everolimus profile

ID Source	ID
PubMed CID	6442177
CHEMBL ID	1908360
CHEBI ID	68478
SCHEMBL ID	4378
MeSH ID	M000602394

Synonym
rad 001
rapamycin, 42-o-(2-hydroxyethyl)-
(1r,9s,12s,15r,16e,18r,19r,21r,23s,24e,26e,28e,30s,32s,35r)-1,18-dihydroxy-12-((1r)-2-((1s,3r,4r)-4-(2-hydroxyethoxy)-3-methoxycyclohexyl)-1-methylethyl)-19,30-dimethoxy-15,17,21,23,29,35-hexamethyl-11,36-dioxa-4-azatricyclo(30.3.1.04,9)hexatriaconta-16,2
(1r,9s,12s,15r,16e,18r,19r,21r,23s,24e,26e,28e,30s,32s,35r)-1,18-dihydroxy-12-((1r)-2-((1s,3r,4r)-4-(2-hydroxyethoxy)-3-methoxycyclohexyl)-1-methylethyl)-19,30-dimethoxy-15,17,21,23,29,35-hexamethyl-11,36-dioxa-4-azatricyclo(30.3.1.0(sup 4,9))hexatriacont
everolimus [usan]
(3s,6r,7e,9r,10r,12r,14s,15e,17e,19e,21s,23s,26r,27r,34as)-9,10,12,13,14,21,22,23,24,25,26,27,32,33,34,34a-hexadecahydro-9,27-dihydroxy-3-((1r)-2-((1s,3r,4r)-4-(2-hydroxyethoxy)-3-methoxycyclohexyl)-1-methylethyl)-10,21-dimethoxy-6,8,12,14,20,26-hexamethy
HY-10218
votubia
nvp-rad-001
sdz-rad
rad-001c
certican
everolimus ,
afinitor
rad-001
zortress
rad ,
DB01590
42-o-(2-hydroxyethyl)rapamycin
40-o-(2-hydroxyethyl)-rapamycin
rad001
nsc733504
NCGC00167512-01
sdz rad
(3s,6r,7e,9r,10r,12r,14s,15e,17e,19e,21s,23s,26r,27r,34as)-9,27-dihydroxy-3-{(2r)-1-[(1s,3r,4r)-4-(2-hydroxyethoxy)-3-methoxycyclohexyl]propan-2-yl}-10,21-dimethoxy-6,8,12,14,20,26-hexamethyl-9,10,12,13,14,21,22,23,24,25,26,27,32,33,34,34a-hexadecahydro-3
bdbm50088378
afinitor disperz
chebi:68478 ,
xience v
hsdb 8255
everolimus [usan:inn:ban]
unii-9hw64q8g6g
tox21_112510
dtxsid0040599 ,
cas-159351-69-6
dtxcid8020599
EVEROLIMUS - RAD001
rad 666
CHEMBL1908360
rad-666
9hw64q8g6g ,
everolimus [orange book]
everolimus [who-dd]
everolimus [ep monograph]
everolimus [inn]
everolimus [jan]
everolimus [mart.]
everolimus [vandf]
everolimus [ema epar]
everolimus [usp-rs]
everolimus [mi]
(1r,9s,12s,15r,16e,18r,19r,21r,23s,24e,26e,28e,30s,35r)-1,18-dihydroxy-12-{(2r)-1-[(1s,3r,4r)-4-(2-hydroxyethoxy)-3-methoxycyclohexyl]propan-2-yl}-19,30-dimethoxy-15,17,21,23,29,35-hexamethyl-11,36-dioxa-4-azatricyclo[30.3.1.0(4,9)]hexatriaconta-16,24,26,
everolimusum
CS-0064
AKOS015850977
40-o-(2-hydroxyethyl)rapamycin
gtpl5889
BRD-K13514097-001-01-2
HKVAMNSJSFKALM-GKUWKFKPSA-N
SCHEMBL4378
Q-101413
rad, sdz
001, rad
everolimus, analytical standard
everolimus (inn)
dihydroxy-[(1r)-2-[(1s,3r,4r)-4-(2-hydroxyethoxy)-3-methoxy-cyclohexyl]-1-methyl-ethyl]-dimethoxy-hexamethyl-[?]pentone
Q421052
AS-16971
BRD-K13514097-001-05-3
42-o-(2-hydroxyethyl)-rapamycin
EX-A2057
everolimus; rad001; sdz-rad
(1r,9s,12s,15r,16e,18r,19r,21r,23s,24e,26e,28e,30s,35r)-1,18-dihydroxy-12-((2r)-1-((1s,3r,4r)-4-(2-hydroxyethoxy)-3-methoxycyclohexyl)propan-2-yl)-19,30-dimethoxy-15,17,21,23,29,35-hexamethyl-11,36-dioxa-4-azatricyclo(30.3.1.0(4,9))hexatriaconta-16,24,26,
everolimus tablets
afinitordisperz
everolimus (usp-rs)
everolimus (mart.)
(3s,6r,7e,9r,10r,12r,14s,15e,17e,19e,21s,23s,26r,27r,34as)-9,27-dihydroxy-3-((2r)-1-((1s,3r,4r)-4-(2-hydroxyethoxy)-3-methoxycyclohexyl)propan-2-yl)-10,21-dimethoxy-6,8,12,14,20,26-hexamethyl-9,10,12,13,14,21,22,23,24,25,26,27,32,33,34,34a-hexadecahydro-3
l04aa18
l01xe10
everolimus (ep monograph)
eve - everolimus

Excerpt	Reference	Relevance
"Everolimus is an mTOR pathway inhibitor with synergistic anti-tumor activity when combined with histone deacetylase inhibitors, such as panobinostat, in preclinical lymphoma models."	( Phase II Study of Single-Agent and Combination Everolimus and Panobinostat in Relapsed or Refractory Diffuse Large B-Cell Lymphoma. Beaven, A; de Castro, C; Diehl, L; Islam, P; Li, Z; Lin, C; Moore, J; Morris, T; Rizzieri, D, 2021)	1.6
"Everolimus is a mammalian target of rapamycin inhibitor/proliferation-signal inhibitor with potent immunosuppressive and anti-proliferative effects."	( An overview of the efficacy and safety of everolimus in adult solid organ transplant recipients. Barten, MJ; Bernhardt, P; De Simone, P; Gawai, A; Gottlieb, J; Pascual, J; Potena, L; Saliba, F; Tedesco-Silva, H, 2022)	1.71
"Everolimus is an inhibitor of serine/ threonine kinase mTOR. "	( Biomarkers of everolimus efficacy in breast cancer therapy. Voutsadakis, IA, 2022)	2.52
"Everolimus is a kind of mammalian target of rapamycin (mTOR) inhibitors. "	( Exosome-mediated miR-7-5p delivery enhances the anticancer effect of Everolimus via blocking MNK/eIF4E axis in non-small cell lung cancer. Fan, S; Liu, S; Luo, J; Ma, J; Ning, Y; Peng, J; Wang, H; Wang, W; Wen, Q; Yang, Y; Zang, H; Zhan, Y; Zheng, H, 2022)	2.4
"Everolimus is an inhibitor of the mammalian target of rapamycin, and its indications include neuroendocrine tumors."	( A case of erythema multiforme-like rash induced by everolimus in a patient with a pancreatic neuroendocrine tumor. Hayama, H; Ito, T; Kubota, Y; Miura, M; Mizuno, Y; Oya, M; Tashiro, A; Tsuneyoshi, M; Ueda, K; Yamashita, A, 2022)	1.69
"Everolimus is a mTOR inhibitor that has been increasingly used in high-risk cardiac rhabdomyomas in recent years. "	( Effect of different dose regimens of everolimus in a series of neonates with giant cardiac rhabdomyomas. Babaoğlu, K; Başar, EZ; Günlemez, A; Usta, E; Yılmaz, EH, 2023)	2.63
"Everolimus is a drug with proven efficacy in the treatment of other conditions related to TS, and some evidence suggests that its use benefits the treatment of refractory epilepsy in these patients."	( Everolimus as a therapeutic option in refractory epilepsy in children with tuberous sclerosis: a systematic review. Dutra, LS; Goes, JS; Menezes, CEG; Morais, LAS; Nery, ES; Portela Filho, MB; Santos, DLD; Serpa, ED, 2023)	3.07
"Everolimus is an oral drug that inhibits mTOR with immunosuppressive and antiproliferative characteristics. "	( Evaluating everolimus for the treatment of breast cancer. Bourbouloux, E; Campone, M; Frenel, JS; Gourmelon, C; Moreau-Bachelard, C; Patsouris, A; Robert, M, )	1.96
"Everolimus is an inhibitor of mammalian target of rapamycin (mTOR) used in both transplantation and cancer treatment (breast, renal and neuroendocrine). "	( First reported double drug-drug interaction in a cancer renal patient under everolimus treatment: therapeutic drug monitoring and review of literature. Bleda-Perez, C; Del Valle-Celiz, PM; Fontanals-Martínez, S; Fort-Casamartina, E; Gonzalo-Diego, N; Muñoz-Sanchez, C; Otero-Torres, S; Prats-Jimenez, J; Rigo-Bonnin, RF, 2023)	2.58
"Everolimus is an active agent in the treatment of prolactinomas that warrants further investigation."	( The treatment of aggressive prolactinomas with everolimus. Geer, EB; Lala, N; Lin, AL; Magge, R; Page-Wilson, G; Tabar, V; Young, RJ, 2023)	2.61
"Everolimus is an alternative second-line therapy, particularly in nonfunctioning NETs and patients with SSTR-negative tumors."	( Systemic Therapy for Tumor Control in Metastatic Well-Differentiated Gastroenteropancreatic Neuroendocrine Tumors: ASCO Guideline. Arshad, J; Basu, S; Bellizzi, AM; Bergsland, EK; Chan, JA; Chauhan, A; Dasari, AN; Del Rivero, J; Gangi, A; Grady, E; Halfdanarson, TR; Howe, JR; Ivanidze, J; Kennedy, EB; Kunz, PL; Lewis, M; Mailman, J; Mittra, ES; Perez, K; Raj, N; Singh, S; Soares, HP; Soulen, MC; Strosberg, JR; Vijayvergia, N; White, SB, 2023)	1.63
"Everolimus is a Food and Drug Administration-approved inhibitor of TORC1."	( Phase 2 clinical trial of TORC1 inhibition with everolimus in men with metastatic castration-resistant prostate cancer. Anand, M; Armstrong, AJ; George, DJ; Halabi, S; Healy, P; Jonasch, D; Madden, JF; Rasmussen, J; Spritzer, C; Wood, SY, 2020)	1.54
"Everolimus is an effective immunosuppressant in organ transplantation without impaired renal function. "	( Efficacy and safety of everolimus treatment on liver transplant recipients: A meta-analysis. Chen, KB; Guan, TW; Lin, YJ; Ou, MY, 2019)	2.27
"Everolimus is a mammalian target of rapamycin (mTOR) inhibitor, which is used in immunosuppressive treatment regimens in solid-organ transplant recipients. "	( Noncontrast Magnetic Resonance Lymphangiography in a Rare Case of Everolimus-Related Lymphedema. Boccanera, D; Cellina, M; Gibelli, D; Menozzi, A; Oliva, G; Soresina, M, 2020)	2.24
"Everolimus is a treatment in NETs that may have antiangiogenic activity."	( Everolimus after hepatic arterial embolisation therapy of metastases from gastrointestinal neuroendocrine tumours: The FFCD 1104-EVACEL-GTE phase II study. Aparicio, T; Barbier, E; Baudin, E; Bouhier-Leporrier, K; Cadiot, G; Caroli-Bosc, FX; Coriat, R; de Baère, T; Di-Fiore, F; Duluc, M; Dupont-Gossart, AC; Gay, F; Ghiringhelli, F; Guimbaud, R; Hentic-Dhome, O; Lecomte, T; Legoux, JL; Lepage, C; Lepere, C; Lombard-Bohas, C; Petorin, C; Smith, D; Walter, T, 2019)	2.68
"Everolimus is a well-established second-line treatment."	( A Phase 4 Study of Everolimus to Evaluate Efficacy and Safety in Patients with Metastatic Renal-Cell Carcinoma after Failure of First-Line Sunitinib or Pazopanib (SUNPAZ). de Geeter, P; Decker, T; Quiering, C; Resch, A; Schmitz, S; Schostak, M, 2020)	1.61
"Everolimus is an mTOR inhibitor, approved as a treatment for cancer and as an immunosuppressant agent in solid organ transplantation; it frequently produces toxic metabolic effects, particularly of the most severe kind. "	( [Lipid lowering treatment of severe hypertriglyceridemia with acute pancreatitis caused by everolimus in a patient with a neuroendocrine tumor]. Anda Apiñániz, E; Castro Unanua, N; De Carlos Artajo, J; Irigaray Echarri, A; Muruzábal Huarte, E; Vera García, R; Zubiría Gortázar, J, 2020)	2.22
"Everolimus is a mammalian target of rapamycin inhibitor and is approved as second-line treatment or beyond for renal cell carcinoma. "	( Human herpesvirus 6 encephalitis in a patient treated with everolimus for renal cell carcinoma. Fitsiori, A; Gantzer, J; Kokkali, S; Oddou, I, 2020)	2.24
"Everolimus is a drug approved for the management of advanced pNETs that can achieve both these goals."	( Should everolimus be stopped after radiological progression in metastatic insulinoma? A "cons" point of view. Amoroso, V; Berruti, A; Consoli, F; Dalla Volta, A; Ferrari, VD; Tovazzi, V, 2020)	1.73
"Everolimus (EVR) is a derivative of sirolimus with a similar mechanism of action. "	( Safety and Efficacy of Everolimus Rescue Treatment After Pediatric Living Donor Liver Transplantation. Bessho, K; Deguchi, K; Kodama, T; Noguchi, Y; Nomura, M; Okuyama, H; Saka, R; Tazuke, Y; Ueno, T; Watanabe, M, )	1.88
"Everolimus is a valid therapeutic option for advanced, progressive, well-differentiated NEN, even in patients with positive FDG-PET findings."	( [ Annibale, B; Franchi, G; Iannicelli, E; Laghi, A; Magi, L; Mazzuca, F; Panzuto, F; Pilozzi, E; Prosperi, D; Rinzivillo, M; Signore, A, 2021)	2.06
"Everolimus is a mTOR inhibitor which demonstrates clinical activity in several solid tumors, especially in kidney cancer after first line TKI anti VEGF treatment and in breast cancer in association with exemesthane after failure of aroamatase inhibitors. "	( [Tolerablity of everolimus in clinical practice: a retrospective study]. Afani, L; Awada, A; Belbaraka, R, 2020)	2.35
"Everolimus is an appropriate first-line choice for somatostatin receptor negative tumors and for any patients with progressive disease."	( Pulmonary Neuroendocrine Tumors: Adjuvant and Systemic Treatments. Halfdanarson, TR; Leventakos, K; Molina, JR; Uprety, D, 2020)	1.28
"Everolimus (Eve) is an immunosuppressive macrolide that is being analyzed in various biological matrices and fluids. "	( Development and validation of a simple and versatile method for the quantification of everolimus loaded in H-ferritin nanocages using UHPLC-MS/MS. Bonizzi, A; Calleri, E; Corsi, F; Cottica, D; Grignani, E; Mazzucchelli, S; Negri, S; Prati, F; Sottani, C, 2020)	2.22
"Everolimus is a safe and effective therapeutic option for renal angiomyolipoma and various manifestations of TSC, which has been reproduced in real life with six years of follow-up."	( Renal angiomyolipoma and tuberous sclerosis complex: long-term safety and efficacy outcomes of Everolimus therapy. Álvarez-Ossorio Fernández, JL; Ledo Cepero, MJ; Ojeda Claro, AV; Ruiz Guerrero, E; Soto Delgado, M, 2021)	2.28
"Everolimus is an immunosuppressant agent used in organ transplantation and, more recently, in cancer therapy. "	( Complex regional pain syndrome in a patient with neuroendocrine tumour under treatment with everolimus. Fernández-Rodríguez, T; Oliver-Noguera, A; Pérez de Amezaga-Tomás, L; Rodríguez-Camacho, JM, 2022)	2.38
"Everolimus is an alternative treatment for several comorbidities, but its early use (< 3 years) requires further study."	( [Tuberous sclerosis complex: analysis of areas of involvement, treatment progress and translation to routine clinical practice in a cohort of paediatric patients]. Aparicio-López, C; Bernardino-Cuesta, B; Cantarín-Extremera, V; de Lucas-Collantes, C; Duat-Rodríguez, A; Hernández-Martín, A; Martín-Villaescusa, C; Melero-Llorente, J; Ruiz-Falcó-Rojas, ML; Tamariz Martel-Moreno, A, 2021)	1.34
"Everolimus is an important drug used for the treatment of NETs."	( Effect of everolimus on the expression of Ki-67 and caspase-3 in patients with neuroendocrine tumors. Cheng, XB; Jin, LD; Li, Y; Yin, HP; Zhang, HY, 2017)	1.58
"Everolimus is a small molecule that inhibits the mammalian target of rapamycin (mTOR) and is used for treatment of various solid tumours and renal transplant rejection prophylaxis. "	( Everolimus-induced nephrotic syndrome precipitated by interaction with voriconazole in a patient with Hodgkin's lymphoma. Pinter-Brown, LC; Tran, PN, 2017)	3.34
"Everolimus is a newer generation mammalian target of rapamycin inhibitor approved for immunosuppressive use in a number of advanced medical conditions. "	( A Case of Everolimus-Induced Eyelid Edema. Rodgers, R; Schear, MJ, )	1.98
"Everolimus is a drug used successfully in a number of different oncology indications, but significant on-target toxicities exist. "	( Continuous low plasma concentrations of everolimus provides equivalent efficacy to oral daily dosing in mouse xenograft models of human cancer. Guthy, D; Laborde, L; McSheehy, P; Oz, F; Ristov, M; Sterker, D, 2017)	2.17
"Everolimus is a standard treatment option for advanced pancreatic neuroendocrine tumors (pNETs). "	( Clinical outcomes of everolimus in patients with advanced, nonfunctioning pancreatic neuroendocrine tumors: a multicenter study in Korea. Bang, S; Cho, JH; Jeong, S; Kim, YT; Lee, JK; Lee, KH; Lee, KJ; Lee, SH; Lee, TH; Lee, WJ; Paik, WH; Ryu, JK; Song, SY; Woo, SM, 2017)	2.22
"Everolimus is a promising candidate that combines immunosuppressive properties with anti-neoplastic effects."	( Everolimus for pediatric patients with acute graft-versus-host disease after hematopoietic stem cell transplantation: A pilot study. Chang, YC; Chao, YH; Peng, CT; Weng, TF; Wu, HP; Wu, KH, 2017)	2.62
"Everolimus is an inhibitor of mammalian target of rapamycin (mTOR), and is available as oral tablets."	( Evaluation of the Effect of Everolimus on Retinal Pigment Epithelial Cells and Experimental Proliferative Vitreoretinopathy. Chen, YH; Ke, MC; Kuo, HK; Kuo, YH; Tseng, YC; Wu, PC, 2018)	1.5
"Everolimus is an inhibitor of the mammalian target of rapamycin (mTOR) that has been approved by the US Food and Drug Administration for the treatment of subependymal giant cell astrocytoma (SEGA) in patients with tuberous sclerosis complex (TSC). "	( Retinal astrocytoma regression in tuberous sclerosis patients treated with everolimus. Ali, A; Tehrani, NN; Zipori, AB, 2018)	2.15
"Everolimus is a mammalian target of rapamycin inhibitor, whose immunosuppressant properties are both desired in transplant patients and unwanted in cancer patients, where it is indicated for its antiproliferative efficacy."	( The immune system as a chronotoxicity target of the anticancer mTOR inhibitor everolimus. Cinar, S; Deniz, G; Giacchetti, S; Kaptan, E; Lévi, F; Li, XM; Okyar, A; Ozsoy, N; Ozturk, D; Ozturk, N; Pala-Kara, Z; Sancar-Bas, S, 2018)	1.43
"Everolimus is a treatment option for hemodialysis patients with metastatic atypical bronchial carcinoid. "	( Efficacy and safety of everolimus treatment in a hemodialysis patient with metastatic atypical bronchial carcinoid: case report and literature review. Brizzi, MP; La Salvia, A; Scagliotti, GV; Sonetto, C; Tampellini, M; Volante, M, 2018)	2.23
"Everolimus (C53H83NO14) is an efficient anti-cancer drug for breast cancer which targets mammalian target of rapamycin (mTOR)."	( Everolimus inhibits breast cancer cell growth through PI3K/AKT/mTOR signaling pathway. Chen, W; Du, L; Li, X; Mu, L; Song, A; Zhang, Y; Zhen, L, 2018)	2.64
"Everolimus is a drug from the class of mammalian target of rapamycin inhibitors used for both immunosuppressant and oncological indications. "	( A pharmacological rationale for improved everolimus dosing in oncology and transplant patients. Burger, DM; de Fijter, JW; Guchelaar, HJ; Moes, DJAR; Reinders, MEJ; Ter Heine, R; van Erp, NP; van Herpen, CM, 2018)	2.19
"Everolimus is an inhibitor of the mammalian target of rapamycin (mTOR) and has been used in combination with calcineurin inhibitors (tacrolimus and cyclosporine) to prevent allograft rejection following organ transplantation. "	( Effect of fluconazole on the pharmacokinetics of everolimus and tacrolimus in a heart transplant recipient: Case report. Matsuda, S; Nakagita, K; Oita, A; Takada, M; Terada, Y; Terakawa, N; Wada, K, 2018)	2.18
"Everolimus (RAD-001) is an orally active rapamycin analogue shown in preclinical data to produce cytostatic cell inhibition, which may be potentially beneficial in treating melanoma. "	( Phase II Study of Everolimus in Metastatic Malignant Melanoma (NCCTG-N0377, Alliance). Allred, JB; Creagan, ET; Erickson, LA; Kaur, JS; Lowe, VJ; Maples, WJ; Markovic, S; Rao, RD; Suman, VJ; Vera Aguilera, J; Windschitl, HE, 2018)	2.26
"Everolimus is an allosteric mTOR inhibitor with efficacy in metastatic RCC."	( Comprehensive Genomic Profiling of Metastatic Tumors in a Phase 2 Biomarker Study of Everolimus in Advanced Renal Cell Carcinoma. Bhatt, RS; Catalano, PJ; Choueiri, TK; Gao, X; George, DJ; Gray, C; Jegede, O; Kwiatkowski, DJ; McDermott, DF; McKay, RR; Novak, J; Signoretti, S, 2018)	1.43
"Everolimus, which is a mammalian target of rapamycin inhibitor, has an anti-fibrosis effect."	( Everolimus Rescue Treatment for Chronic Rejection After Pediatric Living Donor Liver Transplantation: 2 Case Reports. Bessho, K; Hiwatashi, S; Okuyama, H; Saka, R; Takama, Y; Tazuke, Y; Ueno, T; Yamanaka, H, 2018)	2.64
"Everolimus is an inhibitor of mammalian target of rapamycin (mTOR) and reduces the risk of cytomegalovirus (CMV) infection in transplant recipients. "	( Everolimus delayed and suppressed cytomegalovirus DNA synthesis, spread of the infection, and alleviated cytomegalovirus infection. Sato, N; Shiraki, A; Shiraki, K; Takemura, Y; Tan, L; Yanagita, M; Yoshida, Y, 2019)	3.4
"Everolimus is a mammalian target of rapamycin (m-TOR) inhibitor that has been approved for the treatment of hormone receptor-positive advanced breast cancer, metastatic renal cancer, and neuroendocrine tumors. "	( Therapeutic Drug Monitoring of Everolimus in Oncology: Evidences and Perspectives. Falkowski, S; Woillard, JB, 2019)	2.24
"Everolimus is an mTOR (the mammalian target of rapamycin) inhibitor, which is used for the treatment of advanced renal cell carcinoma. "	( Severe gastrointestinal hemorrhage related to everolimus: a case report. Haruki, K; Masubuchi, M; Saito, R; Tsunematsu, M; Watanabe, M; Yanaga, K, 2019)	2.21
"Everolimus (EVR) is a mammalian target of rapamycin (mTOR) inhibitor commonly used for immunosuppression (IS) after liver transplantation (LT). "	( The Effect of Immunosuppression on Coagulation After Liver Transplantation. Achterfeld, A; Bedreli, S; Herzer, K; Katsounas, A; Saner, F; Straub, K; Wedemeyer, H; Willuweit, K, 2019)	1.96
"Everolimus is a mammalian target of rapamycin inhibitor used in the treatment of multiple tumor types, and its most common toxicity, stomatitis, can affect patient quality of life. "	( A single-arm, phase 2 study of steroid-containing mouthwash for the prevention of everolimus-associated stomatitis in multiple tumor types. Adachi, Y; Andoh, M; Gondo, N; Hagiwara, S; Hattori, M; Hijioka, S; Iwata, H; Kotani, H; Mizuno, Y; Sawaki, M; Shimizu, J; Tachi, M; Tatematsu, M; Yoshimura, A; Yoshimura, K, 2019)	2.18
"Everolimus is a mammalian target of rapamycin (mTOR) inhibitor that has cytoreductive effects on subependymal giant cell astrocytoma and renal angiomyolipoma in tuberous sclerosis complex (TSC). "	( [The Efficacy of Everolimus for Refractory Seizures in Childhood Onset Epilepsy with Tuberous Sclerosis Complex]. Baba, S; Enoki, H; Fujimoto, A; Itamura, S; Nishimura, M; Okanari, K; Okanishi, T, 2019)	2.3
"Everolimus is a mammalian target of rapamycin (mTOR) inhibitor approved as an immunosuppressant and for second-line therapy of hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC). "	( Physiologically based pharmacokinetic models for everolimus and sorafenib in mice. Fetterly, GJ; Hylander, BH; Jusko, WJ; Ma, WW; Pawaskar, DK; Repasky, EA; Straubinger, RM, 2013)	2.09
"Everolimus is an immunosuppressant drug used in solid organ transplantation. "	( Comparison of a stable isotope-labeled and an analog internal standard for the quantification of everolimus by a liquid chromatography-tandem mass spectrometry method. Heideloff, C; Payto, D; Wang, S, 2013)	2.05
"Everolimus is a synthetic, orally available analogue of rapamycin that inhibits the activation of mTOR."	( Evaluation of everolimus in renal cell cancer. Amato, R; Stepankiw, M, 2013)	1.47
"Everolimus is a potent immunosuppressive agent that has antiproliferative activities. "	( Clinical everolimus experience in pediatric renal transplant patients. Bulut, IK; Dincel, N; Hoşcoşkun, C; Mir, S; Sezer, TÖ, 2013)	2.25
"Everolimus is a potent, oral inhibitor of the mammalian target of rapamycin (mTOR) that has been investigated in multiple clinical development programs since 1996. "	( Development of everolimus, a novel oral mTOR inhibitor, across a spectrum of diseases. Anak, O; Berg, W; Elmroth, I; Haas, T; Klimovsky, J; Lebwohl, D; Posluszny, J; Sahmoud, T; Saletan, S, 2013)	2.19
"Everolimus is a mammalian target of rapamycin (mTOR) inhibitor approved for the treatment of advanced renal cell carcinoma, pancreatic neuroendocrine tumors, subependymal giant cell astrocytoma associated with tuberous sclerosis complex, renal angiomyolipoma and tuberous sclerosis complex, and, in combination with exemestane, for hormone receptor-positive HER2-negative advanced breast cancer after failure of treatment with letrozole or anastrozole. "	( Management of adverse events in patients with hormone receptor-positive breast cancer treated with everolimus: observations from a phase III clinical trial. Peterson, ME, 2013)	2.05
"Everolimus is an orally administered inhibitor of the mammalian target of rapamycin (mTOR), an intracellular protein kinase downstream of the phosphatidylinositol 3-kinase/AKT pathway involved in key components of tumorigenesis, including cell growth, proliferation, and angiogenesis. "	( Practical management of everolimus-related toxicities in patients with advanced solid tumors. Geberth, M; Grünwald, V; Hörsch, D; Janni, W; Lüftner, D; Pavel, ME; Weber, MM; Weikert, S, 2013)	2.14
"Everolimus is an immunosuppressant and an antiproliferative macrolide agent which is used for coronary stent coating for local inhibition of in-stent restenosis. "	( Everolimus-coated tympanostomy tube on rat tympanic membrane. Akbulut, S; Altintaş, H; Barisik, NO; Berk, D; Sezen, OS, 2013)	3.28
"Everolimus is a widely used oral mTOR inhibitor that has the potential for drug interactions that may affect therapeutic outcomes, produce toxicities, or both. "	( Drug interactions and the pharmacist: focus on everolimus. Grabowsky, JA, )	1.83
"Everolimus is a potent immunosuppressant with several advantages over calcineurin inhibitors, such as good tolerance, preventive effects on cardiovascular morbidity, and mortality and cancer prevention as it inhibits cell proliferation."	( Everolimus monotherapy or combined therapy in liver transplantation: indications and results. Abradelo, M; Alegre, C; Alvaro, E; Calvo, J; Cambra, F; Caso, O; García, M; García-Sesma, A; Jiménez, C; Justo, I; Loinaz, C; Manrique, A; Moreno, E; Sanabria, R, 2013)	3.28
"Everolimus (EVR) is a semi-synthetic mammalian target of rapamycin inhibitor currently under development for liver transplantation (LTx) in combination with reduced exposure tacrolimus (rTAC). "	( mTOR inhibition in liver transplantation: how to dose for effective/safe CNI reduction? Dumortier, T; Fung, J; Junge, G; Schwende, H, 2013)	1.83
"Everolimus is an immunosuppressive drug metabolized by enzymes of the CYP family. "	( The role of CYP2C8 genotypes in dose requirement and levels of everolimus after heart transplantation. Kniepeiss, D; Renner, W; Tscheliessnigg, KH; Wagner, D; Wasler, A, 2013)	2.07
"Everolimus is an mammalian target of rapamycin complex 1 inhibitor with demonstrated benefit in several aspects of TSC."	( Everolimus treatment of refractory epilepsy in tuberous sclerosis complex. Agricola, K; Anderson, AE; Franz, DN; Holland-Bouley, K; Kim, MO; Krueger, DA; Lopez, CM; Mays, M; Tudor, C; Wilfong, AA, 2013)	2.55
"Everolimus is an orally available inhibitor of the mammalian target of rapamycin (mTOR), which has been approved in combination with exemestane for hormone receptor-positive (HR) breast cancer after failure of treatment with non-steroidal aromatase inhibitors. "	( Everolimus: side effect profile and management of toxicities in breast cancer. O'Regan, R; Paplomata, E; Zelnak, A, 2013)	3.28
"Everolimus is a mammalian target of rapamycin inhibitor approved for the treatment of metastatic renal cell carcinoma (mRCC). "	( Pre-treatment neutrophil-to-lymphocyte ratio may be associated with the outcome in patients treated with everolimus for metastatic renal cell carcinoma. Amadori, D; Berardi, R; Burattini, L; Cascinu, S; Conti, A; Cortesi, E; De Giorgi, U; Iacovelli, R; Luca Burgio, S; Muzzonigro, G; Rossi, L; Santoni, M, 2013)	2.05
"Everolimus is a serine-threonine kinase that acts as an inhibitor of mammalian target of rapamycin, which results in reduced growth of cells, angiogenesis, and survival of cells."	( Osteonecrosis of the jaw related to everolimus: a case report. Jung, HD; Jung, YS; Kim, DW; Park, HS, 2013)	1.39
"Everolimus is a derivative of rapamycin and acts as a signal transduction inhibitor."	( The antiproliferative effects of ouabain and everolimus on adrenocortical tumor cells. Barollo, S; Cicala, MV; Iacobone, M; Mantero, F; Mian, C; Mucignat-Caretta, C; Pezzani, R; Radu, C; Redaelli, M; Rubin, B; Salvà, M; Simioni, P, 2014)	1.38
"Everolimus is an oral mammalian target of rapamycin inhibitor approved for advanced renal cell carcinoma (RCC)."	( A phase 1b clinical trial of the multi-targeted tyrosine kinase inhibitor lenvatinib (E7080) in combination with everolimus for treatment of metastatic renal cell carcinoma (RCC). Carter, D; Gold, AM; Hutson, TE; Larkin, J; Michaelson, MD; Molina, AM; Motzer, R; Wood, K, 2014)	1.33
"Everolimus (EVE) is a drug widely used in several renal transplant protocols. "	( Everolimus-induced epithelial to mesenchymal transition in immortalized human renal proximal tubular epithelial cells: key role of heparanase. Gambaro, G; Granata, S; Lupo, A; Masola, V; Onisto, M; Zaza, G, 2013)	3.28
"Everolimus is an oral inhibitor of mTOR complex 1 (mTORC1) with antitumor activity in a variety of cancers."	( Phase II study of everolimus in children and adults with neurofibromatosis type 2 and progressive vestibular schwannomas. Allen, JC; Derman, A; Filatov, A; Giancotti, FG; Goldberg, JD; Golfinos, JG; Hagiwara, M; Hochman, T; Karajannis, MA; Legault, G; Merkelson, A; Roland, JT; Vega, E; Wisoff, JH, 2014)	1.46
"Everolimus is an inhibitor of mammalian target of rapamycin, approved in patients with metastatic renal cell carcinoma. "	( Immunomodulatory effects of everolimus in a long responsive patient with metastatic renal cell carcinoma. Adotevi, O; Borg, C; Laheurte, C; Mansi, L; Pivot, X; Royer, B; Thiery-Vuillemin, A, 2014)	2.14
"Everolimus is an orally administrated mammalian target of rapamycin (mTOR) inhibitor. "	( Therapeutic potential and adverse events of everolimus for treatment of hepatocellular carcinoma - systematic review and meta-analysis. Galli, U; Gao, C; Hatano, E; Houben, P; Lin, S; Petrulionis, M; Richter, S; Schemmer, P; Schultze, D; Winkler, S; Yamanaka, K, 2013)	2.09
"Everolimus is an oral derivative of rapamycin which acts as a signal transduction inhibitor. "	( Everolimus in advanced solid tumors: when to start, early or late? Procopio, G; Pusceddu, S; Tessari, A; Testa, I, )	3.02
"Everolimus is an oral raptor mTOR inhibitor and has shown activity in patients with Waldenstrom's macroglobulinemia (WM). "	( Long-term results of the phase II trial of the oral mTOR inhibitor everolimus (RAD001) in relapsed or refractory Waldenstrom Macroglobulinemia. Bergsagel, PL; Camoriano, J; Chuma, S; DeAngelo, D; Gertz, M; Ghobrial, IM; Hayman, S; Lacy, M; LaPlant, B; Treon, SP; Witzig, TE, 2014)	2.08
"Everolimus is an orally administered mTOR inhibitor. "	( Everolimus prolonged survival in transgenic mice with EGFR-driven lung tumors. Harada, D; Honda, Y; Ichihara, E; Kiura, K; Murakami, T; Ninomiya, T; Ochi, N; Ohashi, K; Takigawa, N; Tanimoto, M; Yasugi, M, 2014)	3.29
"Everolimus is a targeted agent which was effective in several clinical trials and became registered for treatment of hormone receptor positive breast cancer."	( [BOLERO -- another remarkable step in treatment of breast cancer]. Láng, I; Rubovszky, G, 2014)	1.12
"Everolimus is a mammalian target of rapamycin inhibitor and exhibits synergistic immunosuppressive activity with CNI to permit CNI-reduction."	( Everolimus-based calcineurin-inhibitor sparing regimens for kidney transplant recipients: a systematic review and meta-analysis. Chen, P; Deng, R; Li, H; Su, L; Tam, N; Wu, L, 2014)	2.57
"Everolimus (ERL) is an immunosuppressive agent with antitumoral properties."	( Conversion to everolimus dramatically improves the prognosis of de novo malignancies after liver transplantation for alcoholic liver disease. Boillot, O; Decullier, E; Dumortier, J; Guillaud, O; Thimonier, E; Vallin, M; Walter, T, 2014)	1.48
"Everolimus is an orally administered anti-cancer drug that inhibits the mammalian target of rapamycin (mTOR) signal transduction route. "	( [Hyperglycaemia during treatment with everolimus]. Beijnen, JH; Huitema, AD; Opdam, FL; Schellens, JH, 2014)	2.12
"Everolimus is a valid therapeutic option for neuroendocrine tumors (NETs); however, data in a real-world setting outside regulatory trials are sparse. "	( Real-world study of everolimus in advanced progressive neuroendocrine tumors. Ambrosio, MR; Antonuzzo, L; Appetecchia, M; Berruti, A; Brizzi, MP; Campana, D; Cartenì, G; Cascinu, S; Cassano, A; Chiara, S; Colao, A; de Braud, F; Delle Fave, G; Faggiano, A; Falconi, M; Fazio, N; Fontana, A; Funaioli, C; Lugli, F; Luppi, G; Merlano, M; Nobili, E; Nuzzo, C; Panzuto, F; Pastorelli, D; Pusceddu, S; Riccardi, F; Rinzivillo, M; Spada, F; Tomassetti, P; Zaniboni, A; Zatelli, MC, 2014)	2.17
"Everolimus is a novel proliferation signal inhibitor used in immunosuppressive therapies for the prevention of acute and chronic rejection. "	( Latex-enhanced turbidimetric immunoassay for everolimus in whole blood using the Nanopia TDM everolimus assay with the JCA-BM6010 automatic analyzer. Fukushima, N; Hidaka, Y; Kimura, S; Matsui, M; Mori, K; Suehisa, E, 2014)	2.1
"Everolimus (EVL) is an immunosuppressant indicated for allograft rejection and cancer therapy, but with narrow therapeutic window."	( Oral intake of curcumin markedly activated CYP 3A4: in vivo and ex-vivo studies. Chao, PD; Hou, YC; Hsieh, YW; Huang, CY; Peng, YH; Yang, SY; Yu, CP, 2014)	1.12
"Everolimus is an agent frequently associated with specific toxicities. "	( Translational studies within the TAMRAD randomized GINECO trial: evidence for mTORC1 activation marker as a predictive factor for everolimus efficacy in advanced breast cancer. Abadie-Lacourtoisie, S; Arnedos, M; Bachelot, T; Bourcier, AV; Cropet, C; Eymard, JC; Ferrero, JM; Legouffe, E; Levy, C; Lortholary, A; Pujade-Lauraine, E; Spaeth, D; Treilleux, I; Wang, Q, 2015)	2.06
"Everolimus is a mammalian target of rapamycin (mTOR) inhibitor. "	( Efficacy and Safety of Sequential Use of Everolimus in Patients With Metastatic Renal Cell Carcinoma Previously Treated With Bevacizumab With or Without Interferon Therapy: Results From the European AVATOR Study. Emmanouilides, C; Guillot, A; Jacobasch, L; Kelkouli, N; Kim, S; Nguyen Tan Hon, T; Papandreou, C; Schmitz, J; Slimane, K; Theodore, C; Thiery-Vuillemin, A, 2015)	2.13
"Everolimus is an orally administered inhibitor of the mammalian target of rapamycin (mTOR) recommended for patients with metastatic renal cell carcinoma (mRCC) who progressed on previous vascular endothelial growth factor (VEGF) receptor-tyrosine kinase inhibitor therapy. "	( Everolimus in patients with metastatic renal cell carcinoma previously treated with bevacizumab: a prospective multicenter study CRAD001LRU02T. Gurina, L; Manzuk, L; Safina, S; Snegovoy, A; Tsimafeyeu, I; Varlamov, I; Varlamov, S, 2015)	3.3
"Everolimus is a mammalian target of rapamycin inhibitor that has been used for immunosuppression, but its effect on recurrence and survival in HCC patients with a high risk of tumor recurrence has not been examined."	( Everolimus-based immunosuppression in patients with hepatocellular carcinoma at high risk of recurrence after liver transplantation: a case series. Diaz, SP; Ferreiro, AO; Gutiérrez, MG; López, FS; Patiño, MJ; Vazquez-Millán, MA, 2014)	2.57
"Everolimus is an effective and safe treatment option for TSC-related SEGA. "	( Factors affecting response to everolimus therapy for subependymal giant cell astrocytomas associated with tuberous sclerosis. Baranska, D; Dachowska, I; Fendler, W; Jozwiak, S; Kotulska, K; Mlynarski, W; Trelinska, J, 2015)	2.15
"Everolimus (EVE) is an immunosuppressive drug dosed according to therapeutic drug monitoring in renal transplant recipients. "	( Closer to the Site of Action: Everolimus Concentrations in Peripheral Blood Mononuclear Cells Correlate Well With Whole Blood Concentrations. Åsberg, A; Christensen, H; Falck, P; Midtvedt, K; Robertsen, I; Vethe, NT, 2015)	2.15
"Everolimus is a promising pharmacological approach to treat clinically significant inoperable cardiac rhabdomyomas or subependymal giant cell astrocytoma associated with tuberous sclerosis complex during the neonatal period."	( Use of mTOR inhibitor everolimus in three neonates for treatment of tumors associated with tuberous sclerosis complex. Dahdah, N; Goyer, I; Major, P, 2015)	2.17
"Everolimus is an orally-administered inhibitor of the mammalian target of rapamycin."	( The ORCHIDEE study: gathering new evidence on the use of everolimus in clinical practice. Cartenì, G; Floriani, I; Hollander, L; Pappagallo, G; Rizzo, M, )	1.1
"Everolimus is an immunosuppressant drug that was approved for prophylactic use in the United States to prevent organ rejection in adult kidney and liver transplant recipients. "	( Everolimus method comparison between Waters MassTrak™ Immunosuppressants XE (IUO) kit and an in-house laboratory developed LC-MS/MS method in renal transplant patients. Bradshaw, T; Johnson-Davis, KL; Juenke, JM; Thomas, RL, 2015)	3.3
"Everolimus is a recently approved option for posttransplant immunosuppression that spares renal function."	( Update on the management of the liver transplant patient. Fix, OK; Kwong, AJ, 2015)	1.14
"Everolimus is a mammalian target of rapamycin (mTOR) inhibitor approved for the treatment of metastatic renal cell carcinoma (mRCC). "	( The changes of lipid metabolism in advanced renal cell carcinoma patients treated with everolimus: a new pharmacodynamic marker? Ballatore, V; Carteni, G; Cascinu, S; Conti, A; Crucitti, P; Felici, A; Galli, L; Guida, FM; Iacovelli, R; Lugini, A; Milella, M; Modica, D; Ortega, C; Pantano, F; Porta, C; Procopio, G; Rauco, A; Rizzo, M; Russo, A; Santini, D; Santoni, M; Schinzari, G; Silletta, M; Tonini, G; Verzoni, E, 2015)	2.08
"Everolimus (RAD001) is an orally administered mTOR inhibitor that is well known for its antitumor efficacy and that has been approved for the treatment of several solid tumors, including renal cell carcinoma. "	( Successful control of heavily pretreated metastatic gastric cancer with the mTOR inhibitor everolimus (RAD001) in a patient with PIK3CA mutation and pS6 overexpression. Kang, YK; Na, YS; Park, JH; Park, SR; Park, YS; Rhoo, BY; Ryu, MH, 2015)	2.08
"Everolimus is an oral agent that targets the mammalian target of rapamycin (mTOR) pathway. "	( The mTORC1 inhibitor everolimus has antitumor activity in vitro and produces tumor responses in patients with relapsed T-cell lymphoma. Ansell, SM; Colgan, JP; Gupta, M; Habermann, TM; Han, JJ; Inwards, DJ; Johnston, PB; LaPlant, B; Macon, W; Markovic, S; Micallef, IN; Nowakowski, GS; Porrata, LF; Reeder, C; Stenson, M; Tun, HW; Witzig, TE, 2015)	2.18
"Everolimus is a viable option for the treatment of renal dysfunction, and earlier conversion is associated with better recovery of renal function."	( Renal function improvement in liver transplant recipients after early everolimus conversion: A clinical practice cohort study in Spain. Almohalla, C; Bilbao, I; Bustamante, J; Castroagudín, J; Crespo, G; Cuervas-Mons, V; De la Mata, M; Fabregat, J; Gómez, MA; Gonzalez-Dieguez, ML; Guilera, M; Herrero, I; Jimenez, C; Miras, M; Moreno, A; Narvaez, I; Otero, A; Rodrigo, J; Rubín, A; Salcedo, M; Serrano, T, 2015)	1.37
"Everolimus is an mTOR inhibitor approved for use in a number of indications where mTOR overactivation is implicated, including tuberous sclerosis complex."	( Long-Term Everolimus Treatment in Individuals With Tuberous Sclerosis Complex: A Review of the Current Literature. Tran, LH; Zupanc, ML, 2015)	1.54
"Everolimus is a mammalian target of rapamycin (mTOR) inhibitor used in vascular endothelial growth factor (VEGF)-refractory metastatic renal cell carcinoma (mRCC). "	( A Randomised Phase 2 Study of AZD2014 Versus Everolimus in Patients with VEGF-Refractory Metastatic Clear Cell Renal Cancer. Ahmed, I; Boleti, E; Burke, W; Din, O; Geldart, T; Hussain, S; Powles, T; Ralph, C; Robinson, A; Sarker, SJ; Stockdale, A; Sundar, S; Wheater, M; Wimalasingham, A, 2016)	2.14
"Everolimus is an oral inhibitor of the mammalian target of rapamycin pathway, which is aberrantly activated in NSCLC."	( Toxicity and adverse effects of everolimus in the treatment of advanced nonsmall cell lung cancer pretreated with chemotherapy--Chinese experiences. Hu, Y; Jiao, S; Ju, Y; Sun, S; Wang, J, 2015)	1.42
"Everolimus is an mammalian target of rapamycin (mTOR) complex 1 inhibitor that has been successfully used to treat subependymal giant cell astrocytomas and renal angiomyolipomas associated with TSC."	( Rapid resolution of cardiac rhabdomyomas following everolimus therapy. Anwar, S; Choudhry, S; Nguyen, HH, 2015)	1.39
"Everolimus is an approved agent for use after disease progression with vascular endothelial growth factor receptor-tyrosine kinase inhibitors (VEGFR-TKIs) in patients with metastatic renal cell carcinoma. "	( Everolimus Versus Temsirolimus in Metastatic Renal Cell Carcinoma After Progression With Previous Systemic Therapies. Agarwal, AM; Agarwal, N; Gill, DM; Hsu, J; Pal, SK; Patel, SB; Stenehjem, DD; Tantravahi, SK; Vuong, W, 2016)	3.32
"Everolimus appears to be a safe therapeutic option for patients aged <3 years with TSC-associated SEGA. "	( Safety of Everolimus in Patients Younger than 3 Years of Age: Results from EXIST-1, a Randomized, Controlled Clinical Trial. Berkowitz, N; Brechenmacher, T; Franz, DN; Jóźwiak, S; Kotulska, K, 2016)	2.28
"Everolimus (E) is a potent inhibitor of mTOR, a pathway frequently activated in HCC."	( Sorafenib with or without everolimus in patients with advanced hepatocellular carcinoma (HCC): a randomized multicenter, multinational phase II trial (SAKK 77/08 and SASL 29). Bodoky, G; Buehlmann, M; Demeter, G; Dufour, JF; Feilchenfeldt, J; Horber, D; Koeberle, D; Lakatos, G; Li, Q; Montemurro, M; Peck-Radosavljevic, M; Rauch, D; Ribi, K; Roth, AD; Saletti, P; Samaras, P; Tschanz, B; Wagner, AD, 2016)	1.46
"Everolimus is an immunosuppressant agent that has antiproliferative properties and negative effects on wound healing. "	( Extending Myringotomy Patency with Topical Everolimus in Rats. Akbulut, S; Altintas, H; Berk, D; Ozdemir, N, )	1.84
"Everolimus (EVR) is an orally-administered rapamycin analog that selectively inhibits the mammalian target of rapamycin (mTOR) kinase (mainly mTORC1 and likely mTORC2) and the related signaling pathway. "	( Everolimus improves memory and learning while worsening depressive- and anxiety-like behavior in an animal model of depression. Aiello, R; Chimirri, S; Citraro, R; Constanti, A; Crupi, R; Cuzzocrea, S; De Sarro, G; Leo, A; Lippiello, P; Russo, E; Spiga, R, 2016)	3.32
"Everolimus (EVE) is a mammalian target of rapamycin inhibitor (mTOR-I) widely used in transplantation that may determine some severe adverse events, including pulmonary fibrosis. "	( Everolimus-induced epithelial to mesenchymal transition (EMT) in bronchial/pulmonary cells: when the dosage does matter in transplantation. Bellin, G; Carratù, P; Chilosi, M; Ficial, M; Gambaro, G; Granata, S; Lupo, A; Masola, V; Onisto, M; Resta, O; Tomei, P; Ventura, VA; Zaza, G, 2016)	3.32
"Everolimus is a mammalian target of rapamycin inhibitor that has been recently approved for the treatment of patients with advanced progressive pancreatic neuroendocrine tumor. "	( Early Response to Everolimus Therapy Detected on 68Ga-DOTATATE PET/CT in a Patient With Pancreatic Neuroendocrine Tumor. Atmaca, A; Demirag, G; Ozkan, E; Soydal, C; Ucak Semirgin, S; Yapici, O, 2016)	2.21
"Everolimus is a mTOR inhibitor used for the treatment of different solid malignancies. "	( Everolimus pharmacokinetics and its exposure-toxicity relationship in patients with thyroid cancer. de Wit, D; den Hartigh, J; Gelderblom, H; Guchelaar, HJ; Kapiteijn, E; Links, TP; Moes, DJ; Roozen, CF; Schneider, TC; van der Hoeven, JJ; van Erp, NP, 2016)	3.32
"Everolimus (EVR) is a potent mammalian target of rapamycin inhibitor that is used after transplantation and to treat advanced malignancies, as we have done in Taiwan after heart transplantation since 2004."	( Malignancy After Heart Transplantation Under Everolimus Versus Mycophenolate Mofetil Immunosuppression. Chen, YS; Chi, NH; Chou, NK; Huang, SC; Shun, CT; Tsai, JT; Tsao, CI; Wang, CH; Wang, SS; Wang, YJ; Wu, IH; Yu, HY, 2016)	1.42
"Everolimus (EVL) is a novel mTOR-inhibitor similar to sirolimus (SRL) that is used in organ transplant recipients, often in combination with tacrolimus (TAC) or mycophenolate (MPA). "	( Immunoregulatory Effects of Everolimus on In Vitro Alloimmune Responses. Gallon, L; Huang, X; Leventhal, JR; Levitsky, J; Mathew, JM; Miller, J, 2016)	2.17
"Everolimus is an inhibitor of mTOR, approved for treatment of advanced pancreatic neuroendocrine tumors (NETs). "	( The efficacy and safety of everolimus for the treatment of progressive gastroenteropancreatic neuroendocrine tumors: A multi-institution observational study in Taiwan. Chen, JS; Chen, LT; Chen, MH; Chen, YY; Chou, WC; Ku, FC; Liu, CT; Lu, CH; Shan, YS; Su, YL, 2016)	2.17
"Everolimus is a licensed medicine in this patient group, but for a different target of effect."	( The use of everolimus in the treatment of neurocognitive problems in tuberous sclerosis (TRON): study protocol for a randomised controlled trial. Angel, L; Cannings-John, R; Davies, DM; de Vries, PJ; Drew, C; Hood, K; Kirby, N; McDermott, E; McNamara, R; Owen-Jones, E; Randell, E; Sampson, JR; Saxena, A; Smalley, M; Stockwell, L, 2016)	1.55
"Everolimus is an allosteric inhibitor of the mechanistic target of rapamycin complex 1 (mTORC1) widely known for its potent autophagy stimulating properties. "	( Continuous administration of the mTORC1 inhibitor everolimus induces tolerance and decreases autophagy in mice. Apers, S; De Doncker, M; De Meyer, GRY; Kurdi, A; Leloup, A; Lemmens, K; Martinet, W; Neels, H; Timmermans, JP, 2016)	2.13
"Everolimus seems to be an effective treatment option not only for SEGA and AML, but also for TSC-related epilepsies. "	( Efficacy and safety of Everolimus in children with TSC - associated epilepsy - Pilot data from an open single-center prospective study. Abraham, K; Dressler, A; Feucht, M; Gröppel, G; Kasprian, G; Laccone, F; Mühlebner-Fahrngruber, A; Samueli, S; Scholl, T, 2016)	2.19
"Everolimus is a mammalian target of rapamycin (mTOR) inhibitor approved by the US Food and Drug Administration (FDA) and European Medicines Agency (EMA) in 2016 for treatment of adults with progressive, well-differentiated, non-functional NETs of gastrointestinal (GI) or lung origin that are unresectable, locally advanced, or metastatic."	( Budget impact of everolimus for the treatment of progressive, well-differentiated, non-functional neuroendocrine tumors of gastrointestinal or lung origin that are advanced or metastatic. Cai, B; Neary, MP; Nellesen, D; Rose, DB, 2017)	1.52
"Everolimus is a mammalian target of rapamycin inhibitor with both antitumor and radiosensitizing effects."	( Phase 1 Trial of Everolimus and Radiation Therapy for Salvage Treatment of Biochemical Recurrence in Prostate Cancer Patients Following Prostatectomy. Bekelman, JE; Christodouleas, JP; Deville, C; Haas, NB; Mick, R; Narayan, V; Rajendran, R; Subramanian, P; Vapiwala, N, 2017)	1.52
"Everolimus monotherapy is a valid therapeutic option in the relapsed and/or refractory indolent non-Hodgkin lymphoma patients and is well tolerated."	( Efficacy of the oral mTORC1 inhibitor everolimus in relapsed or refractory indolent lymphoma. Ansell, SM; Bennani, NN; Colgan, JP; Ghobrial, IM; Habermann, TM; Inwards, DJ; Johnston, PB; LaPlant, BR; Macon, WR; Markovic, SN; Micallef, IN; Mikhael, JR; Northfelt, DW; Nowakowski, GS; Porrata, LF; Reeder, CB; Witzig, TE, 2017)	1.45
"Everolimus is a more recently developed PSI with molecular structure very similar to that of sirolimus."	( Everolimus-related pulmonary toxicity in heart transplant recipients. de Prada, JA; Expósito, V; Fernández-Valls, M; García-Camarero, T; Gómez-Román, JJ; González-Vilchez, F; Llano-Cardenal, M; Martín-Durán, R; Ruano, J, 2008)	2.51
"Everolimus is an immunosuppressant drug with proven efficacy in transplantation. "	( Everolimus: an update on the mechanism of action, pharmacokinetics and recent clinical trials. Sánchez-Fructuoso, AI, 2008)	3.23
"Everolimus (RAD001) is an orally administered inhibitor of the mammalian target of rapamycin (mTOR), a therapeutic target for metastatic renal cell carcinoma. "	( Efficacy of everolimus in advanced renal cell carcinoma: a double-blind, randomised, placebo-controlled phase III trial. Berg, WJ; Bracarda, S; Escudier, B; Figlin, RA; Grünwald, V; Hollaender, N; Hutson, TE; Kay, A; Lebwohl, D; Motzer, RJ; Oudard, S; Porta, C; Ravaud, A; Thompson, JA; Urbanowitz, G, 2008)	2.17
"Everolimus is a poorly soluble drug and was, therefore, incorporated in an eye-administrable microemulsion. "	( Corneal permeation studies of everolimus microemulsion. Baspinar, Y; Bertelmann, E; Borchert, HH; Buech, G; Pleyer, U; Siebenbrodt, I, 2008)	2.08
"Everolimus is a novel proliferation signal inhibitor that has potent immunosuppressive activity. "	( Prolongation of corneal allograft survival by topical application of everolimus in experimental keratoplasty. Bertelmann, E; Buch, G; Li, XQ; Otasevic, L; Pleyer, U; Schlickeiser, S, 2008)	2.02
"Everolimus is a potential trigger of angioedema."	( [67-year-old patient with speech disorder and dysphagia]. Er, F; Erdmann, E; Nia, AM, 2008)	1.79
"Everolimus is a potent immunosuppressive drug that is as effective as mycophenolate mofetil (MMF) or azathioprine (AZA) in preventing acute transplant rejection when used in combination with cyclosporin A (CyA). "	( Everolimus in liver and lung transplantation. Koch, M, 2009)	3.24
"Everolimus is an orally administered, targeted therapy indicated for the treatment of advanced renal cell carcinoma. "	( Everolimus: in advanced renal cell carcinoma. Garnock-Jones, KP; Keating, GM, 2009)	3.24
"Everolimus is a rapamycin-derived macrolide with immunosuppressive and antiproliferative effects."	( Severe atopic dermatitis treated with everolimus. Bruijnzeel-Koomen, CA; Haeck, IM; Van Velsen, SG, 2009)	1.35
"Everolimus does not seem to be an effective treatment in these two AD patients, either in combination with prednisone or with CsA."	( Severe atopic dermatitis treated with everolimus. Bruijnzeel-Koomen, CA; Haeck, IM; Van Velsen, SG, 2009)	2.07
"Everolimus is an oral agent targeting raptor mTOR (mTORC1)."	( Phase II trial of the oral mammalian target of rapamycin inhibitor everolimus in relapsed or refractory Waldenstrom macroglobulinemia. Anderson, KC; Ansell, SM; Bergsagel, L; Camoriano, J; Chuma, S; Deangelo, D; Dispenzieri, A; Gertz, M; Ghobrial, IM; Harris, B; Hayman, S; Lacy, M; Laplant, B; Leduc, R; Reeder, C; Richardson, PG; Rourke, M; Treon, SP; Witzig, TE, 2010)	1.32
"Everolimus (EVL) is a signal proliferation inhibition that reduces graft vascular disease when used de novo."	( South American Heart Transplantation Registry of patients receiving everolimus in their immunosuppressive regimens. Ahualli, L; Amuchástegui, M; Bortman, GV; Burgos, C; Ceruti, B; Colque, R; Diez, F; Muñoz, J; Perrone, SV; Rodriguez, MC; Sgrosso, JL; Vulcano, N, )	1.09
"Everolimus (RAD001) is an orally administered inhibitor of the mammalian target of rapamycin (mTOR), a therapeutic target for metastatic renal cell carcinoma. "	( Acute cholecystitis in a patient with metastatic renal cell carcinoma treated with everolimus. Baykara, M; Benekli, M; Buyukberber, S; Cetin, B; Coskun, U; Yildiz, R, 2011)	2.04
"Everolimus is an oral antineoplastic agent that targets the raptor mammalian target of rapamycin (mTORC1). "	( A Phase II trial of the oral mTOR inhibitor everolimus in relapsed Hodgkin lymphoma. Ansell, SM; Colgan, JP; Habermann, TM; Inwards, DJ; Johnston, PB; Kabat, BF; Laplant, BR; Micallef, IN; Porrata, LF; Reeder, CB; Roy, V; Witzig, TE, 2010)	2.06
"Everolimus is a novel inhibitor of the mammalian target of rapamycin pathway, which is aberrantly activated in nonsmall cell lung cancer (NSCLC). "	( Phase 1 and pharmacokinetic study of everolimus, a mammalian target of rapamycin inhibitor, in combination with docetaxel for recurrent/refractory nonsmall cell lung cancer. Egorin, MJ; Fu, H; Harvey, RD; Kauh, J; Khuri, FR; Owonikoko, TK; Ramalingam, SS; Saba, N; Shin, DM; Strychor, S; Sun, SY; Tighiouart, M, 2010)	2.08
"Everolimus is an oral rapamycin analog that acts by selectively inhibiting mTOR."	( A phase 2 study of the oral mammalian target of rapamycin inhibitor, everolimus, in patients with recurrent endometrial carcinoma. Broaddus, RR; Burke, TW; Coleman, RL; Gershenson, DM; Johnston, T; Lu, KH; Munsell, M; Ramondetta, LM; Slomovitz, BM; Walker, C; Wolf, J, 2010)	1.32
"Everolimus is a recently developed immunosuppressive drug for patients following solid organ transplantation. "	( Severe stomatitis complicating immune-suppressive switch after cardiac transplantation. Conraads, V; Rodrigus, IE; Vermeulen, T; Vrints, CJ, )	1.57
"Everolimus (RAD001) is a novel mammalian target of rapamycin (mTOR) inhibitor, and anti-proliferative activity in various malignancies has been reported. "	( Schedule-dependent inhibition of T-cell lymphoma cells by cotreatment with the mTOR inhibitor everolimus and anticancer drugs. He, XX; Huang, JJ; Huang, Y; Li, ZM; Lin, TY; Tian, Y; Xiao, J, 2012)	2.04
"Everolimus is an oral agent that targets the raptor mammalian target of rapamycin (mTORC1)."	( A phase II trial of the oral mTOR inhibitor everolimus in relapsed aggressive lymphoma. Ansell, SM; Colgan, JP; Ghobrial, IM; Gupta, M; Habermann, TM; Jacobsen, ED; Johnston, PB; LaPlant, BR; Micallef, IN; Porrata, LF; Reeder, CB; Witzig, TE, 2011)	1.35
"Everolimus is an oral mammalian target of rapamycin (mTOR) inhibitor approved for the management of patients with advanced renal cell carcinoma who progressed on tyrosine kinase inhibitor therapy. "	( Everolimus: a new mammalian target of rapamycin inhibitor for the treatment of advanced renal cell carcinoma. Grgic, T; Hammond, JM; Mis, L, 2011)	3.25
"Everolimus is an immunosuppressant requiring routine monitoring in whole blood. "	( Evaluation of QMS everolimus assay using Hitachi 917 Analyzer: comparison with liquid chromatography/mass spectrometry. Chow, L; Dasgupta, A; Davis, B, 2011)	2.15
"Everolimus is an orally administered inhibitor of the mammalian target of rapamycin that recently received approval from the European Medicines Agency for the treatment of advanced RCC that has progressed on or after treatment with vascular endothelial growth factor (VEGF)-targeted therapy, and from the United States Food and Drug Administration for treatment of advanced RCC after failure of sorafenib or sunitinib."	( Management of adverse events associated with the use of everolimus in patients with advanced renal cell carcinoma. Climent, MA; Creel, P; Dickow, B; Fischer, P; Gornell, SS; Meloni, F; Motzer, RJ; Osanto, S; Porta, C; Ravaud, A; Vaishampayan, U; White, DA, 2011)	1.34
"Everolimus-induced OU is a frequent, recurrent and sometimes harmful complication. "	( Natural history, management and pharmacokinetics of everolimus-induced-oral ulcers: insights into compliance issues. André, F; Ferté, C; Gomez-Roca, C; Gonzales, DB; Goubar, A; Massard, C; Paci, A; Sahmoud, T; Soria, JC; Zizi, M, 2011)	2.06
"Everolimus is a novel inhibitor of the mammalian target of rapamycin pathway, which is aberrantly activated in cancer cell. "	( Phase I trial of capecitabine plus everolimus (RAD001) in patients with previously treated metastatic gastric cancer. Ahn, HK; Baek, KK; Han, B; Kang, WK; Kim, KM; Lee, DJ; Lee, HY; Lee, J; Lee, SJ; Lim, HY; Lim, T; Park, JO; Park, SH; Park, YS, 2011)	2.09
"Everolimus is a proliferation-signal inhibitor which was introduced for heart transplant recipients in 2004. "	( Calcineurin inhibitor-free immunosuppression using everolimus (Certican) after heart transplantation: 2 years' follow-up from the University Hospital Münster. Amler, S; Drees, G; Eckernkemper, S; Engelen, MA; Gunia, S; Rothenburger, M; Rukosujew, A; Sindermann, JR; Stypmann, J; Welp, HA, 2011)	2.06
"Everolimus is an oral mTOR-inhibitor. "	( Phase I and pharmacokinetic study of capecitabine and the oral mTOR inhibitor everolimus in patients with advanced solid malignancies. Beijnen, JH; Deenen, MJ; Klümpen, HJ; Richel, DJ; Schellens, JH; Sparidans, RW; Weterman, MJ; Wilmink, JW, 2012)	2.05
"Everolimus is an oral mTOR kinase inhibitor approved for the treatment of patients with metastatic renal cell carcinoma (mRCC) progressing during or after treatment with vascular endothelial growth factor (VEGF)-targeted agents. "	( [Metastatic renal cell carcinoma treated with everolimus--data from the RENIS Clinical Registry]. Abrahámová, J; Bortlícek, Z; Büchler, T; Budnáková, D; Dusek, L; Fínek, J; Jarkovský, J; Kandrnal, V; Klimes, D; Poprach, A; Vyzula, R, 2011)	2.07
"Everolimus is an orally administered inhibitor of the mammalian target of rapamycin (mTOR). "	( Everolimus: in patients with subependymal giant cell astrocytoma associated with tuberous sclerosis complex. Curran, MP, 2012)	3.26
"Everolimus is a rapamycin analog that inhibits mTOR, but it is more soluble than rapamycin and can be administered orally."	( Clinical review: Current scientific rationale for the use of somatostatin analogs and mTOR inhibitors in neuroendocrine tumor therapy. Billah, SM; Bousquet, C; Caron, P; Chalabi, M; Lasfargues, C; Pyronnet, S; Susini, C; Vezzosi, D, 2012)	1.1
"Everolimus (RAD001) is an mTOR inhibitor that has been successfully used as an immunosuppressant in solid-organ transplantation. "	( Everolimus in combination with cyclosporin a as pre- and posttransplantation immunosuppressive therapy in nonmyeloablative allogeneic hematopoietic stem cell transplantation. Altmann, S; Drewelow, B; Freund, M; Junghanss, C; Lange, S; Mueller, S; Rathsack, S; Vogel, H; Wacke, R; Weirich, V, 2012)	3.26
"Everolimus (RAD001) is an oral antineoplastic agent derived from rapamycin, a macrocyclic lactone antibiotic, targeting the mammalian target of rapamycin (mTOR)."	( mTOR as a target of everolimus in refractory/relapsed Hodgkin lymphoma. Gadaleta, CD; Giannoccaro, M; Guarini, A; Iacobazzi, A; Lapietra, A; Minoia, C; Raimondi, A; Rana, A; Ranieri, G; Silvestris, N, 2012)	1.42
"Everolimus is a mammalian target of rapamycin inhibitor approved for use as an immunosuppressant and antineoplastic agent. "	( Fatal acute pulmonary injury associated with everolimus. Benoit, D; Caes, F; Depuydt, P; Nollet, J; Praet, M, 2012)	2.08
"Everolimus (EVL) is a mammalian target of rapamycin inhibitor, providing a safe and effective immunosuppressive regime after kidney transplantation."	( Everolimus: preventing organ rejection in adult kidney transplant recipients. Dantal, J, 2012)	2.54
"Everolimus is a novel macrolide immunosuppressant used in the prevention of acute and chronic rejection of solid organ transplants. "	( Population pharmacokinetics and pharmacogenetics of everolimus in renal transplant patients. de Fijter, JW; den Hartigh, J; Guchelaar, HJ; Moes, DJ; Press, RR; van der Straaten, T, 2012)	2.07
"Everolimus is an effective agent with several advantages for pediatric solid-organ transplantation. "	( Everolimus in pediatric transplantation. Ahlenstiel, T; Ganschow, R; Pape, L, 2012)	3.26
"Everolimus is an oral mammalian target of rapamycin (mTOR) inhibitor approved by the FDA in May 2011 for the treatment of progressive, advanced pNET. "	( Everolimus: a new treatment option for advanced pancreatic neuroendocrine tumors. Kim, M; O'Bryant, CL; Thompson, LA; Wenger, SD, 2012)	3.26
"The everolimus-eluting stent is a second-generation DES that is very effective for de novo coronary lesions."	( Repeat drug-eluting stent implantation for in-stent restenosis: first- or second-generation stent. Araki, H; Ebara, S; Hoshimoto, K; Isomura, N; Obara, C; Ochiai, M; Okabe, T; Saito, S; Yakushiji, T; Yamamoto, MH; Yamashita, K, 2012)	0.94
"Everolimus is an effective second-line treatment for Taiwanese patients with mRCC. "	( Everolimus in metastatic renal cell carcinoma: preliminary experience from Chang Gung Memorial Hospital. Chang, JW; Chang, YH; Chiang, YJ; Chuang, CK; Hsieh, JJ; Huang, WK; Liaw, CC; Lin, YC; Ou, LY; Pang, ST; Tsai, SI; Wang, HM; Wu, CT; Yang, CH; Yang, CT, )	3.02
"Everolimus is an immunosuppressant that blocks growth factor-mediated proliferation of hematopoietic cells by targeting the mammalian target of rapamycin (mTOR). "	( Interactions of everolimus and sorafenib in whole blood lymphocyte proliferation. Fetterly, GJ; Jusko, WJ; Ma, WW; Pawaskar, DK; Straubinger, RM, 2013)	2.18
"Everolimus (RAD001) is an allosteric mTOR inhibitor that has shown marked efficacy in certain cancers but is unable to completely inhibit mTOR activity."	( RAD001 enhances the potency of BEZ235 to inhibit mTOR signaling and tumor growth. Cao, ZA; Chen, Y; Das, R; Finan, PM; Huang, A; Lehár, J; Li, X; Murphy, LO; Nyfeler, B; Pinzon-Ortiz, M; Pradhan, E; Reddy, A; Schlegel, R; Wang, Z, 2012)	1.1
"Everolimus is a mammalian target of rapamycin (mTOR) inhibitor approved for treatment of renal cell carcinoma, subependymal giant cell astrocytoma, breast cancer, and progressive neuroendocrine tumors of pancreatic origin. "	( Rash to the mTOR inhibitor everolimus: systematic review and meta-analysis. Case, EC; Cerci, FB; Lacouture, ME; Ramirez-Fort, MK; Rosen, AC; Wu, S, 2014)	2.14
"Everolimus is a derivative of sirolimus, and is considered to be free of the latter's pulmonary toxicity. "	( Early everolimus-induced pneumonitis in a renal transplant recipient: A case report. Durlik, M; Gołębiowski, M; Małkowski, P; Miszewska-Szyszkowska, D; Palczewski, P; Sułkowska, K, 2012)	2.3
"Everolimus is an mTOR inhibitor commonly used to treat metastatic pancreatic neuroendocrine tumors (pNETs) and renal cell carcinoma, and for posttransplant immunosuppression. "	( Everolimus causing severe hypertriglyceridemia and acute pancreatitis. Kunz, PL; Subramaniam, S; Zell, JA, 2013)	3.28
"Everolimus appears to be a new effective treatment for patients with metastatic insulinoma and refractory hypoglycemia. "	( Efficacy of everolimus in patients with metastatic insulinoma and refractory hypoglycemia. Baudin, E; Bernard, V; Borson-Chazot, F; Caroli-Bosc, FX; Chougnet, CN; Goichot, B; Guimbaud, R; Lombard-Bohas, C; Niccoli, P; Rohmer, V; Ruszniewski, P; Taquet, MC, 2013)	2.21
"Everolimus is an immunosuppressive macrolide bearing a stable 2-hydroxyethyl chain substitution at position 40 on the sirolimus (rapamycin) structure. "	( Clinical pharmacokinetics of everolimus. Kirchner, GI; Manns, MP; Meier-Wiedenbach, I, 2004)	2.06
"Everolimus is a derivative of sirolimus, a macrocyclic lactone, originally isolated from Streptomyces hygroscopicus. "	( The evolving experience using everolimus in clinical transplantation. Bia, MJ; Formica, RN; Friedman, AL; Lakkis, F; Lorber, KM; Lorber, MI; Smith, JD, 2004)	2.05
"Everolimus is a novel macrolide immunosuppressant that acts as a T-lymphocyte proliferation signal inhibitor. "	( Experience with everolimus. Augustine, JJ; Hricik, DE, 2004)	2.11
"Everolimus is a potent immunosuppressor that inhibits growth factor-stimulated proliferation of hematopoietic and nonhematopoietic cells, including vascular smooth muscle."	( Everolimus: a proliferation signal inhibitor targeting primary causes of allograft dysfunction. Kovarik, JM, 2004)	2.49
"Everolimus is an immunosuppressant that blocks growth factor-mediated proliferation of haematopoietic and nonhaematopoietic cells. "	( Everolimus. Chapman, TM; Perry, CM, 2004)	3.21
"Everolimus is a proliferation inhibitor designed to target chronic rejection, including prevention of acute rejection. "	( Everolimus (Certican) 12-month safety and efficacy versus mycophenolate mofetil in de novo renal transplant recipients. Cretin, N; Dantal, J; Jappe, A; Li, Y; Margreiter, R; Viljoen, HG; Vítko, S; Weimar, W, 2004)	3.21
"Everolimus (Certican) is a novel proliferation signal inhibitor with potent immunosuppressant effects that has been shown to prevent and reverse acute rejection in preclinical models of kidney, heart, and lung transplantation. "	( Introducing everolimus (Certican) in organ transplantation: an overview of preclinical and early clinical developments. Neumayer, HH, 2005)	2.15
"Everolimus is a novel proliferation signal inhibitor used in immunosuppressive therapies for the prevention of acute and chronic rejection. "	( The role of therapeutic monitoring of everolimus in solid organ transplantation. Ensom, MH; Mabasa, VH, 2005)	2.04
"Everolimus is a proliferation signal inhibitor with immunosuppressive activity that may reduce the rate of progression of chronic rejection, bronchiolitis obliterans syndrome (BOS), after lung transplantation. "	( Everolimus versus azathioprine in maintenance lung transplant recipients: an international, randomized, double-blind clinical trial. Aris, R; Glanville, AR; Hmissi, A; Loyd, JE; McGiffin, DC; Pirron, U; Roman, A; Snell, GI; Sole, A; Valentine, VG; Vitulo, P, 2006)	3.22
"Everolimus (Certican) is an orally administered mammalian target of rapamycin inhibitor (proliferation signal inhibitor) derived from sirolimus (rapamycin), which is used as part of immunosuppressant therapy in kidney and heart transplantation. "	( Everolimus: a review of its use in renal and cardiac transplantation. Croom, KF; Dunn, C, 2006)	3.22
"Everolimus is a macrolide immunosuppressive agent with known consistent absorption. "	( Safety, tolerability, and efficacy of everolimus in de novo liver transplant recipients: 12- and 36-month results. Abecassis, M; Calmus, Y; Fischer, L; Freeman, R; Klempnauer, J; Langnas, A; Levy, G; Mayer, D; Nashan, B; Neuhaus, P; Punch, J; Roberts, J; Rogiers, X; Samuel, D; Schmidli, H; Sloof, M; Tuttle-Newhall, E, 2006)	2.05
"Everolimus (RAD) is an mTOR inhibitor closely related to rapamycin. "	( Everolimus (RAD) inhibits in vivo growth of murine squamous cell carcinoma (SCC VII). Khariwala, SS; Kjaergaard, J; Lorenz, R; Shu, S; Strome, M; Van Lente, F, 2006)	3.22
"Everolimus is a novel immunosuppressive agent related to sirolimus. "	( Everolimus: an immunosuppressive agent in transplantation. Kobashigawa, JA; Patel, JK, 2006)	3.22
"Everolimus is a proliferation signal inhibitor (PSI)/mammalian target of rapamycin inhibitor that is structurally similar to sirolimus, but with a number of important pharmacokinetic differences, including a shorter half-life and time to steady state. "	( Everolimus in clinical practice--renal transplantation. Pascual, J, 2006)	3.22
"Everolimus is a potent immunosuppressive agent that has anti-proliferative activity. "	( Long-term cardiovascular risk in transplantation--insights from the use of everolimus in heart transplantation. Eisen, H, 2006)	2.01
"Everolimus is a potent immunosuppressant used in renal transplant therapy, but its effects on renal endothelial cell regeneration after injury are unknown. "	( Everolimus inhibits glomerular endothelial cell proliferation and VEGF, but not long-term recovery in experimental thrombotic microangiopathy. Daniel, C; Endlich, KH; Hugo, C; Johnson, RJ; Keller, K; Kerjaschki, D; Schöcklmann, H, 2006)	3.22
"Everolimus is an orally active derivative of sirolimus. "	( Optimal dosing and duration of oral everolimus to inhibit in-stent neointimal growth in rabbit iliac arteries. Baffour, R; Hellinga, D; Kolodgie, F; Pakala, R; Seabron, R; Virmani, R; Waksman, R, )	1.85
"Everolimus (Certican) is a new immunosuppressant derived from sirolimus (Rapamune) with a 2-hydroxyethyl chain at position 40 of the macrolide ring. "	( Determination of everolimus in whole blood using the Abbott IMx sirolimus microparticle enzyme immunoassay. Bouzas, L; Tutor, JC, 2007)	2.12
"Everolimus is a proliferation signal-inhibitor recently introduced in heart transplant recipients. "	( Calcineurin inhibitor-free immunosuppression using everolimus (Certican) in maintenance heart transplant recipients: 6 months' follow-up. Bara, C; Bruch, C; Hinder, F; Lehmkuhl, H; Rothenburger, M; Schmid, C; Stypmann, J; Suwelack, B; Teerling, E; Wichter, T, 2007)	2.03
"Everolimus is a novel macrolide immunosuppressant developed for the prophylaxis of allogeneic renal or cardiac transplant rejection. "	( Physiologically based pharmacokinetic (PBPK) modeling of everolimus (RAD001) in rats involving non-linear tissue uptake. Kawai, R; Laplanche, R; Meno-Tetang, GM, 2007)	2.03
"Everolimus is an immunosuppressive agent that reduces cardiac allograft vasculopathy. "	( Prevention of acute rejection and allograft vasculopathy by everolimus in cardiac transplants recipients: a 24-month analysis. Abeywickrama, K; Benza, R; Boissonnat, P; Cretin, N; Eisen, HJ; Haverich, A; Hill, J; Laufer, G; Love, R; Parameshwar, J; Pulpón, LA; Renlund, D; Starling, RC; Tuzcu, M; Viganò, M, 2007)	2.02
"Everolimus (RAD001) is an inhibitor of the mammalian target of rapamycin, which is downstream of initial epidermal growth factor receptor signaling."	( Rationale for a phase I trial of erlotinib and the mammalian target of rapamycin inhibitor everolimus (RAD001) for patients with relapsed non small cell lung cancer. Jackman, D; Jänne, PA; Johnson, BE, 2007)	1.28
"Everolimus is an mTOR inhibitor sirolimus analogue, that has proved, to be highly efficacious to prevent acute myocardial rejection and reduce the severity of cardiac allograft vasculopathy in de novo HTx patients."	( Possible role of everolimus in improving renal function in long-term heart transplantation. Fiocchi, R; Fontana, A; Gamba, A; Gandolfi, L; Iacovoni, A; Sebastiani, R, )	1.19
"Everolimus is a new immunosuppressant with antitumoral properties and few side effects, but limited use in liver transplantation. "	( Use of everolimus as a rescue immunosuppressive therapy in liver transplant patients with neoplasms. Bañares, R; Clemente, G; Gomez-Camarero, J; Hernando, A; Lo Iacono, O; Rincon, D; Ripoll, C; Salcedo, M; Sanz, C, 2007)	2.24
"Everolimus is an immunosuppressant used as rejection prophylaxis in patients undergoing transplants. "	( Crossreactivity of isolated everolimus metabolites with the Innofluor Certican immunoassay for therapeutic drug monitoring of everolimus. Arabshahi, L; Boyd, J; Christians, U; Haschke, M; Marbach, P; Roberts, M; Strom, T, 2007)	2.08
"Everolimus is a selective mammalian target of rapamycin (mTOR) inhibitor with promising anticancer activity. "	( Dose- and schedule-dependent inhibition of the mammalian target of rapamycin pathway with everolimus: a phase I tumor pharmacodynamic study in patients with advanced solid tumors. Baselga, J; Burris, H; Calvo, E; Dimitrijevic, S; Hazell, K; Jones, S; Judson, I; Lane, HA; Lebwohl, D; Macarulla, T; Martinelli, E; Ramon y Cajal, S; Ramos, FJ; Rojo, F; Shand, N; Stumm, M; Tabernero, J; Tang, P; Vidal, L; Zoellner, U, 2008)	2.01
"Everolimus is a macrolide immunosuppressant intended for acute rejection prophylaxis after kidney transplantation."	( Population pharmacokinetics of everolimus in de novo renal transplant patients: impact of ethnicity and comedications. Berthier, S; Hsu, CH; Kovarik, JM; McMahon, L; Rordorf, C, 2001)	2.04
"Everolimus is an immunosuppressant intended for use with cyclosporine in acute-rejection prophylaxis following organ transplantation. "	( Differential influence of two cyclosporine formulations on everolimus pharmacokinetics: a clinically relevant pharmacokinetic interaction. Figueiredo, J; Frazier, OL; Kalbag, J; Kovarik, JM; Rordorf, C; Rouilly, M, 2002)	2

Excerpt	Reference	Relevance
"Everolimus has a significant impact on red blood cell parameters in patients with TSC."	( New Insights into Red Blood Cell Microcytosis upon mTOR Inhibitor Administration. Jakubowska, J; Jóźwiak, S; Kotulska, K; Młynarski, W; Pawlik, B; Stolarska, M; Trelińska, J; Wyka, K, 2021)	1.34
"Everolimus has a high single-agent activity of 73% including MR, with a progression free survival of 21 months, indicating that this agent is active in relapsed/refractory WM."	( Long-term results of the phase II trial of the oral mTOR inhibitor everolimus (RAD001) in relapsed or refractory Waldenstrom Macroglobulinemia. Bergsagel, PL; Camoriano, J; Chuma, S; DeAngelo, D; Gertz, M; Ghobrial, IM; Hayman, S; Lacy, M; LaPlant, B; Treon, SP; Witzig, TE, 2014)	1.36
"Everolimus has a favorable pharmacokinetic (PK) profile in early breast cancer studies."	( Evaluating the pharmacokinetics and pharmacodynamics of everolimus for treating breast cancer. Awada, A; Barthélémy, P; Gombos, A, 2015)	1.38
"Everolimus has a mechanism of action similar to that of sirolimus."	( Clinical pharmacokinetics of everolimus. Kirchner, GI; Manns, MP; Meier-Wiedenbach, I, 2004)	1.34
"Everolimus has an appropriate rationale for therapeutic use in combination with erlotinib for patients with NSCLC. "	( Rationale for a phase I trial of erlotinib and the mammalian target of rapamycin inhibitor everolimus (RAD001) for patients with relapsed non small cell lung cancer. Jackman, D; Jänne, PA; Johnson, BE, 2007)	2
"Everolimus has been replaced in the second line setting by these new options."	( [Interdisciplinary recommendations for the treatment of advanced renal cell carcinoma]. Bergmann, L; Doehn, C; Grünwald, V; Gschwend, JE; Ivanyi, P; Kuczyk, MA; Miller, K, 2022)	1.44
"Everolimus (EVR) has been reported to be widely used to prevent the progression of organ fibrosis and graft rejection."	( Everolimus Alleviates Renal Allograft Interstitial Fibrosis by Inhibiting Epithelial-to-Mesenchymal Transition Not Only Chen, H; Fei, S; Gu, M; Gui, Z; Han, Z; Ju, X; Sun, L; Suo, C; Tan, R; Tao, J; Wang, Z; Zhang, H; Zheng, M, 2021)	2.79
"Everolimus has been continued for 6 years without severe side effects."	( A mechanistic target of rapamycin inhibitor, everolimus safely ameliorated lupus nephritis in a patient complicated with tuberous sclerosis. Katada, Y; Ohshima, S; Okita, Y; Saeki, Y; Yoshimura, M, 2023)	1.89
"Everolimus has recently been used to prevent graft rejection in liver transplantation and reduces the incidence of kidney dysfunction caused by calcineurin inhibitors. "	( Population pharmacokinetics of everolimus in adult liver transplant patients: Comparison to tacrolimus disposition and extrapolation to pediatrics. Hata, K; Hatano, E; Hira, D; Hirai, M; Imai, S; Ito, T; Itohara, K; Matsubara, K; Nakagawa, S; Nakagawa, T; Sugimoto, M; Terada, T; Yano, I; Yonezawa, A, 2022)	2.45
"Everolimus (EVE) has been used as a calcineurin inhibitor (CNI) minimization/ elimination agent or to augment immunosuppression in lung transplant recipients (LTR) with CNI-induced nephrotoxicity or neurotoxicity. "	( Rescue Everolimus Post Lung Transplantation is Not Associated With an Increased Incidence of CLAD or CLAD-Related Mortality. Dooley, M; Ivulich, S; Kirkpatrick, C; Paraskeva, M; Paul, E; Snell, G, 2023)	2.81
"Everolimus has shown positive effects on subependymal giant cell astrocytomas, renal angiomyolipoma and refractory seizures associated with tuberous sclerosis complex."	( Everolimus for cardiac rhabdomyomas in children with tuberous sclerosis. The ORACLE study protocol (everOlimus for caRdiac rhAbdomyomas in tuberous sCLErosis): a randomised, multicentre, placebo-controlled, double-blind phase II trial. Bonanato, L; Camacho-Vilchez, J; Da Silva, MVCP; Danos, P; de Abrantes, FF; de Sousa, CF; Diebold, M; Farina, A; Galvani, MAG; Gresse, S; Gutierrez, A; Idris, OEA; Iqbal, F; Jimenez-Pavón, J; Loss, KL; Mahmoud, RAA; Maki, D; Manterola, C; Morón, EM; Nashwan, MWJ; Ortiz-Lopez, R; Parente, DB; Polania, JP; Raquelo-Menegassio, AF; Stein, A; Stelmaszewski, EV; Thompson, L; Victor, C, 2020)	2.72
"Everolimus (EVR) has been approved for the treatment of various advanced cancers and its indications are increasingly expanding. "	( Designing orodispersible films containing everolimus for enhanced compliance and bioavailability. Gao, S; Guan, R; Liu, H; Liu, Y; Ma, Y; Song, W; Yang, Y, 2020)	2.27
"Everolimus has recently been approved by the US Food and Drug Administration and the European Medical Agency for the treatment of refractory seizures associated with TSC starting from the age of 2 years."	( Genetic pathogenesis of the epileptogenic lesions in Tuberous Sclerosis Complex: Therapeutic targeting of the mTOR pathway. Aronica, E; Craiu, D; Curatolo, P; Luinenburg, MJ; Moavero, R; Mühlebner, A, 2022)	1.44
"Everolimus has demonstrated effectiveness in neuroendocrine neoplasms."	( A pilot study of everolimus and radiation for neuroendocrine liver metastases. Chan, DL; Chen, H; Chung, H; Hallet, J; Hudson, J; Law, C; Milot, L; Myrehaug, S; Patel, C; Rodriguez-Freixinos, V; Singh, S, 2021)	1.68
"Everolimus has a significant impact on red blood cell parameters in patients with TSC."	( New Insights into Red Blood Cell Microcytosis upon mTOR Inhibitor Administration. Jakubowska, J; Jóźwiak, S; Kotulska, K; Młynarski, W; Pawlik, B; Stolarska, M; Trelińska, J; Wyka, K, 2021)	1.34
"Everolimus has been shown to be effective for advanced pancreatic neuroendocrine tumours (pNETs), but its positioning in the therapeutic algorithm for pNETs is matter of debate."	( Everolimus as first line therapy for pancreatic neuroendocrine tumours: current knowledge and future perspectives. Colao, A; Faggiano, A; Fanciulli, G; Gallo, M; Malandrino, P; Rota, F, 2017)	3.34
"Everolimus has single-agent activity in lymphoma."	( Adjuvant everolimus in high-risk diffuse large B-cell lymphoma: final results from the PILLAR-2 randomized phase III trial. Belada, D; Bermudez Silva, CD; Bouabdallah, K; Cavalli, F; Costa, LJ; Fan, J; Fayad, L; Hino, M; Ikeda, T; Kattan, JG; Kim, WS; Kuruvilla, J; Larouche, JF; Louveau, AL; Mayer, J; Ogura, M; Ozcan, M; Rigacci, L; Shi, Y; Tobinai, K; Vanazzi, A; Voi, M; Witzig, TE; Wu, C; Zhu, J, 2018)	1.62
"Everolimus has proven to be efficacious in size reduction of cardiac rhabdomyomas in cases when surgical resection is not possible."	( Giant left ventricular rhabdomyoma treated successfully with everolimus: case report and review of literature. Aguinaga-Ríos, M; Cardona-Pérez, JA; Cordero-González, G; Coronado-Zarco, A; Escamilla-Sánchez, KI; Martínez-García, A; Michel-Macías, C, 2018)	2.16
"Everolimus has been shown to overcome endocrine resistance in hormone receptor positive advanced breast cancer patients. "	( Mutational Profile of Metastatic Breast Cancer Tissue in Patients Treated with Exemestane Plus Everolimus. Barbolini, M; Bettelli, S; Caprera, C; Cascinu, S; Conte, PF; Filieri, ME; Guaitoli, G; Kaleci, S; Maiorana, A; Manfredini, S; Moscetti, L; Nasso, C; Omarini, C; Piacentini, F, 2018)	2.14
"Everolimus has been shown to be effective in overcoming hormonal resistance in Lebanese breast cancer patients with results inferior to those reported in the BOLERO-2 population. "	( Efficacy and safety of everolimus in hormone receptor positive breast cancer in a developing country: Real-life single institutional experience. Assi, T; Chebib, R; El Karak, F; El Rassy, E; Farhat, F; Ghosn, M; Hanna, C; Kattan, J; Moussa, T; Tabchi, S, )	1.88
"Everolimus has significant clinical benefit and is well tolerated with reversible side effects as second- or third-line therapy for treating RCC. "	( Evaluation of everolimus in renal cell cancer. Amato, R; Stepankiw, M, 2013)	2.19
"Everolimus conversion has become an excellent choice, offering safety and efficacy with good outcomes."	( Clinical everolimus experience in pediatric renal transplant patients. Bulut, IK; Dincel, N; Hoşcoşkun, C; Mir, S; Sezer, TÖ, 2013)	2.25
"Everolimus has been well tolerated by all."	( Successful everolimus therapy for SEGA in pediatric patients with tuberous sclerosis complex. Adolfo, F; Cappellano, AM; Cavalheiro, S; Covic, A; Paiva, PM; Pinho, R; Saba, N; Senerchia, AA, 2013)	1.5
"Everolimus has effective inhibition on aromatase-overexpressing stem cell in vitro and in vivo."	( Everolimus in combination with letrozole inhibit human breast cancer MCF-7/Aro stem cells via PI3K/mTOR pathway: an experimental study. Hou, G; Liu, J; Liu, Y; Zhang, J; Zhang, S; Zhang, X, 2014)	2.57
"Everolimus has been recently approved as a pharmacotherapy option for TSC patients with subependymal giant-cell astrocytomas (SEGAs) or renal angiomyolipomas (AMLs)."	( Is mTOR inhibition a systemic treatment for tuberous sclerosis? Coniglio, A; Curatolo, P; Garaci, F; Moavero, R, 2013)	1.11
"Everolimus has shown to stop formation and activity of osteoclasts. "	( Everolimus as treatment for breast cancer patients with bone metastases only: results of the phase II RADAR study. Aktas, B; Barinoff, J; Bauerschlag, D; Bischoff, J; Ettl, J; Harbeck, N; Kümmel, S; Lerchenmüller, C; Loibl, S; Lübbe, K; Lück, HJ; Maass, N; Müller, L; Mundhenke, C; Nekljudova, V; Rösel, S; Schmidt, M; Schwedler, K; von Minckwitz, G; Wagner, S, 2013)	3.28
"Everolimus has recently been approved by Food and Drug Administration for graft maintenance in liver transplant recipients. "	( Analytical performance of QMS everolimus assay on ortho Vitros 5,1 FS fusion analyzer: measuring everolimus trough levels for solid organ transplant recipients. Bernard, DW; Chandler, WL; Shu, I; Wang, P; Wright, AM, 2014)	2.13
"Everolimus (EVR) has demonstrated good efficacy after renal transplantation. "	( Outcomes in ethnic minority renal transplant recipients receiving everolimus versus mycophenolate: comparative risk assessment results from a pooled analysis. Delcoro, C; McCague, K; Melancon, K; Mulgaonkar, SP; Shihab, FS; Wiland, A, 2013)	2.07
"Everolimus has demonstrated efficacy in unresectable and progressive pancreatic neuroendocrine tumors, by doubling the median progression free survival (11 versus 4.6 months), with a median time of exposure to everolimus of nine months."	( [Management of metabolic disorders induced by everolimus in patients with differentiated neuroendocrine tumors: expert proposals]. Cariou, B; Coriat, R; François, E; Hammel, P; Hentic, O; Lombard-Bohas, C; N'guyen, T; Niccoli, P; Vergès, B, 2014)	1.38
"Everolimus has important clinical activity in various malignancies, but its use can be complicated by respiratory adverse events. "	( Diagnostic challenges of respiratory adverse events during everolimus treatment. de Boer, M; De Vos, FY; Jansen, A; Tjan-Heijnen, VC; van Herpen, CM; Willemsen, AE, 2014)	2.09
"Everolimus has been shown to reduce the severity and incidence of CAV as measured by first year intravascular ultrasound (IVUS)."	( Cardiac allograft vasculopathy by intravascular ultrasound in heart transplant patients: substudy from the Everolimus versus mycophenolate mofetil randomized, multicenter trial. Cantin, B; Dong, G; Eisen, H; Hill, JA; Kobashigawa, JA; Lopez, P; Nicholls, SJ; Pauly, DF; Ross, H; Starling, RC; Wang, SS, 2013)	1.32
"Everolimus (EVR) has inter-individual pharmacokinetic (PK) variability and a narrow therapeutic index. "	( The impact of genetic polymorphisms, diltiazem, and demographic variables on everolimus trough concentrations in lung transplant recipients. Aquilante, CL; Fish, DN; Kiser, TH; Schoeppler, KE; Zamora, MR, 2014)	2.07
"Everolimus has demonstrated substantial clinical benefit in randomized, controlled, phase III studies leading to approval for the treatment of advanced renal cell carcinoma, advanced neuroendocrine tumors of pancreatic origin, renal angiomyolipoma and subependymal giant-cell astrocytoma associated with tuberous sclerosis complex, as well as advanced hormone-receptor-positive (HR(+)) and human epidermal growth factor receptor-2-negative advanced breast cancer."	( Adverse event management in patients with advanced cancer receiving oral everolimus: focus on breast cancer. Aapro, M; Andre, F; Blackwell, K; Calvo, E; Jahanzeb, M; Papazisis, K; Porta, C; Pritchard, K; Ravaud, A, 2014)	1.36
"Everolimus has been approved for the treatment of pancreatic neuroendocrine tumors (pNETs), metastatic renal cell carcinoma (mRCC), and breast carcinoma."	( Everolimus in advanced solid tumors: when to start, early or late? Procopio, G; Pusceddu, S; Tessari, A; Testa, I, )	2.3
"Everolimus has demonstrated its efficacy in metastatic renal cell carcinoma (mRCC). "	( Impact of everolimus blood concentration on its anti-cancer activity in patients with metastatic renal cell carcinoma. Almotlak, H; Foubert, A; Maurina, T; Montange, D; Montcuquet, P; Mouillet, G; Nerich, V; Nguyen Tan Hon, T; Pivot, X; Royer, B; Stein, U; Thiery-Vuillemin, A, 2014)	2.25
"Everolimus has a high single-agent activity of 73% including MR, with a progression free survival of 21 months, indicating that this agent is active in relapsed/refractory WM."	( Long-term results of the phase II trial of the oral mTOR inhibitor everolimus (RAD001) in relapsed or refractory Waldenstrom Macroglobulinemia. Bergsagel, PL; Camoriano, J; Chuma, S; DeAngelo, D; Gertz, M; Ghobrial, IM; Hayman, S; Lacy, M; LaPlant, B; Treon, SP; Witzig, TE, 2014)	1.36
"Everolimus has been approved by the FDA and the EMA for the treatment of advanced renal cell carcinoma (RCC), subependymal giant cell astrocytoma (SEGA) associated with tuberous sclerosis (TSC), pancreatic neuroendocrine tumors (PNET), in combination with exemestane in advanced hormone-receptor (HR)-positive, HER2-negative breast cancer."	( Everolimus. Hasskarl, J, 2014)	2.57
"Both everolimus and axitinib have been considered standard of care after failure of first-line VEGF-TKI; sorafenib has been proposed as an additional option."	( Improving outcomes in metastatic clear cell renal cell carcinoma by sequencing therapy. Schmidinger, M, 2014)	0.86
"Everolimus has promise as an effective alternative to surgery for subependymal giant cell astrocytomas during early infancy."	( Everolimus Treatment for an Early Infantile Subependymal Giant Cell Astrocytoma With Tuberous Sclerosis Complex. Fukumura, S; Minagawa, K; Takayama, R; Tsutsumi, H; Watanabe, T, 2015)	2.58
"Everolimus has limited clinical activity in advanced MPM patients. "	( SWOG S0722: phase II study of mTOR inhibitor everolimus (RAD001) in advanced malignant pleural mesothelioma (MPM). Gandara, DR; Garland, LL; Mack, PC; Moon, J; Ou, SH; Testa, JR; Tsao, AS; Wozniak, AJ, 2015)	2.12
"Everolimus has a favorable pharmacokinetic (PK) profile in early breast cancer studies."	( Evaluating the pharmacokinetics and pharmacodynamics of everolimus for treating breast cancer. Awada, A; Barthélémy, P; Gombos, A, 2015)	1.38
"Everolimus has also beenrecently studied in HER2 positive locally advanced or metastatic disease in heavily pretreated patients (BOLERO 3 trial)."	( [The drug of the month: everolimus (Afinitor) for the treatment of metastatic breast cancer]. Collignon, J; Jerusalem, G; Rorive, A, 2014)	1.43
"Everolimus has been shown to be an effective HR+/HER2- mBC treatment in both clinical trials and real-world practice. "	( Everolimus use and associated factors among post-menopausal women with hormonal receptor positive/human epidermal growth factor receptor 2 negative metastatic breast cancer. Hao, Y; Li, N; Lin, PL; Signorovitch, JE; Wu, EQ; Xie, J; Zhong, Y; Zhou, Z, 2015)	3.3
"Everolimus (ERL) has become an alternative to calcineurin inhibitors (CNIs) due to its renal-sparing properties, especially in heart transplant (HTx) recipients with kidney dysfunction. "	( Influence of CYP3A5 genetic variation on everolimus maintenance dosing after cardiac transplantation. Englberger, L; Fiedler, GM; Largiadèr, CR; Lesche, D; Mohacsi, P; Setoud, R; Sigurdardottir, V; Sistonen, J, 2015)	2.13
"Everolimus has no nephrotoxicity and is used to treat patients with post-liver transplant chronic renal insufficiency. "	( Everolimus in de novo liver transplant recipients: a systematic review. Deng, HJ; Li, QD; Liu, R; Shen, A; Tang, CY; Wei, XF; Wu, YZ; Wu, ZJ, 2015)	3.3
"Everolimus has been used in patients with hormone receptor-positive breast cancer. "	( Treatment with everolimus for a patient with systemic metastatic breast cancer results in severe pulmonary injury: a case report. Santai, S; Shikai, W; Tao, W; Xiangying, M; Zefei, J, 2017)	2.25
"Everolimus has been used widely in cancer patients and is associated with the development of hyperglycemia. "	( Risk of hyperglycemia attributable to everolimus in cancer patients: A meta-analysis. Shameem, R; Wu, S; Xu, KY, )	1.85
"Everolimus (EVR) has been used widely for the purpose of reducing the dosage of calcineurin inhibitor (CNI), leading to decreasing CNI nephrotoxicity. "	( Effectiveness of the Combination of Everolimus and Tacrolimus With High Dosage of Mizoribine for Living Donor-Related Kidney Transplantation. Harada, S; Ito, T; Koshino, K; Nakamura, T; Nakao, T; Nobori, S; Suzuki, T; Ushigome, H; Yoshimura, N, 2016)	2.15
"Everolimus has activity in relapsed DLBCL."	( Everolimus combined with R-CHOP-21 for new, untreated, diffuse large B-cell lymphoma (NCCTG 1085 [Alliance]): safety and efficacy results of a phase 1 and feasibility trial. Ansell, SM; Colgan, JP; Habermann, TM; Inwards, DJ; Johnston, PB; LaPlant, B; McPhail, E; Micallef, IN; Nowakowski, GS; Witzig, TE, 2016)	2.6
"Everolimus has been shown to have a manageable safety profile, with the most common adverse events being stomatitis, rash, diarrhea, fatigue and infections."	( Everolimus in the treatment of neuroendocrine tumors of the respiratory and gastroenteropancreatic systems. Flaum, N; Mansoor, W; McNamara, MG; Valle, JW, 2016)	2.6
"Everolimus has been used for the treatment of unresectable or metastatic renal cell carcinoma (RCC). "	( Population Pharmacokinetics of Everolimus in Relation to Clinical Outcomes in Patients With Advanced Renal Cell Carcinoma. Fukudo, M; Kamba, T; Masuda, S; Matsubara, K; Ogawa, O; Sato, E; Shinsako, K; Tanaka, A; Yamasaki, T; Yano, I, 2016)	2.16
"Everolimus has clinically relevant antitumor activity in patients with advanced differentiated thyroid cancer. "	( Everolimus in Patients With Advanced Follicular-Derived Thyroid Cancer: Results of a Phase II Clinical Trial. Bos, M; Corver, WE; de Wit, D; Gelderblom, H; Guchelaar, HJ; Kapiteijn, E; Links, TP; Morreau, H; Roozen, IC; Schneider, TC; Smit, JW; van der Hoeven, JJ; van Erp, NP; van Wezel, T, 2017)	3.34
"Everolimus has beneficial effects on UF failure, inflammation, and fibrosis."	( Effects of everolimus as an antiproliferative agent on regression of encapsulating peritoneal sclerosis in a rat model. Bozkurt, D; Duman, S; Ertilav, M; Ok, E; Ozkan, S; Sen, S; Sezak, M; Sipahi, S, 2008)	1.46
"Everolimus has been prescribed both for initial and maintenance therapy after cardiac transplantation. "	( Preliminary experience with conversion from calcineurin inhibitors to everolimus in cardiac transplantation maintenance therapy. Arizón-Muñoz, JM; Benezet-Mazuecos, J; Guisado, A; Jiménez-Díaz, J; Lage-Gallé, E; Martínez, A; Mogollón, MV; Romero-Rodriguez, N; Sánchez-Brotons, JA; Sobrino-Márquez, JM, 2008)	2.02
"Oral everolimus has activity in metastatic breast cancer that is schedule dependent. "	( Randomized phase II study comparing two schedules of everolimus in patients with recurrent/metastatic breast cancer: NCIC Clinical Trials Group IND.163. Chia, S; Clemons, M; Eisen, A; Ellard, SL; Gelmon, KA; Huntsman, D; Kennecke, H; McIntosh, L; Mishaeli, M; Norris, B; Olivo, M; Pritchard, K; Sauerbrei, E; Seymour, L; Taylor, M; Vandenberg, T; Walsh, W, 2009)	1.12
"Everolimus has modest antitumor activity against CLL and can mobilize malignant cells from nodal masses into the peripheral circulation in a subset of CLL patients. "	( The treatment of recurrent/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) with everolimus results in clinical responses and mobilization of CLL cells into the circulation. Call, TG; Habermann, TM; Johnston, PB; LaPlant, BR; Micallef, IN; Witzig, TE; Zent, CS, 2010)	2.02
"Everolimus has shown good results in kidney and heart transplantation, achieving low rates of rejection, of infections, and of tumors compared with calcineurin inhibitors (CNI). "	( Everolimus in lung transplantation in Chile. Alba, A; Parada, MT; Sepúlveda, C, )	3.02
"Everolimus has single-agent activity in relapsed/refractory HL and provides proof-of-concept that targeting the mTOR pathway in HL is clinically relevant."	( A Phase II trial of the oral mTOR inhibitor everolimus in relapsed Hodgkin lymphoma. Ansell, SM; Colgan, JP; Habermann, TM; Inwards, DJ; Johnston, PB; Kabat, BF; Laplant, BR; Micallef, IN; Porrata, LF; Reeder, CB; Roy, V; Witzig, TE, 2010)	1.34
"Everolimus has shown in a randomized phase III trial for patients with metastatic renal cell carcinoma having failed under VEGFR tyrosine kinase inhibitor a significant gain in progression-free survival compared to this obtained with placebo VEGFR (1,8 à 4,6 months; HR: 0.33; P < 0.001)."	( [mTOR inhibitors: temsirolimus and everolimus in the treatment of renal cell carcinoma]. Bernhard, JC; Digue, L; Ferriere, JM; Gross-Goupil, M; Ravaud, A, 2010)	1.36
"Everolimus has single-agent activity in relapsed/refractory aggressive NHL and provides proof-of-concept that targeting the mTOR pathway is clinically relevant."	( A phase II trial of the oral mTOR inhibitor everolimus in relapsed aggressive lymphoma. Ansell, SM; Colgan, JP; Ghobrial, IM; Gupta, M; Habermann, TM; Jacobsen, ED; Johnston, PB; LaPlant, BR; Micallef, IN; Porrata, LF; Reeder, CB; Witzig, TE, 2011)	1.35
"Everolimus has proven efficacy for prevention of rejection in adult de novo renal and cardiac transplant recipient in combination with ciclosporine and corticosteroids. "	( [Level of evidence for therapeutic drug monitoring of everolimus]. Goirand, F; Hulin, A; Royer, B; Saint-Marcoux, F, )	1.82
"Everolimus and sunitinib have been recently introduced as targeted therapies for metastatic pancreatic neuroendocrine tumours."	( New therapeutic options for metastatic malignant insulinomas. de Herder, WW; Feelders, RA; Kwekkeboom, D; van Schaik, E, 2011)	1.09
"Everolimus has been successfully used in solid organ transplantation, especially of the heart and kidney, but much less often in lung transplantation. "	( Long-term use of everolimus in lung transplant patients. Alba, A; Melo, J; Parada, MT; Sepúlveda, C, )	1.91
"Everolimus has previously been shown to have some clinical activity when used as a single agent in NSCLC."	( Everolimus in combination with pemetrexed in patients with advanced non-small cell lung cancer previously treated with chemotherapy: a phase I study using a novel, adaptive Bayesian dose-escalation model. Anrys, B; Boyer, M; Di Scala, L; Dimitrijevic, S; Laack, E; Miller, N; Petrovic, K; Pylvaenaeinen, I; Solomon, B; Vansteenkiste, J; Wolf, J, 2011)	2.53
"Everolimus has potent antifibrotic effects that may potentially affect the clinical course of bronchiolitis obliterans syndrome (BOS) or provide nephroprotective immunosuppressive regimens for lung transplantation."	( A retrospective 12-month study of conversion to everolimus in lung transplant recipients. Borro, JM; Carreño, MC; Roman, A; Santos, F; Solé, A; Ussetti, P; Zurbano, F, 2011)	2.07
"Everolimus therefore has obvious potential in cancer therapy."	( Clinical review: Current scientific rationale for the use of somatostatin analogs and mTOR inhibitors in neuroendocrine tumor therapy. Billah, SM; Bousquet, C; Caron, P; Chalabi, M; Lasfargues, C; Pyronnet, S; Susini, C; Vezzosi, D, 2012)	1.1
"Everolimus has shown preliminary evidence of efficacy as a single-agent in heavily pretreated relapsed/refractory HL, with an overall fair safety profile."	( mTOR as a target of everolimus in refractory/relapsed Hodgkin lymphoma. Gadaleta, CD; Giannoccaro, M; Guarini, A; Iacobazzi, A; Lapietra, A; Minoia, C; Raimondi, A; Rana, A; Ranieri, G; Silvestris, N, 2012)	1.42
"Everolimus has demonstrated antitumor efficacy for various cancers as a result of its inhibition of the mammalian target of rapamycin (mTOR) signaling cascade, which activates cell growth and cell proliferation. "	( Preparation and in vivo evaluation of liposomal everolimus for lung carcinoma and thyroid carcinoma. Iwase, Y; Maitani, Y, 2012)	2.08
"Everolimus has the potential to become an important agent in de novo and maintenance immunotherapy in kidney transplant recipients."	( A drug safety evaluation of everolimus in kidney transplantation. Åsberg, A; Holdaas, H; Midtvedt, K, 2012)	1.39
"Everolimus has been approved for second-line treatment of patients with metastatic renal cell carcinoma (mRCC) after failure of sorafenib or sunitinib. "	( Everolimus in metastatic renal cell carcinoma: preliminary experience from Chang Gung Memorial Hospital. Chang, JW; Chang, YH; Chiang, YJ; Chuang, CK; Hsieh, JJ; Huang, WK; Liaw, CC; Lin, YC; Ou, LY; Pang, ST; Tsai, SI; Wang, HM; Wu, CT; Yang, CH; Yang, CT, )	3.02
"Everolimus, which has greater polarity than sirolimus, was developed in an attempt to improve the pharmacokinetic characteristics of sirolimus, particularly to increase its oral bioavailability."	( Clinical pharmacokinetics of everolimus. Kirchner, GI; Manns, MP; Meier-Wiedenbach, I, 2004)	1.34
"Everolimus has equivalent efficacy to mycophenolate mofetil in reducing the incidence of acute rejection after renal transplantation and superior efficacy to azathioprine after heart transplantation."	( Everolimus: a proliferation signal inhibitor targeting primary causes of allograft dysfunction. Kovarik, JM, 2004)	2.49
"Everolimus has been associated with thrombocytopenia, leucopenia and elevated serum lipids and creatinine."	( Everolimus. Chapman, TM; Perry, CM, 2004)	2.49
"Everolimus has been approved in some European countries and a new drug application has been submitted to the Food and Drug Administration."	( Future immunosuppressive agents in solid-organ transplantation. Cerio, J; Gabardi, S, 2004)	1.04
"Everolimus has been used in conjunction with a new bioabsorbable polymer and gave promising results in initial clinical studies."	( Clinical experiences using everolimus-eluting stents in patients with coronary artery disease. Grube, E; Haase, J; Hofmann, M; Schwarz, F; Störger, H, 2004)	1.34
"Everolimus has recently received approval for immunosuppressive therapy in heart transplant recipients in Austria and Germany. "	( Immunosuppressive therapy with everolimus can be associated with potentially life-threatening lingual angioedema. Berthold, HK; Deyerling, KW; Fuchs, U; Koerfer, R; Minami, K; Tenderich, G; Zittermann, A, 2005)	2.06
"Everolimus has recently shown promise in terms of short- and long-term clinical lung transplant outcomes. "	( Everolimus alters the bronchoalveolar lavage and endobronchial biopsy immunologic profile post-human lung transplantation. Bailey, M; Kotsimbos, TC; Law, L; Levvey, BJ; Orsida, B; Snell, GI; Whitford, HM; Williams, TJ; Zheng, L, 2005)	3.21
"Everolimus has proven efficacy for prevention of rejection in adult de novo renal and cardiac transplant recipients."	( The role of therapeutic monitoring of everolimus in solid organ transplantation. Ensom, MH; Mabasa, VH, 2005)	1.32
"Everolimus has shown to reduce acute cellular rejection and may allow CsA dosage reduction."	( Everolimus and reduced cyclosporine trough levels in maintenance heart transplant recipients. Prenner, G; Schwarz, M; Schweiger, M; Stadlbauer, V; Stiegler, P; Tscheliessnigg, K; Wasler, A, 2006)	2.5
"Everolimus has been shown to be as effective as mycophenolate mofetil in reducing acute rejection in renal transplantation."	( Everolimus: an immunosuppressive agent in transplantation. Kobashigawa, JA; Patel, JK, 2006)	2.5
"Everolimus has an appropriate rationale for therapeutic use in combination with erlotinib for patients with NSCLC. "	( Rationale for a phase I trial of erlotinib and the mammalian target of rapamycin inhibitor everolimus (RAD001) for patients with relapsed non small cell lung cancer. Jackman, D; Jänne, PA; Johnson, BE, 2007)	2
"Everolimus (EVL) has shown a potential to reduce nephrotoxicity associated with cyclosporine (CsA) while providing similar protection against rejection. "	( Higher incidence of acute rejection in renal transplant recipients with low everolimus exposure. Castagneto, M; Citterio, F; Favi, E; Renna, R; Romagnoli, J; Salerno, MP; Spagnoletti, G; Tondolo, V, )	1.8
"Everolimus has recently been introduced into clinical practice with promising perspectives due to its efficacy, lack of nephrotoxicity, and antitumor effects. "	( Evaluation of the efficacy and safety of the conversion from a calcineurin inhibitor to an everolimus-based therapy in maintenance renal transplant patients. Arias, M; Barrientos, A; Calvo, N; Conesa, J; Cotorruelo, J; Gómez-Alamillo, C; Moreno, MA; Rodrigo, E; Ruiz San Millán, JC; Sánchez Fructuoso, A, 2007)	2
"Everolimus (Eve) has shown good efficacy and safety profiles in clinical trials in combination with low doses of cyclosporine but there is limited experience in other modes, especially with calcineurin inhibitor elimination. "	( Use of the new proliferation signal inhibitor everolimus in renal transplant patients in Spain: preliminary results of the EVERODATA registry. Alarcón, A; Andrés, A; Beneyto, I; Cantarell, C; Díaz, JM; Errasti, P; Fernández, A; Morales, JM; Morey, A; Plaza, JJ; Rengel, M; Romero, R; Ruiz, JC; Sánchez, A; Torregrosa, JV; Zárraga, S, 2007)	2.04
"Everolimus has not been assessed in patients with severe hepatic impairment."	( Influence of hepatic impairment on everolimus pharmacokinetics: implications for dose adjustment. Dilzer, SC; Figueiredo, J; Kovarik, JM; Lasseter, K; Reynolds, C; Rordorf, C; Sabia, HD; Zimmermann, H, 2001)	1.31

Excerpt	Reference	Relevance
"Everolimus can enhance the effect of paclitaxel on MDA-MB-231/ADR cells, inhibit cell proliferation, induce apoptosis and arrest cell cycle in the G1 phase mainly by down-regulating the expressions of key proteins in the mTOR signaling pathway."	( Inhibitory effects of everolimus in combination with paclitaxel on adriamycin-resistant breast cancer cell line MDA-MB-231. Li, Q; Liu, P; Shi, C; Wang, X; Xu, T, 2020)	2.32
"Everolimus could inhibit the growth of both total breast cancer cells and sorted stem cells in vitro and in vivo."	( [Drug sensitivity research of mTOR inhibitor on breast cancer stem cells]. Liu, P; Liu, Y; Zhang, J; Zhang, X, 2015)	1.86
"Everolimus appears to suppress the proliferation of fibroblast and thus may provide an effective treatment strategy in glaucoma filtering surgery."	( The Effect of Everolimus on Scar Formation in Glaucoma Filtering Surgery in a Rabbit Model. Aslan, MŞ; Cinik, R; Karaöz, E; Pirhan, D; Subaşı, C; Yüksel, N, 2016)	2.24
"Everolimus might also allow postponement of a neurosurgical resection, making it elective with an overall lower risk."	( Everolimus Alleviates Obstructive Hydrocephalus due to Subependymal Giant Cell Astrocytomas. Carai, A; Curatolo, P; Graziola, F; Marciano, S; Mastronuzzi, A; Moavero, R; Vigevano, F, 2017)	2.62
"Everolimus displays antiproliferative effects on cancer cells, yields antiangiogenic activity in established tumours, and shows synergistic activity with paclitaxel in preclinical models. "	( Safety and pharmacokinetics of paclitaxel and the oral mTOR inhibitor everolimus in advanced solid tumours. Berton Rigaud, D; Bootle, D; Bourbouloux, E; Calvo, F; Campone, M; Dutreix, C; Levy, V; Raymond, E; Shand, N; Zoellner, U, 2009)	2.03
"Everolimus is known to cause ILD; however, its pathology is unclear."	( Granuloma-forming interstitial pneumonia occurring one year after the start of everolimus therapy. Azuma, A; Fukuda, Y; Gemma, A; Kimura, G; Kondo, Y; Kunugi, S; Minegishi, Y; Miura, Y; Narita, K; Saito, Y; Suzuki, Y, 2013)	1.34
"Everolimus displays a potent inhibitory effect on PTLD-derived cells in vitro and in vivo in a dose range leading to prevention of allograft rejection and may prove effective in both the prevention and treatment of PTLDs in transplant patients."	( Immunosuppressive TOR kinase inhibitor everolimus (RAD) suppresses growth of cells derived from posttransplant lymphoproliferative disorder at allograft-protecting doses. Fields, L; Joergensen, J; Korecka, M; Kossev, P; Majewski, M; Schuler, W; Shaw, L; Wasik, MA, 2003)	2.03
"Everolimus patients had lower incidence of efficacy failure compared with azathioprine patients (41.6%, everolimus 1.5 mg; 32.2%, everolimus 3.0 mg; 52.8%, azathioprine). "	( Economic evaluation of everolimus vs. azathioprine at one year after de novo heart transplantation. Cantu, E; Cretin, N; Kaló, Z; Kauf, TL; Radeva, JI; Reed, SD; Schulman, KA, 2005)	2.08
"Everolimus may allow optimization of immunosuppressant regimens in de novo heart transplant patients so that adequate efficacy can be achieved with reduced CNI exposure, thereby protecting kidney function."	( Clinical experience with Certican (everolimus) in de novo heart transplant patients at the Deutsches Herzzentrum Berlin. Hetzer, R; Lehmkuhl, H, 2005)	1.33
"Everolimus displays better efficacy in de novo heart transplant patients than azathioprine for prophylaxis of biopsy-proven acute rejection episodes of at least ISHLT grade 3A (P < .001), of allograft vasculopathy (P < .01), and of CMV infections (P < .01)."	( Recommendations for use of everolimus after heart transplantation: results from a Latin-American Consensus Meeting. Ahualli, L; Amuchastegui, M; Bocchi, EA; Boullon, F; Cerutti, B; Colque, R; Fernandez, D; Fiorelli, A; Olaya, P; Perrone, SV; Vulcado, N, 2006)	1.35
"The everolimus AUC increase with Neoral coadministration was significantly greater than the AUC increase with Sandimmune (p = 0.008)."	( Differential influence of two cyclosporine formulations on everolimus pharmacokinetics: a clinically relevant pharmacokinetic interaction. Figueiredo, J; Frazier, OL; Kalbag, J; Kovarik, JM; Rordorf, C; Rouilly, M, 2002)	1.04

Excerpt	Reference	Relevance
"Everolimus targeted treatment showed good efficacy in patients with recurrence/metastasis."	( ♣Evaluation of clinicopathological profiles and development of a risk model in renal epithelioid angiomyolipoma patients: a large-scale retrospective cohort study. Anwaier, A; Ding, T; Qu, YY; Su, JQ; Tian, X; Wang, Y; Xu, WH; Ye, DW; Zhang, HL, 2022)	1.44
"Everolimus treatment led to a significant and progressive reduction in the cardiac mass volume."	( A case of massive fetal cardiac rhabdomyoma: ultrasound features and management. Balducci, A; Donti, A; Fiorentini, M; Gesuete, V; Montaguti, E; Perolo, A; Pilu, G, 2023)	1.63
"Everolimus showed treatment efficacy and an acceptable safety tolerance with the prevention of side effects in Phase II/III studies."	( Evaluating everolimus for the treatment of breast cancer. Bourbouloux, E; Campone, M; Frenel, JS; Gourmelon, C; Moreau-Bachelard, C; Patsouris, A; Robert, M, )	1.24
"Everolimus (EVE)-based treatment is an option for hormone receptor (HR)-positive and human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer (MBC), but a predictive marker has not yet been established. "	( Relationship Between Daily Dose of Everolimus and Treatment Effect in Patients With Luminal HER2-negative Metastatic Breast Cancer. Horimoto, Y; Ishizuka, Y; Murakami, F; Okazaki, M; Ushiyama, Y; Watanabe, J, 2023)	2.63
"Everolimus as frontline treatment achieves clinical benefits for Chinese patients with mTPBC, which may provide some references for the management of Chinese mTPBC patients."	( Efficacy of everolimus-based therapy in advanced triple-positive breast cancer: Experience from three cancer centers in China. Fan, Y; Jiang, H; Li, Q; Ma, F; Tan, Y; Tian, X; Wang, J; Xu, B; Zhang, P; Zhao, W, 2023)	2.73
"Everolimus treatment had a statistically significant effect on the renal AML volume reduction during follow-up (P < 0.05), and the mean reduction rate of volume for all cases was 56.47 ± 23.32% over 12 weeks."	( Mutational analysis of renal angiomyolipoma associated with tuberous sclerosis complex and the outcome of short-term everolimus therapy. Hao, C; Liu, F; Liu, P; Ni, J; Qin, W; Wang, T; Wu, G; Yan, F; Yang, B; Yang, X; Yu, L; Yuan, J; Zhang, G, 2019)	1.44
"Everolimus is a treatment in NETs that may have antiangiogenic activity."	( Everolimus after hepatic arterial embolisation therapy of metastases from gastrointestinal neuroendocrine tumours: The FFCD 1104-EVACEL-GTE phase II study. Aparicio, T; Barbier, E; Baudin, E; Bouhier-Leporrier, K; Cadiot, G; Caroli-Bosc, FX; Coriat, R; de Baère, T; Di-Fiore, F; Duluc, M; Dupont-Gossart, AC; Gay, F; Ghiringhelli, F; Guimbaud, R; Hentic-Dhome, O; Lecomte, T; Legoux, JL; Lepage, C; Lepere, C; Lombard-Bohas, C; Petorin, C; Smith, D; Walter, T, 2019)	2.68
"Everolimus treatment was continued until disease progression or intolerable toxicity was observed."	( A Phase II Trial of Everolimus in Patients with Advanced Pancreatic Neuroendocrine Carcinoma Refractory or Intolerant to Platinum-Containing Chemotherapy (NECTOR Trial). Asagi, A; Furukawa, M; Furuse, J; Hara, H; Hosokawa, A; Ikeda, M; Kojima, M; Kojima, Y; Mizuno, N; Murohisa, G; Ohkawa, S; Okusaka, T; Okuyama, H; Shioji, K; Yamanaka, T, 2020)	1.6
"Everolimus treatment also led to decreased PD-1 expression on certain T cell subsets."	( Everolimus, an mTORC1/2 inhibitor, in ART-suppressed individuals who received solid organ transplantation: A prospective study. Aweeka, F; Baker, C; Bakkour, S; Busch, MP; Cameron, C; Chu, S; Deeks, SG; Deitchman, AN; Gibson, EA; Henrich, TJ; Hogan, LE; Liegler, T; Milush, J; Richardson, B; Rogers, R; Rutishauser, RL; Schreiner, C; Stock, PG; Thanh, C; Zarinsefat, A, 2021)	2.79
"Everolimus treatment resulted in inhibition of mTORC1 activity in peripheral NK cells, whereas mTORC2 activity was preserved."	( Cutting Edge: mTORC1 Inhibition in Metastatic Breast Cancer Patients Negatively Affects Peripheral NK Cell Maturation and Number. Bachelot, T; Besson, L; Charrier, E; Garin, G; Heudel, PE; Marçais, A; Mayet, R; Mery, B; Morelle, M; Parant, F; Perol, D; Ray-Coquard, I; Rocca, Y; Tredan, O; Viel, S; Villard, M; Walzer, T; You, B, 2021)	1.34
"Everolimus and metformin treated cells were subjected to cytotoxicity and clonogenic assays, western blotting, FACS and metabolic measurements."	( Anti-tumor effects of everolimus and metformin are complementary and glucose-dependent in breast cancer cells. Ariaans, G; Jalving, M; Jong, S; Vries, EG, 2017)	1.49
"Everolimus treatment resulted in rapid reduction in tumor size, symptomatic improvement, and decrease in cerebrospinal fluid protein."	( Acute Management of Symptomatic Subependymal Giant Cell Astrocytoma With Everolimus. Arroyo, MS; Broomall, E; Franz, DN; Krueger, DA; Stevenson, CB, 2017)	2.13
"Everolimus treatment remained safe and effective over approximately 4 years. "	( Everolimus long-term use in patients with tuberous sclerosis complex: Four-year update of the EXIST-2 study. Belousova, E; Berkowitz, N; Bissler, JJ; Brakemeier, S; Budde, K; de Vries, PJ; Frost, MD; Kingswood, JC; Peyrard, S; Radzikowska, E; Sauter, M; Voi, M; Zonnenberg, BA, 2017)	3.34
"Everolimus treatment (1 mg/kg body weight/day) prevented the bone loss observed in OVX mice and concurrently inhibited the metastatic growth of MDA-MB-231 cells by 70% (p < 0.002) while preserving bone mass in an intracardiac model of bone metastasis."	( Concurrent antitumor and bone-protective effects of everolimus in osteotropic breast cancer. Browne, AJ; Chen, D; Göbel, A; Hadji, P; Hofbauer, LC; Kubasch, ML; Rachner, TD; Rauner, M; Stölzel, F, 2017)	1.43
"Everolimus is a standard treatment option for advanced pancreatic neuroendocrine tumors (pNETs). "	( Clinical outcomes of everolimus in patients with advanced, nonfunctioning pancreatic neuroendocrine tumors: a multicenter study in Korea. Bang, S; Cho, JH; Jeong, S; Kim, YT; Lee, JK; Lee, KH; Lee, KJ; Lee, SH; Lee, TH; Lee, WJ; Paik, WH; Ryu, JK; Song, SY; Woo, SM, 2017)	2.22
"Everolimus treatment is seriously hampered by its toxicity profile. "	( Clinical validation study of dried blood spot for determining everolimus concentration in patients with cancer. Brüggemann, RJM; Croes, S; de Beer, YM; Knapen, LM; van Erp, NP; van Herpen, CML; Willemsen, AECAB, 2018)	2.16
"Everolimus is a treatment option for hemodialysis patients with metastatic atypical bronchial carcinoid. "	( Efficacy and safety of everolimus treatment in a hemodialysis patient with metastatic atypical bronchial carcinoid: case report and literature review. Brizzi, MP; La Salvia, A; Scagliotti, GV; Sonetto, C; Tampellini, M; Volante, M, 2018)	2.23
"Everolimus treatment was performed for AML with a maximum diameter of 4 cm."	( Effect of everolimus treatment for regrown renal angiomyolipoma associated with tuberous sclerosis complex after transcatheter arterial embolization. Egawa, S; Endo, K; Hatano, T; Inaba, H; Matsu-Ura, T; Mori, KI; Tamari, M, 2018)	1.6
"Everolimus treatment suppressed the conversion of glutamine and glutamate into glutathione both in vitro and in vivo."	( Inhibition of mTORC1 in pediatric low-grade glioma depletes glutathione and therapeutically synergizes with carboplatin. Alt, J; Arnold, A; Eberhart, CG; Poore, B; Price, A; Raabe, EH; Rubens, JA; Slusher, BS; Yuan, M, 2019)	1.24
"Both everolimus-treated and non-treated mice were sacrificed at several time points, starting 30 min and finishing 7 days after IRI induction."	( Effects of everolimus on oxidative stress in kidney model of ischemia/reperfusion injury. Bajcetic, M; Becker, JU; Kezic, A; Thaiss, F; Tsui, TY, 2013)	1.23
"Everolimus treatment significantly reduced the number of ICAM-1 positive small vessels (66%; p<0.05) and suppressed the infiltration of leucocytes (CD11a (64%), CD18 (42%); p<0.05) and macrophages (ED1; 22%) in the allografts on POD 30. "	( Everolimus's influence on persistent acute rejection after experimental lung transplantation. Brunner, E; Hirt, SW; Lehle, K; Schmid, C; von Suesskind-Schwendi, M, )	3.02
"Everolimus treatment was also able to attenuate the activation of primary stellate cells to their activated form."	( Everolimus is a potent inhibitor of activated hepatic stellate cell functions in vitro and in vivo, while demonstrating anti-angiogenic activities. Chatterjee, S; Dufour, JF; Maheshwari, U; Majumder, S; Manjunathan, R; Piguet, AC; Saran, U, 2014)	2.57
"Everolimus-based salvage treatment of refractory cGVHD results in significant improvement of the NIH Severity Score without impairing control of the malignant disease."	( Salvage therapy with everolimus reduces the severity of treatment-refractory chronic GVHD without impairing disease control: a dual center retrospective analysis. Ammer, J; Ditz, D; Einsele, H; Grigoleit, GU; Holler, E; Kapp, M; Lutz, M; Mielke, S; Schmidhuber, J; Wolff, D, 2014)	1.44
"Everolimus-treated mice displayed a marked reduction in weight gain from the last day of the treatment period."	( Evaluation of the impact of the cancer therapy everolimus on the central nervous system in mice. Anouar, Y; Castel, H; Dubois, M; Gandolfo, P; Hilber, P; Joly, F; Le Joncour, V; Morin, F; Proust, F; Tonon, MC, 2014)	1.38
"Everolimus treatment in TSC patients may lead to life-threatening outcomes, including sepsis and death."	( Complications of mammalian target of rapamycin inhibitor anticancer treatment among patients with tuberous sclerosis complex are common and occasionally life-threatening. Dachowska, I; Fendler, W; Jozwiak, S; Kotulska, K; Mlynarski, W; Trelinska, J, 2015)	1.14
"No everolimus-treated patients experienced renal bleeding."	( Everolimus for renal angiomyolipoma in patients with tuberous sclerosis complex or sporadic lymphangioleiomyomatosis: extension of a randomized controlled trial. Belousova, E; Berkowitz, N; Bissler, JJ; Brakemeier, S; Budde, K; de Vries, PJ; Frost, M; Kingswood, JC; Miao, S; Nonomura, N; Peyrard, S; Radzikowska, E; Sauter, M; Segal, S; Zonnenberg, BA, 2016)	2.39
"With everolimus treatment, the patient's diarrhea resolved and replacement therapy for hypoproteinemia was less frequent."	( Everolimus for Primary Intestinal Lymphangiectasia With Protein-Losing Enteropathy. Fukao, T; Hori, T; Ibuka, T; Kanda, K; Kawamoto, N; Miyazaki, T; Ozeki, M, 2016)	2.33
"Everolimus treatment was stopped, and treated with methylprednisolone and empiric antibiotic therapy for 7 days."	( Treatment with everolimus for a patient with systemic metastatic breast cancer results in severe pulmonary injury: a case report. Santai, S; Shikai, W; Tao, W; Xiangying, M; Zefei, J, 2017)	1.53
"Everolimus treatment improved behavioral deficits in the patient."	( Everolimus improves neuropsychiatric symptoms in a patient with tuberous sclerosis carrying a novel TSC2 mutation. Hwang, SK; Kaang, BK; Lee, JA; Lee, JH; Lee, K; Lee, YS; Lim, CS; Yang, JE, 2016)	2.6
"Everolimus treatment combined with early CNI elimination is associated with increased densities of Tregs 12-months post-HTx compared to patients receiving CNI based regimen. "	( Effect of everolimus initiation and early calcineurin inhibitor withdrawal on myocardial FOXP3+ regulatory T cells in heart transplantation. Andersen, C; Arora, S; Gullestad, L; Gustafsson, F; Mirza, K, 2016)	2.28
"Everolimus treatment disrupts the S6K1-IRS-2/PI3K negative feedback loop, leading to BRAF V600E-dependent activation of ERK and Mcl-1 stabilization in colon cancer cells, which in turn blocks the crosstalk from the death receptor to mitochondria."	( BRAFV600E-dependent Mcl-1 stabilization leads to everolimus resistance in colon cancer cells. Chen, D; He, K; Li, X; Ruan, H; Tong, J; Xu, X; Yu, J; Zhang, L, 2016)	1.41
"Everolimus treatment resulted in significant increases of TCh (from 192.04±40.51mg/dl to 210.74±51.12mg/dl and to 216.69±45.43mg/dl; p=0.0273) and LDL (from 113.21±38.72mg/dl to 133.88±50.71mg/dl and to 141.58±40.67mg/dl; p=0.0006) after three and 12 months respectively."	( Everolimus treatment among patients with tuberous sclerosis affects serum lipid profile. Dachowska, I; Fendler, W; Jóźwiak, S; Kotulska, K; Młynarski, W; Trelińska, J, 2016)	2.6
"Everolimus treatment had a statistically significant effect on the renal AML volume reduction during follow-up (P < 0.05)."	( Effects of everolimus on tuberous sclerosis complex-associated renal angiomyolipoma: A preliminary report. Fan, HC; Hsu, CC; Sheu, JN; Tsai, JD; Tsai, ML; Tung, MC; Wei, CC; Yang, SH, 2017)	1.57
"Everolimus based treatment has meaningful activity in heavily pretreated patients with HR-positive MBC but is associated with considerable toxicity and requirement for dose adjustment."	( Everolimus in heavily pretreated metastatic breast cancer: Is real world experience different? Bajpai, J; Ghosh, J; Gulia, S; Gupta, S; Ramaswamy, A, )	3.02
"Everolimus treatment resulted in reduced neointimal hyperplasia (thickness 3.7+/-1.2 microm) compared to untreated controls (10.1+/-2.5 microm, p=0.008). "	( Everolimus attenuates neointimal hyperplasia in cultured human saphenous vein grafts. Bernecker, OY; Bonatti, JO; Laufer, G; Macfelda, K; Ruttmann-Ulmer, E; Semsroth, S; Stigler, RG; Troppmair, J, 2009)	3.24
"Everolimus single agent treatment significantly inhibited tumor growth relative to control and cyclophosphamide treatment (T/C 19%, p<0.01). "	( mTOR inhibition sensitizes gastric cancer to alkylating chemotherapy in vivo. Cejka, D; Fuereder, T; Preusser, M; Sieghart, W; Strommer, S; Wacheck, V; Werzowa, J, )	1.57
"Everolimus-treated heart and lung transplant patients in the lowest tertile for time posttransplant exhibited mean increases of 7.8 mL/min and 4.9 mL/min, respectively."	( Everolimus with reduced calcineurin inhibitor in thoracic transplant recipients with renal dysfunction: a multicenter, randomized trial. Bergh, CH; Bjørtuft, O; Eiskjaer, H; Ekmehag, B; Fagertun, HE; Gude, E; Gullestad, L; Iversen, M; Jansson, K; Mared, L; Mortensen, SA; Riise, GC; Rundqvist, B; Simonsen, S; Solbu, D, 2010)	2.52
"Everolimus (RAD) treatment was initiated on the day after or 3 days after induction of myocardial infarction (MI) in rats."	( Beneficial effects of Mammalian target of rapamycin inhibition on left ventricular remodeling after myocardial infarction. Bea, F; Bekeredjian, R; Buss, SJ; Hagenmueller, M; Hardt, SE; Izumo, S; Katus, HA; Malekar, P; Muenz, S; Riffel, JH; Schinke-Braun, M; Weiss, CS, 2009)	1.8
"Everolimus-treated mice had significantly less rejection at all time points compared with non-immunosuppressed mice."	( Long-term laryngeal allograft survival using low-dose everolimus. Dan, O; Lott, DG; Lu, L; Strome, M, 2010)	1.33
"Everolimus treatment led to 36% of 6-month progression-free survival (PFS) rate and 31% of 3-month PFS rate."	( Everolimus in renal cell carcinoma. Wang, Y, 2010)	2.52
"The everolimus treatment lasted 20 months (range, 6-60)."	( Everolimus in clinical practice in long-term liver transplantation: an observational study. Argudo, A; Casanovas, T; Peña-Cala, MC, )	2.05
"Everolimus treatment was inefficient at controlling secretion and tumor growth of one ACTH pituitary carcinoma."	( New targeted therapies in pituitary carcinoma resistant to temozolomide. Borson-Chazot, F; Ducray, F; Favrel, V; Honnorat, J; Jouanneau, E; Raverot, G; Trouillas, J; Wierinckx, A, 2012)	1.1
"Everolimus treatment resulted in marked tumor regression, significant improvement in patient's ambulation and cessation of seizures."	( Effective everolimus treatment of inoperable, life-threatening subependymal giant cell astrocytoma and intractable epilepsy in a patient with tuberous sclerosis complex. Jóźwiak, S; Jurkiewicz, E; Kotulska, K; Perek, D; Perek-Polnik, M, 2012)	1.5
"Everolimus treated group (EveG) showed significantly less proteinuria and albuminuria, less glomerular and tubulointerstitial damage and fibrosis, fibroblast activation cell proliferation, when compared with control group (CG), even though the EveG remained with high blood pressure. "	( Delayed mTOR inhibition with low dose of everolimus reduces TGFβ expression, attenuates proteinuria and renal damage in the renal mass reduction model. Arévalo, MA; Boggia, J; Coria, V; Gimenez-Bonafe, P; González-Martínez, F; Grande, MT; Grinyó, J; Herrero-Fresneda, I; Kurdián, M; Lloberas, N; López-Novoa, JM; Malacrida, L; Noboa, O; Torras, J, 2012)	2.09
"Everolimus treatment reduced VEGF-A levels in the supernatant of all cell lines. "	( Measurement of tumor VEGF-A levels with 89Zr-bevacizumab PET as an early biomarker for the antiangiogenic effect of everolimus treatment in an ovarian cancer xenograft model. de Jong, S; de Vries, EG; Kosterink, JG; Lub-de Hooge, MN; Pot, L; Reyners, AK; Schröder, CP; Terwisscha van Scheltinga, AG; Timmer-Bosscha, H; van der Bilt, AR; van der Zee, AG, 2012)	2.03
"Pre-everolimus entry treatment options included exemestane, fulvestrant, and tamoxifen."	( Budget impact analysis of everolimus for the treatment of hormone receptor positive, human epidermal growth factor receptor-2 negative (HER2-) advanced breast cancer in the United States. De, G; Diener, M; Namjoshi, M; Wu, EQ; Xie, J; Yang, H, 2013)	1.17
"Everolimus treatment also induced a significant decrease in Ki67 index and in the phosphorylation levels of the two major effectors of mTOR, p70S6K and 4E-BP1."	( Antitumor effect of everolimus in preclinical models of high-grade gastroenteropancreatic neuroendocrine carcinomas. Benslama, N; Blanc, M; Bollard, J; Couderc, C; Ferraro-Peyret, C; Gouysse, G; Hervieu, V; Lepinasse, F; Poncet, G; Roche, C; Scoazec, JY; Walter, T, 2013)	1.43
"Both everolimus treatment groups significantly reduced in-stent neointimal growth (46% reduction and 42% reduction in intimal thickness in groups 1 and 2, respectively)."	( Oral everolimus inhibits in-stent neointimal growth. Acampado, E; Farb, A; John, M; Kolodgie, FD; Prescott, MF; Virmani, R, 2002)	1.28
"In everolimus-treated patients, mean increases in cyclosporine AUC0-12 ranged from 7% to 43%, which were not significantly different across all dosing cohorts including placebo."	( Influence of everolimus on steady-state pharmacokinetics of cyclosporine in maintenance renal transplant patients. Budde, K; Dantal, J; Fauchald, P; Fritsche, L; Lehne, G; Lison, A; Neumayer, HH; Renders, L; Soulillou, JP; Winkler, M, 2005)	1.21
"Everolimus treatment of established colitis in IL-10-/- mice ameliorated the colitis, probably as a result of decreasing the number of CD4+ T cells in the colonic mucosa and an associated reduction in IFN-gamma production."	( Therapeutic effect of a new immunosuppressive agent, everolimus, on interleukin-10 gene-deficient mice with colitis. Hamanaka, Y; Inoue, M; Ito, T; Kai, Y; Matsuda, C; Matsuda, H; Mizushima, T; Nishida, T; Sawa, Y; Song, J; Tamagawa, H, 2007)	1.31
"Everolimus treatment markedly reduced the number of 5-bromo-2-deoxyuridine-labeled nuclei in cyst epithelia."	( Everolimus retards cyst growth and preserves kidney function in a rodent model for polycystic kidney disease. Le Hir, M; Serra, AL; Wackerle-Men, Y; Wahl, PR; Wu, M; Wuthrich, RP, 2007)	2.5
"Everolimus treatment resulted in immediate inhibition (25-55%) of lymphocyte proliferation in renal-allograft recipients; values returning to baseline by 14 days after cessation of everolimus treatment."	( Pharmacodynamic effects of everolimus on anti-CD3 antibody-stimulated T-lymphocyte proliferation and interleukin-10 synthesis in stable kidney-transplant patients. Böhler, T; Budde, K; Kamar, N; Lichter, S; Neumayer, HH; Schumann, B; Waiser, J, 2008)	1.36
"In everolimus-treated patients for whom rifampin is indicated, alternative agents with less enzyme induction potential than rifampin could be considered. "	( Effect of rifampin on apparent clearance of everolimus. Figueiredo, J; Hartmann, S; Kovarik, JM; Port, A; Rordorf, C; Rouilly, M, 2002)	1.2
"Treatment with everolimus increased survival of mice infected with C."	( Screening the medicine for malaria venture's Pandemic Response Box to identify novel inhibitors of Candida albicans and Candida auris biofilm formation. Ajetunmobi, OH; Badali, H; Chaturvedi, AK; Lopez-Ribot, JL; Najvar, L; Patterson, TF; Vaccaro, A; Wiederhold, NP; Wormley, FL, 2023)	1.25
"Treatment with everolimus and exemestane was discontinued and steroid pulse therapy was initiated; however, she required ventilator management because of the severity of the pneumonia."	( [A Case of Metastatic Breast Cancer That Recovered from Diffuse Alveolar Damage Associated with Everolims]. Hasegawa, T; Hirakawa, K; Kashiwagi, S; Kinoshita, H; Nakamoto, K; Ohira, M; Teraoka, H, 2020)	0.9
"Treatment with everolimus reduced allogeneic fibroproliferation, but had no protective effects on the microvasculature; polymerase chain reaction analysis indicated hypoxic stress and inflammation."	( Microvasculature in murine tracheal allografts after combined therapy with clopidogrel and everolimus. Ensminger, SM; Heim, C; Kuckhahn, A; Nicolls, MR; Ramsperger-Gleixner, M; Weyand, M, 2021)	1.18
"When treated with everolimus, the overall incidence of stomatitis is about two thirds of the patients. "	( Stomatitis in mTOR inhibitors treatment and other targeted cancer therapy, possibilities of infl uencing it, and the use of local corticotherapy. Černá, A; Jánská, V; Kozáková, Š; Liška, J; Vokurka, S, 2020)	0.89
"Treatment with everolimus was stopped due to adverse events in 8 patients (47.1%). "	( Pilot Conversion Study From Mycophenolate Mofetil to Everolimus in Stable ABO-Incompatible Kidney Transplant Recipients: Analysis of 1-Year Follow-Up Data. Iwai, T; Kabei, K; Kumada, N; Kuwabara, N; Naganuma, T; Nakatani, T; Nishide, S; Takemoto, Y; Uchida, J, 2019)	1.12
"Treatment with everolimus supports the expansion of immunosuppressive regulatory T cells (Tregs), which exert a negative effect on antitumor immune responses."	( Metronomic cyclophosphamide attenuates mTOR-mediated expansion of regulatory T cells, but does not impact clinical outcome in patients with metastatic renal cell cancer treated with everolimus. de Gruijl, TD; Haanen, JBAG; Hamberg, P; Helgason, HH; Huijts, CM; Los, M; Lougheed, SM; Polee, MB; Tascilar, M; van der Vliet, HJ; Verheul, HM; Werter, IM, 2019)	1.05
"The treatment with everolimus significantly reduced heme oxygenase-1 expression and increased iNOS mRNA expression when compared to non-treated animals."	( Effects of everolimus on oxidative stress in kidney model of ischemia/reperfusion injury. Bajcetic, M; Becker, JU; Kezic, A; Thaiss, F; Tsui, TY, 2013)	1.1
"Treatment with everolimus or letrozole resulted in growth inhibition of SCs in a dose-dependent manner."	( Everolimus in combination with letrozole inhibit human breast cancer MCF-7/Aro stem cells via PI3K/mTOR pathway: an experimental study. Hou, G; Liu, J; Liu, Y; Zhang, J; Zhang, S; Zhang, X, 2014)	2.18
"Treatment with everolimus, an oral mTOR inhibitor, offers patients a noninvasive pharmacotherapeutic treatment option. "	( Role of mTOR inhibition in the treatment of patients with renal angiomyolipomas. Coombs, EJ, 2013)	0.74
"Treatment with everolimus (10 mg/day) was initiated on POD 32."	( [A case of massive pancreatic neuroendocrine carcinoma successfully treated with surgical resection and postoperative everolimus administration]. Egawa, C; Hamanaka, M; Hashimoto, N; Kagawa, Y; Kato, T; Katsura, Y; Kawashima, H; Kusama, H; Matsushita, K; Mukai, Y; Nakahira, S; Okishiro, M; Sakisaka, H; Suzuki, R; Takeda, Y; Takeno, A; Tamura, S; Taniguchi, H, 2013)	0.94
"Treatment with everolimus significantly enhanced the antitumor activity of trabectedin plus SN-38 or topotecan."	( Combination treatment with trabectedin and irinotecan or topotecan has synergistic effects against ovarian clear cell carcinoma cells. Hamasaki, T; Hisamatsu, T; Kawano, M; Kimura, T; Kishimoto, T; Mabuchi, S; Matsumoto, Y; Sasano, T; Sawada, K; Takahashi, K; Takahashi, R; Takahashi, T, 2014)	0.74
"Treatment with everolimus, resulted in 56% growth inhibition, and a triple combination of SU11274, everolimus and XAV939, resulted in 95% growth inhibition in RU cells."	( Targeting c-Met in melanoma: mechanism of resistance and efficacy of novel combinatorial inhibitor therapy. Bertram, C; Botting, GM; Crees, Z; Etnyre, D; Fong, JT; Girard, J; Jacobs, RJ; Moravec, DN; Puri, N; Rajanna, S; Shambannagari, MR; Stone, AL; Uppada, SB, 2014)	0.74
"Treatment with everolimus was started when he was 10 months old."	( Everolimus Treatment for an Early Infantile Subependymal Giant Cell Astrocytoma With Tuberous Sclerosis Complex. Fukumura, S; Minagawa, K; Takayama, R; Tsutsumi, H; Watanabe, T, 2015)	2.2
"Treatment with everolimus reduces the size of SEGA associated with TSC with an adequate safety profile, and constitutes an alternative to surgery in certain cases."	( [Response to everolimus in patients with giant cell astrocytoma associated to tuberous sclerosis complex]. Baena-Gómez, MA; Camino-León, R; Fernández-Ramos, JA; López-Laso, E; Mateos-González, ME; Peña-Rosa, MJ; Vicente-Rueda, J, 2014)	1.12
"Treatment with everolimus was identified as an independent predictor of longer survival (hazard ratio = 0.34; P = .02)."	( Everolimus-based immunosuppression in patients with hepatocellular carcinoma at high risk of recurrence after liver transplantation: a case series. Diaz, SP; Ferreiro, AO; Gutiérrez, MG; López, FS; Patiño, MJ; Vazquez-Millán, MA, 2014)	2.18
"The treatment with everolimus significantly inhibited cell growth, and significantly reduced the expression of p-mTOR, downstream signaling proteins, and hypoxic related proteins as well as invasion and migration potentials (P < 0.05)."	( Anti-tumor effect of the mammalian target of rapamycin inhibitor everolimus in oral squamous cell carcinoma. Kawakita, A; Kawasaki, G; Naruse, T; Rokutanda, S; Umeda, M; Yamada, S; Yanamoto, S, 2015)	0.97
"Treatment with everolimus induced a clear reduction of transaminases within 2 weeks. "	( Everolimus treatment for patients with autoimmune hepatitis and poor response to standard therapy and drug alternatives in use. Larsen, FS; Ytting, H, 2015)	2.21
"Treatment with everolimus was associated with significant improvement in progression-free survival in patients with progressive lung or gastrointestinal neuroendocrine tumours. "	( Everolimus for the treatment of advanced, non-functional neuroendocrine tumours of the lung or gastrointestinal tract (RADIANT-4): a randomised, placebo-controlled, phase 3 study. Buzzoni, R; Carnaghi, C; Fave, GD; Fazio, N; Kulke, MH; Lahner, H; Oh, DY; Pacaud, LB; Pavel, ME; Raderer, M; Rouyrre, N; Sachs, C; Shimada, Y; Singh, S; Strosberg, J; Tesselaar, M; Tomasek, J; Valle, JW; Van Cutsem, E; Voi, M; Wolin, E; Yao, JC, 2016)	2.23
"Treatment with everolimus resulted in growth inhibition of all stem cells in a dose-dependent manner. "	( [Drug sensitivity research of mTOR inhibitor on breast cancer stem cells]. Liu, P; Liu, Y; Zhang, J; Zhang, X, 2015)	0.77
"Treatment with everolimus in patients with extrapancreatic NETs appears to be a promising strategy that is safe and well tolerated. "	( Efficacy and Safety of Everolimus in Extrapancreatic Neuroendocrine Tumor: A Comprehensive Review of Literature. Agrimi, D; Aversano, M; Bassi, V; Colao, A; Faggiano, A; Giordano, EA; Guarnotta, V; Logoluso, FA; Malandrino, P; Messina, E; Modica, R; Nicastro, V; Nuzzo, V; Sciaraffia, M, 2016)	1.1
"Treatment with everolimus was stopped owing to adverse events in 11 patients (42.3%)."	( Clinical Experience of Late Conversion From Antimetabolites With Standard Exposure Calcineurin Inhibitors to Everolimus With Calcineurin Inhibitor Minimization in Stable Kidney Transplant Recipients With Good Renal Function. Iwai, T; Kabei, K; Kumada, N; Kuwabara, N; Naganuma, T; Nakatanti, T; Nishide, S; Takemoto, Y; Uchida, J; Yamasaki, T, 2016)	0.99
"Treatment with everolimus markedly inhibited the growth of tumors induced by poorly differentiated HAK-1B and KYN-2 cells and phosphorylation of mTOR Ser2481 in vivo."	( Phosphorylation of mTOR Ser2481 is a key target limiting the efficacy of rapalogs for treating hepatocellular carcinoma. Akiba, J; Kawahara, A; Kuwano, M; Murakami, Y; Nishitani, A; Noda, M; Ono, M; Shibata, T; Watari, K; Yano, H, 2016)	0.77
"Treatment of everolimus, the specific mTOR inhibitor, significantly attenuated DDX5-mediated cell proliferation."	( DDX5 promotes gastric cancer cell proliferation in vitro and in vivo through mTOR signaling pathway. Chen, L; Du, C; Hou, MX; Li, DQ; Li, N; Li, SS; Xie, MJ; Yang, Y; Zheng, ZD, 2017)	0.81
"Treatment with everolimus prolongs progression-free survival relative to placebo in patients with metastatic renal cell carcinoma that had progressed on other targeted therapies."	( Efficacy of everolimus in advanced renal cell carcinoma: a double-blind, randomised, placebo-controlled phase III trial. Berg, WJ; Bracarda, S; Escudier, B; Figlin, RA; Grünwald, V; Hollaender, N; Hutson, TE; Kay, A; Lebwohl, D; Motzer, RJ; Oudard, S; Porta, C; Ravaud, A; Thompson, JA; Urbanowitz, G, 2008)	1.08
"Treatment with everolimus was initiated at a mean (SD) of 79.8 (52.7) months (range, 10-163 mo) after transplantation."	( Preliminary experience with conversion from calcineurin inhibitors to everolimus in cardiac transplantation maintenance therapy. Arizón-Muñoz, JM; Benezet-Mazuecos, J; Guisado, A; Jiménez-Díaz, J; Lage-Gallé, E; Martínez, A; Mogollón, MV; Romero-Rodriguez, N; Sánchez-Brotons, JA; Sobrino-Márquez, JM, 2008)	0.92
"Treatment with everolimus at the minimal effective dose was studied in combination with cyclophosphamide at maximum tolerated dose in a human gastric cancer severe combined immunodeficient (SCID) mouse xenograft model. "	( mTOR inhibition sensitizes gastric cancer to alkylating chemotherapy in vivo. Cejka, D; Fuereder, T; Preusser, M; Sieghart, W; Strommer, S; Wacheck, V; Werzowa, J, )	0.48
"Treatment with everolimus allowed a primary response."	( Maintenance immunosuppressive therapy with everolimus preserves humoral immune responses. Bemelman, FJ; Idu, MM; Koch, SD; Minnee, RC; Struijk, GH; ten Berge, IJ; van Donselaar-van der Pant, KA; Zwinderman, AH, 2010)	0.96
"Treatment of everolimus-resistant disease remains largely undefined in metastatic renal cell carcinoma (mRCC). "	( Treatment of everolimus-resistant metastatic renal cell carcinoma with VEGF-targeted therapies. Busch, J; Fenner, M; Ganser, A; Grünwald, V; Seidel, C; Weikert, S, 2011)	1.11
"Treatment of everolimus-resistant disease was associated with a PFS of 5.5 months. "	( Treatment of everolimus-resistant metastatic renal cell carcinoma with VEGF-targeted therapies. Busch, J; Fenner, M; Ganser, A; Grünwald, V; Seidel, C; Weikert, S, 2011)	1.11
"Treatment with everolimus also diminished glomerular hypertrophy."	( Delayed mTOR inhibition with low dose of everolimus reduces TGFβ expression, attenuates proteinuria and renal damage in the renal mass reduction model. Arévalo, MA; Boggia, J; Coria, V; Gimenez-Bonafe, P; González-Martínez, F; Grande, MT; Grinyó, J; Herrero-Fresneda, I; Kurdián, M; Lloberas, N; López-Novoa, JM; Malacrida, L; Noboa, O; Torras, J, 2012)	0.98
"Treatment with everolimus is known to prolong progression-free survival in patients with renal cell carcinoma resistant against tyrosine-kinase inhibitor therapy. "	( [Management of side effects of everolimus treatment for metastatic renal cell carcinoma]. Hongo, F; Mikami, K; Miki, T, 2012)	1.02

