Compounds > temozolomide
Page last updated: 2024-11-04

temozolomide

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Cross-References

ID SourceID
PubMed CID5394
CHEMBL ID810
CHEBI ID72564
SCHEMBL ID3739
MeSH IDM0136562

Synonyms (149)

Synonym
AC-758
BIDD:GT0204
3-methyl-4-oxo-3,4-dihydro-imidazo[5,1-d][1,2,3,5]tetrazine-8-carboxylic acid amide(temozolomide)
3-methyl-4-oxo-3,4-dihydro-imidazo[5,1-d][1,2,3,5]tetrazine-8-carboxylic acid amide
bdbm50034562
AKOS005557098
HMS3269P05
HMS3393O12
AB00639915-08
AB00639915-09
temozolomide [usan:inn:ban]
temozolodida
yf1k15m17y ,
temozolomidum
unii-yf1k15m17y
3-methyl-4-oxo-imidazo[5,1-d][1,2,3,5]tetrazine-8-carboxamide
3-methyl-4-oxo-3,4-dihydroimidazo[5,1-d][1,2,3,5]tetraazine-8-carboxamide
{imidazo[5,1-d]-1,2,3,5-tetrazine-8-carboxamide,} 3, 4-dihydro-3-methyl-4-oxo-
NCI60_003316
sch-52365
mls002701861 ,
nsc362856
temozolomide ,
nsc-362856
temodar (tn) (schering)
85622-93-1
imidazo[5,2,3,5-tetrazine-8-carboxamide, 3,4-dihydro-3-methyl-4-oxo-
methazolastone
temozolomidum [latin]
ccrg 81045
temodal
mb 39831
imidazo(5,1-d)(1,2,3,5)tetrazine-8-carboxamide, 3,4-dihydro-3-methyl-4-oxo-
m&b 39831
3,4-dihydro-3-methyl-4-oxoimidazo(5,1-d)-as-tetrazine-8-carboxamide
temozolodida [spanish]
nsc 362856
3-methyl-4-oxo-3,4-dihydroimidazo(5,1-d)(1,2,3,5)tetrazine-8-carboxamide
c6h6n6o2
sch 52365
brn 5547136
ccrg-81045
m&b-39831
m & b 39831
temodar
ccris 8996
8-carbamoyl-3-methylimidazo(5,1-d)-1,2,3,5-tetrazin-4(3h)-one
3,4-dihydro-3-methyl-4-oxoimidazo(5,1-d)-1,2,3,5-tetrazine-8-carboxamide
temozolomide (jan/usan/inn)
D06067
temodar (tn)
temodal (tn)
MLS001424028
tmz ,
temozolamide
smr000466338
MLS000759447
DB00853
NCGC00167429-02
NCGC00167429-01
3-methyl-4-oxo-3,4-dihydroimidazo[5,1-d][1,2,3,5]tetrazine-8-carboxamide ,
HMS2090B08
HMS2051O12
CHEMBL810 ,
mk-7365
chebi:72564 ,
m-39831
3-methyl-4-oxoimidazo[5,1-d][1,2,3,5]tetrazine-8-carboxamide
STK623541
3-methyl-4-oxo-8-imidazo[5,1-d][1,2,3,5]tetrazinecarboxamide
A841386
3-methyl-4-oxidanylidene-imidazo[5,1-d][1,2,3,5]tetrazine-8-carboxamide
HMS3264I14
4-methyl-5-oxo-2,3,4,6,8-pentazabicyclo[4.3.0]nona-2,7,9-triene-9-carboxamide
cas-85622-93-1
tox21_112433
dtxsid5043714 ,
dtxcid3023714
3,4-dihydro-3-methyl-4-oxoimidazo[5,1-d][1,2,3,5]tetrazine-8-carboxamide
T2744
nsc-759883
pharmakon1600-01502289
nsc759883
temozolomida
HMS2232N13
CCG-100870
HY-17364
FT-0674845
BCP0726000154
FT-0630936
NCGC00167429-05
AM20110227
CS-0943
S1237
3-methyl-4-oxo-3h,4h-imidazo[4,3-d][1,2,3,5]tetrazine-8-carboxamide
gtpl7301
HMS3372K13
temozolomide [ema epar]
temozolomide [usp-rs]
temozolomide [usp monograph]
temozolomide [mart.]
temozolomide [ep monograph]
temozolomide [mi]
temozolomide [who-dd]
temozolomide [inn]
temozolomide [jan]
3,4-dihydro-3-methyl-4-oxoimidazo[5,1-d]-as-tetrazine-8-carboxamide
temozolomide [orange book]
temozolomide [vandf]
temozolomide [usan]
DL-190
AB00639915-06
BPEGJWRSRHCHSN-UHFFFAOYSA-N
3-methyl-4-oxo-3,4-dihydro-imidazo[5,1-d][1,2,3,5]tetrazine-8-carboxylic acid amide (temozolomide)
3-methyl-8-aminocarbonyl-imidazo[5,1-d]-1,2,3,5-tetrazin-4(3h)-one
NC00120
SCHEMBL3739
tox21_112433_1
NCGC00167429-04
KS-1216
Q-201786
3,4-dihydro-3-methyl-4-oxoimidazo[5,1-d]-1,2,3,5-tetrazine-8-carboxamide
AB00639915_11
AB00639915_10
8-carbamoyl-3-methylimidazo[5,1-d]-1,2,3,5-tetrazin-4(3h)-one
mfcd00866492
SR-01000759347-5
sr-01000759347
SR-01000759347-4
temozolomide, united states pharmacopeia (usp) reference standard
temozolomide, vetranal(tm), analytical standard
HMS3654N05
temozolomide, >=98% (hplc)
temozolomide, pharmaceutical secondary standard; certified reference material
HMS3713H16
3-methyl-4-oxo-3,4-dihydroimidazo-[5,1-d][1,2,3,5]tetrazine-8-carboxamide
SW197500-4
BCP03692
3-methyl-4-oxo-3,4-dihydroimidazo[5,1-d][1,2,3,5]tetrazine-8-carboxamide.
HMS3677D06
HMS3413D06
Q425088
BRD-K32107296-001-04-5
EN300-122324
temozolomide 100 microg/ml in acetonitrile
BP-25388
BT164447
temozolomide- bio-x
Z1201620684

Research Excerpts

Overview

Temozolomide (TMZ) is a chemotherapeutic agent that is used in the treatment of glioblastoma and other malignant gliomas. The occurrence of drug resistance limits its antitumor activity.

ExcerptReferenceRelevance
"Temozolomide is a chemotherapeutic agent that is used in the treatment of glioblastoma and other malignant gliomas. "( Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
Banerjee, M; Bernales, S; Chakravarty, S; Dixit, V; Guerrero, J; Gupta, A; Hung, DT; Jangir, R; McCullagh, E; Melkani, P; Middya, S; Olivares, F; Patil, U; Pham, SM; Protter, AA; Rai, R; Raja, M; Riquelme, E; Shrivastava, R; Surya, A; Tripathi, S; Wong, DH; Yadav, S, 2016)		3.32
"Temozolomide (TMZ) is a first-line chemotherapeutic agent used in GBM therapy, but the occurrence of drug resistance limits its antitumor activity."( Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
Chang, JT; Chang, KF; Hsiao, CY; Huang, XF; Huang, YC; Lo, WS; Tsai, NM, 2020)		1.51
"Temozolomide is an oral alkylating agent incorporated in the treatment of glioblastoma multiforme (GBM) that can lead to lymphopenia. "( Temozolomide is a risk factor for invasive pulmonary aspergillosis: A case report and literature review.
Brault, C; Chouaki, T; Maizel, J; Nyga, R; Zerbib, Y, 2021)		3.51
"Temozolomide (TMZ) is a recommended treatment option, but its effects are difficult to predict, and the alternatives are limited."( 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)		1.82
"Temozolomide is an alkylating agent most commonly used with a few other second line options."( Nanomedicine in the treatment of Glioblastoma.
Bukhari, SS; Kishwar Jafri, SK; Shamim, MS, 2021)		1.34
"Temozolomide (TMZ) is a prodrug of 5-(3-methyltriazene-1-yl)imidazole-4-carboxamide (MTIC, short-lived) and used as a first-line therapy drug for glioblastoma multiforme (GBM). "( Visible Light and Glutathione Dually Responsive Delivery of a Polymer-Conjugated Temozolomide Intermediate for Glioblastoma Chemotherapy.
Du, K; Feng, F; Sun, J; Xia, Q, 2021)		2.29
"Temozolomide is an oral alkylating agent used as first line treatment of glioblastoma multiforme (GBM). "( Drug-induced hypersensitivity syndrome following temozolimide for glioblastoma multiforme and the role of desensitization therapy.
Ambur, A; Ambur, L; Khan, L; Nathoo, R, 2022)		2.16
"Temozolomide (TMZ) is a commonly used drug for GBM management."( Extracellular vesicles carry miR-27a-3p to promote drug resistance of glioblastoma to temozolomide by targeting BTG2.
Chen, L; Deng, Q; Guo, S; Hao, P; Hu, S; Li, Z, 2022)		1.67
"Temozolomide (TMZ) is a standard-of-care chemotherapeutic drug for the treatment of glioblastoma (GBM), but TMZ-acquired resistance limits its therapeutic effect. "( Efficacy of Temozolomide-Conjugated Gold Nanoparticle Photothermal Therapy of Drug-Resistant Glioblastoma and Its Mechanism Study.
Chu, L; Liu, X; Sha, C; Sun, K; Sun, Y; Wang, A; Wang, S; Xu, L; Yang, X; Yu, Y; Zhou, L, 2022)		2.54
"Temozolomide (TMZ) is a first-line chemotherapeutic agent for the treatment of glioma. "( The RNA-binding protein fragile-X mental retardation autosomal 1 (FXR1) modulates glioma cells sensitivity to temozolomide by regulating ferroptosis.
Duan, S; Gong, F; Li, Q; Wei, Y, 2022)		2.38
"Temozolomide (TMZ) is a DNA alkylating agent that appears to have a radiosensitizing effect when used in combination with RT and may be worthwhile in meningioma treatment."( Concomitant Temozolomide plus radiotherapy for high-grade and recurrent meningioma: a retrospective chart review.
Belanger, K; Damek, D; Lillehei, KO; Ormond, DR; Ung, TH, 2022)		1.82
"Temozolomide (TMZ) is a chemotherapeutic agent used in glioblastoma and melanoma treatment."( DNA polymerase eta protects human cells against DNA damage induced by the tumor chemotherapeutic temozolomide.
Bastos, AU; de Souza, I; Hoch, NC; Latancia, MT; Leandro, GS; Menck, CFM; Moreno, NC; Ribeiro, VC; Rocha, CRR; Vieira, WKM, 2022)		1.66
"Temozolomide (TMZ) is an imidazotetrazine prodrug used to treat glioblastoma multiforme. "( Temozolomide: An Overview of Biological Properties, Drug Delivery Nanosystems, and Analytical Methods.
Carvalho, SG; Chorilli, M; Di Filippo, LD; Dutra, JAP; Luiz, MT; Tavares Junior, AG, 2022)		3.61
"Temozolomide (TMZ) is a widely used chemotherapeutic drug for glioma."( FOXM1-mediated NUF2 expression confers temozolomide resistance to human glioma cells by regulating autophagy via the PI3K/AKT/mTOR signaling pathway.
Guo, L; Wu, Z, 2022)		1.71
"Temozolomide (TMZ) is a chemotherapeutic agent that has been the first-line standard of care for the aggressive brain cancer glioblastoma (GBM) since 2005. "( Temozolomide-induced guanine mutations create exploitable vulnerabilities of guanine-rich DNA and RNA regions in drug-resistant gliomas.
Alamillo-Ferrer, C; Cheng, SY; Drewry, DH; Erdogdu, B; Goenka, A; Goldlust, SA; Haddad, BR; Hogg, JR; Hu, B; Jin, L; Pertea, M; Pickett, JE; Razaghi, R; Riggins, RB; Sadowski, N; Song, X; Tiek, DM; Timp, W; Wells, CI; Zuercher, WJ, 2022)		3.61
"Temozolomide (TMZ) is a chemotherapeutic drug for the treatment of GBM."( Temozolomide increases heat shock proteins in extracellular vesicles released from glioblastoma cells.
Adıgüzel, Z; Kıyga, E; Önay Uçar, E, 2022)		2.89
"Temozolomide (TMZ) is a first-line chemotherapeutic agent for glioblastoma, but the emergence of drug resistance limits its anti-tumor activity."( GBP3 promotes glioblastoma resistance to temozolomide by enhancing DNA damage repair.
Chen, CC; Chen, Y; Grigore, FN; Jin, J; Lan, Q; Li, M; Li, S; Ma, J; Wang, J; Wang, Q; Wu, G; Xu, H; Zhu, H, 2022)		1.71
"Temozolomide (TMZ) is an auxiliary alkylating agent that is extensively used in conjunction with surgical resection and forms the mainstay of clinical treatment strategies for gliomas."( Regulation of temozolomide resistance via lncRNAs: Clinical and biological properties of lncRNAs in gliomas (Review).
Du, J; Li, S; Peng, C; Peng, F; Xie, X, 2022)		1.8
"Temozolomide (TMZ) is a first-line clinical chemotherapeutic drug."( Piperlongumine-inhibited TRIM14 signaling sensitizes glioblastoma cells to temozolomide treatment.
Chen, KC; Chen, PH; Ho, KH; Kuo, YY; Liu, AJ; Shih, CM, 2022)		1.67
"Temozolomide (TMZ) is a conventional chemotherapeutic drug for glioma, however, its clinical application and efficacy is severely restricted by its drug resistance properties. "( The nanoprodrug of polytemozolomide combines with MGMT siRNA to enhance the effect of temozolomide in glioma.
Li, L; Liu, H; Ma, H; Qian, F; Quan, A; Ren, Y; Wang, L; Xu, H; Yu, R; Zhang, Y, 2023)		2.66
"Temozolomide is an oral alkylating agent that is used as the first line treatment for glioblastoma multiform, and in recurrent anaplastic astrocytoma, as well as having demonstrable activity in patients with metastatic melanoma. "( Is Autophagy Inhibition in Combination with Temozolomide a Therapeutically Viable Strategy?
Elshazly, AM; Gewirtz, DA, 2023)		2.61
"Temozolomide (TMZ) is a first line agent used in the clinic for glioblastoma and it has been useful in increasing patient survival rates."( Efficient delivery of Temozolomide using ultrasmall large-pore silica nanoparticles for glioblastoma.
Ahmed-Cox, A; Akhter, DT; Cao, Y; Fletcher, NL; Janjua, TI; Kavallaris, M; Moniruzzaman, M; Popat, A; Raza, A; Thurecht, KJ, 2023)		1.95
"Temozolomide (TMZ) is a chemotherapy agent used to treat primary central nervous system tumors."( Metastatic Melanoma: A Preclinical Model Standardization and Development of a Chitosan-Coated Nanoemulsion Containing Temozolomide to Treat Brain Metastasis.
Azambuja, JH; Braganhol, E; de Cássia Sant'ana, R; de Souza, PO; Debom, GN; Fachel, FNS; Gelsleichter, NE; Lenz, GS; Michels, LR; Roliano, GG; Teixeira, FC; Teixeira, HF; Visioli, F, 2023)		1.84
"Temozolomide (TMZ) is a DNA alkylating agent that can cross the blood-brain barrier."( Expert opinion on translational research for advanced glioblastoma treatment.
Cui, X; Kang, C; Wang, Q; Wang, Y; Zhou, J, 2023)		1.63
"Temozolomide (TMZ) is a common chemotherapy drug used to treatment of glioblastoma, but drug resistance against this drug is an important barrier to successful treatment of this cancer."( Combination of SIX4-siRNA and temozolomide inhibits the growth and migration of A-172 glioblastoma cancer cells.
Baghbanzadeh, A; Baradaran, B; Barpour, N; Doustvandi, MA; Javadrashid, D; Mohammadpour, ZJ; Mohammadzadeh, R, 2023)		1.92
"Temozolomide (TMZ) is a standard chemotherapeutic for GBM, but TMZ treatment benefits are compromised by chemoresistance."( Identification of the E2F1-RAD51AP1 axis as a key factor in MGMT-methylated GBM TMZ resistance.
Cui, X; Kang, C; Liu, X; Tong, F; Wang, G; Wang, Q; Wang, Y; Zhao, J; Zhou, J, 2023)		1.63
"Temozolomide (TMZ) is a common alkylating chemotherapeutic agent used to treat brain tumors such as glioblastoma multiforme (GBM) and anaplastic astrocytoma. "( LncRNA-associated competing endogenous RNA network analysis uncovered key lncRNAs involved in temozolomide resistance and tumor recurrence of glioblastoma.
Mallick, B; Nayak, R, 2023)		2.57
"Temozolomide (TMZ) is a standard treatment for glioblastoma (GBM) patients. "( Hypoxanthine phosphoribosyl transferase 1 metabolizes temozolomide to activate AMPK for driving chemoresistance of glioblastomas.
Agnihotri, S; Cao, Y; Chen, D; Ding, F; Ge, X; Ge, Z; Huang, G; Ji, J; Lin, F; Lu, Z; Qian, X; Shi, Z; Wang, Q; Wang, X; Yin, J; You, Y; Zhang, J; Zhao, N; Zhou, Q, 2023)		2.6
"Temozolomide (TMZ) is a commonly used chemotherapeutic agent for glioblastoma (GBM), but acquired drug resistance prevents its therapeutic efficacy. "( NFYB increases chemosensitivity in glioblastoma by promoting HDAC5-mediated transcriptional inhibition of SHMT2.
Huang, H; Liu, P; Xie, Y; Zhang, Y, 2023)		2.35
"Temozolomide (TMZ) is an important first-line treatment for glioblastoma (GBM), but there are limitations to TMZ response in terms of durability and dependence on the promoter methylation status of the DNA repair gene O"( Epigenetic Activation of TUSC3 Sensitizes Glioblastoma to Temozolomide Independent of MGMT Promoter Methylation Status.
Berglund, AE; Etame, AB; Macaulay, RJ; Wu, Q, 2023)		2.6
"Temozolomide (TMZ) is a first-line chemotherapeutic agent used against glioblastoma multiforme (GBM), but this disease exhibits recurrence and high lethality. "( miR-140 targeting CTSB signaling suppresses the mesenchymal transition and enhances temozolomide cytotoxicity in glioblastoma multiforme.
Chen, KC; Chen, PH; Cheng, CH; Chou, CM; Ho, KH; Lin, CW; Liu, AJ; Shih, CM, 2019)		2.18
"Temozolomide is an alkylating agent used as the first line of treatment for glioblastoma. "( Temozolomide has anti-tumor effects through the phosphorylation of cPLA
Hara, H; Iwama, T; Nakamura, S; Noda, Y; Ohno, Y; Saio, M; Shimazawa, M; Tsuji, S; Yamada, T, 2019)		3.4
"Temozolomide (TMZ) is a chemotherapy agent used to treat Grade IV astrocytoma, also known as glioblastoma (GBM). "( Simvastatin increases temozolomide-induced cell death by targeting the fusion of autophagosomes and lysosomes.
Aghaei, M; Akbari, M; Albokashy, M; Alizadeh, J; Butterfield, Y; Cole, LK; Eftekharpour, E; Ghavami, S; Hatch, GM; Hombach-Klonisch, S; Islam, MI; Kardami, E; Klonisch, T; Koleini, N; Marzban, H; Samiei, E; Shojaei, S; Thliveris, J; Vosoughi, AR; Xu, F, 2020)		2.32
"Temozolomide (TMZ) is a first-line alkylating agent for glioblastoma multiforme (GBM). "( IGF-1-enhanced miR-513a-5p signaling desensitizes glioma cells to temozolomide by targeting the NEDD4L-inhibited Wnt/β-catenin pathway.
Chen, KC; Chen, PH; Cheng, CH; Chou, CM; Ho, KH; Lee, CC; Shih, CM, 2019)		2.19
"Temozolomide is an oral alkylating agent used for treating several cancers including glioblastoma and melanoma. "( Biomarker-guided implementation of the old drug temozolomide as a novel treatment option for patients with metastatic colorectal cancer.
Benelli, M; de Braud, F; Di Donato, S; Pietrantonio, F; Randon, G; Romagnoli, D, 2020)		2.26
"Temozolomide is a first line anti-tumor drug used for the treatment of patients with Glioblastoma multiforme (GBM). "( Microarray expression profiles and bioinformatics analysis of mRNAs, lncRNAs, and circRNAs in the secondary temozolomide-resistant glioblastoma.
Gao, Y; Guo, R; Li, H; Yang, B; Zhao, C, 2020)		2.21
"Temozolomide is an alkylating agent which is used in glioblastoma treatment. "( Effects of temozolomide on U87MG glioblastoma cell expression of CXCR4, MMP2, MMP9, VEGF, anti-proliferatory cytotoxic and apoptotic properties.
Elieh Ali Komi, D; Kiani, A; Mirabdaly, S; Moini, A; Shakiba, Y, 2020)		2.39
"Temozolomide (TMZ) is a frequently used chemotherapy for glioma; however, chemoresistance is a major problem limiting its effectiveness. "( A
An, W; Attenello, F; Bi, J; Chen, B; Chen, J; Guo, D; He, A; Lu, W; Qian, Y; Shi, J; Shi, T; Wang, W; Zhang, L; Zhao, Z, 2020)		2
"Temozolomide (TMZ) is a drug of choice in glioblastoma treatment. "( Revealing the epigenetic effect of temozolomide on glioblastoma cell lines in therapeutic conditions.
Barciszewska, AM; Barciszewski, J; Belter, A, 2020)		2.28
"Temozolomide (TMZ) is an effective drug for prolonging the overall survival time of patients, while drug-resistance is an important clinical problem at present."( A steroidal saponin form Paris vietnamensis (Takht.) reverses temozolomide resistance in glioblastoma cells via inducing apoptosis through ROS/PI3K/Akt pathway.
Fang, F; Ji, Y; Li, H; Lu, Y; Qiu, P; Tang, H; Zhang, S, 2020)		1.52
"Temozolomide is a drug approved for treating glioblastomas, which has 100% oral bioavailability but gets degraded at physiological pH thus having very short half-life and only 20-30% brain bioavailability. "( Design of temozolomide-loaded proliposomes and lipid crystal nanoparticles with industrial feasible approaches: comparative assessment of drug loading, entrapment efficiency, and stability at plasma pH.
Dubey, SK; Gorantla, S; Khosa, A; Rapalli, VK; Saha, RN; Singhvi, G; Waghule, T, 2021)		2.47
"Temozolomide (TMZ) is a DNA alkylating agent and is currently a first line chemotherapeutic treatment for GBM."( Inhibition of Nrf2 might enhance the anti-tumor effect of temozolomide in glioma cells via inhibition of Ras/Raf/MEK signaling pathway.
Lu, Z; Sun, W; Yu, J; Zhang, W, 2021)		1.59
"Temozolomide is a conventional chemotherapy drug for adjuvant treatment of patients with high-risk gliomas, including grade II to grade IV."( Blockade of Cell Volume Regulatory Protein NKCC1 Increases TMZ-Induced Glioma Apoptosis and Reduces Astrogliosis.
Amankulor, NM; Begum, G; Castro, MG; Ding, D; Dodelson, J; Fiesler, VM; Gayden, J; Guan, X; Hasan, MN; Hu, B; Jia, W; Kohanbash, G; Luo, L; Sun, B; Sun, D, 2020)		1.28
"Temozolomide/etoposide is a feasible candidate as salvage therapy for relapsed osteosarcoma."( Temozolomide and etoposide combination for the treatment of relapsed osteosarcoma.
Adachi, S; Akazawa, R; Arakawa, Y; Hiramatsu, H; Kato, I; Moritake, H; Okamoto, T; Saida, S; Sakamoto, A; Sumiyoshi, S; Takita, J; Umeda, K, 2020)		2.72
"Temozolomide is a first line anti-tumor drug used for the treatment of patients with Glioblastoma multiforme (GBM). "( MicroRNA-128-3p Enhances the Chemosensitivity of Temozolomide in Glioblastoma by Targeting c-Met and EMT.
Guan, F; Guo, R; Li, H; Li, M; Liu, X; Ma, S; Wu, J; Yang, B; Zhao, C, 2020)		2.26
"Temozolomide (TMZ) is a DNA-alkylating agent used for chemo-radiotherapy of glioblastoma, which is also a target cancer for boron neutron capture therapy (BNCT). "( The combined effect of neutron irradiation and temozolomide on glioblastoma cell lines with different MGMT and P53 status.
Ikawa, T; Kinashi, Y; Takahashi, S, 2020)		2.26
"Temozolomide (TMZ) is a life prolonging DNA alkylating agent active against glioblastomas (GBM) in which the O6-methylguanine-DNA methyltransferase (MGMT) gene is silenced by promoter methylation. "( PARP inhibition suppresses the emergence of temozolomide resistance in a model system.
Bering, EA; Black, S; Blough, MD; Cairncross, JG; Liao, J; Maxwell, L; Meode, M; Pedersen, H; Tan, M; Willms, J; Yuan, AL, 2020)		2.26
"Temozolomide (TMZ) is a chemotherapeutic used for the treatment of glioblastoma. "( A co-formulation of interferons type I and II enhances temozolomide response in glioblastoma with unmethylated MGMT promoter status.
Bello-Rivero, I; Leenstra, S; van der Kaaij, M; Vázquez-Blomquist, D; Villarreal, A, 2020)		2.25
"Temozolomide (TMZ) is an alkylating chemotherapy agent used in the clinical treatment of glioblastoma multiforme (GBM) patients. "( Piperine synergistically enhances the effect of temozolomide against temozolomide-resistant human glioma cell lines.
Jeong, S; Jung, S; Oh, JW; Park, GS; Shin, J, 2020)		2.26
"Temozolomide (TMZ) is an oral alkylating agent used for the treatment of glioblastoma and is now becoming a chemotherapeutic option in patients diagnosed with high-risk low-grade gliomas. "( MGMT genomic rearrangements contribute to chemotherapy resistance in gliomas.
Bao, Z; Galán-Ganga, M; Jiang, T; Kim, H; Kroon, P; Liu, H; Mu, Q; Nam, DH; Oldrini, B; Rabadan, R; Rodriguez-Perales, S; Sa, JK; Squatrito, M; Vaquero-Siguero, N; Verhaak, RGW; Wang, J; Wang, Z; Zhang, Y; Zhao, J, 2020)		2
"Temozolomide is an oral DNA-alkylating agent capable of crossing the blood-brain barrier and used as chemotherapy primarily to treat glioblastoma and other brain cancers."( Central diabetes insipidus induced by temozolomide: A report of two cases.
Capes, A; Duck, L; Duprez, T; Labriola, L; Mahiat, C; Whenham, N, 2021)		1.61
"Temozolomide (TMZ) is an oral chemotherapy drug constituting the backbone of chemotherapy regimens utilized as first-line treatment of GBM."( LncRNA NEAT1 promotes malignant phenotypes and TMZ resistance in glioblastoma stem cells by regulating let-7g-5p/MAP3K1 axis.
Bi, CL; Fang, JS; Lan, S; Liu, JF; Yang, ZY; Zhang, MY, 2020)		1.28
"Temozolomide (TMZ) is an oral alkylating agent principally indicated for neurological malignancies including glioblastoma (GBM) and astrocytoma. "( Temozolomide-induced aplastic anaemia: Case report and review of the literature.
Gilbar, PJ; Mangos, HM; Pokharel, K, 2021)		3.51
"Temozolomide (TMZ) is a first-line chemotherapy drug for the treatment of malignant glioma and resistance to it poses a major challenge. "( Regulation of temozolomide resistance in glioma cells via the RIP2/NF-κB/MGMT pathway.
Hu, YH; Jiao, BH; Wang, CY; Wu, JL, 2021)		2.42
"Temozolomide (TMZ) is an effective chemotherapy drug for glioblastoma, but the resistance to TMZ has come to represent a major clinical problem, and its underlying mechanism has yet to be elucidated."( Exosomal connexin 43 regulates the resistance of glioma cells to temozolomide.
Bi, QC; Gan, LJ; Han, XJ; Hong, T; Jiang, LP; Lan, XM; Liu, LH; Tan, RJ; Wei, MJ; Yang, ZJ; Zhang, LL, 2021)		1.58
"Temozolomide (TMZ) is a broad spectrum alkylating agent found effective in the treatment of glioblastoma multiforme, refractory anaplastic astrocytoma, and metastatic melanoma. "( UV spectroscopic method for estimation of temozolomide: Application in stability studies in simulated plasma pH, degradation rate kinetics, formulation design, and selection of dissolution media.
Narayan Saha, R; Singhvi, G; Waghule, T, 2021)		2.33
"Temozolomide (TMZ) is an alkylating agent widely used for glioma treatment."( miR-23b-5p promotes the chemosensitivity of temozolomide via negatively regulating TLR4 in glioma.
Cui, B; Gao, K; Qiao, Y; Wang, T, 2021)		1.6
"Temozolomide (TEM) is an active treatment in metastatic neuroendocrine tumors (NETs). "( Should temozolomide be used on the basis of O
Bagnardi, V; Curigliano, G; Fazio, N; Fumagalli, C; Gervaso, L; Guerini Rocco, E; Laffi, A; Peveri, G; Pisa, E; Rubino, M; Spada, F; Trillo Aliaga, P, 2021)		2.52
"Temozolomide (TMZ) is a first-choice alkylating agent inducted as a gold standard therapy for glioblastoma multiforme (GBM) and astrocytoma. "( Elucidating the mechanisms of Temozolomide resistance in gliomas and the strategies to overcome the resistance.
Kumar, A; Shrivastava, A; Srivastava, C; Tomar, MS, 2021)		2.35
"Temozolomide (TMZ) is an alkylating agent frequently used in well-differentiated metastatic pancreatic neuroendocrine tumors (PNETs) with very variable responses. "( Short article: Evaluation of O6-methylguanine-DNA methyltransferase as a predicting factor of response to temozolomide-based chemotherapy in well-differentiated metastatic pancreatic neuroendocrine tumors.
Caroli-Bosc, FX; Cauchin, E; Dumars, C; Foubert, F; Girot, P; Matysiak-Budnik, T; Mosnier, JF; Muzellec, L; Regenet, N; Senellart, H; Touchefeu, Y, 2017)		2.11
"Temozolomide (TMZ) is a promising chemotherapeutic agent to treat Glioblastoma multiforme (GBM). "( MiR-181b modulates chemosensitivity of glioblastoma multiforme cells to temozolomide by targeting the epidermal growth factor receptor.
Chen, Y; Li, R; Liu, N; Pan, M; Shi, Z; Wang, X; Yan, W; You, Y; Zhang, J, 2017)		2.13
"Temozolomide (TMZ) is an alkylating agent that has been widely used to treat GBM; resistance to this drug is often found."( Cytotoxicity of temozolomide on human glioblastoma cells is enhanced by the concomitant exposure to an extremely low-frequency electromagnetic field (100Hz, 100G).
Abadi, MFS; Ahmadi, M; Akbarnejad, Z; Dini, L; Eskandary, H; Farsinejad, A; Nematollahi-Mahani, SN; Vergallo, C, 2017)		1.52
"Temozolomide (TMZ) is an effective drug for malignant glioma, however, the intracellular and molecular mechanisms behind this anti-cancer effect have yet to be fully understood."( Down-Regulation of AQP4 Expression via p38 MAPK Signaling in Temozolomide-Induced Glioma Cells Growth Inhibition and Invasion Impairment.
Chen, Y; Gao, F; Hou, J; Jiang, R; Kang, L; Li, Y; Liu, H; Liu, X; Yang, M; Yi, Y, 2017)		1.42
"Temozolomide (TMZ) is an alkylating chemotherapeutic agent widely used in anti-glioma treatment. "( Genomic profiling of long non-coding RNA and mRNA expression associated with acquired temozolomide resistance in glioblastoma cells.
Fu, Z; Guo, H; Lian, C; Liu, B; Liu, Y; Xu, N; Yang, Z; Zeng, H, 2017)		2.12
"Temozolomide (TMZ) is an oral alkylating agent that has shown promise in treating aggressive pituitary adenomas and carcinomas that are resistant to other therapies."( Temozolomide therapy for resistant prolactin-secreting pituitary adenomas and carcinomas: a systematic review.
Ahmad, MM; Aldabas, BS; Aljoaib, NN; Almalki, MH; Alotaibi, MJ; Alshahrani, F; Wahedi, TS, 2017)		2.62
"Temozolomide (TMZ) is an alkylating agent previously used in conjunction with doxorubicin (DOX) to treat dogs with relapsed lymphoma. "( Temozolomide alone or in combination with doxorubicin as a rescue agent in 37 cases of canine multicentric lymphoma.
Baines, SJ; Blackwood, L; Elliott, JW; Treggiari, E, 2018)		3.37
"Temozolomide (TMZ) is an integral part of upfront treatment of high-grade gliomas. "( Rechallenge temozolomide in glioma: A case series from India.
Chandrasekaran, A; Epari, S; Gupta, T; Jalali, R; Kothari, R; Pande, N; Patil, VM; Tonse, R, )		1.95
"Temozolomide is an alkylating chemotherapeutic agent used in malignant neuroendocrine neoplasia, melanoma, brain metastases and an essential component of adjuvant therapy in the treatment of glioblastoma multiforme and anaplastic astrocytoma. "( 65 YEARS OF THE DOUBLE HELIX: Treatment of pituitary tumors with temozolomide: an update.
Kovacs, K; Ortiz, LD; Rotondo, F; Syro, LV, 2018)		2.16
"Temozolomide is an oral alkylating cytotoxic drug and like any other alkylating agent can induce side effects."( Severe hematologic temozolomide-related toxicity and lifethreatening infections.
Nikitovic, M; Stepanovic, A, )		1.18
"Temozolomide (TMZ) is an antiangiogenic agent."( Opposite Interplay Between the Canonical WNT/β-Catenin Pathway and PPAR Gamma: A Potential Therapeutic Target in Gliomas.
Guillevin, R; Lecarpentier, Y; Vallée, A; Vallée, JN, 2018)		1.2
"Temozolomide (TMZ) is a standard chemotherapeutic drug used in the treatment of glioblastoma multiforme (GBM); however, resistance to this drug is common. "( Association between SOX9 and CA9 in glioma, and its effects on chemosensitivity to TMZ.
Cheng, Y; Jin, W; Liu, H; Liu, N; Tu, Y; Wang, X; Wang, Z; Xu, X; Yang, H; Zhang, P; Zhang, Y, 2018)		1.92
"Temozolomide (TMZ) is an alkylating agent used for glioblastoma multiforme (GBM) treatment. "( Synergistic effect of temozolomide and thymoquinone on human glioblastoma multiforme cell line (U87MG).
Khazaei, M; Khazaei, MR; Moradi, MT; Pazhouhi, M; Sariri, R, )		1.89
"Temozolomide (TMZ) is a first-line chemotherapeutic drug for malignant gliomas. "( Honokiol enhances temozolomide-induced apoptotic insults to malignant glioma cells via an intrinsic mitochondrion-dependent pathway.
Chen, RM; Chio, CC; Liu, SH; Mohanraj, M; Tai, YT; Yang, ST, 2018)		2.26
"Temozolomide (TMZ) is a drug used to treat GBM, while the survival period of GBM patients with positive treatment remains less than 15 months."( Study on Therapeutic Action and Mechanism of TMZ Combined with RITA Against Glioblastoma.
Cao, Z; Li, L; Wu, Q; Xiao, W; Xie, Q; Zhang, B; Zhao, W; Zhu, L, 2018)		1.2
"Temozolomide (TMZ) is an alkylating agent commonly used as a first‑line treatment for high‑grade glioblastoma. "( Synergistic anticancer effect of acteoside and temozolomide-based glioblastoma chemotherapy.
Choi, DE; Hwang, TW; Jang, TW; Kim, DB; Kim, DH; Kim, GH; Kim, JJ; Moon, M; Park, JH; Yoon, KA, 2019)		2.21
"Temozolomide (TMZ) is a widely used chemotherapeutic agent for glioblastoma multiforme (GBM). "( Momelotinib sensitizes glioblastoma cells to temozolomide by enhancement of autophagy via JAK2/STAT3 inhibition.
Li, A; Liu, T; Xin, Y; Xu, Y, 2019)		2.22
"Temozolomide is a first-line treatment for newly diagnosed glioblastoma. "( Evidence-Based Practice: Temozolomide Beyond Glioblastoma.
Chua, J; Leung, D; Nafziger, E, 2019)		2.26
"Temozolomide (TMZ) is an alkylating agent used in the treatment of high-grade malignant glioma, notably glioblastoma multiforme, the most aggressive form of brain cancer. "( Are There Thresholds in Glioblastoma Cell Death Responses Triggered by Temozolomide?
He, Y; Kaina, B, 2019)		2.19
"Temozolomide (TMZ) is an important agent against GBM."( Inhibition of cyclin E1 overcomes temozolomide resistance in glioblastoma by Mcl-1 degradation.
Chen, Z; Liang, H; Sun, L, 2019)		1.51
"Temozolomide (TMZ) is a frequently used primary chemotherapeutic agent for LGGs."( Comprehensive Analysis Reveals a 4-Gene Signature in Predicting Response to Temozolomide in Low-Grade Glioma Patients.
Chen, Y; He, Z; Wang, Q, )		1.08
"Temozolomide (TMZ) is an alkylating agent widely used to treat cancer, resistance to this drug is often found."( Impact of extremely low-frequency electromagnetic field (100 Hz, 100 G) exposure on human glioblastoma U87 cells during Temozolomide administration.
Ahmadi-Zeidabadi, M; Akbarnejad, Z; Eskandary, H; Esmaeeli, M; Masoumi-Ardakani, Y; Mohammadipoor-Ghasemabad, L, 2019)		1.44
"Temozolomide is an oral chemotherapy used to treat aggressive pituitary tumours since 2006. "( How and when to use temozolomide to treat aggressive pituitary tumours.
Whitelaw, BC, 2019)		2.28
"Temozolomide (TMZ) is an alkylating agent shown to prolong survival in patients with high grade glioma and is routinely used to treat melanoma brain metastases. "( Myeloablative temozolomide enhances CD8⁺ T-cell responses to vaccine and is required for efficacy against brain tumors in mice.
Archer, GE; Bigner, DD; Choi, BD; Cui, X; Flores, C; Herndon, JE; Johnson, LA; Mitchell, DA; Sampson, JH; Sanchez-Perez, LA; Schmittling, RJ; Snyder, D, 2013)		2.19
"Temozolomide is a novel oral chemotherapy drug that penetrates into the brain and purportedly has a low incidence of adverse events."( Temozolomide for high grade glioma.
Garside, R; Grant, R; Hart, MG; Rogers, G; Stein, K, 2013)		2.55
"Temozolomide (TMZ) is an alkylating agent that is the first-line chemotherapy for glioblastoma."( Phase 1/1b study of lonafarnib and temozolomide in patients with recurrent or temozolomide refractory glioblastoma.
Colman, H; Conrad, C; Gilbert, MR; Groves, M; Hsu, S; Kang, S; Levin, V; Liu, D; Liu, V; Puduvalli, V; Yuan, Y; Yung, WK; Yust-Katz, S, 2013)		1.39
"Temozolomide is an oral alkylating agent with proven efficacy in recurrent high-grade glioma. "( Effect of temozolomide on male gametes: an epigenetic risk to the offspring?
Bashamboo, A; Berthaut, I; Deluen, F; Dessolle, L; McElreavey, K; Montjean, D; Morcel, K; Poirot, C; Ravel, C, 2013)		2.23
"Temozolomide (TMZ) is a DNA methylating agent used to treat brain cancer. "( Early Chk1 phosphorylation is driven by temozolomide-induced, DNA double strand break- and mismatch repair-independent DNA damage.
Gaensler, K; Ito, M; Mukherjee, J; Ohba, S; Pieper, RO; Ronen, SM, 2013)		2.1
"Temozolomide (TMZ) is an oral alkylating agent used for the treatment of recurrent or newly diagnosed malignant gliomas with significant survival benefit. "( Temozolomide-related hematologic toxicity.
De Sanctis, V; Enrici, RM; Minniti, G; Scaringi, C, 2013)		3.28
"Temozolomide (TMZ) is an alkylating agent primarily used to treat tumors of the central nervous system. "( Central diabetes insipidus: a previously unreported side effect of temozolomide.
Faje, AT; Klibanski, A; Makimura, H; Miller, KK; Nachtigall, L; Wexler, D, 2013)		2.07
"Temozolomide (TMZ) is an oral alkylating agent used in the treatment of central nervous system neoplasms and metastatic melanoma. "( A phase I, dose-escalation study of cyclical weekly oral temozolomide and weekly PEG-interferon alpha-2b in patients with refractory or advanced solid tumours.
Beelen, AP; Coker, SA; Crosby, NA; Dandamudi, UB; Ernstoff, MS; Fisher, JL; Lewis, LD; Obrocea, M, 2013)		2.08
"Temozolomide (TMZ) is an alkylating agent currently used as first-line therapy for gliomas treatment due to its DNA-damaging effect. "( O6-methylguanine DNA methyltransferase as a promising target for the treatment of temozolomide-resistant gliomas.
Cao, H; Chen, L; Fan, CH; Jiang, G; Liu, WL; Wen, C, 2013)		2.06
"Temozolomide (TMZ) is an alkylating agent used in chemoradiotherapy and adjuvant chemotherapy regimens for treatment of newly diagnosed or recurrent glioblastoma. "( Temozolomide-induced liver damage. A case report.
Becker, F; Fietkau, R; Hecht, M; Schmidtner, J; Semrau, S, 2014)		3.29
"Temozolomide (TMZ) is a promising chemotherapeutic agent for treating glioblastomas. "( miR-125b inhibitor enhance the chemosensitivity of glioblastoma stem cells to temozolomide by targeting Bak1.
Chen, J; Fu, X; Jiang, D; Shi, L; Wan, Y; Wang, Z, 2014)		2.07
"Temozolomide (TMZ) is a first-line chemotherapeutic agent but the efficacy is limited by intrinsic and acquired resistance in GBM."( Triptolide synergistically enhances temozolomide-induced apoptosis and potentiates inhibition of NF-κB signaling in glioma initiating cells.
Chen, YS; Chen, ZP; Guan, S; Guo, CC; Li, WP; Li, WY; Mou, YG; Sai, K; Wang, J; Yang, QY, 2014)		1.4
"Temozolomide (TMZ) is an alkylating agent used for the treatment of glioblastoma multiforme (GBM), the main form of human brain tumours in adults. "( Bak and Mcl-1 are essential for Temozolomide induced cell death in human glioma.
Gratas, C; Oliver, L; Rabé, M; Séry, Q; Vallette, FM, 2014)		2.13
"Temozolomide (TMZ) is an alkylating agent that is widely used in chemotherapy for cancer. "( Progression of O⁶-methylguanine-DNA methyltransferase and temozolomide resistance in cancer research.
Cheng, Q; Jiang, AJ; Jiang, G; Li, LT; Xin, Y; Zheng, JN, 2014)		2.09
"Temozolomide (TMZ) is an oral alkylating agent which is widely used in the treatment of GBM following surgery."( miR-128 and miR-149 enhance the chemosensitivity of temozolomide by Rap1B-mediated cytoskeletal remodeling in glioblastoma.
Cui, Y; Lei, Q; Li, G; She, X; Wang, Z; Wu, M; Xiang, J; Xu, G; Yu, Z, 2014)		1.37
"Temozolomide (TMZ) is an alkylating agent used for the treatment of glioblastoma multiforme (GBM), the most common and deadliest of malignant primary brain tumors."( Glioblastoma multiforme and hepatitis B: do the right thing(s).
Begini, P; Delle Fave, G; Gallina, S; Marignani, M; Minniti, G; Purchiaroni, F, 2014)		1.12
"Temozolomide is an oral alkylating agent with schedule-dependent antitumor activity against high-grade malignancies including high-grade glioma. "( Temozolomide retreatment in a recurrent prolactin-secreting pituitary adenoma: Hormonal and radiographic response.
Laterra, JJ; Salvatori, R; Strowd, RE, 2016)		3.32
"Temozolomide is an increasingly described treatment option for refractory pituitary adenomas and carcinomas. "( Temozolomide retreatment in a recurrent prolactin-secreting pituitary adenoma: Hormonal and radiographic response.
Laterra, JJ; Salvatori, R; Strowd, RE, 2016)		3.32
"Temozolomide (TMZ) is an oral alkylating drug with good tolerability, approved for treatment of malignant gliomas."( Long-term outcome and MGMT as a predictive marker in 24 patients with atypical pituitary adenomas and pituitary carcinomas given treatment with temozolomide.
Andersen, M; Bengtsson, D; Berinder, K; Burman, P; Feldt Rasmussen, U; Hoybye, C; Johannsson, G; Maiter, D; Petersson, M; Ragnarsson, O; Rasmussen, ÅK; Schrøder, HD; van der Lely, AJ, 2015)		1.34
"Temozolomide rechallenge is a treatment option for MGMT promoter-methylated recurrent glioblastoma. "( MGMT Promoter Methylation Is a Strong Prognostic Biomarker for Benefit from Dose-Intensified Temozolomide Rechallenge in Progressive Glioblastoma: The DIRECTOR Trial.
Bähr, O; Felsberg, J; Goldbrunner, R; Hau, P; Herrlinger, U; Homicsko, K; Hüsing, J; Kästner, B; Ketter, R; Kollias, S; Marosi, C; Meixensberger, J; Nikkhah, G; Pichler, J; Platten, M; Reifenberger, G; Sabel, MC; Schlegel, U; Schnell, O; Steinbach, JP; Stupp, R; Tabatabai, G; Tonn, JC; Vajkoczy, P; Weller, M; Wick, A; Wick, W; Wirsching, HG, 2015)		2.08
"Temozolomide (TMZ) is an alkylating agent used for the treatment of glioblastoma. "( The synergistic effect of combination temozolomide and chloroquine treatment is dependent on autophagy formation and p53 status in glioma cells.
Hong, SH; Hong, YK; Joe, YA; Kim, HK; Kim, HS; Lee, NH; Lee, SW; Yi, HY, 2015)		2.13
"Temozolomide (TMZ) is an effective agent for clinical glioma treatment, but the innate and acquired resistance of glioma always limits its application. "( p38 MAPK-dependent Nrf2 induction enhances the resistance of glioma cells against TMZ.
Gu, Y; Liu, J; Ma, L; Qi, J; Yu, W; Zhang, X, 2015)		1.86
"Temozolomide is a chemotherapeutic drug that is mainly used in the treatment of primary glioblastoma multiforme and recurrent high-grade glioma. "( Synthesis of [3-N-(11) C-methyl]temozolomide via in situ activation of 3-N-hydroxymethyl temozolomide and alkylation with [(11) C]methyl iodide.
Eriksson, J; Froklage, FE; Hendrikse, NH; Reijneveld, JC; Schuit, RC; Van Kooij, R; Windhorst, AD, 2015)		2.14
"Temozolomide (TMZ) is an alkylating drug used usually in glioma treatment by inducing the apoptosis in glioma cell. "( Temozolomide may induce cell cycle arrest by interacting with URG4/URGCP in SH-SY5Y neuroblastoma cells.
Avcı, ÇB; Çıtışlı, V; Dodurga, Y; Eroğlu, C; Şatıroğlu-Tufan, NL; Seçme, M, 2015)		3.3
"Temozolomide (TMZ) is an oral, potentially less toxic derivative of dacarbazine, which has shown activity both as a single agent and in combination with other drugs."( Temozolomide in Advanced Neuroendocrine Neoplasms: Pharmacological and Clinical Aspects.
Barberis, M; Berruti, A; Fazio, N; Fumagalli, C; Galdy, S; Kaltsas, G; Koumarianou, A; Kulke, MH; Oberg, K; Spada, F; Strosberg, JR, 2015)		2.58
"Temozolomide (TMZ) is an oral alkylating agent with established effects on the central nervous system of glioblastoma (GBM) patients. "( Do glioma patients derive any therapeutic benefit from taking a higher cumulative dose of temozolomide regimens?: a meta-analysis.
Du, S; Liao, G; Ren, C; Sun, H; Xie, X; Yuan, YW, 2015)		2.08
"Temozolomide is a novel cytotoxic agent currently used as first-line chemotherapy for glioblastoma multiforme (GBM). "( TAZ promotes temozolomide resistance by upregulating MCL-1 in human glioma cells.
Li, A; Li, Z; Lu, H; Luo, R; Tian, T; Zhang, M, 2015)		2.23
"Temozolomide (TMZ) is a promising chemotherapeutic agent for treating glioblastomas. "( PI3K inhibitor combined with miR-125b inhibitor sensitize TMZ-induced anti-glioma stem cancer effects through inactivation of Wnt/β-catenin signaling pathway.
Fei, X; Shi, L; Wang, Z; You, Y, 2015)		1.86
"Temozolomide (TMZ) is an oral alkylating chemotherapeutic agent that prolongs the survival of patients with glioblastoma (GBM). "( A New Epigenetic Mechanism of Temozolomide Action in Glioma Cells.
Barciszewska, AM; Gurda, D; Głodowicz, P; Naskręt-Barciszewska, MZ; Nowak, S, 2015)		2.15
"Temozolomide (TMZ) is an anticancer drug used for the treatment of adult brain tumour and skin cancer. "( Electrochemical monitoring of the interaction between Temozolamide and nucleic acids by using disposable pencil graphite electrodes.
Altay, C; Congur, G; Eksin, E; Erdem, A, 2015)		1.86
"Temozolomide is a standard chemotherapy agent for malignant gliomas, but the efficacy is still not satisfactory. "( Temozolomide reverses doxorubicin resistance by inhibiting P-glycoprotein in malignant glioma cells.
Kanamori, M; Saito, R; Shibahara, I; Sonoda, Y; Sugiyama, S; Tominaga, T; Zhang, R, 2016)		3.32
"Temozolomide (TMZ) is an oral DNA-alkylating agent used for treating patients with glioblastoma. "( Bone morphogenetic protein 7 sensitizes O6-methylguanine methyltransferase expressing-glioblastoma stem cells to clinically relevant dose of temozolomide.
Bui, Y; Cloughesy, TF; Hong, I; Lai, A; Liau, LM; McBride, WH; Menjivar, JC; Nelson, SF; Stream, A; Tso, CL; Tso, JL; Yamada, K; Yang, S; Yong, WH; Zhang, Y, 2015)		2.06
"Temozolomide (TMZ) is an oral alkylating agent that has been used over the past 8 years to treat aggressive pituitary tumors resistant to conventional therapy. "( Temozolomide for aggressive ACTH pituitary tumors: failure of a second course of treatment.
Aller, J; Campderá, M; Estrada, J; Lilienfeld, H; Magallón, R; Martín, P; Palacios, N; Saucedo, G, 2016)		3.32
"Temozolomide is an additional effective therapeutic option for the treatment of aggressive pituitary tumors."( Temozolomide therapy in patients with aggressive pituitary adenomas or carcinomas.
Bogazzi, F; Cannavo, S; Ceccato, F; Curtò, L; De Marinis, L; Iacovazzo, D; Lombardi, G; Losa, M; Mantovani, G; Mazza, E; Minniti, G; Nizzoli, M; Reni, M; Scaroni, C, 2016)		2.6
"Temozolomide is an alkylating agent used along with concurrent radiation therapy in the treatment of glioblastoma. "( Temozolomide-induced biliary ductopenia: a case report.
Balakrishnan, A; Jaglal, M; Ledford, R, 2016)		3.32
"Temozolomide (TMZ) is a standard agent used in the treatment of various types of cancers, including lung carcinoma, but TMZ resistance is common and accounts for many treatment failures. "( miR-487b-5p Regulates Temozolomide Resistance of Lung Cancer Cells Through LAMP2-Medicated Autophagy.
Bao, L; Chen, Y; Feng, J; Han, S; Lv, L; Wang, X; Zhao, H, 2016)		2.19
"Temozolomide is an oral chemotherapy with a favorable side-effect profile that has shown activity against pituitary adenomas."( Is there a role for early chemotherapy in the management of pituitary adenomas?
DeAngelis, LM; Lin, AL; Sum, MW, 2016)		1.16
"Temozolomide (TMZ) is an alkylating agent used to treat glioblastoma. "( Sulfasalazine intensifies temozolomide cytotoxicity in human glioblastoma cells.
Castilho, RF; De Melo, DR; Facchini, G; Ignarro, RS; Lopes-Cendes, I; Rogerio, F; Vieira, AS, 2016)		2.18
"Temozolomide (TMZ) is an alkylating agent that has become the mainstay treatment of the most malignant brain cancer, glioblastoma multiforme (GBM). "( Zinc enhances temozolomide cytotoxicity in glioblastoma multiforme model systems.
Assoulin, M; Constantini, S; Daniels, D; Fisher, T; Freedman, S; Guez, D; Last, D; Mardor, Y; Mehrian-Shai, R; Moshe, I; Pismenyuk, T; Reichardt, JK; Simon, AJ; Toren, A; Yalon, M, 2016)		2.24
"Temozolomide (TMZ) is a DNA-methylating agent."( Current and Future Drug Treatments for Glioblastomas.
Hirose, Y; Ohba, S, 2016)		1.16
"Temozolomide (TMZ) is an oral imidazotetrazine methylating agent which is used for the treatment of glioblastoma multiforme (GBM). "( Acute temozolomide induced liver injury: mixed type hepatocellular and cholestatic toxicity.
Agan, AF; Altınok, AY; Aygun, C; Balaban, Y; Çakır, A, )		2.05
"Temozolomide (TMZ) is an alkylating agent used for the treatment of aggressive forms of brain tumor based on its antitumor actions. "( Temozolomide inhibits cellular growth and motility via targeting ERK signaling in glioma C6 cells.
Gao, S; Liang, J; Wang, W; Wang, Y, 2016)		3.32
"Temozolomide is a commonly used chemotherapy drug and frequently causes lymphocytopenia."( Cutaneous invasive aspergillosis in a patient with glioblastoma receiving long-term temozolomide and corticosteroid therapy.
Hatakeyama, S; Ikeda, T; Morisawa, Y; Norizuki, M; Okabe, T; Onishi, T; Sasahara, T; Suzuki, J; Toshima, M; Yokota, H, 2017)		1.4
"Temozolomide (TMZ) is an alkylating agent used for treatment of brain neoplasms and levetiracetam (LEV) is a commonly used antiepileptic. "( Acute liver injury induced by levetiracetam and temozolomide co-treatment.
Abu Rmeileh, A; Benson, AA; Chen, S; Cohen, J; Daher, S; Khoury, T; Mizrahi, M; Yaari, S, 2017)		2.15
"Temozolomide (TMZ) is a novel cytotoxic agent used as first-line chemotherapy for GBM, however, some individual cells can't be isolated for surgical resection and show treatment-resistance, thus inducing poor prognosis."( MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression.
Chen, C; Chen, W; Ge, XS; He, J; Kong, KK; Li, FC; Li, H; Li, JL; Li, P; Wang, F; Xu, XK, 2017)		1.4
"Temozolomide (TMZ) is an oral imidazotetrazine methylating agent which is used for the treatment of glioblastoma multiforme (GBM). "( Acute temozolomide induced liver injury : Mixed type hepatocellular and cholestatic toxicity.
Agan, AF; Altınok, AY; Aygun, C; Balaban, Y; Çakır, A, )		2.05
"Temozolomide is an alkylating agent which crosses the blood brain barrier and has demonstrated antitumor activity against a broad range of tumor types, including malignant glioma, melanoma, non small cell lung cancer and carcinoma of the ovary and colon."( Phase I trial of weekly docetaxel and daily temozolomide in patients with metastatic disease.
Bukowski, RM; Dreicer, R; Elson, P; Mekhail, T; Olencki, T; Roman, S; Tamaskar, I, 2008)		1.33
"The temozolomide is a promising orally cytotoxic agent used in malignant glioma. "( The safety of the temozolomide in patients with malignant glioma.
Dario, A; Tomei, G, 2006)		1.23
"Temozolomide is a relatively new chemotherapeutic agent frequently associated with selective CD4+ T-lymphocytopenia. "( Disseminated salmonellosis in a patient treated with temozolomide.
Adachi, J; Georgescu, G; Isola, IM; Rolston, K; Youssef, S, 2008)		2.04
"Temozolomide is a novel oral chemotherapeutic drug that penetrates into the brain and has a low incidence of adverse effects."( Temozolomide for high grade glioma.
Garside, R; Grant, R; Hart, MG; Rogers, G; Somerville, M; Stein, K, 2008)		2.51
"Temozolomide is an effective therapy in GBM for prolonging survival and delaying progression as part of primary therapy without impacting on QoL and with a low incidence of early adverse events. "( Temozolomide for high grade glioma.
Garside, R; Grant, R; Hart, MG; Rogers, G; Somerville, M; Stein, K, 2008)		3.23
"Temozolomide is an alkylating agent approved for treatment of glioblastoma in association with radiotherapy."( [Alveolo-interstitial pneumonia due to Temozolamide].
Autret-Leca, E; Beau Salinas, F; Carré, P; de Luca, K; Diot, P; Guilleminault, L; Narciso, B, 2008)		1.79
"Temozolomide (TMZ) is a cytotoxic agent of the imidazotetrazine class, chemically related to dacarbazine. "( Tuberculosis in a patient on temozolomide: a case report.
de Barros e Silva, MJ; de Paiva, TF; Fanelli, MF; Gimenes, DL; Rinck, JA, 2009)		2.09
"Temozolomide is an effective alkylating agent that is increasingly used for the treatment of pediatric brain tumors. "( Treatment-related myelodysplastic syndrome after temozolomide use in a child: first report.
Auger, N; Bhangoo, R; Da Costa, L; Dufour, C; Grill, J; Jullien, M, 2008)		2.04
"Temozolomide is a newly developed chemotherapeutic agent in central nervous system tumors."( Efficacy of temozolomide for recurrent embryonal brain tumors in children.
Chang, KP; Hsu, TR; Wang, CH; Wong, TT, 2009)		1.45
"Temozolomide is a novel cytotoxic agent for malignant gliomas. "( Carboplatin and oral cyclophosphamide combination after temozolomide failure in malignant gliomas.
Benekli, M; Buyukberber, S; Coskun, U; Kaya, AO; Ozturk, B; Uner, A; Yamac, D; Yaman, E; Yildiz, R, )		1.82
"Temozolomide (TMZ) is an oral anticancer agent approved for the treatment of newly diagnosed glioblastoma in combination with radiotherapy. "( Recent approaches to improve the antitumor efficacy of temozolomide.
Graziani, G; Tentori, L, 2009)		2.04
"Temozolomide (TMZ) is an alkylating agent used in the management of gliomas. "( Long-term use of temozolomide: could you use temozolomide safely for life in gliomas?
Bell, D; Khasraw, M; Wheeler, H, 2009)		2.14
"Temozolomide is a new drug which has shown promise in treating malignant gliomas and other difficult-to-treat tumors."( Temozolomide with radiation therapy in high grade brain gliomas: pharmaceuticals considerations and efficacy; a review article.
Beli, I; Chaldeopoulos, D; Fotineas, A; Koukourakis, GV; Kouloulias, V; Kouvaris, J; Maravelis, G; Pantelakos, P; Papadimitriou, C; Zacharias, G, 2009)		2.52
"Temozolomide is an oral alkylating cytotoxic agent of second generation, used in the treatment of high-grade gliomas."( [Prescription guidebook for temozolomide usage in brain tumors].
Borget, I; Brignone, M; Cartalat-Carel, S; Chinot, O; Hassani, Y; Taillandier, L; Taillibert, S; Tilleul, P, 2009)		1.37
"Temozolomide is a well-tolerated oral chemotherapy in patients with malignant DET, including those who have already received treatment. "( Temozolomide: a safe and effective treatment for malignant digestive endocrine tumors.
Couvelard, A; Faivre, S; Hammel, P; Hentic, O; Larroque, B; Lévy, P; Maire, F; Raymond, E; Ruszniewski, P; Yapur, L; Zappa, M, 2009)		3.24
"Temozolomide (TMZ) is an oral alkylating agent with significant activity against glioblastoma multiforme (GBM) and melanoma. "( Non-Hodgkin lymphoma following temozolomide.
Das, P; Dwary, A; Goyal, S; Gupta, D; Mohanti, BK; Muzumder, S; Sharma, A; Thulkar, S, 2009)		2.08
"Temozolomide (TMZ) is an oral alkylating agent that is regarded as a tolerable and effective drug. "( Temozolomide in malignant gliomas: current use and future targets.
Bressler, LR; Seery, TE; Villano, JL, 2009)		3.24
"Temozolomide (TMZ) is a methylating agent used in chemotherapy against glioblastoma. "( DNA ligase IV as a new molecular target for temozolomide.
Kondo, N; McKinnon, PJ; Mori, E; Nakase, H; Ohnishi, K; Ohnishi, T; Sakaki, T; Takahashi, A, 2009)		2.06
"Temozolomide (TMZ) is an alkylating cytostaticum."( Temozolomide treatment of a pituitary carcinoma and two pituitary macroadenomas resistant to conventional therapy.
Andersen, M; Hagen, C; Hansen, S; Schroeder, HD, 2009)		2.52
"Temozolomide (TMZ) is a second-generation alkylating agent that has recently shown some efficacy in stage IV melanoma. "( Temozolomide and cisplatin combination in naive patients with metastatic cutaneous melanoma: results of a phase II multicenter trial.
Bedane, C; Guillet, G; Guillot, B; Mourey, L; Sassolas, B; Tourani, JM; Wierzbicka-Hainaut, E, 2010)		3.25
"Temozolomide is an easily administered, well-tolerated chemotherapeutic option in advanced or recurrent uterine leiomyosarcomas with a reasonable response rate. "( Temozolomide in advanced and recurrent uterine leiomyosarcoma and correlation with o6-methylguanine DNA methyltransferase expression: a case series.
Atkins, KA; Ferriss, JS; Jazaeri, AA; Lachance, JA; Modesitt, SC, 2010)		3.25
"Temozolomide (TMZ) is a pro-drug releasing a DNA alkylating agent that is the most effective drug to treat glial tumors when combined with radiation. "( Temozolomide delivery to tumor cells by a multifunctional nano vehicle based on poly(β-L-malic acid).
Black, KL; Ding, H; Holler, E; Hu, J; Inoue, S; Konda, B; Ljubimova, JY; Patil, R; Portilla-Arias, J; Shin, PK; Wawrowsky, KA, 2010)		3.25
"Temozolomide (TMZ) is a recently introduced alkylating agent that has yielded significant benefits and become a key agent in the treatment of high-grade gliomas."( Gene expression profiling predicts response to temozolomide in malignant gliomas.
Fukushima, T; Katayama, Y; Naruse, N; Ogino, A; Ohta, T; Okamoto, Y; Sano, E; Tsumoto, K; Watanabe, T; Yachi, K; Yoshino, A, 2010)		1.34
"Temozolomide is an oral alkylating agent with established antitumor activity in patients with primary brain tumors and melanoma. "( Dose-dense temozolomide regimens: antitumor activity, toxicity, and immunomodulatory effects.
Hwu, WJ; Neyns, B; Reardon, DA; Tosoni, A, 2010)		2.19
"Temozolomide (TMZ) is a monofunctional methylating agent which is spontaneously activated in aqueous solution into the dacarbazine metabolite 5-(3-methyl-1-triazeno)imidazole-4-carboxamide. "( The use of temozolomide for the treatment of malignant tumors: clinical evidence and molecular mechanisms of action.
Bei, R; Marzocchella, L; Turriziani, M, 2010)		2.19
"Temozolomide (TMZ) is an oral alkylating agent with proven antitumoral activity in preclinical and clinical studies in adults with high-grade glioma (HGG). "( Feasibility study of 21-day-on/7-day-off temozolomide in children with brain tumors.
Barone, G; Lazzareschi, I; Riccardi, R; Ridola, V; Rizzo, D; Ruggiero, A, 2011)		2.08
"Temozolomide is an active agent in metastatic pancreatic endocrine carcinomas. "( First-line chemotherapy with capecitabine and temozolomide in patients with metastatic pancreatic endocrine carcinomas.
Chen, DT; Choi, J; Coppola, D; Fine, RL; Helm, J; Kvols, L; Nasir, A; Strosberg, JR, 2011)		2.07
"Temozolomide (TMZ) is an alkylating agent licensed for treatment of high-grade glioma (HGG). "( Temozolomide versus procarbazine, lomustine, and vincristine in recurrent high-grade glioma.
Beall, S; Brada, M; Collins, VP; Erridge, S; Gabe, R; Gattamaneni, R; Hopkins, K; Lee, SM; Levy, D; Rampling, R; Saran, F; Stenning, S; Thompson, LC, 2010)		3.25
"Temozolomide is an oral alkylating agent approved for the treatment of glioblastoma and anaplastic astrocytoma, and is currently under clinical investigation for the treatment of brain metastases from a variety of cancers. "( Urticarial hypersensitivity reaction caused by temozolomide.
Hsu, MY; Ibrahimi, OA; Kesari, S; Pothiawala, S; Yang, C, 2010)		2.06
"Temozolomide (TMZ) is an oral alkylating agent used for the treatment of high-grade gliomas. "( Acquisition of temozolomide chemoresistance in gliomas leads to remodeling of mitochondrial electron transport chain.
Bailey, SM; Darley-Usmar, VM; Diers, A; Gillespie, GY; Griguer, CE; Landar, A; Markert, JM; McClugage, SG; Nozell, SE; Oliva, CR; Sarkaria, JN, 2010)		2.16
"Temozolomide is an oral alkylating agent approved for glioblastoma multiforme treatment that has only recently shown promise in treating some pituitary tumors."( Temozolomide for corticotroph pituitary adenomas refractory to standard therapy.
Delashaw, JB; Dillard, TH; Fleseriu, M; Gultekin, SH; Neuwelt, EA; Yedinak, CG, 2011)		2.53
"Temozolomide (TMZ) is an oral alkylating agent with demonstrated efficacy as second-line therapy for patients with recurrent anaplastic astrocytoma and glioblastoma multiforme (GBM). "( The outcomes of concomitant radiation plus temozolomide followed by adjuvant temozolomide for newly diagnosed high grade gliomas: the preliminary results of single center prospective study.
Abo Hamar, AH; El-Shorbagy, D; Galal, S; Shawky, H; Zakaria, F, 2009)		2.06
"Temozolomide (TMZ) is an alkylating chemotherapeutic agent that has recently been used in some cases as a new therapeutic tool for pituitary carcinomas and aggressive pituitary adenomas. "( Temozolomide-induced shrinkage of a pituitary carcinoma causing Cushing's disease--report of a case and literature review.
Altavilla, G; Cannavò, S; Curtò, L; Ferraù, F; Granata, F; Hofland, LJ; Longo, M; Pitini, V; Torre, ML; Trimarchi, F, 2010)		3.25
"Temozolomide is a second-generation alkylating chemotherapeutic agent, introduced to therapy of primary brain tumors in the 1990s."( Temozolomide: Expanding its role in brain cancer.
Adair, J; Kiem, HP; Mrugala, MM, 2010)		2.52
"Temozolomide is an alkylating agent recently employed in older patients with newly diagnosed glioblastoma."( Treatment of glioblastoma in elderly patients: an overview of current treatments and future perspective.
Lanzetta, G; Minniti, G, )		0.85
"Temozolomide is an alkylating chemotherapeutic agent used routinely in the management of high grade gliomas."( MGMT immunoexpression in adamantinomatous craniopharyngiomas.
Altuntaş, Y; Aydın, Y; Karaman, O; Müslüman, AM; Ozderya, A; Ozkayalar, H; Oztürk, FY; Tanık, C; Zuhur, SS, 2011)		1.09
"Temozolomide (TMZ) is a DNA-alkylating agent used for the treatment of glioma, astrocytoma, and melanoma."( A novel approach to overcome temozolomide resistance in glioma and melanoma: Inactivation of MGMT by gene therapy.
Jiang, G; Liu, YQ; Pei, DS; Wei, ZP; Xin, Y; Zheng, JN, 2011)		1.38
"Temozolomide (TMZ) is an oral alkylating agent that has been widely used in the treatment of refractory glioma, although inherent and acquired resistance to this drug is common. "( Enhancement of temozolomide-induced apoptosis by valproic acid in human glioma cell lines through redox regulation.
Chang, YJ; Chen, CH; Chung, KT; Ku, MS; Yang, JT, 2011)		2.16
"Temozolomide is an effective treatment for seizure control in patients with brain tumors."( Seizure control: a secondary benefit of chemotherapeutic temozolomide in brain cancer patients.
Hu, A; Kesari, S; Kim, RY; Lee, JW; Nguyen, A; Xu, Z, 2011)		1.34
"Temozolomide (TMZ) is a widely used oral alkylating agent that has been associated with the development of severe hematologic adverse events (HAEs). "( Hematologic adverse events associated with temozolomide.
Abdur, S; Bressler, LR; Letarte, N; Villano, JL; Yu, JM, 2012)		2.08
"Temozolomide (TMZ), is a new alkylating agent with promising antitumour efficacy for malignant gliomas, and the effect of TMZ on GSCs invasion has not been known."( Temozolomide decreases invasion of glioma stem cells by down-regulating TGF-β2.
Jing, Z; Qiu, B; Wang, Y; Wu, A; Zhang, D, 2011)		2.53
"Temozolomide (TMZ) is an oral derivative of dacarbazine that induces DNA damage by methylating nucleotide bases. "( Multicenter phase II trial of temozolomide in mycosis fungoides/sezary syndrome: correlation with O⁶-methylguanine-DNA methyltransferase and mismatch repair proteins.
Baron, J; Dolan, ME; Foss, F; Guitart, J; Kuzel, TM; Pezen, DS; Querfeld, C; Rademaker, A; Rosen, ST; Yarosh, DB, 2011)		2.1
"Temozolomide (TMZ) is an oral alkylating agent with activity in high and LGG."( Using different schedules of Temozolomide to treat low grade gliomas: systematic review of their efficacy and toxicity.
Athanasiou, T; Lashkari, HP; Moreno, L; Saso, S; Zacharoulis, S, 2011)		1.38
"Temozolomide (TMZ) is an alkylating agent that has yielded significant benefits and is a current standard agent in the treatment of malignant gliomas. "( Gene expression profiles predicting the response to IFN-β and a combination of temozolomide and IFN-β in malignant gliomas.
Fukushima, T; Katayama, Y; Ogino, A; Ohta, T; Okamoto, Y; Sano, E; Tashiro, S; Tsumoto, K; Watanabe, T; Yachi, K; Yoshino, A, 2011)		2.04
"Temozolomide is an active drug against gliomas in adults. "( Temozolomide in relapsed pediatric brain tumors: 14 cases from a single center.
Akyüz, C; Büyükpamukçu, M; Demir, HA; Kutluk, T; Varan, A; Yalçin, B, 2012)		3.26
"Temozolomide (TMZ) is a novel cytotoxic alkylating agent for chemotherapy of malignant gliomas. "( Chemoresistance to temozolomide in human glioma cell line U251 is associated with increased activity of O6-methylguanine-DNA methyltransferase and can be overcome by metronomic temozolomide regimen.
Dong, XT; Li, JM; Li, Y; Pan, Q; Wang, HM; Wang, W; Yang, XJ, 2012)		2.15
"Temozolomide (TMZ) is an alkylating agent used for treating gliomas. "( Acquisition of chemoresistance in gliomas is associated with increased mitochondrial coupling and decreased ROS production.
Gillespie, GY; Griguer, CE; Moellering, DR; Oliva, CR, 2011)		1.81
"Temozolomide (TMZ) is an alkylating, antineoplastic agent which is being used to treat cases of refractory anaplastic astrocytoma, newly-diagnosed glioblastoma multiforme and metastatic melanoma. "( Temozolomide-related infections: review of the literature.
Aksoy, S; Altundag, K; Ararat, E; Kizilarslanoglu, MC; Sahin, I; Yildirim, NO, )		3.02
"Temozolomide is an oral chemotherapy agent, which has been used as a salvage therapy to treat aggressive pituitary adenomas and carcinomas, including prolactinomas, unresponsive to all conventional treatment."( Temozolomide in the management of dopamine agonist-resistant prolactinomas.
Aylwin, SJ; Barazi, S; Buchanan, CR; Dworakowska, D; Gilbert, JA; Hampton, T; King, AP; Landau, DB; Lipscomb, D; Riordan-Eva, P; Thomas, NW; Whitelaw, BC, 2012)		2.54
"Temozolomide is an oral alkylating agent with clinical activity against glioblastoma multiforme (GM). "( Temozolomide-associated bronchiolitis obliterans organizing pneumonia successfully treated with high-dose corticosteroid.
Ban, HJ; Chi, SY; Kang, HW; Kim, KS; Kim, TO; Kim, YC; Kim, YI; Kwon, YS; Lim, SC; Oh, IJ, 2012)		3.26
"Temozolomide (TMZ) is an alkylating chemotherapeutic agent that prolongs the survival of patients with glioblastoma. "( Distinct molecular mechanisms of acquired resistance to temozolomide in glioblastoma cells.
Florea, AM; Happold, C; Reifenberger, G; Roth, P; Schmidt, N; Silginer, M; Weller, M; Wick, W, 2012)		2.07
"Temozolomide is an alkylating agent used in the treatment of gliomas and, more recently, aggressive pituitary adenomas and carcinomas. "( Temozolomide in aggressive pituitary adenomas and carcinomas.
Fadul, CE; Horvath, E; Kovacs, K; Ortiz, LD; Rotondo, F; Scheithauer, BW; Syro, LV; Uribe, H, 2012)		3.26
"Temozolomide is an effective agent in HGGs with favorable outcome and low toxicity profile even in advanced age."( Long term experience in high grade glial tumors with temozolomide.
Akmansu, M; Baykara, M; Benekli, M; Buyukberber, S; Coskun, U; Demirci, U; Uner, A; Yamac, D; Yaman, E, )		1.82
"Temozolomide (TMZ) is an oral alkylating agent widely used in the treatment of refractory glioma. "( The synergistic therapeutic effect of temozolomide and hyperbaric oxygen on glioma U251 cell lines is accompanied by alterations in vascular endothelial growth factor and multidrug resistance-associated protein-1 levels.
Cao, K; Li, QY; Lu, PS; Lu, XY; Yuan, ZC, 2012)		2.09
"Temozolomide is an attractive candidate treatment in neuroblastoma with methylated MGMT, especially in central nervous system relapsed cases."( Efficacy of temozolomide in a central nervous system relapse of neuroblastoma with O 6 -methylguanine methyltransferase (MGMT) promoter methylation.
Marutsuka, K; Moritake, H; Nunoi, H; Shimonodan, H; Takeshima, H; Yamada, A; Yokogami, K, 2013)		1.49
"Temozolomide (TMZ) is an antineoplastic alkylating agent with activity against serious and aggressive types of brain tumours. "( In situ electrochemical evaluation of anticancer drug temozolomide and its metabolites-DNA interaction.
Lopes, IC; Oliveira, SC; Oliveira-Brett, AM, 2013)		2.08
"Temozolomide (TMZ) is a prodrug for an alkylating agent used for the treatment of malignant brain tumors. "( An efficient and practical radiosynthesis of [11C]temozolomide.
Carlin, SM; Hooker, JM; Moseley, CK; Neelamegam, R, 2012)		2.07
"Temozolomide is an alkylating agent approved for treating malignant gliomas."( Impact of temozolomide on gonadal function in patients with primary malignant brain tumors.
Blackwood, R; Brown, M; Harmon, M; Lesser, G; Lovato, J; Strowd, RE; Yalcinkaya, T, 2013)		1.51
"Temozolomide (TMZ) is an alkylating agent and was a first-line chemotherapeutic agent for malignant gliomas. "( DNA mismatch repair protein (MSH6) correlated with the responses of atypical pituitary adenomas and pituitary carcinomas to temozolomide: the national cooperative study by the Japan Society for Hypothalamic and Pituitary Tumors.
Amano, K; Arita, K; Asano, K; Fujio, S; Fukuhara, N; Hirohata, T; Hizuka, N; Ikeda, H; Ishii, Y; Isozaki, O; Iwai, Y; Kawamata, T; Matsuno, A; Nishioka, H; Ogawa, Y; Osamura, RY; Sakata, K; Shimatsu, A; Tahara, S; Takano, K; Takano, S; Teramoto, A; Tominaga, A; Yamada, S, 2013)		2.04
"Temozolomide is an imidazotetrazine with a mechanism of action and efficacy similar to dacarbazine (DTIC). "( Temozolomide: a novel oral alkylating agent.
Danson, SJ; Middleton, MR, 2001)		3.2
"Temozolomide (TZM) is a novel methylating agent currently under investigation for treatment of recurrent high-grade gliomas. "( Poly(ADP-ribose) polymerase inhibitor increases growth inhibition and reduces G(2)/M cell accumulation induced by temozolomide in malignant glioma cells.
Graziani, G; Navarra, P; Portarena, I; Scerrati, M; Tentori, L; Torino, F, 2002)		1.97
"Temozolomide is a novel second-generation oral alkylating agent with demonstrated efficacy and safety in patients with recurrent glioblastoma multiforme (GBM) and anaplastic astrocytoma (AA). "( A phase II study of temozolomide in patients with newly diagnosed supratentorial malignant glioma before radiation therapy.
Friedman, HS; Gilbert, MR; Kuttesch, JF; Olson, JJ; Prados, MD; Reaman, GH; Zaknoen, SL, 2002)		2.08
"Temozolomide is a new cytotoxic alkylating agent that has recently been approved in Portugal for the treatment of recurrent high-grade glioma. "( Temozolomide in second-line treatment after prior nitrosurea-based chemotherapy in glioblastoma multiforme: experience from a Portuguese institution.
Albano, J; Cernuda, M; Garcia, I; Lima, L; Oliveira, C; Portela, I; Teixeira, MM, 2002)		3.2
"Temozolomide is an alkylating cytostatic drug that finds increasing application in the treatment of melanoma, anaplastic astrocytoma and glioblastoma multiforme. "( Temozolomide induces apoptosis and senescence in glioma cells cultured as multicellular spheroids.
Arnold, H; Damasceno, R; Günther, W; Pawlak, E; Terzis, AJ, 2003)		3.2
"Temozolomide is a prodrug that undergoes spontaneous chemical degradation at physiologic pH to form the highly reactive alkylating agent, methyl-triazenyl imidazole carboxamide (MTIC). "( Plasma and cerebrospinal fluid pharmacokinetics of intravenous temozolomide in non-human primates.
Balis, FM; Godwin, K; McCully, C; Patel, M, 2003)		2
"Temozolomide (TMZ) is a chemotherapeutic agent used in the treatment of high-grade brain tumors. "( Formation of DNA adducts and induction of lacI mutations in Big Blue Rat-2 cells treated with temozolomide: implications for the treatment of low-grade adult and pediatric brain tumors.
Berger, MS; Bodell, WJ; Gaikwad, NW; Miller, D, 2003)		1.98
"Temozolomide is an imidazotetrazine with a mechanism of action similar to dacarbazine and equivalent activity in melanoma. "( Randomized phase II study of temozolomide given every 8 hours or daily with either interferon alfa-2b or thalidomide in metastatic malignant melanoma.
Arance, A; Ashcroft, L; Clamp, A; Danson, S; Hodgetts, J; Lomax, L; Lorigan, P; Middleton, MR; Ranson, M; Thatcher, N, 2003)		2.05
"Temozolomide (TMZ) is an oral alkylating agent with a good safety profile and proven efficacy in the treatment of malignant glioma. "( Phase I study of temozolamide (TMZ) combined with procarbazine (PCB) in patients with gliomas.
Foster, T; Newlands, ES; Zaknoen, S, 2003)		1.76
"Temozolomide (TMZ) is a lipophilic methylating agent used in the therapy of malignant melanoma and other tumors."( Inhibition of angiogenesis by non-toxic doses of temozolomide.
Kurzen, H; Möhler, T; Näher, H; Schmitt, S, 2003)		1.29
"Temozolomide is an oral alkylating agent that readily crosses the blood-brain barrier and has activity in patients with advanced melanoma. "( A phase I (tumour site-specific) study of carboplatin and temozolomide in patients with advanced melanoma.
Boxall, J; Marples, M; Meyer, T; Napier, MP; Rustin, GJ; Strauss, SJ, 2003)		2.01
"Temozolomide (TMZ) is a DNA methylating agent that has shown promising antitumor activity in recent clinical trials against high grade gliomas, metastatic melanoma, and brain lymphoma. "( Systemic administration of GPI 15427, a novel poly(ADP-ribose) polymerase-1 inhibitor, increases the antitumor activity of temozolomide against intracranial melanoma, glioma, lymphoma.
D'Amati, G; Graziani, G; Kalish, V; Leonetti, C; Portarena, I; Scarsella, M; Tentori, L; Vergati, M; Xu, W; Zhang, J; Zupi, G, 2003)		1.97
"Temozolomide (TMZ) is a DNA alkylating agent currently used as adjuvant treatment for anaplastic astrocytomas. "( Inhibition of DNA repair for sensitizing resistant glioma cells to temozolomide.
Bedwell, J; Germano, IM; Kanzawa, T; Kondo, S; Kondo, Y, 2003)		2
"Temozolomide is an oral alkylating chemotherapy agent licensed for the treatment of recurrent high-grade gliomas, anaplastic astrocytoma (AA) and glioblastoma multiforme (GBM)."( Temozolomide in radio-chemotherapy combined treatment for newly-diagnosed glioblastoma multiforme: phase II clinical trial.
Campanella, C; Costa, A; Fedele, F; Frati, A; Frati, L; Gagliardi, FM; Innocenzi, G; Lanzetta, G; Minniti, G; Nappa, M; Rozzi, A; Salvati, M; Vecchione, A, )		2.3
"Temozolomide is an alkylating agent that mediates its cytotoxic effects via O(6)-methylguanine (O(6)-meG) adducts in DNA and their recognition and processing by the postreplication mismatch repair system (MMR). "( Dual repair modulation reverses Temozolomide resistance in vitro.
Barvaux, VA; Brown, R; Margison, GP; McElhinney, RS; McMurry, TB; Ranson, M, 2004)		2.05
"Temozolomide appears to be an ideal, first-line, single-agent, with a safe profile and demonstrated HQL benefits in patients with high-grade gliomas."( Temozolomide as first-line agent in treating high-grade gliomas: phase II study.
Andreuccetti, M; Benvenuti, L; Buxton, N; Caprio, A; Carnesecchi, S; Chibbaro, S; Faggionato, F; Gagliardi, R; Galli, C; Pulerà, F; Serino, D, )		3.02
"Temozolomide is an oral chemotherapeutic agent with efficacy against malignant gliomas and a favorable safety profile."( Phase II study of temozolomide without radiotherapy in newly diagnosed glioblastoma multiforme in an elderly populations.
Barrie, M; Braguer, D; Chinot, OL; Dufour, H; Figarella-Branger, D; Frauger, E; Grisoli, F; Hoang-Xuan, K; Martin, PM; Moktari, K; Palmari, J; Peragut, JC, 2004)		1.38
"Temozolomide (Temodal) is an oral imidazotetrazine. "( Prolonged schedule of temozolomide (Temodal) plus liposomal doxorubicin (Caelyx) in advanced solid cancers.
Awada, A; de Valeriola, D; Dubuisson, M; Gil, T; Klastersky, J; Moerman, C; Piccart, MJ; Sales, F; Vereecken, P, 2004)		2.08
"Temozolomide is a well-tolerated oral alkylating agent with activity in the CNS. "( Temozolomide for the treatment of brain metastases associated with metastatic melanoma: a phase II study.
Agarwala, SS; Atkins, M; Buzaid, A; Czarnetski, B; Dreno, B; Gore, M; Kirkwood, JM; Rankin, EM; Skarlos, D; Thatcher, N, 2004)		3.21
"Temozolomide is a well-tolerated alkylating agent, that is able to permeate the blood-brain barrier (BBB), and has additive cytotoxicity when given with radiotherapy (RT). "( Salvage chemotherapy with temozolomide in primary CNS lymphomas: preliminary results of a phase II trial.
Abbadessa, A; Bernardi, D; Bordonaro, R; Candela, M; Dell'Oro, S; Ferreri, AJ; Franceschi, E; Latte, G; Mason, W; Pace, A; Perry, J; Reni, M; Stelitano, C; Villa, E; Zaja, F, 2004)		2.07
"Temozolomide is an oral alkylating agent that can cross the blood-brain barrier and in phase II and III trials, patients with advanced metastatic melanoma achieved overall response rates of 13 to 21%."( The effect of temozolomide-based chemotherapy in patients with cerebral metastases from melanoma.
Bafaloukos, D; Briassoulis, E; Christodoulou, C; Fountzilas, G; Gogas, H; Hatzichristou, H; Kalofonos, HP; Linardou, H; Panagiotou, P; Tsoutsos, D, 2004)		1.41
"Temozolomide (TMZ) is a new oral alkylating agent which has proven to be as active as dacarbazine (DTIC) in the treatment of melanoma, but with a lower toxicity. "( Temozolomide and interferon-alpha in metastatic melanoma: a phase II study of the Italian Melanoma Intergroup.
Amaducci, L; Biasco, G; Guida, M; Leoni, M; Michiara, M; Poletti, P; Ravaioli, A; Ridolfi, R; Romanini, A; Sileni, VC, 2004)		3.21
"Temozolomide is an oral alkylating agent shown to have modest efficacy in the treatment of glioblastoma multiforme. "( Transcriptional targeting of adenovirally delivered tumor necrosis factor alpha by temozolomide in experimental glioblastoma.
Gillespie, GY; Kufe, DW; Weichselbaum, RR; Yamini, B; Yu, X, 2004)		1.99
"Temozolomide is an alkylating agent that mediates its cytotoxic effects via O(6)-methylguanine (O(6)-meG) adducts in DNA. "( Sensitization of a human ovarian cancer cell line to temozolomide by simultaneous attenuation of the Bcl-2 antiapoptotic protein and DNA repair by O6-alkylguanine-DNA alkyltransferase.
Barvaux, VA; Gillum, AM; Lorigan, P; Margison, GP; McElhinney, RS; McMurry, TB; Ranson, M, 2004)		2.02
"Temozolomide (TMZ) is a methylating agent with promising antitumor efficacy for the treatment of melanomas and intermediate-grade gliomas. "( The piperidine nitroxide Tempol potentiates the cytotoxic effects of temozolomide in human glioblastoma cells.
Cereda, E; Gariboldi, MB; Monti, E; Ravizza, R, 2004)		2
"Temozolomide seems to be a promising drug in the chemotherapy of malignant gliomas and can be applied as a second line chemotherapy, as well."( Temozolomide chemotherapy of patients with recurrent anaplastic astrocytomas and glioblastomas.
Afra, D; Sipos, L; Vitanovics, D, 2004)		2.49
"Temozolomide (TMZ) is an oral alkylating agent that produces methyl adducts at the 0.6 position of guanine. "( Temozolomide and cisplatin versus temozolomide in patients with advanced melanoma: a randomized phase II study of the Hellenic Cooperative Oncology Group.
Bafaloukos, D; Briassoulis, E; Chalkidou, S; Christodoulou, C; Efstathiou, E; Fountzilas, G; Gogas, H; Iconomou, T; Kalofonos, H; Kouroussis, C; Linardou, E; Panagiotou, P; Polyzos, A; Tsoutsos, D, 2005)		3.21
"Temozolomide (TMZ) is a promising new drug that seems to be effective in patients with recurrent disease."( Adjuvant chemotherapy in the treatment of high grade gliomas.
Brandes, AA; Lonardi, S; Tosoni, A, 2005)		1.05
"Temozolomide (TMZ) is an oral alkylating agent; it produces DNA methyl adducts, which are removed by the DNA repair enzyme AGAT. "( Temozolomide and cisplatin in avdanced malignant melanoma.
Ascierto, PA; Comella, G; Daponte, A; Gravina, A; Melucci, M; Ottaiano, A; Palmieris, G; Scala, S; Simeone, E, )		3.02
"Temozolomide (TMZ) is an alkylating agent that was approved for anaplastic astrocytoma and glioblastoma. "( Optimal role of temozolomide in the treatment of malignant gliomas.
Hegi, ME; Stupp, R; van den Bent, MJ, 2005)		2.12
"Temozolomide (TMZ) is an oral alkylating agent with demonstrated efficacy as therapy for glioblastoma multiforme (GBM) and anaplastic astrocytoma. "( Economic evaluation of temozolomide in the treatment of recurrent glioblastoma multiforme.
Hallinen, T; Kivioja, A; Martikainen, JA; Vihinen, P, 2005)		2.08
"Temozolomide is an oral alkylating agent that has equivalent activity to dacarbazine, but it has the advantage of CNS penetration."( A phase II study of biochemotherapy for advanced melanoma incorporating temozolomide, decrescendo interleukin-2 and GM-CSF.
Anderson, C; Baron, A; Gibbs, P; Gonzalez, R; Lewis, KD; O'Day, S; Richards, J; Russ, P; Weber, J; Zeng, C, 2005)		1.28
"Temozolomide is a DNA-methylating agent used in the treatment of malignant gliomas. "( Poly(ADP-ribose) polymerase-1 inhibition reverses temozolomide resistance in a DNA mismatch repair-deficient malignant glioma xenograft.
Ali-Osman, F; Bigner, DD; Cheng, CL; Dolan, ME; Friedman, HS; Johnson, SP; Keir, ST; Li, H; Modrich, P; Quinn, JA; Salzman, AL; Szabo, C, 2005)		2.02
"Temozolomide is a well-tolerated agent that results in objective responses and stabilisation of disease."( Phase II study of two-weekly temozolomide in patients with high-grade gliomas.
Ashley, D; Cher, L; Dowling, A; Jennens, R; Rosenthal, MA; Wong, S; Woods, AM, 2006)		1.35
"Temozolomide appears to be an ideal, first-line, single-agent, with a safe profile and demonstrated HQL benefits in patients with high-grade gliomas."( Surgery, radiotherapy and temozolomide in treating high-grade gliomas.
Barbarisi, M; Moraci, A; Moraci, M; Parlato, C, 2006)		1.36
"Temozolomide (TMZ) is a methylating agent which prolongs survival when administered during and after radiotherapy in the first-line treatment of glioblastoma and which also has significant activity in recurrent disease. "( O6-methylguanine DNA methyltransferase and p53 status predict temozolomide sensitivity in human malignant glioma cells.
Hermisson, M; Kaina, B; Klumpp, A; Nagel, G; Roos, W; Weller, M; Wick, W; Wischhusen, J, 2006)		2.02
"Temozolomide (TMZ) is an alkylating agent earlier approved for recurrent anaplastic astrocytoma and approved for the treatment of newly diagnosed glioblastoma in the USA and Europe in 2005. "( Temozolomide: a milestone in the pharmacotherapy of brain tumors.
Steinbach, JP; Weller, M; Wick, W, 2005)		3.21
"Temozolomide is an oral alkylating agent that crosses the blood-brain barrier, and has preclinical activity in breast cancer. "( Temozolomide in metastatic breast cancer (MBC): a phase II trial of the National Cancer Institute of Canada - Clinical Trials Group (NCIC-CTG).
Bordeleau, L; Charpentier, D; Crump, M; Eisenhauer, E; Matthews, S; Trudeau, ME; Yelle, L, 2006)		3.22
"Temozolomide is a rapidly absorbed chemotherapeutic agent, achieving significant central nervous system penetration. "( Alternating chemo-immunotherapy with temozolomide and low-dose interleukin-2 in patients with metastatic melanoma.
Hansson, J; Månsson-Brahme, E; Masucci, GV; Nilsson, B; Ragnarsson-Olding, B; Wagenius, G, 2006)		2.05
"Temozolomide is a novel oral alkylating agent, active against metastatic melanoma. "( Phase II multicentre study of temozolomide in combination with interferon alpha-2b in metastatic malignant melanoma.
Crespo, C; del Muro, XG; Filipovich, E; García, M; Germà-Lluch, JR; López, JJ; Pérez, X; Rifà, J; Tres, A; Valladares, M, 2006)		2.07
"Temozolomide is a recently introduced alkylating agent that has yielded a significant benefit in the treatment of high-grade gliomas."( Genetic alterations associated with acquired temozolomide resistance in SNB-19, a human glioma cell line.
Auger, N; Dutrillaux, B; Idbaih, A; Legrier, ME; Poupon, MF; Sanson, M; Thillet, J; Wanherdrick, K, 2006)		1.31
"Temozolomide (TMZ) is a DNA methylating agent that has shown promising antitumor activity against high grade glioma. "( Potentiation of antiglioma effect with combined temozolomide and interferon-beta.
Hong, YK; Joe, YA; Kim, TG; Park, JA, 2006)		2.03
"Temozolomide is an alkylating agent with activity in the treatment of melanoma metastatic to the brain. "( A phase I/II study of lomustine and temozolomide in patients with cerebral metastases from malignant melanoma.
Bate, SC; Beirne, DA; Eisen, TG; Gibbens, IM; Gore, ME; Hughes, SA; Larkin, JM; Patel, PM; Thomas, K, 2007)		2.06
"Temozolomide (TMZ) is a methylating agent that spontaneously decomposes into the active metabolite of dacarbazine, the most effective agent for the systemic treatment of melanoma."( Combined effect of temozolomide and hyperthermia on human melanoma cell growth and O6-methylguanine-DNA methyltransferase activity.
Bonmassar, E; Caporali, S; Caporaso, P; D'Atri, S; Falcinelli, S; Pagani, E; Pepponi, R; Turriziani, M, 2007)		1.39
"Temozolomide is an oral alkylating agent that is considered to be a well-tolerated chemotherapeutic agent."( [Temozolomide, an oral chemotherapeutic agent with potential severe toxicity].
Gijtenbeek, JM; Kappelle, AC; Soetekouw, PM; van der Maazen, RW; van Herpen, CM, 2007)		1.97
"Temozolomide is a novel second-generation alkylating agent that has shown efficacy for the treatment of high-grade gliomas."( [Glioma therapy up-date].
Dalmau, J; de la Fuente, BP; Rosenfeld, M, 2007)		1.06
"Temozolomide is an alkylating agent used frequently in the management of gliomas. "( Prolonged and severe myelosuppression in two patients after low-dose temozolomide treatment- case study and review of literature.
Brown, MP; Selva-Nayagam, S; Singhal, N, 2007)		2.02
"Temozolomide is an oral alkylating agent recently approved for the treatment of glioblastoma multiforme. "( Temozolomide-associated organizing pneumonitis.
Aubrey, MC; Lim, KG; Limper, AH; Maldonado, F, 2007)		3.23
"Temozolomide is an oral cytotoxic agent that has demonstrated its interest in high grade glioma tumors. "( Temozolomide treatment of an adult with a relapsing medulloblastoma.
Bay, JO; Durando, X; Gilliot, O; Irthum, B; Thivat, E; Verrelle, P; Vincent, C, 2007)		3.23
"Temozolomide is an effective chemotherapeutic agent for patients with glioblastoma multiforme, but it induces significant lymphopenia."( Immunological responses in a patient with glioblastoma multiforme treated with sequential courses of temozolomide and immunotherapy: case study.
Aldape, K; Archer, GE; Bigner, DD; Crutcher, L; Dey, M; Gilbert, M; Hassenbusch, SJ; Heimberger, AB; Hussain, SF; Mitchell, DA; Sampson, JH; Sawaya, R; Schmittling, B; Sun, W, 2008)		1.28
"Temozolomide is a methylating agent that is typically administered once daily."( Multi-institutional phase II study of temozolomide administered twice daily in the treatment of recurrent high-grade gliomas.
Alavi, J; Balmaceda, C; Chen, J; Cheung, YK; Fine, RL; Fisher, PG; Pannullo, S; Peereboom, D; Sisti, M, 2008)		1.34
"Temozolomide is an oral alkylating agent used in the treatment of metastatic melanoma. "( Temozolomide-induced desquamative skin rash in a patient with metastatic melanoma.
Neff, WJ; Nystrom, KK; Pick, AM, 2008)		3.23
"Temozolomide is a proautophagic (type II programmed cell death) drug and can thus circumvent part of the glioblastoma resistance to apoptosis."( [The sodium pump could constitute a new target to combat glioblastomas].
Kiss, R; Lefranc, F; Mijatovic, T, 2008)		1.07
"Temozolomide (SCH 52365) is an imidazotetrazine derivative which exhibits broad spectrum activity against murine tumors and is structurally related to dacarbazine (DTIC). "( A phase II study of temozolomide in advanced untreated pancreatic cancer.
Feld, R; Hedley, D; Moore, MJ; Oza, A; Siu, LL, 1998)		2.07
"Temozolomide (TMZ) is a new imidazotetrazine derivative with early clinical activity in glioma and melanoma. "( Phase I trial of temozolomide (NSC 362856) in patients with advanced cancer.
Ames, MM; Buckner, JC; Burch, PA; Dhodapkar, M; Pitot, HC; Reid, JM; Rubin, J; Suman, VJ, 1997)		2.08
"Temozolomide (TMZ) is an oral imidazotetrazinone that is spontaneously converted to 5-(3-methyltriazen-1-yl)imidazole-4-carboxamide (MTIC) at physiological pH. "( A Phase I and pharmacokinetic study of temozolomide and cisplatin in patients with advanced solid malignancies.
Agarwala, SS; Baker, SD; Barrington, R; Britten, CD; Diab, SG; Eckardt, JR; Eckhardt, SG; Fraass, U; Hammond, LA; Johnson, T; Rowinsky, EK; Statkevich, P; Villalona-Calero, M; Von Hoff, DD, 1999)		2.02
"Temozolomide is an imidazotetrazine alkylating agent which undergoes chemical conversion at physiological pH to the active species 5-(3-methyltriazene-1-yl)imidazole-4-carboxamide (MTIC) but is stable at acid pH. "( Effect of gastric pH on the relative oral bioavailability and pharmacokinetics of temozolomide.
Beale, P; Brada, M; Cutler, DL; Judson, I; Marco, A; Moore, S; Reidenberg, P; Statkevich, P, 1999)		1.97
"Temozolomide (TMZ) is a new cytotoxic triazene compound of clinical interest that is able to generate methyl adducts at the O(6)-guanine of DNA, which can be repaired by O(6)-alkylguanine-DNA alkyltransferase (OGAT). "( O(6)-benzylguanine enhances the in vitro immunotoxic activity of temozolomide on natural or antigen-dependent immunity.
Alvino, E; Bonmassar, E; D'Atri, S; Lacal, PM; Nunziata, C; Pagani, E; Pepponi, R, 1999)		1.98
"Temozolomide is a novel, oral, second-generation alkylating agent. "( Temozolomide in early stages of newly diagnosed malignant glioma and neoplastic meningitis.
Friedman, HS, 2000)		3.19
"Temozolomide (TMZ) is a new, orally administered, second-generation imidazotetrazine prodrug with essentially 100% oral bioavailability that has demonstrated meaningful efficacy and an acceptable safety profile in the treatment of patients with recurrent glioblastoma multiforme. "( Future directions in the treatment of malignant gliomas with temozolomide.
Prados, MD, 2000)		1.99
"Temozolomide is a novel methylating agent with proven efficacy against malignant gliomas (MGs) after systemic administration but with dose-limiting myelotoxicity."( Temozolomide delivered by intracerebral microinfusion is safe and efficacious against malignant gliomas in rats.
Archer, GE; Bigner, DD; Friedman, AH; Friedman, HS; Heimberger, AB; Hulette, C; McLendon, RE; Sampson, JH, 2000)		2.47
"Temozolomide (TMZ) is a DNA-methylating agent that has recently been introduced into Phase II and III trials for the treatment of gliomas. "( p53 effects both the duration of G2/M arrest and the fate of temozolomide-treated human glioblastoma cells.
Berger, MS; Hirose, Y; Pieper, RO, 2001)		1.99
"Temozolomide (TMZ) is a methylating agent of the imidotetrazine class, whose cytotoxic product is O(6)-methylguanine DNA adducts, which initiate a futile recycling of the mismatch repair pathway causing DNA strand breaks and apoptotic cell death in mismatch repair proficient cells. "( Temozolomide: the effect of once- and twice-a-day dosing on tumor tissue levels of the DNA repair protein O(6)-alkylguanine-DNA-alkyltransferase.
Gerson, SL; Haaga, J; Liu, L; Majka, S; Spiro, TP; Willson, JK, 2001)		3.2
"Temozolomide is a novel oral alkylating agent that has been approved for the treatment of patients with refractory malignant glioma. "( New approaches for temozolomide therapy: use in newly diagnosed glioma.
Newlands, E; Stupp, R, 2001)		2.08
"Temozolomide is an effective agent in the treatment of recurrent malignant gliomas. "( A phase II study of extended low-dose temozolomide in recurrent malignant gliomas.
Abrey, LE; Bazylewicz, KA; Khan, RB; Malkin, MG; Raizer, JJ, 2002)		2.03
"Temozolomide is a novel oral alkylating agent that is effective against melanoma. "( Temozolomide in combination with docetaxel in patients with advanced melanoma: a phase II study of the Hellenic Cooperative Oncology Group.
Bafaloukos, D; Briassoulis, E; Fountzilas, G; Georgoulias, V; Gogas, H; Kalofonos, Ch; Karabelis, A; Kosmidis, P; Samantas, E; Skarlos, D, 2002)		3.2
"Temozolomide is a novel oral alkylating agent with demonstrated efficacy as second-line therapy for patients with recurrent anaplastic astrocytoma and glioblastoma multiforme (GBM). "( Promising survival for patients with newly diagnosed glioblastoma multiforme treated with concomitant radiation plus temozolomide followed by adjuvant temozolomide.
de Tribolet, N; Dietrich, PY; Janzer, R; Leyvraz, S; Maeder, P; Maillard, I; Meuli, R; Miralbell, R; Mirimanoff, RO; Ostermann Kraljevic, S; Pica, A; Pizzolato, G; Porchet, F; Regli, L; Stupp, R, 2002)		1.97
"Temozolomide (TZM) is a DNA-methylating agent that has recently been introduced into various clinical trials for treatment of solid or hematologic neoplasias, including brain lymphomas. "( Combined treatment with temozolomide and poly(ADP-ribose) polymerase inhibitor enhances survival of mice bearing hematologic malignancy at the central nervous system site.
Bonmassar, E; d'Amati, G; Graziani, G; Leonetti, C; Portarena, I; Scarsella, M; Tentori, L; Zupi, G, 2002)		2.06
"Temozolomide (TMZ) is a newly approved alkylating agent for the treatment of malignant gliomas. "( Biochemical changes associated with a multidrug-resistant phenotype of a human glioma cell line with temozolomide-acquired resistance.
Berman, E; Gallo, JM; Ma, J; Murphy, M; O'Dwyer, PJ; Reed, K, 2002)		1.97
"Temozolomide is a new anticancer agent which in the early clinical investigation has shown promising antitumor activity. "( Influence of O6-methylguanine on DNA damage and cytotoxicity of temozolomide in L1210 mouse leukemia sensitive and resistant to chloroethylnitrosoureas.
Bonfanti, M; Catapano, CV; Citti, L; D'Incalci, M; Taverna, P, 1992)		1.96

Effects

Temozolomide has an established role in treating pituitary tumours which have demonstrated metastases. It may be regarded as the preferred treatment for recurrent anaplastic gliomas after radiotherapy.

Temozolomide (TMZ) has recently been recommended as a novel approach in the management of aggressive pituitary tumors. The drug has an acceptable tolerance in elderly patients with GBM and KPS less than 70.

ExcerptReferenceRelevance
"Temozolomide has an established role in treating pituitary tumours which have demonstrated metastases or which are refractory and progressing, despite all conventional treatment (so-called salvage treatment)."( How and when to use temozolomide to treat aggressive pituitary tumours.
Whitelaw, BC, 2019)		1.56
"Temozolomide treatment has a wide range of efficacy in patients with pituitary carcinoma or locally aggressive pituitary adenoma. "( Salvage therapy with temozolomide in patients with aggressive or metastatic pituitary adenomas: experience in six cases.
Cangi, MG; Gill, AJ; Losa, M; Mazza, E; McCormack, A; Mortini, P; Motta, M; Reni, M; Talarico, A; Terreni, MR, 2010)		2.12
"Temozolomide has an acceptable tolerance in elderly patients with GBM and KPS less than 70. "( Temozolomide in elderly patients with newly diagnosed glioblastoma and poor performance status: an ANOCEF phase II trial.
Barrie, M; Beauchesne, P; Campello, C; Cartalat-Carel, S; Catry-Thomas, I; Chinot, O; Delattre, JY; Ducray, F; Gállego Pérez-Larraya, J; Guillamo, JS; Honnorat, J; Huchet, A; Matta, M; Mokhtari, K; Monjour, A; Taillandier, L; Tanguy, ML, 2011)		3.25
"Temozolomide has an acceptable safety profile and may be regarded as the preferred treatment for recurrent anaplastic gliomas after radiotherapy."( [Favourable result for temozolomide in recurrent high-grade glioma].
Enting, RH; Kros, JM; Sillevis Smitt, PA; Taal, W; van den Bent, MJ; van der Rijt, CD; van Heuvel, I, 2005)		1.36
"Temozolomide has an evolving role in the treatment of high grade gliomas. "( An Australian experience with temozolomide for the treatment of recurrent high grade gliomas.
Ashley, DL; Cher, L; Harris, MT; Rosenthal, MA, 2001)		2.04
"Temozolomide (TMZ) has been widely used in GBM therapy with noticeable side effects."( Cold Plasma Discharge Tube Enhances Antitumoral Efficacy of Temozolomide.
Keidar, M; Keir, ST; Lin, L; Peters, KB; Sherman, JH; Yan, D; Yao, X, 2022)		1.68
"Once temozolomide has failed, there is no recommended treatment option for pituitary carcinomas and aggressive pituitary tumors. "( Immunotherapy in aggressive pituitary tumors and carcinomas: a systematic review.
Ilie, MD; Jouanneau, E; Raverot, G; Vasiljevic, A, 2022)		1.24
"Temozolomide (TMZ) has anti-proliferative and cytotoxic effects and is indicated for glioblastoma multiforme and recurrent mesenchymal astrocytoma."( Progress in research and development of temozolomide brain-targeted preparations: a review.
Chen, J; Fan, W; Fu, Z; Wu, X; Xu, Y; Yang, J, 2023)		1.9
"Temozolomide (TMZ) has been used as standard-of-care for glioblastoma multiforme (GBM), but the resistance to TMZ develops quickly and frequently. "( Involvement of cell shape and lipid metabolism in glioblastoma resistance to temozolomide.
An, YJ; Choo, M; Kim, DH; Kim, HS; Ku, JL; Lee, SK; Mai, VH; Park, CK; Park, S, 2023)		2.58
"Temozolomide has been used in patients with aggressive Nelson's with no consistent results."( Management of Nelson's Syndrome.
Fountas, A; Karavitaki, N, 2022)		1.44
"Temozolomide (TMZ) has been determined to be the chemotherapeutic drug with efficacy for glioblastoma (GBM). "( Ultrasound-excited temozolomide sonosensitization induces necroptosis in glioblastoma.
Song, S; Tong, X; Wang, F; Wang, Y; Wen, B; Wu, H; Wu, Q; Xu, L; Yan, H; Zhou, Y, 2023)		2.68
"Temozolomide (TMZ) has been used in the last 15 years in patients with aggressive pituitary tumors."( Knowing when to discontinue Temozolomide therapy in responding aggressive pituitary tumors and carcinomas: a systematic review and Padua (Italy) case series.
Barbot, M; Bergo, E; Caccese, M; Ceccato, F; Cerretti, G; Lombardi, G; Occhi, G; Padovan, M; Scaroni, C, 2023)		1.93
"Temozolomide (TMZ) has been used as an initial therapy for gliomas."( LncRNA GSCAR promotes glioma stem cell maintenance via stabilizing SOX2 expression.
Chen, M; Chen, Y; Jiang, X; Jin, Z; Li, Y; Liu, B; Pu, J; Shi, Y; Yan, D; Yang, C; Yuan, Y; Zhai, H; Zhang, C; Zhang, Y, 2023)		1.63
"Temozolomide has been mainly used for the treatment of malignant gliomas over a decade."( [Medical Treatments for Malignant Brain Tumor].
Kitamura, Y; Toda, M, 2023)		1.63
"Temozolomide has shown a significant anti-proliferative activity on adrenocortical cancer (ACC) cells in vitro."( Activity and safety of temozolomide in advanced adrenocortical carcinoma patients.
Badalamenti, G; Basile, V; Berruti, A; Cerri, S; Cosentini, D; Dalla Volta, A; Ferrari, VD; Grisanti, S; Incorvaia, L; Laganà, M; Luppi, G; Musso, E; Perotti, P; Rapa, I; Russo, A; Sigala, S; Spallanzani, A; Terzolo, M; Volante, M, 2019)		2.27
"Temozolomide (TMZ) has been the standard-of-care chemotherapy for glioblastoma (GBM) patients for more than a decade. "( Image-based metric of invasiveness predicts response to adjuvant temozolomide for primary glioblastoma.
Bendok, BR; Doyle, T; Hawkins-Daarud, A; Hu, LS; Jackson, PR; Johnston, SK; Massey, SC; Mrugala, MM; Porter, AB; Sarkaria, JN; Singleton, KW; Swanson, KR; Vora, S; White, H; Whitmire, P, 2020)		2.24
"Temozolomide (TMZ) has been used as a first-line drug for the treatment of GBM for over a decade, but its treatment benefits are limited by acquired resistance."( The effect of polysaccharides from Cibotium barometz on enhancing temozolomide-induced glutathione exhausted in human glioblastoma U87 cells, as revealed by
Li, FF; Shi, Y; Wang, N; Wang, SQ; Wang, X; You, YL, 2020)		1.52
"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)		3.51
"Temozolomide (TMZ) has been used to treat glioma."( Circ-VPS18 Knockdown Enhances TMZ Sensitivity and Inhibits Glioma Progression by MiR-370/RUNX1 Axis.
Jia, X; Li, W; Liu, Q; Ma, Q; Wang, X; Yan, P, 2021)		1.34
"Temozolomide (TMZ) has been widely used as a first-line treatment for GBM."( Intranasal Delivery of Temozolomide-Conjugated Gold Nanoparticles Functionalized with Anti-EphA3 for Glioblastoma Targeting.
Li, N; Li, Y; Lv, Y; Sha, C; Sun, K; Tang, S; Wang, A; Wang, L; Yan, X; Yu, Y, 2021)		1.65
"Temozolomide (TMZ) has been shown to determine radiological and biochemical response in malignant PCC/PGLs."( Temozolomide treatment of a malignant pheochromocytoma and an unresectable MAX-related paraganglioma.
Bertorelle, R; Ferrara, AM; Iacobone, M; Lombardi, G; Meringolo, D; Nardin, M; Opocher, G; Pambuku, A; Schiavi, F; Zagonel, V; Zovato, S, 2018)		2.64
"Temozolomide (TMZ) has been considered to be one of the most effective chemotherapeutic agents to prolong the survival of patients with glioblastoma."( Differential Characterization of Temozolomide-Resistant Human Glioma Cells.
Chen, CC; Huang, BR; Lai, SW; Lin, C; Lin, HY; Liu, YS; Lu, DY; Tsai, CF, 2018)		1.48
"Temozolomide has several effects on the immune system that are dependent on mode of delivery and the dosing strategy, which may have unpredicted effects on immunotherapy."( Temozolomide for immunomodulation in the treatment of glioblastoma.
Dastmalchi, F; Karachi, A; Mitchell, DA; Rahman, M, 2018)		2.64
"Temozolomide (TMZ) has been reported to be useful as an adjunctive treatment for some patients."( Early Recognition and Initiation of Temozolomide Chemotherapy for Refractory, Invasive Pituitary Macroprolactinoma with Long-Term Sustained Remission.
Barkhoudarian, G; Eisenberg, A; Kelly, DF; Ogunbameru, R; Palejwala, SK; Wei, H, 2018)		1.48
"Temozolomide has been available to oncologists for over 30 years. "( Role of Temozolomide in the Treatment of Cancers Involving the Central Nervous System.
Grossman, SA; Schreck, KC, 2018)		2.36
"Temozolomide (TMZ) has been successfully used to treat a variety of malignancies, such as glioblastoma multiforme, astrocytoma, non-small-cell lung carcinoma."( Successful treatment with temozolomide in an elderly woman with advanced pulmonary large-cell neuroendocrine carcinoma: A case report.
Dong, XF; Hu, ZL; Lu, YF; Tang, S; Wei, J, 2018)		1.5
"Temozolomide (TMZ) has been proposed in patients with aggressive pituitary neuroendocrine tumors (PitNETs) who do not respond to conventional treatments."( Temozolomide cytoreductive treatment in a giant cabergoline-resistant prolactin-secreting pituitary neuroendocrine tumor.
Albiger, N; Ceccato, F; Lombardi, G; Mazzai, L; Pambuku, A; Rolma, G; Scaroni, C; Zagonel, V, 2019)		2.68
"Temozolomide (TMZ) has been the first-line chemotherapeutic agent used, although to achieve a satisfactory clinical effect."( Synergistic Suppression of Glioblastoma Cell Growth by Combined Application of Temozolomide and Dopamine D2 Receptor Antagonists.
Gao, L; Huang, X; Jiang, X; Li, J; Liu, X; Liu, Z; Zeng, T, 2019)		1.46
"Temozolomide has an established role in treating pituitary tumours which have demonstrated metastases or which are refractory and progressing, despite all conventional treatment (so-called salvage treatment)."( How and when to use temozolomide to treat aggressive pituitary tumours.
Whitelaw, BC, 2019)		1.56
"Temozolomide (TMZ) has established antineoplastic activity in the central nervous system in other disease states, with a favorable toxicity profile."( Temozolomide as a Single Agent Maintenance Therapy in Elderly Patients With Primary CNS Lymphoma.
Brenner, A; Butler, MJ; Faivre, G; Le, I, 2019)		2.68
"Temozolomide (TMZ) has been proposed as a therapeutic option in aggressive pituitary tumors. "( Aggressive silent GH pituitary tumor resistant to multiple treatments, including temozolomide.
Batisse, M; Chazal, J; Durando, X; Kemeny, JL; Maqdasy, S; Montoriol, PF; Raverot, G; Sturm, N; Tauveron, I; Trouillas, J, 2013)		2.06
"Temozolomide (TMZ) has received much attention, notably in the treatment of malignant glioma and malignant melanoma. "( Efficacy and safety between temozolomide alone and temozolomide-based double therapy for malignant melanoma: a meta-analysis.
Jia, HY; Jiang, G; Lei, TC; Li, RH; Liu, YQ; Sun, C, 2014)		2.14
"Temozolomide (TMZ) alone has been proposed as a promising alternative to radiotherapy (RT) in elderly glioblastoma (GBM) patients. "( A meta-analysis of temozolomide versus radiotherapy in elderly glioblastoma patients.
Cai, S; Cheng, JX; Dong, Y; Liu, BL; Yin, AA; Zhang, LH; Zhang, X, 2014)		2.17
"Temozolomide (TMZ) has remained the chemotherapy of choice in patients with glioblastoma multiforme (GBM) primarily due to the lack of more effective drugs. "( Oxidative cytotoxic agent withaferin A resensitizes temozolomide-resistant glioblastomas via MGMT depletion and induces apoptosis through Akt/mTOR pathway inhibitory modulation.
Cohen, MS; Grogan, PT; Sarkaria, JN; Timmermann, BN, 2014)		2.1
"Temozolomide has recently emerged as an alternative option for PCNSL treatment."( MGMT promoter methylation and correlation with protein expression in primary central nervous system lymphoma.
Canal, F; Cavallin, S; Dei Tos, AP; Gherlinzoni, F; Scarpa, M; Scquizzato, E; Stefani, PM; Toffolatti, L, 2014)		1.12
"Temozolomide has demonstrated a 2.5-month increase in overall survival and a 1.9-month increase in progression-free survival, relative to radiotherapy alone."( A review of the economic burden of glioblastoma and the cost effectiveness of pharmacologic treatments.
Hay, JW; Messali, A; Villacorta, R, 2014)		1.12
"Temozolomide (TMZ) has been used for the treatment of glioblastoma."( Inhibition of JNK potentiates temozolomide-induced cytotoxicity in U87MG glioblastoma cells via suppression of Akt phosphorylation.
Chun, W; Kim, SS; Lee, HJ; Lee, JW; Lim, SY; Vo, VA, 2014)		1.41
"Temozolomide (TMZ) has been showed to be an effective chemotherapeutic agent for glioblastoma treatment; however, the response rate is not satisfactory."( Synergistic Anti-Cancer Effects of Icariin and Temozolomide in Glioblastoma.
Guo, H; Guo, M; Wang, Y; Yang, L, 2015)		1.4
"Temozolomide (TMZ) has been widely used in the treatment of glioblastoma (GBM), although inherent or acquired resistance restricts the application. "( Sulforaphane enhances temozolomide-induced apoptosis because of down-regulation of miR-21 via Wnt/β-catenin signaling in glioblastoma.
Lan, F; Pan, Q; Yu, H; Yue, X, 2015)		2.17
"As temozolomide has activity in SCLC, we investigated combination therapy with talazoparib and found marked synergy in vitro and efficacy in vivo, which did not solely depend on SLFN11 or MGMT status."( PARP Inhibitor Activity Correlates with SLFN11 Expression and Demonstrates Synergy with Temozolomide in Small Cell Lung Cancer.
de Stanchina, E; Desmeules, P; Gardner, EE; Lok, BH; Ni, A; Poirier, JT; Powell, SN; Rekhtman, N; Riaz, N; Rudin, CM; Schneeberger, VE; Teicher, BA, 2017)		1.19
"Temozolomide (TMZ) has been shown as an effective treatment option in aggressive pituitary adenomas and carcinomas. "( How effective is temozolomide for treating pituitary tumours and when should it be used?
Halevy, C; Whitelaw, BC, 2017)		2.24
"Temozolomide (TMZ) has demonstrated clinical antitumor activity. "( The safety of temozolomide in the treatment of malignancies.
Hwu, WJ; Patel, SP; Trinh, VA, 2009)		2.16
"Temozolomide has been used with thalidomide to treat gliomas."( Mechanism of thalidomide to enhance cytotoxicity of temozolomide in U251-MG glioma cells in vitro.
Gao, S; Ji, YW; Pan, Q; Yang, XJ; Zhang, WG, 2009)		1.32
"Temozolomide has been used as a standard therapy for the treatment of newly diagnosed glioblastoma multiforme since 2005. "( Effectiveness of temozolomide for primary glioblastoma multiforme in routine clinical practice.
Baumert, BG; Leffers, P; Tjon-A-Fat, H; Twijnstra, A; van Genugten, JA, 2010)		2.14
"Temozolomide has recently been used for atypical adenomas or pituitary carcinomas."( [Recent trends in the pathophysiology and treatment of pituitary adenomas].
Matsuno, A, 2009)		1.07
"Temozolomide (TMZ) has been accepted as a standard antitumor drug for glioma worldwide. "( Flow cytometric analysis for the mechanism of the new antineoplastic agent temozolomide in glioma cells.
Kawamoto, K; Li, Y; Numa, Y; Oishi, T; Oshige, H; Yamahara, T; Zhen, Y, 2010)		2.03
"Temozolomide chemotherapy has become part of the therapy used to treat glioblastoma multiforme and refractory anaplastic astrocytoma. "( Emergence of cytomegalovirus disease in patients receiving temozolomide: report of two cases and literature review.
Aguado, JM; García-Reyne, A; Juan, RS; Lalueza, A; Lizasoain, M; López-Medrano, F; Martínez, P; Meije, Y; Rodríguez, V, 2010)		2.05
"Temozolomide (TM) has anti-tumor activity in patients with malignant glioma. "( Temozolomide/PLGA microparticles plus vatalanib inhibits tumor growth and angiogenesis in an orthotopic glioma model.
Liu, JM; Tang, GS; Wang, Y; Yue, ZJ; Zhang, H; Zhang, YH, 2010)		3.25
"Temozolomide treatment has a wide range of efficacy in patients with pituitary carcinoma or locally aggressive pituitary adenoma. "( Salvage therapy with temozolomide in patients with aggressive or metastatic pituitary adenomas: experience in six cases.
Cangi, MG; Gill, AJ; Losa, M; Mazza, E; McCormack, A; Mortini, P; Motta, M; Reni, M; Talarico, A; Terreni, MR, 2010)		2.12
"Temozolomide has significantly improved the outcome of patients with glioblastoma. "( [Benefit of a prolonged adjuvant treatment with temozolomide for the management of patients with glioblastoma].
Auberdiac, P; Cartier, L; Chargari, C; Forest, F; Fotso, MJ; Magné, N; Malkoun, N; Nuti, C; Pacaut, C; Peoc'h, M; Schmitt, T; Thorin, J, 2011)		2.07
"Temozolomide has shown clinical effect in well-differentiated endocrine carcinomas."( Clinical effect of temozolomide-based chemotherapy in poorly differentiated endocrine carcinoma after progression on first-line chemotherapy.
Busch, C; Knappskog, S; Oberg, K; Sebjornsen, S; Sorbye, H; Welin, S, 2011)		1.42
"Oral temozolomide has shown similar efficacy to dacarbazine in phase III trials with median progression-free survival (PFS) of 2.1 months. "( First-line temozolomide combined with bevacizumab in metastatic melanoma: a multicentre phase II trial (SAKK 50/07).
Cathomas, R; Dummer, R; Gillessen, S; Goldinger, SM; Mamot, C; Michielin, O; Mjhic-Probst, D; Moch, H; Ochsenbein, A; Schläppi, M; Schönewolf, N; Schraml, PH; Seifert, B; Simcock, M; von Moos, R, 2012)		1.28
"Temozolomide has an acceptable tolerance in elderly patients with GBM and KPS less than 70. "( Temozolomide in elderly patients with newly diagnosed glioblastoma and poor performance status: an ANOCEF phase II trial.
Barrie, M; Beauchesne, P; Campello, C; Cartalat-Carel, S; Catry-Thomas, I; Chinot, O; Delattre, JY; Ducray, F; Gállego Pérez-Larraya, J; Guillamo, JS; Honnorat, J; Huchet, A; Matta, M; Mokhtari, K; Monjour, A; Taillandier, L; Tanguy, ML, 2011)		3.25
"Temozolomide (TMZ) has recently been recommended as a novel approach in the management of aggressive pituitary tumors. "( Aggressive silent corticotroph adenoma progressing to pituitary carcinoma: the role of temozolomide therapy.
Cusimano, M; Fadul, CE; Gonzalez, R; Horvath, E; Kovacs, K; Moshkin, O; Ortiz, LD; Rotondo, F; Scheithauer, BW; Syro, LV; Uribe, H, )		1.8
"Temozolomide has activity in relapsed SCLC, particularly for brain metastases. "( Phase II trial of temozolomide in patients with relapsed sensitive or refractory small cell lung cancer, with assessment of methylguanine-DNA methyltransferase as a potential biomarker.
Azzoli, CG; Chan, TA; Fiore, JJ; Ginsberg, MS; Heguy, A; Holodny, AI; Huberman, K; Kadota, K; Kris, MG; Krug, LM; Pietanza, MC; Riely, GJ; Rizvi, NA; Sima, CS; Sumner, DK; Travis, WD, 2012)		2.16
"Temozolomide has quickly become part of the standard of care for the modern treatment of stage IV glioblastoma multiforme since its approval in 2005."( Temozolomide and other potential agents for the treatment of glioblastoma multiforme.
Chow, F; Cremer, N; Kim, W; Nagasawa, DT; Yang, I; Yew, A, 2012)		2.54
"Temozolomide (TMZ) has anti-tumor activity in patients with malignant glioma. "( Combination hyperbaric oxygen and temozolomide therapy in C6 rat glioma model.
Bilir, A; Bozkurt, ER; Dagıstan, Y; Karaca, I; Ozar, E; Toklu, A; Yagmurlu, K, 2012)		2.1
"Temozolomide (TMZ) has become a key therapeutic agent in patients with malignant gliomas; however, its survival benefit remains unsatisfactory. "( Valproic acid downregulates the expression of MGMT and sensitizes temozolomide-resistant glioma cells.
Hou, Y; Jeong, CH; Jeun, SS; Kim, SM; Lim, JY; Park, KY; Ryu, CH; Woo, JS; Yoon, WS, 2012)		2.06
"Temozolomide monotherapy has limited effect in treatment of recurrent neuroendocrine carcinomas. "( Temozolomide as second or third line treatment of patients with neuroendocrine carcinomas.
Federspiel, B; Hansen, CP; Kjaer, A; Knigge, U; Langer, SW; Olsen, IH; Sørensen, JB, 2012)		3.26
"Temozolomide (Temodar) has demonstrated clinical activity against melanoma equivalent to that of intravenous dacarbazine (DTIC). "( Phase II evaluation of temozolomide in metastatic choroidal melanoma.
Bedikian, AY; Eton, O; Papadopoulos, N; Plager, C; Ring, S, 2003)		2.07
"Temozolomide has activity and a favorable safety profile in all dosing schedules tested."( Temozolomide: realizing the promise and potential.
Dolan, ME; Nagasubramanian, R, 2003)		2.48
"Temozolomide has single-agent activity in patients with WHO grade II cerebral glioma, with modest improvement in quality of life and improvement in epilepsy control. "( Phase II study of primary temozolomide chemotherapy in patients with WHO grade II gliomas.
Abson, C; Ashley, S; Brada, M; Britton, J; Gonsalves, A; Hines, F; Sardell, S; Traish, D; Viviers, L; Westbury, C; Wilkins, P, 2003)		2.06
"Temozolomide has shown activity and limited toxicity in patients with primary brain tumors at doses of 150-200 mg/m(2)/day on days 1-5 every 4 weeks. "( Dose-dense regimen of temozolomide given every other week in patients with primary central nervous system tumors.
Abdulkarim, B; Armand, JP; Cioloca, C; Djafari, L; Djazouli, K; Faivre, S; Guillamo, JS; Osorio, M; Parker, F; Raymond, E; Vera, K, 2004)		2.08
"Temozolomide has shown antineoplastic activity against malignant gliomas and more recently was beneficial in one patient with gliomatosis cerebri."( Gliomatosis cerebri: clinical, neurochemical and neuroradiological response to temozolomide administration.
Ambrosetto, P; Barbiroli, B; Cortelli, P; Crinò, L; Franceschi, E; Lodi, R; Setola, E; Tonon, C, 2003)		1.27
"Temozolomide has established activity in the treatment of recurrent glioblastoma multiforme (GBM). "( Phase 2 study of temozolomide and Caelyx in patients with recurrent glioblastoma multiforme.
Ashley, DM; Cher, LM; Chua, SL; Dowling, A; Rosenthal, MA; Wong, SS; Woods, AM, 2004)		2.11
"Temozolomide (TMZ) has demonstrated activity and acceptable toxicity for the treatment of recurrent high-grade gliomas in prospective phase II studies. "( Temozolomide for the treatment of recurrent supratentorial glioma: results of a compassionate use program in Belgium.
Branle, F; Everaert, E; Joosens, E; Menten, J; Neyns, B; Strauven, T, 2004)		3.21
"Temozolomide has been studied in soft-tissue sarcomas with varying dosing schedules. "( Temozolomide in uterine leiomyosarcomas.
Aghajanian, C; Anderson, S, 2005)		3.21
"Temozolomide has promising therapeutic benefit and is well tolerated in patients with metastatic unresectable leiomyosarcoma. "( Temozolomide in uterine leiomyosarcomas.
Aghajanian, C; Anderson, S, 2005)		3.21
"Temozolomide has an acceptable safety profile and may be regarded as the preferred treatment for recurrent anaplastic gliomas after radiotherapy."( [Favourable result for temozolomide in recurrent high-grade glioma].
Enting, RH; Kros, JM; Sillevis Smitt, PA; Taal, W; van den Bent, MJ; van der Rijt, CD; van Heuvel, I, 2005)		1.36
"Temozolomide (TMZ) has shown efficacy in metastatic melanoma equal to that of dacarbazine (DTIC), the standard chemotherapeutic agent for melanoma. "( Temozolomide in combination with interferon-alfa versus temozolomide alone in patients with advanced metastatic melanoma: a randomized, phase III, multicenter study from the Dermatologic Cooperative Oncology Group.
Becker, JC; Dummer, R; Garbe, C; Kaufmann, R; Krengel, S; Kretschmer, L; Leiter, U; Linse, R; Mauch, C; Schadendorf, D; Sebastian, G; Spieth, K; Tilgen, W; Vogt, T; von den Driesch, P, 2005)		3.21
"Temozolomide (TMZ) has shown modest efficacy in the treatment of recurrent brain metastasis (BM). "( Vinorelbine combined with a protracted course of temozolomide for recurrent brain metastases: a phase I trial.
Abrey, LE; Demopoulos, A; Malkin, MG; Omuro, AM; Raizer, JJ, 2006)		2.03
"Temozolomide (TMZ) has shown efficacy in the treatment of metastatic melanoma."( Whole brain irradiation and temozolomide based chemotherapy in melanoma brain metastases.
Castel, T; Conill, C; Domingo-Doménech, J; Gallego, R; Jorcano, S; Malvehy, J; Puig, S; Sánchez, M; Vilella, R, 2006)		1.35
"Temozolomide (TMZ) has demonstrated activity against melanoma and has been investigated as single agent or in combination."( Temozolomide in combination with celecoxib in patients with advanced melanoma. A phase II study of the Hellenic Cooperative Oncology Group.
Fountzilas, G; Frangia, K; Gogas, H; Mantzourani, M; Markopoulos, C; Middleton, M; Panagiotou, P; Papadopoulos, O; Pectasides, D; Polyzos, A; Stavrinidis, I; Tsoutsos, D; Vaiopoulos, G, 2006)		2.5
"Temozolomide has shown some efficacy in metastatic melanoma and recently received extended approval to treat brain tumours. "( Dose-intensified bi-weekly temozolomide in patients with asymptomatic brain metastases from malignant melanoma: a phase II DeCOG/ADO study.
Egberts, F; Garbe, C; Hauschild, A; Kreissig, M; Linse, R; Mohr, P; Schadendorf, D; Thoelke, A; Tilgen, W; Trefzer, U; Ugurel, S; Vogt, T, 2006)		2.07
"Temozolomide (TMZ) has demonstrated activity and acceptable toxicity for the treatment of recurrent malignant gliomas in carious prospective phase II studies. "( [Temozolomide in the treatment of recurrent malignant glioma].
Ishii, N; Iwasaki, Y; Kobayashi, H; Murata, J; Sawamura, Y, 2006)		2.69
"Temozolomide has emerged as a new alternative treatment for PCNSL and constitutes an attractive option for the elderly because of its favorable toxicity profile."( Temozolomide and methotrexate for primary central nervous system lymphoma in the elderly.
Barrie, M; Carnin, C; Chinot, O; Hoang-Xuan, K; Omuro, AM; Taillandier, L, 2007)		2.5
"Temozolomide has proven benefit in grade II/III gliomas progressive following standard therapy and when added to radiation for glioblastoma."( Temozolomide and radiation in low-grade and anaplastic gliomas: temoradiation.
Schiff, D, 2007)		2.5
"Temozolomide (TMZ) has emerged as an active agent against malignant gliomas."( Management of glioblastoma.
Aoki, T; Hashimoto, N; Matsutani, M, 2007)		1.06
"Temozolomide has become the standard of care in newly diagnosed glioblastoma."( [Chemotherapy for brain tumors in adult patients].
Weller, M, 2008)		1.07
"Temozolomide has recently been introduced by Schering-Plough Ltd (Welwyn Garden City, UK) as a new treatment which merits further investigation in this situation."( Temozolomide (Temodal) for treatment of primary brain tumours.
MacConnachie, AM, 2000)		2.47
"Temozolomide, a new drug, has shown promise in treating malignant gliomas and other difficult-to-treat tumors."( Temozolomide and treatment of malignant glioma.
Calvert, H; Friedman, HS; Kerby, T, 2000)		2.47
"Temozolomide has an evolving role in the treatment of high grade gliomas. "( An Australian experience with temozolomide for the treatment of recurrent high grade gliomas.
Ashley, DL; Cher, L; Harris, MT; Rosenthal, MA, 2001)		2.04
"Temozolomide has the potential to be a useful agent in the treatment of a variety of cancers."( Future directions for temozolomide therapy.
Yung, WK, 2001)		1.35
"Temozolomide has shown efficacy in the treatment of metastatic melanoma similar to that of dacarbazine (DTIC), the standard chemotherapy, but with the added benefit of penetration into the central nervous system (CNS). "( Effect of temozolomide on central nervous system relapse in patients with advanced melanoma.
Brampton, MH; Calvert, AH; Middleton, MR; Paul, MJ; Rustin, G; Summers, Y; Thatcher, N, 2002)		2.16

Actions

Temozolomide was chosen because of its previous success when combined with PARP inhibitors, dissimilar to other commonly used chemotherapies. The drug can cause early radiation induced injury which can mimic progressive tumor.

ExcerptReferenceRelevance
"Temozolomide was chosen because of its previous success when combined with PARP inhibitors, dissimilar to other commonly used chemotherapies."( Does PARP Inhibition Sensitize Chondrosarcoma Cell Lines to Chemotherapy or Radiotherapy? Results From a Three-dimensional Spheroid Cell Model.
Boveé, JVMG; Briaire-de Bruijn, IH; Palubeckaitė, I; van den Akker, BEWM; Venneker, S, 2023)		1.63
"Temozolomide plays a role in treating melanoma refractory to immunomodulatory and mitogen-activated protein kinase-targeted approaches, but its efficacy is limited. "( Preclinical Activity of 4-Demethyl-4-cholesteryloxycarbonylpenclomedine in Melanoma.
Benes, EN; Friedlander, P; Jursic, B; Morgan, LR; Rodgers, AH, 2023)		2.35
"Temozolomide may cause thrombocytopenia or neutropenia in 3-4% of glioblastoma patients, respectively. "( MGMT gene variants, temozolomide myelotoxicity and glioma risk. A concise literature survey including an illustrative case.
Altinoz, MA; Bolukbasi, FH; Ekmekci, CG; Elmaci, I; Sari, R; Sav, A; Yenmis, G, 2017)		2.22
"Temozolomide (TMZ) may enhance antitumor immunity in patients with glioblastoma multiforme (GBM). "( Phase I/IIa trial of fractionated radiotherapy, temozolomide, and autologous formalin-fixed tumor vaccine for newly diagnosed glioblastoma.
Abe, T; Hashimoto, K; Ikuta, S; Ishihara, T; Ishikawa, E; Karasawa, K; Maruyama, T; Matsuda, M; Matsumura, A; Matsutani, M; Muragaki, Y; Nakazato, Y; Ohno, T; Tsuboi, K; Uemae, Y; Yamamoto, T, 2014)		2.1
"Temozolomide plays a critical role in curing glioma at present. "( Liposome encapsulated of temozolomide for the treatment of glioma tumor: preparation, characterization and evaluation.
Gao, J; Huang, G; Liu, H; Wang, L; Wang, Z, 2015)		2.16
"Temozolomide can cause early radiation induced injury which can mimic progressive tumor. "( Radiation induced early necrosis in patients with malignant gliomas receiving temozolomide.
Akmansu, M; Benekli, M; Buyukberber, S; Coskun, U; Kaya, AO; Oner, Y; Ozturk, B; Uncu, D; Yaman, E; Yildiz, R, 2010)		2.03
"Temozolomide can cause Pneumocystis pneumonia."( Fatal pneumonia associated with temozolomide therapy in patients with malignant glioma.
Abe, S; Azuma, A; Fujita, K; Gemma, A; Hayashi, H; Kobayashi, K; Kokuho, N; Morimoto, T; Saito, Y; Tanaka, T, 2012)		1.38
"Temozolomide (TMZ) displays efficacy for the treatment of metastatic melanoma."( [Temozolomide in patients with melanoma brain metastases treated with whole brain irradiation].
Castel, T; Conill, C; Fernández-Ibiza, J; Malvehy, J; Puig, S; Sánchez, M, 2004)		1.96
"Temozolomide appears to produce few serious adverse effects and may also have a positive impact on health-related quality of life."( A rapid and systematic review of the effectiveness of temozolomide for the treatment of recurrent malignant glioma.
Cave, C; Dinnes, J; Huang, S; Milne, R, 2002)		1.28

Treatment

Temozolomide (TMZ) treatment efficacy in glioblastoma (GBM) has been limited by resistance. Treatment induced cell cycle arrest, diminished cell viability, migration, invasion, and angiogenesis.

ExcerptReferenceRelevance
"Temozolomide-based treatment was administered to 64 of 68 (94.1%) patients, whereas RT + procarbazine, lomustine (CCNU), and vincristine (PCV) were applied in 2 of 69 (3.5%) patients."( Early Postoperative Treatment versus Initial Observation in CNS WHO Grade 2 and 3 Oligodendroglioma: Clinical Outcomes and DNA Methylation Patterns.
Aichholzer, M; Berghoff, AS; Dieckmann, K; Furtner, J; Goldberger, S; Hatziioannou, T; Heller, G; Leibetseder, A; Mair, MJ; Pichler, J; Preusser, M; Puhr, R; Tomasich, E; von Oertzen, T; Weis, S; Widhalm, G; Wöhrer, A, 2022)		1.44
"Temozolomide treatment in 156/171 patients resulted in complete response in 9.6%, partial response in 30.1%, stable disease in 28.1%, and progressive disease in 32.2% of the patients."( Aggressive pituitary tumours and carcinomas, characteristics and management of 171 patients.
Burman, P; Dekkers, OM; Losa, M; McCormack, A; Petersenn, S; Popovic, V; Raverot, G; Theodoropoulou, M; Trouillas, J, 2022)		1.44
"Temozolomide treatment induced cell cycle arrest, diminished cell viability, migration, invasion, and angiogenesis, and increased apoptosis and autophagy in glioblastoma, which was counteracted by overexpressing LINC00470 or SOX4 but was further promoted by LINC00470 knockdown."( Temozolomide protects against the progression of glioblastoma via SOX4 downregulation by inhibiting the LINC00470-mediated transcription factor EGR2.
Cui, Y; He, J; Li, W; Liu, P; Ma, W; Wang, M; Zhang, M, 2023)		3.07
"Temozolomide (TMZ) treatment is the mainstay drug for GBM despite the rapid development of resistance in mesenchymal GBM."( NADPH Oxidase Subunit CYBB Confers Chemotherapy and Ferroptosis Resistance in Mesenchymal Glioblastoma via Nrf2/SOD2 Modulation.
Fong, IH; Lin, CM; Liu, HW; Setiawan, SA; Su, IC; Su, YK; Yadav, VK; Yeh, CT, 2023)		1.63
"Temozolomide (TMZ) treatment efficacy in glioblastoma (GBM) has been limited by resistance. "( EPIC-0307-mediated selective disruption of PRADX-EZH2 interaction and enhancement of temozolomide sensitivity to glioblastoma via inhibiting DNA repair and MGMT.
Cui, X; Fang, C; Hong, B; Kang, C; Tan, Y; Tian, S; Wang, C; Wang, Q; Xiao, M; Xin, L; Xu, C; Xu, J; Yuan, X; Zhao, J; Zhu, Y, 2023)		2.58
"Pre-temozolomide treatment, these data were 5.2 cm3 (IQR 1.9-12.3), 89.3% and 14.3% (2 intracranial and 2 spinal metastases)."( Efficacy and safety of temozolomide in the treatment of aggressive pituitary neuroendocrine tumours in Spain.
Araujo-Castro, M; Biagetti, B; Cámara, R; Fajardo, C; García-Centeno, R; Guerrero-Pérez, F; Hanzu, F; Iglesias, P; Lamas, C; Mora, M; Remon-Ruiz, P; Soto, A, 2023)		1.7
"Temozolomide (TMZ) treatment efficacy in glioblastoma (GBM) patients has been limited by resistance in the clinic. "( Albumin-bound paclitaxel augment temozolomide treatment sensitivity of glioblastoma cells by disrupting DNA damage repair and promoting ferroptosis.
Huang, G; Li, Z; Qi, S; Qu, S; Wang, K; Ye, R; Yi, GZ; Zhang, H; Zhang, W; Zhu, T, 2023)		2.63
"Temozolomide is used for treatment in high-risk groups with low treatment response of neuroblastomas."( Selenium enhances TRPA1 channel-mediated activity of temozolomide in SH-SY5Y neuroblastoma cells.
Övey, İS; Özkal, B, 2020)		1.53
"Temozolomide (TMZ) treatment failed to induce apoptotic death in shBeclin1-transfected cells, contrary to control."( Autophagy inhibition reinforces stemness together with exit from dormancy of polydisperse glioblastoma stem cells.
Antonietti, P; Barthout, E; Battu, S; Begaud, G; Bessette, B; Brunel, A; Deluche, E; Durand, S; Hombourger, S; Jauberteau, MO; Kögel, D; Lalloué, F; Saada, S; Verdier, M, 2021)		1.34
"SD temozolomide treatment resulted in an upregulation of markers of T-cell exhaustion such as LAG-3 and TIM-3 in lymphocytes which was not seen with MD temozolomide. "( Modulation of temozolomide dose differentially affects T-cell response to immune checkpoint inhibition.
Azari, H; Dastmalchi, F; Flores, C; Huang, J; Karachi, A; Long, Y; Mitchell, DA; Rahman, M; Sayour, EJ; Yang, C, 2019)		1.5
"Temozolomide treatment inhibited p50 recruitment to its cognate element as a function of Ser329 phosphorylation while concomitantly increasing p53 recruitment."( Temozolomide Treatment Induces lncRNA MALAT1 in an NF-κB and p53 Codependent Manner in Glioblastoma.
Bernal, GM; Cahill, KE; Crawley, CD; Khodarev, NN; Larsen, G; Mansour, NM; Nunez, L; Raleigh, DR; Spretz, R; Szymura, SJ; Uppal, A; Voce, DJ; Weichselbaum, RR; Wu, L; Yamini, B; Zhang, W, 2019)		2.68
"Temozolomide treatment is continued for more than six cycles by 80.5 % of neuro-oncologists: 44.4 % only if there is residual disease; 27.8 % for 12 cycles even in the absence of residual disease; and 8.3 % until progression. "( Should we continue temozolomide beyond six cycles in the adjuvant treatment of glioblastoma without an evidence of clinical benefit? A cost analysis based on prescribing patterns in Spain.
Arranz, JL; Balañá, C; Benavides, M; Bugés, C; Cano, JM; de la Peñas, R; García-Bueno, JM; Gil, M; Lopez, D; Martin, JM; Molina-Garrido, MJ; Perez-Segura, P; Rodriguez, A; Sanz, SM; Sepúlveda, JM; Vaz, MA, 2014)		2.17
"Temozolomide-treated cells had increased methylation of the cytosine-phosphate-guanine islands in the Wnt3a gene promoter, decreased expression of Wnt3a, disrupted glycogen synthase-3 kinase/β-catenin axis, reduced transcriptional activation of ABCB1, and a lower amount and activity of Pgp."( Temozolomide downregulates P-glycoprotein expression in glioblastoma stem cells by interfering with the Wnt3a/glycogen synthase-3 kinase/β-catenin pathway.
Annovazzi, L; Bosia, A; Caldera, V; Campia, I; Ghigo, D; Kopecka, J; Mellai, M; Riganti, C; Salaroglio, IC; Schiffer, D, 2013)		2.55
"Temozolomide treatment of 293_pcDNA3.1 cells intensified the stochastic punctuated genome changes and CNAs, and significantly reduced viability and CFE."( Step-wise and punctuated genome evolution drive phenotype changes of tumor cells.
Andreieva, S; Huleyuk, N; Kavsan, V; Korets, K; Mykytenko, D; Stepanenko, A; Vassetzky, Y, 2015)		1.14
"Temozolomide treatment significantly induced mRNA expression of nearly all investigated EMT markers in T98G glioma cells."( Epithelial-to-mesenchymal transition in paired human primary and recurrent glioblastomas.
Hattermann, K; Held-Feindt, J; Kubelt, C; Mehdorn, HM; Sebens, S, 2015)		1.14
"Temozolomide-treated patients with the rs16906252 T genotype have better survival, irrespective of tumor methylation status."( The MGMT promoter SNP rs16906252 is a risk factor for MGMT methylation in glioblastoma and is predictive of response to temozolomide.
Cloughesy, TF; Ha, W; Hitchins, MP; Lai, A; McDonald, KL; Nguyen, HN; Nowak, AK; Rapkins, RW; Wang, F, 2015)		1.35
"Temozolomide treatment did not affect TPM plasma concentrations in chronically treated patients. "( Temozolomide treatment does not affect topiramate and oxcarbazepine plasma concentrations in chronically treated patients with brain tumor-related epilepsy.
Albani, F; Baruzzi, A; Contin, M; Dinapoli, L; Fabi, A; Jandolo, B; Maschio, M; Pace, A; Zarabla, A, 2008)		3.23
"Temozolomide treatment increased the number of SP cells, and this corresponded to more progenitor-like cells, concurrent with elevated expression of several ABC transporters."( Characterization of a side population of astrocytoma cells in response to temozolomide.
Ang, BT; Chong, KH; Chua, C; See, SJ; Tang, C; Wong, MC; Zaiden, N, 2008)		1.3
"Temozolomide, the standard treatment of gliomas, although not an ABCG2 substrate, increases the SP in glioma cells, especially in cells missing PTEN."( PTEN/PI3K/Akt pathway regulates the side population phenotype and ABCG2 activity in glioma tumor stem-like cells.
Bleau, AM; Brennan, CW; Fomchenko, EI; Hambardzumyan, D; Holland, EC; Huse, JT; Ozawa, T, 2009)		1.07
"Temozolomide treatment may be an effective option for some aggressive pituitary tumors or carcinomas. "( Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience.
Assaker, R; Bernier, M; Borson-Chazot, F; Brue, T; Caron, P; Chabre, O; Chanson, P; Cornélius, A; Cortet-Rudelli, C; de Fraipont, F; Dufour, H; Figarella-Branger, D; François, P; Gaillard, S; Jouanneau, E; Muller, M; Passagia, JG; Raverot, G; Salenave, S; Sturm, N; Trouillas, J, 2010)		3.25
"Temozolomide treatment has a wide range of efficacy in patients with pituitary carcinoma or locally aggressive pituitary adenoma. "( Salvage therapy with temozolomide in patients with aggressive or metastatic pituitary adenomas: experience in six cases.
Cangi, MG; Gill, AJ; Losa, M; Mazza, E; McCormack, A; Mortini, P; Motta, M; Reni, M; Talarico, A; Terreni, MR, 2010)		2.12
"Temozolomide treatment was significantly decreased in tumor tissue intratumoral vessel number / total tumor area level."( Combination hyperbaric oxygen and temozolomide therapy in C6 rat glioma model.
Bilir, A; Bozkurt, ER; Dagıstan, Y; Karaca, I; Ozar, E; Toklu, A; Yagmurlu, K, 2012)		1.38
"Temozolomide-treated control cells activated the DNA damage signal transducers Chk1, Chk2, and p38, leading to Cdc25C and Cdc2 inactivation, prolonged G2 arrest, and loss of clonagenicity by a combination of senescence and mitotic catastrophe."( Akt activation suppresses Chk2-mediated, methylating agent-induced G2 arrest and protects from temozolomide-induced mitotic catastrophe and cellular senescence.
Berger, MS; Hirose, Y; Katayama, M; Mirzoeva, OK; Pieper, RO, 2005)		1.27
"Temozolomide (TMZ) treatment and hyperthermia served as controls."( Irradiation and hypoxia promote homing of haematopoietic progenitor cells towards gliomas by TGF-beta-dependent HIF-1alpha-mediated induction of CXCL12.
Frank, B; Möhle, R; Tabatabai, G; Weller, M; Wick, W, 2006)		1.06
"Temozolomide treatment of high-grade tv-a gliomas provided a 14-day growth delay compared with vehicle controls."( Magnetic resonance imaging determination of tumor grade and early response to temozolomide in a genetically engineered mouse model of glioma.
Hambardzumyan, D; Holland, EC; Kreger, AR; Leopold, WR; McConville, P; Moody, JB; Rehemtulla, A; Ross, BD; Woolliscroft, MJ, 2007)		1.29
"Temozolomide treatment caused a decrease in cellular NAD levels, and this was abolished by the PADPRP inhibitors."( Potentiation of temozolomide-induced cytotoxicity: a comparative study of the biological effects of poly(ADP-ribose) polymerase inhibitors.
Boulton, S; Curtin, NJ; Durkacz, BW; Golding, BT; Griffin, RJ; Pemberton, LC; Porteous, JK, 1995)		1.36
"Temozolomide treatment of TK6 cells brought about efficient cell growth inhibition, G2/M arrest, and apoptosis, as indicated by the results of cytofluorimetric analysis of 5-bromo-2'-deoxyuridine incorporation and DNA content and evaluation of DNA fragmentation."( Involvement of the mismatch repair system in temozolomide-induced apoptosis.
Benincasa, E; Bonmassar, E; D'Atri, S; Graziani, G; Jiricny, J; Lacal, PM; Pagani, E; Tentori, L; Zambruno, G, 1998)		1.28
"Mice treated with temozolomide showed recognition memory impairment, along with hippocampal TNF-α and BDNF mRNA expression level raise, and detection of histological insults in hematoxylin and eosin hippocampal slides."( Effect of l -Dopa in acute temozolomide-induced cognitive impairment in male mice: a possible antineuroinflammatory role.
Ahmadi-Zeidabadi, M; Asadi-Shekaari, M; Esmaeilpour, K; Jafarinejad-Farsangi, S; Pardakhty, A; Salarinejad, A; Shabani, M, 2023)		1.53
"Treatment with Temozolomide and Lomeguatrib, a potent MGMT inhibitor, produced a huge, although transient, blastolysis and complete disappearance of all skin lesions."( Triazene compounds in the treatment of acute myeloid leukemia: a short review and a case report.
Aquino, A; Bernardini, S; Bianchi, A; Bonmassar, E; Bonmassar, L; D'Atri, S; Franzese, O; Lattuada, D; Marchesi, F; Margison, GP; Pascale, E, 2013)		0.73
"Treatment with temozolomide was given."( Nonanaplastic pleomorphic xanthoastrocytoma with meningeal dissemination presenting with bilateral visual loss.
Berciano, J; Delgado-Alvarado, M; García-Castaño, A; Gómez-Román, J; Polo, JM; Rodríguez-Rodríguez, E; Sánchez-Salmón, E, )		0.47
"Retreatment with temozolomide (TMZ) is one treatment option."( Dendritic cell vaccination combined with temozolomide retreatment: results of a phase I trial in patients with recurrent glioblastoma multiforme.
Ancelet, LR; Bauer, E; Dzhelali, M; Findlay, MP; Gasser, O; Hamilton, DA; Hermans, IF; Hunn, MK; Mester, B; Sharples, KJ; Wood, CE, 2015)		1.01
"When treated with temozolomide (TMZ), an oral alkylating chemotherapy drug, most low-grade gliomas (LGG) show an initial volume decrease but this effect is rarely long lasting."( Analysis of temozolomide resistance in low-grade gliomas using a mechanistic mathematical model.
Alentorn, A; Delattre, JY; Ducray, F; Grenier, E; Honnorat, J; Idbaih, A; Kaloshi, G; Mazzocco, P; Ollier, E; Psimaras, D; Ricard, D; Samson, A, 2017)		1.16
"Treatment with temozolomide resulted in a significant improvement in symptoms, a reduction of plasma ACTH to 389 pmol/l and regression of tumour on magnetic resonance imaging scan after four cycles of treatment."( Treatment of Nelson's syndrome with temozolomide.
Alusi, G; Berney, DM; Drake, WM; Evanson, J; Kovacs, K; Monson, JP; Moyes, VJ; Plowman, PN; Sabin, HI, 2009)		0.97
"Treatment with temozolomide alone or in combination with capecitabine and bevacizumab resulted in objective response or stabilization in 71% of PDEC patients who failed on first-line chemotherapy. "( Clinical effect of temozolomide-based chemotherapy in poorly differentiated endocrine carcinoma after progression on first-line chemotherapy.
Busch, C; Knappskog, S; Oberg, K; Sebjornsen, S; Sorbye, H; Welin, S, 2011)		1.05
"Treatment with temozolomide was stopped in 12 patients due to side-effects in general, whereas in only three patients (7.1%) treatment had to be discontinued due to haematological side-effects."( Prolonged administration of temozolomide in adult patients with anaplastic glioma.
Freyschlag, CF; Janzen, E; Lohr, F; Schmieder, K; Seiz, M; Smolczyk, DR; Thomé, C; Tuettenberg, J; Weiss, C; Wenz, F, 2011)		1
"Treatment with temozolomide alone or in combination with capecitabine and bevacizumab has recently shown promising results."( Temozolomide as second or third line treatment of patients with neuroendocrine carcinomas.
Federspiel, B; Hansen, CP; Kjaer, A; Knigge, U; Langer, SW; Olsen, IH; Sørensen, JB, 2012)		2.16
"Treatment with temozolomide and thalidomide was associated with an objective biochemical (chromogranin A) response rate of 40%, and a radiologic response rate of 25% (45% among pancreatic endocrine tumors, 33% among pheochromocytomas, and 7% among carcinoid tumors). "( Phase II study of temozolomide and thalidomide in patients with metastatic neuroendocrine tumors.
Clark, JW; Enzinger, PC; Fuchs, CS; Kulke, MH; Michelini, A; Muzikansky, A; Ryan, DP; Stuart, K; Vincitore, M, 2006)		1.02
"Treatment with temozolomide resulted in relief of clinical symptoms and stabilization of tumour growth for 8 months."( Metastatic medulloblastoma in an adult; treatment with temozolomide.
Bernsen, HJ; Poelen, J; Prick, MJ, 2007)		0.93
"Treatment with temozolomide combined with AMG 102 resulted in increased inhibition of cell growth in vitro compared with treatment with either single agent alone. "( AMG 102, a fully human anti-hepatocyte growth factor/scatter factor neutralizing antibody, enhances the efficacy of temozolomide or docetaxel in U-87 MG cells and xenografts.
Burgess, TL; Coxon, A; Jun, HT; Kendall, R; Radinsky, R; Rex, K; Sun, J, 2007)		0.9
"Treatment with temozolomide was generally well tolerated, with occasionally moderate toxicity. "( A phase II study of temozolomide in hormone-refractory prostate cancer.
Busstra, MB; Catsburg, T; Lang, MS; Mickisch, GH; Schröder, FH; van Brussel, JP, 2000)		0.98
"Treatment with temozolomide was well tolerated."( Phase II study of temozolomide in heavily pretreated cancer patients with brain metastases.
Bacoyiannis, C; Bafaloukos, D; Bamias, A; Christodoulou, C; Karabelis, A; Kosmidis, P; Papakostas, P; Samantas, E; Skarlos, DV, 2001)		0.98
"Treatment with temozolomide is now being explored in patients with newly diagnosed malignant glioma in several ongoing clinical trials, and alternative treatment schedules are being evaluated."( New approaches for temozolomide therapy: use in newly diagnosed glioma.
Newlands, E; Stupp, R, 2001)		0.98

Toxicity

Temozolomide (TMZ) is a widely used oral alkylating agent that has been associated with the development of severe hematologic adverse events (HAEs) In this project, we evaluated the effects of silibinin, a natural plant component of milk thistle seeds, to potentiate toxic effects of chemotherapy drugs.

ExcerptReferenceRelevance
"The effects of treatment of mice with O6-benzylguanine (O6-BeG) on the levels of O6-alkylguanine-DNA alkyltransferase (ATase) in the hematopoietic compartment and on the in vivo sensitivity of hematopoietic progenitor cells to the toxic and clastogenic effects of the antitumor agents 1,3-bis(2-chloroethyl)-nitrosourea (BCNU) and temozolomide were studied."( O6-benzylguanine potentiates the in vivo toxicity and clastogenicity of temozolomide and BCNU in mouse bone marrow.
Ashby, J; Chinnasamy, N; Dexter, TM; Fairbairn, LJ; Hickson, I; Margison, GP; Rafferty, JA; Tinwell, H, 1997)		0.7
" Similar degrees of protection were seen for the methylating agent streptozotocin, but no protection was detected for the chloroethylating agents carmustine or mitozolomide in the samples for which there was protection against the toxic effects of Tz."( Macrophage inflammatory protein 1alpha attenuates the toxic effects of temozolomide in human bone marrow granulocyte-macrophage colony-forming cells.
Chang, J; Clemons, M; Dexter, TM; Heyworth, C; Howell, A; Lord, B; Margison, G; Testa, N; Watson, A, 2000)		0.54
" Potentiation of cytotoxicity was obtained at concentrations of NU1025 and NU1085 that were not toxic per se; however, NU1085 alone was 3-fold more cytotoxic (LC50 values ranged from 83 to 94 microM) than NU1025 alone (LC50 > 900 microM)."( Potentiation of temozolomide and topotecan growth inhibition and cytotoxicity by novel poly(adenosine diphosphoribose) polymerase inhibitors in a panel of human tumor cell lines.
Calvert, AH; Curtin, NJ; Delaney, CA; Durkacz, BW; Hostomsky, Z; Kyle, S; Newell, DR; Wang, LZ; White, AW, 2000)		0.65
"The DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT) has been shown to protect cells from the toxic and mutagenic effect of alkylating agents by removing lesions from the O6 position of guanine."( Effect of O6-benzylguanine on alkylating agent-induced toxicity and mutagenicity. In Chinese hamster ovary cells expressing wild-type and mutant O6-alkylguanine-DNA alkyltransferases.
Cai, Y; Dolan, ME; Ludeman, SM; Pegg, AE; Wu, MH; Xu-Welliver, M, 2000)		0.31
" Temozolomide was safe and well tolerated."( Safety and efficacy of temozolomide in patients with recurrent anaplastic oligodendrogliomas after standard radiotherapy and chemotherapy.
Barrie, M; Braguer, D; Chinot, OL; Dufour, H; Figarella-Branger, D; Grisoli, F; Honore, S; Martin, PM; Muracciole, X, 2001)		1.53
"Temozolomide is safe and effective in the treatment of recurrent AO and AOA."( Safety and efficacy of temozolomide in patients with recurrent anaplastic oligodendrogliomas after standard radiotherapy and chemotherapy.
Barrie, M; Braguer, D; Chinot, OL; Dufour, H; Figarella-Branger, D; Grisoli, F; Honore, S; Martin, PM; Muracciole, X, 2001)		2.06
" This study also analyzed the ratio of the toxic effect of TMZ on MNC and on tumor cells (i."( DNA repair enzymes and cytotoxic effects of temozolomide: comparative studies between tumor cells and normal cells of the immune system.
Alvino, E; Bonmassar, L; D'Atri, S; Falcinelli, S; Fuggetta, MP; Guadagni, F; Lacal, PM; Pagani, E; Passarelli, F; Pepponi, R; Prete, SP; Turriziani, M, 2003)		0.58
"Postoperative radiochemotherapy with 30-33 daily doses of temozolomide (75 mg/m(2)) is safe in patients with malignant glioma."( Efficacy and toxicity of postoperative temozolomide radiochemotherapy in malignant glioma.
Eich, HT; Kocher, M; Kunze, S; Müller, RP; Semrau, R, 2005)		0.84
" CB related adverse events occurring in more than one patient were fatigue, gait disturbance, nystagmus, and confusion."( Convection-enhanced delivery of cintredekin besudotox (interleukin-13-PE38QQR) followed by radiation therapy with and without temozolomide in newly diagnosed malignant gliomas: phase 1 study of final safety results.
Asher, AL; Chang, SM; Croteau, D; Grahn, AY; Husain, SR; Kunwar, S; Lang, FF; Parker, K; Puri, RK; Sampson, JH; Shaffrey, M; Sherman, JW; Vogelbaum, MA, 2007)		0.55
" Thus, the implantation of BCNU wafers prior to TMZ and radiotherapy appears safe in newly diagnosed GBM patients."( A retrospective study of the safety of BCNU wafers with concurrent temozolomide and radiotherapy and adjuvant temozolomide for newly diagnosed glioblastoma patients.
Mitchell, SB; Pan, E; Tsai, JS, 2008)		0.58
" The adverse effects related with TMZ administration are divided in three categories: myelosuppression, non haematologic toxicity, and infections."( The safety of the temozolomide in patients with malignant glioma.
Dario, A; Tomei, G, 2006)		0.67
" Although TMZ is generally safe and acute toxicity is well documented, there are limited data on long-term toxicities."( Long-term use of temozolomide: could you use temozolomide safely for life in gliomas?
Bell, D; Khasraw, M; Wheeler, H, 2009)		0.69
" There were no toxic deaths."( Temozolomide: a safe and effective treatment for malignant digestive endocrine tumors.
Couvelard, A; Faivre, S; Hammel, P; Hentic, O; Larroque, B; Lévy, P; Maire, F; Raymond, E; Ruszniewski, P; Yapur, L; Zappa, M, 2009)		1.8
"The primary objective of this augmental, prospective, uncontrolled phase II multicentre trial was to assess adverse events (AE) associated with malignant glioma resection using 5-aminolevulinic (5-ALA)."( Favorable outcome in the elderly cohort treated by concomitant temozolomide radiochemotherapy in a multicentric phase II safety study of 5-ALA.
Kern, BC; Krex, D; Mehdorn, HM; Nestler, U; Pichlmeier, U; Stockhammer, F; Stummer, W; Vince, GH, 2011)		0.61
" When this regimen was administered to mice containing humanized bone marrow, flow cytometric analyses indicated that the human bone marrow cells were significantly more sensitive to treatment than the murine bone marrow cells and that the regimen was highly toxic to human-derived hematopoietic cells of all lineages (progenitor, lymphoid, and myeloid)."( Humanized bone marrow mouse model as a preclinical tool to assess therapy-mediated hematotoxicity.
Bailey, B; Baluyut, AR; Cai, S; Chan, RJ; Ernstberger, A; Goebel, WS; Jones, DR; Juliar, BE; Mayo, LD; Pollok, KE; Sinn, AL; Wang, H, 2011)		0.37
"Temozolomide (TMZ) is a widely used oral alkylating agent that has been associated with the development of severe hematologic adverse events (HAEs)."( Hematologic adverse events associated with temozolomide.
Abdur, S; Bressler, LR; Letarte, N; Villano, JL; Yu, JM, 2012)		2.08
" Although there is possibly an indication that metronomic regimens of TMZ result in better PFS and response rate when compared to the conventional standard 5 day regimen, insufficient available data and study heterogeneity preclude any safe conclusions."( Using different schedules of Temozolomide to treat low grade gliomas: systematic review of their efficacy and toxicity.
Athanasiou, T; Lashkari, HP; Moreno, L; Saso, S; Zacharoulis, S, 2011)		0.66
"The results suggest that Cyberknife re-treatments are relatively safe using selected dose/fraction schemes."( Efficacy and toxicity of CyberKnife re-irradiation and "dose dense" temozolomide for recurrent gliomas.
Arpa, D; Cardali, S; Conti, A; De Renzis, C; Granata, F; Pontoriero, A; Romanelli, P; Siragusa, C; Tomasello, C; Tomasello, F, 2012)		0.61
" The survival rate, progression-free survival, overall survival time and adverse reactions were observed."( [Efficacy and safety of 3-dimensional conformal radiotherapy combined with temozolomide for glioma].
Tu, Q; Wang, L; Zhou, R; Zhou, W, 2011)		0.6
"The adverse reactions were mild and tolerable."( [Efficacy and safety of 3-dimensional conformal radiotherapy combined with temozolomide for glioma].
Tu, Q; Wang, L; Zhou, R; Zhou, W, 2011)		0.6
" Magnetic resonance imaging and laboratory tests were performed to evaluate the efficacy and adverse reactions."( [Safety and efficacy of three-dimensional conformal radiotherapy combined with temozolomide in treatment of diffuse brainstem gliomas].
Cai, CL; Fang, HH; Kang, JB; Li, FM; Nie, Q, 2011)		0.6
" Hematotoxicity is listed as a frequent adverse drug reaction in the US prescribing information and hepatotoxicity has been reported infrequently in the postmarketing period."( Severe sustained cholestatic hepatitis following temozolomide in a patient with glioblastoma multiforme: case study and review of data from the FDA adverse event reporting system.
Bronder, E; Garbe, E; Herbst, H; Kauffmann, W; Klimpel, A; Orzechowski, HD; Sarganas, G; Thomae, M, 2012)		0.63
"Conformal Radiation yields low grades of MRI assessed neurotoxicity and cognitive disturbance in patients of HGG with no adverse impact on local control and survival."( Survival outcome and neurotoxicity in patients of high-grade gliomas treated with conformal radiation and temozolamide.
Aggarwal, HN; Anand, AK; Babu, AG; Chaudhory, AR; Chaudhury, PS; Jena, A; Negi, PS; Rao, A; Sachdeva, PK; Sinha, SN, )		0.13
"Combining Gliadel wafers and radiochemotherapy with TMZ may carry the risk of increased adverse events (AE)."( Safety and efficacy of Gliadel wafers for newly diagnosed and recurrent glioblastoma.
Anile, C; Balducci, M; Chiesa, S; De Bonis, P; Fiorentino, A; Maira, G; Mangiola, A; Pompucci, A, 2012)		0.38
" The incidence of hematological adverse effects (AE) was recorded for all patients."( Toxicity and survival in primary glioblastoma patients treated with concomitant plus adjuvant temozolomide versus adjuvant temozolomide: results of a single-institution, retrospective, matched-pair analysis.
Bock, HC; Brück, W; Giese, A; Gutenberg, A; Reifenberger, G, 2013)		0.61
" However severe hematologic adverse events (HAEs), including myelodysplastic syndrome and aplastic anemia, have also been reported."( Temozolomide-related hematologic toxicity.
De Sanctis, V; Enrici, RM; Minniti, G; Scaringi, C, 2013)		1.83
"Central diabetes insipidus is a rare but reversible side effect of treatment with TMZ."( Central diabetes insipidus: a previously unreported side effect of temozolomide.
Faje, AT; Klibanski, A; Makimura, H; Miller, KK; Nachtigall, L; Wexler, D, 2013)		0.63
" Although TMZ is considered to be a safe drug, it has been demonstrated to cause severe myelotoxicity; in particular, some case reports and small series studies have reported severe myelotoxicity developing during TMZ and concomitant RT."( Clinical and Genetic Factors Associated With Severe Hematological Toxicity in Glioblastoma Patients During Radiation Plus Temozolomide Treatment: A Prospective Study.
Amadori, A; Berti, F; Bertorelle, R; Della Puppa, A; Farina, P; Lombardi, G; Marcato, R; Rumiato, E; Sacchetto, V; Saggioro, D; Zagonel, V; Zustovich, F, 2015)		0.62
" The evaluating indicators were overall response rate (ORR), 1-year survival rate, and several of the most frequent adverse events."( Efficacy and safety between temozolomide alone and temozolomide-based double therapy for malignant melanoma: a meta-analysis.
Jia, HY; Jiang, G; Lei, TC; Li, RH; Liu, YQ; Sun, C, 2014)		0.7
" The aim of this study was to investigate the benefits and adverse effects of this combined therapy in elderly patients with glioblastoma."( Toxicity and outcome of radiotherapy with concomitant and adjuvant temozolomide in elderly patients with glioblastoma: a retrospective study.
Mukasa, A; Narita, Y; Saito, K; Saito, N; Shibui, S; Shinoura, N; Tabei, Y, 2014)		0.64
"8% of the 618 toxicities were Common Terminology Criteria for Adverse Events (CTCAE) grade 1 or 2, while 15."( Toxicity profile of temozolomide in the treatment of 300 malignant glioma patients in Korea.
Bae, SH; Cho, SY; Kim, CY; Kim, TM; Kim, YH; Kim, YJ; Lee, MM; Lee, SH; Park, CK; Park, MJ, 2014)		0.73
" In this project, we evaluated the effects of silibinin, a natural plant component of milk thistle seeds, to potentiate toxic effects of chemotherapy drugs such as temozolomide, etoposide and irinotecan on LN229, U87 and A172 (P53 and phosphatase and tensin homolog (PTEN) -tumor suppressor-mutated) glioma cell lines."( The effect of silibinin in enhancing toxicity of temozolomide and etoposide in p53 and PTEN-mutated resistant glioma cell lines.
Elhag, R; Mazzio, EA; Soliman, KF, 2015)		0.87
" BBBD temozolomide was toxic in the efficacy study, but there was no evidence of symptomatic neurotoxicity in rats given IA temozolomide."( Intra-arterial administration improves temozolomide delivery and efficacy in a model of intracerebral metastasis, but has unexpected brain toxicity.
Muldoon, LL; Netto, JP; Neuwelt, EA; Pagel, MA, 2016)		1.18
" Data on adverse events (AEs) were collected throughout."( Bevacizumab, temozolomide, and radiotherapy for newly diagnosed glioblastoma: comprehensive safety results during and after first-line therapy.
Chinot, OL; Cloughesy, T; Dhar, S; Garcia, J; Henriksson, R; Mason, W; Nishikawa, R; Pozzi, E; Saran, F; Wick, W, 2016)		0.8
" Patients reported adverse effects in Common Toxicity Criteria for Adverse Events diaries; recorded vomiting, nausea, and rescue medication use in diaries (which were used to assess cRINV-CR); and reported QoL 4 days/week using the Modified Functional Living Index-Emesis (M-FLIE) and Osoba nausea and vomiting/retching modules."( Phase II study to evaluate the safety and efficacy of intravenous palonosetron (PAL) in primary malignant glioma (MG) patients receiving standard radiotherapy (RT) and concomitant temozolomide (TMZ).
Affronti, ML; Allen, K; Desjardins, A; Friedman, HS; Healy, PN; Herndon, JE; Kirkpatrick, J; McSherry, F; Peters, KB; Vredenburgh, JJ; Woodring, S, 2016)		0.63
"Single-dose weekly PAL is a safe and tolerable antiemetic for cRINV prevention in MG patients receiving standard RT and concomitant TMZ."( Phase II study to evaluate the safety and efficacy of intravenous palonosetron (PAL) in primary malignant glioma (MG) patients receiving standard radiotherapy (RT) and concomitant temozolomide (TMZ).
Affronti, ML; Allen, K; Desjardins, A; Friedman, HS; Healy, PN; Herndon, JE; Kirkpatrick, J; McSherry, F; Peters, KB; Vredenburgh, JJ; Woodring, S, 2016)		0.63
" 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
" In conclusion, this work reports at least four compounds (5b, 5e, 5g and 6e) with potential anti-tumor effect against glioblastoma multiform cell presenting activity at low concentrations and safe profile of cytotoxicity."( Thiazolidin-4-ones from 4-(methylthio)benzaldehyde and 4-(methylsulfonyl)benzaldehyde: Synthesis, antiglioma activity and cytotoxicity.
Azambuja, JH; Braganhol, E; Cunico, W; da Silva, CEH; da Silva, DS; de Carvalho, TR; Frizzo, CP; Soares, MSP; Spanevello, RM; Zimmer, GC, 2016)		0.43
" The most common treatment emergent adverse events were ocular: blurred vision, dry eye, keratitis, photophobia, and eye pain."( Efficacy and safety results of ABT-414 in combination with radiation and temozolomide in newly diagnosed glioblastoma.
Ansell, P; Fichtel, L; Fischer, J; Gan, HK; Gomez, E; Holen, KD; Kumthekar, P; Lassman, AB; Lee, HJ; Mandich, H; Merrell, R; Munasinghe, W; Reardon, DA; Roberts-Rapp, L; Scott, AM; Sulman, EP; van den Bent, M; Xiong, H, 2017)		0.69
" ATOR showed similar cytotoxic effect as TMZ to glioma cells, and it may be a safer drug, regarding side effect induction, than chemotherapic agents."( Atorvastatin Promotes Cytotoxicity and Reduces Migration and Proliferation of Human A172 Glioma Cells.
Dal-Cim, T; Lopes, FG; Ludka, FK; Nedel, CB; Oliveira, KA; Tasca, CI, 2018)		0.48
" We aimed to determine whether or not pulse high-dose lapatinib was a safe and tolerable regimen in addition to standard therapy."( Report of safety of pulse dosing of lapatinib with temozolomide and radiation therapy for newly-diagnosed glioblastoma in a pilot phase II study.
Cloughesy, TF; Faiq, N; Green, R; Green, S; Hu, J; Lai, A; Mellinghoff, I; Nghiemphu, PL; Yu, A, 2017)		0.71
"Extended cycles of temozolomide are safe and feasible for Chinese patients with disease responsive to temozolomide."( Feasibility and safety of extended adjuvant temozolomide beyond six cycles for patients with glioblastoma.
Chan, DT; Hsieh, SY; Kam, MK; Loong, HH; Ng, SC; Poon, DM; Poon, WS; Tsang, WK, 2017)		1.04
"00%) had grade 3 adverse events."( Safety and Efficacy of the S-1/Temozolomide Regimen in Patients with Metastatic Neuroendocrine Tumors.
Chi, Y; Zhao, H; Zhao, J, 2018)		0.77
" This review summarizes the mechanism of action, efficacy, and adverse events based on pre-clinical studies and clinical trials for TTF in GBM."( Tumor treating fields: a novel and effective therapy for glioblastoma: mechanism, efficacy, safety and future perspectives.
Zhu, JJ; Zhu, P, 2017)		0.46
" For recurrent GBM, the efficacy of TTF monotherapy was shown to be equivalent in PFS and OS without systemic adverse events when compared to the control group that received best physicians-chosen chemotherapies (EF-11 trial)."( Tumor treating fields: a novel and effective therapy for glioblastoma: mechanism, efficacy, safety and future perspectives.
Zhu, JJ; Zhu, P, 2017)		0.46
"Radiochemotherapy involving cisplatinum-based polychemotherapy is more toxic than radiotherapy in combination with temozolomide."( Concurrent radiotherapy with temozolomide vs. concurrent radiotherapy with a cisplatinum-based polychemotherapy regimen : Acute toxicity in pediatric high-grade glioma patients.
Bison, B; Bojko, S; Gielen, GH; Hoffmann, M; Kortmann, RD; Kramm, CM; Pietsch, T; Seidel, C; von Bueren, AO; Warmuth-Metz, M, 2018)		0.98
" Keratitis was the most common grade 3 adverse event observed in 6/38 (16%) patients; thrombocytopenia was the most common grade 4 event seen in 5/38 (13%) patients."( Safety, pharmacokinetics, and antitumor response of depatuxizumab mafodotin as monotherapy or in combination with temozolomide in patients with glioblastoma.
Ansell, PJ; Butowski, N; Fichtel, L; Fischer, J; Gan, HK; Gomez, EJ; Holen, KD; Kumthekar, P; Lassman, AB; Lee, HJ; Lwin, Z; Mandich, H; Merrell, R; Munasinghe, WP; Reardon, DA; Roberts-Rapp, LA; Scott, AM; van den Bent, M; Wheeler, H; Xiong, H, 2018)		0.69
" Compelling clinical data also support the safety of carmustine wafer implantation (grade A recommendation) in these patients and suggest that observed adverse events can be avoided in experienced neurosurgeon hands."( Carmustine wafer implantation for high-grade gliomas: Evidence-based safety efficacy and practical recommendations from the Neuro-oncology Club of the French Society of Neurosurgery.
Caire, F; Guyotat, J; Menei, P; Metellus, P; Pallud, J; Roux, A, 2017)		0.46
" The observation index of both groups included the short- and long-term clinical efficacies, improvement of symptoms and signs, quality of life (QOL), and adverse responses."( Efficacy and safety of temozolomide plus whole-brain radiotherapy in the treatment of intracranial metastases.
Liu, HP; Wang, JW; Zheng, KB, 2017)		0.77
" Although temozolomide is generally a well tolerated drug, with rare severe toxic effects, sometimes certain toxicities can overcome the life risk of the underlying malignancy."( Severe hematologic temozolomide-related toxicity and lifethreatening infections.
Nikitovic, M; Stepanovic, A, )		0.86
" Common adverse events (AEs) were blurred vision (63%), fatigue (38%), and photophobia (35%)."( Safety and efficacy of depatuxizumab mafodotin + temozolomide in patients with EGFR-amplified, recurrent glioblastoma: results from an international phase I multicenter trial.
Ansell, PJ; Bain, E; Butowski, N; Gan, HK; Gomez, E; Holen, KD; Kumthekar, P; Lassman, AB; Lee, HJ; Lwin, Z; Maag, D; Merrell, R; Mikkelsen, T; Nabors, LB; Papadopoulos, KP; Penas-Prado, M; Reardon, DA; Roberts-Rapp, L; Scott, AM; Simes, J; van den Bent, MJ; Walbert, T; Wheeler, H; Xiong, H, 2019)		0.77
" 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)		0.7
"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)		0.7
"Treatments for advanced melanoma are associated with different adverse events (AEs), which may be costly to manage."( Direct costs associated with adverse events of systemic therapies for advanced melanoma: Systematic literature review.
Chmielowski, B; Copley-Merriman, C; Liu, FX; Mauskopf, J; Stevinson, K; Wang, J; Zimovetz, EA, 2018)		0.48
"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)		0.73
" Together, our results suggest that trehalose, a safe nutrient supplement able to cross the blood-brain barrier, is a promising candidate, worthy to be further explored in vivo, to augment the therapeutic efficacy of TMZ and RT in melanoma brain metastases."( Trehalose inhibits cell proliferation and amplifies long-term temozolomide- and radiation-induced cytotoxicity in melanoma cells: A role for autophagy and premature senescence.
Allavena, G; Del Bello, B; Maellaro, E; Miracco, C; Pirtoli, L; Tini, P; Valacchi, G; Volpi, N, 2019)		0.75
"our data underline re-RT as a safe and feasible treatment with limited rate of toxicity, and a combined ones as a better option for selected patients."( Re-irradiation for recurrent glioma: outcome evaluation, toxicity and prognostic factors assessment. A multicenter study of the Radiation Oncology Italian Association (AIRO).
Alongi, F; Amelio, D; Borzillo, V; Ciammella, P; Clerici, E; di Monale, MB; Draghini, L; Fariselli, L; Ferrarese, F; Fiorentino, A; Galaverni, M; Krengli, M; Livi, L; Magrini, S; Maranzano, E; Masini, L; Minniti, G; Muto, P; Navarria, P; Pasqualetti, F; Pinzi, V; Scartoni, D; Scoccianti, S; Scorsetti, M; Tomatis, S, 2019)		0.51
" The procedure was well-tolerated, with no adverse clinical or radiologic events related to the procedure."( Blood-Brain Barrier Opening in Primary Brain Tumors with Non-invasive MR-Guided Focused Ultrasound: A Clinical Safety and Feasibility Study.
Alkins, R; Bethune, A; Heyn, C; Huang, Y; Hynynen, K; Ironside, S; Lipsman, N; Mainprize, T; Meng, Y; Perry, J; Sahgal, A; Trudeau, M, 2019)		0.51
"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)		0.76
" We retrieved evidence on treatment-related grade III/IV adverse events, progression-free survival (PFS) and overall survival (OS)."( A systematic literature review and network meta-analysis of effectiveness and safety outcomes in advanced melanoma.
Franken, MG; Gheorghe, M; Haanen, JBAG; Leeneman, B; Uyl-de Groot, CA; van Baal, PHM, 2019)		0.51
"00001), with no increase in adverse events (RR = 0."( The efficacy and safety of radiotherapy with adjuvant temozolomide for glioblastoma: A meta-analysis of randomized controlled studies.
Feng, Y; Wang, Y, 2020)		0.81
" The aim of this study was to introduce the Z-scan technique as a fast, accurate, inexpensive, and safe in vitro method to distinguish the cytotoxic effects of various treatments."( Z-scan method to measure the nonlinear optical behavior of cells for evaluating the cytotoxic effects of chemotherapy and hyperthermia treatments.
Ara, MHM; Ardakani, AA; Asgari, H; Ghader, A; Khoei, S; Minaei, SE, 2021)		0.62
" Common nonocular treatment-emergent adverse events (TEAEs) with both second-line and first-line Depatux-M included lymphopenia (42%, 33%, respectively), thrombocytopenia (39%, 47%), alanine aminotransferase increase (29%, 47%), and aspartate aminotransferase increase (24%, 60%); incidence of grade ≥3 TEAEs was 66% and 53%, respectively."( Safety and efficacy of depatuxizumab mafodotin in Japanese patients with malignant glioma: A nonrandomized, phase 1/2 trial.
Asai, K; Beppu, T; Date, I; Kagawa, N; Kanamori, M; Kasai, S; Kobayashi, H; Kumabe, T; Kuroda, J; Matsuda, M; Mishima, K; Muragaki, Y; Nagane, M; Narita, Y; Nishimura, Y; Ocampo, C; Ueki, K; Xiong, H; Yamada, M, 2021)		0.62
"Hematological adverse events (HAEs) are common during treatment for glioblastoma (GBM), usually associated with temozolomide (TMZ)."( Hematological adverse events in the management of glioblastoma.
Butts, AR; Garcia, CR; Jayswal, R; Morgan, RM; Myint, ZW; Villano, JL; Wang, C; Weiss, HL, 2022)		0.93
"9 months) compared to those with other or no adverse events (OS 14."( Hematological adverse events in the management of glioblastoma.
Butts, AR; Garcia, CR; Jayswal, R; Morgan, RM; Myint, ZW; Villano, JL; Wang, C; Weiss, HL, 2022)		0.72
" Only one possibly treatment-related treatment emergent adverse event (TEAE), Grade 1 gingival swelling, was observed."( Safety and tolerability of asunercept plus standard radiotherapy/temozolomide in Asian patients with newly-diagnosed glioblastoma: a phase I study.
Chen, KT; Hsu, PW; Huang, HL; Jung, SM; Ke, YX; Lin, YJ; Toh, CH; Tsai, HC; Tseng, CK; Wei, KC, 2021)		0.86
" In addition, OS, PFS and adverse event (AE) data on ndGBM and recurrent GBM (rGBM) were assessed."( Comparative efficacy and safety of therapeutics for elderly glioblastoma patients: A Bayesian network analysis.
Li, H; Ma, W; Qu, T; Wang, Y; Wu, J; Xia, Y; Xing, H; Zhao, B, 2022)		0.72
"5%) had treatment-emergent adverse events (TEAEs); 72."( Efficacy and Safety of Lanreotide Autogel and Temozolomide Combination Therapy in Progressive Thoracic Neuroendocrine Tumors (Carcinoid): Results from the Phase 2 ATLANT Study.
Amoroso, V; Berruti, A; Brizzi, MP; Colao, A; Faggiano, A; Fazio, N; Ferolla, P; Ghizzoni, S; Giuffrida, D; Houchard, A; Ibrahim, T; La Salvia, A; Marconcini, R; Mazzanti, P; Spada, F; Vaccaro, V; Volante, M, 2023)		1.17
" No unexpected adverse events clinically, or permanent end-organ damage during postmortem examination was identified in glioma subjects who had received standard or prolonged duration of BEV, TMZ or TIB regimen-based chemotherapies except rare events of bone marrow suppression."( Postmortem study of organ-specific toxicity in glioblastoma patients treated with a combination of temozolomide, irinotecan and bevacizumab.
Ballester, LY; Bhattacharjee, MB; Brown, RE; Buja, LM; Chen, L; Glass, WF; Hergenroeder, GW; Hunter, RL; Linendoll, N; Lu, G; Pilichowska, M; Pillai, AK; Rao, M; Tian, X; Wu, JK; Zhang, R; Zhu, JJ; Zhu, P, 2022)		0.94
" The patient's progression free survival time (PFS), total survival time (OS) and adverse reactions were observed by telephone, outpatient reexamination and other follow-up methods."( The efficacy and safety of low-dose temozolomide maintenance therapy in elderly patients with glioblastoma: a retrospective cohort study.
Ge, X; Gong, S; Guo, J; Tao, Q; Zhu, T, 2022)		1
" The main adverse reactions were digestive tract reactions and hematological toxicity."( The efficacy and safety of low-dose temozolomide maintenance therapy in elderly patients with glioblastoma: a retrospective cohort study.
Ge, X; Gong, S; Guo, J; Tao, Q; Zhu, T, 2022)		1
"In general, for elderly patients with good Karnofsky Performance Scale (KPS) scores, further reducing TMZ to maintain chemotherapy after the standard STUPP regimen may improve the PFS and OS to a certain extent, with tolerable adverse reactions and reduced cost."( The efficacy and safety of low-dose temozolomide maintenance therapy in elderly patients with glioblastoma: a retrospective cohort study.
Ge, X; Gong, S; Guo, J; Tao, Q; Zhu, T, 2022)		1
" A multicenter phase II trial was designed to determine: (1) the success rate of manufacturing the Aivita GBM vaccine (AV-GBM-1), (2) Adverse Events (AE) associated with AV-GBM-1 administration, and (3) survival."( Phase 2 study of AV-GBM-1 (a tumor-initiating cell targeted dendritic cell vaccine) in newly diagnosed Glioblastoma patients: safety and efficacy assessment.
Abedi, M; Aiken, RD; Bota, DA; Bota, PG; Carrillo, JA; Dillman, RO; Duma, CM; Hsieh, C; Hsu, FPK; Keirstead, HS; Kesari, S; Kong, XT; LaRocca, RV; Nistor, GI; Piccioni, DE; Taylor, TH, 2022)		0.72
" The primary endpoints were skin, neurological and psychiatric adverse events."( Safety and efficacy of tumour-treating fields (TTFields) therapy for newly diagnosed glioblastoma in Japanese patients using the Novo-TTF System: a prospective post-approval study.
Arakawa, Y; Kanamori, M; Mukasa, A; Muragaki, Y; Narita, Y; Nishikawa, R; Tanaka, S; Yamaguchi, S; Yamasaki, F, 2023)		0.91
" The most common tumour-treating-fields-therapy-related adverse event was beneath-array local skin reaction (60% of patients)."( Safety and efficacy of tumour-treating fields (TTFields) therapy for newly diagnosed glioblastoma in Japanese patients using the Novo-TTF System: a prospective post-approval study.
Arakawa, Y; Kanamori, M; Mukasa, A; Muragaki, Y; Narita, Y; Nishikawa, R; Tanaka, S; Yamaguchi, S; Yamasaki, F, 2023)		0.91
" Safety was determined by the number of treatment-related adverse events."( Antisecretory factor is safe to use as add-on treatment in newly diagnosed glioblastoma.
Belting, M; Bengzon, J; Cederberg, D; Darabi, A; Edvardsson, C; Ehinger, E; Kopecky, J; Siesjö, P; Tomasevic, G; Visse, E, 2023)		0.91
"No serious treatment-related adverse events were observed."( Antisecretory factor is safe to use as add-on treatment in newly diagnosed glioblastoma.
Belting, M; Bengzon, J; Cederberg, D; Darabi, A; Edvardsson, C; Ehinger, E; Kopecky, J; Siesjö, P; Tomasevic, G; Visse, E, 2023)		0.91
"We conclude that Salovum is safe to use as an add-on treatment for GBM."( Antisecretory factor is safe to use as add-on treatment in newly diagnosed glioblastoma.
Belting, M; Bengzon, J; Cederberg, D; Darabi, A; Edvardsson, C; Ehinger, E; Kopecky, J; Siesjö, P; Tomasevic, G; Visse, E, 2023)		0.91
" The most common adverse events were leukocytopenia (66."( Safety and Efficacy of Anlotinib Hydrochloride Plus Temozolomide in Patients with Recurrent Glioblastoma.
Bu, L; Cai, J; Chen, Q; Huang, K; Meng, X; Weng, Y; Xu, Q; Zhan, R; Zhang, L; Zheng, X, 2023)		1.16
" Adverse effects occurred in 18 patients (14 mild and 4 moderate or severe)."( Efficacy and safety of temozolomide in the treatment of aggressive pituitary neuroendocrine tumours in Spain.
Araujo-Castro, M; Biagetti, B; Cámara, R; Fajardo, C; García-Centeno, R; Guerrero-Pérez, F; Hanzu, F; Iglesias, P; Lamas, C; Mora, M; Remon-Ruiz, P; Soto, A, 2023)		1.22

Pharmacokinetics

This method was used successfully to perform brain and plasma pharmacokinetic studies of temozolomide in mice after intraperitoneal administration. The enhanced hematologic toxicity resulting from combining O(6)BG with temozlomide does not appear to be the result of a pharmacokinetics interaction between the agents.

ExcerptReferenceRelevance
" The half-life of the drug in the tumors was approximately 60 min."( Pharmacokinetics of the 13C labeled anticancer agent temozolomide detected in vivo by selective cross-polarization transfer.
Artemov, D; Bhujwalla, ZM; Glickson, JD; Griffiths, JR; Judson, IR; Leach, MO; Maxwell, RJ, 1995)		0.54
"We conclude that spectral analysis provides important pharmacokinetic information about radiolabeled anti-cancer drugs with relatively few model assumptions."( Pharmacokinetic assessment of novel anti-cancer drugs using spectral analysis and positron emission tomography: a feasibility study.
Brock, CS; Cunningham, VJ; Harte, RJ; Jones, T; Matthews, JC; Meikle, SR; Price, P; Wells, P, 1998)		0.3
" Plasma samples were obtained on days 1 and 2 to evaluate the pharmacokinetic parameters of TMZ alone and in combination with CDDP."( A Phase I and pharmacokinetic study of temozolomide and cisplatin in patients with advanced solid malignancies.
Agarwala, SS; Baker, SD; Barrington, R; Britten, CD; Diab, SG; Eckardt, JR; Eckhardt, SG; Fraass, U; Hammond, LA; Johnson, T; Rowinsky, EK; Statkevich, P; Villalona-Calero, M; Von Hoff, DD, 1999)		0.57
"Fifteen patients with advanced cancer were enrolled of which 12 were evaluable, all of whom had pharmacokinetic blood sampling."( Effect of gastric pH on the relative oral bioavailability and pharmacokinetics of temozolomide.
Beale, P; Brada, M; Cutler, DL; Judson, I; Marco, A; Moore, S; Reidenberg, P; Statkevich, P, 1999)		0.53
" There was no difference in the pharmacokinetic parameters of temozolomide or MTIC with or without the concomitant administration of ranitidine."( Effect of gastric pH on the relative oral bioavailability and pharmacokinetics of temozolomide.
Beale, P; Brada, M; Cutler, DL; Judson, I; Marco, A; Moore, S; Reidenberg, P; Statkevich, P, 1999)		0.77
" Statistical analyses of pharmacokinetic and pharmacodynamic end points in the control and TNP-470 treatment groups were completed by nonparametric tests."( Pharmacodynamic-mediated reduction of temozolomide tumor concentrations by the angiogenesis inhibitor TNP-470.
Chu, J; Gallo, JM; Li, S; Ma, J; Pulfer, S; Reed, K, 2001)		0.58
" It is proposed that the net balance of antiangiogenic drug-mediated pharmacodynamic actions will determine how drug disposition in tumors may be affected."( Pharmacodynamic-mediated effects of the angiogenesis inhibitor SU5416 on the tumor disposition of temozolomide in subcutaneous and intracerebral glioma xenograft models.
Gallo, JM; Guo, P; Li, S; Ma, J; Reed, K, 2003)		0.54
"To construct a population pharmacokinetic model for temozolomide (TMZ), a novel imidazo-tetrazine methylating agent and its metabolites MTIC and AIC in infants and children with primary central nervous system tumors."( Population pharmacokinetics of temozolomide and metabolites in infants and children with primary central nervous system tumors.
Fouladi, M; Gajjar, A; Heideman, RL; Kirstein, MN; Nair, G; Panetta, JC; Stewart, CF; Wilkinson, M, 2003)		0.86
"We evaluated the pharmacokinetics of TMZ and MTIC in 39 children (20 boys and 19 girls) with 132 pharmacokinetic studies (109 in the training set and 23 in the validation set)."( Population pharmacokinetics of temozolomide and metabolites in infants and children with primary central nervous system tumors.
Fouladi, M; Gajjar, A; Heideman, RL; Kirstein, MN; Nair, G; Panetta, JC; Stewart, CF; Wilkinson, M, 2003)		0.6
"To characterize and compare pharmacokinetic parameters in children and adults treated with temozolomide (TMZ) administered for 5 days in three doses daily, and to evaluate the possible relationship between AUC values and hematologic toxicity."( Pharmacokinetics of temozolomide given three times a day in pediatric and adult patients.
Barone, C; Caldarelli, M; Cefalo, G; Garrè, ML; Lazzareschi, I; Madon, E; Maira, G; Massimino, M; Mastrangelo, S; Mazzarella, G; Riccardi, A; Riccardi, R; Ridola, V; Ruggiero, A; Sandri, A, 2003)		0.86
"TMZ pharmacokinetic parameters were characterized in pediatric and adult patients with primary central nervous system tumors treated with doses ranging from 120 to 200 mg/m2 per day, divided into three doses daily for 5 days."( Pharmacokinetics of temozolomide given three times a day in pediatric and adult patients.
Barone, C; Caldarelli, M; Cefalo, G; Garrè, ML; Lazzareschi, I; Madon, E; Maira, G; Massimino, M; Mastrangelo, S; Mazzarella, G; Riccardi, A; Riccardi, R; Ridola, V; Ruggiero, A; Sandri, A, 2003)		0.64
"No difference appears to exist between pharmacokinetic parameters in adults and children when TMZ is administered in three doses daily."( Pharmacokinetics of temozolomide given three times a day in pediatric and adult patients.
Barone, C; Caldarelli, M; Cefalo, G; Garrè, ML; Lazzareschi, I; Madon, E; Maira, G; Massimino, M; Mastrangelo, S; Mazzarella, G; Riccardi, A; Riccardi, R; Ridola, V; Ruggiero, A; Sandri, A, 2003)		0.64
" The population pharmacokinetic analysis was performed with nonlinear mixed-effect modeling software."( Plasma and cerebrospinal fluid population pharmacokinetics of temozolomide in malignant glioma patients.
Buclin, T; Csajka, C; Decosterd, LA; Lejeune, F; Leyvraz, S; Ostermann, S; Stupp, R, 2004)		0.56
"This is the first human pharmacokinetic study on TMZ to quantify CSF penetration."( Plasma and cerebrospinal fluid population pharmacokinetics of temozolomide in malignant glioma patients.
Buclin, T; Csajka, C; Decosterd, LA; Lejeune, F; Leyvraz, S; Ostermann, S; Stupp, R, 2004)		0.56
" To that end, a novel method, based on physiologically based hybrid pharmacokinetic models, is presented to predict human tumor drug concentrations."( Pharmacokinetic model-predicted anticancer drug concentrations in human tumors.
Bookman, MA; Gallo, JM; Guo, P; Li, S; Ma, J; Orlansky, A; Pulfer, S; Vicini, P; Zhou, F, 2004)		0.32
"To develop a pharmacokinetic limited sampling model (LSM) for temozolomide and its metabolite MTIC in infants and children."( Development of a pharmacokinetic limited sampling model for temozolomide and its active metabolite MTIC.
Freeman, BB; Gajjar, A; Iacono, LC; Kirstein, MN; Nair, G; Panetta, JC; Stewart, CF, 2005)		0.81
" This accounted for prior distribution of temozolomide and MTIC pharmacokinetic parameters based on full pharmacokinetic sampling from 38 patients with 120 pharmacokinetic studies (dosage range 145-200 mg/m(2) per day orally)."( Development of a pharmacokinetic limited sampling model for temozolomide and its active metabolite MTIC.
Freeman, BB; Gajjar, A; Iacono, LC; Kirstein, MN; Nair, G; Panetta, JC; Stewart, CF, 2005)		0.84
" Furthermore, PARP activity was not inhibited by temozolomide treatment and this newly validated pharmacodynamic assay is therefore suitable for use in a proof-of-principle phase I trial a PARP-1 inhibitor in combination with temozolomide."( Temozolomide pharmacodynamics in patients with metastatic melanoma: dna damage and activity of repair enzymes O6-alkylguanine alkyltransferase and poly(ADP-ribose) polymerase-1.
Boddy, AV; Calvert, AH; Curtin, NJ; Harris, AL; Hickson, I; Jones, C; Margison, GP; McGown, G; McHugh, P; Middleton, MR; Newell, DR; Olsen, A; Plummer, ER; Thorncroft, M; Watson, AJ, 2005)		2.03
" Although this approach is promising, there has not been any attempt to define optimal metronomic dosing regimens by integrating pharmacokinetic (PK) with pharmacodynamic (PD) measurements."( Preclinical pharmacokinetic and pharmacodynamic evaluation of metronomic and conventional temozolomide dosing regimens.
Gallo, JM; Guo, P; Nuthalapati, S; Wang, X; Zhou, Q, 2007)		0.56
" Because significant obstacles prevent making these measurements in humans, development of a predictive pharmacokinetic model would be of great value to the translation of preclinical data to the clinic."( Predicting human tumor drug concentrations from a preclinical pharmacokinetic model of temozolomide brain disposition.
Gallo, JM; Guo, P; Kruh, GD; Vicini, P; Wang, X; Zhou, Q, 2007)		0.56
" The resultant data provided the framework to develop a hybrid physiologically based pharmacokinetic model for temozolomide in brain."( Predicting human tumor drug concentrations from a preclinical pharmacokinetic model of temozolomide brain disposition.
Gallo, JM; Guo, P; Kruh, GD; Vicini, P; Wang, X; Zhou, Q, 2007)		0.77
"A physiologically based pharmacokinetic modeling approach offers a means to translate preclinical to clinical characteristics of drug disposition in target tissues and, thus, a means to select appropriate drug dosing regimens for achieving optimal target tissue drug concentrations."( Predicting human tumor drug concentrations from a preclinical pharmacokinetic model of temozolomide brain disposition.
Gallo, JM; Guo, P; Kruh, GD; Vicini, P; Wang, X; Zhou, Q, 2007)		0.56
"The pharmacokinetic and safety profile of TMZ in Japanese patients was comparable to that in Caucasians."( Pharmacokinetic study of temozolomide on a daily-for-5-days schedule in Japanese patients with relapsed malignant gliomas: first study in Asians.
Adachi, J; Aoki, T; Matsutani, M; Mishima, K; Mizutani, T; Nishikawa, R; Nojima, K, 2007)		0.64
" The mean clearance of temozolomide was 107 mL/min/m2, with a volume of distribution of 20 L/m2 and half-life of 109 minutes."( Phase I pharmacokinetic and pharmacodynamic study of temozolomide in pediatric patients with refractory or recurrent leukemia: a Children's Oncology Group Study.
Adamson, PC; Berg, SL; Blaney, SM; Delaney, SM; Dolan, ME; Hedge, M; Horton, TM; Ingle, AM; Thompson, PA; Weiss, HL; Wu, MF, 2007)		0.9
" Pharmacokinetic analyses revealed lowered exposures and enhanced clearance among patients on EIAEDs."( Safety and pharmacokinetics of dose-intensive imatinib mesylate plus temozolomide: phase 1 trial in adults with malignant glioma.
Desjardins, A; Egorin, MJ; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; Lagattuta, TF; McLendon, R; Quinn, JA; Reardon, DA; Rich, JN; Salvado, AJ; Sathornsumetee, S; Vredenburgh, JJ, 2008)		0.58
" pharmacokinetic data on 670 drugs representing, to our knowledge, the largest publicly available set of human clinical pharmacokinetic data."( Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
Lombardo, F; Obach, RS; Waters, NJ, 2008)		0.35
"We conducted a phase I and pharmacokinetic study of the epidermal growth factor receptor (EGFR) inhibitor erlotinib as a single agent and in combination with temozolomide in children with refractory solid tumors."( Pediatric phase I and pharmacokinetic study of erlotinib followed by the combination of erlotinib and temozolomide: a Children's Oncology Group Phase I Consortium Study.
Adamson, PC; Blaney, SM; Dancey, JE; Gilbertson, RJ; Hamilton, M; Ingle, AM; Jakacki, RI; Krailo, MD; Tersak, J; Voss, SD, 2008)		0.76
" Pharmacokinetic studies and ERBB-receptor expression and signaling studies were performed."( Pediatric phase I and pharmacokinetic study of erlotinib followed by the combination of erlotinib and temozolomide: a Children's Oncology Group Phase I Consortium Study.
Adamson, PC; Blaney, SM; Dancey, JE; Gilbertson, RJ; Hamilton, M; Ingle, AM; Jakacki, RI; Krailo, MD; Tersak, J; Voss, SD, 2008)		0.56
"The enhanced hematologic toxicity resulting from combining O(6)BG with temozolomide does not appear to be the result of a pharmacokinetic interaction between the agents."( Pharmacokinetics of temozolomide administered in combination with O6-benzylguanine in children and adolescents with refractory solid tumors.
Aikin, AA; Balis, FM; Cole, DE; Fox, E; Meany, HJ; Warren, KE, 2009)		0.91
" This method was used successfully to perform brain and plasma pharmacokinetic studies of temozolomide in mice after intraperitoneal administration."( Development of a new UPLC-MSMS method for the determination of temozolomide in mice: application to plasma pharmacokinetics and brain distribution study.
Farinotti, R; Fernandez, C; Goldwirt, L; Zahr, N, 2013)		0.85
"Cabozantinib at a dose of 40 mg daily with RT plus TMZ and post-RT TMZ for patients with newly diagnosed high-grade glioma was generally well tolerated, and demonstrated no pharmacokinetic interactions with concurrent TMZ."( Phase 1 dose escalation trial of the safety and pharmacokinetics of cabozantinib concurrent with temozolomide and radiotherapy or temozolomide after radiotherapy in newly diagnosed patients with high-grade gliomas.
Chamberlain, MC; Cloughesy, T; Desjardins, A; Glantz, M; Mikkelsen, T; Reardon, DA; Schiff, D; Wen, PY, 2016)		0.65
" Pharmacokinetic parameters were estimated using non-compartmental analysis."( Plasma and cerebrospinal fluid pharmacokinetics of select chemotherapeutic agents following intranasal delivery in a non-human primate model.
Cruz, R; Figg, WD; League-Pascual, JC; Lester-McCully, CM; Peer, CJ; Rodgers, L; Ronner, L; Shandilya, S; Warren, KE, 2017)		0.46
" This phase I study evaluated the pharmacokinetics and mass balance of veliparib administered alone and in combination with temozolomide, and assessed any potential pharmacokinetic drug-drug interaction between veliparib and temozolomide."( Clinical Pharmacokinetics and Mass Balance of Veliparib in Combination with Temozolomide in Subjects with Nonhematologic Malignancies.
Giranda, V; Munasinghe, W; Nuthalapati, S; Xiong, H, 2018)		0.92
" No pharmacokinetic interaction was observed when veliparib and temozolomide were administered together."( Clinical Pharmacokinetics and Mass Balance of Veliparib in Combination with Temozolomide in Subjects with Nonhematologic Malignancies.
Giranda, V; Munasinghe, W; Nuthalapati, S; Xiong, H, 2018)		0.95
"We recently reported an acceptable safety and pharmacokinetic profile of depatuxizumab mafodotin (depatux-m), formerly called ABT-414, plus radiation and temozolomide in newly diagnosed glioblastoma (arm A)."( Safety, pharmacokinetics, and antitumor response of depatuxizumab mafodotin as monotherapy or in combination with temozolomide in patients with glioblastoma.
Ansell, PJ; Butowski, N; Fichtel, L; Fischer, J; Gan, HK; Gomez, EJ; Holen, KD; Kumthekar, P; Lassman, AB; Lee, HJ; Lwin, Z; Mandich, H; Merrell, R; Munasinghe, WP; Reardon, DA; Roberts-Rapp, LA; Scott, AM; van den Bent, M; Wheeler, H; Xiong, H, 2018)		0.89
" Depatux-m demonstrated a linear pharmacokinetic profile."( Safety, pharmacokinetics, and antitumor response of depatuxizumab mafodotin as monotherapy or in combination with temozolomide in patients with glioblastoma.
Ansell, PJ; Butowski, N; Fichtel, L; Fischer, J; Gan, HK; Gomez, EJ; Holen, KD; Kumthekar, P; Lassman, AB; Lee, HJ; Lwin, Z; Mandich, H; Merrell, R; Munasinghe, WP; Reardon, DA; Roberts-Rapp, LA; Scott, AM; van den Bent, M; Wheeler, H; Xiong, H, 2018)		0.69
"Depatux-m alone or in combination with temozolomide demonstrated an acceptable safety and pharmacokinetic profile in glioblastoma."( Safety, pharmacokinetics, and antitumor response of depatuxizumab mafodotin as monotherapy or in combination with temozolomide in patients with glioblastoma.
Ansell, PJ; Butowski, N; Fichtel, L; Fischer, J; Gan, HK; Gomez, EJ; Holen, KD; Kumthekar, P; Lassman, AB; Lee, HJ; Lwin, Z; Mandich, H; Merrell, R; Munasinghe, WP; Reardon, DA; Roberts-Rapp, LA; Scott, AM; van den Bent, M; Wheeler, H; Xiong, H, 2018)		0.96
" We aimed to describe the development and comparison of 2 population pharmacokinetic modeling approaches."( An Integrated Population Pharmacokinetic Model Versus Individual Models of Depatuxizumab Mafodotin, an Anti-EGFR Antibody Drug Conjugate, in Patients With Solid Tumors Likely to Overexpress EGFR.
Bain, E; Friedel, A; Menon, RM; Mensing, S; Mittapalli, RK; Stodtmann, S; Xiong, H, 2019)		0.51
"Preclinical pharmacokinetic studies evaluated olaparib tissue distribution in rats and tumor-bearing mice."( Pharmacokinetics, safety, and tolerability of olaparib and temozolomide for recurrent glioblastoma: results of the phase I OPARATIC trial.
Carruthers, R; Chalmers, AJ; Cruickshank, G; Dunn, L; Erridge, S; Godfrey, L; Halford, S; Hanna, C; Jackson, A; Jefferies, S; Kurian, KM; McBain, C; McCormick, A; Pittman, M; Sleigh, R; Strathdee, K; Watts, C; Williams, K, 2020)		0.8
" TMZ concentration in blood, brain and tumor was detected using liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) and then pharmacokinetic parameters were calculated."( Essential oil of Ligusticum chuanxiong Hort. Regulated P-gp protein and tight junction protein to change pharmacokinetic parameters of temozolomide in blood, brain and tumor.
Hu, PY; Liu, SS; Liu, XJ; Shuai, SY; Yang, M; Yue, PF; Zhang, GS; Zheng, Q, 2022)		0.92

Compound-Compound Interactions

Zotiraciclib combined with temozolomide is safe in patients with recurrent high-grade astrocytomas. This phase I study evaluated the pharmacokinetics and mass balance of veliparib.

