic acid : The pharmacologically active (6S)-stereoisomer of 5-formyltetrahydrofolic acid.		24.455811935-formyltetrahydrofolic acidantineoplastic agent;
metabolite
guanine
[no description available]		8.89922-aminopurines;
oxopurine;
purine nucleobase		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
inosine
[no description available]		2.0510inosines;
purines D-ribonucleoside		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
folic acid
folcysteine: used to promote fertility in chickens. vitamin B9 : Any B-vitamin that exhibits biological activity against vitamin B9 deficiency. Vitamin B9 refers to the many forms of folic acid and its derivatives, including tetrahydrofolic acid (the active form), methyltetrahydrofolate (the primary form found in blood), methenyltetrahydrofolate, folinic acid amongst others. They are present in abundance in green leafy vegetables, citrus fruits, and animal products. Lack of vitamin B9 leads to anemia, a condition in which the body cannot produce sufficient number of red blood cells. Symptoms of vitamin B9 deficiency include fatigue, muscle weakness, and pale skin.		10.83175folic acids;
N-acyl-amino acid		human metabolite;
mouse metabolite;
nutrient
rifampin
Rifampin: A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)		3.8330cyclic ketal;
hydrazone;
N-iminopiperazine;
N-methylpiperazine;
rifamycins;
semisynthetic derivative;
zwitterion		angiogenesis inhibitor;
antiamoebic agent;
antineoplastic agent;
antitubercular agent;
DNA synthesis inhibitor;
EC 2.7.7.6 (RNA polymerase) inhibitor;
Escherichia coli metabolite;
geroprotector;
leprostatic drug;
neuroprotective agent;
pregnane X receptor agonist;
protein synthesis inhibitor
clozapine
Clozapine: A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent.. clozapine : A benzodiazepine that is 5H-dibenzo[b,e][1,4]diazepine substituted by a chloro group at position 8 and a 4-methylpiperazin-1-yl group at position 11. It is a second generation antipsychotic used in the treatment of psychiatric disorders like schizophrenia.		3.5920benzodiazepine;
N-arylpiperazine;
N-methylpiperazine;
organochlorine compound		adrenergic antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
GABA antagonist;
histamine antagonist;
muscarinic antagonist;
second generation antipsychotic;
serotonergic antagonist;
xenobiotic
dacarbazine
(E)-dacarbazine : A dacarbazine in which the N=N double bond adopts a trans-configuration.		15.215410dacarbazine
didanosine
Didanosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. Didanosine is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase; ddI is then metabolized to dideoxyadenosine triphosphate, its putative active metabolite.. didanosine : A purine 2',3'-dideoxyribonucleoside that is inosine in which the hydroxy groups at both the 2' and the 3' positions on the sugar moiety have been replaced by hydrogen. An antiviral drug, it is used as a medication to treat HIV/AIDS.		3.5920purine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
EC 2.4.2.1 (purine-nucleoside phosphorylase) inhibitor;
geroprotector;
HIV-1 reverse transcriptase inhibitor
ganciclovir
[no description available]		3.59202-aminopurines;
oxopurine		antiinfective agent;
antiviral drug
valacyclovir
Valacyclovir: A prodrug of acyclovir that is used in the treatment of HERPES ZOSTER and HERPES SIMPLEX VIRUS INFECTION of the skin and mucous membranes, including GENITAL HERPES.		3.6620L-valyl esterantiviral drug
sildenafil
sildenafil : A pyrazolo[4,3-d]pyrimidin-7-one having a methyl substituent at the 1-position, a propyl substituent at the 3-position and a 2-ethoxy-5-[(4-methylpiperazin-1-yl)sulfonyl]phenyl group at the 5-position.		3.5920piperazines;
pyrazolopyrimidine;
sulfonamide		EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
olanzapine
Olanzapine: A benzodiazepine derivative that binds SEROTONIN RECEPTORS; MUSCARINIC RECEPTORS; HISTAMINE H1 RECEPTORS; ADRENERGIC ALPHA-1 RECEPTORS; and DOPAMINE RECEPTORS. It is an antipsychotic agent used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER; and MAJOR DEPRESSIVE DISORDER; it may also reduce nausea and vomiting in patients undergoing chemotherapy.. olanzapine : A benzodiazepine that is 10H-thieno[2,3-b][1,5]benzodiazepine substituted by a methyl group at position 2 and a 4-methylpiperazin-1-yl group at position 4.		3.930benzodiazepine;
N-arylpiperazine;
N-methylpiperazine		antiemetic;
dopaminergic antagonist;
histamine antagonist;
muscarinic antagonist;
second generation antipsychotic;
serotonergic antagonist;
serotonin uptake inhibitor
penciclovir
penciclovir : A member of the class of 2-aminopurines that is guanine in which the hydrogen at position 9 is substituted by a 4-hydroxy-3-(hydroxymethyl)but-1-yl group. An antiviral drug, it is administered topically for treatment of herpes labialis. A prodrug, famciclovir, is used for oral administration.		2.05102-aminopurines;
propane-1,3-diols		antiviral drug
oxypurinol
Oxypurinol: A xanthine oxidase inhibitor.. alloxanthine : A pyrazolopyrimidine that is 4,5,6,7-tetrahydro-H-pyrazolo[3,4-d]pyrimidine substituted by oxo groups at positions 4 and 6.		2.0510pyrazolopyrimidinedrug metabolite;
EC 1.17.3.2 (xanthine oxidase) inhibitor
raltitrexed
[no description available]		9.01270N-acyl-amino acid
vardenafil
vardenafil : The sulfonamide resulting from formal condensation of the sulfo group of 4-ethoxy-3-(5-methyl-7-propylimidazo[5,1-f][1,2,4]triazin-4(1H)-one-2-yl)benzenesulfonic acid and the secondary amino group of 4-ethylpiperazine.		3.2310imidazotriazine;
N-alkylpiperazine;
N-sulfonylpiperazine		EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
vasodilator agent
allopurinol
Allopurinol: A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.. allopurinol : A bicyclic structure comprising a pyrazole ring fused to a hydroxy-substituted pyrimidine ring.		3.5920nucleobase analogue;
organic heterobicyclic compound		antimetabolite;
EC 1.17.3.2 (xanthine oxidase) inhibitor;
gout suppressant;
radical scavenger
citrovorum factor
[no description available]		3.2310tetrahydrofolic acid
leucovorin
5-formyltetrahydrofolic acid : A formyltetrahydrofolic acid in which the formyl group is located at position 5.		3.5920formyltetrahydrofolic acidEscherichia coli metabolite;
mouse metabolite
rifapentine
rifapentine: cyclopentyl derivative of rifampicin		3.5420N-alkylpiperazine;
N-iminopiperazine;
rifamycins		antitubercular agent;
leprostatic drug
alanosine
[no description available]		2.0510
bl 4162a
anagrelide: imidazoquinazoline derivative which lowers platelet count probably by inhibiting thrombopoiesis and reduces platelet aggregation; used for thrombocythemia; structure in first source. anagrelide : A 1,5-dihydroimidazo[2,1-]quinazoline having an oxo substituent at the 2-position and chloro substituents at the 6- and 7-positions.		3.5920imidazoquinazolineanticoagulant;
antifibrinolytic drug;
cardiovascular drug;
platelet aggregation inhibitor
tegaserod
tegaserod: a nonbenzamide 5-hydroxytryptamine(4) agonist; used in treatment of irritable bowel syndrome; marketing suspended 2007 in US due to higher incidence of MI, stroke, and unstable angina; structure given in first source		3.2310carboxamidine;
guanidines;
hydrazines;
indoles		gastrointestinal drug;
serotonergic agonist
pemetrexed
pemetrexed disodium : An organic sodium salt that is the disodium salt of N-{4-[2-(2-amino-4-oxo-4,7-dihydro-1H-pyrrolo[2,3-d]pyrimidin-5-yl)ethyl]benzoyl}-L-glutamic acid. Inhibits thymidylate synthase (TS), 421 dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT).		14.25112N-acyl-L-glutamic acid;
pyrrolopyrimidine		antimetabolite;
antineoplastic agent;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
EC 2.1.1.45 (thymidylate synthase) inhibitor;
EC 2.1.2.2 (phosphoribosylglycinamide formyltransferase) inhibitor
tirapazamine
Tirapazamine: A triazine derivative that introduces breaks into DNA strands in hypoxic cells, sensitizing tumor cells to the cytotoxic activity of other drugs and radiation.. tirapazamine : A member of the class of benzotriazines that is 1,2,4-benzotriazine carrying an amino substituent at position 3 and two oxido substituents at positions 1 and 4.		2.0510aromatic amine;
benzotriazines;
N-oxide		antibacterial agent;
antineoplastic agent;
apoptosis inducer
sildenafil citrate
Sildenafil Citrate: A PHOSPHODIESTERASE TYPE-5 INHIBITOR; VASODILATOR AGENT and UROLOGICAL AGENT that is used in the treatment of ERECTILE DYSFUNCTION and PRIMARY PULMONARY HYPERTENSION.. sildenafil citrate : The citrate salt of sildenafil.		4.7421citrate saltEC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
valganciclovir
Valganciclovir: A ganciclovir prodrug and antiviral agent that is used to treat CYTOMEGALOVIRUS RETINITIS in patients with AIDS, and for the prevention of CYTOMEGALOVIRUS INFECTIONS in organ transplant recipients who have received an organ from a CMV-positive donor.. valganciclovir : The L-valinyl ester of ganciclovir, into which it is rapidly converted by intestinal and hepatic esterases. It is a synthetic analogue of 2'-deoxyguanosine.		3.2310L-valyl ester;
purines		antiviral drug;
prodrug
aprepitant
Aprepitant: A morpholine neurokinin-1 (NK1) receptor antagonist that is used in the management of nausea and vomiting caused by DRUG THERAPY, and for the prevention of POSTOPERATIVE NAUSEA AND VOMITING.. aprepitant : A morpholine-based antiemetic, which is or the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of highly emetogenic cancer chemotherapy. Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors.		5.0121(trifluoromethyl)benzenes;
cyclic acetal;
morpholines;
triazoles		antidepressant;
antiemetic;
neurokinin-1 receptor antagonist;
peripheral nervous system drug;
substance P receptor antagonist
fosaprepitant
fosaprepitant: a pro-drug form of aprepitant. fosaprepitant : A morpholine derivative that is the (1R)-1-[3,5-bis(trifluoromethyl)phenyl]ethyl ether of (3-{[(2R,3S)-3-(4-fluorophenyl)-2-hydroxymorpholin-4-yl]methyl}-5-oxo-4,5-dihydro-1H-1,2,4-triazol-1-yl)phosphonic acid.		5.0121(trifluoromethyl)benzenes;
cyclic acetal;
morpholines;
phosphoramide;
triazoles		antiemetic;
neurokinin-1 receptor antagonist;
prodrug
rifabutin
[no description available]		3.5920
zd 9331
ZD 9331: BGC9331 was formerly known as ZD9331; structure in first source		210
8-hydroxy-2'-deoxyguanosine
8-Hydroxy-2'-Deoxyguanosine: Common oxidized form of deoxyguanosine in which C-8 position of guanine base has a carbonyl group.. 8-hydroxy-2'-deoxyguanosine : Guanosine substituted at the purine 8-position by a hydroxy group. It is used as a biomarker of oxidative DNA damage.		2.2110guanosinesbiomarker
febantel
febantel: structure		2.0510aryl sulfide
levomefolate calcium
levomefolate calcium: an ingredient in Contraceptives, Oral, Combined. levomefolate calcium : An organic calcium salt of (6S)-5-methyltetrahydrofolic acid.		3.2310organic calcium saltantidepressant
sta 9090
[no description available]		2.110ring assembly;
triazoles
bmn 673
talazoparib: inhibits both PARP1 and PARP2; structure in first source		3.711
fenobam
fenobam: in USAN fenobam refers to monohydrate		2.0510ureas
pyrimidinones
Pyrimidinones: Heterocyclic compounds known as 2-pyrimidones (or 2-hydroxypyrimidines) and 4-pyrimidones (or 4-hydroxypyrimidines) with the general formula C4H4N2O.		6.1451
ConditionIndicatedRelationship StrengthStudiesTrials
Colorectal Cancer
[description not available]		028.081,307619
Colorectal Neoplasms
Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.		135.625,2282,476
Leukemia L 1210
[description not available]		02.0110
Carcinoma, Non-Small Cell Lung
[description not available]		08.37159
Cancer of Cervix
[description not available]		010.592011
Cancer of Lung
[description not available]		017.4514762
Carcinoma, Non-Small-Cell Lung
A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.		110.37159
Uterine Cervical Neoplasms
Tumors or cancer of the UTERINE CERVIX.		112.592011
Lung Neoplasms
Tumors or cancer of the LUNG.		119.4514762
Metastase
[description not available]		026.6872557
Diarrhea
An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.		021.24226168
Neoplasm Metastasis
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.		128.6872557
Neutropenia
A decrease in the number of NEUTROPHILS found in the blood.		022.2611277
Acute Liver Injury, Drug-Induced
[description not available]		06.0191
Chemical and Drug Induced Liver Injury
A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, herbal and dietary supplements and chemicals from the environment.		06.0191
Adverse Drug Event
[description not available]		018.7912670
Drug-Related Side Effects and Adverse Reactions
Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.		018.7912670
Experimental Neoplasms
[description not available]		05.78110
Congenital Zika Syndrome
[description not available]		02.2510
Disease Models, Animal
Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.		07.36220
Zika Virus Infection
A viral disease transmitted by the bite of AEDES mosquitoes infected with ZIKA VIRUS. Its mild DENGUE-like symptoms include fever, rash, headaches and ARTHRALGIA. The viral infection during pregnancy, in rare cases, is associated with congenital brain and ocular abnormalities, called Congenital Zika Syndrome, including MICROCEPHALY and may also lead to GUILLAIN-BARRE SYNDROME.		02.2510
Adenocarcinoma, Basal Cell
[description not available]		027.341,242832
Cancer of Duodenum
[description not available]		03.4160
Cancer of Jejunum
[description not available]		05.6761
Adenocarcinoma
A malignant epithelial tumor with a glandular organization.		129.341,242832
Cancer of Esophagus
[description not available]		022.96361216
Cancer of Stomach
[description not available]		027.831,205873
Esophageal Neoplasms
Tumors or cancer of the ESOPHAGUS.		129.321,083648
Stomach Neoplasms
Tumors or cancer of the STOMACH.		135.364,8203,492
Carcinoma, Anaplastic
[description not available]		017.9212981
Peritoneal Carcinomatosis
[description not available]		016.238843
Carcinoma
A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm and not a synonym for cancer.		119.9212981
Peritoneal Neoplasms
Tumors or cancer of the PERITONEUM.		118.238843
Hypertriglyceridemia
A condition of elevated levels of TRIGLYCERIDES in the blood.		06.22170
Cancer of Pancreas
[description not available]		023.55449192
Pancreatic Neoplasms
Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).		128.31898384
Neuroendocrine Tumors
Tumors whose cells possess secretory granules and originate from the neuroectoderm, i.e., the cells of the ectoblast or epiblast that program the neuroendocrine system. Common properties across most neuroendocrine tumors include ectopic hormone production (often via APUD CELLS), the presence of tumor-associated antigens, and isozyme composition.		120.8619224
Cardiac Toxicity
[description not available]		08.87270
Cardiac Diseases
[description not available]		017.086850
Heart Diseases
Pathological conditions involving the HEART including its structural and functional abnormalities.		017.086850
Cardiotoxicity
Damage to the HEART or its function secondary to exposure to toxic substances such as drugs used in CHEMOTHERAPY; IMMUNOTHERAPY; or RADIATION.		08.87270
Cancer of Colon
[description not available]		022.42405123
Colonic Neoplasms
Tumors or cancer of the COLON.		127.18810246
Cancer of Liver
[description not available]		022.03446149
Local Neoplasm Recurrence
[description not available]		023.36500230
Liver Neoplasms
Tumors or cancer of the LIVER.		124.03446149
Nasopharyngeal Carcinoma
A carcinoma that originates in the EPITHELIUM of the NASOPHARYNX and includes four subtypes: keratinizing squamous cell, non-keratinizing, basaloid squamous cell, and PAPILLARY ADENOCARCINOMA. It is most prevalent in Southeast Asian populations and is associated with EPSTEIN-BARR VIRUS INFECTIONS. Somatic mutations associated with this cancer have been identified in NPCR, BAP1, UBAP1, ERBB2, ERBB3, MLL2, PIK3CA, KRAS, NRAS, and ARID1A genes.		014.535942
Cancer of Nasopharynx
[description not available]		014.836747
Nasopharyngeal Neoplasms
Tumors or cancer of the NASOPHARYNX.		116.836747
ER-Negative PR-Negative HER2-Negative Breast Cancer
[description not available]		028.681,14866
Breast Cancer
[description not available]		032.062,432685
Breast Neoplasms
Tumors or cancer of the human BREAST.		138.467,2962,055
Triple Negative Breast Neoplasms
Breast neoplasms that do not express ESTROGEN RECEPTORS; PROGESTERONE RECEPTORS; and do not overexpress the NEU RECEPTOR/HER-2 PROTO-ONCOGENE PROTEIN.		130.681,14866
T-Cell Lymphoma
[description not available]		02.3110
Lymphoma, T-Cell
A group of heterogeneous lymphoid tumors representing malignant transformations of T-lymphocytes.		02.3110
Chemotherapy-Induced Acral Erythema
[description not available]		020.66192104
Hand-Foot Syndrome
Chemotherapy-induced dermal side effects that are associated with the use of various CYTOSTATIC AGENTS. Symptoms range from mild ERYTHEMA and/or PARESTHESIA to severe ulcerative dermatitis with debilitating pain involving typically palmoplantar and intertriginous areas. These cutaneous manifestations are sometimes accompanied by nail anomalies.		122.66192104