Excerpt	Reference	Relevance
" There were no significant between-group differences in the composite endpoint of BPAR, graft loss or death, nor any significant between-group differences in adverse events in either study."	( Everolimus with optimized cyclosporine dosing in renal transplant recipients: 6-month safety and efficacy results of two randomized studies. Alves Filho, G; Bernhardt, P; Bourbigot, B; Cambi, V; Campbell, S; Civati, G; Cretin, N; Eris, J; Esmeraldo, R; Garcia, VD; Geissler, J; Haas, T; Jappe, A; Leone, J; Magee, JC; Pascual, J; Rigotti, P; Tedesco, H; Vitko, S; Whelchel, J, 2004)	1.77
" Adverse events were higher in everolimus-treated patients especially at the 4-mg/day dose, but there was no difference in the incidence of thrombocytopenia or leukopenia between all groups and renal function as determined by serum creatinine, and creatinine clearance remained stable to 36 months in everolimus-treated patients."	( Safety, tolerability, and efficacy of everolimus in de novo liver transplant recipients: 12- and 36-month results. Abecassis, M; Calmus, Y; Fischer, L; Freeman, R; Klempnauer, J; Langnas, A; Levy, G; Mayer, D; Nashan, B; Neuhaus, P; Punch, J; Roberts, J; Rogiers, X; Samuel, D; Schmidli, H; Sloof, M; Tuttle-Newhall, E, 2006)	0.89
"To date there is a substantial experience with rapamycin conversion in stable renal transplant recipients with respect to the procedure of conversion, initial doses, and target blood levels as well as adverse events, but in the case of Everolimus there is almost no experience with conversion and calcineurin inhibitor (CNI) withdrawal."	( Conversion to everolimus in kidney transplant recipients: a safe and simple procedure. Arias, M; Barrientos, A; Calvo, N; Conesa, J; Cotorruelo, JG; Gómez-Alamillo, C; Rodrigo, E; Ruiz, JC; Sanchez-Fructuoso, A, 2006)	0.88
" We describe our experience in a series of 78 stable renal transplant patients who were switched to Everolimus with complete and quick elimination of the CNI: the procedure of conversion, pharmacokinetic results after conversion, evolution of renal parameters (renal function, proteinuria, and others), and safety data (acute rejection and adverse events)."	( Evaluation of the efficacy and safety of the conversion from a calcineurin inhibitor to an everolimus-based therapy in maintenance renal transplant patients. Arias, M; Barrientos, A; Calvo, N; Conesa, J; Cotorruelo, J; Gómez-Alamillo, C; Moreno, MA; Rodrigo, E; Ruiz San Millán, JC; Sánchez Fructuoso, A, 2007)	0.78
"mTOR inhibitors were safe immunosuppressive drugs whose side effects were controlled and easily managed."	( Efficacy, tolerance, and safety of mammalian target of rapamycin inhibitors as rescue immunosuppressants in liver transplantation. Alamo, JM; Barrera, L; Bernal, C; Casado, MD; Cordero, E; Gomez-Bravo, MA; Jimenez, R; Marin, LM; Sanchez-Moreno, L; Sousa, JM; Suarez, G; Suarez-Grau, JM, )	0.13
", re-introduction of CNI), incidence of adverse events, and mortality up to one year after OLT."	( A therapeutic exploratory study to determine the efficacy and safety of calcineurin-inhibitor-free de-novo immunosuppression after liver transplantation: CILT. Goralczyk, AD; Lorf, T; Obed, A; Ramadori, G; Schnitzbauer, A; Tsui, TY, 2010)	0.36
" Adverse events led to study drug discontinuation in 17 IE patients (26."	( Efficacy and safety of de novo or early everolimus with low cyclosporine in deceased-donor kidney transplant recipients at specified risk of delayed graft function: 12-month results of a randomized, multicenter trial. Bayle, F; Berthoux, F; Cassuto, E; Charpentier, B; Dantal, J; Di Giambattista, F; Genin, R; Glotz, D; Kossari, N; Lefrançois, N; Legendre, C; Merville, P; Moal, MC; Moulin, B; Quéré, S; Rerolle, JP; Rostaing, L; Toupance, O; Westeel, PF, 2010)	0.63
" Tolerable dose, need for supportive treatments, and early signals for toxic effect were evaluated in a planned safety analysis of 270 patients."	( Integrating bevacizumab, everolimus, and lapatinib into current neoadjuvant chemotherapy regimen for primary breast cancer. Safety results of the GeparQuinto trial. Blohmer, JU; Costa, SD; Eidtmann, H; Fasching, PA; Fehm, T; Gerber, B; Hanusch, C; Hilfrich, J; Kreienberg, R; Loibl, S; Nekljudova, V; Solbach, C; Strumberg, D; Untch, M; von Minckwitz, G, 2011)	0.67
"mTORi treatment was prematurely eliminated due to adverse events in 112 patients."	( Comparative analysis of adverse events requiring suspension of mTOR inhibitors: everolimus versus sirolimus. Arias, M; Calvo Romero, N; Gómez Alamillo, C; Pérez-Flores, I; Ruiz, JC; Sánchez-Fructuoso, AI, 2010)	0.59
"03) and a 43% decrease in major adverse cardiovascular events, cardiac death, myocardial infarction, or ischemic-driven target lesion revascularization (9."	( Long-term (three-year) safety and efficacy of everolimus-eluting stents compared to paclitaxel-eluting stents (from the SPIRIT III Trial). Applegate, RJ; Caputo, R; Cutlip, DE; Doostzadeh, J; Farhat, N; Hermiller, JB; Lansky, AJ; Sood, P; Stone, GW; Sudhir, K; Williams, JE; Yaqub, M; Yu, S, 2011)	0.63
" The rapid introduction of novel treatment options into clinical practice within a relatively short time frame has created some new challenges pertaining to adverse event (AE) management in patients with advanced RCC."	( Treatment-associated adverse event management in the advanced renal cell carcinoma patient treated with targeted therapies. Ravaud, A, 2011)	0.37
"In April 2009, an expert group of 11 physicians and clinical nurses met to discuss the management of selected adverse events associated with the use of everolimus for the treatment of metastatic renal cell carcinoma (mRCC)."	( Management of adverse events associated with the use of everolimus in patients with advanced renal cell carcinoma. Climent, MA; Creel, P; Dickow, B; Fischer, P; Gornell, SS; Meloni, F; Motzer, RJ; Osanto, S; Porta, C; Ravaud, A; Vaishampayan, U; White, DA, 2011)	0.81
" Guidance for management of these adverse events is provided."	( Management of adverse events associated with the use of everolimus in patients with advanced renal cell carcinoma. Climent, MA; Creel, P; Dickow, B; Fischer, P; Gornell, SS; Meloni, F; Motzer, RJ; Osanto, S; Porta, C; Ravaud, A; Vaishampayan, U; White, DA, 2011)	0.62
" Patients were closely monitored for the development of serious and grades 3/4 adverse events (AEs)."	( An international expanded-access programme of everolimus: addressing safety and efficacy in patients with metastatic renal cell carcinoma who progress after initial vascular endothelial growth factor receptor-tyrosine kinase inhibitor therapy. Anak, O; Bavbek, SE; Blank, CU; Bodrogi, I; Bono, P; Booth, J; Castellano, D; Grünwald, V; Hawkins, R; Karakiewicz, PI; Knox, JJ; Larkin, J; Lee, SH; Machiels, JP; Miller, K; Pirotta, N; Rha, SY; Rosamilia, M, 2012)	0.64
" The most common severe adverse event probably related to sorafenib was diarrhea (12."	( Efficacy and safety of sorafenib in combination with mammalian target of rapamycin inhibitors for recurrent hepatocellular carcinoma after liver transplantation. Bustamante, J; Castroagudin, JF; Garralda, E; Gomez-Martin, C; Herrero, I; Matilla, A; Salcedo, M; Sangro, B; Testillano, M, 2012)	0.38
" We sought to determine the causes, incidence, risk factors, and consequences of withdrawal due to adverse events of PSIs in maintenance heart transplantation."	( Withdrawal of proliferation signal inhibitors due to adverse events in the maintenance phase of heart transplantation. Almenar, L; Arizon Del Prado, JM; Brossa, V; Crespo-Leiro, MG; Delgado, JF; Diaz-Molina, B; Gomez-Bueno, M; Gonzalez-Vilchez, F; Lambert, JL; Martínez-Dolz, L; Mirabet, S; Paniagua, MJ; Perez-Villa, F; Roig, E; Ruiz-Cano, MJ; Segovia, J; Vazquez de Prada, JA, 2012)	0.38
"In this large cohort of maintenance heart transplant recipients taking a PSI, 16% withdrew treatment in the first year, and 25% had stopped PSI due to severe adverse events by the fourth year."	( Withdrawal of proliferation signal inhibitors due to adverse events in the maintenance phase of heart transplantation. Almenar, L; Arizon Del Prado, JM; Brossa, V; Crespo-Leiro, MG; Delgado, JF; Diaz-Molina, B; Gomez-Bueno, M; Gonzalez-Vilchez, F; Lambert, JL; Martínez-Dolz, L; Mirabet, S; Paniagua, MJ; Perez-Villa, F; Roig, E; Ruiz-Cano, MJ; Segovia, J; Vazquez de Prada, JA, 2012)	0.38
" This has raised challenges in the management of adverse events (AEs) associated with the six targeted agents approved in RCC-sorafenib, sunitinib, pazopanib, bevacizumab (in combination with interferon alpha), temsirolimus, and everolimus."	( Targeted therapies for renal cell carcinoma: review of adverse event management strategies. Eisen, T; Escudier, B; Izzedine, H; Mulders, P; Pyle, L; Robert, C; Sternberg, CN; Zbinden, S, 2012)	0.56
" Everolimus was generally well tolerated in elderly patients, and most adverse events were grade 1 or 2 in severity."	( Efficacy and safety of everolimus in elderly patients with metastatic renal cell carcinoma: an exploratory analysis of the outcomes of elderly patients in the RECORD-1 Trial. Anak, O; Bracarda, S; Calvo, E; Climent, MA; Escudier, B; Grünwald, V; Hutson, TE; Kim, D; Motzer, RJ; Osanto, S; Panneerselvam, A; Porta, C; Ravaud, A; Vaishampayan, U, 2012)	1.6
"The XIENCE V stent is safe and effective with low TLR and stent thrombosis rates."	( SPIRIT Women, evaluation of the safety and efficacy of the XIENCE V everolimus-eluting stent system in female patients: referral time for coronary intervention and 2-year clinical outcomes. Grinfeld, L; Li, D; Mauri i Ferré, F; Mikhail, GW; Modena, MG; Morice, MC; Papeleu, P; Rutledge, D; Strasser, RH; Stuteville, M; Sudhir, K; Windecker, S, 2012)	0.61
" The data of studies and major outcomes include changes in patients' glomerular filtration rate (GFR), urinary protein, total kidney volume (TKV), cyst volume, parenchymal volume, and lipid profile and the frequency of adverse events."	( Efficacy and safety of mTOR inhibitor therapy in patients with early-stage autosomal dominant polycystic kidney disease: a meta-analysis of randomized controlled trials. Chen, J; He, Q; Ji, S; Lin, C, 2012)	0.38
"Based on the current limited clinical trials, this study suggests that short-duration mTOR inhibitor therapy is relatively safe to slow down the increase in kidney volume in patients with early-stage ADPKD, but it has limited impact on slowing down the decrease in GFR."	( Efficacy and safety of mTOR inhibitor therapy in patients with early-stage autosomal dominant polycystic kidney disease: a meta-analysis of randomized controlled trials. Chen, J; He, Q; Ji, S; Lin, C, 2012)	0.38
" Most adverse events are present for a short time after the introduction of everolimus, and are manageable."	( A drug safety evaluation of everolimus in kidney transplantation. Åsberg, A; Holdaas, H; Midtvedt, K, 2012)	0.9
" Correlates of major adverse cardiac events and ST were identified."	( Safety and efficacy of everolimus-eluting stents versus sirolimus-eluting stents in women. Badr, S; Barbash, IM; Dvir, D; Kitabata, H; Loh, JP; Pichard, AD; Sardi, G; Torguson, R; Waksman, R; Xue, Z, 2013)	0.7
" Dose reduction because of adverse events or intolerance was required in 91% of patients after 26 ± 11 days from the start of treatment."	( Adverse events affect sorafenib efficacy in patients with recurrent hepatocellular carcinoma after liver transplantation: experience at a single center and review of the literature. Airoldi, A; Belli, LS; Cordone, G; Gentiluomo, M; Mancuso, A; Vangeli, M; Viganò, R; Zavaglia, C, 2013)	0.39
" Adverse events were mostly grade 1 or 2; no patients discontinued treatment because of adverse events."	( Efficacy and safety of everolimus for subependymal giant cell astrocytomas associated with tuberous sclerosis complex (EXIST-1): a multicentre, randomised, placebo-controlled phase 3 trial. Bebin, EM; Belousova, E; Cauwel, H; Curatolo, P; de Vries, PJ; Flamini, JR; Ford, JP; Franz, DN; Frost, M; Jozwiak, S; Kohrman, MH; Kuperman, R; Lebwohl, D; Sahmoud, T; Shah, G; Sparagana, S; Thiele, EA; Whittemore, VH; Witt, O; Wu, JY, 2013)	0.7
"In a placebo-controlled trial, the median time to radiologic documentation of cancer worsening or death was extended by about 6 months, although patients experienced many, often serious, adverse effects."	( Everolimus 10 mg and pancreatic neuroendocrine tumours: many adverse effects and uncertain benefit. , 2012)	1.82
" All serious and grade 3/4 adverse events and grade 1/2 adverse events leading to a change in drug administration were reported."	( Safety of everolimus by treatment duration in patients with advanced renal cell cancer in an expanded access program. Anak, O; Bahl, A; Bavbek, S; Bracarda, S; Grünwald, V; Karakiewicz, P; Kim, D; Ou, YC; Panneerselvam, A; Rha, SY; van den Eertwegh, AJ, 2013)	0.79
" First occurrence of adverse events presented early in the treatment course for most patients."	( Safety of everolimus by treatment duration in patients with advanced renal cell cancer in an expanded access program. Anak, O; Bahl, A; Bavbek, S; Bracarda, S; Grünwald, V; Karakiewicz, P; Kim, D; Ou, YC; Panneerselvam, A; Rha, SY; van den Eertwegh, AJ, 2013)	0.79
" All patients reported ≥1 adverse event (AE), mostly grade 1/2 in severity, consistent with that previously reported, and none led to everolimus discontinuation."	( Everolimus long-term safety and efficacy in subependymal giant cell astrocytoma. Agricola, K; Care, MM; Franz, DN; Krueger, DA; Mays, M; Tudor, C, 2013)	2.04
"Everolimus therapy is safe and effective for longer term (median exposure 34."	( Everolimus long-term safety and efficacy in subependymal giant cell astrocytoma. Agricola, K; Care, MM; Franz, DN; Krueger, DA; Mays, M; Tudor, C, 2013)	3.28
" The primary endpoint was major adverse cardiac events."	( Safety and efficacy of everolimus- versus sirolimus-eluting stents: a systematic review and meta-analysis of 11 randomized trials. Hahn, S; Hofma, SH; Kandzari, DE; Kang, HJ; Kang, SH; Kim, HS; Koo, BK; Lee, HY; Lim, WH; Oh, BH; Park, KW; Park, YB; Shin, DH; Van Boven, AJ; Velders, MA; Yang, HM, 2013)	0.7
" Common grade 3/4 adverse events were anemia (20%), hyperglycemia (13%), increased gamma-glutamyltransferase (11%), hyponatremia (8%), dyspnea (8%), hypertriglyceridemia (6%), and lymphopenia (6%)."	( Safety and efficacy of everolimus in Chinese patients with metastatic renal cell carcinoma resistant to vascular endothelial growth factor receptor-tyrosine kinase inhibitor therapy: an open-label phase 1b study. Gogov, S; Guo, J; Huang, Y; Jappe, A; Pirotta, N; Qin, S; Straub, P; Sun, Y; Wang, H; Ye, Z; Zhang, X; Zhou, F, 2013)	0.7
" Although everolimus is generally well tolerated, as with most therapies administered in an advanced cancer setting, drug-related adverse events (AEs) inevitably occur."	( Management of adverse events in patients with hormone receptor-positive breast cancer treated with everolimus: observations from a phase III clinical trial. Peterson, ME, 2013)	1.01
" End points were major adverse cardiovascular events (MACE: defined as the composite of death, myocardial infarction, or target lesion revascularization), target vessel revascularization, and definite stent thrombosis at 1 year."	( Safety and efficacy outcomes of overlapping second-generation everolimus-eluting stents versus first-generation drug-eluting stents. Badr, S; Barbash, IM; Chen, F; Dvir, D; Kent, KM; Kitabata, H; Loh, JP; Minha, S; Pendyala, LK; Pichard, AD; Satler, LF; Suddath, WO; Torguson, R; Waksman, R, 2013)	0.63
" This review will focus on the adverse events reported with everolimus in breast cancer trials and will provide practical guidelines for the management of these adverse events."	( Everolimus: side effect profile and management of toxicities in breast cancer. O'Regan, R; Paplomata, E; Zelnak, A, 2013)	2.07
" The most common adverse events (AEs) were hypertriglyceridemia and anemia, similar to Western patients."	( Efficacy and safety of everolimus in Korean patients with metastatic renal cell carcinoma. Ahn, JB; Kim, HS; Kim, KH; Lee, HJ; Rha, SY; Shin, SJ; Yoon, SH, 2013)	0.7
"Patients who had been treated with everolimus for advanced renal cell carcinoma at 39 Japanese medical centers between January 2010 and November 2011 were retrospectively investigated to assess adverse events and the time to treatment failure."	( Adverse event profile and dose modification of everolimus for advanced renal cell carcinoma in real-world Japanese clinical practice. Azuma, H; Kanayama, HO; Miki, T; Nakatani, T; Nishimura, K; Nonomura, N; Nozawa, M; Tomita, Y; Tsujihata, M; Ueda, T; Uemura, H; Yoshioka, T, 2013)	0.92
"01) after experiencing adverse events."	( Adverse event profile and dose modification of everolimus for advanced renal cell carcinoma in real-world Japanese clinical practice. Azuma, H; Kanayama, HO; Miki, T; Nakatani, T; Nishimura, K; Nonomura, N; Nozawa, M; Tomita, Y; Tsujihata, M; Ueda, T; Uemura, H; Yoshioka, T, 2013)	0.65
"The adverse event profile of everolimus may differ between Japanese and Caucasian patients."	( Adverse event profile and dose modification of everolimus for advanced renal cell carcinoma in real-world Japanese clinical practice. Azuma, H; Kanayama, HO; Miki, T; Nakatani, T; Nishimura, K; Nonomura, N; Nozawa, M; Tomita, Y; Tsujihata, M; Ueda, T; Uemura, H; Yoshioka, T, 2013)	0.94
" Everolimus along with mycophenolate mofetil or azathioprine and prednisolone as a maintenance immunosuppressive therapy was found to be effective and safe in patients with CNIs withdrawal either due to CAN or CNIT."	( Safety and efficacy of everolimus in chronic allograft nephropathy. Dakshinamurty, KV; Das, U, 2013)	1.61
" Adverse events (AEs) of special interest (all grades) that occurred more frequently with EVE than with PBO included stomatitis, infections, rash, pneumonitis, and hyperglycemia."	( Safety and efficacy of everolimus with exemestane vs. exemestane alone in elderly patients with HER2-negative, hormone receptor-positive breast cancer in BOLERO-2. Baselga, J; Bourgeois, H; Burris, HA; Campone, M; Csöszi, T; Dakhil, S; Gnant, M; Gonzalez Martin, A; Heng, D; Hortobagyi, GN; Ito, Y; Noguchi, S; Osborne, K; Panneerselvam, A; Piccart, M; Pritchard, KI; Puttawibul, P; Rugo, HS; Sahmoud, T; Srimuninnimit, V; Taran, T, 2013)	0.7
" However, a low rate of tumor reduction and some adverse events have been pointed out."	( Therapeutic potential and adverse events of everolimus for treatment of hepatocellular carcinoma - systematic review and meta-analysis. Galli, U; Gao, C; Hatano, E; Houben, P; Lin, S; Petrulionis, M; Richter, S; Schemmer, P; Schultze, D; Winkler, S; Yamanaka, K, 2013)	0.65
"Mammalian target of rapamycin (mTOR) inhibitors are associated with dermatological adverse events."	( Everolimus-induced human keratinocytes toxicity is mediated by STAT3 inhibition. Bito, T; Hirai, M; Hirano, T; Kume, M; Makimoto, H; Mukai, A; Nishigori, C; Uda, A; Yamamoto, K; Yamashita, K, 2013)	1.83
" Adverse events led to temporary SORA discontinuation in 2 patients (28."	( Efficacy and safety of combination therapy with everolimus and sorafenib for recurrence of hepatocellular carcinoma after liver transplantation. Bargellini, I; Bartolozzi, C; Campani, D; Carrai, P; Cioni, D; Crocetti, L; De Simone, P; Della Pina, C; Filipponi, F; Ghinolfi, D; Lencioni, R; Leonardi, G; Pezzati, D; Pollina, L, )	0.39
"Everolimus has important clinical activity in various malignancies, but its use can be complicated by respiratory adverse events."	( Diagnostic challenges of respiratory adverse events during everolimus treatment. de Boer, M; De Vos, FY; Jansen, A; Tjan-Heijnen, VC; van Herpen, CM; Willemsen, AE, 2014)	2.09
" We report on the incidence, time course, severity, and resolution of treatment-emergent adverse events (AEs) as well as incidence of dose modifications during the extended follow-up of this study."	( Incidence and time course of everolimus-related adverse events in postmenopausal women with hormone receptor-positive advanced breast cancer: insights from BOLERO-2. Baselga, J; Bauly, H; Burris, HA; Chouinard, E; Csoszi, T; Eakle, J; El-Hashimy, M; Feng, W; Geberth, M; Gnant, M; Hortobagyi, G; Noguchi, S; Perez, A; Piccart, M; Pritchard, KI; Puttawibul, P; Rugo, HS; Srimuninnimit, V; Taran, T, 2014)	0.69
" End points included probable or definite stent thrombosis and major adverse cardiovascular events (MACE), defined as a composite of all-cause death, Q-wave myocardial infarction, and target lesion revascularization up to 3 years."	( Long-term safety and efficacy of second-generation everolimus-eluting stents compared to other limus-eluting stents and bare metal stents in patients with acute coronary syndrome. Kitabata, H; Loh, JP; Magalhaes, MA; Omar, A; Pendyala, LK; Pichard, AD; Satler, LF; Suddath, WO; Torguson, R; Waksman, R, 2014)	0.65
"We discuss clinically relevant everolimus-related adverse events from the phase III studies, including stomatitis, noninfectious pneumonitis, rash, selected metabolic abnormalities, and infections, with focus on appropriate clinical management of these events and specific considerations in patients with breast cancer."	( Adverse event management in patients with advanced cancer receiving oral everolimus: focus on breast cancer. Aapro, M; Andre, F; Blackwell, K; Calvo, E; Jahanzeb, M; Papazisis, K; Porta, C; Pritchard, K; Ravaud, A, 2014)	0.92
"The majority of adverse events experienced during everolimus therapy are of mild to moderate severity."	( Adverse event management in patients with advanced cancer receiving oral everolimus: focus on breast cancer. Aapro, M; Andre, F; Blackwell, K; Calvo, E; Jahanzeb, M; Papazisis, K; Porta, C; Pritchard, K; Ravaud, A, 2014)	0.89
"As with all orally administered agents, education of both physicians and patients in the management of adverse events for patients receiving everolimus is critical to achieving optimal exposure and clinical benefit."	( Adverse event management in patients with advanced cancer receiving oral everolimus: focus on breast cancer. Aapro, M; Andre, F; Blackwell, K; Calvo, E; Jahanzeb, M; Papazisis, K; Porta, C; Pritchard, K; Ravaud, A, 2014)	0.84
"Nineteen patients who discontinued treatment with vascular endothelial growth factor receptor-tyrosine kinase inhibitors because of disease progression or adverse events were administered everolimus."	( Efficacy of everolimus in patients with advanced renal cell carcinoma refractory or intolerant to VEGFR-TKIs and safety compared with prior VEGFR-TKI treatment. Fujioka, T; Iwasaki, K; Kato, R; Kato, Y; Matsuura, T; Obara, W, 2014)	0.97
" Two patients discontinued everolimus treatment because of adverse events."	( Efficacy of everolimus in patients with advanced renal cell carcinoma refractory or intolerant to VEGFR-TKIs and safety compared with prior VEGFR-TKI treatment. Fujioka, T; Iwasaki, K; Kato, R; Kato, Y; Matsuura, T; Obara, W, 2014)	1.08
" The adverse event profiles of everolimus and vascular endothelial growth factor receptor-tyrosine kinase inhibitors were different."	( Efficacy of everolimus in patients with advanced renal cell carcinoma refractory or intolerant to VEGFR-TKIs and safety compared with prior VEGFR-TKI treatment. Fujioka, T; Iwasaki, K; Kato, R; Kato, Y; Matsuura, T; Obara, W, 2014)	1.07
" At 2 years, the incidence of major adverse cardiovascular events was 13."	( Long-term safety and efficacy of the everolimus-eluting stent compared to first-generation drug-eluting stents in contemporary clinical practice. Badr, S; Barbash, IM; Ben-Dor, I; Loh, JP; Minha, S; Pichard, AD; Satler, LF; Torguson, R; Waksman, R, 2014)	0.68
" Two patients required dose reduction due to adverse events."	( Activity and safety of RAD001 (everolimus) in patients affected by biliary tract cancer progressing after prior chemotherapy: a phase II ITMO study. Alabiso, O; Bajetta, E; Bertolini, A; Buzzoni, R; Cantore, M; Ciarlo, A; De Braud, F; Iannacone, C; Mambrini, A; Mazzaferro, V; Platania, M; Pusceddu, S; Turco, C, 2014)	0.69
"Small vessel diameter and long lesion length are independently associated with increased risk of adverse cardiac events after drug-eluting stent implantation."	( Two-year safety and effectiveness of the platinum chromium everolimus-eluting stent for the treatment of small vessels and longer lesions. Allocco, DJ; Cannon, LA; Dawkins, KD; Dens, J; Dubois, CL; Feldman, RL; Lee, TC; Meredith, IT; Mooney, MR; Pompili, VJ; Rabinowitz, AC; Saito, S; Stone, GW; Teirstein, PS, 2015)	0.66
" Thus, the adverse effects, described hereby, may be considered as « positive events », predicting efficacy, and thus looked for… Moreover, the sequential approach, with new drugs, emphasizes the need of defining the optimal sequence."	( [Revision of therapeutic index for targeted treatment in kidney cancer: What if toxicity could predict efficacy?]. Brugères-Chakiba, C; Chaminade, A; Grellety, T; Gross-Goupil, M; Ravaud, A; Roubaud, G, 2014)	0.4
"05) in the incidence of discontinuations and serious adverse events between the groups."	( Safety and efficacy of the early introduction of everolimus with reduced-exposure cyclosporine a in de novo kidney recipients. Ha, J; Huh, KH; Kim, YH; Kim, YL; Kim, YS; Oh, CK, 2015)	0.67
" Because adverse events (AEs) associated with everolimus might differ from AEs that oncologists who treat patients with BC are more familiar with, everolimus AEs and their effective management are reviewed in this article."	( Adverse event management of mTOR inhibitors during treatment of hormone receptor-positive advanced breast cancer: considerations for oncologists. Yardley, DA, 2014)	0.66
" Discontinuation due to adverse events occurred in three everolimus patients (7."	( Efficacy and safety of conversion from cyclosporine to everolimus in living-donor kidney transplant recipients: an analysis from the ZEUS study. Arns, W; Budde, K; Eisenberger, U; Hauser, IA; Heller, K; Klehr, HU; Lehner, F; May, C; Mühlfeld, A; Nadalin, S; Paulus, EM; Porstner, M; Reinke, P; Sommerer, C; Stahl, R; Stangl, M; Suwelack, B; Witzke, O; Wolters, HH; Wüthrich, RP; Zeier, M, 2014)	0.9
" However, as other immunosuppressive drugs, mTOR-I may induce the development of several adverse effects (e."	( [Extra-renal adverse effects of mTOR inhibitors: know them to optimize their use in renal transplantation]. Caletti, C; Granata, S; Lupo, A; Tomei, P; Zaza, G, )	0.13
" Adverse clinical events were independently adjudicated."	( Safety of second-generation drug-eluting stents three years after randomised use in the TWENTE trial. de Man, FH; Doggen, CJ; Lam, MK; Linssen, GC; Louwerenburg, JH; Löwik, MM; Sen, H; Stoel, MG; Tandjung, K; van Houwelingen, KG; von Birgelen, C, 2015)	0.42
" In patients with biliary tract cancer, everolimus is safe but associated with a higher incidence of adverse events."	( Safety profile and treatment response of everolimus in different solid tumors: an observational study. Bajetta, E; Biondani, P; Buzzoni, R; Damato, A; de Braud, F; DeBraud, F; Garanzini, E; Grassi, P; Procopio, G; Pusceddu, S; Testa, I; Verzoni, E, 2014)	0.94
" This study estimates the costs of managing adverse events (AEs) during EVE + EXE therapy and single-agent chemotherapy in Western Europe."	( Cost of adverse events during treatment with everolimus plus exemestane or single-agent chemotherapy in patients with advanced breast cancer in Western Europe. Campone, M; Faust, E; Gao, H; Kageleiry, A; Signorovitch, JE; Yang, H; Zhang, J, 2014)	0.66
" The most costly adverse event among all patients treated with EVE + EXE was anemia (on average €152 per patient)."	( Cost of adverse events during treatment with everolimus plus exemestane or single-agent chemotherapy in patients with advanced breast cancer in Western Europe. Campone, M; Faust, E; Gao, H; Kageleiry, A; Signorovitch, JE; Yang, H; Zhang, J, 2014)	0.66
" The purpose of this study is to compare the adverse event profiles of both agents and to estimate the risk factors for non-infectious pneumonitis in patients with advanced renal cell carcinoma on the basis of our real-world clinical experience."	( Differences in adverse event profiles between everolimus and temsirolimus and the risk factors for non-infectious pneumonitis in advanced renal cell carcinoma. Anai, S; Fujimoto, K; Fukasawa, S; Hongo, F; Miki, T; Nakatani, T; Nozawa, M; Ohzeki, T; Tamada, S; Uemura, H, 2015)	0.68
" Chi-squared test and univariate and multivariate logistic regression analyses were performed to investigate the differences in adverse event profiles and the risk factors associated with non-infectious pneumonitis, respectively."	( Differences in adverse event profiles between everolimus and temsirolimus and the risk factors for non-infectious pneumonitis in advanced renal cell carcinoma. Anai, S; Fujimoto, K; Fukasawa, S; Hongo, F; Miki, T; Nakatani, T; Nozawa, M; Ohzeki, T; Tamada, S; Uemura, H, 2015)	0.68
"Our findings suggest that adverse event profiles may differ between everolimus and temsirolimus and that non-infectious pneumonitis may occur more frequently in patients treated with everolimus than temsirolimus."	( Differences in adverse event profiles between everolimus and temsirolimus and the risk factors for non-infectious pneumonitis in advanced renal cell carcinoma. Anai, S; Fujimoto, K; Fukasawa, S; Hongo, F; Miki, T; Nakatani, T; Nozawa, M; Ohzeki, T; Tamada, S; Uemura, H, 2015)	0.91
" Amenorrhea occurred as a rare adverse event of everolimus."	( Amenorrhea as a rare drug-related adverse event associated with everolimus for pancreatic neuroendocrine tumors. Ito, H; Kawaguchi, Y; Kawashima, Y; Maruno, A; Mine, T; Ogawa, M, 2014)	0.9
"Biodegradable-polymer drug-eluting stents (BP-DES) were developed to be as effective as second-generation durable-polymer drug-eluting stents (DP-DES) and as safe >1 year as bare-metal stents (BMS)."	( Long-term efficacy and safety of biodegradable-polymer biolimus-eluting stents: main results of the Basel Stent Kosten-Effektivitäts Trial-PROspective Validation Examination II (BASKET-PROVE II), a randomized, controlled noninferiority 2-year outcome tria Alber, H; Buser, P; Conen, D; Eberli, F; Galatius, S; Gilgen, N; Hoffmann, A; Jeger, R; Kaiser, C; Kurz, DJ; Moccetti, T; Müller, C; Naber, C; Pedrazzini, G; Pfisterer, M; Rickenbacher, P; Rickli, H; Skov Jensen, J; Steiner, M; Vogt, DR; Von Felten, S; Vuillomenet, A; Wadt Hansen, K; Wanitschek, M; Weilenmann, D, 2015)	0.42
" We analyzed several variables associated with this treatment, including patient characteristics, time from liver transplantation to conversion to everolimus, immunosuppression regimens before and after conversion, treatment efficacy, adverse events, and discontinuation after conversion."	( Immunosuppression based on everolimus in liver transplant recipients with severe early post-transplantation neurotoxicity. Bilbao, I; Caralt, M; Castells, L; Charco, R; Dopazo, C; Lazaro, J; Sapisochin, G, 2014)	0.9
" Patients were followed up to 2 years for major adverse cardiac events (MACE)."	( Safety and efficacy of everolimus-eluting stents compared with first-generation drug-eluting stents in patients undergoing primary percutaneous coronary intervention. Baker, NC; Escárcega, RO; Lipinski, MJ; Magalhaes, MA; Minha, S; Pichard, AD; Satler, LF; Suddath, WO; Torguson, R; Waksman, R, )	0.44
" All grades of common adverse events (AEs) were consistent with the known safety profile of everolimus."	( Efficacy and Safety of Sequential Use of Everolimus in Patients With Metastatic Renal Cell Carcinoma Previously Treated With Bevacizumab With or Without Interferon Therapy: Results From the European AVATOR Study. Emmanouilides, C; Guillot, A; Jacobasch, L; Kelkouli, N; Kim, S; Nguyen Tan Hon, T; Papandreou, C; Schmitz, J; Slimane, K; Theodore, C; Thiery-Vuillemin, A, 2015)	0.9
"There is a probable causal relationship between the study medication and the reported serious adverse events."	( Phase II study evaluating efficacy and safety of everolimus with letrozole for management of advanced (unresectable or metastatic) non-small cell lung cancer after failure of platinum-based treatment: a preliminary analysis of toxicity. Brown, MP; Singhal, N; Vatandoust, S, 2015)	0.67
" Adverse events led to discontinuation of everolimus and CNI in 32."	( Renal, efficacy and safety outcomes following late conversion of kidney transplant patients from calcineurin inhibitor therapy to everolimus: the randomized APOLLO study. Arns, W; Baeumer, D; Budde, K; Haller, H; May, C; Porstner, M; Rath, T; Reinke, P; Sommerer, C; Suwelack, B; Witzke, O, 2015)	0.89
" The analyzed clinical parameters were the 1-year rates of death, Q-wave myocardial infarction (MI), target lesion revascularization (TLR), target vessel revascularization (TVR), definite stent thrombosis (ST) and major adverse cardiac event (MACE) defined as the composite of death, MI, or TLR at 1-year."	( Safety and efficacy of limus-eluting stents and balloon angioplasty for sirolimus-eluting in-stent restenosis. Chen, F; Kitabata, H; Mahmoudi, M; Ota, H; Pichard, AD; Satler, LF; Suddath, WO; Torguson, R; Waksman, R, 2015)	0.42
" Other objectives are: to assess the incidence of treated biopsy-proven acute rejection, graft loss, or death; the incidences of components of the composite efficacy endpoint; renal function via estimated glomerular filtration rate using various formulae (MDRD-4, Nankivell, Cockcroft-Gault, chronic kidney disease epidemiology collaboration and Hoek formulae); the incidence of proteinuria; the incidence of adverse events and serious adverse events; the incidence and severity of cytomegalovirus and HCV infections and HCV-related fibrosis."	( Evaluating the efficacy, safety and evolution of renal function with early initiation of everolimus-facilitated tacrolimus reduction in de novo liver transplant recipients: Study protocol for a randomized controlled trial. Braun, F; Dworak, M; Nashan, B; Schemmer, P; Schlitt, H; Wimmer, P, 2015)	0.64
" Procedural and in-hospital clinical outcomes were examined in addition to the 1-year primary endpoint of death, myocardial infarction, and target lesion revascularization (major adverse cardiac events [MACE])."	( Safety and Effectiveness of Everolimus-Eluting Stents in Chronic Total Coronary Occlusion Revascularization: Results From the EXPERT CTO Multicenter Trial (Evaluation of the XIENCE Coronary Stent, Performance, and Technique in Chronic Total Occlusions). Grantham, JA; Kandzari, DE; Karmpaliotis, D; Kini, AS; Larracas, C; Lembo, NJ; Lombardi, W; Moses, JW; Nicholson, WJ; Orr, C; Popma, JJ; Rutledge, DR; Tummala, PE; Wang, J, 2015)	0.71
"4%), treatment with EES was associated with significantly lower composite adverse events for both intent-to-treat (18."	( Safety and Effectiveness of Everolimus-Eluting Stents in Chronic Total Coronary Occlusion Revascularization: Results From the EXPERT CTO Multicenter Trial (Evaluation of the XIENCE Coronary Stent, Performance, and Technique in Chronic Total Occlusions). Grantham, JA; Kandzari, DE; Karmpaliotis, D; Kini, AS; Larracas, C; Lembo, NJ; Lombardi, W; Moses, JW; Nicholson, WJ; Orr, C; Popma, JJ; Rutledge, DR; Tummala, PE; Wang, J, 2015)	0.71
" The analyzed clinical parameters were the 1-year rates of death, Q-wave myocardial infarction (MI), target lesion revascularization (TLR), target vessel revascularization (TVR), definite stent thrombosis (ST) and major adverse cardiac events (MACE) defined as the composite of death, MI, or TLR at 1-year."	( Safety and efficacy of everolimus-eluting stents for bare-metal in-stent restenosis. Mahmoudi, M; Ota, H; Pichard, AD; Satler, LF; Suddath, WO; Torguson, R; Waksman, R, )	0.44
"The most frequent side-effect of CNIs is nephrotoxicity, which in the long term can contribute, to allograft deterioration."	( The safety of calcineurin inhibitors for kidney-transplant patients. Malvezzi, P; Rostaing, L, 2015)	0.42
"gov updated to Mar 2014 with safety [major adverse cardiac events (MACE)], all-cause mortality, non-fatal myocardial infarction (MI), stent thrombosis (ST) and efficacy [target vessel revascularization (TVR), target lesion revascularization (TLR), target vessel failure (TVF), target lesion failure (TLF)] endpoints and follow-up of ≥12 months were identified."	( Safety and efficacy of everolimus-eluting stent versus zotarolimus-eluting stent: A meta-analysis of randomized controlled clinical trials and observational studies. Gu, H; Hua, K; Li, W; Wang, Y; Yang, J, 2015)	0.73
"Sirolimus should not be started within the first month after liver transplantation (LT) because of an increased risk of adverse outcomes."	( Everolimus is safe within the first month after liver transplantation. Barrera, P; Briceño, J; Ciria, R; De la Mata, M; Ferrín, G; González, V; Guerrero-Misas, M; Montero, JL; Pérez-Medrano, I; Poyato, A; Pozo, JC; Rodríguez-Perálvarez, M; Sánchez-Frías, M, 2015)	1.86
"Everolimus combined with reduced tacrolimus proved to be safe within the first month after LT."	( Everolimus is safe within the first month after liver transplantation. Barrera, P; Briceño, J; Ciria, R; De la Mata, M; Ferrín, G; González, V; Guerrero-Misas, M; Montero, JL; Pérez-Medrano, I; Poyato, A; Pozo, JC; Rodríguez-Perálvarez, M; Sánchez-Frías, M, 2015)	3.3
"In pediatric renal transplantation, an everolimus-based regimen with low-dose cyclosporine yields comparable four year results as a standard regimen, but with a different side effect profile."	( Efficacy and Safety of an Everolimus- vs. a Mycophenolate Mofetil-Based Regimen in Pediatric Renal Transplant Recipients. Ahlenstiel-Grunow, T; Bald, M; Brunkhorst, LC; Burmeister, G; Fichtner, A; Höcker, B; Krupka, K; Pape, L; Tönshoff, B; Zapf, A, 2015)	0.99
" Endpoints analyzed included: (1) the composite of all-cause death and non-fatal myocardial infarction (MI); and (2) the composite safety endpoint of major adverse cardiovascular events (MACEs), including death, MI and symptom-driven target lesion revascularization (TLR)."	( Evaluation of the Safety of Everolimus-Eluting Bioresorbable Vascular Scaffold (BVS) Implantation in Patients With Chronic Total Coronary Occlusions: Acute Procedural and Short-Term Clinical Results. Colombo, A; Erdogan, E; Goktekin, O; Latib, A; Panoulas, VF; Sato, K; Shah, I; Tastan, A; Uyarel, H; Yamac, AH, 2015)	0.71
"Treatment of CTOs with BVS seems to be safe and effective, with a high technical success rate and acceptable MACE at short-term follow-up."	( Evaluation of the Safety of Everolimus-Eluting Bioresorbable Vascular Scaffold (BVS) Implantation in Patients With Chronic Total Coronary Occlusions: Acute Procedural and Short-Term Clinical Results. Colombo, A; Erdogan, E; Goktekin, O; Latib, A; Panoulas, VF; Sato, K; Shah, I; Tastan, A; Uyarel, H; Yamac, AH, 2015)	0.71
" Theoretically, since vessel scaffolding is temporary and no permanent implant remains in the vessel, BRSs, as opposed to metal stents, once degraded would no longer be potential triggers for stent-related adverse events or side effects."	( Evaluation of the short- and long-term safety and therapy outcomes of the everolimus-eluting bioresorbable vascular scaffold system in patients with coronary artery stenosis: Rationale and design of the German-Austrian ABSORB RegIstRy (GABI-R). Achenbach, S; Biermann, J; Hamm, CW; Kastner, J; Limbourg, T; Mehilli, J; Münzel, T; Naber, C; Nef, H; Neumann, T; Pfannebecker, T; Richardt, G; Schmermund, A; Schneider, S; Wiebe, J; Wöhrle, J; Zahn, R, )	0.36
" To provide optimal prevention and management strategies, it is crucial that clinicians are aware of the adverse events (AEs) associated with mTOR inhibition."	( Dosing and Safety Implications for Oncologists When Administering Everolimus to Patients With Hormone Receptor-Positive Breast Cancer. Rugo, HS, 2016)	0.67
" No unexpected adverse events were reported."	( Retrospective analysis on safety and efficacy of everolimus in treatment of metastatic renal cancer patients receiving dialysis. Cosmai, L; del Giovane, C; Di Lorenzo, G; Donati, D; Guida, A; Masini, C; Mighali, P; Milella, M; Porta, C; Prati, V; Sabbatini, R; Santoni, M, 2015)	0.67
"Everolimus appears to be safe in mRCC patients with renal impairment or end-stage renal disease requiring dialysis."	( Retrospective analysis on safety and efficacy of everolimus in treatment of metastatic renal cancer patients receiving dialysis. Cosmai, L; del Giovane, C; Di Lorenzo, G; Donati, D; Guida, A; Masini, C; Mighali, P; Milella, M; Porta, C; Prati, V; Sabbatini, R; Santoni, M, 2015)	2.11
" The increased incidence of serious adverse events in early studies halted the enthusiasm as a kidney sparing alternative to calcineurin inhibitors (CNI)."	( Safety of mTOR inhibitors in adult solid organ transplantation. Campistol, JM; Diekmann, F; Ventura-Aguiar, P, 2016)	0.43
"In the authors' opinion, mTOR inhibitors are a safe alternative to standard immunosuppression therapy with CNI and mycophenolate/azathioprine."	( Safety of mTOR inhibitors in adult solid organ transplantation. Campistol, JM; Diekmann, F; Ventura-Aguiar, P, 2016)	0.43
"Everolimus-based immunosuppression regimen without corticosteroids and/or induction immediately after liver transplantation seems to be safe and effective when administered with low doses of calcineurin-inhibitor or mycophenolate; although these findings require further investigation, these regimens could avoid adverse effects of standard immunosuppression regimens with higher doses."	( The efficacy and safety of mammalian target of rapamycin inhibitors ab initio after liver transplantation without corticosteroids or induction therapy. Angelico, R; Belardi, C; Cillis, A; Katari, R; Manzia, TM; Mogul, A; Orlando, G; Quaranta, C; Sforza, D; Tariciotti, L; Tisone, G; Toti, L, 2016)	1.88
"In percutaneous coronary intervention (PCI) patients new-generation drug-eluting stent (DES) has reduced adverse events in comparison to early-generation DES."	( Three-year efficacy and safety of new- versus early-generation drug-eluting stents for unprotected left main coronary artery disease insights from the ISAR-LEFT MAIN and ISAR-LEFT MAIN 2 trials. Byrne, RA; Cassese, S; Fusaro, M; Ibrahim, T; Kastrati, A; Kreutzer, J; Kufner, S; Laugwitz, KL; Mehilli, J; Schunkert, H; Tiroch, K; Tölg, R; Valgimigli, M; Xhepa, E, 2016)	0.43
" The primary endpoint was the composite of death, myocardial infarction (MI), target lesion revascularization and stroke (MACCE, major adverse cardiac and cerebrovascular event)."	( Three-year efficacy and safety of new- versus early-generation drug-eluting stents for unprotected left main coronary artery disease insights from the ISAR-LEFT MAIN and ISAR-LEFT MAIN 2 trials. Byrne, RA; Cassese, S; Fusaro, M; Ibrahim, T; Kastrati, A; Kreutzer, J; Kufner, S; Laugwitz, KL; Mehilli, J; Schunkert, H; Tiroch, K; Tölg, R; Valgimigli, M; Xhepa, E, 2016)	0.43
" The novel combination of everolimus and exemestane has been shown to prolong progression-free survival but with increased adverse events compared to exemestane alone."	( Occurrence and characterization of everolimus adverse events during first and subsequent cycles in the treatment of metastatic breast cancer. Berger, MJ; Mrozek, E; Phillips, G; Vargo, CA, 2016)	1.01
" The most common adverse events leading to dose reduction or interruption was stomatitis (57."	( Occurrence and characterization of everolimus adverse events during first and subsequent cycles in the treatment of metastatic breast cancer. Berger, MJ; Mrozek, E; Phillips, G; Vargo, CA, 2016)	0.71
" This early onset of adverse events requires thorough patient education and close clinical monitoring during the first 28 days of therapy."	( Occurrence and characterization of everolimus adverse events during first and subsequent cycles in the treatment of metastatic breast cancer. Berger, MJ; Mrozek, E; Phillips, G; Vargo, CA, 2016)	0.71
"Everolimus appears to be a safe therapeutic option for patients aged <3 years with TSC-associated SEGA."	( Safety of Everolimus in Patients Younger than 3 Years of Age: Results from EXIST-1, a Randomized, Controlled Clinical Trial. Berkowitz, N; Brechenmacher, T; Franz, DN; Jóźwiak, S; Kotulska, K, 2016)	2.28
" Given that increasing number of patients with TSC receive mTOR inhibitors, the issue of adverse events associated with this therapy becomes practically important."	( Management of side effects of mTOR inhibitors in tuberous sclerosis patients. Jóźwiak, S; Kotulska, K; Sadowski, K, 2016)	0.43
" Primary endpoint was a composite of major adverse cardiac events (MACE), including cardiac death, myocardial infarction (MI), target vessel revascularization (TVR), and definite stent thrombosis."	( Safety and Efficacy of Everolimus- Versus Sirolimus-Eluting Stents: 5-Year Results From SORT OUT IV. Berencsi, K; Christiansen, EH; Hansen, HS; Hansen, KN; Jensen, LO; Junker, A; Kaltoft, A; Krusell, L; Lassen, JF; Maeng, M; Ravkilde, J; Thayssen, P; Tilsted, HH, 2016)	0.74
" Conversion to MPS was associated with a higher incidence of adverse events."	( Efficacy and Safety of Elective Conversion From Sotrastaurin (STN) to Tacrolimus (TAC) or Mycophenolate (MPS) in Stable Kidney Transplant Recipients. Aguiar, W; Campos, E; Cristelli, M; Felipe, C; Ferreira, A; Franco, M; Gerbase de Lima, M; Hannun, P; Medina-Pestana, J; Sandes-Freitas, T; Tedesco-Silva, H, 2016)	0.43
" Most adverse events were either grade 1 or 2 and easy manageable with a dose reduction or temporary interruption and only rarely requiring discontinuation."	( Efficacy and Safety of Everolimus in Extrapancreatic Neuroendocrine Tumor: A Comprehensive Review of Literature. Agrimi, D; Aversano, M; Bassi, V; Colao, A; Faggiano, A; Giordano, EA; Guarnotta, V; Logoluso, FA; Malandrino, P; Messina, E; Modica, R; Nicastro, V; Nuzzo, V; Sciaraffia, M, 2016)	0.74
"Treatment with everolimus in patients with extrapancreatic NETs appears to be a promising strategy that is safe and well tolerated."	( Efficacy and Safety of Everolimus in Extrapancreatic Neuroendocrine Tumor: A Comprehensive Review of Literature. Agrimi, D; Aversano, M; Bassi, V; Colao, A; Faggiano, A; Giordano, EA; Guarnotta, V; Logoluso, FA; Malandrino, P; Messina, E; Modica, R; Nicastro, V; Nuzzo, V; Sciaraffia, M, 2016)	1.1
" No severe adverse events were usually reported and discontinuation was rarely required; thus, everolimus should be considered a valid therapeutic option for extrapancreatic NETs."	( Efficacy and Safety of Everolimus in Extrapancreatic Neuroendocrine Tumor: A Comprehensive Review of Literature. Agrimi, D; Aversano, M; Bassi, V; Colao, A; Faggiano, A; Giordano, EA; Guarnotta, V; Logoluso, FA; Malandrino, P; Messina, E; Modica, R; Nicastro, V; Nuzzo, V; Sciaraffia, M, 2016)	0.96
" The most common adverse events (AEs) were asthenia, hypertension, and diarrhea."	( Safety and clinical activity of vascular endothelial growth factor receptor (VEGFR)-tyrosine kinase inhibitors after programmed cell death 1 inhibitor treatment in patients with metastatic clear cell renal cell carcinoma. Amin, A; Doyle, J; Geynisman, DM; Hammers, HJ; McDermott, DF; Motzer, R; Nadal, R; Plimack, ER; Rini, B; Viudez, A; Voss, MH; Weinstock, M; Zhang, Z, 2016)	0.43
" Many patients treated with the registered fixed 10 mg dose once daily are in need of dose interruptions, reductions or treatment discontinuation due to severe adverse events."	( Everolimus pharmacokinetics and its exposure-toxicity relationship in patients with thyroid cancer. de Wit, D; den Hartigh, J; Gelderblom, H; Guchelaar, HJ; Kapiteijn, E; Links, TP; Moes, DJ; Roozen, CF; Schneider, TC; van der Hoeven, JJ; van Erp, NP, 2016)	1.88
" Although the pleural effusion reduced markedly after 5 weeks, stomatitis, diarrhea, melena, and interstitial pneumonia occurred as adverse events."	( [An Elderly Patient with Metastatic Breast Cancer Who Developed Severe Adverse Events such as Stomatitis and Interstitial Pneumonia after Everolimus plus Exemestane Treatment]. Goto, Y; Kimura, M; Sakiyama, K; Yoshida, T, 2016)	0.64
" Adverse events observed were stomatitis (35."	( The efficacy and safety of everolimus for the treatment of progressive gastroenteropancreatic neuroendocrine tumors: A multi-institution observational study in Taiwan. Chen, JS; Chen, LT; Chen, MH; Chen, YY; Chou, WC; Ku, FC; Liu, CT; Lu, CH; Shan, YS; Su, YL, 2016)	0.73
" The primary objective was safety of EVE plus EXE based on frequency of adverse events (AEs), and serious AEs (SAEs)."	( Safety of everolimus plus exemestane in patients with hormone-receptor-positive, HER2-negative locally advanced or metastatic breast cancer progressing on prior non-steroidal aromatase inhibitors: primary results of a phase IIIb, open-label, single-arm, e Bianchetti, S; Camozzi, M; Ciruelos, EM; Conte, P; Gavila, JG; Generali, D; Jerusalem, G; Lang, I; Lorizzo, K; Mardiak, J; Mariani, G; Martin, M; Michelotti, A; Montemurro, F; Naume, B; Neven, P; Simoncini, E; Tjan-Heijnen, VC, 2016)	0.84
" The most common grade 3-4 adverse events were haematological; the most common of these was grade 4 neutropenia in 18 (75%) of 24 patients."	( Everolimus combined with R-CHOP-21 for new, untreated, diffuse large B-cell lymphoma (NCCTG 1085 [Alliance]): safety and efficacy results of a phase 1 and feasibility trial. Ansell, SM; Colgan, JP; Habermann, TM; Inwards, DJ; Johnston, PB; LaPlant, B; McPhail, E; Micallef, IN; Nowakowski, GS; Witzig, TE, 2016)	1.88
"Due to toxic events, everolimus dosage was reduced to 5 mg in 27% of patients."	( Safety analysis, association with response and previous treatments of everolimus and exemestane in 181 metastatic breast cancer patients: A multicenter Italian experience. Cortesi, E; D'Onofrio, L; Fabbri, MA; Gamucci, T; Giuliani, R; Iezzi, L; Magri, V; Mancini, ML; Marchetti, P; Mauri, M; Mentuccia, L; Moscetti, L; Natoli, C; Pizzuti, L; Ramponi, S; Roma, CL; Ruggeri, EM; Santini, D; Sini, V; Sperduti, I; Vaccaro, A; Vici, P, 2016)	0.99
"The association of everolimus and exemestane has confirmed to be a safe and effective treatment for endocrine sensitive MBC patients even in routine clinical practice."	( Safety analysis, association with response and previous treatments of everolimus and exemestane in 181 metastatic breast cancer patients: A multicenter Italian experience. Cortesi, E; D'Onofrio, L; Fabbri, MA; Gamucci, T; Giuliani, R; Iezzi, L; Magri, V; Mancini, ML; Marchetti, P; Mauri, M; Mentuccia, L; Moscetti, L; Natoli, C; Pizzuti, L; Ramponi, S; Roma, CL; Ruggeri, EM; Santini, D; Sini, V; Sperduti, I; Vaccaro, A; Vici, P, 2016)	1
" We summarize the nephrotoxic and diabetogenic mechanisms of mTORi after pancreas transplant, the alternatives to minimize these effects, and report on other adverse events."	( mTOR inhibitors in pancreas transplant: adverse effects and drug-drug interactions. Fernandes-Silva, G; Ivani de Paula, M; Rangel, ÉB, 2017)	0.46
"To systematically review relevant literature comparing the oncological outcomes and adverse events of different systemic therapies for patients with metastatic non-ccRCC."	( A Systematic Review and Meta-analysis Comparing the Effectiveness and Adverse Effects of Different Systemic Treatments for Non-clear Cell Renal Cell Carcinoma. Albiges, L; Bensalah, K; Bex, A; Canfield, SE; Dabestani, S; Fernández-Pello, S; Giles, RH; Hofmann, F; Hora, M; Kuczyk, MA; Lam, TB; Ljungberg, B; Marconi, L; Merseburger, AS; Powles, T; Staehler, M; Tahbaz, R; Volpe, A, 2017)	0.46
" Sunitinib was associated with more Grade 3-4 adverse events than everolimus, although this was not statistically significant."	( A Systematic Review and Meta-analysis Comparing the Effectiveness and Adverse Effects of Different Systemic Treatments for Non-clear Cell Renal Cell Carcinoma. Albiges, L; Bensalah, K; Bex, A; Canfield, SE; Dabestani, S; Fernández-Pello, S; Giles, RH; Hofmann, F; Hora, M; Kuczyk, MA; Lam, TB; Ljungberg, B; Marconi, L; Merseburger, AS; Powles, T; Staehler, M; Tahbaz, R; Volpe, A, 2017)	0.69
"Patients with diabetes and coronary artery disease remain at high risk for adverse cardiovascular events after percutaneous coronary intervention."	( Efficacy and safety of everolimus and zotarolimus-eluting stents versus first-generation drug-eluting stents in patients with diabetes: A meta-analysis of randomized trials. Baber, U; Bavishi, C; Dangas, GD; Kini, AS; Moreno, P; Panwar, S; Pirrotta, S; Sharma, SK; Tamis-Holland, J, 2017)	0.77
" Efficacy [target vessel revascularization (TVR) and target lesion revascularization (TLR)] and safety [major adverse cardiac events (MACE), all-cause and cardiac mortality, myocardial infarction, stent thrombosis] outcomes were evaluated."	( Efficacy and safety of everolimus and zotarolimus-eluting stents versus first-generation drug-eluting stents in patients with diabetes: A meta-analysis of randomized trials. Baber, U; Bavishi, C; Dangas, GD; Kini, AS; Moreno, P; Panwar, S; Pirrotta, S; Sharma, SK; Tamis-Holland, J, 2017)	0.77
"In patients with diabetes and coronary artery disease undergoing stenting, EES is the most efficacious and safe DES."	( Efficacy and safety of everolimus and zotarolimus-eluting stents versus first-generation drug-eluting stents in patients with diabetes: A meta-analysis of randomized trials. Baber, U; Bavishi, C; Dangas, GD; Kini, AS; Moreno, P; Panwar, S; Pirrotta, S; Sharma, SK; Tamis-Holland, J, 2017)	0.77
" There was not a substantial difference in graft loss, mortality, and the occurrence of adverse events (AEs) or serious AEs."	( Efficacy and Safety of Everolimus for Maintenance Immunosuppression of Kidney Transplantation: A Meta-Analysis of Randomized Controlled Trials. Lei, K; Li, J; Liu, D; Liu, J; Xu, Q; You, R; Zhang, C; Zhu, L, 2017)	0.77
"The aim of this systematic review and meta-analysis was to evaluate the efficacy-related events and adverse events of 2 different doses of everolimus in kidney transplant recipients."	( Safety and Efficacy of Two Different Doses of Everolimus in Kidney Transplantation: a Systematic Review and Meta-Analysis. Arab-Zozani, M; Ghoddoosi Nejad, D; Hasanpoor, E; Kakemam, E; Mahdavi-Mazdeh, M; Sokhanvar, M, 2016)	0.89
" The relative risk (RR) and 95% confidence interval (CI) for treated efficacy-related events and adverse events were collected to calculate pooled measures."	( Safety and Efficacy of Two Different Doses of Everolimus in Kidney Transplantation: a Systematic Review and Meta-Analysis. Arab-Zozani, M; Ghoddoosi Nejad, D; Hasanpoor, E; Kakemam, E; Mahdavi-Mazdeh, M; Sokhanvar, M, 2016)	0.69
" Both adverse events were rarely severe and were managed easily and efficiently."	( A prospective observational study on the evaluation of everolimus-related adverse events in metastatic renal cell carcinoma after first-line anti-vascular endothelial growth factor therapy: the AFINITE study in France. Albiges, L; Eymard, JC; Guillot, A; Joly, F; Kelkouli, N; Laguerre, B; Lebret, T; Nguyen, T; Ravaud, A; Rolland, F; Slimane, K; Spaeth, D, 2017)	0.7
" However, due to the historical predominance of everolimus in the oncology setting, some physicians who treat TSC patients may be unfamiliar with everolimus-associated adverse events (AEs) and appropriate management strategies."	( Management of everolimus-associated adverse events in patients with tuberous sclerosis complex: a practical guide. Davies, M; Kingswood, JC; Saxena, A, 2017)	1.07
"This meta-analysis explores the relationship between the everolimus minimum (Cmin) and maximum (Cmax) exposure and the risk for pulmonary adverse events (AEs) in Japanese versus non-Japanese patients."	( Relationship between Pulmonary Adverse Events and Everolimus Exposure in Japanese and Non-Japanese Patients: A Meta-Analysis of Oncology Trials. Bouillaud, E; Fan, J; Gallo, J; Ito, T; Jerusalem, G; Noguchi, S; Nonomura, N; Ohno, N; Ohtsu, A; Ravaud, A; Shinohara, N, 2017)	0.95
" The commonly observed adverse events and laboratory abnormalities were stomatitis (49."	( Efficacy and safety of sequential use of everolimus in Japanese patients with advanced renal cell carcinoma after failure of first-line treatment with vascular endothelial growth factor receptor tyrosine kinase inhibitor: a multicenter phase II clinical t Akaza, H; Fujimoto, K; Hinotsu, S; Kimura, G; Kishida, T; Nozawa, M; Oyama, M; Ozono, S; Shimozuma, K; Sugiyama, T; Tokuda, N, 2017)	0.72
" In the everolimus arm of the Asian subset, the most common adverse events of any grade were stomatitis (62."	( Efficacy and safety of everolimus in combination with trastuzumab and paclitaxel in Asian patients with HER2+ advanced breast cancer in BOLERO-1. Feng, J; Hurvitz, S; Jiang, Z; Lee, KS; Liu, D; Ng, TY; Noel-Baron, F; Ridolfi, A; Ringeisen, F; Shao, Z; Shen, K; Toi, M; Tseng, LM; Wang, X; Xu, B; Zhang, Q, 2017)	1.2
"1%), and adverse events (AEs) (16."	( Everolimus Plus Exemestane in Advanced Breast Cancer: Safety Results of the BALLET Study on Patients Previously Treated Without and with Chemotherapy in the Metastatic Setting. Ascione, G; Barone, CA; Bighin, C; Bordonaro, R; Cazzaniga, ME; Cognetti, F; Foglietta, J; Frassoldati, A; Generali, D; Goffredo, F; Ionta, MT; Latini, L; Mafodda, A; Mariani, G; Michelotti, A; Minisini, AM; Molino, A; Montemurro, F; Nolè, F; Nuzzo, F; Piacentini, F; Piovano, P; Portera, G; Riccardi, F; Roila, F; Romito, S; Sartori, D; Schirone, A; Simoncini, EL; Testore, F; Vici, P, 2017)	1.9
" Thus, it is important to assess even the potential of cumulative and additive toxic effects among the drugs."	( Everolimus Plus Exemestane in Advanced Breast Cancer: Safety Results of the BALLET Study on Patients Previously Treated Without and with Chemotherapy in the Metastatic Setting. Ascione, G; Barone, CA; Bighin, C; Bordonaro, R; Cazzaniga, ME; Cognetti, F; Foglietta, J; Frassoldati, A; Generali, D; Goffredo, F; Ionta, MT; Latini, L; Mafodda, A; Mariani, G; Michelotti, A; Minisini, AM; Molino, A; Montemurro, F; Nolè, F; Nuzzo, F; Piacentini, F; Piovano, P; Portera, G; Riccardi, F; Roila, F; Romito, S; Sartori, D; Schirone, A; Simoncini, EL; Testore, F; Vici, P, 2017)	1.9
"Women with acute myocardial infarction (MI) undergoing mechanical reperfusion remain at increased risk of adverse cardiac events and mortality compared with their male counterparts."	( Long-term Safety and Efficacy of New-Generation Drug-Eluting Stents in Women With Acute Myocardial Infarction: From the Women in Innovation and Drug-Eluting Stents (WIN-DES) Collaboration. Baber, U; Camenzind, E; Chieffo, A; Dangas, GD; Faggioni, M; Farhan, S; Galatius, S; Giustino, G; Harari, R; Itchhaporia, D; Jeger, RV; Kandzari, D; Kastrati, A; Kim, HS; Kimura, T; Leon, MB; Mehran, R; Mehta, L; Morice, MC; Sartori, S; Serruys, PW; Sharma, M; Smits, PC; Sorrentino, S; Stefanini, GG; Steg, PG; Stone, GW; Valgimigli, M; Von Birgelen, C; Weisz, G; Wijns, W; Windecker, S, 2017)	0.46
" Grade 3-4 adverse events (AEs) were reported in 37."	( Efficacy and safety of Everolimus and Exemestane in hormone-receptor positive (HR+) human-epidermal-growth-factor negative (HER2-) advanced breast cancer patients: New insights beyond clinical trials. The EVA study. Airoldi, M; Arcangeli, V; Artale, S; Atzori, F; Ballerio, A; Bianchi, GV; Blasi, L; Campidoglio, S; Cazzaniga, ME; Ciccarese, M; Clivio, L; Cursano, MC; Fabi, A; Ferrari, L; Ferzi, A; Ficorella, C; Frassoldati, A; Fumagalli, A; Garrone, O; Gebbia, V; Generali, D; La Verde, N; Maur, M; Michelotti, A; Moretti, G; Musolino, A; Palumbo, R; Piezzo, M; Pistelli, M; Porpiglia, M; Sartori, D; Scavelli, C; Schirone, A; Torri, V; Turletti, A; Valerio, MR; Vici, P; Zambelli, A, 2017)	0.77
" The combination is safe and the best response could be obtained in patients receiving the full dose of EVE and/or after hormone-therapy as Fulvestrant in ABC."	( Efficacy and safety of Everolimus and Exemestane in hormone-receptor positive (HR+) human-epidermal-growth-factor negative (HER2-) advanced breast cancer patients: New insights beyond clinical trials. The EVA study. Airoldi, M; Arcangeli, V; Artale, S; Atzori, F; Ballerio, A; Bianchi, GV; Blasi, L; Campidoglio, S; Cazzaniga, ME; Ciccarese, M; Clivio, L; Cursano, MC; Fabi, A; Ferrari, L; Ferzi, A; Ficorella, C; Frassoldati, A; Fumagalli, A; Garrone, O; Gebbia, V; Generali, D; La Verde, N; Maur, M; Michelotti, A; Moretti, G; Musolino, A; Palumbo, R; Piezzo, M; Pistelli, M; Porpiglia, M; Sartori, D; Scavelli, C; Schirone, A; Torri, V; Turletti, A; Valerio, MR; Vici, P; Zambelli, A, 2017)	0.77
"A meta-analysis of randomized controlled trials (RCTs) was performed to examine the risk of everolimus discontinuation due to related and unrelated adverse events (AE) in cancer patients."	( Discontinuation of Everolimus Due to Related and Unrelated Adverse Events in Cancer Patients: A Meta-Analysis. Garcia, CA; Rogers, SC; Wu, S, 2017)	1
" The most common grade 1-2 adverse events with a suspected association with long-acting pasireotide monotherapy were diarrhoea (15 [37%] of 41), hyperglycaemia (17 [41%]), and weight loss (8 [20%]); those with a suspected association with everolimus monotherapy were stomatitis (26 [62%] of 42) and diarrhoea (16 [38%]); and those suspected to be associated with combination treatment were hyperglycaemia (27 [66%] of 41]), diarrhoea (19 [46%]), and asthenia (8 [20%])."	( Efficacy and safety of long-acting pasireotide or everolimus alone or in combination in patients with advanced carcinoids of the lung and thymus (LUNA): an open-label, multicentre, randomised, phase 2 trial. Baudin, E; Berruti, A; Brizzi, MP; Buikhuisen, W; Damiano, V; De Castro, J; Do Cao, C; Ferolla, P; Gislimberti, G; Grohé, C; Grønbæk, H; Léna, H; Lombard-Bohas, C; Mansoor, W; Mazieres, J; Meyer, T; Minotti, V; Öberg, K; Reed, N; Singh, N; Stankovic, M; Tiseo, M, 2017)	0.89
" The objectives of this analysis were to evaluate the safety profile of this combination in a subset of Spanish patients in the BALLET trial and to characterize grade 3 and 4 adverse events (AEs) in routine clinical practice in Spain."	( Safety of everolimus plus exemestane in patients with hormone-receptor-positive, HER2-negative locally advanced or metastatic breast cancer: results of phase IIIb BALLET trial in Spain. Beliera, A; Carabantes, F; Ciruelos, E; Fernández, Y; Fonseca, R; García-Sáenz, JA; Gavilá, J; Martínez de Dueñas, E; Martínez-Jáñez, N; Murillo, L; Vidal, M, 2018)	0.88
"PtCr-EES demonstrated comparable safety and effectiveness to CoCr-EES through 5 years of follow-up, with low rates of stent thrombosis and other adverse events."	( Long-Term Safety and Efficacy of Platinum Chromium Everolimus-Eluting Stents in Coronary Artery Disease: 5-Year Results From the PLATINUM Trial. Allocco, DJ; Bouchard, A; Carrié, D; Dawkins, KD; Dens, J; Dubois, CL; Farah, B; Feldman, RL; Hagiwara, N; Kelly, CR; Meredith, IT; Pompili, V; Rabinowitz, A; Saito, S; Stone, GW; Teirstein, PS, 2017)	0.71
" In addition, EVR plus low-dose CNI regimen could reduce the rate of cytomegalovirus and infection, whereas a lower rate of other adverse events were noted in MMF plus standard-dose CNI regimen."	( Efficacy and safety of everolimus plus low-dose calcineurin inhibitor vs. mycophenolate mofetil plus standard-dose calcineurin inhibitor in renal transplant recipients: A systematic review and meta-analysis . Deng, J; He, L; Jiang, W; Yang, B, 2018)	0.79
"Lesion length is a major predictor of adverse outcomes after percutaneous coronary intervention."	( Treatment with 48-mm everolimus-eluting stents : Procedural safety and 12-month patient outcome. Arshad, MKM; Ho, HH; Jafary, FH; Loh, JKK; Ong, PJL; Tan, CK; Tin, ZL; Watson, T, 2019)	0.83
"The Xience 48-mm EES device appears to be safe and efficacious with a low clinical event rate at the 12-month follow-up."	( Treatment with 48-mm everolimus-eluting stents : Procedural safety and 12-month patient outcome. Arshad, MKM; Ho, HH; Jafary, FH; Loh, JKK; Ong, PJL; Tan, CK; Tin, ZL; Watson, T, 2019)	0.83
" The most common all-grade adverse events(AEs)were stomatitis(82%) and non-infectious lung disease(27%)."	( [Efficacy and Safety of Everolimus plus Exemetane in Postmenopausal Endocrine-Responsive Metastatic Breast Cancer Patients]. Kubo, H; Maeda, N; Nagano, H; Nagashima, Y; Sakamoto, K; Sato, Y; Suzuki, N; Takeda, S; Yamamoto, S, 2017)	0.76
" Adverse events were noted in four patients: infection, stomatitis, and increased triglycerides."	( Efficacy and safety of everolimus in patients younger than 12 months with congenital subependymal giant cell astrocytoma. Ehara, E; Kawawaki, H; Kuki, I; Kunihiro, N; Matsusaka, Y; Okazaki, S; Yoshida, Y, 2018)	0.79
" This shift has markedly changed adverse event profiles, compared to cytotoxic chemotherapy, affecting a diverse range of organ systems."	( Everolimus is a new anti-cancer molecule: Metabolic side effects as lipid disorders and hyperglycemia. Baldelli, R; Di Giacinto, P; Lenzi, A; Morviducci, L; Nardone, MR; Ramponi, S; Rizza, L; Rota, F; Tubili, C; Zuppi, P, 2018)	1.92
" The most frequent grade 3/4 adverse events were stomatitis (8."	( Efficacy and safety of everolimus plus exemestane in postmenopausal women with hormone receptor-positive, human epidermal growth factor receptor 2-negative locally advanced or metastatic breast cancer: Results of the single-arm, phase IIIB 4EVER trial. Decker, T; Distelrath, A; Fasching, PA; Hadji, P; Janni, W; Kreuzeder, J; Kurbacher, CM; Lüftner, D; Lux, MP; Marmé, F; Mundhenke, C; Muth, M; Quiering, C; Schneeweiss, A; Stoetzer, O; Taran, FA; Tesch, H, 2019)	0.82
" Data collection included demographic and clinical information including reason(s) for initiating treatment with mTOR inhibitors, treatment duration, dosing, and corresponding serum trough levels, response to treatment, and adverse events (AE)."	( Short-term safety of mTOR inhibitors in infants and very young children with tuberous sclerosis complex (TSC): Multicentre clinical experience. Bruns, S; Capal, JK; Curatolo, P; de Vries, P; Devinsky, O; Ess, K; Franz, DN; Jansen, AC; Jozwiak, S; Koenig, MK; Krueger, DA; Lawson, J; Mowat, D; Narayanan, V; Ramos, F; Tzadok, M; Wong, M, 2018)	0.48
" Further studies are necessary to determine if the F-FDG PET/CT could early predict adverse effects of mTOR inhibitors."	( Everolimus-induced pulmonary toxicity: Findings on 18F-FDG PET/CT imaging. Bruna-Muraille, C; Dejust, S; Eymard, JC; Morland, D; Papathanassiou, D; Savoye, AM; Yazbek, G, 2018)	1.92
" Although lenvatinib is associated with favorable efficacy, it is associated with adverse events (AEs) that the clinician will have to closely monitor for and proactively manage."	( Managing the adverse events associated with lenvatinib therapy in radioiodine-refractory differentiated thyroid cancer. Cabanillas, ME; Takahashi, S, 2019)	0.51
"Within the safety population (everolimus 1014, MPA 1012), adverse events with a suspected relation to study drug occurred in 62."	( Safety of Everolimus With Reduced Calcineurin Inhibitor Exposure in De Novo Kidney Transplants: An Analysis From the Randomized TRANSFORM Study. Adel Bakr, M; Basic-Jukic, N; Bernhardt, P; Buchler, M; Cassuto, E; Chadban, S; Citterio, F; Cruzado, JM; Garcia, VD; Hernandez Gutierrez, MP; Kim, DY; Kuypers, D; Pascual, J; Russ, G; Sommerer, C; Soo Kim, M; Tedesco-Silva, H; Uyen, HD; Viklicky, O, 2019)	1.2
"De novo everolimus with reduced-exposure CNI yielded a comparable incidence, though a distinctly different pattern, of adverse events versus current standard of care."	( Safety of Everolimus With Reduced Calcineurin Inhibitor Exposure in De Novo Kidney Transplants: An Analysis From the Randomized TRANSFORM Study. Adel Bakr, M; Basic-Jukic, N; Bernhardt, P; Buchler, M; Cassuto, E; Chadban, S; Citterio, F; Cruzado, JM; Garcia, VD; Hernandez Gutierrez, MP; Kim, DY; Kuypers, D; Pascual, J; Russ, G; Sommerer, C; Soo Kim, M; Tedesco-Silva, H; Uyen, HD; Viklicky, O, 2019)	1.35
" Supraflex seems a safe and effective alternative drug-eluting stent to other stents in clinical practice."	( Safety and efficacy of a sirolimus-eluting coronary stent with ultra-thin strut for treatment of atherosclerotic lesions (TALENT): a prospective multicentre randomised controlled trial. Cequier, A; Chang, CC; Choudhury, A; Colombo, A; de Winter, RJ; Gil, RJ; Hofma, S; Hoye, A; Ijsselmuiden, S; Iniguez, A; Kaul, U; Kogame, N; Kukreja, N; Mathur, A; Merkely, B; Modolo, R; Moreno, R; Onuma, Y; Petrov, I; Prokopczuk, J; Serra, A; Serruys, PW; Smits, PC; Soliman, O; Spitzer, E; Tonev, G; Tonino, P; Ungi, I; Walsh, S; Zaman, A; Zurakowski, A, 2019)	0.51
"This retrospective multicenter study demonstrates that mTOR inhibitor treatment with everolimus is safe in TSC patients under the age of 2 years and shows beneficial effects on cardiac manifestations, SEGA size and early epilepsy."	( Safety and efficacy of mTOR inhibitor treatment in patients with tuberous sclerosis complex under 2 years of age - a multicenter retrospective study. Bernhard, MK; Brösse, I; Gorenflo, M; Hahn, A; Hethey, S; Hoffmann, GF; Kaiser, O; Kölker, S; Kreuzaler, P; Merkenschlager, A; Milde, T; Möckel, A; Roser, T; Saffari, A; Schlump, JU; Serfling, A; Spiegler, J; Syrbe, S; van Tilburg, CM; Wagner, R; Wiemer-Kruel, A; Wilken, B; Witt, O; Ziegler, A, 2019)	0.74
"Patients with diabetes mellitus are prone to increased adverse outcomes after percutaneous coronary intervention, even with contemporary drug-eluting stents."	( Efficacy and Safety of Ultrathin, Bioresorbable-Polymer Sirolimus-Eluting Stents Versus Thin, Durable-Polymer Everolimus-Eluting Stents for Coronary Revascularization of Patients With Diabetes Mellitus. Kandzari, D; Kolm, P; Koolen, JJ; Lipinski, MJ; Saito, S; Shlofmitz, E; Torguson, R; Waksman, R; Windecker, S, 2019)	0.73
" Through planned 4-year follow-up, the primary composite endpoint of major adverse cardiac events (MACE; death, myocardial infarction [MI] and target lesion revascularization) and rates of individual component endpoints and stent thrombosis were determined."	( Late-term safety and effectiveness of everolimus-eluting stents in chronic total coronary occlusion revascularization: Final 4-year results from the evaluation of the XIENCE coronary stent, Performance, and Technique in Chronic Total Occlusions (EXPERT CT Grantham, JA; Kandzari, DE; Karmpaliotis, D; Kini, AS; Lembo, NJ; Lombardi, W; McGreevy, R; Moses, JW; Nicholson, WJ; Orr, C; Popma, JJ; Tummala, PE; Wang, J; Zhao, W, 2019)	0.78
"A comprehensive survey of real-world adverse event reporting with conditions for approval under the Pharmaceuticals and Medical Devices Act identified 490 cases of ST with EES."	( Patient and lesion characteristics in late/very late stent thrombosis with everolimus-eluting stents from real-world adverse event reporting. Handa, N; Ho, M; Ishii, K; Koike, K; Konishi, A; Mitsutake, Y; Mochizuki, S, 2020)	0.79
" Data collection from adverse event reporting could be a helpful strategy for evaluation of this serious but rare complication."	( Patient and lesion characteristics in late/very late stent thrombosis with everolimus-eluting stents from real-world adverse event reporting. Handa, N; Ho, M; Ishii, K; Koike, K; Konishi, A; Mitsutake, Y; Mochizuki, S, 2020)	0.79
" The outcomes of interest were biopsy-proven acute rejection (BPAR), graft loss, death, renal function and adverse events."	( Efficacy and safety of everolimus treatment on liver transplant recipients: A meta-analysis. Chen, KB; Guan, TW; Lin, YJ; Ou, MY, 2019)	0.82
" The risk of any adverse event was increased by everolimus combined with reduced CNI therapy (RR = 1."	( Efficacy and safety of everolimus treatment on liver transplant recipients: A meta-analysis. Chen, KB; Guan, TW; Lin, YJ; Ou, MY, 2019)	1.08
" This regimen might be associated with an increased risk of adverse events, which needs to be elucidated further."	( Efficacy and safety of everolimus treatment on liver transplant recipients: A meta-analysis. Chen, KB; Guan, TW; Lin, YJ; Ou, MY, 2019)	0.82
" Fifteen patients in the sunitinib group and 13 in the pazopanib group experienced adverse events."	( A Phase 4 Study of Everolimus to Evaluate Efficacy and Safety in Patients with Metastatic Renal-Cell Carcinoma after Failure of First-Line Sunitinib or Pazopanib (SUNPAZ). de Geeter, P; Decker, T; Quiering, C; Resch, A; Schmitz, S; Schostak, M, 2020)	0.89
" Therefore, we aimed to evaluate long-term adverse events in HBR patients undergoing percutaneous coronary intervention with cobalt-chromium everolimus-eluting stent implantation."	( Long-Term Safety and Efficacy of Durable Polymer Cobalt-Chromium Everolimus-Eluting Stents in Patients at High Bleeding Risk: A Patient-Level Stratified Analysis From Four Postapproval Studies. Angiolillo, DJ; Baber, U; Bangalore, S; Bhatt, DL; Chandiramani, R; Claessen, BE; Ge, J; Guedeney, P; Hermiller, J; Kozuma, K; Krucoff, M; Liu, Y; Makkar, R; Mehran, R; Neumann, FJ; Rau, V; Saito, S; Seth, A; Sorrentino, S; Valgimigli, M; Vogel, B; Wang, J, 2020)	1
"Everolimus is administered to patients with metastatic renal cell carcinoma in full daily dose of 10 mg or in reduced daily dose of 5 mg in case adverse effect occurred."	( Management of metabolic adverse effects of everolimus in patients with renal carcinoma. Gregorová, J; Holečková, P; Žáková, K, 2019)	2.22
"The combination of everolimus and buparlisib is safe and well-tolerated at the RP2D of 5 and 60 mg on a continuous daily schedule."	( A Phase I Study of Safety, Pharmacokinetics, and Pharmacodynamics of Concurrent Everolimus and Buparlisib Treatment in Advanced Solid Tumors. Akce, M; Alese, OB; Bilen, MA; Carthon, B; Chen, Z; Collins, H; El-Rayes, BF; Harris, WB; Harvey, RD; Khuri, FR; Kudchagkar, RR; Lawson, DH; Lewis, C; Lonial, S; Owonikoko, TK; Ramalingam, SS; Shaib, WL; Sica, GL; Steuer, CE; Wu, C; Zhang, C, 2020)	1.11
"2%) adverse events (AEs)."	( Efficacy and safety of everolimus plus exemestane in patients with HR+, HER2- advanced breast cancer progressing on/after prior endocrine therapy in routine clinical practice: Primary results from the non-interventional study, STEPAUT. Bartsch, R; Egle, D; Gnant, M; Greil, R; Haslbauer, F; Helfgott, R; Hennebelle, M; Hock, K; Hubalek, M; Lang, A; Marth, C; Mraz, B; Öhler, L; Petru, E; Pfeiler, G; Redl, A; Steger, GG; Tinchon, C, 2020)	0.87
" Aims of this study were to evaluate the progression of renal dysfunction after discontinuation of CNIs and to monitor for major adverse events after therapy change."	( Long-Term Effects of the Replacement of Calcineurin Inhibitors With Everolimus and Mycophenolate in Patients With Calcineurin Inhibitor-Related Nephrotoxicity. Acquaro, M; Cattadori, B; D'Armini, AM; Ghio, S; Greco, A; Guida, S; Klersy, C; Pelenghi, S; Pellegrini, C; Raineri, C; Scelsi, L; Turco, A; Visconti, LO, 2020)	0.79
" Adverse events and changes in lipid panel profile, pulmonary function tests, and VEGF-D were assessed."	( A phase II clinical trial of the Safety Of Simvastatin (SOS) in patients with pulmonary lymphangioleiomyomatosis and with tuberous sclerosis complex. Courtwright, AM; Dorgan, D; Fleck, V; Kotloff, R; Kreider, M; Krymskaya, VP; McCormack, FX, 2020)	0.56
" The most common adverse events were peripheral edema (30%), cough (30%), and diarrhea (30%)."	( A phase II clinical trial of the Safety Of Simvastatin (SOS) in patients with pulmonary lymphangioleiomyomatosis and with tuberous sclerosis complex. Courtwright, AM; Dorgan, D; Fleck, V; Kotloff, R; Kreider, M; Krymskaya, VP; McCormack, FX, 2020)	0.56
"The combination of simvastatin with mTORi in LAM patients is safe and well-tolerated from an adverse events perspective."	( A phase II clinical trial of the Safety Of Simvastatin (SOS) in patients with pulmonary lymphangioleiomyomatosis and with tuberous sclerosis complex. Courtwright, AM; Dorgan, D; Fleck, V; Kotloff, R; Kreider, M; Krymskaya, VP; McCormack, FX, 2020)	0.56
" The objectives of this analysis were to provide additional information on the safety profile of this schedule depending on prior anticancer therapies and to characterize the time course of adverse events (AEs) and serious AEs (SAEs) of clinical interest throughout the study period."	( Everolimus plus exemestane in hormone-receptor-positive, HER2-negative locally advanced or metastatic breast cancer: incidence and time course of adverse events in the phase IIIb BALLET population. Ciruelos, E; Conte, P; Gavila, J; Generali, D; Jerusalem, G; Lang, I; Martin, M; Martínez-Serrano, MJ; Montemurro, F; Neven, P; Perelló, MF; Tjan-Heijnen, VCG, 2020)	2
" Lipid metabolism disorder was the most common adverse event (69."	( Safety and efficacy of sirolimus combined with endocrine therapy in patients with advanced hormone receptor-positive breast cancer and the exploration of biomarkers. Guan, X; Li, C; Li, H; Li, L; Liu, B; Ma, F; Qian, H; Rong, G; Sun, X; Wang, W; Xu, B; Yi, Z; Zhai, J, 2020)	0.56
" In 21 patients, EVR dose, trough level, outcomes, and adverse effects were assessed."	( Safety and Efficacy of Everolimus Rescue Treatment After Pediatric Living Donor Liver Transplantation. Bessho, K; Deguchi, K; Kodama, T; Noguchi, Y; Nomura, M; Okuyama, H; Saka, R; Tazuke, Y; Ueno, T; Watanabe, M, )	0.44
"In this single-center, prospective, randomized study, adverse events (AEs), serious AEs (SAEs), viral infections, laboratory abnormalities, dose reductions, and temporary or permanent discontinuation of the immunosuppressant were compared among patients receiving r-ATG/EVR (n = 85), BAS/EVR (n = 102), and BAS/MPS (n = 101)."	( Immunosuppressive Drug-Associated Adverse Event Profiles in De Novo Kidney Transplant Recipients Receiving Everolimus and Reduced Tacrolimus Doses. Felipe, CR; Medina Pestana, JO; Miranda, TA; Santos, RHN; Tedesco-Silva Junior, H, 2020)	0.77
" Common (>5%) grade ≥3 adverse events included rash (19%), neutropenia (19%), hypokalaemia (11%) and fatigue (9%)."	( Phase 1 safety and pharmacodynamic study of lenalidomide combined with everolimus in patients with advanced solid malignancies with efficacy signal in adenoid cystic carcinoma. Alese, OB; Bilen, MA; Carthon, BC; Chen, Z; El-Rayes, BF; Harris, WB; Harvey, RD; Hossain, MS; Khuri, FR; Lawson, DH; Lewis, C; Lonial, S; Owonikoko, TK; Ramalingam, SS; Shaib, W; Steuer, CE; Waller, EK; Wu, C; Zhang, C, 2020)	0.79
"Results of this IPD analysis suggest that the BP-SES with ultrathin struts is as safe as and more efficacious than DP-EES in the overall cohort and especially in small vessels."	( Individual patient data analysis of the BIOFLOW study program comparing safety and efficacy of a bioresorbable polymer sirolimus eluting stent to a durable polymer everolimus eluting stent. Kandzari, DE; Koolen, J; Lefèvre, T; Richardt, G; Saito, S; Slagboom, T; Toelg, R; Waltenberger, J, 2021)	0.82
" The treatment effects and adverse events were compared between the two groups."	( Efficacy and safety of low-dose everolimus treatment for renal angiomyolipoma associated with tuberous sclerosis complex. Endo, K; Hatano, T; Tamari, M, 2021)	0.9
"The present study demonstrates that low-dose everolimus treatment is safe and effective for TSC-associated AML."	( Efficacy and safety of low-dose everolimus treatment for renal angiomyolipoma associated with tuberous sclerosis complex. Endo, K; Hatano, T; Tamari, M, 2021)	1.16
" Primary endpoint was occurrence of any major adverse cardiac event (MACE) up to 12 months' follow-up."	( Safety and performance of everolimus-eluting stents comprising of biodegradable polymers with ultrathin stent platforms. Bolinera, SV; Byrapaneni, S; Chilukuri, M; Gangasani, S; Pamidimukkala, V; Polavarapu, A; Polavarapu, N; Polavarapu, RS; Reddy, SS; Tharaknath, VR, 2020)	0.86
"Conversion to an EVL-based therapy after pediatric HTX is a safe immunosuppressive regime without increasing risk of acute rejection or CMV-infection."	( Conversion to everolimus in pediatric heart transplant recipients is a safe treatment option with an impact on cardiac allograft vasculopathy and renal function. Dalla Pozza, R; Fernandez Rodriguez, S; Fischer, M; Grimm, K; Haas, NA; Jakob, A; Kozlik-Feldmann, R; Lehner, A; Orban, M; Rosenthal, LL; Ulrich, SM, 2021)	0.98
"There are limited real-world data available regarding adverse events (AEs) of immunosuppressants."	( Mtor inhibitors associated with higher cardiovascular adverse events-A large population database analysis. Abagyan, R; Nguyen, VN; Tsunoda, SM, 2021)	0.62
" Absence of complications such as bleeding or glomerular filtration rate decline in the long term, with a favorable safety profile, without interruptions and with mild-moderate, non-cumulative adverse effects, mostly within the first year of treatment."	( Renal angiomyolipoma and tuberous sclerosis complex: long-term safety and efficacy outcomes of Everolimus therapy. Álvarez-Ossorio Fernández, JL; Ledo Cepero, MJ; Ojeda Claro, AV; Ruiz Guerrero, E; Soto Delgado, M, 2021)	0.84
"Everolimus is a safe and effective therapeutic option for renal angiomyolipoma and various manifestations of TSC, which has been reproduced in real life with six years of follow-up."	( Renal angiomyolipoma and tuberous sclerosis complex: long-term safety and efficacy outcomes of Everolimus therapy. Álvarez-Ossorio Fernández, JL; Ledo Cepero, MJ; Ojeda Claro, AV; Ruiz Guerrero, E; Soto Delgado, M, 2021)	2.28
" VAN + EV combination is safe and active in refractory solid tumors."	( Safety and activity of vandetanib in combination with everolimus in patients with advanced solid tumors: a phase I study. Amini, B; Bhatt, T; Cascone, T; Conley, AP; Drobnitzky, N; Falchook, GS; Fu, S; Hess, KR; Heymach, JV; Hong, DS; Janku, F; Karp, D; Meric-Bernstam, F; Naing, A; Piha-Paul, SA; Ryan, AJ; Sacks, RL; Sherman, SI; Subbiah, IM; Subbiah, V, 2021)	0.87
" A landmark progression-free survival (PFS) analysis by central review was performed for patients treated for at least 16 weeks (n = 308) and according to the occurrence of any-grade adverse events (AEs) within this treatment period."	( Relationship between metabolic toxicity and efficacy of everolimus in patients with neuroendocrine tumors: A pooled analysis from the randomized, phase 3 RADIANT-3 and RADIANT-4 trials. Buzzoni, R; Carnaghi, C; Fazio, N; Herbst, F; Kulke, MH; Pavel, ME; Ridolfi, A; Strosberg, J; Valle, JW; Yao, JC, 2021)	0.87
" Additionally, neutropenia, diarrhoea and fatigue were the most common adverse events caused by these drugs, followed by pain, nausea, decreased appetite, anaemia and vomiting."	( Efficacy and safety of targeted drugs in advanced or metastatic gastric and gastroesophageal junction cancer: A network meta-analysis. Ge, L; Gong, H; Hou, L; Jin, X; Leng, G; Li, C; Li, T; Liu, Y; Ma, L; Niu, S; Su, Y; Zhang, H; Zhang, L; Zhao, L, 2022)	0.72
"In the TWILIGHT trial, ticagrelor monotherapy after a short course of dual antiplatelet therapy (DAPT) was shown to be a safe bleeding avoidance strategy in high-risk patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stents (DES)."	( Safety and efficacy of ticagrelor monotherapy according to drug-eluting stent type: the TWILIGHT-STENT study. Angiolillo, DJ; Baber, U; Briguori, C; Camaj, A; Cao, D; Cohen, D; Collier, T; Dangas, G; Dudek, D; Escaned, J; Gibson, CM; Gil, R; Giustino, G; Goel, R; Han, YL; Huber, K; Kastrati, A; Kaul, U; Kornowski, R; Krucoff, MW; Kunadian, V; Mehran, R; Mehta, S; Moliterno, DJ; Nicolas, J; Ohman, EM; Oldroyd, KG; Pocock, S; Sardella, G; Sartori, S; Sharma, S; Shlofmitz, R; Steg, PG; Weisz, G; Witzenbichler, B; Zhang, Z, 2022)	0.72
" Patients in the 14-mg arm were to be uptitrated to lenvatinib 18 mg at cycle 2, day 1, barring intolerable grade 2 or any grade ≥3 treatment-emergent adverse events (TEAEs) requiring dose reduction occurring in the first 28-d cycle."	( Assessing the Safety and Efficacy of Two Starting Doses of Lenvatinib Plus Everolimus in Patients with Renal Cell Carcinoma: A Randomized Phase 2 Trial. Alekseev, B; Binder, TA; Castellano, D; Ciuleanu, T; Glen, H; Heng, DYC; Koralewski, P; Lee, JL; O'Hara, K; Pal, SK; Parnis, F; Peng, L; Puente, J; Rha, SY; Smith, AD; Stroyakovskiy, D; Sunela, K, 2022)	0.95
"As for adverse events (AEs) caused by everolimus, findings from clinical trials and post-marketing surveillance have reported interstitial lung disease, hyperglycaemia, cardiovascular disease, etc."	( Comprehensive analysis of everolimus-induced adverse events using the Japanese real-world database. Fujiwara, M; Nakano, K; Shimizu, T; Uchida, M; Uesawa, Y, 2022)	1.29
"Data reported between April 2004 and June 2021 in the Japanese Adverse Drug Event Report database were extracted for use."	( Comprehensive analysis of everolimus-induced adverse events using the Japanese real-world database. Fujiwara, M; Nakano, K; Shimizu, T; Uchida, M; Uesawa, Y, 2022)	1.02
"Among the top 30 adverse events, 23 adverse event signals were detected and classified into seven categories: lung-related AEs, haematological-related AEs, cancer progression, blood glucose-related AEs, hepatic-related AEs, renal-related AEs and others."	( Comprehensive analysis of everolimus-induced adverse events using the Japanese real-world database. Fujiwara, M; Nakano, K; Shimizu, T; Uchida, M; Uesawa, Y, 2022)	1.02
"A comprehensive survey of adverse events associated with everolimus administration using the pharmacovigilance database revealed that pulmonary and haematological AEs are frequently reported."	( Comprehensive analysis of everolimus-induced adverse events using the Japanese real-world database. Fujiwara, M; Nakano, K; Shimizu, T; Uchida, M; Uesawa, Y, 2022)	1.27
" The Absorb everolimus-eluting BVS was safe and showed the favorable clinical outcomes in both patency and TLR, especially in infrapopliteal disease with heavy calcification."	( Efficacy and Safety of Absorb Everolimus-Eluting Bioresorbable Vascular Scaffold in Peripheral Artery Disease: A Single-Arm Meta-Analysis. Fan, W; Feng, B; Li, L; Pei, J; Shi, W; Tan, J; Yu, B; Yuan, G, 2023)	1.58
"The 48mm-EES is safe and effective to treat long coronary lesions, including CTOs, and provides attractive cost-effectiveness by limiting multiple stenting."	( Safety and efficacy of 48 mm Xience Xpedition everolimus-eluting stent for the treatment of long coronary lesions. Arroyo, D; Benamer, H; Champagne, S; Chevalier, B; Garot, P; Gautier, A; Hovasse, T; Lefèvre, T; Neylon, A; Sanguineti, F; Unterseeh, T, 2022)	0.98
" The mainstay of treatment is with multiple anti-seizure medications (ASMs); however, the ASMs themselves can be associated with psychobehavioural adverse events, and effects (negative or positive) on cognition and sleep."	( Psychobehavioural and Cognitive Adverse Events of Anti-Seizure Medications for the Treatment of Developmental and Epileptic Encephalopathies. Schubert-Bast, S; Strzelczyk, A, 2022)	0.72
" For grade ≥ 3 adverse events (AEs), compared with placebo, lenvatinib plus everolimus showed worse safety than all other treatments except for lenvatinib (placebo vs."	( Optimizing targeted drug selection in combination therapy for patients with advanced or metastatic renal cell carcinoma: A systematic review and network meta-analysis of safety. Bi, X; Cao, C; Jiang, W; Shang, B; Shi, H; Shou, J; Wu, J; Xie, R; Zhou, A, 2023)	1.14
"4%) grade 3 or higher treatment-related adverse events occurred in the combination group, vorolanib group and everolimus group, respectively."	( Efficacy and safety of vorolanib plus everolimus in metastatic renal cell carcinoma: A three-arm, randomised, double-blind, multicentre phase III study (CONCEPT). Chen, K; Chen, P; Ding, L; Fu, C; Guo, H; Guo, J; He, C; He, Z; Hu, Z; Ji, Z; Jiang, K; Li, G; Li, X; Liu, B; Liu, Y; Liu, Z; Luo, H; Qin, S; Sheng, X; Shi, B; Tu, X; Wang, G; Wang, L; Wang, Y; Wang, Z; Wei, Q; Wu, B; Wu, D; Yao, X; Ye, D; Yuan, X; Zhang, D; Zhang, Y; Zhao, Y; Zhou, A; Zhou, F; Zou, Q, 2023)	1.39
"Literature is limited comparing adverse effects (AEs) of the proliferation signal inhibitors (PSIs) sirolimus (SRL) and everolimus (EVL) in pediatric heart transplant (HTx) recipients."	( Assessment of the adverse effects of sirolimus versus everolimus in pediatric heart transplant recipients. Ahmed, H; Albers, EL; Friedland-Little, JM; Hong, BJ; Kemna, MS; Law, YM; Newland, DM; Rosete, BE; Spencer, KL, 2023)	1.37
" In patients with PD-L1+ve and -ve ccRCC, niv, atezolizumab, ipi, and pembrolizumab were safe and effective alone and when combined with cabozantinib, tivozanib, axitinib, levantinib, and pegilodecakin."	( Efficacy and Safety of Checkpoint Inhibitors in Clear Cell Renal Cell Carcinoma: A Systematic Review of Clinical Trials. Aiman, W; Ali, MA; Butt, SK; Farrukh, M; Fatima, A; Garg, I; Habib, R; Kashif, T; Khan, H; Naveed, M; Niaz, R; Saeed, M; Zubair, H, 2023)	0.91
" To determine the safety and efficacy of MTKI therapy in children, adolescents and young adults (AYAs), we conducted a retrospective study on adverse events and treatment outcomes."	( Safety and efficacy of multiple tyrosine kinase inhibitors in pediatric/adolescent and young adult patients with relapsed or refractory osteosarcomas: A single-institution retrospective analysis. Arakawa, A; Iwata, S; Kawai, A; Kobayashi, E; Kumamoto, T; Maniwa, J; Nakajima, M; Ogawa, C; Shirakawa, N; Sugiyama, M; Tanimura, K; Tao, K; Watanabe, Y; Yoneda, A, 2023)	0.91
" The incidence of treatment-related grade 3 nonhematological adverse events was 14."	( Safety and efficacy of multiple tyrosine kinase inhibitors in pediatric/adolescent and young adult patients with relapsed or refractory osteosarcomas: A single-institution retrospective analysis. Arakawa, A; Iwata, S; Kawai, A; Kobayashi, E; Kumamoto, T; Maniwa, J; Nakajima, M; Ogawa, C; Shirakawa, N; Sugiyama, M; Tanimura, K; Tao, K; Watanabe, Y; Yoneda, A, 2023)	0.91
" MTKI therapies, particularly regorafenib, against pediatric relapsed osteosarcoma can suppress tumor growth and prolong PFS with tolerable adverse events."	( Safety and efficacy of multiple tyrosine kinase inhibitors in pediatric/adolescent and young adult patients with relapsed or refractory osteosarcomas: A single-institution retrospective analysis. Arakawa, A; Iwata, S; Kawai, A; Kobayashi, E; Kumamoto, T; Maniwa, J; Nakajima, M; Ogawa, C; Shirakawa, N; Sugiyama, M; Tanimura, K; Tao, K; Watanabe, Y; Yoneda, A, 2023)	0.91
" While this finding is limited by the sample size and warrants prospective verification, initiating therapy at a reduced dose might be practicable and safe in a distinct subset of patients."	( Does the dose matter? Antiproliferative efficacy and toxicity of everolimus in patients with neuroendocrine tumors - Experiences from a tertiary referral center. Haug, A; Kiesewetter, B; Kretschmer-Chott, E; Macheiner, S; Mazal, P; Melhorn, P; Raderer, M; Wolff, L, 2023)	1.15
"The randomised double-blinded placebo-controlled EXIST-1-3 studies have showed everolimus effective with adverse effects reported as acceptable in treatment of symptoms in patients with tuberous sclerosis complex (TSC), although evidence of outcomes in clinical practice remains limited."	( Effectiveness and safety of everolimus treatment in patients with tuberous sclerosis complex in real-world clinical practice. Christensen, J; Cockerell, I; Grenaa Frederiksen, M; Heimdal, K; Hoei-Hansen, CE; Holst, L; Issa-Epe, AI; Johannessen Landmark, C; Lund, C; Nedregaard, B; Nærland, T; Solhoff, R, 2023)	1.43
" Adverse effects were reported in 61 of 64 patients (95%) after a median treatment duration of 31 months (range 0-106), with oral ulceration/stomatitis (63%) and upper respiratory tract infections (38%) being the most common."	( Effectiveness and safety of everolimus treatment in patients with tuberous sclerosis complex in real-world clinical practice. Christensen, J; Cockerell, I; Grenaa Frederiksen, M; Heimdal, K; Hoei-Hansen, CE; Holst, L; Issa-Epe, AI; Johannessen Landmark, C; Lund, C; Nedregaard, B; Nærland, T; Solhoff, R, 2023)	1.2
" Close follow-up is needed for this group, especially for children and patients who may not be able to report adverse effects."	( Effectiveness and safety of everolimus treatment in patients with tuberous sclerosis complex in real-world clinical practice. Christensen, J; Cockerell, I; Grenaa Frederiksen, M; Heimdal, K; Hoei-Hansen, CE; Holst, L; Issa-Epe, AI; Johannessen Landmark, C; Lund, C; Nedregaard, B; Nærland, T; Solhoff, R, 2023)	1.2

Excerpt	Reference	Relevance
" On both study days Cmax, and tmax of cyclosporin were not significantly different."	( Pharmacokinetics of SDZ RAD and cyclosporin including their metabolites in seven kidney graft patients after the first dose of SDZ RAD. Blick, S; Franzke, A; Jacobsen, W; Kirchner, GI; Manns, MP; Mueller, L; Sewing, KF; Vidal, C; Wagner, S; Winkler, M, 2000)	0.31
" The interindividual pharmacokinetic variability for AUC was 85."	( Longitudinal assessment of everolimus in de novo renal transplant recipients over the first post-transplant year: pharmacokinetics, exposure-response relationships, and influence on cyclosporine. Boger, R; Cambon, N; Gerbeau, C; Kahan, BD; Kaplan, B; Kovarik, JM; Lorber, M; Rordorf, C; Rouilly, M; Winkler, M, 2001)	0.61
" Recipients with bile diversion demonstrated lower peak concentration (Cmax) than those without, but overall drug exposure (AUC) was not altered."	( Pharmacokinetics and tolerability of 40-0-[2-hydroxyethyl]rapamycin in de novo liver transplant recipients. Campestrini, J; Grant, D; Kovarik, JM; Levy, GA; Paradis, K; Smith, T, 2001)	0.31
" h/ml) and 84% prolonged half-life (79 +/- 42 versus 43 +/- 18 hours) in subjects with hepatic impairment."	( Influence of hepatic impairment on everolimus pharmacokinetics: implications for dose adjustment. Dilzer, SC; Figueiredo, J; Kovarik, JM; Lasseter, K; Reynolds, C; Rordorf, C; Sabia, HD; Zimmermann, H, 2001)	0.59
"The authors assessed the mutual influence of the immunosuppressant everolimus (Certican) and the HMG-CoA reductase inhibitors atorvastatin and pravastatin when coadministered based on pharmacokinetic and pharmacodynamic measures."	( Pharmacokinetic and pharmacodynamic assessments of HMG-CoA reductase inhibitors when coadministered with everolimus. Berthier, S; Hartmann, S; Hubert, M; Kovarik, JM; Rordorf, C; Rosenkranz, B; Schneider, W, 2002)	0.76
" Compared with adults from a previous study, apparent clearance (L/h) and distribution volume (L) were lower in pediatric patients, whereas the elimination half-life was similar."	( Single-dose pharmacokinetics and tolerability of everolimus in stable pediatric renal transplant patients. Boger, R; Cambon, N; Ettenger, R; Hoyer, PF; Kovarik, JM; Lemire, J; Mahan, J; McMahon, L; Van Damme-Lombaerts, R; Webb, NA, 2002)	0.57
" Everolimus half-life was reduced significantly, from an average of 32 hours to 24 hours."	( Effect of rifampin on apparent clearance of everolimus. Figueiredo, J; Hartmann, S; Kovarik, JM; Port, A; Rordorf, C; Rouilly, M, 2002)	1.49
" Cmax and AUC were evaluated by standard bioequivalence testing to determine relative bioavailability and to quantify the effect of food."	( Clinical development of an everolimus pediatric formulation: relative bioavailability, food effect, and steady-state pharmacokinetics. Berthier, S; Ettenger, R; Hoyer, PF; Kovarik, JM; Langholff, WK; Marion, AS; McMahon, L; Noe, A; Rordorf, C, 2003)	0.62
" Pharmacokinetic data consisted of 4014 everolimus trough concentrations (Cmin) obtained in all patients and 659 area under the concentration-time curve (AUC) -profiles obtained at months 2, 3, and 6 in a subset of 261 patients."	( Pharmacokinetics of an everolimus-cyclosporine immunosuppressive regimen over the first 6 months after kidney transplantation. Berthier, S; Dantal, J; Hsu, CH; Kahan, BD; Kaplan, B; Kovarik, JM; McMahon, L; Rordorf, C; Silva, HT, 2003)	0.9
" We used median-effect analysis to characterize exposure-response associations between everolimus average Cmin vs freedom from biopsy-confirmed acute rejection; maximum cholesterol, low density lipoprotein, triglyceride, and creatinine levels; and minimum leukocyte and platelet counts."	( Everolimus in de novo cardiac transplantation: pharmacokinetics, therapeutic range, and influence on cyclosporine exposure. Dorent, R; Eisen, H; Hsu, CH; Kovarik, JM; Mancini, D; Rordorf, C; Rouilly, M; Vigano, M, 2003)	1.98
" Everolimus Cmin averaged 9-11 ng/mL in the immediate cyclosporine group over the first 3 months."	( Influence of delayed initiation of cyclosporine on everolimus pharmacokinetics in de novo renal transplant patients. Bettoni-Ristic, O; Civati, G; Dantal, J; Kovarik, JM; Rizzo, G; Rordorf, C; Rouilly, M, 2003)	1.48
" Everolimus, which has greater polarity than sirolimus, was developed in an attempt to improve the pharmacokinetic characteristics of sirolimus, particularly to increase its oral bioavailability."	( Clinical pharmacokinetics of everolimus. Kirchner, GI; Manns, MP; Meier-Wiedenbach, I, 2004)	1.52
" The secondary objective was to assess the pharmacokinetic profile of two different formulations (capsule and tablet) of everolimus."	( Tolerability and steady-state pharmacokinetics of everolimus in maintenance renal transplant patients. Budde, K; Dantal, J; Fauchald, P; Fritsche, L; Hauser, IA; Lehne, G; Lison, A; Neumayer, HH; Soulillou, JP; Winkler, M, 2004)	0.78
" Pharmacodynamic assessment showed a relationship between drug exposure and thrombocytopenia."	( Tolerability and steady-state pharmacokinetics of everolimus in maintenance renal transplant patients. Budde, K; Dantal, J; Fauchald, P; Fritsche, L; Hauser, IA; Lehne, G; Lison, A; Neumayer, HH; Soulillou, JP; Winkler, M, 2004)	0.58
" The role of immunosuppressants in post-transplant outcome is crucial, and associations between exposure-related pharmacokinetic parameters and clinical outcome have been made for several drugs in this class."	( Pharmacokinetics of immunosuppressants: a perspective on ethnic differences. Dirks, NL; Huth, B; Meibohm, B; Yates, CR, 2004)	0.32
" The objective of this randomized, double-blind, placebo-controlled, dose-escalating Phase 1 study was to evaluate the pharmacokinetic profile of different dosing regimens of everolimus."	( Pharmacokinetics of the immunosuppressant everolimus in maintenance renal transplant patients. Budde, K; Fritsche, L; Glander, P; Neumayer, HH; Slowinski, T; Waiser, J, 2005)	0.79
" Everolimus half-life was only prolonged to a minor extent (32 +/- 6 vs."	( Pharmacokinetic interaction between verapamil and everolimus in healthy subjects. Allison, MJ; Beyer, D; Bizot, MN; Jiang, Q; Kovarik, JM; Schmouder, RL, 2005)	1.49
"When CsA pharmacokinetic profiles were considered, the CsA dose requirement was not lower in Chinese patients receiving everolimus than that in patients receiving azathioprine."	( Influence of everolimus on cyclosporine Neoral pharmacokinetics in Chinese de novo cardiac transplant recipients. Chi, NH; Chou, NK; Hsu, RB; Ko, WJ; Tsao, CI; Wang, CH; Wang, SS; Wu, FL, 2006)	0.91
"2 ng/mL, Cmax 10."	( Differential pharmacokinetic interaction of tacrolimus and cyclosporine on everolimus. Curtis, JJ; Hricik, DE; Kovarik, JM; Pescovitz, MD; Scantlebury, V; Vasquez, A, 2006)	0.56
" The aim of this work was to characterize the disposition kinetics of everolimus in rats by physiologically based pharmacokinetic (PBPK) modeling."	( Physiologically based pharmacokinetic (PBPK) modeling of everolimus (RAD001) in rats involving non-linear tissue uptake. Kawai, R; Laplanche, R; Meno-Tetang, GM, 2007)	0.82
"To use preclinical and clinical pharmacokinetic (PK)/pharmacodynamic (PD) modeling to predict optimal clinical regimens of everolimus, a novel oral mammalian target of rapamycin (mTOR) inhibitor, to carry forward to expanded phase I with tumor biopsy studies in cancer patients."	( Identifying optimal biologic doses of everolimus (RAD001) in patients with cancer based on the modeling of preclinical and clinical pharmacokinetic and pharmacodynamic data. Boulay, A; Hattenberger, M; Hazell, K; Judson, I; Kovarik, JM; Lane, HA; O'Reilly, T; Raymond, E; Shand, N; Stephan, C; Tanaka, C; Thomas, G; Zumstein-Mecker, S, 2008)	0.82
" In order to identify a rationally based dose and schedule for cancer treatment, we have conducted a tumor pharmacodynamic phase I study in patients with advanced solid tumors."	( Dose- and schedule-dependent inhibition of the mammalian target of rapamycin pathway with everolimus: a phase I tumor pharmacodynamic study in patients with advanced solid tumors. Baselga, J; Burris, H; Calvo, E; Dimitrijevic, S; Hazell, K; Jones, S; Judson, I; Lane, HA; Lebwohl, D; Macarulla, T; Martinelli, E; Ramon y Cajal, S; Ramos, FJ; Rojo, F; Shand, N; Stumm, M; Tabernero, J; Tang, P; Vidal, L; Zoellner, U, 2008)	0.57
"We performed a dose-escalation study in advanced cancer patients administering oral everolimus 5 to 30 mg/wk, with pharmacokinetic (PK) and pharmacodynamic (PD) studies."	( Phase I pharmacokinetic and pharmacodynamic study of the oral mammalian target of rapamycin inhibitor everolimus in patients with advanced solid tumors. Brock, C; Burris, HA; Faivre, S; Hazell, K; Jones, S; Judson, I; Kovarik, JM; Lane, HA; O'Donnell, A; Papadimitrakopoulou, V; Raymond, E; Rea, D; Shand, N; Zoellner, U, 2008)	0.79
" Terminal half-life was 30 hours (range, 26 to 38 hours)."	( Phase I pharmacokinetic and pharmacodynamic study of the oral mammalian target of rapamycin inhibitor everolimus in patients with advanced solid tumors. Brock, C; Burris, HA; Faivre, S; Hazell, K; Jones, S; Judson, I; Kovarik, JM; Lane, HA; O'Donnell, A; Papadimitrakopoulou, V; Raymond, E; Rea, D; Shand, N; Zoellner, U, 2008)	0.56
"This article summarizes this analysis, with special focus on the pharmacokinetic characteristics of everolimus and on the results of its use in renal transplantation."	( Everolimus: an update on the mechanism of action, pharmacokinetics and recent clinical trials. Sánchez-Fructuoso, AI, 2008)	2
"To describe the management of a pharmacokinetic interaction between azole antifungals (fluconazole and voriconazole) and everolimus in a patient who underwent an orthotopic liver transplant."	( Pharmacokinetic interaction between everolimus and antifungal triazoles in a liver transplant patient. Adani, GL; Baccarani, U; Baraldo, M; Cojutti, P; Franceschi, L; Furlanut, M; Londero, A; Pea, F; Tavio, M; Viale, P, 2008)	0.83
" This study assessed the safety and the pharmacokinetic interactions of everolimus and paclitaxel in patients with advanced malignancies."	( Safety and pharmacokinetics of paclitaxel and the oral mTOR inhibitor everolimus in advanced solid tumours. Berton Rigaud, D; Bootle, D; Bourbouloux, E; Calvo, F; Campone, M; Dutreix, C; Levy, V; Raymond, E; Shand, N; Zoellner, U, 2009)	0.82
"Treatment of Japanese cancer patients with RAD001 may be undertaken with the expectation that previously determined pharmacokinetic and safety profiles apply."	( Phase I clinical and pharmacokinetic study of RAD001 (everolimus) administered daily to Japanese patients with advanced solid tumors. Doi, T; Kobayashi, K; Kurei, K; Miyazaki, M; Nakagawa, K; Ohtsu, A; Okamoto, I; Tsuya, A, 2010)	0.61
"Comparative pharmacokinetic (PK) analysis of the mTOR inhibitor RAD001 (everolimus) in rats and mice."	( Comparative pharmacokinetics of RAD001 (everolimus) in normal and tumor-bearing rodents. Allegrini, PR; Brueggen, J; Bruelisauer, A; Gschwind, HP; Kawai, R; Kretz, O; Lane, HA; McMahon, L; McSheehy, PM; O'Reilly, T, 2010)	0.86
" Blood concentrations of everolimus were measured up to 240 min, and pharmacokinetic parameters were calculated."	( Effect of itraconazole on the pharmacokinetics of everolimus administered by different routes in rats. Inui, K; Katsura, T; Masuda, S; Sato, E; Yano, I; Yokomasu, A, 2009)	0.91
" Inhibition of glucose metabolism measured by (18)F-FDG PET was postulated to serve as a pharmacodynamic marker in everolimus-treated non-small cell lung cancer (NSCLC) patients."	( Downregulation of 18F-FDG uptake in PET as an early pharmacodynamic effect in treatment of non-small cell lung cancer with the mTOR inhibitor everolimus. Bangard, C; Boellaard, R; Dietlein, M; Dimitrijevic, S; Eschner, W; Giaccone, G; Gross, SH; Hayes, W; Hoekstra, OS; Hoetjes, N; Kobe, C; Lammertsma, AA; Nogová, L; Pellas, T; Schmidt, K; Thomas, RK; Wolf, J; Zander, T, 2009)	0.76
" The present pharmacokinetic sub-study from the SPIRIT III Randomized and Controlled Trial (RCT) was to evaluate systemic exposure of patients to everolimus and to further demonstrate safety following implantation of XIENCE Vstents with everolimus doses ranging from 53 to 181 microg."	( Pharmacokinetic sub-study in the SPIRIT III Randomized and Controlled Trial of XIENCE V everolimus eluting coronary stent system. Bol, C; Cannon, L; Gordon, P; Pierson, W; Saucedo, J; Sood, P; Sudhir, K; Wang, Q, 2010)	0.78
" The authors determined whether a pharmacokinetic interaction occurs between sotrastaurin and everolimus, both of which are substrates and inhibitors of CYP3A4."	( Sotrastaurin and everolimus pharmacokinetics after single-dose coadministration. Antunes, MC; Bartlett, M; Kovarik, JM; Marbach, P; Rordorf, C; van Marle, S; Winter, S, 2010)	0.92
" Clinical and pharmacokinetic data were collected to Day 5 after each treatment."	( Sotrastaurin and everolimus pharmacokinetics after single-dose coadministration. Antunes, MC; Bartlett, M; Kovarik, JM; Marbach, P; Rordorf, C; van Marle, S; Winter, S, 2010)	0.7
"A prospective randomized phase II pharmacokinetic study was conducted comparing two fixed EVL dosages (0."	( Interaction between everolimus and tacrolimus in renal transplant recipients: a pharmacokinetic controlled trial. Brunet, M; Cabello, M; del Castillo, D; Fernández, AM; Grinyó, JM; Pallardó, L; Pascual, J, 2010)	0.68
" The authors conducted a phase 1 and pharmacokinetic study of everolimus and docetaxel for recurrent NSCLC."	( Phase 1 and pharmacokinetic study of everolimus, a mammalian target of rapamycin inhibitor, in combination with docetaxel for recurrent/refractory nonsmall cell lung cancer. Egorin, MJ; Fu, H; Harvey, RD; Kauh, J; Khuri, FR; Owonikoko, TK; Ramalingam, SS; Saba, N; Shin, DM; Strychor, S; Sun, SY; Tighiouart, M, 2010)	0.87
" Full pharmacokinetic studies of everolimus and CsA were studied at the period of 4-8 weeks after CsA reduction."	( Long-term outcome of very early cyclosporine minimization and de novo everolimus therapy in kidney transplant recipients: a pharmacokinetic guided approach. Chalermsanyakorn, P; Jirasiritham, S; Sumethkul, V; Tankee, P, 2010)	0.88
" Primary end points were pharmacokinetic parameters and safety and tolerability."	( Two-dose-level confirmatory study of the pharmacokinetics and tolerability of everolimus in Chinese patients with advanced solid tumors. Cherfi, A; Jappe, A; Shen, L; Wang, H; Wu, Y; Xu, B; Ye, D; Yuan, R, 2011)	0.6
" The observed safety and pharmacokinetic profile of everolimus from this study were consistent with previous studies."	( Two-dose-level confirmatory study of the pharmacokinetics and tolerability of everolimus in Chinese patients with advanced solid tumors. Cherfi, A; Jappe, A; Shen, L; Wang, H; Wu, Y; Xu, B; Ye, D; Yuan, R, 2011)	0.85
"We retrospectively analyzed data from pharmacokinetic studies of patients implanted with an 18-mm DES: Cypher stent (sirolimus, n = 10), Endeavor stent (zotarolimus, n = 7), Xience V stent (everolimus, n = 6), and Nobori stent (biolimus A9, n = 10), in multicenter trials of Japan."	( Comparison of pharmacokinetics of the limus-eluting stents in Japanese patients. Mitsudo, K; Nakamura, M; Otsuka, Y; Saito, S; Shuto, H, 2011)	0.56
" The other pharmacokinetic parameters of four DESs differed according to characteristics of the coated drug."	( Comparison of pharmacokinetics of the limus-eluting stents in Japanese patients. Mitsudo, K; Nakamura, M; Otsuka, Y; Saito, S; Shuto, H, 2011)	0.37
"In Japanese patients, systemic exposure was low, regardless of the type of limus drug eluted from the stents; but specific pharmacokinetic activities were varied according to the drug characteristics, concentration, and DES design."	( Comparison of pharmacokinetics of the limus-eluting stents in Japanese patients. Mitsudo, K; Nakamura, M; Otsuka, Y; Saito, S; Shuto, H, 2011)	0.37
" There was no pharmacokinetic interaction between everolimus and capecitabine."	( Phase I and pharmacokinetic study of capecitabine and the oral mTOR inhibitor everolimus in patients with advanced solid malignancies. Beijnen, JH; Deenen, MJ; Klümpen, HJ; Richel, DJ; Schellens, JH; Sparidans, RW; Weterman, MJ; Wilmink, JW, 2012)	0.86
" We evaluated the safety, biologic activity, and pharmacokinetic profile of oral AEE788, a selective inhibitor of epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF), plus oral RAD001, a mammalian target of rapamycin inhibitor, in glioblastoma patients."	( Pharmacokinetic drug interaction between AEE788 and RAD001 causing thrombocytopenia in patients with glioblastoma. Alfred Yung, WK; Cloughesy, T; Conrad, C; DiLea, C; Dugan, M; Huang, J; Maes, A; Mietlowski, W; Reardon, DA; Rich, J; Yung, L, 2012)	0.38
" The purpose of this study was to measure the pharmacokinetic profile of everolimus following stent implantation."	( Pharmacokinetic analysis after implantation of everolimus-eluting self-expanding stents in the peripheral vasculature. Hausegger, KA; Koppensteiner, R; Lammer, J; Menon, RM; Scheinert, D; Schroë, H; Schwartz, LB; Vermassen, F, 2012)	0.87
" A population pharmacokinetic model was developed and demographic factors and genetic polymorphisms in genes coding for ABCB1, CYP3A5, CYP2C8 and PXR were included as covariates."	( Population pharmacokinetics and pharmacogenetics of everolimus in renal transplant patients. de Fijter, JW; den Hartigh, J; Guchelaar, HJ; Moes, DJ; Press, RR; van der Straaten, T, 2012)	0.63
" The pharmacokinetic limited sampling model (C(trough) and whole blood drug concentration at 2 hours postdose [C(2)]) resulted in a significantly improved prediction of everolimus exposure compared with the widely used C(trough) monitoring."	( Population pharmacokinetics and pharmacogenetics of everolimus in renal transplant patients. de Fijter, JW; den Hartigh, J; Guchelaar, HJ; Moes, DJ; Press, RR; van der Straaten, T, 2012)	0.82
"A two-compartment pharmacokinetic model with lag-time describing the concentration-time profile of oral everolimus in renal transplant patients has been developed using pharmacokinetic modelling."	( Population pharmacokinetics and pharmacogenetics of everolimus in renal transplant patients. de Fijter, JW; den Hartigh, J; Guchelaar, HJ; Moes, DJ; Press, RR; van der Straaten, T, 2012)	0.84
"The aim of this study was, using routine drug monitoring data, to identify patient characteristics that may influence everolimus (EVE) pharmacokinetic parameters and to develop a population pharmacokinetic model to predict EVE whole blood concentrations in cardiac recipients."	( Population pharmacokinetics of everolimus in cardiac recipients: comedications, ABCB1, and CYP3A5 polymorphisms. Antignac, M; Bezian, E; Farinotti, R; Fernandez, C; Goldwirt, L; Lemaitre, F; Urien, S; Varnous, S, 2012)	0.87
" Population pharmacokinetic modeling was carried out using the nonlinear mixed-effects modeling program."	( Population pharmacokinetics of everolimus in cardiac recipients: comedications, ABCB1, and CYP3A5 polymorphisms. Antignac, M; Bezian, E; Farinotti, R; Fernandez, C; Goldwirt, L; Lemaitre, F; Urien, S; Varnous, S, 2012)	0.66
"The pharmacokinetic of EVE in cardiac recipients was best described by a 1-compartment model."	( Population pharmacokinetics of everolimus in cardiac recipients: comedications, ABCB1, and CYP3A5 polymorphisms. Antignac, M; Bezian, E; Farinotti, R; Fernandez, C; Goldwirt, L; Lemaitre, F; Urien, S; Varnous, S, 2012)	0.66
"This study is the first population pharmacokinetic model of EVE in heart transplantation patients."	( Population pharmacokinetics of everolimus in cardiac recipients: comedications, ABCB1, and CYP3A5 polymorphisms. Antignac, M; Bezian, E; Farinotti, R; Fernandez, C; Goldwirt, L; Lemaitre, F; Urien, S; Varnous, S, 2012)	0.66
" Temsirolimus and everolimus have both been associated with improved outcomes in patients with mRCC but, as reviewed in this paper, the pharmacokinetic characteristics of these agents differ in many respects."	( Oral and intravenously administered mTOR inhibitors for metastatic renal cell carcinoma: pharmacokinetic considerations and clinical implications. Boni, JP; Danesi, R; Ravaud, A, 2013)	0.72
" Blood samples for pharmacokinetic assessment were collected at predetermined time points up to 168 hours postdosing."	( Effects of hepatic impairment on the pharmacokinetics of everolimus: a single-dose, open-label, parallel-group study. Anak, O; Bouillaud, E; Kobalava, Z; Kunz, T; Paquet, T; Peveling-Oberhag, J; Sellami, D; Urva, S; Yong, WP; Zeuzem, S, 2013)	0.64
" This study assessed the pharmacokinetics (PK) of everolimus and sorafenib alone and in combination in plasma and tissues, developed physiologically based pharmacokinetic (PBPK) models in mice, and assessed the possibility of PK drug interactions."	( Physiologically based pharmacokinetic models for everolimus and sorafenib in mice. Fetterly, GJ; Hylander, BH; Jusko, WJ; Ma, WW; Pawaskar, DK; Repasky, EA; Straubinger, RM, 2013)	0.9
" These studies provide the basis for pharmacodynamic evaluation of these drugs in patient-derived primary pancreatic adenocarcinomas explants."	( Physiologically based pharmacokinetic models for everolimus and sorafenib in mice. Fetterly, GJ; Hylander, BH; Jusko, WJ; Ma, WW; Pawaskar, DK; Repasky, EA; Straubinger, RM, 2013)	0.64
"There is limited data analyzing the pharmacokinetic (PK) and pharmacodynamic (PD) properties of everolimus (EVR) between African Americans and Caucasians."	( Racial comparisons of everolimus pharmacokinetics and pharmacodynamics in adult kidney transplant recipients. Baliga, P; Belk, L; Bratton, C; Chavin, K; Fleming, J; McGillicuddy, J; Meadows, H; Pilch, N; Srinivas, T; Taber, DJ, 2013)	0.92
" [(18)F]Fluorodeoxyglucose positron emission tomography (FDG-PET) was performed as a pharmacodynamic marker of mTOR inhibition, and dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) was performed as an indicator of tumor perfusion changes, at 3 time points."	( Phase 1 and pharmacodynamic trial of everolimus in combination with cetuximab in patients with advanced cancer. Avadhani, AN; Ciunci, CA; Divgi, CR; Englander, S; Flaherty, KT; Giantonio, BJ; Harlacker, K; Kang, HC; O'Dwyer, PJ; Perini, RF; Redlinger, M; Rosen, MA; Schnall, M; Song, HK; Sun, W; Troxel, A, 2014)	0.68
" Pharmacodynamic biomarkers could be useful in distinguishing between (1) disease resistance that occurs even though mTOR is successfully inhibited (suggesting a need for a different treatment strategy) and (2) resistance that might respond to changes in drug dosage or schedule."	( Ribosomal S6 kinase and AKT phosphorylation as pharmacodynamic biomarkers in patients with myelodysplastic syndrome treated with RAD001. Advani, AS; Bates, J; Kalaycio, M; Maciejewski, J; Mahfouz, RZ; Rybicki, L; Saunthararajah, Y; Sekeres, M; Tripp, B, 2014)	0.4
" Therefore, to evaluate the pharmacodynamic effects of RAD001, S6 and AKT phosphorylation (pS6, pAKT) were measured by peripheral blood flow cytometry."	( Ribosomal S6 kinase and AKT phosphorylation as pharmacodynamic biomarkers in patients with myelodysplastic syndrome treated with RAD001. Advani, AS; Bates, J; Kalaycio, M; Maciejewski, J; Mahfouz, RZ; Rybicki, L; Saunthararajah, Y; Sekeres, M; Tripp, B, 2014)	0.4
" There were no clinical responses despite the biomarker evidence of intended pharmacodynamic effect."	( Ribosomal S6 kinase and AKT phosphorylation as pharmacodynamic biomarkers in patients with myelodysplastic syndrome treated with RAD001. Advani, AS; Bates, J; Kalaycio, M; Maciejewski, J; Mahfouz, RZ; Rybicki, L; Saunthararajah, Y; Sekeres, M; Tripp, B, 2014)	0.4
" No difference of EVL Cmax or Tmax was found after atorvastatin coadministration."	( Effects of atorvastatin on the pharmacokinetics of everolimus among kidney transplant recipients. Avihingsanon, Y; Chancharoenthana, W; Praditpornsilpa, K; Somparn, P; Townamchai, N; Vadcharavivad, S; Wanitchanont, A, 2014)	0.65
" This review focuses on the pharmacokinetic interactions and exposure-response relationships of mTOR inhibitors and tacrolimus (TAC), the most widely used CNI."	( Focus on mTOR inhibitors and tacrolimus in renal transplantation: pharmacokinetics, exposure-response relationships, and clinical outcomes. Christians, U; Kaplan, B; Shihab, F; Smith, L; Wellen, JR, 2014)	0.4
"2459 ng/mL and mean peak concentration was 13."	( Pharmacokinetics of everolimus when combined with cyclosporine in Japanese de novo renal transplant recipients. Goto, N; Hirano, M; Hoshinaga, K; Kusaka, M; Sasaki, H; Uchida, K; Watarai, Y, 2014)	0.73
"The pharmacokinetic characteristics of everolimus in Japanese de novo renal transplant patients did not differ from those previously observed in non-Japanese patients, hence the same dosage of everolimus may be acceptable in Japanese patients."	( Pharmacokinetics of everolimus when combined with cyclosporine in Japanese de novo renal transplant recipients. Goto, N; Hirano, M; Hoshinaga, K; Kusaka, M; Sasaki, H; Uchida, K; Watarai, Y, 2014)	1
"In a pharmacokinetic substudy of the randomized ASSET trial, 46 de novo kidney transplant patients receiving very low (1."	( The pharmacokinetics of everolimus in de novo kidney transplant patients receiving tacrolimus: an analysis from the randomized ASSET study. Christiaans, MH; Kovarik, JM; Pascual, J; Rostaing, L, 2014)	0.71
"At month 12, mean values for tacrolimus trough concentration (C0), peak concentration (Cmax), and AUC0-12 in the very low tacrolimus group were approximately half that in the low tacrolimus group, but everolimus dose, C0, Cmax, and AUC0-12 were virtually identical in both groups."	( The pharmacokinetics of everolimus in de novo kidney transplant patients receiving tacrolimus: an analysis from the randomized ASSET study. Christiaans, MH; Kovarik, JM; Pascual, J; Rostaing, L, 2014)	0.9
" Everolimus has a favorable pharmacokinetic (PK) profile in early breast cancer studies."	( Evaluating the pharmacokinetics and pharmacodynamics of everolimus for treating breast cancer. Awada, A; Barthélémy, P; Gombos, A, 2015)	1.57
"This review article focuses on the biological rationale of using everolimus in breast cancer and on latest advances in the field of everolimus-based combinations with an emphasis on the PK and pharmacodynamic parameters of the drug throughout different studies."	( Evaluating the pharmacokinetics and pharmacodynamics of everolimus for treating breast cancer. Awada, A; Barthélémy, P; Gombos, A, 2015)	0.9
" We studied the pharmacodynamic effects of everolimus in resectable non-small cell lung cancer (NSCLC) to inform further development of these agents in lung cancer."	( A Translational, Pharmacodynamic, and Pharmacokinetic Phase IB Clinical Study of Everolimus in Resectable Non-Small Cell Lung Cancer. Auffermann, WF; Bechara, R; Behera, M; Chen, Z; Deng, X; Force, SD; Fu, H; Fu, RW; Gal, AA; Harvey, RD; Khuri, FR; Kim, S; Mendel, J; Miller, DL; Owonikoko, TK; Pickens, A; Ramalingam, SS; Rogatko, A; Rossi, MR; Saba, NF; Sica, GL; Sun, SY; Tighiouart, M; Torres, WE, 2015)	0.91
" Nevertheless, exposures produced by the initial EVR dose, the steady state pharmacokinetic and long-term safety and tolerability have not been explored in detail."	( Pharmacokinetics and Long-Term Safety and Tolerability of Everolimus in Renal Transplant Recipients Converted From Cyclosporine. de Paula, MI; Felipe, CR; Hannun, PG; Medina-Pestana, JO; Oliveira, NI; Tedesco-Silva, H, 2016)	0.68
" Weekly monitoring of EVR blood concentrations was followed by a full 12 hour pharmacokinetic profile 28 days after conversion."	( Pharmacokinetics and Long-Term Safety and Tolerability of Everolimus in Renal Transplant Recipients Converted From Cyclosporine. de Paula, MI; Felipe, CR; Hannun, PG; Medina-Pestana, JO; Oliveira, NI; Tedesco-Silva, H, 2016)	0.68
"36 l day(-1) , with an elimination half-life of 11."	( Influence of tumour burden on trastuzumab pharmacokinetics in HER2 positive non-metastatic breast cancer. Arnedos, M; Bachelot, T; Bernadou, G; Campone, M; Diéras, V; Gouilleux-Gruart, V; Jimenez, M; Lokiec, F; Merlin, JL; Paintaud, G; Rezai, K; Ternant, D, 2016)	0.43
" The elimination half-life of trastuzumab was shorter in the present population of patients than in metastatic breast cancer patients previously studied."	( Influence of tumour burden on trastuzumab pharmacokinetics in HER2 positive non-metastatic breast cancer. Arnedos, M; Bachelot, T; Bernadou, G; Campone, M; Diéras, V; Gouilleux-Gruart, V; Jimenez, M; Lokiec, F; Merlin, JL; Paintaud, G; Rezai, K; Ternant, D, 2016)	0.43
"A pharmacokinetic interaction between tacrolimus and everolimus was not observed clinically in renal transplant patients."	( Influence of everolimus on the pharmacokinetics of tacrolimus in Japanese renal transplant patients. Akamine, Y; Habuchi, T; Inoue, T; Kagaya, H; Miura, M; Niioka, T; Numakura, K; Saito, M; Satoh, S; Yamamoto, R, 2016)	1.05
" Serial pharmacokinetic sampling was performed on days 1 and 15."	( Everolimus pharmacokinetics and its exposure-toxicity relationship in patients with thyroid cancer. de Wit, D; den Hartigh, J; Gelderblom, H; Guchelaar, HJ; Kapiteijn, E; Links, TP; Moes, DJ; Roozen, CF; Schneider, TC; van der Hoeven, JJ; van Erp, NP, 2016)	1.88
"A semi-physiological pharmacokinetic model for everolimus was developed from pharmacokinetic data from 73 patients by non-linear mixed-effects modeling."	( A Semi-Physiological Population Model to Quantify the Effect of Hematocrit on Everolimus Pharmacokinetics and Pharmacodynamics in Cancer Patients. Burger, DM; de Wit, D; Huitema, AD; Kapiteijn, E; Ter Heine, R; van Erp, NP; van Herpen, CM; Willemsen, A, 2016)	0.92
"A population pharmacokinetic model was developed for everolimus in cancer patients."	( A Semi-Physiological Population Model to Quantify the Effect of Hematocrit on Everolimus Pharmacokinetics and Pharmacodynamics in Cancer Patients. Burger, DM; de Wit, D; Huitema, AD; Kapiteijn, E; Ter Heine, R; van Erp, NP; van Herpen, CM; Willemsen, A, 2016)	0.91
" The objective of this study was to assess the analytical suitability of a commercial kit-based phosphoflow cytometry protocol using whole blood (WBS) to measure the level of phosphorylated S6RP (p-S6RP) in T-cell subsets to study the pharmacodynamic effects of mTOR inhibitors (mTORi)."	( Performance of a phosphoflow assay to determine phosphorylation of S6 ribosomal protein as a pharmacodynamic read out for mTOR inhibition. Abdel-Kahaar, E; Hartmann, B; Kabakchiev, M; Shipkova, M; Wieland, E, 2016)	0.43
" Here, we measured blood concentrations of everolimus to obtain the population pharmacokinetic parameters and to examine the relationship between blood concentration and clinical outcomes."	( Population Pharmacokinetics of Everolimus in Relation to Clinical Outcomes in Patients With Advanced Renal Cell Carcinoma. Fukudo, M; Kamba, T; Masuda, S; Matsubara, K; Ogawa, O; Sato, E; Shinsako, K; Tanaka, A; Yamasaki, T; Yano, I, 2016)	0.98
" Population pharmacokinetic analysis was conducted using the NONMEM software."	( Population Pharmacokinetics of Everolimus in Relation to Clinical Outcomes in Patients With Advanced Renal Cell Carcinoma. Fukudo, M; Kamba, T; Masuda, S; Matsubara, K; Ogawa, O; Sato, E; Shinsako, K; Tanaka, A; Yamasaki, T; Yano, I, 2016)	0.72
"This study reports the first population pharmacokinetic parameters of everolimus in patients with RCC."	( Population Pharmacokinetics of Everolimus in Relation to Clinical Outcomes in Patients With Advanced Renal Cell Carcinoma. Fukudo, M; Kamba, T; Masuda, S; Matsubara, K; Ogawa, O; Sato, E; Shinsako, K; Tanaka, A; Yamasaki, T; Yano, I, 2016)	0.95
"AUC0-4h, peak concentration (Cmax), Cmax/minimum concentration, and peak-trough fluctuation in the resting period were significantly lower than those in the active period (p = 0."	( Circadian pharmacokinetics and limited sampling strategy of everolimus in heart transplant patients . Fukushima, N; Kawabata, A; Kuwahara, T; Matsuda, S; Nakajima, S; Nakatani, T; Sato, T; Seguchi, O; Takada, M; Terada, Y; Wada, K; Watanabe, T; Yanase, M, 2017)	0.7
"Although the proportion of elderly patients among renal transplant recipients has increased, pharmacokinetic (PK) studies of immunosuppressants rarely include older patients."	( Longitudinal Pharmacokinetics of Everolimus When Combined With Low-level of Tacrolimus in Elderly Renal Transplant Recipients. Agena, F; Coelho, V; David-Neto, E; de Almeida Rezende Ebner, P; Galante, NZ; Lemos, FBC; Ramos, F; Romano, P; Triboni, AHK, 2017)	0.74
"2 ng/mL), Cmax (19."	( Longitudinal Pharmacokinetics of Everolimus When Combined With Low-level of Tacrolimus in Elderly Renal Transplant Recipients. Agena, F; Coelho, V; David-Neto, E; de Almeida Rezende Ebner, P; Galante, NZ; Lemos, FBC; Ramos, F; Romano, P; Triboni, AHK, 2017)	0.74
"The objective of the present study was to assess the effect of cyclosporine (CsA) on the pharmacokinetic parameters of mycophenolic acid (MPA), an active mycophenolate mofetil (MMF) metabolite, and to compare with the effect of everolimus (EVR)."	( Influence of cyclosporine and everolimus on the main mycophenolate mofetil pharmacokinetic parameters: Cross-sectional study. Kaduševičius, E; Marquet, P; Noreikaitė, A; Saint-Marcoux, F; Stankevičius, E, 2017)	0.93
" We aimed to develop pharmacokinetic population models and Bayesian estimators based on a limited sampling strategy for estimation of dose interval exposures of everolimus in whole blood and peripheral blood mononuclear cells (PBMCs) in renal transplant recipients."	( A Limited Sampling Strategy to Estimate Exposure of Everolimus in Whole Blood and Peripheral Blood Mononuclear Cells in Renal Transplant Recipients Using Population Pharmacokinetic Modeling and Bayesian Estimators. Åsberg, A; Debord, J; Marquet, P; Robertsen, I; Woillard, JB, 2018)	0.93
" The pharmacokinetic model was developed using non-parametric modeling and its performances and those of the derived Bayesian estimator were evaluated in the validation set."	( A Limited Sampling Strategy to Estimate Exposure of Everolimus in Whole Blood and Peripheral Blood Mononuclear Cells in Renal Transplant Recipients Using Population Pharmacokinetic Modeling and Bayesian Estimators. Åsberg, A; Debord, J; Marquet, P; Robertsen, I; Woillard, JB, 2018)	0.73
"Pharmacodynamic (PD) monitoring may complement routine pharmacokinetic monitoring of mTOR inhibitors (mTORis) in an attempt to better guide individualized sirolimus (SRL) or everolimus (EVR) treatment after organ transplantation."	( Pharmacodynamic Monitoring of mTOR Inhibitors. Brunet, M; Marquet, P; Millán, O; Wieland, E, 2019)	0.71
" Pharmacokinetic assessment was conducted using blood samples collected on cycle 1, days 8 and 15."	( A Phase I Study of Safety, Pharmacokinetics, and Pharmacodynamics of Concurrent Everolimus and Buparlisib Treatment in Advanced Solid Tumors. Akce, M; Alese, OB; Bilen, MA; Carthon, B; Chen, Z; Collins, H; El-Rayes, BF; Harris, WB; Harvey, RD; Khuri, FR; Kudchagkar, RR; Lawson, DH; Lewis, C; Lonial, S; Owonikoko, TK; Ramalingam, SS; Shaib, WL; Sica, GL; Steuer, CE; Wu, C; Zhang, C, 2020)	0.79
" Steady-state pharmacokinetic analysis showed dose-normalized maximum concentrations and AUC values for everolimus and buparlisib in combination to be comparable with single-agent pharmacokinetic."	( A Phase I Study of Safety, Pharmacokinetics, and Pharmacodynamics of Concurrent Everolimus and Buparlisib Treatment in Advanced Solid Tumors. Akce, M; Alese, OB; Bilen, MA; Carthon, B; Chen, Z; Collins, H; El-Rayes, BF; Harris, WB; Harvey, RD; Khuri, FR; Kudchagkar, RR; Lawson, DH; Lewis, C; Lonial, S; Owonikoko, TK; Ramalingam, SS; Shaib, WL; Sica, GL; Steuer, CE; Wu, C; Zhang, C, 2020)	1
" Pharmacokinetic analyses were accompanied by pharmacodynamics assessment of E by FDG-PET."	( Sorafenib and everolimus in patients with advanced solid tumors and KRAS-mutated NSCLC: A phase I trial with early pharmacodynamic FDG-PET assessment. Abdulla, DSY; Backes, H; Behringer, D; Buettner, R; Eichstaedt, M; Fischer, RN; Franklin, J; Frechen, S; Fuhr, U; Gardizi, M; Junge, L; Kaminsky, B; Kinzig, M; Kobe, C; Limburg, M; Mattonet, C; Merkelbach-Bruse, S; Michels, S; Nogova, L; Ouyang, D; Persigehl, T; Rokitta, D; Scheffler, M; Schnell, R; Sörgel, F; Sos, ML; Stelzer, C; Suleiman, AA; Taubert, M; Tian, Y; Wolf, J, 2020)	0.92
" We conducted a phase 1 study in advanced solid tumour patients to assess safety, efficacy and pharmacodynamic (PD) outcomes."	( Phase 1 safety and pharmacodynamic study of lenalidomide combined with everolimus in patients with advanced solid malignancies with efficacy signal in adenoid cystic carcinoma. Alese, OB; Bilen, MA; Carthon, BC; Chen, Z; El-Rayes, BF; Harris, WB; Harvey, RD; Hossain, MS; Khuri, FR; Lawson, DH; Lewis, C; Lonial, S; Owonikoko, TK; Ramalingam, SS; Shaib, W; Steuer, CE; Waller, EK; Wu, C; Zhang, C, 2020)	0.79
" Here, we report a patient who showed high sunitinib concentrations, in addition to pharmacokinetic changes in tacrolimus and everolimus after sunitinib therapy."	( Model-based assessment of pharmacokinetic changes of sunitinib, tacrolimus, and everolimus in a patient with metastatic renal cell carcinoma after renal transplantation. Fujisawa, M; Furukawa, J; Harada, K; Ito, T; Ogawa, S; Omura, T; Yamamoto, K; Yano, I, 2020)	0.99
"This study aimed to evaluate the pharmacokinetic profile and tissue effects of everolimus delivered into arterial wall using biodegradable nanospheres."	( Nanospheres encapsulated everolimus delivery into arterial wall-the tissue pharmacokinetics and vascular response experimental study. Bryła-Wojciechowska, A; Buszman, PE; Buszman, PP; Błachut, A; Gąsior, P; Jelonek, K; Kachel, M; Kasperczyk, J; Kiesz, RS; Krauze, A; Milewski, K; Musiał-Kulik, M; Rousselle, SD; Tellez, A, 2021)	1.15
"A pharmacokinetic study included 28 porcine coronary arterial segments initially injured with balloon angioplasty followed by the local delivery of everolimus encapsulated in nanospheres (EEN) via injection through a microporous delivery catheter."	( Nanospheres encapsulated everolimus delivery into arterial wall-the tissue pharmacokinetics and vascular response experimental study. Bryła-Wojciechowska, A; Buszman, PE; Buszman, PP; Błachut, A; Gąsior, P; Jelonek, K; Kachel, M; Kasperczyk, J; Kiesz, RS; Krauze, A; Milewski, K; Musiał-Kulik, M; Rousselle, SD; Tellez, A, 2021)	1.12
" However, the pharmacokinetic and pharmacodynamic information for EVL combined with TAC is limited."	( Pharmacodynamic Drug-Drug Interaction on Human Peripheral Blood Mononuclear Cells Between Everolimus and Tacrolimus at the Therapeutic Concentration Range in Renal Transplantation. Akashi, I; Akiyama, S; Hirano, T; Iwamoto, H; Kihara, Y; Konno, O; Oda, T; Okihara, M; Osato, S; Takeuchi, H; Tanaka, S; Unezaki, S; Yoshinaga, R, 2021)	0.84
" To this end, we investigated experimentally and assessed computationally the in vitro pharmacodynamic drug-drug interactions of the various dual and triple combinations to assess their subsequent combinatorial effects (synergistic/additive/antagonistic) in a HER2-therapy resistant BC cell line, JIMT-1."	( Experimental and computational assessment of the synergistic pharmacodynamic drug-drug interactions of a triple combination therapy in refractory HER2-positive breast cancer cells. Ait-Oudhia, S; Vaidya, TR, 2022)	0.72
" In this study, a population pharmacokinetic analysis was conducted to improve the individualization of everolimus therapy."	( Population pharmacokinetics of everolimus in adult liver transplant patients: Comparison to tacrolimus disposition and extrapolation to pediatrics. Hata, K; Hatano, E; Hira, D; Hirai, M; Imai, S; Ito, T; Itohara, K; Matsubara, K; Nakagawa, S; Nakagawa, T; Sugimoto, M; Terada, T; Yano, I; Yonezawa, A, 2022)	1.22
"When highly purified cannabidiol (CBD; Epidiolex) and the mammalian target of rapamycin inhibitor everolimus are used concomitantly in the treatment of tuberous sclerosis complex, there is evidence of a pharmacokinetic (PK) interaction, leading to increased everolimus systemic exposure."	( Pharmacokinetic Drug-Drug Interaction With Coadministration of Cannabidiol and Everolimus in a Phase 1 Healthy Volunteer Trial. Berwaerts, J; Chen, C; Critchley, D; Hyland, K; Tayo, B; Thai, C; Wray, L, 2023)	1.35

Excerpt	Reference	Relevance
"The novel immunosuppressant SDZ RAD, 40-0 (2-hydroxyethyl)rapamycin, is an orally active rapamycin analogue developed for use in combination with cyclosporine (Neoral)."	( Suppression of acute rejection in allogeneic rat lung transplantation: a study of the efficacy and pharmacokinetics of rapamycin derivative (SDZ RAD) used alone and in combination with a microemulsion formulation of cyclosporine. Berry, GJ; Boeke, K; Christians, U; Hausen, B; Morris, RE; Segarra, IT, 1999)	0.3
" We hypothesized that chloroquine in combination with tacrolimus and the rapamycin derivative SDZ-RAD can synergistically suppress T cell responses and antigen-presenting cell (APC) function in vitro."	( Evaluation for synergistic suppression of T cell responses to minor histocompatibility antigens by chloroquine in combination with tacrolimus and a rapamycin derivative, SDZ-RAD. Bader, S; Forooghian, F; Gilman, A; HayGlass, KT; Hsiao, CC; Rempel, J; Schultz, KR; Su, WN, 2002)	0.31
"0 mg/day) combined with reduced-exposure CsA (Neoral) in de novo renal transplant patients."	( Concentration-controlled everolimus (Certican): combination with reduced dose calcineurin inhibitors. Pascual, J, 2005)	0.63
"We evaluated the in vitro capacity of FK778, alone or in combination with other immunosuppressive drugs: Tacrolimus (TRL); Sirolimus (SRL), Everolimus (EVL), to inhibit clonal expansion of T-lymphocytes and expression of lymphocyte-activation surface antigens; secondly, we compared the immunosuppressive potential of FK778 combined with TRL, SRL and EVL with the same combinations using Mycophenolic acid (MPA) as antimetabolite."	( Role of FK778 alone or in combination with tacrolimus or mTOR inhibitors as an immunomodulator of immunofunctions: in vitro evaluation of T cell proliferation and the expression of lymphocyte surface antigens. Barceló, JJ; Brunet, M; Fortuna, V; Jiménez, O; Millán, O, )	0.33
" In this study we sought to determine whether the oncolytic adenovirus Delta-24-RGD, in combination with everolimus (RAD001), would result in an enhanced anti-glioma effect in vivo."	( Delta-24-RGD in combination with RAD001 induces enhanced anti-glioma effect via autophagic cell death. Alonso, MM; Bekele, NB; Fueyo, J; Gomez-Manzano, C; Jiang, H; Kondo, S; Lang, FF; Xu, J; Yokoyama, T, 2008)	0.56
" The objective of our study was to evaluate the effects of RAD001 on the growth of CaP in the bone, both alone and in combination with docetaxel and zoledronic acid."	( RAD001 (Everolimus) inhibits growth of prostate cancer in the bone and the inhibitory effects are increased by combination with docetaxel and zoledronic acid. Corey, E; Gross, TS; Morgan, TM; Pitts, TE; Poliachik, SL; Vessella, RL, 2008)	0.78
"In this study, we examined whether cyclosporine was effective when combined with everolimus in clinical heart transplantation (HT)."	( Heart transplantation under cyclosporine or tacrolimus combined with mycophenolate mofetil or everolimus. Chen, YS; Chi, NH; Chou, NK; Huang, SC; Ko, WJ; Sun, CD; Tsao, CI; Wang, CH; Wang, SS; Wu, IH; Yu, HY, 2008)	0.79
"Although EVR and FTY720 monotherapy delayed the progression of CAN, their combination with CsA had no beneficial effect."	( Treatment of chronic allograft nephropathy at late stages using everolimus or FTY720 in combination with cyclosporine. Baumann, M; Heemann, U; Liu, S; Lutz, J; Roos, M; Schmaderer, C; Strobl, M, 2008)	0.58
" 44 (2007) 963-969] and developed a new method, namely the impregnation of sampling paper with a solution of plasma-protein, formic acid and ammonium acetate, in combination with the extraction of the blood spot by filter filtration."	( Therapeutic drug monitoring of everolimus using the dried blood spot method in combination with liquid chromatography-mass spectrometry. Christiaans, M; de Beer, Y; de Jong, GJ; Hoogtanders, K; Neef, C; Stolk, L; van der Heijden, J, 2009)	0.64
"We report a case of a 54-year-old male renal transplant patient who received antifungal azole treatment in combination with the recently introduced immunosuppressant agent everolimus to prevent post-transplantation aspergillosis reactivation."	( Management of metabolic cytochrome P450 3A4 drug-drug interaction between everolimus and azole antifungals in a renal transplant patient. Abboud, I; Antoine, C; Benammar, M; Berge, M; Billaud, EM; Glotz, D; Lefeuvre, S, 2009)	0.78
"In phase I, patients received imatinib (600/800 mg/day) combined with weekly (20 mg) or daily (2."	( A phase I-II study of everolimus (RAD001) in combination with imatinib in patients with imatinib-resistant gastrointestinal stromal tumors. Blay, JY; Demetri, GD; Dumez, H; Hollaender, N; Jappe, A; Morgan, JA; Ray-Coquard, I; Reichardt, P; Schöffski, P, 2010)	0.68
" 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)	0.61
"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)	0.61
" 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)	0.61
"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)	0.61
"The aim was to determine the potential of the allosteric mammalian target of rapamycin inhibitor, everolimus, to act in combination with cytotoxic anticancer compounds in vitro and in vivo."	( Evaluation of the mTOR inhibitor, everolimus, in combination with cytotoxic antitumor agents using human tumor models in vitro and in vivo. Brandt, R; Lane, HA; Lassota, P; McSheehy, PM; O'Reilly, T; Wartmann, M, 2011)	0.87
"VEGF, mTOR, and EGFR inhibitors have demonstrated anti-tumor and anti-angiogenic effects alone and in combination with each other."	( A phase I study of bevacizumab (B) in combination with everolimus (E) and erlotinib (E) in advanced cancer (BEE). Bendell, JC; Blobe, GC; Broadwater, G; Bullock, KE; Gockerman, JP; Howard, LA; Hurwitz, HI; Lager, JJ; Meadows, KL; Morse, MA; O'Neill, MM; Petros, WP; Truax, R; Uronis, HE; Younis, I; Zafar, SY, 2011)	0.62
"The present study was designed to investigate the effect of low-dose calcineurin inhibitor (CNI) tacrolimus combined with a mammalian target of rapamycin (mTOR) inhibitor on renal function in transplant recipients without allograft nephropathy."	( Low-dose calcineurin inhibitor regimen combined with mammalian target of rapamycin inhibitors preserves kidney functions in renal transplant recipients without allograft nephropathy. Gurkan, A; Kacar, S; Karaca, C; Tilif, S; Varılsuha, C, 2010)	0.36
"1 years underwent renal transplantation and were switched to a new second-line treatment of low-dose CNI combined with an mTOR inhibitor, either sirolimus or everolimus."	( Low-dose calcineurin inhibitor regimen combined with mammalian target of rapamycin inhibitors preserves kidney functions in renal transplant recipients without allograft nephropathy. Gurkan, A; Kacar, S; Karaca, C; Tilif, S; Varılsuha, C, 2010)	0.56
"Low-dose CNI combined with an mTOR inhibitor, as a replacement for mycophenolate mofetil or enteric-coated mycophenolate sodium, seemed to prevent renal dysfunction for at least 6 months among renal transplant patients without allograft nephropathy."	( Low-dose calcineurin inhibitor regimen combined with mammalian target of rapamycin inhibitors preserves kidney functions in renal transplant recipients without allograft nephropathy. Gurkan, A; Kacar, S; Karaca, C; Tilif, S; Varılsuha, C, 2010)	0.36
"To determine the feasible dose and schedule for everolimus, an oral mTOR inhibitor, combined with vinorelbine and trastuzumab for patients with HER2-overexpressing metastatic breast cancer pretreated with trastuzumab."	( Phase I trial of oral mTOR inhibitor everolimus in combination with trastuzumab and vinorelbine in pre-treated patients with HER2-overexpressing metastatic breast cancer. Bergh, J; Cardoso, F; Dieras, V; Fasolo, A; Gianni, L; Jerusalem, G; Massacesi, C; Sahmoud, T; Vittori, L; Zhang, Y, 2011)	0.9
" Moreover, trabectedin combined with everolimus may be more efficacious for the management of CCC."	( The activity of trabectedin as a single agent or in combination with everolimus for clear cell carcinoma of the ovary. Hayashi, M; Hisamatsu, T; Kawase, C; Kimura, T; Kurachi, H; Mabuchi, S; Mimura, K; Sawada, K; Takahashi, K; Takahashi, T, 2011)	0.88
" Patients with HER2-overexpressing MBC who had progressed on trastuzumab-based therapy received trastuzumab every 3 weeks in combination with daily everolimus."	( Phase I/II study of trastuzumab in combination with everolimus (RAD001) in patients with HER2-overexpressing metastatic breast cancer who progressed on trastuzumab-based therapy. Booser, DJ; Coviello, J; Ensor, J; Esteva, FJ; Flores, PR; Hortobagyi, GN; Kindelberger, DW; Krop, IE; Moore, JA; Morrow, PK; Nuñez, R; Sahin, AA; Winer, EP; Wulf, GM; Xiong, Y; Yu, D; Zhang, S, 2011)	0.82
"In our study, we investigated the efficacy of everolimus in combination with sildenafil on hemodynamic and morphological parameters in rats with monocrotaline-induced pulmonary hypertension (PH)."	( Effects of everolimus in combination with sildenafil in monocrotaline-induced pulmonary hypertension in rats. Atli, O; Burukoglu, D; Ilgin, S; Sirmagul, B, 2012)	1.03
" Since strong anti-tumor properties became evident with respect to cell growth and adhesion dynamics, the triple drug combination might provide progress in the treatment of advanced prostate cancer."	( Molecular targeting of prostate cancer cells by a triple drug combination down-regulates integrin driven adhesion processes, delays cell cycle progression and interferes with the cdk-cyclin axis. Blaheta, RA; Haferkamp, A; Hudak, L; Juengel, E; Makarević, J; Seibel, JM; Tsaur, I; Waaga-Gasser, A; Wedel, S, 2011)	0.37
" A Bayesian dose-escalation model was used to determine the feasible doses of daily or weekly everolimus combined with pemetrexed (500 mg/m q3w)."	( Everolimus in combination with pemetrexed in patients with advanced non-small cell lung cancer previously treated with chemotherapy: a phase I study using a novel, adaptive Bayesian dose-escalation model. Anrys, B; Boyer, M; Di Scala, L; Dimitrijevic, S; Laack, E; Miller, N; Petrovic, K; Pylvaenaeinen, I; Solomon, B; Vansteenkiste, J; Wolf, J, 2011)	2.03
" Primary objective was to determine the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of AEE788 combined with RAD001."	( Pharmacokinetic drug interaction between AEE788 and RAD001 causing thrombocytopenia in patients with glioblastoma. Alfred Yung, WK; Cloughesy, T; Conrad, C; DiLea, C; Dugan, M; Huang, J; Maes, A; Mietlowski, W; Reardon, DA; Rich, J; Yung, L, 2012)	0.38
"Fifteen patients with metastatic breast cancer were treated with docetaxel (doses of 40-75 mg/m(2) intravenously on day 1 of a 21-day cycle) in combination with everolimus (doses ranging from 20 to 50 mg orally on days 1 and 8 of a 21-day cycle) in a phase 1 trial using the continuous reassessment method to determine maximum tolerated dose."	( A phase 1 study of weekly everolimus (RAD001) in combination with docetaxel in patients with metastatic breast cancer. Booser, D; Brewster, A; Cristofanilli, M; Ensor, J; Giordano, SH; Gladish, G; Gonzalez-Angulo, AM; Hortobagyi, GN; Moore, J; Moulder, S; Murray, JL; Rivera, E; Tran, HT, 2012)	0.88
"Weekly everolimus in combination with docetaxel every 3 weeks was associated with excessive neutropenia and variable clearance of both drugs, making combination therapy unpredictable, even at low doses of both drugs."	( A phase 1 study of weekly everolimus (RAD001) in combination with docetaxel in patients with metastatic breast cancer. Booser, D; Brewster, A; Cristofanilli, M; Ensor, J; Giordano, SH; Gladish, G; Gonzalez-Angulo, AM; Hortobagyi, GN; Moore, J; Moulder, S; Murray, JL; Rivera, E; Tran, HT, 2012)	1.13
" In this study, we investigated the therapeutic efficacy of the tumor-VDA ASA404 (DMXAA, 5,6-dimethylxanthenone-4-acetic acid, or vadimezan) in combination with the mTOR inhibitor everolimus (RAD001) against RCC."	( Vascular disruption in combination with mTOR inhibition in renal cell carcinoma. Azabdaftari, G; Ellis, L; Hammers, H; Lehet, K; Pili, R; Seshadri, M; Shah, P; Sotomayor, P, 2012)	0.57
"25 mg RAD001 twice daily in combination with 15 mg/kg cyclosporin A (CsA) twice daily were identified as appropriate starting doses to achieve the targeted range of RAD001 (3-8 μg/L) when orally administered."	( Everolimus in combination with cyclosporin a as pre- and posttransplantation immunosuppressive therapy in nonmyeloablative allogeneic hematopoietic stem cell transplantation. Altmann, S; Drewelow, B; Freund, M; Junghanss, C; Lange, S; Mueller, S; Rathsack, S; Vogel, H; Wacke, R; Weirich, V, 2012)	1.82
"Treatment with EVR or SRL alone did not cause severe pancreatic dysfunction and renal injury, but when combined with CsA they aggravated CsA-induced pancreatic and renal injury."	( Drug interaction between cyclosporine and mTOR inhibitors in experimental model of chronic cyclosporine nephrotoxicity and pancreatic islet dysfunction. Bae, SK; Choi, BS; Chung, BH; Lim, SW; Piao, SG; Song, JH; Yang, CW, 2012)	0.38
" This finding provides better understanding of the difference between EVR and SRL when combined with CsA treatment."	( Drug interaction between cyclosporine and mTOR inhibitors in experimental model of chronic cyclosporine nephrotoxicity and pancreatic islet dysfunction. Bae, SK; Choi, BS; Chung, BH; Lim, SW; Piao, SG; Song, JH; Yang, CW, 2012)	0.38
"This study evaluated the effects of a mammalian target of mTOR inhibitor everolimus alone or in combination with trastuzumab on stem cells from HER2-overexpressing primary breast cancer cells and the BT474 breast cancer cell line in vitro and in vivo."	( Antitumor effect of the mTOR inhibitor everolimus in combination with trastuzumab on human breast cancer stem cells in vitro and in vivo. Liu, J; Liu, Y; Ma, Y; Zhang, J; Zhang, S; Zhang, X; Zhu, Y, 2012)	0.88
" This analysis evaluated efficacy and safety of everolimus in combination with tamoxifen in patients with mBC resistant to aromatase inhibitors (AIs)."	( Randomized phase II trial of everolimus in combination with tamoxifen in patients with hormone receptor-positive, human epidermal growth factor receptor 2-negative metastatic breast cancer with prior exposure to aromatase inhibitors: a GINECO study. Abadie-Lacourtoisie, S; Allouache, D; Bachelot, T; Bourgier, C; Cropet, C; Debled, M; El Kouri, C; Eymard, JC; Ferrero, JM; Freyer, G; Legouffe, E; Pujade-Lauraine, E; Ray-Coquard, I; Spaëth, D, 2012)	0.93
"The homogeneous stent strut coverage and the low LLL in the MV reflect proper healing characteristics of the TRYTON Stent in combination with the XIENCE-V™ stent."	( Healing responses after bifurcation stenting with the dedicated TRYTON Side-Branch Stent™ in combination with XIENCE-V™ stents: a clinical, angiography, fractional flow reserve, and optical coherence tomography study: the PYTON (Prospective evaluation of Adriaenssens, T; Bennett, J; Coosemans, M; D'hooge, J; Desmet, W; Dubois, C; Ferdinande, B; Sinnaeve, P; Ughi, G; Wiyono, S, 2013)	0.39
"BC cell lines expressing aromatase (AROM) and modeling endocrine-sensitive (MCF7-AROM1) and human epidermal growth factor receptor 2 (HER2)-dependent de novo resistant disease (BT474-AROM3) and long-term estrogen-deprived (LTED) MCF7 cells that had acquired resistance associated with HER2 overexpression were treated in vitro and as subcutaneous xenografts with everolimus (RAD001-mTORC1 inhibitor), in combination with tamoxifen or letrozole."	( Effectiveness and molecular interactions of the clinically active mTORC1 inhibitor everolimus in combination with tamoxifen or letrozole in vitro and in vivo. A'Hern, R; Dowsett, M; Evans, DB; Farmer, I; Ghazoui, Z; Guest, S; Johnston, SR; Lane, HA; Martin, LA; Pancholi, S; Ribas, R; Thornhill, AM; Weigel, MT, 2012)	0.77
" We compared the dose-dependent effects of the structurally related everolimus (EVL) and sirolimus (SRL) alone, and in combination with cyclosporine (CsA), on the rat kidney."	( Everolimus and sirolimus in combination with cyclosporine have different effects on renal metabolism in the rat. Arbelaez, MF; Bohra, R; Brunner, N; Christians, U; Klawitter, J; Lawrence, R; Schmitz, V; Schniedewind, B; Schöning, W; Shokati, T, 2012)	2.06
" We performed an open label phase II study of everolimus, an inhibitor of mammalian target of rapamycin, in combination with rituximab to examine efficacy and tolerability in patients with relapsed/refractory diffuse large B-cell lymphoma."	( Everolimus in combination with rituximab induces complete responses in heavily pretreated diffuse large B-cell lymphoma. Abramson, JS; Armand, P; Barnes, JA; Feng, Y; Fisher, DC; Freedman, A; Hochberg, EP; Jacobsen, E; Joyce, R; LaCasce, AS; Neuberg, D; Rodig, SJ; Sohani, AR, 2013)	2.09
" The aim of the study was to characterize the effects in vitro of mTOR inhibitors, used alone and in combination with JAK2 inhibitors, against MPN cells."	( mTOR inhibitors alone and in combination with JAK2 inhibitors effectively inhibit cells of myeloproliferative neoplasms. Bartalucci, N; Bogani, C; Bosi, A; Guglielmelli, P; Martinelli, S; Tozzi, L; Vannucchi, AM, 2013)	0.39
"We conducted a phase II study of docetaxel in combination with everolimus, a mammalian target of rapamycin (mTOR) inhibitor, for salvage therapy of advanced non-small-cell lung cancer (NSCLC) based on promising preclinical and early-phase clinical data."	( Phase II study of docetaxel in combination with everolimus for second- or third-line therapy of advanced non-small-cell lung cancer. Behera, M; Chen, Z; Fu, H; Gal, AA; Govindan, R; Harvey, RD; Khuri, FR; Klass, CM; Kono, SA; Owonikoko, TK; Ramalingam, SS; Saba, NF; Shin, DM; Sica, G; Subramanian, J; Sun, SY, 2013)	0.89
" The anti-proliferative activity of CDDP used in combination with RAD001 was statistically significant (P<0."	( Everolimus combined with cisplatin has a potential role in treatment of urothelial bladder cancer. Arantes-Rodrigues, R; Colaço, A; Colaço, B; Costa, C; da Silva, VM; Lopes, C; Oliveira, P; Palmeira, C; Pinto-Leite, R; Santos, L, 2013)	1.83
"Patients were treated with everolimus 10 mg daily in combination with sorafenib (dose level 1: 200 mg twice daily; dose level 2: 200 mg per morning, 400 mg per evening) using standard phase I dose escalation design."	( Phase I study of sorafenib in combination with everolimus (RAD001) in patients with advanced neuroendocrine tumors. Chan, JA; Jackson, N; Kulke, MH; Malinowski, P; Mayer, RJ; Regan, E, 2013)	0.94
" Sorafenib 200 mg twice daily in combination with everolimus 10 mg daily was established as the MTD."	( Phase I study of sorafenib in combination with everolimus (RAD001) in patients with advanced neuroendocrine tumors. Chan, JA; Jackson, N; Kulke, MH; Malinowski, P; Mayer, RJ; Regan, E, 2013)	0.9
"Oral everolimus (Afinitor(®)) in combination with exemestane is indicated for the treatment of hormone receptor-positive, human epidermal growth factor receptor (HER) 2-negative advanced breast cancer in postmenopausal women after failure of treatment with letrozole or anastrozole (in the USA) or after recurrence of progression following a nonsteroidal aromatase inhibitor (AI) in women without symptomatic visceral disease (in the EU)."	( Everolimus in combination with exemestane: a review of its use in the treatment of patients with postmenopausal hormone receptor-positive, HER2-negative advanced breast cancer. Dhillon, S, 2013)	2.35
"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)	1.05
"To evaluate everolimus drug-drug and drug-food interactions, with an emphasis on patients with cancer."	( Drug interactions and the pharmacist: focus on everolimus. Grabowsky, JA, )	0.77
" Everolimus, an oral mammalian target of rapamycin (mTOR) inhibitor, is indicated for the treatment in adults with progressive neuroendocrine tumors of pancreatic origin that are unresectable, locally advanced, or metastatic; adults with advanced renal cell carcinoma after failure of treatment with sunitinib or sorafenib; and, recently, postmenopausal women with advanced hormone receptor-positive, human epidermal growth factor receptor 2-negative breast cancer in combination with exemestane after failure of treatment with letrozole or anastrozole."	( Drug interactions and the pharmacist: focus on everolimus. Grabowsky, JA, )	1.3
" This phase I study was designed to determine the maximum tolerated dose (MTD) of everolimus given with sorafenib 400mg twice daily in patients with advanced HCC of Child-Pugh class A liver function who were naive to systemic therapy."	( Phase I study investigating everolimus combined with sorafenib in patients with advanced hepatocellular carcinoma. Brandt, U; Bruix, J; Chen, LT; Finn, RS; Gomez-Martin, C; Kang, YK; Kim, TY; Klümpen, HJ; Kunz, T; Paquet, T; Poon, RT; Rodriguez-Lope, C; Sellami, D; Yau, T, 2013)	0.91
"This study evaluated the effects of an mTOR inhibitor everolimus alone or in combination with letrozole on MCF-7/Aro (MCF-7 cells stably transfected with CYP19) in vitro and in vivo."	( Everolimus in combination with letrozole inhibit human breast cancer MCF-7/Aro stem cells via PI3K/mTOR pathway: an experimental study. Hou, G; Liu, J; Liu, Y; Zhang, J; Zhang, S; Zhang, X, 2014)	2.09
" In this phase 2 multicenter study, adult patients with HER2-positive advanced breast cancer resistant to trastuzumab and pretreated with a taxane received everolimus 10 mg/day in combination with paclitaxel (80 mg/m(2) days 1, 8, and 15 every 4 weeks) and trastuzumab (4 mg/kg loading dose followed by 2 mg/kg weekly), administered in 28-day cycles."	( A phase 2 study of everolimus combined with trastuzumab and paclitaxel in patients with HER2-overexpressing advanced breast cancer that progressed during prior trastuzumab and taxane therapy. André, F; Campone, M; Dalenc, F; El-Hashimy, M; Gligorov, J; Hurvitz, SA; Jhangiani, H; Lincy, J; Llombart, A; Miao, S; Mirshahidi, HR; O'Regan, RM; Sahmoud, T; Soria, JC; Tan-Chiu, E; Taran, T; Tjan-Heijnen, VC, 2013)	0.92
" The recommended phase 2 dose of oral weekly everolimus is 70 mg in combination with standard cetuximab."	( Phase 1 and pharmacodynamic trial of everolimus in combination with cetuximab in patients with advanced cancer. Avadhani, AN; Ciunci, CA; Divgi, CR; Englander, S; Flaherty, KT; Giantonio, BJ; Harlacker, K; Kang, HC; O'Dwyer, PJ; Perini, RF; Redlinger, M; Rosen, MA; Schnall, M; Song, HK; Sun, W; Troxel, A, 2014)	0.94
"Lenvatinib 18 mg combined with everolimus 5 mg was associated with manageable toxicity consistent with individual agents and no new safety signals."	( A phase 1b clinical trial of the multi-targeted tyrosine kinase inhibitor lenvatinib (E7080) in combination with everolimus for treatment of metastatic renal cell carcinoma (RCC). Carter, D; Gold, AM; Hutson, TE; Larkin, J; Michaelson, MD; Molina, AM; Motzer, R; Wood, K, 2014)	0.9
"This phase Ib study aimed to establish the feasible everolimus dose given with standard-dose etoposide plus cisplatin (EP) for extensive-stage small-cell lung cancer (SCLC)."	( A phase Ib dose-escalation study of everolimus combined with cisplatin and etoposide as first-line therapy in patients with extensive-stage small-cell lung cancer. Beck, JT; Besse, B; Camidge, DR; Dimitrijevic, S; Heist, RS; Johnson, BE; Miller, N; Mulatero, C; Papadmitrakopoulou, VA; Petrovic, K; Pylvaenaeinen, I; Schmid, P; Urva, S, 2014)	0.93
"An adaptive Bayesian dose-escalation model and investigator opinion were used to identify feasible daily or weekly everolimus doses given with EP in adults with treatment-naive extensive-stage SCLC."	( A phase Ib dose-escalation study of everolimus combined with cisplatin and etoposide as first-line therapy in patients with extensive-stage small-cell lung cancer. Beck, JT; Besse, B; Camidge, DR; Dimitrijevic, S; Heist, RS; Johnson, BE; Miller, N; Mulatero, C; Papadmitrakopoulou, VA; Petrovic, K; Pylvaenaeinen, I; Schmid, P; Urva, S, 2014)	0.89
"5 mg/day plus G-CSF was the only feasible dose given with standard-dose EP in untreated extensive-stage SCLC."	( A phase Ib dose-escalation study of everolimus combined with cisplatin and etoposide as first-line therapy in patients with extensive-stage small-cell lung cancer. Beck, JT; Besse, B; Camidge, DR; Dimitrijevic, S; Heist, RS; Johnson, BE; Miller, N; Mulatero, C; Papadmitrakopoulou, VA; Petrovic, K; Pylvaenaeinen, I; Schmid, P; Urva, S, 2014)	0.68
" Secondary objectives included evaluation of safety, toxicity and pharmacokinetics of LY2584702 in combination with erlotinib or everolimus."	( A phase Ib trial of LY2584702 tosylate, a p70 S6 inhibitor, in combination with erlotinib or everolimus in patients with solid tumours. Benhadji, KA; Brail, LH; Bumgardner, W; Cohen, EE; Hollebecque, A; Houédé, N; Italiano, A; Massard, C; Miller, J; Soria, JC; Westwood, P, 2014)	0.83
"Patients with advanced solid tumours were treated with a total daily dose of 50-200mg of LY2584702 in combination with erlotinib 150 mg once daily (Arm A) or everolimus 10mg once daily (Arm B)."	( A phase Ib trial of LY2584702 tosylate, a p70 S6 inhibitor, in combination with erlotinib or everolimus in patients with solid tumours. Benhadji, KA; Brail, LH; Bumgardner, W; Cohen, EE; Hollebecque, A; Houédé, N; Italiano, A; Massard, C; Miller, J; Soria, JC; Westwood, P, 2014)	0.82
" Exposure of erlotinib increased when administered in combination with LY2584702."	( A phase Ib trial of LY2584702 tosylate, a p70 S6 inhibitor, in combination with erlotinib or everolimus in patients with solid tumours. Benhadji, KA; Brail, LH; Bumgardner, W; Cohen, EE; Hollebecque, A; Houédé, N; Italiano, A; Massard, C; Miller, J; Soria, JC; Westwood, P, 2014)	0.62
"LY2584702 was not well tolerated when administered with erlotinib, therefore this combination is not feasible."	( A phase Ib trial of LY2584702 tosylate, a p70 S6 inhibitor, in combination with erlotinib or everolimus in patients with solid tumours. Benhadji, KA; Brail, LH; Bumgardner, W; Cohen, EE; Hollebecque, A; Houédé, N; Italiano, A; Massard, C; Miller, J; Soria, JC; Westwood, P, 2014)	0.62
" We evaluated the optimal schedule of oral topotecan in combination with everolimus in patients with endometrial cancer."	( Phase I clinical trial of the mammalian target of rapamycin inhibitor everolimus in combination with oral topotecan for recurrent and advanced endometrial cancer. Abu-Khalaf, MM; Acevedo-Gadea, C; Azodi, M; Higgins, SA; Ratner, E; Rutherford, T; Santin, AD; Schwartz, PE; Silasi, DA; Urva, S, 2014)	0.87
"9 mg/m on days 1 to 5 in combination with oral everolimus 5 mg every other day."	( Phase I clinical trial of the mammalian target of rapamycin inhibitor everolimus in combination with oral topotecan for recurrent and advanced endometrial cancer. Abu-Khalaf, MM; Acevedo-Gadea, C; Azodi, M; Higgins, SA; Ratner, E; Rutherford, T; Santin, AD; Schwartz, PE; Silasi, DA; Urva, S, 2014)	0.89
" The activity and safety of everolimus was assessed in combination with octreotide long-acting repeatable (LAR) in patients with neuroendocrine tumors (NETs) of gastroenteropancreatic and lung origin."	( Everolimus in combination with octreotide long-acting repeatable in a first-line setting for patients with neuroendocrine tumors: an ITMO group study. Aieta, M; Bajetta, E; Bianco, N; Biondani, P; Blanco, G; Catena, L; Fazio, N; Mauri, CM; Pucci, F; Pusceddu, S; Ricci, S; Spada, F; Valente, M, 2014)	2.14
" Treatment-naive patients with advanced well-differentiated NETs of gastroenteropancreatic tract and lung origin received everolimus 10 mg daily, in combination with octreotide LAR 30 mg every 28 days."	( Everolimus in combination with octreotide long-acting repeatable in a first-line setting for patients with neuroendocrine tumors: an ITMO group study. Aieta, M; Bajetta, E; Bianco, N; Biondani, P; Blanco, G; Catena, L; Fazio, N; Mauri, CM; Pucci, F; Pusceddu, S; Ricci, S; Spada, F; Valente, M, 2014)	2.05
"This phase I study investigated the safety, dose-limiting toxicity, and efficacy in three cohorts all treated with the mTOR inhibitor everolimus that was delivered (1) in combination with 5-fluorouracil with leucovorin (5-FU/LV), (2) with mFOLFOX6 (5-FU/LV + oxaliplatin), and (3) with mFOLFOX6 + panitumumab in patients with refractory solid tumors."	( A phase I trial of everolimus in combination with 5-FU/LV, mFOLFOX6 and mFOLFOX6 plus panitumumab in patients with refractory solid tumors. Bernard, S; Davies, JM; Dees, EC; Goldberg, RM; Ivanova, A; Keller, K; McRee, AJ; O'Neil, BH; Sanoff, HG, 2014)	0.93
" Next, a case study is used to illustrate this NMA feasibility assessment process in order to compare everolimus in combination with hormonal therapy to alternative chemotherapies in terms of progression-free survival for women with advanced breast cancer."	( A process for assessing the feasibility of a network meta-analysis: a case study of everolimus in combination with hormonal therapy versus chemotherapy for advanced breast cancer. Cope, S; Jansen, JP; Saletan, S; Schmid, P; Smiechowski, B; Zhang, J, 2014)	0.84
" Several studies have already used RAD001 in combination with calcineurin inhibitors after hematopoietic stem cell transplantation (HSCT)."	( Everolimus in combination with mycophenolate mofetil as pre- and post-transplantation immunosuppression after nonmyeloablative hematopoietic stem cell transplantation in canine littermates. Junghanss, C; Killian, D; Knuebel, G; Knueppel, A; Lange, S; Lindner, I; Machka, C; Murua Escobar, H; Roolf, C; Vogel, H; Wacke, R; Werner, J, 2014)	1.85
"Currently, there are no published data on pharmacokinetics (PK) of everolimus in combination with cyclosporine in Japanese renal transplant patients."	( Pharmacokinetics of everolimus when combined with cyclosporine in Japanese de novo renal transplant recipients. Goto, N; Hirano, M; Hoshinaga, K; Kusaka, M; Sasaki, H; Uchida, K; Watarai, Y, 2014)	0.96
"Platinum-based therapy combined with cetuximab is standard first-line therapy for recurrent or metastatic squamous cell carcinoma of the head and neck (RMSCCHN)."	( Phase 1 and pharmacokinetic study of everolimus in combination with cetuximab and carboplatin for recurrent/metastatic squamous cell carcinoma of the head and neck. Beitler, JJ; Chen, AY; Chen, Z; El-Deiry, M; Harvey, D; Higgins, K; Hurwitz, SJ; Khuri, FR; Kim, S; Kono, SA; Lewis, C; Magliocca, K; Mendel, J; Owonikoko, TK; Ramalingam, SS; Rogerio, J; Saba, NF; Shin, DM; Sun, SY; Wadsworth, T, 2014)	0.68
" By combination with the mTOR inhibitor RAD001, a synergistic effect on cell proliferation was observed in these cell lines."	( The multi-tyrosine kinase inhibitor TKI258, alone or in combination with RAD001, is effective for treatment of human leukemia with BCR-ABL translocation in vitro. Eucker, J; Habbel, P; Li, X; Liu, H; Neumann, C; Scholz, C; Zang, C; Zhou, Y, 2014)	0.4
"TKI258 may become a potent therapeutic agent, either alone or in combination with RAD001, for treatment of BCR-ABL(+) leukemia."	( The multi-tyrosine kinase inhibitor TKI258, alone or in combination with RAD001, is effective for treatment of human leukemia with BCR-ABL translocation in vitro. Eucker, J; Habbel, P; Li, X; Liu, H; Neumann, C; Scholz, C; Zang, C; Zhou, Y, 2014)	0.4
"This phase Ib trial investigated the safety, tolerability, and recommended phase II dose and schedule of the MEK inhibitor trametinib in combination with the mammalian target of rapamycin (mTOR) inhibitor everolimus."	( A phase IB trial of the oral MEK inhibitor trametinib (GSK1120212) in combination with everolimus in patients with advanced solid tumors. Bellew, KM; Bendell, JC; Burris, HA; Cox, DS; Durante, M; Infante, JR; Jones, SF; Le, NT; Papadopoulos, KP; Park, J; Patnaik, A; Rasco, D; Tolcher, AW, 2015)	0.83
" PK assessment did not suggest drug-drug interactions between these two agents."	( A phase IB trial of the oral MEK inhibitor trametinib (GSK1120212) in combination with everolimus in patients with advanced solid tumors. Bellew, KM; Bendell, JC; Burris, HA; Cox, DS; Durante, M; Infante, JR; Jones, SF; Le, NT; Papadopoulos, KP; Park, J; Patnaik, A; Rasco, D; Tolcher, AW, 2015)	0.64
"This study was unable to identify a recommended phase II dose and schedule of trametinib in combination with everolimus that provided an acceptable tolerability and adequate drug exposure."	( A phase IB trial of the oral MEK inhibitor trametinib (GSK1120212) in combination with everolimus in patients with advanced solid tumors. Bellew, KM; Bendell, JC; Burris, HA; Cox, DS; Durante, M; Infante, JR; Jones, SF; Le, NT; Papadopoulos, KP; Park, J; Patnaik, A; Rasco, D; Tolcher, AW, 2015)	0.85
"Azole antifungals, prescribed prophylactically to avoid severe infections in immunosuppressed organ transplant recipients, can interact with drug substrates of CYP3A4."	( Worsening pneumonitis due to a pharmacokinetic drug-drug interaction between everolimus and voriconazole in a renal transplant patient. Amilien, V; Chauvin, B; Eloy, P; Francois, H; Furlan, V; Lecefel, C; Massias, L; Taburet, AM; Wyplosz, B, 2015)	0.65
" The current study will test the hypothesis that MSC treatment, in combination with the mTOR inhibitor everolimus, facilitates tacrolimus withdrawal, reduces fibrosis and decreases the incidence of opportunistic infections compared to standard tacrolimus dose."	( Autologous bone marrow derived mesenchymal stromal cell therapy in combination with everolimus to preserve renal structure and function in renal transplant recipients. Al Huurman, V; Bank, JR; Claas, FH; de Fijter, JW; Dreyer, GJ; Fibbe, WE; Heidt, S; Lindeman, J; Rabelink, TJ; Reinders, ME; Roelen, DL; Roelofs, H; van Kooten, C, 2014)	0.84
" Patients in the MSC treated group will receive two doses of autologous bone marrow derived MSCs IV (target 1,5 x 10(6), Range 1-2 x 10(6) million MSCs per/kg body weight), 7 days apart, 6 and 7 weeks transplantation in combination with everolimus and prednisolone."	( Autologous bone marrow derived mesenchymal stromal cell therapy in combination with everolimus to preserve renal structure and function in renal transplant recipients. Al Huurman, V; Bank, JR; Claas, FH; de Fijter, JW; Dreyer, GJ; Fibbe, WE; Heidt, S; Lindeman, J; Rabelink, TJ; Reinders, ME; Roelen, DL; Roelofs, H; van Kooten, C, 2014)	0.81
"This study will provide information whether MSCs in combination with everolimus can be used for tacrolimus withdrawal, and whether this strategy leads to preservation of renal structure and function in renal recipients."	( Autologous bone marrow derived mesenchymal stromal cell therapy in combination with everolimus to preserve renal structure and function in renal transplant recipients. Al Huurman, V; Bank, JR; Claas, FH; de Fijter, JW; Dreyer, GJ; Fibbe, WE; Heidt, S; Lindeman, J; Rabelink, TJ; Reinders, ME; Roelen, DL; Roelofs, H; van Kooten, C, 2014)	0.86
" Everolimus, an mTOR inhibitor, has shown antitumor benefit in pNETs alone and in combination with octreotide LAR in RADIANT-1 and RADIANT-3 studies."	( Rationale and protocol of the MetNET-1 trial, a prospective, single center, phase II study to evaluate the activity and safety of everolimus in combination with octreotide LAR and metformin in patients with advanced pancreatic neuroendocrine tumors. Bregant, C; Buzzoni, R; Concas, L; de Braud, F; Formisano, B; Leuzzi, L; Pusceddu, S, )	1.25
"This phase I study evaluated the safety and efficacy of the oral mTOR inhibitor everolimus in combination with thoracic radiotherapy followed by consolidation chemotherapy in locally advanced or oligometastatic untreated non-small-cell lung cancer (NSCLC)."	( Phase I trial of everolimus in combination with thoracic radiotherapy in non-small-cell lung cancer. Angevin, E; Angokai, M; Bahleda, R; Besse, B; Deandreis, D; Deutsch, E; Faivre, L; Hennequin, C; Le Péchoux, C; Levy, A; Pignon, JP; Rivera, S; Soria, JC; Tao, Y, 2015)	0.98
"In previously untreated and unselected NSCLC patients, the recommended phase II dose of everolimus in combination with thoracic radiotherapy is 50 mg/week."	( Phase I trial of everolimus in combination with thoracic radiotherapy in non-small-cell lung cancer. Angevin, E; Angokai, M; Bahleda, R; Besse, B; Deandreis, D; Deutsch, E; Faivre, L; Hennequin, C; Le Péchoux, C; Levy, A; Pignon, JP; Rivera, S; Soria, JC; Tao, Y, 2015)	0.98
" We report the first bench-to-bedside evidence that RET inhibitor combined with an mTOR inhibitor is active against brain-metastatic RET-rearranged lung cancer and the first evidence of blood-brain barrier penetration."	( Systemic and CNS activity of the RET inhibitor vandetanib combined with the mTOR inhibitor everolimus in KIF5B-RET re-arranged non-small cell lung cancer with brain metastases. Ali, SM; Berry, J; Cascone, T; Guha-Thakurta, N; Heymach, JV; McMahon, C; Miller, V; Pai, S; Roxas, M; Subbiah, IM; Subbiah, V; Tang, Z, 2015)	0.64
"A number of studies have provided information regarding the risks and benefits of mammalian target of rapamycin inhibitors (mTOR-I) combined with calcineurin inhibitors (CNI) versus mycophenolic acid (MPA)."	( mTOR inhibitor versus mycophenolic acid as the primary immunosuppression regime combined with calcineurin inhibitor for kidney transplant recipients: a meta-analysis. Chen, J; Jiang, Y; Lai, X; Shou, Z; Xiang, S; Xie, X, 2015)	0.42
" Randomized controlled trials comparing mTOR-I to MPA as the primary immunosuppressive regimen in combination with CNI were selected and meta-analyzed."	( mTOR inhibitor versus mycophenolic acid as the primary immunosuppression regime combined with calcineurin inhibitor for kidney transplant recipients: a meta-analysis. Chen, J; Jiang, Y; Lai, X; Shou, Z; Xiang, S; Xie, X, 2015)	0.42
" Notably, mTOR-I had an increased risk of graft loss when combined with CNI, even when combined with a reduced dose of CNI."	( mTOR inhibitor versus mycophenolic acid as the primary immunosuppression regime combined with calcineurin inhibitor for kidney transplant recipients: a meta-analysis. Chen, J; Jiang, Y; Lai, X; Shou, Z; Xiang, S; Xie, X, 2015)	0.42
" We conducted a pilot trial to assess the pharmacokinetics (PK), tolerability, and efficacy of JI-101 in combination with everolimus in advanced cancers, and pharmacodynamics (PD), tolerability, and efficacy of JI-101 in ovarian cancer."	( A pilot study of JI-101, an inhibitor of VEGFR-2, PDGFR-β, and EphB4 receptors, in combination with everolimus and as a single agent in an ovarian cancer expansion cohort. Agarwal, N; Boucher, K; Luebke, A; Patel, J; Sharma, S; Wade, ML; Werner, TL, 2015)	0.84
"To explore the effect of CQ alone or in combination with RAD001, Torin1 or NVP-BEZ235 on autophagy and on NET cell viability, proliferation and apoptosis."	( Abrogation of Autophagy by Chloroquine Alone or in Combination with mTOR Inhibitors Induces Apoptosis in Neuroendocrine Tumor Cells. Avniel-Polak, S; Glaser, B; Gross, DJ; Grozinsky-Glasberg, S; Leibowitz, G; Riahi, Y, 2016)	0.43
"RAD001 combined with ATRA significantly induced NB4-R1 cells differentiation, but RAD001 or ATRA alone did not enhance NB4-R1 differentiation."	( [Everolimus combined with all-trans retinoid acid reverses drug resistance in acute promyelocytic leukemia NB4-R1 cells]. He, Y; Huang, H; Liao, WC; Wang, BS, 2015)	1.33
"RAD001 combined with ATRA can induce cell differentiation, inhibit cell cycle, resulting the reverse of drug resistance in NB4-R1 cells, which is associated with increase of autophagy level and degradation of PML-RARα."	( [Everolimus combined with all-trans retinoid acid reverses drug resistance in acute promyelocytic leukemia NB4-R1 cells]. He, Y; Huang, H; Liao, WC; Wang, BS, 2015)	1.33
"44 g/day or mycophenolate mofetil at 2 g/day) with tacrolimus; in combination with corticosteroids."	( Design and rationale of the ATHENA study--A 12-month, multicentre, prospective study evaluating the outcomes of a de novo everolimus-based regimen in combination with reduced cyclosporine or tacrolimus versus a standard regimen in kidney transplant patien Dragun, D; Hauser, IA; Nashan, B; Schenker, P; Sommerer, C; Suwelack, B; Thaiss, F, 2016)	0.64
"The VERITAS (A Phase 1B open-label study to assess the safety and tolerability of everolimus in combination with eribulin in triple-negative breast cancers) trial (EudraCT number: 2014-000135-17) is a phase Ib, open label, multicenter, dose-escalation, safety, pharmacokinetic, and pharmacodynamic study based on the combination of everolimus with eribulin in sequential cohorts of metastatic triple negative breast cancer (TNBC) patients."	( A Phase Ib Open-Label Study to Assess the Safety and Tolerability of Everolimus in Combination With Eribulin in Triple-Negative Breast Cancers. Bottini, A; Cappelletti, MR; Generali, D; Gobbi, A; Milani, M; Roviello, G; Senti, C; Sigala, S; Strina, C; Zanotti, L, 2016)	0.89
"The primary objective of the study is to identify the recommended dose of everolimus in combination with eribulin."	( A Phase Ib Open-Label Study to Assess the Safety and Tolerability of Everolimus in Combination With Eribulin in Triple-Negative Breast Cancers. Bottini, A; Cappelletti, MR; Generali, D; Gobbi, A; Milani, M; Roviello, G; Senti, C; Sigala, S; Strina, C; Zanotti, L, 2016)	0.9
"The VERITAS trial is expected to determine the recommended dose of everolimus in combination with eribulin in TBNC."	( A Phase Ib Open-Label Study to Assess the Safety and Tolerability of Everolimus in Combination With Eribulin in Triple-Negative Breast Cancers. Bottini, A; Cappelletti, MR; Generali, D; Gobbi, A; Milani, M; Roviello, G; Senti, C; Sigala, S; Strina, C; Zanotti, L, 2016)	0.91
" The primary endpoint of the phase 1 portion of this study was to establish the maximum tolerated dose of everolimus that could be combined with R-CHOP-21."	( Everolimus combined with R-CHOP-21 for new, untreated, diffuse large B-cell lymphoma (NCCTG 1085 [Alliance]): safety and efficacy results of a phase 1 and feasibility trial. Ansell, SM; Colgan, JP; Habermann, TM; Inwards, DJ; Johnston, PB; LaPlant, B; McPhail, E; Micallef, IN; Nowakowski, GS; Witzig, TE, 2016)	2.09
"The mTORC1 inhibitor everolimus given for 14 days in combination with R-CHOP-21 for patients with DLBCL is safe."	( Everolimus combined with R-CHOP-21 for new, untreated, diffuse large B-cell lymphoma (NCCTG 1085 [Alliance]): safety and efficacy results of a phase 1 and feasibility trial. Ansell, SM; Colgan, JP; Habermann, TM; Inwards, DJ; Johnston, PB; LaPlant, B; McPhail, E; Micallef, IN; Nowakowski, GS; Witzig, TE, 2016)	2.2
" 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
" Here, we report in vivo data for OTX015 in combination with the histone deacetylase inhibitor vorinostat, the Bruton's tyrosine kinase inhibitor ibrutinib, the anti-CD20 monoclonal antibody rituximab, and the mTOR inhibitor everolimus in a diffuse large B cell lymphoma model."	( Bromodomain inhibitor OTX015 (MK-8628) combined with targeted agents shows strong in vivo antitumor activity in lymphoma. Bernasconi, E; Bertoni, F; Cascione, L; Cvitkovic, E; Gaudio, E; Odore, E; Ponzoni, M; Rezai, K; Rinaldi, A; Riveiro, E; Stathis, A; Tarantelli, C; Zucca, E, 2016)	0.62
" Some clinically relevant drug-drug interactions are highlighted."	( mTOR inhibitors in pancreas transplant: adverse effects and drug-drug interactions. Fernandes-Silva, G; Ivani de Paula, M; Rangel, ÉB, 2017)	0.46
" In both animal models the anti-lymphoma activity of selinexor is enhanced through combination with DEX or EVER."	( Anti-tumor activity of selective inhibitor of nuclear export (SINE) compounds, is enhanced in non-Hodgkin lymphoma through combination with mTOR inhibitor and dexamethasone. Aboukameel, A; Azmi, AS; Baloglu, E; Bhutani, D; Carlson, R; Elloul, S; Kauffman, M; Mohammad, RM; Muqbil, I; Senapedis, W; Shacham, S; Zonder, J, 2016)	0.43
"To assess safety and efficacy of mammalian target of rapamycin (mTOR) inhibition in combination with liposomal doxorubicin and bevacizumab in patients with advanced metaplastic TNBC."	( Targeting the PI3K/AKT/mTOR Pathway for the Treatment of Mesenchymal Triple-Negative Breast Cancer: Evidence From a Phase 1 Trial of mTOR Inhibition in Combination With Liposomal Doxorubicin and Bevacizumab. Albarracin, C; Basho, RK; Chavez-MacGregor, M; Gilcrease, M; Helgason, T; Herbrich, SM; Hess, KR; Hong, D; Ibrahim, NK; Janku, F; Karp, DD; Koenig, KB; Kurzrock, R; Litton, JK; Meric-Bernstam, F; Moulder, SL; Murray, JL; Murthy, RK; Subbiah, V; Valero, V, 2017)	0.46
" The aim of this study was to evaluate the anti-tumor activity of OTX015 as single agent and in combination with everolimus in TNBC models."	( The bromodomain inhibitor OTX015 (MK-8628) exerts anti-tumor activity in triple-negative breast cancer models as single agent and in combination with everolimus. Astorgues-Xerri, L; Bekradda, M; Beltrame, L; Bertoni, F; Cvitkovic, E; D'Incalci, M; Erba, E; Frapolli, R; Kwee, I; Odore, E; Panini, N; Rezai, K; Rinaldi, A; Riveiro, ME; Vázquez, R, 2017)	0.86
" Future trials examining the use of immunotherapy, both as monotherapy and in combination with VEGF targeted therapy, will likely be a dominant influence in the therapeutic landscape of mRCC."	( Lenvatinib for use in combination with everolimus for the treatment of patients with advanced renal cell carcinoma following one prior anti-angiogenic therapy. Larkin, J; O'Reilly, A, 2017)	0.72
" The changes in steady-state pharmacokinetics of everolimus with BEZ235 highlight potential drug-drug interactions when these two drugs are administered together."	( A Phase Ib Study of the Dual PI3K/mTOR Inhibitor Dactolisib (BEZ235) Combined with Everolimus in Patients with Advanced Solid Malignancies. Beg, MS; Desai, P; Fathallah, H; Karim, NA; Kozma, SC; Mercer, CA; Moorthy, G; Morris, JC; O'Gara, S; Olowokure, O; Rixe, O; Salkeni, MA; Thomas, G; Thomas, HE; Wise-Draper, TM, 2017)	0.93
" In this study, we aim at determining the antitumor efficacy of everolimus alone or in combination with the SSAs octreotide and pasireotide in primary cultures of pNETs."	( Anti-proliferative and anti-secretory effects of everolimus on human pancreatic neuroendocrine tumors primary cultures: is there any benefit from combination with somatostatin analogs? Albertelli, M; Barbieri, F; Barlier, A; Brue, T; Delpero, JR; Ferone, D; Florio, T; Garcia, S; Gerard, C; Mohamed, A; Moutardier, V; Niccoli, P; Poizat, F; Roche, C; Romano, D; Saveanu, A, 2017)	0.95
"Palbociclib is the first cyclin-dependent kinase 4/6 inhibitor approved in the United States for HR+/HER2- advanced/metastatic breast cancer, in combination with letrozole as initial endocrine-based therapy in postmenopausal women or with fulvestrant in women with disease progression following endocrine therapy."	( Comparison of palbociclib in combination with letrozole or fulvestrant with endocrine therapies for advanced/metastatic breast cancer: network meta-analysis. Chirila, C; Colosia, A; Iyer, S; Kaye, JA; Ling, C; Mitra, D; Odom, D, 2017)	0.46
" Patients undergoing hematopoietic stem cell transplantation (HSCT) are exposed to various types of drugs, and understanding how these drugs interact is of the utmost importance."	( Development of an assay for cellular efflux of pharmaceutically active agents and its relevance to understanding drug interactions. Andersson, BS; Hassan, M; Valdez, BC, 2017)	0.46
" Aim of this study was to evaluate pasireotide alone and in combination with everolimus in patients with MTC."	( The antiproliferative effect of pasireotide LAR alone and in combination with everolimus in patients with medullary thyroid cancer: a single-center, open-label, phase II, proof-of-concept study. Aria, M; Camera, L; Chiofalo, MG; Colao, A; Del Prete, M; Faggiano, A; Ferolla, P; Fonti, R; Modica, R; Pezzullo, L; Severino, R; Vitale, G, 2018)	0.94
"To assess the tolerability, safety, pharmacokinetics and antitumor activities of lenvatinib, an oral inhibitor of multiple receptor tyrosine kinases, in combination with everolimus, an inhibitor of mammalian target of rapamycin, in Japanese patients with advanced or metastatic renal cell carcinoma after disease progression with vascular endothelial growth factor-targeted therapy."	( Lenvatinib in combination with everolimus in patients with advanced or metastatic renal cell carcinoma: A phase 1 study. Fujiwara, Y; Ikezawa, H; Matsubara, N; Naito, Y; Nakano, K; Namiki, M; Okude, T; Takahashi, S; Yusa, W, 2018)	0.96
", as a monotherapy or in combination with the known mechanistic target of rapamycin complex 1 (mTORC1) inhibitor, everolimus, against Caki-1 (Von Hippel-Lindau (VHL)+/+) and 786-O (VHL-/-) human RCC cells."	( Novel therapeutic roles of MC-4 in combination with everolimus against advanced renal cell carcinoma by dual targeting of Akt/pyruvate kinase muscle isozyme M2 and mechanistic target of rapamycin complex 1 pathways. Choi, HY; Chung, KH; De, U; Jeon, Y; Kim, HS; Kwak, JH; Lee, BM; Lee, HW; Lee, SJ; Lim, JE; Park, YJ; Rhyu, IJ; Son, JY; Tae, IH; Yoon, S, 2018)	0.94
" However, there is limited available data on Dmab toxicity in combination with AA therapies in patients with kidney cancer."	( Denosumab Toxicity When Combined With Anti-angiogenic Therapies on Patients With Metastatic Renal Cell Carcinoma: A GETUG Study. Albiges, L; Barthélémy, P; Bouleftour, W; Chevreau, C; Culine, S; Espenel, S; Fizazi, K; Gravis, G; Guillot, A; Houede, N; Joly, C; Mahammedi, H; Meriaux, E; Negrier, S; Oriol, M; Pouessel, D; Roubaud, G; Tartas, S; Tinquaut, F; Vassal, C, 2019)	0.51
"The incidence of ONJ was high in this real-life population of patients with mRCC treated with AA therapies combined with Dmab."	( Denosumab Toxicity When Combined With Anti-angiogenic Therapies on Patients With Metastatic Renal Cell Carcinoma: A GETUG Study. Albiges, L; Barthélémy, P; Bouleftour, W; Chevreau, C; Culine, S; Espenel, S; Fizazi, K; Gravis, G; Guillot, A; Houede, N; Joly, C; Mahammedi, H; Meriaux, E; Negrier, S; Oriol, M; Pouessel, D; Roubaud, G; Tartas, S; Tinquaut, F; Vassal, C, 2019)	0.51
" Current studies determined the OATP1B1/1B3-mediated drug-drug interaction (DDI) potential of mammalian target of rapamycin (mTOR) inhibitors, everolimus and sirolimus, using R-value and physiologically based pharmacokinetic models."	( Preincubation With Everolimus and Sirolimus Reduces Organic Anion-Transporting Polypeptide (OATP)1B1- and 1B3-Mediated Transport Independently of mTOR Kinase Inhibition: Implication in Assessing OATP1B1- and OATP1B3-Mediated Drug-Drug Interactions. Alam, K; Crowe, A; Ding, K; Farasyn, T; Hatley, O; Kanyo, J; Lam, TT; Neuhoff, S; Yue, W, 2019)	1.04
" The purpose of the VicTORia trial was to show superiority of everolimus in combination with vinorelbine versus vinorelbine monotherapy as second-line chemotherapy for patients with advanced HER2 negative breast cancer."	( VicTORia: a randomised phase II study to compare vinorelbine in combination with the mTOR inhibitor everolimus versus vinorelbine monotherapy for second-line chemotherapy in advanced HER2-negative breast cancer. Decker, T; Hagen, V; Jaehnig, P; Lerchenmüller, C; Marschner, N; Muendlein, A; Potthoff, K; Rauh, J; Schröder, H; Welt, A, 2019)	0.97
" In MPC/MTT spheroids, treatment with clinically relevant doses of BYL719 alone or in combination with everolimus was highly effective, leading to a significant shrinkage or even a complete collapse of the spheroids."	( Synergistic Highly Potent Targeted Drug Combinations in Different Pheochromocytoma Models Including Human Tumor Cultures. Aristizabal Prada, ET; Auernhammer, CJ; Bechmann, N; Beuschlein, F; Bornstein, SR; Eisenhofer, G; Fankhauser, M; Fassnacht, M; Favier, J; Gieldon, L; Goncalves, J; Grossman, AB; Klink, B; Knösel, T; Lauseker, M; Maurer, J; Nölting, S; Orth, M; Pacak, K; Rank, P; Reincke, M; Rubinstein, G; Spitzweg, C; Spöttl, G; William, D; Ziegler, CG, 2019)	0.73
"Everolimus (EVR) is often administered with cyclosporine A (CsA), according to an established protocol."	( Optimal dose of everolimus administered with tacrolimus in living donor kidney transplantation. Futamura, K; Goto, N; Hiramitsu, T; Ichimori, T; Narumi, S; Okada, M; Tomosugi, T; Watarai, Y, 2019)	2.3
"The mammalian target of rapamycin (mTOR) inhibitor, everolimus, in combination with reduced-exposure calcineurin inhibitor (CNI), has been demonstrated in clinical trials to have comparable efficacy in low-to-moderate immunological risk kidney transplant recipients to the Standard of Care, mycophenolic acid (MPA) in combination with standard-exposure CNI."	( Evidence-based practice: Guidance for using everolimus in combination with low-exposure calcineurin inhibitors as initial immunosuppression in kidney transplant patients. Berger, SP; Chadban, SJ; Citterio, F; Eisenberger, U; Henry, ML; Hesselink, DA; Kamar, N; Legendre, C; Oppenheimer, F; Pascual, J; Rigotti, P; Russ, GR; Sommerer, C; Srinivas, TR; Tedesco-Silva, H; Vincenti, F; Watarai, Y, 2019)	1.03
" We completed a phase I, dose-finding trial for the mTOR inhibitor everolimus combined with the HDAC inhibitor panobinostat in advanced clear cell renal cell carcinoma (ccRCC) patients."	( Phase I study of the mTOR inhibitor everolimus in combination with the histone deacetylase inhibitor panobinostat in patients with advanced clear cell renal cell carcinoma. Adra, N; Chintala, S; Damayanti, N; George, S; Pili, R; Wood, A, 2020)	1.07
" Results The maximum tolerated doses were determined to be vatalanib 1250 mg once daily or 750 mg twice daily in combination with everolimus 10 mg once daily."	( A phase I study of the VEGFR kinase inhibitor vatalanib in combination with the mTOR inhibitor, everolimus, in patients with advanced solid tumors. Adjei, AA; Croghan, GA; Dy, GK; Glockner, J; Hanson, LJ; Molina, JR; Qi, Y; Roos, MM; Tan, AD; Zhu, M, 2020)	0.98
"We aimed to evaluate the therapeutic effects of paclitaxel in combination with mTOR inhibitor everolimus on adriamycin-resistant breast cancer cell line MDA-MB-231 (MDA-MB-231/ADR)."	( Inhibitory effects of everolimus in combination with paclitaxel on adriamycin-resistant breast cancer cell line MDA-MB-231. Li, Q; Liu, P; Shi, C; Wang, X; Xu, T, 2020)	1.09
"To explore the efficacy and safety of everolimus combined with endocrine therapy in patients with hormone receptor (HR)-positive/human epidermal growth factor receptor 2 (HER-2)-negative advanced breast cancer."	( Efficacy of everolimus combined with endocrine therapy in HR-positive/HER-2-negativeadvanced breast cancer. Chen, C; Kong, F; Lu, J; Shan, H; Song, X; Wang, L; Yuan, H, )	0.78
" Of them, 54 patients were treated with everolimus combined with endocrine drugs (Everolimus group), while the other 54 patients underwent endocrine monotherapy (Control group)."	( Efficacy of everolimus combined with endocrine therapy in HR-positive/HER-2-negativeadvanced breast cancer. Chen, C; Kong, F; Lu, J; Shan, H; Song, X; Wang, L; Yuan, H, )	0.78
"Everolimus combined with endocrine therapy has significant clinical efficacy in patients with HR-positive/HER-2-negative advanced breast cancer, and can effectively improve the survival of patients with tolerable adverse reactions."	( Efficacy of everolimus combined with endocrine therapy in HR-positive/HER-2-negativeadvanced breast cancer. Chen, C; Kong, F; Lu, J; Shan, H; Song, X; Wang, L; Yuan, H, )	1.95
" However, the pharmacokinetic and pharmacodynamic information for EVL combined with TAC is limited."	( Pharmacodynamic Drug-Drug Interaction on Human Peripheral Blood Mononuclear Cells Between Everolimus and Tacrolimus at the Therapeutic Concentration Range in Renal Transplantation. Akashi, I; Akiyama, S; Hirano, T; Iwamoto, H; Kihara, Y; Konno, O; Oda, T; Okihara, M; Osato, S; Takeuchi, H; Tanaka, S; Unezaki, S; Yoshinaga, R, 2021)	0.84
"This case suggests that anterior and posterior spinal fusion combined with everolimus therapy can be a therapeutic option for GSD."	( Gorham-Stout Disease Resulting in Spinal Deformity Treated by Fusion Surgery Combined With Everolimus Therapy: A Case Report. Fujita, N; Matsumoto, M; Nagoshi, N; Nakamura, M; Nori, S; Okada, E; Suzuki, S; Toga, A; Tsuji, O; Watanabe, K; Yagi, M, 2021)	1.07
" The primary objective was to determine the maximum tolerated dose (MTD)/recommended dose for expansion (RDE) of ALP in combination with EVE and in combination with EVE and exemestane (EXE) and subsequently assess safety, preliminary efficacy and effect of ALP on the pharmacokinetics of EVE and determine the magnitude of the drug-drug interaction."	( Alpelisib in combination with everolimus ± exemestane in solid tumours: Phase Ib randomised, open-label, multicentre study. Ajipa, O; Andre, F; Beck, JT; Blumenstein, L; Curigliano, G; Donnet, V; Fazio, N; Hubner, RA; Jhaveri, K; Lahner, H; Li, Z; Martin, M; Maur, M; Tortora, G, 2021)	0.91
" There were no clinically relevant drug-drug interactions observed between ALP and EVE."	( Alpelisib in combination with everolimus ± exemestane in solid tumours: Phase Ib randomised, open-label, multicentre study. Ajipa, O; Andre, F; Beck, JT; Blumenstein, L; Curigliano, G; Donnet, V; Fazio, N; Hubner, RA; Jhaveri, K; Lahner, H; Li, Z; Martin, M; Maur, M; Tortora, G, 2021)	0.91
" Pharmacokinetics of ALP, EVE and EXE was largely unchanged in combination with each other."	( Alpelisib in combination with everolimus ± exemestane in solid tumours: Phase Ib randomised, open-label, multicentre study. Ajipa, O; Andre, F; Beck, JT; Blumenstein, L; Curigliano, G; Donnet, V; Fazio, N; Hubner, RA; Jhaveri, K; Lahner, H; Li, Z; Martin, M; Maur, M; Tortora, G, 2021)	0.91
" This study aimed to investigate a 1-year clinical follow-up of a prospective multicenter registry of HCR combined with non-saphenous vein graft surgical bypass and PCI using everolimus-eluting metallic stents (the PRIDE-METAL study)."	( Prospective multicenter registry of hybrid coronary artery revascularization combined with non-saphenous vein graft surgical bypass and percutaneous coronary intervention using everolimus eluting metallic stents (PRIDE-METAL study). Doi, H; Fujita, T; Fuku, Y; Fukui, T; Kinoshita, Y; Komiya, T; Kozuma, K; Okawa, Y; Shimokawa, T; Takanashi, S; Tobaru, T; Tsujita, K; Watanabe, Y, 2022)	1.11
" To this end, we investigated experimentally and assessed computationally the in vitro pharmacodynamic drug-drug interactions of the various dual and triple combinations to assess their subsequent combinatorial effects (synergistic/additive/antagonistic) in a HER2-therapy resistant BC cell line, JIMT-1."	( Experimental and computational assessment of the synergistic pharmacodynamic drug-drug interactions of a triple combination therapy in refractory HER2-positive breast cancer cells. Ait-Oudhia, S; Vaidya, TR, 2022)	0.72
" Four canine melanoma cell lines were treated in vitro with rapamycin and everolimus as sole treatment or combined with carboplatin."	( Investigation of the effects of mTOR inhibitors rapamycin and everolimus in combination with carboplatin on canine malignant melanoma cells. Bernard, S; Mutsaers, AJ; Poon, AC; Tam, PM, 2021)	1.09
"When combined with carboplatin chemotherapy, rapamycin or everolimus treatment was overall synergistic in reducing cell viability."	( Investigation of the effects of mTOR inhibitors rapamycin and everolimus in combination with carboplatin on canine malignant melanoma cells. Bernard, S; Mutsaers, AJ; Poon, AC; Tam, PM, 2021)	1.11
"Inhibition of mTOR by rapalogs, such as rapamycin and everolimus combined with carboplatin chemotherapy may have activity in canine melanoma."	( Investigation of the effects of mTOR inhibitors rapamycin and everolimus in combination with carboplatin on canine malignant melanoma cells. Bernard, S; Mutsaers, AJ; Poon, AC; Tam, PM, 2021)	1.11
" This case report indicated that remdesivir might interact with cytochrome P450 3A4 substrates, such as tacrolimus and everolimus, and elevate their blood concentrations under high inflammatory conditions."	( Drug-drug interaction between remdesivir and immunosuppressant agents in a kidney transplant recipient. Hirai, T; Inoue, T; Iwamoto, T; Mizuta, A; Nishikawa, K; Sasaki, T, 2022)	0.93
" 14 mg daily) in combination with everolimus (5 mg daily), following one prior vascular endothelial growth factor-targeted treatment."	( Health-Related Quality of Life Outcomes With Two Different Starting Doses of Lenvatinib in Combination With Everolimus for Previously Treated Renal Cell Carcinoma. Alekseev, B; Bennett, L; Bergerot, C; Castellano, D; Ciuleanu, T; Glen, H; Heng, D; Koralewski, P; Lyun Lee, J; O'Hara, K; Pal, S; Pan, J; Parnis, F; Puente, J; Stroyakovskiy, D; Sunela, K; Wang, J; Young Rha, S, 2023)	1.4
"The study intended to explore the effects and molecular mechanisms of imatinib combined with everolimus on AtT-20 cells in AtT-20 mouse pituitary tumors."	( Effects of Imatinib Combined With Everolimus on Mouse Pituitary Tumor Cell AtT-20. Lin, Y; Meng, L; Qu, X; Wang, W; Yang, J, 2023)	1.41
"Imatinib combined with everolimus can affect the AtT-20 cell cycle through the signaling pathway of the phosphatidylin-ositol-3-kinase (PI3K)/Akt/ protein kinase A (PKA) system and can inhibit cell proliferation and induce cell apoptosis."	( Effects of Imatinib Combined With Everolimus on Mouse Pituitary Tumor Cell AtT-20. Lin, Y; Meng, L; Qu, X; Wang, W; Yang, J, 2023)	1.5
" Three years and six months after surgery, she was administered octreotide LAR 30 mg per month in combination with everolimus."	( Everolimus in combination with octreotide LAR in thymic atypical carcinoid. Hagui, E; Haneda, H; Nakano, T; Okuda, K; Sakane, T, 2023)	2.56
" A single dose of everolimus 5 mg was well tolerated when administered with multiple doses of CBD."	( Pharmacokinetic Drug-Drug Interaction With Coadministration of Cannabidiol and Everolimus in a Phase 1 Healthy Volunteer Trial. Berwaerts, J; Chen, C; Critchley, D; Hyland, K; Tayo, B; Thai, C; Wray, L, 2023)	1.47
" Patients received a weekly intravenous infusion of xentuzumab (1000 mg) or placebo in combination with everolimus (10 mg/day orally) and exemestane (25 mg/day orally)."	( XENERA-1: a randomised double-blind Phase II trial of xentuzumab in combination with everolimus and exemestane versus everolimus and exemestane in patients with hormone receptor-positive/HER2-negative metastatic breast cancer and non-visceral disease. Baktash, N; Biyukov, T; Blau, S; Burris, HA; Cortes, J; Díaz-Redondo, T; García-Sáenz, JÁ; Hart, L; Jañez, NM; Joaquim, A; Lemieux, J; Massey, D; Morales, S; Neven, P; Rugo, HS; Schmid, P, 2023)	1.35
"While this study demonstrated that xentuzumab could be safely combined with everolimus and exemestane in patients with HR-positive/HER2-negative advanced breast cancer with non-visceral disease, there was no PFS benefit with the addition of xentuzumab."	( XENERA-1: a randomised double-blind Phase II trial of xentuzumab in combination with everolimus and exemestane versus everolimus and exemestane in patients with hormone receptor-positive/HER2-negative metastatic breast cancer and non-visceral disease. Baktash, N; Biyukov, T; Blau, S; Burris, HA; Cortes, J; Díaz-Redondo, T; García-Sáenz, JÁ; Hart, L; Jañez, NM; Joaquim, A; Lemieux, J; Massey, D; Morales, S; Neven, P; Rugo, HS; Schmid, P, 2023)	1.36
" In transplantation, therapeutic drug monitoring (TDM) is recommended due to the potential drug-drug interactions with chronic medications, which can affect everolimus pharmacokinetics."	( First reported double drug-drug interaction in a cancer renal patient under everolimus treatment: therapeutic drug monitoring and review of literature. Bleda-Perez, C; Del Valle-Celiz, PM; Fontanals-Martínez, S; Fort-Casamartina, E; Gonzalo-Diego, N; Muñoz-Sanchez, C; Otero-Torres, S; Prats-Jimenez, J; Rigo-Bonnin, RF, 2023)	1.34