ExcerptReferenceRelevance
" The analysis of cell cycle indicated that the drug combination of TZM and PADPRP inhibitors provoked G1 arrest only in p53+ cells."( Role of wild-type p53 on the antineoplastic activity of temozolomide alone or combined with inhibitors of poly(ADP-ribose) polymerase.
Benincasa, E; Bonmassar, E; Faraoni, I; Franco, D; Graziani, G; Lacal, PM; Tentori, L, 1998)		0.55
" AGT depleting agents in combination with methylating and chloroethylating agents are now in clinical testing, and may result in greater clinical efficacy in metastatic malignant melanoma."( New cytotoxic agents for the treatment of metastatic malignant melanoma: temozolomide and related alkylating agents in combination with guanine analogues to abrogate drug resistance.
Gerson, S; Liu, L; Spiro, T, )		0.36
"The activity of temozolomide combined with irinotecan (CPT-11) was evaluated against eight independent xenografts (four neuroblastomas, three rhabdomyosarcomas, and one glioblastoma)."( Antitumor activity of temozolomide combined with irinotecan is partly independent of O6-methylguanine-DNA methyltransferase and mismatch repair phenotypes in xenograft models.
Brent, TP; Cheshire, PJ; Friedman, HS; Houghton, PJ; Kirstein, MN; Poquette, CA; Richmond, LB; Stewart, CF; Tan, M, 2000)		0.97
" Preclinical and phase I trials have shown the additive or synergistic activity of temozolomide combined with carmustine against solid tumors, including malignant glioma, and the sequence-dependent effects of the combination."( Temozolomide in combination with other cytotoxic agents.
Prados, M, 2001)		1.98
" These results indicate that a careful selection of the antitumor agent has to be made when antitelomerase therapy is combined with chemotherapy."( Inhibition of telomerase increases resistance of melanoma cells to temozolomide, but not to temozolomide combined with poly (adp-ribose) polymerase inhibitor.
Balduzzi, A; Barbarino, M; Biroccio, A; Gold, B; Graziani, G; Levati, L; Lombardi, ML; Portarena, I; Tentori, L; Vergati, M, 2003)		0.56
" Therefore, the authors initiated a Phase I study to determine the pharmacokinetics and safety profile of temozolomide (TMZ), a novel oral alkylating agent known to cross the blood-brain barrier, in combination with interferon alpha-2b (IFN-alpha2b)."( Temozolomide in combination with interferon alpha-2b in patients with metastatic melanoma: a phase I dose-escalation study.
Agarwala, SS; Kirkwood, JM, 2003)		1.98
" This phase I study was designed to evaluate the efficacy and safety of TMZ alone (course 1) and TMZ in combination with PCB in subsequent courses in chemotherapy-naïve patients with malignant glioma."( Phase I study of temozolamide (TMZ) combined with procarbazine (PCB) in patients with gliomas.
Foster, T; Newlands, ES; Zaknoen, S, 2003)		0.32
"To evaluate the efficacy of temozolomide (TMZ) combined with cisplatin (CDDP) in terms of response rate, time to progression (TTP) and overall survival (OS), as well as the tolerability of the regimen in patients with brain metastases from solid tumors."( Temozolomide (TMZ) combined with cisplatin (CDDP) in patients with brain metastases from solid tumors: a Hellenic Cooperative Oncology Group (HeCOG) Phase II study.
Aravantinos, G; Bafaloukos, D; Bamias, A; Carina, M; Christodoulou, C; Klouvas, G; Linardou, H; Skarlos, D, 2005)		2.07
"Patients (n=32) with brain metastases were treated with TMZ 150 mg/m2/day (chemotherapy-pretreated) or 200 mg/m2/day (chemotherapy-naive) for 5 days, combined with CDDP 75 mg/m2 on day 1, every 28 days."( Temozolomide (TMZ) combined with cisplatin (CDDP) in patients with brain metastases from solid tumors: a Hellenic Cooperative Oncology Group (HeCOG) Phase II study.
Aravantinos, G; Bafaloukos, D; Bamias, A; Carina, M; Christodoulou, C; Klouvas, G; Linardou, H; Skarlos, D, 2005)		1.77
"TMZ combined with CDDP is an active and well-tolerated combination in patients with brain metastases from solid tumors."( Temozolomide (TMZ) combined with cisplatin (CDDP) in patients with brain metastases from solid tumors: a Hellenic Cooperative Oncology Group (HeCOG) Phase II study.
Aravantinos, G; Bafaloukos, D; Bamias, A; Carina, M; Christodoulou, C; Klouvas, G; Linardou, H; Skarlos, D, 2005)		1.77
"The aim of this study was to evaluate the efficacy and safety of carmustine (BCNU) in combination with temozolomide as first-line chemotherapy before and after radiotherapy (RT) in patients with inoperable, newly diagnosed glioblastoma multiforme (GBM)."( Temozolomide in combination with BCNU before and after radiotherapy in patients with inoperable newly diagnosed glioblastoma multiforme.
Barrié, M; Braguer, D; Chinot, O; Couprie, C; Dufour, H; Figarella-Branger, D; Grisoli, F; Hoang-Xuan, K; Martin, PM; Muracciole, X; Peragut, JC, 2005)		1.99
" Furthermore, we show that a human haemopoietic cell line (K562) transduced with a retroviral vector encoding MGMT(P140K) is highly resistant to the cytotoxic effects of PaTrin-2 in combination with the methylating agent temozolomide, and that cells expressing MGMT(P140K) can be effectively enriched in vitro following challenge with this drug combination."( The P140K mutant of human O(6)-methylguanine-DNA-methyltransferase (MGMT) confers resistance in vitro and in vivo to temozolomide in combination with the novel MGMT inactivator O(6)-(4-bromothenyl)guanine.
Fairbairn, LJ; Margison, GP; Milsom, MD; Southgate, TD; Woolford, LB, 2006)		0.73
" As the combination with interferon-alfa (IFN-alpha) appears superior to single-agent DTIC regarding response rates, the purpose of this study was to compare TMZ alone and TMZ plus IFN-alpha in terms of objective response (OR), overall survival, and safety in a prospective, randomized, multicenter trial."( Temozolomide in combination with interferon-alfa versus temozolomide alone in patients with advanced metastatic melanoma: a randomized, phase III, multicenter study from the Dermatologic Cooperative Oncology Group.
Becker, JC; Dummer, R; Garbe, C; Kaufmann, R; Krengel, S; Kretschmer, L; Leiter, U; Linse, R; Mauch, C; Schadendorf, D; Sebastian, G; Spieth, K; Tilgen, W; Vogt, T; von den Driesch, P, 2005)		1.77
"Two hundred ninety-four patients with untreated stage IV metastatic melanoma (American Joint Committee on Cancer staging system) were randomly assigned to receive either oral TMZ alone (200 mg/m2/day; days 1 through 5 every 28 days) or in combination with subcutaneous IFN-alpha (5 MU/m2; days 1, 3, and 5 every week)."( Temozolomide in combination with interferon-alfa versus temozolomide alone in patients with advanced metastatic melanoma: a randomized, phase III, multicenter study from the Dermatologic Cooperative Oncology Group.
Becker, JC; Dummer, R; Garbe, C; Kaufmann, R; Krengel, S; Kretschmer, L; Leiter, U; Linse, R; Mauch, C; Schadendorf, D; Sebastian, G; Spieth, K; Tilgen, W; Vogt, T; von den Driesch, P, 2005)		1.77
" In conclusion, temozolomide combined with cisplatin is an active and safe first-line chemotherapy regimen with acceptable and easily manageable toxicities in patients with metastatic melanoma."( Temozolomide in combination with cisplatin in patients with metastatic melanoma: a phase II trial.
Argon, A; Camlica, H; Tas, F; Topuz, E, 2005)		2.12
" Patients with stable or progressive malignant primary glioma received erlotinib alone or combined with temozolomide in this dose-escalation study."( Phase 1 study of erlotinib HCl alone and combined with temozolomide in patients with stable or recurrent malignant glioma.
Burton, E; Butowski, N; Chang, S; Fedoroff, A; Kapadia, A; Kelley, SK; Lamborn, KR; Malec, M; Page, MS; Prados, MD; Rabbitt, J; Xie, D, 2006)		0.8
" The main aims of this phase I trial were to determine an ATase-depleting dose (ADD) of lomeguatrib, a potent pseudosubstrate inhibitor, and to define a suitable dose of temozolomide to be used in combination with lomeguatrib in patients with advanced cancer."( Lomeguatrib, a potent inhibitor of O6-alkylguanine-DNA-alkyltransferase: phase I safety, pharmacodynamic, and pharmacokinetic trial and evaluation in combination with temozolomide in patients with advanced solid tumors.
Bridgewater, J; Dawson, M; Donnelly, D; Gumbrell, L; Halbert, G; Jowle, D; Lee, SM; Margison, GP; McElhinney, RS; McGrath, H; McMurry, TB; Middleton, MR; Ranson, M; Waller, S, 2006)		0.72
"Lomeguatrib was administered at dose levels of 10 to 40 mg/m2 days 1 to 5, as a single agent, and also in combination with temozolomide."( Lomeguatrib, a potent inhibitor of O6-alkylguanine-DNA-alkyltransferase: phase I safety, pharmacodynamic, and pharmacokinetic trial and evaluation in combination with temozolomide in patients with advanced solid tumors.
Bridgewater, J; Dawson, M; Donnelly, D; Gumbrell, L; Halbert, G; Jowle, D; Lee, SM; Margison, GP; McElhinney, RS; McGrath, H; McMurry, TB; Middleton, MR; Ranson, M; Waller, S, 2006)		0.74
" Groups treated with regional temozolomide alone (350 mg/kg), systemic temozolomide with O6BG, or vehicle combined with O6BG showed no significant tumor responses compared with controls."( Modulation of chemotherapy resistance in regional therapy: a novel therapeutic approach to advanced extremity melanoma using intra-arterial temozolomide in combination with systemic O6-benzylguanine.
Abdel-Wahab, OI; Abdel-Wahab, Z; Augustine, C; Cheng, TY; Friedman, HS; Grubbs, E; Ko, SH; Pruitt, SK; Tyler, DS; Ueno, T; Yoshimoto, Y, 2006)		0.82
" We designed a new regimen utilizing dose-intensified, protracted course of TMZ in combination with vinorelbine, a lipophilic large-spectrum agent, in an attempt to improve the efficacy of TMZ."( Vinorelbine combined with a protracted course of temozolomide for recurrent brain metastases: a phase I trial.
Abrey, LE; Demopoulos, A; Malkin, MG; Omuro, AM; Raizer, JJ, 2006)		0.59
" A multicentre phase II study was performed to assess the activity and toxicity of temozolomide in combination with interferon alpha-2b."( Phase II multicentre study of temozolomide in combination with interferon alpha-2b in metastatic malignant melanoma.
Crespo, C; del Muro, XG; Filipovich, E; García, M; Germà-Lluch, JR; López, JJ; Pérez, X; Rifà, J; Tres, A; Valladares, M, 2006)		0.85
" Previously untreated patients received temozolomide administered orally at a dose of 150 mg/m/day for 5 days every 4 weeks, in combination with interferon given continuously subcutaneously twice a week at a dose of 10 MU/m."( Phase II multicentre study of temozolomide in combination with interferon alpha-2b in metastatic malignant melanoma.
Crespo, C; del Muro, XG; Filipovich, E; García, M; Germà-Lluch, JR; López, JJ; Pérez, X; Rifà, J; Tres, A; Valladares, M, 2006)		0.89
"Temozolomide in combination with interferon is a well-tolerated palliative regimen that has moderate activity against metastatic melanoma."( Phase II multicentre study of temozolomide in combination with interferon alpha-2b in metastatic malignant melanoma.
Crespo, C; del Muro, XG; Filipovich, E; García, M; Germà-Lluch, JR; López, JJ; Pérez, X; Rifà, J; Tres, A; Valladares, M, 2006)		2.07
" In contrast, the cytotoxic drug temozolomide, when used in combination with HIF-1alpha knockdown, exhibited a superadditive and likely synergistic therapeutic effect compared with the monotherapy of either treatment alone in the D54MG glioma model."( Hypoxia-inducible factor-1 inhibition in combination with temozolomide treatment exhibits robust antitumor efficacy in vivo.
Albert, DH; Fesik, SW; Li, L; Lin, X; Shen, Y; Shoemaker, AR, 2006)		0.86
"Our results show that the DNA alkylating agent temozolomide exhibits robust antitumor efficacy when used in combination with HIF-1 inhibition in D54MG-derived tumors, suggesting that the combination of temozolomide with HIF-1 inhibitors might be an effective regimen for cancer therapy."( Hypoxia-inducible factor-1 inhibition in combination with temozolomide treatment exhibits robust antitumor efficacy in vivo.
Albert, DH; Fesik, SW; Li, L; Lin, X; Shen, Y; Shoemaker, AR, 2006)		0.83
" 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)		0.59
" Three MMR-proficient melanoma cell clones with low or no MGMT activity were treated daily for 5 days with 50 micromol/l TMZ, alone or in combination with 5 micromol/l BG."( A single cycle of treatment with temozolomide, alone or combined with O(6)-benzylguanine, induces strong chemoresistance in melanoma cell clones in vitro: role of O(6)-methylguanine-DNA methyltransferase and the mismatch repair system.
Alvino, E; Bonmassar, E; Caporali, S; Caporaso, P; Castiglia, D; D'Atri, S; Fischer, F; Jiricny, J; Lacal, PM; Marra, G; Pepponi, R; Zambruno, G, 2006)		0.62
" Randomized studies are needed to explore the role of celecoxib in combination with chemotherapy or as maintenance treatment in these patients."( Temozolomide in combination with celecoxib in patients with advanced melanoma. A phase II study of the Hellenic Cooperative Oncology Group.
Fountzilas, G; Frangia, K; Gogas, H; Mantzourani, M; Markopoulos, C; Middleton, M; Panagiotou, P; Papadopoulos, O; Pectasides, D; Polyzos, A; Stavrinidis, I; Tsoutsos, D; Vaiopoulos, G, 2006)		1.78
"The aim of this study was to investigate the effect of temozolomide (TZM) in combination with X-rays on proliferation and migration in human glioma spheroids."( The inhibition of proliferation and migration of glioma spheroids exposed to temozolomide is less than additive if combined with irradiation.
Fehlauer, F; Muench, M; Rades, D; Richter, E, 2007)		0.82
"To compare results of treatment with temozolomide or dacarbazine, in combination with an anthracycline, in dogs with relapsed or refractory lymphoma."( Efficacy of temozolomide or dacarbazine in combination with an anthracycline for rescue chemotherapy in dogs with lymphoma.
Cadile, CD; Dervisis, NG; Dominguez, PA; Kitchell, BE; Newman, RG; Sarbu, L; Swanson, CN, 2007)		0.99
"The regimen, temozolomide combined with fotemustine, is an active and moderately safe first-line chemotherapy regimen with acceptable and easily manageable toxicities in patients with metastatic melanoma."( Temozolomide in combination with fotemustine in patients with metastatic melanoma.
Camlica, H; Tas, F; Topuz, E, 2008)		2.16
" The effect of ZD6474, a potent inhibitor of VEGF-receptor-2, was evaluated in combination with either radiotherapy or temozolomide."( Effects of the VEGFR inhibitor ZD6474 in combination with radiotherapy and temozolomide in an orthotopic glioma model.
Bergenheim, AT; Bergström, P; Henriksson, R; Johansson, M; Sandström, M, 2008)		0.78
" ZD6474 30 mg/kg was given alone or in combination with radiotherapy 12 Gy x 1 or with temozolomide 100 mg/kg for 3 days."( Effects of the VEGFR inhibitor ZD6474 in combination with radiotherapy and temozolomide in an orthotopic glioma model.
Bergenheim, AT; Bergström, P; Henriksson, R; Johansson, M; Sandström, M, 2008)		0.8
"ZD6474 in combination with radiotherapy significantly decreased tumour area by 66% compared with controls whereas the combination with temozolomide decreased tumour area by 74%."( Effects of the VEGFR inhibitor ZD6474 in combination with radiotherapy and temozolomide in an orthotopic glioma model.
Bergenheim, AT; Bergström, P; Henriksson, R; Johansson, M; Sandström, M, 2008)		0.78
"ZD6474 in combination with two standard modalities in the treatment of malignant glioma, radiotherapy and chemotherapy, markedly decreased the growth of an intracerebral experimental glioma."( Effects of the VEGFR inhibitor ZD6474 in combination with radiotherapy and temozolomide in an orthotopic glioma model.
Bergenheim, AT; Bergström, P; Henriksson, R; Johansson, M; Sandström, M, 2008)		0.58
"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
"To assess interim safety and tolerability of a 10-patient, Phase II pilot study using bevacizumab (BV) in combination with temozolomide (TMZ) and regional radiation therapy (RT) in the up-front treatment of patients with newly diagnosed glioblastoma."( Phase II pilot study of bevacizumab in combination with temozolomide and regional radiation therapy for up-front treatment of patients with newly diagnosed glioblastoma multiforme: interim analysis of safety and tolerability.
Bergsneider, M; Cloughesy, T; Filka, E; Graham, C; Lai, A; Liau, LM; McGibbon, B; Mischel, P; Nghiemphu, PL; Pope, W; Selch, M; Yong, WH, 2008)		0.8
" At this time data are not sufficient to encourage routine off-label use of BV combined with TMZ/RT in the setting of newly diagnosed glioblastoma without longer follow-up, enrollment of additional patients, and thorough efficacy assessment."( Phase II pilot study of bevacizumab in combination with temozolomide and regional radiation therapy for up-front treatment of patients with newly diagnosed glioblastoma multiforme: interim analysis of safety and tolerability.
Bergsneider, M; Cloughesy, T; Filka, E; Graham, C; Lai, A; Liau, LM; McGibbon, B; Mischel, P; Nghiemphu, PL; Pope, W; Selch, M; Yong, WH, 2008)		0.59
"6% and 1/6 rat survived more than 1 year in case of MRT combined with gadolinium injection."( Enhancement of survival of 9L gliosarcoma bearing rats following intracerebral delivery of drugs in combination with microbeam radiation therapy.
Bräuer-Krisch, E; Bravin, A; Keyriläinen, J; Le Duc, G; Régnard, P; Troprès, I, 2008)		0.35
" The article reports safety, efficacy, pharmacokinetic, and pharmacodynamic results of the first-in-class trial of a PARP inhibitor, AG014699, combined with temozolomide in adults with advanced malignancy."( Phase I study of the poly(ADP-ribose) polymerase inhibitor, AG014699, in combination with temozolomide in patients with advanced solid tumors.
Boddy, A; Calvert, H; Curtin, N; Dewji, R; Evans, J; Harris, A; Johnson, P; Jones, C; McHugh, P; Middleton, M; Newell, D; Olsen, A; Plummer, R; Robson, L; Steinfeldt, H; Wang, D; Wilson, R, 2008)		0.76
" Dasatinib in combination with temozolomide more effectively increased the therapeutic efficacy of temozolomide than when dasatinib was combined with carboplatin or irinotecan."( Dasatinib-induced autophagy is enhanced in combination with temozolomide in glioma.
de Groot, J; LaFortune, T; Milano, V; Piao, Y, 2009)		0.88
"To evaluate the toxicity and efficacy of preoperative intensity-modulated radiotherapy (IMRT) combined with temozolomide to improve local tumor control in soft-tissue sarcoma (STS)."( Preoperative intensity-modulated radiotherapy combined with temozolomide for locally advanced soft-tissue sarcoma.
Dinter, DJ; Hohenberger, P; Jakob, J; Ströbel, P; Wenz, F, 2009)		0.81
" Drug combination of TMZ plus BG and PHA-848125 produced additive or synergistic effects on cell growth, depending on the cell line."( The cyclin-dependent kinase inhibitor PHA-848125 suppresses the in vitro growth of human melanomas sensitive or resistant to temozolomide, and shows synergistic effects in combination with this triazene compound.
Alvino, E; Bonmassar, E; Brasca, MG; Caporali, S; Castiglia, D; Ciomei, M; Covaciu, C; D'Atri, S; Garbin, A; Levati, L; Starace, G, 2010)		0.57
" After irradiation of the symptomatic sites, intrathecal liposomal Ara-C every 2-4 weeks was combined with temozolomide 100 mg/m(2) day 1-5/7."( Neoplastic meningitis from breast cancer: feasibility and activity of long-term intrathecal liposomal Ara-C combined with dose-dense temozolomide.
Buhk, JH; Hoffmann, AL; Strik, H, 2009)		0.77
"To evaluate maximum tolerated dose and recommended dose (RD) for phase II studies of topotecan (TPT) combined with temozolomide (TMZ) (TOTEM) in children and adolescents with relapsed or refractory solid malignancies."( Phase I study of topotecan in combination with temozolomide (TOTEM) in relapsed or refractory paediatric solid tumours.
Aerts, I; Chastagner, P; Chatelut, E; Corradini, N; Dias, N; Djafari, L; Frappaz, D; Gentet, JC; Geoerger, B; Landman-Parker, J; Le Deley, MC; Leblond, P; Ndiaye, A; Paci, A; Pasquet, M; Rubie, H; Schmitt, A; Vassal, G, 2010)		0.83
" Our results demonstrate the potential of the anti-IGF-1R antibody alone and in combination with alkylating agents and support the therapeutic development of the AVE1642 for aggressive neuroblastoma."( Anti-insulin-like growth factor 1 receptor antibody EM164 (murine AVE1642) exhibits anti-tumour activity alone and in combination with temozolomide against neuroblastoma.
Brasme, JF; Daudigeos-Dubus, E; Debussche, L; Geoerger, B; Opolon, P; Vassal, G; Venot, C; Vrignaud, P, 2010)		0.56
" Metronomic dosing of temozolomide (TMZ) combined with standard radiotherapy may improve survival by increasing the therapeutic index and anti-angiogenic effect of TMZ."( A multi-centre Canadian pilot study of metronomic temozolomide combined with radiotherapy for newly diagnosed paediatric brainstem glioma.
Bartels, U; Baruchel, S; Bouffet, E; Eisenstat, D; Gammon, J; Huang, A; Hukin, J; Johnston, DL; Samson, Y; Sharp, JR; Stempak, D; Stephens, D; Tabori, U, 2010)		0.93
" This factorial design phase I/II protocol tested dose-dense temozolomide alone and combined with cytostatic agents."( A phase I factorial design study of dose-dense temozolomide alone and in combination with thalidomide, isotretinoin, and/or celecoxib as postchemoradiation adjuvant therapy for newly diagnosed glioblastoma.
Chang, E; Colman, H; Conrad, C; de Groot, J; Giglio, P; Gilbert, MR; Gonzalez, J; Groves, MD; Hess, K; Hunter, K; Levin, V; Mahajan, A; Puduvalli, V; Woo, S; Yung, WK, 2010)		0.86
" On the basis of promising preclinical data, the safety and tolerability of therapy with the mTOR inhibitor RAD001 in combination with radiation (RT) and temozolomide (TMZ) was evaluated in this Phase I study."( North Central Cancer Treatment Group Phase I trial N057K of everolimus (RAD001) and temozolomide in combination with radiation therapy in patients with newly diagnosed glioblastoma multiforme.
Brown, PD; Buckner, JC; Galanis, E; Giannini, C; Jaeckle, KA; McGraw, S; Peller, PJ; Sarkaria, JN; Uhm, JH; Wu, W, 2011)		0.79
"All patients received weekly oral RAD001 in combination with standard chemoradiotherapy, followed by RAD001 in combination with standard adjuvant temozolomide."( North Central Cancer Treatment Group Phase I trial N057K of everolimus (RAD001) and temozolomide in combination with radiation therapy in patients with newly diagnosed glioblastoma multiforme.
Brown, PD; Buckner, JC; Galanis, E; Giannini, C; Jaeckle, KA; McGraw, S; Peller, PJ; Sarkaria, JN; Uhm, JH; Wu, W, 2011)		0.79
" On the basis of these results, the recommended Phase II dosage currently being tested is RAD001 70 mg/week in combination with standard chemoradiotherapy."( North Central Cancer Treatment Group Phase I trial N057K of everolimus (RAD001) and temozolomide in combination with radiation therapy in patients with newly diagnosed glioblastoma multiforme.
Brown, PD; Buckner, JC; Galanis, E; Giannini, C; Jaeckle, KA; McGraw, S; Peller, PJ; Sarkaria, JN; Uhm, JH; Wu, W, 2011)		0.59
"RAD001 in combination with RT/TMZ and adjuvant TMZ was reasonably well tolerated."( North Central Cancer Treatment Group Phase I trial N057K of everolimus (RAD001) and temozolomide in combination with radiation therapy in patients with newly diagnosed glioblastoma multiforme.
Brown, PD; Buckner, JC; Galanis, E; Giannini, C; Jaeckle, KA; McGraw, S; Peller, PJ; Sarkaria, JN; Uhm, JH; Wu, W, 2011)		0.59
"The phase II trial has been prepared to assess the effectiveness of BPA (250 mg/kg)-based NCT combined with X-ray irradiation and temozolomide (75 mg/m(2)) for the treatment of newly diagnosed GBM."( The status of Tsukuba BNCT trial: BPA-based boron neutron capture therapy combined with X-ray irradiation.
Aiyama, H; Endo, K; Ishikawa, E; Kumada, H; Matsumura, A; Mizumoto, M; Nakai, K; Nariai, T; Okumura, T; Shibata, Y; Takada, T; Tsuboi, K; Yamamoto, T; Yoshida, F; Zaboronok, A, 2011)		0.57
" The major differences of our protocol from the other past studies were simultaneous use of both sodium borocapate and boronophenylalanine, and combination with fractionated X-ray irradiation."( Phase II clinical study of boron neutron capture therapy combined with X-ray radiotherapy/temozolomide in patients with newly diagnosed glioblastoma multiforme--study design and current status report.
Hiramatsu, R; Hirota, Y; Kawabata, S; Kirihata, M; Kuroiwa, T; Maruhashi, A; Miyata, S; Miyatake, S; Ono, K; Sakurai, Y; Takekita, Y, 2011)		0.59
" Here, we describe 3 cases of GBM patients treated with autologous formalin-fixed tumor vaccine (AFTV) combined with TMZ."( Pathological changes after autologous formalin-fixed tumor vaccine therapy combined with temozolomide for glioblastoma - three case reports - .
Enomoto, T; Ishikawa, E; Matsumura, A; Morishita, Y; Nakai, K; Ohno, T; Sakamoto, N; Sato, M; Satomi, K; Takano, S; Tsuboi, K; Yamamoto, T, 2011)		0.59
"The primary end point was surpassed showing promising activity of this bevacizumab/temozolomide combination with a favourable toxicity profile."( First-line temozolomide combined with bevacizumab in metastatic melanoma: a multicentre phase II trial (SAKK 50/07).
Cathomas, R; Dummer, R; Gillessen, S; Goldinger, SM; Mamot, C; Michielin, O; Mjhic-Probst, D; Moch, H; Ochsenbein, A; Schläppi, M; Schönewolf, N; Schraml, PH; Seifert, B; Simcock, M; von Moos, R, 2012)		0.99
" The aim of the present study was to evaluate the efficacy and side effects of nimotuzumab in combination with chemotherapy for patients with malignant gliomas."( [Nimotuzumab in combination with chemotherapy for patients with malignant gliomas].
Chen, ZP; Jiang, XB; Mu, YG; Sai, K; Shen, D; Yang, QY; Zhang, XH, 2011)		0.37
" Individualized chemotherapy was administered based on O(6)-methylguanine-DNA methyltransferase (MGMT) expression and previous chemotherapy responses in combined with nimotuzumab."( [Nimotuzumab in combination with chemotherapy for patients with malignant gliomas].
Chen, ZP; Jiang, XB; Mu, YG; Sai, K; Shen, D; Yang, QY; Zhang, XH, 2011)		0.37
"Nimotuzumab in combination with chemotherapy has moderate activity in patients with malignant gliomas and the toxicities are well tolerable, therefore, worth further investigation."( [Nimotuzumab in combination with chemotherapy for patients with malignant gliomas].
Chen, ZP; Jiang, XB; Mu, YG; Sai, K; Shen, D; Yang, QY; Zhang, XH, 2011)		0.37
" In vitro Southern Blot analysis and cytopathic effect assays demonstrate high anti-glioma potency, which was significantly increased in combination with temozolomide (TMZ), daunorubicin and cisplatin."( YB-1 dependent virotherapy in combination with temozolomide as a multimodal therapy approach to eradicate malignant glioma.
Anton, M; Gänsbacher, B; Haczek, C; Holm, PS; Holzmüller, R; Kasajima, A; Lage, H; Mantwill, K; Rognoni, E; Schlegel, J; Schuster, T; Treue, D; Weichert, W, 2011)		0.82
"To study the efficacy and safety of 3-dimensional conformal radiotherapy combined with temozolomide (TMZ) for gliomas."( [Efficacy and safety of 3-dimensional conformal radiotherapy combined with temozolomide for glioma].
Tu, Q; Wang, L; Zhou, R; Zhou, W, 2011)		0.82
" The patients received temozolomide alone,3-dimensional conformal radiotherapy alone,3-dimensional conformal radiotherapy combined with temozolomide in the chemotherapy group,the radiotherapy group and the comprehensive therapy group respectively."( [Efficacy and safety of 3-dimensional conformal radiotherapy combined with temozolomide for glioma].
Tu, Q; Wang, L; Zhou, R; Zhou, W, 2011)		0.91
"Three-dimensional conformal radiotherapy combined with temozolomide is more effective for gliomas than the simple 3-dimensional conformal radiotherapy and the temozolomide chemotherapy alone."( [Efficacy and safety of 3-dimensional conformal radiotherapy combined with temozolomide for glioma].
Tu, Q; Wang, L; Zhou, R; Zhou, W, 2011)		0.85
"To study the safety and efficacy of three-dimensional conformal radiotherapy in combination with temozolomide in treatment of patients with diffuse brainstem glioma."( [Safety and efficacy of three-dimensional conformal radiotherapy combined with temozolomide in treatment of diffuse brainstem gliomas].
Cai, CL; Fang, HH; Kang, JB; Li, FM; Nie, Q, 2011)		0.81
" It is likely that clinical testing of these agents will be in combination with standard therapies to harness the apoptotic potential of both the agents."( The MEK1/2 inhibitor, selumetinib (AZD6244; ARRY-142886), enhances anti-tumour efficacy when combined with conventional chemotherapeutic agents in human tumour xenograft models.
Alferez, D; Davies, BR; Heaton, SP; Heier, A; Holt, SV; Logié, A; Odedra, R; Smith, PD; Wilkinson, RW, 2012)		0.38
"The aim of this study was to identify agents, which would be likely to offer clinical benefit when combined with selumetinib."( The MEK1/2 inhibitor, selumetinib (AZD6244; ARRY-142886), enhances anti-tumour efficacy when combined with conventional chemotherapeutic agents in human tumour xenograft models.
Alferez, D; Davies, BR; Heaton, SP; Heier, A; Holt, SV; Logié, A; Odedra, R; Smith, PD; Wilkinson, RW, 2012)		0.38
" In several models we observed that continuous exposure to selumetinib in combination with docetaxel results in tumour regression."( The MEK1/2 inhibitor, selumetinib (AZD6244; ARRY-142886), enhances anti-tumour efficacy when combined with conventional chemotherapeutic agents in human tumour xenograft models.
Alferez, D; Davies, BR; Heaton, SP; Heier, A; Holt, SV; Logié, A; Odedra, R; Smith, PD; Wilkinson, RW, 2012)		0.38
"The data presented suggests that MEK inhibition in combination with several standard chemotherapeutics or an Aurora B kinase inhibitor is a promising clinical strategy."( The MEK1/2 inhibitor, selumetinib (AZD6244; ARRY-142886), enhances anti-tumour efficacy when combined with conventional chemotherapeutic agents in human tumour xenograft models.
Alferez, D; Davies, BR; Heaton, SP; Heier, A; Holt, SV; Logié, A; Odedra, R; Smith, PD; Wilkinson, RW, 2012)		0.38
" As HSP27 and AKT interact to regulate the activity of each other, we determined whether inhibition of HSP27 was better than targeting SPARC as a therapeutic approach to inhibit both SPARC-induced glioma cell invasion and survival."( Inhibition of HSP27 alone or in combination with pAKT inhibition as therapeutic approaches to target SPARC-induced glioma cell survival.
Brodie, C; Brown, SL; Golembieski, WA; King, DA; Rempel, SA; Schultz, CR, 2012)		0.38
"We conclude that inhibition of HSP27 alone, or in combination with pAKT inhibitor IV, may be an effective therapeutic approach to inhibit SPARC-induced glioma cell invasion and survival in SPARC-positive/PTEN-wildtype and SPARC-positive/PTEN-null tumors, respectively."( Inhibition of HSP27 alone or in combination with pAKT inhibition as therapeutic approaches to target SPARC-induced glioma cell survival.
Brodie, C; Brown, SL; Golembieski, WA; King, DA; Rempel, SA; Schultz, CR, 2012)		0.38
"A retrospective study assessing treatment-related toxicities in tumor-bearing cats treated with temozolomide (TMZ) alone or in combination with doxorubicin was conducted."( Treatment-related toxicities in tumor-bearing cats treated with temozolomide alone or in combination with doxorubicin: a pilot assessment.
Dervisis, NG; Gagnon, J; Kitchell, BE, 2012)		0.84
" The primary objectives of this randomized phase 2 trial were to determine the safety and efficacy of cilengitide when combined with radiation and temozolomide for patients with newly diagnosed glioblastoma multiforme and to select a dose for comparative clinical testing."( A safety run-in and randomized phase 2 study of cilengitide combined with chemoradiation for newly diagnosed glioblastoma (NABTT 0306).
Batchelor, T; Brem, S; Fisher, JD; Grossman, SA; Hegi, ME; Lesser, G; Mikkelsen, T; Nabors, LB; Olsen, J; Peereboom, D; Rosenfeld, MR; Ye, X, 2012)		0.58
"Cilengitide was well tolerated when combined with standard chemoradiation and may improve survival for patients newly diagnosed with glioblastoma multiforme regardless of MGMT methylation status."( A safety run-in and randomized phase 2 study of cilengitide combined with chemoradiation for newly diagnosed glioblastoma (NABTT 0306).
Batchelor, T; Brem, S; Fisher, JD; Grossman, SA; Hegi, ME; Lesser, G; Mikkelsen, T; Nabors, LB; Olsen, J; Peereboom, D; Rosenfeld, MR; Ye, X, 2012)		0.38
" At the time of last relapse, temozolomide was administered alone and combined with external beam radiation therapy."( Temozolomide combined with radiotherapy in the treatment of recurrent cranial meningioma previously treated with multiple surgical resections and two sessions of radiosurgery: a case report and literature review.
Alongi, F; Clerici, E; Navarria, P; Rognone, E; Santoro, A; Scorsetti, M; Simonelli, M, )		1.86
"To evaluate the toxicity and maximum tolerated dose (MTD) of arsenic trioxide (ATO) in combination with temozolomide (TMZ) and radiation therapy (RT) in malignant gliomas."( Phase I study of arsenic trioxide and temozolomide in combination with radiation therapy in patients with malignant gliomas.
Chandler, JP; Grimm, SA; Jovanovic, B; Levy, RM; Marymont, M; McCarthy, K; Muro, K; Newman, SB; Raizer, JJ, 2012)		0.86
"A phase I, dose-finding study of vorinostat in combination with temozolomide (TMZ) was conducted to determine the maximum tolerated dose (MTD), safety, and pharmacokinetics in patients with high-grade glioma (HGG)."( Phase I study of vorinostat in combination with temozolomide in patients with high-grade gliomas: North American Brain Tumor Consortium Study 04-03.
Ames, MM; Chang, SM; Cloughesy, TF; Desideri, S; Drappatz, J; Espinoza-Delgado, I; Gilbert, MR; Kuhn, JG; Lamborn, KR; Lassman, AB; Lee, EQ; Lieberman, FS; McGovern, RM; Prados, MD; Puduvalli, VK; Reid, JM; Robins, HI; Wen, PY; Xu, J; Ye, X; Yung, WK, 2012)		0.87
" Part 1 was a dose-escalation study of vorinostat in combination with TMZ 150 mg/m(2)/day for 5 days every 28 days."( Phase I study of vorinostat in combination with temozolomide in patients with high-grade gliomas: North American Brain Tumor Consortium Study 04-03.
Ames, MM; Chang, SM; Cloughesy, TF; Desideri, S; Drappatz, J; Espinoza-Delgado, I; Gilbert, MR; Kuhn, JG; Lamborn, KR; Lassman, AB; Lee, EQ; Lieberman, FS; McGovern, RM; Prados, MD; Puduvalli, VK; Reid, JM; Robins, HI; Wen, PY; Xu, J; Ye, X; Yung, WK, 2012)		0.63
"In part 1, the MTD of vorinostat administered on days 1 to 7 and 15 to 21 of every 28-day cycle, in combination with TMZ, was 500 mg daily."( Phase I study of vorinostat in combination with temozolomide in patients with high-grade gliomas: North American Brain Tumor Consortium Study 04-03.
Ames, MM; Chang, SM; Cloughesy, TF; Desideri, S; Drappatz, J; Espinoza-Delgado, I; Gilbert, MR; Kuhn, JG; Lamborn, KR; Lassman, AB; Lee, EQ; Lieberman, FS; McGovern, RM; Prados, MD; Puduvalli, VK; Reid, JM; Robins, HI; Wen, PY; Xu, J; Ye, X; Yung, WK, 2012)		0.63
"Vorinostat in combination with temozolomide is well tolerated in patients with HGG."( Phase I study of vorinostat in combination with temozolomide in patients with high-grade gliomas: North American Brain Tumor Consortium Study 04-03.
Ames, MM; Chang, SM; Cloughesy, TF; Desideri, S; Drappatz, J; Espinoza-Delgado, I; Gilbert, MR; Kuhn, JG; Lamborn, KR; Lassman, AB; Lee, EQ; Lieberman, FS; McGovern, RM; Prados, MD; Puduvalli, VK; Reid, JM; Robins, HI; Wen, PY; Xu, J; Ye, X; Yung, WK, 2012)		0.92
" One of the most interesting combinations that have started to become part of the therapeutic arsenal in the daily clinic is dose-dense temozolomide in combination with bevacizumab."( A review of dose-dense temozolomide alone and in combination with bevacizumab in patients with first relapse of glioblastoma.
Bergqvist, M; Bergström, S; Blomquist, E; Ekman, S; Henriksson, R; Johansson, F, 2012)		0.89
" (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)		0.85
" This drug combination significantly impaired the sphere-forming ability of GSCs in vitro and tumor formation in vivo, leading to increase in the overall survival of mice bearing orthotopic inoculation of GSCs."( Effective elimination of cancer stem cells by a novel drug combination strategy.
Chen, G; Colman, H; Feng, L; Huang, P; Keating, MJ; Li, X; Wang, F; Wang, J; Wang, L; Xu, RH; Yuan, S; Zhang, H, 2013)		0.39
" We hypothesized that epigenetic modulators will reverse chemotherapy resistance, and in this article, we report studies that sought to determine the recommended phase 2 dose (RP2D), safety, and efficacy of decitabine (DAC) combined with TMZ."( Safety and efficacy of decitabine in combination with temozolomide in metastatic melanoma: a phase I/II study and pharmacokinetic analysis.
Beumer, JH; Buch, SC; Christner, S; Egorin, MJ; Kirkwood, JM; Lin, Y; Moschos, S; Tarhini, AA; Tawbi, HA, 2013)		0.64
"This study suggests that ABT-888 has the clinical potential to enhance the current standard treatment for GBM, in combination with conventional chemo-radiotherapy."( Evaluation of poly (ADP-ribose) polymerase inhibitor ABT-888 combined with radiotherapy and temozolomide in glioblastoma.
Barazzuol, L; Burnet, NG; Jena, R; Jeynes, JC; Kirkby, KJ; Kirkby, NF; Meira, LB, 2013)		0.61
"Daily oral everolimus (10 mg) combined with both concurrent radiation and temozolomide followed by adjuvant temozolomide is well tolerated, with an acceptable toxicity profile."( RTOG 0913: a phase 1 study of daily everolimus (RAD001) in combination with radiation therapy and temozolomide in patients with newly diagnosed glioblastoma.
Chinnaiyan, P; Corn, BW; Dipetrillo, TA; Mehta, MP; Rojiani, AM; Wen, PY; Wendland, M; Won, M, 2013)		0.84
"To evaluate the efficacy of pulsed low-dose radiation therapy (PLRT) combined with temozolomide (TMZ) as a novel treatment approach for radioresistant glioblastoma multiforme (GBM) in a murine model."( Pulsed versus conventional radiation therapy in combination with temozolomide in a murine orthotopic model of glioblastoma multiforme.
Chunta, JL; Grills, IS; Huang, J; Krueger, SA; Lee, DY; Marples, B; Martinez, AA; Park, SS; Wilson, GD, 2013)		0.85
"Patients treated within a Phase I/II Trial with a carbon ion boost were compared retrospectively with randomly chosen patients treated with photons or photons in combination with TMZ in a retrospective analysis."( Comparison of carbon ion radiotherapy to photon radiation alone or in combination with temozolomide in patients with high-grade gliomas: explorative hypothesis-generating retrospective analysis.
Bruckner, T; Combs, SE; Debus, J; Kamada, T; Kieser, M; Mizoe, JE; Tsujii, H, 2013)		0.61
"To assess objective response rate (ORR) after two cycles of temozolomide in combination with topotecan (TOTEM) in children with refractory or relapsed neuroblastoma."( Phase II study of temozolomide in combination with topotecan (TOTEM) in relapsed or refractory neuroblastoma: a European Innovative Therapies for Children with Cancer-SIOP-European Neuroblastoma study.
Aerts, I; Amoroso, L; Boubaker, A; Casanova, M; Chastagner, P; Courbon, F; Devos, A; Di Giannatale, A; Dias-Gastellier, N; Ducassoul, S; Geoerger, B; Landman-Parker, J; Le Deley, MC; Malekzadeh, K; Mc Hugh, K; Munzer, C; Riccardi, R; Rubie, H; Verschuur, A; Zwaan, CM, 2014)		0.98
" In the present analysis, we retrospectively investigated the feasibility and effectiveness of bevacizumab combined with ICE in patients with glioblastoma at second relapse during ICE treatment."( Retrospective analysis of bevacizumab in combination with ifosfamide, carboplatin, and etoposide in patients with second recurrence of glioblastoma.
Arakawa, Y; Fujimoto, K; Kikuchi, T; Kunieda, T; Miyamoto, S; Mizowaki, T; Murata, D; Takagi, Y; Takahashi, JC, 2013)		0.39
"To determine the maximum tolerated dose of irinotecan administered every 2 weeks, in combination with a fixed and continuous administration of temozolomide, in patients with glioblastoma at first relapse."( A phase I study of irinotecan in combination with metronomic temozolomide in patients with recurrent glioblastoma.
Balañá, C; Gallego, O; García, JL; Iglesias, L; Pérez, P; Reynés, G, 2014)		0.84
" More generally, these results suggest that traditional therapy in combination with local, as opposed to systemic, delivery of angiogenesis inhibitors may be able to increase median survival for patients with glioblastoma."( Local delivery of angiogenesis-inhibitor minocycline combined with radiotherapy and oral temozolomide chemotherapy in 9L glioma.
Bow, H; Brem, H; Hwang, LS; Murray, L; Salditch, Q; Schildhaus, N; Tyler, B; Weingart, J; Xing, J; Ye, X; Zhang, Y, 2014)		0.62
"To evaluate the safety and efficacy of nimotuzumab, a humanized monoclonal antibody specific for the epidermal growth factor receptor (EGFR), in combination with temozolomide (TMZ) and radiation therapy (RT) in the treatment of newly diagnosed glioblastoma (GBM) in Chinese patients."( Nimotuzumab, a humanized monoclonal antibody specific for the EGFR, in combination with temozolomide and radiation therapy for newly diagnosed glioblastoma multiforme: First results in Chinese patients.
Chen, S; Dai, JZ; Pan, L; Sheng, XF; Wang, Y, 2016)		0.85
" During RT, concurrent TMZ was given daily at 75 mg/m(2) for 40-42 days, combined with six weekly infusions of nimotuzumab at a 200 mg dose."( Nimotuzumab, a humanized monoclonal antibody specific for the EGFR, in combination with temozolomide and radiation therapy for newly diagnosed glioblastoma multiforme: First results in Chinese patients.
Chen, S; Dai, JZ; Pan, L; Sheng, XF; Wang, Y, 2016)		0.66
" This phase I open-label, noncontrolled dose escalation study was performed to determine the safety and maximum tolerated dose (MTD) of Sb in combination with radiation therapy (RT) and temozolomide (TMZ) in 17 patients with newly diagnosed high-grade glioma."( Phase I study of sorafenib combined with radiation therapy and temozolomide as first-line treatment of high-grade glioma.
Ben Aissa, A; Bodmer, A; Dietrich, PY; Dunkel, N; Espeli, V; Hottinger, AF; Hundsberger, T; Mach, N; Schaller, K; Squiban, D; Vargas, MI; Weber, DC, 2014)		0.83
"Patients were treated with RT (60 Gy in 2 Gy fractions) combined with TMZ 75 mg m(-2) daily, and Sb administered at three dose levels (200 mg daily, 200 mg BID, and 400 mg BID) starting on day 8 of RT."( Phase I study of sorafenib combined with radiation therapy and temozolomide as first-line treatment of high-grade glioma.
Ben Aissa, A; Bodmer, A; Dietrich, PY; Dunkel, N; Espeli, V; Hottinger, AF; Hundsberger, T; Mach, N; Schaller, K; Squiban, D; Vargas, MI; Weber, DC, 2014)		0.64
"Although Sb can be combined with RT and TMZ, significant side effects and moderate outcome results do not support further clinical development in malignant gliomas."( Phase I study of sorafenib combined with radiation therapy and temozolomide as first-line treatment of high-grade glioma.
Ben Aissa, A; Bodmer, A; Dietrich, PY; Dunkel, N; Espeli, V; Hottinger, AF; Hundsberger, T; Mach, N; Schaller, K; Squiban, D; Vargas, MI; Weber, DC, 2014)		0.64
"Twenty-six patients received CEP-9722 150-1,000 mg/day combined with temozolomide."( Phase 1 dose-escalation study of the PARP inhibitor CEP-9722 as monotherapy or in combination with temozolomide in patients with solid tumors.
Aissat-Daudigny, L; Brown, PD; Cambois, A; Campone, M; Moachon, G; Plummer, R; Stephens, P, 2014)		0.85
"WBRT followed by IMBRT combined with concomitant TMZ is well tolerated, yielding an encouraging objective response rate; however, overall survival improves slightly comparing with RTOG 9508 randomized trial."( Whole brain radiation therapy followed by intensity-modulated boosting treatment combined with concomitant temozolomide for brain metastases from non-small-cell lung cancer.
Jiang, Z; Leng, C; Liang, S; Liu, H; Lu, F; Lu, S; Qi, X; Shi, J; Wang, Q; Wang, S, 2014)		0.62
"2 mg/kg three times weekly for 2 weeks (starting on day 1), in combination with oral panobinostat 10, 20, or 30 mg every 96 h (starting on day 8), and oral temozolomide 150 mg/m(2)/day on days 9 through 13."( Treatment of resistant metastatic melanoma using sequential epigenetic therapy (decitabine and panobinostat) combined with chemotherapy (temozolomide).
Deutsch, J; Frees, M; Laux, D; Leon-Ferre, R; Milhem, M; Smith, BJ; Xia, C, 2014)		0.8
"This triple agent of dual epigenetic therapy in combination with traditional chemotherapy was generally well tolerated by the cohort and appeared safe to be continued in a Phase II trial."( Treatment of resistant metastatic melanoma using sequential epigenetic therapy (decitabine and panobinostat) combined with chemotherapy (temozolomide).
Deutsch, J; Frees, M; Laux, D; Leon-Ferre, R; Milhem, M; Smith, BJ; Xia, C, 2014)		0.61
" Data from phase 2 trials suggest that it has antitumour activity as a single agent in recurrent glioblastoma and in combination with standard temozolomide chemoradiotherapy in newly diagnosed glioblastoma (particularly in tumours with methylated MGMT promoter)."( Cilengitide combined with standard treatment for patients with newly diagnosed glioblastoma with methylated MGMT promoter (CENTRIC EORTC 26071-22072 study): a multicentre, randomised, open-label, phase 3 trial.
Adamska, K; Aldape, KD; Brandes, AA; Erridge, SC; Gorlia, T; Grujicic, D; Gupta, T; Hau, P; Hegi, ME; Herrlinger, U; Hicking, C; Hong, YK; Kim, CY; Kortmann, RD; Lhermitte, B; Markivskyy, A; McBain, C; Nabors, LB; Nam, DH; Perry, J; Picard, M; Pietsch, T; Rao, N; Reardon, DA; Schnell, O; Shen, CC; Steinbach, JP; Stupp, R; Taphoorn, MJ; Tarnawski, R; Thurzo, L; Tonn, JC; van den Bent, MJ; Weller, M; Weyerbrock, A; Wick, W; Wiegel, T, 2014)		0.6
" In the present work, TMZ was combined with a specific SKI, and the cytotoxic effect of each drug alone or in combination was tested on GBM cell lines."( A sphingosine kinase inhibitor combined with temozolomide induces glioblastoma cell death through accumulation of dihydrosphingosine and dihydroceramide, endoplasmic reticulum stress and autophagy.
Choi, J; Kopp-Schneider, A; Noack, J; Régnier-Vigouroux, A; Richter, K, 2014)		0.66
" We reasoned this could be more effective if combined with a vaccine that preferentially targeted TMZ-resistant cells."( Dendritic cell vaccination combined with temozolomide retreatment: results of a phase I trial in patients with recurrent glioblastoma multiforme.
Ancelet, LR; Bauer, E; Dzhelali, M; Findlay, MP; Gasser, O; Hamilton, DA; Hermans, IF; Hunn, MK; Mester, B; Sharples, KJ; Wood, CE, 2015)		0.68
"After a biopsy (6 patients) or a resection (13 patients) of a newly diagnosed GBM, 19 patients received radiotherapy (30 fractions of 2 Gy) in combination with daily TMZ 75 mg/m(2) and BV 10 mg/kg on days 1, 14, and 28, followed by 6 monthly cycles of TMZ 150-200 mg/m(2) on days 1-5."( Bevacizumab in combination with radiotherapy and temozolomide for patients with newly diagnosed glioblastoma multiforme.
Reijneveld, JC; Richel, DJ; Stalpers, LJ; van Furth, WR; van Linde, ME; Verheul, HM; Verhoeff, JJ, 2015)		0.67
"Wee1 regulates key DNA damage checkpoints, and in this study, the efficacy of the Wee1 inhibitor MK-1775 was evaluated in glioblastoma multiforme (GBM) xenograft models alone and in combination with radiation and/or temozolomide."( The Efficacy of the Wee1 Inhibitor MK-1775 Combined with Temozolomide Is Limited by Heterogeneous Distribution across the Blood-Brain Barrier in Glioblastoma.
Agar, NY; Bakken, KK; Calligaris, D; Carlson, BL; Decker, PA; Eckel-Passow, JE; Elmquist, WF; Evans, DL; Gupta, SK; Iyekegbe, DO; Lou, Z; Ma, B; Mueller, D; Pokorny, JL; Pucci, V; Sarkaria, JN; Schroeder, MA; Shumway, SD, 2015)		0.85
"In vitro MK-1775 efficacy alone and in combination with temozolomide, and the impact on DNA damage, was analyzed by Western blotting and γH2AX foci formation."( The Efficacy of the Wee1 Inhibitor MK-1775 Combined with Temozolomide Is Limited by Heterogeneous Distribution across the Blood-Brain Barrier in Glioblastoma.
Agar, NY; Bakken, KK; Calligaris, D; Carlson, BL; Decker, PA; Eckel-Passow, JE; Elmquist, WF; Evans, DL; Gupta, SK; Iyekegbe, DO; Lou, Z; Ma, B; Mueller, D; Pokorny, JL; Pucci, V; Sarkaria, JN; Schroeder, MA; Shumway, SD, 2015)		0.91
" However, there was no sensitizing effect of MK-1775 when combined with temozolomide in vitro."( The Efficacy of the Wee1 Inhibitor MK-1775 Combined with Temozolomide Is Limited by Heterogeneous Distribution across the Blood-Brain Barrier in Glioblastoma.
Agar, NY; Bakken, KK; Calligaris, D; Carlson, BL; Decker, PA; Eckel-Passow, JE; Elmquist, WF; Evans, DL; Gupta, SK; Iyekegbe, DO; Lou, Z; Ma, B; Mueller, D; Pokorny, JL; Pucci, V; Sarkaria, JN; Schroeder, MA; Shumway, SD, 2015)		0.89
" Primary GBM cells were treated with VPA as a monotherapy and in combination with temozolomide and irradiation."( The effect of valproic acid in combination with irradiation and temozolomide on primary human glioblastoma cells.
Cosgrove, L; Day, B; Fay, M; Head, R; Hosein, AN; Lim, YC; Martin, JH; Rose, S; Sminia, P; Stringer, B, 2015)		0.88
" This phase II, randomized, open-label, multicenter trial investigated the efficacy and safety of 2 dose regimens of the selective integrin inhibitor cilengitide combined with standard chemoradiotherapy in patients with newly diagnosed glioblastoma and an unmethylated MGMT promoter."( Two cilengitide regimens in combination with standard treatment for patients with newly diagnosed glioblastoma and unmethylated MGMT gene promoter: results of the open-label, controlled, randomized phase II CORE study.
Ashby, L; Depenni, R; Fink, KL; Grujicic, D; Hegi, ME; Hicking, C; Lhermitte, B; Mazurkiewicz, M; Mikkelsen, T; Nabors, LB; Nam, DH; Perry, JR; Picard, M; Reardon, DA; Salacz, M; Tarnawski, R; Zagonel, V, 2015)		0.42
" Cilengitide was administered intravenously in combination with daily temozolomide (TMZ) and concomitant radiotherapy (RT; wk 1-6), followed by TMZ maintenance therapy (TMZ/RT→TMZ)."( Two cilengitide regimens in combination with standard treatment for patients with newly diagnosed glioblastoma and unmethylated MGMT gene promoter: results of the open-label, controlled, randomized phase II CORE study.
Ashby, L; Depenni, R; Fink, KL; Grujicic, D; Hegi, ME; Hicking, C; Lhermitte, B; Mazurkiewicz, M; Mikkelsen, T; Nabors, LB; Nam, DH; Perry, JR; Picard, M; Reardon, DA; Salacz, M; Tarnawski, R; Zagonel, V, 2015)		0.65
"Standard and intensive cilengitide dose regimens were well tolerated in combination with TMZ/RT→TMZ."( Two cilengitide regimens in combination with standard treatment for patients with newly diagnosed glioblastoma and unmethylated MGMT gene promoter: results of the open-label, controlled, randomized phase II CORE study.
Ashby, L; Depenni, R; Fink, KL; Grujicic, D; Hegi, ME; Hicking, C; Lhermitte, B; Mazurkiewicz, M; Mikkelsen, T; Nabors, LB; Nam, DH; Perry, JR; Picard, M; Reardon, DA; Salacz, M; Tarnawski, R; Zagonel, V, 2015)		0.42
" Abemaciclib antitumor activity was assessed in subcutaneous and orthotopic glioma models alone and in combination with standard of care temozolomide (TMZ)."( Brain Exposure of Two Selective Dual CDK4 and CDK6 Inhibitors and the Antitumor Activity of CDK4 and CDK6 Inhibition in Combination with Temozolomide in an Intracranial Glioblastoma Xenograft.
Ajamie, RT; De Dios, A; Gelbert, LM; Kulanthaivel, P; Raub, TJ; Sanchez-Martinez, C; Sawada, GA; Shannon, HE; Staton, BA; Wishart, GN, 2015)		0.82
" In this study, we found that PI3K inhibitor combined with miR-125b inhibitor caused a marked increase of TMZ-induced GSC proliferation and invasiveness inhibition."( PI3K inhibitor combined with miR-125b inhibitor sensitize TMZ-induced anti-glioma stem cancer effects through inactivation of Wnt/β-catenin signaling pathway.
Fei, X; Shi, L; Wang, Z; You, Y, 2015)		0.42
"The primary aim of this Phase I study was to determine the maximum tolerated dose (MTD) of TPI 287 and the safety and tolerability of TPI 287 alone and in combination with temozolomide (TMZ) in pediatric patients with refractory or recurrent neuroblastoma or medulloblastoma."( A Phase 1 Trial of TPI 287 as a Single Agent and in Combination With Temozolomide in Patients with Refractory or Recurrent Neuroblastoma or Medulloblastoma.
Ashikaga, T; Bergendahl, G; DeSarno, M; Eslin, D; Ferguson, W; Hanna, GK; Higgins, T; Kaplan, J; Kraveka, J; Mitchell, D; Roberts, W; Sholler, GL; Werff, AV, 2016)		0.86
"Eighteen patients were enrolled to a phase I dose escalation trial of weekly intravenous infusion of TPI 287 for two 28-day cycles with toxicity monitoring to determine the MTD, followed by two cycles of TPI 287 in combination with TMZ."( A Phase 1 Trial of TPI 287 as a Single Agent and in Combination With Temozolomide in Patients with Refractory or Recurrent Neuroblastoma or Medulloblastoma.
Ashikaga, T; Bergendahl, G; DeSarno, M; Eslin, D; Ferguson, W; Hanna, GK; Higgins, T; Kaplan, J; Kraveka, J; Mitchell, D; Roberts, W; Sholler, GL; Werff, AV, 2016)		0.67
"We determined the MTD of TPI 287 alone and in combination with temozolomide to be 125 mg/m(2)."( A Phase 1 Trial of TPI 287 as a Single Agent and in Combination With Temozolomide in Patients with Refractory or Recurrent Neuroblastoma or Medulloblastoma.
Ashikaga, T; Bergendahl, G; DeSarno, M; Eslin, D; Ferguson, W; Hanna, GK; Higgins, T; Kaplan, J; Kraveka, J; Mitchell, D; Roberts, W; Sholler, GL; Werff, AV, 2016)		0.91
" Pharmacokinetic testing did not show evidence of drug-drug interaction between irinotecan and alisertib."( Phase I Study of the Aurora A Kinase Inhibitor Alisertib in Combination With Irinotecan and Temozolomide for Patients With Relapsed or Refractory Neuroblastoma: A NANT (New Approaches to Neuroblastoma Therapy) Trial.
Bagatell, R; Courtier, J; Czarnecki, S; DuBois, SG; Fox, E; Goodarzian, F; Groshen, S; Hawkins, R; Kudgus, RA; Lai, H; Malvar, J; Marachelian, A; Maris, JM; Matthay, KK; Mosse, YP; Reid, JM; Shimada, H; Tsao-Wei, D; Wagner, L, 2016)		0.65
" This phase I study aims to evaluate its safety, maximum tolerated dose (MTD), pharmacodynamic effect, and preliminary efficacy when combined with adjuvant temozolomide in GBM patients after standard chemoradiotherapy."( A phase I study to repurpose disulfiram in combination with temozolomide to treat newly diagnosed glioblastoma after chemoradiotherapy.
Campian, JL; DeWees, TA; Gujar, AD; Huang, J; Kim, AH; Lockhart, AC; Tran, DD; Tsien, CI, 2016)		0.87
" We show that GSI in combination with RT and TMZ attenuates proliferation, decreases 3D spheroid growth and results into a marked reduction in clonogenic survival in primary and established glioma cell lines."( NOTCH blockade combined with radiation therapy and temozolomide prolongs survival of orthotopic glioblastoma.
Barbeau, LM; Chalmers, AJ; Eekers, DB; Granton, PV; Groot, AJ; Habets, R; Iglesias, VS; King, H; Prickaerts, J; Short, SC; Theys, J; van Hoof, SJ; Verhaegen, F; Vooijs, M; Yahyanejad, S, 2016)		0.69
" We investigated the pharmacologic characteristics of OTX015 as a single agent and combined with targeted therapy or conventional chemotherapies in glioblastoma cell lines."( OTX015 (MK-8628), a novel BET inhibitor, displays in vitro and in vivo antitumor effects alone and in combination with conventional therapies in glioblastoma models.
Astorgues-Xerri, L; Bekradda, M; Berenguer-Daizé, C; Cayol, M; Cvitkovic, E; Lokiec, F; MacKenzie, S; Noel, K; Odore, E; Ouafik, L; Rezai, K; Riveiro, ME, 2016)		0.43
" Subsequently, each agent was used in combination with CNDAC at fixed concentration ratios."( Mechanism-Based Drug Combinations with the DNA Strand-Breaking Nucleoside Analog CNDAC.
Hargis, S; Jiang, Y; Liu, X; Nowak, B; Plunkett, W, 2016)		0.43
"We observed no survival benefit in young adults (age < 50) with anaplastic glioma when treated with TMZ combined with RT."( Radiation combined with temozolomide contraindicated for young adults diagnosed with anaplastic glioma.
Cai, J; Jiang, T; Li, S; Li, W; Peng, X; Qiu, X; Wang, Y; Wu, C; Yang, P; Yao, K; You, G; Zhang, C; Zhang, W, 2016)		0.74
"To observe the effect of RITA, a small molecule that targets p53, combined with temozolomide (TMZ) on proliferation, colony formation and apoptosis of human glioblastoma U87 cells and explore the underlying mechanism."( [RITA combined with temozolomide inhibits the proliferation of human glioblastoma U87 cells].
Cao, ZX; Feng, XL; He, XY; Song, XP; Wu, QH; Xiao, WW; Zeng, HC; Zhang, B, 2016)		0.98
" RITA combined with TMZ caused a more significant inhibition of U87 cells (29."( [RITA combined with temozolomide inhibits the proliferation of human glioblastoma U87 cells].
Cao, ZX; Feng, XL; He, XY; Song, XP; Wu, QH; Xiao, WW; Zeng, HC; Zhang, B, 2016)		0.76
" The present study used a patient-derived orthotopic xenograft (PDOX) nude-mouse model of melanoma with a BRAF-V600E mutation to determine the efficacy of temozolomide (TEM) combined with tumor-targeting Salmonella typhimurium A1-R."( Tumor-targeting Salmonella typhimurium A1-R combined with temozolomide regresses malignant melanoma with a BRAF-V600E mutation in a patient-derived orthotopic xenograft (PDOX) model.
Chmielowski, B; Dry, SM; Eilber, FC; Hoffman, RM; Igarashi, K; Kawaguchi, K; Kiyuna, T; Li, Y; Murakami, T; Nelson, SD; Russell, TA; Singh, A; Unno, M; Zhang, Y; Zhao, M, 2016)		0.88
" This phase I study evaluated the pharmacokinetics and mass balance of veliparib administered alone and in combination with temozolomide, and assessed any potential pharmacokinetic drug-drug interaction between veliparib and temozolomide."( Clinical Pharmacokinetics and Mass Balance of Veliparib in Combination with Temozolomide in Subjects with Nonhematologic Malignancies.
Giranda, V; Munasinghe, W; Nuthalapati, S; Xiong, H, 2018)		0.92
"This was an open-label, dose-escalation study of veliparib in combination with temozolomide in 42 subjects with nonhematologic malignancies."( Clinical Pharmacokinetics and Mass Balance of Veliparib in Combination with Temozolomide in Subjects with Nonhematologic Malignancies.
Giranda, V; Munasinghe, W; Nuthalapati, S; Xiong, H, 2018)		0.94
"New therapeutic agents in combination with the standard Stupp protocol (a protocol about the temozolomide combined with radiotherapy treatment with glioblastoma was research by Stupp R in 2005) were assessed to evaluate whether they were superior to the Stupp protocol alone, to determine the optimum treatment regimen for patients with newly diagnosed glioblastoma."( The interventional effect of new drugs combined with the Stupp protocol on glioblastoma: A network meta-analysis.
Chen, T; Fu, A; Li, J; Li, M; Song, X; Zhu, J, 2017)		0.67
"The use of novel therapeutic agents in combination with the Stupp protocol were all shown to be superior than the Stupp protocol alone for the treatment of newly diagnosed glioblastoma, ranked as follows: cilengitide 2000mg/5/week, bevacizumab in combination with irinotecan, nimotuzumab, bevacizumab, cilengitide 2000mg/2/week, cytokine-induced killer cell immunotherapy, and the Stupp protocol."( The interventional effect of new drugs combined with the Stupp protocol on glioblastoma: A network meta-analysis.
Chen, T; Fu, A; Li, J; Li, M; Song, X; Zhu, J, 2017)		0.46
"All intervention drugs evaluated in our study were superior to the Stupp protocol alone when used in combination with it."( The interventional effect of new drugs combined with the Stupp protocol on glioblastoma: A network meta-analysis.
Chen, T; Fu, A; Li, J; Li, M; Song, X; Zhu, J, 2017)		0.46
"We evaluated stereotactic volume modulated arc radiotherapy (VMAT) for canine gliomas, alone (radiotherapy [RT]) and in combination with temozolomide (RT + TMZ), compared with palliation."( Frameless stereotactic radiotherapy alone and combined with temozolomide for presumed canine gliomas.
Bianchi, C; Carrara, N; Dolera, M; Finesso, S; Malfassi, L; Marcarini, S; Mazza, G; Pavesi, S; Sala, M; Urso, G, 2018)		0.93
" The aim of this retrospective study was to evaluate the efficacy and toxicity of TMZ in dogs with relapsed multicentric lymphoma that failed multi-agent chemotherapy protocols, and compare the outcome to a group of dogs receiving the same drug in combination with DOX."( Temozolomide alone or in combination with doxorubicin as a rescue agent in 37 cases of canine multicentric lymphoma.
Baines, SJ; Blackwood, L; Elliott, JW; Treggiari, E, 2018)		1.92
" Proliferation, cell cycle, and apoptotic assays were performed with ML00253764, whereas the synergism of the simultaneous combination with temozolomide was evaluated by the combination index method."( Melanocortin Receptor-4 and Glioblastoma Cells: Effects of the Selective Antagonist ML00253764 Alone and in Combination with Temozolomide In Vitro and In Vivo.
Bocci, G; Di Desidero, T; Giuliani, D; Guarini, S; Orlandi, P; Ottani, A; Pacini, S; Pardini, C; Pasqualetti, F; Vaglini, F, 2018)		0.89
" This open-label, single-arm trial evaluated the maximum tolerated dose (MTD; phase I) and efficacy (phase II) of vorinostat combined with standard chemoradiation in newly diagnosed glioblastoma."( Phase I/II trial of vorinostat combined with temozolomide and radiation therapy for newly diagnosed glioblastoma: results of Alliance N0874/ABTC 02.
Ahluwalia, MS; Anderson, SK; Ballman, KV; Buckner, JC; Cerhan, J; Galanis, E; Gerstner, ER; Giannini, C; Grossman, SA; Jaeckle, K; Lee, EQ; Lesser, GJ; Ligon, KL; Loboda, A; Miller, CR; Moore, DF; Nebozhyn, M; Prados, M; Sarkaria, JN; Schiff, D; Wen, PY, 2018)		0.74
"Vorinostat combined with standard chemoradiation had acceptable tolerability in newly diagnosed glioblastoma."( Phase I/II trial of vorinostat combined with temozolomide and radiation therapy for newly diagnosed glioblastoma: results of Alliance N0874/ABTC 02.
Ahluwalia, MS; Anderson, SK; Ballman, KV; Buckner, JC; Cerhan, J; Galanis, E; Gerstner, ER; Giannini, C; Grossman, SA; Jaeckle, K; Lee, EQ; Lesser, GJ; Ligon, KL; Loboda, A; Miller, CR; Moore, DF; Nebozhyn, M; Prados, M; Sarkaria, JN; Schiff, D; Wen, PY, 2018)		0.74
" The aim of our research was the synthesis of a nanocarrier of quercetin combined with temozolomide, to enhance the specificity and efficacy of this anticancer drug commonly used in glioblastoma treatment."( Novel nanohydrogel of hyaluronic acid loaded with quercetin alone and in combination with temozolomide as new therapeutic tool, CD44 targeted based, of glioblastoma multiforme.
Armenia, E; Barbarisi, A; Barbarisi, M; De Sena, G; Iaffaioli, RV; Quagliariello, V; Schiavo, L; Tafuto, S, 2018)		0.92
" The purpose of this study was to evaluate the safety and pharmacokinetics of depatux-m, either in combination with temozolomide in newly diagnosed or recurrent glioblastoma (arm B) or as monotherapy in recurrent glioblastoma (arm C)."( Safety, pharmacokinetics, and antitumor response of depatuxizumab mafodotin as monotherapy or in combination with temozolomide in patients with glioblastoma.
Ansell, PJ; Butowski, N; Fichtel, L; Fischer, J; Gan, HK; Gomez, EJ; Holen, KD; Kumthekar, P; Lassman, AB; Lee, HJ; Lwin, Z; Mandich, H; Merrell, R; Munasinghe, WP; Reardon, DA; Roberts-Rapp, LA; Scott, AM; van den Bent, M; Wheeler, H; Xiong, H, 2018)		0.9
"Depatux-m alone or in combination with temozolomide demonstrated an acceptable safety and pharmacokinetic profile in glioblastoma."( Safety, pharmacokinetics, and antitumor response of depatuxizumab mafodotin as monotherapy or in combination with temozolomide in patients with glioblastoma.
Ansell, PJ; Butowski, N; Fichtel, L; Fischer, J; Gan, HK; Gomez, EJ; Holen, KD; Kumthekar, P; Lassman, AB; Lee, HJ; Lwin, Z; Mandich, H; Merrell, R; Munasinghe, WP; Reardon, DA; Roberts-Rapp, LA; Scott, AM; van den Bent, M; Wheeler, H; Xiong, H, 2018)		0.96
" In vivo, systemic treatment with pacritinib demonstrated blood-brain barrier penetration and led to improved overall median survival in combination with TMZ, in mice orthotopically xenografted with an aggressive recurrent GBM BTIC culture."( The JAK2/STAT3 inhibitor pacritinib effectively inhibits patient-derived GBM brain tumor initiating cells in vitro and when used in combination with temozolomide increases survival in an orthotopic xenograft model.
Aman, A; Cseh, O; Jensen, KV; Luchman, HA; Weiss, S, 2017)		0.65
"This preclinical study demonstrates the efficacy of pacritinib and supports the feasibility of testing pacritinib for the treatment of GBM, in combination with the standard of care TMZ."( The JAK2/STAT3 inhibitor pacritinib effectively inhibits patient-derived GBM brain tumor initiating cells in vitro and when used in combination with temozolomide increases survival in an orthotopic xenograft model.
Aman, A; Cseh, O; Jensen, KV; Luchman, HA; Weiss, S, 2017)		0.65
"We performed C57BL/6 mouse orthotopic glioma model by stereotactic intracranial implantation of glioma cell line GL261, mice were randomly divided into four groups: (1) control group; (2) TMZ group; (3) anti-PD-1 antibody group; (4) TMZ combined with anti-PD-1 antibody group."( Temozolomide combined with PD-1 Antibody therapy for mouse orthotopic glioma model.
Dai, B; Li, J; Qi, N; Zhang, G, 2018)		1.92
"Anti-PD1 antibody combined with TMZ therapy for orthotopic mouse glioma model could significantly improve the survival time of tumor-bear mice."( Temozolomide combined with PD-1 Antibody therapy for mouse orthotopic glioma model.
Dai, B; Li, J; Qi, N; Zhang, G, 2018)		1.92
"To investigate the clinical efficacy of stereotactic radiation therapy combined with temozolomide on recurrent glioma."( [Clinical efficacy of stereotactic radiation therapy combined with temozolomide on recurrent brain glioma].
Jiang, C; Li, X; Liu, S; Tang, S; Zhao, H, 2018)		0.94
"We retrospectively analyzed the safety and efficacy of hypofractionated radiotherapy (45 Gy/15 fr) combined with temozolomide (TMZ) followed by bevacizumab (BEV) salvage treatment in 18 glioblastoma patients aged > 75 years."( Treatment outcomes of hypofractionated radiotherapy combined with temozolomide followed by bevacizumab salvage therapy in glioblastoma patients aged > 75 years.
Kayama, T; Matsuda, KI; Nemoto, K; Sakurada, K; Sonoda, Y, 2018)		0.93
"Hypofractionated radiotherapy combined with TMZ and BEV salvage treatment was found to be safe and effective in glioblastoma patients aged > 75 years."( Treatment outcomes of hypofractionated radiotherapy combined with temozolomide followed by bevacizumab salvage therapy in glioblastoma patients aged > 75 years.
Kayama, T; Matsuda, KI; Nemoto, K; Sakurada, K; Sonoda, Y, 2018)		0.72
" In addition, TMZ could increase the levels of miR-505 and combination with pri-miR-505 and TMZ promoted the suppressive role mediated by miR-505 in GBM cells."( Combination with TMZ and miR-505 inhibits the development of glioblastoma by regulating the WNT7B/Wnt/β-catenin signaling pathway.
Fu, C; Liu, X; Yang, X; Zhang, C, 2018)		0.48
"We performed a retrospective analysis to compare the efficacy of whole brain radiotherapy (WBRT) combined with temozolomide (TMZ) versus WBRT alone as first-line treatment for brain metastases (BM)."( Effectiveness of temozolomide combined with whole brain radiotherapy for non-small cell lung cancer brain metastases.
Fu, L; Guo, D; Jing, W; Kong, L; Yu, J; Zhu, Y, 2018)		1.03
" To evaluate antitumor activity in vivo, 5-aza was administered alone and in combination with temozolomide (TMZ) in a PDX glioma model harboring IDH1 R132H mutation."( Demethylation and epigenetic modification with 5-azacytidine reduces IDH1 mutant glioma growth in combination with temozolomide.
Borodovsky, A; Chan, T; da Costa Rosa, M; Festuccia, WT; Riggins, GJ; Yamashita, AS, 2019)		0.94
"5-Aza provided a survival benefit as a single agent but worked best in combination with TMZ in 2 different IDH1 R132H mutant glioma models."( Demethylation and epigenetic modification with 5-azacytidine reduces IDH1 mutant glioma growth in combination with temozolomide.
Borodovsky, A; Chan, T; da Costa Rosa, M; Festuccia, WT; Riggins, GJ; Yamashita, AS, 2019)		0.72
" Temozolomide (TMZ) is one of them, widely used even in combination with ionizing radiation."( Drug resistance in glioblastoma and cytotoxicity of seaweed compounds, alone and in combination with anticancer drugs: A mini review.
Almeida, T; Azqueta, A; Ferreira, J; Ramos, AA; Rocha, E, 2018)		1.39
" However, their effects and mechanisms of action, alone or in combination with anticancer drugs, namely TMZ, in glioblastoma cell, still few explored and require more attention due to the unquestionable high potential of these marine compounds."( Drug resistance in glioblastoma and cytotoxicity of seaweed compounds, alone and in combination with anticancer drugs: A mini review.
Almeida, T; Azqueta, A; Ferreira, J; Ramos, AA; Rocha, E, 2018)		0.48
" Six patients received temozolomide and 8 received dacarbazine + 5-FU, combined with Endostar."( Effect of Endostar combined with chemotherapy in advanced well-differentiated pancreatic neuroendocrine tumors.
Bai, CM; Cheng, YJ; Gao, X; Meng, CT; Yan, XY; Ying, HY; Zhou, JF; Zhou, N, 2018)		0.79
" Further clinical investigations aimed at elucidating the veliparib exposure-efficacy/safety relationship and optimizing dosing recommendations for maximizing benefit-risk in patients with advanced myeloid malignancies should study veliparib doses ranging up to 120 mg in combination with temozolomide."( Population pharmacokinetics and exposure-response assessment of veliparib co-administered with temozolomide in patients with myeloid leukemias.
Beumer, JH; Chen, A; Gobburu, J; Gojo, I; Gopalakrishnan, M; Greer, JM; Karp, JE; Kiesel, BF; Mehrotra, S; Piekarz, R; Rudek, MA; Singh, R, 2019)		0.91
" This is the first study to evaluate the in vivo efficacy of the intravenous idasanutlin prodrug, RO6839921 (RG7775), both alone and in combination with temozolomide in TP53 wt orthotopic neuroblastoma models."( Preclinical evaluation of the first intravenous small molecule MDM2 antagonist alone and in combination with temozolomide in neuroblastoma.
Berry, P; Bonner, J; Chen, L; Daga, A; Kirk, C; Lunec, J; Newell, DR; Pastorino, F; Ponzoni, M; Thomas, HD; Tweddle, DA; Veal, GJ; Wood, KM; Zhao, Y, 2019)		0.92
" This study aimed to investigate the antitumor effects of natural killer cells in combination with temozolomide as the standard chemotherapeutic agent for glioblastoma."( Ex vivo-expanded highly purified natural killer cells in combination with temozolomide induce antitumor effects in human glioblastoma cells in vitro.
Matsuda, R; Morita, H; Motoyama, Y; Murakami, T; Nakagawa, I; Nakamura, M; Nakase, H; Nakazawa, T; Nishimura, F; Omoto, K; Shida, Y; Tanaka, Y; Tsujimura, T, 2019)		0.96
" The purpose of our study was to explore if PDT combined with TMZ can effectively inhibit glioma cells by influencing NHE1 in vitro."( Photodynamic therapy combined with temozolomide inhibits C6 glioma migration and invasion and promotes mitochondrial-associated apoptosis by inhibiting sodium-hydrogen exchanger isoform 1.
Chen, L; Chi, D; Cong, D; Gao, S; Hu, S; Ji, H; Jia, Y; Jin, J; Liang, B; Zhou, P, 2019)		0.79
"These results demonstrate that PDT combined with TMZ can inhibit C6 cell migration and invasion and promote mitochondrial-associated apoptosis by inhibiting NHE1."( Photodynamic therapy combined with temozolomide inhibits C6 glioma migration and invasion and promotes mitochondrial-associated apoptosis by inhibiting sodium-hydrogen exchanger isoform 1.
Chen, L; Chi, D; Cong, D; Gao, S; Hu, S; Ji, H; Jia, Y; Jin, J; Liang, B; Zhou, P, 2019)		0.79
" The aim of this study was to evaluate the efficacy of moderately hypofractionated simultaneous integrated boost intensity-modulated radiotherapy (SIB-IMRT) combined with temozolomide (TMZ) for the postoperative treatment of GBM."( Efficacy of moderately hypofractionated simultaneous integrated boost intensity-modulated radiotherapy combined with temozolomide for the postoperative treatment of glioblastoma multiforme: a single-institution experience.
Chen, G; Chen, L; Li, G; Li, Q; Luo, W; Lv, S; Zhong, L; Zhou, P, 2019)		0.92
"Moderately hypofractionated SIB-IMRT combined with TMZ is a feasible and safe treatment option with mild toxicity and good PFS and OS."( Efficacy of moderately hypofractionated simultaneous integrated boost intensity-modulated radiotherapy combined with temozolomide for the postoperative treatment of glioblastoma multiforme: a single-institution experience.
Chen, G; Chen, L; Li, G; Li, Q; Luo, W; Lv, S; Zhong, L; Zhou, P, 2019)		0.72
"A novel core‑shell type thermo‑nanoparticle (CSTNP) co‑loaded with temozolomide (TMZ) and the fluorescein new indocyanine green dye IR820 (termed IT‑CSTNPs) was designed and combined with a near‑infrared (NIR) laser to realize its photothermal conversion."( Core‑shell type thermo‑nanoparticles loaded with temozolomide combined with photothermal therapy in melanoma cells.
Hou, X; Jiang, G; Li, X; Liu, W; Liu, Y; Pang, Y; Yang, C, 2019)		1
"The purpose of this study was to evaluate the outcomes of elderly patients (aged ≥75 years) with newly diagnosed glioblastoma (GBM), who were treated with hypofractionated radiotherapy comprising 45 Gy in 15 fractions combined with temozolomide (TMZ) or TMZ and bevacizumab (TMZ/Bev)."( Survival benefits of hypofractionated radiotherapy combined with temozolomide or temozolomide plus bevacizumab in elderly patients with glioblastoma aged ≥ 75 years.
Ichimura, K; Igaki, H; Matsushita, Y; Miyakita, Y; Narita, Y; Ohno, M; Takahashi, M, 2019)		0.94
"Our hypofractionated radiotherapy regimen combined with TMZ or TMZ/Bev showed benefits in terms of OS, PFS, and KPS maintenance with acceptable toxicities in elderly patients with GBM aged ≥75 years."( Survival benefits of hypofractionated radiotherapy combined with temozolomide or temozolomide plus bevacizumab in elderly patients with glioblastoma aged ≥ 75 years.
Ichimura, K; Igaki, H; Matsushita, Y; Miyakita, Y; Narita, Y; Ohno, M; Takahashi, M, 2019)		0.75
" In clinical practice, Chinese doctors often use radiotherapy combined with temozolomide (TMZ) to treat these patients, although large-scale prospective studies are lacking."( Radiotherapy versus radiotherapy combined with temozolomide in high-risk low-grade gliomas after surgery: study protocol for a randomized controlled clinical trial.
Guan, H; He, L; He, Y; Mu, X; Peng, X; Wang, J; Wang, Y, 2019)		1
" The efficacy was significantly improved after lobaplatin combined with pemetrexed, temozolomide and bevacizumab."( Chemotherapy combined with bevacizumab for the treatment of advanced lung adenocarcinoma cancer harboring EGFR-ANXA2, EGFR-RAD51, ATR and BRCA2 mutations: A case report.
Cheng, Y; Huang, Z; Li, H; Liu, J; Liu, Y; Zhang, S; Zhong, R, 2020)		0.78
" Because the free drug cannot pass the blood-brain barrier (BBB), we investigated the use of nanocarriers for transport of the drug through the BBB and its efficacy when combined with radiotherapy and temozolomide (TMZ) in glioma spheroids."( Preclinical evaluation of binimetinib (MEK162) delivered via polymeric nanocarriers in combination with radiation and temozolomide in glioma.
Becerril Aragon, G; Bikhezar, F; de Kruijff, RM; de Vries, HE; Denkova, AG; Gasol Garcia, A; Narayan, RS; Slotman, BJ; Sminia, P; Torrelo Villa, G; van der Meer, AJGM; van der Pol, SMA, 2020)		0.96
" A synergistic effect was found in combination with fractionated irradiation and an additive effect with TMZ on spheroid volume reduction."( Preclinical evaluation of binimetinib (MEK162) delivered via polymeric nanocarriers in combination with radiation and temozolomide in glioma.
Becerril Aragon, G; Bikhezar, F; de Kruijff, RM; de Vries, HE; Denkova, AG; Gasol Garcia, A; Narayan, RS; Slotman, BJ; Sminia, P; Torrelo Villa, G; van der Meer, AJGM; van der Pol, SMA, 2020)		0.77
" Methods This is an open-label, 2-arm Phase 1b/2a study (N = 56) of galunisertib (intermittent dosing: 14 days on/14 days off per cycle of 28 days) in combination with TMZ/RTX (n = 40), versus a control arm (TMZ/RTX, n = 16)."( Phase 1b/2a study of galunisertib, a small molecule inhibitor of transforming growth factor-beta receptor I, in combination with standard temozolomide-based radiochemotherapy in patients with newly diagnosed malignant glioma.
Burkholder, T; Capper, D; Cleverly, AL; Desjardins, A; Estrem, ST; Forsyth, P; Guba, SC; Gueorguieva, I; Lahn, MM; Rodon, J; Suarez, C; Wang, S; Wick, A, 2020)		0.76
" We observe the effects of Si wei xiao xiu yin combined with chemotherapy on the growth of subcutaneous xenografts in nude mice and the expression of miRNA-21 and miRNA-221 in tumor tissues."( New advances on the inhibition of Siwei Xiaoliuyin combined with Temozolomide in glioma based on the regulatory mechanism of miRNA21/221.
Chen, H; Chen, Y; Li, C; Sharma, A; Sharma, HS; Tan, Q; Xie, C; Yang, Y; Zhan, W; Zhang, Z, 2020)		0.8
" They were randomly divided into saline group, traditional Chinese medicine group, temozolomide group and traditional Chinese medicine combined with temozolomide group to observe the changes in body weight, and the tumor weight, length, short diameter, volume of mice."( New advances on the inhibition of Siwei Xiaoliuyin combined with Temozolomide in glioma based on the regulatory mechanism of miRNA21/221.
Chen, H; Chen, Y; Li, C; Sharma, A; Sharma, HS; Tan, Q; Xie, C; Yang, Y; Zhan, W; Zhang, Z, 2020)		1.02
"To some extent, Si wei xiao xiu yin combined with temozolomide can inhibit the growth of subcutaneous xenografts in glioma nude mice."( New advances on the inhibition of Siwei Xiaoliuyin combined with Temozolomide in glioma based on the regulatory mechanism of miRNA21/221.
Chen, H; Chen, Y; Li, C; Sharma, A; Sharma, HS; Tan, Q; Xie, C; Yang, Y; Zhan, W; Zhang, Z, 2020)		1.05
"9% NaCl at a volume of 100 mL administered over a 30-min period every 3 weeks, combined with temozolomide or albumin-bound paclitaxel (nab-paclitaxel) in four patients with ARMM."( Transcatheter arterial infusion of anti-programmed cell death 1 antibody pembrolizumab combined with temozolomide or nab-paclitaxel in patient with primary anorectal malignant melanoma: Four case reports.
Cao, F; Chen, S; Fan, W; Li, D; Ma, W; Qi, H; Shen, L; Song, Z; Wen, X; Wu, Y; Xie, L; Zhang, X, 2020)		0.99
"This was a phase I, two-stage, multicentre, open-label, dose-escalation study of buparlisib in combination with temozolomide and radiotherapy in patients with newly diagnosed glioblastoma."( Phase I, open-label, multicentre study of buparlisib in combination with temozolomide or with concomitant radiation therapy and temozolomide in patients with newly diagnosed glioblastoma.
Beck, JT; DeGroot, J; Donnet, V; El-Hashimy, M; Mason, W; Mills, D; Rodon, JA; Rosenthal, M; Wen, PY, 2020)		1
"The MTD of buparlisib in combination with temozolomide at stage I (adjuvant phase only) was 80 mg/day, which was used as the starting dose in stage II."( Phase I, open-label, multicentre study of buparlisib in combination with temozolomide or with concomitant radiation therapy and temozolomide in patients with newly diagnosed glioblastoma.
Beck, JT; DeGroot, J; Donnet, V; El-Hashimy, M; Mason, W; Mills, D; Rodon, JA; Rosenthal, M; Wen, PY, 2020)		1.05
"Considering that the primary objective of estimating the MTD was not achieved in addition to the observed challenging safety profile of buparlisib in combination with radiotherapy and temozolomide, Novartis decided not to pursue the development of buparlisib in newly diagnosed glioblastoma."( Phase I, open-label, multicentre study of buparlisib in combination with temozolomide or with concomitant radiation therapy and temozolomide in patients with newly diagnosed glioblastoma.
Beck, JT; DeGroot, J; Donnet, V; El-Hashimy, M; Mason, W; Mills, D; Rodon, JA; Rosenthal, M; Wen, PY, 2020)		0.98
"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)		3.51
"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)		2.06
" This study evaluated the efficacy of atorvastatin in combination with standard therapy in patients with glioblastoma."( Atorvastatin in combination with radiotherapy and temozolomide for glioblastoma: a prospective phase II study.
Aldanan, S; Alghareeb, WA; Alhussain, H; AlNajjar, FH; Alsaeed, E; Alsharm, AA; Altwairgi, AK; Balbaid, AAO; Orz, Y, 2021)		0.87
" Therefore, we analyzed the cytotoxic effect of methadone alone and in combination with temozolomide, a DNA-alkylating drug that is first-line used in GBM treatment, utilizing GBM-derived cell lines and a human fibroblast cell line."( Cytotoxic and Senolytic Effects of Methadone in Combination with Temozolomide in Glioblastoma Cells.
Beltzig, L; Haas, B; Kaina, B; Piee-Staffa, A, 2020)		1.02
" Current treatments for glioblastoma patients consist of surgery followed by radiation in combination with temozolomide."( The effect of temozolomide in combination with doxorubicin in glioblastoma cells
Alexandru, O; Artene, SA; Danoiu, S; Dricu, A; Elena Cioc, C; Horescu, C; Sevastre, AS; Stefana Oana, P; Tache, DE; Tuta, C, 2020)		1.13
"To investigate the efficacy and safety of synchronous stereotactic radiotherapy (SRT) with temozolomide (TMZ) combined with whole brain radiotherapy (WBRT) in treating brain metastases originating from non-small cell lung cancer (NSCLC)."( Efficacy of synchronous stereotactic radiotherapy with temozolomide combined with whole brain radiotherapy in treating brain metastases originating from non-small cell lung cancer.
Liu, J; Liu, P; Ren, R; You, D, )		0.6
"Synchronous SRT with TMZ combined with WBRT is effective in treating patients with brain metastases originating from NSCLC, which can effectively improve the survival of patients and has tolerable adverse reactions."( Efficacy of synchronous stereotactic radiotherapy with temozolomide combined with whole brain radiotherapy in treating brain metastases originating from non-small cell lung cancer.
Liu, J; Liu, P; Ren, R; You, D, )		0.38
"In this work, we constructed LPHNs-cRGD for targeting delivery of the CRISPR/Cas9 system, in combination with FUS-MBs to open the BBB."( Gene Therapy for Drug-Resistant Glioblastoma via Lipid-Polymer Hybrid Nanoparticles Combined with Focused Ultrasound.
Chen, J; Cheng, Y; Huang, N; Wang, Z; Yang, Q; Zhou, Y, 2021)		0.62
"Purpose: To investigate the clinical therapeutic effect and safety of thalidomide combined with temozolomide (TMZ) and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z, )		0.61
"Methods: The clinical data of 108 patients with high-grade gliomas undergoing operation in our hospital from September 2014 to December 2016 were retrospectively analyzed, of which 54 received thalidomide combined with TMZ and three-dimensional conformal radiotherapy (thalidomide group) and 54 received TMZ combined with three-dimensional conformal radiotherapy (control group)."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z, )		0.39
"Conclusions: The application of thalidomide combined with TMZ and three-dimensional conformal radiotherapy for high-grade glioma patients after operation can prominently enhance the clinical therapeutic effect, improve patient quality of life, prolong survival, and produce tolerable adverse reactions."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z, )		0.39
"To explore the efficacy and safety of 125 I radioactive seed implantation combined with intermittent hormonal therapy (IHT) in the clinical treatment of moderate- and high-risk non-metastatic prostate cancer."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z, )		0.39
"125 I seed implantation combined with IHT is safe and effective in the clinical treatment of patients with moderate- and high-risk non-metastatic prostate cancer."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z, )		0.39
"To explore the clinical efficacy and safety of bevacizumab combined with temozolomide dose-dense regimen in the treatment of recurrent glioma."( Efficacy of bevacizumab combined with temozolomide dose-dense regimen on recurrent glioma.
Huang, W; Ji, S; Li, J; Liu, Z; Piao, M; Xue, J; Zhu, X, )		0.63
" There were 51 patients undergoing bevacizumab combined with temozolomide treatment (Bevacizumab group), and the remaining 51 patients received temozolomide treatment alone (Control group)."( Efficacy of bevacizumab combined with temozolomide dose-dense regimen on recurrent glioma.
Huang, W; Ji, S; Li, J; Liu, Z; Piao, M; Xue, J; Zhu, X, )		0.64
"Bevacizumab combined with temozolomide can significantly improve the clinical efficacy, increase the quality of life of patients, and delay the progression of recurrent glioma, with tolerable adverse reactions."( Efficacy of bevacizumab combined with temozolomide dose-dense regimen on recurrent glioma.
Huang, W; Ji, S; Li, J; Liu, Z; Piao, M; Xue, J; Zhu, X, )		0.7
"This two-stage phase I trial determined the MTD of zotiraciclib combined with either dose-dense (Arm1) or metronomic (Arm2) temozolomide using a Bayesian Optimal Interval design; then a randomized cohort expansion compared the progression-free survival rate at 4 months (PFS4) of the two arms for an efficient determination of a temozolomide schedule to combine with zotiraciclib at MTD."( Phase I Study of Zotiraciclib in Combination with Temozolomide for Patients with Recurrent High-grade Astrocytomas.
Aboud, O; Ahmad, S; Antony, R; Armstrong, TS; Boris, L; Bryla, C; Burton, EM; Butler, MK; Calvo, KR; Cordova, C; Figg, WD; Fink, D; Gallin, JI; Garren, N; Gilbert, MR; Gonzales, J; Grajkowska, E; Kuhns, DB; Leeper, H; Lindsley, M; Lollo, N; Long Priel, DA; Mendoza, TR; Mentges, K; Pang, Y; Peer, CJ; Penas-Prado, M; Siegel, C; Sissung, TM; Su, YT; Theeler, BJ; Vera, E; Wu, J; Yu, G; Yuan, Y, 2021)		1.08
"Zotiraciclib combined with temozolomide is safe in patients with recurrent high-grade astrocytomas."( Phase I Study of Zotiraciclib in Combination with Temozolomide for Patients with Recurrent High-grade Astrocytomas.
Aboud, O; Ahmad, S; Antony, R; Armstrong, TS; Boris, L; Bryla, C; Burton, EM; Butler, MK; Calvo, KR; Cordova, C; Figg, WD; Fink, D; Gallin, JI; Garren, N; Gilbert, MR; Gonzales, J; Grajkowska, E; Kuhns, DB; Leeper, H; Lindsley, M; Lollo, N; Long Priel, DA; Mendoza, TR; Mentges, K; Pang, Y; Peer, CJ; Penas-Prado, M; Siegel, C; Sissung, TM; Su, YT; Theeler, BJ; Vera, E; Wu, J; Yu, G; Yuan, Y, 2021)		1.17
"The purpose of this study was to compare the clinical efficacy and safety of temozolomide (TMZ) combined with three-dimensional conformal radiotherapy (3D-CRT) and radiotherapy alone after surgery in patients with high-risk low-grade gliomas (LGGs)."( Temozolomide chemotherapy combined with radiotherapy versus radiotherapy alone after surgery in patients with high-risk low-grade gliomas.
Hou, Y; Huan, Y; Li, Y; Liu, X; Zhang, Y, )		1.8
" Patients receiving TMZ chemotherapy combined with radiotherapy were considered as combination group (n=55), while those treated with radiotherapy alone were regarded as control group (n=55)."( Temozolomide chemotherapy combined with radiotherapy versus radiotherapy alone after surgery in patients with high-risk low-grade gliomas.
Hou, Y; Huan, Y; Li, Y; Liu, X; Zhang, Y, )		1.57
" Besides, age <40 years old, complete tumor resection and TMZ chemotherapy combined with radiotherapy after surgery were independent factors affecting the three-year PFS of patients with high-risk LGGs."( Temozolomide chemotherapy combined with radiotherapy versus radiotherapy alone after surgery in patients with high-risk low-grade gliomas.
Hou, Y; Huan, Y; Li, Y; Liu, X; Zhang, Y, )		1.57
"TMZ chemotherapy combined with radiotherapy after surgery in patients with high-risk LGGs can prominently improve clinical efficacy, prolong PFS, and facilitate tolerance to adverse reactions, but not prolong the OS of patients."( Temozolomide chemotherapy combined with radiotherapy versus radiotherapy alone after surgery in patients with high-risk low-grade gliomas.
Hou, Y; Huan, Y; Li, Y; Liu, X; Zhang, Y, )		1.57
" 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)		1.1
" The current study evaluated the role and molecular mechanisms of anlotinib in glioblastoma, and the effects of anlotinib in combination with temozolomide (TMZ)."( Anlotinib combined with temozolomide suppresses glioblastoma growth via mediation of JAK2/STAT3 signaling pathway.
Chen, J; Deng, C; Pan, H; Wang, H; Xu, P, 2022)		1.23
" In our study, we aim to explore the efficacy and safety of temozolomide combined with radiotherapy in the treatment of malignant glioma (MG) and its influence on postoperative complications and survival rate of patients."( Efficacy and Safety of Temozolomide Combined with Radiotherapy in the Treatment of Malignant Glioma.
Li, J; Wei, S, 2022)		1.27
" Non-ionising electromagnetic fields represent an emerging option given the potential advantages of safety, low toxicity and the possibility to be combined with other therapies."( Selective cell cycle arrest in glioblastoma cell lines by quantum molecular resonance alone or in combination with temozolomide.
Astori, G; Belli, R; Bernardi, M; Bozza, A; Catanzaro, D; Celli, P; Chieregato, K; Menarin, M; Merlo, A; Milani, G; Peroni, D; Pozzato, A; Pozzato, G; Raneri, FA; Ruggeri, M; Volpin, L, 2022)		0.93
"It was found that radiotherapy combined with temozolomide administration often increased the size of the original lesion or produced a new glioblastoma lesion."( Apatinib combined with temozolomide treatment for pseudoprogression in glioblastoma: A case report.
Cheng, P; Han, Q; Ma, H; Yang, H; Zhao, M; Zhao, Y, 2022)		1.29
" Based on the genetic testing results, almonertinib combined with anlotinib and temozolomide was administered and obtained 12 months of progression-free survival after the diagnosis of recurrence as the fourth-line treatment."( Almonertinib Combined with Anlotinib and Temozolomide in a Patient with Recurrent Glioblastoma with EGFR L858R Mutation.
Dong, S; Hou, Z; Li, S; Luo, N; Tao, R; Wu, H; Zhang, H; Zhang, X; Zhu, D, 2023)		1.4
" In this paper, we present the effects of juglone alone and in combination with temozolomide on glioblastoma cells."( Juglone in Combination with Temozolomide Shows a Promising Epigenetic Therapeutic Effect on the Glioblastoma Cell Line.
Barciszewska, AM; Belter, A; Gawrońska, I; Giel-Pietraszuk, M; Naskręt-Barciszewska, MZ, 2023)		1.43
" CCK-8 was used to determine the inhibitory rate of Coix group, TMZ group and drug combination group on GBM cells, and the combination index (CI) was calculated to determine whether they had synergistic effect."( Coixendide efficacy in combination with temozolomide in glioblastoma and transcriptome analysis of the mechanism.
Ban, X; Jin, P; Li, Y; Liu, S; Yue, Y; Zhang, L; Zhang, X; Zhao, C; Zhao, Z, 2023)		1.18
"To investigate the effect of Temozolomide combined with intensity modulated radiation therapy on serum factor, immune function and clinical efficacy in postoperative glioma patients."( Effect of Temozolomide Combined with Intensity Modulated Radiation Therapy on Serum Factor, Immune Function and Clinical Efficacy in Postoperative Glioma Patients.
Fan, R; Liu, J; Liu, Z; Yuan, J, 2023)		1.6

Bioavailability

Temozolomide (TMZ) has become the more commonly used analog of DTIC-related oral agents because of its greater bioavailability and ability to cross the blood brain barrier. 10b is aqueous soluble, orally bioavailable across multiple species, and demonstrated good in vivo efficacy in a B16F10 subcutaneous murine melanoma model.

ExcerptReferenceRelevance
" This study evaluated the effect of an increase in gastric pH, through the use of ranitidine, on the oral bioavailability and plasma pharmacokinetics of temozolomide and MTIC."( Effect of gastric pH on the relative oral bioavailability and pharmacokinetics of temozolomide.
Beale, P; Brada, M; Cutler, DL; Judson, I; Marco, A; Moore, S; Reidenberg, P; Statkevich, P, 1999)		0.73
"Temozolomide, an oral cytotoxic agent with approximately 100% bioavailability after one administration, has demonstrated schedule-dependent clinical activity against highly resistant cancers."( Phase I dose-escalation and pharmacokinetic study of temozolomide (SCH 52365) for refractory or relapsing malignancies.
Batra, V; Beale, P; Brada, M; Cutler, D; Dugan, M; Judson, I; Moore, S; Reidenberg, P; Statkevich, P, 1999)		2
"Temozolomide (TMZ) is a new, orally administered, second-generation imidazotetrazine prodrug with essentially 100% oral bioavailability that has demonstrated meaningful efficacy and an acceptable safety profile in the treatment of patients with recurrent glioblastoma multiforme."( Future directions in the treatment of malignant gliomas with temozolomide.
Prados, MD, 2000)		1.99
" Predictable bioavailability and minimal toxicity make temozolomide a candidate for a wide range of clinical testing to evaluate the potential of combination treatments in different tumor types."( Temozolomide and treatment of malignant glioma.
Calvert, H; Friedman, HS; Kerby, T, 2000)		2
" TMZ is an alkylating agent chemically similar to dacarbazine (DTIC) with good oral bioavailability and CNS penetration."( Temozolomide and whole brain irradiation in melanoma metastatic to the brain: a phase II trial of the Cytokine Working Group.
Atkins, B; Clark, I; Dutcher, P; Ernstoff, S; Flaherty, L; Gollob, J; II Smith, W; Johnson, D; Longmate, J; Margolin, K; Sosman, J; Thompson, A; Weber, J; Weiss, G, 2002)		1.76
" We treated 25 stage IV patients with temozolomide - a cytostatic drug with 100% oral bioavailability and considerable penetration of CNS tissue."( [Temozolomide as therapeutic option for patients with metastatic melanoma and poor prognosis].
Christophers, E; Frick, S; Haacke, TC; Hauschild, A; Lischner, S; Rosien, F; Schäfer, F, 2002)		1.5
" Temozolomide, an orally bioavailable alkylating agent that crosses the blood-brain barrier, has activity against brain metastases from both small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) when used as a single agent, but response rates are low."( Use of temozolomide with other cytotoxic chemotherapy in the treatment of patients with recurrent brain metastases from lung cancer.
Ebert, BL; Niemierko, E; Salgia, R; Shaffer, K, 2003)		1.68
" In this work we investigated the effect of association of temozolomide (TMZ), an orally bioavailable alkylating agent, with three chemotherapeutic drugs, liposomal doxorubicin (DOXO), cis-platinum (CDDP)."( Effect of association of temozolomide with other chemotherapic agents on cell growth inhibition in glioma cell lines.
Balzarotti, M; Boiardi, A; Calatozzolo, C; Ciusani, E; Croci, D; Salmaggi, A, 2004)		0.87
" Pharmacokinetics studies revealed that GPI 15427 possesses a substantial oral bioavailability (plasma Cmax after a single dose of 40 mg/kg: 1041+/-516 ng/ml)."( Brain distribution and efficacy as chemosensitizer of an oral formulation of PARP-1 inhibitor GPI 15427 in experimental models of CNS tumors.
Alemu, C; Calvin, D; Graziani, G; Hoover, R; Lapidus, R; Leonetti, C; Morgan, L; Scarsella, M; Tang, Z; Tentori, L; Vergati, M; Woznizk, K; Xu, W; Zhang, J, 2005)		0.33
" TMZ is able to cross the blood brain barrier and is stable at gastric acid pH so it has almost 100% oral bioavailability and is rapidly absorbed after it is taken orally."( Role of temozolomide in pediatric brain tumors.
Barone, G; Maurizi, P; Riccardi, R; Tamburrini, G, 2006)		0.77
" 10b is aqueous soluble, orally bioavailable across multiple species, and demonstrated good in vivo efficacy in a B16F10 subcutaneous murine melanoma model in combination with temozolomide (TMZ) and in an MX-1 breast xenograph model in combination with cisplatin."( Discovery and SAR of 2-(1-propylpiperidin-4-yl)-1H-benzimidazole-4-carboxamide: A potent inhibitor of poly(ADP-ribose) polymerase (PARP) for the treatment of cancer.
Bontcheva-Diaz, V; Bouska, JJ; Donawho, CK; Frost, DJ; Fry, EH; Gandhi, VB; Giranda, VL; Gong, J; Grandel, R; Johnson, EF; Klinghofer, V; Liu, X; Lubisch, W; Luo, Y; Marsh, KC; Olson, AM; Park, CH; Penning, TD; Rosenberg, SH; Shi, Y; Thomas, S; Wernet, W; Zhu, GD, 2008)		0.54
"ABT-888 is a potent, orally bioavailable PARP-1/2 inhibitor shown to potentiate DNA damaging agents."( The PARP inhibitor, ABT-888 potentiates temozolomide: correlation with drug levels and reduction in PARP activity in vivo.
Bontcheva-Diaz, VD; Bouska, JJ; Bukofzer, G; Colon-Lopez, M; Donawho, CK; Frost, DJ; Giranda, VL; Guan, R; Jarvis, K; Johnson, EF; Klinghofer, V; Liu, X; Luo, Y; Olson, A; Palma, JP; Penning, TD; Rodriguez, LE; Rosenberg, SH; Saltarelli, MJ; Shi, Y; Stavropoulos, JA; Zhu, GD, )		0.4
" Although the bioavailability of temozolomide is approximately 100%, pathology or anatomical changes of the gastrointestinal tract may adversely affect absorption, and consequently therapeutic response."( Disposition of temozolomide in a patient with glioblastoma multiforme after gastric bypass surgery.
Beumer, JH; Egorin, MJ; Park, DM; Shah, DD, 2009)		0.99
" In addition, 3a is aqueous soluble, orally bioavailable across multiple species, and demonstrated good in vivo efficacy in a B16F10 subcutaneous murine melanoma model in combination with temozolomide (TMZ) and in an MX-1 breast cancer xenograft model in combination with either carboplatin or cyclophosphamide."( Discovery of the Poly(ADP-ribose) polymerase (PARP) inhibitor 2-[(R)-2-methylpyrrolidin-2-yl]-1H-benzimidazole-4-carboxamide (ABT-888) for the treatment of cancer.
Bontcheva-Diaz, V; Bouska, JJ; Donawho, CK; Frost, DJ; Gandhi, VB; Giranda, VL; Gong, J; Johnson, EF; Klinghofer, V; Liu, X; Luo, Y; Marsh, KC; Olson, AM; Osterling, DJ; Penning, TD; Shi, Y; Zhu, GD, 2009)		0.54
" Thus, our results show that polymeric nanocapsules are able to increase the intratumoral bioavailability of indomethacin and reduce the growth of implanted gliomas."( Indomethacin-loaded nanocapsules treatment reduces in vivo glioblastoma growth in a rat glioma model.
Battastini, AM; Bernardi, A; Braganhol, E; Edelweiss, MI; Figueiró, F; Guterres, SS; Jäger, E; Pohlmann, AR, 2009)		0.35
" Temozolomide's characteristics which make it a candidate for a wide range of clinical testing to evaluate the potential of combination treatments in different tumor types are its predictable bioavailability and minimal toxicity."( Temozolomide with radiation therapy in high grade brain gliomas: pharmaceuticals considerations and efficacy; a review article.
Beli, I; Chaldeopoulos, D; Fotineas, A; Koukourakis, GV; Kouloulias, V; Kouvaris, J; Maravelis, G; Pantelakos, P; Papadimitriou, C; Zacharias, G, 2009)		2.71
" In addition, 22b is orally bioavailable across multiple species, crosses the blood-brain barrier, and appears to distribute into tumor tissue."( Optimization of phenyl-substituted benzimidazole carboxamide poly(ADP-ribose) polymerase inhibitors: identification of (S)-2-(2-fluoro-4-(pyrrolidin-2-yl)phenyl)-1H-benzimidazole-4-carboxamide (A-966492), a highly potent and efficacious inhibitor.
Bontcheva-Diaz, V; Bouska, JJ; Buchanan, FG; Bukofzer, GT; Donawho, CK; Frost, DJ; Fry, EH; Gandhi, VB; Giranda, VL; Gong, J; Johnson, EF; Klinghofer, V; Liu, X; Luo, Y; Marsh, KC; Olson, AM; Osterling, DJ; Park, CH; Penning, TD; Rodriguez, LE; Shi, Y; Thomas, S; Zhu, GD, 2010)		0.36
" Recently, the clinical use of temozolomide (TMZ) has become the more commonly used analog of DTIC-related oral agents because of its greater bioavailability and ability to cross the blood brain barrier."( Quercetin abrogates chemoresistance in melanoma cells by modulating deltaNp73.
Burd, R; Limesand, KH; Mendoza, EE; Mitchell, GC; Radhakrishnan, VM; Sittadjody, S; Thangasamy, T, 2010)		0.65
" Further in vivo experiments on laboratory animals and analysis of absorption rate and side effects are required."( Arsenic trioxide sensitizes cancer stem cells to chemoradiotherapy. A new approach in the treatment of inoperable glioblastoma multiforme.
Cernea, D; Cocis, A; Fischer-Fodor, E; Florian, IS; Ioani, H; Irimie, A; Kacso, G; Petrescu, M; Soritau, O; Timis, T; Tomuleasa, C; Virag, P, )		0.13
" We evaluated the preclinical potential of a novel, orally bioavailable PI3K/mTOR dual inhibitor (XL765) in in vitro and in vivo studies."( Inhibition of PI3K/mTOR pathways in glioblastoma and implications for combination therapy with temozolomide.
Aftab, DT; Berger, MS; Haas-Kogan, DA; James, CD; Mueller, S; Ozawa, T; Polley, MY; Prados, MD; Prasad, G; Sottero, T; Weiss, WA; Yang, X, 2011)		0.59
" Future studies are needed to determine whether VPA increases TMZ bioavailability or acts as an inhibitor of histone deacetylases and thereby sensitizes for radiochemotherapy in vivo."( Prolonged survival with valproic acid use in the EORTC/NCIC temozolomide trial for glioblastoma.
Belanger, K; Bogdahn, U; Brandes, AA; Cairncross, JG; Forsyth, P; Gorlia, T; Lacombe, D; Macdonald, DR; Mason, W; Mirimanoff, RO; Rossetti, AO; Stupp, R; van den Bent, MJ; Vecht, CJ; Weller, M, 2011)		0.61
" This preclinical study sought to test the efficacy of the food additive Triacetin (glyceryl triacetate, GTA) as a novel therapy to increase acetate bioavailability in glioma cells."( Triacetin-based acetate supplementation as a chemotherapeutic adjuvant therapy in glioma.
Davies, MT; Driscoll, HE; Jaworski, DM; Lawler, SE; Long, PM; Penar, PL; Pendlebury, WW; Spees, JL; Teasdale, BA; Tsen, AR; Viapiano, MS, 2014)		0.4
"CNDAC (2'-C-cyano-2'-deoxy-1-β-d-arabino-pentofuranosyl-cytosine, DFP10917) and its orally bioavailable prodrug, sapacitabine, are undergoing clinical trials for hematologic malignancies and solid tumors."( Mechanism-Based Drug Combinations with the DNA Strand-Breaking Nucleoside Analog CNDAC.
Hargis, S; Jiang, Y; Liu, X; Nowak, B; Plunkett, W, 2016)		0.43
" Its high bioavailability (40%~100%) and high tissue distribution in both monkeys and rats were its most important pharmacokinetic features."( Novel PARP1/2 inhibitor mefuparib hydrochloride elicits potent in vitro and in vivo anticancer activity, characteristic of high tissue distribution.
Chen, CH; Chen, XY; Chen, Y; Ding, J; Gao, ZW; He, JX; He, Q; Huan, XJ; Li, XH; Liao, XM; Lu, XL; Miao, ZH; Shen, YY; Song, SS; Su, Y; Sun, YM; Tan, C; Tong, LJ; Wang, M; Wang, YQ; Wang, YT; Xiong, B; Yang, CH; Yang, XY, 2017)		0.46
"Veliparib is a Biopharmaceutical Classification System (BCS) Class 1 compound, with no less than 90% of the dose absorbed and an oral bioavailability of at least 73%."( Clinical Pharmacokinetics and Mass Balance of Veliparib in Combination with Temozolomide in Subjects with Nonhematologic Malignancies.
Giranda, V; Munasinghe, W; Nuthalapati, S; Xiong, H, 2018)		0.71
" Doxorubicin (DOX) is not used in gliomas due to its low bioavailability in the brain; however, new delivery strategies and low doses may be effective in the long term, especially as part of a drug cocktail."( Low Dose of Doxorubicin Potentiates the Effect of Temozolomide in Glioblastoma Cells.
Kipper, FC; Lenz, G; Lopez, PLDC; Silva, AO; Villodre, ES, 2018)		0.73
" Delivery outcomes are evaluated by the bioavailability of free temozolomide across time."( Delivery of liposome encapsulated temozolomide to brain tumour: Understanding the drug transport for optimisation.
Zhan, W, 2019)		1.03
" However, its pharmacological activity is reduced due MTIC low bioavailability in the brain."( Biophysical interaction of temozolomide and its active metabolite with biomembrane models: The relevance of drug-membrane interaction for Glioblastoma Multiforme therapy.
Andrade, S; Coelho, MÁN; Loureiro, JA; Pereira, MC; Ramalho, MJ, 2019)		0.81
"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
" We reported that copper, for the first time, is found to recognize and bind MTIC in the process of TMZ degradation, which means copper can play an important role in enhancing the bioavailability of MTIC derived from TMZ."( Enhanced Copper-Temozolomide Interactions by Protein for Chemotherapy against Glioblastoma Multiforme.
Du, K; Feng, F; Li, X; Shao, F; Sun, J; Sun, Y, 2019)		0.86
"Temozolomide is a drug approved for treating glioblastomas, which has 100% oral bioavailability but gets degraded at physiological pH thus having very short half-life and only 20-30% brain bioavailability."( Design of temozolomide-loaded proliposomes and lipid crystal nanoparticles with industrial feasible approaches: comparative assessment of drug loading, entrapment efficiency, and stability at plasma pH.
Dubey, SK; Gorantla, S; Khosa, A; Rapalli, VK; Saha, RN; Singhvi, G; Waghule, T, 2021)		2.47
" However, low bioavailability and extractive yield limit the clinical applications of XN."( Xanthohumol regulates miR-4749-5p-inhibited RFC2 signaling in enhancing temozolomide cytotoxicity to glioblastoma.
Chen, KC; Chen, PH; Cheng, CH; Ho, KH; Kuo, TC; Lee, CC; Lee, YT; Liu, AJ; Shih, CM, 2020)		0.79
" The main advantages are its high oral bioavailability (almost 100% although the concentration found in the cerebrospinal fluid was approximately 20% of the plasma concentration of TMZ), its lipophilic properties, and small size that confer the ability to cross the blood-brain barrier."( Temozolomide: An Updated Overview of Resistance Mechanisms, Nanotechnology Advances and Clinical Applications.
Cabeza, L; Jiménez-Luna, C; Luque, R; Melguizo, C; Ortiz, R; Perazzoli, G; Prados, J, 2021)		2.06
"Liposomal formulations may improve the solubility and bioavailability of drugs potentially increasing their ability to cross the blood-brain barrier."( Nanoliposomal Irinotecan and Metronomic Temozolomide for Patients With Recurrent Glioblastoma: BrUOG329, A Phase I Brown University Oncology Research Group Trial.
Baekey, J; Carcieri, A; Cielo, D; Disano, D; Donnelly, J; Elinzano, H; MacKinnon, K; Mohler, A; Robison, J; Safran, H; Sturtevant, A; Toms, S; Vatketich, J; Wood, R, 2021)		0.89
" The efficacy and optimal deployment schedule of the orally bioavailable small-molecule tumor checkpoint controller lisavanbulin alone, and in combination with, standards of care were assessed using a panel of IDH-wildtype GBM patient-derived xenografts."( Preclinical modeling in glioblastoma patient-derived xenograft (GBM PDX) xenografts to guide clinical development of lisavanbulin-a novel tumor checkpoint controller targeting microtubules.
Bachmann, F; Bakken, KK; Burgenske, DM; Carlson, BL; Decker, PA; Eckel-Passow, JE; Elmquist, WF; Gampa, G; Giannini, C; He, L; Hu, Z; Kitange, GJ; Kosel, ML; Lane, HA; McSheehy, P; Mladek, AC; Pokorny, JL; Sarkaria, JN; Schmitt-Hoffmann, A; Schroeder, MA; Talele, S; Vaubel, RA, 2022)		0.72
" Therefore, localised approaches that treat GB straight into the tumour site provide an alternative to enhance chemotherapy bioavailability and efficacy, reducing systemic toxicity."( Nek1-inhibitor and temozolomide-loaded microfibers as a co-therapy strategy for glioblastoma treatment.
Arantes, PR; Borges, GR; Braganhol, E; Dalanhol, CS; de Barros Dias, MCH; de Oliveira Merib, J; de Souza, PO; Ferro, MB; Henn, JG; Morás, AM; Moura, DJ; Nugent, M; Reinhardt, LS, 2022)		1.05
" Although these beneficial effects are promising, the efficacy of natural compounds in glioblastoma is limited due to their bioavailability and blood-brain barrier permeability."( Natural Compounds as Promising Adjuvant Agents in The Treatment of Gliomas.
Gigli, G; Leporatti, S; Persano, F, 2022)		0.72
" TMZ is an orally bioavailable prodrug, which is well absorbed from the gastrointestinal tract and is converted to its active alkylating metabolite 5-(3-methyl triazen-1-yl)imidazole-4-carbozamide (MTIC) spontaneously in physiological condition that does not require hepatic involvement."( Temozolomide Efficacy and Metabolism: The Implicit Relevance of Nanoscale Delivery Systems.
Alyautdin, R; Chubarev, V; Grigorevskikh, E; Ismail, N; Merkulov, V; Petrenko, D; Smolyarchuk, E; Sologova, S; Syzrantsev, N, 2022)		2.16
" Although TMZ has shown 100% oral bioavailability and crosses the blood-brain barrier effectively, however it suffers from limitations such as a short half-life (∼1."( Polymeric and small molecule-conjugates of temozolomide as improved therapeutic agents for glioblastoma multiforme.
Chitkara, D; Jatyan, R; Karthik, YG; Mittal, A; Sahel, DK; Singh, P, 2022)		0.98
" However, poor site-specific delivery and bioavailability significantly restrict the efficient permeability of regorafenib to brain lesions and compromise its treatment efficacy."( Brain-Targeted HFn-Cu-REGO Nanoplatform for Site-Specific Delivery and Manipulation of Autophagy and Cuproptosis in Glioblastoma.
Ding, N; Huang, C; Jia, W; Jiang, J; Li, L; Luo, M; Nice, EC; Tian, H; Zhang, H; Zhou, L, 2023)		0.91
"Brain bioavailability of the KDM1A inhibitor (NCD38) was established using LS-MS/MS."( Lysine-specific histone demethylase 1A (KDM1A/LSD1) inhibition attenuates DNA double-strand break repair and augments the efficacy of temozolomide in glioblastoma.
Alejo, S; Brenner, AJ; Chen, Y; Clarke, K; Gilbert, AR; He, Y; Jayamohan, S; Johnson, JD; Lai, Z; Li, W; Lv, Y; Palacios, BE; Pratap, UP; Sareddy, GR; Suzuki, T; Tekmal, RR; Vadlamudi, RK; Venkata, PP; Viswanadhapalli, S; Weldon, K; Ye, Z; Zhao, W; Zheng, S; Zou, Y, 2023)		1.11
" However, due to the short plasma half-life, only 20-30 % brain bioavailability can be achieved using traditional formulations."( Exploring temozolomide encapsulated PEGylated liposomes and lyotropic liquid crystals for effective treatment of glioblastoma: in-vitro, cell line, and pharmacokinetic studies.
Laxmi Swetha, K; Narayan Saha, R; Roy, A; Singhvi, G; Waghule, T, 2023)		1.31

Dosage Studied

Temozolomide has been studied in soft-tissue sarcomas with varying dosing schedules. Pretreatment of mice with O6-benzylguanine increased temozolmide-induced mortality, requiring reduction of the dosage from 1200 to 750 mg/m2 on the single-day regimen.

ExcerptRelevanceReference
" Pretreatment of mice with O6-benzylguanine increased temozolomide-induced mortality, requiring reduction of the dosage from 1200 to 750 mg/m2 on the single-day regimen."( Activity of temozolomide in the treatment of central nervous system tumor xenografts.
Bigner, DD; Catino, JJ; Dolan, ME; Friedman, HS; Keir, S; Marcelli, S; Pegg, AE; Schold, SC, 1995)		0.92
" Comparisons with BCNU were made on both single and multiple dosing schedules, since temozolomide cytotoxicity is highly schedule dependent."( Potentiation of temozolomide and BCNU cytotoxicity by O(6)-benzylguanine: a comparative study in vitro.
May, BL; Newlands, ES; Porteus, JK; Wedge, SR, 1996)		0.86
") was examined using single and daily x5 dosing regimens in athymic mice bearing subcutaneous A375P xenografts."( Effect of single and multiple administration of an O6-benzylguanine/temozolomide combination: an evaluation in a human melanoma xenograft model.
Newlands, ES; Porteous, JK; Wedge, SR, 1997)		0.53
"Thirty-three patients with newly diagnosed glioblastoma multiforme (GBM) and five patients with newly diagnosed anaplastic astrocytoma (AA) were treated with Temodal at a starting dose of 200 mg/m2 daily for 5 consecutive days with repeat dosing every 28 days after the first daily dose."( DNA mismatch repair and O6-alkylguanine-DNA alkyltransferase analysis and response to Temodal in newly diagnosed malignant glioma.
Ashley, DM; Bigner, DD; Bigner, SH; Cokgor, I; Colvin, OM; Dugan, M; Friedman, AH; Friedman, HS; Haglund, MM; Henry, AJ; Kerby, T; Krischer, J; Lovell, S; Marchev, F; McLendon, RE; Modrich, PL; Provenzale, JM; Rasheed, K; Rich, J; Seman, AJ; Stewart, E, 1998)		0.3
" This review discusses the mechanism of action of TMZ and strategies for overcoming pathways of resistance to this promising agent, including the use of TMZ in combination with other chemotherapeutic agents or radiation therapy, and exploration of alternate dosing schedules."( Future directions in the treatment of malignant gliomas with temozolomide.
Prados, MD, 2000)		0.55
" One day after the last dose of vehicle or TNP-470, a steady-state dosing regimen of TMZ was administered with subsequent collection and high-performance liquid chromatography analysis of plasma and either tumor homogenate or tumor microdialysis steady-state TMZ concentrations, and in some cases [5-(3-methyltriazen-1-yl)imidazole-4-carboximide] MTIC, its active metabolite."( Pharmacodynamic-mediated reduction of temozolomide tumor concentrations by the angiogenesis inhibitor TNP-470.
Chu, J; Gallo, JM; Li, S; Ma, J; Pulfer, S; Reed, K, 2001)		0.58
" In this study, we evaluated the relation between TMZ dosing and AGT depletion in patients with deep visceral tumors and in peripheral blood mononuclear cells (PBMCs) to determine whether the dose of TMZ was sufficient to inactivate AGT and lead to therapeutic efficacy."( Temozolomide: the effect of once- and twice-a-day dosing on tumor tissue levels of the DNA repair protein O(6)-alkylguanine-DNA-alkyltransferase.
Gerson, SL; Haaga, J; Liu, L; Majka, S; Spiro, TP; Willson, JK, 2001)		1.75
" For patients with recurrent malignant glioma, temozolomide provides a therapeutic option with a predictable safety profile, clinical efficacy, and convenient dosing that can provide important quality-of-life benefits."( Temozolomide for recurrent high-grade glioma.
Macdonald, DR, 2001)		2.01
" Also under investigation are modifications to the temozolomide dosing schedule, other routes of administration, and treatment regimens that include temozolomide in combination with other chemotherapeutic and biologic agents."( Future directions for temozolomide therapy.
Yung, WK, 2001)		0.88
" The recommended dosage for TEMO for a phase II study of this combination is 200 mg/m2 per day for 5 days."( Phase I study of Gliadel wafers plus temozolomide in adults with recurrent supratentorial high-grade gliomas.
Affronti, ML; Cokgor, L; Early, M; Edwards, S; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; McLendon, RE; Provenzale, JM; Quinn, JA; Rich, JN; Sampson, JH; Stafford-Fox, V; Tourt-Uhlig, S; Zaknoen, S, 2001)		0.58
" The standard dosage is 150-200 mg/m2 per day for 5 days in a 28-day cycle."( A phase II study of extended low-dose temozolomide in recurrent malignant gliomas.
Abrey, LE; Bazylewicz, KA; Khan, RB; Malkin, MG; Raizer, JJ, 2002)		0.59
"To evaluate the antitumor effects and toxicities of whole brain irradiation (WBI) with temozolomide (TMZ) administered by prolonged oral dosing in patients with melanoma metastatic to the brain."( Temozolomide and whole brain irradiation in melanoma metastatic to the brain: a phase II trial of the Cytokine Working Group.
Atkins, B; Clark, I; Dutcher, P; Ernstoff, S; Flaherty, L; Gollob, J; II Smith, W; Johnson, D; Longmate, J; Margolin, K; Sosman, J; Thompson, A; Weber, J; Weiss, G, 2002)		1.98
" This review will focus on the different pharmacological strategies aimed at overcoming tumor resistance to TMZ such as new formulations of the drug or dosing schedules, and combined treatments with other chemotherapeutic agents, modulators of DNA repair systems, or gene therapy."( Pharmacological strategies to increase the antitumor activity of methylating agents.
Graziani, G; Tentori, L, 2002)		0.31
" The drug is well tolerated with dose limiting myelosuppression and thrombocytopenia occurring in less than 10% of patients at current dosage schedules."( The use of temozolomide in recurrent malignant gliomas.
Gaya, A; Greenstein, A; Rees, J; Stebbing, J, 2002)		0.7
" Body surface area-based dosing was statistically significantly associated with a reduction in interpatient variability in drug clearance for only five of the 33 agents: docosahexaenoic acid (DHA)-paclitaxel, 5-fluorouracil/eniluracil, paclitaxel, temozolomide, and troxacitabine."( Role of body surface area in dosing of investigational anticancer agents in adults, 1991-2001.
Baker, SD; Donehower, RC; Grochow, LB; Rowinsky, EK; Schellens, JH; Sparreboom, A; Verweij, J, 2002)		0.5
" For example, Abdelbasit and Plackett proposed an optimal design assuming that the dose-response relationship follows some specified linear models."( Experimental design and sample size determination for testing synergism in drug combination studies based on uniform measures.
Fang, HB; Houghton, PJ; Tan, M; Tian, GL, 2003)		0.32
" The model is fit to serial ANC measurements obtained after TMZ dosing and it is able to explain, among other things, the lag in ANC reduction following a dose of TMZ, the ANC nadir, and the 'rebound effect' observed where the ANC recovers to levels greater than that observed pre-TMZ dose."( A mechanistic mathematical model of temozolomide myelosuppression in children with high-grade gliomas.
Fouladi, M; Gajjar, AJ; Kirstein, MN; Nair, G; Panetta, JC; Stewart, CF, 2003)		0.59
" In the last 2 years, studies have focused on exploring strategies to optimize the efficacy of temozolomide, including evaluating different temozolomide dosing schedules and combining temozolomide with other antineoplastic agents, radiation therapy, or drug resistance-modifying agents."( Temozolomide: realizing the promise and potential.
Dolan, ME; Nagasubramanian, R, 2003)		1.98
" Temozolomide has activity and a favorable safety profile in all dosing schedules tested."( Temozolomide: realizing the promise and potential.
Dolan, ME; Nagasubramanian, R, 2003)		2.67
" Extended TMZ dosing regimens may be superior by delivering the drug continuously at a higher dose over time."( Selective CD4+ lymphopenia in melanoma patients treated with temozolomide: a toxicity with therapeutic implications.
Chapman, PB; Foster, T; Krown, SE; Livingston, PO; Quinn, C; Sepkowitz, KA; Sohn, S; Su, YB; Williams, L; Wolchok, JD, 2004)		0.56
" Alternate temozolomide dosing schedules such as continuous daily administration may enhance antitumor activity through sustained depletion of the DNA repair protein O6-alkylguanine DNA alkyltransferase."( Temozolomide in patients with advanced cancer: phase I and pharmacokinetic study.
Baker, SD; Batra, VK; Cutler, DL; Donehower, RC; Rudek, MA; Statkevich, P, 2004)		2.16
" In phase II of the study, four weeks after completion of RT, a monochemotherapy using TMZ was administered at the dosage of 200 mg/m2/day per 5 days every 28 days for 6 cycles."( Temozolomide in radio-chemotherapy combined treatment for newly-diagnosed glioblastoma multiforme: phase II clinical trial.
Campanella, C; Costa, A; Fedele, F; Frati, A; Frati, L; Gagliardi, FM; Innocenzi, G; Lanzetta, G; Minniti, G; Nappa, M; Rozzi, A; Salvati, M; Vecchione, A, )		1.57
" Median thalidomide dosage was 200 mg/day."( Combined thalidomide and temozolomide treatment in patients with glioblastoma multiforme.
Baumann, F; Baumert, BG; Bernays, RL; Bjeljac, M; Brandner, S; Kollias, SS; Rousson, V; Yonekawa, Y, )		0.43
"The response rate, efficacy, side-effects, reasons for discontinuation of therapy and survival rate of 47 patients treated with temozolomide in combination with two different dosing regimens of IFN-alpha 2b were documented."( Temozolomide and interferon alpha 2b in metastatic melanoma stage IV.
Fialla, R; Forstinger, Ch; Fritsch, P; Hofmann-Wellenhof, R; Kehrer, H; Kerl, H; Kindermann-Glebowski, E; Klein, G; Koller, J; Konrad, K; Kos, C; Lang, A; Mischer, P; Pachinger, W; Pehamberger, H; Raml, J; Ratzinger, G; Richtig, E; Seeber, A; Smolle, J; Steiner, A; Ulmer, H; Wolff, K; Zelger, B, 2004)		1.97
"We conducted a study to determine the dose-limiting toxicity of an extended dosing schedule of temozolomide (TMZ) when used with a fixed dose of BCNU, or 1,3-bis(2-chloroethyl)-1-nitrosourea (carmustine), taking advantage of TMZ's ability to deplete O6-alkylguanine-DNA-alkyltransferase and the synergistic activity of these two agents."( Phase 1 study of 28-day, low-dose temozolomide and BCNU in the treatment of malignant gliomas after radiation therapy.
Abrey, LE; Kleber, M; Malkin, MG; Raizer, JJ, 2004)		0.82
" We develop a maximum likelihood method based on the expectation/conditional maximization (ECM) algorithm to estimate the dose-response relationship while accounting for the informative censoring and the constraints of model parameters."( Repeated-measures models with constrained parameters for incomplete data in tumour xenograft experiments.
Fang, HB; Houghton, PJ; Tan, M; Tian, GL, 2005)		0.33
" Attempts to maximise efficacy have led to manipulation of both dosage and drug scheduling and the evidence for the various strategies is reviewed."( Temozolomide in the treatment of solid tumours: current results and rationale for dosing/scheduling.
Middleton, MR; Payne, MJ; Pratap, SE, 2005)		1.77
"Temozolomide has been studied in soft-tissue sarcomas with varying dosing schedules."( Temozolomide in uterine leiomyosarcomas.
Aghajanian, C; Anderson, S, 2005)		3.21
" Cisplatin-temozolomide combinations are well tolerated without additional toxicity to single-agent treatments; the recommended phase II dosage is 80 mg m(-2) cisplatin and 150 mg m(-2) x 5 temozolomide in heavily treated, and 200 mg m(-2) x 5 temozolomide in less-heavily pretreated children."( Dose finding and O6-alkylguanine-DNA alkyltransferase study of cisplatin combined with temozolomide in paediatric solid malignancies.
Chastagner, P; Couanet, D; Djafari, L; Doz, F; Frappaz, D; Gentet, JC; Geoerger, B; Geoffray, A; Margison, GP; O'Quigley, J; Pein, F; Raquin, MA; Rubie, H; Vassal, G; Wartelle, M; Watson, AJ, 2005)		0.94
"The objective of the study was to evaluate the efficacy and toxicity of Temozolomide (TMZ) administered for 5 consecutive days in three daily dosing in children with recurrent or refractory high-grade glioma."( Phase II trial of temozolomide in children with recurrent high-grade glioma.
Abate, ME; Attinà, G; Caldarelli, M; Cefalo, G; Clerico, A; Colosimo, C; Di Rocco, C; Garré, ML; Lazzareschi, I; Madon, E; Massimino, M; Maurizi, P; Mazzarella, G; Riccardi, R; Ridola, V; Ruggiero, A; Sandri, A, 2006)		0.9
"We identified a transcriptomic signature that predicts a common in vitro and in vivo resistance phenotype to these agents, a proportion of which is imprinted recurrently by gene dosage changes in the resistant glioblastoma genome."( Tumor necrosis factor-alpha-induced protein 3 as a putative regulator of nuclear factor-kappaB-mediated resistance to O6-alkylating agents in human glioblastomas.
Bredel, C; Bredel, M; Duran, GE; Harsh, GR; Juric, D; Recht, LD; Scheck, AC; Sikic, BI; Vogel, H; Yu, RX, 2006)		0.33
" Extended dosing has met with early favourable results."( Exploiting the role of O6-methylguanine-DNA-methyltransferase (MGMT) in cancer therapy.
Middleton, MR; Sabharwal, A, 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)		1.5
" Three patients (12%) were changed to standard temozolomide dosing due to side effects, including intractable nausea (n = 2) and multiple cytopenias (n = 1)."( Toxicity and efficacy of protracted low dose temozolomide for the treatment of low grade gliomas.
Gasco, J; Pouratian, N; Schiff, D; Shaffrey, ME; Sherman, JH, 2007)		0.86
"Dose-limiting adverse effects of thrombocytopenia and leukopenia prevent augmentation of current temozolomide (TMZ) dosing protocols; therefore, we hypothesized that the direct intracranial delivery of TMZ would lead to improved efficacy in an animal model of malignant glioma in an animal model."( Local delivery of temozolomide by biodegradable polymers is superior to oral administration in a rodent glioma model.
Brem, H; Brem, S; Caplan, J; Legnani, F; Li, K; Pradilla, G; Tyler, B, 2007)		0.89
"Metronomic dosed (MD) chemotherapy as opposed to conventional dosed (CD) chemotherapy is considered an alternate strategy to target angiogenesis and limit host toxicity."( Preclinical pharmacokinetic and pharmacodynamic evaluation of metronomic and conventional temozolomide dosing regimens.
Gallo, JM; Guo, P; Nuthalapati, S; Wang, X; Zhou, Q, 2007)		0.56
" Subsequently the tumor recurred and the patient had a dramatic and durable response to standard 5 day dosing of adjuvant temozolomide."( Durable response of a radiation-induced, high-grade cerebellar glioma to temozolomide.
Doherty, LM; Drappatz, J; Kesari, S; Monje, ML; Ramakrishna, NR; Wen, PY; Young, G, 2007)		0.78
" Depending on the intended indication and dosing regimen, PPL can delay or stop development of a compound in the drug discovery process."( Evaluation of a published in silico model and construction of a novel Bayesian model for predicting phospholipidosis inducing potential.
Gehlhaar, D; Greene, N; Johnson, TO; Pelletier, DJ; Tilloy-Ellul, A, )		0.13
"The efficacy of LM and TMZ in the current dosing schedule is similar to that of TMZ alone."( Randomized trial of the combination of lomeguatrib and temozolomide compared with temozolomide alone in chemotherapy naive patients with metastatic cutaneous melanoma.
Baka, S; Beith, J; Davis, ID; Harris, PA; Haydon, A; Hersey, P; Kefford, RF; Margison, GP; McArthur, GA; Middleton, MR; Mortimer, P; Ranson, M; Sabharwal, A; Seebaran, A; Thompson, D; Watson, AJ, 2007)		0.59
" The preclinical pharmacokinetic model was scaled to predict temozolomide concentrations in human CSF, normal brain, and brain tumor, and through a series of Monte Carlo simulations, the accumulation of temozolomide in brain tumors under conditions of altered blood-brain barrier permeability, fractional blood volume, and clinical dosing schedules was evaluated."( Predicting human tumor drug concentrations from a preclinical pharmacokinetic model of temozolomide brain disposition.
Gallo, JM; Guo, P; Kruh, GD; Vicini, P; Wang, X; Zhou, Q, 2007)		0.8
" Through a series of model simulations, it was shown that the brain tumor accumulation of temozolomide varied substantially based on changes in blood-brain barrier permeability and fractional tumor blood volume but minimally based on clinical dosing regimens."( Predicting human tumor drug concentrations from a preclinical pharmacokinetic model of temozolomide brain disposition.
Gallo, JM; Guo, P; Kruh, GD; Vicini, P; Wang, X; Zhou, Q, 2007)		0.78
"A physiologically based pharmacokinetic modeling approach offers a means to translate preclinical to clinical characteristics of drug disposition in target tissues and, thus, a means to select appropriate drug dosing regimens for achieving optimal target tissue drug concentrations."( Predicting human tumor drug concentrations from a preclinical pharmacokinetic model of temozolomide brain disposition.
Gallo, JM; Guo, P; Kruh, GD; Vicini, P; Wang, X; Zhou, Q, 2007)		0.56
"The effects of 'metronomic' or extended chemotherapy dosing schedules (ECS) are mediated through poorly understood anti-angiogenic mechanisms."( Metronomic chemotherapy dosing-schedules with estramustine and temozolomide act synergistically with anti-VEGFR-2 antibody to cause inhibition of human umbilical venous endothelial cell growth.
Greenman, J; Hetherington, JW; Lam, T; Little, S; Maraveyas, A, 2007)		0.58
" Single-dose temozolomide at five dosage levels (267, 355, 472, 628, and 835 mg/m(2)) was given at least 6 h after completion of O(6)-benzylguanine bolus."( Phase I trial of single-dose temozolomide and continuous administration of o6-benzylguanine in children with brain tumors: a pediatric brain tumor consortium report.
Boyett, JM; Broniscer, A; Danks, MK; Friedman, HS; Gajjar, A; Goldman, S; Gururangan, S; Kun, LE; MacDonald, TJ; Packer, RJ; Poussaint, TY; Stewart, CF; Wallace, D, 2007)		1
" Because preclinical studies suggested that a twice-daily dosing schedule might be more effective, the safety and efficacy of twice-daily dosing of temozolomide were studied in patients with recurrent gliomas at their first, second, or third recurrence."( Multi-institutional phase II study of temozolomide administered twice daily in the treatment of recurrent high-grade gliomas.
Alavi, J; Balmaceda, C; Chen, J; Cheung, YK; Fine, RL; Fisher, PG; Pannullo, S; Peereboom, D; Sisti, M, 2008)		0.82
"Twice-daily dosing may enhance the efficacy of temozolomide in the treatment of recurrent gliomas without increasing toxicity."( Multi-institutional phase II study of temozolomide administered twice daily in the treatment of recurrent high-grade gliomas.
Alavi, J; Balmaceda, C; Chen, J; Cheung, YK; Fine, RL; Fisher, PG; Pannullo, S; Peereboom, D; Sisti, M, 2008)		0.87
" It may also allow a reduction in dosage and a decrease in systemic toxicity."( Solid lipid nanoparticles of temozolomide: potential reduction of cardial and nephric toxicity.
Bi, X; Dou, M; Huang, G; Zhang, N, 2008)		0.64
" Lower dosing of TMZ also is associated with a more beneficial toxicity profile."( Radiochemotherapy in patients with primary glioblastoma comparing two temozolomide dose regimens.
Bischof, M; Combs, SE; Debus, J; Edler, L; Rausch, R; Schulz-Ertner, D; Wagner, F; Wagner, J; Welzel, T; Zabel-du Bois, A, 2008)		0.58
" Accordingly, a clinical trial using oral temozolomide (TMZ) and subcutaneous PEG-interferon alpha-2b (PEG) in patients with metastatic melanoma was designed to determine the maximal tolerated dosage of both drugs and the antitumoral response."( Temozolomide associated with PEG-interferon in patients with metastatic melanoma: a multicenter prospective phase I/II study.
Bedane, C; Cupissol, D; Delaunay, M; Dereure, O; Dreno, B; Guillot, B; Khamari, A; Picot, MC, 2008)		2.05
" Further studies using ATO and AA with TMZ with this dosing schedule in advanced melanoma are not warranted."( Phase II trial of arsenic trioxide and ascorbic acid with temozolomide in patients with metastatic melanoma with or without central nervous system metastases.
Bael, TE; Gollob, JA; Peterson, BL, 2008)		0.59
" Imatinib doses up to 1,000 mg/day for 8 consecutive days are well tolerated when combined with standard TMZ dosing for MG patients."( Safety and pharmacokinetics of dose-intensive imatinib mesylate plus temozolomide: phase 1 trial in adults with malignant glioma.
Desjardins, A; Egorin, MJ; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; Lagattuta, TF; McLendon, R; Quinn, JA; Reardon, DA; Rich, JN; Salvado, AJ; Sathornsumetee, S; Vredenburgh, JJ, 2008)		0.58
" Noninvasive imaging of apoptosis facilitates optimization of therapeutic protocols regarding dosing and schedule and enables identification of efficacious combination therapies."( Noninvasive imaging of apoptosis and its application in cancer therapeutics.
Coppola, JM; Rehemtulla, A; Ross, BD, 2008)		0.35
" If further studies are to be performed, emerging data suggest that higher daily doses of lomeguatrib and a dosing period beyond that of TMZ should be evaluated."( A phase II trial of lomeguatrib and temozolomide in metastatic colorectal cancer.
Khan, OA; Levitt, NC; Margison, GP; Michael, M; Middleton, MR; Midgley, R; Mortimer, P; Olver, I; Ranson, M; Watson, AJ, 2008)		0.62
" Several preliminary studies have been initiated to address the issue of resistance and suppression of MGMT activity, and have used alternative temozolomide dosing schedules and O(6)-guanine mimetic agents as substrates for MGMT."( Mechanisms of disease: temozolomide and glioblastoma--look to the future.
Chamberlain, MC; Mrugala, MM, 2008)		0.86
" A variety of dosing schedules that increase the duration of exposure and the cumulative dose of temozolomide are currently being investigated for the treatment of glioma, with the goal of improving antitumor activity and overcoming resistance."( New (alternative) temozolomide regimens for the treatment of glioma.
Platten, M; Weller, M; Wick, W, 2009)		0.9
" The toxicity of the dose-intense pre-RT regimen used in this study may warrant evaluation of other, less intense dosing strategies."( Phase II trial of preirradiation and concurrent temozolomide in patients with newly diagnosed anaplastic oligodendrogliomas and mixed anaplastic oligoastrocytomas: RTOG BR0131.
Berkey, B; Biggs, C; Blumenthal, DT; Brown, P; Giannini, C; Herman, J; Jenkins, R; Macdonald, D; Mehta, M; Peereboom, D; Schultz, C; Suh, JH; Vogelbaum, MA, 2009)		0.61
" Consistent with a functional significance of MGMT induction, treatment of GBM43 with a protracted low-dose TMZ regimen was significantly less effective than a shorter high-dose regimen, while survival for GBM14 was improved with the protracted dosing regimen."( Induction of MGMT expression is associated with temozolomide resistance in glioblastoma xenografts.
Carlson, BL; Decker, PA; Grogan, PT; James, CD; Kitange, GJ; Lamont, JD; Sarkaria, JN; Schroeder, MA; Wu, W, 2009)		0.61
" Extended ABT-888 dosing schedules showed no advantage compared to simultaneous TMZ administration."( The PARP inhibitor, ABT-888 potentiates temozolomide: correlation with drug levels and reduction in PARP activity in vivo.
Bontcheva-Diaz, VD; Bouska, JJ; Bukofzer, G; Colon-Lopez, M; Donawho, CK; Frost, DJ; Giranda, VL; Guan, R; Jarvis, K; Johnson, EF; Klinghofer, V; Liu, X; Luo, Y; Olson, A; Palma, JP; Penning, TD; Rodriguez, LE; Rosenberg, SH; Saltarelli, MJ; Shi, Y; Stavropoulos, JA; Zhu, GD, )		0.4
" The system analysis technique, embodied in the convolution integral, generated an impulse response function that, when convolved with temozolomide plasma concentration input functions, yielded predicted normal brain and brain tumor temozolomide concentration profiles for different temozolomide dosing regimens (75-200 mg/m(2)/d)."( A new model for prediction of drug distribution in tumor and normal tissues: pharmacokinetics of temozolomide in glioma patients.
Aboagye, EO; Brock, CS; Gallo, JM; Price, PM; Rosso, L; Saleem, A; Turkheimer, FE, 2009)		0.77
"O(6)-BG when added to a 1-day dosing regimen of temozolomide was able to restore temozolomide sensitivity in patients with temozolomide-resistant anaplastic glioma, but there seemed to be no significant restoration of temozolomide sensitivity in patients with temozolomide-resistant GBM."( Phase II trial of temozolomide plus o6-benzylguanine in adults with recurrent, temozolomide-resistant malignant glioma.
Bigner, DD; Desjardins, A; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; Jiang, SX; McLendon, RE; Quinn, JA; Reardon, DA; Rich, JN; Sampson, JH; Vredenburgh, JJ; Walker, A, 2009)		0.94
" It has become common practice to re-expose patients to TMZ who had been previously treated with TMZ, or to switch patients to alternative dosing regimens of TMZ when there are signs of relapse or progress on standard TMZ therapeutic regimens."( Rechallenge with temozolomide in patients with recurrent gliomas.
Bogdahn, U; Hau, P; Jauch, T; Pascher, C; Weller, M; Wick, A; Wick, W, 2009)		0.69
"This phase I clinical trial conducted with patients who had recurrent or progressive malignant glioma (MG) was designed to determine the maximum tolerated dose (MTD) and toxicity of three different 5-day dosing regimens of temozolomide (TMZ) in combination with O(6)-benzylguanine (O(6)-BG)."( Phase I trial of temozolomide plus O6-benzylguanine 5-day regimen with recurrent malignant glioma.
Bigner, DD; Desjardins, A; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; Jiang, SX; McLendon, RE; Quinn, JA; Reardon, DA; Rich, JN; Sampson, JH; Vredenburgh, JJ; Walker, A, 2009)		0.88
"Lomeguatrib, an O(6)-methylguanine-DNA methyltransferase inactivator, was evaluated in an extended dosing regimen with temozolomide, designed according to pharmacodynamic data from previous studies."( A phase I study of extended dosing with lomeguatrib with temozolomide in patients with advanced melanoma.
Abdi, E; Beith, J; Corrie, PG; Kefford, RF; Kotasek, D; Margison, GP; Middleton, MR; Mortimer, P; Palmer, C; Ranson, M; Thomas, NP; Watson, AJ, 2009)		0.81
" Early recovery of MGMT activity in tumours suggested that more protracted dosing with LM is required."( O(6)-methylguanine-DNA methyltransferase depletion and DNA damage in patients with melanoma treated with temozolomide alone or with lomeguatrib.
Beith, J; Davis, ID; Haydon, A; Hayward, O; Hersey, P; Kefford, R; Lorigan, P; Margison, GP; McArthur, G; McGown, G; Middleton, MR; Mortimer, P; Ranson, M; Sabharwal, A; Thomson, D; Thorncroft, M; Watson, AJ, 2009)		0.57
" Regarding the dosing schedule and administration scheme, as well as the co-administration with other anticancer drugs, a C score was attributed for the off label situations."( [Prescription guidebook for temozolomide usage in brain tumors].
Borget, I; Brignone, M; Cartalat-Carel, S; Chinot, O; Hassani, Y; Taillandier, L; Taillibert, S; Tilleul, P, 2009)		0.65
"Alternative dosing schedules of temozolomide may improve survival in patients with newly diagnosed glioblastoma (GBM) by increasing the therapeutic index, overcoming common mechanisms of temozolomide resistance, or both."( Randomized phase II trial of chemoradiotherapy followed by either dose-dense or metronomic temozolomide for newly diagnosed glioblastoma.
Abrey, LE; Clarke, JL; DeAngelis, LM; Gavrilovic, I; Hormigo, A; Iwamoto, FM; Karimi, S; Lassman, AB; Nolan, CP; Panageas, K; Sul, J, 2009)		0.86
" Alternative dosing regimens, such as 1-week on/1-week off, or 3-week on/1-week off, that deliver more prolonged exposure have been observed to result in higher cumulative doses than the standard 5-day regimen and may deplete tumor-derived O6-methylguanine-DNA methyltransferase (MGMT) in tumor cells, thus sensitizing tumor cells to the effects of TMZ."( [Treatment of glioma with temozolomide].
Nishikawa, R, 2009)		0.65
" Neither the extent of the initial resection nor dexamethasone dosing was associated with pseudoprogression."( Population-based study of pseudoprogression after chemoradiotherapy in GBM.
Cairncross, JG; de Robles, PA; Dharmawardene, M; Easaw, JC; Forsyth, PA; Hamilton, MG; Magliocco, AM; McIntyre, JB; Parney, IF; Roldán, GB; Scott, JN; Yan, ES, 2009)		0.35
" Afterward, adjuvant TMZ chemotherapy was discontinued in one patient and the dosage of TMZ was reduced in the other."( Patient-tailored, imaging-guided, long-term temozolomide chemotherapy in patients with glioblastoma.
Backes, H; Brunn, A; Burghaus, L; Galldiks, N; Heiss, WD; Jacobs, AH; Kracht, LW; Ullrich, RT, 2010)		0.62
" 44 of the patients underwent chemo-radiotherapy with Temodal dosed 75 mg/m2, and the rest 135 ones received RT alone."( Postoperative chemo-radiotherapy with temodal in patients with glioblastoma multiforme--survival rates and prognostic factors.
Radev, LR; Semerdjieva, ML; Vlaikova, MI; Yaneva, MP, )		0.13
" In addition, various protracted temozolomide dosing schedules have been evaluated as a strategy to further enhance its anti-tumor activity."( Effect of CYP3A-inducing anti-epileptics on sorafenib exposure: results of a phase II study of sorafenib plus daily temozolomide in adults with recurrent glioblastoma.
Bigner, DD; Desjardins, A; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; Janney, D; Marcello, J; McLendon, RE; Peters, K; Reardon, DA; Sampson, JH; Vredenburgh, JJ, 2011)		0.86
" The originally approved temozolomide dosing regimen is 150 to 200 mg/m(2) per day (Days 1 to 5 every 28-day cycle [5 of 28 days])."( Dose-dense temozolomide regimens: antitumor activity, toxicity, and immunomodulatory effects.
Hwu, WJ; Neyns, B; Reardon, DA; Tosoni, A, 2010)		1.05
" Metronomic dosing of temozolomide (TMZ) combined with standard radiotherapy may improve survival by increasing the therapeutic index and anti-angiogenic effect of TMZ."( A multi-centre Canadian pilot study of metronomic temozolomide combined with radiotherapy for newly diagnosed paediatric brainstem glioma.
Bartels, U; Baruchel, S; Bouffet, E; Eisenstat, D; Gammon, J; Huang, A; Hukin, J; Johnston, DL; Samson, Y; Sharp, JR; Stempak, D; Stephens, D; Tabori, U, 2010)		0.93
"Chemoradiotherapy with metronomic dosing of TMZ showed similar toxicity to previous TMZ regimens, and does not appear to improve survival in paediatric DIBSG."( A multi-centre Canadian pilot study of metronomic temozolomide combined with radiotherapy for newly diagnosed paediatric brainstem glioma.
Bartels, U; Baruchel, S; Bouffet, E; Eisenstat, D; Gammon, J; Huang, A; Hukin, J; Johnston, DL; Samson, Y; Sharp, JR; Stempak, D; Stephens, D; Tabori, U, 2010)		0.61
" These combinations appear to be the most promising for in vivo pre-clinical studies, with a view to testing in melanoma patients as a continuous dosing strategy, due to the in vitro additive inhibitory effect on growth seen in both endothelial and cancer cells."( Sorafenib enhances the in vitro anti-endothelial effects of low dose (metronomic) chemotherapy.
Cawkwell, L; Little, SJ; Maraveyas, A; Murray, A; Stanley, P, 2010)		0.36
" On the basis of these results, the recommended Phase II dosage currently being tested is RAD001 70 mg/week in combination with standard chemoradiotherapy."( North Central Cancer Treatment Group Phase I trial N057K of everolimus (RAD001) and temozolomide in combination with radiation therapy in patients with newly diagnosed glioblastoma multiforme.
Brown, PD; Buckner, JC; Galanis, E; Giannini, C; Jaeckle, KA; McGraw, S; Peller, PJ; Sarkaria, JN; Uhm, JH; Wu, W, 2011)		0.59
"After diagnostic surgery or biopsy, treatment with tipifarnib started 5 to 9 days before initiating radiotherapy, twice daily, in 4-week cycles using discontinuous dosing (21 out of 28 days), until toxicity or progression."( A phase I trial of tipifarnib with radiation therapy, with and without temozolomide, for patients with newly diagnosed glioblastoma.
Abrey, L; Chang, SM; Cloughesy, TF; DeAngelis, LM; Demopoulos, A; Drappatz, J; Fine, HA; Fink, K; Kesari, S; Lamborn, KR; Lassman, AB; Lieberman, FS; Malkin, MG; Mehta, MP; Nghiemphu, PL; Prados, MD; Robins, HI; Torres-Trejo, A; Wen, PY, 2011)		0.6
" All patients received TMZ at a dosage of 90 mg/m(2)/day for 42 days to a dose of 59."( Temozolomide in the treatment of children with newly diagnosed diffuse intrinsic pontine gliomas: a report from the Children's Oncology Group.
Bouffet, E; Cohen, KJ; Heideman, RL; Holmes, EJ; Lavey, RS; Pollack, IF; Zhou, T, 2011)		1.81
" We identified melanoma cell lines with different sensitivities to single versus prolonged clinical dosing regimens of temozolomide treatment and assessed a variety of potential resistance mechanisms using this model."( Temozolomide chemoresistance heterogeneity in melanoma with different treatment regimens: DNA damage accumulation contribution.
Boeckmann, L; Emmert, S; Kuschal, C; Nickel, AC; Schaefer, A; Schön, MP; Thomale, J; Thoms, KM, 2011)		2.02
" Cediranib was dosed at 3 mg/kg daily five times a week orally for 2 weeks."( Cediranib enhances control of wild type EGFR and EGFRvIII-expressing gliomas through potentiating temozolomide, but not through radiosensitization: implications for the clinic.
Andersen, B; Dicker, AP; Lawrence, RY; Liu, Y; Wachsberger, PR; Xia, X, 2011)		0.59
" In our case, TMZ administration, despite changing the TMZ dosing regimen to prompt a drug response, was incapable of depleting MGMT stores."( Aggressive silent corticotroph adenoma progressing to pituitary carcinoma: the role of temozolomide therapy.
Cusimano, M; Fadul, CE; Gonzalez, R; Horvath, E; Kovacs, K; Moshkin, O; Ortiz, LD; Rotondo, F; Scheithauer, BW; Syro, LV; Uribe, H, )		0.35
"We conducted a phase I clinical trial of the combination of SCH 66336 with temozolomide administered on the standard 5-day dosing schedule."( A phase I trial of the farnesyl transferase inhibitor, SCH 66336, with temozolomide for patients with malignant glioma.
Coan, AD; Desjardins, A; Friedman, AH; Friedman, HS; Herndon, JE; Peters, KB; Reardon, DA; Threatt, S; Vredenburgh, JJ, 2011)		0.83
" Additional trials are needed to better define the optimal dosing in such patients."( A phase I study of bortezomib and temozolomide in patients with advanced solid tumors.
Chow, W; Chung, V; Cristea, M; Frankel, P; Koehler, S; Leong, L; Lim, D; Martel, C; Morgan, R; Portnow, J; Reckamp, K; Shibata, S; Synold, TW; Twardowski, P, 2012)		0.66
" The growing body of evidence demonstrating the clinical importance of O6-methylguanine methyltransferase (MGMT) has generated a considerable interest in the exploration of strategies to overcome MGMT-mediated resistance to alkylating agents; for example protracted administration of Temozolomide (TMZ) may result in more extensive and sustained depletion of MGMT; for this reason a variety of dosing schedules that increase the duration of exposure and the cumulative dose of TMZ are being investigated for the treatment of patient with recurrent malignant glioma after standard treatment."( Rechallenge with temozolomide in recurrent glioma.
Botturi, A; Fariselli, L; Ferrari, D; Gaviani, P; Lamperti, E; Salmaggi, A; Silvani, A; Simonetti, G, 2011)		0.89
" These may include TMZ concentrations in the brain parenchyma, TMZ dosing schemes, hypoxic microenvironments, niche factors, and the re-acquisition of stem cell properties by non-stem cells."( Chemoresistance of glioblastoma cancer stem cells--much more complex than expected.
Beier, CP; Beier, D; Schulz, JB, 2011)		0.37
" Temozolomide, dosed according to MGMT methylation status, demonstrated modest clinical activity in elderly patients with AML, especially in those presenting with fewer comorbidities and low disease burden."( Tailored temozolomide therapy according to MGMT methylation status for elderly patients with acute myeloid leukemia.
Arber, DA; Coutre, SE; Gotlib, J; Kohrt, HE; Medeiros, BC; Zehnder, JL; Zhang, B, 2012)		1.71
"Seventy-one eligible patients 70 years of age or older with newly diagnosed GBM and a Karnofsky performance status ≥60 were treated with a short course of RT (40 Gy in 15 fractions over 3 weeks) plus TMZ at the dosage of 75 mg/m(2) per day followed by 12 cycles of adjuvant TMZ (150-200 mg/m(2) for 5 days during each 28-day cycle)."( Phase II study of short-course radiotherapy plus concomitant and adjuvant temozolomide in elderly patients with glioblastoma.
Arcella, A; Caporello, P; De Sanctis, V; Enrici, RM; Giangaspero, F; Lanzetta, G; Minniti, G; Salvati, M; Scaringi, C, 2012)		0.61
"A dosage of 10 mg everolimus daily with TMZ 150 mg/m(2)/day for five consecutive days every 28 days in patients is the recommended dose for this regimen."( A phase I study of temozolomide and everolimus (RAD001) in patients with newly diagnosed and progressive glioblastoma either receiving or not receiving enzyme-inducing anticonvulsants: an NCIC CTG study.
Easaw, J; Eisenhauer, E; Kavan, P; Lwin, Z; Macdonald, D; Macneil, M; Mason, WP; McIntosh, L; Thiessen, B; Urva, S, 2012)		0.71
" Scheduling of docetaxel before selumetinib was more beneficial than when selumetinib was dosed before docetaxel and demonstrated a pro-apoptotic phenotype."( The MEK1/2 inhibitor, selumetinib (AZD6244; ARRY-142886), enhances anti-tumour efficacy when combined with conventional chemotherapeutic agents in human tumour xenograft models.
Alferez, D; Davies, BR; Heaton, SP; Heier, A; Holt, SV; Logié, A; Odedra, R; Smith, PD; Wilkinson, RW, 2012)		0.38
" It could therefore be used as an important platform for better prediction of drug dosing and schedule towards personalized medicine."( Towards personalized medicine with a three-dimensional micro-scale perfusion-based two-chamber tissue model system.
Barker, J; Foltz, G; Honkakoski, P; Küblbeck, J; Li, W; Lin, B; Ma, L; Zhang, J; Zhou, C, 2012)		0.38
" Moreover, this class of compounds possesses a generally favorable in vitro ADME profile, along with good exposure levels in plasma and brain following intraperitoneal dosing (30 mg/kg body weight) in mice."( Synthesis, biological evaluation, and structure-activity relationships of a novel class of apurinic/apyrimidinic endonuclease 1 inhibitors.
Dorjsuren, D; Jadhav, A; Maloney, DJ; Rai, G; Simeonov, A; Vyjayanti, VN; Wilson, DM, 2012)		0.38
" These results suggest that GBMs with EGFR amplification are a heterogenous group of tumors and that behavior might differ according to the degree of amplification, although not in a straightforward dose-response manner."( Paradoxical relationship between the degree of EGFR amplification and outcome in glioblastomas.
Bortoluzzi, S; Cieply, K; Fardo, DW; Hamilton, RL; Hobbs, J; Horbinski, C; Nikiforova, MN, 2012)		0.38
"The effectiveness of temozolomide (TMZ) dosing schemes and the "rechallenge" of recurrent glioblastoma (GBM) with TMZ are controversial."( Efficacy of clinically relevant temozolomide dosing schemes in glioblastoma cancer stem cell lines.
Beier, CP; Beier, D; Brawanski, K; Hau, P; Schriefer, B; Schulz, JB; Weis, J, 2012)		0.98
" These data reassuringly suggest that BEV does not significantly change the ECF tumor concentrations of TMZ in either tumor-bearing or normal brain when dosed 36 h prior to TMZ."( The impact of bevacizumab on temozolomide concentrations in intracranial U87 gliomas.
Blakeley, JO; Brastianos, H; Brem, H; Grossman, R; Rudek, MA; Tyler, B; Zadnik, P, 2012)		0.67
" Dose-response and cellular growth assays indicate that erlotinib reduces cell proliferation in all tested cell lines without inducing cytotoxic effects."( EGFR inhibition in glioma cells modulates Rho signaling to inhibit cell motility and invasion and cooperates with temozolomide to reduce cell growth.
Fernández de Mattos, S; Ramis, G; Rodríguez, J; Thomàs-Moyà, E; Villalonga, P, 2012)		0.59
" No DLTs were encountered, but vorinostat dosing could not be escalated further due to thrombocytopenia."( Phase I study of vorinostat in combination with temozolomide in patients with high-grade gliomas: North American Brain Tumor Consortium Study 04-03.
Ames, MM; Chang, SM; Cloughesy, TF; Desideri, S; Drappatz, J; Espinoza-Delgado, I; Gilbert, MR; Kuhn, JG; Lamborn, KR; Lassman, AB; Lee, EQ; Lieberman, FS; McGovern, RM; Prados, MD; Puduvalli, VK; Reid, JM; Robins, HI; Wen, PY; Xu, J; Ye, X; Yung, WK, 2012)		0.63
" 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)		0.6
" It was designed to maximize cytoreduction via high dosing of synergistically interacting agents, while minimizing morbidity in patients with resistant neuroblastoma (NB) and ineligible for clinical trials due to myelosuppression from previous therapy."( 5-day/5-drug myeloablative outpatient regimen for resistant neuroblastoma.
Basu, EM; Cheung, NK; Kramer, K; Kushner, BH; Modak, S; Roberts, SS, 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)		0.93
" In a human GBM xenograft model, a single daily dosage of MB does not activate AMP-activated protein kinase signaling, and no tumor regression was observed."( Reversing the Warburg effect as a treatment for glioblastoma.
Bigner, DD; Choudhury, GR; Ghorpade, A; Keir, ST; Li, W; Liu, R; Poteet, E; Ryou, MG; Simpkins, JW; Tang, L; Wen, Y; Winters, A; Yan, H; Yang, SH; Yuan, F, 2013)		0.39
" Sufficient information on steroid dosing was available in 72 patients included in the final analysis."( Steroid management in newly diagnosed glioblastoma.
Deangelis, LM; Deutsch, MB; Lassman, AB; Panageas, KS, 2013)		0.39
"Temozolomide (TMZ) is important chemotherapy for glioblastoma multiforme (GBM), but the optimal dosing schedule is unclear."( Efficacy of protracted temozolomide dosing is limited in MGMT unmethylated GBM xenograft models.
Anderson, SK; Ballman, KV; Carlson, BL; Cen, L; Decker, PA; Giannini, C; Grogan, PT; Kitange, GJ; Mladek, AC; Pokorny, JL; Sarkaria, JN; Schroeder, MA; Wu, W, 2013)		2.14
"The efficacies of different clinically relevant dosing regimens were compared in a panel of 7 primary GBM xenografts in an intracranial therapy evaluation model."( Efficacy of protracted temozolomide dosing is limited in MGMT unmethylated GBM xenograft models.
Anderson, SK; Ballman, KV; Carlson, BL; Cen, L; Decker, PA; Giannini, C; Grogan, PT; Kitange, GJ; Mladek, AC; Pokorny, JL; Sarkaria, JN; Schroeder, MA; Wu, W, 2013)		0.7
" There was no clear relationship between vorinostat dosage and drug exposure over the dose range studied."( A pediatric phase 1 trial of vorinostat and temozolomide in relapsed or refractory primary brain or spinal cord tumors: a Children's Oncology Group phase 1 consortium study.
Ahern, C; Ames, MM; Blaney, SM; Fouladi, M; Gilbertson, RJ; Horton, T; Hummel, TR; Ingle, AM; McGovern, RM; Reid, JM; Wagner, L; Weigel, B, 2013)		0.65
" Comparisons included no chemotherapy, non-temozolomide chemotherapy or different dosing schedules of temozolomide."( Temozolomide for high grade glioma.
Garside, R; Grant, R; Hart, MG; Rogers, G; Stein, K, 2013)		2.1
" We report five patients who received long-term treatment with TMZ chemotherapy at normal dosing levels."( Long-term treatment with temozolomide in malignant glioma.
Defrates, SR; Lightner, DD; Mannas, JP; Pittman, T; Villano, JL, 2014)		0.71
"Mutagenic and clastogenic effects of some DNA damaging agents such as methyl methanesulfonate (MMS) and ethyl methanesulfonate (EMS) have been demonstrated to exhibit a nonlinear or even "thresholded" dose-response in vitro and in vivo."( Quantitative assessment of the dose-response of alkylating agents in DNA repair proficient and deficient ames tester strains.
Guérard, M; Tang, L; Zeller, A, 2014)		0.4
" Overall, we have verified that TMZ in addition to being an alkylating and cytotoxic chemotherapy, also possess immune modulatory effect in MM patients treated with standard dosage of TMZ."( Immune modulations during chemoimmunotherapy & novel vaccine strategies--in metastatic melanoma and non small-cell lung cancer.
Iversen, TZ, 2013)		0.39
" Patients aged over 70 years with favorable KPS, or patients aged 60-70 years with borderline KPS, should be considered for monotherapy utilizing standard TMZ dosing for patients with MGMT-methylated tumors, and hypofractionated RT (34 Gy in ten fractions or 40 Gy in 15 fractions) for patients with MGMT-unmethylated tumors."( Treatment options and outcomes for glioblastoma in the elderly patient.
Arvold, ND; Reardon, DA, 2014)		0.4
"Temozolomide, when dosed at 50, 25, 10, or 5 mg/kg, 5 days per week, beginning 3 days after inoculation, completely prevented the formation of experimental brain metastases from MGMT-negative 231-BR-EGFP cells."( Profound prevention of experimental brain metastases of breast cancer by temozolomide in an MGMT-dependent manner.
Biernat, W; Duchnowska, R; Gril, B; Hewitt, SM; Hua, E; Jassem, J; Liewehr, DJ; Palmieri, D; Qian, Y; Sosińska-Mielcarek, K; Stark, AM; Steeg, PS; Steinberg, SM; Woditschka, S, 2014)		2.08
" The ECM algorithm for incomplete data is applied to estimating the dose-response relationship in the proposed model."( Modeling sustained treatment effects in tumor xenograft experiments.
Deng, D; Fang, HB; Tan, M; Zhang, T, 2014)		0.4
" In vivo drug efficacy, pharmacokinetics, and pharmacodynamics were analyzed using clinically relevant dosing regimens."( Discordant in vitro and in vivo chemopotentiating effects of the PARP inhibitor veliparib in temozolomide-sensitive versus -resistant glioblastoma multiforme xenografts.
Bakken, KK; Boakye-Agyeman, F; Carlson, BL; Gupta, SK; Kizilbash, SH; Mladek, AC; Reid, J; Sarkaria, JN; Schroeder, MA, 2014)		0.62
"In vitro cytotoxicity assays do not adequately model the therapeutic index of PARP inhibitors, as concentrations of veliparib and TMZ required to sensitize TMZ-resistant cancer cells in vivo cannot be achieved using a tolerable dosing regimen."( Discordant in vitro and in vivo chemopotentiating effects of the PARP inhibitor veliparib in temozolomide-sensitive versus -resistant glioblastoma multiforme xenografts.
Bakken, KK; Boakye-Agyeman, F; Carlson, BL; Gupta, SK; Kizilbash, SH; Mladek, AC; Reid, J; Sarkaria, JN; Schroeder, MA, 2014)		0.62
"The EORTC-NCIC regimen for glioblastoma requires different dosing of temozolomide (TMZ) during radiation and maintenance therapy."( Analyzing temozolomide medication errors: potentially fatal.
Bressler, LR; Gabay, MP; Letarte, N; Long, KE; Stachnik, JM; Villano, JL, 2014)		1.04
" In phase II, participants were randomized (stratified by age and KPS) to receive A, T or AT; A was dosed at 40 mg/day and T at 75 mg/m(2) for 21 of 28 days."( Phase I/randomized phase II study of afatinib, an irreversible ErbB family blocker, with or without protracted temozolomide in adults with recurrent glioblastoma.
Cong, J; Cseh, A; Eisenstat, DD; Fu, Y; Kavan, P; Mason, WP; Mathieu, D; Nabors, LB; Perry, JR; Phuphanich, S; Reardon, DA; Shapiro, W; Wind, S, 2015)		0.63
" We therefore evaluated a 5-day dosing schedule of temozolomide and examined MGMT as a predictive biomarker for temozolomide treatment in SCLC."( Trial of a 5-day dosing regimen of temozolomide in patients with relapsed small cell lung cancers with assessment of methylguanine-DNA methyltransferase.
Bergagnini, I; Drilon, A; Ginsberg, MS; Heguy, A; Holodny, AI; Huberman, K; Kadota, K; Kris, MG; Krug, LM; Pietanza, MC; Riely, GJ; Sima, CS; Sumner, DK; Travis, WD; Zauderer, MG, 2014)		0.93
" Because tasisulam is highly albumin-bound, patients in the tumor-specific confirmation arms were dosed targeting specific albumin-corrected exposure ranges (AUCalb) identified during dose-escalation (3,500 h*μg/mL [75th percentile] for docetaxel, temozolomide, and cisplatin; 4,000 h*μg/mL for gemcitabine and erlotinib)."( An innovative, multi-arm, complete phase 1b study of the novel anti-cancer agent tasisulam in patients with advanced solid tumors.
Becerra, CR; Braiteh, F; Chen, J; Chow, KH; Conkling, PR; Garbo, L; Ilaria, R; Jotte, RM; Richards, DA; Robert-Vizcarrondo, F; Smith, DA; Stephenson, J; Tai, DF; Turner, PK; Von Hoff, DD, 2015)		0.6
" Dose-response analysis of cultured GBM cells revealed that DP68 is more potent than DP86 and TMZ and that DP68 was effective even in cell lines resistant to TMZ."( Evaluation of novel imidazotetrazine analogues designed to overcome temozolomide resistance and glioblastoma regrowth.
Gynther, M; Mladek, AC; Phillips, RM; Ramirez, YP; Rautio, J; Ross, AH; Sakaria, JN; Wheelhouse, RT, 2015)		0.65
" All patients received conformal WBRT (3 Gy × 10-30 Gy), with or without concomitant TMZ administered at a dosage of 75 mg/m(2)/day during the irradiation period."( Phase II randomized study of whole-brain radiation therapy with or without concurrent temozolomide for brain metastases from breast cancer.
Bourgier, C; Cao, KI; Gerber, S; Gobillion, A; Kirova, YM; Le Scodan, R; Lebas, N; Levy, C; Pierga, JY; Savignoni, A, 2015)		0.64
" All patients received the first cycle of TMZ at a dosage of 150 mg/m(2) starting on the second or third postsurgical day."( Long-term therapy with temozolomide is a feasible option for newly diagnosed glioblastoma: a single-institution experience with as many as 101 temozolomide cycles.
Albanese, V; Barbagallo, GM; Caltabiano, R; Certo, F; Lanzafame, S; Longo, A; Motta, F; Palmucci, S; Paratore, S; Parra, HS; Privitera, G; Scaglione, G, 2014)		0.71
"01), and higher posttreatment dosing of corticosteroid (P=."( Standard (60 Gy) or short-course (40 Gy) irradiation plus concomitant and adjuvant temozolomide for elderly patients with glioblastoma: a propensity-matched analysis.
Arcella, A; Bozzao, A; Enrici, RM; Esposito, V; Giangaspero, F; Lanzetta, G; Minniti, G; Pace, A; Scaringi, C; Terrenato, I, 2015)		0.64
" Since TMZ is the most active cytotoxic agent against GBM, and the standard dosing of TMZ has shown favorable safety profile in clinical trials, re-challenge with TMZ in increased dose density schedules for recurrent tumors that have evaded from prior standard TMZ therapy appears to be a rational approach and has been intensively exploited."( Dose-dense temozolomide: is it still promising?
Nagane, M, 2015)		0.81
" Even though dosing and timing might have been the reasons for this failure, it might also be that TREO does not reach the brain in sufficient amount."( Transport of treosulfan and temozolomide across an in-vitro blood-brain barrier model.
Hupert, M; Linz, U; Santiago-Schübel, B; Stab, J; Wagner, S; Wien, S, 2015)		0.71
"8- and 21-fold, respectively, when similarly dosed in P-gp-deficient mice."( Brain Exposure of Two Selective Dual CDK4 and CDK6 Inhibitors and the Antitumor Activity of CDK4 and CDK6 Inhibition in Combination with Temozolomide in an Intracranial Glioblastoma Xenograft.
Ajamie, RT; De Dios, A; Gelbert, LM; Kulanthaivel, P; Raub, TJ; Sanchez-Martinez, C; Sawada, GA; Shannon, HE; Staton, BA; Wishart, GN, 2015)		0.62
" We investigated the maximum tolerated dose (MTD) of iniparib with monthly (m) and continuous (c) temozolomide (TMZ) dosing schedules in patients with malignant gliomas (MG)."( Phase I study of iniparib concurrent with monthly or continuous temozolomide dosing schedules in patients with newly diagnosed malignant gliomas.
Blakeley, JO; Chi, AS; Desideri, S; Emmons, G; Garcia Ribas, I; Grossman, SA; Mikkelsen, T; Nabors, LB; Peereboom, D; Rosenfeld, MR; Supko, JG; Ye, X, 2015)		0.87
" We used these screening methods to evaluate the dependencies of seven patient-derived cell models: three grown on laminin and four grown as neurospheres, against 56 agents in 17-point dose-response curves in 384-well format in triplicate."( High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
deCarvalho, AC; Mikkelsen, T; Quartararo, CE; Reznik, E; Stockwell, BR, 2015)		0.42
"Midazolam causes a hormetic dose-response relationship in human neuroblastoma cells."( Pretreatment but not subsequent coincubation with midazolam reduces the cytotoxicity of temozolomide in neuroblastoma cells.
Bauer, I; Braun, S; Pannen, B; Werdehausen, R, 2015)		0.64
" We confirmed in these studies that after completion of the Q7D×3 dosing of IrC™, but not IRN, the tumor-associated vascular was normalized as compared to untreated tumors."( Determination of an optimal dosing schedule for combining Irinophore C™ and temozolomide in an orthotopic model of glioblastoma.
Anantha, M; Backstrom, I; Bally, MB; Chu, F; Kalra, J; Masin, D; Strutt, D; Verreault, M; Walker, D; Waterhouse, D; Wehbe, M; Yapp, DT, 2015)		0.65
" In comparing DNA damage signaling after dosing with veliparib/TMZ or TMZ alone, increased phosphorylation of damage-responsive proteins (KAP1, Chk1, Chk2, and H2AX) was observed only in MGMT promoter-hypermethylated lines."( Delineation of MGMT Hypermethylation as a Biomarker for Veliparib-Mediated Temozolomide-Sensitizing Therapy of Glioblastoma.
Bakken, KK; Ballman, KV; Boakye-Agyeman, F; Carlson, BL; Cen, L; Decker, PA; Eckel-Passow, JE; Gupta, SK; Jenkins, RB; Kitange, GJ; Kizilbash, SH; Mladek, AC; Pokorny, JL; Reid, JM; Sarkar, G; Sarkaria, JN; Schroeder, MA; Sulman, EP; Verhaak, RG, 2016)		0.66
" This study provides strong scientific rationale for the development of an optimized dosing regimen for a PARP inhibitor with TMZ/IR for upfront treatment of GBM."( Evaluation of Concurrent Radiation, Temozolomide and ABT-888 Treatment Followed by Maintenance Therapy with Temozolomide and ABT-888 in a Genetically Engineered Glioblastoma Mouse Model.
Chenevert, TL; Galbán, CJ; Galbán, S; Heist, KA; Holland, EC; Lemasson, B; Li, Y; Rehemtulla, A; Ross, BD; Tsein, C; Wang, H; Zhu, Y, 2016)		0.71
" Treatment of TMZ along with a sublethal dosage range of SU1498, a chemical inhibitor of the VEGF receptor signaling, induced significant cell death in both TMZ-sensitive and TMZ-resistant GBM cells without changing the status of the MGMT promoter methylation."( Combined inhibition of vascular endothelial growth factor receptor signaling with temozolomide enhances cytotoxicity against human glioblastoma cells via downregulation of Neuropilin-1.
Choi, C; Choi, K; Kim, E; Lee, J; Ryu, SW, 2016)		0.66
" So far, inhibition of angiogenesis by compounds such as bevacizumab, cediranib, enzastaurin or cilengitide as well as alternative dosing schedules of temozolomide did not prolong survival, neither at primary diagnosis nor at recurrent disease."( Pharmacotherapies for the treatment of glioblastoma - current evidence and perspectives.
Gramatzki, D; Roth, P; Seystahl, K; Weller, M, 2016)		0.63
" According with the poor Performance Status (PS = 2) and to reduce the toxicity of the treatment was chosen an intermittent dosing regimen of metronomic temozolomide (75 mg/m(2)/day-one-week-on/on-week-off)."( Metronomic temozolomide as second line treatment for metastatic poorly differentiated pancreatic neuroendocrine carcinoma.
Arcella, A; Ascierto, PA; Cicala, D; De Divitiis, C; Grimaldi, AM; Iaffaioli, RV; Romano, GM; Simeone, E; Tafuto, S; Tatangelo, F; von Arx, C, 2016)		1.02
" In vivo, we implanted the cells orthotopically in nude mice and administered CBL0137 in various dosing regimens to assess brain and tumor accumulation of CBL0137, its effect on tumor cell proliferation and apoptosis, and on survival of mice with and without temozolomide (TMZ)."( Anticancer drug candidate CBL0137, which inhibits histone chaperone FACT, is efficacious in preclinical orthotopic models of temozolomide-responsive and -resistant glioblastoma.
Barone, TA; Burkhart, CA; Gudkov, AV; Gurova, KV; Haderski, G; Plunkett, RJ; Purmal, AA; Safina, A, 2017)		0.84
" As a comparison group 33 patients with bevacizumab for at least 6 months continuously dosed at 10 mg/kg every 2 weeks were selected."( Impact of tapering and discontinuation of bevacizumab in patients with progressive glioblastoma.
Hertenstein, A; Hielscher, T; Menn, O; Platten, M; Wick, A; Wick, W; Wiestler, B; Winkler, F, 2016)		0.43
" Dose-response curves were constructed using cell proliferation and sphere-forming assays."( The effects of tumor treating fields and temozolomide in MGMT expressing and non-expressing patient-derived glioblastoma cells.
Clark, PA; Deming, DA; Gaal, JT; Kuo, JS; Pasch, CA; Robins, HI; Strebe, JK, 2017)		0.72
" Metronomic dosing of cytotoxic chemotherapy has emerged as a promising option to achieve this objective."( Phase I study of low-dose metronomic temozolomide for recurrent malignant gliomas.
Alsop, DC; Callahan, A; Giarusso, B; O'Loughlin, L; Timmons, J; Wong, ET, 2016)		0.71
" As a part of the study, two DNA alkylating agents, methylnitrosourea (MNU) and temozolomide (TMZ), were dosed by single oral gavage at 25, 50, and 100mg/kg body weight."( Evaluation of the mutagenicity of alkylating agents, methylnitrosourea and temozolomide, using the rat Pig-a assay with total red blood cells or reticulocytes.
Ando, M; Inoue, Y; Iwase, Y; Kato, T; Muto, S; Uno, Y; Yamada, K, 2016)		0.89
"6 μg/day) with negligible leakage into the peripheral blood (<100 ng) rendering ~1000 fold differential drug dosage in tumor versus peripheral blood."( Theranostic 3-Dimensional nano brain-implant for prolonged and localized treatment of recurrent glioma.
Ashokan, A; Gowd, GS; Junnuthula, VR; Koyakutty, M; Nair, SV; Panikar, D; Peethambaran, R; Ramachandran, R; Thomas, A; Thomas, J; Unni, AK, 2017)		0.46
"Temozolomide (TMZ) for malignant gliomas is traditionally dosed in 5 out of a 28-day cycle, however alternative regimens exist, including dose-dense."( Long-term daily temozolomide with dose-dependent efficacy in MGMT promotor methylation negative recurrent high-grade astrocytoma.
Howard, TA; Villano, JL; Zhou, Z, 2017)		2.24
" At recurrence, alternate dosing of temozolomide has shown to further deplete methyl-guanine-methyltransferase (MGMT) conferring added activity for patients who have progressed on the standard dosing regimen."( Phase II study of bi-weekly temozolomide plus bevacizumab for adult patients with recurrent glioblastoma.
Ahmadi, MM; Badruddoja, MA; Kuzma, K; Mahadevan, D; Norton, T; Pazzi, M; Sanan, A; Schroeder, K; Scully, T, 2017)		1.02
" Modern techniques, such as intensity-modulated radiation therapy (IMRT) and proton therapy allow for modifications in radiation dosing and delivery while improving conformality and limiting irradiation of normal tissue."( Fractionated Radiotherapy of Intracranial Gliomas.
Ghia, AJ, 2018)		0.48
" Temozolomide has several effects on the immune system that are dependent on mode of delivery and the dosing strategy, which may have unpredicted effects on immunotherapy."( Temozolomide for immunomodulation in the treatment of glioblastoma.
Dastmalchi, F; Karachi, A; Mitchell, DA; Rahman, M, 2018)		2.83
" Dosing optimization (frequency and sequence) is needed prior to additional efficacy studies."( Phase II Study of Iniparib with Concurrent Chemoradiation in Patients with Newly Diagnosed Glioblastoma.
Ahluwalia, MS; Blakeley, JO; Chi, AS; Desideri, S; Eichler, A; Grossman, SA; Mikkelsen, T; Nabors, LB; Ribas, IG; Rosenfeld, MR; Ye, X, 2019)		0.51
" Our results demonstrate benefit of ddTMZ after previous treatment with standard TMZ dosing with no apparent increase in treatment-related toxicities."( Dose-dense temozolomide for recurrent high-grade gliomas: a single-center retrospective study.
Garcia, CR; Gruber, L; Kumar, SS; Lightner, DD; Morgan, RM; Slone, SA; Villano, JL, 2018)		0.87
" To facilitate optimal dosing for such studies, we evaluated the plasma and brain pharmacokinetics (PK) of letrozole in NOD-scid gamma (NSG) mice, which are frequently employed for assessing efficacy against patient-derived tumor cells."( Plasma and brain pharmacokinetics of letrozole and drug interaction studies with temozolomide in NOD-scid gamma mice and sprague dawley rats.
Adams, CH; Arora, P; DasGupta, B; Desai, PB; Gudelsky, G, 2019)		0.74
"These results will guide the optimization of dosing regimen for further development of letrozole for HGG treatment."( Plasma and brain pharmacokinetics of letrozole and drug interaction studies with temozolomide in NOD-scid gamma mice and sprague dawley rats.
Adams, CH; Arora, P; DasGupta, B; Desai, PB; Gudelsky, G, 2019)		0.74
" Further clinical investigations aimed at elucidating the veliparib exposure-efficacy/safety relationship and optimizing dosing recommendations for maximizing benefit-risk in patients with advanced myeloid malignancies should study veliparib doses ranging up to 120 mg in combination with temozolomide."( Population pharmacokinetics and exposure-response assessment of veliparib co-administered with temozolomide in patients with myeloid leukemias.
Beumer, JH; Chen, A; Gobburu, J; Gojo, I; Gopalakrishnan, M; Greer, JM; Karp, JE; Kiesel, BF; Mehrotra, S; Piekarz, R; Rudek, MA; Singh, R, 2019)		0.91
" Overall, RO6839921 had a favourable pharmacokinetic profile consistent with intermittent dosing and was well tolerated alone and in combination."( Preclinical evaluation of the first intravenous small molecule MDM2 antagonist alone and in combination with temozolomide in neuroblastoma.
Berry, P; Bonner, J; Chen, L; Daga, A; Kirk, C; Lunec, J; Newell, DR; Pastorino, F; Ponzoni, M; Thomas, HD; Tweddle, DA; Veal, GJ; Wood, KM; Zhao, Y, 2019)		0.73
" Combinatorial therapy of diosgenin and TMZ significantly reduced the dosage regimen of TMZ and also showed affectivity in hitherto TMZ resistant GBM cells."( Targeting NFE2L2, a transcription factor upstream of MMP-2: A potential therapeutic strategy for temozolomide resistant glioblastoma.
Banerjee, I; Banik, P; Bharti, R; Biswas, A; Das, S; Ghosh, SK; Kumar, U; Mandal, M; Nayak, S; Rajesh, Y, 2019)		0.73
"Using patient-derived glioblastoma stem cell (GSC) cultures from 15 GBM patients, we described stem cell properties of individual cultures, determined the dose-response relationships of the drugs in the CUSP9, and assessed the efficacy the CUSP9 combination with TMZ in concentrations clinically achievable."( The efficacy of a coordinated pharmacological blockade in glioblastoma stem cells with nine repurposed drugs using the CUSP9 strategy.
Grieg, Z; Langmoen, IA; Sandberg, CJ; Skaga, E; Skaga, IØ; Vik-Mo, EO, 2019)		0.51
" These results form part of the basis for the translation of the therapy to patients with GBM but the dosing and timing of delivery will have to be explored in depth both experimentally and clinically."( Convection-enhanced delivery of temozolomide and whole cell tumor immunizations in GL261 and KR158 experimental mouse gliomas.
Darabi, A; Enríquez Pérez, J; Kopecky, J; Siesjö, P; Visse, E, 2020)		0.84
" Side effects associated with chemotherapy delays or modifications included thrombocytopenia (28%) and nausea/vomiting (19%), with temozolomide dosing most frequently modified."( Children with DIPG and high-grade glioma treated with temozolomide, irinotecan, and bevacizumab: the Seattle Children's Hospital experience.
Browd, SR; Cole, BL; Crotty, EE; Ellenbogen, RG; Ermoian, RP; Geyer, JR; Hauptman, JS; Leary, SES; Lee, A; Lockwood, CM; Millard, NE; Ojemann, JG; Olson, JM; Paulson, VA; Sato, AA; Vitanza, NA, 2020)		1.01
"The interaction of temozolomide (TMZ) (the main chemotherapeutic agent for brain tumors) with blood components has not been studied at the molecular level to date, even though such information is essential in the design of dosage forms for optimal therapy."( The Interaction of Temozolomide with Blood Components Suggests the Potential Use of Human Serum Albumin as a Biomimetic Carrier for the Drug.
Encinar, JA; Esquembre, R; Martínez-Tomé, MJ; Mateo, CR; Rubio-Camacho, M, 2020)		1.22
" We have successfully employed temozolomide desensitization followed by metronomic dosing of temozolomide."( Temozolomide desensitization followed by metronomic dosing in patients with hypersensitivity.
Divekar, RD; Johnson, DR; Maddox, DE; Neth, BJ; Ruff, MW; Uhm, JH, 2020)		2.29
"We performed an observational study of 15 patients at Mayo Clinic (Rochester) with a diagnosis of glioma who underwent temozolomide desensitization with subsequent metronomic dosing from May 2012 to January 2017."( Temozolomide desensitization followed by metronomic dosing in patients with hypersensitivity.
Divekar, RD; Johnson, DR; Maddox, DE; Neth, BJ; Ruff, MW; Uhm, JH, 2020)		2.21
"8% of actual body weight calculated body surface area dosing was determined for concurrent phase temozolomide."( Actual body weight dosing of temozolomide and overall survival in patients with glioblastoma.
Chambers, C; Coppens, R; de Robles, P; Dersch-Mills, D; Folkman, F; Ghosh, S; Hsu, PYH; Leckie, C, 2021)		1.13
"Temozolomide doses at full actual body weight calculated body surface area dosing during the concurrent phase is required to achieve a similar median OS as seen in the pivotal trial by Stupp et al."( Actual body weight dosing of temozolomide and overall survival in patients with glioblastoma.
Chambers, C; Coppens, R; de Robles, P; Dersch-Mills, D; Folkman, F; Ghosh, S; Hsu, PYH; Leckie, C, 2021)		2.36
" However, clinical trials show that treatment schedule and drug dosage significantly affect patient survival."( A neuro evolutionary algorithm for patient calibrated prediction of survival in Glioblastoma patients.
Ebrahimi Zade, A; Shahabi Haghighi, S; Soltani, M, 2021)		0.62
"To investigate the toxicity profile and establish an optimal dosing schedule of zotiraciclib with temozolomide in patients with recurrent high-grade astrocytoma."( Phase I Study of Zotiraciclib in Combination with Temozolomide for Patients with Recurrent High-grade Astrocytomas.
Aboud, O; Ahmad, S; Antony, R; Armstrong, TS; Boris, L; Bryla, C; Burton, EM; Butler, MK; Calvo, KR; Cordova, C; Figg, WD; Fink, D; Gallin, JI; Garren, N; Gilbert, MR; Gonzales, J; Grajkowska, E; Kuhns, DB; Leeper, H; Lindsley, M; Lollo, N; Long Priel, DA; Mendoza, TR; Mentges, K; Pang, Y; Peer, CJ; Penas-Prado, M; Siegel, C; Sissung, TM; Su, YT; Theeler, BJ; Vera, E; Wu, J; Yu, G; Yuan, Y, 2021)		1.09
" Once validated, polymorphisms predicting drug metabolism may allow personalized dosing of zotiraciclib."( Phase I Study of Zotiraciclib in Combination with Temozolomide for Patients with Recurrent High-grade Astrocytomas.
Aboud, O; Ahmad, S; Antony, R; Armstrong, TS; Boris, L; Bryla, C; Burton, EM; Butler, MK; Calvo, KR; Cordova, C; Figg, WD; Fink, D; Gallin, JI; Garren, N; Gilbert, MR; Gonzales, J; Grajkowska, E; Kuhns, DB; Leeper, H; Lindsley, M; Lollo, N; Long Priel, DA; Mendoza, TR; Mentges, K; Pang, Y; Peer, CJ; Penas-Prado, M; Siegel, C; Sissung, TM; Su, YT; Theeler, BJ; Vera, E; Wu, J; Yu, G; Yuan, Y, 2021)		0.87
" Prolonged lisavanbulin dosing from RT start until moribund was required for maximal benefit (GBM6: median survival lisavanbulin/RT 90 vs."( Preclinical modeling in glioblastoma patient-derived xenograft (GBM PDX) xenografts to guide clinical development of lisavanbulin-a novel tumor checkpoint controller targeting microtubules.
Bachmann, F; Bakken, KK; Burgenske, DM; Carlson, BL; Decker, PA; Eckel-Passow, JE; Elmquist, WF; Gampa, G; Giannini, C; He, L; Hu, Z; Kitange, GJ; Kosel, ML; Lane, HA; McSheehy, P; Mladek, AC; Pokorny, JL; Sarkaria, JN; Schmitt-Hoffmann, A; Schroeder, MA; Talele, S; Vaubel, RA, 2022)		0.72
" 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)		0.87
"GBM cells proliferation speed is inversely proportional to the irradiation dose and recedes when the dosage is increased, as expected."( Effectiveness of bortezomib and temozolomide for eradication of recurrent human glioblastoma cells, resistant to radiation.
Bryukhovetskiy, I; Pak, O; Sharma, A; Sharma, HS; Shevchenko, V; Zaitsev, S, 2021)		0.9
" Isoeffective dosing to 52."( Dose-escalated accelerated hypofractionation for elderly or frail patients with a newly diagnosed glioblastoma.
Ammirati, M; Arnett, A; Beyer, S; Blakaj, DM; Brown, PD; Chakravarti, A; Elder, JB; Giglio, P; Gondi, V; Goranovich, J; Grecula, J; Hardesty, D; Klamer, B; Lonser, R; Matsui, J; Ong, S; Palmer, JD; Perlow, HK; Pillainayagam, C; Raval, RR; Yaney, A; Yang, M, 2022)		0.72
"Isoeffective dosing to 52."( Dose-escalated accelerated hypofractionation for elderly or frail patients with a newly diagnosed glioblastoma.
Ammirati, M; Arnett, A; Beyer, S; Blakaj, DM; Brown, PD; Chakravarti, A; Elder, JB; Giglio, P; Gondi, V; Goranovich, J; Grecula, J; Hardesty, D; Klamer, B; Lonser, R; Matsui, J; Ong, S; Palmer, JD; Perlow, HK; Pillainayagam, C; Raval, RR; Yaney, A; Yang, M, 2022)		0.72
" There is insufficient data to make a recommendation about which alternative TMZ dosing provides the best benefits."( Congress of Neurological Surgeons systematic review and evidence-based guidelines update on the role of cytotoxic chemotherapy and other cytotoxic therapies in the management of progressive glioblastoma in adults.
Germano, IM; Olson, JJ; Ormond, DR; Wen, P; Ziu, M, 2022)		0.72
" Furthermore, the non-cytolytic and non-cytotoxic metronomic dosage of hydroxyurea and temozolomide had increased the DBM therapy outcome by strengthening anti-tumor capability."( A retrospective observational study on cases of anaplastic brain tumors treated with the Di Bella Method: A rationale and effectiveness.
Borghetto, V; Costanzo, E; Di Bella, G, 2021)		0.84
"8%), requiring a repeated dosing regimen that limits its efficacy and increases adverse events."( Temozolomide: An Overview of Biological Properties, Drug Delivery Nanosystems, and Analytical Methods.
Carvalho, SG; Chorilli, M; Di Filippo, LD; Dutra, JAP; Luiz, MT; Tavares Junior, AG, 2022)		2.16
" Additionally, by lowering the effective dosage of TMZ, the combination liposomes reduced systemic TMZ-induced toxicity, highlighting the preclinical potential of this novel integrative strategy to deliver combination therapies to brain tumors."( Targeted liposomes for combined delivery of artesunate and temozolomide to resistant glioblastoma.
Chai, T; Du, Q; Hanif, S; Ismail, M; Li, Y; Muhammad, P; Shi, B; Yang, W; Zhang, D; Zheng, M, 2022)		0.96
" In a drug screening assay, diffusion of temozolomide and carmustine to hydrogel-encapsulated U87 cells from the perfusion solution is measured, and dose-response curves are generated, demonstrating utility as an in vitro mimic of the glioblastoma microenvironment."( Hydrogel-based microfluidic device with multiplexed 3D in vitro cell culture.
Bruns, J; Chen, D; Clancy, A; Nadella, J; Stealey, S; Timperman, A; Zhang, Y; Zustiak, SP, 2022)		0.99
" We present a novel case of the challenges of dosing temozolomide in a patient with end stage renal disease on peritoneal hemodialysis with unpredictable clearance and toxicities."( Safe administration of temozolomide in end-stage renal disease patients.
Hundal, J; Pereira, MK; Singh, A; Vredenburg, J, 2023)		1.47
" A stepwise increase in the dosage of temozolomide did not increase the risk of toxicity with HD."( Safe administration of temozolomide in end-stage renal disease patients.
Hundal, J; Pereira, MK; Singh, A; Vredenburg, J, 2023)		1.49
[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.
alkylating agentHighly reactive chemical that introduces alkyl radicals into biologically active molecules and thereby prevents their proper functioning. It could be used as an antineoplastic agent, but it might be very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. It could also be used as a component of poison gases.
[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
imidazotetrazineAny organic heterobicyclic compound containing ortho-fused imidazole and tetrazine rings.
monocarboxylic acid amideA carboxamide derived from a monocarboxylic acid.
triazene derivativeA nitrogen molecular entity resulting from the formal substitution of one or more of the hydrogens of triazene.
[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]

Protein Targets (13)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
DNA polymerase kappa isoform 1Homo sapiens (human)Potency21.19230.031622.3146100.0000AID588579
muscleblind-like protein 1 isoform 1Homo sapiens (human)Potency28.18380.00419.962528.1838AID2675
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
polyadenylate-binding protein 1Homo sapiens (human)IC50 (µMol)54.72504.910023.702976.1900AID602259; AID602260
ATP-binding cassette sub-family C member 3Homo sapiens (human)IC50 (µMol)133.00000.63154.45319.3000AID1473740
Multidrug resistance-associated protein 4Homo sapiens (human)IC50 (µMol)133.00000.20005.677410.0000AID1473741
Carbonic anhydrase 12Homo sapiens (human)Ki50.00000.00021.10439.9000AID1425990
Bile salt export pumpHomo sapiens (human)IC50 (µMol)133.00000.11007.190310.0000AID1473738
Tyrosine-protein kinase ABL1Homo sapiens (human)IC50 (µMol)100.00000.00010.712810.0000AID228828
Carbonic anhydrase 1Homo sapiens (human)Ki50.00000.00001.372610.0000AID1425987
Carbonic anhydrase 2Homo sapiens (human)Ki50.00000.00000.72369.9200AID1425988
Tyrosine-protein kinase ABL2Homo sapiens (human)IC50 (µMol)100.00000.00050.14921.0000AID228828
Carbonic anhydrase 9Homo sapiens (human)Ki50.00000.00010.78749.9000AID1425989
Canalicular multispecific organic anion transporter 1Homo sapiens (human)IC50 (µMol)133.00002.41006.343310.0000AID1473739
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (178)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
bile acid and bile salt transportATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transportATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
leukotriene transportATP-binding cassette sub-family C member 3Homo sapiens (human)
monoatomic anion transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transport across blood-brain barrierATP-binding cassette sub-family C member 3Homo sapiens (human)
prostaglandin secretionMultidrug resistance-associated protein 4Homo sapiens (human)
cilium assemblyMultidrug resistance-associated protein 4Homo sapiens (human)
platelet degranulationMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
bile acid and bile salt transportMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transportMultidrug resistance-associated protein 4Homo sapiens (human)
urate transportMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
cAMP transportMultidrug resistance-associated protein 4Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 4Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 4Homo sapiens (human)
guanine nucleotide transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
estrous cycleCarbonic anhydrase 12Homo sapiens (human)
chloride ion homeostasisCarbonic anhydrase 12Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 12Homo sapiens (human)
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of cytosolic calcium ion concentrationTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of ubiquitin-protein transferase activityTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of phospholipase C activityTyrosine-protein kinase ABL1Homo sapiens (human)
mitotic cell cycleTyrosine-protein kinase ABL1Homo sapiens (human)
neural tube closureTyrosine-protein kinase ABL1Homo sapiens (human)
B-1 B cell homeostasisTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of protein phosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
B cell proliferation involved in immune responseTyrosine-protein kinase ABL1Homo sapiens (human)
transitional one stage B cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
mismatch repairTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of DNA-templated transcriptionTyrosine-protein kinase ABL1Homo sapiens (human)
autophagyTyrosine-protein kinase ABL1Homo sapiens (human)
DNA damage responseTyrosine-protein kinase ABL1Homo sapiens (human)
integrin-mediated signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
canonical NF-kappaB signal transductionTyrosine-protein kinase ABL1Homo sapiens (human)
associative learningTyrosine-protein kinase ABL1Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damageTyrosine-protein kinase ABL1Homo sapiens (human)
response to xenobiotic stimulusTyrosine-protein kinase ABL1Homo sapiens (human)
post-embryonic developmentTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of autophagyTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of endothelial cell migrationTyrosine-protein kinase ABL1Homo sapiens (human)
peptidyl-tyrosine phosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
cerebellum morphogenesisTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of cell-cell adhesionTyrosine-protein kinase ABL1Homo sapiens (human)
microspike assemblyTyrosine-protein kinase ABL1Homo sapiens (human)
actin cytoskeleton organizationTyrosine-protein kinase ABL1Homo sapiens (human)
actin filament polymerizationTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of endocytosisTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of cell adhesionTyrosine-protein kinase ABL1Homo sapiens (human)
neuron differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
BMP signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of BMP signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of axon extensionTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of microtubule polymerizationTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of Cdc42 protein signal transductionTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of type II interferon productionTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of interleukin-2 productionTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of actin cytoskeleton organizationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of osteoblast proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
substrate adhesion-dependent cell spreadingTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to oxidative stressTyrosine-protein kinase ABL1Homo sapiens (human)
response to endoplasmic reticulum stressTyrosine-protein kinase ABL1Homo sapiens (human)
platelet-derived growth factor receptor-beta signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
protein modification processTyrosine-protein kinase ABL1Homo sapiens (human)
peptidyl-tyrosine autophosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
Fc-gamma receptor signaling pathway involved in phagocytosisTyrosine-protein kinase ABL1Homo sapiens (human)
neuropilin signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
signal transduction in response to DNA damageTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transductionTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of neuron apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
endothelial cell migrationTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of T cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of vasoconstrictionTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of mitotic cell cycleTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of mitotic cell cycleTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of transcription by RNA polymerase IITyrosine-protein kinase ABL1Homo sapiens (human)
alpha-beta T cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
protein autophosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of fibroblast proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
spleen developmentTyrosine-protein kinase ABL1Homo sapiens (human)
thymus developmentTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
activated T cell proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
T cell receptor signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
B cell receptor signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
neuromuscular process controlling balanceTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of release of sequestered calcium ion into cytosolTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of oxidoreductase activityTyrosine-protein kinase ABL1Homo sapiens (human)
neuron apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of ubiquitin-protein transferase activityTyrosine-protein kinase ABL1Homo sapiens (human)
myoblast proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of stress fiber assemblyTyrosine-protein kinase ABL1Homo sapiens (human)
establishment of localization in cellTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of cell cycleTyrosine-protein kinase ABL1Homo sapiens (human)
mitochondrial depolarizationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of focal adhesion assemblyTyrosine-protein kinase ABL1Homo sapiens (human)
Bergmann glial cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
cardiac muscle cell proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
neuroepithelial cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to hydrogen peroxideTyrosine-protein kinase ABL1Homo sapiens (human)
ERK1 and ERK2 cascadeTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of ERK1 and ERK2 cascadeTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeTyrosine-protein kinase ABL1Homo sapiens (human)
DNA conformation changeTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to lipopolysaccharideTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to transforming growth factor beta stimulusTyrosine-protein kinase ABL1Homo sapiens (human)
response to epinephrineTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of protein serine/threonine kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of cell migration involved in sprouting angiogenesisTyrosine-protein kinase ABL1Homo sapiens (human)
cellular senescenceTyrosine-protein kinase ABL1Homo sapiens (human)
cell-cell adhesionTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of dendrite developmentTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of substrate adhesion-dependent cell spreadingTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of long-term synaptic potentiationTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of hematopoietic stem cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of extracellular matrix organizationTyrosine-protein kinase ABL1Homo sapiens (human)
podocyte apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to dopamineTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of establishment of T cell polarityTyrosine-protein kinase ABL1Homo sapiens (human)
DN4 thymocyte differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
protein localization to cytoplasmic microtubule plus-endTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of microtubule bindingTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of actin filament bindingTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of modification of synaptic structureTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of blood vessel branchingTyrosine-protein kinase ABL1Homo sapiens (human)
activation of protein kinase C activityTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of double-strand break repair via homologous recombinationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of Wnt signaling pathway, planar cell polarity pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of cell motilityTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of endothelial cell apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of T cell migrationTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of cellular senescenceTyrosine-protein kinase ABL1Homo sapiens (human)
epidermal growth factor receptor signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
protein phosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 1Homo sapiens (human)
morphogenesis of an epitheliumCarbonic anhydrase 2Homo sapiens (human)
positive regulation of synaptic transmission, GABAergicCarbonic anhydrase 2Homo sapiens (human)
positive regulation of cellular pH reductionCarbonic anhydrase 2Homo sapiens (human)
angiotensin-activated signaling pathwayCarbonic anhydrase 2Homo sapiens (human)
regulation of monoatomic anion transportCarbonic anhydrase 2Homo sapiens (human)
secretionCarbonic anhydrase 2Homo sapiens (human)
regulation of intracellular pHCarbonic anhydrase 2Homo sapiens (human)
neuron cellular homeostasisCarbonic anhydrase 2Homo sapiens (human)
positive regulation of dipeptide transmembrane transportCarbonic anhydrase 2Homo sapiens (human)
regulation of chloride transportCarbonic anhydrase 2Homo sapiens (human)
carbon dioxide transportCarbonic anhydrase 2Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 2Homo sapiens (human)
positive regulation of cytosolic calcium ion concentrationTyrosine-protein kinase ABL2Homo sapiens (human)
positive regulation of phospholipase C activityTyrosine-protein kinase ABL2Homo sapiens (human)
negative regulation of Rho protein signal transductionTyrosine-protein kinase ABL2Homo sapiens (human)
exploration behaviorTyrosine-protein kinase ABL2Homo sapiens (human)
cell adhesionTyrosine-protein kinase ABL2Homo sapiens (human)
signal transductionTyrosine-protein kinase ABL2Homo sapiens (human)
regulation of autophagyTyrosine-protein kinase ABL2Homo sapiens (human)
positive regulation of neuron projection developmentTyrosine-protein kinase ABL2Homo sapiens (human)
peptidyl-tyrosine phosphorylationTyrosine-protein kinase ABL2Homo sapiens (human)
regulation of endocytosisTyrosine-protein kinase ABL2Homo sapiens (human)
regulation of cell adhesionTyrosine-protein kinase ABL2Homo sapiens (human)
regulation of actin cytoskeleton organizationTyrosine-protein kinase ABL2Homo sapiens (human)
protein modification processTyrosine-protein kinase ABL2Homo sapiens (human)
positive regulation of oxidoreductase activityTyrosine-protein kinase ABL2Homo sapiens (human)
cellular response to retinoic acidTyrosine-protein kinase ABL2Homo sapiens (human)
positive regulation of establishment of T cell polarityTyrosine-protein kinase ABL2Homo sapiens (human)
regulation of cell motilityTyrosine-protein kinase ABL2Homo sapiens (human)
positive regulation of T cell migrationTyrosine-protein kinase ABL2Homo sapiens (human)
epidermal growth factor receptor signaling pathwayTyrosine-protein kinase ABL2Homo sapiens (human)
protein phosphorylationTyrosine-protein kinase ABL2Homo sapiens (human)
response to hypoxiaCarbonic anhydrase 9Homo sapiens (human)
morphogenesis of an epitheliumCarbonic anhydrase 9Homo sapiens (human)
response to xenobiotic stimulusCarbonic anhydrase 9Homo sapiens (human)
response to testosteroneCarbonic anhydrase 9Homo sapiens (human)
secretionCarbonic anhydrase 9Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 9Homo sapiens (human)
xenobiotic metabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
negative regulation of gene expressionCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bile acid and bile salt transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
heme catabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic export from cellCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transepithelial transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
leukotriene transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
monoatomic anion transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (55)

Processvia Protein(s)Taxonomy
ATP bindingATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type bile acid transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATP hydrolysis activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
icosanoid transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
guanine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ATP bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
urate transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
purine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type bile acid transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 12Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 12Homo sapiens (human)
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
supercoiled DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
magnesium ion bindingTyrosine-protein kinase ABL1Homo sapiens (human)
four-way junction DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
bubble DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
phosphotyrosine residue bindingTyrosine-protein kinase ABL1Homo sapiens (human)
DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
transcription coactivator activityTyrosine-protein kinase ABL1Homo sapiens (human)
actin monomer bindingTyrosine-protein kinase ABL1Homo sapiens (human)
nicotinate-nucleotide adenylyltransferase activityTyrosine-protein kinase ABL1Homo sapiens (human)
protein kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
protein tyrosine kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
protein kinase C bindingTyrosine-protein kinase ABL1Homo sapiens (human)
protein bindingTyrosine-protein kinase ABL1Homo sapiens (human)
ATP bindingTyrosine-protein kinase ABL1Homo sapiens (human)
kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
SH3 domain bindingTyrosine-protein kinase ABL1Homo sapiens (human)
syntaxin bindingTyrosine-protein kinase ABL1Homo sapiens (human)
manganese ion bindingTyrosine-protein kinase ABL1Homo sapiens (human)
neuropilin bindingTyrosine-protein kinase ABL1Homo sapiens (human)
SH2 domain bindingTyrosine-protein kinase ABL1Homo sapiens (human)
ephrin receptor bindingTyrosine-protein kinase ABL1Homo sapiens (human)
actin filament bindingTyrosine-protein kinase ABL1Homo sapiens (human)
mitogen-activated protein kinase bindingTyrosine-protein kinase ABL1Homo sapiens (human)
proline-rich region bindingTyrosine-protein kinase ABL1Homo sapiens (human)
delta-catenin bindingTyrosine-protein kinase ABL1Homo sapiens (human)
sequence-specific double-stranded DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
arylesterase activityCarbonic anhydrase 1Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 1Homo sapiens (human)
protein bindingCarbonic anhydrase 1Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 1Homo sapiens (human)
hydro-lyase activityCarbonic anhydrase 1Homo sapiens (human)
cyanamide hydratase activityCarbonic anhydrase 1Homo sapiens (human)
arylesterase activityCarbonic anhydrase 2Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 2Homo sapiens (human)
protein bindingCarbonic anhydrase 2Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 2Homo sapiens (human)
cyanamide hydratase activityCarbonic anhydrase 2Homo sapiens (human)
magnesium ion bindingTyrosine-protein kinase ABL2Homo sapiens (human)
phosphotyrosine residue bindingTyrosine-protein kinase ABL2Homo sapiens (human)
actin monomer bindingTyrosine-protein kinase ABL2Homo sapiens (human)
protein kinase activityTyrosine-protein kinase ABL2Homo sapiens (human)
protein tyrosine kinase activityTyrosine-protein kinase ABL2Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activityTyrosine-protein kinase ABL2Homo sapiens (human)
protein bindingTyrosine-protein kinase ABL2Homo sapiens (human)
ATP bindingTyrosine-protein kinase ABL2Homo sapiens (human)
manganese ion bindingTyrosine-protein kinase ABL2Homo sapiens (human)
actin filament bindingTyrosine-protein kinase ABL2Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 9Homo sapiens (human)
protein bindingCarbonic anhydrase 9Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 9Homo sapiens (human)
molecular function activator activityCarbonic anhydrase 9Homo sapiens (human)
protein bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
organic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type xenobiotic transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP hydrolysis activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (35)

Processvia Protein(s)Taxonomy
plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basal plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basolateral plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
nucleolusMultidrug resistance-associated protein 4Homo sapiens (human)
Golgi apparatusMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
platelet dense granule membraneMultidrug resistance-associated protein 4Homo sapiens (human)
external side of apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneCarbonic anhydrase 12Homo sapiens (human)
membraneCarbonic anhydrase 12Homo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 12Homo sapiens (human)
apical plasma membraneCarbonic anhydrase 12Homo sapiens (human)
plasma membraneCarbonic anhydrase 12Homo sapiens (human)
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
ruffleTyrosine-protein kinase ABL1Homo sapiens (human)
nucleusTyrosine-protein kinase ABL1Homo sapiens (human)
nucleoplasmTyrosine-protein kinase ABL1Homo sapiens (human)
nucleolusTyrosine-protein kinase ABL1Homo sapiens (human)
cytoplasmTyrosine-protein kinase ABL1Homo sapiens (human)
mitochondrionTyrosine-protein kinase ABL1Homo sapiens (human)
cytosolTyrosine-protein kinase ABL1Homo sapiens (human)
actin cytoskeletonTyrosine-protein kinase ABL1Homo sapiens (human)
nuclear bodyTyrosine-protein kinase ABL1Homo sapiens (human)
dendriteTyrosine-protein kinase ABL1Homo sapiens (human)
growth coneTyrosine-protein kinase ABL1Homo sapiens (human)
nuclear membraneTyrosine-protein kinase ABL1Homo sapiens (human)
neuronal cell bodyTyrosine-protein kinase ABL1Homo sapiens (human)
perinuclear region of cytoplasmTyrosine-protein kinase ABL1Homo sapiens (human)
postsynapseTyrosine-protein kinase ABL1Homo sapiens (human)
protein-containing complexTyrosine-protein kinase ABL1Homo sapiens (human)
plasma membraneTyrosine-protein kinase ABL1Homo sapiens (human)
cytosolCarbonic anhydrase 1Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 1Homo sapiens (human)
cytoplasmCarbonic anhydrase 2Homo sapiens (human)
cytosolCarbonic anhydrase 2Homo sapiens (human)
plasma membraneCarbonic anhydrase 2Homo sapiens (human)
myelin sheathCarbonic anhydrase 2Homo sapiens (human)
apical part of cellCarbonic anhydrase 2Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 2Homo sapiens (human)
cytoplasmCarbonic anhydrase 2Homo sapiens (human)
plasma membraneCarbonic anhydrase 2Homo sapiens (human)
apical part of cellCarbonic anhydrase 2Homo sapiens (human)
cytosolTyrosine-protein kinase ABL2Homo sapiens (human)
actin cytoskeletonTyrosine-protein kinase ABL2Homo sapiens (human)
plasma membraneTyrosine-protein kinase ABL2Homo sapiens (human)
nucleolusCarbonic anhydrase 9Homo sapiens (human)
plasma membraneCarbonic anhydrase 9Homo sapiens (human)
membraneCarbonic anhydrase 9Homo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 9Homo sapiens (human)
microvillus membraneCarbonic anhydrase 9Homo sapiens (human)
plasma membraneCarbonic anhydrase 9Homo sapiens (human)
plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
cell surfaceCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
intercellular canaliculusCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (549)

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.
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.
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.
AID1347117qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
AID1347127qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
AID1347122qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
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.
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.
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.
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.
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.
AID1347114qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
AID1347111qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
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.
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.
AID1347113qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
AID1347129qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
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.
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.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347118qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
AID1347128qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
AID1347115qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
AID1347123qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347109qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
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.
AID1347125qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
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.
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.
AID1347126qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
AID1347121qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
AID1347110qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)2018Oncotarget, 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.
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.
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.
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.
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.
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.
AID1347119qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
AID1347112qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
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.
AID1347116qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
AID1347124qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory 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.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID282551Antitumor activity against human NCI non-small cell lung cancer cell line panel2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
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]
AID1683791Antitumor activity against human NCI-H209 cells xenografted in BALB/c nude mouse assessed as PR rate at 50 mg/kg, po QD for 5 consecutive days at start of study and again 14 days later2020Journal of medicinal chemistry, 12-24, Volume: 63, Issue:24
Discovery of Pamiparib (BGB-290), a Potent and Selective Poly (ADP-ribose) Polymerase (PARP) Inhibitor in Clinical Development.
AID1697834Antitumour activity against human DBTRG-05MG cells xenografted in BALB/c nude mouse assessed as reduction in tumour growth at 5 mg/kg, ip for 5 days and measured every 2 days2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1474445Toxicity in BALB/c mouse assessed as change in body weight at 50 mg/kg, po administered once daily via gavage for 5 days measured twice every week up to 11 days (Rvb = 5.32 g)2017European journal of medicinal chemistry, May-26, Volume: 132Discovery of 2-substituted 1H-benzo[d]immidazole-4-carboxamide derivatives as novel poly(ADP-ribose)polymerase-1 inhibitors with in vivo anti-tumor activity.
AID1497082Cytotoxicity against human MDA-MB-231 cells assessed as reduction in cell viability after 72 hrs by MTT assay2018Bioorganic & medicinal chemistry letters, 07-15, Volume: 28, Issue:13
Design, synthesis and biological evaluation of artemisinin derivatives containing fluorine atoms as anticancer agents.
AID1697710Effect on ERK expression in rat RG2 cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697755Induction of apoptosis in human DBTRG-05MG cells assessed as cleaved PARP expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID661465Cytotoxicity against mouse astrocytes assessed as decrease in cell viability at 1 to 100 uM after 48 hrs by Hoechst 33342 staining2012Journal of medicinal chemistry, Mar-08, Volume: 55, Issue:5
Oxaphosphinanes: new therapeutic perspectives for glioblastoma.
AID1537890Cytotoxicity against P-gp knockout patient-isolated primary glioblastoma cells derived neurospheres assessed as reduction in cell viability at 50 uM measured after 72 hrs by chemiluminescence-based assay2019Journal of medicinal chemistry, 04-25, Volume: 62, Issue:8
Carbonic Anhydrase XII Inhibitors Overcome Temozolomide Resistance in Glioblastoma.
AID1736286Selectivity index, ratio of CC50 for Wistar rat astrocytes to EC50 for human U87MG cells2020European journal of medicinal chemistry, Mar-01, Volume: 189Efficient identification of novel anti-glioma lead compounds by machine learning models.
AID1697774Induction of apoptosis in rat RG2 cells assessed as phosphorylated caspace-9 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697687Inhibition of ERK phosphorylation at Tyr204 residues in human DBTRG-05MG cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
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]
AID1697639Induction of cell cycle arrest in human DBTRG-05MG cells assessed as p53 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1876511Induction of apoptosis in human U-87 MG cells assessed as early apoptotic cells at 1.20 uM incubated for 72 hrs by Annexin V-FITC/PI staining based flow cytometry method (Rvb = 2.53 %)2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1825322Cytotoxicity against human U-87 MG cells assessed as cell viability using raw interpretation method2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1697684Effect on JNK expression in human DBTRG-05MG cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
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).
AID1767414Antitumor activity against rat C6 cells inoculated orthotopic Sprague-Dawley rat model assessed as decrease in PGE2 in tumor tissue at 50 mg/kg, ip twice a day treated 3 days after tumor cell injection measured for 13 days after tumor implantation by West
AID1172642Inhibition of cell proliferation of rat C6 cells assessed as cell viability after 72 hrs by sulforhodamine B assay2014Bioorganic & medicinal chemistry letters, Nov-15, Volume: 24, Issue:22
Bioactive triterpenoid saponins and phenolic compounds against glioma cells.
AID1697800Induction of DNA damage in human DBTRG-05MG cells assessed as ATM phosphorylation at ser1981 residues at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1888669Antiproliferative activity against human LN-229 cells assessed as reduction in cell viability at 80 uM up to 7 days by incucyte live cell assay2022Bioorganic & medicinal chemistry, 01-01, Volume: 53Novel structural-related analogs of PFI-3 (SRAPs) that target the BRG1 catalytic subunit of the SWI/SNF complex increase the activity of temozolomide in glioblastoma cells.
AID1697617Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at G0/G1 phase at 206 uM after 24 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 57.81 +/- 1.9%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1876525Induction of apoptosis in human U-251 cells assessed as late apoptotic cells at 6 uM incubated for 72 hrs by Annexin V-FITC/PI staining based flow cytometry method (Rvb =1.31 %)2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1497081Cytotoxicity against human MCF7 cells assessed as reduction in cell viability after 72 hrs by MTT assay2018Bioorganic & medicinal chemistry letters, 07-15, Volume: 28, Issue:13
Design, synthesis and biological evaluation of artemisinin derivatives containing fluorine atoms as anticancer agents.
AID1736284Antiproliferative activity against human U251MG cells assessed as cell growth inhibition measured after 72 hrs by SRB assay2020European journal of medicinal chemistry, Mar-01, Volume: 189Efficient identification of novel anti-glioma lead compounds by machine learning models.
AID667958Growth inhibition of human Hs683 cells after 72 hrs by MTT assay2012European journal of medicinal chemistry, Aug, Volume: 54N-Aryl-N'-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: screening, synthesis of simplified derivatives, and structure-activity relationship analysis.
AID1697733Induction of apoptosis in rat RG2 cells assessed as increase in apoptotic body formation at 206 uM after 48 hrs by TUNEL assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID661466Cytotoxicity against mouse astrocytes assessed as decrease in cell viability at 1 to 100 uM after 48 hrs by propidium iodide incorporation assay2012Journal of medicinal chemistry, Mar-08, Volume: 55, Issue:5
Oxaphosphinanes: new therapeutic perspectives for glioblastoma.
AID1851872Cytotoxicity against human GSC#83 cells assessed as reduction in cell viability at 5 to 50 uM incubated for 24 hrs by MTS assay
AID1876524Induction of apoptosis in human U-251 cells assessed as early apoptotic cells at 6 uM incubated for 72 hrs by Annexin V-FITC/PI staining based flow cytometry method (Rvb =1.96 %)2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
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).
AID348241Antitumor activity against mouse B16F10 cells xenografted in C57BL/6 mouse assessed as growth inhibition at 50 mg/kg/day, po after 14 days relative to control2009Journal of medicinal chemistry, Jan-22, Volume: 52, Issue:2
Discovery of the Poly(ADP-ribose) polymerase (PARP) inhibitor 2-[(R)-2-methylpyrrolidin-2-yl]-1H-benzimidazole-4-carboxamide (ABT-888) for the treatment of cancer.
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).
AID1736311Cytotoxicity against Wistar rat astrocytes assessed as cell growth inhibition at 100 uM measured after 72 hrs by SRB assay2020European journal of medicinal chemistry, Mar-01, Volume: 189Efficient identification of novel anti-glioma lead compounds by machine learning models.
AID102166Cytotoxic potentiation of Topotecan (TP) by the compound in (human colorectal cancer LoVo cell line2002Journal of medicinal chemistry, Nov-07, Volume: 45, Issue:23
Novel tricyclic poly(ADP-ribose) polymerase-1 inhibitors with potent anticancer chemopotentiating activity: design, synthesis, and X-ray cocrystal structure.
AID282550Antitumor activity against human NCI leukemia cell line panel2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1054218Induction of apoptosis in human SK-MEL-30 cells assessed as apoptotic/necrotic cells at 100 uM after 48 hrs by APC-labeled annexin V and 7-AAD staining-based flow cytometric analysis relative to control2013European journal of medicinal chemistry, , Volume: 70Synthesis and evaluation of N-acylamino acids derivatives of triazenes. Activation by tyrosinase in human melanoma cell lines.
AID1777597Stability of the compound in potassium phosphate buffer at pH 7.4 assessed as half life2021Bioorganic & medicinal chemistry letters, 10-15, Volume: 50Model studies towards prodrugs of the glutamine antagonist 6-diazo-5-oxo-l-norleucine (DON) containing a diazo precursor.
AID1697344Acute toxicity in Balb/c mouse xenografted with SW-620 cells assessed as mean weight loss at 50 mg/kg, po qd administered for 5 days measured on day 6 relative to control2020Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19
Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID282485Half life of hydrolysis in phosphate buffer at pH 7.42004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1697465Cytotoxicity against rat RG2 cells assessed as reduction in cell viability after 72 hrs by MTT assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1683790Antitumor activity against human NCI-H209 cells xenografted in BALB/c nude mouse assessed as tumor relapse at 50 mg/kg, po QD for 5 consecutive days at start of study and again 14 days later and measured after 48 days2020Journal of medicinal chemistry, 12-24, Volume: 63, Issue:24
Discovery of Pamiparib (BGB-290), a Potent and Selective Poly (ADP-ribose) Polymerase (PARP) Inhibitor in Clinical Development.
AID1316634Drug level in Sprague-Dawley rat brain at 10 mg/kg, iv after 30 mins by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID73182In vitro cytotoxicity against human lymphoblast cell line (GM892 A).1995Journal of medicinal chemistry, Apr-28, Volume: 38, Issue:9
Antitumor imidazotetrazines. 32. Synthesis of novel imidazotetrazinones and related bicyclic heterocycles to probe the mode of action of the antitumor drug temozolomide.
AID1876510Induction of apoptosis in human U-87 MG cells assessed as viable cells at 1.20 uM incubated for 72 hrs by Annexin V-FITC/PI staining based flow cytometry method (Rvb = 96.84 %)2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1172641Inhibition of cell proliferation of human U251 cells assessed as cell viability after 72 hrs by sulforhodamine B assay2014Bioorganic & medicinal chemistry letters, Nov-15, Volume: 24, Issue:22
Bioactive triterpenoid saponins and phenolic compounds against glioma cells.
AID94799Cytotoxic effect in K562 cells2003Bioorganic & medicinal chemistry letters, Oct-06, Volume: 13, Issue:19
Synthesis of pyrimidinopyridine-triazene conjugates targeted to abl tyrosine kinase.
AID1736297Antitumor activity against C57BL/6 mouse GL261 cells xenografted in C57BL/6 mouse assessed as reduction in tumor volume at 20 mg/kg, ip administered once daily for 10 days starting from 7 days post tumor cell inoculation and measured on day 172020European journal of medicinal chemistry, Mar-01, Volume: 189Efficient identification of novel anti-glioma lead compounds by machine learning models.
AID1595390Induction of morphological changes in mouse GL261 cells assessed as increase in cell circularity at 10 uM incubated for 48 hrs by Hoechst 33258 staining based fluorescence microscopic analysis2019European journal of medicinal chemistry, Jun-15, Volume: 172Targeting gliomas with triazene-based hybrids: Structure-activity relationship, mechanistic study and stability.
AID1316653Ratio of AUC in human brain to plasma by reversed-phase HPLC analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
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.
AID1763423Cytotoxicity against human HL-60 cells by MTT assay2021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Chemical modifications of ergostane-type triterpenoids from Antrodia camphorata and their cytotoxic activities.
AID1888353Induction of DNA damage in human T98G cells assessed as increase in gammaH2AX foci number and size at 94 uM measured after 96 hrs by DAPI staining based immunofluorescence assay
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1308011Growth inhibition of human U87MG cells at 50 uM after 72 hrs by MTS assay relative to control2016Journal of medicinal chemistry, 05-26, Volume: 59, Issue:10
Lead Optimization of 2-Phenylindolylglyoxylyldipeptide Murine Double Minute (MDM)2/Translocator Protein (TSPO) Dual Inhibitors for the Treatment of Gliomas.
AID1763424Cytotoxicity against human U-251 cells by MTT assay2021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Chemical modifications of ergostane-type triterpenoids from Antrodia camphorata and their cytotoxic activities.
AID7471Potentiation factor at 50% growth inhibition (IC50 of compound to that of compound along with PARP inhibitor) in experiment 22000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 9. Synthesis and biological properties of benzimidazole inhibitors of the DNA repair enzyme poly(ADP-ribose) polymerase.
AID282552Antitumor activity against human NCI colon cancer cell line panel2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1167096Inhibition of cell proliferation of human WI38 cells by CCK8 assay2014Journal of medicinal chemistry, Oct-23, Volume: 57, Issue:20
Inhibition of cancer-associated mutant isocitrate dehydrogenases: synthesis, structure-activity relationship, and selective antitumor activity.
AID231797Ratio of cytotoxicity against Raji cells to that of GM892 A cells.1995Journal of medicinal chemistry, Apr-28, Volume: 38, Issue:9
Antitumor imidazotetrazines. 32. Synthesis of novel imidazotetrazinones and related bicyclic heterocycles to probe the mode of action of the antitumor drug temozolomide.
AID1633573Toxicity in human Capan1 cells xenografted Balb athymic Nu/Nu mouse assessed as maximum weight loss at 62.5 mg/kg, iv qd for 5 days2019ACS medicinal chemistry letters, Apr-11, Volume: 10, Issue:4
Discovery of Stereospecific PARP-1 Inhibitor Isoindolinone NMS-P515.
AID1474441Anti-tumor activity against human MX1 cells xenografted in BALB/c mouse assessed as tumor growth inhibition at 50 mg/kg, po administered once daily via gavage for 5 days measured after 11 days relative to control2017European journal of medicinal chemistry, May-26, Volume: 132Discovery of 2-substituted 1H-benzo[d]immidazole-4-carboxamide derivatives as novel poly(ADP-ribose)polymerase-1 inhibitors with in vivo anti-tumor activity.
AID1537888Cytotoxicity against P-gp knockout patient-isolated primary glioblastoma cells derived neurospheres assessed as increase in LDH release at 50 uM measured after 48 hrs by spectrophotometric method2019Journal of medicinal chemistry, 04-25, Volume: 62, Issue:8
Carbonic Anhydrase XII Inhibitors Overcome Temozolomide Resistance in Glioblastoma.
AID1697688Effect on p38 expression in human DBTRG-05MG cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697628Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at G2/M phase at 206 uM after 48 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 20.04 +/- 0.55%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1769430Cytotoxicity against human HaCaT cells assessed as reduction in cell viability incubated for 72 hrs by MTS assay2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Sulfur Analogues of Tyrosine in the Development of Triazene Hybrid Compounds: A New Strategy against Melanoma.
AID1064453Growth inhibition of human MDA-MB-436 cells after 72 hrs by SRB assay2014Bioorganic & medicinal chemistry letters, Jan-15, Volume: 24, Issue:2
Novel PARP-1 inhibitors based on a 2-propanoyl-3H-quinazolin-4-one scaffold.
AID1697467Cytotoxicity against rat CTX TNA2 cells assessed as reduction in cell viability after 48 hrs by MTT assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID766233Chemosensitization of human A2780 cells after 5 days by MTT assay2013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID1767413Antitumor activity against rat C6 cells inoculated orthotopic Sprague-Dawley rat model assessed as increase in E-cadherin in tumor tissue at 50 mg/kg, ip twice a day treated 3 days after tumor cell injection measured for 13 days after tumor implantation b
AID1425998Cytotoxicity against MDCK cells expressing carbonic anhydrase 9 assessed as reduction in cell viability after 72 hrs under normoxic condition by Alamar blue assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID282556Antitumor activity against human NCI renal cancer cell line panel2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1595381Cytotoxicity against mouse GL261 cells assessed as reduction in cell viability incubated for 48 hrs by MTS assay2019European journal of medicinal chemistry, Jun-15, Volume: 172Targeting gliomas with triazene-based hybrids: Structure-activity relationship, mechanistic study and stability.
AID1546668Cytotoxicity against human SW480 cells incubated for 24 hrs by MTT assay2020Journal of natural products, 01-24, Volume: 83, Issue:1
Antcamphorols A-K, Cytotoxic and ROS Scavenging Triterpenoids from
AID1542800Cytotoxicity against human U251MG cells assessed as reduction in cell survival measured after 72 hrs by MTT assay2019Bioorganic & medicinal chemistry, 05-15, Volume: 27, Issue:10
Chemical modifications of imidazole-containing alkoxyamines increase C-ON bond homolysis rate: Effects on their cytotoxic properties in glioblastoma cells.
AID52527Level of AGT activity in COLO 205 cell line2000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 8. Inhibition of O(6)-alkylguanine-DNA alkyltransferase by O(6)-alkenyl-, O(6)-cycloalkenyl-, and O(6)-(2-oxoalkyl)guanines and potentiation of temozolomide cytotoxicity in vitro by O(6)-(1-cyclopentenylmethyl)guanine.
AID1697466Cytotoxicity against rat CTX TNA2 cells assessed as reduction in cell viability after 24 hrs by MTT assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1316633Plasma concentration in Sprague-Dawley rat plasma at 10 mg/kg, iv after 180 mins by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
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).
AID1697640Induction of cell cycle arrest in human DBTRG-05MG cells assessed as p21 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID282487Half life of hydrolysis in deuterated phosphate buffer at pD 7.82004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1697778Induction of apoptosis in rat RG2 cells assessed as phosphorylated PARP expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID474430Antitumor activity against mouse B16F10 cells transplanted in C57BL/6 mouse assessed as tumor volume at 50 mg/kg/day, po administered from day 6 to 10 post transplantation measured on day 18 relative to control2010Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8
Optimization of phenyl-substituted benzimidazole carboxamide poly(ADP-ribose) polymerase inhibitors: identification of (S)-2-(2-fluoro-4-(pyrrolidin-2-yl)phenyl)-1H-benzimidazole-4-carboxamide (A-966492), a highly potent and efficacious inhibitor.
AID1683795Antitumor activity against human NCI-H209 cells xenografted in BALB/c nude mouse assessed as inhibition of tumor growth at 50 mg/kg, po QD for 5 consecutive days at start of study and again 14 days later2020Journal of medicinal chemistry, 12-24, Volume: 63, Issue:24
Discovery of Pamiparib (BGB-290), a Potent and Selective Poly (ADP-ribose) Polymerase (PARP) Inhibitor in Clinical Development.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1426003Cytotoxicity against carbonic anhydrase 9 knockdown MDCK cells assessed as reduction in cell viability incubated for 24 hrs measured after 7 days under hypoxic condition by methylene blue staining based clonogenic survival assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID1054217Induction of apoptosis in human M8 cells assessed as apoptotic/necrotic cells at 50 to 100 uM after 48 hrs by APC-labeled annexin V and 7-AAD staining-based flow cytometric analysis2013European journal of medicinal chemistry, , Volume: 70Synthesis and evaluation of N-acylamino acids derivatives of triazenes. Activation by tyrosinase in human melanoma cell lines.
AID1623800Toxicity in nude BALB/c mouse xenografted with human U87MG cells assessed as reduction in body weight at 50 mg/kg, ip administered for 5 days/week for two cycles2019Journal of medicinal chemistry, 02-14, Volume: 62, Issue:3
Design of Novel Inhibitors of Human Thymidine Phosphorylase: Synthesis, Enzyme Inhibition, in Vitro Toxicity, and Impact on Human Glioblastoma Cancer.
AID1416899Growth inhibition of MGMT-transfected human SNB19 cells expressing MGMT after 7 days by MTT assay
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).
AID1167095Inhibition of neurosphere formation of mouse BXD3752 cells by CCK8 assay2014Journal of medicinal chemistry, Oct-23, Volume: 57, Issue:20
Inhibition of cancer-associated mutant isocitrate dehydrogenases: synthesis, structure-activity relationship, and selective antitumor activity.
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).
AID1763426Cytotoxicity against human MCF7 cells by MTT assay2021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Chemical modifications of ergostane-type triterpenoids from Antrodia camphorata and their cytotoxic activities.
AID282555Antitumor activity against human NCI ovarian carcinoma cell line panel2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1497079Cytotoxicity against human U87 cells assessed as reduction in cell viability after 72 hrs by MTT assay2018Bioorganic & medicinal chemistry letters, 07-15, Volume: 28, Issue:13
Design, synthesis and biological evaluation of artemisinin derivatives containing fluorine atoms as anticancer agents.
AID1697709Inhibition of JNK phosphorylation at Thr183/Tyr185 residues in rat RG2 cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1167093Inhibition of neurosphere formation of human BT142 cells by CCK8 assay2014Journal of medicinal chemistry, Oct-23, Volume: 57, Issue:20
Inhibition of cancer-associated mutant isocitrate dehydrogenases: synthesis, structure-activity relationship, and selective antitumor activity.
AID1317836Antiproliferative activity against drug-resistant human T98G cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1317832Antiproliferative activity against drug-sensitive human Hs683 cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1697707Inhibition of AKT phosphorylation at S473 residues in rat RG2 cells at 206 uM after 48 hrs by Western blot analysis2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID667956Growth inhibition of human U373 cells after 72 hrs by MTT assay2012European journal of medicinal chemistry, Aug, Volume: 54N-Aryl-N'-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: screening, synthesis of simplified derivatives, and structure-activity relationship analysis.
AID1876492Antiproliferative activity against rat C6 cells assessed as inhibition of cell proliferation measured after 72 hrs by CCK8 assay2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1697750Induction of apoptosis in human DBTRG-05MG cells assessed as phosphorylated caspace-9 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697610Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at G2/M phase at 206 uM after 12 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 20.04 +/- 0.55%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697753Induction of apoptosis in human DBTRG-05MG cells assessed as cleaved caspace-3 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697581Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at G0/G1 phase at 206 uM after 24 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 47.16 +/- 1.55%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1497080Cytotoxicity against human SH-SY5Y cells assessed as reduction in cell viability after 72 hrs by MTT assay2018Bioorganic & medicinal chemistry letters, 07-15, Volume: 28, Issue:13
Design, synthesis and biological evaluation of artemisinin derivatives containing fluorine atoms as anticancer agents.
AID1545832Antiproliferative activity against human GBM2 cells assessed as reduction in cell viability after 72 hrs by MTT assay2019European journal of medicinal chemistry, Dec-01, Volume: 1831,2,3-Triazole-containing hybrids as potential anticancer agents: Current developments, action mechanisms and structure-activity relationships.
AID1425999Cytotoxicity against carbonic anhydrase 9 knockdown MDCK cells assessed as reduction in cell viability after 72 hrs under hypoxic condition by Alamar blue assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID1895190Inhibition of sulfatase in human T98G cells assessed as reduction in fluorescence intensity at 25 uM using 2-(2-Morpholinoethyl)-6-(((2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl)oxy)-1H-benzo[de]-isoquinoline-1,3(2H)-dione a2021Journal of medicinal chemistry, 06-24, Volume: 64, Issue:12
New Protocol-Guided Exploitation of a Lysosomal Sulfatase Inhibitor to Suppress Cell Growth in Glioblastoma Multiforme.
AID1697461Cytotoxicity against human DBTRG-05MG cells assessed as reduction in cell viability after 48 hrs by MTT assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1317834Antiproliferative activity against drug-resistant human U251 cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1697573Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at S phase at 206 uM after 12 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 22.76 +/- 1.56%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1623802Anti-angiogenic activity in tumor of human U87MG cells xenografted in nude BALB/c mouse assessed as reduction in number of blood vessels at 50 mg/kg, ip administered for 14 days by hematoxylin and eosin-staining based light microscopy2019Journal of medicinal chemistry, 02-14, Volume: 62, Issue:3
Design of Novel Inhibitors of Human Thymidine Phosphorylase: Synthesis, Enzyme Inhibition, in Vitro Toxicity, and Impact on Human Glioblastoma Cancer.
AID1888667Induction of cell death in human MT330 cells assessed as reduction in cell viability at 50 uM after 3 days by ELISA2022Bioorganic & medicinal chemistry, 01-01, Volume: 53Novel structural-related analogs of PFI-3 (SRAPs) that target the BRG1 catalytic subunit of the SWI/SNF complex increase the activity of temozolomide in glioblastoma cells.
AID1697618Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at S phase at 206 uM after 24 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 20.15 +/- 2.44%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697469Toxicity in BALB/c mouse xenografted with DBTRG-05MG cells assessed as reduction in body weight at 5 mg/kg, ip after 5 days measured every 2 days2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID282558Antitumor activity against human NCI breast cancer cell line panel2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1876563Antitumor activity against human U-87 MG cells xenografted in BALB/c mouse assessed as decrease in tumor volume at 10 mg/kg,ip bid for 1 month2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1262128Antiproliferative activity against human U118MG cells assessed as inhibition of cell growth at 100 uM after 72 hrs by WST1 assay2015European journal of medicinal chemistry, Nov-13, Volume: 105Design and synthesis of 2-oxindole based multi-targeted inhibitors of PDK1/Akt signaling pathway for the treatment of glioblastoma multiforme.
AID1851874Cytotoxicity against human U-251 cells assessed as reduction in cell viability at 10 uM incubated for 24 hrs by MTS assay
AID282554Antitumor activity against NCI human melanoma cell line panel2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1633569Antitumor activity against human Capan1 cells xenografted in Balb athymic Nu/Nu mouse assessed as maximal tumor growth inhibition at 62.5 mg/kg, iv qd for 5 days2019ACS medicinal chemistry letters, Apr-11, Volume: 10, Issue:4
Discovery of Stereospecific PARP-1 Inhibitor Isoindolinone NMS-P515.
AID668219Antiproliferative activity against human A172 cells after 5 days by MTT assay2012Bioorganic & medicinal chemistry letters, Jul-01, Volume: 22, Issue:13
New substituted 4H-chromenes as anticancer agents.
AID1767417Toxicity in rat C6 cells inoculated orthotopic Sprague-Dawley rat model assessed as body weight change at 50 mg/kg, ip twice a day administered for 13 days of tumor implantation
AID766225Chemosensitization of human HCT116 cells after 5 days by MTT assay2013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID1316632Plasma concentration in Sprague-Dawley rat plasma at 10 mg/kg, iv after 90 mins by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1851859Cytotoxicity against human T98G cells assessed as reduction in cell viability at 5 to 50 uM incubated for 24 hrs by MTS assay
AID1697627Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at S phase at 206 uM after 48 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 20.15 +/- 2.44%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697772Induction of apoptosis in rat RG2 cells assessed as Bcl2 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1254863Tumoricidal effect in patient derived GBM 047T cells assessed as reduction in neurosphere formation at 20 uM after 1 to 2 weeks by 3D tumor clonogenic assay2015European journal of medicinal chemistry, Oct-20, Volume: 103Discovery of potent and selective cytotoxic activity of new quinazoline-ureas against TMZ-resistant glioblastoma multiforme (GBM).
AID1697582Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at S phase at 206 uM after 24 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 22.76 +/- 1.56%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID386713Antitumor activity in human SW620 cells xenografted mouse assessed as days to double the relative tumor volume at 50 mg/kg, po once daily for 5 consecutive days2008Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20
4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID441949Antitumor activity against mouse B16F10 cells implanted in C57BL/6 mouse at 50 mg/kg, po QD for 5 days measured on day 122009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Synthesis and evaluation of a new generation of orally efficacious benzimidazole-based poly(ADP-ribose) polymerase-1 (PARP-1) inhibitors as anticancer agents.
AID348240Antitumor activity against mouse B16F10 cells xenografted in C57BL/6 mouse assessed as tumor volume at 50 mg/kg/day, po after 14 days2009Journal of medicinal chemistry, Jan-22, Volume: 52, Issue:2
Discovery of the Poly(ADP-ribose) polymerase (PARP) inhibitor 2-[(R)-2-methylpyrrolidin-2-yl]-1H-benzimidazole-4-carboxamide (ABT-888) for the treatment of cancer.
AID540210Clearance in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID667962Selectivity index, ratio of of IC50 for mouse astrocytes to IC50 for human Hs683 cells2012European journal of medicinal chemistry, Aug, Volume: 54N-Aryl-N'-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: screening, synthesis of simplified derivatives, and structure-activity relationship analysis.
AID712153Prodrug conversion in citrate-phosphate buffer at pH 8 assessed as pseudo-first-order rate constant2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1729709Inhibition of colony formation in human GSC-18 cells assessed as tumor spheres damage at 15 uM after 2 weeks by crystal violet staining based assay2021European journal of medicinal chemistry, Jan-15, Volume: 210Structures/cytotoxicity/selectivity relationship of natural steroidal saponins against GSCs and primary mechanism of tribulosaponin A.
AID1809515Cytotoxicity against human U-87 MG cells assessed as inhibition of cell growth measured after 48 hrs by MTT assay2021Bioorganic & medicinal chemistry letters, 11-01, Volume: 51Non-alkylator anti-glioblastoma agents induced cell cycle G2/M arrest and apoptosis: Design, in silico physicochemical and SAR studies of 2-aminoquinoline-3-carboxamides.
AID1425987Binding affinity to recombinant human carbonic anhydrase 1 after 15 mins by stopped-flow CO2 hydration assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
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]
AID7467Potentiation of growth inhibition of A2780 cells by compound alone in experiment 22000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 9. Synthesis and biological properties of benzimidazole inhibitors of the DNA repair enzyme poly(ADP-ribose) polymerase.
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.
AID1876512Induction of apoptosis in human U-87 MG cells assessed as late apoptotic cells at 1.20 uM incubated for 72 hrs by Annexin V-FITC/PI staining based flow cytometry method (Rvb = 0.42 %)2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1697600Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at S phase at 206 uM after 6 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 20.15 +/- 2.44%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1317833Antiproliferative activity against drug-resistant human U373 cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1697591Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at S phase at 206 uM after 48 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 22.76 +/- 1.56%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1317835Antiproliferative activity against drug-resistant human U87 cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1697706Effect on AKT expression in rat RG2 cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1473739Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1697601Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at G2/M phase at 206 uM after 6 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 20.04 +/- 0.55%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697729Induction of apoptosis in human DBTRG-05MG cells assessed as increase in DNA fragmentation at 206 uM after 48 hrs by TUNEL assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1426000Cytotoxicity against MDCK cells expressing carbonic anhydrase 9 assessed as reduction in cell viability after 72 hrs under hypoxic condition by Alamar blue assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID1054220Induction of apoptosis in human MNT1 cells assessed as apoptotic/necrotic cells at 100 uM after 48 hrs by APC-labeled annexin V and 7-AAD staining-based flow cytometric analysis relative to control2013European journal of medicinal chemistry, , Volume: 70Synthesis and evaluation of N-acylamino acids derivatives of triazenes. Activation by tyrosinase in human melanoma cell lines.
AID475198Antitumor activity against mouse B16F10 cells transplanted in C57BL/6 mouse assessed as tumor volume at 50 mg/kg/day, po administered from day 6 to 10 post transplantation measured on day 16 relative to control2010Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8
Optimization of phenyl-substituted benzimidazole carboxamide poly(ADP-ribose) polymerase inhibitors: identification of (S)-2-(2-fluoro-4-(pyrrolidin-2-yl)phenyl)-1H-benzimidazole-4-carboxamide (A-966492), a highly potent and efficacious inhibitor.
AID454060Cytotoxicity against human HCT116 cells after 4 days2009Bioorganic & medicinal chemistry, Nov-01, Volume: 17, Issue:21
Synthesis of isoquinolinone-based tetracycles as poly (ADP-ribose) polymerase-1 (PARP-1) inhibitors.
AID1507125Antiproliferative activity in human A431 Cells after 72 hrs by SRB assay2017European journal of medicinal chemistry, Aug-18, Volume: 136Designing multi-targeted agents: An emerging anticancer drug discovery paradigm.
AID1830962Antitumor activity against human U-87MG cells xenografted in BALB/c mouse assessed as reduction in tumor volume at 30 mg/kg, po administered once daily for 5 days and measured on day 8 by MRI scanner (Rvb = 202 +/- 120.4 mm3)
AID1697608Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at G0/G1 phase at 206 uM after 12 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 57.81 +/- 1.9%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1537861Cytotoxicity against patient-isolated primary glioblastoma cells derived adherent cells assessed as increase in LDH release at 50 uM measured after 48 hrs by spectrophotometric method2019Journal of medicinal chemistry, 04-25, Volume: 62, Issue:8
Carbonic Anhydrase XII Inhibitors Overcome Temozolomide Resistance in Glioblastoma.
AID1693365Antitumour activity against human U251 cells xenografted in NCr athymic nude nu/nu mouse assessed as decrease in tumour growth at 50 mg/kg once in a week2021Bioorganic & medicinal chemistry, 01-01, Volume: 29The 3-D conformational shape of N-naphthyl-cyclopenta[d]pyrimidines affects their potency as microtubule targeting agents and their antitumor activity.
AID1825321Cytotoxicity against human SH-SY5Y cells assessed as cell viability using raw interpretation method2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1697809Induction of DNA damage in rat RG2 cells assessed as H2A.X phosphorylation at ser139 at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID474425Antitumor activity against mouse B16F10 cells transplanted in C57BL/6 mouse assessed as tumor growth inhibition at 50 mg/kg/day, po administered from day 6 to 10 post transplantation measured on day 12 relative to control2010Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8
Optimization of phenyl-substituted benzimidazole carboxamide poly(ADP-ribose) polymerase inhibitors: identification of (S)-2-(2-fluoro-4-(pyrrolidin-2-yl)phenyl)-1H-benzimidazole-4-carboxamide (A-966492), a highly potent and efficacious inhibitor.
AID1697662Induction of cell cycle arrest in rat RG2 cells assessed as CDK4 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1729711Inhibition of colony formation in human GSC-18 cells assessed as decrease in number of tumor spheres at 15 uM after 2 weeks by crystal violet staining based assay2021European journal of medicinal chemistry, Jan-15, Volume: 210Structures/cytotoxicity/selectivity relationship of natural steroidal saponins against GSCs and primary mechanism of tribulosaponin A.
AID7469Potentiation of growth inhibition of A2780 cells along with 10 uM NU1085 in experiment 22000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 9. Synthesis and biological properties of benzimidazole inhibitors of the DNA repair enzyme poly(ADP-ribose) polymerase.
AID1583449Permeability in dog MDCK2 cells assessed as reduction in barrier integrity measured within 7 hrs by transendothelial electric resistance measurement assay2020Journal of medicinal chemistry, 02-27, Volume: 63, Issue:4
Identification of Parthenolide Dimers as Activators of Pyruvate Kinase M2 in Xenografts of Glioblastoma Multiforme in Vivo.
AID1825342Induction of morphological changes in human U-87 MG cells assessed as membrane blebbing at 1408 uM measured after 72 hrs by phase contrast microscopy2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1876523Induction of apoptosis in human U-251 cells assessed as viable cells at 6 uM incubated for 72 hrs by Annexin V-FITC/PI staining based flow cytometry method (Rvb = 96.22 %)2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1697641Induction of cell cycle arrest in human DBTRG-05MG cells assessed as CDK4 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1316635Drug level in Sprague-Dawley rat brain at 10 mg/kg, iv after 90 mins by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID712156Cytotoxicity against human U251 cells after 5 days by MTT assay2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1546666Cytotoxicity against human U251 cells incubated for 24 hrs by MTT assay2020Journal of natural products, 01-24, Volume: 83, Issue:1
Antcamphorols A-K, Cytotoxic and ROS Scavenging Triterpenoids from
AID1697754Induction of apoptosis in human DBTRG-05MG cells assessed as phosphorylated PARP expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID766232Chemosensitization of MMR-deficient human A2780/CP70 cells after 5 days by MTT assay2013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID1317842Antiproliferative activity against human MES-SA cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1317839Antiproliferative activity against patient-derived TMZ-resistant GBM 031810 cells over-expressing MGMT after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1697642Induction of cell cycle arrest in human DBTRG-05MG cells assessed as CyclinD1 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697728Induction of apoptosis in human DBTRG-05MG cells assessed as increase in chromatin condensation at 206 uM after 48 hrs by TUNEL assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697660Induction of cell cycle arrest in rat RG2 cells assessed as p53 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1054219Induction of apoptosis in human SK-MEL-30 cells assessed as apoptotic/necrotic cells at 50 uM after 48 hrs by APC-labeled annexin V and 7-AAD staining-based flow cytometric analysis relative to control2013European journal of medicinal chemistry, , Volume: 70Synthesis and evaluation of N-acylamino acids derivatives of triazenes. Activation by tyrosinase in human melanoma cell lines.
AID712157Prodrug conversion in citrate-phosphate buffer at pH 8 assessed as half life of compound2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1697665Induction of cell cycle arrest in rat RG2 cells assessed as CyclinA expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID667957Growth inhibition of human T98G cells after 72 hrs by MTT assay2012European journal of medicinal chemistry, Aug, Volume: 54N-Aryl-N'-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: screening, synthesis of simplified derivatives, and structure-activity relationship analysis.
AID1537887Cytotoxicity against patient-isolated primary glioblastoma cells derived adherent cells assessed as reduction in cell viability at 50 uM measured after 72 hrs by chemiluminescence-based assay2019Journal of medicinal chemistry, 04-25, Volume: 62, Issue:8
Carbonic Anhydrase XII Inhibitors Overcome Temozolomide Resistance in Glioblastoma.
AID1623804In-vivo inhibition of cell proliferation in human U87MG cells xenografted in BALB/c nude mouse at 50 mg/kg, ip after 14 days by Ki-67b-staining based assay2019Journal of medicinal chemistry, 02-14, Volume: 62, Issue:3
Design of Novel Inhibitors of Human Thymidine Phosphorylase: Synthesis, Enzyme Inhibition, in Vitro Toxicity, and Impact on Human Glioblastoma Cancer.
AID1497085Cytotoxicity against human L02 cells assessed as reduction in cell viability after 72 hrs by MTT assay2018Bioorganic & medicinal chemistry letters, 07-15, Volume: 28, Issue:13
Design, synthesis and biological evaluation of artemisinin derivatives containing fluorine atoms as anticancer agents.
AID1697464Cytotoxicity against rat RG2 cells assessed as reduction in cell viability after 48 hrs by MTT assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1316647Antitumor activity against human U87MG cells orthotopically xenografted in Harlan nude mouse brain assessed as increase in mouse survival at 50 umol/kg, iv administered once daily for 5 days2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1240666Antitumor activity against human Capan1 cells xenografted in athymic nu/nu mouse assessed as tumor growth inhibition at 50 mg/kg administered for 5 days2015Journal of medicinal chemistry, Sep-10, Volume: 58, Issue:17
Discovery of 2-[1-(4,4-Difluorocyclohexyl)piperidin-4-yl]-6-fluoro-3-oxo-2,3-dihydro-1H-isoindole-4-carboxamide (NMS-P118): A Potent, Orally Available, and Highly Selective PARP-1 Inhibitor for Cancer Therapy.
AID1736280Selectivity index, ratio of CC50 for Wistar rat astrocytes to EC50 for human U-251 MG cells2020European journal of medicinal chemistry, Mar-01, Volume: 189Efficient identification of novel anti-glioma lead compounds by machine learning models.
AID1250159Cytotoxicity against human Glioma cells (HF2885) at 50 uM after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID101599Inhibitory concentration of compound against Mer+ breast tumor cell line MCF-72000Bioorganic & medicinal chemistry letters, Oct-16, Volume: 10, Issue:20
Design and synthesis of a novel water soluble benzotetrazepinone.
AID1830966Antitumor activity against human U-87MG cells xenografted in BALB/c mouse assessed as reduction in tumor volume at 30 mg/kg, po administered once daily for 5 days and measured on day 32 by MRI scanner
AID1416901Growth inhibition of MGMT-transfected human U373 cells expressing MGMT after 7 days by MTT assay
AID209544In vitro cytotoxicity against mouse TLX5 lymphoma cells1995Journal of medicinal chemistry, Apr-28, Volume: 38, Issue:9
Antitumor imidazotetrazines. 32. Synthesis of novel imidazotetrazinones and related bicyclic heterocycles to probe the mode of action of the antitumor drug temozolomide.
AID668217Antiproliferative activity against human U87 cells after 5 days by MTT assay2012Bioorganic & medicinal chemistry letters, Jul-01, Volume: 22, Issue:13
New substituted 4H-chromenes as anticancer agents.
AID1697779Induction of apoptosis in rat RG2 cells assessed as cleaved PARP expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1305718Antitumor activity against MCT1 expressing mouse GL261 cells coexpressing luc2 syngrafted in C57BL/6 mouse assessed as tumor growth inhibition at 20 mg/kg, ip qd2016Bioorganic & medicinal chemistry letters, 07-15, Volume: 26, Issue:14
Coumarin carboxylic acids as monocarboxylate transporter 1 inhibitors: In vitro and in vivo studies as potential anticancer agents.
AID1623803Anti-angiogenic activity in tumor of human U87MG cells xenografted in nude BALB/c mouse assessed as reduction in CD31 staining at 50 mg/kg, ip administered for 14 days by immunohistochemistry2019Journal of medicinal chemistry, 02-14, Volume: 62, Issue:3
Design of Novel Inhibitors of Human Thymidine Phosphorylase: Synthesis, Enzyme Inhibition, in Vitro Toxicity, and Impact on Human Glioblastoma Cancer.
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).
AID1250157Cytotoxicity against human Glioma cells (HF2790) at 50 uM after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1545833Antiproliferative activity against human GBM95 cells assessed as reduction in cell viability after 72 hrs by MTT assay2019European journal of medicinal chemistry, Dec-01, Volume: 1831,2,3-Triazole-containing hybrids as potential anticancer agents: Current developments, action mechanisms and structure-activity relationships.
AID1697619Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at G2/M phase at 206 uM after 24 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 20.04 +/- 0.55%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID712164Cytotoxicity against human DLD1 cells after 5 days by MTT assay2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1200320Antiproliferative activity against human MES-SA/Dx5 cells assessed as reduction in cell viability after 48 hrs by MTT assay2015Journal of medicinal chemistry, Mar-12, Volume: 58, Issue:5
Activity of 2-aryl-2-(3-indolyl)acetohydroxamates against drug-resistant cancer cells.
AID1595387Induction of apoptosis in human SH-SY5Y cells assessed as increase in early apoptotic cells at 10 uM incubated for 48 hrs by annexinV-PE/7-AAD staining based flow cytometric analysis2019European journal of medicinal chemistry, Jun-15, Volume: 172Targeting gliomas with triazene-based hybrids: Structure-activity relationship, mechanistic study and stability.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1416898Growth inhibition of vehicle-transfected human SNB19 cells after 7 days by MTT assay
AID1054221Induction of apoptosis in human MNT1 cells assessed as apoptotic/necrotic cells at 50 uM after 48 hrs by APC-labeled annexin V and 7-AAD staining-based flow cytometric analysis relative to control2013European journal of medicinal chemistry, , Volume: 70Synthesis and evaluation of N-acylamino acids derivatives of triazenes. Activation by tyrosinase in human melanoma cell lines.
AID1876564Antitumor activity against human U-87 MG cells xenografted in BALB/c mouse assessed as decrease in tumor weight at 10 mg/kg,ip bid for 1 month2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1497083Cytotoxicity against human A549 cells assessed as reduction in cell viability after 72 hrs by MTT assay2018Bioorganic & medicinal chemistry letters, 07-15, Volume: 28, Issue:13
Design, synthesis and biological evaluation of artemisinin derivatives containing fluorine atoms as anticancer agents.
AID1767410Antitumor activity against rat C6 cells inoculated orthotopic Sprague-Dawley rat model assessed as reduction tumor weight at 50 mg/kg, ip twice a day treated 3 days after tumor cell injection measured for 13 days after tumor implantation
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID673621Antitumor activity against B16F10 tumor xenografted in C57BL/6 mouse assessed as tumor growth inhibition at 50 mg/kg/day, po administered QD from day 5 to day 10 post-tumor implantation2012Bioorganic & medicinal chemistry, Aug-01, Volume: 20, Issue:15
Discovery and SAR of orally efficacious tetrahydropyridopyridazinone PARP inhibitors for the treatment of cancer.
AID1317841Antiproliferative activity against patient-derived paclitaxel-resistant NCI-H2073 cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1771786Cytotoxicity against human A 172 cells assessed as cell viability measured after 96 hrs by XTT assay2021European journal of medicinal chemistry, Dec-05, Volume: 225Targeted methylation facilitates DNA double strand breaks and enhances cancer suppression: A DNA intercalating/methylating dual-action chimera Amonafidazene.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID766231Chemosensitization of human A2780 cells after 5 days by MTT assay in presence of MGMT inactivator PaTrin22013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID683689Cytotoxicity against human U138MG cells incubated for 48 hrs by MTT assay2012European journal of medicinal chemistry, Nov, Volume: 57Selective cytotoxicity and apoptosis induction in glioma cell lines by 5-oxygenated-6,7-methylenedioxycoumarins from Pterocaulon species.
AID1697713Inhibition of p38 phosphorylation at Tyr182 residues in rat RG2 cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1769428Cytotoxicity against mouse B16-F10 cells assessed as reduction in cell viability incubated for 72 hrs by MTS assay2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Sulfur Analogues of Tyrosine in the Development of Triazene Hybrid Compounds: A New Strategy against Melanoma.
AID712167Cytotoxicity against human A2780 cells after 5 days by MTT assay in presence of 10 uM MGMT inactivator Patrin22012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1697666Induction of cell cycle arrest in rat RG2 cells assessed as CyclinB1 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1335506Cytotoxicity against Wistar rat C6 cells assessed as decrease in cell viability at 100 uM after 72 hrs by MTT assay relative to control2016European journal of medicinal chemistry, Nov-29, Volume: 124Thiazolidin-4-ones from 4-(methylthio)benzaldehyde and 4-(methylsulfonyl)benzaldehyde: Synthesis, antiglioma activity and cytotoxicity.
AID1697463Cytotoxicity against rat RG2 cells assessed as reduction in cell viability after 24 hrs by MTT assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1809101Cytotoxicity effect against human LN-229 cells assessed as cell growth inhibition incubated for 48 hrs by trypan blue exclusion assay2021Journal of medicinal chemistry, 08-12, Volume: 64, Issue:15
Synthesis and Preclinical Validation of Novel Indole Derivatives as a GPR17 Agonist for Glioblastoma Treatment.
AID1317838Antiproliferative activity against patient-derived TMZ-sensitive GBM 090909 cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1697643Induction of cell cycle arrest in human DBTRG-05MG cells assessed as CDK2 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID386714Toxicity in human SW620 cells xenografted mouse assessed as maximum mean body weight loss after 3 days2008Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20
4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID712162Cytotoxicity against human PANC1 cells after 5 days by MTT assay2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID52525Cytotoxicity of compound in COLO 205 cell line2000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 8. Inhibition of O(6)-alkylguanine-DNA alkyltransferase by O(6)-alkenyl-, O(6)-cycloalkenyl-, and O(6)-(2-oxoalkyl)guanines and potentiation of temozolomide cytotoxicity in vitro by O(6)-(1-cyclopentenylmethyl)guanine.
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).
AID1595388Induction of apoptosis in human SH-SY5Y cells assessed as reduction in cell viability at 10 uM incubated for 48 hrs by annexinV-PE/7-AAD staining based flow cytometric analysis2019European journal of medicinal chemistry, Jun-15, Volume: 172Targeting gliomas with triazene-based hybrids: Structure-activity relationship, mechanistic study and stability.
AID1697563Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at G0/G1 phase at 206 uM after 6 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 47.16 +/- 1.55%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID672002Toxicity in C57BL/6 mouse bearing B16F10 tumor assessed as body weight loss at 50 mg/kg/day, po administered QD from day 5 to day 10 post-tumor implantation relative to vehicle-treated control2012Bioorganic & medicinal chemistry, Aug-01, Volume: 20, Issue:15
Discovery and SAR of orally efficacious tetrahydropyridopyridazinone PARP inhibitors for the treatment of cancer.
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).
AID1473740Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID712168Cytotoxicity against human A2780 cells after 5 days by MTT assay2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
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
AID661464Cytotoxicity against mouse astrocytes assessed as decrease in cell viability at 1 to 100 uM after 48 hrs by neutral red incorporation assay2012Journal of medicinal chemistry, Mar-08, Volume: 55, Issue:5
Oxaphosphinanes: new therapeutic perspectives for glioblastoma.
AID1876490Antiproliferative activity against human U-87 MG cells assessed as inhibition of cell proliferation measured after 72 hrs by CCK8 assay2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1697645Induction of cell cycle arrest in human DBTRG-05MG cells assessed as CyclinB1 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1767416Antitumor activity against rat C6 cells inoculated orthotopic Sprague-Dawley rat model assessed as decrease in p-STAT3 in tumor tissue at 50 mg/kg, ip twice a day treated 3 days after tumor cell injection measured for 13 days after tumor implantation by W
AID1254859Tumoricidal effect in patient derived GBM 464T cells assessed as reduction in neurosphere formation at 20 uM after 1 to 2 weeks by 3D tumor clonogenic assay2015European journal of medicinal chemistry, Oct-20, Volume: 103Discovery of potent and selective cytotoxic activity of new quinazoline-ureas against TMZ-resistant glioblastoma multiforme (GBM).
AID282553Antitumor activity against human NCI CNS cancer cell line panel2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1771789Cytotoxicity against human MDA-MB-238 cells assessed as cell viability measured after 96 hrs by XTT assay2021European journal of medicinal chemistry, Dec-05, Volume: 225Targeted methylation facilitates DNA double strand breaks and enhances cancer suppression: A DNA intercalating/methylating dual-action chimera Amonafidazene.
AID1697749Induction of apoptosis in human DBTRG-05MG cells assessed as Bax expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID667960Selectivity index, ratio of IC50 for mouse astrocytes to IC50 for human U373 cells2012European journal of medicinal chemistry, Aug, Volume: 54N-Aryl-N'-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: screening, synthesis of simplified derivatives, and structure-activity relationship analysis.
AID1697752Induction of apoptosis in human DBTRG-05MG cells assessed as phosphorylated caspace-3 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1661315Antiproliferative activity against rat C6 cells assessed as inhibition of cell proliferation at 500 uM after 24 hrs by MTT assay relative to control2020ACS medicinal chemistry letters, Jul-09, Volume: 11, Issue:7
Antiglioma Activity of Aryl and Amido-Aryl Acetamidine Derivatives Targeting iNOS: Synthesis and Biological Evaluation.
AID1317837Antiproliferative activity against drug-resistant human A549 cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1250160Cytotoxicity against human Glioma cells (HF3013) at 50 uM after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1736296Antitumor activity against C57BL/6 mouse GL261 cells xenografted in C57BL/6 mouse assessed as reduction in tumor volume at 20 mg/kg, po administered via gavage once daily for 10 days starting from 7 days post tumor cell inoculation and measured on day 172020European journal of medicinal chemistry, Mar-01, Volume: 189Efficient identification of novel anti-glioma lead compounds by machine learning models.
AID1783998Cytotoxicity against cold atmospheric plasma (CAP)-treated human U-251MG cells assessed as decrease in cell viability treated with CAP for 30 secs followed by incubated with compound for 6 days by alamar blue assay2021European journal of medicinal chemistry, Nov-15, Volume: 224Enhanced pyrazolopyrimidinones cytotoxicity against glioblastoma cells activated by ROS-Generating cold atmospheric plasma.
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).
AID712159Cytotoxicity against human A549 cells after 5 days by MTT assay2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1767411Antitumor activity against rat C6 cells inoculated orthotopic Sprague-Dawley rat model assessed as reduction tumor volume at 50 mg/kg, ip twice a day treated 3 days after tumor cell injection measured for 13 days after tumor implantation
AID766228Ratio of IC50 for human A2780 cells to IC50 for human A2780 cells in presence of MGMT inactivator PaTrin22013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID1316637Ratio of AUC in brain to plasma of Sprague-Dawley rat at 10 mg/kg, iv after 30 to 180 mins by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1697807Induction of DNA damage in rat RG2 cells assessed as Chk2 phosphorylation at Thr68 at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID766226Chemosensitization of MGMT-deficient human SNB19 cells after 5 days by MTT assay2013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID1497084Cytotoxicity against human A375 cells assessed as reduction in cell viability after 72 hrs by MTT assay2018Bioorganic & medicinal chemistry letters, 07-15, Volume: 28, Issue:13
Design, synthesis and biological evaluation of artemisinin derivatives containing fluorine atoms as anticancer agents.
AID1537885Substrate activity at P-gp in patient-isolated primary glioblastoma cells derived neurospheres assessed as reduction in P-gp ATPase activity at 50 uM after 48 hrs by spectrophotometric method2019Journal of medicinal chemistry, 04-25, Volume: 62, Issue:8
Carbonic Anhydrase XII Inhibitors Overcome Temozolomide Resistance in Glioblastoma.
AID1825316Cytotoxicity against human SH-SY5Y cells assessed as cell viability at 2000 uM incubated upto 72 hrs by MTT assay2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1697609Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at S phase at 206 uM after 12 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 20.15 +/- 2.44%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697803Induction of DNA damage in rat RG2 cells assessed as ATR phosphorylation at ser428 residues at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID766227Chemosensitization of human A2058 cells after 5 days by MTT assay2013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID1697730Induction of apoptosis in human DBTRG-05MG cells assessed as increase in apoptotic body formation at 206 uM after 48 hrs by TUNEL assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
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).
AID712158Prodrug conversion in citrate-phosphate buffer at pH 7.4 assessed as half life of compound2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID766230Chemoseinsitizatioin of MMR-deficieint humain A2780/CP70 cells after 5 days by MTT assay in preseince of MGMT iinactivator PaTriin22013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID1316642Cytotoxicity against human U87MG cells assessed as inhibition of cell growth at 100 uM after 72 hrs by MTS assay2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID672001Toxicity in C57BL/6 mouse bearing B16F10 tumor assessed as body weight loss at 50 mg/kg/day, po administered QD from day 5 to day 9 post-tumor implantation relative to vehicle-treated control2012Bioorganic & medicinal chemistry, Aug-01, Volume: 20, Issue:15
Discovery and SAR of orally efficacious tetrahydropyridopyridazinone PARP inhibitors for the treatment of cancer.
AID1316655AUC in Sprague-Dawley rat plasma at 10 mg/kg, iv after 30 to 180 mins by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1181988Cytotoxicity against human HeLa cells assessed as reduction in cell viability after 24 to 48 hrs by MTT assay2014Bioorganic & medicinal chemistry letters, Aug-01, Volume: 24, Issue:15
New benzothieno[3,2-d]-1,2,3-triazines with antiproliferative activity: synthesis, spectroscopic studies, and biological activity.
AID1553327Antiproliferative activity against patient-derived GBM cells assessed as cell viability after 48 hrs by 5-Ethynyl-2'-deoxyuridine incorporation assay2019Bioorganic & medicinal chemistry letters, 09-15, Volume: 29, Issue:18
The synthesis of a novel Crizotinib heptamethine cyanine dye conjugate that potentiates the cytostatic and cytotoxic effects of Crizotinib in patient-derived glioblastoma cell lines.
AID1426002Cytotoxicity against MDCK cells expressing carbonic anhydrase 9 assessed as reduction in cell viability incubated for 24 hrs measured after 7 days under normoxic condition by methylene blue staining based clonogenic survival assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID1316652Drug level in mouse brain assessed as compound level in soluble tissue fraction at 10 uM after 1 hr by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1623798Antitumor activity against human U87MG cells xenografted in BALB/c nude mouse assessed as tumor growth inhibition 50 mg/kg/day, ip administered for 14 days2019Journal of medicinal chemistry, 02-14, Volume: 62, Issue:3
Design of Novel Inhibitors of Human Thymidine Phosphorylase: Synthesis, Enzyme Inhibition, in Vitro Toxicity, and Impact on Human Glioblastoma Cancer.
AID1546667Cytotoxicity against human MCF7 cells incubated for 24 hrs by MTT assay2020Journal of natural products, 01-24, Volume: 83, Issue:1
Antcamphorols A-K, Cytotoxic and ROS Scavenging Triterpenoids from
AID15820Alkylating activity (0.1 mM) was determined at pH 7.4; expressed as OD (540n m)/mM of drug)2003Bioorganic & medicinal chemistry letters, Oct-06, Volume: 13, Issue:19
Synthesis of pyrimidinopyridine-triazene conjugates targeted to abl tyrosine kinase.
AID1426001Cytotoxicity against carbonic anhydrase 9 knockdown MDCK cells assessed as reduction in cell viability incubated for 24 hrs measured after 7 days under normoxic condition by methylene blue staining based clonogenic survival assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID1426004Cytotoxicity against MDCK cells expressing carbonic anhydrase 9 assessed as reduction in cell viability incubated for 24 hrs measured after 7 days under hypoxic condition by methylene blue staining based clonogenic survival assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID668218Antiproliferative activity against human LN18 cells after 5 days by MTT assay2012Bioorganic & medicinal chemistry letters, Jul-01, Volume: 22, Issue:13
New substituted 4H-chromenes as anticancer agents.
AID1486366Cytotoxicity against human MNT1 cells after 72 hrs by MTS assay2017Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15
The selective cytotoxicity of new triazene compounds to human melanoma cells.
AID1316631Plasma concentration in Sprague-Dawley rat plasma at 10 mg/kg, iv after 30 mins by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID712161Cytotoxicity against human HCT116 cells after 5 days by MTT assay2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID588210Human drug-induced liver injury (DILI) modelling dataset from Ekins et al2010Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 38, Issue:12
A predictive ligand-based Bayesian model for human drug-induced liver injury.
AID1663800Antiproliferative activity against human patient derived GBM cells assessed as reduction in cell proliferation up to 100 uM measured after 48 hrs by Edu incorporation assay2020Bioorganic & medicinal chemistry letters, 07-15, Volume: 30, Issue:14
PARP inhibitor cyanine dye conjugate with enhanced cytotoxic and antiproliferative activity in patient derived glioblastoma cell lines.
AID1771779Induction of DNA methylation in human HCT-116 cells assessed as reduction of MGMT expression at 200 uM measured after 48 hrs by Western blot assay relative to control2021European journal of medicinal chemistry, Dec-05, Volume: 225Targeted methylation facilitates DNA double strand breaks and enhances cancer suppression: A DNA intercalating/methylating dual-action chimera Amonafidazene.
AID1697340Antitumor activity against SW-620 cells xenografted in Balb/c mouse assessed as tumor growth suppression at 50 mg/kg, po administered once daily for 5 days2020Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19
Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID712163Cytotoxicity against human HT-29 cells after 5 days by MTT assay2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1888341Antiproliferative activity against human T98G cells assessed as cell growth inhibition incubated for 96 hrs by CellTiter-Glo luminescent cell viability assay
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).
AID1851871Cytotoxicity against human U-251 cells assessed as reduction in cell viability at 5 to 50 uM incubated for 24 hrs by MTS assay
AID1736285Antiproliferative activity against rat C6 cells assessed as cell growth inhibition measured after 72 hrs by SRB assay2020European journal of medicinal chemistry, Mar-01, Volume: 189Efficient identification of novel anti-glioma lead compounds by machine learning models.
AID7468Potentiation of growth inhibition of A2780 cells along with 10 uM NU1085 in experiment 12000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 9. Synthesis and biological properties of benzimidazole inhibitors of the DNA repair enzyme poly(ADP-ribose) polymerase.
AID1771792Induction of DNA methylation in human HCT-116 cells assessed as reduction of MGMT expression at 400 uM measured after 48 hrs by Western blot assay relative to control2021European journal of medicinal chemistry, Dec-05, Volume: 225Targeted methylation facilitates DNA double strand breaks and enhances cancer suppression: A DNA intercalating/methylating dual-action chimera Amonafidazene.
AID1697775Induction of apoptosis in rat RG2 cells assessed as cleaved caspace-9 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1595389Induction of apoptosis in human SH-SY5Y cells assessed as increase in late necrotic cells at 10 uM incubated for 48 hrs by annexinV-PE/7-AAD staining based flow cytometric analysis2019European journal of medicinal chemistry, Jun-15, Volume: 172Targeting gliomas with triazene-based hybrids: Structure-activity relationship, mechanistic study and stability.
AID1623805Induction of apoptosis in human U87MG cells xenografted in BALB/c nude mouse assessed as caspase-3 levels at 50 mg/kg, ip after 14 days by immunohistochemistry2019Journal of medicinal chemistry, 02-14, Volume: 62, Issue:3
Design of Novel Inhibitors of Human Thymidine Phosphorylase: Synthesis, Enzyme Inhibition, in Vitro Toxicity, and Impact on Human Glioblastoma Cancer.
AID1697773Induction of apoptosis in rat RG2 cells assessed as Bax expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1851873Cytotoxicity against human T98G cells assessed as reduction in cell viability at 10 uM incubated for 24 hrs by MTS assay
AID1809102Cytotoxicity effect against human SNB-19 cells assessed as cell growth inhibition incubated for 48 hrs by trypan blue exclusion assay2021Journal of medicinal chemistry, 08-12, Volume: 64, Issue:15
Synthesis and Preclinical Validation of Novel Indole Derivatives as a GPR17 Agonist for Glioblastoma Treatment.
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]
AID766229Ratio of IC50 for MMR-deficient human A2780/CP70 cells to IC50 for human A2780 cells in presence of MGMT inactivator PaTrin22013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID1825341Induction of morphological changes in human U-87 MG cells assessed as appearance of shrunken cell bodies at 1408 uM measured after 72 hrs by phase contrast microscopy2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1316636Drug level in Sprague-Dawley rat brain at 10 mg/kg, iv after 180 mins by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1825320Cytotoxicity against human U-87 MG cells assessed as cell viability at 10000 uM incubated upto 72 hrs by MTT assay2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1474439Anti-tumor activity against human MX1 cells xenografted in BALB/c mouse assessed as tumor weight at 50 mg/kg, po administered once daily via gavage for 5 days measured after 11 days (Rvb = 4.09 +/- 0.64 g)2017European journal of medicinal chemistry, May-26, Volume: 132Discovery of 2-substituted 1H-benzo[d]immidazole-4-carboxamide derivatives as novel poly(ADP-ribose)polymerase-1 inhibitors with in vivo anti-tumor activity.
AID540209Volume of distribution at steady state in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID474420Antitumor activity against mouse B16F10 cells transplanted in C57BL/6 mouse assessed as tumor volume at 50 mg/kg/day, po administered from day 6 to 10 post transplantation measured on day 12 relative to control2010Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8
Optimization of phenyl-substituted benzimidazole carboxamide poly(ADP-ribose) polymerase inhibitors: identification of (S)-2-(2-fluoro-4-(pyrrolidin-2-yl)phenyl)-1H-benzimidazole-4-carboxamide (A-966492), a highly potent and efficacious inhibitor.
AID1317843Antiproliferative activity against human MES-SA/Dx5 cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID1888345Antiproliferative activity against human T98G cells assessed as cell viability at 94 uM incubated for 96 hrs by CellTiter-Glo luminescent cell viability assay relative to control
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]
AID712149Ratio of IC50 for human A2780 cells to IC50 for MMR-deficient human A2780/CP70 cells in presence of 10 uM MGMT inactivator Patrin22012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1767412Antitumor activity against rat C6 cells inoculated orthotopic Sprague-Dawley rat model assessed as tumor growth inhibition at 50 mg/kg, ip twice a day treated 3 days after tumor cell injection measured for 13 days after tumor implantation
AID209983In vitro cytotoxicity against mouse TLX5 lymphoma cells2002Journal of medicinal chemistry, Dec-05, Volume: 45, Issue:25
Antitumor imidazotetrazines. 41. Conjugation of the antitumor agents mitozolomide and temozolomide to peptides and lexitropsins bearing DNA major and minor groove-binding structural motifs.
AID1697776Induction of apoptosis in rat RG2 cells assessed as phosphorylated caspace-3 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1316639Induction of DNA alkylation in human U87MG cells assessed as increase in O6-MedG formation at 10 to 100 uM after 3 hrs by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1763425Cytotoxicity against human SW480 cells by MTT assay2021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Chemical modifications of ergostane-type triterpenoids from Antrodia camphorata and their cytotoxic activities.
AID7470Potentiation factor at 50% growth inhibition (IC50 of compound to that of compound along with PARP inhibitor) in experiment 12000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 9. Synthesis and biological properties of benzimidazole inhibitors of the DNA repair enzyme poly(ADP-ribose) polymerase.
AID1651753Cytotoxicity against human U87MG cells assessed as reduction in cell viability after 48 hrs under hypoxia condition by MTT assay2020Journal of natural products, 04-24, Volume: 83, Issue:4
Boholamide A, an APD-Class, Hypoxia-Selective Cyclodepsipeptide.
AID1316640Induction of DNA alkylation in human U87MG cells assessed as increase in N7-MedG formation after 3 hrs by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1697732Induction of apoptosis in rat RG2 cells assessed as increase in DNA fragmentation at 206 uM after 48 hrs by TUNEL assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697682Effect on AKT expression in human DBTRG-05MG cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1830975Toxicity in BALB/c mouse xenografted with human U-87MG cells assessed as effect on body weight at 30 mg/kg, po administered once daily for 5 days and measured on day 8 (Rvb = 19 +/- 1 g)
AID26696Half-life period in 95% ethanol in diffuse laboratory light at 28 degrees celsius1984Journal of medicinal chemistry, Feb, Volume: 27, Issue:2
Antitumor imidazotetrazines. 1. Synthesis and chemistry of 8-carbamoyl-3-(2-chloroethyl)imidazo[5,1-d]-1,2,3,5-tetrazin-4(3 H)-one , a novel broad-spectrum antitumor agent.
AID1697806Induction of DNA damage in human DBTRG-05MG cells assessed as Chk2 phosphorylation at Thr68 residues at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID668220Cytotoxicity against mouse primary astrocytes after 5 days by MTT assay2012Bioorganic & medicinal chemistry letters, Jul-01, Volume: 22, Issue:13
New substituted 4H-chromenes as anticancer agents.
AID1888347Antiproliferative activity against human T98G cells assessed as cell viability at 375 uM incubated for 96 hrs by CellTiter-Glo luminescent cell viability assay relative to control
AID1825318Cytotoxicity against human U-87 MG cells assessed as cell viability at 100 uM incubated upto 72 hrs by MTT assay2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1200321Antiproliferative activity against human GBM 031810 cells assessed as reduction in cell viability after 48 hrs by MTT assay2015Journal of medicinal chemistry, Mar-12, Volume: 58, Issue:5
Activity of 2-aryl-2-(3-indolyl)acetohydroxamates against drug-resistant cancer cells.
AID1697644Induction of cell cycle arrest in human DBTRG-05MG cells assessed as CyclinA expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1595392Antiinvasive activity in mouse GL261 cells assessed as reduction in cell migration at 10 uM preincubated for 48 hrs and measured after 6 hrs by giemsa staining based Boyden chamber assay2019European journal of medicinal chemistry, Jun-15, Volume: 172Targeting gliomas with triazene-based hybrids: Structure-activity relationship, mechanistic study and stability.
AID1274559Antiproliferative activity against human H4 cells after 48 hrs by MTT assay2015Journal of natural products, Dec-24, Volume: 78, Issue:12
Phomanolides A and B from the Fungus Phoma sp.: Meroterpenoids Derived from a Putative Tropolonic Sesquiterpene via Hetero-Diels-Alder Reactions.
AID1262127Antiproliferative activity against human ANGM-CSS cells assessed as inhibition of cell growth at 100 uM after 72 hrs by WST1 assay2015European journal of medicinal chemistry, Nov-13, Volume: 105Design and synthesis of 2-oxindole based multi-targeted inhibitors of PDK1/Akt signaling pathway for the treatment of glioblastoma multiforme.
AID1783996Cytotoxicity against human U-251MG cells assessed as decrease in cell viability incubated for 6 days by alamar blue assay2021European journal of medicinal chemistry, Nov-15, Volume: 224Enhanced pyrazolopyrimidinones cytotoxicity against glioblastoma cells activated by ROS-Generating cold atmospheric plasma.
AID1250158Cytotoxicity against human Glioma cells (HF2876) at 50 uM after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1697664Induction of cell cycle arrest in rat RG2 cells assessed as CDK2 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697574Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at G2/M phase at 206 uM after 12 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 30.08 +/- 0.1%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID661450Antiproliferative activity against human SF295 cells at 10 uM after 24 hrs by SRB assay2012Journal of medicinal chemistry, Mar-08, Volume: 55, Issue:5
Oxaphosphinanes: new therapeutic perspectives for glioblastoma.
AID1697663Induction of cell cycle arrest in rat RG2 cells assessed as CyclinD1 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1595380Stability of the compound in PBS buffer at pH 7.4 assessed as half life by HPLC analysis2019European journal of medicinal chemistry, Jun-15, Volume: 172Targeting gliomas with triazene-based hybrids: Structure-activity relationship, mechanistic study and stability.
AID26695Half-life period in 95% ethanol in dark at 28 degrees celsius.1984Journal of medicinal chemistry, Feb, Volume: 27, Issue:2
Antitumor imidazotetrazines. 1. Synthesis and chemistry of 8-carbamoyl-3-(2-chloroethyl)imidazo[5,1-d]-1,2,3,5-tetrazin-4(3 H)-one , a novel broad-spectrum antitumor agent.
AID1274558Antiproliferative activity against human U251 cells after 48 hrs by MTT assay2015Journal of natural products, Dec-24, Volume: 78, Issue:12
Phomanolides A and B from the Fungus Phoma sp.: Meroterpenoids Derived from a Putative Tropolonic Sesquiterpene via Hetero-Diels-Alder Reactions.
AID1767415Antitumor activity against rat C6 cells inoculated orthotopic Sprague-Dawley rat model assessed as decrease in VEGF-A in tumor tissue at 50 mg/kg, ip twice a day treated 3 days after tumor cell injection measured for 13 days after tumor implantation by We
AID1697805Induction of DNA damage in rat RG2 cells assessed as Chk1 phosphorylation at ser345 at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697590Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at G0/G1 phase at 206 uM after 48 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 47.16 +/- 1.55%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697777Induction of apoptosis in rat RG2 cells assessed as cleaved caspace-3 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697808Induction of DNA damage in human DBTRG-05MG cells assessed as H2A.X phosphorylation at ser139 residues at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697683Inhibition of AKT phosphorylation at S473 residues in human DBTRG-05MG cells at 206 uM after 48 hrs by Western blot analysis2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1876526Induction of apoptosis in human U-251 cells assessed as necrotic cells at 6 uM incubated for 72 hrs by Annexin V-FITC/PI staining based flow cytometry method (Rvb =0.51 %)2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID661451Antiproliferative activity against human SNB75 cells at 10 uM after 24 hrs by SRB assay2012Journal of medicinal chemistry, Mar-08, Volume: 55, Issue:5
Oxaphosphinanes: new therapeutic perspectives for glioblastoma.
AID1729708Inhibition of colony formation in human GSC-3 cells assessed as tumor spheres damage at 15 uM after 2 weeks by crystal violet staining based assay2021European journal of medicinal chemistry, Jan-15, Volume: 210Structures/cytotoxicity/selectivity relationship of natural steroidal saponins against GSCs and primary mechanism of tribulosaponin A.
AID1697685Inhibition of JNK phosphorylation at Thr183/Tyr185 residues in human DBTRG-05MG cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1316656AUC in Sprague-Dawley rat brain at 10 mg/kg, iv after 30 to 180 mins by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID712165Cytotoxicity against MMR-deficient human A2780/CP70 cells after 5 days by MTT assay2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID7466Potentiation of growth inhibition of A2780 by compound alone in experiment 12000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 9. Synthesis and biological properties of benzimidazole inhibitors of the DNA repair enzyme poly(ADP-ribose) polymerase.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID1200319Antiproliferative activity against human MES-SA cells assessed as reduction in cell viability after 48 hrs by MTT assay2015Journal of medicinal chemistry, Mar-12, Volume: 58, Issue:5
Activity of 2-aryl-2-(3-indolyl)acetohydroxamates against drug-resistant cancer cells.
AID1697802Induction of DNA damage in human DBTRG-05MG cells assessed as ATR phosphorylation at ser428 residues at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1416900Growth inhibition of vehicle-transfected human U373 cells after 7 days by MTT assay
AID1825323Cytotoxicity against human U-87 MG cells using best fit nonlinear regression analysis2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1697686Effect on ERK expression in human DBTRG-05MG cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1254861Tumoricidal effect in patient derived GBM 025T cells assessed as reduction in neurosphere formation at 20 uM after 1 to 2 weeks by 3D tumor clonogenic assay2015European journal of medicinal chemistry, Oct-20, Volume: 103Discovery of potent and selective cytotoxic activity of new quinazoline-ureas against TMZ-resistant glioblastoma multiforme (GBM).
AID1697751Induction of apoptosis in human DBTRG-05MG cells assessed as cleaved caspace-9 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697592Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at G2/M phase at 206 uM after 48 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 30.08 +/- 0.1%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1876491Antiproliferative activity against human U-251 cells assessed as inhibition of cell proliferation measured after 72 hrs by CCK8 assay2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID1316646Antitumor activity against human U87MG cells orthotopically xenografted in Harlan nude mouse brain assessed as induction of slow tumor growth at 50 umol/kg, iv administered once daily for 5 days2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1274557Antiproliferative activity against human SH-SY5Y cells after 48 hrs by MTT assay2015Journal of natural products, Dec-24, Volume: 78, Issue:12
Phomanolides A and B from the Fungus Phoma sp.: Meroterpenoids Derived from a Putative Tropolonic Sesquiterpene via Hetero-Diels-Alder Reactions.
AID1651754Selectivity index, ratio of IC50 for cytotoxicity against human U87MG cells under normoxia condition to IC50 for cytotoxicity against human U87MG cells under hypoxia condition incubated for 48 hrs by MTT assay2020Journal of natural products, 04-24, Volume: 83, Issue:4
Boholamide A, an APD-Class, Hypoxia-Selective Cyclodepsipeptide.
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.
AID282486Half life in plasma2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID588208Literature-mined public compounds from Lowe et al phospholipidosis modelling dataset2010Molecular pharmaceutics, Oct-04, Volume: 7, Issue:5
Predicting phospholipidosis using machine learning.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1888356Induction of apoptosis in human T98G cells assessed as increase in early apoptotic cells at 94 uM measured after 48 to 96 hrs by Annexin V-FITC/PI staining based flow cytometry analysis
AID1736283Antiproliferative activity against human U87MG cells assessed as cell growth inhibition measured after 72 hrs by SRB assay2020European journal of medicinal chemistry, Mar-01, Volume: 189Efficient identification of novel anti-glioma lead compounds by machine learning models.
AID1335505Cytotoxicity against Wistar rat C6 cells assessed as decrease in cell viability at 100 uM after 48 hrs by MTT assay relative to control2016European journal of medicinal chemistry, Nov-29, Volume: 124Thiazolidin-4-ones from 4-(methylthio)benzaldehyde and 4-(methylsulfonyl)benzaldehyde: Synthesis, antiglioma activity and cytotoxicity.
AID1202313Cytotoxicity against human WiDr cells overexpressing MGMT after 48 hrs by trypan blue staining-based hemocytometric analysis2015European journal of medicinal chemistry, , Volume: 96Synthesis and antiproliferative activity of 3-(2-chloroethyl)-5-methyl-6-phenyl-8-(trifluoromethyl)-5,6-dihydropyrazolo[3,4-f][1,2,3,5]tetrazepin-4-(3H)-one.
AID1697599Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at G0/G1 phase at 206 uM after 6 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 57.81 +/- 1.9%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1316644Oral bioavailability in human for 1 to 2 hrs2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1167094Inhibition of neurosphere formation of mouse BXD4687 cells by CCK8 assay2014Journal of medicinal chemistry, Oct-23, Volume: 57, Issue:20
Inhibition of cancer-associated mutant isocitrate dehydrogenases: synthesis, structure-activity relationship, and selective antitumor activity.
AID441950Antitumor activity against mouse B16F10 cells implanted in C57BL/6 mouse at 50 mg/kg, po QD for 5 days measured on day 162009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Synthesis and evaluation of a new generation of orally efficacious benzimidazole-based poly(ADP-ribose) polymerase-1 (PARP-1) inhibitors as anticancer agents.
AID1697708Effect on JNK expression in rat RG2 cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1316650Drug level in rat brain at 103 umol/kg, iv measured 3 hrs post dose by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1736281Selectivity index, ratio of CC50 for Wistar rat astrocytes to EC50 for rat C6 cells2020European journal of medicinal chemistry, Mar-01, Volume: 189Efficient identification of novel anti-glioma lead compounds by machine learning models.
AID1425988Binding affinity to recombinant human carbonic anhydrase 2 after 15 mins by stopped-flow CO2 hydration assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID1769427Cytotoxicity against human MNT-1 cells assessed as reduction in cell viability incubated for 72 hrs by MTS assay2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Sulfur Analogues of Tyrosine in the Development of Triazene Hybrid Compounds: A New Strategy against Melanoma.
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.
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.
AID540213Half life in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID712154Prodrug conversion in citrate-phosphate buffer at pH 7.4 assessed as pseudo-first-order rate constant2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1811267In vivo inhibition of COX2 in ip dosed orthotopic Sprague-Dawley rat model inoculated with C6 cells assessed as reduction in PGE2 production by ELISA2021European journal of medicinal chemistry, Dec-15, Volume: 226N-2-(phenylamino) benzamide derivatives as novel anti-glioblastoma agents: Synthesis and biological evaluation.
AID1697837Antitumour activity against human DBTRG-05MG cells xenografted in BALB/c nude mouse assessed as increase in survival time at 5 mg/kg, ip for 5 days and measured every 2 days2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1623801Anti-angiogenic activity in tumor of human U87MG cells xenografted in nude BALB/c mouse assessed as reduction in VEGF staining at 50 mg/kg, ip administered for 14 days by immunohistochemistry2019Journal of medicinal chemistry, 02-14, Volume: 62, Issue:3
Design of Novel Inhibitors of Human Thymidine Phosphorylase: Synthesis, Enzyme Inhibition, in Vitro Toxicity, and Impact on Human Glioblastoma Cancer.
AID1697731Induction of apoptosis in rat RG2 cells assessed as increase in chromatin condensation at 206 uM after 48 hrs by TUNEL assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1172643Inhibition of cell proliferation of human U87MG cells assessed as cell viability after 72 hrs by sulforhodamine B assay2014Bioorganic & medicinal chemistry letters, Nov-15, Volume: 24, Issue:22
Bioactive triterpenoid saponins and phenolic compounds against glioma cells.
AID1473738Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID84439Cytotoxicity of compound in HT-29 cell line2000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 8. Inhibition of O(6)-alkylguanine-DNA alkyltransferase by O(6)-alkenyl-, O(6)-cycloalkenyl-, and O(6)-(2-oxoalkyl)guanines and potentiation of temozolomide cytotoxicity in vitro by O(6)-(1-cyclopentenylmethyl)guanine.
AID1697583Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at G2/M phase at 206 uM after 24 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 30.08 +/- 0.1%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1425997Cytotoxicity against carbonic anhydrase 9 knockdown MDCK cells assessed as reduction in cell viability after 72 hrs under normoxic condition by Alamar blue assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID667959Growth inhibition of mouse B16F10 cells after 72 hrs by MTT assay2012European journal of medicinal chemistry, Aug, Volume: 54N-Aryl-N'-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: screening, synthesis of simplified derivatives, and structure-activity relationship analysis.
AID1697460Cytotoxicity against human DBTRG-05MG cells assessed as reduction in cell viability after 24 hrs by MTT assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697572Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at G0/G1 phase at 206 uM after 12 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 47.16 +/- 1.55%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID661463Antiproliferative activity against rat C6 cells at 100 uM after 48 hrs by neutral red incorporation assay2012Journal of medicinal chemistry, Mar-08, Volume: 55, Issue:5
Oxaphosphinanes: new therapeutic perspectives for glioblastoma.
AID1697564Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at S phase at 206 uM after 6 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 22.76 +/- 1.56%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1254862Tumoricidal effect in patient derived GBM 448T cells assessed as reduction in neurosphere formation at 20 uM after 1 to 2 weeks by 3D tumor clonogenic assay2015European journal of medicinal chemistry, Oct-20, Volume: 103Discovery of potent and selective cytotoxic activity of new quinazoline-ureas against TMZ-resistant glioblastoma multiforme (GBM).
AID1537886Cytotoxicity against patient-isolated primary glioblastoma cells derived adherent cells assessed as increase in caspase3 cleavage at 50 uM measured after 48 hrs by immunoblotting method2019Journal of medicinal chemistry, 04-25, Volume: 62, Issue:8
Carbonic Anhydrase XII Inhibitors Overcome Temozolomide Resistance in Glioblastoma.
AID1771785Inhibition of DNA Topoisomerase-2 in human MDA-MB-238 cells assessed as generation of DNA double strand breaks measuring gamma-H2AX at incubated for 24 hrs followed by drug washout and measured after 24 to 96 hrs by immunofluorescence assay2021European journal of medicinal chemistry, Dec-05, Volume: 225Targeted methylation facilitates DNA double strand breaks and enhances cancer suppression: A DNA intercalating/methylating dual-action chimera Amonafidazene.
AID1651752Cytotoxicity against human U87MG cells assessed as reduction in cell viability after 48 hrs under normoxia condition by MTT assay2020Journal of natural products, 04-24, Volume: 83, Issue:4
Boholamide A, an APD-Class, Hypoxia-Selective Cyclodepsipeptide.
AID1316651Fraction unbound in mouse brain assessed as compound level in insoluble tissue fraction at 10 uM after 1 hr by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1769429Cytotoxicity against human A-375 cells assessed as reduction in cell viability incubated for 72 hrs by MTS assay2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Sulfur Analogues of Tyrosine in the Development of Triazene Hybrid Compounds: A New Strategy against Melanoma.
AID1825343Induction of morphological changes in human U-87 MG cells assessed as appearance of undergoing apoptosis at 1408 uM measured after 72 hrs by phase contrast microscopy2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID712155Prodrug conversion in citrate-phosphate buffer at pH 4 assessed as pseudo-first-order rate constant2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID766234Half life of the compound at pH 7.42013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID84467Level of AGT activity in HT-29 cell line2000Journal of medicinal chemistry, Nov-02, Volume: 43, Issue:22
Resistance-modifying agents. 8. Inhibition of O(6)-alkylguanine-DNA alkyltransferase by O(6)-alkenyl-, O(6)-cycloalkenyl-, and O(6)-(2-oxoalkyl)guanines and potentiation of temozolomide cytotoxicity in vitro by O(6)-(1-cyclopentenylmethyl)guanine.
AID683688Cytotoxicity against rat C6 cells incubated for 48 hrs by MTT assay2012European journal of medicinal chemistry, Nov, Volume: 57Selective cytotoxicity and apoptosis induction in glioma cell lines by 5-oxygenated-6,7-methylenedioxycoumarins from Pterocaulon species.
AID165776In vitro cytotoxicity against Raji cell line1995Journal of medicinal chemistry, Apr-28, Volume: 38, Issue:9
Antitumor imidazotetrazines. 32. Synthesis of novel imidazotetrazinones and related bicyclic heterocycles to probe the mode of action of the antitumor drug temozolomide.
AID1697626Induction of cell cycle arrest in rat RG2 cells assessed as accumulation at G0/G1 phase at 206 uM after 48 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 57.81 +/- 1.9%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1825311Cytotoxicity against human SH-SY5Y cells using best fit nonlinear regression analysis2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1697711Inhibition of ERK phosphorylation at Tyr204 residues in rat RG2 cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1811285Toxicity in Sprague-Dawley rat inoculated with C6 cells assessed as reduction in body weight at 50 mg/kg, ip bid administered for 14 days2021European journal of medicinal chemistry, Dec-15, Volume: 226N-2-(phenylamino) benzamide derivatives as novel anti-glioblastoma agents: Synthesis and biological evaluation.
AID1697712Effect on p38 expression in rat RG2 cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1771788Cytotoxicity against human NCI-H1299 cells assessed as cell viability measured after 96 hrs by XTT assay2021European journal of medicinal chemistry, Dec-05, Volume: 225Targeted methylation facilitates DNA double strand breaks and enhances cancer suppression: A DNA intercalating/methylating dual-action chimera Amonafidazene.
AID1425990Binding affinity to recombinant human carbonic anhydrase 12 after 15 mins by stopped-flow CO2 hydration assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID712166Cytotoxicity against MMR-deficient human A2780/CP70 cells after 5 days by MTT assay in presence of 10 uM MGMT inactivator Patrin22012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID1697462Cytotoxicity against human DBTRG-05MG cells assessed as reduction in cell viability after 72 hrs by MTT assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697804Induction of DNA damage in human DBTRG-05MG cells assessed as Chk1 phosphorylation at ser345 residues at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1771787Cytotoxicity against human WM 266-4 cells assessed as cell viability measured after 96 hrs by XTT assay2021European journal of medicinal chemistry, Dec-05, Volume: 225Targeted methylation facilitates DNA double strand breaks and enhances cancer suppression: A DNA intercalating/methylating dual-action chimera Amonafidazene.
AID1254860Tumoricidal effect in patient derived GBM 096T cells assessed as reduction in neurosphere formation at 20 uM after 1 to 2 weeks by 3D tumor clonogenic assay2015European journal of medicinal chemistry, Oct-20, Volume: 103Discovery of potent and selective cytotoxic activity of new quinazoline-ureas against TMZ-resistant glioblastoma multiforme (GBM).
AID1825317Cytotoxicity against human SH-SY5Y cells assessed as cell viability at 500 uM incubated upto 72 hrs by MTT assay2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1729710Inhibition of colony formation in human GSC-3 cells assessed as decrease in number of tumor spheres at 15 uM after 2 weeks by crystal violet staining based assay2021European journal of medicinal chemistry, Jan-15, Volume: 210Structures/cytotoxicity/selectivity relationship of natural steroidal saponins against GSCs and primary mechanism of tribulosaponin A.
AID1697748Induction of apoptosis in human DBTRG-05MG cells assessed as Bcl2 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1876513Induction of apoptosis in human U-87 MG cells assessed as necrotic cells at 1.20 uM incubated for 72 hrs by Annexin V-FITC/PI staining based flow cytometry method (Rvb = 0.21 %)2022European journal of medicinal chemistry, Jan-05, Volume: 227Novel piperazine based benzamide derivatives as potential anti-glioblastoma agents inhibiting cell proliferation and cell cycle progression.
AID712160Prodrug conversion in citrate-phosphate buffer at pH 4 assessed as half life of compound2012ACS medicinal chemistry letters, Dec-13, Volume: 3, Issue:12
Strategy for Imidazotetrazine Prodrugs with Anticancer Activity Independent of MGMT and MMR.
AID668216Antiproliferative activity against human T98G cells after 5 days by MTT assay2012Bioorganic & medicinal chemistry letters, Jul-01, Volume: 22, Issue:13
New substituted 4H-chromenes as anticancer agents.
AID1473741Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1595391Induction of morphological changes in mouse GL261 cells assessed as decrease in cell aspect ratio at 10 uM incubated for 48 hrs by Hoechst 33258 staining based fluorescence microscopic analysis2019European journal of medicinal chemistry, Jun-15, Volume: 172Targeting gliomas with triazene-based hybrids: Structure-activity relationship, mechanistic study and stability.
AID1316648Increase in O6-MedG formation in rat brain at 51.5 to 206 umol/kg, iv measured 3 hrs post dose by LC-MS/MS analysis2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
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.
AID1603447Cytotoxicity in TRPV3 expressing human PC3 cells assessed as reduction in cell viability at 200 uM incubated for 24 to 72 hrs by Cell-titer blue assay2019Bioorganic & medicinal chemistry, 06-15, Volume: 27, Issue:12
Natural product-drug conjugates for modulation of TRPV1-expressing tumors.
AID1486367Cytotoxicity against mouse B16F10 cells after 72 hrs by MTS assay2017Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15
The selective cytotoxicity of new triazene compounds to human melanoma cells.
AID1697661Induction of cell cycle arrest in rat RG2 cells assessed as p21 expression at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1537879Down regulation of P-gp expression in patient-isolated primary glioblastoma cells derived neurospheres at 50 uM after 48 hrs by immunoblotting analysis2019Journal of medicinal chemistry, 04-25, Volume: 62, Issue:8
Carbonic Anhydrase XII Inhibitors Overcome Temozolomide Resistance in Glioblastoma.
AID1825319Cytotoxicity against human U-87 MG cells assessed as cell viability at 2000 uM incubated upto 72 hrs by MTT assay2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1250154Cytotoxicity against human Glioma cells (HF2303) at 50 uM after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID348242Antitumor activity against mouse B16F10 cells xenografted in C57BL/6 mouse assessed as tumor volume at 50 mg/kg/day, po after 17 days2009Journal of medicinal chemistry, Jan-22, Volume: 52, Issue:2
Discovery of the Poly(ADP-ribose) polymerase (PARP) inhibitor 2-[(R)-2-methylpyrrolidin-2-yl]-1H-benzimidazole-4-carboxamide (ABT-888) for the treatment of cancer.
AID667961Selectivity index, ratio of IC50 for mouse astrocytes to IC50 for human T98G cells2012European journal of medicinal chemistry, Aug, Volume: 54N-Aryl-N'-(chroman-4-yl)ureas and thioureas display in vitro anticancer activity and selectivity on apoptosis-resistant glioblastoma cells: screening, synthesis of simplified derivatives, and structure-activity relationship analysis.
AID1783997Cytotoxicity against cold atmospheric plasma (CAP)-treated human U-251MG cells assessed as decrease in cell viability treated with CAP for 15 secs followed by incubated with compound for 6 days by alamar blue assay2021European journal of medicinal chemistry, Nov-15, Volume: 224Enhanced pyrazolopyrimidinones cytotoxicity against glioblastoma cells activated by ROS-Generating cold atmospheric plasma.
AID540235Phospholipidosis-negative literature compound
AID228828Inhibition of Abl tyrosine kinase2003Bioorganic & medicinal chemistry letters, Oct-06, Volume: 13, Issue:19
Synthesis of pyrimidinopyridine-triazene conjugates targeted to abl tyrosine kinase.
AID1825335Cytotoxicity against human U-87 MG cells assessed as cell death at 352 uM incubated upto 72 hrs by MTT assay2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1697801Induction of DNA damage in rat RG2 cells assessed as ATM phosphorylation at ser1981 residues at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697565Induction of cell cycle arrest in human DBTRG-05MG cells assessed as accumulation at G2/M phase at 206 uM after 6 hrs by propidium iodide staining based flow cytometric analysis (Rvb = 30.08 +/- 0.1%)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1697689Inhibition of p38 phosphorylation at Tyr182 residues in human DBTRG-05MG cells at 206 uM after 48 hrs by Western blot analysis (Rvb = 1 No_unit)2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
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).
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1425989Binding affinity to recombinant human carbonic anhydrase 9 after 15 mins by stopped-flow CO2 hydration assay2017European journal of medicinal chemistry, Feb-15, Volume: 127New approach of delivering cytotoxic drugs towards CAIX expressing cells: A concept of dual-target drugs.
AID1317840Antiproliferative activity against patient-derived paclitaxel-sensitive NCI-H1993 cells after 48 to 96 hrs by MTT assay2016European journal of medicinal chemistry, Sep-14, Volume: 1205,10b-Ethanophenanthridine amaryllidaceae alkaloids inspire the discovery of novel bicyclic ring systems with activity against drug resistant cancer cells.
AID540212Mean residence time in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1250155Cytotoxicity against human Glioma cells (HF2381) at 50 uM after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
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).
AID1537889Cytotoxicity against P-gp knockout patient-isolated primary glioblastoma cells derived neurospheres assessed as increase in caspase3 cleavage at 50 uM measured after 48 hrs by immunoblotting method2019Journal of medicinal chemistry, 04-25, Volume: 62, Issue:8
Carbonic Anhydrase XII Inhibitors Overcome Temozolomide Resistance in Glioblastoma.
AID282557Antitumor activity against human NCI prostate cancer cell line panel2004Journal of medicinal chemistry, Dec-30, Volume: 47, Issue:27
Synthesis and antitumor activity of methyltriazene prodrugs simultaneously releasing DNA-methylating agents and the antiresistance drug O(6)-benzylguanine.
AID1316654Ratio of AUC in brain to plasma of Sprague-Dawley rat administered as single dose2016Bioorganic & medicinal chemistry letters, 10-15, Volume: 26, Issue:20
Temozolomide analogs with improved brain/plasma ratios - Exploring the possibility of enhancing the therapeutic index of temozolomide.
AID1250156Cytotoxicity against human Glioma cells (HF2476) at 50 uM after 72 hrs by CelltiterGlo assay2015ACS medicinal chemistry letters, Aug-13, Volume: 6, Issue:8
High-Throughput Screening of Patient-Derived Cultures Reveals Potential for Precision Medicine in Glioblastoma.
AID1825315Cytotoxicity against human SH-SY5Y cells assessed as cell viability at 100 uM incubated upto 72 hrs by MTT assay2022Journal of natural products, 01-28, Volume: 85, Issue:1
Cyclotides Chemosensitize Glioblastoma Cells to Temozolomide.
AID1888346Antiproliferative activity against human T98G cells assessed as cell viability at 188 uM incubated for 96 hrs by CellTiter-Glo luminescent cell viability assay relative to control
AID766224Chemosensitization of human SNB19 cells expressing MGMT after 5 days by MTT assay2013Journal of medicinal chemistry, Sep-12, Volume: 56, Issue:17
Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.
AID1697468Cytotoxicity against rat CTX TNA2 cells assessed as reduction in cell viability after 72 hrs by MTT assay2020Journal of natural products, 10-23, Volume: 83, Issue:10
Cedrol, a Sesquiterpene Alcohol, Enhances the Anticancer Efficacy of Temozolomide in Attenuating Drug Resistance via Regulation of the DNA Damage Response and MGMT Expression.
AID1851875Cytotoxicity against human GSC#83 cells assessed as reduction in cell viability at 10 uM incubated for 24 hrs by MTS assay
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.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (5,827)