Mixed Tumor, Malignant
A malignant tumor composed of more than one type of neoplastic tissue. (Dorland, 27th ed)		02.6620
Cancer of Rectum
[description not available]		025.79806454
Rectal Neoplasms
Tumors or cancer of the RECTUM.		132.172,4181,362
Benign Neoplasms
[description not available]		021.65271104
Neoplasms
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.		126.41542208
Emesis
[description not available]		014.885132
Nausea
An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses.		018.3411595
Vomiting
The forcible expulsion of the contents of the STOMACH through the MOUTH.		014.885132
Cancer of Gallbladder
[description not available]		014.133413
Gallbladder Neoplasms
Tumors or cancer of the gallbladder.		118.816826
Cancer of Pituitary
[description not available]		04.4160
Adenoma, Prolactin-Secreting, Pituitary
[description not available]		02.4110
Pituitary Neoplasms
Neoplasms which arise from or metastasize to the PITUITARY GLAND. The majority of pituitary neoplasms are adenomas, which are divided into non-secreting and secreting forms. Hormone producing forms are further classified by the type of hormone they secrete. Pituitary adenomas may also be characterized by their staining properties (see ADENOMA, BASOPHIL; ADENOMA, ACIDOPHIL; and ADENOMA, CHROMOPHOBE). Pituitary tumors may compress adjacent structures, including the HYPOTHALAMUS, several CRANIAL NERVES, and the OPTIC CHIASM. Chiasmal compression may result in bitemporal HEMIANOPSIA.		04.4160
Cancer of Gastrointestinal Tract
[description not available]		014.96221
Dihydropyrimidine Dehydrogenase Deficiency
An autosomal recessive disorder affecting DIHYDROPYRIMIDINE DEHYDROGENASE and causing familial pyrimidinemia. It is characterized by thymine-uraciluria in homozygous deficient patients. Even a partial deficiency in the enzyme leaves individuals at risk for developing severe 5-FLUOROURACIL-associated toxicity.		08.42550
CACH Syndrome
[description not available]		06.26160
Hematochezia
The passage of bright red blood from the rectum. The blood may or may not be mixed with formed stool in the form of blood, blood clots, bloody stool or diarrhea.		05.03140
Gastrointestinal Hemorrhage
Bleeding in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.		05.03140
Adenoma, Basal Cell
[description not available]		03.3960
Nelson Syndrome
A syndrome characterized by HYPERPIGMENTATION, enlarging pituitary mass, visual defects secondary to compression of the OPTIC CHIASM, and elevated serum ACTH. It is caused by the expansion of an underlying ACTH-SECRETING PITUITARY ADENOMA that grows in the absence of feedback inhibition by adrenal CORTICOSTEROIDS, usually after ADRENALECTOMY.		02.3110
Invasiveness, Neoplasm
[description not available]		017.079456
Adenoma
A benign epithelial tumor with a glandular organization.		08.3960
Minimal Disease, Residual
[description not available]		012.583110
Biliary Tract Cancer
[description not available]		017.17237
Biliary Tract Neoplasms
Tumors or cancer in the BILIARY TRACT including the BILE DUCTS and the GALLBLADDER.		121.8214474
Carcinoma, Ductal, Pancreatic
[description not available]		016.596649
Carcinoma, Pancreatic Ductal
Carcinoma that arises from the PANCREATIC DUCTS. It accounts for the majority of cancers derived from the PANCREAS.		118.596649
Benign Neoplasms, Brain
[description not available]		017.8711541
Brain Neoplasms
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.		119.8711541
Disease Exacerbation
[description not available]		023.48436297
Cholangiocellular Carcinoma
[description not available]		014.944616
Bile Duct Cancer
[description not available]		019.524916
Bile Duct Neoplasms
Tumors or cancer of the BILE DUCTS.		014.524916
Cholangiocarcinoma
A malignant tumor arising from the epithelium of the BILE DUCTS.		119.639232
Enteritis
Inflammation of any segment of the SMALL INTESTINE.		04.1450
Enterocolitis
Inflammation of the MUCOSA of both the SMALL INTESTINE and the LARGE INTESTINE. Etiology includes ISCHEMIA, infections, allergic, and immune responses.		05.03110
Hepatitis B Virus Infection
[description not available]		03.7420
Hepatitis B
INFLAMMATION of the LIVER in humans caused by a member of the ORTHOHEPADNAVIRUS genus, HEPATITIS B VIRUS. It is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact.		08.7420
Encephalopathy, Toxic
[description not available]		011.513211
Thyroiditis
Inflammatory diseases of the THYROID GLAND. Thyroiditis can be classified into acute (THYROIDITIS, SUPPURATIVE), subacute (granulomatous and lymphocytic), chronic fibrous (Riedel's), chronic lymphocytic (HASHIMOTO DISEASE), transient (POSTPARTUM THYROIDITIS), and other AUTOIMMUNE THYROIDITIS subtypes.		07.4110
Anal Cancer
[description not available]		011.33306
Carcinoma, Epidermoid
[description not available]		018.714047
Anus Neoplasms
Tumors or cancer of the ANAL CANAL.		113.33306
Carcinoma, Squamous Cell
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)		123.4328094
Coronary Artery Vasospasm
[description not available]		05.37210
Coronary Vasospasm
Spasm of the large- or medium-sized coronary arteries.		05.37210
Pink Eye
[description not available]		02.4110
Conjunctivitis
INFLAMMATION of the CONJUNCTIVA.		07.4110
Hypokalemia
Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)		07.5320
Diabetes Mellitus
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.		03.2150
Diabetes Mellitus, Adult-Onset
[description not available]		03.7130
Innate Inflammatory Response
[description not available]		07.58113
Palmoplantaris Pustulosis
[description not available]		03.8330
Diabetes Mellitus, Type 2
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.		03.7130
Inflammation
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.		012.58113
Psoriasis
A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis.		03.8330
Bowel Incontinence
[description not available]		06.4553
Fecal Incontinence
Failure of voluntary control of the anal sphincters, with involuntary passage of feces and flatus.		06.4553
Peripheral Nerve Diseases
[description not available]		017.268150
Peripheral Nervous System Diseases
Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.		017.268150
Cancer, Second Primary
[description not available]		010.22262
Bladder Cancer
[description not available]		06.26121
Urinary Bladder Neoplasms
Tumors or cancer of the URINARY BLADDER.		18.26121
Carcinoma, Transitional Cell
A malignant neoplasm derived from TRANSITIONAL EPITHELIAL CELLS, occurring chiefly in the URINARY BLADDER; URETERS; or RENAL PELVIS.		02.9940
Cancer of Mouth
[description not available]		04.1150
Mouth Neoplasms
Tumors or cancer of the MOUTH.		04.1150
Arrhythmia
[description not available]		03.7930
Arrhythmias, Cardiac
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.		03.7930
Esophageal Squamous Cell Carcinoma
A carcinoma that originates usually from cells on the surface of the middle and lower third of the ESOPHAGUS. Tumor cells exhibit typical squamous morphology and form large polypoid lesions. Mutations in RNF6, LZTS1, TGFBR2, DEC1, and WWOX1 genes are associated with this cancer.		08.3185
Lupus Erythematosus, Cutaneous, Subacute
[description not available]		04.79110
Lupus Erythematosus, Cutaneous
A form of lupus erythematosus in which the skin may be the only organ involved or in which skin involvement precedes the spread into other body systems. It has been classified into three forms - acute (= LUPUS ERYTHEMATOSUS, SYSTEMIC with skin lesions), subacute, and chronic (= LUPUS ERYTHEMATOSUS, DISCOID).		04.79110
Acquired Agraphia
[description not available]		02.610
Dysarthosis
[description not available]		03.4420
Kidney Failure
A severe irreversible decline in the ability of kidneys to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism.		02.8330
Renal Insufficiency
Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE.		02.8330
Cruveilhier-Baumgarten Syndrome
Liver cirrhosis with intrahepatic portal obstruction, HYPERTENSION, and patent UMBILICAL VEINS.		03.0940
Enlarged Spleen
[description not available]		02.920
Hypertension, Portal
Abnormal increase of resistance to blood flow within the hepatic PORTAL SYSTEM, frequently seen in LIVER CIRRHOSIS and conditions with obstruction of the PORTAL VEIN.		03.0940
Lassitude
[description not available]		014.815141
Fatigue
The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.		014.815141
Hepatocellular Carcinoma
[description not available]		013.716015
Carcinoma, Hepatocellular
A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.		115.716015
Febrile Neutropenia
Fever accompanied by a significant reduction in the number of NEUTROPHILS.		04.8632
Debility
[description not available]		05.2333
Esophageal Varices
[description not available]		02.920
Cirrhosis, Liver
[description not available]		04.0950
Esophageal and Gastric Varices
Dilated blood vessels in the ESOPHAGUS or GASTRIC FUNDUS that shunt blood from the portal circulation (PORTAL SYSTEM) to the systemic venous circulation. Often they are observed in individuals with portal hypertension (HYPERTENSION, PORTAL).		02.920
Liver Cirrhosis
Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.		04.0950
Mucositis
An INFLAMMATION of the MUCOSA with burning or tingling sensation. It is characterized by atrophy of the squamous EPITHELIUM, vascular damage, inflammatory infiltration, and ulceration. It usually occurs at the mucous lining of the MOUTH, the GASTROINTESTINAL TRACT or the airway due to chemical irritations, CHEMOTHERAPY, or radiation therapy (RADIOTHERAPY).		011.57105
Cancer of Cecum
[description not available]		05.2980
Thrombopenia
[description not available]		013.393819
Varices
[description not available]		02.610
Thrombocytopenia
A subnormal level of BLOOD PLATELETS.		013.393819
Varicose Veins
Enlarged and tortuous VEINS.		02.610
Anemia
A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.		011.572817
Cancer of Testis
[description not available]		05.1531
Testicular Neoplasms
Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.		05.1531
Astrocytoma, Grade IV
[description not available]		07.0784
Glioblastoma
A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.		19.0784
Cancer of Intestines
[description not available]		010.54227
Intestinal Neoplasms
Tumors or cancer of the INTESTINES.		010.54227
Cancer of Sigmoid
[description not available]		012.35505
Lymph Node Metastasis
[description not available]		019.8425574
Rhabdomyolysis
Necrosis or disintegration of skeletal muscle often followed by myoglobinuria.		02.7220
Cardiac Rupture, Traumatic
[description not available]		02.610
Recrudescence
[description not available]		011.86569
Complication, Postoperative
[description not available]		010.72326
Postoperative Complications
Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.		010.72326
Erythema
Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of disease processes.		015.32222
Genetic Predisposition
[description not available]		010.66188
Diffuse Parenchymal Lung Disease
[description not available]		03.9740
Lung Diseases, Interstitial
A diverse group of lung diseases that affect the lung parenchyma. They are characterized by an initial inflammation of PULMONARY ALVEOLI that extends to the interstitium and beyond leading to diffuse PULMONARY FIBROSIS. Interstitial lung diseases are classified by their etiology (known or unknown causes), and radiological-pathological features.		03.9740
Cancer of Skin
[description not available]		010.73402
Mycosis Fungoides
A chronic, malignant T-cell lymphoma of the skin. In the late stages, the LYMPH NODES and viscera are affected.		07.610
Skin Neoplasms
Tumors or cancer of the SKIN.		115.23804
Hyperammonemia
Elevated level of AMMONIA in the blood. It is a sign of defective CATABOLISM of AMINO ACIDS or ammonia to UREA.		03.5670
Thyroid Cancer, Anaplastic
[description not available]		02.610
Cancer of the Thyroid
[description not available]		03.3260
Thyroid Neoplasms
Tumors or cancer of the THYROID GLAND.		15.3260
Thyroid Carcinoma, Anaplastic
An aggressive THYROID GLAND malignancy which generally occurs in IODINE-deficient areas in people with previous thyroid pathology such as GOITER. It is associated with CELL DEDIFFERENTIATION of THYROID CARCINOMA (e.g., FOLLICULAR THYROID CARCINOMA; PAPILLARY THYROID CANCER). Typical initial presentation is a rapidly growing neck mass which upon metastasis is associated with DYSPHAGIA; NECK PAIN; bone pain; DYSPNEA; and NEUROLOGIC DEFICITS.		02.610
Cancer of Kidney
[description not available]		013.274124
Adenoma Sebaceum
Facial ANGIOFIBROMA in tuberous sclerosis		02.610
Kidney Neoplasms
Tumors or cancers of the KIDNEY.		117.878248
Tuberous Sclerosis
Autosomal dominant neurocutaneous syndrome classically characterized by MENTAL RETARDATION; EPILEPSY; and skin lesions (e.g., adenoma sebaceum and hypomelanotic macules). There is, however, considerable heterogeneity in the neurologic manifestations. It is also associated with cortical tuber and HAMARTOMAS formation throughout the body, especially the heart, kidneys, and eyes. Mutations in two loci TSC1 and TSC2 that encode hamartin and tuberin, respectively, are associated with the disease.		02.610
Cecitis
[description not available]		02.610
Cholera Infantum
[description not available]		014.944125
Graft-Versus-Host Disease
[description not available]		07.5920
Graft vs Host Disease
The clinical entity characterized by anorexia, diarrhea, loss of hair, leukopenia, thrombocytopenia, growth retardation, and eventual death brought about by the GRAFT VS HOST REACTION.		02.5920
Ascites, Gelatinous
[description not available]		05.8983
Appendiceal Cancer
[description not available]		03.680
Appendiceal Neoplasms
Tumors or cancer of the APPENDIX.		03.680
Pseudomyxoma Peritonei
A peritoneal adenocarcinoma characterized by build-up of MUCUS in the PERITONEAL CAVITY. Mucus secreting cells may attach to the peritoneal lining and continue to secrete mucus. The majority of cases represent tumor spread from a primary low-grade mucinous neoplasm of the APPENDIX (NCI Thesaurus).		17.8983
Adenopathy
[description not available]		02.610
2019 Novel Coronavirus Disease
[description not available]		03.0130
Hematologic Malignancies
[description not available]		02.5320
Hematologic Neoplasms
Neoplasms located in the blood and blood-forming tissue (the bone marrow and lymphatic tissue). The commonest forms are the various types of LEUKEMIA, of LYMPHOMA, and of the progressive, life-threatening forms of the MYELODYSPLASTIC SYNDROMES.		02.5320
Precordial Catch
[description not available]		05.79120
Chest Pain
Pressure, burning, or numbness in the chest.		05.79120
Ileitis
Inflammation of any segment of the ILEUM and the ILEOCECAL VALVE.		04.7640
ANCA-Associated Vasculitides
[description not available]		02.610
Nasal Bleeding
[description not available]		02.610
Disease, Pulmonary
[description not available]		02.6320
Epistaxis
Bleeding from the nose.		02.610
Kidney Diseases
Pathological processes of the KIDNEY or its component tissues.		06.5392
Lung Diseases
Pathological processes involving any part of the LUNG.		02.6320
Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
Group of systemic vasculitis with a strong association with ANCA. The disorders are characterized by necrotizing inflammation of small and medium size vessels, with little or no immune-complex deposits in vessel walls.		02.610
Fusiform Aneurysm
Elongated, spindle-shaped dilation in the wall of blood vessels, usually large ARTERIES with ATHEROSCLEROSIS.		02.610
Aortic Dissection
[description not available]		07.7930
Aneurysm
Pathological outpouching or sac-like dilatation in the wall of any blood vessel (ARTERIES or VEINS) or the heart (HEART ANEURYSM). It indicates a thin and weakened area in the wall which may later rupture. Aneurysms are classified by location, etiology, or other characteristics.		02.610
Leukoencephalopathy Syndrome, Posterior
[description not available]		03.2850
Brain Disorders
[description not available]		03.2550
Absence Seizure
[description not available]		04.1850
Brain Diseases
Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.		15.2550
Seizures
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or seizure disorder.		04.1850
Argentaffinoma
[description not available]		04.1550
Carcinoid Tumor
A usually small, slow-growing neoplasm composed of islands of rounded, oxyphilic, or spindle-shaped cells of medium size, with moderately small vesicular nuclei, and covered by intact mucosa with a yellow cut surface. The tumor can occur anywhere in the gastrointestinal tract (and in the lungs and other sites); approximately 90% arise in the appendix. It is now established that these tumors are of neuroendocrine origin and derive from a primitive stem cell. (From Stedman, 25th ed & Holland et al., Cancer Medicine, 3d ed, p1182)		04.1550
Dermatitis Medicamentosa
[description not available]		010.76324
Malignant Melanoma
[description not available]		03.1650
Hand Dermatosis
[description not available]		013.915220
Foot Dermatoses
Skin diseases of the foot, general or unspecified.		013.854920
Hand Dermatoses