Excerpt	Reference	Relevance
"The new immunosuppressive agent, SDZ-RAD, and its analog rapamycin were examined for intestinal absorption, metabolism, and bioavailability in Wistar rats."	( Absorption and intestinal metabolism of SDZ-RAD and rapamycin in rats. Bruelisauer, A; Crowe, A; Duerr, L; Guntz, P; Lemaire, M, 1999)	0.3
" The rate of absorption of everolimus was not altered by hepatic impairment on the basis of the maximum blood concentration (C(max)) and time to reach C(max) (t(max))."	( Influence of hepatic impairment on everolimus pharmacokinetics: implications for dose adjustment. Dilzer, SC; Figueiredo, J; Kovarik, JM; Lasseter, K; Reynolds, C; Rordorf, C; Sabia, HD; Zimmermann, H, 2001)	0.88
"To quantify the influence of a high-fat meal on the oral bioavailability of the immunosuppressant everolimus in a single-dose study in healthy subjects and to confirm the results in a small food-effect screening assessment in patients with renal transplants who were receiving multiple-dose everolimus."	( Effect of food on everolimus absorption: quantification in healthy subjects and a confirmatory screening in patients with renal transplants. Budde, K; Figueiredo, J; Golor, G; Hartmann, S; Kovarik, JM; Lison, A; Neumayer, HH; Rordorf, C, 2002)	0.87
" As part of the pediatric clinical development program, the relative bioavailability and food effect for the dispersible tablet were evaluated in healthy adult subjects as a prelude to characterizing the steady-state pharmacokinetics in pediatric kidney allograft recipients."	( Clinical development of an everolimus pediatric formulation: relative bioavailability, food effect, and steady-state pharmacokinetics. Berthier, S; Ettenger, R; Hoyer, PF; Kovarik, JM; Langholff, WK; Marion, AS; McMahon, L; Noe, A; Rordorf, C, 2003)	0.62
" Black patients may have lower bioavailability and/or higher clearance of everolimus compared with white patients."	( Pharmacokinetics of an everolimus-cyclosporine immunosuppressive regimen over the first 6 months after kidney transplantation. Berthier, S; Dantal, J; Hsu, CH; Kahan, BD; Kaplan, B; Kovarik, JM; McMahon, L; Rordorf, C; Silva, HT, 2003)	0.86
"The orally bioavailable rapamycin derivative RAD001 (everolimus) targets the mammalian target of rapamycin pathway and possesses potent immunosuppressive and anticancer activities."	( Antitumor efficacy of intermittent treatment schedules with the rapamycin derivative RAD001 correlates with prolonged inactivation of ribosomal protein S6 kinase 1 in peripheral blood mononuclear cells. Beuvink, I; Boulay, A; Haller, R; Heusser, C; Lane, HA; Marti, A; O'Reilly, T; Stephan, C; Stolz, B; Thomas, G; Tobler, S; Zilbermann, F; Zumstein-Mecker, S, 2004)	0.57
" Everolimus is more hydrophilic, exhibits a shorter elimination half-life (approximately 30 hours), and demonstrates greater relative bioavailability compared to sirolimus."	( The evolving experience using everolimus in clinical transplantation. Bia, MJ; Formica, RN; Friedman, AL; Lakkis, F; Lorber, KM; Lorber, MI; Smith, JD, 2004)	1.52
" Compared with sirolimus, everolimus has unique pharmacokinetic characteristics including greater bioavailability and a shorter half-life, allowing more rapid achievement of a steady state."	( Experience with everolimus. Augustine, JJ; Hricik, DE, 2004)	0.97
" Cyclosporine, tacrolimus, sirolimus and everolimus, however, have all been described to exhibit ethnicity-specific differences in bioavailability and/or dose-adjusted systemic exposure, although currently available reports are controversial for some of these drugs."	( Pharmacokinetics of immunosuppressants: a perspective on ethnic differences. Dirks, NL; Huth, B; Meibohm, B; Yates, CR, 2004)	0.59
" RAD001 (everolimus) is a potent, orally bioavailable inhibitor of the mTOR pathway."	( Future directions in the treatment of hormone-sensitive advanced breast cancer: the RAD001 (Everolimus)-letrozole clinical program. Lane, HA; Lebwohl, D, 2006)	0.97
" It is a proliferation signal inhibitor with an improved pharmacokinetic profile and bioavailability compared with sirolimus."	( Everolimus: an immunosuppressive agent in transplantation. Kobashigawa, JA; Patel, JK, 2006)	1.78
" The oral bioavailability value, as estimated with the PBPK, was 12% and was similar to the value obtained by non-compartmental analysis."	( Physiologically based pharmacokinetic (PBPK) modeling of everolimus (RAD001) in rats involving non-linear tissue uptake. Kawai, R; Laplanche, R; Meno-Tetang, GM, 2007)	0.58
" Closer surveillance for posttransplant infections and alterations in drug bioavailability and dosing as well as break-through immunologic responses are required."	( Out with the old, in with the new: immunosuppression minimization in children. Sarwal, MM, 2008)	0.35
" The bioavailability after intraportal and intraintestinal administration were 48."	( Effect of intestinal and hepatic first-pass extraction on the pharmacokinetics of everolimus in rats. Inui, K; Katsura, T; Masuda, S; Sato, E; Yano, I; Yokomasu, A, 2008)	0.57
" NVP-AEW541 is a new, orally bioavailable small molecule inhibitor of the insulin-like growth factor-1 receptor (IGF-1R)."	( Myeloma cell growth inhibition is augmented by synchronous inhibition of the insulin-like growth factor-1 receptor by NVP-AEW541 and inhibition of mammalian target of rapamycin by Rad001. Baumann, P; Franke, D; Hagemeier, H; Mandl-Weber, S; Schmidmaier, R, 2009)	0.35
" The objective of the study was to evaluate the anti-proliferative efficacy of the mTOR inhibitor, rapamycin, and its orally bioavailable analog RAD001 on the GH-secreting pituitary tumor GH3 and MtT/S cells and in human GH-secreting pituitary adenomas (GH-omas) in primary cell cultures."	( Mammalian target of rapamycin inhibitors rapamycin and RAD001 (everolimus) induce anti-proliferative effects in GH-secreting pituitary tumor cells in vitro. Cerovac, V; Cohen, ZR; Gorshtein, A; Hadani, M; Kendler, E; Rubinfeld, H; Shimon, I; Stalla, GK; Theodoropoulou, M, 2009)	0.59
"We conclude that in adult renal transplant recipients, EVL significantly decreases TAC oral bioavailability in a dose-dependent manner."	( Interaction between everolimus and tacrolimus in renal transplant recipients: a pharmacokinetic controlled trial. Brunet, M; Cabello, M; del Castillo, D; Fernández, AM; Grinyó, JM; Pallardó, L; Pascual, J, 2010)	0.68
" Those drugs have low and variable oral bioavailability that is increased when combined with cyclosporine or tacrolimus (TAC)."	( Sirolimus and everolimus intestinal absorption and interaction with calcineurin inhibitors: a differential effect between cyclosporine and tacrolimus. Boussera, B; Lamoureux, F; Marquet, P; Picard, N; Sauvage, FL, 2012)	0.74
" Everolimus was more effective than rapamycin in preventing diabetic nephropathy in vivo, which may be contributed to the fact that everolimus has better bioavailability and a higher oral absorption rate."	( Everolimus vs. rapamycin for treating diabetic nephropathy in diabetic mouse model. Chen, J; Cheng, L; Mao, X, 2011)	2.72
" However, the low water solubility and low bioavailability of everolimus have prevented its clinical development as an anticancer drug."	( Preparation and in vivo evaluation of liposomal everolimus for lung carcinoma and thyroid carcinoma. Iwase, Y; Maitani, Y, 2012)	0.87
" Temsirolimus has discerning features compared with other currently registered drugs, such as its intravenous administration route-providing predictable bioavailability and adherence to treatment-and potential benefit in nonclear cell histologies."	( The clinical potential of temsirolimus in second or later lines of treatment for metastatic renal cell carcinoma. Greil, R; Grünwald, V; Porta, C; Stenner-Liewen, F, 2013)	0.39
"Macrocycles are ideal in efforts to tackle "difficult" targets, but our understanding of what makes them cell permeable and orally bioavailable is limited."	( Macrocyclic drugs and clinical candidates: what can medicinal chemists learn from their properties? Giordanetto, F; Kihlberg, J, 2014)	0.4
"We used wild-type, Abcb1a/1b(-/-), Abcg2(-/-), Abcb1a/1b;Abcg2(-/-), and Cyp3a(-/-) mice to study everolimus oral bioavailability and brain accumulation."	( P-glycoprotein, CYP3A, and plasma carboxylesterase determine brain and blood disposition of the mTOR Inhibitor everolimus (Afinitor) in mice. Beijnen, JH; Cheung, KL; Durmus, S; Fukami, T; Schinkel, AH; Sparidans, RW; Tang, SC; van Vlijmen, BJ; Wagenaar, E; Yokoi, T, 2014)	0.83
" The physicochemical properties, drug release profile, and bioavailability of SD prepared by SW process were also compared to SD prepared by the conventional co-precipitation method."	( Improved oral absorption and chemical stability of everolimus via preparation of solid dispersion using solvent wetting technique. Jang, SW; Kang, MJ, 2014)	0.65
" In conclusion, oral intake of curcumin significantly decreased the bioavailability of EVL, a probe substrate of P-gp/CYP 3A4, mainly through marked activation on CYP 3A4."	( Oral intake of curcumin markedly activated CYP 3A4: in vivo and ex-vivo studies. Chao, PD; Hou, YC; Hsieh, YW; Huang, CY; Peng, YH; Yang, SY; Yu, CP, 2014)	0.4
" Data from large clinical trials have shown that the combination of everolimus , an orally bioavailable mTOR inhibitor with exemestane improves outcome of metastatic breast cancer resistant to non-steroidal aromatase inhibitors."	( Evaluating the pharmacokinetics and pharmacodynamics of everolimus for treating breast cancer. Awada, A; Barthélémy, P; Gombos, A, 2015)	0.9
" The pharmacokinetics, metabolism and bioavailability of EC0565 were studied in normal rats."	( Antiinflammatory Activity of a Novel Folic Acid Targeted Conjugate of the mTOR Inhibitor Everolimus. Cross, VA; Gehrke, MA; Hahn, SJ; Klein, PJ; Kleindl, PJ; Leamon, CP; Low, PS; Lu, Y; Parker, N; Santhapuram, HK; Stinnette, TW; Vaughn, JF; Vlahov, IR; Wang, K; Westrick, E; Wollak, K; You, F, 2015)	0.64
"The aims of this study were to improve in vitro dissolution property of poorly water-soluble everolimus (EVR) for enhanced bioavailability without using organic solvents and characterize the effects of microfluidization and freeze-drying on physicochemical properties of EVR nanosuspension and nanoparticle, respectively."	( Formulation of Nanoparticle Containing Everolimus Using Microfluidization and Freeze-Drying. Hwang, KM; Kang, SY; Kim, SH; Park, ES; Seo, JW; Seok, SH, 2016)	0.92
" Meanwhile, the pharmacokinetics study in vivo confirmed that the delivery of everolimus through the injection of the prodrug can overcome the low bioavailability of oral everolimus."	( Synthesis and evaluation of an injectable everolimus prodrug. Cai, Z; Wang, H; Yu, O; Zheng, S; Zheng, X; Zhu, T, 2017)	0.95
" BEZ235 systemic exposure increased in a dose-proportional manner while oral bioavailability was quite low, which may be related to gastrointestinal-specific toxicity."	( A Phase Ib Study of the Dual PI3K/mTOR Inhibitor Dactolisib (BEZ235) Combined with Everolimus in Patients with Advanced Solid Malignancies. Beg, MS; Desai, P; Fathallah, H; Karim, NA; Kozma, SC; Mercer, CA; Moorthy, G; Morris, JC; O'Gara, S; Olowokure, O; Rixe, O; Salkeni, MA; Thomas, G; Thomas, HE; Wise-Draper, TM, 2017)	0.68
"We found that formulation did not influence bioavailability and that use of >20 mg prednisolone daily increased everolimus clearance."	( A pharmacological rationale for improved everolimus dosing in oncology and transplant patients. Burger, DM; de Fijter, JW; Guchelaar, HJ; Moes, DJAR; Reinders, MEJ; Ter Heine, R; van Erp, NP; van Herpen, CM, 2018)	0.96
" There is growing evidence to suggest that the bioavailability of the potent pro-tumor function of FGFR2 is associated with thrombospondins (TSPs)."	( FGFR2 Promotes Gastric Cancer Progression by Inhibiting the Expression of Thrombospondin4 via PI3K-Akt-Mtor Pathway. Dai, Y; Huang, T; Li, P; Liu, D; Qiu, H; Sun, L; Wang, Y; Xiong, H; Yuan, X; Zou, M, 2018)	0.48
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."	( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019)	0.51
" Being water-insoluble, administration is restricted to the oral route, which results in a low bioavailability of <10%."	( Berunda Polypeptides Carrying Rapalogues Inhibit Tumor mTORC1 Better than Oral Everolimus. MacKay, JA; Peddi, S, 2020)	0.79
" The aim of this study was to develop a novel sublingual orodispersible film loading everolimus for improving patient compliance and enhancing oral bioavailability of EVR."	( Designing orodispersible films containing everolimus for enhanced compliance and bioavailability. Gao, S; Guan, R; Liu, H; Liu, Y; Ma, Y; Song, W; Yang, Y, 2020)	1.05
" Pharmacokinetic studies showed that loading into the sublingual orodispersible films significantly increased the oral bioavailability of EVR."	( Designing orodispersible films containing everolimus for enhanced compliance and bioavailability. Gao, S; Guan, R; Liu, H; Liu, Y; Ma, Y; Song, W; Yang, Y, 2020)	0.82
" Therefore, the aim of this study is to develop a topical nanomicellar formulation of an immunosuppressant drug, everolimus using Soluplus®, a grafted copolymer of polyvinyl caprolactam-polyvinylalcohol-polyethyleneglycol (PVCL-PVA-PEG) for improved permeation through ocular epithelia with minimal or no irritation resulting in enhanced ocular bioavailability at the posterior segments of the eye for the treatment of uveitis."	( A grafted copolymer-based nanomicelles for topical ocular delivery of everolimus: Formulation, characterization, ex-vivo permeation, in-vitro ocular toxicity, and stability study. Aqil, M; Mehra, N; Sultana, Y, 2021)	1.07
" We found that RCC cells are highly dependent on glutamine for proliferation, and this dependence strongly correlated with sensitivity to telaglenstat (CB-839), an investigational, first-in-class, selective, orally bioavailable GLS inhibitor."	( The glutaminase inhibitor telaglenastat enhances the antitumor activity of signal transduction inhibitors everolimus and cabozantinib in models of renal cell carcinoma. Chen, J; Dang, R; Emberley, E; Gross, M; Huang, T; Li, W; MacKinnon, A; Pan, A; Parlati, F; Singh, D; Sotirovska, N; Steggerda, SM; Wang, T, 2021)	0.83
" However, due to the low oral bioavailability and narrow response window of oral everolimus, a new delivery system is urgently needed to overcome the above problems."	( Tip-concentrated microneedle patch delivering everolimus for therapy of multiple sclerosis. Liu, H; Ren, Y; Song, W; Wang, N; Yang, Y, 2022)	1.21
" One phase II trial of the potent orally bioavailable mTOR inhibitor, everolimus, in combination with letrozole demonstrated an unprecedented clinical benefit rate (CBR) of 40% and high objective response rate (RR) of 32% in hormone agnostic endometrial cancers."	( Targeting the PI3K Pathway in Gynecologic Malignancies. Avila, M; Grinsfelder, MO; Pham, M; Westin, SN, 2022)	0.96
" Analogs of rapamycin were developed to improve its pharmacological properties, such as low oral bioavailability and a long half-life."	( Why Is Rapamycin Not a Rapalog? Kuerec, AH; Maier, AB, 2023)	0.91

Excerpt	Relevance	Reference
" in the range of the steep part of its dose-response relationship."	( The peripheral lymphocyte count predicts graft survival in DA to Lewis heterotopic heart transplantation treated with FTY720 and SDZ RAD. Baumlin, Y; Hof, A; Hof, RP; Nikolova, Z, 2000)	0.31
" Potential differences in cyclosporine dosing and pharmacokinetics at different levels of everolimus exposure were assessed in the context of ANOVA."	( Longitudinal assessment of everolimus in de novo renal transplant recipients over the first post-transplant year: pharmacokinetics, exposure-response relationships, and influence on cyclosporine. Boger, R; Cambon, N; Gerbeau, C; Kahan, BD; Kaplan, B; Kovarik, JM; Lorber, M; Rordorf, C; Rouilly, M; Winkler, M, 2001)	0.83
" For a 4-fold range of everolimus doses there were no differential effects on cyclosporine dosing or pharmacokinetics."	( Longitudinal assessment of everolimus in de novo renal transplant recipients over the first post-transplant year: pharmacokinetics, exposure-response relationships, and influence on cyclosporine. Boger, R; Cambon, N; Gerbeau, C; Kahan, BD; Kaplan, B; Kovarik, JM; Lorber, M; Rordorf, C; Rouilly, M; Winkler, M, 2001)	0.92
" Drug efficacy and potency was calculated based on dose-response curves of the drug-mediated decrease in CD4(+)/CD8alpha(+)/CD25(+) cells."	( Coexpression of CD4 and CD8alpha on rat T-cells in whole blood: a sensitive marker for monitoring T-cell immunosuppressive drugs. Diaz-Romero, J; Vogt, G; Weckbecker, G, 2001)	0.31
" There use allows a lower dosage for the calcineurin inhibitor."	( [Immunosuppression, ongoing clinical trials]. Rivalan, J, 2001)	0.31
" This suggested that, although the adult 12-hour dosing interval was appropriate for pediatric patients, they would require reduced dosing based on body size compared with adults."	( Safety and efficacy of TOR inhibitors in pediatric renal transplant recipients. Ettenger, RB; Grimm, EM, 2001)	0.31
" On two occasions, a pharmacokinetic profile was obtained over the dosing interval after drug administration under fasting conditions and after a high-fat meal in a randomized sequence."	( Effect of food on everolimus absorption: quantification in healthy subjects and a confirmatory screening in patients with renal transplants. Budde, K; Figueiredo, J; Golor, G; Hartmann, S; Kovarik, JM; Lison, A; Neumayer, HH; Rordorf, C, 2002)	0.65
" This is a lower therapeutic concentration limit when everolimus is used with conventionally dosed cyclosporine."	( Exposure-response relationships for everolimus in de novo kidney transplantation: defining a therapeutic range. Boger, R; Dantal, J; Kahan, BD; Kaplan, B; Kovarik, JM; Rordorf, C; Tedesco Silva, H; Vitko, S, 2002)	0.84
" Based on this information, pediatric patients will need a dose scaled down for body size, but can probably maintain the same twice-daily dosing schedule used in adults."	( Single-dose pharmacokinetics and tolerability of everolimus in stable pediatric renal transplant patients. Boger, R; Cambon, N; Ettenger, R; Hoyer, PF; Kovarik, JM; Lemire, J; Mahan, J; McMahon, L; Van Damme-Lombaerts, R; Webb, NA, 2002)	0.57
" Successful dosing was confirmed by measuring splenic weight."	( The rapamycin analogue SDZ RAD attenuates bleomycin-induced pulmonary fibrosis in rats. Chambers, RC; Egan, JJ; Goldsack, NR; Hasleton, PS; Howell, DC; Laurent, GJ; Marshall, RP; Simler, NR, 2002)	0.31
" The newest drugs to reach clinical evaluation, sirolimus and everolimus, have been studied in the context of concentration-controlled dosing and there is a good rationale for their measurement."	( Therapeutic drug monitoring of immunosuppressive drugs in kidney transplantation. Holt, DW, 2002)	0.56
" Steady-state concentration-time profiles in pediatric transplant patients receiving the dispersible tablet were comparable to those of adult patients receiving the conventional tablet when both were dosed to yield similar trough concentrations."	( Clinical development of an everolimus pediatric formulation: relative bioavailability, food effect, and steady-state pharmacokinetics. Berthier, S; Ettenger, R; Hoyer, PF; Kovarik, JM; Langholff, WK; Marion, AS; McMahon, L; Noe, A; Rordorf, C, 2003)	0.62
" Weight-adjusted dosing (mg/kg) does not appear warranted."	( Pharmacokinetics of an everolimus-cyclosporine immunosuppressive regimen over the first 6 months after kidney transplantation. Berthier, S; Dantal, J; Hsu, CH; Kahan, BD; Kaplan, B; Kovarik, JM; McMahon, L; Rordorf, C; Silva, HT, 2003)	0.63
" There were no trends in C(min) or AUC versus patient age when everolimus was dosed on a mg/m2 basis."	( Everolimus in pediatric de nova renal transplant patients. Ettenger, R; Hoyer, PF; Kovarik, JM; Lemire, J; Loirat, C; Mahan, J; Mayer, H; Mentser, M; Moeller, V; Niaudet, P; Offner, G; VanDamme-Lombaerts, R; Webb, NJ; Wehr, S, 2003)	2
"These data support the use of body surface area-adjusted dosing for everolimus in pediatric patients."	( Everolimus in pediatric de nova renal transplant patients. Ettenger, R; Hoyer, PF; Kovarik, JM; Lemire, J; Loirat, C; Mahan, J; Mayer, H; Mentser, M; Moeller, V; Niaudet, P; Offner, G; VanDamme-Lombaerts, R; Webb, NJ; Wehr, S, 2003)	2
" At 8 visits during the first 6 months after transplantation, we obtained 2,328 everolimus trough levels (Cmin) and 129 area-under-the-curve (AUC) profiles over the dosing interval in patients treated with everolimus; we collected 3,258 cyclosporine trough concentrations and 174 profiles in all 3 treatment arms."	( Everolimus in de novo cardiac transplantation: pharmacokinetics, therapeutic range, and influence on cyclosporine exposure. Dorent, R; Eisen, H; Hsu, CH; Kovarik, JM; Mancini, D; Rordorf, C; Rouilly, M; Vigano, M, 2003)	1.99
"We quantified the influence of delayed initiation of cyclosporine on everolimus pharmacokinetics in order to provide dosing guidance for kidney transplant patients."	( Influence of delayed initiation of cyclosporine on everolimus pharmacokinetics in de novo renal transplant patients. Bettoni-Ristic, O; Civati, G; Dantal, J; Kovarik, JM; Rizzo, G; Rordorf, C; Rouilly, M, 2003)	0.81
" The synergistic effect allows a dosage reduction that decreases adverse effects."	( Clinical pharmacokinetics of everolimus. Kirchner, GI; Manns, MP; Meier-Wiedenbach, I, 2004)	0.61
" Everolimus dosing was adjusted to maintain a minimum trough level of 3 ng/mL."	( Everolimus with optimized cyclosporine dosing in renal transplant recipients: 6-month safety and efficacy results of two randomized studies. Alves Filho, G; Bernhardt, P; Bourbigot, B; Cambi, V; Campbell, S; Civati, G; Cretin, N; Eris, J; Esmeraldo, R; Garcia, VD; Geissler, J; Haas, T; Jappe, A; Leone, J; Magee, JC; Pascual, J; Rigotti, P; Tedesco, H; Vitko, S; Whelchel, J, 2004)	2.68
" However, optimal cyclosporine exposure can now be achieved through monitoring of cyclosporine levels 2 hours after dosing (C(2) monitoring)."	( Optimizing the immunosuppressive regimen in heart transplantation. Eisen, H; Ross, H, 2004)	0.32
" Cyclosporine dosing began on average at 274 +/- 78 mg bid, was down-titrated in months 2-3 from 181 +/- 80 mg to 81 +/- 33 mg bid, and stabilized at 70 +/- 26 mg bid thereafter."	( Everolimus therapeutic concentration range defined from a prospective trial with reduced-exposure cyclosporine in de novo kidney transplantation. Bizot, MN; Civati, G; Geissler, J; Kovarik, JM; Pascual, J; Schmidli, H; Tedesco, H, 2004)	1.77
"The aims of the current study were to determine whether therapeutic drug monitoring (TDM) might benefit kidney transplant recipients receiving everolimus, and to establish dosage recommendations when everolimus is used in combination with cyclosporine and corticosteroids."	( Therapeutic drug monitoring for everolimus in kidney transplantation using 12-month exposure, efficacy, and safety data. Kovarik, J; Li, Y; Lorber, MI; Mayer, HW; Ponticelli, C; Schmidli, H; Whelchel, J, 2005)	0.81
" The objective of this randomized, double-blind, placebo-controlled, dose-escalating Phase 1 study was to evaluate the pharmacokinetic profile of different dosing regimens of everolimus."	( Pharmacokinetics of the immunosuppressant everolimus in maintenance renal transplant patients. Budde, K; Fritsche, L; Glander, P; Neumayer, HH; Slowinski, T; Waiser, J, 2005)	0.79
" In everolimus-treated patients, mean increases in cyclosporine AUC0-12 ranged from 7% to 43%, which were not significantly different across all dosing cohorts including placebo."	( Influence of everolimus on steady-state pharmacokinetics of cyclosporine in maintenance renal transplant patients. Budde, K; Dantal, J; Fauchald, P; Fritsche, L; Lehne, G; Lison, A; Neumayer, HH; Renders, L; Soulillou, JP; Winkler, M, 2005)	1.26
"All randomised controlled trials (RCTs) and quasi-RCTs where drug regimens containing TOR-I were compared to alternative drug regimens in the immediate post-transplant period were included, without age restriction, dosage or language of report."	( Target of rapamycin inhibitors (TOR-I; sirolimus and everolimus) for primary immunosuppression in kidney transplant recipients. Chapman, JR; Craig, JC; Lee, VW; Webster, AC, 2006)	0.58
" Everolimus has shown to reduce acute cellular rejection and may allow CsA dosage reduction."	( Everolimus and reduced cyclosporine trough levels in maintenance heart transplant recipients. Prenner, G; Schwarz, M; Schweiger, M; Stadlbauer, V; Stiegler, P; Tscheliessnigg, K; Wasler, A, 2006)	2.69
"CsA trough levels and dosage can be significantly reduced in combination with Everolimus without higher rejection rates and with stable kidney function in oHTX patients."	( Everolimus and reduced cyclosporine trough levels in maintenance heart transplant recipients. Prenner, G; Schwarz, M; Schweiger, M; Stadlbauer, V; Stiegler, P; Tscheliessnigg, K; Wasler, A, 2006)	2
" A reduction in MPA dosage at the time of conversion may be necessary to prevent over-immunosuppression."	( Conversion to everolimus in maintenance patients--current clinical strategies. Pohanka, E, 2006)	0.69
"9 ng/mL and area under the curve over a dosing interval (AUC) was 132 +/- 56 ng x h/mL."	( Differential pharmacokinetic interaction of tacrolimus and cyclosporine on everolimus. Curtis, JJ; Hricik, DE; Kovarik, JM; Pescovitz, MD; Scantlebury, V; Vasquez, A, 2006)	0.56
" Basiliximab allows for utilization of lower doses of everolimus with reduced dosing of Neoral)."	( 12-month safety and efficacy of everolimus with reduced exposure cyclosporine in de novo renal transplant recipients. Alves-Filho, G; Bourbigot, B; Cambi, V; Campbell, S; Civati, G; Eris, J; Esmeraldo, R; Garcia, VD; Haas, T; Leone, J; Magee, JC; Pascual, J; Rigotti, P; Tedesco-Silva, H; Vitko, S; Whelchel, J, 2007)	0.87
" TDM of whole-blood concentrations is mandatory for everolimus (ERL) dosage individualisation."	( Comparison of fluorescent polarization immunoassay (FPIA) versus HPLC to measure everolimus blood concentrations in clinical transplantation. Fruehwirth, F; Halwachs-Baumann, G; Khoschsorur, G; Stettin, M; Zelzer, S, 2007)	0.82
"Moderate dosage of everolimus inhibits cystogenesis in Han:SPRD rats."	( Everolimus retards cyst growth and preserves kidney function in a rodent model for polycystic kidney disease. Le Hir, M; Serra, AL; Wackerle-Men, Y; Wahl, PR; Wu, M; Wuthrich, RP, 2007)	2.11
" The results were evaluated by two-way analysis of variance followed by post-hoc tests, and nonlinear regression analysis for dose-response rates."	( Everolimus and mycophenolate mofetil sensitize human pancreatic cancer cells to gemcitabine in vitro: a novel adjunct to standard chemotherapy? Dillmann, S; Henne-Bruns, D; Keller, F; Klug, F; Mayer, JM; Stracke, S; Tuncyurek, P, 2007)	1.78
"5 mg/m2 in cohorts of three to six patients per dosage level."	( Phase I study of everolimus in pediatric patients with refractory solid tumors. Broniscer, A; Fouladi, M; Furman, WL; Gilbertson, RJ; Houghton, PJ; Laningham, F; Luckett, I; Molina, K; O'Shaughnessy, MA; Spunt, SL; Stewart, CF; Wu, J, 2007)	0.68
" It requires blood concentration-guided dosing and is extensively metabolized."	( Crossreactivity of isolated everolimus metabolites with the Innofluor Certican immunoassay for therapeutic drug monitoring of everolimus. Arabshahi, L; Boyd, J; Christians, U; Haschke, M; Marbach, P; Roberts, M; Strom, T, 2007)	0.63
" A growing body of evidence finds that the selection and dosing of immunosuppressive therapies can have great influence on long-term transplantation outcomes."	( Proliferation signal inhibitors in transplantation: questions at the cutting edge of everolimus therapy. Albanell, J; Arns, WA; Campistol, JM; Chapman, JR; Eisen, H; Frigerio, M; Lehmkuhl, H; Marcen, R; Morris, R; Nashan, B; Pascual, J; Pohanka, E; Segovia, J; Valantine, H; Zuckermann, A, 2007)	0.56
" Plasma trough levels of everolimus were determined on a weekly basis before dosing during the first 4 weeks."	( Dose- and schedule-dependent inhibition of the mammalian target of rapamycin pathway with everolimus: a phase I tumor pharmacodynamic study in patients with advanced solid tumors. Baselga, J; Burris, H; Calvo, E; Dimitrijevic, S; Hazell, K; Jones, S; Judson, I; Lane, HA; Lebwohl, D; Macarulla, T; Martinelli, E; Ramon y Cajal, S; Ramos, FJ; Rojo, F; Shand, N; Stumm, M; Tabernero, J; Tang, P; Vidal, L; Zoellner, U, 2008)	0.87
" A dosage of 10 mg/d or 50 mg/wk is recommended for further development."	( Dose- and schedule-dependent inhibition of the mammalian target of rapamycin pathway with everolimus: a phase I tumor pharmacodynamic study in patients with advanced solid tumors. Baselga, J; Burris, H; Calvo, E; Dimitrijevic, S; Hazell, K; Jones, S; Judson, I; Lane, HA; Lebwohl, D; Macarulla, T; Martinelli, E; Ramon y Cajal, S; Ramos, FJ; Rojo, F; Shand, N; Stumm, M; Tabernero, J; Tang, P; Vidal, L; Zoellner, U, 2008)	0.57
"To identify the optimal regimen and dosage of the oral mammalian target of rapamycin inhibitor everolimus (RAD001)."	( Phase I pharmacokinetic and pharmacodynamic study of the oral mammalian target of rapamycin inhibitor everolimus in patients with advanced solid tumors. Brock, C; Burris, HA; Faivre, S; Hazell, K; Jones, S; Judson, I; Kovarik, JM; Lane, HA; O'Donnell, A; Papadimitrakopoulou, V; Raymond, E; Rea, D; Shand, N; Zoellner, U, 2008)	0.78
" PD data prompted investigation of 50 and 70 mg weekly and daily dosing at 5 and 10 mg."	( Phase I pharmacokinetic and pharmacodynamic study of the oral mammalian target of rapamycin inhibitor everolimus in patients with advanced solid tumors. Brock, C; Burris, HA; Faivre, S; Hazell, K; Jones, S; Judson, I; Kovarik, JM; Lane, HA; O'Donnell, A; Papadimitrakopoulou, V; Raymond, E; Rea, D; Shand, N; Zoellner, U, 2008)	0.56
"Metronomic dosing of cytotoxic drugs such as cyclophosphamide has shown anti-angiogenic activity, most likely by inducing hypoxia in tumors."	( Everolimus (RAD001) and anti-angiogenic cyclophosphamide show long-term control of gastric cancer growth in vivo. Cejka, D; Fuereder, T; Preusser, M; Sieghart, W; Strommer, S; Wacheck, V; Werzowa, J; Woehrer, A, 2008)	1.79
" Especially, clinically relevant immunosuppressive drug interactions require prompt identification, intensified monitoring of drug concentrations and adequate dosing responses."	( Influence of interactions between immunosuppressive drugs on therapeutic drug monitoring. Kuypers, DR, 2008)	0.35
" Of note, prompt reduction of the everolimus dosage since the first azole coadministration, coupled with intensive therapeutic drug monitoring, represented a useful strategy to prevent drug overexposure."	( Pharmacokinetic interaction between everolimus and antifungal triazoles in a liver transplant patient. Adani, GL; Baccarani, U; Baraldo, M; Cojutti, P; Franceschi, L; Furlanut, M; Londero, A; Pea, F; Tavio, M; Viale, P, 2008)	0.9
"We studied 56 HT patients who sequentially received PSIs to either withdraw (77%) or reduce the dosage of a calcineurin inhibitor; 42 received everolimus (EVE) and 14 sirolimus (SRL)."	( Tolerance profile of the proliferation signal inhibitors everolimus and sirolimus in heart transplantation. Agüero, J; Almenar, L; Martínez-Dolz, L; Moro, JA; Salvador, A; Sánchez-Lázaro, I, 2008)	0.79
" Closer surveillance for posttransplant infections and alterations in drug bioavailability and dosing as well as break-through immunologic responses are required."	( Out with the old, in with the new: immunosuppression minimization in children. Sarwal, MM, 2008)	0.35
" This phase 2 study assessed the efficacy of daily oral dosing with everolimus in patients with RCC."	( A phase 2 study with a daily regimen of the oral mTOR inhibitor RAD001 (everolimus) in patients with metastatic clear cell renal cell cancer. Amato, RJ; Giessinger, S; Jac, J; Saxena, S; Willis, JP, 2009)	0.82
" These data show that a larger dosage is needed for everolimus than sirolimus to maintain the same trough blood concentration."	( Larger dosage required for everolimus than sirolimus to maintain same blood concentration in two pancreatic islet transplant patients with tacrolimus. Inui, K; Iwanaga, Y; Katsura, T; Masuda, S; Matsumoto, S; Okitsu, T; Sato, E; Shimomura, M; Uemoto, S; Yano, I, 2009)	0.9
" Tacrolimus was dosed seeking a trough blood level of 8 to 10 ng/mL by month 3 and 5 to 8 ng/mL thereafter."	( Prospective clinical trial comparing two immunosuppressive regimens, tacrolimus and mycophenolate mofetil versus everolimus and low-dose cyclosporine, in de novo renal transplant recipients: results at 6 months follow-up. Castagneto, M; Citterio, F; Delreno, F; Favi, E; Gargiulo, A; Romagnoli, J; Spagnoletti, G, 2009)	0.56
" However, considering the wide ranges found for the prediction error of sirolimus and everolimus concentrations, the clinical relevance of this dosing model is weak."	( Sirolimus and everolimus clearance in maintenance kidney and liver transplant recipients: diagnostic efficiency of the concentration/dose ratio for the prediction of trough steady-state concentrations. Bouzas, L; Hermida, J; Tutor, JC, 2010)	0.94
" Cyclosporine or tacrolimus dosage was reduced by 80% (group 1, n = 10) or discontinued (group 2, n = 10)."	( Renal function outcomes in kidney transplant recipients after conversion to everolimus-based immunosuppression regimen with CNI reduction or elimination. Alberú, J; Cataneo-Dávila, A; Correa-Rotter, R; Zúñiga-Varga, J, 2009)	0.58
" Modelling of the PTK/ZK dose-response curve in this model suggested that any effect of everolimus on the PK of PTK/ZK was unlikely to affect efficacy."	( Everolimus and PTK/ZK show synergistic growth inhibition in the orthotopic BL16/BL6 murine melanoma model. Brueggen, J; Lane, HA; Littlewood-Evans, A; McSheehy, PM; O'Reilly, T; Schnell, C; Wood, JM, 2011)	2.03
" Single dosing of everolimus is possible and safe and may achieve better patient compliance to multiple-drug immunosuppressive therapy."	( Conversion of stable kidney transplant recipients from a twice-daily to once-daily everolimus regimen. Bernini, M; Carmellini, M; Collini, A; Ruggieri, G, 2010)	0.92
" Therefore, we investigated whether two commonly used therapeutic drug monitoring methods for everolimus were in agreement and to what extent their differences could lead to differences in dosage advice."	( Liquid chromatography-tandem mass spectrometry outperforms fluorescence polarization immunoassay in monitoring everolimus therapy in renal transplantation. de Fijter, JW; den Hartigh, J; Guchelaar, HJ; Moes, DJ; Press, RR, 2010)	0.79
" Specifically, the use of FPIA can lead to clinically relevant differences in everolimus dosage advice and higher intrapatient variability."	( Liquid chromatography-tandem mass spectrometry outperforms fluorescence polarization immunoassay in monitoring everolimus therapy in renal transplantation. de Fijter, JW; den Hartigh, J; Guchelaar, HJ; Moes, DJ; Press, RR, 2010)	0.8
" In these conditions, use of an equivalent dosage is of particular importance."	( Relationship between everolimus blood concentration assessed using the Innofluor Certican Fluorescence Polarization Immunoassay and the Architect i System sirolimus chemiluminescent microparticle immunoassay. Carvalho, C; Coentrão, L; Oliveira, JG; Pestana, MI; Sampaio, S, 2010)	0.68
" 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)	0.61
"Human T-cell lymphoma cell lines Hut-78 and Jurkat were treated with increasing doses of everolimus, alone or in combination with doxorubicin, etoposide, vincristine, or bortezomib, using different dosing schedules."	( Schedule-dependent inhibition of T-cell lymphoma cells by cotreatment with the mTOR inhibitor everolimus and anticancer drugs. He, XX; Huang, JJ; Huang, Y; Li, ZM; Lin, TY; Tian, Y; Xiao, J, 2012)	0.82
" With certain dosing schedules, everolimus showed synergism with doxorubicin, etoposide, and bortezomib, but antagonism with vincristine."	( Schedule-dependent inhibition of T-cell lymphoma cells by cotreatment with the mTOR inhibitor everolimus and anticancer drugs. He, XX; Huang, JJ; Huang, Y; Li, ZM; Lin, TY; Tian, Y; Xiao, J, 2012)	0.88
" CNI dosage was progressively reduced until discontinuation."	( Tolerability of everolimus-based immunosuppression in maintenance liver transplant recipients. Adham, M; Boillot, O; Dumortier, J; Gagnieu, MC; Giostra, E; Guillaud, O; Mentha, G; Morard, I; Morelon, E; Vallin, M, )	0.48
" Although treatment-associated AEs are common, the majority of AEs reported during clinical trial experiences were grade 1 or 2 in severity and manageable with intervention in the form of supportive measures and/or dosage modification."	( Treatment-associated adverse event management in the advanced renal cell carcinoma patient treated with targeted therapies. Ravaud, A, 2011)	0.37
" Pulsed immunosuppressive dosing can lessen these risks."	( Ten-month laryngeal allograft survival with use of pulsed everolimus and anti-alphabeta T-cell receptor antibody immunosuppression. Dan, O; Khariwala, SS; Lott, DG; Russell, JO; Strome, M, 2011)	0.61
" Short-term perioperative therapy followed by pulsed, tapered dosing is a viable alternative to traditional regimens and may decrease associated risks."	( Ten-month laryngeal allograft survival with use of pulsed everolimus and anti-alphabeta T-cell receptor antibody immunosuppression. Dan, O; Khariwala, SS; Lott, DG; Russell, JO; Strome, M, 2011)	0.61
" The primary end points were determination of a safe dosage of everolimus (phase 1) and progression-free survival (PFS) at 24 weeks (phase 2)."	( Phase 1/2 study of everolimus in advanced hepatocellular carcinoma. Abrams, TA; Blaszkowsky, LS; Borger, DR; Clark, JW; Fuchs, CS; Iafrate, AJ; Jors, KR; Kwak, EL; Meyerhardt, JA; Miksad, R; Muzikansky, A; Ryan, DP; Schrag, D; Zheng, H; Zhu, AX, 2011)	0.94
" The CSA dosage was reduced by 50%."	( Everolimus plus dosage reduction of cyclosporine in cardiac transplant recipients with chronic kidney disease: a two-year follow-up study. Börgermann, J; Fuchs, U; Gummert, JF; Hakim-Meibodi, K; Schulz, U; Zittermann, A, 2011)	1.81
" CMV data from 2004 de novo RTx recipients from three-randomized, prospective, EVR studies A2309 (N = 833), B201 (N = 588) and B251 (N = 583) were retrospectively analyzed to identify differences between two EVR dosing groups and MPA."	( Cytomegalovirus incidence between everolimus versus mycophenolate in de novo renal transplants: pooled analysis of three clinical trials. Brennan, DC; Legendre, C; Mange, K; McCague, K; Patel, D; Shihab, FS; Wiland, A, 2011)	0.65
" Still, there is no consensus considering the recommended dosing and the therapeutic range of MPA."	( Monitoring of mycophenolic acid and kidney function during combined immunosuppressive therapy. Asztalos, L; Ivády, G; Kappelmayer, J; Kovács, AM; Oláh, AV; Varga, E; Varga, J, 2011)	0.37
" Cell growth and proliferation of PC3(res) was similar to that of PC3(par), and late apoptosis increased in PC3(par) but decreased in PC3(res) following treatment with low dosed everolimus."	( The cdk1-cyclin B complex is involved in everolimus triggered resistance in the PC3 prostate cancer cell line. Bartsch, G; Blaheta, RA; Haferkamp, A; Harder, S; Hudak, L; Juengel, E; Kurosch, M; Makarević, J; Tsaur, I; Wiesner, C, 2011)	0.83
"The coadministration of AEE788 and RAD001 in glioblastoma patients caused a clinically significant thrombocytopenia and a higher-than-expected RAD001 area under the curve concentration when dosed at 200 and 5 mg/day, respectively."	( Pharmacokinetic drug interaction between AEE788 and RAD001 causing thrombocytopenia in patients with glioblastoma. Alfred Yung, WK; Cloughesy, T; Conrad, C; DiLea, C; Dugan, M; Huang, J; Maes, A; Mietlowski, W; Reardon, DA; Rich, J; Yung, L, 2012)	0.38
" The first 2 patients developed a dose-limiting toxicity (neutropenic infection), prompting a mandatory dose reduction and PK evaluation of both everolimus and docetaxel for patients enrolled in subsequent dosing cohorts."	( A phase 1 study of weekly everolimus (RAD001) in combination with docetaxel in patients with metastatic breast cancer. Booser, D; Brewster, A; Cristofanilli, M; Ensor, J; Giordano, SH; Gladish, G; Gonzalez-Angulo, AM; Hortobagyi, GN; Moore, J; Moulder, S; Murray, JL; Rivera, E; Tran, HT, 2012)	0.88
"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)	0.99
" There have also been no reports on the increased risk of tuberculosis reactivation after an introduction of a PSI, and experience with everolimus dosing during antituberculosis treatment is very limited."	( Pulmonary embolism and reactivation of tuberculosis during everolimus therapy in a kidney transplant recipient. Fijałkowska-Morawska, JB; Jagodzińska, M; Nowicki, M, )	0.58
"Taxanes remain first line chemotherapy in management of metastatic breast cancer and have a key role in epithelial ovarian cancer, with increasingly common use of weekly paclitaxel dosing regimens."	( Paclitaxel resistance is associated with switch from apoptotic to autophagic cell death in MCF-7 breast cancer cells. Ajabnoor, GM; Coley, HM; Crook, T, 2012)	0.38
" This dosing regimen has an acceptable safety and tolerability profile and appears to have moderate the clinical activity in refractory tumors."	( A phase I study of bevacizumab, everolimus and panitumumab in advanced solid tumors. Alvarez-Secord, A; Anderson, EL; Bendell, JC; Blobe, GC; Gockerman, J; Hurwitz, HI; Meadows, KL; Morse, MA; Ready, NE; Riedel, RF; Starodub, AN; Uronis, HE; Vlahovic, G; Zafar, SY, 2012)	0.66
"A reduction in CNI dosage may lead to a decrease in the occurrence of post-transplant malignancy."	( Effect of immunosuppressive drugs on spontaneous DNA repair in human peripheral blood mononuclear cells. Gafter, U; Gafter-Gvili, A; Herman-Edelstein, M; Malachi, T; Ori, Y; Rozen-Zvi, B; Zingerman, B, 2012)	0.38
" We have developed a model of tumor growth dynamics utilizing serial measurements of the sum of the longest tumor diameters (SLD) from individual RECORD-1 patients to define the dose-response relationship of everolimus."	( Dynamic tumor modeling of the dose-response relationship for everolimus in metastatic renal cell carcinoma using data from the phase 3 RECORD-1 trial. Carter, AA; Chiparus, O; Hollaender, N; Kim, H; Motzer, RJ; Sarr, C; Stein, A; Wang, W, 2012)	0.81
" This allows evaluation of how an actual dosing history and individual covariates impact on the observed drug effect, and offers the possibility of predicting clinical observations as a function of time."	( Dynamic tumor modeling of the dose-response relationship for everolimus in metastatic renal cell carcinoma using data from the phase 3 RECORD-1 trial. Carter, AA; Chiparus, O; Hollaender, N; Kim, H; Motzer, RJ; Sarr, C; Stein, A; Wang, W, 2012)	0.62
"In this pharmacodynamic model of tumor response, everolimus more effectively shrinks target lesions in mRCC when dosed 10 mg daily versus 5 mg daily, although a 5-mg dose still shows an antitumor effect."	( Dynamic tumor modeling of the dose-response relationship for everolimus in metastatic renal cell carcinoma using data from the phase 3 RECORD-1 trial. Carter, AA; Chiparus, O; Hollaender, N; Kim, H; Motzer, RJ; Sarr, C; Stein, A; Wang, W, 2012)	0.87
" Estimated oral clearances of IT decreased on average by 50%, requiring reduced dosing regimens."	( Practical management of boceprevir and immunosuppressive therapy in liver transplant recipients with hepatitis C virus recurrence. Antonini, TM; Barau, C; Bonhomme-Faivre, L; Coilly, A; Duclos-Vallée, JC; Furlan, V; Noël, C; Roche, B; Roque-Afonso, AM; Samuel, D; Taburet, AM, 2012)	0.38
" However, the newer targeted anticancer therapies have different pharmacokinetic (PK) and dosing characteristics compared with traditional cytotoxic drugs, making it possible to estimate the steady-state drug exposure with a single trough-level measurement."	( Evidence for therapeutic drug monitoring of targeted anticancer therapies. Balakrishnar, B; Clements, A; Gao, B; Gurney, H; Wong, M; Yeap, S, 2012)	0.38
"Patients with metastatic renal cell carcinoma refractory to vascular endothelial growth factor receptor-tyrosine kinase inhibitor received everolimus (10 mg once daily), with dosing interruption or modifications allowed for toxicity."	( Safety of everolimus by treatment duration in patients with advanced renal cell cancer in an expanded access program. Anak, O; Bahl, A; Bavbek, S; Bracarda, S; Grünwald, V; Karakiewicz, P; Kim, D; Ou, YC; Panneerselvam, A; Rha, SY; van den Eertwegh, AJ, 2013)	0.99
" The aim of this article is to propose recommendations for the use of everolimus in lung transplant recipients, including indications, dosing schedules and the use of concomitant immunosuppression."	( Recommendations on the use of everolimus in lung transplantation. Borro, JM; Cifrian, JM; de la Torre, M; de Pablo, A; Laporta, R; Monforte, V; Román, A; Santos, F; Solé, A; Ussetti, P; Zurbano, F, 2013)	0.91
" Everolimus was orally dosed at 10 mg daily."	( A phase II study of bevacizumab and everolimus as treatment for refractory metastatic renal cell carcinoma. Barbeau, S; Harshman, LC; McMillian, A; Srinivas, S, 2013)	1.58
" In every case, we recommend to start the selected targeted agents at standard dosage and to pursue therapy as long as possible because the control of disease should be the primary endpoint for the management of mRCC."	( Management of metastatic renal cell carcinoma progressed after sunitinib or another antiangiogenic treatment. Cortesi, E; Iacovelli, R; Mezi, S; Naso, G; Palazzo, A; Pellegrino, D; Trenta, P, 2014)	0.4
"The goal of this study was to assess the pharmacokinetics and safety of everolimus in healthy volunteers with normal hepatic function and patients with mild (Child-Pugh class A), moderate (Child-Pugh class B), and severe (Child-Pugh class C) hepatic impairment in otherwise good health to inform dosing in the clinical setting."	( Effects of hepatic impairment on the pharmacokinetics of everolimus: a single-dose, open-label, parallel-group study. Anak, O; Bouillaud, E; Kobalava, Z; Kunz, T; Paquet, T; Peveling-Oberhag, J; Sellami, D; Urva, S; Yong, WP; Zeuzem, S, 2013)	0.87
" Pharmacokinetically-directed dosing protocols of everolimus and irinotecan were established and used to assess the in vivo antitumor effects of the agents."	( Utilization of quantitative in vivo pharmacology approaches to assess combination effects of everolimus and irinotecan in mouse xenograft models of colorectal cancer. Bradshaw-Pierce, EL; Eckhardt, SG; Gustafson, DL; Kulikowski, G; Merz, AL; Pitts, TM; Selby, H; Serkova, NJ; Weekes, CD, 2013)	0.86
" Combination effects of everolimus and irinotecan were determined in CRC xenograft models using clinically-relevant dosing protocols."	( Utilization of quantitative in vivo pharmacology approaches to assess combination effects of everolimus and irinotecan in mouse xenograft models of colorectal cancer. Bradshaw-Pierce, EL; Eckhardt, SG; Gustafson, DL; Kulikowski, G; Merz, AL; Pitts, TM; Selby, H; Serkova, NJ; Weekes, CD, 2013)	0.92
" Eighty rats were randomly divided into the sham-operated group (n = 20), injury group (n = 20), low dosage of everolimus group (n = 20), and high dosage of everolimus group (n = 20)."	( Oral everolimus inhibits intimal proliferation in injured carotid artery in rats. Feng, RS; Ning, HJ; Shen, DL; Wang, XF; Zhang, JY; Zhao, XY, 2013)	1.12
" The effect depended on dosage and was associated with the reduction of phosphorylation of P70S6K and the eIF-4E expression level."	( Oral everolimus inhibits intimal proliferation in injured carotid artery in rats. Feng, RS; Ning, HJ; Shen, DL; Wang, XF; Zhang, JY; Zhao, XY, 2013)	0.9
" Clinical awareness and early identification of such AEs by oncology nurses are essential to dosing (interruptions, reduction, and treatment discontinuation); quality of life; and, ultimately, patient outcomes."	( Management of adverse events in patients with hormone receptor-positive breast cancer treated with everolimus: observations from a phase III clinical trial. Peterson, ME, 2013)	0.61
"The mammalian target of rapamycin inhibitor everolimus (Zortress®, Certican®) was recently approved in the USA and a number of EU countries for use in combination with a reduced dosage of tacrolimus and corticosteroids for the prophylaxis of organ rejection in adult liver transplant recipients."	( Everolimus: a guide to its use in liver transplantation. Keating, GM; Lyseng-Williamson, KA, 2013)	2.09
"In sequential phase II studies assessing two dosing schedules, patients with metastatic colorectal cancers refractory to bevacizumab-, fluoropyrimidine-, oxaliplatin-, and irinotecan-based regimens received everolimus 70 mg/wk (n = 99) or 10 mg/d (n = 100)."	( Phase II study of everolimus in patients with metastatic colorectal adenocarcinoma previously treated with bevacizumab-, fluoropyrimidine-, oxaliplatin-, and irinotecan-based regimens. Arrowsmith, ER; Bajetta, E; Del Prete, SA; Fuchs, CS; Hwang, J; Jin, J; Malek, K; Ng, K; Ryan, DP; Sedova, M; Sharma, S; Tabernero, J, 2013)	0.91
" Recently, an inhibitor of mammalian target of rapamycin, everolimus (EVL), has emerged as an alternative immunosuppressant drug that may allow CNI dosage reduction and thereby spare renal function."	( Everolimus-incorporated immunosuppressant strategy improves renal dysfunction while maintaining low rejection rates after heart transplantation in Japanese patients. Endo, M; Hatano, M; Imamura, T; Inaba, T; Kagami, Y; Kato, N; Kinugawa, K; Komuro, I; Kyo, S; Maki, H; Minatsuki, S; Muraoka, H; Ono, M; Yao, A, 2013)	2.08
" Tacrolimus is the basic immunosuppressant for patients after a liver transplant and thanks to its prolonged-release dosage form, which due to its simplicity and reliability of use, replaces tacrolimus twice daily early after the transplant and in the longterm administration, will apparently, for a while, defend its position."	( [Immunosuppression after liver transplant, now and in future]. Trunečka, P, 2013)	0.39
" Specifically, we investigated whether the antitumor effect of an mTOR inhibitor could be improved by changing its dosing schedule in RenCa tumor-bearing mice."	( Circadian regulation of mTOR by the ubiquitin pathway in renal cell carcinoma. Akagawa, Y; Fujioka, T; Koyanagi, S; Kuwano, M; Matsunaga, N; Ohdo, S; Okazaki, F; Okazaki, H; Ono, M; Tsurudome, Y, 2014)	0.4
" Additionally, our results suggest that clinicians should administer the adequate dosage of EVE in order to increase efficacy and reduce adverse effects."	( Everolimus-induced epithelial to mesenchymal transition in immortalized human renal proximal tubular epithelial cells: key role of heparanase. Gambaro, G; Granata, S; Lupo, A; Masola, V; Onisto, M; Zaza, G, 2013)	1.83
" The dosage of everolimus had to be increased and refractory status epilepticus followed after 12 days."	( Everolimus for the treatment of subependymal giant cell astrocytoma probably causing seizure aggravation in a child with tuberous sclerosis complex: a case report. Bast, T; Strobl, K; Wiemer-Kruel, A; Woerle, H, 2014)	2.2
" Pharmacodynamic biomarkers could be useful in distinguishing between (1) disease resistance that occurs even though mTOR is successfully inhibited (suggesting a need for a different treatment strategy) and (2) resistance that might respond to changes in drug dosage or schedule."	( Ribosomal S6 kinase and AKT phosphorylation as pharmacodynamic biomarkers in patients with myelodysplastic syndrome treated with RAD001. Advani, AS; Bates, J; Kalaycio, M; Maciejewski, J; Mahfouz, RZ; Rybicki, L; Saunthararajah, Y; Sekeres, M; Tripp, B, 2014)	0.4
"In patients with solid tumours, daily everolimus dosing demonstrated dose proportionality and linear pharmacokinetics."	( Relationship between everolimus exposure and safety and efficacy: meta-analysis of clinical trials in oncology. Anak, O; Cheung, WK; Grosch, K; Ravaud, A; Sellami, DB; Urva, SR, 2014)	0.99
"Data on 2004 renal transplant recipients from three EVR studies were pooled to identify the impact of ethnicity on efficacy outcomes across EVR dosing groups and control groups."	( Outcomes in ethnic minority renal transplant recipients receiving everolimus versus mycophenolate: comparative risk assessment results from a pooled analysis. Delcoro, C; McCague, K; Melancon, K; Mulgaonkar, SP; Shihab, FS; Wiland, A, 2013)	0.63
"Neutropenia after kidney transplant is an adverse event usually treated with a dosage reduction of mycophenolic acid."	( Replacement of mycophenolate acid with everolimus in patients who became neutropenic after renal transplant. Goumenos, DS; Kalliakmani, P; Karavias, D; Kazakopoulos, P; Marangos, M; Papachristou, E; Savvidaki, E; Voliotis, G; Zavvos, V, 2014)	0.67
" One hundred eighteen episodes of neutropenia were recorded, originally treated by reducing the dosage of mycophenolic acid (765 ± 390 mg/d) and administering granulocyte colony-stimulating factor."	( Replacement of mycophenolate acid with everolimus in patients who became neutropenic after renal transplant. Goumenos, DS; Kalliakmani, P; Karavias, D; Kazakopoulos, P; Marangos, M; Papachristou, E; Savvidaki, E; Voliotis, G; Zavvos, V, 2014)	0.67
" However, comparable data regarding clinical outcomes in HTx recipients receiving EVL either with dosage reduction of cyclosporine A (CSA) or with dosage reduction of tacrolimus (TAC) is scarce."	( Clinical outcome in heart transplant recipients receiving everolimus in combination with dosage reduction of the calcineurin inhibitor cyclosporine A or tacrolimus. Ensminger, SM; Fuchs, U; Gummert, JF; Schulz, U; Zittermann, A, 2014)	0.65
"The pharmacokinetic characteristics of everolimus in Japanese de novo renal transplant patients did not differ from those previously observed in non-Japanese patients, hence the same dosage of everolimus may be acceptable in Japanese patients."	( Pharmacokinetics of everolimus when combined with cyclosporine in Japanese de novo renal transplant recipients. Goto, N; Hirano, M; Hoshinaga, K; Kusaka, M; Sasaki, H; Uchida, K; Watarai, Y, 2014)	1
"From 2007 to 2012, six liver transplant recipients underwent nine major abdominal or thoracic surgical procedures without m-TORi discontinuation or specific dosage adjustment."	( Preliminary report of major surgery in liver transplant recipients receiving m-TOR inhibitors without therapeutic discontinuation. Bernard, D; Calmus, Y; Cauchy, F; Conti, F; Perdigao, F; Scatton, O; Schwarz, L; Sepulveda, A; Soubrane, O, 2014)	0.4
"Major surgery in liver transplant recipients receiving m-TOR inhibitors appears both feasible and safe without therapeutic discontinuation or specific dosage adjustment."	( Preliminary report of major surgery in liver transplant recipients receiving m-TOR inhibitors without therapeutic discontinuation. Bernard, D; Calmus, Y; Cauchy, F; Conti, F; Perdigao, F; Scatton, O; Schwarz, L; Sepulveda, A; Soubrane, O, 2014)	0.4
" Early clinical trials of mTOR inhibitors used fixed dosing with no concomitant reduction in calcineurin inhibitor (CNI) exposure, leading to concerns when consistent and marked dyslipidemia was observed."	( mTOR inhibitors and dyslipidemia in transplant recipients: a cause for concern? Holdaas, H; Potena, L; Saliba, F, 2015)	0.42
" Patients were assigned to one of 10 different cohorts, involving either daily dosing with both agents or daily dosing with trametinib and intermittent everolimus dosing."	( A phase IB trial of the oral MEK inhibitor trametinib (GSK1120212) in combination with everolimus in patients with advanced solid tumors. Bellew, KM; Bendell, JC; Burris, HA; Cox, DS; Durante, M; Infante, JR; Jones, SF; Le, NT; Papadopoulos, KP; Park, J; Patnaik, A; Rasco, D; Tolcher, AW, 2015)	0.84
" Additionally, a 3% annual discount rate was applied to costs, and the robustness of the model results was tested by conducting sensitivity analyses, including those on dosing scheme and post-progression treatment costs."	( Lifetime cost of everolimus vs axitinib in patients with advanced renal cell carcinoma who failed prior sunitinib therapy in the US. Casciano, R; Chua, A; Culver, K; Garrison, LP; Gorritz, M; Liu, Z; Pal, S; Perrin, A; Sherman, S; Wang, X, 2015)	0.76
"Everolimus (EVE) is an immunosuppressive drug dosed according to therapeutic drug monitoring in renal transplant recipients."	( Closer to the Site of Action: Everolimus Concentrations in Peripheral Blood Mononuclear Cells Correlate Well With Whole Blood Concentrations. Åsberg, A; Christensen, H; Falck, P; Midtvedt, K; Robertsen, I; Vethe, NT, 2015)	2.15
"Twelve renal transplant recipients (5 men and 7 women) treated with EVE underwent a pharmacokinetic investigation where EVE concentrations in whole blood and in peripheral blood mononuclear cells (PBMC) were determined within a dosing interval."	( Closer to the Site of Action: Everolimus Concentrations in Peripheral Blood Mononuclear Cells Correlate Well With Whole Blood Concentrations. Åsberg, A; Christensen, H; Falck, P; Midtvedt, K; Robertsen, I; Vethe, NT, 2015)	0.71
" Phase I studies indicated 10 mg daily to be the best dosing of everolimus in DLBCL."	( Everolimus in diffuse large B-cell lymphomas. Arcaini, L; Ferrario, A; Maffioli, M; Merli, M; Passamonti, F, 2015)	2.1
" Dosing decisions were based on the probability of experiencing a dose-limiting toxicity (DLT) during the first two 21-day treatment cycles."	( Phase I study of everolimus, cetuximab and irinotecan as second-line therapy in metastatic colorectal cancer. Beck, JT; Brandt, U; Davidson, SJ; Garrett, CR; Hecht, JR; Mackenzie, MJ; Reid, TR; Rizvi, S; Sharma, S, 2015)	0.76
" Administration of RAD is capable of reducing the dosage of coadministrated calcineurin inhibitors (CNI)."	( Histopathologic impacts of everolimus introduction on kidney transplant recipients. Harada, S; Ito, T; Koshino, K; Nakamura, T; Nakao, T; Nobori, S; Suzuki, T; Takata, T; Ushigome, H; Yoshimura, N, 2015)	0.71
" We explored a novel dosing schedule to assess safety, toxicity and activity in patients with advanced solid tumors."	( Phase I combination of pazopanib and everolimus in PIK3CA mutation positive/PTEN loss patients with advanced solid tumors refractory to standard therapy. Bellido, J; Falchook, G; Fu, S; Hong, D; Janku, F; Karp, D; Ke, D; Kurzrock, R; Lim, J; Naing, A; Piha-Paul, S; Rodrigues, HV; Stephen, B; Subbiah, V; Tsimberidou, A; Wheler, J; Zinner, R, 2015)	0.69
" The objective of the model-based work would be the determination of the optimized doses and dosing schedules of everolimus and sorafenib, offering the maximization of the predicted modeled benefit/toxicity ratio in patients with solid tumors."	( Multiparameter Phase I trials: a tool for model-based development of targeted agent combinations--example of EVESOR trial. Barrois, C; Berger, F; Cassier, P; El-Madani, M; Freyer, G; Guitton, J; Hénin, E; Lachuer, J; Lefort, T; Rodriguez-Lafrasse, C; Slimane, K; Tod, M; Valette, PJ; You, B, 2015)	0.63
" Similarly, SUL was able to reverse the hyper-expression of EMT markers induced by high EVE dosage (100 nM) in cells cultured under both normoxic and hypoxic conditions."	( Sulodexide alone or in combination with low doses of everolimus inhibits the hypoxia-mediated epithelial to mesenchymal transition in human renal proximal tubular cells. Bellin, G; Dalla Gassa, A; Gambaro, G; Granata, S; Lupo, A; Masola, V; Onisto, M; Zaza, G, 2015)	0.67
"Our data reveal, for the first time, that sulodexide, alone or combined to low doses of everolimus, may hinder EMT in renal cells following hypoxia or minimize fibrotic complications due to high dosage of mammalian target of rapamycin inhibitors."	( Sulodexide alone or in combination with low doses of everolimus inhibits the hypoxia-mediated epithelial to mesenchymal transition in human renal proximal tubular cells. Bellin, G; Dalla Gassa, A; Gambaro, G; Granata, S; Lupo, A; Masola, V; Onisto, M; Zaza, G, 2015)	0.89
" Coadministration of an mTOR inhibitor could permit lower dosing of chemotherapeutic agents in HCC management, and trials in non-transplant HCC population are exploring combined used with various agents including sorafenib, the vascular endothelial growth factor inhibitor bevacizumab and conventional agents."	( mTOR inhibitor therapy: Does it prevent HCC recurrence after liver transplantation? Duvoux, C; Toso, C, 2015)	0.42
" Current immunosuppression protocols include a combination of calcineurin inhibitors, such as tacrolimus, and antiproliferative agents (most commonly mycophenolate mofetil), with or without different dosing regimens of corticosteroids."	( Current State of Immunosuppression: Past, Present, and Future. Karam, S; Wali, RK, 2015)	0.42
" Therefore, the optimal dosage strategies for mTOR-I and CNI need to be further explored."	( mTOR inhibitor versus mycophenolic acid as the primary immunosuppression regime combined with calcineurin inhibitor for kidney transplant recipients: a meta-analysis. Chen, J; Jiang, Y; Lai, X; Shou, Z; Xiang, S; Xie, X, 2015)	0.42
" The first 3 patients were enrolled onto a 4 + 2 dosing schedule of daily sunitinib 50 mg and weekly everolimus 30 mg."	( A Single-Arm Phase 1b Study of Everolimus and Sunitinib in Patients With Advanced Renal Cell Carcinoma. Armstrong, AJ; George, DJ; Kanesvaran, R; Turnbull, JD; Watt, K; Wolkowiez, MC, 2015)	0.92
" With limited dosing regimens, the antiarthritic activity of EC0565 was found superior to that of etanercept, everolimus and a nontargeted everolimus analog."	( Antiinflammatory Activity of a Novel Folic Acid Targeted Conjugate of the mTOR Inhibitor Everolimus. Cross, VA; Gehrke, MA; Hahn, SJ; Klein, PJ; Kleindl, PJ; Leamon, CP; Low, PS; Lu, Y; Parker, N; Santhapuram, HK; Stinnette, TW; Vaughn, JF; Vlahov, IR; Wang, K; Westrick, E; Wollak, K; You, F, 2015)	0.85
" The authors used a different dosage regime compared to literature and documented rapid tumor regression by 3D echocardiography."	( Oral Everolimus for Treatment of a Giant Left Ventricular Rhabdomyoma in a Neonate-Rapid Tumor Regression Documented by Real Time 3D Echocardiography. Daehnert, I; Hornemann, F; Riede, FT; Seki, H; Syrbe, S; Wagner, R; Weidenbach, M, 2015)	0.93
" Thus, although CNIs remain the major immunosuppressive treatment, their dosage should be minimized by using them with either full-dose MPA or reduced-dose EVR."	( The safety of calcineurin inhibitors for kidney-transplant patients. Malvezzi, P; Rostaing, L, 2015)	0.42
" However, ERL dosing is challenging due to its narrow therapeutic window combined with high interindividual pharmacokinetic variability."	( Influence of CYP3A5 genetic variation on everolimus maintenance dosing after cardiac transplantation. Englberger, L; Fiedler, GM; Largiadèr, CR; Lesche, D; Mohacsi, P; Setoud, R; Sigurdardottir, V; Sistonen, J, 2015)	0.68
"To describe dosing patterns and to compare the drug costs per month spent in progression-free survival (PFS) among patients with advanced renal cell carcinoma (aRCC) treated with everolimus or axitinib following a first tyrosine kinase inhibitor (TKI)."	( Real-world dosing and drug costs with everolimus or axitinib as second targeted therapies for advanced renal cell carcinoma: a retrospective chart review in the US. Jonasch, E; Li, N; Liu, Z; Pal, SK; Perez, JR; Reichmann, WM; Signorovitch, JE; Vogelzang, NJ, 2016)	0.9
" Real-world dosing patterns were summarized."	( Real-world dosing and drug costs with everolimus or axitinib as second targeted therapies for advanced renal cell carcinoma: a retrospective chart review in the US. Jonasch, E; Li, N; Liu, Z; Pal, SK; Perez, JR; Reichmann, WM; Signorovitch, JE; Vogelzang, NJ, 2016)	0.71
" Close monitoring of the everolimus concentrations and corresponding dosage adjustments are necessary until the target levels are achieved during both periods."	( Management of Everolimus and Voriconazole Interaction in Lung Transplant Patients. Elberdín Pazos, L; Martín Herranz, MI; Outeda Macías, M; Salvador Garrido, P, 2016)	1.1
" Using total DNA content as a measure of cell number, growth inhibitory dose-response curves of everolimus were determined at the end of resistance induction and over time after everolimus withdrawal."	( Long-term acquired everolimus resistance in pancreatic neuroendocrine tumours can be overcome with novel PI3K-AKT-mTOR inhibitors. Beyens, M; de Beeck, KO; de Herder, W; Dogan, F; Hofland, LJ; Mortier, G; Pauwels, P; Peeters, M; Van Camp, G; van Koetsveld, PM; Vandamme, T; Vangestel, C, 2016)	0.98
" We analyzed the impact of orally dosed mammalian target of rapamycin inhibitors on abdominal adhesion formation and wound tensile strength in an experimental model."	( Effects of mTOR Inhibitors in Prevention of Abdominal Adhesions. Alwayn, I; Cimen, S; Guler, S; Hart-Matyas, M; Hu, Q; Venkatachalam, AB, 2016)	0.43
" Dosing patterns and adherence to everolimus were summarized."	( Treatment patterns and factors associated with the use of everolimus among post-menopausal women with HR+/HER2- metastatic breast cancer: a retrospective US claims study. Fang, A; Guérin, A; Hao, Y; Kageleiry, A; Koo, V; Li, N; Peeples, M; Tang, D; Wu, EQ, 2016)	0.96
" Dosing algorithms are provided, with suggestions for target ranges in specific settings, and treatment strategies for the most common side effects are proposed."	( Use of everolimus in liver transplantation: The French experience. Calmus, Y; Dharancy, S; Dumortier, J; Durand, F; Duvoux, C; Salamé, E; Saliba, F, 2016)	0.89
" Everolimus was reinitiated in both cases in addition to decreasing the dosage of tacrolimus, and there were no further complications."	( Use of Everolimus After Multivisceral Transplantation: A Report of Two Cases. Jafri, SM; Kazimi, M; Parekh, R; Rao, B; Raoufi, M; Segovia, MC, 2016)	1.8
" Our findings confirm observations from another study in patients with cancer and show us that everolimus is a good candidate for individualized dosing in patients with cancer."	( Everolimus pharmacokinetics and its exposure-toxicity relationship in patients with thyroid cancer. de Wit, D; den Hartigh, J; Gelderblom, H; Guchelaar, HJ; Kapiteijn, E; Links, TP; Moes, DJ; Roozen, CF; Schneider, TC; van der Hoeven, JJ; van Erp, NP, 2016)	2.1
"Everolimus (EVR) has been used widely for the purpose of reducing the dosage of calcineurin inhibitor (CNI), leading to decreasing CNI nephrotoxicity."	( Effectiveness of the Combination of Everolimus and Tacrolimus With High Dosage of Mizoribine for Living Donor-Related Kidney Transplantation. Harada, S; Ito, T; Koshino, K; Nakamura, T; Nakao, T; Nobori, S; Suzuki, T; Ushigome, H; Yoshimura, N, 2016)	2.15
" Further trials addressing the optimal dosage of imatinib and mTORi in kidney transplant recipients are recommended."	( Gastrointestinal stromal tumors in kidney transplant recipients: Report of two cases and literature review. Chan, CK; Chau, KF; Cheng, IK; Cheung, CY; Li, FK; Lo, SH, 2017)	0.46
"Due to toxic events, everolimus dosage was reduced to 5 mg in 27% of patients."	( Safety analysis, association with response and previous treatments of everolimus and exemestane in 181 metastatic breast cancer patients: A multicenter Italian experience. Cortesi, E; D'Onofrio, L; Fabbri, MA; Gamucci, T; Giuliani, R; Iezzi, L; Magri, V; Mancini, ML; Marchetti, P; Mauri, M; Mentuccia, L; Moscetti, L; Natoli, C; Pizzuti, L; Ramponi, S; Roma, CL; Ruggeri, EM; Santini, D; Sini, V; Sperduti, I; Vaccaro, A; Vici, P, 2016)	0.99
" Several recent clinical trials have demonstrated their efficacy in combination with reduced cyclosporine dosing in de novo heart transplant recipients, in particular with everolimus."	( Recent Advances in Mammalian Target of Rapamycin Inhibitor Use in Heart and Lung Transplantation. Fine, NM; Kushwaha, SS, 2016)	0.63
" Second, the question of identifying an optimal dosing strategy for treating with an AI and a cytotoxic agent is addressed."	( Microenvironment-Mediated Modeling of Tumor Response to Vascular-Targeting Drugs. Gevertz, JL, 2016)	0.43
" In nearly half of orally dosed oncolytics poor dissolution is likely to play a major role in low and unpredictable absorption."	( Inventory of oral anticancer agents: Pharmaceutical formulation aspects with focus on the solid dispersion technique. Beijnen, JH; Nuijen, B; Sawicki, E; Schellens, JH, 2016)	0.43
"About 26 patients with solid tumors were treated in four different dosing schedules."	( EVESOR, a model-based, multiparameter, Phase I trial to optimize the benefit/toxicity ratio of everolimus and sorafenib. Badary, OA; Barrois, C; Cassier, P; Colomban, O; El-Demerdash, E; El-Madani, M; El-Shenawy, SM; Freyer, G; Gagnieu, MC; Guitton, J; Hommel-Fontaine, J; Ibrahim, BM; Lefort, T; Maillet, D; Peron, J; Rodriguez-Lafrasse, C; Tod, M; Valette, PJ; You, B, 2017)	0.67
" Calcineurin inhibitor (CNI) dosage was reduced and renal function improved, and mean estimated glomerular filtration rate recovered from 42."	( Experience of Quatro-Therapy With Everolimus to Minimize Calcineurin Inhibitor for Kidney Transplant Recipients. Furuya, R; Irie, S; Matsuoka, H; Matsuzaki, H; Miyajima, S; Miyazaki, T; Nakamura, N; Tanaka, M, )	0.41
" Key aspects of everolimus dosing and safety profile, drawn up by relevant findings, are included, as well as the role of biomarkers to identify subgroups of mBC patients who may best benefit from everolimus treatment."	( Role of everolimus in the treatment of metastatic HER2-negative/HR-positive breast cancer. Pronzato, P, 2017)	1.24
" There is tendency not to interrupt the EVE treatment and keep it either in a dosage of 10 or 5mg/day if the oral damage is tolerable."	( [Everolimus in Daily Clinical Practice Focusing to Oral Mucosa Damage Issues - Single Oncology Centre Experience within the Course of the Year 2016]. Arnetová, V; Fiala, O; Fínek, J; Kališová, K; Korunková, H; Kulhánková, J; Matějka, VM; Svoboda, T; Vokurka, S; Votavová, M, )	1.04
" Within five post-operative days, patients (mean age 50±13 years, 27% women) were randomized to EVR or a standard CsA dosage (CsA group)."	( Effect of everolimus vs calcineurin inhibitors on quality of life in heart transplant recipients during a 3-year follow-up: Results of a randomized controlled trial (SCHEDULE). Andreassen, AK; Arora, S; Dellgren, G; Eiskjaer, H; Grov, I; Gude, E; Gullestad, L; Gustafsson, F; Jansson, K; Karason, K; Rådegran, G; Relbo Authen, A; Solbu, D, 2017)	0.86
" Therefore, with regard to PI3K inhibitors currently in late-stage clinical trials, the identification of appropriate biomarkers of efficacy and the development of optimal combination regimens and dosing schedules are likely to be important for graduation into clinical practice."	( Phosphoinositide 3-kinase (PI3K) pathway inhibitors in solid tumors: From laboratory to patients. Janku, F, 2017)	0.46
" This beneficial treatment option for patients can minimize the drug dosage and the occurrence of adverse events."	( Intermittent everolimus administration for renal angiomyolipoma associated with tuberous sclerosis complex. Egawa, S; Endo, K; Hatano, T; Inaba, H, 2017)	0.82
" The CsA dosage was further reduced to keep a lowest value of serum creatinine and a target EVL level."	( Ten-Year Follow-up of Pharmacokinetics-Guided Very Early Cyclosporine Minimization Synchronized With Everolimus Initiation in De Novo Kidney Transplantation. Jirasiritham, S; Sumethkul, V; Tankee, P; Worawichawong, S, 2017)	0.67
" We created dose-response curves for both compounds."	( Preclinical analysis of MTOR complex 1/2 inhibition in diffuse intrinsic pontine glioma. Amani, V; DeSisto, JA; Donson, A; Flannery, PC; Foreman, N; Green, AL; Hoffman, L; Lemma, RT; Levy, JMM; Moroze, EE; Prince, EW; Venkataraman, S; Vibhakar, R, 2018)	0.48
" Limits of clinical relevance were set at a difference of ± 25%, as this would lead to a different dosing advice."	( Clinical validation study of dried blood spot for determining everolimus concentration in patients with cancer. Brüggemann, RJM; Croes, S; de Beer, YM; Knapen, LM; van Erp, NP; van Herpen, CML; Willemsen, AECAB, 2018)	0.72
" However, toxicity with flat dosing limits its usage."	( Pharmacokinetically-targeted dosed everolimus maintenance therapy in lymphoma patients. Ambinder, RF; Asiama, A; Gladstone, DE; Hurtt, J; Jones, RJ; Sawyer, K; Schoch, LK; Shanbhag, S; Swinnen, LJ; Wagner-Johnston, N; Zahurak, M, 2018)	0.76
"After HDC, everolimus was dosed to serum trough levels (goal 3-15 ng/mL), with quarterly rituximab infusions for 1 year while maintaining < grade II non-hematologic and < grade III hematologic toxicities."	( Pharmacokinetically-targeted dosed everolimus maintenance therapy in lymphoma patients. Ambinder, RF; Asiama, A; Gladstone, DE; Hurtt, J; Jones, RJ; Sawyer, K; Schoch, LK; Shanbhag, S; Swinnen, LJ; Wagner-Johnston, N; Zahurak, M, 2018)	1.15
"Pharmacokinetically-targeted dosing appears to increase everolimus tolerability."	( Pharmacokinetically-targeted dosed everolimus maintenance therapy in lymphoma patients. Ambinder, RF; Asiama, A; Gladstone, DE; Hurtt, J; Jones, RJ; Sawyer, K; Schoch, LK; Shanbhag, S; Swinnen, LJ; Wagner-Johnston, N; Zahurak, M, 2018)	1
"Patients with advanced pNET were randomized (1:1) to oral BEZ235 400 mg twice daily or oral everolimus 10 mg once daily on a continuous dosing schedule."	( Phase II Study of BEZ235 versus Everolimus in Patients with Mammalian Target of Rapamycin Inhibitor-Naïve Advanced Pancreatic Neuroendocrine Tumors. Capdevila, J; Custodio, A; Garcia-Carbonero, R; Grande, E; Guimbaud, R; Hendifar, AE; Klümpen, HJ; Kong, O; Libutti, SK; Lombard-Bohas, C; Meyer, T; Reed, N; Ricci, S; Safina, S; Salazar, R; Salomon, H; Tavorath, R; Walenkamp, A; Yao, JC, 2018)	0.98
" Everolimus toxicity was less severe following dosing at ZT13, as compared to ZT1, as shown with least body weight inhibition in both genders; least reductions in thymus weight both in males (p < 0."	( The immune system as a chronotoxicity target of the anticancer mTOR inhibitor everolimus. Cinar, S; Deniz, G; Giacchetti, S; Kaptan, E; Lévi, F; Li, XM; Okyar, A; Ozsoy, N; Ozturk, D; Ozturk, N; Pala-Kara, Z; Sancar-Bas, S, 2018)	1.62
" We postulate that there is room for improvement of dosing, as the optimal immunosuppressive dose in calcineurin-free regimens is unknown and since the once daily dosing regimen for oncological indications is often associated with treatment-limiting toxicity."	( A pharmacological rationale for improved everolimus dosing in oncology and transplant patients. Burger, DM; de Fijter, JW; Guchelaar, HJ; Moes, DJAR; Reinders, MEJ; Ter Heine, R; van Erp, NP; van Herpen, CM, 2018)	0.75
"We developed a mechanistic population pharmacokinetic model for everolimus in cancer and transplant patients and explored alternative dosing regimens."	( A pharmacological rationale for improved everolimus dosing in oncology and transplant patients. Burger, DM; de Fijter, JW; Guchelaar, HJ; Moes, DJAR; Reinders, MEJ; Ter Heine, R; van Erp, NP; van Herpen, CM, 2018)	0.99
" Waste occurred in 41% of all patients with primary reasons attributed to cancer progression in 25 patients, death in five patients, toxicity in five patients and increase in dosage of targeted therapy in two patients."	( Financial impact of oral chemotherapy wastage on society and the patient. Clamon, G; Meyer, C; Monga, V; Vakiner, B, 2019)	0.51
" Dosing and administration inputs were consistent with approved prescribing information and the clinical trials used to estimate efficacy and safety inputs."	( The Additional Costs per Month of Progression-Free Survival and Overall Survival: An Economic Model Comparing Everolimus with Cabozantinib, Nivolumab, and Axitinib for Second-Line Treatment of Metastatic Renal Cell Carcinoma. Duchesneau, E; Ghate, S; McDonald, E; Messali, A; Perez, JR; Swallow, E, 2018)	0.69
"This study included two cohorts; cohort 1 received 30 mg of everolimus by mouth (PO) weekly, and cohort 2 was dosed with 10 mg of everolimus PO daily."	( Phase II Study of Everolimus in Metastatic Malignant Melanoma (NCCTG-N0377, Alliance). Allred, JB; Creagan, ET; Erickson, LA; Kaur, JS; Lowe, VJ; Maples, WJ; Markovic, S; Rao, RD; Suman, VJ; Vera Aguilera, J; Windschitl, HE, 2018)	1.06
"Key inputs included in the calculation were patient population, dosing information, incidence rates and associated costs of Grade 3/4 AEs, treatment costs (including drug discount programs), and patients' progression-free survival (PFS) as a proxy for length of treatment."	( Cost analysis for different sequential treatment regimens for metastatic renal cell carcinoma in China. Dong, P; Gao, X; Lu, X; Park, SH; Ren, H; Shi, G; Xue, M, 2018)	0.48
" This study was, therefore, designed to determine the optimal dosage and schedule of CTX when combined with everolimus to prevent this potentially detrimental Treg expansion."	( Phase 1 study of everolimus and low-dose oral cyclophosphamide in patients with metastatic renal cell carcinoma. de Gruijl, TD; Goedegebuure, RS; Haanen, JB; Hamberg, P; Huijts, CM; Lougheed, SM; Tascilar, M; van der Vliet, HJ; van Herpen, CM; Verheul, HM; Werter, IM, 2019)	1.07
" After dosing was discontinued, TAC-treated mice showed gradual graft rejection, whereas EVL-treated mice sustained long-term robust chimerism."	( Evaluation of the impact of conventional immunosuppressant on the establishment of murine transplantation tolerance - an experimental study. Fukuda, H; Hirai, T; Ikemiyagi, M; Ishii, R; Ishii, Y; Kanzawa, T; Katsumata, H; Miyairi, S; Okumi, M; Omoto, K; Saiga, K; Tanabe, K; Yokoo, T, 2019)	0.51
"In a multicenter phase 2 study, performed in patients with mRCC not amenable to or progressive on a vascular endothelial growth factor (VEGF)-receptor tyrosine kinase inhibitor (TKI) containing treatment regimen, we assessed whether the addition of this metronomic dosing schedule of cyclophosphamide to therapy with everolimus could result in an improvement of progression-free survival (PFS) after 4 months of treatment."	( Metronomic cyclophosphamide attenuates mTOR-mediated expansion of regulatory T cells, but does not impact clinical outcome in patients with metastatic renal cell cancer treated with everolimus. de Gruijl, TD; Haanen, JBAG; Hamberg, P; Helgason, HH; Huijts, CM; Los, M; Lougheed, SM; Polee, MB; Tascilar, M; van der Vliet, HJ; Verheul, HM; Werter, IM, 2019)	0.88
" Continuous administration of everolimus at a low dose as opposed to high intermittent dosing schedule has greater antitumor efficacy against thyroid cancer xenografts in vivo."	( Evaluation of preclinical efficacy of everolimus and pasireotide in thyroid cancer cell lines and xenograft models. Chen, Z; Khuri, FR; Lallani, SB; Lonial, S; Marcus, A; Martinson, DE; Owonikoko, TK; Sun, SY; Zhang, G, 2019)	1.07
" Substituting leflunomide for mycophenolate sodium and increasing dosage of everolimus has been proposed to solve BK nephropathy."	( Successful Treatment for BK Virus Nephropathy by Leflunomide in a Kidney Transplant Patient: A Case Report. Chen, HA; Chen, YW; Hsu, YH; Hung, LY; Lee, CH; Wu, MS; Wu, MY, 2019)	0.74
" The aim of this study is to characterize the interaction, optimal sequence and dosing of SSA-based and molecularly targeted therapies in PanNET."	( Interaction between somatostatin analogues and targeted therapies in neuroendocrine tumor cells. Egidi, M; Gress, TM; Krug, S; Michl, P; Mordhorst, JP; Moser, F; Rinke, A; Ruffert, C; Theuerkorn, K, 2019)	0.51
" After 3 months, CNIs were discontinued in patients who tolerated everolimus well, while everolimus dosage was increased (blood trough levels, 6-12 ng/ml)."	( Immunosuppressive treatment with everolimus in patients after liver transplant: 4 years of single-center experience. Grąt, M; Janik, M; Moczydłowska, D; Raszeja-Wyszomirska, J; Wasilewicz, MP; Zieniewicz, K, 2019)	1.03
" Everolimus 5 mg PO daily and panobinostat 10 mg PO 3 times weekly (weeks 1 and 2) given in 21-day cycles was the recommended phase II dosing based on their maximum tolerated dose."	( Phase I study of the mTOR inhibitor everolimus in combination with the histone deacetylase inhibitor panobinostat in patients with advanced clear cell renal cell carcinoma. Adra, N; Chintala, S; Damayanti, N; George, S; Pili, R; Wood, A, 2020)	1.74
"All randomised controlled trials (RCTs) and quasi-RCTs in which drug regimens, containing TOR-I commenced within seven days of transplant, were compared to alternative drug regimens, were included without age restriction, dosage or language of report."	( Target of rapamycin inhibitors (TOR-I; sirolimus and everolimus) for primary immunosuppression in kidney transplant recipients. Chapman, JR; Craig, JC; Hahn, D; Hamiwka, LA; Hodson, EM; Lee, VW; Webster, AC, 2019)	0.76
" Post-HTx patient survival in patients, irrespective of the donor risk factors such as donor age, low LVEF, history of cardiac arrest, was equivalent across cohorts, while longer TIT and higher inotrope dosage prior to procurement surgery were significant risk factors for survival."	( Effect of Therapeutic Modification on Outcomes in Heart Transplantation Over the Past Two Decades　- A Single-Center Experience in Japan. Fujita, T; Fukushima, N; Fukushima, S; Ikura, M; Ishibashi-Ueda, H; Iwasaki, K; Kitamura, S; Kobayashi, J; Kuroda, K; Matsuda, S; Mochizuki, H; Nakajima, S; Nakatani, T; Ogawa, H; Seguchi, O; Tadokoro, N; Takenaka, H; Tsujita, K; Watanabe, T; Yanase, M, 2020)	0.56
" In 21 patients a non-osseous biopsy obtained before dosing was useful for continuous scoring, which demonstrated upregulation of several proteins as compared to readings in corresponding primary tumour tissues."	( PI3K pathway protein analyses in metastatic breast cancer patients receiving standard everolimus and exemestane. Beelen, KJ; Boven, E; de Valk, B; Kruger, DT; Linn, SC; Nieuwenhuis, M; Opdam, M; Sanders, J; van der Noort, V, 2020)	0.78
" All patients received everolimus at a dosage of 10 mg/day alone or in association with exemesthane for breast cancer."	( [Tolerablity of everolimus in clinical practice: a retrospective study]. Afani, L; Awada, A; Belbaraka, R, 2020)	1.21
"The EVR-loaded sublingual orodispersible films are a promising, economical, and convenient approach for delivering EVR efficiently in a solid dosage form."	( Designing orodispersible films containing everolimus for enhanced compliance and bioavailability. Gao, S; Guan, R; Liu, H; Liu, Y; Ma, Y; Song, W; Yang, Y, 2020)	0.82
" Discontinuation or dosage reduction of immunosuppressives and other treatment information was documented."	( Clinical course of COVID-19 disease in immunosuppressed renal transplant patients Ateş, ÖF; Çetin, ES; Dheir, H; Fırat, N; Genç, AB; Karabay, O; Köroğlu, M; Muratdağı, G; Özmen, K; Sipahi, S; Tomak, Y; Yaylacı, S, 2021)	0.62
" Herein, we examined the capacity of single oral dosing with everolimus, an FDA-approved inhibitor of the PI3K/Akt effector mTOR, to reduce incubated cocaine-craving and reverse incubation-associated changes in vmPFC kinase activity and mGlu expression."	( Preclinical evidence to support repurposing everolimus for craving reduction during protracted drug withdrawal. Barger, BD; Chiu, AS; Elias, KN; Fabella, AM; Holder, KN; Huerta Sanchez, LL; Jimenez Chavez, CL; Kang, MC; Kippin, TE; Shin, CB; Szumlinski, KK, 2021)	1.12
"Saliva and whole blood samples were taken from patients with cancer, who were treated with everolimus in the dosage of either 10 mg once a day or 5 mg twice a day."	( Everolimus Concentration in Saliva to Predict Stomatitis: A Feasibility Study in Patients with Cancer. Beijnen, JH; Dorlo, TPC; Huitema, ADR; Jacobs, BAW; Molenaar-Kuijsten, L; Rosing, H; Steeghs, N; Thijssen, B; Verheijen, RB, 2022)	2.38
"The study findings support the approved dosing regimen of lenvatinib 18 mg plus everolimus 5 mg daily for patients with advanced RCC."	( Assessing the Safety and Efficacy of Two Starting Doses of Lenvatinib Plus Everolimus in Patients with Renal Cell Carcinoma: A Randomized Phase 2 Trial. Alekseev, B; Binder, TA; Castellano, D; Ciuleanu, T; Glen, H; Heng, DYC; Koralewski, P; Lee, JL; O'Hara, K; Pal, SK; Parnis, F; Peng, L; Puente, J; Rha, SY; Smith, AD; Stroyakovskiy, D; Sunela, K, 2022)	1.18
" The average dosage of everolimus and sirolimus was 2,65mg (±1,78) and 2,75mg (±0,96) in T patients, respectively, versus 8,75mg (±2,26) for everolimus in K patients."	( Pulmonary toxicity of mTOR inhibitors. Comparisons of two populations: Solid organ recipients and cancer patients. Billaud, EM; Gendarme, S; Gibault, L; Guillemain, R; Israël-Biet, D; Lillo-Lelouet, A; Medioni, J; Oudard, S; Pastré, J, )	0.44
"The management of immunosuppressors in solid organ transplantation requires pharmacological therapeutic monitoring with regular adaptation of the dosage to the residual level."	( Sotorasib associated with tacrolimus and everolimus: A significant drug interaction in lung transplant patients. Bedouch, P; Briault, A; Degano, B; Falque, L; Liaigre, L; Orhon, P; Perrier, Q; Raymond, CS; Romand, P, 2022)	0.99
" All drugs were dosed once daily on days 1-21 of each 28-day cycle."	( DTRMWXHS-12, a novel Bruton tyrosine kinase inhibitor, in combination with everolimus and pomalidomide in patients with relapsed/refractory lymphomas: An open-label, multicenter, phase 1a/1b study. Brander, DM; Ding, W; Gui, M; He, W; Huntington, SF; Iqbal, M; Kearney, AS; Koehler, AB; Leis, JF; Mato, AR; McKinlay, TP; Moustafa, MA; Rosenthal, AC; Schuster, SJ; Tun, HW, 2023)	1.14
" The academic EVESOR trial (NCT01932177) was designed to assess alternative doses and intermittent dosing schedules of EVE and SOR combination therapy to improve the benefit-risk ratio for patients with solid tumors."	( Clinical results of the EVESOR trial, a multiparameter phase I trial of everolimus and sorafenib combination in solid tumors. Augu-Denechere, D; Bonnin, N; Calattini, S; Colomban, O; Fontaine, J; Freyer, G; Guitton, J; Lopez, J; Maillet, D; Payen, L; Peron, J; Puszkiel, A; Schwiertz, V; Tartas, S; Tod, M; Varnier, R; You, B, 2023)	1.14
"EVESOR is a multiparameter dose-escalation phase I trial investigating different doses and dosing schedules, with the final objective of generating data for modeling and simulation."	( Clinical results of the EVESOR trial, a multiparameter phase I trial of everolimus and sorafenib combination in solid tumors. Augu-Denechere, D; Bonnin, N; Calattini, S; Colomban, O; Fontaine, J; Freyer, G; Guitton, J; Lopez, J; Maillet, D; Payen, L; Peron, J; Puszkiel, A; Schwiertz, V; Tartas, S; Tod, M; Varnier, R; You, B, 2023)	1.14
"The objective was to develop a pharmacokinetic-pharmacodynamic (PK-PD) model linking everolimus and sorafenib exposure with biomarker dynamics and progression-free survival (PFS) based on data from EVESOR trial in patients with solid tumors treated with everolimus and sorafenib combination therapy and to simulate alternative dosing schedules for sorafenib."	( A PK-PD model linking biomarker dynamics to progression-free survival in patients treated with everolimus and sorafenib combination therapy, EVESOR phase I trial. Augu-Denechere, D; Bonnin, N; Colomban, O; Fontaine, J; Freyer, G; Guitton, J; Lopez, J; Maillet, D; Payen, L; Péron, J; Puszkiel, A; Rousset, P; Tartas, S; Tod, M; Trillet-Lenoir, V; You, B, 2023)	1.35
"Everolimus (5-10 mg once daily, qd) and sorafenib (200-400 mg twice daily, bid) were administered according to four different dosing schedules in 43 solid tumor patients."	( A PK-PD model linking biomarker dynamics to progression-free survival in patients treated with everolimus and sorafenib combination therapy, EVESOR phase I trial. Augu-Denechere, D; Bonnin, N; Colomban, O; Fontaine, J; Freyer, G; Guitton, J; Lopez, J; Maillet, D; Payen, L; Péron, J; Puszkiel, A; Rousset, P; Tartas, S; Tod, M; Trillet-Lenoir, V; You, B, 2023)	2.57
" Nonlinear pharmacokinetics (PKs) were observed in clinical studies after intravenous and oral dosing across a wide dose range, including the efficacious doses of 240 and 480 mg."	( Developing a mechanistic understanding of the nonlinear pharmacokinetics of letermovir and prospective drug interaction with everolimus using physiological-based pharmacokinetic modeling. Asari, K; Chen, D; Cho, CR; Hartmann, G; Kuo, Y; McCrea, JB; Menzel, K; Wang, YH, 2023)	1.12
" Maximum concentration and area under the concentration-time curve (AUC) from time of dosing to the last measurable concentration and extrapolated to infinity, of everolimus in whole blood were estimated using noncompartmental analysis, with geometric mean ratios and 90% confidence intervals for the ratios of everolimus dosed with CBD to everolimus dosed alone."	( Pharmacokinetic Drug-Drug Interaction With Coadministration of Cannabidiol and Everolimus in a Phase 1 Healthy Volunteer Trial. Berwaerts, J; Chen, C; Critchley, D; Hyland, K; Tayo, B; Thai, C; Wray, L, 2023)	1.33
"Heart transplant recipients experience high rates of skin cancer, likely due to greater length or dosage of immunosuppression."	( A review of heart transplant immunosuppressants and nonmelanoma skin cancer. Camacho, I; Dave, Y; Eckembrecher, DG; Eckembrecher, FJ; Nouri, K; Patel, S; Shah, H, 2023)	0.91
" Dose-response assays were used to confirm the antifungal activity of initial hits and establish their potency."	( Screening the medicine for malaria venture's Pandemic Response Box to identify novel inhibitors of Candida albicans and Candida auris biofilm formation. Ajetunmobi, OH; Badali, H; Chaturvedi, AK; Lopez-Ribot, JL; Najvar, L; Patterson, TF; Vaccaro, A; Wiederhold, NP; Wormley, FL, 2023)	0.91
"3) and no difference with regard to dosing was observed (p = ."	( Does the dose matter? Antiproliferative efficacy and toxicity of everolimus in patients with neuroendocrine tumors - Experiences from a tertiary referral center. Haug, A; Kiesewetter, B; Kretschmer-Chott, E; Macheiner, S; Mazal, P; Melhorn, P; Raderer, M; Wolff, L, 2023)	1.15
" We ascertained whether the risk of drug-induced tremor is influenced by the underlying diagnosis, dosing formulations, drug concentrations, and blood monitoring."	( Tremor Induced by Cyclosporine, Tacrolimus, Sirolimus, or Everolimus: A Review of the Literature. Jha, N; Joyce, M; Khalid, U; Lunny, C; Mahboob, O; Nagaraja, N; Shukla, AM; Wagle Shukla, A, 2023)	1.15
"The development and analysis of pharmaceutical formulations often involves the determination of multiple active ingredients in a dosage form."	( Development and Method Validation of Design of Experiments-Optimized Tablet Formulation for Simultaneous Detection of Exemestane and Everolimus. Kumar, A; Kurmi, BD; Singh, D, )	0.34
" Our data might be useful for determining the dosage of EVE in clinical practice."	( Relationship Between Daily Dose of Everolimus and Treatment Effect in Patients With Luminal HER2-negative Metastatic Breast Cancer. Horimoto, Y; Ishizuka, Y; Murakami, F; Okazaki, M; Ushiyama, Y; Watanabe, J, 2023)	1.19

Role	Description
antineoplastic agent	A substance that inhibits or prevents the proliferation of neoplasms.
immunosuppressive agent	An agent that suppresses immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-cells or by inhibiting the activation of helper cells. In addition, an immunosuppressive agent is a role played by a compound which is exhibited by a capability to diminish the extent and/or voracity of an immune response.
mTOR inhibitor	A protein kinase inhibitor of the mammalian target of rapamycin (mTOR), a protein that regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis and transcription. mTOR inhibitors are used to prevent transplant rejection and in treatment of cancer.
anticoronaviral agent	Any antiviral agent which inhibits the activity of coronaviruses.
geroprotector	Any compound that supports healthy aging, slows the biological aging process, or extends lifespan.
[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]

Class	Description
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.
secondary alcohol	A secondary alcohol is a compound in which a hydroxy group, -OH, is attached to a saturated carbon atom which has two other carbon atoms attached to it.
ether	An organooxygen compound with formula ROR, where R is not hydrogen.
cyclic ketone
cyclic acetal	An acetal in the molecule of which the acetal carbon and one or both oxygen atoms thereon are members of a ring.
macrolide lactam	A macrolide in which the macrocyclic lactone ring includes an amide group.
[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	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
USP1 protein, partial	Homo sapiens (human)	Potency	39.8107	0.0316	37.5844	354.8130	AID504865
TDP1 protein	Homo sapiens (human)	Potency	0.0344	0.0008	11.3822	44.6684	AID686978; AID686979
AR protein	Homo sapiens (human)	Potency	20.4377	0.0002	21.2231	8,912.5098	AID743035; AID743036; AID743042; AID743053; AID743054; AID743063
glucocorticoid receptor [Homo sapiens]	Homo sapiens (human)	Potency	14.4381	0.0002	14.3764	60.0339	AID720691; AID720692
pregnane X nuclear receptor	Homo sapiens (human)	Potency	15.8489	0.0054	28.0263	1,258.9301	AID1346985
estrogen nuclear receptor alpha	Homo sapiens (human)	Potency	11.8481	0.0002	29.3054	16,493.5996	AID743069; AID743075; AID743078; AID743080; AID743091
peroxisome proliferator activated receptor gamma	Homo sapiens (human)	Potency	8.5415	0.0010	19.4141	70.9645	AID743094; AID743140
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_a	Homo sapiens (human)	Potency	0.0266	0.0017	23.8393	78.1014	AID743083
vitamin D3 receptor isoform VDRA	Homo sapiens (human)	Potency	39.8107	0.3548	28.0659	89.1251	AID504847
thyroid hormone receptor beta isoform 2	Rattus norvegicus (Norway rat)	Potency	0.0029	0.0003	23.4451	159.6830	AID743065; AID743067
nuclear receptor ROR-gamma isoform 1	Mus musculus (house mouse)	Potency	17.7408	0.0079	8.2332	1,122.0200	AID2546; AID2551
geminin	Homo sapiens (human)	Potency	26.7852	0.0046	11.3741	33.4983	AID624296; AID624297
peripheral myelin protein 22	Rattus norvegicus (Norway rat)	Potency	32.1968	0.0056	12.3677	36.1254	AID624032
Cellular tumor antigen p53	Homo sapiens (human)	Potency	23.7101	0.0023	19.5956	74.0614	AID651631; AID720552
ATPase family AAA domain-containing protein 5	Homo sapiens (human)	Potency	29.4169	0.0119	17.9420	71.5630	AID651632; AID720516
Ataxin-2	Homo sapiens (human)	Potency	26.6032	0.0119	12.2221	68.7989	AID651632
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
ATP-binding cassette sub-family C member 3	Homo sapiens (human)	IC50 (µMol)	84.0000	0.6315	4.4531	9.3000	AID1473740
Multidrug resistance-associated protein 4	Homo sapiens (human)	IC50 (µMol)	95.0000	0.2000	5.6774	10.0000	AID1473741
Bile salt export pump	Homo sapiens (human)	IC50 (µMol)	2.0000	0.1100	7.1903	10.0000	AID1473738
Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)	IC50 (µMol)	100.0000	0.1200	4.0480	10.0000	AID1207371
Serine/threonine-protein kinase mTOR	Homo sapiens (human)	IC50 (µMol)	0.0022	0.0000	0.8575	10.0000	AID1662433; AID1876108; AID1916668
Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)	IC50 (µMol)	100.0000	0.1200	4.0480	10.0000	AID1207371
Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)	IC50 (µMol)	5,714.8051	0.0009	1.9014	10.0000	AID1207465; AID1207496; AID1207525
Sodium channel protein type 5 subunit alpha	Homo sapiens (human)	IC50 (µMol)	415.2415	0.0003	3.6484	9.2000	AID1207311; AID1207342
Regulatory-associated protein of mTOR	Homo sapiens (human)	IC50 (µMol)	0.0000	0.0000	0.1139	0.6600	AID1916668
Canalicular multispecific organic anion transporter 1	Homo sapiens (human)	IC50 (µMol)	11.3000	2.4100	6.3433	10.0000	AID1473739
Target of rapamycin complex subunit LST8	Homo sapiens (human)	IC50 (µMol)	0.0000	0.0000	0.0963	0.6600	AID1916668
Potassium voltage-gated channel subfamily D member 3	Homo sapiens (human)	IC50 (µMol)	10,000.0000	1.4000	5.3500	9.3000	AID1207431
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Bone morphogenetic protein receptor type-1B	Homo sapiens (human)	Kd	30.0000	0.0009	1.1413	3.7000	AID1424922
Cell division cycle 7-related protein kinase	Homo sapiens (human)	Kd	30.0000	0.5110	0.5110	0.5110	AID1424936
Serine/threonine-protein kinase PLK4	Homo sapiens (human)	Kd	30.0000	0.0008	1.5144	9.0000	AID1425121
ATP-dependent RNA helicase DDX3X	Homo sapiens (human)	Kd	30.0000	0.4350	0.4350	0.4350	AID1424975
Pyridoxal kinase	Homo sapiens (human)	Kd	30.0000	0.2860	5.0765	16.4040	AID1425106
Citron Rho-interacting kinase	Homo sapiens (human)	Kd	30.0000	0.0330	3.0646	48.8760	AID1424954
Serine/threonine-protein kinase Chk1	Homo sapiens (human)	Kd	30.0000	0.0028	1.4744	8.7000	AID1424953
Aurora kinase A	Homo sapiens (human)	Kd	30.0000	0.0001	0.7342	9.3000	AID1424917
Cyclin-G-associated kinase	Homo sapiens (human)	Kd	30.0000	0.0003	0.9086	28.6510	AID1425009
Ephrin type-B receptor 6	Homo sapiens (human)	Kd	30.0000	0.0000	1.0768	9.0000	AID1424995
Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)	Kd	30.0000	0.0260	1.3140	2.6020	AID1424896
Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)	Kd	30.0000	0.0020	1.6212	11.4330	AID1425155
Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)	Kd	30.0000	0.0940	1.3910	3.5070	AID1424926
Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)	Kd	30.0000	0.0170	0.3610	0.7050	AID1425097
Eukaryotic translation initiation factor 5B	Homo sapiens (human)	Kd	30.0000	0.2320	0.2320	0.2320	AID1424986
Rho-associated protein kinase 2	Homo sapiens (human)	Kd	30.0000	0.0002	2.7105	56.0660	AID1425158
Serine/threonine-protein kinase ULK1	Homo sapiens (human)	Kd	30.0000	0.0008	1.8410	23.2730	AID1425208
Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)	Kd	30.0000	0.0057	2.0095	12.2010	AID1424997
Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)	Kd	30.0000	0.0170	1.9737	29.9570	AID1425162
U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)	Kd	30.0000	1.3820	1.3820	1.3820	AID1425174
Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)	Kd	30.0000	0.0120	1.6396	7.2000	AID1425161
Serine/threonine-protein kinase 16	Homo sapiens (human)	Kd	30.0000	0.0017	1.2483	9.9690	AID1425179
Serine/threonine-protein kinase 10	Homo sapiens (human)	Kd	30.0000	0.0000	2.9234	57.4530	AID1425177
Serine/threonine-protein kinase D3	Homo sapiens (human)	Kd	30.0000	0.0089	2.2738	23.3410	AID1425137
Structural maintenance of chromosomes protein 2	Homo sapiens (human)	Kd	30.0000	0.2090	0.6575	1.1060	AID1425173
Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)	Kd	30.0000	0.1700	1.5781	8.0000	AID1425050
Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)	Kd	30.0000	0.0082	2.3645	62.7720	AID1425054
Serine/threonine-protein kinase LATS1	Homo sapiens (human)	Kd	30.0000	0.0140	1.8393	10.7330	AID1425033
Serine/threonine-protein kinase PAK 4	Homo sapiens (human)	Kd	30.0000	0.0027	2.5694	30.3710	AID1425100
Tyrosine-protein kinase ABL1	Homo sapiens (human)	Kd	30.0000	0.0000	1.0411	13.4530	AID1424890
Epidermal growth factor receptor	Homo sapiens (human)	Kd	30.0000	0.0001	1.3514	20.8270	AID1424983
High affinity nerve growth factor receptor	Homo sapiens (human)	Kd	30.0000	0.0020	1.3484	9.2000	AID1425094
Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)	Kd	30.0000	0.1840	0.1840	0.1840	AID1425011
ADP/ATP translocase 2	Homo sapiens (human)	Kd	30.0000	0.4510	0.4510	0.4510	AID1425169
Protein kinase C beta type	Homo sapiens (human)	Kd	30.0000	0.0013	2.7081	26.3240	AID1425130
Insulin receptor	Homo sapiens (human)	Kd	30.0000	0.0017	1.0823	7.9060	AID1425026
Tyrosine-protein kinase Lck	Homo sapiens (human)	Kd	30.0000	0.0002	1.1174	24.2210	AID1425034
Tyrosine-protein kinase Fyn	Homo sapiens (human)	Kd	30.0000	0.0008	1.4238	8.4000	AID1425008
Cyclin-dependent kinase 1	Homo sapiens (human)	Kd	30.0000	0.2880	1.4952	3.0490	AID1424937
Glycogen phosphorylase, liver form	Homo sapiens (human)	Kd	30.0000	2.1210	2.1210	2.1210	AID1425146
Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)	Kd	30.0000	0.0048	1.0986	7.4000	AID1425003
Adenine phosphoribosyltransferase	Homo sapiens (human)	Kd	30.0000	0.0290	0.0290	0.0290	AID1424914
Tyrosine-protein kinase Yes	Homo sapiens (human)	Kd	30.0000	0.0003	1.3708	17.1520	AID1425212
Tyrosine-protein kinase Lyn	Homo sapiens (human)	Kd	30.0000	0.0006	1.0485	5.7000	AID1425037
Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)	Kd	30.0000	0.0007	0.8642	27.5420	AID1425154
Insulin-like growth factor 1 receptor	Homo sapiens (human)	Kd	30.0000	0.0010	1.9211	19.2170	AID1425022
Signal recognition particle receptor subunit alpha	Homo sapiens (human)	Kd	30.0000	0.0080	0.0080	0.0080	AID1425176
Cytochrome c1, heme protein, mitochondrial	Homo sapiens (human)	Kd	30.0000	0.2020	0.2020	0.2020	AID1424969
Hepatocyte growth factor receptor	Homo sapiens (human)	Kd	30.0000	0.0002	1.6297	8.5000	AID1425076
Tyrosine-protein kinase HCK	Homo sapiens (human)	Kd	30.0000	0.0003	2.0343	15.9930	AID1425017
Platelet-derived growth factor receptor beta	Homo sapiens (human)	Kd	30.0000	0.0001	1.0050	11.1070	AID1425104
Tyrosine-protein kinase Fgr	Homo sapiens (human)	Kd	30.0000	0.0005	1.0721	7.8000	AID1425005
Serine/threonine-protein kinase A-Raf	Homo sapiens (human)	Kd	30.0000	0.0470	9.6832	33.6550	AID1424915
Glycogen phosphorylase, brain form	Homo sapiens (human)	Kd	30.0000	3.5690	3.5690	3.5690	AID1425145
Breakpoint cluster region protein	Homo sapiens (human)	Kd	30.0000	0.0030	1.2196	17.3640	AID1424919
Serine/threonine-protein kinase pim-1	Homo sapiens (human)	Kd	30.0000	0.0010	1.1393	19.3160	AID1425111
Fibroblast growth factor receptor 1	Homo sapiens (human)	Kd	30.0000	0.0003	1.5581	6.2000	AID1425004
DNA topoisomerase 2-alpha	Homo sapiens (human)	Kd	30.0000	0.0640	0.2750	0.4860	AID1425202
Cyclin-dependent kinase 4	Homo sapiens (human)	Kd	30.0000	0.0033	1.6050	8.6000	AID1424946
ADP/ATP translocase 3	Homo sapiens (human)	Kd	30.0000	0.0060	0.2505	0.4950	AID1425170
Proto-oncogene tyrosine-protein kinase Src	Homo sapiens (human)	Kd	30.0000	0.0002	1.5077	9.6000	AID1425175
cAMP-dependent protein kinase type II-alpha regulatory subunit	Homo sapiens (human)	Kd	30.0000	0.0520	1.7535	3.4550	AID1425128
Serine/threonine-protein kinase B-raf	Homo sapiens (human)	Kd	30.0000	0.0002	1.6258	26.0180	AID1424924
Phosphorylase b kinase gamma catalytic chain, liver/testis isoform	Homo sapiens (human)	Kd	30.0000	0.0001	2.0569	9.5000	AID1425110
Ribosyldihydronicotinamide dehydrogenase [quinone]	Homo sapiens (human)	Kd	30.0000	0.0040	6.7556	88.9030	AID1425093
Tyrosine-protein kinase Fer	Homo sapiens (human)	Kd	30.0000	0.0014	1.3604	8.8000	AID1425002
Protein kinase C alpha type	Homo sapiens (human)	Kd	30.0000	0.0003	1.7922	21.3520	AID1425129
cAMP-dependent protein kinase catalytic subunit alpha	Homo sapiens (human)	Kd	30.0000	0.0039	2.9479	23.2450	AID1425123
General transcription and DNA repair factor IIH helicase subunit XPD	Homo sapiens (human)	Kd	30.0000	0.0020	1.6906	12.0220	AID1424996
Casein kinase II subunit alpha'	Homo sapiens (human)	Kd	30.0000	0.0010	2.5309	28.8720	AID1424968
Ras-related protein Rab-6A	Homo sapiens (human)	Kd	30.0000	0.0330	0.0330	0.0330	AID1425150
Ephrin type-A receptor 1	Homo sapiens (human)	Kd	30.0000	0.0041	1.8000	9.8000	AID1424987
Multifunctional protein ADE2	Homo sapiens (human)	Kd	30.0000	5.4810	5.4810	5.4810	AID1425098
cAMP-dependent protein kinase catalytic subunit gamma	Homo sapiens (human)	Kd	30.0000	0.0020	8.5577	49.2780	AID1425125
cAMP-dependent protein kinase catalytic subunit beta	Homo sapiens (human)	Kd	30.0000	0.0130	0.7408	4.1000	AID1425124
Ferrochelatase, mitochondrial	Homo sapiens (human)	Kd	30.0000	0.2430	6.4343	67.9140	AID1425001
Ribosomal protein S6 kinase beta-1	Homo sapiens (human)	Kd	30.0000	0.0013	1.1805	4.8000	AID1425164
Tyrosine-protein kinase JAK1	Homo sapiens (human)	Kd	30.0000	0.0016	1.2166	7.8000	AID1425030
Cyclin-dependent kinase 2	Homo sapiens (human)	Kd	30.0000	0.0070	1.5179	10.4870	AID1424944
Beta-adrenergic receptor kinase 1	Homo sapiens (human)	Kd	30.0000	0.1700	5.5791	22.4940	AID1424908
Probable ATP-dependent RNA helicase DDX6	Homo sapiens (human)	Kd	30.0000	4.1030	4.1030	4.1030	AID1424977
Mitogen-activated protein kinase 3	Homo sapiens (human)	Kd	30.0000	0.4300	5.2743	9.8000	AID1425061
MAP/microtubule affinity-regulating kinase 3	Homo sapiens (human)	Kd	30.0000	0.0030	3.9689	58.2400	AID1425069
Deoxycytidine kinase	Homo sapiens (human)	Kd	30.0000	0.0120	1.0875	2.1630	AID1424970
Mitogen-activated protein kinase 1	Homo sapiens (human)	Kd	30.0000	0.0001	2.7441	7.3000	AID1425056
Ephrin type-A receptor 2	Homo sapiens (human)	Kd	30.0000	0.0009	1.0752	8.1980	AID1424988
Ephrin type-B receptor 2	Homo sapiens (human)	Kd	30.0000	0.0004	3.1536	53.1980	AID1424992
Non-receptor tyrosine-protein kinase TYK2	Homo sapiens (human)	Kd	30.0000	0.0009	1.5575	8.7000	AID1425207
UMP-CMP kinase	Homo sapiens (human)	Kd	30.0000	0.0030	0.0045	0.0060	AID1424959
Phosphatidylethanolamine-binding protein 1	Homo sapiens (human)	Kd	30.0000	0.0030	0.0030	0.0030	AID1425107
Wee1-like protein kinase	Homo sapiens (human)	Kd	30.0000	0.0014	3.5389	65.1580	AID1425210
Heme oxygenase 2	Homo sapiens (human)	Kd	30.0000	0.1190	0.1190	0.1190	AID1425018
DnaJ homolog subfamily A member 1	Homo sapiens (human)	Kd	30.0000	0.9620	0.9620	0.9620	AID1424980
RAC-alpha serine/threonine-protein kinase	Homo sapiens (human)	Kd	30.0000	0.0006	1.0621	4.4000	AID1424910
RAC-beta serine/threonine-protein kinase	Homo sapiens (human)	Kd	30.0000	0.0021	1.6196	8.7000	AID1424911
Dual specificity protein kinase TTK	Homo sapiens (human)	Kd	30.0000	0.0065	1.6269	8.5000	AID1425205
DNA replication licensing factor MCM4	Homo sapiens (human)	Kd	30.0000	0.6290	0.6290	0.6290	AID1425072
Myosin-10	Homo sapiens (human)	Kd	30.0000	0.2290	0.4935	0.7580	AID1425079
Dual specificity mitogen-activated protein kinase kinase 2	Homo sapiens (human)	Kd	30.0000	0.0039	1.6429	9.6000	AID1425039
Receptor-type tyrosine-protein kinase FLT3	Homo sapiens (human)	Kd	30.0000	0.0002	0.9559	9.9000	AID1425006
Bone morphogenetic protein receptor type-1A	Homo sapiens (human)	Kd	30.0000	0.0600	1.5010	7.0000	AID1424921
Activin receptor type-1B	Homo sapiens (human)	Kd	30.0000	0.0040	1.5110	15.2580	AID1424901
TGF-beta receptor type-1	Homo sapiens (human)	Kd	30.0000	0.0050	2.2785	9.6000	AID1425196
TGF-beta receptor type-2	Homo sapiens (human)	Kd	30.0000	0.0800	1.8351	6.9000	AID1425197
Electron transfer flavoprotein subunit beta	Homo sapiens (human)	Kd	30.0000	0.0120	0.0120	0.0120	AID1424999
Tyrosine-protein kinase CSK	Homo sapiens (human)	Kd	30.0000	0.0010	3.4578	39.5530	AID1424960
Glycine--tRNA ligase	Homo sapiens (human)	Kd	30.0000	0.0400	0.0400	0.0400	AID1425010
Protein kinase C iota type	Homo sapiens (human)	Kd	30.0000	0.0260	9.3316	51.0180	AID1425133
Exosome RNA helicase MTR4	Homo sapiens (human)	Kd	30.0000	2.6070	2.6070	2.6070	AID1425168
Serine/threonine-protein kinase mTOR	Homo sapiens (human)	Kd	0.0020	0.0001	0.5993	9.2000	AID1409403
Tyrosine-protein kinase Tec	Homo sapiens (human)	Kd	30.0000	0.0010	1.0095	8.7000	AID1425193
Tyrosine-protein kinase ABL2	Homo sapiens (human)	Kd	30.0000	0.0002	1.1249	14.9240	AID1424891
Tyrosine-protein kinase FRK	Homo sapiens (human)	Kd	30.0000	0.0003	1.2424	10.8370	AID1425007
G protein-coupled receptor kinase 6	Homo sapiens (human)	Kd	30.0000	1.1890	1.4020	1.6150	AID1425012
Tyrosine-protein kinase SYK	Homo sapiens (human)	Kd	30.0000	0.0070	2.0052	9.2260	AID1425188
26S proteasome regulatory subunit 6B	Homo sapiens (human)	Kd	30.0000	0.0050	0.0050	0.0050	AID1425141
Mitogen-activated protein kinase 8	Homo sapiens (human)	Kd	30.0000	0.0110	2.0965	26.0590	AID1425063
Mitogen-activated protein kinase 9	Homo sapiens (human)	Kd	30.0000	0.0020	1.4596	8.1000	AID1425064
Dual specificity mitogen-activated protein kinase kinase 3	Homo sapiens (human)	Kd	30.0000	0.0050	2.0462	6.6000	AID1425040
Phosphatidylinositol 5-phosphate 4-kinase type-2 alpha	Homo sapiens (human)	Kd	30.0000	0.2080	3.6125	7.0170	AID1425113
Casein kinase I isoform alpha	Homo sapiens (human)	Kd	30.0000	0.0010	2.5756	19.3520	AID1424961
Casein kinase I isoform delta	Homo sapiens (human)	Kd	30.0000	0.0150	2.2270	18.3960	AID1424962
MAP kinase-activated protein kinase 2	Homo sapiens (human)	Kd	30.0000	0.0003	2.0274	14.7420	AID1425065
Elongation factor Tu, mitochondrial	Homo sapiens (human)	Kd	30.0000	0.4640	0.4640	0.4640	AID1425206
Choline-phosphate cytidylyltransferase A	Homo sapiens (human)	Kd	30.0000	0.0410	0.0410	0.0410	AID1425103
Cysteine--tRNA ligase, cytoplasmic	Homo sapiens (human)	Kd	30.0000	0.0120	0.3320	0.6520	AID1424932
Casein kinase I isoform epsilon	Homo sapiens (human)	Kd	30.0000	0.0130	1.4086	12.4090	AID1424963
Very long-chain specific acyl-CoA dehydrogenase, mitochondrial	Homo sapiens (human)	Kd	30.0000	1.6890	1.6890	1.6890	AID1424894
Dual specificity protein kinase CLK1	Homo sapiens (human)	Kd	30.0000	0.0020	1.8791	29.8810	AID1424955
Dual specificity protein kinase CLK2	Homo sapiens (human)	Kd	30.0000	0.0070	1.1384	6.5000	AID1424956
Dual specificity protein kinase CLK3	Homo sapiens (human)	Kd	30.0000	0.0100	2.4499	9.0000	AID1424957
Glycogen synthase kinase-3 alpha	Homo sapiens (human)	Kd	30.0000	0.0060	2.4754	22.5430	AID1425013
Glycogen synthase kinase-3 beta	Homo sapiens (human)	Kd	30.0000	0.0070	1.0057	6.1680	AID1425014
Cyclin-dependent kinase 7	Homo sapiens (human)	Kd	30.0000	0.0025	1.6783	7.7000	AID1424949
Cyclin-dependent kinase 9	Homo sapiens (human)	Kd	30.0000	0.0010	1.6166	9.9010	AID1424950
Ras-related protein Rab-27A	Homo sapiens (human)	Kd	30.0000	4.4930	4.4930	4.4930	AID1425149
Interleukin-1 receptor-associated kinase 1	Homo sapiens (human)	Kd	30.0000	0.0061	1.5252	8.5000	AID1425027
Ribosomal protein S6 kinase alpha-3	Homo sapiens (human)	Kd	30.0000	0.0170	2.8896	37.6050	AID1425160
Serine/threonine-protein kinase Nek2	Homo sapiens (human)	Kd	30.0000	0.1100	1.5649	6.5000	AID1425086
Serine/threonine-protein kinase Nek3	Homo sapiens (human)	Kd	30.0000	0.1700	5.9368	38.0880	AID1425087
Dual specificity mitogen-activated protein kinase kinase 6	Homo sapiens (human)	Kd	30.0000	0.0034	2.3943	6.5000	AID1425043
Serine/threonine-protein kinase PLK1	Homo sapiens (human)	Kd	30.0000	0.0001	0.5711	5.0000	AID1425120
LIM domain kinase 1	Homo sapiens (human)	Kd	30.0000	0.0260	1.7840	21.0890	AID1425035
LIM domain kinase 2	Homo sapiens (human)	Kd	30.0000	0.0570	4.9717	52.0560	AID1425036
Mitogen-activated protein kinase 10	Homo sapiens (human)	Kd	30.0000	0.0010	1.6354	5.9000	AID1425057
Tyrosine--tRNA ligase, cytoplasmic	Homo sapiens (human)	Kd	30.0000	3.3160	3.3160	3.3160	AID1425211
5'-AMP-activated protein kinase subunit gamma-1	Homo sapiens (human)	Kd	30.0000	0.0060	1.4681	10.2120	AID1425126
Ephrin type-B receptor 3	Homo sapiens (human)	Kd	30.0000	0.0069	2.1713	6.4100	AID1424993
Ephrin type-A receptor 5	Homo sapiens (human)	Kd	30.0000	0.0002	1.2100	5.9000	AID1424990
Ephrin type-B receptor 4	Homo sapiens (human)	Kd	30.0000	0.0003	2.1678	26.3990	AID1424994
Ephrin type-A receptor 4	Homo sapiens (human)	Kd	30.0000	0.0012	3.1525	43.9420	AID1424989
Adenylate kinase 2, mitochondrial	Homo sapiens (human)	Kd	30.0000	1.0360	1.0360	1.0360	AID1424909
Adenosine kinase	Homo sapiens (human)	Kd	30.0000	0.0130	1.8368	3.4930	AID1424907
Ras-related protein Rab-10	Homo sapiens (human)	Kd	30.0000	1.3480	1.3480	1.3480	AID1425148
Actin-related protein 3	Homo sapiens (human)	Kd	30.0000	0.0360	2.7735	5.5110	AID1424899
Actin-related protein 2	Homo sapiens (human)	Kd	30.0000	0.0040	0.0040	0.0040	AID1424898
GTP-binding nuclear protein Ran	Homo sapiens (human)	Kd	30.0000	0.7590	0.7590	0.7590	AID1425153
Casein kinase I isoform gamma-2	Homo sapiens (human)	Kd	30.0000	0.0460	1.4506	6.6000	AID1424965
Cyclin-dependent kinase 3	Homo sapiens (human)	Kd	30.0000	0.0080	3.0602	63.6140	AID1424945
Cyclin-dependent kinase 6	Homo sapiens (human)	Kd	30.0000	0.0320	1.2007	3.3560	AID1424948
Cyclin-dependent-like kinase 5	Homo sapiens (human)	Kd	30.0000	0.0430	1.3757	8.3000	AID1424947
Cyclin-dependent kinase 16	Homo sapiens (human)	Kd	30.0000	0.0011	1.5855	10.0000	AID1424941
Cyclin-dependent kinase 17	Homo sapiens (human)	Kd	30.0000	0.0010	0.8233	5.6000	AID1424942
ATP-dependent 6-phosphofructokinase, platelet type	Homo sapiens (human)	Kd	30.0000	0.9830	0.9830	0.9830	AID1425108
Dual specificity mitogen-activated protein kinase kinase 1	Homo sapiens (human)	Kd	30.0000	0.0002	1.1386	8.7730	AID1425038
DNA topoisomerase 2-beta	Homo sapiens (human)	Kd	30.0000	0.1480	1.2270	2.5970	AID1425203
Protein kinase C theta type	Homo sapiens (human)	Kd	30.0000	0.0007	1.6140	7.2000	AID1425134
Activin receptor type-1	Homo sapiens (human)	Kd	30.0000	0.0040	1.4853	16.1210	AID1424900
Macrophage-stimulating protein receptor	Homo sapiens (human)	Kd	30.0000	0.0030	2.0718	8.4000	AID1425078
Focal adhesion kinase 1	Homo sapiens (human)	Kd	30.0000	0.0005	1.2255	13.0390	AID1425142
Protein kinase C delta type	Homo sapiens (human)	Kd	30.0000	0.0002	1.1261	9.2060	AID1425131
Tyrosine-protein kinase BTK	Homo sapiens (human)	Kd	30.0000	0.0006	1.5299	10.1530	AID1424925
Activated CDC42 kinase 1	Homo sapiens (human)	Kd	30.0000	0.0020	1.7138	9.6000	AID1425201
Epithelial discoidin domain-containing receptor 1	Homo sapiens (human)	Kd	30.0000	0.0002	1.6314	71.4840	AID1424972
Mitogen-activated protein kinase kinase kinase kinase 2	Homo sapiens (human)	Kd	30.0000	0.0031	1.4681	14.0430	AID1425052
Serine/threonine-protein kinase 4	Homo sapiens (human)	Kd	30.0000	0.0002	1.7120	25.9020	AID1425185
5'-AMP-activated protein kinase catalytic subunit alpha-1	Homo sapiens (human)	Kd	30.0000	0.0037	1.8913	15.3890	AID1425122
Dual specificity mitogen-activated protein kinase kinase 5	Homo sapiens (human)	Kd	30.0000	0.0002	2.6590	65.6770	AID1425042
Mitogen-activated protein kinase 7	Homo sapiens (human)	Kd	30.0000	0.0420	2.0073	9.9000	AID1425062
Serine/threonine-protein kinase PAK 2	Homo sapiens (human)	Kd	30.0000	0.0031	2.3045	6.0000	AID1425099
Serine/threonine-protein kinase 3	Homo sapiens (human)	Kd	30.0000	0.0002	1.8602	17.5260	AID1425182
Mitogen-activated protein kinase kinase kinase 1	Homo sapiens (human)	Kd	30.0000	0.0970	2.5995	12.4730	AID1425044
Integrin-linked protein kinase	Homo sapiens (human)	Kd	30.0000	0.0200	0.4603	1.3290	AID1425024
Rho-associated protein kinase 1	Homo sapiens (human)	Kd	30.0000	0.0003	1.7555	13.4620	AID1425157
Non-receptor tyrosine-protein kinase TNK1	Homo sapiens (human)	Kd	30.0000	0.0018	1.0064	11.2690	AID1425200
Calcium/calmodulin-dependent protein kinase type II subunit gamma	Homo sapiens (human)	Kd	30.0000	0.0005	1.0209	7.8000	AID1424929
Calcium/calmodulin-dependent protein kinase type II subunit delta	Homo sapiens (human)	Kd	30.0000	0.0003	1.5044	20.3010	AID1424928
Dual specificity tyrosine-phosphorylation-regulated kinase 1A	Homo sapiens (human)	Kd	30.0000	0.0001	2.1016	40.2910	AID1424981
Activin receptor type-2B	Homo sapiens (human)	Kd	30.0000	0.0076	2.7328	9.9000	AID1424902
Bone morphogenetic protein receptor type-2	Homo sapiens (human)	Kd	30.0000	0.0190	2.5917	14.3770	AID1424923
Protein-tyrosine kinase 6	Homo sapiens (human)	Kd	30.0000	0.0043	1.7430	9.0000	AID1425144
cGMP-dependent protein kinase 1	Homo sapiens (human)	Kd	30.0000	0.0016	0.7072	3.8000	AID1425138
Cyclin-dependent kinase 13	Homo sapiens (human)	Kd	30.0000	0.0009	1.2571	4.5180	AID1424940
Inhibitor of nuclear factor kappa-B kinase subunit epsilon	Homo sapiens (human)	Kd	30.0000	0.0051	1.1093	8.3000	AID1425023
Protein-tyrosine kinase 2-beta	Homo sapiens (human)	Kd	30.0000	0.0011	1.9450	30.4140	AID1425143
Maternal embryonic leucine zipper kinase	Homo sapiens (human)	Kd	30.0000	0.0049	2.2835	29.9330	AID1425074
Structural maintenance of chromosomes protein 1A	Homo sapiens (human)	Kd	30.0000	0.3650	0.3650	0.3650	AID1425172
Chromodomain-helicase-DNA-binding protein 4	Homo sapiens (human)	Kd	30.0000	0.0030	0.0030	0.0030	AID1424952
Peroxisomal acyl-coenzyme A oxidase 1	Homo sapiens (human)	Kd	30.0000	0.0140	0.1425	0.2710	AID1424895
Ephrin type-A receptor 7	Homo sapiens (human)	Kd	30.0000	0.0025	1.4445	6.5000	AID1424991
Delta(24)-sterol reductase	Homo sapiens (human)	Kd	30.0000	0.4320	0.4320	0.4320	AID1424978
Ribosomal protein S6 kinase alpha-1	Homo sapiens (human)	Kd	30.0000	0.0280	2.5286	22.7260	AID1425159
Dual specificity testis-specific protein kinase 1	Homo sapiens (human)	Kd	30.0000	0.0330	1.7568	5.6000	AID1425194
Myosin light chain kinase, smooth muscle	Homo sapiens (human)	Kd	30.0000	0.0030	1.2088	7.9000	AID1425081
Mitogen-activated protein kinase 11	Homo sapiens (human)	Kd	30.0000	0.0001	0.4610	3.7430	AID1425058
Serine/threonine-protein kinase STK11	Homo sapiens (human)	Kd	30.0000	0.0030	0.9949	5.9000	AID1425178
Serine/threonine-protein kinase N1	Homo sapiens (human)	Kd	30.0000	0.0013	3.1729	49.8130	AID1425117
Serine/threonine-protein kinase N2	Homo sapiens (human)	Kd	30.0000	0.0018	1.7527	9.9000	AID1425118
Mitogen-activated protein kinase 14	Homo sapiens (human)	Kd	30.0000	0.0000	0.5036	8.5000	AID1425059
Calcium/calmodulin-dependent protein kinase type IV	Homo sapiens (human)	Kd	30.0000	0.0300	1.9215	5.4600	AID1424930
Mitogen-activated protein kinase kinase kinase 11	Homo sapiens (human)	Kd	30.0000	0.0110	1.5639	17.9840	AID1425045
Discoidin domain-containing receptor 2	Homo sapiens (human)	Kd	30.0000	0.0030	1.9888	42.2800	AID1424973
AP2-associated protein kinase 1	Homo sapiens (human)	Kd	30.0000	0.0012	1.3707	13.7110	AID1424889
Myosin light chain kinase 3	Homo sapiens (human)	Kd	30.0000	0.0020	1.6184	10.4240	AID1425082
Putative heat shock protein HSP 90-beta 2	Homo sapiens (human)	Kd	30.0000	2.5660	2.5660	2.5660	AID1425019
Serine/threonine-protein kinase MRCK alpha	Homo sapiens (human)	Kd	30.0000	0.0570	4.5547	14.0200	AID1424933
Serine/threonine-protein kinase MRCK gamma	Homo sapiens (human)	Kd	30.0000	0.0370	1.9625	9.5000	AID1424935
Acyl-CoA dehydrogenase family member 10	Homo sapiens (human)	Kd	30.0000	0.0780	1.6997	3.9570	AID1424892
Serine/threonine-protein kinase N3	Homo sapiens (human)	Kd	30.0000	0.0990	0.7365	1.3740	AID1425119
Serine/threonine-protein kinase ULK3	Homo sapiens (human)	Kd	30.0000	0.0012	1.3350	9.9000	AID1425209
Uncharacterized protein FLJ45252	Homo sapiens (human)	Kd	30.0000	0.0030	1.2292	9.3110	AID1425147
Acyl-CoA dehydrogenase family member 11	Homo sapiens (human)	Kd	30.0000	1.9160	3.0730	4.1470	AID1424893
Serine/threonine-protein kinase/endoribonuclease IRE2	Homo sapiens (human)	Kd	30.0000	0.1160	0.7604	1.5000	AID1424998
Serine/threonine-protein kinase MARK2	Homo sapiens (human)	Kd	30.0000	0.0001	1.8425	11.1030	AID1425068
ATP-dependent RNA helicase DHX30	Homo sapiens (human)	Kd	30.0000	0.0060	0.0060	0.0060	AID1424979
Serine/threonine-protein kinase TAO1	Homo sapiens (human)	Kd	30.0000	0.0004	2.1612	18.7570	AID1425189
STE20-related kinase adapter protein alpha	Homo sapiens (human)	Kd	30.0000	0.3160	1.7208	3.6720	AID1425186
AarF domain-containing protein kinase 1	Homo sapiens (human)	Kd	30.0000	0.0230	3.1137	22.7470	AID1424904
Mitogen-activated protein kinase kinase kinase kinase 3	Homo sapiens (human)	Kd	30.0000	0.0051	1.6413	15.4350	AID1425053
Eukaryotic peptide chain release factor GTP-binding subunit ERF3B	Homo sapiens (human)	Kd	30.0000	0.0030	0.0030	0.0030	AID1425015
Atypical kinase COQ8A, mitochondrial	Homo sapiens (human)	Kd	30.0000	0.0940	5.1673	65.3020	AID1424905
Phosphatidylinositol 5-phosphate 4-kinase type-2 gamma	Homo sapiens (human)	Kd	30.0000	0.0030	2.7522	8.8000	AID1425115
Mitogen-activated protein kinase 15	Homo sapiens (human)	Kd	30.0000	0.0049	0.6880	4.5000	AID1425060
Serine/threonine-protein kinase Nek9	Homo sapiens (human)	Kd	30.0000	0.0160	2.7428	19.6170	AID1425089
Serine/threonine-protein kinase Nek7	Homo sapiens (human)	Kd	30.0000	0.0030	3.6719	8.7000	AID1425088
ATP-dependent RNA helicase DDX1	Homo sapiens (human)	Kd	30.0000	0.0860	0.0860	0.0860	AID1424974
Mitogen-activated protein kinase kinase kinase kinase 1	Homo sapiens (human)	Kd	30.0000	0.0010	0.9378	5.5000	AID1425051
Aurora kinase B	Homo sapiens (human)	Kd	30.0000	0.0020	1.0614	22.8520	AID1424918
MAP/microtubule affinity-regulating kinase 4	Homo sapiens (human)	Kd	30.0000	0.0054	1.1029	4.9000	AID1425070
Serine/threonine-protein kinase Nek1	Homo sapiens (human)	Kd	30.0000	0.1700	2.4294	8.3000	AID1425085
PAS domain-containing serine/threonine-protein kinase	Homo sapiens (human)	Kd	30.0000	1.0670	1.0670	1.0670	AID1425102
Calcium/calmodulin-dependent protein kinase kinase 2	Homo sapiens (human)	Kd	30.0000	0.0000	3.2331	52.8470	AID1424931
EKC/KEOPS complex subunit TP53RK	Homo sapiens (human)	Kd	30.0000	0.3110	1.9519	3.8400	AID1425204
Dual specificity testis-specific protein kinase 2	Homo sapiens (human)	Kd	30.0000	0.0020	0.0020	0.0020	AID1425195
Membrane-associated tyrosine- and threonine-specific cdc2-inhibitory kinase	Homo sapiens (human)	Kd	30.0000	0.0440	0.9285	2.9000	AID1425116
Mitogen-activated protein kinase kinase kinase 5	Homo sapiens (human)	Kd	30.0000	0.0700	6.5647	50.5360	AID1425049
Mitogen-activated protein kinase kinase kinase 3	Homo sapiens (human)	Kd	30.0000	0.0060	1.5331	9.9000	AID1425047
Eukaryotic translation initiation factor 2-alpha kinase 1	Homo sapiens (human)	Kd	30.0000	0.0580	1.9224	4.8360	AID1424984
Nucleolar GTP-binding protein 1	Homo sapiens (human)	Kd	30.0000	0.0090	4.1035	8.1980	AID1425016
Serine/threonine-protein kinase D2	Homo sapiens (human)	Kd	30.0000	0.0081	2.3723	25.0190	AID1425136
NUAK family SNF1-like kinase 2	Homo sapiens (human)	Kd	30.0000	0.0001	0.6774	4.6000	AID1425095
RNA cytidine acetyltransferase	Homo sapiens (human)	Kd	30.0000	1.2400	1.2400	1.2400	AID1425083
Serine/threonine-protein kinase SIK2	Homo sapiens (human)	Kd	30.0000	0.0011	1.8165	41.7950	AID1425166
STE20-like serine/threonine-protein kinase	Homo sapiens (human)	Kd	30.0000	0.0000	3.8573	99.2320	AID1425171
Serine/threonine-protein kinase TAO3	Homo sapiens (human)	Kd	30.0000	0.0002	2.7131	14.1960	AID1425191
dCTP pyrophosphatase 1	Homo sapiens (human)	Kd	30.0000	0.5730	1.7403	3.0540	AID1424971
Dual specificity protein kinase CLK4	Homo sapiens (human)	Kd	30.0000	0.0020	1.4122	8.3000	AID1424958
Casein kinase I isoform gamma-1	Homo sapiens (human)	Kd	30.0000	0.0530	2.0622	5.7000	AID1424964
Phenylalanine--tRNA ligase beta subunit	Homo sapiens (human)	Kd	30.0000	0.0030	0.0045	0.0060	AID1425000
BMP-2-inducible protein kinase	Homo sapiens (human)	Kd	30.0000	0.0022	2.4097	56.0320	AID1424920
Obg-like ATPase 1	Homo sapiens (human)	Kd	30.0000	0.0030	0.0050	0.0070	AID1425096
Interleukin-1 receptor-associated kinase 4	Homo sapiens (human)	Kd	30.0000	0.0017	3.4719	34.1450	AID1425029
Mitogen-activated protein kinase kinase kinase 20	Homo sapiens (human)	Kd	30.0000	0.0023	1.7034	13.6380	AID1425213
Cyclin-dependent kinase 12	Homo sapiens (human)	Kd	30.0000	0.0320	1.8032	5.6350	AID1424939
NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 13	Homo sapiens (human)	Kd	30.0000	3.9200	3.9200	3.9200	AID1425084
Serine/threonine-protein kinase 26	Homo sapiens (human)	Kd	30.0000	0.0074	1.7380	8.3000	AID1425181
Succinate--CoA ligase [ADP-forming] subunit beta, mitochondrial	Homo sapiens (human)	Kd	30.0000	0.0070	0.0070	0.0070	AID1425187
Serine/threonine-protein kinase NLK	Homo sapiens (human)	Kd	30.0000	0.0060	1.0226	4.4000	AID1425090
5'-AMP-activated protein kinase subunit gamma-2	Homo sapiens (human)	Kd	30.0000	0.0050	1.1581	9.1280	AID1425127
Serine/threonine-protein kinase TBK1	Homo sapiens (human)	Kd	30.0000	0.0009	1.7674	49.6010	AID1425192
Septin-9	Homo sapiens (human)	Kd	30.0000	0.0100	0.2430	0.6350	AID1425165
Ribosomal protein S6 kinase alpha-6	Homo sapiens (human)	Kd	30.0000	0.0040	2.4153	23.7620	AID1425163
TRAF2 and NCK-interacting protein kinase	Homo sapiens (human)	Kd	30.0000	0.0047	1.3935	10.0000	AID1425199
Serine/threonine-protein kinase TAO2	Homo sapiens (human)	Kd	30.0000	0.0100	2.0176	12.9420	AID1425190
Long-chain-fatty-acid--CoA ligase 5	Homo sapiens (human)	Kd	30.0000	0.0080	0.6353	1.6900	AID1424897
RAC-gamma serine/threonine-protein kinase	Homo sapiens (human)	Kd	30.0000	0.0025	1.7646	6.2000	AID1424912
Serine/threonine-protein kinase SIK3	Homo sapiens (human)	Kd	30.0000	0.0005	1.5086	10.3180	AID1425167
Mitogen-activated protein kinase kinase kinase 2	Homo sapiens (human)	Kd	30.0000	0.0024	1.3298	6.9000	AID1425046
Thyroid hormone receptor-associated protein 3	Homo sapiens (human)	Kd	30.0000	2.7460	2.7460	2.7460	AID1425198
Mitogen-activated protein kinase kinase kinase kinase 5	Homo sapiens (human)	Kd	30.0000	0.0005	1.9494	50.2140	AID1425055
Receptor-interacting serine/threonine-protein kinase 3	Homo sapiens (human)	Kd	30.0000	0.0110	1.4797	6.7000	AID1425156
Serine/threonine-protein kinase MRCK beta	Homo sapiens (human)	Kd	30.0000	0.0340	3.6252	50.0050	AID1424934
Interleukin-1 receptor-associated kinase 3	Homo sapiens (human)	Kd	30.0000	0.0070	1.7137	25.5810	AID1425028
Casein kinase I isoform gamma-3	Homo sapiens (human)	Kd	30.0000	0.0970	2.3978	8.7000	AID1424966
Mitogen-activated protein kinase kinase kinase 4	Homo sapiens (human)	Kd	30.0000	0.0390	2.3970	8.4000	AID1425048
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
positive regulation of gene expression	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
cartilage condensation	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
ovarian cumulus expansion	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
osteoblast differentiation	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
eye development	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
chondrocyte development	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
inflammatory response	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
central nervous system neuron differentiation	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
proteoglycan biosynthetic process	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
positive regulation of bone mineralization	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
BMP signaling pathway	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
retinal ganglion cell axon guidance	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
positive regulation of chondrocyte differentiation	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
ovulation cycle	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
positive regulation of osteoblast differentiation	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
retina development in camera-type eye	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
endochondral bone morphogenesis	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
positive regulation of cartilage development	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
cellular response to BMP stimulus	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
positive regulation of extrinsic apoptotic signaling pathway via death domain receptors	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
negative regulation of chondrocyte proliferation	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
dorsal/ventral pattern formation	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
protein phosphorylation	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
cellular response to growth factor stimulus	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
G1/S transition of mitotic cell cycle	Cell division cycle 7-related protein kinase	Homo sapiens (human)
positive regulation of cell population proliferation	Cell division cycle 7-related protein kinase	Homo sapiens (human)
positive regulation of nuclear cell cycle DNA replication	Cell division cycle 7-related protein kinase	Homo sapiens (human)
positive regulation of G2/M transition of mitotic cell cycle	Cell division cycle 7-related protein kinase	Homo sapiens (human)
cell cycle phase transition	Cell division cycle 7-related protein kinase	Homo sapiens (human)
cell division	Cell division cycle 7-related protein kinase	Homo sapiens (human)
peptidyl-serine phosphorylation	Cell division cycle 7-related protein kinase	Homo sapiens (human)
double-strand break repair via break-induced replication	Cell division cycle 7-related protein kinase	Homo sapiens (human)
signal transduction	Cell division cycle 7-related protein kinase	Homo sapiens (human)
positive regulation of centriole replication	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
protein phosphorylation	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
centriole replication	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
positive regulation of centriole replication	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
cilium assembly	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
trophoblast giant cell differentiation	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
de novo centriole assembly involved in multi-ciliated epithelial cell differentiation	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
translational initiation	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
chromosome segregation	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
extrinsic apoptotic signaling pathway via death domain receptors	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
response to virus	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
RNA secondary structure unwinding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of gene expression	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
Wnt signaling pathway	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
negative regulation of translation	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of cell growth	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
negative regulation of cell growth	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
negative regulation of protein-containing complex assembly	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of protein autophosphorylation	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of type I interferon production	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
DNA duplex unwinding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of interferon-alpha production	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of interferon-beta production	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
stress granule assembly	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of toll-like receptor 7 signaling pathway	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of toll-like receptor 8 signaling pathway	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
intracellular signal transduction	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of translation in response to endoplasmic reticulum stress	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cytosolic ribosome assembly	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of apoptotic process	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
negative regulation of apoptotic process	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
negative regulation of cysteine-type endopeptidase activity involved in apoptotic process	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of cysteine-type endopeptidase activity involved in apoptotic process	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of viral genome replication	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
innate immune response	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of translation	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of translational initiation	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
lipid homeostasis	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cellular response to arsenic-containing substance	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cellular response to osmotic stress	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of chemokine (C-C motif) ligand 5 production	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of protein serine/threonine kinase activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of canonical Wnt signaling pathway	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
intrinsic apoptotic signaling pathway	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cellular response to virus	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of G1/S transition of mitotic cell cycle	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of NLRP3 inflammasome complex assembly	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
negative regulation of non-canonical NF-kappaB signal transduction	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of non-canonical NF-kappaB signal transduction	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of protein acetylation	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
negative regulation of extrinsic apoptotic signaling pathway via death domain receptors	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
positive regulation of protein K63-linked ubiquitination	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
protein localization to cytoplasmic stress granule	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathway	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
negative regulation of gene expression	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
gamete generation	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cell differentiation	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
pyridoxal 5'-phosphate salvage	Pyridoxal kinase	Homo sapiens (human)
pyridoxal metabolic process	Pyridoxal kinase	Homo sapiens (human)
pyridoxamine metabolic process	Pyridoxal kinase	Homo sapiens (human)
mitotic cell cycle	Citron Rho-interacting kinase	Homo sapiens (human)
mitotic cytokinesis	Citron Rho-interacting kinase	Homo sapiens (human)
positive regulation of cytokinesis	Citron Rho-interacting kinase	Homo sapiens (human)
negative regulation of hippo signaling	Citron Rho-interacting kinase	Homo sapiens (human)
generation of neurons	Citron Rho-interacting kinase	Homo sapiens (human)
neuron apoptotic process	Citron Rho-interacting kinase	Homo sapiens (human)
DNA damage checkpoint signaling	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
G2/M transition of mitotic cell cycle	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
inner cell mass cell proliferation	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
DNA replication	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
DNA repair	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
chromatin remodeling	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
protein phosphorylation	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
apoptotic process	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
DNA damage response	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
nucleus organization	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
mitotic G2 DNA damage checkpoint signaling	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
regulation of double-strand break repair via homologous recombination	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
peptidyl-threonine phosphorylation	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
regulation of cell population proliferation	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
signal transduction in response to DNA damage	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
mitotic G2/M transition checkpoint	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
positive regulation of cell cycle	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
negative regulation of gene expression, epigenetic	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
negative regulation of mitotic nuclear division	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
regulation of mitotic centrosome separation	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
negative regulation of G0 to G1 transition	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
cellular response to mechanical stimulus	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
cellular response to caffeine	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
replicative senescence	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
regulation of signal transduction by p53 class mediator	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
apoptotic process involved in development	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
negative regulation of DNA biosynthetic process	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
protein phosphorylation	Aurora kinase A	Homo sapiens (human)
response to wounding	Aurora kinase A	Homo sapiens (human)
liver regeneration	Aurora kinase A	Homo sapiens (human)
G2/M transition of mitotic cell cycle	Aurora kinase A	Homo sapiens (human)
mitotic cell cycle	Aurora kinase A	Homo sapiens (human)
chromatin remodeling	Aurora kinase A	Homo sapiens (human)
protein phosphorylation	Aurora kinase A	Homo sapiens (human)
apoptotic process	Aurora kinase A	Homo sapiens (human)
spindle organization	Aurora kinase A	Homo sapiens (human)
spindle assembly involved in female meiosis I	Aurora kinase A	Homo sapiens (human)
mitotic centrosome separation	Aurora kinase A	Homo sapiens (human)
anterior/posterior axis specification	Aurora kinase A	Homo sapiens (human)
regulation of G2/M transition of mitotic cell cycle	Aurora kinase A	Homo sapiens (human)
negative regulation of gene expression	Aurora kinase A	Homo sapiens (human)
peptidyl-serine phosphorylation	Aurora kinase A	Homo sapiens (human)
regulation of protein stability	Aurora kinase A	Homo sapiens (human)
negative regulation of protein binding	Aurora kinase A	Homo sapiens (human)
positive regulation of proteasomal ubiquitin-dependent protein catabolic process	Aurora kinase A	Homo sapiens (human)
negative regulation of apoptotic process	Aurora kinase A	Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic process	Aurora kinase A	Homo sapiens (human)
positive regulation of mitotic nuclear division	Aurora kinase A	Homo sapiens (human)
positive regulation of mitotic cell cycle	Aurora kinase A	Homo sapiens (human)
regulation of centrosome cycle	Aurora kinase A	Homo sapiens (human)
protein autophosphorylation	Aurora kinase A	Homo sapiens (human)
cell division	Aurora kinase A	Homo sapiens (human)
centrosome localization	Aurora kinase A	Homo sapiens (human)
cilium disassembly	Aurora kinase A	Homo sapiens (human)
protein localization to centrosome	Aurora kinase A	Homo sapiens (human)
positive regulation of mitochondrial fission	Aurora kinase A	Homo sapiens (human)
positive regulation of oocyte maturation	Aurora kinase A	Homo sapiens (human)
regulation of signal transduction by p53 class mediator	Aurora kinase A	Homo sapiens (human)
neuron projection extension	Aurora kinase A	Homo sapiens (human)
mitotic spindle organization	Aurora kinase A	Homo sapiens (human)
regulation of cytokinesis	Aurora kinase A	Homo sapiens (human)
receptor-mediated endocytosis	Cyclin-G-associated kinase	Homo sapiens (human)
endoplasmic reticulum organization	Cyclin-G-associated kinase	Homo sapiens (human)
Golgi organization	Cyclin-G-associated kinase	Homo sapiens (human)
negative regulation of neuron projection development	Cyclin-G-associated kinase	Homo sapiens (human)
synaptic vesicle uncoating	Cyclin-G-associated kinase	Homo sapiens (human)
protein localization to Golgi apparatus	Cyclin-G-associated kinase	Homo sapiens (human)
intracellular transport	Cyclin-G-associated kinase	Homo sapiens (human)
clathrin coat assembly	Cyclin-G-associated kinase	Homo sapiens (human)
chaperone cofactor-dependent protein refolding	Cyclin-G-associated kinase	Homo sapiens (human)
clathrin coat disassembly	Cyclin-G-associated kinase	Homo sapiens (human)
clathrin-dependent endocytosis	Cyclin-G-associated kinase	Homo sapiens (human)
protein localization to plasma membrane	Cyclin-G-associated kinase	Homo sapiens (human)
Golgi to lysosome transport	Cyclin-G-associated kinase	Homo sapiens (human)
regulation of clathrin coat assembly	Cyclin-G-associated kinase	Homo sapiens (human)
protein phosphorylation	Ephrin type-B receptor 6	Homo sapiens (human)
ephrin receptor signaling pathway	Ephrin type-B receptor 6	Homo sapiens (human)
axon guidance	Ephrin type-B receptor 6	Homo sapiens (human)
fatty acid beta-oxidation using acyl-CoA oxidase	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
lipid homeostasis	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
xenobiotic metabolic process	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
xenobiotic transmembrane transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
bile acid and bile salt transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
glucuronoside transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
xenobiotic transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
transmembrane transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
leukotriene transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
monoatomic anion transmembrane transport	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
transport across blood-brain barrier	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
prostaglandin secretion	Multidrug resistance-associated protein 4	Homo sapiens (human)
cilium assembly	Multidrug resistance-associated protein 4	Homo sapiens (human)
platelet degranulation	Multidrug resistance-associated protein 4	Homo sapiens (human)
xenobiotic metabolic process	Multidrug resistance-associated protein 4	Homo sapiens (human)
xenobiotic transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
bile acid and bile salt transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
prostaglandin transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
urate transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
glutathione transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
cAMP transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
leukotriene transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
monoatomic anion transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
export across plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
transport across blood-brain barrier	Multidrug resistance-associated protein 4	Homo sapiens (human)
guanine nucleotide transmembrane transport	Multidrug resistance-associated protein 4	Homo sapiens (human)
toll-like receptor 2 signaling pathway	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transduction	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of cytokine-mediated signaling pathway	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
adaptive immune response	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of T-helper 1 type immune response	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
apoptotic process	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
inflammatory response	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
signal transduction	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
canonical NF-kappaB signal transduction	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
JNK cascade	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of peptidyl-threonine phosphorylation	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
cytokine-mediated signaling pathway	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of protein ubiquitination	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
lipopolysaccharide-mediated signaling pathway	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of protein binding	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of chemokine production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of interferon-alpha production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of interferon-beta production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of type II interferon production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of interleukin-1 beta production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of interleukin-12 production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of interleukin-2 production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of interleukin-6 production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of tumor necrosis factor production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of stress-activated MAPK cascade	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
immature T cell proliferation in thymus	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of immature T cell proliferation in thymus	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylation	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
toll-like receptor 4 signaling pathway	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
CD4-positive, alpha-beta T cell proliferation	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
defense response to bacterium	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of apoptotic process	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
response to exogenous dsRNA	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
innate immune response	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of T-helper 1 cell differentiation	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of JNK cascade	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylation	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
defense response to Gram-positive bacterium	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
T cell receptor signaling pathway	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of NF-kappaB transcription factor activity	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
protein homooligomerization	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
stress-activated MAPK cascade	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of macrophage cytokine production	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
ERK1 and ERK2 cascade	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascade	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
nucleotide-binding oligomerization domain containing 1 signaling pathway	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
nucleotide-binding oligomerization domain containing 2 signaling pathway	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
response to interleukin-1	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
response to interleukin-12	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
response to interleukin-18	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
cellular response to lipoteichoic acid	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
cellular response to peptidoglycan	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
cellular response to muramyl dipeptide	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
activation of cysteine-type endopeptidase activity	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
xenophagy	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of protein K63-linked ubiquitination	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of xenophagy	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of CD4-positive, alpha-beta T cell proliferation	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transduction	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
chromatin remodeling	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
apoptotic process	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
chromosome segregation	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
regulation of sister chromatid cohesion	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
mitotic spindle assembly checkpoint signaling	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
cell division	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
regulation of chromosome segregation	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
positive regulation of maintenance of mitotic sister chromatid cohesion, centromeric	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
meiotic sister chromatid cohesion, centromeric	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
mitochondrion organization	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial genome maintenance	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial fission	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
neural tube closure	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
apoptotic process	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrion organization	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
inner mitochondrial membrane organization	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
visual perception	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial fusion	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
axonal transport of mitochondrion	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
positive regulation of interleukin-17 production	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
cristae formation	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
negative regulation of apoptotic process	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
GTP metabolic process	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
protein complex oligomerization	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
membrane fusion	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
negative regulation of release of cytochrome c from mitochondria	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
cellular senescence	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
membrane tubulation	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
negative regulation of endoplasmic reticulum stress-induced intrinsic apoptotic signaling pathway	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial inner membrane fusion	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
positive regulation of T-helper 17 cell lineage commitment	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
regulation of translational initiation	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
ribosome assembly	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
translational initiation	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
epithelial to mesenchymal transition	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of protein phosphorylation	Rho-associated protein kinase 2	Homo sapiens (human)
response to ischemia	Rho-associated protein kinase 2	Homo sapiens (human)
aortic valve morphogenesis	Rho-associated protein kinase 2	Homo sapiens (human)
protein phosphorylation	Rho-associated protein kinase 2	Homo sapiens (human)
smooth muscle contraction	Rho-associated protein kinase 2	Homo sapiens (human)
canonical NF-kappaB signal transduction	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of endothelial cell migration	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of cardiac muscle hypertrophy	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of gene expression	Rho-associated protein kinase 2	Homo sapiens (human)
negative regulation of gene expression	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of centrosome duplication	Rho-associated protein kinase 2	Homo sapiens (human)
negative regulation of angiogenesis	Rho-associated protein kinase 2	Homo sapiens (human)
actin cytoskeleton organization	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of cell adhesion	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of cell migration	Rho-associated protein kinase 2	Homo sapiens (human)
cortical actin cytoskeleton organization	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of nervous system process	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of connective tissue growth factor production	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of actin cytoskeleton organization	Rho-associated protein kinase 2	Homo sapiens (human)
negative regulation of myosin-light-chain-phosphatase activity	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of circadian rhythm	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of MAPK cascade	Rho-associated protein kinase 2	Homo sapiens (human)
modulation by host of viral process	Rho-associated protein kinase 2	Homo sapiens (human)
negative regulation of nitric oxide biosynthetic process	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of keratinocyte differentiation	Rho-associated protein kinase 2	Homo sapiens (human)
rhythmic process	Rho-associated protein kinase 2	Homo sapiens (human)
centrosome duplication	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of stress fiber assembly	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of stress fiber assembly	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of focal adhesion assembly	Rho-associated protein kinase 2	Homo sapiens (human)
mRNA destabilization	Rho-associated protein kinase 2	Homo sapiens (human)
negative regulation of biomineral tissue development	Rho-associated protein kinase 2	Homo sapiens (human)
cellular response to testosterone stimulus	Rho-associated protein kinase 2	Homo sapiens (human)
response to transforming growth factor beta	Rho-associated protein kinase 2	Homo sapiens (human)
protein localization to plasma membrane	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of fibroblast growth factor production	Rho-associated protein kinase 2	Homo sapiens (human)
blood vessel diameter maintenance	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of angiotensin-activated signaling pathway	Rho-associated protein kinase 2	Homo sapiens (human)
negative regulation of protein localization to lysosome	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of cellular response to hypoxia	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of amyloid-beta formation	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of protein localization to early endosome	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of amyloid precursor protein catabolic process	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of establishment of endothelial barrier	Rho-associated protein kinase 2	Homo sapiens (human)
negative regulation of bicellular tight junction assembly	Rho-associated protein kinase 2	Homo sapiens (human)
cellular response to acetylcholine	Rho-associated protein kinase 2	Homo sapiens (human)
positive regulation of connective tissue replacement	Rho-associated protein kinase 2	Homo sapiens (human)
response to angiotensin	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of establishment of cell polarity	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of cell motility	Rho-associated protein kinase 2	Homo sapiens (human)
actomyosin structure organization	Rho-associated protein kinase 2	Homo sapiens (human)
peptidyl-threonine phosphorylation	Rho-associated protein kinase 2	Homo sapiens (human)
mitotic cytokinesis	Rho-associated protein kinase 2	Homo sapiens (human)
embryonic morphogenesis	Rho-associated protein kinase 2	Homo sapiens (human)
regulation of cell junction assembly	Rho-associated protein kinase 2	Homo sapiens (human)
Rho protein signal transduction	Rho-associated protein kinase 2	Homo sapiens (human)
autophagosome assembly	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
protein phosphorylation	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
autophagy	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
signal transduction	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
protein localization	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
negative regulation of cell population proliferation	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
positive regulation of autophagy	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
regulation of tumor necrosis factor-mediated signaling pathway	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
macroautophagy	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
regulation of macroautophagy	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
peptidyl-serine phosphorylation	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
peptidyl-threonine phosphorylation	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
neuron projection regeneration	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
neuron projection development	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
negative regulation of protein-containing complex assembly	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
cellular response to nutrient levels	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
response to starvation	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
protein autophosphorylation	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
regulation of protein lipidation	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
positive regulation of autophagosome assembly	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
axon extension	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
autophagy of mitochondrion	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
reticulophagy	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
piecemeal microautophagy of the nucleus	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
negative regulation of collateral sprouting	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
endothelial cell proliferation	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
mRNA catabolic process	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
protein phosphorylation	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
regulation of macroautophagy	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
positive regulation of RNA splicing	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
cellular response to unfolded protein	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
response to endoplasmic reticulum stress	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
cellular response to vascular endothelial growth factor stimulus	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
peptidyl-serine autophosphorylation	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
IRE1-mediated unfolded protein response	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
positive regulation of JUN kinase activity	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
protein autophosphorylation	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
mRNA splicing, via endonucleolytic cleavage and ligation	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stress	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
cellular response to hydrogen peroxide	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
cellular response to glucose stimulus	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
positive regulation of endoplasmic reticulum unfolded protein response	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
insulin metabolic process	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
positive regulation of vascular associated smooth muscle cell proliferation	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
peptidyl-serine trans-autophosphorylation	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
negative regulation of cytokine production	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
chromatin remodeling	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
regulation of DNA-templated transcription	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
protein phosphorylation	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
inflammatory response	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
axon guidance	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
positive regulation of CREB transcription factor activity	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
intracellular signal transduction	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
post-translational protein modification	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
negative regulation of DNA-templated transcription	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
positive regulation of NF-kappaB transcription factor activity	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
interleukin-1-mediated signaling pathway	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
regulation of postsynapse organization	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
peptidyl-serine phosphorylation	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
cis assembly of pre-catalytic spliceosome	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
spliceosome conformational change to release U4 (or U4atac) and U1 (or U11)	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
mRNA splicing, via spliceosome	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
osteoblast differentiation	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
negative regulation of cytokine production	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
chromatin remodeling	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
regulation of DNA-templated transcription	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
protein phosphorylation	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
inflammatory response	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
positive regulation of CREB transcription factor activity	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
intracellular signal transduction	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
post-translational protein modification	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
positive regulation of NF-kappaB transcription factor activity	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
interleukin-1-mediated signaling pathway	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
peptidyl-serine phosphorylation	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Serine/threonine-protein kinase 16	Homo sapiens (human)
protein autophosphorylation	Serine/threonine-protein kinase 16	Homo sapiens (human)
cellular response to transforming growth factor beta stimulus	Serine/threonine-protein kinase 16	Homo sapiens (human)
protein phosphorylation	Serine/threonine-protein kinase 10	Homo sapiens (human)
protein autophosphorylation	Serine/threonine-protein kinase 10	Homo sapiens (human)
lymphocyte aggregation	Serine/threonine-protein kinase 10	Homo sapiens (human)
regulation of lymphocyte migration	Serine/threonine-protein kinase 10	Homo sapiens (human)
protein phosphorylation	Serine/threonine-protein kinase D3	Homo sapiens (human)
protein kinase C-activating G protein-coupled receptor signaling pathway	Serine/threonine-protein kinase D3	Homo sapiens (human)
sphingolipid biosynthetic process	Serine/threonine-protein kinase D3	Homo sapiens (human)
intracellular signal transduction	Serine/threonine-protein kinase D3	Homo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathway	Serine/threonine-protein kinase D3	Homo sapiens (human)
fatty acid metabolic process	Bile salt export pump	Homo sapiens (human)
bile acid biosynthetic process	Bile salt export pump	Homo sapiens (human)
xenobiotic metabolic process	Bile salt export pump	Homo sapiens (human)
xenobiotic transmembrane transport	Bile salt export pump	Homo sapiens (human)
response to oxidative stress	Bile salt export pump	Homo sapiens (human)
bile acid metabolic process	Bile salt export pump	Homo sapiens (human)
response to organic cyclic compound	Bile salt export pump	Homo sapiens (human)
bile acid and bile salt transport	Bile salt export pump	Homo sapiens (human)
canalicular bile acid transport	Bile salt export pump	Homo sapiens (human)
protein ubiquitination	Bile salt export pump	Homo sapiens (human)
regulation of fatty acid beta-oxidation	Bile salt export pump	Homo sapiens (human)
carbohydrate transmembrane transport	Bile salt export pump	Homo sapiens (human)
bile acid signaling pathway	Bile salt export pump	Homo sapiens (human)
cholesterol homeostasis	Bile salt export pump	Homo sapiens (human)
response to estrogen	Bile salt export pump	Homo sapiens (human)
response to ethanol	Bile salt export pump	Homo sapiens (human)
xenobiotic export from cell	Bile salt export pump	Homo sapiens (human)
lipid homeostasis	Bile salt export pump	Homo sapiens (human)
phospholipid homeostasis	Bile salt export pump	Homo sapiens (human)
positive regulation of bile acid secretion	Bile salt export pump	Homo sapiens (human)
regulation of bile acid metabolic process	Bile salt export pump	Homo sapiens (human)
transmembrane transport	Bile salt export pump	Homo sapiens (human)
mitotic chromosome condensation	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
meiotic chromosome condensation	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
meiotic chromosome segregation	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
cell division	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
kinetochore organization	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
positive regulation of chromosome segregation	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
positive regulation of chromosome separation	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
positive regulation of chromosome condensation	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
MAPK cascade	Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)
protein phosphorylation	Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)
signal transduction	Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)
cellular response to stress	Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)
microvillus assembly	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
negative regulation of cell-matrix adhesion	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
protein phosphorylation	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
positive regulation of cell migration	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
positive regulation of ARF protein signal transduction	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
positive regulation of hippo signaling	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
intracellular signal transduction	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
negative regulation of apoptotic process	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
positive regulation of GTPase activity	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
regulation of JNK cascade	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
positive regulation of keratinocyte migration	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
positive regulation of focal adhesion assembly	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
positive regulation of focal adhesion disassembly	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
regulation of MAPK cascade	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
MAPK cascade	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
neuron projection morphogenesis	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
G2/M transition of mitotic cell cycle	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
sister chromatid segregation	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
inner cell mass cell fate commitment	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
inner cell mass cellular morphogenesis	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
protein phosphorylation	Serine/threonine-protein kinase LATS1	Homo sapiens (human)