TimeframeStudies, This Drug (%)All Drugs %
pre-199013 (0.22)18.7374
1990's99 (1.70)18.2507
2000's1139 (19.55)29.6817
2010's3154 (54.13)24.3611
2020's1422 (24.40)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 79.23

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 Index79.23 (24.57)
Research Supply Index8.83 (2.92)
Research Growth Index6.03 (4.65)
Search Engine Demand Index142.86 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (79.23)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials826 (13.73%)5.53%
Reviews623 (10.36%)6.00%
Case Studies541 (9.00%)4.05%
Observational22 (0.37%)0.25%
Other4,002 (66.54%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (854)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Phase 3, Open Label, Randomized, Comparative Study Of CP-675,206 And Either Dacarbazine Or Temozolomide In Patients With Advanced Melanoma [NCT00257205]Phase 3655 participants (Actual)Interventional2006-03-31Completed
A Multi-Center Phase I Dose Escalation Trial to Evaluate Safety and Tolerability of Intra-Arterial Temozolomide for Patients With Advanced Extremity Melanoma Using Normothermic Isolated Limb Infusion [NCT01127594]Phase 129 participants (Actual)Interventional2010-07-31Completed
Phase 11 Study of Cilengitide in Combination With Concurrent Chemotherapy and Radiotherapy Followed by Protracted Daily Low Dose Temozolomide and Low Dose Procarbazine D1 - 20 in Newly Diagnosed Glioblastoma Without Methylation of the MGMT Promoter Gene [NCT01124240]Phase 248 participants (Anticipated)Interventional2009-11-30Recruiting
A Phase 1 Study of Temsirolimus in Combination With Irinotecan and Temozolomide in Children, Adolescents, and Young Adults With Relapsed or Refractory Solid Tumors [NCT01141244]Phase 172 participants (Actual)Interventional2010-06-30Completed
Phase III Trial Comparing Conventional Adjuvant Temozolomide With Dose-Intensive Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT00304031]Phase 31,173 participants (Actual)Interventional2006-01-31Completed
A Phase II Clinical Trial of the Histone Deacetylase Inhibitor Valproic Acid in Combination With Temodar and Radiation Therapy in Patients With High Grade Gliomas: Multi-Institutional Trial [NCT00302159]Phase 243 participants (Actual)Interventional2006-03-31Completed
A Phase I/II Study of High-Dose Calcitriol in Combination With Temozolomide for Patients With Metastatic Melanoma [NCT00301067]Phase 1/Phase 220 participants (Actual)Interventional2005-01-30Completed
A Phase 1/2 Trial Evaluating the Combination of Temozolomide and the Ataxia Telangiectasia and Rad3-Related Inhibitor M1774 [NCT05691491]Phase 1/Phase 258 participants (Anticipated)Interventional2023-09-28Recruiting
Quantitative Magnetic Resonance Spectroscopic Imaging (MRSI) to Predict Early Response to Standard Radiation Therapy (RT)/Temozolomide (TMZ) ± Belinostat Therapy in Newly-Diagnosed Glioblastomas (GBM) [NCT02137759]Phase 229 participants (Actual)Interventional2014-05-07Active, not recruiting
Phase II Trial of Pulse Dosing of Lapatinib in Combination With Temozolomide and Regional Radiation Therapy for Upfront Treatment of Patients With Newly-Diagnosed Glioblastoma Multiforme [NCT01591577]Phase 250 participants (Actual)Interventional2012-12-07Active, not recruiting
An International, Multi-Center, Randomized, Double Blind Placebo Controlled Phase II Study to Evaluate the Safety and Efficacy of Lucanthone Administered as an Adjunct to Radiation and Temozolomide for Primary Therapy of Glioblastoma Multiforme [NCT01587144]Phase 218 participants (Actual)Interventional2012-06-19Terminated(stopped due to Sponsor's decision)
A Phase II Study of Temozolomide for Injection Combined With Epirubicin in the First-line Treatment of Leiomyosarcoma [NCT05204524]28 participants (Anticipated)Interventional2021-08-27Recruiting
A Phase II/III Study of Non Small Cell Lung Cancer Patient With/Without Synchronous Oral Temozolomide Capsules Combine With Intensity Modulated Radiation Therapy With Simultaneous Integrated Boost With Hippocampus Protection [NCT03732482]Phase 2/Phase 3400 participants (Anticipated)Interventional2019-03-01Not yet recruiting
A Phase II Study of Temozolomide, Cisplatin and Nivolumab in MMR-Proficient Colorectal Cancer [NCT04457284]Phase 218 participants (Actual)Interventional2020-11-18Active, not recruiting
A Phase I Study of BRCX014 to Investigate Dose-Ranging Safety and Pharmacokinetics in Adults With Glioblastoma (GBM) and Non-Methylated MGMT Gene Status [NCT03687034]Phase 121 participants (Anticipated)Interventional2019-06-01Not yet recruiting
First Line Standard Therapy of Glioblastoma Multiforme With or Without add-on Treatment With Trivax, an Anti-tumour Immune Therapy Based on Tumour-lysate Charged Dendritic Cells [NCT01213407]Phase 287 participants (Actual)Interventional2010-04-30Completed
A Cancer Research UK Phase I Trial of IMA950 (A Novel Multi-Peptide Vaccine) Plus GM-CSF in Patients With Newly Diagnosed Glioblastoma [NCT01222221]Phase 145 participants (Actual)Interventional2010-07-31Completed
Randomized Trial Assessing the Significance of Bevacizumab in Recurrent Grade II and Grade III Gliomas - The TAVAREC Trial [NCT01164189]Phase 2155 participants (Actual)Interventional2011-02-28Completed
High-Dose Vitamin D in Combination With Chemoradiotherapy in the Treatment of Glioblastoma Multiforme [NCT01181193]Phase 1/Phase 220 participants (Anticipated)Interventional2011-03-31Recruiting
Efficacy and Safety of Tunlametinib Capsules Versus Combination Chemotherapy of Investigator's Choice in Advanced NRAS-mutant Melanoma Patients Who Had Previously Received Immunotherapy [NCT06008106]Phase 3165 participants (Anticipated)Interventional2023-09-22Not yet recruiting
Phase I Trial of Zotiraciclib (TG02) Plus Dose-Dense or Metronomic Temozolomide Followed by Randomized Phase II Trial of Zotiraciclib (TG02) Plus Temozolomide Versus Temozolomide Alone in Adults With Recurrent Anaplastic Astrocytoma and Glioblastoma [NCT02942264]Phase 1/Phase 253 participants (Actual)Interventional2016-12-14Completed
PI3K/mTOR Pathway Activation Selected Phase II Study of Everolimus (RAD001) With and Without Temozolomide in the Treatment of Adult Patients With Supratentorial Low-Grade Glioma [NCT02023905]Phase 227 participants (Actual)Interventional2014-03-19Terminated(stopped due to Sponsor decision)
Phase II Trial of Low-Dose Whole Brain Radiotherapy With Concurrent Temozolomide and Adjuvant Temozolomide in Patients With Newly-Diagnosed Glioblastoma Multiforme [NCT01822275]Phase 224 participants (Actual)Interventional2013-05-31Terminated(stopped due to Poor accrual)
A Phase II, Open-Label Study to Evaluate the Safety, Tolerability, and Efficacy of Disulfiram and Copper Gluconate When Added to Standard Temozolomide Treatment in Patients With Newly Diagnosed Resected Unmethylated Glioblastoma Multiforme [NCT03363659]Phase 215 participants (Actual)Interventional2018-03-28Terminated(stopped due to Investigator decision)
Phase II Study Incorporating Pegylated Interferon In the Treatment For Children With High-Risk Melanoma [NCT00539591]Phase 229 participants (Actual)Interventional2008-05-09Active, not recruiting
International Randomized Phase II Trial of the Combination of Vincristine and Irinotecan With or Without Temozolomide (VI or VIT) in Children and Adults With Refractory or Relapsed Rhabdomyosarcoma [NCT01355445]Phase 2120 participants (Actual)Interventional2012-01-31Completed
A Single-blind, Randomized, Clinical Trial Comparing the Efficacy of 6 Cycles Versus 12 Cycles Temozolomide Regimens in Adjuvant Treatment of Patients With Brain High Grade Glioma [NCT03633552]Phase 362 participants (Anticipated)Interventional2018-03-03Recruiting
Temozolomide and Concomitant Whole Brain Radiotherapy in NSCLC Patients With Brain Metastases: A Randomized Trial [NCT02385136]Phase 1/Phase 2135 participants (Anticipated)Interventional2015-04-30Not yet recruiting
A Phase I/II Study of Ex-Vivo Expanded Allogeneic Universal Donor (UD) TGFbi NK Cell Infusions in Combination With Temozolomide as a Lymphodepleting Agent in Patients With Melanoma Metastatic to the Brain [NCT05588453]Phase 1/Phase 230 participants (Anticipated)Interventional2023-01-01Recruiting
IDH Mutated 1p/19q Intact Lower Grade Glioma Following Resection: Wait Or Treat? IWOT - a Phase III Study [NCT03763422]Phase 319 participants (Actual)Interventional2020-03-16Terminated(stopped due to Poorly recruiting)
A Pilot Study of Chimeric Antigen Receptor (CAR) T Cells Targeting B7-H3 Antigen in Treating Patients With Recurrent and Refractory Glioblastoma [NCT04385173]Phase 112 participants (Anticipated)Interventional2022-12-01Recruiting
Phase 1b Trial of 5-fluorouracil, Leucovorin, Irinotecan in Combination With Temozolomide (FLIRT) and Bevacizumab for the First-line Treatment of Patients With MGMT Silenced, Microsatellite Stable Metastatic Colorectal Cancer. [NCT04689347]Phase 118 participants (Anticipated)Interventional2021-01-01Recruiting
Image-Based Quantitative Assessment of Acute Radiation-Induced Changes in Glioma [NCT03168919]5 participants (Actual)Interventional2016-10-06Terminated(stopped due to PI is leaving institution)
RAPID Feasibility Study: A Pilot Study for the Rapid Infusion of Dinutuximab [NCT05421897]Phase 411 participants (Anticipated)Interventional2022-10-24Recruiting
A Phase I Study of Methoxyamine and Temozolomide in Patients With Advanced Solid Tumors [NCT00892385]Phase 166 participants (Actual)Interventional2007-08-16Completed
A Phase II, Multicenter, Randomized, Double-blind, Placebo-controlled Clinical Study to Evaluate the Efficacy and Safety of Toripalimab Combined With Temozolomide and Cisplatin in the Postoperative Adjuvant Treatment of Completely Resected Mucosal Melanom [NCT04462965]Phase 2294 participants (Anticipated)Interventional2020-05-30Recruiting
Phase I/II Randomized Prospective Trial for Newly Diagnosed GBM, With Upfront Gross Total Resection, Gliadel®, Followed by Temodar® With Concurrent IMRT Versus GK [NCT02085304]Phase 1/Phase 280 participants (Anticipated)Interventional2012-10-31Recruiting
B7-H3-Targeted Chimeric Antigen Receptor (CAR) T Cells in Treating Patients With Recurrent or Refractory Glioblastoma [NCT04077866]Phase 1/Phase 240 participants (Anticipated)Interventional2023-06-01Recruiting
A Pilot Study of the Combination of Nab-paclitaxel, Temozolomide and Bevacizumab in Patients With Metastatic Melanoma With Brain Metastases [NCT02065466]Phase 1/Phase 20 participants (Actual)Interventional2014-07-31Withdrawn(stopped due to lack of accrual)
A Phase I Study of Mebendazole for the Treatment of Pediatric Gliomas [NCT01837862]Phase 1/Phase 236 participants (Anticipated)Interventional2013-10-22Recruiting
PV-10 Intralesional Injection vs Systemic Chemotherapy or Oncolytic Viral Therapy for Treatment of Locally Advanced Cutaneous Melanoma [NCT02288897]Phase 320 participants (Actual)Interventional2015-04-30Terminated(stopped due to Inadequate rate of enrollment)
Expedited Laser Interstitial Thermal Therapy and Chemoradiation for Patients With Newly Diagnosed High Grade Gliomas [NCT02970448]Early Phase 145 participants (Anticipated)Interventional2017-08-24Recruiting
Phase II Trial of Extended-Dosing Temozolomide in Patients With Melanoma [NCT00591370]Phase 251 participants (Actual)Interventional2005-01-31Completed
Linking the Gut Microbiota to the Prognosis of Glioblastoma Multiforme [NCT03631823]200 participants (Anticipated)Observational2018-08-10Not yet recruiting
Safety and Tolerability of Tumor Treating Fields (TTFields) Combined With Chemoradiation in Newly Diagnosed Glioblastoma (Unity) [NCT03705351]Phase 17 participants (Actual)Interventional2019-12-02Active, not recruiting
A Phase 2 Study of Verubulin With Radiation Therapy and Temozolomide in Subjects Newly Diagnosed With Glioblastoma Multiforme [NCT01285414]Phase 25 participants (Actual)Interventional2010-12-31Completed
Phase I Trial of Super-Selective Intraarterial Cerebral Infusion of Temozolomide (Temodar) for Treatment of Newly Diagnosed Glioblastoma Multiforme and Anaplastic Astrocytoma [NCT01180816]Phase 121 participants (Actual)Interventional2010-08-31Completed
Phase 2 Single-Arm, Open Label Study Of Irinotecan In Combination With Temozolomide In Children With Recurrent Or Refractory Medulloblastoma And In Children With Newly Diagnosed High-Grade Glioma. [NCT00404495]Phase 283 participants (Actual)Interventional2007-04-30Completed
A Randomized, Factorial-Design, Phase II Trial of Temozolomide Alone and in Combination With Possible Permutations of Thalidomide, Isotretinoin and/or Celecoxib as Post-Radiation Adjuvant Therapy of Glioblastoma Multiforme [NCT00112502]Phase 2178 participants (Actual)Interventional2005-09-30Completed
Phase I/II Study Of Pre-Irradiation Chemotherapy With Methotrexate, Rituximab, And Temozolomide And Post -Irradiation Temozolomide For Primary Central Nervous System Lymphoma [NCT00068250]Phase 1/Phase 260 participants (Actual)Interventional2003-07-31Completed
The Temozolomide RESCUE Study: A Phase II Trial of Continuous (28/28) Dose-intense Temozolomide (CDIT) Chemotherapy After Progression on Conventional 5/28 Day Temozolomide in Patients With Recurrent Malignant Glioma [NCT00392171]Phase 2120 participants (Actual)Interventional2006-06-09Completed
Extended Schedule, Escalated Dose Temozolomide Versus Dacarbazine in Stage IV Metastatic Melanoma: A Randomized Phase III Study of the EORTC Melanoma Group [NCT00091572]Phase 3859 participants (Actual)Interventional2004-10-20Completed
Intensive Chemotherapy And Immunotherapy In Patients With Newly Diagnosed Primary CNS Lymphoma [NCT00098774]Phase 247 participants (Actual)Interventional2004-10-31Completed
A Phase II Single Arm Interventional Trial Evaluating the Activity and Safety of Combination Between Cabozantinib and Temozolomide in Lung and GEP-NENS Progressive After Everolimus, Sunitinib or PRRT (CABOTEM) [NCT04893785]Phase 235 participants (Anticipated)Interventional2021-06-15Recruiting
A Phase II Pilot Study Of Thalidomide With Temozolomide In Patients With Relapsed Or Progressive Brain Tumors Or Neuroblastoma [NCT00098865]Phase 215 participants (Actual)Interventional2002-09-30Completed
Phase I/IIa Study of Concomitant Radiotherapy With Olaparib and Temozolomide in Unresectable High Grade Gliomas Patients [NCT03212742]Phase 1/Phase 291 participants (Anticipated)Interventional2017-09-04Recruiting
Radiation Versus Temozolomide in Preventing Brain Metastases in Limited Stage Small Cell Lung Cancer [NCT02605811]Phase 2426 participants (Anticipated)Interventional2015-09-30Recruiting
A Phase Ib/II Randomized, Open Label Drug Repurposing Trial of Glutamate Signaling Inhibitors in Combination With Chemoradiotherapy in Patients With Newly Diagnosed Glioblastoma [NCT05664464]Phase 1/Phase 2120 participants (Anticipated)Interventional2023-01-01Recruiting
A Phase 1 Study of Tumor Treating Fields With 5 Day Hypofractionated Stereotactic Radiosurgery and Concurrent and Maintenance Temozolomide in Newly Diagnosed Glioblastoma [NCT04474353]Phase 112 participants (Anticipated)Interventional2021-05-21Recruiting
PHASE 1/2 STUDY TO EVALUATE PALBOCICLIB (IBRANCE®) IN COMBINATION WITH IRINOTECAN AND TEMOZOLOMIDE OR IN COMBINATION WITH TOPOTECAN AND CYCLOPHOSPHAMIDE IN PEDIATRIC PATIENTS WITH RECURRENT OR REFRACTORY SOLID TUMORS [NCT03709680]Phase 2184 participants (Anticipated)Interventional2019-05-24Recruiting
A Pivotal Randomized, Controlled Trial of VAL-083 in Patients With Recurrent Glioblastoma Who Have Failed Standard Temozolomide/Radiation Therapy and Bevacizumab (STAR-3) [NCT03149575]Phase 32 participants (Actual)Interventional2017-10-27Terminated(stopped due to Change in clinical development plan)
Phase 1b/2a Study Combining LY2157299 With Standard Temozolomide-based Radiochemotherapy in Patients With Newly Diagnosed Malignant Glioma [NCT01220271]Phase 1/Phase 275 participants (Actual)Interventional2011-04-30Completed
An International, Randomized, Double-Blind, Controlled Study of Rindopepimut/GM-CSF With Adjuvant Temozolomide in Patients With Newly Diagnosed, Surgically Resected, EGFRvIII-positive Glioblastoma [NCT01480479]Phase 3745 participants (Actual)Interventional2011-11-30Completed
A Phase 2 Randomized Clinical Trial of ABT-888 in Combination With Temozolomide Versus Pegylated Liposomal Doxorubicin Alone in Subjects With Recurrent High Grade Serous Ovarian Cancer [NCT01113957]Phase 2168 participants (Actual)Interventional2010-03-31Completed
Naxitamab and Granulocyte-Macrophage Colony Stimulating Factor in Combination With Irinotecan and Temozolomide in Patients With High-Risk Neuroblastoma With Primary Refractory Disease or in First Relapse. An International, Single-Arm, Multicenter Phase 2 [NCT04560166]Phase 22 participants (Actual)Interventional2021-11-08Terminated(stopped due to Due to business priorities)
Phase I/II Study of Temozolomide and Gleevec (Imatinib Mesylate, Formerly Known as STI571) in Advanced Melanoma [NCT00667953]Phase 1/Phase 232 participants (Actual)Interventional2003-01-31Terminated(stopped due to Difficulty enrolling subjects)
A Phase II Study of CDX-110 With Radiation and Temozolomide in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00458601]Phase 282 participants (Actual)Interventional2007-08-31Completed
A Phase II Randomized,Controlled,Open Label,Multicentre Study of Tegafur Combined With Temozolomide Versus Tegafur Combined With Temozolomide and Thalidomide in Subjects With Advanced Extrapancreatic Neuroendocrine Tumor [NCT03204032]Phase 260 participants (Anticipated)Interventional2016-10-31Recruiting
Phase Ib/II Multicentric Study Combining Glasdegib (PF-04449913) With Temozolomide in Patients With Newly Diagnosed Glioblastoma, Safety and Preliminary Efficacy for the Combination [NCT03466450]Phase 1/Phase 275 participants (Actual)Interventional2018-03-15Active, not recruiting
Pre-operative Radiation Therapy (RT) and Temozolomide (TMZ) in Patients With Newly Diagnosed Glioblastoma. A Phase I Study. (PARADIGMA) [NCT03480867]Phase 10 participants (Actual)Interventional2017-03-31Withdrawn(stopped due to competing study was opened by the surgeon after this trial was opened)
A Phase 1/1b Adaptive Dose Escalation Study of Mycophenolate Mofetil (MMF) in Combination With Standard of Care for Patients With Glioblastoma [NCT05236036]Phase 160 participants (Anticipated)Interventional2022-08-08Recruiting
An Extension Study to Evaluate the Safety of Veliparib in Combination With Temozolomide in Subjects With Solid Tumors. [NCT01193140]Phase 224 participants (Actual)Interventional2010-07-31Completed
Phase I/II Study of LY2228820 With Radiotherapy Plus Concomitant TMZ in the Treatment of Newly Diagnosed Glioblastoma [NCT02364206]Phase 1/Phase 218 participants (Actual)Interventional2015-06-08Completed
Efficacy and Safety of Apatinib Combined With Dose-dense Temozolomide in Recurrent Glioblastoma [NCT03660761]Phase 225 participants (Actual)Interventional2016-03-03Completed
A Large-scale Research for Immunotherapy of Glioblastoma With Autologous Heat Shock Protein gp96 [NCT03650257]Phase 2150 participants (Anticipated)Interventional2019-08-21Recruiting
Bortezomib Sensitization of Recurrent Glioblastoma With Unmethylated MGMT Promoter to Temozolomide Phase 1B/II Study [NCT03643549]Phase 1/Phase 263 participants (Anticipated)Interventional2018-08-30Recruiting
Individualized (Timed) Temozolomide Administration as a Means of Immune Reconstitution in Patients With Metastatic Melanoma [NCT01328535]Phase 225 participants (Actual)Interventional2011-01-31Completed
Randomized, Phase II, Double-Blind, Placebo-Controlled Trial of Conventional Chemoradiation and Adjuvant Temozolomide Plus Cediranib Versus Conventional Chemoradiation and Adjuvant Temozolomide Plus Placebo in Patients With Newly Diagnosed Glioblastoma [NCT01062425]Phase 2261 participants (Actual)Interventional2010-02-26Completed
A Phase 2 Study of Apatinib Combined With Temozolomide in the Treatment of Advanced Melanoma Patients After Conventional Treatment Failure [NCT03422445]Phase 230 participants (Anticipated)Interventional2018-01-08Recruiting
Randomized Double-Blind, Placebo-Controlled Parallel Multi-Center Study to Assess the Efficacy of Cannabidiol (BRCX014) Combined With Standard-Of-Care Treatment in Subjects With Multiple Myeloma, Glioblastoma Multiforme, and GI Malignancies [NCT03607643]Phase 1/Phase 2160 participants (Anticipated)Interventional2019-01-15Not yet recruiting
Prospective Study of Stereotactic Radiosurgery Using Diffusion-Weighted Abnormality Versus Chemotherapy for Recurrent/Progressive Glioblastoma After Second-line Chemotherapy [NCT05718466]Phase 335 participants (Actual)Interventional2010-11-30Completed
Phase II, Multicentre, Open Label Study to Evaluate the Efficacy of the Combination of Lanreotide Autogel 120mg and Temozolomide in Patients With Progressive Gastro-entero-pancreatic Neuroendocrine Tumours (GEP-NET) G1/G2 - A Pilot-Study [NCT02231762]Phase 257 participants (Actual)Interventional2014-10-31Completed
Phase I Pilot Study of Preoperative Chemoradiation for Glioblastoma [NCT02092038]Phase 11 participants (Actual)Interventional2014-11-30Completed
Phase II Trial of Temozolomide for the Treatment of Mycosis Fungoides and the Sezary Syndrome [NCT00004106]Phase 229 participants (Actual)Interventional1998-05-31Terminated(stopped due to Per Data Monitoring Committee given the poor/inadequate accrual.)
Phase I/II Trial of Concurrent RAD001 (Everolimus) With Temozolomide/Radiation Followed by Adjuvant RAD001/Temozolomide in Newly Diagnosed Glioblastoma [NCT01062399]Phase 1/Phase 2279 participants (Actual)Interventional2010-12-31Completed
Phase II Study of Anti-GD2 3F8 Antibody and GM-CSF for High-Risk Neuroblastoma [NCT00072358]Phase 2291 participants (Actual)Interventional2003-07-31Completed
A Study on the Safety and Effectiveness of Temozolomide for Neoadjuvant Treatment of Pheochromocytoma or Paraganglioma Patients [NCT05885386]Phase 220 participants (Anticipated)Interventional2023-04-01Recruiting
Phase I/Ib Study of Sarasar and Temodar in Patients With Recurrent or Temodar-Refractory Glioblastoma Multiforme [NCT00102648]Phase 135 participants (Anticipated)Interventional2004-12-21Active, not recruiting
A Study of BPM31510 With Vitamin K1 in Subjects With Newly Diagnosed Glioblastoma (GB) [NCT04752813]Phase 250 participants (Anticipated)Interventional2023-09-28Recruiting
Phase I/II Study of BGB-290 With Temozolomide in Recurrent Gliomas With IDH1/2 Mutations [NCT03914742]Phase 1/Phase 260 participants (Actual)Interventional2020-01-03Suspended(stopped due to NCI decided to terminate ABTC Consortium due to NCI moving in different direction for Brain Cancer])
A Phase II, Multicenter, Open-Label, Single-Arm Study to Evaluate the Safety, Tolerability, and Efficacy of DIsulfiram and Copper Gluconate in Recurrent Glioblastoma [NCT03034135]Phase 223 participants (Actual)Interventional2017-03-09Completed
A Retrospective Clinical Study of Postoperative Concurrent Chemoradiotherapy Combined With Anti-angiogenic Drugs in the Treatment of Glioblastoma. [NCT03567135]60 participants (Anticipated)Observational2017-10-01Recruiting
Phase 2 Study of Intraventricular Omburtamab-based Radioimmunotherapy for Pediatric Patients With Recurrent Medulloblastoma and Ependymoma [NCT04743661]Phase 262 participants (Anticipated)Interventional2022-04-04Active, not recruiting
A Prospective Cohort to Study the Effect of Postoperative Upfront Temozolomide Chemotherapy on IDH Mutational Low Grade Gliomas in Eloquent Areas [NCT02209428]Phase 254 participants (Actual)Interventional2014-06-30Active, not recruiting
A Randomized Phase II Study of Temozolomide Monotherapy or in Combination With Olaparib in Patients With METHYLATED 06-Methylguanine-DNA Methyltransferase (MGMT) Pre-Treated Triple Negative Breast Cancer (TNBC) [NCT05128734]Phase 240 participants (Anticipated)Interventional2023-12-01Not yet recruiting
A Phase I Trial of Chlorpromazine Together With Standard of Care in New Diagnosis of Glioblastoma [NCT05190315]Phase 110 participants (Actual)Interventional2022-01-28Active, not recruiting
Phase 2 Trial of a Novel Peptide Vaccine (PEP-CMV) Targeting CMV Antigen for Newly Diagnosed Pediatric High-grade Glioma and Diffuse Intrinsic Pontine Glioma and Recurrent Medulloblastoma [NCT05096481]Phase 2120 participants (Anticipated)Interventional2023-12-15Not yet recruiting
Efficacy and Safety of Anlotinib, Irinotecan and Temozolomide in the Treatment of Refractory or Recurrent Neuroblastoma in Children: an Open, Single Arm, Single Center, Phase II Clinical Study [NCT04842526]Phase 227 participants (Anticipated)Interventional2021-04-12Not yet recruiting
A Phase 1b/2, Dose-finding and Expansion Study to Assess the Safety, Tolerability, Pharmacokinetics and Preliminary Efficacy of HTMC0435 With Temozolomide in Patients With Small Cell Lung Cancer [NCT05728619]Phase 1/Phase 264 participants (Anticipated)Interventional2023-02-03Recruiting
A Randomized, Phase I/II Trial of Irinotecan and Temozolomide Compared to Irinotecan and Temozolomide in Combination With TPI 287 in Patients With Primary Refractory or Early Relapsed Neuroblastoma [NCT01505608]Phase 1/Phase 214 participants (Actual)Interventional2011-12-31Terminated(stopped due to Lack of Enrollment)
Randomized Phase III Study of Conventional Versus Hypofractionated Radiotherapy Combined With Temozolomide in Elderly Glioblastoma Patients [NCT05439278]Phase 3268 participants (Anticipated)Interventional2022-08-01Not yet recruiting
Improvement of Functional Outcome for Patients With Newly Diagnosed Grade II or III Glioma With Co-deletion of 1p/19q - IMPROVE CODEL: the NOA-18 Trial [NCT05331521]Phase 3406 participants (Anticipated)Interventional2021-04-07Recruiting
Preoperative Radiosurgery in High Grade Glioma: A Phase I/IIA Clinical Trial: The NeoGlioma Study [NCT05030298]Phase 1/Phase 240 participants (Anticipated)Interventional2023-05-23Recruiting
An Open Label Single Arm Phase II Trial in Patients With Advanced Unresectable Previously Treated Oesophagogastric Adenocarcinoma Which is MGMT Deficient [NCT04984733]Phase 218 participants (Anticipated)Interventional2021-09-28Recruiting
A Phase I Clinical Trial of Selinexor (KPT-330) in Combination With Temozolomide and Radiation Therapy in Patients With Newly Diagnosed Glioblastoma [NCT04216329]Phase 124 participants (Anticipated)Interventional2020-07-07Recruiting
A Multicenter, Randomized, Controlled, Phase III Trial Comparing High-Dose IFN-a2b With Temozolomide Plus Cisplatin as Systemic Adjuvant Therapy for Resected Mucosal Melanoma [NCT03435302]Phase 3204 participants (Anticipated)Interventional2014-02-28Recruiting
A Phase 2, Randomized, Open-Label Study of Anhydrous Enol-Oxaloacetate in Subjects With Newly Diagnosed Glioblastoma Multiforme [NCT04450160]Phase 280 participants (Anticipated)Interventional2020-12-31Not yet recruiting
Phase II Single-Center Study of Bevacizumab in Combination With Temozolomide in Patients With First-Line Metastatic Uveal Melanoma [NCT01217398]Phase 235 participants (Anticipated)Interventional2009-10-31Recruiting
Cilengitide and Metronomic Temozolomide for Relapsed or Refractory High Grade Gliomas or Diffuse Intrinsic Pontine Gliomas in Children and Adolescents - A Phase II Study HIT-HGG-CilMetro - A Clinical Phase II Trial of the HIT-HGG Study Group - [NCT01517776]Phase 228 participants (Actual)Interventional2012-01-31Terminated(stopped due to due to an altered benefit/risk assessment.)
A Pilot Study Using Carboplatin, Vincristine And Temozolomide For Children ≤ 10 Years With Progressive/Symptomatic Low-Grade Gliomas [NCT00077207]66 participants (Actual)Interventional2004-07-31Completed
A Phase Ib/II Study of AZD2171 in Combination With Daily Temozolomide and Radiation in Patients With Newly Diagnosed Glioblastoma Not Taking Enzyme-Inducing Anti-epileptic Drugs [NCT00662506]Phase 1/Phase 246 participants (Actual)Interventional2008-04-30Completed
A Phase I Trial of High-Dose Ascorbate in Glioblastoma Multiforme [NCT01752491]Phase 113 participants (Actual)Interventional2013-04-01Active, not recruiting
A Phase II Trial of Talampanel in Conjunction With Radiation Therapy With Concurrent and Adjuvant Temozolomide in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00267592]Phase 272 participants (Actual)Interventional2005-12-31Completed
A Phase Ⅰb/Ⅱ Study of Fluzoparib (SHR-3162) and Temozolomide With or Without SHR-1316 in Treating Patients With Replapsed Small Cell Lung Cancer [NCT04400188]Phase 1/Phase 225 participants (Actual)Interventional2020-06-11Active, not recruiting
Bioequivalence Study Between Temozolomide Oral Suspension (Ped-TMZ) and Temodal® Capsules [NCT04467346]Phase 136 participants (Actual)Interventional2020-09-25Completed
Comparative Assessment of Methods to Analyze MGMT as a Predictive Factor of Response to Temozolomide in Glioblastomas. [NCT01345370]300 participants (Actual)Observational2009-03-31Completed
Phase II Trial O6-benzylguanine(BG) and Temozolomide(TMZ) Therapy of Glioblastoma Multiforme (GBM) With Infusion of Autologous P140K MGMT+Hematopoietic Progenitors to Protect Hematopoiesis [NCT05052957]Phase 216 participants (Anticipated)Interventional2023-01-20Recruiting
Phase 1/2 Study of TPX-0005 (Repotrectinib) in Combination With Chemotherapy in Pediatric and Young Adult Subjects With Advanced or Metastatic Solid Tumors and Primary Central Nervous System Tumors [NCT05004116]Phase 1/Phase 250 participants (Anticipated)Interventional2021-08-09Recruiting
A Phase 1-2 Dose-escalation and Expansion Study of ST101 in Patients With Advanced Unresectable and Metastatic Solid Tumors [NCT04478279]Phase 1/Phase 2162 participants (Anticipated)Interventional2020-07-01Recruiting
A Pilot Study of Dinutuximab, Sargramostim (GM-CSF), and Isotretinoin in Combination With Irinotecan and Temozolomide in the Post-Consolidation Setting for High-Risk Neuroblastoma [NCT04385277]Phase 234 participants (Actual)Interventional2020-12-31Active, not recruiting
A Phase 2 Randomized Study of Irinotecan/Temozolomide/Dinutuximab With or Without Eflornithine (DFMO) in Children With Relapsed, Refractory or Progressive Neuroblastoma [NCT03794349]Phase 295 participants (Anticipated)Interventional2019-07-08Recruiting
A Phase II/III Randomized Trial of Veliparib or Placebo in Combination With Adjuvant Temozolomide in Newly Diagnosed Glioblastoma With MGMT Promoter Hypermethylation [NCT02152982]Phase 2/Phase 3447 participants (Actual)Interventional2014-12-15Active, not recruiting
A Randomized Phase II/III Study of Vorinostat and Local Irradiation OR Temozolomide and Local Irradiation OR Bevacizumab and Local Irradiation Followed by Maintenance Bevacizumab and Temozolomide in Children With Newly Diagnosed High-Grade Gliomas [NCT01236560]Phase 2/Phase 3101 participants (Actual)Interventional2010-11-15Active, not recruiting
Quality of Life and Neurocognitive Functioning in Diffuse Low-grade Glioma (TEMOIN) [NCT03257618]26 participants (Actual)Interventional2017-07-27Completed
Phase III Trial of CCNU/Temozolomide (TMZ) Combination Therapy vs. Standard TMZ Therapy for Newly Diagnosed MGMT-methylated Glioblastoma Patients [NCT01149109]Phase 3141 participants (Actual)Interventional2010-10-31Completed
A Randomized Phase 3 Study of Antineoplastons A10 and AS2-1 vs. Temozolomide in Subjects With Recurrent and / or Progressive Optic Pathway Glioma After Carboplatin or Cisplatin Therapy [NCT01260103]Phase 30 participants (Actual)Interventional2011-12-31Withdrawn(stopped due to Withdrawn: study halted prematurely, prior to enrollment of first participant)
Phase I/II Study of AGuIX Nanoparticles With Radiotherapy Plus Concomitant Temozolomide in the Treatment of Newly Diagnosed Glioblastoma [NCT04881032]Phase 1/Phase 266 participants (Anticipated)Interventional2022-03-07Recruiting
A Phase I Study of MK-4827 in Combination With Temozolomide in Patients With Advanced Cancer [NCT01294735]Phase 119 participants (Actual)Interventional2011-02-28Completed
A Phase II Open Label Randomised Multicentric Study in Patients With Unresectable Glioblastoma Using Neo-adjuvant Treatment With Two Cycles of Temozolomide Previous Temozolomide Plus Radiation Therapy and Adjuvant Temozolomide vs. Neo-adjuvant Treatment W [NCT01102595]Phase 2102 participants (Actual)Interventional2009-12-31Completed
Phase I Trial of Oral Topotecan Plus Temodar in the Treatment of Patients With Malignant Gliomas [NCT00610571]Phase 162 participants (Actual)Interventional2004-04-30Completed
Phase 1 Trial of RO4929097 in Combination With Standard Radiotherapy and Temozolomide for Newly Diagnosed Malignant Glioma: A Pharmacokinetic and Pharmacodynamic Study [NCT01119599]Phase 122 participants (Actual)Interventional2010-05-31Completed
First-line Chemotherapy With Temozolomide Alone for Non-enhancing Adult Brainstem Gliomas, With a Diffuse Subtype and Showing Clinical and/or Radiological Infiltrative Pattern of Progression [NCT03932981]Phase 260 participants (Anticipated)Interventional2019-07-26Recruiting
Irinotecan and Temozolomide for Advanced Ewing Sarcoma After Failure of Standard Multimodal Therapy [NCT03359005]Phase 260 participants (Anticipated)Interventional2018-02-07Recruiting
NIVOLUMAB Plus IPILIMUMAB and TEMOZOLOMIDE in Combination in Microsatellite Stable (MSS), MGMT Silenced Metastatic Colorectal Cancer (mCRC): the MAYA Study [NCT03832621]Phase 2135 participants (Actual)Interventional2019-03-25Completed
Early Post-surgical Temozolomide Therapy in Patients With High-Grade Gliomas Admitted to Acute Rehabilitation: A Feasibility Study [NCT03796507]Early Phase 10 participants (Actual)Interventional2021-09-01Withdrawn(stopped due to Hiring freeze of research personnel due to COVID pandemic)
Randomized Phase II Study Comparing Two Schedules Of Temozolomide In Combination With Bay 43-9006 In Patients With Advanced Melanoma [NCT00602576]Phase 2169 participants (Actual)Interventional2005-01-01Completed
A Phase II Study of a Temozolomide-Based Chemoradiotherapy Regimen for High-Risk Low-Grade Gliomas [NCT00114140]Phase 2136 participants (Actual)Interventional2005-01-31Completed
A Multicenter Randomized Phase III Study for Recurrent Glioblastoma Comparing Bevacizumab Alone With Dose-dense Temozolomide Followed by Bevacizumab (JCOG1308C, RE-GEND-pIII) [NCT02761070]Phase 3146 participants (Anticipated)Interventional2016-07-11Active, not recruiting
Study of TG02 in Elderly Newly Diagnosed or Adult Relapsed Patients With Anaplastic Astrocytoma or Glioblastoma: A Phase Ib Study [NCT03224104]Phase 171 participants (Actual)Interventional2018-06-12Completed
Dose Finding Phase 1 Study of the Treatment of Metastatic Melanoma With MPC-6827 in Combination With Temozolomide [NCT00609011]Phase 1/Phase 222 participants (Actual)Interventional2008-03-31Completed
Efficacy and Safety of Nimotuzumab in Addition to Radiotherapy and Temozolomide for Cerebral Glioblastoma [NCT03388372]Phase 239 participants (Actual)Interventional2010-08-18Completed
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
A Pilot Study to Assess the Safety, Feasibility, and Preliminary Efficacy of a Neoepitope-based Personalized Vaccine Approach in Patients With Newly Diagnosed Glioblastoma [NCT02510950]Phase 11 participants (Actual)Interventional2015-12-03Terminated(stopped due to Low accrual)
A Study of CIK in Combination With Temozolomide With and Without Radiation in Adults With Stage I-II Malignant Gliomas [NCT02494804]Phase 1/Phase 280 participants (Anticipated)Interventional2015-07-31Not yet recruiting
A Single Arm, Multi-center, Phase II Clinical Trial of Rituximab, Lenalidomide Combined With High-dose Methotrexate and Temozolomide (RL-MT) in the First-line Treatment for Patients With Primary Central Nervous System Lymphoma [NCT04737889]Phase 230 participants (Anticipated)Interventional2021-01-13Recruiting
Randomized Phase II Trial on Fitness- and Comorbidity- Tailored Treatment in Elderly Patients With Newly Diagnosed Primary CNS Lymphoma (FIORELLA Trial) [NCT03495960]Phase 2208 participants (Anticipated)Interventional2019-06-15Recruiting
An Open-Label, Multi-Center Trial of INO-5401 and INO-9012 Delivered by Electroporation (EP) in Combination With REGN2810 in Subjects With Newly-Diagnosed Glioblastoma (GBM) [NCT03491683]Phase 1/Phase 252 participants (Actual)Interventional2018-05-31Active, not recruiting
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
A Randomized, Double Blind Phase II Trial of Surgery, Radiation Therapy Plus Temozolomide and Pembrolizumab With and Without HSPPC-96 in Newly Diagnosed Glioblastoma (GBM) [NCT03018288]Phase 290 participants (Actual)Interventional2017-09-21Completed
A Study of CIK in Combination With Temozolomide With and Without Radiation in Adults With Advanced Malignant Gliomas [NCT02496988]Phase 4120 participants (Anticipated)Interventional2015-07-31Not yet recruiting
A Prospective Trial of NovoTTF-200A Together With Temozolomide and Radiotherapy in Patients With Newly Diagnosed GBM [NCT03780569]10 participants (Anticipated)Interventional2017-04-27Active, not recruiting
Hypofractionated Radiotherapy With Concurrent Temozolomide for Large Brain Metastases: a Multi-center Randomized Phase III Trial [NCT03778541]Phase 3224 participants (Anticipated)Interventional2018-12-03Recruiting
Phase II Clinical Trial of Concomitant Association of Ultrafractionated Brain Irradiation - Temozolomide in Inoperable Primary Glioblastoma Multiforme [NCT03310372]Phase 246 participants (Actual)Interventional2008-02-13Completed
Short Course Chemo-Radiation Therapy for Patients With Newly Diagnosed Glioblastoma: Comparison of Two Established Schedules [NCT04019262]Phase 1/Phase 240 participants (Anticipated)Interventional2021-12-14Recruiting
An Open Label, Multicenter, Phase II Study Evaluating the Safety and Efficacy of Temozolomide Treatment in Patients With Invasive Pituitary Tumors [NCT00601289]Phase 20 participants (Actual)Interventional2009-12-31Withdrawn(stopped due to funding term ended)
A Randomized Phase I/II Study of ABT-888 in Combination With Temozolomide in Recurrent (Temozolomide Resistant) Glioblastoma [NCT01026493]Phase 1/Phase 2257 participants (Actual)Interventional2010-07-31Completed
A Phase 1/2 Open-label Study of Debio 0123 in Combination With Temozolomide in Adult Participants With Recurrent or Progressive Glioblastoma and of Debio 0123 in Combination With Temozolomide and Radiotherapy in Adult Participants With Newly Diagnosed Gli [NCT05765812]Phase 1/Phase 289 participants (Anticipated)Interventional2023-03-01Recruiting
A Phase 2a Study of the Addition of Temozolomide to a Standard Conditioning Regimen for Autologous Stem Cell Transplantation in Relapsed and Refractory Central Nervous System (CNS) Lymphoma [NCT01235793]Phase 211 participants (Actual)Interventional2010-10-14Terminated(stopped due to The clinical trial was terminated due to poor enrollment)
Phase I, Open Label Trial to Explore Safety of Combining BIBW 2992 and Radiotherapy With or Without Temozolomide in Newly Diagnosed GBM [NCT00977431]Phase 136 participants (Actual)Interventional2009-09-17Completed
A Phase I Study of Safety and Tolerability of Acetazolamide With Temozolomide in Adults With Newly Diagnosed MGMT Promoter-Methylated IDH Wildtype Glioblastoma [NCT03011671]Phase 160 participants (Anticipated)Interventional2018-10-03Recruiting
CPT-SIOP-2009: Intercontinental Multidisciplinary Registry and Treatment Optimization Study for Patients With Choroid Plexus Tumors [NCT01014767]Phase 327 participants (Actual)Interventional2009-11-30Terminated(stopped due to PI departure from coordinating institution)
Phase II Trial of Bevacizumab in Combination With Temozolomide and Regional Radiation Therapy for Upfront Treatment of Patients With Newly-diagnosed Glioblastoma Multiforme [NCT01013285]Phase 270 participants (Actual)Interventional2006-06-30Completed
A Phase I Study of Hydroxychloroquine in Combination With Temozolomide in Patients With Advanced Solid Tumors [NCT00714181]Phase 138 participants (Actual)Interventional2008-06-30Completed
Therapeutic Trial for Patients With Ewing Sarcoma Family of Tumor and Desmoplastic Small Round Cell Tumors [NCT01946529]Phase 224 participants (Actual)Interventional2013-12-27Active, not recruiting
Phase II Portion of Multi Phase Study of Sorafenib With Radiation and Temozolomide in Newly Diagnosed Glioblastoma or Gliosarcoma [NCT02599090]Phase 20 participants (Actual)Interventional2008-12-31Withdrawn(stopped due to Multi phase study did not progress to Phase II. Phase I registered as NCT00734526.)
Prospective Pilot Trial to Assess a Multimodal Molecular Targeted Therapy in Children, Adolescent and Young Adults With Relapsed or Refractory High-grade Pineoblastoma [NCT02596828]Phase 24 participants (Actual)Interventional2016-04-30Completed
Cilengitide for Subjects With Newly Diagnosed Glioblastoma and Methylated MGMT Gene Promoter - A Multicenter, Open-label, Controlled Phase III Study, Testing Cilengitide in Combination With Standard Treatment (Temozolomide With Concomitant Radiation Thera [NCT00689221]Phase 3545 participants (Actual)Interventional2008-09-30Completed
A Clinical Study of Standard TEMODAL® Regimen Versus Standard Regimen Plus Early Post-Surgery TEMODAL® Chemotherapy in Treatment on Patients With Newly Diagnosed Glioblastoma Multiforme (GBM) [NCT00686725]Phase 499 participants (Actual)Interventional2008-06-24Completed
A Randomized, Double-Blind, Placebo-Controlled, Multicenter Phase III Trial of Bevacizumab, Temozolomide and Radiotherapy, Followed by Bevacizumab and Temozolomide Versus Placebo, Temozolomide and Radiotherapy Followed by Placebo and Temozolomide in Patie [NCT00943826]Phase 3921 participants (Actual)Interventional2009-06-29Completed
Open-label, Single Center, Uncontrolled Phase I/II Study Evaluating the Safety and Maximum Tolerated Dose of Daily Sorafenib Administered in Combination With Prolonged Temozolomide in Patients With Metastatic Melanoma [NCT00811759]Phase 1/Phase 258 participants (Anticipated)Interventional2007-06-30Active, not recruiting
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 Study of Normal-fractionated Radiotherapy Versus Hypofractionated Radiotherapy Versus Chemotherapy in Patients Over 60 Years With Malignant Glioma [NCT00820963]Phase 370 participants (Anticipated)Interventional2006-07-31Completed
A First-in-Human Clinical Trial of Pharmacologic Ascorbate and Ferumoxytol Combined With Concomitant Temozolomide and External Beam Radiation Therapy for Newly Diagnosed Glioblastoma [NCT04900792]Phase 112 participants (Anticipated)Interventional2023-02-28Active, not recruiting
A Randomized Phase I/II Study of Talazoparib or Temozolomide in Combination With Onivyde in Children With Recurrent Solid Malignancies and Ewing Sarcoma [NCT04901702]Phase 1/Phase 2160 participants (Anticipated)Interventional2021-06-09Recruiting
Phase II Study of Short Course Hypofractionated Proton Beam Therapy Incorporating 18F-DOPA-PET/MRI for Elderly Patients With Newly Diagnosed Glioblastoma [NCT03778294]Phase 243 participants (Actual)Interventional2019-03-28Completed
A Phase I Study of Temozolomide and RAD001C in Patients With Malignant Glioblastoma Multiforme [NCT00387400]Phase 132 participants (Actual)Interventional2007-03-20Completed
Efficacy and Tolerability of Cisplatin Plus Alternating Weekly Temozolomide in Recurrent High-grade Gliomas: A Single-arm Prospective Phase II Clinical Study [NCT02263105]Phase 267 participants (Actual)Interventional2014-10-31Completed
Pilot Study of Concomitant NovoTTF-200A and Temozolomide Chemoradiation for Newly Diagnosed Glioblastoma [NCT03232424]Phase 112 participants (Actual)Interventional2017-07-26Completed
Phase I/II Study to Evaluate the Safety and Clinical Efficacy of Atezolizumab (aPDL1) in Combination With Temozolomide and Radiation in Patients With Newly Diagnosed Glioblastoma (GBM) [NCT03174197]Phase 1/Phase 280 participants (Actual)Interventional2017-06-30Active, not recruiting
A Phase 1b, Open-label, Dose-Finding Study of CC-90010 in Combination With Temozolomide With or Without Radiation Therapy in Subjects With Newly Diagnosed Glioblastoma [NCT04324840]Phase 1194 participants (Anticipated)Interventional2020-07-10Active, not recruiting
A Phase II Trial of Irinotecan and Temozolomide in Combination With Existing High Dose Alkylator Based Chemotherapy for Treatment of Patients With Newly Diagnosed Ewing Sarcoma [NCT01864109]Phase 283 participants (Actual)Interventional2013-05-31Active, not recruiting
A Phase 2 Study of ABT-888 and Temozolomide for Metastatic Breast Cancer and an Expansion Cohort in BRCA1/2 Mutation Carriers [NCT01009788]Phase 264 participants (Actual)Interventional2009-11-30Active, not recruiting
Phase 3b Study for Management of Ocular Side Effects in Subjects With EGFR-amplified Glioblastoma Receiving Depatuxizumab Mafodotin (ABT-414) [NCT03419403]Phase 340 participants (Actual)Interventional2018-07-30Terminated(stopped due to The study was terminated because clinical development of depatuxizumab mafodotin in glioblastoma was stopped due to lack of survival benefit.)
A Phase II Study of Concurrent Radiation and Temozolomide Followed By Temozolomide and CCNU in the Treatment of Children With High-Grade Glioma [NCT00100802]Phase 2118 participants (Actual)Interventional2005-03-21Completed
Addition of Anlotinib Hydrochloride to the Stupp Regimen Versus the Stupp Regimen Alone for Newly Diagnosed Glioblastoma: A Randomized Double-blind Multicenter Prospective Phase II Study [NCT04959500]Phase 2150 participants (Anticipated)Interventional2021-06-10Recruiting
Application of Proteome Profiler Antibody Arrays to Find Angiogenetic Predictors in Glioma Paitents. [NCT03225963]60 participants (Anticipated)Observational2015-08-01Recruiting
INTELLANCE-2: ABT-414 Alone or ABT-414 Plus Temozolomide Versus Lomustine or Temozolomide for Recurrent Glioblastoma: A Randomized Phase 2 Study of the EORTC Brain Tumor Group [NCT02343406]Phase 2266 participants (Actual)Interventional2015-02-17Completed
Iodine-125 Brachytherapy Together With Chemotherapy Compared With Surgical Resection Followed by Concomitant Radiochemotherapy in Patients With Newly Diagnosed Glioblastoma，a Randomized, Open-label, Multi-center Clinical Trial [NCT04856852]84 participants (Anticipated)Interventional2021-06-28Not yet recruiting
A Phase 1 Study to Assess BDTX-1535, an Oral EGFR Inhibitor, in Patients With Glioblastoma or Non-Small Cell Lung Cancer [NCT05256290]Phase 1120 participants (Anticipated)Interventional2022-03-31Recruiting
A Phase 3 Study of Dinutuximab Added to Intensive Multimodal Therapy for Children With Newly Diagnosed High-Risk Neuroblastoma [NCT06172296]Phase 3478 participants (Anticipated)Interventional2024-02-14Not yet recruiting
A Phase II, Open-label, Single-arm, Multi-center Pilot Study to Evaluate the Efficacy and Safety of Whole-brain Radiotherapy With Concomitant Temozolomide in Lung Cancer and Breast Cancer Patients With Brain Metastases [NCT02133677]Phase 224 participants (Anticipated)Interventional2014-05-31Not yet recruiting
A Randomized, Controlled, Open, Multicenter, Phase II/III Clinical Study to Evaluate the Safety and Efficacy of Vebreltinib Enteric Capsules in the Treatment of sGBM/IDH Mutant Glioblastoma Patients With the ZM Fusion Gene (FUGEN). [NCT06105619]Phase 2/Phase 384 participants (Actual)Interventional2018-10-08Active, not recruiting
A Phase Ib Trial of Eribulin in Combination With Irinotecan and Temozolamide in Children With Relapsed or Refractory Solid Tumors [NCT06006273]Phase 1/Phase 248 participants (Anticipated)Interventional2023-08-16Recruiting
CAMPFIRE: Children's and Young Adult Master Protocol for Innovative Pediatric Research [NCT05999994]Phase 2105 participants (Anticipated)Interventional2020-01-22Recruiting
A Phase II Study of Temozolomide and Everolimus (RAD001) Therapy for Metastatic Melanoma [NCT00521001]Phase 249 participants (Actual)Interventional2008-01-31Completed
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 III Trial Comparing Whole Brain Radiation and Stereotactic Radiosurgery Alone Versus With Temozolomide or Erlotinib in Patients With Non-Small Cell Lung Cancer and 1-3 Brain Metastases [NCT00096265]Phase 3126 participants (Actual)Interventional2004-10-06Terminated
A Phase II Study of Pembrolizumab, Olaparib, and Temozolomide in Patients With Glioma [NCT05188508]Phase 257 participants (Anticipated)Interventional2022-01-14Recruiting
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
Phase I/II Study of ZD6474 (Vandetanib) With Radiation Therapy and Concomitant and Adjuvant Temozolomide in Patients With Newly-Diagnosed Glioblastoma [NCT00441142]Phase 1/Phase 2119 participants (Actual)Interventional2007-05-25Completed
Therapy-Optimization Trial and Phase II Study for the Treatment of Relapsed or Refractory of Primitive Neuroectodermal Brain Tumors and Ependymomas in Children and Adolescents [NCT00749723]Phase 2/Phase 3174 participants (Actual)Interventional2006-02-01Completed
Phase I/II Trial for Vaccine Therapy With Dendritic Cells - Transfected With hTERT-, Survivin- and Tumor Cell Derived mRNA + ex Vivo T Cell Expansion and Reinfusion in Patients With Metastatic Malignant Melanoma [NCT00961844]Phase 1/Phase 215 participants (Actual)Interventional2009-08-31Terminated(stopped due to Logistical problems)
A Phase 1 Dose Finding Study of the Safety and Pharmacokinetics of XL184 Administered Orally in Combination With Temozolomide and Radiation Therapy in the First Line Treatment of Subjects With Glioblastoma [NCT00960492]Phase 126 participants (Actual)Interventional2009-09-30Completed
Phase II Study of Temozolomide in Previously Untreated Acute Myeloid Leukemia (AML)/Myelodysplastic Syndrome (MDS) Subjects Unsuitable for Standard Induction Therapy Exhibiting Low MGMT Expression [NCT00687323]Phase 247 participants (Actual)Interventional2007-07-30Completed
Avastin in Combination With Radiation and Temozolomide Followed by Avastin, Temozolomide, and Topotecan for Glioblastoma Multiformes and Gliosarcomas [NCT01004874]Phase 280 participants (Actual)Interventional2009-12-30Completed
A Multi-centre, Two-arm, Randomized, Open, Phase II Study Investigating SentoClone® Compared to Reference Treatment in Advanced Malignant Melanoma [NCT00991250]Phase 2140 participants (Anticipated)Interventional2009-10-31Recruiting
A Phase I/II Trial of Temozolomide and ABT-888 in Subjects With Newly Diagnosed Glioblastoma Multiforme [NCT00770471]Phase 124 participants (Actual)Interventional2009-07-13Completed
Phase 1, Open Label, Multi-Center Study To Evaluate The Safety And Tolerability of CT-322 Administered In Combination With Focal Brain Radiotherapy And Temozolomide To Subjects With Newly Diagnosed Glioblastoma Multiforme [NCT00768911]Phase 130 participants (Anticipated)Interventional2008-10-31Active, not recruiting
"Phase II Pilot Trial of Chemo-Switch Regimen of Biochemotherapy Followed by Daily Low-Dose Temozolomide Plus Sorafenib in Advanced Melanoma" [NCT00673361]Phase 29 participants (Actual)Interventional2007-03-31Terminated
Dose Escalation Radiotherapy With Modulation of Intensity and Integrated Boost in Association With a Temozolomide in the Treatment of Glioblastoma [NCT01043536]Phase 110 participants (Actual)Interventional2009-09-30Completed
A Phase I/II Trial of Hydroxychloroquine in Conjunction With Radiation Therapy and Concurrent and Adjuvant Temozolomide in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00486603]Phase 1/Phase 292 participants (Actual)Interventional2007-10-29Completed
Releasing the Cancer Patient's Immune System From Down-regulation With Timed Delivery of Standard Chemotherapy [NCT00568451]Phase 212 participants (Actual)Interventional2006-06-30Terminated(stopped due to Slow accrual.)
A Randomized Phase II Trial of Temozolomide (TMZ) and Bevacizumab or ABI-007 (ABX)/Carboplatin (CBDCA) and Bevacizumab in Patients With Unresectable Stage IV Malignant Melanoma [NCT00626405]Phase 295 participants (Actual)Interventional2008-08-31Completed
A Phase I/II Trial Of Temozolomide And Vinorelbine For Patients With Recurrent Brain Metastases [NCT00026494]Phase 1/Phase 249 participants (Actual)Interventional2001-07-31Completed
A Phase II Study of the Safety and Efficacy of SVN53-67/M57-KLH (SurVaxM) in Survivin-Positive Newly Diagnosed Glioblastoma [NCT02455557]Phase 266 participants (Actual)Interventional2015-05-04Active, not recruiting
A Phase 2, Multiple-Cohort, Open-Label, International Study of Talazoparib Monotherapy and Talazoparib Plus Temozolomide in Women With Relapsed Ovarian, Fallopian Tube, and Peritoneal Cancer [NCT02836028]Phase 20 participants (Actual)Interventional2016-10-31Withdrawn
A Phase 1/2, Open-label, Dose-exploration and Expansion Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of NTX-301 Monotherapy in Advanced Solid Tumours, and in Combination With Platinum-based Chemotherapy in Advanced Ova [NCT04851834]Phase 1/Phase 212 participants (Actual)Interventional2021-08-25Terminated(stopped due to Study was terminated by IP Holder (collaborator), PinotBio Inc.)
A Prospective Study of Concurrent Chemoradiotherapy With Temozolomide Versus Radiation Therapy Alone in Patients With IDH Wild-type/TERT Promoter Mutation Grade II/III Gliomas [NCT02766270]Early Phase 130 participants (Anticipated)Interventional2016-09-26Recruiting
Radiotherapy Plus Concomitant Temozolomide for Refractory Pituitary Adenomas，A Randomized，Double-blind, Placebo-controlled Phase II Trial [NCT04244708]Phase 2/Phase 3150 participants (Anticipated)Interventional2020-02-10Not yet recruiting
A Randomized Phase 3 Open Label Study of Nivolumab vs Temozolomide Each in Combination With Radiation Therapy in Newly Diagnosed Adult Subjects With Unmethylated MGMT (Tumor O-6-methylguanine DNA Methyltransferase) Glioblastoma (CheckMate 498: CHECKpoint [NCT02617589]Phase 3560 participants (Actual)Interventional2016-03-01Completed
Randomized Phase II Trial of Hypofractionated Dose-Escalated Photon IMRT or Proton Beam Therapy Versus Conventional Photon Irradiation With Concomitant and Adjuvant Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT02179086]Phase 2624 participants (Actual)Interventional2014-10-27Active, not recruiting
A Randomised Phase II Study of NivolUmab and TeMozolomide vs Temozolomide Alone in Newly Diagnosed Elderly Patients With Glioblastoma (NUTMEG) [NCT04195139]Phase 2103 participants (Actual)Interventional2018-02-22Active, not recruiting
Phase II Study of Pembrolizumab (MK-3475) in Combination With Standard Therapy for Newly Diagnosed Glioblastoma [NCT03197506]Phase 252 participants (Actual)Interventional2017-09-15Suspended(stopped due to Temporary closure per protocol design)
A Phase I Study of a Personalized NeoAntigen Cancer Vaccine With Radiotherapy Plus Pembrolizumab/MK-3475 Among Newly Diagnosed Glioblastoma Patients [NCT02287428]Phase 156 participants (Anticipated)Interventional2014-11-30Recruiting
A Randomized Phase III Study of Temozolomide and Short-Course Radiation Versus Short-Course Radiation Alone In The Treatment of Newly Diagnosed Glioblastoma Multiforme in Elderly Patients [NCT00482677]Phase 3562 participants (Actual)Interventional2007-11-14Completed
Phase 2 Study of Nimotuzumab in Combination With Radio-chemotherapy for the Treatment of Brainstem Tumor in Children [NCT02672241]Phase 230 participants (Anticipated)Interventional2016-01-31Recruiting
Clinical Study of Apatinib Combined With Temozolomide in the Treatment of Uncontrolled or Repeated High-grade Gliomas [NCT04253873]Phase 240 participants (Anticipated)Interventional2019-12-16Recruiting
A Phase III Randomized Study of Neuradiab in Combination With External Beam Radiation and Temozolomide Versus External Beam Radiation and Temozolomide in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00615186]Phase 39 participants (Actual)Interventional2008-06-30Terminated(stopped due to Due to delay in site initiation and funding considerations)
Phase I Trail of Temodar Plus O6-Benzylguanine (O6-BG) (NSC 637037) Plus Irinotecan (CPT-11) (NSC 616348) in the Treatment of Patients With Recurrent / Progressive Cerebral Anaplastic Gliomas [NCT00612638]Phase 196 participants (Anticipated)Interventional2005-01-31Completed
A Phase II Study Of Gliadel, Concomitant Temozolomide And Radiation, Followed By Dose Dense Therapy With Temozolomide Plus Bevacizumab For Newly Diagnosed Malignant High Grade Glioma [NCT00660621]Phase 240 participants (Anticipated)Interventional2008-04-30Recruiting
Phase 1 Study of the Combination of Lapatinib and Temozolomide for the Treatment of Progressive Brain Disease in HER-2 Positive Breast Cancer [NCT00614978]Phase 118 participants (Actual)Interventional2008-01-31Completed
A Phase II Study of Multiparametric MR-Guided High Dose Adaptive Radiotherapy With Concurrent Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT04574856]Phase 230 participants (Anticipated)Interventional2020-11-04Recruiting
A 2-part Trial Comparing Overall Survival of Patients With Metastatic Ewing's Sarcoma Treated With Vigil Versus Gemcitabine and Docetaxel and to Determine Safety Profile of Vigil in Combination With Irinotecan and Temozolomide. [NCT02511132]Phase 222 participants (Actual)Interventional2016-02-10Completed
Effectiveness and Safety of Whole-brain Radiotherapy With/Without TMZ Concurrent Chemotherapy or Avoidance of Hippocampus for Patients of Brain Metastases: a Multi-institutional, Randomized Controlled Clinical Trial [NCT02832635]Phase 2256 participants (Anticipated)Interventional2016-07-31Not yet recruiting
Regorafenib in Combination With Temozolomide With or Without Radiotherapy in Patients With Newly Diagnosed MGMT-Methylated, IDH Wild-type Glioblastoma. A Phase I Dose-finding Study [NCT06095375]Phase 136 participants (Anticipated)Interventional2022-07-04Recruiting
A Randomized, Open-Label, Phase 2 Study Evaluating Abemaciclib in Combination With Irinotecan and Temozolomide in Participants With Relapsed or Refractory Ewing's Sarcoma [NCT05440786]Phase 245 participants (Anticipated)Interventional2022-09-20Recruiting
Phase I/II Multicenter Study to Assess Efficacy and Safety of Ribociclib (LEE011) in Combination With Topotecan and Temozolomide (TOTEM) in Pediatric Patients With Relapsed or Refractory Neuroblastoma and Other Solid Tumors [NCT05429502]Phase 1/Phase 2231 participants (Anticipated)Interventional2022-12-27Recruiting
Phase II Clinical Trial of Bavituximab With Radiation and Temozolomide for Patients With Newly Diagnosed Glioblastoma [NCT03139916]Phase 236 participants (Actual)Interventional2017-09-13Completed
Adjuvant Dendritic-Cell Immunotherapy Plus Temozolomide Following Surgery and Chemoradiation in Patients With Newly Diagnosed Glioblastoma [NCT02649582]Phase 1/Phase 220 participants (Anticipated)Interventional2015-12-31Recruiting
Fractionated Stereotactic Radiotherapy Combined With Temozolomide for Refractory Brain Metastases: A Single-arm, Single-center Phase II Trial [NCT02654106]Phase 265 participants (Actual)Interventional2011-10-31Completed
Genetic Variates of Response to Cisplatin, Vinblastine, and Temozolomide (CVT) in Patients With Metastatic Melanoma [NCT00885534]Phase 27 participants (Actual)Interventional2009-04-30Completed
Addition of Anlotinib Hydrochloride to the Stupp Regimen Versus the Stupp Regimen Alone for Newly Diagnosed Glioblastoma: A Randomized Multicenter Prospective Phase II Study [NCT04157478]Phase 2464 participants (Anticipated)Interventional2020-01-31Not yet recruiting
[NCT02772107]Phase 2/Phase 3132 participants (Anticipated)Interventional2015-12-31Recruiting
Multisite Open-label Randomized Phase II Clinical Trial in Newly Diagnosed Glioblastoma Treated by Concurrent Temoradiation and Adjuvant Temozolomide +/- Ultrasound-induced Blood Brain Barrier Opening. [NCT04614493]Phase 266 participants (Anticipated)Interventional2021-09-11Recruiting
Multicenter Phase 2 Evaluation of Temozolomide for Treatment of Brain Metastases of Either Malignant Melanoma, Breast and Non-small Cell Lung Cancer. [NCT00831545]Phase 2162 participants (Actual)Interventional2000-12-01Completed
Vaccination With Autologous Dendritic Cells Loaded With Autologous Tumour Homogenate in Glioblastoma: a Phase II Study [NCT04523688]Phase 228 participants (Anticipated)Interventional2021-03-25Recruiting
A Study to Evaluate the Safety and Efficacy of the Tumor-targeting Human Antibody-cytokine Fusion Protein L19TNF Plus Standard Temozolomide Chemoradiotherapy in Patients With Newly Diagnosed Glioblastoma [NCT04443010]Phase 1/Phase 2226 participants (Anticipated)Interventional2021-01-20Recruiting
A Phase III Randomized Trial of Repeated Superselective Intraarterial Cerebral Infusion (SIACI) of Bevacizumab (Avastin) With Temozolomide and Radiation Compared to Temozolomide and Radiation Alone in Newly Diagnosed Glioblastoma (GBM) [NCT05271240]Phase 3432 participants (Anticipated)Interventional2022-04-27Recruiting
A Phase Ib/II Study of Intermittent Talazoparib Plus Temozolomide in Patients With Metastatic Castration Resistant Prostate Cancer and No Mutations in DNA Damage Repair [NCT04019327]Phase 1/Phase 244 participants (Anticipated)Interventional2019-07-11Recruiting
European Proof-of-Concept Therapeutic Stratification Trial of Molecular Anomalies in Relapsed or Refractory Tumors [NCT02813135]Phase 1/Phase 2460 participants (Anticipated)Interventional2016-08-03Recruiting
A Randomized Phase II Study of Subventricular Zone (SVZ) Irradiation Plus Temozolomide in Newly Diagnosed Glioblastoma Multiforme [NCT02177578]Phase 260 participants (Anticipated)Interventional2014-07-08Recruiting
A Phase II Randomized Trial of Proton Vs. Photon Therapy (IMRT) for Cognitive Preservation in Patients With IDH Mutant, Low to Intermediate Grade Gliomas [NCT03180502]Phase 2120 participants (Anticipated)Interventional2017-08-02Recruiting
Pilot Study of Anlotinib in Combination With STUPP Regimen for Treatment of Patients With Newly Diagnosed Glioblastoma [NCT04119674]Phase 1/Phase 233 participants (Actual)Interventional2019-03-19Completed
A Phase I Study of Oral Carboxyamidotriazole Orotate (CTO) Titrated as a Single Agent in Patients With Advanced or Metastatic Solid Tumors and Titrated in Combination Therapy With Temodar® for Patients With Glioblastoma and Other Recurrent Malignant Gliom [NCT01107522]Phase 1100 participants (Anticipated)Interventional2010-05-31Active, not recruiting
Treatment Strategy for Low-grade Gliomas [NCT00897377]Phase 3500 participants (Anticipated)Interventional2007-12-31Terminated(stopped due to Difficulty in recruiting patients)
(Inhibition of NF-kB Signaling in Melanoma Therapy) A Phase I/II Clinical Trial of PS-341, a Proteasome Inhibitor, in Combination With an Extended Continuous Oral Schedule of Temozolomide in Patients With Advanced Refractory Solid Tumors With the Phase II [NCT00512798]Phase 1/Phase 247 participants (Actual)Interventional2003-06-30Terminated(stopped due to This study was terminated due to lack of efficacy)
A Phase II Study of Irinotecan + Temozolomide in Children With Recurrent Neuroblastoma [NCT00311584]Phase 259 participants (Actual)Interventional2006-04-30Completed
A Phase II, Multicenter, Study for Newly Diagnosed Glioblastomas Using Boron Neutron Capture Therapy, Additional X-ray Treatment and Chemotherapy [NCT00974987]Phase 232 participants (Actual)Interventional2009-09-01Completed
A Phase II Trial of Concurrent Radiation Therapy and Temozolomide Followed by Temozolomide Plus Sorafenib in the First-Line Treatment of Patients With Glioblastoma Multiforme [NCT00544817]Phase 247 participants (Actual)Interventional2007-04-30Completed
Randomized Phase II Study: Temozolomide (TMZ) Concomitant to Radiotherapy Followed by Sequential TMZ in Advanced Non-Small Cell Lung Cancer (NSCLC) Patients With Central Nervous System (CNS) Metastasis Versus Radiotherapy Alone [NCT00266812]Phase 235 participants (Actual)Interventional2005-03-08Terminated(stopped due to Patient target could not be reached within the planned timeframe.)
Phase I Dose Escalation Study of Temozolomide With Autologous Stem Cell Rescue for Patients With Relapsed/Refractory CNS Malignancy Including Isolated Metastatic Disease [NCT00629187]Phase 12 participants (Actual)Interventional2004-04-30Terminated(stopped due to The study was stopped due to lack of adequate enrollment.)
A Single-center, Open-label, Phase 1 Study of Macitentan, Radiotherapy and Temozolomide Concurrent Therapy Followed by Maintenance Therapy With Macitentan and Temozolomide in Subjects With Newly Diagnosed Glioblastoma [NCT02254954]Phase 130 participants (Actual)Interventional2015-01-08Terminated(stopped due to Sponsor decision due to low recruitment)
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
A Phase II/III Randomized, Open-Label Study of Toca 511, A Retroviral Replicating Vector, Combined With Toca FC With Temozolomide and Radiation Followed by Adjuvant Temozolomide and Toca FC Compared to Temozolomide and Radiation Followed by Adjuvant Temoz [NCT04105374]Phase 2/Phase 30 participants (Actual)Interventional2020-01-31Withdrawn(stopped due to NCI approval withdrawn)
Phase 2 Study of Radiation Therapy and Combination Chemotherapy Following Surgery in Treating Children With Newly Diagnosed Medulloblastoma [NCT02681705]Phase 260 participants (Anticipated)Interventional2010-01-31Recruiting
DIRECT (DIsulfiram REsponse as add-on to ChemoTherapy in Recurrent) Glioblastoma: A Randomized Controlled Trial [NCT02678975]Phase 2/Phase 388 participants (Actual)Interventional2017-01-31Completed
A Phase II Study of Dose-Dense Temozolomide and Lapatinib for Recurrent Low-Grade and Anaplastic Supratentorial, Infratentorial and Spinal Cord Ependymoma [NCT00826241]Phase 258 participants (Actual)Interventional2009-01-31Completed
Efficacy and Safety of AP 12009 in Adult Patients With Recurrent or Refractory Anaplastic Astrocytoma or Secondary Glioblastoma as Compared to Standard Chemotherapy Treatment: A Randomized, Actively Controlled, Open Label Clinical Phase III Study. [NCT00761280]Phase 327 participants (Actual)Interventional2008-12-31Terminated(stopped due to Unable to recruit the projected patient number. All analyses are descriptive, only.)
A Randomized, Double-Blind, Placebo-Controlled, Phase 2 Study Evaluating the Efficacy of ABT-888 in Combination With Temozolomide Versus Temozolomide Alone in Subjects With Metastatic Melanoma [NCT00804908]Phase 2346 participants (Actual)Interventional2009-02-28Completed
Phase III Double-blind Placebo-Controlled Trial of Conventional Concurrent Chemoradiation and Adjuvant Temozolomide Plus Bevacizumab Versus Conventional Concurrent Chemoradiation and Adjuvant Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT00884741]Phase 3637 participants (Actual)Interventional2009-04-15Completed
A Phase 2 Study of Pamiparib (BGB-290) Plus Temozolomide for Hereditary Leiomyomatosis and Renal Cell Cancer (HLRCC) [NCT04603365]Phase 20 participants (Actual)Interventional2021-10-18Withdrawn(stopped due to enrollment)
Temodal Capsule All-Case-Registered Surveillance (Designated Drug Use Investigation) - Evaluation of The Safety and Efficacy of Temodal in Patients With Newly Diagnosed Malignant Glioma (Concomitant With Radiotherapy and Then as Monotherapy) and Relapsed [NCT00705198]1,804 participants (Actual)Observational2006-09-30Completed
A Randomized, Multicenter, Double-Blind, Placebo-Controlled, Phase 2b Study to Assess the Safety and Efficacy of IGV-001, an Autologous Cell Immunotherapy With Antisense Oligonucleotide (IMV-001) Targeting IGF-1R, in Newly Diagnosed Patients With Glioblas [NCT04485949]Phase 293 participants (Anticipated)Interventional2023-03-20Recruiting
Effect of rhIL-7-hyFc on Increasing Lymphocyte Counts in Patients With Newly Diagnosed Non-severe Lymphopenic Gliomas Following Radiation and Temzolomide [NCT03687957]Phase 1/Phase 270 participants (Anticipated)Interventional2019-01-04Recruiting
[NCT02330991]Phase 2204 participants (Actual)Interventional2015-01-31Completed
Avastin and Temozolomide Following Radiation and Chemotherapy for Newly Diagnosed Glioblastoma Multiforme: A Phase II Study [NCT00590681]Phase 262 participants (Actual)Interventional2007-02-28Completed
A Non-Randomized, Open-Label, Multi-Center Phase 1/2 Study Evaluating the Safety, Pharmacokinetics and Efficacy of ABT-414 in Japanese Subjects With Malignant Glioma [NCT02590263]Phase 1/Phase 253 participants (Actual)Interventional2015-08-24Completed
Temodal (TMZ) in Concomitant Radiochemotherapy Followed by Sequential TMZ Chemotherapy in Newly Diagnosed Glioblastoma Multiforme Patients - an Observational Program [NCT00725010]64 participants (Actual)Observational2007-04-30Completed
Phase II Trial of Neoadjuvant Temozolomide in Melanoma Patients With Palpable Stage III or IV Disease Undergoing Complete Surgical Resection [NCT00588341]Phase 224 participants (Actual)Interventional2005-09-30Completed
A Phase II Study of Temozolomide (SCH 52365) in the Treatment of Patients With Relapsed Small Cell Lung Cancer [NCT00022711]Phase 27 participants (Actual)Interventional2002-01-31Completed
A Phase 2 Study of Continuous Talazoparib Plus Intermittent Low-Dose Temozolomide in Patients With Relapsed or Refractory Extensive-Stage Small Cell Lung Cancer (TRIO-US L-07) [NCT03672773]Phase 228 participants (Anticipated)Interventional2018-10-31Recruiting
Phase II Study of Temozolomide for Relapsed Sensitive or Refractory Small Cell Lung Cancer [NCT00740636]Phase 292 participants (Actual)Interventional2008-08-31Completed
Phase 2 Single- Arm Studies of Temozolomide in Combination With Topotecan in Refractory and Relapsed Neuroblastoma and Other Paediatric Solid Tumours [NCT00918320]Phase 2129 participants (Actual)Interventional2009-06-30Completed
Aerosol Liposomal 9-Nitro-20(S)-Camptothecin (L9-NC) and Temozolomide in Ewing's Sarcoma and Other Solid Tumors With Lung Involvement [NCT00492141]Phase 1/Phase 210 participants (Actual)Interventional2006-06-30Completed
SCH 52365 Phase II Clinical Study in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00684567]Phase 230 participants (Actual)Interventional2005-09-27Completed
Phase II Trial of Carboplatin, Paclitaxel, and Temozolomide for Patients With Metastatic Melanoma [NCT01009515]Phase 219 participants (Actual)Interventional2009-08-31Terminated(stopped due to Low accrual; target accrual not met)
Benzylguanine-Mediated Tumor Sensitization With Chemoprotected Autologous Stem Cells for Patients With Malignant Gliomas [NCT00669669]Phase 1/Phase 212 participants (Actual)Interventional2009-02-25Terminated(stopped due to Terminated due to loss in funding.)
A Randomized Phase II Trial of Bevacizumab With Irinotecan or Bevacizumab With Temozolomide in Recurrent Glioblastoma [NCT00433381]Phase 2123 participants (Actual)Interventional2007-03-01Completed
Safety and Efficacy of LITT Combined With Early Use of Temozolomide for Recurrent Glioblastomas [NCT05663125]Phase 1/Phase 210 participants (Anticipated)Interventional2022-12-01Active, not recruiting
A Pilot Study of the Addition of Bevacizumab to Vincristine, Oral Irinotecan, and Temozolomide (VOIT Regimen) for Relapsed/Refractory Pediatric Solid Tumors [NCT00786669]Phase 113 participants (Actual)Interventional2008-10-31Completed
SCH 52365 Phase II Clinical Study: A Study on the Efficacy and Safety of Monotherapy With SCH 52365 in Patients With First Relapsed Anaplastic Astrocytoma [NCT00783393]Phase 232 participants (Actual)Interventional2003-05-27Completed
"Randomized Multicentric Phase II Study of Prolonged Adjuvant Temozolomide or Stop and Go in Glioblastoma Patients: The PATSGO Study" [NCT00643825]Phase 264 participants (Anticipated)Interventional2008-01-31Recruiting
Phase Ib/II: Epigenetic Modification of Chemosensitivity and Apoptosis in Metastatic Melanoma: Treatment of a Resistant Disease Using Decitabine, Temozolomide and Panobinostat [NCT00925132]Phase 1/Phase 239 participants (Actual)Interventional2009-12-31Terminated(stopped due to Change in the number of approved drugs for metastatic melanoma)
A Prospective, Multi-center Trial of NovoTTF-100A Together With Temozolomide Compared to Temozolomide Alone in Patients With Newly Diagnosed GBM. [NCT00916409]Phase 3700 participants (Anticipated)Interventional2009-06-30Completed
Phase I Trial of Aflibercept (VEGF Trap) With Radiation Therapy and Concomitant and Adjuvant Temozolomide in Patients With Malignant Glioma [NCT00650923]Phase 161 participants (Actual)Interventional2008-07-31Completed
A Phase 1/1B Dose-Escalation Study to Determine the Safety and Tolerability of SCH 717454 Administered in Combination With Chemotherapy in Pediatric Subjects With Advanced Solid Tumors (Protocol No. 05883) [NCT00960063]Phase 14 participants (Actual)Interventional2009-11-11Terminated(stopped due to Study was terminated for business reasons.)
An Open-label, Phase 1b Study to Evaluate the Safety and Tolerability of Eflornithine Plus Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT05879367]Phase 166 participants (Anticipated)Interventional2023-07-24Recruiting
A Phase I Study of Temozolomide, Oral Irinotecan, and Vincristine for Children With Refractory Solid Tumors [NCT00138216]Phase 142 participants (Actual)Interventional2005-10-31Completed
NOA-04 Randomized Phase III Study of Sequential Radiochemotherapy of Anaplastic Glioma With PCV or Temozolomide [NCT00717210]Phase 3318 participants (Actual)Interventional1999-06-30Completed
A Phase I Study of the Combination of Radiation Therapy (RT), Arsenic Trioxide (ATO) and Temozolomide (TMZ) in Patients With Newly-Diagnosed Glioblastoma Multiforme (GBM) [NCT00720564]Phase 118 participants (Anticipated)Interventional2008-04-30Completed
Phase 2 Study of Dose-Intense Temozolomide in Recurrent Glioblastoma [NCT00657267]Phase 258 participants (Actual)Interventional2008-05-31Completed
A Phase I Trial of Dose Escalation of Metformin in Combination With Vincristine, Irinotecan, and Temozolomide in Children With Relapsed or Refractory Solid Tumors [NCT01528046]Phase 126 participants (Actual)Interventional2012-09-24Completed
A Phase I Study of Sorafenib With Radiation and Temozolomide in Newly Diagnosed Glioblastoma or Gliosarcoma [NCT00734526]Phase 118 participants (Actual)Interventional2008-12-18Terminated
Clinical Study of Evaluating the Safety and Initial Efficacy of XS005 Cell Injection Combined With Stupp Regimen for Adjuvant Chemotherapy in Subjects With Primary Glioblastoma [NCT06147505]Phase 1/Phase 230 participants (Anticipated)Interventional2023-10-29Recruiting
A Phase I Study of Allogeneic Ex Vivo Expanded Gamma Delta (γδ) T Cells (IND # 28460) in Combination With Dinutuximab, Temozolomide, Irinotecan, and Zoledronate in Children With Refractory, Relapsed, or Progressive Neuroblastoma [NCT05400603]Phase 124 participants (Anticipated)Interventional2023-11-06Recruiting
A Randomized, Open-label Pilot Trial to Evaluate the Safety and Efficacy of Carmustine Wafer in Combination With Retifanlimab and Standard Radiation With or Without Temozolomide in Newly-Diagnosed Adult Subjects With Glioblastoma [NCT05083754]Phase 150 participants (Anticipated)Interventional2022-08-31Recruiting
Phase I/II Trial of Dasatinib (Sprycel) With Radiation Therapy and Concomitant and Adjuvant Temozolomide in Patients With Newly-Diagnosed Glioblastoma [NCT00895960]Phase 116 participants (Actual)Interventional2009-05-07Terminated(stopped due to Sponsor withdrew support; Study did not progress to Phase II.)
Radiotherapy Versus Radiotherapy Combined With Temozolomide in High-risk Low-grade Gliomas After Surgery [NCT04316039]Phase 2/Phase 3250 participants (Anticipated)Interventional2018-04-10Recruiting
A Phase 1, Multicenter, Open-Label, Dose Escalation Study of Tandutinib (Formerly MLN518) in Combination With Temozolomide and Bevacizumab Following Concurrent Radiation Therapy and Temozolomide in the Treatment of Patients With Newly Diagnosed Glioblasto [NCT00904852]Phase 130 participants (Anticipated)Interventional2009-06-30Withdrawn
Phase 2 Clinical Trial Treating Relapsed/Recurrent/Refractory Pediatric Solid Tumors With the Genomically-Targeted Agent Erlotinib in Combination With Temozolomide [NCT02689336]Phase 20 participants (Actual)Interventional2016-08-06Withdrawn(stopped due to Could not recruit any participants)
Use of PET/CT Imaging With 18F-fluoroethylcholine (FEC) in the Evaluation of Patients Treated With Radiotherapy and Temozolomide Following a Diagnosis of Glioblastoma Multiforme [NCT00943462]0 participants (Actual)Observational2009-06-30Withdrawn(stopped due to No eligible patients could be recruited.)
A Phase I Study of Cyclic Oral Administration of SCH 52365 for 21 of 28 Days in Patients With Advanced Solid Malignancies [NCT00003708]Phase 132 participants (Actual)Interventional1998-07-31Completed
Phase 1b, Multicenter, Open-Label Study of Marizomib With Temozolomide and Radiotherapy in Patients With Newly Diagnosed WHO Grade IV Malignant Glioma [NCT02903069]Phase 166 participants (Actual)Interventional2016-08-17Completed
A Cancer Research UK Phase I Trial of Olaparib (AZD2281), an Oral PARP Inhibitor, in Combination With Extended Low-Dose Oral Temozolomide in Patients With Relapsed Glioblastoma [NCT01390571]Phase 134 participants (Anticipated)Interventional2011-07-31Completed
A Pilot Study Investigating Neoadjuvant Temozolomide-based Proton Chemoradiotherapy for High-Risk Soft Tissue Sarcomas [NCT00881595]Phase 20 participants (Actual)Interventional2009-02-28Withdrawn(stopped due to No patients accrued since study opened)
A Protocol for the Treatment of Newly Diagnosed Rhabdomyosarcoma Using Molecular Risk Stratification and Liposomal Irinotecan Based Therapy in Children With Intermediate and High Risk Disease [NCT06023641]Phase 1/Phase 2100 participants (Anticipated)Interventional2023-11-30Not yet recruiting
Phase II Study of Two Distinct Tailored Temozolomide Regimens for Patients With Acute Myeloid Leukemia Age > 60 Years and Poor Risk/Refractory Disease [NCT00611247]Phase 242 participants (Actual)Interventional2007-12-31Completed
The Prospective Study of FTD Program and HD-MTX-Ara-C Program Contrast in the Treatment of PCNSL Lymphoma. [NCT05274139]Phase 220 participants (Actual)Interventional2017-03-02Completed
A Phase 2 Clinical Trial of Neoadjuvant Camrelizumab Plus Apatinib and Temozolomide in High Risk Clinical Stage Ⅱ-Ⅲ Acral Melanoma [NCT05512481]Phase 240 participants (Anticipated)Interventional2022-09-13Recruiting
Evaluating the Impact of 18F-DOPA-PET on Radiotherapy Planning for Newly Diagnosed Gliomas [NCT01991977]Phase 291 participants (Actual)Interventional2013-12-31Active, not recruiting
VITAS: Atezolizumab in Combination With Chemotherapy for Pediatric Relapsed/Refractory Solid Tumors: An Open-label, Phase II, Single-arm, Multi-center Trial [NCT04796012]Phase 1/Phase 223 participants (Anticipated)Interventional2023-04-18Recruiting
IPI-Biochemotherapy for Chemonaive Patients With Metastatic Melanoma [NCT01409174]Phase 119 participants (Actual)Interventional2013-02-28Terminated(stopped due to Slow accrual, closed in Phase I.)
A Phase II Study of Gliadel, Concomitant Temozolomide and Radiation, Followed by Metronomic Therapy With Temozolomide for Newly Diagnosed Malignant High Grade Glioma [NCT00548938]Phase 240 participants (Anticipated)Interventional2007-10-31Terminated(stopped due to Principal Investigator has left the institution)
Phase I Biochemotherapy With Cisplatin, Temozolomide, With Increasing Doses of Abraxane, Combined With Interleukin-2 and Interferon in Patients With Metastatic Melanoma [NCT00970996]Phase 110 participants (Actual)Interventional2009-09-30Completed
Radiation Therapy and Concurrent Plus Adjuvant Temsirolimus (CCI-779) Versus Chemo-Irradiation With Temozolomide in Newly Diagnosed Glioblastoma Without Methylation of the MGMT Gene Promoter - A Randomized Multicenter, Open-Label, Phase II Study. [NCT01019434]Phase 2111 participants (Actual)Interventional2009-10-31Completed
Phase II Study of Bi-Weekly Temozolomide Plus Bevacizumab for Adult Patients With Recurrent Glioblastoma Multiforme [NCT00883298]Phase 230 participants (Actual)Interventional2009-04-30Completed
Dose-intensified Rechallenge With Temozolomide, One Week On One Week Off Versus Three Weeks On One Week Off in Patients With Progressive or Recurrent Glioblastoma [NCT00941460]Phase 2105 participants (Actual)Interventional2009-09-30Completed
A Pilot Study of Bevacizumab-Based Therapy in Patients With Newly Diagnosed High-Grade Gliomas and Diffuse Intrinsic Pontine Gliomas [NCT00890786]Early Phase 127 participants (Actual)Interventional2009-05-31Completed
Feasibility Study on Laser Interstitial Thermal Therapy Ablation for the Treatment of Newly Diagnosed Glioblastoma [NCT02880410]Phase 13 participants (Actual)Interventional2017-08-15Terminated(stopped due to Terminated (failure to enroll))
Open-label, Non-randomized, Two-stage Study to Evaluate the Efficacy, Safety, Pharmacokinetics and Pharmacodynamic Effects of PQR309 in Patients With Progressive Glioblastoma [NCT02850744]Phase 210 participants (Actual)Interventional2015-07-31Terminated
Phase I-II Study of Nivolumab in Combination With Temozolomide and Radiotherapy in Children and Adolescents With Newly Diagnosed High-grade Glioma [NCT04267146]Phase 1/Phase 240 participants (Anticipated)Interventional2019-07-15Recruiting
Phase II Study of Capecitabine and Temozolomide for Progressive, Differentiated, Metastatic Neuroendocrine Cancers [NCT00869050]Phase 241 participants (Actual)Interventional2005-08-31Completed
A Phase 1 Dose-Escalation Study of XL765 (SAR245409) in Combination With Temozolomide With and Without Radiation in Subjects With Malignant Gliomas [NCT00704080]Phase 154 participants (Actual)Interventional2008-08-31Completed
A Phase I Dose Per Fraction Escalation Study of Hypofractionated Intensity-Modulated Radiation Therapy (Hypo-IMRT) Combining With Temozolomide (TMZ) Chemotherapy for Patients With Newly Diagnosed Glioblastoma Multiforme (GBM) [NCT00792012]Phase 137 participants (Actual)Interventional2005-11-30Completed
Repurposing the Antipsychotic Drug Chlorpromazine as a Therapeutic Agent in the Combined Treatment of Newly Diagnosed Glioblastoma Multiforme [NCT04224441]Phase 241 participants (Anticipated)Interventional2019-12-15Recruiting
A Phase I Study of ABT-888, an Oral Inhibitor of Poly (ADP-Ribose) Polymerase and Temozolomide in Children With Recurrent/Refractory CNS Tumors [NCT00946335]Phase 131 participants (Actual)Interventional2009-07-31Completed
A Phase I Trial of the Addition of the Farnesyl Transferase Inhibitor, SCH 66336, to Temodar for Patients With Grade 3 and 4 Malignant Gliomas [NCT00612651]Phase 137 participants (Actual)Interventional2005-10-31Completed
A Randomized Phase II Trial With Bevacizumab, Irinotecan and Cerebral Radiotherapy Versus Bevacizumab, Temozolomide and Cerebral Radiotherapy as First Line Treatment for Patients With Glioblastoma Multiforme [NCT00817284]Phase 260 participants (Actual)Interventional2008-11-30Completed
A Phase I Trial of the Protease Inhibitor Nelfinavir and Concurrent Radiation and Temozolomide in Patients With WHO Grade IV Glioma [NCT00915694]Phase 115 participants (Actual)Interventional2009-04-30Terminated(stopped due to Insufficient accrual)
Phase II Treatment of Adults With Primary Malignant Glioma With Irinotecan Plus Temozolomide [NCT00616005]Phase 241 participants (Anticipated)Interventional2005-11-30Completed
Phase I Study of Temozolomide and Intrathecal DepoCyt in Patients With Neoplastic Meningitis [NCT00515788]Phase 111 participants (Actual)Interventional2006-02-28Terminated(stopped due to Study terminated due to slow accrual with no expansion to additional phase.)
A Randomized, Placebo Controlled Phase 3 Study of ABT-414 With Concurrent Chemoradiation and Adjuvant Temozolomide in Subjects With Newly Diagnosed Glioblastoma (GBM) With Epidermal Growth Factor Receptor (EGFR) Amplification (Intellance1) [NCT02573324]Phase 3691 participants (Actual)Interventional2015-01-04Completed
Phase II Trial of Pemetrexed and Temozolomide in Treating Patients With Relapsed PCNSL [NCT01985451]Phase 215 participants (Anticipated)Interventional2013-03-31Active, not recruiting
ESP1/SARC025 Global Collaboration: A Phase I Study of a Combination of the PARP Inhibitor, Niraparib and Temozolomide and/or Irinotecan in Patients With Previously Treated,Incurable Ewing Sarcoma [NCT02044120]Phase 134 participants (Actual)Interventional2014-05-31Completed
A Phase I/II Trial of Temodar in Pediatric Patients and Young Adults With High-Risk or Recurrent Solid Tumors [NCT00005952]Phase 1/Phase 230 participants (Anticipated)Interventional2000-08-31Completed
Phase II Treatment of Children With Newly Diagnosed Malignant Central Nervous System Tumors With Temozolomide Prior to Radiation Therapy [NCT00005955]Phase 20 participants Interventional2000-08-31Completed
A Phase I Study of Temozolomide and CCNU in Pediatric Patients With Newly Diagnosed Incompletely Resected Non-Brainstem High-Grade Gliomas [NCT00006024]Phase 132 participants (Actual)Interventional2000-11-30Completed
Lobaplatin Combined With Etoposide for First-line Treatment in Extensive Stage Sclc Then Benefit Patients Follow up Temozolomide Maintain Therapeutic [NCT02972320]Phase 260 participants (Anticipated)Interventional2016-06-30Recruiting
Phase I Trial of DNA-PK Inhibitor (M3814) in Combination With Radiation and Adjuvant Temozolomide in Newly Diagnosed MGMT Unmethylated Glioblastoma [NCT04555577]Phase 129 participants (Anticipated)Interventional2020-09-20Recruiting
A Phase I, Open Label Study of AT-101 Plus Radiotherapy and Temozolomide and of AT-101 Plus Adjuvant Temozolomide for Patients With Newly-Diagnosed Glioblastoma Multiforme [NCT00390403]Phase 150 participants (Anticipated)Interventional2007-02-28Completed
Phase I Treatment of Adults With Primary Malignant Glioma With Irinotecan (CPT-11) (NSC- #6616348) Plus Temodar (NSC #362856) [NCT00005951]Phase 10 participants Interventional2000-08-31Completed
Phase II Treatment of Adults With Brain Metastases With Temodar [NCT00005954]Phase 20 participants Interventional2000-08-31Completed
Treatment of Patients With Metastatic Malignant Melanoma With Chemobiotherapy With Temozolomide, GM-CSF, IL2, and Interferon Alfa-2b Phase II Trial [NCT00014092]Phase 20 participants Interventional1999-12-31Completed
Intensive Dose Temozolomide Treatment or Temozolomide With Thalidomide Treatment in Recurrent Glioblastoma After Standard Therapy:a Randomized Phase II Trial [NCT00521482]Phase 240 participants (Anticipated)Interventional2007-09-30Not yet recruiting
Phase I Study of Enzastaurin and Temozolomide in Patients With Gliomas [NCT00516607]Phase 128 participants (Actual)Interventional2007-07-31Active, not recruiting
Phase I Study of TTC (Taxotere/Temodar/Cisplatin) in Metastatic Melanoma Patients [NCT00527761]Phase 123 participants (Actual)Interventional2004-08-31Completed
Phase II Study of Gamma Knife Radiosurgery and Temozolomide (Temodar) for Newly Diagnosed Brain Metastases [NCT00582075]Phase 225 participants (Actual)Interventional2002-07-31Completed
Monitoring Anti-angiogenic Therapy in Brain Tumors by Advanced MRI [NCT02843230]30 participants (Actual)Observational2016-08-01Completed
A Phase II Study of Prolonged Daily Temozolomide for Low-Grade Glioma [NCT00165360]Phase 246 participants (Actual)Interventional2001-09-30Completed
"A Pilot Study of Abraxane® (Albumin-bound Paclitaxel) and Temodar® (Temozolomide) Plus Genasense® (Oblimersen Sodium) in Subjects With Advanced Melanoma (The ATG Study)." [NCT00409383]Phase 128 participants (Anticipated)Interventional2006-11-30Active, not recruiting
A Phase II Study of Temozolomide (TMZ) Following Stereotactic Radiosurgery (SRS) for Patients With Newly Diagnosed Brain Metastases [NCT00717275]Phase 23 participants (Actual)Interventional2008-09-30Terminated(stopped due to Slow accrual.)
A Phase II Feasibility Study of Adjuvant Intra-Nodal Autologous Dendritic Cell Vaccination for Newly Diagnosed Glioblastoma Multiforme [NCT00323115]Phase 211 participants (Actual)Interventional2006-05-31Completed
A Phase 2 Study of Temozolomide (SCH 52365) in Subjects With Advanced Aerodigestive Tract Cancers Selected for Methylation of O6-Methyl-Guanine-DNA Methyltransferase (MGMT) Promoter [NCT00423150]Phase 286 participants (Actual)Interventional2007-01-26Terminated
Evaluation of the Irinotecan/Bevacizumab Association as Neo-adjuvant and Adjuvant Treatment of Chemoradiation With Temozolomide for Naive Unresectable Glioblastoma. Phase II Randomized Study With Comparison to Chemoradiation With Temozolomide [NCT01022918]Phase 2134 participants (Actual)Interventional2009-01-31Completed
A Phase 2 Study of O-Benzylguanine (O-BG) and Temozolomide in Patients With Glioblastoma Progressing at Least 3 Months After Completion of Primary Treatment With Radiation Therapy and Temozolomide [NCT00436436]Phase 212 participants (Actual)Interventional2006-11-13Terminated(stopped due to Study closed to accrual after the company chose to stop development of the drug.)
A Phase II Trial of O6-Benzylguanine and Temozolomide in Pediatric Patients With Recurrent or Progressive High-Grade Gliomas and Recurrent or Progressive Brainstem Tumors [NCT00275002]Phase 241 participants (Actual)Interventional2006-02-28Completed
Phase 1/2 Study of Enzastaurin Plus Temozolomide During and Following Radiation Therapy in Patients With Newly Diagnosed Glioblastoma Multiforme or Gliosarcoma [NCT00402116]Phase 1/Phase 272 participants (Actual)Interventional2006-09-30Completed
Phase II Study of Tarceva Plus Temodar During and Following Radiation Therapy in Patients With Newly Diagnosed Glioblastoma Multiforme and Gliosarcoma [NCT00187486]Phase 266 participants (Actual)Interventional2004-08-31Completed
A Phase II Trial of Temozolomide Plus Bevacizumab in Patients With Metastatic Melanoma Involving the Central Nervous System [NCT01048554]Phase 234 participants (Actual)Interventional2009-11-30Completed
TEMOkids Study: A Population Pharmacokinetic, Acceptability and Safety Study for KIMOZO, a Paediatric Oral Suspension of Temozolomide [NCT04610736]Phase 149 participants (Actual)Interventional2021-03-16Active, not recruiting
A Phase I Study of SAHA and Temozolomide in Children With Relapsed or Refractory Primary Brain or Spinal Cord Tumors [NCT01076530]Phase 127 participants (Actual)Interventional2010-02-28Completed
A Modular Phase I/IIa, Open-label, Multi-centre Study to Assess the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics and Preliminary Efficacy of Ascending Doses of AZD9574 as Monotherapy and in Combination With Anti-cancer Agents in Patients With [NCT05417594]Phase 1/Phase 2490 participants (Anticipated)Interventional2022-06-24Recruiting
A Phase 0/1 Pharmacokinetic and Pharmacodynamics and Safety and Tolerability Study of Letrozole in Combination With Standard Therapy in Recurrent High Grade Gliomas [NCT03122197]Early Phase 139 participants (Anticipated)Interventional2017-05-16Recruiting
A PHASE I/II TRIAL OF TEMOZOLOMIDE, MOTEXAFIN GADOLINIUM, AND 60 GY FRACTIONATED RADIATION FOR NEWLY DIAGNOSED SUPRATENTORIAL GLIOBLASTOMA MULTIFORME [NCT00305864]Phase 1/Phase 2118 participants (Actual)Interventional2006-02-09Completed
A Pilot Study Combining ABT-888, an Oral PARP Inhibitor, With Temozolomide in Patients With Metastatic Castration Resistant Prostate Cancer Who Have Failed Up to Two Non-hormonal Systemic Therapies [NCT01085422]Phase 135 participants (Actual)Interventional2010-04-30Completed
A Randomized Controlled Clinical Trial of Temozolomide Plus Apatinib in Newly Diagnosed High-grade Glioma [NCT03741244]Phase 2211 participants (Anticipated)Interventional2019-05-06Recruiting
A Phase I/II Open-Label Study TPI 287 in Combination With Temozolomide in Patients With Metastatic Melanoma [NCT01067066]Phase 121 participants (Actual)Interventional2010-02-03Terminated(stopped due to Phase I/II study halted as Phase I, Low Response Rate)
A Multicenter Randomized Phase III Trial on INTraoperative RAdiotherapy in Newly Diagnosed GliOblastoma Multiforme (INTRAGO II) [NCT02685605]Phase 3314 participants (Anticipated)Interventional2016-12-09Recruiting
Phase 2 Study of Temozolomide as Maintenance Therapy After Initial Induction Chemotherapy in Small Cell Lung Cancer [NCT01900951]Phase 260 participants (Anticipated)Interventional2013-01-31Active, not recruiting
A Pharmacodynamic Study of Proteasome Inhibition by Disulfiram in Patients With Glioblastoma [NCT01907165]Early Phase 121 participants (Actual)Interventional2013-10-10Completed
A Phase 1 Study of ABI-009 (NAB-RAPAMYCIN) in Pediatric Patients With Recurrent or Refractory Solid Tumors, Including CNS Tumors as a Single Agent and in Combination With Temozolomide and Irinotecan [NCT02975882]Phase 133 participants (Actual)Interventional2017-08-15Active, not recruiting
A Phase I Study of Vincristine, Escalating Doses of Irinotecan, Temozolomide and Bevacizumab (Vit-b) in Pediatric and Adolescent Patients With Recurrent or Refractory Solid Tumors of Non-hematopoietic Origin [NCT00993044]Phase 113 participants (Actual)Interventional2009-09-30Completed
An Open-label, Single Arm Study to Explore Whether Potential Image Biomarkers Correlate With Efficacy of Bevacizumab Combined With Conventional Therapy in Newly Diagnosed Glioblastoma [NCT01939574]20 participants (Actual)Interventional2013-08-31Active, not recruiting
Whole Brain Radiotherapy in Combination With Gefitinib (Iressa) or Temozolomide (Temodal) for Brain Metastases From Non-Small Lung Cancer (NSCLC) A Randomized Phase II Trial [NCT00238251]Phase 259 participants (Actual)Interventional2005-05-31Completed
Peptide Targets for Glioblastoma Against Novel Cytomegalovirus Antigens [NCT02864368]Phase 127 participants (Actual)Interventional2016-12-07Terminated(stopped due to Funding)
A Phase 1b Study to Assess the Safety, Tolerability and Clinical Activity of BGB-290 in Combination With Temozolomide (TMZ) in Subjects With Locally Advanced or Metastatic Solid Tumors [NCT03150810]Phase 1/Phase 2139 participants (Actual)Interventional2017-06-28Completed
Phase I Trial of Combination of DNX-2401 (Formerly Named Delta-24-RGD) Oncolytic Adenovirus With a Short Course of Temozolomide for Treatment of Glioblastoma at First Recurrent [NCT01956734]Phase 131 participants (Anticipated)Interventional2013-09-30Completed
A Phase I Study of Metronomic Temozolomide With Abexinostat (PCI-24781) for Patients With Recurrent High Grade Glioma [NCT05698524]Phase 118 participants (Anticipated)Interventional2023-06-26Recruiting
A Phase I/ II Study of Hypofractionated Radiotherapy With Concurrent Temozolomide Followed by Adjuvant Temozolomide in Patients Over 70 Years Old With Newly Diagnosed Glioblastoma [NCT01985087]Phase 1/Phase 240 participants (Anticipated)Interventional2014-09-30Recruiting
Temozolomide Combined With Bevacizumab in Metastatic Melanoma. A Multicenter Phase II Trial [NCT00568048]Phase 262 participants (Actual)Interventional2007-12-31Completed
A Phase I Study Of Irinotecan and Bevacizumab With Temozolomide in Children With Recurrent/Refractory Central Nervous System Tumors [NCT00876993]Phase 126 participants (Actual)Interventional2008-09-30Completed
The Feasibility of Selecting Patient-Specific Biologically Targeted Therapy With Sorafenib, Everolimus, Erlotinib or Dasatinib for Pediatric Patients With Refractory Or Recurrent Brain Tumors [NCT02015728]20 participants (Anticipated)Interventional2013-12-31Active, not recruiting
Phase II Study of Atorvastatin in Combination With Radiotherapy and Temozolomide in Glioblastoma [NCT02029573]Phase 236 participants (Actual)Interventional2014-01-01Completed
Phase I/II Prospective Trial for Newly Diagnosed GBM, With Upfront Gross or Subtotal Resection, Followed by Ketogenic Diet With Radiotherapy and Concurrent Temodar(R) Chemotherapy Followed by Adjuvant Temodar(R) Chemotherapy. [NCT02046187]Phase 1/Phase 214 participants (Actual)Interventional2013-10-31Terminated(stopped due to excessive protocol deviations due to strict nature of diet requirements)
Phase I-II Trial of CPT-11 and Temozolomide (Temodar) in Patients With Recurrent Malignant Glioma [NCT00006025]Phase 10 participants Interventional2001-01-05Completed
Phase I Trial of Temodar Plus O6-Benzylguanine (O6-BG) (NSC 637037) in the Treatment of Patients With Newly Diagnosed (Part 1) or Recurrent/Progressive (Parts 1 and 2) Cerebral Anaplastic Gliomas [NCT00006474]Phase 10 participants Interventional2001-03-31Completed
Phase II Trial of Temozolomide in Patients With Cisplatin-Refractory Germ Cell Tumors [NCT00006043]Phase 20 participants Interventional2000-02-29Completed
Phase II Evaluation of Temozolomide (SCH52365) and Thalidomide for the Treatment of Recurrent and Progressive Glioblastoma Multiforme [NCT00006358]Phase 244 participants (Actual)Interventional2000-06-13Completed
A Phase II Study Of Temozolomide In The Treatment Of Patients With Metastatic Non-Small Cell Lung Cancer [NCT00006877]Phase 230 participants (Actual)Interventional2000-07-31Completed
Phase 1/2 Study of Vincristine and Temozolomide in Combination With PEN-866 for Adolescents and Young Adults With Relapsed or Refractory Solid Tumors [NCT04890093]Phase 1/Phase 264 participants (Anticipated)Interventional2024-01-03Not yet recruiting
Phase II Study Temozolomide for Retinoblastoma Metastatic to the Central Nervous System for Patients From Guatemala [NCT01857752]Phase 23 participants (Actual)Interventional2012-03-31Terminated(stopped due to accrual)
Phase II Treatment of Adults With Newly Diagnosed Supratentorial Glioblastoma Multiforme Treated With Gliadel Wafers, Surgery and Limited Field Radiation Plus Concomitant Temozolomide Followed by Temozolomide [NCT00574964]Phase 250 participants (Anticipated)Interventional2005-10-31Terminated(stopped due to PI left the institution.)
A Pilot Study of Elemene Injectable Emulsion in Treating Patients With Refractory Glioblastoma [NCT04674527]Phase 230 participants (Anticipated)Interventional2021-06-01Not yet recruiting
A Trail of Fluzoparil in Combination With Temozolomide in Patients With Recurrent Glioblastoma [NCT04552977]Phase 250 participants (Anticipated)Interventional2020-09-30Not yet recruiting
Phase II Trial of High Dose Interleukin-2 Followed by Intermittent Low Dose Temozolomide in Patients With Metastatic Malignant Melanoma [NCT01124734]Phase 217 participants (Actual)Interventional2010-05-31Completed
Randomized Phase II Trial of Temozolomide Versus Hyd-Sulfate AZD6244 [NSC 748727] in Patients With Metastatic Uveal Melanoma [NCT01143402]Phase 2120 participants (Actual)Interventional2010-06-30Completed
A Phase II Study of Anlotinib Combined With Dose-dense Temozolomide for the First Recurrent or Progressive Glioblastoma After STUPP Regimen [NCT04547855]Phase 254 participants (Anticipated)Interventional2020-09-11Recruiting
The Combination of Hypofractionated Stereotactic Radiotherapy and Chemoradiotherapy Using Intensity-Modulated Radiotherapy for Newly Diagnosed Glioblastoma Multiforme: A Prospective, Single-Center, Single-Arm Phase II Clinical Trial [NCT04547621]Phase 1/Phase 250 participants (Anticipated)Interventional2020-09-01Active, not recruiting
Phase Ib/II Study of the Gamma-Secretase Inhibitor (GSI) RO4929097 in Combination With Cisplatin, Vinblastine, and Temozolomide (CVT) in Patients With Metastatic Melanoma [NCT01196416]Phase 1/Phase 214 participants (Actual)Interventional2010-08-31Completed
A Phase III Trial of Gleostine® (Lomustine)-Temozolomide Combination Therapy Versus Standard Temozolomide in Patients With Methylated MGMT Promoter Glioblastoma [NCT05095376]Phase 3306 participants (Anticipated)Interventional2021-11-29Recruiting
Apatinib Mesylate Combined With IT Regimen for the Treatment of Recurrent or Refractory Pediatric Neuroblastoma: Multi-center, Single-arm, Phase II Clinical Study. [NCT05027386]Phase 262 participants (Anticipated)Interventional2021-08-26Recruiting
A Phase 0/2 Clinical Trial of Pamiparib in Newly-Diagnosed and Recurrent Glioblastoma Patients [NCT04614909]Early Phase 130 participants (Anticipated)Interventional2021-01-11Recruiting
A Phase I/II Safety Lead in Study of Ex-Vivo Expanded Allogeneic Universal Donor TGFβi NK Cell Infusions in Combination With Irinotecan, Temozolomide, and Dinutuximab in Patients With Relapsed or Refractory Neuroblastoma: The Allo - STING Trial [NCT04211675]Phase 1/Phase 231 participants (Anticipated)Interventional2022-09-01Recruiting
Pilot Study of Safety and Feasibility of Acquiring Hyperpolarized Imaging in Patients With Gliomas [NCT03739411]Phase 1140 participants (Anticipated)Interventional2015-12-09Recruiting
Phase III Trial on Concurrent and Adjuvant Temozolomide Chemotherapy in Non-1p/19q Deleted Anaplastic Glioma. The CATNON Intergroup Trial. [NCT00626990]Phase 3751 participants (Actual)Interventional2007-12-31Active, not recruiting
An International, Randomized, Open-label Phase I/II Study of Vismodegib in Combination With Temozolomide Versus Temozolomide Alone in Adult Patients With Recurrent or Refractory Medulloblastomas Presenting an Activation of the Sonic Hedgehog (SHH) Pathway [NCT01601184]Phase 1/Phase 224 participants (Actual)Interventional2012-06-30Terminated(stopped due to The number of successes is not reached at the end of first stage of the phase II. The study is stopped.)
Phase I Study of ZD6474 and Temozolomide in Patients With Advanced Cancer [NCT00601614]Phase 10 participants (Actual)Interventional2008-01-31Withdrawn(stopped due to no enrollment)
A Single Arm Phase II Study of Bevacizumab and Extended Treatment of Temozolomide in Patients With Recurrent Glioblastoma Multiforme [NCT01115491]Phase 232 participants (Actual)Interventional2010-06-30Completed
Phase II Randomized Multicenter Study Comparing Brain Radiation in Combination With Temozolomide or Radiation Alone in Patients With Brain Metastases From Breast Cancer [NCT00875355]Phase 2100 participants (Anticipated)Interventional2007-11-30Recruiting
A Phase I/II Study of Daily Oral Dosing With Temozolomide and Sunitinib Malate for 6 Weeks of an 8-Week Cycle in Patients With Metastatic and Unresectable Locally-Advanced Malignant Melanoma [NCT01005472]Phase 116 participants (Actual)Interventional2008-12-01Completed
A Phase Ib, Open-Label, Multicenter Trial of Intravenous INO-1001 Plus Oral Temozolomide to Evaluate the Tolerability, Safety, and Pharmacokinetics in Subjects With Newly-Diagnosed or Recurrent Unresectable Stage III or Stage IV Melanoma [NCT00272415]Phase 139 participants (Anticipated)Interventional2005-10-31Terminated
A Phase II, Multi-centre, Open-Label, Parallel Group, Randomised Study To Compare the Efficacy of AZD6244 vs Temozolomide in Patients With Unresectable AJCC Stage 3 or 4 Malignant Melanoma [NCT00338130]Phase 2239 participants (Actual)Interventional2006-07-31Completed
Phase I Trial of a 5-day Regimen of Temodar Plus O6-Benzylguanine (O6-BG) in the Treatment of Patients With Recurrent / Progressive Glioblastoma Multiforme [NCT00612989]Phase 142 participants (Anticipated)Interventional2005-02-28Completed
A Multicenter Randomized Double-blinded Controlled Phase 2 Study Evaluating the Efficacy of Valganciclovir as add-on Therapy in Glioblastoma Patients [NCT04116411]Phase 2220 participants (Anticipated)Interventional2019-09-04Recruiting
Randomized Phase II Neoadjuvant Study of Temozolomide Alone or With Pegylated Interferon-alpha 2b in Patients With Resectable American Joint Committee on Cancer (AJCC) Stage IIIB/IIIC or Stage IV (M1a) Metastatic Melanoma [NCT00525031]Phase 255 participants (Actual)Interventional2006-08-31Completed
Phase III Trial Evaluating Maintenance Treatment Versus Observation in Elderly Patients Suffering From Primary Central Nervous System Lymphoma in Complete Remission After High Dose Methotrexate Based Chemotherapy in First Line [NCT02313389]Phase 3428 participants (Actual)Interventional2015-09-30Active, not recruiting
A Phase II Trial Evaluating the Effects of Bortezomib in Patients With Recurrent Malignant Gliomas Treated Prior to Surgery and Then Bortezomib and Temozolomide Post-operatively [NCT00990652]Phase 210 participants (Actual)Interventional2009-05-31Completed
Phase II Trial of Temodar Plus O6-Benzylguanine (O6-BG) (NSC 637037) in the Treatment of Patients With Temodar-Resistant Malignant Glioma [NCT00613093]Phase 267 participants (Actual)Interventional2002-10-31Completed
A Phase I Dose-Escalation Study Of Azacitidine In Combination With Temozolomide In Patients With Unresectable Or Metastatic Soft Tissue Sarcoma or Malignant Mesothelioma [NCT00629343]Phase 128 participants (Actual)Interventional2007-10-31Active, not recruiting
Phase II Trial of Vaccination With Lysate-loaded, Mature Dendritic Cells Integrated Into Standard Radiochemotherapy in Newly Diagnosed Glioblastoma [NCT03395587]Phase 2136 participants (Anticipated)Interventional2018-03-06Recruiting
A Phase II Study of Gliadel, Concomitant Temozolomide and Radiation, Followed By Dose Dense Therapy With Temozolomide For Newly Diagnosed Malignant High Grade Glioma [NCT00660283]Phase 220 participants (Anticipated)Interventional2009-01-31Active, not recruiting
An Open Label, Randomised, Phase II Study to Investigate the Efficacy and Safety of ALECSAT Treatment as an add-on Therapy to Radiotherapy and Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT02799238]Phase 262 participants (Actual)Interventional2016-03-31Completed
Phase I/Randomized Phase II Trial of Either Dasatinib or Placebo Combined With Standard Chemo-Radiotherapy for Newly Diagnosed Glioblastoma Multiforme (GBM) [NCT00869401]Phase 1/Phase 2217 participants (Actual)Interventional2009-06-30Completed
A Proof-of-concept Clinical Trial Assessing the Safety of the Coordinated Undermining of Survival Paths by 9 Repurposed Drugs Combined With Metronomic Temozolomide (CUSP9v3 Treatment Protocol) for Recurrent Glioblastoma [NCT02770378]Phase 1/Phase 210 participants (Actual)Interventional2016-11-30Completed
Zenapax®-Activated Peptide ImmunoTherapy [ZAP IT] [NCT00626015]Phase 116 participants (Actual)Interventional2007-03-31Completed
Phase II Trial of Molecularly Determined Treatment of Children and Young Adults With Newly Diagnosed Diffuse Intrinsic Pontine Gliomas [NCT01182350]Phase 253 participants (Actual)Interventional2011-09-30Terminated(stopped due to Per design: Stop if fewer than 3 cohorts by molecular classification were with 10 participants or only 1 cohort enrolled at least 15 participants of 50.)
Phase I Study of the Combination of Sorafenib and Radiation Therapy -/+ Temozolomide for the Treatment of Patients With Brain Metastases and Primary Brain Tumors [NCT00639262]Phase 135 participants (Actual)Interventional2008-03-31Completed
[NCT02663440]Phase 241 participants (Anticipated)Interventional2016-01-31Recruiting
Cilengitide in Subjects With Newly Diagnosed Glioblastoma and Unmethylated MGMT Gene Promoter - a Multicenter, Open-label Phase II Study, Investigating Two Cilengitide Regimens in Combination With Standard Treatment (Temozolomide With Concomitant Radiatio [NCT00813943]Phase 2265 participants (Actual)Interventional2009-03-31Completed
Combination of Checkpoint Inhibition and IDO1 Inhibition Together With Standard Radiotherapy or Chemoradiotherapy in Newly Diagnosed Glioblastoma. A Phase 1 Clinical and Translational Trial [NCT04047706]Phase 118 participants (Actual)Interventional2019-08-13Active, not recruiting
[NCT00967330]Phase 2182 participants (Actual)Interventional2010-06-30Completed
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 Multicenter, Open-Label, Randomized, Active-Controlled Parallel Groups Study Comparing the Efficacy and Safety of Temodal vs Semustine in the Treatment of Subjects With Recurrent Glioblastoma or Anaplastic Astrocytoma [NCT00335075]Phase 3151 participants (Actual)Interventional2005-03-02Completed
Phase II Study of Temozolomide (Temodal) in Children Over 1 Year of Age With Relapsed or Refractory High Risk Neuroblastoma [NCT00276679]Phase 20 participants Interventional2003-04-30Completed
Continuous Temozolomide (SCH 52365) in Patients With Advanced or Metastatic Soft Tissue Sarcoma or Metastatic Breast Cancer, Phase II [NCT00194766]Phase 235 participants (Actual)Interventional2000-07-31Completed
Phase II Trial of Temozolomide, Carboplatin and Neupogen in High-Grade Gliomas, Both Newly-Diagnosed and Recurrent [NCT00006263]Phase 20 participants (Actual)Interventional1997-11-30Withdrawn
Phase II Study of 7 Days On/7 Days Off Temozolomide in Patients With High-Grade Glioma [NCT00619112]Phase 260 participants (Actual)Interventional2007-10-31Completed
Phase I/II Trial of the Combination of Decitabine and Temozolomide in the Treatment of Patients With Metastatic Melanoma [NCT00715793]Phase 1/Phase 239 participants (Actual)Interventional2008-06-30Completed
A Phase I Study of ABT-888, an Oral Inhibitor of Poly(ADP-Ribose) Polymerase and Temozolomide in Children With Recurrent/Refractory CNS Tumors [NCT00994071]Phase 19 participants (Actual)Interventional2009-09-22Completed
A Prospective, Single-arm, Single-center, Multi-cohort Phase II Clinical Study of HER2-positive and Triple-negative Breast Cancer Brain Metastases [NCT04303988]Phase 259 participants (Anticipated)Interventional2020-03-30Not yet recruiting
A Randomised Controlled Phase II Trial of Temozolomide With or Without Cannabinoids in Patients With Recurrent Glioblastoma [NCT05629702]Phase 2234 participants (Anticipated)Interventional2023-02-03Recruiting
Phase I/II Study of Vorinostat (Suberoylanilide Hydroxamic Acid [SAHA]), Temozolomide, and Radiation Therapy in Patients With Newly Diagnosed Glioblastoma [NCT00731731]Phase 1/Phase 2125 participants (Actual)Interventional2009-07-10Completed
Randomized Phase II/III Trial of Radiotherapy Plus Concomitant and Adjuvant Temozolomide With or Without Hydroxychloroquine, Rapamycin for Newly Diagnosed Glioblastoma [NCT03008148]Phase 2/Phase 3288 participants (Anticipated)Interventional2018-10-11Recruiting
Primary Chemotherapy With Temozolomide Versus Radiotherapy in Patients With Low Grade Gliomas After Stratification for Genetic 1p Loss: A Phase III Study [NCT00182819]Phase 3709 participants (Actual)Interventional2005-07-31Completed
Phase 1 Study of Temozolomide Associated With Topotecan in Refractory or Relapsed Malignant Tumors in Children and Adolescents [NCT00412503]Phase 10 participants InterventionalCompleted
A Phase 1 Study of Temozolomide in Combination With Targeted Therapy for NSCLC Patients With CNS Progression on Either Osimertinib or Lorlatinib [NCT04541407]Phase 11 participants (Actual)Interventional2020-10-29Completed
Pilot Study of Spectroscopic MRI-Guided, Dose-Escalated Radiation Therapy for Newly-Diagnosed Glioblastoma [NCT03137888]Phase 234 participants (Actual)Interventional2017-09-20Active, not recruiting
The Efficacy and Safety of Temozolomide in Patients With Relapsed or Advanced Anaplastic Oligodendroglioma and Oligoastrocytoma: a Multicenter, Single-arm, Phase II Trial [NCT01847235]Phase 223 participants (Actual)Interventional2013-05-31Completed
IIT2016-17-HU-KETORADTMZ: A Phase 1 Study of a 4-month Ketogenic Diet in Combination With Standard-of-care Radiation and Temozolomide for Patients With Newly/Recently Diagnosed Glioblastoma [NCT03451799]Phase 121 participants (Actual)Interventional2018-04-13Active, not recruiting
Phase I Study of Olaparib and Temozolomide in Adult Patients With Recurrent/Metastatic Ewing's Sarcoma or Rhabdomyosarcoma Following Failure of Prior Chemotherapy [NCT01858168]Phase 193 participants (Anticipated)Interventional2013-07-31Recruiting
A Double-Blind, Placebo-Controlled, Randomised, Phase II Study Evaluating the Efficacy and Safety of Addition of Continuous Multiple Line Bevacizumab Treatment to Lomustine in Second (2nd)-Line Followed by Standard of Care (SOC) in Third (3rd)-Line and Be [NCT01860638]Phase 2296 participants (Actual)Interventional2013-08-19Completed
Positron Emission Tomography With Fluoro-misonidazole (PET-FMISO) in High Grade Gliomas: Assessment of Tumor Hypoxia and Effect of Spinal Cord Stimulation [NCT01868906]Phase 26 participants (Actual)Interventional2013-06-30Terminated(stopped due to Isotope (FMISO) production is no longer available in our country.)
Zanubrutinib Combined With Rituximab and Chemotherapy for Newly-Diagnosed Primary Central Nervous System Large B-Cell Lymphoma Patients Intolerant to Haematopoietic Stem Cell Transplantation [NCT05896007]Phase 229 participants (Anticipated)Interventional2023-07-13Recruiting
A Phase 1/2 Study of Selinexor in Combination With Standard of Care (SoC) Therapy for Newly Diagnosed or Recurrent Glioblastoma [NCT04421378]Phase 1/Phase 274 participants (Actual)Interventional2020-06-08Terminated(stopped due to Upon further consideration of the existing data and the competitive landscape, Karyopharm Therapeutics Inc has decided not to pursue the ongoing development of Selinexor in GBM at this time.)
Avastin in Combination With Temozolomide and Irinotecan for Unresectable or Multifocal Glioblastoma Multiformes and Gliosarcomas [NCT00979017]Phase 241 participants (Actual)Interventional2009-11-30Completed
Phase II Quality of Life Study of Stereotactic RadioSurgery, Temozolomide and Erlotinib Chemotherapy for the Treatment of 1-3 Brain Metastases in Non-small Cell Lung Cancer [NCT00385398]Phase 20 participants (Actual)Interventional2008-07-31Withdrawn(stopped due to lack of funding and drug supply)
High-Dose Methotrexate Plus Steroid Followed by Concurrent Whole Brain Chemoradiation With Temozolomide for Immunocompetent Patients With Primary Central Nervous System Lymphoma - a Phase II Study [NCT00455286]Phase 225 participants Interventional2006-11-30Recruiting
A Phase I Study of Imatinib Mesylate in Combination With Temozolomide in Patients With Malignant Glioma [NCT00354068]Phase 165 participants (Actual)Interventional2004-07-31Completed
A Single-Center, Open-Label, Phase II, Safety and Efficacy Study of Panzem Nanocrystal Colloidal Dispersion Administered Orally in Combination With Protracted Oral Fixed-Dose Temozolomide to Patients With Recurrent Glioblastoma Multiforme [NCT00481455]Phase 215 participants (Actual)Interventional2007-04-30Completed
Phase I Trial Of Temozolomide Combined With The Histone Deacetylase Inhibitor Valproic Acid (VPA) And Whole Brain Radiation Therapy (WBR) For Brain Metastases From Solid Tumors In Adults [NCT00437957]Phase 110 participants (Actual)Interventional2006-12-31Terminated(stopped due to Lack of enrollment)
A Phase II Pilot Trial of Radiation Therapy With Concurrent and Adjuvant Temozolomide, Tamoxifen and Carboplatin (T2C) in the Treatment of Patients With Primary Central Nervous System Malignant Gliomas [NCT00492687]Phase 280 participants (Anticipated)Interventional2006-12-31Recruiting
A Pharmacokinetic and Pharmacogenomic Study of Patients With High-Grade Gliomas Receiving Daily Radiation Therapy and Temozolomide [NCT00471653]10 participants (Actual)Observational2006-11-11Terminated(stopped due to low accrual)
Phase II Trial of Temozolomide in Elderly Patients With Glioblastoma and Poor Performance Status (KPS<70). [NCT01242566]Phase 270 participants (Actual)Interventional2007-07-31Completed
A Randomized Phase II/III Open-Label Study of Ipilimumab and Nivolumab Versus Temozolomide in Patients With Newly Diagnosed MGMT (Tumor O-6-Methylguanine DNA Methyltransferase) Unmethylated Glioblastoma [NCT04396860]Phase 2/Phase 3485 participants (Anticipated)Interventional2020-09-01Active, not recruiting
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
A Phase IIa Study of AdV-tk + Valacyclovir Gene Therapy in Combination With Standard Radiation Therapy for Malignant Gliomas [NCT00589875]Phase 252 participants (Actual)Interventional2007-03-31Completed
Multicenter Randomized Phase II Study of Methotrexate (MTX) and Temozolomide Versus MTX, Procarbazine, Vincristine and Cytarabine for Primary CNS Lymphoma (PCNSL) in the Elderly [NCT00503594]Phase 292 participants (Anticipated)Interventional2007-07-31Recruiting
A Phase I Study of ABT-888 in Combination With Temozolomide (TMZ) in Subjects With Non-Hematologic Malignancies (NHM) and Metastatic Melanoma (MM) [NCT00526617]Phase 141 participants (Actual)Interventional2007-08-31Completed
A Phase II Multi-Centre Study of Concomitant and Prolonged Adjuvant Temozolomide With Radiotherapy in Diffuse Pontine Gliomas [NCT00514397]Phase 243 participants (Anticipated)Interventional2008-01-31Recruiting
A Phase I Study of Temozolomide, Thalidomide, and Lomustine (TTL) in Patients With Metastatic Melanoma in the Brain [NCT00527657]Phase 117 participants (Actual)Interventional2006-02-09Completed
Clinical Analysis of Naxitamab (hu3F8) in the Treatment of Pediatric High Risk or Refractory/ Relapsed Neuroblastoma [NCT06013618]Phase 230 participants (Anticipated)Interventional2023-06-19Recruiting
A Phase I/II Combination Study of NMS-03305293 and Temozolomide in Adult Patients With Recurrent Glioblastoma [NCT04910022]Phase 1/Phase 275 participants (Anticipated)Interventional2021-12-01Recruiting
Temozolomide and Olaparib for O6-Methylguanine DNA Methyltransferase Promoter Hypermethylated Colorectal Cancer [NCT04166435]Phase 211 participants (Actual)Interventional2020-06-17Completed
A Pilot Trial of Irinotecan, Temozolomide and Bevacizumab in Combination With Existing High Dose Alkylator Based Chemotherapy for Treatment of Newly Diagnosed Patients With Desmoplastic Small Round Cell Tumor [NCT01189643]Early Phase 115 participants (Actual)Interventional2010-08-31Active, not recruiting
Temozolomide in Treatment of Patients With Primary Central Nervous System Lymphoma [NCT02934204]Phase 251 participants (Anticipated)Interventional2016-02-29Recruiting
A Phase II Pilot Study of Cyclophosphamide, Doxorubicin, Vincristine Alternating With Irinotecan and Temozolomide in Patients With Newly Diagnosed Metastatic Ewing's Sarcoma [NCT01313884]Phase 23 participants (Actual)Interventional2011-05-31Terminated(stopped due to Study did not reach primary objective; study did not accrue enough patients.)
A Pilot Feasibility Study of Intracerebral Microdialysis to Determine the Neuropharmacokinetics of Temozolomide [NCT00547131]Phase 112 participants (Anticipated)Interventional2006-01-31Completed
A Phase I Study of Bortezomib and Temozolomide in Patients With Refractory Solid Tumors [NCT00544284]Phase 125 participants (Actual)Interventional2005-01-31Completed
Temozolomide Plus Bevacizumab Chemotherapy in Supratentorial Glioblastoma in 70 Years and Older Patients With an Impaired Functional Status (KPS<70) [NCT02898012]Phase 270 participants (Actual)Interventional2010-10-31Completed
A Phase II Trial of Concurrent Sunitinib, Temozolomide and Radiation Therapy Followed by Adjuvant Temozolomide for Newly Diagnosed Glioblastoma Patients With an Unmethylated MGMT Gene Promoter [NCT02928575]Phase 245 participants (Anticipated)Interventional2012-08-31Recruiting
A Phase I/II Study of the Combination of Indoximod and Temozolomide for Adult Patients With Temozolomide-Refractory Primary Malignant Brain Tumors [NCT02052648]Phase 1/Phase 2160 participants (Actual)Interventional2014-03-31Completed
Phase I / II Adaptive Randomized Trial of Vorinostat, Isotretinoin and Temozolomide in Adults With Recurrent Glioblastoma Multiforme [NCT00555399]Phase 1/Phase 2135 participants (Anticipated)Interventional2007-11-28Active, not recruiting
Temozolomide With Irinotecan Versus Temozolomide, Irinotecan Plus Bevacizumab (NSC# 704865) for Recurrent/Refractory Medulloblastoma/CNS PNET of Childhood, a COG Randomized Phase II Screening Trial [NCT01217437]Phase 2108 participants (Actual)Interventional2010-11-22Completed
A Phase 1b/2 Study of Abemaciclib in Combination With Irinotecan and Temozolomide (Part A) and Abemaciclib in Combination With Temozolomide (Part B) in Pediatric and Young Adult Patients With Relapsed/Refractory Solid Tumors and Abemaciclib in Combination [NCT04238819]Phase 1/Phase 2117 participants (Anticipated)Interventional2020-11-09Recruiting
Phase I/II Study of T-DM1 Alone Versus T-DM1 and Metronomic Temozolomide in Secondary Prevention of HER2-Positive Breast Cancer Brain Metastases Following Stereotactic Radiosurgery [NCT03190967]Phase 1/Phase 212 participants (Actual)Interventional2018-04-18Terminated(stopped due to The phase II portion was never started as we could no longer get the drug from the manufacturer.)
A Pilot Study to Assess Feasibility of 5 Fraction Hypofractionated Stereotactic Radiosurgery Along With Standard Temozolomide as a Lymphocyte Sparing Therapy for Glioblastoma Multiforme [NCT03291990]Early Phase 13 participants (Actual)Interventional2017-10-18Completed
Phase I Trial of Vaccination With Autologous Dendritic Cells Pulsed With Lysate Derived From an Allogeneic Glioblastoma Stem-like Cell Line for Patients With Newly Diagnosed or Recurrent Glioblastoma [NCT02010606]Phase 139 participants (Actual)Interventional2014-01-08Completed
Treatment of Newly Diagnosed High-Grade Gliomas in Patients Ages Greater Than or Equal to 3 and Less Than or Equal to 21 Years With a Phase II Irinotecan Window Followed by Radiation Therapy and Temozolomide [NCT00004068]Phase 253 participants (Actual)Interventional1999-03-31Completed
A Randomized Double-Blind, Placebo-Controlled Phase II Study of the Matrix Metalloprotease Inhibitor Prinomastat in Combination With Temozolomide Following Radiation Therapy in Patients Having Newly Diagnosed Glioblastoma Multiforme [NCT00004200]Phase 20 participants Interventional1999-10-31Completed
A Phase 1B, Open-Label, Dose Escalation Study Evaluating the Safety of BSI-201 in Combination With Chemotherapeutic Regimens in Subjects With Advanced Solid Tumors [NCT00422682]Phase 1136 participants (Actual)Interventional2007-01-31Completed
A Phase I, Two-stage, Multi-center, Open Label, Dose-escalation Study of BKM120 in Combination With Adjuvant Temozolomide and With Concomitant Radiation Therapy and Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT01473901]Phase 138 participants (Actual)Interventional2011-12-30Completed
A Phase I Open Label Safety Study to Evaluate the Pharmacokinetic Profile and Tolerance of Mibefradil Dose Finding in Subjects With Recurrent High-Grade Glioma Undergoing Standard, Repeated Temozolomide Treatment [NCT01480050]Phase 128 participants (Actual)Interventional2012-05-31Completed
A Phase I Study Of Cloretazine™ (VNP40101M) And Temozolomide In Patients With Hematologic Malignancies [NCT00098436]Phase 125 participants (Anticipated)Interventional2004-09-30Completed
Phase I Dose Finding Clinical Trial of Combination Paclitaxel, Carboplatin and Temozolomide for Subjects With Solid Tumor Malignancies. [NCT00249964]Phase 115 participants (Actual)Interventional2003-11-30Completed
A Systemic Temozolomide Treatment Of Melanoma Present In The Central Nervous System [NCT00068666]Phase 241 participants (Actual)Interventional2004-01-31Terminated
A Phase II Trial of Combination Thalidomide Plus Temozolomide in Patients With Metastatic Malignant Melanoma [NCT00104988]Phase 264 participants (Actual)Interventional2005-06-30Completed
A Phase III Trial Comparing Whole Brain Radiation (WBRT) and Stereotactic Radiosurgery (SRS) Alone Versus With Temozolomide or Erlotinib in Patients With Non-Small Cell Lung Cancer and 1-3 Brain Metastases [NCT00268684]Phase 3381 participants Interventional2005-05-31Recruiting
A Randomized Controlled Trial of Chemo-Radiotherapy Versus Biomarker-Guided Therapy for Elderly and Frail Patients With Newly Diagnosed Glioblastoma [NCT04765514]Phase 2121 participants (Anticipated)Interventional2022-07-27Recruiting
A Randomized, Open-Label Phase 2 Study of Temozolomide Added to Whole Brain Radiation Therapy Versus Whole Brain Radiation Therapy Alone for the Treatment of Brain Metastasis From Non-Small Cell Lung Cancer [NCT00076856]Phase 295 participants (Actual)Interventional2004-03-31Completed
A Phase II Study of Radiation With Concomitant and Then Sequential Temozolomide in Patients With Newly Diagnosed Supratentorial Malignant Glioma Who Have Undergone Surgery With Gliadel Wafer Insertion [NCT00283543]Phase 240 participants (Anticipated)Interventional2002-09-30Active, not recruiting
A Phase I Trial and Pharmacokinetic Study of Talabostat (PT-100, Val-Boro-Pro) in Combination With Temozolomide or Carboplatin in Pediatric Patients With Relapsed or Refractory Solid Tumors Including Brain Tumors [NCT00303940]Phase 126 participants (Anticipated)Interventional2005-12-31Completed
Phase I Study Of SCH66336 (Lonafarnib), A Farnesyl Protein Transferase Inhibitor In Combination With Temozolomide In Gliomas [NCT00083096]Phase 130 participants (Anticipated)Interventional2004-03-31Active, not recruiting
Treatment of Primary Glioblastoma Multiforme With Cetuximab, Radiotherapy and Temozolomide (GERT) - Phase I/II Trial [NCT00311857]Phase 1/Phase 246 participants Interventional2006-02-28Recruiting
Phase I Study of Convection Enhanced Delivery (CED) of IL13-PE38QQR Infusion After Resection Followed by Radiation Therapy With or Without Temozolomide in Patients With Newly Diagnosed Supratentorial Malignant Glioma [NCT00089427]Phase 124 participants Interventional2004-07-31Completed
A Randomized, Double-Blind, Placebo-Controlled Phase 3 Study of Enzastaurin Added to Temozolomide During and Following Radiation Therapy in Newly Diagnosed Glioblastoma Patients Who Possess the Novel Genomic Biomarker DGM1 [NCT03776071]Phase 3300 participants (Anticipated)Interventional2020-12-16Active, not recruiting
Phase I Study of Ibrutinib With Radiation and Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT03535350]Phase 136 participants (Anticipated)Interventional2018-08-24Active, not recruiting
Phase I Study of Ruxolitinib With Radiation and Temozolomide in Patients With Newly Diagnosed Grade III Gliomas and Glioblastoma [NCT03514069]Phase 160 participants (Actual)Interventional2018-06-05Active, not recruiting
A Phase I Study of CCI-779, and Temozolomide in Combination With Radiation Therapy in Glioblastoma Multiforme [NCT00316849]Phase 156 participants (Actual)Interventional2006-05-31Completed
Doxorubicin Hydrochloride Liposome Combined With Irinotecan (AI Regimen) Versus VIT Regimen in the Treatment of First Relapsed and Refractory Pediatric Rhabdomyosarcoma: a Prospective, Open-label, Randomized Controlled, Phase II Clinical Study [NCT05457829]Phase 288 participants (Anticipated)Interventional2023-12-30Not yet recruiting
Randomized Phase II of TARCEVA™ (Erlotinib) Versus Temozolomide Or BCNU in Patients With Recurrent Glioblastoma Multiforme [NCT00086879]Phase 2110 participants (Actual)Interventional2004-05-31Completed
A Multi-Center Phase III, Randomized, Open-Label Trial of Vigil (Bi-shRNAfurin and GMCSF Augmented Autologous Tumor Cell Immunotherapy) in Combination With Irinotecan and Temozolomide as a Second-Line Regimen for Ewing's Sarcoma [NCT03495921]Phase 332 participants (Actual)Interventional2018-08-21Terminated(stopped due to Slow accrual and as a result, a strategic business decision was made to terminate enrollment.)
DC Migration Study to Evaluate TReg Depletion In GBM Patients With and Without Varlilumab [NCT03688178]Phase 243 participants (Actual)Interventional2020-08-26Active, not recruiting
A Phase I Trial of Pembrolizumab and Vorinostat Combined With Temozolomide and Radiation Therapy for Newly Diagnosed Glioblastoma [NCT03426891]Phase 121 participants (Actual)Interventional2018-03-16Completed
A Phase I Study Of Oral Irinotecan, Temozolomide, Cefixime In Children With Recurrent/Resistant High-Risk Neuroblastoma [NCT00093353]Phase 130 participants (Anticipated)Interventional2004-05-31Completed
A Pilot Study to Evaluate Novel Agents (Temozolomide and Cixutumumab [IMC-A12, Anti-IGF-IR Monoclonal Antibody NSC # 742460]) in Combination With Intensive Multi-agent Interval Compressed Therapy for Patients With High-Risk Rhabdomyosarcoma [NCT01055314]Phase 2175 participants (Actual)Interventional2010-01-31Completed
A Phase II Study Of Radiation Therapy Plus Low Dose Temozolomide Followed By Temozolomide Plus Irinotecan For Glioblastoma Multiforme [NCT00099125]Phase 2170 participants (Actual)Interventional2004-11-30Completed
Phase I Trial of Weekly Docetaxel and Daily Temozolomide in Patients With Metastatic Disease [NCT00401180]Phase 125 participants (Actual)Interventional2002-06-30Completed
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
A Randomized, Multi-Cohort Phase II Trial of Temozolomide and Atezolizumab as Second or Third Line Treatment for Small Cell Lung Cancer [NCT04919382]Phase 256 participants (Anticipated)Interventional2022-01-26Recruiting
A Phase II Study of Bevacizumab in Combination With Temozolomide in Patients With Advanced Neuroendocrine Tumors [NCT00137774]Phase 234 participants (Actual)Interventional2004-11-30Completed
A Phase I Study of Dietary Methionine Restriction and Temodar® (Temozolomide) for the Treatment of Recurrent and Progressive Glioblastoma Multiforme [NCT00508456]Phase 118 participants (Actual)Interventional2004-08-31Terminated(stopped due to Low Accrual)
A Randomized Phase 2/3 Study of Olaparib Plus Temozolomide Versus Investigator's Choice for the Treatment of Patients With Advanced Uterine Leiomyosarcoma After Progression on Prior Chemotherapy [NCT05432791]Phase 2/Phase 3190 participants (Anticipated)Interventional2023-03-30Recruiting
A Phase II Trial to Evaluate the Effect of Low Dose Temozolomide (TMZ) for 2 Weeks on Brain Tumor O-6-methylguanine-DNA Methyltransferase (MGMT) Activity in Patients With Gliomas. [NCT00424554]Phase 240 participants (Actual)Interventional2006-09-26Completed
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
Avastin in Combination With Radiation and Temozolomide, Followed by Avastin, Temozolomide and Irinotecan for Glioblastoma Multiformes and Gliosarcomas [NCT00597402]Phase 2125 participants (Actual)Interventional2007-07-31Completed
Phase II Trial of Velcade (Bortezomib) in Combination With Temozolomide and Regional Radiation Therapy for Upfront Treatment of Patients With Newly-diagnosed Glioblastoma Multiforme [NCT00998010]Phase 224 participants (Actual)Interventional2011-10-03Completed
A Phase II Study of ABT-888, an Inhibitor of Poly(ADP-ribose) Polymerase (PARP) in Combination With Temozolomide in Patients With Heavily Pretreated, Metastatic Colorectal Cancer [NCT01051596]Phase 275 participants (Actual)Interventional2009-09-30Completed
Phase II Trial of Treatment Intensification for IDH Wildtype, Non-Histological Glioblastoma, Gliomas (IDH Wildtype Lower Grade Glioma Treatment Intensification) [NCT04623931]Phase 240 participants (Anticipated)Interventional2020-01-30Recruiting
Phase I / II Adaptive Randomized Trial of Vorinostat, Erlotinib and Temozolomide in Adults With Recurrent Glioblastoma Multiforme [NCT01110876]Phase 1/Phase 221 participants (Actual)Interventional2011-06-30Terminated(stopped due to Unanticipated Toxicities)
Phase I/II Intraventricular DepoCyt (OD # 06-2348) in Glioblastoma (76,730, 11/06) [NCT01044966]Phase 1/Phase 212 participants (Actual)Interventional2009-09-30Terminated(stopped due to The study was terminated due to lack of adequate patient enrollment into trial.)
A Phase II Study of Thalidomide in Combination With Temodar in Patients With Metastatic Neuroendocrine Tumors [NCT00165230]Phase 232 participants Interventional2002-05-31Completed
Neoadjuvant PD-1 in Newly Diagnosed Glioblastoma: A Phase 2 Clinical Trial [NCT04583020]Phase 242 participants (Anticipated)Interventional2020-11-12Recruiting
Multi-national, Open-label, Active-controlled, Randomized Dose-finding Study to Evaluate Efficacy of 2 Doses of AP 12009 in Recurrent Glioma, Administered Intratumorally as Continuous High-flow Microperfusion Over 7 Days Every Other Week [NCT00431561]Phase 2141 participants (Actual)Interventional2003-04-30Completed
A Phase II Study of the PARP Inhibitor Olaparib in Combination With the DNA Damaging Agent Temozolomide for the Treatment of Advanced Uterine Leiomyosarcoma [NCT03880019]Phase 223 participants (Actual)Interventional2019-08-19Active, not recruiting
A Phase I/II Trial of Cloretazine® (VNP40101M) and Temodar® (Temozolomide) for Patients With Malignant Glioma in First Relapse or Progression [NCT00516282]Phase 114 participants (Actual)Interventional2007-08-31Terminated(stopped due to The pharmaceutical collaborator filed for bankruptcy and as a result, the study was unable to move into the phase II portion.)
Temozolomide and Irinotecan Consolidation in Patients With MGMT Silenced, Microsatellite Stable Colorectal Cancer With Persistence of Minimal Residual Disease in Liquid Biopsy After Standard Adjuvant Chemotherapy: the ERASE-TMZ Study [NCT05031975]Phase 235 participants (Anticipated)Interventional2022-05-02Recruiting
An Exploratory Study of PD-1 Antibody(Toripalimab) or Combining With Temozolomide for Injection in the Treatment of Advanced/Metastatic Malignant Melanoma [NCT04884997]Phase 290 participants (Anticipated)Interventional2021-03-07Recruiting
A Phase II Study of Optune (NovoTTF) in Combination With Bevacizumab (BEV) and Temozolomide (TMZ) in Patients With Newly Diagnosed Unresectable Glioblastoma (GBM) [NCT02343549]Phase 213 participants (Actual)Interventional2015-01-31Terminated(stopped due to closed to accrual due to low accrual)
Stereotactic Accelerated Radiotherapy in GlioblastomA (SAGA) [NCT05781321]Phase 2170 participants (Anticipated)Interventional2023-03-23Recruiting
A Randomized Phase 2 Study to Evaluate the Efficacy Between Only Radiotherapy Versus CCRT With Temozolomide in Newly Diagnosed Grade III Gliomas Without 1p/19q Codeletion [NCT01534845]Phase 290 participants (Actual)Interventional2012-03-31Active, not recruiting
Combination of IDO/Survivin Peptide Vaccine, GM-CSF, Imiquimod and Temozolomide Chemotherapy for Patients With Metastatic Malignant Melanoma [NCT01543464]Phase 241 participants (Actual)Interventional2012-05-31Terminated(stopped due to Diminished rectruitment)
Concomitant and Adjuvant Temozolomide and Radiotherapy for Newly Diagnosed Glioblastoma Multiforme - A Randomized Phase III Study [NCT00006353]Phase 3575 participants (Actual)Interventional2000-07-31Completed
Phase II Trial of Continuous Dose Temozolomide in Patients With Newly Diagnosed Pure and Mixed Anaplastic Oligodendroglioma [NCT00400816]Phase 229 participants (Actual)Interventional2005-08-31Completed
Phase II Trial of Salvage Chemotherapy With Temozolomide in Combination With Topotecan for Primary CNS Lymphoma [NCT00109798]0 participants (Actual)Interventional2005-03-31Withdrawn(stopped due to Sub-Investigator reloacted to another institution)
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
Phase 2 Study to Evaluate the Efficacy and Safety of Sintilimab in Combination With Bevacizumab and Temozolomide in Recurrent Glioblastoma (GBM) Patients [NCT05638451]Phase 230 participants (Anticipated)Interventional2023-01-01Not yet recruiting
Temozolomide Versus Temozolomide + Whole Brain Radiation In Stage IV Melanoma Patients With Asymptomatic Brain Metastases [NCT00020839]Phase 323 participants (Actual)Interventional2001-04-30Terminated(stopped due to low accrual)
Phase I/II Trial Of Temozolomide And Carboplatin In Recurrent Glioblastoma Multiforme [NCT00021307]Phase 1/Phase 20 participants (Actual)InterventionalWithdrawn(stopped due to Study not activated.)
Dose Escalation of Temozolomide in Combination With Thiotepa and Carboplatin With Autologous Stem Cell Rescue in Patients With Malignant Brain Tumors With Minimal Residual Disease [NCT00025558]Phase 10 participants Interventional2000-10-31Completed
A Phase I Study Of ZD 1839 And Temozolomide For The Treatment Of Gliomas [NCT00027625]Phase 10 participants Interventional2002-01-28Completed
A Phase II Study of Temozolomide (Temodar) and Peglated Interferon Alfa-2B (PEGIntron) in the Treatment of Advanced Melanoma [NCT00027742]Phase 20 participants Interventional2001-05-31Completed
A Phase II Study of Temozolomide in the Treatment of Children With High Grade Glioma [NCT00028795]Phase 2170 participants (Actual)Interventional2002-12-31Completed
A Phase II Trial Of Pre-Irradiation And Concurrent Temozolomide In Patients With Newly Diagnosed Anaplastic Oligodendrogliomas And Mixed Anaplastic Oligoastrocytomas [NCT00033280]Phase 242 participants (Actual)Interventional2002-07-31Completed
A Phase II Study of Combination Therapy of a Protracted Oral Schedule of Temozolomide and Thalidomide as First-Line or Subsequent Therapy for Patients With Metastatic, Locally Advanced or Unresectable Leiomyosarcoma [NCT00033709]Phase 20 participants Interventional2002-03-31Active, not recruiting
A Phase II Study of Temozolomide and O6-Benzylguanine (O6-BG) in Patients With Temozolomide-Resistant Anaplastic Glioma [NCT00389090]Phase 232 participants (Actual)Interventional2006-10-31Terminated(stopped due to AOI Pharma terminated the license agreement. IND Transferred to NCI)
Phase I Trial of R115777 With Radiation Therapy and Temozolomide in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00049387]Phase 119 participants (Actual)Interventional2002-09-30Completed
Phase I Trial of Temozolomide and O6-Benzylguanine in Pediatric Patients With Recurrent Brain Tumors [NCT00052780]Phase 172 participants (Actual)Interventional2002-10-31Completed
A Phase II Open-label Study Investigating the Efficacy, Safety and Pharmacokinetic Properties of OKN-007 Combined With Temozolomide in Patients With Recurrent Glioblastoma [NCT04388475]Phase 257 participants (Actual)Interventional2020-06-12Active, not recruiting
A Phase II Study Of Temozolomide And Thalidomide In Patients With Metastatic Melanoma In The Brain [NCT00072163]Phase 250 participants (Actual)Interventional2003-10-31Completed
Dose Intensive Chemotherapy for Children Less Than Ten Years of Age Newly-Diagnosed With Malignant Brain Tumors: A Pilot Study of Two Alternative Intensive Induction Chemotherapy Regimens, Followed by Consolidation With Myeloablative Chemotherapy (Thiotep [NCT00392886]Phase 3120 participants (Anticipated)Interventional2004-03-31Active, not recruiting
Investigation of Cannabis For Tolerability and Feasibility in Patients Receiving Concurrent Chemoradiation for Glioblastoma. [NCT03246113]Phase 11 participants (Actual)Interventional2018-03-19Terminated(stopped due to Lack of subject interest due to study design)
Temozolomide For Patients With Cerebral Metastases Who Have Failed Radiation Therapy [NCT00012116]Phase 24 participants (Actual)Interventional2000-10-31Completed
Phase I/II Trial of Temozolomide and Carboplatin in Recurrent Glioblastoma Multiforme [NCT00014105]Phase 1/Phase 20 participants Interventional2000-12-31Active, not recruiting
A Phase-I Study Of Cyclical Oral Administration Of Temozolomide In Combination With PEG12000-Interferon Alfa-2B In Patients With Refractory And/Or Advanced Solid Tumors [NCT00014261]Phase 10 participants Interventional2000-10-31Completed
A Phase I/II Trial of Arsenic Trioxide and Temozolomide in Combination With Radiation Therapy for Patients With Malignant Gliomas [NCT00275067]Phase 1/Phase 250 participants (Anticipated)Interventional2005-05-31Active, not recruiting
Interleukin 12-Primed Activated T Cells As Therapy For Patients With Metastatic Melanoma (Phase I) [NCT00016055]Phase 118 participants (Anticipated)Interventional2000-11-30Active, not recruiting
Phase I/II Study on Concomitant and Adjuvant Temozolomide and Radiotherapy With or Without PTK787/ZK222584 in Newly Diagnosed GBM [NCT00128700]Phase 1/Phase 220 participants (Actual)Interventional2005-06-30Completed
A Phase 3 Clinical Trial to Evaluate the Safety and Efficacy of Treatment With 2 mg Intralesional Allovectin-7® Compared to Dacarbazine (DTIC) or Temozolomide (TMZ) in Subjects With Recurrent Metastatic Melanoma [NCT00395070]Phase 3390 participants (Actual)Interventional2006-10-31Completed
Phase II Evaluation Temozolomide and Farnesyl Transferase Inhibitor (SCH66336) for the Treatment of Recurrent and Progressive Glioblastoma Multiforme [NCT00038493]Phase 223 participants (Actual)Interventional2001-09-21Completed
An Open-label, Phase I Clinical Trial to Assess the Maximum Tolerated Dose (MTD), Safety and Efficacy of BEY1107 in Combination With Temozolomide in Patient With Recurrent or Progressive Glioblastoma Multiforme (GBM) [NCT05769660]Phase 112 participants (Anticipated)Interventional2022-11-29Recruiting
Pilot Trial of an Implantable Microdevice for In Vivo Drug Sensitivity Testing in Patients With Sarcomas [NCT04199026]Early Phase 120 participants (Anticipated)Interventional2024-01-31Not yet recruiting
Phase I Trial and Pharmacokinetic Study of Temozolomide and O6-Benzylguanine in Childhood Solid Tumors [NCT00020150]Phase 10 participants Interventional2000-06-30Completed
A Phase 1b/2a, Multicenter, Open-Label Study of AQ4N in Combination With Radiation Therapy and Temozolomide, to Evaluate the Safety, Tolerability, and Efficacy in Subjects With Newly Diagnosed Glioblastoma Multiforme [NCT00394628]Phase 1/Phase 260 participants (Anticipated)Interventional2006-10-31Recruiting
A Prospective Randomised Trial Comparing Temozolomide With PCV In The Treatment Of Recurrent WHO Astrocytic Tumours Grades III And IV [NCT00052455]Phase 3500 participants (Anticipated)Interventional2002-10-31Completed
A Phase II Study of Temozolomide (SCH 52365) in Subjects With Brain Metastasis From Non-Small-Cell Lung Cancer [NCT00034697]Phase 224 participants (Actual)Interventional2001-06-28Terminated(stopped due to Slow Enrollment)
A Phase II Study of Temozolomide, Thalidomide, and Lomustine in the Treatment of Advanced Melanoma [NCT00072345]Phase 20 participants Interventional2003-07-31Completed
A Pilot and Phase II Study of OSI-774 and Temozolomide in Combination With Radiation Therapy in Glioblastoma Multiforme [NCT00039494]Phase 2171 participants (Anticipated)Interventional2002-12-31Completed
A Phase III, Randomized, Open-Label Study Of IV Edotecarin Vs Temozolomide Or Carmustine (BCNU) Or Lomustine (CCNU) In Patients With Glioblastoma Multiforme At First Relapse After Alkylator-Based (NEO) Adjuvant Chemotherapy [NCT00068952]Phase 3118 participants Interventional2003-08-31Completed
A Phase I Study of Single Agent OSI-774 (Tarceva) (NSC# 718781, IND# 63383) Followed by OSI-774 With Temozolomide for Patients With Selected Recurrent/Refractory Solid Tumors, Including Brain Tumors [NCT00077454]Phase 195 participants (Actual)Interventional2004-02-29Completed
Phase II Study Of Temozolomide, Thalidomide And Celecoxib In Patients With Newly Diagnosed Glioblastoma Multiforme In The Post-Radiation Setting [NCT00047294]Phase 20 participants Interventional2001-04-30Completed
Phase II Study of the Combination of Cisplatin + Temozolomide in Malignant Glial Tumours in Children and Adolescents at Diagnosis or in Relapse [NCT00147160]Phase 287 participants (Anticipated)Interventional2003-10-31Completed
A Phase II Study Of Whole-Brain Radiation Therapy With Thalidomide And Temozolomide In Patients With Newly Diagnosed Brain Metastases [NCT00049361]Phase 20 participants Interventional2004-01-01Completed
Anlotinib Combined With STUPP Protocol as First-line Regimen for MGMT Nonmethylated Glioblastoma: a Multicenter, Open-label, Single-arm, Phase II Clinical Trial [NCT04725214]Phase 233 participants (Anticipated)Interventional2021-01-15Recruiting
A Phase I Trial Of Temozolomide In Pediatric Patients With Refractory/Recurrent Leukemias [NCT00083070]Phase 116 participants (Actual)Interventional2004-03-31Completed
A Phase II Study of Temozolomide (TEMODAR) in the Treatment of Adult Patients With Supratentorial Low Grade Glioma [NCT00313729]Phase 2120 participants (Actual)Interventional1999-05-31Completed
A Phase 1b Trial of Telaglenastat (CB-839) HCI in Combination With Radiation Therapy and Temozolomide in Patients With IDH-Mutated Diffuse Astrocytoma and Anaplastic Astrocytoma [NCT03528642]Phase 140 participants (Anticipated)Interventional2019-05-01Active, not recruiting
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
A Randomized Phase 3 Single Blind Study of Temozolomide Plus Radiation Therapy Combined With Nivolumab or Placebo in Newly Diagnosed Adult Subjects With MGMT-Methylated (Tumor O6-methylguanine DNA Methyltransferase) Glioblastoma [NCT02667587]Phase 3716 participants (Actual)Interventional2016-05-09Active, not recruiting
"A Surgical Window-of-Opportunity and Phase II Trial of Pembrolizumab, Olaparib and Temozolomide in Recurrent Glioblastoma" [NCT05463848]Phase 278 participants (Anticipated)Interventional2022-10-21Recruiting
An Open-Label Phase 1b Dose-Finding Trial Evaluating the Safety of Niraparib and Temozolomide and Atezolizumab in Participants With Advanced Solid Tumors and Expansion to a Phase 2 Trial Comparing the Effects of Niraparib and Temozolomide Plus Atezolizuma [NCT03830918]Phase 1/Phase 274 participants (Anticipated)Interventional2019-03-06Recruiting
Efficacy of a Protracted Temozolomide Schedule in Patients With Progression After Standard Dose Temozolomide for High-grade Gliomas [NCT00575887]Phase 225 participants (Actual)Interventional2006-08-31Completed
A Phase II Study of Irinotecan and Temozolomide in Breast Cancer Patients With Brian Metastases That Have Progressed After Stereotactic Radiosurgery or Whole Brain Radiation [NCT00617539]Phase 230 participants (Actual)Interventional2005-02-28Completed
Phase 0/I Dose Escalation Study of Mycophenolate Mofetil Combined With Radiation Therapy in Glioblastoma [NCT04477200]Phase 168 participants (Anticipated)Interventional2020-08-05Recruiting
A Phase I Study of Metronomic Temozolomide and Intravenous Ascorbic Acid for Patients With Recurrent High Grade Glioma [NCT02168270]Phase 14 participants (Actual)Interventional2014-06-16Terminated
Phase 2 Study of Sorafenib Plus Protracted Temozolomide in Recurrent Glioblastoma Multiforme [NCT00597493]Phase 232 participants (Actual)Interventional2007-09-30Completed
A Complementary Trial of an Immunotherapy Vaccine Against Tumor-Specific EGFRvIII [NCT00643097]Phase 240 participants (Actual)Interventional2007-09-30Completed
Temodal (Temozolomide) Post Marketing Surveillance Protocol [NCT00723827]682 participants (Actual)Observational2008-03-31Completed
Avastin in Combination With Temozolomide for Unresectable or Multifocal Glioblastoma Multiformes and Gliosarcomas [NCT00612339]Phase 241 participants (Actual)Interventional2007-08-31Completed
A Randomized, Open Label, Two-way Crossover, Single Dose Bioequivalence Study Comparing Dralitem® Capsules to the Reference Drug Temodal® Capsules in Patients With Primary Tumors of the Central Nervous System Under Fasting Conditions [NCT02343081]Phase 424 participants (Actual)Interventional2012-01-31Completed
A Phase I Trial of Hypofraction Radiotherapy + Temozolomide in the Treatment of Patients With Glioblastoma Multiforme and Anaplastic Astrocytoma of the Brain [NCT00841555]Phase 19 participants (Actual)Interventional2009-02-13Completed
Phase I Study of Ipilimumab, Nivolumab, and the Combination in Patients With Newly Diagnosed Glioblastoma [NCT02311920]Phase 132 participants (Actual)Interventional2015-04-16Completed
Phase II Trial of Bevacizumab, Radiation Therapy and Temodar Followed by Bevacizumab and Temodar With Continuation of Bevacizumab Beyond Progression (BBP-Bevacizumab Beyond Progression) [NCT01740258]Phase 268 participants (Actual)Interventional2013-01-31Completed
An Open-Label, Phase 2 Efficacy Study of Temozolomide (TMZ) In Advanced Succinate Dehydrogenase (SDH)-Mutant/Deficient Gastrointestinal Stromal Tumor (GIST) [NCT03556384]Phase 223 participants (Actual)Interventional2018-09-12Active, not recruiting
Phase II Study of Combined Temozolomide and Targeted P53 Gene Therapy (SGT-53) for Treatment of Patients With Recurrent Glioblastoma [NCT02340156]Phase 21 participants (Actual)Interventional2014-12-31Terminated
Phase II Study of TRC102 in Combination With Temozolomide for Recurrent Glioblastoma [NCT02395692]Phase 220 participants (Actual)Interventional2015-12-18Terminated(stopped due to Pre-specified response criteria not met to proceed to next stage of study.)
Phase 1-2 Trial Evaluating Metronomic Chemotherapy in Patients With a Relapsed or Refractory Wilms Tumor [NCT05384821]Phase 1/Phase 228 participants (Anticipated)Interventional2022-09-14Recruiting
Phase II Study of Temozolomide and Radiation in Newly Diagnosed GBM Patients After Resection and Insertion of Gliadel® Wafers [NCT00238277]Phase 215 participants (Actual)Interventional2005-02-15Terminated(stopped due to Terminated - due to low accrual)
Clinical Study of an Dendritic and Glioma Cells Fusion Vaccine With IL-12 for Treatment-naïve GBM Patients. [NCT04388033]Phase 1/Phase 210 participants (Anticipated)Interventional2020-12-31Recruiting
Efficacy of Post-radiation Adjuvant Temozolomide Chemotherapy in Residue Low-grade Glioma [NCT01649830]Phase 3290 participants (Anticipated)Interventional2012-07-31Recruiting
A Phase II Trial of Erlotinib With Temozolomide and Concurrent Radiation Therapy Post-Operatively in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00274833]Phase 227 participants (Actual)Interventional2005-10-31Completed
A Pilot Study of Temozolomide and O-Benzylguanine for Treatment of High-Grade Glioma, Using Autologous Peripheral Blood Stem Cells Genetically Modified for Chemoprotection [NCT00253487]0 participants Interventional2005-08-31Completed
Phase 1 Trial in Newly Diagnosed High Grade Glioma With Temozolomide, Radiation, and Minocycline Followed by Adjuvant Minocycline/Temozolomide. (D-TERMINED) [NCT02272270]Phase 125 participants (Actual)Interventional2014-10-27Completed
Intensive Chemotherapy and Immunotherapy in Patients With Newly Diagnosed Primary CNS Lymphoma: A Pilot Study [NCT00416819]10 participants (Actual)Interventional2003-09-30Completed
Phase II Study of Neoadjuvant Chemoradiation for Resectable Glioblastoma (NeoGlio) [NCT04209790]Phase 230 participants (Anticipated)Interventional2020-04-01Recruiting
A Phase Ib Dose Finding Study Assessing Safety and Activity of [177Lu]Lu-DOTA-TATE in Newly Diagnosed Glioblastoma in Combination With Radiotherapy With or Without Temozolomide and in Recurrent Glioblastoma as Single Agent [NCT05109728]Phase 160 participants (Anticipated)Interventional2022-05-10Recruiting
Phase I Trial of Radiation Therapy Plus Temozolomide With MK-3475 in Patients With Newly Diagnosed Glioblastoma (GBM) [NCT02530502]Phase 14 participants (Actual)Interventional2015-09-30Terminated(stopped due to The protocol was amendment to be stopped after phase I (phase 2 removed from protocol))
Pilot Clinical Trial of Allogeneic Tumor Lysate-Pulsed Autologous Dendritic Cell Vaccination in Newly Diagnosed Glioblastoma [NCT01957956]Early Phase 121 participants (Actual)Interventional2013-11-11Completed
Temodar and Sutent as Therapy for Patients With Malignant Melanoma, a Phase I/II Study [NCT00304200]Phase 1/Phase 27 participants (Actual)Interventional2006-03-31Terminated(stopped due to Funding was inadequate to continue; Companies requested closure.)
Phase Ib Dose Finding Study Assessing Safety and Activity of [177Lu]Lu-NeoB in Combination With Radiotherapy and Temozolomide in Subjects With Newly Diagnosed Glioblastoma and as a Single Agent in Recurrent Glioblastoma [NCT05739942]Phase 148 participants (Anticipated)Interventional2024-04-01Not yet recruiting
A Phase 1/1b, Open-label Study in Patients With Recurrent Glioblastoma to Assess the Safety and Tolerability of Macitentan in Combination With Dose-dense Temozolomide [NCT01499251]Phase 175 participants (Anticipated)Interventional2012-01-31Terminated(stopped due to Results did not clearly support continuing development in recurrent GBM)
Temozolomid (One Week on/One Week Off) Versus Strahlentherapie in Der Primärtherapie Anaplastischer Astrozytome Und Glioblastome Bei älteren Patienten: Eine Randomisierte Phase III-Studie (Methvsalem) [NCT01502241]Phase 3412 participants (Actual)Interventional2005-01-31Completed
A Phase 2 Study to Evaluate the Efficacy and Safety of Temozolomide in Advanced Gastrointestinal Stromal Tumor Patients With SDH Deficiency [NCT05661643]Phase 229 participants (Anticipated)Interventional2023-06-30Not yet recruiting
Phase I Trial of Dimethyl Fumarate, Temozolomide, and Radiation Therapy in Glioblastoma Multiforme [NCT02337426]Phase 112 participants (Actual)Interventional2015-02-13Completed
A Target Validation/Phase1 Study of BGB-290 in Combination With Temozolomide in Adolescent and Young Adult IDH1/2 Newly Diagnosed and Recurrent Mutant Gliomas [NCT03749187]Phase 178 participants (Anticipated)Interventional2019-04-03Recruiting
[NCT01702610]50 participants (Actual)Interventional2008-12-31Completed
Phase Ⅱ Trial of Temozolomide Plus Concurrent Whole-Brain Radiation Followed by TNV Regimen as Adjuvant Therapy for Patients With Newly Diagnosed Primary Central Nervous System (CNS) Lymphoma (PCNSL) [NCT01735747]Phase 216 participants (Anticipated)Interventional2008-06-30Active, not recruiting
Phase II Trial of Chemotherapy With Temozolomide in Combination With Topotecan for Central Nervous System (CNS) Metastasis of Solid Tumors [NCT01736800]Phase 20 participants (Actual)Interventional2007-03-31Withdrawn(stopped due to No enrollment and PI requested study termination per IRB system.)
A Phase 1 and Randomized Phase 2 Trial of Selinexor and Temozolomide in Recurrent Glioblastoma [NCT05432804]Phase 1/Phase 297 participants (Anticipated)Interventional2023-03-20Recruiting
Phase 2 Trial of Indoximod With Chemotherapy and Radiation for Children With Progressive Brain Tumors or Newly Diagnosed DIPG [NCT04049669]Phase 2140 participants (Anticipated)Interventional2019-10-02Recruiting
GBM AGILE: Global Adaptive Trial Master Protocol: An International, Seamless Phase II/III Response Adaptive Randomization Platform Trial Designed To Evaluate Multiple Regimens In Newly Diagnosed and Recurrent GBM [NCT03970447]Phase 2/Phase 31,030 participants (Anticipated)Interventional2019-07-30Recruiting
A Phase III Trial on Adjuvant Standard Temozolomide Chemotherapy With or Without Interferon-alpha in Newly Diagnosed High-grade Gliomas [NCT01765088]Phase 3300 participants (Anticipated)Interventional2012-09-30Recruiting
A PHASE II CLINICAL TRIAL FOR THE EVALUATION OF THE EFFICACY OF DISULFIRAM/COPPER COMBINATION AS AN ADJUVANT AND CONCURRENT CHEMOTHERAPY IN THE TREATMENT OF NEWLY DIAGNOSED GLIOBLASTOMA MULTIFORM [NCT01777919]Phase 232 participants (Anticipated)Interventional2017-01-31Not yet recruiting
Oxidative Phosphorylation Targeting In Malignant Glioma Using Metformin Plus Radiotherapy Temozolomide [NCT04945148]Phase 2640 participants (Anticipated)Interventional2023-05-31Not yet recruiting
A Phase 1 Study Evaluating the Safety and Pharmacokinetics of ABT-414 for Subjects With Glioblastoma Multiforme [NCT01800695]Phase 1202 participants (Actual)Interventional2013-04-02Completed
A Phase II Trial of Low Dose Fractionated Radiation Therapy as a Chemo-Potentiator of Salvage Temozolomide for Recurrent Anaplastic Astrocytoma and Glioblastoma Multiforme [NCT01466686]Phase 231 participants (Actual)Interventional2012-09-30Completed
Clinical Trial Phase IIB Randomized, Multicenter, of Continuation or Non Continuation With 6 Cycles of Temozolomide After the First 6 Cycles of Standard First-line Treatment in Patients With Glioblastoma. [NCT02209948]Phase 2166 participants (Actual)Interventional2014-08-22Completed
Temozolomide or Dacarbazine-based Chemotherapy Plus Endostatin in Advanced Pancreatic Neuroendocrine Tumor [NCT01845675]Phase 214 participants (Actual)Interventional2013-04-30Completed
A Phase 2/3 Randomized, Open-Label Study of Toca 511, a Retroviral Replicating Vector, Combined With Toca FC Versus Standard of Care in Subjects Undergoing Planned Resection for Recurrent Glioblastoma or Anaplastic Astrocytoma [NCT02414165]Phase 2/Phase 3403 participants (Actual)Interventional2015-11-30Terminated(stopped due to Sponsor Decision)
Phase II Trial for Patients With Newly Diagnosed Glioblastoma Multiforme (GBM) Treated With Gliadel Followed by Concurrent Radiation Therapy, Temodar and Avastin, Then Followed by Avastin and Temodar Post-Radiation [NCT01186406]Phase 241 participants (Actual)Interventional2011-04-30Terminated(stopped due to Study ended early due to toxicity)
Feasibility of Autologous Stem Cell Collection and Reinfusion in Newly Diagnosed High Grade Gliomas [NCT02976441]Early Phase 10 participants (Actual)Interventional2017-01-31Withdrawn(stopped due to Physician decided not to go through with study)
Phase II Study of ABT-888 and Temozolomide in Patients With Advanced Hepatocellular Carcinoma (HCC) Progressing Following Sorafenib Treatment or Intolerant to Sorafenib [NCT01205828]Phase 216 participants (Actual)Interventional2010-08-31Terminated(stopped due to Lack of efficacy)
The Efficacy and Safety of Temozolomide in Patients With Metastatic Pheochromocytoma or Paraganglioma [NCT05858177]Phase 262 participants (Actual)Interventional2019-10-01Completed
Phase II Study of Combination Treatment of Methotrexate, Ibrutinib, and Temozolomide (MIT Regimen) in Patients With Newly Diagnosed Primary CNS Lymphoma [NCT04514393]Phase 233 participants (Anticipated)Interventional2020-10-10Recruiting
A Phase I Study of Talazoparib (BMN 673) Plus Irinotecan With or Without Temozolomide in Children With Refractory or Recurrent Solid Malignancies [NCT02392793]Phase 143 participants (Actual)Interventional2015-03-25Completed
I-ATTAC: Improved Anti-Tumor Immunotherapy Targeted Against Cytomegalovirus in Patients With Newly-Diagnosed WHO Grade IV Unmethylated Glioma [NCT03927222]Phase 26 participants (Actual)Interventional2019-09-30Terminated(stopped due to Resource shortage)
Phase I Trial of Temozolomide, Bevacizumab Plus Bortezomib for Patients With Recurrent Glioblastoma Multiforme [NCT01435395]Phase 112 participants (Actual)Interventional2011-12-31Completed
Phase I Clinical Study of Safety & Efficacy of DC Vaccine and TMZ for the Treatment of Newly-diagnosed Glioblastoma After Surgery [NCT04968366]Phase 110 participants (Anticipated)Interventional2021-07-30Recruiting
Temozolomide in the Treatment of Advanced Non-Small Cell Lung Carcinoma: Phase II Evaluation in Previously Treated and Chemo-Naive Patients [NCT00005037]Phase 251 participants (Actual)Interventional2000-01-31Completed
A Phase I/II Dose-escalation and Dose-expansion Study of Disulfiram/Copper With Concurrent Radiation Therapy and Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT02715609]Phase 1/Phase 235 participants (Actual)Interventional2016-06-15Active, not recruiting
Prospective, Open Label, Randomized Phase II Trial to Assess a Multimodal Molecular Targeted Therapy in Children, Adolescent and Young Adults With Relapsed or Refractory High-risk Neuroblastoma [NCT01467986]Phase 2130 participants (Actual)Interventional2013-08-31Completed
Phase II Study of the Combination of Cisplatin + Temozolomide in Malignant Glial Tumours in Children and Adolescents at Diagnosis or in Relapse [NCT00360945]Phase 287 participants (Anticipated)Interventional2004-04-30Active, not recruiting
Combination of Bevacizumab, Irinotecan and Temozolomide for Relapsed or Refractory Neuroblastoma: A Phase II Study [NCT01114555]Phase 234 participants (Actual)Interventional2010-04-29Completed
A Phase 1-2 Trial of Temozolomide and Hypofractionated Radiotherapy in Treatment of Supratentorial Glioblastoma Multiforme [NCT01120639]Phase 1/Phase 230 participants (Actual)Interventional2010-04-30Completed
A Phase 2, Historically Controlled Study Testing the Efficacy of TTFields (Optune®) With Adjuvant Temozolomide in High Risk WHO Grade II and III Astrocytomas (FORWARD) [NCT03906448]Phase 21 participants (Actual)Interventional2019-05-20Terminated(stopped due to The study was terminated because the Study Chair/IDE Sponsor and Novocure determined that conducting this trial was not feasible without CMS approval.)
Phase III Study of Radiation Therapy With or Without Temozolomide for Symptomatic or Progressive Low-Grade Gliomas [NCT00978458]Phase 3540 participants (Actual)Interventional2009-11-17Active, not recruiting
Phase II Treatment of Adults and Children With Progressive Low Grade Gliomas With Temodal [NCT00003466]Phase 2100 participants (Anticipated)Interventional1998-03-31Completed
06-benzylguanine (BG) and Temozolomide (TMZ) Therapy of Glioblastoma Multiforme (GBM) in Patients With MGMT Positive Tumors With Infusion of Autologous P140KMGMT+ Hematopoietic Progenitors to Protect Hematopoiesis [NCT01269424]Phase 110 participants (Actual)Interventional2011-11-22Completed
Phase II Evaluation of Temodal (Temozolomide, Schering) in Previously Treated Advanced Sarcomas [NCT00003718]Phase 225 participants (Anticipated)Interventional1998-09-30Active, not recruiting
Second Line Chemotherapy With Temozolomide in Recurrent Oligodendroglial Tumors After PCV-Chemotherapy [NCT00003304]Phase 229 participants (Anticipated)Interventional1998-04-30Completed
A Phase II Study of Temozolomide in the Treatment of Recurrent Malignant Gliomas [NCT00004204]Phase 20 participants Interventional2000-02-29Active, not recruiting
A Pilot Phase II Trial of Temozolomide in Leptomeningeal Metastases [NCT00005812]Phase 212 participants (Actual)Interventional2000-01-31Terminated(stopped due to No objective response documented, protocol terminated after 12 patients.)
A Phase II Trial of Radiation Plus Temozolomide Followed by Adjuvant Temozolomide and Poly-ICLC in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00262730]Phase 297 participants (Actual)Interventional2006-01-31Completed
FaR-RMS: An Overarching Study for Children and Adults With Frontline and Relapsed RhabdoMyoSarcoma [NCT04625907]Phase 1/Phase 21,672 participants (Anticipated)Interventional2020-09-17Recruiting
A Randomised Phase IIb Trial of Bevacizumab Added to Temozolomide ± Irinotecan for Children With Refractory/Relapsed Neuroblastoma - BEACON-Neuroblastoma Trial [NCT02308527]Phase 2225 participants (Actual)Interventional2013-07-31Active, not recruiting
A Randomized Phase 2 Study of Maintenance Temozolomide Versus Observation in Stable or Responding Stage III/IV Non-Small Cell Lung Cancer Patients [NCT00632203]Phase 253 participants (Actual)Interventional2008-03-04Terminated
Temozolomide in Metastatic Breast Cancer Patients at High Risk of Brain Recurrence: Impact on the Incidence of Brain Metastases (STOP) [NCT00638963]Phase 26 participants (Actual)Interventional2008-10-02Terminated(stopped due to Terminated due to poor accrual)
Safety of TAS-102 in Combination With Temozolomide for Metastatic Pancreatic Neuroendocrine Tumors [NCT02943733]Phase 118 participants (Actual)Interventional2017-08-22Terminated(stopped due to closed per sponsor request, for slow enrollment)
A Phase 2 Trial for Patients With Newly Diagnosed High Grade Glioma Treated With Concurrent Radiation Therapy, Temozolomide, and BMX-001 [NCT02655601]Phase 2160 participants (Actual)Interventional2018-09-25Active, not recruiting
Treatment of Adults With Newly Diagnosed Glioblastoma With Partial Brain Radiation Therapy Plus Temozolomide and Chloroquine Followed by Tumor Treating Fields Plus Temozolomide and Chloroquine -- A Pilot Study [NCT04397679]Phase 110 participants (Anticipated)Interventional2021-08-12Recruiting
Phase 1 Study of 9-ING-41, a Glycogen Synthase Kinase 3 Beta (GSK 3β) Inhibitor, as a Single Agent or With Irinotecan, Irinotecan Plus Temozolomide, or With Cyclophosphamide Plus Topotecan in Pediatric Patients With Refractory Malignancies. [NCT04239092]Phase 168 participants (Anticipated)Interventional2020-06-05Active, not recruiting
A Phase I/II Clinical Trial of Autologous CMV-Specific Cytotoxic T Cells for GBM Patients [NCT02661282]Phase 1/Phase 265 participants (Actual)Interventional2016-06-01Completed
A Phase III Trial of Marizomib in Combination With Standard Temozolomide-based Radiochemotherapy Versus Standard Temozolomide-based Radiochemotherapy Alone in Patients With Newly Diagnosed Glioblastoma [NCT03345095]Phase 3749 participants (Actual)Interventional2018-07-26Active, not recruiting
A Phase I/II Study of High-dose L-methylfolate in With Combination Temozolomide and Bevacizumab in Recurrent High Grade Glioma. [NCT01891747]Phase 114 participants (Actual)Interventional2013-07-31Completed
Phase II Study of Ipilimumab Plus Temozolomide in Patients With Metastatic Melanoma [NCT01119508]Phase 264 participants (Actual)Interventional2010-05-31Completed
A Phase II Single Arm Trial Evaluating the Efficacy and Safety of Temozolomide for Second-Line Treatment of Neuroendocrine Carcinomas Progressing After First-Line Platinum- Based Therapy [NCT04122911]Phase 225 participants (Actual)Interventional2017-01-29Completed
A Phase I/II Study of Local Field Irradiation and Temozolomide Followed by Continuous Infusion Plerixafor as an Upfront Therapy for Newly Diagnosed Glioblastoma GBM [NCT01977677]Phase 1/Phase 230 participants (Actual)Interventional2014-11-30Completed
Phase I Trial of BMN 673 and Selected Cytotoxics in Patients With Advanced Solid Tumors [NCT02049593]Phase 144 participants (Actual)Interventional2014-06-12Completed
Phase I/II Study of the Poly (ADP-ribose) Polymerase-1 (PARP-1) Inhibitor BSI-201 in Patients With Newly Diagnosed Malignant Glioma [NCT00687765]Phase 1/Phase 2126 participants (Actual)Interventional2008-07-31Completed
A Randomized Phase II Trial of Concurrent Temozolomide and Radiotherapy Followed by Dose Dense Versus Metronomic Temozolomide and Maintenance Cis-Retinoic Acid for Patients With Newly Diagnosed Glioblastoma and Other Malignant Gliomas [NCT00200161]Phase 2127 participants (Actual)Interventional2005-08-09Completed
Phase I/II Study of Olaparib and Temozolomide in Patients With Recurrent Small Cell Lung Cancer Following Failure of Prior Chemotherapy [NCT02446704]Phase 1/Phase 266 participants (Actual)Interventional2015-10-13Active, not recruiting
Randomized, Phase II Study of Pembrolizumab (MK-3475) Versus Chemotherapy in Patients With Advanced Melanoma (KEYNOTE 002) [NCT01704287]Phase 2540 participants (Actual)Interventional2012-11-20Completed
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
A Phase I Trial of Neoadjuvant Chemoimmunotherapy in Recurrent Glioblastoma [NCT05700955]Phase 130 participants (Anticipated)Interventional2022-11-01Recruiting
An Italian Multicenter Phase II Trial of Metronomic Temozolomide in Unfit Patients With Advanced Neuroendocrine Neoplasms (NENs): MeTe Study [NCT05554003]Phase 246 participants (Anticipated)Interventional2022-01-14Recruiting
A Randomized Phase III Study of Re-Irradiation in Recurrent Glioblastoma [NCT01830101]Phase 30 participants (Actual)Interventional2014-02-28Withdrawn(stopped due to This study will not be proceeding due to lack of funding from anticipated sources)
Efficacy and Safety of Lanreotide ATG 120 mg in Combination With Temozolomide in Subjects With Progressive Well Differentiated Thoracic Neuroendocrine Tumors. A Phase II, Multicentre, Single Arm, Open-label Trial. [NCT02698410]Phase 240 participants (Actual)Interventional2016-07-31Completed
Phase I/II Study of Bevacizumab Plus Daily Temozolomide and Vorinostat for Recurrent Malignant Glioma Patients [NCT00939991]Phase 1/Phase 248 participants (Actual)Interventional2009-10-31Completed
Adjuvant Dendritic Cell Immunotherapy Complementing Conventional Therapy for Pediatric Patients With High-grade Glioma and Diffuse Intrinsic Pontine Glioma [NCT04911621]Phase 1/Phase 210 participants (Anticipated)Interventional2021-09-10Active, not recruiting
A Safety Run-in/Randomized Phase II Trial of EMD 121974 in Conjunction With Concomitant and Adjuvant Temozolomide With Radiation Therapy in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00085254]Phase 1/Phase 2112 participants (Actual)Interventional2005-04-30Completed
Temozolomide, Bevacizumab, Lithium and Radiation Treatment for Newly Diagnosed High Grade Glioma: A Phase II Study [NCT01105702]Phase 228 participants (Actual)Interventional2010-05-31Terminated(stopped due to Due to slow accrual)
A Pilot Phase II Trial of Hypofractionated Intensity-Modulated Radiation Therapy (Hypo-IMRT) Combining With Temozolomide (TMZ) and Bevacizumab for Patients With Newly Diagnosed Glioblastoma Multiforme (GBM) [NCT01209442]Phase 230 participants (Actual)Interventional2010-09-16Completed
Pamiparib and Low Dose Temozolomide In Patients With Platinum Sensitive Biliary Tract Cancer [NCT04796454]Phase 20 participants (Actual)Interventional2022-05-31Withdrawn(stopped due to Company decision)
Patients With IDH1 Positive Recurrent Grade II Glioma Enrolled in a Safety and Immunogenicity Study of Tumor-Specific Peptide Vaccine [NCT02193347]Phase 124 participants (Actual)Interventional2016-01-28Completed
A Phase III Study of Postoperative Early Temozolomide Treatment Plus STUPP Regimen for Newly Diagnosed GBM Multiforme [NCT05600491]Phase 378 participants (Anticipated)Interventional2015-11-08Recruiting
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
A Phase II Study of TEMOZOLOMIDE in Advanced Non-Small Cell Lung Cancer With and Without Brain Metastases [NCT00003062]Phase 270 participants (Anticipated)Interventional1997-07-31Completed
Phase I/II Study of MLN8237 in Combination With Irinotecan and Temozolomide for Patients With Relapsed or Refractory Neuroblastoma [NCT01601535]Phase 1/Phase 254 participants (Actual)Interventional2012-05-31Completed
A Phase II Trial of Temozolomide and BCNU for Anaplastic Gliomas [NCT00003176]Phase 282 participants Interventional1998-03-25Completed
Phase II Treatment of Adults With Newly Diagnosed Primary Malignant Glioblastoma Multiforme With Temodal [NCT00003464]Phase 250 participants (Anticipated)Interventional1997-09-30Completed
Phase II Trial of Temodal 4 Hourly in Progressive Breast Cancer [NCT00005054]Phase 20 participants Interventional1998-05-31Active, not recruiting
A Randomized Phase II Trial of ATN-224 in Combination With Temozolomide or Temozolomide Followed by ATN-224 in Patients With Advanced Melanoma [NCT00383851]Phase 260 participants (Anticipated)Interventional2006-09-30Active, not recruiting
A Phase I/II Study of Temozolamide and Thalidomide in the Treatment of Advanced Melanoma [NCT00005815]Phase 1/Phase 20 participants Interventional1999-12-31Completed
STRONG Trial - Stem Cell Radiotherapy (ScRT) and Temozolomide for Newly Diagnosed High-grade Glioma (HGG): A Prospective, Phase I/II Trial [NCT02039778]4 participants (Actual)Interventional2013-12-31Terminated(stopped due to Poor Accural)
NYU 05-40 PBMTC ONC-032P:High Dose Temozolomide,Thiotepa and Carboplatin With Autologous Stem Cell Rescue (ASCR) Followed by Continuation Therapy With 13-cis-retinoic Acid in Patients With Recurrent/Refractory Malignant Brain Tumors [NCT00528437]Phase 246 participants (Actual)Interventional2005-10-31Completed
Phase II Study of Dose Escalated, Targeted Radiation Therapy Using 3D Magnetic Resonance Spectroscopy Imaging (MRSI) in Newly Diagnosed Glioblastoma [NCT02394665]Phase 21 participants (Actual)Interventional2015-03-31Terminated(stopped due to Lack of Accrual/Enrollment)
Phase II Study of High Dose Radiotherapy and Concurrent Temozolomide Using Biologically-Based Target Volume Definition in Patients With Newly Diagnosed Glioblastoma [NCT02805179]Phase 226 participants (Actual)Interventional2016-09-22Completed
International Cooperative Phase III Trial of the HIT-HGG Study Group for the Treatment of High Grade Glioma, Diffuse Intrinsic Pontine Glioma, and Gliomatosis Cerebri in Children and Adolescents < 18 Years.(HIT-HGG-2013) [NCT03243461]Phase 3167 participants (Anticipated)Interventional2018-07-17Recruiting
Phase Ib Study of Fluzoparib in Combination With Camrelizumab and Temozolomide in Advanced Melanoma With Homologous Recombination (HR) Mutation ，a Single-center Open-label Exploratory Clinical Trial [NCT05983237]Phase 1/Phase 250 participants (Anticipated)Interventional2023-08-31Not yet recruiting
A Randomized Surgical Window of Opportunity Study With Dose Escalation to Evaluate Whether Oral Fluoxetine Can Induce Cytotoxic Lysosomal Stress and Enhance Temozolomide Efficacy in Clinical Glioma [NCT05634707]Early Phase 130 participants (Anticipated)Interventional2023-08-05Recruiting
A Phase II Study of Cabozantinib and Temozolomide in Patients With Unresectable or Metastatic Leiomyosarcoma and Other Soft Tissue Sarcomas [NCT04200443]Phase 272 participants (Actual)Interventional2020-01-14Active, not recruiting
A Phase I/II Trial of Maximal Resection, Local Radiation Boost With Concomitant Temozolomide, Followed by External Radiation Therapy With Concomitant Temozolomide for the Treatment of Newly Diagnosed Glioblastoma Multiforme [NCT00376103]Phase 1/Phase 23 participants (Actual)Interventional2006-08-31Terminated(stopped due to Loss of funding from sponsor)
Phase I Study of Neoadjuvant GMCI Plus Immune Checkpoint Inhibitor Combined With Standard of Care for Newly Diagnosed High-Grade Gliomas [NCT03576612]Phase 136 participants (Anticipated)Interventional2018-02-27Active, not recruiting
A Phase II Study of Temozolomide and Radiation Therapy in Patients With Brain Metastasis From Non-small Cell Lung Cancer (NSCLC) [NCT00080938]Phase 226 participants (Actual)Interventional2005-12-20Completed
Phase II Trial of Continuous Dose Temozolomide in Patients With Newly Diagnosed Anaplastic Oligodendroglioma and Mixed Oligoastrocytoma [NCT00362570]Phase 21 participants (Actual)Interventional2005-05-31Completed
A Multi-Center, Randomized, Double-Blind Phase II Study Comparing ABT-888, a PARP Inhibitor, Versus Placebo With Temozolomide in Patients With Relapsed Sensitive or Refractory Small Cell Lung Cancer [NCT01638546]Phase 297 participants (Actual)Interventional2012-06-30Completed
BrUOG 329: Onivyde (Nanoliposomal Irinotecan) and Metronomic Temozolomide for Patients With Recurrent Glioblastoma: A Phase IB/IIA Brown University Oncology Research Group Study [NCT03119064]Phase 1/Phase 212 participants (Actual)Interventional2017-11-30Terminated(stopped due to lack of response to study therapy)
Dose Intensive Chemotherapy for Children Less Than Ten Years of Age Newly-Diagnosed With Malignant Brain Tumors: A Pilot Study of Two Alternative Intensive Induction Chemotherapy Regimens, Followed by Consolidation With Myeloablative Chemotherapy (Thiotep [NCT00003273]Phase 20 participants (Actual)Interventional1997-11-30Withdrawn
Phase II Treatment of Adults With Newly Diagnosed, Progressive or Recurrent Primary Malignant Anaplastic Oligodendroglioma With Temodal [NCT00003465]Phase 260 participants (Anticipated)Interventional1998-03-31Completed
Mutant MGMT Gene Transfer Into Human Hematopoietic Progenitors to Protect Hematopoiesis During O6-Benzylguanine (BG, NSC 637037) and Carmustine Followed by Temozolomide Therapy of Advanced Solid Tumors [NCT00003567]Phase 18 participants (Actual)Interventional1999-05-31Terminated(stopped due to slow accrual)
A Phase II Study of Temozolomide (SCH 52365, Temodal(R)) for the Treatment of Recurrent Malignant Glioma [NCT00004113]Phase 20 participants Interventional1999-06-30Completed
Phase I (Tumour Site Specific) Study of Carboplatin and Temozolomide in Patients With Advanced Melanoma [NCT00003747]Phase 130 participants (Anticipated)Interventional1998-10-31Active, not recruiting
A Phase I Study of Extended Low Dose Temozolomide (SCH 52365, Temodar (R)) and Carmustine (BCNU) in the Treatment of Malignant Gliomas After Radiation Therapy [NCT00005637]Phase 10 participants Interventional1999-12-31Completed
A Phase II Trial of Intensive Chemotherapy and Autotransplantation for Patients With Newly Diagnosed Anaplastic Oligodendroglioma [NCT00588523]Phase 260 participants (Actual)Interventional2002-09-30Completed
Phase II Study of Dose Intensive Temozolomide in Elderly Adults With Newly Diagnosed Glioblastoma [NCT00365222]Phase 21 participants (Actual)Interventional2006-07-31Terminated(stopped due to IRB Study Closure)
Capecitabine ON Temozolomide Radionuclide Therapy Octreotate Lutetium-177 NeuroEndocrine Tumours Study [NCT02358356]Phase 275 participants (Actual)Interventional2015-11-30Completed
The Efficacy and Safety of Neoadjuvant Toripalimab Combined With Temozolomide in Resectable Stage III Melanoma: A Prospective, Single-center, Phase 2 Clinical Trial [NCT05827770]Phase 220 participants (Anticipated)Interventional2023-05-01Not yet recruiting
Pilot Study to Evaluate the Safety, Tolerability and Effectiveness of Intranasal Administration of Temozolomide in Patients With Glioblastoma (Phase I) [NCT04091503]Phase 130 participants (Actual)Interventional2019-12-20Completed
A Phase I/II Study of ABT-888, An Oral Poly(ADP-ribose) Polymerase Inhibitor, and Concurrent Radiation Therapy, Followed by ABT-888 and Temozolomide, in Children With Newly Diagnosed Diffuse Pontine Gliomas (DIPG) [NCT01514201]Phase 1/Phase 266 participants (Actual)Interventional2012-02-01Completed
A Phase I Trial for the Addition of Chloroquine, an Autophagy Inhibitor, to Concurrent Chemoradiation for Newly Diagnosed Glioblastoma [NCT02378532]Phase 113 participants (Actual)Interventional2016-08-31Completed
A Phase II, Multi-Cohort Trial of Combination Nivolumab and Temozolomide in Recurrent/Refractory Small-Cell Lung Cancer and Advanced Neuroendocrine Tumors [NCT03728361]Phase 255 participants (Actual)Interventional2018-12-31Active, not recruiting
Phase I/II Multicenter Trial of Intra-Arterial Carboplatin and Oral Temozolomide for the Treatment of Recurrent and Symptomatic Residual Brain Metastases. [NCT00362817]Phase 1/Phase 217 participants (Actual)Interventional2004-10-31Completed
SPARE-Scalp Preservation and Radiation Plus Alternating Electric Tumor Treatment Field (NovoTTF, Optune) for Patients With Glioblastoma: A Pilot Study [NCT03477110]Early Phase 130 participants (Actual)Interventional2018-05-04Active, not recruiting
A Phase II Study of the Efficacy of Hypofractionated Radiation Therapy With Bevacizumab and Temozolomide Followed by Maintenance Temozolomide and Bevacizumab for Recurrent High-Grade Gliomas [NCT01478321]Phase 254 participants (Actual)Interventional2011-12-14Terminated(stopped due to Slow accrual to some cohorts)
Temozolomide Plus Vorinostat in Patients With Relapse/Refractory Acute Myeloid Leukemia (AML) [NCT01550224]Phase 223 participants (Actual)Interventional2013-05-01Completed
A Phase II Randomized,Controlled,Open Label,Multicentre Study of Tegafur Combined With Temozolomide Versus Tegafur Combined With Temozolomide and Thalidomide in Subjects With Advanced Pancreatic Neuroendocrine Tumor [NCT03204019]Phase 260 participants (Anticipated)Interventional2016-10-31Recruiting
Phase II Trial of Temozolomide in Patients Affected by Relapsed Sensitive or Refractory Small Cell Lung Cancer With MGMT Methylation (TeRes). GOPAV03 [NCT02477813]Phase 26 participants (Actual)Interventional2015-01-31Terminated(stopped due to Lack of eligible patient recruitment)
Efficacy and Safety of Low Dose Temozolomide Plus Metformin as Combination Chemotherapy Compared With Low Dose Temozolomide Plus Placebo in Patient With Recurrent or Refractory Glioblastoma [NCT03243851]Phase 281 participants (Actual)Interventional2016-11-21Completed
A Prospective Multicenter Randomized Controlled Clinical Trial of Neoadjuvant Temozolomide Combined With Simultaneous Increased Intensity-modulated Radiotherapy in the Treatment of Glioblastoma [NCT04829097]Phase 380 participants (Anticipated)Interventional2020-11-01Recruiting
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
MT-R Followed by Autologous Stem Cells Transplantation in Newly-diagnosed Primary Central Nervous System Lymphoma [NCT02399189]Phase 239 participants (Anticipated)Interventional2014-05-31Recruiting
A Phase I Lead-In to a 2x2x2 Factorial Trial of Temozolomide, Memantine, Mefloquine, and Metformin as Post-Radiation Adjuvant Therapy of Glioblastoma Multiforme [NCT01430351]Phase 1144 participants (Anticipated)Interventional2011-09-14Active, not recruiting
Phase 1 Study of Pazopanib in Combination With Irinotecan and Temozolomide (PAZIT) for Children and Young Adults With Relapsed or Refractory Sarcoma [NCT03139331]Phase 116 participants (Actual)Interventional2017-06-06Completed
Ultra-low Dose Bevacizumab Plus Temozolomide for Recurrent High-grade Gliomas [NCT02416999]30 participants (Anticipated)Interventional2015-05-31Not yet recruiting
A Prospective, Single-center Clinical Study to Explore the Efficacy and Safety of SHR-1701 Combined With Temozolomide in the Treatment of Advanced Melanoma [NCT05106023]Phase 231 participants (Anticipated)Interventional2022-01-21Recruiting
A Phase 2, Open-label Study of ABI-009 (Nab-Rapamycin) in Patients With Recurrent High-grade Glioma and Patients With Newly Diagnosed Glioblastoma [NCT03463265]Phase 262 participants (Actual)Interventional2018-08-01Completed
Evaluation of Overcoming Limited Migration and Enhancing Cytomegalovirus-specific Dendritic Cell Vaccines With Adjuvant TEtanus Pre-conditioning in Patients With Newly-diagnosed Glioblastoma [NCT02366728]Phase 264 participants (Actual)Interventional2015-10-12Completed
Phase 1B Trial of ADI-PEG 20 Plus Radiotherapy and Temozolomide in Subjects With Newly Diagnosed Glioblastoma Multiforme [NCT04587830]Phase 132 participants (Anticipated)Interventional2020-09-14Recruiting
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
Pilot Pharmacokinetic Study of VAL-413 (Orotecan®) in Patients With Recurrent Pediatric Solid Tumors [NCT04337177]Phase 120 participants (Anticipated)Interventional2021-10-25Recruiting
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
Image-derived Prediction of Response to Chemo-radiation in Patients With Glioblastoma [NCT02329795]16 participants (Actual)Observational2014-10-31Terminated(stopped due to Slow accrual)
Phase I Study of Escalated Pharmacologic Dose, of Oral Folinic Acid in Combination With Temozolomide, According to Stupp R. Regimen, in Patients With Operated Grade-IV Astocytoma and a Non-methylated Gene Status of MGMT. [NCT01700569]Phase 124 participants (Actual)Interventional2013-01-31Terminated(stopped due to changing the standard of care)
A Phase II Trial of Continuous Low-Dose Temozolomide for Patients With Recurrent Malignant Glioma [NCT00498927]Phase 247 participants (Actual)Interventional2007-06-30Completed
A Phase II Study of Bevacizumab in Combination With Metronomic Temozolomide for Recurrent Malignant Glioma [NCT00501891]Phase 232 participants (Actual)Interventional2007-07-31Completed
Biochemotherapy With Temozolomide, Velban, Cisplatin, Interleukin-2, Interferon-alpha and Thalidomide for Metastatic Melanoma With Optional Intrathecal Interleukin-2 Treatment [NCT00505635]Phase 25 participants (Actual)Interventional2007-03-31Terminated(stopped due to Slow accrual)
A Phase II Study of Bevacizumab Plus Temodar and Tarceva After Radiation Therapy and Temodar in Patients With Newly Diagnosed Glioblastoma or Gliosarcoma Who Are Stable Following Radiation [NCT00525525]Phase 274 participants (Actual)Interventional2007-09-30Completed
A Longitudinal Assessment of Tumor Evolution in Patients With Brain Cancer [NCT03425292]Phase 149 participants (Actual)Interventional2018-03-01Completed
PPX and Concurrent Radiation for Newly Diagnosed Glioblastoma Without MGMT Methylation: A Randomized Phase II Study [NCT01402063]Phase 263 participants (Actual)Interventional2011-09-30Completed
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 Rituximab and Temozolomide in Recurrent Primary CNS Lymphoma [NCT00248534]Phase 216 participants (Actual)Interventional2005-09-30Terminated(stopped due to slow accrual/lack of resources/low priority due to combining 2 consortia)
PHASE 2, Multi-center, Single Arm Investigation of HSPPC-96 Vaccine With Temozolomide in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT00905060]Phase 270 participants (Actual)Interventional2009-06-29Completed
A Phase 1 Study of Maprotiline in Combination With Tamoxifen and Temozolomide for Recurrent Glioblastoma [NCT04200066]Phase 10 participants (Actual)Interventional2022-06-01Withdrawn(stopped due to One of the drugs for the study is not commercially available.)
Efficacy and Safety of Salvage Treatment With Dose-dense TMZ Plus CDDP in the Patients With Recurrent Malignant Gliomas: a Multicentre,Prospective Clinical Study [NCT01670890]Phase 2120 participants (Anticipated)Interventional2012-08-31Recruiting
A Phase II Study of Intrathecal and Systemic Chemotherapy With Radiation Therapy for Children With Central Nervous System Atypical Teratoid/Rhabdoid Tumor (AT/RT) Tumor [NCT00084838]Phase 225 participants (Actual)Interventional2003-02-28Completed
A Phase II Randomized Trial of Irinotecan/Temozolomide With Temsirolimus (NSC# 683864) or Chimeric 14.18 Antibody (Ch14.18) (NSC# 764038) in Children With Refractory, Relapsed or Progressive Neuroblastoma [NCT01767194]Phase 273 participants (Actual)Interventional2013-02-12Completed
Camrelizumab Plus Apatinib and Temozolomide as First Line Therapy in Advanced Acral Melanoma：a Single-center, Exploratory Clinical Study [NCT04397770]Phase 240 participants (Anticipated)Interventional2020-05-31Not yet recruiting
Treatment of High-grade Gliomas Using Escalating Doses of Hypofractionated Simultaneous Integrated Boost-intensity Modulated Radiation Therapy in Combination With Temozolomide - a Modified Phase I Clinical Trial [NCT03082846]16 participants (Actual)Interventional2014-01-01Completed
A Randomized, Phase 2 Study of the Efficacy and Tolerability of Veliparib in Combination With Temozolomide or Veliparib in Combination With Carboplatin and Paclitaxel Versus Placebo Plus Carboplatin and Paclitaxel in Subjects With BRCA1 or BRCA2 Mutation [NCT01506609]Phase 2294 participants (Actual)Interventional2012-01-23Completed
Phase I/II Evaluation Temozolomide and Farnesyl Transferase Inhibitor ZARNESTRA (R115777) for the Treatment of Recurrent and Progressive Glioblastoma Multiforme [NCT00050986]Phase 1/Phase 255 participants (Actual)Interventional2002-12-31Completed
A Single Arm Clinical Phase Ⅱ Study of Apatinib Combined With Temozolomide and Etoposide Capsules in the Treatment of Recurrent Medulloblastoma in Children [NCT04501718]Phase 244 participants (Anticipated)Interventional2020-10-28Recruiting
A Multi-Center Pilot/Phase I and Phase II Clinical Trial of NG101m Adjuvant Therapy in Newly Diagnosed Glioblastoma Patients [NCT04373785]Phase 1/Phase 252 participants (Anticipated)Interventional2024-01-01Not yet recruiting
Open-label Prospective Study of Recombinant Human Endostatin Combined With Cytotoxic Chemotherapy Regimen in the Treatment of Recurrent Gliomas [NCT04267978]Phase 2109 participants (Anticipated)Interventional2020-02-13Recruiting
Randomized Phase 2b Study of Safety And Efficacy Of TVI-Brain-1 Combined With Conformal Radiotherapy And Temozolomide Vs Standard Therapy In Newly Diagnosed MGMT Negative Glioblastoma Multiforme (GBM) [NCT05685004]Phase 2/Phase 396 participants (Anticipated)Interventional2023-09-15Recruiting
A Phase Ib/II Clinical Study of BBI608 in Combination With Temozolomide for Adult Patients With Recurrent or Progressed Glioblastoma [NCT02315534]Phase 1/Phase 234 participants (Actual)Interventional2015-03-31Completed
A Phase I/II Study of the Combination of Temozolomide and Pazopanib in Advanced Pancreatic Neuroendocrine Tumors (PNET) [NCT01465659]Phase 1/Phase 229 participants (Actual)Interventional2011-12-12Completed
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)
A Phase 1 Trial of RRx-001 in Combination With Irinotecan and Temozolomide for Pediatric Patients With Recurrent or Progressive Malignant Solid and Central Nervous System Tumors [NCT04525014]Phase 124 participants (Anticipated)Interventional2023-01-26Active, not recruiting
A Phase Ib/II, Open-Label, Multi-Center, Dose Escalation and Expansion Study to Evaluate Safety, Tolerability, Pharmacokinetics, and Anti-tumor Activity of IMP4297 in Combination With Temozolomide in Patients With Advanced Solid Tumors and Small Cell Lung [NCT04434482]Phase 1/Phase 2113 participants (Anticipated)Interventional2020-08-07Recruiting
Safety Run-In and Phase II Trial of M7824 and Topotecan or Temozolomide in Relapsed Small Cell Cancers [NCT03554473]Phase 1/Phase 267 participants (Anticipated)Interventional2018-09-11Recruiting
Phase Ib, Open-label, Multicenter, Intrapatient Dose-escalation Clinical Trial to Assess the Safety Profile of the TN-TC11G (THC+CBD) Combination With Temozolomide and Radiotherapy in Patients With Newly-diagnosed Glioblastoma [NCT03529448]Phase 1/Phase 230 participants (Anticipated)Interventional2023-08-18Recruiting
Pembrolizumab in MMR-Proficient Metastatic Colorectal Cancer Pharmacologically Primed to Trigger Dynamic Hypermutation Status [NCT03519412]Phase 2102 participants (Anticipated)Interventional2019-01-23Active, not recruiting
Molecular Profiling-Based Assignment of Cancer Therapy for Patients With Advanced Solid Tumors [NCT01827384]Phase 2208 participants (Actual)Interventional2014-01-07Completed
An Open Label Phase 1b/2 Study of Orally Administered PLX3397 in Combination With Radiation Therapy and Temozolomide in Patients With Newly Diagnosed Glioblastoma [NCT01790503]Phase 1/Phase 265 participants (Actual)Interventional2013-07-18Completed
Quantitative Assessment of the Early and Late Effects of Radiation and Chemotherapy on Glioblastoma Using Multiple MRI Techniques [NCT00756106]15 participants (Actual)Interventional2008-07-31Terminated(stopped due to Funding ended)
Phase II Study of Bevacizumab and Temozolomide in Elderly Patients With Newly-Diagnosed Glioblastoma [NCT01149850]Phase 250 participants (Actual)Interventional2010-04-28Active, not recruiting
Open Label Randomized Phase II/III Trial of Dendritic Cell Immunotherapy Against Cancer Stem Cells in Glioblastoma Patients Receiving Standard Therapy (DEN-STEM) [NCT03548571]Phase 2/Phase 360 participants (Anticipated)Interventional2018-04-26Active, not recruiting
Phase II Randomized Study: Whole Brain Radiotherapy and Concomitant Temozolomide, Compared With Whole Brain Radiotherapy for Brain Metastases Treatment [NCT01015534]Phase 255 participants (Actual)Interventional2006-01-31Completed
Feasibility Pilot Study of OKN-007 in Combination With Adjuvant Temozolomide Chemoradiotherapy in Patients With Newly Diagnosed Glioblastoma [NCT03587038]Phase 127 participants (Actual)Interventional2018-09-03Active, not recruiting
A Pilot Study of SGT-53 in Conjunction With Irradiation and Chemotherapy in Children With Recurrent or Progressive CNS Malignancies [NCT03554707]Early Phase 16 participants (Anticipated)Interventional2022-06-30Not yet recruiting
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
An Open-Label, Multicenter, First-in-Human, Phase 1 Dose-Escalation and Multicohort Expansion Study of INBRX-109 in Subjects With Locally Advanced or Metastatic Solid Tumors Including Sarcomas [NCT03715933]Phase 1240 participants (Anticipated)Interventional2018-10-10Recruiting
Phase II Study of Temozolomide in Unresectable or Metastatic Gastrointestinal Stromal Tumors (GIST) [NCT00005597]Phase 225 participants (Actual)Interventional2000-04-30Completed
A Phase I Study of PRK787/ZK 222584 in Combination With Daily Temozolomide and Radiation in Patients With Newly Diagnosed Glioblastoma [NCT00385853]Phase 119 participants (Actual)Interventional2006-09-30Completed
First Line Chemotherapy With Temozolomide in Recurrent Oligodendroglial Tumors, a Phase II Trial [NCT00003731]Phase 239 participants (Actual)Interventional1998-12-31Completed
A Prospective, Multi-Institutional Phase II Trial Evaluating Temozolomide vs. Temozolomide and Olaparib for Advanced Pheochromocytoma and Paraganglioma [NCT04394858]Phase 276 participants (Anticipated)Interventional2021-03-17Recruiting
A Randomized, Open-label, Multicentric, Two-arm Pivotal Trial of SonoCloud-9 Combined With Carboplatin (CBDCA) vs Standard of Care Lomustine (CCNU) or Temozolomide (TMZ) in Patients Undergoing Planned Resection for First Recurrence Glioblastoma. [NCT05902169]Phase 3560 participants (Anticipated)Interventional2023-11-05Not yet recruiting
Phase I/II Study of RAD001 in Combination With Temozolomide in Patients With Advanced Pancreatic Neuroendocrine Tumors [NCT00576680]Phase 1/Phase 243 participants (Actual)Interventional2008-05-31Completed
Phase II Study of Bevacizumab Plus Either Temozolomide or Etoposide for (GBM) Patients Who Have Failed Bevacizumab Plus Irinotecan [NCT00613028]Phase 223 participants (Actual)Interventional2008-04-30Completed
A Phase 1 Multicenter, Dose-escalation Study of LY573636-sodium in Combination With 1) Gemcitabine HCl or 2) Docetaxel or 3) Temozolomide or 4) Cisplatin, or 5) Erlotinib in Patients With Advanced Solid Tumors [NCT01284335]Phase 1234 participants (Actual)Interventional2008-07-31Terminated(stopped due to Study was terminated due to the termination of tasisulam development.)
A Phase II Study of Bevacizumab, Temozolomide and Hypofractionated Radiotherapy for Patients With Newly Diagnosed Malignant Glioma [NCT00782756]Phase 240 participants (Actual)Interventional2008-10-28Completed
Using Proton Magnetic Resonance Spectroscopy (MRS) to Predict Response of Vorinostat Treatment in Glioblastoma [NCT01342757]12 participants (Actual)Interventional2010-12-31Completed
A Phase II Open-Label, Randomized, Multi-Centre Comparative Study Of Bevacizumab-Based Therapy In Paediatric Patients With Newly Diagnosed Supratentorial, Infratentorial Cerebellar, or Peduncular High-Grade Glioma [NCT01390948]Phase 2124 participants (Actual)Interventional2011-10-18Completed
Everolimus and Temozolomide as 1-line Treatment in Advanced Gastroenteropancreatic Neuroendocrine Carcinoma (G3) With a Ki67 of 20-55% [NCT02248012]Phase 238 participants (Actual)Interventional2014-12-31Completed
A Multicenter, Open-Label, Randomized Study of NovoTTF-200A Alone and Combined With Temozolomide in Patients With Low-Grade Gliomas [NCT02507232]Early Phase 12 participants (Actual)Interventional2017-04-17Terminated(stopped due to low enrollment)
A Phase I Trial of Indoximod and Temozolomide-Based Therapy for Children With Progressive Primary Brain Tumors [NCT02502708]Phase 181 participants (Actual)Interventional2015-10-31Completed
An Open, Single-center Clinical Study of Surufatinib Combined With Temozolomide and S-1 in the First-line Treatment of Advanced Neuroendocrine Tumors [NCT06038461]Phase 1/Phase 240 participants (Anticipated)Interventional2023-09-15Not yet recruiting
A Phase II Study Analyzing Pulsed Reduced Dose Radiotherapy in Upfront Glioblastoma (PRORADGLIO Study) [NCT04747145]Phase 238 participants (Anticipated)Interventional2021-06-03Recruiting
Phase 1b/2a Single-center, Open-label, Dose Escalation Study to Evaluate the Safety, Tolerability, and Efficacy of MN-166 (Ibudilast) and Temozolomide Combination Treatment in Patients With Newly Diagnosed or Recurrent Glioblastoma [NCT03782415]Phase 1/Phase 250 participants (Anticipated)Interventional2018-12-29Active, not recruiting
Phase 2, Single Arm, Historically Controlled Study Testing The Safety and Efficacy of Adjuvant Temozolomide Plus TTFields (Optune®) Plus Pembrolizumab in Patients With Newly Diagnosed Glioblastoma (2-THE-TOP) [NCT03405792]Phase 231 participants (Actual)Interventional2018-02-23Active, not recruiting
Phase II Study of Hu3F8, Irinotecan/Temozolomide and Sargramostim (HITS) Chemoimmunotherapy for High-Risk Neuroblastoma [NCT03189706]Early Phase 148 participants (Actual)Interventional2017-06-12Active, not recruiting
Post Marketing Surveillance of Radiotherapy With Concomitant and Adjuvant Chemotherapy With Temozolomide for Patients With Newly Diagnosed and Operated Glioblastoma Multiforme [NCT00704808]180 participants (Actual)Observational2006-05-31Completed
Phase I/II Evaluation of Everolimus (RAD001), Radiation and Temozolomide (TMZ) Followed by Adjuvant Temozolomide and Everolimus in Newly Diagnosed Glioblastoma [NCT00553150]Phase 1/Phase 2122 participants (Actual)Interventional2009-03-31Completed
Study With High Doses of Chemotherapy, Radiotherapy and Consolidation Therapy With Ciclofosfamide and Anticyclooxygenase 2, for the Metastatic Ewing Sarcoma [NCT02727387]Phase 2155 participants (Actual)Interventional2009-06-01Completed
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
Phase III Intergroup Study of Radiotherapy With Concomitant and Adjuvant Temozolomide Versus Radiotherapy With Adjuvant PCV Chemotherapy in Patients With 1p/19q Co-deleted Anaplastic Glioma or Low Grade Glioma [NCT00887146]Phase 3360 participants (Anticipated)Interventional2009-09-30Recruiting
Phase I Trial of R115777 With Radiation Therapy and Temozolomide in Patients With Newly Diagnosed Glioblastoma Multiforme [NCT02227901]Phase 119 participants (Actual)Interventional2002-09-30Completed
A Phase 1B Study of the Safety of LAM561 Administered Orally in Combination With Temozolomide (TMZ) and Radiation Therapy or With TMZ Alone in the First Line Treatment of Subjects With Glioblastoma [NCT03867123]Phase 118 participants (Actual)Interventional2018-12-04Completed
A Multi-Center, Open-Label, Phase I/II Study of GEM1777 in Combination With Temozolomide Administered Every 4 Weeks to Patients With Metastatic Melanoma [NCT00724841]Phase 1/Phase 21 participants (Actual)Interventional2008-06-30Terminated(stopped due to Study terminated prematurely due to financial contraints.)
A Randomized, Open-Label, Multicenter, Phase III Study of HX008 (a Humanized Monoclonal Antibody Against PD-1) Plus Transcatheter Arterial Chemoembolization (TACE) in the First-Line Treatment of Subjects With Stage IV (M1c) Melanoma That is Metastatic to [NCT05647954]Phase 3350 participants (Anticipated)Interventional2022-12-31Not yet recruiting
INdividualized Screening Trial of Innovative Glioblastoma Therapy (INSIGhT) [NCT02977780]Phase 2250 participants (Anticipated)Interventional2017-02-09Recruiting
High-Risk Neuroblastoma Study 2 of SIOP-Europa-Neuroblastoma (SIOPEN) [NCT04221035]Phase 3800 participants (Anticipated)Interventional2019-11-05Recruiting
"Medical Treatment of High-Risk Neurofibromas in Patients With Type 1 Neurofibromatosis: A Clinical Trial of Sequential Medical Therapies" [NCT00846430]Phase 29 participants (Actual)Interventional2008-10-31Completed
A Phase II Study of Concurrent Radiation Therapy, Temozolomide, and Bevacizumab Followed by Bevacizumab/Everolimus in the First-line of Treatment of Patients With Glioblastoma Multiforme [NCT00805961]Phase 268 participants (Actual)Interventional2009-01-31Completed
International Multicenter Phase I Trial of Hydroxyurea in Combination With Dose-Intense Temozolomide in Recurrent Glioblastoma [NCT03463733]Phase 154 participants (Anticipated)Interventional2018-03-02Recruiting
A Clinical Study of Supra-early Post-Surgery Chemotherapy Plus Standard TEMODAL® Regimen Versus Standard TEMODAL® Regimen in the Treatment on Patients With Newly Diagnosed Glioblastoma Multiforme [NCT02520635]180 participants (Anticipated)Observational2015-01-31Recruiting
G-FORCE-1: An Open-Label Phase 1 Two Part Dose Escalation Trial of RRx-001 Concurrent With Radiation and Temozolomide and RRx-001 + Temozolomide Post-RT In Newly Diagnosed Glioblastoma and Anaplastic Gliomas With Intact 1p/19q Chromosomes [NCT02871843]Phase 119 participants (Actual)Interventional2017-02-14Completed
Rapid Analysis and Response Evaluation of Combination Anti-Neoplastic Agents in Rare Tumors (RARE CANCER) Trial: RARE 2 Talazoparib and Temozolomide [NCT05142241]Phase 234 participants (Anticipated)Interventional2022-07-11Recruiting
Anticancer Therapeutic Vaccination Using Telomerase-derived Universal Cancer Peptides in Glioblastoma [NCT04280848]Phase 256 participants (Anticipated)Interventional2020-05-26Active, not recruiting
A Phase 2 Study of Veliparib (ABT-888) and Local Irradiation, Followed by Maintenance Veliparib and Temozolomide, in Patients With Newly Diagnosed High-Grade Glioma (HGG) Without H3 K27M or BRAFV600 Mutations [NCT03581292]Phase 238 participants (Actual)Interventional2018-11-06Active, not recruiting
A Phase 1 Study of Pevonedistat (MLN4924), a NEDD8 Activating Enzyme (NAE) Inhibitor, in Combination With Temozolomide and Irinotecan in Pediatric Patients With Recurrent or Refractory Solid Tumors [NCT03323034]Phase 130 participants (Actual)Interventional2018-01-11Active, 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
Pharmacological Ascorbate Combined With Radiation and Temozolomide in Glioblastoma Multiforme: A Phase 2 Trial [NCT02344355]Phase 290 participants (Anticipated)Interventional2017-03-13Active, not recruiting
Phase I Study of AZD1775 (Adavosertib) With Radiation and Temozolomide in Patients With Newly Diagnosed Glioblastoma and Evaluation of Intratumoral Drug Distribution in Patients With Recurrent Glioblastoma [NCT01849146]Phase 174 participants (Actual)Interventional2013-08-19Active, not recruiting
A Phase I Study of the PARP Inhibitor ABT-888 in Combination With Temozolomide in Acute Leukemias [NCT01139970]Phase 166 participants (Actual)Interventional2010-05-21Active, not recruiting
A Phase I Study of Vorinostat (Suberoylanilide Hydroxamic Acid [SAHA]) in Combination With Temozolomide in Patients With Malignant Gliomas [NCT00268385]Phase 183 participants (Actual)Interventional2005-12-16Active, not recruiting
A Phase Ib/II, Open-label Study of NBM-BMX as Monotherapy or in Combination With Radiotherapy and Temozolomide in Subjects With Solid Tumors or Newly Diagnosed Glioblastoma [NCT06012695]Phase 1/Phase 279 participants (Anticipated)Interventional2023-08-11Recruiting
Feasibility of Evaluating Abemaciclib Neuropharmacokinetics of Diffuse Midline Glioma Using Intratumoral Microdialysis [NCT05413304]Phase 17 participants (Anticipated)Interventional2023-04-07Recruiting
Randomized Phase II Study Comparing the MET Inhibitor Cabozantinib to Temozolomide/Dacarbazine in Ocular Melanoma [NCT01835145]Phase 247 participants (Actual)Interventional2013-07-31Completed
A Phase 1/2 Study of BMN 673, an Oral Poly(ADP-Ribose) Polymerase Inhibitor, Plus Temozolomide in Children With Refractory or Recurrent Malignancies [NCT02116777]Phase 1/Phase 240 participants (Actual)Interventional2014-05-16Completed
Phase II Study of High-Dose Rituximab Combined With Temozolomide as Treatment for Patients With Primary CNS Lymphoma [NCT02113007]Phase 22 participants (Actual)Interventional2014-07-31Terminated(stopped due to Closed early due to slow accrual.)
Brain Interstitium Temozolomide Concentration Pre and Post Regadenoson Administration [NCT02389738]Early Phase 16 participants (Actual)Interventional2015-02-28Completed
A Randomized Feasibility Study Evaluating Temozolomide Chronotherapy for High Grade Glioma [NCT02781792]Phase 242 participants (Actual)Interventional2016-08-11Active, not recruiting
A Follow-Up Study to Add Whole Brain Radiotherapy (WBRT) to Standard Temozolomide Chemo-Radiotherapy in Newly Diagnosed Glioblastoma (GBM) Treated With 4 Weeks of Continuous Infusion Plerixafor [NCT03746080]Phase 220 participants (Anticipated)Interventional2018-12-04Recruiting
Phase I / II Study of the Combination of Doxycycline With Temozolomide and Ipilimumab in Patients With Metastatic Melanoma [NCT01590082]Phase 1/Phase 212 participants (Actual)Interventional2012-11-30Terminated(stopped due to Accrual slow due to alternate trials and treatment options.)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00026494 (1) [back to overview]Radiographic Response Assessed by Macdonald Criteria Every 2 Months
NCT00050986 (1) [back to overview]Maximal Tolerating Dose (MTD for Phase I)
NCT00068250 (4) [back to overview]Phase II: Pre-irradiation Chemotherapy Tumor Response Rate (Including Phase I Patients at Same Dose)
NCT00068250 (4) [back to overview]Number of Phase I Participants Experiencing Toxicity
NCT00068250 (4) [back to overview]Phase II: Overall Survival Rate at 2 Years (Including Phase I Patients at Same Dose)
NCT00068250 (4) [back to overview]Phase II: Progression-free Survival (Including Phase I Patients at Same Dose)
NCT00077207 (6) [back to overview]Number of Participants Who Experienced a Grade 3 or 4 Thrombocytopenia and/or Neutropenia.
NCT00077207 (6) [back to overview]Number of Participants Who Experienced Toxic Death
NCT00077207 (6) [back to overview]Percent Probability of Progression-free Survival (PFS)
NCT00077207 (6) [back to overview]Percentage Probability of Event-free Survival (EFS)
NCT00077207 (6) [back to overview]Short Term Feasibility Success
NCT00077207 (6) [back to overview]Long Term Feasibility Success
NCT00080938 (4) [back to overview]1-year Neurologic (Central Nervous System, CNS) Progression Free Rate
NCT00080938 (4) [back to overview]Number of Patients With Intracranial Response
NCT00080938 (4) [back to overview]Overall Survival Time
NCT00080938 (4) [back to overview]Time to Non-CNS (Systemic) Progression
NCT00084838 (19) [back to overview]Grade 3-4 Pulmonary Events
NCT00084838 (19) [back to overview]2-yr Overall Survival
NCT00084838 (19) [back to overview]Grade 3-4 Allergy/Immunology
NCT00084838 (19) [back to overview]Grade 3-4 Auditory/Hearing Events
NCT00084838 (19) [back to overview]Grade 3-4 Blood/Bone Marrow Events
NCT00084838 (19) [back to overview]Grade 3-4 Hepatic Events
NCT00084838 (19) [back to overview]Grade 3-4 Pain Events
NCT00084838 (19) [back to overview]Grade 3-4 Cardiovascular Events
NCT00084838 (19) [back to overview]Grade 3-4 Constitutional Events
NCT00084838 (19) [back to overview]Pre-Radiation Therapy Chemotherapeutic Response
NCT00084838 (19) [back to overview]Grade 3-4 Renal/Genitourinary Events
NCT00084838 (19) [back to overview]Grade 3-4 Dermatology Events
NCT00084838 (19) [back to overview]Grade 3-4 Neurology Events
NCT00084838 (19) [back to overview]Grade 3-4 Muscloskeletal Events
NCT00084838 (19) [back to overview]Grade 3-4 Gastrointestinal Events
NCT00084838 (19) [back to overview]Grade 3-4 Hemorrhage Events
NCT00084838 (19) [back to overview]Grade 3/4 Events
NCT00084838 (19) [back to overview]Grade 3-4 Metabolic/Laboratory Events
NCT00084838 (19) [back to overview]Grade 3-4 Infection/Febrile Neutropenia Events
NCT00085254 (5) [back to overview]Dose Limiting Toxicities of EMD + RT and TMZ
NCT00085254 (5) [back to overview]Overall Survival (Phase II)
NCT00085254 (5) [back to overview]Overall Survival Based on Dose Level - Phase 2
NCT00085254 (5) [back to overview]Maximum Tolerated or Tolerable Dose (MTD) - 3 Pre-defined Doses
NCT00085254 (5) [back to overview]Frequency of Hematologic and Nonhematologic Adverse Events
NCT00091572 (4) [back to overview]Progression Free Survival
NCT00091572 (4) [back to overview]Overall Survival
NCT00091572 (4) [back to overview]Objective Response Rate in Subjects With Measurable Lesions
NCT00091572 (4) [back to overview]Duration of Objective Response
NCT00096265 (6) [back to overview]Change in Steroid Dependence at Six Months
NCT00096265 (6) [back to overview]Change in Performance Status at Six Months
NCT00096265 (6) [back to overview]Change in Functional Assessment of Cancer Therapy-Brain (FACT-Br) Score at 3 Months
NCT00096265 (6) [back to overview]Quality-adjusted Survival as Measured by EuroQol 5-dimension Instrument
NCT00096265 (6) [back to overview]Rate of CNS Progression (One Year)
NCT00096265 (6) [back to overview]Overall Survival
NCT00098774 (4) [back to overview]4 Year Overall Survival Rate
NCT00098774 (4) [back to overview]Change From Baseline in Mini-Mental Status Evaluation at 4 Months
NCT00098774 (4) [back to overview]Complete Response Rate After Remission Induction
NCT00098774 (4) [back to overview]4 Year Progression Free Rate
NCT00098865 (3) [back to overview]Overall Response
NCT00098865 (3) [back to overview]Therapy Completion Rate
NCT00098865 (3) [back to overview]Overall Survival
NCT00100802 (2) [back to overview]One Year Overall Survival
NCT00100802 (2) [back to overview]Occurrence of Death Attributable to Complications of Protocol Therapy
NCT00112502 (10) [back to overview]Median Overall Survival (OS) Comparison of Doublet Versus Triplet Therapy
NCT00112502 (10) [back to overview]Median Overall Survival (OS) Comparison of Celecoxib Arms Versus no Celecoxib Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) of Individual Arms
NCT00112502 (10) [back to overview]Median Overall Survival (OS) Comparison of Thalidomide Arms Versus no Thalidomide Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) Comparison of Celecoxib Arms Versus no Celecoxib Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) Comparison of Doublet Versus Triplet Therapy
NCT00112502 (10) [back to overview]Median Overall Survival (OS) Comparison of Isotretinoin Arms Versus no Isotretinoin Arms
NCT00112502 (10) [back to overview]Overall Survival of Individual Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) Comparison of Isotretinoin Arms Versus no Isotretinoin Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) Comparison of Thalidomide Arms Versus no Thalidomide Arms
NCT00114140 (5) [back to overview]Neurocognitive Function
NCT00114140 (5) [back to overview]Progression-free Survival
NCT00114140 (5) [back to overview]Overall Survival Rate at 3 Years
NCT00114140 (5) [back to overview]Survival and Progression-free Survival by O(6)-Methylguanine-DNA Methyltransferase (MGMT) Methylation Status
NCT00114140 (5) [back to overview]Quality of Life as Measured by the Functional Assessment of Cancer Therapy Scale With Brain Module (FACT-BR)
NCT00187486 (2) [back to overview]Overall Survival
NCT00187486 (2) [back to overview]Progression Free Survival
NCT00200161 (2) [back to overview]Progression Free Survival at 6 Months
NCT00200161 (2) [back to overview]12 Month Overall Survival of Patients With Newly Diagnosed Glioblastoma Multiforme Treated With Concurrent Temozolomide and Radiotherapy Followed by Dose Dense or Metronomic Dosing of Temozolomide and Maintenance Cis-retinoic Acid.
NCT00248534 (4) [back to overview]Number of Participants Alive at 3 Years
NCT00248534 (4) [back to overview]Percentage of Participants With Objective Response
NCT00248534 (4) [back to overview]6-month Progression-free Survival
NCT00248534 (4) [back to overview]1 Year Overall Survival Rate
NCT00262730 (1) [back to overview]Survival
NCT00266812 (1) [back to overview]Number of Participants With Progression-free Survival (6 Month)
NCT00275002 (2) [back to overview]Percentage of Participants With an Objective Response (Complete Response or Partial Response)
NCT00275002 (2) [back to overview]Number of Patients With Grade 3 or 4 Adverse Events at Least Possibly Related to the Combination of O6-benzylguanine and Temozolomide
NCT00301067 (6) [back to overview]Overall Response Rate
NCT00301067 (6) [back to overview]Number and Frequency of Dose Limiting Toxicities (DLTs) With High-dose Calcitriol in Combination With Temozolomide
NCT00301067 (6) [back to overview]Overall Survival (OS) Stratified by Vitamin D-Receptor (VDR) Gene Polymorphisms
NCT00301067 (6) [back to overview]Number of Patients With Toxicity
NCT00301067 (6) [back to overview]Time to Progression
NCT00301067 (6) [back to overview]Overall Survival
NCT00302159 (6) [back to overview]Percentage of Participants With Overall Survival at 6, 12, and 24 Months
NCT00302159 (6) [back to overview]Percentage of Participants With Progression Free Survival at 6, 12, and 24 Months
NCT00302159 (6) [back to overview]Median Progression Free Survival.
NCT00302159 (6) [back to overview]Median Overall Survival
NCT00302159 (6) [back to overview]Number of Participants With Adverse Events
NCT00302159 (6) [back to overview]Number of Participants With Best Response
NCT00304031 (18) [back to overview]Mean Neurocognitive Function (NCF) Composite Score Over Time
NCT00304031 (18) [back to overview]Median Progression-free Survival Time by MGMT Status
NCT00304031 (18) [back to overview]Determination of Impactful Baseline Instruments on Overall Survival
NCT00304031 (18) [back to overview]Median Overall Survival Time by MGMT Status
NCT00304031 (18) [back to overview]Median Progression-free Survival (PFS) Time
NCT00304031 (18) [back to overview]Mean MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score Over Time
NCT00304031 (18) [back to overview]Change From Baseline in Mean EORTC QLQ-C30 Global Health Status
NCT00304031 (18) [back to overview]Overall Survival Status by Progression Status at 6 Months
NCT00304031 (18) [back to overview]Number of Participants With Deterioration From Baseline in MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score at Cycle 4
NCT00304031 (18) [back to overview]Number of Participants With Deterioration From Baseline in MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Interference Score at Cycle 4
NCT00304031 (18) [back to overview]Median Overall Survival Time
NCT00304031 (18) [back to overview]Mean Neurocognitive Function (NCF) Composite Score at Cycle 10 for Participants Without Progression After 6 Months of Adjuvant Therapy
NCT00304031 (18) [back to overview]Mean MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score at Cycle 10 for Participants Without Progression After 6 Months of Adjuvant Therapy
NCT00304031 (18) [back to overview]Mean EORTC QLQ-C30 Global Health Status Score at Cycle 10 for Participants Without Progression After 6 Months of Adjuvant Therapy
NCT00304031 (18) [back to overview]Mean Change From Baseline in MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score at Mid-cyle for Cycle 4
NCT00304031 (18) [back to overview]Mean Change From Baseline in MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score at Mid-cyle for Cycle 1
NCT00304031 (18) [back to overview]Mean Change From Baseline in EORTC QLQ-C30 Global Health Status Score at Mid-cyle for Cycle 4
NCT00304031 (18) [back to overview]Mean Change From Baseline in EORTC QLQ-C30 Global Health Status Score at Mid-cyle for Cycle 1
NCT00305864 (3) [back to overview]Progression-free Survival (Phase II)
NCT00305864 (3) [back to overview]Median Overall Survival (Phase II)
NCT00305864 (3) [back to overview]Maximum Tolerated Dose of MGd (Phase I)
NCT00311584 (1) [back to overview]Overall Response - Complete Response (CR), Very Good Partial Response (VGPR) and Partial Response (PR)
NCT00313729 (3) [back to overview]Response Rate (Complete and Partial Response)
NCT00313729 (3) [back to overview]Safety Profile
NCT00313729 (3) [back to overview]Time to Tumor Progression
NCT00323115 (13) [back to overview]Number of Enzyme-linked Immunosorbent Spots (ELISPOT) - Correlation Between Immunological Parameters and Efficacy - Median
NCT00323115 (13) [back to overview]Number of Participants With Evaluable Data: Feasibility of Vaccination
NCT00323115 (13) [back to overview]Evaluation of T Cell Characteristics
NCT00323115 (13) [back to overview]Number of Participants With Significant Difference in Tumor Volume Size Pre- and Postvaccination: Neuroimaging and Tumor Assessment
NCT00323115 (13) [back to overview]Overall Survival Duration: Efficacy Parameters
NCT00323115 (13) [back to overview]Progression Free Survival (PFS)
NCT00323115 (13) [back to overview]Frequency of CD4+ and CD8+ T Cells - the Proportion of Cells in the Parent Population Responding to Glioblastoma Multiforme (GBM) - Mean
NCT00323115 (13) [back to overview]Frequency of CD4+ and CD8+ T Cells - the Proportion of Cells in the Parent Population Responding to Glioblastoma Multiforme (GBM) - Median
NCT00323115 (13) [back to overview]Percentage of Tumor-specific T-cells - Correlation Between Immunological Parameters and Efficacy- Mean
NCT00323115 (13) [back to overview]Percentage of Tumor-specific T-cells - Correlation Between Immunological Parameters and Efficacy- Median
NCT00323115 (13) [back to overview]Tumor-specific Cytotoxic T-cell Response
NCT00323115 (13) [back to overview]Number of Adverse Events: Toxicity Profile of Intra-nodal DC/Tumor Lysate Vaccination
NCT00323115 (13) [back to overview]Number of Enzyme-linked Immunosorbent Spots (ELISPOT) - Correlation Between Immunological Parameters and Efficacy - Mean
NCT00362817 (5) [back to overview]Analyze Patients Time to Progression
NCT00362817 (5) [back to overview]Determine the Overall Survival of Patients
NCT00362817 (5) [back to overview]The Incidence and Severity of Centeral Nervous System (CNS) Toxicities
NCT00362817 (5) [back to overview]Determine the Cause of Death of Patients After Treatment
NCT00362817 (5) [back to overview]Affects of Response Rate of Chemotherapy With Intra-arterial Carboplatin and Oral Temozolomide
NCT00392171 (1) [back to overview]Percentage of Participants Surviving at Six Months of Treatment Without Evidence of Disease Progression.
NCT00402116 (11) [back to overview]Number of Participants Undergoing Magnetic Resonance Imaging/Magnetic Resonance Spectroscopy (MRI/MRS) for Clinical Evaluation at Baseline
NCT00402116 (11) [back to overview]Phase 1 and 2- Pharmacokinetics: Area Under the Concentration-Time Curve During 1 Dosing Interval at Steady State (AUCτ,ss) for Enzastaurin, LY326020 and Total Analyte (Enzastaurin + LY326020) When Enzastaurin Administered With or Without Temozolomide
NCT00402116 (11) [back to overview]Phase 1 - Number of Participants With Adverse Events (AEs)
NCT00402116 (11) [back to overview]M.D. Anderson Symptom Inventory - Brain Tumor (MDASI-BT)
NCT00402116 (11) [back to overview]Phase 1 and 2 - Progression-Free Survival (PFS)
NCT00402116 (11) [back to overview]Phase 1- Pharmacokinetics (PK): Maximum Observed Drug Concentration During 1 Dosing Interval at Steady State (Cmax,ss) for Enzastaurin, LY326020, and Total Analyte (Enzastaurin + LY326020) When Enzastaurin Administered With or Without Temozolomide
NCT00402116 (11) [back to overview]Functional Assessment of Cancer Therapy - Brain (FACT-Br)
NCT00402116 (11) [back to overview]Phase 1 and Phase 2 - Overall Survival (OS)
NCT00402116 (11) [back to overview]Phase 1- Determination of the Maximum Tolerated Dose (MTD) of Enzastaurin
NCT00402116 (11) [back to overview]Phase 2 - Number of Participants With Adverse Events (AEs)
NCT00402116 (11) [back to overview]Phase 1 and 2: Association Between Biomarkers and Clinical Outcome
NCT00404495 (6) [back to overview]Percentage of Participants With Objective Response of Complete Response or Partial Response
NCT00404495 (6) [back to overview]Percentage of Participants With Objective Response of Complete Response or Partial Response, Investigator's Assessment
NCT00404495 (6) [back to overview]Time to Treatment Failure (TTF)
NCT00404495 (6) [back to overview]Time to Tumor Progression (TTP)
NCT00404495 (6) [back to overview]Duration of Response
NCT00404495 (6) [back to overview]Overall Survival (OS)
NCT00423150 (1) [back to overview]Tumor Responses (Complete and Partial Response)
NCT00424554 (3) [back to overview]Tolerability: Number of Participants Discontinuing Treatment Due to Adverse Events (AE)
NCT00424554 (3) [back to overview]MethylGuanine-DNA MethylTransferase [MGMT] Activity Measured From the Tumor Tissue During Surgery
NCT00424554 (3) [back to overview]Safety: Number of Participants Who Experienced Grade 3 or 4 Toxicities
NCT00433381 (8) [back to overview]Change in Perfusion MRI Markers at Week 8 as Predictors of 12mo Overall Survival (OS)
NCT00433381 (8) [back to overview]Agreement Between Local Interpretation and Central Interpretation of Standard MRI
NCT00433381 (8) [back to overview]Change in Perfusion MRI Markers at Week 16 as Predictors of 12mo Overall Survival (OS)
NCT00433381 (8) [back to overview]Accuracy of Local PFS 6-mo Interpretation Using Central Review PFS-6 as the Reference Standard
NCT00433381 (8) [back to overview]Count/Percentage of Patients Discontinuing Treatment Due to Treatment-related Medical Complications(Bevacizumab and Temozolomide Arm)
NCT00433381 (8) [back to overview]Count/Percentage of Patients Progression-free at 6 Months for Bevacizumab and Irinotecan Hydrochloride Arm
NCT00433381 (8) [back to overview]Count/Percentage of Patients Progression-free at 6 Months for Bevacizumab and Temozolomide Arm
NCT00433381 (8) [back to overview]Change in Perfusion MRI Markers at Week 2 as Predictors of 12mo Overall Survival (OS)
NCT00436436 (1) [back to overview]Toxicity as Assessed by the Common Terminology Criteria in Adverse Events (CTCAE v 3)
NCT00441142 (5) [back to overview]PHASE I: Percentage of Grade 3-5 Treatment-Related Adverse Events
NCT00441142 (5) [back to overview]Number of Participants That Experienced a Dose-limiting Toxicity (DLT)
NCT00441142 (5) [back to overview]Median Progression-free Survival (PFS), as Calculated by the # of Months Patients Remain Progression-free
NCT00441142 (5) [back to overview]Median Overall Survival (OS) of Phase II Patients
NCT00441142 (5) [back to overview]PHASE II: Percentage of Grade 3-5 Treatment-Related Adverse Events
NCT00482677 (3) [back to overview]Methylation Status of the O6-methylguanine-DNA Methyltransferase Promoter
NCT00482677 (3) [back to overview]Overall Survival
NCT00482677 (3) [back to overview]Progression-free Survival
NCT00486603 (10) [back to overview](Phase II) Overall Survival
NCT00486603 (10) [back to overview](Phase II) Number of Participants With Grade 3 and 4 Toxicity
NCT00486603 (10) [back to overview](Phase I) Number of Participants Who Experienced Dose Limiting Toxicity (DLT)
NCT00486603 (10) [back to overview]Pharmocodynamics as Determined by Number of Participants With Autophagy Inhibition in Relation to Maximal Concentration (Cmax) of HCQ
NCT00486603 (10) [back to overview]PK of Hydroxychloroquine as Measured by Oral Clearance (Liters/Hour) From Central Compartment (CL/F)
NCT00486603 (10) [back to overview]PK of Hydroxychloroquine as Measured by Volume of Distribution of Central Compartment (V/F)
NCT00486603 (10) [back to overview](Phase I) Maximum Tolerated Dose (MTD) of Hydroxychloroquine (HCQ)
NCT00486603 (10) [back to overview]PK of Hydroxychloroquine as Measured by First-order Absorption Rate Constant (Ka)
NCT00486603 (10) [back to overview]PK of Hydroxychloroquine as Measured by Distribution Volume of Peripheral Compartment (V2/F)
NCT00486603 (10) [back to overview]Pharmacokinetics (PK) of Hydroxychloroquine as Measured by Lag Time (Tlag)
NCT00498927 (2) [back to overview]Progression-free Survival (PFS) Rate at 6 Months
NCT00498927 (2) [back to overview]Overall Survival
NCT00501891 (4) [back to overview]Incidence and Severity of CNS Hemorrhage and Systemic Hemorrhage
NCT00501891 (4) [back to overview]Incidence of Grade ≥ 4 Hematologic or Grade ≥ 3 Non-hematologic Toxicity
NCT00501891 (4) [back to overview]6-Month Progression-free Survival
NCT00501891 (4) [back to overview]Response Rate
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
NCT00505635 (1) [back to overview]Time to Progression (TTP)
NCT00512798 (5) [back to overview]Optimal Doses of Temozolomide and Bortezomib (Phase I)
NCT00512798 (5) [back to overview]Patients With Clinical Anti-tumor Activity (Phase I)
NCT00512798 (5) [back to overview]Patients With Inhibition of NF-kB (Phase II)
NCT00512798 (5) [back to overview]Patients With Inhibition in NF-kB Activation (Phase I)
NCT00512798 (5) [back to overview]Number of Patients With Clinical Anti-tumor Activity Phase II)
NCT00521001 (4) [back to overview]9-week Progression-free Survival Rate
NCT00521001 (4) [back to overview]Confirmed Response Rate (Complete Response and Partial Response)
NCT00521001 (4) [back to overview]Survival Time
NCT00521001 (4) [back to overview]Time to Disease Progression
NCT00525525 (3) [back to overview]Unexpected Toxicities During First 2 Cycles of Study Drug
NCT00525525 (3) [back to overview]Progression-free Survival
NCT00525525 (3) [back to overview]Overall Survival (OS)
NCT00539591 (23) [back to overview]Mean Total PedsQL 3.0 Scores for Child Cancer Quality of Life (QoL) Assessments (Stratum B)
NCT00539591 (23) [back to overview]Mean Total PedsQL 3.0 Scores for Parent Cancer Quality of Life (QoL) Assessments (Stratum A)
NCT00539591 (23) [back to overview]Mean Total PedsQL 3.0 Scores for Parent Cancer Quality of Life (QoL) Assessments (Stratum B)
NCT00539591 (23) [back to overview]Apparent Clearance (CL) of Pegylated Interferon ɑ-2B
NCT00539591 (23) [back to overview]Mean Total PedsQL 4.0 Scores for Child Quality of Life (QoL) Assessments (Stratum A)
NCT00539591 (23) [back to overview]Mean Total PedsQL 4.0 Scores for Child Quality of Life (QoL) Assessments (Stratum B)
NCT00539591 (23) [back to overview]Volume of Central Compartment (Vc) of Interferon ɑ-2b
NCT00539591 (23) [back to overview]Tumor Response Rate
NCT00539591 (23) [back to overview]Mean Total PedsQL 4.0 Scores for Parent Quality of Life Assessments (Stratum A)
NCT00539591 (23) [back to overview]Mean Total PedsQL 4.0 Scores for Parent Quality of Life Assessments (Stratum B)
NCT00539591 (23) [back to overview]Median Steady State Trough Concentration of Pegylated Interferon ɑ-2B
NCT00539591 (23) [back to overview]Number of Patients Who Experience Toxicity at or Above the Target Toxicity for Stratum A Patients
NCT00539591 (23) [back to overview]Half-Life of Interferon ɑ-2b
NCT00539591 (23) [back to overview]Volume of Central Compartment (Vc) of Pegylated Interferon ɑ-2B
NCT00539591 (23) [back to overview]Systemic Clearance (CL) of Interferon ɑ-2B
NCT00539591 (23) [back to overview]Probability of Event-free Survival (EFS) of Stratum A Participants
NCT00539591 (23) [back to overview]Number of Patients Who Experience Toxicity at or Above the Target Toxicity for Strata B1 and B2
NCT00539591 (23) [back to overview]Mean Total PedsQL 3.0 Scores for Child Cancer Quality of Life (QoL) Assessments (Stratum A)
NCT00539591 (23) [back to overview]BRIEF Psychological Assessment (Stratum A)
NCT00539591 (23) [back to overview]BASC-2 Psychological Assessment (Stratum A)
NCT00539591 (23) [back to overview]ɑ Half Life of Pegylated Interferon ɑ-2B
NCT00539591 (23) [back to overview]Area Under the Curve (AUC) of Pegylated Interferon ɑ-2B
NCT00539591 (23) [back to overview]Area Under the Curve (AUC) of Interferon ɑ-2b
NCT00544817 (3) [back to overview]Progression-free Survival
NCT00544817 (3) [back to overview]Objective Response
NCT00544817 (3) [back to overview]Overall Survival
NCT00553150 (6) [back to overview]Overall Survival Time
NCT00553150 (6) [back to overview]Overall Survival at 12 Months (Phase II)
NCT00553150 (6) [back to overview]Maximum Tolerated Dose (MTD) of Everolimus (RAD001) in Combination With Temozolomide (TMZ) and 3D-conformal Radiotherapy (RT) or Intensity-modulated Radiotherapy (IMRT) Followed by Adjuvant TMZ With or Without RAD001 (Phase I)
NCT00553150 (6) [back to overview]Time to Progression (Phase II)
NCT00553150 (6) [back to overview]Response Rate, as Measured in Patients Receiving FLT-PET Imaging (Phase II)
NCT00553150 (6) [back to overview]Progression-free-survival at 6 Months (Phase II)
NCT00568451 (3) [back to overview]Time to Disease Progression
NCT00568451 (3) [back to overview]Survival Time
NCT00568451 (3) [back to overview]Number of Participants With an Objective Tumor Status of Either a Complete Response(CR) or Partial Response (PR), According to RECIST (Response Evaluation Criteria in Solid Tumors) Criteria
NCT00575887 (1) [back to overview]Progression-free Survival at 6-months
NCT00576680 (3) [back to overview]To Determine the Safety and Tolerability of This Drug Combination.
NCT00576680 (3) [back to overview]Progression-free Survival
NCT00576680 (3) [back to overview]Response Rate
NCT00582075 (2) [back to overview]Percentage of Participants With Distant Brain Failure (DBF) at One Year
NCT00582075 (2) [back to overview]Overall Survival
NCT00588341 (1) [back to overview]Overall Objective Response (Complete Response or Partial Response)
NCT00588523 (2) [back to overview]Progession Free Survival
NCT00588523 (2) [back to overview]Number of Participants Evaluated for Toxicities
NCT00590681 (5) [back to overview]Objective Response
NCT00590681 (5) [back to overview]Overall Survival
NCT00590681 (5) [back to overview]Safety of Avastin in Combination With Temozolomide in This Study Population
NCT00590681 (5) [back to overview]Duration of Response
NCT00590681 (5) [back to overview]Progression-free Survival (PFS)
NCT00591370 (3) [back to overview]Duration of Objective Clinical Responses
NCT00591370 (3) [back to overview]Overall Survival
NCT00591370 (3) [back to overview]Determine the Overall Objective Response Rate (CR and PR).
NCT00597402 (4) [back to overview]Number of Patients Experiencing a Central Nervous System (CNS) Hemorrhage or a Systemic Hemorrhage
NCT00597402 (4) [back to overview]12-month Progression-free Survival (PFS)
NCT00597402 (4) [back to overview]16-month Overall Survival (OS)
NCT00597402 (4) [back to overview]Number of Patients Experiencing a Grade ≥ 4 Hematologic or Grade ≥ 3 Non-hematologic Toxicity
NCT00597493 (5) [back to overview]Safety and Toxicity of Combination
NCT00597493 (5) [back to overview]Pharmacokinetics: T-max
NCT00597493 (5) [back to overview]Pharmacokinetics: C-max
NCT00597493 (5) [back to overview]Pharmacokinetics: AUC-24
NCT00597493 (5) [back to overview]6 Month Progression Free Survival (PFS)
NCT00602576 (3) [back to overview]Overall Survival Rate
NCT00602576 (3) [back to overview]Rate of 6 Month Progression-Free Survival
NCT00602576 (3) [back to overview]Response Rate
NCT00611247 (3) [back to overview]Toxicity Profile: Total Number of Drug-related Serious Adverse Events
NCT00611247 (3) [back to overview]Toxicity Profile: Individual Subjects With Drug-related SAEs
NCT00611247 (3) [back to overview]Response Rate (CR + CRi + LFS)
NCT00612339 (1) [back to overview]Response Rate
NCT00613028 (5) [back to overview]Radiographic Response
NCT00613028 (5) [back to overview]Median Progression-free Survival (PFS)
NCT00613028 (5) [back to overview]Median Overall Survival (OS)
NCT00613028 (5) [back to overview]Grade 3 or Greater, Treatment Related, Non-hematologic Toxicities.
NCT00613028 (5) [back to overview]The Primary Outcome Measure is 6 Month Progression-free Survival.
NCT00617539 (5) [back to overview]Overall Time of Survival
NCT00617539 (5) [back to overview]Number of Patients Whose Circulating Tumor Cells (CTCs) Decreased From >5 to <5 CTCs Per 7.5 mL
NCT00617539 (5) [back to overview]Number of Patients With Objective Treatment Response (Complete or Partial) in the CNS
NCT00617539 (5) [back to overview]Time to First Progression in CNS
NCT00617539 (5) [back to overview]Number of Patients Experiencing a Clinical Benefit
NCT00619112 (7) [back to overview]Progression-free Survival (PFS) Based on Tumor MGMT (O(6)-Methylguanine-DNA Methyltransferase) Promoter Methylation Status.
NCT00619112 (7) [back to overview]Patients With Tumors With Functional Alterations of the Mismatch Repair (MMR) System
NCT00619112 (7) [back to overview]6 Month Progression-free Survival
NCT00619112 (7) [back to overview]Patients Progressing 6 Months After Temozolomide is Voluntarily Discontinued
NCT00619112 (7) [back to overview]Overall Survival
NCT00619112 (7) [back to overview]Patients Progressing After Two First-line Adjuvant Courses of Temozolomide
NCT00619112 (7) [back to overview]Patients Progressing Within 6 Months After 6th Adjuvant Course of Temozolomide
NCT00626405 (3) [back to overview]Tumor Response Rate, Calculated as a Percentage Along With it's 95% Confidence Interval
NCT00626405 (3) [back to overview]Progression-free Survival at 6 Months
NCT00626405 (3) [back to overview]Overall Survival
NCT00626990 (2) [back to overview]Progression-free Survival
NCT00626990 (2) [back to overview]Overall Survival as Measured From the Day of Randomization
NCT00632203 (5) [back to overview]Tolerability of Maintenance Temozolomide
NCT00632203 (5) [back to overview]Time to Radiological Central Nervous System (CNS) Progression
NCT00632203 (5) [back to overview]Overall Survival
NCT00632203 (5) [back to overview]Number of Participants Who Had Brain Metastases
NCT00632203 (5) [back to overview]Time to Progression
NCT00638963 (5) [back to overview]Number of Days on Temozolomide Treatment
NCT00638963 (5) [back to overview]Number of Participants Who Had at Least One Treatment Omission During Treatment
NCT00638963 (5) [back to overview]Total Dose of Temozolomide Taken
NCT00638963 (5) [back to overview]Number of Participants Who Completed the Third Cycle of Treatment
NCT00638963 (5) [back to overview]Number of Participants Who Had at Least One Dose Reduction During Treatment
NCT00643097 (4) [back to overview]Humoral and Cellular Immune Response
NCT00643097 (4) [back to overview]Clinical Efficacy of Vaccination, in Terms of Progression-free Survival (PFS)
NCT00643097 (4) [back to overview]Response to Vaccination
NCT00643097 (4) [back to overview]Toxicity to PEP-3 Vaccine Immunization
NCT00657267 (4) [back to overview]Radiographic Response
NCT00657267 (4) [back to overview]6 Month Progression Free Survival
NCT00657267 (4) [back to overview]Time to Progression.
NCT00657267 (4) [back to overview]Overall Survival
NCT00667953 (2) [back to overview]Response
NCT00667953 (2) [back to overview]Safety - Grade 3 or 4 Adverse Events
NCT00669669 (10) [back to overview]Response Rate
NCT00669669 (10) [back to overview]Time to Progression
NCT00669669 (10) [back to overview]Duration of Response
NCT00669669 (10) [back to overview]Gene Transfer Efficiency After Chemotherapy
NCT00669669 (10) [back to overview]Gene Transfer Efficiency
NCT00669669 (10) [back to overview]Number of Participants Dose-limiting Toxicity (DLT)
NCT00669669 (10) [back to overview]Number of Participants That Survived
NCT00669669 (10) [back to overview]Number of Participants With Chemoprotection
NCT00669669 (10) [back to overview]Number of Participants With Chemoselection
NCT00669669 (10) [back to overview]Number of Participants With Retrovirus or Leukemia
NCT00684567 (5) [back to overview]Adverse Events With an Incidence of Greater Than or Equal to 20%
NCT00684567 (5) [back to overview]Number of Participants With Progression Free Survival (PFS) for 1 Year
NCT00684567 (5) [back to overview]Number of Participants With a Response (Complete Response [CR] + Partial Response [PR]) in Terms of Overall Tumor Response
NCT00684567 (5) [back to overview]Abnormal Changes in Laboratory Test Values With an Incidence of Greater Than or Equal to 20%
NCT00684567 (5) [back to overview]Adverse Drug Reactions With an Incidence of Greater Than or Equal to 20%
NCT00686725 (9) [back to overview]Relationship Between MGMT Status and Therapy Response: Overall Survival Rate for the MGMT Positive Group
NCT00686725 (9) [back to overview]Relationship Between MGMT Status and Therapy Response: Overall Survival Rate for the MGMT Negative Group
NCT00686725 (9) [back to overview]Relationship Between O6-methylguanine-DNA Methyltransferase (MGMT) Status and Therapy Response: Overall Survival for the MGMT Positive Group
NCT00686725 (9) [back to overview]Relationship Between MGMT Status and Therapy Response: PFS for the MGMT Positive Group
NCT00686725 (9) [back to overview]Relationship Between MGMT Status and Therapy Response: PFS for the MGMT Negative Group
NCT00686725 (9) [back to overview]Objective Tumor Assessment After Surgery: Overall Response
NCT00686725 (9) [back to overview]Relationship Between MGMT Status and Therapy Response: Overall Survival for the MGMT Negative Group
NCT00686725 (9) [back to overview]Progression-Free Survival (PFS)
NCT00686725 (9) [back to overview]Overall Survival (OS)
NCT00687323 (7) [back to overview]Number of Participants With CR, PR, or MLFS Who Received Modified Low Dose Maintenance Therapy (100 mg/m^2/Day x21 Days of Each 28 Day Cycle) and Experienced Toxicity
NCT00687323 (7) [back to overview]Number of Previously Untreated Participants With Low O6-Methylguanine Methyltransferase (MGMT) Expression
NCT00687323 (7) [back to overview]Clinical Response at the End of Temozolomide Induction
NCT00687323 (7) [back to overview]Progression-free Survival for Participants Achieving PR, MLSF, or MR
NCT00687323 (7) [back to overview]Overall Survival (OS) in Participants Achieving CR or CRp and Proceeding to Reduced Dose-intensity Maintenance Therapy With Temozolomide
NCT00687323 (7) [back to overview]Duration of Response in Participants Achieving Complete Response (CR) and Proceeding to Reduced Dose-intensity Maintenance Therapy With Temozolomide
NCT00687323 (7) [back to overview]Relapse-free Survival in Participants Achieving CR or CRp and Proceeding to Reduced Dose-intensity Maintenance Therapy With Temozolomide
NCT00689221 (11) [back to overview]European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Brain Module (EORTC QLQ-BN20) Sub-scale Scores
NCT00689221 (11) [back to overview]European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ-C30) Sub-scale Scores
NCT00689221 (11) [back to overview]Number of Participants With Adverse Events (AEs), Serious AEs, Treatment-Related AEs, Treatment-Related Serious AEs, AEs Leading to Death, Treatment Related AEs Leading to Death, AEs of Grade 3 or 4 and Treatment Related AEs of Grade 3 or 4
NCT00689221 (11) [back to overview]Number of Participants With AEs Belonging to Standardized Medical Dictionary for Regulatory Activities (MedDRA) Queries (SMQs) Thromboembolic Events and Hemorrhage With NCI-CTC Toxicity Grade 3 or 4
NCT00689221 (11) [back to overview]Number of Participants With Change From Baseline in Work Status at End of Study
NCT00689221 (11) [back to overview]Progression Free Survival (PFS) Time - Investigator and Independent Read
NCT00689221 (11) [back to overview]Maximum Observed Plasma Concentration (Cmax)
NCT00689221 (11) [back to overview]EuroQol 5-Dimensions (EQ-5D) Questionnaire Index
NCT00689221 (11) [back to overview]Overall Survival (OS) Time
NCT00689221 (11) [back to overview]Area Under the Plasma Concentration Curve From Time 0 to 6 Hours (AUC [0-6]) After Dose
NCT00689221 (11) [back to overview]Time to Maximum Plasma Concentration (Tmax)
NCT00704808 (1) [back to overview]Median Progression Free Survival After Primary Surgical Treatment, Concomitant and Adjuvant Chemotherapy With Temozolomide, for Patients With Newly Diagnosed Glioblastoma Multiforme
NCT00715793 (8) [back to overview]Disease Control Rate (DCR)
NCT00715793 (8) [back to overview]Percentage of Participants That Experienced a Dose Limiting Toxicity (DLT)
NCT00715793 (8) [back to overview]Recommended Phase 2 Dose (RP2D) of DAC + TMZ
NCT00715793 (8) [back to overview]Progression-free Survival (PFS)
NCT00715793 (8) [back to overview]Overall Response Rate (ORR)
NCT00715793 (8) [back to overview]Overall Survival (OS)
NCT00715793 (8) [back to overview]1-year Overall Survival (OS) Rate
NCT00715793 (8) [back to overview]6-month Progression-free Survival (PFS) Rate
NCT00723827 (5) [back to overview]Number of Participants Experiencing Unexpected Adverse Drug Reactions (ADRs)
NCT00723827 (5) [back to overview]Number of Temozolomide Drug Interactions
NCT00723827 (5) [back to overview]Number of Temozolomide Misuse or Abuse Events
NCT00723827 (5) [back to overview]Efficacy: Number of Participants Experiencing Complete Response (CR), Partial Response (PR), or Stable Disease(SD)
NCT00723827 (5) [back to overview]Number of Participants Experiencing Adverse Events (AEs)
NCT00725010 (2) [back to overview]Number of Participants Who Discontinued Due to Toxicity
NCT00725010 (2) [back to overview]Safety: Number of Adverse Events in the Indicated Categories
NCT00731731 (5) [back to overview]Incidence of Adverse Events, Based on CTC (Common Toxicity Criteria) Severity Grade
NCT00731731 (5) [back to overview]Overall Survival at 15 Months (Phase II)
NCT00731731 (5) [back to overview]Time to Tumor Progression (Phase II)
NCT00731731 (5) [back to overview]Maximum Tolerated Dose of Vorinostat, Defined as the Dose at Which Fewer Than One-third of Patients Experience DLTs, Graded According to NCI CTCAE (Common Toxicity Criteria for Adverse Effects) Version 3.0 (Phase I)
NCT00731731 (5) [back to overview]Incidence of Adverse Events, as Per NCI CTCAE Version 3.0 (Phase II)
NCT00740636 (1) [back to overview]The Objective Overall Response
NCT00756106 (4) [back to overview]Permeability-surface Area Product Before, During, and After Chemoradiotherapy
NCT00756106 (4) [back to overview]Relative Cerebral Blood Volume as Measured by Perfusion-weighted MRI Before, During, and After Chemoradiotherapy
NCT00756106 (4) [back to overview]Relative Cerebral Blood Flow as Measured by Perfusion-weighted MRI Before, During, and After Chemoradiotherapy
NCT00756106 (4) [back to overview]Apparent Diffusion Coefficient Before, During, and After Chemoradiotherapy
NCT00761280 (12) [back to overview]Disease Progression at 10, 12, 14, 16, 18, 21, and 24 Months by Independent Review in the Intent-to-treat Population - Number of Participants
NCT00761280 (12) [back to overview]Survival Rate at 12, 18, and 21 Months in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)
NCT00761280 (12) [back to overview]Survival Rate at 24 Months in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)
NCT00761280 (12) [back to overview]Survival at 24 Months in the Intent-to-treat Population - Number of Participants
NCT00761280 (12) [back to overview]Tumor Control Rate (CR+PR+SD) by Independent Review in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)
NCT00761280 (12) [back to overview]Survival at 12, 18, and 21 Months in the Intent-to-treat Population - Number of Participants
NCT00761280 (12) [back to overview]Median Duration of Response (Days) by Independent Review (Descriptive Analysis, Only)
NCT00761280 (12) [back to overview]Median Overall Survival (Days) From Randomization in the Intent-to-treat Population (Descriptive Analysis, Only)
NCT00761280 (12) [back to overview]Median Time to Progression (Days) by Independent Review for the Intent-to-treat Population (Descriptive Analysis, Only)
NCT00761280 (12) [back to overview]Response Category by Independent Review in the Intent-to-treat Population - Number of Participants
NCT00761280 (12) [back to overview]Overall Response Rate (CR+PR) by Independent Review in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)
NCT00761280 (12) [back to overview]Disease Progression Rate at 10, 12, 14, 16, 18, 21, and 24 Months by Independent Review in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)
NCT00782756 (2) [back to overview]Progression Free Survival
NCT00782756 (2) [back to overview]Number of Participants With Adverse Events
NCT00804908 (8) [back to overview]12-Month Overall Survival (OS) Rate
NCT00804908 (8) [back to overview]Disease Control Rate
NCT00804908 (8) [back to overview]Objective Response Rate
NCT00804908 (8) [back to overview]Overall Survival (OS): Time to Event
NCT00804908 (8) [back to overview]Progression-Free Survival (PFS): Time to Event
NCT00804908 (8) [back to overview]Time to Disease Progression
NCT00804908 (8) [back to overview]Time to Neurological/Brain Metastases Progression
NCT00804908 (8) [back to overview]6-month Progression-Free Survival Rate
NCT00805961 (4) [back to overview]Number of Participants Experiencing Toxicity After This Novel Multimodality Regimen
NCT00805961 (4) [back to overview]Objective Response Rate of Patients With Glioblastoma Multiforme Following Treatment With This Novel Multimodality Regimen
NCT00805961 (4) [back to overview]Overall Survival of Patients With Glioblastoma Multiforme Following Treatment With This Novel Multimodality Regimen
NCT00805961 (4) [back to overview]Progression-free Survival (PFS)
NCT00813943 (12) [back to overview]Overall Survival (OS) Time
NCT00813943 (12) [back to overview]Number of Participants With AEs Belonging to Standardized Medical Dictionary for Regulatory Activities (MedDRA) Queries (SMQs) Thromboembolic Events and Hemorrhage With NCI-CTC Toxicity Grade 3 or 4
NCT00813943 (12) [back to overview]Apparent Terminal Rate Constant
NCT00813943 (12) [back to overview]Apparent Volume of Distribution During the Terminal Phase (Vz) and Apparent Volume of Distribution at Steady State (Vss)
NCT00813943 (12) [back to overview]Area Under the Plasma Concentration-Time Curve From Time 0 to Infinity (AUC [0-infinity]) and Area Under the Plasma Concentration-Time Curve From Time 0 to 24 Hours (AUC [0-24])
NCT00813943 (12) [back to overview]Plasma Clearance (CL)
NCT00813943 (12) [back to overview]Maximum Observed Plasma Concentration (Cmax)
NCT00813943 (12) [back to overview]Progression Free Survival (PFS) Time - Investigator and Independent Read
NCT00813943 (12) [back to overview]Time to Maximum Plasma Concentration (Tmax) and Terminal Elimination Half-Life (t1/2)
NCT00813943 (12) [back to overview]Number of Participants With Adverse Events (AEs), Serious AEs, Treatment-Related AEs, Treatment-Related Serious AEs, AEs Leading to Death, Treatment-Related AEs Leading to Death, AEs of Grade 3 or 4 and Treatment-Related AEs of Grade 3 or 4
NCT00813943 (12) [back to overview]Mean Residence Time From Time 0 to Infinity (MRT [0-infinity])
NCT00813943 (12) [back to overview]Plasma Concentration at Pre-dose (Cpre) and Plasma Concentration at End of Infusion (CT)
NCT00826241 (3) [back to overview]Number of Participants With an Overall Response (Complete Response or Partial Response) Assessed by the MacDonald Criteria
NCT00826241 (3) [back to overview]Time to Progression
NCT00826241 (3) [back to overview]Number of Participants With Serious and Non-Serious Adverse Events Assessed by the Common Terminology Criteria in Adverse Events (CTCAE v4.0)
NCT00841555 (3) [back to overview]Time Spent in a Karnofsky Performance Status of 60-100%
NCT00841555 (3) [back to overview]Survival Time
NCT00841555 (3) [back to overview]Maximum Tolerated Dose(MTD)of Temozolomide(TMZ)
NCT00846430 (4) [back to overview]Response by MRI Measurements
NCT00846430 (4) [back to overview]No Reported Psychological Toxicity Based Upon Psychological Evaluations
NCT00846430 (4) [back to overview]Improvement of Symptoms and Pain
NCT00846430 (4) [back to overview]At Least 50% Shrinkage in Tumor Measurements by Physical Examination
NCT00869050 (2) [back to overview]Number of Participants With Complete Response (CR)
NCT00869050 (2) [back to overview]Number of Participants With Partial Response (PR)
NCT00869401 (4) [back to overview]Overall Survival
NCT00869401 (4) [back to overview]Objective Response
NCT00869401 (4) [back to overview]Progression-free Survival
NCT00869401 (4) [back to overview]The Number of Dose Limiting Toxicities(DLT) in Order to Determine Maximum Tolerable Dose(MTD) of Dasatinib Combined With Radiation and Temozolomide in This Patient Population.
NCT00876993 (3) [back to overview]Measurement of Number of Adverse Events
NCT00876993 (3) [back to overview]To Provide Safety and Efficacy Data for to Recommend Further Larger Studies.
NCT00876993 (3) [back to overview]2 Year Event Free Survival With Children Treated With This Regimen.
NCT00884741 (3) [back to overview]Progression-free Survival (PFS)
NCT00884741 (3) [back to overview]Overall Survival (OS)
NCT00884741 (3) [back to overview]Incidence of Grade 3 and Higher Treatment-related Toxicity as Assessed by the National Cancer Institute Common Terminology Criteria for Adverse Events (AEs) Version 3.0
NCT00885534 (1) [back to overview]Overall Response to CVT Chemotherapy.
NCT00905060 (4) [back to overview]Median Overall Survival
NCT00905060 (4) [back to overview]Median PD-L1 Positivity in Circulating Myeloid Cells
NCT00905060 (4) [back to overview]Median Progression Free Survival (PFS)
NCT00905060 (4) [back to overview]Number of Participants With Treatment-Related Adverse Events of Any Grade
NCT00925132 (2) [back to overview]Phase 2 -Number of Patients With a Decrease in Tumor Size Using RECIST and CHOI's Criteria
NCT00925132 (2) [back to overview]Phase I - Number of Participants With Dose Limiting Toxicities (DLTs) at a Given Dose Level
NCT00939991 (6) [back to overview]Phase II: Median Overall Survival (OS)
NCT00939991 (6) [back to overview]Phase II: Median Progression-free Survival (PFS)
NCT00939991 (6) [back to overview]Phase II: Radiographic Response.
NCT00939991 (6) [back to overview]Phase II: Number of Patients With Grade 2 or Greater, Treatment-related Toxicities
NCT00939991 (6) [back to overview]Phase I: Determination of the Maximum Tolerated Dose (MTD)
NCT00939991 (6) [back to overview]Phase II: 6-month Progression-free Survival (PFS)
NCT00943826 (7) [back to overview]Co-Primary: Overall Survival (OS)
NCT00943826 (7) [back to overview]Co-Primary: Progression-free Survival (PFS) as Assessed by Investigator
NCT00943826 (7) [back to overview]Kaplan-Meier (KM) Estimate of One Year Overall Survival
NCT00943826 (7) [back to overview]Kaplan-Meier (KM) Estimate of Two Year Overall Survival
NCT00943826 (7) [back to overview]PFS as Assessed by an Independent Review Facility
NCT00943826 (7) [back to overview]PFS in Participants With Stable/Improved Health Related Quality of Life (HRQoL) Based on European Organization for Research & Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) Core 30 (C30)(EORTC QLQ-C30) & EORTC QLQ Brain Neoplasm 20 (BN20)
NCT00943826 (7) [back to overview]Number of Participants With Non-Serious Adverse Events, Serious Adverse Events and Death
NCT00960063 (3) [back to overview]Best Overall Response Based on Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00960063 (3) [back to overview]Number of Participants Who Developed Anti-robatumumab Antibodies
NCT00960063 (3) [back to overview]Number of Participants With Dose Limiting Toxicities
NCT00967330 (12) [back to overview]Percentage of Participants Who Discontinued
NCT00967330 (12) [back to overview]Overall Survival (OS)
NCT00967330 (12) [back to overview]Change From Baseline for Mini-Mental Status Examination (MMSE) at Baseline, Post-Baseline (up to Month 30)
NCT00967330 (12) [back to overview]Percentage of Participants Achieving Progression-Free Survival (PFS) Without Disease Progression or Death at 6 Months
NCT00967330 (12) [back to overview]Percentage of Participants Who Received Corticosteroid for Glioblastoma
NCT00967330 (12) [back to overview]Number of Participants With A Best Overall Response (BOR) of Complete Response (CR) and With A BOR of CR or Partial Response (PR)
NCT00967330 (12) [back to overview]Change From Baseline in European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ - C30) at Baseline, Post-Baseline (up to Month 30)
NCT00967330 (12) [back to overview]Progression-Free Survival (PFS)
NCT00967330 (12) [back to overview]Percentage of Participants With Response on FLAIR Imaging
NCT00967330 (12) [back to overview]Time to Treatment Failure
NCT00967330 (12) [back to overview]Change From Baseline for EORTC QLQ Brain Neoplasm 20 (BN20) at Baseline, Post-Baseline (up to Month 30)
NCT00967330 (12) [back to overview]Change From Baseline for Karnofsky Performance Status (KPS) Score at Baseline, Post-Baseline (up to Month 30)
NCT00977431 (5) [back to overview]Concentration of Afatinib in Plasma at Steady State Pre-dose on Days 8, 15 and 29
NCT00977431 (5) [back to overview]Number of Patients With Investigator Defined Dose Limiting Toxicities (DLT) During the RT Phase
NCT00977431 (5) [back to overview]The Objective Tumour Response According to the Macdonald Criteria
NCT00977431 (5) [back to overview]Maximum Tolerated Dose (MTD) of Afatinib
NCT00977431 (5) [back to overview]Incidence and Intensity of Adverse Events (AE) According to Common Terminology Criteria of Adverse Events (CTCAE v.3.0)
NCT00979017 (5) [back to overview]Response Rate
NCT00979017 (5) [back to overview]Incidence and Severity of Central Nervous System (CNS) Hemorrhage and Systemic Hemorrhage
NCT00979017 (5) [back to overview]Median Overall Survival (OS)
NCT00979017 (5) [back to overview]Median Progression-free Survival (PFS)
NCT00979017 (5) [back to overview]Incidence of Grade ≥ 4 Hematologic and ≥ Grade 3 Non-hematologic Toxicities
NCT00990652 (5) [back to overview]Number of Patients Surviving Without Disease Progression After 6 Months
NCT00990652 (5) [back to overview]Number of Participants Achieving a Response to Treatment (Either Complete or Partial Response) as Defined by MacDonald Criteria
NCT00990652 (5) [back to overview]Number of Grade 1, 2, 3, 4, and 5 Adverse Events Observed During Study Treatment (Defined by CTCAE v 3.0)
NCT00990652 (5) [back to overview]Overall Survival Rate at 6 Months
NCT00990652 (5) [back to overview]Overall Survival (in Days)
NCT00993044 (1) [back to overview]Dose Limiting Toxicity
NCT00998010 (5) [back to overview]Overall Survival
NCT00998010 (5) [back to overview]Survival at 1 Year
NCT00998010 (5) [back to overview]Toxicity Assessed According to the NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.
NCT00998010 (5) [back to overview]Tumor Progression as Assessed by Magnetic Resonance Imaging (MRI) and Neurologic Exam
NCT00998010 (5) [back to overview]Time to Progression
NCT01004874 (6) [back to overview]One and Two Year Overall Survival
NCT01004874 (6) [back to overview]Median Overall Survival
NCT01004874 (6) [back to overview]6-month Progression-free Survival
NCT01004874 (6) [back to overview]Median Progression-free Survival
NCT01004874 (6) [back to overview]Number of Patients Experiencing a Greater Than or Equal to Grade 4 Hematologic or a Greater Than or Equal to Grade 3 Non-hematologic Toxicity
NCT01004874 (6) [back to overview]Number of Patients Experiencing a Central Nervous System (CNS) Hemorrhage or a Systemic Hemorrhage
NCT01009515 (4) [back to overview]Objective Response Rate (ORR)
NCT01009515 (4) [back to overview]Overall Survival
NCT01009515 (4) [back to overview]Time to Progression
NCT01009515 (4) [back to overview]Safety Profile
NCT01013285 (5) [back to overview]Median Overall Survival (OS) Based on the MGMT Promoter Methylation Status
NCT01013285 (5) [back to overview]Overall Survival
NCT01013285 (5) [back to overview]Radiographic Response (When Evaluable)
NCT01013285 (5) [back to overview]Time to Disease Progression
NCT01013285 (5) [back to overview]Progression-free Survival at 6 Months
NCT01015534 (4) [back to overview]Objective Response Rates. Assessed With Cranial MRI
NCT01015534 (4) [back to overview]Overall Survival
NCT01015534 (4) [back to overview]Survival Free of Brain Metastases Progression (PFS of BM)
NCT01015534 (4) [back to overview]Number of Grade 3-4 Adverse Events (AE) That Are Definitely or Probably Related to Both Groups of Treatment.
NCT01026493 (4) [back to overview]Phase 1: Maximum Tolerated Dose (MTD)
NCT01026493 (4) [back to overview]Phase II: 6-month Progression-free Survival (PFS) Rate for Patients With Measurable Disease After Surgery
NCT01026493 (4) [back to overview]Phase II: Objective Response (Partial and Complete Response) Rate for Patients With Measurable Disease After Surgery
NCT01026493 (4) [back to overview]Phase II: Overall Survival (OS)
NCT01044966 (5) [back to overview]Progression Free Survival
NCT01044966 (5) [back to overview]Proportion of Patients With Recurrent GBM Treated With ITV DepoCyt in Combination With Oral Temozolomide Who Are Progression-free at 16 Weeks.
NCT01044966 (5) [back to overview]Response Rate of Drug Treatment
NCT01044966 (5) [back to overview]Quality of Life Outcomes Measurement
NCT01044966 (5) [back to overview]Number of Participants With Treatment-related Adverse Events as Assessed by CTCAE v4.0
NCT01051596 (4) [back to overview]Percent of Patients With Disease Control
NCT01051596 (4) [back to overview]Percent of Patients With an Objective Response
NCT01051596 (4) [back to overview]Median Progression-free Survival Time
NCT01051596 (4) [back to overview]Overall Survival
NCT01055314 (5) [back to overview]Feasibility of the Addition of Cixutumumab to Chemotherapy Determined by Patient Enrollment
NCT01055314 (5) [back to overview]Event-Free Survival
NCT01055314 (5) [back to overview]Response Rate (CR + PR)
NCT01055314 (5) [back to overview]Incidence of Adverse Events Assessed by Common Terminology Criteria for Adverse Events Version 4.0
NCT01055314 (5) [back to overview]Feasibility of the Addition of Temozolomide to Chemotherapy Determined by Patient Enrollment
NCT01062399 (5) [back to overview]Phase II: Overall Survival (OS)
NCT01062399 (5) [back to overview]Phase I: Distribution of Worst Adverse Event Grade
NCT01062399 (5) [back to overview]Phase II: Distribution of Worst Adverse Event Grade
NCT01062399 (5) [back to overview]Phase I: Number of Patients With Dose-limiting Toxicity (DLT)
NCT01062399 (5) [back to overview]Phase II: Progression-free Survival (PFS)
NCT01062425 (4) [back to overview]6-month Progression-free Survival Rate
NCT01062425 (4) [back to overview]Overall Survival (OS)
NCT01062425 (4) [back to overview]Progression-free Survival (PFS)
NCT01062425 (4) [back to overview]Incidence of Grade 3+ Toxicities
NCT01105702 (3) [back to overview]Median Progression-Free Survival (PFS)
NCT01105702 (3) [back to overview]Median Overall Survival (OS)
NCT01105702 (3) [back to overview]Number of Patients With Grade 3 or 4 Adverse Events
NCT01110876 (1) [back to overview]Maximum Tolerated Dose (MTD) of Vorinostat in Combination With Escalating Doses of Erlotinib and Temozolomide
NCT01114555 (1) [back to overview]Number of Participants With Treatment Related Toxicity
NCT01115491 (6) [back to overview]Overall Survival - Percentage of Participants With an Event
NCT01115491 (6) [back to overview]Progression-Free Survival (PFS) - Percentage of Participants With an Event
NCT01115491 (6) [back to overview]PFS: Probability of Remaining Progression Free at 24 Weeks After Beginning the Study
NCT01115491 (6) [back to overview]PFS - Time to Event
NCT01115491 (6) [back to overview]Percentage of Participants Achieving an Overall Response of Complete Response (CR) or Partial Response (PR)
NCT01115491 (6) [back to overview]Overall Survival - Time to Event
NCT01119508 (1) [back to overview]6-Month Progression-Free Survival (PFS) Rate
NCT01120639 (10) [back to overview]Quality of Life by Brain-20 Survey
NCT01120639 (10) [back to overview]Quality of Life by European Organisation for Research and Treatment of Cancer (EORTC-QLQ C30) Survey
NCT01120639 (10) [back to overview]Quality of Life by MD Anderson Symptom Inventory - Brain Tumor (MDASI-BT) Survey
NCT01120639 (10) [back to overview]Overall Survival (OS)
NCT01120639 (10) [back to overview]Number of Acute Toxicity Within 30 Days
NCT01120639 (10) [back to overview]Long-term Toxicity After More Than 30 Days
NCT01120639 (10) [back to overview]Treatment Failure Analysis
NCT01120639 (10) [back to overview]Progression-free Survival
NCT01120639 (10) [back to overview]Number of Dose-limiting Toxicities (DLTs)
NCT01120639 (10) [back to overview]Percent of Participants With Radiographic Response
NCT01124734 (3) [back to overview]Duration of Response to High-Dose Interleukin-2 (H-D IL-2) Followed by Low Dose Temozolomide
NCT01124734 (3) [back to overview]Safety and Toxicity of H-D IL-2 Followed by Low Dose Temozolomide
NCT01124734 (3) [back to overview]Effect of High Dose IL2 Followed by Low Dose Temozolomide on Lymphocyte Subsets (Autoimmune Biomarkers)
NCT01143402 (2) [back to overview]Progression-free Survival (PFS) (Evaluable Randomized Patients)
NCT01143402 (2) [back to overview]Median Overall Survival (Evaluable Randomized Patients)
NCT01182350 (8) [back to overview]Grade 3-4 Post-Procedural Surgery-Related Toxicity Rate
NCT01182350 (8) [back to overview]9-month Overall Survival (OS) Rate
NCT01182350 (8) [back to overview]Feasibility Rate of Molecular Approach to Therapy
NCT01182350 (8) [back to overview]Rate of Lethal Complications From Surgery
NCT01182350 (8) [back to overview]Number of Participants With Grade 3-4 Treatment-Related Toxicity Over Chemoradiation Therapy
NCT01182350 (8) [back to overview]Median Progression Free Survival (PFS)
NCT01182350 (8) [back to overview]Delay in Radiation Therapy Start
NCT01182350 (8) [back to overview]9-month Overall Survival (OS) Rate by Molecular Cohort
NCT01186406 (4) [back to overview]Unacceptable Toxicity Related to the Treatment Regimen
NCT01186406 (4) [back to overview]Median Progression-free Survival
NCT01186406 (4) [back to overview]Median Overall Survival
NCT01186406 (4) [back to overview]21-month Overall Survival
NCT01196416 (9) [back to overview]Cycle 1 Mean Day 2 Trough/Pharmacokinetics of Gamma-secretase Inhibitor RO4929097 in Combination With Temozolomide (Phase IB)
NCT01196416 (9) [back to overview]Participants Evaluated for Toxicity
NCT01196416 (9) [back to overview]Progression-free Survival (Phase II)
NCT01196416 (9) [back to overview]Maximum Tolerated Dose for RO4929097
NCT01196416 (9) [back to overview]Number of Participants With Presence or Absence of Markers of Notch Signalling Pathway Inhibition in Patient Tumors (Phase Ib)
NCT01196416 (9) [back to overview]Overall Survival (Phase II)
NCT01196416 (9) [back to overview]Cycle 1 AUC/Pharmacokinetics of Gamma-secretase Inhibitor RO4929097 in Combination With Temozolomide (Phase IB)
NCT01196416 (9) [back to overview]Cycle 1 C Max/Pharmacokinetics of Gamma-secretase Inhibitor RO4929097 in Combination With Temozolomide (Phase IB)
NCT01196416 (9) [back to overview]Maximum-tolerated Dose for Cisplatin, Vinblastine and TMZ
NCT01205828 (4) [back to overview]Overall Survival
NCT01205828 (4) [back to overview]Clinical Benefit Rate
NCT01205828 (4) [back to overview]Progression Free Survival
NCT01205828 (4) [back to overview]Number of Participants Who Had Grade 3 or 4 Adverse Events
NCT01209442 (2) [back to overview]6-month Progression-free Survival
NCT01209442 (2) [back to overview]Overall Survival, Measured From the Day of Initial Diagnosis (Biopsy or Surgery) to the Time of Death From Any Cause.
NCT01217437 (3) [back to overview]Response
NCT01217437 (3) [back to overview]Event-free Survival
NCT01217437 (3) [back to overview]Overall Survival
NCT01235793 (2) [back to overview]One-year Progression-free Survival and Overall Survival
NCT01235793 (2) [back to overview]Safest Dose of Temozolomide for the DRBEAT Regimen
NCT01236560 (4) [back to overview]Event-free Survival
NCT01236560 (4) [back to overview]Cumulative Incidence of Disease Progression in Each Treatment Arm
NCT01236560 (4) [back to overview]Maximum Tolerated Dose (MTD) of Vorinostat
NCT01236560 (4) [back to overview]Overall Survival
NCT01284335 (8) [back to overview]Percentage of Participants With a Complete (CR) or Partial Response (PR) (Best Overall Tumor Response)
NCT01284335 (8) [back to overview]Percentage of Participants With a Complete (CR) or Partial Response (PR) (Best Overall Tumor Response)
NCT01284335 (8) [back to overview]Pharmacokinetic (PK): Concentration Maximum (Cmax)
NCT01284335 (8) [back to overview]Percentage of Participants With a Complete (CR) or Partial Response (PR) (Best Overall Tumor Response)
NCT01284335 (8) [back to overview]PK: Area Under the Curve Albumin (AUCalb)
NCT01284335 (8) [back to overview]Number of Participants With Dose-Limiting Toxicities Cycle 1
NCT01284335 (8) [back to overview]Number of Participants With a Clinically Significant Effects
NCT01284335 (8) [back to overview]Percentage of Participants With a Complete (CR) or Partial Response (PR) (Best Overall Tumor Response)
NCT01328535 (4) [back to overview]Toxicity, Assessed Using National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) Version 4.0 (v4)
NCT01328535 (4) [back to overview]Progression-Free Survival at 4 Months
NCT01328535 (4) [back to overview]Progression-Free Survival
NCT01328535 (4) [back to overview]Overall Survival
NCT01342757 (3) [back to overview]Measurable Change on Magnetic Resonance Spectroscopy Imaging After Vorinostat Administration
NCT01342757 (3) [back to overview]Proportion of Patients With Magnetic Resonance Spectroscopy (MRS) Response to Initial Vorinostat by MRI and MRS Scans as Determined by Spectroscopic Index
NCT01342757 (3) [back to overview]Mean Change in Metabolite Levels
NCT01390948 (16) [back to overview]Percentage of Participants With EFS as Determined by the CRRC at 1 Year
NCT01390948 (16) [back to overview]Health Status as Measured by the Health Utility Index (HUI)
NCT01390948 (16) [back to overview]Health Status as Measured by the Health Utility Index (HUI)
NCT01390948 (16) [back to overview]Number of Dose Administrations of TMZ and Bevacizumab in the Concurrent Phase
NCT01390948 (16) [back to overview]Percentage of Participants Who Completed >/= 90% of Planned Radiotherapy and TMZ Administrations
NCT01390948 (16) [back to overview]Percentage of Participants With a Treatment Delay or Discontinuation
NCT01390948 (16) [back to overview]Percentage of Participants With EFS as Determined by the CRRC at 6 Months
NCT01390948 (16) [back to overview]Concordance Between Structural Versus Multimodal Imaging for CRRC-Assessed Event-Free Survival
NCT01390948 (16) [back to overview]EFS as Assessed by the Investigator
NCT01390948 (16) [back to overview]Event-Free Survival (EFS) as Assessed by the Central Radiology Review Committee (CRRC)
NCT01390948 (16) [back to overview]Neurological Psychological Function as Measured by the Wechsler Scale
NCT01390948 (16) [back to overview]Number of Radiotherapy Dose Administrations in the Concurrent Phase
NCT01390948 (16) [back to overview]Objective Response Rate (ORR)
NCT01390948 (16) [back to overview]Overall Survival
NCT01390948 (16) [back to overview]Percentage of Participants With 1-Year Survival
NCT01390948 (16) [back to overview]Percentage of Participants With an Adverse Event (AE)
NCT01402063 (1) [back to overview]Progression Free Survival PPX/RT Versus TMZ/RT for Patients With GBM Without Methylation
NCT01465659 (7) [back to overview]Number of Patients Who Experience Toxicity Events Undergoing This Treatment.
NCT01465659 (7) [back to overview]Progression Free Survival (PFS)
NCT01465659 (7) [back to overview]Determine the Maximum Tolerated Dose (MTD) of Temozolomide in Combination With 400 mg Pazopanib in Patients With Advanced Pancreatic Neuroendocrine Tumor (PNET) in Phase I
NCT01465659 (7) [back to overview]Plasma Temozolomide Concentration in the Blood at Various Timepoints After Administration
NCT01465659 (7) [back to overview]Overall Survival (OS)
NCT01465659 (7) [back to overview]Overall Response Rate (ORR) in Patients With Advanced Neuroendocrine Tumors (PNET) Treated With Temozolomide and Pazopanib Combination Treatment at the RP2D in Phase II
NCT01465659 (7) [back to overview]Number of Patients Experiencing Response to Treatment or Stable Disease (Disease Control Rate)
NCT01466686 (4) [back to overview]Overall Survival Rate
NCT01466686 (4) [back to overview]Number of Patients With Neurologic Toxicity
NCT01466686 (4) [back to overview]Number of Patients With Hematologic Toxicities
NCT01466686 (4) [back to overview]Progression Free Survival Rate
NCT01478321 (6) [back to overview]Safety Profile for Patients With Recurrent High Grade Malignant Gliomas Treated With Concurrent Radiation, Temozolomide, and Bevacizumab Followed by Adjuvant Temozolomide and Bevacizumab
NCT01478321 (6) [back to overview]Overall Survival (OS) for Patients With Recurrent High Grade Malignant Gliomas Treated With Concurrent Radiation, Temozolomide, and Bevacizumab Followed by Adjuvant Temozolomide and Bevacizumab.
NCT01478321 (6) [back to overview]Median Progression Free Survival (PFS) for Patients With Recurrent High Grade Malignant Gliomas Treated With Concurrent Radiation, Temozolomide, and Bevacizumab Followed by Adjuvant Temozolomide and Bevacizumab
NCT01478321 (6) [back to overview]Percentage of Patients With Progression Free Survival (PFS) at 6 Months and 12 Months
NCT01478321 (6) [back to overview]Patient Reported Quality of Life (QOL)
NCT01478321 (6) [back to overview]Overall Survival (OS) at 6 Months and 12 Months for Patients With Recurrent High Grade Malignant Gliomas Treated With Concurrent Radiation, Temozolomide, and Bevacizumab Followed by Adjuvant Temozolomide and Bevacizumab.
NCT01505608 (3) [back to overview]Overall Response Rate (ORR) of Participants Using RECIST Criteria
NCT01505608 (3) [back to overview]Number of Participants With Adverse Events as a Measure of Safety and Tolerability
NCT01505608 (3) [back to overview]Progression Free Survival (PFS) of Participants Using Days Until Progression
NCT01506609 (5) [back to overview]Progression-Free Survival (PFS)
NCT01506609 (5) [back to overview]Clinical Benefit Rate (CBR) at Week 18
NCT01506609 (5) [back to overview]Overall Survival (OS)
NCT01506609 (5) [back to overview]Objective Response Rate (ORR)
NCT01506609 (5) [back to overview]Change From Baseline at Week 18 in European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Chemotherapy-Induced Peripheral Neuropathy Module (EORTC QLQ-CIPN20) Sensory Subscale Score
NCT01514201 (14) [back to overview]Overall Survival
NCT01514201 (14) [back to overview]Trough for Veliparib [Pharmacokinetic Parameter]
NCT01514201 (14) [back to overview]Levels of Urinary Biomarkers
NCT01514201 (14) [back to overview]Maximum Concentration of Veliparib (Cmax) on Days 1 and 4 (Measured in ng/mL) [Pharmacokinetic Parameter]
NCT01514201 (14) [back to overview]Percentage of Participants With Significant Changes in Poly(ADP-ribose) Polymerase (PARP) Levels Post-Veliparib, as Measured in Peripheral Blood Monocytes (PBMCs)
NCT01514201 (14) [back to overview]Percentage of Participants Observed to Have Unacceptable Toxicity During the Intra-patient Dose Escalation of Temozolomide During Maintenance Therapy (Feasibility Analysis Population)
NCT01514201 (14) [back to overview]Terminal Half-life (t1/2) for Veliparib [Pharmacokinetic Parameter]
NCT01514201 (14) [back to overview]Mean Apparent Clearance (CL/F) for Veliparib [Pharmacokinetic Parameter]
NCT01514201 (14) [back to overview]Progression-free Survival (PFS)
NCT01514201 (14) [back to overview]Percentage of Patients With Pseudo Progression
NCT01514201 (14) [back to overview]Apparent Volume of Distribution (Vd/F) for Veliparib [Pharmacokinetic Parameter]
NCT01514201 (14) [back to overview]Maximum Concentration of Veliparib (Cmax) on Day 1 (Measured in μM) [Pharmacokinetic Parameter]
NCT01514201 (14) [back to overview]Maximum-tolerated Dose of Veliparib Defined as Highest Dose Level With Fewer Than 2 Dose Limiting Toxicities in 6 Patients as Assessed by the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.0 (Phase I)
NCT01514201 (14) [back to overview]Number of Phase I Patients Who Experienced Dose Limiting Toxicities (DLTs)
NCT01525082 (6) [back to overview]Treatment-related Toxicity
NCT01525082 (6) [back to overview]O6-methylguanine DNA Methyltransferase (MGMT) Status by Immunohistochemistry (IHC)
NCT01525082 (6) [back to overview]O6-methylguanine DNA Methyltransferase (MGMT) by Promoter Methylation
NCT01525082 (6) [back to overview]Progression-free Survival (PFS)
NCT01525082 (6) [back to overview]Overall Survival (OS)
NCT01525082 (6) [back to overview]Radiographic Response (RR)
NCT01550224 (9) [back to overview]Treatment Failure (TF)
NCT01550224 (9) [back to overview]Relapse-Free Survival (RFS) at 2 Years
NCT01550224 (9) [back to overview]Partial Remission (PR)
NCT01550224 (9) [back to overview]Overall Survival (OS) at 2 Years
NCT01550224 (9) [back to overview]Disease-free Survival (DFS) at 2 Years
NCT01550224 (9) [back to overview]Cytogenetic Response (CyR)
NCT01550224 (9) [back to overview]Morphologic Leukemia-free State (MLFS)
NCT01550224 (9) [back to overview]Complete Remission (CR)
NCT01550224 (9) [back to overview]Complete Remission With Incomplete Blood Count Recovery (CRp)
NCT01590082 (1) [back to overview]Overall Participant Response
NCT01601535 (13) [back to overview]Maximum Tolerated Dose (MTD) When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma
NCT01601535 (13) [back to overview]One Year Progression Free Survival Rate
NCT01601535 (13) [back to overview]Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Alisertib AUC
NCT01601535 (13) [back to overview]Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Irinotecan Clearance
NCT01601535 (13) [back to overview]AURKA Genotype
NCT01601535 (13) [back to overview]Aurora A Expression
NCT01601535 (13) [back to overview]Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Alisertib Day 4 Trough, Day 5 Trough and Cmax
NCT01601535 (13) [back to overview]Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Alisertib Tmax and Half-life
NCT01601535 (13) [back to overview]Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Irinotecan AUC, APC AUC, SN-38 AUC, and SN-38G AUC
NCT01601535 (13) [back to overview]Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Irinotecan Cmax, APC Cmax, SN-38 Cmax, and SN-38G Cmax
NCT01601535 (13) [back to overview]Response Rate for Patients With Relapsed or Refractory Neuroblastoma Treated With MLN8237, Irinotecan, and Temozolomide at the Identified MTD
NCT01601535 (13) [back to overview]UGT1A1 Genotype
NCT01601535 (13) [back to overview]Dose Limiting Toxicity (DLT) Data Associated With the Determination of the Recommended Phase 2 Dose
NCT01638546 (4) [back to overview]Number of Participants With Adverse Events
NCT01638546 (4) [back to overview]Overall Response (ORR) by RECIST 1.1 Criteria
NCT01638546 (4) [back to overview]Overall Survival
NCT01638546 (4) [back to overview]Progression-free Survival, Calculated as the Proportion of Patients Alive and Without Evidence of Disease
NCT01704287 (10) [back to overview]Best Overall Response (BOR) - Initial Treatment Period
NCT01704287 (10) [back to overview]Progression-free Survival (PFS) - Initial Treatment Period
NCT01704287 (10) [back to overview]Overall Response Rate (ORR) - Initial Treatment Period
NCT01704287 (10) [back to overview]Number of Participants Who Experienced an Adverse Event (AE) - Overall Study
NCT01704287 (10) [back to overview]Number of Participants Who Discontinued Study Drug Due to an Adverse Event (AE) - Overall Study
NCT01704287 (10) [back to overview]Interim Overall Survival (OS) - Initial Treatment Period
NCT01704287 (10) [back to overview]Final Overall Survival (OS) - Initial Treatment Period
NCT01704287 (10) [back to overview]Duration of Response (DOR) - Initial Treatment Period
NCT01704287 (10) [back to overview]Best Overall Response (BOR) - Switch-to-Pembrolizumab Treatment Period
NCT01704287 (10) [back to overview]Final Overall Survival (OS) By Programmed Cell Death-Ligand 1 (PD-L1) Tumor Expression Status - Initial Treatment Period
NCT01740258 (3) [back to overview]Progression-free Survival (PFS)
NCT01740258 (3) [back to overview]Overall Survival
NCT01740258 (3) [back to overview]Toxicity: Percentage of Subjects With Unacceptable Toxicities
NCT01767194 (2) [back to overview]Percentage of Randomized Patients Who Are Responders
NCT01767194 (2) [back to overview]Percentage of Patients in the Dinutuximab Arm Who Are Responders
NCT01781403 (4) [back to overview]Pathological Complete Response
NCT01781403 (4) [back to overview]Toxicity(Adeverse Event)
NCT01781403 (4) [back to overview]Recommended Dose (RD)
NCT01781403 (4) [back to overview]Maximum Tolerated Dose (MTD)
NCT01790503 (11) [back to overview]Summary of the Median Progression-free Survival (mPFS) in the Study Group Compared With Historical Control From Medical Literature
NCT01790503 (11) [back to overview]Number of Patients With Clinically Significant Abnormal Chemistry and Hematology Values Reported as Adverse Events by Preferred Term in Phase 1b of the Modified Intent-To-Treat Population
NCT01790503 (11) [back to overview]Summary of the Median Progression-free Survival (mPFS) by Subgroups in the Modified Intent-To-Treat Population on the Recommended Phase 2 Dose
NCT01790503 (11) [back to overview]Overview of Most Frequent System Organ Classes Reported in Phase 2 of the Modified Intent-To-Treat Population
NCT01790503 (11) [back to overview]Overview of Most Frequent System Organ Classes Reported in Phase 1b of the Modified Intent-To-Treat Population
NCT01790503 (11) [back to overview]Summary of the Median Progression-free Survival (mPFS) in the Combined 800 mg, 5 Days/Week Dose Group
NCT01790503 (11) [back to overview]Number of Patients With Clinically Significant Abnormal Chemistry and Hematology Values Reported as Adverse Events by Preferred Term in Phase 2, the Combined RP2D Groups in Phase 1b, and in the Study Overall Modified Intent-To-Treat Population
NCT01790503 (11) [back to overview]Summary of the Overall Survival in the Study Group Compared With Historical Control From Medical Literature
NCT01790503 (11) [back to overview]Summary of Best Overall Response by Subgroups in the Modified Intent-To-Treat Population on the Recommended Phase 2 Dose
NCT01790503 (11) [back to overview]Summary of the Overall Survival in The Study Population
NCT01790503 (11) [back to overview]Summary of the Overall Survival by Subgroups in the Modified Intent-To-Treat Population on the Recommended Phase 2 Dose
NCT01822275 (2) [back to overview]Ability to Calculate the Efficacy of Low-dose Whole Brain RT (WBRT) in Patients With GBM
NCT01822275 (2) [back to overview]Radiographic (CT-MRI) Response Assessment and Treatment Failure Patterns of Patients With GBM
NCT01824875 (3) [back to overview]Proportion of Patients With Response
NCT01824875 (3) [back to overview]Progression-free Survival
NCT01824875 (3) [back to overview]Overall Survival
NCT01827384 (3) [back to overview]Number of Participants With an Objective Response
NCT01827384 (3) [back to overview]Proportion of Participants With 4 Month Progression-free Survival (PFS)
NCT01827384 (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)
NCT01835145 (5) [back to overview]Proportion of Patients Without a Progression Free Survival Event at 4 Months (PFS4)
NCT01835145 (5) [back to overview]Percentage of Patients Who Experienced Grade 3+ Adverse Events Regardless of Attribution
NCT01835145 (5) [back to overview]Overall Survival (OS)
NCT01835145 (5) [back to overview]Confirmed Response Rate as Determined by the RECIST Criteria (Version 1.1)
NCT01835145 (5) [back to overview]PFS
NCT01946529 (1) [back to overview]Response to Window Therapy (2 Courses) for Group B (High-risk) - ESFT Participants
NCT01977677 (2) [back to overview]Participants Alive and Without Disease Progression At 6 Months After the Start of the Irradiation
NCT01977677 (2) [back to overview]Dose-limiting Toxicity
NCT01991977 (1) [back to overview]Proportion of Grade IV MGMT Un-methylated Patients That Experience Confirmed-progression-free Survival at 6 Months (CPFS6)
NCT02023905 (6) [back to overview]Progression-Free Survival Rate (PFS) (Arm 3)
NCT02023905 (6) [back to overview]Progression-Free Survival Rate (PFS) (Arms 1 and 2)
NCT02023905 (6) [back to overview]Rate of Reduction in Seizures
NCT02023905 (6) [back to overview]Median Progression Free Survival (PFS)
NCT02023905 (6) [back to overview]Objective Response Rate (ORR)
NCT02023905 (6) [back to overview]Overall Survival Rate (OS)
NCT02039778 (2) [back to overview]Number of Participants With Adverse Events as a Measure of Safety and Tolerability
NCT02039778 (2) [back to overview]Overall Survival
NCT02113007 (1) [back to overview]Number of Participants With Serious and Non-serious Adverse Events as a Measure of Safety.
NCT02116777 (18) [back to overview]C Max of Talazoparib
NCT02116777 (18) [back to overview]C Max of Talazoparib in Combination With Temozolomide
NCT02116777 (18) [back to overview]C Max of Temozolomide in Combination With Talazoparib
NCT02116777 (18) [back to overview]Clearance of Temozolomide in Combination With Talazoparib
NCT02116777 (18) [back to overview]Half-life of Temozolomide in Combination With Talazoparib
NCT02116777 (18) [back to overview]Number of Ewing/Peripheral PNET Participants in Phase 2 With Complete Response (CR) or Partial Response (PR)
NCT02116777 (18) [back to overview]Number of Solid Tumor Patients With Complete Response (CR) or Partial Response (PR)
NCT02116777 (18) [back to overview]T Max of Talazoparib
NCT02116777 (18) [back to overview]T Max of Talazoparib in Combination With Temozolomide
NCT02116777 (18) [back to overview]T Max of Temozolomide in Combination With Talazoparib
NCT02116777 (18) [back to overview]The Number of Participants With Dose Limiting Toxicities to Determine the Maximum Tolerated Dose of Temozolomide and Talazoparib Combination Therapy
NCT02116777 (18) [back to overview]Clearance of Talazoparib in Combination With Temozolomide
NCT02116777 (18) [back to overview]AUC of Talazoparib in Combination With Temozolomide
NCT02116777 (18) [back to overview]Accumulation Half-life of Talazoparib in Combination With Temozolomide.
NCT02116777 (18) [back to overview]Accumulation Ratio of Talazoparib in Combination With Temozolomide
NCT02116777 (18) [back to overview]All Cycle 1 Toxicities >=Grade 3
NCT02116777 (18) [back to overview]AUC of Talazoparib
NCT02116777 (18) [back to overview]AUC of Temozolomide in Combination With Talazoparib
NCT02152982 (5) [back to overview]Overall Survival (OS)
NCT02152982 (5) [back to overview]Objective Tumor Response
NCT02152982 (5) [back to overview]Interaction With Optune Device
NCT02152982 (5) [back to overview]Progression-free Survival (PFS)
NCT02152982 (5) [back to overview]Overall Adverse Event Rates for Grade 3 or Higher Adverse Events
NCT02193347 (2) [back to overview]Percentage of Participants With an Unacceptable Toxicity
NCT02193347 (2) [back to overview]Percentage of Patients With a Positive Vaccine Response After 3 Post-Surgery Vaccines as Measured by IFNγ ELIspot
NCT02209948 (6) [back to overview]Median Overall Survival (OS) by Arm and MGMT Methylation Status
NCT02209948 (6) [back to overview]Progresion Free Survival Median Values
NCT02209948 (6) [back to overview]Overall Survival
NCT02209948 (6) [back to overview]Progression Free Survival at 6 Month
NCT02209948 (6) [back to overview]Number of Participants With Adverse Effects
NCT02209948 (6) [back to overview]Median Progression-free Survival (PFS) by Arm and MGMT Methylation Status
NCT02231762 (18) [back to overview]DCR After 12 Months
NCT02231762 (18) [back to overview]Disease Control Rate (DCR) After 6 Months
NCT02231762 (18) [back to overview]Duration of Response (DoR) Within 12 Months
NCT02231762 (18) [back to overview]Progression-Free Survival (PFS) Within 12 Months
NCT02231762 (18) [back to overview]Time To Response (TtR) Within 12 Months
NCT02231762 (18) [back to overview]The Number of Subjects With a Symptomatic Response After 12 Months - Maintenance Phase
NCT02231762 (18) [back to overview]The Number of Subjects With a Biochemical Response Using CgA Levels After 12 Months
NCT02231762 (18) [back to overview]The Number of Subjects With a Biochemical Response Using 5-Hydroxy-Indol-Amino-Acid (HIAA) Levels After 6 Months
NCT02231762 (18) [back to overview]The Number of Subjects With a Symptomatic Response After 6 Months
NCT02231762 (18) [back to overview]The Number of Subjects With a Biochemical Response Using 5-HIAA Levels After 12 Months
NCT02231762 (18) [back to overview]DCR by O6-methylguanine-DNA Methyl-transferase (MGMT) Expression and Methylation and Somatostatin Receptor (SSTR) Expression After 6 Months
NCT02231762 (18) [back to overview]Quality of Life Gastrointestinal Neuroendocrine Tumour 21 Questionnaire (QLQ-GI.NET21): Mean Change From Baseline at 6 Months
NCT02231762 (18) [back to overview]QoL Questionnaire QLQ-GI.NET21: Mean Change From Baseline at 12 Months
NCT02231762 (18) [back to overview]Pharmacokinetic (PK) Results: Lanreotide ATG 120 mg Serum Concentrations Within 12 Months
NCT02231762 (18) [back to overview]European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life (QoL) Core 30 Questionnaire (QLQ-C30): Mean Change From Baseline at 6 Months
NCT02231762 (18) [back to overview]EORTC QoL Questionnaire QLQ-C30: Mean Change From Baseline at 12 Months
NCT02231762 (18) [back to overview]QoL Questionnaire QLQ-GI.NET21: Mean Change From Baseline at 12 Months
NCT02231762 (18) [back to overview]The Number of Subjects With a Biochemical Response Using Chromogranin-A (CgA) Levels After 6 Months
NCT02288897 (6) [back to overview]Number of Participants With Adverse Events
NCT02288897 (6) [back to overview]Overall Survival (OS)
NCT02288897 (6) [back to overview]Complete Response Rate (CRR)
NCT02288897 (6) [back to overview]Progression-free Survival (PFS)
NCT02288897 (6) [back to overview]Change in Domain Scores From Baseline Using the Patient Reported Skindex-16 Instrument
NCT02288897 (6) [back to overview]Duration of Complete Response (DCR)
NCT02315534 (7) [back to overview]Pharmacokinetic Profile of BBI608 and Temozolomide When Administered in Combination With Temozolomide as Assessed by the Area Under the Curve
NCT02315534 (7) [back to overview]Dose-limiting Toxicities (DLTs)
NCT02315534 (7) [back to overview]Progression Free Survival (PFS)-6
NCT02315534 (7) [back to overview]Overall Survival (OS)
NCT02315534 (7) [back to overview]Disease Control Rate (DCR)
NCT02315534 (7) [back to overview]Progression Free Survival (PFS)-12
NCT02315534 (7) [back to overview]Overall Response Rate (ORR)
NCT02340156 (1) [back to overview]Incidence of Treatment-Emergent Adverse Events
NCT02343081 (5) [back to overview]AUC0-∞
NCT02343081 (5) [back to overview]Kel
NCT02343081 (5) [back to overview]AUC0-t
NCT02343081 (5) [back to overview]T1/2
NCT02343081 (5) [back to overview]Cmax
NCT02343406 (11) [back to overview]Pediatric Study: Half-life (t1/2) Observed for ABT-414
NCT02343406 (11) [back to overview]Pediatric Study: Area Under the Concentration-time-curve (AUC) Observed for Unconjugated Cys-mcMMAF
NCT02343406 (11) [back to overview]Pediatric Study: Area Under the Concentration-time Curve (AUC) Observed for ABT-414
NCT02343406 (11) [back to overview]Adult Study: Objective Response Rate (ORR)
NCT02343406 (11) [back to overview]Adult Study: Progression-Free Survival (PFS)
NCT02343406 (11) [back to overview]Adult Study: Overall Survival in the Subgroup With Epidermal Growth Factor Receptor (EGFRvIII) Mutation
NCT02343406 (11) [back to overview]Pediatric Study: Percentage of Participants With Adverse Events From the First Visit Until 49 Days After the Last Dose of Study Drug
NCT02343406 (11) [back to overview]Adult Study: Overall Survival (OS)
NCT02343406 (11) [back to overview]Pediatric Study: Maximum Observed Serum Concentration (Cmax) of ABT-414
NCT02343406 (11) [back to overview]Pediatric Study: Maximum Observed Plasma Concentration (Cmax) of Cys-mcMMAF
NCT02343406 (11) [back to overview]Pediatric Study: Half-life (t1/2) Observed for Cys-mcMMAF
NCT02343549 (7) [back to overview]Overall Survival (OS)
NCT02343549 (7) [back to overview]Progression Free Survival (PFS)
NCT02343549 (7) [back to overview]Duration of Response
NCT02343549 (7) [back to overview]Number of Participants With 12-Month Survival
NCT02343549 (7) [back to overview]Duration of Disease Control
NCT02343549 (7) [back to overview]Number of Participants With Disease Control
NCT02343549 (7) [back to overview]Number of Participants With Objective Response
NCT02366728 (7) [back to overview]Median Overall Survival in CMV Negative Participants
NCT02366728 (7) [back to overview]Median Overall Survival
NCT02366728 (7) [back to overview]Percentage of 111In-labeled Dendritic Cells Migrating to the Inguinal Lymph Nodes
NCT02366728 (7) [back to overview]Median Progression-free Survival in CMV Positive Participants
NCT02366728 (7) [back to overview]Median Progression-free Survival in CMV Negative Participants
NCT02366728 (7) [back to overview]Median Progression-free Survival
NCT02366728 (7) [back to overview]Median Overall Survival in CMV Positive Participants
NCT02389738 (1) [back to overview]Change in AUC0-18 of the Temozolomide Concentration (AUC-T) in Brain Interstitium Before and After Regadenoson Infusion
NCT02395692 (5) [back to overview]Progression-free Survival at 6 Months
NCT02395692 (5) [back to overview]Toxicity as Assessed by Number of Participants Who Experienced Adverse Events
NCT02395692 (5) [back to overview]Progression-free Survival
NCT02395692 (5) [back to overview]Overall Survival
NCT02395692 (5) [back to overview]Objective Response as Assessed by Response Assessment in Neuro-Oncology (RANO) Criteria (Arm 1 and Arm 2)
NCT02455557 (2) [back to overview]Overall Survival
NCT02455557 (2) [back to overview]Progression-free Survival (PFS)
NCT02511132 (3) [back to overview]Progression Free Survival
NCT02511132 (3) [back to overview]Overall Survival
NCT02511132 (3) [back to overview]Number of Participants With Adverse Events Determined by Laboratory Assessments and Physical Examinations
NCT02573324 (9) [back to overview]Deterioration Free Survival in M.D. Anderson Symptom Inventory Brain Tumor Module (MDASI-BT) Symptom Severity Score
NCT02573324 (9) [back to overview]Progression-Free Survival (PFS)
NCT02573324 (9) [back to overview]PFS for EGFRvIII-Mutated Tumor Subgroup
NCT02573324 (9) [back to overview]Overall Survival (OS)
NCT02573324 (9) [back to overview]OS for the O6-methylguaninemethlytransferese (MGMT) Unmethylated Group
NCT02573324 (9) [back to overview]OS for the MGMT Methylated Group
NCT02573324 (9) [back to overview]OS for the Epidermal Growth Factor Receptor (EGFR)vIII-Mutated Tumor Subgroup
NCT02573324 (9) [back to overview]Deterioration Free Survival in Neurocognitive Functioning on the Hopkins Verbal Learning Test Revised (HVLT-R) Total Recall Score
NCT02573324 (9) [back to overview]Deterioration Free Survival in MDASI-BT Symptom Interference Score
NCT02617589 (4) [back to overview]Kaplan-Meier Plot of Overall Survival (OS) - Extended Collection
NCT02617589 (4) [back to overview]Kaplan-Meier Plot of Progression Free Survival
NCT02617589 (4) [back to overview]Overall Survival Rate at 24 Months
NCT02617589 (4) [back to overview]Overall Survival (OS)
NCT02661282 (8) [back to overview]Progression Free Survival (PFS) (Newly Diagnosed Glioblastoma Cohort)- Phase II
NCT02661282 (8) [back to overview]Progression Free Survival (PFS) (Recurrent Glioblastoma Cohort) at 6 Months- Phase II
NCT02661282 (8) [back to overview]Time to Progression (Recurrent Glioblastoma Cohort)- Phase II
NCT02661282 (8) [back to overview]Overall Survival (OS) (Newly Diagnosed Glioblastoma Cohort)- Phase II
NCT02661282 (8) [back to overview]Maximum Tolerated Dose (MTD) (Recurrent Glioblastoma Participant Cohort)- Phase I
NCT02661282 (8) [back to overview]Median Duration of Response (Newly Diagnosed Glioblastoma Cohort)- Phase II
NCT02661282 (8) [back to overview]Number of Participants With Immunological Effects in Tumor Tissue (Recurrent Glioblastoma Cohort)- Phase II
NCT02661282 (8) [back to overview]Overall Objective Response Rate (ORR) (Newly Diagnosed Glioblastoma Cohort)- Phase II
NCT02667587 (5) [back to overview]Progression-free Survival (PFS) Determined by BICR
NCT02667587 (5) [back to overview]Progression Free Survival (PFS) Based on Investigator Assessment
NCT02667587 (5) [back to overview]Overall Survival (OS) Rates at 12 Months
NCT02667587 (5) [back to overview]Overall Survival (OS)
NCT02667587 (5) [back to overview]Overall Survival (OS) Rates at 24 Months
NCT02698410 (15) [back to overview]Median Time to Progression (TTP) Assessed Locally and Centrally
NCT02698410 (15) [back to overview]Median Progression Free Survival (PFS) Assessed Locally and Centrally
NCT02698410 (15) [back to overview]DCR Assessed Centrally at Month 9
NCT02698410 (15) [back to overview]Median Time to Response (TTR) Assessed Locally and Centrally
NCT02698410 (15) [back to overview]Neuron-Specific Enolase (NSE) and CgA Biomarker Levels
NCT02698410 (15) [back to overview]Percentage of Biochemical Responders According to Chromogranin A (CgA) Plasma Levels
NCT02698410 (15) [back to overview]Best Overall Response (BOR) Assessed Locally and Centrally
NCT02698410 (15) [back to overview]DCR Assessed Locally and Centrally at Month 12
NCT02698410 (15) [back to overview]Disease Control Rate (DCR) Assessed Locally at Month 9
NCT02698410 (15) [back to overview]DCR Assessed Locally and Centrally at Month 9 by Carcinoid Type
NCT02698410 (15) [back to overview]Coefficient of Agreement Between Central and Local Assessment of Tumor Radiological Response at Month 9
NCT02698410 (15) [back to overview]Objective Response Rate (ORR) Assessed Locally and Centrally at Months 9 and 12
NCT02698410 (15) [back to overview]Influence of Biomarkers Expression on Locally and Centrally Assessed DCR at Months 9 and 12
NCT02698410 (15) [back to overview]Influence of Biomarkers Expression on Locally and Centrally Assessed PFS
NCT02698410 (15) [back to overview]Median Duration of Response (DOR) Assessed Locally and Centrally
NCT02805179 (6) [back to overview]Median Change in Tumor Volume From Baseline to Mid-radiation Treatment (Week 4)
NCT02805179 (6) [back to overview]Median Progression-free Survival
NCT02805179 (6) [back to overview]Percentage of Patients With Failure; Central or In-field vs. Marginal or Distant
NCT02805179 (6) [back to overview]Percentage of Patients That Experienced Deterioration in Quality of Life (QOL)
NCT02805179 (6) [back to overview]Overall Survival at 12 Months
NCT02805179 (6) [back to overview]Median Overall Survival
NCT02864368 (2) [back to overview]Immunologic Response as Measured by Peak Number of T Cells That Secrete IFNγ by ELISPOT in Response to Component A of PEP-CMV
NCT02864368 (2) [back to overview]Percentage of Participants With Treatment-related Adverse Events
NCT02942264 (6) [back to overview]% of Participants Free of Disease Progression at 4mos Treated w/Zotiraciclib at the Maximum Tolerated Dose in Combination Temozolomide w/Dose Dense Temozolomide Schedules in Adult Patients With Recurrent Anaplastic Astrocytoma or Glioblastoma/Gliosarcoma
NCT02942264 (6) [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)
NCT02942264 (6) [back to overview]Phase I: Maximum Tolerated Dose (MTD) of Zotiraciclib (TG02) in Combination of Metronomic (mn) Temozolomide (TMZ) in Adult Patients With Recurrent Anaplastic Astrocytoma or Glioblastoma/Gliosarcoma
NCT02942264 (6) [back to overview]Phase I: Maximum Tolerated Dose (MTD) of Zotiraciclib in Combination With Dose Dense (dd) Temozolomide (TMZ) in Adult Patients With Recurrent Anaplastic Astrocytoma or Glioblastoma/Gliosarcoma
NCT02942264 (6) [back to overview]Phase I: Number of Participants With a Dose-limiting Toxicity (DLT)
NCT02942264 (6) [back to overview]% of Participants Free of Disease Progression at 4mos Treated w/Zotiraciclib at the Maximum Tolerated Dose (MTD) in Combination With the Metronomic (mn) Temozolomide (TMZ) in Adult Patients With Recurrent Anaplastic Astrocytoma or Glioblastoma/Gliosarcoma
NCT02975882 (4) [back to overview]Area Under the Serum of Nanoparticle Albumin-bound Rapamycin Concentration Curve
NCT02975882 (4) [back to overview]Number of Patients With Cycle 1 and 2 Dose Limiting Toxicities Attributable to Nanoparticle Albumin-bound Rapamycin
NCT02975882 (4) [back to overview]Number of Patients With Adverse Events
NCT02975882 (4) [back to overview]Number of Patients With Antitumor Activity of Nanoparticle Albumin-bound Rapamycin
NCT03034135 (6) [back to overview]Objective Response Rate
NCT03034135 (6) [back to overview]Overall Survival
NCT03034135 (6) [back to overview]Median Duration of Overall Survival
NCT03034135 (6) [back to overview]Progression Free Survival
NCT03034135 (6) [back to overview]Median Progression Free Survival
NCT03034135 (6) [back to overview]Number of Participants With Serious Adverse Events
NCT03119064 (3) [back to overview]Toxicities
NCT03119064 (3) [back to overview]Response
NCT03119064 (3) [back to overview]Determination of Maximum Tolerated Dose (MTD)
NCT03168919 (4) [back to overview]Time to Progression
NCT03168919 (4) [back to overview]Changes of Tumor Angiogenesis
NCT03168919 (4) [back to overview]Changes of Tumor Cellularity
NCT03168919 (4) [back to overview]Changes of Tumor Volume
NCT03190967 (6) [back to overview]Phase I: Number of Participants With Serious and/or Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0)
NCT03190967 (6) [back to overview]Phase I: Number of Participants With Dose Limiting Toxicity (DLTs) at Each Dose Level
NCT03190967 (6) [back to overview]Phase I: Standard Time to Progression (TTP)
NCT03190967 (6) [back to overview]Phase I: Median Survival
NCT03190967 (6) [back to overview]Phase I: Maximum Tolerated Dose (MTD) of Temozolomide (TMZ) When Used With T-DM1 (Ado-trastuzumab)
NCT03190967 (6) [back to overview]Phase I: Number of Participants With Grade 3 and/or Grade 4 Adverse Events
NCT03323034 (8) [back to overview]Number of Participants With Grade 3 or Greater Toxicities Associated With Pevonedistat in Combination With Irinotecan and Temozolomide
NCT03323034 (8) [back to overview]Anti-tumor Activity of Pevonedistat in Combination With Irinotecan and Temozolomide
NCT03323034 (8) [back to overview]AUC of Pevonedistat in Combination With Irinotecan and Temozolomide
NCT03323034 (8) [back to overview]C Max of Pevonedistat in Combination With Irinotecan and Temozolomide
NCT03323034 (8) [back to overview]Clearance of Pevonedistat in Combination With Irinotecan and Temozolomide
NCT03323034 (8) [back to overview]Half-life of Pevonedistat in Combination With Irinotecan and Temozolomide
NCT03323034 (8) [back to overview]MTD/RP2D of Pevonedistat in Combination With Irinotecan and Temozolomide
NCT03323034 (8) [back to overview]T Max of Pevonedistat in Combination With Irinotecan and Temozolomide
NCT03363659 (2) [back to overview]6 Months Progression Free Survival (PFS)
NCT03363659 (2) [back to overview]Overall Survival
NCT03419403 (10) [back to overview]Number of Participants With Depatuxizumab Mafodotin Dose Modifications to Ocular Side Effects After Bandage Contact Lens (BCL) Intervention
NCT03419403 (10) [back to overview]Percentage of Participants Who Required a Change in Ocular Side Effect (OSE) Management
NCT03419403 (10) [back to overview]Maximum Change From Baseline on the Logarithm of the Minimum Angle of Resolution (LogMAR) Scale
NCT03419403 (10) [back to overview]Change From Baseline In Logarithm of the Minimum Angle of Resolution (LogMAR) Scale After Bandage Contact Lens (BCL) Intervention
NCT03419403 (10) [back to overview]Time to Bandage Contact Lens (BCL) Intervention
NCT03419403 (10) [back to overview]Cumulative Dose of Depatuxizumab Mafodotin Received During Chemoradiation and During Adjuvant Treatment
NCT03419403 (10) [back to overview]Treatment-Emergent Corneal Epithelial Adverse Event (CEAE) Grade at Each Visit
NCT03419403 (10) [back to overview]Treatment Emergent Corneal Epithelial Adverse Event (CEAE) Grade at Each Visit After Bandage Contact Lens (BCL) Intervention
NCT03419403 (10) [back to overview]Number of Participants With Depatuxizumab Mafodotin Dose Modifications Due to Ocular Side Effects (OSE)
NCT03419403 (10) [back to overview]Change From Baseline In Logarithm of the Minimum Angle of Resolution (LogMAR) Scale After Bandage Contact Lens (BCL) Intervention
NCT03463265 (5) [back to overview]PFS Rate at 6 Months and 12 Months
NCT03463265 (5) [back to overview]OS at 12 Months
NCT03463265 (5) [back to overview]OS
NCT03463265 (5) [back to overview]ORR
NCT03463265 (5) [back to overview]Median PFS
NCT03495921 (4) [back to overview]Overall Response Rate (ORR)
NCT03495921 (4) [back to overview]Overall Survival (OS)
NCT03495921 (4) [back to overview]Vigil Manufacture Success Rate: Number of Participants Eligible for Treatment on the Main Study.
NCT03495921 (4) [back to overview]Progression Free Survival (PFS)
NCT03778294 (2) [back to overview]Overall Survival (OS)
NCT03778294 (2) [back to overview]Progression Free Survival
NCT03880019 (2) [back to overview]Number of Patients Experiencing Adverse Events
NCT03880019 (2) [back to overview]Confirmed Objective Response Rate (ORR) (Complete Response + Partial Response)
NCT03930771 (4) [back to overview]Number of Subjects With Radiographic Response, as Defined by the RECIST Criteria.
NCT03930771 (4) [back to overview]Safety, as Measured by the Number of Subjects With at Least One AE
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]Effect of the CAP and TMZ Combination on Pituitary Function, Measured by Changes in Pituitary Hormone Secretion in Patients
NCT04166435 (3) [back to overview]Progression Free Survival
NCT04166435 (3) [back to overview]Count of Participants With Adverse Events Greater or Equal to 3
NCT04166435 (3) [back to overview]Overall Survival
NCT05718466 (3) [back to overview]Overall Survival
NCT05718466 (3) [back to overview]Local Tumor Control
NCT05718466 (3) [back to overview]Progression Free Survival