Skin diseases involving the HANDS.		013.915220
Melanoma
A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)		16.14150
Genetic Diseases, X-Chromosome Linked
[description not available]		02.2110
Hypogammaglobulinemia
[description not available]		02.2110
Agammaglobulinemia
An immunologic deficiency state characterized by an extremely low level of generally all classes of gamma-globulin in the blood.		02.2110
Hypocalcemia
Reduction of the blood calcium below normal. Manifestations include hyperactive deep tendon reflexes, Chvostek's sign, muscle and abdominal cramps, and carpopedal spasm. (Dorland, 27th ed)		02.2110
Body-Weight Trajectory
A general pattern of body weight gain or loss over many years. Weight change trajectory is influenced by several determinants in children and adults.		03.5911
Carcinoma, Ductal, Breast
An invasive (infiltrating) CARCINOMA of the mammary ductal system (MAMMARY GLANDS) in the human BREAST.		013.636412
Acid Aspiration Syndrome
[description not available]		02.2110
Flaccid Quadriplegia
[description not available]		02.2110
Anterior Horn Cell Disease
[description not available]		02.5120
Pneumonia, Aspiration
A type of lung inflammation resulting from the aspiration of food, liquid, or gastric contents into the upper RESPIRATORY TRACT.		02.2110
Motor Neuron Disease
Diseases characterized by a selective degeneration of the motor neurons of the spinal cord, brainstem, or motor cortex. Clinical subtypes are distinguished by the major site of degeneration. In AMYOTROPHIC LATERAL SCLEROSIS there is involvement of upper, lower, and brainstem motor neurons. In progressive muscular atrophy and related syndromes (see MUSCULAR ATROPHY, SPINAL) the motor neurons in the spinal cord are primarily affected. With progressive bulbar palsy (BULBAR PALSY, PROGRESSIVE), the initial degeneration occurs in the brainstem. In primary lateral sclerosis, the cortical neurons are affected in isolation. (Adams et al., Principles of Neurology, 6th ed, p1089)		02.5120
Apical Ballooning Syndrome
[description not available]		04.0240
Takotsubo Cardiomyopathy
A transient left ventricular apical dysfunction or ballooning accompanied by electrocardiographic (ECG) T wave inversions. This abnormality is associated with high levels of CATECHOLAMINES, either administered or endogenously secreted from a tumor or during extreme stress.		04.0240
Jaundice, Cholestatic
[description not available]		02.2110
Jaundice, Obstructive
Jaundice, the condition with yellowish staining of the skin and mucous membranes, that is due to impaired BILE flow in the BILIARY TRACT, such as INTRAHEPATIC CHOLESTASIS, or EXTRAHEPATIC CHOLESTASIS.		02.2110
Inflammatory Breast Cancer
[description not available]		02.5820
Inflammatory Breast Neoplasms
Metastatic breast cancer characterized by EDEMA and ERYTHEMA of the affected breast due to LYMPHATIC METASTASIS and eventual obstruction of LYMPHATIC VESSELS by the cancer cells.		14.5820
Dermatitis, Radiation-Induced
[description not available]		07.45161
Radiodermatitis
A cutaneous inflammatory reaction occurring as a result of exposure to ionizing radiation.		07.45161
Hepatic Veno Occlusive Disease
[description not available]		04.2860
Hepatic Veno-Occlusive Disease
Liver disease that is caused by injuries to the ENDOTHELIAL CELLS of the vessels and subendothelial EDEMA, but not by THROMBOSIS. Extracellular matrix, rich in FIBRONECTINS, is usually deposited around the HEPATIC VEINS leading to venous outflow occlusion and sinusoidal obstruction.		04.2860
Lymphocytopenia
[description not available]		05.2943
Lymphopenia
Reduction in the number of lymphocytes.		05.2943
Neoplasms, Bone Marrow
[description not available]		02.2110
Bone Marrow Neoplasms
Neoplasms located in the bone marrow. They are differentiated from neoplasms composed of bone marrow cells, such as MULTIPLE MYELOMA. Most bone marrow neoplasms are metastatic.		02.2110
Dermatomyositis, Adult Type
[description not available]		02.8730
Dermatomyositis
A subacute or chronic inflammatory disease of muscle and skin, marked by proximal muscle weakness and a characteristic skin rash. The illness occurs with approximately equal frequency in children and adults. The skin lesions usually take the form of a purplish rash (or less often an exfoliative dermatitis) involving the nose, cheeks, forehead, upper trunk, and arms. The disease is associated with a complement mediated intramuscular microangiopathy, leading to loss of capillaries, muscle ischemia, muscle-fiber necrosis, and perifascicular atrophy. The childhood form of this disease tends to evolve into a systemic vasculitis. Dermatomyositis may occur in association with malignant neoplasms. (From Adams et al., Principles of Neurology, 6th ed, pp1405-6)		02.8730
Proteinuria
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.		02.8230
Central Retinal Edema, Cystoid
[description not available]		02.2110
Macular Edema
Fluid accumulation in the outer layer of the MACULA LUTEA that results from intraocular or systemic insults. It may develop in a diffuse pattern where the macula appears thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with various underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, DIABETIC RETINOPATHY, and posterior segment inflammatory disease. (From Survey of Ophthalmology 2004; 49(5) 470-90)		02.2110
Margins of Excision
The edges of tissue removed in a surgery for assessment of the effectiveness of a surgical procedure in achieving the local control of a neoplasm and the adequacy of tumor removal. When the margin is negative or not involved by tumor (e.g., CANCER) it suggests all of the tumor has been removed by the surgery.		09.5104
Exanthem
[description not available]		07.3253
Exanthema
Diseases in which skin eruptions or rashes are a prominent manifestation. Classically, six such diseases were described with similar rashes; they were numbered in the order in which they were reported. Only the fourth (Duke's disease), fifth (ERYTHEMA INFECTIOSUM), and sixth (EXANTHEMA SUBITUM) numeric designations survive as occasional synonyms in current terminology.		07.3253
Mucositis, Oral
[description not available]		017.617361
Anorexia
The lack or loss of APPETITE accompanied by an aversion to food and the inability to eat. It is the defining characteristic of the disorder ANOREXIA NERVOSA.		011.62421
Stomatitis
INFLAMMATION of the soft tissues of the MOUTH, such as MUCOSA; PALATE; GINGIVA; and LIP.		022.617361
Nervous System Disorders
[description not available]		09.99118
Nervous System Diseases
Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.		09.99118
Bone Cancer
[description not available]		016.648647
Bone Neoplasms
Tumors or cancer located in bone tissue or specific BONES.		016.648647
Heart Disease, Ischemic
[description not available]		05.7570
Myocardial Ischemia
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).		05.7570
Intestinal Obstruction
Any impairment, arrest, or reversal of the normal flow of INTESTINAL CONTENTS toward the ANAL CANAL.		03.3460
Colonic Inertia
Symptom characterized by the passage of stool once a week or less.		03.6411
Colicky Pain
[description not available]		05.9242
Constipation
Infrequent or difficult evacuation of FECES. These symptoms are associated with a variety of causes, including low DIETARY FIBER intake, emotional or nervous disturbances, systemic and structural disorders, drug-induced aggravation, and infections.		03.6411
Abdominal Pain
Sensation of discomfort, distress, or agony in the abdominal region.		05.9242
Libman-Sacks Disease
[description not available]		03.4420
Lupus Erythematosus, Systemic
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.		03.4420
Bone Fractures
[description not available]		03.1710
Disbacteriosis
[description not available]		03.1710
Bacterial Disease
[description not available]		03.1710
Bacterial Infections
Infections by bacteria, general or unspecified.		03.1710
Fractures, Bone
Breaks in bones.		03.1710
Hormone-Dependent Neoplasms
[description not available]		08.886
EBV Infections
[description not available]		02.2510
Epstein-Barr Virus Infections
Infection with human herpesvirus 4 (HERPESVIRUS 4, HUMAN); which may facilitate the development of various lymphoproliferative disorders. These include BURKITT LYMPHOMA (African type), INFECTIOUS MONONUCLEOSIS, and oral hairy leukoplakia (LEUKOPLAKIA, HAIRY).		02.2510
Granulomas
[description not available]		02.2510
Granuloma
A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents.		07.2510
Diarrheogenic Islet Cell Tumor
[description not available]		02.2510
Hepatitis, Viral, Non-A, Non-B, Parenterally-Transmitted
[description not available]		02.4920
Hepatitis C
INFLAMMATION of the LIVER in humans caused by HEPATITIS C VIRUS, a single-stranded RNA virus. Its incubation period is 30-90 days. Hepatitis C is transmitted primarily by contaminated blood parenterally and is often associated with transfusion and intravenous drug abuse. However, in a significant number of cases, the source of hepatitis C infection is unknown.		02.4920
Carcinoma, Colloid
[description not available]		09.25253
Signet Ring Cell Carcinoma
[description not available]		08.95183
Adenocarcinoma, Mucinous
An adenocarcinoma producing mucin in significant amounts. (From Dorland, 27th ed)		09.25253
Carcinoma, Signet Ring Cell
A poorly differentiated adenocarcinoma in which the nucleus is pressed to one side by a cytoplasmic droplet of mucus. It usually arises in the gastrointestinal system.		08.95183
Injuries, Radiation
[description not available]		09.35236
Colon Cancer, Familial Nonpolyposis
[description not available]		02.9130
Cancer of ILEUM
[description not available]		05.5151
Cancer of Ovary
[description not available]		010.992711
Colorectal Neoplasms, Hereditary Nonpolyposis
A group of autosomal-dominant inherited diseases in which COLON CANCER arises in discrete adenomas. Unlike FAMILIAL POLYPOSIS COLI with hundreds of polyps, hereditary nonpolyposis colorectal neoplasms occur much later, in the fourth and fifth decades. HNPCC has been associated with germline mutations in mismatch repair (MMR) genes. It has been subdivided into Lynch syndrome I or site-specific colonic cancer, and LYNCH SYNDROME II which includes extracolonic cancer.		02.9130
Ovarian Neoplasms
Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.		115.465422
Carcinoma, Neuroendocrine
A group of carcinomas which share a characteristic morphology, often being composed of clusters and trabecular sheets of round blue cells, granular chromatin, and an attenuated rim of poorly demarcated cytoplasm. Neuroendocrine tumors include carcinoids, small (oat) cell carcinomas, medullary carcinoma of the thyroid, Merkel cell tumor, cutaneous neuroendocrine carcinoma, pancreatic islet cell tumors, and pheochromocytoma. Neurosecretory granules are found within the tumor cells. (Segen, Dictionary of Modern Medicine, 1992)		110.48161
Sensitivity and Specificity
Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)		08.74287
Response Evaluation Criteria in Solid Tumors
An internationally recognized set of published rules used for evaluation of cancer treatment that define when tumors found in cancer patients improve, worsen, or remain stable during treatment. These criteria are based specifically on the response of the tumor(s) to treatment, and not on the overall health status of the patient resulting from treatment.		010.31712
Blood Diseases
[description not available]		014.743926
Hematologic Diseases
Disorders of the blood and blood forming tissues.		014.743926
Ectropion
The turning outward (eversion) of the edge of the eyelid, resulting in the exposure of the palpebral conjunctiva. (Dorland, 27th ed)		07.2510
Paraneoplastic Syndromes
In patients with neoplastic diseases a wide variety of clinical pictures which are indirect and usually remote effects produced by tumor cell metabolites or other products.		03.9240
Cells, Neoplasm Circulating
[description not available]		09.75168
Androgen-Independent Prostatic Cancer
[description not available]		02.2510
Prostatic Neoplasms, Castration-Resistant
Tumors or cancer of the PROSTATE which can grow in the presence of low or residual amount of androgen hormones such as TESTOSTERONE.		14.2510
Infections, Coronavirus
[description not available]		02.6620
Pneumonia, Viral
Inflammation of the lung parenchyma that is caused by a viral infection.		02.6620
Coronavirus Infections
Virus diseases caused by the CORONAVIRUS genus. Some specifics include transmissible enteritis of turkeys (ENTERITIS, TRANSMISSIBLE, OF TURKEYS); FELINE INFECTIOUS PERITONITIS; and transmissible gastroenteritis of swine (GASTROENTERITIS, TRANSMISSIBLE, OF SWINE).		02.6620
Infectious Myelitis
[description not available]		02.6620
Idiopathic Inflammatory Myopathies
[description not available]		02.5820
Myositis
Inflammation of a muscle or muscle tissue.		02.5820
Spinal Neoplasms
New abnormal growth of tissue in the SPINE.		02.2510
Blood Clot
[description not available]		02.8630
Thrombosis
Formation and development of a thrombus or blood clot in the blood vessel.		02.8630
Microsatellite Instability
The occurrence of highly polymorphic mono- and dinucleotide MICROSATELLITE REPEATS in somatic cells. It is a form of genome instability associated with defects in DNA MISMATCH REPAIR.		09.92174
Central Nervous System Neoplasm
[description not available]		06.5144
Central Nervous System Neoplasms
Benign and malignant neoplastic processes that arise from or secondarily involve the brain, spinal cord, or meninges.		18.5144
Breast Cancer, Male
[description not available]		010.35117
Breast Neoplasms, Male
Any neoplasms of the male breast. These occur infrequently in males in developed countries, the incidence being about 1% of that in females.		112.35117
Actinic Keratosis
[description not available]		09.1450
Carcinoma, Basal Cell, Pigmented
[description not available]		04.5850
Carcinoma, Basal Cell
A malignant skin neoplasm that seldom metastasizes but has potentialities for local invasion and destruction. Clinically it is divided into types: nodular, cicatricial, morphaic, and erythematoid (pagetoid). They develop on hair-bearing skin, most commonly on sun-exposed areas. Approximately 85% are found on the head and neck area and the remaining 15% on the trunk and limbs. (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1471)		04.5850
Keratosis, Actinic
White or pink lesions on the arms, hands, face, or scalp that arise from sun-induced DNA DAMAGE to KERATINOCYTES in exposed areas. They are considered precursor lesions to superficial SQUAMOUS CELL CARCINOMA.		04.1450
Cardiomyopathies, Primary
[description not available]		04.230
Cardiomyopathies
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).		04.230
Abnormal Movements
[description not available]		02.3110
Lower Urinary Tract Symptom
[description not available]		02.2510
Impotence
[description not available]		02.2510
Sex Disorders
[description not available]		03.620
Dyspareunia
Recurrent genital pain occurring during, before, or after SEXUAL INTERCOURSE in either the male or the female.		02.2510
Erectile Dysfunction
The inability in the male to have a PENILE ERECTION due to psychological or organ dysfunction.		02.2510
Sexual Dysfunction, Physiological
Physiological disturbances in normal sexual performance in either the male or the female.		03.620
Leukocytopenia
[description not available]		011.663921
Leukopenia
A decrease in the number of LEUKOCYTES in a blood sample below the normal range (LEUKOCYTE COUNT less than 4000).		011.663921
Neoplasms, Bronchial
[description not available]		03.1710
Bronchial Neoplasms
Tumors or cancer of the BRONCHI.		03.1710
Hepatic Infarct
[description not available]		03.1710
Necrosis
The death of cells in an organ or tissue due to disease, injury or failure of the blood supply.		09.21104
Adrenocortical Carcinoma
A malignant neoplasm of the ADRENAL CORTEX. Adrenocortical carcinomas are unencapsulated anaplastic (ANAPLASIA) masses sometimes exceeding 20 cm or 200 g. They are more likely to be functional than nonfunctional, and produce ADRENAL CORTEX HORMONES that may result in hypercortisolism (CUSHING SYNDROME); HYPERALDOSTERONISM; and/or VIRILISM.		05.942
Adrenal Cortex Cancer
[description not available]		06.0652
Adrenal Cortex Neoplasms
Tumors or cancers of the ADRENAL CORTEX.		06.0652
Shingles
[description not available]		03.6930
Herpes Zoster
An acute infectious, usually self-limited, disease believed to represent activation of latent varicella-zoster virus (HERPESVIRUS 3, HUMAN) in those who have been rendered partially immune after a previous attack of CHICKENPOX. It involves the SENSORY GANGLIA and their areas of innervation and is characterized by severe neuralgic pain along the distribution of the affected nerve and crops of clustered vesicles over the area. (From Dorland, 27th ed)		03.6930
Ascites
Accumulation or retention of free fluid within the peritoneal cavity.		03.0440
Carcinoma, Lobular
A type of BREAST CANCER where the abnormal malignant cells form in the lobules, or milk-producing glands, of the breast.		08.92188
Hyperglycemia, Postprandial
Abnormally high BLOOD GLUCOSE level after a meal.		04.4340