Process	via Protein(s)	Taxonomy
protein serine/threonine kinase activity	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
transmembrane receptor protein serine/threonine kinase activity	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
transmembrane signaling receptor activity	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
protein binding	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
ATP binding	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
BMP binding	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
SMAD binding	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
metal ion binding	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
BMP receptor activity	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
transforming growth factor beta receptor activity, type I	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
protein kinase activity	Cell division cycle 7-related protein kinase	Homo sapiens (human)
protein binding	Cell division cycle 7-related protein kinase	Homo sapiens (human)
ATP binding	Cell division cycle 7-related protein kinase	Homo sapiens (human)
kinase activity	Cell division cycle 7-related protein kinase	Homo sapiens (human)
metal ion binding	Cell division cycle 7-related protein kinase	Homo sapiens (human)
protein serine kinase activity	Cell division cycle 7-related protein kinase	Homo sapiens (human)
protein serine/threonine kinase activity	Cell division cycle 7-related protein kinase	Homo sapiens (human)
protein serine/threonine kinase activity	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
protein binding	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
ATP binding	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
identical protein binding	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
protein serine kinase activity	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
DNA binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
DNA helicase activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
RNA binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
RNA helicase activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
mRNA binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
GTPase activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
protein binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
ATP binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
transcription factor binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
poly(A) binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
eukaryotic initiation factor 4E binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
ATP hydrolysis activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
ribonucleoside triphosphate phosphatase activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
translation initiation factor binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
RNA strand annealing activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
signaling adaptor activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
RNA stem-loop binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
gamma-tubulin binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
ribosomal small subunit binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
CTPase activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
protein serine/threonine kinase activator activity	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cadherin binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
mRNA 5'-UTR binding	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
magnesium ion binding	Pyridoxal kinase	Homo sapiens (human)
ATP binding	Pyridoxal kinase	Homo sapiens (human)
zinc ion binding	Pyridoxal kinase	Homo sapiens (human)
pyridoxal kinase activity	Pyridoxal kinase	Homo sapiens (human)
pyridoxal phosphate binding	Pyridoxal kinase	Homo sapiens (human)
potassium ion binding	Pyridoxal kinase	Homo sapiens (human)
sodium ion binding	Pyridoxal kinase	Homo sapiens (human)
lithium ion binding	Pyridoxal kinase	Homo sapiens (human)
protein homodimerization activity	Pyridoxal kinase	Homo sapiens (human)
transcription coactivator binding	Citron Rho-interacting kinase	Homo sapiens (human)
protein serine/threonine kinase activity	Citron Rho-interacting kinase	Homo sapiens (human)
protein binding	Citron Rho-interacting kinase	Homo sapiens (human)
ATP binding	Citron Rho-interacting kinase	Homo sapiens (human)
SH3 domain binding	Citron Rho-interacting kinase	Homo sapiens (human)
protein kinase binding	Citron Rho-interacting kinase	Homo sapiens (human)
PDZ domain binding	Citron Rho-interacting kinase	Homo sapiens (human)
protein serine/threonine kinase inhibitor activity	Citron Rho-interacting kinase	Homo sapiens (human)
metal ion binding	Citron Rho-interacting kinase	Homo sapiens (human)
scaffold protein binding	Citron Rho-interacting kinase	Homo sapiens (human)
protein serine kinase activity	Citron Rho-interacting kinase	Homo sapiens (human)
protein kinase activity	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
protein serine/threonine kinase activity	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
protein binding	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
ATP binding	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
protein domain specific binding	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
histone H3T11 kinase activity	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
protein serine kinase activity	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
protein kinase activity	Aurora kinase A	Homo sapiens (human)
protein serine/threonine kinase activity	Aurora kinase A	Homo sapiens (human)
protein serine/threonine/tyrosine kinase activity	Aurora kinase A	Homo sapiens (human)
protein binding	Aurora kinase A	Homo sapiens (human)
ATP binding	Aurora kinase A	Homo sapiens (human)
protein kinase binding	Aurora kinase A	Homo sapiens (human)
ubiquitin protein ligase binding	Aurora kinase A	Homo sapiens (human)
histone H3S10 kinase activity	Aurora kinase A	Homo sapiens (human)
protein heterodimerization activity	Aurora kinase A	Homo sapiens (human)
protein serine kinase activity	Aurora kinase A	Homo sapiens (human)
molecular function activator activity	Aurora kinase A	Homo sapiens (human)
protein serine/threonine kinase activity	Cyclin-G-associated kinase	Homo sapiens (human)
protein binding	Cyclin-G-associated kinase	Homo sapiens (human)
ATP binding	Cyclin-G-associated kinase	Homo sapiens (human)
cyclin binding	Cyclin-G-associated kinase	Homo sapiens (human)
protein-folding chaperone binding	Cyclin-G-associated kinase	Homo sapiens (human)
protein serine kinase activity	Cyclin-G-associated kinase	Homo sapiens (human)
clathrin binding	Cyclin-G-associated kinase	Homo sapiens (human)
ephrin receptor activity	Ephrin type-B receptor 6	Homo sapiens (human)
protein binding	Ephrin type-B receptor 6	Homo sapiens (human)
ATP binding	Ephrin type-B receptor 6	Homo sapiens (human)
signaling receptor activity	Ephrin type-B receptor 6	Homo sapiens (human)
transmembrane-ephrin receptor activity	Ephrin type-B receptor 6	Homo sapiens (human)
FAD binding	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
flavin adenine dinucleotide binding	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
pristanoyl-CoA oxidase activity	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
fatty acid binding	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
ATP binding	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type xenobiotic transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
glucuronoside transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type bile acid transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ATP hydrolysis activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ATPase-coupled transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
xenobiotic transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
icosanoid transmembrane transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
ABC-type transporter activity	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
guanine nucleotide transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
protein binding	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATP binding	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type xenobiotic transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
urate transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
purine nucleotide transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type bile acid transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
efflux transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATP hydrolysis activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
glutathione transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATPase-coupled transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
xenobiotic transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
ABC-type transporter activity	Multidrug resistance-associated protein 4	Homo sapiens (human)
protein serine/threonine kinase activity	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activity	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
signaling receptor binding	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
protein binding	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
ATP binding	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
LIM domain binding	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
signaling adaptor activity	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
identical protein binding	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
protein homodimerization activity	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
CARD domain binding	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
caspase binding	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
protein serine kinase activity	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
JUN kinase kinase kinase activity	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
protein kinase activity	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
protein serine/threonine kinase activity	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
protein binding	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
ATP binding	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
protein serine kinase activity	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
histone H2A kinase activity	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
magnesium ion binding	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
GTPase activity	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
protein binding	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
GTP binding	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
phosphatidic acid binding	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
GTPase-dependent fusogenic activity	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
membrane bending activity	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
cardiolipin binding	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
microtubule binding	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
tRNA binding	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
RNA binding	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
translation initiation factor activity	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
GTPase activity	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
protein binding	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
GTP binding	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
metal ion binding	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
protease binding	Rho-associated protein kinase 2	Homo sapiens (human)
RNA binding	Rho-associated protein kinase 2	Homo sapiens (human)
protein serine/threonine kinase activity	Rho-associated protein kinase 2	Homo sapiens (human)
structural molecule activity	Rho-associated protein kinase 2	Homo sapiens (human)
protein binding	Rho-associated protein kinase 2	Homo sapiens (human)
ATP binding	Rho-associated protein kinase 2	Homo sapiens (human)
small GTPase binding	Rho-associated protein kinase 2	Homo sapiens (human)
metal ion binding	Rho-associated protein kinase 2	Homo sapiens (human)
tau protein binding	Rho-associated protein kinase 2	Homo sapiens (human)
tau-protein kinase activity	Rho-associated protein kinase 2	Homo sapiens (human)
endopeptidase activator activity	Rho-associated protein kinase 2	Homo sapiens (human)
Rho-dependent protein serine/threonine kinase activity	Rho-associated protein kinase 2	Homo sapiens (human)
protein serine kinase activity	Rho-associated protein kinase 2	Homo sapiens (human)
protein serine/threonine kinase activity	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
protein binding	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
ATP binding	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
small GTPase binding	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
identical protein binding	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
protein-containing complex binding	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
GTPase binding	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
protein serine kinase activity	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
magnesium ion binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
RNA endonuclease activity	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
protein serine/threonine kinase activity	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
platelet-derived growth factor receptor binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
protein binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
ATP binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
enzyme binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
Hsp70 protein binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
identical protein binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
protein homodimerization activity	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
ADP binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
Hsp90 protein binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
protein serine kinase activity	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
unfolded protein binding	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
magnesium ion binding	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
protein serine/threonine kinase activity	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
protein tyrosine kinase activity	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
protein binding	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
ATP binding	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
histone H3S10 kinase activity	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
histone H3S28 kinase activity	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
histone H2AS1 kinase activity	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
protein serine kinase activity	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
RNA binding	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
RNA helicase activity	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
helicase activity	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
protein binding	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
ATP binding	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
ATP hydrolysis activity	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
identical protein binding	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
magnesium ion binding	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
protein serine/threonine kinase activity	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
ribosomal protein S6 kinase activity	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
protein binding	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
ATP binding	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
histone H3S10 kinase activity	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
histone H3S28 kinase activity	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
protein serine kinase activity	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Serine/threonine-protein kinase 16	Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activity	Serine/threonine-protein kinase 16	Homo sapiens (human)
protein binding	Serine/threonine-protein kinase 16	Homo sapiens (human)
ATP binding	Serine/threonine-protein kinase 16	Homo sapiens (human)
protein serine kinase activity	Serine/threonine-protein kinase 16	Homo sapiens (human)
protein serine/threonine kinase activity	Serine/threonine-protein kinase 16	Homo sapiens (human)
protein serine/threonine kinase activity	Serine/threonine-protein kinase 10	Homo sapiens (human)
protein binding	Serine/threonine-protein kinase 10	Homo sapiens (human)
ATP binding	Serine/threonine-protein kinase 10	Homo sapiens (human)
identical protein binding	Serine/threonine-protein kinase 10	Homo sapiens (human)
protein homodimerization activity	Serine/threonine-protein kinase 10	Homo sapiens (human)
protein serine kinase activity	Serine/threonine-protein kinase 10	Homo sapiens (human)
diacylglycerol-dependent serine/threonine kinase activity	Serine/threonine-protein kinase D3	Homo sapiens (human)
protein binding	Serine/threonine-protein kinase D3	Homo sapiens (human)
ATP binding	Serine/threonine-protein kinase D3	Homo sapiens (human)
kinase activity	Serine/threonine-protein kinase D3	Homo sapiens (human)
metal ion binding	Serine/threonine-protein kinase D3	Homo sapiens (human)
protein serine kinase activity	Serine/threonine-protein kinase D3	Homo sapiens (human)
protein serine/threonine kinase activity	Serine/threonine-protein kinase D3	Homo sapiens (human)
protein binding	Bile salt export pump	Homo sapiens (human)
ATP binding	Bile salt export pump	Homo sapiens (human)
ABC-type xenobiotic transporter activity	Bile salt export pump	Homo sapiens (human)
bile acid transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
canalicular bile acid transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
carbohydrate transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
ABC-type bile acid transporter activity	Bile salt export pump	Homo sapiens (human)
ATP hydrolysis activity	Bile salt export pump	Homo sapiens (human)
single-stranded DNA binding	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
protein binding	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
ATP binding	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
ATP hydrolysis activity	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
chromatin binding	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
magnesium ion binding	Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)
MAP kinase kinase kinase activity	Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)
protein binding	Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)
ATP binding	Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)
protein serine kinase activity	Mitogen-activated protein kinase kinase kinase 6	Homo sapiens (human)
creatine kinase activity	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
protein serine/threonine kinase activity	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
protein binding	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
ATP binding	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
microtubule binding	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
MAP kinase kinase kinase kinase activity	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
protein serine kinase activity	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
magnesium ion binding	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
protein serine/threonine kinase activity	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
protein binding	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
ATP binding	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
protein kinase binding	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
nuclear estrogen receptor binding	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
protein serine kinase activity	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
protein kinase activity	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
protein serine/threonine kinase activity	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
protein binding	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
ATP binding	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
cadherin binding involved in cell-cell adhesion	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
protein serine kinase activity	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
supercoiled DNA binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
magnesium ion binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
four-way junction DNA binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
bubble DNA binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
phosphotyrosine residue binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
DNA binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
transcription coactivator activity	Tyrosine-protein kinase ABL1	Homo sapiens (human)
actin monomer binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
nicotinate-nucleotide adenylyltransferase activity	Tyrosine-protein kinase ABL1	Homo sapiens (human)
protein kinase activity	Tyrosine-protein kinase ABL1	Homo sapiens (human)
protein tyrosine kinase activity	Tyrosine-protein kinase ABL1	Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activity	Tyrosine-protein kinase ABL1	Homo sapiens (human)
protein kinase C binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
protein binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
ATP binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
kinase activity	Tyrosine-protein kinase ABL1	Homo sapiens (human)
SH3 domain binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
syntaxin binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
manganese ion binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
neuropilin binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
SH2 domain binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
ephrin receptor binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
actin filament binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
mitogen-activated protein kinase binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
proline-rich region binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
delta-catenin binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
sequence-specific double-stranded DNA binding	Tyrosine-protein kinase ABL1	Homo sapiens (human)
epidermal growth factor receptor activity	Epidermal growth factor receptor	Homo sapiens (human)
virus receptor activity	Epidermal growth factor receptor	Homo sapiens (human)
chromatin binding	Epidermal growth factor receptor	Homo sapiens (human)
double-stranded DNA binding	Epidermal growth factor receptor	Homo sapiens (human)
MAP kinase kinase kinase activity	Epidermal growth factor receptor	Homo sapiens (human)
protein tyrosine kinase activity	Epidermal growth factor receptor	Homo sapiens (human)
transmembrane receptor protein tyrosine kinase activity	Epidermal growth factor receptor	Homo sapiens (human)
transmembrane signaling receptor activity	Epidermal growth factor receptor	Homo sapiens (human)
epidermal growth factor receptor activity	Epidermal growth factor receptor	Homo sapiens (human)
integrin binding	Epidermal growth factor receptor	Homo sapiens (human)
protein binding	Epidermal growth factor receptor	Homo sapiens (human)
calmodulin binding	Epidermal growth factor receptor	Homo sapiens (human)
ATP binding	Epidermal growth factor receptor	Homo sapiens (human)
enzyme binding	Epidermal growth factor receptor	Homo sapiens (human)
kinase binding	Epidermal growth factor receptor	Homo sapiens (human)
protein kinase binding	Epidermal growth factor receptor	Homo sapiens (human)
protein phosphatase binding	Epidermal growth factor receptor	Homo sapiens (human)
protein tyrosine kinase activator activity	Epidermal growth factor receptor	Homo sapiens (human)
transmembrane receptor protein tyrosine kinase activator activity	Epidermal growth factor receptor	Homo sapiens (human)
ubiquitin protein ligase binding	Epidermal growth factor receptor	Homo sapiens (human)
identical protein binding	Epidermal growth factor receptor	Homo sapiens (human)
cadherin binding	Epidermal growth factor receptor	Homo sapiens (human)
actin filament binding	Epidermal growth factor receptor	Homo sapiens (human)
ATPase binding	Epidermal growth factor receptor	Homo sapiens (human)
epidermal growth factor binding	Epidermal growth factor receptor	Homo sapiens (human)
protein tyrosine kinase activity	High affinity nerve growth factor receptor	Homo sapiens (human)
transmembrane receptor protein tyrosine kinase activity	High affinity nerve growth factor receptor	Homo sapiens (human)
GPI-linked ephrin receptor activity	High affinity nerve growth factor receptor	Homo sapiens (human)
neurotrophin p75 receptor binding	High affinity nerve growth factor receptor	Homo sapiens (human)
protein binding	High affinity nerve growth factor receptor	Homo sapiens (human)
ATP binding	High affinity nerve growth factor receptor	Homo sapiens (human)
nerve growth factor receptor activity	High affinity nerve growth factor receptor	Homo sapiens (human)
kinase binding	High affinity nerve growth factor receptor	Homo sapiens (human)
identical protein binding	High affinity nerve growth factor receptor	Homo sapiens (human)
protein homodimerization activity	High affinity nerve growth factor receptor	Homo sapiens (human)
nerve growth factor binding	High affinity nerve growth factor receptor	Homo sapiens (human)
neurotrophin binding	High affinity nerve growth factor receptor	Homo sapiens (human)
neurotrophin receptor activity	High affinity nerve growth factor receptor	Homo sapiens (human)
transcription cis-regulatory region binding	Cellular tumor antigen p53	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
cis-regulatory region sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
core promoter sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
TFIID-class transcription factor complex binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
protease binding	Cellular tumor antigen p53	Homo sapiens (human)
p53 binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
chromatin binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription factor activity	Cellular tumor antigen p53	Homo sapiens (human)
mRNA 3'-UTR binding	Cellular tumor antigen p53	Homo sapiens (human)
copper ion binding	Cellular tumor antigen p53	Homo sapiens (human)
protein binding	Cellular tumor antigen p53	Homo sapiens (human)
zinc ion binding	Cellular tumor antigen p53	Homo sapiens (human)
enzyme binding	Cellular tumor antigen p53	Homo sapiens (human)
receptor tyrosine kinase binding	Cellular tumor antigen p53	Homo sapiens (human)
ubiquitin protein ligase binding	Cellular tumor antigen p53	Homo sapiens (human)
histone deacetylase regulator activity	Cellular tumor antigen p53	Homo sapiens (human)
ATP-dependent DNA/DNA annealing activity	Cellular tumor antigen p53	Homo sapiens (human)
identical protein binding	Cellular tumor antigen p53	Homo sapiens (human)
histone deacetylase binding	Cellular tumor antigen p53	Homo sapiens (human)
protein heterodimerization activity	Cellular tumor antigen p53	Homo sapiens (human)
protein-folding chaperone binding	Cellular tumor antigen p53	Homo sapiens (human)
protein phosphatase 2A binding	Cellular tumor antigen p53	Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor binding	Cellular tumor antigen p53	Homo sapiens (human)
14-3-3 protein binding	Cellular tumor antigen p53	Homo sapiens (human)
MDM2/MDM4 family protein binding	Cellular tumor antigen p53	Homo sapiens (human)
disordered domain specific binding	Cellular tumor antigen p53	Homo sapiens (human)
general transcription initiation factor binding	Cellular tumor antigen p53	Homo sapiens (human)
molecular function activator activity	Cellular tumor antigen p53	Homo sapiens (human)
promoter-specific chromatin binding	Cellular tumor antigen p53	Homo sapiens (human)
protein binding	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
GTP binding	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
metal ion binding	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
G-protein beta/gamma-subunit complex binding	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
G protein-coupled receptor binding	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
GTPase activity	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
adenine nucleotide transmembrane transporter activity	ADP/ATP translocase 2	Homo sapiens (human)
RNA binding	ADP/ATP translocase 2	Homo sapiens (human)
ATP:ADP antiporter activity	ADP/ATP translocase 2	Homo sapiens (human)
protein binding	ADP/ATP translocase 2	Homo sapiens (human)
proton transmembrane transporter activity	ADP/ATP translocase 2	Homo sapiens (human)
adenine transmembrane transporter activity	ADP/ATP translocase 2	Homo sapiens (human)
oxidative phosphorylation uncoupler activity	ADP/ATP translocase 2	Homo sapiens (human)
ubiquitin protein ligase binding	ADP/ATP translocase 2	Homo sapiens (human)
chromatin binding	Protein kinase C beta type	Homo sapiens (human)
protein serine/threonine kinase activity	Protein kinase C beta type	Homo sapiens (human)
diacylglycerol-dependent serine/threonine kinase activity	Protein kinase C beta type	Homo sapiens (human)
protein kinase C binding	Protein kinase C beta type	Homo sapiens (human)
calcium channel regulator activity	Protein kinase C beta type	Homo sapiens (human)
protein binding	Protein kinase C beta type	Homo sapiens (human)
ATP binding	Protein kinase C beta type	Homo sapiens (human)
zinc ion binding	Protein kinase C beta type	Homo sapiens (human)
nuclear receptor coactivator activity	Protein kinase C beta type	Homo sapiens (human)
histone H3T6 kinase activity	Protein kinase C beta type	Homo sapiens (human)
histone binding	Protein kinase C beta type	Homo sapiens (human)
nuclear androgen receptor binding	Protein kinase C beta type	Homo sapiens (human)
protein serine kinase activity	Protein kinase C beta type	Homo sapiens (human)
amyloid-beta binding	Insulin receptor	Homo sapiens (human)
protein tyrosine kinase activity	Insulin receptor	Homo sapiens (human)
insulin receptor activity	Insulin receptor	Homo sapiens (human)
insulin-like growth factor receptor binding	Insulin receptor	Homo sapiens (human)
protein binding	Insulin receptor	Homo sapiens (human)
ATP binding	Insulin receptor	Homo sapiens (human)
GTP binding	Insulin receptor	Homo sapiens (human)
protein domain specific binding	Insulin receptor	Homo sapiens (human)
insulin-like growth factor I binding	Insulin receptor	Homo sapiens (human)
insulin-like growth factor II binding	Insulin receptor	Homo sapiens (human)
cargo receptor activity	Insulin receptor	Homo sapiens (human)
phosphatidylinositol 3-kinase binding	Insulin receptor	Homo sapiens (human)
insulin binding	Insulin receptor	Homo sapiens (human)
insulin receptor substrate binding	Insulin receptor	Homo sapiens (human)
protein-containing complex binding	Insulin receptor	Homo sapiens (human)
PTB domain binding	Insulin receptor	Homo sapiens (human)
phosphotyrosine residue binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
protein tyrosine kinase activity	Tyrosine-protein kinase Lck	Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activity	Tyrosine-protein kinase Lck	Homo sapiens (human)
protein serine/threonine phosphatase activity	Tyrosine-protein kinase Lck	Homo sapiens (human)
protein binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
ATP binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
phospholipase activator activity	Tyrosine-protein kinase Lck	Homo sapiens (human)
protein kinase binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
protein phosphatase binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
SH2 domain binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
T cell receptor binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
CD4 receptor binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
CD8 receptor binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
identical protein binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
phospholipase binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
phosphatidylinositol 3-kinase binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
ATPase binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
signaling receptor binding	Tyrosine-protein kinase Lck	Homo sapiens (human)
protein tyrosine kinase activity	Tyrosine-protein kinase Fyn	Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activity	Tyrosine-protein kinase Fyn	Homo sapiens (human)
protein binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
ATP binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
phospholipase activator activity	Tyrosine-protein kinase Fyn	Homo sapiens (human)
enzyme binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
type 5 metabotropic glutamate receptor binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
identical protein binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
alpha-tubulin binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
phospholipase binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
transmembrane transporter binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
metal ion binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
ephrin receptor binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
tau protein binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
tau-protein kinase activity	Tyrosine-protein kinase Fyn	Homo sapiens (human)
growth factor receptor binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
scaffold protein binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
disordered domain specific binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
signaling receptor binding	Tyrosine-protein kinase Fyn	Homo sapiens (human)
virus receptor activity	Cyclin-dependent kinase 1	Homo sapiens (human)
chromatin binding	Cyclin-dependent kinase 1	Homo sapiens (human)
protein kinase activity	Cyclin-dependent kinase 1	Homo sapiens (human)
protein serine/threonine kinase activity	Cyclin-dependent kinase 1	Homo sapiens (human)
cyclin-dependent protein serine/threonine kinase activity	Cyclin-dependent kinase 1	Homo sapiens (human)
protein binding	Cyclin-dependent kinase 1	Homo sapiens (human)
ATP binding	Cyclin-dependent kinase 1	Homo sapiens (human)
RNA polymerase II CTD heptapeptide repeat kinase activity	Cyclin-dependent kinase 1	Homo sapiens (human)
kinase activity	Cyclin-dependent kinase 1	Homo sapiens (human)
cyclin binding	Cyclin-dependent kinase 1	Homo sapiens (human)
Hsp70 protein binding	Cyclin-dependent kinase 1	Homo sapiens (human)
histone kinase activity	Cyclin-dependent kinase 1	Homo sapiens (human)
cyclin-dependent protein kinase activity	Cyclin-dependent kinase 1	Homo sapiens (human)
protein serine kinase activity	Cyclin-dependent kinase 1	Homo sapiens (human)
purine nucleobase binding	Glycogen phosphorylase, liver form	Homo sapiens (human)
protein binding	Glycogen phosphorylase, liver form	Homo sapiens (human)
ATP binding	Glycogen phosphorylase, liver form	Homo sapiens (human)
glucose binding	Glycogen phosphorylase, liver form	Homo sapiens (human)
glycogen phosphorylase activity	Glycogen phosphorylase, liver form	Homo sapiens (human)
AMP binding	Glycogen phosphorylase, liver form	Homo sapiens (human)
vitamin binding	Glycogen phosphorylase, liver form	Homo sapiens (human)
bile acid binding	Glycogen phosphorylase, liver form	Homo sapiens (human)
identical protein binding	Glycogen phosphorylase, liver form	Homo sapiens (human)
linear malto-oligosaccharide phosphorylase activity	Glycogen phosphorylase, liver form	Homo sapiens (human)
SHG alpha-glucan phosphorylase activity	Glycogen phosphorylase, liver form	Homo sapiens (human)
pyridoxal phosphate binding	Glycogen phosphorylase, liver form	Homo sapiens (human)
protein tyrosine kinase activity	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activity	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
protein binding	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
ATP binding	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
microtubule binding	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
immunoglobulin receptor binding	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
phosphatidylinositol binding	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
adenine phosphoribosyltransferase activity	Adenine phosphoribosyltransferase	Homo sapiens (human)
protein binding	Adenine phosphoribosyltransferase	Homo sapiens (human)
AMP binding	Adenine phosphoribosyltransferase	Homo sapiens (human)
adenine binding	Adenine phosphoribosyltransferase	Homo sapiens (human)
phosphotyrosine residue binding	Tyrosine-protein kinase Yes	Homo sapiens (human)
protein tyrosine kinase activity	Tyrosine-protein kinase Yes	Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activity	Tyrosine-protein kinase Yes	Homo sapiens (human)
protein binding	Tyrosine-protein kinase Yes	Homo sapiens (human)
ATP binding	Tyrosine-protein kinase Yes	Homo sapiens (human)
enzyme binding	Tyrosine-protein kinase Yes	Homo sapiens (human)

Process	via Protein(s)	Taxonomy
plasma membrane	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
dendrite	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
neuronal cell body	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
receptor complex	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
HFE-transferrin receptor complex	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
plasma membrane	Bone morphogenetic protein receptor type-1B	Homo sapiens (human)
nucleus	Cell division cycle 7-related protein kinase	Homo sapiens (human)
nucleoplasm	Cell division cycle 7-related protein kinase	Homo sapiens (human)
cytoplasm	Cell division cycle 7-related protein kinase	Homo sapiens (human)
intercellular bridge	Cell division cycle 7-related protein kinase	Homo sapiens (human)
mitotic spindle	Cell division cycle 7-related protein kinase	Homo sapiens (human)
nucleus	Cell division cycle 7-related protein kinase	Homo sapiens (human)
cytoplasm	Cell division cycle 7-related protein kinase	Homo sapiens (human)
XY body	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
nucleolus	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
centrosome	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
centriole	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
cleavage furrow	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
deuterosome	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
procentriole	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
procentriole replication complex	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
nucleus	Serine/threonine-protein kinase PLK4	Homo sapiens (human)
eukaryotic translation initiation factor 3 complex	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cytosolic small ribosomal subunit	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cytoplasm	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
extracellular region	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
nucleus	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
nucleoplasm	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cytoplasm	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
centrosome	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cytosol	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
plasma membrane	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cytoplasmic stress granule	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
lamellipodium	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
cell leading edge	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
secretory granule lumen	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
extracellular exosome	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
ficolin-1-rich granule lumen	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
NLRP3 inflammasome complex	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
nucleus	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
P granule	ATP-dependent RNA helicase DDX3X	Homo sapiens (human)
extracellular region	Pyridoxal kinase	Homo sapiens (human)
nucleus	Pyridoxal kinase	Homo sapiens (human)
nucleoplasm	Pyridoxal kinase	Homo sapiens (human)
cytosol	Pyridoxal kinase	Homo sapiens (human)
secretory granule lumen	Pyridoxal kinase	Homo sapiens (human)
specific granule lumen	Pyridoxal kinase	Homo sapiens (human)
extracellular exosome	Pyridoxal kinase	Homo sapiens (human)
cytosol	Pyridoxal kinase	Homo sapiens (human)
cytosol	Citron Rho-interacting kinase	Homo sapiens (human)
membrane	Citron Rho-interacting kinase	Homo sapiens (human)
chromosome, telomeric region	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
condensed nuclear chromosome	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
extracellular space	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
nucleus	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
nucleoplasm	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
replication fork	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
cytoplasm	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
centrosome	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
intracellular membrane-bounded organelle	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
chromatin	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
protein-containing complex	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
nucleus	Serine/threonine-protein kinase Chk1	Homo sapiens (human)
spindle microtubule	Aurora kinase A	Homo sapiens (human)
nucleus	Aurora kinase A	Homo sapiens (human)
nucleoplasm	Aurora kinase A	Homo sapiens (human)
centrosome	Aurora kinase A	Homo sapiens (human)
centriole	Aurora kinase A	Homo sapiens (human)
spindle	Aurora kinase A	Homo sapiens (human)
cytosol	Aurora kinase A	Homo sapiens (human)
postsynaptic density	Aurora kinase A	Homo sapiens (human)
microtubule cytoskeleton	Aurora kinase A	Homo sapiens (human)
basolateral plasma membrane	Aurora kinase A	Homo sapiens (human)
midbody	Aurora kinase A	Homo sapiens (human)
spindle pole centrosome	Aurora kinase A	Homo sapiens (human)
ciliary basal body	Aurora kinase A	Homo sapiens (human)
germinal vesicle	Aurora kinase A	Homo sapiens (human)
axon hillock	Aurora kinase A	Homo sapiens (human)
pronucleus	Aurora kinase A	Homo sapiens (human)
perinuclear region of cytoplasm	Aurora kinase A	Homo sapiens (human)
mitotic spindle	Aurora kinase A	Homo sapiens (human)
meiotic spindle	Aurora kinase A	Homo sapiens (human)
mitotic spindle pole	Aurora kinase A	Homo sapiens (human)
glutamatergic synapse	Aurora kinase A	Homo sapiens (human)
spindle pole centrosome	Aurora kinase A	Homo sapiens (human)
chromosome passenger complex	Aurora kinase A	Homo sapiens (human)
spindle midzone	Aurora kinase A	Homo sapiens (human)
kinetochore	Aurora kinase A	Homo sapiens (human)
Golgi apparatus	Cyclin-G-associated kinase	Homo sapiens (human)
cytosol	Cyclin-G-associated kinase	Homo sapiens (human)
focal adhesion	Cyclin-G-associated kinase	Homo sapiens (human)
membrane	Cyclin-G-associated kinase	Homo sapiens (human)
clathrin-coated vesicle	Cyclin-G-associated kinase	Homo sapiens (human)
vesicle	Cyclin-G-associated kinase	Homo sapiens (human)
intracellular membrane-bounded organelle	Cyclin-G-associated kinase	Homo sapiens (human)
perinuclear region of cytoplasm	Cyclin-G-associated kinase	Homo sapiens (human)
presynapse	Cyclin-G-associated kinase	Homo sapiens (human)
vesicle	Cyclin-G-associated kinase	Homo sapiens (human)
cytoplasm	Cyclin-G-associated kinase	Homo sapiens (human)
intracellular membrane-bounded organelle	Cyclin-G-associated kinase	Homo sapiens (human)
extracellular region	Ephrin type-B receptor 6	Homo sapiens (human)
cytosol	Ephrin type-B receptor 6	Homo sapiens (human)
plasma membrane	Ephrin type-B receptor 6	Homo sapiens (human)
plasma membrane	Ephrin type-B receptor 6	Homo sapiens (human)
dendrite	Ephrin type-B receptor 6	Homo sapiens (human)
peroxisome	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
peroxisomal matrix	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
cytosol	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
membrane	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
peroxisome	Peroxisomal acyl-coenzyme A oxidase 3	Homo sapiens (human)
plasma membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
basal plasma membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
basolateral plasma membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
membrane	ATP-binding cassette sub-family C member 3	Homo sapiens (human)
nucleolus	Multidrug resistance-associated protein 4	Homo sapiens (human)
Golgi apparatus	Multidrug resistance-associated protein 4	Homo sapiens (human)
plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
basolateral plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
apical plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
platelet dense granule membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
external side of apical plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
plasma membrane	Multidrug resistance-associated protein 4	Homo sapiens (human)
plasma membrane	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
cytoplasm	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
endoplasmic reticulum	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
cytosol	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
cytoskeleton	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
vesicle	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
protein-containing complex	Receptor-interacting serine/threonine-protein kinase 2	Homo sapiens (human)
kinetochore	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
nucleoplasm	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
cytosol	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
membrane	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
intracellular membrane-bounded organelle	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
outer kinetochore	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
kinetochore	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
nucleus	Mitotic checkpoint serine/threonine-protein kinase BUB1	Homo sapiens (human)
nucleoplasm	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrion	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial outer membrane	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial inner membrane	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial intermembrane space	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
cytosol	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
membrane	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial crista	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
dendrite	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
axon cytoplasm	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial intermembrane space	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
cytoplasm	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
microtubule	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
mitochondrial membrane	Dynamin-like 120 kDa protein, mitochondrial	Homo sapiens (human)
nucleus	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
cytoplasm	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
cytosol	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
synapse	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
cytoplasm	Eukaryotic translation initiation factor 5B	Homo sapiens (human)
nucleus	Rho-associated protein kinase 2	Homo sapiens (human)
centrosome	Rho-associated protein kinase 2	Homo sapiens (human)
cytosol	Rho-associated protein kinase 2	Homo sapiens (human)
plasma membrane	Rho-associated protein kinase 2	Homo sapiens (human)
cytoplasmic ribonucleoprotein granule	Rho-associated protein kinase 2	Homo sapiens (human)
centrosome	Rho-associated protein kinase 2	Homo sapiens (human)
cytoskeleton	Rho-associated protein kinase 2	Homo sapiens (human)
cytoplasm	Rho-associated protein kinase 2	Homo sapiens (human)
cytoplasm	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
phagophore assembly site	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
autophagosome membrane	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
cytoplasm	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
mitochondrial outer membrane	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
autophagosome	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
endoplasmic reticulum membrane	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
axon	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
phagophore assembly site membrane	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
recycling endosome	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
omegasome membrane	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
Atg1/ULK1 kinase complex	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
phagophore assembly site	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
autophagosome	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
phagophore assembly site membrane	Serine/threonine-protein kinase ULK1	Homo sapiens (human)
nuclear inner membrane	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
cytoplasm	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
mitochondrion	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
endoplasmic reticulum	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
endoplasmic reticulum membrane	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
Ire1 complex	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
AIP1-IRE1 complex	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
IRE1-TRAF2-ASK1 complex	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
IRE1-RACK1-PP2A complex	Serine/threonine-protein kinase/endoribonuclease IRE1	Homo sapiens (human)
nucleus	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
nucleoplasm	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
cytoplasm	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
nucleoplasm	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
cytoplasm	Ribosomal protein S6 kinase alpha-5	Homo sapiens (human)
nucleus	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
nucleoplasm	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
membrane	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
U4/U6 x U5 tri-snRNP complex	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
spliceosomal complex	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
U5 snRNP	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
U2-type precatalytic spliceosome	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
U2-type catalytic step 1 spliceosome	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
catalytic step 2 spliceosome	U5 small nuclear ribonucleoprotein 200 kDa helicase	Homo sapiens (human)
nucleus	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
nucleoplasm	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
cytosol	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
synapse	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
cytoplasm	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
nucleoplasm	Ribosomal protein S6 kinase alpha-4	Homo sapiens (human)
nucleoplasm	Serine/threonine-protein kinase 16	Homo sapiens (human)
Golgi-associated vesicle	Serine/threonine-protein kinase 16	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase 16	Homo sapiens (human)
plasma membrane	Serine/threonine-protein kinase 16	Homo sapiens (human)
perinuclear region of cytoplasm	Serine/threonine-protein kinase 16	Homo sapiens (human)
Golgi apparatus	Serine/threonine-protein kinase 16	Homo sapiens (human)
cytoplasm	Serine/threonine-protein kinase 16	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase 10	Homo sapiens (human)
plasma membrane	Serine/threonine-protein kinase 10	Homo sapiens (human)
specific granule membrane	Serine/threonine-protein kinase 10	Homo sapiens (human)
extracellular exosome	Serine/threonine-protein kinase 10	Homo sapiens (human)
cytoplasm	Serine/threonine-protein kinase 10	Homo sapiens (human)
nucleoplasm	Serine/threonine-protein kinase D3	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase D3	Homo sapiens (human)
plasma membrane	Serine/threonine-protein kinase D3	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase D3	Homo sapiens (human)
basolateral plasma membrane	Bile salt export pump	Homo sapiens (human)
Golgi membrane	Bile salt export pump	Homo sapiens (human)
endosome	Bile salt export pump	Homo sapiens (human)
plasma membrane	Bile salt export pump	Homo sapiens (human)
cell surface	Bile salt export pump	Homo sapiens (human)
apical plasma membrane	Bile salt export pump	Homo sapiens (human)
intercellular canaliculus	Bile salt export pump	Homo sapiens (human)
intracellular canaliculus	Bile salt export pump	Homo sapiens (human)
recycling endosome	Bile salt export pump	Homo sapiens (human)
recycling endosome membrane	Bile salt export pump	Homo sapiens (human)
extracellular exosome	Bile salt export pump	Homo sapiens (human)
membrane	Bile salt export pump	Homo sapiens (human)
nuclear chromosome	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
condensed chromosome	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
condensed nuclear chromosome	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
condensin complex	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
nucleus	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
nucleoplasm	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
nucleolus	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
cytoplasm	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
cytosol	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
extracellular exosome	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
condensed chromosome	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
chromatin	Structural maintenance of chromosomes protein 2	Homo sapiens (human)
cytoplasm	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
cytoplasm	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
focal adhesion	Mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens (human)
cytoplasm	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
spindle pole	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
nucleus	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
centrosome	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
midbody	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
spindle pole	Serine/threonine-protein kinase LATS1	Homo sapiens (human)
Golgi apparatus	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
cytosol	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
adherens junction	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
focal adhesion	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
cytoplasm	Serine/threonine-protein kinase PAK 4	Homo sapiens (human)
ruffle	Tyrosine-protein kinase ABL1	Homo sapiens (human)
nucleus	Tyrosine-protein kinase ABL1	Homo sapiens (human)
nucleoplasm	Tyrosine-protein kinase ABL1	Homo sapiens (human)
nucleolus	Tyrosine-protein kinase ABL1	Homo sapiens (human)
cytoplasm	Tyrosine-protein kinase ABL1	Homo sapiens (human)
mitochondrion	Tyrosine-protein kinase ABL1	Homo sapiens (human)
cytosol	Tyrosine-protein kinase ABL1	Homo sapiens (human)
actin cytoskeleton	Tyrosine-protein kinase ABL1	Homo sapiens (human)
nuclear body	Tyrosine-protein kinase ABL1	Homo sapiens (human)
dendrite	Tyrosine-protein kinase ABL1	Homo sapiens (human)
growth cone	Tyrosine-protein kinase ABL1	Homo sapiens (human)
nuclear membrane	Tyrosine-protein kinase ABL1	Homo sapiens (human)
neuronal cell body	Tyrosine-protein kinase ABL1	Homo sapiens (human)
perinuclear region of cytoplasm	Tyrosine-protein kinase ABL1	Homo sapiens (human)
postsynapse	Tyrosine-protein kinase ABL1	Homo sapiens (human)
protein-containing complex	Tyrosine-protein kinase ABL1	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase ABL1	Homo sapiens (human)
endosome	Epidermal growth factor receptor	Homo sapiens (human)
plasma membrane	Epidermal growth factor receptor	Homo sapiens (human)
ruffle membrane	Epidermal growth factor receptor	Homo sapiens (human)
Golgi membrane	Epidermal growth factor receptor	Homo sapiens (human)
extracellular space	Epidermal growth factor receptor	Homo sapiens (human)
nucleus	Epidermal growth factor receptor	Homo sapiens (human)
cytoplasm	Epidermal growth factor receptor	Homo sapiens (human)
endosome	Epidermal growth factor receptor	Homo sapiens (human)
endoplasmic reticulum membrane	Epidermal growth factor receptor	Homo sapiens (human)
plasma membrane	Epidermal growth factor receptor	Homo sapiens (human)
focal adhesion	Epidermal growth factor receptor	Homo sapiens (human)
cell surface	Epidermal growth factor receptor	Homo sapiens (human)
endosome membrane	Epidermal growth factor receptor	Homo sapiens (human)
membrane	Epidermal growth factor receptor	Homo sapiens (human)
basolateral plasma membrane	Epidermal growth factor receptor	Homo sapiens (human)
apical plasma membrane	Epidermal growth factor receptor	Homo sapiens (human)
cell junction	Epidermal growth factor receptor	Homo sapiens (human)
clathrin-coated endocytic vesicle membrane	Epidermal growth factor receptor	Homo sapiens (human)
early endosome membrane	Epidermal growth factor receptor	Homo sapiens (human)
nuclear membrane	Epidermal growth factor receptor	Homo sapiens (human)
membrane raft	Epidermal growth factor receptor	Homo sapiens (human)
perinuclear region of cytoplasm	Epidermal growth factor receptor	Homo sapiens (human)
multivesicular body, internal vesicle lumen	Epidermal growth factor receptor	Homo sapiens (human)
intracellular vesicle	Epidermal growth factor receptor	Homo sapiens (human)
protein-containing complex	Epidermal growth factor receptor	Homo sapiens (human)
receptor complex	Epidermal growth factor receptor	Homo sapiens (human)
Shc-EGFR complex	Epidermal growth factor receptor	Homo sapiens (human)
basal plasma membrane	Epidermal growth factor receptor	Homo sapiens (human)
early endosome	High affinity nerve growth factor receptor	Homo sapiens (human)
late endosome	High affinity nerve growth factor receptor	Homo sapiens (human)
plasma membrane	High affinity nerve growth factor receptor	Homo sapiens (human)
cell surface	High affinity nerve growth factor receptor	Homo sapiens (human)
endosome membrane	High affinity nerve growth factor receptor	Homo sapiens (human)
dendrite	High affinity nerve growth factor receptor	Homo sapiens (human)
early endosome membrane	High affinity nerve growth factor receptor	Homo sapiens (human)
late endosome membrane	High affinity nerve growth factor receptor	Homo sapiens (human)
neuronal cell body	High affinity nerve growth factor receptor	Homo sapiens (human)
recycling endosome membrane	High affinity nerve growth factor receptor	Homo sapiens (human)
protein-containing complex	High affinity nerve growth factor receptor	Homo sapiens (human)
receptor complex	High affinity nerve growth factor receptor	Homo sapiens (human)
axon	High affinity nerve growth factor receptor	Homo sapiens (human)
plasma membrane	High affinity nerve growth factor receptor	Homo sapiens (human)
nuclear body	Cellular tumor antigen p53	Homo sapiens (human)
nucleus	Cellular tumor antigen p53	Homo sapiens (human)
nucleoplasm	Cellular tumor antigen p53	Homo sapiens (human)
replication fork	Cellular tumor antigen p53	Homo sapiens (human)
nucleolus	Cellular tumor antigen p53	Homo sapiens (human)
cytoplasm	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrion	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrial matrix	Cellular tumor antigen p53	Homo sapiens (human)
endoplasmic reticulum	Cellular tumor antigen p53	Homo sapiens (human)
centrosome	Cellular tumor antigen p53	Homo sapiens (human)
cytosol	Cellular tumor antigen p53	Homo sapiens (human)
nuclear matrix	Cellular tumor antigen p53	Homo sapiens (human)
PML body	Cellular tumor antigen p53	Homo sapiens (human)
transcription repressor complex	Cellular tumor antigen p53	Homo sapiens (human)
site of double-strand break	Cellular tumor antigen p53	Homo sapiens (human)
germ cell nucleus	Cellular tumor antigen p53	Homo sapiens (human)
chromatin	Cellular tumor antigen p53	Homo sapiens (human)
transcription regulator complex	Cellular tumor antigen p53	Homo sapiens (human)
protein-containing complex	Cellular tumor antigen p53	Homo sapiens (human)
nucleoplasm	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
cytoplasm	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
centrosome	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
cytosol	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
plasma membrane	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
membrane	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
dendrite	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
midbody	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
cell body	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
synapse	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
extracellular exosome	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
neuronal dense core vesicle	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
extracellular vesicle	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
heterotrimeric G-protein complex	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
cytoplasm	Guanine nucleotide-binding protein G(i) subunit alpha-2	Homo sapiens (human)
nucleus	ADP/ATP translocase 2	Homo sapiens (human)
mitochondrion	ADP/ATP translocase 2	Homo sapiens (human)
mitochondrial inner membrane	ADP/ATP translocase 2	Homo sapiens (human)
plasma membrane	ADP/ATP translocase 2	Homo sapiens (human)
membrane	ADP/ATP translocase 2	Homo sapiens (human)
mitochondrial nucleoid	ADP/ATP translocase 2	Homo sapiens (human)
mitochondrial permeability transition pore complex	ADP/ATP translocase 2	Homo sapiens (human)
MMXD complex	ADP/ATP translocase 2	Homo sapiens (human)
nucleus	Protein kinase C beta type	Homo sapiens (human)
nucleoplasm	Protein kinase C beta type	Homo sapiens (human)
cytoplasm	Protein kinase C beta type	Homo sapiens (human)
centrosome	Protein kinase C beta type	Homo sapiens (human)
cytosol	Protein kinase C beta type	Homo sapiens (human)
plasma membrane	Protein kinase C beta type	Homo sapiens (human)
brush border membrane	Protein kinase C beta type	Homo sapiens (human)
calyx of Held	Protein kinase C beta type	Homo sapiens (human)
extracellular exosome	Protein kinase C beta type	Homo sapiens (human)
presynaptic cytosol	Protein kinase C beta type	Homo sapiens (human)
spectrin	Protein kinase C beta type	Homo sapiens (human)
nuclear envelope	Insulin receptor	Homo sapiens (human)
nuclear lumen	Insulin receptor	Homo sapiens (human)
lysosome	Insulin receptor	Homo sapiens (human)
late endosome	Insulin receptor	Homo sapiens (human)
plasma membrane	Insulin receptor	Homo sapiens (human)
caveola	Insulin receptor	Homo sapiens (human)
external side of plasma membrane	Insulin receptor	Homo sapiens (human)
endosome membrane	Insulin receptor	Homo sapiens (human)
membrane	Insulin receptor	Homo sapiens (human)
dendrite membrane	Insulin receptor	Homo sapiens (human)
neuronal cell body membrane	Insulin receptor	Homo sapiens (human)
extracellular exosome	Insulin receptor	Homo sapiens (human)
insulin receptor complex	Insulin receptor	Homo sapiens (human)
receptor complex	Insulin receptor	Homo sapiens (human)
plasma membrane	Insulin receptor	Homo sapiens (human)
axon	Insulin receptor	Homo sapiens (human)
pericentriolar material	Tyrosine-protein kinase Lck	Homo sapiens (human)
immunological synapse	Tyrosine-protein kinase Lck	Homo sapiens (human)
cytosol	Tyrosine-protein kinase Lck	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase Lck	Homo sapiens (human)
membrane raft	Tyrosine-protein kinase Lck	Homo sapiens (human)
extracellular exosome	Tyrosine-protein kinase Lck	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase Lck	Homo sapiens (human)
membrane raft	Tyrosine-protein kinase Fyn	Homo sapiens (human)
dendrite	Tyrosine-protein kinase Fyn	Homo sapiens (human)
nucleus	Tyrosine-protein kinase Fyn	Homo sapiens (human)
mitochondrion	Tyrosine-protein kinase Fyn	Homo sapiens (human)
endosome	Tyrosine-protein kinase Fyn	Homo sapiens (human)
cytosol	Tyrosine-protein kinase Fyn	Homo sapiens (human)
actin filament	Tyrosine-protein kinase Fyn	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase Fyn	Homo sapiens (human)
postsynaptic density	Tyrosine-protein kinase Fyn	Homo sapiens (human)
dendrite	Tyrosine-protein kinase Fyn	Homo sapiens (human)
perikaryon	Tyrosine-protein kinase Fyn	Homo sapiens (human)
cell body	Tyrosine-protein kinase Fyn	Homo sapiens (human)
membrane raft	Tyrosine-protein kinase Fyn	Homo sapiens (human)
perinuclear region of cytoplasm	Tyrosine-protein kinase Fyn	Homo sapiens (human)
perinuclear endoplasmic reticulum	Tyrosine-protein kinase Fyn	Homo sapiens (human)
glial cell projection	Tyrosine-protein kinase Fyn	Homo sapiens (human)
Schaffer collateral - CA1 synapse	Tyrosine-protein kinase Fyn	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase Fyn	Homo sapiens (human)
mitochondrial matrix	Cyclin-dependent kinase 1	Homo sapiens (human)
chromosome, telomeric region	Cyclin-dependent kinase 1	Homo sapiens (human)
nucleus	Cyclin-dependent kinase 1	Homo sapiens (human)
nucleoplasm	Cyclin-dependent kinase 1	Homo sapiens (human)
mitochondrion	Cyclin-dependent kinase 1	Homo sapiens (human)
endoplasmic reticulum membrane	Cyclin-dependent kinase 1	Homo sapiens (human)
centrosome	Cyclin-dependent kinase 1	Homo sapiens (human)
cytosol	Cyclin-dependent kinase 1	Homo sapiens (human)
spindle microtubule	Cyclin-dependent kinase 1	Homo sapiens (human)
membrane	Cyclin-dependent kinase 1	Homo sapiens (human)
midbody	Cyclin-dependent kinase 1	Homo sapiens (human)
extracellular exosome	Cyclin-dependent kinase 1	Homo sapiens (human)
mitotic spindle	Cyclin-dependent kinase 1	Homo sapiens (human)
cyclin A1-CDK1 complex	Cyclin-dependent kinase 1	Homo sapiens (human)
cyclin A2-CDK1 complex	Cyclin-dependent kinase 1	Homo sapiens (human)
cyclin B1-CDK1 complex	Cyclin-dependent kinase 1	Homo sapiens (human)
cyclin-dependent protein kinase holoenzyme complex	Cyclin-dependent kinase 1	Homo sapiens (human)
cytoplasm	Cyclin-dependent kinase 1	Homo sapiens (human)
nucleus	Cyclin-dependent kinase 1	Homo sapiens (human)
extracellular region	Glycogen phosphorylase, liver form	Homo sapiens (human)
cytosol	Glycogen phosphorylase, liver form	Homo sapiens (human)
secretory granule lumen	Glycogen phosphorylase, liver form	Homo sapiens (human)
extracellular exosome	Glycogen phosphorylase, liver form	Homo sapiens (human)
ficolin-1-rich granule lumen	Glycogen phosphorylase, liver form	Homo sapiens (human)
cytoplasm	Glycogen phosphorylase, liver form	Homo sapiens (human)
cytoplasmic vesicle	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
cytoplasm	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
Golgi apparatus	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
cytosol	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
focal adhesion	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
cytoplasmic side of plasma membrane	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
microtubule cytoskeleton	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase Fes/Fps	Homo sapiens (human)
extracellular region	Adenine phosphoribosyltransferase	Homo sapiens (human)
nucleoplasm	Adenine phosphoribosyltransferase	Homo sapiens (human)
cytoplasm	Adenine phosphoribosyltransferase	Homo sapiens (human)
cytosol	Adenine phosphoribosyltransferase	Homo sapiens (human)
secretory granule lumen	Adenine phosphoribosyltransferase	Homo sapiens (human)
extracellular exosome	Adenine phosphoribosyltransferase	Homo sapiens (human)
cytoplasm	Adenine phosphoribosyltransferase	Homo sapiens (human)
Golgi apparatus	Tyrosine-protein kinase Yes	Homo sapiens (human)
centrosome	Tyrosine-protein kinase Yes	Homo sapiens (human)
cytosol	Tyrosine-protein kinase Yes	Homo sapiens (human)
actin filament	Tyrosine-protein kinase Yes	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase Yes	Homo sapiens (human)
focal adhesion	Tyrosine-protein kinase Yes	Homo sapiens (human)
extracellular exosome	Tyrosine-protein kinase Yes	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase Yes	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase Lyn	Homo sapiens (human)
cytoplasmic side of plasma membrane	Tyrosine-protein kinase Lyn	Homo sapiens (human)
nucleus	Tyrosine-protein kinase Lyn	Homo sapiens (human)
cytoplasm	Tyrosine-protein kinase Lyn	Homo sapiens (human)
lysosomal membrane	Tyrosine-protein kinase Lyn	Homo sapiens (human)
Golgi apparatus	Tyrosine-protein kinase Lyn	Homo sapiens (human)
cytosol	Tyrosine-protein kinase Lyn	Homo sapiens (human)
plasma membrane	Tyrosine-protein kinase Lyn	Homo sapiens (human)
adherens junction	Tyrosine-protein kinase Lyn	Homo sapiens (human)
mitochondrial crista	Tyrosine-protein kinase Lyn	Homo sapiens (human)
endocytic vesicle membrane	Tyrosine-protein kinase Lyn	Homo sapiens (human)
intracellular membrane-bounded organelle	Tyrosine-protein kinase Lyn	Homo sapiens (human)
membrane raft	Tyrosine-protein kinase Lyn	Homo sapiens (human)
perinuclear region of cytoplasm	Tyrosine-protein kinase Lyn	Homo sapiens (human)
extracellular exosome	Tyrosine-protein kinase Lyn	Homo sapiens (human)
glutamatergic synapse	Tyrosine-protein kinase Lyn	Homo sapiens (human)
postsynaptic specialization, intracellular component	Tyrosine-protein kinase Lyn	Homo sapiens (human)
integrin alpha2-beta1 complex	Tyrosine-protein kinase Lyn	Homo sapiens (human)
plasma membrane	Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)
early endosome	Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)
plasma membrane	Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)
endosome membrane	Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)
dendrite	Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)
neuronal cell body	Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)
receptor complex	Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)
plasma membrane protein complex	Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)
axon	Proto-oncogene tyrosine-protein kinase receptor Ret	Homo sapiens (human)
plasma membrane	Insulin-like growth factor 1 receptor	Homo sapiens (human)
caveola	Insulin-like growth factor 1 receptor	Homo sapiens (human)
membrane	Insulin-like growth factor 1 receptor	Homo sapiens (human)
T-tubule	Insulin-like growth factor 1 receptor	Homo sapiens (human)