Radiographic Response Assessed by Macdonald Criteria Every 2 Months

All patients will have their tumor measurements recorded at baseline and at the time of each MRI scan. Lesions must be measured in two dimensions. (NCT00026494)
Timeframe: 2 years

,,,
Interventionparticipants (Number)
Stable Disease (SD)Progression of Disease (POD)Partial Response (PR)Minor Response (MR)Complete Response (CR)
15mg/m2 - Vinorelbine32000
20mg/m2 - Vinorelbine21100
25mg/m2 - Vinorelbine411010
30mg/m2 - Vinorelbine312001

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Maximal Tolerating Dose (MTD for Phase I)

"Phase I Dose limiting toxicity evaluation at end of first cycle based on blood tests every two weeks and participants' subjective and objective symptoms.~Start Dose Level 100 mg/m² Temozolomide once daily + 400 mg ZARNESTRA twice daily; Dose Level 1 100 mg/m² Temozolomide once daily + 500 mg ZARNESTRA twice daily; Dose Level 2 150 mg/m² Temozolomide once daily + 500 mg ZARNESTRA twice daily; Dose Level 3 150 mg/m² Temozolomide once daily + 600 mg ZARNESTRA twice daily; Dose Level 4 150 mg/m² Temozolomide once daily + 800 mg ZARNESTRA twice daily" (NCT00050986)
Timeframe: End of first cycle (4 weeks) evaluation

Interventionparticipants (Number)
Dose Level 1Dose Level 2Dose Level 3Dose Level 4
Temozolomide and R1157773363

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Phase II: Pre-irradiation Chemotherapy Tumor Response Rate (Including Phase I Patients at Same Dose)

Tumor response was centrally reviewed. Complete response: Disappearance of all enhancing tumor, the patient must be off steroid therapy and neurologically stable or improved; partial response: ≥ 50% decrease in enhancing tumor; progressive disease: ≥ 25% increase in a lesion, progressive or newly emergent meningeal or ocular disease. (Please note that this outcome measure is considered a secondary endpoint for the Phase II component of the study, but that the patients from Phase I that were treated at the same dose level are included, as indicated in the treatment arm descriptions. ) (NCT00068250)
Timeframe: From start of treatment to 10 weeks if RT received, to 15 weeks if not.

InterventionParticipants (Count of Participants)
Complete ResponsePartial ResponseProgressive DiseaseNot evaluable
Combined Temozolomide 100mg Arms181223

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Number of Phase I Participants Experiencing Toxicity

A dose limiting toxicity (DLT) is defined as any grade 3 or 4 non-hematological toxicity (other than grade 3 nausea/vomiting) or any hematological toxicity resulting in the discontinuation of temozolomide. Toxicity evaluation for this dose escalation includes all toxicities occurring prior to the start of radiation therapy. If the patient did not receive radiation therapy, then toxicity evaluation included all toxicities occurring through week 15. Any grade 5 toxicity would result in immediate suspension of accrual. (NCT00068250)
Timeframe: From start of treatment to 10 weeks if radiation therapy received, to 15 weeks if not.

InterventionParticipants (Count of Participants)
Phase I: Temozolomide 100mg1
Phase I: Temozolomide150 mg3

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Phase II: Overall Survival Rate at 2 Years (Including Phase I Patients at Same Dose)

Survival time is defined as time from registration to date of death from any cause and is estimated by the Kaplan-Meier method. Patients last known to be alive are censored at the date of last contact. (Please note that this outcome measure is considered the primary endpoint for the Phase II component of the study, but that the patients from Phase I that were treated at the same dose level are included, as indicated in the treatment arm descriptions. ) (NCT00068250)
Timeframe: Analysis occured after all patients have been on study for 2 years. Maximum follow-up at time of analysis was 8.5 years.

Interventionpercentage of participants (Number)
Combined Temozolomide 100mg Arms80.8

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Phase II: Progression-free Survival (Including Phase I Patients at Same Dose)

Progression is defined as greater than 25% increase in enhancing tumor or the appearance of new lesions in the brain, eye, or the appearance of a new positive cerebrospinal fluid (CSF) cytology. The patient may be neurologically stable or worse and on stable or increasing doses of corticosteroid. Progression-free survival time is defined as time from registration to the date of progression, death, or last known follow-up (censored). Progression-free survival rates are estimated using the Kaplan-Meier method. (Please note that this outcome measure is considered a secondary endpoint for the Phase II component of the study, but that the patients from Phase I that were treated at the same dose level are included, as indicated in the treatment arm descriptions. ) (NCT00068250)
Timeframe: Analysis occured after all patients have been on study for 2 years. Maximum follow-up at time of analysis was 8.5 years.

Interventionyears (Median)
Combined Temozolomide 100mg Arms5.4

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Number of Participants Who Experienced a Grade 3 or 4 Thrombocytopenia and/or Neutropenia.

Occurence of grade 3 or 4 thrombocytopenia or neutropenia while receiving protocol therapy. (NCT00077207)
Timeframe: Up to 18 months of protocol therapy

InterventionParticipants (Count of Participants)
Carboplatin, Vincristine Sulfate, Temozolomide)43

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Number of Participants Who Experienced Toxic Death

Primary safety endpoints are (1) the occurrence of toxic death, which is death during treatment that is not primarily attributable to disease progression, and (2) the occurrence of grade 4 allergy to carboplatin. (NCT00077207)
Timeframe: Up to 6 years after the start of protocol therapy

InterventionParticipants (Count of Participants)
Carboplatin, Vincristine Sulfate, Temozolomide)0

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Percent Probability of Progression-free Survival (PFS)

Percentage probability of being alive and without the occurrence of disease progression 3 years following enrollment. (NCT00077207)
Timeframe: 3 years

InterventionPercent probability PFS (Number)
Carboplatin, Vincristine Sulfate, Temozolomide)60.59

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Percentage Probability of Event-free Survival (EFS)

Percentage probability of being alive and without the occurrence of disease progression or second malignant neoplasm 6 years following enrollment. (NCT00077207)
Timeframe: Six years

Interventionpercent probability EFS (Number)
Carboplatin, Vincristine Sulfate, Temozolomide)40.89

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Short Term Feasibility Success

"Success is defined as the completion of induction plus one cycle of maintenance within 24 weeks of enrollment without more than a 25% reduction in either carboplatin or temozolomide dosage.~Failure to complete the induction and one cycle of maintenance within 24 weeks counts as a short-term-feasibility failure." (NCT00077207)
Timeframe: 24 weeks

Interventionparticipants (Number)
Treatment (Carboplatin, Vincristine Sulfate, Temozolomide)25

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Long Term Feasibility Success

"Success is defined as the completion of induction plus four cycles of maintenance within 60 weeks of enrollment without more than a 25% reduction in either carboplatin or temozolomide dosage.~If the participant completes all therapy within 60 weeks the patient is a long-term feasibility success. As such, a patient who experiences short term feasibility failure can be classified as a long-term feasibility success." (NCT00077207)
Timeframe: 60 weeks

Interventionparticipants (Number)
Treatment (Carboplatin, Vincristine Sulfate, Temozolomide)41

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1-year Neurologic (Central Nervous System, CNS) Progression Free Rate

1-year CNS progression free rate is the percentage of patients who had no CNS progression after being followed for 1 year . Progressive disease (CNS) was defined as a 25% or greater increase in the sum of the product(s) of the maximal cross-sections on MRI scan, reappearance of any lesion that has disappeared, development of any new lesion(s), stable disease with a deterioration of neurologic exam, or clear worsening of any evaluable disease. (NCT00080938)
Timeframe: assessed every 3 months for 2 years

Interventionpercentage of participants (Number)
Temozolamide and Radiation90.5

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Number of Patients With Intracranial Response

Response was assessed per Response Evaluation Criteria in Solid Tumor (RECIST) by brain MRI in the 21 eligible and treated patients.Complete response (CR): complete disappearance of the clinically detectable malignant brain metastasis(es) being followed on MRI scan off corticosteroids and a stable or improving neurologic exam. Partial response (PR): greater than or equal to a 50% reduction in the sum of the product(s) of the maximal cross-sections on MRI scan with a stable or decreasing dose of corticosteroids and a stable or improving neurologic exam. Response = CR + PR (NCT00080938)
Timeframe: assessed every cycle while on treatment, then every 3 months for 2 years

Interventionparticipants (Number)
Temozolamide and Radiation3

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Overall Survival Time

Overall survival (months) was calculated from time of protocol entry to time of death from any cause. Patients alive at last follow-up were censored. The 21 eligible and treated patients were included in the analysis. (NCT00080938)
Timeframe: assessed every 3 months for 2 years

Interventionmonths (Median)
Temozolamide and Radiation7

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Time to Non-CNS (Systemic) Progression

Time to non-CNS progression was calculated from time of protocol entry to time of first systemic progressive disease or death. Patients alive and non-CNS progression-free at last follow-up were censored. Disease progression was defined as at least a 20% increase in the sum of the longest diameters of target lesions, taking as reference the baseline sum longest diameter (per RECIST criteria). Development of new lesions in non-CNS sites also constituted non-CNS progression. The 21 eligible and treated patients were included in the analysis. (NCT00080938)
Timeframe: assessed every 3 months for 2 years

Interventionmonths (Median)
Temozolamide and Radiation3.2

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Grade 3-4 Pulmonary Events

All Grade 3-4 Pulmonary events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)4

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2-yr Overall Survival

Overall survival is defined as the time from date of diagnosis to death or date of last follow-up. 2-year overall survival is the probability of patients remaining alive at 2-years from study entry estimated using Kaplan-Meier (KM) methods which censors patients at date of last follow-up. Precision of this conditional probability estimate was measured in terms of standard error. Median OS, the original primary endpoint, was not estimable based on the Kaplan-Meier method because of insufficient follow-up. (NCT00084838)
Timeframe: Patients are followed for survival up to 5 yrs post-therapy completion or death; As of this analysis, median follow-up among survivors was 31 months with the longest follow-up being 40 months.

Interventionprobability (Number)
Multi-agent Intrathecal and Systemic CT With RT (Modified IRS0.70

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Grade 3-4 Allergy/Immunology

All Grade 3-4 Allergy/Immunology events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)1

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Grade 3-4 Auditory/Hearing Events

All Grade 3-4 Auditory/Hearing events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)8

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Grade 3-4 Blood/Bone Marrow Events

"All Grade 3-4 Blood/Bone Marrow events based on CTCAEv2 as reported on case report forms.~Arm Name" (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)564

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Grade 3-4 Hepatic Events

All Grade 3-4 Hepatic events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)8

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Grade 3-4 Pain Events

All Grade 3-4 Pain events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)31

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Grade 3-4 Cardiovascular Events

All Grade 3-4 Cardiovascular events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)6

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Grade 3-4 Constitutional Events

All Grade 3-4 Constitutional events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)22

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Pre-Radiation Therapy Chemotherapeutic Response

"Response pre-RT/post-CT was defined as follows with overall response defined as achieving PR or CR.~Complete Response (CR): Complete resolution of all initially demonstrable tumor on MRI or CT evaluation w/o appearance of any new areas of disease; negative CSF cytology. Partial Response (PR): >/= 50% decrease in the sum of the products of the maximum perpendicular diameters of the tumor (sum LD) relative to baseline w/o appearance of any new areas of disease; CSF cytology unchanged from that at diagnosis or clearing after being initially positive Stable Disease (SD): <50% decrease in the sum LD w/o appearance of any new areas of disease; CSF cytology unchanged from that at diagnosis or clearing after being initially positive Progressive Disease (PD): >/= 25% increase in the sum LD relative to baseline, or the appearance of any new areas of disease or appearance of positive cytology after two consecutive negative samples." (NCT00084838)
Timeframe: Assessed at study entry and pre-RT/post-CT at week 7.

Interventionproportion of evaluable patients (Number)
Multi-agent Intrathecal and Systemic CT With RT (Modified IRS0.58

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Grade 3-4 Renal/Genitourinary Events

All Grade 3-4 Renal/Genitourinary events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)4

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Grade 3-4 Dermatology Events

All Grade 3-4 Dermatology events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)3

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Grade 3-4 Neurology Events

All Grade 3-4 Neurology events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)45

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Grade 3-4 Muscloskeletal Events

All Grade 3-4 Muscloskeletal events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)8

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Grade 3-4 Gastrointestinal Events

All Grade 3-4 Gastrointestinal events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)139

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Grade 3-4 Hemorrhage Events

All Grade 3-4 Hemorrhage events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)1

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Grade 3/4 Events

All Grade 3-4 events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)1021

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Grade 3-4 Metabolic/Laboratory Events

All Grade 3-4 Metabolic/Laboratory events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)128

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Grade 3-4 Infection/Febrile Neutropenia Events

All Grade 3-4 Infection/Febrile Neutropenia events based on CTCAEv2 as reported on case report forms. (NCT00084838)
Timeframe: Assessed during therapy up to 30 days post-therapy completion which is approximately 55 weeks for patients who completed therapy.

Interventionadverse events (Number)
Multi-agent Intrathecal and Systemic CT With RT (Mod IRS III)49

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Dose Limiting Toxicities of EMD + RT and TMZ

"pts will be evaluated from first dose through end of initiation cycle. (6 weeks of RT+TMZ +EMD and 4 weeks of EMD alone) to review dose limiting toxicity (DLT) using Common Terminology Criteria for Adverse Events (CTCAE) version 4.0 (Phase I)~DLT defined as: Known TMZ hematological toxicities will not be considered dose limiting.~Nonhematological toxicities Grades 3-4 severity (except nausea and vomiting without sufficient antiemetic prophylaxis)" (NCT00085254)
Timeframe: 10 weeks

Interventionparticipants (Number)
Arm 1 500mg (Safety Run In)0
ARM 2 1000mg (Safety run-in)0
Arm 3 2000mg (Safety Run-In)0

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Overall Survival (Phase II)

The overall survival is calculated from time of histological diagnosis to death occurance - median based on all 112 patients, all dose levels (NCT00085254)
Timeframe: up to 36 months

Interventionmonths (Median)
Arm 4 (Overall Study)19.7

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Overall Survival Based on Dose Level - Phase 2

survival calculated from date of initial histologic diagnosis and occurence of death. Pts at 500mg dose compared against Pts treated at 2000mg dose. Calculated using median (NCT00085254)
Timeframe: Up to 3 years

Interventionmonths (Median)
Arm 1 - Phase 2 (Treatment 1)17.4
Arm 2 - Phase 2 (Treatment 2)20.8

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Maximum Tolerated or Tolerable Dose (MTD) - 3 Pre-defined Doses

"pts will be evaluated from first dose through end of initiation cycle. (6 weeks of RT+TMZ +EMD and 4 weeks of EMD alone) to review any dose limiting toxicity (DLT) using Common Terminology Criteria for Adverse Events (CTCAE) version 4.0 (safety run-in)~DLT defined as: Known TMZ hematological toxicities will not be considered dose limiting.~cohorts at these 3 defined doses: 500mg, 1000mg and 2000mg MTD defined as: dose producing DLT in 2 out of 6 patients or dose level below the dose which produced DLT in >/= 2 out of 3 patients, or in >/= 3 out of 6 patients If no MTD (maximum tolerable dose) was defined through 3 steps of dose escalation, phase 2 will proceed with a randomized treatment allocation of the two pre-specified dosage arms: low dose; 500mg and high dose; 2000mg" (NCT00085254)
Timeframe: 10 weeks

Interventionmg (Number)
Arm 1 - Safety Run InNA

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Frequency of Hematologic and Nonhematologic Adverse Events

The proportion of patients with grade 3 and grade 4 hematologic and non hematologic adverse events per CTCAE 4.0 (NCT00085254)
Timeframe: Up to 1 year

InterventionNumber of grade 3 or 4 events (Number)
Arm 1- Phase 2 (500mg)48
Arm 2 - Phase 2 (2000mg)35

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Progression Free Survival

Progression free survival was defined as the time from the date of randomization to the date of disease progression or the date of death regardless of the cause. (NCT00091572)
Timeframe: Treatment continued until disease progression or unacceptable toxicity. Patients will be followed for survival.

InterventionMonths (Median)
Temozolomide2.30
Dacarbazine2.17

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Overall Survival

Overall Survival was defined as the time from the date of randomization to the date of death from any cause. (NCT00091572)
Timeframe: The final analysis was to be performed when at least 616 deaths had occurred.

InterventionMonths (Median)
Temozolomide9.13
Dacarbazine9.36

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Objective Response Rate in Subjects With Measurable Lesions

Based on investigator's assessment of response in subjects with measurable lesions. Objective response = complete response + partial response. Complete response = disappearance of all target lesions. Partial response = at least a 30% decrease in the sum of longest diameter of target lesions taking as reference the baseline sum longest diameter. (NCT00091572)
Timeframe: Treatment continued until disease progression or unacceptable toxicity.

InterventionRatio (Median)
Temozolomide0.14
Dacarbazine0.10

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Duration of Objective Response

Duration of objective response was measured from the time the criteria were met for complete response or partial response to the first date that recurrent or progressive disease was objectively documented. (NCT00091572)
Timeframe: Treatment continued until disease progression or unacceptable toxicity.

InterventionMonths (Median)
Temozolomide4.34
Dacarbazine8.31

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Change in Steroid Dependence at Six Months

Daily steroid dose will be collected at baseline and follow-up, as one of the following: 0-4 mg, >4 to ≤ 8 mg, >8 to ≤12 mg, and >12 mg. Change from baseline at six months will be evaluated to have decreased, remained stable, or increased, based on these categories. (NCT00096265)
Timeframe: From randomization to six months.

,,
InterventionParticipants (Count of Participants)
DecreaseStableIncrease
Erlotinib + WBRT + SRS1061
Temozolomide + WBRT + SRS1044
WBRT + SRS12104

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Change in Performance Status at Six Months

Compared between two treatment arms using a two-group chi-squared test. Zubrod score will be collected at baseline and follow-up. The Zubrod performance score runs from 0 to 5, with 0 denoting perfect health and 5 death. Change from baseline is calculated as 6-month value - baseline value. Patients with a baseline score who have died by six months will be included in the analysis with a score of 5 at six months. (NCT00096265)
Timeframe: From randomization to six months.

,,
InterventionParticipants (Count of Participants)
Improvement (decrease)Stable (no change)Deterioration (increase)
Erlotinib + WBRT + SRS3230
Temozolomide + WBRT + SRS1430
WBRT + SRS01921

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Change in Functional Assessment of Cancer Therapy-Brain (FACT-Br) Score at 3 Months

The Functional Assessment of Cancer Therapy-Brain (FACT-Br) is a 19-item self-report instrument designed to measure multidimensional quality of life in patients with brain cancer. It is to be administered with the FACT-General. There are 5 responses options, with 0=Not a lot and 4=Very much. All items are added together to obtain a total score, which ranges from 0 to 76. Certain items must be reversed before it is added by subtracting the response from 4. It requires at least 50% of the items to be completed while the overall response rate of the FACT-Br including the FACT-G must be greater than 80%. If items are missing, the subscale scores can be prorated. A higher score indicates better QOL. A change of 5 points will be considered a minimal clinically meaningful change. Change from baseline at three months (3 month score - baseline score) will be categorized as improvement if increased, stable if no change, or deterioration if decreased. (NCT00096265)
Timeframe: From randomization to three months.

,,
InterventionParticipants (Count of Participants)
Deterioration/DecreaseStableImprovement/Increase
Erlotinib + WBRT + SRS1161
Temozolomide + WBRT + SRS1024
WBRT + SRS1286

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Quality-adjusted Survival as Measured by EuroQol 5-dimension Instrument

Quality-adjusted life years (QALY) incorporate the societal-based utilities of health states into expected life years for a health condition. The QALY model is QALY(h,y) where h is a health state and y is the years of life. Higher quality-adjusted life year values represent a better outcome. A patient's health state will be determined from the index score of the EQ-5D-5L patient questionnaire.The EQ-5D-5L is a 2-part self-assessment questionnaire, a 5-item index score and a visual analogue scale, but only the index score is used for quality-adjusted survival. The index score has 5 items (mobility, self care, usual activities, pain/discomfort, anxiety/depression) each with 5 problem levels (1-none to 5-extreme). The 5-item index score is transformed into a utility score between 0 (worst health state) and 1 (best health state). (NCT00096265)
Timeframe: From randomization to last follow-up, up to 48.1 months. Analysis occurs after all patients have been potentially followed for 9 months.

InterventionQuality-adjusted life years (Mean)
WBRT + SRS16.9
Temozolomide + WBRT + SRS15.9
Erlotinib + WBRT + SRS14.4

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Rate of CNS Progression (One Year)

CNS progression is defined as any increase in perpendicular bi-dimensional tumor area for any of the 1-3 tracked brain metastases, by any amount, or the appearance of any new brain metastasis on a follow-up MRI (SRS planning scan will not be used to evaluate CNS progression). For lesions smaller than 1 cm in maximum diameter, a maximum increase of 50% in perpendicular bi-dimensional treatment area is necessary to score as progression. This caveat is included to account for potential variability in measurement, which is most susceptible to proportionate errors at smaller sizes. For greater than 1 cm lesions, the definition uses a 25% rule for change. Rates of CNS progression estimated by the cumulative incidence method, with death treated as a competing risk. (NCT00096265)
Timeframe: From randomization to last follow-up, up to 48.1 months. Analysis occurs after all patients have been potentially followed for 9 months.

Interventionpercentage of participants (Number)
WBRT + SRS34.1
Temozolomide + WBRT + SRS47.4
Erlotinib + WBRT + SRS27.4

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Overall Survival

Survival time is defined as time from randomization to date of death from any cause and estimated by the Kaplan-Meier method. Patients last known to be alive are censored at date of last contact. (NCT00096265)
Timeframe: From randomization to date of death or last follow-up, up to 48.1 months. Analysis occurs after all patients have been potentially followed for 9 months.

Interventionmonths (Median)
WBRT + SRS13.4
Temozolomide + WBRT + SRS6.3
Erlotinib + WBRT + SRS6.1

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4 Year Overall Survival Rate

Percentage of patients who were alive at 4 years. The 4-year survival rate was estimated using the Kaplan Meier method. (NCT00098774)
Timeframe: 4 years

Interventionpercentage of participants (Number)
Intensive Combination Chemo & Immunotherapy65

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Change From Baseline in Mini-Mental Status Evaluation at 4 Months

Neurologic functioning will be assessed using the Mini-Mental Status Evaluation (MMSE), a standardized, bedside tool for evaluation of higher mental function. This assessment is based on a 30-point scale (0-30) with higher scores associated with better performance. (NCT00098774)
Timeframe: Baseline & month 4

Interventionunits on a scale (Median)
Baseline Score4 month ScoreChange from Baseline
Intensive Combination Chemo & Immunotherapy27281

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Complete Response Rate After Remission Induction

Response is assessed by investigator according to Revised Response Criteria for Malignant Lymphoma. Complete response requires disappearance of all evidence of disease. (NCT00098774)
Timeframe: 4 months

Interventionpercentage of participants (Number)
Intensive Combination Chemo & Immunotherapy66

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4 Year Progression Free Rate

"Percentage of patients who were progression free at 4 years. The 4-year progression free rate was estimated using the Kaplan Meier method.~Relapse was assessed by investigator according to Revised Response Criteria for Malignant Lymphoma. Progression required a 25% increase of previous area of gadolinium enhancement, appearance of new areas of T1 gadolinium enhancement or new appearance of malignant cells in the spinal fluid or new tumor appearance in other sites of the body" (NCT00098774)
Timeframe: 4 years

Interventionpercentage of participants (Number)
Intensive Combination Chemo & Immunotherapy48

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Overall Response

"Overall response is the best response during 6 months of therapy measured by radiographic response.~Complete Response (CR): Disappearance of all detectable tumors by imaging, if initially positive, as well as 2 consecutively negative CSF cytologic examinations (if the initial cytology was positive).~Partial Response (PR): > 50% reduction in the sum of the products of the maximum perpendicular diameter of all measurable lesions; or 2 consecutively negative CSF cytologies and a < 50% reduction in tumor size.~Stable Disease (SD): < 50% reduction in the sum of the products of the maximum perpendicular diameters of all measurable lesions, and persistently negative or positive CSF cytology Progressive Disease (PD): > 25% increase in the size of any measurable lesion, the appearance of a new radiographically demonstrable lesion, or the conversion of negative CSF cytology to positive, as confirmed by at least one repeat CSF cytology" (NCT00098865)
Timeframe: Assessed every 8 weeks while on treatment and every 3 months for one year off-study

Interventionparticipants (Number)
Partial ResponseStable DiseaseProgressive DiseaseUnevaluable
Thalidomide and Temozolomide1941

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Therapy Completion Rate

Feasibility in this study was defined as completion of 6 months of thalidomide with temozolomide therapy. The corresponding therapy completion rate is defined as the proportion of patients who completed 6 months of therapy. (NCT00098865)
Timeframe: 6 months

Interventionproportion of participants (Number)
Thalidomide and Temozolomide.40

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Overall Survival

Time from registration to death. Patients alive at last follow-up were censored. (NCT00098865)
Timeframe: Assessed after treatment discontinued every 3 months up to 2 years.

Interventionmonths (Median)
Thalidomide and Temozolomide12.8

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One Year Overall Survival

Estimated one year survival using the Kaplan-Meier methodology. (NCT00100802)
Timeframe: One year

InterventionEstimated probability (Number)
Surgery, Chemoradiotherapy, Rest, Maintenance, FUP0.7208

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Occurrence of Death Attributable to Complications of Protocol Therapy

Number of deaths due to complications of protocol therapy. (NCT00100802)
Timeframe: While receiving protocol therapy (up to 301 days excluding delays) or within 30 days of Termination of Protocol Therapy

Interventionpatients (Number)
Surgery, Chemoradiotherapy, Rest, Maintenance, FUP1

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Median Overall Survival (OS) Comparison of Doublet Versus Triplet Therapy

Doublet (2 agents) versus Triplet (3 agents) therapy analysis: We compared the median OS outcome of participants in arms II, III, IV, versus participants in arms V, VI and VII. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Doublet (2 Agents): Arm II, Arm III and Arm IV17.0
Triplet (3 Agents): Arm V, Arm VI and Arm VII20.1

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Median Overall Survival (OS) Comparison of Celecoxib Arms Versus no Celecoxib Arms

Celecoxib versus not Celecoxib analysis: We compared the median OS outcome of participants in arms III, V, VI and VIII, versus participants in arms I, II, IV and VII. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Celecoxib: Arm III, Arm V, Arm VI and Arm VIII20.2
No Celecoxib: Arm I, Arm II, Arm IV and Arm VII17.1

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Median Progression-Free Survival (PFS) of Individual Arms

Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Arm I: TMZ10.5
Arm II: TMZ + Thalidomide7.7
Arm III: TMZ + Celecoxib13.4
Arm IV: TMZ + Isotretinoin6.5
Arm V: TMZ + Isotretinoin + Celecoxib11.6
Arm VI: TMZ + Thalidomide + Celecoxib7.9
Arm VII: TMZ + Thalidomide + Isotretinoin6.2
Arm VIII: TMZ + Thalidomide + Isotretinoin + Celecoxib5.8

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Median Overall Survival (OS) Comparison of Thalidomide Arms Versus no Thalidomide Arms

Thalidomide versus not Thalidomide analysis: We compared the median OS outcome of participants in arms II, VI, VII and VIII, versus participants in arms I, III, IV and V. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Thalidomide: Arm II, Arm VI, Arm VII and Arm VIII18.3
No Thalidomide: Arm I, Arm III, Arm IV and Arm V17.4

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Median Progression-Free Survival (PFS) Comparison of Celecoxib Arms Versus no Celecoxib Arms

Celecoxib versus not Celecoxib analysis: We compared the median PFS outcome of participants in arms III, V, VI and VIII, versus participants in arms I, II, IV and VII. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Celecoxib: Arm III, Arm V, Arm VI and Arm VIII8.3
No Celecoxib: Arm I, Arm II, Arm IV and Arm VII7.4

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Median Progression-Free Survival (PFS) Comparison of Doublet Versus Triplet Therapy

Doublet (2 agents) versus Triplet (3 agents) therapy analysis: We compared the median PFS outcome of participants in arms II, III, IV, versus participants in arms V, VI and VII. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Doublet (2 Agents): Arm II, Arm III and Arm IV8.3
Triplet (3 Agents): Arm V, Arm VI and Arm VII8.2

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Median Overall Survival (OS) Comparison of Isotretinoin Arms Versus no Isotretinoin Arms

Isotretinoin versus not Isotretinoin analysis: We compared the median OS outcome of participants in arms IV, V, VII and VIII, versus participants in arms I, II, III and VI. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Isotretinoin: Arm IV, Arm V, Arm VII and ARM VIII17.1
No Isotretinoin: Arm I, Arm II, Arm III and ARM VI19.9

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Overall Survival of Individual Arms

Overall Survival (OS) was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Arm I: TMZ21.2
Arm II: TMZ + Thalidomide17.4
Arm III: TMZ + Celecoxib18.1
Arm IV: TMZ + Isotretinoin11.7
Arm V: TMZ + Isotretinoin + Celecoxib23.1
Arm VI: TMZ + Thalidomide + Celecoxib20.2
Arm VII: TMZ + Thalidomide + Isotretinoin17.9
Arm VIII: TMZ + Thalidomide + Isotretinoin + Celecoxib18.5

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Median Progression-Free Survival (PFS) Comparison of Isotretinoin Arms Versus no Isotretinoin Arms

Isotretinoin versus not Isotretinoin analysis: We compared the median PFS outcome of participants in arms IV, V, VII and VIII, versus participants in arms I, II, III and VI. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Isotretinoin: Arm IV, Arm V, Arm VII and Arm VIII6.6
No Isotretinoin: Arm I, Arm II, Arm III and Arm VI9.1

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Median Progression-Free Survival (PFS) Comparison of Thalidomide Arms Versus no Thalidomide Arms

Thalidomide versus not Thalidomide analysis: Comparison of median PFS outcome of participants in arms II, VI, VII and VIII, versus participants in arms I, III, IV and V. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up, up to one year (12 study cycles).

Interventionmonths (Median)
Thalidomide: Arm II, Arm VI, Arm VII and Arm VIII7.6
No Thalidomide: Arm I, Arm III, Arm IV and Arm V8.7

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Neurocognitive Function

"Hopkins Verbal Learning Test (HVLT) is a test measuring learning memory retrieval, and memory consolidation processes.; Controlled Oral Word Association Test (COWAT) is a test of phonemic verbal fluency. The patient produces as many words as possible in 1 min. (each) for a specific letter (C, F, L or P, R, W).; Trail Making Test (TMT) is a measure of visuospatial scanning, attention, sequencing, and speed in Part A (TMT A) and executive function in Part B (TMT B). Patients must connect the dots either in a numbered sequence or alternating letters and numbers. Difference between pre-treatment baseline and follow-up assessment scores determined by the reliable change (RC) index, using a 90% confidence interval to designate statistically significant change." (NCT00114140)
Timeframe: Baseline, 6 months, and 12 months.

,
Interventionparticipants (Number)
HVLT Recall Status: DeteriorationHVLT Recall Status: No changeHVLT Recall Status: ImprovementCOWA Status: DeteriorationCOWA Status: No changeCOWA Status: ImprovementTMT A Status: DeteriorationTMT A Status: No changeTMT A Status: ImprovementTMT B Status: DeteriorationTMT B Status: No changeTMT B Status: Improvement
Temozolomide + Radiation Therapy (RT) at 12 Months82215328127241472215
Temozolomide + Radiation Therapy (RT) at 6 Months1126131426152411112711

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Progression-free Survival

"Progressive Disease (PD) is defined as 25% or > increase in the cross-sectional area of enhancing or non-enhancing tumor on consecutive MRI scans, or any new area(s) of tumor. Under exceptional circumstances, disease progression may be declared in the absence of an increase in tumor size based on clinical deterioration including the need for increasing doses of steroid and/or a worsening Karnofsky Performance Status(KPS) / Neurologic Function Score(NFS). Progression-free survival time is defined as time from registration to date of progressive disease or death from any cause and is estimated by the Kaplan-Meier method. Patients last known to be alive are censored at the date of last contact. Median survival time is reported." (NCT00114140)
Timeframe: From registration to last follow-up, up to 7.1 years. Analysis occurs after all patients have been on study for at least 3 years.

Interventionyears (Median)
Temozolomide + Radiation Therapy (RT)4.5

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Overall Survival Rate at 3 Years

Survival time is defined as time from registration to date of death from any cause and is estimated by the Kaplan-Meier method. Patients last known to be alive are censored at the date of last contact. This analysis was planned to occur when all patients had been potentially followed for at least 3 years. (NCT00114140)
Timeframe: Registration to 3 years

Interventionpercentage of participants (Number)
Temozolomide + Radiation Therapy (RT)73.1

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Survival and Progression-free Survival by O(6)-Methylguanine-DNA Methyltransferase (MGMT) Methylation Status

"Survival time is defined as time from registration to date of death from any cause. Progressive Disease (PD) is defined as 25% or > increase in the cross-sectional area of enhancing or non-enhancing tumor on consecutive MRI scans, or any new area(s) of tumor. Under exceptional circumstances, disease progression may be declared in the absence of an increase in tumor size based on clinical deterioration including the need for increasing doses of steroid and/or a worsening Karnofsky Performance Status(KPS) / Neurologic Function Score(NFS). Survival and progression-free survival are estimated by the Kaplan-Meier method. Patients last known to be alive are censored at the date of last contact." (NCT00114140)
Timeframe: Registration to 3 years

,
Interventionyears (Median)
Overall SurvivalProgression-free Survival
Temozolomide + Radiation Therapy (RT) - MethylatedNANA
Temozolomide + Radiation Therapy (RT) - Unmethylated3.02.0

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Quality of Life as Measured by the Functional Assessment of Cancer Therapy Scale With Brain Module (FACT-BR)

Functional Assessment of Cancer Therapy Scale with brain module (FACT-BR): a 50-question self-report questionnaire contains the following domains (scales): Physical well-being (7 questions totalling 0-28), social/family well-being (7 questions totalling 0-28), emotional well-being (6 questions totalling 0-24), functional well-being (7 questions totalling 0-28) and brain cancer subscale which contains concerns relevant to patients with brain tumors (19 questions totalling 0-76). Each question has a value 0-4. For some questions a higher indicates better outcome and others are the opposite. The former are summed as is, the latter are reversed in value before adding, such that each domain ranges from 0 to 4 multiplied by the number of questions in the domain, with 0 indicating worst and the highest possible value indicating best outcome. The FACT-Br total (0-184) is obtained by adding all domains together if the overall question response rate is greater than 80%. (NCT00114140)
Timeframe: Baseline, 6 months, and 12 months.

,,
Interventionunits on a scale (Median)
Physical Well-BeingSocial/Family Well-BeingEmotional Well-BeingFunctional Well-BeingBrain Cancer SubscaleFACT-Br Total
Temozolomide + Radiation Therapy (RT) at 12 Months2324.323.019.559.0140.0
Temozolomide + Radiation Therapy (RT) at 6 Months2224.020.018.052.0129.9
Temozolomide + Radiation Therapy (RT) at Baseline2324.518.517.054.0135.3

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Overall Survival

Patients were monitored until death (NCT00187486)
Timeframe: assessment of survival was every 2 months, up to 181 weeks

Interventionmonths (Median)
Temodar Plus Tarceva Plus Radiotherapy19

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Progression Free Survival

Progression based on MR imaging using the Modified McDonnald Criteria defined as 25% increase in sum of products of all measured lesions or any new lesion (NCT00187486)
Timeframe: every 2 months measure by MR imaging, up to 39 months

Interventionmonths (Median)
Temodar Plus Tarceva Plus Radiotherapy8.2

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Progression Free Survival at 6 Months

(NCT00200161)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Metronomic Therapy Cohort46
Dose-Dense Therapy Cohort56

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12 Month Overall Survival of Patients With Newly Diagnosed Glioblastoma Multiforme Treated With Concurrent Temozolomide and Radiotherapy Followed by Dose Dense or Metronomic Dosing of Temozolomide and Maintenance Cis-retinoic Acid.

(NCT00200161)
Timeframe: until death or date of last follow up, an average of 12 months

Interventionpercentage of participants (Number)
Metronomic Therapy Cohort69
Dose-Dense Therapy Cohort80

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Number of Participants Alive at 3 Years

The intent was to measure Median Overall Survival at 3 years, however only one participant was analyzable at this time point. Therefore, the number of participants who survived is reported instead. (NCT00248534)
Timeframe: 3 years

InterventionParticipants (Count of Participants)
IV Rituximab1

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Percentage of Participants With Objective Response

Objective response rate of the combination of Rituximab and TMZ (NCT00248534)
Timeframe: 2 months

Interventionpercent of participants (Number)
IV Rituximab14

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6-month Progression-free Survival

"Scan at 6 months~Complete response: Complete disappearance of all tumor on MRI scan, off all glucocorticoids with stable or improving neurological exam minimum of 4 wks~Partial response: Greater than or equal 50% reduction in tumor size on MRI, on sable or decreasing glucocorticoids with stable or improving neurological exam for a minimum of 4 wks.~Progressive disease: Progressive neurological abnormalities not explained by other causes or greater than 25% increase in size of tumor or if new lesion.~Stable disease: Clinical status and MRI does not qualify for complete response, partial response or progression" (NCT00248534)
Timeframe: 6 months

Interventionpercentage of participants (Number)
IV Rituximab13

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1 Year Overall Survival Rate

(NCT00248534)
Timeframe: 1 year

Interventionpercentage of participants (Number)
IV Rituximab71

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Survival

survival time is defined from time of histological diagnosis to death occurrence. (NCT00262730)
Timeframe: 30 months

Interventionmonths (Mean)
Treatment Arm - All Subjects17.2

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Number of Participants With Progression-free Survival (6 Month)

The occurrence of progression will be compared between the study groups by Kaplan-Meier curves. Responsiveness to temozolomide will be evaluated by brain Magnetic Resonance Imanging (MRI)/Computed Tomography (CT), thorax CT, and Quality of Life (QoL) assessments. Progression-free is defined as <25% increase in tumor size on CT or MRI. (NCT00266812)
Timeframe: 6 months

InterventionParticipants (Number)
Chemotherapy With Temozolomide and Radiotherapy8
Radiotherapy Alone8

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Percentage of Participants With an Objective Response (Complete Response or Partial Response)

The primary endpoint is to assess the percentage of participants with a sustained objective response (complete response (CR) or partial response (PR)). Response is assessed by magnetic resonance imaging (MRI) per the following criteria: CR - disappearance of tumor and PR - ≥50% reduction in tumor based on the maximal cross-sectional measurements. The response must be sustained for at least 8 weeks, and the date of the confirmed sustained response is the date at which the response was first noted by MRI. (NCT00275002)
Timeframe: Week 8, 16, 24, 32, and 40 after starting therapy

InterventionPercent of Participants (Number)
Recurrent High-Grade Gliomas4
Recurrent Brain Stem Tumors0

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Overall Response Rate

"Overall Response Rate (ORR) is defined as percentage of patients who's best response to treatment is complete response plus those with partial response.~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." (NCT00301067)
Timeframe: From the start of treatment, every 2 cycles where 1 cycle equals 28 days, for a maximum of 12 cycles

InterventionParticipants (Count of Participants)
Temozolomide and Calcitriol (Cohort 1-3+Expansion)2

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Number and Frequency of Dose Limiting Toxicities (DLTs) With High-dose Calcitriol in Combination With Temozolomide

"Determine number and frequency of dose limiting toxicities (DLT) of high-dose calcitriol when administered with temozolomide in patients with metastatic melanoma for up to 12 cycles of therapy, where 1 cycle equals 28 days.~3 patients per dose cohort will be entered into the trial at doses of 0.2, 0.3, and 0.5 mcg/kg of calcitriol administered orally. If 1 patient experiences dose limiting toxicity (DLT) at any dose, that dose cohort will be expanded to a maximum of 6 patients. If 1 additional patient experiences DLT at that dose stratum, further dose escalation will cease and the dose cohort immediately preceding the dose cohort where the 2 experiences of DLT occurred will be considered the MTD. If no additional patients experience DLT, dose escalation to the next higher dose stratum will take place.~DLT is defined as National Cancer Institute Common Toxicity Criteria, version 3.0 grade 3 toxicity determined to be related to calcitriol." (NCT00301067)
Timeframe: From start of treatment, up to 12 cycles where 1 cycle equals 28 days

InterventionDLT (Number)
Cohort 1 - Temozolomide and Calcitriol0
Cohort 2 - Temozolomide and Calcitriol0
Cohort 3 - Temozolomide and Calcitriol0

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Overall Survival (OS) Stratified by Vitamin D-Receptor (VDR) Gene Polymorphisms

Investigate the relationship between vitamin D-receptor (VDR) gene polymorphisms in Taq1 and Fok1 (analyzed from baseline blood sample) and Overall Survival (OS). VDR gene analysis was completed using PCR-RFLP based assays. (NCT00301067)
Timeframe: at baseline and until death from any cause up to 6 and half years

InterventionMonths (Median)
VDR genotype (tt+/-ff)non tt+/-ff VDR genotype
Temozolomide and Calcitriol (Cohort 1-3+Expansion)3.87.4

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Number of Patients With Toxicity

"Toxicity will be assessed for each patient on a seven-day on/seven-day off temozolomide in combination with high-dose calcitriol for every 2 weeks for up to 12 cycles where 1 cycle equals 28 days. Toxicity will be assessed during treatment according to the National Cancer Institute's Common Toxicity Criteria for adverse events version 3.0 (CTCAE v3.0) and defined by any toxicity determined to be at least possibly related to either study drug (temozolomide or calcitriol).~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~Grade 3 and grade 4 toxicities where relatedness to either study drug could not be ruled out were collected and recorded only." (NCT00301067)
Timeframe: From the start of treatment and every 2 weeks for a maximum of 12 cycles, and 30 days post last treatment, where 1 cycle equals 28 days

,,,
Interventionparticipants (Number)
ThrombocytopeniaVascularNauseaVomitingLeukopeniaFatigueAnemiaLymphopeniaHemorrhageRashAnorexia
Cohort 1 - Temozolomide and Calcitriol11000000000
Cohort 2 - Temozolomide and Calcitriol00000000000
Cohort 3 - Temozolomide and Calcitriol00111000000
Expansion - Temozolomide and Calcitriol11001122111

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Time to Progression

Time to progression (TTP) is measured from the start of treatment until the time of first documentation of disease progression. (NCT00301067)
Timeframe: From the start of treatment, until progressive disease, up to 12 months

InterventionMonths (Median)
Temozolomide and Calcitriol (Cohort 1-3+Expansion)1.81

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Overall Survival

Overall Survival (OS) will be measured from first day of treatment until death of any cause. Patients still alive at the last data cut off point will be censored. (NCT00301067)
Timeframe: From the first day of treatment until death from any cause, up to a maximum of 6 and half years

InterventionMonths (Median)
Temozolomide and Calcitriol (Cohort 1-3+Expansion)5.5

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Percentage of Participants With Overall Survival at 6, 12, and 24 Months

Percentage of participants who were alive at 6, 12, and 24 months. (NCT00302159)
Timeframe: 6, 12, and 24 months

Interventionpercentage of participants (Number)
6 months12 months24 months
Valproic Acid978656

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Percentage of Participants With Progression Free Survival at 6, 12, and 24 Months

Percentage of participants who were progression free by 6, 12, or 24 months. Progressive disease is a >25% increase in contrast enhancing tumor volume documented at the initiation of treatment on protocol. (NCT00302159)
Timeframe: 6, 12, and 24 months

Interventionpercentage of participants (Number)
6 months12 months24 months
Valproic Acid704338

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Median Progression Free Survival.

Progression free survival is the interval from initiation of treatment on protocol to symptomatic or radiographic progression. Progressive disease is a >25% increase in contrast enhancing tumor volume documented at the initiation of treatment on protocol. (NCT00302159)
Timeframe: up to 51 months

Interventionmonths (Median)
Valproic Acid10.5

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Median Overall Survival

Survival is the interval from the initiation of treatment on protocol to date of death. (NCT00302159)
Timeframe: up to 63.8 months

Interventionmonths (Median)
Valproic Acid29.6

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Number of Participants With Adverse Events

Here is the number of participants with adverse events. For a detailed list of adverse events, see the adverse event module. (NCT00302159)
Timeframe: 6 years, 7 months and 27 days

Interventionparticipants (Number)
Valproic Acid43

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Number of Participants With Best Response

Best response recorded from the start of treatment until disease progression/recurrence. Complete response is complete resolution of all contrast enhancing tumor documented at initiation of treatment on protocol, with no appearance of new lesions. Partial response is a >50% reduction in the contrast enhancing tumor volume documented at the initiation of treatment on protocol. Minor response is a >25%, but <50% reduction in the contrast enhancing tumor volume documented at the initiation of treatment on protocol. Stable disease is a change in tumor size less than MR but not demonstrating progressive disease. Progressive disease is a >25% increase in contrast enhancing tumor volume documented at the initiation of treatment on protocol. Not evaluable means the participant cannot be evaluated (e.g., quality of scan). (NCT00302159)
Timeframe: up to 63.8 months

Interventionparticipants (Number)
Complete ResponsePartial ResponseMinor ResponseStable DiseaseProgressive DiseaseNot Evaluable
Valproic Acid0002779

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Mean Neurocognitive Function (NCF) Composite Score Over Time

The NCF Composite score is the arithmetic mean of the HVLT-R (Free Recall, Delayed Recall, Delayed Recognition), TMTA, TMTB, and COWA scores, all of which are standardized, adjusting for age, education, and gender as necessary, such that mean is 0 and standard deviation is 1. A participant must have at least 5 of the 6 scores. A higher composite score indicates better neurocognitive function. (NCT00304031)
Timeframe: Baseline, 10, 22, and 46 weeks

,
Interventionscore on a scale (Mean)
BaselineWeek 10 (Cycle 1)Week 22 (Cycle 4)Week 46 (Cycle 10)
Conventional Adjuvant TMZ-1.2-1.3-1.1-1.0
Dose-dense Adjuvant TMZ-1.5-1.45-1.3-1.2

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Median Progression-free Survival Time by MGMT Status

Progression is defined as greater than 25% increase in tumor area (two diameters) provided that the patient has not had his/her dose of steroids decreased since the last evaluation period. Progression-free survival time is defined as time from registration to the date of first progression, death, or last known follow-up (censored). Progression-free survival rates are estimated using the Kaplan-Meier method. A concomitant decrease in steroid dose will rule out a progression designation during the first 2 months after completion of radiation therapy. Tumor tissue submitted at baseline was analyzed to determine MGMT (O[6]-methylguanine-DNA methyltransferase) promoter methylation status (methylated / unmethylated). Analysis occurred after 647 deaths were reported. (NCT00304031)
Timeframe: From randomization to last follow-up. Maximum follow-up at time of analysis was 4.4 years.

,
Interventionmonths (Median)
Unmethylated MGMTMethylated MGMT
Conventional Adjuvant TMZ5.16.5
Dose-dense Adjuvant TMZ6.010.1

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Determination of Impactful Baseline Instruments on Overall Survival

Overall survival time is defined as time from registration/randomization to the date of death from any cause or last known follow-up (censored). Overall survival rates are estimated by the Kaplan-Meier method. The European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ]-C30 subscales are calculated as the mean of component items, then standardized such that subscale scores range from 0 to 100. A high score for a functional scale represents a healthy level of functioning. Controlled Oral Word Association (COWA) score is the sum of correct responses with a range of 0 to infinity. A higher score indicates better functioning. Hopkins Verbal Learning Test - Revised (HVLT-R) score ranges from 0 to 36 for total recall is 0 to 36, 0 to 12 for delayed recall, and -12 to 12 for recognition. A higher score indicates better functioning. (NCT00304031)
Timeframe: From randomization to last follow-up. Maximum follow-up at time of analysis was 4.4 years.

Interventionmonths (Median)
Both Arms Combined17.5

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Median Overall Survival Time by MGMT Status

Overall survival time is defined as time from randomization 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. Tumor tissue submitted at baseline was analyzed to determine MGMT (O[6]-methylguanine-DNA methyltransferase) promoter methylation status (methylated / unmethylated). Analysis occurred after 647 deaths were reported. (NCT00304031)
Timeframe: From randomization to last follow-up. Maximum follow-up at time of analysis was 4.4 years.

,
Interventionmonths (Median)
Unmethylated MGMTMethylated MGMT
Conventional Adjuvant TMZ14.621.4
Dose-dense Adjuvant TMZ13.320.2

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Median Progression-free Survival (PFS) Time

Progression is defined as greater than 25% increase in tumor area (two diameters) provided that the patient has not had his/her dose of steroids decreased since the last evaluation period. Progression-free survival time is defined as time from registration to the date of first progression, death, or last known follow-up (censored). Progression-free survival rates are estimated using the Kaplan-Meier method. A concomitant decrease in steroid dose will rule out a progression designation during the first 2 months after completion of radiation therapy. Analysis occurred after 647 deaths were reported. (NCT00304031)
Timeframe: From randomization to last follow-up. Maximum follow-up at time of analysis was 4.4 years.

Interventionmonths (Median)
Conventional Adjuvant TMZ5.5
Dose-dense Adjuvant TMZ6.7

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Mean MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score Over Time

The MDASI-BT is a 28-item patient-reported outcome measure assessing symptom severity and resulting interference with daily living in brain cancer patients. All items range from 0 (not present) to 10 (as bad as you can imagine). The symptom severity score is the average of the symptom severity items, given a specified minimum numbers were completed. (NCT00304031)
Timeframe: Baseline, 10, 12, 22, 24, and 46 weeks

,
Interventionscore on a scale (Mean)
BaselineWeek 10 (Cycle 1)Week 12 (Cycle 1.5)Week 22 (Cycle 4)Week 24 (Cycle 4.5)Week 46 (Cycle 10)
Conventional Adjuvant TMZ1.31.41.61.01.01.2
Dose-dense Adjuvant TMZ1.11.41.51.21.11.1

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Change From Baseline in Mean EORTC QLQ-C30 Global Health Status

"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 was calculated as time point value - baseline value with a positive change value indicating improved QOL from baseline." (NCT00304031)
Timeframe: Baseline, 10,12, 22, 24, and 46 weeks

,
Interventionscore on a scale (Mean)
Week 10 (Cycle 1)Week 12 (Cycle 1.5)Week 22 (Cycle 4)Week 24 (Cycle 4.5)Week 46 (Cycle 10)
Conventional Adjuvant TMZ0.0-4.63.9-2.85.4
Dose-dense Adjuvant TMZ-2.9-2.7-4.4-0.7-1.9

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Overall Survival Status by Progression Status at 6 Months

Overall survival time is defined as time from registration to the date of death from any cause or last known follow-up (censored). Overall survival rates are estimated by the Kaplan-Meier method. Progression is defined as greater than 25% increase in tumor area (two diameters) provided that the patient has not had his/her dose of steroids decreased since the last evaluation period. (NCT00304031)
Timeframe: From randomization to last follow-up. Maximum follow-up at time of analysis was 4.4 years.

Interventionmonths (Median)
No Progression at 6 Months20.7
Progression at 6 Months10.1

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Number of Participants With Deterioration From Baseline in MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score at Cycle 4

The MDASI-BT is a 28-item patient-reported outcome measure assessing symptom severity and resulting interference with daily living in brain cancer patients. All items range from 0 (not present) to 10 (as bad as you can imagine). The symptom severity score is the average of the symptom severity items, given a specified minimum numbers were completed. A score worse than baseline by at least one is considered deterioration. (NCT00304031)
Timeframe: baseline and cycle 4 (approximately 22 weeks)

InterventionParticipants (Count of Participants)
Conventional Adjuvant TMZ5
Dose-dense Adjuvant TMZ11

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Number of Participants With Deterioration From Baseline in MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Interference Score at Cycle 4

The MDASI-BT is a 28-item patient-reported outcome measure assessing symptom severity and resulting interference with daily living in brain cancer patients. All items range from 0 (did not interfere) to 10 (interfered completely). The symptom interference score is the average of the symptom interference items, given a specified minimum numbers were completed. A score worse than baseline by at least one is considered deterioration. (NCT00304031)
Timeframe: baseline and cycle 4 (approximately 22 weeks)

InterventionParticipants (Count of Participants)
Conventional Adjuvant TMZ7
Dose-dense Adjuvant TMZ13

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Median Overall Survival Time

Overall survival time is defined as time from registration/randomization 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. Analysis occurred after 647 deaths were reported. (NCT00304031)
Timeframe: From randomization to last follow-up. Maximum follow-up at time of analysis was 4.4 years.

Interventionmonths (Median)
Conventional Adjuvant TMZ16.6
Dose-dense Adjuvant TMZ14.9

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Mean Neurocognitive Function (NCF) Composite Score at Cycle 10 for Participants Without Progression After 6 Months of Adjuvant Therapy

The NCF Composite score is the arithmetic mean of the Hopkins Verbal Learning Test - Revised (HVLT-R) (Free Recall, Delayed Recall, Delayed Recognition), Trail Making Test Part A (TMTA), Trail Making Test Part B (TMTB), and Controlled Oral Word Association (COWA) test scores, all of which are standardized, adjusting for age, education, and gender as necessary, such that mean is 0 and standard deviation is 1. A participant must have at least 5 of the 6 scores. A higher composite score indicates better neurocognitive function. (NCT00304031)
Timeframe: Baseline and cycle 10 (approximately 46 weeks)

Interventionscore on a scale (Mean)
Conventional Adjuvant TMZ-0.95
Dose-dense Adjuvant TMZ-1.19

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Mean MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score at Cycle 10 for Participants Without Progression After 6 Months of Adjuvant Therapy

The MDASI-BT is a 28-item patient-reported outcome measure assessing symptom severity and resulting interference with daily living in brain cancer patients. All items range from 0 (not present) to 10 (as bad as you can imagine). The symptom severity score is the average of the symptom severity items, given a specified minimum numbers were completed. (NCT00304031)
Timeframe: Baseline and cycle 10 (approximately 46 weeks)

Interventionscore on a scale (Mean)
Conventional Adjuvant TMZ1.17
Dose-dense Adjuvant TMZ1.18

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Mean EORTC QLQ-C30 Global Health Status Score at Cycle 10 for Participants Without Progression After 6 Months of Adjuvant Therapy

"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)." (NCT00304031)
Timeframe: Baseline and cycle 10 (approximately 46 weeks)

Interventionscore on a scale (Mean)
Conventional Adjuvant TMZ73.3
Dose-dense Adjuvant TMZ69.7

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Mean Change From Baseline in MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score at Mid-cyle for Cycle 4

The MDASI-BT is a 28-item patient-reported outcome measure assessing symptom severity and resulting interference with daily living in brain cancer patients. All items range from 0 (not present) to 10 (as bad as you can imagine). The symptom severity score is the average of the symptom severity items, given a specified minimum numbers were completed. A score worse than baseline by at least one is considered deterioration. Change is calculated as time point - baseline such that a positive change value indicates worse symptoms compared to baseline. (NCT00304031)
Timeframe: Baseline and mid-cycle 4 (approximately 24 weeks)

Interventionscore on a scale (Mean)
Conventional Adjuvant TMZ-0.23
Dose-dense Adjuvant TMZ0.19

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Mean Change From Baseline in MD Anderson Symptom Inventory Brain Tumor (MDASI-BT) Symptom Severity Score at Mid-cyle for Cycle 1

The MDASI-BT is a 28-item patient-reported outcome measure assessing symptom severity and resulting interference with daily living in brain cancer patients. All items range from 0 (not present) to 10 (as bad as you can imagine). The symptom severity score is the average of the symptom severity items, given a specified minimum numbers were completed. A score worse than baseline by at least one is considered deterioration. Change is calculated as time point - baseline such that a positive change value indicates worse symptoms compared to baseline. (NCT00304031)
Timeframe: Baseline and mid-cycle 1 (approximately 12 weeks)

Interventionscore on a scale (Mean)
Conventional Adjuvant TMZ0.48
Dose-dense Adjuvant TMZ0.39

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Mean Change From Baseline in EORTC QLQ-C30 Global Health Status Score at Mid-cyle for Cycle 4

"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 is calculated as time point - baseline such that a positive change value indicates worse symptoms compared to baseline." (NCT00304031)
Timeframe: Baseline and mid-cycle 4 (approximately 24 weeks)

Interventionscore on a scale (Mean)
Conventional Adjuvant TMZ-2.78
Dose-dense Adjuvant TMZ-0.72

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Mean Change From Baseline in EORTC QLQ-C30 Global Health Status Score at Mid-cyle for Cycle 1

"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 is calculated as time point - baseline such that a positive change value indicates worse symptoms compared to baseline." (NCT00304031)
Timeframe: Baseline and mid-cycle 1 (approximately 12 weeks)

Interventionscore on a scale (Mean)
Conventional Adjuvant TMZ-4.58
Dose-dense Adjuvant TMZ-2.63

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Progression-free Survival (Phase II)

Progression will be defined as a > 25% increase in tumor area. Progression-free survival time was defined as the time from baseline to date of death from any cause. Patients last known to be alive are censored at date of last contact. (NCT00305864)
Timeframe: From randomization to date of progression, death, or last follow-up. Analysis occurs after all patients have been potentially followed for at least 18 months. Patients were followed up to 54.3 months.

Interventionmonths (Median)
All MGd 5mg/kg Patients (Phase I and II Arms Combined)7.6

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Median Overall Survival (Phase II)

Survival time was defined as the time from baseline to date of death from any cause. Patients last known to be alive are censored at date of last contact. (NCT00305864)
Timeframe: From randomization to date of death or last follow-up. Analysis occurs after all patients have been potentially followed for at least 18 months. Patients were followed up to 54.3 months

InterventionMonths (Median)
All MGd 5mg/kg Patients (Phase I and II Arms Combined)15.6

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Maximum Tolerated Dose of MGd (Phase I)

"Patients were to be followed for a minimum of 90 days from the start of radiation therapy (RT) and carefully evaluated with respect to treatment morbidity. A dose limiting toxicity (DLT) was defined as a grade 4 neurologic adverse event (AE) considered to be related to treatment occurring within 21 days of the conclusion of RT. For each dose level, up to seven patients were to be accrued to assure that there would be six eligible for treatment adverse event evaluation. A dose level of MGd was considered acceptable if no more than 1 patient of the 6 experience a DLT. If the current level was considered acceptable, then dose escalation occurred. Otherwise, the preceding dose level would be declared the maximum tolerated dose (MTD). The MTD would be used for the Phase II arm.~Rating scale: 0 = not the MTD, 1 = MTD" (NCT00305864)
Timeframe: From start of radiation therapy to 90 days,

Interventionunits on a scale (Number)
Phase I: MGd 3 mg/kg0
Phase I: MGd 4 mg/kg0
Phase I: 5 mg/kg1

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Overall Response - Complete Response (CR), Very Good Partial Response (VGPR) and Partial Response (PR)

"The patient's best overall response obtained during Reporting Periods 1 and 2 will be scored as best response. Patients enrolled on Stratum 1 with bone marrow disease, a responder has no tumor cells detectable by routine morphology on 2 subsequent bilateral bone marrow aspirates and biopsies done at least 3 weeks apart. For patients enrolled on stratum 1 with MIBG only disease, response will be assessed using the Curie scale. Patients who have complete resolution of all MIBG positive lesions (CR) or resolution of at least one MIBG positive lesion with persistence of other lesions (PR) will be considered responders. For Stratum 2 a responder is defined to be a patient who achieves a best overall response of CR, VGPR or PR from CT/MRI scans from central review using (RECIST) Response Evaluation Criteria in Solid Tumor. A responder is defined to be a patient who achieves a best overall response of CR (Complete Response), VGPR (Very Good Partial Response) or PR (Partial Response)." (NCT00311584)
Timeframe: up to 6 courses of therapy, or about 6 months

Interventionparticipants (Number)
Disease Eval by Bone Marrow or MIBG (Irinotecan/Temozolomide)5
Disease Measurable by CT or MRI Scan (Irinotecan/Temozolomide)3

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Response Rate (Complete and Partial Response)

"Assessment of treatment response was determined by MRI in conjunction with neurological examination and steroid requirement assessment derived from Macdonald's criteria. Complete response was defined as complete disappearance of lesion on consecutive MRI scans with stable or improved neuro exam and steroids. Partial response was defined as a 50% reduction in lesion size or that tumor burden was definitely better than prior scan with stable or improved neuro exam and steroids." (NCT00313729)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Temozolomide7

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Safety Profile

Number of participants with treatment related grade 2-4 adverse events as defined by CTCAE 3.0 (NCT00313729)
Timeframe: Time from registration up to 13 months

InterventionParticipants (Count of Participants)
Temozolomide12

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Time to Tumor Progression

Progressive disease was defined as definite enlargement of any existing lesion or any new lesion based on modified Macdonald's criteria. (NCT00313729)
Timeframe: time from registration until date of the first documented progression, an average of 1 year

Interventionyears (Median)
Temozolomide3.8

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Number of Enzyme-linked Immunosorbent Spots (ELISPOT) - Correlation Between Immunological Parameters and Efficacy - Median

Pre- and post-vaccine immune assay results (Tumor-specific T-cell Responses) are summarized on a continuous scale as mean. (NCT00323115)
Timeframe: Day 7 (pre-vaccination) and Day 42 (post-vaccination)

Interventionspots (Median)
Pre-Vaccine0
Post-Vaccine0

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Number of Participants With Evaluable Data: Feasibility of Vaccination

To determine the feasibility of this approach, the investigators hypothesize that at least 2/3 of the patients included in the study will be evaluable, meaning that the participants would have received the 3 vaccinations with immunologic outcome parameters measured before and after vaccination. Therefore a maximum of 15 patients would be enrolled in the study to obtain 10 evaluable patients. If after enrolling 15 patients the investigators are unable to obtain 10 evaluable patients, the investigators would consider this approach not feasible. (NCT00323115)
Timeframe: Through enrollment, approximately 2 years

InterventionParticipants (Count of Participants)
Vaccine10

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Evaluation of T Cell Characteristics

Peripheral blood obtained before starting radiation/ temozolomide (TMZ), and at first and second leukapheresis will be used to do lymphocyte phenotyping. We will determine percentages of CD3+/CD8+/CD45RO+ (memory T-cells), CD3+/CD8+/CD28- (CD8 suppressor T cell phenotype), and CD4+/CD25+ cells at those 3 time points. An anti-human Foxp3 antibody will be used to determine if the CD4+/CD25+ cells are T regulatory cells (TREG) and how the compartmental shift correlates with immunoresponse by other immune parameters as well as to efficacy. (NCT00323115)
Timeframe: Before starting radiation/Temozolomide and at Day 7 and Day 42.

,,
Interventionpercentage of cells (Mean)
% of CD3+/CD8+/CD45RO+ (memory T-cells)% CD3+/CD8+/CD28- (CD8 suppressor T cell phenotype%CD4+/CD25+ cells% of are T regulatory cells (TREG)
Vaccine - Before Starting Radiation/TMZ30.834.614.94.0
Vaccine - First Leukapheresis25.830.514.13.5
Vaccine - Second Leukapheresis19.323.711.81.2

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Number of Participants With Significant Difference in Tumor Volume Size Pre- and Postvaccination: Neuroimaging and Tumor Assessment

Patients with evidence of evaluable enhancing disease on contrast-enhanced MRI performed within four weeks of study entry will be evaluated for response rate. Patients will be evaluated for objective tumor assessments by gadolinium-enhanced magnetic resonance imaging (Gd-MRI). Comparisons of objective assessments, excluding progressive disease, are based upon major changes in tumor size on the Gd-MRI compared to the baseline scan. Determination of progressive disease is based upon comparison to the previous scan with volumetric analysis. (NCT00323115)
Timeframe: baseline and 4 weeks

InterventionParticipants (Count of Participants)
Vaccine0

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Overall Survival Duration: Efficacy Parameters

Overall survival will also be followed. Survival will be assessed from the date of surgery to the date of patient death, due to any cause, or to the last date the patient was known to be alive. (NCT00323115)
Timeframe: Approximately 42 months

InterventionMonths (Median)
Vaccine28

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Progression Free Survival (PFS)

Progression-free survival will be assessed for each patient as the time from surgery until the patient reaches objective disease progression by MRI criteria. Death will be regarded as a progression event in those patients that die before disease progression. Patients without documented objective progression at the time of the analysis will be censored at the date of their last objective tumor assessment. Since disease free survival and overall survival are secondary endpoints all patients will be followed until death or for a period of 5 years following enrollment. (NCT00323115)
Timeframe: Approximately 42 months

InterventionMonths (Median)
Vaccine9.5

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Frequency of CD4+ and CD8+ T Cells - the Proportion of Cells in the Parent Population Responding to Glioblastoma Multiforme (GBM) - Mean

Pre- and post-vaccine immune assay results (Tumor-specific T-cells ) are summarized on a continuous scale as mean. (NCT00323115)
Timeframe: Day 7 (pre-vaccination) and Day 42 (post-vaccination)

,
Interventionproportion of cells (Mean)
Precursor frequency of CD4+ T cellsPrecursor frequency of CD8+ T cells
Post-Vaccine0.010.003
Pre-Vaccine0.0050.001

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Frequency of CD4+ and CD8+ T Cells - the Proportion of Cells in the Parent Population Responding to Glioblastoma Multiforme (GBM) - Median

Pre- and post-vaccine immune assay results (Tumor-specific T-cells ) are summarized on a continuous scale as median. (NCT00323115)
Timeframe: Day 7 (pre-vaccination) and Day 42 (post-vaccination).

,
Interventionproportion of cells (Median)
Precursor frequency of CD4+ T cellsPrecursor frequency of CD8+ T cells
Post-Vaccine0.010.001
Pre-Vaccine0.0030.001

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Percentage of Tumor-specific T-cells - Correlation Between Immunological Parameters and Efficacy- Mean

Pre- and post-vaccine immune assay results (Tumor-specific T-cell Responses) are summarized on a continuous scale as median. IFN = interferon. (NCT00323115)
Timeframe: Day 7 (pre-vaccination) and Day 42 (post-vaccination)

,
Interventionpercentage of cells (Mean)
Percentage of CD4+ proliferating and IFNPercentage of CD8+ proliferating and IFN
Post-Vaccine0.880.92
Pre-Vaccine0.380.45

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Percentage of Tumor-specific T-cells - Correlation Between Immunological Parameters and Efficacy- Median

Pre- and post-vaccine immune assay results (Tumor-specific T-cell Responses) are summarized on a continuous scale as median. (NCT00323115)
Timeframe: Day 7 (pre-vaccination) and Day 42 (post-vaccination)

,
Interventionpercentage of cells (Median)
Percentage of CD4+ proliferating and IFNPercentage of CD8+ proliferating and IFN
Post-Vaccine0.250.25
Pre-Vaccine0.150.27

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Tumor-specific Cytotoxic T-cell Response

MRI & pheresis post vaccine (NCT00323115)
Timeframe: Day 42

Intervention10^9 cells/L (Median)
No. CD4+No. CD8+
Vaccine0.4960.4836

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Number of Adverse Events: Toxicity Profile of Intra-nodal DC/Tumor Lysate Vaccination

Adverse events attributed to vaccination. Collected and attributed adverse events at each study visit; monitored participants for adverse events for two hours following vaccination procedure. (NCT00323115)
Timeframe: Until death or approximately 24 months after diagnosis

Interventionattributable adverse events (Number)
Vaccine1

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Number of Enzyme-linked Immunosorbent Spots (ELISPOT) - Correlation Between Immunological Parameters and Efficacy - Mean

Pre- and post-vaccine immune assay results (Tumor-specific T-cell Responses) are summarized on a continuous scale as mean. (NCT00323115)
Timeframe: Day 7 (pre-vaccination) and Day 42 (post-vaccination)

Interventionspots (Mean)
Pre-Vaccine1.40
Post-Vaccine44.2

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Analyze Patients Time to Progression

"Responses to treatment was determined by comparing new enhanced MRI scans with those obtained at the previous evaluation (i.e., 2 treatment cycles ago) or with the pre-IA chemotherapy baseline scan, if it is the first follow-up MRI scan during treatment.~MRI is the neuro-imaging modality of choice, since it is more accurate than CT for small tumors, multiple tumors, and tumors in the posterior fossa.58 The methodology used (techniques and equipment) must be identical for all scans. Lesions should be measured as the largest diameter seen on scan and the largest diameter perpendicular to that dimension." (NCT00362817)
Timeframe: up to 60 weeks

Interventionweeks (Mean)
Temozolomide & Intra-Arterial (IA) Carboplatin22.6

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Determine the Overall Survival of Patients

From the time of protocol initiation (NCT00362817)
Timeframe: up to 64 weeks

Interventionweeks (Mean)
Temozolomide & Intra-Arterial (IA) Carboplatin25.2

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The Incidence and Severity of Centeral Nervous System (CNS) Toxicities

To determine the incidence and severity of CNS toxicity in patients treated with intra-arterial carboplatin and oral temozolomide. (NCT00362817)
Timeframe: up to 24 weeks

Interventionpatients (Number)
Temozolomide & Intra-Arterial (IA) Carboplatin0

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Determine the Cause of Death of Patients After Treatment

To determine the cause of death (i.e., CNS tumor versus systemic disease progression) in patients after treatment. (NCT00362817)
Timeframe: up to 1 year

Interventionpatients (Number)
CNS tumorSystemic disease progression
Temozolomide & Intra-Arterial (IA) Carboplatin07

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Affects of Response Rate of Chemotherapy With Intra-arterial Carboplatin and Oral Temozolomide

Response was evaluated by MRI Criteria (MacDonald Criteria). The MacDonald criteria for determining tumor progression is determined through assessing the increase in size of an enhancing tumor on consecutive MRI scans and clinical assessment. Complete response occurs when there is a disappearance of all enhancing tumor on consecutive MRI scans at least one month apart. Partial response occurs at a >50% reduction in size of enhancing tumor on consecutive MRI scans at least one month apart. Progressive disease occurs when there is a >25% increase in size of enhancing tumor on consecutive MRI scans. Stable disease occurs in all remaining situations. (NCT00362817)
Timeframe: up to 1 year

Interventionpercentage of patients with response (Number)
Temozolomide & Intra-Arterial (IA) Carboplatin42.8

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Percentage of Participants Surviving at Six Months of Treatment Without Evidence of Disease Progression.

Progression-free survival as determined by Kaplan-Meier method. (NCT00392171)
Timeframe: 6 months

InterventionPercentage of Participants (Number)
Anaplastic Glioma (n=28)Early Glioblastoma Multiforme (GBM) (n=33)Extended Glioblastoma Multiforme (GBM) (n=27)Rechallenge Glioblastoma Multiforme (GBM) (n=28)
Temozolomide35.727.37.435.7

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Number of Participants Undergoing Magnetic Resonance Imaging/Magnetic Resonance Spectroscopy (MRI/MRS) for Clinical Evaluation at Baseline

Number of patients having MRI/MRS for clinical evaluation with baseline assessment. (NCT00402116)
Timeframe: Each radiologic assessment (up to 12 cycles, 28 days per cycle)

InterventionParticipants (Count of Participants)
Phase 2 - 250 mg35

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Phase 1 and 2- Pharmacokinetics: Area Under the Concentration-Time Curve During 1 Dosing Interval at Steady State (AUCτ,ss) for Enzastaurin, LY326020 and Total Analyte (Enzastaurin + LY326020) When Enzastaurin Administered With or Without Temozolomide

AUCτ,ss was calculated using concentration versus time data of enzastaurin, LY326020, and total analyte (enzastaurin + LY326020). Data are reported as Geometric Mean and Geometric Coefficient of Variation (%). (NCT00402116)
Timeframe: Phase 1, Cycle 1 Day 22, Cycle 2 Day 5 of a 28 day Cycle; Phase 2, Cycle 1 Day 22 of a 28 day Cycle

,,,,
Interventionnmol•h/L (Geometric Mean)
EnzastaurinLY326020Total Analyte
Enzastaurin 250 mg + Temozolomide5270738012800
Enzastaurin 250 mg Phase 15390726012800
Enzastaurin 250 mg Phase 277201280021400
Enzastaurin 500 mg16600424021300
Enzastaurin 500 mg + Temozolomide10100865018900

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Phase 1 - Number of Participants With Adverse Events (AEs)

Summaries of serious AEs (SAEs) and all other non-serious AEs are located in the Reported Adverse Event Module. (NCT00402116)
Timeframe: Every cycle (up to 12 cycles, 28 days per cycle)

InterventionParticipants (Count of Participants)
Phase 1- Cohort 1 (250 mg Enzastaurin)0
Phase 1 Cohort 2 (500 mg Enzastaurin )1

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M.D. Anderson Symptom Inventory - Brain Tumor (MDASI-BT)

General and brain tumor-specific symptoms each assessed on a scale of 0 to 10, with a higher score representing higher symptom burden. The 4 symptom scales reported as changing over the course of the study are listed here. (NCT00402116)
Timeframe: Every cycle (up to 12 cycles, 28 days per cycle)

,,,
Interventionunits on a scale (Mean)
BaselineRadiation therapy visitCycle 1Cycle 2Cycle 3Cycle 4Cycle 5Cycle 6Cycle 7Cycle 8Cycle 9Cycle 10Cycle 11Cycle 12
Enzastaurin 250 mg Phase 1 and 2 Combined-Appetite0.31.01.61.81.41.00.60.70.70.51.00.40.20.4
Enzastaurin 250 mg Phase 1 and 2 Combined-Concentration1.21.41.81.91.51.51.61.21.31.11.11.20.91.2
Enzastaurin 250 mg Phase 1 and 2 Combined-Memory1.82.22.42.52.01.92.11.61.41.41.81.51.61.2
Enzastaurin 250 mg Phases 1 and 2 Combined-Fatigue2.43.33.63.73.22.63.32.92.82.62.81.93.01.7

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Phase 1 and 2 - Progression-Free Survival (PFS)

PFS was defined as the time from date of first dose to the first observation of disease progression, or death due to any cause. (NCT00402116)
Timeframe: Baseline to measured progressive disease (up to 12 cycles, 28 days per cycle)

Interventionmonths (Median)
250 mg Enzastaurin Phases 1 and 2 Combined10.6

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Phase 1- Pharmacokinetics (PK): Maximum Observed Drug Concentration During 1 Dosing Interval at Steady State (Cmax,ss) for Enzastaurin, LY326020, and Total Analyte (Enzastaurin + LY326020) When Enzastaurin Administered With or Without Temozolomide

Cmax,ss was calculated using concentration versus time data of enzastaurin, LY326020, and Total Analyte (enzastaurin + LY326020) when 250 mg or 500 mg enzastaurin was administered alone or with 75 mg/m^2 temozolomide. Data are reported as Geometric Mean and Geometric Coefficient of Variation (%). (NCT00402116)
Timeframe: Cycle 1 Day 22, Cycle 2 Day 5, 28 days per Cycle

,,,
Interventionnanomole per liter (nmol/L) (Geometric Mean)
EnzastaurinLY326020Total Analyte
Enzastaurin 250 mg504370853
Enzastaurin 250 mg + Temozolomide458392821
Enzastaurin 500 mg13501981570
Enzastaurin 500 mg + Temozolomide7194651010

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Functional Assessment of Cancer Therapy - Brain (FACT-Br)

Total FACT-Br score includes physical well-being, social/family well-being, emotional well-being, functional well-being and additional concerns related to brain tumors. The score ranges 0 to 200, with a higher score representing better quality of life. (NCT00402116)
Timeframe: Every cycle (up to 12 cycles, 28 days per cycle)

Interventionunits on a scale (Mean)
Baseline visitRadiation therapy visitCycle 1Cycle 2Cycle 3Cycle 4Cycle 5Cycle 6Cycle 7Cycle 8Cycle 9Cycle 10Cycle 11Cycle 12
250 mg Enzastaurin Phases 1 and 2 Combined153.5156.1151.9152.0158.9158.8158.3159.0164.1163.6162.0159.3158.2163.5

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Phase 1 and Phase 2 - Overall Survival (OS)

OS is the time from surgical diagnosis to the date of death from any cause. For participants who were alive, OS was censored at the last contact. (NCT00402116)
Timeframe: Baseline to death from any cause (Up to 48 weeks)

Interventionmonths (Median)
250 mg Enzastaurin Phases 1 and 2 Combined18.3

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Phase 1- Determination of the Maximum Tolerated Dose (MTD) of Enzastaurin

Phase 1- dose escalation of enzastaurin in 2 cohorts up to 6 participants each in order to assess MTD. After radiation/enzastaurin 250 mg per day/temozolomide 75 mg/m^2 therapy, if no more than 1 of 6 patients experienced a dose-limiting toxicity (DLT) or tumor progression, participants completed one 28-day cycle. If no significant toxicity after the first cycle, participants received subsequent cycles. If no more than 1 of the 6 patients treated at 250 mg of enzastaurin experienced a DLT, up to 6 more patients could be entered at escalated dose cohort of enzastaurin (500 mg). (NCT00402116)
Timeframe: Until MTD can be determined (up to 12 cycles, 28 days per cycle)

Interventionmilligrams (mg) (Number)
Phase 1 Participants250

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Phase 2 - Number of Participants With Adverse Events (AEs)

Summaries of serious AEs (SAEs) and all other non-serious AEs are located in the Reported Adverse Event Module. (NCT00402116)
Timeframe: Every cycle (28 days per cycle)

InterventionParticipants (Count of Participants)
Phase 2 - 250 mg Enzastaurin22

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Phase 1 and 2: Association Between Biomarkers and Clinical Outcome

Phosphorylated-S6 (pS6) ribosomal protein is a biomarker that's being investigated as a potential marker for clinical outcome using 2211 or 2215 antibody to pS6. Reported here are the hazard ratios and 95% confidence intervals (CIs) for participants for whom an pS6 immunohistochemistry (IHC) score was available. The IHC assays were scored using a 0 to +3 scoring system (no positive staining was scored 0; at least 25% immunoreactivity of cells was scored +1; 26% to 75% was scored +2; and 76% or greater was scored +3). Hazard ratio (HR) > 1 indicates worse outcome for that IHC score. (NCT00402116)
Timeframe: Baseline, Cycle 2, end of study (up to 12 cycles, 28 days per cycle)

InterventionHazard ratio (Number)
S6 2211 scoreS6 2215 score
250 mg Enzastaurin Phases 1 and 2 Combined1.701.69

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Percentage of Participants With Objective Response of Complete Response or Partial Response

Percentage of participants with objective response based assessment of confirmed complete response (CR) or confirmed partial response (PR). CR persisted on repeat imaging study at least (≥) 4 weeks after initial documentation of response. PR, for bidimensionally measurable disease, was a decrease by ≥50% of the sum of the products of the largest perpendicular diameters of all measurable lesions as determined by 2 observations not less than 4 weeks apart. Best overall response recorded any time while the participant was receiving treatment. External Response Review Committee (ERRC) assessment. (NCT00404495)
Timeframe: Baseline to 1 Year (medulloblastoma), Baseline to 6 Weeks (high-grade glioma)

Interventionpercentage of participants (Number)
Temozolomide + Irinotecan for Medulloblastoma32.6
Temozolomide + Irinotecan for High-Grade Glioma0

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Percentage of Participants With Objective Response of Complete Response or Partial Response, Investigator's Assessment

Percentage of participants with objective response based assessment of confirmed CR or confirmed PR. CR persisted on repeat imaging study ≥4 weeks after initial documentation of response. PR, in case of bidimensionally measurable disease, was a decrease by ≥50% of the sum of the products of the largest perpendicular diameters of all measurable lesions as determined by 2 observations not less than 4 weeks apart. Best overall response could be recorded any time while the participant was receiving treatment. Investigator's assessment. (NCT00404495)
Timeframe: Baseline to 1 Year (medulloblastoma), Baseline to 6 Weeks (high-grade glioma)

Interventionpercentage of participants (Number)
Temozolomide + Irinotecan for Medulloblastoma34.9
Temozolomide + Irinotecan for High-Grade Glioma11.8

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Time to Treatment Failure (TTF)

TTF was defined as the time from the date of first dose of study treatment to the date of the first documentation of progressive disease (PD), the date of treatment discontinuation except completion of treatment, or date of death due to cancer. Investigator's assessment. (NCT00404495)
Timeframe: Baseline to Date of Treatment Failure (Up to 1 Year)

Interventionmonths (Median)
Temozolomide + Irinotecan for Medulloblastoma3.8
Temozolomide + Irinotecan for High-Grade Glioma1.6

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Time to Tumor Progression (TTP)

TTP was defined as the time in months from start of study treatment to first documentation of objective tumor progression or death due to cancer, whichever came first. TTP was calculated as (first event date minus the date of first dose of study medication plus 1) divided by 7 multiplied by 4.33. Tumor progression was determined from oncologic assessment data (where data met the criteria for PD). Investigator's assessment. (NCT00404495)
Timeframe: Baseline to Date of Progression (Up to 1 Year)

Interventionmonths (Median)
Temozolomide + Irinotecan for Medulloblastoma5.6
Temozolomide + Irinotecan for High-Grade Glioma1.6

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Duration of Response

Median duration (50%) of tumor response for participants with objective disease response: who have not progressed or died due to any cause; with a response and subsequent progression or death due to any cause for duration of response (DR). DR was 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 occurred first. DR (calculated in Weeks) = (the end date for DR minus first subsequent confirmed CR or PR plus 1) divided by 7. Investigator's assessment. (NCT00404495)
Timeframe: Baseline to Date of Tumor Response (Up to 1 Year)

Interventionweeks (Median)
Temozolomide + Irinotecan for Medulloblastoma22.4
Temozolomide + Irinotecan for High-Grade Glioma36.3

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Overall Survival (OS)

Time in months from the start of study treatment to date of death due to any cause. OS was calculated as (the death date minus the date of first dose of study medication plus 1) divided by 7 multiplied by 4.33. Death was determined from adverse event data (where outcome was death) or from follow-up contact data (where the participant current status was death). Investigator's assessment. (NCT00404495)
Timeframe: Baseline to Date of Death (Up to 1 Year After Treatment)

Interventionmonths (Median)
Temozolomide + Irinotecan for Medulloblastoma16.7
Temozolomide + Irinotecan for High-Grade Glioma9.4

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Tumor Responses (Complete and Partial Response)

"Tumor response rate was based on Response Evaluation Criteria in Solid Tumors (RECIST).~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." (NCT00423150)
Timeframe: From start of treatment until participant's disease progression, intolerable toxicity or death, which ever comes first

InterventionParticipants (Number)
Number of participants with Complete ResponseNumber of participants with Partial Response
Temozolomide05

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Tolerability: Number of Participants Discontinuing Treatment Due to Adverse Events (AE)

An AE was defined as any event which was adverse, including what were commonly described as adverse or undesirable experiences, adverse events, adverse reactions, side effects, or death due to any cause associated with, or observed in conjunction with the use of a drug, biological product, or device in humans, whether or not considered related to the use of that product. Additionally, any event which was associated with, or observed in conjunction with product overdose whether accidental or intentional, or product abuse and/or withdrawal was also considered an AE. (NCT00424554)
Timeframe: 12 months

Interventionparticipants (Number)
Temozolomide (TMZ)0
No Intervention0

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MethylGuanine-DNA MethylTransferase [MGMT] Activity Measured From the Tumor Tissue During Surgery

An experimental assay was developed to measure MGMT levels. (NCT00424554)
Timeframe: 14 days

Interventionfmol/mg of proteins (Mean)
Temozolomide (TMZ)333.7
No Intervention105.1

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Safety: Number of Participants Who Experienced Grade 3 or 4 Toxicities

"Grade 3 was defined as severe per Common Terminology Criteria for Adverse Events (CTCAE).~Grade 4 was defined as life-threatening per CTCAE." (NCT00424554)
Timeframe: 12 months

,
Interventionparticipants (Number)
Grade 3Grade 4
No Intervention00
Temozolomide (TMZ)40

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Change in Perfusion MRI Markers at Week 8 as Predictors of 12mo Overall Survival (OS)

To assess the potential role of perfusion MRI as a prognostic indicator for 12-month OS based on the change in MRI markers evaluated before treatment and 8 weeks following initiation of protocol treatment. Percent change in mean tumor relative cerebral blood volume (rCBV) derived from dynamic susceptibility contrast (DSC) MRI normalized to white matter (nRCBV) and standardized rCBV (sRCBV) between baseline and week 8 are the prognostic indicators. (NCT00433381)
Timeframe: Baseline and 8 weeks

InterventionArea Under the Curve (AUC) (Number)
nRCBV (%change @ week8)sRCBV (%change @ week8)
DSC 8-week Participants0.4700.561

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Agreement Between Local Interpretation and Central Interpretation of Standard MRI

Local and central interpretations of the standard MRI were assessed for progression and survival at all available imaging (baseline visit, week 2, and after every 2 cycles of treatment, and at termination of treatment). Patients who suffer clinical progression without radiographic confirmation of progression were considered to have progressive disease in determination of PFS-6. Subjects participated in the MR substudies regardless of therapeutic intervention (NCT00433381)
Timeframe: baseline visit, week 2, after every 2 cycles of treatment, and at termination of treatment

InterventionParticipants (Count of Participants)
Local Read72402959Central Read72402959
PFS <= 6moPFS >= 6mo
Standard MRI Local and Central Evaluation62
Standard MRI Local and Central Evaluation41
Standard MRI Local and Central Evaluation55
Standard MRI Local and Central Evaluation48

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Change in Perfusion MRI Markers at Week 16 as Predictors of 12mo Overall Survival (OS)

To assess the potential role of perfusion MRI as a prognostic indicator for 12-month OS based on the change in MRI markers evaluated before treatment and 16 weeks following initiation of protocol treatment. Percent change in mean tumor relative cerebral blood volume (rCBV) derived from dynamic susceptibility contrast (DSC) MRI normalized to white matter (nRCBV) and standardized rCBV (sRCBV) between baseline and week 16 are the prognostic indicators. (NCT00433381)
Timeframe: Baseline and 16 Weeks

InterventionArea Under the Curve (AUC) (Number)
nRCBV (%change @ week16)sRCBV (%change @ week16)
DSC 16-week Participants0.7620.905

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Accuracy of Local PFS 6-mo Interpretation Using Central Review PFS-6 as the Reference Standard

Local reads were treated as the test and central reads were treated as the reference standard. Thus, a participant meeting the definition of progression on any standard MRI central interpretation (baseline visit, week 2, after every 2 cycles of treatment, and at termination of treatment) was considered positive for PFS-6. Therefore, a true positive is defined as a positive local interpretation for a subject with a positive central read. (NCT00433381)
Timeframe: baseline visit, week 2, after every 2 cycles of treatment, and at termination of treatment

InterventionParticipants (Count of Participants)
Local Read (Test)72402959Central Read (Reference)72402959
PFS-6 NegativePFS-6 Positive
Standard MRI Local and Central Evaluation62
Standard MRI Local and Central Evaluation41
Standard MRI Local and Central Evaluation48
Standard MRI Local and Central Evaluation55

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Count/Percentage of Patients Progression-free at 6 Months for Bevacizumab and Irinotecan Hydrochloride Arm

Progression defined as ≥ 25% increase in the size of enhancing tumor or any new tumor; or neurologically worse, and steroids stable or increased. Percentage is calculated by taking the number of patients who have survived 6 months without progression of study disease after study registration in the numerator. The denominator consists of all patients except those who were found retrospectively to be ineligible or who were lost to follow-up after less than 6 months. (NCT00433381)
Timeframe: From randomization to six months.

InterventionParticipants (Count of Participants)
Arm II (Bevacizumab and Irinotecan Hydrochloride)22

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Count/Percentage of Patients Progression-free at 6 Months for Bevacizumab and Temozolomide Arm

Progression defined as ≥ 25% increase in the size of enhancing tumor or any new tumor; or neurologically worse, and steroids stable or increased. Percentage is calculated by taking the number of patients who have survived 6 months without progression of study disease after study registration in the numerator. The denominator consists of all patients except those who were found retrospectively to be ineligible or who were lost to follow-up after less than 6 months. (NCT00433381)
Timeframe: From randomization to six months.

InterventionParticipants (Count of Participants)
Arm I (Bevacizumab and Temozolomide)23

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Change in Perfusion MRI Markers at Week 2 as Predictors of 12mo Overall Survival (OS)

To assess the potential role of perfusion MRI as a prognostic indicator for 12-month OS based on the change in MRI markers evaluated before treatment and 2 weeks following initiation of protocol treatment. Percent change in mean tumor relative cerebral blood volume (rCBV) derived from dynamic susceptibility contrast (DSC) MRI normalized to white matter (nRCBV) and standardized rCBV (sRCBV) between baseline and week 2 are the prognostic indicators. (NCT00433381)
Timeframe: Baseline and 2 Weeks

InterventionArea Under the Curve (AUC) (Number)
nRCBV (%change @ week2)sRCBV (%change @ week2)
DSC 2-week Participants0.850.825

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Toxicity as Assessed by the Common Terminology Criteria in Adverse Events (CTCAE v 3)

Here is the number of participants with adverse events. For a detailed list of adverse events, see the adverse event module. Adverse events were assessed by the Common Terminology Criteria in Adverse Events (CTCAE)v3. (NCT00436436)
Timeframe: 18 months and 4 days

InterventionParticipants (Count of Participants)
O6-benzylguanine & Temozolomide in Glioblastoma12

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Number of Participants That Experienced a Dose-limiting Toxicity (DLT)

The primary outcome of Phase I of this trial was to determine the maximum tolerated dose (MTD) of ZD6474 (Vandetanib) in patients with newly-diagnosed glioblastomas multiforme (GBM) and gliosarcomas who are also receiving radiation therapy with concomitant and adjuvant temozolomide. The MTD is the dose level at which 0/6 or 1/6 patients experience a dose-limiting toxicity (DLT) with the next higher dose having at least 2/3 or 2/6 patients encountering DLT. (NCT00441142)
Timeframe: 2 years

InterventionParticipants (Number)
Phase I: Dose Level -1: RT + TMZ + Vandetanib @ 200 mg/Day3
Phase I: Dose Level -2: RT + TMZ + Vandetanib @ 100 mg/Day0

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Median Progression-free Survival (PFS), as Calculated by the # of Months Patients Remain Progression-free

A secondary outcome of Phase II of this trial is the median progression-free survival (PFS), as calculated by the # of months patients remain progression-free (NCT00441142)
Timeframe: 3 years

Interventionmonths (Median)
Phase II: Arm A (Control Group: RT + TMZ)6.2
Phase II: Arm B (Experimental Group: RT + TMZ + Vandetanib)7.7

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Median Overall Survival (OS) of Phase II Patients

The primary outcome of Phase II of this trial was to determine the efficacy of ZD6474 (Vandetanib) in combination with radiation therapy and concomitant and adjuvant temozolomide in patients with newly-diagnosed GBM and gliosarcomas as measured by overall survival and median survival. (NCT00441142)
Timeframe: 3 years

Interventionmonths (Median)
Phase II: Arm A (Control Group: RT + TMZ)15.9
Phase II: Arm B (Experimental Group: RT + TMZ + Vandetanib)16.6

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Methylation Status of the O6-methylguanine-DNA Methyltransferase Promoter

Overall survival for patients by Methylation status of the O6-methylguanine-DNA methyltransferase promoter (NCT00482677)
Timeframe: 7 years

InterventionMonths (Median)
Temozolomide13.47
Radiation7.69

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Overall Survival

Time from date of randomization to the date of death of any causes, or censored at last known alive date. (NCT00482677)
Timeframe: 7 years

InterventionMonths (Median)
Temozolomide9.33
Radiation7.62

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Progression-free Survival

Time from date of randomization to the date of disease progression or death whichever came first, or censored at last disease assessment date. (NCT00482677)
Timeframe: 7 years

InterventionMonths (Median)
Temozolomide5.29
Radiation3.94

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(Phase II) Overall Survival

Number of months alive after end of study participation (NCT00486603)
Timeframe: 2 years

Interventionmonths (Median)
Phase 2: RT + TMZ + HCQ15.6

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(Phase II) Number of Participants With Grade 3 and 4 Toxicity

Number of participants experiencing Grade 3 and 4 toxicity, as defined by CTCAE v3.0, with a possible, probable or definite relationship to HCQ, TMZ or both (NCT00486603)
Timeframe: up to 2 years

InterventionParticipants (Count of Participants)
Phase 2: RT + TMZ + HCQ22

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(Phase I) Number of Participants Who Experienced Dose Limiting Toxicity (DLT)

Dose limiting toxicity defined as: Any DLT must be a toxicity considered at least possibly related to HCQ. DLTs will include any possibly, probably, or definitely HCQ-related Grade 3 or 4 toxicity. Known or reasonably suspected TMZ hematological toxicities will not be considered dose limiting unless the treating physician considers the toxicity to be exacerbated by HCQ. Nonhematological toxicities: Any Grades 3-4 severity (except nausea and vomiting without sufficient antiemetic prophylaxis) (NCT00486603)
Timeframe: 10 weeks

InterventionParticipants (Count of Participants)
Phase 1: RT+TMZ+HCQ - 200mg0
Phase 1: RT+TMZ+HCQ - 400mg0
Phase 1: RT+TMZ+HCQ - 600mg0
Phase 1: RT+TMZ+HCQ - 800mg3

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Pharmocodynamics as Determined by Number of Participants With Autophagy Inhibition in Relation to Maximal Concentration (Cmax) of HCQ

Autophagy inhibition is represented by an increase in autophagic vacuoles (AV) in participants with at least 2 peripheral blood mononuclear cell samples that were amenable to EM. (NCT00486603)
Timeframe: up to 9 weeks

,
InterventionParticipants (Count of Participants)
AV IncreaseNo AV Increase
HCQ Cmax <= 1785 ng/mL1012
HCQ Cmax>1785 ng/mL126

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PK of Hydroxychloroquine as Measured by Oral Clearance (Liters/Hour) From Central Compartment (CL/F)

The population model PK parameters do not specifically represent steady-state values, as they were determined from multiple repeated single doses taken from multiple repeated doses taken by the individual patient during their period on the study. To obtain steady state PK parameters, individual estimates were simulated from the population model. (NCT00486603)
Timeframe: up to 276 days

InterventionL/hr (Mean)
Phase 2: RT + TMZ + HCQ11.85

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PK of Hydroxychloroquine as Measured by Volume of Distribution of Central Compartment (V/F)

The population model PK parameters do not specifically represent steady-state values, as they were determined from multiple repeated single doses taken from multiple repeated doses taken by the individual patient during their period on the study. To obtain steady state PK parameters, individual estimates were simulated from the population model. (NCT00486603)
Timeframe: up to 276 days

InterventionLiters (Mean)
Phase 2: RT + TMZ + HCQ483.96

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(Phase I) Maximum Tolerated Dose (MTD) of Hydroxychloroquine (HCQ)

Number of participants who tolerated doses of HCQ without dose limiting toxicity. The highest dose at which participants did not experience dose limiting toxicity was determined as the MTD. (NCT00486603)
Timeframe: 10 weeks

InterventionParticipants (Count of Participants)
200mg400mg600mg800mg
Phase 1 - Dose Finding3730

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PK of Hydroxychloroquine as Measured by First-order Absorption Rate Constant (Ka)

The population model PK parameters do not specifically represent steady-state values, as they were determined from multiple repeated single doses taken from multiple repeated doses taken by the individual patient during their period on the study. To obtain steady state PK parameters, individual estimates were simulated from the population model. (NCT00486603)
Timeframe: up to 276 days

Interventionhours (Mean)
Phase 2: RT + TMZ + HCQ0.51

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PK of Hydroxychloroquine as Measured by Distribution Volume of Peripheral Compartment (V2/F)

The population model PK parameters do not specifically represent steady-state values, as they were determined from multiple repeated single doses taken from multiple repeated doses taken by the individual patient during their period on the study. To obtain steady state PK parameters, individual estimates were simulated from the population model. (NCT00486603)
Timeframe: up to 276 days

InterventionLiters (Mean)
Phase 2: RT + TMZ + HCQ963

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Pharmacokinetics (PK) of Hydroxychloroquine as Measured by Lag Time (Tlag)

The population model PK parameters do not specifically represent steady-state values, as they were determined from multiple repeated single doses taken from multiple repeated doses taken by the individual patient during their period on the study. To obtain steady state PK parameters, individual estimates were simulated from the population model. (NCT00486603)
Timeframe: up to 276 days

Interventionhour (Mean)
Phase 2: RT + TMZ + HCQ1.06

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Progression-free Survival (PFS) Rate at 6 Months

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. (NCT00498927)
Timeframe: at 6 months

Interventionpercentage of participants (Number)
Temozolomide19

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Overall Survival

All patients will have their tumor measurements recorded at baseline and at the time of each MRI scan. Lesions must be measured in two dimensions. The dose of gadolinium must be held constant from scan to scan. Macdonald criteria will be used for assessment of tumor response. (NCT00498927)
Timeframe: 2 years

Interventionmonths (Median)
Temozolomide7

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Incidence and Severity of CNS Hemorrhage and Systemic Hemorrhage

Number of participants experiencing a Central Nervous System (CNS) hemorrhage or systemic hemorrhage (NCT00501891)
Timeframe: 27 months

Interventionparticipants (Number)
CNS HemorrhageSystemic Hemorrhage
Bevacizumab and Metronomic Temozolomide00

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Incidence of Grade ≥ 4 Hematologic or Grade ≥ 3 Non-hematologic Toxicity

Number of participants experiencing a grade ≥4 hematologic or grade ≥3 non-hematologic toxicity (NCT00501891)
Timeframe: 27 months

Interventionparticipants (Number)
Grade ≥ 4 hematologic toxicitiesGrade ≥ 3 non-hematologic toxicities
Bevacizumab and Metromonic Temozolomide014

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6-Month Progression-free Survival

Percentage of participants surviving six months from the start of study treatment without progression of disease. PFS was defined as the time from the date of study treatment initiation to the date of the first documented progression according to the Macdonald criteria, or to death due to any cause. [Optional: Macdonald criteria are standard criteria in neuro-oncology. Tumor assessment was made according to the adapted MacDonald criteria based on the combined evaluation of: 1) assessment of the MRI scan for measurable, evaluable, and new lesions (made by the independent external expert too), 2) overall assessment of neurological performance (made by the investigator), 3) concomitant steroid use (as reported by the investigator).] (NCT00501891)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Bevacizumab and Metronomic Temozolomide18.8

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Response Rate

The number of participants with complete or partial response as determined by a modification of the Macdonald criteria. Complete response was defined as complete disappearance on MR/CT of all enhancing tumor and mass effect, off all corticosteroids (or receiving only adrenal replacement doses), accompanied by a stable or improving neurologic examination, and maintained for at least 4 weeks. Partial Response was defined as greater than or equal to 50% reduction in tumor size on MR/CT by bi-dimensional measurement, on a stable or decreasing dose of corticosteroids, accompanied by a stable or improving neurologic examination, and maintained for at least 4 weeks. (NCT00501891)
Timeframe: 27 months

InterventionNumber of participants (Number)
Bevacizumab and Metronomic Temozolomide9

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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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Time to Progression (TTP)

TTP defined as the time from date of first dose of study medication to first documentation of objective tumor progression in days. Response evaluation by Response Evaluation Criteria in Solid Tumors (RECIST) done following 2 cycles and 3 cycles. Progression is defined, using RECIST, as a measurable increase in the smallest dimension of any target or non-target lesion, or the appearance of new lesions, since baseline. (NCT00505635)
Timeframe: Following two 21 day cycles until disease progression

Interventiondays (Geometric Mean)
Biochemotherapy With Temozolomide93.2

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Optimal Doses of Temozolomide and Bortezomib (Phase I)

The optimal biologic dose (OBD) defined as the dose that achieves the greatest degree of inhibition of NF-κB activation in peripheral blood mononuclear cells when co-administered with Temozolomide (NCT00512798)
Timeframe: up to 42 days

Interventionmg/m2 (Number)
bortezomibtemozolomide
Phase I1.375

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Patients With Clinical Anti-tumor Activity (Phase I)

Per RECIST criteria v. 1.0: measurable lesions: complete response (CR) disappearance of target lesions, partial response (PR) > 30% decrease in the sum of the longest diameter (LD) of target lesions, progressive disease (PD) > 20% increase in the sum of the LD of target lesions or appearance of new lesions, stable disease (SD) neither sufficient decrease nor increase of the sum of smallest sum of the LD of target lesions (NCT00512798)
Timeframe: every 9 weeks up to a maximum of 54 weeks

Interventionparticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressive Disease
Phase I04114

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Patients With Inhibition of NF-kB (Phase II)

Patient with a minimum of 50% reduction from baseline on day 8 or day 29 in NF-kB, measured by picograms/milliliter in peripheral mononuclear blood cells (NCT00512798)
Timeframe: at baseline, on day 8 and on day 29

Interventionparticipants (Number)
Phase II0

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Patients With Inhibition in NF-kB Activation (Phase I)

Patient with a minimum of 50% reduction from baseline on day 8 or day 29 in NF-kB, measured by picograms/milliliter in peripheral mononuclear blood cells (NCT00512798)
Timeframe: at baseline, on day 8 and on day 29

Interventionparticipants (Number)
Phase I0

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Number of Patients With Clinical Anti-tumor Activity Phase II)

Per RECIST criteria v. 1.0: measurable lesions: complete response (CR) disappearance of target lesions, partial response (PR) > 30% decrease in the sum of the longest diameter (LD) of target lesions, progressive disease (PD) > 20% increase in the sum of the LD of target lesions or appearance of new lesions, stable disease (SD) neither sufficient decrease nor increase of the sum of smallest sum of the LD of target lesions. Patients with CR + PR + SD (NCT00512798)
Timeframe: every 9 weeks to a maximum of 54 weeks

Interventionparticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressive Disease
Phase II01522

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9-week Progression-free Survival Rate

The primary endpoint of this trial is the 9 week PFS rate. A patient is a success if they are progression free at their cycle 2 evaluation (approximately 9 weeks post registration). All patients, who meet the eligibility criteria, sign a consent form, and start treatment will be included in the evaluation of the 9-week PFS rate (evaluable patients). 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 using the properties of the binomial distribution. If some patients are lost to follow up prior to their cycle 2 evaluation, the Kaplan-Meier method will be used to estimate the 9 week PFS rate. 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. (NCT00521001)
Timeframe: at 9 weeks

Interventionproportion of patients (Number)
Everolimus + Temozolomide0.44

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Confirmed Response Rate (Complete Response and Partial Response)

Confirmed response rates will be evaluated by dividing the number of confirmed responders (i.e. patients that achieve a CR or PR on consecutive evaluations) by the total number of evaluable patients. Confidence intervals for the true response rate will be calculated using the properties of the binomial distribution. (NCT00521001)
Timeframe: Up to 5 years

Interventionpercentage of confirmed responses (Number)
Everolimus + Temozolomide8.3

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Survival Time

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. (NCT00521001)
Timeframe: Time from registration to death due to any cause; Up to 5 years

Interventionmonths (Median)
Everolimus + Temozolomide8.6

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Time to Disease Progression

Time to disease progression is defined as the time from registration to the earliest date documentation of disease progression. 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. 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. (NCT00521001)
Timeframe: Time from registration to the earliest date documentation of disease progression; Up to 5 years

Interventionmonths (Median)
Everolimus + Temozolomide2.4

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Unexpected Toxicities During First 2 Cycles of Study Drug

Unexpected severe study-related adverse events (NCT00525525)
Timeframe: Within 8 weeks of initiating study therapy

InterventionEvents (Number)
Safety Lead-in Group0

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Progression-free Survival

Progression-free survival was defined from the date of diagnosis to the date that progressive disease was first observed on imaging, or the date at which nonreversible neurologic progression or permanently increased corticosteroid requirement, death from any cause, or early discontinuation of treatment. Imaging guidelines were used to evaluate progression: (i) 25% increase in the sum of products of all measurable lesions over the smallest sum observed (over baseline if no decrease) using the same techniques as baseline; (ii) clear worsening of any assessable disease; (iii) appearance of any new lesion/site; and (iv) clear clinical worsening or failure to return for evaluation as a result of death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00525525)
Timeframe: Approximately 6 months to 1 year

Interventionmonths (Median)
Efficacy Group13.5

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Overall Survival (OS)

Overall survival was defined from the date of diagnosis to date of death from any cause (NCT00525525)
Timeframe: Approximately 6-24 months

Interventionmonths (Median)
Efficacy Group19.8

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Mean Total PedsQL 3.0 Scores for Child Cancer Quality of Life (QoL) Assessments (Stratum B)

QoL assessments were completed using Pediatrics Cancer Quality of Life Inventory (PedsQL v3.0). Scale range is 0-100 with higher scores reflecting better quality of life. (NCT00539591)
Timeframe: Weeks 2, 4, 8, 12, and 24; and End of therapy at 6 months and 12 months post

Interventionunits on a scale (Number)
Week 292.8
Week 490.1
Week 893.2
Week 1279.6
End of Therapy67.4

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Mean Total PedsQL 3.0 Scores for Parent Cancer Quality of Life (QoL) Assessments (Stratum A)

QoL assessments were completed using Pediatrics Cancer Quality of Life Inventory (PedsQL v3.0). Scale range is 0-100 with higher scores reflecting better quality of life. (NCT00539591)
Timeframe: Weeks 2, 4, 8, 12, and 24; and End of therapy at 6 months and 12 months post

Interventionunits on a scale (Mean)
Week 273.2
Week 475.1
Week 881.4
Week 1278.7
Week 2481.6
End of Therapy85.6
6 Months After End of Therapy85.0
12 Months After End of Therapy89.1

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Mean Total PedsQL 3.0 Scores for Parent Cancer Quality of Life (QoL) Assessments (Stratum B)

QoL assessments were completed using Pediatrics Cancer Quality of Life Inventory (PedsQL v3.0). Scale range is 0-100 with higher scores reflecting better quality of life. (NCT00539591)
Timeframe: Weeks 2, 4, 8, 12, and 24; and End of therapy at 6 months and 12 months post

Interventionunits on a scale (Number)
Week 267.7
Week 471.4

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Apparent Clearance (CL) of Pegylated Interferon ɑ-2B

"Pharmacokinetic (PK) analysis of pegylated ɑ-2b included only Stratum A patients who had PK studies performed.~Samples were analyzed for pegylated interferon ɑ-2b concentrations by using the VeriKine Human Interferon Alpha ELISA Kit following the manufacturer's instructions, and concentration-time data were analyzed by nonlinear-mixed effects modeling as implemented in NONMEM." (NCT00539591)
Timeframe: Before first dose, and 24, 96 and 168 hours after dose during weeks 5 and 28

Interventionml/hr/kg (Median)
Peginterferon ɑ-2b/Non-Pegylated Interferon ɑ-2b19.8

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Mean Total PedsQL 4.0 Scores for Child Quality of Life (QoL) Assessments (Stratum A)

QoL assessments were completed using Pediatrics Quality of Life Inventory (PedsQL v4.0). Scale range is 0-100 with higher scores reflecting better quality of life. PedsQL 4.0 healthy sample normative mean ± SD for child report = 83.0 ± 14.8. (NCT00539591)
Timeframe: Pretherapy; Weeks 2, 4, 8, 12, and 24; and End of therapy at 6 months and 12 months post

Interventionunits on a scale (Mean)
Pretherapy75.5
Week 271.6
Week 477.2
Week 879.3
Week 1277.8
Week 2480.6
End of Therapy80.4
6 Months After End of Therapy87.5
12 Months After End of Therapy91.0

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Mean Total PedsQL 4.0 Scores for Child Quality of Life (QoL) Assessments (Stratum B)

QoL assessments were completed using Pediatrics Quality of Life Inventory (PedsQL v4.0). Scale range is 0-100 with higher scores reflecting better quality of life. PedsQL 4.0 healthy sample normative mean ± SD for child report = 83.0 ± 14.8. (NCT00539591)
Timeframe: Pretherapy; Weeks 2, 4, 8, 12, and 24; and End of therapy at 6 months and 12 months post

Interventionunits on a scale (Number)
Pretherapy90.3
Week 293.1
Week 472.8
Week 879.2
Week 1268.1
End of Therapy65.6

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Volume of Central Compartment (Vc) of Interferon ɑ-2b

Samples were analyzed for interferon ɑ-2b concentrations by using the VeriKine Human Interferon Alpha ELISA Kit following the manufacturer's instructions, and concentration-time data were analyzed by nonlinear-mixed effects modeling as implemented in NONMEM. (NCT00539591)
Timeframe: Before first dose, and 1, 2, 4, 6, 8, 12, and 24 hours postinfusion

Interventionl/m^2 (Median)
Interferon ɑ-2b25.1

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Tumor Response Rate

Tumor response rate of stratum B1 participants was evaluated after 1 treatment course of temozolomide plus peginterferon ɑ-2b. Complete response (CR) and partial response (PR) confirmed with repeated scan at least 4 weeks apart following completion of course 1 therapy. CR defined as disappearance of all target and non-target lesions with no new lesions detected. If available, no disease must be detected by immunocytology or serum tumor markers. PR defined as at least 30% decrease in disease measurement compared to disease measurement at study entry with no new lesions detected. Progressive disease (PD) defined as at least 20% increase in the disease measurement compared to the smallest disease measurement recorded since start of treatment, or appearance of one or more new lesions. Stable disease defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD compared to smallest disease measurement since start of treatment. (NCT00539591)
Timeframe: 8 weeks

Interventionparticipants (Number)
Progressive DiseaseClinical Remission
Stratum B120

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Mean Total PedsQL 4.0 Scores for Parent Quality of Life Assessments (Stratum A)

QoL assessments were completed using Pediatrics Quality of Live Inventory (PedsQL v4.0). Scale range is 0-100 with higher scores reflecting better quality of life. PedsQL 4.0 healthy sample normative mean ± SD for parent report = 87.6 ± 12.3. (NCT00539591)
Timeframe: Pretherapy; Weeks 2, 4, 8, 12, and 24; and End of therapy at 6 months and 12 months post

Interventionunits on a scale (Mean)
Pretherapy70.3
Week 271.8
Week 474.4
Week 879.1
Week 1279.0
Week 2482.2
End of Therapy87.5
6 Months After End of Therapy86.0
12 Months After End of Therapy87.3

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Mean Total PedsQL 4.0 Scores for Parent Quality of Life Assessments (Stratum B)

QoL assessments were completed using Pediatrics Quality of Live Inventory (PedsQL v4.0). Scale range is 0-100 with higher scores reflecting better quality of life. PedsQL 4.0 healthy sample normative mean ± SD for parent report = 87.6 ± 12.3. (NCT00539591)
Timeframe: Pretherapy; Weeks 2, 4, 8, 12, and 24; and End of therapy at 6 months and 12 months post

Interventionunits on a scale (Number)
Pretherapy77.6
Week 272.2
Week 489.1

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Median Steady State Trough Concentration of Pegylated Interferon ɑ-2B

"The pharmacokinetic (PK) analysis of pegylated ɑ-2b included only patients within Stratum A who had PK studies performed.~Samples were analyzed for pegylated interferon ɑ-2b concentrations by using the VeriKine Human Interferon Alpha ELISA Kit following the manufacturer's instructions, and concentration-time data were analyzed by nonlinear-mixed effects modeling as implemented in NONMEM." (NCT00539591)
Timeframe: Before first dose, and 24, 96 and 168 hours after dose during weeks 5 and 28

Interventionpcg/ml (Median)
Peginterferon ɑ-2b/Non-Pegylated Interferon ɑ-2b52.8

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Number of Patients Who Experience Toxicity at or Above the Target Toxicity for Stratum A Patients

"The objective was to study the feasibility and safety of administering peginterferon a-2b weekly for 48 weeks following the initial induction phase to Stratum A participants.~Accrual was suspended during the 48-week course if 2 or more of 6, 4 or more of 12, 6 or more of 18, 8 or more of 24, 10 or more of 30 participants experienced target toxicity defined as:~Grade 4 non-hematologic (non-hem) toxicity that does not resolve to ≤grade 1 within 2 weeks from the time next dose is due and is determined to be probably or definitely related to protocol therapy~Grade 4 non-hem toxicity that is NOT constitutional symptoms (fever, chills, fatigue and/or pain)~Grade 3 elevations in creatinine or BUN that are determined to be probably or definitely related to protocol therapy~Grade 4 cardiopulmonary toxicity that is determined to be probably or definitely related to protocol therapy~Grade 4 mood alteration (suicidal ideation; danger to self or others)" (NCT00539591)
Timeframe: 52 weeks

Interventionparticipants (Number)
Grade 4 non-hem toxicityGrade 4 non-hem/NOT constitutionalGrade 3 elevations in creatinine or BUNGrade 4 cardiopulmonary toxicityGrade 4 mood alteration
Peginterferon ɑ-2b/Non-pegylated Interferon ɑ-2b20001

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Half-Life of Interferon ɑ-2b

Samples were analyzed for interferon ɑ-2b concentrations by using the VeriKine Human Interferon Alpha ELISA Kit following the manufacturer's instructions, and concentration-time data were analyzed by nonlinear-mixed effects modeling as implemented in NONMEM. (NCT00539591)
Timeframe: Before first dose, and 1, 2, 4, 6, 8, 12, and 24 hours postinfusion

Interventionhours (Median)
ɑ half-lifeß half-life
Peginterferon ɑ-2b/Non-Pegylated Interferon ɑ-2b0.714.7

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Volume of Central Compartment (Vc) of Pegylated Interferon ɑ-2B

"Pharmacokinetic (PK) analysis of pegylated ɑ-2b included only Stratum A patients who had PK studies performed.~Samples were analyzed for pegylated interferon ɑ-2b concentrations by using the VeriKine Human Interferon Alpha ELISA Kit following the manufacturer's instructions, and concentration-time data were analyzed by nonlinear-mixed effects modeling as implemented in NONMEM." (NCT00539591)
Timeframe: Before first dose, and 24, 96 and 168 hours after dose during weeks 5 and 28

Interventionml/kg (Median)
Peginterferon ɑ-2b/Non-Pegylated Interferon ɑ-2b772

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Systemic Clearance (CL) of Interferon ɑ-2B

Samples were analyzed for interferon ɑ-2b concentrations by using the VeriKine Human Interferon Alpha ELISA Kit following the manufacturer's instructions, and concentration-time data were analyzed by nonlinear-mixed effects modeling as implemented in NONMEM. (NCT00539591)
Timeframe: Before first dose, and 1, 2, 4, 6, 8, 12, and 24 hours postinfusion

Interventionl/hr/m^2 (Median)
Interferon ɑ-2b15.3

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Probability of Event-free Survival (EFS) of Stratum A Participants

The probability of EFS was estimated as time to first event (relapse, death or second malignancy). As of April 2016, 21 out of 23 participants had no events. The EFS rate was estimated by Kaplan-Meier method. (NCT00539591)
Timeframe: 3 years from diagnosis

Interventionprobability (Number)
Peginterferon ɑ-2b/Non-pegylated Interferon ɑ-2b0.913

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Number of Patients Who Experience Toxicity at or Above the Target Toxicity for Strata B1 and B2

"The objective was to assess the safety of temozolomide administered in combination with peginterferon a-2b in Stratum B participants.~Accrual was suspended any time during therapy if 2 or more of 6, 4 or more of 12, 6 or more of 18, 8 or more of 24, 10 or more of 30 participants experienced target toxicity defined as:~Grade 4 non-hematologic (non-hem) toxicity that does not resolve to ≤grade 1 within 2 weeks from the time next dose is due and is determined to be probably or definitely related to protocol therapy~Grade 4 non-hem toxicity that is NOT constitutional symptoms (fever, chills, fatigue and/or pain)~Grade 3 elevations in creatinine or BUN that are determined to be probably or definitely related to protocol therapy~Grade 4 cardiopulmonary toxicity that is determined to be probably or definitely related to protocol therapy~Grade 4 mood alteration (suicidal ideation; danger to self or others)" (NCT00539591)
Timeframe: 52 weeks

Interventionparticipants (Number)
Temozolomide/Peginterferon ɑ-2b With Measureable Disease0
Temozolomide/Peginterferon ɑ-2b Without Measureable Disease0

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Mean Total PedsQL 3.0 Scores for Child Cancer Quality of Life (QoL) Assessments (Stratum A)

QoL assessments were completed using Pediatrics Cancer Quality of Life Inventory (PedsQL v3.0). Scale range is 0-100 with higher scores reflecting better quality of life. (NCT00539591)
Timeframe: Weeks 2, 4, 8, 12, and 24; and End of therapy at 6 months and 12 months post

Interventionunits on a scale (Mean)
Week 271.1
Week 476.1
Week 879.2
Week 1278.5
Week 2477.1
End of Therapy77.0
6 Months After End of Therapy83.7
12 Months After End of Therapy85.4

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BRIEF Psychological Assessment (Stratum A)

The Behavioral Rating Inventory of Executive Function (BRIEF) was administered to parents, assessing for any effects on behavior or mood in children undergoing study therapy. The global executive composite (GEC) T-score (range 0-100) is reported for the BRIEF assessment. Higher scores reflect poorer executive function. (NCT00539591)
Timeframe: Pretherapy, Week 4, Week 24, End of Therapy, and 6 Months Post End of Therapy

InterventionT score (Mean)
Pretherapy47.9
Week 450.8
Week 2448.6
End of Therapy47.6
6 Months After End of Therapy42.6

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BASC-2 Psychological Assessment (Stratum A)

The Behavioral Assessment System for Children, 2nd Edition (BASC-2) was administered to parents, assessing for any effects on behavior or mood in children undergoing study therapy. The behavior system index (BSI) T-score (range 0-100) is reported for the BASC-2 assessment. Higher scores reflect greater behavioral problems. (NCT00539591)
Timeframe: Pretherapy, Week 4, Week 24, End of Therapy, and 6 Months Post End of Therapy

InterventionT score (Mean)
Pretherapy44.9
Week 445.9
Week 2444.2
End of Therapy47.2
6 Months After End of Therapy42.3

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ɑ Half Life of Pegylated Interferon ɑ-2B

"Pharmacokinetic (PK) analysis of pegylated ɑ-2b included only Stratum A patients who had PK studies performed.~Samples were analyzed for pegylated interferon ɑ-2b concentrations by using the VeriKine Human Interferon Alpha ELISA Kit following the manufacturer's instructions, and concentration-time data were analyzed by nonlinear-mixed effects modeling as implemented in NONMEM." (NCT00539591)
Timeframe: Before first dose, and 24, 96 and 168 hours after dose during weeks 5 and 28

Interventionhours (Median)
Peginterferon ɑ-2b/Non-Pegylated Interferon ɑ-2b24.8

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Area Under the Curve (AUC) of Pegylated Interferon ɑ-2B

"Pharmacokinetic (PK) analysis of pegylated ɑ-2b included only Stratum A patients who had PK studies performed.~Samples were analyzed for pegylated interferon ɑ-2b concentrations by using the VeriKine Human Interferon Alpha ELISA Kit following the manufacturer's instructions, and concentration-time data were analyzed by nonlinear-mixed effects modeling as implemented in NONMEM. AUC is given as Time 0 through infinity." (NCT00539591)
Timeframe: Before first dose, and 24, 96 and 168 hours after dose during weeks 5 and 28

Interventionpcg * hr/ml (Median)
Week 5 - First Dose50556
Week 28 - Steady State48480

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Area Under the Curve (AUC) of Interferon ɑ-2b

Samples were analyzed for interferon ɑ-2b concentrations by using the VeriKine Human Interferon Alpha ELISA Kit following the manufacturer's instructions, and concentration-time data were analyzed by nonlinear-mixed effects modeling as implemented in NONMEM. AUC is given as Time 0 to infinity. (NCT00539591)
Timeframe: Before first dose, and 1, 2, 4, 6, 8, 12, and 24 hours postinfusion

Interventionpcg * hr/ml (Median)
Peginterferon ɑ-2b/Non-Pegylated Interferon ɑ-2b5026

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Progression-free Survival

Defined as the duration of time from start of treatment to time of progression or death, whichever comes first. (NCT00544817)
Timeframe: 18 months

InterventionMonths (Median)
Combination Therapy6

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Objective Response

"The number of patients with complete or partial responses measured from the time of initial response to documented tumor progression. Radiologic response was defined using the Macdonald criteria.~The Macdonald criteria divides response into 4 types of response based on imaging (MRI) and clinical features, as follows: 1) complete response (CR); 2) partial response (PR); 3) stable disease (SD); and 4) progression (PD).~Criteria:~CR: disappearance of all enhancing disease (measurable and non-measurable) sustained for at least 4 weeks, no new lesions. No corticosteroids, clinically stable or improved.~PR: >=50% decrease of all measurable enhancing lesions, sustained for at least 4 weeks, no new lesions. Stable or reduced corticosteroids, clinically stable or improved.~SD: does not qualify for complete response, partial response or progression. Clinically stable.~PD: >= 25% increase in enhancing lesions, any new lesions. Clinical deterioration." (NCT00544817)
Timeframe: every 8 weeks until disease progression, estimated 18 months

Interventionparticipants (Number)
Combination Therapy13

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Overall Survival

Defined as Day 1 of protocol treatment to date of death from any cause. (NCT00544817)
Timeframe: 18 months

InterventionMonths (Median)
Combination Therapy12

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Overall Survival 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. (NCT00553150)
Timeframe: Up to 15 years

Interventionmonths (Median)
Phase II15.8

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Overall Survival at 12 Months (Phase II)

"The primary endpoint is overall survival at 12 months (OS12) after entry into this study. The proportion of successes will be estimated using the binomial point estimator (number of successes divided by the total number of evaluable patients) and the binomial 95% confidence interval estimated. A patient who is evaluable and survive more than 12 months (i.e. 365 days or more) after start of therapy will be classified as a success. Patients who die within 12 months after start of therapy will be considered to have failed." (NCT00553150)
Timeframe: at 12 months

Interventionproportion of participants (Number)
Phase II0.64

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Maximum Tolerated Dose (MTD) of Everolimus (RAD001) in Combination With Temozolomide (TMZ) and 3D-conformal Radiotherapy (RT) or Intensity-modulated Radiotherapy (IMRT) Followed by Adjuvant TMZ With or Without RAD001 (Phase I)

Patients were assessed during RT for dose-limiting toxicities (DLT), which were defined as failure to deliver greater than 75% of the planned doses of TMZ or RAD001 during RT, interruption of RT for more than 5 days because of toxicity, or the following: >= Grade 3 diarrhea or skin rash; >= Grade 4 neutropenia, leukopenia, or thrombocytopenia; >= Grade 4 hypertriglyceridemia, hypercholesterolemia, or hyperglycemia despite optimal medial management, other >= 3 non-hematologic events; or >= Grade 4 radiation dermatitis. Maximum tolerated dose (MTD) was defined a priori as the highest dose level at which 0 or 1 of 6 patients developed DLTs. The number of patients who developed DLTs are reported here by dose level, with the MTD reported in the statistical analysis section. (NCT00553150)
Timeframe: Up to 49 days

Interventionparticipants who developed DLTs (Number)
Phase I: Dose Level 01
Phase I: Dose Level 11
Phase I: Dose Level 21

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Time to Progression (Phase II)

Time-to-disease progression is defined as the time from start of study therapy to documentation of disease progression. Patients who die without documentation of progression will be considered to have had tumor progression at the time of death unless there is documented evidence that no progression occurred before death. Patients who fail to return for evaluation after beginning therapy will be censored for progression on the last day of therapy. Patients who experience major treatment violations will be censored for progression on the date of treatment violation occurred. The time-to-progression distribution will be estimated using the Kaplan-Meier method. Progression is defined as at least a 25% increase in product of perpendicular diameters of contrast enhancement or mass or unequivocal increase in size of contrast enhancement or increase in mass effect as agreed upon independently by primary physician and quality control physicians or appearance of new lesions. (NCT00553150)
Timeframe: Up to 5 years

Interventionmonths (Median)
Phase II6.4

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Response Rate, as Measured in Patients Receiving FLT-PET Imaging (Phase II)

The response rate is defined as the percentage of patients receiving F-fluorothymidine positron emission tomography (FLT-PET) imaging whose cancer shrinks or disappears after treatment. A reduction in standardized uptake value (SUV) of 30% or greater in the T1-post-gadolinium scan volume of interest (T1-gad VOI) or the total tumor VOI will be considered a responsive tumor. (NCT00553150)
Timeframe: Up to 5 years

Interventionpercentage of participants (Number)
Phase II44.4

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Progression-free-survival at 6 Months (Phase II)

Progression-free-survival at 6 months: is the proportion of patients alive and progression-free at 6 months after start of regimen. This proportion will be estimated using the binomial point estimator and the binomial 95% confidence interval estimated. Progression is defined as at least a 25% increase in product of perpendicular diameters of contrast enhancement or mass or unequivocal increase in size of contrast enhancement or increase in mass effect as agreed upon independently by primary physician and quality control physicians or appearance of new lesions. (NCT00553150)
Timeframe: at 6 months

Interventionproportion of participants (Number)
Phase II0.52

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Time to Disease Progression

Time to disease progression was defined as the time from registration to documentation of disease progression. Disease progression was measured according to the RECIST criteria. Progression: At least a 20 percent increase in the sum of of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT00568451)
Timeframe: up to 2 years

InterventionDays (Median)
Overall74

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Survival Time

Survival time was defined as the time from registration to death due to any cause. (NCT00568451)
Timeframe: up to 2 years

InterventionMonths (Median)
Overall12.5

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Number of Participants With an Objective Tumor Status of Either a Complete Response(CR) or Partial Response (PR), According to RECIST (Response Evaluation Criteria in Solid Tumors) Criteria

"Response that was noted on 2 consecutive evaluations for at least 4 weeks apart.~CR: Disappearance of all target lesions; PR: At least a 30 percent of decrease in the sum of the longest diameter (LD) of target lesions taking as reference the baseline sum LD. Target lesions: All measurable lesions up to a maximum of 10 lesions representative of all involved organs." (NCT00568451)
Timeframe: Every other cycle of therapy (cycle=4 weeks) for the first 6 cycles of treatment

Interventionparticipants (Number)
TMZ (Previously Treated)0
TMZ (Chemo Naive)2

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Progression-free Survival at 6-months

(NCT00575887)
Timeframe: Until progression

Interventionpercentage of participants (Number)
Temozolomide17.3

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To Determine the Safety and Tolerability of This Drug Combination.