Coma, Hyperglycemic Hyperosmolar Nonketotic
[description not available]		02.3110
Hyperglycemia
Abnormally high BLOOD GLUCOSE level.		04.4340
Cancer of Digestive System
[description not available]		07.563
Digestive System Neoplasms
Tumors or cancer of the DIGESTIVE SYSTEM.		07.563
Drug-Induced Stevens Johnson Syndrome
[description not available]		03.0340
Stevens-Johnson Syndrome
Rare cutaneous eruption characterized by extensive KERATINOCYTE apoptosis resulting in skin detachment with mucosal involvement. It is often provoked by the use of drugs (e.g., antibiotics and anticonvulsants) or associated with PNEUMONIA, MYCOPLASMA. It is considered a continuum of Toxic Epidermal Necrolysis.		03.0340
Infections, Staphylococcal
[description not available]		02.3110
Staphylococcal Infections
Infections with bacteria of the genus STAPHYLOCOCCUS.		02.3110
Hypomelanosis
[description not available]		02.4110
Hypopigmentation
A condition caused by a deficiency or a loss of melanin pigmentation in the epidermis, also known as hypomelanosis. Hypopigmentation can be localized or generalized, and may result from genetic defects, trauma, inflammation, or infections.		07.4110
Cancer of the Vulva
[description not available]		03.711
Vulvar Neoplasms
Tumors or cancer of the VULVA.		03.711
Amazon Black Fever
[description not available]		02.4110
Hepatitis D
INFLAMMATION of the LIVER in humans caused by HEPATITIS DELTA VIRUS, a defective RNA virus that can only infect HEPATITIS B patients. For its viral coating, hepatitis delta virus requires the HEPATITIS B SURFACE ANTIGENS produced by these patients. Hepatitis D can occur either concomitantly with (coinfection) or subsequent to (superinfection) hepatitis B infection. Similar to hepatitis B, it is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact.		02.4110
Licheniform Eruptions
[description not available]		02.7830
Allergy, Drug
[description not available]		05.8881
Drug Hypersensitivity
Immunologically mediated adverse reactions to medicinal substances used legally or illegally.		05.8881
Cardiovascular Stroke
[description not available]		09.42104
Acute Disease
Disease having a short and relatively severe course.		06.92150
Myocardial Infarction
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).		09.42104
Extramembranous Glomerulopathy
[description not available]		02.1510
Nephrotic Syndrome
A condition characterized by severe PROTEINURIA, greater than 3.5 g/day in an average adult. The substantial loss of protein in the urine results in complications such as HYPOPROTEINEMIA; generalized EDEMA; HYPERTENSION; and HYPERLIPIDEMIAS. Diseases associated with nephrotic syndrome generally cause chronic kidney dysfunction.		02.1510
Glomerulonephritis, Membranous
A type of glomerulonephritis that is characterized by the accumulation of immune deposits (COMPLEMENT MEMBRANE ATTACK COMPLEX) on the outer aspect of the GLOMERULAR BASEMENT MEMBRANE. It progresses from subepithelial dense deposits, to basement membrane reaction and eventual thickening of the basement membrane.		02.1510
Angiogenesis, Pathologic
[description not available]		012.77345
Adenoma, alpha-Cell
[description not available]		02.1510
Icterus
[description not available]		02.5420
Jaundice
A clinical manifestation of HYPERBILIRUBINEMIA, characterized by the yellowish staining of the SKIN; MUCOUS MEMBRANE; and SCLERA. Clinical jaundice usually is a sign of LIVER dysfunction.		07.5420
Cancer of the Thymus
[description not available]		07.1262
Thymus Neoplasms
Tumors or cancer of the THYMUS GLAND.		07.1262
Deep Vein Thrombosis
[description not available]		04.8671
Venous Thrombosis
The formation or presence of a blood clot (THROMBUS) within a vein.		04.8671
Cancer of Mediastinum
[description not available]		02.5220
Paraganglioma, Gangliocytic
[description not available]		02.5120
Mediastinal Neoplasms
Tumors or cancer of the MEDIASTINUM.		02.5220
Paraganglioma
A neural crest tumor usually derived from the chromoreceptor tissue of a paraganglion, such as the carotid body, or medulla of the adrenal gland (usually called a chromaffinoma or pheochromocytoma). It is more common in women than in men. (Stedman, 25th ed; from Segen, Dictionary of Modern Medicine, 1992)		07.5120
Carcinoma, Squamous Cell of Head and Neck
[description not available]		05.9183
Cancer of Head
[description not available]		011.673313
Squamous Cell Carcinoma of Head and Neck
The most common type of head and neck carcinoma that originates from cells on the surface of the NASAL CAVITY; MOUTH; PARANASAL SINUSES, SALIVARY GLANDS, and LARYNX. Mutations in TNFRSF10B, PTEN, and ING1 genes are associated with this cancer.		112.9183
Head and Neck Neoplasms
Soft tissue tumors or cancer arising from the mucosal surfaces of the LIP; oral cavity; PHARYNX; LARYNX; and cervical esophagus. Other sites included are the NOSE and PARANASAL SINUSES; SALIVARY GLANDS; THYROID GLAND and PARATHYROID GLANDS; and MELANOMA and non-melanoma skin cancers of the head and neck. (from Holland et al., Cancer Medicine, 4th ed, p1651)		116.196626
Congenital Familial Lymphedema
[description not available]		03.5311
Lymphedema
Edema due to obstruction of lymph vessels or disorders of the lymph nodes.		03.5311
Blood Pressure, High
[description not available]		08.97104
Hypertension
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.		013.97104
Acute Kidney Failure
[description not available]		03.0140
Acute Kidney Injury
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.		03.0140
Nail Diseases
Diseases of the nail plate and tissues surrounding it. The concept is limited to primates.		06.51101
Cancer Syndromes, Hereditary
[description not available]		04.8721
Alcoholic Liver Diseases
[description not available]		02.1510
Liver Diseases, Alcoholic
Liver diseases associated with ALCOHOLISM. It usually refers to the coexistence of two or more subentities, i.e., ALCOHOLIC FATTY LIVER; ALCOHOLIC HEPATITIS; and ALCOHOLIC CIRRHOSIS.		02.1510
Foot Diseases
Anatomical and functional disorders affecting the foot.		02.5320
Nevi, Melanocytic
[description not available]		02.4620
Nevus, Pigmented
A nevus containing melanin. The term is usually restricted to nevocytic nevi (round or oval collections of melanin-containing nevus cells occurring at the dermoepidermal junction of the skin or in the dermis proper) or moles, but may be applied to other pigmented nevi.		02.4620
Aneurysm, Arteriovenous
[description not available]		02.1510
HPV Infection
[description not available]		04.5530
Actinic Reticuloid Syndrome
[description not available]		04.2360
Keratoacanthoma
A benign, non-neoplastic, usually self-limiting epithelial lesion closely resembling squamous cell carcinoma clinically and histopathologically. It occurs in solitary, multiple, and eruptive forms. The solitary and multiple forms occur on sunlight exposed areas and are identical histologically; they affect primarily white males. The eruptive form usually involves both sexes and appears as a generalized papular eruption.		03.0610
Papillomavirus Infections
Neoplasms of the skin and mucous membranes caused by papillomaviruses. They are usually benign but some have a high risk for malignant progression.		04.5530
Paronychia
An inflammatory reaction involving the folds of the skin surrounding the fingernail. It is characterized by acute or chronic purulent, tender, and painful swellings of the tissues around the nail, caused by an abscess of the nail fold. The pathogenic yeast causing paronychia is most frequently Candida albicans. Saprophytic fungi may also be involved. The causative bacteria are usually Staphylococcus, Pseudomonas aeruginosa, or Streptococcus. (Andrews' Diseases of the Skin, 8th ed, p271)		08.8421
Angiolymphoid Hyperplasia with Eosinophilia
Solitary or multiple benign cutaneous nodules comprised of immature and mature vascular structures intermingled with endothelial cells and a varied infiltrate of eosinophils, histiocytes, lymphocytes, and mast cells.		02.1710
Adiadochokinesis
[description not available]		02.9740
Cerebellar Ataxia
Incoordination of voluntary movements that occur as a manifestation of CEREBELLAR DISEASES. Characteristic features include a tendency for limb movements to overshoot or undershoot a target (dysmetria), a tremor that occurs during attempted movements (intention TREMOR), impaired force and rhythm of diadochokinesis (rapidly alternating movements), and GAIT ATAXIA. (From Adams et al., Principles of Neurology, 6th ed, p90)		07.9740
Remission, Spontaneous
A spontaneous diminution or abatement of a disease over time, without formal treatment.		02.9940
Liver Steatosis
[description not available]		04.1631
Fatty Liver
Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of TRIGLYCERIDES, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of FATTY ACIDS.		09.1631
Abdomen, Acute
A clinical syndrome with acute abdominal pain that is severe, localized, and rapid in onset. Acute abdomen may be caused by a variety of disorders, injuries, or diseases.		02.1710
Acute Edematous Pancreatitis
[description not available]		02.7530
Pancreatitis
INFLAMMATION of the PANCREAS. Pancreatitis is classified as acute unless there are computed tomographic or endoscopic retrograde cholangiopancreatographic findings of CHRONIC PANCREATITIS (International Symposium on Acute Pancreatitis, Atlanta, 1992). The two most common forms of acute pancreatitis are ALCOHOLIC PANCREATITIS and gallstone pancreatitis.		02.7530
Dystonia
An attitude or posture due to the co-contraction of agonists and antagonist muscles in one region of the body. It most often affects the large axial muscles of the trunk and limb girdles. Conditions which feature persistent or recurrent episodes of dystonia as a primary manifestation of disease are referred to as DYSTONIC DISORDERS. (Adams et al., Principles of Neurology, 6th ed, p77)		03.730
Adenocarcinoma Of Kidney
[description not available]		012.623625
Carcinoma, Renal Cell
A heterogeneous group of sporadic or hereditary carcinoma derived from cells of the KIDNEYS. There are several subtypes including the clear cells, the papillary, the chromophobe, the collecting duct, the spindle cells (sarcomatoid), or mixed cell-type carcinoma.		114.623625
Multiple Primary Neoplasms
[description not available]		05.4480
Cardiac Failure
[description not available]		04.0950
Heart Failure
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.		09.0950
Aging
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.		05.0730
Palsy
[description not available]		02.1510
Paralysis
A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45)		02.1510
Christmas Disease
[description not available]		02.1510
Hemophilia B
A deficiency of blood coagulation factor IX inherited as an X-linked disorder. (Also known as Christmas Disease, after the first patient studied in detail, not the holy day.) Historical and clinical features resemble those in classic hemophilia (HEMOPHILIA A), but patients present with fewer symptoms. Severity of bleeding is usually similar in members of a single family. Many patients are asymptomatic until the hemostatic system is stressed by surgery or trauma. Treatment is similar to that for hemophilia A. (From Cecil Textbook of Medicine, 19th ed, p1008)		02.1510
Eosinophilia, Tropical
[description not available]		02.1710
Sycosis
[description not available]		02.1710
Bullous Dermatoses
[description not available]		02.1710
Eosinophilia
Abnormal increase of EOSINOPHILS in the blood, tissues or organs.		02.1710
Folliculitis
Inflammation of follicles, primarily hair follicles.		07.1710
Chemotherapy-Induced Febrile Neutropenia
FEVER accompanied by a significant reduction in NEUTROPHIL count associated with CHEMOTHERAPY.		05.3641
Carcinomatous Meningitis
[description not available]		03.4820
Meningeal Carcinomatosis
Primary or secondary neoplasm in the ARACHNOID or SUBARACHNOID SPACE. It appears as a diffuse fibrotic thickening of the MENINGES associated with variable degrees of inflammation.		03.4820
Common Bile Duct Neoplasms
Tumor or cancer of the COMMON BILE DUCT including the AMPULLA OF VATER and the SPHINCTER OF ODDI.		08.97146
Dermatitis
Any inflammation of the skin.		02.4820
Anastomotic Leak
Breakdown of the connection and subsequent leakage of effluent (fluids, secretions, air) from a SURGICAL ANASTOMOSIS of the digestive, respiratory, genitourinary, and cardiovascular systems. Most common leakages are from the breakdown of suture lines in gastrointestinal or bowel anastomosis.		03.2150
Cardiovascular Diseases
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.		06.5661
Micrometastases, Neoplasm
[description not available]		02.1710
Affective Psychosis, Bipolar
[description not available]		02.1710
Bipolar Disorder
A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence.		02.1710
Acinar Carcinoma
[description not available]		02.4620
Carcinoma, Acinar Cell
A malignant tumor arising from secreting cells of a racemose gland, particularly the salivary glands. Racemose (Latin racemosus, full of clusters) refers, as does acinar (Latin acinus, grape), to small saclike dilatations in various glands. Acinar cell carcinomas are usually well differentiated and account for about 13% of the cancers arising in the parotid gland. Lymph node metastasis occurs in about 16% of cases. Local recurrences and distant metastases many years after treatment are common. This tumor appears in all age groups and is most common in women. (Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1240; from DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p575)		02.4620
Pleuropericarditis
Inflammation of both the PERICARDIUM and the PLEURA.		03.1210
Pericarditis
Inflammation of the PERICARDIUM from various origins, such as infection, neoplasm, autoimmune process, injuries, or drug-induced. Pericarditis usually leads to PERICARDIAL EFFUSION, or CONSTRICTIVE PERICARDITIS.		08.1210
Chromosome Deletion
Actual loss of portion of a chromosome.		06.4931
Drug Overdose
Accidental or deliberate use of a medication or street drug in excess of normal dosage.		03.2350
Liver Dysfunction
[description not available]		05.660
Liver Diseases
Pathological processes of the LIVER.		05.660
Sigmoid Colon Diseases
[description not available]		02.4920
Abscess
Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection.		02.1710
Bleeding
[description not available]		04.5790
Hemorrhage
Bleeding or escape of blood from a vessel.		04.5790
Neoplasms, Sweat Gland
[description not available]		02.7630
Cancer of the Urinary Tract
[description not available]		02.2110
Ache
[description not available]		010.51913
Pain
An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.		010.51913
Vascular Diseases
Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.		03.5911
Dermatoses
[description not available]		09.74114
Skin Diseases
Diseases involving the DERMIS or EPIDERMIS.		09.74114
Adverse Effects, Long Term
[description not available]		02.2110
Obesity
A status with BODY WEIGHT that is grossly above the recommended standards, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).		05.942
Sarcopenia
Progressive decline in muscle mass due to aging which results in decreased functional capacity of muscles.		02.5520
Melena
The black, tarry, foul-smelling FECES that contain degraded blood.		02.1710
Cytomegalic Inclusion Disease
[description not available]		02.2110
Colitis
Inflammation of the COLON section of the large intestine (INTESTINE, LARGE), usually with symptoms such as DIARRHEA (often with blood and mucus), ABDOMINAL PAIN, and FEVER.		03.9240
Cytomegalovirus Infections
Infection with CYTOMEGALOVIRUS, characterized by enlarged cells bearing intranuclear inclusions. Infection may be in almost any organ, but the salivary glands are the most common site in children, as are the lungs in adults.		02.2110
Ulcer
A lesion on the surface of the skin or a mucous surface, produced by the sloughing of inflammatory necrotic tissue.		02.2110
Lacrimal Duct Obstruction
Interference with the secretion of tears by the lacrimal glands. Obstruction of the LACRIMAL SAC or NASOLACRIMAL DUCT causing acute or chronic inflammation of the lacrimal sac (DACRYOCYSTITIS). It is caused also in infants by failure of the nasolacrimal duct to open into the inferior meatus and occurs about the third week of life. In adults occlusion may occur spontaneously or after injury or nasal disease. (Newell, Ophthalmology: Principles and Concepts, 7th ed, p250)		07.5520
Hypermelanosis
[description not available]		03.6590
Hyperpigmentation
Excessive pigmentation of the skin, usually as a result of increased epidermal or dermal melanin pigmentation, hypermelanosis. Hyperpigmentation can be localized or generalized. The condition may arise from exposure to light, chemicals or other substances, or from a primary metabolic imbalance.		03.6590
Kussmaul Aphasia
[description not available]		02.2110
Cerebellar Diseases
Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include dysmetria, GAIT ATAXIA, and MUSCLE HYPOTONIA.		02.5120
Cancer of Spleen
[description not available]		02.8130
Epithelial Ovarian Cancer
[description not available]		03.5911