Assay ID	Title	Year	Journal	Article
AID1296008	Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening	2020	SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1	Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1346986	P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987	P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1876329	Antiviral activity against MERS-CoV infected in 1 hr pretreated human Huh-7 cells assessed as inhibition of viral growth at 10 uM measured after 48 hrs by plaque reduction assay relative to control	2022	Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2	Kinases as Potential Therapeutic Targets for Anti-coronaviral Therapy.
AID1425005	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425174	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718215	Elimination half life in C57BL/6J mouse plasma at 10 mg/kg, po administered as single dose by mass spectrometry based UHPLC analysis
AID1424992	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425117	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425203	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718226	AUC (0 to 8 hrs) in C57BL/6J mouse brain at 10 mg/kg, po administered as single dose by mass spectrometry based UHPLC analysis
AID1425000	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425060	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424925	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1153720	Cytotoxicity against human COLO205 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Jun-23, Volume: 81	Benzofuran derivatives as anticancer inhibitors of mTOR signaling.
AID1424929	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425147	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424505	Antitumor activity in renal cell carcinoma patient without previous VEGFR TKI treatment assessed as progression free survival (Rvb = 1.9 months)	2017	European journal of medicinal chemistry, Dec-15, Volume: 142	Recent developments in small molecule therapies for renal cell carcinoma.
AID1425122	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1409403	Binding affinity to mTOR FKBP12 site (unknown origin)	2018	Journal of medicinal chemistry, 11-21, Volume: 61, Issue:22	Discovery and Preclinical Characterization of 5-[4,6-Bis({3-oxa-8-azabicyclo[3.2.1]octan-8-yl})-1,3,5-triazin-2-yl]-4-(difluoromethyl)pyridin-2-amine (PQR620), a Highly Potent and Selective mTORC1/2 Inhibitor for Cancer and Neurological Disorders.
AID1662433	Inhibition of mTOR in HEK293 cells	2020	Journal of medicinal chemistry, 09-24, Volume: 63, Issue:18	p62/SQSTM1, a Central but Unexploited Target: Advances in Its Physiological/Pathogenic Functions and Small Molecular Modulators.
AID1424937	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425010	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425170	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425164	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424960	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1207342	Inhibition of fast sodium current (INa) in HEK293 cells transfected with human Nav1.5 measured using IonWorks Quattro automated patch clamp platform
AID1425188	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1876111	Cytotoxicity against human Huh-7 cells	2022	Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2	Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1425024	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424948	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424922	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425159	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718223	Cmax in C57BL/6J mouse brain at 10 mg/kg, po administered as single dose by mass spectrometry based UHPLC analysis
AID1425115	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424955	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425161	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425107	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424949	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1153724	Inhibition of mTORC1 in human COLO205 cells assessed as reduction of S6 phosphorylation at 0.1 to 8 uM after 24 hrs by Western blotting	2014	European journal of medicinal chemistry, Jun-23, Volume: 81	Benzofuran derivatives as anticancer inhibitors of mTOR signaling.
AID1425104	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425202	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1071501	Cytotoxicity against human Caki1 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1424915	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718218	Cmax in C57BL/6J mouse plasma at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1424947	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425128	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424897	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424975	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425072	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425133	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425046	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1065394	Oral bioavailability in human	2014	Journal of medicinal chemistry, Jan-23, Volume: 57, Issue:2	Macrocyclic drugs and clinical candidates: what can medicinal chemists learn from their properties?
AID1424959	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424506	Antitumor activity in renal cell carcinoma patient with 2 previous VEGFR TKI treatment assessed as progression free survival (Rvb = 1.8 months)	2017	European journal of medicinal chemistry, Dec-15, Volume: 142	Recent developments in small molecule therapies for renal cell carcinoma.
AID1424956	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1207402	Inhibition of slow delayed inward rectifying potassium current (Iks) in Chinese Hamster Ovary (CHO) cells transfected with KCNQ1 / Kv1.7 / KvLQT1 and KCNE1/minK measured using IonWorks automated patch clamp platform
AID1425050	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425088	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425026	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1153721	Inhibition of mTORC1 in human SK-HEP1 cells assessed as reduction of S6 phosphorylation at 0.1 to 8 uM after 24 hrs by Western blotting	2014	European journal of medicinal chemistry, Jun-23, Volume: 81	Benzofuran derivatives as anticancer inhibitors of mTOR signaling.
AID1425137	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1207282	Inhibition of long-lasting type calcium current (ICaL) in HEK293 cells (alpha1C/beta2a/alpha2delta1) cells measured using IonWorks Barracuda automated patch clamp platform
AID1236017	Induction of autophagic punctation in human A549 cells assessed as increase of puncta with p62 at 5 uM after 6 hrs by immunofluorescence staining-based microscopic analysis relative to control	2015	Journal of natural products, Jul-24, Volume: 78, Issue:7	Bisleuconothine A Induces Autophagosome Formation by Interfering with AKT-mTOR Signaling Pathway.
AID1207311	Inhibition of fast sodium current (INa) in Chinese Hamster Ovary (CHO) K1 cells transfected with human Nav1.5 measured using IonWorks Quattro automated patch clamp platform
AID1425173	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425012	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424928	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425068	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425197	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424970	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425078	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425087	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424969	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425127	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424988	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424991	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718230	Elimination half life in C57BL/6J mouse brain at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1207371	Inhibition of slow delayed inward rectifying potassium current (Iks) in Chinese Hamster Ovary (CHO) cells expressing hKvLQT1/hminK measured using IonWorks Quattro automated patch clamp platform
AID1425019	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425204	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425053	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425083	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424912	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425210	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425001	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424944	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425064	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425195	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425044	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424923	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425193	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718225	Elimination half life in C57BL/6J mouse brain at 10 mg/kg, po administered as single dose by mass spectrometry based UHPLC analysis
AID1425136	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425168	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424983	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425029	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425150	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473740	Inhibition 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 assay	2013	Toxicological 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.
AID1425080	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1236023	Inhibition of AKT in human A549 cells assessed as downregulation of PRAS40 phosphorylation at thr246 at 5 uM after 3 to 12 hrs by Western blot analysis	2015	Journal of natural products, Jul-24, Volume: 78, Issue:7	Bisleuconothine A Induces Autophagosome Formation by Interfering with AKT-mTOR Signaling Pathway.
AID1425062	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473910	Ratio of drug concentration at steady state in human at 0.25 to 20 mg, po after 24 hrs to IC50 for human BSEP overexpressed in Sf9 insect cells	2013	Toxicological 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.
AID1424950	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425014	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424926	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425102	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1071500	Cytotoxicity against human HT-29 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1424918	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424965	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425004	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473912	Ratio of drug concentration at steady state in human at 0.25 to 20 mg, po after 24 hrs to IC50 for human MRP3 overexpressed in Sf9 insect cells	2013	Toxicological 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.
AID1424909	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718232	Clearance in C57BL/6J mouse brain at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1424908	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425171	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425097	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424940	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473739	Inhibition 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 assay	2013	Toxicological 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.
AID1718222	Clearance in C57BL/6J mouse plasma at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1425106	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425063	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1236019	Inhibition of mTOR phosphorylation at ser2448 in human A549 cells at 5 uM after 3 to 24 hrs by Western blot analysis	2015	Journal of natural products, Jul-24, Volume: 78, Issue:7	Bisleuconothine A Induces Autophagosome Formation by Interfering with AKT-mTOR Signaling Pathway.
AID1424979	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424905	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425153	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425038	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425018	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425074	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425054	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1236012	Induction of autophagy in human A549 cells assessed as increase in conversion of LC3-1 to LC3-2 at 5 uM after 6 hrs by Western blot analysis	2015	Journal of natural products, Jul-24, Volume: 78, Issue:7	Bisleuconothine A Induces Autophagosome Formation by Interfering with AKT-mTOR Signaling Pathway.
AID1425201	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1153726	Inhibition of mTORC1 in human COLO205 cells assessed as AKT phosphorylation at Ser473 at 0.1 to 8 uM after 24 hrs by Western blotting	2014	European journal of medicinal chemistry, Jun-23, Volume: 81	Benzofuran derivatives as anticancer inhibitors of mTOR signaling.
AID1425166	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424958	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473908	AUC in human at 0.25 to 20 mg, po QD after 24 hrs	2013	Toxicological 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.
AID1153719	Cytotoxicity against human HOP62 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Jun-23, Volume: 81	Benzofuran derivatives as anticancer inhibitors of mTOR signaling.
AID1425144	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424935	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1207431	Inhibition of transient outward potassium current (Ito) current in Chinese Hamster Ovary (CHO) K1 cells expressing human Kv4.3 measured using IonWorks Quattro automated patch clamp platform
AID1071505	Cytotoxicity against human COLO205 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1424896	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425059	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1876110	Cytotoxicity against human HaCaT cells	2022	Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2	Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1425175	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425198	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424892	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID706794	Increase in allograft survival in stringent Dark Agouti to Lewis rat heterotopic vascular heart allotransplantation model assessed as allograft mean survival time at 0.3 mg/kg, po qd (Rvb = 6 days)	2012	Journal of medicinal chemistry, Nov-26, Volume: 55, Issue:22	An oral sphingosine 1-phosphate receptor 1 (S1P(1)) antagonist prodrug with efficacy in vivo: discovery, synthesis, and evaluation.
AID1425149	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425108	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425206	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1153725	Inhibition of mTORC1 in human COLO205 cells assessed as reduction of 4-EBP1 phosphorylation at 0.1 to 8 uM after 24 hrs by Western blotting	2014	European journal of medicinal chemistry, Jun-23, Volume: 81	Benzofuran derivatives as anticancer inhibitors of mTOR signaling.
AID1425042	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1875901	Antiviral activity against MERS-CoV infected in 1 hr pretreated human Huh-7 cells at 10 uM relative to control	2022	Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2	Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1424917	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424984	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424978	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425051	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1876108	Inhibition of mTOR (unknown origin)	2022	Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2	Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1583277	Protection against C57BL/6J mouse model of neuronal mTOR hyperactivity assessed as survival rate at 6 mg/kg, ip administered on postnatal day 22 daily and measured on postnatal day 52 (Rvb = 48 %)	2020	Journal of medicinal chemistry, 02-13, Volume: 63, Issue:3	Discovery of a Brain-Penetrant ATP-Competitive Inhibitor of the Mechanistic Target of Rapamycin (mTOR) for CNS Disorders.
AID1425176	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425095	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425103	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718267	Toxicity in Tsc1-GFAP knockout Balb/c mouse assessed as change in body weight at 10 mg/kg, po
AID1424933	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424914	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424890	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425002	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425035	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425189	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425140	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424977	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424993	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424987	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718213	Cmax in C57BL/6J mouse plasma at 10 mg/kg, po administered as single dose by mass spectrometry based UHPLC analysis
AID1424994	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473741	Inhibition 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 assay	2013	Toxicological 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.
AID1718231	AUC (0 to 8 hrs) in C57BL/6J mouse brain at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1425185	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425118	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425027	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425090	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424920	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718262	Protection against Tsc1-GFAP knockout induced mortality in Balb/c mouse assessed as increase in survival rate at 10 mg/kg, po administered as single dose
AID1424911	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718214	Tmax in C57BL/6J mouse plasma at 10 mg/kg, po administered as single dose by mass spectrometry based UHPLC analysis
AID1424971	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424973	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425116	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1474166	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index	2016	Drug 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.
AID1425073	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425213	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425003	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1876090	Antiviral activity against MERS-CoV at 10 uM relative to control	2022	Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2	Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1424968	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1916668	Inhibition of mTORC1 (unknown origin)	2022	European journal of medicinal chemistry, Aug-05, Volume: 238	Contemporary mTOR inhibitor scaffolds to diseases breakdown: A patent review (2015-2021).
AID1425138	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425043	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1071502	Cytotoxicity against human ColoR cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1425179	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425007	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425154	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425022	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424921	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425208	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425061	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424967	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425045	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424931	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1236021	Inhibition of mTOR in human A549 cells assessed as downregulation of p70S6K phosphorylation at thr389 at 5 uM after 3 to 24 hrs by Western blot analysis	2015	Journal of natural products, Jul-24, Volume: 78, Issue:7	Bisleuconothine A Induces Autophagosome Formation by Interfering with AKT-mTOR Signaling Pathway.
AID1425156	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425132	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424899	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424900	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425030	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424972	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424898	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425119	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718229	Tmax in C57BL/6J mouse brain at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1718220	Elimination half life in C57BL/6J mouse plasma at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1425099	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425191	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425056	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425049	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425016	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425039	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718217	Clearance in C57BL/6J mouse plasma at 10 mg/kg, po administered as single dose by mass spectrometry based UHPLC analysis
AID1425036	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425181	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425211	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425177	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425143	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425160	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425113	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1071503	Cytotoxicity against human HCT116 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1207465	Inhibition of rapid delayed inward rectifying potassium current (IKr) in Chinese hamster ovary (CHO) K1 cells stably expressing hERG measured using IonWorks Quattro automated patch clamp platform
AID1424942	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424919	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424910	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1207559	Inhibition of long-lasting type calcium current (hICa) in Chinese Hamster Ovary (CHO) cells expressing hCav1.2 measured using IonWorks Quattro automated patch clamp platform
AID1425098	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424907	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473909	Drug concentration at steady state in human at 0.25 to 20 mg, po QD after 24 hrs	2013	Toxicological 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.
AID1425192	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425196	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718219	Tmax in C57BL/6J mouse plasma at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1876109	Cytotoxicity against human HeLa cells	2022	Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2	Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1425142	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425081	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425100	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425089	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425124	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425126	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1153722	Inhibition of mTORC1 in human SK-HEP1 cells assessed as reduction of 4-EBP1 phosphorylation at 0.1 to 8 uM after 24 hrs by Western blotting	2014	European journal of medicinal chemistry, Jun-23, Volume: 81	Benzofuran derivatives as anticancer inhibitors of mTOR signaling.
AID1425121	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424954	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425172	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424997	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424985	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425028	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425190	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424503	Antitumor activity in patient with metastatic renal cell carcinoma assessed as progression free survival	2017	European journal of medicinal chemistry, Dec-15, Volume: 142	Recent developments in small molecule therapies for renal cell carcinoma.
AID1424893	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425163	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425082	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425017	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1153723	Inhibition of mTORC1 in human SK-HEP1 cells assessed as AKT phosphorylation at Ser473 at 0.1 to 8 uM after 24 hrs by Western blotting	2014	European journal of medicinal chemistry, Jun-23, Volume: 81	Benzofuran derivatives as anticancer inhibitors of mTOR signaling.
AID1424962	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718243	In vivo inhibition of PI3Kalpha in C57BL/6J mouse assessed as increase in plasma glucose concentration at 10 mg/kg, po measured after 8 hrs by glucoseoxidase-peroxide coupled colorimetric assay
AID1424889	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1071499	Cytotoxicity against human OVCAR3 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1425199	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425182	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424986	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425169	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425048	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425131	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425162	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425096	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424936	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424946	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425057	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425047	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425008	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424934	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424930	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425055	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425187	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424963	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425079	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718247	In vivo inhibition of mTORC1 signalling in C57BL/6J mouse assessed as reduction in RPS6 phosphorylation at S235/236 residue in cortex at 10 mg/kg, po incubated for 30 mins by Western blot analysis
AID1424974	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425155	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425037	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425058	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424894	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425040	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425141	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425013	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424952	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424999	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425157	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425178	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425186	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425212	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425129	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1071495	Cytotoxicity against human HOP62 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1425023	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473913	Ratio of drug concentration at steady state in human at 0.25 to 20 mg, po after 24 hrs to IC50 for human MRP4 overexpressed in Sf9 insect cells	2013	Toxicological 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.
AID1425200	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425093	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424902	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425086	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424485	Antitumor activity in patient with metastatic renal cell carcinoma assessed as overall survival	2017	European journal of medicinal chemistry, Dec-15, Volume: 142	Recent developments in small molecule therapies for renal cell carcinoma.
AID1424996	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425069	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425209	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425167	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1236011	Prevention of autophagosome degradation in human A549 cells assessed as upregulation of p62 expression at 5 uM after 6 hrs by Western blot analysis	2015	Journal of natural products, Jul-24, Volume: 78, Issue:7	Bisleuconothine A Induces Autophagosome Formation by Interfering with AKT-mTOR Signaling Pathway.
AID1424981	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424957	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718245	In vivo inhibition of PI3Kalpha C57BL/6J mouse assessed as increase in plasma insulin concentration at 10 mg/kg, po measured after 8 hrs by ELISA
AID1207496	Inhibition of rapid delayed inward rectifying potassium current (IKr) in Chinese hamster ovary (CHO) cells stable expressing hERG measured using IonWorks Barracuda automated patch clamp platform
AID1071498	Cytotoxicity against human DU145 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1425125	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718224	Tmax in C57BL/6J mouse brain at 10 mg/kg, po administered as single dose by mass spectrometry based UHPLC analysis
AID1425070	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424895	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424924	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425034	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425205	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1153718	Cytotoxicity against human SQ20B cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Jun-23, Volume: 81	Benzofuran derivatives as anticancer inhibitors of mTOR signaling.
AID1718216	AUC (0 to 8 hrs) in C57BL/6J mouse plasma at 10 mg/kg, po administered as single dose by mass spectrometry based UHPLC analysis
AID1207525	Inhibition of rapid delayed inward rectifying potassium current (IKr) measured using manual patch clamp assay
AID1425111	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425148	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425123	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1236016	Induction of autophagic punctation in human A549 cells assessed as increase of puncta with LC3 at 5 uM after 6 hrs by immunofluorescence staining-based microscopic analysis relative to control	2015	Journal of natural products, Jul-24, Volume: 78, Issue:7	Bisleuconothine A Induces Autophagosome Formation by Interfering with AKT-mTOR Signaling Pathway.
AID1424998	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425207	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425025	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425134	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424891	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424939	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425194	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425130	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473738	Inhibition 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 assay	2013	Toxicological 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.
AID1425110	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425011	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424945	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425105	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424904	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718221	AUC (0 to 8 hrs) in C57BL/6J mouse plasma at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1424989	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1474167	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status	2016	Drug 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.
AID1425076	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425094	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1718228	Cmax in C57BL/6J mouse brain at 10 mg/kg, po administered once a day for 4 consecutive days by mass spectrometry based UHPLC analysis
AID1425006	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424976	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425145	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424932	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1583253	Inhibition of oversizing of mouse primary cortical neuron harboring TSC1 deletion mutant at 20 nM incubated for 7 days by immunofluorescence assay	2020	Journal of medicinal chemistry, 02-13, Volume: 63, Issue:3	Discovery of a Brain-Penetrant ATP-Competitive Inhibitor of the Mechanistic Target of Rapamycin (mTOR) for CNS Disorders.
AID1425158	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425165	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1473911	Ratio of drug concentration at steady state in human at 0.25 to 20 mg, po after 24 hrs to IC50 for human MRP2 overexpressed in Sf9 insect cells	2013	Toxicological 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.
AID1425015	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1875938	Antiviral activity against MERS-CoV infected in human Huh-7 cells at 10 uM relative to control	2022	Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2	Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1425084	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425033	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425146	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425120	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424953	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425085	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424941	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1071497	Cytotoxicity against human SKHEP1 cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1425052	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425071	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1071513	Cytotoxicity against human SQ20B cells after 72 hrs by MTT assay	2014	European journal of medicinal chemistry, Mar-03, Volume: 74	Benzofuran derivatives as a novel class of inhibitors of mTOR signaling.
AID1424966	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424901	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424990	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424964	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424995	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424980	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1425065	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1424961	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID1583252	Inhibition of overgrowth of mouse primary cortical neuron harboring TSC1 deletion mutant at 20 nM incubated for 7 days by immunofluorescence assay	2020	Journal of medicinal chemistry, 02-13, Volume: 63, Issue:3	Discovery of a Brain-Penetrant ATP-Competitive Inhibitor of the Mechanistic Target of Rapamycin (mTOR) for CNS Disorders.
AID1425009	Kinobeads (epsilon), multiple immobilized ATP-competitive broad spectrum kinase inhibitors, used to assess residual binding of ~300 proteins simultaneously from cell lysate in the presence of a compound. Quantitative readout performed by mass spectrometry	2017	Science (New York, N.Y.), 12-01, Volume: 358, Issue:6367	The target landscape of clinical kinase drugs.
AID504749	qHTS profiling for inhibitors of Plasmodium falciparum proliferation	2011	Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043	Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1345726	Human mechanistic target of rapamycin kinase (FRAP subfamily)	1998	Transplantation proceedings, Aug, Volume: 30, Issue:5	Chemical modification of rapamycin: the discovery of SDZ RAD.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	0 (0.00)	18.7374
1990's	20 (0.37)	18.2507
2000's	596 (10.97)	29.6817
2010's	3917 (72.11)	24.3611
2020's	899 (16.55)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	1,289 (22.89%)	5.53%
Reviews	767 (13.62%)	6.00%
Case Studies	596 (10.58%)	4.05%
Observational	147 (2.61%)	0.25%
Other	2,832 (50.29%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (895)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
Outcome-related Factors in Patients With Metastatic Renal Cell Carcinoma Treated With Everolimus After Failure of a First-line Treatment With VEGF Inhibitor [NCT02338570]	Phase 4	31 participants (Actual)	Interventional	2015-07-31	Terminated(stopped due to Stopped on November 16th 2016, because of recruitment failure.)
A Phase 1b Trial of ARV-471 in Combination With Everolimus in Patients With ER+, HER2- Advanced or Metastatic Breast Cancer [NCT05501769]	Phase 1	32 participants (Anticipated)	Interventional	2022-09-08	Recruiting
An Open-label, Phase II, Single-arm Study of Everolimus in Combination With Letrozole in the Treatment of Postmenopausal Women With Estrogen Receptor Positive HER2 Negative Metastatic or Locally Advanced Breast Cancer [NCT01698918]	Phase 2	202 participants (Actual)	Interventional	2013-03-07	Completed
Phase I Study of the Combination of Bevacizumab, Everolimus and LBH589 (BEL) for the Treatment of Advanced Solid Tumors [NCT01055795]	Phase 1	14 participants (Actual)	Interventional	2010-03-31	Completed
Phase II Trial on Efficacy of mTOR Inhibitor RAD001 as Maintenance Therapy for Patients Above 60 Years in Mantle Cell Lymphoma After First and Second Line Chemotherapy [NCT00727207]	Phase 2	35 participants (Anticipated)	Interventional	2008-05-31	Terminated(stopped due to Lack of participations (8 of 25))
Phase II Study of Everolimus in Children and Adolescents With Refractory or Relapsed Osteosarcoma [NCT01216826]	Phase 2	20 participants (Anticipated)	Interventional	2011-03-31	Recruiting
A Phase IB/II Study of Second Line Therapy With Panitumumab, Irinotecan and Everolimus (PIE) in Metastatic Colorectal Cancer With KRAS WT [NCT01139138]	Phase 1/Phase 2	49 participants (Actual)	Interventional	2010-06-30	Completed
Randomized Phase II Study of Sorafenib With or Without Everolimus in Patients With Radioactive Iodine Refractory Hurthle Cell Thyroid Cancer [NCT02143726]	Phase 2	35 participants (Actual)	Interventional	2014-10-01	Active, not recruiting
A Twelve-month, Multicenter, Open-label, Randomized Study of the Safety, Tolerability and Efficacy of Everolimus With IL-2 Receptor Antagonist, Corticosteroids and Two Different Exposure Levels of Tacrolimus in de Novo Renal Transplant Recipients [NCT00369161]	Phase 4	228 participants (Actual)	Interventional	2006-06-30	Completed
Everolimus Added to Long Acting Octreotide as a Volume Reducing Treatment of Polycystic Livers [NCT01157858]	Phase 2	44 participants (Actual)	Interventional	2010-06-30	Completed
[NCT01167530]	Phase 1	36 participants (Anticipated)	Interventional	2008-03-31	Recruiting
An Open Label Multi-Center Phase II Study of RAD001 in Advanced Thyroid Cancer [NCT01164176]	Phase 2	40 participants (Actual)	Interventional	2010-03-31	Completed
A Phase Ib, Open-label Study to Evaluate RAD001 as Monotherapy Treatment in Chinese Patients With Advanced Pulmonary Neuroendocrine Tumor [NCT01175096]	Phase 1/Phase 2	20 participants (Anticipated)	Interventional	2010-07-31	Active, not recruiting
Hormone Receptor Positive Disease Across Solid Tumor Types: A Phase I Study of Single-Agent Hormone Blockade and Combination Approaches With Targeted Agents to Provide Synergy and Overcome Resistance [NCT01197170]	Phase 1	277 participants (Actual)	Interventional	2010-09-07	Completed
A Phase II Study of the Mammalian Target of Rapamycin (mTOR) Inhibitor RAD001 in Combination With Imatinib Mesylate in Patients With Previously Treated Advanced Renal Carcinoma [NCT00331409]	Phase 2	23 participants (Actual)	Interventional	2006-01-31	Completed
A Randomized Three Arm Phase II Study of (1) Everolimus, (2) Estrogen Deprivation Therapy (EDT) With Leuprolide + Letrozole and (3) Everolimus + EDT in Patients With Unresectable Fibrolamellar Hepatocellular Carcinoma (FLL-HCC) [NCT01642186]	Phase 2	28 participants (Actual)	Interventional	2012-07-12	Completed
A Clinical Evaluation of the Everolimus Eluting Bioresorbable Vascular Scaffold System (BVS) for the Treatment of Subjects With Critical Limb Ischemia (CLI) From Occlusive Vascular Disease of the Tibial Arteries [NCT01341340]		2 participants (Actual)	Interventional	2011-11-30	Terminated(stopped due to Discontinued due to poor enrollment. Insufficient number of patients enrolled to permit a statistically rigorous assessment of safety and efficacy.)
2-phased Randomized Comparison Between PromusTMElementTM Versus Xience PRIME® Stent [NCT01581515]	Phase 4	100 participants (Anticipated)	Interventional	2012-01-31	Recruiting
NOBORI Biolimus-Eluting Versus XIENCE/PROMUS Everolimus-eluting Stent Trial [NCT01303640]	Phase 4	3,235 participants (Actual)	Interventional	2011-05-31	Completed
BARIS - BIBF1120 and RAD001 in Solid Tumors. A Phase I Trial to Evaluate the Safety and Tolerability of Combined BIBF 1120 and RAD001 in Solid Tumors and to Determine the Maximum Tolerated Dose (MTD) of the Combination [NCT01349296]	Phase 1	18 participants (Actual)	Interventional	2012-07-31	Completed
A Phase II, Randomized Two-Arm Study of Everolimus and Letrozole, +/- Ribociclib (LEE011) in Patients With Advanced or Recurrent Endometrial Carcinoma [NCT03008408]	Phase 2	99 participants (Anticipated)	Interventional	2017-08-18	Recruiting
Assessment of Neointimal Stent Strut Coverage and Endothelial Function After Second Generation Drug-Eluting Stent Systems [NCT01073111]		0 participants (Actual)	Interventional	2010-04-30	Withdrawn
Multicenter International Durability and Safety of Sirolimus in LAM Trial (MIDAS) [NCT02432560]		600 participants (Anticipated)	Observational	2015-03-31	Recruiting
Phase II Study of the IGF-1 Inhibitor Pasireotide Lar in Combination With the m-TOR Inhibitor Everolimus in Patients With Relapsed/Refractory Multiple Myeloma [NCT01234974]	Phase 2	0 participants (Actual)	Interventional	2010-12-31	Withdrawn(stopped due to Study never undertaken)
Dose-finding Study of CAELYXTM and RAD001 in Patients With Advanced Solid Tumors [NCT01148628]	Phase 1	54 participants (Actual)	Interventional	2007-10-31	Active, not recruiting
A Phase II/III Clinical Study to Evaluate the Efficacy and Safety of Fruquintinib in Combination With Sintilimab Versus Axitinib or Everolimus as Second-line Treatment for Locally Advanced or Metastatic Renal Cell Carcinoma [NCT05522231]	Phase 2/Phase 3	264 participants (Anticipated)	Interventional	2022-10-27	Recruiting
Phase II Study of RAD001monotherapy in Patients With Unresectable Adenoid Cystic Carcinoma [NCT01152840]	Phase 2	33 participants (Actual)	Interventional	2008-07-31	Completed
Comparison of the Efficacy and Safety of New Platform Everolimus-eluting Coronary Stent System (Promus Element) With Zotarolimus-eluting Coronary Stent System (Endeavor Resolute) and Triple Anti-platelet Therapy With Double-dose Clopidogrel Anti-platelet [NCT01267734]	Phase 4	3,750 participants (Anticipated)	Interventional	2010-06-30	Recruiting
A 6-Month Open Pilot Study to Investigate the Safety and Tolerability of Immediate Conversion From Calcineurin Inhibitor Tacrolimus to Everolimus in Stable Maintenance Renal Transplant Recipients [NCT01269684]	Phase 4	0 participants (Actual)	Interventional	2008-08-31	Withdrawn(stopped due to No patient has never been included in the trial)
Phase I Trial of Gemcitabine and Split-Dose Cisplatin Plus Everolimus (RAD001) in Patients With Advanced Solid Tumor Malignancies [NCT01182168]	Phase 1	12 participants (Actual)	Interventional	2010-08-31	Completed
An Observational Safety Evaluation of Patients Treated With the NEVO™ Sirolimus-eluting Coronary Stent. [NCT01202058]	Phase 3	156 participants (Actual)	Interventional	2010-08-31	Terminated(stopped due to The NEVO™ stent will not be commercialized. Cordis decided to close the study after 1 years. This decision took the absence of safety signals into account.)
Phase I Study of Anti-IGF-1R Monoclonal Antibody, IMC-A12, and mTOR Inhibitor, Everolimus, in Advanced Low to Intermediate Grade Neuroendocrine Carcinoma [NCT01204476]	Phase 1	27 participants (Actual)	Interventional	2010-10-31	Completed
Phase II Study of Everolimus (RAD001, Afinitor®) for Children With Recurrent or Progressive Ependymoma [NCT02155920]	Phase 2	11 participants (Actual)	Interventional	2015-02-28	Completed
Effect of the Inhibition of the Mammalian Target of Rapamycin on Metabolism and Exercise. [NCT01561404]	Phase 4	3 participants (Actual)	Interventional	2011-09-30	Terminated(stopped due to lack of potential patients)
A Phase II Trial of Everolimus and Bevacizumab in Advanced Non-Clear Cell Renal Cell Carcinoma (RCC) [NCT01399918]	Phase 2	57 participants (Actual)	Interventional	2011-07-31	Completed
A Phase II Study on Everolimus, an mTOR Inhibitor (Oral Formulation), With Octreotide LAR® in Adult Patients With Advanced, Non-functioning, Well-differentiated Gastrointestinal Neuroendocrine Tumours (GI NET) [NCT01567488]	Phase 2	43 participants (Actual)	Interventional	2011-06-08	Completed
A Prospective, Active Control, Open-label, Multinational, Randomized Clinical Trial Comparing Single Long BioMimeTM Morph Coronary Stent System vs. Two Overlapping Xience Family Coronary Stent Systems to Evaluate Safety and Performance in Patients With Lo [NCT03721614]		200 participants (Anticipated)	Interventional	2019-09-15	Not yet recruiting
A Phase I/II Trial of RAD001/Capecitabine in Refractory Gastric Cancer [NCT01099527]	Phase 1/Phase 2	59 participants (Actual)	Interventional	2009-10-31	Completed
A Phase I Study of Oral Administration of mTOR Inhibitor Everolimus (RAD001) in Association With Cisplatin and Radiotherapy for the Treatment of Locally Advanced Cervix Cancer [NCT01217177]	Phase 1	14 participants (Actual)	Interventional	2011-12-31	Completed
Phase II Study of Everolimus in Children and Adolescents With Refractory or Relapsed Rhabdomyosarcoma and Other Soft Tissue Sarcomas [NCT01216839]	Phase 2	20 participants (Anticipated)	Interventional	2011-03-31	Recruiting
RANDOMIZED TRIAL OF ZOTAROLIMUS- AND EVEROLIMUS-ELUTING STENTS REGARDING STENT COVERAGE ASSESSED BY OCT [NCT01230723]	Phase 4	30 participants (Anticipated)	Interventional	2010-10-31	Active, not recruiting
Comparison of the Everolimus Eluting (XIENCE-V®, XIENCE-Prime® or PROMUS® Stent) With the Biolimus A9 Eluting NOBORI® Stent in All-comers: a Randomized Open Label Study [NCT01233453]	Phase 4	2,700 participants (Anticipated)	Interventional	2009-01-31	Active, not recruiting
A New Strategy Regarding Discontinuation of Dual Antiplatelet; Real Safety and Efficacy of a 3-month Dual Antiplatelet Therapy Following Zotarolimus-eluting Stents Implantation (RESET Trial) [NCT01145079]	Phase 4	982 participants (Actual)	Interventional	2009-05-31	Completed
Comparison of the Efficacy of Everolimus-Eluting Versus Zotarolimus-Eluting Stent for Coronary Lesions in Acute Myocardial Infarction [NCT01347554]	Phase 4	461 participants (Actual)	Interventional	2009-01-31	Completed
A Phase I and Surgical Study of Ribociclib and Everolimus (RAD001) in Children With Recurrent or Refractory Malignant Brain Tumors [NCT03387020]	Phase 1	22 participants (Actual)	Interventional	2018-01-13	Completed
Clinical Outcome of de Novo Everolimus-based Immunosuppressive Therapy for Renal Transplantation Using Rituximab Induction [NCT01312064]	Phase 4	2 participants (Actual)	Interventional	2011-04-30	Terminated(stopped due to Difficulty collecting)
A Phase Ib, Multi-center, Open-label Study to Evaluate the Safety of RAD001 in Chinese Patients With Metastatic Renal Cell Cancer Who Are Intolerant of or Who Have Progressed Despite Treatment With VEGF-targeted Therapies [NCT01152801]	Phase 1	64 participants (Actual)	Interventional	2010-05-31	Completed
A Phase II Study of Everolimus and Sorafenib in Patients With Metastatic Differentiated Thyroid Cancer Who Have Progressed on Sorafenib Alone [NCT01263951]	Phase 2	35 participants (Actual)	Interventional	2010-11-30	Active, not recruiting
An Open Label, Single Arm Trial to Characterize Patients With Metastatic Renal Cell Carcinoma Treated With Everolimus After Failure of the First VEGF-targeted Therapy [NCT01266837]	Phase 4	64 participants (Actual)	Interventional	2011-03-31	Completed
A Multicenter Phase II Study to Evaluate the Clinical Activity and the Safety Profile of Everolimus (RAD001) in Marginal Zone B-cell Lymphomas (MZL) EudraCT Number 2009-011725-14 [NCT01164267]	Phase 2	30 participants (Actual)	Interventional	2010-03-31	Completed
Evaluation of Late Clinical Events After Drug-eluting Versus Bare-metal Stents in Patients at Risk: BAsel Stent Kosten Effektivitäts Trial - PROspective Validation Examination Part II (BASKET-PROVE II) [NCT01166685]	Phase 4	2,291 participants (Actual)	Interventional	2010-04-30	Completed
Pilot Study of Everolimus in the Treatment of Neoplasms in Patients With Peutz-Jeghers Syndrome [NCT01178151]	Phase 2	0 participants (Actual)	Interventional	2010-10-31	Withdrawn(stopped due to No patients)
Polyomavirus BK Nephropathy After Renal Transplantation: Randomized Clinical Trial to Demonstrate That Switching to mTOR Inhibitor is More Effective Than a Reduction of Immunosuppressive Therapy [NCT01289301]	Phase 4	124 participants (Anticipated)	Interventional	2011-10-31	Not yet recruiting
Targeted Therapy Selection Based on Tumor Tissue Kinase Activity Profiles for Patients With Advanced Solid Malignancies, an Exploratory Study [NCT01190241]		45 participants (Actual)	Interventional	2010-08-31	Terminated
Z-SEA-SIDE: Sirolimus Versus Everolimus Versus Zotarolimus-eluting Stent Assessment in Bifurcated Lesions and Clinical SIgnificance of Residual siDE-branch Stenosis [NCT01200693]	Phase 4	80 participants (Actual)	Interventional	2008-11-30	Completed
A Phase I/II Study of RAD001 Combined With CHOP in Newly Diagnosed Peripheral T-cell Lymphomas [NCT01198665]	Phase 1/Phase 2	46 participants (Actual)	Interventional	2010-07-31	Completed
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 2	27 participants (Actual)	Interventional	2014-03-19	Terminated(stopped due to Sponsor decision)
Phase I Study of the Combination of Axitinib (AX) Plus Everolimus (EV) in Patients With Malignant Advanced Solid Tumors [NCT01334073]	Phase 1	19 participants (Actual)	Interventional	2011-03-31	Completed
A Phase I Dose Escalation Study of the mTOR Inhibitor Everolimus (RAD001) and Erlotinib Concurrently With Radiation Therapy in the Re-Irradiation Setting for Head and Neck Cancer [NCT01332279]	Phase 1	0 participants (Actual)	Interventional	2011-04-30	Withdrawn(stopped due to Pharmaceutical co. withdrew support. Study was never activated and did not accrue any patients.)
CRAD001X2401: Treatment Plan for an Individual Patient With Recurrent Uterine Papillary Serous Carcinoma (UPSC) With PIK3CA Gene Mutation [NCT03285802]	Phase 2/Phase 3	1 participants (Actual)	Interventional	2017-09-07	Completed
A Six-month, Prospective, Single-center, Pilot Study Determining the Pharmacokinetics and Effectiveness of Twice-daily Tacolimus and Everolimus Regimen Convert to Once-daily Tacrolimus and Everolimus Regimen in Liver Transplant Patients [NCT03256864]	Phase 4	10 participants (Actual)	Interventional	2016-01-31	Completed
mTor-inhibitor (EVERolimus) Based Immunosuppressive Strategies for CNI Minimisation in OLD for Old Renal Transplantation [NCT01028092]	Phase 3	327 participants (Actual)	Interventional	2009-03-31	Completed
Phase I/II Trial of Everolimus in Combination With Lonafarnib in Progeria [NCT02579044]	Phase 1/Phase 2	80 participants (Anticipated)	Interventional	2015-12-31	Enrolling by invitation
Everolimus-eluting Bioresorbable Vascular Scaffold System in the Treatment of Cardiac Allograft Vasculopathy in Heart Transplant Recipients: A Prospective Multicenter Pilot Study [NCT02377648]	Phase 4	34 participants (Actual)	Interventional	2015-01-31	Completed
An Open-Label Phase I/II Safety and Efficacy Study of Itacitinib In Combination With Everolimus In Subjects With Relapsed/Refractory Classical Hodgkin Lymphoma [NCT03697408]	Phase 1/Phase 2	23 participants (Actual)	Interventional	2019-02-11	Active, not recruiting
Phase I Trial of Ribociclib in Combination With Everolimus and Dexamethasone in Children and Young Adults With Relapsed Acute Lymphoblastic Leukemia [NCT03740334]	Phase 1	45 participants (Anticipated)	Interventional	2019-01-30	Active, not recruiting
A Neoadjuvant Phase II Trial of Aromatase Inhibitors in Combination With Everolimus in Postmenopausal Women With Hormone Receptor Positive/HER2 Negative Breast Cancers With Low and Intermediate Risk (< 25) Oncotype Dx Recurrence Scores [NCT02236572]	Phase 2	17 participants (Actual)	Interventional	2014-11-29	Terminated(stopped due to Phase 2 of recruitment was contingent on 5 of 15 patients responding, which did not occur.)
DUrable Polymer-based STent CHallenge of Promus Element Versus ReSolute Integrity (DUTCH PEERS): Randomized Multicenter Trial in All Comers Population Treated Within Eastern NeThErlands-2 (TWENTE-2) [NCT01331707]	Phase 4	1,811 participants (Actual)	Interventional	2010-11-30	Completed
Biomarkers Predicting Successful Tacrolimus Withdrawal and Everolimus (Zortress) Monotherapy Early After Liver Transplantation [NCT02736227]		28 participants (Actual)	Interventional	2016-03-31	Completed
A Randomized, Double-Blind, Placebo-Controlled Phase 2 Study Comparing CB-839 in Combination With Everolimus (CBE) vs. Placebo With Everolimus (PboE) in Patients With Advanced or Metastatic Renal Cell Carcinoma (RCC) [NCT03163667]	Phase 2	69 participants (Actual)	Interventional	2017-09-06	Completed
Treatment of Neuroendocrine Tumors (NETs) With Combination of Everolimus and Radiolabeled Somatostatin Analogue [NCT03629847]	Phase 1/Phase 2	30 participants (Anticipated)	Interventional	2012-12-31	Recruiting
Clinical Evaluation of Everolimus (a Rapamycin Analog) in Restoring Salivary Gland Function to Patients Treated With Radiotherapy for Head and Neck Cancer [NCT03578432]	Early Phase 1	2 participants (Actual)	Interventional	2018-05-04	Terminated(stopped due to UACC-PHX is no longer able to support the study and Novartis is unable to provide drug beyond December 2019.)
To Evaluate Prevention Effect Of Everolimus and Low-dose Tacrolimus in Comparison With Standard-dose Tacrolimus Therapy With Mycophenolic Acid on the New Onset Diabetes Mellitus After Transplantation in the Renal Allograft Recipients [NCT02036554]	Phase 4	234 participants (Anticipated)	Interventional	2013-03-31	Recruiting
Study of ABSORB Stent in Acute Coronary Syndrome [NCT02071342]		300 participants (Anticipated)	Observational	2013-09-30	Recruiting
Everolimus in Association With Very Low-dose Tacrolimus Versus Enteric-coated Mycophenolate Sodium With Low-dose Tacrolimus in de Novo Renal Transplant Recipients - A Prospective Single Center Study [NCT02084446]	Phase 4	120 participants (Actual)	Interventional	2012-12-31	Completed
DORA: A Phase I and Randomized Phase II Study of Docetaxel and RAD001 (Everolimus) in Advanced/Recurrent or Metastatic Squamous Cell Carcinoma of the Head and Neck [NCT01313390]	Phase 1/Phase 2	4 participants (Actual)	Interventional	2009-06-30	Terminated(stopped due to Lack of recruitment)
SPIRIT III: A Clinical Evaluation of the Investigational Device XIENCE V® Everolimus Eluting Coronary Stent System (EECSS) in the Treatment of Subjects With de Novo Native Coronary Artery Lesions [NCT00180479]	Phase 3	1,002 participants (Actual)	Interventional	2005-06-30	Completed
Enzalutamide Plus Everolimus in Men With Metastatic Castrate-Resistant Prostate Cancer: A Phase I Study With a Maximum Tolerated Dose Expansion Cohort [NCT02125084]	Phase 1	38 participants (Actual)	Interventional	2014-10-31	Completed
Prospective, Randomized Trial of Belatacept Switch in Renal Transplant Recipients With Delayed Graft Function [NCT02134288]	Early Phase 1	8 participants (Actual)	Interventional	2014-04-30	Terminated(stopped due to Drug unavailability due to a manufacturing transition.)
Phase I/II Study of Induction Chemotherapy With Weekly RAD001, Carboplatin and Paclitaxel in Unresectable or Inoperable Locally Advanced Head and Neck Squamous Cell Carcinoma (HNSCC) [NCT01333085]	Phase 1/Phase 2	49 participants (Actual)	Interventional	2009-10-31	Completed
Differentiating Sirolimus and Everolimus in Combination With Calcineurin Inhibitors in Long-term Maintenance of Kidney Transplant Patients - The Effects on Vascular Endothelial and Kidney Function. The DESIRE Study. [NCT02062892]	Phase 4	0 participants (Actual)	Interventional	2013-12-31	Withdrawn(stopped due to Patients meeting the inclusion/ exclusion criteria did not agree to participate. It became obvious that recruitment goals could not be met.)
The Effect of Everolimus on the Pharmacokinetics of Tacrolimus in Renal Transplant Patients, and the Effect of ABCB1、CYP3A4、CYP3A5、PORGenetic Polymorphism on the Two Drugs [NCT02077556]	Phase 4	14 participants (Actual)	Interventional	2014-04-30	Completed
Phase I Study of Everolimus (RAD001) in Combination With Lenalidomide in Patients With Advanced Solid Malignancies Enriched for Renal Cell Carcinoma [NCT01218555]	Phase 1	44 participants (Actual)	Interventional	2010-09-09	Completed
Efficacy and Safety of Induction Strategies Combined With Low Tacrolimus Exposure in Kidney Transplant Recipients Receiving Everolimus or Sodium Mycophenolate [NCT01354301]	Phase 4	300 participants (Actual)	Interventional	2011-05-31	Completed
To Compare the Safety and Performance of MeRes100 Sirolimus Eluting BioResorbable Vascular Scaffold System Versus Contemporary DES Platforms in Patients With de Novo Coronary Artery Lesions [NCT05417893]		1,872 participants (Anticipated)	Interventional	2022-10-15	Not yet recruiting
Assessment of Vessel Healing After DES Implantation With STEMI, NSTEMI and Stable/Unstable Angina Patients: a Randomized Study Between Everolimus and Biolimus A9-eluting Stents: an Optical Coherence Tomography (OCT) and Intravascular Ultrasound Tissue Cha [NCT01065519]		64 participants (Actual)	Interventional	2009-06-30	Completed
A Phase 2 Study of Panobinostat in Combination With Everolimus for Children and Young Adults With Gliomas Harboring H3.3 or H3.1 K27M Mutation [NCT03632317]	Phase 2	0 participants (Actual)	Interventional	2019-10-31	Withdrawn(stopped due to low accrual)
A Phase Ib/II Randomized Study of BI 836845 in Combination With Exemestane and Everolimus Versus Exemestane and Everolimus Alone in Women With Locally Advanced or Metastatic Breast Cancer [NCT02123823]	Phase 1	164 participants (Actual)	Interventional	2014-05-15	Completed
RIBS IV (Restenosis Intra-stent of Drug-eluting Stents: Paclitaxel-eluting Balloon vs Everolimus-eluting Stent). A Prospective, Multicenter and Randomized Clinical Trial [NCT01239940]	Phase 4	310 participants (Anticipated)	Interventional	2010-01-31	Recruiting
Phase I Study of Carboplatin, Pegylated Liposomal Doxorubicin (PLD) and Everolimus in Patients With Platinum-Sensitive Epithelial Ovarian, Fallopian Tube or Primary Peritoneal Cancer in First Relapse [NCT01281514]	Phase 1	21 participants (Actual)	Interventional	2010-12-14	Completed
Percutaneous Treatment of LONG Native Coronary Lesions With Drug-Eluting Stent-V:Everolimus-eluting(PROMUS-ELEMENT) vs. Biolimus A9-Eluting(NOBORI) Stents [NCT01186120]	Phase 4	500 participants (Actual)	Interventional	2010-08-31	Completed
Percutaneous Treatment of LONG Native Coronary Lesions With Drug-Eluting Stent-III: Sirolimus vs. Everolimus-eluting Stent [NCT01078038]	Phase 4	451 participants (Actual)	Interventional	2008-06-30	Completed
ABSORB PHYSIOLOGY Clinical Investigation: Clinical Evaluation of the Short and Long-Term Effects of the Abbott Vascular Everolimus-Eluting Bioresorbable Vascular Scaffold on Coronary Artery Blood Flow and Physiological Responsiveness [NCT01308346]		1 participants (Actual)	Interventional	2011-11-30	Terminated(stopped due to Due to a challenging protocol inclusion/ exclusion criteria, only one subject was enrolled since the trial was initiated in June 2011.)
A Single Arm, Multicenter Phase II Study of Everolimus in Patients With Metastatic Colorectal Adenocarcinoma Whose Cancer Has Progressed Despite Prior Therapy With an Anti-EGFR Antibody (if Appropriate), Bevacizumab, Fluoropyrimidine, Oxaliplatin, and Iri [NCT00419159]	Phase 2	199 participants (Actual)	Interventional	2006-12-31	Completed
A Randomized, Double-blind Placebo-controlled, Multicenter Phase III Study in Patients With Advanced Carcinoid Tumor Receiving Octreotide Depot and Everolimus 10 mg/Day or Octreotide Depot and Placebo [NCT00412061]	Phase 3	429 participants (Actual)	Interventional	2006-12-31	Completed
A Phase I/II Trial of Fixed Doses of Daily Gefitinib With Escalating Doses of Daily RAD001 in Advanced Non-Small Cell Lung Cancer [NCT00096486]	Phase 1/Phase 2	74 participants (Actual)	Interventional	2004-05-31	Completed
A Phase I/ II, Non-randomized, Feasibility/ Safety and Efficacy Study of the Combination of Everolimus, Cetuximab and Capecitabine in Patients With Metastatic Pancreatic Cancer [NCT01077986]	Phase 1/Phase 2	35 participants (Actual)	Interventional	2009-08-31	Completed
A Phase I/II, Non-randomized, Multi-center, Dose-escalating, Two-stage Efficacy and Feasibility Study of the Combination of Everolimus and Capecitabine in Patients With Advanced Malignancies [NCT01079702]	Phase 1/Phase 2	35 participants (Anticipated)	Interventional	2008-04-30	Recruiting
Impact and Efficacy of Everolimus Rescue Immunosuppression in the Treatment of Chronic Allograft Dysfunction in Renal Transplant Recipients [NCT01046045]	Phase 4	17 participants (Actual)	Interventional	2008-04-30	Completed
A Phase I Study of Combination Anticancer Therapy of Paclitaxel and Everolimus for Relapsed or Refractory Small Cell Lung Cancer [NCT01079481]	Phase 1	21 participants (Actual)	Interventional	2009-12-31	Completed
Drug Eluting Balloon Angioplasty in Tunisian Population Versus Everolimus Platinum Chrome Stent [NCT05516446]		290 participants (Anticipated)	Interventional	2021-08-25	Recruiting
Targeting of Renal Cell Cancer With Specific Inhibitors: A Model for Selective Adaptive Medicine Based on Molecular Alterations [NCT02560012]	Phase 2	4 participants (Actual)	Interventional	2016-01-04	Terminated(stopped due to Loss of laboratory performing molecular analysis)
A Randomized, Open-Label (Formerly Double-Blind), Phase 2 Trial to Assess Safety and Efficacy of Lenvatinib at Two Different Starting Doses (18 mg vs. 14 mg QD) in Combination With Everolimus (5 mg QD) in Renal Cell Carcinoma Following One Prior VEGF-Targ [NCT03173560]	Phase 2	343 participants (Actual)	Interventional	2017-08-17	Active, not recruiting
Phase II Study of Oral PRednisone 5 mg Bid Plus EVerolimus in Patients With Metastatic Renal Cell Cancer After Failure of Vascular Endothelial Growth Factor Receptor-tyrosine Kinase Inhibitors [NCT02479490]	Phase 2	8 participants (Actual)	Interventional	2015-09-22	Terminated
A Phase 2, Open-label Study to Evaluate the Efficacy and Safety of Single-Agent MLN0128 and the Combination of MLN0128+MLN1117 Compared With Everolimus in the Treatment of Adult Patients With Advanced or Metastatic Clear-Cell Renal Cell Carcinoma That Has [NCT02724020]	Phase 2	96 participants (Actual)	Interventional	2016-06-30	Completed
P2 Efficacy Evaluation of Sabizabulin Monotherapy Versus Active Control for Treatment of ER+HER2- MBC in Patients Who Have Shown Previous Disease Progression on a Nonsteroidal Aromatase Inhibitor, Fulvestrant and CDK 4/6 Inhibitor [NCT05079360]	Phase 2	0 participants (Actual)	Interventional	2023-03-15	Withdrawn(stopped due to Decided to halt and will potentially reopen in the future.)
Autophagy Inhibition to Augment Mammilian Target of Rapamycin (mTOR) Inhibition: A Phase I/II Trial of RAD001 and Hydroxychloroquine (HCQ) in Patients With Previously Treated Renal Cell Carcinoma [NCT01510119]	Phase 1/Phase 2	40 participants (Actual)	Interventional	2011-09-30	Completed
A Randomized, Controlled, Open Label, Two Arms, Exploratory Study to Evaluate the Effect of Everolimus on Histologically Assessed Fibrosis Progression (Ishak-Knodell) in Liver Transplant Recipients With Recurrent Hepatitis C Viral Infection as Compared to [NCT00582738]	Phase 2	43 participants (Actual)	Interventional	2007-12-31	Terminated
[NCT02449538]	Phase 2	10 participants (Actual)	Interventional	2015-02-28	Completed
Clinical Evaluation of a Bioresorbable Sirolimus-eluting Coronary Scaffold in the Treatment of Patients With Denovo Coronary Artery Lesion (NeoVas): Randomized Controlled Trial [NCT02305485]		560 participants (Anticipated)	Interventional	2014-11-30	Active, not recruiting
A Multicenter, Randomized Phase ll Study of Letrozole Versus Letrozole Plus Everolimus for Hormone Receptor-PositivePremenopausal Women With Recurrent or Metastatic Breast Cancer on Goserelin Treatment After Progression on Tamoxifen [NCT02313051]	Phase 2	200 participants (Anticipated)	Interventional	2014-12-31	Not yet recruiting
A Phase II Randomized, Double-Blinded Evaluation of Oral Everolimus (RAD001) Plus Bevacizumab vs. Oral Placebo Plus Bevacizumab in the Treatment of Recurrent or Persistent Epithelial Ovarian, Fallopian Tube or Primary Peritoneal Cancer [NCT00886691]	Phase 2	150 participants (Actual)	Interventional	2010-12-27	Completed
A Phase I Study of Everolimus (mTOR Inhibitor) and OSI-906 (Dual IGFR and IR Tyrosine Kinase Inhibitor) for the Treatment of Patients With Refractory Metastatic Colorectal Cancer [NCT01154335]	Phase 1	18 participants (Actual)	Interventional	2010-07-31	Completed
A Phase 1b/2a Study Of Palbociclib In Combination With Everolimus And Exemestane In Postmenopausal Women With Estrogen Receptor Positive and HER2 Negative Metastatic Breast Cancer [NCT02871791]	Phase 1/Phase 2	41 participants (Actual)	Interventional	2016-08-24	Completed
Ovarian Suppression Plus Letrozole Plus Everolimus for Hormone Receptor-Positive, Tamoxifen and Ovarian Suppression Pretreated, Premenopausal Women With Recurrent or Metastatic Breast Cancer[LEO] [NCT02344550]	Phase 2	137 participants (Actual)	Interventional	2014-01-31	Completed
Prospective Multicenter Randomized Openlabel Study to Evaluate the Benefit on Renal Function at 12months Post-transplantation of Immunosuppressive Treatment With Withdrawal of Calcineurin Inhibitor at 3months and Combining Mycophenolate Sodium-Everolimus [NCT02334488]	Phase 3	329 participants (Actual)	Interventional	2014-12-11	Completed
Phase I/II Study of Weekly Abraxane and RAD001 in Women With Locally Advanced or Metastatic Breast Cancer. A Study of the Cancer Institute of New Jersey Oncology Group (CINJOG) [NCT00934895]	Phase 1/Phase 2	27 participants (Actual)	Interventional	2009-07-15	Terminated(stopped due to Closed early due to slow accrual)
Phase II Single Arm Trial With Combination of Everolimus and Letrozole in Treatment of Platinum Resistant Relapse or Refractory or Persistent Ovarian Cancer/Endometrial Cancer (CRAD001CUS242T) [NCT02188550]	Phase 2	20 participants (Anticipated)	Interventional	2014-06-30	Recruiting
Molecular Determinants for Therapy Response on Renal Cell Carcinoma [NCT02208128]		4 participants (Anticipated)	Interventional	2014-05-31	Recruiting
Drug-Eluting Balloon Versus Drug-eluting Stent On de Novo coRonary Artery Disease in Patients With High Bleeding Risk [NCT04885816]		5 participants (Actual)	Interventional	2021-04-20	Terminated(stopped due to Slow recruitment)
CERTICOEUR a Secondary Prevention Study of Skin Cancers in Heart Transplant Patients. An Open Labelled Randomized Everolimus vs Calcineurin Inhibitors Multicenter Trial [NCT00799188]	Phase 3	175 participants (Actual)	Interventional	2008-10-31	Active, not recruiting
A Phase II, Open-Label, Randomized Study of GDC-0980 Versus Everolimus in Patients With Metastatic Renal Cell Carcinoma Who Have Progressed on or Following VEGF-Targeted Therapy [NCT01442090]	Phase 2	85 participants (Actual)	Interventional	2011-10-31	Completed
Phase I Study of Pasireotide (SOM230) in Combination With RAD001 in Patients With Advanced Neuroendocrine Tumors [NCT00804336]	Phase 1	22 participants (Actual)	Interventional	2008-10-31	Completed
Safety and Tolerability of Everolimus as Second-line Treatment in Poorly Differentiated Neuroendocrine Carcinoma / Neuroendocrine Carcinoma G3 (WHO 2010) and Neuroendocrine Tumor G3 - an Investigator Initiated Phase II Study [NCT02113800]	Phase 2	40 participants (Actual)	Interventional	2015-08-31	Completed
Phase I/II Trial of Concurrent RAD001 (Everolimus) With Temozolomide/Radiation Followed by Adjuvant RAD001/Temozolomide in Newly Diagnosed Glioblastoma [NCT01062399]	Phase 1/Phase 2	279 participants (Actual)	Interventional	2010-12-31	Completed
Pet Imaging as a Biomarker of Everolimus Added Value in Hormone Refractory postmenopausaL Women [NCT02028364]	Phase 2	55 participants (Actual)	Interventional	2014-01-12	Completed
A Single Arm, Phase Ib Study of RAD001 and Sunitinib in Patients With Advanced Renal Cell Carcinoma [NCT00788060]	Phase 1	5 participants (Actual)	Interventional	2008-10-31	Completed
Activity and Safety of Everolimus in Combination With Octreotide LAR and Metformin in Patients With Advanced Pancreatic Well-differentiated Neuroendocrine Tumors (pWDNETs): a Phase II, Open, Monocentric, Prospective Study [NCT02294006]	Phase 2	26 participants (Actual)	Interventional	2014-06-30	Active, not recruiting
Phase I Combination of Pazopanib and Everolimus in PI3KCA Mutation Positive/PTEN Loss Patients With Advanced Solid Tumors Refractory to Standard Therapy [NCT01430572]	Phase 1	62 participants (Actual)	Interventional	2011-10-07	Completed
Intracoronary Analysis of Cardiac Allograft Vasculopathy in Comparison to Coronary Artery Disease by Means of Optical Coherence Tomography [NCT02254668]	Phase 4	278 participants (Anticipated)	Interventional	2013-12-31	Recruiting
N-of-1 Trial of Actionable Target Identification in Metastatic Cancer for Palliative Systemic Therapy [NCT02142036]	Phase 2	50 participants (Actual)	Interventional	2014-05-31	Completed
Treatment of Canadian Men and Pre/Postmenopausal Women With ER+ Advanced Breast Cancer in the Real-World Setting With Hormone Therapy ± Targeted Therapy [NCT02753686]		440 participants (Actual)	Observational [Patient Registry]	2016-03-15	Completed
BIOTRONIK-Safety and Clinical Performance of the Drug Eluting Resorbable Coronary MAGnesium Scaffold System (DREAMS 3G) in the Treatment of Subjects With de Novo Lesions in Native Coronary Arteries: BIOMAG-II: A Randomized Controlled Trial [NCT05540223]		1,859 participants (Anticipated)	Interventional	2024-04-30	Not yet recruiting
Biomarker and Tumor Cell Culture-Driven Pilot Trial for Treatment of Recurrent Glioblastoma [NCT05432518]	Early Phase 1	10 participants (Anticipated)	Interventional	2023-06-27	Recruiting
Aflac LL1602 ENCERT: A Phase 1 Trial Using Everolimus in Combination With Nelarabine, Cyclophosphamide and Etoposide in Relapsed T Cell Lymphoblastic Leukemia/Lymphoma [NCT03328104]	Phase 1	8 participants (Actual)	Interventional	2018-07-24	Completed
Everolimus (Afinitor) in Patients With Metastatic Renal Cell Carcinoma Following Progression on Prior Bevacizumab Treatment [NCT02056587]	Phase 4	37 participants (Actual)	Interventional	2011-11-30	Completed
Multi-center, Single Arm, Open-label, Phase 4 STudy to Evaluate the Efficacy and Safety of CertiroBELL® Tablet Plus TAcrolimus in Primary Living Donor Liver Transplant Recipients [NCT04867720]	Phase 4	112 participants (Anticipated)	Interventional	2021-03-16	Recruiting
A Randomized, Open-Label, Phase 3 Study of Nivolumab (BMS-936558) vs. Everolimus in Subjects With Advanced or Metastatic Clear-Cell Renal Cell Carcinoma Who Have Received Prior Anti-Angiogenic Therapy [NCT01668784]	Phase 3	821 participants (Actual)	Interventional	2012-10-09	Completed
PhaseII Study of Ribociclib and Everolimus Following Radiotherapy in Pediatric and Young Adult Patients Newly Diagnosed With HGG Including DIPG, Which Harbor Alterations of the Cell Cycle and/or PI3K/mTOR Pathways [NCT05843253]	Phase 2	100 participants (Anticipated)	Interventional	2024-01-15	Not yet recruiting
Serial Measurements of Molecular and Architectural Responses to Therapy (SMMART) Trial: PRIME [NCT03878524]	Phase 1	2 participants (Actual)	Interventional	2020-04-01	Active, not recruiting
A 12 Month, Multicenter, Randomized, Parallel, Open-label Study, to Evaluate Renal Function and Efficacy of Everolimus With Basiliximab and Cyclosporine Microemulsion Discontinuation at 3 Month Post-transplant Versus Minimization, in de Novo Kidney Transp [NCT00154284]	Phase 3	114 participants (Actual)	Interventional	2005-07-31	Completed
A Phase I-II Trial of Everolimus and Sorafenib in Patients With Recurrent High-Grade Gliomas [NCT01434602]	Phase 1/Phase 2	86 participants (Actual)	Interventional	2012-10-02	Completed
A Prospective, Randomized, Double-blind, Placebo-Controlled Phase Ⅱ Study to Evaluate the Efficacy of Adjunctive Everolimus Treatment in Patients With Refractory Epilepsy [NCT05613166]	Phase 2	108 participants (Anticipated)	Interventional	2022-11-30	Recruiting
A Prospective, Active Control Open Label, Multicentre Randomized Clinical Trial for Comparison Between BioMime Sirolimus Eluting Stent of Meril Life Sciences and Xience Everolimus Eluting Stent of Abbott Vascular Inc. to Evaluate Efficacy and Safety in Co [NCT02112981]		256 participants (Actual)	Interventional	2014-11-05	Active, not recruiting
Evaluation of Acute Rejection Rates in de Novo Renal Transplant Recipients Following Thymoglobulin Induction, CNI-free, Nulojix (Belatacept)-Based Immunosuppression [NCT02137239]	Phase 2	58 participants (Actual)	Interventional	2015-12-31	Completed
An Open-labelled Multicenter Randomized Study on the Efficacy of Everolimus in Reducing Total Native Kidney Volume in Kidney Transplanted Patients With Autosomal Dominant Polycystic Kidney Disease [NCT02134899]	Phase 3	3 participants (Actual)	Interventional	2014-10-14	Completed
Phase 1 Study of Everolimus in Combination With Brentuximab Vedotin in Patients With Relapsed or Refractory Hodgkin Lymphoma [NCT02254239]	Phase 1	10 participants (Actual)	Interventional	2016-02-04	Terminated(stopped due to funding withdrawal)
Phase I/II Trial With Sorafenib in Combination With RAD001 Administered Orally in Patients With Advanced Solid Tumors, Selected on the Base of Molecular Targets [NCT01226056]	Phase 1/Phase 2	45 participants (Anticipated)	Interventional	2009-03-31	Suspended(stopped due to toxicity (protocol amendment under approval))
Multi-center, Open-label, Prospective, Randomized, Parallel Group Study Investigating a CNI-free Regimen With Enteric-Coated Mycophenolate Sodium (EC-MPS) and Everolimus in Comparison to Standard Therapy With Enteric-Coated Mycophenolate Sodium (EC-MPS) a [NCT00154310]	Phase 4	300 participants (Actual)	Interventional	2005-06-30	Completed
A Single Arm, Multicenter, Phase II Trial of RAD001 as Monotherapy in the Palliative Treatment of Patients With Locally Advanced or Metastatic Transitional Cell Carcinoma After Failure of Platinum-based Chemotherapy [NCT00714025]	Phase 2	40 participants (Actual)	Interventional	2008-11-30	Completed
A Phase I Study of TS-1, Cisplatin & RAD001 (Everolimus) [NCT01096199]	Phase 1	35 participants	Interventional		Terminated
[NCT02616848]	Phase 1	1 participants (Anticipated)	Interventional	2015-11-30	Recruiting
A Prospective Multicenter Post Market Trial to Assess the Safety and Effectiveness of the Firehawk™ Rapamycin Target Eluting Cobalt Chromium Coronary Stent System (Firehawk™ Stent System) for the Treatment of Atherosclerotic Lesion(s) [NCT02520180]		1,653 participants (Actual)	Interventional	2015-12-31	Completed
A Phase II Study to Investigate the Efficacy of RAD001 (Afinitor®, Everolimus) in Patients With Irresectable Recurrent or Metastatic Differentiated, Undifferentiated (Anaplastic) and Medullary Thyroid Carcinoma [NCT01118065]	Phase 2	42 participants (Anticipated)	Interventional	2010-05-31	Recruiting
Phase I Study of mTOR Inhibitor RAD001 in Combination With IGF-1R Inhibitor AMG479 for Patients With Advanced Solid Tumors [NCT01122199]	Phase 1	27 participants (Actual)	Interventional	2010-05-14	Completed
A Phase II Study of Lenvatinib in Combination With Everolimus in Patients With Advanced Carcinoid Tumors [NCT03950609]	Phase 2	36 participants (Actual)	Interventional	2019-07-30	Active, not recruiting
EMBER: A Phase 1a/1b Study of LY3484356 Administered as Monotherapy and in Combination With Anticancer Therapies for Patients With ER+ Locally Advanced or Metastatic Breast Cancer and Other Select Non-Breast Cancers [NCT04188548]	Phase 1	500 participants (Anticipated)	Interventional	2019-12-10	Active, not recruiting
Optical Coherence Tomography Assessment of Intimal Tissue and Malapposition: A Randomized Comparison of the Biolimus A9-eluting and Everolimus-eluting Coronary Stents [NCT01137019]	Phase 3	80 participants (Anticipated)	Interventional	2010-10-31	Active, not recruiting
An Angiogenic Study in Patients With Well/Moderately Differentiated Metastatic Pancreatic Neuroendocrine Tumors Treated With Everolimus [NCT02305810]	Phase 2	54 participants (Actual)	Interventional	2013-09-30	Completed
A 12 Month, Single-center, Open-label, Randomized-controlled Trial to Investigate Efficacy, Safety and Tolerability of Everolimus in Combination With Cyclosporine A and Corticosteroid in de Novo Transplant Recipients of Expanded Criteria Donor Kidneys or [NCT02314312]	Phase 3	48 participants (Anticipated)	Interventional	2012-01-31	Active, not recruiting
Managed Access Program (MAP) Cohort Treatment Plan CRAD001Y2002M to Provide Access to Afinitor for Patients With Advanced Hormone Receptor Positive (HR+) Breast Cancer [NCT05108740]		0 participants	Expanded Access		No longer available
Phase IV, Single Arm Study of Safety and Efficacy of Everolimus in Chinese Adults With Tuberous Sclerosis Complex Who Have Renal Angiomyolipoma Not Requiring Immediate Surgery [NCT03525834]	Phase 4	40 participants (Actual)	Interventional	2018-11-09	Completed
Clinical Trial Program of a Medical Instrument Product [NCT01157455]	Phase 4	1,900 participants (Anticipated)	Interventional	2010-05-31	Recruiting
Comparison of Biolimus-eluting Biodegradable Polymer, Everolimus-eluting and Sirolimus-eluting Coronary Stents [NCT01268371]	Phase 4	1,462 participants (Anticipated)	Interventional	2010-12-31	Active, not recruiting
An Open Label, Time-To-Event Continuous Reassessment Method, Phase I/II Study of the Mammalian Target of Rapamycin (mTOR) Inhibitor RAD001 in Combination With Imatinib (Gleevec) in Patients With Chronic Phase Chronic Myeloid Leukemia (CML) With Persistent [NCT01188889]	Phase 1/Phase 2	0 participants (Actual)	Interventional	2013-09-30	Withdrawn(stopped due to Unable to obtain sufficient funding.)
A Pilot Study of Neo-Adjuvant Everolimus in Patients With Advanced Renal Cell Carcinoma Undergoing Definitive Therapy With Radical Nephrectomy, or Cytoreductive Nephrectomy - Analysis of Serum and Tissue Biomarkers [NCT01107509]		20 participants (Actual)	Interventional	2010-10-01	Completed
Precision Platform Study of HR+/ HER2-advanced Breast Cancer Based on SNF Typing (A Prospective, Open-label, Multi-center, Phase II Platform Study) [NCT05594095]	Phase 2	140 participants (Anticipated)	Interventional	2022-12-30	Recruiting
A Single Arm, Multicenter Single Stage Phase II Trial of RAD001 as Monotherapy in the Treatment of Metastatic Non Syndromic Neuro-endocrine Tumors [NCT00688623]	Phase 2	73 participants (Actual)	Interventional	2009-06-24	Completed
A Single-center,Randomized,Open-label,12 Months Study,2 Parallel Group to Compare the Efficacy of Everolimus Combination + Tacrolimus in Regression of Left Ventricular Hypertrophy vs Tacrolimus + MMF in Renal Transplant Patients [NCT03415750]	Phase 4	20 participants (Actual)	Interventional	2016-11-30	Completed
RIBS V (Restenosis Intra-stent of Bare Metal Stents: Paclitaxel-eluting Balloon vs Everolimus-eluting Stent). A Prospective, Multicenter and Randomized Clinical Trial [NCT01239953]	Phase 4	190 participants (Actual)	Interventional	2010-01-31	Active, not recruiting
Alterations in Cognitive Function and Cerebral Blood Flow After Conversion From Calcineurin Inhibitors to Everolimus [NCT03413722]		30 participants (Anticipated)	Observational	2018-02-01	Recruiting
Phase II Study of RAD001monotherapy in Patients With Unresectable Pheochromocytoma or Extra-adrenal Paraganglioma or Non-functioning Carcinoid [NCT01152827]	Phase 2	33 participants (Actual)	Interventional	2008-07-31	Completed
An Open-label Phase I Study Evaluating the Safety and Tolerability of Pasireotide LAR in Combination With Everolimus in Advanced Metastatic NETs - The COOPERATE-1 Study [NCT01263353]	Phase 1	36 participants (Actual)	Interventional	2010-11-30	Completed
Phase II Trial of Lapatinib and RAD-001 for HER2 Positive Metastatic Breast Cancer [NCT01283789]	Phase 2	23 participants (Actual)	Interventional	2011-02-28	Active, not recruiting
A Phase II Study With Tumor Molecular Pharmacodynamic (MPD) Evaluation of Oral mTOR-inhibitor Everolimus (RAD001) 10 mg Daily in Patients Suffering From Classic or Endemic Kaposi's Sarcoma [NCT01412515]	Phase 2	11 participants (Actual)	Interventional	2008-06-30	Terminated(stopped due to results from interim analysis conducted to study interruption)
An Open, Single Centre, Randomised, Parallel Group Study to Investigate Three Different Immunosuppressive Regimens for de Novo Renal Transplant Recipients: A Comparison of a Sirolimus / EC-MPS (Myfortic) / Tacrolimus Regimen, an Everolimus / EC-MPS / Tacr [NCT01183247]	Phase 4	63 participants (Actual)	Interventional	2008-07-31	Completed
A Phase IIIb, Multi-center, Open-label Study of RAD001 in Combination With EXemestane in Post-menopausal Women With EStrogen Receptor Positive, Human Epidermal Growth Factor Receptor 2 Negative Locally Advanced or Metastatic Breast Cancer [NCT03176238]	Phase 3	235 participants (Actual)	Interventional	2013-03-29	Completed
Safety and Feasibility of Bioabsorbable Everolimus-Eluting Stents for Patients With Internal Pudendal Artery-Related Arteriogenic Erectile Dysfunction (PERFECT-ABSORB) [NCT02492386]	Phase 2/Phase 3	15 participants (Anticipated)	Interventional	2015-07-31	Not yet recruiting
A Phase I and Feasibility Study of Everolimus (RAD001) Plus R-CHOP for New Untreated Diffuse Large B-Cell Lymphoma (DLBCL) [NCT01334502]	Phase 1	26 participants (Actual)	Interventional	2012-03-31	Completed
A Phase I/II Study Investigating the Combination of RAD001 and Rituximab in Patients With Non-Hodgkin's Lymphomas [NCT01567475]	Phase 1	21 participants (Actual)	Interventional	2011-12-31	Completed
89Zr-bevacizumab PET Imaging as Predictive Biomarker for Everolimus Efficacy in Patients With Neuroendocrine Tumors [NCT01338090]		14 participants (Actual)	Observational	2010-04-30	Completed
A Safety and Tolerability Study of RAD001 (mTOR Inhibitor) in Combination With Two Dosing Schedules of LBH589B (Histone Deacetylase Inhibitor) in Solid Tumors/ Lymphomas With Enrichment for EBV-Driven Tumors [NCT01341834]	Phase 1	49 participants (Actual)	Interventional	2010-03-31	Active, not recruiting
A Phase 1 Dose Escalation and Expansion Study of AZD9833 Alone or in Combination With Palbociclib or Everolimus in Chinese Patients With Oestrogen Receptor Positive (ER+), Human Epidermal Growth Factor Receptor 2 Negative (HER2-) Metastatic Breast Cancer [NCT04818632]	Phase 1	28 participants (Actual)	Interventional	2021-11-12	Completed
The Rome Trial From Histology to Target: the Road to Personalize Target Therapy and Immunotherapy [NCT04591431]	Phase 2	400 participants (Actual)	Interventional	2020-10-07	Active, not recruiting
An Open-Label, Single-Arm, Phase II Study of RAD001 in Patients With Mantle Cell Lymphoma Who Are Refractory or Intolerant to Velcade® (Bortezomib) [NCT00702052]	Phase 2	58 participants (Actual)	Interventional	2008-08-22	Completed
Prospective Randomized Trial of Everolimus- and Zotarolimus-eluting Stents for Treatment of Unprotected Left Main Coronary Artery Disease: ISAR-LEFT-MAIN-2 [NCT00598637]	Phase 4	650 participants (Actual)	Interventional	2007-12-31	Completed
A Randomized Phase III, Double-blind, Placebo-controlled, Multi-center Study to Evaluate the Efficacy and Safety of Everolimus (RAD001) in Adult Patients With Advanced Hepatocellular Carcinoma After Failure of Sorafenib Treatment - The EVOLVE-1 Study [NCT01035229]	Phase 3	546 participants (Actual)	Interventional	2010-04-30	Completed
A Phase II Study of RAD001 (Everolimus) and Pasireotide (SOM230) LAR in Patients With Advanced Uveal Melanoma [NCT01252251]	Phase 2	14 participants (Actual)	Interventional	2010-11-30	Completed
A Phase I/IIB Study of Combination Weekly Carboplatin, Cetuximab and Dose Escalation of RAD001 in Recurrent Metastatic Squamous Cell Carcinoma of the Head and Neck (SCCHN) [NCT01283334]	Phase 1/Phase 2	20 participants (Actual)	Interventional	2011-01-31	Completed
A Phase Ib/II Study of Cisplatin, Paclitaxel, and RAD001 in Patients With Metastatic Breast Cancer [NCT01031446]	Phase 1/Phase 2	55 participants (Actual)	Interventional	2009-10-31	Completed
NET RETREAT: A Phase II Study of 177 Lutetium-DOTATATE Retreatment vs. Everolimus in Metastatic/Unresectable Midgut NET [NCT05773274]	Phase 2	100 participants (Anticipated)	Interventional	2024-03-01	Recruiting
Phase II Open Label Study of RAD001 (Everolimus) in Combination With Letrozole in the Treatment of Postmenopausal Women With Locally Advanced or Metastatic, Estrogen Receptor Positive Breast Cancer, After Failure of Tamoxifen and/or Anastrozole and/or Let [NCT01231659]	Phase 2	72 participants (Actual)	Interventional	2011-08-09	Completed
A Randomized Phase III, Double-blind, Placebo-controlled Multicenter Trial of Daily Everolimus in Combination With Trastuzumab and Vinorelbine, in Pretreated Women With HER2/Neu Over-expressing Locally Advanced or Metastatic Breast Cancer. [NCT01007942]	Phase 3	569 participants (Actual)	Interventional	2009-10-31	Completed
Early vs. Delayed EVERolimus in de Novo HEART Transplant Recipients: Optimization of the Safety/Efficacy Profile (EVERHEART Study) [NCT01017029]	Phase 4	182 participants (Actual)	Interventional	2009-09-30	Completed
MEGALiT - a Multicenter, Basket and Umbrella Explorative Trial on the Efficacy and Safety of Molecular Profile Selected Commercially Available Targeted Anti-cancer Drugs in Patients With Advanced Cancers Progressive on Standard Therapy [NCT04185831]	Phase 2	154 participants (Anticipated)	Interventional	2020-10-20	Recruiting
Once-a-day Regimen or Steroid Withdrawal in de Novo Kidney Transplant Recipients Treated With Everolimus, Cyclosporine and Steroids: a 12-month, Prospective, Randomized, Multicenter, Open-label Study. The EVIDENCE Study (EVerolImus Once-a-Day rEgimen With [NCT01023815]	Phase 3	330 participants (Actual)	Interventional	2009-04-30	Completed
A Single Arm, Multicenter Phase II Trial of RAD001 as Monotherapy in the Treatment of Advanced Papillary Renal Cell Cancer [NCT00688753]	Phase 2	92 participants (Actual)	Interventional	2009-07-31	Completed
A Dose-Escalation Study to Evaluate the Safety and Tolerability of SCH 717454 in Combination With Different Treatment Regimens in Subjects With Advanced Solid Tumors (Phase 1B/2; Protocol No. P04722) [NCT00954512]	Phase 1/Phase 2	15 participants (Actual)	Interventional	2009-09-25	Terminated(stopped due to This study was terminated for business reasons.)
Phase II Study of RAD001 and Bevacizumab in Recurrent Ovarian, Peritoneal, and Fallopian Tube Cancer An Investigator-initiated, Single-institution Trial at Magee-Womens Hospital [NCT01031381]	Phase 2	50 participants (Actual)	Interventional	2010-09-30	Completed
Phase II Clinical Trial of the Combination of RAD001 and Erlotinib in Patients With Recurrent Squamous Cell Carcinoma of the Head and Neck [NCT00942734]	Phase 2	49 participants (Actual)	Interventional	2009-07-31	Completed
A Phase II Study of Everolimus (RAD001) for Children With Chemotherapy and/or Radiation-Refractory Progressive or Recurrent Low-Grade Gliomas [NCT00782626]	Phase 2	23 participants (Actual)	Interventional	2009-06-30	Completed
Efficiency of Everolimus for the Treatment of Kidney Transplanted Patients Presenting a Missing Self-induced Natural Killer Cells Mediated (NK-mediated) Rejection [NCT03955172]		20 participants (Anticipated)	Interventional	2020-12-03	Recruiting
Phase I/II Study of RAD001 in Patients With Relapsed or Refractory Acute Myeloid Leukemia, Acute Lymphocytic Leukemia, Chronic Myeloid Leukemia in Blastic-Phase, Agnogenic Myeloid Metaplasia, Chronic Lymphocytic Leukemia, T-Cell Leukemia, or Mantle Cell L [NCT00081874]	Phase 1/Phase 2	29 participants (Actual)	Interventional	2004-04-30	Completed
A Randomized Controlled, Open Labeled, Two Arm, Study of Addition of Everolimus to Standard of Care in Carcinoma Gallbladder [NCT05833815]	Phase 2/Phase 3	56 participants (Anticipated)	Interventional	2022-11-01	Recruiting
A Randomized Double-Blind, Placebo-Controlled Study of Everolimus in Combination With Exemestane in the Treatment of Postmenopausal Women With Estrogen Receptor Positive Locally Advanced or Metastatic Breast Cancer Who Are Refractory to Letrozole or Anast [NCT00863655]	Phase 3	724 participants (Actual)	Interventional	2009-06-03	Completed
Comparison of the Efficacy of Everolimus-Eluting Versus Sirolimus-Eluting Stent for Coronary Lesions [NCT00698607]	Phase 4	1,466 participants (Anticipated)	Interventional	2008-06-30	Active, not recruiting
Phase 1b Study of ARN 509 Plus Everolimus in Men With Progressive Metastatic Castration-Resistant Prostate Cancer After Treatment With Abiraterone Acetate [NCT02106507]	Phase 1	9 participants (Actual)	Interventional	2014-04-30	Completed
A Single-armed, Open-labeled and Single-centered Phase II Trial of Everolimus in Selected Patients With Metastatic Melanoma: Efficacy and Safety Study [NCT01960829]	Phase 2	60 participants (Anticipated)	Interventional	2013-09-30	Recruiting
Dried Blood SPOT Analysis of Everolimus in Cancer Patients [NCT02809404]		75 participants (Actual)	Observational	2015-06-30	Completed
Phase II Multicenter Study Evaluating the Tolerability and Efficacy of RAD001 (Everolimus) in Patients With Relapsed or Metastatic Endometrial Cancer [NCT00870337]	Phase 2	44 participants (Actual)	Interventional	2008-03-31	Completed
A Randomized, Open-label Phase II Trial Comparing Durable Overall Response Rate at 56 Days in Patients With Steroid-resistant Severe Acute GvHD After Allogeneic HSCT Treated With Decidual Stromal Cells or Best Available Treatment [NCT05132166]	Phase 2	50 participants (Anticipated)	Interventional	2021-12-22	Active, not recruiting
Randomized Phase II Trial of Lutetium Lu 177 Dotatate Versus Everolimus in Somatostatin Receptor Positive Bronchial Neuroendocrine Tumors [NCT04665739]	Phase 2	108 participants (Anticipated)	Interventional	2023-02-03	Recruiting
A Phase I Study of Temozolomide and RAD001C in Patients With Malignant Glioblastoma Multiforme [NCT00387400]	Phase 1	32 participants (Actual)	Interventional	2007-03-20	Completed
A Randomized Phase II Study of Two Different Schedules of RAD001C in Patients With Recurrent/Metastatic Breast Cancer [NCT00255788]	Phase 2	49 participants (Actual)	Interventional	2005-05-10	Completed
Bioresorbable Vascular Scaffold in Patient With ST Elevation Myocardial Infarction: a Randomized Comparison With Everolimus Eluting Stent [NCT02151929]	Phase 4	100 participants (Actual)	Interventional	2013-05-31	Completed
A National Multicentre Randomized Study Comparing the Early Versus Delayed Administration of Everolimus in de Novo Kidney Transplant Recipients at Risk of Delayed Graft Function [NCT00154297]	Phase 4	139 participants (Actual)	Interventional	2005-06-30	Completed
Combination Treatment With Everolimus, Letrozole and Trastuzumab in Hormone Receptor and HER2/Neu-Positive Patients With Advanced Metastatic Breast Cancer and Other Solid Tumors: Evaluating Synergy and Overcoming Resistance [NCT02152943]	Phase 1	37 participants (Actual)	Interventional	2014-07-17	Completed
Phase II Study of Everolimus (RAD001) in Metastatic Transitional Cell Carcinoma of the Urothelium [NCT00805129]	Phase 2	46 participants (Actual)	Interventional	2008-12-05	Completed
Comprehensive Imaging and Interventional Therapy Studies for Arteriogenic Erectile Dysfunction and Lower Urinary Tract Symptoms: A Multi-modality, Multi-Specialty Collaborative Study (PERFECT Program) [NCT02178761]		300 participants (Anticipated)	Interventional	2012-10-31	Recruiting
Multi-center, Open-label, Randomized Controlled Phase 4 Study to Evaluate the Efficacy and Safety of CertiroBell® Compared With Mycophenolate Mofetil in Primary Living Donor Liver Transplant Recipients. [NCT04471441]	Phase 4	150 participants (Anticipated)	Interventional	2020-06-30	Recruiting
An Open-label, Randomized Phase 3 Study of MK-6482 Versus Everolimus in Participants With Advanced Renal Cell Carcinoma That Has Progressed After Prior PD-1/L1 and VEGF-Targeted Therapies [NCT04195750]	Phase 3	736 participants (Anticipated)	Interventional	2020-02-27	Active, not recruiting
MAINtenance Afinitor: A Randomized Trial Comparing Maintenance Aromatase Inhibitors (AIs) + Everolimus (Afinitor) vs AIs in Hormone Receptor Positive (HR+) Metastatic Breast Cancer Patients With Disease Control After First Line Chemotherapy [NCT02511639]	Phase 3	110 participants (Actual)	Interventional	2014-07-30	Completed
Effects of Everolimus in Left Ventricular Hypertrophy After Conversion From Azathioprine: A Pilot Study [NCT02493465]	Phase 4	50 participants (Anticipated)	Interventional	2015-07-31	Recruiting
6-month, Open-label, Randomized, Multicenter, Prospective, Controlled Study to Evaluate the Efficacy, Safety and Tolerability of Everolimus in de Novo Renal Transplant Recipients Participating in the Eurotransplant Senior Program [NCT00956293]	Phase 4	207 participants (Actual)	Interventional	2009-07-31	Terminated(stopped due to The study was terminated because the required sample size of 240-260 de novo senior renal transplant patients was not achieved within a reasonable time.)
Protection of Renal Function After Liver Transplant Using Everolimus Monotherapy as the Immunosuppression Regimen [NCT04063865]	Phase 3	14 participants (Actual)	Interventional	2019-05-09	Terminated(stopped due to Study was larger than expected and became a burden to faculty and staff resources.)
Comparison of Titanium-Nitride-Oxide Coated Bio-Active-Stent (Optimax™) to the Drug (Everolimus) -Eluting Stent (Synergy™) in Acute Coronary Syndrome [NCT02049229]	Phase 4	1,800 participants (Anticipated)	Interventional	2014-01-31	Recruiting
Sequential Two-agent Assessment in Renal Cell Carcinoma Therapy: The START Trial [NCT01217931]	Phase 2	180 participants (Actual)	Interventional	2011-01-19	Active, not recruiting
A Phase Ib Dose-finding Study of BYL719 Plus Everolimus and BYL719 Plus Everolimus Plus Exemestane in Patients With Advanced Solid Tumors, With Dose-expansion Cohorts in Renal Cell Cancer (RCC), Pancreatic Neuroendocrine Tumors (pNETs), and Advanced Breas [NCT02077933]	Phase 1	79 participants (Actual)	Interventional	2014-05-14	Completed
Combination of Everolimus and 177Lu-DOTATATE in the Treatment of Grades 2 and 3 Refractory Meningioma: a Phase IIb Clinical Trial [NCT06126588]	Phase 2	28 participants (Anticipated)	Interventional	2024-03-01	Not yet recruiting
AN OBSERVATIONAL REAL-WORLD STUDY OF THE SYSTEMIC TREATMENT OF WELL-DIFFERENTIATED, UNRESECTABLE OR METASTATIC, PROGRESSIVE PANCREATIC NEUROENDOCRINE TUMOURS (PNET): A STUDY OF MORBIDITY AND MORTALITY AT 2 YEARS [NCT02264665]		144 participants (Actual)	Observational	2015-05-12	Completed
XIENCE V® Everolimus Eluting Coronary Stent System USA Post- Approval Study (XIENCE V® USA DAPT Cohort) (XVU-AV DAPT) [NCT01106534]	Phase 4	870 participants (Actual)	Interventional	2009-08-31	Completed
MicroRNA Expression in Everolimus-based Versus Tacrolimus-based Maintenance Immunosuppressive Regimens in Kidney Transplantation [NCT02091973]		50 participants (Anticipated)	Interventional	2010-06-30	Recruiting
Randomized Clinical Comparison of Everolimus-Eluting SYNERGY® and Biolimus-Eluting BioMatrix NeoFlex® Coronary Stents in Non-Selected Patients With Ischemic Heart Disease [NCT02093845]		2,800 participants (Actual)	Interventional	2014-02-10	Active, not recruiting
Phosphatidylinositol 3-kinase (PI3K) Pathway Analysis in Tumor Tissue and Circulating DNA to Obtain Further Insight in the Efficacy of Everolimus When Combined With Exemestane: A Side-study Protocol Attached to Standard Treatment With Everolimus and Exeme [NCT02109913]		175 participants (Anticipated)	Interventional	2014-03-31	Active, not recruiting
A Phase I Study of LDE225 in Combination With Everolimus in Patients With Advanced Gastroesophageal Adenocarcinoma [NCT02138929]	Phase 1	25 participants (Actual)	Interventional	2014-11-10	Completed
Phase I Study of the Pan-ERBB Inhibitor Neratinib Given in Combination With Everolimus, Palbociclib, or Trametinib in Advanced Cancer Subjects With EGFR Mutation/Amplification, HER2 Mutation/Amplification, or HER3/4 Mutation or KRAS Mutation [NCT03065387]	Phase 1	93 participants (Actual)	Interventional	2017-10-31	Active, not recruiting
Phase 1 Study of Lenvatinib in Combination With Everolimus in Subjects With Unresectable Advanced or Metastatic RCC [NCT02454478]	Phase 1	7 participants (Actual)	Interventional	2015-07-01	Completed
Etiology of the Platelet-Cancer Metastatic Pathway - A Study of Inflammatory Markers, Platelet Characteristics and Metastatic Surrogates in Cancer Patients and Controls [NCT02450175]		50 participants (Anticipated)	Interventional	2014-06-30	Recruiting
Comparison of Safety and Efficacy of de Novo Everolimus Plus Low Dose of Cyclosporine With Standard Dose of Cyclosporine Plus Cellcept on CMV and BK Virus Infections Prevention in Renal Transplant Patients [NCT04906304]		35 participants (Actual)	Interventional	2020-01-01	Completed
Prospective, Multicenter, Randomized, Open-label, Phase 2, Lasting 12 Weeks, Evaluating the Pharmacodynamics, Efficacy and Safety of Basiliximab in de Novo Adult Renal Transplant Patients at Low Risk Receiving Either a Cumulative Dose of Basiliximab of 40 [NCT01596062]	Phase 2	16 participants (Actual)	Interventional	2012-03-31	Completed
Treg Adoptive Therapy in Subclinical Inflammation in Kidney Transplantation (CTOT-21) [NCT02711826]	Phase 1/Phase 2	14 participants (Anticipated)	Interventional	2016-09-20	Completed
Phase II Study of RAD001 Plus Octreotide Depot in Patients With Metastatic or Unresectable Low Grade Neuroendocrine Carcinoma (Carcinoid, Islet Cell) [NCT00113360]	Phase 2	67 participants (Actual)	Interventional	2005-01-31	Completed
A Phase II Study of RAD001 in Patients With Recurrent Endometrial Cancer [NCT00087685]	Phase 2	35 participants (Actual)	Interventional	2004-06-30	Completed
A Prospective, Open Label, Multi-center Trial of Firehawk™ Coronary Stent System in the Treatment of Coronary Chronic Total Occlusion Lesion(s) by Optical Coherent Tomography (OCT) and Coronary Angiography [NCT03040934]		196 participants (Actual)	Interventional	2017-11-10	Active, not recruiting
Precision Treatment of Luminal Advanced Breast Cancer Based on Molecular Subtyping [NCT04355858]	Phase 2	319 participants (Anticipated)	Interventional	2020-05-01	Recruiting
Open-label Study on Treatment of Primary Aldosteronism With Everolimus [NCT03174171]	Phase 2	12 participants (Actual)	Interventional	2017-05-22	Completed
Proof of Concept for Lenvatinib and Everolimus Prior to Nephrectomy in Eligible Patients With Local and Metastatic Renal Cell Carcinoma (RCC) [NCT03324373]	Phase 1	11 participants (Actual)	Interventional	2019-03-20	Active, not recruiting
Phase II Study of Erlotinib and RAD001 (Everolimus) in Patients With Previously Treated Advanced Pancreatic Cancer [NCT00640978]	Phase 2	16 participants (Actual)	Interventional	2008-03-31	Terminated(stopped due to Significant Adverse Effects - Futility)
Evaluation of RAD001 as Therapy for Patients With Systemic Mastocytosis [NCT00449748]	Phase 2	10 participants (Actual)	Interventional	2007-04-30	Completed
A Phase I Trial to Evaluate Acute and Late Toxicities of Concurrent Treatment With Everolimus (RAD001) and Radio-Hormonotherapy in High-risk Prostate Cancer.(RHOMUS) [NCT00943956]	Phase 1	30 participants (Actual)	Interventional	2009-01-31	Completed
A Phase II Study of Temozolomide and Everolimus (RAD001) Therapy for Metastatic Melanoma [NCT00521001]	Phase 2	49 participants (Actual)	Interventional	2008-01-31	Completed
A Phase II, Single-Arm Study of RAD001 (Everolimus), Letrozole, and Metformin in Patients With Advanced or Recurrent Endometrial Carcinoma [NCT01797523]	Phase 2	62 participants (Actual)	Interventional	2013-10-07	Active, not recruiting
Optical Coherence Tomography Assessment of Gender diVersity In Primary Angioplasty: The OCTAVIA Trial [NCT02577965]	Phase 4	140 participants (Actual)	Interventional	2011-03-31	Completed
ComparisiOn of Neointimal coVerage betwEen zotaRolimus Eluting Stent and Everolimus Eluting Stent Using Optical Coherence Tomography at 9 Months (COVER OCT) [NCT00894062]	Phase 4	40 participants (Actual)	Interventional	2008-12-31	Completed
COREV : A Multi-center, Randomized, Open-label Study Evaluating the Efficacy on Renal Function of Everolimus in Heart Transplant Recipients With Established Chronic Renal Failure [NCT00716573]	Phase 4	120 participants (Actual)	Interventional	2008-09-16	Completed
AngiographiC Evaluation of the Everolimus-Eluting Stent in Chronic Total Occlusions - the ACE-CTO Study [NCT01012869]	Phase 4	100 participants (Anticipated)	Interventional	2009-11-30	Completed
Impact of Cyclosporine or Steroid Withdrawal at 3 Months Post Transplantation on Graft Function, Patient Survival and Cardiovascular Surrogate Markers the First 5 Years After Renal Transplantation. [NCT00903188]	Phase 4	152 participants (Anticipated)	Interventional	2008-10-31	Recruiting
Phase 1b/3 Global, Randomized, Controlled, Open-label Trial Comparing Treatment With RYZ101 to Standard of Care Therapy in Subjects With Inoperable, Advanced, SSTR+, Well-differentiated GEP-NETs That Have Progressed Following Prior 177Lu-SSA Therapy [NCT05477576]	Phase 3	288 participants (Anticipated)	Interventional	2022-03-24	Recruiting
A Phase 1b/2 Study of Ibrutinib Combination Therapy in Selected Advanced Gastrointestinal and Genitourinary Tumors [NCT02599324]	Phase 1/Phase 2	263 participants (Actual)	Interventional	2015-12-01	Completed
A Single Arm, Multi-center Phase II Trial to Evaluate Paclitaxel Plus RAD001 in Urothelial Carcinoma After Failure of Prior Platin-based Chemotherapy [NCT00933374]	Phase 2	28 participants (Actual)	Interventional	2009-07-31	Terminated(stopped due to delayed recruitment)
A Phase II Trial of LEE011 in Combination With Everolimus in the Treatment of Advanced Well Differentiated Neuroendocrine Tumors of Foregut Origin [NCT03070301]	Phase 2	21 participants (Actual)	Interventional	2017-02-27	Active, not recruiting
Phase II Trial of Everolimus (RAD001) in Relapsed/Refractory Lymphoma [NCT00436618]	Phase 2	277 participants (Actual)	Interventional	2005-08-31	Completed
A Phase Ib/II Study Investigating the Combination of Everolimus With Trastuzumab and Paclitaxel in Patients With HER2-overexpressing Metastatic Breast Cancer [NCT00426556]	Phase 1	88 participants (Actual)	Interventional	2007-07-31	Completed
Phase I Everolimus Dose Finding Study for the Treatment of Stage IV or Recurrent, Non-resectable, Cervical Cancer With Standard Whole Pelvic Radiation Therapy in Combination With Weekly Cisplatin and Daily Everolimus [NCT00967928]	Phase 1	0 participants (Actual)	Interventional	2009-12-31	Withdrawn(stopped due to Lack of enrollment)
A Prospective Multicenter Open-label Randomized Study to Assess Efficacy and Safety of Everolimus in Combination With Cyclosporine Microemulsion Versus Everolimus Without Calcineurine Inhibitor in Combination With Enteric-coated Mycophenolate Sodium (EC-M [NCT00425308]	Phase 3	30 participants (Actual)	Interventional	2006-10-31	Completed
Multiple Ascending Dose (MAD) Phase Ib/II Study of the mTOR Inhibitor (RAD001) in Combination With the IGF-1R Antagonist (R1507) for the Treatment of Patients With Advanced Solid Tumors [NCT00985374]	Phase 1	11 participants (Actual)	Interventional	2009-11-30	Terminated
A Phase I/Ib Dose Escalation and Biomarker Study of Ceritinib (LDK378) in Combination With Everolimus in Patients With Locally Advanced or Metastatic Solid Tumors With an Expansion in NSCLC Characterized by Abnormalities in Anaplastic Lymphoma Kinase (ALK [NCT02321501]	Phase 1	37 participants (Actual)	Interventional	2016-06-22	Active, not recruiting
Efficacy and Safety of Anti-cytomegalovirus Prophylaxis Versus Pre-emptive Approaches With Valganciclovir in Heart Transplant Recipients Treated With Everolimus or Mycophenolate. A Randomized Open-label Study for Prevention of Cardiaca Allograft Vasculopa [NCT00966836]	Phase 3	100 participants (Anticipated)	Interventional	2009-04-30	Recruiting
A Randomized Study of mTOR Inhibition by RAD001 (Everolimus) in Invasive Breast Cancer Patients After Pre-operative Use of Anthracycline and/or Taxane-based Chemotherapy [NCT01088893]	Phase 2	50 participants (Anticipated)	Interventional	2009-11-30	Recruiting
Evaluation of the Early Conversion From a Calcineurin Inhibitor-based Immunosuppressive Regimen to Everolimus in de Novo Renal Transplant Recipients, a Multicenter Experience [NCT01609673]		1 participants (Actual)	Interventional	2013-03-31	Terminated(stopped due to The inclusion of proposed sample turned to be infeasible due to Ethical Non-approval of 2 research sites and another site no transplant activity since 2012.)
Antiangiogenic Treatment of Advanced or Metastatic Hepatocellular Cancer (HCC) - An Open Label, Stratified, Single-arm Phase II Study of Bevacizumab and RAD001 [NCT00775073]	Phase 2	33 participants (Actual)	Interventional	2008-10-31	Completed
A Prospective, Randomized, Single Center Pilot Study Comparing Patient and Graft Survival, Adverse Events and Tolerability of Zortress® (Everolimus) Versus Rapamune® (Sirolimus) in Combination With Low Dose Neoral® (Cyclosporine) Dosed by C2 Monitoring, i [NCT01976390]		60 participants (Actual)	Interventional	2013-10-01	Completed
A Phase Ib, Open-label Study to Evaluate RAD001 as Monotherapy Treatment in Chinese Patients With Advanced Pulmonary Neuroendocrine Tumor [NCT01324492]	Phase 1	16 participants (Actual)	Interventional	2010-12-31	Completed
Phase II Trial of RAD001 (Everolimus) in Previously Treated Small Cell Lung Cancer [NCT00374140]	Phase 2	40 participants (Actual)	Interventional	2006-10-31	Completed
Phase I Trial of Carboplatin and Etoposide in Combination With Everolimus (RAD001) in Advanced Solid Tumors, With Emphasis on Small Cell Lung Cancer (SCLC) [NCT00807755]	Phase 1	5 participants (Actual)	Interventional	2009-03-31	Terminated(stopped due to Number of known toxicities observed despite a treatment-naïve population)
A Phase I Dose Finding Study of RAD001 in Combination With Capecitabine and Oxaliplatin (XELOX) in Patients With Advanced Gastric Cancer [NCT01049620]	Phase 1	40 participants (Actual)	Interventional	2010-02-28	Completed
A Two Parts, Biomarker Study to Identify Genetic Aberrations Predictive for Response on Everolimus in Solid Tumors Without Regular Treatment Options (CPCT-03) [NCT01566279]		73 participants (Actual)	Interventional	2012-08-31	Completed
Nordic Everolimus (Certican) Trial in Heart and Lung Transplantation: Results at 24 Months [NCT00377962]	Phase 4	282 participants (Actual)	Interventional	2005-12-31	Completed
Multicentric Study of GOELAMS Phase I Evaluation of RAD001 in Association With Aracytine and Daunorubicine in AML Treatment in Patients Less Than 65 Years in Relapse More Than One Year After First Complete Remission [NCT01074086]	Phase 1	31 participants (Actual)	Interventional	2008-02-29	Completed
A Phase I/II Study of RAD001 and Radiation Therapy in Patients With Brain Metastasis From Non-small Cell Lung Cancer (NSCLC) [NCT00892801]	Phase 1	5 participants (Actual)	Interventional	2009-05-31	Terminated(stopped due to Terminated due to low accrual. Study was closed to accrual prematurely and did not continue on to Phase II.)
Safety and Efficacy of Cemiplimab (PD-1 Blockade) in Selected Organ Transplant Recipients With Advanced Cutaneous Squamous Cell Carcinoma (CONTRAC) [NCT04339062]	Phase 1	12 participants (Anticipated)	Interventional	2020-07-15	Active, not recruiting
A Multi-Centered Randomized Phase II Study Comparison of Single-Agent Carboplatin vs the Combination of Carboplatin and Everolimus for the Treatment of Advanced Triple-Negative Breast Cancer [NCT02531932]	Phase 2	62 participants (Anticipated)	Interventional	2015-12-16	Active, not recruiting
A Single-centre Study of Certican (Everolimus) as Prophylaxis for Graft-versus-Host Disease Following Post-Transplantation Cyclophosphamide After Allogeneic Stem Cell Transplantation [NCT02812940]	Phase 2	19 participants (Actual)	Interventional	2016-04-30	Completed
Comparison of the Vasomotor Function and Myocardial Flow in Patients Treated [NCT02738658]	Phase 4	70 participants (Actual)	Interventional	2015-03-01	Completed
Everolimus (RAD001) in Combination With Intravenous Carboplatin in Taxane- and Anthracycline-pretreated Patients With Progressive Metastatic Breast Cancer [NCT00930475]	Phase 1/Phase 2	54 participants (Anticipated)	Interventional	2009-02-28	Recruiting
Pharmacokinetics of Everolimus and Enteric-Coated Mycophenolatesodium Before and After Withdrawal of Cyclosporine in Stable Renal Transplant Patients [NCT00443937]	Phase 4	15 participants (Anticipated)	Interventional	2004-01-31	Completed
Spirit Small Vessel Registry (SPIRIT SV) [NCT00783796]		150 participants (Actual)	Interventional	2008-10-31	Terminated(stopped due to Study stopped at 3 years. Funding for trial withdrawn by sponsor.)
Everolimus-Eluting Stent in the Treatment of Bifurcation Lesions: Comparison of Main Vessel Stent to Main Vessel and Side Branch Stent [NCT00916695]	Phase 4	332 participants (Anticipated)	Interventional	2009-06-30	Recruiting
An Open-Label Controlled Study of Adjunctive Everolimus (RAD 001) Therapy for Epilepsy in Children With Sturge-Weber Syndrome [NCT01997255]	Phase 2	0 participants (Actual)	Interventional	2014-04-30	Withdrawn(stopped due to Site did not want to pursue study)
PROlonging Dual Antiplatelet Treatment In Patients With Coronary Artery Disease After Graded Stent-induced Intimal Hyperplasia studY [NCT00611286]	Phase 4	1,700 participants (Anticipated)	Interventional	2006-12-31	Completed
Precise Targeted Therapy for Refractory HER2 Positive Advanced Breast Cancer Based on Genome Signature and Drug Sensitivity of PDO Model [NCT05429684]	Phase 3	120 participants (Anticipated)	Interventional	2021-01-01	Recruiting
A Multicenter, Randomized, Double-blind, Phase II Study to Evaluate the Tolerability of an Induction Dose Escalation of Everolimus in Patients With Metastatic Breast Cancer [NCT02387099]	Phase 2	156 participants (Actual)	Interventional	2015-05-31	Completed
A Randomized, Double-blind, Multi-center Phase III Study Comparing Everolimus (RAD001) Plus Best Supportive Care Versus Placebo Plus Best Supportive Care in Patients With Advanced Gastric Cancer After Progression on 1 or 2 Prior Systemic Chemotherapy [NCT00879333]	Phase 3	656 participants (Actual)	Interventional	2009-07-31	Completed
The Landscape of ESR1 Mutations in Asian Estrogen Receptor-positive Metastatic Breast Cancer Patients Detected by Liquid Biopsy and Impact on Hormonal Therapy-based Treatments [NCT04212702]		123 participants (Actual)	Observational	2017-05-22	Active, not recruiting
A Multicentre, Open-label, Randomised, Controlled Study of Molecularly Precision Target Therapy Based on Tumor Molecular Profiling With GEMOX in Advanced or Recurrent Extrahepatic Cholangiocarcinoma and Gallbladder Carcinoma [NCT02836847]	Phase 2	152 participants (Anticipated)	Interventional	2016-07-31	Recruiting
Genomics-Based Target Therapy for Children With Relapsed or Refractory Malignancy [NCT02638428]	Phase 2	90 participants (Anticipated)	Interventional	2015-12-31	Recruiting
Phase IV Study of the Choice of Optimal Strategy for Bifurcation Lesions With Normal Side Branch [NCT00694005]	Phase 4	504 participants (Actual)	Interventional	2008-01-31	Completed
A Phase 1 Trial of the Combination of Everolimus (RAD001) and Bortezomib (VELCADE) for Relapsed or Refractory Lymphoma [NCT00671112]	Phase 1	30 participants (Actual)	Interventional	2008-06-30	Terminated(stopped due to Treatment ineffective)
Certican® (Everolimus) Against Cytomegalovirus Disease in Renal Transplant Patients [NCT00828503]	Phase 2	40 participants (Anticipated)	Interventional	2008-12-31	Recruiting
Everolimus and Mycophenolate Sodium as GvHD Prophylaxis in Allogeneic Stem Cell Transplantation [NCT00856505]	Phase 1/Phase 2	38 participants (Anticipated)	Interventional	2008-03-31	Recruiting
A Phase 1 Dose Escalation and Expansion Study of AZD9833 Alone or in Combination in Women With ER-positive, HER2-negative Advanced Breast Cancer (SERENA-1) [NCT03616587]	Phase 1	386 participants (Anticipated)	Interventional	2018-10-11	Recruiting
A Multicenter, Open-label, Phase I Clinical Study to Evaluate the Safety, Pharmacokinetics, and Antitumor Efficacy of SIM0270 Alone or in Combination in Subjects With ER-positive, HER-2 Negative Locally Advanced or Metastatic Breast Cancer [NCT05293964]	Phase 1	210 participants (Anticipated)	Interventional	2022-05-18	Recruiting
A Randomized Phase 2 Study of MK-2206 in Comparison With Everolimus in Refractory Renal Cell Carcinoma [NCT01239342]	Phase 2	43 participants (Actual)	Interventional	2011-01-27	Terminated
XENERA™1: A Multi-centre, Double-blind, Placebo-controlled, Randomised Phase II Trial to Compare Efficacy of Xentuzumab in Combination With Everolimus and Exemestane Versus Everolimus and Exemestane in Women With HR+ / HER2- Metastatic Breast Cancer and N [NCT03659136]	Phase 2	103 participants (Actual)	Interventional	2018-11-28	Completed
European Proof-of-Concept Therapeutic Stratification Trial of Molecular Anomalies in Relapsed or Refractory Tumors [NCT02813135]	Phase 1/Phase 2	460 participants (Anticipated)	Interventional	2016-08-03	Recruiting
Phase II Randomized Multicenter Study of Everolimus as Maintenance Therapy for Metastatic Neuroendocrine Carcinoma With Pulmonary or Gastroenteropancreatic Origin [NCT02687958]	Phase 2	30 participants (Actual)	Interventional	2015-05-31	Active, not recruiting
An Exploratory Study Evaluating FDG-PET as a Predictive Marker for mTOR Directed Therapy With RAD001 in Metastatic Renal Cell Cancer [NCT00529802]	Phase 2	60 participants (Actual)	Interventional	2007-09-30	Completed
A Phase I/Ib, Open-label, Multi-center Study of DFF332 as a Single Agent and in Combination With Everolimus or IO Agents in Patients With Advanced/Relapsed ccRCC and Other Malignancies With HIF2α Stabilizing Mutations [NCT04895748]	Phase 1	40 participants (Actual)	Interventional	2021-11-30	Active, not recruiting
An Umbrella Trial Based on Molecular Pathway for Patients With Unresectable Locally Advanced or Metastatic Triple Negative Breast Cancer (FUTURE SUPER) [NCT04395989]	Phase 2	139 participants (Actual)	Interventional	2020-07-28	Active, not recruiting
A 36 Month Multi-center, Open Label, Randomized, Comparator Study to Evaluate the Efficacy and Safety of Everolimus Immunosuppression Treatment in Liver Transplantation for Hepatocellular Carcinoma Exceeding Milan Criteria [NCT02081755]	Phase 4	336 participants (Anticipated)	Interventional	2014-03-31	Active, not recruiting
Phase I, Open Label, Dose Escalation Study of the Safety, Tolerability, and Pharmacokinetics of the Combination RAD001 Plus Docetaxel in Patients With Metastatic Breast Cancer [NCT00253318]	Phase 1	15 participants (Actual)	Interventional	2005-11-01	Terminated(stopped due to Toxicity and Lack of Efficacy)
An Open-label, Multicenter Phase II Study to Compare the Efficacy and Safety of RAD001 as First-line Followed by Second-line Sunitinib Versus Sunitinib as First-line Followed by Second-line RAD001 in the Treatment of Patients With Metastatic Renal Cell Ca [NCT00903175]	Phase 2	471 participants (Actual)	Interventional	2009-10-31	Completed
Multi-center, Open-label, Prospective, Randomized, Parallel Group, Long-term Study Investigating a Standard Regimen in de Novo Kidney Transplant Patients Versus a CNI-free Regimen and a CNI-low Dose Regimen [NCT00514514]	Phase 3	802 participants (Actual)	Interventional	2007-07-31	Completed
A Phase I Trial of the IGF-1R Antibody AMG 479 in Combination With Everolimus (RAD001) and Panitumumab in Patients With Advanced Cancer (The RAP Trial) [NCT01061788]	Phase 1	43 participants (Actual)	Interventional	2010-04-30	Completed
A Randomized Double-blind Phase III Study of RAD001 10 mg/d Plus Best Supportive Care Versus Placebo Plus Best Supportive Care in the Treatment of Patients With Advanced Pancreatic Neuroendocrine Tumor (NET) [NCT00510068]	Phase 3	410 participants (Actual)	Interventional	2007-07-31	Completed
Phase I Trial of Everolimus, Gemcitabine, and Cisplatin for Patients With Solid Tumors Refractory to Standard Therapy [NCT00949949]	Phase 1	38 participants (Actual)	Interventional	2009-09-30	Completed
A 24-month, Multi-center, Randomized, Open-label, Non-inferiority Study of Efficacy and Safety Comparing Two Exposures of Concentration-controlled Everolimus With Reduced Cyclosporine Versus 3.0 g Mycophenolate Mofetil With Standard Dose Cyclosporine in d [NCT00300274]	Phase 3	721 participants (Actual)	Interventional	2006-01-31	Completed
Phase III Placebo-Controlled Trial to Evaluate Dexamethasone Use for Everolimus-Induced Oral Stomatitis: Prevention Versus Early Treatment Approaches: MIST (My Individualized Stomatitis Treatment) [NCT03839940]	Phase 3	39 participants (Actual)	Interventional	2019-02-15	Terminated(stopped due to Severe lack of accrual)
A Phase I/II Study of RAD001 With Docetaxel in the Treatment of Metastatic, Androgen Independent Prostate Cancer [NCT00459186]	Phase 1/Phase 2	19 participants (Actual)	Interventional	2005-11-30	Completed
A Phase I Study Evaluating the Combination of the Deacetylase Inhibitor, LBH589 Plus the mTOR Inhibitor RAD001, in Relapsed and Refractory Adult Patients With Lymphoma [NCT00962507]	Phase 1	11 participants (Actual)	Interventional	2009-07-31	Completed
An Open-label, Single-dose Study to Assess the Pharmacokinetics of Oral Everolimus (Afinitor®) in Subjects With Impaired Hepatic Function [NCT00968591]	Phase 1	34 participants (Actual)	Interventional	2009-11-30	Completed
An Open Label, Stratified, Single-arm Phase II Study of Everolimus in Patients With Advanced Pancreatic Neuroendocrine Tumor (NET) After Failure of Cytotoxic Chemotherapy [NCT00363051]	Phase 2	160 participants (Actual)	Interventional	2006-06-30	Completed
Post-Approval Study of the PROMUS PREMIERTM Everolimus-Eluting Platinum Chromium Coronary Stent System in China [NCT03273023]		2,059 participants (Actual)	Observational [Patient Registry]	2018-01-11	Active, not recruiting
A Randomized, Double-blind, Placebo-controlled Study of Everolimus in the Treatment of Patients With Subependymal Giant Cell Astrocytomas (SEGA) Associated With Tuberous Sclerosis Complex (TSC) [NCT00789828]	Phase 3	117 participants (Actual)	Interventional	2009-08-31	Completed
A Randomized Controlled Trial of Everolimus-eluting Stents and Paclitaxel-eluting Stents for Coronary Revascularization in Daily Practice: The COMPARE Trial [NCT01016041]	Phase 3	1,800 participants (Actual)	Interventional	2007-02-28	Completed
Open Label Randomized Clinical Trial of Standard Neoadjuvant Chemotherapy (Paclitaxel Followed by FEC) Versus the Combination of Paclitaxel and RAD001 Followed by FEC in Women With Triple Receptor-Negative Breast Cancer (CRAD001C24101) [NCT00499603]	Phase 2	62 participants (Actual)	Interventional	2007-07-31	Active, not recruiting
A Phase I Study of BKM120 and Everolimus in Advanced Solid Malignancies [NCT01470209]	Phase 1	43 participants (Actual)	Interventional	2012-01-31	Completed
A Clinical Evaluation of the Bioabsorbable Everolimus Eluting Coronary Stent System (BVS EECSS) in the Treatment of Patients With de Novo Native Coronary Artery Lesions. [NCT00856856]		101 participants (Actual)	Interventional	2009-03-31	Completed
A Phase II Trial of RAD001 in Triple Negative Metastatic Breast Cancer [NCT00827567]	Phase 2	6 participants (Actual)	Interventional	2009-04-30	Terminated(stopped due to Slow accrual)
A Phase I Trial of the mTOR Inhibitor RAD001 in Combination With VEGF Receptor Tyrosine Kinase Inhibitor PTK787/ZK 222584 in Patients With Advanced Solid Tumors [NCT00655655]	Phase 1	96 participants (Anticipated)	Interventional	2004-12-31	Completed
A Phase Ib Study Investigating the Combination of RAD001 With Cisplatin and Etoposide in Patients With Extensive-stage Small-cell Lung Cancer Not Previously Treated With Chemotherapy [NCT00466466]	Phase 1	20 participants (Actual)	Interventional	2007-04-30	Completed
A Randomized Comparison of the Supralimus® Stent With the Xience V™ Stent in the Treatment of Patients With de Novo Native Coronary Artery Lesions [NCT00917163]	Phase 4	13 participants (Actual)	Interventional	2009-07-31	Terminated(stopped due to due to unavoidable circumstances relating to logistic issues and regulatory processes in various countries causing unacceptable delays.)
A Two-step Phase 1 Study Investigating the Combination of RAD001 With Carboplatin, Paclitaxel and Bevacizumab in Non-small-cell Lung Cancer (NSCLC) Patients Not Treated Previously With Systemic Therapy [NCT00457119]	Phase 1	69 participants (Actual)	Interventional	2007-02-28	Completed
CLEVER Pilot Trial: A Phase II Pilot Trial of HydroxyChLoroquine, EVErolimus or the Combination for Prevention of Recurrent Breast Cancer [NCT03032406]	Phase 2	54 participants (Actual)	Interventional	2017-01-23	Active, not recruiting
A Phase I Trial of RAD001 (Everolimus) and Avastin(R) (Bevacizumab) in Children With Recurrent Solid Tumors [NCT00756340]	Phase 1	16 participants (Actual)	Interventional	2008-07-31	Completed
A Randomized, Double-blind, Placebo-controlled Study of RAD0001 in the Treatment of Angiomyolipoma in Patients With Either Tuberous Sclerosis Complex (TSC) or Sporadic Lymphangioleiomyomatosis (LAM) [NCT00790400]	Phase 3	118 participants (Actual)	Interventional	2009-04-30	Completed
A Randomized Phase III, Double-Blind, Placebo-Controlled Multicenter Trial of Everolimus in Combination With Trastuzumab and Paclitaxel, as First Line Therapy in Women With HER2 Positive Locally Advanced or Metastatic Breast Cancer [NCT00876395]	Phase 3	719 participants (Actual)	Interventional	2009-09-10	Completed
Phase IV Study of Optimal Stenting Strategy For True Bifurcation Lesions [NCT00693251]	Phase 4	420 participants (Actual)	Interventional	2008-01-31	Completed
Everolimus in Combination With Rituximab for Relapsed/Refractory Diffuse Large B Cell Lymphoma [NCT00869999]	Phase 2	26 participants (Actual)	Interventional	2009-05-31	Completed
Long Term Follow Up for RAD001 Therapy of Angiomyolipomata in Patients With Tuberous Sclerosis Complex and Sporadic Lymphangioleiomyomatosis [NCT00792766]	Phase 1/Phase 2	20 participants (Actual)	Interventional	2008-12-31	Completed
Phase II Trial of mTOR Inhibitor, Everolimus (RAD001), in Malignant Pleural Mesothelioma (MPM) [NCT00770120]	Phase 2	61 participants (Actual)	Interventional	2008-12-31	Completed
A Phase II Trial of RAD001 Plus Bevacizumab in the Treatment of Patients With Metastatic Melanoma [NCT00591734]	Phase 2	57 participants (Actual)	Interventional	2008-01-31	Completed
Open Label Phase II Study of Everolimus (RAD001) in Patients With Segmental Overgrowth Syndrome [NCT02569125]	Phase 2	0 participants (Actual)	Interventional	2016-01-31	Withdrawn(stopped due to Change in supply of study medication)
A Multi-center, Randomized, Open-label, Parallel Group Study Investigating the Renal Tolerability, Efficacy and Safety of a CNI-free Regimen (Everolimus and MPA) Versus a CNI-regimen With Everolimus in Heart Transplant Recipients [NCT00862979]	Phase 4	162 participants (Actual)	Interventional	2009-02-24	Completed
A Randomized, Open-label, Multi-center Phase II Study to Compare Bevacizumab Plus RAD001 Versus Interferon Alfa-2a Plus Bevacizumab for the First-line Treatment of Patients With Metastatic Clear Cell Carcinoma of the Kidney [NCT00719264]	Phase 2	365 participants (Actual)	Interventional	2008-11-12	Completed
Multicenter, Triple-arm, Single-stage, Phase II Trial to Determine the Preliminary Efficacy and Safety of RAD001 in Patients With Histological Evidence of Progressive or Metastatic Bone or Soft Tissue Sarcomas [NCT00767819]	Phase 2	71 participants (Actual)	Interventional	2008-03-31	Completed
A Phase II Study of Combined Fulvestrant (Faslodex) and Everolimus in Advanced/Metastatic Breast Cancer After Aromatase Inhibitor Failure [NCT00570921]	Phase 2	33 participants (Actual)	Interventional	2008-04-30	Completed
Randomized Comparison Between Sirolimus-eluting and Everolimus-eluting Coronary Stents in Chronic Coronary Occlusions [NCT00793221]	Phase 3	207 participants (Actual)	Interventional	2008-11-30	Completed
Phase 1 Study of the Combination of CM082 With Everolimus in Patients With Metastatic Renal Cell Carcinoma (RCC): Safety, Tolerability, Pharmacokinetics, and Preliminary Efficacy [NCT02577458]	Phase 1	18 participants (Anticipated)	Interventional	2015-09-30	Recruiting
Phase I/II Study of Hyper-CVAD Plus RAD001 (Everolimus) for Patients With Relapsed or Refractory Acute Lymphocytic Leukemia (ALL) [NCT00968253]	Phase 1/Phase 2	24 participants (Actual)	Interventional	2009-11-30	Completed
Phase II Trial of EVEROLIMUS ± Trastuzumab in Hormone-Refractory Metastatic Breast Cancer [NCT00912340]	Phase 2	70 participants (Actual)	Interventional	2009-05-31	Completed
A Phase 2b Randomized Trial of Autologous Dendritic Cell Immunotherapy (CMN-001) Plus Standard Treatment of Advanced Renal Cell Carcinoma [NCT04203901]	Phase 2	16 participants (Actual)	Interventional	2020-07-22	Terminated(stopped due to Strategic corporate decision)
A Phase 0/II Study of Ribociclib (LEE011) in Combination With Everolimus in Preoperative Rb-Intact Recurrent High-Grade Glioma Patients Scheduled for Resection to Evaluate Central Nervous System (CNS) Penetration [NCT03834740]	Early Phase 1	27 participants (Actual)	Interventional	2018-12-21	Completed
A Phase I Study of Capecitabine, Oxaliplatin, Bevacizumab, and RAD001 (XELOX-A-Ev) for Subjects With Advanced Solid Tumors [NCT00849550]	Phase 1	32 participants (Actual)	Interventional	2009-07-31	Completed
A Phase I Study of Ribociclib and Everolimus Following Radiation Therapy in Children With Newly Diagnosed Non-biopsied Diffuse Pontine Gliomas (DIPG) and RB+ Biopsied DIPG and High Grade Gliomas (HGG) [NCT03355794]	Phase 1	19 participants (Actual)	Interventional	2017-11-14	Completed
A Phase II Study Evaluating The Efficacy And Tolerability Of Everolimus (RAD001) In Combination With Trastuzumab And Vinorelbine In The Treatment Of Progressive HER2-Positive Breast Cancer Brain Metastases [NCT01305941]	Phase 2	32 participants (Actual)	Interventional	2011-09-30	Completed
An Open-Label Phase I Study of the Safety of and Efficacy of RAD001 in Combination With Lenalidomide in the Treatment of Subjects With Relapsed and Relapsed/Refractory Multiple Myeloma [NCT00729638]	Phase 1	28 participants (Actual)	Interventional	2008-06-30	Completed
Harmonizing Optimal Strategy for Treatment of Coronary Atherosclerotic Lesions- Registry-based Study on the Effect and Safety of Xience Xpedition™/Alpine™, Everolimus-eluting Stent for Coronary Atherosclerotic Lesions: HOST-Alpine Registry [NCT02845804]		1,533 participants (Anticipated)	Observational [Patient Registry]	2015-07-31	Recruiting
An Open-label, Multi-center Phase 2 Study to Evaluate Everolimus as Monotherapy Treatment for Patients With Metastatic Recurrent and/or Unresectable Renal Cell Carcinoma (EVERMORE). [NCT01206764]	Phase 4	143 participants (Actual)	Interventional	2009-11-11	Completed
An Extension to a 12-month, Open-label, Randomised, Multicenter, Sequential Cohort, Dose Finding Study to Evaluate the Efficacy, Safety and Tolerability of Oral AEB071 Versus Cyclosporine in Combination With Everolimus, Basiliximab and Corticosteroids in [NCT00820911]	Phase 2	175 participants (Actual)	Interventional	2008-09-30	Completed
Extension Study to the Multicenter, Open-label, Randomized, Controlled Study CRAD001H2304 to Evaluate the Long-term Efficacy and Safety of Concentration-controlled Everolimus in Liver Transplant Recipient [NCT01150097]	Phase 3	284 participants (Actual)	Interventional	2010-03-31	Completed
A 24 Month, Multicenter, Open-label, Randomized, Controlled Study to Evaluate the Efficacy and Safety of Concentration-controlled Everolimus to Eliminate or to Reduce Tacrolimus Compared to Tacrolimus in de Novo Liver Transplant Recipients [NCT00622869]	Phase 3	719 participants (Actual)	Interventional	2008-01-31	Completed
A Clinical Evaluation of Everolimus Eluting Coronary Stents in the Treatment of Patients With ST-segment Elevation Myocardial Infarction.EXAMINATION Study [NCT00828087]		1,504 participants (Actual)	Interventional	2008-12-31	Completed
A Phase I Study of the Weekly Oral RAD001 in Combination With Oral Topotecan in Patients With Advanced or Recurrent Endometrial Cancers [NCT00703807]	Phase 1	10 participants (Actual)	Interventional	2008-12-31	Completed
Phase I/II Study of Combination Everolimus (RAD001), and Rituximab (Rituxan), OR Everolimus, Bortezomib (Velcade, PS-341), and Rituximab in Patients With Relapsed and/or Relapsed/Refractory Waldenstrom's Macroglobulinemia [NCT01125293]	Phase 1/Phase 2	46 participants (Actual)	Interventional	2010-04-30	Terminated(stopped due to Per protocol, Phase II is to be terminated early if a less than 5% of the Phase II participants observe a Very Good Partial Response or Better in the first 23 participants enrolled to Phase II.)
Phase I Dose Escalation of Gleevec in Combination With RAD001 Plus Hydroxyurea for Patients With Recurrent Malignant Glioma [NCT00613132]	Phase 1	78 participants (Actual)	Interventional	2005-05-31	Completed
A 24-month, Multi-center, Open-label, Randomized, Controlled Trial to Investigate Efficacy, Safety and Evolution of Cardiovascular Parameters in de Novo Renal Transplant Recipients After Early Calcineurin Inhibitor to Everolimus Conversion [NCT01114529]	Phase 3	828 participants (Actual)	Interventional	2010-08-09	Completed
A Phase I/II Study of the Histone Deacetylase (HDAC) Inhibitor LBH589 (Panobinostat) in Combination With mTOR Inhibitor RAD001 (Everolimus) in Patients With Relapsed Multiple Myeloma or Lymphoma [NCT00918333]	Phase 1/Phase 2	124 participants (Actual)	Interventional	2009-06-30	Completed
A Phase I Dose Escalation Study of RAD001 Administered in Patients With Relapsed or Refractory Non-Hodgkin's Lymphoma [NCT00622258]	Phase 1	13 participants (Actual)	Interventional	2008-03-31	Completed
Phase I Study of Sorafenib in Combination With RAD001 in Patients With Advanced Neuroendocrine Tumors [NCT00942682]	Phase 1	21 participants (Actual)	Interventional	2009-07-31	Completed
An Open-Label, Single Arm, Pilot Study of the Renal Safety of Everolimus in Addition to Neoral® in Cardiac Transplant Recipients With Established Allograft Vasculopathy [NCT00097968]	Phase 3	0 participants	Interventional	2004-08-31	Completed
A Phase I Study of Radiation Therapy (IMRT) + RAD001 (Everolimus) + Cisplatin for Patients With Head and Neck Cancer [NCT00858663]	Phase 1	13 participants (Actual)	Interventional	2009-03-31	Completed
A Randomized, Phase 2 Study to Assess the Safety and Efficacy of CRLX101 in Combination With Bevacizumab in Patients With Metastatic Renal Cell Carcinoma (RCC) Versus Standard of Care (SOC) (Investigator's Choice) [NCT02187302]	Phase 2	115 participants (Actual)	Interventional	2014-07-31	Completed
Observational Study Evaluating Efficacy, Tolerability and Treatment Algorithm of Advanced Renal Cell Cancer Patients Under Afinitor Treatment [NCT01390519]		30 participants (Actual)	Observational	2011-06-30	Completed
EndothelIal progeNitor Cell Capture steNt With 1-mOnth Dual Antiplatelet Therapy Versus eVerolimus-eluting Stent With stAndard 12-month Dual anTIplatelet Therapy in Elderly (≥ 70 Year) With Stable corONary Artery Disease - INNOVATION Trial [NCT01394848]	Phase 4	1 participants (Actual)	Interventional	2011-10-31	Terminated(stopped due to Previous other study including EPC capture stent raised the issue of safety (significant high incidence of instent restenosis))
A Multicenter, Open-labeled, Randomized Controlled Trial Comparing Three 2nd Generation Drug-Eluting Stents in Real-World Practice [NCT01397175]		1,960 participants (Actual)	Interventional	2013-01-16	Terminated(stopped due to Slow enrollment)
The DESTINY Trial: a Prospective Randomized Multicenter Trial Comparing the Implant of a Drug Eluting Stent (XIENCE V, Abbott Vascular) vs. a Bare Metal Stent (MULTILINK VISION, Abbott Vascular) in the Critically Ischemic Lower Leg [NCT00510393]	Phase 2	140 participants (Actual)	Interventional	2008-03-31	Completed
Efficacy and Safety of Certican® in Combination With Myfortic® in Adult Renal Allograft Recipients Following Calcineurin Inhibitor Withdrawal at Week 16 Compared to Patients Who Are Maintained on Tacrolimus and Myfortic® [NCT01399242]	Phase 4	40 participants (Anticipated)	Interventional	2011-08-31	Not yet recruiting
A Randomized Phase II Study to Explore the Efficacy and Feasibility of Upfront Bi-monthly Rotations Between Everolimus and Pazopanib in Patients With Advanced or Metastatic Clear Cell Renal Cancer [NCT01408004]	Phase 2	101 participants (Actual)	Interventional	2011-11-30	Completed
A Therapeutic Exploratory Study to Determine the Efficacy and Safety of Calcineurin-Inhibitor-Free De-novo Immunosuppression After Liver Transplantation [NCT00890253]	Phase 2	29 participants (Anticipated)	Interventional	2010-01-31	Recruiting
Randomized Comparison of Biolimus-Eluting and Everolimus-Eluting Stents With Optical Coherence Tomography Guided Stent Implantation in ST Elevation Myocardial Infarction.A 9-Month Angiographic and Optical Coherence Tomography Follow-up. [NCT00888758]	Phase 4	400 participants (Anticipated)	Interventional	2009-05-31	Not yet recruiting
Multi-center, Open-label, Prospective, Randomized, Parallel Group Study Investigating a CNI-free Regimen With Enteric-coated Mycophenolate Sodium and Everolimus in Comparison to Standard Therapy With Enteric-coated Mycophenolate Sodium and Ciclosporin Mic [NCT00332839]	Phase 4	93 participants (Actual)	Interventional	2005-11-30	Terminated(stopped due to The trial was terminated early due to slow enrollment. It was determined that the planned sample size of 300 could not be achieved.)
Randomized Phase I/II of Rapamycin Analog, RAD001, in Advanced Hepatocellular Carcinoma - With a Pharmacokinetic Study of RAD001 [NCT00390195]	Phase 1/Phase 2	134 participants (Anticipated)	Interventional	2006-10-31	Recruiting
Prospective and Randomized Study to Evaluate the Effect of Everolimus in the Clinical and Intra-Cardiac Ecography Progression of Heart Graft Vascular Illness. [NCT00695344]	Phase 4	52 participants (Actual)	Interventional	2006-01-31	Active, not recruiting
A Phase II Trial Using RAD001 for Patients With Radioiodine Refractory Thyroid Cancer [NCT00936858]	Phase 2	50 participants (Actual)	Interventional	2009-07-31	Completed
A Phase II Study of Carboplatin (CBDCA), Paclitaxel (TAXOL), and Everolimus (RAD001) in Previously Untreated Patients With Measurable Disease With Cancer of Unknown Primary (CUP) [NCT00936702]	Phase 2	46 participants (Actual)	Interventional	2009-09-30	Completed
A Phase II Neo-Adjuvant Study of Cisplatin, Paclitaxel With or Without RAD001 in Patients With Triple-negative Locally Advanced Breast Cancer. [NCT00930930]	Phase 2	145 participants (Actual)	Interventional	2009-06-30	Completed
SEA-SIDE: Sirolimus Versus Everolimus-eluting Stent Randomized Assessment in Bifurcated Lesions and Clinical SIgnificance of Residual siDE-branch Stenosis [NCT00697372]	Phase 4	150 participants (Actual)	Interventional	2007-09-30	Completed
Everolimus-Eluting Bioresorbable Scaffolds Versus Everolimus-Eluting Metallic Stents for Diffuse Long Coronary Artery Disease [NCT02831205]	Phase 4	800 participants (Anticipated)	Interventional	2016-07-31	Terminated(stopped due to Due to current BVS safety issue)
SORAVE-Sorafenib and Everolimus in Solid Tumors. A Phase I Clinical Trial to Evaluate the Safety of Combined Sorafenib and Everolimus Treatment in Patients With Relapsed Solid Tumors [NCT00933777]	Phase 1	36 participants (Actual)	Interventional	2009-07-31	Completed
An Open-label, Single-arm Phase II Study of RAD001 in Patients With Relapsed/Refractory Classical Hodgkin Lymphoma [NCT01022996]	Phase 2	57 participants (Actual)	Interventional	2009-12-31	Completed
XIENCE V® Everolimus Eluting Coronary Stent System (EECSS) USA Post-Approval Study [NCT00676520]		8,053 participants (Actual)	Observational	2008-07-31	Completed
An Open-label Phase I/II (Proof of Concept) Trial of an Combination of Nilotinib (AMN 107) and RAD001 in Patients With Acute Myeloid Leukemia [NCT00762632]	Phase 1/Phase 2	40 participants (Anticipated)	Interventional	2007-12-31	Completed
AERO: Adjuvant EveRolimus Outcomes in Laryngotracheal Stenosis [NCT05153668]	Early Phase 1	20 participants (Anticipated)	Interventional	2022-09-30	Active, not recruiting
A 12-month, Multicenter, Randomized, Open-label Study to Investigate Efficacy and Safety of Concentration Controlled Everolimus With Reduced Dose Cyclosporine A Versus Mycophenolate Mofetil With Standard Dose Cyclosporine A in de Novo Renal Transplant Adu [NCT00658320]	Phase 3	122 participants (Actual)	Interventional	2008-02-29	Completed
A Randomized, Double-blind, Placebo-controlled, Multi-center Phase III Study of RAD001 Adjuvant Therapy in Poor Risk Patients With Diffuse Large B-Cell Lymphoma (DLBCL) of RAD001 Versus Matching Placebo After Patients Have Achieved Complete Response With [NCT00790036]	Phase 3	742 participants (Actual)	Interventional	2009-07-24	Completed
A Phase Ib Trial of LEE011 in Combination With Everolimus (RAD001) and Exemestane in the Treatment of Postmenopausal Women With Hormone Receptor Positive, HER2 Negative Locally Advanced or Metastatic Breast Cancer [NCT01857193]	Phase 1	132 participants (Actual)	Interventional	2013-09-06	Completed
Randomized Comparison of Coronary Artery Bypass Surgery and Everolimus-Eluting Stent Implantation in the Treatment of Patients With Multivessel Coronary Artery Disease (BEST) [NCT00997828]		888 participants (Actual)	Interventional	2008-07-28	Terminated(stopped due to Problem with recruitment of subjects)
A Phase 1 Open Label/ Phase 2 Randomized, Double-blind, Multicenter Study Investigating the Combination of RAD001 and Sorafenib (Nexavar®) in Patients With Advanced Hepatocellular Carcinoma [NCT00828594]	Phase 1	130 participants (Actual)	Interventional	2008-12-31	Terminated
Neoadjuvant Everolimus (RAD001)for Advanced RCC Before Cytoreductive Nephrectomy, With Correlative Tumor Studies (Protocol #: 06-08-20-01) [NCT00831480]	Phase 2	15 participants (Actual)	Interventional	2011-04-30	Terminated(stopped due to Difficulty in accrual and by the order of the cancer center.)
An Open-Label, Dose-Escalation, Phase IB II Study to Investigate the Safety, Pharmacokinetics, Pharmacodynamics and Clinical Activity of the MEK Inhibitor GSK1120212 in Combination With Oral Everolimus in Subjects With Solid Tumors [NCT00955773]	Phase 1	64 participants (Actual)	Interventional	2009-08-17	Completed
A Phase II Trial of Short-Term Everolimus (RAD001) to Predict Response in Women With Operable Breast Cancer [NCT00855114]	Phase 2	0 participants (Actual)	Interventional	2008-07-31	Withdrawn(stopped due to Withdrawn due to no accrual)
Phase II Study of RAD001 in Advanced Cholangiocarcinoma [NCT00973713]	Phase 2	27 participants (Anticipated)	Interventional	2009-09-30	Recruiting
Rapalogues for Autism Phenotype in TSC: A Feasibility Study [NCT01929642]	Phase 2	3 participants (Actual)	Interventional	2013-07-31	Completed
Everolimus First-line Therapy in Non-rapidly Progressive Castration Resistant Prostate Cancer (CRPC). A Multicenter Phase II Trial. [NCT00976755]	Phase 2	37 participants (Actual)	Interventional	2009-09-14	Completed
Everolimus for the Treatment of Uveitis Unresponsive to Cyclosporine A [NCT00803816]	Phase 2	12 participants (Actual)	Interventional	2007-11-30	Completed
Master Protocol for Mantle Cell Lymphoma A Multicenter Phase II Trial Testing Everolimus (RAD001) for the Treatment of Patients With Relapsed or Therapy Resistant Mantle Cell Lymphoma [NCT00516412]	Phase 2	35 participants (Actual)	Interventional	2007-08-31	Completed
A Single Arm, Prospective, Open-label, Pilot Study to Assess Effects of the Switch From Sirolimus to Everolimus in Stable Maintenance Renal Transplant Patients Receiving a Calcineurin Inhibitor Free Regimen [NCT00170820]	Phase 4	20 participants	Interventional	2005-02-28	Completed
A One-year Multicenter, Randomized, Open-label Study of the Safety and Efficacy of Everolimus Versus Mycophenolate Mofetil in Combination With Reduced Dose Cyclosporine Microemulsion in Maintenance Heart Transplant Recipients [NCT00170859]	Phase 4	0 participants	Interventional	2004-08-31	Completed
ABILITY Diabetes Global [NCT04236609]		3,050 participants (Actual)	Interventional	2020-06-15	Active, not recruiting
A Facilitated Access Program to Provide Everolimus (RAD) Maintenance for Patients Completing Therapy in RAD Trials in Solid Organ Transplantation [NCT00149981]		0 participants	Expanded Access		No longer available
Phase I Clinical Trial of RAD001 in Combination With CP-751,871 in Patients With Advanced Sarcomas and Other Malignant Neoplasms [NCT00927966]	Phase 1	21 participants (Actual)	Interventional	2009-07-31	Completed
Phase I Study Evaluating the Chemosensitizing Effect of Everolimus Administered With Cytarabine and Daunorubicin in Patients With Acute Myeloid Leukemia in Relapse [NCT00544999]	Phase 1	21 participants (Anticipated)	Interventional	2007-09-30	Recruiting
EXecutive Randomized Controlled Trial (RCT): XIENCE V® Everolimus Eluting Coronary Stent System (XIENCE V® EECSS) in the Treatment of the Specific Setting of Patients With Multi-vessel Coronary Artery Disease. [NCT00531011]	Phase 4	200 participants (Actual)	Interventional	2007-09-30	Completed
A 3-Armed Prospective Randomized Controlled, Open-Labeled Phase II Trial to Evaluate Late Introduction of Cyclosporine or Everolimus Versus a 5-day Delay of Cyclosporine in Combination With MMF in Liver Transplant Recipients With MELD-Scores≥25 [NCT01023542]	Phase 2/Phase 3	45 participants (Anticipated)	Interventional	2011-06-30	Recruiting
Randomized Evaluation of Sirolimus-eluting Versus Everolimus-eluting Stent Trial [NCT01035450]	Phase 4	3,206 participants (Actual)	Interventional	2010-02-28	Completed
A Randomized, Double-blind, Placebo-controlled, Multicenter Phase III Study to Compare the Safety and Efficacy of RAD001 Plus Best Supportive Care (BSC) Versus BSC Plus Placebo in Patients With Metastatic Carcinoma of the Kidney Which Has Progressed on VE [NCT00410124]	Phase 3	416 participants (Actual)	Interventional	2006-11-30	Completed
A Multicenter, Randomized, Placebo-controlled, Double-blind Study on the Efficacy, Safety and Tolerability of Everolimus in Preventing End-stage Renal Disease (ESRD) in Patients With Autosomal Dominant Polycystic Kidney Disease (ADPKD) [NCT00414440]	Phase 4	431 participants (Actual)	Interventional	2006-12-31	Completed
SPIRIT IV Clinical Trial: Clinical Evaluation of the XIENCE V® Everolimus Eluting Coronary Stent System in the Treatment of Subjects With de Novo Native Coronary Artery Lesions [NCT00307047]	Phase 3	3,687 participants (Actual)	Interventional	2006-08-31	Completed
Phase I Study of Daily RAD001 Administered Orally in Combination With Mitomycin C, Administered Every Three Weeks to Patients With Advanced Gastric Cancer or Cancer of the Esophagogastric Junction [NCT01042782]	Phase 1	16 participants (Actual)	Interventional	2008-01-31	Completed
A 6-month, Multicenter, Randomized, Open-label Study of Safety and Efficacy of Everolimus-based Regimen Versus Calcineurin Inhibitor (CNI)-Based Regimen in Maintenance Liver Transplant Recipients [NCT00267189]	Phase 3	145 participants (Actual)	Interventional	2005-11-30	Completed
A Prospective, Open-label, Controlled Multicenter Trial to Assess the Efficacy and Safety of an Induction Regimen of Cyclosporine Micro Emulsion, Enteric-coated Mycophenolate Sodium (EC-MPS) and Corticosteroids, Followed by Administration of Everolimus an [NCT00371826]	Phase 4	126 participants (Actual)	Interventional	2006-03-31	Completed
A Randomised Fase I/II Trial With Irinotecan, Cetuximab and Everolimus (ICE)Compared to Capecitabine and Oxaliplatin (CapOx) for Patients With Gemcitabin Resistant Pancreatic Cancer [NCT01042028]	Phase 1/Phase 2	39 participants (Actual)	Interventional	2010-01-31	Terminated(stopped due to Emergence of FOLFIRINOX and slow recruitment)
AN INTERVENTIONAL, OPEN-LABEL, RANDOMIZED, MULTICENTER PHASE 3 STUDY OF PF-07220060 PLUS FULVESTRANT COMPARED TO INVESTIGATOR'S CHOICE OF THERAPY IN PARTICIPANTS OVER 18 YEARS OF AGE WITH HORMONE RECEPTOR-POSITIVE, HER2-NEGATIVE ADVANCED/METASTATIC BREAST [NCT06105632]	Phase 3	510 participants (Anticipated)	Interventional	2023-12-15	Not yet recruiting
Presentation of Renal Function in Liver Transplant Recipients With Certican Therapy: PROTECT Study A Twelve-month, Multicenter, Randomized, Open-label Study of Safety, Tolerability and Efficacy of Certican-based Regimen Versus Calcineurin Inhibitor-based [NCT00378014]	Phase 3	276 participants (Actual)	Interventional	2006-08-31	Completed
A Phase I Trial Using RAD001 With Weekly Cisplatin and Radiation Therapy in Patients With Locally Advanced Head and Neck Cancer [NCT01058408]	Phase 1	3 participants (Actual)	Interventional	2010-02-28	Terminated
The Real-World Endeavor Resolute Versus XIENCE V Drug-Eluting SteNt Study: Head-to-head Comparison of Clinical Outcome After Implantation of Second Generation Drug-eluting Stents in a Real World Scenario [NCT01066650]	Phase 4	1,391 participants (Actual)	Interventional	2008-06-30	Completed
Efficacy and Safety Study Comparing Concentration-controlled Everolimus in Two Doses (1.5 and 3.0 mg/Day Starting Doses) With Reduced Cyclosporine Versus 1.44 g Mycophenolic Acid (as Sodium Salt) With Standard Dose Cyclosporine in de Novo Renal Transplant [NCT00251004]	Phase 3	833 participants (Actual)	Interventional	2005-10-31	Completed
A Phase I Dose Escalation Study of RAD001 in Combination With Chemotherapy and Radiation in Patients With NSCLC [NCT01063478]	Phase 1	3 participants (Actual)	Interventional	2010-02-28	Terminated(stopped due to Poor accrual)
Exploring the Activity of RAD001 in Vestibular Schwannomas and Meningiomas [NCT01880749]	Early Phase 1	5 participants (Actual)	Interventional	2013-06-30	Completed
Effect of Rotational Atherectomy on Balloon-resistant Calcified Coronary Lesion the During a Long-term Follow-up Study [NCT01887704]		240 participants (Actual)	Interventional	2010-01-31	Completed
Phase II Study Assessing Everolimus as Fist Line Treatment in Patients With Metastatic Kidney Cancer of Bad Prognosis [NCT01888042]	Phase 2	61 participants (Actual)	Interventional	2011-07-31	Terminated
[NCT01895049]	Phase 4	171 participants (Actual)	Interventional	2013-08-31	Completed
EVESOR: a Phase 1 Trial of Everolimus and Sorafenib to Assess the Impact of Doses and Administration Sequences on Pharmacokinetic and Pharmacodynamic Effects of the Combination [NCT01932177]	Phase 1	60 participants (Anticipated)	Interventional	2013-04-30	Recruiting
Regulatory T Cell Modulation in Kidney Transplantation With Biologic Blockade of Dual Effector Pathways, CD28 and IL-6 (CTOT-24) [NCT04066114]	Phase 1/Phase 2	10 participants (Actual)	Interventional	2019-12-11	Completed
A Phase Ib Trial of Gemcitabine and Cisplatin With RAD001 in Patients With Metastatic Triple Negative Breast Cancer Proceeding to an Open Label Randomized Phase II Trial Comparing Gemcitabine/Cisplatin With or Without RAD001. [NCT01939418]	Phase 1/Phase 2	23 participants (Actual)	Interventional	2013-08-31	Terminated(stopped due to slow recruitment)
Intracoronary Scaffold Assessment a Randomised Evaluation of Absorb in Myocardial Infarction (ISAR-Absorb MI) A Prospective, Randomized Trial of BVS Veruss EES in Patients Undergoing Coronary Stenting for Myocardial Infarction [NCT01942070]		262 participants (Actual)	Interventional	2013-09-30	Active, not recruiting
Influence of Exceptional Patient Characteristics on Everolimus Exposure [NCT01948960]	Phase 4	56 participants (Actual)	Interventional	2013-08-31	Completed
Combination of Everolimus and Octreotide LAR in Aggressive Recurrent Meningiomas. [NCT02333565]	Phase 2	20 participants (Actual)	Interventional	2015-01-22	Completed
TRON: A Randomised, Double Blind, Placebo-controlled Study of RAD001 (Everolimus) in the Treatment of Neurocognitive Problems in Tuberous Sclerosis [NCT01954693]	Phase 2	48 participants (Anticipated)	Interventional	2012-06-30	Active, not recruiting
Treatment of Drug-Eluting Stent REstenosis Using Drug-Eluting STents vs. Drug-COated Balloon for Preventing REcurrent In-Stent Restenosis [NCT01967199]	Phase 4	175 participants (Actual)	Interventional	2013-04-18	Terminated
A Phase Ib/II, Open-Label, Multicenter, Randomized Umbrella Study Evaluating the Efficacy and Safety of Multiple Treatment Combinations in Patients With Breast Cancer (MORPHEUS- BREAST CANCER) [NCT04802759]	Phase 1/Phase 2	510 participants (Anticipated)	Interventional	2021-06-20	Recruiting
A Phase I Trial of Sirolimus or Everolimus or Temsirolimus (mTOR Inhibitor) and Vorinostat (Histone Deacetylase Inhibitor) in Patients With Advanced Cancer [NCT01087554]	Phase 1	249 participants (Anticipated)	Interventional	2010-03-31	Active, not recruiting
A Single Center, Open-label, Randomized, Controlled Pilot Trial to Evaluate the Efficacy and Safety of Everolimus Conversion Versus Standard Immunosuppression in Liver Transplant Recipients [NCT01998789]	Phase 2	50 participants (Anticipated)	Interventional	2013-10-31	Recruiting
A Phase I/II Trial of an Oral MTOR Protein Kinase Inhibitor (Everolimus, RAD001) in Combination With an Oral EGFR Tyrosine Kinase Inhibitor (Erlotinib, Tarceva™) In Patients With Metastatic Breast Cancer [NCT00574366]	Phase 1	14 participants (Actual)	Interventional	2005-12-31	Completed
Strut Coverage With SYNERGY Stents and Bioresorbable Vascular Scaffold in Acute Myocardial Infarction: An Intracoronary Optical Coherence Tomography Randomized Study [NCT02890589]		22 participants (Actual)	Interventional	2016-07-31	Completed
A Randomized Phase II Trial of Carboplatin, Paclitaxel, Bevacizumab, With or Without Everolimus for Therapy of Metastatic Malignant Melanoma [NCT00976573]	Phase 2	149 participants (Actual)	Interventional	2010-04-30	Completed
Phase IV, Open-label, Multi-center, Single-arm Study of the Safety and Efficacy of Everolimus (Afinitor) in Adult Patients With Local Advanced or Metastatic, Well Differentiated Progressive Pancreatic Neuroendocrine Tumors (pNET) in China. [NCT02842749]	Phase 4	61 participants (Actual)	Interventional	2016-03-14	Active, not recruiting
A Randomized Prospective, Multicentric, Open Label, Phase II Study Aiming to Evaluate the Efficacity and Safety of EVEROLIMUS as Neo-adjuvant Therapy in Patients With Primary or Relapsed Chondrosarcomas [NCT02008019]	Phase 2	57 participants (Anticipated)	Interventional	2014-08-14	Suspended(stopped due to The study was suspended since july 27th 2016 because of unavailability of Everolimus)
A Pilot Study of Genomic Sequencing Guided Individualized Therapy in Gastrointestinal Cancers [NCT02013089]		50 participants (Anticipated)	Interventional	2013-12-31	Recruiting
Multicenter Comparison of Early and Late Vascular Responses to Everolimus-eluting Cobalt-CHromium Stent and Platelet AggregatioN studIeS for TreatMent of Acute Myocardial Infarction: MECHANISM-AMI [NCT02014753]		100 participants (Anticipated)	Observational	2014-04-30	Completed
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)	Interventional	2013-12-31	Active, not recruiting
Incidence and Predictors for Late Acquired Stent Malaposition of Drug-Eluting-Stents With Second-Generation Permanent and Biodegradable Polymer-Coatings - a Prospective, Randomized Comparison Using Optical Coherence Tomography [NCT02018991]	Phase 4	69 participants (Actual)	Interventional	2010-10-31	Completed
Observational Study of Everolimus in Combination With Exemestane in Postmenopausal Patients With Hormone Receptor-positive, HER 2-negative Advanced Breast Cancer [NCT02023359]		7 participants (Actual)	Observational	2013-12-31	Completed
A Phase II Open-label Pilot Study Evaluating the Maintenance Therapy With Exemestane Plus Everolimus After Induction Chemotherapy in Patients With Hormone-receptor Positive Metastatic Breast Cancer [NCT02025712]	Phase 2	35 participants (Anticipated)	Interventional		Not yet recruiting
A Multicenter, Open-label, Randomized, Phase 3 Trial to Compare the Efficacy and Safety of Lenvatinib in Combination With Everolimus or Pembrolizumab Versus Sunitinib Alone in First-Line Treatment of Subjects With Advanced Renal Cell Carcinoma (CLEAR) [NCT02811861]	Phase 3	1,069 participants (Actual)	Interventional	2016-10-13	Active, not recruiting
Phase Ib, Open-label, Multi-center Study to Characterize the Safety, Tolerability and Pharmacodynamics (PD) of PDR001 in Combination With LCL161, Everolimus (RAD001) or Panobinostat (LBH589) [NCT02890069]	Phase 1	298 participants (Actual)	Interventional	2016-10-14	Completed
A Phase I/II Study of Preoperative (Neoadjuvant) Combination of Letrozole (Femara), Everolimus (Afinitor), and TRC105 in Postmenopausal Women With Newly Diagnosed Local or Locally Advanced Potentially Resectable Hormone-Receptor Positive and Her2 Negative [NCT02520063]	Phase 1/Phase 2	15 participants (Actual)	Interventional	2016-02-01	Completed
Phase II Study of Everolimus (RAD001) for the Treatment of Malignant Pleural Mesothelioma With Merlin/NF2 Loss as a Biomarker to Predict Sensitivity [NCT01024946]	Phase 2	11 participants (Actual)	Interventional	2009-12-31	Completed
Combination of Antiangiogenic Therapy Using the mTOR-inhibitor RAD001 and Low Dose Chemotherapy for Locally Advanced and/or Metastatic Pancreatic Cancer - a Dose Finding Study [NCT00560963]	Phase 1/Phase 2	21 participants (Actual)	Interventional	2007-10-31	Completed
A Phase III Trials Program Exploring the Integration of Bevacizumab, Everolimus (RAD001), and Lapatinib Into Current Neoadjuvant Chemotherapy Regimes for Primary Breast Cancer [NCT00567554]	Phase 3	2,600 participants (Actual)	Interventional	2007-10-31	Completed
Phase Ib/II Evaluation of RAD001 With Docetaxel and Bevacizumab in Patients With Metastatic Androgen Independent Prostate Cancer [NCT00574769]	Phase 1/Phase 2	27 participants (Actual)	Interventional	2010-02-17	Completed
A Phase I Study of Bevacizumab, Everolimus, and Panitumumab for Patients With Advanced Solid Tumors [NCT00586443]	Phase 1	56 participants (Actual)	Interventional	2007-11-30	Completed
Assessment of Everolimus in Addition to Calcineurin Inhibitors Reduction in Maintenance Renal Transplant Recipients [NCT00170846]	Phase 4	394 participants (Actual)	Interventional	2005-02-28	Completed
A Phase I/II Study of the Raf Kinase/VEGFR Inhibitor Sorafenib in Combination With the mTOR Inhibitor RAD001 (Everolimus) in Patients With Relapsed Non-Hodgkin Lymphoma, Hodgkin Lymphoma, or Multiple Myeloma [NCT00474929]	Phase 1/Phase 2	103 participants (Actual)	Interventional	2007-08-29	Completed
A Phase I Study to Investigate the Safety and Clinical Activity of Idelalisib in Combination With Chemotherapeutic Agents, Immunomodulatory Agents and Anti-CD20 mAb in Subjects With Relapsed or Refractory Indolent B-cell Non-Hodgkin Lymphoma, Mantle Cell [NCT01088048]	Phase 1	241 participants (Actual)	Interventional	2010-03-25	Completed
Everolimus for Treatment of Disfiguring Cutaneous Lesions in Neurofibromatosis1- CRAD001CUS232T [NCT02332902]	Phase 2	24 participants (Actual)	Interventional	2015-02-28	Completed
Expanded Access to Everolimus, for an Individual Patient With GIST (Gastrointestinal Stromal Tumors)(CTMS#18-0019) [NCT03493152]		0 participants	Expanded Access		Temporarily not available
A Randomized Phase II Study of Fulvestrant in Combination With the Dual mTOR Inhibitor AZD2014 or Everolimus or Fulvestrant Alone in Estrogen Receptor-positive Advanced or Metastatic Breast Cancer [NCT02216786]	Phase 2	333 participants (Actual)	Interventional	2014-01-31	Active, not recruiting
PNOC021: A Phase I Trial Evaluating the Combination of Trametinib and Everolimus in Pediatric and Young Adult Patients With Recurrent Low-Grade Gliomas and High Grade Gliomas [NCT04485559]	Phase 1	50 participants (Anticipated)	Interventional	2020-12-09	Recruiting
A Phase 1b Study of Abemaciclib in Combination With Therapies for Patients With Metastatic Breast Cancer [NCT02057133]	Phase 1	198 participants (Anticipated)	Interventional	2014-03-10	Active, not recruiting
A Feasibility Trial of Everolimus (RAD001),an mTOR Inhibitor, Given in Combination With Multiagent Re-Induction Chemotherapy in Pediatric Patients With Relapsed Acute Lymphoblastic Leukemia (ALL) [NCT01523977]	Phase 1	22 participants (Actual)	Interventional	2011-11-30	Completed
A Phase II Study of RAD001 in the Treatment of Patients With Plexiform Neurofibromas (PN) Associated With Neurofibromatosis Type 1 (NF1) [NCT01365468]	Phase 2	9 participants (Actual)	Interventional	2012-04-30	Terminated(stopped due to Poor patients' accrual)
Multicenter, Open-label, Randomized, 24 Months Follow-up, Two Arm Study to Compare the Efficacy of Everolimus in Improving the Cardiovascular Profile in a Regimen With Mycophenolic Acid vs. a Regimen of CNI+MPA in Maintenance Renal Transplant Recipients. [NCT01169701]	Phase 4	71 participants (Actual)	Interventional	2010-08-31	Completed
Intracoronary Stenting and Angiographic Results: Test Efficacy of 3 Limus-Eluting STents (ISAR-TEST 4): Prospective, Randomized Trial of 3-limus Agent-eluting Stents With Different Polymer Coatings [NCT00598676]	Phase 4	2,600 participants (Actual)	Interventional	2007-09-30	Completed
A Multi-centric, Open-label, Phase II Study Investigating the Combination of Afinitor With Paclitaxel and Carboplatin in First Line Treatment of Patients With Advanced (Stage IV) Large Cell Lung Cancer With Neuroendocrine Differentiation (LC-NEC) [NCT01317615]	Phase 4	49 participants (Actual)	Interventional	2011-04-30	Completed
An Open Label Randomized Phase II Study of SOM230 and Everolimus in Castrate-Resistant, Chemotherapy-Naïve Prostate Cancer Patients [NCT01313559]	Phase 2	6 participants (Actual)	Interventional	2011-06-30	Terminated(stopped due to Slow accrual)
A Phase I/II Clinical Trial of the mTor Inhibitor RAD001 (Everolimus) in Combination With Lenalidomide (Revlimid) for Patients With Relapsed or Refractory Lymphoid Malignancy [NCT01075321]	Phase 1/Phase 2	58 participants (Actual)	Interventional	2011-01-10	Completed
Phase II Trial of Everolimus or Everolimus Plus Paclitaxel as First-line Therapy in Cisplatin-ineligible Patients With Advanced Urothelial Carcinoma: Hoosier Cancer Research Network GU10-147 [NCT01215136]	Phase 2	36 participants (Actual)	Interventional	2010-12-31	Terminated(stopped due to Lack of Accrual)
A Phase I Study of RAD001 (Everolimus) + Docetaxel + Cisplatin as Induction Chemotherapy in Patients With Local-Regional Advanced Head and Neck Cancer [NCT00935961]	Phase 1	18 participants (Actual)	Interventional	2009-07-31	Completed
Multicentre, Open Study for the Setting up of Population Pharmacokinetic Models and Bayesian Estimators for Individual Dose Adjustment of Immunosuppressive Drugs (Cyclosporine, Tacrolimus, Mycophenolate Mofetil, Everolimus) During the First Year Post-graf [NCT00812786]	Phase 4	42 participants (Actual)	Interventional	2007-07-31	Completed
A Randomized, Double-masked, Parallel Group Study to Assess the Efficacy of Oral Everolimus, Either Alone or Added to Lucentis, in Patients With Neovascular Age-related Macular Degeneration [NCT00857259]	Phase 2	16 participants (Actual)	Interventional	2009-02-28	Terminated
Sorafenib Alone or in Combination With Everolimus in Patients With Unresectable Hepatocellular Carcinoma. A Randomized Multicenter Phase II Trial. [NCT01005199]	Phase 2	106 participants (Actual)	Interventional	2009-11-30	Completed
Expanded Cohort of Patients With Refractory Metastatic Colorectal Cancer (MCRC) Treated With Bevacizumab and Everolimus [NCT00597506]	Phase 2	50 participants (Actual)	Interventional	2007-10-31	Completed
A Phase I Open Label/Phase II Randomized, Double-Blind, Multicenter Trial Investigating the Combination of Everolimus and TransArterial ChemoEmbolization (TACE) With Doxorubicin in Patients With Hepatocellular Carcinoma [NCT01009801]	Phase 1/Phase 2	27 participants (Actual)	Interventional	2010-02-28	Terminated(stopped due to due to slow patient recruitement.)
Everolimus on CKD (Chronic Kidney Disease) Progression in ADPKD Patients [NCT01009957]	Phase 2/Phase 3	71 participants (Actual)	Interventional	2008-06-30	Terminated(stopped due to After primary completition date, experimental drug was no longer available)
A Phase II, Randomized, Multi-center Study, Assessing Value of Adding Everolimus (RAD001) to Trastuzumab as Preoperative Therapy of HER-2 Positive Primary Breast Cancer Amenable to Surgery. [NCT00674414]	Phase 2	82 participants (Actual)	Interventional	2008-04-30	Terminated(stopped due to IDMC decision due to accrual issue (82 pts accrued / 120 expected))
A Phase III, Randomized, Open-Label, Multicenter Study Evaluating the Efficacy and Safety of Giredestrant Plus Everolimus Compared With The Physician's Choice of Endocrine Therapy Plus Everolimus in Patients With Estrogen Receptor-Positive, HER2-Negative, [NCT05306340]	Phase 3	320 participants (Anticipated)	Interventional	2022-08-03	Recruiting
LAte Stent Strut APPosition and COverage After Drug-Eluting Stent ImplantaTIOn by Optical Coherence Tomography in PatieNts With Acute Myocardial Infarction II(APPOSITION-AMI II) [NCT02770651]		69 participants (Anticipated)	Observational	2016-05-31	Enrolling by invitation
Everolimus Versus Sunitinib Therapy in Patients With Advanced Non-clear Cell Renal Cell Carcinoma [NCT01185366]	Phase 2	73 participants (Actual)	Interventional	2010-08-31	Terminated
XIENCE V® Everolimus Eluting Coronary Stent System India Post-marketing Single-Arm Study [NCT00631228]		1,000 participants (Actual)	Observational	2008-06-30	Completed
Phase I/II Study of BNC105P in Combination With Everolimus or Following Everolimus For Progressive Metastatic Clear Cell Renal Cell Carcinoma Following Prior Tyrosine Kinase Inhibitors [NCT01034631]	Phase 1/Phase 2	154 participants (Actual)	Interventional	2010-01-31	Completed
Phase II Study of Cisplatinum and Everolimus in Patients With Metastatic or Unresectable Neuroendocrine Carcinomas (NEC) of Extrapulmonary Origin [NCT02695459]	Phase 2	39 participants (Actual)	Interventional	2016-03-30	Active, not recruiting
Everolimus-eluting Bioresorbable Vascular Scaffolds Versus Everolimus-eluting Stents in Patients With Chronic Total Occlusion [NCT02739685]		17 participants (Actual)	Interventional	2016-09-30	Terminated(stopped due to Slow enrollment, access to devices)
A 12 Month, Multi-center, Randomized, Open-label Non-inferiority Study Comparing Safety and Efficacy of Concentration-controlled Everolimus With Low Dose Tacrolimus to Mycophenolate Mofetil With Standard Dose Tacrolimus in de Novo Renal Transplant Recipie [NCT01025817]	Phase 3	613 participants (Actual)	Interventional	2010-01-31	Completed
A Sequential Phase I Study Of The Combination Of Everolimus (Rad001) With 5-Fu/Lv (De Gramont), Folfox6, And Folfox6/Panitumumab In Patients With Refractory Solid Malignancies [NCT00610948]	Phase 1	74 participants (Actual)	Interventional	2008-03-31	Completed
Everolimus (RAD001) Therapy for Epilepsy in Patients With Tuberous Sclerosis Complex [NCT01070316]	Phase 1/Phase 2	20 participants (Actual)	Interventional	2010-01-31	Completed
A Phase I Dose Finding Study of Everolimus (RAD001) in Elderly Patients With Acute Myeloid Leukemia (AML) Unfit for Intensive Induction Chemotherapy [NCT00636922]	Phase 1	40 participants (Anticipated)	Interventional	2010-02-28	Active, not recruiting
A Phase II Biomarker Trial of Everolimus in Patients With Advanced Renal Cell Carcinoma [NCT00827359]	Phase 2	25 participants (Actual)	Interventional	2009-03-31	Completed
A Phase 2 Study to Evaluate the Efficacy of Epigenetic Modulation in Relapsed/Refractory Diffuse Large B-Cell Lymphoma (DLBCL) [NCT00978432]	Phase 2	50 participants (Actual)	Interventional	2012-02-29	Terminated(stopped due to The toxicity seemed to outweigh the benefit.)
Selection of Chemoradiotherapy Based on Response to Induction Chemotherapy - a Phase II Study in Locally Advanced Squamous Cell Carcinoma of Head and Neck [NCT01133678]	Phase 2	50 participants (Actual)	Interventional	2010-05-04	Terminated(stopped due to Primary endpoint reached futility boundary)
An Open-Label, Multi-Center, Expanded Access Study of RAD001 in Patients With Metastatic Carcinoma of the Kidney Who Are Intolerant of or Have Progressed Despite Any AvailableVascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitor Therapy [NCT00655252]		0 participants	Expanded Access		No longer available
Phase II Study of RAD001 in a Neoadjuvant Setting in Men With Intermediate or High Risk Prostate Cancer [NCT00657982]	Phase 2	15 participants (Anticipated)	Interventional	2008-04-30	Recruiting
Efficacy and Safety of Certican® (Everolimus) in Combination With Myfortic® (EC-MPS, Enteric-coated Mycophenolate Sodium) After Early CNI Elimination Versus Myfortic® in Combination With Prograf® in Renal Transplant Recipients [NCT00965094]	Phase 4	36 participants (Actual)	Interventional	2009-12-31	Completed
Topical Everolimus Versus Placebo for the Treatment of Facial Angiofibromas in Patients With Tuberous Sclerosis Complex. A Phase II/III, Multicentre, Randomized, Double-blind, Placebo-controlled Study of 3 Doses of Topical Everolimus. [NCT02860494]	Phase 2/Phase 3	0 participants (Actual)	Interventional	2020-12-31	Withdrawn(stopped due to Pharmaceutical and financial difficulties)
A Phase I Study of Cisplatin, Paclitaxel, and RAD001 Patients With Metastatic Breast Cancer [NCT00680758]	Phase 1	18 participants (Actual)	Interventional	2008-05-31	Completed
An Expanded Phase I Study of Pazopanib and Everolimus in Patients With Advanced Solid Tumors and Previously Treated Advanced Urothelial Cancer [NCT01184326]	Phase 1	23 participants (Actual)	Interventional	2011-01-31	Completed
A Randomized, Double-blind, Placebo Controlled, Phase II Study of Everolimus in Combination With Exemestane in the Treatment of Chinese Postmenopausal Women With Estrogen Receptor Positive, HER-2 Negative, Locally Advanced, Recurrent, or Metastatic Breast [NCT03312738]	Phase 2	159 participants (Actual)	Interventional	2017-09-15	Completed
[NCT02796157]		950 participants (Anticipated)	Interventional	2016-06-30	Recruiting
Phase II Examination of Irinotecan, Cetuximab and Everolimus to Chemotherapy Resistent Patients With Metastatic Colorectal Cancer and KRAS Mutations or After Progression With KRAS Wildtype on Irinotecan and Cetuximab - Effect and Biological Markers [NCT01387880]	Phase 2	100 participants (Actual)	Interventional	2010-01-31	Completed
A Single Arm, Multicenter Phase II a Trial of RAD001 as Monotherapy in the Treatment of Neurofibromatosis 1 Related Internal Plexiform Neurofibromas That Cannot be Removed by Surgery [NCT01412892]	Phase 2	30 participants (Actual)	Interventional	2011-04-30	Completed
Terapia Con Everolimus Nel Trapianto de Novo di Fegato: Uno Studio Multicentrico Randomizzato [NCT01423708]	Phase 2	117 participants (Anticipated)	Interventional	2010-02-28	Recruiting
A Phase 1b/2 Study of Retaspimycin HCl (IPI-504) in Combination With Everolimus in Patients With KRAS Mutant NSCLC [NCT01427946]	Phase 1/Phase 2	47 participants (Actual)	Interventional	2011-07-31	Completed
Plasmonic Photothermal and Stem Cell Therapy of Atherosclerosis With The Use of Gold Nanoparticles With Iron Oxide-Silica Shells Versus Stenting [NCT01436123]	Phase 1	62 participants (Actual)	Interventional	2010-12-31	Terminated(stopped due to The study was terminated under the political pressure of the Federal Security Service of the Russian Federation (FSB) and the Russian Society of Cardiology)
P3 Efficacy Evaluation of Enobosarm in Combo With Abemaciclib Compared to Estrogen Blocking Agent for 2nd Line Treatment of ER+HER2- MBC in Patients Who Have Shown Previous Disease Progression on an Estrogen Blocking Agent Plus Palbociclib [NCT05065411]	Phase 3	186 participants (Anticipated)	Interventional	2022-04-11	Active, not recruiting
A Phase I Study of Weekly Low-Dose Cisplatin Plus Escalating Doses of Oral RAD001(Everolimus) for Patients With Advanced Solid Tumors [NCT00423865]	Phase 1	30 participants (Actual)	Interventional	2006-11-30	Completed
Multicenter, Randomized, Open-label Trial to Evaluate the Safety, Tolerability and Efficacy of Two Regimens of Everolimus Plus Cyclosporine Microemulsion, Given According to Different Blood Target Levels, in de Novo Renal Transplant Recipients [NCT00170885]	Phase 4	0 participants	Interventional	2005-05-31	Completed
A Phase II Trial of RAD001 in Patients With Recurrent Glioblastoma Multiforme [NCT00515086]	Phase 2	41 participants (Actual)	Interventional	2007-08-31	Terminated(stopped due to Early termination due to slow enrollment and protocol-defined stopping rule.)
RESOLUTE-III All-comers Trial: A Randomized Comparison of a Zotarolimus-Eluting Stent With an Everolimus-Eluting Stent for Percutaneous Coronary Intervention [NCT00617084]	Phase 4	2,292 participants (Actual)	Interventional	2008-04-30	Completed
Phase II Study of Low-dose RAD001(Everolimus) Plus Cisplatin and HDFL (Weekly 24-Hour Infusion of High-dose 5-Fluorouracil and Leucovorin) Chemotherapy for First-line Treatment of Unresectable, Recurrent or Metastatic Gastric Cancer [NCT00632268]	Phase 2	40 participants (Actual)	Interventional	2008-02-29	Completed
A Randomised Pilot Study of Neoadjuvant Everolimus Plus Letrozole Compared With FEC in Postmenopausal Patients With ER-positive, HER2-negative Breast Cancer [NCT02742051]	Phase 2	40 participants (Actual)	Interventional	2016-06-30	Completed
A Phase 1 Study of RAD001 in Combination w/ Cetuximab and Cisplatin as First-line Therapy in Recurrent & Metastatic Squamous Cell Cancer of the Head & Neck [NCT01009346]	Phase 1/Phase 2	9 participants (Actual)	Interventional	2009-10-31	Terminated(stopped due to Toxicity)
Phase II Trial of RAD001 in Relapsed/Refractory Multiple Myeloma [NCT00618345]	Phase 2	35 participants (Anticipated)	Interventional	2005-03-31	Completed
A Phase I Pilot Study of the Oral mTOR Inhibitor RAD001 in Combination With Capecitabine for Metastatic Breast Cancer [NCT00473005]	Phase 1	18 participants (Actual)	Interventional	2007-08-31	Terminated(stopped due to Principal Investigator (Dr. Guardino) left Stanford)
A Pilot, Rapid Sequencing of First Line Cabozantinib, Ipilimumab and Nivolumab, and Lenvatinib and Everolimus in Patients With Metastatic or Unresectable Clear Cell Renal Cell Carcinoma [NCT05188118]	Early Phase 1	20 participants (Anticipated)	Interventional	2023-02-24	Recruiting
An Open-Label, Single-arm, Phase Ib/II Study of AEB071 (a Protein Kinase C Inhibitor) and Everolimus (mTOR Inhibitor) in Patients With CD79-mutant or ABC Subtype Diffuse Large B-Cell Lymphoma [NCT01854606]	Phase 1	31 participants (Actual)	Interventional	2013-12-05	Completed
[NCT01856374]	Phase 4	60 participants (Actual)	Interventional	2011-08-31	Completed
Phase II Study of the Levonorgestrel Intrauterine Device Alone or in Combination With the mTORC1 Inhibitor, Everolimus, for the Treatment of Complex Atypical Hyperplasia and Stage Ia Grade 1 Endometrial Cancer [NCT02397083]	Phase 2	270 participants (Anticipated)	Interventional	2015-09-23	Recruiting
[NCT01857843]	Phase 4	160 participants (Actual)	Interventional	2009-11-30	Completed
Amsterdam Investigator-initiateD Absorb Strategy All-comers Trial (AIDA Trial): A Clinical Evaluation Comparing the Efficacy and Performance of ABSORB™ Everolimus Eluting Bioresorbable Vascular Scaffold Strategy Versus the XIENCE Family (XIENCE PRIME™ or [NCT01858077]		1,845 participants (Actual)	Interventional	2013-08-31	Active, not recruiting
Open Label, Non-randomized, Phase 2 Study Investigating the Effect of RAD001 Monotherapy in Patients With Advanced NSCLC Previously Treated With Either Chemotherapy Only or With Chemotherapy and EGFR Inhibitor(s) [NCT00124280]	Phase 2	85 participants (Actual)	Interventional	2005-07-31	Completed
Phase I Study of TheraSphere and Everolimus Among Patients With Neuroendocrine Tumors and Liver Only or Liver Dominant Disease [NCT01864070]	Phase 1	0 participants (Actual)	Interventional	2014-05-31	Withdrawn
Everolimus (RAD001)Therapy of Giant Cell Astrocytomas in Patients With Tuberous Sclerosis Complex [NCT00411619]	Phase 1/Phase 2	28 participants (Actual)	Interventional	2007-01-31	Completed
SCHEDULE - Scandinavian Heart Transplant Everolimus de Novo Study With Early CNI Avoidance [NCT01266148]	Phase 4	115 participants (Actual)	Interventional	2009-11-30	Completed
Phase III Multicenter Open-label Randomized Clinical Trial Comparing Everolimus and Low Dose Tacrolimus to Tacrolimus and Mycophenolate Mofetil at 6 mo Post-Transplant to Prevent Long-term Complications After Pediatric Heart Transplantation [NCT03386539]	Phase 3	211 participants (Actual)	Interventional	2018-01-29	Active, not recruiting
A Pilot Study Comparing the Safety and Efficacy of Zortress (Everolimus) With Low Dose Tacrolimus to Early Conversion to Calcineulin Inhibitor-Free Regimen and Mycophenolic Acid With Standard Dose Tacrolimus in Recipients of ECD/DCD Kidneys [NCT01878786]	Phase 2/Phase 3	25 participants (Actual)	Interventional	2013-06-30	Terminated(stopped due to Interim results suggested a concern for patient outcomes and safety)
Pilot Study of mTOR Inhibitor Therapy for Treatment of Intestinal Polyps in Peutz-Jeghers Syndrome [NCT00811590]	Phase 2	3 participants (Actual)	Interventional	2008-11-30	Terminated(stopped due to The study was ended early due to low enrollment.)
Phase IB/II Study of Pasireotide, Everolimus and Selective Internal Radioembolization Therapy (SIRT) for Unresectable Neuroendocrine Hepatic Metastases [NCT01469572]	Phase 1	13 participants (Actual)	Interventional	2011-12-31	Completed
Randomized Comparison of the Effects of PLatinum Chromium Everolimus-eluting Stent vs. cobAlT Chromium Everolimus-eluting Stent on inFlammatOry maRkers and Endothelial daMage - The PLATFORM Trial [NCT01489202]	Phase 4	100 participants (Anticipated)	Interventional	2014-09-30	Not yet recruiting
A Single Arm, Single Center, Phase II Trial of RAD001 as Monotherapy in the Treatment of Neurofibromatosis Type 2 - Related Vestibular Schwannoma [NCT01490476]	Phase 2	10 participants (Actual)	Interventional	2012-01-31	Completed
Phase I/IIB Study of Induction Chemotherapy With XELOX, Followed by Radiation Therapy and Dose Escalation of RAD001 in Patients With Esophageal Cancer [NCT01490749]	Phase 1	17 participants (Actual)	Interventional	2012-02-29	Completed
A Phase 1/2 Study of Lenvatinib in Combination With Everolimus in Recurrent and Refractory Pediatric Solid Tumors, Including CNS Tumors [NCT03245151]	Phase 1/Phase 2	64 participants (Actual)	Interventional	2017-11-16	Completed
PhaseII,Open-label,Pilot Study Evaluating the Safety+Efficacy of Certican ® in the Prevention of Chronic Graft-versus-host Disease+Late Pulmonary Complications After Allogeneic Hematopoietic Cell Transplantation Blood [NCT01509560]	Phase 2	21 participants (Actual)	Interventional	2011-11-01	Completed
Phase I/II Trial of RAD001 Plus Nexavar® For Patients With Metastatic Renal Cell Carcinoma [NCT00448149]	Phase 1/Phase 2	55 participants (Actual)	Interventional	2006-12-31	Completed
A Combined Phase 1 and 2 Study Investigating the Combination of RAD001 and Erlotinib in Patients With Advanced NSCLC Previously Treated Only With Chemotherapy [NCT00456833]	Phase 1	248 participants (Actual)	Interventional	2005-06-30	Completed
Reduction or Discontinuation of Calcineurine Inhibitors With Conversion to Everolimus-Based Immunosuppresion to Alleviate Chronic Allograft Nephropathy (CAN) in Kidney Transplant Recipients: A Prospective Randomized Study [NCT00443508]	Phase 4	60 participants	Interventional	2007-02-28	Recruiting
RAD001 Therapy of Angiomyolipomata in Patients With Tuberous Sclerosis Complex and Sporadic Lymphangioleiomyomatosis [NCT00457964]	Phase 1/Phase 2	36 participants (Actual)	Interventional	2005-08-31	Completed
A Phase II Randomized, Double-blinded, Multicenter Asian Study Investigating the Combination of Transcatheter Arterial Chemoembolization (TACE) and Oral Everolimus (RAD001, Afinitor®) in Localised Unresectable Hepatocellular Carcinoma (HCC) - The TRACER S [NCT01379521]	Phase 2	65 participants (Actual)	Interventional	2011-06-30	Terminated(stopped due to The study was terminated due to low enrollment. This resulted in the study being underpowered and inconclusive.)
[NCT01605721]	Phase 4	2,000 participants (Anticipated)	Interventional	2011-05-31	Recruiting
An Open-label, Multicenter Phase 1 Study Investigating the Combination of RAD001, Cetuximab and Irinotecan as Second-line Therapy After FOLFOX (or XELOX) Plus Bevacizumab (if Given as Part of Local Standard Practice) in Patient With Metastatic Colorectal [NCT00478634]	Phase 1	19 participants (Actual)	Interventional	2007-05-31	Completed
Comparison Between Drug-Eluting Stents for the Treatment of the Diffuse Type In-Stent Restenosis After Drug-Eluting Stents Implantation: Sirolimus-Eluting vs. Paclitaxel-Eluting Stents [NCT00485030]	Phase 4	60 participants (Actual)	Interventional	2007-03-31	Completed
A 12 Month Open-label, Randomized, Multicenter, Sequential Cohort-group, Dose Finding Study to Evaluate the Efficacy, Safety and Tolerability of Oral AEB071 Versus Cyclosporine in Combination With Everolimus, Basiliximab and Corticosteroids in de Novo Adu [NCT00504543]	Phase 2	311 participants (Actual)	Interventional	2007-07-31	Completed
A 2-year Extension to a 1-year Multicenter, Randomized, Open Label, Parallel Group Study of the Safety, Tolerability and Efficacy of Two Doses (1.5 and 3 mg/Day) of Everolimus With Steroids and Optimized Administration of Cyclosporine in de Novo Renal Tra [NCT00531063]	Phase 3	237 participants (Anticipated)	Interventional	2001-11-30	Completed
Phase I / Randomized Phase II Study of Second Line Therapy With Irinotecan and Cetuximab With or Without RAD001, an Oral mTOR Inhibitor for Patients With Metastatic Colorectal Cancer: Hoosier Oncology Group GI05-102 [NCT00522665]	Phase 1/Phase 2	41 participants (Actual)	Interventional	2007-08-31	Completed
A 2 Year Extension to a 1 Year Multicenter, Randomized, Open Label, Parallel Group Study of the Safety, Tolerability and Efficacy of Two Doses (1.5 and 3 mg/Day) of Everolimus (RAD001) With Basiliximab, Corticosteroids and Optimized Administration of Cycl [NCT00531440]	Phase 3	256 participants (Actual)	Interventional	2001-11-30	Completed
A Prospective, Multi-Center, Single-Blinded, Randomized Trial of the Sirolimus-Eluting Iron Bioresorbable Coronary Scaffold System in Patients With Coronary Artery Disease: IRONMAN-II [NCT05206084]		518 participants (Actual)	Interventional	2022-03-10	Active, not recruiting
Phase 2 Study Assessing the Tolerance and Efficacy of Tamoxifen Alone Versus the Association Tamoxifen-RAD001 (Everolimus) in Patients With Anti-aromatase Resistant Breast Metastatic Cancer [NCT01298713]	Phase 2	111 participants (Actual)	Interventional	2008-03-31	Completed
A Phase 1b/2 Study of Imatinib in Combination With Everolimus in Synovial Sarcoma [NCT01281865]	Phase 1/Phase 2	14 participants (Actual)	Interventional	2011-01-31	Completed
Comparison of Everolimus- and Biolimus-Eluting Stents With Everolimus-Eluting Bioresorbable Vascular Scaffold Stents [NCT01711931]	Phase 4	240 participants (Actual)	Interventional	2012-10-31	Completed
Ph1 Study of the Safety, PK, and PDn of Escalating Oral Doses of the Glutaminase Inhibitor CB-839, as a Single Agent and in Combination With Standard Chemotherapy in Patients With Advanced and/or Treatment-Refractory Solid Tumors [NCT02071862]	Phase 1	210 participants (Actual)	Interventional	2014-02-28	Completed
Phase IV: Effect of Everolimus and CNI Minimalization on Renal Function. [NCT00596557]	Phase 4	20 participants (Actual)	Interventional	2008-02-29	Completed
Phase I-II Study of Trastuzumab in Combination With RAD001 in Patients With HER-2 Overexpressing, PTEN-deficient Metastatic Breast Cancer Progressing on Trastuzumab-Based Therapy [NCT00317720]	Phase 1/Phase 2	40 participants (Actual)	Interventional	2006-04-30	Completed
An Exploratory, Open-label, Non-randomized, Within-patient Multiple Dose-escalation Safety, Tolerability, PK and Efficacy Trial of RAD001 (Everolimus) in Patients With Lymphangioleiomyomatosis [NCT01059318]	Phase 2	24 participants (Actual)	Interventional	2010-01-31	Completed
A Multi Center Randomized Control Study of MeRes100 Sirolimus Eluting BioResorbable Vascular Scaffold System in Treatment of Coronary Artery Disease Patients: MeRes - China. [NCT03454724]		484 participants (Anticipated)	Interventional	2020-01-01	Not yet recruiting
Cytokines Evaluation in Early Calcineurin Inhibitors Withdrawn on Renal Transplant [NCT01239472]	Phase 4	30 participants (Actual)	Interventional	2011-01-31	Completed
A Single-arm, Open-label and Multi-center Phase I Study on Safety, Tolerance and Pharmacokinetics of HRS-8080 Tablets Monotherapy and Combined With Other Anti-cancer Therapy in Patients With Metastatic or Local Advanced Breast Cancer [NCT05189717]	Phase 1	156 participants (Anticipated)	Interventional	2022-02-17	Enrolling by invitation
Phase I Trial of Everolimus, Pomalidomide and Dexamethasone in Patients With Relapsed/Refractory Multiple Myeloma [NCT01889420]	Phase 1	1 participants (Actual)	Interventional	2014-07-31	Terminated(stopped due to Low accrual)
Zortress (Everolimus) to Prevent Alloantibody Formation in Patients With Late Stage Renal Allograft Failure: The Everolimus-Transplant Exit Strategy Trial (E-TEST) [NCT01636466]	Phase 3	1 participants (Actual)	Interventional	2013-06-30	Terminated(stopped due to Feasibility)
ABSORB II RANDOMIZED CONTROLLED TRIAL A Clinical Evaluation to Compare the Safety, Efficacy and Performance of ABSORB Everolimus Eluting Bioresorbable Vascular Scaffold System Against XIENCE Everolimus Eluting Coronary Stent System in the Treatment of Sub [NCT01425281]		501 participants (Actual)	Interventional	2011-11-30	Completed
A Phase II Study to Evaluate the Safety and Efficacy of RAD001 Plus Erlotinib in Patients With Well- to Moderately-Differentiated Neuroendocrine Tumors [NCT00843531]	Phase 2	17 participants (Actual)	Interventional	2009-06-25	Terminated(stopped due to Low Accrual)
Randomized Open Label Study to Compare the Efficacy and Safety of Everolimus Followed by Chemotherapy With Streptozotocin- Fluorouracilo (STZ-5FU) Upon Progression or the Reverse Sequence, in Advanced Progressive Pancreatic NETs (pNETs) [NCT02246127]	Phase 3	141 participants (Actual)	Interventional	2014-10-27	Completed
A Phase 3, Randomized, Controlled Study of Cabozantinib (XL184) vs Everolimus in Subjects With Metastatic Renal Cell Carcinoma That Has Progressed After Prior VEGFR Tyrosine Kinase Inhibitor Therapy [NCT01865747]	Phase 3	658 participants (Actual)	Interventional	2013-06-30	Completed
A Randomized, Double-Blind, Placebo-Controlled Phase II Trial of Weekly Paclitaxel/Bevacizumab +/- Everolimus as First-Line Chemotherapy for Patients With HER2-Negative Metastatic Breast Cancer (MBC) [NCT00915603]	Phase 2	113 participants (Actual)	Interventional	2009-07-31	Completed
The Efficacy and Safety of CM082 Combined With Everolimus in Chinese Patients With Metastatic Renal Cell Carcinoma: a Randomized, Double-blind, Double Dummy, Multicenter Study [NCT03095040]	Phase 3	390 participants (Anticipated)	Interventional	2016-12-16	Active, not recruiting
A Phase I/II Study of LEE011 Plus Everolimus in Patients With Metastatic Pancreatic Adenocarcinoma Refractory to Chemotherapy [NCT02985125]	Phase 1/Phase 2	44 participants (Anticipated)	Interventional	2017-05-04	Active, not recruiting
A Phase II Study of Everolimus in Combination With Paclitaxel and Carboplatin in Patients With Metastatic Melanoma [NCT01014351]	Phase 2	70 participants (Actual)	Interventional	2010-02-28	Completed
5, 6 or 7 Year Follow-up Control After the SCHEDULE Study (SCANDINAVIAN HEART TRANSPLANT EVEROLIMUS DE NOVO STUDY WITH EARLY CNI AVOIDANCE) [NCT02864706]	Phase 4	95 participants (Actual)	Interventional	2016-01-18	Completed
Conversion From MPA to Zortress (Everolimus) for GI Toxicity Post-renal Transplantation [NCT02974686]	Phase 4	1 participants (Actual)	Interventional	2016-11-30	Terminated(stopped due to low recruitment)
A Phase I-II, Open-label Study of RAD001 in Combination With Glivec®/Gleevec™ (Imatinib) in Patients With Glivec/Gleevec-refractory/Resistant Gastrointestinal Stromal Tumors. [NCT01275222]	Phase 1/Phase 2	117 participants (Actual)	Interventional	2002-11-13	Completed
Randomized ph. II Study to Explore Efficacy and Feasibility of Upfront Rotations Between SUNitinib and Everolimus vs Sequential Treatment of 1st lIne Sunitinib & 2nd Line EverolimuS Until Progression in Pats Met. Clear Cell Renal Cancer [NCT01784978]	Phase 2	41 participants (Actual)	Interventional	2013-02-12	Terminated(stopped due to Lack of recruitment)
A Prospective, Single-center, Open-label, Pilot Study to Investigate the Effect of Switching to Certican® in Viremia of Hepatitis C Virus in Adult Renal Allograft Recipients. [NCT01469884]	Phase 4	30 participants (Actual)	Interventional	2011-11-30	Completed
A Phase II Trial of RAD001 (Everolimus) for 2nd Line Treatment After Failure of Fluoropyrimidine Plus Platinum Chemotherapy in Patients With Metastatic or Recurrent Gastric Cancer With pS6 Ser 240/4 Expression [NCT01482299]	Phase 2	45 participants (Actual)	Interventional	2011-11-30	Completed
Six-month, Multicenter, Randomized, Open-label Study of the Safety, Tolerability and Efficacy of Two Neoral Doses in Addition to Certican and Steroids in de Novo Heart Transplant Recipients [NCT00098007]	Phase 3	199 participants (Actual)	Interventional	2004-08-09	Completed
Multicenter Trial of the Safety & Efficacy of Certican in Pediatric de Novo Renal Transplant Patients [NCT00098241]	Phase 3	45 participants (Anticipated)	Interventional	2000-06-30	Completed
Phase II Trial Of RAD-001 In Metastatic Malignant Melanoma [NCT00098553]	Phase 2	53 participants (Actual)	Interventional	2005-04-30	Completed
Randomized 2x2 Factorial Trial Comparing the Cre8 Amphilimus-sirolimus Eluting Stent vs. the Synergy Everolimus-eluting Stent and a Personalized vs. Standard Duration of Dual Antiplatelet Therapy in All-comers Patients Undergoing Percutaneous Coronary Int [NCT04135989]	Phase 4	2,106 participants (Anticipated)	Interventional	2020-01-01	Active, not recruiting
Pilot Study on the Determination of Intratumoral Concentrations of Kinase Inhibitors in Patients With Advanced Solid Malignancies. [NCT01636908]		43 participants (Actual)	Interventional	2011-08-31	Completed
A Phase 2, Double-blind, Randomized, Placebo-controlled, Multi-center Study Assessing the Value of Adding Everolimus to Letrozole as Preoperative Therapy of Primary Breast Cancer in Postmenopausal Women [NCT00107016]	Phase 2	267 participants (Actual)	Interventional	2005-03-31	Completed
A One-Year, Single-Center, Prospective, Open-Label Study of the Safety, Tolerability, and Preliminary Efficacy of Anti-Thymocyte Globulin, Cyclosporine, and RAD in Type 1 Diabetic Islet Transplant Recipients [NCT00286624]	Phase 1/Phase 2	6 participants (Actual)	Interventional	2003-03-31	Completed
Levels of Circulating Tumor DNA as a Predictive Marker for Early Switch in Treatment for Patients With Metastatic (Stage IV) Breast Cancer: A Phase 2 Randomized, Open-Label Study [NCT05826964]	Phase 2	500 participants (Anticipated)	Interventional	2023-06-12	Recruiting
XIENCE Skypoint Large Vessel Post Approval Study [NCT05423379]		100 participants (Anticipated)	Observational	2022-09-14	Recruiting
Multicenter Randomized Two-arms Study Evaluating the BK Viral Clearance in Kidney Transplant Recipients With BK Viremia After Reduction of Immunosuppression Alone vs. Reduction of Immunosuppression and Replacement of Mycophenolate Mofetil by Everolimus [NCT03216967]	Phase 4	130 participants (Actual)	Interventional	2018-01-15	Active, not recruiting
A Phase 2 Study of Dasatinib in Combination With Everolimus for Children With Gliomas Harboring PDGFR Alterations [NCT03352427]	Phase 2	3 participants (Actual)	Interventional	2017-12-06	Terminated(stopped due to Low accrual)
A Phase I-II, Study of RAD001 in Combination With Imatinib (Glivec®/Gleevec™) in Patients With Chronic Myelogenous Leukemia (CML) in Chronic Phase Who Are Not In Complete Cytogenetic Response to Imatinib-Alone at Study Entry [NCT00093639]	Phase 1/Phase 2	0 participants	Interventional	2004-08-31	Completed
A Phase I Study Investigating Everolimus and Dovitinib in Metastatic Clear Cell Renal Cancer [NCT01714765]	Phase 1	17 participants (Actual)	Interventional	2011-04-30	Completed
Phase II Study Evaluating the Combination of Everolimus and Sorafenib in the Treatment of Thyroid Cancer [NCT01141309]	Phase 2	41 participants (Actual)	Interventional	2010-06-30	Active, not recruiting
Reservoir-Based Polymer-Free Amphilimus-Eluting Stent Versus Polymer-Based Everolimus-Eluting Stent in Diabetic Patients (RESERVOIR) Trial [NCT01710748]	Phase 3	112 participants (Anticipated)	Interventional	2012-10-31	Active, not recruiting
A Phase IB/II Multicenter, Two-Arm, Dose-Escalation Study of Oral AEE788 Administered in Combination With Oral RAD001 on a Continuous Once Daily Dosing Schedule in Adult Patients With First or Second Recurrent or Relapsing Glioblastoma Multiforme [NCT00107237]	Phase 1/Phase 2	16 participants (Actual)	Interventional	2003-10-31	Completed
RADAR: A Randomized Discontinuation Phase II Study to Determine the Efficacy of RAD001 in Breast Cancer Patients With Bone Metastases [NCT00466102]	Phase 2	130 participants (Anticipated)	Interventional	2006-12-31	Active, not recruiting
Monocenter, Double Blinded, Prospective, Randomized Placebo Controlled Study Investigating Prevention of Major Adverse Cardiac Events (MACEs) Within 6 Months by Systemic Treatment With Everolimus After Coronary Intervention With Bare Metal Stents in Patie [NCT00426049]	Phase 3	484 participants	Interventional	2006-10-31	Recruiting
Phase II Study of RAD001 (Everolimus) in Patient's With Metastatic Renal Cell Cancer [NCT00446368]	Phase 2	66 participants (Actual)	Interventional	2005-05-31	Completed
Prophylaxis of the Graft-Versus-Host-Disease in Patients After Allogeneic Stem Cell Transplantation With a Combination of Tacrolimus and Everolimus [NCT00117702]	Phase 2/Phase 3	24 participants (Actual)	Interventional	2005-10-31	Terminated(stopped due to safety reasons)
A Single Arm, Open-label Multicenter Phase II Trial of Everolimus in Patients With Relapsed/Refractory Germ Cell Cancer [NCT01242631]	Phase 2	25 participants (Actual)	Interventional	2010-11-30	Completed
SPIRIT V: A Clinical Evaluation of the XIENCE V® Everolimus Eluting Coronary Stent System in the Treatment of Patients With de Novo Coronary Artery Lesions [NCT00402272]	Phase 4	2,700 participants (Actual)	Interventional	2006-11-30	Completed
Phase I Study of Patupilone and RAD001 in Patients With Refractory Solid Tumor Malignancy [NCT00496600]	Phase 1	42 participants (Actual)	Interventional	2007-07-31	Completed
A Phase II Study of Everolimus in Combination With Imatinib in Metastatic Melanoma [NCT00402662]	Phase 2	3 participants (Actual)	Interventional	2006-02-28	Terminated(stopped due to unexpected level of toxicity)
A Randomized, Double-blind, Multi-center Phase III Study Evaluating Paclitaxel With and Without RAD001 in Patients With Gastric Carcinoma Who Have Progressed After Therapy With a Fluoropyrimidine-containing Regimen [NCT01248403]	Phase 3	300 participants (Actual)	Interventional	2011-10-31	Completed
A Phase I Study Investigating the Combination of RAD001 With Standard Induction and Consolidation Therapy in Older Patients With Newly Diagnosed Acute Myeloid Leukemia (AML) [NCT01154439]	Phase 1	11 participants (Actual)	Interventional	2010-10-31	Completed
Efficacy and Safety of Everolimus to SAve REnal Function (SAREFU) in Long Term Heart Transplanted Patients [NCT00505102]	Phase 4	200 participants (Anticipated)	Interventional	2007-01-31	Active, not recruiting
PNOC 001: Phase II Study of Everolimus for Recurrent or Progressive Low-grade Gliomas in Children [NCT01734512]	Phase 2	65 participants (Actual)	Interventional	2012-12-13	Active, not recruiting
Trial of RAD001 in Patients With Operable Non-Small Cell Lung Cancer (NSCLC) [NCT00401778]	Phase 1	33 participants (Actual)	Interventional	2006-11-30	Completed
A Phase 1b Trial of LY2584702 in Combination With Erlotinib or Everolimus in Patients With Solid Tumors [NCT01115803]	Phase 1	29 participants (Actual)	Interventional	2010-03-31	Terminated(stopped due to Primary objective has been met; safety and pharmacokinetics have been characterized.)
Circulating Tumor Cells and Tumor DNA in HCC and NET - Patient-specific Biomarkers for Clinical Decision Support and Tailored Relapse Diagnostics [NCT02973204]		167 participants (Actual)	Observational [Patient Registry]	2016-11-30	Completed
Phase II Trial of Bicalutamide and RAD001 in Patients With Hormone-Independent Prostatic Adenocarcinoma (HIPC) After the First-Line Androgen Deprivation Therapy [NCT00814788]	Phase 2	24 participants (Actual)	Interventional	2008-12-31	Completed
Phase I/II of Panobinostat (LBH589) Plus Everolimus (RAD001) in Patients With Relapsed and Refractory Lymphoma [NCT00967044]	Phase 1/Phase 2	31 participants (Actual)	Interventional	2009-11-30	Completed
Phase II Study of Everolimus (RAD001) in Primary Therapy of Waldenstrom's Macroglobulinemia [NCT00976248]	Phase 2	33 participants (Actual)	Interventional	2009-11-30	Completed
[NCT01093300]	Phase 4	264 participants (Anticipated)	Interventional		Not yet recruiting
Randomized Phase III Trial Comparing Everolimus Versus Everolimus Plus Bevacizumab for Advanced Renal Cell Carcinoma Progressing After Treatment With Tyrosine Kinase Inhibitors [NCT01198158]	Phase 3	77 participants (Actual)	Interventional	2010-09-15	Terminated
Efficacy, Safety and Patient-reported Outcomes of Peptide Receptor Radionuclide Therapy With 177Lu-edotreotide Compared to Everolimus in Somatostatin Receptor Positive Neuroendocrine Tumors of the Lung and Thymus. [NCT05918302]	Phase 3	120 participants (Anticipated)	Interventional	2023-10-27	Recruiting
Clinical Evaluation of mTORC1 Inhibition for Geroprotection [NCT05835999]	Phase 2	86 participants (Anticipated)	Interventional	2023-03-24	Recruiting
A Phase I Dose Escalation Study With Everolimus in Combination With Cyclosporine A and Prednisolone for the Treatment of Acute GVHD After Allogeneic Hematopoietic Stem Cell Transplantation [NCT00373815]	Phase 1	10 participants (Anticipated)	Interventional	2006-09-30	Terminated(stopped due to high incidence of TTP, poor recrual)
Phase III Randomized, Placebo-Controlled Clinical Trial Evaluating the Use of Adjuvant Endocrine Therapy +/- One Year of Everolimus in Patients With High-Risk, Hormone Receptor-Positive and HER2/Neu Negative Breast Cancer [NCT01674140]	Phase 3	1,939 participants (Actual)	Interventional	2013-09-12	Active, not recruiting
Prospective Randomised Study Comparing Efficacy of Treatment Coronary In-stent Restenosis Using Drug Eluting Paclitaxel-coated Balloon and Drug Eluting Stent With Everolimus. [NCT01735825]		199 participants (Actual)	Interventional	2012-01-31	Completed
An Open-Label, Multicenter, Phase 1b/2 Study of E7080 Alone, and in Combination With Everolimus in Subjects With Unresectable Advanced or Metastatic Renal Cell Carcinoma Following One Prior VEGF-Targeted Treatment [NCT01136733]	Phase 1/Phase 2	173 participants (Actual)	Interventional	2010-08-05	Completed
Phase II Trial of RAD001 Plus Carboplatin in Patients With Triple-Negative Metastatic Breast Cancer [NCT01127763]	Phase 2	25 participants (Actual)	Interventional	2010-06-30	Completed
A Phase Ib Study Investigating the Combination of Everolimus With Trastuzumab and Vinorelbine in Patients With HER2-overexpressing Metastatic Breast Cancer [NCT00426530]	Phase 1	50 participants (Actual)	Interventional	2007-02-28	Completed
A Phase I Study Investigating the Combination of Everolimus With Pemetrexed in Patients With Advanced Non Small Cell Lung Cancer (NSCLC) Previously Treated With Chemotherapy [NCT00434174]	Phase 1	48 participants (Actual)	Interventional	2006-12-31	Completed
A Study to Evaluate the Safety and Performance of the Dynalink®-E, Everolimus Eluting Peripheral Stent System for Treating Atherosclerotic de Novo or Restenotic Native Superficial Femoral and Proximal Popliteal Artery Lesions [NCT00475566]		104 participants (Actual)	Interventional	2007-05-31	Completed
A Pilot Study to Evaluate Feasibility and Safety of Early Switch to Everolimus From Cyclosporine in de Novo Renal Transplant [NCT00464399]	Phase 3	20 participants	Interventional	2006-09-30	Completed
Immune Monitoring to Facilitate Belatacept Monotherapy [NCT04177095]	Phase 4	17 participants (Actual)	Interventional	2020-02-11	Completed
A Single Arm, Multi-center Phase II Study of RAD001 in Patients With Advanced Gastric Carcinoma Whose Cancer Has Progressed Despite Prior Treatment [NCT00519324]	Phase 2	54 participants (Actual)	Interventional	2007-08-31	Completed
Phase I/II Study of Paclitaxel / Carboplatin / RAD001 as First Line Therapy for Advanced Adenocarcinoma of the Stomach [NCT01514110]	Phase 1/Phase 2	35 participants (Actual)	Interventional	2008-01-23	Completed
Hybrid Sirolimus-eluting Stent With Bioresorbable Polymer Versus Everolimus-eluting Stent With Durable Polymer for Total Coronary Occlusions in Native Coronary Arteries (PRISON-IV) [NCT01516723]	Phase 3	330 participants (Anticipated)	Interventional	2012-02-29	Active, not recruiting
Randomized Phase II Study to Compare Vinorelbine In Combination With the mTOR Inhibitor Everolimus vs. Vinorelbin Monotherapy for Second-line Treatment in Advanced Breast Cancer [NCT01520103]	Phase 2	139 participants (Actual)	Interventional	2012-01-31	Completed
Impact of Two Prednisone-free Maintenance Immunosuppressive Regimens With Reduced Dose FK506+Everolimus vs. Standard Dose Tacrolimus (FK506)+ Mycophenolate Mofetil (MMF) on Subpopulation of T and B Cells, Renal Allograft Function and Gene Expression Profi [NCT01653847]		88 participants (Actual)	Interventional	2013-02-28	Completed
A Phase II Single Arm Study to Evaluate the Safety and Efficacy of RAD001 as Monotherapy in Treatment naïve Advanced Cholangiocarcinoma [NCT01525719]	Phase 2	40 participants (Anticipated)	Interventional	2012-01-31	Active, not recruiting
Phase I-II Randomized Prospective Double-blind Multi-center Trial on the Effects of a Short Course of Oral Everolimus on Infarct Size, Left Ventricular Remodeling and Inflammation in Patients With Acute ST-Elevation Myocardial Infarction [NCT01529554]	Phase 1/Phase 2	150 participants (Actual)	Interventional	2015-01-08	Completed
Phase 1 Trial of the Mammalian Target of Rapamycin (mTOR) Inhibitor Everolimus Plus Radiation Therapy (RT) for Salvage Treatment of Biochemical Recurrence in Prostate Cancer Patients Following Prostatectomy [NCT01548807]	Phase 1	19 participants (Actual)	Interventional	2010-09-30	Completed
A Single-arm, Open Label Phase II Study of RAD001 in Soft Tissue Extremity and/or Retroperitoneal Sarcomas [NCT01048723]	Phase 2	2 participants (Actual)	Interventional	2010-01-31	Terminated(stopped due to Novartis terminated funding)
Trametinib Combined With Everolimus and Lenvatinib in the Treatment of Recurrent/Refractory Advanced Solid Tumors: a Phase II Clinical Trial [NCT04803318]	Phase 2	100 participants (Anticipated)	Interventional	2021-01-01	Recruiting
A Trial of Maintenance Rituximab With mTor Inhibition After High-dose Consolidative Therapy in CD20+, B-cell Lymphomas, Gray Zone Lymphoma, and Hodgkin's Lymphoma [NCT01665768]	Phase 2	56 participants (Actual)	Interventional	2012-09-30	Completed
Phase II Study of Everolimus in Patients With Advanced Solid Malignancies With TSC1, TSC2, NF1, NF2, or STK11 Mutations [NCT02352844]	Phase 2	12 participants (Actual)	Interventional	2015-10-07	Completed
A Ph2 Randomized Trial to Evaluate the Safety Preliminary Efficacy and Biomarker Response of Host Directed Therapies Added to Rifabutin-modified Standard Therapy in Adults With Drug-Sensitive Smear-Positive Pulmonary TB [NCT02968927]	Phase 2	200 participants (Actual)	Interventional	2016-11-30	Active, not recruiting
Phase II Expansion Cohorts Studies of a Novel Triple Combination Therapy, DTRM-555, in Patients With Relapsed/Refractory Chronic Lymphocytic Leukemia or Relapsed/Refractory Non-Hodgkin's Lymphomas [NCT04305444]	Phase 2	120 participants (Anticipated)	Interventional	2020-04-24	Recruiting
Phase II Study of Everolimus in Refractory Testicular Germ Cell Cancer. [NCT01466231]	Phase 2	15 participants (Actual)	Interventional	2011-11-30	Completed
Phase I Study of Bevacizumab in Combination With Everolimus and Erlotinib in Advanced Cancer [NCT00276575]	Phase 1	65 participants (Actual)	Interventional	2005-03-31	Completed
Pilot Trial of an Implantable Microdevice for In Vivo Drug Sensitivity Testing in Patients With Sarcomas [NCT04199026]	Early Phase 1	20 participants (Anticipated)	Interventional	2024-01-31	Not yet recruiting
Envarsus® Tablets Administered Once Daily in Combination With Everolimus in Elderly De-novo Kidney Transplant Recipients: Open-label, Multicentre, Single-arm, Pharmacokinetic and Clinical Study [NCT02970630]	Phase 2	28 participants (Actual)	Interventional	2017-01-31	Completed
A Single Arm, Monocenter Phase II Trial of RAD001 as Monotherapy in the Treatment of Neurofibromatosis Type 2 - Related Vestibular Schwannoma [NCT01345136]	Phase 2	4 participants (Actual)	Interventional	2015-07-01	Active, not recruiting
Immunosuppressive Therapy With Certican (Everolimus) After Lung Transplantation [NCT00402532]	Phase 3	190 participants (Actual)	Interventional	2005-03-31	Completed
An Open Label, Randomised Phase II Study, Comparing AZD2014 Versus Everolimus With Advanced Metastatic Renal Cancer and Progression on VEGF Targeted Therapy [NCT01793636]	Phase 2	49 participants (Actual)	Interventional	2013-02-28	Terminated(stopped due to Inferior efficacy of study drug in renal indication.)
A 12-month, Multicenter, Randomized, Open-label Non-inferiority Study of Renal Function and Efficacy Comparing Concentration-controlled Certican (1.5 mg/Day Starting Dose) With Reduced Neoral Dose Versus MMF With Standard Neoral Dose in de Novo Heart Tran [NCT00150046]	Phase 3	176 participants (Anticipated)	Interventional	2004-12-31	Completed
Prospective Randomized Study to Characterize Risk Factors of Polyomavirus-related Transplant Nephropathy and the Impact of Three Immunosuppressive Regimens on Nephropathy Incidence [NCT00160966]	Phase 4	108 participants (Actual)	Interventional	2004-09-30	Completed
A One Year, Multicenter, Open-Label, Single Arm, Pilot Study of the Renal Safety of Everolimus in Addition to Cyclosporine Microemulsion in Cardiac Transplant Recipients. [NCT00170794]	Phase 3	0 participants	Interventional	2004-09-30	Completed
A Prospective, Multicenter, Open Label, Randomized Study of the Safety, Tolerability and Efficacy of Everolimus (RAD001) With Basiliximab, Corticosteroids and Lower Levels Versus Higher Levels of Tacrolimus in de Novo Renal Transplant Recipients [NCT00170833]	Phase 3	80 participants	Interventional	2003-11-30	Completed
A Clinical Evaluation of the XIENCE V® Everolimus Eluting Coronary Stent System in the Treatment of Patients With de Novo Native Coronary Artery Lesions [NCT00180310]	Phase 3	300 participants (Actual)	Interventional	2005-07-31	Completed
Phase I Trial of RAD001C (Everolimus) in Pediatric Patients With Recurrent Refractory Solid Tumors or Brain Tumors [NCT00187174]	Phase 1	41 participants (Actual)	Interventional	2004-10-31	Completed
Polymorphism of the Cytochrome P450-system and the MDR-system in Renal Transplants Receiving the Immunosuppressive Drugs Tacrolimus, Sirolimus, Everolimus or Cyclosporine A [NCT00223054]		200 participants (Actual)	Observational	2005-03-31	Completed
Effects of Zortress® + Tacrolimus vs. Standard Immunosuppression on Progression of Coronary Artery Calcifications and Bone Disease in de Novo Renal Transplant Recipients [NCT01612299]		0 participants (Actual)	Interventional	2012-05-31	Withdrawn(stopped due to Funding was withdrawn for this study by the sponsor.)
Efficacy and Safety of Precision Therapy in Refractory Tumor (Long March Pathway) [NCT03239015]	Phase 2	300 participants (Anticipated)	Interventional	2017-01-01	Recruiting
A Brief Dose Escalation Followed by a Phase 2 Study of RAD001 in Combination With Trastuzumab in HER2-Positive Metastatic Breast Cancer [NCT00458237]	Phase 1/Phase 2	11 participants (Actual)	Interventional	2007-04-30	Completed
Single Arm, Single Center, Prospective, Phase II Clinical Study of Anlotinib Hydrochloride Capsule Combined With Everolimus in the First-line Treatment of Advanced Non Clear Cell Renal Cell Carcinoma [NCT05124431]	Phase 2	30 participants (Anticipated)	Interventional	2021-12-31	Not yet recruiting
Randomized Phase II Study of Two Different Doses of RAD-001 (Everolimus) as Neo-Adjuvant Therapy in Patients With Localized Prostate Cancer [NCT00526591]	Phase 2	17 participants (Actual)	Interventional	2007-09-30	Terminated(stopped due to Slow accrual)
Study Examining the PROMUS Element Everolimus-eluting Stent in Multi-center Coronary Intervention of Complex Arterial Lesion Subsets [NCT01670318]		800 participants (Anticipated)	Interventional	2012-08-31	Recruiting
A Phase II Randomized, Double-blind, Placebo-controlled Trial of Radium-223 Dichloride in Combination With Exemestane and Everolimus Versus Placebo in Combination With Exemestane and Everolimus When Administered to Metastatic HER2 Negative Hormone Recepto [NCT02258451]	Phase 2	283 participants (Actual)	Interventional	2015-06-04	Completed
Everolimus as Treatment After Embolization or Chemoembolization for Liver Metastases From Digestive Endocrine Tumors [NCT01678664]	Phase 2	74 participants (Actual)	Interventional	2012-10-31	Completed
A 3-Arm Randomized Phase II Trial Evaluating Single Agent and Combined Efficacy of Pasireotide and Everolimus in Adult Patients With Radioiodine-Refractory Differentiated and Medullary Thyroid Cancer [NCT01270321]	Phase 2	42 participants (Actual)	Interventional	2010-11-30	Completed
A Single Arm, Two Center, Phase II Study of RAD001 in Patients With Metastatic, Hormone-Refractory Prostate Cancer [NCT00629525]	Phase 2	35 participants (Actual)	Interventional	2005-08-31	Completed
An 18 Month Extension to the Multicenter, Randomized, Open-label Trial (NCT00170885) to Evaluate the Safety, Tolerability, and Efficacy of Two Regimens of Everolimus Plus Cyclosporine Microemulsion, Given According to Different Blood Target Levels, in de [NCT01276457]	Phase 3	223 participants (Actual)	Interventional	2006-05-31	Completed
A Phase 2 Trial of RAD001(Everolimus) in Low and Intermediate-1 Risk Myelodysplastic Syndrome [NCT00809185]	Phase 2	7 participants (Actual)	Interventional	2005-11-30	Terminated(stopped due to slow accrual)
Phase II Trial of RAD001 in Patients With Recurrent Low Grade Glioma [NCT00823459]	Phase 2	58 participants (Actual)	Interventional	2009-01-23	Completed
Comparison Between Abluminal Biodegradable Polymer Ultrathin Sirolimus-eluting Stent and Durable-polymer Everolimus-eluting Stent (GENOSS Randomized Clinical Trial) [NCT05444452]		850 participants (Anticipated)	Interventional	2022-04-24	Recruiting
Study to Investigate Outcome of Individualized Treatment Based on Pharmacogenomic Profiling & Ex Vivo Drug Sensitivity Testing of Patient-derived Organoids in Patients With Metastatic Colorectal Cancer [NCT05725200]	Phase 2	40 participants (Anticipated)	Interventional	2022-09-27	Recruiting
A Multicenter, Two Arms, Randomized, Open Label Clinical Phase IV Study Investigating the Proportion of CMV Seropositive Kidney Transplant Recipients Who Will Develop a CMV Infection Within the First 6 Months Post-transplantation When Treated With an Immu [NCT02328963]	Phase 4	186 participants (Actual)	Interventional	2014-05-02	Completed
Neoadjuvant Phase II Study Of Everolimus Plus Cisplatin In Triple Negative Breast Cancer Patients With Residual Disease After Standard Chemotherapy [NCT01931163]	Phase 2	24 participants (Actual)	Interventional	2013-07-31	Completed
A Phase I Trial of Escalating Dose of RAD001 in Combination With PKC412 in Patients With Relapsed, Refractory or Poor Prognosis AML or MDS [NCT00819546]	Phase 1	29 participants (Anticipated)	Interventional	2009-01-31	Active, not recruiting
A Study in Adults on Pre LT Dialysis With Basiliximab, Delayed Tacrolimus (TAC), Mycophenolate (MMF), Steroids (Grp 1) vs. Basiliximab, Delayed TAC, MMF, Steroids, With Everolimus 30d Post LT(Grp 2), vs. TAC, MMF, Steroids (Grp 3). [NCT04104438]	Phase 4	90 participants (Anticipated)	Interventional	2021-01-15	Recruiting
AXITINIB IN ADVANCED / METASTATIC RENAL CELL CARCINOMA - A NON-INTERVENTIONAL STUDY OF REAL WORLD TREATMENT OUTCOMES IN PATIENTS RECEIVING 2ND LINE AXITINIB AFTER 1ST LINE SUNITINIB (ADONIS) [NCT02184416]		573 participants (Actual)	Observational	2014-10-31	Completed
A Phase II Multicenter Trial of RAD001 in Patients With Metastatic or Recurrent Sarcomas [NCT01830153]	Phase 2	41 participants (Actual)	Interventional	2010-04-30	Completed
An Open-label Randomized Controlled Clinical Trial to Assess the Efficacy and Safety of the Conversion to Everolimus 3 Months After Kidney Transplantation. [NCT01608412]	Phase 4	120 participants (Anticipated)	Interventional	2012-02-29	Recruiting
Placebo-Controlled, Randomized, Prospective and Multicenter Trial of Everolimus in Castrated Resistant Prostate Cancer Patients With PI3K-AKT-mTOR Signaling Pathway Deficiency [NCT03580239]	Phase 3	120 participants (Anticipated)	Interventional	2019-01-01	Not yet recruiting
Phase IV, Prospective Single Arm Study of Safety and Efficacy of Votubia (Everolimus) in Taiwanese Adults With Tuberous Sclerosis Complex Who Have Renal Angiomyolipoma [NCT05252585]	Phase 4	10 participants (Anticipated)	Interventional	2023-05-01	Recruiting
Phase II Trial of Carboplatin and Everolimus (RAD001) in Metastatic Castrate Resistant Prostate Cancer (CRPC) Pretreated With Docetaxel Chemotherapy. [NCT01051570]	Phase 2	26 participants (Actual)	Interventional	2010-02-28	Completed
PTK787/ZK222584 and RAD001 for Patients With Advanced Solid Tumors [NCT00303732]	Phase 1	37 participants (Actual)	Interventional	2004-12-31	Completed
Bioabsorbable Vascular Solutions First in Man Clinical Investigation: A Clinical Evaluation of the Bioabsorbable Vascular Solutions Everolimus Eluting Coronary Stent System (BVS EECSS) in the Treatment of Patients With Single de Novo Native Coronary Arter [NCT00300131]		30 participants (Actual)	Observational	2006-03-31	Completed
An Open-label, Multi-center Phase I Dose-finding Study of RAD001 (Everolimus, Afinitor®) in Combination With BEZ235 in Patients With Advanced Solid Tumors [NCT01482156]	Phase 1	46 participants (Actual)	Interventional	2012-01-31	Completed
Safety and Efficacy of Low-dose Cyclosporine in Association With Everolimus to Minimize Renal Dysfunction in Heart Transplant Recipients [NCT00420537]	Phase 4	34 participants (Actual)	Interventional	2006-09-30	Terminated(stopped due to A cluster of adverse events in everolimus arm was noted.)
Phase II Trial of RAD001 in Patients With Refractory Colorectal Cancer [NCT00337545]	Phase 2	22 participants (Actual)	Interventional	2006-05-31	Completed
A Phase 1b/2, Open-Label Umbrella Study To Evaluate Safety And Efficacy Of Elacestrant In Various Combination In Patients With Metastatic Breast Cancer [NCT05563220]	Phase 1/Phase 2	322 participants (Anticipated)	Interventional	2023-01-24	Recruiting
Open Label Multicenter Randomized Trial Comparing Standard Immunosuppression With Tacrolimus and Mycophenolate Mofetil With a Low Exposure Tacrolimus Regimen in Combination With Everolimus in de Novo Renal Transplantation in Elderly Patient [NCT03797196]	Phase 4	374 participants (Anticipated)	Interventional	2019-07-29	Active, not recruiting
PREVENT: a Prospective, Multi-center, Monitored Trial Investigating the Implant of the Promus Everolimus-Eluting Stent System in Critically Ischemic Lesions BTK [NCT01500070]	Phase 2	70 participants (Anticipated)	Interventional	2012-08-31	Completed
An Open, Randomized Phase III Study of Everolimus With Investigator's Choice of Chemotherapy Versus Chemotherapy in The First-Line Treatment of Luminal Androgen Receptor (LAR) Subtype With PI3K/AKT/mTOR Pathway Mutation of Locally Recurrent Inoperable or [NCT05954442]	Phase 3	203 participants (Anticipated)	Interventional	2023-09-13	Recruiting
A Dose Escalation, Single Arm, Phase 1b-2 Combination Study of BEZ235 With Everolimus to Determine the Safety, Pharmacodynamics and Pharmacokinetics in Subjects With Advanced Solid Malignancies [NCT01508104]	Phase 1	19 participants (Actual)	Interventional	2012-01-31	Terminated(stopped due to funding)
The Beneficial Role of Percutaneous Coronary Intervention Over Optimal Medical Therapy in Elderly Patients (Age > 75 Years Old) With Coronary Artery Disease: a Randomized Controlled Study [NCT01508663]	Phase 4	1,600 participants (Anticipated)	Interventional	2010-08-31	Recruiting
TITANIC-XV Trial: Prospective, Multicenter and Randomized Trial (Bioactive Bare Metal Titanium Stent Versus Everolimus Drug Eluting Stent) [NCT01510509]	Phase 4	0 participants	Interventional	2009-01-31	Active, not recruiting
A Phase I Trial of Anakinra (IL-1 Receptor Antagonist) or Denosumab (Anti-RANKL Monoclonal Antibody) in Combination With Everolimus (mTOR Inhibitor) in Patients With Advanced Malignancies [NCT01624766]	Phase 1	57 participants (Actual)	Interventional	2012-06-19	Completed
Mono Centre, Open Label Proof of Concept Study SOM230 in Progressive Medullary Thyroid Cancer Patients and the Combination With RAD001 Upon Progression [NCT01625520]	Phase 2	19 participants (Actual)	Interventional	2012-02-29	Completed
A Phase IIIB, Multi-Center, Open Label Study For Postmenopausal Women With Estrogen Receptor Positive Locally Advanced or Metastatic Breast Cancer Treated With Everolimus (RAD001) in Combination With Exemestane: 4EVER - Efficacy, Safety, Health Economics, [NCT01626222]	Phase 3	301 participants (Actual)	Interventional	2012-06-30	Completed
Immunosuppression in Renal Transplantation in The Elderly: Time to Rethink. - nEverOld Study [NCT01631058]	Phase 4	90 participants (Anticipated)	Interventional	2012-07-31	Recruiting
A Phase I Evaluation of Cetuximab and RAD001 in Patients With Solid Tumors [NCT01637194]	Phase 1	12 participants (Actual)	Interventional	2008-11-30	Completed
Effect of Different Therapeutic Strategies on Regulatory T Cells in Kidney Transplantation: a Randomized Study [NCT01640743]		58 participants (Actual)	Interventional	2010-03-31	Completed
Phase II Multicenter Single-arm Study Evaluating the Safety and Efficacy of Everolimus as a First-line Treatment in Newly-diagnosed Patients With Advanced GI Neuroendocrine Tumors. [NCT01648465]	Phase 2	25 participants (Actual)	Interventional	2012-08-06	Terminated
Certican (Everolimus) for Recipients of Kidney From HLA-identical Living Donors [NCT01653041]	Phase 4	47 participants (Actual)	Interventional	2012-08-31	Completed
Phase II Single Arm Study of Everolimus and Pasireotide (SOM230) in Patients With Advanced or Metastatic Hepatocellular Carcinoma (HCC) [NCT01488487]	Phase 2	24 participants (Actual)	Interventional	2011-12-31	Completed
"Effects of the Use of de Novo Everolimus for the Expression of Cytokines in Kidneys From Extended Criteria Donors and With Delayed Graft Function" [NCT01663805]	Phase 4	80 participants (Anticipated)	Interventional	2012-01-31	Recruiting
Randomized Comparison of Everolimus Eluting Stents and Sirolimus Eluting Stent in Patients With ST Elevation Myocardial Infarction (STEMI) (RaCES-MI Trial) [NCT01684982]	Phase 4	500 participants (Actual)	Interventional	2007-04-30	Completed
Phase I/II Study of RAD001 and Intravesical Gemcitabine in BCG-Refractory Primary or Secondary Carcinoma In Situ of the Bladder [NCT01259063]	Phase 1/Phase 2	33 participants (Actual)	Interventional	2010-12-31	Completed
An Open Label, Single Arm Trial to Evaluate Patients With Metastatic Renal Cell Carcinoma Treated With Everolimus After Failure of First Line Therapy With Sunitinib or Pazopanib [NCT01514448]	Phase 4	29 participants (Actual)	Interventional	2012-05-21	Completed
Phase I Dose Escalation Study of Everolimus, Pemetrexed, Carboplatin, and Bevacizumab in Stage IV Non-Squamous Non-Small Cell Lung Cancer [NCT01700400]	Phase 1	13 participants (Actual)	Interventional	2012-09-30	Completed
[NCT01706471]	Phase 4	60 participants (Actual)	Interventional	2009-06-30	Completed
An Unicenter, Prospective, Randomized, Pilot Study Comparing the Effect of Everolimus-containing Versus mTOR Inhibitor Free Immunosuppression in the Evolution of Hepatitis C Fibrosis After Liver Transplantation. [NCT01707849]	Phase 3	18 participants (Actual)	Interventional	2012-10-31	Completed
Phase 2 Study of Everolimus Therapy in Patients With Birt-Hogg-Dube Syndrome (BHD)-Associated Kidney Cancer or Sporadic Chromophobe Renal Cancer [NCT02504892]	Phase 2	3 participants (Actual)	Interventional	2015-07-21	Terminated(stopped due to Study was terminated due to slow, insufficient accrual.)
A Comparison of Blood and Tissue Biomarkers Before and After Nephrectomy in the First-line Setting With Everolimus in Patients With Locally Advanced or Metastatic Renal Cell Carcinoma [NCT01715935]	Phase 2	25 participants (Actual)	Interventional	2012-06-30	Completed
Efficacy of RAD001/Everolimus in Autism and NeuroPsychological Deficits in Children With Tuberous Sclerosis Complex [NCT01730209]	Phase 2/Phase 3	60 participants (Anticipated)	Interventional	2012-11-30	Recruiting
A Prospective, Open-label, Multicenter, Randomized Phase II Trial: Sequential Therapy With BEvacizumab, RAd001 (Everolimus) and Tyrosinekinase Inhibitors (TKI) in Metastatic Renal Cell Carcinoma (mRCC) (BERAT Study) [NCT01731158]	Phase 2	22 participants (Actual)	Interventional	2012-10-31	Completed
A Randomized Proof-of-concept Phase II Trial Comparing Therapy Based on Tumor Molecular Profiling Versus Conventional Therapy in Patients With Refractory Cancer. [NCT01771458]	Phase 2	742 participants (Actual)	Interventional	2012-10-31	Active, not recruiting
A Multicenter Randomized, Double Blind, Placebo- Controlled, Phase II Study to Compare Endocrine Treatment Alone Versus Endocrine Treatment With Everolimus in Patients With HR+/HER2- Metastatic Breast Cancer and Progression After Previous Treatment With E [NCT01773460]	Phase 3	3 participants (Actual)	Interventional	2013-07-31	Terminated(stopped due to Study was stopped terminated early due to low recruitment.)
Apposition Assessed Using Optical Coherence Tomography of Chromium Stents Eluting Everolimus From Cobalt Versus Platinum Alloy Platforms. [NCT01776567]	Phase 4	60 participants (Anticipated)	Interventional	2012-07-31	Recruiting
Drug Interaction and Pharmacokinetic Assessment of Everolimus When Coadministered With Atorvastatin in Renal Transplantation Recipient [NCT01780948]		18 participants (Actual)	Interventional	2012-09-30	Completed
Phase 1b/2 Single-arm Trial Evaluating the Combination of Lapatinib, Everolimus and Capecitabine for the Treatment of Patients With HER2-positive Metastatic Breast Cancer With CNS Progression After Trastuzumab [NCT01783756]	Phase 1/Phase 2	9 participants (Actual)	Interventional	2013-06-26	Completed
A Multicentre Phase III Trial to Determine the Efficacy of RAD 001 (Everolimus, Afinitor) as Second Line Therapy in Patients With Transitional Cell Carcinoma TCC of the Urothelium Which Failed or Progressed After First Line Chemotherapy [NCT01801137]	Phase 2	54 participants (Actual)	Interventional	2011-06-30	Completed
A Phase II, Open Label, Non-randomized Study of Second or Third Line Treatment With the Combination of Sorafenib and Everolimus in Patients Affected by Relapsed and Non-resectable High-grade Osteosarcoma [NCT01804374]	Phase 2	38 participants (Actual)	Interventional	2011-06-30	Completed
Prospective Evaluation of the Efficacy and Safety of Zortress (Everolimus)/Myfortic (Enteric Coated Mycophenolate Sodium) Conversion in High MELD Liver Transplantation [NCT01807767]		0 participants (Actual)	Interventional	2013-03-31	Withdrawn(stopped due to funding was withdrawn)
Drug- Drug Interaction Study of JI-101 & Everolimus in Advanced Solid Tumors, Expansion Pharmacodynamic Study of JI-101 in Advanced Low Grade Endocrine Tumors, Ovarian Cancers or K-RAS Mutant Colon Cancers [NCT01149434]	Phase 1/Phase 2	19 participants (Actual)	Interventional	2010-09-30	Terminated(stopped due to Lack of drug efficacy)
Sirolimus-coated Balloon Versus Drug-eluting Stent in Native Coronary Vessels [NCT04893291]		1,820 participants (Anticipated)	Interventional	2021-11-16	Recruiting
Randomized Double-Blind Phase 2 Trial Of RAD001 For Neurocognition In Individuals With Tuberous Sclerosis Complex [NCT01289912]	Phase 2	52 participants (Actual)	Interventional	2011-01-31	Completed
PHASE II TRIAL OF THE mTOR INHIBITOR EVEROLIMUS IN RELAPSED OR REFRACTORY CUTANEOUS T-CELL LYMPHOMA (CTCL) [NCT01637090]	Phase 2	3 participants (Actual)	Interventional	2012-06-30	Terminated(stopped due to Poor enrollment)
A Phase II Study of Lenvatinib Plus Everolimus Versus Cabozantinib in Patients With Metastatic Renal Cell Carcinoma That Progressed on A PD-1/PD-L1 Checkpoint Inhibitor [NCT05012371]	Phase 2	90 participants (Anticipated)	Interventional	2022-02-16	Recruiting
Phase II Trial of Lapatinib in Combination With Everolimus in Triple Negative Metastatic or Locally Advanced Breast Cancer [NCT01272141]	Phase 2	5 participants (Actual)	Interventional	2010-12-31	Terminated(stopped due to Slow accrual, Funding stopped)
A Phase 1b/2, Protocol Evaluating the Safety, Tolerability, Pharmacokinetics, and Efficacy of Sotorasib Monotherapy and in Combination With Other Anti-cancer Therapies in Subjects With Advanced Solid Tumors With KRAS p.G12C Mutation (CodeBreak 101) [NCT04185883]	Phase 1/Phase 2	1,143 participants (Anticipated)	Interventional	2019-12-17	Recruiting
A Randomized Comparison of a Sirolimus-eluting Stent With Biodegradable Polymer Versus an Everolimus-eluting Stent With a Durable Polymer for Percutaneous Coronary Revascularization [NCT01443104]		2,119 participants (Actual)	Interventional	2012-02-29	Completed
Phase 1 Pilot Study Using Autologous CD4+CD25+FoxP3+ T Regulatory Cells and Campath-1H to Induce Renal Transplant Tolerance [NCT01446484]	Phase 1/Phase 2	30 participants (Anticipated)	Interventional	2011-10-31	Recruiting
Women's Triple-Negative First-Line Study: A Phase II Trial of Liposomal Doxorubicin, Bevacizumab and Everolimus (DAE) in Patients With Localized Triple-Negative Breast Cancer (TNBC) With Tumors Predicted Insensitive to Standard Neoadjuvant Chemotherapy [NCT02456857]	Phase 2	17 participants (Actual)	Interventional	2016-01-12	Completed
Phase 1-2 Study of Everolimus and Low-dose Cyclophosphamide in Patients With Metastatic Renal Cell Cancer. [NCT01462214]	Phase 1/Phase 2	96 participants (Anticipated)	Interventional	2011-10-31	Completed
Phase II Trial of Bevacizumab(Avastin) and RAD001(Everolimus)in the Treatment of Patients With Advanced Clear Cell Renal Carcinoma [NCT00323739]	Phase 2	80 participants (Actual)	Interventional	2006-05-31	Completed
A Phase II Trial of RAD001 and Bicalutamide for Androgen Independent Prostate Cancer [NCT00630344]	Phase 2	36 participants (Actual)	Interventional	2008-02-29	Completed
Prospective, Multicenter, Randomized Open Study to Evaluate the Progression of Renal Graft Fibrosis According to the Epithelial-mesenchymal Transition (EMT) in de Novo Renal Transplant Recipients Treated Either by a CNI Free Immunosuppressive Regimen With [NCT01079143]	Phase 3	194 participants (Actual)	Interventional	2009-09-30	Completed
German-Austrian Register to Evaluate the Short and Long-term Safety and Therapy Outcomes of the ABSORB Everolimus-eluting Bioresorbable Vascular Scaffold System in Patients With Coronary Artery Stenosis [NCT02066623]		3,330 participants (Actual)	Observational [Patient Registry]	2013-11-08	Completed
A Phase II Trial of the Combination of Bevacizumab and Everolimus in Patients With Refractory, Progressive Intracranial Meningioma [NCT00972335]	Phase 2	18 participants (Actual)	Interventional	2010-01-31	Terminated(stopped due to Study terminated early due to slow accrual)
A Phase 2 Trial of Letrozole and Everolimus in Relapsed Hormone Receptor Positive Ovarian, Fallopian Tube or Primary Peritoneal Carcinomas [NCT02283658]	Phase 2	20 participants (Actual)	Interventional	2014-11-14	Completed
BIOTRONIK - A Prospective Randomized Multicenter Study to Assess the SaFety and Effectiveness of the Orsiro SiroLimus Eluting Coronary Stent System in the Treatment Of Subjects With up to Three De Novo or Restenotic Coronary Artery Lesions - V [NCT02389946]		1,334 participants (Actual)	Interventional	2015-05-31	Completed
Phase Ib Trial of mFOLFOX6 and Everolimus (NSC-733504) in Patients With Metastatic Gastroesophageal Adenocarcinoma [NCT01231399]	Phase 1/Phase 2	6 participants (Actual)	Interventional	2012-02-29	Completed
A 12-month, Multi-center, Open-label, Randomized, Controlled Study to Evaluate Efficacy/Safety and Evolution of Renal Function of Everolimus in Co-exposure With Tacrolimus in de Novo Liver Transplant Recipients [NCT01551212]	Phase 4	339 participants (Actual)	Interventional	2012-05-24	Completed
BrUOG-H&N-229-RAD001, Cisplatin and Concurrent Radiation for Locally Advanced, Inoperable Head and Neck Cancer: A PHASE I STUDY- Novartis CRAD001CUS134T [NCT01057277]	Phase 1	3 participants (Actual)	Interventional	2009-12-31	Terminated(stopped due to Pharmaceutical co- re aligned their specialties- no longer will fund H&N ca)
XIENCE V Everolimus Eluting Coronary Stent System (EECSS) China: Post-Approval, Single-Arm Study [NCT01249027]		2,605 participants (Actual)	Observational	2010-11-30	Completed
A Phase I/II Study of the HDAC Inhibitor LBH-589 in Combination With the mTOR Inhibitor Everolimus (RAD001) in Metastatic Renal Cell Carcinoma [NCT01582009]	Phase 1/Phase 2	26 participants (Actual)	Interventional	2010-03-31	Terminated(stopped due to pts off study, PI left institute)
A Phase 1 Study of Fosbretabulin in Combination With Everolimus in Neuroendocrine Tumors (Grades 1-3) That Have Progressed After at Least One Prior Regimen for Metastatic Disease [NCT03014297]	Phase 1	17 participants (Actual)	Interventional	2017-03-06	Terminated(stopped due to Part I completed. Part 2 will not be done due to sponsor decision.)
An Open-label, Multi-center Long-term Safety Roll-over Study in Patients With Tuberous Sclerosis Complex (TSC) and Refractory Seizures Who Are Judged by the Investigator to Benefit From Continued Treatment With Everolimus After Completion of Study CRAD001 [NCT02962414]	Phase 3	206 participants (Actual)	Interventional	2017-06-08	Active, not recruiting
A Phase II Study of RAD001 (Everolimus) for Children With NeurF1 and Chemotherapy-Refractory Radiographic Progressive Low Grade Gliomas [NCT01158651]	Phase 2	23 participants (Actual)	Interventional	2010-07-10	Completed
Randomized Phase II Study of Everolimus Alone Versus Everolimus Plus Bevacizumab in Patients With Locally Advanced or Metastatic Pancreatic Neuroendocrine Tumors [NCT01229943]	Phase 2	150 participants (Actual)	Interventional	2010-10-15	Completed
A Single-arm, Multicenter, Phase 2 Trial to Evaluate Efficacy and Safety of Lenvatinib in Combination With Everolimus in Subjects With Unresectable Advanced or Metastatic Non Clear Cell Renal Cell Carcinoma (nccRCC) Who Have Not Received Any Chemotherapy [NCT02915783]	Phase 2	41 participants (Actual)	Interventional	2017-02-20	Completed
Circulating FGF21 Levels and Efficacy of Exemestane, Everolimus and Metformin in Postmenopausal Women With Hormone Receptor Positive Metastatic Breast Cancer and BMI >/= 25 [NCT01627067]	Phase 2	23 participants (Actual)	Interventional	2012-09-30	Terminated(stopped due to Komen Foundation Funding Terminated)
A Prospective, Open-label, Controlled, Randomized Study to Evaluate the Safety and Efficacy of Switching Calcineurin Inhibitor to Everolimus After 90 to 150 Days After Kidney Transplantation in Adults, Maintaining Corticosteroid and Mycophenolate Sodium C [NCT01455649]	Phase 4	30 participants (Anticipated)	Interventional	2011-11-30	Not yet recruiting
A 12-month, Multicenter, Open Label, Randomized, Controlled Study to Evaluate the Efficacy, Tolerability and Safety of Early Introduction of Everolimus, Reduced CNI, and Early Steroid Elimination Compared to Standard CNI, Mycophenolate Mofetil and Steroid [NCT01544491]	Phase 3	106 participants (Actual)	Interventional	2012-08-17	Completed
Preservation of Renal Function After Liver Transplant for Patients With Pre-existing Chronic Kidney Disease or Peri-operative Acute Kidney Injury Using Everolimus Plus Mycophenolate Mofetil Immunosuppression Regimen [NCT04258423]	Phase 3	4 participants (Actual)	Interventional	2019-12-19	Terminated(stopped due to Study was larger than expected and became a burden to faculty and staff resources.)
Phase II Study of Everolimus (RAD001) in Children and Adults With Neurofibromatosis Type 2 [NCT01419639]	Phase 2	10 participants (Actual)	Interventional	2011-10-31	Completed
A Prospective, Randomized, Double-blind, Placebo-controlled Cross Over Study Investigating the Anti-epileptic Efficacy of Afinitor (Everolimus) in Patients With Refractory Seizures Who Have Focal Cortical Dysplasia Type II (FCD II) [NCT03198949]	Phase 2	23 participants (Actual)	Interventional	2018-05-24	Completed
An Open Label, Single-Centre, Pilot Study for Radiosensitization of Everolimus With External Beam Radiotherapy for the Treatment of Metastatic Neuroendocrine Liver Metastasis [NCT02205515]	Phase 1/Phase 2	17 participants (Actual)	Interventional	2016-03-31	Completed
Phase II Study of Everolimus in Patients With Thymoma and Thymic Carcinoma Previously Treated With Chemotherapy [NCT02049047]	Phase 2	41 participants (Actual)	Interventional	2011-02-28	Completed
Safety and Efficacy of Everolimus Transition in Minimizing Progressive Graft Dysfunction and Interstitial Fibrosis in Adult Kidney Transplant Recipients [NCT02096107]	Phase 4	60 participants (Actual)	Interventional	2014-02-28	Completed
Observationnal Multicenter Study on a Prospective Cohort of Kidney Transplanted Patients Receiving a Year After Transplant an Extended Releasing Tacrolimus-Everolimus Association [NCT03228576]		16 participants (Actual)	Observational	2017-04-14	Terminated(stopped due to No recruitment)
A Randomized Double-Blind Controlled Trial of Everolimus in Individuals With PTEN Mutations (RAD001XUS257T) [NCT02991807]	Phase 1/Phase 2	46 participants (Actual)	Interventional	2017-06-12	Completed
Phase 2 Study of the mTOR Inhibitor Everolimus in Combination With Bevacizumab in Patients With Sporadic and Neurofibromatosis Type 1 (NF1) Related Refractory Malignant Peripheral Nerve Sheath Tumors [NCT01661283]	Phase 2	25 participants (Actual)	Interventional	2012-09-30	Completed
Safer mTOR Inhibition for Human Geroprotection [NCT05949658]	Phase 1	72 participants (Anticipated)	Interventional	2024-01-31	Not yet recruiting
Study of Efficacy of Everolimus Combined With First-line Endocrine Therapy for HR+/HER2- (Open, Randomized, Phase II ) [NCT05949541]	Phase 2	265 participants (Anticipated)	Interventional	2023-07-31	Not yet recruiting
A Phase III Randomized Open-label Multi-center Study of Ruxolitinib vs. Best Available Therapy in Patients With Corticosteroid-refractory Chronic Graft vs Host Disease After Allogeneic Stem Cell Transplantation (REACH3) [NCT03112603]	Phase 3	330 participants (Actual)	Interventional	2017-06-29	Completed
A Phase 1/2 Study for the Safety, Efficacy, Pharmacokinetic and Pharmacodynamics Evaluation of Amcenestrant (SAR439859), Administered Orally as Monotherapy, Then in Combination With Other Anti-cancer Therapies in Postmenopausal Women With Estrogen Recepto [NCT03284957]	Phase 1/Phase 2	136 participants (Actual)	Interventional	2017-09-20	Active, not recruiting
The Efficacy of Everolimus With Reduced-dose Tacrolimus Versus Reduced-dose Tacrolimus in Treatment of BK Virus Infection in Kidney Transplantation Recipient [NCT04542733]		50 participants (Anticipated)	Interventional	2021-02-10	Recruiting
Phase I Study of Everolimus + Bendamustine in Patients With Relapsed/Refractory Hematological Malignancies [NCT02240719]	Phase 1	20 participants (Actual)	Interventional	2014-10-31	Completed
A Phase I/II Study of RAD001, FOLFOX and Bevacizumab in Treatment of Colorectal Carcinoma [NCT01047293]	Phase 1/Phase 2	47 participants (Actual)	Interventional	2010-05-31	Completed
A Phase I Trial of VS-6766 (RO5126766) (a Dual RAF/MEK Inhibitor) Exploring Intermittent, Oral Dosing Regimens in Patients With Solid Tumours or Multiple Myeloma, With an Expansion to Explore Intermittent Dosing in Combination With Everolimus [NCT02407509]	Phase 1	104 participants (Anticipated)	Interventional	2013-06-17	Recruiting
A Phase 1 Trial of Vandetanib (a Multi-Kinase Inhibitor of EGFR, VEGFR, and RET Inhibitor) in Combination With Everolimus (an mTOR Inhibitor) in Advanced Cancer [NCT01582191]	Phase 1	153 participants (Actual)	Interventional	2012-05-14	Active, not recruiting
EVEREST: EVErolimus for Renal Cancer Ensuing Surgical Therapy, A Phase III Study [NCT01120249]	Phase 3	1,545 participants (Actual)	Interventional	2011-04-01	Active, not recruiting
"Extension Study to the Open-label Phase I Study Evaluating the Safety and Tolerability of Pasireotide LAR in Combination With Everolimus in Advanced Metastatic NETs - The COOPERATE-1 Study" [NCT01590199]	Phase 1	18 participants (Actual)	Interventional	2012-05-18	Completed
A Prospective, Open-label Study to Assess Safety of Certican in Kidney Transplant Patients [NCT01594268]	Phase 4	54 participants (Actual)	Interventional	2012-03-31	Completed
An Open-label, Multi-center, Expanded Access Study of Everolimus in Participants With Advanced Neuroendocrine Tumors (NETs) (Core Study) and an Extension Study to the Open-label, Multi-center, Expanded Access Study of Everolimus in Patients With Advanced [NCT01595009]	Phase 4	246 participants (Actual)	Interventional	2011-04-27	Completed
Randomized, Multicenter, Open-label, Comparative Study of Efficacy and Safety of Treatment With a Calcineurin Inhibitor (CNI), Associating Myfortic ® and Neoral ® Compared to a CNI-free Treatment, Combining Myfortic ® and Certican ® , in Adult Patients Wi [NCT01595984]	Phase 3	90 participants (Actual)	Interventional	2012-05-03	Active, not recruiting
A Phase I Dose-Escalation Study of the BRAF Inhibitor Vemurafenib (Zelboraf®) in Combination With an mTOR Inhibitor, Everolimus (Afinitor®) or Temsirolimus (Torisel®), in Subjects With Advanced Cancer [NCT01596140]	Phase 1	27 participants (Actual)	Interventional	2012-12-18	Completed
Biological Medicine for Diffuse Intrinsic Pontine Glioma (DIPG) Eradication [NCT05476939]	Phase 3	368 participants (Anticipated)	Interventional	2022-09-29	Recruiting
A Randomized Non-Comparative Multicenter Phase II Study of Everolimus/Sorafenib or Sunitinib in Patients With Metastatic Renal Cell Carcinoma (RCC) [NCT01616186]	Phase 2	0 participants (Actual)	Interventional	2012-07-31	Withdrawn
A Controlled Randomized Open-label Multicenter Study Evaluating if Early Conversion to Everolimus (Certican) From Cyclosporine (Neoral) in de Novo Renal Transplant Recipients Can Improve Long-term Renal Function and Slow Down the Progression of Chronic Al [NCT00634920]	Phase 4	204 participants (Actual)	Interventional	2008-03-31	Completed
A Phase I/II Study of Sorafenib and Everolimus in Patients With Advanced Solid Tumors and Gemcitabine-Refractory Metastatic Pancreatic Cancer [NCT00981162]	Phase 1	12 participants (Actual)	Interventional	2009-08-31	Completed
A Multicenter, Open-label, Randomized, Phase I/II Clinical Trial Comparing Safety and Durable Overall Response Day 56 in Patients With Steroid Resistent Acute GvHD After Allogeneic Hematopoietic Stem Cell Transplant Treated With DSC or BAT [NCT04118556]	Phase 1/Phase 2	50 participants (Anticipated)	Interventional	2021-12-01	Recruiting
XIENCE PRIME SV Everolimus Eluting Coronary Stent Japan Post Marketing Surveillance [NCT02513719]		312 participants (Actual)	Observational	2013-05-13	Completed
Phase I Study Evaluating the Combination of Lapatinib (GW572016; NSC-727989) and Everolimus (RAD001) in Patients With Advanced Solid Tumors [NCT00352443]	Phase 1	66 participants (Actual)	Interventional	2006-09-30	Completed
Randomized Comparison of Dual Drug-Eluting Cilotax Stent and Everolimus -Eluting Stent Implantation for DE Novo Coronary Artery DisEase in Patients With DIABETES Mellitus [NCT01515228]	Phase 4	291 participants (Actual)	Interventional	2012-01-31	Completed
A Pilot Study to Investigate Pharmacokinetic Characteristics of Everolimus in Patients Treated With Tacrolimus-Based Immunosuppression in De Novo Kidney Transplantation [NCT00325325]	Phase 2	40 participants	Interventional	2006-01-31	Recruiting
A Phase I/II Study of RAD001 and AV-951 in Patients With Refractory, Metastatic Colorectal Cancer [NCT01058655]	Phase 1/Phase 2	56 participants (Actual)	Interventional	2010-02-28	Completed
Phase II Study of RAD001 for Treatment of Refractory, Recurrent, Locally Advanced Squamous Cell Carcinoma of the Head and Neck [NCT01051791]	Phase 2	13 participants (Actual)	Interventional	2010-01-31	Terminated
Expanded Access to Everolimus, for an Individual Patient With Uterine Sarcoma (CTMS#18-0020) [NCT03493165]		0 participants	Expanded Access		Available
A Phase II Trial of Everolimus for Cancer Patients With Inactivating Mutations in TSC1 or TSC2 or Activating MTOR Mutations [NCT02201212]	Phase 2	30 participants (Actual)	Interventional	2014-09-30	Completed
A Prospective, Single Blind, Multi-center, Randomized Trial to Compare the TAXUS Element™ Coronary Stent System Against the XIENCE Prime™ Coronary Stent System in the Treatment of a Diabetic Patient PopulatiOn in India [NCT03125772]		1,830 participants (Actual)	Interventional	2011-06-30	Completed
Phase II Open Label Study of Everolimus in Combination With Anti-estrogen Therapy in Hormone Receptor-Positive HER2-Negative Advanced Breast Cancer [NCT02291913]	Phase 2	48 participants (Actual)	Interventional	2014-12-18	Completed
A Phase II Trial of Mutation-Targeted Therapy With Sunitinib or Everolimus in Patients With Advanced Low-or Intermediate Grade Neuroendocrine Tumors of the Gastrointestinal Tract and Pancreas With or Without Cytoreductive Surgery [NCT02315625]	Phase 2	16 participants (Actual)	Interventional	2015-04-08	Terminated(stopped due to Study closed due to poor accrual.)
A Phase II Study of Letrozole and RAD001 (Everolimus) in Patients With Advanced or Recurrent Endometrial Cancer [NCT01068249]	Phase 2	42 participants (Actual)	Interventional	2010-04-30	Active, not recruiting
An Open Label, Multi-center Everolimus Roll-over Protocol for Patients Who Have Completed a Previous Novartis-sponsored Everolimus Study and Are Judged by the Investigator to Benefit From Continued Everolimus Treatment. [NCT02017860]	Phase 2	4 participants (Actual)	Interventional	2014-01-16	Completed
12 Month, Multi-center, Open-label, Prospective, Randomized, Parallel Group Study Investigating a Standard Regimen in de Novo Kidney Transplant Patients Versus a Certican® Based Regimen Either in Combination With Cyclosporin A or Tacrolimus [NCT01843348]	Phase 3	612 participants (Actual)	Interventional	2012-12-27	Completed
An Open-label, Multi-center Everolimus Roll-over Protocol for Patients Who Have Completed a Previous Novartis-sponsored Everolimus Study and Are Judged by the Investigator to Benefit From Continued Everolimus Treatment [NCT01789281]	Phase 4	34 participants (Actual)	Interventional	2013-05-14	Completed
De Novo Everolimus Versus Tacrolimus in Combination With Mofetil Mycophenolate and Low Dose Corticosteroids to Reduce Tacrolimus Induced Nephrotoxicity in Liver Transplantation: a Prospective, Multicentric, Randomised Study [NCT02909335]	Phase 3	0 participants (Actual)	Interventional	2016-11-30	Withdrawn
A Randomized Prospective Trial of Conversion to Everolimus Therapy From Calcineurin Inhibitor Based Maintenance Immunosuppression in Association With Mycophenolic Acid in Liver Transplantation: Examination of Impact on Long Term Renal Function. [NCT01936519]		24 participants (Actual)	Interventional	2013-12-16	Completed
The Safety of Simvastatin (SOS) in Patients With Pulmonary Lymphangioleiomyomatosis (LAM) and With Tuberous Sclerosis Complex (TSC) [NCT02061397]	Phase 1/Phase 2	10 participants (Actual)	Interventional	2014-03-31	Completed
Phase II Trial of Ribociclib in Combination With Everolimus in Advanced Dedifferentiated Liposarcoma (DDL) and Leiomyosarcoma (LMS) [NCT03114527]	Phase 2	48 participants (Actual)	Interventional	2017-08-08	Active, not recruiting
Randomized, Double Blind, Multicentric Phase III Trial Evaluating the Safety and Benefit of Adding Everolimus to Adjuvant Hormone Therapy in Women With High Risk of Relapse, ER+ and HER2- Primary Breast Cancer Who Remain Free of Disease After Receiving at [NCT01805271]	Phase 3	1,278 participants (Actual)	Interventional	2013-03-31	Active, not recruiting
A Randomized, Double-Blinded, Placebo-Controlled Phase II Study of Adjuvant Everolimus Following the Resection of Metastatic Pancreatic Neuroendocrine Tumors to the Liver [NCT02031536]	Phase 2	2 participants (Actual)	Interventional	2014-04-10	Terminated(stopped due to Slow accrual)
A Phase I Study of Sorafenib and RAD001 in Patients With Metastatic Renal Cell Carcinoma [NCT00384969]	Phase 1	21 participants (Actual)	Interventional	2006-10-31	Completed
Impact of Everolimus on HIV Persistence Post Kidney (and Kidney/Pancreas) or Liver Transplant [NCT02429869]	Phase 4	10 participants (Actual)	Interventional	2016-02-24	Completed
Once-daily Regimen With Envarsus® to Optimize Immunosuppression Management and Outcomes in Kidney Transplant Recipients [NCT02954198]		40 participants (Actual)	Interventional	2016-12-01	Completed
Phase I/II Trial of Sorafenib (Nexavar) and RAD001 (Everolimus)in the Treatment of Patients With Advanced Clear Cell Renal Cell Carcinoma [NCT00392821]	Phase 1/Phase 2	78 participants (Actual)	Interventional	2006-12-31	Completed
Genetically-informed Therapy for ER+ Breast Cancer in a Post-CDK4/6 Inhibitor Setting: a Phase II Umbrella Study (GERTRUDE) [NCT05933395]	Phase 2	135 participants (Anticipated)	Interventional	2023-10-10	Recruiting
Continuous Access to Advanced and Metastatic Renal Cell Carcinoma Therapy With Everolimus Post Pazopanib Treatment [NCT01545817]	Phase 2	74 participants (Actual)	Interventional	2012-04-19	Terminated(stopped due to As the therapeutic landscape in renal cell carcinoma is changing, it has become apparent that information gained so far by CATChEz study is sufficient.)