To determine the safety and tolerability of RAD001 when given in combination with temozolomide in patients with advanced pancreatic neuroendocrine tumors. (NCT00576680)
Timeframe: 2 years

InterventionParticipants (Count of Participants)
Grade 3 or 4 LymphopeniaGrade 3 or 4 thrombocytopeniaGrade 3 or 4 mucositisGrade 3 or 4 hyperglycemiaGrade 3 or 4 AST IncreaseGrade 3 or 4 Leukocyte decrease
Temozolomide and Everolimus1971847

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Progression-free Survival

To determine progression-free survival when RAD001 is given in combination with temozolomide in patients with advanced pancreatic neuroendocrine tumors. Progression-free survival is defined as time from start of therapy until disease progression, as defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST), as 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 death. (NCT00576680)
Timeframe: 2 years

Interventionmonths (Median)
Temozolomide and Everolimus15.4

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Response Rate

To determine the objective response rate by RECIST criteria of RAD001 in combination with temozolomide in patients with advanced pancreatic neuroendocrine tumors. Partial response (PR) by these criteria is 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. Progressive disease (PD) is 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 the treatment started or the appearance of one or more new lesions. Stable Disease (SD) is defined as neither sufficient decrease to qualify for partial response nor sufficient increase to qualify for progressive disease, taking as reference the smallest sum longest diameter since the treatment started. (NCT00576680)
Timeframe: 2 years

InterventionParticipants (Count of Participants)
Temozolomide and Everolimus16

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Percentage of Participants With Distant Brain Failure (DBF) at One Year

Patients developing distant brain failure (DBF) at one year. An approximation method was used to arrive at the reported percentage. (NCT00582075)
Timeframe: 1 years

Interventionpercentage of participants (Number)
Radiosurgery 15-24 Gy + Adjuvant Temozolomide37

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Overall Survival

(NCT00582075)
Timeframe: 2 years

Interventionweeks (Median)
Radiosurgery 15-24 Gy + Adjuvant Temozolomide31

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Overall Objective Response (Complete Response or Partial Response)

"The Response Evaluation Criteria in Solid Tumors (RECIST) will be used to determine treatment response.~Clinical Complete Response (CRc) Disappearance of all target lesions and non-measurable disease.~Pathological Complete Response (CRp) A CRc in which a lymph node dissection done after completing temozolomide treatment shows no pathological evidence of melanoma. Partial Response (PR) A greater or equal then 30% in the sum of the longest diameter of all target lesions relative to baseline measurement" (NCT00588341)
Timeframe: 2 years

Interventionparticipants (Number)
Complete Response (CR)Partial Response (PR)Non Responder
Treatment2215

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Progession Free Survival

To determine the duration of disease control of newly diagnosed pure and mixed anaplastic oligodendrogliomas treated with dose-intensive chemotherapy requiring hematopoietic stem cell support. (NCT00588523)
Timeframe: 2 years

Intervention% of participants without progression (Number)
Participants With Newly Diagnosed Anaplastic Oligodendroglioma85.7

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Number of Participants Evaluated for Toxicities

(NCT00588523)
Timeframe: up to 2 years

InterventionParticipants (Count of Participants)
Participants With Newly Diagnosed Anaplastic Oligodendroglioma60

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Objective Response

The best clinical response rates determined and 95% confidence intervals obtained using the exact binomial distribution. (NCT00590681)
Timeframe: Up to 3 years

Interventionpercentage of participants (Number)
Complete ResponsePartial ResponseStable DiseaseProgression
Treatment22.519.411.36.5

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Overall Survival

(NCT00590681)
Timeframe: Up to 3 years

Interventionyears (Median)
Treatment1.68

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Safety of Avastin in Combination With Temozolomide in This Study Population

Toxicity rates (limited toxicity to grade 4+) (NCT00590681)
Timeframe: Up to 3 years

InterventionParticipants (Count of Participants)
ApneaBone infectionCreatine phosphokinase increasedDICDeathDepressionFatigueFebrile neutropeniaHypocalcemiaIschemia cerebrovascularLeukocytesLeukopeniaMetabolicMusculoskeletalNeutrophilsPlateletsPleural effusionProteinuriaSeizureSoft tissue infectionThrombosisLymphopenia
Treatment1111111111121122121111

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Duration of Response

Duration of response time from the first assessment of CR or PR until disease progression or death from any cause, whichever occurs first, event-free survival probability at two years assessed by Kaplan-Meier survivor function (NCT00590681)
Timeframe: Up to 2 years

Interventionprobability (Number)
Treatment38.8

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Progression-free Survival (PFS)

(NCT00590681)
Timeframe: Up to 3 years

Interventionyears (Median)
Treatment0.96

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Duration of Objective Clinical Responses

Duration of Response (Objective Clinical Responses) (NCT00591370)
Timeframe: 24 weeks after ending treatment

Interventionmonths (Median)
Temozolomide (TMZ)7.7

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Overall Survival

Overall survival at 18 months post treatment (NCT00591370)
Timeframe: 18 months after ending treatment

Interventionpercentage of participants (Number)
Temozolomide (TMZ)27

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Determine the Overall Objective Response Rate (CR and PR).

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. (NCT00591370)
Timeframe: From start of treatment through 24 weeks after ending treatment

Interventionparticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgression of Disease
Temozolomide (TMZ)061627

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Number of Patients Experiencing a Central Nervous System (CNS) Hemorrhage or a Systemic Hemorrhage

Number of times a CNS hemorrhage or systemic hemorrhage was experienced (NCT00597402)
Timeframe: 55 months

Interventionparticipants (Number)
Gr.2 Central Nervous System (CNS) HemorrhageGr.3 Central Nervous System (CNS) HemorrhageGr.4 Central Nervous System (CNS) HemorrhageGr.5 Central Nervous System (CNS) HemorrhageGr.2 Systemic HemorrhageGr.3 Systemic HemorrhageGr.4 Systemic HemorrhageGr.5 Systemic Hemorrhage
Avastin, Radiation, Temozolomide, and Irinotecan10101000

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12-month Progression-free Survival (PFS)

Percentage of participants surviving twelve months from the start of study treatment without progression of disease. PFS was defined as the time from the date of study treatment initiation to the date of the first documented progression according to the Macdonald criteria, or to death due to any cause. (NCT00597402)
Timeframe: 12 months

Interventionpercentage of participants (Number)
Avastin, Radiation, Temozolomide, and Irinotecan63.2

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16-month Overall Survival (OS)

Percentage of participants surviving sixteen months from the start of study treatment. OS was defined as the time from the date of study treatment initiation to the date of death due to any cause. (NCT00597402)
Timeframe: 16 months

Interventionpercentage of participants (Number)
Avastin, Radiation, Temozolomide, and Irinotecan64.8

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Number of Patients Experiencing a Grade ≥ 4 Hematologic or Grade ≥ 3 Non-hematologic Toxicity

Number of times a grade ≥ 4 hematologic or grade ≥ 3 non-hematologic toxicity was experienced (NCT00597402)
Timeframe: 55 months

Interventionparticipants (Number)
Grade ≥ 4 Hematologic ToxicitiesGrade ≥3 Non-hematologic Toxicities
Avastin, Radiation, Temozolomide, and Irinotecan2049

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Safety and Toxicity of Combination

Number of participants experiencing a toxicity of at least grade 3 that was deemed possibly, probably, or definitely related to the treatment. (NCT00597493)
Timeframe: 16 months

Interventionparticipants (Number)
Sorafenib + Temozolomide19

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Pharmacokinetics: T-max

Blood sampling for sorafenib pharmacokinetics was performed on days 1 and 28 of cycle 1 and was obtained before and at 0.5, 1, 2, 4, 6, 8, and 24 h after the morning dose. T-max refers to time to maximum concentration. The pharmacokinetics of those patients taking enzyme-inducing antiepileptic drugs (EIAED) and those who were not were analyzed separately. (NCT00597493)
Timeframe: 13 months

Interventionhours (Median)
EIAEDs-Day 18.2
EIAEDs-Day 282.1
Non-EIAEDs-Day 124.0
Non-EIAEDs-Day 284.2

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Pharmacokinetics: C-max

Blood sampling for sorafenib pharmacokinetics was performed on days 1 and 28 of cycle 1 and was obtained before and at 0.5, 1, 2, 4, 6, 8, and 24 h after the morning dose. C-max refers to maximum plasma concentration. The pharmacokinetics of those patients taking enzyme-inducing antiepileptic drugs (EIAED) and those who were not were analyzed separately. (NCT00597493)
Timeframe: 13 months

Interventionug/L (Geometric Mean)
EIAEDs-Day 13397.3
EIAEDs-Day 283813.9
Non-EIAEDs-Day 13155.1
Non-EIAEDs-Day 288118.8

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Pharmacokinetics: AUC-24

Blood sampling for sorafenib pharmacokinetics was performed on days 1 and 28 of cycle 1 and was obtained before and at 0.5, 1, 2, 4, 6, 8, and 24 h after the morning dose. AUC-24 refers to area under the plasma concentration-time curve from 0 to 24 hours. The pharmacokinetics of those patients taking enzyme-inducing antiepileptic drugs (EIAEDs) and those who were not were analyzed separately. (NCT00597493)
Timeframe: 13 months

Interventionug*H/L (Geometric Mean)
EIAEDs-Day 145309.7
EIAEDs-Day 2847148.2
Non-EIAEDs-Day 145238.7
Non-EIAEDs-Day 28128820.8

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6 Month Progression Free Survival (PFS)

Percentage of participants surviving six months from the start of study treatment without progression of disease. PFS was defined as the time from the date of study treatment initiation to the date of the first documented progression according to the Macdonald criteria, or to death due to any cause. (NCT00597493)
Timeframe: 6 months

Interventionpercentage of patients (Number)
Sorafenib + Temozolomide9.4

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Overall Survival Rate

(NCT00602576)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Arm A12
Arm B18
Arm C5
Arm D17

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Rate of 6 Month 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 (NCT00602576)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Arm A18
Arm B15
Arm C4
Arm D12

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Response Rate

Response Rate as defined by 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. (NCT00602576)
Timeframe: Approximately 3 years

InterventionParticipants (Count of Participants)
Arm A8
Arm B6
Arm C0
Arm D8

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Response Rate (CR + CRi + LFS)

"Response determined per European LeukemiaNet response criteria:~CR = bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; absolute neutrophil count > 1.0 x 10e9/L; platelet count > 100 x 10e9/L; and independence of red cell transfusions.~CRi = all CR criteria except for residual neutropenia (< 1.0 x 10e9/L) or thrombocytopenia (< 100 x 10e9/L)].~Morphologic leukemia-free state (LFS) = bone marrow blasts <5%; absence of blasts with Auer rods; absence of extramedullary disease; with no hematologic recovery required.~Relapse = bone marrow blasts >5%; reappearance of blasts in the blood; or development of extramedullary disease." (NCT00611247)
Timeframe: up to 2 months

Interventionparticipants (Number)
Methylated AGAT Promoter (Group 1)3
Un-Methylated AGAT Promoter (Group 2)10

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Response Rate

The proportion of subjects with complete or partial response as determined by a modification of the RANO (Response Assessment in Neuro-Oncology) criteria. A confirmation of response was not required. Complete Response was defined as complete disappearance on MR/CT of all enhancing tumor and mass effect, off all corticosteroids (or receiving only adrenal replacement doses), accompanied by a stable or improving neurologic examination, and maintained for at least 4 weeks. Partial Response was defined as greater than or equal to 50% reduction in tumor size on MR/CT by bi-dimensional measurement, on a stable or decreasing dose of corticosteroids, accompanied by a stable or improving neurologic examination, and maintained for at least 4 weeks. (NCT00612339)
Timeframe: 4 months

Interventionpercentage of patients (Number)
Avastin and Temozolomide24.4

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Radiographic Response

Percentage of participants with an objective response (complete response or partial response) based on modified Macdonald criteria. (NCT00613028)
Timeframe: 41 months

Interventionpercentage of participants (Number)
Temozolomide Arm0
Etoposide Arm0

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Median Progression-free Survival (PFS)

Time in months from the start of study treatment to the date of first progression according to Macdonald criteria, or to death due to any cause. Patients alive who had not progressed as of the last follow-up had PFS censored at the last follow-up date. Median PFS was estimated using a Kaplan-Meier curve. (NCT00613028)
Timeframe: 41 months

Interventionweeks (Median)
Temozolomide Arm4.1
Etoposide Arm8.1

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Median Overall Survival (OS)

Time in months from the start of study treatment to date of death due to any cause. Patients alive as of the last follow-up had OS censored at the last follow-up date. Median OS was estimated using a Kaplan-Meier curve. (NCT00613028)
Timeframe: 41 months

Interventionweeks (Median)
Temozolomide Arm12.6
Etoposide Arm19

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Grade 3 or Greater, Treatment Related, Non-hematologic Toxicities.

Incidence of ≥Grade 3 treatment related, non-hematologic toxicity (NCT00613028)
Timeframe: 41 months

Interventionparticipants (Number)
Temozolomide Arm1
Etoposide Arm2

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The Primary Outcome Measure is 6 Month Progression-free Survival.

Percentage of participants surviving six months from the start of study treatment without progression of disease. PFS was defined as the time from the date of study treatment initiation to the date of the first documented progression according to the Macdonald criteria, or to death due to any cause. (NCT00613028)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Temozolomide Arm0
Etoposide Arm7.7

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Overall Time of Survival

Time from initiation of study participation until death (NCT00617539)
Timeframe: Time from initiation of study participation until death or up to 3 years

InterventionDays (Median)
Irinotecan and Temozolomide146

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Number of Patients Whose Circulating Tumor Cells (CTCs) Decreased From >5 to <5 CTCs Per 7.5 mL

CTCs were measured in blood using the Cellsearch(R) assay in 14 of the 20 patients measured at baseline (NCT00617539)
Timeframe: CTCs drawn on cycle 1 day 1, collection at 8 week intervals on patients who did not progress on their 8 week scans up to 2 years

Interventionparticipants (Number)
Irinotecan and Temozolomide1

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Number of Patients With Objective Treatment Response (Complete or Partial) in the CNS

Imaging was performed at 8-week intervals to assess response to treatment. Patients with known or suspected leptomeningeal disease were deemed to have a complete response if CSF cytology converted to negative (if positive at baseline) and all meningeal enhancement or nodularity of brain and/or spine MRI resolved. A modified RECIST 1.0 criteria was used to assess CNS response for patients with new or progressing brain metastases. In this modified RECIST criteria, CNS lesions <1cm were not considered measurable, but were considered evaluable for response and progression. Progressive disease for patients with lesions <1 cm was defined as follows: growth of a lesion from less than or equal to 5 mm to greater than or equal to 10mm; or, growth of a 6-9 mm lesion by at least 5 mm in the case of non-target parenchymal brain metastases. (NCT00617539)
Timeframe: Baseline scan prior to study entry was performed within 14 days of cycle 1 day 1, then every 8 weeks from then until disease progression or up to 2 years

InterventionParticipants (Count of Participants)
Irinotecan and Temozolomide2

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Time to First Progression in CNS

"Imaging at 8-week intervals to assess response to treatment. A modified RECIST 1.0 criteria was used to assess response and time to progression in the CNS for patients with progressing brain metastases. In this modified RECIST criteria, CNS lesions <1cm were not considered measurable, but were considered evaluable for response and progression. Progressive disease for patients with lesions <1 cm was defined as follows: growth of a lesion from less than or equal to 5 mm to greater than or equal to 10mm; or, growth of a 6-9 mm lesion by at least 5 mm in the case of non-target parenchymal brain metastases.~If patient did not come back for a follow up scan after clinical deterioration, patient was only considered stable up to the time of the last scan per protocol and time to progression would be from cycle 1 day 1 to the last scan they completed that was stable." (NCT00617539)
Timeframe: Baseline scan prior to study entry was performed within 14 days of cycle 1 day 1, then every 8 weeks from then until disease progression or up to 2 years

InterventionDays (Median)
Irinotecan and Temozolomide70

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Number of Patients Experiencing a Clinical Benefit

The number of patients experiencing a clinical benefit is the sum of patients with an objective response plus patients with stable disease at ≥ 16 weeks from cycle 1 day 1 (first day of treatment). If a patient did not come back for a follow up scan after clinical deterioration, then they were only considered stable up to the time of the last scan they had per protocol. (NCT00617539)
Timeframe: From 1 day 1 (first day of treatment) every 8 weeks until scan shows disease progression or up to 2 years

InterventionParticipants (Count of Participants)
Irinotecan and Temozolomide7

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Progression-free Survival (PFS) Based on Tumor MGMT (O(6)-Methylguanine-DNA Methyltransferase) Promoter Methylation Status.

Progression-free survival data (obtained for Primary Outcome Measure) was correlated with tumor MGMT (O(6)-methylguanine-DNA methyltransferase) promoter methylation status, obtained from patients as part of the study. (NCT00619112)
Timeframe: First day of treatment until progression or until 6 months mark

Interventionweeks (Median)
Glioblastoma With Methylated MGMT8.14
Glioblastoma With Unmethylated MGMT7.57
Grade III Glioma With Methylated MGMT38.1
Grade III Glioma With Unmethylated MGMT48.6

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Patients With Tumors With Functional Alterations of the Mismatch Repair (MMR) System

PCR analysis of tumor tissue for microsatellite instability (MSI). Tissue was obtained during surgeries prior this study. (NCT00619112)
Timeframe: prior to start of study

InterventionParticipants (Count of Participants)
Glioblastoma0
Grade III Glioma0

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6 Month Progression-free Survival

Efficacy of dose-intense temozolomide treatment schedule, as measured by 6 months progression-free survival (NCT00619112)
Timeframe: First day of treatment until progression or until 6 months mark

Interventionpercentage of patients (Number)
Glioblastoma10
Grade III Glioma50

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Patients Progressing 6 Months After Temozolomide is Voluntarily Discontinued

(NCT00619112)
Timeframe: From beginning of voluntarily temozolomide discontinued up to 6 months

InterventionParticipants (Count of Participants)
Glioblastoma4
Grade III Glioma4

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Overall Survival

(NCT00619112)
Timeframe: up to 2 years after treatment

Interventionweeks (Median)
Glioblastoma21.6
Grade III Glioma100.6

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Patients Progressing After Two First-line Adjuvant Courses of Temozolomide

(NCT00619112)
Timeframe: After two first-line adjuvant courses of temozolomide

InterventionParticipants (Count of Participants)
Glioblastoma3
Grade III Glioma0

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Patients Progressing Within 6 Months After 6th Adjuvant Course of Temozolomide

(NCT00619112)
Timeframe: Within 6 months after 6th adjuvant course of temozolomide

InterventionParticipants (Count of Participants)
Glioblastoma4
Grade III Glioma1

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Tumor Response Rate, Calculated as a Percentage Along With it's 95% Confidence Interval

"A confirmed tumor response is defined to be a Complete Response or Partial Response noted~> as the objective status on 2 consecutive evaluations at least 8~> weeks apart. The proportion of tumor responses will be~> estimated by the number of confirmed tumor responses divided~> by the total number of evaluable patients.~> 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.~> Progression (PD): At least a 20% increase in the sum 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. responses will be calculated assuming that the number of~> confirmed tumor responses follows a binomial distribution." (NCT00626405)
Timeframe: Up to 5 years

Interventionpercentage of patients with response (Number)
Arm I23.8
Arm II33.3

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Progression-free Survival at 6 Months

The primary endpoint is the 6 month post registration Progression-free survival (PFS) rate. Progression-free survival time is defined as the time from registration to documentation of disease progression using the RECIST criteria. Patients who died without documentation of disease progression will be considered to have progressed at death unless there is sufficient documented evidence to conclude no progression occurred prior to death. All patients, who meet the eligibility criteria, sign a consent form, and start treatment will be included in the evaluation of the 6 month PFS rate. (NCT00626405)
Timeframe: at 6 months

Intervention% of patients alive and progression free (Number)
Arm I32.8
Arm II56.1

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Overall Survival

Overall 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. (NCT00626405)
Timeframe: Up to 5 years

InterventionMonths (Median)
Arm I12.3
Arm II13.9

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Progression-free Survival

Disease progression is defined as radiological or neurological/clinical progression (whichever occurs first); progression free survival (PFS) is the time interval between the date of randomization and the date of disease progression or death whichever occurs first. If neither event has been observed, the patient is censored at the date of the last follow up examination. Radiological progression was defined as increase of contrast enhancing area on MRI or CT scans of more than 25% as measured by two perpendicular diameters compared to the smallest measurements ever recorded for the same lesion by the same technique. The appearance of new lesions with or without contrast enhancement Neurological/clinical progression was defined as:decrease in WHO performance status,deterioration of neurological functions,appearance of signs/symptoms of increased intracranial pressure,and/or start of corticosteroid or increase of corticosteroid dosage by 50% for control of neurological symptoms. (NCT00626990)
Timeframe: from randomization till the date of disease progression or death (time till death is up to 10.9 years after patient enrollment in the study)

InterventionMonths (Median)
Absence of Concomitant TMZ20.9
Presence of Concomitant TMZ33.02
Absence of Adjuvant TMZ19.09
Presence of Adjuvant TMZ42.81

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Overall Survival as Measured From the Day of Randomization

The duration of survival is the time interval between randomization and the date of death due to any cause. Patients not reported dead or lost to follow up will be censored at the date of the last follow up examination. (NCT00626990)
Timeframe: from date from enrollment till the date of death (time till death is up to 10.9 years after patient enrollment in the study)

InterventionMonths (Median)
Absence of Concomitant Temozolomide (TMZ)60.42
Presence of Concomitant Temozolomide (TMZ)66.92
Absence of Adjuvant Temozolomide (TMZ)46.92
Presence of Adjuvant Temozolomide (TMZ)82.33

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Tolerability of Maintenance Temozolomide

Tolerability was defined as number of participants with any adverse event leading to study discontinuation and/or study drug discontinuation. (NCT00632203)
Timeframe: from Cycle 1 Day 1 of Standard First Line Systemic Therapy to the last time of follow-up (up to 6 cycles (168 days) of study treatment)

Interventionparticipants (Number)
Temozolomide Treatment5
ObservationNA

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Time to Radiological Central Nervous System (CNS) Progression

"Defined as CNS progression as measured by MRI.~Time to CNS progression was analyzed using the Kaplan-Meier method." (NCT00632203)
Timeframe: from Cycle 1 Day 1 of Standard First Line Systemic Therapy to radiological progression or the last known CNS progression-free date

Interventionmonths (Median)
Temozolomide TreatmentNA
ObservationNA

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Overall Survival

The overall survival was analyzed using the Kaplan-Meier method. (NCT00632203)
Timeframe: from Cycle 1 Day 1 of Standard First Line Systemic Therapy to the last time of follow-up

Interventionmonths (Median)
Temozolomide Treatment27.14
Observation22.54

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Number of Participants Who Had Brain Metastases

Brain Metastases were defined as radiological evidence of brain metastases on magnetic resonance imaging (MRI). (NCT00632203)
Timeframe: Up to 12 months (as measured from day 1 of cycle 1 of standard first-line systemic chemotherapy)

Interventionparticipants (Number)
Temozolomide Treatment4
Observation3

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Time to Progression

"The time to progression (per response evaluation criteria in solid tumors [RECIST]) was analyzed using the Kaplan-Meier method.~Definitions of response per RECIST:~Complete Response (CR): Disappearance of all target lesions.~Partial Response (PR): A decrease of at least 30% in the sum of the longest~diameter of target lesions.~Progressive Disease (PD): An increase of at least 20% in the sum of the longest~diameter of target lesions.~Stable Disease (SD): Neither sufficient shrinkage to qualify for partial response nor sufficient increase to qualify for progressive disease." (NCT00632203)
Timeframe: from Cycle 1 Day 1 of Standard First Line Systemic Therapy to progression or up to 6 cycles (168 days) of study treatment

Interventionmonths (Median)
Temozolomide Treatment11.70
Observation10.68

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Number of Days on Temozolomide Treatment

This outcome measure was only applicable to the temozolomide arm; the observation arm was therefore not analyzed. (NCT00638963)
Timeframe: Baseline to 24 Weeks

InterventionDays (Mean)
Temozolomide75

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Number of Participants Who Had at Least One Treatment Omission During Treatment

This outcome measure was only applicable to the temozolomide arm; the observation arm was therefore not analyzed. (NCT00638963)
Timeframe: Baseline to 24 Weeks

InterventionParticipants (Number)
Temozolomide2

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Total Dose of Temozolomide Taken

This outcome measure was only applicable to the temozolomide arm; the observation arm was therefore not analyzed. (NCT00638963)
Timeframe: Baseline to 24 Weeks

InterventionMilligrams (Mean)
Temozolomide9791.9

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Number of Participants Who Completed the Third Cycle of Treatment

This outcome measure was only applicable to the temozolomide arm; the observation arm was therefore not analyzed. (NCT00638963)
Timeframe: Baseline to 24 Weeks

InterventionParticipants (Number)
Temozolomide2

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Number of Participants Who Had at Least One Dose Reduction During Treatment

This outcome measure was only applicable to the temozolomide arm; the observation arm was therefore not analyzed. (NCT00638963)
Timeframe: Baseline to 24 Weeks

InterventionParticipants (Number)
Temozolomide3

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Humoral and Cellular Immune Response

Number of patients that developed a delayed-type hypersensitivity (DTH) response at following vaccination. Any skin reaction in response to the intradermal injection of the antigen was measured and recorded. A positive skin test was defined as > 5 mm induration (swelling). (NCT00643097)
Timeframe: 26 months

Interventionparticipants (Number)
Arm I (ACTIVATE)3
Arm II (ACT II STD)0
Arm III (ACT II DI)7

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Clinical Efficacy of Vaccination, in Terms of Progression-free Survival (PFS)

"Time in months from the start of study treatment to the date of first progression according to Macdonald criteria, or to death due to any cause. Patients alive who had not progressed as of the last follow-up had PFS censored at the last follow-up date. Median PFS was estimated using a Kaplan-Meier curve.~Macdonald criteria are standard criteria in neuro-oncology. Tumor assessment was made according to the adapted MacDonald criteria based on the combined evaluation of: 1) assessment of the MRI scan for measurable, evaluable, and new lesions (made by the independent external expert too), 2) overall assessment of neurological performance (made by the investigator), 3) concomitant steroid use (as reported by the investigator)." (NCT00643097)
Timeframe: 58 months

Interventionmonths (Median)
Arm I (ACTIVATE)14.2
Arm II (ACT II STD)12.1
Arm III (ACT II DI)11.6

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Response to Vaccination

The objective is to assess the duration of immunosuppressive cytokine secretion and to identify a receptive interval for active immunotherapy. Immunosuppression will determined by monitoring a panel of immunosuppressive serum/plasma cytokines longitudinally and by determining the response of each patient to Recombivax Hepatitis B (HB) vaccination. Response is defined as seropositive or seronegative to the Hepatitis B surface antigen. (NCT00643097)
Timeframe: 26 months

InterventionMonths (Mean)
Arm I (ACTIVATE)NA
Arm II (ACT II STD)NA
Arm III (ACT II DI)NA

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Toxicity to PEP-3 Vaccine Immunization

To assess for any potential toxicity to the PEP-3 vaccine immunization in patients with newly diagnosed glioblastoma, Common Terminology Criteria for Adverse Events (CTCAE) version 3.0 was used to tabulate any toxicities attributable to PEP-3. The number of patients with toxicity attributable to vaccine while on study are tabulated. (NCT00643097)
Timeframe: 26 months

Interventionparticipants (Number)
Arm I (ACTIVATE)4
Arm II (ACT II STD)1
Arm III (ACT II DI)7

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Radiographic Response

Responders on study are those with a best response of either CR or PR. Per Modified Macdonald Criteria for lesions assessed by MRI/CT: Complete Response (CR) = Complete disappearance of all measurable and evaluable disease, no new lesions, no evidence of non-evaluable disease, with no steroids. Partial Response (PR) >/= 50% decrease under baseline in the sum of products of perpendicular diameters of all measurable lesions, no progression of evaluable disease, no new lesions, with steroid dose @ time of response NCT00657267)
Timeframe: From patient registration until end of study, assessed up to 54 months

Interventionpercentage of participants evaluated (Number)
Partial Response13
Complete Response0

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6 Month Progression Free Survival

Progression is defined using Modified Macdonald Criteria , using a >/= 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR clear clinical worsening or failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00657267)
Timeframe: 6 months

Interventionpercentage of evaluable participants (Number)
12 Cycles of Dose-Dense Temozolomide (Single Arm Study)11

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Time to Progression.

Progression is defined using Modified Macdonald Criteria , using a >/= 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR clear clinical worsening or failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00657267)
Timeframe: From patient registration until end of study, assessed up to 54 months

Interventiondays (Median)
12 Cycles of Dose-Dense Temozolomide (Single Arm Study)56

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Overall Survival

(NCT00657267)
Timeframe: From patient registration until end of study, assessed up to 54 months

Interventionmonths (Median)
12 Cycles of Dose-Dense Temozolomide (Single Arm Study)11.7

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Response

Response rate by RECIST (NCT00667953)
Timeframe: through study completion, an average of 1 year

InterventionParticipants (Count of Participants)
Arm A:1

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Safety - Grade 3 or 4 Adverse Events

Number of reported grade 3 or 4 adverse events (NCT00667953)
Timeframe: through study completion, an average of 1 year

InterventionAdverse Events (Number)
Arm A:20

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Response Rate

Number of patients with reduction in tumor burden of a predefined amount (NCT00669669)
Timeframe: Up to 66 months

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)1

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Time to Progression

From the first day of treatment (transplant) until unequivocal progression is documented, assessed up to 66 months. (NCT00669669)
Timeframe: Up to 66 months.

Interventionmonths (Median)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)5.5

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Duration of Response

From the onset of temozolomide to the date at which unequivocal disease progression, assessed up to 65 months. (NCT00669669)
Timeframe: Up to 65 months

Interventionmonths (Median)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)4.5

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Gene Transfer Efficiency After Chemotherapy

Assessed by gene marking in peripheral blood after chemoselection. Gene marking is assessed in whole blood by quantitative PCR and reported as a vector copy number (VCN) or the average copies of integrated transgene per cell. The units here will be reported as copies/cell. (NCT00669669)
Timeframe: Up to 59 months

Interventioncopies/cell (Mean)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)0.50

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Gene Transfer Efficiency

Assessed by gene marking in peripheral blood prior to chemoselection. Gene marking is assessed in whole blood by quantitative PCR and reported as a vector copy number (VCN) or the average copies of integrated transgene per cell. The units here will be reported as copies/cell. (NCT00669669)
Timeframe: Up to 59 months

Interventioncopies/cell (Mean)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)0.78

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Number of Participants Dose-limiting Toxicity (DLT)

Defined as any grade 4 nonhematopoietic toxicity that is likely related to the investigational procedures (Part I) (NCT00669669)
Timeframe: Up to 6 weeks after infusion

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)1

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Number of Participants That Survived

From the first day of treatment until death, assessed up to 74 months. (NCT00669669)
Timeframe: Up to 74 months

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)0

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Number of Participants With Chemoprotection

assessed by the ability to increase the Temozolomide dose beyond 472 mg/m^2 (NCT00669669)
Timeframe: Up to 66 months

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)2

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Number of Participants With Chemoselection

assessed by the increase in peripheral blood Vector Copy Number (VCN), the average copies of integrated transgene per cell, after chemotherapy (NCT00669669)
Timeframe: Up to 59 months

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)4

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Number of Participants With Retrovirus or Leukemia

Replication competent retrovirus or diagnosis of leukemia (NCT00669669)
Timeframe: Up to 2 years after infusion

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy, Autologous Stem Cell Transplant)0

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Adverse Events With an Incidence of Greater Than or Equal to 20%

Safety was assessed from the start of administration during the concomitant radiotherapy phase until 30 days after the completion of administration of monotherapy. Adverse events were classified under the system organ class using MedDRA-J Version 11.0. (NCT00684567)
Timeframe: until 30 days after the completion of administration of monotherapy

InterventionParticipants (Number)
alopecianauseaanorexiaconstipationmalaiserashweight decreasedheadachevomitingdry skinnasopharyngitisdiarrheaconvulsionpruritusneutrophil count decreasedwound complication
Radiotherapy/Temozolomide251717151411111098877666

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Number of Participants With Progression Free Survival (PFS) for 1 Year

Administration of SCH 52365 was continued until progression was observed (progression was judged by the investigator based on MRI and clinical symptoms). (NCT00684567)
Timeframe: 1 year after the start of admininstration in the concomitant radiotherapy phase

InterventionParticipants (Number)
Radiotherapy/Temozolomide11

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Number of Participants With a Response (Complete Response [CR] + Partial Response [PR]) in Terms of Overall Tumor Response

"CR = measurable lesion disappeared.~PR = total sum of lesions measurable in bidimension decreased by 50% or more on whole and no secondary progression attributable to tumor was noted. No onset of new lesion." (NCT00684567)
Timeframe: 1 year after the start of administration in the concomitant radiotherapy phase

InterventionParticipants (Number)
Radiotherapy/Temozolomide6

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Abnormal Changes in Laboratory Test Values With an Incidence of Greater Than or Equal to 20%

Safety was assessed from the start of administration during the concomitant radiotherapy phase until 30 days after the completion of administration of monotherapy. (NCT00684567)
Timeframe: until 30 days after the completion of administration of monotherapy

InterventionParticipants (Number)
lymphocyte count decreasedwhite blood cell count decreasedeosinophil percentage increased
Radiotherapy/Temozolomide241410

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Adverse Drug Reactions With an Incidence of Greater Than or Equal to 20%

Safety was assessed from the start of administration during the concomitant radiotherapy phase until 30 days after the completion of administration of monotherapy. (NCT00684567)
Timeframe: until 30 days after the completion of administration of monotherapy

InterventionParticipants (Number)
constipationnauseavomitingneutrophil count decreasedweight decreasedmalaiseanorexia
Radiotherapy/Temozolomide151166679

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Relationship Between MGMT Status and Therapy Response: Overall Survival Rate for the MGMT Positive Group

"MGMT was measured by IHC.~OS rate was defined as the percentage of participants who were still alive 6, 12, & 18 months after starting study treatment.~OS was calculated by the Kaplan-Meier method." (NCT00686725)
Timeframe: 6, 12, & 18 months

,
Interventionpercentage of participants (Number)
6 months12 months18 months
Temozolomide + Radiation80.869.336.9
Temozolomide Alone, Then Temozolomide + Radiation89.282.866.2

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Relationship Between MGMT Status and Therapy Response: Overall Survival Rate for the MGMT Negative Group

"MGMT was measured by IHC.~OS rate was defined as the percentage of participants who were still alive 6, 12, & 18 months after starting study treatment.~OS was calculated by the Kaplan-Meier method." (NCT00686725)
Timeframe: 6, 12, & 18 months

,
Interventionpercentage of participants (Number)
6 months12 months18 months
Temozolomide + Radiation87.557.744.9
Temozolomide Alone, Then Temozolomide + Radiation95.881.426.7

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Relationship Between O6-methylguanine-DNA Methyltransferase (MGMT) Status and Therapy Response: Overall Survival for the MGMT Positive Group

"MGMT was measured by immunohistochemistry (IHC).~OS was defined as the length of time from the start of treatment that 1/2 of the participants were still alive.~OS was calculated by the Kaplan-Meier method." (NCT00686725)
Timeframe: Up to 2 years

Interventionmonths (Median)
Temozolomide + Radiation14.4
Temozolomide Alone, Then Temozolomide + Radiation17.49

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Relationship Between MGMT Status and Therapy Response: PFS for the MGMT Positive Group

"MGMT was measured by IHC.~PFS: The length of time during and after treatment that a participant lived with the cancer but it does not get worse.~PFS was calculated by the Kaplan-Meier method." (NCT00686725)
Timeframe: Up to 2 years

Interventionmonths (Median)
Temozolomide + Radiation10.04
Temozolomide Alone, Then Temozolomide + Radiation11.19

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Relationship Between MGMT Status and Therapy Response: PFS for the MGMT Negative Group

"MGMT was measured by IHC.~PFS: The length of time during and after treatment that a participant lived with the cancer but it does not get worse.~PFS was calculated by the Kaplan-Meier method." (NCT00686725)
Timeframe: Up to 2 years

Interventionmonths (Median)
Temozolomide + Radiation11.11
Temozolomide Alone, Then Temozolomide + Radiation10.46

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Objective Tumor Assessment After Surgery: Overall Response

"Overall response was based on neuroimaging (magnetic resonance imaging [MRI]), clinical neurological examination, and steroid administration.~It was assessed as follows:~Complete Response (CR): Disappearance of all enhancing tumor (measurable~or non-measurable), no corticosteroid use, and neurologically stable or~improved.~Partial Response (PR): ≥50% reduction in size of enhancing tumor~(measurable or non-measurable) for any measurable lesions or definite~improvement for any non-measurable lesions, corticosteroid dosage stable or~reduced, and neurologically stable or improved.~Progressive Disease (PD): ≥25% increase in contrast enhancement for any~measurable lesions or definite worsening for any non-measurable lesions, or~any new tumor on MRI scans, at an increased dose of corticosteroid, with or without neurologic progression. Clinical or radiological worsening resulting from other than tumor factors were excluded.~Stable Disease (SD): All other situations." (NCT00686725)
Timeframe: Up to 2 years

,
Interventionparticipants (Number)
CRPRSDPDNo overall response data available
Temozolomide + Radiation103835
Temozolomide Alone, Then Temozolomide + Radiation004741

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Relationship Between MGMT Status and Therapy Response: Overall Survival for the MGMT Negative Group

"MGMT was measured by IHC.~OS was defined as the length of time from the start of treatment that 1/2 of the participants were still alive.~OS was calculated by the Kaplan-Meier method." (NCT00686725)
Timeframe: Up to 2 years

Interventionmonths (Median)
Temozolomide + Radiation13.81
Temozolomide Alone, Then Temozolomide + Radiation15.12

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Progression-Free Survival (PFS)

"PFS was defined as the length of time from randomization to disease progression (the length of time during which the cancer did not get worse) or death.~PFS was calculated by the Kaplan-Meier method." (NCT00686725)
Timeframe: Up to 2 years

Interventionmonths (Median)
Temozolomide + Radiation10.38
Temozolomide Alone, Then Temozolomide + Radiation8.74

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Overall Survival (OS)

"OS was defined as the time from randomization to death.~OS was calculated by the Kaplan-Meier method." (NCT00686725)
Timeframe: Up to 2 years

Interventionmonths (Median)
Temozolomide + Radiation13.17
Temozolomide Alone, Then Temozolomide + Radiation17.58

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Number of Participants With CR, PR, or MLFS Who Received Modified Low Dose Maintenance Therapy (100 mg/m^2/Day x21 Days of Each 28 Day Cycle) and Experienced Toxicity

Toxicity was defined as any adverse event experienced by a participant regardless of causal relationship with study treatment. An adverse event (AE) was defined as any untoward medical occurrence in a participant administered a pharmaceutical product, biologic (at any dose), or medical device, which did not necessarily have a causal relationship with the treatment. Adverse events may have included the onset of new illness and/or the exacerbation of preexisting conditions. (NCT00687323)
Timeframe: From first dose to 30 days after last dose of study drug (up to 67 weeks)

Interventionparticipants (Number)
Temozolomide1

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Number of Previously Untreated Participants With Low O6-Methylguanine Methyltransferase (MGMT) Expression

Low MGMT expression was defined as MGMT/β-actin ratio < 0.2. MGMT & β-actin are cancer biomarkers. (NCT00687323)
Timeframe: Baseline

Interventionparticipants (Number)
Temozolomide81

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Clinical Response at the End of Temozolomide Induction

"Complete Response (CR): < 5% blasts in normocellular bone marrow (BM); Absolute Neutrophil Count (ANC) > 1.0 x 10^9/L, platelets > 100 x 10^9/L, and no extramedullary disease.~CR with incomplete platelet recovery (CRp): All the criteria of CR but with platelets < 100 x 10^9/L but ≥ 50 x 10^9/L and platelet transfusion independent.~Morphologic leukemia-free state (MLFS): complete clearance of blasts from marrow and blood, but criteria for CR or CRp not met.~Partial response (PR): decrease ≥ 50% BM blasts. Minimal Response (MR): decrease ≥ 25% but <50% BM blasts." (NCT00687323)
Timeframe: at the end of each cycle (approximately 4 weeks post start of cycle), up to a maximum 63 weeks

Interventionparticipants (Number)
CRCRpMLFSPRMR
Temozolomide102487

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Progression-free Survival for Participants Achieving PR, MLSF, or MR

Progression-free survival was defined as time to disease progression. Morphologic leukemia-free state (MLFS): complete clearance of blasts from marrow and blood, but criteria for CR or CRp not met. Partial response (PR): decrease ≥ 50% BM blasts. Minimal Response (MR): decrease ≥ 25% but <50% BM blasts. (NCT00687323)
Timeframe: Start of treatment until disease progression [up to 1 year after treatment ends (up to 115 weeks)]

Interventionmonths (Median)
Temozolomide1.6

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Overall Survival (OS) in Participants Achieving CR or CRp and Proceeding to Reduced Dose-intensity Maintenance Therapy With Temozolomide

"OS was defined as the time from start of treatment until death or end of study.~Complete Response (CR): < 5% blasts in normocellular bone marrow (BM); Absolute Neutrophil Count (ANC) > 1.0 x 10^9/L, platelets > 100 x 10^9/L, and no extramedullary disease. CR with incomplete platelet recovery (CRp): All the criteria of CR but with platelets < 100 x 10^9/L but ≥ 50 x 10^9/L and platelet transfusion independent." (NCT00687323)
Timeframe: Start of treatment until death or end of study [up to 1 year after treatment ends (up to 115 weeks)]

Interventionmonths (Median)
Temozolomide21.4

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Duration of Response in Participants Achieving Complete Response (CR) and Proceeding to Reduced Dose-intensity Maintenance Therapy With Temozolomide

Complete Response (CR): < 5% blasts in normocellular bone marrow (BM); Absolute Neutrophil Count (ANC) > 1.0 x 10^9/L, platelets > 100 x 10^9/L, and no extramedullary disease. (NCT00687323)
Timeframe: Up to 1 year after treatment ends (up to 115 weeks)

InterventionDays (Median)
Temozolomide408

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Relapse-free Survival in Participants Achieving CR or CRp and Proceeding to Reduced Dose-intensity Maintenance Therapy With Temozolomide

Relapse-free survival was defined as time to disease progression. Complete Response (CR): < 5% blasts in normocellular bone marrow (BM); Absolute Neutrophil Count (ANC) > 1.0 x 10^9/L, platelets > 100 x 10^9/L, and no extramedullary disease. CR with incomplete platelet recovery (CRp): All the criteria of CR but with platelets < 100 x 10^9/L but ≥ 50 x 10^9/L and platelet transfusion independent. (NCT00687323)
Timeframe: Start of treatment until disease progression [up to 1 year after treatment ends (up to 115 weeks)]

Interventionmonths (Median)
Temozolomide10.5

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European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Brain Module (EORTC QLQ-BN20) Sub-scale Scores

The QLQ-BN20 is a questionnaire specifically designed as the QLQ-C30 supplement for the evaluation of quality of life in brain tumor participants. It includes 4 multi-item sub-scales: future uncertainty, visual disorder, motor dysfunction, communication deficits, and 7 single-item scales: headaches, seizures, drowsiness, itchy skin, hair loss, weakness of legs, and bladder control. All items are rated on a 4-point Likert-type scale ('1=not at all', '2=a little', '3=quite a bit' and '4=very much'), and are linearly transformed to a 0-100 scale, with higher scores indicating more severe symptoms. (NCT00689221)
Timeframe: Up to 50 months

,
Interventionunits on a scale (Mean)
Future Uncertainty (n=68, 86)Visual Disorder (n=68, 85)Motor Dysfunction (n=68, 86)Communication Deficit (n=68, 86)Headaches (n=68, 86)Seizures (n=68, 87)Drowsiness (n=66, 87)Itchy Skin (n=68, 86)Hair Loss (n=66, 86)Weakness of Legs (n=67, 85)Bladder Control (n=67, 85)
Cilengitide + Temozolomide + Radiotherapy44.4912.9927.4526.1425.989.3138.389.8013.1324.3819.40
Temozolomide + Radiotherapy39.3117.7823.3919.9621.718.0535.2513.5715.1220.3910.20

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European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC QLQ-C30) Sub-scale Scores

The EORTC QLQ-C30 is a questionnaire including following sub-scales: global health status, functional scales (physical functioning, role functioning, emotional functioning, cognitive functioning, and social activity), symptom scales (fatigue, nausea and vomiting, and pain) and single items (dyspnoea, insomnia, appetite loss, constipation, diarrhoea and financial difficulties). Scores are averaged for each scale and transformed to 0-100 scale; higher score indicates better quality of life on global health status and functional scales and worse quality of life on symptom scales and financial difficulty scale. (NCT00689221)
Timeframe: Up to 50 months

,
Interventionunits on a scale (Mean)
Global Health Status (n=71, 92)Physical Functioning (n=71, 92)Role Functioning (n=71, 92)Emotional Functioning (n=71, 93)Cognitive Functioning (n=70, 93)Social Activity (n=71, 93)Fatigue (n=71, 92)Nausea and Vomiting (n=71, 93)Pain (n=71, 93)Dyspnoea (n=71, 92)Insomnia (n=71, 91)Appetite Loss (n=71, 92)Constipation (n=71, 93)Diarrhoea (n=70, 92)Financial Difficulties (n=71, 93)
Cilengitide + Temozolomide + Radiotherapy54.3465.7056.3467.4964.0556.3444.3710.3322.3015.9620.6621.1318.786.6727.23
Temozolomide + Radiotherapy55.4367.4656.3467.0065.4162.7239.737.7124.3713.0420.5115.9413.984.3522.94

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Number of Participants With AEs Belonging to Standardized Medical Dictionary for Regulatory Activities (MedDRA) Queries (SMQs) Thromboembolic Events and Hemorrhage With NCI-CTC Toxicity Grade 3 or 4

Thromboembolic events (standardized MedDRA query [SMQ]) Grade 3 or 4 AEs encompassed hemiparesis and cerebrovascular accident, pulmonary embolism, and deep vein thrombosis. Thromboembolic events (SMQ) of any grade and of Grade 3 or 4 were generally more frequent in the Cilengitide + Temozolomide/Radiotherapy group than in the Temozolomide/Radiotherapy group but were still in the expected range of this patient population The severity of AEs was assessed according to the National Cancer Institute-Common Toxicity Criteria (NCI-CTCAE) (version 3.0): Grade 1=mild, Grade 2=moderate, Grade 3=severe, Grade 4=life threatening or disabling. Note: Death (Grade 5) was regarded as an outcome. (NCT00689221)
Timeframe: Time from first dose up to 28 days after last dose of study treatment, reported between day of first participant randomized, that is, Sep 2008 until cut-off date (19 Nov 2012)

,
InterventionParticipants (Number)
SMQ:Thromboembolic eventsSMQ: Hemorrhage
Cilengitide + Temozolomide + Radiotherapy354
Temozolomide + Radiotherapy234

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Number of Participants With Change From Baseline in Work Status at End of Study

Number of participants with change from baseline in work status (working full time [FT], part-time [PT], unemployed/retired [U/R]) at end of study (EOS) (up to cut-off date, [19 Nov 2012]) was reported. For the category 'part-time', the following sub-categories were defined: part-time due to basic disease (PT1); part-time not due to basic disease (PT2); part-time reason not known (PT3). (NCT00689221)
Timeframe: Baseline, End of study (up to cut-off date, [19 Nov 2012])

,
Interventionparticipants (Number)
Baseline: FT, EOS: FTBaseline: FT, EOS: PT1Baseline: FT, EOS: PT2Baseline: FT, EOS: PT3Baseline: FT, EOS: U/RBaseline: PT1, EOS: FTBaseline: PT1, EOS: PT1Baseline: PT1, EOS: PT2Baseline: PT1, EOS: PT3Baseline: PT1, EOS: U/RBaseline: PT2, EOS: FTBaseline: PT2, EOS: PT1Baseline: PT2, EOS: PT2Baseline: PT2, EOS: PT3Baseline: PT2, EOS: U/RBaseline: PT3, EOS: FTBaseline: PT3, EOS: PT1Baseline: PT3, EOS: PT2Baseline: PT3, EOS: PT3Baseline: PT3, EOS: U/RBaseline: U/R, EOS: FTBaseline: U/R, EOS: PT1Baseline: U/R, EOS: PT2Baseline: U/R, EOS: PT3Baseline: U/R, EOS: U/RBaseline: Missing, EOS: FTBaseline: Missing, EOS: PT1Baseline: Missing, EOS: PT2Baseline: Missing, EOS: PT3Baseline: Missing, EOS: U/RBaseline: Missing, EOS: Missing
Cilengitide + Temozolomide + Radiotherapy3210243300900015000005510199000011
Temozolomide + Radiotherapy61002221001210004000008710191000011

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Progression Free Survival (PFS) Time - Investigator and Independent Read

"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. Investigator read is the assessment of all imaging by the treating physician at the local trial site and Independent Read is the assessment of all imaging centrally by an Independent Review Committee (IRC). Investigator's assessed progression according to MacDonald criteria and IRC by Response Assessment in Neuro-Oncology Working Group (RANO) criteria using Gadolinium-enhanced magnetic resonance imaging.~Investigator and IRC read: Progression is defined as greater than 25 percent increase in the sum of the product of the largest perpendicular diameters of enhancing tumor compared to the smallest prior sum, or Worsening of an evaluable lesion(s),or Marked increase in T2/FLAIR non-enhancing lesions (IRC only) or Any new lesion" (NCT00689221)
Timeframe: Time from randomization to disease progression, death or last tumor assessment, reported between day of first participant randomized, that is, Sep 2008 until cut-off date, (19 Nov 2012)

,
InterventionMonths (Median)
PFS Time: Investigator readPFS Time: Independent read
Cilengitide + Temozolomide + Radiotherapy13.510.6
Temozolomide + Radiotherapy10.77.9

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Maximum Observed Plasma Concentration (Cmax)

The Cmax for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2.1. (NCT00689221)
Timeframe: Day 1 of Week -1

Interventionnanogram per milliliter (ng/mL) (Mean)
Cilengitide + Temozolomide + Radiotherapy167363.2

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EuroQol 5-Dimensions (EQ-5D) Questionnaire Index

The EuroQuol-5D (EQ-5D) questionnaire is a measure of health status that provides a simple descriptive profile and a single index value. The optional part of the questionnaire was not applied. The EQ-5D defines health in terms of mobility, self-care, usual activities, pain/discomfort and anxiety/depression. The 5 items are combined to generate health profiles. These profiles were converted to a continuous single index score using a one to one matching. The lowest possible score is -0.594 (death) and the highest is 1.00 (full health). (NCT00689221)
Timeframe: Up to 50 months

Interventionunits on a scale (Mean)
Cilengitide + Temozolomide + Radiotherapy0.598
Temozolomide + Radiotherapy0.623

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Overall Survival (OS) Time

The OS time is defined as the time (in months) 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. (NCT00689221)
Timeframe: Time from randomization to death or last day known to be alive, reported between day of first participant randomized, that is, Sep 2008 until cut-off date, (19 Nov 2012)

InterventionMonths (Median)
Cilengitide + Temozolomide + Radiotherapy26.3
Temozolomide + Radiotherapy26.3

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Area Under the Plasma Concentration Curve From Time 0 to 6 Hours (AUC [0-6]) After Dose

The AUC (0-6) for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2.1. (NCT00689221)
Timeframe: Day 1 of Week -1

Interventionhour*ng/mL (Mean)
Cilengitide + Temozolomide + Radiotherapy295171.2

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Time to Maximum Plasma Concentration (Tmax)

The Tmax for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2.1. (NCT00689221)
Timeframe: Day 1 of Week -1

Interventionhours (Mean)
Cilengitide + Temozolomide + Radiotherapy1.029

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Median Progression Free Survival After Primary Surgical Treatment, Concomitant and Adjuvant Chemotherapy With Temozolomide, for Patients With Newly Diagnosed Glioblastoma Multiforme

(NCT00704808)
Timeframe: After primary surgical treatment and concomitant and adjuvant chemotherapy with temozolomide

InterventionMonths (Median)
Temozolomide9.57

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Disease Control Rate (DCR)

Using RECIST v1.0 criteria, disease control rate (DCR) was determined by the number of participants with complete response (CR) + the number of participants with partial response (PR) + the number of participants with stable disease (SD) / the number of participants with complete response (CR) + the number of participants with partial response (PR) + the number of participants with stable disease (SD) + the number of participants with progressive disease (PD). Per RECIST v1.0 criteria (assessed by MRI or CT): Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), neither sufficient shrinkage to qualify for a Partial Response (PR) nor sufficient increase to to qualify for Progressive Disease (PD); PD, 20% increase in the sum if target lesion or the appearance of new lesions; Complete Response (CR), Disappearance of all target lesions. (NCT00715793)
Timeframe: Up to 30 months

Interventionpercentage of participants (Number)
DAC (Decitabine) + TMZ (Temozolomide)61

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Percentage of Participants That Experienced a Dose Limiting Toxicity (DLT)

Dose-limiting toxicities (DLTs) were defined as grade 4 neutropenia or thrombocytopenia which lasts >7 days; grade 3 or 4 febrile neutropenia; grade 3 or greater non-hematological toxic effects. (NCT00715793)
Timeframe: Up to 26 months

Interventionpercentage of participants (Number)
Dose Level 1:DAC (Decitabine) 0.075 mg/kg + TMZ (Temozolomide)0
Dose Level 2:DAC (Decitabine) 0.15 mg/kg + TMZ (Temozolomide)17

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Progression-free Survival (PFS)

PFS was defined as the time from study entry until the documented radiological or symptomatic progression. Per RECIST v1.0 criteria (assessed by MRI or CT): Progressive Disease (PD); PD, 20% increase in the sum if target lesion or the appearance of new lesions. (NCT00715793)
Timeframe: Up to 42 months

Interventionmonths (Median)
DAC (Decitabine) + TMZ (Temozolomide)3.4

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Overall Response Rate (ORR)

Using RECIST v1.0 criteria, overall response rate (ORR) was determined by the number of participants with complete response (CR) + the number of participants with partial response (PR) / the number of participants with complete response (CR) + the number of participants with partial response (PR) + the number of participants with stable disease (SD) + the number of participants with progressive disease (PD), multiplied by 100. Per RECIST v1.0 criteria (assessed by MRI or CT): Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), neither sufficient shrinkage to qualify for a Partial Response (PR) nor sufficient increase to to qualify for Progressive Disease (PD); PD, 20% increase in the sum if target lesion or the appearance of new lesions; Complete Response (CR), Disappearance of all target lesions. (NCT00715793)
Timeframe: Up to 30 months

Interventionpercentage of participants (Number)
DAC (Decitabine) + TMZ (Temozolomide)18

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Overall Survival (OS)

OS was defined as the time from study entry until the death or date of last contract. (NCT00715793)
Timeframe: Up to 42 months

Interventionmonths (Median)
DAC (Decitabine) + TMZ (Temozolomide)12.4

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1-year Overall Survival (OS) Rate

Percentage of patients alive at one year (number of patients alive / total number of evaluable (analyzed) patients). (NCT00715793)
Timeframe: 12 months

Interventionpercentage of participants (Number)
DAC (Decitabine) + TMZ (Temozolomide)56

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6-month Progression-free Survival (PFS) Rate

(NCT00715793)
Timeframe: 6 months

Interventionpercentage of participants (Number)
DAC (Decitabine) + TMZ (Temozolomide)32.4

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Number of Participants Experiencing Unexpected Adverse Drug Reactions (ADRs)

An unexpected ADR was defined as an adverse reaction, whose nature, severity, specificity, or outcome is not consistent with the term or description used in the applicable product information. (NCT00723827)
Timeframe: Complete study duration & 30 days after completion (up to approximately 7.5 months)

Interventionparticipants (Number)
All Participants49

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Number of Temozolomide Drug Interactions

Drug interaction was defined as a chemical or physiological reaction that can occur when two different drugs are taken together. (NCT00723827)
Timeframe: Complete study duration & 30 days after completion (up to approximately 7.5 months)

Interventionevents (Number)
All Participants5

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Number of Temozolomide Misuse or Abuse Events

"Drug abuse was defined as the use of the study drug for a non-therapeutic effect.~Misuse was defined as use of the study medication in a way that was not prescribed." (NCT00723827)
Timeframe: Complete study duration & 30 days after completion (up to approximately 7.5 months)

InterventionEvents (Number)
All Participants1

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Efficacy: Number of Participants Experiencing Complete Response (CR), Partial Response (PR), or Stable Disease(SD)

The response ratings were based on the judgment of the investigator. (NCT00723827)
Timeframe: Complete study duration (up to approximately 6.5 months)

Interventionparticipants (Number)
CRPRSD
All Participants82143322

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Number of Participants Experiencing Adverse Events (AEs)

An AE was defined as any unfavorable and unintended sign, symptom, or disease temporally associated with the use of vaccine, whether or not considered related to the medicinal product. (NCT00723827)
Timeframe: Complete study duration & 30 days after completion (up to approximately 7.5 months)

Interventionparticipants (Number)
All Participants324

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Number of Participants Who Discontinued Due to Toxicity

(NCT00725010)
Timeframe: Weekly during the concomitant treatment phase, and then monthly during the monotherapy phase

InterventionParticipants (Number)
Temozolomide+Radiotherapy8
Temozolomide Alone1

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Safety: Number of Adverse Events in the Indicated Categories

(NCT00725010)
Timeframe: Weekly during the concomitant treatment phase, and then monthly during the monotherapy phase

,
InterventionAdverse Events (Number)
Unlikely Related to TemozolomidePossibly Related to TemozolomideProbably Related to Temozolomide
Temozolomide Alone101
Temozolomide+Radiotherapy351422

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Incidence of Adverse Events, Based on CTC (Common Toxicity Criteria) Severity Grade

Safety variables will be summarized by descriptive statistics. Adverse Events (AEs) that occur will be reported for each phase and dose level and described in terms of incidence and severity. Parameters will be described based on the CTC severity grading. Distribution by CTC severity grade and clinical relevance will be given. (NCT00731731)
Timeframe: Up to 5 years

Interventionparticipants evaluable for toxicity (Number)
Phase I, Dose Level 012
Phase I, Dose Level 13
Phase II107

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Overall Survival at 15 Months (Phase II)

The primary endpoint will be survival status at 15 months (OS15). In addition, survival will be estimated using a Kaplan-Meier curve. For this analysis, patients who are still alive at the time of analysis have survival time censored at the last contact date. (NCT00731731)
Timeframe: Time from study registration to the date of death from any cause, assessed up to 5 years

Interventionpercentage of phase II patients (Number)
Phase II54.6

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Time to Tumor Progression (Phase II)

Progression free survival time will be defined from date of registration to date of progression or death. (NCT00731731)
Timeframe: Up to 5 years

Interventionmonths (Median)
Phase II8.05

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Incidence of Adverse Events, as Per NCI CTCAE Version 3.0 (Phase II)

"The maximum grade for each type of treatment-related adverse event will be recorded for each patient, and frequency tables for each arm will be reviewed to determine patterns. In addition, we will review all adverse event data that is graded as 3, 4, or 5 and classified as either unrelated or unlikely to be related to study treatment in the event of an actual relationship developing." (NCT00731731)
Timeframe: Up to 5 years

Interventionparticipants evaluable for toxicity (Number)
Phase I, Dose Level 012
Phase I, Dose Level 13
Phase II107

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The Objective Overall Response

"The objective response is defined as all complete responses and partial responses based on the modified RECIST.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. 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." (NCT00740636)
Timeframe: 2 years

,
Interventionparticipants (Number)
Partial Response (PR)Stable Disease (SD)Progression of Disease (POD)Complete Response (CR)
200 mg/m2/Day for 5 Days (23 Days Off tx). 28 Day Cycles.7790
75 mg/m2/Day for 21 Days (7 Days Off tx). 28 Day Cycles.1219311

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Permeability-surface Area Product Before, During, and After Chemoradiotherapy

"Permeability-surface Area Product (Ktrans). Ktrans reflects the efflux rate of contrast from blood plasma into the tissue extravascular extracellular space (EES). Ktrans was assessed using post-contrast T1-weighted images. Multiple images were used to assess each participant at every time-point and the median value for each participant was calculated by time-point. The data presented represent the average of those median values at each time-point.~CRT: Chemoradiotherapy Cx: The cycle number TMZ: temozolomide" (NCT00756106)
Timeframe: Baseline, weekly during treatment, monthly following treatment for up to six months

Interventionmin ^-1 (Mean)
Baseline 1Baseline 2Week 1 CRTWeek 2 CRTWeek 3 CRTWeek 4 CRTWeek 5 CRTWeek 6 CRTPre-C1 TMZPre-C2 TMZPre-C3 TMZPre-C4 TMZPre-C5 TMZPre-C6 TMZPost-TMZ
Temozolomide and Radiation Therapy0.0530.0390.0550.0480.0550.0530.0580.0590.0630.0420.0500.0580.0560.0600.032

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Relative Cerebral Blood Volume as Measured by Perfusion-weighted MRI Before, During, and After Chemoradiotherapy

"Relative cerebral blood volume (rCBV) is the blood volume in the region of interest (ROI) divided by the blood volume in the symmetrical region on the other side of the normal brain (control region). CBV was assessed using spin-echo post-contrast T1-weighted images. Multiple images were used to assess each participant at every time-point and the median value for each participant was calculated by time-point. The data presented represent the average of those median values at each time-point. The baseline value was measured twice (representing baseline 1 and 2) to make sure that the value was reproducible and to account for any variation attributable to measurement variation.~CRT: Chemoradiotherapy Cx: The cycle number TMZ: temozolomide" (NCT00756106)
Timeframe: Baseline, weekly during treatment, monthly following treatment for up to six months

Interventionratio (Mean)
Baseline 1Baseline 2Week 1 CRTWeek 2 CRTWeek 3 CRTWeek 4 CRTWeek 5 CRTWeek 6 CRTPre-C1 TMZPre-C2 TMZPre-C3 TMZPre-C4 TMZPre-C5 TMZPre-C6 TMZPost-TMZ
Temozolomide and Radiation Therapy0.880.900.951.00.880.830.860.760.680.610.590.650.610.640.32

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Relative Cerebral Blood Flow as Measured by Perfusion-weighted MRI Before, During, and After Chemoradiotherapy

"Relative cerebral blood flow (rCBF) is the blood flow rate (the volume of blood passing through the specified are over a specified period of time) in the region of interest (ROI) divided by the blood flow rate in the symmetrical region on the other side of the normal brain (control region). CBF was assessed using spin-echo post-contrast T1-weighted images. CBF was assessed using spin-echo post-contrast T1-weighted images. Multiple images were used to assess each participant at every time-point and the median value for each participant was calculated by time-point. The data presented represent the average of those median values at each time-point. The baseline value was measured twice (representing baseline 1 and 2) to make sure that the value was reproducible and to account for any variation attributable to measurement variation.~CRT: Chemoradiotherapy Cx: The cycle number TMZ: temozolomide" (NCT00756106)
Timeframe: Baseline, weekly during treatment, monthly following treatment for up to six months

Interventionratio (Mean)
Baseline 1Baseline 2Week 1 CRTWeek 2 CRTWeek 3 CRTWeek 4 CRTWeek 5 CRTWeek 6 CRTPre-C1 TMZPre-C2 TMZPre-C3 TMZPre-C4 TMZPre-C5 TMZPre-C6 TMZPost-TMZ
Temozolomide and Radiation Therapy0.830.860.920.940.800.790.830.730.630.590.600.600.520.470.37

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Apparent Diffusion Coefficient Before, During, and After Chemoradiotherapy

"Apparent diffusion coefficient (ADC) is a measure of the magnitude of diffusion (of water molecules) within tissue. ADC was assessed using post-contrast T1-weighted images. Multiple images were used to assess each participant at every time-point and the median value for each participant was calculated by time-point. The data presented represent the average of those median values at each time-point.~CRT: Chemoradiotherapy Cx: The cycle number TMZ: temozolomide" (NCT00756106)
Timeframe: Baseline, weekly during treatment, monthly following treatment for up to six months

Interventionmm2/s (Mean)
Baseline 1Baseline 2Week 1 CRTWeek 2 CRTWeek 3 CRTWeek 4 CRTWeek 5 CRTWeek 6 CRTPre-C1 TMZPre-C2 TMZPre-C3 TMZPre-C4 TMZPre-C5 TMZPre-C6 TMZPost-TMZ
Temozolomide and Radiation Therapy0.001100.001130.001060.001100.001180.001220.001250.001250.001320.001270.001080.001330.001480.001790.00140

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Disease Progression at 10, 12, 14, 16, 18, 21, and 24 Months by Independent Review in the Intent-to-treat Population - Number of Participants

"Tumor response was classified based on the (neuro-)radiologist's evaluation:~Complete Response (CR): Disappearance of all enhancing tumor on consecutive MRI scans at least 1 month apart, off steroids, neurologically stable or improved.~Partial Response (PR): ≥50% reduction in size of enhancing tumor on consecutive MRI scans at least 1 month apart, steroids stable or reduced, neurologically stable or improved.~Progressive Disease (PD): ≥25% increase in size of enhancing tumor or any new tumor on MRI scans, steroids stable or increased, neurologically worse.~Stable Disease (SD): all other situations.~Based on clinical and imaging data, an independent neuro-oncologist made the final assessment of Progressed versus Not Progressed. Participants who had MRI assessment results missing or unknown were UNK or missing, and were treated as Progressed for the purposes of the calculation." (NCT00761280)
Timeframe: 10, 12, 14, 16, 18, 21, and 24 months

,
Interventionparticipants (Number)
Progressed at 10 monthsNot progressed at 10 monthsStatus unknown / missing at 10 monthsLost to follow-up at 10 monthsProgressed at 12 monthsNot progressed at 12 monthsStatus unknown / missing at 12 monthsLost to follow-up at 12 monthsProgressed at 14 monthsNot progressed at 14 monthsStatus unknown / missing at 14 monthsLost to follow-up at 14 monthsProgressed at 16 monthsNot progressed at 16 monthsStatus unknown / missing at 16 monthsLost to follow-up at 16 monthsProgressed at 18 monthsNot progressed at 18 monthsStatus unknown / missing at 18 monthsLost to follow-up at 18 monthsProgressed at 21 monthsNot progressed at 21 monthsStatus unknown / missing at 21 monthsLost to follow-up at 21 monthsProgressed at 24 monthsNot progressed at 24 monthsStatus unknown / missing at 24 monthsLost to follow-up at 24 months
Chemotherapy5071507150715071507150715071
Trabedersen 10 µM7340725072507250725071607160

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Survival Rate at 12, 18, and 21 Months in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)

Survival rate was defined as the proportion of participants known to be alive at each time-point from randomization. Participants with unknown or missing status were considered treatment failures, i.e., assumed to be dead. (NCT00761280)
Timeframe: 12, 18, and 21 months

,
Interventionpercentage of participants (Number)
Survival rates at 12 monthsSurvival rates at 18 monthsSurvival rates at 21 months
Chemotherapy53.838.523.1
Trabedersen 10 µM57.142.935.7

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Survival Rate at 24 Months in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)

Survival rate was defined as the proportion of participants known to be alive at 24 months from randomization. If a participant's status was unknown and there was no follow-up information available, they were categorized as 'Died' for the purposes of the analysis. (NCT00761280)
Timeframe: 24 months

Interventionpercentage of participants (Number)
Trabedersen 10 µM28.6
Chemotherapy15.4

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Survival at 24 Months in the Intent-to-treat Population - Number of Participants

"Survival status was assessed at 24 months from randomization. Participants with unknown or missing status were considered treatment failures, i.e., assumed to be dead. The category Lost to / insufficient follow-up includes participants who were alive at last data collection point but did not yet have enough follow-up time to reach the 24 month time point." (NCT00761280)
Timeframe: 24 months

,
Interventionparticipants (Number)
AliveDiedLost to/insufficient follow-up
Chemotherapy256
Trabedersen 10 µM473

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Tumor Control Rate (CR+PR+SD) by Independent Review in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)

Tumor control rate was defined as the proportion of participants assessed as having Complete Response (CR), Partial Response (PR), or Stable Disease (SD). Participants with unknown or missing response were treated as non-responders. (NCT00761280)
Timeframe: Up to 24 months

Interventionpercentage of participants (Number)
Trabedersen 10 µM28.6
Chemotherapy53.8

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Survival at 12, 18, and 21 Months in the Intent-to-treat Population - Number of Participants

"Survival status was assessed at each time-point from randomization. Participants with unknown or missing status were considered treatment failures, i.e., assumed to be dead. The category Lost to follow-up for each time-point includes participants who were alive at the last data collection point but did not yet have enough follow-up time to reach the time point." (NCT00761280)
Timeframe: 12, 18, and 21 months

,
Interventionparticipants (Number)
Alive at 12 monthsDied at 12 monthsLost to follow-up at 12 monthsAlive at 18 monthsDied at 18 monthsLost to follow-up at 18 monthsAlive at 21 monthsDied at 21 monthsLost to follow-up at 21 months
Chemotherapy715535355
Trabedersen 10 µM851671572

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Median Duration of Response (Days) by Independent Review (Descriptive Analysis, Only)

"Duration of response was defined as the time from the first documentation of confirmed response (Complete Response, CR, or Partial Response, PR) to the first signs of Progressive Disease (PD), as assessed by the study neuro-oncologist. Median Duration of Response was calculated by Kaplan-Meier estimate.~Censoring rules were:~at the date of randomization -- participants without baseline assessments, or for those with no post-baseline timor assessments who were discontinued for other than progressive disease or death.~at the date of last tumor assessment -- discontinuation other than PD or death, or if a new treatment was started prior to disease progression~at the date of death or last tumor assessment -- death or PD after one missed tumor assessment~at the date of last tumor assessment -- death or PD after more than one missed tumor assessment~at the date of last tumor assessment -- participants on ongoing treatment at data cut-off" (NCT00761280)
Timeframe: Up to 24 months

Interventiondays (Median)
Trabedersen 10 µMNA
ChemotherapyNA

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Median Overall Survival (Days) From Randomization in the Intent-to-treat Population (Descriptive Analysis, Only)

Median overall survival was defined as the date of randomization to the date of death. If a participant's status was unknown and there was no follow-up information available, they were categorized as 'Died' for the purposes of the analysis. Analysis was by Kaplan-Meier estimation. (NCT00761280)
Timeframe: Up to 24 months

Interventiondays (Median)
Trabedersen 10 µM458.0
Chemotherapy584.5

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Median Time to Progression (Days) by Independent Review for the Intent-to-treat Population (Descriptive Analysis, Only)

Time to progression was calculated from the date of randomization to the date of the first documented tumor progression. Participants who did not progress or died were censored at the last tumor assessment date or the date of start of a new anti-tumor treatment or death. (NCT00761280)
Timeframe: Up to 24 months

Interventiondays (Median)
Trabedersen 10 µM57.0
Chemotherapy153.5

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Response Category by Independent Review in the Intent-to-treat Population - Number of Participants

"Tumor response was classified based on the (neuro-)radiologist's evaluation according to the Macdonald Response Criteria for bidimensionally measurable disease as outlined below:~Complete Response (CR): Disappearance of all enhancing tumor on consecutive MRI scans at least 1 month apart, off steroids, neurologically stable or improved.~Partial Response (PR): ≥50% reduction in size of enhancing tumor on consecutive MRI scans at least 1 month apart, steroids stable or reduced, neurologically stable or improved.~Progressive Disease (PD): ≥25% increase in size of enhancing tumor or any new tumor on MRI scans, steroids stable or increased, neurologically worse.~Stable Disease (SD): all other situations.~Two qualified neuro-radiologists reviewed scans at each MRI time point, with adjudication of discrepancies by a third reviewer. Their findings and clinical information were independently reviewed by a neuro-oncologist, who made the assessment of overall response." (NCT00761280)
Timeframe: Up to 24 months

,
Interventionparticipants (Number)
Complete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive Disease (PD)UnknownMissing
Chemotherapy016132
Trabedersen 10 µM022712

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Overall Response Rate (CR+PR) by Independent Review in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)

Overall response rate was the proportion of participants with a best response of Complete Response (CR) or Partial Response (PR) observed from the start of treatment until disease progression. (NCT00761280)
Timeframe: Up to 24 months

Interventionpercentage of participants (Number)
Trabedersen 10 µM14.3
Chemotherapy7.7

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Disease Progression Rate at 10, 12, 14, 16, 18, 21, and 24 Months by Independent Review in the Intent-to-treat Population - Percentage of Participants (Descriptive Analysis, Only)

"Tumor response was classified based on the (neuro-)radiologist's evaluation:~Complete Response (CR): Disappearance of all enhancing tumor on consecutive MRI scans at least 1 month apart, off steroids, neurologically stable or improved.~Partial Response (PR): ≥50% reduction in size of enhancing tumor on consecutive MRI scans at least 1 month apart, steroids stable or reduced, neurologically stable or improved.~Progressive Disease (PD): ≥25% increase in size of enhancing tumor or any new tumor on MRI scans, steroids stable or increased, neurologically worse.~Stable Disease (SD): all other situations.~Based on clinical and imaging data, an independent neuro-oncologist made the final assessment of Progressed versus Not Progressed. Participants who had MRI assessment results missing or unknown were UNK or missing, and were treated as Progressed for the purposes of the calculation." (NCT00761280)
Timeframe: 10, 12, 14, 16, 18, 21 and 24 months

,
Interventionpercentage of participants (Number)
Progression rate at 10 monthsProgression rate at 12 monthsProgression rate at 14 monthsProgression rate at 16 monthsProgression rate at 18 monthsProgression rate at 21 monthsProgression rate at 24 months
Chemotherapy100.0100.0100.0100.0100.0100.0100.0
Trabedersen 10 µM78.685.785.785.785.792.992.9

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Progression Free Survival

(NCT00782756)
Timeframe: through study completion, an average of 1 year

Interventionmonths (Median)
RT, With Temozolomide and Bevacizumab10

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Number of Participants With Adverse Events

Safety assessments and toxicity grading will follow CTCAE Version 4 Grade (NCT00782756)
Timeframe: through study completion, an average of 1 year

InterventionParticipants (Count of Participants)
RT, With Temozolomide and Bevacizumab40

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12-Month Overall Survival (OS) Rate

The 12-month overall survival rate was defined as the percentage of participants surviving at 12 months. The distribution of 12-month OS rate was estimated using Kaplan-Meier methodology. Point estimates and 95% CIs for the quartiles for the PFS distribution are provided. Per protocol, because neither the ABT-888 20 mg BID + TMZ nor ABT-888 40 mg BID + TMZ treatment groups were statistically significantly better than the Placebo + TMZ treatment group for the primary endpoint of PFS, confirmatory statistical testing was not continued for any secondary endpoints, regardless of the observed P values. (NCT00804908)
Timeframe: Per protocol, survival was to be assessed every 4 weeks or as needed after participant is registered as off-study for up to 18 months. The maximum observed follow-up at the overall survival analysis time was 21.0 months.

Interventionpercentage of participants (Number)
Placebo for ABT-888 BID + TMZ QD52.6
ABT-888 20 mg BID + TMZ QD43.5
ABT-888 40 mg BID + TMZ QD54.1

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Disease Control Rate

The disease control rate was defined as the percentage of participants who had at least stable disease (complete response, partial response, or stable disease) through the end of Week 8. Per protocol, because neither the ABT-888 20 mg BID + TMZ nor ABT-888 40 mg BID + TMZ treatment groups were statistically significantly better than the Placebo + TMZ treatment group for the primary endpoint of PFS, confirmatory statistical testing was not continued for any secondary endpoints, regardless of the observed P values. (NCT00804908)
Timeframe: Week 8

Interventionpercentage of participants (Number)
Placebo for ABT-888 BID + TMZ QD48.7
ABT-888 20 mg BID + TMZ QD62.9
ABT-888 40 mg BID + TMZ QD59.1

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Objective Response Rate

The objective response rate was defined as the percentage of participants with a confirmed CR or PR per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by computed tomography (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. Per protocol, because neither the ABT-888 20 mg BID + TMZ nor ABT-888 40 mg BID + TMZ treatment groups were statistically significantly better than the Placebo + TMZ treatment group for the primary endpoint of PFS, confirmatory statistical testing was not continued for any secondary endpoints, regardless of the observed P values. (NCT00804908)
Timeframe: Every 2 cycles (8 weeks) until disease progression was observed or another reason for discontinuation of assessments was identified by the investigator. The maximum observed followup duration at the progression-free survival analysis time was 9.7 months.

Interventionpercentage of participants (Number)
Placebo for ABT-888 BID + TMZ QD7.0
ABT-888 20 mg BID + TMZ QD10.3
ABT-888 40 mg BID + TMZ QD9.6

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Overall Survival (OS): Time to Event

OS was defined as the number of days from the date the participant was randomized to the date of death. All deaths were included, whether the participant was still taking or had discontinued study drug. If a participant had not died and was lost to follow-up, then data were censored at the last study visit or contact date, or date the participant was last known to be alive, whichever was later; if the participant was not lost to follow-up, then data were censored at the last study visit or contact date, whichever was later. The distribution of OS was estimated for each treatment group using Kaplan-Meier methodology. Point estimates and 95% CIs for the quartiles for the OS distribution are provided. Per protocol, because neither the ABT-888 20 mg BID + TMZ nor ABT-888 40 mg BID + TMZ groups were statistically significantly better than the Placebo + TMZ group for the primary endpoint of PFS, confirmatory statistical testing was not continued for any secondary endpoints. (NCT00804908)
Timeframe: Per protocol, survival follow-up information was to be obtained every 3 months for up to 18 months after the final visit for the subject. The maximum observed follow-up at the overall survival analysis time was 21.0 months.

,,
Interventiondays (Number)
25th Percentile50th percentile75th percentile
ABT-888 20 mg BID + TMZ QD204327NA
ABT-888 40 mg BID + TMZ QD181412NA
Placebo for ABT-888 BID + TMZ QD207390559

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Progression-Free Survival (PFS): Time to Event

PFS: the number of days from the date that the participant was randomized to the date the participant experienced a confirmed event of disease progression (radiological, as determined by the central imaging center; or clinical, as determined by the investigator), or to the date of death (all causes of mortality) if disease progression was not reached. All events were included whether the participant was still taking or had discontinued study drug. Events of death were included for participants who had not experienced a confirmed event of disease progression, provided the death occurred within 8 weeks of the last available disease progression assessment. The distribution of PFS, as determined by the central imaging center (radiological)/ investigator (clinical), was estimated for each treatment group using Kaplan-Meier methodology. Point estimates and 95% confidence intervals (95% CIs) for the quartiles for the PFS distribution are provided. (NCT00804908)
Timeframe: Every Cycle (28 Days) until disease progression was observed or another reason for discontinuation of assessments was identified by the investigator. The maximum observed followup duration at the progression-free survival analysis time was 9.7 months.

,,
Interventiondays (Number)
25th Percentile50th Percentile75th Percentile
ABT-888 20 mg BID + TMZ QD56113225
ABT-888 40 mg BID + TMZ QD53110226
Placebo for ABT-888 BID + TMZ QD5460163

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Time to Disease Progression

The distribution of time to disease progression, as determined by the central imaging center (radiological)/ investigator (clinical), was estimated for each treatment group using Kaplan-Meier methodology. Point estimates and 95% CIs for the quartiles for the PFS distribution are provided. Per protocol, because neither the ABT-888 20 mg BID + TMZ nor ABT-888 40 mg BID + TMZ treatment groups were statistically significantly better than the Placebo + TMZ treatment group for the primary endpoint of PFS, confirmatory statistical testing was not continued for any secondary endpoints, regardless of the observed P values. (NCT00804908)
Timeframe: Every Cycle (28 Days), until disease progression was observed or another reason for discontinuation of assessments was identified by the investigator. The maximum observed followup duration at the progression-free survival analysis time was 9.7 months.

,,
Interventiondays (Number)
25th Percentile50th percentile75th percentile
ABT-888 20 mg BID + TMZ QD56113225
ABT-888 40 mg BID + TMZ QD53110226
Placebo for ABT-888 BID + TMZ QD5460163

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Time to Neurological/Brain Metastases Progression

Time to neurological/brain metastases progression, defined as the number of days from the date of randomization to the date the participant experienced an event of neurological/brain metastases progression, was estimated using Kaplan-Meier methodology. Point estimates and 95% CIs for the quartiles for the distribution are provided. All events of progression were included, regardless of whether the event occurred while the participant was still taking study drug. If a participant did not experience an event, data were censored at the date of the last available brain CT scan. For participants with no postbaseline brain CT scans, data were censored at randomization. Per protocol, because neither the ABT-888 20 mg BID + TMZ nor ABT-888 40 mg BID + TMZ groups were statistically significantly better than the Placebo + TMZ group for the primary endpoint of PFS, confirmatory statistical testing was not continued for any secondary endpoints, regardless of the observed P values. (NCT00804908)
Timeframe: Every 2 cycles (8 weeks) until disease progression was observed or another reason for discontinuation of assessments was identified by the investigator. The maximum observed followup duration at the progression-free survival analysis time was 9.7 months.

,,
Interventiondays (Number)
25th Percentile50th percentile75th percentile
ABT-888 20 mg BID + TMZ QD119NANA
ABT-888 40 mg BID + TMZ QD184184NA
Placebo for ABT-888 BID + TMZ QD60NANA

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6-month Progression-Free Survival Rate

The 6-month progression-free survival rate was defined as the percentage of participants without disease progression at 6 months.The distribution of 6-month progression-free survival rate, as determined by the central imaging center (radiological)/ investigator (clinical), was estimated using Kaplan-Meier methodology. Point estimates and 95% CIs for the quartiles for the PFS distribution are provided. Per protocol, because neither the ABT-888 20 mg BID + TMZ nor ABT-888 40 mg BID + TMZ treatment groups were statistically significantly better than the Placebo + TMZ treatment group for the primary endpoint of PFS, confirmatory statistical testing was not continued for any secondary endpoints, regardless of the observed P values. (NCT00804908)
Timeframe: Every Cycle (28 Days) until disease progression was observed or another reason for discontinuation of assessments was identified by the investigator. The maximum observed followup duration at the progression-free survival analysis time was 9.7 months.

Interventionpercentage of participants (Number)
Placebo for ABT-888 BID + TMZ QD19.1
ABT-888 20 mg BID + TMZ QD32.8
ABT-888 40 mg BID + TMZ QD30.7

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Number of Participants Experiencing Toxicity After This Novel Multimodality Regimen

The toxicity assessments were made according to the common terminology criteria for adverse events (CTCAE version 3.0) of the National Cancer Institute. Number of participants with Grade 1 to 5 adverse events are reported here. (NCT00805961)
Timeframe: 18 months

InterventionParticipants (Count of Participants)
Overall Study53

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Objective Response Rate of Patients With Glioblastoma Multiforme Following Treatment With This Novel Multimodality Regimen

Response to treatment was assessed by MRI using the MacDonald criteria based on the assessment of the MRI scan for measurable, evaluable, and new lesions. The objective response rate is defined as the proportion of patients with improvement and or decreased extent of lesions compared to baseline. (NCT00805961)
Timeframe: 18 months

InterventionParticipants (Count of Participants)
Overall Study31

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Overall Survival of Patients With Glioblastoma Multiforme Following Treatment With This Novel Multimodality Regimen

Overall survival was defined as the interval from the first day of study treatment until the date of death. (NCT00805961)
Timeframe: 18 months

InterventionMonths (Number)
Overall Study13.9

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Progression-free Survival (PFS)

Progression-free survival is defined as the duration of time from start of treatment to time of progression or death, whichever comes first. (NCT00805961)
Timeframe: 18 months

InterventionMonths (Median)
Overall Study11.3

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Overall Survival (OS) Time

The OS time is defined as the time (in months) 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. (NCT00813943)
Timeframe: Time from randomization to death or last day known to be alive, reported between day of first participant randomized, that is, Jun 2009 until cut-off date, (07 Feb 2013)

InterventionMonths (Median)
Cilengitide (2-times Weekly) + Temozolomide + Radiotherapy16.3
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy14.5
Temozolomide + Radiotherapy13.4

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Number of Participants With AEs Belonging to Standardized Medical Dictionary for Regulatory Activities (MedDRA) Queries (SMQs) Thromboembolic Events and Hemorrhage With NCI-CTC Toxicity Grade 3 or 4

Thromboembolic events (standardized MedDRA query [SMQ]) Grade 3 or 4 AEs encompassed hemiparesis and cerebrovascular accident, pulmonary embolism, and deep vein thrombosis. Thromboembolic events (SMQ) of any grade and of Grade 3 or 4 were generally more frequent in the Cilengitide + Temozolomide/Radiotherapy group than in the Temozolomide/Radiotherapy group but were still in the expected range of this patient population The severity of AEs was assessed according to the National Cancer Institute-Common Toxicity Criteria (NCI-CTCAE) (version 3.0): Grade 1=mild, Grade 2=moderate, Grade 3=severe, Grade 4=life threatening or disabling. Note: Death (Grade 5) was regarded as an outcome. (NCT00813943)
Timeframe: Time from first dose up to 28 days after last dose of study treatment, reported between day of first participant randomized, that is, Jun 2009 until cut-off date (07 Feb 2013)

,,
InterventionParticipants (Number)
SMQ: Thromboembolic eventsSMQ:Hemorrhage
Cilengitide (2-times Weekly) + Temozolomide + Radiotherapy173
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy100
Temozolomide + Radiotherapy121

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Apparent Terminal Rate Constant

The apparent terminal rate constant for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2. Cilengitide plasma concentrations were determined after dosing on Day 1 (single dose) and Day 5 (repeated doses) of Week 1. (NCT00813943)
Timeframe: Days 1 and 5 of Week 1

Interventionper hour (Mean)
Day 1 (Single dose)Day 5 (Repeated doses)
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy0.320.32

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Apparent Volume of Distribution During the Terminal Phase (Vz) and Apparent Volume of Distribution at Steady State (Vss)

The Vz (after single dose) and Vss (after repeated doses) for cilengitide were calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2. Cilengitide plasma concentrations were determined after dosing on Day 1 (single dose) and Day 5 (repeated doses) of Week 1. (NCT00813943)
Timeframe: Days 1 and 5 of Week 1

Interventionliter (Mean)
VzVss
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy24.719.2

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Area Under the Plasma Concentration-Time Curve From Time 0 to Infinity (AUC [0-infinity]) and Area Under the Plasma Concentration-Time Curve From Time 0 to 24 Hours (AUC [0-24])

The AUC (0-infinity) and AUC (0-24) for cilengitide were calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2. Cilengitide plasma concentrations were determined after dosing on Day 1 (single dose) and Day 5 (repeated doses) of Week 1. (NCT00813943)
Timeframe: Days 1 and 5 of Week 1

Interventionhour*ng/mL (Mean)
AUC (0-infinity): Day 1 (Single dose)AUC (0-infinity): Day 5 (Repeated Doses)AUC (0-24): Day 1 (Single dose)AUC (0-24): Day 5 (Repeated doses)
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy280944335263269941316137

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Plasma Clearance (CL)

The CL for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2. Cilengitide plasma concentrations were determined after dosing on Day 1 (single dose) and Day 5 (repeated doses) of Week 1. (NCT00813943)
Timeframe: Days 1 and 5 of Week 1

Interventionmilliliter per minute (Mean)
Day 1 (Single dose)Day 5 (Repeated doses)
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy125.7109.3

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Maximum Observed Plasma Concentration (Cmax)

The Cmax for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2. Cilengitide plasma concentrations were determined after dosing on Day 1 (single dose) and Day 5 (repeated doses) of Week 1. (NCT00813943)
Timeframe: Days 1 and 5 of Week 1

Interventionnanogram per milliliter (ng/mL) (Mean)
Day 1 (Single dose)Day 5 (Repeated doses)
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy108527150873

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Progression Free Survival (PFS) Time - Investigator and Independent Read

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. Investigator read is the assessment of all imaging by the treating physician at the local trial site. Independent Read is the assessment of all imaging centrally by an Independent Review Committee (IRC). (NCT00813943)
Timeframe: Time from randomization to disease progression, death or last tumor assessment, reported between day of first participant randomized, that is, Jun 2009 until cut-off date, (07 Feb 2013)

,,
InterventionMonths (Median)
PFS Time: Independent readPFS Time: Investigator read
Cilengitide (2-times Weekly) + Temozolomide + Radiotherapy5.66.4
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy5.97.5
Temozolomide + Radiotherapy4.16.0

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Time to Maximum Plasma Concentration (Tmax) and Terminal Elimination Half-Life (t1/2)

The Tmax and t1/2 for cilengitide were calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2. Cilengitide plasma concentrations were determined after dosing on Day 1 (single dose) and Day 5 (repeated doses) of Week 1. (NCT00813943)
Timeframe: Days 1 and 5 of Week 1

Interventionhours (Mean)
Tmax: Day 1 (Single dose)Tmax: Day 5 (Repeated doses)t1/2: Day 1 (Single dose)t1/2: Day 5 (Repeated doses)
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy0.971.172.382.44

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Mean Residence Time From Time 0 to Infinity (MRT [0-infinity])

The MRT (0-infinity) for cilengitide was calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2. Cilengitide plasma concentrations were determined after dosing on Day 1 (single dose) and Day 5 (repeated doses) of Week 1. (NCT00813943)
Timeframe: Days 1 and 5 of Week 1

Interventionhour (Mean)
Day 1 (Single dose)Day 5 (Repeated doses)
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy2.82.9

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Plasma Concentration at Pre-dose (Cpre) and Plasma Concentration at End of Infusion (CT)

The Cpre and CT for cilengitide were calculated by non-compartmental analysis using the computer program WinNonlin, Version 6.2. Cilengitide plasma concentrations were determined after dosing on Day 1 (single dose) and Day 5 (repeated doses) of Week 1. (NCT00813943)
Timeframe: Days 1 and 5 of Week 1

Interventionng/mL (Mean)
Cpre: Day 1 (Single dose)Cpre: Day 5 (Repeated doses)CT: Day 1 (Single dose)CT: Day 5 (Repeated doses)
Cilengitide (5-times Weekly) + Temozolomide + Radiotherapy6372.7286.0108045.5157470.0

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Number of Participants With an Overall Response (Complete Response or Partial Response) Assessed by the MacDonald Criteria

Anti-tumor activity as determined by the overall response (Complete response (CR) or partial response (PR)) was assessed by the MacDonald criteria. Complete response is complete resolution of all lesions. The patient cannot be on any corticosteroids with the exception of adrenal replacement doses. Partial response is ≥50% reduction in the sum of products of all measurable lesions over baseline sum observed using the same techniques as baseline. The patient must be on a stable or decreased dose of corticosteroids to be evaluable for response. (NCT00826241)
Timeframe: 4 weeks

InterventionParticipants (Count of Participants)
Complete ResponsePartial Response
Temozolomide + Lapatinib28

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Time to Progression

Time to progression defined as progressive disease, toxicity at a level of severity that precludes the patient continuing on the protocol, or death. Progression is a 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00826241)
Timeframe: Assessed every two months till disease progression, up to 4 years

InterventionMonths (Median)
Temozolomide + Lapatinib7.8

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Number of Participants With Serious and Non-Serious Adverse Events Assessed by the Common Terminology Criteria in Adverse Events (CTCAE v4.0)

Here is the count of participants with serious and non-serious adverse events assessed by the Common Terminology Criteria in 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. (NCT00826241)
Timeframe: Date treatment consent signed to date off study, approximately 111 months and 26 days

InterventionParticipants (Count of Participants)
Temozolomide + Lapatinib50

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Time Spent in a Karnofsky Performance Status of 60-100%

Time spent in a KPS ≥70 was calculated from the date of diagnosis of Karonofsky Performance Status decline (KPS<70) or censored at the last date the patient was known with KPS ≥70. The KPS higher scores indicates normal activity status. (NCT00841555)
Timeframe: up to 12-16 months

Interventionmonths (Median)
Hypofractionation Radiotherapy+Temozolomide8.1

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Survival Time

All patients will be followed to death. Active follow-up with disease evaluation with scans will be terminated if the patient's physician deems it in the patient's interest not to continue or upon patient request. (NCT00841555)
Timeframe: up to 2 years

Interventionmonths (Median)
Hypofractionation Radiotherapy+Temozolomide12.7

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Maximum Tolerated Dose(MTD)of Temozolomide(TMZ)

This study is designed as a phase I dose escalation trial using the Standard Method of dose escalation of three patients per dose level to determine the MTD of TMZ (up to 75 mg/m 2 /day) when TMZ is used with HIMRT for patients with glioblastoma multiforme(GBM) or Anaplastic Astrocytoma(AA)of the brain. The 3 dose levels will be evaluated using the standard method to determine if either represents an MTD based on DLT. If DLT is not observed at all doses level, the greater of the three levels will be recommended for phase II evaluations of treatment effect. (NCT00841555)
Timeframe: up to 12-16 months

Interventionmg/m^2 (Number)
Hypofractionation Radiotherapy+Temozolomide75

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Response by MRI Measurements

partial response by RICST criteria is defined as >50% tumor shrinkage (NCT00846430)
Timeframe: evaluated 6, 12 and 24 months compared to baseline

Interventionparticipants (Number)
Partial Response at 6 monthsComplete Response at 6 monthsLess than Partial Response at 6 monthsPartial Response at 12 monthsComplete Response at 12 monthsLess than Partial Response at 12 monthsPartial Response at 24 monthsComplete Response at 24 monthsLess than Partial Response at 24 monthsno longer participating at 24 months
Open-Label Intervention0182164113

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No Reported Psychological Toxicity Based Upon Psychological Evaluations

Psychological toxicity defined as suicidal ideation (NCT00846430)
Timeframe: Psychological evaluation at 24 months

InterventionParticipants (Count of Participants)
Open-Label Intervention8

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Improvement of Symptoms and Pain

Subjects will be evaluated for pain and Quality of Life scores (NCT00846430)
Timeframe: Monthly physical exam first three months and then every three months after, for up to 36 months

InterventionParticipants (Count of Participants)
Open-Label Intervention9

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At Least 50% Shrinkage in Tumor Measurements by Physical Examination

(NCT00846430)
Timeframe: Monthly physical exam first three months and then every three months after, for up to 36 months

InterventionParticipants (Count of Participants)
Open-Label Intervention7

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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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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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Overall Survival

Overall survival (OS) is the primary endpoint and is defined as the time from study registration to time of death due to any cause. All patients who meet the eligibility criteria, have signed a consent form, and have received at least one dose of the regimens will be considered evaluable. Patients who are lost to follow-up will be censored at the date of their last follow-up. Patients still alive at the time of analysis will be censored. Only Phase II was evaluated for survival (NCT00869401)
Timeframe: Up to 5 years post treatment

InterventionMonths (Median)
Group 1 (Phase II) Dasatinib + Radiation + Temozolomide15.6
Group 2 (Phase II) Placebo + Radiation + Temozolomide19.3

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Objective Response

Objective response to treatment will be determined by a combination of the results of neurological exam and the MRI and/or CT measurement of the tumor at each evaluation as is used for all NCCTG neuro-oncology trials. The proportion of patients in each response category will be summarized. Only phase II patients were evaluated for response. (NCT00869401)
Timeframe: Up to 5 years post treatment

,
InterventionProportion of participants (Number)
ProgressionStableREGRPartial ResponseComplete Response
Group 1 (Phase II) Dasatinib + Radiation + Temozolomide.31.59.08.020
Group 2 (Phase II) Placebo + Radiation + Temozolomide.19.73.02.060

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Progression-free Survival

Progression-free survival (PFS) is defined as the time from study registration to the date of first observation of disease progression or death due to any cause (whichever comes first). If a patient has not progressed or died, progression-free survival is censored at the time of last follow-up. Only Phase II patients were evaluated for Progression-free survival (NCT00869401)
Timeframe: Up to 5 years post treatment

InterventionMonths (Median)
Group 1 (Phase II) Dasatinib + Radiation + Temozolomide6.2
Group 2 (Phase II) Placebo + Radiation + Temozolomide7.8

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The Number of Dose Limiting Toxicities(DLT) in Order to Determine Maximum Tolerable Dose(MTD) of Dasatinib Combined With Radiation and Temozolomide in This Patient Population.

Doselimiting toxicity will be defined as: Adverse event at least possibly related to the study medication. All by CTCAE v3.0 criteria: Greater than or equal to grade 3: diarrhea or skin rash or desquamation or (other) clinically relevant non-hematological adverse event or non-hematologic adverse event at least possibly due to drug therapy. Or greater than or equal to grade 4: neutropenia or leukopenia or thrombocytopenia or radiation dermatitis or hematologic adverse event OR failure to administer greater than 75% of dasatinib TMZ or interruption of RT for more than 5 days due to adverse events.OR severe acute central nervous system deterioration attributable to TMZ, RT and or dasatinib which cannot be controlled with corticosteroid administration. The MTD for this study will be defined as the highest safely tolerated dose level where at most 1 out of 6 patients experience DLT with the next higher dose having at least 2 patients out of a maximum of 6 patients experience DLT. (NCT00869401)
Timeframe: Every cycle from first dose to end of rest period prior cycle 3

Interventionparticipants with Dose Limiting Toxicits (Number)
Dose Level 0 Phase I1
Dose Level 0-A Phase I0
Dose Level 1 Phase I1

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Measurement of Number of Adverse Events

Collect and grade the all of the adverse events to evaluate for safety. This data was collected for the first 2 cycles for each participant. (NCT00876993)
Timeframe: Two 28-day cycles

,,,,
InterventionAdverse events (Number)
Grade 1 adverse eventsGrade 2 adverse eventsGrade 3 adverse eventsGrade 4 adverse events
Cohort 1 - Dose Level 14431
Cohort 2 - Dose Level 06310
Cohort 3 - Dose Level 13310
Cohort 4 - Dose Level 25540
Cohort 5 - Dose Level 13210

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To Provide Safety and Efficacy Data for to Recommend Further Larger Studies.

Number participants with grade 3 and 4 hematologic and non-hematologic toxicities. All toxicities are for end of cycle 2. (NCT00876993)
Timeframe: Two 28 day cycles

,,,,
InterventionParticipants (Count of Participants)
Grade 3 & 4 Blood/Bone MarrowGrade 3 & 4 GastrointestinalGrade 3 & 4 Metabolic/LaboratoryGrade 3 & 4 Musculoskelatal/Soft TissueGrade 3 & 4 NeurologyGrade 3 & 4 PainGrade 3 & 4 VascularGrade 3 & 4 Other
Cohort 1 - Dose Level 120001101
Cohort 2 - Dose Level 000000010
Cohort 3 - Dose Level 101000000
Cohort 4 - Dose Level 211113200
Cohort 5 - Dose Level 110000000

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2 Year Event Free Survival With Children Treated With This Regimen.

2 year actual event free survival.with children treated with this protocol (NCT00876993)
Timeframe: 2 year

InterventionCount of participants (Number)
Cohort 1 - Dose Level 14
Cohort 2 - Dose Level 06
Cohort 3 - Dose Level 13
Cohort 4 - Dose Level 25
Cohort 5 - Dose Level 13

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Progression-free Survival (PFS)

Progression-free survival was defined as time from randomization to date of progression, death, or last follow-up, and was estimated by the Kaplan-Meier method. Patients last known to be alive were censored at the date of last contact. This analysis was planned to occur when 390 deaths had been reported. (NCT00884741)
Timeframe: From randomization to date of progression, death, or last follow-up for progression-free survival. Analysis occurs after all 390 deaths have been reported.

Interventionmonths (Median)
Randomized Arm 1: TMZ+RT + Placebo7.3
Randomized Arm 2: TMZ+RT + Bevacizumab10.7

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Overall Survival (OS)

Survival time was defined as time from randomization to date of death from any cause and was estimated by the Kaplan-Meier method. Patients last known to be alive were censored at the date of last contact. This analysis was planned to occur when 390 deaths had been reported. (NCT00884741)
Timeframe: From randomization to date of death or last follow-up. Analysis occurs after all 390 deaths have been reported.

Interventionmonths (Median)
Randomized Arm 1: TMZ+RT + Placebo16.1
Randomized Arm 2: TMZ+RT + Bevacizumab15.7

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Overall Response to CVT Chemotherapy.

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 (NCT00885534)
Timeframe: 2 years

Interventionparticipants (Number)
Partial ResponseStable Disease
Cisplatin, Vinblastine, Temozolomide15

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Median Overall Survival

Overall survival is defined as the time from surgical resection to death of any cause. (NCT00905060)
Timeframe: Up to 3 years

Interventionmonths (Median)
Protein Peptide-Complex (HSPPC-96)23.8

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Median PD-L1 Positivity in Circulating Myeloid Cells

Circulating myeloid cells (CD45+/CD11b+) obtained from patients at the time of surgery were analyzed for PD-L1 expression to determine the percent of myeloid cells positive for PD-L1 (cut off for positivity determined relative to Fluorescence Minus One (FMO) and isotype control). (NCT00905060)
Timeframe: Up to 53 Weeks

Interventionpercentage of PD-L1 positivity (Median)
Protein Peptide-Complex (HSPPC-96)54.5

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Median Progression Free Survival (PFS)

PFS is defined as the duration of progression-free survival from the time from resection until either documented disease progression or death (NCT00905060)
Timeframe: Up to 3 years

Interventionmonths (Median)
Protein Peptide-Complex (HSPPC-96)18

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Phase 2 -Number of Patients With a Decrease in Tumor Size Using RECIST and CHOI's Criteria

"Tumor response rate was assessed using RECIST criteria in which a complete response was the disappearance of all target lesions; Partial response was a 30% decrease in the sum of the longest dimension (LD) of target lesions, relative to baseline measurement; Progressive disease was an increase of 20% or more in the sum of the LD of target lesions; and Stable disease was a decrease in tumor size of less than 30% or increase of less than 20%.~Tumor response rate was also assessed using CHOI's criteria in which a response was a 10% decrease in tumor size or a 15% decrease in tumor density on contrast-enhanced computed tomography scan.~Tumor response rates were assessed in order to determine effectiveness of the treatment regimen which was defined by the response rate of at least 30% as measured by either the RECIST or Choi's criteria, and ineffective if the rate is less than 15% on both." (NCT00925132)
Timeframe: 12 weeks (2 cycles)

InterventionParticipants (Count of Participants)
Progressive Disease (PD)Stable Disease (SD)
Phase II:Decitabine 0.2 mg/kg +Panobinostat 30mg +Temozolomide125

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Phase I - Number of Participants With Dose Limiting Toxicities (DLTs) at a Given Dose Level

"A DLT was any Grade 4 toxicity for neutrophils or platelets for ≥ 7 days, Grade 3 toxicity for neutrophils for ≥ 21 days, any Grade 3 solid organ toxicity not explainable by another cause (e.g. neurotoxicity, GI toxicity), metabolic/laboratory toxicity (≥10 x ULN AST) for ≥ 14 days, any Grade 4 infection or QTcF> 500msec EKG. DLTs were assessed according to the Common Toxicity Criteria for Adverse Events (CTCAE) version 3.0.~All adverse events were collected and graded to determine DLTs as assessed according to the Common Toxicity Criteria for Adverse Events (CTCAE) version 3.0. DLTs were assessed to determine the recommended Decitabine and Panobinostat dose for the Phase II portion of the trial." (NCT00925132)
Timeframe: 6 weeks (one full cycle)

InterventionParticipants (Count of Participants)
Cohort 1: Experienced DLTCohort 2: Experienced DLTCohort 3: Experienced DLTCohort 4: Experienced DLT
Phase I Dose Escalation0000

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Phase II: Median Overall Survival (OS)

Phase II: Time in months from the start of study treatment to date of death due to any cause. Patients alive as of the last follow-up had OS censored at the last follow-up date. Median OS was estimated using a Kaplan-Meier curve. (NCT00939991)
Timeframe: 3 years

Interventionmonths (Median)
Phase II12.5

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Phase II: Median Progression-free Survival (PFS)

Phase II: Time in months from the start of study treatment to the date of first progression according to RANO criteria, or to death due to any cause. Per RANO, progression is a ≥ 25% increase in the sum of the products of perpendicular diameters of enhancing lesions, any new lesion or clinical deterioration. Patients alive who had not progressed as of the last follow-up had PFS censored at the last follow-up date. Median PFS was estimated using a Kaplan-Meier curve. (NCT00939991)
Timeframe: 3 years

Interventionmonths (Median)
Phase II6.7

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Phase II: Radiographic Response.

The percentage of participants with a complete or partial response as determined by modified Response Assessment in Neuro-Oncology (RANO) criteria. A confirmation of response was not required. Complete Response (CR) was defined as complete disappearance on MR/CT of all enhancing tumor and mass effect, off all corticosteroids (or receiving only adrenal replacement doses) and accompanied by a stable or improving neurologic examination. Partial Response (PR) was defined as greater than or equal to 50% reduction in tumor size on MR/CT by bi-dimensional measurement, on a stable or decreasing dose of corticosteroids and accompanied by a stable or improving neurologic examination. Tumor assessments were done at baseline, the end of the first cycle (4 weeks), then the end of every second cycle (every 8 weeks) thereafter. (NCT00939991)
Timeframe: 3 years

Interventionpercentage of participants (Number)
Phase II56

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Phase I: Determination of the Maximum Tolerated Dose (MTD)

The MTD is based upon dose-limiting toxicities (DLTs) experienced during Cycle 1 of treatment. The MTD is the dose level at which 0/6 or 1/6 patients experience DLT with at least two patients experiencing DLT at the next higher dose level. Using Common Terminology Criteria for Adverse Events (CTCAE) version 3.0, DLTs are defined as: Grade 4 neutropenia lasting greater than 5 days; Grade 3 thrombocytopenia; the occurrence of non-hematologic Grade 3 or greater drug-related adverse events excluding Grade ≥ 3 elevation in alkaline phosphatase, Grade ≥ 3 nausea or vomiting unless occurring despite the use of standard anti-emetics or Grade 3 diarrhea unless occurring despite standard anti-diarrheal therapy; > 14 day delay to re-treat due to failure to resolve drug-related toxicity to re-treatment criteria or pre-treatment baseline. (NCT00939991)
Timeframe: Cycle 1 (28 days)

Interventionmg (Number)
Phase I Dose Escalation400

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Phase II: 6-month Progression-free Survival (PFS)

Phase II: Percentage of participants surviving six months from the start of study treatment without progression of disease. PFS was defined as the time from the date of study treatment initiation to the date of the first documented progression according to RANO criteria, or to death due to any cause. Per RANO, progression is a ≥ 25% increase in the sum of the products of perpendicular diameters of enhancing lesions, any new lesion or clinical deterioration. (NCT00939991)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Phase II53.8

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Co-Primary: Overall Survival (OS)

Overall Survival was defined as the time from randomization to death due to any cause. (NCT00943826)
Timeframe: Randomization until OS Event (Until data cutoff= 28 February 2013 [up to 42.2 months])

InterventionMonths (Median)
Bevacizumab + RT + Temozolomide16.8
Placebo + RT + Temozolomide16.7

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Co-Primary: Progression-free Survival (PFS) as Assessed by Investigator

PFS is defined as time from randomization to disease progression (PD) or death. PD was assessed using adapted Macdonald response criteria (modified World Health Organization [WHO] criteria) based on 3 components: radiological tumor assessments using Magnetic Resonance Imaging [MRI] scans,neurological assessment and changes in corticosteroid use. PD is assessed as greater than or equal to(>=) 25% increase in sum of products of the longest diameters of all index lesions (enhancing,measurable) compared with the smallest recorded sum (nadir); or unequivocal PD of existing non-index lesions (non-enhancing and enhancing,non-measurable); or unequivocal appearance of new lesions); or neurological worsening (if corticosteroid dose is stable or increased) compared to neurological evaluation at previous disease assessment with no need for a confirmatory scan. Participants without a PFS event were censored at last disease assessment. (NCT00943826)
Timeframe: Randomization until PFS Event [Until data cutoff= 31 March 2012 (up to 31.4 months)

InterventionMonths (Median)
Bevacizumab + RT + Temozolomide10.6
Placebo + RT + Temozolomide6.2

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Kaplan-Meier (KM) Estimate of One Year Overall Survival

KM estimate of one year overall survival (probability to survive for at least 1 year) was reported. Corresponding 95% confidence interval (CI) was calculated using Greenwood's formula. (NCT00943826)
Timeframe: Randomization until Overall Survival Event (Until data cutoff= 28 February 2013 [up to 42.2 months])

Interventionprobability of being alive (Number)
Bevacizumab + RT + Temozolomide0.72
Placebo + RT + Temozolomide0.66

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Kaplan-Meier (KM) Estimate of Two Year Overall Survival

KM estimate of two year overall survival was reported (probability to survive for at least 2 years). Corresponding 95% CI was calculated using Greenwood's formula. (NCT00943826)
Timeframe: Randomization until Overall Survival Event (Until data cutoff= 28 February 2013 [up to 42.2 months])

Interventionprobability of being alive (Number)
Bevacizumab + RT + Temozolomide0.34
Placebo + RT + Temozolomide0.30

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PFS as Assessed by an Independent Review Facility

An Independent Review Facility reviewed the MRI scans used by investigator to evaluate radiological tumor response. PFS is defined as time from randomization to PD or death. PD was assessed using adapted Macdonald response (modified WHO) criteria based on 3 components: radiological tumor assessments using MRI scans, neurological assessment and changes in corticosteroid use. PD is assessed as >=25% increase in sum of products of the longest diameters of all index lesions (enhancing, measurable) compared with the smallest recorded sum (nadir); or unequivocal PD of existing non-index lesions (non-enhancing and enhancing, non-measurable); or unequivocal appearance of new lesions); or neurological worsening (if corticosteroid dose is stable or increased) compared to neurological evaluation at previous disease assessment with no need for a confirmatory scan. Participants without a PFS event were censored at last disease assessment. (NCT00943826)
Timeframe: Randomization until PFS Event (Until data cutoff= 31 March 2012 [up to 29.5 months])

InterventionMonths (Median)
Bevacizumab + RT +Temozolomide8.4
Placebo + RT + Temozolomide4.3

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Number of Participants With Non-Serious Adverse Events, Serious Adverse Events and Death

An adverse event (AE) 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 AE.A serious adverse event (SAE) 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. Non-serious adverse events (Non-SAEs) included all AEs except SAEs (non-SAEs = all AEs - SAEs). Nine participants randomized to the Placebo+RT+Temozolomide arm incorrectly received at least 1 dose of bevacizumab and were added to the Bevacizumab+RT+Temozolomide arm for Safety. (NCT00943826)
Timeframe: Randomization until study completion (Until data cutoff= 09 Sep 2015 [up to 64 months])

,
InterventionParticipants (Number)
Non-SAEsSAEsDeath
Bevacizumab + RT + Temozolomide437179335
Placebo + RT + Temozolomide412115337

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Best Overall Response Based on Response Evaluation Criteria in Solid Tumors (RECIST)

All measurable lesions up to a maximum of 5 lesions per organ and 10 lesions in total, representative of all involved organs were to be identified as target lesions. Data were to be collected at Screening, every 6 weeks and at 30 days after the final dose of robatumumab or the standard treatment assigned (whichever was last). The best overall response was to be the best response recorded from the start of the treatment until disease progression/recurrence. Complete Response (CR): Disappearance of all target lesions; Partial Response (PR): >30% decrease in the sum of the longest diameter (LD) of target lesions; Progressive Disease (PD): >20% increase in the sum of the LD of target lesions 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. (NCT00960063)
Timeframe: Screening, every 6 weeks and at ~30 days after last dose of study drug (Up to ~10.3 months)

,
InterventionParticipants (Number)
Complete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive Disease (PD)
Ifosfamide+Etoposide+Robatumumab0201
Temozolomide+Irinotecan+Robatumumab0100

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Number of Participants Who Developed Anti-robatumumab Antibodies

The incidence of anti-robatumumab antibodies was to be assessed. Only participants who had a negative pre-treatment sample and a post-treatment sample were considered to be evaluable. If a participant had a single sample considered positive in the anti-robatumumab antibody assay (with the exception of pre-treatment positive participants), then they would be counted as positive in the immunogenicity assessment. (NCT00960063)
Timeframe: Prior to 1st and 8th doses of robatumumab, ~30 days after last dose of study drug, and 4 months after last dose of study drug (Up to ~13.3 months)

InterventionParticipants (Number)
Temozolomide+Irinotecan+Robatumumab0
Ifosfamide+Etoposide+Robatumumab0

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Number of Participants With Dose Limiting Toxicities

Dose-limiting toxicity was defined by the following adverse events (AEs) that were considered possibly or probably related to either robatumumab or to its interaction with the chemotherapy regimen assigned: neutropenia (Grade 4 for >1 week that did not resolve prior to Day 1 of the next cycle; Grade 3-4 neutropenia with Grade ≥2 fever lasting 3 days; neutropenic infection; failure to recover to study entry/eligibility criteria laboratory requirement levels that resulted in a delay of 14 days between treatment cycles), thrombocytopenia (Grade 4 for >1 week that did not resolve prior to Day 1 of the next cycle; Grade 3-4 requiring a platelet transfusion on 2 separate days within a cycle) or all other AEs (Grade ≥3 [any duration] not ameliorable by supportive or symptomatic measures). The National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE version 4.0) was to be used to grade AEs. (NCT00960063)
Timeframe: Up to ~30 days after last dose of study drug (Up to ~10.3 months)

InterventionParticipants (Number)
Temozolomide+Irinotecan+Robatumumab1
Ifosfamide+Etoposide+Robatumumab3

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Percentage of Participants Who Discontinued

Discontinuation was defined as the percentage of participants who permanently discontinued treatment in either treatment arm. Percentage of participant with individual discontinuation reason are reported. CNS: central nervous system; CTCAE: Common Terminology Criteria for Adverse Events . Other reason refers to any other reason than the specified ones. (NCT00967330)
Timeframe: From baseline until death (up to 4.5 years)

,
Interventionpercentage of participants (Number)
Persisting non-hematological toxicity CTCAE Grade3CNS hemorrhagic event (CTCAE Grade >1)Gastro-intestinal perforation (CTCAE Grade 1-4)OtherParticipant's wishProgressive diseaseProteinuria (nephrotic syndrome) (CTCAE Grade 4)RegularRepeated CTCAE Grade 4 hematological toxicityVenous thrombosis/embolismWound dehiscence requiring medical interventionWound dehiscence requiring surgical intervention
Bevacizumab + Irinotecan00.90.99.5674.10.91.700.90.94.3
Temozolomide1.9005.65.657.4027.80.9000

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Overall Survival (OS)

Overall survival was defined as the time from randomization to death from any cause. OS was estimated using Kaplan-Meier method. (NCT00967330)
Timeframe: From baseline until death (up to 4.5 years)

InterventionMonths (Median)
Bevacizumab + Irinotecan16.64
Temozolomide17.30

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Change From Baseline for Mini-Mental Status Examination (MMSE) at Baseline, Post-Baseline (up to Month 30)

The MMSE briefly measures orientation to time and place, immediate recall, short-term verbal memory, calculation, language and construct ability. Each area tested had a designated point value, the total score can range from 0 to 30, with a higher score indicating better function. (NCT00967330)
Timeframe: Baseline, Post-Baseline (up to Month 30)

,
Interventionunits on a scale (Least Squares Mean)
Orientation to time and placeImmediate recallRepetitions requiredCalculationsShort-term verbal memoryLanguage and construct abilityTotal Score
Bevacizumab + Irinotecan-0.01771-0.00264-0.05763-0.21530.2012-0.1254-0.2871
Temozolomide-0.2110-0.032190.08530-0.21200.1634-0.2057-0.5999

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Percentage of Participants Achieving Progression-Free Survival (PFS) Without Disease Progression or Death at 6 Months

Progression-free survival was defined as the time from randomization to objective tumor progression or death from any cause, whichever came first. Progression was defined as 25 percent (%) increase in size of enhancing tumor or any new tumor on gadolinium contrast agent magnetic resonance imaging (Gd-MRI) scans, or neurologically worse, and steroids stable or increased. Percentage of participants achieving PFS without disease progression or death was reported. (NCT00967330)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Bevacizumab + Irinotecan79.31
Temozolomide42.59

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Percentage of Participants Who Received Corticosteroid for Glioblastoma

Participants used corticosteroids for the glioblastoma condition. Corticosteroids included dexamethasone, methylprednisone, fortecortin, hydrocortisone, urbason, and prednisolone. (NCT00967330)
Timeframe: From baseline to Month 6

Interventionpercentage of participants (Number)
Bevacizumab + Irinotecan80.0
Temozolomide78.7

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Number of Participants With A Best Overall Response (BOR) of Complete Response (CR) and With A BOR of CR or Partial Response (PR)

BOR was defined as the best response observed for a participant during assessment. Number of participants who had BOR as CR and number of participants who had BOR as CR or PR were reported. Complete response was defined as disappearance of all enhancing tumor on consecutive Gd-MRI scans at least 1 month apart, off steroids, and neurologically stable or improved. Partial response was defined as 50% reduction in size of enhancing tumor on consecutive Gd-MRI scans at least 1 month apart, steroids stable or reduced, and neurologically stable or improved. (NCT00967330)
Timeframe: 4 week after radiotherapy (RT) (up to Week 4), >4 Week after RT (up to Week 8) and Month 6

,
Interventionparticipants (Number)
CR at 4 weeks after RT (n=110,46)CR at >4 weeks after RT (n=95,35)CR at Month 6 (n=91,28)CR or PR at 4 Week after RT (n=110,46)CR or PR at >4 Week after RT (n=95,35)CR or PR at Month 6 (n=91,28)
Bevacizumab + Irinotecan1111342185
Temozolomide211633

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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) at Baseline, Post-Baseline (up to Month 30)

The EORTC QLQ-C30 incorporates: 5 functional scales (physical, role, cognitive, emotional, and social); 9 symptom scales (fatigue, pain, nausea and vomiting, dyspnea, 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 for Global Qol/functional scales=better level of functioning or a higher score for symptom scale=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. (NCT00967330)
Timeframe: Baseline, Post-Baseline (up to Month 30)

,
Interventionunits on a scale (Least Squares Mean)
Physical FunctioningRole FunctioningEmotional FunctioningCognitive FunctioningSocial FunctioningGlobal health Status /QoL (ql)FatiqueNausea/VomittingPainDyspnoeaInsomniaAppetite lossConstipationDiarrhoeaFinancial Problems
Bevacizumab + Irinotecan-8.3513-0.76352.2774-2.0188-6.2324-3.11345.52288.955710.68763.7134-2.626613.74238.02306.02304.8435
Temozolomide-6.2511-2.23392.2547-3.8401-4.61980.38552.17794.75971.59260.5046-7.502610.96014.0855-0.14552.1140

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Progression-Free Survival (PFS)

Progression-free survival was defined as the time from randomization to objective tumor progression or death from any cause, whichever came first. Progression was defined as 25% increase in size of enhancing tumor or any new tumor on Gd-MRI scans, or neurologically worse, and steroids stable or increased. PFS was estimated using Kaplan-Meier method. (NCT00967330)
Timeframe: From baseline to the end of the study (up to 4.5 years)

InterventionMonths (Median)
Bevacizumab + Irinotecan9.74
Temozolomide5.99

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Percentage of Participants With Response on FLAIR Imaging

"FLAIR lesions were determined as stable, progressive or decreased. FLAIR lesions was determined as progressive only if they were not be attributed to causes apart from tumor infiltration (sequelae of radiation therapy, demyelination, ischemia, infection, seizures, or other treatment effects). Percentage of participants are based on ITT population.~Dis.=Discontinuation." (NCT00967330)
Timeframe: At screening, Baseline, Month 6 and Therapy Discontinuation (Up to 4.5 years)

,
Interventionpercentage of participants (Number)
Screening: Initial Flair Lesion (n=116,54)Screening:Stable Flair Lesion (n=116,54)Baseline:Decreased FLAIR Lesions (n=105,46)Baseline:Initial FLAIR Lesions (n=105,46)Baseline:Progressive FLAIR Lesions (n=105,46)Baseline: Stable FLAIR Lesions (n=105,46)Month 6:Progressive FLAIR Lesions (n=91,28)Month 6: Stable FLAIR Lesions (n=91,28)Therapy Dis.:Decreased FLAIR Lesions (n=55,31)Therapy Dis.:Progressiv FLAIR Lesions (n=55,31)Therapy Dis.:Stable FLAIR Lesions (n=55,31)
Bevacizumab + Irinotecan72.417.216.418.114.741.416.462.10.929.317.2
Temozolomide72.216.720.418.511.135.222.229.60.027.829.6

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Time to Treatment Failure

(NCT00967330)
Timeframe: From baseline until end of study (up to 4.5 years)

Interventionyears (Median)
Bevacizumab + IrinotecanNA
TemozolomideNA

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Change From Baseline for EORTC QLQ Brain Neoplasm 20 (BN20) at Baseline, Post-Baseline (up to Month 30)

EORTC QLQ-BN20 consisted of 20 items assessing visual disorders, motor dysfunction, communication deficit, various disease symptoms (e.g. headaches and seizures), treatment toxicities (e.g. hair loss) and future uncertainty. All of the 20 items are rated on a 4 point Likert scale from 1=not at all, 2=a little, 3=quite a bit and 4=very much, and were linearly transformed to a 0-100 scale, with higher scores indicating more severe symptoms. (NCT00967330)
Timeframe: Baseline, Post-Baseline (up to Month 30)

,
Interventionunits on a scale (Least Squares Mean)
Future uncertaintyVisual disorderMotor dysfunctionCommunication deficitHeadachesDrowsinesHair lossItchy skinWeakness of legsBladder control
Bevacizumab + Irinotecan-5.2779-2.08695.44164.74404.390511.720411.92355.48828.95861.5020
Temozolomide-8.5478-3.2026.54294.6431-3.93898.28057.33286.46907.92451.9710

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Change From Baseline for Karnofsky Performance Status (KPS) Score at Baseline, Post-Baseline (up to Month 30)

KPS is an 11-level score (0, 10, 20, 30, 40, 50, 60, 70, 80, 90, and 100) which ranges between 0 (death) to 100 (complete healthy status); a higher score represents a higher ability to perform daily tasks. Deterioration in KPS was defined as decrease of 20 or more points in KPS score. (NCT00967330)
Timeframe: Baseline, Post-Baseline (up to Month 30)

Interventionunits on a scale (Least Squares Mean)
Bevacizumab + Irinotecan-3.3399
Temozolomide-5.4909

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Concentration of Afatinib in Plasma at Steady State Pre-dose on Days 8, 15 and 29

Concentration of afatinib in plasma at steady state pre-dose (Cpre,ss) on days 8, 15 and 29. (NCT00977431)
Timeframe: Pharmacokinetic blood sample were taken at 5 minutes before drug on days 8, 15 and 29 and 1, 3 and 6 hours after drug administration on day 15

,,,,
Interventionnanograms per milliliter (ng/mL) (Geometric Mean)
Cpre, ss, 8Cpre, ss, 15Cpre, ss, 29
Afatinib 20 mg, Radiotherapy - Regimen U4.94.45.0
Afatinib 20 Milligram, Radiotherapy + Temozolomide - Regimen M4.45.65.3
Afatinib 30 mg, Radiotherapy + Temozolomide - Regimen M10.79.617.8
Afatinib 40 mg, Radiotherapy - Regimen U16.718.916.1
Afatinib 40 mg, Radiotherapy + Temozolomide - Regimen M15.716.817.4

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Number of Patients With Investigator Defined Dose Limiting Toxicities (DLT) During the RT Phase

"Adverse event (AE) related to afatinib with any one criteria; Hematological: Common terminology criteria for adverse events (CTCAE) Grade 4 neutropenia (Absolute neutrophil count, including bands <500/cubic millimeter (mm³)) for >7 days, CTCAE Grade 3 or 4 neutropenia of any duration associated with fever >38.3 Celsius, CTCAE Grade 3 thrombocytopenia (platelet count <50000 - 25000/mm³), All other toxicities of CTCAE Grade ≥3 leading interruption of treatment > 14 days.~Non-hematological: CTCAE Grade ≥3 nausea or vomiting despite appropriate use of standard anti-emetics for ≥3 days, CTCAE Grade ≥3 diarrhea despite appropriate use of standard anti-diarrheal therapy for ≥3 days, CTCAE Grade ≥3 rash despite standard medical management and lasting >7 days, CTCAE Grade ≥2 cardiac left ventricular function, CTCAE Grade ≥2 worsening of renal function as measured by serum creatinine, newly developed proteinuria or decrease in glomerular filtration rate, All other toxicities of CTCAE Grade ≥3. (NCT00977431)
Timeframe: 6 weeks

InterventionParticipants (Number)
Afatinib 20 Milligram, Radiotherapy + Temozolomide - Regimen M1
Afatinib 30 mg, Radiotherapy + Temozolomide - Regimen M0
Afatinib 40 mg, Radiotherapy + Temozolomide - Regimen M2
Afatinib 20 mg, Radiotherapy - Regimen U0
Afatinib 40 mg, Radiotherapy - Regimen U1

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The Objective Tumour Response According to the Macdonald Criteria

Objective response was defined as a best overall response of complete response (CR) or partial response (PR). The best overall response was the best overall response to trial medication according to the Macdonald criteria recorded since the first administration of trial medication and until the earliest of disease progression, death, or start of further anti-cancer treatment. Tumour response was assessed based on local radiological image evaluation by the investigators according to the Macdonald criteria: Complete Response (CR): Disappearance of all enhancing tumour on consecutive Magnetic resonance imaging (MRI) scans at least 28 days apart, off steroids, and neurologically stable or improved. Partial Response (PR): At least 50% reduction in size of enhancing tumour on consecutive MRI scans at least 28 days apart, steroids stable or reduced, and neurologically stable or improved. (NCT00977431)
Timeframe: From the first administration of trial medication until 4 weeks after the last administration of trial medication, up to approximately 338 weeks

,,,,
InterventionParticipants (Number)
NoYesMissing
Afatinib 20 mg, Radiotherapy - Regimen U300
Afatinib 20 Milligram, Radiotherapy + Temozolomide - Regimen M520
Afatinib 30 mg, Radiotherapy + Temozolomide - Regimen M330
Afatinib 40 mg, Radiotherapy - Regimen U1012
Afatinib 40 mg, Radiotherapy + Temozolomide - Regimen M502

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Maximum Tolerated Dose (MTD) of Afatinib

The MTD was defined as the highest afatinib dose level, at which no more than 1 out of 6 patients experienced drug-related DLT, i.e. the highest afatinib dose with a DLT incidence ≤17%. A separate MTD was determined for afatinib and RT (Regimen U), and for afatinib, TMZ, and RT (Regimen M). (NCT00977431)
Timeframe: 6 weeks

InterventionMilligram (mg) (Number)
Total - Regimen M30
Total - Regimen U40

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Incidence and Intensity of Adverse Events (AE) According to Common Terminology Criteria of Adverse Events (CTCAE v.3.0)

Incidence and intensity of adverse events (AE) according to Common Terminology Criteria of Adverse Events (CTCAE v.3.0). The CTCAE grades are: 1 (mild AE), 2 (moderate AE), 3 (severe AE), 4 (life-threatening or disabling AE), 5 (death related to AE). (NCT00977431)
Timeframe: From the first administration of trial medication until 4 weeks after the last administration of trial medication, up to approximately 338 weeks

,,,,
InterventionParticipants (Number)
Grade 1Grade 2Grade 3Grade 4Grade 5
Afatinib 20 mg, Radiotherapy - Regimen U01200
Afatinib 20 Milligram, Radiotherapy + Temozolomide - Regimen M00430
Afatinib 30 mg, Radiotherapy + Temozolomide - Regimen M02400
Afatinib 40 mg, Radiotherapy - Regimen U12523
Afatinib 40 mg, Radiotherapy + Temozolomide - Regimen M11410

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Response Rate

The percentage of participants with a complete or partial response as determined by a modification of the Response Assessment in Neuro-Oncology (RANO) criteria. Complete Response (CR) was defined as complete disappearance on MR/CT of all enhancing tumor and mass effect, off all corticosteroids (or receiving only adrenal replacement doses) and accompanied by a stable or improving neurologic examination. Partial Response (PR) was defined as greater than or equal to 50% reduction in tumor size on MR/CT by bi-dimensional measurement, on a stable or decreasing dose of corticosteroids and accompanied by a stable or improving neurologic examination. Per the criteria, confirmation of response was required. Response rate = CR+PR. (NCT00979017)
Timeframe: 4 months

Interventionpercentage of participants (Number)
Avastin in Combination With Temozolomide and Irinotecan22

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Incidence and Severity of Central Nervous System (CNS) Hemorrhage and Systemic Hemorrhage

Incidence and severity of CNS hemorrhage and systemic hemorrhage- The adverse events for this study were collected using Common Terminology Criteria for Adverse Events (CTCAE) version 3.0, and have been converted to CTCAE version 4.0 for entry into ClinicalTrials.gov. (NCT00979017)
Timeframe: 4 months

Interventionparticipants (Number)
CNS hemorrhage (grade 3)Systemic hemorrhage (all grade 3)
Avastin in Combination With Temozolomide and Irinotecan13

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Median Overall Survival (OS)

Time in months from the start of study treatment to the date of death due to any cause. Patients alive as of the last follow-up had OS censored at the last follow-up date. Median OS was estimated using a Kaplan-Meier curve. (NCT00979017)
Timeframe: 36 months

Interventionmonths (Median)
Avastin in Combination With Temozolomide and Irinotecan12

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Median Progression-free Survival (PFS)

Time in months from the start of study treatment to the date of first progression according to RANO criteria, or to death due to any cause. Per RANO, progression is a ≥ 25% increase in the sum of the products of perpendicular diameters of enhancing lesions, worsening T2/FLAIR, any new lesion, or clinical deterioration. Patients alive who had not progressed as of the last follow-up had PFS censored at the last follow-up date. Median PFS was estimated using a Kaplan-Meier curve. (NCT00979017)
Timeframe: 36 months

Interventionmonths (Median)
Avastin in Combination With Temozolomide and Irinotecan8.6

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Incidence of Grade ≥ 4 Hematologic and ≥ Grade 3 Non-hematologic Toxicities

Incidence of treatment-related, grade ≥ 4 hematologic and ≥ grade 3 non-hematologic toxicities- The adverse events for this study were collected using Common Terminology Criteria for Adverse Events (CTCAE) version 3.0, and have been converted to CTCAE version 4.0 for entry into ClinicalTrials.gov. (NCT00979017)
Timeframe: 4 months

Interventionparticipants (Number)
Grade > or = to 4 hematologic toxicityGrade > or = to 3 non-hematologic toxicity
Avastin in Combination With Temozolomide and Irinotecan717

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Number of Patients Surviving Without Disease Progression After 6 Months

"Patients will be monitored from date of first treatment to the date of first observation of progressive disease, non-reversible neurologic progression or increasing steroid requirements, death due to any cause, or early discontinuation of treatment. Progression-free survival will be defined as the absence of any of the above after 6 months.~Progression (defined by MacDonald Criteria) is a 25% increase in the sum of products of all measurable lesions over smallest sum observed compared to baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to the cancer)." (NCT00990652)
Timeframe: From date of first treatment until disease progression, death, or early discontinuation of treatment (up to 24 months)

Interventionparticipants (Number)
Bortezomib + Temozolomide0

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Number of Participants Achieving a Response to Treatment (Either Complete or Partial Response) as Defined by MacDonald Criteria

"This measure was assessed only in patients who had residual tumor post-operatively. Per MacDonald Criteria:~Complete Response requires complete disappearance of all measurable & evaluable disease, no new lesions, no evidence of non-evaluable disease, and only minimal or no use of steroids.~Partial Response is defined as >= 50% decrease compared to baseline in the sum of products of perpendicular diameters of all measurable lesions, no progression of evaluable disease, and no new lesions. Responders must be on the same or decreasing doses of steroid.~Response was assessed by imaging (MRI or CT with contrast)." (NCT00990652)
Timeframe: Day of treatment post-surgery and then approximately every 8 weeks thereafter until off treatment

Interventionparticipants (Number)
Bortezomib + Temozolomide0

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Number of Grade 1, 2, 3, 4, and 5 Adverse Events Observed During Study Treatment (Defined by CTCAE v 3.0)

"Adverse events (AEs) were graded according to the National Cancer Institute's Common Toxicity Criteria for Adverse Events (CTCAE) version 3.0. In general, AEs are 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" (NCT00990652)
Timeframe: Days 1, 4, 8 pre-surgery, and then at the start of every cycle (approximately every 4 weeks) post-surgery while on treatment

Interventionadverse events (Number)
Grade 1Grade 2Grade 3Grade 4Grade 5
Bortezomib + Temozolomide80301110

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Overall Survival Rate at 6 Months

The rate of overall survival at 6 months (regardless of disease progression) was calculated. (NCT00990652)
Timeframe: After 6 months on study

Interventionpercentage of participants (Number)
Bortezomib + Temozolomide69

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Overall Survival (in Days)

(NCT00990652)
Timeframe: Days 1, 4, 8 pre-surgery, once per cycle (every 4 weeks) while on treatment post-surgery, and then every 3 months up to 2 years during follow-up

Interventiondays (Median)
Bortezomib + Temozolomide248

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Dose Limiting Toxicity

Number of participants with dose limiting toxicity events (NCT00993044)
Timeframe: 2 years

Interventionparticipants (Number)
Single Arm2

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Overall Survival

Estimate the overall survival in subjects with newly-diagnosed glioblastoma (GBM) treated with bortezomib/temozolomide/radiation followed by bortezomib/temozolomide for 24 cycles until progression is detected or for up to 24 cycles (~2 years). (NCT00998010)
Timeframe: 2 years

Interventionmonths (Mean)
Experimental19.1

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Survival at 1 Year

Overall Survival at 12 months from completion of radiation treatment (NCT00998010)
Timeframe: 1 year

Interventionpercentage of participants (Median)
Experimental87.5

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Toxicity Assessed According to the NCI Common Terminology Criteria for Adverse Events (CTCAE) Version 3.

(NCT00998010)
Timeframe: 2 years

InterventionParticipants (Count of Participants)
Radiotherapy phase72241098Post Radiotherapy phase72241098Follow-up phase72241098
Grade 4 Toxicity< Grade 3 ToxicityGrade 3 toxicity
Experimental6
Experimental1
Experimental17
Experimental7
Experimental0
Experimental24

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Tumor Progression as Assessed by Magnetic Resonance Imaging (MRI) and Neurologic Exam

MRI will be done 2 weeks after completion of radiation and then every 8 weeks. Neurologic exam to be performed every 2 weeks during radiation therapy, then every every 4 weeks after radiation is completed. (NCT00998010)
Timeframe: at 6, 12, 18 and 24 months from completion of radiation treatment.

Interventionpercentage of participants (Median)
Progression Free Survival rate at 6 monthsProgression Free Survival rate at 12 monthsProgression Free Survival rate at 18 monthsProgression Free Survival rate at 24 moths
Experimental54.229.225.025

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Time to Progression

"Median time to tumor progression. Because many newly-diagnosed patients are likely not to have evaluable disease due to gross total resections. A 7-point scale was used to guide Magnetic resonance imaging (MRI) assessment to determine progression in this study. A -2 or -3 assessment will be taken as progression.~The 7-point scale is listed below. complete resolution of tumor: 3 tumor definitely smaller: 2 tumor probably smaller: 1 tumor unchanged: 0 tumor probably worse: -1 tumor definitely worse: -2 new lesion: -3" (NCT00998010)
Timeframe: From the completion of radiation treatment to tumor progression

Interventionmonths (Median)
Experimental6.2

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One and Two Year Overall Survival

Time in months from the start of study treatment to date of death due to any cause. Patients alive as of the last follow-up had OS censored at the last follow-up date. (NCT01004874)
Timeframe: One year and two years

Interventionpercentage of participants (Number)
One year Overall SurvivalTwo year Overall Survival
Bevacizumab, XRT, Temozolomide, Topotecan73.835.6

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Median Overall Survival

OS was defined as time in months from the start of study treatment to date of death due to any cause. Patients alive as of the last follow-up had OS censored at the last follow-up date. Median OS was estimated using a Kaplan-Meier curve. (NCT01004874)
Timeframe: 27 months

Interventionmonths (Median)
Bevacizumab, XRT, Temozolomide, Topotecan17.2

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6-month Progression-free Survival

Percentage of participants surviving six months from the start of study treatment without progression of disease. PFS was defined as the time from the date of study treatment initiation to the date of the first documented progression according to the Macdonald criteria, or to death due to any cause. (NCT01004874)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Bevacizumab, XRT, Temozolomide, Topotecan88.8

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Median Progression-free Survival

PFS was defined as time in months from the start of study treatment to the date of first progression according to Macdonald criteria, or to death due to any cause. Patients alive who had not progressed as of the last follow-up had PFS censored at the last follow-up date. Median PFS was estimated using a Kaplan-Meier curve. (NCT01004874)
Timeframe: 27 months

Interventionmonths (Median)
Bevacizumab, XRT, Temozolomide, Topotecan11.1

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Number of Patients Experiencing a Greater Than or Equal to Grade 4 Hematologic or a Greater Than or Equal to Grade 3 Non-hematologic Toxicity

Number of times a grade ≥4 hematologic or grade ≥3 non-hematologic toxicity was experienced (NCT01004874)
Timeframe: 27 months

Interventionparticipants (Number)
Greater than equal Gr.4 hematologic toxicitesGreater than equal Gr.3 non-hematologic toxicites
Bevacizumab, XRT, Temozolomide, Topotecan2317

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Number of Patients Experiencing a Central Nervous System (CNS) Hemorrhage or a Systemic Hemorrhage

Number of times a CNS hemorrhage or systemic hemorrhage was experienced (NCT01004874)
Timeframe: 27 months

Interventionparticipants (Number)
Grade 2 central nervous system (CNS) hemorrhageGrade 3 CNS hemorrhageGrade 4 CNS hemorrhage
Bevacizumab, XRT, Temozolomide, Topotecan102

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Objective Response Rate (ORR)

Tumor response is evaluated according to Response Evaluation Criteria in Solid Tumors (RECIST) (version 1.0). Target lesions are assessed by physical exam and/or computerized tomography (CT): 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. The Objective Response Rate (ORR) is the sum of the percentages of patients achieving CR or PR. (NCT01009515)
Timeframe: 6 months

Interventionparticipants (Number)
Complete response (CR)Partial response (PR)Stable diseaseProgressive disease (PD)ORR (CR + PR)
Chemotherapy Combination130124

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Overall Survival

The time from treatment initiation to death by any cause. (NCT01009515)
Timeframe: 2 years

Interventionweeks (Median)
Chemotherapy Combination47

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Time to Progression

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 physical exam or computerized tomography (CT): 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. (NCT01009515)
Timeframe: 2 years

Interventionweeks (Median)
Chemotherapy Combination31

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Safety Profile

All toxicities encountered during the study by patients who receive at least one on-study treatment will be graded according to the NCI CTCAE (Version 3.0). The number of patients experiencing adverse events will be reported according to grade. (NCT01009515)
Timeframe: Up to 30 days after last on-study treatment, for up to 2 years

Interventionparticipants (Number)
Fatigue (Grade 1-2)Fatigue (Grade 3-4)Fever (Grade 1-2)Fever (Grade 3-4)Weight loss (Grade 1-2)Weight loss (Grade 3-4)Anorexia (Grade 1-2)Anorexia (Grade 3-4)Diarrhea (Grade 1-2)Diarrhea (Grade 3-4)Aspartate aminotransferase increased (Grade 1-2)Aspartate aminotransferase increased (Grade 3-4)Vomiting (Grade 1-2)Vomiting (Grade 3-4)Gastrointestinal Bleed (Grade 1-2)Gastrointestinal Bleed (Grade 3-4)Nausea (Grade 1-2)Nausea (Grade 3-4)Alanine aminotransferase increased (Grade 1-2)Alanine aminotransferase increased (Grade 3-4)Hyperbilirubinemia (Grade 1-2)Hyperbilirubinemia (Grade 3-4)Neutropenia (Grade 1-2)Neutropenia (Grade 3-4)Anemia (Grade 1-2)Anemia (Grade 3-4)Lymphopenia (Grade 1-2)Lymphopenia (Grade 3-4)Leukopenia (Grade 1-2)Leukopenia (Grade 3-4)Thrombocytopenia (Grade 1-2)Thrombocytopenia (Grade 3-4)Hyperglycemia (Grade 1-2)Hyperglycemia (Grade 3-4)Hypophosphatemia (Grade 1-2)Hypophosphatemia (Grade 3-4)Hypokalemia (Grade 1-2)Hypokalemia (Grade 3-4)Hyponatremia (Grade 1-2)Hyponatremia (Grade 3-4)Chest wall pain (Grade 1-2)Chest wall pain (Grade 3-4)Bone pain (Grade 1-2)Bone pain (Grade 3-4)Muscle weakness, lower limb (Grade 1-2)Muscle weakness, lower limb (Grade 3-4)Joint pain (Grade 1-2)Joint pain (Grade 3-4)Drowsiness (Grade 1-2)Drowsiness (Grade 3-4)Peripheral Sensory Neuropathy (Grade 1-2)Peripheral Sensory Neutropenia (Grade 3-4)Pericardial effusion (Grade 1-2)Pericardial effusion (Grade 3-4)Edema limbs (Grade 1-2)Edema limbs (Grade 3-4)Alopecia (Grade 1-2)Alopecia (Grade 3-4)Rash (Grade 1-2)Rash (Grade 3-4)Dry mouth (Grade 1-2)Dry mouth (Grade 3-4)
Chemotherapy Combination910101105121210112020103240417030310130301120201001300110804030

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Median Overall Survival (OS) Based on the MGMT Promoter Methylation Status

IDH1 and MGMT methylation are important independent prognostic biomarkers that have to be included in a Cox regression model. In addition, subgroup analysis could reveal differential sensitivities to the treatment arm. The MGMT promoter methylation status, IDH1 mutation status were not available for all of the control samples. Therefore, only the samples with both info available were included in the analysis. Baseline analysis results are included in the Baseline Characteristics module. (NCT01013285)
Timeframe: 2 years

,
Interventionmonths (Median)
Median Overall survival of MGMT MethylatedMedian Overall survival of MGMT Unmethylated
Historical Control UCLA/KPLA26.718.2
Treatment Arm24.715.9

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Overall Survival

(NCT01013285)
Timeframe: 2 years

InterventionMonths (Median)
Treatment Arm19.6
Historical Control UCLA/KPLA21.1

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Radiographic Response (When Evaluable)

"Radiation therapy (RT) median from diagnosis to RT. Patients will have brain MRI evaluation of response and progression every 8 weeks starting from the day 56 scan obtained 2 weeks after completion of radiation and daily temozolomide and assessment will be conducted on a 7-point scale. This scale is expected to be more useful in this study because many newly-diagnosed patients are likely not to have evaluable disease due to gross total resections. Determination of whether progression occurs based on the day 56 scan will take into account the untreated window between baseline MRI and day of 1 of study.~7 Point Likert Scale: 3 to -3, 3 means complete resolution of tumor, and -3 means new lesion. A -2 or -3 assessment will be taken as tumor progression.~complete resolution of tumor: 3~tumor resolved 3 tumor definitely smaller: 2 tumor probably smaller: 1 tumor unchanged: 0 tumor probably worse: -1 tumor definitely worse: -2 New Lesion: -3" (NCT01013285)
Timeframe: 2 years

InterventionWeeks (Median)
Treatment Arm4.14
Historical Control UCLA/KPLA5

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Time to Disease Progression

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. (NCT01013285)
Timeframe: 2 years

InterventionMonths (Median)
Treatment Arm13.6
Historical Control UCLA/KPLA7.6

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Progression-free Survival at 6 Months

participants who were alive and disease progression free at 6 months (NCT01013285)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Treatment Arm88.4
Historical Control UCLA/KPLA58.3

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Objective Response Rates. Assessed With Cranial MRI

"Objective Response (OR) encompassed the number of participants with Complete Response (CR) and the number of participants with Partial Response (PR). CR is the disappearance of all brain metastases, assessed between two or more cranial MRI. PR is at least a 30% decrease in the sum of the longest diameter of the brain metastases, taking as reference the baseline sum longest diameter, assessed between two or more cranial MRI.~Objective Response Rate (ORR) is the ratio between the number of participants with objective response and the total number of participants." (NCT01015534)
Timeframe: 90 days

InterventionPercentage of participants with OR (Number)
Whole Brain Irradiation and Temozolomide78.6
Whole Brain Irradiation48.1

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Overall Survival

Overall survival:Time in months measured from treatment initiation until the date of death or the date of last follow-up. (NCT01015534)
Timeframe: 1 year

InterventionMonths of Overall Survival (Median)
Whole Brain Irradiation and Temozolomide8
Whole Brain Irradiation8.1

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Survival Free of Brain Metastases Progression (PFS of BM)

Progression free survival of brain metastases is the survival of participants without progressive brain metastases or without neurological symptoms. The progressive brain metastases (PBM) were evaluated with cranial MRI. The PBM were defined as an increase of at least 20% 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 metastases. (NCT01015534)
Timeframe: at 90 days

InterventionPercentage of Participants (Number)
Whole Brain Irradiation and Temozolomide88.7
Whole Brain Irradiation83.7

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Phase 1: Maximum Tolerated Dose (MTD)

Dose limiting toxicity (DLT) = any of the following events within 1st 8 weeks of treatment attributable to study drugs: Any grade (gr) 3/4 thrombocytopenia, gr 4 anemia, gr 3 neutropenia with fever (>100.4). gr 4 neutropenia lasting > 7 days; Any non-hematologic (NH) gr 3+ toxicity (TOX), excluding alopecia, despite maximal medical therapy (MLT); NH TOX such as rash, nausea, vomiting, diarrhea, mucositis, hypophosphatemia, and hypertension will only be considered DLTs if they remain gr 3+ despite MLT; 2nd occurrence of thromboembolism; Failure to recover from TOX (<= gr 1) to be eligible for re-treatment with study drugs <= 14 days of last dose of either drug; Any episode of non-infectious radiologically observed pneumonitis gr 2-4 any duration. Dose level will be considered acceptable if <= 1 of the 1st 6 eligible patients experiences a DLT. If current level is considered acceptable, dose escalation occurs. Otherwise preceding acceptable dose level will be declared the MTD. (NCT01026493)
Timeframe: Start of treatment to 8 weeks.

Interventionparticipants (Number)
Phase I: Dose Level 11
Phase I: Dose Level 2a0
Phase I: Dose Level 2b1
Phase I: Dose Level 31

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Phase II: 6-month Progression-free Survival (PFS) Rate for Patients With Measurable Disease After Surgery

For patients with measureable disease after surgery: Progression defined as ≥ 25% increase in size of enhancing tumor or any new tumor; or neurologically worse, and steroids stable/increased. Bevacizumab (BEV)-naïve group: p0= 15% as estimate of 6-mo. PFS [null hypothesis (NH)], p1= 30%, with a 15% absolute increase [alternative hypothesis (AH)]. Error rates of 10% alpha and 10% beta. If <= 11 patients experience 6-month PFS of the first 53 analyzable patients, then do not reject the null hypothesis that the 6-month PFS rate of experimental arm is less than 15%; BEV-failure group: p0 = 2% as a conservative estimate of 6-month PFS [NH], p1 = 15%, with a 13% absolute increase [AH]. Using first 26 analyzable subjects for each experimental arm, there is >= 90% power to detect >= 15% increase at a significance level of 0.10, using a 1-sided binomial test. If >= 2 patients (8%) are progression free at 6 mo., then claim this regimen to be promising in the patient group. (NCT01026493)
Timeframe: Randomization to 6 months.

Interventionparticipants (Number)
Phase II: Arm 1/BEV-NAIVE9
Phase II: Arm 2/BEV-NAIVE9
Phase II: Arm 1/BEV-FAILURE1
Phase II: Arm 2/BEV-FAILURE1

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Phase II: Objective Response (Partial and Complete Response) Rate for Patients With Measurable Disease After Surgery

Response and progression will be evaluated using standard criteria for patients with malignant gliomas (Macdonald 1990). Partial response and complete response are centrally reviewed. (NCT01026493)
Timeframe: Analysis occurs after all patients have been on study for at 6 months. (Patients are followed from randomization to death or study termination whichever occurs first.)

Interventionpercentage of participants (Number)
Phase II: Arm 1/BEV-NAIVE0
Phase II: Arm 2/BEV-NAIVE3.8
Phase II: Arm 1/BEV-FAILURE5.3
Phase II: Arm 2/BEV-FAILURE0

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Phase II: Overall Survival (OS)

Survival time is defined as time from randomization to date of death from any cause and is estimated by the Kaplan-Meier method. Patients last known to be alive are censored at the date of last contact. This analysis was planned to occur when all patients had been potentially followed for at least 6 months. (NCT01026493)
Timeframe: Analysis occurs after all patients have been on study for at 6 months. (Patients are followed from randomization to death or study termination whichever occurs first.)

Interventionmonths (Median)
Phase II: Arm 1/BEV-NAIVE10.3
Phase II: Arm 2/BEV-NAIVE10.7
Phase II: Arm 1/BEV-FAILURE4.7
Phase II: Arm 2/BEV-FAILURE4.7

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Progression Free Survival

The progression free survival of patients receiving study drug will be recorded. 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. (NCT01044966)
Timeframe: At 6 months

InterventionParticipants (Count of Participants)
ITV DepoCyt + Temozolomide2

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Proportion of Patients With Recurrent GBM Treated With ITV DepoCyt in Combination With Oral Temozolomide Who Are Progression-free at 16 Weeks.

Eligibility of patients with GBM that are able to receive study drug to estimate the proportion of patients with recurrent GBM treated with ITV DepoCyt in combination with oral temozolomide who are progression-free at 16 weeks. 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. (NCT01044966)
Timeframe: 16 weeks

InterventionParticipants (Count of Participants)
ITV DepoCyt + Temozolomide12

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Response Rate of Drug Treatment

Those responding to study drug will be recorded. Response will be defined as stable neurological examination in conjunction with the absence of progression as defined above. (NCT01044966)
Timeframe: 52 weeks

InterventionParticipants (Count of Participants)
ITV DepoCyt + Temozolomide2

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Quality of Life Outcomes Measurement

"Participants recorded are those who had an improvement in QOL score, QOL outcomes will be assessed and recorded using the EORTC QLQ C30 version 3.~This 30 question questionnaire will be used to asses our patient overall feeling of well-being during the trial. Questions to assess quality of life are measured from 1-4 with the following graded values:~Not at all~A little~Quite a bit~Very much Lower total scores are consistent with better quality of life and changes of greater or equal to 10 points are considered a significant change in quality of life." (NCT01044966)
Timeframe: 52 weeks

InterventionParticipants (Count of Participants)
ITV DepoCyt + Temozolomide2

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Percent of Patients With Disease Control

Disease control rate defined as stable disease, partial response, or complete response according to the Response Evaluation Criteria in Solid Tumors (RECIST). (NCT01051596)
Timeframe: 2 months

InterventionParticipants (Count of Participants)
ABT-888 and Temozolomide18

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Percent of Patients With an Objective Response

Objective response rate defined as partial response or complete response according to RECIST criteria (NCT01051596)
Timeframe: 2 months

InterventionParticipants (Count of Participants)
ABT-888 and Temozolomide2

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Median Progression-free Survival Time

Progression-free survival defines as the time in days from study study entry until progression or death (NCT01051596)
Timeframe: 1 year

InterventionMonths (Median)
ABT-888 and Temozolomide1.8

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Overall Survival

Overall survival defined as the time in days from study entry until death (NCT01051596)
Timeframe: 1 year

InterventionMonths (Median)
ABT-888 and Temozolomide6.6

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Feasibility of the Addition of Cixutumumab to Chemotherapy Determined by Patient Enrollment

Proportion of no Grade 3+ cardiac toxicity. (NCT01055314)
Timeframe: From start to week 26 of therapy

InterventionProportion of Participants (Number)
IMC-A120.9390

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Event-Free Survival

Probability of no relapse, secondary malignancy, or death after 3 years in the study. (NCT01055314)
Timeframe: 3 years

InterventionProbability (Number)
IMC-A120.1627
Temozolomide0.1919

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Response Rate (CR + PR)

Proportion of patients with complete or partial response. Complete Response (CR): Complete disappearance of the tumor confirmed at > 4 weeks. Partial Response (PR): At least 64% decrease in volume compared to the measurement obtained at study enrollment; Overall Response (OR) = CR + PR. (NCT01055314)
Timeframe: From the start of treatment until a maximum of 2 cycles (21 days per cycle) of treatment in the absence of disease progression or unacceptable toxicities

InterventionProportion of Participants (Number)
IMC-A120.7667
Temozolomide0.7846

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Incidence of Adverse Events Assessed by Common Terminology Criteria for Adverse Events Version 4.0

Number of patients with grade 3+ adverse events (AE) during therapy. (Grade 3+) = (Grade 3 + Grade 4 + Grade 5) . Grade 3: Severe and undesirable AE; Grade 4: Life threatening or disabling AE; Grade 5: Death related to AE. (NCT01055314)
Timeframe: Up to 54 weeks

InterventionParticipants (Number)
IMC-A1289
Temozolomide61

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Feasibility of the Addition of Temozolomide to Chemotherapy Determined by Patient Enrollment

Proportion of no Grade 4+ non-hematologic toxicity. (NCT01055314)
Timeframe: From start to week 26 of therapy

InterventionProportion of Participants (Number)
Temozolomide0.7097

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Phase II: Overall Survival (OS)

Overall survival time is defined as time from/randomization to the date of death from any cause and is estimated by the Kaplan-Meier method. Patients last known to be alive are censored at the date of last contact. (NCT01062399)
Timeframe: Analysis occured after 134 events (progression or death) were reported. Patients were followed from randomization to death or study termination whichever occurs first, up to 36.7 months.

Interventionmonths (Median)
Ph II: RT + TMZ21.2
Ph II: RT + TMZ + RAD00116.5

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Phase I: Distribution of Worst Adverse Event Grade

"AE reporting in Phase I was split up by treatment timing: concurrent treatment (RT, TMZ, RAD001); post-RT treatment (TMZ, RAD001) along with all AE's reported in follow-up.~The worst/highest grade of any adverse event reported in each time period was determined for each patient. The percentage of patients in each grade level is reported. Adverse events are graded using CTCAE v4.0. Grade refers to the severity of the AE. The CTCAE v4.0 assigns Grades 1 through 5 with unique clinical descriptions of severity for each AE based on this general guideline: 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." (NCT01062399)
Timeframe: Analysis occured after 134 events (progression or death) were reported. Patients were followed from randomization to death or study termination whichever occurs first, up to 36.7 months.

,,
Interventionpercentage of participants (Number)
Concurrent treatment: Grade 1Concurrent treatment: Grade 2Concurrent treatment: Grade 3Concurrent treatment: Grade 4Concurrent treatment: Grade 5Post-RT treatment: Grade 1Post-RT treatment: Grade 2Post-RT treatment: Grade 3Post-RT treatment: Grade 4Post-RT treatment: Grade 5
Ph I: RT + TMZ + RAD001 10 mg/Day12.50.087.50.00.00.0100.00.00.00.0
Ph I: RT + TMZ + RAD001 2.5 mg/Day0.00.050.050.00.00.00.071.414.314.3
Ph I: RT + TMZ + RAD001 5 mg/Day11.133.344.411.10.00.042.928.60.00.0

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Phase II: Distribution of Worst Adverse Event Grade

The worst/highest grade of any adverse event reported was determined for each patient. The percentage of patients in each grade level is reported. Adverse events are graded using CTCAE v4.0. Grade refers to the severity of the AE. The CTCAE v4.0 assigns Grades 1 through 5 with unique clinical descriptions of severity for each AE based on this general guideline: 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. (NCT01062399)
Timeframe: Analysis occured after 134 events (progression or death) were reported. Patients were followed from randomization to death or study termination whichever occurs first, up to 36.7 months.

,
Interventionpercentage of patients (Number)
Grade 1Grade 2Grade 3Grade 4Grade 5
Ph II: RT + TMZ00332
Ph II: RT + TMZ + RAD00103501

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Phase I: Number of Patients With Dose-limiting Toxicity (DLT)

DLT is defined as any of the following events occurring during the first 8 weeks of treatment with RAD001 and temozolomide and attributable to the study drugs: any grade 3 or 4 thrombocytopenia, grade 4 anemia, or grade 4 neutropenia lasting more than 7 days; any non-hematologic grade 3 or greater adverse event (AE), excluding alopecia, despite maximal medical therapy; any grade 4 radiation-induced skin changes; failure to recover from adverse events to be eligible for re-treatment with RAD001 and temozolomide within 14 days of the last dose of either drug; or any episode of non-infectious pneumonitis grade 2, 3, or 4 of any duration. Adverse events are graded using CTCAE v4.0. Grade refers to the severity of the AE. The CTCAE v4.0 assigns Grades 1 through 5 with unique clinical descriptions of severity for each AE based on this general guideline: 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 (NCT01062399)
Timeframe: From start of treatment to eight weeks.

InterventionParticipants (Count of Participants)
Ph I: RT + TMZ + RAD001 2.5 mg/Day2
Ph I: RT + TMZ + RAD001 5 mg/Day2
Ph I: RT + TMZ + RAD001 10 mg/Day2

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Phase II: Progression-free Survival (PFS)

Using the Response Assessment in Neuro- Oncology (RANO) criteria, the progression is defined by any of the following: > 25% increase in sum of the products of perpendicular diameters of enhancing lesions compared to the smallest tumor measurement obtained either at baseline (if no decrease) or best response, on stable or increasing doses of corticosteroids; Significant increase in T2/FLAIR non-enhancing lesion on stable or increasing doses of corticosteroids compared to baseline scan or best response following initiation of therapy, not due to co-morbid events; Any new lesion; Clear clinical deterioration not attributable to other causes apart from the tumor or changes in corticosteroid dose; Failure to return for evaluation due to death or deteriorating condition; Clear progression of non-measurable disease. PFS time is defined as time from registration to date of progression, death, or last known follow-up (censored). PFS rates are estimated using the Kaplan-Meier method. (NCT01062399)
Timeframe: Analysis occured after 134 events (progression or death) were reported. Patients were followed from randomization to death or study termination whichever occurs first, up to 36.7 months.

Interventionmonths (Median)
Ph II: RT + TMZ10.2
Ph II: RT + TMZ + RAD0018.2

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6-month Progression-free Survival Rate

Six-month progression-free survival is the rate of patients who have NOT progressed at six months, where progressive disease is defined as any of the following: ≥ 25% increase in sum of the products of perpendicular diameters of enhancing lesions; any new lesion; or clinical deterioration. Progression will be determined by central review of MRI exams, assessed using MacDonald criteria for progression versus response on 2D T1 and T2 weighted images. (NCT01062425)
Timeframe: From randomization to 6 months.

Interventionpercentage of participants (Number)
Placebo, TMZ, and RT24.5
Cediranib, TMZ, and RT46.6

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Overall Survival (OS)

OS will be estimated using the Kaplan-Meier method and differences between treatment arms will be tested using the log rank test. Multivariate analyses with the Cox proportional hazard model for OS will be performed with the stratification variables as fixed variables to assess the treatment effect adjusting patient-specific risk factors. (NCT01062425)
Timeframe: From randomization to time of death due to any cause. Patients are followed until death. Analysis occurs after all patients have been potentially followed for six months.

InterventionMonths (Median)
Placebo, TMZ, and RT13.8
Cediranib, TMZ, and RT14.5

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Progression-free Survival (PFS)

Progression-free survival time is defined as time from randomization to date of first progression or death from any cause and is estimated by the Kaplan-Meier method. Patients last known to be alive without progression are censored at the date of last contact. Progression is defined as any of the following: ≥ 25% increase in sum of the products of perpendicular diameters of enhancing lesions; any new lesion; or clinical deterioration. (NCT01062425)
Timeframe: From randomization to time of first progression or death due to any cause. Patients are followed until death. Analysis occurs after all patients have been potentially followed for six months.

InterventionMonths (Median)
Placebo, TMZ, and RT2.7
Cediranib, TMZ, and RT6.2

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Incidence of Grade 3+ Toxicities

The number of patients with reported grade 3 and higher treatment-related toxicities as assessed by Common Terminology Criteria for Adverse Events version 4.0 (NCT01062425)
Timeframe: From randomization to six months.

Interventionparticipants (Number)
Placebo, TMZ, and RT35
Cediranib, TMZ, and RT77

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Median Progression-Free Survival (PFS)

PFS defined as time from date of diagnosis to most recent follow up, disease progression, or death. Disease progress defined as either clinical deterioration or radiographic progressive disease on magnetic resonance imaging (MRI) per updated response assessment in neuro-oncology criteria (Wen, et al). (NCT01105702)
Timeframe: Up to 50 months

Interventionmonths (Median)
TBL/RT9.4

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Median Overall Survival (OS)

OS defined as time from diagnosis to most recent follow up or death. (NCT01105702)
Timeframe: Up to 50 months

Interventionmonths (Median)
TBL/RT18.5

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Number of Patients With Grade 3 or 4 Adverse Events

Adverse events evaluated per CTCAE 3 (NCT01105702)
Timeframe: The whole time while on treatment and 30 days after the treatment

,
Interventionparticipants (Number)
DermatitisDVTNeurologicPneumoniaRashCoughHyponatremiaGastrointestinalFebril NeutropeniaNeutropeniaThrombocytopeniaSomnolence
Grade 3113111120111
Grade 4000000001010

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Maximum Tolerated Dose (MTD) of Vorinostat in Combination With Escalating Doses of Erlotinib and Temozolomide

"Phase I assessment MTD Vorinostat in combination with escalating doses of Erlotinib and Temozolomide using conventional phase I design where 3 enrolled into first dose level, monitored for 3 weeks and if no dose-limiting toxicity (DLT) seen, 3 more enrolled at next dosage level. If 2/6 participants experience DLT, the previous (lower) dosage level declared MTD of vorinostat in combination with Erlotinib and Temozolomide.~A maximum of 4 dosage levels utilized with deescalation by 2 dose levels if DLT is seen at the starting dose level. If no DLT noted after dose escalation to Level 4, these doses utilized as MTD for phase II." (NCT01110876)
Timeframe: Evaluated with each 28 day (+2 days) cycle, up to 24 weeks

Interventionmg (Number)
Vorinostat (mg) twice/dayErlotinib (mg)
Phase I Group 1: Vorinostat + Erlotinib + Temozolomide200200

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Overall Survival - Percentage of Participants With an Event

Overall survival was defined as the time transpired (in weeks) between the date of the participant's inclusion in the trial until the date of his/her death by any cause. Participants that were alive at the time the analysis was performed were censored on the date of last contact. (NCT01115491)
Timeframe: BL, every 28 days, until death or end-of-study, an average of 32 weeks

Interventionpercentage of participants (Number)
Bevacizumab + Temozolomide75.00

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Progression-Free Survival (PFS) - Percentage of Participants With an Event

PFS was defined as the time, in weeks, from the date of inclusion in the study to the date of the first documentation of disease progression or death of the participant due to any cause. Participants that did not have an event at the time the analysis was performed were censored at the date of last contact. Participants that began a treatment other than those planned in this study (bevacizumab or temozolomide) were censored on the start date of the new treatment. (NCT01115491)
Timeframe: Baseline (BL), every 28 days, until progression, death or end-of-study, an average of 32 weeks

Interventionpercentage of participants (Number)
Bevacizumab + Temozolomide96.88

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PFS: Probability of Remaining Progression Free at 24 Weeks After Beginning the Study

(NCT01115491)
Timeframe: BL, 24 weeks (after 6th cycle)

Interventionsurvival probability (Number)
Bevacizumab + Temozolomide0.30000

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PFS - Time to Event

PFS was defined as the time, in weeks, from the date of inclusion in the study to the date of the first documentation of disease progression or death of the participant due to any cause. Participants that did not have an event at the time the analysis was performed were censored at the date of last contact. Participants that began a treatment other than those planned in this study (bevacizumab or temozolomide) were censored on the start date of the new treatment. PFS was estimated using the Kaplan-Meier method. (NCT01115491)
Timeframe: BL, every 28 days, until progression, death or end-of-study, an average of 32 weeks

Interventionweeks (Median)
Bevacizumab + Temozolomide18.29

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Percentage of Participants Achieving an Overall Response of Complete Response (CR) or Partial Response (PR)

Overall response was defined as the percentage of participants who obtained CR or PR using adapted MacDonald criteria. CR: disappearance of all index and non-index lesions, confirmed no less than 4 weeks after assessment, no evidence of disease progression; corticosteroid dosage at or below 20 mg hydrocortisone daily; no neurological changes or an improvement as compared to last disease assessment. PR was defined as: Fifty percent or greater decrease in the sum of products of the larger diameter and the larger perpendicular diameter of all index lesions confirmed no less than 4 weeks after assessment, no evidence of disease progression and the absence of progressive, or non-evaluable disease status for non-index legions; unchanged, or decreased corticosteroid dose as compared to the last disease assessment; no neurological changes or an improvement as compared to the neurological examination at last disease assessment. (NCT01115491)
Timeframe: BL, every 28 days, until progression, death or end-of-study, an average of 32 weeks

Interventionpercentage of participants (Number)
Bevacizumab + Temozolomide40.6

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Overall Survival - Time to Event

Overall survival was defined as the time transpired (in weeks) between the date of the participant's inclusion in the trial until the date of his/her death by any cause. Participants that were alive at the time the analysis was performed were censored on the date of last contact. Median overall survival was estimated using the Kaplan-Meier method. (NCT01115491)
Timeframe: BL, every 28 days, until death or end-of-study, an average of 32 weeks

Interventionweeks (Median)
Bevacizumab + Temozolomide31.43

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6-Month Progression-Free Survival (PFS) Rate

6-month progression free survival rate is defined as the number of participants without progression per RECIST 1.0 6 months after starting study treatment. (NCT01119508)
Timeframe: 6 Months

Interventionparticipants (Number)
Ipilimumab + Temozolomide29

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Quality of Life by Brain-20 Survey

"Brain-20 (BN-20) quality of life surveys were administered at study entry and 12 months after treatment initiation to assess health-related quality of life (HR-QOL). The Brain-20 (BN-20) quality of life survey has 20 questions and responses are on scale of 1 to 4 with 1 indicating not at all (most favorable) and 4 indicating very much (least favorable). The total score can range from 20 to 80, and the result is expressed as the difference from baseline (study entry) to 12 months after the start of treatment. The outcome is stratified by Planning Target Volume (PTV) < 60 cm³ or 60 to 150 cm³, and expressed as the mean with 95% confidence interval." (NCT01120639)
Timeframe: 12 months

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Interventionscore on a scale (Mean)
Planning Target Volume (PTV) <60 CM3Planning Target Volume (PTV) 60-150CM3
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide66.640.7
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide40.755.5
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide18.559.2
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide44.425.9

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Quality of Life by European Organisation for Research and Treatment of Cancer (EORTC-QLQ C30) Survey

"European Organization for Research and Treatment of Cancer (EORTC-QLQ C30) quality of life surveys were administered at study entry and 12 months after treatment initiation to assess health-related quality of life (HR-QOL). The EORTC-QLQ C30 survey has 30 questions and responses are on scale of 1 to 4 with 1 indicating not at all and 4 indicating very much. The total score can range from 30 to 120. The outcome is stratified by Planning Target Volume (PTV) < 60 cm³ or 60 to 150 cm³, and is expressed as the mean of the difference from baseline to 12 months, with 95% confidence interval." (NCT01120639)
Timeframe: 12 Months

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Interventionscore on a scale (Mean)
Planning Target Volume (PTV) <60 CM3Planning Target Volume (PTV) 60-150CM3
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide41.641.6
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide58.352.7
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide80.544.4
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide53.351.3

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Quality of Life by MD Anderson Symptom Inventory - Brain Tumor (MDASI-BT) Survey

"MD Anderson Symptom Inventory - Brain Tumor (MDASI-BT) quality of life surveys were administered at study entry and 12 months after treatment initiation to assess health-related quality of life (HR-QOL). MDASI-BT quality of life survey has 23 questions and responses are on scale of 0 to 10 with 0 indicating did not interfere (most favorable) and 10 indicating interfered completely (least favorable). A participant's overall score is computed as the mean of that participant's individual scores, and can range 0 to 10. The outcome is stratified by Planning Target Volume (PTV) < 60 cm³ or 60 to 150 cm³, and expressed as the mean difference from baseline with 95% confidence interval. A positive value for the mean indicates worsening quality of life." (NCT01120639)
Timeframe: 12 months

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Interventionscore on a scale (Mean)
Planning Target Volume (PTV) <60 CM3Planning Target Volume (PTV) 60-150CM3
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide5.23.7
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide2.03.2
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide2.82.3
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide3.23.6

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Overall Survival (OS)

Overall survival (OS) was assessed as those participants remaining alive with any tumor status following radiotherapy after 20 months. The outcome is stratified by Planning Target Volume (PTV) < 60 cm³ or 60 to 150 cm³, and expressed as the median value with 95% confidence interval. (NCT01120639)
Timeframe: 20 Months.

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InterventionMonths (Median)
Planning Target Volume (PTV) <60 CM3Planning Target Volume (PTV) 60-150CM3
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide17.610.1
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide19.911.3
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide48.317.6
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide10.211.6

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Number of Acute Toxicity Within 30 Days

"Acute toxicity is defined as treatment-related adverse events that occur within 30 days of receiving radiotherapy. National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) v4.0 is used to grade adverse events. The non-stratified outcome is reported as number of treatment-related adverse events observed for each radiotherapy dose level.~Acute toxicity is based on radiotherapy dose level not tumor volume, and is reported by radiotherapy dose level only." (NCT01120639)
Timeframe: 30 days

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Interventionadverse events (Number)
CTCAE Grade 1CTCAE Grade 2CTCAE Grade 3CTCAE Grade 4CTCAE Grade 5All grades
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide500005
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide200002
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide211004
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide400116

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Long-term Toxicity After More Than 30 Days

"Long-term toxicity is defined as treatment-related adverse events (any grade or any Body System) that occur ≥ 30 days after receiving radiotherapy. National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) v4.0 is used to grade adverse events. The non-stratified outcome is reported as number of treatment-related adverse events observed for each dose level.~Long-term toxicity is based on radiotherapy dose level not tumor volume, and is reported by radiotherapy dose level only." (NCT01120639)
Timeframe: 12 months

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InterventionNumber of adverse events (Number)
CTCAE Grade 1CTCAE Grade 2CTCAE Grade 3CTCAE Grade 4All grades
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide00303
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide01405
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide11103
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide11316

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Treatment Failure Analysis

"Treatment failure in individual participants, ie, tumor recurrence or metastasis, can be described by the location relative to the first treatment failure (ie, infield, marginal, or distal), as further defined below.~Failure pattern is defined as tumor recurrence or metastasis relative to the primary lesion that is~Infield: at tumor or within 5 mm~Marginal: > 5 mm or ≤ 20 mm from tumor~Distal: > 20 mm from tumor~The outcome will be reported as the number of participants who failed treatment for each type of failure, ie, infield, marginal, or distal failure." (NCT01120639)
Timeframe: 18 months

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InterventionParticipants (Count of Participants)
In-FieldMarginalDistal
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide213
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide501
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide211
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide812

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Progression-free Survival

Progression-free survival (PFS) following radiotherapy, measured in months. Progressive disease (PD) is defined as: New tumor lesion, or > 25% increase in the product of the 2 greatest diameters of target lesion, as determined by computed tomography (CT) or magnetic resonance imaging (MRI), provided that within 2 months of completion of radiotherapy, the participant has not had a decrease in steroid dose since the last evaluation. The outcome is expressed as the median with 95% confidence interval for each cohort. (NCT01120639)
Timeframe: 18 Months.

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InterventionMonths (Median)
Planning Target Volume (PTV) <60 CM3Planning Target Volume (PTV) 60-150CM3
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide13.47.2
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide10.56.5
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide33.58.8
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide3.94.0

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Number of Dose-limiting Toxicities (DLTs)

"The maximum-tolerated dose (MTD) of study treatment (temozolomid plus hypofractionated radiotherapy administered as 5 fractions) is defined as either:~The highest radiation dose per protocol, or~The radiation dose at which dose-limiting toxicities (DLTs) occurred in ≥ 2 of 3 participants at a dose level, and/or ≥ 2 of 6 participants, at a dose level.~Dose-limiting toxicity (DLT) was defined as a treatment-related (with possible, probable or definite attribution) Grade 3 to 5 CNS toxicity [Common Terminology Criteria for Adverse Events (CTCAE) v4] occurring within 30 days of stereotactic radiosurgery (SRS).~The non-stratified outcome is reported as the number of DLTs observed in by radiation dose and by strata (Planning Target Volume (PTV) < 60 cm³ and from 60 to 150 cm³)." (NCT01120639)
Timeframe: 30 days

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InterventionNumber of DLT observed (Number)
Planning Target Volume (PTV) < 60 cm³Planning Target Volume (PTV) 60 to 150 cm³
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide00
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide00
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide00
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide11

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Percent of Participants With Radiographic Response

"Radiographic response rate was assessed following radiotherapy until disease progression. Response is considered to be the sum and proportion participants that achieved a complete response (CR); partial response (PR); or minor response (MR). The outcome is expressed as a number without dispersion for each cohort.~CR: Tumor is no longer detected by computed tomography (CT) or magnetic resonance imaging (MRI).~PR: Decrease in the product of the two greatest diameters > 50%, as determined by CT or MRI, with no new lesions, and the same or lower dose of dexamethasone.~MR: Decrease in the product of the two greatest diameters < 50%, as determined by CT or MRI, and neither PR nor PD.~PD: New tumor lesion, or > 25% increase in the product of the two greatest diameters of target lesion, as determined by CT or MRI, provided that within 2 months of completion of radiotherapy, the participant has not had a decrease in steroid dose since the last evaluation." (NCT01120639)
Timeframe: 6 months

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InterventionPercentage of participants (Number)
Planning Target Volume (PTV) <60 CM3Planning Target Volume (PTV) 60-150CM3
Stereotactic Radiosurgery (25 Gray x 5 Fractions)+Temozolomide10066.7
Stereotactic Radiosurgery (30 Gray x 5 Fractions)+Temozolomide10066.7
Stereotactic Radiosurgery (35 Gray x 5 Fractions)+Temozolomide10066.7
Stereotactic Radiosurgery (40 Gray x 5 Fractions)+Temozolomide33.316.7

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Duration of Response to High-Dose Interleukin-2 (H-D IL-2) Followed by Low Dose Temozolomide

Duration of response is defined as the length (measured in days) from the date of best response to the date of progression (if any), or to the date of last follow-up (if no progression is observed). The duration of response is applicable for those CR/MR/PR/SD subjects only. (NCT01124734)
Timeframe: 8 years

InterventionDays (Mean)
Course 1 Cycle 1 and Cycle 2432.88

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Safety and Toxicity of H-D IL-2 Followed by Low Dose Temozolomide

Safety and toxicity in this study population was evaluated using the NCI Common Toxicity Criteria. The unit of measure is the number of study participants with one or more unexpected and related (even remotely) SAE. (NCT01124734)
Timeframe: 2 years

InterventionParticipants (Count of Participants)
Course 1 Cycle 10
Course 1 Cycle 20

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Effect of High Dose IL2 Followed by Low Dose Temozolomide on Lymphocyte Subsets (Autoimmune Biomarkers)

The effect outcome is measured by the change in percentage of circulating lymphocyte cells (autoimmune biomarkers) that express the noted phenotype. This percentage change is determined by comparing the values obtained within 7 days of participant going off treatment against the baseline values. (NCT01124734)
Timeframe: 2 years

,
InterventionPercentage of Cells (Mean)
%CCR7- CD45RO+ of CD4+ Effector Memory%CCR7- CD45RO+ of CD8+ Effector Memory%CCR7- CD45RO- of CD4+ Effector Memory RA+%CCR7- CD45RO- of CD8+ Effector Memory RA+%CD25+FoxP3+ of CD4+ (Tregs)
% of Cells Expressing Phenotype Pre-treatment (BASELINE).36.31.09.46.10
% of Cells Expressing Phenotype Within 7 Days of Off-treatment.36.34.08.40.09

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Progression-free Survival (PFS) (Evaluable Randomized Patients)

The primary analysis will be performed among the Gnaq/Gna11 mutant patients. A stratified logrank test will be performed stratified by mutation status, M stage, and number of prior systemic therapies for metastatic disease. Due to the potential for a large number of strata and small strata sizes, the standard asymptotic stratified logrank test will be verified for robustness utilizing a permutation reference distribution. (NCT01143402)
Timeframe: The time from randomization to the earlier date of objective disease progression per Response Evaluation Criteria In Solid Tumors (RECIST) criteria or death due to any cause in the absence of progression, assessed up to 5 years

Interventionweeks (Median)
Arm I (Temozolomide)7
Arm II (Selumetinib)15.9

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Median Overall Survival (Evaluable Randomized Patients)

The primary analysis will be performed among the Gnaq/Gna11 mutant patients. A stratified logrank test will be performed stratified by mutation status, M stage, and number of prior systemic therapies for metastatic disease. Due to the potential for a large number of strata and small strata sizes, the standard asymptotic stratified logrank test will be verified for robustness utilizing a permutation reference distribution. (NCT01143402)
Timeframe: The time from randomization to death due to any cause, assessed up to 5 years

InterventionMonths (Median)
Arm I (Temozolomide)9.1
Arm II (Selumetinib)11.8

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Grade 3-4 Post-Procedural Surgery-Related Toxicity Rate

Grade 3-4 post-procedural surgery-related toxicity rate is the percentage of participants experiencing at least one grade 3-4 adverse event (AE) during the post-procedural time frame of 14 days attributable to the surgical procedure based on NCI Common Toxicity Criteria for Adverse Events version 4 (CTCAEv4). (NCT01182350)
Timeframe: 2 weeks

Interventionpercentage of participants (Number)
All Biopsied Participants10.0

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9-month Overall Survival (OS) Rate

9-month overall survival is the percentage of participants remaining alive 9 months from registration. (NCT01182350)
Timeframe: 9 months

Interventionpercentage of participants (Number)
All Patients Starting Assigned Chemoradiation64.4

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Feasibility Rate of Molecular Approach to Therapy

Feasibility rate of the molecular strategy is based on the percentage of participants either with inadequate tissue from surgical biopsy to confirm DIPG diagnosis and/or with uninterpretable results for identification of EGFR overexpression and MGMT methylation status. (NCT01182350)
Timeframe: 3 weeks

Interventionpercentage of participants (Number)
All Biopsied Participants92.0

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Rate of Lethal Complications From Surgery

The rate of lethal complications from surgery is the percentage of participants dying as a result of surgery. (NCT01182350)
Timeframe: 2 weeks

Interventionpercentage of participants (Number)
All Biopsied Participants0.0

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Median Progression Free Survival (PFS)

PFS based on the Kaplan-Meier method is defined as the duration of time [months (m)] from study entry to documented disease progression (PD) or death. Participants alive without PD are censored at the date of last disease assessment. For intrinsic pontine brainstem gliomas, only one lesion/mass is present at diagnosis. Comparisons of maximal 2-dimensional measurements, TxW (product of the longest diameter [width (W)] and its longest perpendicular diameter [transverse (T)]) are used to assess response for this target lesion. PD is 25% or more increase, taking as reference the smallest product observed since the start of treatment, or the appearance of one or more new lesions. (NCT01182350)
Timeframe: Disease assessments using a standard CNS imaging protocol occurred chemoradiation cycles 1 and 2, every other maintenance cycle, every 3 months post-treatment year 1 then annually until PD or therapy change; In this study cohort, follow-up was up to 34m.

Interventionmonths (Median)
All Patients Starting Assigned Chemoradiation8

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Delay in Radiation Therapy Start

The number of participants delaying the start of radiation therapy by more than 3 weeks due to complications as a result of surgical biopsy to obtain diagnostic tumor sample. (NCT01182350)
Timeframe: 3 weeks

InterventionParticipants (Count of Participants)
All Biopsied Participants1

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9-month Overall Survival (OS) Rate by Molecular Cohort

9-month OS rate is the percentage of participants alive at 9 months from registration. (NCT01182350)
Timeframe: 9 months

Interventionpercentage of participants (Number)
Cohort 1: MGMT-/EGFR-66.7
Cohort 2: MGMT-/EGFR+57.1
Cohort 3. MGMT+/EGFR-50.0
Cohort 4. MGMT+/EGFR+100

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Median Progression-free Survival

Progression-free survival was defined as the time in months from the date study treatment started until the date of progression or the date of death if death occurred before progression, or until the date of last follow-up if alive without progression. Kaplan-Meier methods were used to estimate progression-free survival. (NCT01186406)
Timeframe: 21 months

Interventionmonths (Median)
Gliadel, Radiation Therapy, Avastin, Temodar11.3

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Median Overall Survival

Overall survival was defined as the time in months from the start of SRS to the date of death or last contact if alive. Kaplan-Meier methods were used to estimate overall survival. (NCT01186406)
Timeframe: 21 months

Interventionmonths (Median)
Gliadel, Radiation Therapy, Avastin, Temodar19.4

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21-month Overall Survival

The percentage of participants alive at 21 months after the start of study treatment. Overall survival was calculated from the date study treatment started until the date of death or the date of last follow-up if alive. Kaplan-Meier methods were used to estimate overall survival. (NCT01186406)
Timeframe: 21 months

Interventionpercentage of participants (Number)
Gliadel, Radiation Therapy, Avastin, Temodar40.9

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Cycle 1 Mean Day 2 Trough/Pharmacokinetics of Gamma-secretase Inhibitor RO4929097 in Combination With Temozolomide (Phase IB)

(NCT01196416)
Timeframe: At Day 2 of Cycle 1

Interventionng/mL (Mean)
Treatment (RO4929097, Cisplatin, Vinblastine, Temozolomide)129

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Participants Evaluated for Toxicity

Number of patients with AE's as assessed by NCI CTCAE v. 4.0 Please see Adverse Events section for specifics. (NCT01196416)
Timeframe: Up to 30 days post-treatment

InterventionParticipants (Count of Participants)
Treatment (RO4929097, Cisplatin, Vinblastine, Temozolomide)14

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Progression-free Survival (Phase II)

Progression-free survival curves will be generated using Kaplan-Meier methodology. (NCT01196416)
Timeframe: Time from start of treatment to time of progression or death, whichever occurs first, assessed up to 2 years

Interventionmonths (Median)
Treatment (RO4929097, Cisplatin, Vinblastine, Temozolomide)2.7

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Maximum Tolerated Dose for RO4929097

based on the incidence of dose-limiting toxicity as assessed the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.0 (Phase IB) (NCT01196416)
Timeframe: 21 days

Interventionmg/day (Number)
Treatment (RO4929097, Cisplatin, Vinblastine, Temozolomide)15

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Number of Participants With Presence or Absence of Markers of Notch Signalling Pathway Inhibition in Patient Tumors (Phase Ib)

The association of response or clinical benefit with the presence or absence of markers of pathway inhibition in patient tumors will be tested using Fisher's exact test. (NCT01196416)
Timeframe: 2 weeks

InterventionParticipants (Count of Participants)
Insufficient tissue to asses any changeSig decrease in post-treatment cleaved Notch
Treatment (RO4929097, Cisplatin, Vinblastine, Temozolomide)14

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Overall Survival (Phase II)

Overall response rate (complete [CR] or partial response [PR]) according to RECIST version 1.1 (NCT01196416)
Timeframe: Up to 2 years

Interventionparticipants (Number)
Partial ResponseStable DiseaseProgression of Disease
Treatment (RO4929097, Cisplatin, Vinblastine, Temozolomide)356

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Cycle 1 AUC/Pharmacokinetics of Gamma-secretase Inhibitor RO4929097 in Combination With Temozolomide (Phase IB)

(NCT01196416)
Timeframe: Days 4 and 5

Interventionhr·ng/mL (Mean)
Treatment (RO4929097, Cisplatin, Vinblastine, Temozolomide)5410

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Cycle 1 C Max/Pharmacokinetics of Gamma-secretase Inhibitor RO4929097 in Combination With Temozolomide (Phase IB)

(NCT01196416)
Timeframe: At Cycle 1

Interventionng/mL (Mean)
Treatment (RO4929097, Cisplatin, Vinblastine, Temozolomide)301

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Maximum-tolerated Dose for Cisplatin, Vinblastine and TMZ

"based on the incidence of dose-limiting toxicity as assessed the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.0 (Phase IB)~Data is not yet available, as it's currently being analyzed." (NCT01196416)
Timeframe: 21 days

Interventionmg/m2 (Number)
CisplatinVinblastineTemozolomide
Treatment (RO4929097, Cisplatin, Vinblastine, Temozolomide)201.2150

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Overall Survival

the number of months between a patient's enrollment and his/her date of death (NCT01205828)
Timeframe: 2 years

Interventionmonths (Median)
ABT-888 and Temozolomide13.1

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Clinical Benefit Rate

complete response at any time + partial response at any time + stable disease after 8 weeks of treatment based on RECIST Criteria (NCT01205828)
Timeframe: 8 weeks

Interventionparticipants (Number)
ABT-888 and Temozolomide3

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Progression Free Survival

The number of months between a patient's enrollment and his/her disease progression (NCT01205828)
Timeframe: 2 years

Interventionmonths (Median)
ABT-888 and Temozolomide1.9

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Number of Participants Who Had Grade 3 or 4 Adverse Events

Record of all toxicities graded according to the NCI CTCAE version 3.0 (NCT01205828)
Timeframe: 6 months

Interventionparticipants (Number)
ABT-888 and Temozolomide5

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6-month Progression-free Survival

To use 6-month progression-free survival to assess the efficacy of the combination of hypofractionated IMRT delivering 60 Gy over 2 weeks with concurrent bevacizumab and temozolomide followed by 6 cycles of adjuvant bevacizumab and temozolomide. (NCT01209442)
Timeframe: 6 months

Interventionmonths (Median)
RT With Temozolomide and Bevacizumab90

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Overall Survival, Measured From the Day of Initial Diagnosis (Biopsy or Surgery) to the Time of Death From Any Cause.

(NCT01209442)
Timeframe: follow up for life

Interventionmonths (Median)
RT With Temozolomide and Bevacizumab16.3

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Response

Patient's best response during protocol therapy coded as complete response, partial response or no response. (NCT01217437)
Timeframe: Up to 12 cycles of therapy (11 months)

,
InterventionParticipants (Count of Participants)
Complete ResponsePartial ResponseNo Response
Arm I (Temozolomide, Irinotecan Hydrochloride)01632
Arm II (Temozolomide, Irinotecan Hydrochloride, Bevacizumab)81424

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Event-free Survival

Percentage Probability of remaining event-free 5 years after enrollment estimated by the method of Kaplan and Meier (NCT01217437)
Timeframe: Up to 5 years after enrollment

Interventionpercent probability (Number)
Arm I (Temozolomide, Irinotecan Hydrochloride)1.85
Arm II (Temozolomide, Irinotecan Hydrochloride, Bevacizumab)15.4

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Overall Survival

Percentage Probability of remaining alive 5 years after enrollment estimated by the method of Kaplan and Meier (NCT01217437)
Timeframe: Up to 5 years after enrollment

Interventionpercent probability (Number)
Arm I (Temozolomide, Irinotecan Hydrochloride)2.43
Arm II (Temozolomide, Irinotecan Hydrochloride, Bevacizumab)13.6

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One-year Progression-free Survival and Overall Survival

"Efficacy of the DRBEAT Regimen will be assessed by analysis of~one-year progression-free survival (PFS), defined as the time interval from maximal response from therapy to tumor regrowth, progression*, or death, (*Progression is defined as meeting the response criteria listed in Table 4: Response Criteria for Primary Central Nervous System Lymphoma according to Abrey LE, Batchelor TT, Ferreri AJM et al.)~and~Overall survival, defined as the time interval between the date of transplant and the date of death from any cause." (NCT01235793)
Timeframe: (1) One Year (2) Until date of death from any cause, assessed up to 2 years

InterventionDays (Median)
Progression Free SurvivalOverall Survival
DRBEAT Regimen132564

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Safest Dose of Temozolomide for the DRBEAT Regimen

Safety will be assessed using a dose escalation design for temozolomide's use to determine the target dose and also to evaluate any and all acute treatment related toxicities. During the course of patient follow up and therapy, toxicities will be evaluated, particularly as the investigators will be determining the target dose of temozolomide. One of the major criteria for dose limiting toxicity for the study will be any Grade 3 or 4 nonhematologic toxicity from a list of commonly expected toxicities associated with autologous transplantation and temozolomide. (NCT01235793)
Timeframe: One Year

Interventiondose in mg/m^2 (Number)
DRBEAT Regimen773.25

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Event-free Survival

Time from enrollment to disease progression, diagnosis of a second malignant neoplasm, death or last follow-up, whichever occurs first. Disease progression is evaluated according to the COG criteria for measurement of brain tumors and is defined to be a ≥ 25% increase in the product of perpendicular diameters of ANY target lesion, taking as reference the smallest product observed since the start of treatment; OR the appearance of one or more new lesions, OR worsening neurologic status not explained by causes unrelated to tumor progression (e.g., anticonvulsant or corticosteroid toxicity, electrolyte disturbances, sepsis, hyperglycemia, presumed post-therapy swelling etc) PLUS any increase in tumor cross-sectional area (or tumor volume). (NCT01236560)
Timeframe: 1 year after enrollment

Interventionpercent probability (Number)
Feasibility (Vorinostat)33.3
Arm I (Vorinostat, Phase II Arm A)41.3
Arm II (Temozolomide, Phase II Arm B)59.3
Arm III (Bevacizumab, Phase II Arm C)43.8

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Cumulative Incidence of Disease Progression in Each Treatment Arm

Cumulative incidence of progression where death from any cause prior to progression and diagnosis of a second malignant neoplasm prior to progression are considered competing events. Disease progression is evaluated according to the COG criteria for measurement of brain tumors and is defined to be a ≥ 25% increase in the product of perpendicular diameters of ANY target lesion, taking as reference the smallest product observed since the start of treatment; OR the appearance of one or more new lesions, OR worsening neurologic status not explained by causes unrelated to tumor progression (e.g., anticonvulsant or corticosteroid toxicity, electrolyte disturbances, sepsis, hyperglycemia, presumed post-therapy swelling etc) PLUS any increase in tumor cross-sectional area (or tumor volume). (NCT01236560)
Timeframe: 1 year after enrollment

Interventionpercent probability (Number)
Feasibility (Vorinostat)67
Arm I (Vorinostat, Phase II Arm A)59
Arm II (Temozolomide, Phase II Arm B)53
Arm III (Bevacizumab, Phase II Arm C)37

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Maximum Tolerated Dose (MTD) of Vorinostat

The dose of vorinostat in mg/sq m/day to be administered with combination chemotherapy and radiation therapy. (NCT01236560)
Timeframe: 10 weeks

Interventionmg/sq m (Number)
Feasibility (Vorinostat)230

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Overall Survival

Time from enrollment to death or last follow-up, whichever occurs first. (NCT01236560)
Timeframe: 1 year after enrollment

Interventionpercent probability (Number)
Feasibility (Vorinostat)33.3
Arm I (Vorinostat, Phase II Arm A)82.2
Arm II (Temozolomide, Phase II Arm B)85.2
Arm III (Bevacizumab, Phase II Arm C)67.3

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

Best overall tumor response was evaluated using Response Evaluation Criteria In Solid Tumors (RECIST, version 1.0) criteria. Complete Response (CR) was defined as the disappearance of all target lesions; Partial Response (PR) was defined as at least a 30% decrease in sum of longest diameter of target lesions. (NCT01284335)
Timeframe: Baseline to Study Completion (Up to 2 years)

Interventionpercentage of participants (Number)
Non-Small Cell Lung Cancer (NSCLC)Other
Arm B* Tasisulam + Docetaxel Dose Confirmation20.06.3

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

Best overall tumor response was evaluated using Response Evaluation Criteria In Solid Tumors (RECIST, version 1.0) criteria. Complete Response (CR) was defined as the disappearance of all target lesions; Partial Response (PR) was defined as at least a 30% decrease in sum of longest diameter of target lesions. (NCT01284335)
Timeframe: Baseline to Study Completion (Up to 2 years)

Interventionpercentage of participants (Number)
Non-Small Cell Lung Cancer (NSCLC)OtherPancreasSmall Cell Lung Cancer (SCLC)
Arm D Tasisulam + Cisplatin Dose Confirmation5.010.007.1

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Pharmacokinetic (PK): Concentration Maximum (Cmax)

Cycle 2: predose,1h start of infusion, end of infusion, 30min,2h,4h,6h,22h,166h,334h,698h end of infusion. (NCT01284335)
Timeframe: Cycle 1: predose,0,30min,1h start of infusion, end of infusion, 30min,2h,4h,6h,22h,166h,334h,698h end of infusion.

Interventionmicrograms per milliliter (µg/mL) (Geometric Mean)
Cycle 1Cycle 2
Tasisulam306250

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

Best overall tumor response was evaluated using Response Evaluation Criteria In Solid Tumors (RECIST, version 1.0) criteria. Complete Response (CR) was defined as the disappearance of all target lesions; Partial Response (PR) was defined as at least a 30% decrease in sum of longest diameter of target lesions. (NCT01284335)
Timeframe: Baseline to Study Completion (Up to 2 years)

,
Interventionpercentage of participants (Number)
Non-Small Cell Lung Cancer (NSCLC)OtherPancreas
Arm A Tasisulam + Gemcitabine Dose Confirmation0.014.313.3
Arm E Tasisulam + Erlotinib Dose Confirmation0.014.30.0

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PK: Area Under the Curve Albumin (AUCalb)

Cycle 2: predose,1h start of infusion, end of infusion, 30min,2h,4h,6h,22h,166h,334h,698h end of infusion. (NCT01284335)
Timeframe: Cycle 1: predose,0,30min,1h start of infusion, end of infusion, 30min,2h,4h,6h,22h,166h,334h,698h end of infusion.

Interventionmicrograms*hour/milliliter (µg*h/mL) (Geometric Mean)
Cycle 1Cycle 2
Tasisulam946648

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Number of Participants With Dose-Limiting Toxicities Cycle 1

A Dose-Limiting Toxicity (DLT) is defined as an Adverse Event (AE) that is likely related to the study medication or combination, and fulfills any one of the following criteria: Common Terminology Criteria for Adverse Events (CTCAE, Version 3.0) Grade 4 neutropenia lasting more than 5 days. Grade 4 neutropenia with fever or Grade 4 thrombocytopenia, regardless of duration; Grade ≥3 thrombocytopenia with bleeding, regardless of duration; Grade ≥3 nonhematologic toxicity (excluding nausea/vomiting or diarrhea that can be controlled with medication, and alopecia). Grade 3 electrolyte toxicity (for example, hypokalemia, hypophosphatemia) will not be considered a DLT unless it is considered related to the study drug or combination and does not resolve with standard replacement treatments within 42 days after Cycle 1 Day 1. A summary of other nonserious AEs and all Serious Adverse Events (SAE), regardless of causality is located in the Reported Adverse Event section. (NCT01284335)
Timeframe: Baseline to Cycle 1 (Up to Day 28)

InterventionParticipants (Count of Participants)
Arm A Tasisulam + Gemcitabine Dose Escalation4
Arm A Tasisulam + Gemcitabine Dose Confirmation0
Arm B* Tasisulam + Docetaxel Dose Escalation4
Arm B1 Tasisulam + Docetaxel Dose Escalation4
Arm B2 Tasisulam + Docetaxel Dose Escalation3
Arm B2 Tasisulam + Docetaxel Dose Confirmation0
Arm C Tasisulam + Temozolomide Dose Escalation3
Arm C Tasisulam + Temozolomide Dose Confirmation0
Arm D* Tasisulam + Cisplatin Dose Escalation0
Arm D Tasisulam + Cisplatin Dose Escalation2
Arm D Tasisulam + Cisplatin Dose Confirmation0
Arm E Tasisulam + Erlotinib Dose Escalation1
Arm E Tasisulam + Erlotinib Dose Confirmation0

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Number of Participants With a Clinically Significant Effects

Clinically significant effects are reported if a Grade 3 or higher treatment emergent adverse event (TEAE) and observed in ≥10% of participants or a toxicity possibly related to study drug based on Common Terminology Criteria for Adverse Events (CTCAE). A summary of other nonserious AEs and all SAEs, regardless of causality is located in the Reported Adverse Event section. (NCT01284335)
Timeframe: Baseline to Study Completion (Up to 2 years)

,,,,,,,,,,,,
InterventionParticipants (Count of Participants)
TEAE >/= Grade 3Toxicity >/= Grade 3
Arm A Tasisulam + Gemcitabine Dose Confirmation1818
Arm A Tasisulam + Gemcitabine Dose Escalation1513
Arm B* Tasisulam + Docetaxel Dose Escalation04
Arm B1 Tasisulam + Docetaxel Dose Escalation05
Arm B2 Tasisulam + Docetaxel Dose Confirmation1926
Arm B2 Tasisulam + Docetaxel Dose Escalation1618
Arm C Tasisulam + Temozolomide Dose Confirmation66
Arm C Tasisulam + Temozolomide Dose Escalation1113
Arm D Tasisulam + Cisplatin Dose Confirmation3030
Arm D Tasisulam + Cisplatin Dose Escalation87
Arm D* Tasisulam + Cisplatin Dose Escalation01
Arm E Tasisulam + Erlotinib Dose Confirmation77
Arm E Tasisulam + Erlotinib Dose Escalation55

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

Best overall tumor response was evaluated using Response Evaluation Criteria In Solid Tumors (RECIST, version 1.0) criteria. Complete Response (CR) was defined as the disappearance of all target lesions; Partial Response (PR) was defined as at least a 30% decrease in sum of longest diameter of target lesions. (NCT01284335)
Timeframe: Baseline to Study Completion (Up to 2 years)

Interventionpercentage of participants (Number)
Other
Arm C Tasisulam + Temozolomide Dose Confirmation0.0

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Toxicity, Assessed Using National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) Version 4.0 (v4)

"The maximum grade for each type of toxicity will be recorded for each patient, and frequency tables will be reviewed to determine toxicity patterns within patient groups. In addition, we will review all adverse event data that is graded as 3, 4, or 5 and classified as either unrelated or unlikely to be related to study treatment in the event of an actual relationship developing. The overall toxicity rates (percentages) for grade 3 or higher adverse events considered at least possibly related to treatment are reported below." (NCT01328535)
Timeframe: Up to 2 years

Interventionpercentage of patients (Number)
FatigueFebrile NeutropeniaNeutrophil Count DecreasedPlatelet Count DecreasedSepsisUrinary Tract InfectionWhite Blood Cell DecreasedAbdominal Infection
Treatment (Individualized Chemotherapy)4.28.38.3254.24.28.34.2

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Progression-Free Survival at 4 Months

The distribution of time to progression will be estimated using the method of Kaplan-Meier and the 4 month progression-free rate (percentage) will be provided. Progression is defined as: At least one of the following must be true: At least one new malignant lesion, which also includes any lymph node that was normal at baseline (< 1.0 cm short axis) and increased to ≥ 1.0 cm short axis during follow-up. At least a 20% increase in PBSD (sum of the longest diameter for all target lesions plus the sum of the short axis of all the target lymph nodes at current evaluation) taking as reference the MSD. In addition, the PBSD must also demonstrate an absolute increase of at least 0.5 cm from the MSD. (NCT01328535)
Timeframe: Time from registration to the earliest date of documentation of disease progression, assessed at 4 months

Interventionpercentage of patients (Number)
Treatment (Timed Individualized Chemotherapy)22.2

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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 as:At least one of the following must be true: At least one new malignant lesion, which also includes any lymph node that was normal at baseline (< 1.0 cm short axis) and increased to ≥ 1.0 cm short axis during follow-up. At least a 20% increase in PBSD (sum of the longest diameter for all target lesions plus the sum of the short axis of all the target lymph nodes at current evaluation) taking as reference the MSD (Section 11.41). In addition, the PBSD must also demonstrate an absolute increase of at least 0.5 cm from the MSD. The median and 95% confidence intervals are estimated using the Kaplan-Meier estimator. (NCT01328535)
Timeframe: Up to 2 years

Interventionmonths (Median)
Treatment (Timed Individualized Chemotherapy)3.4
Treatment (Untimed Individualized Chemotherapy)7.2

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Overall Survival

Overall survival time is defined as the time from randomization to death due to any cause. The median and 95% confidence intervals are estimated using the Kaplan-Meier estimator. (NCT01328535)
Timeframe: Up to 2 years

Interventionmonths (Median)
Treatment (Timed Individualized Chemotherapy)23.1
Treatment (Untimed Individualized Chemotherapy)17.5

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Measurable Change on Magnetic Resonance Spectroscopy Imaging After Vorinostat Administration

Changes in magnetic resonance spectroscopic imaging signal and semiquantitative analysis of inositol, choline, lactate, and N-acetyl aspartate (NAA) signal are measured. The values for each of these metabolites are normalized to baseline at one and nine weeks. The values of all the metabolites at one week are added and this is the magnetic resonance spectroscopic index for one week. This is done again at nine weeks. The number is unitless and there is no range limit. Positive values represent normalization of tumor metabolism and negative values suggest no improvement or worsening of metabolic character. (NCT01342757)
Timeframe: 9 weeks

InterventionSpectroscopic index (Mean)
Arm I0

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Proportion of Patients With Magnetic Resonance Spectroscopy (MRS) Response to Initial Vorinostat by MRI and MRS Scans as Determined by Spectroscopic Index

Changes in magnetic resonance spectroscopic imaging signal and semiquantitative analysis of inositol, choline, lactate, and N-acetylaspartate signal are measured. The values for each of these metabolites are normalized to baseline at one and nine weeks. The values of all the metabolites at one week are added and this is the magnetic resonance spectroscopic index for one week. This is done again at nine weeks. The number is unitless and there is no range limit. Positive values represent normalization of tumor metabolism and negative values suggest no improvement or worsening of metabolic character. (NCT01342757)
Timeframe: 9 weeks

Interventionparticipants (Number)
Arm I0

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Mean Change in Metabolite Levels

Baseline MRS was performed 1-3 days before initiation of treatment. Follow-up MRS studies were performed at day 7. A standard quadrature head coil was used to collect MR data. The change of metabolite level in choline (Cho) and N-acetyl aspartate (NAA) were calculated in ratio by (metabolite after treatment / metabolite before treatment - 1). The reported ratios represent the Cho-to-NAA ratio at day 7 compared with day 0. (NCT01342757)
Timeframe: Baseline to 1 week

InterventionCho/NAA Ratios (Mean)
Metabolic RespondersMetabolic Non-Responders
Arm I-0.150.29

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Percentage of Participants With EFS as Determined by the CRRC at 1 Year

EFS was defined as the time from randomisation to the earliest occurrence of any of the following: tumor progression, tumor recurrence, second primary non- HGG malignancy or death attributable to any cause. Tumor assessments were conducted using MRI and reviewed by the site-independent CRRC using RANO criteria. Tumor progression was defined as clear clinical progression or >/= 25% increase in the sum of the products of perpendicular diameters of the contrast enhancing lesions compared with the smallest tumor measurement obtained either at baseline (if no decrease was observed) or best response and with the subject on stable or increasing doses of corticosteroids. Tumor recurrence was defined as recurrence after tumor was completely resected (no disease present at baseline). EFS was estimated using the Kaplan-Meier method. (NCT01390948)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Chemoradiation + TMZ48.37
Chemoradiation + Bevacizumab + TMZ38.28

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Health Status as Measured by the Health Utility Index (HUI)

HUI is a preference-based, multi-attitude, health-related instrument specifically developed for use with children. HUI consists of eight attributes of health status: vision, hearing, speech, ambulation, dexterity, emotion, cognition and pain. Each attribute had 5 or 6 levels varying from highly impaired to normal. Each of the eight health dimensions was tested separately and a composite score ranging between 1 (perfect health) and 0 (death) was obtained for participants aged 5 years or older. (NCT01390948)
Timeframe: Baseline, Cycle 6 of the adjuvant phase, end of treatment (approximately 58 weeks post-baseline), and yearly during the follow-up period (maximum 5 years in follow-up)

Interventionunits on a scale (Mean)
BaselineCycle 6, Day 1End of TreatmentYearly Follow-Up 1Yearly Follow-up 2Additional Safety Follow-Up (Visit 2)Additional Safety Follow-Up (Visit 4)Additional Safety Follow-Up (Visit 6)Additional Safety Follow-Up (Visit 8)End of Study
Chemoradiation + Bevacizumab + TMZ0.7300.7790.8200.9260.7930.9010.8300.4900.9300.790

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Health Status as Measured by the Health Utility Index (HUI)

HUI is a preference-based, multi-attitude, health-related instrument specifically developed for use with children. HUI consists of eight attributes of health status: vision, hearing, speech, ambulation, dexterity, emotion, cognition and pain. Each attribute had 5 or 6 levels varying from highly impaired to normal. Each of the eight health dimensions was tested separately and a composite score ranging between 1 (perfect health) and 0 (death) was obtained for participants aged 5 years or older. (NCT01390948)
Timeframe: Baseline, Cycle 6 of the adjuvant phase, end of treatment (approximately 58 weeks post-baseline), and yearly during the follow-up period (maximum 5 years in follow-up)

Interventionunits on a scale (Mean)
BaselineCycle 6, Day 1End of TreatmentYearly Follow-Up 1Yearly Follow-up 2Additional Safety Follow-Up (Visit 2)Additional Safety Follow-Up (Visit 4)Additional Safety Follow-Up (Visit 6)End of Study
Chemoradiation + TMZ0.7130.7850.8320.9060.7370.7840.8141.0000.647

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Number of Dose Administrations of TMZ and Bevacizumab in the Concurrent Phase

Number of doses were assessed for the concurrent phase, which is the treatment period after the initial treatment phase and including the subsequent treatment break of approximately 4 weeks. (NCT01390948)
Timeframe: Beginning of the concurrent phase to end of treatment break (10 weeks)

,
Interventionnumber of dose administrations (Median)
TMZBevacizumab
Chemoradiation + Bevacizumab + TMZ42.06.0
Chemoradiation + TMZ42.0NA

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Percentage of Participants Who Completed >/= 90% of Planned Radiotherapy and TMZ Administrations

(NCT01390948)
Timeframe: From the time of randomization of the first participant to the date of clinical cutoff (approximately 60 months)

,
Interventionpercentage of participants (Number)
RadiotherapyTMZ
Chemoradiation + Bevacizumab + TMZ98.388.3
Chemoradiation + TMZ94.685.7

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Percentage of Participants With a Treatment Delay or Discontinuation

(NCT01390948)
Timeframe: From the time of randomization of the first participant to the date of clinical cutoff (approximately 60 months)

,
Interventionpercentage of participants (Number)
AE leading to dose modification/interruptionAE leading to withdrawal from treatment
Chemoradiation + Bevacizumab + TMZ71.721.7
Chemoradiation + TMZ60.75.4

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Percentage of Participants With EFS as Determined by the CRRC at 6 Months

EFS was defined as the time from randomisation to the earliest occurrence of any of the following: tumor progression, tumor recurrence, second primary non- HGG malignancy or death attributable to any cause. Tumor assessments were conducted using MRI and reviewed by the site-independent CRRC using RANO criteria. Tumor progression was defined as clear clinical progression or >/= 25% increase in the sum of the products of perpendicular diameters of the contrast enhancing lesions compared with the smallest tumor measurement obtained either at baseline (if no decrease was observed) or best response and with the subject on stable or increasing doses of corticosteroids. Tumor recurrence was defined as recurrence after tumor was completely resected (no disease present at baseline). EFS was estimated using the Kaplan-Meier method. (NCT01390948)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Chemoradiation + TMZ66.46
Chemoradiation + Bevacizumab + TMZ68.43

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Concordance Between Structural Versus Multimodal Imaging for CRRC-Assessed Event-Free Survival

Concordance is presented as the percentage of participants with concordance between assessments. EFS concordance was defined as event Structural assessment and Diffusion Perfusion assessment occurs within 28 days or no event Structural and no Diffusion Perfusion. (NCT01390948)
Timeframe: Up to 12 months

Interventionpercentage of participants (Number)
Chemoradiation + TMZ96.6
Chemoradiation + Bevacizumab + TMZ87.1

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EFS as Assessed by the Investigator

EFS was defined as the time from randomisation to the earliest occurrence of any of the following: tumor progression, tumor recurrence, second primary non-HGG malignancy or death attributable to any cause. Tumor assessments were conducted using MRI and reviewed by the investigator using RANO criteria. Tumor progression was defined as clear clinical progression or >/= 25% increase in the sum of the products of perpendicular diameters of the contrast enhancing lesions compared with the smallest tumor measurement obtained either at baseline (if no decrease was observed) or best response and with the participant on stable or increasing doses of corticosteroids. Tumor recurrence was defined as recurrence after tumor was completely resected (no disease present at baseline). EFS was estimated using the Kaplan-Meier method. (NCT01390948)
Timeframe: From the time of randomization to the date of any defined event (up to 12 months)

Interventionmonths (Median)
Chemoradiation + TMZ11.79
Chemoradiation + Bevacizumab + TMZ11.27

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Event-Free Survival (EFS) as Assessed by the Central Radiology Review Committee (CRRC)

EFS was defined as the time from randomisation to the earliest occurrence of any of the following: tumor progression, tumor recurrence, second primary non- HGG malignancy or death attributable to any cause. Tumor assessments were conducted using magnetic resonance imaging (MRI) and reviewed by the site-independent CRRC using Response Assessment in Neuro-Oncology (RANO) criteria. Tumor progression was defined as clear clinical progression or >/= 25% increase in the sum of the products of perpendicular diameters of the contrast enhancing lesions compared with the smallest tumor measurement obtained either at baseline (if no decrease was observed) or best response and with the subject on stable or increasing doses of corticosteroids. Tumor recurrence was defined as recurrence after tumor was completely resected (no disease present at baseline). EFS was estimated using the Kaplan-Meier method. (NCT01390948)
Timeframe: From the time of randomization to the date of any defined event (up to 12 months)

Interventionmonths (Median)
Chemoradiation + TMZ11.79
Chemoradiation + Bevacizumab + TMZ8.21

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Neurological Psychological Function as Measured by the Wechsler Scale

The Wechsler Intelligence Scale for Children version IV (WISC-IV) was used to generate a full scale intelligence quotient (IQ) which represents a child's general intellectual ability. The average IQ score is 100, with lower scores representing lower intellectual ability. (NCT01390948)
Timeframe: End of treatment (approximately 58 weeks post-baseline)

Interventionunits on a scale (Mean)
Chemoradiation + TMZ92.0
Chemoradiation + Bevacizumab + TMZ97.0

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Number of Radiotherapy Dose Administrations in the Concurrent Phase

Number of doses were assessed for the concurrent phase, which is the treatment period after the initial treatment phase and including the subsequent treatment break of approximately 4 weeks. (NCT01390948)
Timeframe: Beginning of the concurrent phase to end of treatment break (10 weeks)

InterventionGrays (Median)
Chemoradiation + TMZ54.0
Chemoradiation + Bevacizumab + TMZ54.0

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Objective Response Rate (ORR)

ORR was defined as the percentage of participants with a complete response (CR) or partial response (PR) determined on two consecutive occasions >/= 4 weeks apart. Tumor assessments were conducted using MRI and reviewed by the site-independent CRRC using RANO criteria. The following were needed to qualify as CR: complete disappearance of all measurable enhancing lesions sustained for at least 4 weeks by MRI, no steroids above physiological levels, clinical status stable or improved compared to baseline. The following were needed to qualify as PR: ≥ 50% decrease from baseline in the sum of products of perpendicular diameters of all measurable enhancing lesions sustained for at least 4 weeks by MRI, steroid dose not increased compared to baseline, clinical status stable or improved compared to baseline. (NCT01390948)
Timeframe: From the time of randomization to the date of any defined event (up to 12 months)

Interventionpercentage of participants (Number)
Chemoradiation + TMZ40
Chemoradiation + Bevacizumab + TMZ41.7

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Overall Survival

Overall Survival was defined as the time of diagnosis to the date of death due to any cause. Overall Survival was estimated using the Kaplan-Meier method. (NCT01390948)
Timeframe: From the time of randomization to the date of death (up to approximately 60 months)

Interventionmonths (Median)
Chemoradiation + TMZ20.27
Chemoradiation + Bevacizumab + TMZ18.30

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Percentage of Participants With 1-Year Survival

1-year survival was estimated using the Kaplan-Meier method. (NCT01390948)
Timeframe: 1 year after end of treatment

Interventionpercentage of participants (Number)
Chemoradiation + TMZ67.69
Chemoradiation + Bevacizumab + TMZ74.83

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Percentage of Participants With an Adverse Event (AE)

An AE 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. (NCT01390948)
Timeframe: From the time of randomization of the first participant to the date of clinical cutoff (approximately 60 months)

Interventionpercentage of participants (Number)
Chemoradiation + TMZ100
Chemoradiation + Bevacizumab + TMZ98.3

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Progression Free Survival PPX/RT Versus TMZ/RT for Patients With GBM Without Methylation

"MRI response evaluated by RANO criteria~Complete Response (CR): Circumstance when the enhancing tumor is no longer seen by neuroimaging, with the patient off all steroids or on adrenal maintenance only; CR will be coded only if confirmed by a second CT/MR scan performed a minimum of 4 weeks after the initial scan coding a response.~Partial Response (PR): Decrease of > 50% in the product of two diameters. Patients should be receiving stable or decreasing doses of steroids. PR will be coded only if confirmed by a second CT/MR scan performed a minimum of 4 weeks after the initial scan.~Progression (P): A > 25% increase in tumor area (two diameters) provided that the patient has not had his/her dose of steroids decreased since the last evaluation period. This will not need a confirmatory scan. A concomitant decrease in steroid dose will rule out a progression designation during the first 2 months after completion of XRT." (NCT01402063)
Timeframe: Q 3 months on study then Q3 months in f/u for yr 1, q 4 months yr 2, q 6 months for approximately 4 ys.

Interventionparticipants (Number)
Radiation Plus PPX(CT210331
Radiation + Temozolomide15

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Number of Patients Who Experience Toxicity Events Undergoing This Treatment.

"Safety and toxicity will be reported in the number of patients who experience adverse events during treatment, graded using CTCAE 4.03.~In general the severity of an AE is graded as follows:~Mild (grade 1): the event causes discomfort without disruption of normal daily activities.~Moderate (grade 2): the event causes discomfort that affects normal daily activities.~Severe (grade 3): the event makes the patient unable to perform normal daily activities or significantly affects his/her clinical status.~Life-threatening (grade 4): the patient was at risk of death at the time of the event. Fatal (grade 5): the event caused death." (NCT01465659)
Timeframe: During treatment and up to one month post last dose of study drug. Range of cycles completed by patients was 1-41 where one cycle =28 days.

,,,
Interventionpatients (Number)
Any AEAE related to treatmentSAESAE related to treatmentGrade 5 SAECame off treatment due to an AE
Cohort -1 -Temozolomide 100 mg/m2 and Pazopanib 400 mg553113
Cohort -2 - Temozolomide 75 mg/m2 and Pazopanib 400 mg661103
Cohort 1 - Temozolomide 150 mg/m2 and Pazopanib 400 mg773303
Phase II -Temozolomide 75 mg/m2 and Pazopanib 400 mg11111102

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Progression Free Survival (PFS)

PFS will be defined as will be defined as the time from the first study treatment to the first occurrence of progression or death. Progressive disease will be assessed using RECIST v1.1 criteria where in general the following definition is true: At least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum recorded on study AND an absolute increase in the sum of at least 5 mm OR the appearance of one or more new lesions (NCT01465659)
Timeframe: Baseline and after every 2 cycles of treatment (8 weeks) for up to 40 months

Interventionmonths (Median)
Cohort 1/Cohort -1/Cohort -2 - Temozolomide and Pazopanib9.38

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Determine the Maximum Tolerated Dose (MTD) of Temozolomide in Combination With 400 mg Pazopanib in Patients With Advanced Pancreatic Neuroendocrine Tumor (PNET) in Phase I

"MTD and recommended phase II dose (RP2D) determination for the combination of temozolomide in combination with 400mg pazopanib in patients with advanced PNET will be achieved using a standard 3+3 dose escalation/de-escalation design. After each 3 patients are enrolled into the study, further enrollment will be temporarily suspended until safety has been reviewed for the first 28 days of treatment to determine if dose limiting toxicities have been experienced by patients and if a further 3 patients should be enrolled at the current dose or dose escalation/de-escalation for the next 3 patients should occur." (NCT01465659)
Timeframe: After 28 days (1 cycle of treatment)

Interventionmg/m2 (Number)
Cohort 1/Cohort -1/Cohort -2 - Temozolomide and Pazopanib75

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Plasma Temozolomide Concentration in the Blood at Various Timepoints After Administration

"For the Six Patients in Phase I portion who are enrolled in the PK cohort: Blood will be drawn on Day 1 before beginning treatment and again at 10 minutes, 30 minutes, 1, 2, 3, 4, 6 and 8 hours after beginning treatment. On Day 2- 24 hours after the first dose from Day 1, and again 10 minutes, 30 minutes, 1, 2, 3, 4, 6 and 8 hours after taking the second dose. Day 3 - 24 hours after the second dose from Day 2.~Cycle 1 Day 1 only temozolomide will be taken by the patient and on Cycle 2 Day 2, temozolomide and pazopanib will be taken by the patient. Data that was collected but not analyzed. The data that was collected is reported below in raw form." (NCT01465659)
Timeframe: Multiple timepoints during Days 1-3 of cycle 1 and cycle 2 (1 cycle =28 days)

Interventionng/mL (Number)
Patient #1 : Cycle 1 Day 1 at time 0 hoursPatient #1 : Cycle 1 Day 1 at time 0.17 hoursPatient #1 : Cycle 1 Day 1 at time 0.5 hoursPatient #1 : Cycle 1 Day 1 at time 1 hoursPatient #1 : Cycle 1 Day 1 at time 2 hoursPatient #1 : Cycle 1 Day 1 at time 3 hoursPatient #1 : Cycle 1 Day 1 at time 4 hoursPatient #1 : Cycle 1 Day 1 at time 6 hoursPatient #1 : Cycle 1 Day 1 at time 8 hoursPatient #1 : Cycle 1 Day 1 at time 24 hoursPatient #1 : Cycle 2 Day 1 at time 0 hoursPatient #1 : Cycle 2 Day 1 at time 0.17 hoursPatient #1 : Cycle 2 Day 1 at time 0.5 hoursPatient #1 : Cycle 2 Day 1 at time 1 hoursPatient #1 : Cycle 2 Day 1 at time 2 hoursPatient #1 : Cycle 2 Day 1 at time 3 hoursPatient #1 : Cycle 2 Day 1 at time 4 hoursPatient #1 : Cycle 2 Day 1 at time 6 hoursPatient #1 : Cycle 2 Day 1 at time 8 hoursPatient #1 : Cycle 2 Day 1 at time 24 hoursPatient #2 : Cycle 1 Day 1 at time 0 hoursPatient #2 : Cycle 1 Day 1 at time 0.17 hoursPatient #2 : Cycle 1 Day 1 at time 0.5 hoursPatient #2 : Cycle 1 Day 1 at time 1 hoursPatient #2 : Cycle 1 Day 1 at time 2 hoursPatient #2 : Cycle 1 Day 1 at time 3 hoursPatient #2 : Cycle 1 Day 1 at time 4 hoursPatient #2 : Cycle 1 Day 1 at time 6 hoursPatient #2 : Cycle 1 Day 1 at time 8 hoursPatient #2 : Cycle 1 Day 1 at time 24 hoursPatient #2 : Cycle 2 Day 1 at time 0 hoursPatient #2 : Cycle 2 Day 1 at time 0.17 hoursPatient #2 : Cycle 2 Day 1 at time 0.5 hoursPatient #2 : Cycle 2 Day 1 at time 1 hoursPatient #2 : Cycle 2 Day 1 at time 2 hoursPatient #2 : Cycle 2 Day 1 at time 3 hoursPatient #2 : Cycle 2 Day 1 at time 4 hoursPatient #2 : Cycle 2 Day 1 at time 6 hoursPatient #2 : Cycle 2 Day 1 at time 8 hoursPatient #2 : Cycle 2 Day 1 at time 24 hoursPatient #3 : Cycle 1 Day 1 at time 0 hoursPatient #3 : Cycle 1 Day 1 at time 0.17 hoursPatient #3 : Cycle 1 Day 1 at time 0.5 hoursPatient #3 : Cycle 1 Day 1 at time 1 hoursPatient #3 : Cycle 1 Day 1 at time 2 hoursPatient #3 : Cycle 1 Day 1 at time 3 hoursPatient #3 : Cycle 1 Day 1 at time 4 hoursPatient #3 : Cycle 1 Day 1 at time 6 hoursPatient #3 : Cycle 1 Day 1 at time 8 hoursPatient #3 : Cycle 1 Day 1 at time 24 hoursPatient #3 : Cycle 2 Day 1 at time 0 hoursPatient #3 : Cycle 2 Day 1 at time 0.17 hoursPatient #3 : Cycle 2 Day 1 at time 0.5 hoursPatient #3 : Cycle 2 Day 1 at time 1 hoursPatient #3 : Cycle 2 Day 1 at time 2 hoursPatient #3 : Cycle 2 Day 1 at time 3 hoursPatient #3 : Cycle 2 Day 1 at time 4 hoursPatient #3 : Cycle 2 Day 1 at time 6 hoursPatient #3 : Cycle 2 Day 1 at time 8 hoursPatient #3 : Cycle 2 Day 1 at time 24 hoursPatient #4 : Cycle 1 Day 1 at time 0 hoursPatient #4 : Cycle 1 Day 1 at time 0.17 hoursPatient #4 : Cycle 1 Day 1 at time 0.5 hoursPatient #4 : Cycle 1 Day 1 at time 1 hoursPatient #4 : Cycle 1 Day 1 at time 2 hoursPatient #4 : Cycle 1 Day 1 at time 3 hoursPatient #4 : Cycle 1 Day 1 at time 4 hoursPatient #4 : Cycle 1 Day 1 at time 6 hoursPatient #4 : Cycle 1 Day 1 at time 8 hoursPatient #4 : Cycle 1 Day 1 at time 24 hoursPatient #4 : Cycle 2 Day 1 at time 0 hoursPatient #4 : Cycle 2 Day 1 at time 0.17 hoursPatient #4 : Cycle 2 Day 1 at time 0.5 hoursPatient #4 : Cycle 2 Day 1 at time 1 hoursPatient #4 : Cycle 2 Day 1 at time 2 hoursPatient #4 : Cycle 2 Day 1 at time 3 hoursPatient #4 : Cycle 2 Day 1 at time 4 hoursPatient #4 : Cycle 2 Day 1 at time 6 hoursPatient #4 : Cycle 2 Day 1 at time 8 hoursPatient #4 : Cycle 2 Day 1 at time 24 hoursPatient #5 : Cycle 1 Day 1 at time 0 hoursPatient #5 : Cycle 1 Day 1 at time 0.17 hoursPatient #5 : Cycle 1 Day 1 at time 0.5 hoursPatient #5 : Cycle 1 Day 1 at time 1 hoursPatient #5 : Cycle 1 Day 1 at time 2 hoursPatient #5 : Cycle 1 Day 1 at time 3 hoursPatient #5 : Cycle 1 Day 1 at time 4 hoursPatient #5 : Cycle 1 Day 1 at time 6 hoursPatient #5 : Cycle 1 Day 1 at time 8 hoursPatient #5 : Cycle 1 Day 1 at time 24 hoursPatient #5 : Cycle 2 Day 1 at time 0 hoursPatient #5 : Cycle 2 Day 1 at time 0.17 hoursPatient #5 : Cycle 2 Day 1 at time 0.5 hoursPatient #5 : Cycle 2 Day 1 at time 1 hoursPatient #5 : Cycle 2 Day 1 at time 2 hoursPatient #5 : Cycle 2 Day 1 at time 3 hoursPatient #5 : Cycle 2 Day 1 at time 4 hoursPatient #5 : Cycle 2 Day 1 at time 6 hoursPatient #5 : Cycle 2 Day 1 at time 8 hoursPatient #5 : Cycle 2 Day 1 at time 24 hoursPatient #6a : Cycle 1 Day 1 at time 0 hoursPatient #6a : Cycle 1 Day 1 at time 0.17 hoursPatient #6a : Cycle 1 Day 1 at time 0.5 hoursPatient #6a : Cycle 1 Day 1 at time 1 hoursPatient #6a : Cycle 1 Day 1 at time 2 hoursPatient #6a : Cycle 1 Day 1 at time 3 hoursPatient #6a : Cycle 1 Day 1 at time 4 hoursPatient #6a : Cycle 1 Day 1 at time 6 hoursPatient #6a : Cycle 1 Day 1 at time 8 hoursPatient #6a : Cycle 1 Day 1 at time 24 hoursPatient #6a : Cycle 2 Day 1 at time 0 hoursPatient #6a : Cycle 2 Day 1 at time 0.17 hoursPatient #6a : Cycle 2 Day 1 at time 0.5 hoursPatient #6a : Cycle 2 Day 1 at time 1 hoursPatient #6a : Cycle 2 Day 1 at time 2 hoursPatient #6a : Cycle 2 Day 1 at time 3 hoursPatient #6a : Cycle 2 Day 1 at time 4 hoursPatient #6a : Cycle 2 Day 1 at time 6 hoursPatient #6a : Cycle 2 Day 1 at time 8 hoursPatient #6a : Cycle 2 Day 1 at time 24 hours
Temozolomide 75 mg/m2 and Pazopanib 400 mg0091.8425.5462583210.51054400025.290.8516.525551915499.900054.9494660.5557.599105.5109.500041.61151490961.5382.5510.5109.500052716702440202414667183174.34.124190921302490193315867613284.7503.64923025280517651430686.53831.22.42.33.01.61.0123360261012253285019.1177227275829.59251145819.544.20108166.5188.5422.5716.510701180744.536.70459.530552720173514701195499.52511.5067.740952135209514451025.5324.5192.51.3

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Overall Survival (OS)

OS is defined as the time from first study treatment until death from any cause. (NCT01465659)
Timeframe: Baseline and after every 2 cycles of treatment (8 weeks) and up to 60 months

Interventionmonths (Median)
Cohort 1/Cohort -1/Cohort -2 - Temozolomide and Pazopanib24.2

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Overall Response Rate (ORR) in Patients With Advanced Neuroendocrine Tumors (PNET) Treated With Temozolomide and Pazopanib Combination Treatment at the RP2D in Phase II

"Overall response rate will be determined by the number of patients who's best response as assessed by RECIST 1.1 is complete response (CR) and partial response (PR) in patients with PNET that are enrolled at the recommended phase II dose (RP2D) (PK cohort included).~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 diameters." (NCT01465659)
Timeframe: After two cycles of treatment (8 weeks)

InterventionParticipants (Count of Participants)
Phase II -Temozolomide 75 mg/m2 and Pazopanib 400 mg0

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Number of Patients Experiencing Response to Treatment or Stable Disease (Disease Control Rate)

"Disease Control Rate (DCR) is defined as the number of patients demonstrating the complete response, partial response or stable disease.~In general the following is true:~Complete Response (CR) Disappearance of all target lesions. Disappearance of all non-target lesions and normalization of tumor marker level.~Partial Response (PR) At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters Stable Disease (SD) Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease, taking as reference the smallest sum of diameters while on study" (NCT01465659)
Timeframe: After every 2 courses of treatment (8 weeks) for up to 41 cycles where 1 cycle =28 days.