Carcinoma, Ovarian Epithelial
A malignant neoplasm that originates in cells on the surface EPITHELIUM of the ovary and is the most common form of ovarian cancer. There are five histologic subtypes: papillary serous, endometrioid, mucinous, clear cell, and transitional cell. Mutations in BRCA1, OPCML, PRKN, PIK3CA, AKT1, CTNNB1, RRAS2, and CDH1 genes are associated with this cancer.		03.5911
Neoplasms, Cystic, Mucinous, and Serous
Neoplasms containing cyst-like formations or producing mucin or serum.		03.5911
Chromosome Inversion
An aberration in which a chromosomal segment is deleted and reinserted in the same place but turned 180 degrees from its original orientation, so that the gene sequence for the segment is reversed with respect to that of the rest of the chromosome.		02.2110
Acute Myelogenous Leukemia
[description not available]		02.7830
Leukemia, Myeloid, Acute
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.		02.7830
Deficiency, Vitamin D
[description not available]		03.5911
Vitamin D Deficiency
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)		03.5911
Neoplasms, Otorhinolaryngologic
[description not available]		03.8621
Anogenital Type Verrucous Carcinoma
[description not available]		03.1210
Angiogranuloma
[description not available]		02.9940
Neuropathy, Paraneoplastic
[description not available]		03.420
Cystitis
Inflammation of the URINARY BLADDER, either from bacterial or non-bacterial causes. Cystitis is usually associated with painful urination (dysuria), increased frequency, urgency, and suprapubic pain.		03.9121
Proctitis
INFLAMMATION of the MUCOUS MEMBRANE of the RECTUM, the distal end of the large intestine (INTESTINE, LARGE).		06.0374
Lethargy
A general state of sluggishness, listless, or uninterested, with being tired, and having difficulty concentrating and doing simple tasks. It may be related to DEPRESSION or DRUG ADDICTION.		02.0810
Carcinoma, Thymic
[description not available]		03.3920
Encephalitis, JC Polyomavirus
[description not available]		02.0810
Leukoencephalopathy, Progressive Multifocal
An opportunistic viral infection of the central nervous system associated with conditions that impair cell-mediated immunity (e.g., ACQUIRED IMMUNODEFICIENCY SYNDROME and other IMMUNOLOGIC DEFICIENCY SYNDROMES; HEMATOLOGIC NEOPLASMS; IMMUNOSUPPRESSION; and COLLAGEN DISEASES). The causative organism is JC Polyomavirus (JC VIRUS) which primarily affects oligodendrocytes, resulting in multiple areas of demyelination. Clinical manifestations include DEMENTIA; ATAXIA; visual disturbances; and other focal neurologic deficits, generally progressing to a vegetative state within 6 months. (From Joynt, Clinical Neurology, 1996, Ch26, pp36-7)		02.0810
Thymoma
A neoplasm originating from thymic tissue, usually benign, and frequently encapsulated. Although it is occasionally invasive, metastases are extremely rare. It consists of any type of thymic epithelial cell as well as lymphocytes that are usually abundant. Malignant lymphomas that involve the thymus, e.g., lymphosarcoma, Hodgkin's disease (previously termed granulomatous thymoma), should not be regarded as thymoma. (From Stedman, 25th ed)		08.3920
Blood Poisoning
[description not available]		02.1110
Asystole
[description not available]		03.3560
Heart Arrest
Cessation of heart beat or MYOCARDIAL CONTRACTION. If it is treated within a few minutes, heart arrest can be reversed in most cases to normal cardiac rhythm and effective circulation.		03.3560
Sepsis
Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.		02.1110
Brain Stem Neoplasms, Primary
[description not available]		03.4711
Glial Cell Tumors
[description not available]		04.4122
Glioma
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)		17.5444
Brain Stem Neoplasms
Benign and malignant intra-axial tumors of the MESENCEPHALON; PONS; or MEDULLA OBLONGATA of the BRAIN STEM. Primary and metastatic neoplasms may occur in this location. Clinical features include ATAXIA, cranial neuropathies (see CRANIAL NERVE DISEASES), NAUSEA, hemiparesis (see HEMIPLEGIA), and quadriparesis. Primary brain stem neoplasms are more frequent in children. Histologic subtypes include GLIOMA; HEMANGIOBLASTOMA; GANGLIOGLIOMA; and EPENDYMOMA.		03.4711
Thromboembolism, Venous
[description not available]		02.7730
Embolism, Pulmonary
[description not available]		05.0731
Pulmonary Embolism
Blocking of the PULMONARY ARTERY or one of its branches by an EMBOLUS.		05.0731
Venous Thromboembolism
Obstruction of a vein or VEINS (embolism) by a blood clot (THROMBUS) in the blood stream.		02.7730
Dyslipidemia
[description not available]		02.4720
Dyslipidemias
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.		02.4720
Acute Promyelocytic Leukemia
[description not available]		07.830
Leukemia, Promyelocytic, Acute
An acute myeloid leukemia in which abnormal PROMYELOCYTES predominate. It is frequently associated with DISSEMINATED INTRAVASCULAR COAGULATION.		02.830
Fasciitis, Necrotizing
A fulminating bacterial infection of the deep layers of the skin and FASCIA. It can be caused by many different organisms, with STREPTOCOCCUS PYOGENES being the most common.		02.0810
Atypical Ductal Hyperplasia
[description not available]		04.1631
Carcinoma, Intraductal, Noninfiltrating
A noninvasive (noninfiltrating) carcinoma of the breast characterized by a proliferation of malignant epithelial cells confined to the mammary ducts or lobules, without light-microscopy evidence of invasion through the basement membrane into the surrounding stroma.		04.1631
Experimental Mammary Neoplasms
[description not available]		04.260
Idiopathic Parkinson Disease
[description not available]		02.0810
Congenital Stiff-Man Syndrome
[description not available]		02.0810
Parkinson Disease
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)		02.0810
Stiff-Person Syndrome
A condition characterized by persistent spasms (SPASM) involving multiple muscles, primarily in the lower limbs and trunk. The illness tends to occur in the fourth to sixth decade of life, presenting with intermittent spasms that become continuous. Minor sensory stimuli, such as noise and light touch, precipitate severe spasms. Spasms do not occur during sleep and only rarely involve cranial muscles. Respiration may become impaired in advanced cases. (Adams et al., Principles of Neurology, 6th ed, p1492; Neurology 1998 Jul;51(1):85-93)		02.0810
Chronic Pancreatitis
[description not available]		07.0810
MODS
[description not available]		02.0810
Multiple Organ Failure
A progressive condition usually characterized by combined failure of several organs such as the lungs, liver, kidney, along with some clotting mechanisms, usually postinjury or postoperative.		02.0810
Pancreatitis, Chronic
INFLAMMATION of the PANCREAS that is characterized by recurring or persistent ABDOMINAL PAIN with or without STEATORRHEA or DIABETES MELLITUS. It is characterized by the irregular destruction of the pancreatic parenchyma which may be focal, segmental, or diffuse.		02.0810
B16 Melanoma
[description not available]		07.0810
Infection, Postoperative Wound
[description not available]		02.4920
Autosomal Chromosome Disorders
[description not available]		0310
Cirrhosis
[description not available]		02.7730
Cholangiitis, Sclerosing
[description not available]		02.110
Fibrosis
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.		07.7730
Cholangitis, Sclerosing
Chronic inflammatory disease of the BILIARY TRACT. It is characterized by fibrosis and hardening of the intrahepatic and extrahepatic biliary ductal systems leading to bile duct strictures, CHOLESTASIS, and eventual BILIARY CIRRHOSIS.		02.110
Articulation Disorders
Disorders of the quality of speech characterized by the substitution, omission, distortion, and addition of phonemes.		02.1110
Capillary Leak Syndrome
A condition characterized by recurring episodes of fluid leaking from capillaries into extra-vascular compartments causing hematocrit to rise precipitously. If not treated, generalized vascular leak can lead to generalized EDEMA; SHOCK; cardiovascular collapse; and MULTIPLE ORGAN FAILURE.		02.110
Bilirubinemia
[description not available]		06.6473
Adrenocorticotropic Hormone, Inappropriate Secretion
[description not available]		02.110
ACTH-Producing Pituitary Adenoma
[description not available]		02.4820
Pituitary ACTH Hypersecretion
A disease of the PITUITARY GLAND characterized by the excess amount of ADRENOCORTICOTROPIC HORMONE secreted. This leads to hypersecretion of cortisol (HYDROCORTISONE) by the ADRENAL GLANDS resulting in CUSHING SYNDROME.		02.110
Complication, Intraoperative
[description not available]		04.821
Shock, Cardiogenic
Shock resulting from diminution of cardiac output in heart disease.		03.3820
Cognition Disorders
Disorders characterized by disturbances in mental processes related to learning, thinking, reasoning, and judgment.		03.4811
Depression
Depressive states usually of moderate intensity in contrast with MAJOR DEPRESSIVE DISORDER present in neurotic and psychotic disorders.		03.4811
Acquired Metabolic Diseases, Brain
[description not available]		02.0810
Primary Peritonitis
[description not available]		02.0810
Peritonitis
INFLAMMATION of the PERITONEUM lining the ABDOMINAL CAVITY as the result of infectious, autoimmune, or chemical processes. Primary peritonitis is due to infection of the PERITONEAL CAVITY via hematogenous or lymphatic spread and without intra-abdominal source. Secondary peritonitis arises from the ABDOMINAL CAVITY itself through RUPTURE or ABSCESS of intra-abdominal organs.		02.0810
Intestinal Perforation
Opening or penetration through the wall of the INTESTINES.		04.3770
Abscess, Abdominal
[description not available]		02.830
Abdominal Abscess
An abscess located in the abdominal cavity, i.e., the cavity between the diaphragm above and the pelvis below. (From Dorland, 27th ed)		02.830
Cancer of Endocrine Gland
[description not available]		06.1132
Endocrine Gland Neoplasms
Tumors or cancer of the ENDOCRINE GLANDS.		06.1132
Autoimmune Thrombocytopenia
[description not available]		02.4720
Purpura, Thrombocytopenic, Idiopathic
Thrombocytopenia occurring in the absence of toxic exposure or a disease associated with decreased platelets. It is mediated by immune mechanisms, in most cases IMMUNOGLOBULIN G autoantibodies which attach to platelets and subsequently undergo destruction by macrophages. The disease is seen in acute (affecting children) and chronic (adult) forms.		02.4720
Deficiency, Folic Acid
[description not available]		03.0310
Folic Acid Deficiency
A nutritional condition produced by a deficiency of FOLIC ACID in the diet. Many plant and animal tissues contain folic acid, abundant in green leafy vegetables, yeast, liver, and mushrooms but destroyed by long-term cooking. Alcohol interferes with its intermediate metabolism and absorption. Folic acid deficiency may develop in long-term anticonvulsant therapy or with use of oral contraceptives. This deficiency causes anemia, macrocytic anemia, and megaloblastic anemia. It is indistinguishable from vitamin B 12 deficiency in peripheral blood and bone marrow findings, but the neurologic lesions seen in B 12 deficiency do not occur. (Merck Manual, 16th ed)		03.0310
Brain Swelling
[description not available]		03.3820
Brain Edema
Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)		03.3820
Thromboembolism
Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.		09.78106
Asymptomatic Conditions
[description not available]		02.110
Colonic Diseases
Pathological processes in the COLON region of the large intestine (INTESTINE, LARGE).		03.730
Cholecystoduodenal Fistula
[description not available]		02.110
Urinary Bladder Fistula
An abnormal passage in the URINARY BLADDER or between the bladder and any surrounding organ.		02.4820
Ductal Carcinoma
[description not available]		06.4182
Carcinoma, Ductal
Malignant neoplasms involving the ductal systems of any of a number of organs, such as the MAMMARY GLANDS, the PANCREAS, the PROSTATE, or the LACRIMAL GLAND.		06.4182
Symptom Cluster
[description not available]		014.234415
Syndrome
A characteristic symptom complex.		014.234415
Oculopharyngeal Dystrophy
[description not available]		02.110
Chronic Idiopathic Intestinal Pseudo-Obstruction
[description not available]		02.110
External Ophthalmoplegia
[description not available]		02.110
Encephalomyopathies, Mitochondrial
[description not available]		02.110
Intestinal Pseudo-Obstruction
A type of ILEUS, a functional not mechanical obstruction of the INTESTINES. This syndrome is caused by a large number of disorders involving the smooth muscles (MUSCLE, SMOOTH) or the NERVOUS SYSTEM.		02.110
Muscular Dystrophy, Oculopharyngeal
An autosomal dominant hereditary disease that presents in late in life and is characterized by DYSPHAGIA and progressive ptosis of the eyelids. Mutations in the gene for POLY(A)-BINDING PROTEIN II have been associated with oculopharyngeal muscular dystrophy.		02.110
Coagulation, Disseminated Intravascular
[description not available]		03.0110
Disseminated Intravascular Coagulation
A disorder characterized by procoagulant substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders. A majority of the patients manifest skin lesions, sometimes leading to PURPURA FULMINANS.		03.0110
Malignant Fibrohistiocytic Tumors
[description not available]		02.110
Histiocytoma, Malignant Fibrous
The most commonly diagnosed soft tissue sarcoma. It is a neoplasm with a fibrohistiocytic appearance found chiefly in later adult life, with peak incidence in the 7th decade.		02.110
Dehiscence, Surgical Wound
[description not available]		05.0531
Viral Diseases
[description not available]		02.110
Virus Diseases
A general term for diseases caused by viruses.		02.110
Cancer of Prostate
[description not available]		08.591710
Cancer of Endometrium
[description not available]		03.8921
Prostatic Neoplasms
Tumors or cancer of the PROSTATE.		08.591710
Endometrial Neoplasms
Tumors or cancer of ENDOMETRIUM, the mucous lining of the UTERUS. These neoplasms can be benign or malignant. Their classification and grading are based on the various cell types and the percent of undifferentiated cells.		03.8921
Pulmonary Arterial Remodeling
[description not available]		02.110
Choriocarcinoma
A malignant metastatic form of trophoblastic tumors. Unlike the HYDATIDIFORM MOLE, choriocarcinoma contains no CHORIONIC VILLI but rather sheets of undifferentiated cytotrophoblasts and syncytiotrophoblasts (TROPHOBLASTS). It is characterized by the large amounts of CHORIONIC GONADOTROPIN produced. Tissue origins can be determined by DNA analyses: placental (fetal) origin or non-placental origin (CHORIOCARCINOMA, NON-GESTATIONAL).		03.3820
Cryptogenic Fibrosing Alveolitis
[description not available]		02.1110
Idiopathic Pulmonary Fibrosis
A common interstitial lung disease of unknown etiology, usually occurring between 50-70 years of age. Clinically, it is characterized by an insidious onset of breathlessness with exertion and a nonproductive cough, leading to progressive DYSPNEA. Pathological features show scant interstitial inflammation, patchy collagen fibrosis, prominent fibroblast proliferation foci, and microscopic honeycomb change.		02.1110
Gasser Syndrome
[description not available]		03.3920
Hemolytic-Uremic Syndrome
A syndrome that is associated with microvascular diseases of the KIDNEY, such as RENAL CORTICAL NECROSIS. It is characterized by hemolytic anemia (ANEMIA, HEMOLYTIC); THROMBOCYTOPENIA; and ACUTE RENAL FAILURE.		03.3920
Coronary Thrombosis
Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.		03.6630
Intussusception
A form of intestinal obstruction caused by the PROLAPSE of a part of the intestine into the adjoining intestinal lumen. There are four types: colic, involving segments of the LARGE INTESTINE; enteric, involving only the SMALL INTESTINE; ileocecal, in which the ILEOCECAL VALVE prolapses into the CECUM, drawing the ILEUM along with it; and ileocolic, in which the ileum prolapses through the ileocecal valve into the COLON.		03.4320
Dysesthesia
[description not available]		012.46285
Erythroderma, Sezary
[description not available]		03.0110
Leukemia, Lymphocytic, Chronic, T Cell
[description not available]		03.0110
Sezary Syndrome
A form of cutaneous T-cell lymphoma manifested by generalized exfoliative ERYTHRODERMA; PRURITUS; peripheral lymphadenopathy, and abnormal hyperchromatic mononuclear (cerebriform) cells in the skin, LYMPH NODES, and peripheral blood (Sezary cells).		03.0110
Leukemia, Prolymphocytic, T-Cell
A lymphoid leukemia characterized by a profound LYMPHOCYTOSIS with or without LYMPHADENOPATHY, hepatosplenomegaly, frequently rapid progression, and short survival. It was formerly called T-cell chronic lymphocytic leukemia.		03.0110
Epithelial Neoplasms
[description not available]		04.4222
Abnormalities, Autosome
[description not available]		02.110
Weight Reduction
[description not available]		010.45381
Weight Loss
Decrease in existing BODY WEIGHT.		010.45381
Gastritis
Inflammation of the GASTRIC MUCOSA, a lesion observed in a number of unrelated disorders.		02.4620
Deafness, Transitory