Effect of the Introduction of mTor Inhibitors in the Activation of the Cytomegalovirus (CMV) -Specific Cellular Immune Response to Control Viral Replication in Kidney Transplant Patients [NCT04936971]	Phase 4	46 participants (Anticipated)	Interventional	2021-09-30	Not yet recruiting
A Randomized, Multicenter Study of Belatacept, Everolimus, rATG and Early Steroid Withdrawal Versus Belatacept, Mycophenolate, rATG and Chronic Steroids in Renal Transplantation [NCT04849533]	Phase 4	120 participants (Anticipated)	Interventional	2021-04-09	Recruiting
Evaluation of WSS and Neointimal Healing Following Percutaneous Coronary Intervention of Angulated Vessels With Resolute® Integrity Zotarolimus Eluting Coronary Stent Compared to XIENCE Xpedition® Everolimus Eluting Coronary Stent [NCT02098876]		86 participants (Actual)	Interventional	2014-05-31	Completed
Fulvestrant Followed by Everolimus Plus Exemestane vs Examestane and Everolimus Followed by Fulvestrant in Postmenopausal Women With HR+ and HER2- Locally Advanced (LABC) or Metastatic Breast Cancer (MBC) Previously Treated With NSAI [NCT02404051]	Phase 3	745 participants (Anticipated)	Interventional	2015-12-31	Recruiting
A Randomized, Open-label Phase II Multicenter Study Evaluating the Efficacy of Oral Everolimus Alone or in Combination With Pasireotide LAR i.m. in Advanced Progressive Pancreatic Neuroendocrine Tumors (PNET) - The COOPERATE-2 Study [NCT01374451]	Phase 2	160 participants (Actual)	Interventional	2011-06-30	Terminated(stopped due to The study was stopped for not meeting the primary endpoint for PFS.)
Evaluation of Oral Care to Prevent Oral Mucositis in Estrogen Receptor Positive Metastatic Breast Cancer Patients Treated With Everolimus: Phase III Randomized Control Trial [NCT02376985]	Phase 3	174 participants (Actual)	Interventional	2015-03-26	Completed
GCC 0901- A Phase II Study of Letrozole in Combination With Lapatinib Followed by an Addition of Everolimus in Postmenopausal Women With Advanced Endocrine Resistant Breast Cancer [NCT01499160]	Phase 2	7 participants (Actual)	Interventional	2012-05-31	Terminated(stopped due to low accrual)
Mechanisms and Treatment of Chronic Allograft Injury (CAI) Due to Calcineurin Inhibitor (CNI) Toxicity [NCT01473732]		2 participants (Actual)	Interventional	2012-03-31	Terminated(stopped due to terminated after 2 patients due to difficulty in enrollment)
An Open-label, Multicenter Phase II Study to Examine the Efficacy and Safety of Everolimus as Second-line Therapy in the Treatment of Patients With Metastatic Renal Cell Carcinoma [NCT01491672]	Phase 2	134 participants (Actual)	Interventional	2011-11-30	Completed
UPCC 36315 A Phase II Study Of Everolimus (RAD001) And Lenvatinib (E7080) In Patients With Metastatic Differentiated Thyroid Cancer Who Have Progressed on Lenvatinib Alone [NCT03139747]	Phase 2	5 participants (Actual)	Interventional	2017-04-03	Suspended(stopped due to lack of accrual reevaluating feasibility)
A Phase I/II Study of RAD001 in Advanced Hepatocellular Carcinoma [NCT00516165]	Phase 1/Phase 2	28 participants (Actual)	Interventional	2007-08-31	Completed
Exploratory Study of Avastin (Bevacizumab) and RAD001 (Everolimus) in Advanced Low or Intermediate Grade Neuroendocrine Carcinoma (AVF3961s) (CRAD001C2481) [NCT00607113]	Phase 2	41 participants (Actual)	Interventional	2008-01-31	Completed
A 2-arm, Prospective, Randomized, Controlled, Open-label, 12 Month Phase III Trial to Evaluate the Efficacy Regarding Renal Function of Everolimus in Combination With a Centre Specific Standard Immunosuppressive Regimen Consisting of CNI, Purinantagonists [NCT01404325]	Phase 3	130 participants (Actual)	Interventional	2012-02-01	Completed
A Phase II Study to Evaluate the Efficacy of RAD001 in Metastatic Non-clear Cell Renal Cell Carcinoma [NCT00830895]	Phase 2	49 participants (Actual)	Interventional	2009-01-31	Completed
A Randomized Phase II Study of Afinitor (RAD001) vs. Sutent (Sunitinib) in Patients With Metastatic Non-Clear Cell Renal Cell Carcinoma (ASPEN) [NCT01108445]	Phase 2	131 participants (Actual)	Interventional	2010-09-30	Completed
An Open Label, randomIzed Controlled Prospective Multicenter Two Arm Phase IV Trial to Determine Patient Preference for Everolimus in Combination With Exemestane or Capecitabine in Combination With Bevacizumab for Advanced (Inoperable or Metastatic) HER2- [NCT02248571]	Phase 4	85 participants (Actual)	Interventional	2014-08-31	Completed
A Pilot Study To Evaluate The Effects of Everolimus on Brain mTOR Activity and Cortical Hyperexcitability in TSC and FCD [NCT02451696]	Phase 2	15 participants (Actual)	Interventional	2014-01-31	Completed
A Randomized Phase II Trial of Everolimus and Letrozole or Hormonal Therapy (Tamoxifen/Medroxyprogesterone Acetate) in Women With Advanced, Recurrent, or Persistent Endometria Carcinoma [NCT02228681]	Phase 2	74 participants (Actual)	Interventional	2015-02-28	Active, not recruiting
Treatment of Relapsed/Refractory Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL) With Everolimus (RAD001) and Alemtuzumab: A Phase I/II Study [NCT00935792]	Phase 1/Phase 2	28 participants (Actual)	Interventional	2009-07-31	Completed
Randomized Phase II Trial of Everolimus Versus Placebo as Adjuvant Therapy in Patients With Locally Advanced Squamous Cell Cancer of the Head and Neck (SCCHN) [NCT01111058]	Phase 2	52 participants (Actual)	Interventional	2010-04-30	Terminated(stopped due to Slow accrual)
Healing Responses After Treatment of Bare Metal Stent Restenosis With Implantation of an Everolimus-eluting Xience V Stent Versus Use of a Paclitaxel-eluting Balloon: Optical Coherence Tomography Study [NCT01065532]		50 participants (Anticipated)	Interventional	2009-05-31	Completed
A Phase I/II Drug Withdrawal Study of Alloantigen-Specific Tregs in Liver Transplantation [NCT03654040]	Phase 1/Phase 2	30 participants (Actual)	Interventional	2021-04-22	Terminated(stopped due to The study was terminated by the Sponsor prior to any participants receiving the investigational product.)
Long-term Follow-up Study to Monitor the Growth and Development of Pediatric Patients Previously Treated With Everolimus in Study CRAD001M2301 [NCT02338609]	Phase 4	15 participants (Actual)	Interventional	2014-12-17	Active, not recruiting
A Phase II Study of the mTOR Inhibitor RAD001 in Previously Treated Patients With Unresectable or Metastatic Adenocarcinoma of the Esophagus and Stomach [NCT00985192]	Phase 2	49 participants (Actual)	Interventional	2009-09-30	Completed
An Exploratory Evaluation of Early Use of Everolimus (EVE) on Tacrolimus (TAC)-Based Immunosuppressive Regiment vs. Mycophenolate Sodium (MPS) on Cytomegalovirus (CMV) Infection in Renal Transplant Recipients. [NCT01927588]	Phase 4	50 participants (Anticipated)	Interventional	2013-08-31	Not yet recruiting
A Prospective, Randomized, Placebo-controlled, Multicenter, International Phase I/II Trial of RAD001 (Everolimus) in Combination With DHAP as Induction Therapy in Patients With Relapsed or Refractory Hodgkin Lymphoma (HL) [NCT01453504]	Phase 1/Phase 2	73 participants (Actual)	Interventional	2012-08-31	Completed
A Randomized, Double-blind, Multicenter, Phase III Study of Everolimus (RAD001) Plus Best Supportive Care Versus Placebo Plus Best Supportive Care in the Treatment of Patients With Advanced NET of GI or Lung Origin [NCT01524783]	Phase 3	302 participants (Actual)	Interventional	2012-03-30	Completed
Signal TrAnsduction Pathway Activity Analysis in OVarian cancER [NCT03458221]	Phase 2/Phase 3	148 participants (Anticipated)	Interventional	2023-01-31	Recruiting
Phase II Study of Single Agent RAD001 in Patients With Colon Cancer and Activating Mutations in the PI3KCA Gene [NCT00390364]	Phase 2	1 participants (Actual)	Interventional	2006-10-31	Terminated(stopped due to Withdrawn due to low accrual)
Phase I/II Trial of RAD001 Plus Docetaxel in Patients With Metastatic or Recurrent Non-Small Cell Lung Cancer [NCT00406276]	Phase 1/Phase 2	28 participants (Actual)	Interventional	2006-11-30	Terminated(stopped due to data analysis showed insufficient drug efficacy)
Molecular Profiling-Based Assignment of Cancer Therapy for Patients With Advanced Solid Tumors [NCT01827384]	Phase 2	208 participants (Actual)	Interventional	2014-01-07	Completed
A Phase II Study of Sporadic Angiomyolipomas (AMLs) Growth Kinetics While on Everolimus Therapy [NCT02539459]	Phase 2	20 participants (Actual)	Interventional	2015-09-23	Terminated(stopped due to Extreme toxicity, met toxicity stopping rules)
Randomised Comparison of Two Different Immunosuppressive Regimens on Progression of Arteriosclerosis in Renal Transplant Patients. [NCT01276834]	Phase 4	13 participants (Actual)	Interventional	2010-09-30	Terminated(stopped due to insufficient patients enrolled)
A Phase 1 Evaluation of the Safety and Tolerability of Niraparib in Combination With Everolimus in Advanced Gynecologic Malignancies and Breast Cancer [NCT03154281]	Phase 1	24 participants (Anticipated)	Interventional	2017-07-17	Active, not recruiting
A Phase IV Multicentre, Open Label Study of Postmenopausal Women With Oestrogen Receptor Positive Locally Advanced or Metastatic Breast Cancer Treated With Everolimus (RAD001) in Combination With Exemestane, With Exploratory Epigenetic Marker Analysis [NCT01743560]	Phase 4	52 participants (Actual)	Interventional	2013-01-31	Completed
A Phase 1b, Open-label, Dose-escalation Study to Evaluate the Safety and Tolerability of SGN-75 in Combination With Everolimus in Patients With CD70-positive Metastatic Renal Cell Carcinoma [NCT01677390]	Phase 1	4 participants (Actual)	Interventional	2012-08-31	Terminated
Multicenter, Prospective, Open-label, Controlled, Randomized, Parallel Groups Study to Evaluate the Renal Function of Adult Liver Transplant Recipients Treated With Two Everolimus-based Immunosuppressive Regimens (Tacrolimus Withdrawal vs. Minimization) U [NCT02115113]	Phase 3	78 participants (Actual)	Interventional	2014-03-28	Completed
A Phase I/II Trial to Assess the Tolerability of RAD 001 With Gefitinib in Patients With Glioblastoma Multiforme and Prostate Cancer and Efficacy in Patients With Castrate Metastatic Prostate Cancer [NCT00085566]	Phase 1/Phase 2	61 participants (Actual)	Interventional	2004-03-31	Completed
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 3	202 participants (Anticipated)	Interventional	2021-12-21	Recruiting
A Phase I/II Drug Withdrawal Study of Alloantigen-Specific Tregs in Liver Transplantation (ITN073ST) [NCT03577431]	Phase 1/Phase 2	9 participants (Anticipated)	Interventional	2019-03-29	Active, not recruiting
Ten-year Follow-up of the Clinical Evaluation of Everolimus-Eluting Coronary Stents in the Treatment of Patients With ST-segment Elevation Myocardial Infarction: EXAMINATION-EXTEND Trial [NCT04462315]		1,498 participants (Actual)	Observational	2015-05-01	Completed
A Prospective, Pilot Trial to Evaluate Safety and Tolerability of Everolimus for the Prevention of BK and CMV Viremia in HLA Sensitized Kidney Transplant Recipients [NCT01911546]	Phase 2	20 participants (Actual)	Interventional	2013-06-30	Completed
Evaluate the Continued Safety and Effectiveness of the XIENCE PRIME EECSS in a Cohort of Real-world Patients Receiving the XIENCE PRIME EECSS During Commercial Use. [NCT01894152]		2,002 participants (Actual)	Observational	2013-07-31	Completed
Phase II Study of RAD001 in Previously Treated Patients With Metastatic Pancreatic Cancer [NCT00409292]	Phase 2	33 participants (Actual)	Interventional	2007-01-31	Completed
PLATINUM: A Prospective, Randomized, Multicenter Trial to Assess an Everolimus-Eluting Coronary Stent System (PROMUS Element™) for the Treatment of up to Two De Novo Coronary Artery Lesions - Pharmacokinetics Sub-trial [NCT01510327]	Phase 3	22 participants (Actual)	Interventional	2009-10-31	Completed
Phase I/II Study of RAD001 in Combination With Temozolomide in Patients With Advanced Pancreatic Neuroendocrine Tumors [NCT00576680]	Phase 1/Phase 2	43 participants (Actual)	Interventional	2008-05-31	Completed
Treatment of Refractory Metastatic Renal Cell Carcinoma With Bevacizumab and RAD001 (Everolimus) [NCT00651482]	Phase 2	10 participants (Actual)	Interventional	2008-08-31	Terminated(stopped due to slow accrual)
Phase I/IB Trial of Eribulin and Everolimus in Patients With Triple Negative Metastatic Breast Cancer [NCT02120469]	Phase 1	27 participants (Actual)	Interventional	2014-10-01	Completed
A Phase II Study of RAD001 (Everolimus) in Patients With Fluoropyrimidine and Platinum-refractory Advanced Gastric Cancer [NCT00729482]	Phase 2	54 participants (Actual)	Interventional	2008-07-31	Completed
A 24-month, Single Center, Pilot, Open Label, Controlled Trial to Evaluate the Efficacy and Safety of Calcineurin-inhibitor Reduction With Conversion at 2 Months to Reduced Dose Tacrolimus/Everolimus in Adult Renal Transplant Recipients Following Campath® [NCT01935128]	Phase 4	55 participants (Actual)	Interventional	2013-07-03	Completed
A 3-month, Multicenter, Randomized, Open Label Study to Evaluate the Impact of Early Versus Delayed Introduction of Everolimus on Wound Healing in de Novo Kidney Transplant Recipients With a Follow-up Evaluation at 12 Month After Transplant (NEVERWOUND St [NCT01410448]	Phase 3	383 participants (Actual)	Interventional	2011-11-30	Completed
Everolimus and Temozolomide as 1-line Treatment in Advanced Gastroenteropancreatic Neuroendocrine Carcinoma (G3) With a Ki67 of 20-55% [NCT02248012]	Phase 2	38 participants (Actual)	Interventional	2014-12-31	Completed
Safety and Efficacy of Mycophenolic Acid Withdrawal With Conversion to Zortress (Everolimus) in Renal Transplant Recipients With BK Virus Infection [NCT01624948]	Phase 4	40 participants (Actual)	Interventional	2012-09-30	Completed
MEK114375: A Rollover Study to Provide Continued Treatment With GSK1120212 to Subjects With Solid Tumors or Leukemia [NCT01376310]	Phase 2	159 participants (Actual)	Interventional	2010-11-02	Terminated(stopped due to Company Decision)
Randomized Comparison of the Biolimus-eluting Biomatrix Neoflex™ og Everolimus-eluting SYNERGY™ Stents in All-comer Patients With Ischemic Heart Disease - The OCT SORT-OUT VIII [NCT02253108]		160 participants (Anticipated)	Interventional	2014-05-31	Active, not recruiting
A Phase I/II Study of X-82, an Oral Anti-VEGFR Tyrosine Kinase Inhibitor, With Everolimus for Patients With Pancreatic Neuroendocrine Tumors [NCT01784861]	Phase 1/Phase 2	23 participants (Actual)	Interventional	2013-05-03	Terminated(stopped due to Pharmaceutical company decision)
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 2	122 participants (Actual)	Interventional	2009-03-31	Completed
Comparison of the Efficacy and Safety of Sirolimus, Everolimus or Mycophenolate in Renal Transplant Recipients Receiving Induction With Anti-thymocyte Globulin, Tacrolimus and Prednisone [NCT03468478]	Phase 4	1,209 participants (Actual)	Interventional	2017-06-18	Completed
Randomized, Double-Blind, Placebo-Controlled Phase II Trial of Fulvestrant (Faslodex) Plus Everolimus in Post-Menopausal Patients With Hormone-Receptor Positive Metastatic Breast Cancer Resistant to Aromatase Inhibitor Therapy [NCT01797120]	Phase 2	131 participants (Actual)	Interventional	2013-05-31	Completed
Multicenter 3-arm Trial to Evaluate the Efficacy and Safety of Pasireotide LAR or Everolimus Alone or in Combination in Patients With Well Differentiated Neuroendocrine Carcinoma of the Lung and Thymus - LUNA Trial [NCT01563354]	Phase 2	124 participants (Actual)	Interventional	2013-08-16	Completed
A 24-month Multi-center, Open-label, Randomized, Controlled Study to Evaluate the Evolution of Renal Function in Maintenance Liver Transplant Recipients Receiving Either RAD001 (Everolimus) Plus Reduced TAC or RAD001 (Everolimus) Plus Mycophenolate Mofeti [NCT03596970]	Phase 3	0 participants (Actual)	Interventional	2015-09-30	Withdrawn
Biological Medicine for Diffuse Intrinsic Pontine Glioma (DIPG) Eradication [NCT02233049]	Phase 2	250 participants (Anticipated)	Interventional	2014-10-31	Recruiting
Phase II Evaluation of Real-Time, Pharmacokinetically Guided Everolimus in Patients With Hormone Receptor Positive Breast Cancer, Pancreatic Neuroendocrine Tumors (PNET), and Renal Cell Carcinoma [NCT02273752]	Phase 2	2 participants (Actual)	Interventional	2014-11-30	Terminated(stopped due to Slow accrual)
A Prospective Cohort, Open, Phase II Clinical Study of Chidamide/Everolimus Combined With Endocrine Therapy for PIK3CA Wild-type/Mutant Hormone Receptor Positive/Human Epidermal Growth Factor Receptor 2 Negative Advanced Breast Cancer [NCT05983107]	Phase 2	102 participants (Anticipated)	Interventional	2023-07-20	Recruiting
A Multi-institutional Phase I and Biomarker Study of Everolimus Added to Combined Hormonal and Radiation Therapy for High Risk Prostate Cancer [NCT01642732]	Phase 1	1 participants (Actual)	Interventional	2012-10-31	Terminated(stopped due to Lack of accrual and funding expires in June, 2014.)
Randomized, Open-Label Trial of Tacrolimus/Everolimus vs. Tacrolimus/Enteric-Coated Mycophenolate Sodium to Prevent Biopsy-Proven Acute Rejection and Chronic Allograft Injury in Adult, Primary Kidney Transplantation [NCT01680861]	Phase 3	32 participants (Actual)	Interventional	2012-11-30	Completed
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 2	68 participants (Actual)	Interventional	2009-01-31	Completed
A Phase I/II, Single Arm, Open-label Study of Ribociclib in Combination With Everolimus + Exemestane in the Treatment of Men and Postmenopausal Women With HR+, HER2- Locally Advanced or Metastatic Breast Cancer Following Progression on a CDK 4/6 Inhibitor [NCT02732119]	Phase 1/Phase 2	104 participants (Actual)	Interventional	2016-06-14	Completed
A Multicenter, Dose-finding Study to Determine if Oral BEZ235 Alone or in Combination With RAD001 Decreases the Incidence of Respiratory Tract Infections in Elderly Subjects [NCT03373903]	Phase 2	652 participants (Actual)	Interventional	2017-11-15	Active, not recruiting
Precision Treatment of Refractory Triple Negative Breast Cancer Based on Molecular Subtyping --FUSCC-TNBC- Umbrella Trial [NCT03805399]	Phase 1/Phase 2	140 participants (Anticipated)	Interventional	2018-10-18	Recruiting
Fulvestrant Alone Versus Fulvestrant and Everolimus Versus Fulvestrant, Everolimus and Anastrozole: A Phase III Randomized Placebo-Controlled Trial in Postmenopausal Patients [NCT02137837]	Phase 3	37 participants (Actual)	Interventional	2014-05-31	Terminated(stopped due to lack of accrual)
Japan-USA Harmonized Assessment by Randomized, Multi-Center Study of OrbusNEich's Combo StEnt (Japan-USA HARMONEE): Assessment of a Novel DES Platform For Percutaneous Coronary Revascularization in Patients With Ischemic Coronary Disease and NSTEMI Acute [NCT02073565]		572 participants (Actual)	Interventional	2014-02-28	Completed
A National, Multi-center, Randomized, Open Label Study to Evaluate the Efficacy and Safety of Everolimus Combined With Enteric-coated Mycophenolate Sodium Compared to the Standard Treatment Combining Tacrolimus and Enteric-coated Mycophenolate Sodium in d [NCT01625377]	Phase 3	188 participants (Actual)	Interventional	2012-12-31	Completed
A 24-month, Multi-center, Single Arm, Prospective Study to Evaluate Renal Function, Efficacy, Safety and Tolerability of Everolimus in Combination With Reduced Exposure Cyclosporine or Tacrolimus in Paediatric Liver Transplant Recipients. [NCT01598987]	Phase 3	56 participants (Actual)	Interventional	2012-10-31	Completed
A Phase II, Single Arm Study of the Use of Steroid-based Mouthwash to Prevent Stomatitis in Postmenopausal Women With Advanced or Metastatic Hormone Receptor Positive Breast Cancer Being Treated With Everolimus Plus Exemestane [NCT02069093]	Phase 2	92 participants (Actual)	Interventional	2014-05-31	Completed
A Prospective, Randomised, Controlled, Open-label, Multicentre Phase III Study to Evaluate Efficacy and Safety of Peptide Receptor Radionuclide Therapy (PRRT) With 177Lu-Edotreotide Compared to Targeted Molecular Therapy With Everolimus in Patients With I [NCT03049189]	Phase 3	309 participants (Actual)	Interventional	2017-02-02	Active, not recruiting
A Two-period, Multicenter, Randomized, Open-label, Phase II Study Evaluating the Clinical Benefit of a Maintenance Treatment Targeting Tumor Molecular Alterations in Patients With Progressive Locally-advanced or Metastatic Solid Tumors [NCT02029001]	Phase 2	560 participants (Anticipated)	Interventional	2014-03-31	Recruiting
A Phase I Study of RAD001 and Sunitinib in Metastatic Renal Cell Carcinoma Patients [NCT00422344]	Phase 1	20 participants (Actual)	Interventional	2006-10-31	Completed
A Randomized, Open-label, Single-dose, Two-way Crossover Clinical Trial to Investigate the Pharmacokinetic and Safety After Oral Administration of SVG101(Dispersible Tablet of Everolimus) 5mg and Afinitor 5mg in Healthy Adults [NCT05490095]	Phase 1	26 participants (Actual)	Interventional	2021-07-23	Completed
A 24 Month, Randomized, Controlled, Study to Evaluate the Efficacy and Safety of Concentration-controlled Everolimus Plus Reduced Tacrolimus Compared to Standard Tacrolimus in Recipients of Living Donor Liver Transplants and Long Term Extension to Evaluat [NCT01888432]	Phase 3	285 participants (Actual)	Interventional	2013-09-25	Completed
Donor-Alloantigen-Reactive Regulatory T Cell (darTreg) Therapy in Liver Transplantation (RTB-002) [NCT02188719]	Phase 1	15 participants (Actual)	Interventional	2014-12-17	Terminated(stopped due to The trial could not be completed within the grant timeline.)
Randomized Phase II Study of BEZ235 or Everolimus in Advanced Pancreatic Neuroendocrine Tumors [NCT01628913]	Phase 2	62 participants (Actual)	Interventional	2012-10-31	Terminated(stopped due to This trial was terminated based on an interim analysis as BEZ235 did not demonstrate a progression free survival advantage to everolimus treatment.)
A Three-arm, Randomized, Open Label, Phase II Study of Everolimus in Combination With Exemestane Versus Everolimus Alone Versus Capecitabine in the Treatment of Postmenopausal Women With Estrogen Receptor Positive, Locally Advanced, Recurrent, or Metastat [NCT01783444]	Phase 2	309 participants (Actual)	Interventional	2013-02-26	Completed
Phase II Study of Everolimus Beyond Progression in Postmenopausal Women With Advanced, Hormone Receptor Positive Breast Cancer [NCT02269670]	Phase 2	3 participants (Actual)	Interventional	2014-11-25	Terminated(stopped due to Slow to accrual)
A Three-arm, Randomized, Double-blind, Placebo-controlled Study of the Efficacy and Safety of Two Trough-ranges of Everolimus as Adjunctive Therapy in Patients With Tuberous Sclerosis Complex (TSC) Who Have Refractory Partial-onset Seizures [NCT01713946]	Phase 3	366 participants (Actual)	Interventional	2013-04-29	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00085566 (1) [back to overview]	Overall Objective Response
NCT00087685 (2) [back to overview]	Clinical Benefit Rate
NCT00087685 (2) [back to overview]	Number of Participants With Objective Response Plus Stable Disease Rate (CR + PR + SD)
NCT00096486 (1) [back to overview]	Overall Objective Response
NCT00113360 (1) [back to overview]	Progression Free Survival (PFS)
NCT00154284 (4) [back to overview]	Calculated Creatinine Clearance at 6 Month and 12 Month
NCT00154284 (4) [back to overview]	Number of Participants With Biopsy-proven Acute Rejection (BPAR) Episodes, Graft Loss, Death or Loss to Follow-up
NCT00154284 (4) [back to overview]	Renal Function Measured by Calculated Glomerular Filtration Rate (GFR Calculated According to the Nankivell Formula)
NCT00154284 (4) [back to overview]	Serum Creatinine at Month 6 and 12
NCT00154297 (6) [back to overview]	Number of Participants With Any Wound Healing Disorder During the 12-month Treatment Period
NCT00154297 (6) [back to overview]	Number of Participants Considered in Failure for the Primary Failure Endpoint at 6 Months Post-transplantation.
NCT00154297 (6) [back to overview]	Number of Participants Considered in Failure for the Primary Failure Endpoint at 3 Months
NCT00154297 (6) [back to overview]	Number of Participants Considered in Failure for the Primary Failure Endpoint at 12 Months Post-transplantation.
NCT00154297 (6) [back to overview]	Number of Participants Who Underwent Any Dialysis Within the 12-month Treatment Period
NCT00154297 (6) [back to overview]	Duration of Dialysis
NCT00154310 (5) [back to overview]	Number of Participants With Occurrence of Treatment Failures
NCT00154310 (5) [back to overview]	Number of Participants With Occurrence of Biopsy Proven Acute Rejection (BPAR), Graft Loss or Death
NCT00154310 (5) [back to overview]	Number of Participants Who Experienced an Adverse Event or Serious Adverse Event
NCT00154310 (5) [back to overview]	Changes in Cardiovascular Risk From Month 4.5 to Final Assessment at Month 12
NCT00154310 (5) [back to overview]	Renal Function (Nankivell Formula) at Month 12 Post Transplantation.
NCT00170846 (3) [back to overview]	Number of Participants With Safety Parameters
NCT00170846 (3) [back to overview]	Change in mGFR by Baseline Calculated Creatinine Clearance (Cockcroft-Gault Formula)
NCT00170846 (3) [back to overview]	Renal Function Assessed by Measured GFR (mGFR)
NCT00180479 (44) [back to overview]	Target Vessel Failure (TVF)
NCT00180479 (44) [back to overview]	% Volume Obstruction (% VO)
NCT00180479 (44) [back to overview]	Acute Success: Clinical Device
NCT00180479 (44) [back to overview]	Acute Success: Clinical Procedure
NCT00180479 (44) [back to overview]	Distal Late Loss
NCT00180479 (44) [back to overview]	In-segment % Angiographic Binary Restenosis (% ABR) Rate
NCT00180479 (44) [back to overview]	In-segment % Diameter Stenosis (% DS)
NCT00180479 (44) [back to overview]	In-stent % Angiographic Binary Restenosis (% ABR) Rate
NCT00180479 (44) [back to overview]	In-stent % Diameter Stenosis (% DS)
NCT00180479 (44) [back to overview]	In-stent Late Loss
NCT00180479 (44) [back to overview]	Ischemia Driven Major Adverse Cardiac Event (MACE)
NCT00180479 (44) [back to overview]	Ischemia Driven Major Adverse Cardiac Event (MACE)
NCT00180479 (44) [back to overview]	Ischemia Driven Major Adverse Cardiac Event (MACE)
NCT00180479 (44) [back to overview]	Ischemia Driven Major Adverse Cardiac Event (MACE)
NCT00180479 (44) [back to overview]	Ischemia Driven Major Adverse Cardiac Event (MACE)
NCT00180479 (44) [back to overview]	Ischemia Driven Major Adverse Cardiac Event (MACE)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00180479 (44) [back to overview]	Ischemia Driven Major Adverse Cardiac Event(MACE)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00180479 (44) [back to overview]	Ischemia Driven Major Adverse Cardiac Event (MACE)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00180479 (44) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00180479 (44) [back to overview]	Major Secondary Endpoint: Ischemia Driven Target Vessel Failure (ID-TVF)
NCT00180479 (44) [back to overview]	Persisting Incomplete Stent Apposition, Late-acquired Incomplete Stent Apposition, Aneurysm, Thrombosis, and Persisting Dissection
NCT00180479 (44) [back to overview]	Primary Endpoint: In-segment Late Loss (LL)
NCT00180479 (44) [back to overview]	Proximal Late Loss
NCT00180479 (44) [back to overview]	Target Vessel Failure (TVF)
NCT00180479 (44) [back to overview]	Target Vessel Failure (TVF)
NCT00180479 (44) [back to overview]	Target Vessel Failure (TVF)
NCT00180479 (44) [back to overview]	Target Vessel Failure (TVF)
NCT00180479 (44) [back to overview]	Target Vessel Failure (TVF)
NCT00180479 (44) [back to overview]	Target Vessel Failure (TVF)
NCT00251004 (4) [back to overview]	Number of Participants With Composite Efficacy Endpoints - 12 Month Analysis
NCT00251004 (4) [back to overview]	Percentage of Participants With the Composite Incidence of Graft Loss, Death or Loss to Follow up at 12 Months Post-transplantation
NCT00251004 (4) [back to overview]	Non-inferiority Analysis of Renal Function, Calculated by Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula
NCT00251004 (4) [back to overview]	Non-inferiority Analysis on Percentage of Participants With Composite Efficacy Endpoints
NCT00267189 (3) [back to overview]	Percentage of Patients With Efficacy Failure (Biopsy Proven Acute Rejection [BPAR], Graft Loss or Death)
NCT00267189 (3) [back to overview]	Mean Change From Baseline in Cockcroft-Gault Calculated Creatinine Clearance (CrCl)
NCT00267189 (3) [back to overview]	Number of Patients With Discontinuation of Study Medication
NCT00300274 (10) [back to overview]	Percentage of Participants With Biopsy-proven Acute Rejection (BPAR of ISHLT Grade ≥ 3A), Acute Rejection (AR) Associated With Hemodynamic Compromise (HDC), Graft Loss/Re-transplant and Death at Month 24
NCT00300274 (10) [back to overview]	Renal Function Measured by Glomerular Filtration Rate (GFR) at 12 Months
NCT00300274 (10) [back to overview]	Renal Function Calculated by Glomerular Filtration Rate (GFR) at 24 Months
NCT00300274 (10) [back to overview]	Percentage of Participants With Graft Loss/Re-transplant, Death or Loss to Follow-up at 24 Months
NCT00300274 (10) [back to overview]	Percentage of Participants With Graft Loss/Re-transplant, Death or Loss to Follow-up at 12 Months
NCT00300274 (10) [back to overview]	Percentage of Participants With Composite Efficacy Failure at 24 Months
NCT00300274 (10) [back to overview]	Percentage of Participants With Composite Efficacy Failure at 12 Months
NCT00300274 (10) [back to overview]	Percentage of Participants With Cardiac Allograft Vasculopathy (CAV) at Month 12
NCT00300274 (10) [back to overview]	Percentage of Participants With Biopsy-proven Acute Rejection (BPAR of ISHLT Grade ≥ 3A), Acute Rejection Associated With Hemodynamic Compromise (HDC), Graft Loss/Re-transplant and Death at Month 12
NCT00300274 (10) [back to overview]	Change From Baseline in the Average Maximum Intimal Thickness at Month 12
NCT00307047 (66) [back to overview]	Ischemia Driven Major Adverse Cardiac Events (MACE)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Failure (TLF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Failure (TLF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Failure (TLF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Failure (TLF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Failure (TLF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Revascularization (TLR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Revascularization (TLR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Revascularization (TLR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Revascularization (TLR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Revascularization (TLR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Revascularization (TLR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Failure (TVF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Failure (TVF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Failure (TVF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Failure (TVF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Failure (TVF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Failure (TVF)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Revascularization (TVR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Revascularization (TVR)
NCT00307047 (66) [back to overview]	All Cause Mortality
NCT00307047 (66) [back to overview]	All Cause Mortality
NCT00307047 (66) [back to overview]	All Cause Mortality
NCT00307047 (66) [back to overview]	All Cause Mortality
NCT00307047 (66) [back to overview]	All Cause Mortality
NCT00307047 (66) [back to overview]	Acute Success (Clinical Procedure)
NCT00307047 (66) [back to overview]	Acute Success (Clinical Device)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Revascularization (TVR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Revascularization (TVR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Revascularization (TVR)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Vessel Revascularization (TVR)
NCT00307047 (66) [back to overview]	Ischemia Driven Major Adverse Cardiac Events (MACE)
NCT00307047 (66) [back to overview]	Protocol Defined Stent Thrombosis Rate
NCT00307047 (66) [back to overview]	Protocol Defined Stent Thrombosis Rate
NCT00307047 (66) [back to overview]	Protocol Defined Stent Thrombosis Rate
NCT00307047 (66) [back to overview]	Protocol Defined Stent Thrombosis Rate
NCT00307047 (66) [back to overview]	All Myocardial Infarction (MI)
NCT00307047 (66) [back to overview]	Ischemia Driven Target Lesion Failure (TLF)
NCT00307047 (66) [back to overview]	Protocol Defined Stent Thrombosis Rate
NCT00307047 (66) [back to overview]	Ischemia Driven Major Adverse Cardiac Events (MACE)
NCT00307047 (66) [back to overview]	Ischemia Driven Major Adverse Cardiac Events (MACE)
NCT00307047 (66) [back to overview]	Ischemia Driven Major Adverse Cardiac Events (MACE)
NCT00307047 (66) [back to overview]	Ischemia Driven Major Adverse Cardiac Events (MACE)
NCT00307047 (66) [back to overview]	Definite + Probable Stent Thrombosis Rate Based on ARC Definition
NCT00307047 (66) [back to overview]	Definite + Probable Stent Thrombosis Rate Based on ARC Definition
NCT00307047 (66) [back to overview]	Definite + Probable Stent Thrombosis Rate Based on ARC Definition
NCT00307047 (66) [back to overview]	Definite + Probable Stent Thrombosis Rate Based on ARC Definition
NCT00307047 (66) [back to overview]	Definite + Probable Stent Thrombosis Rate Based on Academic Research Consortium (ARC) Definition
NCT00307047 (66) [back to overview]	Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)
NCT00307047 (66) [back to overview]	Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)
NCT00307047 (66) [back to overview]	Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)
NCT00307047 (66) [back to overview]	Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)
NCT00307047 (66) [back to overview]	Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)
NCT00307047 (66) [back to overview]	Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)
NCT00307047 (66) [back to overview]	Cardiac Death or Target Vessel MI Rate
NCT00307047 (66) [back to overview]	Cardiac Death or Target Vessel MI Rate
NCT00307047 (66) [back to overview]	Cardiac Death or Target Vessel MI Rate
NCT00307047 (66) [back to overview]	Cardiac Death or Target Vessel MI Rate
NCT00307047 (66) [back to overview]	Cardiac Death or Target Vessel MI Rate
NCT00307047 (66) [back to overview]	Cardiac Death or Target Vessel MI Rate
NCT00307047 (66) [back to overview]	All MI
NCT00307047 (66) [back to overview]	All MI
NCT00307047 (66) [back to overview]	All MI
NCT00307047 (66) [back to overview]	All MI
NCT00307047 (66) [back to overview]	All MI
NCT00307047 (66) [back to overview]	All Cause Mortality
NCT00317720 (2) [back to overview]	Clinical Benefit Response Rate (CBR)
NCT00317720 (2) [back to overview]	Optimal Dose of RAD001 in Combination With Trastuzumab (Phase I)
NCT00323739 (2) [back to overview]	Progression Free Survival (PFS), the Length of Time, in Months, That Patients Were Alive From Their First Date of Protocol Treatment Until Worsening of Their Disease
NCT00323739 (2) [back to overview]	Overall Survival (OS), the Length of Time, in Months, That Patients Were Alive From Their First Date of Protocol Treatment Until Death
NCT00331409 (5) [back to overview]	Median Time to Progression
NCT00331409 (5) [back to overview]	Number of Participants With Adverse Events
NCT00331409 (5) [back to overview]	Number of Subjects That Demonstrated a Reduction in Tumor Measurements.
NCT00331409 (5) [back to overview]	Overall Number of Participants Who Achieve a Response Rate (Complete Response, Partial Response, and Stable Disease) at 3 Months
NCT00331409 (5) [back to overview]	Progression-free Survival at 3 Months
NCT00332839 (1) [back to overview]	Number of Participants Who Experienced Adverse Events and Death
NCT00363051 (11) [back to overview]	Everolimus Trough Level Determination by Pharmacokinetics Parameter in Both Strata (Stratum 1 and 2)
NCT00363051 (11) [back to overview]	Objective Response Rate: Percentage of Participants With Best Over All Response of Complete Response or Partial Response by Central Radiology Review (Stratum 1) Based on Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00363051 (11) [back to overview]	Objective Response Rate: Percentage of Participants With Best Over All Response of Complete Response or Partial Response by Central Radiology Review (Stratum 2) Based on Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00363051 (11) [back to overview]	Time to Overall Survival (OS) (Stratum 2)
NCT00363051 (11) [back to overview]	Time to Progression Free Survival (PFS) Per Central Radiology Review (Stratum 2)
NCT00363051 (11) [back to overview]	Time to Overall Survival (OS)(Stratum 1)
NCT00363051 (11) [back to overview]	Time to Progression Free Survival (PFS) Per Central Radiology Review (Stratum 1)
NCT00363051 (11) [back to overview]	Effect of Octreotide Depot on the Trough Concentrations of Everolimus
NCT00363051 (11) [back to overview]	Number of Participants With Adverse Events (AEs), Death, Serious Adverse Events (SAEs) [Stratum 2]
NCT00363051 (11) [back to overview]	Number of Participants With Adverse Events (AEs), Death, Serious Adverse Events (SAEs)[Stratum 1]
NCT00363051 (11) [back to overview]	Duration of Overall Response (Stratum 1) Based on Response Evaluation Criteria in Solid Tumors (RECIST)- Central Radiology Review
NCT00369161 (3) [back to overview]	Number of Participants With Incidence of Biopsy-proven Acute Rejection (BPAR)
NCT00369161 (3) [back to overview]	Renal Function Assessed by Calculated Glomerular Filtration Rate (cGFR)
NCT00369161 (3) [back to overview]	Percentage of Participants With Efficacy Failure
NCT00371826 (39) [back to overview]	Number of Participants With Wound Problems(12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Sub Clinical Acute Rejection (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Sub Clinical Acute Rejection (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Post Transplant Diabetes Mellitus (PTDM) and Impaired Fasting Glucose (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Notable Abnormalities in Total Cholesterol and Triglycerides as Measurement of Effect of Treatment on Cardiovascular Health (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Notable Abnormalities in Total Cholesterol and Triglycerides as Measurement of Effect of Treatment on Cardiovascular Health (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Notable Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) as Measurement of Effect of Treatment on Cardiovascular Health (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Notable Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) as Measurement of Effect of Treatment on Cardiovascular Health (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With New Onset Diabetes Mellitus After Transplantation (NODAT) and Impaired Fasting Glucose (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Histological Evidence Chronic Allograft Nephropathy (CAN) (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Histological Evidence Chronic Allograft Nephropathy (CAN) (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Employment Status (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Employment Status (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Composite Endpoint of Treatment Failure (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Biopsy Proven Acute Rejection (BPAR) Per Treatment Group (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Biopsy Proven Acute Rejection (BPAR) Influenced by Demographic Characteristics and Morbidities (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Biopsy Proven Acute Rejection (BPAR) Influenced by Demographic Characteristics and Morbidities (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Any Wound Problems (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Antibody-mediated Rejection Per Treatment Group (36 Months Analysis)
NCT00371826 (39) [back to overview]	Mean Urine Albumin/Creatinine Ratio [ACR] as Measurement of Proteinuria (36 Months Analysis)
NCT00371826 (39) [back to overview]	Mean Short-form 36 Health Survey (SF-36) Score as a Measure of Quality of Life Assessment (36 Months Analysis)
NCT00371826 (39) [back to overview]	Mean Short-form 36 Health Survey (SF-36) Score as a Measure of Quality of Life Assessment (12 Months Analysis)
NCT00371826 (39) [back to overview]	Mean Serum Creatinine (36 Months Analysis)
NCT00371826 (39) [back to overview]	Creatinine Clearance Calculated by the Cockcroft-Gault Formula (36 Months Analysis)
NCT00371826 (39) [back to overview]	Change in Bone Mineral Density Between Week 2 and Month 24 (36 Months Analysis)
NCT00371826 (39) [back to overview]	Calculated Glomerular Filtration Rate (cGFR) After Kidney Transplant to Evaluate Kidney Function (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Erythropoietin Usage (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Erythropoietin Usage (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Composite Endpoint of Treatment Failure (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Biopsy Proven Acute Rejection (BPAR) Per Treatment Group (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants With Antibody-mediated Rejection Per Treatment Group (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants Hospitalized for Reasons Other Than Primary Transplantation (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Participants Hospitalized for Reasons Other Than Primary Transplantation (12 Months Analysis)
NCT00371826 (39) [back to overview]	Mean Urine Albumin/Creatinine Ratio (ACR) as Measurement of Proteinuria (12 Months Analysis)
NCT00371826 (39) [back to overview]	Mean Serum Creatinine (12 Months Analysis)
NCT00371826 (39) [back to overview]	Creatinine Clearance (CrCl) Calculated by the Cockcroft-Gault Formula (12 Months Analysis)
NCT00371826 (39) [back to overview]	Calculated Glomerular Filtration Rate (cGFR) After Kidney Transplant to Evaluate Kidney Function (12 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Patient Survival and Graft Survival (36 Months Analysis)
NCT00371826 (39) [back to overview]	Number of Patient Survival and Graft Survival (12 Months Analysis)
NCT00374140 (4) [back to overview]	Progression-free Survival
NCT00374140 (4) [back to overview]	Overall Survival
NCT00374140 (4) [back to overview]	Objective Response Rate
NCT00374140 (4) [back to overview]	Determine the Proportion of Previously Treated Small Cell Lung Cancer (SCLC) Patients Whose Disease Has Not Progressed Following 6-weeks (2 Cycles) of Treatment With RAD001.
NCT00377962 (12) [back to overview]	Number of Patients With Biopsy-proven Acute Rejection From Month 12 to End of Study (Month 24)
NCT00377962 (12) [back to overview]	Number of Patients in Need of Dialysis From Month 12 to End of Study (Month 24)
NCT00377962 (12) [back to overview]	Mean Days of Hospitalization From Baseline to End of Study (Month 24)
NCT00377962 (12) [back to overview]	Change in Forced Vital Capacity (FVC) From Baseline to End of Study (Month 24) in the Lung Transplant Subgroup
NCT00377962 (12) [back to overview]	Change in Forced Expiratory Volume in 1 Second (FEV1) From Baseline to End of Study (Month 24) in the Lung Transplant Subgroup
NCT00377962 (12) [back to overview]	Number of Patients Who Died and Number of Patients With Graft Loss From Month 12 to End of Study (Month 24)
NCT00377962 (12) [back to overview]	Change in Measured Glomerular Filtration Rate (mGFR) From Baseline to Month 12
NCT00377962 (12) [back to overview]	Change in Left Ventricular Function (Diameter and Thickness Parameters) From Baseline to End of Study (Month 24) in the Heart Transplant Subgroup
NCT00377962 (12) [back to overview]	Change in Left Ventricular Function (Filling and Ejection Fraction Parameters) From Baseline to End of Study (Month 24) in the Heart Transplant Subgroup
NCT00377962 (12) [back to overview]	Change in Measured Glomerular Filtration Rate (mGFR) From Baseline to End of Study (Month 24)
NCT00377962 (12) [back to overview]	Number of Patients Discontinued From the Study Due to Adverse Events From Month 12 to End of Study (Month 24)
NCT00377962 (12) [back to overview]	Change in Serum Creatinine From Baseline to End of Study (Month 24)
NCT00378014 (9) [back to overview]	Number of Patients Who Experienced Adverse Events, Serious Adverse Events and Death
NCT00378014 (9) [back to overview]	Incidence of Efficacy Failure
NCT00378014 (9) [back to overview]	Incidence of the Need for a Change in the Immunosuppressive Regimen
NCT00378014 (9) [back to overview]	Patient and Graft Survival
NCT00378014 (9) [back to overview]	Renal Function (cGFR)
NCT00378014 (9) [back to overview]	Hepatitis C Virus (HCV) Replication in HCV-positive Patients
NCT00378014 (9) [back to overview]	Number of Patients Who Experienced Adverse Events, Serious Adverse Events and Death
NCT00378014 (9) [back to overview]	Incidence of Treated BPAR
NCT00378014 (9) [back to overview]	Calculated Glomerular Filtration Rate (cGFR)
NCT00390364 (1) [back to overview]	Response Rate: The Total Number of Participants With Progression of Disease
NCT00392821 (2) [back to overview]	Progression-Free Survival for Patients Treated at MTD/Phase II Dose Level
NCT00392821 (2) [back to overview]	Overall Response Rate (ORR) of Patients Treated at MTD/Phase II Dose Level
NCT00401778 (3) [back to overview]	Clinical Response as Assessed Metabolically by Changes in Positron Emission Tomography (PET) Scan Between Baseline and Immediately Prior to Surgery.
NCT00401778 (3) [back to overview]	Effects of RAD001 on the Regulation of Key Proteins Involved With the Mammalian Target of Rapamycin (mTOR) Axis in Tumor Specimens and Buccal Mucosa in Patients With Operable Non-small Cell Lung Cancer (NSCLC).
NCT00401778 (3) [back to overview]	Duration of Hospital Stay Following Surgery.
NCT00406276 (2) [back to overview]	Time to Progression:Time Period (in Months) From Study Entry Until Disease Progression, Death, or Last Date of Contact.
NCT00406276 (2) [back to overview]	Number of Subjects Showing Partial Response and Stable Disease With the Combination of RAD001 and Docetaxel.
NCT00409292 (4) [back to overview]	To Assess the Safety of RAD001 in Patients With Metastatic Pancreatic Cancer
NCT00409292 (4) [back to overview]	to Assess Overall Survival Associated With RAD001 in This Patient Population.
NCT00409292 (4) [back to overview]	To Assess Progression-free Survival of RAD001 at Two Months in Patients With Metastatic Pancreatic Cancer Whose Disease Has Progressed on Gemcitabine Chemotherapy.
NCT00409292 (4) [back to overview]	to Assess Response Rate Associated With RAD001 in This Patient Population.
NCT00410124 (13) [back to overview]	Time to Definitive Deterioration of the FKS-DRS Risk Score by at Least 2 Score Units Using Kaplan-Meier Method, by Treatment.
NCT00410124 (13) [back to overview]	Progressive Free Survival (PFS) in Patients Who Receive RAD001 Plus Best Supportive Care(BSC) Versus Patients Who Receive Matching Placebo Plus BSC
NCT00410124 (13) [back to overview]	Overall Survival (OS) Assessed by the Monthly Overall Survival Assessments
NCT00410124 (13) [back to overview]	Pharmacokinetics of RAD001: Time of the Last Quantifiable Concentration in a Dosing Interval - (Tlast)
NCT00410124 (13) [back to overview]	Pharmacokinetics of RAD001: Time at Which C-Max Occurs (t-Max)
NCT00410124 (13) [back to overview]	Pharmacokinetics of RAD001: Normalized to Body Surface Area (CL/F)
NCT00410124 (13) [back to overview]	Pharmacokinetics of RAD001: Area Under Curve (AUC) in a Dosing Interval From Time-zero to Time of the Last Quantifiable Concentration. (AUC 0-tlast)
NCT00410124 (13) [back to overview]	Duration of Response in Patients Who Receive RAD001 Plus BSC Versus Placebo Plus BSC
NCT00410124 (13) [back to overview]	Best Overall Response Rate in Patients Who Receive RAD001 Plus BSC Versus Matching Placebo Plus BSC
NCT00410124 (13) [back to overview]	Analysis of Time to Definitive Deterioration of the Global Health Status/QoL Scale(QL) Scores of the EORTC QLQ-30 Questionnaire by at Least 10 Percent Using Kaplan Meier Method, by Treatment.
NCT00410124 (13) [back to overview]	Pharmacokinetics of RAD001: Apparent Systemic Clearance From Blood Following Extravascular Administration (CL/F)
NCT00410124 (13) [back to overview]	Pharmacokinetics of RAD001:Peak Concentration in a Dosing Interval (C-max); Pre-dose Concentration at 24-h Time Point in Dosing Interval (C-min) and Average Concentration in a Dosing Interval =(C-avg)
NCT00410124 (13) [back to overview]	Time to Definitive Deterioration of the Physical Functioning Scale (PF)Score of the EORTC QLQ-C30 Questionnaire by at Least 10 Percent Using Kaplan_Meier Method, by Treatment.
NCT00411619 (2) [back to overview]	Overall Reduction in SEGA Tumor Volume.
NCT00411619 (2) [back to overview]	Number With Observed Adverse Side Effects
NCT00412061 (7) [back to overview]	Overall Survival Using Kaplan-Meier Methodology
NCT00412061 (7) [back to overview]	Progression Free Survival (PFS) as Per Adjudicated Central Review by Baseline 5-hydroxyindoleacetic Acid (5-HIAA) Level
NCT00412061 (7) [back to overview]	Number of Patients With Adverse Events (AEs), Clinically Notable AE, Death, Serious Adverse Events (SAEs) (Double-Blind Phase)
NCT00412061 (7) [back to overview]	Progression Free Survival (PFS) as Per Adjudicated Central Radiology Review
NCT00412061 (7) [back to overview]	Best Overall Response Rate as Per Adjudicated Central Radiology Review Based on Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00412061 (7) [back to overview]	Progression Free Survival (PFS) as Per Adjudicated Central Review by Baseline Chromogranin A (CgA)
NCT00412061 (7) [back to overview]	Number of Patients With Adverse Events (AEs), Clinically Notable AE, Death, Serious Adverse Events (SAEs) (Open Label Phase)
NCT00414440 (5) [back to overview]	Course of Calculated GFR (mL/Min/1.73 m^2) From Month 24 to Month 60
NCT00414440 (5) [back to overview]	Changes in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP)
NCT00414440 (5) [back to overview]	Calculated GFR, Change From Baseline at Month 60 by Baseline cGFR
NCT00414440 (5) [back to overview]	Primary Efficacy Analysis of Total Kidney Volume (mITT Set, Multiple Imputation)
NCT00414440 (5) [back to overview]	Calculated GFR (mL/Min/1.73 m^2), Change From Baseline by Visit
NCT00419159 (13) [back to overview]	Biomarkers Predictive of Clinical Benefit (DCR by PTEN ) on Everolimus (RAD001) 10mg/Day
NCT00419159 (13) [back to overview]	Biomarker Predictive of Clinical Benefit (DCR by KRAS) on Everolimus (RAD001) 70 mg/Week
NCT00419159 (13) [back to overview]	Biomarkers Predictive of Clinical Benefit (Median PFS and OS by PTEN ) on Everolimus (RAD001) 10mg/Day
NCT00419159 (13) [back to overview]	Biomarker Predictive of Clinical Benefit (DCR by KRAS) on Everolimus (RAD001) 10 mg/Day
NCT00419159 (13) [back to overview]	Number of Patients Who Died, Had an Serious Adverse Event (SAE), Had Grade 3 to 4 Adverse Event (AE), Discontinued Due to an AE, or Had a Clinical Notable AE by Treatment (tr).
NCT00419159 (13) [back to overview]	Disease Control Rate (DCR) and Objective Response Rate (ORR) According to the Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00419159 (13) [back to overview]	Biomarkers Predictive of Clinical Benefit (Median PFS and OS by PTEN ) on Everolimus (RAD001) 70mg/Week
NCT00419159 (13) [back to overview]	The Number of Participants With Best Overall Response According to Response Evaluation Criteria in Solid Tumors (RECIST)
NCT00419159 (13) [back to overview]	Biomarkers Predictive of Clinical Benefit (Median PFS and OS by KRAS) on Everolimus (RAD001) 10mg/Day
NCT00419159 (13) [back to overview]	Progression-free Survival (PFS)
NCT00419159 (13) [back to overview]	Biomarkers Predictive of Clinical Benefit (Median PFS and OS by KRAS ) on Everolimus (RAD001) 70mg/Week
NCT00419159 (13) [back to overview]	Overall Survival (OS)
NCT00419159 (13) [back to overview]	Biomarkers Predictive of Clinical Benefit (DCR by PTEN ) on Everolimus (RAD001) 70mg/Week
NCT00425308 (12) [back to overview]	Number of Participants With Biopsy-proven Acute Rejection (BPAR) at Month 6 and Month 12.
NCT00425308 (12) [back to overview]	Number of Participants With Treatment Failures Assessed by Biopsy-proven Acute Rejection (BPAR), Graft Loss/Re-transplantation, Death or Lost to Follow-up at Month 12.
NCT00425308 (12) [back to overview]	Change in the Glomerular Filtration Rate Estimated by Iohexol Plasma Clearance 12 Months After Randomization Between the 2 Groups of Patients Who Completed Trial
NCT00425308 (12) [back to overview]	Change in Glomerular Filtration Rate Estimated by Iohexol Plasma Clearance 12 Months After Randomization Between the 2 Groups of Patients.
NCT00425308 (12) [back to overview]	Assessing Cardiovascular Risk Factors Based on Fasting C-reactive Protein (CRP).
NCT00425308 (12) [back to overview]	Assessing Cardiovascular Risk Factors Based on Fasting Triglycerides.
NCT00425308 (12) [back to overview]	Assessing Cardiovascular Risk Factors Based on Fasting Total Cholesterol.
NCT00425308 (12) [back to overview]	Assessing Cardiovascular Risk Factors Based on Fasting High-density Lipoprotein (HDL) Cholesterol, Low-density Lipoprotein (LDL) Cholesterol.
NCT00425308 (12) [back to overview]	Change in Renal Function Assessed by Creatinine Clearance at Month 3, Month 6 and Month 12
NCT00425308 (12) [back to overview]	Change in Renal Function Assessed by Proteinuria at Month 3, Month 6 and Month 12
NCT00425308 (12) [back to overview]	Change in Renal Function Assessed by Serum Creatinine at Month 3, Month 6 and Month 12
NCT00425308 (12) [back to overview]	Assessing Cardiovascular Risk Factors Based on Fasting Glucose.
NCT00426556 (4) [back to overview]	Phase I: Best Overall Response (BOR)
NCT00426556 (4) [back to overview]	Phase II: Progression Free Survival (PFS)
NCT00426556 (4) [back to overview]	Phase II: Overall Survival (OS)
NCT00426556 (4) [back to overview]	Phase II: Overall Response Rate
NCT00436618 (4) [back to overview]	Progression-free Survival
NCT00436618 (4) [back to overview]	Tumor Response, Defined by Disease: Chronic Lymphocytic Leukemia(CLL): Clinical Complete or Complete or Nodular Partial or Partial Remission, Waldenstrom: Complete or Partial Response, All Others: Complete or Complete Unconfirmed or Partial Response.
NCT00436618 (4) [back to overview]	Time to Progression
NCT00436618 (4) [back to overview]	Overall Survival
NCT00449748 (1) [back to overview]	Number of Participants With Objective Response
NCT00458237 (2) [back to overview]	Clinical Response Rate
NCT00458237 (2) [back to overview]	Maximum Tolerated Dose (MTD)
NCT00459186 (2) [back to overview]	Number of Patients Free of Dose Limiting Toxicity
NCT00459186 (2) [back to overview]	Response Based on PET Scan
NCT00474929 (4) [back to overview]	Survival Time
NCT00474929 (4) [back to overview]	Progression Free Survival
NCT00474929 (4) [back to overview]	Number of Participants Reporting a Dose Limiting Toxicity (DLT)
NCT00474929 (4) [back to overview]	Proportion of Confirmed Tumor Responses
NCT00499603 (3) [back to overview]	Participant Responses Per Treatment Arm at 12 Weeks
NCT00499603 (3) [back to overview]	Number Participants With Inhibition of PI3K/PTEN/AKT Pathway at 48 Hours
NCT00499603 (3) [back to overview]	Participant Responses Per Treatment Arm at 24 Weeks
NCT00510068 (18) [back to overview]	Progression Free Survival According to Neuron Specific Enolase Tumor Marker (NSE) Baseline Level and According to NSE Early Response
NCT00510068 (18) [back to overview]	Progression Free Survival According to Ki-67 Levels Categorized as: Less Than or Equal to 2%, > 2% to Less Than or Equal to 5% and > 5%
NCT00510068 (18) [back to overview]	Progression Free Survival According to Chromogramin A Tumor Marker (CgA) Baseline Level and According to CgA Early Response
NCT00510068 (18) [back to overview]	Plasma Angiogenesis Marker: Vascular Endothelial Growth Factor (VEGF)
NCT00510068 (18) [back to overview]	Plasma Angiogenesis Marker: Soluble Vascular Endothelial Growth Factor Receptor 1 (sVEGFR1)
NCT00510068 (18) [back to overview]	Plasma Angiogenesis Marker: Placental Growth Factor (PLGF)
NCT00510068 (18) [back to overview]	Evaluation of Pharmacokinetics (PK) Parameter: CL/F
NCT00510068 (18) [back to overview]	Plasma Angiogenesis Marker: Basic Fibroblast Growth Factor (bFGF)
NCT00510068 (18) [back to overview]	Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs) (Open-label Period)
NCT00510068 (18) [back to overview]	Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs)
NCT00510068 (18) [back to overview]	Evaluation of Pharmacokinetics (PK) Parameters: Cmax, Cmin
NCT00510068 (18) [back to overview]	Evaluation of Pharmacokinetics (PK) Parameter: Tmax -Time to Maximum (Peak) Drug Concentration
NCT00510068 (18) [back to overview]	Overall Survival
NCT00510068 (18) [back to overview]	Percentage of Participants With Objective Response Rate ( CR {Complete Response} OR PR {Partial Response})
NCT00510068 (18) [back to overview]	Time to Progression Free Survival (PFS) Based as Per Investigator Using Kaplan-Meier Methodology
NCT00510068 (18) [back to overview]	Analysis of Time to Definitive Deterioration of WHO Performance Status Using Kaplan-Meier
NCT00510068 (18) [back to overview]	Evaluation of Pharmacokinetics (PK) Parameter: AUC0-t Last
NCT00510068 (18) [back to overview]	Plasma Angiogenesis Marker: Soluble Vascular Endothelial Growth Factor Receptor 2 (sVEGFR2)
NCT00514514 (13) [back to overview]	Efficacy Event Data After Month 12 to Month 60
NCT00514514 (13) [back to overview]	Efficacy Event Data Baseline 2 (Month 3) to Month 12
NCT00514514 (13) [back to overview]	Efficacy Event Data From Baseline 2 (Month 3) to Month 6
NCT00514514 (13) [back to overview]	Change From BL2 (Month 3) to Month 12 in Cardiovascular Risk (Framingham Score; 10-year Cardiovascular Risk)
NCT00514514 (13) [back to overview]	GFR at Month 60 Utilizing Cockcroft-Gault Formula
NCT00514514 (13) [back to overview]	GFR at Month 12 Utilizing Cockcroft-Gault Formula
NCT00514514 (13) [back to overview]	GFR at Month 12 Utilizing Modification of Diet in Renal Disease (MDRD) Method
NCT00514514 (13) [back to overview]	Mean Change in Serum Creatinine From Month 3 to Month 60
NCT00514514 (13) [back to overview]	GFR at Month 60 Utilizing Modification of Diet in Renal Disease (MDRD) Method
NCT00514514 (13) [back to overview]	GFR Calculated Via Nankivell Formula at Month 60
NCT00514514 (13) [back to overview]	GFR Via Nankivell Formula at Month 12 - All Regimens
NCT00514514 (13) [back to overview]	GFR Via Nankivell Method at Month 12 - CNI-Free vs Standard Regimen
NCT00514514 (13) [back to overview]	Mean Change in Serum Creatinine From Month 3 to Month 12
NCT00515086 (4) [back to overview]	Surgery Group: Progression-free Survival
NCT00515086 (4) [back to overview]	No Surgery Group: Progression Free Survival
NCT00515086 (4) [back to overview]	Surgery Group: Number of Participants With Adverse Events
NCT00515086 (4) [back to overview]	No Surgery Group: Best Overall Tumor Response
NCT00516165 (6) [back to overview]	Time to Progression
NCT00516165 (6) [back to overview]	Progression-free Survival Rate at 24 Weeks
NCT00516165 (6) [back to overview]	Overall Survival
NCT00516165 (6) [back to overview]	Number of Patients With Adverse Events Who Were Treated With RAD001 for Advanced HCC
NCT00516165 (6) [back to overview]	Maximum Tolerated Dose of RAD001 in Patients With Advanced Hepatocellular Carcinoma (HCC).
NCT00516165 (6) [back to overview]	Overall Response Rate
NCT00521001 (4) [back to overview]	Time to Disease Progression
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
NCT00526591 (3) [back to overview]	Change in PSA
NCT00526591 (3) [back to overview]	Proportion of Patients Who Are P0 (i.e., no Clinically Detectable Tumor in the Pathologic Specimen) at Surgery
NCT00526591 (3) [back to overview]	Toxicity Profile of Each Dose (Number of Patients With Worst Grade Toxicity)
NCT00529802 (2) [back to overview]	Percent Change in FDG-PETUptake Following 2 Weeks of Therapy
NCT00529802 (2) [back to overview]	Relative Tumor Size Change Following 8 Weeks of Therapy.
NCT00531011 (19) [back to overview]	Revascularizations
NCT00531011 (19) [back to overview]	Distal Minimum Lumen Diameter (MLD).
NCT00531011 (19) [back to overview]	In-stent Late Loss (LL)
NCT00531011 (19) [back to overview]	In-stent Minimum Lumen Diameter (MLD).
NCT00531011 (19) [back to overview]	Composite Rate of Cardiac Death, Myocardial Infarction (MI, Both Q-wave and Non Q-wave), and Ischemia-driven Target Lesion Revascularization (TLR) .
NCT00531011 (19) [back to overview]	Composite Rate of All Death, MI (Q-wave and Non Q-wave), and Target Vessel Revascularization (TVR).
NCT00531011 (19) [back to overview]	Device Success
NCT00531011 (19) [back to overview]	Composite Endpoint of All Death, MI (Q-wave and Non Q-wave), and TVR.
NCT00531011 (19) [back to overview]	Procedural Success
NCT00531011 (19) [back to overview]	Adjudicated Stent Thrombosis.
NCT00531011 (19) [back to overview]	Adjudicated Stent Thrombosis.
NCT00531011 (19) [back to overview]	Composite Endpoint of Cardiac Death, MI (Q-wave and Non Q-wave), and Ischemia-driven TLR .
NCT00531011 (19) [back to overview]	Lesion Success
NCT00531011 (19) [back to overview]	In-segment Binary Restenosis Rate
NCT00531011 (19) [back to overview]	In-segment Late Loss (LL)
NCT00531011 (19) [back to overview]	In-segment Minimum Lumen Diameter (MLD).
NCT00531011 (19) [back to overview]	In-stent Binary Restenosis Rate
NCT00531011 (19) [back to overview]	Proximal Minimum Lumen Diameter (MLD).
NCT00531011 (19) [back to overview]	Revascularizations
NCT00553150 (6) [back to overview]	Overall Survival Time
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]	Progression-free-survival at 6 Months (Phase II)
NCT00553150 (6) [back to overview]	Response Rate, as Measured in Patients Receiving FLT-PET Imaging (Phase II)
NCT00553150 (6) [back to overview]	Overall Survival at 12 Months (Phase II)
NCT00553150 (6) [back to overview]	Time to Progression (Phase II)
NCT00570921 (3) [back to overview]	Time to Progression
NCT00570921 (3) [back to overview]	Objective Response Rates
NCT00570921 (3) [back to overview]	Clinical Benefit Rate
NCT00576680 (3) [back to overview]	Response Rate
NCT00576680 (3) [back to overview]	Progression-free Survival
NCT00576680 (3) [back to overview]	To Determine the Safety and Tolerability of This Drug Combination.
NCT00582738 (9) [back to overview]	Percentage of Patients in Each Study Arm With Increase of ≥1 Point in the Ishak-Knodell Staging Score in Fibrosis
NCT00582738 (9) [back to overview]	Change From Baseline in Fibrosis Staging Score (Measured by the Ishak-Knodell Staging Score) Between Baseline and 24 Months Post-transplant.
NCT00582738 (9) [back to overview]	Comparison of Renal Function (Glomerular Filtration Rate [GFR] Calculated Using the Modification of Diet in Renal Disease Study Group [MDRD] Formula) Between Study Groups
NCT00582738 (9) [back to overview]	Percentage of Patients With Death, Graft Loss and Biopsy Proven Acute Rejection (BPAR) Between Study Groups
NCT00582738 (9) [back to overview]	Number of Patients With Events (Progression to Cirrhosis, Retransplantation, HCV Related Death, First BPAR, Graft Loss)at 12 and 24 Months
NCT00582738 (9) [back to overview]	Comparison of the Effect of Both Regimens on the Inflammatory (Acti-test) and Fibrosis (Fibro-test) Components of Fibrosure, and on Fibrosis Area Assessed by Histomorphometry
NCT00582738 (9) [back to overview]	Comparison of the Effect of Both Regimens in the Necroinflammatory Grading Score (Ishak-Knodell) (Portal Inflammation)
NCT00582738 (9) [back to overview]	Change From Baseline in Hepatitis C Virus (HCV) Ribonucleic Acid (RNA) Viral Load at 12 and 24 Months Post Randomization
NCT00582738 (9) [back to overview]	Change From Baseline in Fibrosis Metavir Scoring at 12 and 24 Months Post Randomization
NCT00591734 (3) [back to overview]	Objective Response Rate (ORR)
NCT00591734 (3) [back to overview]	Overall Survival Rate
NCT00591734 (3) [back to overview]	Progression-free Survival
NCT00597506 (2) [back to overview]	Progression Free Survival (PFS)
NCT00597506 (2) [back to overview]	Overall Response
NCT00607113 (1) [back to overview]	Net Change Relative to Baseline in Tumor Blood Flow
NCT00617084 (2) [back to overview]	In-Stent Percent Diameter Stenosis
NCT00617084 (2) [back to overview]	Target Lesion Failure
NCT00622869 (4) [back to overview]	Incidence Rate of Composite Efficacy Failure From Randomization to Month 24
NCT00622869 (4) [back to overview]	Incidence Rate of Composite Efficacy Failure From Randomization to Month 12
NCT00622869 (4) [back to overview]	Incidence Rate of Treated Biopsy Proven Acute Rejection (tBPAR) at Months 12 and 24
NCT00622869 (4) [back to overview]	Change in Renal Function From Randomization to Months 12 and 24
NCT00629525 (5) [back to overview]	Biochemical Response Rate
NCT00629525 (5) [back to overview]	Clinical Response
NCT00629525 (5) [back to overview]	Molecular Response
NCT00629525 (5) [back to overview]	Progression Free Survival
NCT00629525 (5) [back to overview]	Pathologic Response
NCT00630344 (6) [back to overview]	Incidence of Grade 4 Treatment-Related Toxicity
NCT00630344 (6) [back to overview]	Incidence of Grade 1-3 Treatment-Related Fatigue Toxicity
NCT00630344 (6) [back to overview]	Time to Progression (TTP)
NCT00630344 (6) [back to overview]	Incidence of Grade 1-3 Treatment-Related Mucositis Toxicity
NCT00630344 (6) [back to overview]	Incidence of Grade 1-3 Treatment-Related Rash Toxicity
NCT00630344 (6) [back to overview]	Overall Response Rate
NCT00634920 (19) [back to overview]	Progression of Measured Glomerular Filtration Rate
NCT00634920 (19) [back to overview]	Percentage of Participants With Treatment Failures
NCT00634920 (19) [back to overview]	Percentage of Participants With Graft Loss or Death
NCT00634920 (19) [back to overview]	Percentage of Participants With Biopsy Proven Acute Rejection (BPAR)
NCT00634920 (19) [back to overview]	Percentage of Participants on Lipid-lowering Drugs
NCT00634920 (19) [back to overview]	Percentage of Participants Who Had Donor Specific Antibodies (DSA)
NCT00634920 (19) [back to overview]	Percentage of Participants Who Developed CAN (Chronic Allograft Nephropathy)
NCT00634920 (19) [back to overview]	Time to First Malignancy
NCT00634920 (19) [back to overview]	Measured Glomerular Filtration Rate
NCT00634920 (19) [back to overview]	Calculated Glomerular Filtration Rate
NCT00634920 (19) [back to overview]	Health-related Quality of Life (QoL) as Measured by EuroQoL EQ-5D
NCT00634920 (19) [back to overview]	Lipid Profile for Apolipoprotein
NCT00634920 (19) [back to overview]	Lipid Profile for HDL-C, LDL-C,Total Cholesterol, and Triglycerides
NCT00634920 (19) [back to overview]	Number of Lipid-lowering Drugs Taken
NCT00634920 (19) [back to overview]	Percentage of Participants on Antihypertensive Drugs
NCT00634920 (19) [back to overview]	Time to Treatment Failure
NCT00634920 (19) [back to overview]	Measured Glomerular Filtration Rate
NCT00634920 (19) [back to overview]	Proteinuria (Measured as Urine Albumin/Creatinine Ratio (mg/mmol))
NCT00634920 (19) [back to overview]	Number of Antihypertensive Drugs Taken
NCT00640978 (1) [back to overview]	Number of Participants Surviving at 6 Months
NCT00651482 (9) [back to overview]	Progression-free Survival (PFS)
NCT00651482 (9) [back to overview]	Overall Survival (OS)
NCT00651482 (9) [back to overview]	Number of Subjects With Drug-related SAEs
NCT00651482 (9) [back to overview]	Objective Response (OR)
NCT00651482 (9) [back to overview]	Objective Response (OR) Duration
NCT00651482 (9) [back to overview]	Time-to-Treatment Failure (TTF)
NCT00651482 (9) [back to overview]	Total Number of Drug-related SAEs
NCT00651482 (9) [back to overview]	Treatment Discontinuation Due to Disease Progression
NCT00651482 (9) [back to overview]	Treatment Discontinuation Due to Toxicity
NCT00658320 (10) [back to overview]	Core Study: Number of Patients With Composite Efficacy Endpoint
NCT00658320 (10) [back to overview]	Extension Study: Renal Function Measured by Calculated Glomerular Filtration Rate (cGFR) Using the Modification of Diet in Renal Disease (MDRD) Formula
NCT00658320 (10) [back to overview]	Core Study: Renal Function Measured by Calculated Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula
NCT00658320 (10) [back to overview]	Core Study: Number Participants With Combined Graft Loss, Death or Loss to Follow-up
NCT00658320 (10) [back to overview]	Extension Study: Renal Function Measured by Calculated Glomerular Filtration Rate (cGFR) Using the Modification of Diet in Renal Disease (MDRD) Formula
NCT00658320 (10) [back to overview]	Extension Study: Renal Function Measured by Calculated Glomerular Filtration Rate (GFR) Using the Nankivell Formula
NCT00658320 (10) [back to overview]	Extension Study: Number of Participants With Combined Efficacy Endpoint: Graft Loss, Death, Loss to Follow-up and/or Treated Biopsy Proven Acute Rejection (BPAR)
NCT00658320 (10) [back to overview]	Extension Study: Number of Participants With Adverse Events and Serious Adverse Events
NCT00658320 (10) [back to overview]	Extension Study: Everolimus Trough Levels
NCT00658320 (10) [back to overview]	Extension Study: Cyclosporine Trough Levels
NCT00676520 (42) [back to overview]	Death (Cardiac Death, Vascular Death, and Non-cardiovascular Death)
NCT00676520 (42) [back to overview]	Death (Cardiac Death, Vascular Death, and Non-cardiovascular Death)
NCT00676520 (42) [back to overview]	Death (Cardiac Death, Vascular Death, and Non-cardiovascular Death)
NCT00676520 (42) [back to overview]	Dual Antiplatelet Medication Usage
NCT00676520 (42) [back to overview]	Composite Rate of Cardiac Death, Any MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Target Lesion Revascularization (TLR) (PCI and CABG)
NCT00676520 (42) [back to overview]	Any MI (Q-wave and Non Q-wave)
NCT00676520 (42) [back to overview]	Any MI (Q-wave and Non Q-wave)
NCT00676520 (42) [back to overview]	Any MI (Q-wave and Non Q-wave)
NCT00676520 (42) [back to overview]	Dual Antiplatelet Medication Usage
NCT00676520 (42) [back to overview]	Dual Antiplatelet Therapy Non-compliance Through 1 Year
NCT00676520 (42) [back to overview]	Major Bleeding Complications
NCT00676520 (42) [back to overview]	Major Bleeding Complications
NCT00676520 (42) [back to overview]	Major Bleeding Complications
NCT00676520 (42) [back to overview]	Major Bleeding Complications
NCT00676520 (42) [back to overview]	Composite Rate of Cardiac Death, Any MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Target Lesion Revascularization (TLR) (PCI and CABG)
NCT00676520 (42) [back to overview]	Composite Rate of Cardiac Death and MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Clinically-indicated Target Lesion Revascularization (CI-TLR) (PCI and CABG) (This Composite Endpoint is Also Denoted as TLF)
NCT00676520 (42) [back to overview]	Patient Health Status, Physical Limitations Assessed Using the SAQ (Seattle Angina Questionaire)
NCT00676520 (42) [back to overview]	Patient Health Status, Physical Limitations Assessed Using the SAQ (Seattle Angina Questionaire)
NCT00676520 (42) [back to overview]	SAQ (Seattle Angina Questionaire)
NCT00676520 (42) [back to overview]	SAQ (Seattle Angina Questionaire)
NCT00676520 (42) [back to overview]	Composite Rate of Cardiac Death and MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Clinically-indicated Target Lesion Revascularization (CI-TLR) (PCI and CABG) (This Composite Endpoint is Also Denoted as TLF)
NCT00676520 (42) [back to overview]	Composite Rate of Cardiac Death and MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Clinically-indicated Target Lesion Revascularization (CI-TLR) (PCI and CABG) (This Composite Endpoint is Also Denoted as TLF)
NCT00676520 (42) [back to overview]	Composite Rate of Cardiac Death and Any Myocardial Infarction (MI)
NCT00676520 (42) [back to overview]	Composite Rate of Cardiac Death and Any MI (Q-wave and Non Q-wave)
NCT00676520 (42) [back to overview]	Composite Rate of All Death, Any MI (Q-wave and Non Q-wave) and Any Repeat Revascularization (Percutaneous Coronary Intervention [PCI] and Coronary Artery Bypass Graft [CABG])
NCT00676520 (42) [back to overview]	SAQ (Seattle Angina Questionaire)
NCT00676520 (42) [back to overview]	Composite Rate of All Death, Any MI (Q-wave and Non Q-wave) and Any Repeat Revascularization (Percutaneous Coronary Intervention [PCI] and Coronary Artery Bypass Graft [CABG])
NCT00676520 (42) [back to overview]	Composite Rate of All Death, Any MI (Q-wave and Non Q-wave) and Any Repeat Revascularization (Percutaneous Coronary Intervention [PCI] and Coronary Artery Bypass Graft [CABG])
NCT00676520 (42) [back to overview]	Patient Health Status, Physical Limitations Assessed Using the SAQ (Seattle Angina Questionaire)
NCT00676520 (42) [back to overview]	Composite Rate of All Death and Any MI (Q-wave and Non Q-wave)
NCT00676520 (42) [back to overview]	Composite Rate of All Death and Any MI (Q-wave and Non Q-wave)
NCT00676520 (42) [back to overview]	Composite Rate of Cardiac Death, Any MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Target Lesion Revascularization (TLR) (PCI and CABG)
NCT00676520 (42) [back to overview]	Procedural Success
NCT00676520 (42) [back to overview]	Revascularization (Target Lesion, Target Vessel [TVR], and Non-target Vessel) (PCI and CABG)
NCT00676520 (42) [back to overview]	Revascularization (Target Lesion, Target Vessel [TVR], and Non-target Vessel) (PCI and CABG)
NCT00676520 (42) [back to overview]	Composite Rate of All Death and Any MI (Q-wave and Non Q-wave)
NCT00676520 (42) [back to overview]	Composite Rate of Cardiac Death and Any MI (Q-wave and Non Q-wave)
NCT00676520 (42) [back to overview]	Clinical Device Success
NCT00676520 (42) [back to overview]	Dual Antiplatelet Medication Usage
NCT00676520 (42) [back to overview]	Stent Thrombosis (Definite and Probable) Rate as Defined by ARC (Academic Research Constortium).
NCT00676520 (42) [back to overview]	Dual Antiplatelet Medication Usage
NCT00676520 (42) [back to overview]	Revascularization (Target Lesion, Target Vessel [TVR], and Non-target Vessel) (PCI and CABG)
NCT00688623 (7) [back to overview]	Overall Survival (OS) for Per Protocol (PP) and ITT Sets
NCT00688623 (7) [back to overview]	Percentage of Participants With a Overall Response Rate With a Complete Response (CR) or Partial Response (PR) at 12 Months ITT Set
NCT00688623 (7) [back to overview]	Percentage of Participants With Disease Control Rate (DCR) at 12 Months for Per Protocol (PP) and ITT Sets
NCT00688623 (7) [back to overview]	Percentage of Participants' Best Overall Response Rate at 12 Months - Per Protocol Set (PP)
NCT00688623 (7) [back to overview]	Duration of Progression Free Survival (PFS) for Per Protocol (PP) and ITT Sets
NCT00688623 (7) [back to overview]	Percentage of Participants With Objective Response Rate at 12 Months - Per Protocol Set (PP)
NCT00688623 (7) [back to overview]	Percentage of Participants With Objective Response Rate at 12 Months ITT Set
NCT00688753 (6) [back to overview]	Objective Response Rate
NCT00688753 (6) [back to overview]	To Evaluate Efficacy of RAD001 as Monotherapy for the Treatment of Papillary Renal Cancer. Efficacy is Defined as the Percentage of Patients Progression-free at 6 Months.
NCT00688753 (6) [back to overview]	Duration of Response
NCT00688753 (6) [back to overview]	Median Progression Free Survival
NCT00688753 (6) [back to overview]	Disease Control Rate (SD + PR + CR)
NCT00688753 (6) [back to overview]	Incidence of Adverse Events, Serious Adverse Events, and Death.
NCT00702052 (5) [back to overview]	Disease Control Rate (DCR)
NCT00702052 (5) [back to overview]	Progression Free Survival (PFS)
NCT00702052 (5) [back to overview]	Overall Survival
NCT00702052 (5) [back to overview]	Overall Response Rate (ORR)
NCT00702052 (5) [back to overview]	Number of Participants With At Least One Adverse Event (AE) and Serious Adverse Event (SAE)
NCT00719264 (8) [back to overview]	Best Overall Response in Participants Who Received RAD001 Plus Bevacizumab Versus Participants Who Received IFN Plus Bevacizumab
NCT00719264 (8) [back to overview]	Time to Definitive Deterioration of the Functional Assessment of Cancer Therapy Kidney Symptom Index, Disease Related Symptoms (FKSI-DRS) Risk Score by at Least 2 Score Units
NCT00719264 (8) [back to overview]	Response Duration Differences in Participants Who Received RAD001 Plus Bevacizumab Versus Participants Who Received IFN Plus Bevacizumab
NCT00719264 (8) [back to overview]	Overall Survival (OS) Treatment Effect in Participants Who Received RAD001 Plus Bevacizumab Versus Participants Who Received IFN Plus Bevacizumab
NCT00719264 (8) [back to overview]	Duration of Exposure of RAD001 in Participants Randomized to the Treatment Combination of RAD001 and Bevacizumab
NCT00719264 (8) [back to overview]	Progression-free Survival (PFS) of Participants Who Received RAD001 Plus Bevacizumab Versus Participants Who Received IFN Plus Bevacizumab
NCT00719264 (8) [back to overview]	Time to Definitive Deterioration of the Global Health Status and the Physical Functioning (PF) Subscale Scores of the European Organization for the Research and Treatment of Cancer (EORTC)-Core Quality of Life Questionnaire (QLQ-C30) by at Least 10%
NCT00719264 (8) [back to overview]	Number of Participants Who Experienced Adverse Events (AEs), Serious Adverse Events and Deaths
NCT00729482 (4) [back to overview]	Number of Participants With Adverse Events
NCT00729482 (4) [back to overview]	Overall Survival
NCT00729482 (4) [back to overview]	Progression-free Survival Rate at 4-month (16 Weeks)
NCT00729482 (4) [back to overview]	Response Rate
NCT00767819 (6) [back to overview]	Objective Tumor Response Rates (Complete Response and Partial Response) at Week 16 (ITT)
NCT00767819 (6) [back to overview]	Best Overall Response Rates by Week 16 (ITT)
NCT00767819 (6) [back to overview]	Time to Progression (TTP) (ITT)
NCT00767819 (6) [back to overview]	Percentage of Participants With Progression-free Survival (PFS) at 16 Weeks
NCT00767819 (6) [back to overview]	Percentage of Participants With Overall Survival (OS) at Week 16 (ITT)
NCT00767819 (6) [back to overview]	Percentage of Participants With Duration of Response (CR, PR, SD) at 16 Weeks.
NCT00770120 (4) [back to overview]	Frequency and Severity of Toxicities
NCT00770120 (4) [back to overview]	Response
NCT00770120 (4) [back to overview]	Progression-Free Survival
NCT00770120 (4) [back to overview]	Overall Survival
NCT00782626 (1) [back to overview]	Overall Response
NCT00783796 (99) [back to overview]	Cardiac Death/MI
NCT00783796 (99) [back to overview]	Cardiac Death/ All MI /CI-TLR
NCT00783796 (99) [back to overview]	Cardiac Death/ All MI /CI-TLR
NCT00783796 (99) [back to overview]	Cardiac Death/ All MI /CI-TLR
NCT00783796 (99) [back to overview]	Cardiac Death/ All MI /CI-TLR
NCT00783796 (99) [back to overview]	Cardiac Death/ All MI /CI-TLR
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)
NCT00783796 (99) [back to overview]	All TVR (CI and Non-CI)
NCT00783796 (99) [back to overview]	All TVR (CI and Non-CI)
NCT00783796 (99) [back to overview]	Clinically Indicated Target Lesion Revascularization (CI-TLR)
NCT00783796 (99) [back to overview]	Clinically Indicated Target Vessel Revascularization
NCT00783796 (99) [back to overview]	Clinically Indicated Target Vessel Revascularization
NCT00783796 (99) [back to overview]	Clinically Indicated Target Vessel Revascularization
NCT00783796 (99) [back to overview]	Clinically Indicated Target Vessel Revascularization
NCT00783796 (99) [back to overview]	All TVR (CI and Non-CI)
NCT00783796 (99) [back to overview]	Clinically Indicated Target Vessel Revascularization (TVR)
NCT00783796 (99) [back to overview]	Composite Rate of Cardiac Death, Target Vessel Myocardial Infarction (MI) (Per Protocol Definition) & Clinically Indicated Target Lesion Revascularization (CI-TLR).
NCT00783796 (99) [back to overview]	All TVR (CI and Non-CI)
NCT00783796 (99) [back to overview]	All TVR (CI and Non-CI)
NCT00783796 (99) [back to overview]	All TLR (CI and Non-CI)
NCT00783796 (99) [back to overview]	All TLR (CI and Non-CI)
NCT00783796 (99) [back to overview]	All TLR (CI and Non-CI)
NCT00783796 (99) [back to overview]	All TLR (CI and Non-CI)
NCT00783796 (99) [back to overview]	All TLR (CI and Non-CI)
NCT00783796 (99) [back to overview]	All Death/ All MI/All Coronary Revascularization
NCT00783796 (99) [back to overview]	All Death/ All MI/All Coronary Revascularization
NCT00783796 (99) [back to overview]	All Death/ All MI/All Coronary Revascularization
NCT00783796 (99) [back to overview]	All Death/ All MI/All Coronary Revascularization
NCT00783796 (99) [back to overview]	All Death/ All MI/All Coronary Revascularization
NCT00783796 (99) [back to overview]	All Death (Cardiac, Vascular, Non-cardiovascular)
NCT00783796 (99) [back to overview]	All Death (Cardiac, Vascular, Non-cardiovascular)
NCT00783796 (99) [back to overview]	All Death (Cardiac, Vascular, Non-cardiovascular)
NCT00783796 (99) [back to overview]	All Death (Cardiac, Vascular, Non-cardiovascular)
NCT00783796 (99) [back to overview]	All Death (Cardiac, Vascular, Non-cardiovascular)
NCT00783796 (99) [back to overview]	All Coronary Revascularization (TVR and Non-TVR)
NCT00783796 (99) [back to overview]	All Coronary Revascularization (TVR and Non-TVR)
NCT00783796 (99) [back to overview]	All Coronary Revascularization (TVR and Non-TVR)
NCT00783796 (99) [back to overview]	All Coronary Revascularization (TVR and Non-TVR)
NCT00783796 (99) [back to overview]	All Coronary Revascularization (TVR and Non-TVR)
NCT00783796 (99) [back to overview]	Clinically Indicated Target Lesion Revascularization (CI-TLR)
NCT00783796 (99) [back to overview]	Composite Rate of Cardiac Death, Target Vessel Myocardial Infarction (MI) (Per Protocol Definition) & Clinically Indicated Target Lesion Revascularization (CI-TLR).
NCT00783796 (99) [back to overview]	Device Success (Per Lesion Basis, for Target Lesions Treated by 2.25 mm XIENCE V EECS With or Without Planned Overlap)
NCT00783796 (99) [back to overview]	Distal % Diameter Stenosis
NCT00783796 (99) [back to overview]	Distal Angiographic Binary Restenosis (ABR) Rate
NCT00783796 (99) [back to overview]	Distal Late Loss
NCT00783796 (99) [back to overview]	In-segment % Diameter Stenosis
NCT00783796 (99) [back to overview]	In-segment Angiographic Binary Restenosis (ABR) Rate
NCT00783796 (99) [back to overview]	In-segment Late Loss (LL)
NCT00783796 (99) [back to overview]	In-stent % Diameter Stenosis
NCT00783796 (99) [back to overview]	In-stent Angiographic Binary Restenosis (ABR) Rate
NCT00783796 (99) [back to overview]	In-Stent Late Loss
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)
NCT00783796 (99) [back to overview]	Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)
NCT00783796 (99) [back to overview]	Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)
NCT00783796 (99) [back to overview]	Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)
NCT00783796 (99) [back to overview]	Clinically Indicated Target Lesion Revascularization (CI-TLR)
NCT00783796 (99) [back to overview]	Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)
NCT00783796 (99) [back to overview]	Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)
NCT00783796 (99) [back to overview]	Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Clinically Indicated Target Lesion Revascularization (CI-TLR)
NCT00783796 (99) [back to overview]	Clinically Indicated Target Lesion Revascularization (CI-TLR)
NCT00783796 (99) [back to overview]	Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Procedural Success (Per Subject Basis, for ALL Target and Non-target Lesions)
NCT00783796 (99) [back to overview]	Proximal % Diameter Stenosis
NCT00783796 (99) [back to overview]	Proximal Angiographic Binary Restenosis (ABR) Rate
NCT00783796 (99) [back to overview]	Proximal Late Loss
NCT00783796 (99) [back to overview]	Stent Thrombosis (ARC Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (ARC Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (ARC Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (ARC Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (ARC Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (ARC Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (ARC Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (ARC Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (ARC Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (Protocol Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (Protocol Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (Protocol Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (Protocol Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (Protocol Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (Protocol Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (Protocol Defined)
NCT00783796 (99) [back to overview]	Stent Thrombosis (Protocol Defined)
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Cardiac Death/MI
NCT00783796 (99) [back to overview]	Cardiac Death/MI
NCT00783796 (99) [back to overview]	Cardiac Death/MI
NCT00783796 (99) [back to overview]	Cardiac Death/MI
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per ARC)
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)
NCT00783796 (99) [back to overview]	Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)
NCT00783796 (99) [back to overview]	Composite Rate of Cardiac Death, Target Vessel Myocardial Infarction (MI) (Per Protocol Definition) & Clinically Indicated Target Lesion Revascularization (CI-TLR).
NCT00789828 (11) [back to overview]	Everolimus Blood Concentration (C2h) at 2 Hours Post Dose
NCT00789828 (11) [back to overview]	Everolimus Trough Concentrations (Cmin) at 24 Hours After Last Dose
NCT00789828 (11) [back to overview]	Percentage of Participants With Renal Impairment During Core Period
NCT00789828 (11) [back to overview]	Change From Baseline in Frequency of Total Seizure Events Per 24 Hours at Week 24 in Both Core and Extension Period
NCT00789828 (11) [back to overview]	Duration of SEGA Response
NCT00789828 (11) [back to overview]	Duration of Skin Lesion Response in Everolimus Treated Participants
NCT00789828 (11) [back to overview]	Percentage of Participants With Best Overall Subependymal Giant Cell Astrocytomas (SEGA) Response
NCT00789828 (11) [back to overview]	Percentage of Participants With Skin Lesions Assessed Using Physician's Global Assessement Overall Score
NCT00789828 (11) [back to overview]	Time to SEGA Progression
NCT00789828 (11) [back to overview]	Time to SEGA Response
NCT00789828 (11) [back to overview]	Time to SEGA Worsening
NCT00790036 (3) [back to overview]	Disease-free Survival (DFS)
NCT00790036 (3) [back to overview]	Lymphoma-specific Survival (LSS)
NCT00790036 (3) [back to overview]	Overall Survival (OS)
NCT00790400 (10) [back to overview]	Angiomyolipoma Response Rate as Per Central Radiology Review
NCT00790400 (10) [back to overview]	Duration of Angiomyolipoma Response - Only Everolimus Patients With Angiomyolipoma Response
NCT00790400 (10) [back to overview]	Duration of Skin Lesion Response - Only Everolimus Patients With Best Overall Skin Lesion Response of Complete Clinical Response (CCR) or Partial Response (PR)
NCT00790400 (10) [back to overview]	Skin Lesion Response Rate as Per Investigator (Only Patients With at Least One Skin Lesion at Baseline)
NCT00790400 (10) [back to overview]	Time to Angiomyolipoma Progression as Per Central Radiology Review
NCT00790400 (10) [back to overview]	Time to Angiomyolipoma Response - Only Everolimus Patients With Angiomyolipoma Response
NCT00790400 (10) [back to overview]	Change From Baseline in Plasma Angiogenic Molecules - Vascular Endothelial Growth Factor (VEGF) Marker
NCT00790400 (10) [back to overview]	Everolimus Blood Concentrations (C2h) at 2 Hours Post-dose
NCT00790400 (10) [back to overview]	Everolimus Trough Concentrations (Cmin)
NCT00790400 (10) [back to overview]	Percentage of Participants With Renal Impairment
NCT00805129 (2) [back to overview]	Proportion of Pretreatment Primary Tumor Samples With mTOR Pathway Markers
NCT00805129 (2) [back to overview]	Number of Participants Evaluated for Toxicity
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)
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
NCT00809185 (3) [back to overview]	Number of Participants With Bone Marrow Morphology and Cytogenetics Pre- and Post-therapy
NCT00809185 (3) [back to overview]	Number of Patients With Either a Major or Minor Erythroid Response (Hemoglobin Change From Baseline Measure)
NCT00809185 (3) [back to overview]	Number of Dose- and Non-dose-limiting Toxicities
NCT00814788 (3) [back to overview]	Progression-free Survival
NCT00814788 (3) [back to overview]	Overall Survival
NCT00814788 (3) [back to overview]	PSA Response Rate
NCT00823459 (5) [back to overview]	Progression-free Survival at 6 Months.
NCT00823459 (5) [back to overview]	To Assess the Correlation of Activation of the PI3K/mTOR Pathway With Survival
NCT00823459 (5) [back to overview]	Objective Response Rate (ORR) in Patients Treated With RAD001.
NCT00823459 (5) [back to overview]	Overall Survival (OS) in Patients Treated With RAD001.
NCT00823459 (5) [back to overview]	RAD001 Safety Profile in Patients With Recurrent LLG
NCT00827359 (3) [back to overview]	Best Overall Response by PI3K-AKT-MTOR Mutation
NCT00827359 (3) [back to overview]	Median Progression Free Survival
NCT00827359 (3) [back to overview]	Best Overall Response Rate
NCT00831480 (1) [back to overview]	Disease Progression Diagnosed by Biopsy
NCT00843531 (3) [back to overview]	Objective Response Rate (ORR)
NCT00843531 (3) [back to overview]	Number of Patients With Dose-limiting Toxicity (DLT)
NCT00843531 (3) [back to overview]	Duration of Objective Response
NCT00856856 (194) [back to overview]	In-scaffold Percent Diameter Stenosis (%DS)
NCT00856856 (194) [back to overview]	In-scaffold Percent Diameter Stenosis (%DS)
NCT00856856 (194) [back to overview]	In-scaffold Percent Diameter Stenosis (%DS)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00856856 (194) [back to overview]	Ischemia Driven Target Vessel Revascularization (ID-TVR)
NCT00856856 (194) [back to overview]	Late Incomplete Apposition
NCT00856856 (194) [back to overview]	Late Incomplete Apposition
NCT00856856 (194) [back to overview]	Late Incomplete Apposition
NCT00856856 (194) [back to overview]	Late Incomplete Apposition
NCT00856856 (194) [back to overview]	Luminal Volume
NCT00856856 (194) [back to overview]	Luminal Volume
NCT00856856 (194) [back to overview]	Luminal Volume
NCT00856856 (194) [back to overview]	Luminal Volume
NCT00856856 (194) [back to overview]	Mean Flow Area
NCT00856856 (194) [back to overview]	Mean Flow Area
NCT00856856 (194) [back to overview]	Mean Flow Area
NCT00856856 (194) [back to overview]	Mean Flow Area
NCT00856856 (194) [back to overview]	Mean Luminal Area
NCT00856856 (194) [back to overview]	Mean Luminal Area
NCT00856856 (194) [back to overview]	Mean Luminal Area
NCT00856856 (194) [back to overview]	Mean Luminal Area
NCT00856856 (194) [back to overview]	Mean Luminal Diameter
NCT00856856 (194) [back to overview]	Mean Luminal Diameter
NCT00856856 (194) [back to overview]	Mean Luminal Diameter
NCT00856856 (194) [back to overview]	Mean Luminal Diameter
NCT00856856 (194) [back to overview]	Mean Reference Area
NCT00856856 (194) [back to overview]	Mean Reference Area
NCT00856856 (194) [back to overview]	Mean Reference Area
NCT00856856 (194) [back to overview]	Mean Reference Area
NCT00856856 (194) [back to overview]	Mean Scaffold Area
NCT00856856 (194) [back to overview]	Mean Scaffold Area
NCT00856856 (194) [back to overview]	Mean Scaffold Diameter
NCT00856856 (194) [back to overview]	Mean Scaffold Diameter
NCT00856856 (194) [back to overview]	Mean Stent Area
NCT00856856 (194) [back to overview]	Mean Stent Diameter
NCT00856856 (194) [back to overview]	Mean Strut Core Area
NCT00856856 (194) [back to overview]	Mean Strut Core Area
NCT00856856 (194) [back to overview]	Mean Strut Core Area
NCT00856856 (194) [back to overview]	Minimum Flow Area
NCT00856856 (194) [back to overview]	Minimum Flow Area
NCT00856856 (194) [back to overview]	Minimum Flow Area
NCT00856856 (194) [back to overview]	Minimum Flow Area
NCT00856856 (194) [back to overview]	Minimum Luminal Area
NCT00856856 (194) [back to overview]	Minimum Luminal Area
NCT00856856 (194) [back to overview]	Minimum Luminal Area
NCT00856856 (194) [back to overview]	Minimum Luminal Area
NCT00856856 (194) [back to overview]	Minimum Luminal Diameter
NCT00856856 (194) [back to overview]	Minimum Luminal Diameter
NCT00856856 (194) [back to overview]	Minimum Luminal Diameter
NCT00856856 (194) [back to overview]	Minimum Luminal Diameter (MLD)
NCT00856856 (194) [back to overview]	Minimum Scaffold Area
NCT00856856 (194) [back to overview]	Minimum Scaffold Area
NCT00856856 (194) [back to overview]	Minimum Scaffold Diameter
NCT00856856 (194) [back to overview]	Minimum Scaffold Diameter
NCT00856856 (194) [back to overview]	Minimum Stent Area
NCT00856856 (194) [back to overview]	Minimum Stent Diameter
NCT00856856 (194) [back to overview]	Myocardial Infarction
NCT00856856 (194) [back to overview]	Myocardial Infarction
NCT00856856 (194) [back to overview]	Myocardial Infarction
NCT00856856 (194) [back to overview]	Myocardial Infarction
NCT00856856 (194) [back to overview]	Myocardial Infarction
NCT00856856 (194) [back to overview]	Myocardial Infarction
NCT00856856 (194) [back to overview]	Number of Struts in Side Branch
NCT00856856 (194) [back to overview]	Number of Struts in Side Branch
NCT00856856 (194) [back to overview]	Number of Struts in Side Branch
NCT00856856 (194) [back to overview]	Number of Struts in Side Branch
NCT00856856 (194) [back to overview]	Number of Struts Per BVS
NCT00856856 (194) [back to overview]	Number of Struts Per BVS
NCT00856856 (194) [back to overview]	Number of Struts Per BVS
NCT00856856 (194) [back to overview]	Number of Struts Per BVS
NCT00856856 (194) [back to overview]	Percent (%) Lumen Area Stenosis
NCT00856856 (194) [back to overview]	Percent (%) Lumen Area Stenosis
NCT00856856 (194) [back to overview]	Percent (%) Lumen Area Stenosis
NCT00856856 (194) [back to overview]	Percent (%) Lumen Area Stenosis
NCT00856856 (194) [back to overview]	Persisting Dissection
NCT00856856 (194) [back to overview]	Persisting Dissection
NCT00856856 (194) [back to overview]	Persisting Dissection
NCT00856856 (194) [back to overview]	Persisting Dissection
NCT00856856 (194) [back to overview]	Persisting Dissection
NCT00856856 (194) [back to overview]	Persisting Incomplete Apposition
NCT00856856 (194) [back to overview]	Persisting Incomplete Apposition
NCT00856856 (194) [back to overview]	Persisting Incomplete Apposition
NCT00856856 (194) [back to overview]	Persisting Incomplete Apposition
NCT00856856 (194) [back to overview]	Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 1 Year
NCT00856856 (194) [back to overview]	Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 180 Days
NCT00856856 (194) [back to overview]	Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 2 Years
NCT00856856 (194) [back to overview]	Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 3 Years
NCT00856856 (194) [back to overview]	Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 5 Years
NCT00856856 (194) [back to overview]	Scaffold Thrombosis
NCT00856856 (194) [back to overview]	Scaffold Thrombosis
NCT00856856 (194) [back to overview]	Scaffold Thrombosis
NCT00856856 (194) [back to overview]	Scaffold Thrombosis
NCT00856856 (194) [back to overview]	Scaffold Thrombosis
NCT00856856 (194) [back to overview]	Scaffold Thrombosis
NCT00856856 (194) [back to overview]	Scaffold Volume
NCT00856856 (194) [back to overview]	Scaffold Volume
NCT00856856 (194) [back to overview]	Stent Volume
NCT00856856 (194) [back to overview]	Strut Volume
NCT00856856 (194) [back to overview]	Strut Volume
NCT00856856 (194) [back to overview]	Strut Volume
NCT00856856 (194) [back to overview]	Thrombus
NCT00856856 (194) [back to overview]	Thrombus
NCT00856856 (194) [back to overview]	Thrombus
NCT00856856 (194) [back to overview]	Thrombus
NCT00856856 (194) [back to overview]	Thrombus
NCT00856856 (194) [back to overview]	Tissue Coverage Area BVS (Neointimal Area)
NCT00856856 (194) [back to overview]	Tissue Coverage Area BVS (Neointimal Area)
NCT00856856 (194) [back to overview]	Tissue Coverage Area BVS (Neointimal Area)
NCT00856856 (194) [back to overview]	Tissue Coverage Area Classical
NCT00856856 (194) [back to overview]	Tissue Coverage Area Classical
NCT00856856 (194) [back to overview]	Tissue Coverage Area Classical
NCT00856856 (194) [back to overview]	Tissue Coverage Obstruction Volume BVS
NCT00856856 (194) [back to overview]	Tissue Coverage Obstruction Volume BVS
NCT00856856 (194) [back to overview]	Tissue Coverage Obstruction Volume BVS
NCT00856856 (194) [back to overview]	Ischemia Driven Target Lesion Revascularization (ID-TLR)
NCT00856856 (194) [back to overview]	Tissue Coverage Obstruction Volume Classical
NCT00856856 (194) [back to overview]	Tissue Coverage Obstruction Volume Classical
NCT00856856 (194) [back to overview]	Tissue Coverage Volume BVS
NCT00856856 (194) [back to overview]	Tissue Coverage Volume BVS
NCT00856856 (194) [back to overview]	Tissue Coverage Volume BVS
NCT00856856 (194) [back to overview]	Tissue Coverage Volume Classical
NCT00856856 (194) [back to overview]	Tissue Coverage Volume Classical
NCT00856856 (194) [back to overview]	Tissue Coverage Volume Classical
NCT00856856 (194) [back to overview]	Volume Obstruction (VO)
NCT00856856 (194) [back to overview]	Volume Obstruction (VO)
NCT00856856 (194) [back to overview]	Volume Obstruction (VO)
NCT00856856 (194) [back to overview]	Volume Obstruction (VO)
NCT00856856 (194) [back to overview]	Vasomotion Analysis: In-scaffold Mean Luminal Diameter
NCT00856856 (194) [back to overview]	Cardiac Death
NCT00856856 (194) [back to overview]	Clinical Device Success (Per Lesion)
NCT00856856 (194) [back to overview]	Clinical Procedure Success (Per Patient)
NCT00856856 (194) [back to overview]	Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 1 Year
NCT00856856 (194) [back to overview]	Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 180 Days
NCT00856856 (194) [back to overview]	Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 2 Years
NCT00856856 (194) [back to overview]	Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 3 Years
NCT00856856 (194) [back to overview]	Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 5 Years
NCT00856856 (194) [back to overview]	Hierarchical Major Adverse Cardiac Event (MACE)
NCT00856856 (194) [back to overview]	Hierarchical Major Adverse Cardiac Event (MACE)
NCT00856856 (194) [back to overview]	Hierarchical Major Adverse Cardiac Event (MACE)
NCT00856856 (194) [back to overview]	Hierarchical Major Adverse Cardiac Event (MACE)
NCT00856856 (194) [back to overview]	Hierarchical Major Adverse Cardiac Event (MACE)
NCT00856856 (194) [back to overview]	Hierarchical Major Adverse Cardiac Event (MACE)
NCT00856856 (194) [back to overview]	Hierarchical Major Adverse Cardiac Event (MACE)
NCT00856856 (194) [back to overview]	Hierarchical Major Adverse Cardiac Event (MACE)
NCT00856856 (194) [back to overview]	Hierarchical Target Vessel Failure (TVF)
NCT00856856 (194) [back to overview]	Hierarchical Target Vessel Failure (TVF)
NCT00856856 (194) [back to overview]	Hierarchical Target Vessel Failure (TVF)
NCT00856856 (194) [back to overview]	Hierarchical Target Vessel Failure (TVF)
NCT00856856 (194) [back to overview]	Hierarchical Target Vessel Failure (TVF)
NCT00856856 (194) [back to overview]	Hierarchical Target Vessel Failure (TVF)
NCT00856856 (194) [back to overview]	Hierarchical Target Vessel Failure (TVF)
NCT00856856 (194) [back to overview]	Hierarchical Target Vessel Failure (TVF)
NCT00856856 (194) [back to overview]	In-scaffold Angiographic Binary Restenosis (ABR)
NCT00856856 (194) [back to overview]	In-scaffold Angiographic Binary Restenosis (ABR)
NCT00856856 (194) [back to overview]	In-scaffold Angiographic Binary Restenosis (ABR)
NCT00856856 (194) [back to overview]	In-scaffold Angiographic Binary Restenosis (ABR)
NCT00856856 (194) [back to overview]	In-scaffold Angiographic Binary Restenosis (ABR)
NCT00856856 (194) [back to overview]	In-scaffold Late Loss (LL): In-scaffold MLD Post-procedure - In-scaffold MLD at 2 Years
NCT00856856 (194) [back to overview]	In-scaffold Late Loss (LL): In-scaffold MLD Post-procedure - In-scaffold MLD at 3 Years
NCT00856856 (194) [back to overview]	In-scaffold Late Loss (LL): In-scaffold MLD Post-procedure - In-scaffold MLD at 5 Years
NCT00856856 (194) [back to overview]	In-scaffold Late Loss: In-scaffold MLD Post-procedure - In-scaffold MLD at 1 Year
NCT00856856 (194) [back to overview]	In-scaffold Late Loss: In-scaffold MLD Post-procedure - In-scaffold MLD at 180 Days
NCT00856856 (194) [back to overview]	Tissue Coverage Obstruction Volume Classical
NCT00856856 (194) [back to overview]	% of Acutely Covered Struts
NCT00856856 (194) [back to overview]	% of Acutely Covered Struts
NCT00856856 (194) [back to overview]	% of Covered Struts (150 µm)
NCT00856856 (194) [back to overview]	% of Uncovered Struts (150 µm)
NCT00856856 (194) [back to overview]	% of Uncovered Struts (150 µm)
NCT00856856 (194) [back to overview]	% of Uncovered Struts (150 µm)
NCT00856856 (194) [back to overview]	Aneurysm
NCT00856856 (194) [back to overview]	Aneurysm
NCT00856856 (194) [back to overview]	Aneurysm
NCT00856856 (194) [back to overview]	Aneurysm
NCT00856856 (194) [back to overview]	Aneurysm
NCT00856856 (194) [back to overview]	Cardiac Death
NCT00856856 (194) [back to overview]	Cardiac Death
NCT00856856 (194) [back to overview]	Cardiac Death
NCT00856856 (194) [back to overview]	Cardiac Death
NCT00856856 (194) [back to overview]	Cardiac Death
NCT00856856 (194) [back to overview]	In-scaffold Percent Diameter Stenosis (%DS)
NCT00856856 (194) [back to overview]	In-scaffold Percent Diameter Stenosis (%DS)
NCT00857259 (2) [back to overview]	Change in Visual Acuity From Baseline to Week 4 in Patients Treated With Everolimus
NCT00857259 (2) [back to overview]	Change in Central Retinal Thickness From Baseline to Week 4, as Measured by Optical Coherence Tomography (OCT)
NCT00862979 (6) [back to overview]	Occurrence of Treatment Failures From Month 6 to 9 and Month 9 to 18
NCT00862979 (6) [back to overview]	Calculated Glomerular Filtration Rate (cGFR) According to Cockcroft-Gault at Month 12 and 18
NCT00862979 (6) [back to overview]	Serum Creatinine at Month 6, 8, 9, 10 12 and 18
NCT00862979 (6) [back to overview]	Reciprocal Creatinine Slope Between Month 6 and Month 18
NCT00862979 (6) [back to overview]	Calculated Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula at Month 18
NCT00862979 (6) [back to overview]	Occurrence of Major Cardiac Events (MACE) From Month 6 to 18
NCT00863655 (12) [back to overview]	Overall Response Rate (ORR)
NCT00863655 (12) [back to overview]	Estradiol Plasma Concentrations
NCT00863655 (12) [back to overview]	Clinical Benefit Rate (CBR)
NCT00863655 (12) [back to overview]	Duration of Response (Among Participants With Best Overall Response of CR or PR) Estimated Per Kaplan-Meier
NCT00863655 (12) [back to overview]	Overall Survival (OS) by Number of Deaths
NCT00863655 (12) [back to overview]	Progression-free Survival (PFS) Based on Local Radiology Review of Tumor Assessments.
NCT00863655 (12) [back to overview]	Overall Survival (OS) by Median
NCT00863655 (12) [back to overview]	Proportion of Patients With no Deterioration of Eastern Cooperative Oncology Group Performance Status (ECOG PS) Using Kaplan-Meier
NCT00863655 (12) [back to overview]	Proportion of Patients With Having no Overall Response Based on Investigator Assessment
NCT00863655 (12) [back to overview]	Patient-reported Outcomes (PROs): Time to Deterioration of PRO Scores Using Kaplan Meier - EORTC QLQ-C30
NCT00863655 (12) [back to overview]	Exemestane Concentrations at Week 4
NCT00863655 (12) [back to overview]	Everolimus Concentrations at Week 4
NCT00869999 (3) [back to overview]	Progression-free Survival
NCT00869999 (3) [back to overview]	Duration of Overall Response
NCT00869999 (3) [back to overview]	Overall Response Rate
NCT00876395 (17) [back to overview]	Clinical Benefit Rate (CBR) Equal to or Greater Than 24 Weeks - Full Population
NCT00876395 (17) [back to overview]	Clinical Benefit Rate (CBR) Equal to or Greater Than 24 Weeks - HR-negative Population
NCT00876395 (17) [back to overview]	Overall Response Rate (ORR) - HR-negative Population
NCT00876395 (17) [back to overview]	Overall Survival (OS) - Full Population
NCT00876395 (17) [back to overview]	Time to Overall Response Based on Investigator - HR-negative Population
NCT00876395 (17) [back to overview]	Time to Overall Response Based on Investigator - Full Population
NCT00876395 (17) [back to overview]	Everolimus Blood Level Concentrations at Steady States for Everolimus
NCT00876395 (17) [back to overview]	Overall Response (OR) - Full Population
NCT00876395 (17) [back to overview]	Overall Response (OR) - HR-negative Population
NCT00876395 (17) [back to overview]	Paclitaxel Plasma Concentrations
NCT00876395 (17) [back to overview]	Time to Deterioration of Eastern Cooperative Oncology Group Performance Status (ECOG-PS) Score - HR-negative Population
NCT00876395 (17) [back to overview]	Time to Deterioration of Eastern Cooperative Oncology Group Performance Status (ECOG-PS) Score - Full Population
NCT00876395 (17) [back to overview]	Progression-free Survival (PFS) Per Investigators' Assessment Based on Local Radiology Review - Full Population
NCT00876395 (17) [back to overview]	Trastuzumab Serum Concentrations
NCT00876395 (17) [back to overview]	Overall Response Rate (ORR) - Full Population
NCT00876395 (17) [back to overview]	Progression-free Survival (PFS) Per Investigators' Assessment Based on Local Radiology Review - (Hormone Receptor (HR)-Negative Population
NCT00876395 (17) [back to overview]	Overall Survival (OS) - HR-negative Population
NCT00879333 (7) [back to overview]	Patient Reported Outcome (PRO): Time to Definitive Deterioration of European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire 30 (EORTC QLQ-C30) Scores
NCT00879333 (7) [back to overview]	Overall Response Rate (ORR)
NCT00879333 (7) [back to overview]	Progression Free Survival (PFS)
NCT00879333 (7) [back to overview]	Overall Survival (OS)
NCT00879333 (7) [back to overview]	Time to Definitive Deterioration of Eastern Cooperative Oncology Group Performance Status (ECOG PS) Score
NCT00879333 (7) [back to overview]	Everolimus Steady State Concentraions at Predose (Cmin) and Cmax at Week 5
NCT00879333 (7) [back to overview]	Everolimus Steady State Concentraions at Predose (Cmin) and Cmax by Region Asia vs. Rest of the World (ROW) at Week 5
NCT00886691 (5) [back to overview]	Progression-free Survival
NCT00886691 (5) [back to overview]	The Proportion of Patients With Measurable Disease Who Have Objective Tumor Responses by Treatment.
NCT00886691 (5) [back to overview]	Percentage of Participants With at Least One Cancer Antigen 125 (CA-125) Response
NCT00886691 (5) [back to overview]	Characterize and Compare Progression-free Survival and Overall Survival in Patients With Measurable Disease (RECIST Criteria) and Patients With Detectable (Non-measurable) Disease
NCT00886691 (5) [back to overview]	Incidence of Adverse Events as Assessed by Common Terminology Criteria for Adverse Events Version 4.0 (CTCAE v4.0)
NCT00903175 (13) [back to overview]	Time to Definitive Deterioration of the Global Health Status/QoL Scores of the EORTC QLQ-C30 by First-Line Drug
NCT00903175 (13) [back to overview]	Overall Response Rate (ORR) - First -Line (1-L)
NCT00903175 (13) [back to overview]	Time to Definitive Deterioration of the Physical Functioning Scale of the EORTC QLQ-C30 - by First and Second-Line Drugs Combined
NCT00903175 (13) [back to overview]	Time to Definitive Deterioration of the Global Health Status/QoL Scores of the EORTC QLQ-C30 by First and Second-Line Drugs Combined
NCT00903175 (13) [back to overview]	Time to Definitive Deterioration of the FKSI-DRS Risk Score by at Least 3 Score Units by First-line Drug
NCT00903175 (13) [back to overview]	Time to Definitive Deterioration of the FKSI-DRS Risk Score by at Least 3 Score Units by First and Second-line Drugs Combined
NCT00903175 (13) [back to overview]	Time to Definitive Deterioration of the Fatigue Scale of the EORTC QLQ-C30 by First-Line Drug
NCT00903175 (13) [back to overview]	Time to Definitive Deterioration of the Fatigue Scale of the EORTC QLQ-C30 by First and Second-Line Drugs Combined
NCT00903175 (13) [back to overview]	Progression-free Survival Combined (PFS-C)
NCT00903175 (13) [back to overview]	Progression Free Survival First-Line (PFS 1-L)
NCT00903175 (13) [back to overview]	Overall Survival (OS)
NCT00903175 (13) [back to overview]	Duration of Response (DoR) - First-Line (1-L)
NCT00903175 (13) [back to overview]	Time to Definitive Deterioration of the Physical Functioning (PF) Scale of the EORTC QLQ-C30 - by First-Line (1L) Drug
NCT00912340 (2) [back to overview]	Progression-free Survival (PFS) Until First Progression
NCT00912340 (2) [back to overview]	Progression-free Survival (PFS) in Patients Who Crossed Over
NCT00915603 (5) [back to overview]	Number of Patients With Treatment-related Adverse Events (AEs) as a Measure of Safety and Tolerability
NCT00915603 (5) [back to overview]	Duration of Response (DOR)
NCT00915603 (5) [back to overview]	Overall Response Rate (ORR)
NCT00915603 (5) [back to overview]	Overall Survival (OS)
NCT00915603 (5) [back to overview]	Progression-Free Survival (PFS)
NCT00918333 (5) [back to overview]	Number of Phase I Participants With Dose-Limiting Toxicity Events (Phase I)
NCT00918333 (5) [back to overview]	Overall Response Rate (Phase II)
NCT00918333 (5) [back to overview]	Duration of Response (Phase II)
NCT00918333 (5) [back to overview]	Progression-free Survival (Phase II)
NCT00918333 (5) [back to overview]	Overall Survival Time (Phase II)
NCT00930930 (4) [back to overview]	Number of Patients With Pathological Complete Response
NCT00930930 (4) [back to overview]	Clinical Tumor Response to Neoadjuvant Therapy as Measured by Ultrasound Immediately Before Surgery
NCT00930930 (4) [back to overview]	Number of Patients With Each Worst-grade Toxicity Response
NCT00930930 (4) [back to overview]	Number of Patients That Underwent Breast Conservation Surgery
NCT00934895 (1) [back to overview]	To Determine the Maximum Tolerated Dose (MTD) of RAD001 in Combination of Weekly Abraxane and Determine the Phase II Dose of RAD001.
NCT00935792 (7) [back to overview]	Progression-free Survival
NCT00935792 (7) [back to overview]	Clinical Response (Complete or Partial Remission)
NCT00935792 (7) [back to overview]	Survival Time
NCT00935792 (7) [back to overview]	Time to Subsequent Therapy
NCT00935792 (7) [back to overview]	Duration of Response
NCT00935792 (7) [back to overview]	Test the Safety and Tolerability of the Combination of Everolimus and Alemtuzumab.
NCT00935792 (7) [back to overview]	Number of Participants With Dose-Limiting Toxicities
NCT00936702 (5) [back to overview]	Duration of Response
NCT00936702 (5) [back to overview]	Overall Survival
NCT00936702 (5) [back to overview]	Percentage of Participants With Confirmed Tumor Responses
NCT00936702 (5) [back to overview]	Progression-free Survival
NCT00936702 (5) [back to overview]	Time to Treatment Failure
NCT00936858 (4) [back to overview]	Median Overall Survival
NCT00936858 (4) [back to overview]	Median Progression Free Survival
NCT00936858 (4) [back to overview]	Objective Response Rate
NCT00936858 (4) [back to overview]	Mean Change in Quality of Life [Medullary Thyroid Cancer Population Only]
NCT00942734 (1) [back to overview]	12-Week Progression-Free Survival (PFS)
NCT00954512 (2) [back to overview]	Part 1: Number of Participants Who Experienced One or More Adverse Events (AEs)
NCT00954512 (2) [back to overview]	Part 2: Number of Participants With Each Type of Response Evaluation Criteria in Solid Tumors (RECIST)-Determined Overall Best Response
NCT00956293 (1) [back to overview]	Number of Participants Who Experienced Adverse Events, Serious Adverse Events and Death
NCT00965094 (5) [back to overview]	Change in Renal Function (Creatinine Slope)
NCT00965094 (5) [back to overview]	Participants Who Had Occurrence of Biopsy Proven Acute Rejection, Graft Loss or Death.
NCT00965094 (5) [back to overview]	Participants Who Had Occurrence of Treatment Failure.
NCT00965094 (5) [back to overview]	Assessment of GFR by the Cockcroft-Gault Method (LOCF)
NCT00965094 (5) [back to overview]	Renal Function Assessed as Glomerula Filtration Rate (GFR) - Nankivell Method - 9 Months After Renal Transplantation (LOCF)
NCT00967044 (1) [back to overview]	Maximum Tolerated Dose (MTD) of Everolimus With Panobinostat
NCT00968253 (3) [back to overview]	Overall Response Rate (OR) Where OR = CR + CRp + CRi
NCT00968253 (3) [back to overview]	Participant Responses by Daily Dose Level Assignment (RAD001 5 mg, 10 mg and MTD 5 mg)
NCT00968253 (3) [back to overview]	Maximum Tolerated Dose [MTD] Determination by Number of Participants With Dose Limiting Toxicity (DLT)
NCT00972335 (2) [back to overview]	Progression-free Survival (PFS), in the Treatment of Patients With Refractory Meningioma.
NCT00972335 (2) [back to overview]	To Evaluate the Toxicity of Bevacizumab/Everolimus in Patients With Recurrent Meningioma.
NCT00976248 (3) [back to overview]	Time to Next Therapy With Single Agent RAD001 Therapy in Previously Untreated WM
NCT00976248 (3) [back to overview]	Overall Response Rate of RAD001 in Patients With Previously Untreated WM
NCT00976248 (3) [back to overview]	Time to Progression With Single Agent RAD001 Therapy in Previously Untreated WM.
NCT00976573 (4) [back to overview]	Confirmed Tumor Response Rate (Complete Response [CR] or Partial Response [PR]) According to Response Evaluation Criteria in Solid Tumors (RECIST) Criteria
NCT00976573 (4) [back to overview]	Progression-free Survival
NCT00976573 (4) [back to overview]	Overall Survival Time
NCT00976573 (4) [back to overview]	Toxicity
NCT00978432 (2) [back to overview]	Overall Response Rate
NCT00978432 (2) [back to overview]	Summary of Adverse Events (AEs)
NCT00985192 (6) [back to overview]	Biomarker Correlations: Time to Progression
NCT00985192 (6) [back to overview]	Efficacy in Terms of Progression Free Response
NCT00985192 (6) [back to overview]	Overall Disease-control Rate in Patients With Previously Treated Unresectable or Metastatic Adenocarcinoma of the Upper Gastrointestinal Tract Treated With Everolimus.
NCT00985192 (6) [back to overview]	Overall Survival
NCT00985192 (6) [back to overview]	Biomarker Correlations: Progression Free Survival
NCT00985192 (6) [back to overview]	Observed Biomarkers
NCT01007942 (9) [back to overview]	Vinorelbine Blood Concentrations by Leading Dose and Time Point
NCT01007942 (9) [back to overview]	Trastuzumab Blood Concentrations by Leading Dose and Time Point
NCT01007942 (9) [back to overview]	Progressive-free Survival (PFS) Per Investigator Assessment
NCT01007942 (9) [back to overview]	Overall Survival (OS)
NCT01007942 (9) [back to overview]	Overall Response Rate (ORR)
NCT01007942 (9) [back to overview]	Median Time to Deterioration of the ECOG Performance Status Score
NCT01007942 (9) [back to overview]	Clinical Benefit Rate (CBR)
NCT01007942 (9) [back to overview]	Everolimus Blood Concentrations by Leading Dose and Time Point
NCT01007942 (9) [back to overview]	PRO: Time to Deterioration in Global Health Status/QoL Domain Score of the European Organization for the Research and Treatment of Cancer (EORTC)-Core Quality of Life Questionnaire (QLQ-C30) (by at Least 10%)
NCT01009346 (2) [back to overview]	Progression Free Survival (PFS) of RAD001 in Combination With Weekly Cetuximab and Cisplatin.
NCT01009346 (2) [back to overview]	Maximum Tolerated Dose (MTD) of RAD001 in Combination With Cetuximab and Cisplatin.
NCT01014351 (3) [back to overview]	Overall Survival (OS)
NCT01014351 (3) [back to overview]	Objective Response Rate (ORR)
NCT01014351 (3) [back to overview]	Progression-free Survival (PFS)
NCT01017029 (6) [back to overview]	Absolute and Percent Frequencies of Patients With LDL ≥ 100 mg/mL at 1, 3 and 6 Months, by Treatment Group
NCT01017029 (6) [back to overview]	Participants With at Least One Occurrence of Safety Composite Endpoint After 6 Months by Treatment Group
NCT01017029 (6) [back to overview]	Participants With at Least One Occurrence of Composite Treatment Failure Events
NCT01017029 (6) [back to overview]	Hazard Cox's Model Analysis of Pericardial/Pleural Effusions
NCT01017029 (6) [back to overview]	Partcipants With at Least One Occurrence of Each Safety Composite Endpoint Event After 6 Months by Treatment Group
NCT01017029 (6) [back to overview]	Participants With CMV Infection and CMV Syndrome/Disease After 6 Months by Treatment Group
NCT01022996 (6) [back to overview]	Overall Response Rate (ORR) Based on the Assessments by Investigator
NCT01022996 (6) [back to overview]	Disease Control Rate (DCR)
NCT01022996 (6) [back to overview]	Duration of Disease Control
NCT01022996 (6) [back to overview]	Progression Free Survival (PFS) by Kaplan-Meier Estimate
NCT01022996 (6) [back to overview]	Time to Overall Response (TTR) Per Kaplan-Meier Estimate
NCT01022996 (6) [back to overview]	Duration of Overall Response (DoR)
NCT01023815 (6) [back to overview]	Treatment Failure Rate
NCT01023815 (6) [back to overview]	Number of Participants With Graft and Patient Survival After Randomization
NCT01023815 (6) [back to overview]	Changes in the Estimated Glomerular Filtration Rate (eGFR) Between Randomization (Month 3) and Month 12
NCT01023815 (6) [back to overview]	Biopsy Proven Acute Rejection (BPAR) Rate Between Randomization and Month 12
NCT01023815 (6) [back to overview]	Change in Serum Creatinine
NCT01023815 (6) [back to overview]	Change in Estimated Creatine Clearance
NCT01024946 (1) [back to overview]	To Determine the Rate of Clinical Benefit (i.e. Rate of Complete or Partial Response Plus Stable Disease) at 16 Weeks for Patients With Malignant Mesothelioma Treated With Everolimus as Second or Third Line Therapy.
NCT01025817 (7) [back to overview]	Number of Participants With Incidence of Proteinuria Events
NCT01025817 (7) [back to overview]	Number of Participants With Incidence Rates of BKV Viremia, BKV Viruria, or BKV Nephropathy
NCT01025817 (7) [back to overview]	Number of Participants With Incidence of Adverse Events, Serious Adverse Events, and Tacrolimus-associated Adverse Events
NCT01025817 (7) [back to overview]	Number of Participants With Incidence of CMV (Viremia, Syndrome and Disease)
NCT01025817 (7) [back to overview]	Estimated Glomerular Filtration Rate (eGFR)
NCT01025817 (7) [back to overview]	Number of Participants With Incidence of Composite Efficacy Failure
NCT01025817 (7) [back to overview]	Number of Participants With Incidence of New Onset of Diabetes Mellitus
NCT01031381 (2) [back to overview]	Total Number of Participants Experienced a Response (Complete Response+Partial Response+Stable Disease)
NCT01031381 (2) [back to overview]	Progression-free Survival (PFS) at 6-months
NCT01031446 (6) [back to overview]	Patients With Overall Response
NCT01031446 (6) [back to overview]	Maximum Feasible Dose in Milligrams Per Meter Squared of Body Surface Area (mg/m2) of Cisplatin and Paclitaxel for Women With Metastatic Breast Cancer
NCT01031446 (6) [back to overview]	Time to Progression in Patients With Metastatic Basal-like Breast Cancer.
NCT01031446 (6) [back to overview]	Time to Progression
NCT01031446 (6) [back to overview]	Patients With Progression-free Survival
NCT01031446 (6) [back to overview]	Maximum Feasible Dose in mg of RAD001 (Everolimus)for Women With Metastatic Breast Cancer
NCT01034631 (10) [back to overview]	Exploratory Objective: Correlation of PFS With Biomarkers
NCT01034631 (10) [back to overview]	Phase II: Response Rate With Combination Therapy Compared to Everolimus Alone
NCT01034631 (10) [back to overview]	Phase I: Toxicities of BNC105P in Combination With Everolimus.
NCT01034631 (10) [back to overview]	Phase II: Adverse Events of Everolimus and BNC105P When Administered as a Combination or Sequential Regimen.
NCT01034631 (10) [back to overview]	Phase I: Response Rate of BNC105P in Combination With Everolimus.
NCT01034631 (10) [back to overview]	Geometric Mean Half-life of BNC105 and BNC105P in Combination With Everolimus.
NCT01034631 (10) [back to overview]	Phase I: Maximum Tolerated Dose of BNC105P in Combination With Everolimus.
NCT01034631 (10) [back to overview]	Phase II: 6-month Progression Free Survival (PFS) With the Addition of BNC105P to Everolimus.
NCT01034631 (10) [back to overview]	Phase II: Overall Survival
NCT01034631 (10) [back to overview]	Phase II: Progression Free Survival (PFS) With BNC105P Alone in Patients After Progressing on Everolimus.
NCT01035229 (7) [back to overview]	Time to Tumor Progression (TTP)
NCT01035229 (7) [back to overview]	Time to Definitive Deterioration of EORTC QLQ-C30 Scores
NCT01035229 (7) [back to overview]	Time to Definitive Deterioration of ECOG Performance Score (PS) Score
NCT01035229 (7) [back to overview]	Pharmacokinetics Assessments - Cmin
NCT01035229 (7) [back to overview]	Pharmacokinetics Assessments - Cmax
NCT01035229 (7) [back to overview]	Percentage of Participants With Disease Control Rate (DCR)
NCT01035229 (7) [back to overview]	Overall Survival (OS)
NCT01047293 (2) [back to overview]	Evaluate Safety of the Combination at a Daily Dosing of 2.5mg RAD001, 5 mg RAD001 or 10 mg RAD001 (Phase 1 Part)
NCT01047293 (2) [back to overview]	Progression Free Survival at Six Months
NCT01051570 (6) [back to overview]	PSA Response Rate
NCT01051570 (6) [back to overview]	Association of PSA Response Rate With Correlative Markers (Phospho mTOR, pAKT, and p70S6)
NCT01051570 (6) [back to overview]	Overall Survival
NCT01051570 (6) [back to overview]	Pharmacokinetics: Observed Carboplatin AUC Was Estimated Based on the Concentration in the 2.75-h Sample.
NCT01051570 (6) [back to overview]	Time to Progression (TTP)
NCT01051570 (6) [back to overview]	Number of Participants With Toxicity as Measured by NCI CTCAE v3.0 Criteria
NCT01051791 (4) [back to overview]	Overall Survival (OS)
NCT01051791 (4) [back to overview]	Progression Free Survival (PFS)
NCT01051791 (4) [back to overview]	Objective Response Rate (ORR)
NCT01051791 (4) [back to overview]	Clinical Benefit Rate (CBR)
NCT01057277 (1) [back to overview]	Response
NCT01058655 (6) [back to overview]	Overall Survival (OS) [Phase II]
NCT01058655 (6) [back to overview]	Everolimus Maximum Tolerated Dose (MTD) [Phase I]
NCT01058655 (6) [back to overview]	Dose Limiting Toxicity (DLT) [Phase I]
NCT01058655 (6) [back to overview]	Disease Control Rate (DCR) [Phase II]
NCT01058655 (6) [back to overview]	Tivozanib Maximum Tolerated Dose (MTD) [Phase I]
NCT01058655 (6) [back to overview]	Progression-Free Survival (PFS) [Phase II]
NCT01059318 (8) [back to overview]	Change From Baseline in Forced Vital Capacity (FVC)
NCT01059318 (8) [back to overview]	Change From Baseline in Forced Expiratory Volume in 1 Second (FEV1)
NCT01059318 (8) [back to overview]	Change From Baseline in Extended Pulmonary Function Testing
NCT01059318 (8) [back to overview]	Change From Baseline in 6-minute Walk Test Score to Measure Exercise Capacity
NCT01059318 (8) [back to overview]	Change From Baseline in Carbon Monoxide Diffusing Capacity (DLCO)
NCT01059318 (8) [back to overview]	Mean Trough (C0,ss) and Peak (C2,ss) Drug Concentration at Steady State
NCT01059318 (8) [back to overview]	Change From Baseline in Vascular Endothelial Growth Factor-D (VEGF-D) Concentrations
NCT01059318 (8) [back to overview]	Change From Baseline in Oxygen Saturation
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: Overall Survival (OS)
NCT01062399 (5) [back to overview]	Phase II: Progression-free Survival (PFS)
NCT01062399 (5) [back to overview]	Phase I: Distribution of Worst Adverse Event Grade
NCT01068249 (5) [back to overview]	Number of Participants With Disease Progression
NCT01068249 (5) [back to overview]	Number of Participants With Objective Response Rate
NCT01068249 (5) [back to overview]	Number of Participants With Adverse Events (All Grades)
NCT01068249 (5) [back to overview]	Median Overall Survival (OS)
NCT01068249 (5) [back to overview]	Median Progression Free Survival (PFS)
NCT01070316 (2) [back to overview]	Reduction in Seizure Frequency
NCT01070316 (2) [back to overview]	Number of Participants Continuing Study Medication Over Time
NCT01075321 (5) [back to overview]	Number of Patients Reporting Dose-Limiting Toxicity (DLT) (Phase I)
NCT01075321 (5) [back to overview]	Duration of Response for All Eligible Patients
NCT01075321 (5) [back to overview]	Overall Survival for All Eligible Patients
NCT01075321 (5) [back to overview]	Time to Treatment Failure for All Eligible Patients
NCT01075321 (5) [back to overview]	Progression-Free Survival For All Eligible Patients
NCT01079143 (18) [back to overview]	Change in Interstitial Fibrosis/Tabular Atrophy (IF/TA) Grade
NCT01079143 (18) [back to overview]	Number of Participants With Progression of Renal Graft Fibrosis (Primary Comparison - ITT Population
NCT01079143 (18) [back to overview]	Number of Participants With Progression of Renal Fibrosis Using Numerical Quantification
NCT01079143 (18) [back to overview]	Number of Participants With Epithelial-mesenchymal Transition (EMT) Status
NCT01079143 (18) [back to overview]	Number of Participants With Epithelial-mesenchymal Transition (EMT) Score
NCT01079143 (18) [back to overview]	Interstitial Fibrosis/Tabular Atrophy (IF/TA)
NCT01079143 (18) [back to overview]	Incidence (Number) of BPAR
NCT01079143 (18) [back to overview]	Change in EMT Score
NCT01079143 (18) [back to overview]	Incidence (Number) of Subclinical Rejections and Borderline Lesions
NCT01079143 (18) [back to overview]	Change in Urine Protein/Creatinine Ratio (Without Imputation)
NCT01079143 (18) [back to overview]	Change From Baseline (M3) in Estimated Glomerular Filtration Rate (eGFR)
NCT01079143 (18) [back to overview]	Change in Estimated Glomerular Filtration Rate (eGFR) at M12 From Baseline (M3) - ANCOVA Model
NCT01079143 (18) [back to overview]	Incidence (Number) of Participants With Graft Losses
NCT01079143 (18) [back to overview]	Type of Biopsy Proven Acute Rejection (BPAR)
NCT01079143 (18) [back to overview]	Treatment Failures
NCT01079143 (18) [back to overview]	Change in Percentage of Interstitial Fibrosis (IF) by Numerical Quantification
NCT01079143 (18) [back to overview]	Severity of BPAR
NCT01079143 (18) [back to overview]	Risk Factors of IF/TA Progression
NCT01088048 (15) [back to overview]	Plasma Concentration of Lenalidomide
NCT01088048 (15) [back to overview]	Plasma Concentration of Everolimus
NCT01088048 (15) [back to overview]	Plasma Concentration of Bendamustine
NCT01088048 (15) [back to overview]	Toxicity of Administration of IDELA
NCT01088048 (15) [back to overview]	Time to Response
NCT01088048 (15) [back to overview]	Progression-free Survival
NCT01088048 (15) [back to overview]	Overall Survival
NCT01088048 (15) [back to overview]	Overall Response Rate
NCT01088048 (15) [back to overview]	Duration of Response
NCT01088048 (15) [back to overview]	Duration of Exposure to IDELA
NCT01088048 (15) [back to overview]	Plasma Concentration of IDELA (Cohort 6)
NCT01088048 (15) [back to overview]	Plasma Concentration of IDELA (Cohort 7)
NCT01088048 (15) [back to overview]	Sub-study: Plasma Concentration of IDELA (Cohorts 1-4)
NCT01088048 (15) [back to overview]	Plasma Concentration of IDELA (Cohort 4)
NCT01088048 (15) [back to overview]	Plasma Concentration of IDELA (Cohort 1, Cohorts 2 and 3, Cohort 5)
NCT01108445 (15) [back to overview]	Percentage of Participants With Stable Disease (SD)
NCT01108445 (15) [back to overview]	Percentage of Participants With Adverse Events
NCT01108445 (15) [back to overview]	Overall Response Rate
NCT01108445 (15) [back to overview]	Median OS
NCT01108445 (15) [back to overview]	12 Week Clinical Benefit Rate as Percentage
NCT01108445 (15) [back to overview]	Median Duration of Response (CR, PR, and SD)
NCT01108445 (15) [back to overview]	Change in Quality-of-life
NCT01108445 (15) [back to overview]	Change in Quality-of-life
NCT01108445 (15) [back to overview]	Progression Free Survival Rates
NCT01108445 (15) [back to overview]	PFS Expressed in Months
NCT01108445 (15) [back to overview]	Best Tumor Shrinkage as a Percentile in Each Arm
NCT01108445 (15) [back to overview]	Time-to-new Metastatic Disease in Each Treatment Arm
NCT01108445 (15) [back to overview]	Anti-tumor Activity as Measured by Median Progression Free Survival Time
NCT01108445 (15) [back to overview]	Overall Survival Rates
NCT01108445 (15) [back to overview]	Change in Quality-of-life
NCT01111058 (5) [back to overview]	Site of Progression: Distant
NCT01111058 (5) [back to overview]	Site of Progression: Local-regional
NCT01111058 (5) [back to overview]	Site of Progression: Unknown
NCT01111058 (5) [back to overview]	2 Year Progression Free Survival Rate
NCT01111058 (5) [back to overview]	Number of Participants With Toxicity
NCT01114529 (4) [back to overview]	Estimated Glomerular Filtration Rate (eGFR)
NCT01114529 (4) [back to overview]	Incidence of Composite Efficacy Endpoint for Each Arm at Month 12 and Month 24
NCT01114529 (4) [back to overview]	Comparison of Incidence Rates of Efficacy Endpoints Between Treatment Arms (Full Analysis Set - 24 Month Analysis)
NCT01114529 (4) [back to overview]	Change in Left Ventricular Mass Index (LVMi) From Randomization to Month 12 and Month 24
NCT01115803 (7) [back to overview]	Percentage of Participants Achieving Complete Response (CR) or Partial Response (PR) [Response Rate (RR)]
NCT01115803 (7) [back to overview]	Number of Participants With Complete Response (CR), Partial Response (PR) or Stable Disease (SD) [Best Overall Response (BOR) (CR+PR+SD)]
NCT01115803 (7) [back to overview]	Number of Participants Who Died Due to Progressive Disease Within 30 Days of Study Drug Discontinuation
NCT01115803 (7) [back to overview]	Pharmacokinetics, Maximum Observed Plasma Concentration (Cmax) of LY2584702
NCT01115803 (7) [back to overview]	Pharmacokinetics, Area Under the Concentration Time Curve (AUC)
NCT01115803 (7) [back to overview]	Clinically Significant Effects (Number of Participants With Adverse Events)
NCT01115803 (7) [back to overview]	Recommended Dose for Phase 2 Studies
NCT01125293 (10) [back to overview]	PTEN Mutation Rate [Phase II]
NCT01125293 (10) [back to overview]	Very-good-partial-response-or-better Rate [Phase II]
NCT01125293 (10) [back to overview]	Treatment-Emergent Sensory Neuropathy Rate [Phase I]
NCT01125293 (10) [back to overview]	Phase II Duration of Response (DoR)
NCT01125293 (10) [back to overview]	Phase II Overall Response Rate
NCT01125293 (10) [back to overview]	2 Year Progression-free-survival [Phase II]
NCT01125293 (10) [back to overview]	2-year Time-to-progression Probability (TTP) [Phase II]
NCT01125293 (10) [back to overview]	Everolimus Dose Limiting Toxicity (DLT) [Phase I]
NCT01125293 (10) [back to overview]	Everolimus Maximum Tolerated Dose (MTD) Stage A [Phase I]
NCT01125293 (10) [back to overview]	Everolimus Maximum Tolerated Dose (MTD) Stage B [Phase I]
NCT01127763 (4) [back to overview]	Median Progression-free Survival Time
NCT01127763 (4) [back to overview]	Toxicity Profile-Non Hematological
NCT01127763 (4) [back to overview]	Toxicity Profile-Hematological
NCT01127763 (4) [back to overview]	Clinical Benefit Rate (Complete Response, Partial Response, and Stable Disease That Lasts More Than 6 Months)
NCT01133678 (1) [back to overview]	Tumor Responses
NCT01136733 (16) [back to overview]	Summary of Plasma Concentrations of Lenvatinib for Sparse Pharmacokinetic (PK) Sampling for Phase 1b and Phase 2
NCT01136733 (16) [back to overview]	Maximum Concentration of Everolimus (Cmax) in Blood When Administered Alone or in Combination With Lenvatinib
NCT01136733 (16) [back to overview]	Phase 2: Objective Response Rate (ORR)
NCT01136733 (16) [back to overview]	Phase 2: Overall Survival (OS)
NCT01136733 (16) [back to overview]	Phase 1b: Number of Participants With Dose-limiting Toxicity (DLT)
NCT01136733 (16) [back to overview]	Area Under the Blood Concentration-Time Curve From 0 to 24 Hours for Everolimus When Administered Alone or in Combination With Lenvatinib
NCT01136733 (16) [back to overview]	Phase 1b: Maximum Tolerated Dose (MTD) and Recommended Phase 2 (RP2) Dose
NCT01136733 (16) [back to overview]	Area Under the Plasma Concentration-Time Curve From 0 to 24 Hours (AUC(0-24)) for Lenvatinib When Administered Alone or in Combination With Everolimus
NCT01136733 (16) [back to overview]	Phase 2: Progression-Free Survival (PFS)
NCT01136733 (16) [back to overview]	Summary of Blood Concentrations of Everolimus for Sparse PK Sampling for Phase 1b and Phase 2
NCT01136733 (16) [back to overview]	Clinical Benefit Rate (CBR)
NCT01136733 (16) [back to overview]	Disease Control Rate (DCR)
NCT01136733 (16) [back to overview]	Time to Cmax (Tmax) for Everolimus When Administered Alone or in Combination With Lenvatinib
NCT01136733 (16) [back to overview]	Durable Stable Disease (SD) Rate
NCT01136733 (16) [back to overview]	Maximum Concentration (Cmax) of Lenvatinib in Plasma When Administered Alone or in Combination With Everolimus
NCT01136733 (16) [back to overview]	Time to Cmax (Tmax) for Lenvatinib When Administered Alone or in Combination With Everolimus
NCT01149434 (6) [back to overview]	Effect of RAD001 on Pharmacokinetics AUC(0-inf) of JI-101
NCT01149434 (6) [back to overview]	Progression Free-Survival in the Ovarian Cancer Cohort
NCT01149434 (6) [back to overview]	Safety and Tolerability of JI-101
NCT01149434 (6) [back to overview]	Effect of JI 101 on Pharmacokinetics Area Under Curve (AUC) (0-inf) of RAD001
NCT01149434 (6) [back to overview]	Tumor Response in the Ovarian Cancer Cohort
NCT01149434 (6) [back to overview]	Tumor Response
NCT01150097 (6) [back to overview]	Incidence Rate of Composite Efficacy Failure Defined as Treated Biopsy Proven Acute Rejection (tBPAR ), Graft Loss or Death
NCT01150097 (6) [back to overview]	Incidence Rate of Composite Efficacy Failure Defined as Graft Loss or Death
NCT01150097 (6) [back to overview]	Change in Renal Function
NCT01150097 (6) [back to overview]	Incidence Rate of Composite Efficacy Failure Defined as Graft Loss or Death
NCT01150097 (6) [back to overview]	Incidence Rate of tBPAR
NCT01150097 (6) [back to overview]	Incidence Rate of Composite Efficacy Failure Defined as Treated Biopsy Proven Acute Rejection (tBPAR ), Graft Loss or Death
NCT01154335 (4) [back to overview]	Progression-Free Survival (PFS)
NCT01154335 (4) [back to overview]	Response Rate
NCT01154335 (4) [back to overview]	To Determine the Maximum Tolerated Dose (MTD) of the Combination of OSI-906 and Everolimus for the Treatment of Patients With Refractory Metastatic Colorectal Cancer.
NCT01154335 (4) [back to overview]	Overall Survival (OS)
NCT01158651 (2) [back to overview]	Common Terminology Criteria for Adverse Events (CTCAE) Events
NCT01158651 (2) [back to overview]	RAD001 Response Rate Based on 2D MRI Change From Baseline
NCT01169701 (14) [back to overview]	Change From Baseline in Cardiovascular Biomarkers, C-reactive Protein (CRP)
NCT01169701 (14) [back to overview]	Percentage of Participants With Biopsy-proven Acute Rejection (BPAR), Graft Loss, Death and Lost to Follow up
NCT01169701 (14) [back to overview]	Change From Baseline in the Cardiovascular Biomarker, Type 1 Procollagen Amino-terminal-propeptide (PINP)
NCT01169701 (14) [back to overview]	Renal Function as Measured by Estimated Glomerular Filtration Rate (eGFR)
NCT01169701 (14) [back to overview]	Renal Function Measured by Serum Creatinine
NCT01169701 (14) [back to overview]	Change From Baseline in the Cardiovascular Biomarker, N-terminal Pro-brain Natriuretic Peptide Fraction (NT-proBNP)
NCT01169701 (14) [back to overview]	Change From Baseline in the Cardiovascular Biomarker, Glycosylated Hemoglobin (HbA1c)
NCT01169701 (14) [back to overview]	Change From Baseline in Cardiovascular Biomarkers: Troponin I and Collagen Type 1 C-telopeptide (ICTP)
NCT01169701 (14) [back to overview]	Change From Baseline in the Cardiovascular Biomarker, Myeloperoxidase (MPO)
NCT01169701 (14) [back to overview]	Renal Function as Measured by Creatinine Clearance
NCT01169701 (14) [back to overview]	Pulse Wave Velocity (PWV)
NCT01169701 (14) [back to overview]	Change From Baseline in Left Ventricular Mass Index (LVMI)
NCT01169701 (14) [back to overview]	Percentage of Participants With Major Cardiovascular Events (MACE)
NCT01169701 (14) [back to overview]	Change From Baseline in Mean 24 Hour Systolic and Diastolic Blood Pressure
NCT01184326 (7) [back to overview]	Grade 4 Treatment-Related Toxicity Rate [Dose Finding]
NCT01184326 (7) [back to overview]	Dose Limiting Toxicity (DLT) [Phase I Dose Finding]
NCT01184326 (7) [back to overview]	Objective Response Rate [Expansion]
NCT01184326 (7) [back to overview]	Median Progression-Free Survival [Expansion]
NCT01184326 (7) [back to overview]	Mean Duration of Response [Expansion]
NCT01184326 (7) [back to overview]	Grade 4 Treatment-Related Toxicity Rate [Expansion]
NCT01184326 (7) [back to overview]	Maximum Tolerated Dose (MTD) [Phase I Dose Finding]
NCT01185366 (5) [back to overview]	Progression Free Survival (PFS) for First Line Medication
NCT01185366 (5) [back to overview]	Number of Participants Who Experienced Either a Grade 3 or 4 Adverse Event
NCT01185366 (5) [back to overview]	Number of Participants With Best Overall Response for First Line Medication
NCT01185366 (5) [back to overview]	Overall Survival of the First Line Therapy
NCT01185366 (5) [back to overview]	Progression Free Survival (PFS) for Crossover Medication
NCT01198158 (4) [back to overview]	Toxicities, Graded According to the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.0
NCT01198158 (4) [back to overview]	Progression-free Survival (PFS)
NCT01198158 (4) [back to overview]	Objective Response Rate (CR + PR)
NCT01198158 (4) [back to overview]	Overall Survival (OS)
NCT01206764 (5) [back to overview]	Disease Control Rate (Stable Disease [SD] + Partial Response [PR] + Complete Response [CR]);
NCT01206764 (5) [back to overview]	PFS (Progression-Free Survival)
NCT01206764 (5) [back to overview]	Overall Survival
NCT01206764 (5) [back to overview]	Objective Response Rate (ORR; Where ORR = CR + PR)
NCT01206764 (5) [back to overview]	Duration of Response (DOR)
NCT01215136 (4) [back to overview]	Number of Adverse Events as a Measure of Safety and Tolerability
NCT01215136 (4) [back to overview]	Response Rate of Single-Agent Everolimus and Everolimus + Paclitaxel
NCT01215136 (4) [back to overview]	Progression Free Survival
NCT01215136 (4) [back to overview]	Overall Survival
NCT01229943 (3) [back to overview]	Progression Free Survival
NCT01229943 (3) [back to overview]	Overall Survival (OS)
NCT01229943 (3) [back to overview]	Overall Response Rate
NCT01231399 (4) [back to overview]	Progression-free Survival
NCT01231399 (4) [back to overview]	Overall Survival
NCT01231399 (4) [back to overview]	Number of Subject With Overall Response
NCT01231399 (4) [back to overview]	Maximum Tolerated Dose (MTD) of Everolimus
NCT01231659 (6) [back to overview]	Disease Control Rate (DCR)
NCT01231659 (6) [back to overview]	Median Time to Overall Survival (OS)
NCT01231659 (6) [back to overview]	Median Time to Progression-Free Survival (PFS)
NCT01231659 (6) [back to overview]	Percentage of Participants With Overall Response Rate (ORR)
NCT01231659 (6) [back to overview]	All Collected Deaths
NCT01231659 (6) [back to overview]	Long-term Safety and Tolerability
NCT01239342 (4) [back to overview]	Median Overall Survival (OS) in Months
NCT01239342 (4) [back to overview]	Summary of Selected Toxicities Grade 3 or Greater Toxicity Based on the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.0
NCT01239342 (4) [back to overview]	Median Progression Free Survival (PFS) in Months
NCT01239342 (4) [back to overview]	Overall Response Rate (ORR) Defined as Complete Response (CR) + Partial Response (PR)
NCT01239472 (2) [back to overview]	Evaluation of Renal Function
NCT01239472 (2) [back to overview]	Cytokines Evaluation
NCT01249027 (66) [back to overview]	Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)
NCT01249027 (66) [back to overview]	Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)
NCT01249027 (66) [back to overview]	Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)
NCT01249027 (66) [back to overview]	Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)
NCT01249027 (66) [back to overview]	Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)
NCT01249027 (66) [back to overview]	Number of Participants Experiencing Death
NCT01249027 (66) [back to overview]	Number of Participants Experiencing Death
NCT01249027 (66) [back to overview]	Number of Participants Experiencing Death
NCT01249027 (66) [back to overview]	Number of Participants Experiencing Death
NCT01249027 (66) [back to overview]	Number of Participants With All Target Lesion Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With All Target Lesion Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With All Target Lesion Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With All Target Lesions Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With All Target Lesions Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With All Target Vessel Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With All Target Vessel Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With All Target Vessel Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With All Target Vessel Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With All Target Vessel Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death and Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death and Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death and Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death and Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death and Any MI
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)
NCT01249027 (66) [back to overview]	Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)
NCT01249027 (66) [back to overview]	Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)
NCT01249027 (66) [back to overview]	Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)
NCT01249027 (66) [back to overview]	Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)
NCT01249027 (66) [back to overview]	Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))
NCT01249027 (66) [back to overview]	Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))
NCT01249027 (66) [back to overview]	Number of Participants Experiencing Death
NCT01249027 (66) [back to overview]	Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))
NCT01249027 (66) [back to overview]	Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))
NCT01249027 (66) [back to overview]	Number of Participants With Major Bleeding Complications (According to GUSTO Classification)
NCT01249027 (66) [back to overview]	Number of Participants With Major Bleeding Complications (According to GUSTO Classification)
NCT01249027 (66) [back to overview]	Number of Participants With Major Bleeding Complications (According to GUSTO Classification)
NCT01249027 (66) [back to overview]	Number of Participants With Major Bleeding Complications (According to GUSTO Classification)
NCT01249027 (66) [back to overview]	Number of Participants With Major Bleeding Complications (According to GUSTO Classification)
NCT01249027 (66) [back to overview]	Number of Participants With Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Revascularization
NCT01249027 (66) [back to overview]	Number of Participants With Target Lesion Failure (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Target Lesion Failure (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Target Lesion Failure (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Target Lesion Failure (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Target Lesion Failure (TLF) (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)
NCT01249027 (66) [back to overview]	Number of Participants With Stent Thrombosis
NCT01249027 (66) [back to overview]	Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))
NCT01252251 (3) [back to overview]	Number of Participants With Stable Disease (SD)
NCT01252251 (3) [back to overview]	Median Progression Free Survival(PFS)
NCT01252251 (3) [back to overview]	Median Overall Survival (OS)
NCT01259063 (5) [back to overview]	Survival of Patients Treated
NCT01259063 (5) [back to overview]	Complete Response (CR) Rate
NCT01259063 (5) [back to overview]	Phase I - Dose-limiting Toxicity (DLT)
NCT01259063 (5) [back to overview]	Phase II - Patients Who Are Free of Disease at 1 Year
NCT01259063 (5) [back to overview]	Phase I - Maximum Tolerated Dose (MTD)
NCT01266148 (11) [back to overview]	Number of Rejections Leading to Hemodynamic Compromise
NCT01266148 (11) [back to overview]	Measured Glomerular Filtration Rate (mGFR), 12 Months After Heart Transplantation
NCT01266148 (11) [back to overview]	Average Level of Protenuria at Week 52
NCT01266148 (11) [back to overview]	Change in Quality of Life - Euro Quality of Life 5D (EQ-5D)
NCT01266148 (11) [back to overview]	Change in Calculated Glomerular Filtration Rate From Pre-transplantation to Week 52
NCT01266148 (11) [back to overview]	Progression of Chronic Allograft Vasculopathy (CAV) Based on Maximal Intimal Thickness (MIT) From Baseline to Week 52
NCT01266148 (11) [back to overview]	Progression of Chronic Allograft Vasculopathy (CAV) Based on Incidence of Chronic Allograft Vasculopathy (CAV) From Baseline to Week 52
NCT01266148 (11) [back to overview]	Occurrence of Treatment Failures up to 12 Months After Transplant
NCT01266148 (11) [back to overview]	Calculated Glomerular Filtration Rate From Pre-Transplantation to Week 52
NCT01266148 (11) [back to overview]	Lipid Profile at 12 Months
NCT01266148 (11) [back to overview]	Change in Quality of Life Assessed by SF-36 (Minnesota Living With Heart Failure Questionnaire ([MLHF)]) From Pre-transplant to Week 52 of Treatment
NCT01270321 (2) [back to overview]	Number of Participants With Progression-free Survival
NCT01270321 (2) [back to overview]	Number of Participants With Response Per Responsive Evaluation Criteria in Solid Tumors Criteria (RECIST v1.0)
NCT01275222 (8) [back to overview]	All Collected Deaths
NCT01275222 (8) [back to overview]	4-Month Progression-free Survival (PFS) Rate - Phase II
NCT01275222 (8) [back to overview]	Best Overall Response (BOR) as Assessed by Overall Response (Complete Response (CR) & Partial Response (PR)) - Phase I & II
NCT01275222 (8) [back to overview]	Number of Participants With Adverse Events (AEs): Phase I & II
NCT01275222 (8) [back to overview]	Overall Survival (OS) - Phase I & II
NCT01275222 (8) [back to overview]	Progression-free Survival (PFS) - Phase II
NCT01275222 (8) [back to overview]	Trough Concentrations for RAD001 and for Imatinib - Phase II
NCT01275222 (8) [back to overview]	Trough Concentrations for RAD001 and for Imatinib - Phase II
NCT01276457 (4) [back to overview]	Renal Function Assessed by Creatinine Clearance
NCT01276457 (4) [back to overview]	Number of Participants Who Died, Number of Participants Who Lost Their Graft, and Number of Participants Who Died or Lost Their Graft
NCT01276457 (4) [back to overview]	Number of Participants With Adverse Events (AE), Serious Adverse Events (SAE) or Deaths
NCT01276457 (4) [back to overview]	Number of Participants With Biopsy-proven Acute Rejection
NCT01281865 (1) [back to overview]	Response Rate (CR + PR) Assessed by RECIST 1.1 (Phase II)
NCT01283334 (2) [back to overview]	Progression-free Survival (PFS)
NCT01283334 (2) [back to overview]	To Measure the Safety and Clinical Effectiveness of the Combination of Carboplatin, Cetuximab and RAD001 in Patients With Advanced (Recurrent or Metastatic) Head and Neck Cancer
NCT01289912 (6) [back to overview]	Evaluation of the Efficacy of RAD001 on Neurocognition in Patients With TSC Compared With Placebo.
NCT01289912 (6) [back to overview]	Evaluation of the Safety of RAD001 on Neurocognition in Patients With TSC Compared With Placebo in Patients With TSC.
NCT01289912 (6) [back to overview]	Comparison of Autism Spectrum Disorders Features Between Patients Taking RAD001 vs. Placebo
NCT01289912 (6) [back to overview]	Comparison of Behavioral Problems Between Patients Taking RAD001 vs Placebo
NCT01289912 (6) [back to overview]	Evaluation of the Efficacy of RAD001 on Neurocognition (Cambridge Neuropsychological Test Automated Battery) in Patients With TSC Compared With Placebo.
NCT01289912 (6) [back to overview]	Comparison of Academic Skills Between Patients Taking RAD001 vs. Placebo
NCT01305941 (9) [back to overview]	Extracranial Response
NCT01305941 (9) [back to overview]	Time to Intracranial Progression.
NCT01305941 (9) [back to overview]	Toxicity
NCT01305941 (9) [back to overview]	Overall Survival
NCT01305941 (9) [back to overview]	Intracranial Response Rate- MacDonald Criteria
NCT01305941 (9) [back to overview]	Functional Assessment of Cancer Therapy- Brain (FACT-Br) Change From Baseline to Assess Impact of Everolimus in Combination With Trastuzumab and Vinorelbine on Quality of Life
NCT01305941 (9) [back to overview]	Intracranial Objective Response Rate- Modified RECIST Criteria
NCT01305941 (9) [back to overview]	Functional Assessment Cancer Therapy- Breast (FACT-B) From Baseline to 9 Weeks of Treatment to Assess Impact of Everolimus in Combination With Trastuzumab and Vinorelbine on Quality of Life
NCT01305941 (9) [back to overview]	Extracranial Time to Progression
NCT01313559 (4) [back to overview]	Number of Participants Without New Bone Lesions After 12 Weeks of Treatment
NCT01313559 (4) [back to overview]	Number of Participants With > 50% Decline From Baseline PSA Level
NCT01313559 (4) [back to overview]	Number of Participants With Progression Free Survival (PFS) Based on RECIST 1.1 Criteria
NCT01313559 (4) [back to overview]	Number of Participants Alive and Progression Free After 12 Weeks of Treatment
NCT01317615 (6) [back to overview]	Percentage of Participants Progression-free
NCT01317615 (6) [back to overview]	Overall Survival (OS)
NCT01317615 (6) [back to overview]	Percentage of Participants With Disease Control Rate (DCR)
NCT01317615 (6) [back to overview]	Progression Free Survival (PFS)
NCT01317615 (6) [back to overview]	Percentage of Participants With Overall Response Rate (ORR)
NCT01317615 (6) [back to overview]	Percentage of Participants Progression-free
NCT01347554 (4) [back to overview]	Any Bleeding
NCT01347554 (4) [back to overview]	Device-oriented Composite Outcome
NCT01347554 (4) [back to overview]	Device-oriented Composite Outcome
NCT01347554 (4) [back to overview]	Stent Thrombosis
NCT01365468 (3) [back to overview]	Number of Patients With Objective Radiographic Responses Based on Volumetric MRI Measurements (In Stratum 2 Only)
NCT01365468 (3) [back to overview]	Number of Patients With Adverse Events Assessed by Common Toxicity Criteria for Adverse Events (CTCAE) V.04
NCT01365468 (3) [back to overview]	Time to Disease Progression (TTP) Based on Change in Volumetric MRI Measurements in Children and Adults (In Stratum I Only)
NCT01374451 (10) [back to overview]	Overall Survival (OS) Using Kaplan Meier Method
NCT01374451 (10) [back to overview]	Progression-free Survival (PFS) Per Local Radiological Review
NCT01374451 (10) [back to overview]	Summary of Pharmacokinetics (PK) for Everolimus for AUClast
NCT01374451 (10) [back to overview]	Summary of Pharmacokinetics (PK) for Everolimus for CL/F
NCT01374451 (10) [back to overview]	Summary of Pharmacokinetics (PK) for Everolimus for Cmax and Cmin
NCT01374451 (10) [back to overview]	Summary of Pharmacokinetics (PK) for Everolimus for Tmax
NCT01374451 (10) [back to overview]	Safety and Tolerability Profile of Everolimus Alone or in Combination With Pasireotide LAR
NCT01374451 (10) [back to overview]	Summary of Pasireotide Concentrations Following Intramuscular Injection of Pasireotide LAR 60mg
NCT01374451 (10) [back to overview]	Objective Response Rate (ORR) as Per Radiology Review
NCT01374451 (10) [back to overview]	Disease Control Rate (DCR) as Per Radiology Review
NCT01376310 (1) [back to overview]	Number of Participants With Adverse Events
NCT01379521 (3) [back to overview]	Time to Progression (TTP) Based on the Modified RECIST Criteria
NCT01379521 (3) [back to overview]	Percentage of Participants With a Decrease in the Sum of the of Longest Diameters (SLD) of Target Lesions From Baseline to 30 Months
NCT01379521 (3) [back to overview]	Overall Survival (OS)
NCT01399918 (3) [back to overview]	Participants Evaluated for Toxicity
NCT01399918 (3) [back to overview]	Secondary Endpoint Will be the Overall Response Rate (ORR)
NCT01399918 (3) [back to overview]	To Evaluate the Efficacy of Combining Everolimus and Bevacizumab in Patients With Advanced RCC of Non-clear Cell Histology
NCT01404325 (26) [back to overview]	Incidence of Bacterial, Viral, and Fungal Infections at Month 12
NCT01404325 (26) [back to overview]	Incidence of Acute Rejection Episodes at Month 6 and Month 12
NCT01404325 (26) [back to overview]	High-Density Lipoprotein (HDL)Cholesterol Levels at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Exercise Capacity 6-Minute Walk Test(6MWT) at Month 6 and Month 12
NCT01404325 (26) [back to overview]	Calculated Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Calculated Glomerular Filtration Rate (cGFR) According to Cystatin C-based Hoek's Formula at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Calculated Glomerular Filtration Rate (cGFR) According to Chronic Kidney Disease Epidemiology Collaboration (CKD EPI) at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Adherence to Target Ranges of Tacrolimus at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Adherence to Target Ranges of Everolimus at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Adherence to Target Ranges of Cyclosporine A (CsA) at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Calculated Glomerular Filtration Rate (cGFR) According to Chronic Kidney Disease Epidemiology Collaboration (CKD EPI) at 12 Months
NCT01404325 (26) [back to overview]	Calculated Glomerular Filtration Rate (cGFR) According to Cockcroft-Gault at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Trough Levels of Everolimus at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Trough Levels of Tacrolimus at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Incidence of Patients Experiencing a Decline in GFR of < 10, 10-15, 15-20, 20-25 and > 25 mL/Min From Baseline to Month 6 and 12.
NCT01404325 (26) [back to overview]	Trough Levels of Cyclosporine A (CsA) at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Triglyceride Levels at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Total Cholesterol Levels at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Quality of Life (QoL, SF36) at Month 6 and Month 12
NCT01404325 (26) [back to overview]	Incidence of Treated Arterial Hypertension up to Month 12
NCT01404325 (26) [back to overview]	Incidence of Renal Replacement Therapy at Month 6 and Month 12
NCT01404325 (26) [back to overview]	Incidence of Graft Loss/Re-transplantation at Month 6 and Month 12
NCT01404325 (26) [back to overview]	Low-Density Lipoprotein (LDL)Cholesterol Levels at Month 1, 3, 6, 9, 12
NCT01404325 (26) [back to overview]	Incidence of Diabetes Mellitus up to Month 12
NCT01404325 (26) [back to overview]	Incidence of Death at Month 6 and Month 12
NCT01404325 (26) [back to overview]	Incidence of Bronchiolitis Obliterans Syndrome (BOS) at Month 6 and Month 12
NCT01410448 (17) [back to overview]	Change From Baseline in Serum Creatinine - ITT
NCT01410448 (17) [back to overview]	Change From Baseline in Serum Creatinine - Modified ITT
NCT01410448 (17) [back to overview]	Percentage of Participants With Proteinuria
NCT01410448 (17) [back to overview]	Percentage of Participants Who Experienced Treatment Failure - Worst-case Scenario
NCT01410448 (17) [back to overview]	Percentage of Participants With a New Onset of Diabetes
NCT01410448 (17) [back to overview]	Percentage of Participants With a New Onset of Malignancy
NCT01410448 (17) [back to overview]	Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) (Calculated With Modified Diet in Renal Disease (MDRD)-4 Formula - ITT
NCT01410448 (17) [back to overview]	Percentage of Participants With Acute Rejection (AR)
NCT01410448 (17) [back to overview]	Participant/Graft Survival Rate: Percentage of Participants With Failure Events of Death or Graft Loss - Worst-case Scenario
NCT01410448 (17) [back to overview]	Percentage of Participants Without Wound Healing Complications - Worst-case Scenario
NCT01410448 (17) [back to overview]	Duration of DGF
NCT01410448 (17) [back to overview]	Patient Survival Rate: Percentage of Deaths - Worst-case Scenario
NCT01410448 (17) [back to overview]	Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) (Calculated With Modified Diet in Renal Disease (MDRD)-4 Formula - Modified ITT
NCT01410448 (17) [back to overview]	Percentage of Participants Without Wound Healing Complications - Worst-case Scenario
NCT01410448 (17) [back to overview]	Graft Survival Rate: Percentage of Participants With Graft Loss - Worst-case Scenario
NCT01410448 (17) [back to overview]	Percentage of Participants With BPAR - Worst-case Scenario
NCT01410448 (17) [back to overview]	Percentage of Participants With Delayed Graft Function (DGF) -
NCT01419639 (3) [back to overview]	Audiologic Response
NCT01419639 (3) [back to overview]	Change in Tumor Size From Baseline
NCT01419639 (3) [back to overview]	Radiographic Response
NCT01425281 (106) [back to overview]	Number of Participants With All Revascularization
NCT01425281 (106) [back to overview]	Number of Participants With All Revascularization
NCT01425281 (106) [back to overview]	Number of Participants With All Revascularization
NCT01425281 (106) [back to overview]	Number of Participants With DMR (All Death, All MI, All Revascularization)
NCT01425281 (106) [back to overview]	Number of Participants With DMR (All Death, All MI, All Revascularization)
NCT01425281 (106) [back to overview]	Number of Participants With DMR (All Death, All MI, All Revascularization)
NCT01425281 (106) [back to overview]	Number of Participants With DMR (All Death, All MI, All Revascularization)
NCT01425281 (106) [back to overview]	Number of Participants With DMR (All Death, All MI, All Revascularization)
NCT01425281 (106) [back to overview]	Number of Participants With DMR (All Death, All MI, All Revascularization)
NCT01425281 (106) [back to overview]	Number of Participants With DMR (All Death, All MI, All Revascularization)
NCT01425281 (106) [back to overview]	Number of Participants With DMR (All Death, All MI, All Revascularization)
NCT01425281 (106) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Non Target Vessel Revascularization (Non-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Non Target Vessel Revascularization (Non-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Non Target Vessel Revascularization (Non-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Non Target Vessel Revascularization (Non-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Non Target Vessel Revascularization (Non-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Non Target Vessel Revascularization (Non-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Non-Target Vessel Revascularization (Non-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Procedural Success
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, Target Vessel Myocardial Infarction (TV-MI), ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Failure (TLF) (Cardiac Death,(Target Vessel Myocardial Infarction(TV-MI), ID-TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Revascularization (TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Revascularization (TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Revascularization (TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Revascularization (TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Revascularization (TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Revascularization (TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Revascularization (TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Lesion Revascularization (TLR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Revascularization (TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Revascularization (TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Revascularization (TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Revascularization (TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Revascularization (TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Revascularization (TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Revascularization (TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Target Vessel Revascularization (TVR)
NCT01425281 (106) [back to overview]	Number of Participants With Acute Stent/Scaffold Thrombosis
NCT01425281 (106) [back to overview]	Number of Participants With Acute/Subacute Stent/Scaffold Thrombosis
NCT01425281 (106) [back to overview]	Number of Participants With Cumulative Stent/Scaffold Thrombosis
NCT01425281 (106) [back to overview]	Number of Participants With Late Stent/Scaffold Thrombosis
NCT01425281 (106) [back to overview]	Number of Participants With Subacute Stent/Scaffold Thrombosis
NCT01425281 (106) [back to overview]	Number of Participants With Very Late Stent/Scaffold Thrombosis
NCT01425281 (106) [back to overview]	Number of Participants With Non Target Vessel Revascularization (Non-TVR)
NCT01425281 (106) [back to overview]	Absolute Difference (3 Years Post Nitrate- 3 Years Pre Nitrate) In-Scaffold Mean Lumen Diameter (MLD)
NCT01425281 (106) [back to overview]	Absolute Difference (3 Years Post-nitrate - Post Procedure Post-nitrate) In-Scaffold Minimum Lumen Diameter
NCT01425281 (106) [back to overview]	Device Success
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing All Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing Cardiac Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing Cardiac Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing Cardiac Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing Cardiac Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing Cardiac Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing Cardiac Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing Cardiac Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants Experiencing Cardiac Death/All MI
NCT01425281 (106) [back to overview]	Number of Participants With All Myocardial Infarction (Per Protocol Definition)
NCT01425281 (106) [back to overview]	Number of Participants With All Myocardial Infarction (Per Protocol Definition)
NCT01425281 (106) [back to overview]	Number of Participants With All Myocardial Infarction (Per Protocol Definition)
NCT01425281 (106) [back to overview]	Number of Participants With All Myocardial Infarction (Per Protocol Definition)
NCT01425281 (106) [back to overview]	Number of Participants With All Myocardial Infarction (Per Protocol Definition)
NCT01425281 (106) [back to overview]	Number of Participants With All Myocardial Infarction (Per Protocol Definition)
NCT01425281 (106) [back to overview]	Number of Participants With All Myocardial Infarction (Per Protocol Definition)
NCT01425281 (106) [back to overview]	Number of Participants With All Myocardial Infarction (Per Protocol Definition)
NCT01425281 (106) [back to overview]	Number of Participants With All Revascularization
NCT01425281 (106) [back to overview]	Number of Participants With All Revascularization
NCT01425281 (106) [back to overview]	Number of Participants With All Revascularization
NCT01425281 (106) [back to overview]	Number of Participants With All Revascularization
NCT01425281 (106) [back to overview]	Number of Participants With All Revascularization
NCT01434602 (16) [back to overview]	Maximum Tolerated Dose of Sorafenib for Participants With Recurrent Malignant Gliomas
NCT01434602 (16) [back to overview]	Median Amount of Time a Participant Survives After Therapy for Participants With Recurrent Malignant Glioma (Group A, Group B, and Group C) Treated With Everolimus and Sorafenib Measured From the Time of Study Enrollment
NCT01434602 (16) [back to overview]	Median Amount of Time Participants Survives Without Disease Progression for Groups A, B, and C Treated With Everolimus and Sorafenib
NCT01434602 (16) [back to overview]	Number of Participants With a Dose-limiting Toxicity (DLT)
NCT01434602 (16) [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)
NCT01434602 (16) [back to overview]	Percentage of Participants Who Survived Without Disease Progression at 3 Months After Treatment for Glioblastoma Participants With Prior Bevacizumab Exposure
NCT01434602 (16) [back to overview]	Rate of Participants Symptom Interference With Function
NCT01434602 (16) [back to overview]	Percentage of Participants Who Survived Without Disease Progression at 6 Months After Treatment for Anaplastic Glioma (AG) Participants With no Prior Bevacizumab Exposure
NCT01434602 (16) [back to overview]	Percentage of Participants Who Survived Without Disease Progression at 6 Months After Treatment for Glioblastoma Participants With no Prior Bevacizumab Exposure
NCT01434602 (16) [back to overview]	Objective Response for Participants With Recurrent Malignant Gliomas (Group A, Group B, and Group C) Treated With Everolimus and Sorafenib
NCT01434602 (16) [back to overview]	Rate of Participants Symptom Severity
NCT01434602 (16) [back to overview]	Rate of Participants Symptom Severity
NCT01434602 (16) [back to overview]	Rate of Participants Symptom Severity
NCT01434602 (16) [back to overview]	Rate of Participants Symptom Interference With Function
NCT01434602 (16) [back to overview]	Rate of Participants Symptom Interference With Function
NCT01434602 (16) [back to overview]	Maximum Tolerated Dose of Everolimus for Participants With Recurrent Malignant Gliomas
NCT01488487 (4) [back to overview]	Number of Individuals Experiencing Toxicity
NCT01488487 (4) [back to overview]	Objective Response Rate (ORR)
NCT01488487 (4) [back to overview]	Time to Progression (TTP)
NCT01488487 (4) [back to overview]	Overall Survival (OS)
NCT01491672 (6) [back to overview]	Duration of Response (DoR)
NCT01491672 (6) [back to overview]	Clinical Benefit Rate (CBR)
NCT01491672 (6) [back to overview]	Duration of PFS for Each First-line Treatment Cohort
NCT01491672 (6) [back to overview]	Progression-free Survival (PFS) - All Participants
NCT01491672 (6) [back to overview]	Overall Survival (OS)
NCT01491672 (6) [back to overview]	Objective Response Rate (ORR)
NCT01499160 (2) [back to overview]	Clinical Benefit Rate of Patients Treated With the Combination of Letrozole and Lapatinib and Then After Progression, Treated With Everolimus, Letrozole and Lapatinib.
NCT01499160 (2) [back to overview]	PROGRESSION FREE SURVIVAL TUMOR ASSESSMENT
NCT01510327 (14) [back to overview]	Myocardial Infarction (MI) Related to the Target Vessel
NCT01510327 (14) [back to overview]	Maximum Observed Everolimus Blood Concentration (Cmax)
NCT01510327 (14) [back to overview]	Definite + Probable Stent Thrombosis Rate Based on Academic Research Consortium (ARC) Definition
NCT01510327 (14) [back to overview]	Definite + Probable Stent Thrombosis Rate Based on Academic Research Consortium (ARC) Definition
NCT01510327 (14) [back to overview]	Definite + Probable Stent Thrombosis (ST) Rate Based on Academic Research Consortium (ARC) Definition
NCT01510327 (14) [back to overview]	Area Under the Concentration Versus Time Curve (AUC 0-t) Everolimus
NCT01510327 (14) [back to overview]	Area Under the Concentration Versus Time Curve (AUC 0-infinity) Everolimus
NCT01510327 (14) [back to overview]	Area Under the Concentration Versus Time Curve (AUC 0-24), Everolimus
NCT01510327 (14) [back to overview]	All Death
NCT01510327 (14) [back to overview]	Time of Occurrence of Maximum Everolimus Concentration (Tmax)
NCT01510327 (14) [back to overview]	Total Blood Clearance - Everolimus (CL)
NCT01510327 (14) [back to overview]	Terminal Phase Half-life (t1/2) Everolimus
NCT01510327 (14) [back to overview]	Target Vessel Revascularization (TVR)
NCT01510327 (14) [back to overview]	Target Lesion Revascularization (TLR)
NCT01514448 (4) [back to overview]	Overall Survival (OS) of Patients Treated With Everolimus After Failure of First-line Sunitinib or Pazopanib Therapy up to 48 Months
NCT01514448 (4) [back to overview]	Percentage of Patients With Overall Response Rate (ORR) Treated With Everolimus After Failure of First-line Sunitinib or Pazopanib Therapy at Month 6
NCT01514448 (4) [back to overview]	Percentage of Progression-free Patients by Month 6
NCT01514448 (4) [back to overview]	Progression-Free Survival (PFS) as the Time Interval Between First Intake of Everolimus and First Documented Disease Progression or Death Due to Any Cause at 24 Months
NCT01524783 (10) [back to overview]	Time to Definitive Deterioration in Functional Assessment of Cancer Therapy - General (FACT-G) Questionnaire Total Score
NCT01524783 (10) [back to overview]	Overall Survival (OS)
NCT01524783 (10) [back to overview]	Disease Control Rate (DCR) Based on Modified RECIST 1.0 and as Per Central Radiology Assessment
NCT01524783 (10) [back to overview]	Pharmacokinetics (PK): Predose Concentration (Cmin) of Everolimus at Day 29
NCT01524783 (10) [back to overview]	Overall Response Rate (ORR) as Per Modified RECIST 1.0 According to Central Evaluation
NCT01524783 (10) [back to overview]	Time to Definitive Deterioration in World Health Organization (WHO) Performance Status (PS) Change
NCT01524783 (10) [back to overview]	Probability of Participants Remaining Event-Free in Progression-Free Survival (PFS) Based on Central Radiology Assessment
NCT01524783 (10) [back to overview]	Change From Baseline in Neuron Specific Enolase (NSE) Levels
NCT01524783 (10) [back to overview]	Change From Baseline in Chromogranin A (CgA) Levels
NCT01524783 (10) [back to overview]	All Collected Deaths
NCT01544491 (11) [back to overview]	Incidence of Biopsy Proven Antibody Mediated Rejection.
NCT01544491 (11) [back to overview]	Number of Participants Having Reached the Composite Efficacy Endpoint of Biopsy-proven Acute Rejection
NCT01544491 (11) [back to overview]	To Evaluate Renal Function, Assessed by Glomerular Filtration Rate (eGFR) and Estimated by the Schwartz Formula (Extended), at Month 12
NCT01544491 (11) [back to overview]	Chronic Allograft Nephropathy / Interstitial Fibrosis and Tubular Atrophy
NCT01544491 (11) [back to overview]	Composite Efficacy Endpoint
NCT01544491 (11) [back to overview]	Evaluation of Evolution of Renal Allograft Function Over Time
NCT01544491 (11) [back to overview]	Growth/Development : Weight, Height, BMI : Change From Baseline
NCT01544491 (11) [back to overview]	To Evaluate Renal Function, Assessed by Glomerular Filtration Rate (eGFR) and Estimated by the Schwartz Formula (Abbreviated), at Month 12 and 36
NCT01544491 (11) [back to overview]	To Evaluate the Severity of BPAR (Acute T-cell Mediated Rejection Only) (Banff 2009)
NCT01544491 (11) [back to overview]	To Evaluate the Time to Event of BPAR
NCT01544491 (11) [back to overview]	Proteinuria (Urinary Protein/Creatinine Ratio)
NCT01545817 (7) [back to overview]	Overall Survival From the Start (OSS) of Study Treatment
NCT01545817 (7) [back to overview]	Overall Survival of Everolimus (OSE)
NCT01545817 (7) [back to overview]	Progression Free Survival (PFS) Rates
NCT01545817 (7) [back to overview]	Objective Response Rate (ORR) for the Pazopanib Treatment Period Using RECIST
NCT01545817 (7) [back to overview]	Objective Response Rate (ORR) for the Everolimus Treatment Period Using RECIST
NCT01545817 (7) [back to overview]	Progression Free Survival (PFS) for the Everolimus Treatment Period Using RECIST
NCT01545817 (7) [back to overview]	PFS for the Pazopanib Treatment Period Using RECIST
NCT01551212 (6) [back to overview]	Incidence of HCV Related Fibrosis
NCT01551212 (6) [back to overview]	Estimated GFR - PP Set
NCT01551212 (6) [back to overview]	Estimated Glomerular Filtration Rate (GFR)
NCT01551212 (6) [back to overview]	Incidence of de Novo HCC Malignancies
NCT01551212 (6) [back to overview]	Number of Participants With HCV
NCT01551212 (6) [back to overview]	Percentage of Participants With Treated Biopsy Proven Acute Rejection (BPAR), Graft Loss or Death
NCT01563354 (12) [back to overview]	Biochemical Response Rate (BRR) for 5HIAA Levels
NCT01563354 (12) [back to overview]	Duration of Biochemical Response (DBR), by Treatment (Full Analysis Set)
NCT01563354 (12) [back to overview]	Summary of Duration of Response (Months)
NCT01563354 (12) [back to overview]	Percentage of Participants Progression-free at 9 Months Based on Response Evaluation Criteria In Solid Tumors v1.1 (RECIST v1.1)
NCT01563354 (12) [back to overview]	12-month Disease Control Rate (DCR) and Objective Response Rate (ORR)
NCT01563354 (12) [back to overview]	Summary of Progression-free Survival (PFS) Based on RECIST v1.1
NCT01563354 (12) [back to overview]	Biochemical Response Rate (BRR) for Chromogranin A (CgA) Levels
NCT01563354 (12) [back to overview]	Kaplan-Meier Estimates of Progression-free Survival (PFS)
NCT01563354 (12) [back to overview]	Summary of Time to Response (Months)
NCT01563354 (12) [back to overview]	Kaplan-Meier Event-free Probability Estimate for Biochemical Progression-free Survival Based on CgA Levels
NCT01563354 (12) [back to overview]	Kaplan-Meier Event-free Probability Estimate Based on CgA Levels
NCT01563354 (12) [back to overview]	Summary of Biochemical Progression-free Survival Based on CgA Levels by Treatment
NCT01582009 (5) [back to overview]	Number of Participants With an Adverse Event.
NCT01582009 (5) [back to overview]	Number of Participants With Clinical Response
NCT01582009 (5) [back to overview]	Progression-free Survival (PFS)
NCT01582009 (5) [back to overview]	Median Progression Free Survival
NCT01582009 (5) [back to overview]	6-month Overall Survival Rate
NCT01595009 (16) [back to overview]	Mean EORTC QLQ-G.I. NET21 Score (Core)
NCT01595009 (16) [back to overview]	Change in EORTC QLQ-G.I. NET21 Score at the End of Treatment From Baseline (Baseline = First Day of Treatment in the Extension) (E1)
NCT01595009 (16) [back to overview]	Number and Percentage of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs) and Deaths During the Extension Phase (E1)
NCT01595009 (16) [back to overview]	Investigator-assessed Best Overall Response During the Extension Phase (E1)
NCT01595009 (16) [back to overview]	Number and Percentage of Participants With Ratings of 'no Problem, 'Some Problem' and 'Extreme Problem' in the EuroQol Five Dimensions Questionnaire (EQ-5D) (Core)
NCT01595009 (16) [back to overview]	Number and Percentage of Participants With Ratings of 'no Problem, 'Some Problem' and 'Extreme Problem' in the EuroQol Five Dimensions Questionnaire (EQ-5D) (Core)
NCT01595009 (16) [back to overview]	Change in EORTC QLQ-G.I. NET21 Score at the End of Treatment From Baseline (Baseline = First Day of Treatment in the Extension) (E1)
NCT01595009 (16) [back to overview]	Investigator-assessed Progression Free Survival (PFS) (E1)
NCT01595009 (16) [back to overview]	Investigator-assessed Progression Free Survival (PFS) (Core)
NCT01595009 (16) [back to overview]	Change in European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30 (EORTC QLQ-C30) Score at the End of Treatment From Baseline (Baseline = First Day of Treatment in the Extension) (E1)
NCT01595009 (16) [back to overview]	Mean European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30 (EORTC QLQ-C30) Score (Core)
NCT01595009 (16) [back to overview]	Mean EQ-5D Visual Analogue Scale (VAS) Score (Core)
NCT01595009 (16) [back to overview]	Mean EORTC QLQ-G.I. NET21 Score (Core)
NCT01595009 (16) [back to overview]	Number and Percentage of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs) and Deaths (Core)
NCT01595009 (16) [back to overview]	Change in EuroQol Five Dimensions Questionnaire (EQ-5D) Score at the End of Treatment From Baseline (Baseline = First Day of Treatment in the Extension) (E1)
NCT01595009 (16) [back to overview]	Investigator-assessed Best Overall Response (Core)
NCT01596062 (9) [back to overview]	Estimated Glomerular Filtration Rate (eGFR) at Day 8 and Week 24
NCT01596062 (9) [back to overview]	AUC of Basiliximab Binding to CD25 Receptors From Day 0 to Day 84
NCT01596062 (9) [back to overview]	Area Under the Curve (AUC) of CD25 Saturation by Basiliximab From Day 0 to Day 84
NCT01596062 (9) [back to overview]	Saturation Rate of CD25 Antigen Saturation by Basiliximab
NCT01596062 (9) [back to overview]	Percentage of Participants With Biopsy Proven Acute Rejection (BPAR) According to Type and Severity
NCT01596062 (9) [back to overview]	Percentage of Participants With of Biopsy Proven Acute Rejection (BPAR)
NCT01596062 (9) [back to overview]	Percentage of T-cells That Bind Basiliximab to CD25 Receptors
NCT01596062 (9) [back to overview]	Proportion of CD3+, CD4+, CD8+, CD19+ and CD56+ T Cells
NCT01596062 (9) [back to overview]	Percentage of Participants With of Treatment Failures
NCT01598987 (7) [back to overview]	Growth Development - Height at Baseline and Month 24
NCT01598987 (7) [back to overview]	Growth Development - Height at Baseline and Month 12
NCT01598987 (7) [back to overview]	Change From Baseline in Estimated Glomerular Filtration Rate - Month 12
NCT01598987 (7) [back to overview]	Change From Baseline in Estimated Glomerular Filtration Rate - Month 24
NCT01598987 (7) [back to overview]	Kaplan-Meier Estimates for Failure Rates of Efficacy Endpoints
NCT01598987 (7) [back to overview]	Growth Development - Weight at Baseline and Month 24
NCT01598987 (7) [back to overview]	Growth Development - Weight at Baseline and Month 12
NCT01624948 (6) [back to overview]	Evidence of Reduction of BK Viruria and/or Clearance of BK Viremia
NCT01624948 (6) [back to overview]	Proteinuria
NCT01624948 (6) [back to overview]	p70S6 Kinase Phosphorylation
NCT01624948 (6) [back to overview]	Cholesterol
NCT01624948 (6) [back to overview]	Evaluation for the Development of BK Virus Nephropathy or Doubling of BK Viremia Levels
NCT01624948 (6) [back to overview]	Median Between the Calculated Mean Residual Expression of NFAT-regulated Genes
NCT01625377 (13) [back to overview]	Change From Baseline (Randomization) in Serum Creatinine
NCT01625377 (13) [back to overview]	Number of Patients With Treated or Not Treated Biopsy Proven Acute Rejection (BPAR)
NCT01625377 (13) [back to overview]	Change From Baseline (Randomization) in Creatinine Clearance Estimated Using the Adjusted Cockcroft-Gault Formula
NCT01625377 (13) [back to overview]	Change From Baseline (Randomization) in Glomerular Filtration Rate Estimated by CKD-EPI Formula
NCT01625377 (13) [back to overview]	Change From Baseline (Randomization) in Renal Function
NCT01625377 (13) [back to overview]	Change From Baseline (Randomization) in Urine Protein/Creatinine Ratio
NCT01625377 (13) [back to overview]	Change From Baseline (Randomization) in Glomerular Filtration Rate Estimated by Abbreviated Modification of Diet in Renal Disease (MDRD) Formula
NCT01625377 (13) [back to overview]	Number of Patients in Different Stages of Chronic Kidney Diseases According to the K/DOQI Classification System
NCT01625377 (13) [back to overview]	Number of Patients Reported With Different Categories of Severity of BPAR According to Banff Classification
NCT01625377 (13) [back to overview]	Number of Patients With Any Adverse Events, Serious Adverse Events, Death and Premature Discontinuation
NCT01625377 (13) [back to overview]	Number of Patients With Death or Graft Loss
NCT01625377 (13) [back to overview]	Number of Patients With Treated or Untreated BPAR With RAI Score Greater Than 3
NCT01625377 (13) [back to overview]	Number of Patients With Treatment Failures
NCT01627067 (5) [back to overview]	Overall Survival (OS)
NCT01627067 (5) [back to overview]	Progression-Free Survival (PFS)
NCT01627067 (5) [back to overview]	Compare Overall Survival (OS) Between the Number of Obese and Overweight Participants
NCT01627067 (5) [back to overview]	Compare Progression Free Survival (PFS) Between the Number of Obese and Overweight Participants
NCT01627067 (5) [back to overview]	Number of Participants With Response
NCT01628913 (1) [back to overview]	Progression Free Survival (PFS)
NCT01637090 (5) [back to overview]	Efficacy of Treatment
NCT01637090 (5) [back to overview]	Progression-free Survival
NCT01637090 (5) [back to overview]	Effect of mTOR on Tumors
NCT01637090 (5) [back to overview]	Time to Response
NCT01637090 (5) [back to overview]	Number of Participants With Adverse Events as a Measure of Safety and Tolerability
NCT01642186 (5) [back to overview]	Median PFS
NCT01642186 (5) [back to overview]	Number of Participants With One or More Adverse Events/Toxicity
NCT01642186 (5) [back to overview]	Number of Participants With Tissue Biomarkers Collected
NCT01642186 (5) [back to overview]	Percentage of Participants With Stable Disease
NCT01642186 (5) [back to overview]	Median Overall Survival (OS)
NCT01653847 (5) [back to overview]	Change in T Cell & B Cell Generation
NCT01653847 (5) [back to overview]	Renal Allograft Survival
NCT01653847 (5) [back to overview]	Patient Survival
NCT01653847 (5) [back to overview]	Acute Rejection
NCT01653847 (5) [back to overview]	Change in Glomerular Filtration Rate (GFR)
NCT01661283 (3) [back to overview]	Vascular Endothelial Growth Factor (VEGF) and Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) Levels at Baseline and Pre-Cycles 3 and 5
NCT01661283 (3) [back to overview]	Clinical Benefit Rate (Complete Response, Partial Response, and Stable Disease at ≥ 4 Months Using World Health Organization (WHO) Criteria) of Everolimus in Combination With Bevacizumab
NCT01661283 (3) [back to overview]	Number of Participants With Response Stratified by Individuals With Sporadic or NF1 Associated MPNST
NCT01665768 (2) [back to overview]	Safety as Assessed by Avoidance of Grade 3-4 Adverse Events
NCT01665768 (2) [back to overview]	Event Free Survival (EFS)
NCT01668784 (11) [back to overview]	Number of Participants With Abnormal Hematology and Serum Chemistry Laboratory Parameters by Worse CTC Grade - SI Units
NCT01668784 (11) [back to overview]	Number of Participants Meeting Marked Laboratory Abnormality Criteria in Specific Liver and Thyroid Tests
NCT01668784 (11) [back to overview]	Overall Survival (OS) at Primary Endpoint
NCT01668784 (11) [back to overview]	Investigator-assessed Objective Response Rate (ORR)
NCT01668784 (11) [back to overview]	Extended Collection to Post Hoc Overall Survival (OS)
NCT01668784 (11) [back to overview]	Investigator-assessed Duration of Objective Response
NCT01668784 (11) [back to overview]	Number of Participants With Serious Adverse Events, Death, Discontinuation Due to Adverse Events
NCT01668784 (11) [back to overview]	Investigator-assessed Time of Progression-free Survival (PFS)
NCT01668784 (11) [back to overview]	Percentage of Participants With Disease-related Symptom Progression (DRSP)
NCT01668784 (11) [back to overview]	Overall Survival (OS) by Programmed Death-Ligand 1 (PD-L1) Expression Level
NCT01668784 (11) [back to overview]	Investigator-assessed Time to Objective Response
NCT01674140 (4) [back to overview]	Distant Recurrence-Free Survival (DRFS)
NCT01674140 (4) [back to overview]	Invasive Disease-Free Survival (IDFS)
NCT01674140 (4) [back to overview]	Overall Survival (OS)
NCT01674140 (4) [back to overview]	Toxicity Based on Common Terminology Criteria for Adverse Events (CTCAE) Version 4.0, Assessed up to 10 Years.
NCT01680861 (7) [back to overview]	Incidence of Chronic Allograft Nephropathy (CAI) at 12 Months Post-transplant
NCT01680861 (7) [back to overview]	BPAR (Biopsy-proven Acute Rejection) Incidence During the First 12 Months Post-transplant
NCT01680861 (7) [back to overview]	Discontinuance of Any Study Medication (Tacrolimus, Everolimus, or EC-MPS)
NCT01680861 (7) [back to overview]	eGFR (Calculated Glomerular Filtration Rate), i.e., Renal Function, at 1 Month Post-transplant.
NCT01680861 (7) [back to overview]	eGFR (Renal Function) at 6 Months Post-transplant
NCT01680861 (7) [back to overview]	eGFR (Renal Function) at Month 3 Post-transplant
NCT01680861 (7) [back to overview]	Graft Loss (Return to Permanent Dialysis or Death)
NCT01698918 (23) [back to overview]	First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Overall Health at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	First-line Treatment: Progression-free Survival (PFS)
NCT01698918 (23) [back to overview]	First-line Treatment: Overall Response Rate (ORR)
NCT01698918 (23) [back to overview]	First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Mouth and Throat Soreness Limiting Swallowing, Drinking, Eating, Talking and Sleeping at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Mouth Pain Severity Affecting Daily Activities at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Mouth Pain Severity at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	First-line Treatment: Duration of First Stomatitis Based on OSDQ
NCT01698918 (23) [back to overview]	First-line Treatment (Stomatitis Sub-study): Duration of First Stomatitis Based on OSDQ
NCT01698918 (23) [back to overview]	First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Mouth and Throat Soreness at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Mouth and Throat Soreness Limiting Swallowing, Drinking, Eating, Talking and Sleeping at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	First-line Treatment: Clinical Benefit Rate (CBR)
NCT01698918 (23) [back to overview]	All Collected Deaths
NCT01698918 (23) [back to overview]	Second-line Treatment: Progression-free Survival (PFS)
NCT01698918 (23) [back to overview]	First-line Treatment (Stomatitis Sub-study): Time to First Stomatitis Episode as Assessed by the OSDQ
NCT01698918 (23) [back to overview]	First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Mouth and Throat Soreness at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	First-line Treatment: Time to First Stomatitis Episode as Assessed by the Oral Stomatitis Daily Questionnaire (OSDQ)
NCT01698918 (23) [back to overview]	First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Mouth Pain Severity Affecting Daily Activities at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Mouth Pain Severity at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	Second-line Treatment: Overall Response Rate (ORR)
NCT01698918 (23) [back to overview]	First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Overall Health at the End of the First Stomatitis Episode
NCT01698918 (23) [back to overview]	Second-line Treatment: Clinical Benefit Rate (CBR)
NCT01698918 (23) [back to overview]	Number of Participants With Clinical Benfit During Extension Phase
NCT01698918 (23) [back to overview]	Overall Survival (OS)
NCT01713946 (22) [back to overview]	Seizure Free Rates by Time Window
NCT01713946 (22) [back to overview]	Long Term Evaluation: Relationship Between Seizure Frequency and Time-normalized Everolimus Concentration at Trough (Cmin,TN) - Repeated Measures Analysis
NCT01713946 (22) [back to overview]	Core Phase: Median Percentage Change From Baseline in Seizure Frequency by Time Normalized Minimum Concentration
NCT01713946 (22) [back to overview]	Core Phase: Food & Drug Administration (FDA): Percentage Change From Baseline in Partial Onset-seizure Frequency
NCT01713946 (22) [back to overview]	Core Phase: Percentage of Patients With at Least a 25% Reduction in Seizure Frequency
NCT01713946 (22) [back to overview]	Core Phase: Impact of Everolimus on Anti-epileptic Drugs (AEDs) Concentrations
NCT01713946 (22) [back to overview]	Percentage of Seizure-free Patients During the Maintenance Period of the Core Phase
NCT01713946 (22) [back to overview]	Core Phase: Change From Baseline in the Overall Vineland-II Adaptive Behavior Composite (ABC) Score
NCT01713946 (22) [back to overview]	Long Term Evaluation: Incidence of Suicide Attempt, Suicidal Ideation or Behavior During Core Phase Per Columbia Suicide Severity Rating Scale (C-SSRS) Outcomes
NCT01713946 (22) [back to overview]	Core Phase: Response Rate in Seizure Frequency by Time Normalized Minimum Concentration
NCT01713946 (22) [back to overview]	Core Phase: European Medicine Agency (EMA): Seizure Frequency Response Rate
NCT01713946 (22) [back to overview]	Core Phase: Changes From Baseline in Number of Seizure-free Days
NCT01713946 (22) [back to overview]	Core Phase: Change From Baseline in the QOLIE-31-P Overall Quality-of-life Score for Patients Aged >=18 Years
NCT01713946 (22) [back to overview]	Long Term Evaluation: Effect of Everolimus Over Time in the Overall Wechsler Nonverbal Composite Score
NCT01713946 (22) [back to overview]	Long Term Evaluation: Effect of Everolimus Over Time in the Overall Vineland-II Adaptive Behavior Composite (ABC) Score
NCT01713946 (22) [back to overview]	Core Phase: Probability That a Patient Remains On-treatment up to a Specified Time Point
NCT01713946 (22) [back to overview]	Core Phase: Incidence of Suicide Attempt, Suicidal Ideation or Behavior During Core Phase Per Columbia Suicide Severity Rating Scale (C-SSRS) Outcomes
NCT01713946 (22) [back to overview]	Core Phase: Distribution of Reduction From Baseline in Seizure Frequency
NCT01713946 (22) [back to overview]	Core Phase: Change From Baseline in the QOLIE-AD-48 Overall Quality-of-life Score for Patients >=11 to 18 Years
NCT01713946 (22) [back to overview]	Core Phase: Change From Baseline in Wechsler Nonverbal Composite Score
NCT01713946 (22) [back to overview]	Long Term Evaluation: Percentage Change From Start of Everolimus in Seizure Frequency by Time Window
NCT01713946 (22) [back to overview]	Core Phase: Change From Baseline in the QOLCE Overall Quality-of-life Score for Patients <11 Years
NCT01734512 (1) [back to overview]	Percentage of Participants With Progression Free Survival at 6 Months
NCT01743560 (10) [back to overview]	Overall Survival (OS) Events (Number of Deaths) - FAS
NCT01743560 (10) [back to overview]	Overall Survival (OS) - % Event-free Probability Estimate - FAS
NCT01743560 (10) [back to overview]	Change From Baseline EORTC Quality of Life Questionnaire of Cancer Patients QLQ-C30 at Each Time Point
NCT01743560 (10) [back to overview]	Progression-free Survival (PFS) - % Event-free Probability Estimate - FAS
NCT01743560 (10) [back to overview]	Progression-free Survival (PFS) Events as Per Investigators - FAS
NCT01743560 (10) [back to overview]	Change From Baseline in EuroQoL 5-dimension Visual Analogue Scores - FAS
NCT01743560 (10) [back to overview]	Overall Response Rate of Everolimus and Exemestane Treatment in Postmenopausal Women With Hormone Receptor Positive Locally Advanced or Metastatic Breast Cancer
NCT01743560 (10) [back to overview]	Progression-free Survival (PFS) by Median Time in Weeks as Per Investigators - FAS
NCT01743560 (10) [back to overview]	Percentage of Patient Responses in EuroQoL 5-dimension Questionnaire - FAS
NCT01743560 (10) [back to overview]	Best Overall Response of Everolimus and Exemestane Treatment in Postmenopausal Women With Hormone Receptor Positive Locally Advanced or Metastatic Breast Cancer
NCT01783444 (9) [back to overview]	Mean Change in Treatment Satisfaction Questionnaire for Medication (TSQM) Between Week 3 and 12
NCT01783444 (9) [back to overview]	Time to Eastern Cooperative Oncology Group (ECOG) Performance Deterioration
NCT01783444 (9) [back to overview]	Time to 10% Definitive Deterioration in the Global Health Status / Quality of Life
NCT01783444 (9) [back to overview]	Progression Free Survival (PFS) - Everolimus Plus Exemestane Versus Capecitabine Alone
NCT01783444 (9) [back to overview]	Progression Free Survival (PFS) - Everolimus Plus Exemestane Versus Everolimus Alone
NCT01783444 (9) [back to overview]	Clinical Benefit Rate (CBR)
NCT01783444 (9) [back to overview]	Overall Response Rate (ORR)
NCT01783444 (9) [back to overview]	All Collected Deaths
NCT01783444 (9) [back to overview]	Overall Survival (OS)
NCT01784861 (8) [back to overview]	Disease Stabilization Rate - Phase II
NCT01784861 (8) [back to overview]	Progression Free Survival (PFS) - Phase II
NCT01784861 (8) [back to overview]	Recommended Phase II Dose of X-82
NCT01784861 (8) [back to overview]	Number of Participants With Toxicity - Phase II
NCT01784861 (8) [back to overview]	Overall Toxicities - Phase I
NCT01784861 (8) [back to overview]	Number of Participants With Dose Limiting Toxicities - Phase I
NCT01784861 (8) [back to overview]	Objective Response Rate (Complete Response + Partial Response) - Phase II
NCT01784861 (8) [back to overview]	Overall Survival - Phase II
NCT01789281 (2) [back to overview]	Percentage of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT01789281 (2) [back to overview]	Percentage of Patients With Clinical Benefit
NCT01797120 (4) [back to overview]	Clinical Benefit Rate
NCT01797120 (4) [back to overview]	Objective Response Rate
NCT01797120 (4) [back to overview]	Overall Survival
NCT01797120 (4) [back to overview]	Progression-free 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)
NCT01843348 (11) [back to overview]	Percent of Participants With Delayed Graft Function by Day
NCT01843348 (11) [back to overview]	Glomular Filtration Rate (GFR) mL/Min Via Cockcroft- Gault Method at Month 12 Post Transplant
NCT01843348 (11) [back to overview]	Glomular Filtration Rate (GFR) Via Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) Method at Month 12 Post Transplant
NCT01843348 (11) [back to overview]	Glomular Filtration Rate (GFR) Via Modification of Diet in Renal Disease (MDRD) Method at Month 12 Post Transplant
NCT01843348 (11) [back to overview]	Duration of Wound Healing
NCT01843348 (11) [back to overview]	Glomular Filtration Rate (GFR) mL/Min Via Nankivell Method at Month 12 - Standard Regimen vs Certican Regimens
NCT01843348 (11) [back to overview]	Percent of Participants With Delayed Graft Function and Slow Graft Function
NCT01843348 (11) [back to overview]	Percent of Participants With Viral Infections
NCT01843348 (11) [back to overview]	Percent of Participants With Wound Healing Complications During Study
NCT01843348 (11) [back to overview]	Percentage of Participants With Composite Treatment Failure Endpoints - Difference Between Groups at Month 12
NCT01843348 (11) [back to overview]	Percentage of Participants With Treatment Failure Endpoints at Month 12
NCT01865747 (3) [back to overview]	Objective Response Rate (ORR)
NCT01865747 (3) [back to overview]	Overall Survival (OS)
NCT01865747 (3) [back to overview]	Progression-free Survival (PFS)
NCT01888432 (16) [back to overview]	Composite Efficacy Failure of Treated Biopsy in Everolimus With Reduced Tacrolimus Group Compared to Standard Tacrolimus in Patients From Japan Only
NCT01888432 (16) [back to overview]	Number of Participants With Composite of tBPAR, Graft Loss, and Death
NCT01888432 (16) [back to overview]	Number of Participants With Time to Recurrence of HCC in Subjects With a Diagnosis of HCC at the Time of Liver Transplantation
NCT01888432 (16) [back to overview]	Compare Renal Function Over Time Assessed by the Change by eGFR, Post-randomization
NCT01888432 (16) [back to overview]	Renal Function by Estimated Glomerular Filtration Rate (eGFR) From Randomization
NCT01888432 (16) [back to overview]	Number of Subjects Experiencing Adverse Events/Infections by SOC
NCT01888432 (16) [back to overview]	Number of Participants With Composite Efficacy Failure of Treated Biopsy Proven Acute Rejection, Graft Loss or Death in Everolimus With Reduced Tacrolimus Group Compared to Standard Tacrolimus
NCT01888432 (16) [back to overview]	Compare Incidence of tAR
NCT01888432 (16) [back to overview]	Renal Function by Estimated Glomerular Filtration Rate (All Extension Patients)
NCT01888432 (16) [back to overview]	Compare Incidence of a Composite of Death or Graft Loss
NCT01888432 (16) [back to overview]	Compare Incidence of AR
NCT01888432 (16) [back to overview]	Compare Incidence of BPAR
NCT01888432 (16) [back to overview]	Compare Incidence of Death
NCT01888432 (16) [back to overview]	Compare Incidence of Graft Loss
NCT01888432 (16) [back to overview]	Compare Incidence of Notable Safety Events (SAEs, Infections and Serious Infections Leading to Premature Discontinuation)
NCT01888432 (16) [back to overview]	Compare Incidence of tBPAR
NCT01894152 (38) [back to overview]	Number of All Death (Cardiac, Vascular, and Non-cardiovascular)
NCT01894152 (38) [back to overview]	Number of All Deaths, Myocardial Infarction, Any Repetitive Revascularization Composite Endpoints
NCT01894152 (38) [back to overview]	Number of Participants With All Target Vessel Revascularization (TVR)
NCT01894152 (38) [back to overview]	Number of Participants With All TLR
NCT01894152 (38) [back to overview]	Number of Participants With All TLR
NCT01894152 (38) [back to overview]	Number of Participants With ID-TVR (TLR and TVR, Non-target Lesion)
NCT01894152 (38) [back to overview]	Number of Participants With Cardiac Death and All Myocardial Infarction (MI) (Q-wave and Non-Q Wave) Composite Endpoint
NCT01894152 (38) [back to overview]	Number of Participants With All TVR (TLR and TVR, Non-target Lesion)
NCT01894152 (38) [back to overview]	Number of Participants With ID-TVR (TLR and TVR, Non-target Lesion)
NCT01894152 (38) [back to overview]	Number of Participants With Target Lesion Failure (TLF)
NCT01894152 (38) [back to overview]	Number of Participants With Sub-acute Stent Thrombosis
NCT01894152 (38) [back to overview]	Number of Participants With ID-TVR, Non-target Lesion
NCT01894152 (38) [back to overview]	Number of Participants With ID-TVR, Non-target Lesion
NCT01894152 (38) [back to overview]	Number of Participants With Late Stent Thrombosis
NCT01894152 (38) [back to overview]	Number of Participants With Overall Stent Thrombosis
NCT01894152 (38) [back to overview]	Number of All Death (Cardiac, Vascular, and Non-cardiovascular)
NCT01894152 (38) [back to overview]	Number of Participants With Early Stent Thrombosis
NCT01894152 (38) [back to overview]	Number of All Deaths, Myocardial Infarction, Any Repetitive Revascularization Composite Endpoints
NCT01894152 (38) [back to overview]	Number of Participants With All TVR (TLR and TVR, Non-target Lesion)
NCT01894152 (38) [back to overview]	Number of Participants With Target Lesion Failure (TLF)
NCT01894152 (38) [back to overview]	Number of Participants With Very Late Stent Thrombosis
NCT01894152 (38) [back to overview]	Number of Participants With Acute Stent Thrombosis
NCT01894152 (38) [back to overview]	Number of Participants With Target Vessel Failure (ID-TVF) (Cardiac Death, All Myocardial Infarctions and Ischemia-driven Target Vessel Revascularization)
NCT01894152 (38) [back to overview]	Number of Participants With Target Vessel ARC MI
NCT01894152 (38) [back to overview]	Number of Participants With Target Vessel ARC MI
NCT01894152 (38) [back to overview]	Number of Participants With Composite Rate of All Deaths and Myocardial Infarctions (MI)
NCT01894152 (38) [back to overview]	Number of Participants With ID-TLR
NCT01894152 (38) [back to overview]	Number of Participants With ID-TLR
NCT01894152 (38) [back to overview]	Number of Participants With Target Vessel Failure (ID-TVF) (Cardiac Death, All Myocardial Infarctions and Ischemia-driven Target Vessel Revascularization)
NCT01894152 (38) [back to overview]	Number of Participants With Cardiogenic Death, Target Vessel Blood Flow Myocardial Infarction, Target Lesion Revascularization Composite Endpoint
NCT01894152 (38) [back to overview]	Number of Participants With Cardiogenic Death, Target Vessel Blood Flow Myocardial Infarction, Target Lesion Revascularization Composite Endpoint
NCT01894152 (38) [back to overview]	Number of Participants With Composite Rate of All Deaths and Myocardial Infarctions (MI)
NCT01894152 (38) [back to overview]	Number of Participants With All Target Vessel Revascularization (TVR)
NCT01894152 (38) [back to overview]	Number of Participants With All Revascularization (Target Lesion, Target Vessel, and Non-target Vessel) (PCI and Coronary Artery Bypass Graft [CABG])
NCT01894152 (38) [back to overview]	Number of Participants With All Revascularization (Target Lesion, Target Vessel, and Non-target Vessel) (PCI and Coronary Artery Bypass Graft [CABG])
NCT01894152 (38) [back to overview]	Number of Participants With All Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)
NCT01894152 (38) [back to overview]	Number of Participants With All Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)
NCT01894152 (38) [back to overview]	Number of Participants With Cardiac Death and All Myocardial Infarction (MI) (Q-wave and Non-Q Wave) Composite Endpoint
NCT01911546 (4) [back to overview]	The Number of Polyoma BK Viremia Patients
NCT01911546 (4) [back to overview]	The Number of CMV Viremia
NCT01911546 (4) [back to overview]	Incidence of Cell Mediated Rejection (CMR)
NCT01911546 (4) [back to overview]	Incidence of Antibody Mediated Rejection (ABMR)
NCT01929642 (7) [back to overview]	Frequency of Seizures Assessed by Total Number of Seizures
NCT01929642 (7) [back to overview]	Feasibility Measurements of Parental Stress
NCT01929642 (7) [back to overview]	Cognitive Function as Assessed by the Capute Scale
NCT01929642 (7) [back to overview]	Caregiver Burden
NCT01929642 (7) [back to overview]	Number of Participants With Compliance to the Treatment Protocol.
NCT01929642 (7) [back to overview]	Total Number of Aggressions or Self-injuries
NCT01929642 (7) [back to overview]	Repetitive Behavior
NCT01931163 (1) [back to overview]	Tumor Response
NCT01935128 (20) [back to overview]	Leukopenia
NCT01935128 (20) [back to overview]	Infection Requiring Hospitalization
NCT01935128 (20) [back to overview]	Impaired Glucose Tolerance
NCT01935128 (20) [back to overview]	Graft Survival
NCT01935128 (20) [back to overview]	Gastrointestinal Complaints
NCT01935128 (20) [back to overview]	Development of Donor Specific Antibody
NCT01935128 (20) [back to overview]	Cytomegalovirus
NCT01935128 (20) [back to overview]	BK Nephropathy
NCT01935128 (20) [back to overview]	BK Infection
NCT01935128 (20) [back to overview]	Biopsy Proven Acute Rejection
NCT01935128 (20) [back to overview]	Cardiovascular Complications
NCT01935128 (20) [back to overview]	Lipid Levels
NCT01935128 (20) [back to overview]	Thrombocytopenia
NCT01935128 (20) [back to overview]	Renal Function
NCT01935128 (20) [back to overview]	Proteinuria
NCT01935128 (20) [back to overview]	Pneumonitis
NCT01935128 (20) [back to overview]	Patient Survival
NCT01935128 (20) [back to overview]	Neurotoxicity
NCT01935128 (20) [back to overview]	Mouth Ulcers
NCT01935128 (20) [back to overview]	Malignancies
NCT01936519 (6) [back to overview]	Recipient and Donor Genotyping for Selected Variants of CYP3A5, ABCB1 (MDR1), and CYP4A Genes
NCT01936519 (6) [back to overview]	Renal Function as Measured by 24 Hour Urine Creatinine Clearance
NCT01936519 (6) [back to overview]	Renal Function as Measured by Cockcroft Gault Creatinine Clearance
NCT01936519 (6) [back to overview]	Renal Function as Measured by Iothalamate Clearance
NCT01936519 (6) [back to overview]	Renal Function as Measured by Modification of Diet in Renal Disease (MDRD) Estimated Glomerular Filtration Rate (eGFR)
NCT01936519 (6) [back to overview]	Renal Function as Measured by Serum Creatinine Level
NCT01976390 (1) [back to overview]	Number of Participants With Composite Endpoint of Graft Survival (Non-death Censored) and Biopsy Proven Acute Rejection at 1 Year
NCT02017860 (1) [back to overview]	Number of Pariticipants With Adverse Events as a Measure of Safety and Tolerability
NCT02023905 (6) [back to overview]	Rate of Reduction in Seizures
NCT02023905 (6) [back to overview]	Progression-Free Survival Rate (PFS) (Arms 1 and 2)
NCT02023905 (6) [back to overview]	Progression-Free Survival Rate (PFS) (Arm 3)
NCT02023905 (6) [back to overview]	Overall Survival Rate (OS)
NCT02023905 (6) [back to overview]	Median Progression Free Survival (PFS)
NCT02023905 (6) [back to overview]	Objective Response Rate (ORR)
NCT02031536 (2) [back to overview]	Overall Survival (OS)
NCT02031536 (2) [back to overview]	Disease Free Survival (DFS)
NCT02061397 (2) [back to overview]	Safety of Simvastatin in the Treatment of LAM-S and LAM-TS Patients
NCT02061397 (2) [back to overview]	Percent Predicted FEV1
NCT02069093 (6) [back to overview]	Time to Resolution of Stomatitis From Grade 2 or Greater to Grade 1 or Less
NCT02069093 (6) [back to overview]	Blood Concentration of Everolimus and Exemestane
NCT02069093 (6) [back to overview]	Dose Intensity of Everolimus and Exemestane
NCT02069093 (6) [back to overview]	Number of Participants With All Grades of Stomatitis
NCT02069093 (6) [back to overview]	Number of Participants With Stomatitis Grade ≥ 2
NCT02069093 (6) [back to overview]	Median Number of Mouthwashes Per Day
NCT02073565 (4) [back to overview]	Percentage of Healthy Tissue Coverage That Was Greater Than 40 Micrometers
NCT02073565 (4) [back to overview]	Number of Patients Exhibiting Human Antimurine Antibody (HAMA) Reaction
NCT02073565 (4) [back to overview]	Number of Participants With Target Vessel Failure (TVF)
NCT02073565 (4) [back to overview]	Number of Patients With Clinically and Functionally Ischemia-Driven Target Lesion Revascularization (TLR)
NCT02096107 (6) [back to overview]	Adverse Drug Reactions
NCT02096107 (6) [back to overview]	Percentage of Participants Discontinuing or Modifying Immunosuppressant Use
NCT02096107 (6) [back to overview]	Kidney Allograft Survival
NCT02096107 (6) [back to overview]	Infection
NCT02096107 (6) [back to overview]	Renal Function Measured by Estimated Glomerular Filtration Rate (eGFR)
NCT02096107 (6) [back to overview]	Kidney Allograft Fibrosis Assessment
NCT02098876 (8) [back to overview]	In Stent: Mean Thickness of Strut Coverage at Follow up
NCT02098876 (8) [back to overview]	In Stent Mean Cross-sectional Area of Neo-intimal Tissue Coverage
NCT02098876 (8) [back to overview]	Stent Edge -Change in Plaque Area (Efficacy Endpoint) at 5 mm Proximal and Distal to Stent.
NCT02098876 (8) [back to overview]	In Stent: Plaque Prolapse Post-PCI (In-Stent Mechanistic Endpoint)
NCT02098876 (8) [back to overview]	Stent Edge: Percent Area With Low Wall Shear Stress (WSS) at Stent Edges Post-PCI (Mechanistic Endpoint)
NCT02098876 (8) [back to overview]	In-Stent: Degree of Vascular Straightening Post-percutaneous Coronary Intervention (PCI) (In-Stent Mechanistic Endpoint)
NCT02098876 (8) [back to overview]	In-Stent: Percent Area of Low Wall Shear Stress (WSS)-(In-Stent Mechanistic Endpoint)
NCT02098876 (8) [back to overview]	Stent Edge: Degree of Vascular Straightening Post-percutaneous Coronary Intervention (PCI) at the Stent Edges (Stent Edge Mechanistic Endpoint)
NCT02115113 (3) [back to overview]	Renal Function Assessed by Estimated Glomerular Filtartion Rate (eGFR)
NCT02115113 (3) [back to overview]	Percentage of Participants With Treated Biopsy Proven Acute Rejection (tBPAR) Acute Rejection (AR), Graft Loss (GL) or Death (D)
NCT02115113 (3) [back to overview]	Change From Baseline (Randomization) in Serum Creatinine at 12 Months Post-transplant
NCT02120469 (5) [back to overview]	Number of Subjects With Disease Progression Using the Response Evaluation Criteria in Solid Tumors (RECIST) Version 1.1 (Phase IB)
NCT02120469 (5) [back to overview]	Number of Participants With Grade 3 or Higher Toxicities (Phase IB)
NCT02120469 (5) [back to overview]	Number of Participants Experiencing a Dose Limiting Toxicity (DLT) (Phase I) and the Recommended Phase IB Dose (RP2D)
NCT02120469 (5) [back to overview]	Median Progression Free Survival (Phase IB)
NCT02120469 (5) [back to overview]	Median Overall Survival (Phase IB)
NCT02137239 (28) [back to overview]	Absolute Values of Blood Pressure: Mean
NCT02137239 (28) [back to overview]	Absolute Calculated Glomerular Filtration Rate (cGFR): Mean
NCT02137239 (28) [back to overview]	Time to Clinically-suspected Biopsy-proven Acute Rejection (CSBPAR).
NCT02137239 (28) [back to overview]	Percentage of Participants With Serious Adverse Events (SAEs)
NCT02137239 (28) [back to overview]	Percentage of Participants With Adverse Events (AEs)
NCT02137239 (28) [back to overview]	Percentage of Particpants With Laboratory Test Abnormalities (LTAs)
NCT02137239 (28) [back to overview]	Urine Protein Creatinine Ratio (UPr/Cr)
NCT02137239 (28) [back to overview]	Treatment Differences in Therapeutic Modalities
NCT02137239 (28) [back to overview]	Time to Event: Graft Loss and Death
NCT02137239 (28) [back to overview]	Percentage of Participants With New Onset Diabetes After Transplant
NCT02137239 (28) [back to overview]	Percentage of Participants With Events of Special Interest (ESIs)
NCT02137239 (28) [back to overview]	Percentage of Participants With Donor Specific Anti-HLA Antibodies (DSA)
NCT02137239 (28) [back to overview]	Percentage of Participants With De Novo Donor Specific Anti-HLA Antibodies (DSA)
NCT02137239 (28) [back to overview]	Percentage of Participants With BANFF Grade by Severity Grades. BANFF Type (Grade) for Acute/Active Rejection
NCT02137239 (28) [back to overview]	Percentage of Clinically-suspected Biopsy-proven Acute Rejection (CSBPAR) at 6 Months
NCT02137239 (28) [back to overview]	Number of Participants Who Survive With a Functioning Graft
NCT02137239 (28) [back to overview]	Number of Participants Who Experience Graft Loss Post Transplant
NCT02137239 (28) [back to overview]	Number of Participants Deaths Post Transplant
NCT02137239 (28) [back to overview]	Median Calculated Glomerular Filtration Rate (cGFR)
NCT02137239 (28) [back to overview]	Mean Changes From Baseline Values of Lipid Values
NCT02137239 (28) [back to overview]	Mean Changes From Baseline Values for Blood Pressure
NCT02137239 (28) [back to overview]	Mean Change From Month 3 in cGFR
NCT02137239 (28) [back to overview]	Mean and Mean Change From Baseline in Whole Blood HbA1c
NCT02137239 (28) [back to overview]	Mean and Mean Change From Baseline in Blood Glucose
NCT02137239 (28) [back to overview]	Clinically-suspected Biopsy-proven Acute Rejection (CSBPAR) at 6, 12 and 24 Months
NCT02137239 (28) [back to overview]	Absolute Values of Fasting Lipid Values: Median
NCT02137239 (28) [back to overview]	Absolute Values of Fasting Lipid Values: Mean
NCT02137239 (28) [back to overview]	Absolute Values of Blood Pressure: Median
NCT02137837 (8) [back to overview]	Progression-free Survival (Fulvestrant Versus Fulvestrant + Everolimus + Anastrozole)
NCT02137837 (8) [back to overview]	Progression Free Survival (Fulvestrant + Everolimus vs Fulvestrant + Everolimus + Anastrozole)
NCT02137837 (8) [back to overview]	Overall Survival
NCT02137837 (8) [back to overview]	Molecular Determinants of Response in Circulating Tumor Cells: CTC-ETI
NCT02137837 (8) [back to overview]	Clinical Benefit Rate
NCT02137837 (8) [back to overview]	Number of Patients With Gr 3 Through 5 Adverse Events That Are Related to Study Drugs
NCT02137837 (8) [back to overview]	Response Rate
NCT02137837 (8) [back to overview]	Progression-Free Survival (Fulvestrant vs Fulvestrant + Everolimus )
NCT02143726 (4) [back to overview]	Progression Free Survival
NCT02143726 (4) [back to overview]	Overall Survival
NCT02143726 (4) [back to overview]	Confirmed Response Rate
NCT02143726 (4) [back to overview]	Number of Participants With Grade 3 or Higher Adverse Events
NCT02188719 (5) [back to overview]	Percent of Participants With Grade 3 or Higher Infectious Adverse Event(s)
NCT02188719 (5) [back to overview]	Percent of Participants With Adverse Events (AEs) Attributable to the Donor Alloantigen Reactive Tregs (darTregs) Infusion
NCT02188719 (5) [back to overview]	Percent of Participants With Grade 2 or Higher Hematologic Adverse Events (AEs) of Anemia, Neutropenia, and/or Thrombocytopenia
NCT02188719 (5) [back to overview]	Percent of Participants With Biopsy-Proven Acute and/or Chronic Rejection
NCT02188719 (5) [back to overview]	Percent of Participants With Grade 3 or Higher Wound Complication(s) Adverse Event(s)
NCT02201212 (5) [back to overview]	Progression-free Survival
NCT02201212 (5) [back to overview]	Duration of Response
NCT02201212 (5) [back to overview]	Toxicity Rate
NCT02201212 (5) [back to overview]	Objective Response Rate
NCT02201212 (5) [back to overview]	Overall Survival
NCT02228681 (4) [back to overview]	Median Survival
NCT02228681 (4) [back to overview]	Frequency of Response
NCT02228681 (4) [back to overview]	Frequency and Severity of CTCAE (Common Toxicity Criteria for Adverse Events) Version 4
NCT02228681 (4) [back to overview]	Median Progression-free Survival
NCT02236572 (2) [back to overview]	PEPI Score
NCT02236572 (2) [back to overview]	Participant Ability to Tolerate Study Treatment With Minimal Side Effects
NCT02258451 (15) [back to overview]	Symptomatic Skeletal Event-free Survival (SSE-FS)
NCT02258451 (15) [back to overview]	Number of Participants With Hematological Toxicities: Worst Grade Under Treatment (From First Dosing Till Primary Analysis)
NCT02258451 (15) [back to overview]	Number of Participants With Hematological Toxicities: Worst Grade Under Treatment
NCT02258451 (15) [back to overview]	Number of Participants With Treatment-emergent Adverse Events (TEAEs) (From First Dosing Till Primary Analysis)
NCT02258451 (15) [back to overview]	Radiological Progression-free Survival (rPFS)
NCT02258451 (15) [back to overview]	Number of Participants With Post-treatment Chemotherapy Related Adverse Events (From First Dosing Till Primary Analysis)
NCT02258451 (15) [back to overview]	Number of Participants With Post-treatment Chemotherapy Related Adverse Events
NCT02258451 (15) [back to overview]	Number of Participants With New Primary Malignancies
NCT02258451 (15) [back to overview]	Number of Participants With New Primary Malignancies During Study Treatment Till Primary Analysis
NCT02258451 (15) [back to overview]	Time to Cytotoxic Chemotherapy
NCT02258451 (15) [back to overview]	Time to Opiate Use for Cancer Pain
NCT02258451 (15) [back to overview]	Overall Survival
NCT02258451 (15) [back to overview]	Percentage of Participants With Pain Improvement
NCT02258451 (15) [back to overview]	Number of Participants With Treatment-emergent Adverse Events (TEAEs)
NCT02258451 (15) [back to overview]	Time to Pain Progression
NCT02264665 (13) [back to overview]	Mean of Number of Tumor Assessment Visits - Based on Targeted Therapy Group and Other Treatments Group at Inclusion
NCT02264665 (13) [back to overview]	Number of Participants With Adverse Events Leading to Death - Based on Treatment Received At-least Once During the Study
NCT02264665 (13) [back to overview]	OS Rate at 2 Years- Based on Targeted Therapy Group and Other Treatments Group at Inclusion
NCT02264665 (13) [back to overview]	Number of Participants Who Had a Change in Their Treatment - Based on Targeted Therapy Group and Other Treatments Group at Inclusion
NCT02264665 (13) [back to overview]	Overall Survival (OS) Rate at 2 Years - Based on Type of Treatment at Inclusion
NCT02264665 (13) [back to overview]	PFS at 2 Years Assessed by Investigator Per RECIST v1.1 - Based on Targeted Therapy Group and Other Treatments Group at Inclusion
NCT02264665 (13) [back to overview]	Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs), Treatment Related AEs, SAEs and SAEs With Common Terminology Criteria For Adverse Events (CTCAE) 3, 4 and 5, v4.0-Based on Treatment Received At-least Once During Study
NCT02264665 (13) [back to overview]	Number of Participants With Adverse Events Leading to Discontinuation of Treatment - Based on Treatment Received At-least Once During the Study
NCT02264665 (13) [back to overview]	Number of Participants With Different Types of Investigation Used for Tumor Assessment - Based on Targeted Therapy Group and Other Treatments Group at Inclusion
NCT02264665 (13) [back to overview]	Number of Participants With Types of Main Lines of Treatment Received During the Follow-up - Based on Targeted Therapy Group and Other Treatments Group at Inclusion
NCT02264665 (13) [back to overview]	Number of Main Lines of Treatment Received During the Study - Based on Targeted Therapy Group and Other Treatments Group at Inclusion
NCT02264665 (13) [back to overview]	Number of Combined Main Lines of Treatments Received - Based on Targeted Therapy Group and Other Treatments Group at Inclusion
NCT02264665 (13) [back to overview]	Progression-Free Survival (PFS) at 2 Years Assessed by Investigator Per Response Evaluation Criteria in Solid Tumors (RECIST) Version (v) 1.1 - Based on Type of Treatment at Inclusion
NCT02283658 (6) [back to overview]	Progression Free Survival (PFS)
NCT02283658 (6) [back to overview]	Percentage of Participants With CA-125 Response
NCT02283658 (6) [back to overview]	Percentage of Patients Alive and Progression Free Survival at 12 Weeks
NCT02283658 (6) [back to overview]	Confirmed Response Rate, Estimated Using RECIST 1.1 Criteria
NCT02283658 (6) [back to overview]	Overall Suravival(OS)
NCT02283658 (6) [back to overview]	Number of Participants Experiencing Adverse Events
NCT02291913 (6) [back to overview]	Median Time From First Occurrence of CR or PR to Disease Progression or Death Also Called Duration of Response (DOR)
NCT02291913 (6) [back to overview]	Median Progression Free Survival (PFS)
NCT02291913 (6) [back to overview]	Number of Patients With Adverse Events (AEs) as a Measure of Safety and Tolerability
NCT02291913 (6) [back to overview]	Number of Patients With an Objective Response (CR or PR) Also Called the Overall Response Rate (ORR).
NCT02291913 (6) [back to overview]	Number of Participants With CR, PR, or 6 Months of SD Also Called Clinical Benefit Rate (CBR)
NCT02291913 (6) [back to overview]	Median Overall Survival (OS)
NCT02315625 (5) [back to overview]	Overall Survival
NCT02315625 (5) [back to overview]	Number of Participants With Serious and Non-Serious Adverse Events
NCT02315625 (5) [back to overview]	Number of Participants With an Overall Response
NCT02315625 (5) [back to overview]	Median Survival Time (MST)
NCT02315625 (5) [back to overview]	Median Amount of Time Subject Survives Without Disease Progression After Treatment
NCT02332902 (2) [back to overview]	3D Photographic Measurement of Surface Volume of Cutaneous Neurofibroma Lesion
NCT02332902 (2) [back to overview]	Number of Participants With Grade 3-4 Adverse Events
NCT02352844 (3) [back to overview]	Mutations Associated With Therapeutic Response
NCT02352844 (3) [back to overview]	Response Rate (RR)
NCT02352844 (3) [back to overview]	Genetic Changes Associated With Disease Progression
NCT02389946 (10) [back to overview]	Number of Lesions With Lesion Success
NCT02389946 (10) [back to overview]	Number of Participants With Procedure Success
NCT02389946 (10) [back to overview]	Number of Participants With TLF and Individual TLF Components
NCT02389946 (10) [back to overview]	Percentage of Participants With Target Lesion Failure (TLF) at 12 Months Post-Index Procedure by Bayesian Estimation
NCT02389946 (10) [back to overview]	Number of Participants With MACE and Individual MACE Components
NCT02389946 (10) [back to overview]	Number of Participants With Myocardial Infarction
NCT02389946 (10) [back to overview]	Number of Participants With Myocardial Infarction or Cardiac Death
NCT02389946 (10) [back to overview]	Number of Participants With Stent Thrombosis
NCT02389946 (10) [back to overview]	Number of Participants With Target Vessel Failure (TVF) and Individual TVF Components
NCT02389946 (10) [back to overview]	Number of Lesions With Device Success
NCT02429869 (3) [back to overview]	Plasma HIV RNA
NCT02429869 (3) [back to overview]	Cell-associated Total HIV RNA
NCT02429869 (3) [back to overview]	Cell-associated HIV DNA
NCT02451696 (5) [back to overview]	Blood Total VEGF Levels (Not Only VEGF-D)
NCT02451696 (5) [back to overview]	mTOR Brain Tissue-S6 Phosphate by Western Blot
NCT02451696 (5) [back to overview]	Number of Patients With Adverse Events
NCT02451696 (5) [back to overview]	HMGB1 Expression in Brain Tissue
NCT02451696 (5) [back to overview]	Blood Everolimus Levels
NCT02454478 (11) [back to overview]	Objective Response Rate (ORR)
NCT02454478 (11) [back to overview]	Tss,Max: Time to Reach the Maximum Plasma Concentration (Cmax) at Steady State for Levatinib and Everolimus
NCT02454478 (11) [back to overview]	Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)
NCT02454478 (11) [back to overview]	Number of Participants With the Minimum Percent Change From Baseline in the Sum of Diameters of Target Lesions
NCT02454478 (11) [back to overview]	Disease Control Rate (DCR)
NCT02454478 (11) [back to overview]	Number of Participants With Best Overall Response (BOR)
NCT02454478 (11) [back to overview]	Css,Max: Maximum Observed Plasma Concentration at Steady State for Levatinib and Everolimus
NCT02454478 (11) [back to overview]	Cmax: Maximum Observed Plasma Concentration for Levatinib and Everolimus
NCT02454478 (11) [back to overview]	Tmax: Time to Reach the Maximum Plasma Concentration (Cmax) for Levatinib and Everolimus
NCT02454478 (11) [back to overview]	Number of Participants Who Experienced Any Dose Limiting Toxicity (DLT)
NCT02454478 (11) [back to overview]	AUC 0-t: Area Under the Concentration-time Curve From Zero (Pre-dose) to Time of Last Quantifiable Concentration for Levatinib and Everolimus
NCT02504892 (4) [back to overview]	Count of Participants With Non-serious Adverse Events Assessed by the Common Terminology Criteria in Adverse Events (CTCAE v4.0)
NCT02504892 (4) [back to overview]	Progression-free Survival (PFS)
NCT02504892 (4) [back to overview]	Overall Response Rate With Everolimus Treatment.
NCT02504892 (4) [back to overview]	Overall Survival (OS)
NCT02513719 (97) [back to overview]	Number of Participants With All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With Myocardial Infarction
NCT02513719 (97) [back to overview]	Number of Participants With Myocardial Infarction
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or Target Vessel MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or Target Vessel MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or Target Vessel MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or Target Vessel MI
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Failure
NCT02513719 (97) [back to overview]	Number of Participants With Myocardial Infarction
NCT02513719 (97) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE)
NCT02513719 (97) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE)
NCT02513719 (97) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE)
NCT02513719 (97) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE)
NCT02513719 (97) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE)
NCT02513719 (97) [back to overview]	Number of Participants With Major Adverse Cardiac Events (MACE)
NCT02513719 (97) [back to overview]	Number of Participants With Hemorrhage
NCT02513719 (97) [back to overview]	Number of Participants With Hemorrhage
NCT02513719 (97) [back to overview]	Number of Participants With Hemorrhage
NCT02513719 (97) [back to overview]	Number of Participants With Hemorrhage
NCT02513719 (97) [back to overview]	Number of Participants With Hemorrhage
NCT02513719 (97) [back to overview]	Number of Participants With Hemorrhage
NCT02513719 (97) [back to overview]	Number of Participants With Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Death or MI
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or Target-Vessel MI
NCT02513719 (97) [back to overview]	Net Gain: In-stent, In-segment
NCT02513719 (97) [back to overview]	Late Loss(LL): In-stent,In-segment,Proximal, and Distal
NCT02513719 (97) [back to overview]	Acute Gain: In-stent,In-segment
NCT02513719 (97) [back to overview]	Success Rate: XIENCE PRIME Implant Success by Patient
NCT02513719 (97) [back to overview]	Success Rate: Percentage of Lesions With Procedural Success
NCT02513719 (97) [back to overview]	Success Rate: Percentage of Devices With Implant Success
NCT02513719 (97) [back to overview]	Percent Diameter Stenosis (%DS)
NCT02513719 (97) [back to overview]	Percent Diameter Stenosis (%DS)
NCT02513719 (97) [back to overview]	Percent Diameter Stenosis (%DS)
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Failure
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Failure
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Failure
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Failure
NCT02513719 (97) [back to overview]	Number of Participants With Target Vessel Failure
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Failure
NCT02513719 (97) [back to overview]	Number of Participants With Cardiac Death or Target Vessel-MI
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Failure
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Failure
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Failure
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Failure
NCT02513719 (97) [back to overview]	Number of Participants With Target Lesion Failure
NCT02513719 (97) [back to overview]	Number of Participants With Stent Thrombosis: Very Late
NCT02513719 (97) [back to overview]	Number of Death
NCT02513719 (97) [back to overview]	Number of Death
NCT02513719 (97) [back to overview]	Number of Death
NCT02513719 (97) [back to overview]	Number of Death
NCT02513719 (97) [back to overview]	Number of Death
NCT02513719 (97) [back to overview]	Number of Death
NCT02513719 (97) [back to overview]	Number of Participants With All Death/All MI/All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With All Death/All MI/All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With All Death/All MI/All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With All Death/All MI/All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With All Death/All MI/All Revascularization
NCT02513719 (97) [back to overview]	Number of Participants With Stent Thrombosis: Subacute
NCT02513719 (97) [back to overview]	Number of Participants With Stent Thrombosis: Late
NCT02513719 (97) [back to overview]	Number of Participants With Stent Thrombosis: Acute
NCT02513719 (97) [back to overview]	Number of Participants With Non-target Vessel Revascularization (Non-TVR)
NCT02513719 (97) [back to overview]	Number of Participants With Non-target Vessel Revascularization (Non-TVR)
NCT02513719 (97) [back to overview]	Number of Participants With Non-target Vessel Revascularization (Non-TVR)
NCT02513719 (97) [back to overview]	Number of Participants With Non-target Vessel Revascularization (Non-TVR)
NCT02513719 (97) [back to overview]	Number of Participants With Non-target Vessel Revascularization (Non-TVR)
NCT02513719 (97) [back to overview]	Number of Participants With Non-target Vessel Revascularization (Non-TVR)
NCT02513719 (97) [back to overview]	Number of Participants With Myocardial Infarction
NCT02513719 (97) [back to overview]	Number of Participants With Myocardial Infarction
NCT02513719 (97) [back to overview]	Number of Participants With Myocardial Infarction
NCT02513719 (97) [back to overview]	Number of Participants With All Death/All MI/All Revascularization
NCT02520063 (1) [back to overview]	Number of Participants Who Experienced Dose-limiting Toxicities
NCT02539459 (2) [back to overview]	Number of Patients With Tumor Volume Reduction Greater Than 25%
NCT02539459 (2) [back to overview]	Safety and Tolerability of Everolimus in Patients With Sporadic AML
NCT02560012 (1) [back to overview]	Number of Participants Who Progressed
NCT02599324 (19) [back to overview]	Phase 1b: Terminal Elimination Rate Constant (λz) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4
NCT02599324 (19) [back to overview]	Phase 1b: Area Under the Concentration-Time Curve to Last Observed Time Point (AUClast) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4
NCT02599324 (19) [back to overview]	Phase 1b: Apparent Total Clearance at Steady-State (CLss/F) for Ibrutinib in Cohorts 1 to 4
NCT02599324 (19) [back to overview]	Phase 1b: Terminal Elimination Rate Constant (λz) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4
NCT02599324 (19) [back to overview]	Phase 1b: Terminal Elimination Half-Life (t1/2term) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4
NCT02599324 (19) [back to overview]	Phase 1b: Observed Maximum Concentration (Cmax) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4
NCT02599324 (19) [back to overview]	Phase 1b: Disease Control Rate (DCR) in Cohorts 1 to 6
NCT02599324 (19) [back to overview]	Phase 1b: Number of Participants With Dose-Limiting Toxicities (DLTs) in Cohorts 1 to 6
NCT02599324 (19) [back to overview]	Phase 1b: ORR in Cohorts 1 to 6
NCT02599324 (19) [back to overview]	Phase 1b/2 RP2D: DCR in Cohorts 1 to 6
NCT02599324 (19) [back to overview]	Phase 1b/2 RP2D: Duration of Response (DOR) in Cohorts 1 to 6
NCT02599324 (19) [back to overview]	Phase 1b/2 RP2D: ORR in Cohorts 1 and 2
NCT02599324 (19) [back to overview]	Phase 1b/2 RP2D: Overall Response Rate (ORR) as Assessed by Investigator in Cohorts 3 to 6
NCT02599324 (19) [back to overview]	Phase 1b/2 RP2D: Overall Survival (OS) in Cohorts 1 to 6
NCT02599324 (19) [back to overview]	Phase 1b/2 RP2D: PFS in Cohorts 3 to 6
NCT02599324 (19) [back to overview]	Phase 1b/2 RP2D: Progression-Free Survival (PFS) as Assessed by Investigator in Cohorts 1 and 2
NCT02599324 (19) [back to overview]	Phase 1b: Area Under the Concentration-Time Curve From Time 0 to Hour 24 (AUC0-24h) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4
NCT02599324 (19) [back to overview]	Phase 1b: Time of Last Observed Concentration (Tlast) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4
NCT02599324 (19) [back to overview]	Phase 1b: Time to Cmax (Tmax) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4
NCT02724020 (7) [back to overview]	Number of Participants With Treatment-Emergent Adverse Events (TEAEs)
NCT02724020 (7) [back to overview]	Objective Response Rate (ORR)
NCT02724020 (7) [back to overview]	Overall Survival (OS)
NCT02724020 (7) [back to overview]	Progression-Free Survival (PFS)
NCT02724020 (7) [back to overview]	Time-to-progression (TTP)
NCT02724020 (7) [back to overview]	Clinical Benefit Rate (CBR)
NCT02724020 (7) [back to overview]	CBR With SD Duration of at Least 16 Weeks
NCT02732119 (12) [back to overview]	Duration of Overall Response (DOR) by Group - Phase II
NCT02732119 (12) [back to overview]	Participants With Dose Limiting Toxicities by Preferred Term in Cycle 1 (28 Days) - in Phase I
NCT02732119 (12) [back to overview]	Everolimus Pharmacokinetic Plasma Concentrations by Cohort - Phase I
NCT02732119 (12) [back to overview]	Everolimus Pharmacokinetic Plasma Concentrations - Phase II
NCT02732119 (12) [back to overview]	Clinical Benefit Rate as Per Central Review by Group- Phase II
NCT02732119 (12) [back to overview]	Clinical Benefit Rate as Per Central Review by Dose Cohort - Phase I
NCT02732119 (12) [back to overview]	Clinical Benefit Rate as Per Central Review by Dose Cohort - Phase I
NCT02732119 (12) [back to overview]	Best Overall Responses (BOR) Summary Table as Per Central Review by Group - Phase II
NCT02732119 (12) [back to overview]	Time to Definitive Deterioration of ECOG Performance Status in One Category of the Score by Group - Phase II
NCT02732119 (12) [back to overview]	Summary of Progression-free Survival (PFS) (Months), as Per Central Review by Group - Phase II
NCT02732119 (12) [back to overview]	Overall Survival (OS) by Group - Phase II
NCT02732119 (12) [back to overview]	Best Overall Responses (BOR) Summary Table as Per Central Review by Cohort - Phase I
NCT02736227 (1) [back to overview]	Amount of Treg Cells Observed in Peripheral Blood in Patients With and Without Rejection
NCT02811861 (1) [back to overview]	Progression-free Survival (PFS) by Independent Imaging Review (IIR)
NCT02864706 (8) [back to overview]	Measured Glomerular Filtration Rate (mGFR)
NCT02864706 (8) [back to overview]	Progression of Cardiac Allograft Vasculopathy (CAV) Recorded by Intravascular Ultrasound (IVUS)
NCT02864706 (8) [back to overview]	Change From Baseline in Visual Analog Scale (VAS)
NCT02864706 (8) [back to overview]	Change From Baseline in the Euro Quality of Life 5D
NCT02864706 (8) [back to overview]	Number of Participants With Beck Depression Inventory (BDI)
NCT02864706 (8) [back to overview]	Quality of Life by SF-36 Change From Pre-transplantation to 5-7 Year Follow-up
NCT02864706 (8) [back to overview]	Percent of Participants With Incidence of Coronary Allograft Vasculopathy (CAV)
NCT02864706 (8) [back to overview]	Myocardial Structure and Function
NCT02871791 (5) [back to overview]	Duration of Response (DOR) [Phase 2a]
NCT02871791 (5) [back to overview]	Median Progression Free Survival (PFS) [Phase 2a]
NCT02871791 (5) [back to overview]	Overall Response Rate (ORR) [Phase 2a]
NCT02871791 (5) [back to overview]	Clinical Benefit Rate (CBR) [Phase 2a]
NCT02871791 (5) [back to overview]	Disease Control Rate (DCR) [Phase 2a]
NCT02915783 (3) [back to overview]	Overall Survival (OS)
NCT02915783 (3) [back to overview]	Objective Response Rate (ORR)
NCT02915783 (3) [back to overview]	Progression-free Survival (PFS)
NCT02954198 (4) [back to overview]	Percent of Participants Experiencing Acute Allograft Rejection
NCT02954198 (4) [back to overview]	Subject Specific Change on Medication Side Effect Scale
NCT02954198 (4) [back to overview]	Self-reported Medication Adherence From Baseline to 6 Months.
NCT02954198 (4) [back to overview]	Percent of Participants Who Experienced Kidney Transplant Graft Loss
NCT03112603 (24) [back to overview]	Percentage of Participants With a ≥ 50% Reduction in Daily Corticosteroid Dose
NCT03112603 (24) [back to overview]	t1/2 of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]	Tmax of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]	Vz/F of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]	Rate of Failure-free Survival (FFS)
NCT03112603 (24) [back to overview]	CL/F of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]	Cmax of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]	Change From Baseline in Functional Assessment of Cancer Therapy - Bone Marrow Transplantation (FACT-BMT)
NCT03112603 (24) [back to overview]	Change From Baseline in EQ-5D-5L
NCT03112603 (24) [back to overview]	AUClast of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]	Best Overall Response (BOR) at Cycle 7 Day 1
NCT03112603 (24) [back to overview]	BOR During Cross-over Treatment With Ruxolitinib
NCT03112603 (24) [back to overview]	Duration of Response Through Study Completion
NCT03112603 (24) [back to overview]	Efficacy of Ruxolitinib Versus Investigator's Choice Best Available Therapy (BAT) in Participants With Moderate or Severe Steroid Refractory Chronic Graft Versus Host Disease (SR-cGvHD) Assessed by Overall Response Rate (ORR) at the Cycle 7 Day 1 Visit
NCT03112603 (24) [back to overview]	Number of Participants With Any Treatment-emergent Adverse Event (TEAE)
NCT03112603 (24) [back to overview]	AUCinf of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]	Utilization of Medical Resources
NCT03112603 (24) [back to overview]	Rate of Participants With Clinically Relevant Improvement of the Modified Lee cGvHD Symptom Scale Score
NCT03112603 (24) [back to overview]	ORR at the End of Cycle 3
NCT03112603 (24) [back to overview]	Rate of FFS at Study Completion
NCT03112603 (24) [back to overview]	Overall Survival (OS)
NCT03112603 (24) [back to overview]	Cumulative Incidence of Malignancy Relapse/Recurrence (MR)
NCT03112603 (24) [back to overview]	Cumulative Incidence of Non-relapse Mortality (NRM)
NCT03112603 (24) [back to overview]	Percentage of Participants Successfully Tapered Off of All Corticosteroids
NCT03163667 (2) [back to overview]	Overall Survival (OS)
NCT03163667 (2) [back to overview]	Progression Free Survival (PFS)
NCT03173560 (15) [back to overview]	Health-Related Quality of Life (HRQoL) Assessed by Functional Assessment of Cancer Therapy Kidney Syndrome Index-Disease-Related Symptoms (FKSI-DRS) Scores
NCT03173560 (15) [back to overview]	Health-Related Quality of Life (HRQoL) Assessed by Functional Assessment of Cancer Therapy Kidney Syndrome Index-Disease-Related Symptoms (FKSI-DRS) Scores
NCT03173560 (15) [back to overview]	HRQoL Assessed by European Organization for the Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-C30 Scores
NCT03173560 (15) [back to overview]	HRQoL Assessed by European Quality of Life (EuroQol) Five-Dimensional, 3-Level (EQ-5D-3L) Index Score and Visual Analogue Scale (VAS)
NCT03173560 (15) [back to overview]	Overall Survival (OS)
NCT03173560 (15) [back to overview]	Number of Participants With TEAEs and Serious TEAEs
NCT03173560 (15) [back to overview]	HRQoL Assessed by European Organization for the Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-C30 Scores
NCT03173560 (15) [back to overview]	Objective Response Rate (ORR)
NCT03173560 (15) [back to overview]	HRQoL Assessed by European Quality of Life (EuroQol) Five-Dimensional, 3-Level (EQ-5D-3L) Index Score and Visual Analogue Scale (VAS)
NCT03173560 (15) [back to overview]	Objective Response Rate at Week 24 (ORR24W)
NCT03173560 (15) [back to overview]	Percentage of Participants With Intolerable Grade 2 or Any Grade >=Grade 3 TEAEs Within 24 Weeks
NCT03173560 (15) [back to overview]	Percentage of Participants Who Discontinued Treatment Due to Toxicity
NCT03173560 (15) [back to overview]	Progression-free Survival (PFS)
NCT03173560 (15) [back to overview]	Progression-free Survival After Next Line of Therapy (PFS2)
NCT03173560 (15) [back to overview]	Time to Treatment Failure Due to Toxicity
NCT03176238 (5) [back to overview]	Percentage of Participants Response Rates (Best Overall and Overall)
NCT03176238 (5) [back to overview]	Summary of Number of Participants With Treatment Emergent Adverse Events (TEAE) - All Grades
NCT03176238 (5) [back to overview]	Percent of Participants Event-free Probability Estimates of Deterioration of Eastern Cooperative Oncology Group (ECOG) Performance Status
NCT03176238 (5) [back to overview]	Percentage of Participants Clinical Benefit Rate
NCT03176238 (5) [back to overview]	Progression Free Survival (PFS)
NCT03245151 (18) [back to overview]	Phase 2: Objective Response Rate (ORR)
NCT03245151 (18) [back to overview]	Phase 2: Number of Participants With Any Treatment-emergent Serious Adverse Event (TESAE)
NCT03245151 (18) [back to overview]	Phase 2: Number of Participants With Any Treatment-emergent Adverse Event (TEAE)
NCT03245151 (18) [back to overview]	Phase 1: Disease Control Rate (DCR)
NCT03245151 (18) [back to overview]	Phase 2: Duration of Response (DOR)
NCT03245151 (18) [back to overview]	Phase 2: Disease Control Rate (DCR)
NCT03245151 (18) [back to overview]	Phase 2: Clinical Benefit Rate (CBR)
NCT03245151 (18) [back to overview]	Phase 1: Recommended Phase 2 Dose (RP2D) of Lenvatinib in Combination With Everolimus
NCT03245151 (18) [back to overview]	Phase 1: Objective Response Rate (ORR)
NCT03245151 (18) [back to overview]	Phase 1: Number of Participants With Any Treatment-emergent Serious Adverse Event (TESAE)
NCT03245151 (18) [back to overview]	Phase 1: Number of Participants With Any Treatment-emergent Adverse Event (TEAE)
NCT03245151 (18) [back to overview]	Phase 1: Maximum Tolerated Dose (MTD) of Lenvatinib in Combination With Everolimus
NCT03245151 (18) [back to overview]	Phase 1: Clinical Benefit Rate (CBR)
NCT03245151 (18) [back to overview]	Phase 1: Trough Concentrations (Ctrough) of Everolimus When Administered in Combination With Lenvatinib
NCT03245151 (18) [back to overview]	Phase 1: Time to Reach Maximum Plasma Concentration (Cmax) of Lenvatinib (Tmax)
NCT03245151 (18) [back to overview]	Phase 1: Maximum Plasma Concentration of Lenvatinib (Cmax)
NCT03245151 (18) [back to overview]	Phase 1: Area Under the Plasma Concentration-time Curve From Time Zero to Time of Last Quantifiable Concentration of Lenvatinib (AUC[0-t Hours])
NCT03245151 (18) [back to overview]	Phase 2: Objective Response Rate (ORR) at Week 16
NCT03352427 (5) [back to overview]	Progression-free Survival in Participants With Newly Diagnosed High-grade Glioma (HGG)
NCT03352427 (5) [back to overview]	Progression-free Survival in Participants With Newly Diagnosed Diffuse Intrinsic Pontine Glioma (DIPG)
NCT03352427 (5) [back to overview]	Overall Survival
NCT03352427 (5) [back to overview]	Overall Response Rate (OR) (Partial Response or Better) in Participants With Refractory or Recurrent Glioma
NCT03352427 (5) [back to overview]	Overall Survival
NCT03387020 (8) [back to overview]	Ribociclib Half-Life as Obtained From the Phase 1 Study
NCT03387020 (8) [back to overview]	Maximum Tolerated Dose of Ribociclib and Everolimus
NCT03387020 (8) [back to overview]	Average Tumor and Plasma Concentrations of Ribociclib for the Surgical Study
NCT03387020 (8) [back to overview]	Everolimus Half Life as Obtained From the Phase 1 Study
NCT03387020 (8) [back to overview]	Objective Responses (Complete Response + Partial Response)
NCT03387020 (8) [back to overview]	Percent Change in ki67 Between Archival and Post-treatment Tissue
NCT03387020 (8) [back to overview]	Everolimus AUC (Area Under the Plasma Concentration Versus Time Curve) as Obtained From the Phase I Study
NCT03387020 (8) [back to overview]	Ribociclib AUC (Area Under the Plasma Concentration Versus Time Curve) as Obtained From the Patients Who Received Phase I Defined Treatment
NCT03468478 (1) [back to overview]	Incidence of Cytomegalovirus Infection or Disease
NCT03525834 (5) [back to overview]	Percentage of Participants With Best Overall Response (BOR) Status of Angiomyolipoma (AML) Response During Maximum Treatment Duration of 48 Weeks
NCT03525834 (5) [back to overview]	Percentage of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT03525834 (5) [back to overview]	Percentage of Participants With Best Overall Response Status of Angiomyolipoma (AML) Progression During Maximum Treatment Duration of 48 Weeks
NCT03525834 (5) [back to overview]	Percentage of Participants With Severe Renal Impairment
NCT03525834 (5) [back to overview]	Percentage of Participants With NCI CTCA Grade 3/4 Serum Creatinine
NCT03659136 (6) [back to overview]	Duration of Disease Control (DC)
NCT03659136 (6) [back to overview]	Overall Survival (OS)
NCT03659136 (6) [back to overview]	Progression Free Survival (PFS)
NCT03659136 (6) [back to overview]	Time to Pain Progression or Intensification of Pain Palliation
NCT03659136 (6) [back to overview]	Number of Participants With Objective Response (OR)
NCT03659136 (6) [back to overview]	Number of Patients With Disease Control (DC)
NCT03839940 (7) [back to overview]	Severity of Mouth Pain Scores by Ethnicity
NCT03839940 (7) [back to overview]	Severity of Mouth Pain Scores by Sex
NCT03839940 (7) [back to overview]	Incidence Rate of the mTOR Inhibitor-associated Stomatitis (mIAS)-Related Pain Based on Daily Self-reports Via the Numerical Analogue Scale by Ethnicity.
NCT03839940 (7) [back to overview]	Incidence Rate of the mTOR Inhibitor-associated Stomatitis (mIAS)-Related Pain Based on Daily Self-reports Via the Numerical Analogue Scale by Race
NCT03839940 (7) [back to overview]	Incidence Rate of the mTOR Inhibitor-associated Stomatitis (mIAS)-Related Pain Based on Daily Self-reports Via the Numerical Analogue Scale by Sex
NCT03839940 (7) [back to overview]	Severity of Mouth Pain Scores
NCT03839940 (7) [back to overview]	Severity of Mouth Pain Scores by Race
NCT04177095 (6) [back to overview]	Incidence of Acute Rejection
NCT04177095 (6) [back to overview]	Incidence of de Novo Donor Specific Antibodies
NCT04177095 (6) [back to overview]	Rate of New-onset Proteinuria
NCT04177095 (6) [back to overview]	Survival
NCT04177095 (6) [back to overview]	Incidence of Acute Rejection
NCT04177095 (6) [back to overview]	Increase in eGFR