InterventionParticipants (Count of Participants)
Cohort 1/Cohort -1/Cohort -2 - Temozolomide and Pazopanib20

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Overall Survival Rate

Overall survival rate is calculated as the median number of months that patients were alive for the cohort (NCT01466686)
Timeframe: up to 12 months after completion of temozolomide (48 weeks of treatment)

Interventionmonths (Median)
Temozolomide With Low Dose Fractionated Radiation Therapy9.6

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Number of Patients With Neurologic Toxicity

The number of patients with reported grade 3+ neurologic toxicities (NCT01466686)
Timeframe: Approximately every month from study start until 48 weeks, and then up to 12 months after completion of temozolomide at 3, 6, and 12 months follow up

InterventionParticipants (Count of Participants)
Temozolomide With Low Dose Fractionated Radiation Therapy6

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Number of Patients With Hematologic Toxicities

The number of patients with grade 3+ hematologic toxicities. (NCT01466686)
Timeframe: Approximately every month from study start until 48 weeks, and then up to 12 months after completion of temozolomide at 3, 6, and 12 months follow up

InterventionParticipants (Count of Participants)
Temozolomide With Low Dose Fractionated Radiation Therapy8

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Progression Free Survival Rate

Progression free survival rate is calculated as the median number of months for the cohort until patient's disease worsened/progressed (NCT01466686)
Timeframe: up to 12 months after completion of temozolomide (48 weeks of treatment)

Interventionmonths (Median)
Temozolomide With Low Dose Fractionated Radiation Therapy7.3

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Safety Profile for Patients With Recurrent High Grade Malignant Gliomas Treated With Concurrent Radiation, Temozolomide, and Bevacizumab Followed by Adjuvant Temozolomide and Bevacizumab

"Toxicity will be assessed using the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) version 4.0 criteria on Day 1 of every treatment cycle and by patient report while on study treatment and up to 30 days after the last treatment. Grade 1 - 4 adverse events (AE) where the relationship between the AE and at least one of the study drugs were considered to be definite, probable or possible, were collected and graded as:~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" (NCT01478321)
Timeframe: Completed weekly during initial phase of 5 weeks and 2 weeks recovery, then every cycle during adjuvant therapy where 1 cycle =8 weeks (for up to 7 cycles)

Interventionparticipants (Number)
Lymphopenia : Grade 1Lymphopenia : Grade 2Lymphopenia : Grade 3Lymphopenia : Grade 4Fatigue : Grade 1Fatigue : Grade 2Fatigue : Grade 3Fatigue : Grade 4Thrombocytopenia : Grade 1Thrombocytopenia : Grade 2Thrombocytopenia : Grade 3Thrombocytopenia : Grade 4Anemia : Grade 1Anemia : Grade 2Anemia : Grade 3Anemia : Grade 4Constipation : Grade 1Constipation : Grade 2Constipation : Grade 3Constipation : Grade 4Hypertension : Grade 1Hypertension : Grade 2Hypertension : Grade 3Hypertension : Grade 4Neutropenia : Grade 1Neutropenia : Grade 2Neutropenia : Grade 3Neutropenia : Grade 4Epistaxis : Grade 1Epistaxis : Grade 2Epistaxis : Grade 3Epistaxis : Grade 4Thromboembolism : Grade 1Thromboembolism : Grade 2Thromboembolism : Grade 3Thromboembolism : Grade 4Proteinuria : Grade 1Proteinuria : Grade 2Proteinuria : Grade 3Proteinuria : Grade 4Wound Complication : Grade 1Wound Complication : Grade 2Wound Complication : Grade 3Wound Complication : Grade 4
Treatment (Radiation, Chemotherapy, Monoclonal Antibody)412419510812171108100061023003000011000200020

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Overall Survival (OS) for Patients With Recurrent High Grade Malignant Gliomas Treated With Concurrent Radiation, Temozolomide, and Bevacizumab Followed by Adjuvant Temozolomide and Bevacizumab.

Data will be analyzed using Kaplan-Meier curves. OS is defined as the time from first re-irradiation treatment until death from any cause. (NCT01478321)
Timeframe: From treatment initiation and every 8 weeks for up to 53.5 months

InterventionMonths (Median)
Treatment (Radiation, Chemotherapy, Monoclonal Antibody)8.5

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Median Progression Free Survival (PFS) for Patients With Recurrent High Grade Malignant Gliomas Treated With Concurrent Radiation, Temozolomide, and Bevacizumab Followed by Adjuvant Temozolomide and Bevacizumab

Progression Free Survival (PFS) is defined as the time from the first study treatment to the first occurrence of disease progression or death. Data will be analyzed using Kaplan-Meier curves. Tumor measurements and assessments will be based on Updated Response Assessment Criteria of High Grade Gliomas- Neuro-Oncology Working Group (RANO criteria). Tumor assessments may include either a CT or MRI scan of the brain, however the same method should be used throughout the treatment period for each patient. In general, progressive disease is defined as any of the following: ≥ 25% increase in T1 gadolinium enhancing disease, increase in T2/Flair, new lesions present or decrease in clinical status. (NCT01478321)
Timeframe: Range from treatment initiation 0.4-26.9 months

InterventionMonths (Median)
Treatment (Radiation, Chemotherapy, Monoclonal Antibody)5.5

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Percentage of Patients With Progression Free Survival (PFS) at 6 Months and 12 Months

Progression Free Survival is defined as the time from the first study treatment to the first occurrence of disease progression or death. Data will be analyzed using Kaplan-Meier curves. Tumor measurements and assessments will be based on Updated Response Assessment Criteria of High Grade Gliomas- Neuro-Oncology Working Group (RANO criteria). Tumor assessments may include either a CT or MRI scan of the brain, however the same method should be used throughout the treatment period for each patient. In general, progressive disease is defined as any of the following: ≥ 25% increase in T1 gadolinium enhancing disease, increase in T2/Flair, new lesions present or decrease in clinical status (NCT01478321)
Timeframe: At 6 and 12 months after the start of treatment

Interventionpercentage of patients with PFS (Number)
6 Months12 Months
Treatment (Radiation, Chemotherapy, Monoclonal Antibody)4812

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Patient Reported Quality of Life (QOL)

"Questionnaires were completed before treatment (baseline) at the end of treatment (EOT) and after Cycle 1 and Cycle 2 of treatment (Initial phase of treatment =5 weeks + approximately 2 weeks recovery then adjuvant therapy where 1 cycle = 8 weeks). The following questionnaires were completed by patients to evaluate quality of life (QOL) at these timepoints:~FACT-Fatigue - scores from 1 to 4 with 1=not at all and 4=very much, the higher the score the more fatigue reported by the patient.~FACT-Brain (FACT Br) which included - Physcial Well-being (PWB), Social/Family Well-being (SWB), Emotional Well-being (EWB), and Functional Well-being (FWB).~Patients gave scores from 0 to 4 with 0=not at all and 4=very much, the higher the score the better the QOL reported by the patient." (NCT01478321)
Timeframe: Completed before treatment (baseline) after Cycle 1 (approximately week 15) and Cycle 2 (approximately week 23)of adjuvant treatment and at the end of treatment (up to 7 cycles of adjuvant treatment, where 1 cycle =8 weeks)

Interventionscore on a scale (Mean)
FACT-BR Total : BaselineFACT-BR Total : EOTFACT-BR Total : Post Cycle 1FACT-BR Total : Post Cycle 2FACT-BR PWB : BaselineFACT-BR PWB : EOTFACT-BR PWB : Post Cycle 1FACT-BR PWB : Post Cycle 2FACT-BR SWB : BaselineFACT-BR SWB : EOTFACT-BR SWB : Post Cycle 1FACT-BR SWB : Post Cycle 2FACT-BR EWB : BaselineFACT-BR EWB : EOTFACT-BR EWB : Post Cycle 1FACT-BR EWB : Post Cycle 2FACT-FWB : BaselineFACT-FWB : EOTFACT-FWB : Post Cycle 1FACT-FWB: Post Cycle 2FACIT-Fatigue: BaselineFACIT-Fatigue: EOTFACIT-Fatigue: Post Cycle 1FACIT-Fatigue: Post Cycle 2
Treatment (Radiation, Chemotherapy, Monoclonal Antibody)130.4106.9133.0131.422.021.621.721.122.222.923.023.715.916.517.217.715.917.817.018.335.630.334.436.2

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Overall Survival (OS) at 6 Months and 12 Months for Patients With Recurrent High Grade Malignant Gliomas Treated With Concurrent Radiation, Temozolomide, and Bevacizumab Followed by Adjuvant Temozolomide and Bevacizumab.

Data will be analyzed using Kaplan-Meier curves. OS is defined as the time from first re-irradiation treatment until death from any cause. Percentages of patients alive at that 6 months and 12 months will be calculated from the Kaplan-Meier curve. (NCT01478321)
Timeframe: At 6 and 12 months from start of treatment

Interventionpercentage of patients alive (Number)
6 Months12 Months
Treatment (Radiation, Chemotherapy, Monoclonal Antibody)6728

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Overall Response Rate (ORR) of Participants Using RECIST Criteria

"Phase I portion of trial- All patients enrolled to recieve TPI+I+TMZ. These patients will be added to the Phase II patients that were randomized to Arm B- Arm with TPI 287 (recieved same tx as Phase I participatns).~Phase II portion of trial- TPatients enrolled to this portion (different patients than enrolled to Phase 1) were randomized to Arm A: I+TMZ OR Arm B: TPI+I+TMZ 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." (NCT01505608)
Timeframe: 3 years

Interventionparticipants (Number)
Arm A- Temozolomide and Irinotecan0
Phase I Patients + Phase II Assigned Arm B- Tmz +I+ TPI 2872

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Number of Participants With Adverse Events as a Measure of Safety and Tolerability

"To determine the safety and tolerability of TPI 287 in combination with Irinotecan and Temozolomide (TPI+I+TMZ) in pediatric and young adult patients with primary refractory or recurrent Neuroblastoma.~Phase I patients were all enrolled to receive TPI 287. Phase 2 is where randomization began. Patients were different patients than the Phase 1 patients. Below all patients that received TPI 287 are included in the TPI 287 group. This includes Phase I patients and the Phase 2 patients randomized to TPI 287." (NCT01505608)
Timeframe: 6 months

Interventionparticipants (Number)
TPI 2877
Arm A- TMZ + Irinotecan Only0

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Progression Free Survival (PFS) of Participants Using Days Until Progression

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 (NCT01505608)
Timeframe: 3 years

InterventionDays (Number)
Arm A- Temozolomide and Irinotecan22
Arm B- Temozolomide/Irinotecan + TPI 287125

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Progression-Free Survival (PFS)

PFS is defined as the number of months from the date the participant was randomized to the date of radiographic progression as determined by the central imaging center, or to the date of all cause deaths within 63 days of last tumor assessment if disease progression was not reached. (NCT01506609)
Timeframe: Radiographic evaluation every 9 weeks, clinical evaluation every cycle (data cutoff date: 04 March 2016); maximum duration of follow up for PFS was 34 months.

Interventionmonths (Median)
Group 2 Placebo + Carboplatin/Paclitaxel12.3
Group 2 Veliparib + Carboplatin/Paclitaxel14.1
Group 2 Veliparib + TMZ7.4

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Clinical Benefit Rate (CBR) at Week 18

"CBR: percentage of participants who were progression-free at 18 weeks, defined as complete response (CR), partial response (PR), stable disease (SD) or non-CR/non-disease progression (PD) per Response Evaluation Criteria in Solid Tumors [RECIST] 1.1.~CR: The disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 0 mm. PR: >= 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters (SOD). PD: >= 20% increase in the SOD of target lesions, taking as reference the smallest SOD recorded since the treatment started (baseline or after) or the appearance of >=1 new lesions. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD since the treatment started (baseline or after)." (NCT01506609)
Timeframe: Week 18

Interventionpercentage of participants (Number)
Group 2 Placebo + Carboplatin/Paclitaxel87.0
Group 2 Veliparib + Carboplatin/Paclitaxel90.7
Group 2 Veliparib + TMZ73.0

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Overall Survival (OS)

Time to death for a given participant was defined as the number of months from the day the participant is randomized to the date of the participant's death. All events of death were included, regardless of whether the event occurs while the participant was still taking study drug, or after the participant discontinued study drug. If a participant had not died, then the data will be censored at the date when the participant was last known to be alive. (NCT01506609)
Timeframe: From Cycle 1 Day 1 until participant's death or 3 years post discontinuation (data cutoff date: 04 March 2016); maximum duration of follow up for OS was 72 months.

Interventionmonths (Median)
Group 2 Placebo + Carboplatin/Paclitaxel25.4
Group 2 Veliparib + Carboplatin/Paclitaxel28.3
Group 2 Veliparib + TMZ19.1

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Objective Response Rate (ORR)

The objective response rate, defined as percentage of participants with a confirmed CR or PR based on RECIST 1.1 criteria. CR: The disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 0 mm. PR: >= 30% decrease in the sum of diameters of target lesions, taking as reference the baseline SODs. (NCT01506609)
Timeframe: Radiographic evaluation every 9 weeks, clinical evaluation every cycle (data cutoff date: 04 March 2016); maximum duration of follow up for ORR was 34 months.

Interventionpercentage of participants (Number)
Group 2 Placebo + Carboplatin/Paclitaxel61.3
Group 2 Veliparib + Carboplatin/Paclitaxel77.8
Group 2 Veliparib + TMZ28.6

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Change From Baseline at Week 18 in European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Chemotherapy-Induced Peripheral Neuropathy Module (EORTC QLQ-CIPN20) Sensory Subscale Score

EORTC QLQ-CIPN20 sensory subscale score was calculated following the standard scoring algorithm, transformed to a 0 (low quality of life) to 100 (best quality of life) scale. A positive change from baseline indicates improvement. (NCT01506609)
Timeframe: Baseline, Week 18

Interventionscore on a scale (Mean)
Group 2 Placebo + Carboplatin/Paclitaxel13.94
Group 2 Veliparib + Carboplatin/Paclitaxel11.24

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Overall Survival

Overall survival was defined as the interval from date on treatment to date of death from any cause or to date of last follow-up. Patients who had not failed (died) at the time of analyses were censored at their last date of contact. The method of Kaplan and Meier was used to estimate overall survival. The 3-year estimate with a 95% confidence interval is reported. (NCT01514201)
Timeframe: Time from initiation of therapy to the date of death from any cause or to the date patient was known to be alive for surviving patients, assessed to up to 3 years

InterventionPercent probability (Number)
Phase II Patients + Phase I MTD Patients5.3

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Trough for Veliparib [Pharmacokinetic Parameter]

During course 1, blood samples were collected pre-veliparib on day 1, at 0.5, 1, 2, and 6-8 hours after the first dose, pre-veliparib on day 4 (steady state), and 2 hours after the morning dose. Veliparib concentrations were measured using a liquid chromatography tandem mass spectrometry assay and pharmacokinetic parameters were evaluated using a non-compartmental analysis. (NCT01514201)
Timeframe: Up to day 4

Interventionng/mL (Mean)
Phase I, Dose Level 1 (50 mg)58
Phase I, Dose Level 2 (65 mg)140
Phase I, Dose Level 3 (85 mg)163
Phase II (MTD)84

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Levels of Urinary Biomarkers

Urine samples were analyzed for a panel of biomarkers. Netrin-1 levels were determined by ELISA. Levels of matrix metalloproteinase 3 (MMP3) and basic fibroblast growth factor (bFGF) were analyzed using custom Luminex® screening assays. Tissue inhibitor of metalloproteinase 1 (TIMP1) levels were analyzed using a Luminex® performance assay. Protein concentrations are given in picograms per microgram (pg/μg), and were determined by dividing the concentration of the target protein in the sample (pg/mL) by the concentration of total protein in the sample (μg/mL) as a normalization measure. (NCT01514201)
Timeframe: Baseline to up to 3 years

,,,
Interventionpg/μg (Median)
MMP3 at pre-studyMMP3 at week 10-11MMP3 at week 18MMP3 at week 26Netrin-1 at pre-studyNetrin-1 at week 10-11Netrin-1 at week 18Netrin-1 at week 26TIMP1 at pre-studyTIMP1 at week 10-11TIMP1 at week 18TIMP1 at week 26bFGF at pre-studybFGF at week 10-11bFGF at week 18bFGF at week 26
Phase I, Dose Level 1 (50 mg)2.01.44.32.90.10.10.30.43.46.210.77.33.13.610.37.7
Phase I, Dose Level 2 (65 mg)1.01.01.70.40.10.10.10.29.911.97.75.21.92.13.50.9
Phase I, Dose Level 3 (85 mg)0.00.80.71.00.10.10.00.010.812.314.832.81.21.81.31.1
Phase II (MTD)1.12.62.33.00.10.00.10.07.37.57.110.74.53.54.44.5

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Maximum Concentration of Veliparib (Cmax) on Days 1 and 4 (Measured in ng/mL) [Pharmacokinetic Parameter]

During course 1, blood samples were collected pre-veliparib on day 1, at 0.5, 1, 2, and 6-8 hours after the first dose, pre-veliparib on day 4 (steady state), and 2 hours after the morning dose. Veliparib concentrations were measured using a liquid chromatography tandem mass spectrometry assay and pharmacokinetic parameters were evaluated using a non-compartmental analysis. Cmax measures the highest concentration of drug. (NCT01514201)
Timeframe: Up to day 4

,,,
Interventionng/mL (Mean)
Day 1, Cmax (ng/mL)Day 4, Cmax (ng/mL)
Phase I, Dose Level 1 (50 mg)519409
Phase I, Dose Level 2 (65 mg)843788
Phase I, Dose Level 3 (85 mg)1074954
Phase II (MTD)844717

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Percentage of Participants With Significant Changes in Poly(ADP-ribose) Polymerase (PARP) Levels Post-Veliparib, as Measured in Peripheral Blood Monocytes (PBMCs)

Blood samples were collected from patients and assessed pre- and post-Veliparib to assess treatment-induced changes. A significant change in PBMC PARP level was arbitrarily defined as a >50% increase or decrease from the pre-treatment level, documented at week 6 and/or week 11 after starting protocol therapy. (NCT01514201)
Timeframe: Baseline and up to 11 weeks

Interventionpercentage of participants (Number)
Phase I, Dose Level 1 (50 mg)100
Phase I, Dose Level 2 (65 mg)100
Phase I, Dose Level 3 (85 mg)75
Phase II (MTD)36

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Percentage of Participants Observed to Have Unacceptable Toxicity During the Intra-patient Dose Escalation of Temozolomide During Maintenance Therapy (Feasibility Analysis Population)

Unacceptable toxicities during maintenance included events at least possibly attributable to Veliparib and temozolomide (TMZ) such as any grade 4 non-hematologic toxicity, any grade 3 non-hematologic toxicity with some exceptions (e.g., grade 3 nausea/vomiting <5 days, grade 3 fever or infection <5 days), grade 3+ thrombocytopenia, grade 4 neutropenia, delay >14 days in starting subsequent cycle due to neutrophil <1,000/mm3 or platelet <100,000/mm3. Maintenance therapy was initiated with 25 mg/m2 Veliparib and 135 mg/m2 of TMZ, with the possibility to escalate TMZ to 175 mg/m2 and 200 mg/m2 in courses 2 and 3, respectively, if no unacceptable toxicities occurred following one course of treatment at each of the dose levels to be tested. Intra-patient dose escalation to a given dose (135, 175, or 200 mg/m2) was halted based on rules employed in 3+3 designs. This dose escalation was intended for all patients but was halted early, during the phase I portion, as it was not well tolerated. (NCT01514201)
Timeframe: 28 days per treatment cycle

Intervention% of participants (Number)
Dose Level 1 (135 mg/m2)9
Dose Level 2 (175 mg/m2)40
Dose Level 3 (200 mg/m2)67

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Terminal Half-life (t1/2) for Veliparib [Pharmacokinetic Parameter]

During course 1, blood samples were collected pre-veliparib on day 1, at 0.5, 1, 2, and 6-8 hours after the first dose, pre-veliparib on day 4 (steady state), and 2 hours after the morning dose. Veliparib concentrations were measured using a liquid chromatography tandem mass spectrometry assay and pharmacokinetic parameters were evaluated using a non-compartmental analysis. (NCT01514201)
Timeframe: Up to day 4

InterventionHour (Mean)
Phase I, Dose Level 1 (50 mg)5.18
Phase I, Dose Level 2 (65 mg)2.62
Phase I, Dose Level 3 (85 mg)4.45
Phase II (MTD)2.18

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Mean Apparent Clearance (CL/F) for Veliparib [Pharmacokinetic Parameter]

During course 1, blood samples were collected pre-veliparib on day 1, at 0.5, 1, 2, and 6-8 hours after the first dose, pre-veliparib on day 4 (steady state), and 2 hours after the morning dose. Veliparib concentrations were measured using a liquid chromatography tandem mass spectrometry assay and pharmacokinetic parameters were evaluated using a non-compartmental analysis. (NCT01514201)
Timeframe: Up to day 4

InterventionL/m^2/h (Mean)
Phase I, Dose Level 1 (50 mg)16.1
Phase I, Dose Level 2 (65 mg)13.2
Phase I, Dose Level 3 (85 mg)15.8
Phase II (MTD)11.7

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Progression-free Survival (PFS)

PFS was defined as the interval from date of treatment initiation to date of first event (disease progression or relapse, second malignancy or death from any cause). Patients who had not failed at the time of analyses were censored at their last date of contact. The method of Kaplan and Meier was used to estimate PFS. A 3-year estimate with a 95% confidence interval is reported. (NCT01514201)
Timeframe: Time from initiation of treatment to the earliest date of failure (disease progression, death from any cause, or second malignancy), assessed up to 3 years

InterventionPercent probability (Number)
Phase II Patients + Phase I MTD Patients2.9

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Percentage of Patients With Pseudo Progression

For participants that showed possible tumor progression (pseudo progression) on magnetic resonance imaging (MRI) during the first 6 months of therapy, treating physicians had the option of allowing patients to remain on therapy and repeating the disease assessment in 4-6 weeks. If the repeat MRI at 4-6 weeks showed disease progression, the patient was noted to have true disease progression (and the progression date corresponded to that of the first MRI). If the repeat MRI at 4-6 weeks did not show disease progression, then the patient was noted to have pseudo progression. The percentage of patients observed to have experienced pseudo progression was provided with a 95% confidence interval. (NCT01514201)
Timeframe: Up to 6 months

InterventionPercentage of participants (Number)
Phase I, Dose Level 1 (50 mg)33.3
Phase I, Dose Level 2 (65 mg)16.7
Phase I, Dose Level 3 (85 mg)0
Phase II (MTD)12.8

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Apparent Volume of Distribution (Vd/F) for Veliparib [Pharmacokinetic Parameter]

During course 1, blood samples were collected pre-veliparib on day 1, at 0.5, 1, 2, and 6-8 hours after the first dose, pre-veliparib on day 4 (steady state), and 2 hours after the morning dose. Veliparib concentrations were measured using a liquid chromatography tandem mass spectrometry assay and pharmacokinetic parameters were evaluated using a non-compartmental analysis. (NCT01514201)
Timeframe: Up to day 4

InterventionL/m^2 (Mean)
Phase I, Dose Level 1 (50 mg)75.4
Phase I, Dose Level 2 (65 mg)56.1
Phase I, Dose Level 3 (85 mg)63.9
Phase II (MTD)73.1

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Maximum Concentration of Veliparib (Cmax) on Day 1 (Measured in μM) [Pharmacokinetic Parameter]

During course 1, blood samples were collected pre-veliparib on day 1, at 0.5, 1, 2, and 6-8 hours after the first dose, pre-veliparib on day 4 (steady state), and 2 hours after the morning dose. Veliparib concentrations were measured using a liquid chromatography tandem mass spectrometry assay and pharmacokinetic parameters were evaluated using a non-compartmental analysis. Cmax measures the highest concentration of drug. (NCT01514201)
Timeframe: Day 1

InterventionμM (Mean)
Phase I, Dose Level 1 (50 mg)2.12
Phase I, Dose Level 2 (65 mg)3.45
Phase I, Dose Level 3 (85 mg)4.40
Phase II (MTD)3.45

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Maximum-tolerated Dose of Veliparib Defined as Highest Dose Level With Fewer Than 2 Dose Limiting Toxicities in 6 Patients as Assessed by the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.0 (Phase I)

The traditional 3+3 dose finding algorithm was used to estimate the maximum-tolerated dose of veliparib given concurrently with radiation therapy. The dose-limiting toxicity observation period was the first 10 weeks of therapy. Dose-limiting toxicities included any grade 4 non-hematologic toxicity, any grade 3 non-hematologic toxicity with a few exceptions (see section 5.2.1.2 of the protocol document), any grade 2 non-hematologic toxicity that persisted for >7 days and considered medically significant that required treatment interruption; grade 3 or higher thrombocytopenia or grade 4 neutropenia; and any Veliparib related adverse event that led to a dose reduction or the permanent cessation of therapy. (NCT01514201)
Timeframe: 10 weeks

Interventionmg/m2/dose BID (Number)
Phase I Patients65

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Number of Phase I Patients Who Experienced Dose Limiting Toxicities (DLTs)

DLTs were defined as any of the following adverse events that were at least possibly attributable to Veliparib observed during the dose finding phase (the first 10 weeks of therapy). Hematologic dose limiting toxicities included grade 3 and higher thrombocytopenia or grade 4 neutropenia. Non-hematologic dose limiting toxicities included any grade 4 non-hematologic toxicity, any grade 3 non-hematologic toxicity with some exceptions (e.g., nausea and vomiting of <5 days; fever or infection of <5 days; hypophosphatemia, hypokalemia, hypocalcemia or hypomagnesemia responsive to oral supplementation; elevation of transaminases that return to levels meeting eligibility criteria within 7 days), or any grade non-hematologic toxicity that persisted for >7 days and considered medically significant or sufficiently intolerable by patients that required treatment interruption. (NCT01514201)
Timeframe: 10 weeks

InterventionParticipants (Count of Participants)
Phase I, Dose Level 1 (50 mg)1
Phase I, Dose Level 2 (65 mg)0
Phase I, Dose Level 3 (85 mg)3

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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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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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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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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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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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Treatment Failure (TF)

"Treatment failure (TF) is defined as failing to achieve either a complete remission (CR) or partial remission (PR) after induction chemotherapy. The outcome is reported as the percentage without dispersion of participants in Groups 1 and 2 that experienced TF. CR and PR are defined as the following.~CR = < 5% blasts in bone marrow aspirate containing marrow spicules; > 200 nucleated cells no blasts with Auer rods; no persistence of extramedullary disease absolute neutrophil count (ANC) ≥ 1,000/µL platelets (PLT) ≥ 100,000/µL~PR = 5% to 25% blasts (must be ≥ 50% reduction of blasts) in bone marrow aspirate containing marrow spicules; > 200 nucleated cells no blasts with Auer rods no persistence of extramedullary disease absolute neutrophil count (ANC) ≥ 1,000/µL platelets (PLT) ≥ 100,000/µL" (NCT01550224)
Timeframe: up to 10 weeks

InterventionParticipants (Count of Participants)
Participant Group 1 (Methylated MGMT Promoter)3
Participant Group 2 (Non-methylated MGMT Promoter)20

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Relapse-Free Survival (RFS) at 2 Years

"Relapse-free survival (RFS) is defined as survival after complete response (CR) or (PR) without further disease progression. RFS is reported as the percentage without dispersion of participants in Groups 1 and 2 that experienced CR or PR, and were alive without progression 2 years after induction chemotherapy. CR and PR are defined as the following.~CR = < 5% blasts in bone marrow aspirate containing marrow spicules; > 200 nucleated cells no blasts with Auer rods; no persistence of extramedullary disease absolute neutrophil count (ANC) ≥ 1,000/µL platelets (PLT) ≥ 100,000/µL~PR = 5% to 25% blasts (must be ≥ 50% reduction of blasts) in bone marrow aspirate containing marrow spicules; > 200 nucleated cells no blasts with Auer rods no persistence of extramedullary disease absolute neutrophil count (ANC) ≥ 1,000/µL platelets (PLT) ≥ 100,000/µL" (NCT01550224)
Timeframe: 2 years

InterventionParticipants (Count of Participants)
Participant Group 1 (Methylated MGMT Promoter)0
Participant Group 2 (Non-methylated MGMT Promoter)0

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Partial Remission (PR)

"Partial remission (PR) is reported as the percentage without dispersion of participants in Groups 1 and 2 that demonstrated PR. PR is defined as all of the following.~PR = 5% to 25% blasts (must be ≥ 50% reduction of blasts) in bone marrow aspirate containing marrow spicules; > 200 nucleated cells no blasts with Auer rods no persistence of extramedullary disease absolute neutrophil count (ANC) ≥ 1,000/µL platelets (PLT) ≥ 100,000/µL" (NCT01550224)
Timeframe: up to 10 weeks

InterventionParticipants (Count of Participants)
Participant Group 1 (Methylated MGMT Promoter)0
Participant Group 2 (Non-methylated MGMT Promoter)0

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Overall Survival (OS) at 2 Years

Overall Survival (OS) is defined as survival regardless of clinical status. OS is reported as the percentage without dispersion of participants in Groups 1 and 2 that remained alive 2 years after induction chemotherapy. (NCT01550224)
Timeframe: 2 years

InterventionParticipants (Count of Participants)
Participant Group 1 (Methylated MGMT Promoter)0
Participant Group 2 (Non-methylated MGMT Promoter)0

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Disease-free Survival (DFS) at 2 Years

"Disease-Free Survival (DFS) is defined as survival after complete response (CR) without disease progression. DFS is reported as the percentage without dispersion of participants in Groups 1 and 2 that experienced CR and were alive without progression (ie, without disease) 2 years after induction chemotherapy. CR is defined as all of the following.~CR = < 5% blasts in bone marrow aspirate containing marrow spicules; > 200 nucleated cells no blasts with Auer rods; no persistence of extramedullary disease absolute neutrophil count (ANC) ≥ 1,000/µL platelets (PLT) ≥ 100,000/µL" (NCT01550224)
Timeframe: 2 years

InterventionParticipants (Count of Participants)
Participant Group 1 (Methylated MGMT Promoter)0
Participant Group 2 (Non-methylated MGMT Promoter)0

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Cytogenetic Response (CyR)

"Cytogenetic response (CyR) is defined as complete remission (CR), PLUS a documented decrease or absence of cytogenetic abnormalities, when analyzed microscopically for 20 cellular metaphases (actively dividing cells). The outcome is reported as the percentage without dispersion of participants in Groups 1 and 2 that demonstrated CyR. CR is defined as all of the following.~CR = < 5% blasts in bone marrow aspirate containing marrow spicules; > 200 nucleated cells no blasts with Auer rods; no persistence of extramedullary disease absolute neutrophil count (ANC) ≥ 1,000/µL platelets (PLT) ≥ 100,000/µL" (NCT01550224)
Timeframe: up to 10 weeks

InterventionParticipants (Count of Participants)
Participant Group 1 (Methylated MGMT Promoter)0
Participant Group 2 (Non-methylated MGMT Promoter)0

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Morphologic Leukemia-free State (MLFS)

"The rate of morphologic leukemia-free state (MLFS) is reported as the percentage without dispersion of participants in Groups 1 and 2 that achieve MLFS. The outcome is reported as the percentage without dispersion of participants in Groups 1 and 2 that demonstrated MLFS. This assessment is independent of absolute neutrophil count (ANC) or platelets (PLT) recovery status. MLFS is defined below.~MLFS = < 5% blasts in bone marrow aspirate containing marrow spicules > 200 nucleated cells no blasts with Auer rods no persistence of extramedullary disease" (NCT01550224)
Timeframe: up to 10 weeks

InterventionParticipants (Count of Participants)
Participant Group 1 (Methylated MGMT Promoter)0
Participant Group 2 (Non-methylated MGMT Promoter)1

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Complete Remission (CR)

"This study evaluates the clinical efficacy of temozolomide + vorinostat as administered to Groups 1 and 2, assessed as the rate of complete remission [CR, aka morphologic complete remission (mCR)], defined as the morphologic leukemia-free state (MLFS), WITH absolute neutrophil count (ANC) ≥ 1,000/µL AND platelets (PLT) ≥ 100,000/µL. The outcome is reported as the percentage without dispersion of participants in Groups 1 and 2 that demonstrated CR. CR is defined as all of the following.~MLFS = < 5% blasts in bone marrow aspirate containing marrow spicules > 200 nucleated cells no blasts with Auer rods no persistence of extramedullary disease ANC = ≥ 1,000/µL PLT = ≥ 100,000/µL" (NCT01550224)
Timeframe: up to 10 weeks

InterventionParticipants (Count of Participants)
Participant Group 1 (Methylated MGMT Promoter)0
Participant Group 2 (Non-methylated MGMT Promoter)0

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Complete Remission With Incomplete Blood Count Recovery (CRp)

"The rate of complete remission with incomplete blood count recovery (CRp) for Groups 1 and 2 was assessed as the rate of morphologic leukemia-free state (MLFS) but with EITHER residual neutropenia (ANC < 1,000/µL) OR residual thrombocytopenia (PLT < 100,000/µL). MLFS is defined as follows.~MLFS = < 5% blasts in bone marrow aspirate containing marrow spicules > 200 nucleated cells no blasts with Auer rods no persistence of extramedullary disease" (NCT01550224)
Timeframe: up to 10 weeks

InterventionParticipants (Count of Participants)
Participant Group 1 (Methylated MGMT Promoter)0
Participant Group 2 (Non-methylated MGMT Promoter)1

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Overall Participant Response

Number of participants with response according to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 criteria. Complete Response (CR): Disappearance all target lesions; Any pathological lymph nodes must be <10mm in short axis. Partial Response (PR): >30% decrease in sum of diameters of target lesions, reference baseline sum of diameters (e.g. percent change from baseline). Stable Disease (SD): Neither sufficient shrinkage for PR nor sufficient increase for progressive disease. Progressive Disease (PD): >20% increase in sum of diameters of target lesions, reference smallest sum of diameters recorded since treatment started (e.g. percent change from nadir, where nadir defined as smallest sum of diameters recorded since treatment start). In addition, sum must have an absolute increase from nadir of 5mm. Not Applicable (NA): No target lesions at baseline. Not Evaluable (NE): Cannot be classified by 1 of 5 preceding definitions. (NCT01590082)
Timeframe: 2 cycles, up to 7 weeks

InterventionParticipants (Count of Participants)
Complete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive Disease (PD)Not Evaluable (NE)
Phase I: Doxycycline, Ipilimumab, and Temozolomide00361

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Maximum Tolerated Dose (MTD) When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma

The MTD was the highest dose level tested at which fewer than two of six patients had first course DLT. Hematologic DLT was defined as grade 4 neutropenia for more than 7 days, need for platelet transfusion for a platelet count of less than 20,000/mL twice within a 7-day period, or greater than 14-day delay in the start of a subsequent course because of neutropenia or thrombocytopenia. Nonhematologic DLT was defined as any nonhematologic toxicity that delayed the start of a subsequent cycle by more than 14 days or any grade ≥3 toxicity with the exception of the following grade 3 toxicities: nausea, vomiting, anorexia, or dehydration resolving to grade ≤ 2 within 72 hours; increase in hepatic transaminase or electrolyte abnormality resolving to grade ≤ 1 within 7 days; diarrhea persisting for less than 72 hours; fever; infection; or febrile neutropenia. DLT definitions included only toxicities deemed at least possibly related to therapy. (NCT01601535)
Timeframe: 21 days, from study day 1

Interventionmg/m^2 (Number)
Phase I60

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One Year Progression Free Survival Rate

To determine the progression free survival rates for patients with relapsed or refractory neuroblastoma treated with MLN8237, irinotecan, and temozolomide at the identified MTD (NCT01601535)
Timeframe: 1 Years after completion of study

InterventionParticipants (Count of Participants)
Ph 24

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Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Alisertib AUC

Outcomes included Alisertib, irinotecan, APC, SN-38, and SN-38G. APC, SN-38, and SN-38G are metabolites of irinotecan. (NCT01601535)
Timeframe: 1st week of cycle 1

InterventionµM•hour (Median)
DL 128.15
DL 1B21
DL 2B30.71
DL 3B47.73
Oral Solution58.15

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Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Irinotecan Clearance

Outcomes included Alisertib, irinotecan, APC, SN-38, and SN-38G. APC, SN-38, and SN-38G are metabolites of irinotecan. (NCT01601535)
Timeframe: 1st week of cycle 1

InterventionL/h (Median)
DL 114.0
DL 1B15.7
DL 2B10.4
DL 3B16.0
Ph 212.6
Oral Solution10.3

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AURKA Genotype

To explore whether AURKA genotype is associated with antitumor activity in children with refractory neuroblastoma treated with the combination of MLN8237, irinotecan, and temozolomide. (NCT01601535)
Timeframe: Day 7 of cycle 1

,
Interventionparticipants (Number)
AurkA Codon 31 Summary HAurkA Codon 31 Summary VAurkA Codon 31 Summary WAurkA Codon 31 Summary MissingAurkA Codon 57 Summary HAurkA Codon 57 Summary WAurkA Codon 57 Summary Missing
Objective Non-Responders912210102210
Objective Responders3054354

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Aurora A Expression

To explore whether MYCN status and markers of expression of Aurora A in archival tumor tissue are associated with the antitumor activity of the combination of MLN8237, irinotecan, and temozolomide (NCT01601535)
Timeframe: From date of study enrollment to the date of progression or withdrawal from the study, up to 34 cycles (about 2 years).

,
Interventionparticipants (Number)
MYCN AmplifiedMYCN not AmplifiedMYCN MissingMYCN Amplified or Myc PositiveMYCN Non-amplified and Myc NegativeMYCN or Myc MissingAurora A protein PositiveAurora A protein NegativeAurora A protein Missing
Objective Non-Responders14244161115101418
Objective Responders192255246

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Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Alisertib Day 4 Trough, Day 5 Trough and Cmax

Outcomes included Alisertib, irinotecan, APC, SN-38, and SN-38G. APC, SN-38, and SN-38G are metabolites of irinotecan. (NCT01601535)
Timeframe: 1st week of cycle 1

,,,,
InterventionµM (Median)
Alisertib Day 4 troughAlisertib Day 5 troughAlisertib Cmax
DL 10.480.372.56
DL 1B0.350.362.39
DL 2B0.30.23.77
DL 3B0.730.694.94
Oral Solution0.470.588.66

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Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Alisertib Tmax and Half-life

Outcomes included Alisertib, irinotecan, APC, SN-38, and SN-38G. APC, SN-38, and SN-38G are metabolites of irinotecan. (NCT01601535)
Timeframe: 1st week of cycle 1

,,,,
Interventionhour (Median)
Alisertib TmaxAlisertib Half-life
DL 12.047.20
DL 1B1.748.61
DL 2B2.56.19
DL 3B2.528.54
Oral Solution28.34

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Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Irinotecan AUC, APC AUC, SN-38 AUC, and SN-38G AUC

Outcomes included Alisertib, irinotecan, APC, SN-38, and SN-38G. APC, SN-38, and SN-38G are metabolites of irinotecan. (NCT01601535)
Timeframe: 1st week of cycle 1

,,,,,
Interventionh·ng/mL (Median)
Irinotecan AUCAPC AUCSN-38 AUCSN-38G AUC
DL 13,70257163.2206.5
DL 1B2,68047752.997.6
DL 2B3,95751180.8141.8
DL 3B2,61541872.0134.4
Oral Solution3,12161656.7136
Ph 23,53351190.0132

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Pharmacokinetics When Given Together With Fixed Doses of Irinotecan and Temozolomide in Children and Young Adults With Relapsed or Refractory Neuroblastoma: Irinotecan Cmax, APC Cmax, SN-38 Cmax, and SN-38G Cmax

Outcomes included Alisertib, irinotecan, APC, SN-38, and SN-38G. APC, SN-38, and SN-38G are metabolites of irinotecan. (NCT01601535)
Timeframe: 1st week of cycle 1

,,,,,
Interventionng/mL (Median)
Irinotecan CmaxAPC CmaxSN-38 CmaxSN-38G Cmax
DL 172261.29.518.2
DL 1B70359.812.616.9
DL 2B1,23855.812.013.8
DL 3B78443.411.713.0
Oral Solution73251.48.2615.2
Ph 288157.110.412.8

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Response Rate for Patients With Relapsed or Refractory Neuroblastoma Treated With MLN8237, Irinotecan, and Temozolomide at the Identified MTD

Response was graded according to version 1.2 of the NANT response criteria that classifies patients as having one of the following overall response categories based upon underlying response at soft tissue sites, MIBG positive sites, and bone marrow disease: complete response (CR); CR with minimal residual disease (CR-MRD); partial response (PR); minor response (MR); stable disease (SD); and progressive disease (PD). These criteria utilize RECIST criteria for measurable tumors, Curie score for MIBG scan response, and bone marrow (BM) morphology. BM response was graded as CR (required two time points to confirm), CR unconfirmed (one time point only), CR-MRD (bone marrow involvement < 5% at study entry with negative follow-up biopsies), SD, or PD. Patients with at least SD or better underwent central review of MIBG scans, CT scans, and bone marrow pathology slides. Overall responses of CR, CR-MRD, or PR were considered objective responses. (NCT01601535)
Timeframe: Cycles repeated every 21 days for up to 34 cycles.

InterventionParticipants (Count of Participants)
Complete Response (CR)CR-Minimal Residual Disease (MRD)Partial Response (PR)Minor ResponseStable DiseaseProgressive DiseaseResponse Rate (CR + CR-MRD + PR)
Ph 20042854

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UGT1A1 Genotype

To explore whether UGT1A1 genotype is associated with toxicity in children with refractory neuroblastoma treated with the combination of MLN8237, irinotecan, and temozolomide (NCT01601535)
Timeframe: Day 7 of cycle 1

,,,
Interventionparticipants (Number)
UGT1A1 66UGT1A1 67UGT1A1 77UGT1A1 Missing
DLT in Any Cycle No91116
DLT in Any Cycle Yes8649
First Cycle DLT No1514212
First Cycle DLT Yes2333

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Number of Participants With Adverse Events

Tabulated According to the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.0. Summary level. (NCT01638546)
Timeframe: From the start of treatment until 30 days from coming off treatment

InterventionParticipants (Count of Participants)
Arm I (Veliparib and Temozolomide)52
Arm II (Placebo and Temozolomide)45

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Overall Response (ORR) by RECIST 1.1 Criteria

Corresponding exact two-sided 95% confidence intervals will be calculated and reported in both arms of the study. Comparisons between treatment arms will be performed using Fisher-exact test. (NCT01638546)
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 4 months

Interventionparticipants (Number)
Arm I (Veliparib and Temozolomide)20
Arm II (Placebo and Temozolomide)6

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Overall Survival

Estimated in each treatment group using Kaplan-Meier method. Group comparisons will be performed using log-rank test. (NCT01638546)
Timeframe: From randomization to time of death

Interventionmonths (Median)
Arm I (Veliparib and Temozolomide)8.2
Arm II (Placebo and Temozolomide)7

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Progression-free Survival, Calculated as the Proportion of Patients Alive and Without Evidence of Disease

Compared across the two arms using a Fisher exact test. (NCT01638546)
Timeframe: From randomization to time of progression or death, whichever occurs first, assessed at 4 months

Interventionparticipants (Number)
Arm I (Veliparib and Temozolomide)18
Arm II (Placebo and Temozolomide)11

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Best Overall Response (BOR) - Initial Treatment Period

BOR was assessed by independent radiology review using RECIST 1.1 and was recorded from randomization until the last imaging assessment in this period. Response categories included: Complete Response (CR): disappearance of all target lesions; Partial Response (PR): at least a 30% decrease in the sum of diameters of target lesions; Progressive Disease (PD): at least a 20% increase in the sum of diameters of target lesions; and Stable Disease (SD): neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. BOR for the Initial Treatment Period was based on IRO. BOR for participants during the Initial Treatment Period is presented. (NCT01704287)
Timeframe: Up to approximately 36 months (Through Final Analysis database cutoff date of 16-Nov-2015)

,,
InterventionPercentage of Participants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressive DiseaseNot EvaluableNo DiseaseNo Assessment
Investigator-Choice Chemotherapy (ICC)0.04.519.061.515.10.00.0
Pembrolizumab 10 mg/kg7.220.414.947.59.90.00.0
Pembrolizumab 2 mg/kg3.318.916.746.713.30.60.6

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Progression-free Survival (PFS) - Initial Treatment Period

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 Response Criteria in Solid Tumors version 1.1 (RECIST 1.1), 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. In addition to the relative increase of 20%, the sum must have also demonstrated an absolute increase of at least 5 mm. Note: The appearance of one or more new lesions was also considered PD. Analysis of PFS was based on an integrated radiology and oncology (IRO) assessment and was not planned or conducted for the switch-to-pembrolizumab treatment groups. Median PFS based on the product limit (Kaplan-Meier) method for censored data is presented. This was the final analysis for PFS. (NCT01704287)
Timeframe: Up to approximately 36 months (Through Final Analysis database cutoff date of 16-Nov-2015)

InterventionMonths (Median)
Pembrolizumab 2 mg/kg2.9
Pembrolizumab 10 mg/kg3.0
Investigator-Choice Chemotherapy (ICC)2.8

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Overall Response Rate (ORR) - Initial Treatment Period

ORR was defined as the percentage of participants who had a 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) as assessed using RECIST 1.1. Analysis of ORR was not planned or conducted for the switch-to-pembrolizumab treatment groups. The percentage of participants who experienced a CR or PR is presented. This was the final analysis for ORR. (NCT01704287)
Timeframe: Up to approximately 36 months (Through Final Analysis database cutoff date of 16-Nov-2015)

InterventionPercentage of Participants (Number)
Pembrolizumab 2 mg/kg22.2
Pembrolizumab 10 mg/kg27.6
Investigator-Choice Chemotherapy (ICC)4.5

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Number of Participants Who Experienced an Adverse Event (AE) - Overall Study

An AE was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of study drug, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a pre-existing condition which was temporally associated with the use of study drug, was also an AE. Participants were included in the treatment group in which an AE was experienced. The number of participants who experienced at least one AE is presented. (NCT01704287)
Timeframe: Up to approximately 75 months (Through End of Trial Analysis database cutoff date of 31-Jan-2019)

InterventionParticipants (Count of Participants)
Pembrolizumab 2 mg/kg172
Pembrolizumab 10 mg/kg179
ICC Only71
ICC→Pembrolizumab 2 mg/kg52
ICC→Pembrolizumab 10 mg/kg45
ICC→Pembrolizumab 2 mg/kg (After Switch to Pembrolizumab)53
ICC→Pembrolizumab 10 mg/kg (After Switch to Pembrolizumab)41

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Number of Participants Who Discontinued Study Drug Due to an Adverse Event (AE) - Overall Study

An AE was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the study drug, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a pre-existing condition which is temporally associated with the use of study drug, was also an AE. The number of participants who discontinued study drug due to an AE is presented. (NCT01704287)
Timeframe: Up to approximately 75 months (Through End of Trial Analysis database cutoff date of 31-Jan-2019)

InterventionParticipants (Count of Participants)
Pembrolizumab 2 mg/kg29
Pembrolizumab 10 mg/kg33
ICC Only13
ICC→Pembrolizumab 2 mg/kg1
ICC→Pembrolizumab 10 mg/kg1
ICC→Pembrolizumab 2 mg/kg (After Switch to Pembrolizumab)4
ICC→Pembrolizumab 10 mg/kg (After Switch to Pembrolizumab)4

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Interim Overall Survival (OS) - Initial Treatment Period

OS was defined as the time from randomization to death due to any cause. Analysis of OS was not planned or conducted for the switch-to-pembrolizumab treatment groups. Median OS based on the product-limit (Kaplan-Meier) method for censored data is presented. This was the interim analysis for OS. (NCT01704287)
Timeframe: Up to approximately 36 months (Through Final Analysis database cutoff date of 16-Nov-2015)

InterventionMonths (Median)
Pembrolizumab 2 mg/kg13.4
Pembrolizumab 10 mg/kg14.7
Investigator-Choice Chemotherapy (ICC)11.0

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Final Overall Survival (OS) - Initial Treatment Period

OS was defined as the time from randomization to death due to any cause. Analysis of OS was not planned or conducted for the switch-to-pembrolizumab treatment groups. Median OS duration based on the product-limit (Kaplan-Meier) method for censored data is presented. This was the final analysis for OS. (NCT01704287)
Timeframe: Up to approximately 75 months (Through End of Trial Analysis database cutoff date of 31-Jan-2019)

InterventionMonths (Median)
Pembrolizumab 2 mg/kg13.4
Pembrolizumab 10 mg/kg14.7
Investigator-Choice Chemotherapy (ICC)11.0

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Duration of Response (DOR) - Initial Treatment Period

For participants who demonstrated a confirmed response (Complete Response [CR]: disappearance of all target lesions or Partial Response [PR]: ≥30% decrease in the sum of diameters of target lesions) per RECIST 1.1, DOR was defined as the time from first documented evidence of CR or PR until disease progression 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. DOR analysis was based on IRO assessment. Analysis of DOR was not planned or analyzed for the switch-to-pembrolizumab treatment groups. Median DOR for participants who demonstrated a confirmed response is presented. (NCT01704287)
Timeframe: Up to approximately 36 months (Through Final Analysis database cutoff date of 16-Nov-2015)

InterventionMonths (Median)
Pembrolizumab 2 mg/kg22.8
Pembrolizumab 10 mg/kgNA
Investigator-Choice Chemotherapy (ICC)6.8

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Best Overall Response (BOR) - Switch-to-Pembrolizumab Treatment Period

The BOR was assessed using RECIST 1.1 and was recorded from the start of the second line of study drug (pembrolizumab) until the last imaging assessment in this period. Response categories included: Complete Response (CR): disappearance of all target lesions; Partial Response (PR): at least a 30% decrease in the sum of diameters of target lesions; Progressive Disease (PD): at least a 20% increase in the sum of diameters of target lesions; and Stable Disease (SD): neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. For the switch-to-pembrolizumab treatment groups, BOR was based on independent review committee (IRC) assessment. The BOR for switched-to pembrolizumab treatment groups is presented. (NCT01704287)
Timeframe: Up to approximately 36 months (Through Final Analysis database cutoff date of 16-Nov-2015)

,
InterventionPercentage of Participants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressive DiseaseNot EvaluableNo Assessment
ICC→Pembrolizumab 10 mg/kg4.413.311.155.613.32.2
ICC→Pembrolizumab 2 mg/kg1.917.015.154.711.30.0

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Final Overall Survival (OS) By Programmed Cell Death-Ligand 1 (PD-L1) Tumor Expression Status - Initial Treatment Period

OS was defined as the time from randomization to death due to any cause. Participants with an Allred Proportion Score (APS) ≥2 (membranous staining in ≥1% of cells for PD-L1) were considered to be PD-L1 Positive and participants with an APS of 0 or 1 were considered to be PD-L1 Negative. Analysis of OS was not planned or conducted for the switch-to-pembrolizumab treatment groups. Median OS duration based on the product-limit (Kaplan-Meier) method for censored data by PD-L1 tumor expression status is presented. (NCT01704287)
Timeframe: Up to approximately 75 months (Through End of Trial Analysis database cutoff date of 31-Jan-2019)

,,
InterventionMonths (Median)
PD-L1 PositivePD-L1 Negative
Investigator-Choice Chemotherapy (ICC)12.19.3
Pembrolizumab 10 mg/kg17.513.4
Pembrolizumab 2 mg/kg15.010.5

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Progression-free Survival (PFS)

To assess the effect on progression-free survival of continuing bevacizumab treatment after disease progression in patients treated with bevacizumab from the time of initiation of treatment to the first occurrence of progression, or death (NCT01740258)
Timeframe: 5 Years

Interventionmonths (Median)
Bevaczimab, Radiation Therapy, Temozolomide9.9

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Overall Survival

To assess the effect on overall survival of continuing bevacizumab treatment after disease progression in patients treated with bevacizumab from the time of first diagnosis of grade IV malignant glioma. (NCT01740258)
Timeframe: 5 Years

Interventionmonths (Median)
Bevaczimab, Radiation Therapy, Temozolomide17.8

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Toxicity: Percentage of Subjects With Unacceptable Toxicities

"The occurrence of ≥ grade 2 CNS (central nervous system) hemorrhage or grade 4 or 5 non-hematologic toxicity is defined as being unacceptable. Unacceptable toxicity rates of 5% or less are considered desirable, while rates of 20% or greater are considered as undesirable." (NCT01740258)
Timeframe: 5 Years

Interventionpercentage of participants (Number)
Bevaczimab, Radiation Therapy, Temozolomide11.8

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Percentage of Randomized Patients Who Are Responders

The percentage of patients who are responders will be tabulated, including a 95% confidence interval on the response rate. Responders are defined as patients who achieve a best overall response of complete response (CR), very good partial response (VGPR), or partial response (PR) per the International Neuroblastoma Response Criteria (INRC). Per INRC: CR= Disappearance of all target lesions. No evidence of tumor at any site; VGPR= >90% decrease of the disease measurement for CT/MRI target lesions. All pre-existing bone lesions with CR by MIBG; MIBG scan can be stable disease (SD) or CR in soft tissue lesions corresponding to lesions on CT/MRI. CR in bone marrow. No new sites of tumor; PR= >=30% decrease in the disease measurement for CT/MRI target lesions. Bone marrow with CR. MIBG with either PR/CR in bone lesions; MIBG may be SD or CR in soft tissue lesions corresponding to lesions on CT/MRI. Homovanillic acid (HVA)/Vanillylmandelic acid (VMA) may still be elevated. (NCT01767194)
Timeframe: Up to the first 6 cycles of treatment

InterventionPercentage of patients (Number)
Arm I (Temozolomide, Irinotecan Hydrochloride, Temsirolimus)5.6
Arm II (Temozolomide, Irinotecan Hydrochloride, Dinutuximab)52.9

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Percentage of Patients in the Dinutuximab Arm Who Are Responders

Percentage of patients who are responders to therapy with dinutuximab will be tabulated, including a 95% confidence interval on the response rate. Responders are defined as patients who achieve a best overall response of complete response (CR), very good partial response (VGPR), or partial response (PR) per the International Neuroblastoma Response Criteria (INRC). Per INRC: CR= Disappearance of all target lesions. No evidence of tumor at any site; VGPR= >90% decrease of disease measurement for CT/MRI target lesions. All pre-existing bone lesions with CR by MIBG; MIBG scan can be stable disease (SD) or CR in soft tissue lesions corresponding to lesions on CT/MRI. CR in bone marrow. No new sites of tumor; PR= ≥30% decrease in disease measurement for CT/MRI target lesions. Bone marrow with CR. MIBG with either PR/CR in bone lesions; MIBG may be SD or CR in soft tissue lesions corresponding to lesions on CT/MRI. Homovanillic acid (HVA)/ Vanillylmandelic acid (VMA) may still be elevated. (NCT01767194)
Timeframe: Up to the first 6 cycles of treatment

InterventionPercentage of patients (Number)
Arm II (Temozolomide, Irinotecan Hydrochloride, Dinutuximab)41.2

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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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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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Summary of the Median Progression-free Survival (mPFS) in the Study Group Compared With Historical Control From Medical Literature

mPFS was based on model parameters estimated by maximum likelihood with a Newton-Raphson algorithm. The Radiation Therapy Oncology Group (RTOG) 0525 study was the main historical control used for statistical analysis. Additionally, RTOG-0825 was also used to support this outcome measure. (NCT01790503)
Timeframe: Assessed from date of first dose administered to date of first documented progression or date of death from any cause, whichever came first, assessed up to 4 years 4 months.

Interventionmonths (Median)
RP2D7.7
RP2D-0525 (Cycle 1, Day 1)7.6
RP2D-08257.0
RP2D-0525 (Rest Period, Day 15)6.1

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Number of Patients With Clinically Significant Abnormal Chemistry and Hematology Values Reported as Adverse Events by Preferred Term in Phase 1b of the Modified Intent-To-Treat Population

(NCT01790503)
Timeframe: Baseline up to 30 days after last dose, up to 4 years 4 months

,,,,,,,,
InterventionParticipants (Count of Participants)
ThrombocytopeniaNeutropeniaAnaemiaLymphopeniaAST increasedPlatelet count decreasedNeutrophil count decreasedLeukopeniaFebrile neutropeniaALT increasedBone marrow failureHaemolysisWhite blood cell decreasedLymphocyte count decreased
Phase 1b Dose Escalation - 600 mg00000000000100
Phase 1b Dose Escalation - 600 mg/1000 mg00001001010000
Phase 1b Dose Escalation - 600 mg/600 mg10110010000000
Phase 1b Dose Escalation - 600 mg/800 mg11010001000000
Phase 1b Dose Escalation - 800 mg (5 Days)11000100000001
Phase 1b Dose Escalation - 800 mg/1000 mg11112100110000
Phase 1b Dose Escalation - 800 mg/600 mg00000000000000
Phase 1b Dose Escalation - 800 mg/800 mg10000000000000
Phase 1b Dose Escation - 800 mg (No Adjuvant Therapy)11100120101010

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Overview of Most Frequent System Organ Classes Reported in Phase 2 of the Modified Intent-To-Treat Population

(NCT01790503)
Timeframe: Baseline up to 30 days after last dose, up to 4 years 4 months

,,,
InterventionParticipants (Count of Participants)
General Disorders and Administration SiteSkin and Subcutaneous Tissue DisordersNervous System DisordersGastrointestinal DisordersMetabolism and Nutrition DisordersPsychiatric DisordersInvestigationsMusculoskeletal and Connective Tissue DisordersBlood and Lymphatic System DisordersInjury, Poisoning, and Procedural ComplicationsEye DisordersVascular DisordersRespiratory, Thoracic, and Mediastinal DisordersRenal and Urinary DisordersCardiac DisordersEndocrine DisordersEar and Labyrinth DisordersReproductive System and Breast DisordersNeoplasms Benign, Malignant, and UnspecifiedHepatobiliary DisordersImmune System Disorders
Combined 800 mg, 5 Days/Week47454341302727251818161816138753211
Phase 2 - 800 mg1312121286972664322110010
Phase 2 - 800 mg/800 mg2424222116171213141079775532201
Phase 2 Total3736343324232120161613131097642211

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Overview of Most Frequent System Organ Classes Reported in Phase 1b of the Modified Intent-To-Treat Population

(NCT01790503)
Timeframe: Baseline up to 30 days after last dose, up to 4 years 4 months

,,,,,,,,
InterventionParticipants (Count of Participants)
General Disorders and Administrative SiteNervous System DisordersSkin and Subcutaneous Tissue DisordersGastrointestinal DisordersMetabolism and Nutrition DisordersPsychiatric DisordersInfections and InfestationsInvestigationsRespiratory, Thoracic, and Mediastinal DisordersMusculoskeletal and Connective Tissue DisordersBlood and Lymphatic Tissue DisordersVascular DisordersRenal and Urinary DisordersEye DisordersInjury, Poisoning, and Procedural ComplicationsEar and LabyrinthEndocrine DisordersCardiac DisordersHepatobiliary DisordersReproductive System and Breast DisordersImmune System DisordersNeoplasms Benign, Malignant, and Unspecified
Phase 1b Dose Escalation - 600 mg1221121101111011000000
Phase 1b Dose Escalation - 600 mg/1000 mg1111111110100000000000
Phase 1b Dose Escalation - 600 mg/600 mg2333321110101110000000
Phase 1b Dose Escalation - 600 mg/800 mg0111110000100000000000
Phase 1b Dose Escalation - 800 mg5443211233121100010000
Phase 1b Dose Escalation - 800 mg/1000 mg5555435432133221100100
Phase 1b Dose Escalation - 800 mg/600 mg1100010101000000000000
Phase 1b Dose Escalation - 800 mg/800 mg1010100000100000000000
Phase 1b Dose Escation - 800 mg3212213321121101101000

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Summary of the Median Progression-free Survival (mPFS) in the Combined 800 mg, 5 Days/Week Dose Group

Progression was determined by Response Assessment in Neuro-Oncology (RANO) criteria and progression-free survival (PFS) was analyzed based on the non-parametric Kaplan-Meier method. (NCT01790503)
Timeframe: Assessed from date of first dose administered to date of first documented progression or date of death from any cause, whichever came first, assessed up to 4 years 4 months.

Interventionmonths (Median)
mITT RP2DPP RP2D
Combined 800 mg, 5 Days/Week6.76.9

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Number of Patients With Clinically Significant Abnormal Chemistry and Hematology Values Reported as Adverse Events by Preferred Term in Phase 2, the Combined RP2D Groups in Phase 1b, and in the Study Overall Modified Intent-To-Treat Population

(NCT01790503)
Timeframe: Baseline up to 30 days after last dose, up to 4 years 4 months

,,,
InterventionParticipants (Count of Participants)
NeutropeniaThrombocytopeniaAnaemiaALT increasedAST increasedPlatelet count decreasedLymphopeniaWhite blood cell count decreasedNeutrophil count decreasedLeukopeniaFebrile neutropeniaLymphocyte count decreasedBlood alkaline phosphatase increasedBlood creatinine increasedDRESSLiver function test abnormalBone marrow failureHaemolysisBlood bilirubin increasedBlood iron decreased
Combined 800 mg, 5 Days/Week96788745222333110111
Phase 2 - 800 mg11154111011131110010
Phase 2 - 800 mg/800 mg63522424210102000001
Phase 2 Total74676535221233110011

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Summary of the Overall Survival in the Study Group Compared With Historical Control From Medical Literature

Overall Survival was calculated using a parametric model. The Radiation Therapy Oncology Group (RTOG) 0525 study was the main historical control used for statistical analysis. Additionally, RTOG-0825 was also used to support this outcome measure (NCT01790503)
Timeframe: Assessed from date of first dose administered to the date of death from any cause, assessed up to 4 years 4 months.

Interventionmonths (Median)
RP2D18.8
RP2D-0525 (Cycle 1, Day 1)20.2
RP2D-082517.0
RP2D-0525 (Rest Period, Day 15)16.9

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Summary of the Overall Survival in The Study Population

Overall Survival (OS) was defined as the number of days from the first day of treatment (C1D1) to the date of death and analyzed using a non-parametric Kaplan Meier method. (NCT01790503)
Timeframe: Assessed from date of first dose administered to date of death from any cause, assessed up to 4 years 4 months

Interventionmonths (Median)
mITT RP2DPP RP2D
Combined 800 mg, 5 Days/Week13.112.4

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Ability to Calculate the Efficacy of Low-dose Whole Brain RT (WBRT) in Patients With GBM

"Median survival (in months from time of diagnosis to date of death) was calculated and reported below.~It is very difficult to draw efficacy outcomes for outcome measure #1 and #2 because of incomplete enrollment." (NCT01822275)
Timeframe: 5 years

Interventionmonths (Median)
Low Dose WBRT10

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Radiographic (CT-MRI) Response Assessment and Treatment Failure Patterns of Patients With GBM

"To determine the radiographic response and treatment failure patterns with the combination therapy. This would be measured through imaging that was collected from baseline to follow-up. If unable to meet statistical requirements, response assessment and treatment patterns will be unable to be determined.~It is very difficult to draw efficacy outcomes for outcome measure #1 and #2 because of incomplete enrollment." (NCT01822275)
Timeframe: 5 years

Interventionparticipants (Number)
Low Dose WBRT4

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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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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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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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Number of Participants With an Objective Response

ORR is the proportion of participants with a complete response (CR) or partial response (PR) per the Response Evaluation Criteria in Solid Tumors (RECIST). Complete Response is disappearance of all tumors. Partial Response is at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum of diameters. (NCT01827384)
Timeframe: Up to 30 days after completion of study treatment, up to 75 months

,,,,,,,,,,,,
InterventionParticipants (Count of Participants)
Complete ResponsePartial Response
TAC1 -> TAC400
TAC200
TAC2 -> TAC100
TAC2 -> TAC300
TAC301
TAC3 -> TAC100
TAC3 -> TAC1 -> TAC400
TAC3 -> TAC400
TAC400
TAC4 -> TAC100
TAC4 -> TAC200
TAC4 -> TAC300
Treatment Assignment Code 1 (TAC1)00

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Proportion of Participants With 4 Month Progression-free Survival (PFS)

Time from random assignment to progression or death from any cause (whichever comes first). Progression was measured by the Response Evaluation Criteria in Solid Tumors (RECIST). Progression is at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. And the appearance of one or more new lesions is also considered progressions. (NCT01827384)
Timeframe: 4 months

Interventionproportion of participants (Number)
Treatment Assignment Code 1 (TAC1)0.23
TAC1 -> TAC40.00
TAC20.22
TAC2 -> TAC10.00
TAC2 -> TAC31.00
TAC30.41
TAC3 -> TAC10.50
TAC3 -> TAC1 -> TAC40.00
TAC3 -> TAC40.00
TAC40.13
TAC4 -> TAC10.29
TAC4 -> TAC20.00
TAC4 -> TAC30.00

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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. (NCT01827384)
Timeframe: Date treatment consent signed to date off study, approx. 73months (m) & 21day (d); 4m & 11d; 61m & 8d; 4m & 11d; 10m & 11d; 72m & 29d; 13m & 11d; 6m & 13d; 29m & 18d; 48m & 25d; 49m & 5d; 4m &7d; 15m & 5d; and 75m &13d, for each group respectively.

InterventionParticipants (Count of Participants)
Treatment Assignment Code 1 (TAC1)13
TAC1 -> TAC41
TAC29
TAC2 -> TAC11
TAC2 -> TAC31
TAC322
TAC3 -> TAC12
TAC3 -> TAC1 -> TAC41
TAC3 -> TAC42
TAC415
TAC4 -> TAC17
TAC4 -> TAC21
TAC4 -> TAC32
Participants Enrolled But Not Treated2

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Proportion of Patients Without a Progression Free Survival Event at 4 Months (PFS4)

A patient will be declared a PFS4 success if they are on study and progression free for at least 4 months. Progression 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, with an absolute increase of at least 5 mm. The appearance of one or more new lesions is also considered progression. The success for each arm will be calculated independently as the number of successes divided by the total number of evaluable patients. A one-sided chi-squared test for a difference in PFS4 proportions will be used to test for a difference between arms. (NCT01835145)
Timeframe: At 4 months

Interventionproportion of participants (Number)
Arm I (Cabozantinib-s-malate).323
Arm II (Temozolomide or Dacarbazine).267

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Percentage of Patients Who Experienced Grade 3+ Adverse Events Regardless of Attribution

percentage of patients who experienced grade 3+ adverse events regardless of attribution, graded according to the National Cancer Institute CTCAE version 4.0 (NCT01835145)
Timeframe: Up to 2 years

Interventionpercentage of patients (Number)
Arm I (Cabozantinib-s-malate)51.6
Arm II (Temozolomide or Dacarbazine)20

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Overall Survival (OS)

The distribution of OS time will be estimated using the method of Kaplan Meier. (NCT01835145)
Timeframe: Number of days from registration until death, assessed up to 2 years

Interventionmonths (Median)
Arm I (Cabozantinib-s-malate)6.3
Arm II (Temozolomide or Dacarbazine)7.2

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Confirmed Response Rate as Determined by the RECIST Criteria (Version 1.1)

The confirmed response rates will be estimated by dividing the number of confirmed responders by the number of evaluable patients. 95% confidence intervals will be calculated. (NCT01835145)
Timeframe: Up to 2 years

InterventionParticipants (Count of Participants)
Arm I (Cabozantinib-s-malate)0
Arm II (Temozolomide or Dacarbazine)0

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PFS

The distribution of PFS time will be estimated using the method of Kaplan Meier and is defined as the number of days from registration until disease progression (or death). Progression 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, with an absolute increase of at least 5 mm. The appearance of one or more new lesions is also considered progression. (NCT01835145)
Timeframe: Number of days from registration until disease progression (or death), assessed up to 2 years

Interventionmonths (Median)
Arm I (Cabozantinib-s-malate)2.0
Arm II (Temozolomide or Dacarbazine)1.9

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Response to Window Therapy (2 Courses) for Group B (High-risk) - ESFT Participants

Response rate will be defined as the proportion of patients who achieved complete response or partial response (CR+PR) using the World Health Organization (WHO) criteria evaluated after two initial courses of temsirolimus, temozolomide and irinotecan in previously untreated patients with high risk Ewing Sarcoma Family of Tumor (ESFT). Participants who are treated in Group B with Desmoplastic Small Round Cell Tumor (DSRCT) or those who do not receive window therapy will not be included in this analysis. (NCT01946529)
Timeframe: at 6 weeks after start of therapy (after 2 initial courses)

Interventionparticipants (Number)
Partial Response (PR)Stable disease (no response) (NR)Progressive Disease (PD)
Group B (High Risk) - ESFT381

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Participants Alive and Without Disease Progression At 6 Months After the Start of the Irradiation

Progression free survival based on the Response Assessment for Neuro-Oncology (RANO) criteria, using both clinical examinations and MRIs with and without contrast summarized with Kaplan Meier estimates. (NCT01977677)
Timeframe: 6 months from start of irradiation

InterventionParticipants (Count of Participants)
Escalation: Plerixafor 200 mcg/kg/Day3
Escalation: Plerixafor 400 mcg/kg/Day5
Expansion: Plerixafor 400 mcg/kg/Day19

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Dose-limiting Toxicity

Dose Limiting Toxicity is defined as defined as any hematologic or on-hematologic adverse events grade 3 or higher using the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.0 with a suspected causal relationship to Plerixafor (including electrocardiogram changes indicative of ischemia, ventricular tachycardia) (NCT01977677)
Timeframe: Up to 30 days post plerixafor

InterventionParticipants (Count of Participants)
Escalation: Plerixafor 200 mcg/kg/Day0
Escalation: Plerixafor 400 mcg/kg/Day0
Expansion: Plerixafor 400 mcg/kg/Day0

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Proportion of Grade IV MGMT Un-methylated Patients That Experience Confirmed-progression-free Survival at 6 Months (CPFS6)

"The proportion of Grade IV MGMT un-methylated patients that experience confirmed-progression-free survival at 6 months (CPFS6). Progression is defined by any of the following:~≥25% increase in the sum of products of perpendicular diameters of enhancing lesions compared to the smallest tumor measurement obtained either at baseline or best response, on stable or increasing doses of corticosteroids~Significant increase in T2/FLAIR non-enhancing lesion on stable or increasing doses of corticosteroids compared to baseline scan or best response following initiation of therapy, not due to co-morbid events~Any new lesion~Clear clinical deterioration not attributable to other causes apart from the tumor or changes in corticosteroid dose.~Failure to return for evaluation due to death or deteriorating condition~Clear progression of non-measurable disease" (NCT01991977)
Timeframe: Time from registration to the confirmed disease progression, assessed at 6 months

Interventionproportion of participants (Number)
Diagnostic (PET, pMRI, DTI, IMRT, Temozolomide)0.795

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Progression-Free Survival Rate (PFS) (Arm 3)

Participants will be analyzed based on intention to treat using the Response Assessment in Neuro-Oncology (RANO) criteria for progression. Based on RANO criteria, a responder is defined using both radiographic and clinical criteria. Complete response (CR) or Partial Response (PR) will be first assessed by radiographic changes as determined by an improvement of the bi-dimensional evaluation of the tumor size. In addition, changes in neurologic function and steroid use will be considered. Analyses will be performed after all participants enrolled in arm 3 have completed 38 months on study, or whenever the progression status of all participants has been established, whichever comes first. Kaplan-Meier estimates and the associated 95% CIs will be calculated for the 38-month PFS. (NCT02023905)
Timeframe: Up to 38 Months

Interventionpercentage of participants (Number)
Arm 3: Everolimus (1p/19q Co-deletion Present)55.5

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Progression-Free Survival Rate (PFS) (Arms 1 and 2)

Participants will be analyzed based on intention to treat using the Response Assessment in Neuro-Oncology (RANO) criteria for progression. Based on RANO criteria, a responder is defined using both radiographic and clinical criteria. Complete response (CR) or Partial Response (PR) will be first assessed by radiographic changes as determined by an improvement of the bi-dimensional evaluation of the tumor size. In addition, changes in neurologic function and steroid use will be considered. Analyses will be performed after all enrolled participants in arm 1 or arm 2 have completed 33 months on study, or whenever the progression status of all participants has been established, whichever comes first. Kaplan-Meier estimates and the associated 95% confidence intervals (CI) will be calculated for the 33-month PFS separately for the two arms. (NCT02023905)
Timeframe: Up to 33 Months

Interventionpercentage of participants (Number)
Arm 1: Everolimus31
Arm 2: Everolimus and TemozolomideNA

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Rate of Reduction in Seizures

To assess the reduction in seizure rate the investigator will compare the seizure rate on study to that experienced one month prior to enrolling in the study. The RANO low grade gliomas (LGG) guideline will be used to assess reduction of seizures, which calls a 50% or more reduction number of monthly seizures an 'improvement'; a 50% or more increase a worsening'; and anything less than 50% in either direction a 'stable seizure rate'. (NCT02023905)
Timeframe: Up to 36 Months

Interventionpercentage of participants (Number)
Arm 1: Everolimus25
Arm 2: Everolimus and TemozolomideNA
Arm 3: Everolimus (1p/19q Co-deletion Present)50

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Median Progression Free Survival (PFS)

Participants will be analyzed based on an intention to treat model. PFS is defined as the time from first objective response to the time of disease progression or death using the Response Assessment in Neuro-Oncology (RANO) criteria to determine progression. If the participant does not have an event of disease progression or recurrence nor has the patient died, the participant's data will be censored at the date of last contact with the patient. Kaplan-Meier estimates and the associated 95% CIs will be calculated. (NCT02023905)
Timeframe: Up to 84 Months

Interventionmonths (Median)
Arm 1: Everolimus25.8
Arm 2: Everolimus and TemozolomideNA
Arm 3: Everolimus (1p/19q Co-deletion Present)43.6

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Objective Response Rate (ORR)

Overall response rate (ORR) is the percentage of patients who achieved a best response of complete response (CR) or partial response (PR) out of all assigned patients. Based on the best objective status as assessed by the Response Assessment in Neuro-Oncology (RANO) criteria. Using RANO criteria, a responder is defined by radiographic and clinical criteria. Complete response or PR will be first assessed by radiographic changes as determined by an improvement of the bi-dimensional evaluation of the tumor size. In addition, changes in neurologic function and steroid use will be considered. The point estimate and the associated 2-sided 95% CI for the response rate separately for the three arms. (NCT02023905)
Timeframe: Up to 36 Months

Interventionpercentage of participants (Number)
Arm 1: Everolimus0
Arm 2: Everolimus and TemozolomideNA
Arm 3: Everolimus (1p/19q Co-deletion Present)11

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Overall Survival Rate (OS)

Participants will be analyzed based on an intention to treat model. Overall survival is defined as the first day of treatment until death or study completion, whichever comes first. Kaplan-Meier estimates and the associated 95% CIs will be calculated by treatment arm. (NCT02023905)
Timeframe: Up to 84 Months

Interventionpercentage of participants (Number)
Arm 1: EverolimusNA
Arm 2: Everolimus and TemozolomideNA
Arm 3: Everolimus (1p/19q Co-deletion Present)NA

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Number of Participants With Adverse Events as a Measure of Safety and Tolerability

The short-and long-term toxicity of ScRT (and compare to historical controls). (NCT02039778)
Timeframe: 36 months

InterventionParticipants (Count of Participants)
Stem Cell Radiotherapy and Temozolomide4

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Overall Survival

The overall survival of patients with newly diagnosed high-grade glioma (HGG) treated with concurrent ScRT and temozolomide, followed by post-radiation temozolomide (and compare to historical controls). (NCT02039778)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Stem Cell Radiotherapy and Temozolomide1

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Number of Participants With Serious and Non-serious Adverse Events as a Measure of Safety.

Patients in the safety lead-in part of the study were monitored for up to 2 treatment cycles (4 weeks) to assure there were no unexpected or prohibitive toxicities. A non-serious adverse event is any untoward medical occurrence. A serious adverse event (SAE) is an event that meets one or more of the following: results in death; is life-threatening; requires inpatient hospitalization or prolongation of existing hospitalization; results in persistent or significant disability/incapacity; is a congenital anomaly/birth defect; requires intervention to prevent permanent impairment or damage. Specific AE and SAE terms are provided in the Adverse event module. (NCT02113007)
Timeframe: up to 4 weeks

Interventionparticipants (Number)
Adverse EventsSerious Adverse Events
Rituximab Plus Temozolomide21

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C Max of Talazoparib

Median with minimum and maximum for the time at which the maximum (peak) serum concentration occurs. (NCT02116777)
Timeframe: Cycle 1 Day 1 pre-dose, and 1, 2, 4, 8 and 24 hours after the first talazoparib dose.

Interventionng/mL (Median)
Treatment (Talazoparib, Temozolomide): Phase 14670

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C Max of Talazoparib in Combination With Temozolomide

Median with minimum and maximum for the time at which the maximum (peak) serum concentration occurs. (NCT02116777)
Timeframe: Cycle 1 Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the talazoparib dose

Interventionpg/ml (Median)
Treatment (Talazoparib, Temozolomide): Phase 116450

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C Max of Temozolomide in Combination With Talazoparib

Median with minimum and maximum for the maximum (peak) serum concentration. (NCT02116777)
Timeframe: Cycle 1 Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the temozolomide dose

Interventionng/mL (Median)
Treatment (Talazoparib, Temozolomide): Phase 11234.1

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Clearance of Temozolomide in Combination With Talazoparib

Median with minimum and maximum for the rate of elimination of the drug. (NCT02116777)
Timeframe: Cycle 1 Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the temozolomide dose

InterventionL/hr/m² (Median)
Treatment (Talazoparib, Temozolomide): Phase 16.49

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Half-life of Temozolomide in Combination With Talazoparib

Median with minimum and maximum for the time required for the serum concentration to fall to 50% of its starting dose. (NCT02116777)
Timeframe: Cycle 1 Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the temozolomide dose

InterventionHours (Median)
Treatment (Talazoparib, Temozolomide): Phase 11.74

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Number of Ewing/Peripheral PNET Participants in Phase 2 With Complete Response (CR) or Partial Response (PR)

Frequency of Ewing sarcoma and peripheral PNET participants with Complete Response (CR) or Partial Response (PR) per the Response Evaluation Criteria In Solid Tumors (RECIST) (NCT02116777)
Timeframe: Up to 24 months

InterventionParticipants (Count of Participants)
Treatment (Talazoparib, Temozolomide): Phase 20

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Number of Solid Tumor Patients With Complete Response (CR) or Partial Response (PR)

Frequency of solid tumor participants with Complete Response (CR) or Partial Response (PR) per the Response Evaluation Criteria In Solid Tumors (RECIST) (NCT02116777)
Timeframe: Up to 24 months

InterventionParticipants (Count of Participants)
Treatment (Talazoparib, Temozolomide): Phase 11

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T Max of Talazoparib

Median with minimum and maximum for the time at which the maximum (peak) serum concentration occurs. (NCT02116777)
Timeframe: Cycle 1 Day 1 pre-dose, and 1, 2, 4, 8 and 24 hours after the first talazoparib dose.

InterventionHours (Median)
Treatment (Talazoparib, Temozolomide): Phase 12

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T Max of Talazoparib in Combination With Temozolomide

Median with minimum and maximum for the time at which the maximum (peak) serum concentration occurs. (NCT02116777)
Timeframe: Cycle 1 Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the talazoparib dose

InterventionHours (Median)
Treatment (Talazoparib, Temozolomide): Phase 11.04

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T Max of Temozolomide in Combination With Talazoparib

Median with minimum and maximum for the time at which the maximum (peak) serum concentration occurs. (NCT02116777)
Timeframe: Cycle 1 Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the temozolomide dose

InterventionHours (Median)
Treatment (Talazoparib, Temozolomide): Phase 11.03

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The Number of Participants With Dose Limiting Toxicities to Determine the Maximum Tolerated Dose of Temozolomide and Talazoparib Combination Therapy

The Maximum Tolerated Dose (MTD) reflects the highest dose of Talazoparib (BMN 673) when combined with a dose of temozolomide that did not cause a Grade 3 or higher toxicity in children with refractory or recurrent solid tumors. (NCT02116777)
Timeframe: 28 days

InterventionParticipants (Count of Participants)
400 mcg/m²/Dose BMN 673 QD+20mg/m²/Dose TEM,Max 800 mcg/Day0
400 mcg/m²/Dose BMN 673 BID+20mg/m²/Dose TEM,Max 800 mcg/Day0
600 mcg/m²/Dose BMN 673 BID+20mg/m²/Dose TEM,Max 1000 mcg/Day1
600 mcg/m²/Dose BMN 673 BID+30mg/m²/Dose TEM, Max 1000 mcg/Day2
600 mcg/m²/Dose BMN 673 BID+40mg/m²/Dose TEM, Max 1000 mcg/Day2
600 mcg/m²/doseBMN 673 BID+55mg/m²/Dose TEM, Max 1000 mcg/Day2
600 mcg/m²/Dose BMN 673 BID+30 mg/m²/Dose TEM,Max 1000 mcg/Day0

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Clearance of Talazoparib in Combination With Temozolomide

Median with minimum and maximum for the rate of elimination of the drug. (NCT02116777)
Timeframe: Cycle 1 Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the talazoparib dose

InterventionL/hr/m² (Median)
Treatment (Talazoparib, Temozolomide): Phase 13.08

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AUC of Talazoparib in Combination With Temozolomide

Median with minimum and maximum area under the drug concentration over time curve (NCT02116777)
Timeframe: Cycle 1 Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the talazoparib dose

Interventionh•µg/L (Median)
Treatment (Talazoparib, Temozolomide): Phase 182.08
Treatment (Talazoparib, Temozolomide): Phase 1173.08

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Accumulation Half-life of Talazoparib in Combination With Temozolomide.

Median with minimum and maximum for the time required for the serum concentration to fall to 50% of its starting dose. (NCT02116777)
Timeframe: Cycle 1 Day 1 pre-dose, and 1, 2, 4 and 8 hours after the first talazoparib dose. Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the talazoparib dose

InterventionHours (Median)
Treatment (Talazoparib, Temozolomide): Phase 146.8

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Accumulation Ratio of Talazoparib in Combination With Temozolomide

Median with minimum and maximum of the accumulation ratio. (NCT02116777)
Timeframe: Cycle 1 Day 1 pre-dose, and 1, 2, 4 and 8 hours after the first talazoparib dose. Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the talazoparib dose

InterventionRatio (Median)
Treatment (Talazoparib, Temozolomide): Phase 13.34

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All Cycle 1 Toxicities >=Grade 3

The number of patients with at least one toxicity (DLT or non-DLT) in cycle 1 that is at least possibly attributable to study agent (NCT02116777)
Timeframe: Up to 28 days

InterventionParticipants (Count of Participants)
400 mcg/m²/Dose BMN 673 QD+20mg/m²/Dose TEM,Max 800 mcg/Day0
400 mcg/m²/Dose BMN 673 BID+20mg/m²/Dose TEM,Max 800 mcg/Day0
600 mcg/m²/Dose BMN 673 BID+20mg/m²/Dose TEM,Max 1000 mcg/Day2
600 mcg/m²/Dose BMN 673 BID+30mg/m²/Dose TEM, Max 1000 mcg/Day7
600 mcg/m²/Dose BMN 673 BID+40mg/m²/Dose TEM, Max 1000 mcg/Day5
600 mcg/m²/doseBMN 673 BID+55mg/m²/Dose TEM, Max 1000 mcg/Day3
600 mcg/m²/Dose BMN 673 BID+30mg/m²/Dose TEM,Max 1000 mcg/Day5

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AUC of Talazoparib

Median with minimum and maximum for the area under the drug concentration over time curve. (NCT02116777)
Timeframe: Cycle 1 Day 1 pre-dose, and 1, 2, 4 and 8 hours after the first talazoparib dose

Interventionh•µg/L (Median)
Treatment (Talazoparib, Temozolomide): Phase 117.55

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AUC of Temozolomide in Combination With Talazoparib

Median with minimum and maximum for the area under the drug concentration over time curve. (NCT02116777)
Timeframe: Cycle 1 Day 5 or 6 pre-dose, and 1, 2, 4 and 8 hours after the temozolomide dose.

Interventionh•µg/L (Median)
Treatment (Talazoparib, Temozolomide): Phase 14352.16

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Overall Survival (OS)

The distribution of OS for each arm will be estimated using the Kaplan-Meier method and compared with a stratified logrank test. (NCT02152982)
Timeframe: 83 months

Interventionmonths (Median)
Arm I (Temozolomide, Veliparib)24.8
Arm II (Temozolomide, Placebo)28.1

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Objective Tumor Response

"Defined as complete response (CR) or partial response (PR) as specified in the Revised Assessment in Neuro-Oncology criteria. An objective tumor response will be evaluated for each patient and the tumor response count will be summarized for each arm and compared using the Chi-square test. For CR, all of the following must be true:~disappearance of all enhancing measurable and non-measurable disease; no new enhancing lesions; stable or improved non-enhancing lesions; patients must be off corticosteroids; stable or improved clinically~A PR requires all of the following: > 50% decrease in sum of products of perpendicular diameters of all measurable enhancing lesions compared with baseline; no progression of non-measurable disease; no new lesions; stable or improved non-enhancing lesions on same or lower dose of corticosteroids compared with baseline scan; steroid dose should be same or lower compared with baseline scan; stable or improved clinically" (NCT02152982)
Timeframe: 5 years

InterventionParticipants (Count of Participants)
Arm I (Temozolomide, Veliparib)34
Arm II (Temozolomide, Placebo)37

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Interaction With Optune Device

Cox proportional hazards model will be used to evaluate whether there is a potential interaction between the treatment arm and the Optune device. If an interaction is detected, separate analyses of treatment effect (using Cox models) will be done for patients treated with the Optune device and patients who were not treated with the Optune device. (NCT02152982)
Timeframe: 5 years

,
Interventionparticipants (Number)
Reporting actual Optune useNo actual Optune use
Arm I (Temozolomide, Veliparib)33125
Arm II (Temozolomide, Placebo)33135

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Progression-free Survival (PFS)

"The distribution of PFS for each arm will be estimated using the Kaplan-Meier method, and be compared using Cox proportional hazard models with all stratification factors adjusted. Progression (PD): Defined by any of the following:~> 25% increase in sum of products of perpendicular diameters of enhancing lesions, compared with the smallest tumor measurement obtained either at baseline or best response~Significant increase in T2/FLAIR non-enhancing lesion on stable or increasing doses of corticosteroids compared with baseline scan or best response after therapy initiation (stable doses of steroids include patient not on steroids) not caused by comorbid events~Any new lesion~Clear clinical deterioration not attributable to other causes apart from tumor or change in corticosteroid dose~Failure to return for evaluation as a result of death or deteriorating condition~Clear progression of non-measurable disease" (NCT02152982)
Timeframe: 83 months

Interventionmonths (Median)
Arm I (Temozolomide, Veliparib)12.1
Arm II (Temozolomide, Placebo)13.2

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Overall Adverse Event Rates for Grade 3 or Higher Adverse Events

Assessed using National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0 (version 5 beginning April 1, 2018). The overall adverse event rates for grade 3 or higher adverse events will be summarized and be compared using Chi-Square or Fisher's Exact tests between treatment arms. The maximum grade for each type of treatment-related adverse event will be recorded for each patient, and frequency tables for each arm will be reviewed to determine patterns. Treatment-related adverse events will be tabulated for each arm. (NCT02152982)
Timeframe: 5 years

Interventionparticipants with at least 1 grade 3+ AE (Number)
Arm I (Temozolomide, Veliparib)94
Arm II (Temozolomide, Placebo)137

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Percentage of Participants With an Unacceptable Toxicity

The percentage of patients who experience an unacceptable toxicity defined as any Grade 3 toxicity at least possibly attributed to the vaccine (or vaccine + TMZ and/or RT) that does not resolve to baseline within 3 weeks, any Grade 3 hypersensitivity reactions requiring steroids, any Grade 4 toxicity, including neurologic events not due to progressive disease, or any life threatening-event not attributable to concomitant medication, co-morbid event, or disease progression. (NCT02193347)
Timeframe: Date of consent through 2 months after the last vaccination

Interventionpercentage of participants (Number)
PEPIDH1M Vaccine0

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Percentage of Patients With a Positive Vaccine Response After 3 Post-Surgery Vaccines as Measured by IFNγ ELIspot

Assess the immunogenicity of the PEPIDH1M vaccine with adjuvant TMZ using ELISpot. This will be done by finding the difference between the number of SFC after 3 post-surgery vaccines and the number of SFC at baseline for each evaluable subject. Immunogenicity will then be summarized by the percentage of evaluable subjects who have a positive vaccine response after 3 post-surgery vaccines. A response will be considered positive if the difference in SFC measurement is greater than 20 SFC per 10^6 lymphocytes after determining the level of detection in the IDH ELISpot. (NCT02193347)
Timeframe: From time of pheresis #1, one day prior to first pre-surgery vaccine dose, until the time of the third post-surgery vaccination, an expected average of 24 weeks after study initiation

InterventionPercentage of evaluable participants (Number)
PEPIDH1M Vaccine42.86

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Median Overall Survival (OS) by Arm and MGMT Methylation Status

Median OS depending on treatment arm in patients with methylated MGMT (NCT02209948)
Timeframe: Through the whole study. 4 years. The median follow up for each patient was 33.4 months

Interventionmonths (Median)
Temozolomide20.7
Without Treatment27.1

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Progresion Free Survival Median Values

It will be measured following Response assessment in neuro-oncology (RANO) guidelines: progression-free survival (NCT02209948)
Timeframe: Through the whole study. 4 years. The median follow up for each patient was 33.4 months

Interventionmonths (Median)
Temozolomide9.5
Without Treatment7.77

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Overall Survival

Time between start of treatment and death (NCT02209948)
Timeframe: Through the whole study. 4 years. The median follow up for each patient was 33.4 months

Interventionmonths (Median)
Temozolomide18.2
Without Treatment23.3

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Progression Free Survival at 6 Month

"Percentage of patients without progression of disease and time between start of treatment and progression of disease.~The progression disease is defined as the time from the date of randomization to the date of progression defined according to the RANO criteria." (NCT02209948)
Timeframe: 6 month

Interventionpercentage of patients (Number)
Temozolomide61.3
Without Treatment55.7

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Number of Participants With Adverse Effects

Total number of patients presenting adverse events, stratified by type of event and grade. Adverse Events of special interest: Only relevant differences in toxicity by arm. (NCT02209948)
Timeframe: Through the whole study. 4 years

InterventionParticipants (Count of Participants)
Lymphopenia72025836Lymphopenia72025835Thrombocytopenia72025835Thrombocytopenia72025836Nausea and vomiting72025835Nausea and vomiting72025836Fatigue72025836Fatigue72025835Leucopenia72025835Leucopenia72025836
Grade 1-2Grade 3-4not affected
Temozolomide52
Without Treatment33
Temozolomide3
Temozolomide25
Without Treatment46
Temozolomide36
Without Treatment17
Temozolomide2
Temozolomide42
Without Treatment62
Temozolomide30
Without Treatment10
Without Treatment0
Temozolomide50
Without Treatment69
Temozolomide35
Without Treatment21
Temozolomide0
Temozolomide45
Without Treatment58
Temozolomide29
Without Treatment20
Temozolomide1
Without Treatment59

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Median Progression-free Survival (PFS) by Arm and MGMT Methylation Status

Median Progression Free Survival depending on treatment arm in patients with MGMT methylation (NCT02209948)
Timeframe: Through the whole study. 4 years. The median follow up for each patient was 33.4 months

Interventionmonths (Median)
Temozolomide11.4
Without Treatment8.5

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DCR After 12 Months

"All tumour assessments were performed using the RECIST criteria (1.1). CT-scan or MRI could be used for as method of tumour measurement and the same method of tumour measurement was used throughout the study for each subject. CT scans/MRI were performed at screening or baseline visit then at baseline, weeks 12, 24, 36, 48 (end of study) and at study withdrawal or at anytime during the study in the case of any clinical or biological signs of tumour progression.~The DCR was defined as the proportion of subjects with a response of CR, PR or SD after 6 months combination treatment followed by either 6 months of lanreotide ATG 120 mg maintenance treatment or no treatment. The DCR was described in the ITT population along with its 95% CI and was compared to 45% with an exact binomial proportion test. The LOCF method was used to replace missing assessments at the end of the maintenance phase." (NCT02231762)
Timeframe: 12 months

Interventionpercentage of subjects (Number)
Maintenance Phase - Functioning NET, Lanreotide54.5
Maintenance Phase - Non-functioning NET, Lanreotide71.4
Maintenance Phase - Non-functioning NET, No Treatment41.7

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Disease Control Rate (DCR) After 6 Months

"All tumour assessments were performed using the Response Evaluation Criteria In Solid Tumours (RECIST) criteria (1.1). Computer Tomography (CT-scan) or Magnetic Resonance Imaging (MRI) could be used for as method of tumour measurement and the same method of tumour measurement was used throughout the study for each subject. CT scans/MRI were performed at screening or baseline visit then at weeks 12, 24 and at early withdrawal or at anytime during the study in the case of any clinical or biological signs of tumour progression.~The DCR was defined as the proportion of subjects with a response of CR, PR or SD after 6 months of combination treatment and was described in the ITT population along with its 95% Confidence Interval (CI) and was compared to 45% with an exact binomial proportion test. The Last Observation Carried Forward (LOCF) method was used to replace missing assessments at the end of the combination phase." (NCT02231762)
Timeframe: 6 months

Interventionpercentage of subjects (Number)
Combination Phase73.5

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Duration of Response (DoR) Within 12 Months

"The DoR is an estimation of the time from first documented objective response (CR or PR) to the first date of progressive disease (PD) or death due to disease progression for subjects who experienced an objective response within the first 12 months of treatment (combination and maintenance phases).~The Kaplan-Meier method was used to estimate the median DoR and its 95% CI for subjects in the ITT population who had an objective response." (NCT02231762)
Timeframe: 12 months

Interventionmonths (Median)
Intention-to-treat (ITT) PopulationNA

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Progression-Free Survival (PFS) Within 12 Months

"PFS was defined as the time from the date of treatment start to the date of the first documented disease progression or death due to any cause within the first 12 months of treatment. If a subject had not progressed or died after 12 months of treatment or when any further anti-neoplastic therapy was received, PFS was censored at the time of the last tumour assessment before the analysis cut-off date or the anti-neoplastic therapy date.~A Kaplan-Meier estimate of the PFS was calculated to determine the number of subjects at risk. Median PFS time (50% of subjects who would not progress or die) of the ITT population is presented along with 95 % CI." (NCT02231762)
Timeframe: 12 months

Interventionmonths (Median)
Intention-to-treat (ITT) Population11.1

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Time To Response (TtR) Within 12 Months

"TtR was defined as the time from the date of treatment start to the date of the first documented objective response (CR or PR) within the first 12 months of treatment (combination and maintenance phases). A Kaplan Meier estimate of the TtR survival function was constructed.~The Kaplan-Meier method was used to estimate the median TtR and its 95% CI for subjects in the ITT population (50% of subjects were expected to have a CR or PR at this time)." (NCT02231762)
Timeframe: 12 months

Interventionmonths (Median)
Intention-to-treat (ITT) PopulationNA

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The Number of Subjects With a Symptomatic Response After 12 Months - Maintenance Phase

"Symptomatic response was evaluated as absolute change from baseline in the number of episodes of the lead symptoms (i.e. diarrhoea and flushing) using the mean of the last 3 days before the visit, at each visit, as compared to baseline.~Symptomatic responses were categorised as: Reduction, Increase or Stability of occurrences of diarrhoea / Reduction, Increase or Stability of occurrences of flushing.~The number of subjects in each response category at week 48 (end of study) is presented. Analysis was only carried out on subjects in the ITT population with functioning NET." (NCT02231762)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Diarrhoea - ReductionDiarrhoea - IncreaseDiarrhoea - StabilityDiarrhoea - MissingFlushing - ReductionFlushing - IncreaseFlushing - StabilityFlushing - Missing
Maintenance Phase - Functioning NET, Lanreotide41332333

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The Number of Subjects With a Biochemical Response Using CgA Levels After 12 Months

"Blood samples for CgA blood tumour marker analysis were taken at baseline, weeks 12, 24, 36, 48 (end of study) and at early withdrawal. The biochemical response after 12 months combination and maintenance treatment was estimated for subjects with abnormal CgA levels at baseline. Abnormal CgA levels were defined as above the upper limit of normal range (≥100 mcg/L).~Biochemical response based on CgA levels was categorised as: PR (decrease of CgA ≥50 % compared to the baseline CgA), SD (decrease < 50% or an increase ≤ 25% compared to the baseline CgA) or PD (defined as an increase ≥ 25%, compared to the baseline CgA).~The number of subjects in each response category at each time point in the maintenance phase is presented. Analysis was only carried out on subjects in the ITT population who had abnormal CgA at baseline." (NCT02231762)
Timeframe: 12 months

,,
InterventionParticipants (Count of Participants)
Week 24 - PDWeek 24 - SDWeek 24 - PRWeek 24 - MissingWeek 36 - PDWeek 36 - SDWeek 36 - PRWeek 36 - MissingWeek 48 - PDWeek 48 - SDWeek 48 - PRWeek 48 - MissingEarly Withdrawal - PDEarly Withdrawal - SDEarly Withdrawal - PREarly Withdrawal - Missing
Maintenance Phase - Functioning NET, Lanreotide2300120010101002
Maintenance Phase - Non-functioning NET, Lanreotide1431141112202010
Maintenance Phase - Non-functioning NET, No Treatment2232324023101010

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The Number of Subjects With a Biochemical Response Using 5-Hydroxy-Indol-Amino-Acid (HIAA) Levels After 6 Months

"Urine samples for 5-HIAA urinary tumour marker analysis were taken at at baseline, weeks 12, 24and early withdrawal.~Biochemical response based on 5-HIAA levels was categorised as: Response (5-HIAA reduction compared to baseline) or Progression (5-HIAA increase compared to baseline).~The number of subjects in each response category at each time point in the combination phase is presented. Analysis was only carried out on subjects in the ITT population with functioning NET." (NCT02231762)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Week 12 - ProgressionWeek 12 - ResponseWeek 12 - Not evaluableWeek 12 - MissingWeek 24 - ProgressionWeek 24 - ResponseWeek 24 - Not evaluableWeek 24 - MissingEarly Withdrawal - ProgressionEarly Withdrawal - ResponseEarly Withdrawal - Not EvaluableEarly Withdrawal - Missing
Combination Phase - Functioning NET461663130107

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The Number of Subjects With a Symptomatic Response After 6 Months

"Symptomatic response was evaluated as absolute change from baseline in the number of episodes of the lead symptoms (i.e. diarrhoea and flushing) using the mean of the last 3 days before the visit, at each visit, as compared to baseline.~Symptomatic responses were categorised as: Reduction, Increase or Stability of occurrences of diarrhoea / Reduction, Increase or Stability of occurrences of flushing.~The number of subjects in each response category at week 24 (end of the combination phase) is presented. Analysis was only carried out on subjects in the ITT population with functioning NET." (NCT02231762)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Diarrhoea - ReductionDiarrhoea - IncreaseDiarrhoea - StabilityDiarrhoea - MissingFlushing - ReductionFlushing - IncreaseFlushing - StabilityFlushing - Missing
Combination Phase - Functioning NET42564436

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The Number of Subjects With a Biochemical Response Using 5-HIAA Levels After 12 Months

"Urine samples for 5-HIAA urinary tumour marker analysis were taken at baseline, weeks 12, 24, 36, 48 (end of study) and early withdrawal.~Biochemical response based on 5-HIAA levels was categorised as: Response (5-HIAA reduction compared to baseline) or Progression (5-HIAA increase compared to baseline).~The number of subjects in each response category at each time point in the maintenance phase is presented. Analysis was only carried out on subjects in the ITT population with functioning NET." (NCT02231762)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Week 24 - ProgressionWeek 24 - ResponseWeek 24 - Not evaluableWeek 24 - MissingWeek 36 - ProgressionWeek 36 - ResponseWeek 36 - Not evaluableWeek 36 - MissingWeek 48 - ProgressionWeek 48 - ResponseWeek 48 - Not evaluableWeek 48 - MissingEarly Withdrawal - ProgressionEarly Withdrawal - ResponseEarly Withdrawal - Not evaluableEarly Withdrawal - Missing
Maintenance Phase - Functioning NET, Lanreotide6311330342020003

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DCR by O6-methylguanine-DNA Methyl-transferase (MGMT) Expression and Methylation and Somatostatin Receptor (SSTR) Expression After 6 Months

"In all subjects whose tumour tissue was available, MGMT expression/methylation and SSTR expression was analysed. After 6 months, the DCR (SD+PR+CR) by MGMT methylation and expression and by SSTR 2a and SSTR 5 expression was evaluated.~DCR in response to MGMT methylation and expression results are presented. SSTR 2a and SSTR 5 expression is categorised as: No Receptors, Cytoplasmatic Expression (CE), Focal Expression (FE), Complete Circumferent Membrane Expression (CCME).~The DCR was defined as the proportion of subjects with a response of CR, PR or SD after 6 months of combination treatment within each methylation/expression category. The DCR was described in the ITT population along with its 95% CI and was compared to 45% with an exact binomial proportion test." (NCT02231762)
Timeframe: 6 months

Interventionpercentage of subjects (Number)
MGMT MethylationMGMT No methylationMGMT ExpressionMGMT No expressionSSTR 2a FESSTR 2a CCMESSTR 5 - No ReceptorsSSTR 5 CESSTR 5 FE
Combination Phase100.084.690.970.086.772.775.0100.081.8

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Quality of Life Gastrointestinal Neuroendocrine Tumour 21 Questionnaire (QLQ-GI.NET21): Mean Change From Baseline at 6 Months

Subjects were instructed to complete the QLQ-GI.NET21 questionnaire at baseline, weeks 12, 24 or at early withdrawal. It contained 21 questions that used a 4-point scale (1 = Not at all, 2 = A little, 3 = Quite a bit, 4 = Very much) to evaluate 3 defined multi-item symptom scales (endocrine, gastrointestinal and treatment related side effects), 2 single item symptoms (bone/muscle pain and concern about weight loss), 2 psychosocial scales (social function and disease-related worries) and 2 other single items (sexuality and communication). Each individual subscore was transformed to range from 0 to 100. The mean change from baseline at week 24 (end of combination phase) is presented with a higher score representing a higher level response. Thus, a better level of functioning/a worse level of symptoms. (NCT02231762)
Timeframe: 6 months

InterventionUnits on a scale (Mean)
Endocrine symptomsGastrointestinal (G.I.) symptomsTreatment related symptomsSocial functionDisease related worriesMuscle/bone pain symptomsBody imageWeight gainInformation/communication functionSexual function
Combination Phase-1.05.73.62.31.61.00.0-11.8-9.4-4.8

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QoL Questionnaire QLQ-GI.NET21: Mean Change From Baseline at 12 Months

Subjects were instructed to complete the QLQ-GI.NET21 questionnaire at baseline, weeks 12, 24, 36, 48 (end of study) or at early withdrawal. It contained 21 questions that used a 4-point scale (1 = Not at all, 2 = A little, 3 = Quite a bit, 4 = Very much) to evaluate 3 defined multi-item symptom scales (endocrine, gastrointestinal and treatment related side effects), 2 single item symptoms (bone/muscle pain and concern about weight loss), 2 psychosocial scales (social function and disease-related worries) and 2 other single items (sexuality and communication). Answers were converted into grading scale, with values between 0 and 100. Each individual subscore was transformed to range from 0 to 100. The mean change from baseline at week 48 (end of study) is presented with a higher score representing a higher level response. Thus, a better level of functioning/a worse level of symptoms. (NCT02231762)
Timeframe: 12 months

Interventionunits on a scale (Mean)
Endocrine symptomsG.I. symptomsSocial functionDisease related worriesMuscle/bone pain symptomsBody imageWeight gainInformation/communication functionSexual function
Maintenance Phase - Non-functioning NET, No Treatment1.66.7-6.3-3.24.84.8-9.5-4.80.0

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Pharmacokinetic (PK) Results: Lanreotide ATG 120 mg Serum Concentrations Within 12 Months

"Lanreotide ATG levels were measured in a subset of subjects to evaluate if temozolomide co-treatment had an impact on lanreotide serum concentration over a 12 month period.~Blood samples were collected for the determination of lanreotide ATG in serum at baseline, weeks 4, 12, 24 and 48 (end of study).~The concentrations of lanreotide ATG in serum were determined by a validated radioimmunoassay analysis method with a lower limit of quantitation of 0.08 nanograms [ng]/mL).~Serum concentrations of lanreotide ATG at each of the time points in the combination and maintenance phase are presented. Only subjects with data available for analysis are presented." (NCT02231762)
Timeframe: Baseline (week 1) and weeks 4, 12, 24 and 48

Interventionng/mL (Mean)
BaselineWeek 4Week 12Week 24Week 48
PK Subset0.442.455.065.833.68

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European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life (QoL) Core 30 Questionnaire (QLQ-C30): Mean Change From Baseline at 6 Months

Subjects were instructed to complete the QLQ-C30 questionnaire at baseline, weeks 12, 24 or at early withdrawal. The first 28 questions used a 4-point scale (1=not at all, 2=a little, 3=quite a bit, 4=very much) for evaluating 5 functional scales (physical, role, emotional, cognitive, social), 3 symptom scales (fatigue, nausea/vomiting, pain) & 6 other single items. The last 2 questions represented subject's assessment of overall health & quality of life, coded on a 7-point scale (1=very poor to 7=excellent). The mean change from baseline at week 24 (end of the combination phase) is presented for global health status (scoring of questions 29 & 30) and 5 functional scales, 3 symptom scales and other single items (scoring of questions 1 to 28). Each individual subscore was transformed to range from 0 to 100. A higher score represents a higher level response. Thus, a better QoL/a better level of functioning/a worse level of symptoms. (NCT02231762)
Timeframe: 6 months

Interventionunits on a scale (Mean)
Global health statusPhysical functioningRole functioningEmotional functioningCognitive functioningSocial functioningFatigueNausea and vomitingPainDyspnoeaInsomniaAppetite lossConstipationDiarrhoeaFinancial difficulties
Combination Phase-4.9-9.6-8.3-4.7-5.9-11.86.96.9-1.012.70.02.06.9-3.92.9

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EORTC QoL Questionnaire QLQ-C30: Mean Change From Baseline at 12 Months

Subjects were instructed to complete QLQ-C30 questionnaire at baseline, weeks 12, 24, 36, 48 (end of study) or at early withdrawal. The first 28 questions used a 4-point scale (1=not at all, 2=a little, 3=quite a bit, 4=very much) for evaluating 5 functional scales (physical, role, emotional, cognitive, social), 3 symptom scales (fatigue, nausea/vomiting, pain) & 6 other single items. The last 2 questions represented subject's assessment of overall health & quality of life, coded on a 7-point scale (1=very poor to 7=excellent). The mean change from baseline at week 48 (end of study) is presented for global health status (scoring of questions 29 & 30) and 5 functional scales, 3 symptom scales and other single items (scoring of questions 1 to 28). Each individual subscore was transformed to range from 0 to 100. A higher score represents a higher level response. Thus, a better QoL/a better level of functioning/a worse level of symptoms. (NCT02231762)
Timeframe: 12 months

,,
Interventionunits on a scale (Mean)
Global health statusPhysical functioningRole functioningEmotional functioningCognitive functioningSocial functioningFatigueNausea and vomitingPainDyspnoeaInsomniaAppetite lossConstipationDiarrhoeaFinancial difficulties
Maintenance Phase - Functioning NET, Lanreotide-11.78.03.315.03.313.3-22.2-10.0-13.3-8.3-13.30.020.0-40.06.7
Maintenance Phase - Non-functioning NET, Lanreotide-3.1-12.5-2.1-6.2-2.1-22.9-9.74.24.24.2-8.30.0-4.28.34.2
Maintenance Phase - Non-functioning NET, No Treatment-7.1-11.4-7.1-6.02.4-4.84.82.49.59.516.714.3-4.80.09.5

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QoL Questionnaire QLQ-GI.NET21: Mean Change From Baseline at 12 Months

Subjects were instructed to complete the QLQ-GI.NET21 questionnaire at baseline, weeks 12, 24, 36, 48 (end of study) or at early withdrawal. It contained 21 questions that used a 4-point scale (1 = Not at all, 2 = A little, 3 = Quite a bit, 4 = Very much) to evaluate 3 defined multi-item symptom scales (endocrine, gastrointestinal and treatment related side effects), 2 single item symptoms (bone/muscle pain and concern about weight loss), 2 psychosocial scales (social function and disease-related worries) and 2 other single items (sexuality and communication). Answers were converted into grading scale, with values between 0 and 100. Each individual subscore was transformed to range from 0 to 100. The mean change from baseline at week 48 (end of study) is presented with a higher score representing a higher level response. Thus, a better level of functioning/a worse level of symptoms. (NCT02231762)
Timeframe: 12 months

,
Interventionunits on a scale (Mean)
Endocrine symptomsG.I. symptomsTreatment related symptomsSocial functionDisease related worriesMuscle/bone pain symptomsBody imageWeight gainInformation/communication functionSexual function
Maintenance Phase - Functioning NET, Lanreotide-13.3-4.00.0-6.7-6.7-6.70.0-20.00.00.0
Maintenance Phase - Non-functioning NET, Lanreotide-5.60.0-11.19.71.44.24.29.50.00.0

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The Number of Subjects With a Biochemical Response Using Chromogranin-A (CgA) Levels After 6 Months

"Blood samples for CgA blood tumour marker analysis were taken at baseline, weeks 12, 24 and at early withdrawal. The biochemical response after 6 months combination treatment was estimated for subjects with abnormal CgA levels at baseline. Abnormal CgA levels were defined as above the upper limit of normal range (≥100 micrograms/litre [mcg/L]).~Biochemical response based on CgA levels was categorised as: PR (decrease of CgA ≥ 50%, compared to the baseline CgA), SD (decrease < 50 % or an increase ≤25%, compared to the baseline CgA) or PD (defined as an increase ≥25 %, compared to the baseline CgA).~The number of subjects in each response category at each time point in the combination phase is presented. Analysis was only carried out on subjects in the ITT population who had abnormal CgA at baseline." (NCT02231762)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Week 12- PDWeek 12 - SDWeek 12- PRWeek 12 - MissingWeek 24 - PDWeek 24 - SDWeek 24 - PRWeek 24 - MissingEarly Withdrawal - PDEarly Withdrawal - SDEarly Withdrawal - PREarly Withdrawal - Missing
Combination Phase815101597012114

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Number of Participants With Adverse Events

Safety and tolerability were assessed by monitoring the frequency, duration, severity and attribution of adverse events and evaluating changes in laboratory values and vital signs. (NCT02288897)
Timeframe: Assessed every 4 weeks until 28 days after last treatment; median duration of treatment was 11.8 and 9.5 weeks in each treatment group, respectively.

InterventionParticipants (Count of Participants)
PV-1014
Chemotherapy or Oncolytic Viral Therapy8

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Overall Survival (OS)

OS was documented at 12 week intervals commencing on withdrawal from active study participation. Documentation was made by subject clinic visit or other personal contact, telephonic contact, review of medical records, or other unequivocal evidence of survival status. OS was estimated via Kaplan-Meier analysis, and was defined as the interval from randomization to death; subjects who did not have an event of death were censored at their last assessment date. (NCT02288897)
Timeframe: Assessed every 12 weeks upon withdrawal from active study participation until death, withdrawal of consent, or study termination; median follow-up time for survival was 82.4 weeks, maximum was 167.0 weeks.

InterventionMonths (Median)
PV-10NA
Chemotherapy or Oncolytic Viral TherapyNA

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Complete Response Rate (CRR)

CRR was assessed using RECIST v1.1 criteria, and required disappearance of all target and non-target lesions. (NCT02288897)
Timeframe: Assessed every 12 weeks until disease progression, withdrawal of consent, or study termination; median follow-up time for CRR was 26.6 weeks, maximum was 125.8 weeks.

InterventionParticipants (Count of Participants)
PV-103
Chemotherapy or Oncolytic Viral Therapy2

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Progression-free Survival (PFS)

"PFS was estimated via Kaplan-Meier analysis using Response Evaluation Criteria In Solid Tumors (RECIST v1.1) criteria. Subjects who did not have an event of progression or death were censored at their last assessment date.~Assessment of progression was performed by the sponsor based on review of lesion measurement and clinical progression data reported by each investigator. Events signaling progression included increase in size and/or number of study lesions, onset of visceral metastatic disease, and death. For target lesions (assigned prior to randomization), complete response (CR) required disappearance of all target lesions; partial response (PR) required >= 30% decrease in sum of the longest diameter (SLD) of all target lesions; progressive disease (PD) required >=20% increase in SLD of target lesions. Non-target lesions were followed for CR, PD, or non-CR/non-PD status using equivalent thresholds. Progression occurred when PD was observed in either target or non-target lesion." (NCT02288897)
Timeframe: Assessed every 12 weeks until disease progression, withdrawal of consent, or study termination; progression detected between formal assessments was documented at the time of detection; median follow-up time for PFS was 26.6 weeks, maximum was 125.8 weeks.

InterventionMonths (Median)
PV-106.1
Chemotherapy or Oncolytic Viral Therapy8.6

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Change in Domain Scores From Baseline Using the Patient Reported Skindex-16 Instrument

In this exploratory endpoint, changes in Skindex-16 self-assessment scores were evaluated vs Day 1 baseline domain scores: symptom domain (items 1-4); emotional domain (items 5-11); and functioning domain (items 12-16). The Skindex-16 instrument solicits response to the extent of bother during the preceding week by 16 items (e.g., itching, hurting, worry, impact on daily activities), using a score from 0 (never bothered) to 6 (always bothered) for each item. Item scores are transformed to 0 to 100 scale, and domain scores are calculated as the average of the item scores comprising the domain. A lower domain score at baseline signifies lower impact of that domain; a decrease in domain score from baseline signifies improvement in that domain. Median baseline score and change from baseline over the study interval is presented for each domain. (NCT02288897)
Timeframe: Assessed at baseline (Day 1 at start of study treatment) and at the end of each treatment cycle (every 4 or 6 weeks) until disease progression, withdrawal of consent, or study termination; median follow-up time was 26.6 weeks, maximum was 125.8 weeks.

,
InterventionScores on a Scale (0-100) (Median)
Baseline Symptom Domain ScoreChange in Symptom Domain Score from BaselineBaseline Emotional Domain ScoreChange in Emotional Domain Score from BaselineBaseline Functioning Domain ScoreChange in Functioning Domain Score from Baseline
Chemotherapy or Oncolytic Viral Therapy18.8-6.316.7-4.88.36.7
PV-102.1-2.120.2-10.11.7-1.7

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Duration of Complete Response (DCR)

DCR was estimated via Kaplan-Meier analysis for participants achieving a complete response, and was defined as the interval from first complete response to disease progression or death; responders who did not have an event of progression or death were censored at their last assessment date. Complete response was assessed using RECIST v1.1 criteria, and required disappearance of all target and non-target lesions. (NCT02288897)
Timeframe: Assessed every 12 weeks until disease progression, withdrawal of consent, or study termination; median follow-up time for DCR was 26.7 weeks, maximum was 77.7 weeks.

InterventionMonths (Median)
PV-10NA
Chemotherapy or Oncolytic Viral TherapyNA

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Pharmacokinetic Profile of BBI608 and Temozolomide When Administered in Combination With Temozolomide as Assessed by the Area Under the Curve

The area under the curve of BBI608, from time 0 to the last quantifiable concentration, calculated by a combination of linear and logarithmic trapezoidal methods (linear up/log down method) (NCT02315534)
Timeframe: On Day 1 and Day 5 after the first dosing, prior to dosing and 1, 2, 3, 5, 5h40m (day 1 only), 6, 7, 8 and 24 hours after first dose of BBI608

Interventionh*ng/ml (Geometric Mean)
Candidates Whom Surgery is Recommended4820
Candidates Whom Surgery is Not Recommended4200

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Dose-limiting Toxicities (DLTs)

Number of patients who experienced a dose limiting toxicity following a dosing of BBI608 (NCT02315534)
Timeframe: 28 days after first administration of combination treatment (BBI608+TMZ)

InterventionParticipants (Count of Participants)
Candidates Whom Surgery is Recommended.0
Candidates Whom Surgery is Not Recommended0

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Progression Free Survival (PFS)-6

To assess the effect of BBI608 + temozolomide (TMZ) therapy defined as the percentage of patients who have survived without objective disease progression for at least 6 months after treatment per neuro-oncology (RANO) criteria who had evaluable disease at baseline. PFS-6 is defined as the percentage of patients who survived without objective disease progression per RANO criteria for at least 6 months after treatment. (NCT02315534)
Timeframe: From the time of exposure to study drug to first objective documentation of disease progression or death due to any cause, assessed up to 6 months

Interventionpercentage of participants (Number)
Candidates Whom Surgery is Not Recommended.28.07

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Overall Survival (OS)

To assess the effect of BBI608 + temozolomide (TMZ) on the overall survival of patients with recurrent or progressive glioblastoma multiforme (GBM) who had not received prior treatment with bevacizumab or other anti-vascular endothelial growth factor agents who either were eligible or not eligible for surgical resection. (NCT02315534)
Timeframe: From the time of exposure to study drug to death from any cause. If patient discontinued study drug, they were assessed the first 3 months after discontinuation, then every 3 months up to 1 year, then every 6 months thereafter until death.

Interventionmonths (Median)
Candidates Whom Surgery is Not Recommended8.05

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Disease Control Rate (DCR)

To assess the percentage of patients that had evaluable disease at baseline with a documented complete response, partial response, and stable disease (CR + PR + SD) based on the Response Assessment in Neuro-Oncology (RANO) criteria out of all patients who received at least one dose of any study drug and had evaluable disease at baseline. (NCT02315534)
Timeframe: 4 weeks

Interventionpercentage of patients (Number)
Candidates Whom Surgery is Not Recommended30

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Progression Free Survival (PFS)-12

To assess the effect of BBI608 + temozolomide (TMZ) therapy defined as the percentage of patients who have survived without objective disease progression for at least 12 months after treatment per neuro-oncology (RANO) criteria who had evaluable disease at baseline. PFS-12 is defined as the percentage of patients who survived without objective disease progression per RANO criteria for at least 12 months after treatment. (NCT02315534)
Timeframe: From the time of exposure to study drug to first objective documentation of disease progression or death due to any cause, up to 12 months

Interventionpercentage of participants (Number)
Candidates Whom Surgery is Not Recommended16.84

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Overall Response Rate (ORR)

The proportion of patients with a documented complete response and partial response (CR + PR) based on RANO criteria. (NCT02315534)
Timeframe: 4 weeks

Interventionpercentage (Number)
Candidates Whom Surgery is Not Recommended3

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Incidence of Treatment-Emergent Adverse Events

The safety of the combination of SGT-53 and Temozolomide was assessed by analysis of adverse experiences, clinical laboratory tests and physical examinations. (NCT02340156)
Timeframe: Study drug initiation through 30 days after the last dose of study drug or EOS, whichever is later, approximately 90 days.

InterventionParticipants (Number)
SeizureElectrocardiogram QT corrected interval prolongedSkin ulceration
SGT-53 With Temozolomide111

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AUC0-∞

Extent of absorption of Temozolomide from time (0) to infinity (∞) will be measured after oral administration of the test product (Dralitem®, Monte Verde S.A.) or the reference product (Temodal®, Schering-Plough). (NCT02343081)
Timeframe: 0, 0.25, 0.5, 0.75, 1.0, 1.25, 1.5, 1.75, 2.0, 2.5, 3.0, 4.0, 6.0, 8.0, 10.0 hours on Days 3 and 4

Interventionmcg*h/mL (Mean)
Temodal31.817
Dralitem32.290

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Kel

Rate at which Temozolomide is removed from the body. (NCT02343081)
Timeframe: 0, 0.25, 0.5, 0.75, 1.0, 1.25, 1.5, 1.75, 2.0, 2.5, 3.0, 4.0, 6.0, 8.0, 10.0 hours on Days 3 and 4

Intervention1/h (Mean)
Temodal0.3743
Dralitem0.3691

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AUC0-t

Extent of absorption of Temozolomide from time (0) to the last quantifiable concentration (t) will be measured after the oral administration of the test product (Dralitem®, Monte Verde S.A.) or the reference product (Temodal®, Schering-Plough) (NCT02343081)
Timeframe: 0, 0.25, 0.5, 0.75, 1.0, 1.25, 1.75, 2.0, 2.5, 3.0, 4.0, 6.0, 8.0, 10.0 hours on Days 3 and 4

Interventionmcg*h/mL (Mean)
Temodal30.796
Dralitem31.104

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T1/2

Time required for Temozolomide plasma concentration to decrease by 50% (NCT02343081)
Timeframe: 0, 0.25, 0.5, 0.75, 1.0, 1.25, 1.5, 1.75, 2.0, 2.5, 3.0, 4.0, 6.0, 8.0, 10.0 hours on Days 3 and 4

Interventionhours (Mean)
Temodal1.87
Dralitem1.89

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Cmax

Rate of absorption of Temozolomide (Cmax) will be measured after the oral administration of the test product (Dralitem®, Monte Verde S.A.) or the reference product (Temodal®, Schering-Plough). (NCT02343081)
Timeframe: 0, 0.25, 0.5, 0.75, 1.0, 1.25, 1.5, 1.75, 2.0, 2.5, 3.0, 4.0, 6.0, 8.0, 10.0 hours on Days 3 and 4

Interventionmcg/mL (Mean)
Temodal11.108
Dralitem10.575

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Pediatric Study: Half-life (t1/2) Observed for ABT-414

Half-life is the calculated time it takes for half of the drug to leave the body. (NCT02343406)
Timeframe: Samples collected Cycle 1 Days 1, 2,3,5,8,15; Cycle 2 Day 1; Cycle 3 Day 1; Cycle 5 Day 1; Day 1 of every two cycles starting with Cycle 5; and 35 days after the last dose

Interventiondays (Mean)
ABT-414_ Pediatric9.0

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Pediatric Study: Area Under the Concentration-time-curve (AUC) Observed for Unconjugated Cys-mcMMAF

AUC is a measure of how long and how much drug or drug metabolite is present in the body after dosing. The AUC of Cys-mcMMAF, a toxic metabolite of depatuxizumab mafodotin, in the pediatric population was measured following treatment to confirm that this was comparable to adults, and that the dosing levels are appropriate for a pediatric population. (NCT02343406)
Timeframe: Samples collected Cycle 1 Days 1, 2, 3, 5, 8

Interventionng*h/mL (Mean)
ABT-414_ Pediatric14.1

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Pediatric Study: Area Under the Concentration-time Curve (AUC) Observed for ABT-414

AUC is a measure of how long and how much drug is present in the body after dosing. The AUC of depatuxizumab mafodotin (ABT-414) in the pediatric population was measured following treatment to confirm that this was comparable to adults, and that the dosing levels are appropriate for a pediatric population. (NCT02343406)
Timeframe: Samples collected Cycle 1 Days 1, 2,3,5,8,15; Cycle 2 Day 1; Cycle 3 Day 1; Cycle 5 Day 1; Day 1 of every two cycles starting with Cycle 5; and 35 days after the last dose

Interventionµg*h/mL (Mean)
ABT-414_ Pediatric3170

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Adult Study: Objective Response Rate (ORR)

The objective response rate (ORR) included best overall responses - complete response (CR) and partial response (PR) - assessed by the independent review committee per response assessment in neurooncology criteria (RANO) criteria from the date of randomization until disease progression or death, whichever came first. All objective responses (CR and PR) must be have been confirmed by repeat MRI 4 weeks after the first time when CR or PR is identified. Any subject who did not meet CR or PR including those who did not have post-baseline radiological assessments was considered a nonresponder. (NCT02343406)
Timeframe: Every 8 weeks at each assessment of disease, up to 28 months

Interventionpercentage of participants (Number)
ABT-414/Temozolomide14.3
ABT-414_adult7.7
Control (Temozolomide/Lomustine)4.4

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Adult Study: Progression-Free Survival (PFS)

Progression-free survival was assessed per response assessment in neuro-oncology criteria (RANO) criteria and assessed by an independent review committee and was defined as the length of time during and after the treatment of a disease, that the participant lived with the disease but did not get worse. (NCT02343406)
Timeframe: Measured every 8 weeks from date of randomization until the date of first objective progression or subject's death, whichever occurred first, up to 2 years

,,
Interventionmonths (Number)
25th quartile50th quartile75th quartile
ABT-414_adult1.51.93.5
ABT-414/Temozolomide1.82.74.9
Control (Temozolomide/Lomustine)1.61.94.2

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Adult Study: Overall Survival in the Subgroup With Epidermal Growth Factor Receptor (EGFRvIII) Mutation

Overall Survival (OS) was defined as time from randomization to death due to any cause, regardless of whether the event occurred on or off study drug (depatuxizumab mafodotin/temozolomide/lomustine) for all randomized participants that had the Epidermal Growth Factor Receptor (EGFRvIII) mutation. (NCT02343406)
Timeframe: From the date of randomization up to the date of participant's death; participants who completed treatment were to be assessed every 12 weeks, up to 28 months

,,
Interventionmonths (Number)
25th quartile50th quartile75th quartile
ABT-414_adult5.08.413.9
ABT-414/Temozolomide6.39.414.4
Control (Temozolomide/Lomustine)4.77.512.4

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Pediatric Study: Percentage of Participants With Adverse Events From the First Visit Until 49 Days After the Last Dose of Study Drug

The severity of each adverse event was rated according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE Version 4.0) (NCT02343406)
Timeframe: From participant's first visit until 49 days after the participant's last dose of study drug, up to 63 weeks

Interventionpercentage of participants (Number)
ABT-414_ Pediatric100

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Adult Study: Overall Survival (OS)

Overall Survival (OS) was defined as time from randomization to death due to any cause, regardless of whether the event occurred on or off study drug (depatuxizumab mafodotin/temozolomide/lomustine). (NCT02343406)
Timeframe: From the date of randomization up to the date of participant's death; participants who completed treatment were to be assessed every 12 weeks, up to 28 months.

,,
Interventionmonths (Number)
25th quartile50th quartile75th quartile
ABT-414_adult4.67.915.5
ABT-414/Temozolomide5.79.616.9
Control (Temozolomide/Lomustine)4.98.212.6

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Pediatric Study: Maximum Observed Serum Concentration (Cmax) of ABT-414

Cmax is the peak concentration that a drug achieves in a specified compartment after the drug has been administrated and before administration of a second dose. (NCT02343406)
Timeframe: Samples collected Cycle 1 Days 1, 2,3,5,8,15; Cycle 2 Day 1; Cycle 3 Day 1; Cycle 5 Day 1; Day 1 of every two cycles starting with Cycle 5; and 35 days after the last dose

Interventionµg/mL (Mean)
ABT-414_ Pediatric31.4

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Pediatric Study: Maximum Observed Plasma Concentration (Cmax) of Cys-mcMMAF

Cmax is the peak concentration that a drug or drug metabolite achieves in a specified compartment after the drug has been administrated and before administration of a second dose. Cys-mcMMAF is a toxic metabolite of depatuxizumab mafodotin. (NCT02343406)
Timeframe: Samples collected Cycle 1 Days 1, 2, 3, 5, 8

Interventionng/mL (Mean)
ABT-414_ Pediatric0.272

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Pediatric Study: Half-life (t1/2) Observed for Cys-mcMMAF

Half-life is the calculated time it takes for half of the drug or drug metabolite to leave the body. CysmcMMAF is a toxic metabolite of depatuxizumab mafodotin. (NCT02343406)
Timeframe: Samples collected Cycle 1 Days 1, 2, 3, 5, 8

Interventiondays (Mean)
ABT-414_ Pediatric11.2

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Overall Survival (OS)

Overall survival was defined as the duration from the initiation of chemoradiation therapy to the date of death from any cause. Subjects who were alive or lost to follow-up at the time of the analysis were be censored at the last known date they were alive. (NCT02343549)
Timeframe: From date of treatment start to date of death, or censored as described above; assessed for approximately 5 years

Interventionmonths (Median)
Planned RT + TMZ + BEV + NovoTTF100A Device9.9

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Progression Free Survival (PFS)

Progression-Free Survival (PFS) is defined as duration of time from initiation of chemoradiation therapy to first occurrence of either progressive disease (PD) or death. PD must be objectively determined as per RANO criteria (Updated Response Assessment Criteria for High Grade Gliomas, where PD is defined as a 25% increase in sum of products of diameters from nadir), where date of PD is date of assessment that identified PD. If subject died without documented PD, date of progression will be date of death. For surviving subjects who do not have documented PD, PFS will be censored at date of last radiologic assessment. For subjects who receive subsequent anti-cancer therapy prior to documented PD, PFS will be censored at the date of last radiologic assessment prior to the commencement of subsequent therapy. Subjects who have an initial PFS event immediately following 2 or more consecutive missed assessments will be censored at date of last assessment prior to missed assessments. (NCT02343549)
Timeframe: From date of treatment start to date of progression/death, or censored as described above; assessed for approximately 2 years.

Interventionmonths (Median)
Planned RT + TMZ + BEV + NovoTTF100A Device7.9

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Duration of Response

Duration of response (DOR) was measured from the time RANO criteria are met for CR or PR (whichever is first recorded) until the first occurrence of either progressive disease or death. PD must be objectively determined as per RANO criteria (Updated Response Assessment Criteria for High Grade Gliomas, where PD is defined as a 25% increase in sum of products of diameters from nadir), where PD date is assessment date that identified PD. If subject died without PD, PD date was death date. For surviving subjects who didn't have documented PD, DOR was censored at last radiologic assessment. For subjects who receive subsequent anti-cancer therapy prior to documented PD, DOR was censored at last radiologic assessment prior to commencement of subsequent therapy. Subjects who had an initial PD event immediately following 2 or more consecutive missed assessments were censored at last assessment prior to missed assessments. DOR was only calculated for subjects with a best response of PR or CR. (NCT02343549)
Timeframe: From date of first response to date of progression/death, or censored as described above; assessed for approximately 2 years.

Interventionmonths (Median)
Planned RT + TMZ + BEV + NovoTTF100A Device8.1

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Number of Participants With 12-Month Survival

Twelve-month survival was determined for each subject as a binary variable indicating whether or not the subject was alive at 12 months from initiation of chemoradiation. Determination of this endpoint occurs after the subject has at least 12 months of follow-up, unless they have died sooner. (NCT02343549)
Timeframe: Evaluated over 12 months

InterventionParticipants (Count of Participants)
Planned RT + TMZ + BEV + NovoTTF100A Device3

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Duration of Disease Control

Duration of disease control (DoDC) was measured from the time of initiation of chemoradiation therapy until the first occurrence of either progressive disease or death. PD must be objectively determined as per RANO criteria (Updated Response Assessment Criteria for High Grade Gliomas, where PD is defined as a 25% increase in sum of products of diameters from nadir), where PD date is assessment date that identified PD. If subject died without PD, PD date was death date. For surviving subjects who didn't have documented PD, DoDC was censored at last radiologic assessment. For subjects who receive subsequent anti-cancer therapy prior to documented PD, DoDC was censored at last radiologic assessment prior to commencement of subsequent therapy. Subjects who had an initial PD event immediately following 2 or more consecutive missed assessments were censored at last assessment prior to missed assessments. DoDC was calculated only for subjects with a best overall response of SD or better. (NCT02343549)
Timeframe: From date of treatment start to date of progression/death, or censored as described above; assessed for approximately 2 years.

Interventionmonths (Median)
Planned RT + TMZ + BEV + NovoTTF100A Device7.9

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Number of Participants With Disease Control

Disease control was determined for each subject indicating whether or not they achieved an overall response of stable disease (SD) or better by RANO criteria (where a CR is indicated by disappearance of all target and non target lesions, a PR is indicated by >= 50% decrease in sum of products of diameters of target lesions with baseline as reference, and SD is neither sufficient shrinkage to qualify for PR nor sufficient growth, >=25%, to indicate progression). (NCT02343549)
Timeframe: From enrollment to best response while on study treatment; subjects remained on treatment until disease progression or death or unacceptable toxicity (subjects were on treatment for an average of 7 months).

InterventionParticipants (Count of Participants)
Planned RT + TMZ + BEV + NovoTTF100A Device9

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Number of Participants With Objective Response

Objective response was determined for each subject as a binary variable indicating whether or not the subject achieved a best overall response of complete response (CR) or partial response (PR) as determined by the Updated Response Assessment Criteria for High Grade Gliomas (RANO; where CR is indicated by disappearance of all target lesions and PR is indicated by >=50% decrease in the sum of products of diameters of target lesions with baseline as reference). Best responses of CR or PR must be confirmed by a subsequent radiologic assessment. (NCT02343549)
Timeframe: From enrollment to best response while on study treatment; subjects remained on treatment until disease progression or death or unacceptable toxicity (subjects were on treatment for an average of 7 months)

InterventionParticipants (Count of Participants)
Planned RT + TMZ + BEV + NovoTTF100A Device3

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Median Overall Survival in CMV Negative Participants

Median overall survival will be estimated in the subset of participants that are CMV negative. Overall survival will be defined as the time in months between randomization and death, or last follow-up if alive. Kaplan-Meier methods will be used to estimate overall survival. (NCT02366728)
Timeframe: Up to 72 months (from the time of randomization of the first patient until approximately 31 months after randomization of the last patient)

Interventionmonths (Median)
Group I: Unpulsed DC Pre-conditioning13.4
Group II: Tetanus Pre-conditioning16.7

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Median Overall Survival

Overall survival will be defined as the time in months between randomization and death, or last follow-up if alive. Kaplan-Meier methods will be used to estimate overall survival. (NCT02366728)
Timeframe: Up to 72 months (from the time of randomization of the first patient until approximately 31 months after randomization of the last patient)

Interventionmonths (Median)
Group I: Unpulsed DC Pre-conditioning16
Group II: Tetanus Pre-conditioning20
Group III: Basiliximab and Tetanus Pre-conditioning19

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Percentage of 111In-labeled Dendritic Cells Migrating to the Inguinal Lymph Nodes

Within Groups I and II only, the percentage of 111In-labeled DCs migrating to the inguinal lymph nodes from the initial injection sites in the left and right groin at 48 hours post-vaccination #4 will be calculated. (NCT02366728)
Timeframe: For each patient, migration studies will occur after vaccination #4 which occurs approximately 7 months after study consent.

Interventionpercentage of cells (Median)
Group I: Unpulsed DC Pre-conditioning6.0
Group II: Tetanus Pre-conditioning9

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Median Progression-free Survival in CMV Positive Participants

Median progression-free survival will be estimated in the subset of participants that are CMV positive. Progression-free survival will be defined as the time in months between randomization and disease progression or death. Participants alive without disease progression will be censored at the time of their last follow-up. Kaplan-Meier methods will be used to estimate progression-free survival. (NCT02366728)
Timeframe: Up to 72 months (from the time of randomization of the first patient until approximately 31 months after randomization of the last patient)

Interventionmonths (Median)
Group I: Unpulsed DC Pre-conditioning6.5
Group II: Tetanus Pre-conditioning6.8

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Median Progression-free Survival in CMV Negative Participants

Median progression-free survival will be estimated in the subset of participants that are CMV negative. Progression-free survival will be defined as the time in months between randomization and disease progression or death. Participants alive without disease progression will be censored at the time of their last follow-up. Kaplan-Meier methods will be used to estimate progression-free survival. (NCT02366728)
Timeframe: Up to 72 months (from the time of randomization of the first patient until approximately 31 months after randomization of the last patient)

Interventionmonths (Median)
Group I: Unpulsed DC Pre-conditioning5.9
Group II: Tetanus Pre-conditioning5.8

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Median Progression-free Survival

Progression-free survival will be defined as the time in months between randomization and disease progression or death. Participants alive without disease progression will be censored at the time of their last follow-up. Kaplan-Meier methods will be used to estimate progression-free survival. (NCT02366728)
Timeframe: Up to 72 months (from the time of randomization of the first patient until approximately 31 months after randomization of the last patient)

Interventionmonths (Median)
Group I: Unpulsed DC Pre-conditioning6.5
Group II: Tetanus Pre-conditioning6.7
Group III: Basiliximab and Tetanus Pre-conditioning7.1

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Median Overall Survival in CMV Positive Participants

Median overall survival will be estimated in the subset of participants that are CMV positive. Overall survival will be defined as the time in months between randomization and death, or last follow-up if alive. Kaplan-Meier methods will be used to estimate overall survival. (NCT02366728)
Timeframe: Up to 72 months (from the time of randomization of the first patient until approximately 31 months after randomization of the last patient)

Interventionmonths (Median)
Group I: Unpulsed DC Pre-conditioning16.5
Group II: Tetanus Pre-conditioning23.8

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Change in AUC0-18 of the Temozolomide Concentration (AUC-T) in Brain Interstitium Before and After Regadenoson Infusion

The AUC-T for each day will be estimated by the trapezoid rule, based on the number of time points available for the particular evaluable patient. The PK variables will be tabulated and descriptive statistics calculated pre and post Regadenoson. The difference of AUCs will be summarized by mean and standard deviation or median and range if there is large variation from patient to patient. Means and standard deviation or mean and range will be presented for Cmax and AUC(inf) for each group. Graphic method will be used to display the difference for individual patient and all five patients. (NCT02389738)
Timeframe: 18 hours post temozolomide administration

Interventionpercentage of AUC (Mean)
Temozolomide alone AUC brain/plasmaTemozolomide/Regadenoson AUC brain/plasma
BBB Disruption With Regadenoson19.118.0

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Progression-free Survival at 6 Months

Will be analyzed using standard descriptive statistical methods. (NCT02395692)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Treatment (Methoxyamine, Temozolomide)2

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Toxicity as Assessed by Number of Participants Who Experienced Adverse Events

Number of participants who experience adverse events graded 3 or higher as defined by National Cancer Institute CTCAE v4.0. (NCT02395692)
Timeframe: Up to 30 days following the last dose of study drug

InterventionParticipants (Count of Participants)
Treatment (Methoxyamine, Temozolomide)19

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Progression-free Survival

Will be analyzed using standard descriptive statistical methods. 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 (NCT02395692)
Timeframe: Up to at least 2 years

Interventionmonths (Median)
Treatment (Methoxyamine, Temozolomide)2

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Overall Survival

Will be analyzed using standard descriptive statistical methods. (NCT02395692)
Timeframe: Up to at least 2 years

Interventionmonths (Median)
Treatment (Methoxyamine, Temozolomide)11

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Objective Response as Assessed by Response Assessment in Neuro-Oncology (RANO) Criteria (Arm 1 and Arm 2)

"To test the hypothesis that the combination treatment of temozolomide and methoxyamine will achieve 30% radiographic response rate (partial response + complete response) in patients with first recurrence of glioblastoma.~Per Response Assessment in Neuro-Oncology (RANO) Criteria: 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." (NCT02395692)
Timeframe: Up to at least 2 years

InterventionParticipants (Count of Participants)
Arm1 Methoxyamine&Temozolomide (Bevacizumab-naïve)0

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Overall Survival

The median overall survival estimated using the Kaplan-Meier methods. Estimates of quantities such as median survival will be obtained. Corresponding confidence intervals will be computed. (NCT02455557)
Timeframe: Date of diagnosis until (1) date of death or (2) the last date patient known alive (if death is not observed), assessed up to 2 years

Interventionmonths (Median)
Treatment (SurVaxM, Temozolomide)25.8

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Progression-free Survival (PFS)

The 6-month progression-free survival (PFS6) estimated using the Kaplan-Meier methods. PFS6 is defined as the percentage of patients without tumor progression or death from any cause 6 months after the date of diagnosis by biopsy. Corresponding confidence intervals will be computed. (NCT02455557)
Timeframe: Date of diagnosis to the date of first observed disease progression or death due to any cause, assessed at 6 months

Interventionpercentage of participants (Number)
Treatment (SurVaxM, Temozolomide)95

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Progression Free Survival

Progression Free Survival (PFS) is defined as the time from randomization to the event of disease recurrence/progression defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) or death due to any cause. To determine the progression free survival of subjects dosed with Vigil immunotherapy in combination with irinotecan and temozolomide. (NCT02511132)
Timeframe: Estimated median 1.3 years

InterventionParticipants (Count of Participants)
Part 1: Vigil Alone5
Part 1: Gemicitabine and Docetaxel6
Part 2: Vigil in Combination With Temozolomide and Irinotecan9

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Overall Survival

OS is defined as time from randomization to death or to the date of last follow-up. The date of last follow-up confirming survival will be used as the censoring date for subjects who are alive and/or do not have a known date of death. (NCT02511132)
Timeframe: Estimated median 2 years

InterventionParticipants (Count of Participants)
Part 1: Vigil Alone3
Part 1: Gemcitabine and Docetaxel6
Part 2: Vigil in Combination With Temozolomide and Irinotecan5

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Number of Participants With Adverse Events Determined by Laboratory Assessments and Physical Examinations

"To determine safety profile of Vigil immunotherapy in combination with irinotecan and temozolomide with 30 days of last dose in patients with metastatic Ewing's sarcoma refractory or intolerant to at least 1 prior line of systemic chemotherapy.~• To determine safety profile of Vigil immunotherapy in combination with irinotecan and temozolimidetemozolomide in patients with metastatic Ewing's sarcoma refractory or intolerant to at least 1 prior line of systemic chemotherapy." (NCT02511132)
Timeframe: 30 days of last treatment dosing

InterventionParticipants (Count of Participants)
Part 1: Vigil Alone5
Part 1: Gemcitabine and Docetaxel6
Part 2: Vigil in Combination With Temozolomide and Irinotecan9

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Deterioration Free Survival in M.D. Anderson Symptom Inventory Brain Tumor Module (MDASI-BT) Symptom Severity Score

The MDASI-BT assesses the severity of multiple brain tumor-related symptoms and the impact of these symptoms on daily functioning in the last 24 hours. It consists of 22 symptom items and 6 interference items, each rated from 0 to 10. MDASI-BT symptom severity score is defined as average over 13 core symptom items and 9 brain tumor symptom items, with a total score of 0 to 10, with higher score indicating worse symptoms/interference. Changes in symptom severity score were classified into 3 categories: improved (≤ -1), stable (> -1 and < 1), and deteriorated (≥ 1). Deterioration is defined as satisfying the deterioration criteria (i.e., increase in symptom severity score by ≥ 1 unit) without further improvement (i.e., failing to satisfy deterioration criteria) within 8 weeks or occurrence of death. (NCT02573324)
Timeframe: Overall median duration of follow-up was 15.5 months (range: 0.1, 35.6).

Interventionmonths (Median)
Placebo, Radiation and TMZ11.0
Depatuxizumab Mafodotin, Radiation and TMZ6.1

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Progression-Free Survival (PFS)

PFS will be defined as the number of days from the date of randomization to the date of earliest disease progression based on Response Assessment in Neuro-Oncology (RANO) criteria (see Wen et al. J Clin Oncol. 2010 Apr 10;28(11):1963-72) or to the date of death, if disease progression does not occur. (NCT02573324)
Timeframe: Overall median duration of follow-up was 15.5 months (range: 0.1, 35.6).

Interventionmonths (Median)
Placebo, Radiation and TMZ6.3
Depatuxizumab Mafodotin, Radiation and TMZ8.0

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PFS for EGFRvIII-Mutated Tumor Subgroup

PFS will be defined as the number of days from the date of randomization to the date of earliest disease progression based on Response Assessment in Neuro-Oncology (RANO) criteria or to the date of death, if disease progression does not occur. (NCT02573324)
Timeframe: Overall median duration of follow-up was 15.5 months (range: 0.1, 35.6).

Interventionmonths (Median)
Placebo, Radiation and TMZ5.9
Depatuxizumab Mafodotin, Radiation and TMZ8.3

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Overall Survival (OS)

Time to OS is defined as the number of days from the date of randomization to the date of death due to any cause. (NCT02573324)
Timeframe: Overall median duration of follow-up was 15.5 months (range: 0.1, 35.6).

Interventionmonths (Median)
Placebo, Radiation and TMZ18.7
Depatuxizumab Mafodotin, Radiation and TMZ18.9

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OS for the O6-methylguaninemethlytransferese (MGMT) Unmethylated Group

"Time to OS is defined as the number of days from the date of randomization to the date of death due to any cause.~Unmethylated MGMT promoter is associated with a worse prognosis in GBM" (NCT02573324)
Timeframe: Overall median duration of follow-up was 15.5 months (range: 0.1, 35.6).

Interventionmonths (Median)
Placebo, Radiation and TMZ16.2
Depatuxizumab Mafodotin, Radiation and TMZ16.1

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OS for the MGMT Methylated Group

Time to OS is defined as the number of days from the date of randomization to the date of death due to any cause. (NCT02573324)
Timeframe: Overall median duration of follow-up was 15.5 months (range: 0.1, 35.6).

Interventionmonths (Median)
Placebo, Radiation and TMZNA
Depatuxizumab Mafodotin, Radiation and TMZ25.4

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OS for the Epidermal Growth Factor Receptor (EGFR)vIII-Mutated Tumor Subgroup

Time to OS is defined as the number of days from the date of randomization to the date of death due to any cause. (NCT02573324)
Timeframe: Overall median duration of follow-up was 15.5 months (range: 0.1, 35.6).

Interventionmonths (Median)
Placebo, Radiation and TMZ18.2
Depatuxizumab Mafodotin, Radiation and TMZ19.8

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Deterioration Free Survival in Neurocognitive Functioning on the Hopkins Verbal Learning Test Revised (HVLT-R) Total Recall Score

The HVLT-R consists of 3 parts. Free call has a range of 0 to 36, delayed recall has a range from 0 to 12, and delayed recognition has a range of -12 to 12. Higher scores indicating better function in all 3 parts. When scoring the HVLT-R, the 3 learning trials are combined to calculate a total recall score (range -12 to 60). Deterioration is defined as satisfying the deterioration criteria (i.e., decrease in HVLT-R total recall score by 5 units) without further improvement within 8 weeks or occurrence of death. (NCT02573324)
Timeframe: Overall median duration of follow-up was 15.5 months (range: 0.1, 35.6).

Interventionmonths (Median)
Placebo, Radiation and TMZ13.2
Depatuxizumab Mafodotin, Radiation and TMZ10.7

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Deterioration Free Survival in MDASI-BT Symptom Interference Score

The MDASI-BT assesses the severity of multiple brain tumor-related symptoms and the impact of these symptoms on daily functioning in the last 24 hours. It consists of 22 symptom items and 6 interference items, each rated from 0 to 10. MDASI-BT symptom interference score is defined as an average of 6 interference items, with a total score of 0 to 10, where higher scores indicate worse interference. Changes in symptom interference score were classified into 3 categories: improved (≤ -1), stable (> -1 and < 1), and deteriorated (≥ 1). Deterioration is defined as satisfying the deterioration criteria (i.e., increase in symptom interference score by ≥ 1 unit) without further improvement (i.e., failing to satisfy deterioration criteria) within 8 weeks or occurrence of death. (NCT02573324)
Timeframe: Overall median duration of follow-up was 15.5 months (range: 0.1, 35.6).

Interventionmonths (Median)
Placebo, Radiation and TMZ9.7
Depatuxizumab Mafodotin, Radiation and TMZ6.1

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Kaplan-Meier Plot of Overall Survival (OS) - Extended Collection

OS was defined as the time between the date of randomization and the date of death due to any cause. A participant who has not died was censored at the last known alive date. Note: This outcome measure represents an updated version of the primary endpoint to include additional data collection that has occurred after the primary completion date (assessments were made until March 4, 2022). (NCT02617589)
Timeframe: From randomization to the date of death due to any cause (up to approximately 6 years)

InterventionMonths (Median)
Nivolumab + Radiation Therapy13.34
Temozolomide + Radiation Therapy14.92

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Kaplan-Meier Plot of Progression Free Survival

PFS was defined as the time from randomization to the date of the first documented tumor progression or death due to any cause. Participants who did not have disease progression or who did not die were censored at the date of last tumor assessment. Participants who did not have any on study tumor assessment and did not have tumor progression or die were censored at the randomization date. Participants who started any subsequent anti-cancer therapy without a prior reported progression were censored at the last tumor assessment prior to initiation of the subsequent anti-cancer therapy. Participants who had surgical resection post start of study treatment were censored at the last tumor assessment date prior to initiation of surgical resection. PFS was determined by investigator reported response based on the Radiologic Assessment in Neuro-Oncology criteria. (NCT02617589)
Timeframe: From randomization to the date of the first documented tumor progression or death due to any cause (up to approximately 6 years)

InterventionMonths (Median)
Nivolumab + Radiation Therapy6.01
Temozolomide + Radiation Therapy6.21

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Overall Survival Rate at 24 Months

The overall survival (OS) rate of (nivolumab + radiation therapy) and (temozolomide + radiation therapy) estimated as Kaplan-Meier probability of survival at 24 months. OS was defined as the time between the date of randomization and the date of death due to any cause. A participant who has not died was censored at the last known alive date. (NCT02617589)
Timeframe: At 24 Months

InterventionPercentage of participants (Number)
Nivolumab + Radiation Therapy10.6
Temozolomide + Radiation Therapy21.2

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Overall Survival (OS)

OS is defined as the time between the date of randomization and the date of death due to any cause. A participant who has not died will be censored at the last known alive date. (NCT02617589)
Timeframe: up to 3 years

InterventionMonths (Median)
Nivolumab + Radiation Therapy13.40
Temozolomide + Radiation Therapy14.88

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Progression Free Survival (PFS) (Newly Diagnosed Glioblastoma Cohort)- Phase II

Progression free survival is defined as time in weeks from start of study treatment to first documentation of objective tumor progression or up to death due to any cause, whichever occurs first. (NCT02661282)
Timeframe: At 6 months

Interventionweeks (Median)
Phase II: Newly Diagnosed Dose Level 1 x 10^819

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Progression Free Survival (PFS) (Recurrent Glioblastoma Cohort) at 6 Months- Phase II

Progression-free survival (PFS) is defined as the time from study enrollment until the time of first disease progression, relapse, or death due to disease. Patients who are alive without progression or relapse will be censored at the time of last contact. The point estimate of 6-month progression-free survival (PFS6) will be analyzed. Kaplan-Meier curves will be generated and median survival time will be derived. (NCT02661282)
Timeframe: 6 months

Interventionmonths (Number)
Phase II: Recurrent Glioblastoma Dose Level 1 x 10^82.5

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Time to Progression (Recurrent Glioblastoma Cohort)- Phase II

The length of time from the date of diagnosis or the start of treatment for a disease until the disease starts to get worse or spread to other parts of the body. (NCT02661282)
Timeframe: Baseline to disease progression, assessed up to 4 years

Interventionmonths (Number)
Phase II: Recurrent Glioblastoma Dose Level 1 x 10^82.5

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Overall Survival (OS) (Newly Diagnosed Glioblastoma Cohort)- Phase II

Overall Survival is defined as the time from definitive histological diagnosis until the time of death. (NCT02661282)
Timeframe: Time from definitive histological diagnosis until death

Interventionweeks (Median)
Phase II: Newly Diagnosed Dose Level 1 x 10^824

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Maximum Tolerated Dose (MTD) (Recurrent Glioblastoma Participant Cohort)- Phase I

The number of participants who were treated at the respective dose level without DLT (NCT02661282)
Timeframe: Up to 42 days

Interventionparticipants (Number)
Phase I: Recurrent Glioblastoma Dose Level 5 x 10^63
Phase I: Recurrent Glioblastoma Dose Level 1 x 10^73
Phase I: Recurrent Glioblastoma Dose Level 5 x 10^73
Phase I: Recurrent Glioblastoma (MTD) Dose Level 1 x 10^87

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Median Duration of Response (Newly Diagnosed Glioblastoma Cohort)- Phase II

Cox proportional hazard regression will be employed for multivariate analysis. (NCT02661282)
Timeframe: Baseline to response, assessed up to 4 years

Interventionmonths (Median)
Phase II: Newly Diagnosed Dose Level 1 x 10^85.3

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Number of Participants With Immunological Effects in Tumor Tissue (Recurrent Glioblastoma Cohort)- Phase II

Descriptive statistics will be used to summarize immunological effect. To evaluate the tumor-mediated immune suppression at the effector location, the markers (interferon, interleukin-2, and tumor necrosis factor alpha, perforin, granzyme B) will be measured for immune responses in the tumor microenvironment rather than in the peripheral blood. (NCT02661282)
Timeframe: Up to 4 years

InterventionParticipants (Count of Participants)
Phase II: Recurrent Glioblastoma Dose Level 1 x 10^81

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Overall Objective Response Rate (ORR) (Newly Diagnosed Glioblastoma Cohort)- Phase II

The number of participants with stable disease according to Response Evaluation Criteria in Solid Tumors (RECIST). (NCT02661282)
Timeframe: Up to 4 years

InterventionParticipants (Count of Participants)
Phase II: Newly Diagnosed Dose Level 1 x 10^83

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Progression-free Survival (PFS) Determined by BICR

The time from randomization to the date of the first documented tumor progression or death by any cause. PFS will be determined by a Blinded Independent Central Review (BICR) assessed based on Radiologic Assessment in Neuro-Oncology (RANO) criteria. Specifically, RANO response criteria indicates that within the first 12 weeks of completion of radiotherapy, progression can only be assessed if the majority of the new enhancement is outside of the radiation field or if there is pathologic confirmation of progressive disease. (NCT02667587)
Timeframe: From randomization to the date of the first documented tumor progression or death by any cause. (up to approximately 4.5 years)

InterventionMonths (Median)
Radiotherapy, Temozolomide Plus Nivolumab10.64
Radiotherapy, Temozolomide Plus Placebo10.32

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Progression Free Survival (PFS) Based on Investigator Assessment

The time from randomization to the date of the first documented tumor progression or death by any cause. PFS will be determined by investigator assessment based Radiologic Assessment in Neuro-Oncology (RANO) criteria. Specifically, RANO response criteria indicates that within the first 12 weeks of completion of radiotherapy, progression can only be assessed if the majority of the new enhancement is outside of the radiation field or if there is pathologic confirmation of progressive disease. (NCT02667587)
Timeframe: From randomization to the date of the first documented tumor progression or death by any cause. (up to approximately 4.5 years)

InterventionMonths (Median)
Radiotherapy, Temozolomide Plus Nivolumab14.09
Radiotherapy, Temozolomide Plus Placebo15.18

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Overall Survival (OS) Rates at 12 Months

Overall Survival (OS) rate is defined as the percentage of participants surviving at 12 months (NCT02667587)
Timeframe: From randomization to 12 months after first dose

Interventionpercentage of participants (Number)
Radiotherapy, Temozolomide Plus Nivolumab82.7
Radiotherapy, Temozolomide Plus Placebo87.7

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Overall Survival (OS)

The time from the date of randomization to the date of death. who have not died by the end of the study will be censored to last known date alive. OS is assessed in the randomized population with no corticosteroids at baseline population and in the overall randomized population. (NCT02667587)
Timeframe: From randomization to date of death (up to approximately 4.5 years)

,
InterventionMonths (Median)
All randomized participantsAll randomized participants without baseline corticosteroids
Radiotherapy, Temozolomide Plus Nivolumab28.9131.34
Radiotherapy, Temozolomide Plus Placebo32.0732.99

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Overall Survival (OS) Rates at 24 Months

Overall Survival (OS) rate is defined as the percentage of participants surviving at 24 months (NCT02667587)
Timeframe: From randomization to 24 months after first dose

Interventionpercentage of participants (Number)
Radiotherapy, Temozolomide Plus Nivolumab55.9
Radiotherapy, Temozolomide Plus Placebo63.3

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Median Time to Progression (TTP) Assessed Locally and Centrally

The TTP was defined as the time from first treatment administration to the first objective tumor progression (PD) according to RECIST criteria v 1.1. The TTP was assessed locally by the investigator and centrally by an independent radiologist. The distribution of TTP times was estimated using the Kaplan-Meier method. The TTP of participants who were lost to follow-up, and those who had not progressed at end of study were censored at the date of the last disease assessment. (NCT02698410)
Timeframe: From Day 1 up to end of study, 52 weeks

Interventionweeks (Median)
Local assessmentCentral assessment
Lanreotide ATG Plus Temozolomide37.137.1

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Median Progression Free Survival (PFS) Assessed Locally and Centrally

The PFS was defined as the time from the first treatment administration to disease progression according to RECIST criteria v 1.1 or death from any cause. The PFS was assessed locally by the investigator and centrally by an independent radiologist. The distribution of PFS times was estimated using the Kaplan-Meier method. The PFS of participants who were lost to follow-up and those who had not progressed at end of study were censored at the date of the last disease assessment. (NCT02698410)
Timeframe: From Day 1 up to end of study, 52 weeks

Interventionweeks (Median)
Local assessmentCentral assessment
Lanreotide ATG Plus Temozolomide37.137.1

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DCR Assessed Centrally at Month 9

The DCR was defined as SD, PR or CR according to RECIST criteria v1.1. A second set of the original computed tomography (CT) scan images were used for a centralized RECIST v1.1 assessment by an independent radiologist. (NCT02698410)
Timeframe: Up to Month 9

Interventionpercentage of participants (Number)
Lanreotide ATG Plus Temozolomide28.2

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Median Time to Response (TTR) Assessed Locally and Centrally

The TTR was defined as the time from first treatment administration to the first objective tumor response (PR or CR according to RECIST criteria v 1.1). The TTR was assessed locally by the investigator and centrally by an independent radiologist. The distribution of TTR was estimated using the Kaplan-Meier method. The TTR of participants who were lost to follow-up or died prior to any objective tumor response were censored at the date of the last disease assessment. (NCT02698410)
Timeframe: From Day 1 up to end of study, 52 weeks

Interventionweeks (Median)
Local assessmentCentral assessment
Lanreotide ATG Plus TemozolomideNANA

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Neuron-Specific Enolase (NSE) and CgA Biomarker Levels

The NSE and CgA levels were classified according to ULN as follows: < 1 ULN, 1-2 ULN and > 2 ULN. Baseline was defined as value at Day 1. Percentages are based on the number of participants in the ITT/Safety population who attended the visit with non-missing observations. (NCT02698410)
Timeframe: Baseline and Weeks 4, 12, 24, 36 and 52

Interventionpercentage of participants (Number)
CgA: Baseline: <1 ULNCgA: Baseline: 1-2 ULNCgA: Baseline: >2 ULNCgA: Week 4: <1 ULNCgA: Week 4: 1-2 ULNCgA: Week 4: >2 ULNCgA: Week 12: <1 ULNCgA: Week 12: 1-2 ULNCgA: Week 12: >2 ULNCgA: Week 24: <1 ULNCgA: Week 24: 1-2 ULNCgA: Week 24: >2 ULNCgA: Week 36: <1 ULNCgA: Week 36: 1-2 ULNCgA: Week 36: >2 ULNCgA: Week 52: <1 ULNCgA: Week 52: 1-2 ULNCgA: Week 52: >2 ULNNSE: Baseline: <1 ULNNSE: Baseline: 1-2 ULNNSE: Baseline: >2 ULNNSE: Week 4: <1 ULNNSE: Week 4: 1-2 ULNNSE: Week 4: >2 ULNNSE: Week 12: <1 ULNNSE: Week 12: 1-2 ULNNSE: Week 12: >2 ULNNSE: Week 24: <1 ULNNSE: Week 24: 1-2 ULNNSE: Week 24: >2 ULNNSE: Week 36: <1 ULNNSE: Week 36: 1-2 ULNNSE: Week 36: >2 ULNNSE: Week 52: <1 ULNNSE: Week 52: 1-2 ULNNSE: Week 52: >2 ULN
Lanreotide ATG Plus Temozolomide40.015.045.034.322.942.946.417.935.730.025.045.031.312.556.327.39.163.665.025.010.062.925.711.478.617.93.680.010.010.087.56.36.363.618.218.2

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Percentage of Biochemical Responders According to Chromogranin A (CgA) Plasma Levels

Participants with baseline CgA plasma levels greater than the upper limit of normal (ULN) were assessed for a biochemical response. A biochemical responder was defined as a participant who had a decrease of CgA >= 50% compared to baseline, while biochemical SD was defined as a decrease < 50% or an increase <= 25% compared to baseline. Biochemical non-responders had an increase >25% compared to baseline. Baseline was defined as value at Day 1. (NCT02698410)
Timeframe: Baseline (Day 1) and Week 4, 12, 24, 36 and 52

Interventionpercentage of participants (Number)
Week 4: RespondersWeek 4: SDWeek 4: Non-respondersWeek 12: RespondersWeek 12: SDWeek 12: Non-respondersWeek 24: RespondersWeek 24: SDWeek 24: Non-respondersWeek 36: RespondersWeek 36: SDWeek 36: Non-respondersWeek 52: RespondersWeek 52: SDWeek 52: Non-responders
Lanreotide ATG Plus Temozolomide27.359.113.637.537.525.023.130.846.236.427.336.412.550.037.5

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Best Overall Response (BOR) Assessed Locally and Centrally

The BOR was defined as the highest OR achieved by the participant from the time of first treatment until disease progression/recurrence or the end of study according to RECIST criteria v1.1 and was classified as: CR > PR > Non-CR/Non-progressive disease (NCR/NPD) > SD > PD > ND > not evaluable (NE). The BOR was assessed locally by the investigator and centrally by an independent radiologist. Percentages are based on the number of participants in the ITT/Safety population with non-missing observations. (NCT02698410)
Timeframe: From Day 1 up to end of study, 52 weeks

Interventionpercentage of participants (Number)
Local assessment: CRLocal assessment: PRLocal assessment: SDLocal assessment: NCR/NPDLocal assessment: PDLocal assessment: NELocal assessment: Not applicableCentral assessment: CRCentral assessment: PRCentral assessment: SDCentral assessment: NCR/NPDCentral assessment: PDCentral assessment: NECentral assessment: Not applicable
Lanreotide ATG Plus Temozolomide07.771.8020.500013.265.82.615.802.6

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DCR Assessed Locally and Centrally at Month 12

The DCR was defined as SD, PR or CR according to RECIST criteria v1.1. The DCR was assessed locally by the investigator and centrally by an independent radiologist. (NCT02698410)
Timeframe: Month 12

Interventionpercentage of participants (Number)
Local assessmentCentral assessment
Lanreotide ATG Plus Temozolomide17.515.4

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Disease Control Rate (DCR) Assessed Locally at Month 9

Responders were participants who showed disease control according to Response Evaluation Criteria in Solid Tumors (RECIST) criteria v 1.1 assessed locally by the investigator. The DCR was defined as complete response (CR), partial response (PR) or stable disease (SD) according to RECIST criteria v1.1. A sensitivity analysis-1 of local DCR was performed excluding participants withdrawn before 9 months with reason other than progressive disease (PD) or missing assessment and considering participants with PD prior or at 9 months as failures. In addition, a sensitivity analysis-2 was performed in order to consider assessments done between 7.5 and 10.5 months as 9 months assessments when 9-month assessment was missing using same methodology, i.e. considering PD prior or at 9 months and participants withdrawn with other or missing reasons as failures. (NCT02698410)
Timeframe: Up to Month 9; for sensitivity analysis-2, up to 10.5 months

Interventionpercentage of participants (Number)
DCR at Month 9Sensitivity analysis-1Sensitivity analysis-2
Lanreotide ATG Plus Temozolomide35.045.245.0

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DCR Assessed Locally and Centrally at Month 9 by Carcinoid Type

The influence of type of carcinoid [typical, atypical and undetermined carcinoid neuroendocrine tumors (NET)] on the local and central DCR at 9 months was analysed. Typical carcinoids were defined with absent foci of necrosis and mitotic count < 2 mitoses/2 millimeters^2 (mm^2); atypical carcinoids were defined with presence of foci of necrosis and/or 2 mitoses/2 mm^2 <= mitotic count <= 10 mitoses/2 mm^2; and carcinoid NET were defined as confirmed carcinoid without foci of necrosis and/or mitotic count reported. The DCR was assessed locally by the investigator and centrally by an independent radiologist. (NCT02698410)
Timeframe: Up to Month 9

Interventionpercentage of participants (Number)
Local assessment: Typical carcinoidLocal assessment: Atypical carcinoidLocal assessment: Carcinoid NETCentral assessment: Typical carcinoidCentral assessment: Atypical carcinoidCentral assessment: Carcinoid NET
Lanreotide ATG Plus Temozolomide12.547.627.3035.036.4

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Coefficient of Agreement Between Central and Local Assessment of Tumor Radiological Response at Month 9

Differences between central radiology review and local investigator review were assessed according to the DCR status and the number of agreements and disagreements between the evaluators (central versus local) along with the p-values from the kappa test. A kappa statistic was used to evaluate the concordance between the central and the local review. (NCT02698410)
Timeframe: Month 9

Interventionkappa coefficient (Number)
Lanreotide ATG Plus Temozolomide0.71

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Objective Response Rate (ORR) Assessed Locally and Centrally at Months 9 and 12

The ORR was defined as the percentage of participants with CR or PR according to RECIST criteria v1.1. The ORR was assessed locally by the investigator and centrally by an independent radiologist. The ORR was based on the participants with PD prior to 9 and 12 months with respectively PD at 9 and 12 months, and participants withdrawn before the assessment for reason other than PD or missing as failures. (NCT02698410)
Timeframe: Months 9 and 12

Interventionpercentage of participants (Number)
Local assessment: Month 9Local assessment: Month 12Central assessment: Month 9Central assessment: Month 12
Lanreotide ATG Plus Temozolomide2.52.55.12.6

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Influence of Biomarkers Expression on Locally and Centrally Assessed DCR at Months 9 and 12

The following biomarkers were investigated: Immunohistochemistry assay SSTR2 including HER-2 score (0, 1+, 2+, 3+ and +ve versus -ve); H-score (from 0 to 300 as quantitative variable and +ve versus -ve); IRS score (from 0 to 12 and reference for odds ratio was 0-1). Ki67 index (from 0% to 100% and reference for odds ratio was 4%-25%). MGMT expression including percentage of +ve nuclei stained and methylated sites and H-score (from 0 to 300 as quantitative variable). For all these categories, higher score indicates a higher expression of biomarkers. Carcinoid type (typical or NET) was also investigated. Prognostic value of biomarkers expression at screening on DCR were assessed locally and centrally using univariate logistic regression models. (NCT02698410)
Timeframe: Screening period, Months 9 and 12

Interventionodds ratio (Number)
Month 9: Local: SSTR2: HER-2 score; +ve (2+, 3+)Month 9: Local: SSTR2: H-score; +ve (>= 50)Month 9: Local: SSTR2: IRS score; 2-3Month 9: Local: SSTR2: IRS score; 4-8Month 9: Local: SSTR2: IRS score; 9-12Month 9: Local: Ki67: <4Month 9: Local: Ki67: >=25Month 9:Local: MGMT: +ve nuclei stained; +ve(>=5%)Month 9: Local: MGMT: Methylated sites; +ve (>10%)Month 9: Local: MGMT: H-scoreMonth 9: Local: Carcinoid type: TypicalMonth 9: Local: Carcinoid type: Carcinoid NETMonth 9: Central: SSTR2: HER-2 score; +ve (2+, 3+)Month 9: Central: SSTR2: H-score; +ve (>= 50)Month 9: Central: SSTR2: IRS score; 2-3Month 9: Central: SSTR2: IRS score; 4-8Month 9: Central: SSTR2: IRS score; 9-12Month 9: Central: Ki67: <4Month 9: Central: Ki67: >=25Month 9:Central:MGMT:+ve nuclei stained; +ve(>=5%)Month 9:Central: MGMT: Methylated sites; +ve(>10%)Month 9: Central: MGMT: H-scoreMonth 9: Central: Carcinoid type: TypicalMonth 9: Central: Carcinoid type: Carcinoid NETMonth 12: Local: SSTR2: HER-2 score; +ve (2+, 3+)Month 12: Local: SSTR2: H-score; +ve (>= 50)Month 12: Local: SSTR2: IRS score; 2-3Month 12: Local: SSTR2: IRS score; 4-8Month 12: Local: SSTR2: IRS score; 9-12Month 12: Local: Ki67: <4Month 12: Local: Ki67: >=25Month 12:Local:MGMT: +ve nuclei stained; +ve(>=5%)Month 12: Local: MGMT: Methylated sites; +ve(>10%)Month 12: Local: MGMT: H-scoreMonth 12: Local: Carcinoid type: TypicalMonth 12: Local: Carcinoid type: Carcinoid NETMonth 12: Central: SSTR2: HER-2 score; +ve(2+, 3+)Month 12: Central: SSTR2: H-score; +ve (>= 50)Month 12: Central: SSTR2: IRS score; 2-3Month 12: Central: SSTR2: IRS score; 4-8Month 12: Central: SSTR2: IRS score; 9-12Month 12: Central: Ki67: <4Month 12: Central: Ki67: >=25Month 12:Central:MGMT:+ve nuclei stained;+ve(>=5%)Month 12:Central: MGMT: Methylated sites;+ve(>10%)Month 12: Central: MGMT: H-scoreMonth 12: Central: Carcinoid type: TypicalMonth 12: Central: Carcinoid type: Carcinoid NET
Lanreotide ATG Plus Temozolomide0.900.78NA0.6712.00NA1.67NA3.250.990.160.411.402.253.000.6712.00NANA0.505.001.00NA1.063.004.40NA0.7010.50NANA0.202.130.990.460.322.083.00NANA10.50NANA0.143.000.990.570.40

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Influence of Biomarkers Expression on Locally and Centrally Assessed PFS

The following biomarkers were investigated: Immunohistochemistry assay human somatostatin receptors 2 (SSTR2) including human epidermal growth factor receptor 2 (HER-2) score [0, 1+, 2+, 3+ and positive (+ve) versus negative (-ve)]; hormone receptor score (H-score) (from 0 to 300 as quantitative variable and +ve versus -ve); immunoreactive score (IRS) score (from 0 to 12 and reference for hazard ratio was 0-1). Ki67 index (from 0% to 100% and reference for hazard ratio was 4%-25%). O^6-methylguanine-DNA methyltransferase (MGMT) expression including percentage of +ve nuclei stained and methylated sites and H-score (from 0 to 300 as quantitative variable). For all these categories, higher score indicates a higher expression of biomarkers. Carcinoid type (typical or NET) was also investigated. Prognostic value of biomarkers expression at screening on PFS were assessed locally and centrally using univariate cox proportional hazard models. (NCT02698410)
Timeframe: From Screening period (-4 weeks) up to Week 52

Interventionhazard ratio (Number)
Local: SSTR2: HER-2 score; +ve (2+, 3+)Local: SSTR2: H-score; +ve (>= 50)Local: SSTR2: IRS score; 2-3Local: SSTR2: IRS score; 4-8Local: SSTR2: IRS score; 9-12Local: Ki67: <4Local: Ki67: >=25Local: MGMT: +ve nuclei stained; +ve (>=5%)Local: MGMT: Methylated sites; +ve (>10%)Local: MGMT: H-scoreLocal: Carcinoid type: TypicalLocal: Carcinoid type: Carcinoid NETCentral: SSTR2: HER-2 score; +ve (2+, 3+)Central: SSTR2: H-score; +ve (>= 50)Central: SSTR2: IRS score; 2-3Central: SSTR2: IRS score; 4-8Central: SSTR2: IRS score; 9-12Central: Ki67: <4Central: Ki67: >=25Central: MGMT: +ve nuclei stained; +ve (>=5%)Central: MGMT: Methylated sites; +ve (>10%)Central: MGMT: H-scoreCentral: Carcinoid type: TypicalCentral: Carcinoid type: Carcinoid NET
Lanreotide ATG Plus Temozolomide0.710.660.310.900.121.081.682.060.411.001.051.590.500.360.780.880.100.002.752.110.731.000.990.61

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Median Duration of Response (DOR) Assessed Locally and Centrally

The DOR was defined as the time from onset of the first objective tumor response (PR or CR) to objective tumor progression (PD) according to RECIST criteria v 1.1. The DOR was assessed locally by the investigator and centrally by an independent radiologist. (NCT02698410)
Timeframe: From Day 1 up to end of study, 52 weeks

Interventionweeks (Median)
Local assessmentCentral assessment
Lanreotide ATG Plus TemozolomideNANA

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Median Change in Tumor Volume From Baseline to Mid-radiation Treatment (Week 4)

Tumor volume will be measured by diffusion MRI and perfusion MRI before treatment start and at mid-treatment. (NCT02805179)
Timeframe: Baseline to Week 4

Interventioncubic centimeters (Median)
High Dose Chemoradiation-2.9

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Median Progression-free Survival

From start of RT until disease progression or death, or until date of last imaging follow-up, estimated using Kaplan-Meier. Progression is defined by any of the following: >= 25% increase in sum of the products of perpendicular diameters of enhancing lesions (compared with baseline if no decrease) on stable or increasing doses of corticosteroids; a significant increase in T2/FLAIR non-enhancing lesions on stable or increasing doses of corticosteroids compared with baseline scan or best response after initiation of therapy, not due to comorbid events; appearance of any new lesions; clear progression of non-measurable lesions; or definite clinical deterioration not attributable to causes other than tumor, or to decrease in corticosteroid dose. When pathologic confirmation was unavailable, progression was defined as worsening enhancement based on imaging with or without adjunctive advanced imaging including perfusion MRI or magnetic resonance spectroscopy, when clinically indicated. (NCT02805179)
Timeframe: Median follow-up time was 26 months

Interventionmonths (Median)
all eligible patients who completed dose-intensified chemo-radiationonly patients who were boosted to both diffusion and perfusion
High Dose Chemoradiation1012

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Percentage of Patients With Failure; Central or In-field vs. Marginal or Distant

"Failures will be classified as central or in-field, marginal or distant based on previously published criteria. 1) central, in which 95% or more of the recurrent tumor volume (Vrecur) was within D95, the region treated to high dose (95% of the prescription dose); 2) in-field, in which 80% or more of Vrecur was within the D95 isodose surface; 3) marginal, when between 20 and 80% of Vrecur was inside the D95 surface; 4) outside, in which less than 20% of Vrecur was inside the D95 surface." (NCT02805179)
Timeframe: Median 26 months

Interventionpercentage of participants (Number)
central or in-fieldnon-central/non-in-field (marginal or distant)
High Dose Chemoradiation3169

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Percentage of Patients That Experienced Deterioration in Quality of Life (QOL)

Percentage of patients that experienced deterioration in QOL per the European Organization for Research and Treatment of Cancer, Quality of Life Questionnaire (EORTC QLQ-C30). EORTC QLQ-C30 is a 30-item questionnaire to assess the overall quality of life in cancer patients. EORTC QLQ-C30 includes functional scales (physical, role, cognitive, emotional, and social), global health status, symptom scales (fatigue, pain, nausea/vomiting), and other (dyspnea, 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 are averaged, and transformed to 0-100 scale; higher score=better level of physical functioning. (NCT02805179)
Timeframe: Baseline to 1 and 7 months

Interventionpercentage of participants (Number)
at 1 monthat 7 months
High Dose Chemoradiation2633

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Overall Survival at 12 Months

Percentage of patients alive at 12 months after completion of chemoradiation (NCT02805179)
Timeframe: 12 months after completion of chemoradiation

Interventionpercentage of participants (Number)
all eligible patients who completed dose-intensified chemo-radiationonly patients who were boosted to both diffusion and perfusion
High Dose Chemoradiation7492

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Median Overall Survival

Median overall survival in months (NCT02805179)
Timeframe: Median follow-up time was 26 months

Interventionmonths (Median)
all eligible patients who completed dose-intensified chemo-radiationonly patients who were boosted to both diffusion and perfusion
High Dose Chemoradiation2020

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Immunologic Response as Measured by Peak Number of T Cells That Secrete IFNγ by ELISPOT in Response to Component A of PEP-CMV

"The primary analysis will focus on patients who have follow-up immunologic monitoring after the 3rd vaccination with component A alone and before initiation of the second TMZ/vaccine cycle. Such a patient is considered evaluable for the immunologic response primary analyses.~The Wilcoxon rank sum test will compare treatment groups with regard to the median peak number of T cells that secrete IFNγ by ELISPOT in response to component A of PEP-CMV. Analyses will include only those patients who have an assessment of immune response after receiving 3 vaccinations." (NCT02864368)
Timeframe: Through study completion, an average of 1.5 years

InterventionT cells (Median)
5-day TMZ: Component A Alone57.5
21-day TMZ: Component A Alone71.25

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% of Participants Free of Disease Progression at 4mos Treated w/Zotiraciclib at the Maximum Tolerated Dose in Combination Temozolomide w/Dose Dense Temozolomide Schedules in Adult Patients With Recurrent Anaplastic Astrocytoma or Glioblastoma/Gliosarcoma

We first determined the maximum tolerated dose (MTDs) in each ARM and we then performed the cohort expansion at the MTD in both ARMs separately, until we treated a total of 18 participants at this dose in each ARM. PFS is defined as the duration of time from start of registration to time of progression or death, whichever comes first. Progression was assessed by the Response Assessment in Neuro-Oncology Criteria (RANO). Progression is ≥25% increase in tumor volume compared to baseline in the sum of the products of perpendicular diameters of enhancing lesions compared with the smallest measurement obtained either at baseline or best response with the participant on stable or increasing doses of steroids. Significant increase in T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) non-enhancing lesions with the participant on stable or increasing doses of steroids (not caused by comorbid events). Any new lesions. (NCT02942264)
Timeframe: 4 months

Interventionpercentage of participants (Number)
All Participants40

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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. (NCT02942264)
Timeframe: Date treatment consent signed to date off study, approximately 15mo(m)/8days(d), 26m, 7m/26d, 13m/17d, 11m/30d, 12m/6d, 19m/11d, 9m/28d and 18m/21d for Group 1-9 respectively.

InterventionParticipants (Count of Participants)
ARM 1 Dose Level 0 - (Starting Dose)6
ARM 1 Dose Level 1 - (Dose Escalation)13
ARM 2 Dose Level 0 (Starting Dose)3
ARM 2 Dose 1 - (Dose Escalation)6
ARM 2 Dose 0 - (Dose De-escalation)3
ARM 2 Dose Level II - (Dose Escalation)2
ARM 2 Dose Level I - (Dose De-escalation)7
ARM 1 Dose Level 1 (MTD Level in ARM1)6
ARM 2 Dose Level 1 (MTD Level in ARM2)7

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Phase I: Maximum Tolerated Dose (MTD) of Zotiraciclib (TG02) in Combination of Metronomic (mn) Temozolomide (TMZ) in Adult Patients With Recurrent Anaplastic Astrocytoma or Glioblastoma/Gliosarcoma

Maximum tolerated dose of metronomic (mn) Zotiraciclib (TG02) was assessed using the Bayesian Optimal Interval (BOIN) design. The MTD is defined as the dose for which the isotonic estimate of the toxicity rate is closest to the target toxicity rate of 0.35. If there are ties, we select the higher dose level when the isotonic estimate is lower than the target toxicity rate; and we select the lower dose level when the isotonic estimate is greater than the target toxicity rate of 0.35. (NCT02942264)
Timeframe: 4 weeks after initiation of treatment

Interventionmg/day (Number)
All Participants250

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Phase I: Maximum Tolerated Dose (MTD) of Zotiraciclib in Combination With Dose Dense (dd) Temozolomide (TMZ) in Adult Patients With Recurrent Anaplastic Astrocytoma or Glioblastoma/Gliosarcoma

Maximum tolerated dose of Zotiraciclib (TG02) in combination with dose dense Temozolomide (TMZ) was assessed using the Bayesian Optimal Interval (BOIN) design. The MTD is defined as the dose for which the isotonic estimate of the toxicity rate is closest to the target toxicity rate of 0.35. If there are ties, we select the higher dose level when the isotonic estimate is lower than the target toxicity rate; and we select the lower dose level when the isotonic estimate is greater than the target toxicity rate of 0.35. (NCT02942264)
Timeframe: 4 weeks after initiation of treatment

Interventionmg/day (Number)
All Participants250

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Phase I: Number of Participants With a Dose-limiting Toxicity (DLT)

DLT is defined as any adverse events attributed to the study drug. For example, Grade 4 neutropenia lasting 5 days or more. Febrile neutropenia defined as grade 3-4 neutropenia with fever ≥38.5ºC and/or infection requiring antibiotic or antifungal treatment. Nausea or vomiting that responds to symptomatic therapy and lasts ≤7 days. Fatigue that responds to symptomatic therapy and lasts ≤7 days. And weight gain (in patients on steroids). (NCT02942264)
Timeframe: 4 weeks after initiation of treatment

InterventionParticipants (Count of Participants)
ARM 1 Dose Level 0 - (Starting Dose)1
ARM 1 Dose Level 1 - (Dose Escalation)3
ARM 2 Dose Level 0 (Starting Dose)0
ARM 2 Dose 1 - (Dose Escalation)3
ARM 2 Dose 0 - (Dose De-escalation)1
ARM 2 Dose Level II - (Dose Escalation)1
ARM 2 Dose Level I - (Dose De-escalation)4

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% of Participants Free of Disease Progression at 4mos Treated w/Zotiraciclib at the Maximum Tolerated Dose (MTD) in Combination With the Metronomic (mn) Temozolomide (TMZ) in Adult Patients With Recurrent Anaplastic Astrocytoma or Glioblastoma/Gliosarcoma

We first determined the MTDs in each ARM and we then performed the cohort expansion at the MTD in both ARMs separately, until we treated a total of 18 participants at this dose in each ARM. PFS is defined as the duration of time from start of registration to time of progression or death, whichever comes first. Progression was assessed by the Response Assessment in Neuro-Oncology Criteria (RANO). Progression is ≥25% increase in tumor volume compared to baseline in the sum of the products of perpendicular diameters of enhancing lesions compared with the smallest measurement obtained either at baseline or best response with the participant on stable or increasing doses of steroids. Significant increase in T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) non-enhancing lesions with the participant on stable or increasing doses of steroids (not caused by comorbid events). Any new lesions. (NCT02942264)
Timeframe: 4 months

Interventionpercentage of participants (Number)
All Participants25

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Area Under the Serum of Nanoparticle Albumin-bound Rapamycin Concentration Curve

Median with minimum and maximum values of the area under the drug concentration over time curve stratified by dose level. (NCT02975882)
Timeframe: Days 1, 2, 3, 4, and 8

Interventionhr*ng/mL (Mean)
Stratum Cohort With Dose Level 113654
Stratum Cohort With Dose Level -19532
Stratum Cohort With Dose Level -28666
PK Cohort With Dose Level -27988.5

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Number of Patients With Cycle 1 and 2 Dose Limiting Toxicities Attributable to Nanoparticle Albumin-bound Rapamycin

Number of patients with cycle 1 and 2 dose limiting toxicities possibly, probably, or definitely attributable with nanoparticle albumin-bound rapamycin stratified by dose level. (NCT02975882)
Timeframe: Up to 42 days

InterventionParticipants (Count of Participants)
Stratum Cohort With Dose Level 11
Stratum Cohort With Dose Level -12
Stratum Cohort With Dose Level -21
PK Cohort With Dose Level -21

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Number of Patients With Adverse Events

The number of patients with adverse events that are at least possibly attributable to nanoparticle albumin-bound rapamycin stratified by dose level. (NCT02975882)
Timeframe: Up to 24 months

InterventionParticipants (Count of Participants)
Stratum Cohort With Dose Level 14
Stratum Cohort With Dose Level -112
Stratum Cohort With Dose Level -28
PK Cohort With Dose Level -25

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Number of Patients With Antitumor Activity of Nanoparticle Albumin-bound Rapamycin

The number of response-evaluable patients with best overall response of complete response (CR), disappearance of all target lesions; or partial response (PR), >=50% decrease in the sum of the products of the two perpendicular diameters of all target lesions (up to 5), while on study therapy stratified by dose level; Overall response (OR)=CR+PR. (NCT02975882)
Timeframe: Up to 24 months

InterventionParticipants (Count of Participants)
Stratum Cohort With Dose Level 11
Stratum Cohort With Dose Level -10
Stratum Cohort With Dose Level -20
PK Cohort With Dose Level -20

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Objective Response Rate

ORR will be defined as the percentage of patients with complete response (CR) or partial response (PR) according to the RANO criteria. (NCT03034135)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Complete responsePartial Response
DSF-Cu00

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Overall Survival

Percentage of patients that are alive (NCT03034135)
Timeframe: 6 months and 12 months

Interventionpercentage of participants (Number)
6 months12 months
DSF-Cu6135

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Median Duration of Overall Survival

Duration of overall survival for patients that are alive (NCT03034135)
Timeframe: 14 months

Interventionmonths (Median)
DSF-Cu7.1

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Progression Free Survival

Percentage of patients that are free from progressive disease per RANO criteria (NCT03034135)
Timeframe: 6 months

Interventionpercentage of participants (Number)
DSF-Cu14

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Median Progression Free Survival

Duration of progression free survival according to RANO criteria (NCT03034135)
Timeframe: 12 months

Interventionmonths (Median)
DSF-Cu1.7

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Number of Participants With Serious Adverse Events

Number of Participants with Grade 3 and 4 serious adverse events (NCT03034135)
Timeframe: 14 months

InterventionParticipants (Count of Participants)
DSF-Cu2

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Toxicities

Treatment emergent toxicities of nanoliposomal irinotecan with continuous low-dose temozolomide using CTCAE version 4.03, grades 2 through 4 (NCT03119064)
Timeframe: Baseline through 30 days post off study treatment

,
Interventionevents (Number)
NeutropeniaALT/ASTHypokalemiaHypophosphatemiaNauseaFatigueDiarrheaAnorexiaDehydrationUrticaria
Dose 10211120001
Dose 21110222220

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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." (NCT03119064)
Timeframe: Every 2 months on study treatment then very 3 months once treatment has stopped, until progression of disease up to 2 years.

,
Interventionparticipants (Number)
Partial ResponseProgressive Disease
Dose 118
Dose 212

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Determination of Maximum Tolerated Dose (MTD)

To evaluate the maximum tolerated dose of nanoliposomal irinotecan with continuous low-dose temozolomide for patients with recurrent glioblastoma. (NCT03119064)
Timeframe: Every two weeks for 4 weeks

Interventionmg/m^2 (Number)
All Participants50

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Time to Progression

Percentage change of the Cho/NAA, ADC and nCBV from baseline to the end of radiation therapy, RT will be used for assessment of time to progression. (NCT03168919)
Timeframe: From Baseline through 24 months.

Interventiondays (Mean)
Chemoradiation Arm465

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Changes of Tumor Angiogenesis

Perfusion MRI will be used for assessment of tumor angiogenesis (with median normalized cerbral blood volume, nCBV) during the course of fractionated radiation treatment. (NCT03168919)
Timeframe: From baseline to 6 weeks

InterventionmL/100 gm of brain tissue (Mean)
baselineEarly in therapy (At 2 weeks in therapy)Late therapy (At 4 weeks in therapy)At completion (At 6 weeks from baseline)
Chemoradiation Arm3.783.351.581.2

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Changes of Tumor Cellularity

Diffusion MRI will be used for assessment of measures tumor cellularity (with minimum apparent diffusion co-efficent, ADC) during the course of fractionated radiation treatment. (NCT03168919)
Timeframe: From baseline to 6 weeks

Interventionmm^2/sec (Mean)
BaselineEarly in therapy (At 2 weeks in therapy)Late therapy (At 4 weeks in therapy)At completion (At 6 weeks from baseline)
Chemoradiation Arm0.0006750.0007980.0008420.001144

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Changes of Tumor Volume

MRI will be used for assessment of measures tumor volume. (NCT03168919)
Timeframe: From baseline Up to 6 weeks

Interventioncm3 (Mean)
BaselineEarly in therapy (At 2 weeks in therapy)Late therapy (At 4 weeks in therapy)At completion (At 6 weeks from baseline)
Chemoradiation Arm6.13.792.662.16

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Phase I: 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. (NCT03190967)
Timeframe: Date treatment consent signed to date off study, approximately 44 months and 27 days for level 1, 28 months and 10 days for level 2, and 40 months and 8 days for level 3.

InterventionParticipants (Count of Participants)
Level 1 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 30 mg/m^23
Level 2 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 40 mg/m^23
Level 3 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 50 mg/m^26

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Phase I: Number of Participants With Dose Limiting Toxicity (DLTs) at Each Dose Level

Number of participants with DLTs at each dose level 30 days after treatment. A DLT is defined as grade 3 or higher non-hematologic adverse events excluding grade 3 hypertension controlled with anti-hypertensive therapy; or grade 3 asymptomatic electrolytes imbalance; grade 3 endocrinopathy; grade 3 asymptomatic increase in aspartate aminotransferase or alanine aminotransferase; and transient (lasting less than <48 hours) nausea, emesis, or diarrhea if corrected with conservative measures within 24-48 hours. A hematologic grade 4 neutropenia of ≥ 7 days duration, grade ≥ 3 thrombocytopenia, and all other grade 4 hematologic toxicities excluding grade 4 lymphopenia, or leukopenia in the absence of grade 3 or higher neutropenia. Grade 3 is severe. Grade 4 is life-threatening. (NCT03190967)
Timeframe: After first cycle of treatment, up to 30 days

InterventionParticipants (Count of Participants)
Level 1 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 30 mg/m^20
Level 2 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 40 mg/m^20
Level 3 Phase I:Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 50 mg/m^20

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Phase I: Standard Time to Progression (TTP)

TTP is the time between the first day of treatment to the day of disease progression. Progression was assessed using the Response Evaluation Criteria in Solid Tumors (RECIST). Progression is at least a 25% increase in the sum of products of all measurable lesions over smallest sum observed, clear worsening of any evaluable disease, appearance of any new lesion/site, or failure to return for evaluation due to death or deteriorating condition. (NCT03190967)
Timeframe: From first day of treatment to the day of disease progression, an average of 15 months.

InterventionMonths (Mean)
Level 1 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 30 mg/m^26.95
Level 2 Phase I:Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 40 mg/m^216.26
Level 3 Phase I:Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 50 mg/m^217.46

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Phase I: Median Survival

Median amount of time participants survives after therapy. Survival compared between the two arms and Kaplan-Meier curves constructed with a two-tailed log-rank test used to compare the arms. (NCT03190967)
Timeframe: From date of first therapy until death, an average of 40.79 months

InterventionMonths (Median)
Level 1 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 30 mg/m^237.8
Level 2 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 40 mg/m^248.4
Level 3 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 50 mg/m^238.5

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Phase I: Maximum Tolerated Dose (MTD) of Temozolomide (TMZ) When Used With T-DM1 (Ado-trastuzumab)

Maximum tolerated dose of TMZ when used in combination with T-DM1. MTD is defined as the dose level at which 0 or 1 participant in 6 has a dose limiting toxicity (DLT). A DLT is defined as grade 3 or higher non-hematologic adverse events excluding grade 3 hypertension controlled with anti-hypertensive therapy; or grade 3 asymptomatic electrolytes imbalance; grade 3 endocrinopathy; grade 3 asymptomatic increase in aspartate aminotransferase or alanine aminotransferase; and transient (lasting less than <48 hours) nausea, emesis, or diarrhea if corrected with conservative measures within 24-48 hours. A hematologic grade 4 neutropenia of ≥ 7 days duration, grade ≥ 3 thrombocytopenia, and all other grade 4 hematologic toxicities excluding grade 4 lymphopenia, or leukopenia in the absence of grade 3 or higher neutropenia. Grade 3 is severe. Grade 4 is life-threatening. (NCT03190967)
Timeframe: first 21 days of treatment

Interventionmg/m^2 (Number)
All Participants40

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Phase I: Number of Participants With Grade 3 and/or Grade 4 Adverse Events

Adverse events were assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0). Grade 3 is severe. Grade 4 is life-threatening. (NCT03190967)
Timeframe: Evaluated at the beginning of every cycle while on study, for an average of 9.6 months (range 2.8-33.9 months).

,,
InterventionParticipants (Count of Participants)
Grade 3 AnemiaGrade 3 Aspartate aminotransferase increasedGrade 3 CD4 lymphocytes decreasedGrade 3 DysphasiaGrade 3 HypokalemiaGrade 3 Lymphocyte count decreasedGrade 3 Neoplasms benign, malignant and unspecified (incl cysts and polyps) - Malignant Neoplasm-CMLGrade 3 Neutrophil count decreasedGrade 3 Platelet count decreasedGrade 3 Surgical and medical procedures - Other, Lap Cholecystectomy/Hernia RepairGrade 3 White blood cell decreasedGrade 4 White blood cell decreasedGrade 4 CD4 lymphocytes decreasedGrade 4 Lymphocyte count decreasedGrade 5
Level 1 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 30 mg/m^2001101000000000
Level 2 Phase I: Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 40 mg/m^2101002000000000
Level 3 Phase I:Ado-trastuzumab (T-DMI) 3.6 mg/kg + Temozolomide (TMZ) 50 mg/m^2015015111110220

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Number of Participants With Grade 3 or Greater Toxicities Associated With Pevonedistat in Combination With Irinotecan and Temozolomide

Frequency of patients who experience at least one grade 3 or higher toxicity that is at least possibly attributable to pevonedistat using the Common Terminology Criteria for Adverse Events version 5.0 by dose level stratified by study part and dose level. (NCT03323034)
Timeframe: Up to 3 years 8 months

InterventionParticipants (Count of Participants)
Part A Dose Level 1: 15 mg/m^25
Part A Dose Level 2: 20 mg/m^24
Part A Dose Level 3: 25 mg/m^26
Part A Dose Level 4: 35 mg/m^22
Part A PK Dose Level 4: 35 mg/m^24

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Anti-tumor Activity of Pevonedistat in Combination With Irinotecan and Temozolomide

Frequency of disease response (best overall response of partial or complete response) assessed 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 by dose level. (NCT03323034)
Timeframe: Up to 4 years

InterventionParticipants (Count of Participants)
Part A Dose Level 1: 15 mg/m^21
Part A Dose Level 2: 20 mg/m^21
Part A Dose Level 3: 25 mg/m^20
Part A Dose Level 4: 35 mg/m^20
Part A PK Dose Level 4: 35 mg/m^20

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AUC of Pevonedistat in Combination With Irinotecan and Temozolomide

Median (range) of the area under the drug concentration over time (pre-dose and then 0, 1, 2, 4, 6-8, and 24-hours post-dose infusion) curve stratified by study part and dose level. (NCT03323034)
Timeframe: Up to 10 days

Interventionhr*ng/mL (Median)
Part A Dose Level 1: 15 mg/m^2803
Part A Dose Level 2: 20 mg/m^2973.5
Part A Dose Level 3: 25 mg/m^21340
Part A Dose Level 4: 35 mg/m^22018.5
Part A PK Dose Level 4: 35 mg/m^21957

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C Max of Pevonedistat in Combination With Irinotecan and Temozolomide

Median (Range) for the maximum (peak) serum concentration by dose level stratified by study part and dose level. (NCT03323034)
Timeframe: Up to 10 days

Interventionng/mL (Median)
Part A Dose Level 1: 15 mg/m^2156
Part A Dose Level 2: 20 mg/m^2218.5
Part A Dose Level 3: 25 mg/m^2303.5
Part A Dose Level 4: 35 mg/m^2419
Part A PK Dose Level 4: 35 mg/m^2363.8

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Clearance of Pevonedistat in Combination With Irinotecan and Temozolomide

Median (Range) for the rate of elimination of the drug by dose level stratified by study part and dose level. (NCT03323034)
Timeframe: Up to 10 days

InterventionL/hr/m^2 (Median)
Part A Dose Level 1: 15 mg/m^218.8
Part A Dose Level 2: 20 mg/m^220.8
Part A Dose Level 3: 25 mg/m^218.9
Part A Dose Level 4: 35 mg/m^217.5
Part A PK Dose Level 4: 35 mg/m^217.9

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Half-life of Pevonedistat in Combination With Irinotecan and Temozolomide

Median (Range) for the time required for the serum concentration to fall to 50% of its starting dose by dose level stratified by study part and dose level. (NCT03323034)
Timeframe: Up to 10 days

Interventionhours (Median)
Part A Dose Level 1: 15 mg/m^25.3
Part A Dose Level 2: 20 mg/m^25
Part A Dose Level 3: 25 mg/m^25.2
Part A Dose Level 4: 35 mg/m^24.7
Part A PK Dose Level 4: 35 mg/m^26.1

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MTD/RP2D of Pevonedistat in Combination With Irinotecan and Temozolomide

The maximum tolerated dose (MTD) or recommended phase 2 dose (RP2D) will be the maximum dose at which fewer than one-third of patients experience dose limiting toxicities. (NCT03323034)
Timeframe: Up to 28 days

Interventionmg/m^2 (Number)
Treatment (Pevonedistat, Temozolomide, Irinotecan)35

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T Max of Pevonedistat in Combination With Irinotecan and Temozolomide

Median (Range) for the time at which the maximum (peak) serum concentration occurs by dose level stratified by study part and dose level. (NCT03323034)
Timeframe: Up to 10 days

Interventionhours (Median)
Part A Dose Level 1: 15 mg/m^21.
Part A Dose Level 2: 20 mg/m^21
Part A Dose Level 3: 25 mg/m^21
Part A Dose Level 4: 35 mg/m^21.1
Part A PK Dose Level 4: 35 mg/m^21.1

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6 Months Progression Free Survival (PFS)

To determine 6 month PFS of patients with unmethylated glioblastoma treated with DSF-Cu in combination with concurrent radiation and temozolomide. This was assessed by the number of participants who did not have disease progression and were alive at 6 months. (NCT03363659)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Open Label1

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Overall Survival

Overall Survival will be assessed as a number of participants alive at 1 and 2 years. (NCT03363659)
Timeframe: 1 and 2 years

InterventionParticipants (Count of Participants)
1 Year2 Years
Open Label92

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Number of Participants With Depatuxizumab Mafodotin Dose Modifications to Ocular Side Effects After Bandage Contact Lens (BCL) Intervention

Dose modifications included depatuxizumab mafodotin withdrawal, interruption, and reductions in dose initiated due to OSEs after BCL intervention. (NCT03419403)
Timeframe: From the last assessment prior to BCL intervention to the end of BCL intervention, up to 38 weeks

Interventionparticipants (Number)
Standard Steroids2
Standard Steroids + Vasoconstrictor + Cold Compress1
Enhanced Steroids + Vasoconstrictor + Cold Compress0

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Percentage of Participants Who Required a Change in Ocular Side Effect (OSE) Management

Inadequate control of ocular side effects (OSE) was defined as either a ≥ 3-line decline from baseline (≥ +0.3 on LogMAR scale) in visual acuity (with baseline correction determined at the screening ophthalmology visit)) or ≥ Grade 3 OSE severity on the Corneal Epithelial Adverse Event (CEAE) scale. (NCT03419403)
Timeframe: Within 8 weeks after the initial dose of depatuxizumab mafodotin

,,
Interventionpercentage of participants (Number)
Bilateral visionVision in worst eye
Enhanced Steroids + Vasoconstrictor + Cold Compress41.750.0
Standard Steroids50.064.3
Standard Steroids + Vasoconstrictor + Cold Compress27.372.7

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Maximum Change From Baseline on the Logarithm of the Minimum Angle of Resolution (LogMAR) Scale

The LogMAR scale measures visual acuity on a continuous scale, with a LogMAR value of 0 equivalent to 20/20 visual acuity. Normal vision is considered to be from -0.2 - 0.1; higher values indicate visual impairment. The baseline observation is defined as the last non-missing measurement collected prior to the first dose of depatuxizumab mafodotin. (NCT03419403)
Timeframe: Within 8 weeks after the initial dose of depatuxizumab mafodotin

,,
Interventionunits on a scale (Mean)
Bilateral visionVision in worst eye
Enhanced Steroids + Vasoconstrictor + Cold Compress0.2720.430
Standard Steroids0.3530.482
Standard Steroids + Vasoconstrictor + Cold Compress0.4020.528

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Change From Baseline In Logarithm of the Minimum Angle of Resolution (LogMAR) Scale After Bandage Contact Lens (BCL) Intervention

The change on the LogMAR Scale from last assessment prior to BCL intervention to 2 weeks after BCL intervention was calculated. The LogMAR scale measures visual acuity on a continuous scale, with a LogMAR value of 0 equivalent to 20/20 visual acuity. Normal vision is considered to be from -0.2 - 0.1; higher values indicate visual impairment. (NCT03419403)
Timeframe: From the last assessment prior to BCL intervention to 2 weeks after BCL intervention

,
Interventionunits on a scale (Mean)
Within 8 weeks of first dose: Bilateral visionWithin 8 weeks of first dose: Vision in worst eyeWithin 8 weeks of first adjuvant dose: Bilateral visionWithin 8 weeks of first adjuvant dose: Vision in worst eye
Standard Steroids0.3250.435-0.1-0.1
Standard Steroids + Vasoconstrictor + Cold Compress0.130.520.410.33

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Time to Bandage Contact Lens (BCL) Intervention

The time to initiation of bandage contact lenses for those participants who required intervention due to inadequate control of ocular side effects (OSE) was calculated. (NCT03419403)
Timeframe: Up to 9 months after the first dose of depatuxizumab mafodotin

Interventionmonths (Median)
Standard SteroidsNA
Standard Steroids + Vasoconstrictor + Cold Compress3.6
Enhanced Steroids + Vasoconstrictor + Cold Compress2.1

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Cumulative Dose of Depatuxizumab Mafodotin Received During Chemoradiation and During Adjuvant Treatment

The cumulative dose of depatuxizumab mafodotin administered was tabulated. (NCT03419403)
Timeframe: Up to 9 months

Interventionmg/kg (Mean)
Standard Steroids8.5
Standard Steroids + Vasoconstrictor + Cold Compress10.5
Enhanced Steroids + Vasoconstrictor + Cold Compress7.0

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Treatment-Emergent Corneal Epithelial Adverse Event (CEAE) Grade at Each Visit

The corneal epithelial adverse event (CEAE) rating scale is designed to record symptoms associated with corneal epitheliopathy caused by antibody-drug conjugates and to grade the severity of findings. The overall CEAE grade is measured on a scale of 0 to 5, with higher values being more severe, reflecting the impact of corneal abnormalities on visual activities of daily living (ADLs). Additional detailed information is collected for specific domains that are commonly affected, with the following ranges (each in order of increasing severity): ocular discomfort (0 - 4), photophobia (0 - 3), and reading (1 - 3). (NCT03419403)
Timeframe: Up to 47 weeks

,,
InterventionParticipants (Count of Participants)
Week 1: Grade 0Week 1: Grade 1Week 3: Grade 0Week 3: Grade 1Week 3: Grade 2Week 5: Grade 0Week 5: Grade 1Week 5: Grade 2Week 5: Grade 3Week 7: Grade 0Week 7: Grade 1Week 7: Grade 2Week 7: Grade 3Week 9: Grade 0Week 9: Grade 1Week 9: Grade 2Week 9: Grade 3Week 11: Grade 0Week 11: Grade 1Week 11: Grade 2Week 11: Grade 3Week 11: Grade 4Week 13: Grade 1Adj Week 1: Grade 0Adj Week 1: Grade 1Adj Week 1: Grade 2Adj Week 1: Grade 3Adj Week 5: Grade 0Adj Week 5: Grade 1Adj Week 5: Grade 2Adj Week 5: Grade 3Adj Week 9: Grade 0Adj Week 9: Grade 1Adj Week 9: Grade 2Adj Week 9: Grade 3Adj Week 13: Grade 0Adj Week 13: Grade 1Adj Week 13: Grade 2Adj Week 13: Grade 3Adj Week 17: Grade 0Adj Week 17: Grade 1Adj Week 17: Grade 2Adj Week 21: Grade 1Adj Week 21: Grade 2Adj Week 25: Grade 1Adj Week 25: Grade 2Adj Week 29: Grade 2Adj Week 29: Grade 4
Enhanced Steroids + Vasoconstrictor + Cold Compress517312622205210411031010220201001200020100100000
Standard Steroids10141001714034211320221110131014100210021002020110
Standard Steroids + Vasoconstrictor + Cold Compress835600532046002500100001320230112211220013032101

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Treatment Emergent Corneal Epithelial Adverse Event (CEAE) Grade at Each Visit After Bandage Contact Lens (BCL) Intervention

The corneal epithelial adverse event (CEAE) rating scale is designed to record symptoms associated with corneal epitheliopathy caused by antibody-drug conjugates and to grade the severity of findings. The overall CEAE grade is measured on a scale of 0 to 5, with higher values being more severe, reflecting the impact of corneal abnormalities on visual activities of daily living (ADLs). Additional detailed information is collected for specific domains that are commonly affected, with the following ranges (each in order of increasing severity): ocular discomfort (0 - 4), photophobia (0 - 3), and reading (1 - 3). (NCT03419403)
Timeframe: From the last assessment prior to BCL intervention to the end of BCL intervention, up to 38 weeks

,,
InterventionParticipants (Count of Participants)
Week 5: Grade 1Week 7: Grade 2Week 9: Grade 2Week 11: Grade 2Week 11: Grade 3Week 13: Grade 1Adj Week 1: Grade 1Adj Week 1: Grade 2Adj Week 5: Grade 0Adj Week 5: Grade 1Adj Week 5: Grade 2Adj Week 5: Grade 3Adj Week 9: Grade 0Adj Week 9: Grade 1Adj Week 9: Grade 2Adj Week 9: Grade 3Adj Week 13: Grade 0Adj Week 13: Grade 1Adj Week 13: Grade 2Adj Week 13: Grade 3Adj Week 17: Grade 1Adj Week 17: Grade 2Adj Week 21: Grade 2Adj Week 25: Grade 1Adj Week 25: Grade 2Adj Week 29: Grade 2
Enhanced Steroids + Vasoconstrictor + Cold Compress00120011101001100010000000
Standard Steroids21101100001100010011012011
Standard Steroids + Vasoconstrictor + Cold Compress01100000110010002100111100

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Number of Participants With Depatuxizumab Mafodotin Dose Modifications Due to Ocular Side Effects (OSE)

Dose modifications included depatuxizumab mafodotin withdrawal, interruption, and reductions in dose initiated due to OSEs. (NCT03419403)
Timeframe: From the first dose of study drug until 49 days after last depatuxizumab mafodotin administration, up to 47 weeks

InterventionParticipants (Count of Participants)
Standard Steroids2
Standard Steroids + Vasoconstrictor + Cold Compress3
Enhanced Steroids + Vasoconstrictor + Cold Compress2

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Change From Baseline In Logarithm of the Minimum Angle of Resolution (LogMAR) Scale After Bandage Contact Lens (BCL) Intervention

The change on the LogMAR Scale from last assessment prior to BCL intervention to 2 weeks after BCL intervention was calculated. The LogMAR scale measures visual acuity on a continuous scale, with a LogMAR value of 0 equivalent to 20/20 visual acuity. Normal vision is considered to be from -0.2 - 0.1; higher values indicate visual impairment. (NCT03419403)
Timeframe: From the last assessment prior to BCL intervention to 2 weeks after BCL intervention

Interventionunits on a scale (Mean)
Within 8 weeks of first dose: Bilateral visionWithin 8 weeks of first dose: Vision in worst eye
Enhanced Steroids + Vasoconstrictor + Cold Compress0.540.867

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PFS Rate at 6 Months and 12 Months

"Progression-free survival rate at 6 months and 12 months was calculated as the proportion of patients who were progression-free and alive at 6 and 12 months, respectively.~Progression is assessed according to Response Assessment in Neuro-Oncology (RANO) 2010 criteria based on MRI imaging, and includes ≥25% increase in the sum of the products of perpendicular diameters of enhancing lesions (compared with baseline if no decrease) on stable or increasing doses of corticosteroids." (NCT03463265)
Timeframe: 6 and 12 months

,,,,,
Interventionpercentage of patients (Number)
PFS at 6 monthsPFS at 12 months
Arm A, Cohort 1: Nab-sirolimus in Patients With Recurrent High Grade Glioma0.00.0
Arm A, Cohort 2: Nab-sirolimus + Temozolomide in Patients With Recurrent High Grade Glioma75.050.0
Arm A, Cohort 3: Nab-sirolimus + Bevacizumab in Patients With Recurrent High Grade Glioma37.512.5
Arm A, Cohort 4: Nab-sirolimus + Lomustine in Patients With Recurrent High Grade Glioma25.00.0
Arm A, Cohort 5: Nab-sirolimus + Marizomib in Patients With Recurrent High Grade Glioma10.00.0
Arm B: Nab-sirolimus + Temozolomide + Radiotherapy in Patients With Newly Diagnosed Glioblastoma76.936.4

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OS at 12 Months

Overall Survival rate at 12 months (NCT03463265)
Timeframe: 12 months

Interventionpercentage of patients (Number)
Arm A, Cohort 1: Nab-sirolimus in Patients With Recurrent High Grade Glioma0.0
Arm A, Cohort 2: Nab-sirolimus + Temozolomide in Patients With Recurrent High Grade Glioma66.7
Arm A, Cohort 3: Nab-sirolimus + Bevacizumab in Patients With Recurrent High Grade Glioma25.0
Arm A, Cohort 4: Nab-sirolimus + Lomustine in Patients With Recurrent High Grade Glioma25.0
Arm A, Cohort 5: Nab-sirolimus + Marizomib in Patients With Recurrent High Grade Glioma0.0
Arm B: Nab-sirolimus + Temozolomide + Radiotherapy in Patients With Newly Diagnosed Glioblastoma53.8

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OS

Median Overall Survival (NCT03463265)
Timeframe: Through study completion (up to 48 months)

Interventionmonths (Median)
Arm A, Cohort 1: Nab-sirolimus in Patients With Recurrent High Grade Glioma7.2
Arm A, Cohort 2: Nab-sirolimus + Temozolomide in Patients With Recurrent High Grade Glioma13.8
Arm A, Cohort 3: Nab-sirolimus + Bevacizumab in Patients With Recurrent High Grade Glioma6.8
Arm A, Cohort 4: Nab-sirolimus + Lomustine in Patients With Recurrent High Grade Gliom7.5
Arm A, Cohort 5: Nab-sirolimus + Marizomib in Patients With Recurrent High Grade Glioma6.7
Arm B: Nab-sirolimus + Temozolomide + Radiotherapy in Patients With Newly Diagnosed Glioblastoma13.3

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ORR

Objective overall response rate (ORR, according to Response Assessment in Neuro-Oncology [RANO]) by investigator-assessed radiologic review and defined as the proportion of patients who achieved a confirmed partial response (PR) or confirmed complete response (CR) per RANO 2010 criteria. PR is defined as greater than or equal to 50% decrease compared with baseline in the sum of products of perpendicular diameters of all measurable enhancing lesions sustained for at least 4 weeks. (NCT03463265)
Timeframe: Through study completion (up to 48 months)

Interventionpercentage of patients (Number)
Arm A, Cohort 1: Nab-sirolimus in Patients With Recurrent High Grade Glioma0
Arm A, Cohort 2: Nab-sirolimus + Temozolomide in Patients With Recurrent High Grade Glioma0
Arm A, Cohort 3: Nab-sirolimus + Bevacizumab in Patients With Recurrent High Grade Glioma0
Arm A, Cohort 4: Nab-sirolimus + Lomustine in Patients With Recurrent High Grade Glioma0
Arm A, Cohort 5: Nab-sirolimus + Marizomib in Patients With Recurrent High Grade Glioma0
Arm B: Nab-sirolimus + Temozolomide + Radiotherapy in Patients With Newly Diagnosed Glioblastoma11.5

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Median PFS

"Progression-free Survival defined as number of months from the date of the first dose of study drug to the first observation of a disease progression or death due to any cause.~Progression is assessed according to Response Assessment in Neuro-Oncology (RANO) 2010 criteria based on MRI imaging, and includes ≥25% increase in the sum of the products of perpendicular diameters of enhancing lesions (compared with baseline if no decrease) on stable or increasing doses of corticosteroids." (NCT03463265)
Timeframe: Through study completion (up to 48 months)

Interventionmonths (Median)
Arm A, Cohort 1: Nab-sirolimus in Patients With Recurrent High Grade Glioma1.7
Arm A, Cohort 2: Nab-sirolimus + Temozolomide in Patients With Recurrent High Grade Glioma11.3
Arm A, Cohort 3: Nab-sirolimus + Bevacizumab in Patients With Recurrent High Grade Glioma3.1
Arm A, Cohort 4: Nab-sirolimus + Lomustine in Patients With Recurrent High Grade Glioma3.8
Arm A, Cohort 5: Nab-sirolimus + Marizomib in Patients With Recurrent High Grade Glioma1.7
Arm B: Nab-sirolimus + Temozolomide + Radiotherapy in Patients With Newly Diagnosed Glioblastoma7.5

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Overall Response Rate (ORR)

ORR is defined as the proportion of participants who have prolonged stable disease or a partial or complete response or complete response to therapy according to RECIST 1.1. (NCT03495921)
Timeframe: 6 months after treatment with Vigil.

InterventionProportion of participants. (Number)
Group A: Vigil in Combination With Irinotecan and Temozolomide0
Group B: Irinotecan and Temozolomide0

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Overall Survival (OS)

OS is defined as time from randomization to death or to the date of last follow-up. The date of last follow-up confirming survival will be used as the censoring date for subjects who are alive and/or do not have a known date of death. (NCT03495921)
Timeframe: From date of randomization until date of death from any cause, whichever came first (assessed up to 3 years).

InterventionMonths (Median)
Group A: Vigil in Combination With Irinotecan and Temozolomide16.1
Group B: Irinotecan and Temozolomide3.3

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Vigil Manufacture Success Rate: Number of Participants Eligible for Treatment on the Main Study.

Participants were considered eligible for treatment, if the tissue submitted to Gradalis met all criteria, including manufacturing product release criteria. (NCT03495921)
Timeframe: From manufacturing start date until 4 weeks post manufacturing for each tissue procurement (assessed up to 17 months).

InterventionParticipants (Count of Participants)
Total Number of Tissue Procurements4

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Progression Free Survival (PFS)

Progression Free Survival (PFS) is defined as the time from randomization to the event of disease recurrence/progression according to Response Evaluation Criteria In Solid Tumors (RECIST) criteria (version 1.1) for target lesions and assessed CT/MRI by local investigator. (NCT03495921)
Timeframe: From date of randomization until the date of first documented progression (assessed up to 3 years).