[description not available]		03.4811
Hearing Loss
A general term for the complete or partial loss of the ability to hear from one or both ears.		03.4811
Amaurosis
[description not available]		02.110
Blindness
The inability to see or the loss or absence of perception of visual stimuli. This condition may be the result of EYE DISEASES; OPTIC NERVE DISEASES; OPTIC CHIASM diseases; or BRAIN DISEASES affecting the VISUAL PATHWAYS or OCCIPITAL LOBE.		02.110
Lung Adenocarcinoma
[description not available]		04.4111
Adenocarcinoma of Lung
A carcinoma originating in the lung and the most common lung cancer type in never-smokers. Malignant cells exhibit distinct features such as glandular epithelial, or tubular morphology. Mutations in KRAS, EGFR, BRAF, and ERBB2 genes are associated with this cancer.		04.4111
Delayed Hypersensitivity
[description not available]		04.441
Carcinoma, Adenosquamous
A mixed adenocarcinoma and squamous cell or epidermoid carcinoma.		04.7821
Ileus
A condition caused by the lack of intestinal PERISTALSIS or INTESTINAL MOTILITY without any mechanical obstruction. This interference of the flow of INTESTINAL CONTENTS often leads to INTESTINAL OBSTRUCTION. Ileus may be classified into postoperative, inflammatory, metabolic, neurogenic, and drug-induced.		03.250
Adrenal Cancer
[description not available]		05.6261
Hepatitis
INFLAMMATION of the LIVER.		02.110
Thoracic Neoplasms
New abnormal growth of tissue in the THORAX.		05.8442
Pelvic Pain
Pain in the pelvic region of genital and non-genital origin.		02.1510
Ventricular Fibrillation
A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in HEART VENTRICLES. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (SYNCOPE). It is one of the major electrocardiographic patterns seen with CARDIAC ARREST.		03.0240
Cancer of Pelvis
[description not available]		03.511
Adenocarcinoma, Clear Cell
An adenocarcinoma characterized by the presence of varying combinations of clear and hobnail-shaped tumor cells. There are three predominant patterns described as tubulocystic, solid, and papillary. These tumors, usually located in the female reproductive organs, have been seen more frequently in young women since 1970 as a result of the association with intrauterine exposure to diethylstilbestrol. (From Holland et al., Cancer Medicine, 3d ed)		03.511
Cystadenocarcinoma, Serous
A malignant cystic or semicystic neoplasm. It often occurs in the ovary and usually bilaterally. The external surface is usually covered with papillary excrescences. Microscopically, the papillary patterns are predominantly epithelial overgrowths with differentiated and undifferentiated papillary serous cystadenocarcinoma cells. Psammoma bodies may be present. The tumor generally adheres to surrounding structures and produces ascites. (From Hughes, Obstetric-Gynecologic Terminology, 1972, p185)		03.511
Carcinoma, Small Cell Lung
[description not available]		02.1310
Acneiform Eruptions
Visible efflorescent lesions of the skin caused by acne or resembling acne. (Dorland, 28th ed, p18, 575)		02.1310
Small Cell Lung Carcinoma
A form of highly malignant lung cancer that is composed of small ovoid cells (SMALL CELL CARCINOMA).		02.1310
Frigidity
[description not available]		03.511
Sexual Dysfunctions, Psychological
Disturbances in sexual desire and the psychophysiologic changes that characterize the sexual response cycle and cause marked distress and interpersonal difficulty. (APA, DSM-IV, 1994)		03.511
Carcinoma, Oat Cell
[description not available]		02.1110
Carcinoma, Small Cell
An anaplastic, highly malignant, and usually bronchogenic carcinoma composed of small ovoid cells with scanty neoplasm. It is characterized by a dominant, deeply basophilic nucleus, and absent or indistinct nucleoli. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1286-7)		02.1110
Curling Ulcer
Acute stress DUODENAL ULCER, usually observed in patients with extensive third-degree burns.		02.1310
Duodenal Ulcer
A PEPTIC ULCER located in the DUODENUM.		02.1310
Adenoma, Villous
An adenoma of the large intestine. It is usually a solitary, sessile, often large, tumor of colonic mucosa composed of mucinous epithelium covering delicate vascular projections. Hypersecretion and malignant changes occur frequently. (Stedman, 25th ed)		02.4820
Blood Loss, Surgical
Loss of blood during a surgical procedure.		02.7930
Sarcoma, Epithelioid
[description not available]		02.7430
Sarcoma
A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant.		07.7430
Alcohol Problem
[description not available]		02.1310
Experimental Lung Inflammation
Inflammation of any part, segment or lobe, of the lung parenchyma.		04.1331
Alcohol Drinking
Behaviors associated with the ingesting of ALCOHOLIC BEVERAGES, including social drinking.		02.1310
Pneumonia
Infection of the lung often accompanied by inflammation.		04.1331
Alcohol-Related Disorders
Disorders related to or resulting from abuse or misuse of alcohol.		02.1310
Neoplasm Metastasis, Unknown Primary
[description not available]		07.3155
Allodynia
[description not available]		02.1110
Erythermalgia
[description not available]		02.1110
Erythromelalgia
A peripheral arterial disease that is characterized by the triad of ERYTHEMA, burning PAIN, and increased SKIN TEMPERATURE of the extremities (or red, painful extremities). Erythromelalgia may be classified as primary or idiopathic, familial or non-familial. Secondary erythromelalgia is associated with other diseases, the most common being MYELOPROLIFERATIVE DISORDERS.		02.1110
C gattii Infection
[description not available]		02.1110
Cerebral Cryptococcosis
[description not available]		02.1110
Cryptococcosis
Fungal infection caused by genus CRYPTOCOCCUS.		02.1110
Meningitis, Cryptococcal
Meningeal inflammation produced by CRYPTOCOCCUS NEOFORMANS, an encapsulated yeast that tends to infect individuals with ACQUIRED IMMUNODEFICIENCY SYNDROME and other immunocompromised states. The organism enters the body through the respiratory tract, but symptomatic infections are usually limited to the lungs and nervous system. The organism may also produce parenchymal brain lesions (torulomas). Clinically, the course is subacute and may feature HEADACHE; NAUSEA; PHOTOPHOBIA; focal neurologic deficits; SEIZURES; cranial neuropathies; and HYDROCEPHALUS. (From Adams et al., Principles of Neurology, 6th ed, pp721-2)		02.1110
Carcinoma, Papillary
A malignant neoplasm characterized by the formation of numerous, irregular, finger-like projections of fibrous stroma that is covered with a surface layer of neoplastic epithelial cells. (Stedman, 25th ed)		06.3751
Cachexia
General ill health, malnutrition, and weight loss, usually associated with chronic disease.		09.1431
Alopecia Cicatrisata
[description not available]		016.225955
Alopecia
Absence of hair from areas where it is normally present.		016.225955
Appetite Disorders
[description not available]		03.511
Feeding and Eating Disorders
A group of disorders characterized by physiological and psychological disturbances in appetite or food intake.		03.511
Hypercalciuria
Excretion of abnormally high level of CALCIUM in the URINE, greater than 4 mg/kg/day.		02.520
Kidney Tubular Transport, Inborn Error
[description not available]		02.520
Nephrocalcinosis
A condition characterized by calcification of the renal tissue itself. It is usually seen in distal RENAL TUBULAR ACIDOSIS with calcium deposition in the DISTAL KIDNEY TUBULES and the surrounding interstitium. Nephrocalcinosis causes RENAL INSUFFICIENCY.		02.520
Chronic Illness
[description not available]		02.1310
Complications of Diabetes Mellitus
[description not available]		02.1310
Chronic Disease
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care (Dictionary of Health Services Management, 2d ed). For epidemiological studies chronic disease often includes HEART DISEASES; STROKE; CANCER; and diabetes (DIABETES MELLITUS, TYPE 2).		02.1310
Chronic Kidney Failure
[description not available]		02.4920
Kidney Failure, Chronic
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.		02.4920
Cancer of the Uterus
[description not available]		03.0310
Uterine Neoplasms
Tumors or cancer of the UTERUS.		03.0310
Infection
[description not available]		03.5111
Infections
Invasion of the host organism by microorganisms or their toxins or by parasites that can cause pathological conditions or diseases.		03.5111
Cancer of Larynx
[description not available]		02.1310
Cancer of Pharynx
[description not available]		02.1310
Laryngeal Neoplasms
Cancers or tumors of the LARYNX or any of its parts: the GLOTTIS; EPIGLOTTIS; LARYNGEAL CARTILAGES; LARYNGEAL MUSCLES; and VOCAL CORDS.		02.1310
Pharyngeal Neoplasms
Tumors or cancer of the PHARYNX.		02.1310
Agnogenic Myeloid Metaplasia
[description not available]		02.1310
Pancytopenia
Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets.		02.5420
Primary Myelofibrosis
A de novo myeloproliferation arising from an abnormal stem cell. It is characterized by the replacement of bone marrow by fibrous tissue, a process that is mediated by CYTOKINES arising from the abnormal clone.		02.1310
Bone Marrow Diseases
Diseases involving the BONE MARROW.		03.420
Benign Meningeal Neoplasms
[description not available]		06.13111
Meningeal Neoplasms
Benign and malignant neoplastic processes that arise from or secondarily involve the meningeal coverings of the brain and spinal cord.		06.13111
Yolk Sac Tumor
[description not available]		02.1510
Endodermal Sinus Tumor
An unusual and aggressive tumor of germ-cell origin that reproduces the extraembryonic structures of the early embryo. It is the most common malignant germ cell tumor found in children. It is characterized by a labyrinthine glandular pattern of flat epithelial cells and rounded papillary processes with a central capillary (Schiller-Duval body). The tumor is rarely bilateral. Before the use of combination chemotherapy, the tumor was almost invariably fatal. (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1189)		02.1510
Pregnancy
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.		02.9840
Dysmyelopoietic Syndromes
[description not available]		03.0410
Myelodysplastic Syndromes
Clonal hematopoietic stem cell disorders characterized by dysplasia in one or more hematopoietic cell lineages. They predominantly affect patients over 60, are considered preleukemic conditions, and have high probability of transformation into ACUTE MYELOID LEUKEMIA.		03.0410
Abnormalities, Drug-Induced
Congenital abnormalities caused by medicinal substances or drugs of abuse given to or taken by the mother, or to which she is inadvertently exposed during the manufacture of such substances. The concept excludes abnormalities resulting from exposure to non-medicinal chemicals in the environment.		02.1310
Asthenia
Clinical sign or symptom manifested as debility, or lack or loss of strength and energy.		06.0565
Genetic Skin Diseases
[description not available]		02.5520
Skin Ulcer
An ULCER of the skin and underlying tissues.		04.0950
Choroid Neoplasms
Tumors of the choroid; most common intraocular tumors are malignant melanomas of the choroid. These usually occur after puberty and increase in incidence with advancing age. Most malignant melanomas of the uveal tract develop from benign melanomas (nevi).		02.4720
Cardiac Arrest, Sudden
[description not available]		02.1510
Death, Sudden, Cardiac
Unexpected rapid natural death due to cardiovascular collapse within one hour of initial symptoms. It is usually caused by the worsening of existing heart diseases. The sudden onset of symptoms, such as CHEST PAIN and CARDIAC ARRHYTHMIAS, particularly VENTRICULAR TACHYCARDIA, can lead to the loss of consciousness and cardiac arrest followed by biological death. (from Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., 2005)		02.1510
Genital Diseases, Male
Pathological processes involving the male reproductive tract (GENITALIA, MALE).		02.520
Penile Diseases
Pathological processes involving the PENIS or its component tissues.		02.1510
Granulocytic Leukemia, Chronic
[description not available]		02.4820
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.		02.4820
Gastric Diseases
[description not available]		03.0610
Esophageal Fistula
Abnormal passage communicating with the ESOPHAGUS. The most common type is TRACHEOESOPHAGEAL FISTULA between the esophagus and the TRACHEA.		02.1310
Aortic Diseases
Pathological processes involving any part of the AORTA.		02.1310
Sister Joseph's Nodule
[description not available]		02.4920
Inguinal Hernia
[description not available]		02.4820
Hernia, Inguinal
An abdominal hernia with an external bulge in the GROIN region. It can be classified by the location of herniation. Indirect inguinal hernias occur through the internal inguinal ring. Direct inguinal hernias occur through defects in the ABDOMINAL WALL (transversalis fascia) in Hesselbach's triangle. The former type is commonly seen in children and young adults; the latter in adults.		02.4820
Pancreatic Fistula
Abnormal passage communicating with the PANCREAS.		02.1510
Postpartum Amenorrhea
[description not available]		03.8521
Amenorrhea
Absence of menstruation.		03.8521
Pyrexia
[description not available]		06.0765
Fever
An abnormal elevation of body temperature, usually as a result of a pathologic process.		06.0765
Canine Diseases
[description not available]		02.4420
Atypical Lipomatous Tumor
[description not available]		02.0410
Liposarcoma
A malignant tumor derived from primitive or embryonal lipoblastic cells. It may be composed of well-differentiated fat cells or may be dedifferentiated: myxoid (LIPOSARCOMA, MYXOID), round-celled, or pleomorphic, usually in association with a rich network of capillaries. Recurrences are common and dedifferentiated liposarcomas metastasize to the lungs or serosal surfaces. (From Dorland, 27th ed; Stedman, 25th ed)		02.0410
Body Weight
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.		08.3475
Neoplasms, Pleural
[description not available]		05.9151
Animal Mammary Carcinoma
[description not available]		02.9610
Agranulocytosis
A decrease in the number of GRANULOCYTES; (BASOPHILS; EOSINOPHILS; and NEUTROPHILS).		04.1331
Granuloma, Hodgkin
[description not available]		02.0510
Hodgkin Disease
A malignant disease characterized by progressive enlargement of the lymph nodes, spleen, and general lymphoid tissue. In the classical variant, giant usually multinucleate Hodgkin's and REED-STERNBERG CELLS are present; in the nodular lymphocyte predominant variant, lymphocytic and histiocytic cells are seen.		02.0510
Carcinoma, Large Cell
A tumor of undifferentiated (anaplastic) cells of large size. It is usually bronchogenic. (From Dorland, 27th ed)		03.8321
Cardiomyopathy, Congestive
[description not available]		03.8221
Incompetence, Pulmonary Valve
[description not available]		02.0510
Cardiomyopathy, Dilated
A form of CARDIAC MUSCLE disease that is characterized by ventricular dilation, VENTRICULAR DYSFUNCTION, and HEART FAILURE. Risk factors include SMOKING; ALCOHOL DRINKING; HYPERTENSION; INFECTION; PREGNANCY; and mutations in the LMNA gene encoding LAMIN TYPE A, a NUCLEAR LAMINA protein.		03.8221
Muscle Disorders
[description not available]		04.9140
Muscular Diseases
Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.		04.9140
Brachial Paresis
[description not available]		02.0510
Onycholysis
Separation of nail plate from the underlying nail bed. It can be a sign of skin disease, infection (such as ONYCHOMYCOSIS) or tissue injury.		03.3720
Ptosis, Eyelid
[description not available]		02.4620
Day Blindness
[description not available]		02.4620
Blepharoptosis
Drooping of the upper lid due to deficient development or paralysis of the levator palpebrae muscle.		02.4620
Overweight
A status with BODY WEIGHT that is above certain standards. In the scale of BODY MASS INDEX, overweight is defined as having a BMI of 25.0-29.9 kg/m2. Overweight may or may not be due to increases in body fat (ADIPOSE TISSUE), hence overweight does not equal over fat.		02.9610
Autoimmune Diabetes
[description not available]		02.9610
Infections, Helicobacter
[description not available]		02.9610
Diabetes Mellitus, Type 1
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.		02.9610
Helicobacter Infections
Infections with organisms of the genus HELICOBACTER, particularly, in humans, HELICOBACTER PYLORI. The clinical manifestations are focused in the stomach, usually the gastric mucosa and antrum, and the upper duodenum. This infection plays a major role in the pathogenesis of type B gastritis and peptic ulcer disease.		02.9610
Soft Tissue Neoplasms
Neoplasms of whatever cell type or origin, occurring in the extraskeletal connective tissue framework of the body including the organs of locomotion and their various component structures, such as nerves, blood vessels, lymphatics, etc.		010.451412
Facial Dermatoses
Skin diseases involving the FACE.		02.7330
Microglossia
[description not available]		02.0510
Incontinentia Pigmenti Achromians
[description not available]		02.4520
HIV Coinfection
[description not available]		02.7430
HIV Infections
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).		02.7430