Overall Objective Response

Response will be evaluated in this study using the new international criteria Response Evaluation Criteria in Solid Tumors (RECIST) (NCT00085566)
Timeframe: 2 years

Intervention	participants (Number)
	Partial Response (PR)	Stable Disease (SD)	Progression of Disease (POD)
RAD 001 30 mg	0	0	3
RAD 001 50 mg	0	1	2
RAD 001 70 mg	2	15	26

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Clinical Benefit Rate

Clinical benefit rate (CBR) is defined as the objective response rate plus the proportion of participants with prolonged stable disease (SD), e.g. nonprogression at 20 weeks. Objective response rate (ORR), determined by tumor assessments from radiological tests or physical examination using Response Evaluation Criteria In Solid Tumors (RECIST). (NCT00087685)
Timeframe: 20 weeks

Intervention	percentage of participants (Number)
RAD001	21

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Number of Participants With Objective Response Plus Stable Disease Rate (CR + PR + SD)

Response determined by tumor assessments from radiological tests or physical examination using Response Evaluation Criteria In Solid Tumors (RECIST). Complete Response (CR): Disappearance of all target and non-target lesions and no evidence of new lesions documented by two disease assessments at least 4 weeks apart. Partial Response (PR): At least 30% decrease in sum of the longest dimensions (LD) of all target measurable lesions taking as reference the baseline sum of LD. Stable Disease (SD): Any condition not meeting the above criteria. The minimum duration for the SD will be 8 weeks. If the participant has stable disease at the time of the first radiographic evaluation, he/she will be considered to have stable disease. Progressive Disease (PD): At least a 20% increase in the sum of LD of target lesions taking as reference the smallest sum LD or the appearance of new lesions within 8 weeks of study entry. (NCT00087685)
Timeframe: 8 weeks

Intervention	participants (Number)
	Complete Response (CR)	Partial Response (PD)	Stable Disease (SD)	Progressive Disease (PD)
RAD001	0	0	14	17

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Overall Objective Response

Determine efficacy of the combination oral daily gefitinib and oral daily RAD001 in patients with advanced NSCLC. Response and progression will be evaluated in this study using the international criteria proposed by the Response Evaluation Criteria in Solid Tumors (RECIST). (NCT00096486)
Timeframe: 2 years

,,,

Intervention	participants (Number)
	Partial Response (PR)	Stable Disease (SD)	Progression of Disease (POD)	Not Evaluable/ Evaluable for Toxicity Only
Phase I: RAD001 10 mg, Gefitinib 250 mg	1	1	1	1
Phase I: RAD001 5 mg, Gefitinib 250 mg	1	1	4	0
Phase II: Cohort I no Prior Conventional Chemotherapy	3	9	11	1
Phase II: Cohort II One or More Prior Chemotherapy	2	15	18	1

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Progression Free Survival (PFS)

PFS is measured from date of trial entry until documented progression of disease or death from any cause. PFS is measured by computed tomography (CT) scans or magnetic resonance imaging (MRI) performed at baseline and after every three cycles. (NCT00113360)
Timeframe: PFS assessed every 12 weeks (at the end of every 3 cycles) or more frequently if clinically indicated

Intervention	Weeks (Median)
RAD001 Plus Octreotide Depot	60

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Calculated Creatinine Clearance at 6 Month and 12 Month

"Creatinine clearance calculated by Cockcroft-Gault formula and summarized by mean, and standard deviation. Cockcroft-Gault formula to calculate Creatinine Clearance (CrCl[mL/min]) is shown below:~CrCl[mL/min] = (140 - A) * W / (72 * C) * R. Where A is age at sample date [years], W is body weight at specific visit [kg], C is the serum concentration of creatinine [mg/dL], R = 1 if the patient is male and = 0.85 if female." (NCT00154284)
Timeframe: 6 month and 12 months

Intervention	mL/min (Mean)
	6 Month	12 Month
Everolimus (Certican) With Cyclosporine (Neoral) Continuation	63.6	65.6
Everolimus (Certican) With Cyclosporine (Neoral) Withdrawal	72.9	72.3

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Number of Participants With Biopsy-proven Acute Rejection (BPAR) Episodes, Graft Loss, Death or Loss to Follow-up

Renal biopsies were collected for all cases of suspected acute rejection. For these cases, regardless of initiation of anti-rejection treatment, a graft core biopsy had been performed within 48 hours. These biopsies were listed on the Kidney Allograft Biopsy eCRF and the results used for patient management for BPAR. Graft loss was defined as the allograft was presumed to be lost on the day the patient started dialysis and was not able to subsequently be removed from dialysis as well as re-transplant. BPAR, graft loss, death, or loss to follow-up was analyzed by means of frequency tables. (NCT00154284)
Timeframe: Month 12

Intervention	Participants (Number)
	Biopsy-proven Acute Rejection (BPAR)	Graft Loss	Death	Loss to Follow-up
Everolimus (Certican) With Cyclosporine (Neoral) Continuation	10	0	0	0
Everolimus (Certican) With Cyclosporine (Neoral) Withdrawal	10	0	0	0

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Renal Function Measured by Calculated Glomerular Filtration Rate (GFR Calculated According to the Nankivell Formula)

"Nankivell's formula for calculated GFR is shown below:~GFR [mL/min] = 6.7/C + W/4 - UREA/2 - 100/H2+ 35 (25 for females). Where W is body weight at specific visit [kg], H is height at specific visit [m], C is the serum concentration of creatinine [mmol/L], and UREA is the serum concentration of urea [mmol/L]. UREA was calculated from blood urea nitrogen (BUN) lab data by: UREA = 2.1441*BUN. If a GFR value from Nankivell formula was less than 10 [mL/min], then the value was assigned as 10 [mL/min]." (NCT00154284)
Timeframe: At Month 3 and Month 12

Intervention	mL/min per 1.73 m^2 (Mean)
	GFR at 3 months (Pre-randomization)	GFR at 12 months
Everolimus (Certican) With Cyclosporine (Neoral) Continuation	68.5	63.6
Everolimus (Certican) With Cyclosporine (Neoral) Withdrawal	69.2	68.3

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Serum Creatinine at Month 6 and 12

serum creatinine summarized by mean and standard deviation (NCT00154284)
Timeframe: 6 month and 12 months

Intervention	µmol/L (Mean)
	6 Month	12 Month
Everolimus (Certican) With Cyclosporine (Neoral) Continuation	139.1	135.6
Everolimus (Certican) With Cyclosporine (Neoral) Withdrawal	120.1	123.0

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Number of Participants With Any Wound Healing Disorder During the 12-month Treatment Period

A wound was considered healed if all the suture material and staples were removed and the wound was intact by 3 weeks. Any wound opened beyond this point, infected, drained fluid or herniated was considered not healed. (NCT00154297)
Timeframe: Month 12

Intervention	Participants (Number)
	Any wound healing disorder -Total	Wound healing disorder related to transplant	Wound healing disorder unrelated to transplant
Delayed Everolimus	32	28	6
Immediate Everolimus	28	26	2

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Number of Participants Considered in Failure for the Primary Failure Endpoint at 6 Months Post-transplantation.

"The primary efficacy variable was the primary failure endpoint at 6 months defined as the occurrence of one or more of the following events within the first 6 months:~delayed graft function (DGF), defined as the need for dialysis within the first 7 days post-transplantation excluding the first day post-transplantation~efficacy failure (biopsy proven acute rejection (BPAR), graft loss, death or loss to follow-up)~wound healing disorder related to initial transplant surgery" (NCT00154297)
Timeframe: at 6 Month post-transplantation

Intervention	Participants (Number)
	Failure at month 6 - Total	Dialysis within first 7 days	Efficacy failure (Total)	--BPAR	--Graft Loss	--Death	--Lost to follow-up (composite efficacy endpoint)	Wound healing disorder	Loss to follow-up for the primary failure endpoint
Delayed Everolimus	48	18	22	13	4	2	4	28	3
Immediate Everolimus	39	16	17	10	5	4	0	25	0

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Number of Participants Considered in Failure for the Primary Failure Endpoint at 3 Months

"In Failure, is at least one of these events occurred within the first 3 months: delayed graft function(DGF), (need for dialysis within the first 7 days,minus day one,post-transplantation); Biopsy proven acute rejection (BPAR), Graft loss, (allograft was presumed lost on the day the patient started and not removable from dialysis). Death; Loss to follow-up; Wound healing disorder(Any wound related to the kidney transplantation being opened beyond 3 weeks, or infected, or drained fluid or herniated was considered not healed)." (NCT00154297)
Timeframe: Month 3

Intervention	Participants (Number)
	Failure at month 3 - Total	Dialysis within first 7 days	Efficacy failure (Total)	--BPAR	--Graft Loss	--Death	--Lost to follow-up (composite efficacy endpoint)	Wound healing disorder	Loss to follow-up for the primary failure endpoint
Delayed Everolimus	47	18	15	7	3	2	4	28	3
Immediate Everolimus	36	16	14	7	5	4	0	24	0

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Number of Participants Considered in Failure for the Primary Failure Endpoint at 12 Months Post-transplantation.

"The primary efficacy variable was the primary failure endpoint at 12 months defined as the occurrence of one or more of the following events within the first 12 months:~delayed graft function (DGF), defined as the need for dialysis within the first 7 days post-transplantation excluding the first day post-transplantation~efficacy failure (biopsy proven acute rejection (BPAR), graft loss, death or loss to follow-up)~wound healing disorder related to initial transplant surgery" (NCT00154297)
Timeframe: at 12 Month post-transplantation

Intervention	Participants (Number)
	Failure at month 12 - Total	Dialysis within first 7 days	Efficacy failure (Total)	--BPAR	--Graft Loss	--Death	--Lost to follow-up (composite efficacy endpoint)	Wound healing disorder	Loss to follow-up for the primary failure endpoint
Delayed Everolimus	49	18	25	15	5	2	5	28	3
Immediate Everolimus	42	16	22	13	6	5	0	26	0

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Number of Participants Who Underwent Any Dialysis Within the 12-month Treatment Period

The number of patients who underwent any dialysis within the 12-month treatment period. (NCT00154297)
Timeframe: Month 12

Intervention	Participants (Number)
Immediate Everolimus	16
Delayed Everolimus	24

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Duration of Dialysis

The mean duration in days of any dialysis session that occurred within the 12 month treatment period. (NCT00154297)
Timeframe: 12 months

Intervention	Days (Mean)
Immediate Everolimus	11.9
Delayed Everolimus	7.8

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Number of Participants With Occurrence of Treatment Failures

Treatment failures defined as a composite endpoint of biopsy proven acute rejection, graft loss, death, loss to follow up and discontinuations due to lack of efficacy or toxicity, or conversion to another regimen (at least one condition must be present). (NCT00154310)
Timeframe: up to or at Month 12

Intervention	Participants (Number)
	Treatment failure: Yes	Treatment failure: No
Cyclosporine + Mycophenolate Sodium	23	123
Everolimus + Mycophenolate Sodium	29	125

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Number of Participants With Occurrence of Biopsy Proven Acute Rejection (BPAR), Graft Loss or Death

The number of participants with occurrence of biopsy proven acute rejection (BPAR), graft loss, or death up to Month 12 during the randomized treatment period. BPAR was defined as a biopsy graded IA, IB, IIA, IIB or III according to Banff 97 classification. A graft core biopsy was performed prior to 24 hours following initiation of graft rejection therapy. The allograft is presumed to be lost on the day the patient starts dialysis and was not able to subsequently be removed from dialysis. If the patient underwent a graft nephrectomy, then the day of nephrectomy was the day of graft loss. (NCT00154310)
Timeframe: Up to Month 12

Intervention	Participants (Number)
	BPAR: Yes	BPAR: No	Graft Loss: Yes	Graft Loss: No	Death: Yes	Death: No
Cyclosporine + Mycophenolate Sodium	5	141	0	146	1	145
Everolimus + Mycophenolate Sodium	15	139	0	154	0	154

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Number of Participants Who Experienced an Adverse Event or Serious Adverse Event

Additional information about the number of participants who experienced Adverse Events (greater than 5%) or Serious Adverse Events can be found in the Adverse Event section. (NCT00154310)
Timeframe: Aes from end of core study period (month 12) to end of follow-up period (month 60)

Intervention	Participants (Number)
	Adverse Events	Serious Adverse Events
Cyclosporine + Mycophenolate Sodium	145	86
Everolimus + Mycophenolate Sodium	155	95

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Changes in Cardiovascular Risk From Month 4.5 to Final Assessment at Month 12

An updated 1991 Framingham coronary prediction algorithm was used to estimate the total risk of developing coronary heart diseases (CHD) over the course of 10 years. Risk was calculated separately for male and females. To calculate risk, points were assigned for each of the following risk factors: age, levels of LDL cholesterol, HDL cholesterol, blood pressure, cigarette smoking, and diabetes mellitus. The sum of the individual risk factor points gives a total point score, which ranges from -5 to 18 for men and -16 to 24 for women. Higher points indicate a higher risk for CHD. (NCT00154310)
Timeframe: Month 4.5 and Month 12

Intervention	Points (Mean)
	Male (n= 55, 37)	Female (n= 22, 35)	Total Population (n= 77, 72)
Cyclosporine + Mycophenolate Sodium	0.1	0.8	0.4
Everolimus + Mycophenolate Sodium	0.5	0.0	0.4

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Renal Function (Nankivell Formula) at Month 12 Post Transplantation.

Renal function at the end of the trial assessed as mean absolute values of the glomerular filtration rate (GFR) calculated by Nankivell formula 12 months after renal transplantation. The Nankivell formula: GFR = 6.7 / Scr + BW / 4 - Surea / 2-100 / (height)^2 + C ; where Scr is the serum creatinine concentration expressed in mmol/L, BW the body weight in kg, Surea the serum urea in mmol/L, height in m, and the constant C is 35 for male and 25 for female patients. Estimated GFR is expressed in mL/min per 1.73m^2. (NCT00154310)
Timeframe: at Month 12 post transplantation

Intervention	mL/min /1.73m^2 (Mean)
Everolimus + Mycophenolate Sodium	71.84
Cyclosporine + Mycophenolate Sodium	61.24

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Number of Participants With Safety Parameters

The selected safety parameters (such as hypertension, hyperlipidemia, diabetes mellitus, anemia, malignancies ) were derived based on adverse events preferred terms defined in the analysis plan. (NCT00170846)
Timeframe: 24 months

Intervention	Participants (Number)
	Hypertension, Yes	Hypertension, No	Hyperlipidemia, Yes	Hyperlipidemia, No	Diabetes mellitus, Yes	Diabetes mellitus, No	Anemia, Yes	Anemia, No	Malignancies, Yes	Malignancies, No
Group A: No RAD	6	117	6	117	4	119	25	98	7	116
Group B : CNI Withdrawal	13	114	18	109	6	121	45	82	9	118
Group C: CNI Reduction	9	135	11	133	7	137	46	98	11	133

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Change in mGFR by Baseline Calculated Creatinine Clearance (Cockcroft-Gault Formula)

"Cockcroft-Gault formula (CrCl):~Creatinine Clearance [mL/min] = CrCl (males) = (140 - A) * W / (72 * C) (males), CrCl (females) = CrCl (males) * 0.85,~Where:~A is age [years]~W is body weight [kg]~C is the serum concentration of creatinine [mg/dL]" (NCT00170846)
Timeframe: Baseline and 24 months

Intervention	mL/min (Mean)
	Baseline CrCl(CG) ≤ 50 :(n= 32, 28, 32):- Change	Baseline CrCl(CG) > 50 : (n=31, 29, 39):-Change
Group A: No RAD	1.55	-2.55
Group B : CNI Withdrawal	-5.75	7.32
Group C: CNI Reduction	0.82	-0.24

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Renal Function Assessed by Measured GFR (mGFR)

The acceptable methods for GFR measurement were Chromium 51-Ethylenediaminetetra acetic acid (Cr-EDTA), Technetium 99-Diethylenetriaminepentacetic acid (Tc-DTPA), Iohexol clearance Inuline clearance and Iothalamate clearance. The method should have been consistent for a given patient at every time point. (NCT00170846)
Timeframe: 24 months

Intervention	mL/min/1.73m^2 (Mean)
Group A: No RAD	46.02
Group B : CNI Withdrawal	48.00
Group C: CNI Reduction	46.60

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Target Vessel Failure (TVF)

"The composite endpoint comprised of:~Cardiac death (death in which a cardiac cause cannot be excluded)~Myocardial infarction (MI, classified as Q-wave and non-Q wave)~Ischemia-driven target lesion revascularization (TLR) by CABG or PCI~Ischemia-driven target vessel revascularization (TVR) by CABG or PCI" (NCT00180479)
Timeframe: 5 years

Intervention	percentage of participants (Number)
XIENCE V® EECSS	20.3
TAXUS® EXPRESS2™ ECSS	26.6

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% Volume Obstruction (% VO)

Defined as stent intimal hyperplasia and calculated as 100*(Stent Volume - Lumen Volume)/Stent Volume by IVUS. (NCT00180479)
Timeframe: at 240 days

Intervention	percent of volume obstruction (Mean)
XIENCE V® EECSS	6.91
TAXUS® EXPRESS2™ ECSS	11.21

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Acute Success: Clinical Device

Successful delivery and deployment of 1st implanted study stent/s @ the intended target lesion and successful withdrawal of the stent delivery system with final residual stenosis < 50%. (NCT00180479)
Timeframe: In-hospital

Intervention	percentage of participants (Number)
XIENCE V® EECSS	98.3
TAXUS® EXPRESS2™ ECSS	98.7

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Acute Success: Clinical Procedure

Successful delivery and deployment of study stent/s @ the intended target lesion and successful withdrawal of the stent delivery system with final residual stenosis < 50%. (NCT00180479)
Timeframe: In-hospital

Intervention	percentage of participants (Number)
XIENCE V® EECSS	98.5
TAXUS® EXPRESS2™ ECSS	97.3

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Distal Late Loss

Distal MLD post-procedure minus distal MLD at follow-up (distal defined as within 5 mm of healthy tissue distal to stent placement) (NCT00180479)
Timeframe: 240 days

Intervention	millimeters (Mean)
XIENCE V® EECSS	0.09
TAXUS® EXPRESS2™ ECSS	0.10

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In-segment % Angiographic Binary Restenosis (% ABR) Rate

Percent of subjects with a follow-up in-segment percent diameter stenosis of ≥ 50% per QCA (NCT00180479)
Timeframe: 240 days

Intervention	percentage of participants (Number)
XIENCE V® EECSS	4.7
TAXUS® EXPRESS2™ ECSS	8.9

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In-segment % Diameter Stenosis (% DS)

Within the margins of the stent, 5 mm proximal and 5 mm distal to the stent, the value calculated as 100 * (1 - in-segment MLD/RVD) using the mean values from two orthogonal views (when possible) by QCA. (NCT00180479)
Timeframe: 240 days

Intervention	percent of in-segment diameter stenosis (Mean)
XIENCE V® EECSS	18.77
TAXUS® EXPRESS2™ ECSS	22.82

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In-stent % Angiographic Binary Restenosis (% ABR) Rate

Percent of subjects with a follow-up in-stent percent diameter stenosis of ≥ 50% per quantitative coronary angiography (QCA) (NCT00180479)
Timeframe: at 240 days

Intervention	percentage of participants (Number)
XIENCE V® EECSS	2.3
TAXUS® EXPRESS2™ ECSS	5.7

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In-stent % Diameter Stenosis (% DS)

In-stent: Within the margins of the stent, the value calculated as 100 * (1 - in-stent MLD/RVD) using the mean values from two orthogonal views (when possible) by QCA. (NCT00180479)
Timeframe: at 240 days

Intervention	percent diameter stenosis (Mean)
XIENCE V® EECSS	5.92
TAXUS® EXPRESS2™ ECSS	10.30

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In-stent Late Loss

In-stent MLD post-procedure minus in-stent MLD at follow-up (in-stent defined as within the margins of the stent) (NCT00180479)
Timeframe: at 240 days

Intervention	millimeters (Mean)
XIENCE V® EECSS	0.16
TAXUS® EXPRESS2™ ECSS	0.30

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Ischemia Driven Major Adverse Cardiac Event (MACE)

"The composite endpoint comprised of:~Cardiac death~Myocardial infarction (MI, classified as Q-wave and non-Q wave)~Ischemia-driven target lesion revascularization (TLR) by CABG or PCI" (NCT00180479)
Timeframe: 1 year

Intervention	percentage of participants (Number)
XIENCE V® EECSS	6.0
TAXUS® EXPRESS2™ ECSS	10.3

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Ischemia Driven Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	5.0
TAXUS® EXPRESS2™ ECSS	8.8

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Ischemia Driven Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	9.7
TAXUS® EXPRESS2™ ECSS	16.4

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Ischemia Driven Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	1.3
TAXUS® EXPRESS2™ ECSS	3.0

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Ischemia Driven Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	12.8
TAXUS® EXPRESS2™ ECSS	18.5

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Ischemia Driven Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	14.4
TAXUS® EXPRESS2™ ECSS	22.0

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

"Revascularization @ target lesion associated w/ any of following:~(+) functional ischemia study Ischemic symptoms & angiographic diameter stenosis ≥50% by core lab quantitative coronary angiography (QCA) Revascularization of a target lesion w/ angiographic diameter stenosis ≥70% by core laboratory QCA without angina or (+) functional study" (NCT00180479)
Timeframe: 1 years

Intervention	percentage of participants (Number)
XIENCE V® EECSS	3.4
TAXUS® EXPRESS2™ ECSS	5.6

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	1.5
TAXUS® EXPRESS2™ ECSS	2.1

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Ischemia Driven Major Adverse Cardiac Event(MACE)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	7.7
TAXUS® EXPRESS2™ ECSS	13.8

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	5.7
TAXUS® EXPRESS2™ ECSS	9.2

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	2.7
TAXUS® EXPRESS2™ ECSS	5.0

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	5.7
TAXUS® EXPRESS2™ ECSS	9.2

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	0.4
TAXUS® EXPRESS2™ ECSS	0.3

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	8.0
TAXUS® EXPRESS2™ ECSS	10.6

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	8.9
TAXUS® EXPRESS2™ ECSS	12.9

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

"Revascularization at the target vessel associated with any of the following~Positive functional ischemia study~Ischemic symptoms and angiographic diameter stenosis ≥ 50% by core laboratory QCA~Revascularization of a target vessel with angiographic diameter stenosis ≥ 70% by core laboratory QCA without angina or positive functional study~Derived from Non-Hierarchical Subject Counts of Adverse Events" (NCT00180479)
Timeframe: 1 year

Intervention	percentage of participants (Number)
XIENCE V® EECSS	3.1
TAXUS® EXPRESS2™ ECSS	4.7

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	1.2
TAXUS® EXPRESS2™ ECSS	1.8

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	4.9
TAXUS® EXPRESS2™ ECSS	6.6

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	2.9
TAXUS® EXPRESS2™ ECSS	4.1

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	6.7
TAXUS® EXPRESS2™ ECSS	8.9

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	0.3
TAXUS® EXPRESS2™ ECSS	0.9

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Ischemia Driven Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	2.9
TAXUS® EXPRESS2™ ECSS	5.2

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	7.8
TAXUS® EXPRESS2™ ECSS	9.6

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	8.8
TAXUS® EXPRESS2™ ECSS	11.9

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Major Secondary Endpoint: Ischemia Driven Target Vessel Failure (ID-TVF)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	7.2
TAXUS® EXPRESS2™ ECSS	9.0

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Persisting Incomplete Stent Apposition, Late-acquired Incomplete Stent Apposition, Aneurysm, Thrombosis, and Persisting Dissection

"Incomplete Apposition (Persisting & Late acquired): Failure to completely appose vessel wall w/ ≥1 strut separated from vessel wall w/ blood behind strut per ultrasound. Aneurysm: Abnormal vessel expansion ≥ 1.5 of reference vessel diameter. Thrombus: Protocol & ARC definition.~Persisting dissection @ follow-up, present post-procedure." (NCT00180479)
Timeframe: at 240 days

Intervention	percentage of participants (Number)
XIENCE V® EECSS	24.4
TAXUS® EXPRESS2™ ECSS	14.0

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Primary Endpoint: In-segment Late Loss (LL)

In-segment minimal lumen diameter (MLD) post-procedure minus (-) in segment MLD at 240 day follow-up and 5 mm proximal and 5mm distal to the stent equals Late Loss. MLD defined: The average of two orthogonal views (when possible) of the narrowest point within the area of assessment. (NCT00180479)
Timeframe: 240 days

Intervention	millimeters (Mean)
XIENCE V® EECSS	0.14
TAXUS® EXPRESS2™ ECSS	0.28

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Proximal Late Loss

Proximal Minimum Lumen Diameter (MLD) post-procedure minus proximal MLD at follow-up (proximal defined as within 5 mm of healthy tissue proximal to stent placement) (NCT00180479)
Timeframe: at 240 days

Intervention	millimeters (Mean)
XIENCE V® EECSS	0.12
TAXUS® EXPRESS2™ ECSS	0.20

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Target Vessel Failure (TVF)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	8.6
TAXUS® EXPRESS2™ ECSS	11.6

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Target Vessel Failure (TVF)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	4.1
TAXUS® EXPRESS2™ ECSS	5.5

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Target Vessel Failure (TVF)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	11.3
TAXUS® EXPRESS2™ ECSS	16.4

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Target Vessel Failure (TVF)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	14.3
TAXUS® EXPRESS2™ ECSS	20.0

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Target Vessel Failure (TVF)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	1.6
TAXUS® EXPRESS2™ ECSS	3.3

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Target Vessel Failure (TVF)

Intervention	percentage of participants (Number)
XIENCE V® EECSS	18.5
TAXUS® EXPRESS2™ ECSS	22.5

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Number of Participants With Composite Efficacy Endpoints - 12 Month Analysis

The primary efficacy endpoint was the 12 month analysis of primary efficacy failure defined as a composite endpoint including treated biopsy proven acute rejection (BPAR), graft loss, death or loss to follow-up. A treated BPAR episode was defined as a biopsy graded IA, IB, IIA, IIB, or III that was treated with anti-rejection therapy. Graft loss was defined as the allograft was presumed to be lost on the day the patient started dialysis and was not able to subsequently be removed from dialysis as well as re-transplant. (NCT00251004)
Timeframe: 12 months

Intervention	Participants (Number)
	Composite Endpoint (n)	--Death	--Graft Loss	--Treated BPAR	--Lost to follow up
Control Group	70	6	9	50	9
High-dose Everolimus Group	60	9	13	38	6
Low-dose Everolimus Group	75	8	13	48	12

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Percentage of Participants With the Composite Incidence of Graft Loss, Death or Loss to Follow up at 12 Months Post-transplantation

"Graft loss was defined as graft loss (the allograft was presumed to be lost on the day the patient started dialysis and was not able to subsequently be removed from dialysis) and re-transplant.~A loss to follow-up patient in the composite endpoint of graft loss, death or loss to follow-up (the main secondary efficacy endpoint) was a patient who did not experience graft loss or death from day 1 and whose last day of contact was prior to study day 316." (NCT00251004)
Timeframe: 12 months

Intervention	Percentage of participants (Number)
Low-dose Everolimus Group	11.6
High-dose Everolimus Group	9.7
Control Group	9.4

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Non-inferiority Analysis of Renal Function, Calculated by Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula

"Modification of Diet in Renal Disease (MDRD) formula is:~GFR [mL/min/1.73m^2] = 186.3*(C^-1.154)*(A^-0.203)*G*R where~C is the serum concentration of creatinine [mg/dL],~A is patient age at sample collection date [years],~G=0.742 when gender is female, otherwise G=1,~R=1.21 when race is black, otherwise R=1" (NCT00251004)
Timeframe: at 12 months

Intervention	mL/min/1.73m^2 (Number)
Low-dose Everolimus Group	54.66
High-dose Everolimus Group	51.41
Control Group	52.24

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Non-inferiority Analysis on Percentage of Participants With Composite Efficacy Endpoints

The primary efficacy endpoint was the 12 month analysis of primary efficacy failure defined as a composite endpoint including treated biopsy proven acute rejection (BPAR), graft loss, death or loss to follow-up. In the definition of composite efficacy failure, loss to follow-up includes patients who did not experience treated BPAR, graft loss or death on or after day 1 and whose last day of contact was prior to day 316, the start day of the 12 month visit window. (NCT00251004)
Timeframe: 12 months

Intervention	Percentage of Participants (Number)
Low-dose Everolimus Group	27.1
High-dose Everolimus Group	21.5
Control Group	25.3

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Percentage of Patients With Efficacy Failure (Biopsy Proven Acute Rejection [BPAR], Graft Loss or Death)

The composite efficacy failure endpoint encompasses at least one of: biopsy proven acute rejection, graft loss, or death for the patient. BPAR was defined as a clinically suspected acute rejection confirmed by biopsy. Acute rejection episodes were recorded as Liver Allograft Rejection. The allograft was presumed to be lost if a patient had a liver retransplant or died. (NCT00267189)
Timeframe: 6 months

Intervention	Percentage of patients (Number)
	Composite efficacy failure (total)	Biopsy proven acute rejection	Graft Loss	Death
Group 1 (Everolimus)	2.8	1.4	0	1.4
Group 2 (Control)	1.4	1.4	0	0

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Mean Change From Baseline in Cockcroft-Gault Calculated Creatinine Clearance (CrCl)

"The primary variable was renal function assessed by calculated creatinine clearance using the Cockcroft-Gault formula, and was assessed at all visits.~CrCl[mL/min] = (140 - A) * W / (72 * C) * R. Where A is age at sample date [years], W is body weight at specific visit [kg], C is the serum concentration of creatinine [mg/dL], R = 1 if the patient is male and = 0.85 if female." (NCT00267189)
Timeframe: From baseline to 6 months

Intervention	mL/min (Mean)
Group 1 (Everolimus)	0.99
Group 2 (Control)	2.26

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Number of Patients With Discontinuation of Study Medication

(NCT00267189)
Timeframe: 6 months

Intervention	Patients (Number)
	Total # of discontinuation of study medication	Adverse Event	Patient withdrew consent	Abnormal laboratory value(s)	Administrative problems
Group 1 (Everolimus)	18	14	2	1	1
Group 2 (Control)	1	0	1	0	0

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Percentage of Participants With Biopsy-proven Acute Rejection (BPAR of ISHLT Grade ≥ 3A), Acute Rejection (AR) Associated With Hemodynamic Compromise (HDC), Graft Loss/Re-transplant and Death at Month 24

"Identification of acute rejections was based on the local pathologist's evaluation of endomyocardial biopsy slides.~Hemodynamic compromise was present if 1 or more of the following were met: Ejection fraction ≤ 30% or 25% lower than Baseline or Fractional shortening ≤ 20% or 25% lower than Baseline, and/ or use of inotropic treatment." (NCT00300274)
Timeframe: 24 Months

Intervention	Percentage of participants (Number)
	AR associated with HDC	BPAR of ISHLT grade ≥ 3A	Death	Graft loss/re-transplant
Everolimus 1.5 mg	4.3	24.1	10.6	2.5
Everolimus 3.0 mg	3.6	28.6	11.9	3.0
Mycophenolate Mofetil	5.2	27.3	9.2	3.7

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Renal Function Measured by Glomerular Filtration Rate (GFR) at 12 Months

"GFR was calculated using the Modification of Diet and Renal Disease (MDRD) formula:~GFR [mL/min/1.73m^2] = 186.3*(C^-1.154)*(A^-0.203)*G*R where C is the serum concentration of creatinine [mg/dL] A is age [years] G=0.742 when gender is female, otherwise G=1 R=1.21 when race is black, otherwise R=1" (NCT00300274)
Timeframe: 12 Months

Intervention	mL/min/1.73^2 (Mean)
Everolimus 1.5 mg	59.21
Everolimus 3.0 mg	59.78
Mycophenolate Mofetil	64.37

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Renal Function Calculated by Glomerular Filtration Rate (GFR) at 24 Months

"GFR was calculated using the Modification of Diet and Renal Disease (MDRD) formula:~GFR [mL/min/1.73m^2] = 186.3*(C^-1.154)*(A^-0.203)*G*R~C is the serum concentration of creatinine [mg/dL] A is age [years] G=0.742 when gender is female, otherwise G=1 R=1.21 when race is black, otherwise R=1" (NCT00300274)
Timeframe: 24 Months

Intervention	mL/min/1.73^2 (Mean)
Everolimus 1.5 mg	59.50
Everolimus 3.0 mg	61.84
Mycophenolate Mofetil	64.52

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Percentage of Participants With Graft Loss/Re-transplant, Death or Loss to Follow-up at 24 Months

Loss to follow-up for this composite endpoint included participants who did not experience graft loss/re-transplant or death and whose last day of contact was prior to Day 631 (start day of 24 Month visit window). (NCT00300274)
Timeframe: 24 Months

Intervention	Percentage of participants (Number)
Everolimus 1.5 mg	15.2
Everolimus 3.0 mg	16.1
Mycophenolate Mofetil	15.1

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Percentage of Participants With Graft Loss/Re-transplant, Death or Loss to Follow-up at 12 Months

Loss to follow-up for this composite endpoint included participants who did not experience graft loss/re-transplant or death and whose last day of contact was prior to Day 316 (start day of the Month 12 visit window). (NCT00300274)
Timeframe: 12 Months

Intervention	Percentage of participants (Number)
Everolimus 1.5 mg	11.7
Everolimus 3.0 mg	11.9
Mycophenolate Mofetil	8.9

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Percentage of Participants With Composite Efficacy Failure at 24 Months

"Composite efficacy failure was defined as Biopsy Proven Acute Rejection (BPAR) of International Society for Heart and Lung Transplantation grade ≥ 3A, Acute Rejection associated with Hemodynamic Compromise, Graft loss/Retransplant, Death or Loss to follow-up.~Identification of acute rejections was based on the local pathologist's evaluation of endomyocardial biopsy slides.~Hemodynamic compromise was present if 1 or more of the following were met: Ejection fraction ≤ 30% or 25% lower than Baseline or Fractional shortening ≤ 20% or 25% lower than Baseline and/or use of inotropic treatment." (NCT00300274)
Timeframe: 24 Months

Intervention	Percentage of participants (Number)
Everolimus 1.5 mg	39.4
Everolimus 3.0 mg	41.1
Mycophenolate Mofetil	41.3

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Percentage of Participants With Composite Efficacy Failure at 12 Months

"Composite efficacy failure was defined as Biopsy Proven Acute Rejection(BPAR) of International Society for Heart and Lung Transplantation(ISHLT) grade ≥3A, Acute Rejection associated with Hemodynamic Compromise, Graft loss/Retransplant, Death or Loss to follow-up.~Identification of acute rejection was based on the local pathologist's evaluation of endomyocardial biopsy slides.~Hemodynamic compromise was present if 1 or more of the following were met: Ejection fraction ≤30% or 25% lower than Baseline or Fractional shortening ≤20% or 25% lower than Baseline and/or use of inotropic treatment." (NCT00300274)
Timeframe: 12 Months

Intervention	Percentage of participants (Number)
Everolimus 1.5 mg	35.1
Everolimus 3.0 mg	35.1
Mycophenolate Mofetil	33.6

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Percentage of Participants With Cardiac Allograft Vasculopathy (CAV) at Month 12

Cardiac allograft vasculopathy is defined as a 0.5 mm increase in maximum intimal thickness as measured by Intravascular Ultrasound (IVUS) in at least one matched slice between baseline and Month 12. (NCT00300274)
Timeframe: 12 Months

Intervention	Percentage of participants (Number)
Everolimus 1.5 mg	12.5
Everolimus 3.0 mg	21.6
Mycophenolate Mofetil	26.7

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Percentage of Participants With Biopsy-proven Acute Rejection (BPAR of ISHLT Grade ≥ 3A), Acute Rejection Associated With Hemodynamic Compromise (HDC), Graft Loss/Re-transplant and Death at Month 12

"Identification of acute rejections was based on the local pathologist's evaluation of endomyocardial biopsy slides.~Hemodynamic compromise was present if 1 or more of the following were met: Ejection fraction ≤ 30% or 25% lower than Baseline or Fractional shortening ≤ 20% or 25% lower than Baseline, and/or use of inotropic treatment." (NCT00300274)
Timeframe: 12 Months

Intervention	Percentage of participants (Number)
	AR associated with HDC	BPAR of ISHLT ≥ 3A	Death	Graft loss/re-transplant
Everolimus 1.5 mg	3.9	22.3	7.8	1.4
Everolimus 3.0 mg	3.0	25.6	10.1	3.0
Mycophenolate Mofetil	2.6	24.7	4.8	1.8

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Change From Baseline in the Average Maximum Intimal Thickness at Month 12

Maximum intimal thickness was assessed using Intravascular Ultrasound (IVUS). IVUS is a technique for taking ultrasound pictures of the wall of an artery from inside the artery itself. It shows the thickness of the artery wall and any narrowing of the artery. (NCT00300274)
Timeframe: Baseline, Month 12

Intervention	mm (Mean)
Everolimus 1.5 mg	0.03
Everolimus 3.0 mg	0.04
Mycophenolate Mofetil	0.07

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Ischemia Driven Major Adverse Cardiac Events (MACE)

Patients determined to have had a MACE event, defined as one of the following events: Cardiac death, myocardial infarction, and TLR (NCT00307047)
Timeframe: 30 days

Intervention	Percentage of participants (Number)
XIENCE V®	1.6
TAXUS™ EXPRESS 2™	2.7

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Ischemia Driven Target Lesion Failure (TLF)

Percentage of participants with the determination of TLF. TLF is the composite of cardiac death, target vessel myocardial infarction, and ischemic driven target lesion revascularization (TLR). (NCT00307047)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
XIENCE V®	4.2
TAXUS™ EXPRESS 2™	6.8

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Ischemia Driven Target Lesion Failure (TLF)

Intervention	Percentage of participants (Number)
XIENCE V®	2.5
TAXUS™ EXPRESS 2™	5.1

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Ischemia Driven Target Lesion Failure (TLF)

Intervention	Percentage of participants (Number)
XIENCE V®	7.0
TAXUS™ EXPRESS 2™	10.0

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Ischemia Driven Target Lesion Failure (TLF)

Intervention	Percentage of participants (Number)
XIENCE V®	3.4
TAXUS™ EXPRESS 2™	6.1

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Ischemia Driven Target Lesion Failure (TLF)

Intervention	Percentage of participants (Number)
XIENCE V®	1.6
TAXUS™ EXPRESS 2™	2.7

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Ischemia Driven Target Lesion Revascularization (TLR)

"Revascularization of a target lesion associated with any of the following:~positive functional ischemia study~ischemic symptoms and angiographic minimal lumen diameter stenosis ≥ 50% by core laboratory quantitative coronary angiography (QCA)~angiographic diameter stenosis ≥ 70% by core laboratory QCA without either ischemic symptoms or a positive functional study" (NCT00307047)
Timeframe: 1 year

Intervention	percentage of participants (Number)
XIENCE V®	2.5
TAXUS™ EXPRESS 2™	4.6

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Ischemia Driven Target Lesion Revascularization (TLR)

Intervention	percentage of participants (Number)
XIENCE V®	1.1
TAXUS™ EXPRESS 2™	3.2

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Ischemia Driven Target Lesion Revascularization (TLR)

Intervention	percentage of participants (Number)
XIENCE V®	4.4
TAXUS™ EXPRESS 2™	6.9

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Ischemia Driven Target Lesion Revascularization (TLR)

Intervention	percentage of participants (Number)
XIENCE V®	1.9
TAXUS™ EXPRESS 2™	4.1

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Ischemia Driven Target Lesion Revascularization (TLR)

Intervention	percentage of participants (Number)
XIENCE V®	6.3
TAXUS™ EXPRESS 2™	7.9

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Ischemia Driven Target Lesion Revascularization (TLR)

Intervention	percentage of participants (Number)
XIENCE V®	0.4
TAXUS™ EXPRESS 2™	1.1

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Ischemia Driven Target Vessel Failure (TVF)

Defined as the composite endpoint comprised of cardiac death (CD), myocardial infarction (MI), TLR, and TVR (NCT00307047)
Timeframe: 1 year

Intervention	percentage of participants (Number)
XIENCE V®	5.6
TAXUS™ EXPRESS 2™	7.9

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Ischemia Driven Target Vessel Failure (TVF)

Defined as the composite endpoint comprised of cardiac death (CD), myocardial infarction (MI), TLR, and TVR (NCT00307047)
Timeframe: 180 days

Intervention	percentage of participants (Number)
XIENCE V®	3.4
TAXUS™ EXPRESS 2™	6.2

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Ischemia Driven Target Vessel Failure (TVF)

Defined as the composite endpoint comprised of cardiac death (CD), myocardial infarction (MI), TLR, and TVR (NCT00307047)
Timeframe: 2 years

Intervention	percentage of participants (Number)
XIENCE V®	9.6
TAXUS™ EXPRESS 2™	11.8

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Ischemia Driven Target Vessel Failure (TVF)

Defined as the composite endpoint comprised of cardiac death (CD), myocardial infarction (MI), TLR, and TVR (NCT00307047)
Timeframe: 270 days

Intervention	percentage of participants (Number)
XIENCE V®	4.6
TAXUS™ EXPRESS 2™	7.2

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Ischemia Driven Target Vessel Failure (TVF)

Defined as the composite endpoint comprised of cardiac death (CD), myocardial infarction (MI), TLR, and TVR (NCT00307047)
Timeframe: 3 years

Intervention	percentage of participants (Number)
XIENCE V®	13.3
TAXUS™ EXPRESS 2™	14.5

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Ischemia Driven Target Vessel Failure (TVF)

Defined as the composite endpoint comprised of cardiac death (CD), myocardial infarction (MI), TLR, and TVR (NCT00307047)
Timeframe: 30 days

Intervention	percentage of participants (Number)
XIENCE V®	1.9
TAXUS™ EXPRESS 2™	3.1

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Ischemia Driven Target Vessel Revascularization (TVR)

"Revascularization of a lesion within the target vessel associated with any of the following:~positive functional ischemia study~ischemic symptoms and an angiographic minimal lumen diameter stenosis ≥ 50% by core laboratory quantitative coronary angiography (QCA)~angiographic diameter stenosis ≥ 70% by core laboratory QCA without either ischemic symptoms or a positive functional study" (NCT00307047)
Timeframe: 1 year

Intervention	percentage of participants (Number)
XIENCE V®	3.9
TAXUS™ EXPRESS 2™	5.9

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Ischemia Driven Target Vessel Revascularization (TVR)

Intervention	percentage of participants (Number)
XIENCE V®	1.9
TAXUS™ EXPRESS 2™	4.3

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All Cause Mortality

(NCT00307047)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
XIENCE V®	3.4
TAXUS™ EXPRESS 2™	5.2

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All Cause Mortality

(NCT00307047)
Timeframe: 270 days

Intervention	Percentage of participants (Number)
XIENCE V®	0.7
TAXUS™ EXPRESS 2™	0.9

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All Cause Mortality

(NCT00307047)
Timeframe: 2 years

Intervention	Percentage of participants (Number)
XIENCE V®	2.1
TAXUS™ EXPRESS 2™	2.7

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All Cause Mortality

(NCT00307047)
Timeframe: 180 days

Intervention	Percentage of participants (Number)
XIENCE V®	0.5
TAXUS™ EXPRESS 2™	0.6

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All Cause Mortality

(NCT00307047)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
XIENCE V®	1.0
TAXUS™ EXPRESS 2™	1.3

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Acute Success (Clinical Procedure)

Successful delivery and deployment of the study stent or stents at the intended target lesion and successful withdrawal of the stent delivery system with attainment of final residual stenosis of less than 50% of the target lesion by QCA (by visual estimation if QCA unavailable) and/or using any adjunctive device without the occurrence of major adverse cardiac event (MACE) during the hospital stay with a maximum of first seven days following the index procedure. In multiple lesion setting all lesions must meet clinical procedure success. (NCT00307047)
Timeframe: Acute: At time of index procedure

Intervention	Percentage of success (Number)
XIENCE V®	98.6
TAXUS™ EXPRESS 2™	98.1

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Acute Success (Clinical Device)

Successful delivery and deployment of the first implanted study stent (in overlapping stent setting a successful delivery and deployment of the first and second study stents) at the intended target lesion and successful withdrawal of the stent delivery system with attainment of final residual stenosis of less than 50% of the target lesion by QCA (by visual estimation if QCA unavailable). Bailout subjects will be included as device success only if the above criteria for clinical device are met. (NCT00307047)
Timeframe: Acute: At time of index procedure

Intervention	Percent of success (Number)
XIENCE V®	92.0
TAXUS™ EXPRESS 2™	90.7

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Ischemia Driven Target Vessel Revascularization (TVR)

Intervention	percentage of participants (Number)
XIENCE V®	7.0
TAXUS™ EXPRESS 2™	8.9

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Ischemia Driven Target Vessel Revascularization (TVR)

Intervention	percentage of participants (Number)
XIENCE V®	3.0
TAXUS™ EXPRESS 2™	5.3

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Ischemia Driven Target Vessel Revascularization (TVR)

Intervention	percentage of participants (Number)
XIENCE V®	10.1
TAXUS™ EXPRESS 2™	10.6

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Ischemia Driven Target Vessel Revascularization (TVR)

Intervention	percentage of participants (Number)
XIENCE V®	0.7
TAXUS™ EXPRESS 2™	1.6

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Ischemia Driven Major Adverse Cardiac Events (MACE)

Patients determined to have had a MACE event, defined as one of the following events: Cardiac death, myocardial infarction, and TLR (NCT00307047)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
XIENCE V®	9.8
TAXUS™ EXPRESS 2™	12.3

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Protocol Defined Stent Thrombosis Rate

"ST will be categorized as acute (≤ 1day), subacute (>1 day to ≤ 30 days) and late (>30 days) and will be defined as any of the following:~Clinical presentation of acute coronary syndrome with angiographic evidence of ST~In the absence of angiography, any unexplained death, or acute MI (S-T segment elevation or new Q-wave)* in the distribution of the target lesion within 30 days *(Non-specific S-T/T changes, and cardiac enzyme elevations do not suffice) Any thromboses that occur less than 30 days after the index procedure will not be counted as restenosis." (NCT00307047)
Timeframe: 0-393 days

Intervention	Percentage of participants (Number)
XIENCE V®	0.17
TAXUS™ EXPRESS 2™	0.85

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Protocol Defined Stent Thrombosis Rate

Intervention	Percentage of participants (Number)
XIENCE V®	0.12
TAXUS™ EXPRESS 2™	0.57

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Protocol Defined Stent Thrombosis Rate

Intervention	Percentage of participants (Number)
XIENCE V®	0.52
TAXUS™ EXPRESS 2™	1.23

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Protocol Defined Stent Thrombosis Rate

Intervention	Percentage of participants (Number)
XIENCE V®	0.04
TAXUS™ EXPRESS 2™	0.34

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All Myocardial Infarction (MI)

(NCT00307047)
Timeframe: 30 days

Intervention	Percentage of participants (Number)
XIENCE V®	1.5
TAXUS™ EXPRESS 2™	2.1

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Ischemia Driven Target Lesion Failure (TLF)

Intervention	Percentage of participants (Number)
XIENCE V®	9.5
TAXUS™ EXPRESS 2™	11.9

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Protocol Defined Stent Thrombosis Rate

Intervention	Percentage of participants (Number)
XIENCE V®	0.79
TAXUS™ EXPRESS 2™	1.99

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Ischemia Driven Major Adverse Cardiac Events (MACE)

Patients determined to have had a MACE event, defined as one of the following events: Cardiac death, myocardial infarction, and TLR (NCT00307047)
Timeframe: 270 days

Intervention	Percentage of participants (Number)
XIENCE V®	3.5
TAXUS™ EXPRESS 2™	6.2

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Ischemia Driven Major Adverse Cardiac Events (MACE)

Patients determined to have had a MACE event, defined as one of the following events: Cardiac death, myocardial infarction, and TLR (NCT00307047)
Timeframe: 2 years

Intervention	Percentage of participants (Number)
XIENCE V®	7.2
TAXUS™ EXPRESS 2™	10.2

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Ischemia Driven Major Adverse Cardiac Events (MACE)

Patients determined to have had a MACE event, defined as one of the following events: Cardiac death, myocardial infarction, and TLR (NCT00307047)
Timeframe: 180 days

Intervention	Percentage of participants (Number)
XIENCE V®	2.6
TAXUS™ EXPRESS 2™	5.3

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Ischemia Driven Major Adverse Cardiac Events (MACE)

Patients determined to have had a MACE event, defined as one of the following events: Cardiac death, myocardial infarction, and TLR (NCT00307047)
Timeframe: 1 years

Intervention	Percentage of participants (Number)
XIENCE V®	4.2
TAXUS™ EXPRESS 2™	6.9

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Definite + Probable Stent Thrombosis Rate Based on ARC Definition

"ARC: Academic Research Consortium-defines ST as a cumulative value at the different time points and with the different seperate time points. Time 0 is defined as the time point after the guiding catheter has been removed. Acute*: 0-24 hours post implantation Subacute*: >24 hours-30 days post Late†: 30 days-1 year post Very late stent thrombosis†: >1 year post~* Acute/subacute can also be replaced by early ST. Early ST (0-30 days) is currently used in the community.~† Including primary as well as secondary late ST; secondary late ST is after a target segment revascularization." (NCT00307047)
Timeframe: 31-393 days

Intervention	Percentage of participants (Number)
XIENCE V®	0.13
TAXUS™ EXPRESS 2™	0.42

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Definite + Probable Stent Thrombosis Rate Based on ARC Definition

Intervention	Percentage of participants (Number)
XIENCE V®	0.48
TAXUS™ EXPRESS 2™	1.32

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Definite + Probable Stent Thrombosis Rate Based on ARC Definition

Intervention	Percentage of participants (Number)
XIENCE V®	0.62
TAXUS™ EXPRESS 2™	1.73

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Definite + Probable Stent Thrombosis Rate Based on ARC Definition

Intervention	Percentage of participants (Number)
XIENCE V®	0.29
TAXUS™ EXPRESS 2™	1.10

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Definite + Probable Stent Thrombosis Rate Based on Academic Research Consortium (ARC) Definition

Intervention	Percentage of participants (Number)
XIENCE V®	0.16
TAXUS™ EXPRESS 2™	0.74

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Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)

(NCT00307047)
Timeframe: 30 days

Intervention	Percentage of participants (Number)
XIENCE V®	2.4
TAXUS™ EXPRESS 2™	3.6

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Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)

(NCT00307047)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
XIENCE V®	21.4
TAXUS™ EXPRESS 2™	22.5

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Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)

(NCT00307047)
Timeframe: 270 days

Intervention	Percentage of participants (Number)
XIENCE V®	7.2
TAXUS™ EXPRESS 2™	9.3

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Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)

(NCT00307047)
Timeframe: 2 years

Intervention	Percentage of participants (Number)
XIENCE V®	15.5
TAXUS™ EXPRESS 2™	16.2

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Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)

(NCT00307047)
Timeframe: 180 days

Intervention	Percentage of participants (Number)
XIENCE V®	5.5
TAXUS™ EXPRESS 2™	7.5

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Composite Endpoint of All Deaths, All MI, All Revascularizations (DMR)

(NCT00307047)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
XIENCE V®	9.0
TAXUS™ EXPRESS 2™	10.5

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Cardiac Death or Target Vessel MI Rate

(NCT00307047)
Timeframe: 30 days

Intervention	Percentage of participants (Number)
XIENCE V®	1.5
TAXUS™ EXPRESS 2™	2.1

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Cardiac Death or Target Vessel MI Rate

(NCT00307047)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
XIENCE V®	4.1
TAXUS™ EXPRESS 2™	5.5

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Cardiac Death or Target Vessel MI Rate

(NCT00307047)
Timeframe: 270 days

Intervention	Percentage of participants (Number)
XIENCE V®	2.1
TAXUS™ EXPRESS 2™	3.0

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Cardiac Death or Target Vessel MI Rate

(NCT00307047)
Timeframe: 2 years

Intervention	Percentage of participants (Number)
XIENCE V®	3.2
TAXUS™ EXPRESS 2™	4.3

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Cardiac Death or Target Vessel MI Rate

(NCT00307047)
Timeframe: 180 days

Intervention	Percentage of participants (Number)
XIENCE V®	1.8
TAXUS™ EXPRESS 2™	2.8

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Cardiac Death or Target Vessel MI Rate

(NCT00307047)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
XIENCE V®	2.2
TAXUS™ EXPRESS 2™	3.2

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All MI

(NCT00307047)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
XIENCE V®	3.1
TAXUS™ EXPRESS 2™	4.7

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All MI

(NCT00307047)
Timeframe: 270 days

Intervention	Percentage of participants (Number)
XIENCE V®	1.8
TAXUS™ EXPRESS 2™	3.0

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All MI

(NCT00307047)
Timeframe: 2 years

Intervention	Percentage of participants (Number)
XIENCE V®	2.6
TAXUS™ EXPRESS 2™	3.9

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All MI

(NCT00307047)
Timeframe: 180 days

Intervention	Percentage of participants (Number)
XIENCE V®	1.6
TAXUS™ EXPRESS 2™	2.9

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All MI

(NCT00307047)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
XIENCE V®	1.9
TAXUS™ EXPRESS 2™	3.1

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All Cause Mortality

(NCT00307047)
Timeframe: 30 days

Intervention	Percentage of participants (Number)
XIENCE V®	0.0
TAXUS™ EXPRESS 2™	0.2

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Clinical Benefit Response Rate (CBR)

Efficacy measured by the clinical benefit response rate (CBR), defined as confirmed Complete Response (CR) plus Partial Response (PR) at any time plus Persistent Stable Disease (pSD). Confirmed CR is defined as disappearance of all target lesions at the time of radiographic evaluation; pSD was defined as SD lasting 24 weeks. Complete Response (CR): disappearance of all target lesions, and Partial Response (PR): at least a 30% decrease in the sum of longest diameter (LD) of target lesions taking as a reference the baseline sum LD. Stable Disease (SD): neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease taking as references the smallest sum LD since the treatment started. (NCT00317720)
Timeframe: 6 weeks

Intervention	percentage of partcipants (Number)
	CBR	CR	PR	pSD
Trastuzumab + RAD001	34	0	15	19

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Optimal Dose of RAD001 in Combination With Trastuzumab (Phase I)

"In Phase I, two dose levels of RAD001 were studied: 10 mg (dose level 1) and 5 mg (dose level -1) where each dose was evaluated after cycle 1. At MDACC, the Continual Reassessment Method (CRM) for determining Maximum Tolerated Dose (MTD) was applied to the two predefined RAD001 dose levels; and at DFCI/BIDMC, a 3 x 3 study design was utilized.~Optimal dose defined as the dose most closely associated with a toxicity rate of 0.20, and toxicity defined as any grade 3 or 4 toxicity (based on Common Terminology Criteria (CTC) version 3.0 except fatigue. Participants underwent clinical evaluation every 3 weeks (one cycle) and radiologic evaluations every 6 weeks. After the second cycle, participants underwent a radiologic evaluation using the same imaging technique used at initial evaluation (ie, computed tomography or magnetic resonance imaging)." (NCT00317720)
Timeframe: Following two 3 week cycles of therapy

Intervention	mg (Number)
Trastuzumab + RAD001	10

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Progression Free Survival (PFS), the Length of Time, in Months, That Patients Were Alive From Their First Date of Protocol Treatment Until Worsening of Their Disease

(NCT00323739)
Timeframe: 18 months

Intervention	Months (Median)
Bevacizumab and Everolimus	8.1

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Overall Survival (OS), the Length of Time, in Months, That Patients Were Alive From Their First Date of Protocol Treatment Until Death

(NCT00323739)
Timeframe: 18 months

Intervention	Months (Median)
Bevacizumab and Everolimus	18.5

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Median Time to Progression

(NCT00331409)
Timeframe: Time to progression

Intervention	months (Median)
Everolimus and Imatinib Mesylate	2.9

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Number of Participants With Adverse Events

"Toxicity assessments will be obtained as follows:~Cycle 1: Weeks 1,2,3 Cycle 2: Weeks 6,9 Cycle 3: Weeks 12, 15 Cycle 4: Weeks 18, 21 Cycle 5: Weeks 24, 27 Cycle 6+: Every visit during these cycles~Safety assessments will consist of evaluating adverse events and serious adverse events." (NCT00331409)
Timeframe: Duration of study, Up to 4 years

Intervention	participants (Number)
Everolimus and Imatinib Mesylate	19

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Number of Subjects That Demonstrated a Reduction in Tumor Measurements.

Number of subjects that received at least one post-baseline scan that demonstrated a reduction in sum target lesions per Response Evaluation Criteria in Solid Tumors (RECIST) criteria. (NCT00331409)
Timeframe: Up to 4 years

Intervention	Participants (Count of Participants)
Everolimus and Imatinib Mesylate	5

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Overall Number of Participants Who Achieve a Response Rate (Complete Response, Partial Response, and Stable Disease) at 3 Months

(NCT00331409)
Timeframe: Up to 4 years

Intervention	participants (Number)
Everolimus and Imatinib Mesylate	18

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Progression-free Survival at 3 Months

(NCT00331409)
Timeframe: 3 months post 1st dose

Intervention	months (Median)
Everolimus and Imatinib Mesylate	2.9

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Number of Participants Who Experienced Adverse Events and Death

Participants were monitored for adverse events, serious adverse events and deaths thorughout the prospective and follow-up phases of the study. (NCT00332839)
Timeframe: 12 months

Intervention	Participants (Number)
	Adverse events (serious and non-serious)	Serious adverse events	Deaths
Calcineurin Inhibitor (CNI) Group	44	11	1
Certican Group	44	12	1

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Everolimus Trough Level Determination by Pharmacokinetics Parameter in Both Strata (Stratum 1 and 2)

For all patients in both strata, a blood sample for everolimus trough level determination will be collected immediately prior to the everolimus administration on Cycle 1 Day 15, Cycle 2 Day 1, and every month thereafter. A treatment cycle was defined as 28 days of consecutive daily treatment with everolimus and treatment continued until tumor progression. It is critical that patients not take their daily everolimus dose before the sample is drawn. (NCT00363051)
Timeframe: Cycle 1 Day 15

Intervention	ng/ml (Mean)
Stratum 1: Everolimus 10 mg	15.7
Stratum 2: Everolimus 10 mg + Octreotide Depot	17.3

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Objective Response Rate: Percentage of Participants With Best Over All Response of Complete Response or Partial Response by Central Radiology Review (Stratum 1) Based on Response Evaluation Criteria in Solid Tumors (RECIST)

Objective response rate was defined by RECIST criteria: Partial response (PR) must have ≥ 30% decrease in the sum of longest diameter of all target lesions, from the baseline sum. Complete response (CR) must have disappearance of all target and non-target lesions. For CR or PR, tumor measurements must be confirmed by 2nd assessments within 4 weeks. Progression = 20% increase in the sum of longest diameter of all target lesions, from smallest sum of longest diameter of all target lesions recorded at or after baseline; or a new lesion; or progression of non-target lesions. (NCT00363051)
Timeframe: from date of randomization/start of treatment until first documented response confirmed 4 weeks later( at least 3 months)

Intervention	percentage of participants (Number)
Stratum 1: Everolimus 10 mg	9.6

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Objective Response Rate: Percentage of Participants With Best Over All Response of Complete Response or Partial Response by Central Radiology Review (Stratum 2) Based on Response Evaluation Criteria in Solid Tumors (RECIST)

Intervention	percentage of participants (Number)
Stratum 2: Everolimus 10 mg + Octreotide Depot	4.4

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Time to Overall Survival (OS) (Stratum 2)

"Overall survival measures the time of survival , with any response or disease progression, until death. The OS is defined as the time from date of start of treatment to date of death due to any cause.~If a patient is not known to have died, survival was censored at the date of last contact. In each treatment stratum, the Kaplan-Meier estimate of the overall survival function was constructed." (NCT00363051)
Timeframe: from randomisation to dates of disease progression, death from any cause, reported between day of first patient randomised, 26 June 2006, until cut-off date 13 April 2012

Intervention	months (Median)
Stratum 2: Everolimus 10 mg + Octreotide Depot	38.77

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Time to Progression Free Survival (PFS) Per Central Radiology Review (Stratum 2)

"Progression free survival (PFS) is defined as the time from randomization to the date of first documented disease progression or death from any cause. The Kaplan-Meier estimate of the PFS survival function was constructed.~Median PFS was obtained and displayed along with 95% confidence intervals." (NCT00363051)
Timeframe: from randomisation to dates of disease progression, death from any cause or last tumor assessment, reported between day of first patient randomised, 26 June 2006, until cut-off date 13 September 2010

Intervention	Months (Median)
Stratum 2: Everolimus 10 mg + Octreotide Depot	16.69

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Time to Overall Survival (OS)(Stratum 1)

Intervention	months (Median)
Stratum 1: Everolimus 10 mg	28.78

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Time to Progression Free Survival (PFS) Per Central Radiology Review (Stratum 1)

Intervention	Months (Median)
Stratum 1: Everolimus 10 mg	9.69

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Effect of Octreotide Depot on the Trough Concentrations of Everolimus

The effect of Octreotide Depot on the trough concentrations of everolimus was assessed at Cycle 1 Day 15. (NCT00363051)
Timeframe: Cycle 1 Day 1, Cycle 2 Day 1

Intervention	ng/ml (Mean)
	Cycle 1 Day 1 (pre-treatment baseline) (n=37)	Cycle 2 Day 1 (n= 38)
Stratum 2: Everolimus 10 mg + Octreotide Depot	3.2	3.7

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Number of Participants With Adverse Events (AEs), Death, Serious Adverse Events (SAEs) [Stratum 2]

Adverse events are defined as any unfavorable and unintended diagnosis, symptom, sign (including an abnormal laboratory finding), syndrome or disease which either occurs during study, having been absent at baseline, or, if present at baseline, appears to worsen. Serious adverse events are any untoward medical occurrences that result in death, are life threatening, require (or prolong) hospitalization, cause persistent or significant disability/incapacity, result in congenital anomalies or birth defects, or are other conditions which in judgment of investigators represent significant hazards. (NCT00363051)
Timeframe: on or after the day of the first intake of study treatment to starting no later than 28 days after study treatment discontinuation, at least every month

Intervention	Participants (Number)
	Adverse Events	Death	Serious Adverse Events
Stratum 2: Everolimus 10 mg + Octreotide Depot	45	2	27

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Number of Participants With Adverse Events (AEs), Death, Serious Adverse Events (SAEs)[Stratum 1]

Intervention	Participants (Number)
	Adverse Events	Death	Serious Adverse Events
Stratum 1: Everolimus 10 mg	115	10	63

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Duration of Overall Response (Stratum 1) Based on Response Evaluation Criteria in Solid Tumors (RECIST)- Central Radiology Review

"Duration of overall response applies only to patients whose best overall response was complete response (CR) or partial response (PR):~Complete Response (CR) = at least two determinations of CR at least 4 weeks apart before progression.~Partial response (PR) = at least two determinations of PR or better at least 4 weeks apart before progression.~Progression = 20% increase in the sum of the longest diameter of all target lesions, from the smallest sum of longest diameter of all target lesions recorded at or after baseline; or a new lesion; or progression of non-target lesions" (NCT00363051)
Timeframe: from date of first documented confirmed response to time to progression, at least 3 months

Intervention	Months (Median)
Stratum 1: Everolimus 10 mg	10.64

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Number of Participants With Incidence of Biopsy-proven Acute Rejection (BPAR)

Biopsy-proven acute rejection (BPAR) was defined as a clinically suspected acute rejection confirmed by biopsy (performed by the local pathologist). For all clinically suspected rejection episodes a graft core biopsy must have been performed before or within a 24 hour period from the initiation of anti-rejection therapy. (NCT00369161)
Timeframe: from Month 4 through to Month 12

Intervention	participants (Number)
Very Low Dose Tacrolimus	2
Low Dose Tacrolimus	1

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Renal Function Assessed by Calculated Glomerular Filtration Rate (cGFR)

"Renal function was assessed by calculated glomerular filtration rate (cGFR) using Modification of Diet in Renal Disease (MDRD)formula.~GFR [mL/min/1.73m^2] = 186.3*(C-1.154)*(A-0.203)*G*R, where:~C is the serum concentration of creatinine [mg/dL],~A is patient age at sample collection date [years],~G=0.742 when gender is female, otherwise G=1,~R=1.21 when race is black, otherwise R=1" (NCT00369161)
Timeframe: 12 months post -transplant

Intervention	mL/min/1.73m^2 (Mean)
Very Low Dose Tacrolimus	57.07
Low Dose Tacrolimus	51.73

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Percentage of Participants With Efficacy Failure

Efficacy failure was a composite of BPAR, graft loss, death or lost to follow-up. BPAR was defined as a clinically suspected acute rejection confirmed by biopsy (performed by the local pathologist). For all clinically suspected rejection episodes a graft core biopsy must have been performed before or within a 24 hour period from the initiation of anti-rejection therapy. An allograft was presumed to be lost on the day a patient started dialysis and was unable to subsequently be removed from dialysis. If the patient underwent a graft nephrectomy, the day of nephrectomy was the day of graft loss. (NCT00369161)
Timeframe: Month 12

Intervention	percentage of participants (Number)
	Efficacy failure (Composite)	BPAR	Graft loss or death	Graft Loss	Death	Lost To Follow-up
Low Dose Tacrolimus	4.3	1.1	2.2	1.1	1.1	1.1
Very Low Dose Tacrolimus	6.7	2.7	4.0	1.3	2.7	0.0

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Number of Participants With Wound Problems(12 Months Analysis)

Patients with any wound healing problem such as infection related to kidney surgery, dehiscence, lymphocele, hernia, seroma, hematoma, ureteral anastomotic complication and other were reported in this analysis. (NCT00371826)
Timeframe: At Month 12

Intervention	Participants (Number)
	Any wound healing problem	Infection related to kidney surgery	Dehiscence	Lymphocele	Hernia	Seroma	Hematoma	Ureteral anastomotic complication	Other
Calcineurin Inhibitor (CNI) Withdrawal	16	2	3	3	3	4	4	2	3
CNI+MPA+ Steroid	15	4	2	4	2	9	0	1	1
Steroid Withdrawal	9	3	2	3	1	3	2	1	0

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Number of Participants With Sub Clinical Acute Rejection (36 Months Analysis)

"Based on Banff 97 criteria, sub clinical acute rejection can be:~GRADE IA - Cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of moderate tubulitis (>4 mononuclear cells/tubular cross section or group of 10 tubular cells).~GRADE IB - Cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of moderate tubulitis (>10 mononuclear cells/tubular cross section or group of 10 tubular cells).~GRADE IIA - Cases with significant interstitial infiltration and mild to moderate intimal arteritis (v1).~GRADE IIB - Cases with moderate to severe intimal arteritis comprising >25% of the luminal area (v2).~GRADE III - Cases with transmural arteritis or fibrinoid change and necrosis of medial smooth muscle cells (v3).~Borderline' category is used when no intimal arteritis is present, but there are foci of mild tubulitis (1 to 4 mononuclear cells/tubular cross section)." (NCT00371826)
Timeframe: At Month 36

Intervention	Participants (Number)
	Month 36: NO	Month 36: Borderline	Month 36: Grade IA	Month 36: Grade IB	Month 36: Grade IIA	Month 36: Grade IIB	Month 36: Grade III	Month 36: Not Done
Calcineurin Inhibitor (CNI) Withdrawal	9	1	0	0	0	0	0	8
CNI+MPA+ Steroid	15	1	1	0	0	0	0	14
Steroid Withdrawal	2	0	0	0	0	0	0	1

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Number of Participants With Sub Clinical Acute Rejection (12 Months Analysis)

"Based on Banff 97 criteria, sub clinical acute rejection can be:~GRADE IA - Cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of moderate tubulitis (>4 mononuclear cells/tubular cross section or group of 10 tubular cells).~GRADE IB - Cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of moderate tubulitis (>10 mononuclear cells/tubular cross section or group of 10 tubular cells).~GRADE IIA - Cases with significant interstitial infiltration and mild to moderate intimal arteritis (v1).~GRADE IIB - Cases with moderate to severe intimal arteritis comprising >25% of the luminal area (v2).~GRADE III - Cases with transmural arteritis or fibrinoid change and necrosis of medial smooth muscle cells (v3).~Borderline category is used when no intimal arteritis is present, but there are foci of mild tubulitis (1 to 4 mononuclear cells/tubular cross section)." (NCT00371826)
Timeframe: At Month 12

Intervention	Participants (Number)
	NO	Borderline	Grade IA	Grade IB	Grade IIA	Grade IIB	Grade III	Not Done
Calcineurin Inhibitor (CNI) Withdrawal	20	2	1	0	0	0	0	7
CNI+MPA+ Steroid	29	2	0	1	0	0	0	8
Steroid Withdrawal	5	2	0	0	0	0	0	3

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Number of Participants With Post Transplant Diabetes Mellitus (PTDM) and Impaired Fasting Glucose (12 Months Analysis)

"The symptoms of post transplant diabetes mellitus (PTDM) and impaired fasting glucose are defined as any of the following conditions:~Patients receiving glucose lowering treatment~Fasting plasma glucose (FPG) >= 126 mg/dL on 2 separate occasions~Hemoglobin subtype A1c (HbA1c) > 6.5%~Diabetes reported as treatment emergent AE with end date > Day 15" (NCT00371826)
Timeframe: At Month 12

Intervention	Participants (Number)
	Glucose lowering treatment	FPG >= 126 mg/dL on 2 separate occasions	HbA1c > 6.5%	Diabetes as treatment emergent AE	Any of the above symptoms
Calcineurin Inhibitor (CNI) Withdrawal	10	6	12	8	19
CNI+MPA+ Steroid	9	0	3	2	10
Steroid Withdrawal	5	5	5	3	8

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Number of Participants With Notable Abnormalities in Total Cholesterol and Triglycerides as Measurement of Effect of Treatment on Cardiovascular Health (36 Months Analysis)

"Notable abnormal total cholesterol is defined as : High: >= 9.1 mmol/L , normal range is 0.00 - 5.17 mmol/L~Notable abnormal triglycerides is defined as : High: >= 8.5 mmol/L, normal range is 0.30 - 2.00 mmol/L" (NCT00371826)
Timeframe: Overall Post Baseline up to month 36

Intervention	Participants (Number)
	Total Cholesterol: High	Triglycerides : High
Calcineurin Inhibitor (CNI) Withdrawal	6	0
CNI+MPA+ Steroid	0	1
Steroid Withdrawal	1	0

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Number of Participants With Notable Abnormalities in Total Cholesterol and Triglycerides as Measurement of Effect of Treatment on Cardiovascular Health (12 Months Analysis)

Intervention	Participants (Number)
	Total Cholesterol: High (n = 48, 47,30)	Triglycerides : High (n= 48, 46, 30)
Calcineurin Inhibitor (CNI) Withdrawal	6	1
CNI+MPA+ Steroid	0	0
Steroid Withdrawal	3	0

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Number of Participants With Notable Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) as Measurement of Effect of Treatment on Cardiovascular Health (36 Months Analysis)

"Notable abnormal systolic blood pressure is defined as :~Either an increase of >=30 that results in >=180 or >200 (mm/Hg)~OR a decrease of >=30 that results in <=90 or <75 (mm/Hg) from baseline~Notable abnormal diastolic blood pressure is defined as :~Either an increase of >=20 that results in >=105 or >115 (mm/Hg)~OR a decrease of >=20 that results in <=50 or <40 (mm/Hg) from baseline" (NCT00371826)
Timeframe: Baseline, Overall post baseline up to Month 36

Intervention	Participants (Number)
	SBP: >=180 mm/Hg or 200 mm/Hg	SBP: < = 90 mm/Hg or < 200 mm/Hg	DBP : >=105 mm/Hg or >115 mm/Hg	DBP: <=50 mm/Hg or <40 mm/Hg
Calcineurin Inhibitor (CNI) Withdrawal	3	1	2	1
CNI+MPA+ Steroid	4	0	5	4
Steroid Withdrawal	1	0	1	0

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Number of Participants With Notable Abnormal Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) as Measurement of Effect of Treatment on Cardiovascular Health (12 Months Analysis)

"Notable abnormal systolic blood pressure is defined as :~Either an increase of >=30 that results in >=180 or >200 (mm/Hg)~OR a decrease of >=30 that results in <=90 or <75 (mm/Hg)from baseline~Notable abnormal diastolic blood pressure is defined as :~Either an increase of >=20 that results in >=105 or >115 (mm/Hg)~OR a decrease of >=20 that results in <=50 or <40 (mm/Hg) from baseline" (NCT00371826)
Timeframe: Baseline, Overall post-baseline up to 12 month

Intervention	Participants (Number)
	SBP: >=180 mm/Hg or 200 mm/Hg	SBP: < = 90 mm/Hg or < 200 mm/Hg	DBP : >=105 mm/Hg or >115 mm/Hg	DBP: <=50 mm/Hg or <40 mm/Hg
Calcineurin Inhibitor (CNI) Withdrawal	5	1	3	1
CNI+MPA+ Steroid	5	0	6	4
Steroid Withdrawal	7	0	5	0

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Number of Participants With New Onset Diabetes Mellitus After Transplantation (NODAT) and Impaired Fasting Glucose (36 Months Analysis)

"The symptoms of new onset diabetes mellitus after transplantation (NODAT) and impaired fasting glucose are defined as any of the following conditions:~Patients receiving glucose lowering treatment~2 fasting plasma glucose (FPG) values >= 126 mg/dL or 2 random plasma glucose (RPG) values >= 200 mg/dL or FPG value >= 126 mg/dL and 1 RPG value >= 200 mg/dL~Diabetes reported as treatment emergent AE with end date > Day 15" (NCT00371826)
Timeframe: At Month 36

Intervention	Participants (Number)
	Glucose lowering treatment	FPG or RPG	Diabetes as treatment emergent AE	Any of the above symptoms
Calcineurin Inhibitor (CNI) Withdrawal	5	3	5	6
CNI+MPA+ Steroid	10	2	4	11
Steroid Withdrawal	2	1	2	2

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Number of Participants With Histological Evidence Chronic Allograft Nephropathy (CAN) (36 Months Analysis)

"Chronic rejection is characterized by a slow progressive decline in renal function and is typically preceded by the histological picture of chronic allograft nephropathy. The presence of biopsy confirmed Grade I, II or III chronic allograft nephropathy by Banff 97 criteria was assessed on all optional biopsies obtained for clinical suspicion of chronic rejection.~Data summarized by 3 categories. Yes - Patients with histological evidence of CAN ; No - Patients with histological evidence of CAN and Not Done - Central protocol defined kidney allograft biopsies were not done." (NCT00371826)
Timeframe: At Month 36

Intervention	Participants (Number)
	YES	NO	Not Done
Calcineurin Inhibitor (CNI) Withdrawal	2	8	8
CNI+MPA+ Steroid	1	16	14
Steroid Withdrawal	1	1	1

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Number of Participants With Histological Evidence Chronic Allograft Nephropathy (CAN) (12 Months Analysis)

"A per-protocol biopsy was performed at Baseline and Month 12 and read by an independent blinded pathologist in order to assess chronic allograft nephropathy. Chronic rejection is characterized by a slow progressive decline in renal function and is typically preceded by the histological picture of chronic allograft nephropathy. The presence of biopsy confirmed Grade I, II or III chronic allograft nephropathy by Banff 97 criteria was assessed on all optional biopsies obtained for clinical suspicion of chronic rejection.~Data summarized by 3 categories. Yes - Patients with histological evidence of CAN ; No - Patients with histological evidence of CAN and Not Done - Central protocol defined kidney allograft biopsies were not done." (NCT00371826)
Timeframe: At Month 12

Intervention	Participants (Number)
	YES	NO	Not Done
Calcineurin Inhibitor (CNI) Withdrawal	8	15	7
CNI+MPA+ Steroid	6	26	8
Steroid Withdrawal	2	5	3

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Number of Participants With Employment Status (36 Months Analysis)

"The various employment status reported are:~Employed/self employed full time~Employed part time~Unemployed~Homemaker~Volunteer~Permanently disabled~Non-permanently disable~Retired~Other" (NCT00371826)
Timeframe: At screening (at day 0 +/- 7 days ), At Month 36

Intervention	Participants (Number)
	Screening visit: Employed/self employed full time	Month 36: Employed/self employed full time	Screening visit: Employed part time	Month 36: Employed part time	Screening visit: Unemployed	Month 36: Unemployed	Screening visit: Homemaker	Month 36 : Homemaker	Screening visit: Permanently disabled	Month 36: Permanently disabled	Screening visit: Non-permanently disabled	Month 36: Non-permanently disabled	Screening visit: Retired	Month 36: Retired	Screening visit: Other	Month 36: Other
Calcineurin Inhibitor (CNI) Withdrawal	5	4	4	3	5	3	3	3	0	0	0	0	0	0	1	1
CNI+MPA+ Steroid	10	10	7	4	7	6	3	3	1	1	1	1	2	2	0	0
Steroid Withdrawal	1	1	0	0	1	0	1	1	0	0	0	0	0	0	0	0

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Number of Participants With Employment Status (12 Months Analysis)

Intervention	Participants (Number)
	Screening visit: Employed/self employed full time	Month 12: Employed/self employed full time	Screening visit: Employed part time	Month 12: Employed part time	Screening visit: Unemployed	Month 12: Unemployed	Screening visit: Homemaker	Month 12 : Homemaker	Screening visit: Volunteer	Month 12: Volunteer	Screening visit: Permanently disabled	Month 12: Permanently disabled	Screening visit: Non-permanently disabled	Month 12: Non-permanently disabled	Screening visit: Retired	Month 12: Retired	Screening visit: Other	Month 12: Other
Calcineurin Inhibitor (CNI) Withdrawal	18	6	9	3	10	6	3	2	1	1	2	1	1	1	4	1	1	1
CNI+MPA+ Steroid	21	14	7	5	8	1	5	5	0	0	2	2	2	0	2	2	0	0
Steroid Withdrawal	9	2	4	0	10	6	5	2	0	0	0	0	0	0	1	0	1	0

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Number of Participants With Composite Endpoint of Treatment Failure (36 Months Analysis)

"Composite endpoint of treatment failure includes biopsy-proven acute rejection (BPAR), graft loss, death and loss-to-follow-up. A BPAR is defined as a biopsy graded IA, IB, IIA, IIB, or III as per Banff 97 classification.~The allograft was presumed to be lost on the day the patient started dialysis and was not able to subsequently be removed from dialysis. If the patient underwent a graft nephrectomy, then the day of nephrectomy was the day of graft loss." (NCT00371826)
Timeframe: At Month 12, 24 and 36

Intervention	Participants (Number)
	At Month 12	At Month 24	At Month 36
Calcineurin Inhibitor (CNI) Withdrawal	4	6	7
CNI+MPA+ Steroid	4	6	10
Steroid Withdrawal	0	0	0

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Number of Participants With Biopsy Proven Acute Rejection (BPAR) Per Treatment Group (36 Months Analysis)

A biopsy-proven acute rejection is defined as a biopsy graded IA, IB, IIA, IIB, or III as per Banff 97 classification. (NCT00371826)
Timeframe: At Month 12, 24 and 36

Intervention	Participants (Number)
	At Month 12	At Month 24	At Month 36
Calcineurin Inhibitor (CNI) Withdrawal	4	5	6
CNI+MPA+ Steroid	4	5	8
Steroid Withdrawal	0	0	0

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Number of Participants With Biopsy Proven Acute Rejection (BPAR) Influenced by Demographic Characteristics and Morbidities (36 Months Analysis)

The influence of demographic characteristics and comorbidities on incidence of BPAR were analyzed in the following way: Demographic characteristics were age (<55 years, ≥55 years), Expanded Criteria Donor [ECD] organ (donor age >60 years or donor non heart-beating and donor age >50), gender, living vs. deceased donor, Body Mass Index (BMI) classes (underweight <18.5, normal 18.5 - <25.0, overweight 25.0 - <30.0, obesity 30.0 and above), years on dialysis before transplantation (<1, 1-5, >5 years). Comorbidities were diabetes, hypertension, cardiovascular diseases/events, nephrosclerosis, glomerulonephritis/glomerular disease, polycystic disease, and Cytomegalovirus status. (NCT00371826)
Timeframe: At Month 36

Intervention	Participants (Number)
	Age < 55 years	Age > = 55 years	ECD Organ	NO ECD Organ	Male	Female	Living donor	Deceased donor	BMI < 18.5	BMI 18.5 - <25	BMI 25 - <30	BMI >= 30	Years on dialysis before transplantation: None	< 1 Year on dialysis before transplantation	1 - 5 Years on dialysis before transplantation	> 5 Years on dialysis before transplantation	Diabetes mellitus: No	Diabetes mellitus: Yes	Hypertension: No	Hypertension: Yes	Cardiovascular disease : No	Cardiovascular disease: Yes	Nephrosclerosis: No	Nephrosclerosis: Yes	Glomerulonephritis/glomerular disease : No	Glomerulonephritis/glomerular disease: Yes	Cytomegalovirus : Negative	Cytomegalovirus : Positive
Calcineurin Inhibitor (CNI) Withdrawal	6	0	0	6	4	2	5	1	1	1	4	0	0	3	2	1	3	3	1	5	3	3	6	0	4	2	1	5
CNI+MPA+ Steroid	7	1	0	8	7	1	6	2	0	3	4	1	1	4	2	1	6	2	1	7	5	3	7	1	7	1	4	4
Steroid Withdrawal	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0

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Number of Participants With Biopsy Proven Acute Rejection (BPAR) Influenced by Demographic Characteristics and Morbidities (12 Months Analysis)

The influence of demographic characteristics and comorbidities on incidence of BPAR were analyzed in the following way: Demographic characteristics were age (<55 years, ≥55 years), Expanded criteria Donor (ECD) organ (donor age >60 years or donor non heart-beating and donor age >50), gender, living vs. deceased donor, Body Mass Index (BMI) classes (underweight <18.5, normal 18.5 - <25.0, overweight 25.0 - <30.0, obesity 30.0 and above), years on dialysis before transplantation (<1, 1-5, >5 years). Comorbidities were diabetes, hypertension, cardiovascular diseases/events, nephrosclerosis, glomerulonephritis/glomerular disease, polycystic disease, and Cytomegalovirus status. (NCT00371826)
Timeframe: At Month 12

Intervention	Participants (Number)
	Age < 55 years	Age > = 55 years	ECD Organ	NO ECD Organ	Male	Female	Living donor	Deceased donor	BMI < 18.5	BMI 18.5 - <25	BMI 25 - <30	BMI >= 30	Years on dialysis before transplantation: None	< 1 Year on dialysis before transplantation	1 - 5 Years on dialysis before transplantation	> 5 Years on dialysis before transplantation	Diabetes mellitus: No	Diabetes mellitus: Yes	Hypertension: No	Hypertension: Yes	Cardiovascular disease : No	Cardiovascular disease: Yes	Nephrosclerosis: No	Nephrosclerosis: Yes	Glomerulonephritis/glomerular disease : No	Glomerulonephritis/glomerular disease: Yes	Cytomegalovirus : Negative	Cytomegalovirus : Positive
Calcineurin Inhibitor (CNI) Withdrawal	11	4	3	12	11	4	9	6	0	5	8	2	1	3	8	3	10	5	2	13	4	11	15	0	8	7	2	13
CNI+MPA+ Steroid	5	1	0	6	6	0	6	0	1	2	3	0	0	3	1	2	4	2	1	5	3	3	6	0	5	1	2	4
Steroid Withdrawal	4	1	2	3	4	1	2	3	0	3	1	1	0	1	2	2	4	1	0	5	2	3	4	1	3	2	0	5

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Number of Participants With Any Wound Problems (36 Months Analysis)

Intervention	Participants (Number)
	At Month 12	At Month 24	At Month 36
Calcineurin Inhibitor (CNI) Withdrawal	6	9	10
CNI+MPA+ Steroid	11	13	13
Steroid Withdrawal	2	2	2

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Number of Participants With Antibody-mediated Rejection Per Treatment Group (36 Months Analysis)

(NCT00371826)
Timeframe: At Month 12, 24 and 36

Intervention	Participants (Number)
	At Month 12	At Month 24	At Month 36
Calcineurin Inhibitor (CNI) Withdrawal	1	1	1
CNI+MPA+ Steroid	0	0	2
Steroid Withdrawal	0	0	0

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Mean Urine Albumin/Creatinine Ratio [ACR] as Measurement of Proteinuria (36 Months Analysis)

Proteinuria is measured by spot morning urine Albumin/Creatinine Ratio [ACR]. When the ACR is more than or equal to 30 mg/mmol then it is known as proteinuria. (NCT00371826)
Timeframe: At Month 12, 18, 24 and 36

Intervention	mg/mmol (Mean)
	At 12 Month (n = 18, 32, 2)	At 18 Month (n= 17, 31, 2)	At 24 Month ( n= 16, 29, 1)	At 36 Month ( n= 15, 25, 0)
Calcineurin Inhibitor (CNI) Withdrawal	23.5	28.2	30.0	30.6
CNI+MPA+ Steroid	8.1	8.1	6.6	23.4
Steroid Withdrawal	4.8	5.3	7.0	NA

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Mean Short-form 36 Health Survey (SF-36) Score as a Measure of Quality of Life Assessment (36 Months Analysis)

"SF-36 measures impact of disease on overall quality of life (QoL). 36-item survey has 8 subscales. The 8 subscales are : Physical functioning (PF), Role-physical (RP), Bodily pain (BP), General health (GH), Vitality (VT), Social functioning (SF), Role-emotional (RE) and Mental health (MH).~Score for each sub-scale has been standardized with the use of norm-based methods based on assessment of the general U.S. population free of chronic conditions. Scores range from 1-100 with a mean=50 and a standard deviation=10. A higher score indicates less impact on QoL." (NCT00371826)
Timeframe: At Month 24

Intervention	units on a scale (Mean)
	Physical functioning (PF)	Role-physical (RP)	Bodily pain (BP)	General health (GH)	Vitality (VT)	Social Functioning (SF)	Role-emotional (RE)	Mental health (MH)
Calcineurin Inhibitor (CNI) Withdrawal	84.3	75.0	81.6	71.6	70.0	85.9	72.9	77.5
CNI+MPA+ Steroid	87.6	77.4	85.0	69.8	72.7	80.6	83.9	77.9
Steroid Withdrawal	90.0	100.0	84.0	67.0	60.0	68.8	33.3	62.0

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Mean Short-form 36 Health Survey (SF-36) Score as a Measure of Quality of Life Assessment (12 Months Analysis)

"SF-36 measures impact of disease on overall quality of life (QoL). 36-item survey has 8 subscales. The 8 subscales are: Physical functioning (PF), Role-physical (RP), Bodily pain (BP), General health (GH), Vitality (VT), Social functioning (SF), Role-emotional (RE) and Mental health (MH).~Score for eash sub-scale has been standardized with the use of norm-based methods based on assessment of the general U.S. population free of chronic conditions. Scores range from 1-100 with a mean=50 and a standard deviation=10. A higher score indicates less impact on QoL." (NCT00371826)
Timeframe: At Month 12

Intervention	units on a scale (Mean)
	Physical functioning (PF)	Role-physical (RP)	Bodily pain (BP)	General health (GH)	Vitality (VT)	Social Functioning (SF)	Role-emotional (RE)	Mental health (MH)
Calcineurin Inhibitor (CNI) Withdrawal	78.7	72.9	73.6	67.1	62.7	74.5	72.2	73.3
CNI+MPA+ Steroid	76.9	78.2	81.5	71.2	72.4	81.1	81.1	79.1
Steroid Withdrawal	82.0	100.0	96.8	86.8	85.0	97.5	100.0	92.8

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Mean Serum Creatinine (36 Months Analysis)

(NCT00371826)
Timeframe: At Month 12, 18, 24 and 36

Intervention	umol/L (Mean)
	At Month 12 (n= 23, 39, 4)	At Month 18 (n= 22, 36, 4)	At Month 24 (n = 23, 36, 4)	At Month 36 (n= 19, 35, 3)
Calcineurin Inhibitor (CNI) Withdrawal	112.7	113.6	119.9	119.4
CNI+MPA+ Steroid	123.0	121.4	123.7	131.8
Steroid Withdrawal	146.8	146.3	146.5	176.0

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Creatinine Clearance Calculated by the Cockcroft-Gault Formula (36 Months Analysis)

"Creatinine clearance were calculated according to the Cockcroft-Gault formula:~CrCl (males) = (140-A) × BW/(72 × Cr) CrCl (females) = CrCl (males) × 0.85 where A is age [years], BW is body weight [kg], and Cr is the serum concentration of creatinine [mg/dL].~The Cockcroft-Gault formula estimates creatinine clearance based on serum creatinine level, body weight, and age." (NCT00371826)
Timeframe: At Month 12, 24 and 36

Intervention	mL/min (Mean)
	At Month 12 (n= 23, 39, 4)	At Month 18 (n=22, 36, 4)	At Month 24 (n= 23, 36, 4)	At Month 36 (n= 23, 39, 4)
Calcineurin Inhibitor (CNI) Withdrawal	69.8	69.9	65.6	66.3
CNI+MPA+ Steroid	71.7	73.7	72.8	67.5
Steroid Withdrawal	63.7	66.2	63.7	62.7

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Change in Bone Mineral Density Between Week 2 and Month 24 (36 Months Analysis)

Measurements of bone mineral density (BMD) by Dual Energy X-ray Absorptiometry (DEXA) were done at Week 2 and Month 24. Change in BMD between week 2 and Month 24 were done for neck of femur and lumbar spine. (NCT00371826)
Timeframe: Week 2, Month 24

Intervention	g/cm^2 (Mean)
	Neck of Femur (Month 24- Week 2)	Lumbar Spine (Month 24 - Week 2)
Calcineurin Inhibitor (CNI) Withdrawal	0.2	-0.0
CNI+MPA+ Steroid	-0.1	-0.1
Steroid Withdrawal	-0.1	-0.0

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Calculated Glomerular Filtration Rate (cGFR) After Kidney Transplant to Evaluate Kidney Function (36 Months Analysis)

The glomerular filtration rate (GFR) was calculated by the Nankivell formula: GFR = 6.7 / Scr + BW / 4 - Surea / 2-100 / (height)^ 2 + C where Scr is the serum creatinine concentration expressed in mmol/L, BW the body weight in kg, Surea the serum urea in mmol/L, height in m, and the constant C is 35 for male and 25 for female patients. (NCT00371826)
Timeframe: At Month 24 and 36

Intervention	mL/min per 1.73 m^2 (Mean)
	Month 24 (n= 23, 36, 4)	Month 36 (n= 19, 35, 3)
Calcineurin Inhibitor (CNI) Withdrawal	69.5	71.6
CNI+MPA+ Steroid	71.8	69.1
Steroid Withdrawal	67.0	61.0

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Number of Participants With Erythropoietin Usage (36 Months Analysis)

(NCT00371826)
Timeframe: Month 36

Intervention	participants (Number)
Calcineurin Inhibitor (CNI) Withdrawal	5
CNI+MPA+ Steroid	7
Steroid Withdrawal	2

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Number of Participants With Erythropoietin Usage (12 Months Analysis)

(NCT00371826)
Timeframe: Month 12

Intervention	participants (Number)
Calcineurin Inhibitor (CNI) Withdrawal	20
CNI+MPA+ Steroid	10
Steroid Withdrawal	8

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Number of Participants With Composite Endpoint of Treatment Failure (12 Months Analysis)

Intervention	Participants (Number)
Calcineurin Inhibitor (CNI) Withdrawal	16
CNI+MPA+ Steroid	8
Steroid Withdrawal	11

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Number of Participants With Biopsy Proven Acute Rejection (BPAR) Per Treatment Group (12 Months Analysis)

A biopsy-proven acute rejection is defined as a biopsy graded IA, IB, IIA, IIB, or III as per Banff 97 classification. (NCT00371826)
Timeframe: At Month 12

Intervention	Participants (Number)
Calcineurin Inhibitor (CNI) Withdrawal	15
CNI+MPA+ Steroid	6
Steroid Withdrawal	5

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Number of Participants With Antibody-mediated Rejection Per Treatment Group (12 Months Analysis)

(NCT00371826)
Timeframe: At Month 12

Intervention	Participants (Number)
Calcineurin Inhibitor (CNI) Withdrawal	5
CNI+MPA+ Steroid	2
Steroid Withdrawal	2

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Number of Participants Hospitalized for Reasons Other Than Primary Transplantation (36 Months Analysis)

This analysis is reporting number of participants hospitalized for reasons (such as acute rejection, infection, gastrointestinal (GI) events, cardiovascular event, metabolic disorder and Other) other than primary transplantation. (NCT00371826)
Timeframe: Month 36

Intervention	Participants (Number)
Calcineurin Inhibitor (CNI) Withdrawal	16
CNI+MPA+ Steroid	30
Steroid Withdrawal	1

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Number of Participants Hospitalized for Reasons Other Than Primary Transplantation (12 Months Analysis)

Intervention	Participants (Number)
Calcineurin Inhibitor (CNI) Withdrawal	34
CNI+MPA+ Steroid	31
Steroid Withdrawal	13

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Mean Urine Albumin/Creatinine Ratio (ACR) as Measurement of Proteinuria (12 Months Analysis)

Proteinuria is measured by spot morning urine Albumin/Creatinine Ratio [ACR]. When the ACR is more than or equal to 30 mg/mmol then it is known as proteinuria. (NCT00371826)
Timeframe: At Month 12

Intervention	mg/mg (Mean)
Calcineurin Inhibitor (CNI) Withdrawal	0.2
CNI+MPA+ Steroid	0.1
Steroid Withdrawal	0.1

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Mean Serum Creatinine (12 Months Analysis)

(NCT00371826)
Timeframe: At Month 12

Intervention	umol/L (Mean)
Calcineurin Inhibitor (CNI) Withdrawal	118.9
CNI+MPA+ Steroid	161.0
Steroid Withdrawal	148.6

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Creatinine Clearance (CrCl) Calculated by the Cockcroft-Gault Formula (12 Months Analysis)

Intervention	mL/min (Mean)
Calcineurin Inhibitor (CNI) Withdrawal	66.1
CNI+MPA+ Steroid	67.8
Steroid Withdrawal	63.2

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Calculated Glomerular Filtration Rate (cGFR) After Kidney Transplant to Evaluate Kidney Function (12 Months Analysis)

Intervention	mL/min per 1.73 m^2 (Mean)
Calcineurin Inhibitor (CNI) Withdrawal	65.2
CNI+MPA+ Steroid	69.3
Steroid Withdrawal	66.9

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Number of Patient Survival and Graft Survival (36 Months Analysis)

(NCT00371826)
Timeframe: At Month 12, 24 and 36

Intervention	Participants (Number)
	Month 12: Patient Survival	Month 12: Graft Survival	Month 24: Patient Survival	Month 24: Graft Survival	Month 36: Patient Survival	Month 36: Graft Survival
Calcineurin Inhibitor (CNI) Withdrawal	23	23	23	23	23	23
CNI+MPA+ Steroid	39	39	39	39	39	39
Steroid Withdrawal	4	4	4	4	4	4

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Number of Patient Survival and Graft Survival (12 Months Analysis)

(NCT00371826)
Timeframe: At Month 12

Intervention	Participants (Number)
	Patient Survival	Graft Survival
Calcineurin Inhibitor (CNI) Withdrawal	49	49
CNI+MPA+ Steroid	46	45
Steroid Withdrawal	30	30

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Progression-free Survival

(NCT00374140)
Timeframe: From entry into trial to up to 60 months

Intervention	months (Median)
RAD001 (Everolimus)	1.3

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Overall Survival

(NCT00374140)
Timeframe: From entry in trial to up to 60 months

Intervention	months (Median)
RAD001 (Everolimus)	6.7

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Objective Response Rate

Number of patients for which response to treatment was observed / total number of patients. (NCT00374140)
Timeframe: From beginning of treatment up to 60 months

Intervention	percentage of participants (Number)
RAD001 (Everolimus)	3

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Determine the Proportion of Previously Treated Small Cell Lung Cancer (SCLC) Patients Whose Disease Has Not Progressed Following 6-weeks (2 Cycles) of Treatment With RAD001.

(NCT00374140)
Timeframe: Two cycles of treatment with RAD001 (~6 weeks)

Intervention	percentage of participants (Number)
RAD001 (Everolimus)	26

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Number of Patients With Biopsy-proven Acute Rejection From Month 12 to End of Study (Month 24)

Biopsy-proved acute rejection was defined as a treated acute rejection confirmed by biopsy, graded locally according to the International Society for Heart & Lung Transplantation (ISHLT) criteria. A treated acute rejection was defined as an acute rejection clinically suspected, whether biopsy-proven or not, which had been treated and confirmed by the investigator according to the response to therapy. (NCT00377962)
Timeframe: Month 12 to end of study (Month 24)

Intervention	Participants (Number)
Everolimus + CNI Reduction	6
Control	5

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Number of Patients in Need of Dialysis From Month 12 to End of Study (Month 24)

(NCT00377962)
Timeframe: Month 12 to end of study (Month 24)

Intervention	Participants (Number)
Everolimus + CNI Reduction	0
Control	2

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Mean Days of Hospitalization From Baseline to End of Study (Month 24)

(NCT00377962)
Timeframe: Baseline to end of study (Month 24)

Intervention	Days (Mean)
Everolimus + CNI Reduction	8.5
Control	16.2

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Change in Forced Vital Capacity (FVC) From Baseline to End of Study (Month 24) in the Lung Transplant Subgroup

Forced vital capacity (FVC) was measured by spirometry conducted according to internationally accepted standards. FVC is the volume delivered during an expiration made as forcefully and completely as possible starting from full inspiration. A positive change score indicates improved lung function. (NCT00377962)
Timeframe: Baseline to end of study (Month 24)

Intervention	Liters (Mean)
Everolimus + CNI Reduction	-0.2
Control	-0.1

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Change in Forced Expiratory Volume in 1 Second (FEV1) From Baseline to End of Study (Month 24) in the Lung Transplant Subgroup

Forced expiratory volume in 1 second (FEV1) was measured by spirometry conducted according to internationally accepted standards. FEV1 is the volume delivered in the first second of a forced vital capacity (FVC) maneuver. A positive change score indicates improved lung function. (NCT00377962)
Timeframe: Baseline to end of study (Month 24)

Intervention	Liters (Mean)
Everolimus + CNI Reduction	-0.2
Control	-0.1

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Number of Patients Who Died and Number of Patients With Graft Loss From Month 12 to End of Study (Month 24)

Number of patients not alive and number of patients with loss of their graft. (NCT00377962)
Timeframe: Month 12 to end of study (Month 24)

Intervention	Participants (Number)
	Death	Graft Loss
Control	0	0
Everolimus + CNI Reduction	3	0

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Change in Measured Glomerular Filtration Rate (mGFR) From Baseline to Month 12

Renal function was assessed by determining the measured glomerular filtration rate (mGFR) using creatinine ethylenediamine tetraacetic acid (Cr-EDTA) clearance or an equivalent method. A positive change score indicates improved renal function. (NCT00377962)
Timeframe: Baseline to Month 12

Intervention	mL/min (Mean)
	Baseline	Month 12	Change from Baseline
Control	48.0	47.5	-0.5
Everolimus + CNI Reduction	48.6	53.2	4.6

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Change in Left Ventricular Function (Diameter and Thickness Parameters) From Baseline to End of Study (Month 24) in the Heart Transplant Subgroup

Left ventricular function was assessed by echocardiography which was performed according to local routine practice. Echocardiography parameters were left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), interventricular septal wall thickness (IVSTd), and posterior wall thickness (PWTd). A positive change score indicates improved left ventricular function. (NCT00377962)
Timeframe: Baseline to end of study (Month 24)

Intervention	cm (Mean)
	LVEDD	LVESD	IVSTd	PWTd
Control	-0.0	0.1	-0.1	-0.1
Everolimus + CNI Reduction	-0.1	0.1	-0.4	-0.5

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Change in Left Ventricular Function (Filling and Ejection Fraction Parameters) From Baseline to End of Study (Month 24) in the Heart Transplant Subgroup

Left ventricular function was assessed by echocardiography which was performed according to local routine practice. Echocardiography parameters were filling fraction (FF) and ejection fraction (EF). A positive change score indicates improved left ventricular function. (NCT00377962)
Timeframe: Baseline to end of study (Month 24)

Intervention	percentage (Mean)
	EF	FF
Control	0.1	0
Everolimus + CNI Reduction	-0.6	0

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Change in Measured Glomerular Filtration Rate (mGFR) From Baseline to End of Study (Month 24)

Intervention	mL/min (Mean)
	Month 0	Month 24	Change
Control	49.1	46.8	-2.4
Everolimus + CNI Reduction	49.3	52.5	3.2

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Number of Patients Discontinued From the Study Due to Adverse Events From Month 12 to End of Study (Month 24)

(NCT00377962)
Timeframe: Month 12 to end of study (Month 24)

Intervention	Participants (Number)
	Total discontinued due to AE(s)	Pulmonary embolism	Skin problems	Hypercholesterolemia	Stroke	Muscular pain	Diarrhea	Edema
Control	0	0	0	0	0	0	0	0
Everolimus + CNI Reduction	8	2	1	1	1	1	1	1

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Change in Serum Creatinine From Baseline to End of Study (Month 24)

Renal function was assessed by determining serum creatinine using standard laboratory methods. A positive change score indicates improved renal function. (NCT00377962)
Timeframe: Baseline to end of study (Month 24)

Intervention	μmol/L (Mean)
	Month 0	Month 24	Change
Control	129	132	3
Everolimus + CNI Reduction	126	126	0

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Number of Patients Who Experienced Adverse Events, Serious Adverse Events and Death

Patients with all (serious and non-serious) adverse events, serious adverse events and death were reported. (NCT00378014)
Timeframe: Month 12 to Month 59 post-baseline

Intervention	Number of participants (Number)
	Adverse Events (serious and non-serious)	Serious Adverse Events	Deaths
Calcineurin Inhibitor (CNI)	40	28	2
Everolimus	41	26	1

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Incidence of Efficacy Failure

Efficacy failure was defined as the composite endpoint of biopsy-proven acute rejection (BPAR), graft loss, death, lost to follow-up (from any reason), whichever occurred first. Incidence of efficacy failure was estimated using crude rate estimation (relative frequency). (NCT00378014)
Timeframe: Month 11

Intervention	Percentage of participants (Number)
Everolimus	20.8
Calcineurin Inhibitor (CNI)	20.4

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Incidence of the Need for a Change in the Immunosuppressive Regimen

The incidence of any changes in the immunosuppressive regimen other than allowed in the study protocol (for example, introduction of Mycophenolic acid (MPA) or sirolimus) was estimated using crude rate estimation (relative frequency). (NCT00378014)
Timeframe: Month 11

Intervention	Percentage of participants (Number)
Everolimus	80.2
Calcineurin Inhibitor (CNI)	73.5

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Patient and Graft Survival

Patient survival was defined as the time from date of randomization to date of death from any cause. If a patient was not known to have died, patient survival was censored as the date of last contact. Graft survival was defined as the time from the date of randomization to the date of graft loss. If a patient was not known to suffer from a graft loss or died without graft loss, time to graft loss was censored with date of last contact or date of death, respectively. Patient and graft survival were analyzed using the Kaplan Meier method. (NCT00378014)
Timeframe: Month 11

Intervention	Percentage of Participants (Number)
	Death	Graft loss
Calcineurin Inhibitor (CNI)	4.1	2.1
Everolimus	4.3	2.2

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Renal Function (cGFR)

This outcome measure evaluated renal function by assessing the calculated GFR based on the Cockcroft-Gault formula. (NCT00378014)
Timeframe: Month 5

Intervention	mL/min (Mean)
Everolimus	88.7
Calcineurin Inhibitor (CNI)	82.9

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Hepatitis C Virus (HCV) Replication in HCV-positive Patients

HCV ribonucleic acid (RNA) was measured by real time reverse transcriptase polymerase chain reaction (PCR; copies per mL). (NCT00378014)
Timeframe: Baseline, Month 5

Intervention	Percentage of participants (Number)
	Baseline, negative	Baseline, positive	Baseline, not done	Month 5, negative	Month 5, positive	Month 5, not done
Calcineurin Inhibitor (CNI)	55.3	0.0	44.7	38.2	13.2	48.7
Everolimus	64.5	0.0	35.5	62.9	1.6	35.5

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Number of Patients Who Experienced Adverse Events, Serious Adverse Events and Death

Patients with all (serious and non-serious) adverse events, serious adverse events and death were reported. (NCT00378014)
Timeframe: From randomization to Month 11

Intervention	Number of participants (Number)
	Adverse Events (serious and non-serious)	Serious Adverse Events	Deaths
Calcineurin Inhibitor (CNI)	96	58	4
Everolimus	98	67	4

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Incidence of Treated BPAR

The incidence of treated BPAR was estimated using crude rate estimation (relative frequency). (NCT00378014)
Timeframe: Month 11

Intervention	Percentage of Participants (Number)
Everolimus	13.5
Calcineurin Inhibitor (CNI)	10.2

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Calculated Glomerular Filtration Rate (cGFR)

This outcome measure evaluated renal function by assessing the calculated GFR based on the Cockcroft-Gault formula. (NCT00378014)
Timeframe: Month 11

Intervention	mL/min (Mean)
Everolimus	87.9
Calcineurin Inhibitor (CNI)	84.1

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Response Rate: The Total Number of Participants With Progression of Disease

"To determine response rate and time to tumor progression of patients with colorectal cancer and mutations in the PI3KCA gene who are treated with RAD001. Response and progression will be evaluated in this study using the international criteria proposed by the Response Evaluation Criteria in Solid Tumors (RECIST) Committee.~Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions assessed by CT (or MRI): Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesion. 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 lesion.~The outcome measure will be the total number of subjects who show progression of disease." (NCT00390364)
Timeframe: 1 month

Intervention	participants with progression of disease (Number)
RAD0001	1

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Progression-Free Survival for Patients Treated at MTD/Phase II Dose Level

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. Progression-free survival was defined as the interval from the date of study entry until the date of tumor progression or death for the patients treated at the MTD/Phase II dose level. This outcome measure is reported for all patients treated at the same dose level and is not separated into Phase I and Phase II. The phase I and phase II results are not separated out as the timing of their enrollment (early in phase 1 or later phase II) is not relevant to the outcome measure. (NCT00392821)
Timeframe: 18 months

Intervention	Months (Median)
RAD001 and Sorafenib	5.45

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Overall Response Rate (ORR) of Patients Treated at MTD/Phase II Dose Level

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI or CT: 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 Rate (ORR) = Percentage of Patients Who Experience an Objective Response (CR+ PR) to Treatment. In oncology, this outcome measure is reported for all patients treated at the same dose level and is not separated into Phase I and Phase II. The phase I and phase II results are not separated out as the timing of their enrollment (early in phase 1 or later phase II) is not relevant to the outcome measure. (NCT00392821)
Timeframe: 18 months

Intervention	percentage of evaluable patients (Number)
RAD001 and Sorafenib	13

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Clinical Response as Assessed Metabolically by Changes in Positron Emission Tomography (PET) Scan Between Baseline and Immediately Prior to Surgery.

All patients had baseline imaging in a fasted state with 18F-2-fluoro-2-deoxy-D-glucose fluorodeoxyglucose (18FDG)-PET scan and a repeat scan at 3 to 4 weeks later using routine clinical protocol for patient preparation, radiotracer administration and data acquisition. The repeat imaging occurred no longer than 24 hours before surgical resection. (NCT00401778)
Timeframe: Day 21

Intervention	percentage of patients (Number)
	Stable metabolic disease (SMD)	Progressive metabolic disease (PM)
Control	78	22
Everolimus 10 mg	50	50
Everolimus 5 mg	64	36

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Effects of RAD001 on the Regulation of Key Proteins Involved With the Mammalian Target of Rapamycin (mTOR) Axis in Tumor Specimens and Buccal Mucosa in Patients With Operable Non-small Cell Lung Cancer (NSCLC).

Changes in the expression of key signaling proteins in the mTOR/phosphatidylinositol 3-kinase (PI3K) pathway were determined by immunohistochemistry using previously published protocols and manufacturers' recommendations for antigen retrieval and antibody dilution along with positive and negative controls. Two investigators assessed protein expression jointly by light microscopy. The degree of expression was assessed by intensity (0, 1+, 2+, 3+) and percentage of cell staining in line with published algorithm. A derivative score (immunoscore) ranging between 0 and 300 was calculated as the product of intensity and percent cell staining. (NCT00401778)
Timeframe: 6 months

Intervention	% change in immunoscore (Mean)
	S6	pS6	pS6/S6	pMTOR	p4E-BP1	p70s6k	p70s6k Cytoplasmic	p70s6k Nuclear	pe1f4e	PAKT Nuclear	PAKT Cytoplasmic	Bim
Control	-36.06	-41.25	-85.75	-6.58	-95.37	25	-19.17	-3.33	-50	-33.33	200	-11.76
Everolimus 10 mg	-77.03	-47.21	128.57	-63.82	-78.75	-78.62	305.37	223.43	-27.13	0	-25	-21.76
Everolimus 5 mg	-13.69	-61.57	-100	30	150	137.14	0.56	135	2.78	NA	NA	NA

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Duration of Hospital Stay Following Surgery.

(NCT00401778)
Timeframe: 6 months

Intervention	days (Median)
Control	5
Everolimus 5 or 10 mg	5

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Time to Progression:Time Period (in Months) From Study Entry Until Disease Progression, Death, or Last Date of Contact.

"Period from study entry until disease progression, death, or last date of contact.~Progressive Disease: Appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions." (NCT00406276)
Timeframe: 6 months

Intervention	Months (Median)
Docetaxel/RAD001	4.42

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Number of Subjects Showing Partial Response and Stable Disease With the Combination of RAD001 and Docetaxel.

"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 of LD.~Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for Progressive disease (PD), taking as reference the smallest sum Longest diameter(LD) since treatment started." (NCT00406276)
Timeframe: 6 weeks

Intervention	participants (Number)
	Partial response	Stable disease	Disease Progression
Docetaxel/RAD001	2	15	7

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To Assess the Safety of RAD001 in Patients With Metastatic Pancreatic Cancer

Patients were followed for the duration of their time on treatment and 30 days after their last dose of RAD001. The number of patients with treatment-related adverse events are reported. (NCT00409292)
Timeframe: Patients were followed for the duration of their time on treatment and 30 days after their last dose of RAD001.

Intervention	participants (Number)
RAD001	33

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to Assess Overall Survival Associated With RAD001 in This Patient Population.

Overall survival was defined as the time from study entry until death from any cause. (NCT00409292)
Timeframe: 2 years

Intervention	months (Median)
RAD001	4.5

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To Assess Progression-free Survival of RAD001 at Two Months in Patients With Metastatic Pancreatic Cancer Whose Disease Has Progressed on Gemcitabine Chemotherapy.

"The Outcome Measure is reporting the number of participants experiencing Progression-free Survival at 2 months after treatment.~The study was designed with a primary end point of progression-free survival (PFS), defined as the time from study entry to documentation of progressive disease or death from any cause. On the basis of prior studies of second-line treatment in metastatic pancreatic cancer, we estimated that such treatment has been associated with a median PFS of 2 months. Our study design used a one-stage design with a target accrual of 35 eligible patients, with the assumption that an improvement in PFS at 2 months from 50% to 71% would warrant further study in this patient population." (NCT00409292)
Timeframe: two months

Intervention	participants (Number)
RAD001	23

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to Assess Response Rate Associated With RAD001 in This Patient Population.

The secondary objectives of the study were to assess tumor response rate and overall survival. Patients were required to have measurable disease per Response Evaluation Criteria in Solid Tumors (RECIST). Per RECIST, for target lesions assessed by CT: Complete Response (CR) is Disappearance of all target lesions; Partial Response (PR) is >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) equals CR + PR. (NCT00409292)
Timeframe: 2 years

Intervention	participants (Number)
	Stable Disease as Best Response	Progressive Disease as Best Response
RAD001	7	22

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Time to Definitive Deterioration of the FKS-DRS Risk Score by at Least 2 Score Units Using Kaplan-Meier Method, by Treatment.

"The Functional Assessment of Cancer Therapy - Kidney Symptom Index, Disease Related Symptoms (FKSI-DRS) is a set of items to assess symptoms experienced by patients with advanced kidney cancer. These symptoms include fatigue, pain, weight loss, dyspnea, cough, fever and hematuria. There were 4 response categories (1=Not at all, 2= A little, 3=Quite a bit, 4=Very much), sum of item responses can range from 0 to 36. 0= severely symptomatic patient and the highest score is an asymptomatic patient. Definitive deterioration of the FKSI-DRS score was defined as a decrease by at least 2 units compared to baseline, with no later increase above this threshold observed during the study. A single measure reporting a decrease of at least 2 units was considered definitive only if it is the last one available for the patient. Time to definitive deterioration is the number of days between the date of randomization and the date of the assessment at which definitive deterioration is seen." (NCT00410124)
Timeframe: "Baseline and every 28 days under treatment and at discontinuation from RAD001 until 28Feb2008 cutoff date"

Intervention	months (Median)
RAD001 +BSC	4.76
Placebo + BSC	3.84

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Progressive Free Survival (PFS) in Patients Who Receive RAD001 Plus Best Supportive Care(BSC) Versus Patients Who Receive Matching Placebo Plus BSC

Progression Free survival is defined as the time from randomization to the date of first documented disease progression or death from any cause. The primary statistical analysis of PFS was based on central radiological assessments using a one-sided stratified log-rank test. Radiological assessments: every 8 weeks (+/-1 week) during the first year and every 12 weeks (+/- 1 week) during the second year and thereafter and at the end of the study. Kaplan-Meier methodology was used to estimate the median PFS for each treatment group. (NCT00410124)
Timeframe: Time from randomization to dates of disease progression, death from any cause or last tumor assessment reported between date of first patient randomized until 28Feb2008 cut of date.

Intervention	Months (Median)
RAD001 +BSC	4.90
Placebo + BSC	1.87

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Overall Survival (OS) Assessed by the Monthly Overall Survival Assessments

Overall survival (OS) was defined as the time from date of randomization to date of death due to any cause. Kaplan-Meier methodology was used to estimate the median overall survival for each treatment group (NCT00410124)
Timeframe: Assessed every month up to 2 years after the last patient was randomized into the study from the date of randomization to the time of death. (Data cutoff was 15Nov2009)

Intervention	Months (Median)
RAD001 +BSC	13.57
Placebo + BSC	13.01

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Pharmacokinetics of RAD001: Time of the Last Quantifiable Concentration in a Dosing Interval - (Tlast)

Blood samples will be collected by direct venipuncture during regularly scheduled visits according to the collection plan provided in the study protocol. (NCT00410124)
Timeframe: At pre-dose and post-dose: 1 hour, 2 hour, 5 hour, 24 hour of Cycle 1 Day 1, Cycle 1 Day 15 and at pre-dose from Cycle 2 (Day 1) and all subsequent treatment cycles until data cut-off 28Feb2008.

Intervention	hour (Median)
Day 1	24.0
Day 15	24.0

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Pharmacokinetics of RAD001: Time at Which C-Max Occurs (t-Max)

Blood samples will be collected by direct venipuncture during regularly scheduled visits according to the collection plan provided in the study protocol. (NCT00410124)
Timeframe: At pre-dose and post-dose: 1 hour, 2 hour, 5 hour, 24 hour of Cycle 1 Day 1, Cycle 1 Day 15 and at pre-dose of From Cycle 2 (Day 1) and all subsequent treatment cycles until data cut-off 28Feb2008.

Intervention	h (Median)
Day 1	1.0
Day 15	1.0

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Pharmacokinetics of RAD001: Normalized to Body Surface Area (CL/F)

Intervention	L/hour/m^2 (Mean)
Day 15	7.5

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Pharmacokinetics of RAD001: Area Under Curve (AUC) in a Dosing Interval From Time-zero to Time of the Last Quantifiable Concentration. (AUC 0-tlast)

Intervention	ng.h/mL (Mean)
Day 1	455.0
Day 15	729.1

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Duration of Response in Patients Who Receive RAD001 Plus BSC Versus Placebo Plus BSC

Duration of overall response (CR or PR) applies only to patients whose Best Overall Response (BOR) was Complete Response (CR) or Partial Response (PR). The start date is the date of first documented response (CR or PR) and the end date is the date of event defined as the first documented progression or death. Radiological assessments: every 8 weeks (+/-1 week) during the first year and every 12 weeks (+/- 1 week) during the second year and thereafter and at the end of the study. (NCT00410124)
Timeframe: Time from randomization to dates of disease progression, death from any cause or last tumor assessment reported, between date of first patient randomized until 28Feb2008 cutoff date

Intervention	months (Median)
RAD001 +BSC	NA

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Best Overall Response Rate in Patients Who Receive RAD001 Plus BSC Versus Matching Placebo Plus BSC

The Best Overall Response rate (BOR) is defined as the percentage of patients having achieved confirmed Complete Response + Partial Response. Complete Response (CR) = at least two determinations of CR at least 4 weeks apart before progression. • Partial response (PR) = at least two determinations of PR or better at least 4 weeks apart before progression. Radiological assessments: every 8 weeks (+/-1 week) during the first year and every 12 weeks (+/- 1 week) during the second year and thereafter and at the end of the study. (NCT00410124)
Timeframe: Time from randomization to dates of disease progression, death from any cause or last tumor assessment reported, between date of first patient randomized until 28Feb2008 cutoff date

Intervention	Percentage of Participants (Number)
RAD001 +BSC	1.8
Placebo + BSC	0.0

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Analysis of Time to Definitive Deterioration of the Global Health Status/QoL Scale(QL) Scores of the EORTC QLQ-30 Questionnaire by at Least 10 Percent Using Kaplan Meier Method, by Treatment.

The European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) contains 30 items. These include a global health status/QoL scale, five functional scales, three symptom scales, and six single items. Global health status / QoL scale (QL), consisting of 2 questions each scored from 1 (very poor) to 7 (excellent), and with possible scores ranging from 2 to 14. Higher score indicates better functioning. Definitive deterioration by at least 10% is defined as a decrease in score by at least 10% compared to baseline, with no increase above this threshold observed during the course of the study. A single measure reporting a decrease of at least 10% is considered definitive only if it is the last one available for the patient. Time to definitive deterioration is the number of days between the date of randomization and date of assessment at which definitive deterioration is seen. (NCT00410124)
Timeframe: "Baseline and every 28 days under treatment and at discontinuation from RAD001 until 28Feb2008 cutoff date"

Intervention	months (Median)
RAD001 +BSC	4.76
Placebo + BSC	3.91

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Pharmacokinetics of RAD001: Apparent Systemic Clearance From Blood Following Extravascular Administration (CL/F)

Blood samples will be collected by direct venipuncture during regularly scheduled visits according to the collection plan provided in the study protocol.Apparent oral clearance of RAD001 (CL/F) was calculated using AUC in a dosing interval of 24 hours (AUC0-24hours) value on Day 15 as: CL/F = dose/ AUC0-τ (NCT00410124)
Timeframe: At pre-dose and post-dose: 1 hour, 2 hour, 5 hour, 24 hour of Cycle 1 Day 1, Cycle 1 Day 15 and at pre-dose from Cycle 2 (Day 1) and all subsequent treatment cycles until data cut-off 28Feb2008.

Intervention	L/hour (Mean)
Day 15	15.4

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Pharmacokinetics of RAD001:Peak Concentration in a Dosing Interval (C-max); Pre-dose Concentration at 24-h Time Point in Dosing Interval (C-min) and Average Concentration in a Dosing Interval =(C-avg)

Blood samples will be collected by direct venipuncture during regularly scheduled visits according to the collection plan provided in the study protocol. C-avg= Area under curve (AUC) in a dosing interval from time-zero to time of the last quantifiable concentration (AUC0-tlast)/ time of the last quantifiable concentration in a dosing interval (tlast) (NCT00410124)
Timeframe: At pre-dose and post-dose: 1 hour, 2 hour, 5 hour, 24 hour of Cycle 1 Day1, Cycle 1 Day 15 and at pre-dose from Cycle 2(day1) and all subsequent treatment cycles up until data cut-off 28 Feb 2008.

Intervention	ng/mL (Mean)
	C-max	C-min	C-avg
Day 1	68.1	7.9	19.0
Day 15	76.7	19.8	30.4

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Time to Definitive Deterioration of the Physical Functioning Scale (PF)Score of the EORTC QLQ-C30 Questionnaire by at Least 10 Percent Using Kaplan_Meier Method, by Treatment.

The EORTC QLQ-C30 contains 30 items. These include five functional scales (physical, role, emotional, social and cognitive functioning), three symptom scales fatigue, pain, nausea, and vomiting), a global health status/QoL scale, and six single items (dyspnea, diarrhea, constipation, anorexia, insomnia and financial impact). Physical Functioning (PF) sub-scale, consisting of 5 questions each scored from 1 (not at all) to 4 (very much), and with possible values ranging from 5 to 20. Definitive deterioration by at least 10% is defined as a decrease in score by at least 10% compared to baseline, with no later increase above this threshold observed during the course of the study. A single measure reporting a decrease of at least 10% is considered definitive only if it is the last one available for the patient. Time to definitive deterioration is the number of days between the date of randomization and the date of the assessment at which definitive deterioration is seen. (NCT00410124)
Timeframe: "Baseline and every 28 days under treatment and at discontinuation from RAD001 until 28Feb2008 cutoff date"

Intervention	months (Median)
RAD001 +BSC	5.06
Placebo + BSC	4.57

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Overall Reduction in SEGA Tumor Volume.

(NCT00411619)
Timeframe: During the entire study

Intervention	participants (Number)
	# with reductions > 30% relative to baseline	# with reductions > 50% relative to baseline
Everolimus	14	12

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Number With Observed Adverse Side Effects

(NCT00411619)
Timeframe: During the entire study

Intervention	participants (Number)
	Upper Respiratory Tract Infection	Stomatitis	Sinusitis	Mouth Ulceration	Cellulitis	Diarrhoea	Gastroenteritis	Otitis Media	Pyrexia	Vomiting	Acne	Convulsion	Nasopharyngitis	Rhinitis Allergic	Conjunctivitis	Pharyngitis	Rash	Constipation	Cough	Dermatitis Acneiform	Dermatitis Contact	Excoriation	Laceration	Nasal Congestion	Otitis Externa	Abnormal Behaviour	Body Tinea	Dry Skin	Pneumonia	Skin Infection	Urinary Tract Infection
Everolimus	26	25	15	14	12	12	12	11	10	10	9	9	9	9	8	8	8	7	7	7	7	7	7	7	7	6	6	6	6	6	6

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Overall Survival Using Kaplan-Meier Methodology

Overall survival was defined as the time from the date of randomization to the date of death from any cause. If a patient was not known to have died, survival was censored at the date of last contact. Kaplan-Meier methodology was used to estimate the median overall survival for each treatment group. (NCT00412061)
Timeframe: Months 12, 24, 36, 48

Intervention	Percentage of Participants (Number)
	12 Months	24 Months	36 Months	48 Months
Octreotide+ Everolimus	80.5	57.0	42.9	38.0
Octreotide+ Placebo Followed by Open Label Arm	81.8	63.6	48.5	41.6

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Progression Free Survival (PFS) as Per Adjudicated Central Review by Baseline 5-hydroxyindoleacetic Acid (5-HIAA) Level

5-HIAA levels in urine are frequently elevated in patients with advanced carcinoid tumors. Baseline levels of 5-HIAA in urine were defined as 'High' if they exceeded the median value, and 'Low' if they were lower than or equal to the median. (NCT00412061)
Timeframe: If elevated at baseline, evaluated every cycle visit (28 days/cycle) reported between day of first patient randomised, 10 January 2007, until cut-off date 02 April 2010

Intervention	Months (Median)
	5-HIAA <=median (n=93,96)	5-HIAA > median (n=94,95)
Octreotide+ Everolimus	21.75	13.83
Octreotide+ Placebo	13.90	8.41

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Number of Patients With Adverse Events (AEs), Clinically Notable AE, Death, Serious Adverse Events (SAEs) (Double-Blind Phase)

AEs are defined as any unfavorable and unintended diagnosis, symptom, sign (including an abnormal laboratory finding), syndrome or disease which either occurs during study, having been absent at baseline, or, if present at baseline, appears to worsen. SAEs are any untoward medical occurrences that result in death, are life threatening, require (or prolong) hospitalization, cause persistent or significant disability/incapacity, result in congenital anomalies or birth defects, or are other conditions which in judgment of investigators represent significant hazards. (NCT00412061)
Timeframe: From first day of treatment up to 28 days after last day of treatment in double blind

Intervention	Patients (Number)
	Clinically notable AE	Grade 3-4 Adverse Events	On treatment death	Serious adverse events
Octreotide+ Everolimus	208	162	19	126
Octreotide+ Placebo	146	109	11	74

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Progression Free Survival (PFS) as Per Adjudicated Central Radiology Review

Progression free survival (PFS) is defined as the time from randomization to the date of first documented disease progression or death from any cause. The primary analysis of PFS was based on the independent central adjudicated assessment using Kaplan-Meier method. (NCT00412061)
Timeframe: Time from randomisation to dates of disease progression, death from any cause or last tumor assessment, reported between day of first patient randomised, 10 January 2007, until cut-off date 02 April 2010

Intervention	Months (Median)
Octreotide+ Everolimus	16.43
Octreotide+ Placebo	11.33

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Best Overall Response Rate as Per Adjudicated Central Radiology Review Based on Response Evaluation Criteria in Solid Tumors (RECIST)

The best overall response rate is defined as the percentage of patients having achieved confirmed Complete Response + Partial Response. Complete Response (CR) = at least two determinations of CR at least 4 weeks apart before progression. • Partial response (PR) = at least two determinations of PR or better at least 4 weeks apart before progression. (NCT00412061)
Timeframe: Time from randomisation to dates of disease progression, death from any cause or last tumor assessment, reported between day of first patient randomised, 10 January 2007, until cut-off date 02 April 2010

Intervention	Percentage of patients (Number)
Octreotide+ Everolimus	2.3
Octreotide+ Placebo	1.9

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Progression Free Survival (PFS) as Per Adjudicated Central Review by Baseline Chromogranin A (CgA)

"Serum CgA levels in urine are frequently elevated in patients with advanced carcinoid tumors. Baseline levels of serum CgA were characterized relative to the upper limited of normal (ULN). CgA levels exceeding 2 x ULN were considered to be 'Elevated'; otherwise considered as Non-elevated." (NCT00412061)
Timeframe: If elevated at baseline, evaluated every cycle visit (28 days/cycle) reported between day of first patient randomised, 10 January 2007, until cut-off date 02 April 2010

Intervention	Months (Median)
	CgA<=2x ULN (n=60,78)	CgA>2x ULN (n=152,130)
Octreotide+ Everolimus	31.31	13.93
Octreotide+ Placebo	20.07	8.41

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Number of Patients With Adverse Events (AEs), Clinically Notable AE, Death, Serious Adverse Events (SAEs) (Open Label Phase)

Intervention	Patients (Number)
	Clinically notable AE	Grade 3-4 Adverse Events	On treatment death	Serious adverse events
Everolimus Open Label Arm	154	115	22	93

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Course of Calculated GFR (mL/Min/1.73 m^2) From Month 24 to Month 60

Course of calculated GFR (mL/min/1.73 m^2) at Months 24, 36, 48 and 60 (NCT00414440)
Timeframe: Months 24, 36, 48 and 60

Intervention	mL/min/1.73 m^2 (Mean)
	Month 24	Month 36	Month 48	Month 60
Everolimus	43.9	42.6	39.6	37.7
Placebo	48.8	44.9	42.7	37.6

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Changes in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP)

Changes in systolic blood pressure (SBP) and diastolic blood pressure (DBP), at baseline and then months 12 and 24 (NCT00414440)
Timeframe: Baseline, Months 12 and 24

Intervention	mmHG (Mean)
	Baseline SBP	Month 12 SBP	Month 24 SBP	Baseline DBP	Month 12 DBP	Month 24 DBP
Everolimus	136	134	134	88	86	85
Placebo	135	134	134	88	86	85

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Calculated GFR, Change From Baseline at Month 60 by Baseline cGFR

Change in renal function was assessed by the estimated Glomerular Filtration Rate (eGFR) using the abbreviated (4 variables) Modification of Diet in Renal Disease (MDRD-4) formula which was developed by the MDRD Study Group and has been validated in patients with chronic kidney disease. The MDRD-4 formula used for the eGFR calculation is: eGFR (mL/min/1.73m^2) = 186.3*(C^-1.154)*(A^-0.203)*G*R, where C is the serum concentration of creatinine (mg/dL), A is age (years), G=0.742 when gender is female, otherwise G=1, R=1.21 when race is black, otherwise R=1. The changes in renal function were analyzed via analysis of covariance (ANCOVA) with treatment, pre-transplant hepatitis C virus status and randomization eGFR as covariates. Based on these ANCOVA analyses, the least-squares mean and standard errors of change were reported. (NCT00414440)
Timeframe: Months 24, 36, 48 and 60

Intervention	mL/min/1.73 m^2 (Mean)
	>70 mL/min/1.73 m^2 n=11, 18	≤70 mL/min/1.73 m^2 n=53, 57	>60 mL/min/1.73 m^2 n=21.26	≤60 mL/min/1.73 m^2 n=43,49	>50 mL/min/1.73 m^2 n=36,39	≤50 mL/min/1.73 m^2 n=28, 36
Everolimus	-14.8	-16.1	-17.0	-15.3	-19.0	-11.8
Placebo	-20.5	-15.6	-20.0	-15.1	-19.4	-14.0

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Primary Efficacy Analysis of Total Kidney Volume (mITT Set, Multiple Imputation)

Everolimus (RAD001) compared to placebo with respect to the change from baseline in total kidney volume at Month 24. (NCT00414440)
Timeframe: Baseline, Month 24

Intervention	mL (Mean)
Everolimus	230.1
Placebo	300.8

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Calculated GFR (mL/Min/1.73 m^2), Change From Baseline by Visit

Change in renal function was assessed by the Glomerular Filtration Rate (GFR) using the abbreviated (4 variables) Modification of Diet in Renal Disease (MDRD-4) formula which was developed by the MDRD Study Group and has been validated in patients with chronic kidney disease. The MDRD-4 formula used for the eGFR calculation is: eGFR (mL/min/1.73m^2) = 186.3*(C^-1.154)*(A^-0.203)*G*R, where C is the serum concentration of creatinine (mg/dL), A is age (years), G=0.742 when gender is female, otherwise G=1, R=1.21 when race is black, otherwise R=1. The changes in renal function were analyzed via analysis of covariance (ANCOVA) with treatment, pre-transplant hepatitis C virus status and randomization eGFR as covariates. Based on these ANCOVA analyses, the least-squares mean and standard errors of change were reported. (NCT00414440)
Timeframe: Months 3, 6, 9, 12, 18 and 24

Intervention	mL/min/1.73m^2 (Mean)
	Week 1	Week 2	Week 4	Month 3	Month 6	Month 9	Month 12	Month 18	Month 24
Everolimus	2.0	1.7	0.6	-0.5	-2.3	-4.6	-5.4	-7.7	-8.9
Placebo	-0.9	-0.9	-1.2	-2.4	-2.2	-2.4	-3.2	-5.5	-7.7

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Biomarkers Predictive of Clinical Benefit (DCR by PTEN ) on Everolimus (RAD001) 10mg/Day

The efficacy variable that was compared in the biomarker analysis is DCR within the Everolimus (RAD001) 10mg/day arm in the analysis not adjusted for prognostic factors: from archival tumor tissue (and additionally from a biopsy at a metastatic site, if available), collected during screening: PTEN loss (imunohistochemistry, IHC), phosphoAKT (IHC), phosphoS6 (IHC), and p53 (IHC). From blood plasma, collected at screening then on day 1 at cycles 2, 3 and 4, and at the end of treatment: blood lactate dehydrogenase (LDH) isoenzyme fractionation and serum levels of sVEGFR2, bFGF, PLGF and VEGF. (NCT00419159)
Timeframe: Screening and Day 1 of cycles 2, 3, 4 and end of treatment

Intervention	percentage of participants (Number)
PTEN Expression Low/Everolimus (RAD001) 10 mg/Day	26.9
PTEN Expression Normal/Everolimus (RAD001) 10 mg/Day	26.1

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Biomarker Predictive of Clinical Benefit (DCR by KRAS) on Everolimus (RAD001) 70 mg/Week

The efficacy variable compared in this biomarker analysis is disease control rate (DCR) within the 70mg/week arm in the analysis not adjusted for prognostic factors: from archival tumor tissue (and additionally from a biopsy at a metastatic site, if available), collected during screening: KRAS gene mutation. From blood plasma, collected at screening then on day 1 at cycles 2, 3 and 4, and at the end of treatment: blood lactate dehydrogenase (LDH) isoenzyme fractionation and serum levels of sVEGFR2, bFGF, PLGF and VEGF. (NCT00419159)
Timeframe: Screening and Day 1 of cycles 2, 3, 4 and end of treatment

Intervention	percentage of participants (Number)
KRAS Mutation/Everolimus (RAD001) 70 mg/Week	33.3
KRAS Wildtype/Everolimus (RAD001) 70 mg/Week	21.7

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Biomarkers Predictive of Clinical Benefit (Median PFS and OS by PTEN ) on Everolimus (RAD001) 10mg/Day

The efficacy variable that was compared in the biomarker analysis are PFS & OS within the Everolimus (RAD001) 10mg/day arm in the analysis not adjusted for prognostic factors: from archival tumor tissue (and additionally from a biopsy at a metastatic site, if available), collected during screening: PTEN loss (imunohistochemistry, IHC), phosphoAKT (IHC), phosphoS6 (IHC), and p53 (IHC). From blood plasma, collected at screening then on day 1 at cycles 2, 3 and 4, and at the end of treatment: blood lactate dehydrogenase (LDH) isoenzyme fractionation and serum levels of sVEGFR2, bFGF, PLGF and VEGF. (NCT00419159)
Timeframe: Screening and Day 1 of cycles 2, 3, 4 and end of treatment

Intervention	months (Median)
	Median PFS	Median OS
PTEN Expression Low/Everolimus (RAD001) 10 mg/Day	1.81	10.38
PTEN Expression Normal/Everolimus (RAD001) 10 mg/Day	1.68	6.34

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Biomarker Predictive of Clinical Benefit (DCR by KRAS) on Everolimus (RAD001) 10 mg/Day

The efficacy variable compared in this biomarker analysis is disease control rate (DCR) within the 10mg/day arm in the analysis not adjusted for prognostic factors: from archival tumor tissue (and additionally from a biopsy at a metastatic site, if available), collected during screening: KRAS gene mutation. From blood plasma, collected at screening then on day 1 at cycles 2, 3 and 4, and at the end of treatment: blood lactate dehydrogenase (LDH) isoenzyme fractionation and serum levels of sVEGFR2, bFGF, PLGF and VEGF. (NCT00419159)
Timeframe: Screening and Day 1 of cycles 2, 3, 4 and end of treatment

Intervention	percentage of participants (Number)
KRAS Mutation/Everolimus (RAD001) 10 mg/Day	17.1
KRAS Wildtype/Everolimus (RAD001) 10 mg/Day	35.0

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Number of Patients Who Died, Had an Serious Adverse Event (SAE), Had Grade 3 to 4 Adverse Event (AE), Discontinued Due to an AE, or Had a Clinical Notable AE by Treatment (tr).

Toxicity assessed using the NIH-NCI Common Terminology Criteria for Adverse Events, Version 3.0 (CTCAEv3.0). On treatment death defined as deaths occurring no more than 28 days after the discontinuation of study treatment. (NCT00419159)
Timeframe: From the first day of treatment until 28 days after discontinuation of study treatment

Intervention	Participants (Number)
	Deaths	On-treatment Death	SAE regardless of relationship to study treatment	SAE with suspected relationship to study treatment	AE Grade 3-4, regardless of relationship to study	AE Grade 3-4, suspected relationship to study tr	AE leading to discontinuation	Clinically notable adverse event
Everolimus (RAD001) 10 mg/Day	65	14	22	6	50	26	20	76
Everolimus (RAD001) 70 mg/Week	86	11	34	7	58	31	9	85

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Disease Control Rate (DCR) and Objective Response Rate (ORR) According to the Response Evaluation Criteria in Solid Tumors (RECIST)

"RECIST (Response Evaluation Criteria In Solid Tumors) is a set of published rules that define when cancer patients improve (respond), stay the same (stable) or worsen (progression) during treatments.~Disease Control Rate (DCR) defined as the percentage of participants with Disease Control best overall response (complete response, partial response or stable disease)and Objective Response Rate (ORR) defined as the percentage of participants with best overall Objective Response (complete response or partial response)." (NCT00419159)
Timeframe: Imaging every 8 weeks

Intervention	Percentage of participants (Number)
	Disease Control Rate (DCR)	Objective Response Rate (ORR)
Everolimus (RAD001) 10 mg/Day	32.4	0
Everolimus (RAD001) 70 mg/Week	31.0	0

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Biomarkers Predictive of Clinical Benefit (Median PFS and OS by PTEN ) on Everolimus (RAD001) 70mg/Week

The efficacy variable that was compared in the biomarker analysis are PFS & OS within the Everolimus (RAD001) 70mg/Week arm in the analysis not adjusted for prognostic factors: from archival tumor tissue (and additionally from a biopsy at a metastatic site, if available), collected during screening: PTEN loss (imunohistochemistry, IHC), phosphoAKT (IHC), phosphoS6 (IHC), and p53 (IHC). From blood plasma, collected at screening then on day 1 at cycles 2, 3 and 4, and at the end of treatment: blood lactate dehydrogenase (LDH) isoenzyme fractionation and serum levels of sVEGFR2, bFGF, PLGF and VEGF. (NCT00419159)
Timeframe: Screening and Day 1 of cycles 2, 3, 4 and end of treatment

Intervention	months (Median)
	Median PFS	Median OS
PTEN Expression Low/Everolimus (RAD001) 70 mg/Week	1.71	5.98
PTEN Expression Normal/Everolimus (RAD001) 70 mg/Week	1.77	4.37

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The Number of Participants With Best Overall Response According to Response Evaluation Criteria in Solid Tumors (RECIST)

"RECIST (Response Evaluation Criteria In Solid Tumors) is a set of published rules that define when cancer patients improve (respond), stay the same (stable) or worsen (progression) during treatments.~Best Over Response (BOR): Complete Response (CR, No lesions), Partial Response (PR, 30% decrease in lesions), and Stable Disease (SD, none of the above)" (NCT00419159)
Timeframe: Imaging every 8 weeks

Intervention	Participants (Number)
	Complete Response (CR)	Partial Response (PR)	Stable Disease (SD)	Progressive Disease (PD)	Disease Control (CR or PR or SD)	Objective Response (CR or PR)	Unknown
Everolimus (RAD001) 10 mg/Day	0	0	26	55	26	0	19
Everolimus (RAD001) 70 mg/Week	0	0	25	58	25	0	16

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Biomarkers Predictive of Clinical Benefit (Median PFS and OS by KRAS) on Everolimus (RAD001) 10mg/Day

The efficacy variable that was compared in the biomarker analysis are Median progression free survival (PFS) and overall survival (OS) within the Everolimus (RAD001) 10mg/day arm in the analysis not adjusted for prognostic factors: from archival tumor tissue (and additionally from a biopsy at a metastatic site, if available), collected during screening: KRAS gene mutation. From blood plasma, collected at screening then on day 1 at cycles 2, 3 and 4, and at the end of treatment: blood lactate dehydrogenase (LDH) isoenzyme fractionation and serum levels of sVEGFR2, bFGF, PLGF and VEGF. (NCT00419159)
Timeframe: Screening and Day 1 of cycles 2, 3, 4 and end of treatment

Intervention	months (Median)
	Median PFS	Median OS
KRAS Mutation/Everolimus (RAD001) 10 mg/Day	1.71	5.59
KRAS Wildtype/Everolimus (RAD001) 10 mg/Day	1.77	7.06

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Progression-free Survival (PFS)

Duration in months from the date of first study treatment to the date of the first documented disease progression or death due to any cause. (NCT00419159)
Timeframe: Imaging every 8 weeks

Intervention	Months (Median)
Everolimus (RAD001) 70 mg/Week	1.77
Everolimus (RAD001) 10 mg/Day	1.77

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Biomarkers Predictive of Clinical Benefit (Median PFS and OS by KRAS ) on Everolimus (RAD001) 70mg/Week

The efficacy variable that was compared in the biomarker analysis are Median progression free survival (PFS) and overall survival (OS) within the Everolimus (RAD001) 70mg/week arm in the analysis not adjusted for prognostic factors: from archival tumor tissue (and additionally from a biopsy at a metastatic site, if available), collected during screening: KRAS gene mutation. From blood plasma, collected at screening then on day 1 at cycles 2, 3 and 4, and at the end of treatment: blood lactate dehydrogenase (LDH) isoenzyme fractionation and serum levels of sVEGFR2, bFGF, PLGF and VEGF. (NCT00419159)
Timeframe: Screening and Day 1 of cycles 2, 3, 4 and end of treatment

Intervention	months (Median)
	Median PFS	Median OS
KRAS Mutation/Everolimus (RAD001) 70 mg/Week	1.77	6.18
KRAS Wildtype/Everolimus (RAD001) 70 mg/Week	1.71	4.90

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Overall Survival (OS)

Overall survival defined as the time from date of first study treatment to the date of death due to any cause. (NCT00419159)
Timeframe: Every 3 months

Intervention	Months (Median)
Everolimus (RAD001) 70 mg/Week	4.90
Everolimus (RAD001) 10 mg/Day	5.88

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Biomarkers Predictive of Clinical Benefit (DCR by PTEN ) on Everolimus (RAD001) 70mg/Week

The efficacy variable that was compared in the biomarker analysis is DCR within the Everolimus (RAD001) 70mg/week arm in the analysis not adjusted for prognostic factors: from archival tumor tissue (and additionally from a biopsy at a metastatic site, if available), collected during screening: PTEN loss (imunohistochemistry, IHC), phosphoAKT (IHC), phosphoS6 (IHC), and p53 (IHC). From blood plasma, collected at screening then on day 1 at cycles 2, 3 and 4, and at the end of treatment: blood lactate dehydrogenase (LDH) isoenzyme fractionation and serum levels of sVEGFR2, bFGF, PLGF and VEGF. (NCT00419159)
Timeframe: Screening and Day 1 of cycles 2, 3, 4 and end of treatment

Intervention	percentage of participants (Number)
PTEN Expression Low/Everolimus (RAD001) 70 mg/Week	20.9
PTEN Expression Normal/Everolimus (RAD001) 70 mg/Week	33.3

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Number of Participants With Biopsy-proven Acute Rejection (BPAR) at Month 6 and Month 12.

(NCT00425308)
Timeframe: Month 6 and 12

Intervention	participants (Number)
	Yes: treatment failure Month 6	No: treatment failure Month 6	Yes: treatment failure Month 12	No: treatment failure Month 12
Cyclosporine	0	0	1	12
Enteric-coated Mycophenolate Sodium (EC-MPS)	0	0	0	14

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Number of Participants With Treatment Failures Assessed by Biopsy-proven Acute Rejection (BPAR), Graft Loss/Re-transplantation, Death or Lost to Follow-up at Month 12.

(NCT00425308)
Timeframe: Month 12

Intervention	participants (Number)
	BPAR 12 months	Graft Loss 12 months	Death 12 months	Lost to Follow-up 12 months
Cyclosporine	1	0	1	0
Enteric-coated Mycophenolate Sodium (EC-MPS)	0	0	0	0

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Change in the Glomerular Filtration Rate Estimated by Iohexol Plasma Clearance 12 Months After Randomization Between the 2 Groups of Patients Who Completed Trial

Primary efficacy endpoint: between treatment analysis of change in iohexol plasmatic clearance (mL/min) from baseline to Month 12 (M12) (NCT00425308)
Timeframe: From Baseline to Month 12

Intervention	(mL/min) (Least Squares Mean)
Cyclosporine	1.46
Enteric-coated Mycophenolate Sodium (EC-MPS)	12.00

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Change in Glomerular Filtration Rate Estimated by Iohexol Plasma Clearance 12 Months After Randomization Between the 2 Groups of Patients.

Primary efficacy endpoint: between treatment analysis of change in iohexol plasmatic clearance (mL/min) from baseline to Month 12 (M12) (NCT00425308)
Timeframe: From Baseline to Month 12

Intervention	(mL/min) (Least Squares Mean)
Cyclosporine	-4.07
Enteric-coated Mycophenolate Sodium (EC-MPS)	10.30

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Assessing Cardiovascular Risk Factors Based on Fasting C-reactive Protein (CRP).