InterventionMonths (Median)
Group A: Vigil in Combination With Irinotecan and Temozolomide2.8
Group B: Irinotecan and Temozolomide9.1

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Overall Survival (OS)

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 utilizing exact binomial methodology. The distribution of survival time will be estimated using the method of Kaplan-Meier (1958). (NCT03778294)
Timeframe: Time from registration to death due to any cause, assessed up to 12 months

Interventionproportion of successes (Number)
Treatment (18F-DOPA, PET/MRI, PET/CT, Temozolomide)0.54

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Progression Free Survival

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 utilizing exact binomial methodology. (NCT03778294)
Timeframe: At 12 months after radiation therapy

Interventionproportion of successes (Number)
Treatment (18F-DOPA, PET/MRI, PET/CT, Temozolomide)0.72

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Number of Patients Experiencing Adverse Events

Recorded at each clinical visit and will be categorized according to National Cancer Institute Common Terminology Criteria for Adverse Events version 5.0. Number of patients experiencing a grade 3 or greater adverse event will be reported. (NCT03880019)
Timeframe: Up to 2 years after study treatment

InterventionParticipants (Count of Participants)
Treatment (Olaparib, Temozolomide)20

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Confirmed Objective Response Rate (ORR) (Complete Response + Partial Response)

Will be measured by Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 criteria assessed by MRI: 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 (<1 cm); Partial Response (PR), at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters. A response rate of 10% is considered inactive and unworthy of further study. A response rate of 35% would be promising for further study among patients with advanced uterine leiomyosarcoma (LMS) treated with at least one prior systemic regimen. A response rate of 35% for the temozolomide (TMZ) + poly(adenosine diphosphate[ADP]-ribose) polymerase inhibitor (PARPi) combination would also be suggestive of superior efficacy over TMZ monotherapy in sarcoma. Will be reported with a 95% confidence interval. (NCT03880019)
Timeframe: Within first 6 months of study treatment

InterventionParticipants (Count of Participants)
Treatment (Olaparib, Temozolomide)5

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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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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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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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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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Progression Free Survival

To estimate the progression free survival (PFS), patients will be followed for up to 24 months. (NCT04166435)
Timeframe: Up to 2 years from last treatment

Interventionmonths (Median)
Temozolomide + Olaparib3

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Count of Participants With Adverse Events Greater or Equal to 3

To determine the safety of TMZ in combination with olaparib, the number of participants with ≥ grade 3 treatment related adverse events by CTCAE v5.0 coding will be assessed. (NCT04166435)
Timeframe: Up to 2 years from last treatment

InterventionParticipants (Count of Participants)
Temozolomide + Olaparib7

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Overall Survival

To estimate overall survival (OS), patients will be followed for up to 24 months. (NCT04166435)
Timeframe: Up to 2 years from last treatment

Interventionmonths (Median)
Temozolomide + Olaparib9.4

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Overall Survival

(NCT05718466)
Timeframe: 12 months

Interventionmonths (Median)
Fractionated Radiosurgery and Bevacizumab7.2
Bev With Chemo4.8

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Local Tumor Control

(NCT05718466)
Timeframe: 2 months

InterventionParticipants (Count of Participants)
Fractionated Radiosurgery and Bevacizumab14
Bev With Chemo4

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Progression Free Survival

(NCT05718466)
Timeframe: 12 months

Interventionmonths (Median)
Fractionated Radiosurgery and Bevacizumab5.1
Bev With Chemo1.8