Congenital Thrombotic Thrombocytopenic Purpura
[description not available]		02.9710
Purpura, Thrombotic Thrombocytopenic
An acquired, congenital, or familial disorder caused by PLATELET AGGREGATION with THROMBOSIS in terminal arterioles and capillaries. Clinical features include THROMBOCYTOPENIA; HEMOLYTIC ANEMIA; AZOTEMIA; FEVER; and thrombotic microangiopathy. The classical form also includes neurological symptoms and end-organ damage, such as RENAL FAILURE. Mutations in the ADAMTS13 PROTEIN gene have been identified in familial cases.		02.9710
Genome Instability
[description not available]		03.3820
Adult Fanconi Syndrome
[description not available]		02.0510
Angor Pectoris
[description not available]		03.2860
Atrioventricular Nodal Re-Entrant Tachycardia
[description not available]		02.0510
Angina Pectoris
The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.		03.2860
Tachycardia, Ventricular
An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).		02.0510
Bleb
[description not available]		02.4420
Hematoma, Subdural, Cranial
[description not available]		02.0510
Hematoma, Subdural, Intracranial
Accumulation of blood in the SUBDURAL SPACE over the CEREBRAL HEMISPHERE.		02.0510
Menopause
The last menstrual period. Permanent cessation of menses (MENSTRUATION) is usually defined after 6 to 12 months of AMENORRHEA in a woman over 45 years of age. In the United States, menopause generally occurs in women between 48 and 55 years of age.		02.9610
Condition, Preneoplastic
[description not available]		02.4620
Precancerous Conditions
Pathological conditions that tend eventually to become malignant.		02.4620
Adenocarcinoma, Scirrhous
An adenocarcinoma with a hard (Greek skirrhos, hard) structure owing to the formation of dense connective tissue in the stroma. (From Dorland, 27th ed)		04.0650
Gangrene
Death and putrefaction of tissue usually due to a loss of blood supply.		03.4411
Carcinoma, Intraepithelial
[description not available]		04.1231
Carcinoma in Situ
A lesion with cytological characteristics associated with invasive carcinoma but the tumor cells are confined to the epithelium of origin, without invasion of the basement membrane.		04.1231
Aneurysm, Aortic
[description not available]		02.0510
Aortic Aneurysm
An abnormal balloon- or sac-like dilatation in the wall of AORTA.		02.0510
HbS Disease
[description not available]		02.0510
Anemia, Sickle Cell
A disease characterized by chronic hemolytic anemia, episodic painful crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S.		02.0510
Cramp
[description not available]		02.0510
Muscle Cramp
A sustained and usually painful contraction of muscle fibers. This may occur as an isolated phenomenon or as a manifestation of an underlying disease process (e.g., UREMIA; HYPOTHYROIDISM; MOTOR NEURON DISEASE; etc.). (From Adams et al., Principles of Neurology, 6th ed, p1398)		02.0510
Anemia, Hypoplastic
[description not available]		02.9710
Tooth Discoloration
Any change in the hue, color, or translucency of a tooth due to any cause. Restorative filling materials, drugs (both topical and systemic), pulpal necrosis, or hemorrhage may be responsible. (Jablonski, Dictionary of Dentistry, 1992, p253)		02.9710
Anemia, Aplastic
A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.		02.9710
Mesothelioma
A tumor derived from mesothelial tissue (peritoneum, pleura, pericardium). It appears as broad sheets of cells, with some regions containing spindle-shaped, sarcoma-like cells and other regions showing adenomatous patterns. Pleural mesotheliomas have been linked to exposure to asbestos. (Dorland, 27th ed)		16.7421
Anaphylactic Reaction
[description not available]		02.4620
Anaphylaxis
An acute hypersensitivity reaction due to exposure to a previously encountered ANTIGEN. The reaction may include rapidly progressing URTICARIA, respiratory distress, vascular collapse, systemic SHOCK, and death.		02.4620
Dysphagia
[description not available]		02.7630
Breathlessness
[description not available]		06.3751
Breathing Sounds
[description not available]		02.0510
Hoarseness
An unnaturally deep or rough quality of voice.		02.0510
Deglutition Disorders
Difficulty in SWALLOWING which may result from neuromuscular disorder or mechanical obstruction. Dysphagia is classified into two distinct types: oropharyngeal dysphagia due to malfunction of the PHARYNX and UPPER ESOPHAGEAL SPHINCTER; and esophageal dysphagia due to malfunction of the ESOPHAGUS.		02.7630
Dyspnea
Difficult or labored breathing.		06.3751
Respiratory Sounds
Noises, normal and abnormal, heard on auscultation over any part of the RESPIRATORY TRACT.		02.0510
Rectovaginal Fistula
An abnormal anatomical passage between the RECTUM and the VAGINA.		02.0510
Anal Fistula
[description not available]		02.0510
Atrophy
Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.		02.4620
Airflow Obstruction, Chronic
[description not available]		02.0510
Arteriosclerosis, Coronary
[description not available]		02.0510
Arthritis, Degenerative
[description not available]		02.0510
Carotid Artery Narrowing
[description not available]		02.0510
Coronary Artery Disease
Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.		02.0510
Osteoarthritis
A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans.		02.0510
Carotid Stenosis
Narrowing or stricture of any part of the CAROTID ARTERIES, most often due to atherosclerotic plaque formation. Ulcerations may form in atherosclerotic plaques and induce THROMBUS formation. Platelet or cholesterol emboli may arise from stenotic carotid lesions and induce a TRANSIENT ISCHEMIC ATTACK; CEREBROVASCULAR ACCIDENT; or temporary blindness (AMAUROSIS FUGAX). (From Adams et al., Principles of Neurology, 6th ed, pp 822-3)		02.0510
Pulmonary Disease, Chronic Obstructive
A disease of chronic diffuse irreversible airflow obstruction. Subcategories of COPD include CHRONIC BRONCHITIS and PULMONARY EMPHYSEMA.		14.0510
Acidosis, Renal Tubular, Type I
[description not available]		02.9710
Acidosis, Renal Tubular
A group of genetic disorders of the KIDNEY TUBULES characterized by the accumulation of metabolically produced acids with elevated plasma chloride, hyperchloremic metabolic ACIDOSIS. Defective renal acidification of URINE (proximal tubules) or low renal acid excretion (distal tubules) can lead to complications such as HYPOKALEMIA, hypercalcinuria with NEPHROLITHIASIS and NEPHROCALCINOSIS, and RICKETS.		02.9710
Age-Related Osteoporosis
[description not available]		02.0610
Hangman Fracture
[description not available]		02.0610
Osteoporosis
Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis (OSTEOPOROSIS, POSTMENOPAUSAL) and age-related or senile osteoporosis.		02.0610
Spinal Fractures
Broken bones in the vertebral column.		02.0610
Sensation Disorders
Disorders of the special senses (i.e., VISION; HEARING; TASTE; and SMELL) or somatosensory system (i.e., afferent components of the PERIPHERAL NERVOUS SYSTEM).		03.8521
Adenoma, Pleomorphic
A benign, slow-growing tumor, most commonly of the salivary gland, occurring as a small, painless, firm nodule, usually of the parotid gland, but also found in any major or accessory salivary gland anywhere in the oral cavity. It is most often seen in women in the fifth decade. Histologically, the tumor presents a variety of cells: cuboidal, columnar, and squamous cells, showing all forms of epithelial growth. (Dorland, 27th ed)		02.0510
Cancer of Salivary Gland
[description not available]		02.0510
Salivary Gland Neoplasms
Tumors or cancer of the SALIVARY GLANDS.		02.0510
Blood Pressure, Low
[description not available]		03.4411
Hypotension
Abnormally low BLOOD PRESSURE that can result in inadequate blood flow to the brain and other vital organs. Common symptom is DIZZINESS but greater negative impacts on the body occur when there is prolonged depravation of oxygen and nutrients.		03.4411
Angina at Rest
[description not available]		02.4420
Angina, Unstable
Precordial pain at rest, which may precede a MYOCARDIAL INFARCTION.		02.4420
Abdominal Aortic Aneurysm
[description not available]		02.0510
Aortic Aneurysm, Abdominal
An abnormal balloon- or sac-like dilatation in the wall of the ABDOMINAL AORTA which gives rise to the visceral, the parietal, and the terminal (iliac) branches below the aortic hiatus at the diaphragm.		02.0510
Extrasystole, Ventricular
[description not available]		02.0610
Abdominal Cramps
[description not available]		02.0610
Elevated Cholesterol
[description not available]		02.0610
Hypercholesterolemia
A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.		02.0610
BOOP
[description not available]		02.0510
Glioblastoma with Sarcomatous Component
[description not available]		02.0610
Gliosarcoma
Rare mixed tumors of the brain and rarely the spinal cord which contain malignant neuroectodermal (glial) and mesenchymal components, including spindle-shaped fibrosarcoma cells. These tumors are highly aggressive and present primarily in adults as rapidly expanding mass lesions. They may arise in tissue that has been previously irradiated. (From Br J Neurosurg 1995 Apr;9(2):171-8)		02.0610
Chronic Insomnia
[description not available]		04.3611
Sleep Initiation and Maintenance Disorders
Disorders characterized by impairment of the ability to initiate or maintain sleep. This may occur as a primary disorder or in association with another medical or psychiatric condition.		04.3611
Chromosomal Instability
An increased tendency to acquire CHROMOSOME ABERRATIONS when various processes involved in chromosome replication, repair, or segregation are dysfunctional.		02.9710
Islet Cell Tumor, Malignant
[description not available]		06.3590
Carcinoma, Islet Cell
A primary malignant neoplasm of the pancreatic ISLET CELLS. Usually it involves the non-INSULIN-producing cell types, the PANCREATIC ALPHA CELLS and the pancreatic delta cells (SOMATOSTATIN-SECRETING CELLS) in GLUCAGONOMA and SOMATOSTATINOMA, respectively.		18.3590
Neoplasms, Squamous Cell
Neoplasms of the SQUAMOUS EPITHELIAL CELLS. The concept does not refer to neoplasms located in tissue composed of squamous elements.		04.1531
Colitis, Ischemic
Inflammation of the COLON due to colonic ISCHEMIA resulting from alterations in systemic circulation or local vasculature.		02.0610
Rupture, Spontaneous
Tear or break of an organ, vessel or other soft part of the body, occurring in the absence of external force.		02.0510
Scalp Dermatoses
Skin diseases involving the SCALP.		02.0610
Allergic Alveolitis, Extrinsic
[description not available]		02.0610
Alveolitis, Fibrosing
[description not available]		03.3820
Alveolitis, Extrinsic Allergic
A common interstitial lung disease caused by hypersensitivity reactions of PULMONARY ALVEOLI after inhalation of and sensitization to environmental antigens of microbial, animal, or chemical sources. The disease is characterized by lymphocytic alveolitis and granulomatous pneumonitis.		02.0610
Pulmonary Fibrosis
A process in which normal lung tissues are progressively replaced by FIBROBLASTS and COLLAGEN causing an irreversible loss of the ability to transfer oxygen into the bloodstream via PULMONARY ALVEOLI. Patients show progressive DYSPNEA finally resulting in death.		03.3820
Fifth Phacomatosis
[description not available]		02.0610
Basal Cell Nevus Syndrome
Hereditary disorder consisting of multiple basal cell carcinomas, odontogenic keratocysts, and multiple skeletal defects, e.g., frontal and temporoparietal bossing, bifurcated and splayed ribs, kyphoscoliosis, fusion of vertebrae, and cervicothoracic spina bifida. Genetic transmission is autosomal dominant.		02.0610
Lymphangitis
A lymphatic disease characterized by INFLAMMATION of LYMPHATIC VESSELS.		02.0610
Pleurisy
INFLAMMATION of PLEURA, the lining of the LUNG. When PARIETAL PLEURA is involved, there is pleuritic CHEST PAIN.		02.0610
Branch Vein Occlusion
[description not available]		02.0710
Retinal Vein Occlusion
Blockage of the RETINAL VEIN. Those at high risk for this condition include patients with HYPERTENSION; DIABETES MELLITUS; ATHEROSCLEROSIS; and other CARDIOVASCULAR DISEASES.		02.0710
Aura
[description not available]		02.7430
Epilepsy
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)		02.7430
Neuritis
A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include PAIN; PARESTHESIAS; PARESIS; or HYPESTHESIA.		03.4511
Diffuse Large B-Cell Lymphoma
[description not available]		02.0610
Lymphoma, Large B-Cell, Diffuse
Malignant lymphoma composed of large B lymphoid cells whose nuclear size can exceed normal macrophage nuclei, or more than twice the size of a normal lymphocyte. The pattern is predominantly diffuse. Most of these lymphomas represent the malignant counterpart of B-lymphocytes at midstage in the process of differentiation.		02.0610
Acute Coronary Syndrome
An episode of MYOCARDIAL ISCHEMIA that generally lasts longer than a transient anginal episode that ultimately may lead to MYOCARDIAL INFARCTION.		02.4620
Gastrointestinal Stromal Neoplasm
[description not available]		02.0610
Gastrointestinal Stromal Tumors
All tumors in the GASTROINTESTINAL TRACT arising from mesenchymal cells (MESODERM) except those of smooth muscle cells (LEIOMYOMA) or Schwann cells (SCHWANNOMA).		02.0610
Neoplasms, Vascular
[description not available]		03.8321
Haim-Monk Syndrome
[description not available]		03.4511
Acrospiroma
A rare cutaneous tumor of apocrine or eccrine SWEAT GLAND origin. It is most commonly found on the extremities and is usually benign. It appears as a solitary nodule or cyst and may be solid or produce a watery discharge. It is related to POROMA except in acrospiroma it does not involve the epidermis. There is no indication that heredity or external agents cause these tumors.		02.0610
Hyponatremia
Deficiency of sodium in the blood; salt depletion. (Dorland, 27th ed)		03.4611
Cancer of the Tongue
[description not available]		02.0610
Tongue Neoplasms
Tumors or cancer of the TONGUE.		02.0610
Acquired Autoimmune Hemolytic Anemia
[description not available]		03.6630
Anemia, Hemolytic, Autoimmune
Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.		03.6630
Electrocardiogram QT Prolonged
[description not available]		02.0610
Long QT Syndrome
A condition that is characterized by episodes of fainting (SYNCOPE) and varying degree of ventricular arrhythmia as indicated by the prolonged QT interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are ROMANO-WARD SYNDROME and JERVELL-LANGE NIELSEN SYNDROME.		02.0610
Abnormal Karyotype
A variation from the normal set of chromosomes characteristic of a species.		02.0710
Chromosomal Translocation
[description not available]		02.0710
Dehydration
The condition that results from excessive loss of water from a living organism.		02.0710
Death, Sudden
The abrupt cessation of all vital bodily functions, manifested by the permanent loss of total cerebral, respiratory, and cardiovascular functions.		02.0710
Infections, Pseudomonas
[description not available]		03.8910
Microbial Superinvasion
[description not available]		03.8910
Pseudomonas Infections
Infections with bacteria of the genus PSEUDOMONAS.		03.8910
Bacteremia
The presence of viable bacteria circulating in the blood. Fever, chills, tachycardia, and tachypnea are common acute manifestations of bacteremia. The majority of cases are seen in already hospitalized patients, most of whom have underlying diseases or procedures which render their bloodstreams susceptible to invasion.		04.2920
Bradyarrhythmia
[description not available]		02.9910
Bradycardia
Cardiac arrhythmias that are characterized by excessively slow HEART RATE, usually below 50 beats per minute in human adults. They can be classified broadly into SINOATRIAL NODE dysfunction and ATRIOVENTRICULAR BLOCK.		02.9910
Fibrosis, Radiation
[description not available]		03.4511
Esophagitis
INFLAMMATION, acute or chronic, of the ESOPHAGUS caused by BACTERIA, chemicals, or TRAUMA.		03.4511
Radiation Pneumonitis
Inflammation of the lung due to harmful effects of ionizing or non-ionizing radiation.		03.4511
Retroperitoneal Neoplasms
New abnormal growth of tissue in the RETROPERITONEAL SPACE.		02.0710
Orbital Neoplasms
Neoplasms of the bony orbit and contents except the eyeball.		02.4420
Kahler Disease
[description not available]		02.0710
Multiple Myeloma
A malignancy of mature PLASMA CELLS engaging in monoclonal immunoglobulin production. It is characterized by hyperglobulinemia, excess Bence-Jones proteins (free monoclonal IMMUNOGLOBULIN LIGHT CHAINS) in the urine, skeletal destruction, bone pain, and fractures. Other features include ANEMIA; HYPERCALCEMIA; and RENAL INSUFFICIENCY.		02.0710
Amyotonia Congenita
[description not available]		02.0710
Neuromuscular Diseases
A general term encompassing lower MOTOR NEURON DISEASE; PERIPHERAL NERVOUS SYSTEM DISEASES; and certain MUSCULAR DISEASES. Manifestations include MUSCLE WEAKNESS; FASCICULATION; muscle ATROPHY; SPASM; MYOKYMIA; MUSCLE HYPERTONIA, myalgias, and MUSCLE HYPOTONIA.		02.0710
Esophageal Perforation
An opening or hole in the ESOPHAGUS that is caused by TRAUMA, injury, or pathological process.		02.0710
Prosthesis Durability
[description not available]		02.0710
Muscle Contraction