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SubstanceRelationship StrengthStudiesTrialsClassesRoles
ethylene dichloride
ethylene dichloride: RN given refers to 1,2-isomer; structure given in first source. 1,2-dichloroethane : A member of the class of chloroethanes substituted by two chloro groups at positions 1 and 2.		2.0510chloroethaneshepatotoxic agent;
mutagen;
non-polar solvent
alpha-hydroxyglutarate
2-hydroxyglutarate : A dicarboxylic acid anion obtained by deprotonation of at least one of the carboxy groups of 2-hydroxyglutaric acid.. 2-hydroxyglutaric acid : A 2-hydroxydicarboxylic acid that is glutaric acid in which one hydrogen alpha- to a carboxylic acid group is substituted by a hydroxy group.		2.57202-hydroxydicarboxylic acid;
dicarboxylic fatty acid		metabolite;
mouse metabolite
4-hydroxyphenylacetic acid
4-hydroxyphenylacetic acid : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is substituted by a 4-hydroxyphenyl group.		2.1510monocarboxylic acid;
phenols		fungal metabolite;
human metabolite;
mouse metabolite;
plant metabolite
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.		4.61514-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
ethylene glycol
Ethylene Glycol: A colorless, odorless, viscous dihydroxy alcohol. It has a sweet taste, but is poisonous if ingested. Ethylene glycol is the most important glycol commercially available and is manufactured on a large scale in the United States. It is used as an antifreeze and coolant, in hydraulic fluids, and in the manufacture of low-freezing dynamites and resins.. ethanediol : Any diol that is ethane or substituted ethane carrying two hydroxy groups.. ethylene glycol : A 1,2-glycol compound produced via reaction of ethylene oxide with water.		2.0510ethanediol;
glycol		metabolite;
mouse metabolite;
solvent;
toxin
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.		2.5320monocarboxylic 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
acetone
methyl ketone : A ketone of formula RC(=O)CH3 (R =/= H).		2.610ketone body;
methyl ketone;
propanones;
volatile organic compound		EC 3.5.1.4 (amidase) inhibitor;
human metabolite;
polar aprotic solvent
adenine
[no description available]		9.52806-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
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.		3.1950acridines;
aromatic ether;
organochlorine compound;
tertiary amino compound		antimalarial;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor
benzene
[no description available]		4.811aromatic annulene;
benzenes;
volatile organic compound		carcinogenic agent;
environmental contaminant;
non-polar solvent
benzoic acid
Benzoic Acid: A fungistatic compound that is widely used as a food preservative. It is conjugated to GLYCINE in the liver and excreted as hippuric acid.. benzoic acid : A compound comprising a benzene ring core carrying a carboxylic acid substituent.. aromatic carboxylic acid : Any carboxylic acid in which the carboxy group is directly bonded to an aromatic ring.		2.1310benzoic acidsalgal 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
betaine
glycine betaine : The amino acid betaine derived from glycine.		3.5920amino-acid betaine;
glycine derivative		fundamental metabolite
carbamates
[no description available]		2.3110amino-acid anion
aminooxyacetic acid
Aminooxyacetic Acid: A compound that inhibits aminobutyrate aminotransferase activity in vivo, thereby raising the level of gamma-aminobutyric acid in tissues.. (aminooxy)acetic acid : A member of the class of hydroxylamines that is acetic acid substituted at postion 2 by an aminooxy group. It is a compound which inhibits aminobutyrate aminotransferase activity in vivo, resulting in increased levels of gamma-aminobutyric acid in tissues.		2.0810amino acid;
hydroxylamines;
monocarboxylic acid		anticonvulsant;
EC 2.6.1.19 (4-aminobutyrate--2-oxoglutarate transaminase) inhibitor;
EC 4.2.1.22 (cystathionine beta-synthase) inhibitor;
nootropic agent
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).		2.9830alkane;
gas molecular entity;
mononuclear parent hydride;
one-carbon compound		bacterial metabolite;
fossil fuel;
greenhouse gas
choline
[no description available]		5.81112cholinesallergen;
Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
neurotransmitter;
nutrient;
plant metabolite;
Saccharomyces cerevisiae metabolite
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.		2.0710halide anion;
monoatomic chlorine		cofactor;
Escherichia coli metabolite;
human metabolite
coumarin
2H-chromen-2-one: coumarin derivative		2.0710coumarinsfluorescent dye;
human metabolite;
plant metabolite
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).		5.341monohydroxybenzoic acidalgal metabolite;
antifungal agent;
antiinfective agent;
EC 1.11.1.11 (L-ascorbate peroxidase) inhibitor;
keratolytic drug;
plant hormone;
plant metabolite
phloroglucinol
Phloroglucinol: A trinitrobenzene derivative with antispasmodic properties that is used primarily as a laboratory reagent.. phloroglucinol : A benzenetriol with hydroxy groups at position 1, 3 and 5.		3.2710benzenetriol;
phenolic donor		algal metabolite
gallic acid
gallate : A trihydroxybenzoate that is the conjugate base of gallic acid.		2.2110trihydroxybenzoic acidantineoplastic agent;
antioxidant;
apoptosis inducer;
astringent;
cyclooxygenase 2 inhibitor;
EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor;
geroprotector;
human xenobiotic metabolite;
plant metabolite
4-aminophenol
4-aminophenol: RN given refers to parent cpd. 4-aminophenol : An amino phenol (one of the three possible isomers) which has the single amino substituent located para to the phenolic -OH group.		2.0510aminophenolallergen;
metabolite
dihydrolipoic acid
dihydrolipoic acid: RN given refers to parent cpd without isomeric designation. dihydrolipoic acid : A thio-fatty acid that is reduced form of lipoic acid. A potent antioxidant shown to directly destroy superoxide, hydroperoxy and hydroxyl radicals; also has neuroprotective and anti-tumour effects.. dihydrolipoate : The conjugate base of dihydrolipoic acid.		2.1110thio-fatty acidantioxidant;
human metabolite;
neuroprotective agent
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.		3.8630aromatic ketone;
monochlorobenzenes;
secondary amino compound		antidepressant;
environmental contaminant;
xenobiotic
4-aminoimidazole
4-aminoimidazole: structure in first source. 4-aminoimidazole : An aminoimidazole that is 1H-imidazole substituted by an amino group at position 4.		2.610aminoimidazole
methylmalonic acid
Methylmalonic Acid: A malonic acid derivative which is a vital intermediate in the metabolism of fat and protein. Abnormalities in methylmalonic acid metabolism lead to methylmalonic aciduria. This metabolic disease is attributed to a block in the enzymatic conversion of methylmalonyl CoA to succinyl CoA.. methylmalonic acid : A dicarboxylic acid that is malonic acid in which one of the methylene hydrogens is substituted by a methyl group.		2.110C4-dicarboxylic acidhuman metabolite
malic acid
malic acid : A 2-hydroxydicarboxylic acid that is succinic acid in which one of the hydrogens attached to a carbon is replaced by a hydroxy group.. 2-hydroxydicarboxylic acid : Any dicarboxylic acid carrying a hydroxy group on the carbon atom at position alpha to the carboxy group.		2.55202-hydroxydicarboxylic acid;
C4-dicarboxylic acid		food acidity regulator;
fundamental metabolite
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.		4.0840amino acid zwitterion;
epsilon-amino acid;
omega-amino fatty acid		antifibrinolytic drug;
hematologic agent;
metabolite
creatine
[no description available]		4.7361glycine derivative;
guanidines;
zwitterion		geroprotector;
human metabolite;
mouse metabolite;
neuroprotective agent;
nutraceutical
cytosine
[no description available]		9.9660aminopyrimidine;
pyrimidine nucleobase;
pyrimidone		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
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.		9.351802-hydroxy monocarboxylic acidalgal metabolite;
Daphnia magna 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.		340sulfoxide;
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		2.4620aldehyde;
one-carbon compound		allergen;
carcinogenic agent;
disinfectant;
EC 3.5.1.4 (amidase) inhibitor;
environmental contaminant;
Escherichia coli metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
hexachlorocyclohexane
Lindane: An organochlorine insecticide made up of greater than 99% gamma-Hexachlorocyclohexane. It has been used as a pediculicide and scabicide, and shown to cause cancer.. beta-hexachlorocyclohexane : The beta-isomer of hexachlorocyclohexane.		2.0510chlorocyclohexane
glycine
[no description available]		2.5320alpha-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
glycolic acid
glycolic acid: RN given refers to parent cpd. glycolic acid : A 2-hydroxy monocarboxylic acid that is acetic acid where the methyl group has been hydroxylated.		7.21102-hydroxy monocarboxylic acid;
primary alcohol		keratolytic drug;
metabolite
hydroquinone
[no description available]		2.0510benzenediol;
hydroquinones		antioxidant;
carcinogenic agent;
cofactor;
Escherichia coli metabolite;
human xenobiotic metabolite;
mouse metabolite;
skin lightening agent
dihydroxyphenylalanine
Dihydroxyphenylalanine: A beta-hydroxylated derivative of phenylalanine. The D-form of dihydroxyphenylalanine has less physiologic activity than the L-form and is commonly used experimentally to determine whether the pharmacological effects of LEVODOPA are stereospecific.. dopa : A hydroxyphenylalanine carrying hydroxy substituents at positions 3 and 4 of the benzene ring.		5.8241hydroxyphenylalanine;
non-proteinogenic alpha-amino acid;
tyrosine derivative		human metabolite
thioctic acid
Thioctic Acid: An octanoic acid bridged with two sulfurs so that it is sometimes also called a pentanoic acid in some naming schemes. It is biosynthesized by cleavage of LINOLEIC ACID and is a coenzyme of oxoglutarate dehydrogenase (KETOGLUTARATE DEHYDROGENASE COMPLEX). It is used in DIETARY SUPPLEMENTS.		2.1110dithiolanes;
heterocyclic fatty acid;
thia fatty acid		fundamental metabolite;
geroprotector
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.		2.4110alkyl alcohol;
one-carbon compound;
primary alcohol;
volatile organic compound		amphiprotic solvent;
Escherichia coli metabolite;
fuel;
human metabolite;
mouse metabolite;
Mycoplasma genitalium metabolite
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.		2.4620cyclitol;
hexol
melatonin
[no description available]		8.2550acetamides;
tryptamines		anticonvulsant;
central nervous system depressant;
geroprotector;
hormone;
human metabolite;
immunological adjuvant;
mouse metabolite;
radical scavenger
nickel
Nickel: A trace element with the atomic symbol Ni, atomic number 28, and atomic weight 58.69. It is a cofactor of the enzyme UREASE.. nickel ion : A nickel atom having a net electric charge.. nickel atom : Chemical element (nickel group element atom) with atomic number 28.		4.811metal allergen;
nickel group element atom		epitope;
micronutrient
niacinamide
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.		9.26196pyridine 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.		4.1140pyridine 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
nitroxyl
nitroxyl: hydroxamic acid oxidized to nitroxyl free radical. nitroxyl : A nitrogen oxoacid consisting of an oxygen atom double-bonded to an NH group.		4.811nitrogen oxoacid
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.		2.0510pyrimidinemonocarboxylic acidEscherichia coli metabolite;
metabolite;
mouse metabolite
oxaloacetic acid
Oxaloacetic Acid: A dicarboxylic acid ketone that is an important metabolic intermediate of the CITRIC ACID CYCLE. It can be converted to ASPARTIC ACID by ASPARTATE TRANSAMINASE.. oxaloacetic acid : An oxodicarboxylic acid that is succinic acid bearing a single oxo group.		4.9340C4-dicarboxylic acid;
oxo dicarboxylic acid		geroprotector;
metabolite
oxalic acid
Oxalic Acid: A strong dicarboxylic acid occurring in many plants and vegetables. It is produced in the body by metabolism of glyoxylic acid or ascorbic acid. It is not metabolized but excreted in the urine. It is used as an analytical reagent and general reducing agent.. oxalic acid : An alpha,omega-dicarboxylic acid that is ethane substituted by carboxyl groups at positions 1 and 2.		2.0710alpha,omega-dicarboxylic acidalgal metabolite;
human metabolite;
plant metabolite
oxamic acid
Oxamic Acid: Amino-substituted glyoxylic acid derivative.. oxamic acid : A dicarboxylic acid monoamide resulting from the formal condensation of one of the carboxy groups of oxalic acid with ammonia.		3.5110dicarboxylic acid monoamideEscherichia coli 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.		2.4720aminobenzoic 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
phenethylamine
phenethylamine: RN given refers to parent cpd; structure in Merck Index, 9th ed, #7016. 2-phenylethylamine : A phenylethylamine having the phenyl substituent at the 2-position.		2.3110alkaloid;
aralkylamine;
phenylethylamine		Escherichia coli metabolite;
human metabolite;
mouse metabolite
phosphorylcholine
Phosphorylcholine: Calcium and magnesium salts used therapeutically in hepatobiliary dysfunction.. phosphocholine : The phosphate of choline; and the parent compound of the phosphocholine family.		4.670phosphocholinesallergen;
epitope;
hapten;
human metabolite;
mouse metabolite
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.		4.2750monocarboxylic 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).		3.8630hydroxymethylpyridine;
methylpyridines;
monohydroxypyridine;
vitamin B6		cofactor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
pyruvic acid
Pyruvic Acid: An intermediate compound in the metabolism of carbohydrates, proteins, and fats. In thiamine deficiency, its oxidation is retarded and it accumulates in the tissues, especially in nervous structures. (From Stedman, 26th ed). pyruvic acid : A 2-oxo monocarboxylic acid that is the 2-keto derivative of propionic acid. It is a metabolite obtained during glycolysis.		2.79302-oxo monocarboxylic acidcofactor;
fundamental metabolite
quinolinic acid
Quinolinic Acid: A metabolite of tryptophan with a possible role in neurodegenerative disorders. Elevated CSF levels of quinolinic acid are correlated with the severity of neuropsychological deficits in patients who have AIDS.. pyridinedicarboxylic acid : Any member of the class of pyridines carrying two carboxy groups.. quinolinic acid : A pyridinedicarboxylic acid that is pyridine substituted by carboxy groups at positions 2 and 3. It is a metabolite of tryptophan.		2.0810pyridinedicarboxylic acidEscherichia coli metabolite;
human metabolite;
mouse metabolite;
NMDA receptor agonist
sarcosine
cocobetaine: N-alkyl-betaine; cause of shampoo dermatitis		2.0810N-alkylglycine zwitterion;
N-alkylglycine;
N-methyl-amino acid;
N-methylglycines		Escherichia coli metabolite;
glycine receptor agonist;
glycine transporter 1 inhibitor;
human metabolite;
mouse metabolite
sulfites
Sulfites: Inorganic salts of sulfurous acid.. sulfites : Any sulfurous acid derivative that is a salt or an ester of sulfurous acid.. organosulfonate oxoanion : An organic anion obtained by deprotonation of the sufonate group(s) of any organosulfonic acid.. sulfite : A sulfur oxoanion that is the conjugate base of hydrogen sulfite (H2SO3).		2.110divalent inorganic anion;
sulfur oxide;
sulfur oxoanion
succinic acid
Succinic Acid: A water-soluble, colorless crystal with an acid taste that is used as a chemical intermediate, in medicine, the manufacture of lacquers, and to make perfume esters. It is also used in foods as a sequestrant, buffer, and a neutralizing agent. (Hawley's Condensed Chemical Dictionary, 12th ed, p1099; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1851). succinic acid : An alpha,omega-dicarboxylic acid resulting from the formal oxidation of each of the terminal methyl groups of butane to the corresponding carboxy group. It is an intermediate metabolite in the citric acid cycle.		5.0321alpha,omega-dicarboxylic acid;
C4-dicarboxylic acid		anti-ulcer drug;
fundamental metabolite;
micronutrient;
nutraceutical;
radiation protective agent
taurine
[no description available]		7.3110amino sulfonic acid;
zwitterion		antioxidant;
Escherichia coli metabolite;
glycine receptor agonist;
human metabolite;
mouse metabolite;
nutrient;
radical scavenger;
Saccharomyces cerevisiae metabolite
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.		3.8630primary alcohol;
vitamin B1		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
thymine
[no description available]		2.1310pyrimidine nucleobase;
pyrimidone		Escherichia coli metabolite;
human metabolite;
mouse metabolite
toluene
methylbenzene : Any alkylbenzene that is benzene substituted with one or more methyl groups.		5.6551methylbenzene;
toluenes;
volatile organic compound		cholinergic antagonist;
fuel additive;
neurotoxin;
non-polar solvent
uracil
2,4-dihydroxypyrimidine: a urinary biomarker for bipolar disorder		5.9670pyrimidine nucleobase;
pyrimidone		allergen;
Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
prodrug;
Saccharomyces cerevisiae metabolite
uric acid
Uric Acid: An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.. uric acid : An oxopurine that is the final oxidation product of purine metabolism.. 6-hydroxy-1H-purine-2,8(7H,9H)-dione : A tautomer of uric acid having oxo groups at C-2 and C-8 and a hydroxy group at C-6.. 7,9-dihydro-1H-purine-2,6,8(3H)-trione : An oxopurine in which the purine ring is substituted by oxo groups at positions 2, 6, and 8.		4.811uric acidEscherichia coli metabolite;
human metabolite;
mouse 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.		10.8561isourea;
monocarboxylic acid amide;
one-carbon compound		Daphnia magna metabolite;
Escherichia coli metabolite;
fertilizer;
flour treatment agent;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae 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
pk 11195
PK-11195 : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 1-(2-chlorophenyl)isoquinoline-3-carboxylic acid with the amino group of sec-butylmethylamine		2.1110aromatic amide;
isoquinolines;
monocarboxylic acid amide;
monochlorobenzenes		antineoplastic agent
1-(3-chlorophenyl)piperazine
1-(3-chlorophenyl)piperazine: supposed metabolite of TRAZODONE; RN given refers to parent cpd; structure. 1-(3-chlorophenyl)piperazine : A N-arylpiperazine that is piperazine carrying a 3-chlorophenyl substituent at position 1. It is a metabolite of the antidepressant drug trazodone.		2.4620monochlorobenzenes;
N-arylpiperazine		drug metabolite;
environmental contaminant;
serotonergic agonist;
xenobiotic
n-(3-(aminomethyl)benzyl)acetamidine
N-(3-(aminomethyl)benzyl)acetamidine: structure in first source. N-[3-(aminomethyl)benzyl]acetamidine : An aralkylamine that is Nbenzylacetamidine substituted at position 3 on the benzene ring by an aminomethyl group. An inhibitor of nitric oxide synthase.		2.2510aralkylamine;
carboxamidine;
primary amino compound		angiogenesis inhibitor;
EC 1.14.13.39 (nitric oxide synthase) inhibitor;
geroprotector
2,4-dinitrophenol
2,4-Dinitrophenol: A toxic dye, chemically related to trinitrophenol (picric acid), used in biochemical studies of oxidative processes where it uncouples oxidative phosphorylation. It is also used as a metabolic stimulant. (Stedman, 26th ed). dinitrophenol : Members of the class of nitrophenol carrying two nitro substituents.. 2,4-dinitrophenol : A dinitrophenol having the nitro groups at the 2- and 4-positions.		2.0510dinitrophenolallergen;
antiseptic drug;
bacterial xenobiotic metabolite;
geroprotector;
oxidative phosphorylation inhibitor
3-aminobenzamide
[no description available]		9.981benzamides;
substituted aniline		EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
3-methylcholanthrene
Methylcholanthrene: A carcinogen that is often used in experimental cancer studies.. 3-methylcholanthrene : A pentacyclic ortho- and peri-fused polycyclic arene consisting of a dihydrocyclopenta[ij]tetraphene ring system with a methyl substituent at the 3-position.		2.0510ortho- and peri-fused polycyclic arenearyl hydrocarbon receptor agonist;
carcinogenic agent
enprofylline
enprofylline : Xanthine bearing a propyl substituent at position 3. A bronchodilator, it is used for the symptomatic treatment of asthma and chronic obstructive pulmonary disease, and in the management of cerebrovascular insufficiency, sickle cell disease, and diabetic neuropathy.		2.0410oxopurineanti-arrhythmia drug;
anti-asthmatic drug;
bronchodilator agent;
non-steroidal anti-inflammatory drug
4-(2-aminoethyl)benzenesulfonylfluoride
[no description available]		2.0110
phenytoin
[no description available]		9.0740imidazolidine-2,4-dioneanticonvulsant;
drug allergen;
sodium channel blocker;
teratogenic agent
hydroxyindoleacetic acid
(5-hydroxyindol-3-yl)acetic acid : A member of the class of indole-3-acetic acids that is indole-3-acetic acid substituted by a hydroxy group at C-5.		3.1510indole-3-acetic acidsdrug metabolite;
human metabolite;
mouse metabolite
tacrine
Tacrine: A cholinesterase inhibitor that crosses the blood-brain barrier. Tacrine has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the treatment of Alzheimer's disease and other central nervous system disorders.. tacrine : A member of the class of acridines that is 1,2,3,4-tetrahydroacridine substituted by an amino group at position 9. It is used in the treatment of Alzheimer's disease.		3.1750acridines;
aromatic amine		EC 3.1.1.7 (acetylcholinesterase) inhibitor
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.		3.8630aromatic 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.		4.6780acetamides;
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)		5.08120monocarboxylic 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.		2.4620acetophenones;
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
alaproclate
alaproclate: specific 5-hydroxytryptamine uptake inhibitors; RN given refers to (DL)-isomer		3.2310alpha-amino acid ester
albendazole
[no description available]		6.1951aryl 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).		4.0840phenols;
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		3.8630monocarboxylic 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.		3.5820imidazoles;
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.		3.5820organochlorine compound;
triazolobenzodiazepine		anticonvulsant;
anxiolytic drug;
GABA agonist;
muscle relaxant;
sedative;
xenobiotic
alprenolol
Alprenolol: One of the ADRENERGIC BETA-ANTAGONISTS used as an antihypertensive, anti-anginal, and anti-arrhythmic agent.. alprenolol : A secondary alcohol that is propan-2-ol substituted by a 2-allylphenoxy group at position 1 and an isopropylamino group at position 3. It is a beta-adrenergic antagonist used as a antihypertensive, anti-arrhythmia and a sympatholytic agent.		2.4620secondary alcohol;
secondary amino compound		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
sympatholytic agent
altretamine
Altretamine: A hexamethyl-2,4,6-triamine derivative of 1,3,5-triazine.		3.8130triamino-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		4.0840adamantanes;
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.		2.4620aromatic 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.		3.8730acetamides;
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.		3.2310diamine;
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.		2.7630dicarboximide;
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]		4.2650dimethylxanthineadenosine 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.		4.42601-benzofurans;
aromatic ketone;
organoiodine compound;
tertiary amino compound		cardiovascular drug
dan 2163
[no description available]		2.0810aromatic amide;
aromatic amine;
benzamides;
pyrrolidines;
sulfone		environmental contaminant;
second generation antipsychotic;
xenobiotic
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.		4.2650carbotricyclic compound;
tertiary amine		adrenergic uptake inhibitor;
antidepressant;
environmental contaminant;
tropomyosin-related kinase B receptor agonist;
xenobiotic
amlexanox
amlexanox: SRA-A antagonist;structure given in first source. amlexanox : A pyridochromene-derived monocarboxylic acid having an amino substituent at the 2-position, an oxo substituent at the 5-position and an isopropyl substituent at the 7-position.		2.0810monocarboxylic acid;
pyridochromene		anti-allergic agent;
anti-ulcer drug;
non-steroidal anti-inflammatory drug
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.		4.0840dihydropyridine;
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.		3.8730dibenzooxazepineadrenergic 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.		3.1750acridines;
aromatic ether;
sulfonamide		antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
anastrozole
[no description available]		3.8730nitrile;
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
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.		2.4720anthracenesantipsoriatic
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.		2.7430pyrazoloneantipyretic;
cyclooxygenase 3 inhibitor;
environmental contaminant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
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.		4.89100benzoic 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.		2.4720benzimidazoles;
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.		4.2650ethanolamines;
monocarboxylic acid amide;
propanolamine		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
environmental contaminant;
sympatholytic agent;
xenobiotic
aurintricarboxylic acid
Aurintricarboxylic Acid: A dye which inhibits protein biosynthesis at the initial stages. The ammonium salt (aluminon) is a reagent for the colorimetric estimation of aluminum in water, foods, and tissues.. aurintricarboxylic acid : A member of the class of quinomethanes that is 3-methylidene-6-oxocyclohexa-1,4-diene-1-carboxylic acid in which the methylidene hydrogens are replaced by 4-carboxy-3-hydroxyphenyl groups. The trisodium salt is the biological stain 'chrome violet CG' while the triammonium salt is 'aluminon'.		2.1510monohydroxybenzoic acid;
quinomethanes;
tricarboxylic acid		fluorochrome;
histological dye;
insulin-like growth factor receptor 1 antagonist
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.		4.2750aryl sulfide;
C-nitro compound;
imidazoles;
thiopurine		antimetabolite;
antineoplastic agent;
carcinogenic agent;
DNA synthesis inhibitor;
hepatotoxic agent;
immunosuppressive agent;
prodrug
azelastine
azelastine: azeptin is azelastine hydrochloride; structure; eye drop formulation effective in relieving symptoms of allergic conjunctivitis; do not confuse with 5-loxin which is an extract of Boswellia. azelastine : A phthalazine compound having an oxo substituent at the 1-position, a 1-methylazepan-4-yl group at the 2-position and a 4-chlorobenzyl substituent at the 4-position.		2.0410monochlorobenzenes;
phthalazines;
tertiary amino compound		anti-allergic agent;
anti-asthmatic drug;
bronchodilator agent;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
H1-receptor antagonist;
platelet aggregation inhibitor
baclofen
[no description available]		3.8730amino 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
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
benzamide
benzamide : An aromatic amide that consists of benzene bearing a single carboxamido substituent. The parent of the class of benzamides.		2.0510benzamides
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.		4.09401-benzofurans;
aromatic ketone		uricosuric drug
benzocaine
Benzocaine: A surface anesthetic that acts by preventing transmission of impulses along NERVE FIBERS and at NERVE ENDINGS.. dextran sulfate sodium : An organic sodium salt of dextran sulfate. It induces colitis in mice.. benzocaine : A benzoate ester having 4-aminobenzoic acid as the acid component and ethanol as the alcohol component. A surface anaesthetic, it is used to suppress the gag reflex, and as a lubricant and topical anaesthetic on the larynx, mouth, nasal cavity, respiratory tract, oesophagus, rectum, urinary tract, and vagina.		2.0810benzoate ester;
substituted aniline		allergen;
antipruritic drug;
sensitiser;
topical anaesthetic
betaxolol
[no description available]		3.5820propanolamineantihypertensive 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
bevantolol
bevantolol: structure given in first source. bevantolol : A propanolamine that is 3-aminopropane-1,2-diol in which the hydrogen of the primary hydroxy group is substituted by 3-methylphenyl and one of the hydrogens attached to the nitrogen is substituted by 2-(3,4-dimethoxyphenyl)ethyl. A beta1 adrenoceptor antagonist, it has been shown to be as effective as other beta-blockers for the treatment of angina pectoris and hypertension.		2.0410propanolamineanti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
calcium channel blocker
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.		4.2750(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.		2.4720biphenyls;
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.		3.5820piperidines;
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)		3.6120diarylmethane
bisoprolol
Bisoprolol: A cardioselective beta-1 adrenergic blocker. It is effective in the management of HYPERTENSION and ANGINA PECTORIS.		3.8630secondary alcohol;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
sympatholytic agent
bithionol
Bithionol: Halogenated anti-infective agent that is used against trematode and cestode infestations.. bithionol : An aryl sulfide that is diphenyl sulfide in which each phenyl group is substituted at position 2 by hydroxy and at positions 3 and 5 by chlorine. A fungicide and anthelmintic, it was used in various topical drug products for the treatment of liver flukes, but withdrawn after being shown to be a potent photosensitizer with the potential to cause serious skin disorders.		2.0510aryl sulfide;
bridged diphenyl antifungal drug;
bridged diphenyl fungicide;
dichlorobenzene;
organochlorine pesticide;
polyphenol		antifungal agrochemical;
antiplatyhelmintic drug
bromazepam
Bromazepam: One of the BENZODIAZEPINES that is used in the treatment of ANXIETY DISORDERS.		2.0410organic molecular entity
bromhexine
Bromhexine: A mucolytic agent used in the treatment of respiratory disorders associated with viscid or excessive mucus. (From Martindale, The Extra Pharmacopoeia, 30th ed, p744). bromhexine : A substituted aniline that is 2,4-dibromoaniline which is substituted at position 6 by a [cyclohexyl(methyl)amino]methyl group. It is used (as the monohydrochloride salt) as a mucolytic for the treatment of respiratory disorders associated with productive cough (i.e. a cough characterised by the production of sputum).		2.0510organobromine compound;
substituted aniline;
tertiary amino compound		mucolytic
bromopride
bromopride: RN given refers to parent cpd; structure		2.4620benzamides
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
bronopol
[no description available]		2.0810nitro compound
brotizolam
brotizolam: structure		2.4520organic molecular entity
buflomedil
buflomedil: RN given refers to parent cpd; synonym LL 1656 refers to HCl; structure		2.0410aromatic ketone
bumetanide
[no description available]		4.4260amino acid;
benzoic acids;
sulfonamide		diuretic;
EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor
bunazosin
bunazosin: structure		2.0410quinazolines
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.		2.7430aromatic 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.		4.0840azaspiro 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]		5.49110methanesulfonate 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]		4.7990purine 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.		9.5770aromatic ether;
nitrile;
polyether;
tertiary amino compound
metrizoate
Metrizoic Acid: A diagnostic radiopaque that usually occurs as the sodium salt.		2.0410monocarboxylic acidradioopaque medium
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.		3.8830benzimidazolecarboxylic acid;
biphenylyltetrazole		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
cannabinol
Cannabinol: A physiologically inactive constituent of Cannabis sativa L.		2.1110dibenzopyran
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.		6.1691dibenzoazepine;
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
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.		3.5920carbamate estermuscle relaxant
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.		17.9716432N-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.		2.4720carbazoles;
organochlorine compound		EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug;
photosensitizing agent
carvedilol
[no description available]		4.0840carbazoles;
secondary alcohol;
secondary amino compound		alpha-adrenergic antagonist;
antihypertensive agent;
beta-adrenergic antagonist;
cardiovascular drug;
vasodilator agent
carbonyl cyanide m-chlorophenyl hydrazone
Carbonyl Cyanide m-Chlorophenyl Hydrazone: A proton ionophore. It is commonly used as an uncoupling agent and inhibitor of photosynthesis because of its effects on mitochondrial and chloroplast membranes.. CCCP : A member of the class of monochlorobenzenes that is benzene substituted by 2-(1,3-dinitrilopropan-2-ylidene)hydrazinyl and chloro groups at positions 1 and 3, respectively. It is a mitochondrial depolarizing agent that induces reactive oxygen species mediated cell death.		2.830hydrazone;
monochlorobenzenes;
nitrile		antibacterial agent;
geroprotector;
ionophore
celecoxib
[no description available]		10.84285organofluorine compound;
pyrazoles;
sulfonamide;
toluenes		cyclooxygenase 2 inhibitor;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
cefixime
Cefixime: A third-generation cephalosporin antibiotic that is stable to hydrolysis by beta-lactamases.. cefixime : A third-generation cephalosporin antibiotic bearing vinyl and (2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-[(carboxymethoxy)imino]acetamido groups at positions 3 and 7, respectively, of the cephem skeleton. It is used in the treatment of gonorrhoea, tonsilitis, pharyngitis, bronchitis, and urinary tract infections.		3.4711
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.		4.5370aromatic 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		3.5920diarylmethane
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.		4.0840benzodiazepine
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.		7.96181aminoquinoline;
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.		4.0840monochlorobenzenes;
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.		4.5670organochlorine 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.		4.2650monochlorobenzenes;
N-sulfonylurea		hypoglycemic agent;
insulin secretagogue
chlorthalidone
Chlorthalidone: A benzenesulfonamide-phthalimidine that tautomerizes to a BENZOPHENONES form. It is considered a thiazide-like diuretic.		3.8730isoindoles;
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.		4.09401,3-benzoxazoles;
heteroaryl hydroxy compound;
organochlorine compound		muscle relaxant;
sedative
cifenline
[no description available]		2.4620diarylmethane
ciclopirox
[no description available]		2.7730cyclic hydroxamic acid;
hydroxypyridone antifungal drug;
pyridone		antibacterial agent;
antiseborrheic
ciglitazone
ciglitazone: structure given in second source; PPAR agonist used for type II diabetes. ciglitazone : An aromatic ether that consists of 1,3-thiazolidine-2,4-dione with position 5 substituted by a 4-[(1-methylcyclohexyl)methoxy]benzyl group. A selective PPARgamma agonist.		2.4720aromatic ether;
thiazolidinone		antineoplastic agent;
insulin-sensitizing drug
cilostazol
[no description available]		3.6120lactam;
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.		9.5470aliphatic 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.		2.0510cinnolines;
oxacycle;
oxo carboxylic acid		antibacterial drug;
antiinfective agent
ciprofibrate
[no description available]		2.9840cyclopropanes;
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.		4.0840aminoquinoline;
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.		2.4620benzamides
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.		4.42602-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.		2.4720monohydroxyquinoline;
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.		2.47201,4-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.		2.4720monochlorobenzenes;
phenazines		dye;
leprostatic drug;
non-steroidal anti-inflammatory drug
clofibrate
angiokapsul: contains clofibrate & insoitolnicotinate		4.2750aromatic ether;
ethyl ester;
monochlorobenzenes		anticholesteremic drug;
antilipemic drug;
geroprotector;
PPARalpha agonist
clomiphene
[no description available]		4.0940tertiary 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.		4.2650dibenzoazepineanticoronaviral 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.		3.58201,4-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.		3.8630clonidine;
imidazoline
4-chloro-N-(2,6-dimethyl-1-piperidinyl)-3-sulfamoylbenzamide
[no description available]		2.0810sulfonamide
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.		3.58201,4-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]		3.8630conazole antifungal drug;
imidazole antifungal drug;
imidazoles;
monochlorobenzenes		antiinfective agent;
environmental contaminant;
xenobiotic
cromolyn
cromoglycic acid : A dicarboxylic acid that is the bis-chromone derivative of glycerol. It is effective as a mast cell stabilizer.		2.0510chromones;
dicarboxylic acid		anti-asthmatic drug;
calcium channel blocker
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]		4.2650substituted aniline;
sulfone		anti-inflammatory drug;
antiinfective agent;
antimalarial;
leprostatic drug
deferiprone
Deferiprone: A pyridone derivative and iron chelator that is used in the treatment of IRON OVERLOAD in patients with THALASSEMIA.. deferiprone : A member of the class of 4-pyridones that is pyridin-4(1H)-one substituted at positions 1 and 2 by methyl groups and at position 3 by a hydroxy group. A lipid-soluble iron-chelator used for treatment of thalassaemia.		7.13104-pyridonesiron chelator;
protective agent
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.		3.8630acyclic 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.		4.2650dibenzoazepine;
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
nordazepam
Nordazepam: An intermediate in the metabolism of DIAZEPAM to OXAZEPAM. It may have actions similar to those of diazepam.. nordazepam : A 1,4-benzodiazepinone having phenyl and chloro substituents at positions 5 and 7 respectively; it has anticonvulsant, anxiolytic, muscle relaxant and sedative properties but is used primarily in the treatment of anxiety.		2.04101,4-benzodiazepinone;
organochlorine compound		anticonvulsant;
anxiolytic drug;
GABA modulator;
human metabolite;
sedative
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.		3.8630primary 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.		8.8930alpha-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.		9.57701,4-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.		4.0840benzothiadiazine;
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.		4.2650amino 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
3,4-dihydroxybenzohydroxamic acid
[no description available]		2.0110benzoic acids
diethylcarbamazine
Diethylcarbamazine: An anthelmintic used primarily as the citrate in the treatment of filariasis, particularly infestations with Wucheria bancrofti or Loa loa.		2.0510N-carbamoylpiperazine;
N-methylpiperazine
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.		4.2650monohydroxybenzoic acid;
organofluorine compound		non-narcotic analgesic;
non-steroidal anti-inflammatory drug
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.		3.5920dithiol;
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.		3.8630ether;
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.		4.0940piperidines;
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.		4.0840monocarboxylic acid amide;
pyridines;
tertiary amino compound		anti-arrhythmia drug
disulfiram
[no description available]		9.14173organic 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.		11.04384branched-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
racemetirosine
alpha-Methyltyrosine: 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. (Martindale, The Extra Pharmacopoeia, 30th ed)		2.9410
domperidone
Domperidone: A specific blocker of dopamine receptors. It speeds gastrointestinal peristalsis, causes prolactin release, and is used as antiemetic and tool in the study of dopaminergic mechanisms.. domperidone : 1-[3-(Piperidin-1-yl)propyl]-1,3-dihydro-2H-benzimidazol-2-one in which the 4-position of the piperidine ring is substituted by a 5-chloro-1,3-dihydro-2H-benzimidazol-2-on-1-yl group. A dopamine antagonist, it is used as an antiemetic for the short-term treatment of nausea and vomiting, and to control gastrointestinal effects of dopaminergic drugs given in the management of parkinsonism. The free base is used in oral suspensions, while the maleate salt is used in tablet preparations.		2.4620benzimidazoles;
heteroarylpiperidine		antiemetic;
dopaminergic antagonist
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.		4.0940aromatic 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.		3.8630morpholines;
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.		3.5820aromatic 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.		4.0840dibenzooxepine;
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.		3.5920aromatic 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.		3.5820oxopurine;
propane-1,2-diols		bronchodilator agent;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
muscle relaxant;
vasodilator agent
ebastine
[no description available]		2.0810organic molecular entity
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
ellipticine
ellipticine : A organic heterotetracyclic compound that is pyrido[4,3-b]carbazole carrying two methyl substituents at positions 5 and 11.		3.3110indole alkaloid;
organic heterotetracyclic compound;
organonitrogen heterocyclic compound;
polycyclic heteroarene		antineoplastic agent;
plant metabolite
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.		7.610trihydroxyanthraquinoneantineoplastic 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.		2.75301,8-naphthyridine derivative;
amino acid;
fluoroquinolone antibiotic;
monocarboxylic acid;
N-arylpiperazine;
quinolone antibiotic		antibacterial drug;
DNA synthesis inhibitor
erythrosine
Fluoresceins: A family of spiro(isobenzofuran-1(3H),9'-(9H)xanthen)-3-one derivatives. These are used as dyes, as indicators for various metals, and as fluorescent labels in immunoassays.		2.520
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
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.		4.0840aromatic 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.		3.8730dicarboximide;
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
ethyl loflazepate
ethyl loflazepate: structure given in first source		2.0510organic molecular entity
ethylenediamine
ethylenediamine: RN given refers to parent cpd; edamine is the recommended contraction for the ethylenediamine radical. ethylenediamine : An alkane-alpha,omega-diamine in which the alkane is ethane.		2.1510alkane-alpha,omega-diamineGABA agonist
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.		3.61201,1-bis(phosphonic acid)antineoplastic agent;
bone density conservation agent;
chelator
etilefrine
Etilefrine: A phenylephrine-related beta-1 adrenergic and alpha adrenergic agonist used as a cardiotonic and antihypotensive agent.		2.0410phenols
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]		3.87302-aminopurines;
acetate ester		antiviral drug;
prodrug
carbonyl cyanide p-trifluoromethoxyphenylhydrazone
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone: A proton ionophore that is commonly used as an uncoupling agent in biochemical studies.. carbonyl cyanide p-trifluoromethoxyphenylhydrazone : A hydrazone that is hydrazonomalononitrile in which one of the hydrazine hydrogens is substituted by a p-trifluoromethoxyphenyl group.		2.0510aromatic ether;
hydrazone;
nitrile;
organofluorine compound		ATP synthase inhibitor;
geroprotector;
ionophore
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.		4.0840carbamate esteranticonvulsant;
neuroprotective agent
4-biphenylylacetic acid
biphenyl-4-ylacetic acid : A monocarboxylic acid in which one of the alpha-hydrogens is substituted by a biphenyl-4-yl group. An active metabolite of fenbufen, it is used as a topical medicine to treat muscle inflammation and arthritis.		2.0810biphenyls;
monocarboxylic acid		non-steroidal anti-inflammatory drug
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.		4.0840dichlorobenzene;
dihydropyridine;
ethyl ester;
methyl ester		anti-arrhythmia drug;
antihypertensive agent;
calcium channel blocker;
vasodilator agent
fenfluramine
Fenfluramine: A centrally active drug that apparently both blocks serotonin uptake and provokes transport-mediated serotonin release.. fenfluramine : A secondary amino compound that is 1-phenyl-propan-2-amine in which one of the meta-hydrogens is substituted by trifluoromethyl, and one of the hydrogens attached to the nitrogen is substituted by an ethyl group. It binds to the serotonin reuptake pump, causing inhbition of serotonin uptake and release of serotonin. The resulting increased levels of serotonin lead to greater serotonin receptor activation which in turn lead to enhancement of serotoninergic transmission in the centres of feeding behavior located in the hypothalamus. This suppresses the appetite for carbohydrates. Fenfluramine was used as the hydrochloride for treatment of diabetes and obesity. It was withdrawn worldwide after reports of heart valve disease and pulmonary hypertension.		2.0510(trifluoromethyl)benzenes;
secondary amino compound		appetite depressant;
serotonergic agonist;
serotonin uptake inhibitor
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		4.4260aromatic 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
berotek
Fenoterol: A synthetic adrenergic beta-2 agonist that is used as a bronchodilator and tocolytic.. fenoterol : A member of the class resorcinols that is 5-(1-hydroxyethyl)benzene-1,3-diol in which one of the methyl hydrogens is replaced by a 1-(4-hydroxyphenyl)propan-2-amino group. A beta2-adrenergic agonist, it is used (as the hydrobromide salt) as a bronchodilator in the management of reversible airway obstruction.		2.4520resorcinols;
secondary alcohol;
secondary amino compound		beta-adrenergic agonist;
bronchodilator agent;
sympathomimetic agent;
tocolytic agent
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		2.0410azaspiro 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.		2.4520anilide;
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.		3.5920piperidines;
tertiary amine		anti-allergic agent;
H1-receptor antagonist
fipexide
fipexide: regulates dopaminergic systems at macromolecular level		3.5920benzodioxoles
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).		4.0840aromatic ether;
monocarboxylic acid amide;
organofluorine compound;
piperidines		anti-arrhythmia drug
fleroxacin
Fleroxacin: A broad-spectrum antimicrobial fluoroquinolone. The drug strongly inhibits the DNA-supercoiling activity of DNA GYRASE.. fleroxacin : A fluoroquinolone antibiotic that is 4-oxo-1,4-dihydroquinoline which is substituted at positions 1, 3, 6, 7 and 8 by 2-fluoroethyl, carboxy, fluoro, 4-methylpiperazin-1-yl and fluoro groups, respectively. It is active against many Gram-positive and Gram-negative bacteria.		2.4620difluorobenzene;
fluoroquinolone antibiotic;
monocarboxylic acid;
N-alkylpiperazine;
quinolines		antibacterial drug;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
topoisomerase IV inhibitor
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.		4.5670conazole 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.		6.9881aminopyrimidine;
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.		2.4620aromatic 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.		4.2650ethyl 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.		2.45201,4-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.		3.8730benzoic 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.		20.08589nucleobase 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.		4.99110(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.		3.8630fluorobiphenyl;
monocarboxylic acid		antipyretic;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
fluspirilene
Fluspirilene: A long-acting injectable antipsychotic agent used for chronic schizophrenia.		2.0510diarylmethane
flutamide
Flutamide: An antiandrogen with about the same potency as cyproterone in rodent and canine species.		4.2750(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.		3.8630carboxylic acid;
one-carbon compound;
phosphonic acids		antiviral drug;
geroprotector;
HIV-1 reverse transcriptase inhibitor;
sodium-dependent Pi-transporter inhibitor
furafylline
[no description available]		2.1110oxopurine
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.		4.4260chlorobenzoic 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.		3.8630gamma-amino acidanticonvulsant;
calcium channel blocker;
environmental contaminant;
xenobiotic
gemfibrozil
[no description available]		4.2750aromatic 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.		2.7630N-sulfonylureahypoglycemic agent;
insulin secretagogue;
radical scavenger
glimepiride
glimepiride: structure given in first source		4.0840sulfonamide
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.		3.8730aromatic 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.		2.4620piperidines
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.		4.2750monochlorobenzenes;
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.		8.6480
granisetron
[no description available]		3.5820aromatic 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.		3.8730acetamides
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.		3.7120carboxamidine;
guanidines;
one-carbon compound
1-(5-isoquinolinesulfonyl)-2-methylpiperazine
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine: A specific protein kinase C inhibitor, which inhibits superoxide release from human neutrophils (PMN) stimulated with phorbol myristate acetate or synthetic diacylglycerol.. 1-(5-isoquinolinesulfonyl)-2-methylpiperazine : A member of the class of N-sulfonylpiperazines that is 2-methylpiperazine substituted at position 1 by a 5-isoquinolinesulfonyl group.		2.1710isoquinolines;
N-sulfonylpiperazine		EC 2.7.11.13 (protein kinase C) inhibitor
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.		7.520isoquinolines;
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.		9.5870aromatic 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.		2.4620bridged 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.		2.5320phosphocholines;
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.		2.4520barbiturates
homochlorocyclizine
homochlorocyclizine: RN given refers to parent cpd		2.0510diarylmethane
hycanthone
Hycanthone: Potentially toxic, but effective antischistosomal agent, it is a metabolite of LUCANTHONE.. hycanthone : A thioxanthen-9-one compound having a hydroxymethyl substituent at the 1-position and a 2-[(diethylamino)ethyl]amino substituent at the 4-position. It was formerly used (particularly as the monomethanesulfonic acid salt) as a schistosomicide for individual or mass treatement of infection with Schistosoma haematobium and S. mansoni, but due to its toxicity and concern about possible carcinogenicity, it has been replaced by other drugs such as praziquantel.		2.0510thioxanthenesmutagen;
schistosomicide drug
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.		3.8630azaarene;
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.		4.2950benzothiadiazine;
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.		3.8730benzothiadiazine;
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.		8.4572aminoquinoline;
organochlorine compound;
primary alcohol;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antimalarial;
antirheumatic drug;
dermatologic drug
hydroxyurea
[no description available]		7.59132one-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.		3.8630hydroxyether;
monochlorobenzenes;
N-alkylpiperazine		anticoronaviral agent;
antipruritic drug;
anxiolytic drug;
dermatologic drug;
H1-receptor antagonist
hypericin
[no description available]		7.4420
ibudilast
[no description available]		7.2110pyrazolopyridine
ibuprofen
Midol: combination of cinnamedrine, phenacetin, aspirin & caffeine		4.0840monocarboxylic 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.		3.8630primary 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.		4.4260benzenes;
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]		2.05101,4-benzoquinones;
primary alcohol		antioxidant;
ferroptosis inhibitor
ifosfamide
[no description available]		7.71183ifosfamidesalkylating 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.		9.780dibenzoazepineadrenergic 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.		4.2650bipyridinesEC 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.		3.8730indoles;
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.		6.8571aromatic 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.		2.7530benzenedicarboxamide;
organoiodine compound		environmental contaminant;
radioopaque medium;
xenobiotic
iopromide
iopromide: structure given in first source. iopromide : A dicarboxylic acid diamide that consists of N-methylisophthalamide bearing three iodo substituents at positions 2, 4 and 6, a methoxyacetyl substituent at position 5 and two 2,3-dihydroxypropyl groups attached to the amide nitrogens. A water soluble x-ray contrast agent for intravascular administration.		2.0410dicarboxylic acid diamide;
organoiodine compound		environmental contaminant;
nephrotoxic agent;
radioopaque medium;
xenobiotic
iothalamic acid
Iothalamic Acid: A contrast medium in diagnostic radiology with properties similar to those of diatrizoic acid. It is used primarily as its sodium and meglumine (IOTHALAMATE MEGLUMINE) salts.		2.0410organic molecular entity
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]		4.0940carbohydrazide;
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.		4.2650azaspiro 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)		3.5920benzenes
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).		4.4160carbohydrazideantitubercular 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.		2.0510secondary 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.		3.8630catechols;
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.		4.0840benzoxadiazole;
dihydropyridine;
isopropyl ester;
methyl ester
itraconazole
[no description available]		4.0840piperazines
juglone
juglone: structure. juglone : A hydroxy-1,4-naphthoquinone that is 1,4-naphthoquinone in which the hydrogen at position 5 has been replaced by a hydroxy group. A plant-derived 1,4-naphthoquinone with confirmed antibacterial and antitumor activities.		7.610hydroxy-1,4-naphthoquinonegeroprotector;
herbicide;
reactive oxygen species generator
nsc 664704
kenpaullone: inhibits CDK1/cyclin B; structure in first source. kenpaullone : An indolobenzazepine that is paullone in which the hydrogen at position 9 is replaced by a bromo substituent. It is an ATP-competitive inhibitor of cyclin-dependent kinases (CDKs) and glycogen synthase kinase 3beta (GSK3beta).		2.2110indolobenzazepine;
lactam;
organobromine compound		cardioprotective agent;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor;
EC 2.7.11.26 (tau-protein kinase) inhibitor;
geroprotector
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.		4.0840cyclohexanones;
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.		2.7530aromatic 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.		5.99100dichlorobenzene;
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.		4.0840benzophenones;
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.		3.5820amino acid;
aromatic ketone;
monocarboxylic acid;
pyrrolizines;
racemate		analgesic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
ketotifen
Ketotifen: A cycloheptathiophene blocker of histamine H1 receptors and release of inflammatory mediators. It has been proposed for the treatment of asthma, rhinitis, skin allergies, and anaphylaxis.. ketotifen : An organic heterotricyclic compound that is 4,9-dihydro-10H-benzo[4,5]cyclohepta[1,2-b]thiophen-10-one which is substituted at position 4 by a 1-methylpiperidin-4-ylidene group. A blocker of histamine H1 receptors with a stabilising action on mast cells, it is used (usually as its hydrogen fumarate salt) for the treatment of asthma, where it may take several weeks to exert its full effect.		2.0510cyclic ketone;
olefinic compound;
organic heterotricyclic compound;
organosulfur heterocyclic compound;
piperidines;
tertiary amino compound		anti-asthmatic drug;
H1-receptor antagonist
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.		4.4260benzamides;
benzenes;
phenols;
primary carboxamide;
salicylamides;
secondary alcohol;
secondary amino compound
lamotrigine
[no description available]		3.87301,2,4-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.		4.0840benzimidazoles;
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.		2.0510benzochromenone;
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.		4.0940(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]		4.3250nitrile;
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.		2.4720aromatic 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]		16.379721N-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.		3.5920monocarboxylic 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.		3.8730benzocycloheptapyridine;
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.		3.5820benzodiazepine
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		4.4360biphenylyltetrazole;
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
2-(4-morpholinyl)-8-phenyl-4h-1-benzopyran-4-one
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one: specific inhibitor of phosphatidylinositol 3-kinase; structure in first source		3.3660chromones;
morpholines;
organochlorine compound		autophagy inhibitor;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
geroprotector
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.		4.2650anthracenes
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
edaravone
[no description available]		2.0410pyrazoloneantioxidant;
radical scavenger
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.		9.5670aromatic 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.		3.8630diarylmethane
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.		5.431aminobenzoic 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
meclofenamate sodium anhydrous
[no description available]		2.0510organic sodium salt
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.		4.0940aminobenzoic 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]		10.8661adamantanes;
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.		2.75301,4-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.		4.0840ethyl 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.		3.8630piperidinecarboxamidedrug 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)		4.0840organic 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.		3.8630amino 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.		3.5920phenothiazines;
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.		8.44213guanidinesenvironmental contaminant;
geroprotector;
hypoglycemic agent;
xenobiotic
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.		11.181benzenes;
diarylmethane;
ketone;
tertiary amino compound
methapyrilene
Methapyrilene: Histamine H1 antagonist with sedative action used as a hypnotic and in allergies.. methapyrilene : A member of the class of ethylenediamine derivatives that is ethylenediamine in which one of the nitrogens is substituted by two methyl groups, and the other nitrogen is substituted by a 2-pyridyl group and a (2-thienyl)methyl group.		2.7430ethylenediamine derivativeanti-allergic agent;
carcinogenic agent;
H1-receptor antagonist;
sedative
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
methoxyamine
methoxyamine: analytical reagent for aldehydes and ketones; strong irritant, can probably produce methemoglobinemia; RN given refers to parent cpd; structure		5.29120organooxygen compound
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
nocodazole
[no description available]		3.6120aromatic ketone;
benzimidazoles;
carbamate ester;
thiophenes		antimitotic;
antineoplastic agent;
microtubule-destabilising agent;
tubulin modulator
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.		2.5220benzoate ester;
methyl ester;
salicylates		flavouring agent;
insect attractant;
metabolite
methyl methanesulfonate
[no description available]		4.12150methanesulfonate esteralkylating agent;
apoptosis inducer;
carcinogenic agent;
genotoxin;
mutagen
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.		4.0840beta-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.		4.0840benzamides;
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.		3.8630organochlorine 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.		4.0840aromatic 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.		4.2650C-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.		4.4130aromatic 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.		3.8730aromatic 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.		2.7530dibenzoazepineadrenergic 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.		2.4620dichlorobenzene;
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.		9.2750imidazobenzodiazepine;
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]		3.5820bipyridines;
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.		4.0940dialkylarylamine;
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.		4.0840benzazepine;
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.		4.9860diarylmethane
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.		11.1591dihydroxyanthraquinoneanalgesic;
antineoplastic agent
moclobemide
Moclobemide: A reversible inhibitor of monoamine oxidase type A; (RIMA); (see MONOAMINE OXIDASE INHIBITORS) that has antidepressive properties.. moclobemide : A member of the class of benzamides that is benzamide substituted by a chloro group at position 4 and a 2-(morpholin-4-yl)ethyl group at the nitrogen atom. It acts as a reversible monoamine oxidase inhibitor and is used in the treatment of depression.		2.4620benzamides;
monochlorobenzenes;
morpholines		antidepressant;
environmental contaminant;
xenobiotic
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.		3.9330monocarboxylic 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]		2.7830benzamides;
carbamate ester;
primary amino compound;
pyridines;
substituted aniline		antineoplastic agent;
apoptosis inducer;
EC 3.5.1.98 (histone deacetylase) inhibitor
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
acecainide
Acecainide: A major metabolite of PROCAINAMIDE. Its anti-arrhythmic action may cause cardiac toxicity in kidney failure.. N-acetylprocainamide : A benzamide obtained via formal condensation of 4-acetamidobenzoic acid and 2-(diethylamino)ethylamine.		2.4620acetamides;
benzamides		anti-arrhythmia drug
ethylmaleimide
Ethylmaleimide: A sulfhydryl reagent that is widely used in experimental biochemical studies.		2.2510maleimidesanticoronaviral agent;
EC 1.3.1.8 [acyl-CoA dehydrogenase (NADP(+))] inhibitor;
EC 2.1.1.122 [(S)-tetrahydroprotoberberine N-methyltransferase] inhibitor;
EC 2.7.1.1 (hexokinase) inhibitor
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]		3.6120tetralins
nalidixic acid
[no description available]		4.09401,8-naphthyridine derivative;
monocarboxylic acid;
quinolone antibiotic		antibacterial drug;
antimicrobial agent;
DNA synthesis inhibitor
naratriptan
naratriptan: structure given in first source		3.5820heteroarylpiperidine;
sulfonamide;
tryptamines		serotonergic agonist;
vasoconstrictor agent
nefazodone
nefazodone: may be useful as an opiate adjunct		4.2650aromatic ether;
monochlorobenzenes;
N-alkylpiperazine;
N-arylpiperazine;
triazoles		alpha-adrenergic antagonist;
analgesic;
antidepressant;
serotonergic antagonist;
serotonin uptake inhibitor
nefopam
Nefopam: Non-narcotic analgesic chemically similar to ORPHENADRINE. Its mechanism of action is unclear. It is used for the relief of acute and chronic pain. (From Martindale, The Extra Pharmacopoeia, 30th ed, p26). nefopam : A racemate comprising equal amounts of (R)- and (S)-nefopam. The hydrochloride is a centrally acting non-opiate analgesic commonly used for the treatment of moderate to severe pain.. 5-methyl-1-phenyl-3,4,5,6-tetrahydro-1H-2,5-benzoxazocine : A member of the class of benzoxazocines that is 3,4,5,6-tetrahydro-1H-2,5-benzoxazocine substituted by phenyl and methyl groups at positions 1 and 5 respectively.		2.4620benzoxazocine;
tertiary amino compound
neostigmine
Neostigmine: A cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike PHYSOSTIGMINE, does not cross the blood-brain barrier.. neostigmine : A quaternary ammonium ion comprising an anilinium ion core having three methyl substituents on the aniline nitrogen, and a 3-[(dimethylcarbamoyl)oxy] substituent at position 3. It is a parasympathomimetic which acts as a reversible acetylcholinesterase inhibitor.		2.0810quaternary ammonium ionantidote to curare poisoning;
EC 3.1.1.7 (acetylcholinesterase) inhibitor
netropsin
Netropsin: A basic polypeptide isolated from Streptomyces netropsis. It is cytotoxic and its strong, specific binding to A-T areas of DNA is useful to genetics research.		2.4320
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.		4.0840cyclopropanes;
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.		9.1240benzenes;
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
niclosamide
Niclosamide: An antihelmintic that is active against most tapeworms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p48). niclosamide : A secondary carboxamide resulting from the formal condensation of the carboxy group of 5-chlorosalicylic acid with the amino group of 2-chloro-4-nitroaniline. It is an oral anthelmintic drug approved for use against tapeworm infections.		7.2510benzamides;
C-nitro compound;
monochlorobenzenes;
salicylanilides;
secondary carboxamide		anthelminthic drug;
anticoronaviral agent;
antiparasitic agent;
apoptosis inducer;
molluscicide;
piscicide;
STAT3 inhibitor
nifedipine
Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.		4.2650C-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.		4.0940aromatic 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.		4.26502-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.		4.2650C-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).		2.75301,4-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.		2.7530C-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.		3.5920nitroglycerolexplosive;
muscle relaxant;
nitric oxide donor;
prodrug;
tocolytic agent;
vasodilator agent;
xenobiotic
nizatidine
[no description available]		3.86301,3-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.		3.8630isoquinolinesdopamine 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.		3.8730fluoroquinolone 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.		4.2650organic tricyclic compound;
secondary amine		adrenergic uptake inhibitor;
analgesic;
antidepressant;
antineoplastic agent;
apoptosis inducer;
drug metabolite
5-nitro-2-(3-phenylpropylamino)benzoic acid
5-nitro-2-(3-phenylpropylamino)benzoic acid: structure given in first source; chloride channel antagonist		2.1310nitrobenzoic acid
ns 1619
NS 1619: structure given in first source. NS 1619 : A member of the class of benzimidazoles that is 1,3-dihydro-2H-benzimidazol-2-one in which the hydrogens at positions 1 and 5 are replaced are replaced by 2-hydroxy-5-(trifluoromethyl)phenyl and trifluoromethyl groups, respectively. It is an opener/activator of the large-conductance calcium-activated potassium channel (Bkca).		2.0510(trifluoromethyl)benzenes;
benzimidazoles;
phenols		potassium channel opener
n-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide: structure given in first source. NS-398 : A C-nitro compound that is N-methylsulfonyl-4-nitroaniline bearing an additional cyclohexyloxy substituent at position 2.		2.4110aromatic ether;
C-nitro compound;
sulfonamide		antineoplastic agent;
cyclooxygenase 2 inhibitor
nu2058
NU2058: structure in first source		210
o(6)-benzylguanine
O(6)-benzylguanine: a suicide inhibitor of O(6)-methylguanine-DNA methyltransferase activity		12.496510
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.		6.18513-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.		4.4260aromatic 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.		7.5682carbazoles
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.		2.17101,3,5-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.		4.09401,3-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.		3.86301,4-benzodiazepinone;
organochlorine compound		anxiolytic drug;
environmental contaminant;
xenobiotic
oxethazaine
[no description available]		2.0510amino acid amide
oxibendazole
oxibendazole: structure		2.0510benzimidazoles;
carbamate ester
oxidopamine
Oxidopamine: A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.. oxidopamine : A benzenetriol that is phenethylamine in which the hydrogens at positions 2, 4, and 5 on the phenyl ring are replaced by hydroxy groups. It occurs naturally in human urine, but is also produced as a metabolite of the drug DOPA (used for the treatment of Parkinson's disease).		2.0510benzenetriol;
catecholamine;
primary amino compound		drug metabolite;
human metabolite;
neurotoxin
oxiracetam
oxiracetam: structure in first source		2.0410organonitrogen compound;
organooxygen compound
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.		3.8730acetylenic 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.		3.8630aminobenzoic acid;
phenols		antitubercular agent
pamidronate
[no description available]		9.1140phosphonoacetic 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.		3.8630aromatic 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.		4.3150benzylisoquinoline alkaloid;
dimethoxybenzene;
isoquinolines		antispasmodic drug;
vasodilator agent
4-dichlorobenzene
dichlorobenzene : Any member of the class of chlorobenzenes carrying two chloro groups at unspecified positions.. 1,4-dichlorobenzene : A dichlorobenzene carrying chloro groups at positions 1 and 4.		2.0510dichlorobenzeneinsecticide
pargyline
Pargyline: A monoamine oxidase inhibitor with antihypertensive properties.		2.0510aromatic amine
pd 98059
2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one: inhibits MAP kinase kinase (MEK) activity, p42 MAPK and p44 MAPK; structure in first source. 2-(2-amino-3-methoxyphenyl)chromen-4-one : A member of the class of monomethoxyflavones that is 3'-methoxyflavone bearing an additional amino substituent at position 2'.		2.110aromatic amine;
monomethoxyflavone		EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
geroprotector
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.		4.09401,3-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.		3.8730aromatic 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.		3.8630barbituratesGABAA receptor agonist
pentoxifylline
[no description available]		4.0840oxopurine
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.		3.8630piperidinescardiovascular 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.		4.0840N-(2-hydroxyethyl)piperazine;
N-alkylpiperazine;
organochlorine compound;
phenothiazines		antiemetic;
dopaminergic antagonist;
phenothiazine antipsychotic drug
phenacetin
Saridon: contains phenacetin, caffeine, propyphenazone & pyrithyldione		3.1550acetamides;
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.		4.2650barbituratesanticonvulsant;
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
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.		3.5920primary 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
oxophenylarsine
oxophenylarsine: inhibits protein-tyrosine-phosphatase. phenylarsine oxide : An arsine oxide derived from phenylarsine.		2.1310arsine oxidesantineoplastic agent;
apoptosis inducer;
EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor
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.		2.4620pyrazolidinesantirheumatic 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		2.4520organohalogen compound;
pyrimidines
pifithrin
pifithrin: a tetrahydrobenzothiazol; inhibitor of P53 that protects mice from the side effects of cancer therapy; structure in first source		2.9640aromatic ketone
pimobendan
pimobendan: produces arterial & venous dilatation in dogs; structure given in first source		2.0410benzimidazoles;
pyridazinone		cardiotonic drug;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
vasodilator agent
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)		2.7530pyridines
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.		4.0840indoles;
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.		6.1651aromatic 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.		2.5120N-acylpiperazine;
organobromine compound;
tertiary carboxamide		alkylating agent;
antineoplastic agent
piracetam
Piracetam: A compound suggested to be both a nootropic and a neuroprotective agent.		6.290organonitrogen compound;
organooxygen compound
piretanide
piretanide: potent inhibitor of chloride transport; structure		2.0410aromatic ether
piribedil
Piribedil: A dopamine D2 agonist. It is used in the treatment of parkinson disease, particularly for alleviation of tremor. It has also been used for circulatory disorders and in other applications as a D2 agonist.		2.0810N-arylpiperazine
polythiazide
[no description available]		3.2310benzothiadiazine
4-aminobenzoic acid
para-Aminobenzoates: Benzoic acids, salts, or esters that contain an amino group attached to carbon number 4 of the benzene ring structure.. 4-aminobenzoate : An aromatic amino-acid anion that is the conjugate base of 4-aminobenzoic acid.		3.0640aminobenzoate;
aromatic amino-acid anion		Escherichia coli metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
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
ono 1078
pranlukast: SRS-A antagonist; leukotriene D4 receptor antagonist		2.0810chromones
pyranoprofen
pyranoprofen: RN given refers to unlabled parent cpd; structure given in first source		2.0810pyridochromene
praziquantel
azinox: Russian drug		4.0940isoquinolines
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.		4.0840aromatic ether;
furans;
monocarboxylic acid amide;
piperazines;
quinazolines		alpha-adrenergic antagonist;
antihypertensive agent;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
prilocaine
Prilocaine: A local anesthetic that is similar pharmacologically to LIDOCAINE. Currently, it is used most often for infiltration anesthesia in dentistry.. prilocaine : An amino acid amide in which N-propyl-DL-alanine and 2-methylaniline have combined to form the amide bond; used as a local anaesthetic.		2.0410amino acid amide;
monocarboxylic acid amide		anticonvulsant;
local anaesthetic
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.		4.0840aminoquinoline;
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.		4.0940pyrimidoneanticonvulsant;
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.		4.2650benzoic 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.		2.4620dithioketal;
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.		4.2650benzamidesanti-arrhythmia drug;
platelet aggregation inhibitor;
sodium channel blocker
procaine
Procaine: A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016).. procaine : A benzoate ester, formally the result of esterification of 4-aminobenzoic acid with 2-diethylaminoethanol but formed experimentally by reaction of ethyl 4-aminobenzoate with 2-diethylaminoethanol.		2.0510benzoate ester;
substituted aniline;
tertiary amino compound		central nervous system depressant;
drug allergen;
local anaesthetic;
peripheral nervous system drug
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.		15.096319benzamides;
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.		4.0840N-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.		3.8730pyrrolidines;
tertiary alcohol		antidyskinesia agent;
antiparkinson drug;
muscarinic antagonist
promazine
Promazine: A phenothiazine with actions similar to CHLORPROMAZINE but with less antipsychotic activity. It is primarily used in short-term treatment of disturbed behavior and as an antiemetic.. promazine : A phenothiazine deriative in which the phenothiazine tricycle has a 3-(dimethylaminopropyl) group at the N-10 position.		2.4520phenothiazines;
tertiary amine		antiemetic;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
H1-receptor antagonist;
muscarinic antagonist;
phenothiazine antipsychotic drug;
serotonergic 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.		4.2650phenothiazines;
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.		3.8730aromatic 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
propidium
Propidium: Quaternary ammonium analog of ethidium; an intercalating dye with a specific affinity to certain forms of DNA and, used as diiodide, to separate them in density gradients; also forms fluorescent complexes with cholinesterase which it inhibits.		3.0640phenanthridines;
quaternary ammonium ion		fluorochrome;
intercalator
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.		9.4660phenolsanticonvulsant;
antiemetic;
intravenous anaesthetic;
radical scavenger;
sedative
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.		4.5670naphthalenes;
propanolamine;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
anxiolytic drug;
beta-adrenergic antagonist;
environmental contaminant;
human blood serum metabolite;
vasodilator agent;
xenobiotic
propyl gallate
Propyl Gallate: Antioxidant for foods, fats, oils, ethers, emulsions, waxes, and transformer oils.		7.1510trihydroxybenzoic acid
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]		3.5820pyridinium ion
pyrimethamine
Maloprim: contains above 2 cpds		6.9381aminopyrimidine;
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.		8.930benzimidazoles;
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.		3.59201-benzothiophenes;
aromatic ketone;
N-oxyethylpiperidine;
phenols		bone density conservation agent;
estrogen antagonist;
estrogen receptor modulator
ranitidine
[no description available]		2.9740aralkylamine
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.		9.4660benzothiazoles
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.		4.58701,2-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		3.5820tryptaminesanti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
rofecoxib
[no description available]		4.5551butenolide;
sulfone		analgesic;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
rolipram
[no description available]		2.5220pyrrolidin-2-onesantidepressant;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor
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.		3.2310benzoate 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 202190
4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole: structure given in first source; inhibits p38 MAP kinase		2.0110imidazoles;
organofluorine compound;
phenols;
pyridines		apoptosis inducer;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
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.		9.4322N-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.		4.0840pyrimidines;
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
sodium fluoride
[no description available]		4.811fluoride saltmutagen
risedronic acid
Risedronic Acid: A pyridine and diphosphonic acid derivative that acts as a CALCIUM CHANNEL BLOCKER and inhibits BONE RESORPTION.		3.8730pyridines
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.		4.2650ethanolamines;
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.		2.0410long-chain fatty acid;
saturated fatty acid;
straight-chain saturated fatty acid		algal metabolite;
Daphnia magna metabolite;
human metabolite;
plant metabolite
imatinib
[no description available]		4.2550aromatic amine;
benzamides;
N-methylpiperazine;
pyridines;
pyrimidines		antineoplastic agent;
apoptosis inducer;
tyrosine kinase inhibitor
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).		9.49155dicarboxylic 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
sulfabenzamide
sulfabenzamide : A sulfonamide containing a benzamido substituent on nitrogen. An antibacterial/antimicrobial, it is often used in conjunction with sulfathiazole and sulfacetamide as a topical, intravaginal antibacterial preparation.		2.0510benzenes;
sulfonamide antibiotic;
sulfonamide		antibacterial drug;
antimicrobial drug
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.		3.8630sulfonamide 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.		2.9740isoxazoles;
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]		2.7830substituted aniline;
sulfonamide antibiotic;
sulfonamide		antibacterial agent;
drug allergen;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
sulfanitran
[no description available]		2.0810sulfonamide
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.		2.4820primary 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.		9.8190
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.		2.7430pyrazolidines;
sulfoxide		uricosuric drug
sulfisoxazole
Sulfisoxazole: A short-acting sulfonamide antibacterial with activity against a wide range of gram- negative and gram-positive organisms.. sulfisoxazole : A sulfonamide antibacterial with an oxazole substituent. It has antibiotic activity against a wide range of gram-negative and gram-positive organisms.		2.4620isoxazoles;
sulfonamide antibiotic;
sulfonamide		antibacterial drug;
drug allergen
sulfobromophthalein
Sulfobromophthalein: A phenolphthalein that is used as a diagnostic aid in hepatic function determination.		2.05102-benzofurans;
organobromine compound;
organosulfonic acid;
phenols		dye
sulforaphane
sulforaphane: from Cardaria draba L.. sulforaphane : An isothiocyanate having a 4-(methylsulfinyl)butyl group attached to the nitrogen.		2.5220isothiocyanate;
sulfoxide		antineoplastic agent;
antioxidant;
EC 3.5.1.98 (histone deacetylase) inhibitor;
plant metabolite
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.		4.2650sulfonamide;
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.		2.4520aromatic 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.		4.0440naphthalenesulfonic 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.		2.9740N-arylpiperazine;
organofluorine compound;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antiinfective agent;
antimicrobial agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
tazarotene
tazarotene: a topical acetylenic retinoid; a topical kerytolytic. tazarotene : The ethyl ester of tazarotenic acid. A prodrug for tazarotenic acid, it is used for the treatment of psoriasis, acne, and sun-damaged skin.		2.0810acetylenic compound;
ethyl ester;
pyridines;
retinoid;
thiochromane		keratolytic drug;
prodrug;
teratogenic agent
tegafur
[no description available]		3.8430organohalogen compound;
pyrimidines
telenzepine
telenzepine: structure given in first source		2.0510benzodiazepine
temazepam
Temazepam: A benzodiazepine that acts as a GAMMA-AMINOBUTYRIC ACID modulator and anti-anxiety agent.		3.5920benzodiazepine
terazosin
Terazosin: induces decreased blood pressure; used in the treatment of benign prostatic hyperplasia		3.8730furans;
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.		4.0840phenylethanolamines;
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.		2.9940diarylmethane
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.		14.123417phthalimides;
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.		9.1140phenothiazines;
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).		11.791aziridines
tiapride
[no description available]		2.0810benzamides
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.		3.8630monochlorobenzenes;
thienopyridine		anticoagulant;
fibrin modulating drug;
hematologic agent;
P2Y12 receptor antagonist;
platelet aggregation inhibitor
tilorone
Tilorone: An antiviral agent used as its hydrochloride. It is the first recognized synthetic, low-molecular-weight compound that is an orally active interferon inducer, and is also reported to have antineoplastic and anti-inflammatory actions.. tilorone : A member of the class of fluoren-9-ones that is 9H-fluoren-9-one which is substituted by a 2-(diethylamino)ethoxy group at positions 2 and 7. It is an interferon inducer and a selective alpha7 nicotinic acetylcholine receptor (alpha7 nAChR) agonist. Its hydrochloride salt is used as an antiviral drug.		2.4720aromatic ether;
diether;
fluoren-9-ones;
tertiary amino compound		anti-inflammatory agent;
antineoplastic agent;
antiviral agent;
interferon inducer;
nicotinic acetylcholine receptor agonist
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.		3.8730imidazolesantiamoebic 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.		4.0840benzothiadiazole;
imidazoles		alpha-adrenergic agonist;
muscle relaxant
nikethamide
Nikethamide: A central nervous system stimulant. It was formerly used in the treatment of barbiturate overdose but is now considered to be of no value for such purposes and may be dangerous. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1229)		2.0810pyridinecarboxamide
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.		3.8630N-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.		4.2650N-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.		3.5920aromatic ketone;
monocarboxylic acid;
pyrroles		EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug
tolnaftate
[no description available]		2.0810monothiocarbamic esterantifungal 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)		2.0510aromatic 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.		3.8630aromatic ether;
tertiary alcohol;
tertiary amino compound
tranexamic acid
Tranexamic Acid: Antifibrinolytic hemostatic used in severe hemorrhage.		3.8630amino 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.		4.0840monochlorobenzenes;
N-alkylpiperazine;
N-arylpiperazine;
triazolopyridine		adrenergic antagonist;
antidepressant;
anxiolytic drug;
H1-receptor antagonist;
sedative;
serotonin uptake inhibitor
triacetin
Triacetin: A triglyceride that is used as an antifungal agent.. triacetin : A triglyceride obtained by acetylation of the three hydroxy groups of glycerol. It has fungistatic properties (based on release of acetic acid) and has been used in the topical treatment of minor dermatophyte infections.		2.110triglycerideadjuvant;
antifungal drug;
food additive carrier;
food emulsifier;
food humectant;
fuel additive;
plant metabolite;
solvent
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.		3.8730pteridinesdiuretic;
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.		3.5820triazolobenzodiazepinesedative
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]		3.9330N-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.		3.8630oxazolidinoneanticonvulsant;
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.		4.2650aminopyrimidine;
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.		3.8630
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.		3.8630dibenzoazepine;
tertiary amino compound		antidepressant;
environmental contaminant;
xenobiotic
tripelennamine
Tripelennamine: A histamine H1 antagonist with low sedative action but frequent gastrointestinal irritation. It is used to treat ASTHMA; HAY FEVER; URTICARIA; and RHINITIS; and also in veterinary applications. Tripelennamine is administered by various routes, including topically.		2.0510aromatic amine
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.		4.0940chromanes;
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
troxipide
troxipide: RN given refers to parent cpd		2.3110benzamides
thenoyltrifluoroacetone
Thenoyltrifluoroacetone: Chelating agent and inhibitor of cellular respiration.		2.0810
tyramine
[no description available]		3.6120monoamine 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.		3.2310aminopyridine;
indolecarboxamide;
N-acylpiperazine;
sulfonamide		antiviral drug;
HIV-1 reverse transcriptase inhibitor
undecylenic acid
undecylenic acid: a fatty acid with a terminal double bond. 10-undecenoic acid : An undecenoic acid having its double bond in the 10-position. It is derived from castor oil and is used for the treatment of skin problems.. undecenoic acid : A C11, straight-chain fatty acid carrying a C=C double bond at any position.		2.0810undecenoic acidantifungal drug;
plant metabolite
urapidil
[no description available]		2.4620piperazines
urethane
[no description available]		7.1510carbamate esterfungal metabolite;
mutagen
venlafaxine
venlafaxine : A tertiary amino compound that is N,N-dimethylethanamine substituted at position 1 by a 1-hydroxycyclohexyl and 4-methoxyphenyl group.		4.0840cyclohexanols;
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]		3.8730gamma-amino acidanticonvulsant;
EC 2.6.1.19 (4-aminobutyrate--2-oxoglutarate transaminase) inhibitor
viloxazine
Viloxazine: A morpholine derivative used as an antidepressant. It is similar in action to IMIPRAMINE.		2.0410aromatic ether
pirinixic acid
pirinixic acid: structure		2.4720aryl sulfide;
organochlorine compound;
pyrimidines
ici 204,219
zafirlukast: a leukotriene D4 receptor antagonist		4.0940carbamate 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.		3.8730nitrile;
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.		4.0840imidazopyridinecentral nervous system depressant;
GABA agonist;
sedative
zomepirac
zomepirac: RN given refers to parent cpd; structure		2.0510aromatic ketone;
monocarboxylic acid;
monochlorobenzenes;
pyrroles		cardiovascular drug;
non-steroidal anti-inflammatory drug
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.		3.61201,2-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.		2.4620monochloropyridine;
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.		9.5370mitomycinalkylating agent;
antineoplastic agent
oxyphenonium
Oxyphenonium: A quaternary ammonium anticholinergic agent with peripheral side effects similar to those of ATROPINE. It is used as an adjunct in the treatment of gastric and duodenal ulcer, and to relieve visceral spasms. The drug has also been used in the form of eye drops for mydriatic effect.		2.0510acylcholine
corticosterone
[no description available]		2.151011beta-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone		human metabolite;
mouse metabolite
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.		5.057011beta-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
lysergic acid diethylamide
Lysergic Acid Diethylamide: Semisynthetic derivative of ergot (Claviceps purpurea). It has complex effects on serotonergic systems including antagonism at some peripheral serotonin receptors, both agonist and antagonist actions at central nervous system serotonin receptors, and possibly effects on serotonin turnover. It is a potent hallucinogen, but the mechanisms of that effect are not well understood.. lysergic acid diethylamide : An ergoline alkaloid arising from formal condensation of lysergic acid with diethylamine.		2.0510ergoline alkaloid;
monocarboxylic acid amide;
organic heterotetracyclic compound		dopamine agonist;
hallucinogen;
serotonergic agonist
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.		3.8730alkaloid 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.		2.7430beta-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).		3.8630glucitolcathartic;
Escherichia coli metabolite;
food humectant;
human metabolite;
laxative;
metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite;
sweetening agent
thymidine
[no description available]		2.4110pyrimidine 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.		2.4620nucleoside analogue;
organofluorine compound;
pyrimidine 2'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
antiviral drug;
radiosensitizing agent
piperonyl butoxide
[no description available]		2.0510benzodioxolespesticide synergist
benzimidazole
1H-benzimidazole : The 1H-tautomer of benzimidazole.		2.1310benzimidazole;
polycyclic heteroarene
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
isoproterenol hydrochloride
[no description available]		2.0510catechols
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.		2.0510ammonium 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.		3.86303-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.		3.8730non-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.		4.779011-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.		3.863017-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.		7.833017-oxo steroid;
3beta-hydroxy-Delta(5)-steroid;
androstanoid		androgen;
human metabolite;
mouse metabolite
promazine hydrochloride
[no description available]		2.0510hydrochloride
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.		3.8630penicillin allergen;
penicillin		antibacterial drug;
drug allergen;
epitope
idoxuridine
[no description available]		2.0510organoiodine compound;
pyrimidine 2'-deoxyribonucleoside		antiviral drug;
DNA synthesis inhibitor
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.		3.8630pilocarpineantiglaucoma 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.		3.86302-halophenol;
amino acid zwitterion;
iodophenol;
iodothyronine		human metabolite;
mouse metabolite;
thyroid hormone
carbon tetrachloride
Carbon Tetrachloride: A solvent for oils, fats, lacquers, varnishes, rubber waxes, and resins, and a starting material in the manufacturing of organic compounds. Poisoning by inhalation, ingestion or skin absorption is possible and may be fatal. (Merck Index, 11th ed). tetrachloromethane : A chlorocarbon that is methane in which all the hydrogens have been replaced by chloro groups.		2.7630chlorocarbon;
chloromethanes		hepatotoxic agent;
refrigerant
serine
Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from GLYCINE or THREONINE. It is involved in the biosynthesis of PURINES; PYRIMIDINES; and other amino acids.. serine : An alpha-amino acid that is alanine substituted at position 3 by a hydroxy group.		7.7730L-alpha-amino acid;
proteinogenic amino acid;
serine family amino acid;
serine zwitterion;
serine		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
chloramphenicol
Amphenicol: Chloramphenicol and its derivatives.		4.2650C-nitro compound;
carboxamide;
diol;
organochlorine compound		antibacterial drug;
antimicrobial agent;
Escherichia coli metabolite;
geroprotector;
Mycoplasma genitalium metabolite;
protein synthesis inhibitor
aspartic acid
Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter.. aspartic acid : An alpha-amino acid that consists of succinic acid bearing a single alpha-amino substituent. L-aspartic acid : The L-enantiomer of aspartic acid.		4.7361aspartate family amino acid;
aspartic acid;
L-alpha-amino acid;
proteinogenic amino acid		Escherichia coli metabolite;
mouse metabolite;
neurotransmitter
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.		11.7391amino 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
lysine
Lysine: An essential amino acid. It is often added to animal feed.. lysine : A diamino acid that is caproic (hexanoic) acid bearing two amino substituents at positions 2 and 6.. L-lysine : An L-alpha-amino acid; the L-isomer of lysine.		3.6270aspartate family amino acid;
L-alpha-amino acid zwitterion;
L-alpha-amino acid;
lysine;
organic molecular entity;
proteinogenic amino acid		algal metabolite;
anticonvulsant;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
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]		4.2650acetate 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.		4.0840carbamate 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.		3.155017-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
tubocurarine
Tubocurarine: A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.. tubocurarine : A benzylisoquinoline alkaloid muscle relaxant which constitutes the active component of curare.. isoquinoline alkaloid : Any alkaloid that has a structure based on an isoquinoline nucleus. They are derived from the amino acids like tyrosine and phenylalanine.		2.0810bisbenzylisoquinoline alkaloiddrug allergen;
muscle relaxant;
nicotinic antagonist
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.		4.0840aporphine 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
promethazine hydrochloride
[no description available]		2.0510hydrochlorideanti-allergic agent;
anticoronaviral agent;
antiemetic;
antipruritic drug;
geroprotector;
H1-receptor antagonist;
local anaesthetic;
sedative
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
adenosine diphosphate
Adenosine Diphosphate: Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.		2.6920adenosine 5'-phosphate;
purine ribonucleoside 5'-diphosphate		fundamental metabolite;
human metabolite
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.		2.4520azabicycloalkene;
beta-lactam antibiotic allergen;
carboxylic acid;
cephalosporin;
semisynthetic derivative;
thiophenes		antibacterial drug;
antimicrobial agent
uridine
[no description available]		2.4920uridinesdrug 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.		4.0840kanamycinsbacterial 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.		2.7330pyrimidine 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.		3.4511monohydroxyquinoline;
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		3.1650amino 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
tyrosine
Tyrosine: A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.. tyrosine : An alpha-amino acid that is phenylalanine bearing a hydroxy substituent at position 4 on the phenyl ring.		7.61153amino acid zwitterion;
erythrose 4-phosphate/phosphoenolpyruvate family amino acid;
L-alpha-amino acid;
proteinogenic amino acid;
tyrosine		EC 1.3.1.43 (arogenate dehydrogenase) inhibitor;
fundamental metabolite;
micronutrient;
nutraceutical
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.		3.5920quaternary 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
methoxamine hydrochloride
[no description available]		2.0510dimethoxybenzene
methicillin
Methicillin: One of the PENICILLINS which is resistant to PENICILLINASE but susceptible to a penicillin-binding protein. It is inactivated by gastric acid so administered by injection.. methicillin : A penicillin that is 6-aminopenicillanic acid in which one of the amino hydrogens is replaced by a 2,6-dimethoxybenzoyl group.		2.0410penicillin allergen;
penicillin		antibacterial drug
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
methylene blue
Methylene Blue: A compound consisting of dark green crystals or crystalline powder, having a bronze-like luster. Solutions in water or alcohol have a deep blue color. Methylene blue is used as a bacteriologic stain and as an indicator. It inhibits GUANYLATE CYCLASE, and has been used to treat cyanide poisoning and to lower levels of METHEMOGLOBIN.. methylene blue : An organic chloride salt having 3,7-bis(dimethylamino)phenothiazin-5-ium as the counterion. A commonly used dye that also exhibits antioxidant, antimalarial, antidepressant and cardioprotective properties.		2.520organic chloride saltacid-base indicator;
antidepressant;
antimalarial;
antimicrobial agent;
antioxidant;
cardioprotective agent;
EC 1.4.3.4 (monoamine oxidase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
EC 4.6.1.2 (guanylate cyclase) inhibitor;
fluorochrome;
histological dye;
neuroprotective agent;
physical tracer
ethyl methanesulfonate
Ethyl Methanesulfonate: An antineoplastic agent with alkylating properties. It also acts as a mutagen by damaging DNA and is used experimentally for that effect.. ethyl methanesulfonate : A methanesulfonate ester resulting from the formal condensation of methanesulfonic acid with ethanol.		2.110methanesulfonate esteralkylating agent;
antineoplastic agent;
carcinogenic agent;
genotoxin;
mutagen;
teratogenic agent
aniline
[no description available]		2.1510anilines;
primary arylamine
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
dimethylnitrosamine
Dimethylnitrosamine: A nitrosamine derivative with alkylating, carcinogenic, and mutagenic properties. It causes serious liver damage and is a hepatocarcinogen in rodents.		2.0510nitrosaminegeroprotector;
mutagen
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
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.		2.4620lactose
primaquine phosphate
[no description available]		2.0510
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.		9.44212aspartate family amino acid;
L-alpha-amino acid;
methionine zwitterion;
methionine;
proteinogenic amino acid		antidote to paracetamol poisoning;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical
1,2-dipalmitoylphosphatidylcholine
1,2-Dipalmitoylphosphatidylcholine: Synthetic phospholipid used in liposomes and lipid bilayers to study biological membranes. It is also a major constituent of PULMONARY SURFACTANTS.		2.1710
phenylalanine
Phenylalanine: An essential aromatic amino acid that is a precursor of MELANIN; DOPAMINE; noradrenalin (NOREPINEPHRINE), and THYROXINE.. L-phenylalanine : The L-enantiomer of phenylalanine.. phenylalanine : An aromatic amino acid that is alanine in which one of the methyl hydrogens is substituted by a phenyl group.		3.4811amino acid zwitterion;
erythrose 4-phosphate/phosphoenolpyruvate family amino acid;
L-alpha-amino acid;
phenylalanine;
proteinogenic amino acid		algal metabolite;
EC 3.1.3.1 (alkaline phosphatase) inhibitor;
Escherichia coli metabolite;
human xenobiotic metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
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.		4.6780alkaloid;
colchicine		anti-inflammatory agent;
gout suppressant;
mutagen
gallamine triethiodide
Gallamine Triethiodide: A synthetic nondepolarizing blocking drug. The actions of gallamine triethiodide are similar to those of TUBOCURARINE, but this agent blocks the cardiac vagus and may cause sinus tachycardia and, occasionally, hypertension and increased cardiac output. It should be used cautiously in patients at risk from increased heart rate but may be preferred for patients with bradycardia. (From AMA Drug Evaluations Annual, 1992, p198)		2.0510
mebanazine
mebanazine: RN given refers to parent cpd without isomeric designation; structure		3.2310benzenes
uracil mustard
Uracil Mustard: Nitrogen mustard derivative of URACIL. It is a alkylating antineoplastic agent that is used in lymphatic malignancies, and causes mainly gastrointestinal and bone marrow damage.		2.0510aminouracil;
nitrogen mustard
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.		3.5820penicillinantibacterial agent;
antibacterial drug
cycloheximide
Cycloheximide: Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.. cycloheximide : A dicarboximide that is 4-(2-hydroxyethyl)piperidine-2,6-dione in which one of the hydrogens attached to the carbon bearing the hydroxy group is replaced by a 3,5-dimethyl-2-oxocyclohexyl group. It is an antibiotic produced by the bacterium Streptomyces griseus.		2.4720antibiotic fungicide;
cyclic ketone;
dicarboximide;
piperidine antibiotic;
piperidones;
secondary alcohol		anticoronaviral agent;
bacterial metabolite;
ferroptosis inhibitor;
neuroprotective agent;
protein synthesis inhibitor
chloroform
Chloroform: A commonly used laboratory solvent. It was previously used as an anesthetic, but was banned from use in the U.S. due to its suspected carcinogenicity.. chloroform : A one-carbon compound that is methane in which three of the hydrogens are replaced by chlorines.		2.7430chloromethanes;
one-carbon compound		carcinogenic agent;
central nervous system drug;
inhalation anaesthetic;
non-polar solvent;
refrigerant
triamcinolone diacetate
triamcinolone diacetate: lysyl oxidase antagonist; Polcortolon may also refers to triamcinolone		2.0810corticosteroid hormone
gliotoxin
Gliotoxin: A fungal toxin produced by various species of Trichoderma, Gladiocladium fimbriatum, Aspergillus fumigatus, and Penicillium. It is used as an immunosuppressive agent.. gliotoxin : A pyrazinoindole with a disulfide bridge spanning a dioxo-substituted pyrazine ring; mycotoxin produced by several species of fungi.		2.2510dipeptide;
organic disulfide;
organic heterotetracyclic compound;
pyrazinoindole		antifungal agent;
EC 2.5.1.58 (protein farnesyltransferase) inhibitor;
immunosuppressive agent;
mycotoxin;
proteasome inhibitor
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.		2.462017beta-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.		4.5640beta-lactam antibiotic;
penicillin allergen;
penicillin		antibacterial drug
mannitol
[no description available]		4.4760mannitolallergen;
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]		11.51244beta-D-arabinoside;
monosaccharide derivative;
pyrimidine nucleoside		antimetabolite;
antineoplastic agent;
antiviral agent;
immunosuppressive agent
asparagine
Asparagine: A non-essential amino acid that is involved in the metabolic control of cell functions in nerve and brain tissue. It is biosynthesized from ASPARTIC ACID and AMMONIA by asparagine synthetase. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed). asparagine : An alpha-amino acid in which one of the hydrogens attached to the alpha-carbon of glycine is substituted by a 2-amino-2-oxoethyl group.		2.110amino acid zwitterion;
asparagine;
aspartate family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
medroxyprogesterone acetate
[no description available]		34020-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
valine
Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway.. valine : A branched-chain amino acid that consists of glycine in which one of the hydrogens attached to the alpha-carbon is substituted by an isopropyl group.. L-valine : The L-enantiomer of valine.		5.8721L-alpha-amino acid zwitterion;
L-alpha-amino acid;
proteinogenic amino acid;
pyruvate family amino acid;
valine		algal metabolite;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
Saccharomyces cerevisiae metabolite
threonine
Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins.. threonine : An alpha-amino acid in which one of the hydrogens attached to the alpha-carbon of glycine is substituted by a 1-hydroxyethyl group.		2.0610amino acid zwitterion;
aspartate family amino acid;
L-alpha-amino acid;
proteinogenic amino acid;
threonine		algal metabolite;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
mestranol
[no description available]		2.462017beta-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]		3.07403'-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.		2.7830erythrose 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.		4.9860arginine;
glutamine family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		biomarker;
Escherichia coli metabolite;
micronutrient;
mouse metabolite;
nutraceutical
acetylene
[no description available]		2.6920alkyne;
gas molecular entity;
terminal acetylenic compound
methyl iodide
methyl iodide: RN given refers to unlabeled cpd with MF of CH3-I. iodomethane : A member of the class of iodomethanes that is methane in which one of the hydrogens is replaced by iodine.		7.1110iodomethanes;
methyl halides		fumigant insecticide
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.		2.110aliphatic 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.		2.0510monocarboxylic acid;
organochlorine compound		carcinogenic agent;
metabolite;
mouse metabolite
trifluoroacetic acid
Trifluoroacetic Acid: A very strong halogenated derivative of acetic acid. It is used in acid catalyzed reactions, especially those where an ester is cleaved in peptide synthesis.. trifluoroacetic acid : A monocarboxylic acid that is the trifluoro derivative of acetic acid.		2.0210fluoroalkanoic acidhuman xenobiotic metabolite;
NMR chemical shift reference compound;
reagent
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.		2.753011beta-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
phencyclidine
Phencyclidine: A hallucinogen formerly used as a veterinary anesthetic, and briefly as a general anesthetic for humans. Phencyclidine is similar to KETAMINE in structure and in many of its effects. Like ketamine, it can produce a dissociative state. It exerts its pharmacological action through inhibition of NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE). As a drug of abuse, it is known as PCP and Angel Dust.. phencyclidine : A member of the class of piperidines that is piperidine in which the nitrogen is substituted with a 1-phenylcyclohexyl group. Formerly used as an anaesthetic agent, it exhibits both hallucinogenic and neurotoxic effects.		4.9921benzenes;
piperidines		anaesthetic;
neurotoxin;
NMDA receptor antagonist;
psychotropic drug
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
dimethyl sulfate
dimethyl sulfate: RN given refers to unlabeled cpd; structure. dimethyl sulfate : The dimethyl ester of sulfuric acid.		2.420alkyl sulfatealkylating agent;
immunosuppressive agent
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)		3.5920primary amino compound;
triol		buffer
triparanol
Triparanol: Antilipemic agent with high ophthalmic toxicity. According to Merck Index, 11th ed, the compound was withdrawn from the market in 1962 because of its association with the formation of irreversible cataracts.		2.0510stilbenoidanticoronaviral agent
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.		2.4620chloroethenesinhalation anaesthetic;
mouse metabolite
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.		10.1721alpha,beta-unsaturated monocarboxylic acidmetabolite
dichloroacetic acid
[no description available]		2.7630monocarboxylic 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
rhodamine b
rhodamine B: RN & N1 from 9th CI Form Index; RN given refers to parent cpd; structure in Merck Index, 9th ed, #7973; TETRAETHYLRHODAMINE was see RHODAMINES 1975-93; use RHODAMINES to search TETRAETHYLRHODAMINE 1975-93. rhodamine B : An organic chloride salt having N-[9-(2-carboxyphenyl)-6-(diethylamino)-3H-xanthen-3-ylidene]-N-ethylethanaminium as the counterion. An amphoteric dye commonly used as a fluorochrome.		5.1421organic chloride salt;
xanthene dye		fluorescent probe;
fluorochrome;
histological dye
cyclizine
Cyclizine: A histamine H1 antagonist given by mouth or parenterally for the control of postoperative and drug-induced vomiting and in motion sickness. (From Martindale, The Extra Pharmacopoeia, 30th ed, p935). cyclizine : An N-alkylpiperazine in which one nitrogen of the piperazine ring is substituted by a methyl group, while the other is substituted by a diphenylmethyl group.		2.4620N-alkylpiperazineantiemetic;
central nervous system depressant;
cholinergic antagonist;
H1-receptor antagonist;
local anaesthetic
methylprednisolone
Methylprednisolone: A PREDNISOLONE derivative with similar anti-inflammatory action.. 6alpha-methylprednisolone : The 6alpha-stereoisomer of 6-methylprednisolone.		5.08706-methylprednisolone;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antiemetic;
environmental contaminant;
neuroprotective agent;
xenobiotic
rotenone
Derris: A plant genus of the family FABACEAE. The root is a source of rotenoids (ROTENONE) and flavonoids. Some species of Pongamia have been reclassified to this genus and some to MILLETTIA. Some species of Deguelia have been reclassified to this genus.. rotenoid : Members of the class of tetrahydrochromenochromene that consists of a cis-fused tetrahydrochromeno[3,4-b]chromene skeleton and its substituted derivatives. The term was originally restricted to natural products, but is now also used to describe semi-synthetic and fully synthetic compounds.		2.4720organic heteropentacyclic compound;
rotenones		antineoplastic agent;
metabolite;
mitochondrial NADH:ubiquinone reductase inhibitor;
phytogenic insecticide;
piscicide;
toxin
9,10-anthraquinone
9,10-anthraquinone : An anthraquinone that is anthracene in which positions 9 and 10 have been oxidised to carbonyls.		2.610anthraquinone
diquat
Diquat: A contact herbicide used also to produce desiccation and defoliation. (From Merck Index, 11th ed). diquat : The organic cation formed formally by addition of an ethylene bridge between the nitrogen atoms of 2,2'-bipyridine. Most often available as the dibromide.		2.0510organic cationdefoliant;
herbicide
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
carbazole
carbazole: structure in first source		7.1110carbazole
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.		3.5820penicillin 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.		4.0840glucitol derivative;
nitrate ester		nitric oxide donor;
vasodilator agent
n-vinyl-2-pyrrolidinone
N-vinyl-2-pyrrolidinone: monomer of POVIDONE; structure given in first source		4.811pyrrolidin-2-ones
thymol
Thymol: A phenol obtained from thyme oil or other volatile oils used as a stabilizer in pharmaceutical preparations, and as an antiseptic (antibacterial or antifungal) agent.. thymol : A phenol that is a natural monoterpene derivative of cymene.		2.4110monoterpenoid;
phenols		volatile oil component
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
quinoxalines
quinoxaline : A naphthyridine in which the nitrogens are at positions 1 and 4.		4.1631mancude organic heterobicyclic parent;
naphthyridine;
ortho-fused heteroarene
tolonium chloride
Tolonium Chloride: A phenothiazine that has been used as a hemostatic, a biological stain, and a dye for wool and silk. Tolonium chloride has also been used as a diagnostic aid for oral and gastric neoplasms and in the identification of the parathyroid gland in thyroid surgery.. tolonium chloride : An organic chloride salt having 3-amino-7-(dimethylamino)-2-methylphenothiazin-5-ium (tolonium) as the counterion. It is a blue nuclear counterstain that can be used to demonstrate Nissl substance and is also useful for staining mast cell granules, both in metachromatic and orthochromatic techniques.		2.0810
xanthenes
Xanthenes: Compounds with three aromatic rings in linear arrangement with an OXYGEN in the center ring.		2.5520xanthene
phenothiazine
10H-phenothiazine : The 10H-tautomer of phenothiazine.		2.0510phenothiazineferroptosis inhibitor;
plant metabolite;
radical scavenger
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-bromophenol
bromophenol : A halophenol that is any phenol containing one or more covalently bonded bromine atoms.		2.0510bromophenolmarine metabolite
trehalose
alpha,alpha-trehalose : A trehalose in which both glucose residues have alpha-configuration at the anomeric carbon.		7.2110trehaloseEscherichia coli metabolite;
geroprotector;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
ethylbenzene
[no description available]		4.811alkylbenzene
quinuclidines
Quinuclidines: A class of organic compounds which contain two rings that share a pair of bridgehead carbon atoms and contains an amine group.		4.9942quinuclidines;
saturated organic heterobicyclic parent
pyridostigmine bromide
Pyridostigmine Bromide: A cholinesterase inhibitor with a slightly longer duration of action than NEOSTIGMINE. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants.		2.0510pyridinium salt
4,4'-diaminodiphenylmethane
4,4'-diaminodiphenylmethane: RN given refers to parent cpd; structure. 4,4'-diaminodiphenylmethane : An aromatic amine that is diphenylmethane substituted at the 4-position of each benzene ring by an amino group.		2.0510aromatic amineallergen;
carcinogenic agent
phenylisothiocyanate
phenylisothiocyanate: structure. phenyl isothiocyanate : An isothiocyanate having a phenyl group attached to the nitrogen; used for amino acid sequencing in the Edman degradation.		2.0510isothiocyanateallergen;
reagent
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
4-bromophenol
4-bromophenol : A bromophenol containing only hydroxy and bromo substituents that are para to one another.		2.0510bromophenolhuman urinary metabolite;
human xenobiotic metabolite;
marine metabolite;
mouse metabolite;
persistent organic pollutant;
rat metabolite
acrolein
[no description available]		2.2110enalherbicide;
human xenobiotic metabolite;
toxin
2-bromoethylamine
[no description available]		2.0510
allyl alcohol
allyl alcohol: structure. allylic alcohol : An alcohol where the hydroxy group is attached to a saturated carbon atom adjacent to a double bond (R groups may be H, organyl, etc.).. allyl alcohol : A propenol in which the C=C bond connects C-2 and C-3. It is has been found in garlic (Allium sativum). Formerly used as a herbicide for the control of various grass and weed seeds.		2.0510primary allylic alcohol;
propenol		antibacterial agent;
fungicide;
herbicide;
insecticide;
plant metabolite
bromobenzene
[no description available]		2.0510bromoarene;
bromobenzenes;
volatile organic compound		hepatotoxic agent;
mouse metabolite;
non-polar solvent
n-pentanoic acid
n-pentanoic acid: RN given refers to unlabeled parent cpd. valeric acid : A straight-chain saturated fatty acid containing five carbon atoms.		2.0510short-chain fatty acid;
straight-chain saturated fatty acid		plant metabolite
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.		9.28181pyrrole;
secondary amine
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.		4.2550mancude organic heteromonocyclic parent;
monocyclic heteroarene;
thiophenes;
volatile organic compound		non-polar solvent
isopropyl myristate
isopropyl myristate: used for microemulsions; structure		2.0310fatty acid ester
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.		2.4520peptide 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
imipramine hydrochloride
[no description available]		2.0510hydrochlorideantidepressant
neostigmine bromide
neostigmine bromide : The bromide salt of neostigmine.		2.4520bromide 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.		4.1340biguanidesantineoplastic 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.		2.4620barbituratesanticonvulsant
edrophonium chloride
edrophonium chloride : The chloride salt of edrophonium. A reversible inhibitor of cholinesterase with a rapid onset (30-60 seconds after injection) but a short duration of action (5-15 minutes), it 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.		2.0510chloride salt;
quaternary ammonium salt		antidote;
diagnostic agent;
EC 3.1.1.8 (cholinesterase) inhibitor
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.		5.0121aminoglycosideallergen;
antibacterial drug;
Escherichia coli metabolite
isoquinoline
[no description available]		7.4110azaarene;
isoquinolines;
mancude organic heterobicyclic parent;
ortho-fused heteroarene
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.		2.9940anthrapyrazole;
aromatic ketone;
cyclic ketone		antineoplastic agent;
c-Jun N-terminal kinase inhibitor;
geroprotector
di-n-pentyl phthalate
dipentyl phthalate : A phthalate ester that is the dipentyl ester of benzene-1,2-dicarboxylic acid.		2.0510diester;
phthalate ester		plasticiser
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.		2.8230hexosamine;
secondary amino compound
cinchophen
cinchophen: was heading 1963-94; ACIPHENOCHINOLIUM was see CHINOPHEN 1978-94; use QUINOLINES to search CINCHOPHEN 1966-94		3.8630quinolines
phenazopyridine hydrochloride
phenazopyridine hydrochloride : A hydrochloride obtained by combining phenazopyridine with one equivalent of hydrochloric acid. A local anesthetic that has topical analgesic effect on mucosa lining of the urinary tract. Its use is limited by problems with toxicity (primarily blood disorders) and potential carcinogenicity.		2.0510hydrochloridecarcinogenic agent;
local anaesthetic;
non-narcotic analgesic
tetrracaine hydrochloride
leocaine: a crystal beta-modification of the beta-dimethylaminoethyl ether of n-butylaminobenzoic acid hydrochloride		2.0510benzoate ester
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
diphenhydramine hydrochloride
Antitussive Agents: Agents that suppress cough. They act centrally on the medullary cough center. EXPECTORANTS, also used in the treatment of cough, act locally.. diphenhydramine hydrochloride : The hydrochloride salt of diphenhydramine.		2.0510hydrochloride;
organoammonium salt		anti-allergic agent;
antiemetic;
antiparkinson drug;
antipruritic drug;
H1-receptor antagonist;
local anaesthetic;
muscarinic antagonist;
sedative
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.		3.5820penicillin allergen;
penicillin		antibacterial drug
ditiocarb
Ditiocarb: A chelating agent that has been used to mobilize toxic metals from the tissues of humans and experimental animals. It is the main metabolite of DISULFIRAM.. diethyldithiocarbamic acid : A member of the class of dithiocarbamic acids that is diethylcarbamic acid in which both of the oxygens are replaced by sulfur.		2.3110dithiocarbamic acidschelator;
copper chelator
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.		3.5820acetylenic 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
catechin
Catechin: An antioxidant flavonoid, occurring especially in woody plants as both (+)-catechin and (-)-epicatechin (cis) forms.. catechin : Members of the class of hydroxyflavan that have a flavan-3-ol skeleton and its substituted derivatives.. rac-catechin : A racemate comprising equimolar amounts of (+)- and (-)-catechin. (+)-catechin : The (+)-enantiomer of catechin and a polyphenolic antioxidant plant metabolite.		8.1750catechinantioxidant;
plant metabolite
tripelennamine hydrochloride
[no description available]		2.0510
perylene
Perylene: A 20-carbon dibenz(de,kl)anthracene that can be viewed as a naphthalene fused to a phenalene or as dinaphthalene. It is used as fluorescent lipid probe in the cytochemistry of membranes and is a polycyclic hydrocarbon pollutant in soil and water. Derivatives may be carcinogenic.. perylene : An ortho- and peri-fused polycyclic arene comprising of five benzene rings that is anthracene in which the d,e and k,l sides are fused to benzene rings.		2.0310ortho- and peri-fused polycyclic arene;
perylenes
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.		15.576323azaarene;
mancude organic heterobicyclic parent;
ortho-fused heteroarene;
quinazolines
acridines
Acridines: Compounds that include the structure of acridine.. acridine : A polycyclic heteroarene that is anthracene in which one of the central CH groups is replaced by a nitrogen atom.		3.8130acridines;
mancude organic heterotricyclic parent;
polycyclic heteroarene		genotoxin
indazoles
Indazoles: A group of heterocyclic aromatic organic compounds consisting of the fusion of BENZENE and PYRAZOLES.		7.38121indazole
adamantane
Adamantane: A tricyclo bridged hydrocarbon.		2.610adamantanes;
polycyclic alkane
cyclopentane
Cyclopentanes: A group of alicyclic hydrocarbons with the general formula R-C5H9.. cyclopentanes : Cyclopentane and its derivatives formed by substitution.		2.3110cycloalkane;
cyclopentanes;
volatile organic compound		non-polar solvent
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.		2.6620isoxazoles;
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.		2.21101,3-oxazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
thiazoles
[no description available]		6.691611,3-thiazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
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.		9163diazine;
pyrazines		Daphnia magna metabolite
ethynodiol diacetate
Ethynodiol Diacetate: A synthetic progestational hormone used alone or in combination with estrogens as an oral contraceptive (CONTRACEPTIVES, ORAL).		2.0510steroid ester;
terminal acetylenic compound		contraceptive drug;
estrogen receptor modulator;
synthetic oral contraceptive
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
hydrazine
diamine : Any polyamine that contains two amino groups.		8.0782azane;
hydrazines		EC 4.3.1.10 (serine-sulfate ammonia-lyase) inhibitor
chlormadinone acetate
Chlormadinone Acetate: An orally active synthetic progestational hormone used often in combinations as an oral contraceptive (CONTRACEPTIVES, ORAL).		2.0510corticosteroid hormone
pirinitramide
Pirinitramide: A diphenylpropylamine with intense narcotic analgesic activity of long duration. It is a derivative of MEPERIDINE with similar activity and usage.		2.0410nitrile
edrophonium bromide
[no description available]		2.0410
norchlorcyclizine
norchlorcyclizine: RN given refers to parent cpd		2.0510
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
monocrotaline
Monocrotaline: A pyrrolizidine alkaloid and a toxic plant constituent that poisons livestock and humans through the ingestion of contaminated grains and other foods. The alkaloid causes pulmonary artery hypertension, right ventricular hypertrophy, and pathological changes in the pulmonary vasculature. Significant attenuation of the cardiopulmonary changes are noted after oral magnesium treatment.		2.0510pyrrolizidine alkaloid
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.		3.8730mixturebronchodilator 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.		8.91152N-glycosyl-1,3,5-triazine;
nucleoside analogue		antineoplastic agent
phenyramidol
phenyramidol: considered as a drug that possibly causes hepatotoxicity		2.0510aminopyridine
diazomethane
Diazomethane: A diazonium compound with the formula CH2N2.. diazomethane : The simplest diazo compound, in which a diazo group is attached to a methylene group.		2.0210diazo compoundalkylating agent;
antineoplastic agent;
carcinogenic agent;
poison
carbutamide
Carbutamide: A sulfonylurea antidiabetic agent with similar actions and uses to CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277)		2.0510benzenes;
sulfonamide
pseudoephedrine hydrochloride
pseudoephedrine hydrochloride : A hydrochloride that is the monohydrochloride salt of pseudoephedrine.		2.0510hydrochlorideplant metabolite
fluocinonide
Fluocinonide: A topical glucocorticoid used in the treatment of ECZEMA.		2.0510organic molecular entity
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.		3.8730benzazepine 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
aminoimidazole carboxamide
Aminoimidazole Carboxamide: An imidazole derivative which is a metabolite of the antineoplastic agents BIC and DIC. By itself, or as the ribonucleotide, it is used as a condensation agent in the preparation of nucleosides and nucleotides. Compounded with orotic acid, it is used to treat liver diseases.. 5-aminoimidazole-4-carboxamide : An aminoimidazole in which the amino group is at C-5 with a carboxamido group at C-4.		4.3541aminoimidazole;
monocarboxylic acid amide		mouse metabolite
bucladesine
[no description available]		2.05103',5'-cyclic purine nucleotide;
butanamides;
butyrate ester		agonist;
cardiotonic drug;
vasodilator agent
procarbazine hydrochloride
procarbazine hydrochloride : A hydrochloride obtained by combining procarbazine with one equivalent of hydrochloric acid. 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.		2.4720hydrochlorideantineoplastic agent
N-[(2-chlorophenyl)methyl]-1-[4-[[(2-chlorophenyl)methylamino]methyl]cyclohexyl]methanamine
[no description available]		2.0510aromatic amine
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)		2.974011beta-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
prenylamine
Prenylamine: A drug formerly used in the treatment of angina pectoris but superseded by less hazardous drugs. Prenylamine depletes myocardial catecholamine stores and has some calcium channel blocking activity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1406)		2.0510diarylmethane
trifluoroacetic anhydride
[no description available]		2.0210
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
cyproterone acetate
[no description available]		2.753020-oxo steroid;
3-oxo-Delta(4) steroid;
acetate ester;
chlorinated steroid;
steroid ester		androgen antagonist;
geroprotector;
progestin
lithocholic acid
Lithocholic Acid: A bile acid formed from chenodeoxycholate by bacterial action, usually conjugated with glycine or taurine. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as cholagogue and choleretic.. lithocholic acid : A monohydroxy-5beta-cholanic acid with a alpha-hydroxy substituent at position 3. It is a bile acid obtained from chenodeoxycholic acid by bacterial action.. lithocholate : A bile acid anion that is the conjugate base of lithocholic acid.		2.4620bile acid;
C24-steroid;
monohydroxy-5beta-cholanic acid		geroprotector;
human metabolite;
mouse metabolite
hydantoins
Hydantoins: Compounds based on imidazolidine dione. Some derivatives are ANTICONVULSANTS.. imidazolidine-2,4-dione : An imidazolidinone with oxo groups at position 2 and 4.		4.811imidazolidine-2,4-dione
chlorphentermine
Chlorphentermine: A sympathomimetic agent that was formerly used as an anorectic. It has properties similar to those of DEXTROAMPHETAMINE. It has been implicated in lipid storage disorders and pulmonary hypertension. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1223)		2.0510amphetamines
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.		3.86301-benzyl-3-(dimethylamino)-2-methyl-1-phenylpropyl propanoatemu-opioid receptor agonist;
opioid analgesic
ketobemidone
ketobemidone: structure		2.0410piperidines
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.		3.8630bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
aloe emodin
aloe emodin: structure distinct from emodin; this does not mean emodin from aloe. Aloe emodin : A dihydroxyanthraquinone that is chrysazin carrying a hydroxymethyl group at position 3. It has been isolated from plant species of the genus Aloe.		3.9220aromatic primary alcohol;
dihydroxyanthraquinone		antineoplastic agent;
plant metabolite
emetine
Emetine: The principal alkaloid of ipecac, from the ground roots of Uragoga (or Cephaelis) ipecacuanha or U. acuminata, of the Rubiaceae. It is used as an amebicide in many different preparations and may cause serious cardiac, hepatic, or renal damage and violent diarrhea and vomiting. Emetine inhibits protein synthesis in EUKARYOTIC CELLS but not PROKARYOTIC CELLS.. emetine : A pyridoisoquinoline comprising emetam having methoxy substituents at the 6'-, 7'-, 10- and 11-positions. It is an antiprotozoal agent and emetic. It inhibits SARS-CoV2, Zika and Ebola virus replication and displays antimalarial, antineoplastic and antiamoebic properties.		2.4720isoquinoline alkaloid;
pyridoisoquinoline		antiamoebic agent;
anticoronaviral agent;
antiinfective agent;
antimalarial;
antineoplastic agent;
antiprotozoal drug;
antiviral agent;
autophagy inhibitor;
emetic;
expectorant;
plant metabolite;
protein synthesis inhibitor
osthol
osthol: from Cnidium monnieri and Angelica pubescens (both Apiaceae); structure given in first source		2.2510botanical anti-fungal agent;
coumarins		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.		2.66201,4-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
melarsoprol
Melarsoprol: Arsenical used in trypanosomiases. It may cause fatal encephalopathy and other undesirable side effects.		7.1510triazines
carvacrol
carvacrol : A phenol that is a natural monoterpene derivative of cymene. An inhibitor of bacterial growth, it is used as a food additive. Potent activator of the human ion channels transient receptor potential V3 (TRPV3) and A1 (TRPA1).		2.4110botanical anti-fungal agent;
p-menthane monoterpenoid;
phenols		agrochemical;
antimicrobial agent;
flavouring agent;
TRPA1 channel agonist;
volatile oil component
caprolactone
hexano-6-lactone : A epsilon-lactone that is oxepane substituted by an oxo group at position 2.		7.1510epsilon-lactone
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.		5.5951
thiazolidines
Thiazolidines: Reduced (protonated) form of THIAZOLES. They can be oxidized to THIAZOLIDINEDIONES.		2.830thiazolidine
mustard gas
Mustard Gas: Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed).. bis(2-chloroethyl) sulfide : An ethyl sulfide that is diethyl sulfide in which a hydrogen from each of the terminal methyl groups is replaced by a chlorine. It is a powerful vesicant regulated under the Chemical Weapons Convention.		2.2110ethyl sulfide;
organochlorine compound		alkylating agent;
carcinogenic agent;
vesicant
oleanolic acid
[no description available]		2.110hydroxy monocarboxylic acid;
pentacyclic triterpenoid		plant metabolite
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
hematoxylin
Hematoxylin: A dye obtained from the heartwood of logwood (Haematoxylon campechianum Linn., Leguminosae) used as a stain in microscopy and in the manufacture of ink.		2.4110organic heterotetracyclic compound;
oxacycle;
polyphenol;
tertiary alcohol		histological dye;
plant metabolite
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.		4.1340furonaphthodioxole;
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]		8.662017alpha-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		3.6120diarylmethane
copper gluconate
Gluconates: Derivatives of gluconic acid (the structural formula HOCH2(CHOH)4COOH), including its salts and esters.		3.1810organic molecular entity
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.		2.4520thiazoles
perillyl alcohol
perillyl alcohol: inhibits geranylgeranyl transferase; structure in first source. perillyl alcohol : A limonene monoterpenoid consists of a cyclohexene ring substituted by a hydroxymethyl and a prop-1-en-2-yl group at positions 1 and 4 respectively. It is a constituent of a variety of essential oils including lavender.		5.0181limonene monoterpenoidplant metabolite;
volatile oil component
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.		4.1140amphetamines;
secondary amine		central nervous system stimulant;
environmental contaminant;
neurotoxin;
psychotropic drug;
xenobiotic
aminoacetonitrile
Aminoacetonitrile: Cyanomethylamine.		2.0610
levocarnitine
(R)-carnitine : The (R)-enantiomer of carnitine.		3.2310carnitineantilipemic drug;
nootropic agent;
nutraceutical;
Saccharomyces cerevisiae metabolite;
water-soluble vitamin (role)
sulfanilylurea
sulfanilylurea: antimicrobial agent; structure		3.2310benzenes;
sulfonamide
eosine yellowish-(ys)
Eosine Yellowish-(YS): A versatile red dye used in cosmetics, pharmaceuticals, textiles, etc., and as tissue stain, vital stain, and counterstain with HEMATOXYLIN. It is also used in special culture media.. eosin YS dye : An organic sodium salt that is 2',4',5',7'-tetrabromofluorescein in which the carboxy group and the phenolic hydroxy group have been deprotonated and the resulting charge is neutralised by two sodium ions.		2.4110organic sodium salt;
organobromine compound		fluorochrome;
histological dye
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.		2.5320organic chloride saltanthelminthic drug;
antibacterial agent;
antifungal agent;
antiseptic drug;
histological dye
amitriptyline hydrochloride
[no description available]		2.0510organic tricyclic compound
1-naphthylisothiocyanate
1-Naphthylisothiocyanate: A tool for the study of liver damage which causes bile stasis and hyperbilirubinemia acutely and bile duct hyperplasia and biliary cirrhosis chronically, with changes in hepatocyte function. It may cause skin and kidney damage.		2.7630isothiocyanateinsecticide
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.		2.4820
aniline mustard
Aniline Mustard: Alkylating anti-neoplastic agent.		1.9610
lithium carbonate
Lithium Carbonate: A lithium salt, classified as a mood-stabilizing agent. Lithium ion alters the metabolism of BIOGENIC MONOAMINES in the CENTRAL NERVOUS SYSTEM, and affects multiple neurotransmission systems.		2.0410carbonate salt;
lithium salt		antimanic drug
malachite green
malachite green: RN given refers to parent cpd; structure. malachite green : An organic chloride salt that is the monochloride salt of malachite green cation. Used as a green-coloured dye, as a counter-stain in histology, and for its anti-fungal properties in aquaculture.		2.2110organic chloride saltantibacterial agent;
antifungal drug;
carcinogenic agent;
environmental contaminant;
fluorochrome;
histological dye;
teratogenic agent
lactulose
[no description available]		3.5920glycosylfructosegastrointestinal drug;
laxative
isoxsuprine hydrochloride
[no description available]		2.0510alkylbenzene
diphenylamine
Diphenylamine: In humans it may be irritating to mucous membranes. Methemoglobinemia has been produced experimentally. In veterinary use, it is one of active ingredients in topical agents for prevention and treatment of screwworm infestation. An indicator in tests for nitrate poisoning.. diphenylamine : An aromatic amine containing two phenyl substituents. It has been used as a fungicide for the treatment of superficial scald in apples and pears, but is no longer approved for this purpose within the European Union.		2.0510aromatic amine;
bridged diphenyl fungicide;
secondary amino compound		antifungal agrochemical;
antioxidant;
carotogenesis inhibitor;
EC 1.3.99.29 [phytoene desaturase (zeta-carotene-forming)] inhibitor;
ferroptosis inhibitor;
radical scavenger
betaine hydrochloride
[no description available]		2.0510
megestrol acetate
[no description available]		2.472020-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.		4.2850acetylcysteine;
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
3-hydroxyacetanilide
metacetamol : A derivative of phenol which has an acetamido substituent located meta to the phenolic -OH group. It is a non-toxic regioisomer of paracetamol with analgesic properties, but has never been marketed as a drug.		2.0510acetamides;
phenols		non-narcotic analgesic
methoxyacetic acid
methoxyacetic acid: RN given refers to parent cpd. methoxyacetic acid : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by a methoxy group.		2.0510ether;
monocarboxylic acid		antineoplastic agent;
apoptosis inducer;
human xenobiotic metabolite;
mutagen
c.i. 42510
Rosaniline Dyes: Compounds that contain the triphenylmethane aniline structure found in rosaniline. Many of them have a characteristic magenta color and are used as COLORING AGENTS.. basic fuchsin : A four-component mixture of chemically related dyes comprising pararosanilin, rosanilin, magenta II and new fuchsin in varying amounts. rosanilin : A hydrochloride that is the monohydrochloride of 4-[(4-aminophenyl)(4-iminocyclohexa-2,5-dien-1-ylidene)methyl]-2-methylaniline. One of the major constituents of Basic fuchsin, together with pararosanilin, magenta II and new fuchsin.		2.2110
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.		4.4260cyclic ketone;
erythromycin
perfluoropentane
perfluoropentane: inert expander of tissue spaces, liquid at room temperature, but gaseous at body temperatures; used in experimental eye surgery; structure. perfluoropentane : A fluorocarbon that is pentane in which all of the hydrogens have been replaced by fluorines.		2.610fluoroalkane;
fluorocarbon		radioopaque medium;
ultrasound contrast agent
methylnitrosourea
Methylnitrosourea: A nitrosourea compound with alkylating, carcinogenic, and mutagenic properties.. N-methyl-N-nitrosourea : A member of the class of N-nitrosoureas that is urea in which one of the nitrogens is substituted by methyl and nitroso groups.		8.360N-nitrosoureasalkylating agent;
carcinogenic agent;
mutagen;
teratogenic agent
2-chloroethyl ethyl sulfide
[no description available]		2.2110
hydroxychloroquine sulfate
[no description available]		2.0810
ethylnitrosourea
Ethylnitrosourea: A nitrosourea compound with alkylating, carcinogenic, and mutagenic properties.. N-ethyl-N-nitrosourea : A member of the class of N-nitrosoureas that is urea in which one of the nitrogens is substituted by ethyl and nitroso groups.		1.9910N-nitrosoureasalkylating agent;
carcinogenic agent;
genotoxin;
mutagen
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.		6.014117beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
terminal acetylenic compound		contraceptive drug;
female contraceptive drug;
progestin;
synthetic oral contraceptive
lormetazepam
lormetazepam: RN given refers to cpd with specified locant for methyl group; structure given in first source. lormetazepam : A 1,4-benzodiazepinone compound having a methyl substituent at the 1-position, a hydroxy substituent at the 3-position, a 2-chlorophenyl group at the 5-position and a chloro substituent at the 7-position.		2.04101,4-benzodiazepinone;
organochlorine compound		sedative
vinblastine
[no description available]		3.1650
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]		14.25447pyrimidine 2'-deoxyribonucleosideEscherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
cyproheptadine hydrochloride (anhydrous)
cyproheptadine hydrochloride (anhydrous) : The hydrochloride salt of cyproheptadine. Note that the drug named cyproheptadine hydrochloride generally refers to cyproheptadine hydrochloride sesquihydrate.		2.0510hydrochloride
estradiol valerate
[no description available]		2.0510steroid ester
ethambutol hydrochloride
ethambutol dihydrochloride : The dihydrchloride salt of ethambutol. A bacteriostatic antimycobacterial drug, it is effective against Mycobacterium tuberculosis and some other mycobacteria. It is used in combination with other antituberculous drugs in the treatment of pulmonary and extrapulmonary tuberculosis; resistant strains of M. tuberculosis are readily produced if ethambutol dihydrochloride is used alone.		2.0810hydrochlorideantitubercular agent
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.		3.5820ethanolamines;
ethylenediamine derivative		antitubercular agent;
environmental contaminant;
xenobiotic
calcium peroxide
[no description available]		4.811calcium oxides
durapatite
Durapatite: The mineral component of bones and teeth; it has been used therapeutically as a prosthetic aid and in the prevention and treatment of osteoporosis.. hydroxylapatite : A phosphate mineral with the formula Ca5(PO4)3(OH).		2.0710
manganese dioxide
[no description available]		4.811manganese molecular entity;
metal oxide
zinc oxide
Zinc Oxide: A mild astringent and topical protectant with some antiseptic action. It is also used in bandages, pastes, ointments, dental cements, and as a sunblock.		10.1221zinc molecular entity
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.		5.8783
antimycin a
[no description available]		2.0810benzamides;
formamides;
macrodiolide;
phenols		antifungal agent;
mitochondrial respiratory-chain inhibitor;
piscicide
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.		4.0840glycopeptideantibacterial drug;
antimicrobial agent;
bacterial 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.		5.4641alpha-tocopherolalgal metabolite;
antiatherogenic agent;
anticoagulant;
antioxidant;
antiviral agent;
EC 2.7.11.13 (protein kinase C) inhibitor;
immunomodulator;
micronutrient;
nutraceutical;
plant metabolite
tocopherols
[no description available]		2.1310
pregnenolone carbonitrile
Pregnenolone Carbonitrile: A catatoxic steroid and microsomal enzyme inducer having significant effects on the induction of cytochrome P450. It has also demonstrated the potential for protective capability against acetaminophen-induced liver damage.		2.0810aliphatic nitrile
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.		3.5920monocarboxylic acidEC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
hepatotoxic agent;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
metylperon
metylperon: RN given refers to parent cpd		2.4620aromatic ketone
metaxalone
[no description available]		3.2310aromatic 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.		3.8630cyclic acetal;
cyclic hemiketal;
cyclic ketone;
pyranobenzodioxin;
secondary alcohol;
secondary amino compound		antibacterial drug;
antimicrobial agent;
bacterial metabolite
paraquat
Paraquat: A poisonous dipyridilium compound used as contact herbicide. Contact with concentrated solutions causes irritation of the skin, cracking and shedding of the nails, and delayed healing of cuts and wounds.. paraquat : An organic cation that consists of 4,4'-bipyridine bearing two N-methyl substituents loctated at the 1- and 1'-positions.		2.4620organic cationgeroprotector;
herbicide
s,n,n'-tripropylthiocarbamate
Reward: An object or a situation that can serve to reinforce a response, to satisfy a motive, or to afford pleasure.. vernolate : A monounsaturated fatty acid anion that is the conjugate base of vernolic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.		2.3110tertiary amine
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.		8.26102benzochromene;
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
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.		4.1140benzimidazoles;
heteroarylpiperidine;
organofluorine compound		antidyskinesia agent;
dopaminergic antagonist;
first generation antipsychotic;
H1-receptor antagonist;
serotonergic antagonist
benperidol
Benperidol: A butyrophenone with general properties similar to those of HALOPERIDOL. It has been used in the treatment of aberrant sexual behavior. (From Martindale, The Extra Pharmacopoeia, 30th ed, p567)		2.0410aromatic ketone
methylprednisolone hemisuccinate
Methylprednisolone Hemisuccinate: A water-soluble ester of METHYLPREDNISOLONE used for cardiac, allergic, and hypoxic emergencies.		2.0610corticosteroid hormone;
hemisuccinate
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
chlordesmethyldiazepam
[no description available]		2.0410benzodiazepine
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		4.4260dihydrofuran;
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.		2.4520organofluorine 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.		3.8730dichlorobenzene;
penicillin		antibacterial drug
fluorescein-5-isothiocyanate
Fluorescein-5-isothiocyanate: Fluorescent probe capable of being conjugated to tissue and proteins. It is used as a label in fluorescent antibody staining procedures as well as protein- and amino acid-binding techniques.. fluorescein 5-isothiocyanate : The 5-isomer of fluorescein isothiocyanate. Acts as a fluorescent probe capable of being conjugated to tissue and proteins; used as a label in fluorescent antibody staining procedures as well as protein- and amino acid-binding techniques.		2.1510fluorescein isothiocyanate
mannose
mannopyranose : The pyranose form of mannose.		7.4110D-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.		3.231017alpha-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(4) steroid;
tertiary alpha-hydroxy ketone		antineoplastic agent;
appetite enhancer;
contraceptive drug;
progestin;
synthetic oral contraceptive
tranylcypromine
Tranylcypromine: A propylamine formed from the cyclization of the side chain of amphetamine. This monoamine oxidase inhibitor is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in panic and phobic disorders. (From AMA Drug Evaluations Annual, 1994, p311). tranylcypromine : A racemate comprising equal amounts of (1R,2S)- and (1S,2R)-2-phenylcyclopropan-1-amine. An irreversible monoamine oxidase inhibitor that is used as an antidepressant (INN tranylcypromine).. (1R,2S)-tranylcypromine : A 2-phenylcyclopropan-1-amine that is the (1R,2S)-enantiomer of tranylcypromine.		2.58202-phenylcyclopropan-1-amine
streptomycin
[no description available]		4.0840antibiotic antifungal drug;
antibiotic fungicide;
streptomycins		antibacterial drug;
antifungal agrochemical;
antimicrobial agent;
antimicrobial drug;
bacterial metabolite;
protein synthesis inhibitor
nitroxoline
nitroxoline: structure in Merck Index, 9th ed, #6475; RN given refers to parent cpd. nitroxoline : A monohydroxyquinoline in which the hydroxy group is positioned at C-8 with a nitro group trans to it at C-5.		2.6120C-nitro compound;
monohydroxyquinoline		antifungal agent;
antiinfective agent;
antimicrobial agent;
renal agent
clonidine hydrochloride
[no description available]		2.0510dichlorobenzene
cladribine
[no description available]		4.4260organochlorine compound;
purine 2'-deoxyribonucleoside		antineoplastic agent;
immunosuppressive agent
ethylene dimethanesulfonate
ethylene dimethanesulfonate: antispermatogenic agent; structure		2.0510
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.		3.5820penicillin 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
noxiptilin
noxiptilin: proposed tricyclic antidepressent; minor descriptor (75-86); on line & INDEX MEDICUS search DIBENZOCYCLOHEPTENES (75-86); RN given refers to parent cpd		2.0510organic tricyclic compound
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
buthionine sulfoximine
Buthionine Sulfoximine: A synthetic amino acid that depletes glutathione by irreversibly inhibiting gamma-glutamylcysteine synthetase. Inhibition of this enzyme is a critical step in glutathione biosynthesis. It has been shown to inhibit the proliferative response in human T-lymphocytes and inhibit macrophage activation. (J Biol Chem 1995;270(33):1945-7). 2-amino-4-(S-butylsulfonimidoyl)butanoic acid : A non-proteinogenic alpha-amino acid that is homocysteine in which the thiol group carries an oxo, imino and butyl groups.. S-butyl-DL-homocysteine (S,R)-sulfoximine : A sulfoximide that is the sulfoximine derivative of an analogue of DL-methionine in which the S-methyl group is replaced by S-butyl.		3.1850diastereoisomeric mixture;
homocysteines;
non-proteinogenic alpha-amino acid;
sulfoximide		EC 6.3.2.2 (glutamate--cysteine ligase) inhibitor;
ferroptosis inducer
metocurine
metocurine: from Chinese herb Cyclea hainanensis Mrr		2.0810isoquinolines
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.		2.4520penicillin allergen;
penicillin		antibacterial drug
clomacran
clomacran: RN given refers to parent cpd; structure		3.5920acridines
mexiletine hydrochloride
mexiletine hydrochloride : A hydrochloride composed of equimolar amounts of mexiletine and hydrogen chloride.		2.0510hydrochlorideanti-arrhythmia drug
beclomethasone dipropionate
beclomethasone dipropionate : A steroid ester comprising beclomethasone having propionyl groups at the 17- and 21-positions.		2.452011beta-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(1),Delta(4)-steroid;
chlorinated steroid;
corticosteroid;
enone;
glucocorticoid;
propanoate ester;
steroid ester		anti-arrhythmia drug;
anti-asthmatic drug;
anti-inflammatory drug;
prodrug
vidarabine
adenine arabinoside : A purine nucleoside in which adenine is attached to arabinofuranose via a beta-N(9)-glycosidic bond.		2.4620beta-D-arabinoside;
purine nucleoside		antineoplastic agent;
bacterial metabolite;
nucleoside antibiotic
iprindole
Iprindole: A tricyclic antidepressant that has actions and uses similar to those of AMITRIPTYLINE, but has only weak antimuscarinic and sedative effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p257)		2.0510indoles
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.		3.5820azobenzenes;
dicarboxylic acid		non-steroidal anti-inflammatory drug;
prodrug
nimorazole
Nimorazole: An antitrichomonal agent which is effective either topically or orally and whose urinary metabolites are also trichomonicidal.		7.3110C-nitro compound;
imidazoles
tiadenol
tiadenol: structure		2.0510aliphatic sulfide
terodiline
[no description available]		2.0410diarylmethane
1-(4-carboxyphenyl)-3,3-dimethyltriazene
1-(4-carboxyphenyl)-3,3-dimethyltriazene: RN given refers to parent cpd		2.0410
metoclopramide hydrochloride
metoclopramide hydrochloride : A hydrate that is the monohydrate form of metoclopramide monohydrochloride.		2.0510
etidronate disodium
etidronate disodium : An organic sodium salt resulting from the replacement of two protons from etidronic acid (one from from each of the phosphonic acid groups) by sodium ions.		2.0810organic sodium saltantineoplastic agent;
bone density conservation agent;
chelator
lanthanum
[no description available]		7.2510f-block element atom;
lanthanoid atom;
scandium group element atom
lutetium
Lutetium: An element of the rare earth family of metals. It has the atomic symbol Lu, atomic number 71, and atomic weight 175.		3.6320d-block element atom;
lanthanoid atom
manganese
Manganese: A trace element with atomic symbol Mn, atomic number 25, and atomic weight 54.94. It is concentrated in cell mitochondria, mostly in the pituitary gland, liver, pancreas, kidney, and bone, influences the synthesis of mucopolysaccharides, stimulates hepatic synthesis of cholesterol and fatty acids, and is a cofactor in many enzymes, including arginase and alkaline phosphatase in the liver. (From AMA Drug Evaluations Annual 1992, p2035). manganese(4+) : A manganese cation that is monoatomic and has a formal charge of +4.		4.811elemental manganese;
manganese group element atom		Escherichia coli metabolite;
micronutrient
mercury
Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to MERCURY POISONING. Because of its toxicity, the clinical use of mercury and mercurials is diminishing.. mercury(0) : Elemental mercury of oxidation state zero.		4.811elemental mercury;
zinc group element atom		neurotoxin
molybdenum
Molybdenum: A metallic element with the atomic symbol Mo, atomic number 42, and atomic weight 95.95. It is an essential trace element, being a component of the enzymes xanthine oxidase, aldehyde oxidase, and nitrate reductase.		521chromium group element atommicronutrient
osmium
Osmium: A very hard, gray, toxic, and nearly infusible metal element, atomic number 76, atomic weight 190.2, symbol Os.		2.1710iron group element atom;
platinum group metal 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.		2.5920elemental platinum;
nickel group element atom;
platinum group metal 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.		4.811copper 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.		5.1421titanium group element atom
gadolinium
Gadolinium: An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors.		5.9671f-block element atom;
lanthanoid 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.		6.47111copper group element atom;
elemental gold
hafnium
Hafnium: A metal element of atomic number 72 and atomic weight 178.49, symbol Hf.		2.3110titanium 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.		2.9740pyrimidine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
HIV-1 reverse transcriptase inhibitor
galactosamine
2-amino-2-deoxy-D-galactopyranose : The pyranose form of D-galactosamine.. D-galactosamine : The D-stereoisomer of galactosamine.		4.811D-galactosamine;
primary amino compound		toxin
metocurine iodide
[no description available]		2.0410aromatic ether
hypochlorous acid
Hypochlorous Acid: An oxyacid of chlorine (HClO) containing monovalent chlorine that acts as an oxidizing or reducing agent.. hypochlorous acid : A chlorine oxoacid with formula HOCl; a weak, unstable acid, it is the active form of chlorine in water.		2.0110chlorine oxoacid;
reactive oxygen species		EC 2.5.1.18 (glutathione transferase) inhibitor;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
human metabolite
camptothecin
NSC 100880: carboxylate (opened lactone) form of camptothecin; RN refers to (S)-isomer; structure given in first source		23.6515049delta-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.		4.811metal sulfate;
zinc molecular entity		fertilizer
tricalcium phosphate
tricalcium phosphate: a form of tricalcium phosphate used as bioceramic bone replacement material; see also records for alpha-tricalcium phosphate, beta-tricalcium phosphate, calcium phosphate; apatitic tricalcium phosphate Ca9(HPO4)(PO4)5(OH) is the calcium orthophosphate leading to beta tricalcium phosphate Ca3(PO4)2 (b-TCP). calcium phosphate : A calcium salt composed of calcium and phosphate/diphosphate ions; present in milk and used for the mineralisation of calcified tissues.		4.811calcium phosphate
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
potassium sulfate
potassium sulfate: RN given refers to cpd with MF of K2-H2SO4		2.110inorganic potassium salt;
potassium salt
deuterium
Deuterium: The stable isotope of hydrogen. It has one neutron and one proton in the nucleus.		2.0510dihydrogen
poloxalene
Poloxalene: A copolymer of polyethylene and polypropylene ether glycol. It is a non-ionic polyol surface-active agent used medically as a fecal softener and in cattle for prevention of bloat.. pluronic : A triblock copolymer composed of a central hydrophobic chain of poly(propylene oxide) flanked by two hydrophilic chains of poly(ethylene oxide).		2.2110epoxide
sodium selenite
disodium selenite : An inorganic sodium salt composed of sodium and selenite ions in a 2:1 ratio.		2.3110inorganic sodium salt;
selenite salt		nutraceutical
cadmium chloride
Cadmium Chloride: A cadmium halide in the form of colorless crystals, soluble in water, methanol, and ethanol. It is used in photography, in dyeing, and calico printing, and as a solution to precipitate sulfides. (McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed). cadmium dichloride : A cadmium coordination entity in which cadmium(2+) and Cl(-) ions are present in the ratio 2:1. Although considered to be ionic, it has considerable covalent character to its bonding.		2.0410cadmium coordination entity
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
rhamnose
[no description available]		2.110L-rhamnose
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
carbendazim
carbendazim: carcinogen when combined with sodium nitrite; principle metabolite of thiophanate methyl & benomyl; structure. carbendazim : A member of the class of benzimidazoles that is 2-aminobenzimidazole in which the primary amino group is substituted by a methoxycarbonyl group. A fungicide, carbendazim controls Ascomycetes, Fungi Imperfecti, and Basidiomycetes on a wide variety of crops, including bananas, cereals, cotton, fruits, grapes, mushrooms, ornamentals, peanuts, sugarbeet, soybeans, tobacco, and vegetables.		2.0510benzimidazole fungicide;
benzimidazoles;
benzimidazolylcarbamate fungicide;
carbamate ester		antifungal agrochemical;
antinematodal drug;
metabolite;
microtubule-destabilising agent
mafenide acetate
[no description available]		2.0810carboxylic acid
ethionine
L-ethionine : An S-ethylhomocysteine that has S-configuration at the chiral centre.		2.4620S-ethylhomocysteineantimetabolite;
carcinogenic agent
titanium dioxide
titanium dioxide: used medically as protectant against externally caused irritation & sunlight; high concentrations of dust may cause irritation to respiratory tract; RN given refers to titanium oxide (TiO2); structure. titanium dioxide : A titanium oxide with the formula TiO2. A naturally occurring oxide sourced from ilmenite, rutile and anatase, it has a wide range of applications.		5.321titanium oxidesfood colouring
apazone
Apazone: An anti-inflammatory agent used in the treatment of rheumatoid arthritis. It also has uricosuric properties and has been used to treat gout.. apazone : A member of the class of benzotriazines that is 1,2-dihydro-1,2,4-benzotriazine bearing a dimethylamino substitutent at position 3 and a methyl substituent at position 7 and in which the nitrogens at positions 1 and 2 are both acylated by a carboxy group of propylmalonic acid.		2.0410benzotriazinesnon-steroidal anti-inflammatory drug;
uricosuric drug
misonidazole
Misonidazole: A nitroimidazole that sensitizes normally radio-resistant hypoxic cells to radiation. It may also be directly cytotoxic to hypoxic cells and has been proposed as an antineoplastic.		7.0710
diacerein
diacerein: chelates with bivalent metals; a quinone which possesses redox properties; metabolized to active rhein; proposed mechanisms include inhibiting IL1 and metalloproteinases; called a slow acting symptomatic drug in osteoarthritis; no effect of cyclooxygenase;		2.0810anthraquinone
cloforex
cloforex: carbamic ethyl ester of chlorphentermine; structure in Negwer, 5th ed, #2275		2.0510amphetamines
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.		3.8630selegiline;
terminal acetylenic compound		geroprotector
selegiline hydrochloride, (r)-isomer
[no description available]		2.0810hydrochloride;
terminal acetylenic compound		antiparkinson drug;
dopaminergic agent;
EC 1.4.3.4 (monoamine oxidase) inhibitor
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.		2.05106-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]		2.4720monocarboxylic acid amide;
sulfone		antimicrobial agent;
immunosuppressive agent
pancuronium bromide
pancuronium bromide : A bromide salt consisting of two bromide ions and one pancuronium dication.		2.0810bromide saltcholinergic antagonist;
muscle relaxant;
nicotinic antagonist
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.		3.5820beta-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		2.4520glucitol derivative;
nitrate ester		nitric oxide donor;
vasodilator agent
tetradecanoylphorbol acetate
Tetradecanoylphorbol Acetate: A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.. phorbol ester : Esters of phorbol, originally found in croton oil (from Croton tiglium, of the family Euphorbiaceae). A number of phorbol esters possess activity as tumour promoters and activate the mechanisms associated with cell growth. Some of these are used in experiments as activators of protein kinase C.. phorbol 13-acetate 12-myristate : A phorbol ester that is phorbol in which the hydroxy groups at the cyclopropane ring juction (position 13) and the adjacent carbon (position 12) have been converted into the corresponding acetate and myristate esters. It is a major active constituent of the seed oil of Croton tiglium. It has been used as a tumour promoting agent for skin carcinogenesis in rodents and is associated with increased cell proliferation of malignant cells. However its function is controversial since a decrease in cell proliferation has also been observed in several cancer cell types.		2.4120acetate ester;
diester;
phorbol ester;
tertiary alpha-hydroxy ketone;
tetradecanoate ester		antineoplastic agent;
apoptosis inducer;
carcinogenic agent;
mitogen;
plant metabolite;
protein kinase C agonist;
reactive oxygen species generator
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.		2.0810C-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.		4.094017beta-hydroxy steroid;
terminal acetylenic compound		anti-estrogen;
estrogen antagonist;
geroprotector
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
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.		4.4460aminoglycoside antibiotic;
anthracycline;
p-quinones;
tetracenequinones		antineoplastic agent;
bacterial metabolite
cephapirin
Cephapirin: Cephalosporin antibiotic, partly plasma-bound, that is effective against gram-negative and gram-positive organisms.. cephapirin : A cephalosporin with acetoxymethyl and 2(pyridin-4-ylsulfanyl)acetamido substituents at positions 3 and 7, respectively, of the cephem skeleton. It is used (as its sodium salt) as an antibiotic, being effective against gram-negative and gram-positive organisms.		2.0410cephalosporinantibacterial drug
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.		3.6120nucleoside analogue;
organofluorine compound;
purine arabinonucleoside monophosphate		antimetabolite;
antineoplastic agent;
antiviral agent;
DNA synthesis inhibitor;
immunosuppressive agent;
prodrug
disopyramide phosphate
[no description available]		2.0510organoammonium phosphate
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.		3.8930indole alkaloidantidyskinesia agent;
antiparkinson drug;
dopamine agonist;
hormone antagonist
methylformamide
N-methylformamide : A member of the class of formamides having a N-methyl substituent.		1.9710formamides
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.		4.0940bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
pregnanolone
Pregnanolone: A pregnane found in the urine of pregnant women and sows. It has anesthetic, hypnotic, and sedative properties.. 3alpha-hydroxy-5beta-pregnan-20-one : The 3alpha-stereoisomer of 3-hydroxy-5beta-pregnan-20-one.		2.52203-hydroxy-5beta-pregnan-20-one;
3alpha-hydroxy steroid		human metabolite;
intravenous anaesthetic;
sedative
butylated hydroxytoluene
2,6-di-tert-butyl-4-methylphenol : A member of the class of phenols that is 4-methylphenol substituted by tert-butyl groups at positions 2 and 6.		2.0510phenolsantioxidant;
ferroptosis inhibitor;
food additive;
geroprotector
benzonidazole
benzonidazole: used in treatment of Chagas' disease. benznidazole : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of (2-nitroimidazol-1-yl)acetic acid with the aromatic amino group of benzylamine. Used for treatment of Chagas disease.		2.0810C-nitro compound;
imidazoles;
monocarboxylic acid amide		antiprotozoal drug
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
du-21220
Ritodrine: An adrenergic beta-2 agonist used to control PREMATURE LABOR.. 4-[2-[[1-hydroxy-1-(4-hydroxyphenyl)propan-2-yl]amino]ethyl]phenol : A secondary amino compound that is 4-(2-amino-1-hydroxypropyl)phenol in which one of the hydrogens attached to the nitrogen is replaced by a 2-(4-hydroxyphenyl)ethyl group.		2.0410benzyl alcohols;
polyphenol;
secondary alcohol;
secondary amino compound
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.		3.5370
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.		5.2860glutamic 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]		3.1810pyrimidine 2',3'-dideoxyribonucleoside
ribostamycin
Ribostamycin: A broad-spectrum antimicrobial isolated from Streptomyces ribosifidicus.. ribostamycin : An amino cyclitol glycoside that is 4,6-diaminocyclohexane-1,2,3-triol having a 2,6-diamino-2,6-dideoxy-alpha-D-glucosyl residue attached at position 1 and a beta-D-ribosyl residue attached at position 2. It is an antibiotic produced by Streptomyces ribosidificus (formerly S. thermoflavus).		2.0410amino cyclitol glycoside;
aminoglycoside antibiotic		antibacterial drug;
antimicrobial agent;
metabolite
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.		3.8630beta-lactam antibiotic allergen;
cephalosporin;
tetrazoles;
thiadiazoles		antibacterial drug
adenosine diphosphate ribose
Adenosine Diphosphate Ribose: An ester formed between the aldehydic carbon of RIBOSE and the terminal phosphate of ADENOSINE DIPHOSPHATE. It is produced by the hydrolysis of nicotinamide-adenine dinucleotide (NAD) by a variety of enzymes, some of which transfer an ADP-ribosyl group to target proteins.		2.920ADP-sugarEscherichia coli metabolite;
mouse metabolite
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.		4.2650penicillin 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.		4.0840timololanti-arrhythmia drug;
antiglaucoma drug;
antihypertensive agent;
beta-adrenergic antagonist
indoramin
Indoramin: An alpha-1 adrenergic antagonist that is commonly used as an antihypertensive agent.		2.7530tryptamines
tramadol
Tramadol: A narcotic analgesic proposed for severe pain. It may be habituating.. tramadol : A racemate consisting of equal amounts of (R,R)- and (S,S)-tramadol. A centrally acting synthetic opioid analgesic, used (as the hydrochloride salt) to treat moderately severe pain. The (R,R)-enantiomer exhibits ten-fold higher analgesic potency than the (S,S)-enantiomer. Originally developed by Gruenenthal GmbH and launched in 1977, it was subsequently isolated from the root bark of the South African tree Nauclea latifolia.. (R,R)-tramadol : A 2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanol in which both stereocentres have R-configuration; the (R,R)-enantiomer of the racemic opioid analgesic tramadol, it exhibits ten-fold higher analgesic potency than the (S,S)-enantiomer.		7.69202-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanoladrenergic uptake inhibitor;
antitussive;
capsaicin receptor antagonist;
delta-opioid receptor agonist;
kappa-opioid receptor agonist;
metabolite;
mu-opioid receptor agonist;
muscarinic antagonist;
nicotinic antagonist;
NMDA receptor antagonist;
opioid analgesic;
serotonergic antagonist;
serotonin uptake inhibitor
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.		10.6551cyclic 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.		3.6120catechols;
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.		2.0410oxazolidinone;
primary alcohol;
toluenes
moricizine hydrochloride
moricizine hydrochloride : A hydrochloride salt obtained from equimola amounts of moricizine and hydrogen chloride.		2.0510hydrochlorideanti-arrhythmia drug
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
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.		3.8630amino 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.		5.0770azide;
pyrimidine 2',3'-dideoxyribonucleoside		antimetabolite;
antiviral drug;
HIV-1 reverse transcriptase inhibitor
feprazone
Feprazone: A pyrazole that has analgesic, anti-inflammatory, and antipyretic properties. It has been used in mild to moderate pain, fever, and inflammation associated with musculoskeletal and joint disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p15)		2.0810organic molecular entity
pirprofen
pirprofen: anti-inflammatory agent used in therapy of rheumatoid arthritis; prostaglandin synthetase inhibitor; more potent than indomethacin; structure		3.8630pyrroline
sisomicin
Sisomicin: Antibiotic produced by Micromonospora inyoensis. It is closely related to gentamicin C1A, one of the components of the gentamicin complex (GENTAMICINS).		2.0410amino cyclitol glycoside;
aminoglycoside antibiotic;
beta-L-arabinoside;
monosaccharide derivative
serentil
mesoridazine besylate : The benzenesulfonate salt of mesoridazine prepared using equimolar amounts of mesoridazine and benzenesulfonic acid.		2.0510organosulfonate saltdopaminergic antagonist;
first generation antipsychotic
amdinocillin
Amdinocillin: An amidinopenicillanic acid derivative with broad spectrum antibacterial action.. mecillinam : A penicillin in which the 6beta substituent is [(azepan-1-yl)methylidene]amino; an extended-spectrum penicillin antibiotic that binds specifically to penicillin binding protein 2 (PBP2), and is only considered to be active against Gram-negative bacteria.		2.0410penicillinantibacterial drug;
antiinfective agent
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.		3.1550amino 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).		14.03729taxane diterpenoid;
tetracyclic diterpenoid		antineoplastic agent;
human metabolite;
metabolite;
microtubule-stabilising agent
etoposide
[no description available]		14.18689beta-D-glucoside;
furonaphthodioxole;
organic heterotetracyclic compound		antineoplastic agent;
DNA synthesis inhibitor
propafenone hydrochloride
propafenone hydrochloride : A hydrochloride that is the monohydrochloride salt of propafenone. It is a class 1C antiarrhythmic drug with local anesthetic effects, and is used in the management of supraventricular and ventricular arrhythmias.		2.0510hydrochlorideanti-arrhythmia drug
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
ticarcillin
Ticarcillin: An antibiotic derived from penicillin similar to CARBENICILLIN in action.. ticarcillin : A penicillin compound having a 6beta-[(2R)-2-carboxy-2-thiophen-3-ylacetyl]amino side-group.		2.0410penicillin allergen;
penicillin		antibacterial drug
trimazosin
trimazosin: RN given refers to parent cpd; structure		2.0410N-arylpiperazine
penbutolol
Penbutolol: A nonselective beta-blocker used as an antihypertensive and an antianginal agent.		3.2310ethanolamines
ribavirin
Rebetron: Rebetron is tradename		4.54701-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
adinazolam
adinazolam: structure in first source. adinazolam : A triazolo[4,3-a][1,4]benzodiazepine having a dimethylaminomethyl group at the 1-position, a phenyl group at the 6-position and a chloro substituent at the 8-position.		2.0410triazolobenzodiazepineanticonvulsant;
antidepressant;
anxiolytic drug;
sedative
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.		4.2650alpha-D-glucoside;
amino cyclitol glycoside;
aminoglycoside;
carboxamide		antibacterial drug;
antimicrobial agent;
nephrotoxin
tolamolol
[no description available]		2.0410
carbidopa
[no description available]		2.0510catechols;
hydrate;
hydrazines;
monocarboxylic acid		antidyskinesia agent;
antiparkinson drug;
dopaminergic agent;
EC 4.1.1.28 (aromatic-L-amino-acid decarboxylase) inhibitor
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.		3.8630beta-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.		3.8630aromatic 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.		4.2650L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid		alpha-adrenergic agonist;
antihypertensive agent;
hapten;
peripheral nervous system drug;
sympatholytic agent
tocainide
Tocainide: An antiarrhythmic agent which exerts a potential- and frequency-dependent block of SODIUM CHANNELS.. tocainide : A monocarboxylic acid amide in which 2,6-dimethylphenylaniline and isobutyric acid have combined to form the amide bond; used as a local anaesthetic.		2.0410monocarboxylic acid amideanti-arrhythmia drug;
local anaesthetic;
sodium channel blocker
sulbenicillin
Sulbenicillin: Semisynthetic penicillin-type antibiotic.. sulbenicillin : A penicillin antibiotic having a 6beta-[phenyl(sulfo)acetamido] side-chain.		2.0410penicillin
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.		2.7430
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.		4.08405-[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
nimustine
Nimustine: Antineoplastic agent especially effective against malignant brain tumors. The resistance which brain tumor cells acquire to the initial effectiveness of this drug can be partially overcome by the simultaneous use of membrane-modifying agents such as reserpine, calcium antagonists such as nicardipine or verapamil, or the calmodulin inhibitor, trifluoperazine. The drug has also been used in combination with other antineoplastic agents or with radiotherapy for the treatment of various neoplasms.. nimustine : 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-amino-2-methylpyrimidin-5-ylmethyl] group. An antineoplastic agent especially effective against malignant brain tumors.		9.03293aminopyrimidine;
N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent
nonachlazine
Nonachlazine: Coronary vasodilator with a novel mechanism of action; proposed as antianginal agent.		2.0510
lonidamine
lonidamine: structure. lonidamine : A member of the class of indazoles that is 1H-indazole that is substituted at positions 1 and 3 by 2,4-dichlorobenzyl and carboxy groups, respectively.		2.7630dichlorobenzene;
indazoles;
monocarboxylic acid		antineoplastic agent;
antispermatogenic agent;
EC 2.7.1.1 (hexokinase) inhibitor;
geroprotector
vecuronium bromide
Vecuronium Bromide: Monoquaternary homolog of PANCURONIUM. A non-depolarizing neuromuscular blocking agent with shorter duration of action than pancuronium. Its lack of significant cardiovascular effects and lack of dependence on good kidney function for elimination as well as its short duration of action and easy reversibility provide advantages over, or alternatives to, other established neuromuscular blocking agents.. vecuronium bromide : The organic bromide salt of a 5alpha-androstane compound having 3alpha-acetoxy-, 17beta-acetoxy-, 2beta-piperidinino- and 16beta-N-methylpiperidinium substituents.		2.4620organic bromide salt;
quaternary ammonium salt		muscle relaxant;
neuromuscular agent;
nicotinic antagonist
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
ng-nitroarginine methyl ester
NG-Nitroarginine Methyl Ester: A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.		3.710alpha-amino acid ester;
L-arginine derivative;
methyl ester;
N-nitro compound		EC 1.14.13.39 (nitric oxide synthase) inhibitor
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.		3.86301,3-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
permethrin
hemoglobin Atlanta-Coventry: Leu replaced by Pro at beta75 and Leu deleted at beta141		2.4620cyclopropanecarboxylate 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
vindesine
Vindesine: Vinblastine derivative with antineoplastic activity against CANCER. Major side effects are myelosuppression and neurotoxicity. Vindesine is used extensively in chemotherapy protocols (ANTINEOPLASTIC COMBINED CHEMOTHERAPY PROTOCOLS).		4.3130methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
primary carboxamide;
tertiary alcohol;
tertiary amino compound;
vinca alkaloid		antineoplastic agent
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
flecainide acetate
flecainide acetate : An acetate salt obtained by combining flecainide with one molar equivalent of acetic acid. An antiarrhythmic agent used to prevent and treat tachyarrhythmia (abnormal fast rhythm of the heart).		2.0510acetate saltanti-arrhythmia drug
meptazinol
Meptazinol: A narcotic antagonist with analgesic properties. It is used for the control of moderate to severe pain.		2.0410azepanes
nicardipine hydrochloride
[no description available]		2.0510dihydropyridinegeroprotector
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		3.6120benzamides;
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.		3.5820anilide;
ether;
piperidines;
thiophenes		anaesthesia adjuvant;
intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic
acarbose
[no description available]		3.6120tetrasaccharide 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.		3.5820aminopyridine;
N-sulfonylurea;
secondary amino compound		antihypertensive agent;
loop diuretic
medroxalol
medroxalol: RN given refers to parent cpd without isomeric designation		2.0410salicylamides
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.		4.6880aminoglycoside;
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
cefmetazole
Cefmetazole: A semisynthetic cephamycin antibiotic with a broad spectrum of activity against both gram-positive and gram-negative microorganisms. It has a high rate of efficacy in many types of infection and to date no severe side effects have been noted.. cefmetazole : A second-generation cephalosporin antibiotic having N(1)-methyltetrazol-5-ylthiomethyl, {[(cyanomethyl)sulfanyl]acetyl}amino and methoxy side-groups at positions 3, 7beta and 7alpha respectively of the parent cephem bicyclic structure.		2.0410cephalosporinantibacterial drug
desflurane
Desflurane: A fluorinated ether that is used as a volatile anesthetic for maintenance of general anesthesia.		2.0510organofluorine compoundinhalation anaesthetic
indacrinone
indacrinone: polyvalent saluretic; RN given refers to parent cpd without isomeric designation; structure		2.0510
lorcainide
[no description available]		2.4620acetamides
idarubicin
Idarubicin: An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA.		4.5740anthracycline antibiotic;
deoxy hexoside;
monosaccharide derivative
eniluracil
eniluracil: structure in first source; inactivates dihydropyrimidine dehydrogenase		5.2230pyrimidone
ceforanide
ceforanide: RN given refers to (6R-(trans))-isomer. ceforanide : A second-generation cephalosporin antibiotic with {[1-(carboxymethyl)-1H-tetrazol-5-yl]sulfanyl}methyl and 2-(aminomethyl)phenylacetamido groups at positions 3 and 7, respectively, of the cephem skeleton. It is effective against many coliforms, including Escherichia coli, Klebsiella, Enterobacter and Proteus, and most strains of Salmonella, Shigella, Hemophilus, Citrobacter and Arizona species.		2.0410cephalosporinantibacterial drug
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.		3.8630penicillin 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.		4.0840aromatic 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.		5.3190alkanethiol;
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.		3.8630cephalosporinantibacterial drug
staurosporine
[no description available]		2.0810indolocarbazole alkaloid;
organic heterooctacyclic compound		apoptosis inducer;
bacterial metabolite;
EC 2.7.11.13 (protein kinase C) inhibitor;
geroprotector
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.		2.4720one-carbon compound;
organic sodium salt		antiviral drug
n-(2-chloroethyl)-n-nitrosoacetamide
N-(2-chloroethyl)-N-nitrosoacetamide: structure given in first source		3.1310
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.		3.5820diester;
quaternary ammonium ion		muscle relaxant;
nicotinic antagonist
atracurium besylate
atracurium besylate : The bisbenzenesulfonate salt of atracurium.		2.0810organosulfonate salt;
quaternary ammonium salt		muscle relaxant;
nicotinic antagonist
butoconazole nitrate
butoconazole nitrate : An organic nitrate salt obtained by reaction of equimolar amounts of butaconazole and nitric acid. An antifungal agent, it is used in gynaecology for treatment of vulvovaginal infections caused by Candida species, particularly Candida albicans.		2.0510aryl sulfide;
conazole antifungal drug;
imidazole antifungal drug;
imidazoles;
organic nitrate salt
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.		2.4520cephalosporin;
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.		2.4720nitrate ester;
pyridinecarboxamide		potassium channel opener;
vasodilator agent
endralazine
BQ 22-708: RN given refers to parent cpd		2.0410benzamides
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
pergolide mesylate
pergolide mesylate : A methanesulfonate salt obtained from pergolide by mixing eqimolar amount of pergolide and methanesulfonic acid. A dopamine D2 receptor agonist which also has D1 and D2 agonist properties, it is used 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.		2.0810methanesulfonate saltantiparkinson drug;
dopamine agonist;
geroprotector
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.		4.2650cephalosporinantibacterial 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.		2.4520benzamides;
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		2.0810benzofurans
fenoldopam mesylate
[no description available]		2.0810benzazepine
fialuridine
[no description available]		3.5920
amonafide
xanafide: salt formulation of amonafide; DNA-intercalating agent and topoisomerase II inhibitor		2.3110isoquinolines
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.		3.8730cephalosporinantibacterial drug;
drug allergen
pefloxacin
Pefloxacin: A synthetic broad-spectrum fluoroquinolone antibacterial agent active against most gram-negative and gram-positive bacteria.. pefloxacin : A quinolone that is 4-oxo-1,4-dihydroquinoline which is substituted at positions 1, 3, 6 and 7 by ethyl, carboxy, fluorine, and 4-methylpiperazin-1-yl groups, respectively.		2.4620fluoroquinolone antibiotic;
monocarboxylic acid;
N-alkylpiperazine;
N-arylpiperazine;
quinolone antibiotic;
quinolone		antibacterial drug;
antiinfective agent;
DNA synthesis inhibitor
mitoxantrone hydrochloride
[no description available]		2.0510hydrochlorideantineoplastic agent
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.		3.5820monocarboxylic acid amide;
piperidines		central nervous system depressant;
intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic;
peripheral nervous system drug
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.		4.2650
recainam
recainam: structure given in first source		2.0410
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).		9.4360delta-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		2.4620aminopyridine
tolrestat
tolrestat: RN & structure given in first source		3.5920naphthalenesEC 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.		2.7530aromatic ketone
stepronin
[no description available]		2.0810N-acyl-amino acid
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.		4.4660delta-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
idazoxan
Idazoxan: A benzodioxane-linked imidazole that has alpha-2 adrenoceptor antagonist activity.. idazoxan : A benzodioxine that is 2,3-dihydro-1,4-benzodioxine in which one of the hydrogens at position 2 has been replaced by a 4,5-dihydro-1H-imidazol-2-yl group.		2.4620benzodioxine;
imidazolines		alpha-adrenergic antagonist
remoxipride
Remoxipride: An antipsychotic agent that is specific for dopamine D2 receptors. It has been shown to be effective in the treatment of schizophrenia.		2.4620dimethoxybenzene
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.		3.86303-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.		12.56110N-acylureaantineoplastic agent;
antiparkinson drug;
dopamine agonist
bambuterol
bambuterol: selective inhibitor of butyrylcholinesterase & acetylcholinesterase. bambuterol : A carbamate ester that is terbutaline in which both of the phenolic hydroxy groups have been protected as the corresponding N,N-dimethylcarbamates. A long acting beta-adrenoceptor agonist used in the treatment of asthma, it is a prodrug for terbutaline.		2.4520carbamate ester;
phenylethanolamines		anti-asthmatic drug;
beta-adrenergic agonist;
bronchodilator agent;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
prodrug;
sympathomimetic agent;
tocolytic agent
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.		2.4720hydrochlorideadrenergic uptake inhibitor;
antidepressant
atomoxetine
atomoxetine : A secondary amino compound having methyl and 3-(2-methylphenoxy)-3-phenylpropan-1-yl substituents.		3.8630aromatic 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.		4.0940dicarboxylic acid monoester;
ethyl ester;
isoquinolines;
tertiary carboxamide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
alpidem
[no description available]		3.5920imidazoles
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.		4.1403-oxo-Delta(4) steroid;
acetylenic compound;
tertiary amino compound		abortifacient;
contraceptive drug;
hormone antagonist;
synthetic oral contraceptive
itraconazole
Itraconazole: A triazole antifungal agent that inhibits cytochrome P-450-dependent enzymes required for ERGOSTEROL synthesis.. itraconazole : An N-arylpiperazine that is cis-ketoconazole in which the imidazol-1-yl group is replaced by a 1,2,4-triazol-1-yl group and in which the actyl group attached to the piperazine moiety is replaced by a p-[(+-)1-sec-butyl-5-oxo-1,5-dihydro-4H-1,2,4-triazol-4-yl]phenyl group. A potent P-glycoprotein and CYP3A4 inhibitor, it is used as an antifungal drug for the treatment of various fungal infections, including aspergillosis, blastomycosis, candidiasis, chromoblastomycosis, coccidioidomycosis, cryptococcosis, histoplasmosis, and sporotrichosis.		7.5420aromatic ether;
conazole antifungal drug;
cyclic ketal;
dichlorobenzene;
dioxolane;
N-arylpiperazine;
triazole antifungal drug;
triazoles		EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor;
Hedgehog signaling pathway inhibitor;
P450 inhibitor
trospectomycin
trospectomycin: active against Neisseria gonorrhoeae; RN refers to 2R-(2alpha,4abeta,5abeta,6beta,7beta,8beta,9beta,9alpha,9aalpha,10abeta)-(9CI)-isomer		2.4520dioxanes
fosphenytoin
fosphenytoin: structure given in first & second source		3.2310imidazolidine-2,4-dione
fluorodopa f 18
fluorodopa F 18: RN given refers to (L)-isomer		5.6231(18)F radiopharmaceutical;
6-fluoro-L-dopa
salmeterol xinafoate
Salmeterol Xinafoate: A selective ADRENERGIC BETA-2 RECEPTOR agonist that functions as a BRONCHODILATOR when administered by inhalation. It is used to manage the symptoms of ASTHMA and CHRONIC OBSTRUCTIVE PULMONARY DISEASE.		5.0421naphthoic acid
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.		3.87303-oxo steroid;
aza-steroid;
delta-lactam		androgen antagonist;
antihyperplasia drug;
EC 1.3.1.22 [3-oxo-5alpha-steroid 4-dehydrogenase (NADP(+))] inhibitor
imiquimod
Imiquimod: A topically-applied aminoquinoline immune modulator that induces interferon production. It is used in the treatment of external genital and perianal warts, superficial CARCINOMA, BASAL CELL; and ACTINIC KERATOSIS.. imiquimod : An imidazoquinoline fused [4,5-c] carrying isobutyl and amino substituents at N-1 and C-4 respectively. A prescription medication, it acts as an immune response modifier and is used to treat genital warts, superficial basal cell carcinoma, and actinic keratosis.		2.0810imidazoquinolineantineoplastic agent;
interferon inducer
cyclodisone
cyclodisone: structure given in first source		1.9710
sematilide
sematilide: RN refers to HCl; structure given in first source		2.0410
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.		3.5820aromatic ether;
ethanolamines;
methyl ester;
secondary alcohol;
secondary amino compound
temafloxacin
temafloxacin: structure given in first source. temafloxacin : A racemate comprising equimolar amounts of (R)- and (S)-temafloxacin. Both enantiomers both exhibit similar pharmacological profiles. Temafloxacin was briefly used (either as the free base or as the hydrochloride salt) as an antibacterial drug but was withdrawn worldwide in 1992 following reports of serious side effects, including severe hypoglycaemia, haemolytic anaemia, liver and kidney dysfunction, anaphylaxis, and death.. 1-(2,4-difluorophenyl)-6-fluoro-7-(3-methylpiperazin-1-yl)-4-oxo-1,4-dihydroquinoline-3-carboxylic acid : A quinolone that is 4-oxo-1,4-dihydroquinoline-3-carboxylic acid which is substituted at positions 1, 6, and 7 by 2,4-difluorophenyl, fluorine, and 3-methylpiperazin-1-yl groups, respectively.		2.0510amino acid;
monocarboxylic acid;
N-arylpiperazine;
organofluorine compound;
quinolone antibiotic;
quinolone;
secondary amino compound;
tertiary amino compound
clinafloxacin
clinafloxacin: structure given in first source; RN given is for monoHCl		2.4520quinolines
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.		2.0810heteroarylpiperidine;
imidazolidinone;
organochlorine compound;
organofluorine compound;
phenylindole		alpha-adrenergic antagonist;
H1-receptor antagonist;
second generation antipsychotic;
serotonergic antagonist
adapalene
Adapalene: A naphthalene derivative that has specificity for RETINOIC ACID RECEPTORS. It is used as a DERMATOLOGIC AGENT for the treatment of ACNE.. adapalene : A naphthoic acid that is CD437 in which the phenolic hydroxy group has been converted to its methyl ether.		2.0810adamantanes;
monocarboxylic acid;
naphthoic acid		dermatologic drug;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor;
non-steroidal anti-inflammatory drug
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.		3.58206-aminopurines;
ether;
phosphonic acids		antiviral drug;
DNA synthesis inhibitor;
drug metabolite;
HIV-1 reverse transcriptase inhibitor;
nephrotoxic agent
loxiglumide
loxiglumide: cholecystokinin receptor antagonist; RN refers to (+-)-isomer; structure in first source		2.0410organic molecular entity
aromasil
[no description available]		3.612017-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]		2.7530fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone
zileuton
[no description available]		4.44601-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.		3.5920methyl 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.		4.0840phosphonic 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.		3.5820beta-amino acid;
piperidinemonocarboxylic acid;
tertiary amino compound;
thiophenes		anticonvulsant;
GABA reuptake inhibitor
mibefradil
Mibefradil: A benzimidazoyl-substituted tetraline that selectively binds and inhibits CALCIUM CHANNELS, T-TYPE.		10.2941tetralinsT-type calcium channel blocker
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.		9.75333pyranoindolizinoquinolineantineoplastic 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.		4.2650aromatic amino acid;
benzophenones;
organobromine compound;
substituted aniline		non-narcotic analgesic;
non-steroidal anti-inflammatory drug
gemcitabine hydrochloride
[no description available]		2.0810hydrochloride;
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.		9.68172organofluorine 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
temoporfin
temoporfin: used as PHOTOCHEMOTHERAPY		2.1110
ibutilide
ibutilide: RN & structure in first source; RN refers to the fumarate salt		3.5820benzenes;
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.		3.8730aromatic 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.		3.5820alpha-amino acid ester;
anilide;
monocarboxylic acid amide;
piperidinecarboxylate ester		intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic;
sedative
atorvastatin calcium anhydrous
[no description available]		2.0810organic calcium salt
atorvastatin
[no description available]		5.8561aromatic amide;
dihydroxy monocarboxylic acid;
monofluorobenzenes;
pyrroles;
statin (synthetic)		environmental contaminant;
xenobiotic
lamivudine
[no description available]		4.4160monothioacetal;
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 hydrochloride
Duloxetine Hydrochloride: A thiophene derivative and selective NEUROTRANSMITTER UPTAKE INHIBITOR for SEROTONIN and NORADRENALINE (SNRI). It is an ANTIDEPRESSIVE AGENT and ANXIOLYTIC, and is also used for the treatment of pain in patients with DIABETES MELLITUS and FIBROMYALGIA.. (S)-duloxetine hydrochloride : A duloxetine hydrochloride in which the duloxetine moiety has S configuration.		2.0810duloxetine hydrochlorideantidepressant
duloxetine
[no description available]		3.5920duloxetine
irinotecan
[no description available]		19.3618360carbamate 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.		4.2650biphenylyltetrazole;
monocarboxylic acid amide;
monocarboxylic acid		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
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.		3.5820
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
zanamivir
Zanamivir: A guanido-neuraminic acid that is used to inhibit NEURAMINIDASE.		2.0410guanidinesantiviral agent;
EC 3.2.1.18 (exo-alpha-sialidase) inhibitor
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.		3.8730oxazolidinone;
tryptamines		anti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
3-iodobenzylguanidine
3-Iodobenzylguanidine: A guanidine analog with specific affinity for tissues of the sympathetic nervous system and related tumors. The radiolabeled forms are used as antineoplastic agents and radioactive imaging agents. (Merck Index, 12th ed) MIBG serves as a neuron-blocking agent which has a strong affinity for, and retention in, the adrenal medulla and also inhibits ADP-ribosyltransferase.		3.5720organoiodine compound
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.		2.47206-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.		3.6120monothioacetal;
nucleoside analogue;
organofluorine compound;
pyrimidone		antiviral drug;
HIV-1 reverse transcriptase inhibitor
tasosartan
tasosartan: angiotensin II antagonist; structure given in first source		3.5920biphenyls
saquinavir monomethanesulfonate
[no description available]		2.0510organic molecular entity
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.		3.5820L-tyrosine derivative;
piperidines;
sulfonamide		anticoagulant;
fibrin modulating drug;
platelet glycoprotein-IIb/IIIa receptor antagonist
capecitabine
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.. 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.		16.589413carbamate ester;
cytidines;
organofluorine compound		antimetabolite;
antineoplastic agent;
prodrug
adenosine
quinquefolan B: isolated from roots of Panax quinquefolium L.; RN not in Chemline 10/87; RN from Toxlit		6.97111adenosines;
purines D-ribonucleoside		analgesic;
anti-arrhythmia drug;
fundamental metabolite;
human metabolite;
vasodilator agent
allyl formate
[no description available]		2.0510
4-propionyloxy-4-phenyl-n-methylpiperidine
4-propionyloxy-4-phenyl-N-methylpiperidine: causes parkinsonism; structure in first source		2.0810
acridine orange
Acridine Orange: A cationic cytochemical stain specific for cell nuclei, especially DNA. It is used as a supravital stain and in fluorescence cytochemistry. It may cause mutations in microorganisms.. acridine orange : Fluorescent dye useful for cell cycle determination. It is cell-permeable, and interacts with DNA and RNA by intercalation or electrostatic attractions respectively.. acridine orange free base : A member of the class of aminoacridines that is acridine carrying two dimethylamino substituents at positions 3 and 6. The hydrochloride salt is the fluorescent dye 'acridine orange', used for cell cycle determination.		340aminoacridines;
aromatic amine;
tertiary amino compound		fluorochrome;
histological dye
paroxetine hydrochloride
paroxetine hydrochloride : The hydrochloride salt of paroxetine. It is an antidepressant drug.		2.0810hydrochlorideantidepressant;
anxiolytic drug;
hepatotoxic agent;
P450 inhibitor;
serotonin uptake inhibitor
desferrioxamine b mesylate
desferrioxamine B mesylate : A methanesulfonate salt obtained by reaction of desferrioxamine B with one molar equivalent of methanesulfonic acid. It is an iron-chelating medicine used to remove excess iron from the body. It binds to iron in the blood, which is then passed out in the urine.		2.0510methanesulfonate saltantidote;
ferroptosis inhibitor;
iron chelator
bupropion hydrochloride
[no description available]		2.4720aromatic ketone
cisatracurium
cisatracurium: RN refers to (1R-(1alpha,2alpha(1'R*,2'R*)))-isomer. cisatracurium : A diester that is the (1R,1'R,2R,2'R)-diastereoisomer of atracurium, a quaternary ammonium ion consisting of pentane-1,5-diol with both hydroxy functions bearing 3-[1-(3,4-dimethoxybenzyl)-6,7-dimethoxy-2-methyl-3,4-dihydroisoquinolinium-2(1H)-yl]propanoyl groups. The active species in the skeletal muscle relaxant cisatracurium besylate.		2.0410diester;
quaternary ammonium ion		muscle relaxant;
nicotinic antagonist
halofuginone
[no description available]		2.0510quinazolines
diltiazem hydrochloride
Carex: fluoride (1.8%) containing varnish; no further information available 8/91. diltiazem hydrochloride : A hydrochloride salt resulting from the reaction of equimolar amounts of diltiazem and hydrogen chloride. A calcium-channel blocker and vasodilator, it is used in the management of angina pectoris and hypertension.		2.0510hydrochlorideantihypertensive agent;
calcium channel blocker;
vasodilator agent
trazodone hydrochloride
Triticum: A plant genus of the family POACEAE that is the source of EDIBLE GRAIN. A hybrid with rye (SECALE CEREALE) is called TRITICALE. The seed is ground into FLOUR and used to make BREAD, and is the source of WHEAT GERM AGGLUTININS.. trazodone hydrochloride : A hydrochloride salt prepared from equimolar amounts of trazodone and hydrogen chloride.		2.4720hydrochlorideadrenergic antagonist;
antidepressant;
H1-receptor antagonist;
sedative;
serotonin uptake inhibitor
fosinoprilat
fosinoprilat: active phosphinic acid metabolite of prodrug fosenopril, which is activated by esterases in vivo; structure given in first source; binds zinc with phosphinic acid group. fosinoprilat : A phosphinic acid-containing N-acyl derivative of (4S)-cyclohexyl-L-proline. An inhibitor of angiotensin converting enzyme (ACE), it is used as the phosphinate ester pro-drug fosinopril for treatment of hypertension and chronic heart failure.		2.0410L-proline derivative;
phosphinic acids		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
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.		3.8630
verapamil hydrochloride
verapamil hydrochloride : A racemate comprising equimolar amounts of dexverapamil hydrochloride and (S)-verapamil hydrochloride.		2.0510
cefprozil
[no description available]		3.8630cephalosporin;
semisynthetic derivative		antibacterial drug
doxazosin mesylate
Cardura: Trade name in United States.		2.0810methanesulfonate saltgeroprotector
ciprofloxacin hydrochloride anhydrous
[no description available]		2.0510hydrochlorideantibacterial drug;
antiinfective agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
topoisomerase IV inhibitor
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.		3.8730acetylenic 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.		6.4671aryl sulfide;
benzamides;
organic heterobicyclic compound;
phenols;
secondary alcohol;
tertiary amino compound		antineoplastic agent;
HIV protease inhibitor
amantadine hydrochloride
[no description available]		2.0510hydrochlorideantiviral agent;
dopamine agonist;
NMDA receptor antagonist
doxapram hydrochloride
[no description available]		2.0510hydrochloridecentral nervous system stimulant
methionine methyl ester
[no description available]		3.6930
glucose, (beta-d)-isomer
beta-D-glucose : D-Glucopyranose with beta configuration at the anomeric centre.. (1->4)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->4) linkages.. (1->3)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->3) linkages.		5.741D-glucopyranoseepitope;
mouse metabolite
mevastatin
mevastatin: antifungal metabolite from Penicillium brevicopactum; potent inhibitory activity to sterol synthesis; structure. mevastatin : A carboxylic ester that is pravastatin that is lacking the allylic hydroxy group. A hydroxymethylglutaryl-CoA reductase inhibitor (statin) isolated from Penicillium citrinum and from Penicillium brevicompactum, its clinical use as a lipid-regulating drug ceased following reports of toxicity in animals.		2.08102-pyranones;
carboxylic ester;
hexahydronaphthalenes;
polyketide;
statin (naturally occurring)		antifungal agent;
apoptosis inducer;
EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor;
fungal metabolite;
Penicillium metabolite
bupivacaine hydrochloride
bupivacaine hydrochloride (anhydrous) : A racemate composed of equimolar amounts of dextrobupivacaine hydrochloride and levobupivacaine hydrochloride. The monohydrate form is commonly used as a local anaesthetic.. 1-butyl-N-(2,6-dimethylphenyl)piperidine-2-carboxamide hydrochloride : A hydrochloride obtained by combining 1-butyl-N-(2,6-dimethylphenyl)piperidine-2-carboxamide with one molar equivalent of hydrochloric acid.		2.0810hydrochloride;
racemate		adrenergic antagonist;
amphiphile;
EC 3.1.1.8 (cholinesterase) inhibitor;
EC 3.6.3.8 (Ca(2+)-transporting ATPase) inhibitor;
local anaesthetic
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.		3.2310aromatic ketone;
chlorobenzophenone;
monocarboxylic acid		drug metabolite;
marine xenobiotic metabolite
1,5-anhydroglucitol
1,5-anhydroglucitol: structure. 1,5-anhydro-D-glucitol : An anhydro sugar of D-glucitol.		2.0510anhydro sugarhuman metabolite
thiazolyl blue
thiazolyl blue: RN & II refers to bromide. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide : The bromide salt of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium.		3.2960organic bromide saltcolorimetric reagent;
dye
betulinic acid
[no description available]		2.7630hydroxy 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
baicalin
[no description available]		2.110dihydroxyflavone;
glucosiduronic acid;
glycosyloxyflavone;
monosaccharide derivative		antiatherosclerotic agent;
antibacterial agent;
anticoronaviral agent;
antineoplastic agent;
antioxidant;
cardioprotective agent;
EC 2.7.7.48 (RNA-directed RNA polymerase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
ferroptosis inhibitor;
neuroprotective agent;
non-steroidal anti-inflammatory drug;
plant metabolite;
prodrug
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.		3.930azacycloalkane;
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]		3.8730carbamate 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.		3.2310acetamides;
amino acid ester;
cyclohexenecarboxylate ester;
primary amino compound		antiviral drug;
EC 3.2.1.18 (exo-alpha-sialidase) inhibitor;
environmental contaminant;
prodrug;
xenobiotic
allicin
[no description available]		7.2510botanical anti-fungal agent;
sulfoxide		antibacterial agent
5-methylcytosine
5-Methylcytosine: A methylated nucleotide base found in eukaryotic DNA. In ANIMALS, the DNA METHYLATION of CYTOSINE to form 5-methylcytosine is found primarily in the palindromic sequence CpG. In PLANTS, the methylated sequence is CpNpGp, where N can be any base.. 5-methylcytosine : A pyrimidine that is a derivative of cytosine, having a methyl group at the 5-position.		4.4850methylcytosine;
pyrimidines		human metabolite
epigallocatechin gallate
epigallocatechin gallate: a steroid 5alpha-reductase inhibitor and antimutagen in green tea (Camellia sinensis). (-)-epigallocatechin 3-gallate : A gallate ester obtained by the formal condensation of gallic acid with the (3R)-hydroxy group of (-)-epigallocatechin.		8.1750flavans;
gallate ester;
polyphenol		antineoplastic agent;
antioxidant;
apoptosis inducer;
geroprotector;
Hsp90 inhibitor;
neuroprotective agent;
plant metabolite
n-acetylaspartic acid
N-acetyl-L-aspartic acid : An N-acyl-L-aspartic acid in which the acyl group is specified as acetyl.		4.5851N-acetyl-L-amino acid;
N-acyl-L-aspartic acid		antioxidant;
human metabolite;
mouse metabolite;
nutraceutical;
rat metabolite
fluorexon
fluorexon: structure		2.520xanthene dyefluorochrome
salvin
salvin: a biocyclic diterpenoid; from sage and rosemary (Lamiaceae)		2.2110abietane diterpenoid;
carbotricyclic compound;
catechols;
monocarboxylic acid		angiogenesis modulating agent;
anti-inflammatory agent;
antineoplastic agent;
antioxidant;
apoptosis inducer;
food preservative;
HIV protease inhibitor;
plant metabolite
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.		9.4403methylguaninemutagen
dobutamine hydrochloride
dobutamine hydrochloride : The hydrochloride salt of dobutamine. A beta1-adrenergic receptor agonist that has cardiac stimulant action without evoking vasoconstriction or tachycardia, it is used to increase the contractility of the heart in the management of acute heart failure.		2.0510hydrochloridebeta-adrenergic agonist;
cardiotonic drug;
sympathomimetic agent
ticlopidine hydrochloride
[no description available]		2.0810hydrochloride
epirubicin hydrochloride
[no description available]		2.0810
glutathione disulfide
Glutathione Disulfide: A GLUTATHIONE dimer formed by a disulfide bond between the cysteine sulfhydryl side chains during the course of being oxidized.		2.4620glutathione derivative;
organic disulfide		Escherichia coli metabolite;
mouse metabolite
hypusine
hypusine: N-terminal amino alcohol deriv of Lys occurring in bovine brain & in the urine of children with familial hyperlysinemia; minor descriptor (75-82); online & Index Medicus search LYSINE/AA (75-82). hypusine : An L-lysine derivative that is L-lysine bearing a (2R)-4-amino-2-hydroxybutyl substituent at position N(6).		2.5720
iopamidol
Iopamidol: A non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiological procedures.. iopamidol : A benzenedicarboxamide compound having N-substituted carbamoyl groups at the 1- and 3-positions, iodo substituents at the 2-, 4- and 6-positions and a (2S)-2-hydroxypropanamido group at the 5-position.		2.4520benzenedicarboxamide;
organoiodine compound;
pentol		environmental contaminant;
radioopaque medium;
xenobiotic
sulconazole, mononitrate, (+-)-isomer
[no description available]		2.0510conazole antifungal drug;
imidazole antifungal drug;
organic nitrate salt
histamine phosphate
histamine phosphate : A phosphate salt that is the diphosphate salt of histamine.		3.2310phosphate salthistamine agonist
cedrol
cedrol: a cyclic terpenoid from cedarwood oil; 8-epicedrol is an epimer		7.2510cedrane sesquiterpenoid;
tertiary alcohol
imipramine n-oxide
imipramine N-oxide: RN given refers to parent cpd; structure		2.0410dibenzooxazepine
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
ebrotidine
ebrotidine: an H2-receptor antagonist and gastric mucosa protector		3.2310sulfonamide
mizolastine
[no description available]		2.0510benzimidazoles
tallimustine
tallimustine: structure given in first source		3.0910
dexloxiglumide
dexloxiglumide: a CCK receptor antagonist; structure given in first source		2.0410glutamic acid derivative
intoplicine
intoplicine: structure in first source		2.4520pyridoindole
pazufloxacin
[no description available]		2.0810quinolines
repaglinide
[no description available]		3.8730piperidines
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.		4.2650benzimidazoles;
biphenyls;
carboxybiphenyl		angiotensin receptor antagonist;
antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
environmental contaminant;
xenobiotic
hexestrol bis(diethylaminoethyl ether)
hexestrol bis(diethylaminoethyl ether): minor descriptor (75-84); on-line & Index Medicus search HEXESTROL/AA (75-84); RN given refers to parent cpd without isomeric designation		2.0510stilbenoid
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.		2.4520fenfluramineappetite depressant;
serotonergic agonist;
serotonin uptake inhibitor
2-methoxyestradiol
2-methoxy-17beta-estradiol : A 17beta-hydroxy steroid, being 17beta-estradiol methoxylated at C-2.		2.472017beta-hydroxy steroid;
3-hydroxy steroid		angiogenesis modulating agent;
antimitotic;
antineoplastic agent;
human metabolite;
metabolite;
mouse metabolite
naphthalimides
Naphthalimides: Compounds with three fused rings that appear like a naphthalene fused to piperidone or like a benz(de)isoquinoline-1,3-dione (not to be confused with BENZYLISOQUINOLINES which have a methyl separating the naphthyl from the benzyl rings). Members are CYTOTOXINS.		2.3110
synthalin a
synthalin A: RN given refers to parent cpd; structure. synthalin : A hydrochloride resulting from the reaction of decamethylenediguanidine with 2 mol eq. of hydrogen chloride.. synthalin A : A member of the class of guanidines that is decane having guanidino groups at the 1- and 10-positions.		2.0510guanidineshepatotoxic agent;
hypoglycemic agent;
nephrotoxin
ethinyl estradiol-17-sulfate
ethinyl estradiol-17-sulfate: RN given refers to the (17alpha)-isomer		2.0410
4-(diethylamino)benzaldehyde
4-(diethylamino)benzaldehyde : A member of the class of benzaldehydes carrying a diethylamino substituent at position 4.		2.0710aromatic amine;
benzaldehydes;
tertiary amino compound		EC 1.2.1.3 [aldehyde dehydrogenase (NAD(+))] inhibitor
1h-imidazo(4,5-b)pyridine
1H-imidazo(4,5-b)pyridine: structure given in first source. 4-azabenzimidazole : The [4,5-b]-fused isomer of imidazopyridine.		2.0210imidazopyridine
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.		3.74901,2,3-triazole
delphinidin
Paraffin: A mixture of solid hydrocarbons obtained from petroleum. It has a wide range of uses including as a stiffening agent in ointments, as a lubricant, and as a topical anti-inflammatory. It is also commonly used as an embedding material in histology.. delphinidin chloride : An anthocyanidin chloride that has delphinidin as the cationic counterpart.		2.0210anthocyanidin chloride
trimethobenzamide monohydrochloride
[no description available]		2.0510
amiloride hydrochloride
amiloride hydrochloride dihydrate : A hydrate that is the dihydrate of amiloride hydrochloride.		2.0510hydratediuretic;
sodium channel blocker
miconazole nitrate
miconazole nitrate : A racemate composed of equimolar amounts of (R)- and (S)-miconazole nitrate. An antifungal used for the treatment of athlete's foot, jock itch, ringworm and other fungal skin infections. It inhibits the synthesis of ergosterol, a critical component of fungal cell membranes.		2.0810
disobutamide
[no description available]		2.0510acetamides
ethinylestradiol-3-sulfate
ethinylestradiol-3-sulfate: binds to albumin at 2 sites		2.041017beta-hydroxy steroid;
steroid sulfate		antineoplastic agent;
estrogen
econazole nitrate
econazole nitrate : A racemate composed of equimolar amounts of (R)- and (S)-econazole nitrate. Used to treat skin infections such as athlete's foot, jock itch, ringworm and other fungal skin infections.		2.0510
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)		8.421432-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.		10.0870dichlorobenzene;
secondary amino compound;
tetralins		antidepressant;
serotonin uptake inhibitor
lomefloxacin hydrochloride
lomefloxacin hydrochloride : The hydrochloride salt of lomefloxacin. It is administered by mouth to treat bacterial infections including bronchitis and urinary tract infections. It is also used topically as eye drops for the treatment of bacterial conjunctivitis, and as ear drops for the treatment of otitis externa and otitis media.		2.0510hydrochlorideantimicrobial agent;
antitubercular agent;
photosensitizing agent
picosulfate sodium
picosulfate sodium: contains two active ingredients, sodium picosulfate and magnesium citrate, which are both laxatives; structure		2.0510aryl sulfate;
pyridines
cefcanel
cefcanel: RN given refers to (6R-(6 alpha,7 beta(R*)))-isomer; structure		2.0410
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.		9.43601,1-bis(phosphonic acid);
imidazoles		bone density conservation agent
epristeride
epristeride: structure given in first source		2.0410steroid acid
talinolol
[no description available]		2.0410ureas
artemisinin
(+)-artemisinin : A sesquiterpene lactone obtained from sweet wormwood, Artemisia annua, which is used as an antimalarial for the treatment of multi-drug resistant strains of falciparum malaria.		3.9330organic peroxide;
sesquiterpene lactone		antimalarial;
plant metabolite
brinzolamide
brinzolamide: an antiglaucoma agent		2.0810sulfonamide;
thienothiazine		antiglaucoma drug;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
dienogest
[no description available]		2.051017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
aliphatic nitrile;
steroid hormone		progesterone receptor agonist;
progestin;
synthetic oral contraceptive
flunoxaprofen
flunoxaprofen: structure given in first source. flunoxaprofen : A monocarboxylic acid that is propionic acid substituted at position 2 by a 2-(4-chlorophenyl)-1,3-benzoxazol-5-yl group (the S-enantiomer). Although it was shown to be effective in treatment of rheumatoid arthritis and osteoarthritis, the clinical use of flunoxaprofen was discontinued due to possible hepatotoxic side-effects.		2.05101,3-benzoxazoles;
monocarboxylic acid;
organofluorine compound		antirheumatic drug;
hepatotoxic agent;
non-steroidal anti-inflammatory drug;
protein kinase C agonist
tianeptine
tianeptine: structure given in first source. tianeptine : A racemate comprising of equimolar amounts of (R)- and (S)-tianeptine. It is an atypical antidepressant used in Europe to treat patients who respond poorly to selective serotonin reuptake inhibitors (SSRIs).. 7-[(3-chloro-6-methyl-5,5-dioxido-6,11-dihydrodibenzo[c,f][1,2]thiazepin-11-yl)amino]heptanoic acid : A member of the class of dibenzothiazepines that is 3-chloro-6-methyl-6,11-dihydrodibenzo[c,f][1,2]thiazepine 5,5-dioxide substituted by a (6-carboxyhexyl)amino group at position 11.. (S)-tianeptine : The S-enantiomer of tianeptine.		2.0510dibenzothiazepine;
monocarboxylic acid;
organochlorine compound
drospirenone
drospirenone: a progestational compound with antimineralocorticoid and antiandrogenic activity; structure given in first source		2.08103-oxo-Delta(4) steroid;
steroid lactone		aldosterone antagonist;
contraceptive drug;
progestin
artemether
Artemether: An artemisinin derivative that is used in the treatment of MALARIA.. artemether : An artemisinin derivative that is artemisinin in which the lactone has been converted to the corresponding lactol methyl ether. It is used in combination with lumefantrine as an antimalarial for the treatment of multi-drug resistant strains of falciparum malaria.		2.0810artemisinin derivative;
cyclic acetal;
organic peroxide;
semisynthetic derivative;
sesquiterpenoid		antimalarial
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
denaverine
denaverine: RN given refers to parent cpd; structure		2.0410diarylmethane
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
diprafenone
diprafenone: structure given in first source		2.0410aromatic compound
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.		3.5820chromanes;
diol;
organofluorine compound;
secondary alcohol;
secondary amino compound
uk 68798
[no description available]		3.8730aromatic ether;
sulfonamide;
tertiary amino compound		anti-arrhythmia drug;
potassium channel blocker
ljc 10627
biapenem: structure given in first source. biapenem : A carbapenem antibiotic in which the azetidine and pyrroline rings carry 1-hydroxymethyl and pyrazolo[1,2-a][1,2,4]triazolium-6-ylthio substituents respectively.		2.0410carbapenems;
organic sulfide;
pyrazolotriazole		antibacterial drug
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.		3.61201,2-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.		3.8630razoxaneantineoplastic agent;
cardiovascular drug;
chelator;
immunosuppressive agent
masoprocol
Masoprocol: A potent lipoxygenase inhibitor that interferes with arachidonic acid metabolism. The compound also inhibits formyltetrahydrofolate synthetase, carboxylesterase, and cyclooxygenase to a lesser extent. It also serves as an antioxidant in fats and oils.. masoprocol : The meso-form of nordihydroguaiaretic acid. An antioxidant found in the creosote bush, Larrea divaricata, it is a potent lipoxygenase inhibitor that interferes with arachidonic acid metabolism. It also inhibits (though to a lesser extent) formyltetrahydrofolate synthetase, carboxylesterase, and cyclooxygenase.		2.5820nordihydroguaiaretic acidantineoplastic agent;
hypoglycemic agent;
lipoxygenase inhibitor;
metabolite
loxapine succinate
[no description available]		2.0810succinate saltgeroprotector
tocophersolan
tocophersolan: RN given refers to parent cpd		2.0310tocol
loperamide hydrochloride
loperamide hydrochloride : A hydrochloride obtained by combining loperamide with one equivalent of hydrochloric acid. Used for treatment of diarrhoea resulting from gastroenteritis or inflammatory bowel disease.		2.0510hydrochlorideanticoronaviral agent;
antidiarrhoeal drug;
mu-opioid receptor agonist
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.		4.2750conazole antifungal drug;
difluorobenzene;
pyrimidines;
tertiary alcohol;
triazole antifungal drug		P450 inhibitor
betamipron
[no description available]		2.4620organonitrogen compound;
organooxygen compound
bufuralol
bufuralol: RN given refers to cpd without isomeric designation; structure		2.0410benzofurans
ranimustine
ranimustine: RN given refers to (alpha)-(D)-isomer; structure		2.0510organic molecular entity
uroxatral
[no description available]		2.0810hydrochloride
mitozolomide
mitozolomide: RN & structure given in first source		6.48200
aceclofenac
[no description available]		3.6120amino 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
clociguanil
clociguanil: RN given refers to parent cpd; structure		2.0510
nitrefazole
[no description available]		3.2310imidazoles
panipenem
panipenem: synthetic cpd; structure given in first source		2.0410organic molecular entity
perindoprilat
perindoprilat : A dipeptide obtained by formal condensation of one of the carboxy groups of N-[(1S)-1-carboxyethyl]-L-norvaline with the amino group of (2S,3aS,7aS)-octahydroindole-2-carboxylic acid. The major active metabolite of perindopril.		2.0410dicarboxylic acid;
dipeptide;
L-alanine derivative;
organic heterobicyclic compound		antihypertensive agent;
drug metabolite;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
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
thiocolchicoside
[no description available]		2.0810glycoside
terlipressin
terlivaz: first FDA approved injection to improve kidney function in adults with hepatorenal syndrome (HRS) with rapid reduction in kidney function.		2.0510polypeptide
avarol
avarol: RN given refers to parent cpd; extract from Dysidea avara(sea sponge)		2.1710
avarone
avarone: antileukemic agent; isolated from Dysidea avara		2.1710
7-hydroxystaurosporine
[no description available]		2.7330
methotrimeprazine
Methotrimeprazine: A phenothiazine with pharmacological activity similar to that of both CHLORPROMAZINE and PROMETHAZINE. It has the histamine-antagonist properties of the antihistamines together with CENTRAL NERVOUS SYSTEM effects resembling those of chlorpromazine. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604). methotrimeprazine : A member of the class of phenothiazines that is 10H-phenothiazine substituted by a (2R)-3-(dimethylamino)-2-methylpropyl group and a methoxy group at positions 10 and 2 respectively.		2.0410phenothiazines;
tertiary amine		anticoronaviral agent;
cholinergic antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
non-narcotic analgesic;
phenothiazine antipsychotic drug;
serotonergic antagonist
magnolol
[no description available]		7.610biphenyls
honokiol
[no description available]		3.0840biphenyls
isoflavone
[no description available]		2.0510isoflavones
betulin
betulin: isolated from various white birch bark (BETULA). betulin : A pentacyclic triterpenoid that is lupane having a double bond at position 20(29) as well as 3beta-hydroxy and 28-hydroxymethyl substituents.		2.6920diol;
pentacyclic triterpenoid		analgesic;
anti-inflammatory agent;
antineoplastic agent;
antiviral agent;
metabolite
clevudine
[no description available]		2.0510
lycorine
lycorine: from bulbs of LYCORIS & other plants; RN given refers to (1 alpha,2 beta)-isomer; structure in Merck Index, 9th ed, #5444. lycorine : An indolizidine alkaloid that is 3,12-didehydrogalanthan substituted by hydroxy groups at positions and 2 and a methylenedioxy group across positions 9 and 10. Isolated from Crinum asiaticum, it has been shown to exhibit antimalarial activity.		2.6320indolizidine alkaloidanticoronaviral agent;
antimalarial;
plant metabolite;
protein synthesis inhibitor
gentamicin c1
[no description available]		2.0510
9-aminocamptothecin
[no description available]		2.0410pyranoindolizinoquinoline
sch 34343
Sch 34343: structure given in first source; RN given refers to (5R-(5alpha,6alpha))-isomer		2.0410
grepafloxacin
grepafloxacin: structure in first source		2.0510fluoroquinolone antibiotic;
quinolines;
quinolone antibiotic
squalamine
squalamine: from dogfish shark Squalus acanthias; structure given in first source		2.0410bile acid
2-(4'-methylpiperazino-1-methyl)-1,3-diazafluoranthene 1-oxide
2-(4'-methylpiperazino-1-methyl)-1,3-diazafluoranthene 1-oxide: structure		2.0510
3-methylbenzotriazin-4-one
3-methylbenzotriazin-4-one: structure given in first source		5.7122
tetrandrine
tetrandrine: a bisbenzylisoquinoline that exhibits antifibrogenic activity		2.0510bisbenzylisoquinoline alkaloid;
isoquinolines
3-deazaneplanocin
3-deazaneplanocin: S-adenosylhomocysteine hydrolase antagonist		7.6920
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.		3.6120carbapenems
o(6)-methyl-2'-deoxyguanosine
O(6)-methyl-2'-deoxyguanosine: RN given refers to (beta)-isomer. O(6)-methyl-2'-deoxyguanosine : A purine 2'-deoxyribonucleoside having O(6)-methylguanine as the nucleobase.		2.0510purine 2'-deoxyribonucleoside
calpeptin
[no description available]		2.2510amino acid amide
eburicoic acid
eburicoic acid: structure		2.2510
corilagin
corilagin: isolated from Geranii herba. corilagin : An ellagitannin with a hexahydroxydiphenoyl group bridging over the 3-O and 6-O of the glucose core.		2.3110ellagitannin;
gallate ester		antihypertensive agent;
antioxidant;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
non-steroidal anti-inflammatory drug
2-naphthylisothiocyanate
[no description available]		2.0510
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.		3.5820hydroxy-1,2-naphthoquinone
irinotecan hydrochloride
irinotecan hydrochloride (anhydrous) : A hydrochloride obtained by combining irinotecan with one molar equivalent of hydrochloric acid. Used (in the form of its trihydrate) in combination with fluorouracil and leucovorin, for the treatment of patients with metastatic adenocarcinoma of the pancreas after disease progression following gemcitabine-based therapy. It is converted via hydrolysis of the carbamate linkage to its active metabolite, SN-38, which is ~1000 times more active.		2.1110hydrochlorideantineoplastic agent;
apoptosis inducer;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
prodrug
1-(2-chloroethyl)-1-nitrosourea
[no description available]		1.9910
5-(3-methyl-1-triazeno)imidazole-4-carboxamide
5-(3-methyl-1-triazeno)imidazole-4-carboxamide: structure; RN given refers to parent cpd. MTIC : A monocarboxylic acid amide that is dacarbazine in which one of the methyl groups is replaced by a hydrogen. It is the active metabolite of dacarbazine, and is also produced by spontaneous hydrolysis of temozolomide in the body.		9.57205imidazoles;
monocarboxylic acid amide;
triazene derivative		alkylating agent;
antineoplastic agent
bendamustine hydrochloride
[no description available]		3.5311
rivastigmine
[no description available]		3.5820carbamate ester;
tertiary amino compound		cholinergic drug;
EC 3.1.1.8 (cholinesterase) inhibitor;
neuroprotective agent
frovatriptan
[no description available]		3.5820carbazoles
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.		3.5820indoles;
N-alkylpyrrolidine;
sulfone		non-steroidal anti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
rosiglitazone
[no description available]		4.9360aminopyridine;
thiazolidinediones		EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
insulin-sensitizing drug
tamiflu
[no description available]		2.0810phosphate salt
6-amino-5-bromouracil
[no description available]		2.2110
bexarotene
[no description available]		3.8730benzoic acids;
naphthalenes;
retinoid		antineoplastic agent
s20098
[no description available]		2.0810acetamides
flunisolide
flunisolide: flunisolide HFA is a formulation of flunisolide using hydrofluoroalkane (HFA) as propellant in place of chlorofluorocarbon (CFC) ones		2.081011beta-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
cyclic ketal;
fluorinated steroid;
primary alpha-hydroxy ketone		anti-asthmatic drug;
anti-inflammatory drug;
immunosuppressive agent
1-ethyl-2-benzimidazolinone
1-ethyl-2-benzimidazolinone: structure in first source		2.1310imidazoles
chloroquine diphosphate
[no description available]		2.0510
orphenadrine citrate
orphenadrine citrate : A citrate salt which comprises equimolar amounts of orphenadrine and citric acid.		2.0510citrate saltH1-receptor antagonist;
muscarinic antagonist;
muscle relaxant;
NMDA receptor antagonist;
parasympatholytic
ketorolac tromethamine
Ketorolac Tromethamine: A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is a non-steroidal anti-inflammatory agent used for analgesia for postoperative pain and inhibits cyclooxygenase activity.. ketorolac tromethamine : An organoammonium salt resulting from the mixture of equimolar amounts of ketorolac and tromethamine (tris). It has potent non-sedating analgesic and moderate anti-inflammatory effects. It is used in the short-term management of post-operative pain, and in eye drops to relieve the ocular itching associated with seasonal allergic conjunctivitis.		2.4720organoammonium saltanalgesic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor
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.		4.4260macrolide 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.		2.75303-(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
n-(3,5-dichlorophenyl)succinimide
N-(3,5-dichlorophenyl)succinimide: nephrotoxic; post-treatment enhanced induction of renal cell tumors in rats by dimethylnitrosamine, pre-treatment inhibited induction of tumors, & alone caused interstitial nephritis but no tumors		2.0510pyrrolidines
fibrinogen
Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.. D-iditol : The D-enantiomer of iditol.		5.0821iditolfungal metabolite
moexipril
[no description available]		3.2310peptide
phentolamine mesylate
[no description available]		2.0510
oxybutynin hydrochloride
[no description available]		2.0510hydrochloride
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.		2.2110amino acid zwitterion;
homocysteine;
serine family amino acid		fundamental metabolite;
mouse metabolite
gliquidone
gliquidone: structure; RN given refers to parent cpd		2.0810isoquinolines
cordium
bepridil hydrochloride monohydrate : The hydrochloride monohydrate of bepridril.		2.0510hydrate;
hydrochloride
fluoromisonidazole
[no description available]		7.0710
mci 9038
[no description available]		3.5820peptide
lopinavir
[no description available]		2.4720amphetamines;
dicarboxylic acid diamide		anticoronaviral agent;
antiviral drug;
HIV protease inhibitor
firefly luciferin
Firefly Luciferin: A benzothaizole which is oxidized by LUCIFERASES, FIREFLY to cause emission of light (LUMINESCENCE).. Photinus luciferin : A 1,3-thiazolemonocarboxylic acid consisting of 3,5-dihydrothiophene-4-carboxylic acid having a 6-hydroxybenzothiazol-2-yl group at the 2-position.		2.06101,3-thiazolemonocarboxylic acid;
benzothiazoles;
imidothioate		luciferin
erythrose
D-erythrose : The D-enantiomer of erythrose.		2.610erythroseplant metabolite
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.		2.8230D-glucuronic acidalgal metabolite
o(6)-n-butylguanine
[no description available]		210
6-ethylguanine
6-ethylguanine: found in rat brain DNA		2.420
diosgenin
[no description available]		3.31103beta-sterol;
hexacyclic triterpenoid;
sapogenin;
spiroketal		antineoplastic agent;
antiviral agent;
apoptosis inducer;
metabolite
clomesone
clomesone: structure & RN given in first source		1.9710
taurineamide
taurineamide: structure in first source		2.2110
moxifloxacin hydrochloride
moxifloxacin hydrochloride : A hydrochloride comprising equimolar amounts of moxifloxacin and hydrogen chloride.		2.0810hydrochlorideantibacterial drug
n-methyladenosine
N-methyladenosine: is a inhibitor of cell differentiation. N(6)-methyladenosine : A methyladenosine compound with one methyl group attached to N(6) of the adenine nucleobase.		2.7220methyladenosine
1,2-distearoylphosphatidylethanolamine
1,2-distearoylphosphatidylethanolamine: RN given refers to cpd without isomeric designation. 1,2-distearoylphosphatidylethanolamine : A phosphatidylethanolamine in which the phosphatidyl acyl group at C-1 and C-2 is stearoyl.		2.1310phosphatidylethanolamine zwitterion;
phosphatidylethanolamine		human 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.		3.612017beta-hydroxy steroid;
3-hydroxy steroid;
organofluorine compound;
sulfoxide		antineoplastic agent;
estrogen antagonist;
estrogen receptor antagonist
mafosfamide
mafosfamide: RN given refers to cis-(+-)-isomer		7.0310
hydrogen sulfite
[no description available]		2.110sulfur oxoanionhuman metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
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.		6.3741
mizoribine
[no description available]		2.0810imidazolesanticoronaviral agent
u 73122
1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione: structure given in first source. U-73122 : An aza-steroid that is 3-O-methyl-17beta-estradiol in which the 17beta-hydroxy group is replaced by a 6-(maleimid-1-yl)hexylamino group. An inibitor of phospholipase C.		2.0510aromatic ether;
aza-steroid;
maleimides		EC 3.1.4.11 (phosphoinositide phospholipase C) inhibitor
fotemustine
fotemustine: structure given in first source. fotemustine : A racemate comprising equimolar amounts of (R)- and (S)-fotemustine. It is an alkylating agent used in the treatment of malignant melanoma.. diethyl (1-{[(2-chloroethyl)(nitroso)carbamoyl]amino}ethyl)phosphonate : A member of the class of N-nitrosoureas that is ethyl diethylphosphonate in the hydrogen at position 1 of the ethyl group attached to the phosphorus has been replaced by a [(2-chloroethyl)(nitroso)carbamoyl]amino group.		10.9328N-nitrosoureas;
organic phosphonate;
organochlorine compound
arginyl-glycyl-aspartic acid
arginyl-glycyl-aspartic acid: amino acid sequence of basic unit of widespread cellular recognition system		3.2550oligopeptide
imipenem, anhydrous
Imipenem: Semisynthetic thienamycin that has a wide spectrum of antibacterial activity against gram-negative and gram-positive aerobic and anaerobic bacteria, including many multiresistant strains. It is stable to beta-lactamases. Clinical studies have demonstrated high efficacy in the treatment of infections of various body systems. Its effectiveness is enhanced when it is administered in combination with CILASTATIN, a renal dipeptidase inhibitor.. imipenem : A broad-spectrum, intravenous beta-lactam antibiotic of the carbapenem subgroup.		2.0410beta-lactam antibiotic allergen;
carbapenems;
zwitterion		antibacterial drug
sr141716
[no description available]		2.4720amidopiperidine;
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.		4.2650primary alcohol;
pyrimidines;
sulfonamide		antihypertensive agent;
endothelin receptor antagonist
paxilline
paxilline: structure given in first source; RN given refers to (2R-(2alpha,4bbeta,6aalpha,12bbeta,12calpha,14abeta))-isomer. paxilline : An indole diterpene alkaloid with formula C27H33NO4 isolated from Penicillium paxilli. It is a potent inhibitor of large conductance Ca2(+)- and voltage-activated K(+) (BK)-type channels.		3.1310diterpene alkaloid;
enone;
organic heterohexacyclic compound;
terpenoid indole alkaloid;
tertiary alcohol		anticonvulsant;
Aspergillus metabolite;
EC 3.6.3.8 (Ca(2+)-transporting ATPase) inhibitor;
genotoxin;
geroprotector;
mycotoxin;
Penicillium metabolite;
potassium channel blocker
selenomethionine
[no description available]		2.0510amino acid zwitterion;
selenomethionine		plant metabolite
artesunic acid
[no description available]		4.7680
racecadotril
racecadotril: parenterally active enkephalinase inhibitor		2.0810N-acyl-amino acid
n-(2'-(dimethylamino)ethyl)acridine-4-carboxamide
[no description available]		3.1110
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
2'-5'-oligoadenylate trimer
2',5'-oligoadenylate: inhibits protein synthesis in cell-free systems		2.0310
asulacrine
asulacrine: derivative of amsacrine; structure given in first source		2.0410acridines
hydroxycotinine
hydroxycotinine: metabolite of nicotine; RN given refers to (S)-isomer; structure. trans-3-hydroxycotinine : An N-alkylpyrrolidine that is cotinine substituted at position C-3 by a hydroxy group (the 3R,5S-diastereomer).		2.0410N-alkylpyrrolidine;
pyridines;
pyrrolidin-2-ones;
pyrrolidine alkaloid
fingolimod hydrochloride
Fingolimod Hydrochloride: A sphingosine-derivative and IMMUNOSUPPRESSIVE AGENT that blocks the migration and homing of LYMPHOCYTES to the CENTRAL NERVOUS SYSTEM through its action on SPHINGOSINE 1-PHOSPHATE RECEPTORS. It is used in the treatment of MULTIPLE SCLEROSIS.. fingolimod hydrochloride : The hydrochloride salt of 2-amino-2-[2-(4-octylphenyl) ethyl]-1,3-propanediol (fingolimod).		2.8330hydrochlorideimmunosuppressive agent;
prodrug;
sphingosine-1-phosphate receptor agonist
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
triptolide
[no description available]		7.110diterpenoid;
epoxide;
gamma-lactam;
organic heteroheptacyclic compound		antispermatogenic agent;
plant metabolite
quinaprilat
quinaprilat: metabolite of quinapril. quinaprilat : A dicarboxylic acid resulting from the hydrolysis of the ethyl ester group of quinapril to give the corresponding dicarboxylic acid. The active angiotensin-converting enzyme inhibitor (ACE inhibitor) of the prodrug quinapril.		2.0410dicarboxylic acid;
isoquinolines;
tertiary carboxamide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
vasodilator agent
2-hydroxyimipramine
2-hydroxyimipramine: RN given refers to parent cpd		2.0410dibenzoazepine
parthenolide
[no description available]		2.9130germacranolide
tamibarotene
tamibarotene: has retinoid-binding activity. tamibarotene : A dicarboxylic acid monoamide resulting from the condensation of one of the carboxy groups of terephthalic acid with the amino group of 5,5,8,8-tetramethyl-5,6,7,8-tetrahydronaphthalen-2-amine.		2.0510dicarboxylic acid monoamide;
retinoid;
tetralins		antineoplastic agent;
retinoic acid receptor alpha/beta agonist
ecteinascidin 743
[no description available]		4.2650acetate 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
deoxyglucose
Deoxyglucose: 2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.. deoxyglucose : A deoxyhexose comprising glucose having at least one hydroxy group replaced by hydrogen.		2.4720
tadalafil
[no description available]		3.6120benzodioxoles;
pyrazinopyridoindole		EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
5-hydroxydopamine
5-hydroxydopamine: RN given refers to parent cpd		2.0510catecholamine
homoorientin
homoorientin: isolated from Swertia japonica; structure given in first source		4.811flavone C-glycoside;
tetrahydroxyflavone		antineoplastic agent;
radical scavenger
liquiritigenin
liquiritigenin: structure given in first source; isolated from Pterocarpus marsupium. 4',7-dihydroxyflavanone : A dihydroxyflavanone in which the two hydroxy substituents are located at positions 4' and 7.. liquiritigenin : A dihydroxyflavanone compound having the two hydroxy substituents at the 4'- and 7-positions. Isolated from the root of Glycyrrhizae uralensis, it is a selective agonist for oestrogen receptor beta.		2.11104',7-dihydroxyflavanonehormone agonist;
plant metabolite
tanshinone
tanshinone: from root of Salvia miltiorrhiza Bunge; RN given refers to tanshinone I; cardioprotective agent and neuroprotective agent		7.2110abietane diterpenoidanticoronaviral agent
3'-o-(4-benzoyl)benzoyladenosine 5'-triphosphate
3'-O-(4-benzoyl)benzoyladenosine 5'-triphosphate: purinergic receptors agonist; structure given in first source		2.1110purine ribonucleoside triphosphate
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
4-s-cysteaminylphenol
[no description available]		2.3110
nitisinone
[no description available]		3.5920(trifluoromethyl)benzenes;
C-nitro compound;
cyclohexanones;
mesotrione		EC 1.13.11.27 (4-hydroxyphenylpyruvate dioxygenase) inhibitor
plavix
[no description available]		2.0810azaheterocycle sulfate salt;
organoammonium sulfate salt		anticoagulant;
P2Y12 receptor antagonist;
platelet aggregation 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.		5.9942hydroxamic acid;
secondary carboxamide		antineoplastic agent;
matrix metalloproteinase inhibitor
asiatic acid
[no description available]		2.1110monocarboxylic acid;
pentacyclic triterpenoid;
triol		angiogenesis modulating agent;
metabolite
clofarabine
[no description available]		4.0940adenosines;
organofluorine compound		antimetabolite;
antineoplastic agent
dioscin
[no description available]		2.3110hexacyclic triterpenoid;
spiroketal;
spirostanyl glycoside;
trisaccharide derivative		anti-inflammatory agent;
antifungal agent;
antineoplastic agent;
antiviral agent;
apoptosis inducer;
EC 1.14.18.1 (tyrosinase) inhibitor;
hepatoprotective agent;
metabolite
elacridar
Elacridar: inhibitor of MDR1 PROTEIN; structure given in first source		2.110
n'-(2-chloroethyl)-n-(2-(methylsulfonyl)ethyl)-n'-nitrosourea
N'-(2-chloroethyl)-N-(2-(methylsulfonyl)ethyl)-N'-nitrosourea: structure given in first source		3.0910
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.		3.8730benzothiazoles;
diamine		antidyskinesia agent;
antiparkinson drug;
dopamine agonist;
radical scavenger
lexitropsin
lexitropsin: structure given in first source; information reading oligopeptide		7.0110
valdecoxib
[no description available]		3.9330isoxazoles;
sulfonamide		antipyretic;
antirheumatic drug;
cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
hydroquinidine
hydroquinidine: urinary quinine metabolite; RN given refers to (9S)-isomer; structure in Merck Index, 9th ed, #4703		2.610cinchona alkaloid
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-fluorodopa
5-fluorodopa: RN given refers to (DL)-isomer; DOPA might be a specific substance which would allow a distinction to be made between normal & abnormal brain capillaries by means of external gamma-ray detection; structure		2.0810
rc 3095
bombesin (6-14), Tpi(6)-Leu(13)-psi(CH2NH)-Leu(14)-: an antagonist of bombesin		2.0510
celastrol
[no description available]		7.0510monocarboxylic acid;
pentacyclic triterpenoid		anti-inflammatory drug;
antineoplastic agent;
antioxidant;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
Hsp90 inhibitor;
metabolite
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.		14.23143methanesulfonate 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.		3.5820indoles;
sulfonamide;
tertiary amine		non-steroidal anti-inflammatory drug;
serotonergic agonist;
vasoconstrictor agent
mk 0663
[no description available]		2.7930bipyridines;
organochlorine compound;
sulfone		cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
gefitinib
[no description available]		11.06203aromatic 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
c & b metabond
Super-bond: an adhesive resin composed of 4-methacryloxyethyltrimellitic anhydride (4-META), methylmethacrylates (MMA) and tri-n-butylborane (TBB)		2.1110
polytrimethylene carbonate
trimethylene carbonate: structure in first source		2.3110
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.		3.6120benzocycloheptapyridineanti-allergic agent;
cholinergic antagonist;
drug metabolite;
H1-receptor antagonist
iguratimod
iguratimod: an immunosuppressive agent		7.2110organic molecular entity
1,4,7-triazacyclononane-n,n',n''-triacetic acid
1,4,7-triazacyclononane-N,N',N''-triacetic acid: structure given in first source		3.711
teloxantrone
teloxantrone: structure given in first source		3.0910
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
o(6)-benzyl-2'-deoxyguanosine
[no description available]		2.9340
lestaurtinib
[no description available]		2.0510indolocarbazole
ethazolastone
ethazolastone: structure given in first source		5.62100
methotrexate
[no description available]		12.9358dicarboxylic 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
estrone-3-o-sulfamate
estrone-3-O-sulfamate: a steroid sulfatase inhibitor		2.3110
cyanidin
cyanidin: RN given refers to parent cpd; structure. cyanidin cation : An anthocyanidin cation that is flavylium substituted at positions 3, 3', 4', 5 and 7 by hydroxy groups.		2.41105-hydroxyanthocyanidinantioxidant;
metabolite;
neuroprotective agent
2-methacryloyloxyethyl phosphorylcholine
[no description available]		2.1710
tamsulosin
[no description available]		3.58205-(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]		340penicillanic acids
olmesartan medoxomil
Olmesartan Medoxomil: An ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to manage HYPERTENSION.		3.8730biphenyls
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
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
abiraterone
[no description available]		2.08103beta-hydroxy-Delta(5)-steroid;
3beta-sterol;
pyridines		antineoplastic agent;
EC 1.14.99.9 (steroid 17alpha-monooxygenase) inhibitor
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.		3.61201,3-thiazolemonocarboxylic acid;
aromatic ether;
nitrile		EC 1.17.3.2 (xanthine oxidase) inhibitor
dilevalol
(R,R)-labetalol : A 2-hydroxy-5-{1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl}benzamide that has 1R,2R-configuration.		2.04102-hydroxy-5-{1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl}benzamide
cd 437
CD 437: selective for retinoic acid receptors gamma. CD437 : A naphthoic acid that is 6-phenylnaphthylene-2-carboxyic acid in which the phenyl substituent has been substituted at positions 3 and 4 by adamant-1-yl and hydroxy groups, respectively. It acts as a selective agonist of retinoic acid receptor (RAR)gamma and induces cell cycle arrest and apoptosis in various cancer cells.		2.0510adamantanes;
monocarboxylic acid;
naphthoic acid;
phenols		apoptosis inducer;
retinoic acid receptor gamma agonist
beta-lactams
2-azetidinone: structure in first source. azetidin-2-one : An unsubstituted beta-lactam compound.. beta-lactam : A lactam in which the amide bond is contained within a four-membered ring, which includes the amide nitrogen and the carbonyl carbon.		2.0110beta-lactam antibiotic allergen;
beta-lactam
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
lexapro
Lexapro: Trade name of escitalopram, the active S-enantiomer of the racemic citalopram.		2.0810
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]		2.7430hydrate;
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.		8.97124secondary alpha-hydroxy ketone;
tetracyclic diterpenoid		antimalarial;
antineoplastic agent;
photosensitizing agent
3,4-dihydro-5-methyl-1(2h)-isoquinolinone
3,4-dihydro-5-methyl-1(2H)-isoquinolinone: structure given in first source		2.420isoquinolines
perifosine
[no description available]		8.8530ammonium betaine;
phospholipid		EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
irofulven
irofulven: structure in first source		2.0410cyclohexenones
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.		5.13524-{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
ym 872
YM 872: structure in first source		2.0410
cositecan
cositecan: structure in first source		2.0510pyranoindolizinoquinoline
nsc-141549
[no description available]		2.0510
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.		4.42609-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).		3.8730azetidines;
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.		3.5820carbapenemcarboxylic acid;
pyrrolidinecarboxamide		antibacterial drug
dx 8951
[no description available]		2.0410pyranoindolizinoquinoline
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.		3.8730amino acid;
monocarboxylic acid;
organochlorine compound;
organofluorine compound;
secondary amino compound		cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
cilomilast
[no description available]		2.0410methoxybenzenes
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).		3.5820benzazepineaquaretic;
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		2.4520
vatalanib
[no description available]		6.0832monochlorobenzenes;
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
sabarubicin
sabarubicin: structure given in first source		2.0410
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.		4.0740aromatic 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		3.5820dihydropyridine
jtt 501
JTT 501: an insulin sensitizer; structure in first source		2.0510
solifenacin
[no description available]		3.5820isoquinolines
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.		3.2310methyl phenyl(piperidin-2-yl)acetateadrenergic agent
xamoterol
Xamoterol: A phenoxypropanolamine derivative that is a selective beta-1-adrenergic agonist.		2.4620morpholines
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.		4.0940methoxynaphthalene;
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
olmesartan
olmesartan: an active metabolite of CS 866		2.0510biphenylyltetrazoleangiotensin receptor antagonist;
antihypertensive agent
telbivudine
[no description available]		3.6120pyrimidine 2'-deoxyribonucleosideantiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
tipifarnib
[no description available]		8.4511imidazoles;
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.		4.84302,6-diaminopurinesantiviral drug;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
matteucinol
matteucinol: isolated from leaves of Rhododendron simsii; structure given in first source. matteucinol : A dihydroxyflavanone that is (2S)-flavanone with hydroxy groups at positions 5 and 7, methyl groups at positions 6 and 8 and a methoxy group at position 4'.		7.41104'-methoxyflavanones;
dihydroxyflavanone;
monomethoxyflavanone		plant metabolite;
radical scavenger
abanoquil
[no description available]		2.0410
ly 300164
talampanel: AMPA receptor antagonist		3.8421benzodioxoles
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.		3.5820antibiotic antifungal drug;
azamacrocycle;
echinocandin;
heterodetic cyclic peptide;
semisynthetic derivative
avasimibe
[no description available]		2.0510monoterpenoid
anacardic acid
anacardic acid: isolated from Anacardium occidentale; monophenol monooxygenase inhibitor. anacardic acid : A hydroxybenzoic acid that is salicylic acid substituted by a pentadecyl group at position 6. It is a major component of cashew nut shell liquid and exhibits an extensive range of bioactivities.		2.2110hydroxy monocarboxylic acid;
hydroxybenzoic acid		anti-inflammatory agent;
antibacterial agent;
anticoronaviral agent;
apoptosis inducer;
EC 2.3.1.48 (histone acetyltransferase) inhibitor;
EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor;
neuroprotective agent;
plant metabolite
boswellic acid
boswellic acid: ursane type; RN given refers to (3alpha,4beta)-isomer; active principle of salai guggal; see also record for salai guggal		7.2110triterpenoid
aminopterin
Aminopterin: A folic acid derivative used as a rodenticide that has been shown to be teratogenic.		3.0910dicarboxylic acidEC 1.5.1.3 (dihydrofolate reductase) inhibitor;
mutagen
4-(2-aminoethyl)benzenesulfonamide
[no description available]		2.2110
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.		9.1231biotins;
vitamin B7		coenzyme;
cofactor;
Escherichia coli metabolite;
fundamental metabolite;
human metabolite;
mouse metabolite;
nutraceutical;
prosthetic group;
Saccharomyces cerevisiae metabolite
isofuranodiene
isofuranodiene: structure		7.2110
angiotensin ii
Giapreza: injectable form of angiotensin II used to increase blood pressure in adult patients with septic or other distributive shock. Ile(5)-angiotensin II : An angiotensin II that acts on the central nervous system (PDB entry: 1N9V).		4.811amino acid zwitterion;
angiotensin II		human 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.		4.2650
ropivacaine
Ropivacaine: An anilide used as a long-acting local anesthetic. It has a differential blocking effect on sensory and motor neurons.. ropivacaine : The piperidinecarboxamide obtained by the formal condensation of N-propylpipecolic acid and 2,6-dimethylaniline.. (S)-ropivacaine : A piperidinecarboxamide-based amide-type local anaesthetic (amide caine) in which (S)-N-propylpipecolic acid and 2,6-dimethylaniline are combined to form the amide bond.		2.0410piperidinecarboxamide;
ropivacaine		local anaesthetic
sb 203580
[no description available]		2.4520imidazoles;
monofluorobenzenes;
pyridines;
sulfoxide		EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
geroprotector;
Hsp90 inhibitor;
neuroprotective agent
enzastaurin
[no description available]		6.6873indoles;
maleimides
1-(3-c-ethynylribopentofuranosyl)uracil
1-(3-C-ethynylribopentofuranosyl)uracil: structure given in first source		2.1310
erlotinib
[no description available]		4.4130aromatic ether;
quinazolines;
secondary amino compound;
terminal acetylenic compound		antineoplastic agent;
epidermal growth factor receptor antagonist;
protein kinase inhibitor
erlotinib hydrochloride
[no description available]		12.031711hydrochloride;
terminal acetylenic compound		antineoplastic agent;
protein kinase inhibitor
cilengitide
Cilengitide: an alphaVbeta3 integrin antagonist that paralyzes cancer cells		11.43207oligopeptide
organophosphonates
hydrogenphosphite : A divalent inorganic anion resulting from the removal of a proton from two of the hydroxy groups of phosphorous acid.		4.811divalent inorganic anion;
phosphite ion
l 694,458
DMP 777: structure given in first source		2.0510
melagatran
[no description available]		2.0410azetidines;
carboxamidine;
dicarboxylic acid monoamide;
non-proteinogenic alpha-amino acid;
secondary amino compound		anticoagulant;
EC 3.4.21.5 (thrombin) inhibitor;
serine protease inhibitor
aflatoxin b1
Aflatoxin B1: A potent hepatotoxic and hepatocarcinogenic mycotoxin produced by the Aspergillus flavus group of fungi. It is also mutagenic, teratogenic, and causes immunosuppression in animals. It is found as a contaminant in peanuts, cottonseed meal, corn, and other grains. The mycotoxin requires epoxidation to aflatoxin B1 2,3-oxide for activation. Microsomal monooxygenases biotransform the toxin to the less toxic metabolites aflatoxin M1 and Q1.. aflatoxin B1 : An aflatoxin having a tetrahydrocyclopenta[c]furo[3',2':4,5]furo[2,3-h]chromene skeleton with oxygen functionality at positions 1, 4 and 11.		2.0510aflatoxin;
aromatic ether;
aromatic ketone		carcinogenic agent;
human metabolite
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.		2.4620acetate 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
tesaglitazar
tesaglitazar: structure in first source		2.0410
ramelteon
ramelteon: melatonin MT1/MT2 receptor agonist		3.6120indanes
lapatinib
[no description available]		9.0584furans;
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.		3.8730benzoic acids;
monocarboxylic acid;
phenols;
triazoles		iron chelator
bms204352
BMS204352: a calcium-sensitive opener of maxi-K potassium channels; structure in first source		2.4620
fosfluconazole
fosfluconazole: prodrug of fluconazole		2.0410conazole antifungal drug;
triazole antifungal drug;
triazoles		prodrug
tbc-11251
sitaxsentan: endothelin A receptor antagonist; structure in first source		3.8730benzodioxoles
tolvaptan
[no description available]		3.6120benzazepine;
benzenedicarboxamide		aquaretic;
vasopressin receptor antagonist
sorafenib
[no description available]		11.31216(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]		6.8651aromatic amine;
dicarboximide;
isoindoles;
piperidones		angiogenesis inhibitor;
antineoplastic agent;
immunomodulator
nutlin 3
[no description available]		2.1310stilbenoid
regadenoson
[no description available]		10.3231purine 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.		3.6120N-acyl-amino acid
cp 101,606
traxoprodil mesylate: a selective NMDA antagonist; structure given in first source		2.0410
1-methylpropyl-2-imidazolyl disulfide
1-methylpropyl-2-imidazolyl disulfide: a thioredoxin inhibitor with antineoplastic activity		2.1710imidazoles
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
fludrocortisone acetate
fludrocortisone acetate : An acetate ester resulting from the formal condensation of the primary hydroxy group of fludrocortisone with acetic acid. A synthetic corticosteroid, it has glucocorticoid actions about 10 times as potent as hydrocortisone, while its mineralocorticoid actions are over 100 times as potent. It is used in partial replacement therapy for primary and secondary adrenocortical insufficiency in Addison's disease and for the treatment of salt-losing adrenal hyperplasia.		2.051011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(4) steroid;
acetate ester;
fluorinated steroid;
mineralocorticoid;
tertiary alpha-hydroxy ketone
gossypol acetic acid
[no description available]		3.240
vincaleukoblastine
[no description available]		3.930acetate 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
lanosterol
[no description available]		2.211014alpha-methyl steroid;
3beta-sterol;
tetracyclic triterpenoid		bacterial metabolite;
human metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
vincristine sulfate
[no description available]		2.4720organic sulfate saltantineoplastic agent;
geroprotector
anisomycin
Anisomycin: An antibiotic isolated from various Streptomyces species. It interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.. (-)-anisomycin : An antibiotic isolated from various Streptomyces species. It interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.		2.3110monohydroxypyrrolidine;
organonitrogen heterocyclic antibiotic		anticoronaviral agent;
antimicrobial agent;
antineoplastic agent;
antiparasitic agent;
bacterial metabolite;
DNA synthesis inhibitor;
protein synthesis inhibitor
benzofurans
Benzofurans: Compounds that contain a BENZENE ring fused to a furan ring.		2.5320
benzarone
benzarone: antihemorrhagic agent; structure		3.59201-benzofurans
nsc-89199
estramustine phosphate : A steroid phosphate which is the 17-O-phospho derivative of estramustine.		2.0410carbamate ester;
organochlorine compound;
steroid phosphate
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.		9.084017beta-hydroxy steroid;
carbamate ester;
organochlorine compound		alkylating agent;
antineoplastic agent;
radiation protective agent
Gamabufogenin
gamabufotalin: antiangiogenic, main active compound isolated from Chinese medicine Chansu; structure in first source		2.2510steroid lactone
withaferin a
withaferin A: an antiestrogen and phytogenic antineoplastic agent isolated from leaves of Withania somnifera Dun.; structure. withaferin A : A withanolide that is 5,6:22,26-diepoxyergosta-2,24-diene-1,26-dione substituted by hydroxy groups at positions 4 and 27 (the 4beta,5beta,6beta,22R stereoisomer). Isolated from Physalis longifolia, it exhibits cytotoxic activity.		7.11027-hydroxy steroid;
4-hydroxy steroid;
delta-lactone;
enone;
epoxy steroid;
ergostanoid;
primary alcohol;
secondary alcohol;
withanolide		antineoplastic agent;
apoptosis inducer
phenethicillin
phenethicillin: minor descriptor (85); major descriptor (63-84); on-line search PENICILLIN, PHENOXYMETHYL/AA (66-85); Index Medicus search PHENETHICILLIN (63-84); RN given refers to (2S-(2alpha,5alpha,6beta))-isomer. phenethicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-phenoxypropanamido group.		2.0410penicillin allergen;
penicillin
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.		2.4620aromatic 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
acivicin
[no description available]		2.4520isoxazoles;
non-proteinogenic L-alpha-amino acid;
organochlorine compound		antileishmanial agent;
antimetabolite;
antimicrobial agent;
antineoplastic agent;
EC 2.3.2.2 (gamma-glutamyltransferase) inhibitor;
glutamine antagonist;
metabolite
elesclomol
[no description available]		3.3110carbohydrazide;
thiocarbonyl compound		antineoplastic agent;
apoptosis inducer
u-104
SLC-0111: a carbonic anhydrase inhibitor; structure in first source		2.5820
wortmannin
[no description available]		2.4320acetate ester;
cyclic ketone;
delta-lactone;
organic heteropentacyclic compound		anticoronaviral agent;
antineoplastic agent;
autophagy inhibitor;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
geroprotector;
Penicillium metabolite;
radiosensitizing agent
withanolides
Withanolides: Ergostane derivatives of 28 carbons with oxygens at C1, C22, and C26 positions and the side chain cyclized. They are found in WITHANIA plant genus and have cytotoxic and other effects.		2.110
trimethoprim, sulfamethoxazole drug combination
Trimethoprim, Sulfamethoxazole Drug Combination: A drug combination with broad-spectrum antibacterial activity against both gram-positive and gram-negative organisms. It is effective in the treatment of many infections, including PNEUMOCYSTIS PNEUMONIA in AIDS.. co-trimoxazole : A two-component mixture comprising trimethoprim and sulfamethoxazole.		3.0540
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.		2.9340carbamate 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
2,5-bis(5-hydroxymethyl-2-thienyl)furan
[no description available]		2.5720thiophenes
bortezomib
[no description available]		10.72245amino 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.		4.7801,3-thiazoles;
carbamate ester;
carboxamide;
L-valine derivative;
ureas		antiviral drug;
environmental contaminant;
HIV protease inhibitor;
xenobiotic
jib-04
JIB-04: structure in first source		2.1510
acetogenins
Acetogenins: Polyketides of up to a few dozen carbons in length, formed by chain extension of multiple PROPIONATES and oxygenated to form tetrahydrofuran and lactone rings along the length of the chain. They are found in ANNONACEAE and other PLANTS. Related compounds cyclize to MACROLIDES.		2.610
nexavar
[no description available]		2.0510organosulfonate salt
gant 61
GANT 61: a sonic hedgehog pathway inhibitor and Gli inhibitor; structure in first source. GANT61 : An aminal that is hexahydropyrimidine which is substituted on each nitrogen by a 2-(dimethylamino)benzyl group, and at the aminal carbon by a pyridin-4-yl group. A Hedgehog signaling pathway and Gli protein inhibitor.		2.5820aminal;
dialkylarylamine;
pyridines;
substituted aniline;
tertiary amino compound		antineoplastic agent;
apoptosis inducer;
glioma-associated oncogene inhibitor;
Hedgehog signaling pathway inhibitor
leupeptins
Leupeptins: A group of acylated oligopeptides produced by Actinomycetes that function as protease inhibitors. They have been known to inhibit to varying degrees trypsin, plasmin, KALLIKREINS, papain and the cathepsins.		2.110
carboplatin
[no description available]		14.185112
bradykinin
[no description available]		2.110oligopeptidehuman blood serum metabolite;
vasodilator agent
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.		2.7530D-glucosamineEscherichia coli metabolite;
geroprotector;
mouse metabolite
carnosine
polaprezinc: stimulates bone growth		7.2110amino acid zwitterion;
dipeptide		anticonvulsant;
antineoplastic agent;
antioxidant;
Daphnia magna metabolite;
geroprotector;
human metabolite;
mouse metabolite;
neuroprotective agent
mevalonic acid
Mevalonic Acid: A dihydroxy monocarboxylic acid and precursor in the biosynthetic pathway known as the mevalonate pathway, which produces terpenes and steroids that are vital for diverse cellular functions.. mevalonic acid : A racemate composed of equimolar amounts of (R)- and (S)-mevalonic acid.. (R)-mevalonic acid : The (R)-enantiomer of mevalonic acid.		2.6103,5-dihydroxy-3-methylpentanoic acid
naringenin
(S)-naringenin : The (S)-enantiomer of naringenin.		7.4110(2S)-flavan-4-one;
naringenin		expectorant;
plant metabolite
epiglucan
epiglucan: a highly side-chain/branched alkali-insoluble cell wall glucan from fungus such as Epicoccum nigrum, Botrytis cinerea, ascomycetes & basidiomycetes; also isolated S-4001 from Lei Wan (polyporus mylitiae), HA-beta-glucan from mushroom Pleutotus ostreatus (Fr.) Quel., and translam from seaweed Laminaria cichorioides; with commercially important functional properties including emulsification and friction reduction.		2.3110
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
ouabain
Ouabain: A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like DIGITALIS. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-EXCHANGING ATPASE.. cardiac glycoside : Steroid lactones containing sugar residues that act on the contractile force of the cardiac muscles.. ouabain : A steroid hormone that is a multi-hydroxylated alpha-L-rhamnosyl cardenoloide. It binds to and inhibits the plasma membrane Na(+)/K(+)-ATPase (sodium pump). It has been isolated naturally from Strophanthus gratus.		2.11011alpha-hydroxy steroid;
14beta-hydroxy steroid;
5beta-hydroxy steroid;
alpha-L-rhamnoside;
cardenolide glycoside;
steroid hormone		anti-arrhythmia drug;
cardiotonic drug;
EC 2.3.3.1 [citrate (Si)-synthase] inhibitor;
EC 3.1.3.41 (4-nitrophenylphosphatase) inhibitor;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor;
EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor;
ion transport inhibitor;
plant metabolite
puromycin
[no description available]		2.0510puromycinsantiinfective agent;
antimicrobial agent;
antineoplastic agent;
EC 3.4.11.14 (cytosol alanyl aminopeptidase) inhibitor;
EC 3.4.14.2 (dipeptidyl-peptidase II) inhibitor;
nucleoside antibiotic;
protein synthesis inhibitor
tartaric acid
tartaric acid: RN given refers to cpd with unspecified isomeric designation. D-tartaric acid : The D-enantiomer of tartaric acid.		2.0710tartaric acidEscherichia coli 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.		3.8730coformycinsantimetabolite;
antineoplastic agent;
Aspergillus metabolite;
bacterial metabolite;
EC 3.5.4.4 (adenosine deaminase) inhibitor
taurolithocholic acid
Taurolithocholic Acid: A bile salt formed in the liver from lithocholic acid conjugation with taurine, usually as the sodium salt. It solubilizes fats for absorption and is itself absorbed. It is a cholagogue and choleretic.. taurolithocholic acid : The bile acid taurine conjugate of lithocholic acid.		2.0510bile acid taurine conjugate;
monocarboxylic acid amide		human metabolite
(+)-limonene
(4R)-limonene : An optically active form of limonene having (4R)-configuration.		2.0510limoneneplant metabolite
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.		4.5570cinchona 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.		4.0840alpha,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.		3.86301-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.		3.8630beta-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.		2.7530cardenolide glycosideEC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor
moxalactam disodium
[no description available]		2.0510
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.		4.0840L-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.		3.5820acetate ester;
steroid ester		cholinergic antagonist;
muscle relaxant;
nicotinic antagonist
rocuronium
Rocuronium: An androstanol non-depolarizing neuromuscular blocking agent. It has a mono-quaternary structure and is a weaker nicotinic antagonist than PANCURONIUM.. rocuronium : A 5alpha-androstane compound having 3alpha-hydroxy-, 17beta-acetoxy-, 2beta-morpholino- and 16beta-N-allyllyrrolidinium substituents.		2.04103alpha-hydroxy steroid;
acetate ester;
androstane;
morpholines;
quaternary ammonium ion;
tertiary amino compound		drug allergen;
muscle relaxant;
neuromuscular agent
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.		4.08402,6-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.		2.7430
trimethaphan camsylate
trimethaphan camsylate : The (S)-camphorsulfonate salt of trimethaphan.		2.0510
perindopril erbumine
[no description available]		2.0810addition compoundantihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
miglitol
[no description available]		3.8730piperidines
mometasone furoate
Mometasone Furoate: A pregnadienediol derivative ANTI-ALLERGIC AGENT and ANTI-INFLAMMATORY AGENT that is used in the management of ASTHMA and ALLERGIC RHINITIS. It is also used as a topical treatment for skin disorders.		2.051011beta-hydroxy steroid;
2-furoate ester;
20-oxo steroid;
3-oxo-Delta(1),Delta(4)-steroid;
organochlorine compound;
steroid ester		anti-allergic agent;
anti-inflammatory drug
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
rocuronium bromide
rocuronium bromide : The organic bromide salt of a 5alpha androstane compound having 3alpha-hydroxy-, 17beta-acetoxy-, 2beta-morpholino- and 16beta-N-allyllyrrolidinium substituents.		2.0810organic bromide salt;
quaternary ammonium salt		muscle relaxant;
neuromuscular agent
nortriptyline hydrochloride
[no description available]		2.0510organic tricyclic compoundgeroprotector
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.		2.4620aminoglycoside sulfate salt;
erythromycin derivative		enzyme inhibitor
kanamycin sulfate
[no description available]		2.0510aminoglycoside sulfate saltantibacterial drug;
geroprotector
paromomycin sulfate
paromomycin sulfate : An aminoglycoside sulfate salt resulting from the treatment of paromomycin with sulfuric acid. A broad-spectrum antibiotic, it is used 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.		2.0510
linezolid
[no description available]		3.8730acetamides;
morpholines;
organofluorine compound;
oxazolidinone		antibacterial drug;
protein synthesis inhibitor
hemanthamine
[no description available]		2.1310alkaloid
euphol
euphol: from Euphorbia acaulis Roxb.; structure given in first source		7.2110triterpenoid
furostanol i
furostanol I: from Dioscorea deltoidea; intermediate in in vivo diosgenin biosynthesis; structure given in first source. protodioscin : A spirostanyl glycoside that consists of the trisaccharide alpha-L-Rha-(1->4)-[alpha-L-Rha-(1->2)]-beta-D-Glc attached to position 3 of 26-(beta-D-glucopyranosyloxy)-3beta,22-dihydroxyfurost-5-ene via a glycosidic linkage. Found in several plant species including yams, asparagus and funugreek.		2.3110beta-D-glucoside;
cyclic hemiketal;
pentacyclic triterpenoid;
steroid saponin;
trisaccharide derivative		metabolite
cyclopamine
[no description available]		3.3760piperidinesglioma-associated oncogene inhibitor
lignans
Lignans: A class of dibenzylbutane derivatives which occurs in higher plants and in fluids (bile, serum, urine, etc.) in man and other animals. These compounds, which have a potential anti-cancer role, can be synthesized in vitro by human fecal flora. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)		3.2750
acriflavine
Acriflavine: 3,6-Diamino-10-methylacridinium chloride mixt. with 3,6-acridinediamine. Fluorescent dye used as a local antiseptic and also as a biological stain. It intercalates into nucleic acids thereby inhibiting bacterial and viral replication.		7.4110
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
chloramphenicol palmitate
chloramphenicol palmitate: RN given refers to ((R-(R*,R*))-isomer)		2.0510hexadecanoate ester
clindamycin phosphate
[no description available]		3.2310
sodium arsenite
sodium arsenite : An inoganic sodium salt with formula with formula NaAsO2.		2.110arsenic molecular entity;
inorganic sodium salt		antibacterial agent;
antifungal agent;
antineoplastic agent;
carcinogenic agent;
herbicide;
insecticide;
rodenticide
actinonin
actinonin: natural hydroxamic acid, pseudopeptide antibiotic isolated from Streptomyces species; structure		7.4110
hamayne
hamayne: structure in first source		2.1310alkaloid
calcium pantothenate
[no description available]		2.0510polymer
pemirolast potassium salt
[no description available]		2.0810
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.		3.61203-oxo-Delta(4) steroid;
epoxy steroid;
gamma-lactone;
methyl ester;
organic heteropentacyclic compound;
oxaspiro compound;
steroid acid ester		aldosterone antagonist;
antihypertensive agent
tolterodine
[no description available]		3.8630tertiary amineantispasmodic drug;
muscarinic antagonist;
muscle relaxant
doxorubicin hydrochloride
[no description available]		2.9940anthracycline
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		2.4720organic molecular entity
loteprednol etabonate
Loteprednol Etabonate: An androstadiene derivative corticosteroid that is used as an ANTI-ALLERGIC AGENT for the treatment of inflammatory and allergic eye conditions.		2.081011beta-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
etabonate ester;
organochlorine compound;
steroid acid ester;
steroid ester		anti-inflammatory drug
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.		3.58201-benzofurans;
monocarboxylic acid amide;
pyrrolidines		antispasmodic drug;
muscarinic antagonist
fluticasone propionate
fluticasone propionate : A trifluorinated corticosteroid that consists of 6alpha,9-difluoro-11beta,17alpha-dihydroxy-17beta-{[(fluoromethyl)sulfanyl]carbonyl}-16-methyl-3-oxoandrosta-1,4-diene bearing a propionyl substituent at position 17; has anti-inflammatory, anti-asthmatic and anti-allergic activity.		2.462011beta-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
corticosteroid;
fluorinated steroid;
propanoate ester;
steroid ester;
thioester		adrenergic agent;
anti-allergic agent;
anti-asthmatic drug;
anti-inflammatory drug;
bronchodilator agent;
dermatologic drug
betadex
beta-Cyclodextrins: Cyclic GLUCANS consisting of seven (7) glucopyranose units linked by 1,4-glycosidic bonds.		2.6620cyclodextrin
acarbose
[no description available]		2.4520amino cyclitol;
glycoside
maleic acid
maleic acid: RN given refers to parent cpd(Z)-isomer which is maleic acid; all RR's given refer to (Z)-isomer; (E)-isomer is fumaric acid. maleic acid : A butenedioic acid in which the double bond has cis- (Z)-configuration.		2.0510butenedioic acidalgal metabolite;
mouse metabolite;
plant metabolite
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		7.7220antibiotic 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.		8.78122retinoic 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
arachidonic acid
icosa-5,8,11,14-tetraenoic acid : Any icosatetraenoic acid with the double bonds at positions 5, 8, 11 and 14.. arachidonate : A long-chain fatty acid anion resulting from the removal of a proton from the carboxy group of arachidonic acid.		2.0610icosa-5,8,11,14-tetraenoic acid;
long-chain fatty acid;
omega-6 fatty acid		Daphnia galeata metabolite;
EC 3.1.1.1 (carboxylesterase) inhibitor;
human metabolite;
mouse metabolite
resveratrol
trans-resveratrol : A resveratrol in which the double bond has E configuration.		5.08120resveratrolantioxidant;
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).		3.8630retinol;
vitamin A		human metabolite;
mouse metabolite;
plant metabolite
cyanoginosin lr
cyanoginosin LR: cyclic heptapeptide from cyanobacterium Microcystis aeruginosa. microcystin-LR : A microcystin consisting of D-alanyl, L-leucyl, (3S)-3-methyl-D-beta-aspartyl,L-arginyl, 2S,3S,4E,6E,8S,9S)-3-amino-4,5,6,7-tetradehydro-9-methoxy-2,6,8-trimethyl-10-phenyldecanoyl, D-gamma-glutamyl, and 2,3-didehydro-N-methylalanyl residues joined into a 25-membered macrocycle. Produced by the cyanobacterium Microcystis aeruginosa, it is the most studied of the microcystins.		2.0510microcystinbacterial metabolite;
EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
environmental contaminant;
xenobiotic
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.		2.7630octadec-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.		4.2750macrolide lactambacterial metabolite;
immunosuppressive agent
pectins
Pectins: High molecular weight polysaccharides present in the cell walls of all plants. Pectins cement cell walls together. They are used as emulsifiers and stabilizers in the food industry. They have been tried for a variety of therapeutic uses including as antidiarrheals, where they are now generally considered ineffective, and in the treatment of hypercholesterolemia.. alpha-D-galacturonic acid : The alpha-anomer of D-galacturonic acid.		2.1310D-galactopyranuronic acid
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.		2.7430dihydroxy 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).		3.8630dihydroxy 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.		3.0140benzoate 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.		4.13402-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.		2.0810alpha,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.		4.0840
keratan sulfate
Keratan Sulfate: A sulfated mucopolysaccharide initially isolated from bovine cornea. At least two types are known. Type I, found mostly in the cornea, contains D-galactose and D-glucosamine-6-O-sulfate as the repeating unit; type II, found in skeletal tissues, contains D-galactose and D-galactosamine-6-O-sulfate as the repeating unit.. keratan sulfate : A sulfated glycosaminoglycan, a linear polymer that consists of the repeating disaccharide [3)-beta-Gal-(1->4)-beta-GlcNAc-(1->] and containing sulfo groups located at random positions.. keratan 6'-sulfate : A keratan sulfate with random sulfation at the 6'-position.		2.1110
lycopene
[no description available]		2.0810acyclic caroteneantioxidant;
plant metabolite
fosfomycin
Fosfomycin: An antibiotic produced by Streptomyces fradiae.. fosfomycin : A phosphonic acid having an (R,S)-1,2-epoxypropyl group attached to phosphorus.		3.8630epoxide;
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.		4.4260macrolide antibioticantibacterial drug;
environmental contaminant;
xenobiotic
drf 2725
ragaglitazar: a phenoxazine analogue of phenyl propanoic acid; Ragaglitazar is a coligand of PPARalpha and PPARgamma		2.4620
n(1)-guanyl-1,7-diaminoheptane
N(1)-guanyl-1,7-diaminoheptane: inhibits deoxyhypusine synthase. 2-(7-aminoheptyl)guanidine : A member of the class of guanidines in which the imino hydrogen of guanidine itself has been replaced by a 7-aminoheptyl group. It is an inhibitor of deoxyhypusine synthase activity (GO:0034038).		2.0710guanidines;
primary amino compound		antineoplastic agent;
EC 2.5.1.46 (deoxyhypusine synthase) inhibitor
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
bms 214662
7-cyano-2,3,4,5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3-(phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-benzodiazepine: a farnesyltransferase inhibitor; structure in first source. BMS-214662 : A member of the class of benzodiazepines that is 2,3,4,5-tetrahydro-1H-1,4-benzodiazepine substituted by (1H-imidazol-5-yl)methyl, benzyl, (thiophen-2-yl)sulfonyl, and cyano groups at positions 1, 3R, 4 and 7, respectively. It is a potent inhibitor of farnesyltransferase (IC50 = 1.35nM) which was under clinical development for the treatment of solid tumors.		2.0410benzenes;
benzodiazepine;
imidazoles;
nitrile;
sulfonamide;
thiophenes		antineoplastic agent;
apoptosis inducer;
EC 2.5.1.58 (protein farnesyltransferase) inhibitor
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).		3.5520epothilone;
epoxide		antineoplastic agent;
metabolite;
microtubule-stabilising agent;
tubulin modulator
eptifibatide
[no description available]		3.5820homodetic 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
gs 4071
GS 4071: The acid form.. oseltamivir acid : A cyclohexenecarboxylic acid that is cyclohex-1-ene-1-carboxylic acid which is substituted at positions 3, 4, and 5 by pentan-3-yloxy, acetamido, and amino groups, respectively (the 3R,4R,5S enantiomer). An antiviral drug, it is used as the corresponding ethyl ester prodrug, oseltamivir, to slow the spread of influenza.		2.0410acetate ester;
amino acid;
cyclohexenecarboxylic acid;
primary amino compound		antiviral drug;
EC 3.2.1.18 (exo-alpha-sialidase) inhibitor;
marine xenobiotic metabolite
fluciclovine f-18
fluciclovine F-18: A radioactive diagnostic agent used for the detection of recurrent prostate cancer by POSITRON EMISSION TOMOGRAPHY; structure in first source.		310
decitabine
[no description available]		8.911522'-deoxyribonucleoside
sm 8668
Sch 39304: Sch 42427 is the active entantiomer of the antifungal agent Sch 39304 which consists of Sch 42426 & Sch 42427; Sch 42426, the (S,S)-isomer, is inactive		2.0410
teniposide
[no description available]		4.2650aromatic 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
iridoids
Iridoids: A type of MONOTERPENES, derived from geraniol. They have the general form of cyclopentanopyran, but in some cases, one of the rings is broken as in the case of secoiridoid. They are different from the similarly named iridals (TRITERPENES).		2.2110
troxacitabine
troxacitabine: shows good anti-HIV activity without cytotoxicity		3.3420carbohydrate derivative;
nucleobase-containing molecular entity
valrubicin
[no description available]		2.4720anthracycline;
trifluoroacetamide
cefamandole
Cefamandole: Semisynthetic wide-spectrum cephalosporin with prolonged action, probably due to beta-lactamase resistance. It is used also as the nafate.. cefamandole : A cephalosporin compound having (R)-mandelamido and N-methylthiotetrazole side-groups.		2.0410cephalosporin;
semisynthetic derivative		antibacterial drug
artenimol
[no description available]		3.6920
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)		4.4360actinomycinmutagen
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).		2.71301,3-thiazoles;
C-glycosyl compound;
monocarboxylic acid amide		antineoplastic agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
prodrug
azaserine
Azaserine: Antibiotic substance produced by various Streptomyces species. It is an inhibitor of enzymatic activities that involve glutamine and is used as an antineoplastic and immunosuppressive agent.. azaserine : A carboxylic ester resulting from the formal condensation of the carboxy group of diazoacetic acid with the alcoholic hydroxy group of L-serine. An antibiotic produced by a Streptomyces species.		2.4620carboxylic ester;
diazo compound;
L-serine derivative;
non-proteinogenic L-alpha-amino acid		antifungal agent;
antimetabolite;
antimicrobial agent;
antineoplastic agent;
glutamine antagonist;
immunosuppressive agent;
metabolite
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.		11.62151L-phenylalanine derivative;
nitrogen mustard;
non-proteinogenic L-alpha-amino acid;
organochlorine compound		alkylating agent;
antineoplastic agent;
carcinogenic agent;
drug allergen;
immunosuppressive agent
sitafloxacin
[no description available]		2.0410fluoroquinolone antibiotic;
quinolines;
quinolone antibiotic
benzyloxycarbonylleucyl-leucyl-leucine aldehyde
benzyloxycarbonylleucyl-leucyl-leucine aldehyde: proteasome inhibitor. N-benzyloxycarbonyl-L-leucyl-L-leucyl-L-leucinal : A tripeptide that is L-leucyl-L-leucyl-L-leucine in which the C-terminal carboxy group has been reduced to the corresponding aldehyde and the N-terminal amino group is protected as its benzyloxycarbonyl derivative.		2.110amino aldehyde;
carbamate ester;
tripeptide		proteasome inhibitor
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.		3.8630nucleoside analogue;
phosphonic acids		antiviral drug;
drug metabolite;
HIV-1 reverse transcriptase inhibitor
posaconazole
[no description available]		3.6120aromatic ether;
conazole antifungal drug;
N-arylpiperazine;
organofluorine compound;
oxolanes;
triazole antifungal drug;
triazoles		trypanocidal drug
dibekacin
Dibekacin: Analog of KANAMYCIN with antitubercular as well as broad-spectrum antimicrobial properties.. dibekacin : A kanamycin that is kanamycin B lacking the 3- and 4-hydroxy groups on the 2,6-diaminosugar ring.		2.4520kanamycinsantibacterial agent;
protein synthesis inhibitor
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.		2.4720C-nitro compound;
delta-lactone;
pyranoindolizinoquinoline;
semisynthetic derivative;
tertiary alcohol		antineoplastic agent;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
prodrug
terameprocol
[no description available]		2.5820lignan
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.		3.8630antibiotic antifungal drug;
echinocandin		antiinfective agent
shikonin
shikonin: a naphthazarin; has antineoplastic and angiogenesis inhibiting activities		2.9830hydroxy-1,4-naphthoquinone
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
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.		3.5920one-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.		3.5920arsenic 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.		2.06102-bromocarboxylic acid;
monocarboxylic acid;
organochlorine compound
11-mercaptoundecanoic acid
[no description available]		2.1110
tolfenamic acid
tolfenamic acid: structure. tolfenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 3-chloro-2-methylphenyl group. Tolfenamic acid is used specifically for relieving the pain of migraine. It also shows anticancer activity.		2.3110aminobenzoic acid;
organochlorine compound;
secondary amino compound		EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
idarubicin hydrochloride
[no description available]		2.0510anthracycline
sr 90107
fondaparinux sodium : An organic sodium salt, being the decasodium salt of fondaparinux.		3.2310
carbenoxolone sodium
Carbenoxolone: An agent derived from licorice root. It is used for the treatment of digestive tract ulcers, especially in the stomach. Antidiuretic side effects are frequent, but otherwise the drug is low in toxicity.		2.0510triterpenoid
carbenoxolone
[no description available]		2.0510
meglumine iodipamide
[no description available]		3.2310organoammonium saltradioopaque medium
alpha-asarone
asarone: structure in Merck Index, 9th ed, #847. asarone : A phenylpropanoid that is benzene substituted by methoxy groups at positions 1, 2 and 4 and a propen-1-yl group at position 5. It has been isolated from Acorus.. alpha-asarone : The trans-isomer of asarone.		2.5720asaroneanticonvulsant;
GABA modulator
glycosides
[no description available]		2.1710
sinapinic acid
sinapinic acid: a matrix for matrix-assisted laser desorption technique for protein MW determination; a constituent of propolis. trans-sinapic acid : A sinapic acid in which the double bond has trans-configuration.		2.1510sinapic acidMALDI matrix material;
plant metabolite
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)		12.13594isomethyleugenol
piplartine
piplartine: Antineoplastic Agent, Phytogenic; alkaloid from Piper; structure in first source		2.4110cinnamamides;
dicarboximide
retinaldehyde
Retinaldehyde: A diterpene derived from the carotenoid VITAMIN A which functions as the active component of the visual cycle. It is the prosthetic group of RHODOPSIN (i.e., covalently bonded to ROD OPSIN as 11-cis-retinal). When stimulated by visible light, rhodopsin transforms this cis-isomer of retinal to the trans-isomer (11-trans-retinal). This transformation straightens-out the bend of the retinal molecule and causes a change in the shape of rhodopsin triggering the visual process. A series of energy-requiring enzyme-catalyzed reactions convert the 11-trans-retinal back to the cis-isomer.. all-trans-retinal : A retinal in which all four exocyclic double bonds have E- (trans-) geometry.		3.4511retinal;
vitamin A		gap junctional intercellular communication inhibitor;
human metabolite;
mouse metabolite
piperine
piperine : A N-acylpiperidine that is piperidine substituted by a (1E,3E)-1-(1,3-benzodioxol-5-yl)-5-oxopenta-1,3-dien-5-yl group at the nitrogen atom. It is an alkaloid isolated from the plant Piper nigrum.		7.2510benzodioxoles;
N-acylpiperidine;
piperidine alkaloid;
tertiary carboxamide		food component;
human blood serum metabolite;
NF-kappaB inhibitor;
plant metabolite
stilbenes
Stilbenes: Organic compounds that contain 1,2-diphenylethylene as a functional group.. trans-stilbene : The trans-isomer of stilbene.		4.88100stilbene
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
xanthohumol
xanthohumol: from hop plant, Humulus lupulus. xanthohumol : A member of the class of chalcones that is trans-chalcone substituted by hydroxy groups at positions 4, 2' and 4', a methoxy group at position 6' and a prenyl group at position 3'. Isolated from Humulus lupulus, it induces apoptosis in human malignant glioblastoma cells.		7.2510aromatic ether;
chalcones;
polyphenol		anti-HIV-1 agent;
antineoplastic agent;
antiviral agent;
apoptosis inducer;
EC 2.3.1.20 (diacylglycerol O-acyltransferase) inhibitor;
metabolite
p-hydroxycinnamaldehyde
p-hydroxycinnamaldehyde: an antibacterial substance from the saw fly, Acantholyda parki S.; structure in first source. 4-hydroxycinnamaldehyde : A cinnamaldehyde that is (E)-cinnamaldehyde substituted at position 4 on the phenyl ring by a hydroxy group.		2.2110cinnamaldehydesapoptosis inducer;
EC 1.14.13.39 (nitric oxide synthase) inhibitor;
plant metabolite
discodermolide
[no description available]		2.0510diterpenoid
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.		7.0182olefinic 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.		3.6120vasopressincardiovascular 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
mezlocillin
Mezlocillin: Semisynthetic ampicillin-derived acylureido penicillin. It has been proposed for infections with certain anaerobes and may be useful in inner ear, bile, and CNS infections.. mezlocillin : A penicillin in which the substituent at position 6 of the penam ring is a (2R)-2-[3-(methanesulfonyl)-2-oxoimidazolidine-1-carboxamido]-2-phenylacetamido group.		2.0410penicillin allergen;
penicillin		antibacterial drug
trilostane
trilostane: inhibits conversion of pregnenolone to progesterone; adrenal blocking agent used in treatment of Cushing's syndrome. trilostane : An epoxy steroid that is 3,17beta-dihydroxy-5alpha-androst-2-ene-2-carbonitrile in which the oxygen of the epoxy group is joined to the 4alpha and 5 alpha positions.		2.081017beta-hydroxy steroid;
3-hydroxy steroid;
androstanoid;
epoxy steroid;
nitrile		abortifacient;
antineoplastic agent;
EC 1.1.1.210 [3beta(or 20alpha)-hydroxysteroid dehydrogenase] inhibitor
tropisetron
Tropisetron: An indole derivative and 5-HT3 RECEPTOR antagonist that is used for the prevention of nausea and vomiting.. tropisetron : An indolyl carboxylate ester obtained by formal condensation of the carboxy group of indole-3-carboxylic acid with the hydroxy group of tropine.		2.0410indolyl carboxylic acid
tram 34
TRAM 34: inhibits IKCa1; structure in first source		2.5220organochlorine compound
leuprolide acetate
leuprolide acetate : An acetate salt obtained by combining the nonapeptide leuprolide with acetic acid. A long lasting GnRH analog, LH-Rh agonist. It is a synthetic nonapeptide analogue of gonadotropin-releasing hormone, and is used as a subcutaneous hydrogel implant for the treatment of prostate cancer and for the suppression of gonadal sex hormone production in children with central precocious puberty.		2.0810acetate saltantineoplastic agent;
gonadotropin releasing hormone agonist
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.		2.0410oligopeptideanti-estrogen;
antineoplastic agent;
gonadotropin releasing hormone agonist
fludarabine
[no description available]		2.4520purine 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.		4.0840pyrimidinethioneantidote 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]		4.1140
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.		4.6140ethyl 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.		4.5770aryl thiol;
purines;
thiocarbonyl compound		anticoronaviral agent;
antimetabolite;
antineoplastic agent
1-methyltryptophan
1-methyltryptophan: an immunomodulator. 1-methyltryptophan : A tryptophan derivative that is tryptophan carrying a single methyl substituent at position 1 on the indole.		2.1310indolyl carboxylic acid
levosulpiride
(S)-(-)-sulpiride : An optically active form of sulpiride having (S)-configuration. The active enantiomer of the racemic drug sulpiride. Selective D2-like dopamine antagonist (Ki values are ~ 0.015. ~ 0.013, 1, ~ 45 and ~ 77 muM at D2, D3, D4, D1 and D5 receptors respectively).		2.0810sulpirideantidepressant;
antiemetic;
antipsychotic agent;
dopaminergic antagonist
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
cotinine
Cotinine: The N-glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. It thus serves as a biomarker of exposure to tobacco SMOKING. It has CNS stimulating properties.. (-)-cotinine : An N-alkylpyrrolidine that consists of N-methylpyrrolidinone bearing a pyridin-3-yl substituent at position C-5 (the 5S-enantiomer). It is an alkaloid commonly found in Nicotiana tabacum.		2.0410N-alkylpyrrolidine;
pyridines;
pyrrolidin-2-ones;
pyrrolidine alkaloid		antidepressant;
biomarker;
human xenobiotic metabolite;
plant metabolite
flunarizine
Flunarizine: Flunarizine is a selective calcium entry blocker with calmodulin binding properties and histamine H1 blocking activity. It is effective in the prophylaxis of migraine, occlusive peripheral vascular disease, vertigo of central and peripheral origin, and as an adjuvant in the therapy of epilepsy.		2.3110diarylmethane
thiothixene
[no description available]		3.5920N-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.		3.6120zopiclonecentral 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.		4.43190aromatic 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
thiohydantoins
Thiohydantoins: Sulfur analogs of hydantoins with one or both carbonyl groups replaced by thiocarbonyl groups.		4.811
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.		4.26501,3-dihydroimidazole-2-thionesantithyroid drug
cinnarizine
Cinnarizine: A piperazine derivative having histamine H1-receptor and calcium-channel blocking activity with vasodilating and antiemetic properties but it induces PARKINSONIAN DISORDERS.		2.0810diarylmethane;
N-alkylpiperazine;
olefinic compound		anti-allergic agent;
antiemetic;
calcium channel blocker;
geroprotector;
H1-receptor antagonist;
histamine antagonist;
muscarinic antagonist
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.		4.2750monocarboxylic 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.		2.7830capsaicinoidnon-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
epalrestat
epalrestat : A monocarboxylic acid that is 1,3-thiazolidine which is substituted on the nitrogen by a carboxymethyl group, at positions 2 and 4 by thioxo and oxo groups, respectively, and at position 5 by a 2-methyl-3-phenylprop-2-en-1-ylidene group. It is an inhibitor of aldose reductase (which catalyses the conversion of glucose to sorbitol) and is used for the treatment of some diabetic complications, including neuropathy.		2.0810monocarboxylic acid;
thiazolidines		EC 1.1.1.21 (aldehyde reductase) inhibitor
drotaverin
drotaverin: Hungarian drug; RN given refers to parent cpd; structure		2.4620isoquinolines
chlorogenic acid
caffeoylquinic acid: Antiviral Agent; structure in first source. chlorogenate : A monocarboxylic acid anion that is the conjugate base of chlorogenic acid; major species at pH 7.3.		5.9632cinnamate ester;
tannin		food component;
plant metabolite
fatostatin
fatostatin: inhibits activation of SREBP; structure in first source		2.610thiazoles
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.		4.54702-aminopurinesanticoronaviral agent;
antimetabolite;
antineoplastic agent
(1R,2S)-tranylcypromine hydrochloride
(1R,2S)-tranylcypromine hydrochloride : A hydrochloride obtained by combining (1R,2S)-tranylcypromine with one equivalent of hydrochloric acid.		2.0510hydrochloride
tacrine hydrochloride
[no description available]		2.0510
thiourea
Thiourea: A photographic fixative used also in the manufacture of resins. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance may reasonably be anticipated to be a carcinogen (Merck Index, 9th ed). Many of its derivatives are ANTITHYROID AGENTS and/or FREE RADICAL SCAVENGERS.. thiourea : The simplest member of the thiourea class, consisting of urea with the oxygen atom substituted by sulfur.		10.6541one-carbon compound;
thioureas;
ureas		antioxidant;
chromophore
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
D-fructopyranose
[no description available]		3.8421cyclic hemiketal;
D-fructose;
fructopyranose		sweetening agent
thioacetamide
Thioacetamide: A crystalline compound used as a laboratory reagent in place of HYDROGEN SULFIDE. It is a potent hepatocarcinogen.. thioacetamide : A thiocarboxamide consiting of acetamide having the oxygen replaced by sulfur.		2.4620thiocarboxamidehepatotoxic agent
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.		4.0840cardenolide glycoside;
steroid saponin		anti-arrhythmia drug;
cardiotonic drug;
EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor;
epitope
streptozocin
[no description available]		4.0840
tamoxifen
[no description available]		9.71235stilbenoid;
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
stattic
[no description available]		2.55201-benzothiophenes;
C-nitro compound;
sulfone		antineoplastic agent;
radiosensitizing agent;
STAT3 inhibitor
cancidas
[no description available]		3.5820
apcin
apcin: inhibits the anaphase-promoting complex; structure in first source		7.3110
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.		2.472011alpha-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.		3.5820carbohydrate-containing antibiotic;
L-proline derivative;
monocarboxylic acid amide;
pyrrolidinecarboxamide;
S-glycosyl compound		antimicrobial agent;
bacterial metabolite
valinomycin
Valinomycin: A cyclododecadepsipeptide ionophore antibiotic produced by Streptomyces fulvissimus and related to the enniatins. It is composed of 3 moles each of L-valine, D-alpha-hydroxyisovaleric acid, D-valine, and L-lactic acid linked alternately to form a 36-membered ring. (From Merck Index, 11th ed) Valinomycin is a potassium selective ionophore and is commonly used as a tool in biochemical studies.. valinomycin : A twelve-membered cyclodepsipeptide composed of three repeating D-alpha-hydroxyisovaleryl-D-valyl-L-lactoyl-L-valyl units joined in sequence. An antibiotic found in several Streptomyces strains.		2.4920cyclodepsipeptide;
macrocycle		antimicrobial agent;
antiviral agent;
bacterial metabolite;
potassium ionophore
thiopental
Thiopental: A barbiturate that is administered intravenously for the induction of general anesthesia or for the production of complete anesthesia of short duration.. thiopental : A barbiturate, the structure of which is that of 2-thiobarbituric acid substituted at C-5 by ethyl and sec-pentyl groups.		2.0410barbituratesanticonvulsant;
drug allergen;
environmental contaminant;
intravenous anaesthetic;
sedative;
xenobiotic
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.		5.2331C-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]		4.2650
latoconazole
latoconazole: RN refers to cpd without isomeric designation; latoconazole is (E)-isomer; structure given in first source		2.0810conazole antifungal drug;
imidazole antifungal drug
maraviroc
[no description available]		3.6120tropane alkaloid
toremifene citrate
[no description available]		2.0810stilbenoidanticoronaviral agent
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.		4.4130aromatic ether;
organochlorine compound;
tertiary amine		antineoplastic agent;
bone density conservation agent;
estrogen antagonist;
estrogen receptor modulator
u 0126
U 0126: protein kinase kinase inhibitor; structure in first source		3.8930aryl sulfide;
dinitrile;
enamine;
substituted aniline		antineoplastic agent;
antioxidant;
apoptosis inducer;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
osteogenesis regulator;
vasoconstrictor agent
telaprevir
[no description available]		2.0510cyclopentapyrrole;
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).		3.8730beta-D-arabinoside;
monosaccharide derivative;
purine nucleoside		antineoplastic agent;
DNA synthesis inhibitor;
prodrug
2-[(2-ethoxyphenoxy)-phenylmethyl]morpholine
[no description available]		2.0410aromatic ether
lomeguatrib
[no description available]		8.16185
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.		7.1510alkali metal atom
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]		3.5820indolyl carboxylic acid
or 1259
[no description available]		2.4520hydrazone;
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		2.7530steroidestrogen
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.		4.140beta-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]		4.0840cinchona alkaloidantimalarial;
muscle relaxant;
non-narcotic analgesic
amrubicin
amrubicin: structure in first source; a 9-amino-anthracycline antibiotic. amrubicin : A synthetic anthracycline antibiotic with molecular formula C25H25NO9. A specific inhibitor of topoisomerase II, it is used (particularly as the hydrochloride salt) in the treatment of cancer, especially lung cancer, where it is a prodrug for the active metabolite, ambrucinol.		2.2110anthracycline antibiotic;
methyl ketone;
primary amino compound;
quinone;
tetracenes		antineoplastic agent;
prodrug;
topoisomerase II inhibitor
2'-cyano-2'-deoxyarabinofuranosylcytosine
2'-cyano-2'-deoxyarabinofuranosylcytosine: structure given in first source; RN given is for mono HCl		2.1310
e 7010
E 7010: inhibits tubulin polymerization; structure given in first source		3.3110sulfonamide
isepamicin
[no description available]		2.0410
ifetroban
ifetroban: thromboxane receptor antagonist; structure given in first source; a 7-oxabicyclo(2.2.1)heptane derivative		2.0410benzenes;
monocarboxylic acid
lamifiban
lamifiban: a nonpeptide glycoprotein IIb/IIIa antagonist; prevents platelet loss during experimental cardiopulmonary bypass		2.0410N-acylglycine
fospropofol
[no description available]		3.2310alkylbenzene
azilect
[no description available]		2.0810
rasagiline
[no description available]		3.2310indanes;
secondary amine;
terminal acetylenic compound		EC 1.4.3.4 (monoamine oxidase) inhibitor;
neuroprotective agent
safingol
safingol: RN given refers to the (R-(R*,S*))-isomer		2.110amino alcohol
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).		9.57701,3-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
laromustine
laromustine: has antineoplastic activity		10.0431
zd 6474
CH 331: structure in first source		6.7983aromatic ether;
organobromine compound;
organofluorine compound;
piperidines;
quinazolines;
secondary amine		antineoplastic agent;
tyrosine kinase inhibitor
telavancin
telavancin: an anti-infective agent; structure in first source. telavancin : A glycopeptide that is vancomycin substituted at position N-3'' by a 2-(decylamino)ethyl group and at position C-29 by a (phosphonomethyl)aminomethyl group. Used as its hydrochloride salt for treatment of adults with complicated skin and skin structure infections caused by bacteria.		2.0410glycopeptideantibacterial drug;
antimicrobial agent
salinomycin
salinomycin: from Streptomyces albus; RN given refers to parent cpd; structure		3.9230polyketide;
spiroketal		animal growth promotant;
potassium ionophore
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.		2.5720
silybin
[no description available]		2.0510
ovalbumin
Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily.		3.711
crocin
crocin: a free radical scavenger		2.610
mtt formazan
MTT formazan: a blue MEM-insoluble mitochondrial byproduct; used to determine viability of cells with active mitochondrial dehydrogenase enzymes		2.1110
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 225002
[no description available]		2.3110nitrophenol
minoxidil sulfate ester
minoxidil sulfate ester: metabolite of minoxidil; structure given 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.		3.240
stx-0119
STX-0119: antineoplastic; structure in first source		2.8230
sodium borohydride
sodium borohydride: RN given refers to parent cpd		3.4811inorganic sodium salt;
metal tetrahydridoborate
sitagliptin
sitagliptin : A triazolopyrazine that exhibits hypoglycemic activity.		3.8730triazolopyrazine;
trifluorobenzene		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
environmental contaminant;
hypoglycemic agent;
serine proteinase inhibitor;
xenobiotic
flosequinan
[no description available]		2.0510quinolines
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.		4.26502-nitrophenols;
benzophenones;
catechols		antiparkinson drug;
EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
tetrathiomolybdate
tetrathiomolybdate: RN given refers to (MoS4)-2; chelates copper; inhibits CopB copper ATPase and cytokine proteins important for angiogenesis; structure		2.0510
ganhuangenin
ganhuangenin: flavonoid from Scutellaria rehderiana; lipid peroxide antagonist		2.110
ku 55933
2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one: specific inhibitor of the ataxia-telangiectasia mutated kinase ATM; structure in first source		2.9940
sphingosine
sphing-4-enine : A sphingenine in which the C=C double bond is located at the 4-position.. sphingenine : A 2-aminooctadecene-1,3-diol having (2S,3R)-configuration.. sphingoid : Sphinganine, its homologs and stereoisomers, and the hydroxy and unsaturated derivatives of these compounds.. 2-aminooctadec-4-ene-1,3-diol : A 2-aminooctadecene-1,3-diol having its double bond at position 4.		7.7830sphing-4-eninehuman metabolite;
mouse metabolite
quercetin
[no description available]		4.181507-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
ubiquinone q2
Ubiquinone Q2: interacts with iron atom to form acceptor quinone complex; RN given refers to cpd with unspecified isomeric designation		2.1710ubiquinones
bilirubin
[no description available]		4.7421biladienes;
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.		2.5220prostaglandins 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
biochanin a
[no description available]		2.69204'-methoxyisoflavones;
7-hydroxyisoflavones		antineoplastic agent;
EC 3.5.1.99 (fatty acid amide hydrolase) inhibitor;
phytoestrogen;
plant metabolite;
tyrosine kinase inhibitor
formononetin
[no description available]		2.93304'-methoxyisoflavones;
7-hydroxyisoflavones		phytoestrogen;
plant metabolite
luteolin
[no description available]		5.08213'-hydroxyflavonoid;
tetrahydroxyflavone		angiogenesis inhibitor;
anti-inflammatory agent;
antineoplastic agent;
apoptosis inducer;
c-Jun N-terminal kinase inhibitor;
EC 2.3.1.85 (fatty acid synthase) inhibitor;
immunomodulator;
nephroprotective agent;
plant metabolite;
radical scavenger;
vascular endothelial growth factor receptor antagonist
7,3'-dihydroxy-4'-methoxyisoflavone
7,3'-dihydroxy-4'-methoxyisoflavone: isolated from Astragali radix; structure in first source. calycosin : A member of the class of 7-hydroxyisoflavones that is 7-hydroxyisoflavone which is substituted by an additional hydroxy group at the 3' position and a methoxy group at the 4' position.		2.69204'-methoxyisoflavones;
7-hydroxyisoflavones		antioxidant;
metabolite
calcitriol
dihydroxy-vitamin D3: as a major in vitro metabolite of 1alpha,25-dihydroxyvitamin D3, produced in primary cultures of neonatal human keratinocytes		3.8730D3 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
leukotriene b4
Leukotriene B4: The major metabolite in neutrophil polymorphonuclear leukocytes. It stimulates polymorphonuclear cell function (degranulation, formation of oxygen-centered free radicals, arachidonic acid release, and metabolism). (From Dictionary of Prostaglandins and Related Compounds, 1990). leukotriene B4 : A leukotriene composed of (6Z,8E,10E,14Z)-icosatetraenoic acid having (5S)- and (12R)-hydroxy substituents. It is a lipid mediator of inflammation that is generated from arachidonic acid via the 5-lipoxygenase pathway.		2.2110dihydroxy monocarboxylic acid;
hydroxy polyunsaturated fatty acid;
leukotriene;
long-chain fatty acid		human metabolite;
mouse metabolite;
plant metabolite;
vasoconstrictor agent
retinol palmitate
retinol palmitate: RN given refers to parent cpd; structure. retinyl palmitate : A palmitate ester of retinol with undefined geometry about the C=C bonds.. all-trans-retinyl palmitate : An all-trans-retinyl ester obtained by formal condensation of the carboxy group of palmitic (hexadecanoic acid) with the hydroxy group of all-trans-retinol. It is used in cosmetic products to treat various skin disorders such as acne, skin aging, wrinkles, dark spots, and also protect against psoriasis.		2.0510all-trans-retinyl ester;
retinyl palmitate		antioxidant;
Escherichia coli metabolite;
human xenobiotic metabolite
hymecromone
Hymecromone: A coumarin derivative possessing properties as a spasmolytic, choleretic and light-protective agent. It is also used in ANALYTICAL CHEMISTRY TECHNIQUES for the determination of NITRIC ACID.		2.610hydroxycoumarinantineoplastic agent;
hyaluronic acid synthesis inhibitor
alprostadil
[no description available]		2.4720prostaglandins 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.		3.8730hydroxy 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.		2.5220D3 vitamins;
hydroxy seco-steroid;
seco-cholestane;
secondary alcohol;
steroid hormone		geroprotector;
human metabolite
rutin
Hydroxyethylrutoside: Monohydroxyethyl derivative of rutin. Peripheral circulation stimulant used in treatment of venous disorders.		7.5220disaccharide derivative;
quercetin O-glucoside;
rutinoside;
tetrahydroxyflavone		antioxidant;
metabolite
gamma-linolenic acid
gamma-Linolenic Acid: An omega-6 fatty acid produced in the body as the delta 6-desaturase metabolite of linoleic acid. It is converted to dihomo-gamma-linolenic acid, a biosynthetic precursor of monoenoic prostaglandins such as PGE1. (From Merck Index, 11th ed). gamma-linolenic acid : A C18, omega-6 acid fatty acid comprising a linolenic acid having cis- double bonds at positions 6, 9 and 12.		2.0610linolenic acid;
omega-6 fatty acid		human metabolite;
mouse metabolite;
plant metabolite
alpha-linolenic acid
linolenic acid : A two-membered subclass of octadecatrienoic acid comprising the (9Z,12Z,15Z)- and (6Z,9Z,12Z)-isomers. Linolenic acids are nutrients essential to the formation of prostaglandins and are also used in making paints and synthetic resins.. linolenate : A polyunsaturated fatty acid anion obtained by deprotonation of the carboxy group of either alpha- or gamma-linolenic acid.		2.610linolenic acid;
omega-3 fatty acid		micronutrient;
mouse metabolite;
nutraceutical
harmine
Harmine: Alkaloid isolated from seeds of PEGANUM HARMALA; ZYGOPHYLLACEAE. It is identical to banisterine, or telepathine, from Banisteria caapi and is one of the active ingredients of hallucinogenic drinks made in the western Amazon region from related plants. It has no therapeutic use, but (as banisterine) was hailed as a cure for postencephalitic PARKINSON DISEASE in the 1920's.. harmine : A harmala alkaloid in which the harman skeleton is methoxy-substituted at C-7.		3.3110harmala alkaloidanti-HIV agent;
EC 1.4.3.4 (monoamine oxidase) inhibitor;
metabolite
genistein
[no description available]		2.69207-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.		4.0840antibiotic 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.		2.4520oxapenamantibacterial 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.		4.084011beta-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.		3.8730
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.		4.0840dicarboxylic acid;
imidazoles;
thiophenes		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
montelukast
montelukast: a leukotriene D4 receptor antagonist		4.0840aliphatic 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.		3.5820isoquinolines
timolol maleate
(S)-timolol maleate : The maleic acid salt of the active (S)-enantiomer of timolol, comprising equimolar amounts of (S)-timolol and maleic acid.		2.0510maleate saltanti-arrhythmia drug;
antiglaucoma drug;
antihypertensive agent;
beta-adrenergic antagonist
brompheniramine maleate
brompheniramine maleate : The maleic acid salt of brompheniramine. A histamine H1 receptor antagonist, it is used for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.		2.4720maleate saltanti-allergic agent
chlorpheniramine maleate
[no description available]		2.0510organic molecular entity
clemastine fumarate
clemastine fumarate : The fumaric acid salt of clemastine. An antihistamine with antimuscarinic and moderate sedative properties, it is used for the symptomatic relief of allergic conditions such as rhinitis, urticaria, conjunctivitis and in pruritic (severe itching) skin conditions.		2.0510fumarate saltanti-allergic agent;
antipruritic drug;
H1-receptor antagonist;
muscarinic antagonist
dexchlorpheniramine maleate
[no description available]		2.0810organic molecular entity
methylergonovine maleate
[no description available]		2.0510ergoline alkaloidgeroprotector
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.		3.8730carboxylic 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.		4.26502-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]		3.5820hydroxy 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
fucoxanthin
fucoxanthin: RN given refers to (3S,3'S,5R,5'R,6S,6'R)-isomer. fucoxanthin : An epoxycarotenol that is found in brown seaweed and which exhibits anti-cancer, anti-diabetic, anti-oxidative and neuroprotective properties.		3.2710
esculetin
esculetin: used in filters for absorption of ultraviolet light; structure. esculetin : A hydroxycoumarin that is umbelliferone in which the hydrogen at position 6 is substituted by a hydroxy group. It is used in filters for absorption of ultraviolet light.		2.0710hydroxycoumarinantioxidant;
plant metabolite;
ultraviolet filter
esculin
[no description available]		2.0710beta-D-glucoside;
hydroxycoumarin		antioxidant;
metabolite
7-hydroxycoumarin
7-oxycoumarin: derivatives have anti-oxidant properties. umbelliferone : A hydroxycoumarin that is coumarin substituted by a hydroxy group ay position 7.		2.0710hydroxycoumarinfluorescent probe;
food component;
plant metabolite
humulene
humulene: structure given in first source. (1E,4E,8E)-alpha-humulene : The (1E,4E,8E)-isomer of alpha-humulene.		4.811alpha-humulene
oleuropein
oleuropein: iridoid isolated from leaves and fruit of Olea and Ligustrum (Oleaceae). oleuropein : A secoiridoid glycoside that is the methyl ester of 3,4-dihydro-2H-pyran-5-carboxylic acid which is substituted at positions 2, 3, and 4 by hydroxy, ethylidene, and carboxymethyl groups, respectively and in which the anomeric hydroxy group at position 2 has been converted into its beta-D-glucoside and the carboxylic acid moiety of the carboxymethyl substituent has been converted to the corresponding 3,4-dihydroxyphenethyl ester (the 2S,3E,4S stereoisomer). The most important phenolic compound present in olive cultivars.		2.2110beta-D-glucoside;
catechols;
diester;
methyl ester;
pyrans;
secoiridoid glycoside		anti-inflammatory agent;
antihypertensive agent;
antineoplastic agent;
antioxidant;
apoptosis inducer;
NF-kappaB inhibitor;
nutraceutical;
plant metabolite;
radical scavenger
diosmin
[no description available]		2.0510dihydroxyflavanone;
disaccharide derivative;
glycosyloxyflavone;
monomethoxyflavone;
rutinoside		anti-inflammatory agent;
antioxidant
hispidulin
hispidulin : A monomethoxyflavone that is scutellarein methylated at position 6.		2.5920monomethoxyflavone;
trihydroxyflavone		anti-inflammatory agent;
anticonvulsant;
antineoplastic agent;
antioxidant;
apoptosis inducer;
plant metabolite
myricetin
[no description available]		2.17107-hydroxyflavonol;
hexahydroxyflavone		antineoplastic agent;
antioxidant;
cyclooxygenase 1 inhibitor;
food component;
geroprotector;
hypoglycemic agent;
plant 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
rosmarinic acid
rosmarinic acid: RN given refers to parent cpd; promote OT project. (R)-rosmarinic acid : A stereoisomer of rosmarinic acid having (R)-configuration.. rosmarinic acid : The 1-carboxy-2-(2,4-dihydroxyphenyl)ethyl ester of trans-caffeic acid.		2.110rosmarinic acidgeroprotector;
plant metabolite
salvianolic acid a
salvianolic acid A: a nootropic depside from Salvia miltiorrhizia		7.4110stilbenoid
acteoside
acteoside: a protein kinase C inhibitor with hepatoprotective, anti-asthmatic, and analgesic activities; a phenylethanoid glycoside related to isoacteoside; from leaves of Lippia multiflora (Verbenaceae). acteoside : A glycoside that is the alpha-L-rhamnosyl-(1->3)-beta-D-glucoside of hydroxytyrosol in which the hydroxy group at position 4 of the glucopyranosyl moiety has undergone esterification by formal condensation with trans-caffeic acid.		7.2110catechols;
cinnamate ester;
disaccharide derivative;
glycoside;
polyphenol		anti-inflammatory agent;
antibacterial agent;
antileishmanial agent;
neuroprotective agent;
plant metabolite
ellagic acid
[no description available]		2.6320catechols;
cyclic ketone;
lactone;
organic heterotetracyclic compound;
polyphenol		antioxidant;
EC 1.14.18.1 (tyrosinase) inhibitor;
EC 2.3.1.5 (arylamine N-acetyltransferase) inhibitor;
EC 2.4.1.1 (glycogen phosphorylase) inhibitor;
EC 2.5.1.18 (glutathione transferase) inhibitor;
EC 2.7.1.127 (inositol-trisphosphate 3-kinase) inhibitor;
EC 2.7.1.151 (inositol-polyphosphate multikinase) inhibitor;
EC 2.7.4.6 (nucleoside-diphosphate kinase) inhibitor;
EC 2.7.7.7 (DNA-directed DNA polymerase) inhibitor;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
food additive;
fungal metabolite;
geroprotector;
plant metabolite;
skin lightening agent
flupenthixol
cis-flupenthixol : A flupenthixol in which the double bond adopts a cis-configuration.		2.0510flupenthixoldopaminergic antagonist
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		2.4520homodetic cyclic peptide
estradiol-17 beta-glucuronide
17beta-estradiol 17-glucosiduronic acid : A steroid glucosiduronic acid that consists of 17beta-estradiol having a beta-glucuronyl residue attached at position 17 via a glycosidic linkage.		2.05103-hydroxy steroid;
steroid glucosiduronic acid
l 660,711
[no description available]		2.0810quinolines
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.		2.8130ubiquinonesantioxidant;
ferroptosis inhibitor;
human metabolite
travoprost
Travoprost: A cloprostenol derivative that is used as an ANTIHYPERTENSIVE AGENT in the treatment of OPEN-ANGLE GLAUCOMA and OCULAR HYPERTENSION.. travoprost : The isopropyl ester of prostaglandin F2alpha in which the pentyl group is replaced by a 3-(trifluoromethyl)phenoxymethyl group. A synthetic analogue of prostaglandin F2alpha, ophthalmic solutions of travoprost are used as a topical medication for controlling the progression of open-angle glaucoma and ocular hypertension, by reducing intraocular pressure. It is a pro-drug; the isopropyl ester group is hydrolysed by esterases in the cornea to the biologically active free acid, fluprostenol.		2.0810(trifluoromethyl)benzenes;
isopropyl ester;
prostaglandins Falpha		antiglaucoma drug;
antihypertensive agent;
ophthalmology drug;
prodrug;
prostaglandin receptor agonist
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.		2.4720amidobenzoic 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
imipenem
[no description available]		2.0810carbapenems
etretinate
retinoid : Oxygenated derivatives of 3,7-dimethyl-1-(2,6,6-trimethylcyclohex-1-enyl)nona-1,3,5,7-tetraene and derivatives thereof.		2.4720enoate 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.		9.83145retinoic 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
ketotifen fumarate
ketotifen fumarate : An organoammonium salt consisting of equimolar amounts of ketotifen(1+) and fumarate(1-) ions. A blocker of histamine H1 receptors with a stabilising action on mast cells, it is a non-bronchodilator anti-asthmatic drug.		2.0810organoammonium saltanti-asthmatic drug;
H1-receptor antagonist
epoprostenol
[no description available]		3.2310prostaglandins Imouse metabolite
indocyanine green
[no description available]		3.58201,1-diunsubstituted alkanesulfonate;
benzoindole;
cyanine dye
dinoprost tromethamine
[no description available]		2.0810organic molecular entity
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
rosuvastatin calcium
S 4522: structure in first source		2.0810N-acyl-15-methylhexadecasphinganine-1-phosphoethanolamine;
organic calcium salt		anti-inflammatory agent;
cardioprotective agent;
CETP inhibitor
terbinafine hydrochloride
terbinafine hydrochloride : A hydrochloride obtained by reaction of terbinafine with one molar equivalent of hydrogen chloride.		2.0810allylamine antifungal drug;
hydrochloride		EC 1.14.13.132 (squalene monooxygenase) inhibitor;
P450 inhibitor
ethamolin
monoethanolamine oleate: used for treatment of pyogenic granuloma		3.2310long-chain fatty acid
alatrofloxacin mesylate
[no description available]		3.5920
sphingosine 1-phosphate
sphingosine 1-phosphate: RN given refers to (R-(R*,S*-(E)))-isomer; RN for cpd without isomeric designation not available 8/89. sphingosine 1-phosphate : A phosphosphingolipid that consists of sphingosine having a phospho group attached at position 1		2.5820sphingoid 1-phosphatemouse metabolite;
signalling molecule;
sphingosine-1-phosphate receptor agonist;
T-cell proliferation inhibitor;
vasodilator agent
codeine
[no description available]		3.8630morphinane 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		4.2650homodetic 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
mitolactol
Mitolactol: Alkylating antineoplastic toxic to bone marrow; used in breast cancer, also in combination with other drugs.		3.2310alcohol;
organobromine compound
phenoxybenzamine hydrochloride
[no description available]		2.0510organic molecular entity
natamycin
[no description available]		2.4720antibiotic 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.		4.0940acitretin;
alpha,beta-unsaturated monocarboxylic acid;
retinoid		keratolytic drug
dothiepin
[no description available]		2.0510dothiepin
estropipate
estropipate: used therapeutically in menopausal patients		3.2310piperazinium salt;
steroid sulfate
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.		3.5820morphinane 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.		8.78181pyrrolidin-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.		3.5920carbacephem;
zwitterion		antibacterial drug;
antimicrobial agent
nabilone
nabilone: cannabinol deriv; RN given refers to cpd without isomeric designation; structure		3.2310
nalmefene
nalmefene: RN given refers to 5-alpha isomer		2.7530morphinane alkaloid
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.		4.0840morphinane 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.		3.8730organic 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.		3.2310phylloquinones;
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.		13.3408antibiotic 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.		10.6551cyclic 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
irosustat
irosustat: Antineoplastic Agents, Hormonal; a tricyclic sulfamate ester; structure in first source		2.3110
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.		2.9940dihydroxyflavone;
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.		3.8630morphinane 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]		2.4720
acipimox
acipimox: lipolysis inhibitor		2.0810pyrazinecarboxylic acid
atosiban
[no description available]		2.0810oligopeptide
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
bimatoprost
Bimatoprost: A cloprostenol-derived amide that is used as an ANTIHYPERTENSIVE AGENT in the treatment of OPEN-ANGLE GLAUCOMA and OCULAR HYPERTENSION.		2.0810monocarboxylic acid amideantiglaucoma drug;
antihypertensive agent
cicaprost
cicaprost: RN given refers to (3aS-(2E,3aalpha,4alpha(3R*,4R*),5beta,6aalpha))-isomer		2.0410monoterpenoid
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.		3.6920heterodetic cyclic peptidediagnostic agent;
renal agent;
vasopressin receptor agonist
dexmedetomidine
[no description available]		3.5820medetomidinealpha-adrenergic agonist;
analgesic;
non-narcotic analgesic;
sedative
fluticasone
Fluticasone: A STEROID with GLUCOCORTICOID RECEPTOR activity that is used to manage the symptoms of ASTHMA; ALLERGIC RHINITIS, and ATOPIC DERMATITIS.. fluticasone : A trifluorinated corticosteroid used in the form of its propionate ester for treatment of allergic rhinitis.		4.81111beta-hydroxy steroid;
17alpha-hydroxy steroid;
3-oxo-Delta(4) steroid;
corticosteroid;
fluorinated steroid;
thioester		anti-allergic agent;
anti-asthmatic drug
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.		3.2310organic 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.		2.4520carbobicyclic compound;
monocarboxylic acid;
secondary alcohol		platelet aggregation inhibitor;
vasodilator agent
latanoprost
Latanoprost: A prostaglandin F analog used to treat OCULAR HYPERTENSION in patients with GLAUCOMA.. latanoprost : A prostaglandin Falpha that is the isopropyl ester prodrug of latanoprost free acid. Used in the treatment of open-angle glaucoma and ocular hypertension.		2.0810isopropyl ester;
prostaglandins Falpha;
triol		antiglaucoma drug;
antihypertensive agent;
EC 4.2.1.1 (carbonic anhydrase) inhibitor;
prodrug
n-(n-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester
DAPT : A dipeptide consisting of alanylphenylglycine derivatised as a 3,5-difluorophenylacetamide at the amino terminal and a tert-butyl ester at the carboxy terminal. A gamma-secretase inhibitor.		2.0510carboxylic ester;
difluorobenzene;
dipeptide;
tert-butyl ester		EC 3.4.23.46 (memapsin 2) inhibitor
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.		3.5820organic 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.		3.8730phenylalanine derivative
vinorelbine
[no description available]		4.0840acetate 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
bufothionine
bufothionine: has antineoplastic activity; found in Cinobufacini, and extract derived from the toad Bufo bufo gargarizans cantor; structure in first source		7.2110
andrographolide
[no description available]		2.2110carbobicyclic compound;
gamma-lactone;
labdane diterpenoid;
primary alcohol;
secondary alcohol		anti-HIV agent;
anti-inflammatory drug;
antineoplastic agent;
metabolite
icariin
[no description available]		7.1110flavonols;
glycosyloxyflavone		antioxidant;
bone density conservation agent;
EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
phytoestrogen
5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one
5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one: isolated from the Chinese herb Scutellariae radix. oroxylin A : A dihydroxy- and monomethoxy-flavone in which the hydroxy groups are positioned at C-5 and C-7 and the methoxy group is at C-6.		2.6320dihydroxyflavone;
monomethoxyflavone		antineoplastic agent;
EC 1.14.13.39 (nitric oxide synthase) inhibitor
1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3h-cyclopenta(c)quinolin-8-yl)ethanone
1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone: G-1 was able to induce both c-fos expression and proliferation in the ERalpha-negative/GPR30-positive SKBR3 breast cancer cells, the requirement for ERalpha expression in GPR30/EGFR signaling may depend on the specific cellular context of different tumor types		2.3110agonist
furazolidone
[no description available]		2.4620
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.		4.0840(trifluoromethyl)benzenes;
5-methoxyvalerophenone O-(2-aminoethyl)oxime		antidepressant;
anxiolytic drug;
serotonin uptake inhibitor
casein kinase ii
Casein Kinase II: A ubiquitous casein kinase that is comprised of two distinct catalytic subunits and dimeric regulatory subunit. Casein kinase II has been shown to phosphorylate a large number of substrates, many of which are proteins involved in the regulation of gene expression.		2.6620
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		2.0510aminoquinoline;
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.		2.4420olefinic 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]		9.94201monocarboxylic 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]		8.2650aminopyridine;
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]		2.3110stilbenoid
fosbretabulin
fosbretabulin: a microtubule destabilizing agent isolated from Combretum caffrum; structure in first source		2.0610
stilbamidine
stilbamidine: RN given refers to parent cpd		2.0510
romidepsin
depsipeptide : A natural or synthetic compound having a sequence of amino and hydroxy carboxylic acid residues (usually alpha-amino and alpha-hydroxy acids), commonly but not necessarily regularly alternating.		2.0410cyclodepsipeptide;
heterocyclic antibiotic;
organic disulfide		antineoplastic agent;
EC 3.5.1.98 (histone deacetylase) inhibitor
stellettin b
stellettin B: from the marine sponge Rhabdastrella globostellata; structure in first source		2.610
6,7-dihydroxyflavone
6,7-dihydroxyflavone: intensifies effect of antibiotics on Staphylococcus aureus; structure in first source		2.3110
bay 11-7082
(E)-3-tosylacrylonitrile : A nitrile that is acrylonitrile in which the hydrogen located beta,trans to the cyano group is replaced by a tosyl group. It is an inhibitor of cytokine-induced IkappaB-alpha phosphorylation in cells.		7.6620nitrile;
sulfone		apoptosis inducer;
EC 2.7.11.10 (IkappaB kinase) inhibitor;
EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor;
non-steroidal anti-inflammatory drug;
platelet aggregation inhibitor
(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.		4.2650dihydroxy monocarboxylic acid;
indoles;
organofluorine compound
molsidomine
[no description available]		2.4720ethyl ester;
morpholines;
oxadiazole;
zwitterion		antioxidant;
apoptosis inhibitor;
cardioprotective agent;
nitric oxide donor;
vasodilator agent
octylmethoxycinnamate
[no description available]		2.0510cinnamate ester
levorphanol
Levorphanol: A narcotic analgesic that may be habit-forming. It is nearly as effective orally as by injection.		3.2310morphinane alkaloid
strontium
Strontium: An element of the alkaline earth family of metals. It has the atomic symbol Sr, atomic number 38, and atomic weight 87.62.		4.811alkaline earth metal atom
bismuth
Bismuth: A metallic element that has the atomic symbol Bi, and atomic number 83. Its principal isotope is Bismuth 209.		5.0321metal atom;
pnictogen
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)		5.7473metalloid 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.		6.5951cyclopropanes;
morphinane-like compound;
organic heteropentacyclic compound		antidote to opioid poisoning;
central nervous system depressant;
environmental contaminant;
mu-opioid receptor antagonist;
xenobiotic
morphine-6-glucuronide
morphine-6-glucuronide: RN given refers to (5alpha,6alpha)-isomer		2.0410morphinane alkaloid
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.		3.8730morphinane alkaloidantitussive;
kappa-opioid receptor agonist;
mu-opioid receptor agonist;
opioid analgesic
cefodizime
cefodizime: RN given refers to (6R-(6alpha,7beta(Z)))-isomer. cefodizime : A cephalosporin compound having 5-(carboxymethyl)-4-methyl-1,3-thiazol-2-yl]sulfanyl}methyl and [2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups located at positions 3 and 7 respectively.		2.04101,3-thiazoles;
cephalosporin;
oxime O-ether		antibacterial drug;
EC 1.14.18.1 (tyrosinase) inhibitor
methylnaltrexone
methylnaltrexone: RN given refers to parent cpd(5alpha)-isomer		2.0410phenanthrenes
cefixime
[no description available]		4.0840cephalosporinantibacterial drug;
drug allergen
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.		4.2650dipeptideEC 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.		3.8730azabicycloalkane;
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.		4.0840dicarboxylic acid diamide;
N-(2-hydroxyethyl)piperazine;
piperazinecarboxamide		HIV protease inhibitor
sulfur
Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight [32.059; 32.076]. It is found in the amino acids cysteine and methionine.		4.811chalcogen;
nonmetal atom		macronutrient
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)		3.5920styrenes
enalapril maleate
enalapril maleate : The maleic acid salt of enalapril. It contains one molecule of maleic acid for each molecule of enalapril. Following oral administration, the ethyl ester group of enalapril is hydrolysed to afford the corresponding carboxylic acid, enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor. Enalapril is thus a prodrug for enalaprilat (which, unlike enalapril, is not absorbed by mouth), and its maleate is used 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.		2.0810maleate saltantihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
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
vinblastine sulfate
[no description available]		2.0510
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]		3.5920
n-methylscopolamine bromide
scopolamine methobromide : A quaternary ammonium salt resulting from the reaction of the amino group of scopolamine with methyl bromide.		3.2310
dimyristoylphosphatidylcholine
1,2-di-O-myristoyl-sn-glycero-3-phosphocholine : A 1,2-diacyl-sn-glycero-3-phosphocholine where the two phosphatidyl acyl groups are specified as tetradecanoyl (myristoyl).. dimyristoyl phosphatidylcholine : A phosphatidylcholine where the phosphatidyl acyl groups are specified as tetradecanoyl (myristoyl).		2.21101,2-diacyl-sn-glycero-3-phosphocholine;
phosphatidylcholine 28:0;
tetradecanoate ester		antigen;
mouse metabolite
fumarates
Fumarates: Compounds based on fumaric acid.. fumarate(2-) : A C4-dicarboxylate that is the E-isomer of but-2-enedioate(2-)		2.4110butenedioate;
C4-dicarboxylate		human metabolite;
metabolite;
Saccharomyces cerevisiae metabolite
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.		3.7130cysteiniumfundamental metabolite
silicon
Silicon: A trace element that constitutes about 27.6% of the earth's crust in the form of SILICON DIOXIDE. It does not occur free in nature. Silicon has the atomic symbol Si, atomic number 14, and atomic weight [28.084; 28.086].		2.9330carbon group element atom;
metalloid atom;
nonmetal atom
dextromethorphan hydrobromide
dextromethorphan hydrobromide : The hydrobromide and monohydrate of the antitussive drug dextromethorphan.		2.0510hydrate;
hydrobromide
indinavir sulfate
[no description available]		2.0510azaheterocycle sulfate salt
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.		4.0840dicarboxylic acid;
dipeptide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
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.		2.0510dicarboxylic acid monoester;
dipeptide;
ethyl ester;
imidazolidines;
N-acylurea;
secondary amino compound		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
demethoxycurcumin
demethoxycurcumin: corresponds to curcumin with one methoxy group replaced by hydrogen; isolated from rhizomes of Curcuma longa. demethoxycurcumin : A beta-diketone that is curcumin in which one of the methoxy groups is replaced by hydrogen. It is found in Curcuma zedoaria and Etlingera elatior.		7.8230beta-diketone;
diarylheptanoid;
enone;
polyphenol		anti-inflammatory agent;
antineoplastic agent;
metabolite
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.		2.0510monocarboxylic 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.		3.8630amidoxime;
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]		3.58203-(carbamoyloxymethyl)cephalosporin;
furans;
oxime O-ether		drug allergen
ceftriaxone
[no description available]		3.86301,2,4-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.		3.5820cephalosporin;
oxime O-ether		antibacterial drug
hr 810
cefpirome: structure in first source. cefpirome : A fourth-generation cephalosporin antibiotic having 6,7-dihydro-5H-cyclopenta[b]pyridinium-1-ylmethyl and [(2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups located at positions 3 and 7 respectively.		2.0410cephalosporin;
cyclopentapyridine
pafuramidine
pafuramidine: a prodrug of furamidine		3.2310
ceftazidime
[no description available]		4.0840cephalosporin;
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.		3.8730dicarboxylic 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
talaporfin
Talaporfin: effective tumor localizer that brings about the selective degradation of tumor tissue following light exposure; structure given in first source		7.110
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.		3.6120gamma-amino acidanticonvulsant;
calcium channel blocker
cefetamet
cefetamet: active against Neisseria gonorrhoeae; structure given in first source. cefetamet : A cephalosporin compound having methyl and [(2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side-groups; a cephalosporin antibiotic active against Neisseria gonorrhoeae.		2.0410cephalosporin
alvimopan anhydrous
alvimopan: mu opioid receptor antagonist; intended to treat constipation in patients taking opiates for pain		3.6120peptide
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
triolein
Triolein: (Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.. triolein : A triglyceride formed by esterification of the three hydroxy groups of glycerol with oleic acid. Triolein is one of the two components of Lorenzo's oil.		7.3110triglycerideCaenorhabditis elegans metabolite;
plant metabolite
guanabenz acetate
[no description available]		2.0510dichlorobenzenegeroprotector
guanabenz
Guanabenz: An alpha-2 selective adrenergic agonist used as an antihypertensive agent.		2.3110dichlorobenzene
famotidine
[no description available]		4.42601,3-thiazoles;
guanidines;
sulfonamide		anti-ulcer drug;
H2-receptor antagonist;
P450 inhibitor
fenoterol
fenoterol hydrobromide : The hydrobromide salt of fenoterol. A beta2-adrenergic agonist, it is used as a bronchodilator in the management of reversible airway obstruction.		2.0510hydrobromidebeta-adrenergic agonist;
bronchodilator agent;
sympathomimetic agent
carbocyanines
Carbocyanines: Compounds that contain three methine groups. They are frequently used as cationic dyes used for differential staining of biological materials.		3.0430cyanine dye;
organic iodide salt		fluorochrome
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.		3.86301,3-thiazoles;
cephalosporin;
oxime O-ether		antibacterial drug;
drug allergen
aztreonam
[no description available]		4.0840beta-lactam antibiotic allergen;
monobactam		antibacterial drug;
drug allergen;
EC 2.4.1.129 (peptidoglycan glycosyltransferase) inhibitor
apaziquone
apaziquone: structure given in first source; RN given refers to (E)-isomer		3.0910indoles
su 1498
SU 1498: structure in first source. SU1498 : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of (2E)-2-cyano-3-[4-hydroxy-3,5-di(propan-2-yl)phenyl]prop-2-enoic acid with the amino group of 3-phenylpropylamine.		2.1310enamide;
monocarboxylic acid amide;
nitrile;
phenols;
secondary carboxamide		vascular endothelial growth factor receptor antagonist
ammonium sulfate
Ammonium Sulfate: Sulfuric acid diammonium salt. It is used in CHEMICAL FRACTIONATION of proteins.. ammonium sulfate : An inorganic sulfate salt obtained by reaction of sulfuric acid with two equivalents of ammonia. A high-melting (decomposes above 280degreeC) white solid which is very soluble in water (70.6 g/100 g water at 0degreeC; 103.8 g/100 g water at 100degreeC), it is widely used as a fertilizer for alkaline soils.		2.0510ammonium salt;
inorganic sulfate salt		fertilizer
barium titanate(iv)
barium titanate(IV): RN given refers to parent cpd		2.2110
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
cci 15641
[no description available]		2.0810cephalosporin
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.		2.2110carboxamidine;
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
ginkgolide b
[no description available]		2.0410
selenium
Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.97. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of GLUTATHIONE PEROXIDASE.		2.8630chalcogen;
nonmetal atom		micronutrient
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.		8.7120alkaline earth metal atom
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.		6.2352azabicycloalkane;
delta-lactam;
organic heterotricyclic compound		antiemetic;
serotonergic antagonist
epoprostenol sodium
[no description available]		2.0510prostanoid
tenofovir disoproxil fumarate
tenofovir disoproxil fumarate : A fumarate salt prepared from equimolar amounts of tenofovir disoproxil and fumaric acid. It is used in combination therapy for the treatment of HIV infection.		2.0810fumarate saltantiviral drug;
HIV-1 reverse transcriptase inhibitor;
prodrug
cefatrizine
Cefatrizine: Orally active semisynthetic cephalosporin antibiotic with broad-spectrum activity.. cefatrizine : A cephalosporin compound having (1H-1,2,3-triazol-4-ylsulfanyl)methyl and [(2R)-2-amino-2-(4-hydroxyphenyl)]acetamido side-groups. An antibacterial drug first prepared in the 1970s, it has more recently been found to be an inhibitor of eukaryotic elongation factor-2 kinase (eEF2K), which is known to regulate apoptosis, autophagy and ER stress in many types of human cancers.		2.0410amino acid amide;
carboxylic acid;
cephalosporin;
phenols;
semisynthetic derivative;
triazoles		antibacterial drug;
EC 2.7.11.20 (elongation factor 2 kinase) inhibitor
diphenoxylate hydrochloride
diphenoxylate hydrochloride : The hydrochloride salt of diphenoxylate.		2.0510hydrochlorideantidiarrhoeal drug
eniporide
eniporide: inhibits NHE-1 isoform; structure in first source		2.0410
dexbrompheniramine maleate
dexbrompheniramine maleate : The maleic acid salt of the (pharmacologically active) (S)-(+)-enantiomer of brompheniramine. A histamine H1 receptor antagonist, it is used for the symptomatic relief of allergic conditions, including rhinitis and conjunctivitis.		2.0810brompheniramine maleateanti-allergic agent;
H1-receptor antagonist
ethoglucid
imidazole mustard: inhibitor of purine nucleoside synthesis; minor descriptor (77-84); on-line & Index Medicus search NITROGEN MUSTARD COMPOUNDS (77-84); RN given refers to parent cpd		1.9710
cilastatin
[no description available]		2.0410carboxamide;
L-cysteine derivative;
non-proteinogenic L-alpha-amino acid;
organic sulfide		EC 3.4.13.19 (membrane dipeptidase) inhibitor;
environmental contaminant;
protease inhibitor;
xenobiotic
13-cis-retinal
13-cis-retinal : A retinal in which the double bond alpha- to the aldehyde group has cis configuration, whilst the remaining acyclic double bonds have trans configuration.		3.4511retinalhuman metabolite
rifaximin
[no description available]		3.6120acetate ester;
cyclic ketal;
lactam;
macrocycle;
organic heterohexacyclic compound;
rifamycins;
semisynthetic derivative		antimicrobial agent;
gastrointestinal drug;
orphan drug
bafilomycin a1
bafilomycin A1: from Streptomyces griseus; structure given in first source. bafilomycin A1 : The most used of the bafilomycins, a family of toxic macrolide antibiotics derived from Streptomyces griseus.		2.7730cyclic hemiketal;
macrolide antibiotic;
oxanes		apoptosis inducer;
autophagy inhibitor;
bacterial metabolite;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor;
EC 3.6.3.14 (H(+)-transporting two-sector ATPase) inhibitor;
ferroptosis inhibitor;
fungicide;
potassium ionophore;
toxin
ergonovine maleate
ergometrine maleate : A maleate salt resulting form the reaction of equimolar amounts of maleic acid and ergometrine. It is used in the active management of the third stage of labour, and to prevent or treat postpartum of postabortal haemorrhage caused by uterine atony: by maintaining uterine contraction and tone, blood vessels in the uterine wall are compressed and blood flow reduced.		2.0510maleate saltdiagnostic agent;
oxytocic
rhizoxin
rhizoxin: from Rhizopus chinensis; causal agent of rice seedling blight; structure given in first source. rhizoxin : An macrolide antibiotic isolated from the pathogenic plant fungus Rhizopus microsporus. It also exhibits antitumour and antimitotic activity.		3.09101,3-oxazoles;
epoxide;
macrolide antibiotic		antimitotic;
antineoplastic agent;
metabolite
lumefantrine
Lumefantrine: A fluorene derivative that is used in combination with ARTEMETHER for the treatment of MALARIA (see ARTEMETHER-LUMEFANTRINE DRUG COMBINATION).. lumefantrine : A member of the class of fluorenes that is 9-(p-chlorobenzylidene)-9H-fluorene which is substitutec by chlorine at positions 2 and 7, and by a 2-(dibutylamino)-1-hydroxyethyl group at position 4. An antimalarial drug used in combination with artemether for the treatment of multi-drug resistant strains of falciparum malaria.		7.2510fluorenes;
monochlorobenzenes;
secondary alcohol;
tertiary amine		antimalarial
1,2-dioleoylphosphatidylserine
1,2-dioleoylphosphatidylserine: RN given in first source; RN given refers to (R-(Z,Z))-isomer; RN for cpd without isomeric designation not available 6/90. 1,2-dioleoyl-sn-glycero-3-phospho-L-serine : A 3-sn-phosphatidyl L-serine in which the phosphatidyl acyl groups are both oleoyl.. phosphatidylserine(18:1/18:1) : A 3-sn-phosphatidyl-L-serine in which the 1- and 2-acyl groups are octadecenoyl groups.		2.110phosphatidylserine(18:1/18:1)mouse metabolite
pregna-4,17-diene-3,16-dione
pregna-4,17-diene-3,16-dione: steroid from guggulu extract; RN & N1 from C1 Form index; RN given refers to cpd without isomeric designation; structure in first source; antagonist of farnesoid X receptor		2.6103-hydroxy steroidandrogen
everolimus
[no description available]		13.54309cyclic acetal;
cyclic ketone;
ether;
macrolide lactam;
primary alcohol;
secondary alcohol		anticoronaviral agent;
antineoplastic agent;
geroprotector;
immunosuppressive agent;
mTOR inhibitor
ixabepilone
[no description available]		4.59401,3-thiazoles;
beta-hydroxy ketone;
epoxide;
lactam;
macrocycle		antineoplastic agent;
microtubule-destabilising agent
ovatodiolide
ovatodiolide: from Anisomeles indica; structure in first source		7.2110
4,5-di-O-caffeoylquinic acid
[no description available]		2.110quinic acid
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.		2.4520penicillin allergen;
penicillin;
semisynthetic derivative		antibacterial drug
tanespimycin
CP 127374: analog of herbimycin A		2.74301,4-benzoquinones;
ansamycin;
carbamate ester;
organic heterobicyclic compound;
secondary amino compound		antineoplastic agent;
apoptosis inducer;
Hsp90 inhibitor
furanodienone
furanodienone: an antineoplastic agent that suppresses estrogen receptor alpha (ERalpha) signaling; structure in first source		7.2110germacrane sesquiterpenoid
verlukast
verlukast: LTD4 receptor antagonist		2.0410
cefpodoxime proxetil
cefpodoxime proxetil: structure given in first source; prodrug for cefpodoxime. cefpodoxime proxetil : The 1-[(isopropoxycarbonyl)oxy]ethyl (proxetil) ester prodrug of cefpodoxime. After swallowing, hydrolysis of the ester group occurs in the intestinal epithelium, to release active cefpodoxime in the bloodstream. It is used to treat acute otitis media, pharyngitis, and sinusitis.		2.0810carboxylic acid;
carboxylic ester;
cephalosporin		antibacterial drug;
prodrug
ceftizoxime
[no description available]		3.5820cephalosporinantibacterial drug
1-methyl-d-lysergic acid butanolamide
[no description available]		3.2310ergot alkaloid;
monocarboxylic acid amide		serotonergic antagonist;
sympatholytic agent;
vasoconstrictor agent
carumonam
carumonam: structure given in first source; RN given refers to (2S-(2alpha,3alpha(Z))-isomer. carumonam : An N-sulfonated monobactam antibiotic.		2.0410monobactamantibacterial drug
beta-escin
[no description available]		2.9630
fluphenazine
[no description available]		2.0810
s-nitroso-n-acetylpenicillamine
S-Nitroso-N-Acetylpenicillamine: A sulfur-containing alkyl thionitrite that is one of the NITRIC OXIDE DONORS.		2.2110nitroso compound;
nitrosothio compound		nitric oxide donor;
vasodilator agent
dantrolene sodium
dantrolene sodium (anhydrous) : The anhydrous sodium salt of dantrolene.		2.4620
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.		4.2650imidazolidine-2,4-dione;
nitrofuran antibiotic;
organonitrogen heterocyclic antibiotic;
organooxygen heterocyclic antibiotic		antibacterial drug;
antiinfective agent;
hepatotoxic agent
ca 074 methyl ester
[no description available]		2.110
nifurtimox
Nifurtimox: A nitrofuran thiazine that has been used against TRYPANOSOMIASIS.		2.0510nitrofuran antibiotic
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)		3.4470gadolinium coordination entityMRI contrast agent
ergoline
Ergolines: A series of structurally-related alkaloids that contain the ergoline backbone structure.. ergoline : An indole alkaloid whose structural skeleton is found in many naturally occurring and synthetic ergolines which are known to bind to neurotransmitter receptors, such as dopamine, noradrenaline and serotonin receptors and function as unselective agonists or antagonists at these receptors.		4.3730diamine;
ergoline alkaloid;
indole alkaloid fundamental parent;
indole alkaloid;
organic heterotetracyclic compound
sq-23377
Ionomycin: A divalent calcium ionophore that is widely used as a tool to investigate the role of intracellular calcium in cellular processes.. ionomycin : A very long-chain fatty acid that is docosa-10,16-dienoic acid which is substituted by methyl groups at positions 4, 6, 8, 12, 14, 18 and 20, by hydroxy groups at positions 11, 19 and 21, and by a (2',5-dimethyloctahydro-2,2'-bifuran-5-yl)ethanol group at position 21. An ionophore produced by Streptomyces conglobatus, it is used in research to raise the intracellular level of Ca(2+) and as a research tool to understand Ca(2+) transport across biological membranes.		2.1310cyclic ether;
enol;
polyunsaturated fatty acid;
very long-chain fatty acid		calcium ionophore;
metabolite
eritoran
eritoran : A lipid A derivative used for the treatment of severe sepsis.		2.0410lipid As
dantrolene
[no description available]		3.8630
fk 866
N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide: inhibits nicotinamide phosphoribosyltransferase; structure in first source		2.830benzamides;
N-acylpiperidine
roxithromycin
(E)-roxithromycin : A major geometrical isomer of roxithromycin.		2.4720roxithromycinenvironmental contaminant;
xenobiotic
cefdinir
[no description available]		3.6120cephalosporin;
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
bisoprolol, fumarate (1:1) salt
[no description available]		2.0810
artesunate
artesunic acid: RN given for (3R-(3alpha,5abeta,6beta,8abeta,9alpha,10alpha,12beta,(2aR*))-isomer; succinic ester of artemether		4.6140artemisinin derivative;
cyclic acetal;
dicarboxylic acid monoester;
hemisuccinate;
semisynthetic derivative;
sesquiterpenoid		antimalarial;
antineoplastic agent;
ferroptosis inducer
edatrexate
edatrexate: structure given in first source		3.0910glutamic acid derivative
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
ginsenoside rb2
[no description available]		2.11012beta-hydroxy steroid;
beta-D-glucoside;
disaccharide derivative;
ginsenoside;
tetracyclic triterpenoid		antiviral agent;
hypoglycemic agent;
plant metabolite
lanreotide
[no description available]		2.0510
etoposide phosphate
[no description available]		2.0810furonaphthodioxole
dexniguldipine
niguldipine: structure given in first source; clinical modulator of multidrug resistance		2.0410diarylmethane
ciclesonide
ciclesonide: nasal spray approved for seasonal and perennial allergic rhinitis		2.0810organic molecular entity
perfosfamide
[no description available]		210
napsagatran
napsagatran: structure given in first source		2.0410
temsirolimus
[no description available]		3.8730macrolide 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.		3.6120(trifluoromethyl)benzenes;
aza-steroid;
delta-lactam		antihyperplasia drug;
EC 1.3.1.22 [3-oxo-5alpha-steroid 4-dehydrogenase (NADP(+))] inhibitor
beta-elemene
beta-elemene: increases tumor cell immunogenicity by inducing, at least in part, elevated expression of heat shock protein 70 on tumor cell surface. beta-elemene : A sesquiterpene that consists of cyclohexane bearing methyl and vinyl substituents at position 1 as well as two isopropenyl substituents at positions 2 and 4.. (-)-beta-elemene : The (-)-enantiomer of beta-elemene that has (1S,2S,4R)-configuration.		3.0340beta-elemeneantineoplastic agent
tekturna
[no description available]		2.0810fumarate saltantihypertensive agent
pd 184352
2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide: inhibits MAP kinase kinase; structure in first source		2.0810aminobenzoic acid
lu 208075
ambrisentan: an ET(A) receptor antagonist and antihypertensive agent; studied for use in pulmonary arterial hypertension		3.5920diarylmethane
bms188797
[no description available]		2.0410
bibx 1382bs
BIBX 1382BS: an ErbB receptor kinase inhibitor; no further information available 4/2001		3.2310substituted aniline
vildagliptin
[no description available]		2.0810amino acid amide
fesoterodine
fesoterodine: a muscarinic antagonist for treatment of overactive bladder		3.2310diarylmethane
abt-510
NAc-Sar-Gly-Val-(d-allo-Ile)-Thr-Nva-Ile-Arg-ProNEt: has antiangiogenic and antineoplastic activity; structure in first source		3.4411
panobinostat
Panobinostat: An indole and hydroxamic acid derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used as an antineoplastic agent in combination with BORTEZOMIB and DEXAMETHASONE for the treatment of MULTIPLE MYELOMA.. panobinostat : A hydroxamic acid obtained by formal condensation of the carboxy group of (2E)-3-[4-({[2-(2-methylindol-3-yl)ethyl]amino}methyl)phenyl]prop-2-enoic acid with the amino group of hydroxylamine. A histone deacetylase inhibitor used (as its lactate salt) in combination with bortezomib and dexamethasone for the treatment of multiple myeloma.		5.4241cinnamamides;
hydroxamic acid;
methylindole;
secondary amino compound		angiogenesis modulating agent;
antineoplastic agent;
EC 3.5.1.98 (histone deacetylase) inhibitor
bromopyruvate
[no description available]		2.11102-oxo monocarboxylic acid anion
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
staurosporine
staurosporinium : Conjugate acid of staurosporine.		2.4420ammonium ion derivative
bufalin
bufalin: cardiotonic; powerful anesthetic & one of the active constituents of the Chinese drug ch'an su(senso); in Japan prepared from skin of Bufo bufo garfarizans; RN given refers to (3beta,5beta)-isomer. bufalin : A 14beta-hydroxy steroid that is bufan-20,22-dienolide having hydroxy substituents at the 5beta- and 14beta-positions. It has been isolated from the skin of the toad Bufo bufo.		2.211014beta-hydroxy steroid;
3beta-hydroxy steroid		animal metabolite;
anti-inflammatory agent;
antineoplastic agent;
cardiotonic drug
hypericum
Hypericum: Genus of perennial plants in the family CLUSIACEAE (sometimes classified as Hypericaceae). Herbal and homeopathic preparations are used for depression, neuralgias, and a variety of other conditions. Hypericum contains flavonoids; GLYCOSIDES; mucilage, TANNINS; volatile oils (OILS, ESSENTIAL), hypericin and hyperforin.. 6-formamidopenicillanic acid : A penicillanic acid having a (6R)-formamido substituent.		2.0510penicillanic acids
taxane
taxane: produced by Taxomyces andreanae		4.6630diterpene;
terpenoid fundamental parent
sl 327
SL 327: a MEK inhibitor. SL-327 : A nitrile that is acrylonitrile in which the hydrogen attached to the same carbon as the cyano group has been replaced by an o-(trifluoromethyl)phenyl group, while the remaining hydrogens of the ethenyl group have been replaced by amino and (4-aminophenyl)sulfanyl groups. The configuration of the double bond is not specified. It is an inhibitor of MEK1 and MEK2.		2.0610
sgd 301-76
[no description available]		2.0810conazole antifungal drug;
imidazole antifungal drug;
organic nitrate salt		antiinfective agent
fluvoxamine maleate
[no description available]		2.0810(trifluoromethyl)benzenes
formazans
Formazans: Colored azo compounds formed by the reduction of tetrazolium salts. Employing this reaction, oxidoreductase activity can be determined quantitatively in tissue sections by allowing the enzymes to act on their specific substrates in the presence of tetrazolium salts.		2.1110
thioacetazone
Thioacetazone: A thiosemicarbazone that is used in association with other antimycobacterial agents in the initial and continuation phases of antituberculosis regimens. Thiacetazone containing regimens are less effective than the short-course regimen recommended by the International Union Against Tuberculosis and are used in some developing countries to reduce drug costs. (From Martindale, The Extra Pharmacopoeia, 30th ed, p217). thiosemicarbazone : A hydrazone resulting from the formal condensation of an aldehyde or ketone with the non-thioacylated nitrogen of thiosemicarbazide or its substituted derivatives.		2.0810
azimilide
azimilide: structure given in first source; RN given refers to dihydrochloride		2.0410imidazolidine-2,4-dione
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.		3.6120benzimidazoles;
sulfoxide
gemifloxacin mesylate
gemifloxacin mesylate : The mesylate salt of gemifloxacin.		2.0810methanesulfonate saltantimicrobial agent;
topoisomerase IV inhibitor
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
iniparib
[no description available]		10.6732carbonyl compound;
organohalogen compound
2-hydroxy-9-cis-octadecenoic acid
2-hydroxy-9-cis-octadecenoic acid: designed to modify the lipid organization of the membrane. 2-hydroxyoleic acid : A 2-hydroxy fatty acid that is oleic acid which carries a hydroxy group at position 2. It is an orally bioavailable synthetic hydroxylated fatty acid which modulates the lipid content of cancer cell membranes and induces cell cycle arrest and apoptosis in several cancer cell lines.		2.07102-hydroxy fatty acid;
hydroxy monounsaturated fatty acid;
long-chain fatty acid		antihypertensive agent;
antineoplastic agent;
apoptosis inducer
eflucimibe
eflucimibe: a powerful and systemic acylcoenzyme A: cholesterol acyltransferase inhibitor		2.0510
givinostat
[no description available]		7.610carbamate ester
ginsenoside f1
ginsenoside F1: from ginseng. ginsenoside F1 : A ginsenoside found in Panax species that is dammarane which is substituted by hydroxy groups at the 3beta, 6alpha, 12beta and 20 pro-S positions, in which the hydroxy group at position 20 has been converted to the corresponding beta-D-glucopyranoside, and in which a double bond has been introduced at the 24-25 position.		2.11012beta-hydroxy steroid;
3beta-hydroxy-4,4-dimethylsteroid;
3beta-hydroxy steroid;
6alpha-hydroxy steroid;
beta-D-glucoside;
ginsenoside;
tetracyclic triterpenoid		apoptosis inhibitor;
plant metabolite
tomopenem
[no description available]		2.0410
bms345541
4(2'-aminoethyl)amino-1,8-dimethylimidazo(1,2-a)quinoxaline: structure in first source		2.0510quinoxaline derivative
6-(7-nitro-2,1,3-benzoxadiazol-4-ylthio)hexanol
6-(7-nitro-2,1,3-benzoxadiazol-4-ylthio)hexanol: a specific glutathione S-transferase inhibitor; structure in first source		7.0610
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.		8.511aromatic 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
pd 0325901
mirdametinib: has antineoplastic activity; appears to be a MEK inhibitor. PD 0325901 : A hydroxamic acid ester that is benzhydroxamic acid (N-hydroxybenzamide) in which the hydroxamic acid group has been converted to the corresponding 2,3-dihydroxypropyl ester and in which the benzene ring has been substituted at position 2 by a (2-fluoro-4-iodophenyl)amino group and at positions 3 and 4 by fluorines (the R enantiomer).		2.0510difluorobenzene;
hydroxamic acid ester;
monofluorobenzenes;
organoiodine compound;
propane-1,2-diols;
secondary amino compound		antineoplastic agent;
EC 2.7.12.2 (mitogen-activated protein kinase kinase) inhibitor
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.		3.9930oligopeptide
18f-fluoroethyl-l-tyrosine
(18F)fluoroethyltyrosine: structure in first source		4.1931
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
ml 00253764
2-(2-(2-(5-bromo-2-methoxyphenyl)ethyl)-3-fluorophenyl)-4,5-dihydro-1H-imidazole: structure in first source		2.1710
px-866
PX-866: inhibitor of phosphoinositide-3-kinase signaling with antitumor activity; structure in first source. PX-866 : An organic heterotetracyclic compound that is obtained from wortmanin via aminolysis of its furan ring by diallyl amine.		7.2110acetate ester;
delta-lactone;
organic heterotetracyclic compound;
tertiary amino compound		EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
bb-83698
BB-83698: peptide deformylase inhibitor		2.0410
gambogic acid
gambogic acid: RN given refers to (1R-(1alpha,1(Z),3abeta,5alpha,11beta,14aS*))-isomer		3.3110pyranoxanthonesmetabolite
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
abt-770
ABT-770: structure in first source		2.0510
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
rivaroxaban
Rivaroxaban: A morpholine and thiophene derivative that functions as a FACTOR XA INHIBITOR and is used in the treatment and prevention of DEEP-VEIN THROMBOSIS and PULMONARY EMBOLISM. It is also used for the prevention of STROKE and systemic embolization in patients with non-valvular ATRIAL FIBRILLATION, and for the prevention of atherothrombotic events in patients after an ACUTE CORONARY SYNDROME.. rivaroxaban : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-chlorothiophene-2-carboxylic acid with the amino group of 4-{4-[(5S)-5-(aminomethyl)-2-oxo-1,3-oxazolidin-3-yl]phenyl}morpholin-3-one. An anticoagulant used for prophylaxis of venous thromboembolism in patients with knee or hip replacement surgery.		2.0810aromatic amide;
lactam;
monocarboxylic acid amide;
morpholines;
organochlorine compound;
oxazolidinone;
thiophenes		anticoagulant;
EC 3.4.21.6 (coagulation factor Xa) inhibitor
zotarolimus
zotarolimus: synthetic analog of rapamycin; structure in first source		2.0410lactam;
macrolide
treosulfan
treosulfan: immunosuppressant; RN given refers to (S-(R*,R*))-isomer		7.1110methanesulfonate ester
molindone hydrochloride
[no description available]		2.0510indoles
pi103
PI103: pyridofuropyrimidine antineoplastic; a potent inhibitor of class I phosphatidylinositide 3-kinases (PI3K); structure in first soruce		2.5320aromatic amine;
morpholines;
organic heterotricyclic compound;
phenols;
tertiary amino compound		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
mTOR inhibitor
dapagliflozin
[no description available]		2.610aromatic ether;
C-glycosyl compound;
monochlorobenzenes		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
9-n-(1-propyl)erythromyclamine
9-N-(1-propyl)erythromyclamine: structure given in first source		2.0510
mart-1 antigen
MART-1 Antigen: A melanosome-specific protein that plays a role in the expression, stability, trafficking, and processing of GP100 MELANOMA ANTIGEN, which is critical to the formation of Stage II MELANOSOMES. The protein is used as an antigen marker for MELANOMA cells.		2.2510
ginsenoside rb1
[no description available]		2.110ginsenoside;
glycoside;
tetracyclic triterpenoid		anti-inflammatory drug;
anti-obesity agent;
apoptosis inhibitor;
neuroprotective agent;
plant metabolite;
radical scavenger
gentamicin sulfate
[no description available]		2.4520
bn 52020
[no description available]		2.0410
hki 272
[no description available]		2.0810nitrile;
quinolines		antineoplastic agent;
tyrosine kinase inhibitor
adh-1 pepide
ADH-1 pepide: a cyclic pentapeptide and N-cadherin antagonist targeting cancer vascularization		2.1110
ginsenoside f2
ginsenoside F2: isolated from the leaves of Panax ginseng. ginsenoside F2 : A ginsenoside found in Panax species that is dammarane which is substituted by hydroxy groups at the 3beta, 12beta and 20 pro-S positions, in which the hydroxy groups at positions 3 and 20 have been converted to the corresponding beta-D-glucopyranosides, and in which a double bond has been introduced at the 24-25 position.		2.11012beta-hydroxy steroid;
beta-D-glucoside;
ginsenoside;
tetracyclic triterpenoid		antineoplastic agent;
apoptosis inducer;
plant metabolite
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.		7.8330ginsenoside;
glycoside;
tetracyclic triterpenoid		angiogenesis modulating agent;
antineoplastic agent;
apoptosis inducer;
plant metabolite
motexafin gadolinium
[no description available]		7.9142
perampanel
perampanel : A member of the class of bipyridines that is 2,3'-bipyridin-6'-one substituted at positions 1' and 5' by phenyl and 2-cyanophenyl groups respectively. Used as an adjunctive therapy for the treatment of partial-onset seizures in patients with epilepsy.		2.930bipyridines;
nitrile;
pyridone		AMPA receptor antagonist;
anticonvulsant
tofacitinib
tofacitinib : A pyrrolopyrimidine that is pyrrolo[2,3-d]pyrimidine substituted at position 4 by an N-methyl,N-(1-cyanoacetyl-4-methylpiperidin-3-yl)amino moiety. Used as its citrate salt to treat moderately to severely active rheumatoid arthritis.		2.0810N-acylpiperidine;
nitrile;
pyrrolopyrimidine;
tertiary amino compound		antirheumatic drug;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
rucaparib
AG14447: Poly(ADP-ribose) polymerase inhibitor; structure in first source		12122azepinoindole;
caprolactams;
organofluorine compound;
secondary amino compound		antineoplastic agent;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
cediranib
[no description available]		8.2673aromatic ether
6h-thieno[3,2-f][1,2,4]triazolo[4,3-a][1,4]diazepine-6-acetamide, 4-(4-chlorophenyl)-n-(4-hydroxyphenyl)-2,3,9-trimethyl-, (6s)-
[no description available]		2.1310organonitrogen heterocyclic compound;
organosulfur heterocyclic compound
pasireotide
pasireotide : A six-membered homodetic cyclic peptide composed from L-phenylglycyl, D-tryptophyl, L-lysyl, O-benzyl-L-tyrosyl, L-phenylalanyl and modified L-hydroxyproline residues joined in sequence. A somatostatin analogue with pharmacologic properties mimicking those of the natural hormone somatostatin; used (as its diaspartate salt) for treatment of Cushing's disease.		6.6170homodetic cyclic peptide;
peptide hormone		antineoplastic agent
3,4-dihydro-5-(4-(1-piperidinyl)butoxy)-1(2h)-isoquinolinone
[no description available]		2.0510
cp 31398
CP 31398: structure in first source		2.0610
aluminum oxide
Aluminum Oxide: An oxide of aluminum, occurring in nature as various minerals such as bauxite, corundum, etc. It is used as an adsorbent, desiccating agent, and catalyst, and in the manufacture of dental cements and refractories.		4.811
azacosterol
Azacosterol: Diaza derivative of cholesterol which acts as a hypocholesteremic agent by blocking delta-24-reductase, which causes the accumulation of desmosterol.		2.0510
opuntiol
opuntiol: structure in first source		2.3110
hispolon
hispolon: structure given in first source		3.4110
ly-2157299
LY-2157299: an orally active transforming growth factor beta receptor (TGF-beraR) kinase inhibitor. LY-2157299 : A pyrrolopyrazole that is 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazole which is substituted at positions 2 and 3 by 6-methylpyridin-2-yl and 6-(aminocarbonyl)quinolin-4-yl groups, respectively. A Transforming growth factor-betaRI (TGF-betaRI) kinase inhibitor, it blocks TGF-beta-mediated tumor growth in glioblastoma.		4.9921aromatic amide;
methylpyridines;
monocarboxylic acid amide;
pyrrolopyrazole;
quinolines		antineoplastic agent;
TGFbeta receptor antagonist
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.		10.3860aminopyrimidine;
indazoles;
sulfonamide		angiogenesis modulating agent;
antineoplastic agent;
tyrosine kinase inhibitor;
vascular endothelial growth factor receptor antagonist
azd 6244
AZD 6244: a MEK inhibitor		6.0352benzimidazoles;
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
bibw 2992
[no description available]		6.4472aromatic ether;
enamide;
furans;
monochlorobenzenes;
organofluorine compound;
quinazolines;
secondary carboxamide;
tertiary amino compound		antineoplastic agent;
tyrosine kinase inhibitor
artenimol
artenimol: derivative of antimalarial drug artemisinin (quinghaosu)		2.4820
erteberel
erteberel: an estrogen receptor beta agonist		2.1310
trans-sodium crocetinate
trans-sodium crocetinate: vitamin A-analog that increases diffusivity of oxygen in aqueous solutions, including plasma		7.0510
binimetinib
binimetinib : A member of the class of benzimidazoles that is 1-methyl-1H-benzimidazole which is substituted at positions 4, 5, and 6 by fluorine, (4-bromo-2-fluorophenyl)nitrilo, and N-(2-hydroxyethoxy)aminocarbonyl groups, respectively. It is a MEK1 and MEK2 inhibitor (IC50= 12 nM). Approved by the FDA for the treatment of patients with unresectable or metastatic melanoma with a BRAF V600E or V600K mutation in combination with encorafenib.		8.7320benzimidazoles;
bromobenzenes;
hydroxamic acid ester;
monofluorobenzenes;
secondary amino compound		antineoplastic agent;
apoptosis inducer;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
az10606120
AZ10606120: a P2X7 receptor antagonist		2.610
ngr peptide
[no description available]		2.2110
2'-benzoyloxycinnamaldehyde
2'-benzoyloxycinnamaldehyde: induces apoptosis in cancer cells; possible antineoplastic agent		2.2110
amg 009
AMG 009: an anti-inflammatory agent; structure in first source		2.0810
oxadiazoles
Oxadiazoles: Compounds containing five-membered heteroaromatic rings containing two carbons, two nitrogens, and one oxygen atom which exist in various regioisomeric forms.		3.3660
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.		2.0510acetate ester;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
semisynthetic derivative;
vinca alkaloid		antineoplastic agent
cefotaxime sodium
[no description available]		2.0810organic sodium salt
ly 341495
LY 341495: structure in first source		2.5520
baci-im
[no description available]		3.8630homodetic cyclic peptide;
polypeptide;
zwitterion		antibacterial agent;
antimicrobial agent
ucn 1028 c
calphostin C: structure given in first source; isolated from Cladosporium cladosporioides		1.9810
ribose
ribopyranose : The pyranose form of ribose.		2.6920D-ribose;
ribopyranose
prosapogenin a
[no description available]		2.3110steroid saponin
aplysin
aplysin: Antineoplastic Agents, Alkylating, derived from Laurencia tristicha; structure in first source		7.110
regorafenib
[no description available]		8.1130(trifluoromethyl)benzenes;
aromatic ether;
monochlorobenzenes;
monofluorobenzenes;
phenylureas;
pyridinecarboxamide		antineoplastic agent;
hepatotoxic agent;
tyrosine kinase inhibitor
acetyl-11-ketoboswellic acid
acetyl-11-ketoboswellic acid: a 5-lipoxygenase inhibitor; structure given in first source		3.5911triterpenoid
calpain inhibitor iii
calpain inhibitor III: potential anticataract drug		2.2110
wp1066
[no description available]		2.0610
erastin
erastin: an antineoplastic agent; structure in first source. erastin : A member of the class of quinazolines that is quinazolin-4(3H)-one in which the hydrogens at positions 2 and 3 are replaced by 1-{4-[(4-chlorophenoxy)acetyl]piperazin-1-yl}ethyl and 2-ethoxyphenyl groups, respectively. It is an inhibitor of voltage-dependent anion-selective channels (VDAC2 and VDAC3) and a potent ferroptosis inducer.		7.5220aromatic ether;
diether;
monochlorobenzenes;
N-acylpiperazine;
N-alkylpiperazine;
quinazolines;
tertiary carboxamide		antineoplastic agent;
ferroptosis inducer;
voltage-dependent anion channel inhibitor
abt-737
[no description available]		7.7930aromatic amine;
aryl sulfide;
biphenyls;
C-nitro compound;
monochlorobenzenes;
N-arylpiperazine;
N-sulfonylcarboxamide;
secondary amino compound;
tertiary amino compound		anti-allergic agent;
anti-inflammatory agent;
antineoplastic agent;
apoptosis inducer;
B-cell lymphoma 2 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
fg-4592
roxadustat: structure in first source. roxadustat : An N-acylglycine resulting from the formal condensation of the amino group of glycine with the carboxy group of 4-hydroxy-1-methyl-7-phenoxyisoquinoline-3-carboxylic acid. It is an inhibitor of hypoxia inducible factor prolyl hydroxylase (HIF-PH).		2.4110aromatic ether;
isoquinolines;
N-acylglycine		EC 1.14.11.2 (procollagen-proline dioxygenase) inhibitor;
EC 1.14.11.29 (hypoxia-inducible factor-proline dioxygenase) inhibitor
mp470
[no description available]		2.2110N-arylpiperazine
zk-219477
sagopilone: has antineoplastic activity		2.0510macrolide
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
Dihydrotanshinone I
dihydrotanshinone I: extracted from Radix Salviae		2.1510abietane diterpenoidanticoronaviral agent
nutlin-3a
nutlin 3: an MDM2 antagonist; structure in first source		3.0240stilbenoid
abt 869
[no description available]		2.0310aromatic amine;
indazoles;
phenylureas		angiogenesis inhibitor;
antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
arq 197
[no description available]		2.3110indoles
lbw242
LBW242: proapoptotic IAP inhibitor; low MW Smac (Second mitochondria-derived activator of caspases) mimetic; structure in first source		2.0610
3-bromo-2-oxopropionate-1-propyl ester
3-bromo-2-oxopropionate-1-propyl ester: glycolysis inhibitor		2.0810
2,5-dimethylcelecoxib
2,5-dimethylcelecoxib: non-COX-2 inhibitory structural analog of celecoxib		2.5420
carfilzomib
[no description available]		4.811epoxide;
morpholines;
tetrapeptide		antineoplastic agent;
proteasome inhibitor
tpi-287
TPI-287: a microtubule-stabilizing agent; structure in first source		4.4822
cytidine diphosphate choline
[no description available]		2.0510nucleotide-(amino alcohol)s;
phosphocholines		human metabolite;
mouse metabolite;
neuroprotective agent;
psychotropic drug;
Saccharomyces cerevisiae metabolite
sitagliptin phosphate
Sitagliptin Phosphate: A pyrazine-derived DIPEPTIDYL-PEPTIDASE IV INHIBITOR and HYPOGLYCEMIC AGENT that increases the levels of the INCRETIN hormones GLUCAGON-LIKE PEPTIDE-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). It is used in the treatment of TYPE 2 DIABETES.		2.610
milnacipran
[no description available]		3.2310acetamides
crizotinib
Crizotinib: A piperidine and aminopyridine derivative that acts as an inhibitor of RECEPTOR PROTEIN-TYROSINE KINASES, including ANAPLASTIC LYMPHOMA KINASE (ALK) and HEPATOCYTE GROWTH FACTOR RECEPTOR (HGFR; c-Met). It is used in the treatment of NON-SMALL CELL LUNG CANCER.. crizotinib : A 3-[1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(piperidin-4-yl)pyrazol-4-yl]pyridin-2-amine that has R configuration at the chiral centre. The active enantiomer, it acts as a kinase inhibitor and is used for the treatment of patients with locally advanced or metastatic non-small cell lung cancer (NSCLC)		2.21103-[1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(piperidin-4-yl)pyrazol-4-yl]pyridin-2-amineantineoplastic agent;
biomarker;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
vindesine
[no description available]		2.4520
cgp 57380
CGP 57380: inhibits the mitogen-activated protein kinase-interacting kinase Mnk1		2.1310pyrazolopyrimidine
zstk474
ZSTK-474 : A triamino-1,3,5-triazine that is 1,3,5-triazine in which two of the hydrogens have been replaced by morpholin-4-yl groups while the third hydrogen has been replaced by a 2-(difluoromethyl)benzimidazol-1-yl group. It is an inhibitor of phosphatidylinositol 3-kinase.		7.4110benzimidazoles;
morpholines;
organofluorine compound;
triamino-1,3,5-triazine		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
ly2109761
[no description available]		7.0610
ginsenoside rd
ginsenoside Rd: RN refers to (3beta,12beta)-isomer. ginsenoside Rd : A ginsenoside found in Panax ginseng and Panax japonicus var. major that is (20S)-ginsenoside Rg3 in which the hydroxy group at position 20 has been converted to its beta-D-glucopyranoside.		2.110beta-D-glucoside;
ginsenoside;
tetracyclic triterpenoid		anti-inflammatory drug;
apoptosis inducer;
immunosuppressive agent;
neuroprotective agent;
plant metabolite;
vulnerary
trametinib
[no description available]		6.2951acetamides;
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
gpi 15427
[no description available]		2.4320
losartan potassium
Erythropoietin: Glycoprotein hormone, secreted chiefly by the KIDNEY in the adult and the LIVER in the FETUS, that acts on erythroid stem cells of the BONE MARROW to stimulate proliferation and differentiation.		2.4620
hypoglycin a
hypoglycin: RN given refers to cpd without isomeric designation. hypoglycin A : A diastereoisomeric mixture of (2S,4R)- and (2S,4S)- hypoglycin A, found in the edible part of the fruit of the Ackee, Blighia sapida (where the 2S,4R diastereoisomer is more dominant (17% d.e.) than its 2S,4S counterpart) as well as in the sycamore maple tree (Acer pseudoplatanus).		2.0510L-alpha-amino acid
sesone
7-deazaxanthine: structure in first source		2.2110
empagliflozin
[no description available]		4.811aromatic ether;
C-glycosyl compound;
monochlorobenzenes;
tetrahydrofuryl ether		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
at 13387
(2,4-dihydroxy-5-isopropylphenyl)-(5-(4-methylpiperazin-1-ylmethyl)-1,3-dihydroisoindol-2-yl)methanone: structure in first source. onalespib : A member of the class of isoindoles that is isoindole in which the amino group has been acylated by a 2,4-dihydroxy-5-isopropylbenzoyl group and in which position 5 of the isoidole moiety has been substituted by a (4-methylpiperazin-1-yl)methyl group. A second-generation Hsp90 inhibitor.		2.6320benzamides;
isoindoles;
N-alkylpiperazine;
resorcinols;
tertiary carboxamide		antineoplastic agent;
Hsp90 inhibitor
veliparib
[no description available]		12.284817benzimidazolesEC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
sepharose
agarose : A linear polysaccharide made up from alternating D-galactose and 3,6-anhydro-alpha-L-galactopyranose residues joined by alpha-(1->3)- and beta-(1->4)-linkages.		2.1710
indocyanine green
Indocyanine Green: A tricarbocyanine dye that is used diagnostically in liver function tests and to determine blood volume and cardiac output.		3.14401,1-diunsubstituted alkanesulfonate;
benzoindole;
cyanine dye
scopolamine hydrobromide
[no description available]		3.5820
dactolisib
dactolisib: antineoplastic agent that inhibits both phosphatidylinositol 3-kinase and mTOR. dactolisib : An imidazoquinoline that is 3-methyl-2-oxo-2,3-dihydro-1H-imidazo[4,5-c]quinoline substituted at position 1 by a 4-(1-cyanoisopropyl)phenyl group and at position 8 by a quinolin-3-yl group. A dual PI3K/mTOR inhibitor used in cancer treatment.		3.0240imidazoquinoline;
nitrile;
quinolines;
ring assembly;
ureas		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
mTOR inhibitor
pituitrin
Pituitrin: A substance or extract from the neurohypophysis (PITUITARY GLAND, POSTERIOR).		2.3110
n4-(2,2-dimethyl-3-oxo-4h-pyrid(1,4)oxazin-6-yl)-5-fluoro-n2-(3,4,5-trimethoxyphenyl)-2,4-pyrimidinediamine
N4-(2,2-dimethyl-3-oxo-4H-pyrid(1,4)oxazin-6-yl)-5-fluoro-N2-(3,4,5-trimethoxyphenyl)-2,4-pyrimidinediamine: a spleen tyrosine kinase (Syk) inhibitor; structure in first source		2.2110
pf 03491390
[no description available]		2.0510
ginsenoside rc
[no description available]		2.11012beta-hydroxy steroid;
beta-D-glucoside;
disaccharide derivative;
ginsenoside;
tetracyclic triterpenoid		hypoglycemic agent;
plant metabolite
ginsenoside rb3
[no description available]		2.11012beta-hydroxy steroid;
beta-D-glucoside;
disaccharide derivative;
ginsenoside;
tetracyclic triterpenoid		antidepressant;
antioxidant;
cardioprotective agent;
neuroprotective agent;
NMDA receptor antagonist;
plant metabolite
mefloquine
Mefloquine: A phospholipid-interacting antimalarial drug (ANTIMALARIALS). It is very effective against PLASMODIUM FALCIPARUM with very few side effects.. mefloquine : A racemate composed of (+)-(11R,2'S)- and (-)-(11S,2'R)-enantiomers of mefloquine. An antimalarial agent which acts as a blood schizonticide; its mechanism of action is unknown.		9.2931
SYC-435
SYC-435 : A cyclic hydroxamic acid that is 1-hydroxypyridin-2(1H)-one in which the hydrogens at positions 4 and 6 are substituted by methyl and benzyl groups, respectively. It is a potent inhibitor of mutant isocitrate dehydrogenase 1 (Ki values of 190 nM against R132H mutant and 120 nM against R132C mutant).		2.110benzenes;
cyclic hydroxamic acid;
pyridone		antineoplastic agent;
EC 1.1.1.42 (isocitrate dehydrogenase) inhibitor
curcumol
[no description available]		7.8220sesquiterpenoid
rabeprazole sodium
[no description available]		2.0810organic sodium salt
dehydroeburicoic acid
dehydroeburicoic acid: structure in first source		2.2510bile acid
carbon-11 methionine
carbon-11 methionine: RN refers to L-methionine labeled with carbon-11		4.9342
nad
NAD(1-) : An anionic form of nicotinamide adenine dinucleotide arising from deprotonation of the two OH groups of the diphosphate moiety.		9.67100organophosphate oxoanioncofactor;
human metabolite;
hydrogen acceptor;
Saccharomyces cerevisiae metabolite
dianhydrogalactitol
Dianhydrogalactitol: One of the cytotoxic dihalohexitols that alkylates and cross-links DNA via an epoxide group during all phases of the cell cycle, resulting in a disruption of DNA function and cell cycle arrest. It has antineoplastic activity and also causes bone marrow toxicity.		7.3110
rrx-001
RRx-001: has antineoplastic activity; structure in first source		7.3110
mdv 3100
[no description available]		2.4110(trifluoromethyl)benzenes;
benzamides;
imidazolidinone;
monofluorobenzenes;
nitrile;
thiocarbonyl compound		androgen antagonist;
antineoplastic agent
macitentan
[no description available]		7.1110aromatic ether;
organobromine compound;
pyrimidines;
ring assembly;
sulfamides		antihypertensive agent;
endothelin receptor antagonist;
orphan drug
amodiaquine hydrochloride
[no description available]		2.4620
clindamycin hydrochloride
[no description available]		2.0510S-glycosyl compound
cytochrome c-t
Cytochromes c: Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.		3.7290
bisaramil
[no description available]		2.0410
melitten
Melitten: Basic polypeptide from the venom of the honey bee (Apis mellifera). It contains 26 amino acids, has cytolytic properties, causes contracture of muscle, releases histamine, and disrupts surface tension, probably due to lysis of cell and mitochondrial membranes.		2.2110
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.		3.6120polypeptideanticoagulant;
EC 3.4.21.5 (thrombin) inhibitor
somatostatin
[no description available]		2.0810heterodetic cyclic peptide;
peptide hormone
teicoplanin
teicoplanin A2-1 : A teicoplanin A2 that has (4Z)-dec-4-enoyl as the variable N-acyl group.		2.0410
tachyplesin peptide, tachypleus tridentatus
tachyplesin peptide, Tachypleus tridentatus: isolated from the hemocytes of the horseshoe crab (Tachypleus tridentatus); cationic peptide; 17 amino acid residues given in first source		2.2110
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
hes1 protein, human
HES1 protein, human: RefSeq NM_005524		2.5820
humanin
humanin: suppresses neuronal cell death induced by the Swedish mutant of amyloid precursor protein; suppresses neuronal cell death induced by three different types of FAD genes and amyloid beta; amino acid sequence in first source		7.2110
protegrin-1
protegrin-1: GenBank X84094		2.4110
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.		2.1310
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]		3.1550
ly-146032
[no description available]		3.8730heterodetic cyclic peptide;
lipopeptide antibiotic;
lipopeptide;
macrocycle;
macrolide		antibacterial drug;
bacterial metabolite;
calcium-dependent antibiotics
dalbavancin
[no description available]		2.0410carbohydrate acid derivative;
glycopeptide;
monosaccharide derivative;
semisynthetic derivative		antibacterial drug;
antimicrobial agent
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
warfarin sodium
warfarin sodium : A racemate comprising equal amounts of (R)- and (S)-warfarin sodium. Extensively used as both an anticoagulant drug and as a pesticide against rats and mice.		2.0810
cellulose
DEAE-Cellulose: Cellulose derivative used in chromatography, as ion-exchange material, and for various industrial applications.		4.811glycoside
quinine sulfate
[no description available]		2.0510hydrate
gdc-0973
cobimetinib: has antineoplastic activity; structure in first source. cobimetinib : A member of the class of N-acylazetidines obtained by selective formal condensation of the carboxy group of 3,4-difluoro-2-(2-fluoro-4-iodoanilino)benzoic acid with the secondary amino group from the azetidine ring of 3-[(2S)-piperidin-2-yl]azetidin-3-ol. An inhibitor of mitogen-activated protein kinase that is used (as its fumarate salt) in combination with vemurafenib for the treatment of patients with unresectable or metastatic melanoma.		3.3110aromatic amine;
difluorobenzene;
N-acylazetidine;
organoiodine compound;
piperidines;
secondary amino compound;
tertiary alcohol		antineoplastic agent;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
buparlisib
NVP-BKM120: a pan class I PI3 kinase inhibitor with antineoplastic activity; structure in first source		9.5511aminopyridine;
aminopyrimidine;
morpholines;
organofluorine compound		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
azd 1480
[no description available]		2.5520
pha 848125
N,1,4,4-tetramethyl-8-((4-(4-methylpiperazin-1-yl)phenyl)amino)-4,5-dihydro-1H-pyrazolo(4,3-h)quinazoline-3-carboxamide: a cyclin dependent kinase inhibitor		2.4720
pevonedistat
pevonedistat: a potent and selective inhibitor of NAE (NEDD8-activating enzyme). pevonedistat : A pyrrolopyrimidine that is 7H-pyrrolo[2,3-d]pyrimidine which is substituted by a (1S)-2,3-dihydro-1H-inden-1-ylnitrilo group at position 4 and by a (1S,3S,4S)-3-hydroxy-4-[(sulfamoyloxy)methyl]cyclopentyl group at position 7. It is a potent and selective NEDD8-activating enzyme inhibitor with an IC50 of 4.7 nM, and currently under clinical investigation for the treatment of acute myeloid leukemia (AML) and myelodysplastic syndromes.		2.610cyclopentanols;
indanes;
pyrrolopyrimidine;
secondary amino compound;
sulfamidate		antineoplastic agent;
apoptosis inducer
ku 0063794
Ku 0063794: an mTOR inhibitor; structure in first source		2.110benzyl alcohols;
monomethoxybenzene;
morpholines;
pyridopyrimidine;
tertiary amino compound		antineoplastic agent;
mTOR inhibitor
14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene
14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene: has antineoplastic activity; also inhibits Fms-like tyrosine kinase-3; structure in first source		2.1710
dihydroceramide
dihydroceramide: lacks the 4-5 trans double bond of the sphingosine moiety of ceramides; structure in first source. N-acylsphinganine : A ceramide consisting of sphinganine in which one of the amino hydrogens is substituted by a fatty acyl group.. dihydroceramide : An N-acylsphingoid obtained by formal condensation of the carboxy group of any fatty acid with the amino group of any dihydrosphingoid base.		7.110
pravastatin sodium
pravastatin sodium : An organic sodium salt that is the sodium salt of pravastatin. A reversible inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA), it 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.		2.0810organic sodium salt;
statin (semi-synthetic)		anticholesteremic drug
alendronate sodium
[no description available]		2.0810
sphingosine kinase
[no description available]		3.3760
ubiquinone
Ubiquinone: A lipid-soluble benzoquinone which is involved in ELECTRON TRANSPORT in mitochondrial preparations. The compound occurs in the majority of aerobic organisms, from bacteria to higher plants and animals.		2.5920
gdc 0941
pictrelisib : A sulfonamide composed of indazole, morpholine, and methylsulfonyl-substituted piperazine rings bound to a thienopyrimidine ring.		3.2510indazoles;
morpholines;
piperazines;
sulfonamide;
thienopyrimidine		EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
sl 80.0750
[no description available]		2.0810
calpain
Calpain: Cysteine proteinase found in many tissues. Hydrolyzes a variety of endogenous proteins including NEUROPEPTIDES; CYTOSKELETAL PROTEINS; proteins from SMOOTH MUSCLE; CARDIAC MUSCLE; liver; platelets; and erythrocytes. Two subclasses having high and low calcium sensitivity are known. Removes Z-discs and M-lines from myofibrils. Activates phosphorylase kinase and cyclic nucleotide-independent protein kinase. This enzyme was formerly listed as EC 3.4.22.4.		8.3260
cefotiam hydrochloride
[no description available]		2.0510
ginsenoside rg2
ginsenoside Rg2: structure in first source; RN given refers to (6-deoxy-alpha-L-mannopyranosyl)-isomer. ginsenoside Rg2 : A ginsenoside found in Panax species that is dammarane which is substituted by hydroxy groups at the 3beta, 6alpha, 12beta and 20 pro-S positions, in which the hydroxy group at position 6 has been converted to the corresponding alpha-L-rhamnopyranosyl-(1->2)-beta-D-glucopyranoside, and in which a double bond has been introduced at the 24-25 position.		2.11012beta-hydroxy steroid;
20-hydroxy steroid;
3beta-hydroxy-4,4-dimethylsteroid;
3beta-hydroxy steroid;
beta-D-glucoside;
disaccharide derivative;
ginsenoside;
tetracyclic triterpenoid		anticoagulant;
cardioprotective agent;
plant metabolite
notoginsenoside r2
notoginsenoside R2: from the roots of commercial ginseng		2.110triterpenoid saponin
chitosan
[no description available]		4.03120
technetium tc 99m sestamibi
Technetium Tc 99m Sestamibi: A technetium imaging agent used to reveal blood-starved cardiac tissue during a heart attack.		2.0210
cep 8983
CEP 8983: inhibits PAR polymerase-1 and PAR polymerase-2; structure in first source		3.8521
mesna
Mesna: A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from ANTINEOPLASTIC AGENTS, such as IFOSFAMIDE or CYCLOPHOSPHAMIDE.		3.8730organosulfonic acid
potassium aminobenzoate
[no description available]		2.0510
bucladesine
Bucladesine: A cyclic nucleotide derivative that mimics the action of endogenous CYCLIC AMP and is capable of permeating the cell membrane. It has vasodilator properties and is used as a cardiac stimulant. (From Merck Index, 11th ed). bucladesine : A 3',5'-cyclic purine nucleotide that is the 2'-butanoate ester and 6-N-butanoyl derivative of 3',5'-cyclic AMP.		2.07103',5'-cyclic purine nucleotide
ampicillin sodium
[no description available]		2.0510organic sodium salt
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)
clavulanate potassium
potassium clavulanate : A potassium salt having clavulanate as the counterion. It acts as a suicide inhibitor of bacterial beta-lactamase enzymes and has only weak anitbiotic activity when administered alone. However it can be used in combination with amoxicillin trihydrate (under the trade name Augmentin) for treatment of a variety of bacterial infections, where it prevents antibiotic inactivation by microbial lactamases.		2.0810potassium saltantibacterial drug;
antimicrobial agent;
EC 3.5.2.6 (beta-lactamase) inhibitor
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
piperacillin sodium
[no description available]		2.0810organic sodium salt
monensin
[no description available]		2.0510
sodium iothalamate
[no description available]		3.2310
methicillin sodium
[no description available]		2.0510organic sodium salt
nafcillin sodium
[no description available]		2.0510organic sodium salt
oxacillin sodium
[no description available]		2.4720organic sodium salt
penicillin g sodium
[no description available]		2.0510organic sodium salt
cefamandole nafate
cefamandole sodium : An organic sodium salt that is the sodium salt of cefamandole.		2.0510organic sodium saltantibacterial drug
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
cephapirin sodium
cephapirin sodium : The sodium salt of cephapirin. A first-generation cephalosporin antibiotic, it is effective against gram-negative and gram-positive organisms. Being more resistant to beta-lactamases than penicillins, it is effective agains most staphylococci, though not methicillin-resistant staphylococci.		2.0510cephalosporin;
organic sodium salt		antibacterial drug
sodium cephalothin
[no description available]		2.0510organic sodium salt
cefazolin sodium
cefazolin sodium : A cephalosporin organic sodium salt having [(5-methyl-1,3,4-thiadiazol-2-yl)sulfanyl]methyl and (1H-tetrazol-1-ylacetyl)amino side-groups.		2.0810organic sodium salt
dicloxacillin sodium
[no description available]		2.0510hydrate
azlocillin sodium
[no description available]		2.4720organic sodium salt
chiniofon
Hydroxyquinolines: The 8-hydroxy derivatives inhibit various enzymes and their halogenated derivatives, though neurotoxic, are used as topical anti-infective agents, among other uses.		2.1310
arginine
Teniposide: A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle.. teniposide : A furonaphthodioxole that is a synthetic derivative of podophyllotoxin with anti-tumour activity; causes single- and double-stranded breaks in DNA and DNA-protein cross-links and prevents repair by topoisomerase II binding.		5.6551
olaparib
[no description available]		9.21314cyclopropanes;
monofluorobenzenes;
N-acylpiperazine;
phthalazines		antineoplastic agent;
apoptosis inducer;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
thiostrepton
Thiostrepton: One of the CYCLIC PEPTIDES from Streptomyces that is active against gram-positive bacteria. In veterinary medicine, it has been used in mastitis caused by gram-negative organisms and in dermatologic disorders.. thiostrepton : A heterodetic cyclic peptide, in which the cyclisation step involves a formal lactonisation between the carboxy group of a quinaldic acid-based residue and a secondary alcohol. An antibiotic that inhibits bacterial protein synthesis. Also acts as an antitumor agent.		2.1510
cx 4945
[no description available]		2.3110
mln 8237
MLN 8237: an aurora kinase A inhibitor		4.231benzazepine
gdc 0449
HhAntag691: inhibits the hedgehog pathway and ABC transporters; has antineoplastic activity		5.252benzamides;
monochlorobenzenes;
pyridines;
sulfone		antineoplastic agent;
Hedgehog signaling pathway inhibitor;
SMO receptor antagonist;
teratogenic agent
cep-9722
CEP-9722: a prodrug of the poly(ADP-ribose) polymerase inhibitor CEP-8983		2.0310
pci 32765
ibrutinib: a Btk protein inhibitor. ibrutinib : A member of the class of acrylamides that is (3R)-3-[4-amino-3-(4-phenoxyphenyl)pyrazolo[3,4-d]pyrimidin-1-yl]piperidine in which the piperidine nitrogen is replaced by an acryloyl group. A selective and covalent inhibitor of the enzyme Bruton's tyrosine kinase, it is used for treatment of B-cell malignancies.		2.9330acrylamides;
aromatic amine;
aromatic ether;
N-acylpiperidine;
pyrazolopyrimidine;
tertiary carboxamide		antineoplastic agent;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
mk-1775
adavosertib: a Wee1 kinase inhibitor; structure in first source		8.9721piperazines
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.		5.05212-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamideantineoplastic agent;
apoptosis inducer;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor;
radiosensitizing agent
mk 2206
MK 2206: a protein kinase inhibitor and antineoplastic agent		2.5320organic heterotricyclic compoundEC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
navitoclax
[no description available]		2.5720aryl sulfide;
monochlorobenzenes;
morpholines;
N-sulfonylcarboxamide;
organofluorine compound;
piperazines;
secondary amino compound;
sulfone;
tertiary amino compound		antineoplastic agent;
apoptosis inducer;
B-cell lymphoma 2 inhibitor
quetiapine fumarate
Quetiapine Fumarate: A dibenzothiazepine and ANTIPSYCHOTIC AGENT that targets the SEROTONIN 5-HT2 RECEPTOR; HISTAMINE H1 RECEPTOR, adrenergic alpha1 and alpha2 receptors, as well as the DOPAMINE D1 RECEPTOR and DOPAMINE D2 RECEPTOR. It is used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER and DEPRESSIVE DISORDER.		2.5820fumarate salt
n-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide
N-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide: a Janus kinase 1 and Janus kinase 2 inhibitor; structure in first source. momelotinib : A benzamide obtained by formal condensation of the carboxy group of 4-{2-[4-(morpholin-4-yl)anilino]pyrimidin-4-yl}benzoic acid with the primary amino group of aminoacetonitrile. It is an ATP-competitive JAK1/JAK2 inhibitor with IC50 of 11 nM and 18 nM, respectively. Used for the treatment of patients with intermediate- or high-risk myelofibrosis.		2.2110aminopyrimidine;
benzamides;
morpholines;
nitrile;
secondary amino compound;
tertiary amino compound		anti-anaemic agent;
antineoplastic agent;
apoptosis inducer;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
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.		3.5820oligopeptideantineoplastic agent;
GnRH antagonist
cabozantinib
cabozantinib: a multikinase inhibitor. cabozantinib : A dicarboxylic acid diamide that is N-phenyl-N'-(4-fluorophenyl)cyclopropane-1,1-dicarboxamide in which the hydrogen at position 4 on the phenyl ring is substituted by a (6,7-dimethoxyquinolin-4-yl)oxy group. A multi-tyrosine kinase inhibitor, used (as its malate salt) for the treatment of progressive, metastatic, medullary thyroid cancer.		5.641aromatic ether;
dicarboxylic acid diamide;
organofluorine compound;
quinolines		antineoplastic agent;
tyrosine kinase inhibitor
incb-018424
[no description available]		2.4110nitrile;
pyrazoles;
pyrrolopyrimidine		antineoplastic agent;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
entrectinib
entrectinib: inhibits TRK, ROS1, and ALK receptor tyrosine kinases; structure in first source. entrectinib : A member of the class of indazoles that is 1H-indazole substituted by [4-(4-methylpiperazin-1-yl)-2-(tetrahydro-2H-pyran-4-ylamino)benzoyl]amino and 3,5-difluorobenzyl groups at positions 3 and 5, respectively. It is a potent inhibitor of TRKA, TRKB, TRKC, ROS1, and ALK (IC50 values of 0.1 to 1.7 nM), and used for the treatment of NTRK, ROS1 and ALK gene fusion-positive solid tumours.		2.5920benzamides;
difluorobenzene;
indazoles;
N-methylpiperazine;
oxanes;
secondary amino compound;
secondary carboxamide		antibacterial agent;
antineoplastic agent;
apoptosis inducer;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
(5-(2,4-bis((3s)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol
(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol: a potent, selective, and orally bioavailable ATP-competitive mammalian target of rapamycin kinase inhibitor with in vitro and in vivo antitumor activity; structure in first source		2.1110benzyl alcohols;
morpholines;
pyridopyrimidine;
tertiary amino compound		antineoplastic agent;
apoptosis inducer;
mTOR inhibitor
plx4032
[no description available]		8.41171aromatic ketone;
difluorobenzene;
monochlorobenzenes;
pyrrolopyridine;
sulfonamide		antineoplastic agent;
B-Raf inhibitor
gsk 1363089
GSK 1363089: a multikinase inhibitor that acts on Met, RON, Axl, and VEGFR; structure in first source		3.3110aromatic ether
osilodrostat
Osilodrostat: an orally active aldosterone-synthase inhibitor		4.2210
gw 1000
nabiximols: a combination of the above cpds for treatment of multiple sclerosis pain		6.4842
glycolipids
[no description available]		3.8620
piperidines
Piperidines: A family of hexahydropyridines.		10.22276
6-[(3-aminophenyl)methyl]-4-methyl-2-methylsulfinyl-5-thieno[3,4]pyrrolo[1,3-d]pyridazinone
ML-265: a small molecule activator of PKM2		2.2510organic heterobicyclic compound;
organonitrogen heterocyclic compound;
organosulfur heterocyclic compound
bryostatin 1
bryostatin 1: a protein kinase C activator; macrocyclic lactone from marine Bryozoan Bugula neritina; RN given refers to (1S*-(1R*,3R*,5Z,7S*,8E,11R*,12R*(2E,4E),13E,15R*,17S*(S*),21S*,23S*,25R*))-isomer; structure given in first source; activates protein kinase c. bryostatin 1 : A member of the class of bryostatins that is (17E)-2-oxooxacyclohexacos-17-ene which is substituted by hydroxy groups at positions 4, 10, and 20; an acetoxy group at position 8; methyl groups at positions 9, 9, 18, and 19; 2-methoxy-2-oxoethylidene groups at positions 14 and 24; an (E,E)-octa-2,4-dienoyloxy group at position 21; and with oxygen bridges linking positions 6 to 10, 12 to 16, and 20 to 24. It is one of the most abundant member of the class of bryostatins.		3.0910
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.		3.4560
dabrafenib
[no description available]		5.01401,3-thiazoles;
aminopyrimidine;
organofluorine compound;
sulfonamide		anticoronaviral agent;
antineoplastic agent;
B-Raf inhibitor
cblc137
CBLC137: a FACT histone chaperone inhibitor with antineoplastic activity; structure in first source. CBL0137 : A member of the class of carbazoles that is 9H-carbazole which is substituted by acetyl groups at positions 3 and 6, and by a 2-isopropylethyl group on the nitrogen atom (position 9). It is a modulator of histone chaperone FACT (FAcilitates Chromatin Transcription) - interaction of CBL0137 with the FACT complex results in simultaneous NF-kappa beta suppression, Heat Shock Transcription Factor 1 (HSF1) suppression and p53 activation - and shows antitumour effects in animal models of various cancers.		2.1510aromatic ketone;
carbazoles;
methyl ketone;
secondary amino compound;
tertiary amino compound		antineoplastic agent;
apoptosis inducer;
NF-kappaB inhibitor;
p53 activator
gypenoside XVII
gypenoside XVII : A ginsenoside found in Panax species that is dammarane which is substituted by hydroxy groups at the 3beta, 12beta and 20 pro-S positions, in which the hydroxy groups at positions 3 and 20 have been converted to the corresponding beta-D-glucopyranoside and beta-D-glucopyranosyl-(1->6)-beta-D-glucopyranoside respectively, and in which a double bond has been introduced at the 24-25 position.		2.11012beta-hydroxy steroid;
beta-D-glucoside;
disaccharide derivative;
ginsenoside;
tetracyclic triterpenoid		plant metabolite
apatinib
apatinib: reverses multidrug resistance by inhibiting the efflux function of multiple ATP-binding cassette transporters; structure in first source		7.7872
bal101553
lisavanbulin: a prodrug of BAL27862		2.3110
gx 15-070
obatoclax: a pan-Bcl-2 inhibitor potentially useful in treating mantle cell lymphoma		2.110
abemaciclib
[no description available]		2.8930
(20R)-ginsenoside Rg3
(20R)-ginsenoside Rg3 : A ginsenoside found in Panax japonicus var. major that is dammarane which is substituted by hydroxy groups at the 3beta, 12beta and 20 pro-R 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.		2.110ginsenoside;
glycoside;
tetracyclic triterpenoid		antioxidant;
plant metabolite
gsk923295
GSK923295: an antimotitic agent and CENP-E inhibitor		2.0810
lgk974
LGK974: a potent and specific small-molecule inhibitor of Porcupine (PORCN) acyltransferase. LGK974 : A carboxamide, the structure of which is that of acetamide substituted on carbon by a 2',3-dimethyl-2,4'-bipyridin-5-yl group and on nitrogen by a 5-(pyrazin-2-yl)pyridin-2-yl group. It is a highly potent, selective and orally bioavailable Porcupine inhibitor (a Wnt signalling inhibitor).		2.1110bipyridines;
pyrazines;
pyridines;
secondary carboxamide		Wnt signalling inhibitor
gsk525762a
molibresib: mimicks acetylated histones; structure in first source		2.1510benzodiazepine
alectinib
[no description available]		2.3110aromatic ketone;
morpholines;
nitrile;
organic heterotetracyclic compound;
piperidines		antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
birinapant
birinapant: a Smac mimetic with antineoplastic activity		2.1310dipeptide
nms-p118
NMS-P118: a PARP-1 inhibitor; structure in first source		2.1110
tubastatin a
[no description available]		2.8830hydroxamic acid;
pyridoindole;
tertiary amino compound		EC 3.5.1.98 (histone deacetylase) inhibitor
xl765
[no description available]		8.8921aromatic amine;
aromatic ether;
benzamides;
quinoxaline derivative;
sulfonamide		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
mTOR inhibitor
ve 821
3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide: an antineoplastic agent; structure in first source		2.1510aromatic amide
gsk1210151a
GSK1210151A: inhibitor of the BET family of proteins; structure in first source		2.2510imidazoquinoline
apr-246
eprenetapopt: works in tandem with cisplatin to cause apoptosis of tumor cells; structure in first source		7.3110
acy-1215
ricolinostat: an HDAC6 inhibitor; structure in first source		2.2110pyrimidinecarboxylic acid
rg7388
RG7388: structure in first source		2.6620
o-(2-fluoroethyl)tyrosine
O-(2-fluoroethyl)tyrosine: structure in first source		4.4141
cudc-907
[no description available]		3.6320
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.		5.6651ascorbic 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.		2.4620carbamate 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.		4.4260
chlortetracycline
Chlortetracycline: A TETRACYCLINE with a 7-chloro substitution.. chlortetracycline : A member of the class of tetracyclines with formula C22H23ClN2O8 isolated from Streptomyces aureofaciens.		2.7430
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.		3.8630
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.		9.2950
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.		2.2110monohydroxybenzoateplant 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]		4.2750benzothiazine;
monocarboxylic acid amide;
pyridines		analgesic;
antirheumatic drug;
cyclooxygenase 1 inhibitor;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug
roquinimex
roquinimex: structure in first source		2.4620aromatic amide
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.		2.4620C-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.		4.42601,3-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.		2.7530heteroaryl 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
isoxicam
isoxicam : A monocarboxylic acid amide that is piroxicam in which the pyrid-2-yl group is replaced by a 5-methyl-1,2-oxazol-3-yl group. A non-steroidal anti-inflammatory drug, it was withdrawn from the market in the 1980s following its association with cases of Stevens-Johnson syndrome.		2.7530benzothiazine;
isoxazoles;
monocarboxylic acid amide		antirheumatic drug;
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.		4.2850benzenes;
hydroxycoumarin;
methyl ketone
metastat
tetracycline CMT-3: a non-antimicrobial tetracycline; structure in second source		3.1210
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.		3.8630
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
chlortetracycline hydrochloride
Alexomycin: a thiopeptide; a cyclic peptide antibiotic produced by Streptomyces arginensis isolated from the soil		2.0510
rolitetracycline
Rolitetracycline: A pyrrolidinylmethyl TETRACYCLINE.. rolitetracycline : A derivative of tetracycline in which the amide function is substituted with a pyrrolidinomethyl group.		2.7430
sudoxicam
sudoxicam: proposed ant-inflammatory agent; minor descriptor (75-86); on-line & INDEX MEDICUS search THIAZINES (75-86)		2.0510
methacycline monohydrochloride
[no description available]		2.0510
minocycline hydrochloride
[no description available]		2.4720
demeclocycline hydrochloride
demeclocycline hydrochloride : The hydrochloride salt of demeclocycline. A tetracycline antibiotic, 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.		2.0510
tigecycline
[no description available]		3.8730
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.		2.4720heteroaryl 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		2.1710
agi-5198
AGI-5198: inhibits isocitrate dehydrogenase 1; structure in first source		2.110
byl719
[no description available]		4.811proline derivative
rg2833
RG2833: a histone deacetylase inhibitor; structure in first source		2.1310
cycloviolacin o13
cycloviolacin O13: amino acid sequence in first source		2.4110
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.		7.7530
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.		4.8571
ceritinib
ceritinib: an anaplastic lymphoma kinase inhibitor. ceritinib : A member of the class of aminopyrimidines that is 2,6-diamino-5-chloropyrimidine in which the amino groups at positions 2 and 6 are respectively carrying 2-methoxy-4-(piperidin-4-yl)-5-methylphenyl and 2-(isopropylsulfonyl)phenyl substituents. Used for the treatment of ALK-positive metastatic non-small cell lung cancer.		2.6920aminopyrimidine;
aromatic ether;
organochlorine compound;
piperidines;
secondary amino compound;
sulfone		antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
wnt-c59
2-(4-(2-methylpyridin-4-yl)phenyl)-N-(4-(pyridin-3-yl)phenyl)acetamide: a PORCN acyltransferase inhibitor; structure in first source		2.1110
vx-970
berzosertib: an ATR kinase inhibitor		2.5820sulfonamide
g007-lk
G007-LK: potent and specific small-molecule tankyrase inhibitor; structure in first source		2.1110
3-(6-isobutyl-9-methoxy-1,4-dioxo-1,2,3,4,6,7,12,12a-octahydropyrazino(1',2'-1,6)pyrido(3,4-b)indol-3-yl)propionic acid tert-butyl ester
3-(6-isobutyl-9-methoxy-1,4-dioxo-1,2,3,4,6,7,12,12a-octahydropyrazino(1',2'-1,6)pyrido(3,4-b)indol-3-yl)propionic acid tert-butyl ester: a breast cancer resistance protein (BCRP) inhibitor; structure in first source		2.6320
ajmaline
[no description available]		2.0510
rome
Rome: The capital city of Italy.. (2R)-2-amino-2-(methoxymethyl)-4-(4-octylphenyl)butan-1-ol : A 2-amino-2-(methoxymethyl)-4-(4-octylphenyl)butan-1-ol that has R-configuration. It is a sphingosine kinase-2 inhibitor.		2.11102-amino-2-(methoxymethyl)-4-(4-octylphenyl)butan-1-olEC 2.7.1.91 (sphingosine kinase) inhibitor
agar
Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis.. agar : A complex mixture of polysaccharides extracted from species of red algae. Its two main components are agarose and agaropectin. Agarose is the component responsible for the high-strength gelling properties of agar, while agaropectin provides the viscous properties.		2.4110
glutaminase
[no description available]		7.8630
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.		8.460
fertinex
[no description available]		3.2310
pf-06687252
PF-06687252: a SMARCA2/4 bromodomain inhibitor; structure in first source. PFI-3 : An azabicycloalkane that is (1R,4R)-2,5-diazabicyclo[2.2.1]heptane which is substituted at position 2 by a 3-(2-hydroxyphenyl)-3-oxoprop-1-en-1-yl group and at position 5 by a pyridin-2-yl group. It is a potent and selective inhibitor of polybromo 1 (Kd = 48 nM), SMARCA2 and SMARCA4 (Kd = 89 nM) bromodomains.		2.4110azabicycloalkane;
enone;
phenols;
pyridines
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone: an interleukin-1beta converting enzyme (ICE)-like protease inhibitor		2.0510
nitrophenols
Nitrophenols: PHENOLS carrying nitro group substituents.		2.7930
lewis x antigen
Lewis X Antigen: A trisaccharide antigen expressed on glycolipids and many cell-surface glycoproteins. In the blood the antigen is found on the surface of NEUTROPHILS; EOSINOPHILS; and MONOCYTES. In addition, Lewis X antigen is a stage-specific embryonic antigen.		2.1710
adrenomedullin
Adrenomedullin: A 52-amino acid peptide with multi-functions. It was originally isolated from PHEOCHROMOCYTOMA and ADRENAL MEDULLA but is widely distributed throughout the body including lung and kidney tissues. Besides controlling fluid-electrolyte homeostasis, adrenomedullin is a potent vasodilator and can inhibit pituitary ACTH secretion.		2.7620
daptomycin
[no description available]		3.711
oblimersen
oblimersen: targets the Bcl-2 oncogene good efficacy with low toxicity tumour regressions		10.2131
cycloviolacin o2
[no description available]		2.4110
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).		2.4520
silybin
Silybin: The major active component of silymarin flavonoids extracted from seeds of the MILK THISTLE, Silybum marianum; it is used in the treatment of HEPATITIS; LIVER CIRRHOSIS; and CHEMICAL AND DRUG INDUCED LIVER INJURY, and has antineoplastic activity; silybins A and B are diastereomers.		2.5220
siomycin a
siomycin A: see also records for siomycin & siomycin D1		2.0810
lactoferrin
Lactoferrin: An iron-binding protein that was originally characterized as a milk protein. It is widely distributed in secretory fluids and is found in the neutrophilic granules of LEUKOCYTES. The N-terminal part of lactoferrin possesses a serine protease which functions to inactivate the TYPE III SECRETION SYSTEM used by bacteria to export virulence proteins for host cell invasion.		5.2850
orabase
Orabase: used in therapy of oral mucosal ulcers		8.4785
sc002
SC002: structure in first source		3.6920
lutetium lu 177 dotatate
177Lu-DOTA-octreotate: an somatostatin receptor agonist		3.7120
chondroitin sulfates
Chondroitin Sulfates: Derivatives of chondroitin which have a sulfate moiety esterified to the galactosamine moiety of chondroitin. Chondroitin sulfate A, or chondroitin 4-sulfate, and chondroitin sulfate C, or chondroitin 6-sulfate, have the sulfate esterified in the 4- and 6-positions, respectively. Chondroitin sulfate B (beta heparin; DERMATAN SULFATE) is a misnomer and this compound is not a true chondroitin sulfate.		2.3110
mrk 003
MRK 003: structure in first source		2.0810
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.		3.87302-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.		7.37712-aminopurines;
oxopurine		antimetabolite;
antiviral drug
nu 1025
NU 1064: structure in first source		3.1350phenols;
quinazolines		EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
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.		7.31535-formyltetrahydrofolic acidantineoplastic agent;
metabolite
8-oxodeoxyguanosine triphosphate
8-oxodeoxyguanosine triphosphate: mutagenic nucleotide; hydrolyzed by 8-oxodGTPase to 8-oxodGMP. 8-oxo-dGTP : A purine 2'-deoxyribonucleoside 5'-triphosphate having 8-oxo-7,8-dihydroguanine as the nucleobase.		2.1710purine 2'-deoxyribonucleoside 5'-triphosphatemutagen
deoxyguanosine
[no description available]		9.3270purine 2'-deoxyribonucleoside;
purines 2'-deoxy-D-ribonucleoside		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
deoxyguanosine triphosphate
[no description available]		2.1710deoxyguanosine phosphate;
guanyl deoxyribonucleotide;
purine 2'-deoxyribonucleoside 5'-triphosphate		Arabidopsis thaliana metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
guanine
[no description available]		13.93112132-aminopurines;
oxopurine;
purine nucleobase		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
guanosine
ribonucleoside : Any nucleoside where the sugar component is D-ribose.		7.8130guanosines;
purines D-ribonucleoside		fundamental 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.		5.09120folic acids;
N-acyl-amino acid		human metabolite;
mouse metabolite;
nutrient
3-methyladenine
N3-methyladenine: structure in first source		7.8130
7-methylguanine
7-methylguanine: RN given refers to unlabeled cpd; structure. 7-methylguanine : A methylguanine that is guanine substituted by a methyl group at position 7. It is a metabolite obtained during the methylation of DNA.. 2-imino-7-methyl-1,2,3,7-tetrahydro-6H-purin-6-one : A 7-methylguanine that is 1,2,3,7-tetrahydro-6H-purin-6-one substituted by an imino group at position 2 and a methyl group at position 7.. 2-amino-7-methyl-7H-purin-6-ol : A 7-methylguanine that is 7H-purine substituted by an amino group at position 2, a methyl group at position 7 and a hydroxy group at position 6.. 2-amino-7-methyl-1,7-dihydro-6H-purin-6-one : A 7-methylguanine that is 1,7-dihydro-6H-purin-6-one substituted by an amino group at position 2 and a methyl group at position 7.		3.63307-methylguanine
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)		4.5570cyclic 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.		4.4260benzodiazepine;
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.		30.844,072804dacarbazine
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.		4.2650purine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
EC 2.4.2.1 (purine-nucleoside phosphorylase) inhibitor;
geroprotector;
HIV-1 reverse transcriptase inhibitor
ganciclovir
[no description available]		9.77902-aminopurines;
oxopurine		antiinfective agent;
antiviral drug
valtrex
[no description available]		2.0810organic molecular entity
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.		6.6931L-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.		3.8630piperazines;
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.		9.2850benzodiazepine;
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.		2.45202-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]		4.2350N-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.		3.5820imidazotriazine;
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.		4.4260nucleobase analogue;
organic heterobicyclic compound		antimetabolite;
EC 1.17.3.2 (xanthine oxidase) inhibitor;
gout suppressant;
radical scavenger
citrovorum factor
[no description available]		3.8730tetrahydrofolic acid
leucovorin
5-formyltetrahydrofolic acid : A formyltetrahydrofolic acid in which the formyl group is located at position 5.		3.8630formyltetrahydrofolic acidEscherichia coli metabolite;
mouse metabolite
rifapentine
rifapentine: cyclopentyl derivative of rifampicin		3.6120N-alkylpiperazine;
N-iminopiperazine;
rifamycins		antitubercular agent;
leprostatic drug
alanosine
[no description available]		2.0510
3,4,5-trihydroxybenzamidoxime
3,4,5-trihydroxybenzamidoxime: structure given in first source		2.0110benzenetriol
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		3.5820carboxamidine;
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).		4.6740N-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.		4.0540aromatic 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.		2.0810citrate 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.		6.91111(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.		3.2310(trifluoromethyl)benzenes;
cyclic acetal;
morpholines;
phosphoramide;
triazoles		antiemetic;
neurokinin-1 receptor antagonist;
prodrug
tegaserod maleate
[no description available]		2.0810maleate saltserotonergic agonist
ceftobiprole
ceftobiprole: BAL5788 is Ceftobiprole medocaril sodium. ceftobiprole : A fifth-generation cephalosporin antibiotic having (E)-[(3'R)-2-oxo[1,3'-bipyrrolidin]-3-ylidene]methyl and [(2Z)-2-(5-amino-1,2,4-thiadiazol-3-yl)-2-(hydroxyimino)acetyl]amino side groups located at positions 3 and 7 respectively; developed for the treatment of hospital-acquired pneumonia (HAP, excluding ventilator-associated pneumonia, VAP) and community-acquired pneumonia (CAP).		2.0410cephalosporin;
thiadiazoles		antimicrobial agent
rifabutin
[no description available]		4.2650
xav939
XAV939: selectively inhibits beta-catenin-mediated transcription; structure in first source. XAV939 : A thiopyranopyrimidine in which a 7,8-dihydro-5H-thiopyrano[4,3-d]pyrimidine skeleton is substituted at C-4 by a hydroxy group and at C-2 by a para-(trifluoromethyl)phenyl group.		2.1110(trifluoromethyl)benzenes;
thiopyranopyrimidine		tankyrase inhibitor
hesperadin
[no description available]		2.2110
trypan blue
Trypan Blue: A diazo-naphthalene sulfonate that is widely used as a stain.. trypan blue : An organosulfonate salt that is the tetrasodium salt of 3,3'-[(3,3'-dimethylbiphenyl-4,4'-diyl)didiazene-2,1-diyl]bis(5-amino-4-hydroxynaphthalene-2,7-disulfonic acid).		2.520
methylnitronitrosoguanidine
Methylnitronitrosoguanidine: A nitrosoguanidine derivative with potent mutagenic and carcinogenic properties.. N-methyl-N'-nitro-N-nitrosoguanidine : An N-nitroguanidine compound having nitroso and methyl substituents at the N'-position		5.02150nitroso compoundalkylating agent
8-methylguanosine
8-methylguanosine: structure in first source		2.0810
5-(3-hydroxymethyl-3-methyl-1-triazeno)imidazole-4-carboxamide
5-(3-hydroxymethyl-3-methyl-1-triazeno)imidazole-4-carboxamide: metabolite of dacarbazine; structure in first source		4.0730aromatic amide;
heteroarene
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
bmn 673
talazoparib: inhibits both PARP1 and PARP2; structure in first source		10.7492
pp242
torkinib : A member of the class of pyrazolopyrimidines that is 1H-pyrazolo[3,4-d]pyrimidine substituted by isopropyl, 5-hydroxyindol-2-yl and amino groups at positions 1, 3 and 4 respectively. It is a potent inhibitor of mTOR and exhibits anti-cancer properties.		2.3110aromatic amine;
biaryl;
hydroxyindoles;
phenols;
primary amino compound;
pyrazolopyrimidine		antineoplastic agent;
mTOR inhibitor
7-methyl-2-deoxyguanosine
7-methyl-2-deoxyguanosine: structure given in first source		210
cholestyramine resin
Cholestyramine Resin: A strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium Cl(-) anion.		2.110
chlorotoxin
[no description available]		2.4920
leptin
Leptin: A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.		4.811
pyrimidinones
Pyrimidinones: Heterocyclic compounds known as 2-pyrimidones (or 2-hydroxypyrimidines) and 4-pyrimidones (or 4-hydroxypyrimidines) with the general formula C4H4N2O.		6.6581
phenanthrenes
Phenanthrenes: POLYCYCLIC AROMATIC HYDROCARBONS composed of three fused BENZENE rings.. phenanthrenes : Any benzenoid aromatic compound that consists of a phenanthrene skeleton and its substituted derivatives thereof.		2.5220
ConditionIndicatedRelationship StrengthStudiesTrials
Experimental Leukemia
[description not available]		05.0250
Breast Cancer
[description not available]		016.086229
Breast Neoplasms
Tumors or cancer of the human BREAST.		118.086229
B16 Melanoma
[description not available]		06.84330
Acute Liver Injury, Drug-Induced
[description not available]		09.44263
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.		09.44263
Lipidoses
Conditions characterized by abnormal lipid deposition due to disturbance in lipid metabolism, such as hereditary diseases involving lysosomal enzymes required for lipid breakdown. They are classified either by the enzyme defect or by the type of lipid involved.		02.0510
Innate Inflammatory Response
[description not available]		09.87154
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.		09.87154
Adverse Drug Event
[description not available]		011.23158
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.		011.23158
Benign Neoplasms, Brain
[description not available]		033.155,1822,252
Astrocytoma, Grade IV
[description not available]		032.64,7432,153
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.		139.5415,5466,756
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.		134.64,7432,153
Experimental Neoplasms
[description not available]		08.56460
Glial Cell Tumors
[description not available]		025.671,430183
Central Nervous System Neoplasm
[description not available]		018.8815446
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)		133.25,720732
Central Nervous System Neoplasms
Benign and malignant neoplastic processes that arise from or secondarily involve the brain, spinal cord, or meninges.		120.8815446
Malignant Melanoma
[description not available]		021.4337113
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)		127.771,011339
Benign Neoplasms
[description not available]		018.8514952
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.		123.59298104
ER-Negative PR-Negative HER2-Negative Breast Cancer
[description not available]		03.3760
Cancer of Pancreas
[description not available]		014.27619
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).		116.27619
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.		03.3760
Anemia, Fanconi
[description not available]		02.7830
Fanconi Anemia
Congenital disorder affecting all bone marrow elements, resulting in ANEMIA; LEUKOPENIA; and THROMBOPENIA, and associated with cardiac, renal, and limb malformations as well as dermal pigmentary changes. Spontaneous CHROMOSOME BREAKAGE is a feature of this disease along with predisposition to LEUKEMIA. There are at least 7 complementation groups in Fanconi anemia: FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, and FANCL. (from Online Mendelian Inheritance in Man, http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=227650, August 20, 2004)		02.7830
Experimental Mammary Neoplasms
[description not available]		02.9440
Anoxemia
[description not available]		04.47180
Hypoxia
Sub-optimal OXYGEN levels in the ambient air of living organisms.		04.47180
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.		015.4115913
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
Canine Diseases
[description not available]		07.66115
Cancer of Pituitary
[description not available]		011.951311
Craniopharyngioma, Adamantinous
[description not available]		03.7330
Craniopharyngioma
A benign pituitary-region neoplasm that originates from Rathke's pouch. The two major histologic and clinical subtypes are adamantinous (or classical) craniopharyngioma and papillary craniopharyngioma. The adamantinous form presents in children and adolescents as an expanding cystic lesion in the pituitary region. The cystic cavity is filled with a black viscous substance and histologically the tumor is composed of adamantinomatous epithelium and areas of calcification and necrosis. Papillary craniopharyngiomas occur in adults, and histologically feature a squamous epithelium with papillations. (From Joynt, Clinical Neurology, 1998, Ch14, p50)		03.7330
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.		118.951311
Local Neoplasm Recurrence
[description not available]		024.09647213
Allergic Bronchopulmonary Mycosis
[description not available]		03.2310
Anemia, Hypoplastic
[description not available]		04.8110
Anemia, Aplastic
A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.		04.8110
Disease Exacerbation
[description not available]		028.841,7961,587
Angiogenesis, Pathologic
[description not available]		013.4607
Invasiveness, Neoplasm
[description not available]		013.821127
Hyperprolactinaemia
[description not available]		03.7530
Hypergonadotropic Hypogonadism
[description not available]		04.0720
Disruptive, Impulse Control, and Conduct Disorders
Disorders whose essential features are the failure to resist an impulse, drive, or temptation to perform an act that is harmful to the individual or to others. Individuals experience an increased sense of tension prior to the act and pleasure, gratification or release of tension at the time of committing the act.		03.2310
Adenoma, Prolactin-Secreting, Pituitary
[description not available]		07.91310
Galactorrhea
Excessive or inappropriate LACTATION in females or males, and not necessarily related to PREGNANCY. Galactorrhea can occur either unilaterally or bilaterally, and be profuse or sparse. Its most common cause is HYPERPROLACTINEMIA.		03.2310
Hyperprolactinemia
Increased levels of PROLACTIN in the BLOOD, which may be associated with AMENORRHEA and GALACTORRHEA. Relatively common etiologies include PROLACTINOMA, medication effect, KIDNEY FAILURE, granulomatous diseases of the PITUITARY GLAND, and disorders which interfere with the hypothalamic inhibition of prolactin release. Ectopic (non-pituitary) production of prolactin may also occur. (From Joynt, Clinical Neurology, 1992, Ch36, pp77-8)		03.7530
Hypogonadism
Condition resulting from deficient gonadal functions, such as GAMETOGENESIS and the production of GONADAL STEROID HORMONES. It is characterized by delay in GROWTH, germ cell maturation, and development of secondary sex characteristics. Hypogonadism can be due to a deficiency of GONADOTROPINS (hypogonadotropic hypogonadism) or due to primary gonadal failure (hypergonadotropic hypogonadism).		04.0720
Pregnancy
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.		013.75114
Carcinoma, Non-Small Cell Lung
[description not available]		014.954721
Cancer of Lung
[description not available]		017.6111834
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.		116.954721
Lung Neoplasms
Tumors or cancer of the LUNG.		119.6111834
Benign Meningeal Neoplasms
[description not available]		09.96404
Astroblastoma
[description not available]		09315
Meningeal Neoplasms
Benign and malignant neoplastic processes that arise from or secondarily involve the meningeal coverings of the brain and spinal cord.		09.96404
Neoplasms, Neuroepithelial
Neoplasms composed of neuroepithelial cells, which have the capacity to differentiate into NEURONS, oligodendrocytes, and ASTROCYTES. The majority of craniospinal tumors are of neuroepithelial origin. (From Dev Biol 1998 Aug 1;200(1):1-5)		09315
Neurilemoma
[description not available]		02.3110
Benign Cranial Nerve Neoplasms
[description not available]		02.5820
Neurilemmoma
A neoplasm that arises from SCHWANN CELLS of the cranial, peripheral, and autonomic nerves. Clinically, these tumors may present as a cranial neuropathy, abdominal or soft tissue mass, intracranial lesion, or with spinal cord compression. Histologically, these tumors are encapsulated, highly vascular, and composed of a homogenous pattern of biphasic fusiform-shaped cells that may have a palisaded appearance. (From DeVita Jr et al., Cancer: Principles and Practice of Oncology, 5th ed, pp964-5)		02.3110
Thrombopenia
[description not available]		015.887348
Thrombocytopenia
A subnormal level of BLOOD PLATELETS.		015.887348
DRESS Syndrome
[description not available]		02.4110
Exanthem
[description not available]		03.0540
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.		03.0540
Neuroblastoma
A common neoplasm of early childhood arising from neural crest cells in the sympathetic nervous system, and characterized by diverse clinical behavior, ranging from spontaneous remission to rapid metastatic progression and death. This tumor is the most common intraabdominal malignancy of childhood, but it may also arise from thorax, neck, or rarely occur in the central nervous system. Histologic features include uniform round cells with hyperchromatic nuclei arranged in nests and separated by fibrovascular septa. Neuroblastomas may be associated with the opsoclonus-myoclonus syndrome. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2099-2101; Curr Opin Oncol 1998 Jan;10(1):43-51)		115.816312
Rhabdomyosarcoma
A malignant solid tumor arising from mesenchymal tissues which normally differentiate to form striated muscle. It can occur in a wide variety of sites. It is divided into four distinct types: pleomorphic, predominantly in male adults; alveolar (RHABDOMYOSARCOMA, ALVEOLAR), mainly in adolescents and young adults; embryonal (RHABDOMYOSARCOMA, EMBRYONAL), predominantly in infants and children; and botryoidal, also in young children. It is one of the most frequently occurring soft tissue sarcomas and the most common in children under 15. (From Dorland, 27th ed; Holland et al., Cancer Medicine, 3d ed, p2186; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, pp1647-9)		116.16212
Colon Cancer, Familial Nonpolyposis
[description not available]		02.7730
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.		02.7730
Adenoma, Basal Cell
[description not available]		011.6701
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.		05.0860
Adenoma
A benign epithelial tumor with a glandular organization.		011.6701
Colorectal Cancer
[description not available]		019.71167116
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.		126501348
Cell Transformation, Neoplastic
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.		06.16280
Cancer of Liver
[description not available]		014.194912
Liver Neoplasms
Tumors or cancer of the LIVER.		014.194912
Debility
[description not available]		02.6920
Germinoblastoma
[description not available]		016.287036
Lymphoma
A general term for various neoplastic diseases of the lymphoid tissue.		118.287036
Lymphocytopenia
[description not available]		011.88305
Lymphopenia
Reduction in the number of lymphocytes.		011.88305
Encephalitis, JC Polyomavirus
[description not available]		02.4110
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)		02.4110
Bone Cancer
[description not available]		08.56221
Osteogenic Sarcoma
[description not available]		05.8571
Bone Neoplasms
Tumors or cancer located in bone tissue or specific BONES.		08.56221
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)		05.8571
Anaplastic Astrocytoma
[description not available]		019.4621449
Astrocytoma
Neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors. Fibrillary astrocytomas are the most common type and may be classified in order of increasing malignancy (grades I through IV). In the first two decades of life, astrocytomas tend to originate in the cerebellar hemispheres; in adults, they most frequently arise in the cerebrum and frequently undergo malignant transformation. (From Devita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2013-7; Holland et al., Cancer Medicine, 3d ed, p1082)		124.242898
Sarcoma, Epithelioid
[description not available]		010.08167
Sarcoma
A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant.		114.533214
Abnormalities, Autosome
[description not available]		04.2260
Anaplastic Oligodendroglioma
[description not available]		017.1210921
Chromosome Deletion
Actual loss of portion of a chromosome.		010.92326
Oligodendroglioma
A relatively slow-growing glioma that is derived from oligodendrocytes and tends to occur in the cerebral hemispheres, thalamus, or lateral ventricle. They may present at any age, but are most frequent in the third to fifth decades, with an earlier incidence peak in the first decade. Histologically, these tumors are encapsulated, relatively avascular, and tend to form cysts and microcalcifications. Neoplastic cells tend to have small round nuclei surrounded by unstained nuclei. The tumors may vary from well-differentiated to highly anaplastic forms. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2052; Adams et al., Principles of Neurology, 6th ed, p655)		123.4532763
Carcinogenesis
The origin, production or development of cancer through genotypic and phenotypic changes which upset the normal balance between cell proliferation and cell death. Carcinogenesis generally requires a constellation of steps, which may occur quickly or over a period of many years.		010.17374
Cancer of Skin
[description not available]		018.2415556
Skin Neoplasms
Tumors or cancer of the SKIN.		120.2415556
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.		123.536936
Complication, Postoperative
[description not available]		09.04143
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.		09.04143
Bladder Cancer
[description not available]		05.4851
Urinary Bladder Neoplasms
Tumors or cancer of the URINARY BLADDER.		05.4851
Carcinoma, Transitional Cell
A malignant neoplasm derived from TRANSITIONAL EPITHELIAL CELLS, occurring chiefly in the URINARY BLADDER; URETERS; or RENAL PELVIS.		02.4110
Cancer of Colon
[description not available]		08.31212
Cancer of Rectum
[description not available]		08.9797
Colonic Neoplasms
Tumors or cancer of the COLON.		08.31212
Rectal Neoplasms
Tumors or cancer of the RECTUM.		110.9797
Hypermelanosis
[description not available]		02.4110
Microglossia
[description not available]		02.4110
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.		07.4110
Deficiency, Mental
[description not available]		02.4110
Intellectual Disability
Subnormal intellectual functioning which originates during the developmental period. This has multiple potential etiologies, including genetic defects and perinatal insults. Intelligence quotient (IQ) scores are commonly used to determine whether an individual has an intellectual disability. IQ scores between 70 and 79 are in the borderline range. Scores below 67 are in the disabled range. (from Joynt, Clinical Neurology, 1992, Ch55, p28)		02.4110
P carinii Pneumonia
[description not available]		04.690
Pneumonia, Pneumocystis
A pulmonary disease in humans occurring in immunodeficient or malnourished patients or infants, characterized by DYSPNEA, tachypnea, and HYPOXEMIA. Pneumocystis pneumonia is a frequently seen opportunistic infection in AIDS. It is caused by the fungus PNEUMOCYSTIS JIROVECII. The disease is also found in other MAMMALS where it is caused by related species of Pneumocystis.		04.690
Emesis
[description not available]		014.424228
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.		014.624630
Vomiting
The forcible expulsion of the contents of the STOMACH through the MOUTH.		014.424228
Ewing Sarcoma
[description not available]		010.04315
Neutropenia
A decrease in the number of NEUTROPHILS found in the blood.		018.754223
Sarcoma, Ewing
A malignant tumor of the bone which always arises in the medullary tissue, occurring more often in cylindrical bones. The tumor occurs usually before the age of 20, about twice as frequently in males as in females.		112.04315
Angioblastic Meningioma
[description not available]		06.19111
Meningioma
A relatively common neoplasm of the CENTRAL NERVOUS SYSTEM that arises from arachnoidal cells. The majority are well differentiated vascular tumors which grow slowly and have a low potential to be invasive, although malignant subtypes occur. Meningiomas have a predilection to arise from the parasagittal region, cerebral convexity, sphenoidal ridge, olfactory groove, and SPINAL CANAL. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2056-7)		06.19111
Glioblastoma with Sarcomatous Component
[description not available]		010.76314
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)		112.76314
Carcinoma, Anaplastic
[description not available]		09.67372
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.		09.67372
Carcinoma, Small Cell Lung
[description not available]		09.49144
Small Cell Lung Carcinoma
A form of highly malignant lung cancer that is composed of small ovoid cells (SMALL CELL CARCINOMA).		111.49144
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).		09.3131
Kaposi Disease
[description not available]		02.4920
Xeroderma Pigmentosum
A rare, pigmentary, and atrophic autosomal recessive disease. It is manifested as an extreme photosensitivity to ULTRAVIOLET RAYS as the result of a deficiency in the enzyme that permits excisional repair of ultraviolet-damaged DNA.		02.4920
Argentaffinoma
[description not available]		09.24162
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)		116.24162
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)		19.72151
Absence Seizure
[description not available]		010.9267
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.		010.9267
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).		03.811
Benign Cerebellar Neoplasms
[description not available]		09.03325
Arachnoidal Cerebellar Sarcoma, Circumscribed
[description not available]		013.074415
Medulloblastoma
A malignant neoplasm that may be classified either as a glioma or as a primitive neuroectodermal tumor of childhood (see NEUROECTODERMAL TUMOR, PRIMITIVE). The tumor occurs most frequently in the first decade of life with the most typical location being the cerebellar vermis. Histologic features include a high degree of cellularity, frequent mitotic figures, and a tendency for the cells to organize into sheets or form rosettes. Medulloblastoma have a high propensity to spread throughout the craniospinal intradural axis. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2060-1)		115.074415
Leiomyosarcoma, Epithelioid
[description not available]		07.4792
Cancer of the Uterus
[description not available]		07.7283
Leiomyosarcoma
A sarcoma containing large spindle cells of smooth muscle. Although it rarely occurs in soft tissue, it is common in the viscera. It is the most common soft tissue sarcoma of the gastrointestinal tract and uterus. The median age of patients is 60 years. (From Dorland, 27th ed; Holland et al., Cancer Medicine, 3d ed, p1865)		07.4792
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.		06.6573
Uterine Neoplasms
Tumors or cancer of the UTERUS.		07.7283
Adrenal Cancer
[description not available]		08.93171
Paraganglioma, Gangliocytic
[description not available]		06.3130
Pheochromocytoma, Extra-Adrenal
[description not available]		07.51111
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)		06.3130
Pheochromocytoma
A usually benign, well-encapsulated, lobular, vascular tumor of chromaffin tissue of the ADRENAL MEDULLA or sympathetic paraganglia. The cardinal symptom, reflecting the increased secretion of EPINEPHRINE and NOREPINEPHRINE, is HYPERTENSION, which may be persistent or intermittent. During severe attacks, there may be HEADACHE; SWEATING, palpitation, apprehension, TREMOR; PALLOR or FLUSHING of the face, NAUSEA and VOMITING, pain in the CHEST and ABDOMEN, and paresthesias of the extremities. The incidence of malignancy is as low as 5% but the pathologic distinction between benign and malignant pheochromocytomas is not clear. (Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1298)		07.51111
Diabetes Mellitus, Adult-Onset
[description not available]		05.1831
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.		05.1831
Brill-Symmers Disease
[description not available]		05.1221
Lymphoma, Follicular
Malignant lymphoma in which the lymphomatous cells are clustered into identifiable nodules within the LYMPH NODES. The nodules resemble to some extent the GERMINAL CENTER of lymph node follicles and most likely represent neoplastic proliferation of lymph node-derived follicular center B-LYMPHOCYTES.		05.1221
Leukemia, Plasmacytic
[description not available]		02.4110
Leukemia, Plasma Cell
A rare, aggressive variant of MULTIPLE MYELOMA characterized by the circulation of excessive PLASMA CELLS in the peripheral blood. It can be a primary manifestation of multiple myeloma or develop as a terminal complication during the disease.		02.4110
Kidney Diseases
Pathological processes of the KIDNEY or its component tissues.		05.1431
Anaplastic Ependymoma
[description not available]		011.652510
Ependymoma
Glioma derived from EPENDYMOGLIAL CELLS that tend to present as malignant intracranial tumors in children and as benign intraspinal neoplasms in adults. It may arise from any level of the ventricular system or central canal of the spinal cord. Intracranial ependymomas most frequently originate in the FOURTH VENTRICLE and histologically are densely cellular tumors which may contain ependymal tubules and perivascular pseudorosettes. Spinal ependymomas are usually benign papillary or myxopapillary tumors. (From DeVita et al., Principles and Practice of Oncology, 5th ed, p2018; Escourolle et al., Manual of Basic Neuropathology, 2nd ed, pp28-9)		113.652510
Gastrointestinal Stromal Neoplasm
[description not available]		02.610
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).		14.610
(pPNET) Peripheral Primitive Neuroectodermal Tumors
[description not available]		05.05100
Neuroectodermal Tumors, Primitive, Peripheral
A group of highly cellular primitive round cell neoplasms which occur extracranially in soft tissue and bone and are derived from embryonal neural crest cells. These tumors occur primarily in children and adolescents and share a number of characteristics with EWING SARCOMA.		17.05100
Acid Aspiration Syndrome
[description not available]		02.4110
Pneumonia, Aspiration
A type of lung inflammation resulting from the aspiration of food, liquid, or gastric contents into the upper RESPIRATORY TRACT.		02.4110
Diffuse Mixed Small and Large Cell Lymphoma
[description not available]		08.47162
Lymphoma, Non-Hodgkin
Any of a group of malignant tumors of lymphoid tissue that differ from HODGKIN DISEASE, being more heterogeneous with respect to malignant cell lineage, clinical course, prognosis, and therapy. The only common feature among these tumors is the absence of giant REED-STERNBERG CELLS, a characteristic of Hodgkin's disease.		08.47162
Chronic Illness
[description not available]		06.2491
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).		06.2491
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.		08.2991
Injuries, Radiation
[description not available]		010.5243
2019 Novel Coronavirus Disease
[description not available]		09.55128
Recrudescence
[description not available]		016.026833
Cancer of Intestines
[description not available]		07.07132
Intestinal Neoplasms
Tumors or cancer of the INTESTINES.		07.07132
Cancer, Second Primary
[description not available]		09.21262
Chronic Kidney Failure
[description not available]		03.5240
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.		03.5240
Chondrosarcoma
A slowly growing malignant neoplasm derived from cartilage cells, occurring most frequently in pelvic bones or near the ends of long bones, in middle-aged and old people. Most chondrosarcomas arise de novo, but some may develop in a preexisting benign cartilaginous lesion or in patients with ENCHONDROMATOSIS. (Stedman, 25th ed)		02.6620
Carcinoma, Squamous Cell of Head and Neck
[description not available]		02.610
Cancer of Head
[description not available]		012.672625
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.		02.610
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)		012.672625
Dysplastic Nevus Syndrome, Hereditary
[description not available]		05.7461
Behavior Disorders
[description not available]		03.0120
Mental Disorders
Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function.		03.0120
EBV Infections
[description not available]		03.830
Antibody Deficiency Syndrome
[description not available]		02.610
Duncan Disease
[description not available]		02.5820
Immunologic Deficiency Syndromes
Syndromes in which there is a deficiency or defect in the mechanisms of immunity, either cellular or humoral.		02.610
Lymphoproliferative Disorders
Disorders characterized by proliferation of lymphoid tissue, general or unspecified.		02.5820
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).		03.830
Cancer of Ovary
[description not available]		06.21121
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.		18.21121
Cancer of Kidney
[description not available]		011.692113
Adenoma Sebaceum
Facial ANGIOFIBROMA in tuberous sclerosis		02.610
Kidney Neoplasms
Tumors or cancers of the KIDNEY.		011.692113
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
Cognitive Decline
[description not available]		03.4760
Age-Related Memory Disorders
[description not available]		03.1140
Memory Disorders
Disturbances in registering an impression, in the retention of an acquired impression, or in the recall of an impression. Memory impairments are associated with DEMENTIA; CRANIOCEREBRAL TRAUMA; ENCEPHALITIS; ALCOHOLISM (see also ALCOHOL AMNESTIC DISORDER); SCHIZOPHRENIA; and other conditions.		03.1140
Cognitive Dysfunction
Diminished or impaired mental and/or intellectual function.		03.4760
Cortical Lewy Body Disease
[description not available]		02.610
Lewy Body Disease
A neurodegenerative disease characterized by dementia, mild parkinsonism, and fluctuations in attention and alertness. The neuropsychiatric manifestations tend to precede the onset of bradykinesia, MUSCLE RIGIDITY, and other extrapyramidal signs. DELUSIONS and visual HALLUCINATIONS are relatively frequent in this condition. Histologic examination reveals LEWY BODIES in the CEREBRAL CORTEX and BRAIN STEM. SENILE PLAQUES and other pathologic features characteristic of ALZHEIMER DISEASE may also be present. (From Neurology 1997;48:376-380; Neurology 1996;47:1113-1124)		02.610
Neoplastic Processes
The pathological mechanisms and forms taken by tissue during degeneration into a neoplasm and its subsequent activity.		03.0120
Ataxia Telangiectasia Syndrome
[description not available]		02.610
Ataxia Telangiectasia
An autosomal recessive inherited disorder characterized by choreoathetosis beginning in childhood, progressive CEREBELLAR ATAXIA; TELANGIECTASIS of CONJUNCTIVA and SKIN; DYSARTHRIA; B- and T-cell immunodeficiency, and RADIOSENSITIVITY to IONIZING RADIATION. Affected individuals are prone to recurrent sinobronchopulmonary infections, lymphoreticular neoplasms, and other malignancies. Serum ALPHA-FETOPROTEINS are usually elevated. (Menkes, Textbook of Child Neurology, 5th ed, p688) The gene for this disorder (ATM) encodes a cell cycle checkpoint protein kinase and has been mapped to chromosome 11 (11q22-q23).		02.610
Depression
Depressive states usually of moderate intensity in contrast with MAJOR DEPRESSIVE DISORDER present in neurotic and psychotic disorders.		08.3250
Carcinoma, Large Cell
A tumor of undifferentiated (anaplastic) cells of large size. It is usually bronchogenic. (From Dorland, 27th ed)		02.8230
Adenohypophyseal Diseases
[description not available]		02.610
Pituitary Diseases
Disorders involving either the ADENOHYPOPHYSIS or the NEUROHYPOPHYSIS. These diseases usually manifest as hypersecretion or hyposecretion of PITUITARY HORMONES. Neoplastic pituitary masses can also cause compression of the OPTIC CHIASM and other adjacent structures.		02.610
Cardiovascular Diseases
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.		07.9654
C gattii Infection
[description not available]		03.4820
Cryptococcosis
Fungal infection caused by genus CRYPTOCOCCUS.		03.4820
Pleural Effusion
Presence of fluid in the pleural cavity resulting from excessive transudation or exudation from the pleural surfaces. It is a sign of disease and not a diagnosis in itself.		02.6120
Genetic Predisposition
[description not available]		07.91111
Brain Disorders
[description not available]		05.5390
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.		17.5390
Adrenocorticotropic Hormone, Inappropriate Secretion
[description not available]		06.97110
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.		06.97110
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.		02.8930
Muscular Weakness
[description not available]		02.830
Muscle Weakness
A vague complaint of debility, fatigue, or exhaustion attributable to weakness of various muscles. The weakness can be characterized as subacute or chronic, often progressive, and is a manifestation of many muscle and neuromuscular diseases. (From Wyngaarden et al., Cecil Textbook of Medicine, 19th ed, p2251)		02.830
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.		02.9130
Benign Supratentorial Neoplasms
[description not available]		012.234415
Brain Stem Neoplasms, Primary
[description not available]		012.844114
DIPG Brain Tumors
[description not available]		07.1452
Diffuse Intrinsic Pontine Glioma
A rare, aggressive brain tumor that forms in the GLIAL CELLS in the PONS.		19.1452
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.		114.844114
Drug Refractory Epilepsy
[description not available]		02.2510
Extravascular Hemolysis
[description not available]		02.2510
Hemolysis
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.		02.2510
Cytomegalic Inclusion Disease
[description not available]		06.66111
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.		18.66111
Cytomegalovirus
A genus of the family HERPESVIRIDAE, subfamily BETAHERPESVIRINAE, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS.		010.6961
Metastase
[description not available]		018.0310541
Neoplasm Metastasis
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.		120.0310541
Lung Adenocarcinoma
[description not available]		02.8430
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.		02.8430
Blood Pressure, High
[description not available]		06.2771
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.		06.2771
Proteinuria
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.		04.2430
Brain Swelling
[description not available]		09.15124
Aura
[description not available]		06.4491
Bilateral Headache
[description not available]		05.8112
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)		09.15124
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)		06.4491
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.		05.8112
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)		04.4241
Adenocarcinoma, Basal Cell
[description not available]		07.46171
Barrett Epithelium
[description not available]		02.2510
Cancer of Esophagus
[description not available]		05.3941
Adenocarcinoma
A malignant epithelial tumor with a glandular organization.		07.46171
Barrett Esophagus
A condition with damage to the lining of the lower ESOPHAGUS resulting from chronic acid reflux (ESOPHAGITIS, REFLUX). Through the process of metaplasia, the squamous cells are replaced by a columnar epithelium with cells resembling those of the INTESTINE or the salmon-pink mucosa of the STOMACH. Barrett's columnar epithelium is a marker for severe reflux and precursor to ADENOCARCINOMA of the esophagus.		02.2510
Esophageal Neoplasms
Tumors or cancer of the ESOPHAGUS.		05.3941
Cancer of the Retina
[description not available]		02.5220
Cancer of Eye
[description not available]		09.18104
Anxiety
Feelings or emotions of dread, apprehension, and impending disaster but not disabling as with ANXIETY DISORDERS.		07.6320
Diarrheogenic Islet Cell Tumor
[description not available]		02.2510
ACTH-Producing Pituitary Adenoma
[description not available]		07.58180
Necrosis
The death of cells in an organ or tissue due to disease, injury or failure of the blood supply.		010.66284
Desmoplastic Small Cell Tumor
[description not available]		02.8530
Desmoplastic Small Round Cell Tumor
A rare, aggressive soft tissue sarcoma that primarily affects adolescents and young adults. It is most commonly found in the abdomen.		14.8530
Infections, Coronavirus
[description not available]		04.9921
Pneumonia, Viral
Inflammation of the lung parenchyma that is caused by a viral infection.		04.9921
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).		04.9921
Spinal Neoplasms
New abnormal growth of tissue in the SPINE.		04.4980
Astrocytosis
[description not available]		02.2510
Anal Cancer
[description not available]		02.520
Anus Neoplasms
Tumors or cancer of the ANAL CANAL.		02.520
Orphan Diseases
Rare diseases that have not been well studied.		03.520
Central Diabetes Insipidus
[description not available]		02.8730
Diabetes Insipidus, Neurogenic
A genetic or acquired polyuric disorder caused by a deficiency of VASOPRESSINS secreted by the NEUROHYPOPHYSIS. Clinical signs include the excretion of large volumes of dilute URINE; HYPERNATREMIA; THIRST; and polydipsia. Etiologies include HEAD TRAUMA; surgeries and diseases involving the HYPOTHALAMUS and the PITUITARY GLAND. This disorder may also be caused by mutations of genes such as ARVP encoding vasopressin and its corresponding neurophysin (NEUROPHYSINS).		02.8730
Diffuse Large B-Cell Lymphoma
[description not available]		04.580
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.		04.580
Intradural-Extramedullary Spinal Cord Neoplasms
[description not available]		010.62274
Spinal Cord Neoplasms
Benign and malignant neoplasms which occur within the substance of the spinal cord (intramedullary neoplasms) or in the space between the dura and spinal cord (intradural extramedullary neoplasms). The majority of intramedullary spinal tumors are primary CNS neoplasms including ASTROCYTOMA; EPENDYMOMA; and LIPOMA. Intramedullary neoplasms are often associated with SYRINGOMYELIA. The most frequent histologic types of intradural-extramedullary tumors are MENINGIOMA and NEUROFIBROMA.		112.62274
Multiple Primary Neoplasms
[description not available]		04.02130
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.		07.6375
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.		02.3110
Allergic Reaction
[description not available]		02.7830
Hypersensitivity
Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen.		07.7830
Neoplasms, Bronchial
[description not available]		04.3840
Bronchial Neoplasms
Tumors or cancer of the BRONCHI.		04.3840
Attachment Loss, Periodontal
[description not available]		04.6211
Chemical Dependence
[description not available]		04.6211
Cerebral Infarction, Middle Cerebral Artery
[description not available]		04.9421
Osteoarthritis of Knee
[description not available]		04.6211
Deafness, Transitory
[description not available]		04.6211
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.		04.6211
Complications of Diabetes Mellitus
[description not available]		07.9464
Acute Kidney Failure
[description not available]		07.9254
Fatty Liver, Nonalcoholic
[description not available]		04.6211
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.		04.9621
Ancylostomiasis
Infection of humans or animals with hookworms of the genus ANCYLOSTOMA. Characteristics include anemia, dyspepsia, eosinophilia, and abdominal swelling.		04.6211
Auricular Fibrillation
[description not available]		04.6211
Bladder Disorder, Neurogenic
[description not available]		04.6211
Acute Brain Injuries
[description not available]		05.422
Carcinoma, Epidermoid
[description not available]		05.2941
Cerebral Ischemia
[description not available]		04.9421
Caries, Dental
[description not available]		04.6211
Alloxan Diabetes
[description not available]		04.6211
Fistula
Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body.		04.6211
Cancer of Gastrointestinal Tract
[description not available]		08.3973
Focal Segmental Glomerulosclerosis
[description not available]		04.6211
Cardiac Failure
[description not available]		07.7444
Bleeding
[description not available]		04.7821
Hepatocellular Carcinoma
[description not available]		011.9952
Infections, Klebsiella
[description not available]		04.6211
Cirrhosis, Liver
[description not available]		04.921
Liver Dysfunction
[description not available]		04.8621
Mitral Incompetence
[description not available]		04.6211
Kahler Disease
[description not available]		05.0731
Cardiomyopathies, Primary
[description not available]		05.3522
Morbid Obesity
[description not available]		04.8221
Arthritis, Degenerative
[description not available]		04.6211
Pocket, Periodontal
[description not available]		04.6211
Pericementitis
[description not available]		04.6211
Condition, Preneoplastic
[description not available]		04.8421
Cancer of Prostate
[description not available]		08.71105
Embolism, Pulmonary
[description not available]		06.2243
Acute Respiratory Distress Syndrome
[description not available]		04.6211
Linear Skull Fracture
[description not available]		04.6211
Cancer of Stomach
[description not available]		014.352522
Nicotine Addiction
[description not available]		04.6211
Zoonoses
Diseases of non-human animals that may be transmitted to HUMANS or may be transmitted from humans to non-human animals.		04.8421
Coxarthrosis
[description not available]		04.6211
Injury, Ischemia-Reperfusion
[description not available]		07.7444
MPTP Neurotoxicity Syndrome
[description not available]		04.6211
Shoulder Injuries
Injuries involving the SHOULDERS and SHOULDER JOINT.		04.6211
Hemorrhage, Gingival
[description not available]		04.6211
Acute Disease
Disease having a short and relatively severe course.		08.34102
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.		04.6211
Biliary Tract Diseases
Diseases in any part of the BILIARY TRACT including the BILE DUCTS and the GALLBLADDER.		04.6211
Urinary Bladder, Neurogenic
Dysfunction of the URINARY BLADDER due to disease of the central or peripheral nervous system pathways involved in the control of URINATION. This is often associated with SPINAL CORD DISEASES, but may also be caused by BRAIN DISEASES or PERIPHERAL NERVE DISEASES.		04.6211
Brain Injuries
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.		05.422
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)		05.2941
Brain Ischemia
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.		04.9421
Dental Caries
Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp.		04.6211
Diabetes Mellitus
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.		04.8621
Gingival Hemorrhage
The flowing of blood from the marginal gingival area, particularly the sulcus, seen in such conditions as GINGIVITIS, marginal PERIODONTITIS, injury, and ASCORBIC ACID DEFICIENCY.		04.6211
Glomerulosclerosis, Focal Segmental
A clinicopathological syndrome or diagnostic term for a type of glomerular injury that has multiple causes, primary or secondary. Clinical features include PROTEINURIA, reduced GLOMERULAR FILTRATION RATE, and EDEMA. Kidney biopsy initially indicates focal segmental glomerular consolidation (hyalinosis) or scarring which can progress to globally sclerotic glomeruli leading to eventual KIDNEY FAILURE.		04.6211
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.		07.7444
Hemorrhage
Bleeding or escape of blood from a vessel.		04.7821
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.		18.9952
Ischemia
A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.		04.6211
Klebsiella Infections
Infections with bacteria of the genus KLEBSIELLA.		04.6211
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.		04.921
Liver Diseases
Pathological processes of the LIVER.		04.8621
Mitral Valve Insufficiency
Backflow of blood from the LEFT VENTRICLE into the LEFT ATRIUM due to imperfect closure of the MITRAL VALVE. This can lead to mitral valve regurgitation.		04.6211
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.		05.0731
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).		05.3522
Obesity, Morbid
The condition of weighing two, three, or more times the ideal weight, so called because it is associated with many serious and life-threatening disorders. In the BODY MASS INDEX, morbid obesity is defined as having a BMI greater than 40.0 kg/m2.		04.8221
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.		04.6211
Periodontal Pocket
An abnormal extension of a gingival sulcus accompanied by the apical migration of the epithelial attachment and bone resorption.		04.6211
Periodontitis
Inflammation and loss of connective tissues supporting or surrounding the teeth. This may involve any part of the PERIODONTIUM. Periodontitis is currently classified by disease progression (CHRONIC PERIODONTITIS; AGGRESSIVE PERIODONTITIS) instead of age of onset. (From 1999 International Workshop for a Classification of Periodontal Diseases and Conditions, American Academy of Periodontology)		04.6211
Precancerous Conditions
Pathological conditions that tend eventually to become malignant.		04.8421
Prostatic Neoplasms
Tumors or cancer of the PROSTATE.		110.71105
Pulmonary Embolism
Blocking of the PULMONARY ARTERY or one of its branches by an EMBOLUS.		06.2243
Respiratory Distress Syndrome
A syndrome characterized by progressive life-threatening RESPIRATORY INSUFFICIENCY in the absence of known LUNG DISEASES, usually following a systemic insult such as surgery or major TRAUMA.		04.6211
Stomach Neoplasms
Tumors or cancer of the STOMACH.		014.352522
Tobacco Use Disorder
Tobacco used to the detriment of a person's health or social functioning. Tobacco dependence is included.		04.6211
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.		05.2821
Osteoarthritis, Hip
Noninflammatory degenerative disease of the hip joint which usually appears in late middle or old age. It is characterized by growth or maturational disturbances in the femoral neck and head, as well as acetabular dysplasia. A dominant symptom is pain on weight-bearing or motion.		04.6211
Reperfusion Injury
Adverse functional, metabolic, or structural changes in tissues that result from the restoration of blood flow to the tissue (REPERFUSION) following ISCHEMIA.		07.7444
Substance-Related Disorders
Disorders related to substance use or abuse.		04.6211
Infarction, Middle Cerebral Artery
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.		04.9421
Osteoarthritis, Knee
Noninflammatory degenerative disease of the knee joint consisting of three large categories: conditions that block normal synchronous movement, conditions that produce abnormal pathways of motion, and conditions that cause stress concentration resulting in changes to articular cartilage. (Crenshaw, Campbell's Operative Orthopaedics, 8th ed, p2019)		04.6211
Hearing Loss
A general term for the complete or partial loss of the ability to hear from one or both ears.		04.6211
Lipid Metabolism Disorders
Pathological conditions resulting from abnormal anabolism or catabolism of lipids in the body.		04.6211
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.		07.9254
Non-alcoholic Fatty Liver Disease
Fatty liver finding without excessive ALCOHOL CONSUMPTION.		04.6211
Acquired Nephrogenic Diabetes Insipidus
[description not available]		02.3110
Interstitial Nephritis
[description not available]		07.3110
Nephritis, Interstitial
Inflammation of the interstitial tissue of the kidney. This term is generally used for primary inflammation of KIDNEY TUBULES and/or surrounding interstitium. For primary inflammation of glomerular interstitium, see GLOMERULONEPHRITIS. Infiltration of the inflammatory cells into the interstitial compartment results in EDEMA, increased spaces between the tubules, and tubular renal dysfunction.		02.3110
B-Cell Chronic Lymphocytic Leukemia
[description not available]		02.2510
Leukemia, Lymphocytic, Chronic, B-Cell
A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.		02.2510
T-Cell Lymphoma
[description not available]		07.7220
Lymphoma, T-Cell
A group of heterogeneous lymphoid tumors representing malignant transformations of T-lymphocytes.		02.7220
Pancytopenia
Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets.		07.2781
Hepatitis B Virus Infection
[description not available]		03.3260
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.		03.3260
Body Weight
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.		010.91100
Disbacteriosis
[description not available]		02.2510
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.		05.6532
Neoplasms, Pleural
[description not available]		05.0831
Hemangiopericytoma
A tumor composed of spindle cells with a rich vascular network, which apparently arises from pericytes, cells of smooth muscle origin that lie around small vessels. Benign and malignant hemangiopericytomas exist, and the rarity of these lesions has led to considerable confusion in distinguishing between benign and malignant variants. (From Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1364)		03.7530
Solitary Fibrous Tumors
Rare neoplasms of mesenchymal origin, usually benign, and most commonly involving the PLEURA (see SOLITARY FIBROUS TUMOR, PLEURAL). They also are found in extrapleural sites.		04.4340
Benign Infratentorial Neoplasms
[description not available]		02.5720
Cancer of Duodenum
[description not available]		03.711
Cancer of Gallbladder
[description not available]		03.711
Gallbladder Neoplasms
Tumors or cancer of the gallbladder.		03.711
Fibrosarcoma
A sarcoma derived from deep fibrous tissue, characterized by bundles of immature proliferating fibroblasts with variable collagen formation, which tends to invade locally and metastasize by the bloodstream. (Stedman, 25th ed)		03.7930
Hypothermia, Accidental
[description not available]		02.3110
Hypothermia
Lower than normal body temperature, especially in warm-blooded animals.		02.3110
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)		08.24294
Cells, Neoplasm Circulating
[description not available]		04.9421
Adrenal Cortex Cancer
[description not available]		02.5920
Adrenal Cortex Neoplasms
Tumors or cancers of the ADRENAL CORTEX.		02.5920
Aerobic Glycolysis, Oncologic
[description not available]		02.3110
Angiosarcoma
[description not available]		02.3110
Hemangiosarcoma
A rare malignant neoplasm characterized by rapidly proliferating, extensively infiltrating, anaplastic cells derived from blood vessels and lining irregular blood-filled or lumpy spaces. (Stedman, 25th ed)		02.3110
Aging
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.		04.4270
Elevated ICP (Intracranial Pressure)
[description not available]		03.1850
Apraxia
[description not available]		02.3110
Apraxias
A group of cognitive disorders characterized by the inability to perform previously learned skills that cannot be attributed to deficits of motor or sensory function. The two major subtypes of this condition are ideomotor (see APRAXIA, IDEOMOTOR) and ideational apraxia, which refers to loss of the ability to mentally formulate the processes involved with performing an action. For example, dressing apraxia may result from an inability to mentally formulate the act of placing clothes on the body. Apraxias are generally associated with lesions of the dominant PARIETAL LOBE and supramarginal gyrus. (From Adams et al., Principles of Neurology, 6th ed, pp56-7)		02.3110
Intracranial Hypertension
Increased pressure within the cranial vault. This may result from several conditions, including HYDROCEPHALUS; BRAIN EDEMA; intracranial masses; severe systemic HYPERTENSION; PSEUDOTUMOR CEREBRI; and other disorders.		03.1850
Symptom Cluster
[description not available]		03.7330
Syndrome
A characteristic symptom complex.		08.7330
Diffuse Parenchymal Lung Disease
[description not available]		04.5551
Atherogenesis
[description not available]		03.711
Atheroma
[description not available]		03.711
Idiopathic Parkinson Disease
[description not available]		03.9121
Infections, Staphylococcal
[description not available]		03.711
Bacterial Endocarditides
[description not available]		03.711
Endocarditis, Bacterial
Inflammation of the ENDOCARDIUM caused by BACTERIA that entered the bloodstream. The strains of bacteria vary with predisposing factors, such as CONGENITAL HEART DEFECTS; HEART VALVE DISEASES; HEART VALVE PROSTHESIS IMPLANTATION; or intravenous drug use.		03.711
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)		03.9121
Staphylococcal Infections
Infections with bacteria of the genus STAPHYLOCOCCUS.		03.711
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.		04.5551
Atherosclerosis
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.		03.711
Amphetamine Abuse
[description not available]		02.3110
Amphetamine-Related Disorders
Disorders related or resulting from use of amphetamines.		02.3110
Diabetic Cardiomyopathies
Diabetes complications in which VENTRICULAR REMODELING in the absence of CORONARY ATHEROSCLEROSIS and hypertension results in cardiac dysfunctions, typically LEFT VENTRICULAR DYSFUNCTION. The changes also result in myocardial hypertrophy, myocardial necrosis and fibrosis, and collagen deposition due to impaired glucose tolerance.		03.2310
Bacterial Disease
[description not available]		02.4720
Bacterial Infections
Infections by bacteria, general or unspecified.		02.4720
Anemia
A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.		012.072322
Deep Vein Thrombosis
[description not available]		04.7132
Brain Thrombosis
[description not available]		02.1510
Venous Thrombosis
The formation or presence of a blood clot (THROMBUS) within a vein.		04.7132
Acute Stress Disorders
[description not available]		02.1510
Depression, Endogenous
[description not available]		02.5520
Depressive Disorder
An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent.		02.5520
Stress Disorders, Traumatic, Acute
A class of traumatic stress disorders that is characterized by the significant dissociative states seen immediately after overwhelming trauma. By definition it cannot last longer than 1 month, if it persists, a diagnosis of post-traumatic stress disorder (STRESS DISORDERS, POST-TRAUMATIC) is more appropriate.		02.1510
Chromosomal Translocation
[description not available]		02.830
African Sleeping Sickness
[description not available]		02.1510
Trypanosomiasis, African
A disease endemic among people and animals in Central Africa. It is caused by various species of trypanosomes, particularly T. gambiense and T. rhodesiense. Its second host is the TSETSE FLY. Involvement of the central nervous system produces African sleeping sickness. Nagana is a rapidly fatal trypanosomiasis of horses and other animals.		02.1510
Hematologic Malignancies
[description not available]		04.5251
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.		16.5251
Adenoma, alpha-Cell
[description not available]		02.1510
Icterus
[description not available]		02.5220
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.		02.5220
Genome Instability
[description not available]		03.0540
CACH Syndrome
[description not available]		03.7330
Rhabdomyoma
A benign tumor derived from striated muscle. It is extremely rare, generally occurring in the tongue, neck muscles, larynx, uvula, nasal cavity, axilla, vulva, and heart. These tumors are treated by simple excision. (Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1354)		03.5611
Carditis
[description not available]		02.1510
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.		02.1510
Histoplasma capsulatum Infection
[description not available]		02.1310
Opportunistic Infections
An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression.		010.68110
Fungal Lung Diseases
[description not available]		02.1310
Blastomycosis, North American
[description not available]		02.1310
Blastomycosis
A fungal infection that may appear in two forms: 1, a primary lesion characterized by the formation of a small cutaneous nodule and small nodules along the lymphatics that may heal within several months; and 2, chronic granulomatous lesions characterized by thick crusts, warty growths, and unusual vascularity and infection in the middle or upper lobes of the lung.		07.1310
Histoplasmosis
Infection resulting from exposure to the fungus HISTOPLASMA. It is worldwide in distribution and particularly common in the central and eastern states, especially areas around the Ohio and Mississippi River valleys.		07.1310
Rhabdomyosarcoma 2
[description not available]		02.7830
Rhabdomyosarcoma, Alveolar
A form of RHABDOMYOSARCOMA occurring mainly in adolescents and young adults, affecting muscles of the extremities, trunk, orbital region, etc. It is extremely malignant, metastasizing widely at an early stage. Few cures have been achieved and the prognosis is poor. Alveolar refers to its microscopic appearance simulating the cells of the respiratory alveolus. (Holland et al., Cancer Medicine, 3d ed, p2188)		14.7830
Polyploid
[description not available]		02.5420
Carcinomatous Meningitis
[description not available]		04.0850
Colicky Pain
[description not available]		03.0610
Abdominal Pain
Sensation of discomfort, distress, or agony in the abdominal region.		03.0610
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.		04.0850
Stomatitis, Vesicular
[description not available]		02.1510
Action Tremor
[description not available]		02.1710
Tremor
Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of CEREBELLAR DISEASES, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of PARKINSON DISEASE.		02.1710
Leukocytopenia
[description not available]		09.821412
Leukopenia
A decrease in the number of LEUKOCYTES in a blood sample below the normal range (LEUKOCYTE COUNT less than 4000).		09.821412
Breast Cancer, Male
[description not available]		04.8221
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.		04.8221
Anaplasia
Loss of structural differentiation and useful function of neoplastic cells.		03.8621
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).		02.1510
Benign Optic Nerve Neoplasm
[description not available]		03.1850
Ganglioglioma
Rare indolent tumors comprised of neoplastic glial and neuronal cells which occur primarily in children and young adults. Benign lesions tend to be associated with long survival unless the tumor degenerates into a histologically malignant form. They tend to occur in the optic nerve and white matter of the brain and spinal cord.		04.9580
Neoplasms, Skull
[description not available]		02.1710
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.		02.1710
Connective and Soft Tissue Neoplasms
[description not available]		02.1510
Cerebral Primitive Neuroectodermal Tumor
[description not available]		011.522210
Neuroectodermal Tumors, Primitive
A group of malignant tumors of the nervous system that feature primitive cells with elements of neuronal and/or glial differentiation. Use of this term is limited by some authors to central nervous system tumors and others include neoplasms of similar origin which arise extracranially (i.e., NEUROECTODERMAL TUMORS, PRIMITIVE, PERIPHERAL). This term is also occasionally used as a synonym for MEDULLOBLASTOMA. In general, these tumors arise in the first decade of life and tend to be highly malignant. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2059)		011.522210
Blood Loss, Postoperative
[description not available]		02.5420
Cyst
[description not available]		02.1710
Disseminated Superficial Actinic Porokeratosis
[description not available]		07.1710
Porokeratosis
A heritable disorder of faulty keratinization characterized by the proliferation of abnormal clones of KERATINOCYTES and lesions showing varying atrophic patches surrounded by an elevated, keratotic border. These keratotic lesions can progress to overt cutaneous neoplasm. Several clinical variants are recognized, including porokeratosis of Mibelli, linear porokeratosis, disseminated superficial actinic porokeratosis, palmoplantar porokeratosis, and punctate porokeratosis.		07.1710
Minimal Disease, Residual
[description not available]		07.44124
Chromosomal Duplication
[description not available]		02.1710
Autoimmune Chronic Hepatitis
[description not available]		03.0910
Hepatitis, Autoimmune
A chronic self-perpetuating hepatocellular INFLAMMATION of unknown cause, usually with HYPERGAMMAGLOBULINEMIA and serum AUTOANTIBODIES.		03.0910
Apoplexy
[description not available]		02.5920
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)		07.5920
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.		02.4620
Cancer of Pelvis
[description not available]		02.5220
Experimental Radiation Injuries
[description not available]		02.5920
Cushing's Syndrome
[description not available]		04.3320
Ectopic ACTH Syndrome
[description not available]		04.3420
ACTH Syndrome, Ectopic
Symptom complex due to ACTH production by non-pituitary neoplasms.		04.3420
Cushing Syndrome
A condition caused by prolonged exposure to excess levels of cortisol (HYDROCORTISONE) or other GLUCOCORTICOIDS from endogenous or exogenous sources. It is characterized by upper body OBESITY; OSTEOPOROSIS; HYPERTENSION; DIABETES MELLITUS; HIRSUTISM; AMENORRHEA; and excess body fluid. Endogenous Cushing syndrome or spontaneous hypercortisolism is divided into two groups, those due to an excess of ADRENOCORTICOTROPIN and those that are ACTH-independent.		04.3320
Bilateral Wilms Tumor
[description not available]		02.5420
Wilms Tumor
A malignant kidney tumor, caused by the uncontrolled multiplication of renal stem (blastemal), stromal (STROMAL CELLS), and epithelial (EPITHELIAL CELLS) elements. However, not all three are present in every case. Several genes or chromosomal areas have been associated with Wilms tumor which is usually found in childhood as a firm lump in a child's side or ABDOMEN.		19.5420
Blood Diseases
[description not available]		010.54249
Hematologic Diseases
Disorders of the blood and blood forming tissues.		010.54249
Fibromatosis
[description not available]		03.0910
Fasting Hypoglycemia
HYPOGLYCEMIA expressed in the postabsorptive state, after prolonged FASTING, or an overnight fast.		03.0910
Fibroma
A benign tumor of fibrous or fully developed connective tissue.		03.0910
Hypoglycemia
A syndrome of abnormally low BLOOD GLUCOSE level. Clinical hypoglycemia has diverse etiologies. Severe hypoglycemia eventually lead to glucose deprivation of the CENTRAL NERVOUS SYSTEM resulting in HUNGER; SWEATING; PARESTHESIA; impaired mental function; SEIZURES; COMA; and even DEATH.		08.0910
Infections, Salmonella
[description not available]		02.4920
Acute Myelogenous Leukemia
[description not available]		09.8176
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.		111.8176
Academic Disorder, Developmental
[description not available]		02.2110
Learning Disabilities
Conditions characterized by a significant discrepancy between an individual's perceived level of intellect and their ability to acquire new language and other cognitive skills. These may result from organic or psychological conditions. Relatively common subtypes include DYSLEXIA, DYSCALCULIA, and DYSGRAPHIA.		02.2110
Peritoneal Carcinomatosis
[description not available]		07.7754
Peritoneal Neoplasms
Tumors or cancer of the PERITONEUM.		07.7754
Adenocarcinoma Of Kidney
[description not available]		06.6573
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.		06.6573
Cancer of Digestive System
[description not available]		04.3541
Digestive System Neoplasms
Tumors or cancer of the DIGESTIVE SYSTEM.		04.3541
Nerve Pain
[description not available]		02.2110
Neuralgia
Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.		02.2110
Encephalopathy, Toxic
[description not available]		04.1830
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.		05.0931
Cancer of Muscle
[description not available]		03.4520
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
Dendritic Cell Sarcoma, Follicular
Sarcoma of FOLLICULAR DENDRITIC CELLS most often found in the lymph nodes. This rare neoplasm occurs predominately in adults.		02.2110
Aspergillus Infection
[description not available]		02.5820
Brain Abscess
A circumscribed collection of purulent exudate in the brain, due to bacterial and other infections. The majority are caused by spread of infected material from a focus of suppuration elsewhere in the body, notably the PARANASAL SINUSES, middle ear (see EAR, MIDDLE); HEART (see also ENDOCARDITIS, BACTERIAL), and LUNG. Penetrating CRANIOCEREBRAL TRAUMA and NEUROSURGICAL PROCEDURES may also be associated with this condition. Clinical manifestations include HEADACHE; SEIZURES; focal neurologic deficits; and alterations of consciousness. (Adams et al., Principles of Neurology, 6th ed, pp712-6)		07.7830
Aspergillosis
Infections with fungi of the genus ASPERGILLUS.		02.5820
Chordoma
A malignant tumor arising from the embryonic remains of the notochord. It is also called chordocarcinoma, chordoepithelioma, and notochordoma. (Dorland, 27th ed)		07.2110
Ptosis, Eyelid
[description not available]		02.4520
Diplopia
A visual symptom in which a single object is perceived by the visual cortex as two objects rather than one. Disorders associated with this condition include REFRACTIVE ERRORS; STRABISMUS; OCULOMOTOR NERVE DISEASES; TROCHLEAR NERVE DISEASES; ABDUCENS NERVE DISEASES; and diseases of the BRAIN STEM and OCCIPITAL LOBE.		02.4820
Blepharoptosis
Drooping of the upper lid due to deficient development or paralysis of the levator palpebrae muscle.		02.4520
Mixed Pineocytoma-Pineoblastoma
[description not available]		03.8940
Pinealoma
Neoplasms which originate from pineal parenchymal cells that tend to enlarge the gland and be locally invasive. The two major forms are pineocytoma and the more malignant pineoblastoma. Pineocytomas have moderate cellularity and tend to form rosette patterns. Pineoblastomas are highly cellular tumors containing small, poorly differentiated cells. These tumors occasionally seed the neuroaxis or cause obstructive HYDROCEPHALUS or Parinaud's syndrome. GERMINOMA; CARCINOMA, EMBRYONAL; GLIOMA; and other neoplasms may arise in the pineal region with germinoma being the most common pineal region tumor. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2064; Adams et al., Principles of Neurology, 6th ed, p670)		15.8940
Lymph Node Metastasis
[description not available]		08.35193
Cancer of the Vulva
[description not available]		02.4520
Cancer of the Vagina
[description not available]		02.7430
Vaginal Neoplasms
Tumors or cancer of the VAGINA.		02.7430
Vulvar Neoplasms
Tumors or cancer of the VULVA.		02.4520
Complex and Mixed Neoplasms
[description not available]		02.520
Neoplasms, Complex and Mixed
Neoplasms composed of more than one type of neoplastic tissue.		02.520
Hemangioma, Capillary
A dull red, firm, dome-shaped hemangioma, sharply demarcated from surrounding skin, usually located on the head and neck, which grows rapidly and generally undergoes regression and involution without scarring. It is caused by proliferation of immature capillary vessels in active stroma, and is usually present at birth or occurs within the first two or three months of life. (Dorland, 27th ed)		02.0810
Hypesthesia
Absent or reduced sensitivity to cutaneous stimulation.		02.0810
Lassitude
[description not available]		09.53109
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.		09.53109
Brain Ventricular Neoplasms
[description not available]		03.8840
Cafe-au-Lait Spots with Pulmonic Stenosis
[description not available]		02.7830
Neurofibromatosis 1
An autosomal dominant inherited disorder (with a high frequency of spontaneous mutations) that features developmental changes in the nervous system, muscles, bones, and skin, most notably in tissue derived from the embryonic NEURAL CREST. Multiple hyperpigmented skin lesions and subcutaneous tumors are the hallmark of this disease. Peripheral and central nervous system neoplasms occur frequently, especially OPTIC NERVE GLIOMA and NEUROFIBROSARCOMA. NF1 is caused by mutations which inactivate the NF1 gene (GENES, NEUROFIBROMATOSIS 1) on chromosome 17q. The incidence of learning disabilities is also elevated in this condition. (From Adams et al., Principles of Neurology, 6th ed, pp1014-18) There is overlap of clinical features with NOONAN SYNDROME in a syndrome called neurofibromatosis-Noonan syndrome. Both the PTPN11 and NF1 gene products are involved in the SIGNAL TRANSDUCTION pathway of Ras (RAS PROTEINS).		14.7830
Inappropriate GH Secretion Syndrome (Acromegaly)
[description not available]		03.420
Acromegaly
A condition caused by prolonged exposure to excessive HUMAN GROWTH HORMONE in adults. It is characterized by bony enlargement of the FACE; lower jaw (PROGNATHISM); hands; FEET; HEAD; and THORAX. The most common etiology is a GROWTH HORMONE-SECRETING PITUITARY ADENOMA. (From Joynt, Clinical Neurology, 1992, Ch36, pp79-80)		08.420
Community Acquired Infection
[description not available]		02.0810
Neoplasm Metastasis, Unknown Primary
[description not available]		04.3541
Carcinoma, Oat Cell
[description not available]		06.3551
Cancer of Parotid
[description not available]		02.0810
Parotid Neoplasms
Tumors or cancer of the PAROTID GLAND.		02.0810
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)		06.3551
Uveal Neoplasms
Tumors or cancer of the UVEA.		05.6361
Polyuria
Urination of a large volume of urine with an increase in urinary frequency, commonly seen in diabetes (DIABETES MELLITUS; DIABETES INSIPIDUS).		02.0810
Polydipsia
Excessive thirst manifested by excessive fluid intake. It is characteristic of many diseases such as DIABETES MELLITUS; DIABETES INSIPIDUS; and NEPHROGENIC DIABETES INSIPIDUS. The condition may be psychogenic in origin.		02.0810
B-Cell Lymphoma
[description not available]		05.8480
Lymphoma, B-Cell
A group of heterogeneous lymphoid tumors generally expressing one or more B-cell antigens or representing malignant transformations of B-lymphocytes.		05.8480
Neoplasm Seeding
The local implantation of tumor cells by contamination of instruments and surgical equipment during and after surgical resection, resulting in local growth of the cells and tumor formation.		02.4720
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.		07.520
Cancer of Nasopharynx
[description not available]		04.3641
Nasopharyngeal Neoplasms
Tumors or cancer of the NASOPHARYNX.		04.3641
Complex Partial Epilepsy
[description not available]		02.0810
Epilepsy, Complex Partial
A disorder characterized by recurrent partial seizures marked by impairment of cognition. During the seizure the individual may experience a wide variety of psychic phenomenon including formed hallucinations, illusions, deja vu, intense emotional feelings, confusion, and spatial disorientation. Focal motor activity, sensory alterations and AUTOMATISM may also occur. Complex partial seizures often originate from foci in one or both temporal lobes. The etiology may be idiopathic (cryptogenic partial complex epilepsy) or occur as a secondary manifestation of a focal cortical lesion (symptomatic partial complex epilepsy). (From Adams et al., Principles of Neurology, 6th ed, pp317-8)		02.0810
Pneumothorax, Primary Spontaneous
[description not available]		02.7830
Rupture, Spontaneous
Tear or break of an organ, vessel or other soft part of the body, occurring in the absence of external force.		02.4420
Synovioma
[description not available]		02.5220
Pneumothorax
An accumulation of air or gas in the PLEURAL CAVITY, which may occur spontaneously or as a result of trauma or a pathological process. The gas may also be introduced deliberately during PNEUMOTHORAX, ARTIFICIAL.		02.7830
Sarcoma, Synovial
A malignant neoplasm arising from tenosynovial tissue of the joints and in synovial cells of tendons and bursae. The legs are the most common site, but the tumor can occur in the abdominal wall and other trunk muscles. There are two recognized types: the monophasic (characterized by sheaths of monotonous spindle cells) and the biphasic (characterized by slit-like spaces or clefts within the tumor, lined by cuboidal or tall columnar epithelial cells). These sarcomas occur most commonly in the second and fourth decades of life. (From Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1363)		02.5220
Neurocytoma
A benign brain tumor composed of neural elements which most often arise from the SEPTUM PELLUCIDUM and the walls of the lateral ventricles. Immunohistochemistry and electron microscopy evaluations may reveal expression of neuron specific enolase and synaptophysin and cells containing microtubuli, neurosecretory granules, and presynaptic vesicles. (From Acta Med Port 1994 Feb;7(2):113-9)		02.110
Cognition Disorders
Disorders characterized by disturbances in mental processes related to learning, thinking, reasoning, and judgment.		06.16110
Brain Damage, Chronic
A condition characterized by long-standing brain dysfunction or damage, usually of three months duration or longer. Potential etiologies include BRAIN INFARCTION; certain NEURODEGENERATIVE DISORDERS; CRANIOCEREBRAL TRAUMA; ANOXIA, BRAIN; ENCEPHALITIS; certain NEUROTOXICITY SYNDROMES; metabolic disorders (see BRAIN DISEASES, METABOLIC); and other conditions.		02.5120
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.		02.5220
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.		02.110
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.		02.110
Acute Lymphoid Leukemia
[description not available]		06.592
Precursor Cell Lymphoblastic Leukemia-Lymphoma
A neoplasm characterized by abnormalities of the lymphoid cell precursors leading to excessive lymphoblasts in the marrow and other organs. It is the most common cancer in children and accounts for the vast majority of all childhood leukemias.		06.592
Lymphocytosis
Excess of normal lymphocytes in the blood or in any effusion.		03.3820
Encephalitis, Viral
Inflammation of brain parenchymal tissue as a result of viral infection. Encephalitis may occur as primary or secondary manifestation of TOGAVIRIDAE INFECTIONS; HERPESVIRIDAE INFECTIONS; ADENOVIRIDAE INFECTIONS; FLAVIVIRIDAE INFECTIONS; BUNYAVIRIDAE INFECTIONS; PICORNAVIRIDAE INFECTIONS; PARAMYXOVIRIDAE INFECTIONS; ORTHOMYXOVIRIDAE INFECTIONS; RETROVIRIDAE INFECTIONS; and ARENAVIRIDAE INFECTIONS.		02.110
Encephalitis Infection
[description not available]		02.110
Acromegaly Due To Pituitary Adenoma
[description not available]		03.8920
Flaccid Quadriplegia
[description not available]		02.110
Cacosmia
[description not available]		02.1110
Taste Disorder, Anterior Tongue
[description not available]		02.1110
Friedreich Disease
[description not available]		02.110
Friedreich Ataxia
An autosomal recessive disease, usually of childhood onset, characterized pathologically by degeneration of the spinocerebellar tracts, posterior columns, and to a lesser extent the corticospinal tracts. Clinical manifestations include GAIT ATAXIA, pes cavus, speech impairment, lateral curvature of spine, rhythmic head tremor, kyphoscoliosis, congestive heart failure (secondary to a cardiomyopathy), and lower extremity weakness. Most forms of this condition are associated with a mutation in a gene on chromosome 9, at band q13, which codes for the mitochondrial protein frataxin. (From Adams et al., Principles of Neurology, 6th ed, p1081; N Engl J Med 1996 Oct 17;335(16):1169-75) The severity of Friedreich ataxia associated with expansion of GAA repeats in the first intron of the frataxin gene correlates with the number of trinucleotide repeats. (From Durr et al, N Engl J Med 1996 Oct 17;335(16):1169-75)		02.110
Androgen-Independent Prostatic Cancer
[description not available]		04.411
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.		16.411
Brain Hemorrhage, Cerebral
[description not available]		03.8940
Cerebral Hemorrhage
Bleeding into one or both CEREBRAL HEMISPHERES including the BASAL GANGLIA and the CEREBRAL CORTEX. It is often associated with HYPERTENSION and CRANIOCEREBRAL TRAUMA.		08.8940
Chronic Insomnia
[description not available]		02.110
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.		02.110
Hyperoxia
An abnormal increase in the amount of oxygen in the tissues and organs.		02.4920
Drug-Induced Stevens Johnson Syndrome
[description not available]		02.4720
Erythema
Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of disease processes.		03.8521
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.		07.4720
Dermatitis, Radiation-Induced
[description not available]		02.110
Radiodermatitis
A cutaneous inflammatory reaction occurring as a result of exposure to ionizing radiation.		02.110
Thoracic Neoplasms
New abnormal growth of tissue in the THORAX.		03.0110
Day Blindness
[description not available]		02.7830
Adult Optic Nerve Glioma
[description not available]		03.1850
Optic Nerve Glioma
Glial cell derived tumors arising from the optic nerve, usually presenting in childhood.		15.1850
Dysmyelopoietic Syndromes
[description not available]		07.73112
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.		19.73112
Cerebral Nocardiosis
[description not available]		02.1110
Hepatic Failure
[description not available]		07.4720
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)		02.4720
Cranial Nerve V Diseases
[description not available]		02.1110
Common Bile Duct Diseases
Diseases of the COMMON BILE DUCT including the AMPULLA OF VATER and the SPHINCTER OF ODDI.		02.110
Infectious Myelitis
[description not available]		02.110
Paralysis, Legs
[description not available]		02.4620
Paraplegia
Severe or complete loss of motor function in the lower extremities and lower portions of the trunk. This condition is most often associated with SPINAL CORD DISEASES, although BRAIN DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; and MUSCULAR DISEASES may also cause bilateral leg weakness.		02.4620
Granulomatosis, Lymphomatoid
[description not available]		02.110
Carcinoid Heart Disease
Cardiac manifestation of gastrointestinal CARCINOID TUMOR that metastasizes to the liver. Substances secreted by the tumor cells, including SEROTONIN, promote fibrous plaque formation in ENDOCARDIUM and its underlying layers. These deposits cause distortion of the TRICUSPID VALVE and the PULMONARY VALVE eventually leading to STENOSIS and valve regurgitation.		03.9410
Asymptomatic Conditions
[description not available]		03.0310
Chromosome Instability Syndromes
[description not available]		02.1110
Cancer, Embryonal
[description not available]		04.9342
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.		04.9342
Chromosomal Instability
An increased tendency to acquire CHROMOSOME ABERRATIONS when various processes involved in chromosome replication, repair, or segregation are dysfunctional.		03.3820
Thromboembolism
Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.		04.7721
Bile Duct Obstruction
[description not available]		04.5650
Cholestasis
Impairment of bile flow due to obstruction in small bile ducts (INTRAHEPATIC CHOLESTASIS) or obstruction in large bile ducts (EXTRAHEPATIC CHOLESTASIS).		04.5650
Neoplasms, Nervous System
[description not available]		02.4420
Brain Hemorrhage
[description not available]		02.1110
Motor Disorders
Motor skills deficits that significantly and persistently interfere with ACTIVITIES OF DAILY LIVING appropriate to chronological age. (from DSM-5)		02.1110
Psychoses
[description not available]		02.4920
Infection, Postoperative Wound
[description not available]		02.1110
Psychotic Disorders
Disorders in which there is a loss of ego boundaries or a gross impairment in reality testing with delusions or prominent hallucinations. (From DSM-IV, 1994)		02.4920
Intracranial Hemorrhages
Bleeding within the SKULL, including hemorrhages in the brain and the three membranes of MENINGES. The escape of blood often leads to the formation of HEMATOMA in the cranial epidural, subdural, and subarachnoid spaces.		02.1110
Hyperglycemia, Postprandial
Abnormally high BLOOD GLUCOSE level after a meal.		02.5220
Hyperglycemia
Abnormally high BLOOD GLUCOSE level.		02.5220
Abdominal Epilepsy
[description not available]		02.4620
Epilepsies, Partial
Conditions characterized by recurrent paroxysmal neuronal discharges which arise from a focal region of the brain. Partial seizures are divided into simple and complex, depending on whether consciousness is unaltered (simple partial seizure) or disturbed (complex partial seizure). Both types may feature a wide variety of motor, sensory, and autonomic symptoms. Partial seizures may be classified by associated clinical features or anatomic location of the seizure focus. A secondary generalized seizure refers to a partial seizure that spreads to involve the brain diffusely. (From Adams et al., Principles of Neurology, 6th ed, pp317)		02.4620
Breathlessness
[description not available]		02.7730
Dyspnea
Difficult or labored breathing.		02.7730
Allergy, Drug
[description not available]		03.1750
Drug Hypersensitivity
Immunologically mediated adverse reactions to medicinal substances used legally or illegally.		03.1750
Central Nervous System Disease
[description not available]		04.7621
Central Nervous System Diseases
Diseases of any component of the brain (including the cerebral hemispheres, diencephalon, brain stem, and cerebellum) or the spinal cord.		04.7621
Mycosis Fungoides
A chronic, malignant T-cell lymphoma of the skin. In the late stages, the LYMPH NODES and viscera are affected.		03.8821
Adenomatous Polyposis Coli, Familial
[description not available]		03.0310
Adenomatous Polyposis Coli
A polyposis syndrome due to an autosomal dominant mutation of the APC genes (GENES, APC) on CHROMOSOME 5. The syndrome is characterized by the development of hundreds of ADENOMATOUS POLYPS in the COLON and RECTUM of affected individuals by early adulthood.		03.0310
Cancer of Paranasal Sinus
[description not available]		02.1110
Paranasal Sinus Neoplasms
Tumors or cancer of the PARANASAL SINUSES.		02.1110
Adenovirus Infections
[description not available]		02.1310
Adenoviridae Infections
Virus diseases caused by the ADENOVIRIDAE.		02.1310
Colonic Inertia
Symptom characterized by the passage of stool once a week or less.		05.0633
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.		05.0633
Delirium of Mixed Origin
[description not available]		02.1310
Leukocytosis
A transient increase in the number of leukocytes in a body fluid.		02.1310
Acute Necrotizing Encephalitis, Herpetic
[description not available]		02.5120
Delirium
A disorder characterized by CONFUSION; inattentiveness; disorientation; ILLUSIONS; HALLUCINATIONS; agitation; and in some instances autonomic nervous system overactivity. It may result from toxic/metabolic conditions or structural brain lesions. (From Adams et al., Principles of Neurology, 6th ed, pp411-2)		02.1310
Encephalitis, Herpes Simplex
An acute (or rarely chronic) inflammatory process of the brain caused by SIMPLEXVIRUS infections which may be fatal. The majority of infections are caused by human herpesvirus 1 (HERPESVIRUS 1, HUMAN) and less often by human herpesvirus 2 (HERPESVIRUS 2, HUMAN). Clinical manifestations include FEVER; HEADACHE; SEIZURES; HALLUCINATIONS; behavioral alterations; APHASIA; hemiparesis; and COMA. Pathologically, the condition is marked by a hemorrhagic necrosis involving the medial and inferior TEMPORAL LOBE and orbital regions of the FRONTAL LOBE. (From Adams et al., Principles of Neurology, 6th ed, pp751-4)		02.5120
Bile Duct Diseases
Diseases in any part of the ductal system of the BILIARY TRACT from the smallest BILE CANALICULI to the largest COMMON BILE DUCT.		02.1310
Bilirubinemia
[description not available]		02.1310
Anasarca
[description not available]		03.8621
Edema
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.		03.8621
Bone Marrow Failure
[description not available]		02.1310
Bone Marrow Diseases
Diseases involving the BONE MARROW.		06.1841
Marchiafava-Micheli Syndrome
[description not available]		02.1310
Bone Marrow Failure Disorders
Inherited or acquired diseases characterized by insufficient and/or dysplastic blood cells.		02.1310
Hemoglobinuria, Paroxysmal
A condition characterized by the recurrence of HEMOGLOBINURIA caused by intravascular HEMOLYSIS. In cases occurring upon cold exposure (paroxysmal cold hemoglobinuria), usually after infections, there is a circulating antibody which is also a cold hemolysin. In cases occurring during or after sleep (paroxysmal nocturnal hemoglobinuria), the clonal hematopoietic stem cells exhibit a global deficiency of cell membrane proteins.		02.1310
Dysembryoma
[description not available]		03.8840
Teratoma
A true neoplasm composed of a number of different types of tissue, none of which is native to the area in which it occurs. It is composed of tissues that are derived from three germinal layers, the endoderm, mesoderm, and ectoderm. They are classified histologically as mature (benign) or immature (malignant). (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1642)		03.8840
Rhabdoid Tumor
A rare but highly lethal childhood tumor found almost exclusively in infants. Histopathologically, it resembles RHABDOMYOSARCOMA but the tumor cells are not of myogenic origin. Although it arises primarily in the kidney, it may be found in other parts of the body. The rhabdoid cytomorphology is believed to be the expression of a very primitive malignant cell. (From Holland et al., Cancer Medicine, 3d ed, p2210)		04.0650
Alopecia Cicatrisata
[description not available]		03.8521
Alopecia
Absence of hair from areas where it is normally present.		03.8521
Carcinoma, Lewis Lung
A carcinoma discovered by Dr. Margaret R. Lewis of the Wistar Institute in 1951. This tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse. The tumor does not appear to be grossly hemorrhagic and the majority of the tumor tissue is a semifirm homogeneous mass. (From Cancer Chemother Rep 2 1972 Nov;(3)1:325) It is also called 3LL and LLC and is used as a transplantable malignancy.		02.7330
Neoplasm Regression, Spontaneous
Disappearance of a neoplasm or neoplastic state without the intervention of therapy.		02.1310
Clerambault Syndrome
[description not available]		02.1510
Altidudinal Hemianopia
[description not available]		02.1310
Adenohypophyseal Hyposecretion
[description not available]		02.520
Diabetes Insipidus
A disease that is characterized by frequent urination, excretion of large amounts of dilute URINE, and excessive THIRST. Etiologies of diabetes insipidus include deficiency of antidiuretic hormone (also known as ADH or VASOPRESSIN) secreted by the NEUROHYPOPHYSIS, impaired KIDNEY response to ADH, and impaired hypothalamic regulation of thirst.		02.1310
Hypopituitarism
Diminution or cessation of secretion of one or more hormones from the anterior pituitary gland (including LH; FOLLICLE STIMULATING HORMONE; SOMATOTROPIN; and CORTICOTROPIN). This may result from surgical or radiation ablation, non-secretory PITUITARY NEOPLASMS, metastatic tumors, infarction, PITUITARY APOPLEXY, infiltrative or granulomatous processes, and other conditions.		02.520
Infection
[description not available]		03.3520
Infections
Invasion of the host organism by microorganisms or their toxins or by parasites that can cause pathological conditions or diseases.		03.3520
Arthritides, Bacterial
[description not available]		02.0410
Focal Infection
An infection at a specific location that may spread to another region of the body.		02.0410
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.		02.0410
Dermatitis Medicamentosa
[description not available]		04.3541
Aplasia Pure Red Cell
[description not available]		02.0510
Pulmonary Consumption
[description not available]		02.0510
Red-Cell Aplasia, Pure
Suppression of erythropoiesis with little or no abnormality of leukocyte or platelet production.		02.0510
Tuberculosis, Pulmonary
MYCOBACTERIUM infections of the lung.		02.0510
Choked Disk
[description not available]		03.6630
Papilledema
Swelling of the OPTIC DISK, usually in association with increased intracranial pressure, characterized by hyperemia, blurring of the disk margins, microhemorrhages, blind spot enlargement, and engorgement of retinal veins. Chronic papilledema may cause OPTIC ATROPHY and visual loss. (Miller et al., Clinical Neuro-Ophthalmology, 4th ed, p175)		03.6630
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.		02.0510
Bewilderment
[description not available]		02.0510
Cancer of the Tonsil
[description not available]		02.0510
Tonsillar Neoplasms
Tumors or cancer of the PALATINE TONSIL.		02.0510
Allergic Alveolitis, Extrinsic
[description not available]		02.4520
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.		02.4520
Pachymeningitis
[description not available]		03.3420
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)		08.3420
Cancer of Endocrine Gland
[description not available]		02.0510
Endocrine Gland Neoplasms
Tumors or cancer of the ENDOCRINE GLANDS.		02.0510
Carcinoma, Basal Cell, Pigmented
[description not available]		02.0510
Cancer of Spleen
[description not available]		02.0510
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)		02.0510
HIV Coinfection
[description not available]		02.9610
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).		02.9610
Cancer of Testis
[description not available]		05.0752
Testicular Neoplasms
Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.		05.0752
Experimental Lung Inflammation
Inflammation of any part, segment or lobe, of the lung parenchyma.		04.7721
Pneumonia
Infection of the lung often accompanied by inflammation.		09.7721
Alveolitis, Fibrosing
[description not available]		02.0510
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.		02.0510
Leucocythaemia
[description not available]		08.41113
Leukemia
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)		110.41113
Chloasma
[description not available]		02.0510
Neurocutaneous Disorders
[description not available]		02.0510
Melanosis
Disorders of increased melanin pigmentation that develop without preceding inflammatory disease.		02.0510
Brain Hemorrhage, Putaminal
[description not available]		02.0510
Choroid Plexus Neoplasms, Primary
[description not available]		02.4620
Choroid Plexus Neoplasms
Benign or malignant tumors which arise from the choroid plexus of the ventricles of the brain. Papillomas (see PAPILLOMA, CHOROID PLEXUS) and carcinomas are the most common histologic subtypes, and tend to seed throughout the ventricular and subarachnoid spaces. Clinical features include headaches, ataxia and alterations of consciousness, primarily resulting from associated HYDROCEPHALUS. (From Devita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2072; J Neurosurg 1998 Mar;88(3):521-8)		14.4620
Aneuploid
[description not available]		02.0510
Anoxia, Brain
[description not available]		02.0510
Aesthesioneuroblastoma
[description not available]		02.4420
Cancer of Nose
[description not available]		02.4420
Esthesioneuroblastoma, Olfactory
A malignant olfactory neuroblastoma arising from the olfactory epithelium of the superior nasal cavity and cribriform plate. It is uncommon (3% of nasal tumors) and rarely is associated with the production of excess hormones (e.g., SIADH, Cushing Syndrome). It has a high propensity for multiple local recurrences and bony metastases. (From Holland et al., Cancer Medicine, 3rd ed, p1245; J Laryngol Otol 1998 Jul;112(7):628-33)		02.4420
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.		03.4411
Diverticulitis
Inflammation of a DIVERTICULUM or diverticula.		03.4411
Gastrointestinal Hemorrhage
Bleeding in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.		03.4411
Benign Hypothalamic Neoplasms
[description not available]		02.4720
Cancer, Radiation-Induced
[description not available]		04.9481
Infections, Respiratory
[description not available]		02.0610
Bordetella Infections
Infections with bacteria of the genus BORDETELLA.		02.0610
Respiratory Tract Infections
Invasion of the host RESPIRATORY SYSTEM by microorganisms, usually leading to pathological processes or diseases.		02.0610
Nervous System Disorders
[description not available]		04.5351
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.		04.5351
At-V1
[description not available]		02.0510
Encephalopathy, Hepatic
[description not available]		02.0610
Hepatic Encephalopathy
A syndrome characterized by central nervous system dysfunction in association with LIVER FAILURE, including portal-systemic shunts. Clinical features include lethargy and CONFUSION (frequently progressing to COMA); ASTERIXIS; NYSTAGMUS, PATHOLOGIC; brisk oculovestibular reflexes; decorticate and decerebrate posturing; MUSCLE SPASTICITY; and bilateral extensor plantar reflexes (see REFLEX, BABINSKI). ELECTROENCEPHALOGRAPHY may demonstrate triphasic waves. (From Adams et al., Principles of Neurology, 6th ed, pp1117-20; Plum & Posner, Diagnosis of Stupor and Coma, 3rd ed, p222-5)		07.0610
Hemorrhagic Diathesis
[description not available]		02.0510
Hemorrhagic Disorders
Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).		02.0510
Islet Cell Tumor, Malignant
[description not available]		07.82101
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.		19.82101
Hives
[description not available]		02.0510
Urticaria
A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress.		07.0510
Cranial Nerve II Diseases
[description not available]		02.0510
Optic Nerve Diseases
Conditions which produce injury or dysfunction of the second cranial or optic nerve, which is generally considered a component of the central nervous system. Damage to optic nerve fibers may occur at or near their origin in the retina, at the optic disk, or in the nerve, optic chiasm, optic tract, or lateral geniculate nuclei. Clinical manifestations may include decreased visual acuity and contrast sensitivity, impaired color vision, and an afferent pupillary defect.		02.0510
Cancer of Cervix
[description not available]		02.4420
Uterine Cervical Neoplasms
Tumors or cancer of the UTERINE CERVIX.		02.4420
Myeloproliferative Disorders
Conditions which cause proliferation of hemopoietically active tissue or of tissue which has embryonic hemopoietic potential. They all involve dysregulation of multipotent MYELOID PROGENITOR CELLS, most often caused by a mutation in the JAK2 PROTEIN TYROSINE KINASE.		02.0610
External Ophthalmoplegia
[description not available]		02.7430
Sterility, Female
[description not available]		02.0510
Infertility, Female
Diminished or absent ability of a female to achieve conception.		02.0510
Delayed Hypersensitivity
[description not available]		04.7821
Chromosomal Triplication
[description not available]		02.0610
Adult-Onset Vitelliform Macular Dystrophy
[description not available]		02.0610
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.		03.6630
Cranial Sinus Thrombosis
[description not available]		02.0610
Thromboembolism, Venous
[description not available]		03.8520
Venous Thromboembolism
Obstruction of a vein or VEINS (embolism) by a blood clot (THROMBUS) in the blood stream.		03.8520
Ambulation Disorders, Neurologic
[description not available]		02.4720
Aqueductal Stenosis
[description not available]		03.3160
Carcinosarcoma
A malignant neoplasm that contains elements of carcinoma and sarcoma so extensively intermixed as to indicate neoplasia of epithelial and mesenchymal tissue. (Stedman, 25th ed)		02.0610
Deficiency, Vitamin B 12
[description not available]		02.0610
Vitamin B 12 Deficiency
A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)		02.0610
Developmental Psychomotor Disorders
[description not available]		02.0610
Cancer of Mediastinum
[description not available]		04.6932
Mediastinal Neoplasms
Tumors or cancer of the MEDIASTINUM.		04.6932
Retroperitoneal Neoplasms
New abnormal growth of tissue in the RETROPERITONEAL SPACE.		03.8621
Dermatomycoses
Superficial infections of the skin or its appendages by any of various fungi.		02.0610
Sycosis
[description not available]		02.0610
Keratoderma Blennorrhagicum
[description not available]		02.0610
Hand Dermatosis
[description not available]		02.0610
Folliculitis
Inflammation of follicles, primarily hair follicles.		02.0610
Hand Dermatoses
Skin diseases involving the HANDS.		02.0610
Keratosis
Any horny growth such as a wart or callus.		02.0610
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)		02.0610
Erythroderma, Sezary
[description not available]		03.4511
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).		08.4511
Myxoid Liposarcoma
[description not available]		02.0710
Liposarcoma, Myxoid
A liposarcoma containing round mesenchymal cells and a myxoid extracellular matrix in stroma.		02.0710
Leukoencephalopathy Syndrome, Posterior
[description not available]		02.0610
Asthenia
Clinical sign or symptom manifested as debility, or lack or loss of strength and energy.		03.4611
Brown Tendon Sheath Syndrome
[description not available]		02.0610
Abdominal Neoplasms
New abnormal growth of tissue in the ABDOMEN.		02.4620
Neoplasms, Bone Marrow
[description not available]		02.4620
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.		02.4620
Stretch Marks
[description not available]		02.0710
Striae Distensae
Linear dermal scars accompanied by epidermal atrophy that affects skin that is subjected to continuous stretching. They usually do not cause any significant medical problems, only cosmetic problems.		02.0710
Phlegmon
[description not available]		02.0710
Fungal Diseases
[description not available]		02.0710
Idiopathic Inflammatory Myopathies
[description not available]		02.0710
Cellulitis
An acute, diffuse, and suppurative inflammation of loose connective tissue, particularly the deep subcutaneous tissues, and sometimes muscle, which is most commonly seen as a result of infection of a wound, ulcer, or other skin lesions.		02.0710
Mycoses
Diseases caused by FUNGI.		02.0710
Myositis
Inflammation of a muscle or muscle tissue.		02.0710
Agranulocytosis
A decrease in the number of GRANULOCYTES; (BASOPHILS; EOSINOPHILS; and NEUTROPHILS).		04.7421
Depression, Involutional
Form of depression in those MIDDLE AGE with feelings of ANXIETY.		02.0710
Depressive Disorder, Major
Disorder in which five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure. Symptoms include: depressed mood most of the day, nearly every daily; markedly diminished interest or pleasure in activities most of the day, nearly every day; significant weight loss when not dieting or weight gain; Insomnia or hypersomnia nearly every day; psychomotor agitation or retardation nearly every day; fatigue or loss of energy nearly every day; feelings of worthlessness or excessive or inappropriate guilt; diminished ability to think or concentrate, or indecisiveness, nearly every day; or recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt. (DSM-5)		02.0710
Hepatitis
INFLAMMATION of the LIVER.		07.9910
Complications, Neoplastic Pregnancy
[description not available]		03.6430
BOOP
[description not available]		02.0710
Mucositis, Oral
[description not available]		04.1331
Cat Diseases
Diseases of the domestic cat (Felis catus or F. domesticus). This term does not include diseases of the so-called big cats such as CHEETAHS; LIONS; tigers, cougars, panthers, leopards, and other Felidae for which the heading CARNIVORA is used.		02.0710
Stomatitis
INFLAMMATION of the soft tissues of the MOUTH, such as MUCOSA; PALATE; GINGIVA; and LIP.		04.1331
Ganglioneuroblastoma
A moderately malignant neoplasm composed of primitive neuroectodermal cells dispersed in myxomatous or fibrous stroma intermixed with mature ganglion cells. It may undergo transformation into a neuroblastoma. It arises from the sympathetic trunk or less frequently from the adrenal medulla, cerebral cortex, and other locations. Cervical ganglioneuroblastomas may be associated with HORNER SYNDROME and the tumor may occasionally secrete vasoactive intestinal peptide, resulting in chronic diarrhea.		14.9910
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).		03.420
Cancer of Parathyroid
[description not available]		02.0710
Apoplexy, Pituitary
[description not available]		02.0710
Parathyroid Neoplasms
Tumors or cancer of the PARATHYROID GLANDS.		02.0710
Post-Traumatic Subarachnoid Hemorrhage
[description not available]		02.0710
Arteriovenous Malformations, Cerebral
[description not available]		02.0810
Brachial Paresis
[description not available]		04.0650
Hemorrhage, Subarachnoid
[description not available]		02.0810
Intracranial Arteriovenous Malformations
Congenital vascular anomalies in the brain characterized by direct communication between an artery and a vein without passing through the CAPILLARIES. The locations and size of the shunts determine the symptoms including HEADACHES; SEIZURES; STROKE; INTRACRANIAL HEMORRHAGES; mass effect; and vascular steal effect.		02.0810
Subarachnoid Hemorrhage
Bleeding into the intracranial or spinal SUBARACHNOID SPACE, most resulting from INTRACRANIAL ANEURYSM rupture. It can occur after traumatic injuries (SUBARACHNOID HEMORRHAGE, TRAUMATIC). Clinical features include HEADACHE; NAUSEA; VOMITING, nuchal rigidity, variable neurological deficits and reduced mental status.		02.0810
Leukemia L 1210
[description not available]		03.0950
Liver Steatosis
[description not available]		02.0710
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.		02.0710
Conus Medullaris Syndrome
[description not available]		02.0710
Hydrosyringomyelia
[description not available]		02.0710
Seminoma
A radiosensitive, malignant neoplasm of the testis, thought to be derived from primordial germ cells of the sexually undifferentiated embryonic gonad. There are three variants: classical (typical), the most common type; anaplastic; and spermatocytic. The classical seminoma is composed of fairly well differentiated sheets or cords of uniform polygonal or round cells (seminoma cells), each cell having abundant clear cytoplasm, distinct cell membranes, a centrally placed round nucleus, and one or more nucleoli. In the female, a grossly and histologically identical neoplasm, known as dysgerminoma, occurs. (Dorland, 27th ed)		02.0710
Palmoplantaris Pustulosis
[description not available]		02.0710
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.		02.0710
Cirrhosis
[description not available]		02.0710
Fibrosis
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.		07.0710
MEA 2a
[description not available]		0310
Cancer of the Thymus
[description not available]		07.7664
Thymus Neoplasms
Tumors or cancer of the THYMUS GLAND.		07.7664
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
Cranial Nerve Diseases
Disorders of one or more of the twelve cranial nerves. With the exception of the optic and olfactory nerves, this includes disorders of the brain stem nuclei from which the cranial nerves originate or terminate.		02.9910
Gangliocytoma
[description not available]		02.9910
Vision, Diminished
[description not available]		03.3820
Alogia
[description not available]		02.0710
Aphasia
A cognitive disorder marked by an impaired ability to comprehend or express language in its written or spoken form. This condition is caused by diseases which affect the language areas of the dominant hemisphere. Clinical features are used to classify the various subtypes of this condition. General categories include receptive, expressive, and mixed forms of aphasia.		02.0710
Blood Poisoning
[description not available]		02.4620
Familial Nonmedullary Thyroid Cancer
[description not available]		02.0810
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)		02.0810
Cancer of the Thyroid
[description not available]		02.4620
Hypernatremia
Excessive amount of sodium in the blood. (Dorland, 27th ed)		07.0810
Thyroid Neoplasms
Tumors or cancer of the THYROID GLAND.		02.4620
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.		07.4620
Granulocytic Leukemia, Chronic
[description not available]		04.4851
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.		04.4851
Anemia, Cooley's
[description not available]		02.0110
beta-Thalassemia
A disorder characterized by reduced synthesis of the beta chains of hemoglobin. There is retardation of hemoglobin A synthesis in the heterozygous form (thalassemia minor), which is asymptomatic, while in the homozygous form (thalassemia major, Cooley's anemia, Mediterranean anemia, erythroblastic anemia), which can result in severe complications and even death, hemoglobin A synthesis is absent.		02.0110
Cholera Infantum
[description not available]		04.3722
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).		03.8121
African Lymphoma
[description not available]		02.6930
Di Guglielmo Disease
[description not available]		02.8940
Burkitt Lymphoma
A form of undifferentiated malignant LYMPHOMA usually found in central Africa, but also reported in other parts of the world. It is commonly manifested as a large osteolytic lesion in the jaw or as an abdominal mass. B-cell antigens are expressed on the immature cells that make up the tumor in virtually all cases of Burkitt lymphoma. The Epstein-Barr virus (HERPESVIRUS 4, HUMAN) has been isolated from Burkitt lymphoma cases in Africa and it is implicated as the causative agent in these cases; however, most non-African cases are EBV-negative.		02.6930
Leukemia, Erythroblastic, Acute
A myeloproliferative disorder characterized by neoplastic proliferation of erythroblastic and myeloblastic elements with atypical erythroblasts and myeloblasts in the peripheral blood.		02.8940
B-Cell Leukemia
[description not available]		02.0110
Germinoma
A malignant neoplasm of the germinal tissue of the GONADS; MEDIASTINUM; or pineal region. Germinomas are uniform in appearance, consisting of large, round cells with vesicular nuclei and clear or finely granular eosinophilic-staining cytoplasm. (Stedman, 265th ed; from DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, pp1642-3)		04.0931
Orbital Neoplasms
Neoplasms of the bony orbit and contents except the eyeball.		02.0210
Cavernous Sinus Thrombophlebitis
[description not available]		02.0210
Dermatitis, Contact, Phototoxic
[description not available]		02.4320
Pyrexia
[description not available]		05.2541
Fever
An abnormal elevation of body temperature, usually as a result of a pathologic process.		05.2541
Arachnoid Cysts
Intracranial or spinal cavities containing a cerebrospinal-like fluid, the wall of which is composed of arachnoidal cells. They are most often developmental or related to trauma. Intracranial arachnoid cysts usually occur adjacent to arachnoidal cistern and may present with HYDROCEPHALUS; HEADACHE; SEIZURES; and focal neurologic signs. (From Joynt, Clinical Neurology, 1994, Ch44, pp105-115)		02.9410
Angioma
A vascular anomaly due to proliferation of blood or lymphatic vessels that forms a tumor-like mass. Vessels in the angioma may or may not be dilated.		02.0210
Kerion Celsi
An inflammatory manifestation of tinea capitis with a pronounced swelling that develops into suppurative central and indurated peripheral area called kerion.		02.0210
Hemangioma
A vascular anomaly due to proliferation of BLOOD VESSELS that forms a tumor-like mass. The common types involve CAPILLARIES and VEINS. It can occur anywhere in the body but is most frequently noticed in the SKIN and SUBCUTANEOUS TISSUE. (from Stedman, 27th ed, 2000)		02.0210
Tinea Capitis
Ringworm of the scalp and associated hair mainly caused by species of MICROSPORUM; TRICHOPHYTON; and EPIDERMOPHYTON, which may occasionally involve the eyebrows and eyelashes.		02.0210
Chondrosarcoma, Mesenchymal
A rare aggressive variant of chondrosarcoma, characterized by a biphasic histologic pattern of small compact cells intermixed with islands of cartilaginous matrix. Mesenchymal chondrosarcomas have a predilection for flat bones; long tubular bones are rarely affected. They tend to occur in the younger age group and are highly metastatic. (DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1456)		02.9410
Sterility, Male
[description not available]		02.0210
Infertility, Male
The inability of the male to effect FERTILIZATION of an OVUM after a specified period of unprotected intercourse. Male sterility is permanent infertility.		02.0210
Cardiac Cancer
[description not available]		02.4320
Cutaneous T-Cell Lymphoma
[description not available]		08.4111
Lymphoma, T-Cell, Cutaneous
A group of lymphomas exhibiting clonal expansion of malignant T-lymphocytes arrested at varying stages of differentiation as well as malignant infiltration of the skin. MYCOSIS FUNGOIDES; SEZARY SYNDROME; LYMPHOMATOID PAPULOSIS; and PRIMARY CUTANEOUS ANAPLASTIC LARGE CELL LYMPHOMA are the best characterized of these disorders.		03.4111
Cerebellar Diseases
Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include dysmetria, GAIT ATAXIA, and MUSCLE HYPOTONIA.		02.0210
Acute Onset Vascular Dementia
[description not available]		02.9410
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)		02.9410
P carinii Infection
[description not available]		05.2822
Pneumocystis Infections
Infections with species in the genus PNEUMOCYSTIS, a fungus causing interstitial plasma cell pneumonia (PNEUMONIA, PNEUMOCYSTIS) and other infections in humans and other MAMMALS. Immunocompromised patients, especially those with AIDS, are particularly susceptible to these infections. Extrapulmonary sites are rare but seen occasionally.		05.2822
Drug Overdose
Accidental or deliberate use of a medication or street drug in excess of normal dosage.		02.0310
Granulocytic Leukemia
[description not available]		05.0331
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.		05.0331
Delayed Effects, Prenatal Exposure
[description not available]		02.0310
Arthropathies
[description not available]		03.4111
Joint Diseases
Diseases involving the JOINTS.		03.4111
Cancer of Mouth
[description not available]		05.5932
Mouth Neoplasms
Tumors or cancer of the MOUTH.		05.5932
Infections, Listeria
[description not available]		02.0310
Kaposi Sarcoma
[description not available]		02.0310
Sarcoma, Kaposi
A multicentric, malignant neoplastic vascular proliferation characterized by the development of bluish-red cutaneous nodules, usually on the lower extremities, most often on the toes or feet, and slowly increasing in size and number and spreading to more proximal areas. The tumors have endothelium-lined channels and vascular spaces admixed with variably sized aggregates of spindle-shaped cells, and often remain confined to the skin and subcutaneous tissue, but widespread visceral involvement may occur. Kaposi's sarcoma occurs spontaneously in Jewish and Italian males in Europe and the United States. An aggressive variant in young children is endemic in some areas of Africa. A third form occurs in about 0.04% of kidney transplant patients. There is also a high incidence in AIDS patients. (From Dorland, 27th ed & Holland et al., Cancer Medicine, 3d ed, pp2105-7) HHV-8 is the suspected cause.		02.0310
Fibroid
[description not available]		02.0310
Leiomyoma
A benign tumor derived from smooth muscle tissue, also known as a fibroid tumor. They rarely occur outside of the UTERUS and the GASTROINTESTINAL TRACT but can occur in the SKIN and SUBCUTANEOUS TISSUE, probably arising from the smooth muscle of small blood vessels in these tissues.		02.0310
Intestinal Diseases
Pathological processes in any segment of the INTESTINE from DUODENUM to RECTUM.		02.0310
Altered Level of Consciousness
[description not available]		02.0410
Cancer of Larynx
[description not available]		02.0310
Laryngeal Neoplasms
Cancers or tumors of the LARYNX or any of its parts: the GLOTTIS; EPIGLOTTIS; LARYNGEAL CARTILAGES; LARYNGEAL MUSCLES; and VOCAL CORDS.		02.0310
Hypercoagulability
[description not available]		02.9510
Thrombophilia
A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.		02.9510
Shingles
[description not available]		02.0310
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)		02.0310
Hypomelanosis
[description not available]		02.0310
Melanoma, Amelanotic
An unpigmented malignant melanoma. It is an anaplastic melanoma consisting of cells derived from melanoblasts but not forming melanin. (Dorland, 27th ed; Stedman, 25th ed)		02.0310
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.		02.0310
Neoplasms, Skull Base
[description not available]		02.0410
Cardiac Diseases
[description not available]		02.0410
Heart Diseases
Pathological conditions involving the HEART including its structural and functional abnormalities.		02.0410
Cerebral Cryptococcosis
[description not available]		02.0410
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)		02.0410
Ecchymosis
Extravasation of blood into the skin, resulting in a nonelevated, rounded or irregular, blue or purplish patch, larger than a petechia.		02.0410
Blast Phase
[description not available]		03.3711
Leukemia, Megakaryocytic
[description not available]		03.3711
Leukemia, Myeloid, Acute, M4
[description not available]		03.3711
Blast Crisis
An advanced phase of chronic myelogenous leukemia, characterized by a rapid increase in the proportion of immature white blood cells (blasts) in the blood and bone marrow to greater than 30%.		03.3711
Leukemia, Megakaryoblastic, Acute
An acute myeloid leukemia in which 20-30% of the bone marrow or peripheral blood cells are of megakaryocyte lineage. MYELOFIBROSIS or increased bone marrow RETICULIN is common.		03.3711
Leukemia, Myelomonocytic, Acute
A pediatric acute myeloid leukemia involving both myeloid and monocytoid precursors. At least 20% of non-erythroid cells are of monocytic origin.		03.3711
Genito-urinary Cancer
[description not available]		01.9910
Urogenital Neoplasms
Tumors or cancer of the UROGENITAL SYSTEM in either the male or the female.		01.9910
Neuralgia, Sciatic
[description not available]		0210
Sciatica
A condition characterized by pain radiating from the back into the buttock and posterior/lateral aspects of the leg. Sciatica may be a manifestation of SCIATIC NEUROPATHY; RADICULOPATHY (involving the SPINAL NERVE ROOTS; L4, L5, S1, or S2, often associated with INTERVERTEBRAL DISK DISPLACEMENT); or lesions of the CAUDA EQUINA.		0210
Adenocarcinoma, Papillary
An adenocarcinoma containing finger-like processes of vascular connective tissue covered by neoplastic epithelium, projecting into cysts or the cavity of glands or follicles. It occurs most frequently in the ovary and thyroid gland. (Stedman, 25th ed)		0210
Cancer of the Fallopian Tube
[description not available]		0210
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.		1410
Plasma Cell Tumor
[description not available]		04.8340
EHS Tumor
[description not available]		04.8340
Plasmacytoma
Any discrete, presumably solitary, mass of neoplastic PLASMA CELLS either in BONE MARROW or various extramedullary sites.		04.8340