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.		02.0710
Auricular Fibrillation
[description not available]		02.0710
Atrial Fibrillation
Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.		02.0710
Aqueductal Stenosis
[description not available]		02.0710
Osteogenic Sarcoma
[description not available]		02.0710
Osteosarcoma
A sarcoma originating in bone-forming cells, affecting the ends of long bones. It is the most common and most malignant of sarcomas of the bones, and occurs chiefly among 10- to 25-year-old youths. (From Stedman, 25th ed)		02.0710
Addison's Disease
[description not available]		0310
Addison Disease
An adrenal disease characterized by the progressive destruction of the ADRENAL CORTEX, resulting in insufficient production of ALDOSTERONE and HYDROCORTISONE. Clinical symptoms include ANOREXIA; NAUSEA; WEIGHT LOSS; MUSCLE WEAKNESS; and HYPERPIGMENTATION of the SKIN due to increase in circulating levels of ACTH precursor hormone which stimulates MELANOCYTES.		0310
Anoxemia
[description not available]		03.3520
Hypoxia
Sub-optimal OXYGEN levels in the ambient air of living organisms.		08.3520
Muscle Spasm
[description not available]		02.0710
Spasm
An involuntary contraction of a muscle or group of muscles. Spasms may involve SKELETAL MUSCLE or SMOOTH MUSCLE.		02.0710
Female Genital Neoplasms
[description not available]		02.0710
Genital Neoplasms, Female
Tumor or cancer of the female reproductive tract (GENITALIA, FEMALE).		02.0710
Cancer, Radiation-Induced
[description not available]		02.0710
Acute Necrotizing Pancreatitis
[description not available]		02.0710
Multiple Endocrine Neoplasia Type 1
A form of multiple endocrine neoplasia that is characterized by the combined occurrence of tumors in the PARATHYROID GLANDS, the PITUITARY GLAND, and the PANCREATIC ISLETS. The resulting clinical signs include HYPERPARATHYROIDISM; HYPERCALCEMIA; HYPERPROLACTINEMIA; CUSHING DISEASE; GASTRINOMA; and ZOLLINGER-ELLISON SYNDROME. This disease is due to loss-of-function of the MEN1 gene, a tumor suppressor gene (GENES, TUMOR SUPPRESSOR) on CHROMOSOME 11 (Locus: 11q13).		0310
MEA 2a
[description not available]		0310
Anemia, Hemolytic, Acquired
[description not available]		02.4620
Anemia, Hemolytic
A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).		02.4620
Hydronephrosis
Abnormal enlargement or swelling of a KIDNEY due to dilation of the KIDNEY CALICES and the KIDNEY PELVIS. It is often associated with obstruction of the URETER or chronic kidney diseases that prevents normal drainage of urine into the URINARY BLADDER.		07.9910
Necrolytic Migratory Erythema
Recurrent cutaneous manifestation of GLUCAGONOMA characterized by necrolytic polycyclic migratory lesions with scaling borders. It is associated with elevated secretion of GLUCAGON by the tumor. Other conditions with elevated serum glucagon levels such as HEPATIC CIRRHOSIS may also result in similar skin lesions, which are referred to as pseudoglucagonoma syndrome.		02.0810
Freckle, Melanotic
[description not available]		02.0110
Hand Foot and Mouth Disease
[description not available]		03.411
Hand, Foot and Mouth Disease
A mild, highly infectious viral disease of children, characterized by vesicular lesions in the mouth and on the hands and feet. It is caused by coxsackieviruses A.		03.411
Carcinoma, Verrucous
A variant of well-differentiated epidermoid carcinoma that is most common in the oral cavity, but also occurs in the larynx, nasal cavity, esophagus, penis, anorectal region, vulva, vagina, uterine cervix, and skin, especially on the sole of the foot. Most intraoral cases occur in elderly male abusers of smokeless tobacco. The treatment is surgical resection. Radiotherapy is not indicated, as up to 30% treated with radiation become highly aggressive within six months. (Segen, Dictionary of Modern Medicine, 1992)		02.0110
Convulsive Generalized Seizure Disorder
[description not available]		02.0110
Ataxia of Gait
[description not available]		02.0110
Bewilderment
[description not available]		02.0110
Aprosodia
[description not available]		02.0110
Lock Jaw
[description not available]		02.0110
Experimental Hepatoma
[description not available]		02.0110
Pachymeningitis
[description not available]		02.0110
Meningitis
Inflammation of the coverings of the brain and/or spinal cord, which consist of the PIA MATER; ARACHNOID; and DURA MATER. Infections (viral, bacterial, and fungal) are the most common causes of this condition, but subarachnoid hemorrhage (HEMORRHAGES, SUBARACHNOID), chemical irritation (chemical MENINGITIS), granulomatous conditions, neoplastic conditions (CARCINOMATOUS MENINGITIS), and other inflammatory conditions may produce this syndrome. (From Joynt, Clinical Neurology, 1994, Ch24, p6)		07.0110
Weight Gain
Increase in BODY WEIGHT over existing weight.		03.411
Keratoderma Blennorrhagicum
[description not available]		03.1250
Keratosis
Any horny growth such as a wart or callus.		08.1250
Tumour Lysis Syndrome
[description not available]		02.4320
Tumor Lysis Syndrome
A syndrome resulting from cytotoxic therapy, occurring generally in aggressive, rapidly proliferating lymphoproliferative disorders. It is characterized by combinations of hyperuricemia, lactic acidosis, hyperkalemia, hyperphosphatemia and hypocalcemia.		02.4320
Abdominal Neoplasms
New abnormal growth of tissue in the ABDOMEN.		04.6732
Cancer of the Fallopian Tube
[description not available]		03.411
Fallopian Tube Neoplasms
Benign or malignant neoplasms of the FALLOPIAN TUBES. They are uncommon. If they develop, they may be located in the wall or within the lumen as a growth attached to the wall by a stalk.		16.3722
Thyroid Diseases
Pathological processes involving the THYROID GLAND.		02.0210
Hepatic Failure
[description not available]		02.4320
Liver Failure
Severe inability of the LIVER to perform its normal metabolic functions, as evidenced by severe JAUNDICE and abnormal serum levels of AMMONIA; BILIRUBIN; ALKALINE PHOSPHATASE; ASPARTATE AMINOTRANSFERASE; LACTATE DEHYDROGENASES; and albumin/globulin ratio. (Blakiston's Gould Medical Dictionary, 4th ed)		02.4320
Polyneuropathy, Acquired
[description not available]		02.0210
Polyneuropathies
Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.		02.0210
Lymphatic Diseases
Diseases of LYMPH; LYMPH NODES; or LYMPHATIC VESSELS.		02.0210
Eyelid Neoplasms
Tumors of cancer of the EYELIDS.		02.0210
Cold Fingers, Hereditary
[description not available]		02.0210
Raynaud Disease
An idiopathic vascular disorder characterized by bilateral Raynaud phenomenon, the abrupt onset of digital paleness or CYANOSIS in response to cold exposure or stress.		02.0210
Bile Duct Obstruction, Extrahepatic
[description not available]		03.4111
Bile Duct Obstruction, Intrahepatic
[description not available]		03.4111
Cholestasis, Intrahepatic
Impairment of bile flow due to injury to the HEPATOCYTES; BILE CANALICULI; or the intrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC).		03.4111
Carditis
[description not available]		02.9310
Myocarditis
Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.		02.9310
Coronary Artery Stenosis
[description not available]		03.4111
Coronary Stenosis
Narrowing or constriction of a coronary artery.		03.4111
Extravascular Hemolysis
[description not available]		03.4111
Hemolysis
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.		03.4111
Back Ache
[description not available]		02.0110
Back Pain
Acute or chronic pain located in the posterior regions of the THORAX; LUMBOSACRAL REGION; or the adjacent regions.		02.0110
Myelopathy
[description not available]		07.0210
Spinal Cord Diseases
Pathologic conditions which feature SPINAL CORD damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord.		02.0210
Chronic Hepatitis B
[description not available]		03.4111
Hepatitis B, Chronic
INFLAMMATION of the LIVER in humans caused by HEPATITIS B VIRUS lasting six months or more. It is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact.		03.4111
Central Nervous System Disease
[description not available]		02.0310
Coma
A profound state of unconsciousness associated with depressed cerebral activity from which the individual cannot be aroused. Coma generally occurs when there is dysfunction or injury involving both cerebral hemispheres or the brain stem RETICULAR FORMATION.		07.0310
Central Nervous System Diseases
Diseases of any component of the brain (including the cerebral hemispheres, diencephalon, brain stem, and cerebellum) or the spinal cord.		02.0310
Anemia, Hypochromic
Anemia characterized by a decrease in the ratio of the weight of hemoglobin to the volume of the erythrocyte, i.e., the mean corpuscular hemoglobin concentration is less than normal. The individual cells contain less hemoglobin than they could have under optimal conditions. Hypochromic anemia may be caused by iron deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. It can also be caused by infections or other diseases, therapeutic drugs, lead poisoning, and other conditions. (Stedman, 25th ed; from Miale, Laboratory Medicine: Hematology, 6th ed, p393)		02.0210
Atherogenesis
[description not available]		02.0310
Atherosclerosis
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.		02.0310
Hemorrhage, Peptic Ulcer
[description not available]		04.3311
Coagulation Disorders, Blood
[description not available]		02.0310
Blood Coagulation Disorders
Hemorrhagic and thrombotic disorders that occur as a consequence of abnormalities in blood coagulation due to a variety of factors such as COAGULATION PROTEIN DISORDERS; BLOOD PLATELET DISORDERS; BLOOD PROTEIN DISORDERS or nutritional conditions.		02.0310
Cardiac Cancer
[description not available]		02.0310
Cardiac Tamponade
Compression of the heart by accumulated fluid (PERICARDIAL EFFUSION) or blood (HEMOPERICARDIUM) in the PERICARDIUM surrounding the heart. The affected cardiac functions and CARDIAC OUTPUT can range from minimal to total hemodynamic collapse.		02.0310
Coronary Heart Disease
[description not available]		02.0310
Coronary Disease
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.		02.0310
Constitutional Liver Dysfunction
[description not available]		02.0310
Esophageal Diseases
Pathological processes in the ESOPHAGUS.		03.8610
Dermatosclerosis
[description not available]		02.7330
Scleroderma, Localized
A term used to describe a variety of localized asymmetrical SKIN thickening that is similar to those of SYSTEMIC SCLERODERMA but without the disease features in the multiple internal organs and BLOOD VESSELS. Lesions may be characterized as patches or plaques (morphea), bands (linear), or nodules.		02.7330
Aseptic Necrosis of Femur Head
[description not available]		02.0310
Milk-Alkali Syndrome
[description not available]		02.0310
Hypercalcemia
Abnormally high level of calcium in the blood.		02.0310
Foot Injuries
General or unspecified injuries involving the foot.		03.8610
Hand Injuries
General or unspecified injuries to the hand.		03.8610
Deficiency Diseases
A condition produced by dietary or metabolic deficiency. The term includes all diseases caused by an insufficient supply of essential nutrients, i.e., protein (or amino acids), vitamins, and minerals. It also includes an inadequacy of calories. (From Dorland, 27th ed; Stedman, 25th ed)		02.0310
Adenoma, Sweat Gland
A benign neoplasm derived from epithelial cells of sweat glands. (Stedman, 25th ed)		02.0310
Facial Neoplasms
New abnormal growth of tissue in the FACE.		02.0310
Adhesions, Tissue
[description not available]		02.0310
Cancer, Embryonal
[description not available]		03.4211
Neoplasms, Germ Cell and Embryonal
Neoplasms composed of primordial GERM CELLS of embryonic GONADS or of elements of the germ layers of the EMBRYO, MAMMALIAN. The concept does not refer to neoplasms located in the gonads or present in an embryo or FETUS.		03.4211
Cancer of Parotid
[description not available]		02.0310
Parotid Neoplasms
Tumors or cancer of the PAROTID GLAND.		02.0310
Neoplasms, Trophoblastic
[description not available]		02.0310
Granulocytic Leukemia
[description not available]		02.0310
Leukemia, Myeloid
Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.		02.0310
Bilateral Headache
[description not available]		02.0310
Headache
The symptom of PAIN in the cranial region. It may be an isolated benign occurrence or manifestation of a wide variety of HEADACHE DISORDERS.		07.0310
Island Cell Tumor
[description not available]		02.0310
Adenoma, Islet Cell
A benign tumor of the pancreatic ISLET CELLS. Usually it involves the INSULIN-producing PANCREATIC BETA CELLS, as in INSULINOMA, resulting in HYPERINSULINISM.		02.0310
Carcinoma, Medullary
A carcinoma composed mainly of epithelial elements with little or no stroma. Medullary carcinomas of the breast constitute 5%-7% of all mammary carcinomas; medullary carcinomas of the thyroid comprise 3%-10% of all thyroid malignancies. (From Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1141; Segen, Dictionary of Modern Medicine, 1992)		02.4420
Apoplexy
[description not available]		02.0410
Acute Onset Vascular Dementia
[description not available]		02.0410
Dementia, Vascular
An imprecise term referring to dementia associated with CEREBROVASCULAR DISORDERS, including CEREBRAL INFARCTION (single or multiple), and conditions associated with chronic BRAIN ISCHEMIA. Diffuse, cortical, and subcortical subtypes have been described. (From Gerontol Geriatr 1998 Feb;31(1):36-44)		02.0410
Stroke
A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)		02.0410
Iris Neoplasms
Tumors of the iris characterized by increased pigmentation of melanocytes. Iris nevi are composed of proliferated melanocytes and are associated with neurofibromatosis and malignant melanoma of the choroid and ciliary body. Malignant melanoma of the iris often originates from preexisting nevi.		02.0310
Glaucoma
An ocular disease, occurring in many forms, having as its primary characteristics an unstable or a sustained increase in the intraocular pressure which the eye cannot withstand without damage to its structure or impairment of its function. The consequences of the increased pressure may be manifested in a variety of symptoms, depending upon type and severity, such as excavation of the optic disk, hardness of the eyeball, corneal anesthesia, reduced visual acuity, seeing of colored halos around lights, disturbed dark adaptation, visual field defects, and headaches. (Dictionary of Visual Science, 4th ed)		02.0310
Corneal Diseases
Diseases of the cornea.		02.4220
Ataxia
Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharynx, larynx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or PERIPHERAL NERVE DISEASES. Motor ataxia may be associated with CEREBELLAR DISEASES; CEREBRAL CORTEX diseases; THALAMIC DISEASES; BASAL GANGLIA DISEASES; injury to the RED NUCLEUS; and other conditions.		02.9610
Sarcoma, Small Cell
A sarcoma characterized by the presence of small cells, cells measuring 9-14 micrometers with a faint or indistinct rim of cytoplasm and an oval-to-elongated nucleus with relatively dense chromatin. (From Segen, Dictionary of Modern Medicine, 1992)		02.9610
Vitiligo
A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.		02.4220
Endotoxin Shock
[description not available]		04.3411
Shock, Septic
Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.		04.3411
Cold Panniculitis
[description not available]		02.0410
Enlarged Liver
[description not available]		02.0410
Liver Abscess, Pyogenic
Single or multiple areas of PUS due to bacterial infection within the hepatic parenchyma. It can be caused by a variety of BACTERIA, local or disseminated from infections elsewhere such as in APPENDICITIS; CHOLECYSTITIS; PERITONITIS; and after LIVER TRANSPLANTATION.		02.0410
Bacteroides Infections
Infections with bacteria of the genus BACTEROIDES.		02.0410
Lupus Erythematosus, Chronic Cutaneous
[description not available]		02.0410
Lupus Erythematosus, Discoid
A chronic form of cutaneous lupus erythematosus (LUPUS ERYTHEMATOSUS, CUTANEOUS) in which the skin lesions mimic those of the systemic form but in which systemic signs are rare. It is characterized by the presence of discoid skin plaques showing varying degrees of edema, erythema, scaliness, follicular plugging, and skin atrophy. Lesions are surrounded by an elevated erythematous border. The condition typically involves the face and scalp, but widespread dissemination may occur.		02.0410
Anasarca
[description not available]		03.4211
Edema
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.		03.4211
Complications, Neoplastic Pregnancy
[description not available]		02.0410
Ph 1 Chromosome
[description not available]		02.0410
Keratoconjunctivitis Sicca
Drying and inflammation of the conjunctiva as a result of insufficient lacrimal secretion. When found in association with XEROSTOMIA and polyarthritis, it is called SJOGREN'S SYNDROME.		0210
Keratitis
Inflammation of the cornea.		0210
Nail Abnormalities
[description not available]		0210
Hyperkeratosis Palmaris et Plantaris
[description not available]		04.3111
Acquired Neuromyotonia
[description not available]		02.9210
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