Blood chemistry - C-reactive Protein (CRP) (mg/L) (NCT00425308)
Timeframe: From Baseline to Month 3, 6, and 12

Intervention	mg/L (Mean)
	Baseline [N = 13; N = 14]	Month 3 [N = 11; N = 11]	Month 6 [N = 11; N = 9]	Month 12 [N = 14; N = 12]
Cyclosporine	11.4	6.3	8.0	34.2
Enteric-coated Mycophenolate Sodium (EC-MPS)	3.0	10.3	5.6	12.6

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Assessing Cardiovascular Risk Factors Based on Fasting Triglycerides.

(NCT00425308)
Timeframe: From Baseline to Month 1, 3, 6, 9, and 12

Intervention	mmol/L (Mean)
	Baseline [N = 11; N = 14]	Month 1 [N = 10; N = 14]	Month 3 [N = 13; N = 14]	Month 6 [N = 12; N = 12]	Month 9 [N = 10; N = 12]	Month 12 [N = 12; N = 11]
Cyclosporine	2.4	2.1	2.0	1.9	1.9	2.3
Enteric-coated Mycophenolate Sodium (EC-MPS)	1.8	2.0	2.2	2.1	2.2	2.3

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Assessing Cardiovascular Risk Factors Based on Fasting Total Cholesterol.

Blood chemistry - total cholesterol (mmol/L) (NCT00425308)
Timeframe: From Baseline to Month 1, 3, 6, 9, and 12

Intervention	mmol/L (Mean)
	Baseline [N = 13; N = 14]	Month 1 [N = 11; N = 14]	Month 3 [N = 13; N = 14]	Month 6 [N = 12; N = 12]	Month 9 [N = 9; N = 12]	Month 12 [N = 12; N = 11]
Cyclosporine	5.7	5.0	5.3	5.5	5.4	5.6
Enteric-coated Mycophenolate Sodium (EC-MPS)	6.0	5.7	5.6	5.7	5.4	5.8

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Assessing Cardiovascular Risk Factors Based on Fasting High-density Lipoprotein (HDL) Cholesterol, Low-density Lipoprotein (LDL) Cholesterol.

(NCT00425308)
Timeframe: From Baseline to Month 3, 6, and 12

Intervention	mmol/L (Mean)
	Baseline LDL [N = 10; N = 14]	Baseline HDL [N = 10; N = 14]	Month 3 LDL [N = 12; N = 14]	Month 3 HDL [N = 12; N = 13]	Month 6 LDL [N = 12; N = 12]	Month 6 HDL [N = 12; N = 12]	Month 12 LDL [N = 10; N = 11]	Month 12 HDL [N = 10; N = 11]
Cyclosporine	3.4	1.5	3.2	1.7	3.2	1.6	3.0	1.7
Enteric-coated Mycophenolate Sodium (EC-MPS)	3.1	1.5	3.4	1.5	3.3	1.4	3.2	1.5

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Change in Renal Function Assessed by Creatinine Clearance at Month 3, Month 6 and Month 12

Change in creatinine clearance, Nankivell formula (mL/min/1.73m²) from baseline to M12 (NCT00425308)
Timeframe: From Baseline to Month 3, 6, and 12

Intervention	mL/min/1.73m² (Mean)
	Baseline [N = 12; N = 13]	Month 3 [N = 10; N = 14]	Month 6 [N = 10; N = 12]	Month 12 [N = 7; N = 11]
Cyclosporine	56.3	57.3	50.3	48.7
Enteric-coated Mycophenolate Sodium (EC-MPS)	60.3	67.1	68.1	70.1

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Change in Renal Function Assessed by Proteinuria at Month 3, Month 6 and Month 12

Change in proteinuria (g/24h) from baseline to M12 (NCT00425308)
Timeframe: From Baseline to Month 3, 6, and 12

Intervention	g/24h (Mean)
	Baseline [N = 9; N = 10]	Month 3 [N = 9; N = 8]	Month 6 [N = 6; N = 5]	Month 12 [N = 7; N = 10]
Cyclosporine	0.44	0.53	0.44	0.48
Enteric-coated Mycophenolate Sodium (EC-MPS)	0.47	0.24	0.33	0.75

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Change in Renal Function Assessed by Serum Creatinine at Month 3, Month 6 and Month 12

(NCT00425308)
Timeframe: From Baseline to Month 3, 6, and 12

Intervention	µmol/L (Mean)
	Baseline [N = 13; N = 14]	Month 3 [N = 12; N = 14]	Month 6 [N = 12; N = 13]	Month 12 [N = 13; N = 14]
Cyclosporine	161.7	156.6	170.8	227.7
Enteric-coated Mycophenolate Sodium (EC-MPS)	153.2	138.9	139.8	130.4

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Assessing Cardiovascular Risk Factors Based on Fasting Glucose.

Blood chemistry - fasting glycemia (mmol/L) (NCT00425308)
Timeframe: From Baseline to Month 1, 3, 6, 9, and 12

Intervention	mmol/L (Mean)
	Baseline [N = 15; N = 15]	Month 1 [N = 15; N = 15]	Month 3 [N = 14; N = 15]	Month 6 [N = 14; N = 14]	Month 9 [N = 12; N = 13]	Month 12 [N = 14; N = 13]
Cyclosporine	5.5	5.2	5.6	5.5	5.3	4.8
Enteric-coated Mycophenolate Sodium (EC-MPS)	5.2	5.3	5.2	5.1	5.6	5.4

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Phase I: Best Overall Response (BOR)

BOR was determined based on investigator assessment of overall lesion response using RECIST criteria guidelines. BOR = objective responses rate (ORR), disease control rate (DCR) or clinical benefit rate (CBR). ORR = (complete response (CR) or partial response(PR); DCR = (CR or PR or Stable disease (SD); CBR = (CR or PR or SD >= 24 weeks).CR = Disappearance of all target lesions; PR = At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters; SD = Neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for partial disease (PD). PD = At least a 20% increase in the sum of the longest diameter of all measured target lesions, taking as reference the smallest sum of longest diameter of all target lesions recorded at or after baseline. (NCT00426556)
Timeframe: every 8 - 9 weeks until disease progression or a new lesion is identified

Intervention	Percentage of Participants (Number)
	Objective Response Rate (ORR)	Disease Control Rate (DCR)	Clinical Benefit Rate (CBR)
Phase I - RAD001 10mg + PT, Daily	23.5	82.4	47.1
Phase I - RAD001 30mg + PT, Weekly	30.0	80.0	70.0
Phase I - RAD001 5mg + PT, Daily	83.3	83.3	83.3

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Phase II: Progression Free Survival (PFS)

PFS is defined as the time from start of treatment to the date of first documented progression or death due to any cause. If a patient has not had an event, PFS will be censored at the date of last adequate tumor assessment. (NCT00426556)
Timeframe: every 8 - 9 weeks until disease progression or a new lesion is identified

Intervention	Months (Median)
Phase II - RAD001 10mg + PT, Daily	5.52

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Phase II: Overall Survival (OS)

Overall survival (OS) is defined as the time from start of treatment to the date of death due to any cause. If a patient is not known to have died, survival was censored at the last date of contact. OS was to be reported at extension and after 3-year follow-up. The Kaplan-Meier median was used to analyze the OS. (NCT00426556)
Timeframe: every 3 months until death

Intervention	Months (Median)
Phase II - RAD001 10mg + PT, Daily	18.07

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Phase II: Overall Response Rate

The primary objective of this phase II study was to evaluate the efficacy of the dose level/regimen of everolimus recommended from the Phase I with trastuzumab and paclitaxel (PT) therapy in patients with HER2-overexpressing metastatic breast cancer whose disease progressed on/after trastuzumab mono-and/or combination therapy based on the evaluation of objective response rate (ORR) according to Response Evaluation Criteria in Solid Tumors (RECIST). Objective response rate (ORR) was defined as the proportion of patients with a best overall response (BOR) of complete response (CR) or partial response (PR). Only patients with measurable disease (the presence of at least one measurable lesion) at baseline were included in the study. CR = Disappearance of all target lesions; PR = At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters. (NCT00426556)
Timeframe: every 8 - 9 weeks until disease progression or a new lesion is identified

Intervention	Percentage of Participants (Number)
Phase II - RAD001 10mg + PT, Daily	21.8

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Progression-free Survival

"Progression-free survival is defined as the time from registration to the time of progression or death due to any cause. Progression-free survival was estimated using the method of Kaplan-Meier.~Progression is defined as the following:~CLL (subset of patients in the Relapsed Indolent Non-Hodgkin Lymphoma group): >=50% increase in nodes from nadir or >=50% increase in liver/spleen size from nadir.~Waldenstrom (subset of patients in the Uncommon Lymphomas group): >50% lymph node increase in SPD of > 1 node or new nodes, or >50% liver/spleen size increase, or > 25% IgM (by SPEP) increase, or lymphocyte morphology transformation to a more aggressive histology.~All Others: New lesions or >=50% lymph nodes." (NCT00436618)
Timeframe: 5 years

Intervention	years (Median)
Relapsed Aggressive Non-Hodgkin Lymphoma	0.18
Relapsed Indolent Non-Hodgkin Lymphoma	0.60
Uncommon Lymphomas	0.79

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Tumor Response, Defined by Disease: Chronic Lymphocytic Leukemia(CLL): Clinical Complete or Complete or Nodular Partial or Partial Remission, Waldenstrom: Complete or Partial Response, All Others: Complete or Complete Unconfirmed or Partial Response.

"CLL (subset of patients in the Relapsed Indolent Non-Hodgkin Lymphoma group): 50% decrease in peripheral blood lymphocytes, lymphadenopathy, liver/spleen size, presence/absence of constitutional symptoms; plus ≥1 of the following: ≥1500/μL polymorphonuclear leukocytes, >100000/μL platelets, >11.0 g/dL hemoglobin or 50% improvement for these parameters without transfusions.~Waldenstrom (subset of patients in the Uncommon Lymphomas group): >50% reduction in serum immunoglobulin M(IgM) levels (by serum protein electrophoresis (SPEP)) during any point while in this study, and no appearance of new lesions.~All others: at least a 50% decrease in the sum of the products of the greatest diameters (SPD) of the six largest dominant nodes or nodal masses and no increase in the size of other nodes, liver, or spleen and splenic and hepatic nodules must regress by at least 50% in the SPD and no new sites of disease." (NCT00436618)
Timeframe: 5 years

Intervention	percentage of patients in group (Number)
Relapsed Aggressive Non-Hodgkin Lymphoma	26
Relapsed Indolent Non-Hodgkin Lymphoma	35
Uncommon Lymphomas	49

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Time to Progression

The time to progression is defined as the time from registration to the time of progression. The distribution of time to progression was estimated using the method of Kaplan-Meier. (NCT00436618)
Timeframe: 5 years

Intervention	years (Median)
Relapsed Aggressive Non-Hodgkin Lymphoma	0.18
Relapsed Indolent Non-Hodgkin Lymphoma	0.60
Uncommon Lymphomas	0.90

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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 was estimated using the method of Kaplan-Meier. (NCT00436618)
Timeframe: 5 years

Intervention	years (Median)
Relapsed Aggressive Non-Hodgkin Lymphoma	0.66
Relapsed Indolent Non-Hodgkin Lymphoma	2.45
Uncommon Lymphomas	3.41

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Number of Participants With Objective Response

Efficacy reported as objective response. Objective response defined as change in serum tryptase level or bone marrow mast cell percentage. (NCT00449748)
Timeframe: Monthly for first 3 months, then every 3 months

Intervention	Participants (Number)
RAD001	0

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Clinical Response Rate

Best response on treatment was based on RECIST 1.0 criteria with overall clinical response defined as achieving stable disease (SD), partial response (PR) or complete response (CR). Per RECIST 1.0 for target lesions, CR is complete disappearance of all target lesions and PR is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. To be assigned a status of CR or PR, changes in tumor measurements must be confirmed by repeat assessments performed no fewer than 4 weeks after the response. SD is neither CR/PR or progressive disease (PD). PD is at least a 20% increase in sum LD, takings as reference smallest sum LD since treatment started. (NCT00458237)
Timeframe: Disease assessments occurred every 9 weeks (3 cycles) on treatment. Treatment continued until disease progression or unacceptable toxicity. Median duration of treatment was 2.4 months.

Intervention	proportion of participants (Number)
Phase I: Everolimus (Dose Level 2) and Trastuzumab	.67
Phase II: Everolimus (Maximum Tolerated Dose) and Trastuzumab	.80

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Maximum Tolerated Dose (MTD)

"The MTD is determined by the number of patients who experience a dose limiting toxicity (DLT). The MTD is defined as the highest dose at which fewer than one-third of patients experience a DLT. If no DLTs are observed, the MTD is not reached. Dose Limiting Toxicities (DLTs) were defined as follows (CTCAE v4.0):~Any grade 4 hematologic toxicity, excluding anemia.~Any grade 3 or 4 nonhematologic toxicity, except for nausea, vomiting, diarrhea, or hyperlipidemia that responds promptly (within 24 hours for nausea, vomiting, and diarrhea and within 1 week for hyperlipidemia) to appropriate treatment, and except for cardiac toxicity which will be assessed after 12 weeks of treatment.~Need to hold >1 dose of trastuzumab or > 7 doses of RAD001 within the first 3 weeks because of the presence of toxicity." (NCT00458237)
Timeframe: Cycle One (first 21 days of treatment)

Intervention	participants with DLT (Number)
Phase I: Everolimus (Dose Level 1) and Trastuzumab	0
Phase I: Everolimus (Dose Level 2) and Trastuzumab	0

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Number of Patients Free of Dose Limiting Toxicity

"A dose limiting toxicity was defined as an adverse event or laboratory abnormality that occurs to patients on the Phase I portion of the trial, during the first 21 days following the first dose of RAD001/docetaxel during cycle 1, judged to be related to RAD001/docetaxel and meeting any of the following criteria:~Hematologic Toxicity:~CTCAE grade 4 neutropenia > 7 days or any Grade 3 or 4 neutropenia with fever Or CTCAE grade 3 or 4 thrombocytopenia > 7 days~Non-hematologic toxicity:~The occurrence of non-hematologic CTCAE grade 3 or 4 adverse events will be considered dose limiting, except for the following:~CTCAE grade 3 nausea or grade 3 or 4 vomiting CTCAE grade 3 or 4 vomiting will only be considered dose limiting if it occurs despite the use of standard anti-emetics.~CTCAE grade 3 or 4 fever identified with a source (i.e. infection, tumor)~CTCAE grade 3 or 4 alkaline phosphatase." (NCT00459186)
Timeframe: 21 days

Intervention	participants (Number)
RAD001 Followed by RAD001 + Docetaxel	14

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Response Based on PET Scan

Patients were scanned using Positron Emission Tomography (PET) before and after receiving single agent RAD001. Patients were classified as having partial metabolic response, stable metabolic disease, or progressive metabolic disease based on changes in PET imaging from baseline to post-treatment. A positive FDG-PET for the purposes of this study consisted of a visualized area of abnormal increased FDG uptake that matched the anatomic location of an abnormality seen on bone scan or CT. Metabolic response was assessed for percent change in SUVmax according to the criteria of the European Organization for Research and Treatment of Cancer (EORTC) : partial metabolic response (PMR) ≤ -25%; stable metabolic disease (SMD) -25% + 25%; progressive metabolic disease (PMD) > 25%. (NCT00459186)
Timeframe: 10 to 14 days after study entry

Intervention	percentage of participants (Number)
	Partial Metabolic Response	Stable Metabolic Disease	Progressive Metabolic Disease
RAD001 Followed by RAD001 + Docetaxel	22	67	11

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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. (NCT00474929)
Timeframe: Up to 3 years from registration

Intervention	months (Median)
Sorafenib 200 mg Twice Daily, RAD001 5mg Every Day	13.5

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Progression Free Survival

Progression Free Survival is defined as the time from registration to the earliest date documentation of disease progression or death. The distribution of time to disease progression will be estimated using the method of Kaplan-Meier. (NCT00474929)
Timeframe: Up to 3 years from registration

Intervention	months (Median)
Sorafenib 200 mg Twice Daily, RAD001 5mg Every Day	4.6

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Number of Participants Reporting a Dose Limiting Toxicity (DLT)

"The Maximum Tolerated Dose (MTD) is defined as the dose level below the lowest dose that induces dose-limiting toxicity (DLT) in at least one-third of patients (at least 2 of a maximum of 6 new patients). Dose-limiting toxicity (DLT) is defined as an adverse event attributed (definitely, probably, or possibly) in first cycle to the study treatment and meeting the following criteria:~Grade 4 infection~Grade 4 ANC or PLT~Grade 3 or higher non-hematologic adverse event.~NCI Common Terminology Criteria for Adverse Events (CTCAE) v3.0 will be used to assess adverse events. For this endpoint, the number of patients reporting a DLT event are tabulated." (NCT00474929)
Timeframe: First cycle (28 days) of study treatment

Intervention	participants (Number)
Phase I, Dose Level 0	1
Phase I, Dose Level 1	0
Phase I, Dose Level 2	1
Phase I, Dose Level 3	2

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Proportion of Confirmed Tumor Responses

"A confirmed response is defined to be a CR or PR noted as the objective status for eligible patients during cycles 1-12.~Complete Response (CR):~Multiple Myeloma (MM): Negative immunofixation of serum and urine, disappearance of soft tissue plasmacytomas, and normalization of free light chain (FLC) ratio.~Lymphoma: Disappearance of all clinical and radiographic evidence of disease, all lymph nodes of normal size (1.5 cm or less), no splenomegaly.~Partial Response (PR):~MM: 50% reduction of serum or urine M-protein or to less than 200mg/day, a 50% reduction in the difference between involved and uninvolved FLC, and 50% reduction in the size of soft tissue plasmacytoma.~Lymphoma: 50% or greater reduction in sum of the products of the dimension for nodal masses; no increase in liver, spleen or node size; no new sites of disease; and a 50% decrease in lymphocyte count if followed at baseline." (NCT00474929)
Timeframe: Up to 12 cycles of treatment

Intervention	percentage of participants (Number)
	Complete Response (CR)	Partial Response (PR)
Sorafenib 200 mg Twice Daily, RAD001 5mg Every Day	8.5	15.9

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Participant Responses Per Treatment Arm at 12 Weeks

Radiographic criteria of response based on regional ultrasound examination (decrease in size of the primary tumor and/or fatty replacement in regional lymph nodes), and includes partial response and complete response. A decrease in size of the product of the two largest dimensions =/> 50% considered a partial response (PR), and a complete disappearance of the primary tumor by physical exam and or ultrasound and normalization of the lymph nodes by ultrasound will be considered a complete clinical response (CR). Stable Disease (SD) is carcinoma neither decreasing nor increasing in extent or severity, and Progression of disease (PD) defined as 30% increase in size primary tumor and/or lymph nodes on physical exam and/or ultrasound. (NCT00499603)
Timeframe: 12 weeks

Intervention	participants (Number)
	CR	PR	SD	PD
Paclitaxel + FEC	3	5	16	3
Paclitaxel + RAD001 + FEC	0	11	11	1

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Number Participants With Inhibition of PI3K/PTEN/AKT Pathway at 48 Hours

Number of participants with inhibition of the PI3K/PTEN/AKT pathway at 48 hours after the start of treatment, regardless of the status of the pathway at the time of randomization. Molecular changes (inhibition/activation) of the PI3K/PTEN/AKT pathway evaluated using reverse phase protein arrays (RPPA) where fine-needle aspirations (FNAs) from the primary breast cancer obtained pretreatment, and at 48 hours. Bioinformatics cluster analysis of arrays used to define molecular changes as inhibition or activation where pathways called 'active' with presence of 2 or more phosphorilated pathway proteins (pAKT, pmTOR, pGSK3, pS6K1, pS6), and 'inhibited' with one or none phosphorilated pathway proteins present. (NCT00499603)
Timeframe: 48 hours after start of treatment

Intervention	participants (Number)
Paclitaxel + FEC	27
Paclitaxel + RAD001 + FEC	22

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Participant Responses Per Treatment Arm at 24 Weeks

Intervention	participants (Number)
	CR	PR	SD	PD
Paclitaxel + FEC	4	16	7	0
Paclitaxel + RAD001 + FEC	2	11	7	3

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Progression Free Survival According to Neuron Specific Enolase Tumor Marker (NSE) Baseline Level and According to NSE Early Response

"Baseline levels of serum NSE were characterized towards PFS as per local investigator assessment, relative to the upper limited of normal (ULN). NSE levels exceeding ULN were considered to be 'Elevated' otherwise considered as Non-elevated. An 'early response' (applicable to only those patients with elevated levels at baseline) was defined as a decrease of greater than or equal to 30% from baseline to Cycle 2 Day 1 or normalization by Cycle 2 Day 1. NSE is widely expressed in well-differentiated pancreatic NET. NSE is usually expressed in the cytoplasm. Pancreatic NET patients often present with elevated circulating levels of NSE in their blood. Baseline levels of these biomarkers are considered as prognostic factors." (NCT00510068)
Timeframe: Time from randomisation to dates of disease progression, death from any cause or last tumor assessment, reported between day of first patient randomised, 17 August 2007, until cut-off date 28 February 2010

Intervention	Months (Median)
	NSE Levels at baseline: <= ULN (n: 155, 138)	NSE levels at baseline: > ULN (n: 48, 56)	Early NSE response: Response (n: 24, 16)	Early NSE response: Non-Response (n:16, 27)
Everolimus 10 mg/Day	13.86	8.11	8.11	3.79
Placebo	5.36	2.83	3.06	2.58

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Progression Free Survival According to Ki-67 Levels Categorized as: Less Than or Equal to 2%, > 2% to Less Than or Equal to 5% and > 5%

The level of Ki 67 expression for evaluable tumor samples were analyzed towards progression free survival (PFS) as per local investigator assessment. The Ki-67 protein is a cellular marker for proliferation. It is strictly associated with cell proliferation. During interphase, the Ki-67 antigen can be exclusively detected within the cell nucleus, whereas in mitosis most of the protein is relocated to the surface of the chromosomes. Baseline Ki 67 levels were categorized as: less than or equal to 2%, > 2% to less than or equal to 5% and > 5%. (NCT00510068)
Timeframe: Time from randomisation to dates of disease progression, death from any cause or last tumor assessment, reported between day of first patient randomised, 17 August 2007, until cut-off date 28 February 2010

Intervention	Months (Median)
	Ki67 <=2% (n: 7, 17)	2%	Ki67 >5% (n: 20, 22)
Everolimus 10 mg/Day	12.52	10.94	7.69
Placebo	3.68	8.48	3.15

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Progression Free Survival According to Chromogramin A Tumor Marker (CgA) Baseline Level and According to CgA Early Response

"Baseline levels of serum CgA SE were characterized towards progression free survival (PFS) as per local investigator assessment, relative to the upper limited of normal (ULN). CgA levels exceeding 2 x ULN were considered to be 'Elevated' otherwise considered as Non-elevated. An 'early response' (applicable to only those patients with elevated levels at baseline) was defined as a decrease of greater than or equal to 30% from baseline to Cycle 2 Day 1 or normalization by Cycle 2 Day 1. CgA is widely expressed in well-differentiated pancreatic NET. CgA is present in the secretory granules of neuroendocrine cells. Pancreatic NET patients often present with elevated circulating levels of CgA in their blood. Baseline levels of these biomarkers are considered as prognostic factors." (NCT00510068)
Timeframe: Time from randomisation to dates of disease progression, death from any cause or last tumor assessment, reported between day of first patient randomised, 17 August 2007, until cut-off date 28 February 2010

Intervention	Months (Median)
	CgA Levels at baseline: CgA <= 2x ULN (n:121, 97)	CgA levels at baseline: CgA > 2x ULN (n:84, 103)	Early CgA response: Response (n: 48, 22)	Early CgA response: Non-Response (n:40, 82)
Everolimus 10 mg/Day	11.17	8.54	8.54	11.14
Placebo	4.90	4.34	5.70	3.19

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Plasma Angiogenesis Marker: Vascular Endothelial Growth Factor (VEGF)

This biomarker is related to angiogenesis pathway, was analyzed to determine the effects of everolimus on plasma antiangiogenic molecules. (NCT00510068)
Timeframe: Baseline, Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1

Intervention	pg/mL (Mean)
	Baseline (n:198, 195)	Cycle 2 Day 1 (n: 185, 184)	Cycle 3 Day 1 (n: 185, 174)	Cycle 4 Day 1 (n: 171, 159)
Everolimus 10 mg/Day	265.09	243.03	280.18	283.51
Placebo	326.16	326.78	292.27	319.60

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Plasma Angiogenesis Marker: Soluble Vascular Endothelial Growth Factor Receptor 1 (sVEGFR1)

Intervention	pg/mL (Mean)
	Baseline (n:198, 195)	Cycle 2 Day 1 (n: 185, 184)	Cycle 3 Day 1 (n: 185, 174)	Cycle 4 Day 1 (n: 171, 159)
Everolimus 10 mg/Day	264.18	307.46	263.81	258.03
Placebo	256.69	299.03	253.37	242.17

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Plasma Angiogenesis Marker: Placental Growth Factor (PLGF)

Intervention	pg/mL (Mean)
	Baseline (n:198, 195)	Cycle 2 Day 1 (n: 185, 184)	Cycle 3 Day 1 (n: 185, 174)	Cycle 4 Day 1 (n: 171, 159)
Everolimus 10 mg/Day	45.82	25.78	26.55	25.69
Placebo	32.92	35.38	33.84	35.47

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Evaluation of Pharmacokinetics (PK) Parameter: CL/F

The PK parameters for a full PK profile at steady-state were determined in blood using non compartmental methods. The PK parameter clearance of distribution expressed as a function of bioavailability (CL/F). (NCT00510068)
Timeframe: Day 1 of every cycle (28 days/cycle) throughout the study

Intervention	L/h (Mean)
Everolimus 10 mg/Day	20.2
Everolimus 5 mg/Day	10.7

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Plasma Angiogenesis Marker: Basic Fibroblast Growth Factor (bFGF)

Intervention	pg/mL (Mean)
	Baseline (n:198, 195)	Cycle 2 Day 1 (n: 185, 184)	Cycle 3 Day 1 (n: 185, 174)	Cycle 4 Day 1 (n: 171, 159)
Everolimus 10 mg/Day	52.59	38.43	51.97	51.28
Placebo	51.49	58.33	59.08	54.58

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Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs) (Open-label Period)

Adverse events are defined as any unfavorable and unintended diagnosis, symptom, sign (including an abnormal laboratory finding), syndrome or disease which either occurs during study, having been absent at baseline, or, if present at baseline, appears to worsen. Serious adverse events are any untoward medical occurrences that result in death, are life threatening, require (or prolong) hospitalization, cause persistent or significant disability/incapacity, result in congenital anomalies or birth defects, or are other conditions which in judgment of investigators represent significant hazards. (NCT00510068)
Timeframe: on or after the start of open-label study medication until no later than 28 days after open-label study medication discontinuation

Intervention	Participants (Number)
	Adverse events (AEs)	Death	Serious Adverse Events
Everolimus 10 mg/Day	221	122	108

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Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs)

Adverse events are defined as any unfavorable and unintended diagnosis, symptom, sign (including an abnormal laboratory finding), syndrome or disease which either occurs during study, having been absent at baseline, or, if present at baseline, appears to worsen. Serious adverse events are any untoward medical occurrences that result in death, are life threatening, require (or prolong) hospitalization, cause persistent or significant disability/incapacity, result in congenital anomalies or birth defects, or are other conditions which in judgment of investigators represent significant hazards. (NCT00510068)
Timeframe: on or after the start of double-blind study medication until no later than 28 days after double-blind study medication discontinuation

Intervention	Participants (Number)
	Adverse events (AEs)	Death	Serious Adverse Events
Everolimus 10 mg/Day	203	111	84
Placebo	198	23	52

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Evaluation of Pharmacokinetics (PK) Parameters: Cmax, Cmin

The PK parameters for a full PK profile at steady-state were determined in blood using non compartmental methods. The PK parameter: maximum (peak) drug concentration (Cmax) and minimum (trough) drug concentration (Cmin). (NCT00510068)
Timeframe: Day 1 of every cycle (28 days/cycle) throughout the study

Intervention	ng/mL (Mean)
	Cmax	Cmin
Everolimus 10 mg/Day	62.4	9.80
Everolimus 5 mg/Day	27.4	12.2

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Evaluation of Pharmacokinetics (PK) Parameter: Tmax -Time to Maximum (Peak) Drug Concentration

The PK parameters for a full PK profile at steady-state were determined in blood using non compartmental methods. Values for tmax where summarized in median (range). (NCT00510068)
Timeframe: Day 1 of every cycle (28 days/cycle) throughout the study

Intervention	h (Median)
Everolimus 10 mg/Day	1.17
Everolimus 5 mg/Day	3.0

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Overall Survival

Overall survival (OS) was defined as the time from date of randomization to the date of death due to any cause. Analyses were performed using all deaths in the FAS population regardless of whether they were observed during the double-blind treatment period, the open-label treatment period, the post-treatment evaluations, or the survival follow-up period. (NCT00510068)
Timeframe: Baseline, to death- no time limit

Intervention	Months (Median)
Everolimus 10 mg/Day	44.02
Placebo	37.68

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Percentage of Participants With Objective Response Rate ( CR {Complete Response} OR PR {Partial Response})

Objective Response defined by RECIST criteria: Partial response (PR) must have ≥ 30% decrease in the sum of the longest diameter of all target lesions, from the baseline sum. Complete response (CR) must have disappearance of all target and non-target lesions. For CR or PR, tumor measurements must be confirmed by 2nd assessments within 4 weeks . Progression = 20% increase in the sum of the longest diameter of all target lesions, from the smallest sum of longest diameter of all target lesions recorded at or after baseline; or a new lesion; or progression of non-target lesions (NCT00510068)
Timeframe: Time from randomisation to dates of disease progression, death from any cause or last tumor assessment, reported between day of first patient randomised, 17 August 2007, until cut-off date 28 February 2010

Intervention	Percentage of participants (Number)
Everolimus 10 mg/Day	4.8
Placebo	2.0

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Time to Progression Free Survival (PFS) Based as Per Investigator Using Kaplan-Meier Methodology

Progression of disease is defined as the time from study start to the date of first documented progression of disease or death due to any cause. Progression of disease is defined by RECIST criteria: Progression = 20% increase in the sum of the longest diameter of all target lesions, from the smallest sum of longest diameter of all target lesions recorded at or after baseline; or a new lesion; or progression of non-target lesions. (NCT00510068)
Timeframe: Time from randomisation to dates of disease progression, death from any cause or last tumor assessment, reported between day of first patient randomised, 17 August 2007, until cut-off date 28 February 2010

Intervention	Months (Median)
Everolimus 10 mg/Day	11.04
Placebo	4.60

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Analysis of Time to Definitive Deterioration of WHO Performance Status Using Kaplan-Meier

Time to definitive worsening is defined as a definitive increase in performance status from a baseline of 0 or 1 to WHO >= 2, or from a baseline value of 2 to WHO >= 3. If no earlier deterioration, patients were censored at the end of follow-up or at the start of further antineoplastic therapy. Rates of patients with no deterioration at 3 and 6 months were computed using Kaplan-meier method. Grade 0: Able to carry out all activity without restriction; Grade 1: Restricted in physically strenuous activity but ambulatory & able to do light work; Grade 2: Ambulatory & capable of all self-care but unable to carry out any work. Up & about more than 50% of waking hours; Grade 3: Capable of only limited self-care, confined to bed or chair more than 50% of waking hours; Grade 4: Completely disabled & cannot carry on any self-care; totally confined to bed or chair. (NCT00510068)
Timeframe: 3 months, 6 months

Intervention	% of participants with no deterioration (Number)
	Month 3	Month 6
Everolimus 10 mg/Day	94.4	90.6
Placebo	91.8	86.3

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Evaluation of Pharmacokinetics (PK) Parameter: AUC0-t Last

The PK parameters for a full PK profile at steady-state were determined in blood using non compartmental methods. This PK parameter is area under the concentration-time curve from time zero to the time of the last quantifiable concentration (AUC0-t last). (NCT00510068)
Timeframe: Day 1 of every cycle (28 days/cycle) throughout the study

Intervention	ng.h/mL (Mean)
Everolimus 10 mg/Day	594
Everolimus 5 mg/Day	481

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Plasma Angiogenesis Marker: Soluble Vascular Endothelial Growth Factor Receptor 2 (sVEGFR2)

Intervention	pg/mL (Mean)
	Baseline (n:197, 193)	Cycle 2 Day 1 (n: 185, 183)	Cycle 3 Day 1 (n: 185, 173)	Cycle 4 Day 1 (n: 172, 158)
Everolimus 10 mg/Day	30061.30	22691.18	22021.23	21218.17
Placebo	31299.61	30223.21	29264.67	28308.58

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Efficacy Event Data After Month 12 to Month 60

Efficacy events were: Biopsy-proven acute rejection (BPAR), graft loss, death, and treatment failure (defined as composite endpoint of BPAR, graft loss, death, loss to follow-up, discontinuation due to lack of efficacy or due to toxicity). (NCT00514514)
Timeframe: Events starting after Month 12

Intervention	Participants (Number)
	BPAR	Graft loss	Death	Lost to follow-up	Discontinuation due to adverse event	Therapy failure (composite endpoint)
CNI Free Regimen	13	7	4	15	8	35
CNI Low Regimen	12	3	9	13	4	36
Standard Regimen	13	7	7	17	10	38

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Efficacy Event Data Baseline 2 (Month 3) to Month 12

Intervention	Participants (Number)
	BPAR	Graft loss	Death	Lost to follow-up	Discontinuation due to lack of efficacy	Discontinuation due to adverse event	Therapy failure composite
CNI Free Regimen	20	2	2	0	3	44	58
CNI Low Regimen	13	1	2	0	1	27	35
Standard Regimen	13	1	3	0	2	25	34

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Efficacy Event Data From Baseline 2 (Month 3) to Month 6

Intervention	Participants (Number)
	BPAR	Graft loss	Death	Lost to follow-up	Discontinuation due to lack of efficacy	Discontinuation due to adverse event	Therapy failure composite
CNI Free Regimen	15	1	1	0	2	26	37
CNI Low Regimen	10	1	0	0	1	13	19
Standard Regimen	6	0	1	0	1	8	14

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Change From BL2 (Month 3) to Month 12 in Cardiovascular Risk (Framingham Score; 10-year Cardiovascular Risk)

The Framingham Score (based on LDL cholesterol level) estimates the coronary heart disease risk (%) of developing one of the following coronary heart diseases: angina pectoris, myocardial infarction, or coronary disease death, over the course of 10 years. (NCT00514514)
Timeframe: From Baseline 2 (Month 3) to Month 12

Intervention	Percent risk (Mean)
	Baseline 1/Visit 1 (n=165,171,161)	Baseline 2/Month 3 (n=165,171,161)	Month 12 (n=158,166,156)	Change from Baseline 2 to Month 12 (n=158,166,156)
CNI Free Regimen	10.2	8.8	9.1	0.4
CNI Low Regimen	9.5	9.3	8.7	-0.7
Standard Regimen	10.9	10.3	9.4	-0.7

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GFR at Month 60 Utilizing Cockcroft-Gault Formula

Cockcroft-Gault formula: For men: GFR= ((140-age) × body weight in kg)∕(72 x serum creatinine in mg∕dl) For women: GFR= (0.85×(140-age) × body weight in kg)∕(72 x serum creatinine in mg/dl), ), last observation carried forward (LOCF) was used for imputation of missing values, ANCOVA model (NCT00514514)
Timeframe: From randomization at BL2 (Month 3) to Month 60 post-transplant

Intervention	ml/min/1.73m² (Least Squares Mean)
Standard Regimen	55.92
CNI Free Regimen	61.6
CNI Low Regimen	52.91

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GFR at Month 12 Utilizing Cockcroft-Gault Formula

Cockcroft-Gault formula: For men: GFR= ((140-age) × body weight in kg)∕(72 x serum creatinine in mg∕dl)For women: GFR= (0.85×(140-age) × body weight in kg)∕(72 x serum creatinine in mg/dl), ), last observation carried forward (LOCF) was used for imputation of missing values, ANCOVA model (NCT00514514)
Timeframe: From randomization at BL2 (Month 3) to Month 12 post-transplant

Intervention	ml/min/1.73m² (Least Squares Mean)
Standard Regimen	60.18
CNI Free Regimen	64.87
CNI Low Regimen	61.16

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GFR at Month 12 Utilizing Modification of Diet in Renal Disease (MDRD) Method

"Change in GFR (Modification of Diet in Renal Disease calculated using the -MDRD formulat:~For men: GFR = 170 × (serum creatinine -0,999)×(age-0,176) x (urea nitrogen -0,17) × (albumin0,318) For women: GFR = 170 × (serum creatinine -0,999) × (age-0,176) × (urea nitrogen -0,17) x (albumin0,318) × 0.762 with urea nitrogen = urea / 2.144. ), last observation carried forward (LOCF) was used for imputation of missing values, ANCOVA model, with treatment, center, donor type (deceased vs. living) as factors and BL2-value at V4/M3/BL2 as covariate." (NCT00514514)
Timeframe: From randomization at BL2 (Month 3) to Month 12 post-transplant

Intervention	ml/min/1.73m² (Least Squares Mean)
Standard Regimen	50.23
CNI Free Regimen	56.36
CNI Low Regimen	50.24

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Mean Change in Serum Creatinine From Month 3 to Month 60

Change in venous blood serum creatinine. Last observation carried forward (LOCF) was used for imputation of missing values, ANCOVA model (NCT00514514)
Timeframe: From randomization at BL2 (Month 3) to Month 60 post-transplant

Intervention	mg/dl (Least Squares Mean)
Standard Regimen	1.94
CNI Free Regimen	1.69
CNI Low Regimen	2.01

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GFR at Month 60 Utilizing Modification of Diet in Renal Disease (MDRD) Method

Intervention	ml/min/1.73m² (Least Squares Mean)
Standard Regimen	47.56
CNI Free Regimen	53.41
CNI Low Regimen	44.79

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GFR Calculated Via Nankivell Formula at Month 60

Change in GFR using the Nankivell formula (GFR = 6.7 / Scr + BW / 4 - Surea / 2-100 / (height)² + C where where Scr is the serum creatinine concentration expressed in mmol/L, BW the body weight in kilograms, Surea the serum urea in mmol/L, height in m, and the constant C is 35 for male and 25 for female patients. The calculated GFR is expressed in mL/min per 1.73m², last observation carried forward (LOCF) was used for imputation of missing values, ANCOVA model, with treatment, center, donor type (deceased vs. living) as factors and BL2-value at V4/M3/BL2 as covariate. (NCT00514514)
Timeframe: From randomization at BL2 (Month 3) to Month 60

Intervention	ml/min/1.73m² (Least Squares Mean)
Standard Regimen	60.24
CNI Free Regimen	66.98
CNI Low Regimen	58.74

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GFR Via Nankivell Formula at Month 12 - All Regimens

Intervention	ml/min/1.73m² (Least Squares Mean)
Standard Regimen	63.03
CNI Free Regimen	68.59
CNI Low Regimen	63.08

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GFR Via Nankivell Method at Month 12 - CNI-Free vs Standard Regimen

Demonstrate superiority of CNI-Free vs Standard Regimen in GFR using the Nankivell formula (GFR = 6.7 / Scr + BW / 4 - Surea / 2-100 / (height)² + C where where Scr is the serum creatinine concentration expressed in mmol/L, BW the body weight in kilograms, Surea the serum urea in mmol/L, height in m, and the constant C is 35 for male and 25 for female patients. The calculated GFR is expressed in mL/min per 1.73m², last observation carried forward (LOCF) was used for imputation of missing values, ANCOVA model, with treatment, center, donor type (deceased vs. living) as factors and BL2-value at V4/M3/BL2 as covariate. P-values are not adjusted (NCT00514514)
Timeframe: From randomization at BL2 (Month 3) to Month 12 post-transplant

Intervention	ml/min/1.73m² (Least Squares Mean)
Standard Regimen	63.03
CNI Free Regimen	68.59
CNI Low Regimen	63.08

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Mean Change in Serum Creatinine From Month 3 to Month 12

Intervention	mg/dl (Least Squares Mean)
Standard Regimen	1.66
CNI Free Regimen	1.58
CNI Low Regimen	1.76

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Surgery Group: Progression-free Survival

Progression-free survival (PFS) was assessed using Gadolinium chelate-enhanced Magnetic Resonance Imaging (MRI) and based on the Neuro-Oncology Criteria for Tumor Response for CNS tumors. PFS was measured from the first day of treatment after surgery to disease progression or death and is derived using the Kaplan-Meier method. (NCT00515086)
Timeframe: After surgery (within 96 hours), Weeks 4 and 8 and then every 8 weeks after restarting treatment until study discontinuation (Up to 28 weeks)

Intervention	Weeks (Median)
Everolimus 10 mg + Surgery	25.9
Everolimus 5 mg + Surgery	9.1
Everolimus 0 mg + Surgery	NA
Total	14.9

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No Surgery Group: Progression Free Survival

Progression-free survival (PFS) was assessed using Gadolinium chelate-enhanced Magnetic Resonance Imaging (MRI) and based on the Neuro-Oncology Criteria for Tumor Response for CNS tumors. PFS is reported for participants with 1 previous relapse and participants with ≥2 previous relapses. PFS was measured from the first day of treatment to disease progression or death and is derived using the Kaplan-Meier method. (NCT00515086)
Timeframe: First day of treatment to study discontinuation (up to 60 weeks)

Intervention	Weeks (Median)
No Surgery (1 Previous Relapse)	4.14
No Surgery ( ≥ 2 Previous Relapses)	4.14
Total : No Surgery	4.14

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Surgery Group: Number of Participants With Adverse Events

The number of participants with any adverse event by System Organ Class. Additional information about Adverse Events can be found in the Adverse Event Section. (NCT00515086)
Timeframe: First day of treatment to study discontinuation (Up to 28 weeks)

Intervention	Participants (Number)
	Gastrointestinal disorders	Nervous system disorders	General disorders & administration site conditions	Metabolism and nutrition disorders	Blood and lymphatic system disorders	Infections and infestations	Psychiatric disorders	Skin and subcutaneous tissue disorders	Investigations	Injury, poisoning, and procedural complications	Musculoskeletal and connective tissue disorders	Respiratory, thoracic and mediastinal disorders	Renal and urinary disorders	Vascular disorders	Immune system disorders	Eye disorders	Ear and labyrinth disorders	Reproductive system and breast disorders	Cardiac disorders	Endocrine disorders	Surgical and medical procedures	Neoplasms benign, malignant and unspecified
Everolimus 0 mg + Surgery	3	5	5	3	5	3	2	2	1	0	2	2	2	2	1	0	0	0	1	0	0	0
Everolimus 10 mg + Surgery	5	4	4	6	4	4	5	4	3	5	1	0	0	2	1	1	2	0	0	1	1	0
Everolimus 5 mg + Surgery	5	5	4	4	2	2	3	2	1	3	1	2	1	1	1	1	0	1	0	0	0	0

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No Surgery Group: Best Overall Tumor Response

The best overall tumor response is reported for participants with 1 previous relapse and participants with ≥2 previous relapses according to the following categories: Complete Response, Partial Response, Stable Disease and Progressive Disease. Gadolinium chelate-enhanced Magnetic Resonance Imaging (MRI) was used for tumor analysis. The objective assessment of tumor response was evaluated at each site by the designated pathologist based on the Neuro-Oncology criteria for Tumor Response for Central Nervous System (CNS) tumors. (NCT00515086)
Timeframe: First day of treatment to study discontinuation (up to 60 weeks)

Intervention	Participants (Number)
	Complete response + Partial response	Complete response	Partial response	Stable disease	Progressive disease
No Surgery ( ≥ 2 Previous Relapses)	0	0	0	6	6
No Surgery (1 Previous Relapse)	0	0	0	3	7

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Time to Progression

3.9 months with a CI of 21- (NCT00516165)
Timeframe: 2 years

Intervention	month (Median)
RAD001	3.9

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Progression-free Survival Rate at 24 Weeks

"Progression was 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~This information will be collected during two years of patient participation." (NCT00516165)
Timeframe: 2 years

Intervention	months (Median)
RAD001	3.8

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Overall Survival

The median overall survival was 8.4 months (95% CI, 3.9-21.1 months). Only 2 ((8 %) patients were progression-free at 24 weeks. The study did not proceed to the second stage of the phase 2 portion of the study. (NCT00516165)
Timeframe: 2 years

Intervention	months (Median)
RAD001	8.4

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Number of Patients With Adverse Events Who Were Treated With RAD001 for Advanced HCC

Everolimus given at 10 mg/day as a single agent was well tolerated in patients with advanced HCC. (NCT00516165)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
RAD001	28

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Maximum Tolerated Dose of RAD001 in Patients With Advanced Hepatocellular Carcinoma (HCC).

(NCT00516165)
Timeframe: 2 years

Intervention	mg (Number)
RAD001	10

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Overall Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00516165)
Timeframe: 2 years

Intervention	percentage of patient response (Number)
RAD001	4

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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

Intervention	months (Median)
Everolimus + Temozolomide	2.4

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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

Intervention	proportion of patients (Number)
Everolimus + Temozolomide	0.44

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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

Intervention	percentage of confirmed responses (Number)
Everolimus + Temozolomide	8.3

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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

Intervention	months (Median)
Everolimus + Temozolomide	8.6

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Change in PSA

Time-to-event data, such as change in PSA will be summarized using the method of Kaplan and Meier. (NCT00526591)
Timeframe: Up to 16 weeks after start of study

Intervention	ng/mL (Median)
High-dose Cohort	3.5
Low-dose Cohort	3.04

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Proportion of Patients Who Are P0 (i.e., no Clinically Detectable Tumor in the Pathologic Specimen) at Surgery

Specimens are fixed in formalin for 24 hours.Specimens are the cut at 3 mm intervals perpendicular to the rectal surface and the sections are examined grossly and microscopically on routine Hematoxylin and Eosin stain (H&E) (pathologic complete response or P0) will be defined as responders. (NCT00526591)
Timeframe: After 8 weeks of therapy at the time of prostatectomy

Intervention	participants (Number)
Low-dose Cohort	0
High-dose Cohort	0

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Toxicity Profile of Each Dose (Number of Patients With Worst Grade Toxicity)

Toxicity will be assessed using the NIH-NCI Common Terminology Criteria for Adverse Events, version 3.0 (CTCAEv3.0) (NCT00526591)
Timeframe: at daily dose for 8 weeks

Intervention	participants (Number)
	Patients with Grade 3 toxicity	Patients with Grade 4 toxicity
High-dose Cohort	1	0
Low-dose Cohort	2	0

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Percent Change in FDG-PETUptake Following 2 Weeks of Therapy

The secondary objective was to explore whether an early change in FDG-PET uptake is associated with tumor shrinkage. Change in FDG-PET uptake was calculated using the baseline and 2-week FDG-PET scans. (NCT00529802)
Timeframe: 2 weeks

Intervention	% change in avgSUVmax at 2 weeks (Mean)
Patients Evaluable for Secondary Outcome	-29.7

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Relative Tumor Size Change Following 8 Weeks of Therapy.

The primary objective is to determine whether high SUV uptake on FDG-PET is associated with greater tumor shrinkage. Tumor size is defined as the sum of unidimensional tumor measurements from standard CT imaging calculated according to RECIST criteria. Tumor size is measured at baseline and after eight weeks of therapy. Tumor shrinkage is the relative change (%) in tumor size from baseline. (NCT00529802)
Timeframe: 8 weeks

Intervention	Percent change from baseline (Mean)
Low Uptake	1.4
High Uptake	-0.57

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Revascularizations

(TLR/TVR/any revascularization)both ischemia-driven and not ischemia-driven. (NCT00531011)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
XIENCE V	0
TAXUS® Liberté™	0

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Distal Minimum Lumen Diameter (MLD).

Distal refers to the immediate 5 mm outside of the distal end of the stent. (NCT00531011)
Timeframe: at 9 months.

Intervention	millimeters (Mean)
XIENCE V	2.28
TAXUS® Liberté™	2.25

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In-stent Late Loss (LL)

Full Analysis Set (FAS). LL is defined as the difference between the post-procedure (immediately post placement of the stent) minimal lumen diameter (MLD) and the follow-up MLD (at 270 days). In stent is measured within the confines of the stent edges. (NCT00531011)
Timeframe: at 270 days

Intervention	millimeters (Mean)
XIENCE V	0.052
TAXUS® Liberté™	0.238

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In-stent Minimum Lumen Diameter (MLD).

(NCT00531011)
Timeframe: at 9 months.

Intervention	millimeters (Mean)
XIENCE V	2.29
TAXUS® Liberté™	2.17

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Composite Rate of Cardiac Death, Myocardial Infarction (MI, Both Q-wave and Non Q-wave), and Ischemia-driven Target Lesion Revascularization (TLR) .

This measure is a calculation of the percentage of participants who experience any of the components of this composite measure. (NCT00531011)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
XIENCE V	1
TAXUS® Liberté™	2.1

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Composite Rate of All Death, MI (Q-wave and Non Q-wave), and Target Vessel Revascularization (TVR).

(NCT00531011)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
XIENCE V	1
TAXUS® Liberté™	2.1

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Device Success

defined as achievement of a final residual in-stent diameter stenosis of < 30% (visual assessment) using the assigned device only. (NCT00531011)
Timeframe: at the time of PCI

Intervention	percentage of participants (Number)
XIENCE V	97.7
TAXUS® Liberté™	98.2

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Composite Endpoint of All Death, MI (Q-wave and Non Q-wave), and TVR.

(NCT00531011)
Timeframe: 9 months

Intervention	percentage of participants (Number)
XIENCE V	6.8
TAXUS® Liberté™	12.4

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Procedural Success

defined as: residual in-stent %DS of < 30% using a percutaneous method, without cardiac death, Q-wave MI, non Q-wave MI, or repeat revasc of the target during hospitalization. (NCT00531011)
Timeframe: at the time of PCI

Intervention	percentage of participants (Number)
XIENCE V	98.1
TAXUS® Liberté™	97

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Adjudicated Stent Thrombosis.

(NCT00531011)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
XIENCE V	0
TAXUS® Liberté™	0

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Adjudicated Stent Thrombosis.

(NCT00531011)
Timeframe: 9 months

Intervention	percentage of participants (Number)
XIENCE V	0
TAXUS® Liberté™	0

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Composite Endpoint of Cardiac Death, MI (Q-wave and Non Q-wave), and Ischemia-driven TLR .

ITT (NCT00531011)
Timeframe: 9 months

Intervention	percentage of participants (Number)
XIENCE V	4.9
TAXUS® Liberté™	7.2

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Lesion Success

defined as attainment of < 30% residual in-stent stenosis (by visual assessment) using any percutaneous method. (NCT00531011)
Timeframe: at the time of PCI

Intervention	Percentage of participants (Number)
XIENCE V	99.2
TAXUS® Liberté™	99.6

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In-segment Binary Restenosis Rate

"This measures the percentage of patients who have > 50% diameter stenosis of the assessed vessel, within the stent edges~In-segment is measured within the confines of the stent edges plus within 5 mm on either side of the stent." (NCT00531011)
Timeframe: at 9 months

Intervention	percentage of participants (Number)
XIENCE V	6.2
TAXUS® Liberté™	4.6

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In-segment Late Loss (LL)

LL is defined as the difference between the post-procedure (immediately post placement of the stent) minimal lumen diameter (MLD) and the follow-up MLD (at 270 days). In segment LL is measured within the confines of the stent edges and within 5 mm of those edges. (NCT00531011)
Timeframe: at 9 months

Intervention	millimeters (Mean)
XIENCE V	-0.100
TAXUS® Liberté™	0.037

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In-segment Minimum Lumen Diameter (MLD).

(NCT00531011)
Timeframe: at 9 months.

Intervention	millimeters (Mean)
XIENCE V	2.10
TAXUS® Liberté™	2.04

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In-stent Binary Restenosis Rate

This measures the percentage of patients who have > 50% diameter stenosis of the assessed vessel, within the stent edges. (NCT00531011)
Timeframe: at 9 months

Intervention	percentage of participants (Number)
XIENCE V	5.8
TAXUS® Liberté™	3.6

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Proximal Minimum Lumen Diameter (MLD).

Proximal refers to the immediate 5 mm outside of the proximal end of the stent. (NCT00531011)
Timeframe: at 9 months.

Intervention	millimeters (Mean)
XIENCE V	2.67
TAXUS® Liberté™	2.61

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Revascularizations

(TLR/TVR/any revascularization)both ischemia-driven and not ischemia-driven. (NCT00531011)
Timeframe: 9 months

Intervention	percentage of participants (Number)
XIENCE V	5.8
TAXUS® Liberté™	11.3

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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

Intervention	months (Median)
Phase II	15.8

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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

Intervention	participants who developed DLTs (Number)
Phase I: Dose Level 0	1
Phase I: Dose Level 1	1
Phase I: Dose Level 2	1

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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

Intervention	proportion of participants (Number)
Phase II	0.52

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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

Intervention	percentage of participants (Number)
Phase II	44.4

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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

Intervention	proportion of participants (Number)
Phase II	0.64

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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

Intervention	months (Median)
Phase II	6.4

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Time to Progression

(NCT00570921)
Timeframe: Duration of time start of treatment to time of documented progression or death

Intervention	months (Median)
Fulvestrant + Everolimus	7.4

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Objective Response Rates

Intervention	participants (Number)
Fulvestrant + Everolimus	4

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Clinical Benefit Rate

Clinical benefit rate is defined as a complete response, partial response, or stable disease (CR, PR, SD) by Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for a minimum of at least 24 weeks or more. (NCT00570921)
Timeframe: Duration of response or stable disease for 24 weeks or more

Intervention	participants (Number)
Fulvestrant + Everolimus	15

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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

Intervention	Participants (Count of Participants)
Temozolomide and Everolimus	16

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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

Intervention	months (Median)
Temozolomide and Everolimus	15.4

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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

Intervention	Participants (Count of Participants)
	Grade 3 or 4 Lymphopenia	Grade 3 or 4 thrombocytopenia	Grade 3 or 4 mucositis	Grade 3 or 4 hyperglycemia	Grade 3 or 4 AST Increase	Grade 3 or 4 Leukocyte decrease
Temozolomide and Everolimus	19	7	1	8	4	7

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Percentage of Patients in Each Study Arm With Increase of ≥1 Point in the Ishak-Knodell Staging Score in Fibrosis

Ishak-Knodell Score: 0=No fibrosis; 01=Fibrous expansion of some portal areas, with or without short fibrous septa; 02=Fibrous expansion of most portal areas, with or without short fibrous septa; 03=Fibrous expansion of most portal areas, with occasional portal to portal (P-P) bridging; 04=Fibrous expansion of portal areas, with marked bridging (portal to portal (P-P) as well as portal to central (P-C)); 05=Marked bridging (P-P and/or P-C) with occasional nodules (incomplete cirrhosis); 06=Cirrhosis, probable or definite. (NCT00582738)
Timeframe: baseline to month 24

Intervention	percentage of participants (Number)
Standard Treatment	38.9
Everolimus	7.1

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Change From Baseline in Fibrosis Staging Score (Measured by the Ishak-Knodell Staging Score) Between Baseline and 24 Months Post-transplant.

"Ishak-Knodell Score: 0=No fibrosis; 01=Fibrous expansion of some portal areas, with or without short fibrous septa; 02=Fibrous expansion of most portal areas, with or without short fibrous septa; 03=Fibrous expansion of most portal areas, with occasional portal to portal (P-P) bridging; 04=Fibrous expansion of portal areas, with marked bridging (portal to portal (P-P) as well as portal to central (P-C)); 05=Marked bridging (P-P and/or P-C) with occasional nodules (incomplete cirrhosis); 06=Cirrhosis, probable or definite~Decrease in score from baseline indicates improvement" (NCT00582738)
Timeframe: baseline, 24 Months

Intervention	Score on Scale (Median)
CsA-TAC	-0.5
Everolimus	0.0

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Comparison of Renal Function (Glomerular Filtration Rate [GFR] Calculated Using the Modification of Diet in Renal Disease Study Group [MDRD] Formula) Between Study Groups

"GFR Month 9 value if available, otherwise minimal first year post-randomization available value. Imputation rule of missing Month 24 GFR values: GFR Month 18 value if available, otherwise Month 12 GFR is used.~Least square means are from an ANCOVA model containing treatment as factor and baseline eGFR as a covariate." (NCT00582738)
Timeframe: 12 months, 24 months/EOS

Intervention	mL/min/1.73^2 (Least Squares Mean)
	12 Months (n=21, 22)	24 months (n=20, 18)
CsA-TAC	62.2	65.5
Everolimus	65.6	71.6

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Percentage of Patients With Death, Graft Loss and Biopsy Proven Acute Rejection (BPAR) Between Study Groups

(NCT00582738)
Timeframe: 24 Months

Intervention	Percentage of Participants (Number)
	Death	Graft Loss	Acute Rejection (BPAR)
CsA/TAC	0	0	0
Everolimus	4.5	4.5	0.0

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Number of Patients With Events (Progression to Cirrhosis, Retransplantation, HCV Related Death, First BPAR, Graft Loss)at 12 and 24 Months

(NCT00582738)
Timeframe: 12 months, 24 months

Intervention	participants (Number)
	12 months	24 months
CsA-TAC	0	0
Everolimus	0	1

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Comparison of the Effect of Both Regimens on the Inflammatory (Acti-test) and Fibrosis (Fibro-test) Components of Fibrosure, and on Fibrosis Area Assessed by Histomorphometry

"The Fibrosure test is the combination of Fibro-test + Acti-test.~FibroTest (FT) was for the assessment of fibrosis. Fibro test was calculated using an original combination of five highly concentrated serum biochemical markers; alpha2macroglobulin, haptoglobin, apolipoprotein A1, total bilirubin and gammaglutamyltransferase (GGT). FibroTest scores range from 0.00 to 1.00 where 0.0-0.21 is no fibrosis and >= 0.59 is cirrhosis.~Acti-test was calculated using 6 serum biochemical markers; alpha2macroglobulin, haptoglobin, apolipoprotein A1, total bilirubin, GGT and alanine aminotransferase (ALT). ActiTest (AT) was used for the assessment of necroinflammatory activity. Test score ranges from 0.00 to 1.00, where 0.00-0.17 indicates no necrosis and >= 0.61 indicates severe necrosis~If 12-month Actitest value was the last available assessment, the value is used to impute the final staging score(End of Study)" (NCT00582738)
Timeframe: baseline, 12 and 24 months

,,,

Intervention	units on a scale (Median)
	Baseline (n=21,21,21,21)	month 12 (n=20,17, 20, 17)	month 24 (n=1,2,1,2)	end of study [month 24] (n=20,21,20,21)
Everolimus - Summary of Fibrotest by Treatment	0.80	0.80	1.0	0.70
Everolimus -Summary of Actitest by Treatment	0.50	0.50	0.70	0.50
Standard Treatment - Summary of Actitest by Treatment	0.40	0.60	0.60	0.60
Standard Treatment -Summary of Fibrotest by Treatment	0.80	0.80	0.90	0.80

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Comparison of the Effect of Both Regimens in the Necroinflammatory Grading Score (Ishak-Knodell) (Portal Inflammation)

Intervention	Score on a scale (Mean)
	Baseline (n= 18, 14)	Month 12 (n = 18, 14)	Month 24 (n = 8, 5)
CsA-TAC	1.8	1.9	2.1
Everolimus	2.4	1.9	2.0

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Change From Baseline in Hepatitis C Virus (HCV) Ribonucleic Acid (RNA) Viral Load at 12 and 24 Months Post Randomization

End of Study (EOS) endpoint is the last available assessment on or after Month 12. A reduction of at least two logs in HCV RNA viral load was considered as success (NCT00582738)
Timeframe: baseline, 12 months, 24 months/EOS

Intervention	log10 copies/ml (Mean)
	baseline	12 months (n=20, 20)	24 months/EoS (n=20, 20)	Month 12 - baseline (n=20,20)	Monh 24 - baseline (n=20,20)
CsA-TAC	6.6	6.5	6.9	-0.1	0.3
Everolimus	6.4	6.6	6.7	0.2	0.3

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Change From Baseline in Fibrosis Metavir Scoring at 12 and 24 Months Post Randomization

Metavir Score: F0=No fibrosis; F1=Portal fibrosis without septa; F2=Portal fibrosis with rare septa; F3=Numerous septa without cirrhosis Decrease in score from baseline indicates improvement (NCT00582738)
Timeframe: Baseline, 12 months, 24 months

Intervention	Scores on a Scale (Median)
	Baseline (n=18, 14)	Month 12 (n=18, 14)	Month 24 (n=8, 5)	Month 12-Baseline (n=18, 14)	Month 24-Baseline (n=8, 5)
CsA-TAC	1.0	1.0	1.0	0.0	0.0
Everolimus	1.5	1.0	1.0	0.0	0.0

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Objective Response Rate (ORR)

The percentage of patients who experience an objective benefit from treatment (CR+PR). The response categories were assigned using RECIST criteria. Complete Response (CR) = Disappearance of all target lesions ; Partial Response (PR) = >=30% decrease in the sum of the longest diameter of target lesions. (NCT00591734)
Timeframe: 13 months

Intervention	Participants (Count of Participants)
Intervention	7

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Overall Survival Rate

Overall Survival is defined as the length of time, in months, that patients were alive from their first date of protocol treatment until death. For patients who were alive at the time of calculation, follow-up time was censored at date of last contact. The percentage of patients who were alive at 1 year is reported here. This was estimated using the Kaplan Meier method. (NCT00591734)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Intervention	43

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Progression-free Survival

Length of time, in months, that patients were alive from their first date of protocol treatment until worsening of their disease (NCT00591734)
Timeframe: 13 months

Intervention	months (Median)
Intervention	4

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Progression Free Survival (PFS)

8 week PFS (NCT00597506)
Timeframe: interval between start of treatment and 8-week

Intervention	proportion of participants (Number)
Bevacizumab and Everolimus	0.58

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Overall Response

Overall response is composed of complete responses and partial responses. Complete response (CR): disappearance of all target lesions; Partial response: at least a 30 percent decrease in the sum of the longest diameter of the target lesions taking as reference the baseline sum longest diameter. Response is assessed at each subject's restaging, approximately ever 2 months. (NCT00597506)
Timeframe: Measured 1 month after the last treated subject came off treatment

Intervention	percentage of participants (Number)
Bevacizumab and Everolimus	0

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Net Change Relative to Baseline in Tumor Blood Flow

Tumor blood flow (ml/min/100gm) determined by functional computed tomography (CT). Functional computed tomography (CT) at baseline, after first and third cycles (21 day cycles). Change (percentage) calculated as tumor blood flow measured at baseline compared to tumor blood flow measurement taken at end of Cycle 1, week 3 (21 days), and again at end of Cycle 3, Week 9 (63 days). (NCT00607113)
Timeframe: Baseline to end of Cycle 3 (63 days)

Intervention	ml/min/100gm (Mean)
	Baseline to Week 3	Baseline to Week 9
Avastin	-0.44	-0.60
RAD001	-0.12	-0.40

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In-Stent Percent Diameter Stenosis

In Stent Percent Diameter Stenosis at thirteen months. In Stent Percent Diameter Stenosis: measured percent of diameter stenosis at the region of the stent (calculated as 100x(RVD-MLD)/RVD using the mean values from 2 orthogonal views by QCA. RVD (Reference Vessel Diameter): average of normal segments within 10mm proximal and distal to target lesion from 2 orthogonal views using QCA. MLD (Minimal Lumen Diameter): average of 2 orthogonal views of the narrowest point wihtin the area of assessment. MLD measured during QCA by the angiographic core laboratory. (NCT00617084)
Timeframe: 13 Months

Intervention	Percentage diameter stenosis (Mean)
1. Resolute - 12-13 Months	21.65
2. XIENCE V - 12-13 Months	19.76

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Target Lesion Failure

Percentage of participants that had either Cardiac Death, Myocardial Infarction (not clearly attributable to a non-target vessel)or Target Lesion Revascularization (TLR, clinically indicated) after one year. MI: Q MI if new pathological Q waves and chest pain, non Q MI if CK elevated more than two times normal, troponin elevated more than normal, according to ARC definitions. TLR, clinically indicated if associated with ischemic symptoms and angiographic min lumen diameter bigger than fifty percent by QCA or without symptoms and min lumen diameter bigger than seventy percent. Measure average. (NCT00617084)
Timeframe: 12 months

Intervention	percentage of participants (Number)
1. Resolute - 12-13 Months	8.2
2. XIENCE V - 12-13 Months	8.3

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Incidence Rate of Composite Efficacy Failure From Randomization to Month 24

"Composite efficacy failure was defined as treated biopsy proven acute rejection (tBPAR), graft loss, or death.~The incidence rates of composite efficacy failure were estimated with a Kaplan-Meier product-limit formula." (NCT00622869)
Timeframe: Randomization to Month 24

Intervention	Percentage (Number)
Everolimus + Reduced Tacrolimus	10.3
Tacrolimus Elimination	26.0
Tacrolimus Control Arm	12.5

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Incidence Rate of Composite Efficacy Failure From Randomization to Month 12

"Composite efficacy failure was defined as treated biopsy proven acute rejection (tBPAR), graft loss, or death. A BPAR was defined as an acute rejection confirmed by biopsy with a Rejection Activity Index (RAI) score ≥ 3. tBPAR was defined as a BPAR which was treated with anti-rejection therapy. The RAI is used to score liver biopsies with acute rejection and is composed of 3 categories (portal inflammation, bile duct inflammation damage, venous endothelial inflammation) each scored on a scale of 0 (absent) to 3 (severe) by a trained pathologist. The total RAI score = the sum of the scores of the 3 categories and ranges from 0 to 9, with a higher score indicating greater rejection. The graft was presumed to be lost on the day the patient was newly listed for a liver graft, they received a graft re-transplant, or they died.~The incidence rates of composite efficacy failure were estimated with a Kaplan-Meier product-limit formula." (NCT00622869)
Timeframe: Randomization to Month 12

Intervention	Percentage of participants (Number)
Everolimus + Reduced Tacrolimus	6.7
Tacrolimus Elimination	24.2
Tacrolimus Control Arm	9.7

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Incidence Rate of Treated Biopsy Proven Acute Rejection (tBPAR) at Months 12 and 24

"tBPAR was defined as an acute rejection confirmed by biopsy with a Rejection Activity Index (RAI) score ≥ 3, which was treated with anti-rejection therapy. Liver biopsies were collected for all cases of suspected acute rejection preferably within 24 hours, at the latest within 48 hours, whenever clinically possible. The RAI is used to score liver biopsies with acute rejection and is composed of 3 categories (portal inflammation, bile duct inflammation damage, venous endothelial inflammation) each scored on a scale of 0 (absent) to 3 (severe) by a trained pathologist. The total RAI score = the sum of the scores of the 3 categories and ranges from 0 to 9, with a higher score indicating greater rejection. The graft was presumed to be lost on the day the patient was newly listed for a liver graft, they received a graft re-transplant, or they died.~The incidence rates of tBPAR were estimated with a Kaplan-Meier product-limit formula." (NCT00622869)
Timeframe: Randomization to Month 24

Intervention	Percentage (Number)
	Month 12	Month 24
Everolimus + Reduced Tacrolimus	3.0	4.8
Tacrolimus Control Arm	7.2	7.7
Tacrolimus Elimination	18.8	19.9

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Change in Renal Function From Randomization to Months 12 and 24

"Change in renal function was assessed by the estimated Glomerular Filtration Rate (eGFR) using the abbreviated (4 variables) Modification of Diet in Renal Disease (MDRD-4) formula which was developed by the MDRD Study Group and has been validated in patients with chronic kidney disease. The MDRD-4 formula used for the eGFR calculation is: eGFR (mL/min/1.73m^2) = 186.3*(C^-1.154)*(A^-0.203)*G*R, where C is the serum concentration of creatinine (mg/dL), A is age (years), G=0.742 when gender is female, otherwise G=1, R=1.21 when race is black, otherwise R=1.~The changes in renal function were analyzed via analysis of covariance (ANCOVA) with treatment, pre-transplant hepatitis C virus status and randomization eGFR as covariates. Based on these ANCOVA analyses, the least-squares mean and standard errors of change were reported." (NCT00622869)
Timeframe: Randomization to Month 24

Intervention	mL/min/1.73m^2 (Least Squares Mean)
	Month 12 (N=244, 231, 243)	Month 24 (N=245, 231, 243)
Everolimus + Reduced Tacrolimus	-2.23	-7.94
Tacrolimus Control Arm	-10.73	-14.60
Tacrolimus Elimination	-1.51	-4.19

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Biochemical Response Rate

Number of participants with 50% decline in serum PSA from baseline was pre-set as the primary measure of disease response. (NCT00629525)
Timeframe: Patients were followed for a median of 315 days

Intervention	participants (Number)
RAD001	0

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Clinical Response

"The percentage of participants with a complete or partial response as defined by RECIST 1.0. Response Criteria are defined below:~Complete Response: Disappearance of all target lesions Partial Response: 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: 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: Neither sufficient shrinkage to qualify for partial response nor sufficient increase to qualify for progressive disease, taking as reference the smallest sum LD" (NCT00629525)
Timeframe: Patients were followed for a median of 315 days

Intervention	participants (Number)
RAD001	0

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Molecular Response

Functional extent of mTOR inhibition by changes in the phosphorylation status of pS6 in prostate tumors. (NCT00629525)
Timeframe: Patients were followed for a median of 315 days

Intervention	percentage of decrease (Mean)
RAD001	60.11

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Progression Free Survival

Time in months from the start of study treatment to the date of first progression according to RECIST 1.0, 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. (NCT00629525)
Timeframe: Patients were followed for a median of 315 days, with the last patient censored at 1309 days.

Intervention	months (Median)
RAD001	3.58

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Pathologic Response

Number of participants with either a 50% or greater decrease in proliferation index or a 50% or greater increase in apoptotic index (NCT00629525)
Timeframe: Patients were followed for a median of 315 days

Intervention	participants (Number)
RAD001	0

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Incidence of Grade 4 Treatment-Related Toxicity

All grade 4 adverse events (AE) with treatment attribution of possibly, probably or definite based on CTCAEv3 as reported on case report forms were counted. Incidence is the number of patients experiencing at least one treatment-related grade 4 AE of any type during the time of observation. (NCT00630344)
Timeframe: Assessed each cycle during therapy and up to 30 days post-therapy completion which is approximately 1 year for patients in this study cohort.

Intervention	Participants (Count of Participants)
RAD001 + Bicalutamide	0

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Incidence of Grade 1-3 Treatment-Related Fatigue Toxicity

All grade 1-3 fatigue adverse events (AE) with treatment attribution of possible, probable or definite based on CTCAEv3 as reported on case report forms were counted. Incidence is the number of patients experiencing at least one treatment-related grade 1-3 fatigue AE during the time of observation. (NCT00630344)
Timeframe: Assessed each cycle during therapy and up to 30 days post-therapy completion which is approximately 1 year for patients in this study cohort.

Intervention	Participants (Count of Participants)
RAD001 + Bicalutamide	16

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Time to Progression (TTP)

TTP estimated with Kaplan-Meier methods is defined as the time from treatment start to when PSA progression criteria is first met, or the date of measurable or non-measurable disease progression (PD). Absent progression, patients are censored at the date of the last PSA measurement. PSA progression is a ≥25% increase over baseline or nadir PSA, whichever is lowest with a minimum increase of 5 ng/mL. If PSA declines ≥50%, PSA progression is a ≥50% PSA increase above nadir with a minimum increase of 5 ng/mL or back to pretreatment baseline, whichever is lowest. PSA progression requires 2 week confirmation. Per RECIST, PD is at least a 20% increase in sum LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or appearance of new lesions. Non-measurable PD is defined as a worsening bone scan, as indicated by the appearance of two or more new lesions, the appearance of new non-bony metastases or a requirement for radiation therapy. (NCT00630344)
Timeframe: PSA was measured monthly and measurable disease on imaging assessed every 2 cycles in first 8 weeks and every 3 cycles thereafter. In this study cohort, patients were followed on treatment up to approximately 1 year.

Intervention	weeks (Median)
RAD001 + Bicalutamide	8.7

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Incidence of Grade 1-3 Treatment-Related Mucositis Toxicity

All grade 1-3 mucositis adverse events (AE) with treatment attribution of possible, probable or definite based on CTCAEv3 as reported on case report forms were counted. Incidence is the number of patients experiencing at least one treatment-related grade 1-3 mucositis AE during the time of observation. (NCT00630344)
Timeframe: Assessed each cycle during therapy and up to 30 days post-therapy completion which is approximately 1 year for patients in this study cohort.

Intervention	Participants (Count of Participants)
RAD001 + Bicalutamide	20

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Incidence of Grade 1-3 Treatment-Related Rash Toxicity

All grade 1-3 rash adverse events (AE) with treatment attribution of possible, probable or definite based on CTCAEv3 as reported on case report forms were counted. Incidence is the number of patients experiencing at least one treatment-related grade 1-3 rash AE during the time of observation. (NCT00630344)
Timeframe: Assessed each cycle during therapy and up to 30 days post-therapy completion which is approximately 1 year for patients in this study cohort.

Intervention	Participants (Count of Participants)
RAD001 + Bicalutamide	17

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Overall Response Rate

"Overall response rate is the percentage of patients achieving response taking into consideration measurable disease, bone metastases, and PSA. PSA declines in the absence of both measurable disease and the appearance of new bone lesions or a response in measurable disease without an increase in PSA or the appearance of new bone lesions. Patients with stable disease (SD) lasting at least 6 months will also be considered responders.~Per RECIST guidelines, for target lesions, complete response (CR) is complete disappearance of all target lesions and partial response (PR) is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. CR or PR confirmation is required within 4 weeks. Per modified PSAWG2 criteria (Scher H, Halabi S, Tannock I et al. JCO 2008) PSA response is defined as PSA decline ≥ 50% from baseline confirmed by a second measurement at least 4 weeks later." (NCT00630344)
Timeframe: PSA was measured monthly and measurable disease on imaging assessed every 2 cycles in first 8 weeks and every 3 cycles thereafter. In this study cohort, patients were followed on treatment up to approximately 1 year.

Intervention	percentage of patients (Number)
RAD-001 + Bicalutamide	6

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Progression of Measured Glomerular Filtration Rate

Change in renal progression measured by mean mGFR from week 7 to Month 36 (NCT00634920)
Timeframe: Week 7, Week 52, Month 36

Intervention	mL/min/1.73m^2 (Mean)
	Week 7	Week 52	Change from week 7 to Week 52	Month 36	Change from week 7 to Month 36
Control (CsA)	47.8	47.8	0.0	46.1	-1.7
Everolimus (CNI-free)	46.3	51.5	5.6	48.2	1.3

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Percentage of Participants With Treatment Failures

Treatment failure was defined as graft loss or death. (NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	Percentage of participants (Number)
	Month 12: No Failure	Month 12: Failure	Month 24: No Failure	Month 24: Failure	Month 36: No Failure	Month 36: Failure
Control (CsA)	100.0	0.0	98.8	1.2	96.7	3.3
Everolimus (CNI-free)	100.0	0.0	98.8	1.2	98.8	1.2

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Percentage of Participants With Graft Loss or Death

The allograft was presumed to be lost on the day the patient started dialysis and was not able to subsequently be removed from dialysis. If the patient underwent a graft nephrectomy, the day of nephrectomy was the day of graft loss. Graft loss was considered an SAE (serious adverse event). (NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	Percentage of participants (Number)
	Month 12: Event First Year	Month 12: No Event First Year	Month 24: Event Second Year	Month 24: No Event Second Year	Month 36: Event Third Year	Month 36: No Event Third Year
Control (CsA)	0.0	100.0	1.1	98.9	2.2	97.8
Everolimus (CNI-free)	0.0	100.0	1.1	98.9	0.0	100.0

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Percentage of Participants With Biopsy Proven Acute Rejection (BPAR)

A BPAR was defined as a biopsy graded IA, IB, IIA, IIB, or III (Banff 97 classification). Biopsy graded IA: Significant interstitial infiltration (> 25% of parenchyma) and foci of moderate tubulitis (> 4 mononuclear cells/tubular cross section or group of 10 tubular cells). Biopsy grade IB: Significant interstitial infiltration (> 25% of parenchyma) and foci of severe tubulitis (> 10 mononuclear cells/tubular cross section or group of 10 tubular cells). Biopsy grade IIA: Mild to moderate intimal arteritis. Biopsy graded IIB: Severe intimal arteritis comprising > 25% of the lumenal area. (NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	Percentage of participants (Number)
	Month 12: lA	Month 12: lB	Month 12: llA	Month 12: llB	Month 24: lA	Month 24: lB	Month 36: lA	Month 36: lB
Control (CsA)	4.4	0.0	2.2	1.1	4.4	3.3	1.1	0.0
Everolimus (CNI-free)	19.6	10.9	2.2	2.2	5.4	1.1	2.2	1.1

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Percentage of Participants on Lipid-lowering Drugs

(NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	Percentage of participants (Number)
	Month 12	Month 24	Month 36
Control (CsA)	60.0	65.0	63.0
Everolimus (CNI-free)	75.0	78.0	73.0

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Percentage of Participants Who Had Donor Specific Antibodies (DSA)

Venous blood was drawn for donor specific (DSA) measurements prior to transplantation and at the final visit (36 months). The blood sample was first screened for the presence of PRA i.e. donor specific Immunoglobulin-G antibodies against specific HLA antigens. If PRA antibodies were detected, the blood sample was tested for specific DSAs on single antigen Luminex beads (coated with single HLA class I or II molecules). In this way, the specificity of these antibodies could be determined. (NCT00634920)
Timeframe: Month 36

Intervention	Percentage of participants (Number)
	ND (not done)	Negative	Positive
Control (CsA)	9.0	70.0	21.0
Everolimus (CNI-free)	7.0	78.0	15.0

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Percentage of Participants Who Developed CAN (Chronic Allograft Nephropathy)

Assessed by protocol biopsies findings (Banff 1997 lesion scores and morphometry of the interstitial space) (NCT00634920)
Timeframe: Month 12, Month 36

Intervention	Percentage of participants (Number)
	Month 12	Month 36
Control (CsA)	1.0	64.0
Everolimus (CNI-free)	1.0	59.0

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Time to First Malignancy

This is the time to first diagnosed malignancy. Malignancies (skin- or solid cancer) were listed whether they reoccurred in situ, were metastatic or de novo. This is shown as mean time. (NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	Months (Mean)
Everolimus (CNI-free)	35.5
Control (CsA)	35.1

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Measured Glomerular Filtration Rate

Progression of renal function measured by mean mGFR at 36 months after renal TX. The mGFR was measured using Iohexol or Cr-EDTA clearance according to local practice. (NCT00634920)
Timeframe: Month 36

Intervention	mL/min/1.73m^2 (Mean)
Everolimus (CNI-free)	48.2
Control (CsA)	46.1

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Calculated Glomerular Filtration Rate

The GFR was calculated according to the Modification of Diet in Renal Disease Study Group (MDRD) method, the Cockcroft-Gault method, and the Nankivell formula. cGFR was calculated from blood samples collected at predefined time points. (NCT00634920)
Timeframe: Months 12, 36

Intervention	mL/min/1.73m^2 (Mean)
	MDRD M12	MDRD M36	Cockcroft-Gault M12	Cockcroft-Gault M36	Nankivel M12	Nankivel M36
Control (CsA)	60.1	57.4	45.6	42.1	61.8	58.9
Everolimus (CNI-free)	65.0	59.4	45.4	43.1	66.3	61.8

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Health-related Quality of Life (QoL) as Measured by EuroQoL EQ-5D

Health-related QoL was assessed using the EQ-5D questionnaire. The EQ-5D self-report questionnaire consists of the EQ-5D descriptive system that measures health-related quality of life on 5 dimensions (mobility, self-care, usual activities, pain/discomfort, and anxiety/depression) each of which can take one of three responses. The responses record three levels of severity (no problems/moderate problems/severe problems) within a particular EQ-5D dimension. Scores are transformed to a range of 0-1, in which higher scores reflect better health status. (NCT00634920)
Timeframe: Before randomization, Months 12, 36

Intervention	scores on a scale (Mean)
	Before Randomization (Week 7)	Month 12	Month 36
Control (CsA)	0.8693	0.8470	0.8422
Everolimus (CNI-free)	0.8430	0.8155	0.8285

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Lipid Profile for Apolipoprotein

Blood lipid levels of patients in both groups for Apolipoprotein (Apo) A1 and B. (NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	g/L (Mean)
	Month 12: Apolipoprotein A1	Month 24: Apolipoprotein A1	Month 36: Apolipoprotein A1	Month 12: Apolipoprotein B	Month 24: Apolipoprotein B (	Month 36: Apolipoprotein B
Control (CsA)	1.46	1.36	1.56	0.923	1.058	0.934
Everolimus (CNI-free)	1.59	1.55	1.70	0.935	1.178	0.984

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Lipid Profile for HDL-C, LDL-C,Total Cholesterol, and Triglycerides

Blood lipid levels of patients in both groups: HDL-C, LDL-C,Total cholesterol, and triglycerides. (NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	mmol/L (Mean)
	Month 12: HDL Cholesterol	Month 24: HDL Cholesterol	Month 36: HDL Cholesterol	Month 12: LDL Cholesterol	Month 24: LDL Cholesterol	Month 36: LDL Cholesterol	Month 12: Total Cholesterol	Month 24: Total Cholesterol	Month 36: Total Cholesterol	Month 12: Triglycerides	Month 24: Triglycerides	Month 36: Triglycerides
Control (CsA)	1.419	1.409	1.529	3.130	2.925	2.822	5.318	5.112	4.830	1.868	1.757	1.580
Everolimus (CNI-free)	1.486	1.477	1.495	3.569	3.381	3.206	6.091	5.823	5.595	2.461	2.288	2.164

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Number of Lipid-lowering Drugs Taken

(NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	Number of lipid-lowering drugs (Mean)
	Month 12	Month 24	Month 36
Control (CsA)	0.8	0.9	0.8
Everolimus (CNI-free)	0.9	1.0	0.9

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Percentage of Participants on Antihypertensive Drugs

(NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	Percentage of participants (Number)
	Month 12: No antihypertensive drugs	Month 12: Has antihypertensive drugs	Month 24: No antihypertensive drugs	Month 24: Has antihypertensive drugs	Month 36: No antihypertensive drugs	Month 36: Has antihypertensive drugs
Control (CsA)	3.3	96.7	5.3	94.7	12.8	87.2
Everolimus (CNI-free)	9.2	90.8	4.2	95.8	15.6	84.4

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Time to Treatment Failure

Treatment failure was defined as graft loss or death.Time to treatment failure is shown as mean time to treatment failure. (NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	Days (Mean)
Everolimus (CNI-free)	972.7
Control (CsA)	959.5

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Measured Glomerular Filtration Rate

To compare the efficacy between treatment regimens by assessing the difference in renal function evaluated by mean measured glomerular filtration rate (mGFR) 12 months after renal transplantation (TX). The mGFR was measured using Iohexol or Cr-EDTA clearance according to local practice. (NCT00634920)
Timeframe: Month 12

Intervention	mL/min/1.73m^2 (Mean)
Everolimus (CNI-free)	51.5
Control (CsA)	47.8

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Proteinuria (Measured as Urine Albumin/Creatinine Ratio (mg/mmol))

"Proteinuria is when a large amount of protein, that should remain circulating in a person's blood, is spilled into their urine and eliminated from the body." (NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	mg/mmol (Mean)
	Month 12	Month 24	Month 36
Control (CsA)	11.27	24.55	80.73
Everolimus (CNI-free)	17.31	62.83	78.78

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Number of Antihypertensive Drugs Taken

(NCT00634920)
Timeframe: Months 12, 24, 36

Intervention	Number of antihypertensive dugs (Mean)
	Month 12	Month 24	Month 36
Control (CsA)	2.5	2.4	2.2
Everolimus (CNI-free)	2.5	2.5	2.0

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Number of Participants Surviving at 6 Months

Overall survival (OS) at 6 months in participants receiving a combination of Erlotinib and RAD001 who have received previous treatment for advanced pancreatic cancer. OS at 6 months is number of participants alive at 6 months. (NCT00640978)
Timeframe: 6 months

Intervention	Participants (Number)
Erlotinib + RAD001	15

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Progression-free Survival (PFS)

Progression-free survival (PFS) per RECIST criteria (NCT00651482)
Timeframe: 24 months

Intervention	months (Median)
Bevacizumab + RAD001 (Everolimus)	5.1

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Overall Survival (OS)

(NCT00651482)
Timeframe: 44 months

Intervention	months (Median)
Bevacizumab + RAD001 (Everolimus)	21.0

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Objective Response (OR)

Number of subjects with objective response (OR) (NCT00651482)
Timeframe: 24 months

Intervention	participants (Number)
Bevacizumab + RAD001 (Everolimus)	1

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Objective Response (OR) Duration

(NCT00651482)
Timeframe: 24 months

Intervention	weeks (Median)
Bevacizumab + RAD001 (Everolimus)	21.7

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Time-to-Treatment Failure (TTF)

(NCT00651482)
Timeframe: 24 months

Intervention	months (Median)
Bevacizumab + RAD001 (Everolimus)	5.1

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Treatment Discontinuation Due to Disease Progression

Number of subjects whose treatment was discontinued due to disease progression (NCT00651482)
Timeframe: 24 months

Intervention	participants (Number)
Bevacizumab + RAD001 (Everolimus)	6

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Treatment Discontinuation Due to Toxicity

Number of subjects whose treatment was discontinued due to toxicity (NCT00651482)
Timeframe: 24 months

Intervention	participants (Number)
Bevacizumab + RAD001 (Everolimus)	4

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Core Study: Number of Patients With Composite Efficacy Endpoint

"The composite efficacy endpoint consisted of treated biopsy proven acute rejection (BPAR) episodes, graft loss, death or loss to follow-up. A treated BPAR was defined as a biopsy graded IA, IB, IIA, IIB, or III and which was treated with anti-rejection therapy. The allograft was presumed to be lost on the day the patient starts dialysis and was not able to stop dialysis. If the patient underwent a graft nephrectomy, then the day of nephrectomy was considered as the day of graft loss.~For the individual components (including loss of follow-up)of the composite endpoint, patients are counted for the first event to occur." (NCT00658320)
Timeframe: 12 months

Intervention	Participants (Number)
	Composite Efficacy Endpoint	Treated BPAR	Graft Loss	Death	Loss to follow up (see caveats)
Everolimus + Reduced Dose of Cyclosporine	7	3	0	0	4
Mycophenolate Mofetil (MMF) + Standard Dose of Cyclosporine	7	5	0	0	2

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Extension Study: Renal Function Measured by Calculated Glomerular Filtration Rate (cGFR) Using the Modification of Diet in Renal Disease (MDRD) Formula

"Renal function was assessed by glomerular filtration rate (GFR) using the MDRD formula:~GFR [mL/min/1.73m2] = 186.3*(C-1.154)*(A-0.203)*G*R C is the serum concentration of creatinine [mg/dL] A is age [years] G = 0.742 when gender is female, otherwise G=1 R = 1.21 when race is black, otherwise R=1~Loss to follow up (in In Primary Core Outcome Measure) is composite efficacy failure and contains incidence of treated BPAR, graft loss, death or loss to follow-up" (NCT00658320)
Timeframe: Month 24

Intervention	mL/min/1.73m^2 (Median)
Everolimus + Reduced Dose of Cyclosporine	58.90
Mycophenolate Mofetil (MMF) + Standard Dose of Cyclosporine	54.95

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Core Study: Renal Function Measured by Calculated Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula

"Modification of Diet in Renal Disease (MDRD) formula is:~Calculated GFR [mL/min/1.73m^2] = 186.3*(C^-1.154)*(A^-0.203)*G*R where~C is the serum concentration of creatinine [mg/dL],~A is patient age at sample collection date [years],~G=0.742 when gender is female, otherwise G=1,~R=1.21 when race is black, otherwise R=1" (NCT00658320)
Timeframe: Month 12

Intervention	mL/min/1.73m^2 (Median)
Everolimus + Reduced Dose of Cyclosporine	58.00
Mycophenolate Mofetil (MMF) + Standard Dose of Cyclosporine	55.25

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Core Study: Number Participants With Combined Graft Loss, Death or Loss to Follow-up

"The allograft was presumed to be lost on the day the patient starts dialysis and was not able to stop dialysis. If the patient underwent a graft nephrectomy, then the day of nephrectomy was considered as the day of graft loss.~A loss to follow-up in graft loss, death or loss to follow-up is a patient who did not experience graft loss or death and whose last day of contact was prior to Day 316, i.e. prior to the Month 12 visit window." (NCT00658320)
Timeframe: 12 months

Intervention	Participants (Number)
Everolimus + Reduced Dose of Cyclosporine	5
Mycophenolate Mofetil (MMF) + Standard Dose of Cyclosporine	3

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Extension Study: Renal Function Measured by Calculated Glomerular Filtration Rate (cGFR) Using the Modification of Diet in Renal Disease (MDRD) Formula

Intervention	mL/min/1.73m^2 (Median)
Everolimus + Reduced Dose of Cyclosporine	59.80

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Extension Study: Renal Function Measured by Calculated Glomerular Filtration Rate (GFR) Using the Nankivell Formula

"The Nankivell formula was used to calculate GFR at Month 24:~GFR[mL/min]=6.7/C + W/4 - UREA/2 - 100/H^2 + 35 (25 for females) W= body weight [kg] H= height [m] C= serum creatinine [mmol/L] UREA= serum urea [mmolL]" (NCT00658320)
Timeframe: Month 24, Month 48

Intervention	mL/min (Mean)
	Month 24	Month 48 (9,0)
Everolimus + Reduced Dose of Cyclosporine	63.49	60.16
Mycophenolate Mofetil (MMF) + Standard Dose of Cyclosporine	59.24	NA

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Extension Study: Number of Participants With Combined Efficacy Endpoint: Graft Loss, Death, Loss to Follow-up and/or Treated Biopsy Proven Acute Rejection (BPAR)

"Graft loss was defined as the day the patient started dialysis and was not able to subsequently be removed from dialysis or re-transplant.~Loss-to-follow was a patient who did not experience a treated BPAR, graft loss or death and whose last day of contact was prior to Month 24.~A Graft Biopsy was done within 48 hours of suspect rejection. Biopsies were read by the local pathologist according to the updated Banff '97 criteria.~Treated BPAR was based on local laboratory biopsy results and was defined as a biopsy Banff criteria graded IA to III that was treated with anti-rejection therapy." (NCT00658320)
Timeframe: 24 Months

Intervention	Participants (Number)
	Combined Efficacy Endpoint	Treated BPAR	Graft Loss	Death	Loss to follow-up
Everolimus + Reduced Dose of Cyclosporine	4	3	0	0	1
Mycophenolate Mofetil (MMF) + Standard Dose of Cyclosporine	5	5	0	0	0

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Extension Study: Number of Participants With Adverse Events and Serious Adverse Events

Additional information about Adverse Events can be found in the Adverse Event Section. (NCT00658320)
Timeframe: 24 Months

Intervention	Participants (Number)
	Adverse Events	Serious Adverse Events
Everolimus + Reduced Dose of Cyclosporine	50	30
Mycophenolate Mofetil (MMF) + Standard Dose of Cyclosporine	50	30

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Extension Study: Everolimus Trough Levels

Blood was collected at all visits after Day 3 for trough (collected 5 minutes before study drug dose) everolimus levels and was analyzed at a central laboratory using liquid chromatography mass spectrometry. (NCT00658320)
Timeframe: Month 24, Month 48

Intervention	ng/mL (Mean)
	Month 24	Month 48 (n=8)
Everolimus + Reduced Dose of Cyclosporine	5.258	4.408

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Extension Study: Cyclosporine Trough Levels

Blood was collected at all visits after Day 3 for trough (collected 5 minutes before study drug dose) cyclosporine levels and was analyzed at a central laboratory using immunoassay. (NCT00658320)
Timeframe: Month 24, Month 48

Intervention	ng/mL (Mean)
	Month 24	Month 48 (n=7,0)
Everolimus + Reduced Dose of Cyclosporine	54.1	34.2
Mycophenolate Mofetil (MMF) + Standard Dose of Cyclosporine	105.5	NA

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Death (Cardiac Death, Vascular Death, and Non-cardiovascular Death)

(NCT00676520)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	0.4

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Death (Cardiac Death, Vascular Death, and Non-cardiovascular Death)

(NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	1.4

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Death (Cardiac Death, Vascular Death, and Non-cardiovascular Death)

(NCT00676520)
Timeframe: at 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	2.6

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Dual Antiplatelet Medication Usage

"Patient is included if medications (both aspirin and thienopyridine) were taken for at least 1 day during the visit window. The visit window for 14-day visit is 7-21 days, 30-day visit is 23-37 days, 180-day visit is 166-194 days, 1-year visit is 323-407 days, and 2-year visit is 688-772 days.~Adjunctive antiplatelet therapy includes: Aspirin & Thienopyridines (Clopidogrel/Ticlopidine/Prasugrel).~Compliance refers to subjects following prescribed instructions for taking these medications. Therapy interruptions refer to any intervals during which the subject stops taking one or all of the prescribed medications." (NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	86.4

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Composite Rate of Cardiac Death, Any MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Target Lesion Revascularization (TLR) (PCI and CABG)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	3.5

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Any MI (Q-wave and Non Q-wave)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	6.3

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Any MI (Q-wave and Non Q-wave)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	4.7

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Any MI (Q-wave and Non Q-wave)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	3.3

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Dual Antiplatelet Medication Usage

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	89.2

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Dual Antiplatelet Therapy Non-compliance Through 1 Year

Defined as patients who had at least 1 day without using either aspirin or thienopyridine from 1 to 407 days post index procedure. (NCT00676520)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	18.0

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Major Bleeding Complications

by TIMI flow (NCT00676520)
Timeframe: at 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	2.8

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Major Bleeding Complications

by TIMI flow (NCT00676520)
Timeframe: at 14 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	0.6

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Major Bleeding Complications

by TIMI flow (NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	1.8

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Major Bleeding Complications

by TIMI flow (NCT00676520)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	0.7

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Composite Rate of Cardiac Death, Any MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Target Lesion Revascularization (TLR) (PCI and CABG)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	9.6

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Composite Rate of Cardiac Death and MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Clinically-indicated Target Lesion Revascularization (CI-TLR) (PCI and CABG) (This Composite Endpoint is Also Denoted as TLF)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	3.5

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Patient Health Status, Physical Limitations Assessed Using the SAQ (Seattle Angina Questionaire)

"SAQ: 19-item, 5-6-point Likert, questionnaire measuring 5 dimensions of coronary artery disease:~Anginal Stability: whether a patient's symptoms are changing over time. Anginal Frequency: how often a patient is having symptoms now Physical Limitation: how much a patient's condition is hampering his ability to do what he wants to do.~Treatment Satisfaction: how well a patient understands her care and what she thinks of it.~Disease Perception: the overall impact of a patient's condition on a patient's interpersonal relationships and state of mind.~Each dimension is assigns each response an ordinal value, beginning with 1 for the response at the lowest level of functioning, and summing across items within each of the 5 scales. Scale scores then transformed to 0-100 range by subtracting the lowest possible scale score, dividing by the range of the scale and multiplying by 100." (NCT00676520)
Timeframe: at 1 year

Intervention	units on the SAQ scale (Mean)
Subjects Receiving the XIENCE V EECSS	76.0

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Patient Health Status, Physical Limitations Assessed Using the SAQ (Seattle Angina Questionaire)

Intervention	units on the SAQ scale (Mean)
Subjects Receiving the XIENCE V EECSS	75.8

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SAQ (Seattle Angina Questionaire)

Intervention	units on the SAQ scale (Mean)
Physical Limitations	76.0
Angina Stability	54.3
Angina Frequency	90.7
Treatment Satisfaction	92.2
Perception of Disease/Quality of Life	78.0

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SAQ (Seattle Angina Questionaire)

Intervention	units on the SAQ scale (Mean)
Physical Limitations	75.8
Angina Stability	57.3
Angina Frequency	90.1
Treatment Satisfaction	91.4
Perception of Disease/Quality of Life	76.8

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Composite Rate of Cardiac Death and MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Clinically-indicated Target Lesion Revascularization (CI-TLR) (PCI and CABG) (This Composite Endpoint is Also Denoted as TLF)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	6.2

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Composite Rate of Cardiac Death and MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Clinically-indicated Target Lesion Revascularization (CI-TLR) (PCI and CABG) (This Composite Endpoint is Also Denoted as TLF)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	9.4

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Composite Rate of Cardiac Death and Any Myocardial Infarction (MI)

MI= ARC (Academic Research Constortium) defined (NCT00676520)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	7.2

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Composite Rate of Cardiac Death and Any MI (Q-wave and Non Q-wave)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	3.6

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Composite Rate of All Death, Any MI (Q-wave and Non Q-wave) and Any Repeat Revascularization (Percutaneous Coronary Intervention [PCI] and Coronary Artery Bypass Graft [CABG])

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	4.3

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SAQ (Seattle Angina Questionaire)

Intervention	units on the SAQ scale (Mean)
Physical Limitations	70.0
Angina Stability	42.0
Angina Frequency	73.1
Treatment Satisfaction	98.1
Perception of Disease/Quality of Life	55.3

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Composite Rate of All Death, Any MI (Q-wave and Non Q-wave) and Any Repeat Revascularization (Percutaneous Coronary Intervention [PCI] and Coronary Artery Bypass Graft [CABG])

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	9.4

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Composite Rate of All Death, Any MI (Q-wave and Non Q-wave) and Any Repeat Revascularization (Percutaneous Coronary Intervention [PCI] and Coronary Artery Bypass Graft [CABG])

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	14.9

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Patient Health Status, Physical Limitations Assessed Using the SAQ (Seattle Angina Questionaire)

Intervention	units on the SAQ scale (Mean)
Subjects Receiving the XIENCE V EECSS	70.0

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Composite Rate of All Death and Any MI (Q-wave and Non Q-wave)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	3.6

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Composite Rate of All Death and Any MI (Q-wave and Non Q-wave)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	5.8

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Composite Rate of Cardiac Death, Any MI (Q-wave and Non Q-wave) Attributed to the Target Vessel, and Target Lesion Revascularization (TLR) (PCI and CABG)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	6.3

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Procedural Success

(NCT00676520)
Timeframe: acute: post index procedure until hospital discharge

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	97.3

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Revascularization (Target Lesion, Target Vessel [TVR], and Non-target Vessel) (PCI and CABG)

(NCT00676520)
Timeframe: at 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	9.2

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Revascularization (Target Lesion, Target Vessel [TVR], and Non-target Vessel) (PCI and CABG)

(NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	5.0

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Composite Rate of All Death and Any MI (Q-wave and Non Q-wave)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	8.3

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Composite Rate of Cardiac Death and Any MI (Q-wave and Non Q-wave)

MI= Academic Research Consortium (ARC) defined (NCT00676520)
Timeframe: at 180 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	5.4

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Clinical Device Success

(NCT00676520)
Timeframe: acute: post index procedure until hospital discharge

Intervention	percentage of lesions (Number)
Subjects Receiving the XIENCE V EECSS	99.8

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Dual Antiplatelet Medication Usage

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	79.9

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Stent Thrombosis (Definite and Probable) Rate as Defined by ARC (Academic Research Constortium).

"ARC Defines Stent Thrombosis in the following way:~Definite Stent Thrombosis: Angiographic or pathologic confirmation of partial or total thrombotic occlusion within the peri-stent region AND at least ONE of the following, additional criteria:~Acute ischemic symptoms Ischemic ECG changes Elevated cardiac biomarkers~Probable Stent Thrombosis: Any unexplained death within 30 days of stent implantation or any myocardial infarction, which is related to documented acute ischemia in the territory of the implanted stent without angiographic confirmation of stent thrombosis and in the absence of any other obvious cause~Possible Stent Thrombosis Any unexplained death beyond 30 days~For further information on ARC definitions, please refer to the following website: http://circ.ahajournals.org/content/115/17/2344.full#sec-1" (NCT00676520)
Timeframe: up to 1 year

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	0.81

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Dual Antiplatelet Medication Usage

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	89.4

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Revascularization (Target Lesion, Target Vessel [TVR], and Non-target Vessel) (PCI and CABG)

(NCT00676520)
Timeframe: at 30 days

Intervention	percentage of participants (Number)
Subjects Receiving the XIENCE V EECSS	1.1

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Overall Survival (OS) for Per Protocol (PP) and ITT Sets

OS was defined as the time from first study drug administration to death from any cause. If a patient was not known to have died at date of database closure, overall survival was censored at the date of last contact. (NCT00688623)
Timeframe: baseline up to approximately 15 months

Intervention	days (Mean)
	OS for Per protocol set	OS for Intent to treat set
Everolimus	451.8	437.1

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Percentage of Participants With a Overall Response Rate With a Complete Response (CR) or Partial Response (PR) at 12 Months ITT Set

"The best overall response (BOR) was calculated on basis of the tumor of overall lesion response evaluated at each visit. To be assigned a status of PR or CR, changes in tumor measurements had to be confirmed by repeat assessments that should have been performed not less than 4 weeks after the criteria for response were first met. Assessments was based on RECIST criteria 1.0. Measurable disease lesions had to be accurately measured in at least one dimension with longest diameter ≥ 20 mm using conventional techniques or ≥ 10 mm with spiral CT scan (with minimum lesion size no less than double the slice thickness). PR required at least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters.~CR required disappearance of all target and non-target lesions." (NCT00688623)
Timeframe: baseline up to approximately 12 months

Intervention	percentage of participants (Number)
	Complete response (CR)	Partial response	Stable disease (SD)	Progressive disease (PD)	Unknown
Everolimus	0.0	0.0	74.0	16.4	9.6

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Percentage of Participants With Disease Control Rate (DCR) at 12 Months for Per Protocol (PP) and ITT Sets

DCR was based on central radiologic review and is defined as the percentage of patients with a best overall response of 'Complete response' (CR), 'Partial response' (PR) or 'Stable disease' (SD). Relative frequencies together with their exact 2-sided 80% confidence intervals were presented (NCT00688623)
Timeframe: baseline up to approximately 12 months

Intervention	percentage of participants (Number)
	DCR for Per protocol set	DCR for Intent to treat set
Everolimus	56.7	50.7

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Percentage of Participants' Best Overall Response Rate at 12 Months - Per Protocol Set (PP)

Overall response rate (ORR) was based on RECIST central assessment and defined as the percentage of patients with best overall response (BOR) of a confirmed complete response (CR) or partial response (PR). The BOR was calculated on basis of the tumor of overall lesion response evaluated at each visit. To be assigned a status of PR or CR, changes in tumor measurements had to be confirmed by repeat assessments obtained within 4 weeks after the criteria for response were first met. Assessments was based on RECIST criteria 1.0. Measurable disease lesions had to be accurately measured in at least one dimension with longest diameter ≥ 20 mm using conventional techniques or ≥ 10 mm with spiral CT scan (with minimum lesion size no less than double the slice thickness). PR required at least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters. CR required disappearance of all target and non-target lesions. (NCT00688623)
Timeframe: baseline up to approximately 12 months

Intervention	percentage of participants (Number)
	Complete response (CR)	Partial response	Stable disease (SD)	Progressive disease (PD)	Unknown
Everolimus	0.0	0.0	56.7	43.3	0.0

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Duration of Progression Free Survival (PFS) for Per Protocol (PP) and ITT Sets

Duration of PFS was defined as the time from first study drug administration to objective tumor progression or death from any cause. Observations from patients not experiencing tumor progression or death at date of database closure were censored with the date of their last adequate tumor assessment. Progression was either 1) a 20% increase in the sum of the longest diameter of all target lesions, taking as reference the smallest sum of longest diameter of all target lesions recorded at or after baseline or 2) the appearance of a new lesion or 3) the unequivocal progression of non-target lesions. (NCT00688623)
Timeframe: baseline up to approximately 12 months

Intervention	days (Median)
	PFS days for Per protocol set	PFS days for Intent to treat set
Everolimus	185	190

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Percentage of Participants With Objective Response Rate at 12 Months - Per Protocol Set (PP)

Overall Response Rate (ORR) was calculated for total PP population based on central review as confirmatory, primary analysis as well as for ITT population as sensitivity analysis. It was presented with relative frequencies and the exact 2-sided 80% confidence limit (CI) computed using the Clopper-Pearson method). If the lower limit of the CI did not include p0=5%, the hypothesis that p ≤ 5% was rejected. The primary analysis was based on the PP Set (NCT00688623)
Timeframe: baseline up to approximately 12 months

Intervention	percentage of participants (Number)
Everolimus	0.0

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Percentage of Participants With Objective Response Rate at 12 Months ITT Set

Overall Response Rate (ORR) was presented for ITT population as sensitivity analysis. It was presented with relative frequencies and the exact 2-sided 80% confidence limit (CL; computed using the Clopper-Pearson method). If the lower limit of the CI did not include p0=5%, the hypothesis that p ≤ 5% was rejected. (NCT00688623)
Timeframe: baseline up to approximately 12 months

Intervention	percentage of participants (Number)
Everolimus	0.0

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Objective Response Rate

ORR is defined as the proportion of patients with tumor size reduction of a predefined amount and for a minimum time period. Response duration usually is measured from the time of initial response until documented tumor progression (NCT00688753)
Timeframe: End of trial

Intervention	% participants (Number)
	PP Set	ITT Set
RAD001	1.5	1.2

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To Evaluate Efficacy of RAD001 as Monotherapy for the Treatment of Papillary Renal Cancer. Efficacy is Defined as the Percentage of Patients Progression-free at 6 Months.

PFSR at 6 months based on central review (NCT00688753)
Timeframe: 6 mos

Intervention	% participants (Number)
	(PPFF Set, N=44)	(PPSet, N=66)	(ITT Set, N=86)
RAD001	34.1	33.3	32.6

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Duration of Response

The DOR analysis applied only to patients whose overall response was CR or PR and was defined as the time from onset of response (CR/PR) to progression or death from any cause. (NCT00688753)
Timeframe: End of trial

Intervention	days (Median)
	local review PP set	local review ITT set
RAD001	169	226

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Median Progression Free Survival

PFS was defined as the time from first study drug administration to objective tumor progression or death from any cause. (NCT00688753)
Timeframe: End of trial

Intervention	days (Median)
	PP set	ITT set
RAD001	118	113

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Disease Control Rate (SD + PR + CR)

DCR was defined as the proportion of patients with a best overall response of CR, PR or SD and ORR as the percentage of patients with CR or PR (NCT00688753)
Timeframe: 6 mos

Intervention	% Participants (Number)
	PP set	ITT set
RAD001	65.2	65.1

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Incidence of Adverse Events, Serious Adverse Events, and Death.

(NCT00688753)
Timeframe: End of trial

Intervention	% participants (Number)
	Patients with any AE	AE with suspected relation to study drug	AE leading to dose adjustment or interruption	AE leading to permanent discontinuation	AE requiring concomitant medication	Patients with serious adverse event (SAE)	SAE suspected relation to study drug	SAE leading to permanent discontinuation	Patients died
RAD001	100	97.83	53.26	27.17	90.22	46.74	23.91	10.87	10.87

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Disease Control Rate (DCR)

Disease Control Rate was defined as the percentage of participants with best overall disease response of CR or PR or stable disease (SD). CR was defined as complete disappearance of all extranodal lesions. PR was defined as at least a 50% decrease in SPD of all index nodal and extranodal lesions. SD was defined failure to attain the criteria needed for CR or PR and failure to fulfill the criteria for at least a 50% increase in the SPD of all index nodal and extranodal (including splenic and/or hepatic nodules) lesions, taking as reference the smallest sum of the product of the diameters of all index lesions recorded at or after baseline. (NCT00702052)
Timeframe: From date of start of treatment up to disease progression or death (approximately up to 3.8 years)

Intervention	percentage of participants (Number)
Everolimus	69.0

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Progression Free Survival (PFS)

PFS was defined as the time from the date of start of treatment to the date of event defined as the first documented progression or death due to any cause. (NCT00702052)
Timeframe: From date of start of treatment up to disease progression or death (approximately up to 3.8 years)

Intervention	months (Median)
Everolimus	4.40

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Overall Survival

Overall survival was defined as the time from the date of start of study treatment to the date of death due to any cause. (NCT00702052)
Timeframe: From date of start of treatment up to disease progression or death (approximately up to 3.8 years)

Intervention	months (Median)
Everolimus	16.85

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Overall Response Rate (ORR)

Overall response rate was defined as the percentage of participants with a best overall disease response of complete response (CR) or partial response (PR). CR was defined as complete disappearance of all extranodal lesions. PR was defined as at least a 50% decrease in the sum of the product of diameter (SPD) of all index nodal and extranodal lesions. (NCT00702052)
Timeframe: From date of enrollment up to disease progression or death (approximately 3.8 years)

Intervention	percentage of participants (Number)
Everolimus	8.6

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Number of Participants With At Least One Adverse Event (AE) and Serious Adverse Event (SAE)

An AE was defined as any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease associated with the use of study drug, whether or not considered related to the study drug or worsening of pre-existing medical condition, whether or not related to study drug. A SAE was an AE that resulted in any of the following outcomes: death; life threatening; persistent/significant disability/incapacity; initial or prolonged inpatient hospitalization; congenital anomaly/birth defect or was otherwise considered medically important. (NCT00702052)
Timeframe: From the start of the study and 28 days after study drug discontinuation (approximately up to 18 months)

Intervention	Participants (Count of Participants)
	AE	SAE
Everolimus	58	29

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Best Overall Response in Participants Who Received RAD001 Plus Bevacizumab Versus Participants Who Received IFN Plus Bevacizumab

Overall response is defined as the number of participants having achieved confirmed Complete Response (CR) + Partial Response (PR). Confirmed CR = at least two determinations of CR at least 4 weeks apart before progression. Confirmed PR = at least two determinations of PR or better at least 4 weeks apart before progression. CR required a disappearance of all target and non-target lesions. PR required at least a 30% decrease in the sum of the longest diameters of all target lesions, taking as a reference the baseline sum of the longest diameters. Disease progression was defined as: 1) a 20% increase in the sum of the longest diameter of all target lesions, taking as reference the smallest sum of the longest diameters of all target lesions recorded at or after baseline or 2) the appearance of a new lesions or 3) the unequivocal progression of non-target lesions overall. (NCT00719264)
Timeframe: Time from first participant randomized until 31Dec2011, cutoff date.

Intervention	Number of participants (Number)
	Complete response (CR)	Partial response (PR)	Stable disease (SD)	Progressive disease (PD)	Unknown response	Overall objective response (CR+PR)
Bevacizumab, Interferon Alfa-2a (IFN)	1	50	84	26	22	51
Bevacizumab, RAD001 (Everolimus)	0	49	90	25	18	49

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Time to Definitive Deterioration of the Functional Assessment of Cancer Therapy Kidney Symptom Index, Disease Related Symptoms (FKSI-DRS) Risk Score by at Least 2 Score Units

The analysis of this outcome measure was based on the FKSI-DRS scale which is a validated disease-related symptom index containing 9 items that measure symptoms predominantly related to kidney cancer. Each item is scored on a 5-point scale (0 = not at all; 4 = very much). If at least 5 of the 9 questions have been answered, the FKSI-DRS total score is calculated by subtracting nine times the mean of the scores of the answered items from 36. Participants with less than 5 out of the 9 questions answered will have a missing FKSI-DRS total score. The FKSI-DRS total score ranges from 0 (most severe symptoms) to 36 (no symptoms). Definitive deterioration is defined as a decrease by at least 2 units compared to baseline, with no later increase above this threshold observed during the study. A single measure reporting a decrease of at least 2 units was considered definitive only if it is the last one available for the participant. (NCT00719264)
Timeframe: Time from randomization to the date of definitive deterioration (defined as no later increase above the threshold observed during the study), or date of last assessment, reported between date of first patient randomized until 31Dec2011

Intervention	Months (Median)
Bevacizumab, RAD001 (Everolimus)	7.4
Bevacizumab, Interferon Alfa-2a (IFN)	8.0

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Response Duration Differences in Participants Who Received RAD001 Plus Bevacizumab Versus Participants Who Received IFN Plus Bevacizumab

The duration of response, applied only to participants with best overall response at CR or PR, is defined as the number of days between the date of first documented response (CR or PR) and the date of the event: radiological progression as per central review or death due to underlying cancer, whichever occurs first. If no event, participant is censored at the last adequate assessment. (NCT00719264)
Timeframe: Time from first documented response date of radiological progressive disease as per independent central review, death due to underlying cancer, or last tumor assessment, reported between date of first participant randomized until 31Dec2011, cut-off date.

Intervention	Months (Median)
Bevacizumab, RAD001 (Everolimus)	13.3
Bevacizumab, Interferon Alfa-2a (IFN)	11.3

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Overall Survival (OS) Treatment Effect in Participants Who Received RAD001 Plus Bevacizumab Versus Participants Who Received IFN Plus Bevacizumab

Overall survival (OS) was defined as the time of randomization to the date of death due to any cause. (NCT00719264)
Timeframe: Time from randomization to the date of death from any cause, reported between date of first participant randomized and up to 2 years after the last participant randomized (data cutoff: 30Aug2012)

Intervention	Months (Median)
Bevacizumab, RAD001 (Everolimus)	27.1
Bevacizumab, Interferon Alfa-2a (IFN)	27.1

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Duration of Exposure of RAD001 in Participants Randomized to the Treatment Combination of RAD001 and Bevacizumab

This outcome measure was assessed continuously. (NCT00719264)
Timeframe: From the date of the first participant treated until the last patient discontinued the study treatment + 28 days

Intervention	weeks (Median)
Bevacizumab, RAD001 (Everolimus)	37.0

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Progression-free Survival (PFS) of Participants Who Received RAD001 Plus Bevacizumab Versus Participants Who Received IFN Plus Bevacizumab

Tumor response and disease progression were assessed using response evaluation criteria in solid tumors (RECIST), version 1.0. All target and non-target lesions identified at baseline were assessed using the same method, CT scan with contrast or MRI with contrast, throughout the trial. All scans were reviewed by independent, central radiology. Disease progression was defined as: 1) a 20% increase in the sum of the longest diameter of all target lesions, taking as reference the smallest sum of the longest diameters of all target lesions recorded at or after baseline or 2) the appearance of a new lesions or 3) the unequivocal progression of non-target lesions overall. (NCT00719264)
Timeframe: Time from randomization to the date of radiological progressive disease as per independent central review, death from any cause, or last tumor assessment, reported between date of first participant randomized until 31Dec2011, cutoff date.

Intervention	Months (Median)
Bevacizumab, RAD001 (Everolimus)	9.3
Bevacizumab, Interferon Alfa-2a (IFN)	10.0

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Time to Definitive Deterioration of the Global Health Status and the Physical Functioning (PF) Subscale Scores of the European Organization for the Research and Treatment of Cancer (EORTC)-Core Quality of Life Questionnaire (QLQ-C30) by at Least 10%

The EORTC QLQ-C30 contains 30 items. These include five functional scales (physical, role, emotional, social and cognitive functioning), three symptom scales (fatigue, pain, nausea, and vomiting), a global health status/QoL scale, and six single items (dyspnea, diarrhea, constipation, anorexia, insomnia and financial impact). The PF subscale consists of 5 questions each scored from 1 (not at all) to 4 (very much). The score for the PF subscale and global health status range from 0 to 100, with a higher score representing a high level of functioning/high quality of life. Definitive deterioration by at least 10% is defined as a decrease in score by at least 10% compared to baseline, with no later increase above this threshold observed during the course of the study. A single measure reporting a decrease of at least 10% is considered definitive only if it is the last one available for the participant. (NCT00719264)
Timeframe: Time from randomization to the date of definitive deterioration (defined as no later increase above the threshold observed during the study), or date of last assessment, reported between date of first participant randomized until 31Dec2011

Intervention	Months (Median)
	Global health status/QoL	Physical functioning
Bevacizumab, Interferon Alfa-2a (IFN)	7.8	9.0
Bevacizumab, RAD001 (Everolimus)	7.4	8.5

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Number of Participants Who Experienced Adverse Events (AEs), Serious Adverse Events and Deaths

Participants were monitored for adverse events, serious adverse events and deaths throughout the study. Participants were assessed continuously at each 28-day cycle. (NCT00719264)
Timeframe: From the first participant randomized until the last patient discontinued the study treatment + 28 days

Intervention	Participants (Number)
	Adverse events (serious and non-serious)	Serious adverse events	Deaths
Bevacizumab, Interferon Alfa-2a (IFN)	180	76	95
Bevacizumab, RAD001 (Everolimus)	179	79	93

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Number of Participants With Adverse Events

(according to National Cancer Institute Common Terminology Criteria for Adverse Events version 3.0) (NCT00729482)
Timeframe: up to 24 weeks

Intervention	participants (Number)
RAD001	54

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Overall Survival

(NCT00729482)
Timeframe: 1 year

Intervention	Months (Median)
RAD001	8.3

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Progression-free Survival Rate at 4-month (16 Weeks)

progression is definced as a more than 20% increase in one or more lesions or the appearance of any new lesion (NCT00729482)
Timeframe: 4 months (16 weeks)

Intervention	percentage of participants (Number)
RAD001	18.4

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Response Rate

Tumor response is evaluated according to the new guidelines by RECIST criteria (See Appendix D). A complete response (CR) is defined as the disappearance of all evidence of cancer for 4 weeks or longer. A partial response (PR) is defined as a 30% or more reduction in the sum of the longest diameters of target lesions for 4 weeks or longer without any evidence of new lesions or progression of any lesions. Stable disease is defined as less than a 30% reduction or less than a 20% increase in the longest diameters of target lesions without any evidence of new lesions. Progressive disease is defined as a more than 20% increase in one or more lesions or the appearance of any new lesion. (NCT00729482)
Timeframe: 2years

Intervention	percentage of participants (Number)
RAD001	3.7

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Objective Tumor Response Rates (Complete Response and Partial Response) at Week 16 (ITT)

The best overall response is the best response recorded from the start of the treatment until disease progression/recurrence (taking as reference for PD the smallest measurements recorded since the treatment started). In general, the patient's best response assignment will depend on the achievement of both measurement and confirmation criteria. Best lesion response was defined by (Resist Criteria V1 for target and non-target lesions). (NCT00767819)
Timeframe: Baseline up to approximately 16 weeks

Intervention	percentage of participants (Number)
	Complete response	Partial response
Arm 1	0	0
Arm 2	0	0
Arm 3	0	0

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Best Overall Response Rates by Week 16 (ITT)

"The best overall response is the best response recorded from treatment start until disease progression/recurrence (both measurement and confirmation criteria). Best lesion response was defined by (Resist Criteria V1 for target and non-target lesions): Complete Response (CR)=at least two determinations of CR 4 weeks apart before progression, Partial Response (PR)=at least two determinations of CR 4 weeks apart before progression (and not qualifying for a CR), Stable Disease (SD)=at least one SD assessment >6 weeks after start of treatment and Progressive Disease (PD)=Progression or death due to underlying cancer ≤16 weeks after start of treatment. PD without radiologic evidence were classified as progression only, when clear evidence of clinical deterioration was available and patient discontinued due to disease progression. Unknown (UNK) = all other cases." (NCT00767819)
Timeframe: Baseline up to 16 weeks

Intervention	percentage of participants (Number)
	Complete Response	Partial Response	Stable Disease	Progressive Disease	Unknown
Arm 1	0	0	40.5	51.4	8.1
Arm 2	0	0	33.3	62.5	4.2
Arm 3	0	0	100.0	0	0

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Time to Progression (TTP) (ITT)

Time to progression (TTP) was defined as the time from the date of start of treatment to the date of event defined as the first documented progression or death from underlying disease. If a patient had not had an event, TTP was censored at the date of the last adequate tumor assessment, which was the date of Visit 6 (Week 16) for the core phase and the last available tumor assessment for the follow-up phase. TTP was explored by using the Kaplan-Meier method. (NCT00767819)
Timeframe: Baseline up to 16 weeks

Intervention	days (Median)
Arm 1	57
Arm 2	57
Arm 3	499

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Percentage of Participants With Progression-free Survival (PFS) at 16 Weeks

Progression-free Survival (PFS) was defined as the time from the date of start of treatment to the date of event defined as the first documented progression or death from any cause. If a patient had not had an event, PFS was censored at the date of the last adequate tumor assessment at week 16 (NCT00767819)
Timeframe: 16 weeks

Intervention	percentage of participants (Number)
Arm 1	35.1
Arm 2	30.5
Arm 3	100.0

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Percentage of Participants With Overall Survival (OS) at Week 16 (ITT)

Overall survival (OS) was defined as the time from the date of start of treatment to death from any cause. If a patient was not known to have died (was alive), OS was censored at the date of the last contact, which was the date of Visit 6 (Week 16) for the core phase and the last available visit for the follow-up phase. OS was explored by using the Kaplan-Meier method. One death occurred in Arm 3 after Week 16. (NCT00767819)
Timeframe: Baseline up to 16 weeks

Intervention	percentage of participants (Number)
Arm 1	68.8
Arm 2	56.9
Arm 3	100.0

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Percentage of Participants With Duration of Response (CR, PR, SD) at 16 Weeks.

Duration of response (CR, PR or SD) applied only to those patients whose best overall response was CR, PR or SD based on local radiologic assessments and was defined as the time from start of treatment to progression or death from underlying disease. Patients not experiencing progression or death at 16 weeks were censored with the date of their last tumor assessment. Duration of response was explored using the Kaplan-Meier method. (NCT00767819)
Timeframe: Baseline up to 16 weeks

Intervention	percentage of participants (Number)
Arm 1	60
Arm 2	62.5
Arm 3	100

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Frequency and Severity of Toxicities

(NCT00770120)
Timeframe: Weekly during the first 8 weeks of treatment, then every 4 weeks while on treatment, then every 8 weeks until disease progression, then every 6 months thereafter.

Intervention	participants (Number)
	Anorexia	Confusion	Dehydration	Diarrhea	Dyspnea (shortness of breath)	Fatigue (asthenia, lethargy, malaise)	Glucose, serum-high (hyperglycemia)	Hemoglobin	INR (of prothrombin time)	Inf (clin/microbio) w/Gr 3-4 neuts - Lung	Infection with unknown ANC - Lung (pneumonia)	Left ventricular systolic dysfunction	Lymphopenia	Mucositis/stomatitis (clinical exam) - Oral cavity	Mucositis/stomatitis (functional/symp) - Oral cav	Muscle weakness, not d/t neuropathy - body/general	Pneumonitis/pulmonary infiltrates	Rash/desquamation	Triglyceride, serum-high (hypertriglyceridemia)
Everolimus	1	1	2	1	3	6	3	4	1	1	3	1	2	1	1	2	2	1	2

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Response

A response was defined as either a confirmed or unconfirmed complete or partial responses as defined by RECIST. A complete response (CR) was defined as the disappearance of all disease. A partial response (PR) was defined as a >= 30% decrease in the sum of longest diameters of target lesions. A CR or PR was considered confirmed if two consecutive determinations were made at least 4 weeks apart. (NCT00770120)
Timeframe: Every 8 weeks until disease progression, up to 3 years.

Intervention	percentage of overall response rate (Number)
Everolimus	2

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Progression-Free Survival

Progression-Free Survival was defined as the duration from the date of registration until the date of disease progression per RECIST or death due to any cause. Patients known to be alive without evidence of disease progression were censored at the date of last contact. Disease progression was defined as a >= 20% increase over nadir in the sum of longest diameters of target lesions, unequivocal progression of non-target lesions in the opinion of the treating investigator, appearance of new lesions, symptomatic deterioration, or death due to disease (NCT00770120)
Timeframe: Every 8 weeks until disease progression, up to 3 years.

Intervention	months (Median)
Everolimus	3.0

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Overall Survival

Overall survival was defined as the duration between the date of enrollment and the date of death due to any cause. Patients last known to be alive were censored at the date of last contact. (NCT00770120)
Timeframe: Every 8 weeks until disease progression, up to 3 years.

Intervention	months (Median)
Everolimus	6.3

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Overall Response

Overall response is classified as complete response (CR), partial response (PR), stable disease (SD) or Progressive Disease (PD) on therapy.Description: Overall response is classified as complete response (CR), partial response (PR), stable disease (SD) or Progressive Disease (PD) on therapy. Response for target lesions (up to5) is based on 3 dimensions with an elliptical model volume used: 0.5L*W*T; (L) tumor extent in plane perpendicular to the selected plane; (W) longest measurement of the tumor width; (T) transverse measurement perpendicular to the width. CR is disappearance all target and non-target lesions and no new lesions. PR is >/= 65% decrease in sum of the products (referent baseline). PD 40% or more increase in any target lesion (referent smallest product observed on therapy). SD is none of the above. PR and SD classification as long as absent new lesions and unequivocal progression for non-target lesions else PD. (NCT00782626)
Timeframe: Disease evaluations (MRI brain, including volumetric analysis) occurred at baseline, at the end of course 1, every 3 courses during treatment up to 12 courses and at early treatment discontinuation.

Intervention	participants (Number)
	Partial Response	Stable Disease
Everolimus	2	21

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Cardiac Death/MI

This endpoint is a composite of cardiac death and all myocardial infarction per protocol definition. (NCT00783796)
Timeframe: 1 year

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	2.9

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Cardiac Death/ All MI /CI-TLR

This endpoint is a composite of cardiac death, all myocardial infarction (MI)per protocol definition, and clinically-indicated target lesion revascularization (CI-TLR). (NCT00783796)
Timeframe: 30 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	2.1

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Cardiac Death/ All MI /CI-TLR

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	12.1

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Cardiac Death/ All MI /CI-TLR

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	7.2

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Cardiac Death/ All MI /CI-TLR

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	8.3

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Cardiac Death/ All MI /CI-TLR

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	8.1

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Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)

Target vessel myocardial infarction (MI) (MI not clearly attributable to a non-target vessel), including Q-wave MI (new pathologic Q waves) and Non Q-wave MI (elevation of CK to ≥ two times the upper limit normal with elevated CK-MB in the absence of new pathological Q waves). (NCT00783796)
Timeframe: 3 years

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	1.5

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All TVR (CI and Non-CI)

Includes any repeat revascularization intervention after the index procedure by any means (percutaneous or bypass surgery) in the target vessel from the index procedure. (NCT00783796)
Timeframe: 30 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.4

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All TVR (CI and Non-CI)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	8.6

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Clinically Indicated Target Lesion Revascularization (CI-TLR)

Includes clinically indicated repeat revascularization after the index procedure by any means (percutaneous or bypass surgery) of the target lesion. Classification as clinically indicated is done prospectively and verified by angiographic core lab measurement, and requires ≥50% diameter stenosis with ischemic signs or symptoms (positive history of angina pectoris or objective signs of ischemia at rest (ECG changes) or during exercise test or abnormal invasive cardiac functional diagnostic test), or ≥70% diameter stenosis in the absence of the above-mentioned ischemic signs or symptoms. (NCT00783796)
Timeframe: 30 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.0

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Clinically Indicated Target Vessel Revascularization

Includes clinically indicated repeat revascularization after the index procedure by any means (percutaneous or bypass surgery), of the target vessel. Classification as clinically indicated is done prospectively and verified by angiographic core lab measurement, and requires ≥50% diameter stenosis with ischemic signs or symptoms (positive history of angina pectoris or objective signs of ischemia at rest (ECG changes) or during exercise test or abnormal invasive cardiac functional diagnostic test), or ≥70% diameter stenosis in the absence of the above-mentioned ischemic signs or symptoms (per protocol). (NCT00783796)
Timeframe: 3 years

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	12.1

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Clinically Indicated Target Vessel Revascularization

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	8.8

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Clinically Indicated Target Vessel Revascularization

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	9.8

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Clinically Indicated Target Vessel Revascularization

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	7.2

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All TVR (CI and Non-CI)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	11.3

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Clinically Indicated Target Vessel Revascularization (TVR)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.4

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Composite Rate of Cardiac Death, Target Vessel Myocardial Infarction (MI) (Per Protocol Definition) & Clinically Indicated Target Lesion Revascularization (CI-TLR).

This endpoint is a composite of cardiac death, target vessel myocardial infarction per protocol definition, and clinically-indicated target lesion revascularization. (NCT00783796)
Timeframe: 1 year

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	8.1

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All TVR (CI and Non-CI)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	10.3

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All TVR (CI and Non-CI)

Includes any repeat revascularization intervention after the index procedure by any means (percutaneous or bypass surgery) in the target vessel from the index procedure (per protocol). (NCT00783796)
Timeframe: 3 years

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	13.6

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All TLR (CI and Non-CI)

Includes any repeat revascularization intervention after the index procedure by any means (percutaneous or bypass surgery) of the target lesion from the index procedure. This includes interventions classified as clinically indicated, and also includes interventions classified as not clinically indicated. (NCT00783796)
Timeframe: 30 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.7

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All TLR (CI and Non-CI)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	5.8

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All TLR (CI and Non-CI)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	6.8

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All TLR (CI and Non-CI)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	6.6

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All TLR (CI and Non-CI)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	8.3

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All Death/ All MI/All Coronary Revascularization

This endpoint is a composite of all death, all myocardial infarction per protocol definition, and all revascularization. (NCT00783796)
Timeframe: 30 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	3.5

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All Death/ All MI/All Coronary Revascularization

This endpoint is a composite of all death, all myocardial infarction per protocol definition, and all revascularization. (NCT00783796)
Timeframe: 3 years

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	26.5

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All Death/ All MI/All Coronary Revascularization

This endpoint is a composite of all death, all myocardial infarction per protocol definition, and all revascularization. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	15.1

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All Death/ All MI/All Coronary Revascularization

This endpoint is a composite of all death, all myocardial infarction per protocol definition, and all revascularization. (NCT00783796)
Timeframe: 2 years

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	22.6

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All Death/ All MI/All Coronary Revascularization

This endpoint is a composite of all death, all myocardial infarction per protocol definition, and all revascularization. (NCT00783796)
Timeframe: 1 year

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	16.9

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All Death (Cardiac, Vascular, Non-cardiovascular)

All death, including death from cardiac, vascular, and non-cardiovascular causes. (NCT00783796)
Timeframe: 30 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.7

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All Death (Cardiac, Vascular, Non-cardiovascular)

All death, including death from cardiac, vascular, and non-cardiovascular causes. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.4

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All Death (Cardiac, Vascular, Non-cardiovascular)

All death, including death from cardiac, vascular, and non-cardiovascular causes. (NCT00783796)
Timeframe: 2 years

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	1.5

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All Death (Cardiac, Vascular, Non-cardiovascular)

All death, including death from cardiac, vascular, and non-cardiovascular causes. (NCT00783796)
Timeframe: 1 year

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.5

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All Death (Cardiac, Vascular, Non-cardiovascular)

All death, including death from cardiac, vascular, and non-cardiovascular causes (per protocol). (NCT00783796)
Timeframe: 3 years

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	3.8

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All Coronary Revascularization (TVR and Non-TVR)

Includes any revascularization intervention after the index procedure by any means (percutaneous or bypass surgery), including intervention to the target vessel, and intervention to a vessel other than the target vessel. (NCT00783796)
Timeframe: 30 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	2.1

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All Coronary Revascularization (TVR and Non-TVR)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	12.9

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All Coronary Revascularization (TVR and Non-TVR)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	20.3

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All Coronary Revascularization (TVR and Non-TVR)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	14.7

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All Coronary Revascularization (TVR and Non-TVR)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	23.5

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Clinically Indicated Target Lesion Revascularization (CI-TLR)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	5.3

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Composite Rate of Cardiac Death, Target Vessel Myocardial Infarction (MI) (Per Protocol Definition) & Clinically Indicated Target Lesion Revascularization (CI-TLR).

This endpoint is a composite of cardiac death, target vessel myocardial infarction per protocol definition, and clinically-indicated target lesion revascularization. (NCT00783796)
Timeframe: 3 years

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	12.1

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Device Success (Per Lesion Basis, for Target Lesions Treated by 2.25 mm XIENCE V EECS With or Without Planned Overlap)

Successful delivery and deployment of the first study stent intended to be implanted at the intended target lesion (or intended first and second investigational stents for overlapping stents), successful withdrawal of the stent delivery system, and attainment of final residual stenosis of <50%. (NCT00783796)
Timeframe: From start of index procedure to end of index procedure

Intervention	Percentage of Lesions (Number)
2.25mm XIENCE V®	95.21

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Distal % Diameter Stenosis

Value calculated as 100*(1-MLD/RVD) where MLD is minimum lumen diameter and RVD is reference vessel diameter in 5 mm of healthy tissue distal to stent placement. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage (Mean)
2.25mm XIENCE V®	10.4

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Distal Angiographic Binary Restenosis (ABR) Rate

Percentage of patients with target lesions with ≥ 50% diameter stenosis in 5 mm of healthy tissue distal to stent placement at angiographic follow-up. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.0

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Distal Late Loss

Distal minimum lumen diameter (MLD) post-procedure minus distal MLD at angiographic follow-up (distal defined as 5 mm of healthy tissue distal to stent placement). (NCT00783796)
Timeframe: 240 days

Intervention	Millimeter (Mean)
2.25mm XIENCE V®	0.00

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In-segment % Diameter Stenosis

Value calculated as 100*(1-MLD/RVD) where MLD is in-segment minimum lumen diameter and RVD is in-segment reference vessel diameter. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage (Mean)
2.25mm XIENCE V®	20.85

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In-segment Angiographic Binary Restenosis (ABR) Rate

Percentage of patients with target lesions with ≥ 50% in-segment % diameter stenosis at angiographic follow-up. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	9.6

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In-segment Late Loss (LL)

In-segment minimum lumen diameter (MLD) post-procedure minus in-segment MLD at angiographic follow-up. (NCT00783796)
Timeframe: 240 Days

Intervention	Millimeters (Mean)
2.25mm XIENCE V®	0.16

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In-stent % Diameter Stenosis

Value calculated as 100*(1-MLD/RVD) where MLD is in-stent minimum lumen diameter and RVD is in-stent reference vessel diameter. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage (Mean)
2.25mm XIENCE V®	12.86

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In-stent Angiographic Binary Restenosis (ABR) Rate

Percentage of patients with target lesions with ≥ 50% in-stent % diameter stenosis at angiographic follow-up. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	3.8

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In-Stent Late Loss

In-stent minimum lumen diameter (MLD) post-procedure minus in-stent MLD at angiographic follow-up. (NCT00783796)
Timeframe: 240 days

Intervention	Millimeters (Mean)
2.25mm XIENCE V®	0.20

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Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.4

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Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)

Non target vessel myocardial infarction (MI) (MI clearly attributable to a non-target vessel), including Q-wave MI (new pathologic Q waves) and Non Q-wave MI (elevation of CK to ≥ two times the upper limit normal with elevated CK-MB in the absence of new pathological Q waves). (NCT00783796)
Timeframe: 1 year

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.0

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Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	0.0

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Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.0

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Clinically Indicated Target Lesion Revascularization (CI-TLR)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	4.3

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Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	0.0

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Non Target Vessel MI (Q-wave, Non Q-wave)(Per Protocol)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.0

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Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)

ARC defined non-target vessel MI (MI clearly attributable to a non-target vessel): Myocardial Infarction as per Academic Research Consortium standardized definitions (Circulation 2007;115:2344- 2351). (NCT00783796)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
2.25mm XIENCE V®	1.5

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Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	1.5

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Clinically Indicated Target Lesion Revascularization (CI-TLR)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	5.1

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Clinically Indicated Target Lesion Revascularization (CI-TLR)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	6.8

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Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)

Intervention	Percentage of participants (Number)
2.25mm XIENCE V®	1.4

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Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	4.5

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Non Target Vessel MI- Q-wave, Non Q-wave (Per ARC)

Intervention	Percentage of participants (Number)
2.25mm XIENCE V®	0.0

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Procedural Success (Per Subject Basis, for ALL Target and Non-target Lesions)

Achievement of a final in-stent diameter stenosis of <50% using the study device, without the occurence of cardiac death, target vessel myocardial infarction per protocol definition, or repeat revascularization of the target lesion during the hospital stay up to 7 days. (NCT00783796)
Timeframe: From the start of index procedure to end of index procedure

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	97.93

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Proximal % Diameter Stenosis

Value calculated as 100*(1-MLD/RVD) where MLD is minimum lumen diameter and RVD is reference vessel diameter in 5 mm of healthy tissue proximal to stent placement. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage (Mean)
2.25mm XIENCE V®	14.31

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Proximal Angiographic Binary Restenosis (ABR) Rate

Percentage of patients with target lesions with ≥ 50% diameter stenosis in 5 mm of healthy tissue proximal to stent placement at angiographic follow-up. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	2.7

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Proximal Late Loss

Proximal minimum lumen diameter (MLD) post-procedure minus proximal MLD at angiographic follow-up (proximal defined as 5 mm of healthy tissue proximal to stent placement). (NCT00783796)
Timeframe: 240 days

Intervention	Millimeter (Mean)
2.25mm XIENCE V®	0.21

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Stent Thrombosis (ARC Defined)

ARC defined: Stent Thrombosis as per Academic Research Consortium standardized definitions (Circulation 2007;115:2344-2351). Result includes Definite/Probable/Possible. (NCT00783796)
Timeframe: 0 to 1 day (Acute)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.0

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Stent Thrombosis (ARC Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.7

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Stent Thrombosis (ARC Defined)

Stent Thrombosis as per Academic Research Consortium standardized definitions (Circulation 2007;115:2344-2351). Result includes Definite/Probable/Possible. (NCT00783796)
Timeframe: >1 year (Very late)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.0

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Stent Thrombosis (ARC Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.5

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Stent Thrombosis (ARC Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.78

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Stent Thrombosis (ARC Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.0

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Stent Thrombosis (ARC Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	3.08

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Stent Thrombosis (ARC Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	2.17

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Stent Thrombosis (ARC Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	2.29

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Stent Thrombosis (Protocol Defined)

Stent Thrombosis per protocol categorized as acute (≤1 day), subacute (>1 day and ≤30 days), and late (>30 days), and defined as clinical presentation of acute coronary syndrome with angiographic evidence of stent thrombosis, or in absence of angiography, any unexplained death at any time or acute myocardial infarction* (ST segment elevation or new Q-wave) in the distribution of the target lesion within 30 days of the index procedure. (*Non-specific ST/T changes and cardiac enzymes do not suffice.). Result includes Definite/Probable/Possible. (NCT00783796)
Timeframe: > 1 day to 30 days (Subacute)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.7

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Stent Thrombosis (Protocol Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	0.0

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Stent Thrombosis (Protocol Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	2.3

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Stent Thrombosis (Protocol Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.5

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Stent Thrombosis (Protocol Defined)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.5

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Stent Thrombosis (Protocol Defined)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	3.1

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Stent Thrombosis (Protocol Defined)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	2.2

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Stent Thrombosis (Protocol Defined)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	2.27

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Target Vessel MI - Q-wave and Non Q-wave (Per ARC)

ARC defined target vessel MI (MI not clearly attributable to a non-target vessel): Myocardial Infarction as per Academic Research Consortium standardized definitions (Circulation 2007;115:2344- 2351). (NCT00783796)
Timeframe: 1 year

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	6.6

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Target Vessel MI - Q-wave and Non Q-wave (Per ARC)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	6.7

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Target Vessel MI - Q-wave and Non Q-wave (Per ARC)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	6.5

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Cardiac Death/MI

This endpoint is a composite of cardiac death and all myocardial infarction per protocol definition. (NCT00783796)
Timeframe: 30 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	2.1

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Cardiac Death/MI

This endpoint is a composite of cardiac death and all myocardial infarction per protocol definition. (NCT00783796)
Timeframe: 3 years

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	5.3

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Cardiac Death/MI

This endpoint is a composite of cardiac death and all myocardial infarction per protocol definition. (NCT00783796)
Timeframe: 240 days

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	2.9

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Cardiac Death/MI

This endpoint is a composite of cardiac death and all myocardial infarction per protocol definition. (NCT00783796)
Timeframe: 2 years

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	3.0

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Target Vessel MI - Q-wave and Non Q-wave (Per ARC)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	7.5

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Target Vessel MI - Q-wave and Non Q-wave (Per ARC)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	6.3

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Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.5

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Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)

Intervention	percentage of participants (Number)
2.25mm XIENCE V®	1.5

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Target Vessel MI - Q-wave and Non Q-wave (Per Protocol)

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	1.4

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Composite Rate of Cardiac Death, Target Vessel Myocardial Infarction (MI) (Per Protocol Definition) & Clinically Indicated Target Lesion Revascularization (CI-TLR).

This endpoint is a composite of cardiac death, target vessel myocardial infarction per protocol definition, and clinically-indicated target lesion revascularization. (NCT00783796)
Timeframe: 2 years

Intervention	Percentage of Participants (Number)
2.25mm XIENCE V®	8.3

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Everolimus Blood Concentration (C2h) at 2 Hours Post Dose

The participants were assessed for everolimus blood concentration at 2 hours time point after dose administration on the same day, if the participant did not vomit between previous dose and blood sample collection. Tandem liquid chromatography-mass spectrometry method was used for evaluation. C2h values were categorized as < 20 ng/mL, 20-50 ng/mL, and > 50 ng/mL, concentrations below the lower limit of quantification were entered as 0 ng/mL. (NCT00789828)
Timeframe: 2 hours post dose on Week 6, Week 24, Week 48, Week 96, Week 144, and Week 240

Intervention	ng/mL (Mean)
	Week 6 (n= 37, 47)	Week 24 (n= 11, 13)	Week 48 (n= 1, 3)	Week 96 (n= 0, 6)	Week 144 (n= 0, 6)	Week 240 (n= 0, 0)
Everolimus (Core Period)	27.52	38.7	23.2	NA	NA	NA
Everolimus (Extension Period)	27.74	39.25	49.73	31.63	26.33	NA

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Everolimus Trough Concentrations (Cmin) at 24 Hours After Last Dose

The participants were assessed for everolimus trough concentration (Cmin) at 24 hours time point after previous dose administration, at a steady state following 5 days of consistent dosing, if the participant did not vomit within 4 hours of previous dose. Tandem liquid chromatography-mass spectrometry method was used for evaluation. Cmin values were categorized as <5 ng/mL, 5-10 ng/mL, and >10 ng/mL, concentrations below the lower limit of quantification were entered as 0 ng/mL. (NCT00789828)
Timeframe: 24 hours post dose on Week 6, Week 24, Week 48, Week 72, Week 96, Week 144, and Week 240

Intervention	ng/mL (Mean)
	Week 6 (n= 64, 94)	Week 24 (n= 64, 89)	Week 48 (n= 23, 86)	Week 72 (n= 4, 92)	Week 96 (n= 0, 83)	Week 144 (n= 0, 69)	Week 240 (n= 0, 13)
Everolimus (Core Period)	5.8	6.59	7.28	6.08	NA	NA	NA
Everolimus (Extension Period)	6.09	6.86	7.07	7.25	7.09	7.28	5.85

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Percentage of Participants With Renal Impairment During Core Period

Renal function was assessed using glomerular filtration rate (GFR) based on age measure; Modification of Diet in Renal Disease (MDRD) formula for participants aged 18 years or older, defined as GFR equal to 32788*(serum creatinine (micromol/L)^-1.154)*(age^-0.203 )*(0.742, if female)*(1.210, if black), and Schwartz formula for participants less than 18 years defined as GFR equal to 0.41*height (cm)/ Serum creatinine (mg/dL). Participants with severe renal impairment defined as GFR < 30 mL/min/1.73 m^2 and participants with National Cancer Institute's Common Terminology Criteria for Adverse Events (NCI-CTCAE) grade 3/4 serum creatinine were reported. (NCT00789828)
Timeframe: Day 1 up to 28 days after end of treatment (Core period)

Intervention	Percentage of participants (Number)
	Grade 3 or 4	Grade 1 or 2	Grade 0
Everolimus (Core Period)	0	3.8	96.2
Placebo (Core Period)	0	0	100

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Change From Baseline in Frequency of Total Seizure Events Per 24 Hours at Week 24 in Both Core and Extension Period

Seizure frequency per 24 hours was defined as the number of seizures in the electroencephalography (EEG) divided by the number of hours in the EEG, multiplied by 24. Seizure frequency was evaluated using a 24-hour video-EEG. Seizure frequency was listed as missing if the actual EEG recording duration was < 18 hours. (NCT00789828)
Timeframe: Baseline (Core period) to Week 24 (Core period), Baseline (Extension period, Week 24 post-core baseline) to Week 24 (Extension period, Week 48 post-core baseline)

Intervention	Seizure frequency (Mean)
Everolimus (Core Period)	-1.24
Placebo (Core Period)	-0.24
Everolimus (Extension Period)	-6.07

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Duration of SEGA Response

Duration of SEGA response was defined as time from the date of the first documented SEGA response until the date of the first documented SEGA progression. Duration of SEGA response was evaluated only for participants who achieved a SEGA response. The time to SEGA progression was censored if SEGA progression was not observed before the first to occur out of (i) analysis cut-off date (ii) the date when systemic anti-SEGA medication is started, (iii) the date of a SEGA-related surgery or (iv) the date of death. Since, no case of SEGA progression was observed in core study which resulted in censored duration of SEGA response. Only 5 SEGA responders experienced a SEGA progression in extension period. (NCT00789828)
Timeframe: Baseline up to week 48 (end of core period), and end of extension period (up to 4 years)

Intervention	months (Median)
Everolimus (Core Period)	NA
Everolimus (Extension Period)	NA

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Duration of Skin Lesion Response in Everolimus Treated Participants

Duration of skin lesion response was defined as the time from the first skin lesion response until the first skin lesion progression, defined as worsening of lesion by > 25% or more from baseline. (NCT00789828)
Timeframe: Baseline up to week 48 (end of core period), and end of extension period (up to 4 years)

Intervention	months (Median)
Everolimus (Core Period)	NA
Everolimus (Extension Period)	NA

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Percentage of Participants With Best Overall Subependymal Giant Cell Astrocytomas (SEGA) Response

Participants were assessed for SEGA response, defined as 50% reduction from baseline in SEGA volume (where SEGA volume was the sum of the volumes of all target SEGA lesions identified at baseline, and confirmed with a second scan performed approximately 12 weeks later), no unequivocal worsening of non-target SEGA lesions, no new SEGA lesions (≥ 1 cm in longest diameter), and no new or worsening hydrocephalus. Multi-phase brain MRI was utilized to identify SEGA lesions. SEGA response rate was defined as the percentage of participants whose best overall status was SEGA response as determined by Independent Central Radiology Review. The Kaplan-Meier estimate was used for determining time to SEGA response. (NCT00789828)
Timeframe: End of core period (Week 48), and end of extension period (up to 4 years)

Intervention	Percentage of participants (Number)
Everolimus (Core Period)	34.6
Placebo (Core Period)	0.0
Everolimus (Extension Period)	57.7

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Percentage of Participants With Skin Lesions Assessed Using Physician's Global Assessement Overall Score

Skin lesions included hypomelanotic macules, the shagreen patch, periungual or subungual fibromas, facial angiofibromas and/or forehead plaques. Response was evaluated using the Physician's Global Assessment of Clinical Condition (PGA) on a 7-point scale: Grade 0 = complete clinical response, indicated absence of disease, Grade 1, 2, and 3 = partial response, indicated improvements of ≥ 50% but < 100%, Grade 4, 5 = stable disease, indicated some or no improvements of 25% - < 50% and 6 = progressive disease, indicated worse than at baseline evaluation by > 25%. Response rate was determined for participants with ≥ 1 skin lesion at baseline, defined as the percentage of participants with overall status as complete clinical response or partial response. (NCT00789828)
Timeframe: End of core period (Week 48), and end of extension period (up to 4 years)

Intervention	Percentage of participants (Number)
Everolimus (Core Period)	41.7
Placebo (Core Period)	10.5
Everolimus (Extension Period)	58.1

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Time to SEGA Progression

Time to SEGA progression was defined as time between randomisation to time to first SEGA progression. SEGA progression was defined as either one or more of the following criteria: 1. increase from nadir of ≥ 25% in SEGA volume to a value greater than baseline SEGA volume (where SEGA volume is the sum of the volumes of all target SEGA lesions identified at baseline, and nadir is the lowest SEGA volume obtained for the participant previously in the trial), 2. unequivocal worsening of non-target SEGA lesions, 3. appearance of new SEGA lesion ≥ 1.0 cm in longest diameter, 4. new or worsening hydrocephalus. The median TTSP based on central radiology review was not reached in any treatment arms; Only 6 events of SEGA progressions were observed in the placebo group of core period. (NCT00789828)
Timeframe: Baseline up to week 48 (end of core period), and end of extension period (up to 4 years)

Intervention	months (Median)
Everolimus (Core Period)	NA
Placebo (Core Period)	NA
Everolimus (Extension Period)	NA

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Time to SEGA Response

Participants were assessed for time to SEGA response, defined as 50% reduction from baseline in SEGA volume (where SEGA volume was the sum of the volumes of all target SEGA lesions identified at baseline, and confirmed with a second scan performed approximately 12 weeks later), no unequivocal worsening of non-target SEGA lesions, no new SEGA lesions (≥ 1 cm in longest diameter), and no new or worsening hydrocephalus. Multi-phase brain MRI was utilised to identify SEGA lesions. SEGA response rate was defined as the percentage of participants whose best overall status was SEGA response as determined by Independent Central Radiology Review. The Kaplan-Meier estimate was used for determining time to SEGA response. (NCT00789828)
Timeframe: Baseline up to week 48 (end of core period), and end of extension period (up to 4 years)

Intervention	months (Median)
Everolimus (Core Period)	2.99
Everolimus (Extension Period)	5.32

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Time to SEGA Worsening

Time to SEGA worsening was defined as the time from the start of everolimus to date of the first SEGA worsening. SEGA worsening was defined as either; increase from nadir of ≥ 25% in SEGA volume or unequivocal worsening of non-target SEGA lesions, or appearance of new SEGA lesion ≥ 1.0 cm in longest diameter, or new or worsening hydrocephalus. The median value was not reached in either treatment arm of core period as SEGA worsening was observed in less participants (everolimus - 7 and placebo - 8). (NCT00789828)
Timeframe: Baseline up to week 48 (end of core period), and end of extension period (up to 4 years)

Intervention	months (Median)
Everolimus (Core Period)	NA
Placebo (Core Period)	NA
Everolimus (Extension Period)	55.72

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Disease-free Survival (DFS)

DFS was defined as the time from date of randomization to the date of event defined as the first documented relapse of the disease or death due to any cause. Relapse was based on investigator assessment and was assigned only if: It was documented according to Cheson guidelines by an objective radiological assessment method; It was documented by a biopsy proven lymphoma including new or recurrent bone marrow involvement; A new anticancer therapy for lymphoma started with subsequent confirmation of the relapse within 4 weeks of the start of this anticancer therapy (NCT00790036)
Timeframe: From date of randomization to the date of event defined as the first documented recurrence of the disease, or death due to any cause and up to 6 years

Intervention	Percentage of participants (Number)
RAD001 (Everolimus)1	77.8
Placebo	77.0

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Lymphoma-specific Survival (LSS)

LSS was defined as time from randomization to death as a result of lymphoma. (NCT00790036)
Timeframe: From randomization to death documented as a result of lymphoma up to 7 years

Intervention	Percentage of participants (Number)
	2 years	3 years	4 years	5 years	6 years
Placebo	90.5	88.8	86.9	85.4	85.4
RAD001 (Everolimus)1	94.9	93.1	91.6	89.4	89.4

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Overall Survival (OS)

OS was defined as the time from date of randomization to date of death due to any cause. If the patient was not known to have died, survival was censored at the date of the last contact. (NCT00790036)
Timeframe: From date of randomization to date of death due to any cause up to around 7 years

Intervention	Percentage of participants (Number)
	2 years	3 years	4 years	5 years	6 years
Placebo	88.3	83.7	80.7	77.4	77.4
RAD001 (Everolimus)1	90.7	88.0	85.4	83.4	80.3

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Angiomyolipoma Response Rate as Per Central Radiology Review

"Angiomyolipoma response defined as the combination of the following criteria: reduction in angiomyolipoma volume of ≥ 50% relative to baseline, where angiomyolipoma volume was sum of volumes of all target lesions identified at baseline, and with a confirmatory scan performed approximately 12 weeks later (no sooner than 8 weeks later); no new angiomyolipoma lesions ≥ 1.0 cm in longest diameter were identified; there were no kidney increases in volume > 20% from nadir. The patient did not have any angiomyolipoma-related bleeding of ≥ grade 2.~For the everolimus (core/extension periods) treatment group, the baseline means the latest value on or before starting everolimus." (NCT00790400)
Timeframe: From date of randomization until the earliest date of first documented AML progression, date of further anti-AML medication (including open-label Everolimus)/surgery or up to 5.7 years

Intervention	Percentage of Participants (Number)
Everolimus Randomized (Core Period)	41.8
Placebo Randomized (Core Period)	0
Everolimus (Core and/or Extension Period)	58.0

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Duration of Angiomyolipoma Response - Only Everolimus Patients With Angiomyolipoma Response

Duration of angiomyolipoma response was defined as the time from the date of the first documented angiomyolipoma response until the date of the first documented angiomyolipoma progression . Angiomyolipoma response was defined as the combination of the following criteria: reduction in angiomyolipoma volume of ≥ 50% relative to baseline, where angiomyolipoma volume was sum of volumes of all target lesions identified at baseline, and with a confirmatory scan performed approximately 12 weeks later (no sooner than 8 weeks later); no new angiomyolipoma lesions ≥ 1.0 cm in longest diameter were identified; there were no kidney increases in volume > 20% from nadir. The patient did not have any angiomyolipoma-related bleeding of ≥ grade 2. (NCT00790400)
Timeframe: From date of randomization until the earliest date of first documented AML progression, date of further anti-AML medication (including open-label Everolimus)/surgery or up to about 5.7 years

Intervention	months (Median)
Everolimus Randomized (Core Period)	NA
Everolimus (Core and/or Extension Period)	NA

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Duration of Skin Lesion Response - Only Everolimus Patients With Best Overall Skin Lesion Response of Complete Clinical Response (CCR) or Partial Response (PR)

Duration of skin lesion response is defined as the time from the date of the first skin lesion response until the date of the first skin lesion progression, according to the PGA (physician's global assessment of clinical condition). A progression is when the disease is worse than at baseline evaluation by >=25% or more. (NCT00790400)
Timeframe: From date of randomization until the earliest date of first documented AML progression, date of further anti-AML medication (including open-label Everolimus)/surgery or up to about 5.7 years

Intervention	months (Median)
Everolimus Randomized (Core Period)	NA
Everolimus (Core and/or Extension Period)	NA

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Skin Lesion Response Rate as Per Investigator (Only Patients With at Least One Skin Lesion at Baseline)

Skin lesion response rate in the double-blind period was determined only among patients with at least one skin lesion at baseline, and is the percentage of this group of patients with a best overall skin lesion response on the Physician's Global Assessment of Clinical Condition (PGA) of either complete clinical response (CCR) or partial response (PR). A complete clinical response (CCR) requires a grading of 0 indicating the absence of disease (histological confirmation is not required). Grades 1, 2, and 3 constitute partial response, indicating improvement of at least 50 percent, but less than 100 percent improvement. For the everolimus (core/extension periods) treatment group, the baseline means the latest value on or before starting everolimus. (NCT00790400)
Timeframe: From date of randomization until the earliest date of first documented AML progression, date of further anti-AML medication (including open-label Everolimus)/surgery or up to 5.7 years

Intervention	Percentage of participants (Number)
Everolimus Randomized (Core Period)	26
Placebo Randomized (Core Period)	0
Everolimus (Core and/or Extension Period)	68.2

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Time to Angiomyolipoma Progression as Per Central Radiology Review

"Time to angiomyolipoma progression (TTAP) is defined as time from date of randomization to date of first documented angiomyolipoma progression. Angiomyolipoma progression was defined as one or more of the following: Increase from nadir of ≥ 25% in angiomyolipoma volume to value greater than baseline; the appearance of a new angiomyolipoma ≥ 1.0 cm in longest diameter; an increase from nadir of 20% or more in the volume of either kidney to a value greater than baseline; angiomyolipoma-related bleeding grade ≥ 2.~For the everolimus (core/extension periods) treatment group, the time to angiomyolipoma progression is defined starting from the start of everolimus. The baseline means the latest value on or before starting everolimus." (NCT00790400)
Timeframe: From date of randomization until the earliest date of first documented AML progression, date of further anti-AML medication (including open-label Everolimus)/surgery or up to about 5.7 years

Intervention	months (Median)
Everolimus Randomized (Core Period)	NA
Placebo Randomized (Core Period)	11.37
Everolimus (Core and/or Extension Period)	NA

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Time to Angiomyolipoma Response - Only Everolimus Patients With Angiomyolipoma Response

"Time to angiomyolipoma response was defined as the time from the date of randomization until the date of the first documented angiomyolipoma response. Angiomyolipoma response defined as the combination of the following criteria: reduction in angiomyolipoma volume of ≥ 50% relative to baseline, where angiomyolipoma volume was sum of volumes of all target lesions identified at baseline, and with a confirmatory scan performed approximately 12 weeks later (no sooner than 8 weeks later); no new angiomyolipoma lesions ≥ 1.0 cm in longest diameter were identified; no kidney increases in volume > 20% from nadir; no angiomyolipoma-related bleeding of ≥ grade 2.~For the everolimus (core/extension periods) treatment group, the time to angiomyolipoma response is from the start of everolimus. The baseline in the response definition means the latest value on or before starting everolimus." (NCT00790400)
Timeframe: From date of randomization until the earliest date of first documented AML progression, date of further anti-AML medication (including open-label Everolimus)/surgery or up to 5.7 years

Intervention	months (Median)
Everolimus Randomized (Core Period)	2.86
Everolimus (Core and/or Extension Period)	2.89

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Change From Baseline in Plasma Angiogenic Molecules - Vascular Endothelial Growth Factor (VEGF) Marker

Blood samples for biomarker assessment were collected immediately prior to study administration. On-treatment samples was compared to baseline samples with the change from baseline. (NCT00790400)
Timeframe: 4 weeks, 12 weeks, 24 weeks, 36 weeks 48 weeks, 60 weeks, 72 weeks

Intervention	pg/mL (Mean)
	Week 4 (n:56, 28)	Week 12 (n:56, 29)	Week 24 (n:53, 29)	Week 36 (n:26, 18)	Week 48 (n:16, 8)	Week 60 (n:0, 1)	Week 72 (n:0, 1)
Everolimus Randomized (Core Period)	38.7	43.4	31.1	18.0	55.3	NA	NA
Placebo Randomized (Core Period)	17.6	-6.1	-4.3	5.4	3.1	-4.12	-6.1

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Everolimus Blood Concentrations (C2h) at 2 Hours Post-dose

C2h values collected 1-3 hours after dose administration on the same study day, at steady state, and patient did not vomit between taking previous dose and blood collection. Samples collected during the first 4 days of dosing will be excluded from all analyses. (NCT00790400)
Timeframe: 2 hours post-dose administration at Weeks 2, 4, 12, 24, 48

Intervention	ng/mL (Mean)
	2 hours post dose administration at Week 2 (n:55)	2 hours post dose administration at Week 4 (n:49)	2 hours post dose administration at Week 12 (n:56)	2 hours post dose administration at Week 24 (n:50)	2 hours post dose administration at Week 48 (n:14)
Everolimus Randomized (Core Period)	33.38	30.89	34.48	39.27	33.20

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Everolimus Trough Concentrations (Cmin)

Cmin values collected prior to dose administration on the same study day and at 20-28 hours after previous dose, at steady state, and patient did not vomit within 4 hours of previous dose. Samples collected during the first 4 days of dosing were excluded from all analyses. (NCT00790400)
Timeframe: Prior to dosing at weeks 2, 4, 12, 24, 48

Intervention	ng/mL (Mean)
	Prior to dosing at Week 2 (n:43)	Prior to dosing Week 4 (n:44)	Prior to dosing Week 12 (n:49)	Prior to dosing Week 24 (n:46)	Prior to dosing Week 48 (n:15)
Everolimus Randomized (Core Period)	7.63	7.72	8.79	9.37	11.49

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Percentage of Participants With Renal Impairment

Renal Impairment was measured by glomerular filtration rate which was calculated using the Modification of Diet in Renal Disease formula. Percentage of participants with renal impairment was reported. Severe renal impairment was defined as a GFR of <30ml/min/1.73m2. (NCT00790400)
Timeframe: Day 1 up to 28 days after end of treatment

Intervention	Percentage of Participants (Number)
	Glomerular filtration rate <30 ml/min/1.73m^2	Glomerular filtration rate≥ 30 ml/min/1.73m^2
Everolimus (Core and/or Extension Period)	7.1	92.9
Everolimus Randomized (Core Period)	2.5	97.5
Placebo Randomized (Core Period)	7.7	92.3

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Proportion of Pretreatment Primary Tumor Samples With mTOR Pathway Markers

To assess markers for activated mTOR pathway (including phospho-S6 and phospho-4E BP1) in all pre-treatment tissue specimens and correlate with response to treatment and PFS. (NCT00805129)
Timeframe: 25 months

Intervention	Proportion of pretreatment primary tumor (Number)
Everolimus	0.62

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Number of Participants Evaluated for Toxicity

To determine the safety and toxicity of Everolimus (RAD001) in this patient population with toxicities being evaluated by CTCAE v3.0 (NCT00805129)
Timeframe: through study completion, up to 25 months

Intervention	Participants (Count of Participants)
Everolimus	46

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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

Intervention	Months (Number)
Overall Study	13.9

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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

Intervention	Months (Median)
Overall Study	11.3

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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

Intervention	Participants (Count of Participants)
Overall Study	53

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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

Intervention	Participants (Count of Participants)
Overall Study	31

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Number of Participants With Bone Marrow Morphology and Cytogenetics Pre- and Post-therapy

Number of Participants with change in bone marrow morphology and cytogenetics (NCT00809185)
Timeframe: at 2 years of treatment

Intervention	Participants (Count of Participants)
RAD001(Everolimus)	0

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Number of Patients With Either a Major or Minor Erythroid Response (Hemoglobin Change From Baseline Measure)

"Major erythroid response: (1) For patients with a baseline hemoglobin less than 11 g/dL, a major erythroid response is defined as a > 2 g/dL increase in hemoglobin from baseline; or (2) 100% decrease in red blood cell transfusion requirements.~Minor erythroid response: (1) For patients with baseline hemoglobin less than 11 g/dL, a minor erythroid response is defined as an increase in hemoglobin greater than 1 g/dL but less than 2 g/dL from baseline; or (2) > 50% decrease in red blood cell transfusion requirements." (NCT00809185)
Timeframe: 2 years of treatment

Intervention	participants (Number)
	Number of Patients with a Minor Response	Number of Patients with a Major Response
RAD001(Everolimus)	0	0

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Number of Dose- and Non-dose-limiting Toxicities

Number of Dose- and Non-dose-limiting Toxicities at the end of cycle 1 associated with RAD001 (see AE/SAE section for details). (NCT00809185)
Timeframe: at end of one cycle (28 days)

Intervention	events (Number)
RAD001 (Everolimus)	26

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Progression-free Survival

Intervention	months (Median)
Bicalutamide + Everolimus	9.4

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Overall Survival

Overall survival was estimated using the Kaplan-Meier method. (NCT00814788)
Timeframe: Up to 3 years

Intervention	months (Median)
Bicalutamide + Everolimus	28

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PSA Response Rate

The PSA response rate was defined as a 30% reduction in the PSA level from baseline. PSA Working Group consensus criteria combined with radiographic studies were used to determine the proportion of patients with PSA decline. (NCT00814788)
Timeframe: Up to 2 years

Intervention	Participants (Count of Participants)
Bicalutamide + Everolimus	18

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Progression-free Survival at 6 Months.

Number of patients alive without progressive disease at 6 months. Assessment of progression was defined by RANO as a 25% increase in the sum of all the products of measurable lesions, clear worsening of any evaluable disease or any new lesion (NCT00823459)
Timeframe: At 6 months after treatment start

Intervention	Participants (Count of Participants)
	Grade II	Grade III/IV
Daily Intervention With RAD001	39	6

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To Assess the Correlation of Activation of the PI3K/mTOR Pathway With Survival

Survival of patients with p-S6 staining of >19% (activated pathway) (NCT00823459)
Timeframe: 5 years

Intervention	years (Median)
Daily Intervention With RAD001	3.9

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Objective Response Rate (ORR) in Patients Treated With RAD001.

Objective response is defined as complete or partial response as defined by RANO criteria as determined by MRI and steroid requirement. Complete response was defined by disappearance of all measurable disease with minimal or no steroids; a partial response was defined as 50% in sum of all products in perpendicular diameters of all measurable lesions with no new lesions on stable or decreasing steroids. (NCT00823459)
Timeframe: 12 months

Intervention	participants (Number)
Daily Intervention With RAD001	0

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Overall Survival (OS) in Patients Treated With RAD001.

Number of years from the day the patient started treatment until the date of death, an average of 5 years. (NCT00823459)
Timeframe: Time from registration till death, an average of 5 years

Intervention	years (Median)
Daily Intervention With RAD001	5.2

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RAD001 Safety Profile in Patients With Recurrent LLG

Grade 4-5 treatment related adverse events as defined by CTCAE 3.0 (NCT00823459)
Timeframe: 13 months

Intervention	Participants (Count of Participants)
Daily Intervention With RAD001	0

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Best Overall Response by PI3K-AKT-MTOR Mutation

Next generation sequencing was used to identify participants with PI3K-AKT-MTOR mutations. Best overall response rate was analyzed with mutant versus wild-type pathways. Please see Best Overall Response Rate for response definition. (NCT00827359)
Timeframe: Evaluated while on treatment. Up to 36 months

Intervention	percentage of participants (Number)
	Mutation	No Mutations
Treatment	5.6	0

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Median Progression Free Survival

"Progression free survival (PFS) is defined as the time from start of treatment to disease progression (PD) or death from any cause as estimated by Kaplan Meier methods. Patients who have not progressed and are alive are censored at the date the patient is known to be progression-free. Progression is defined by Response Evaluation Criteria In Solid Tumors Criteria 1.1 (RECIST) as follows:~- >20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (including baseline if it's the smallest). The sum must also demonstrate an increase of >5 mm.~OR~-Appearance of new lesions and/or unequivocal progression of non-target lesions. It must be representative of overall disease status change, not a single lesion increase. For patients with PD at the first on-treatment imaging assessment, patients will be allowed to remain on study until confirmation at the next assessment at investigator discretion if patient is benefiting from treatment." (NCT00827359)
Timeframe: Follow-up time was up to 39 months from treatment start date.

Intervention	months (Median)
Treatment	3.8

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Best Overall Response Rate

"The best overall response rate is the percentage of participants achieving complete response (CR) or partial response (PR) as the best response recorded on treatment based on Response Evaluation Criteria In Solid Tumors Criteria (RECIST 1.1) criteria.~CR and PR must meet the following lesion criteria without having any new lesions as well:~Target Lesion:~(CR): Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~(PR): At least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters.~Non-Target Lesion:~(CR): Disappearance of all non-target lesions and normalization of tumor marker level. All lymph nodes must be non-pathological in size (<10 mm short axis).~Non-CR/Non-Progressive Disease: Persistence of one or more non-target lesion(s) and/or maintenance of tumor marker level above the normal limits. Must have PR in target lesion." (NCT00827359)
Timeframe: Evaluated while on treatment. Up to 36 months.

Intervention	percentage of participants (Number)
Treatment	4.2

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Disease Progression Diagnosed by Biopsy

Clinical progression validated by biopsy of metastatic site. Progression-free survival (PFS) will be measured from the post-op treatment start date to either the date the patient is first recorded as having disease progression, or the date of death if the patient dies due to any causes before progression. If a patient is lost to follow-up or removed for toxicities, the patient will be censored as of the last date of contact. Patients who start a new treatment before they progress will be censored as of the date of start of the new treatment. If a patient has not progressed or died, PFS is censored at the date of last follow-up. Patients removed from therapy with everolimus due to toxicities will not be included in the PFS estimation. (NCT00831480)
Timeframe: up to one year

Intervention	participants (Number)
"Neoadjuvant Everolimus RAD001 for Advanced RCC Before Cytore"	9

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Objective Response Rate (ORR)

Objective response is defined as complete response (CR) or partial response (PR) assessed using Response Evaluation Criteria in Solid Tumors (RECIST) criteria. The primary analysis population is based on efficacy-evaluable patients, defined as those patients who receive at least one cycle of RAD001 plus erlotinib and undergo at least one post-baseline response assessment or die while on therapy. (NCT00843531)
Timeframe: Up to 2 years

Intervention	Participants (Count of Participants)
RAD001 Plus Erlotinib	0

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Number of Patients With Dose-limiting Toxicity (DLT)

Primary safety analysis will be conducted after the first 16 patients have had potential for completion of two cycles of protocol therapy. All patients receiving at least one dose of protocol therapy will be included in the analyses. All patients with treatment-related, Grade 3 or higher adverse events according to the NCI Common Terminology Criteria for Adverse Events (CTCAE) version 3 resulting in a DLT will be reported. (NCT00843531)
Timeframe: Up to 9 months

Intervention	Participants (Count of Participants)
RAD001 and Erlotinib	8

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Duration of Objective Response

Duration of objective response will be defined as the time from the initial documentation of response to documented disease progression or death from any cause on study (NCT00843531)
Timeframe: Up to 2 years

Intervention	months (Number)
RAD001 and Erlotinib	NA

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In-scaffold Percent Diameter Stenosis (%DS)

Percent Diameter Stenosis is defined as the value calculated as 100 * (1 - MLD/RVD) using the mean values from two orthogonal views (when possible) by QCA. (NCT00856856)
Timeframe: 2 years

Intervention	percentage of diameter stenosis (Mean)
Absorb BVS	20.94

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In-scaffold Percent Diameter Stenosis (%DS)

Percent Diameter Stenosis is defined as the value calculated as 100 * (1 - MLD/RVD) using the mean values from two orthogonal views (when possible) by QCA. (NCT00856856)
Timeframe: 3 years

Intervention	percentage of diameter stenosis (Mean)
Absorb BVS	23.16

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In-scaffold Percent Diameter Stenosis (%DS)

Percent Diameter Stenosis is defined as the value calculated as 100 * (1 - MLD/RVD) using the mean values from two orthogonal views (when possible) by QCA. (NCT00856856)
Timeframe: 5 years

Intervention	percentage of diameter stenosis (Mean)
Absorb BVS	22.74

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

"ID-TLR is defined as the revascularization at the target lesion associated with any of the following:~Positive functional ischemia study~Ischemic symptoms and angiographic minimal lumen diameter stenosis ≥ 50% by core laboratory quantitative coronary angiography (QCA)~Revascularization of a target lesion with diameter stenosis ≥ 70% by core laboratory QCA without either ischemic symptoms or a positive functional study." (NCT00856856)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Absorb BVS	4.0

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	Percentage of participants (Number)
Absorb BVS	2.0

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	Percentage of participants (Number)
Absorb BVS	2.0

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
Absorb BVS	7.0

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
Absorb BVS	0

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
Absorb BVS	7.1

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
Absorb BVS	8.0

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

"ID-TVR is the revascularization in the target vessel associated with any of the following:~Positive functional ischemia study~Ischemic symptoms and an angiographic minimal lumen diameter stenosis ≥ 50% by core laboratory quantitative coronary angiography (QCA)~Revascularization of a target vessel with diameter stenosis ≥ 70% by core laboratory QCA without either ischemic symptoms or a positive functional study." (NCT00856856)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Absorb BVS	4.0

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	Percentage of participants (Number)
Absorb BVS	2.0

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	Percentage of participants (Number)
Absorb BVS	8.0

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	Percentage of participants (Number)
Absorb BVS	2.0

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	Percentage of participants (Number)
Absorb BVS	10.0

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	Percentage of participants (Number)
Absorb BVS	10.0

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Ischemia Driven Target Vessel Revascularization (ID-TVR)

Intervention	Percentage of participants (Number)
Absorb BVS	11.0

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Late Incomplete Apposition

"Late-Acquired Incomplete Apposition is defined as incomplete apposition of the scaffold at follow-up, which was not present post-procedure.~Incomplete Apposition: Failure of the scaffold to completely appose to the vessel wall after placement is defined as one or more scaffold strut separated from the vessel wall with evidence of blood speckles behind the strut in the ultrasound image." (NCT00856856)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Absorb BVS	3.6

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Late Incomplete Apposition

Intervention	Percentage of participants (Number)
Absorb BVS	7.5

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Late Incomplete Apposition

Intervention	Percentage of participants (Number)
Absorb BVS	2.6

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Late Incomplete Apposition

Intervention	Percentage of participants (Number)
Absorb BVS	7.0

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Luminal Volume

(NCT00856856)
Timeframe: 1 year

Intervention	mm^3 (Mean)
Absorb BVS	106.33

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Luminal Volume

(NCT00856856)
Timeframe: 2 years

Intervention	mm^3 (Mean)
Absorb BVS	107.66

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Luminal Volume

(NCT00856856)
Timeframe: 3 years

Intervention	mm^3 (Mean)
Absorb BVS	103.31

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Luminal Volume

(NCT00856856)
Timeframe: 5 years

Intervention	mm^3 (Mean)
Absorb BVS	106.36

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Mean Flow Area

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	5.90

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Mean Flow Area

(NCT00856856)
Timeframe: 2 years

Intervention	mm^2 (Mean)
Absorb BVS	6.00

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Mean Flow Area

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	6.06

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Mean Flow Area

(NCT00856856)
Timeframe: 5 years

Intervention	mm^2 (Mean)
Absorb BVS	6.21

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Mean Luminal Area

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	5.92

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Mean Luminal Area

(NCT00856856)
Timeframe: 2 years

Intervention	mm^2 (Mean)
Absorb BVS	6.00

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Mean Luminal Area

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	6.06

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Mean Luminal Area

(NCT00856856)
Timeframe: 5 years

Intervention	mm^2 (Mean)
Absorb BVS	6.22

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Mean Luminal Diameter

(NCT00856856)
Timeframe: 1 year

Intervention	mm (Mean)
Absorb BVS	2.71

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Mean Luminal Diameter

(NCT00856856)
Timeframe: 2 years

Intervention	mm (Mean)
Absorb BVS	2.72

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Mean Luminal Diameter

(NCT00856856)
Timeframe: 3 years

Intervention	mm (Mean)
Absorb BVS	2.74

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Mean Luminal Diameter

It is measured during QCA by the Angiographic Core Lab. (NCT00856856)
Timeframe: 5 years

Intervention	mm (Mean)
Absorb BVS	2.77

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Mean Reference Area

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	6.34

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Mean Reference Area

(NCT00856856)
Timeframe: 2 years

Intervention	mm^2 (Mean)
Absorb BVS	6.29

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Mean Reference Area

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	6.24

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Mean Reference Area

(NCT00856856)
Timeframe: 5 years

Intervention	mm^2 (Mean)
Absorb BVS	6.13

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Mean Scaffold Area

(NCT00856856)
Timeframe: 2 years

Intervention	mm^2 (Mean)
Absorb BVS	8.14

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Mean Scaffold Area

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	8.50

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Mean Scaffold Diameter

(NCT00856856)
Timeframe: 2 years

Intervention	mm (Mean)
Absorb BVS	3.19

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Mean Scaffold Diameter

(NCT00856856)
Timeframe: 3 years

Intervention	mm (Mean)
Absorb BVS	3.26

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Mean Stent Area

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	7.42

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Mean Stent Diameter

(NCT00856856)
Timeframe: 1 year

Intervention	mm (Mean)
Absorb BVS	3.06

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Mean Strut Core Area

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	0.17

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Mean Strut Core Area

(NCT00856856)
Timeframe: 2 years

Intervention	mm^2 (Mean)
Absorb BVS	0.15

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Mean Strut Core Area

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	0.19

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Minimum Flow Area

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	4.28

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Minimum Flow Area

(NCT00856856)
Timeframe: 2 years

Intervention	mm^2 (Mean)
Absorb BVS	4.29

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Minimum Flow Area

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	4.45

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Minimum Flow Area

(NCT00856856)
Timeframe: 5 years

Intervention	mm^2 (Mean)
Absorb BVS	4.15

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Minimum Luminal Area

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	4.29

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Minimum Luminal Area

(NCT00856856)
Timeframe: 2 years

Intervention	mm^2 (Mean)
Absorb BVS	4.29

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Minimum Luminal Area

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	4.45

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Minimum Luminal Area

(NCT00856856)
Timeframe: 5 years

Intervention	mm^2 (Mean)
Absorb BVS	4.15

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Minimum Luminal Diameter

The average of two orthogonal views (when possible) of the narrowest point within the area of assessment - in lesion, in scaffold or in segment. MLD is visually estimated during angiography by the Investigator; it is measured during QCA by the Angiographic Core Lab. (NCT00856856)
Timeframe: 2 years

Intervention	mm (Mean)
Absorb BVS	2.30

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Minimum Luminal Diameter

Intervention	mm (Mean)
Absorb BVS	2.34

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Minimum Luminal Diameter

Intervention	mm (Mean)
Absorb BVS	2.25

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Minimum Luminal Diameter (MLD)

Intervention	mm (Mean)
Absorb BVS	2.30

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Minimum Scaffold Area

(NCT00856856)
Timeframe: 2 year

Intervention	mm^2 (Mean)
Absorb BVS	6.33

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Minimum Scaffold Area

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	6.66

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Minimum Scaffold Diameter

(NCT00856856)
Timeframe: 2 years

Intervention	mm (Mean)
Absorb BVS	2.82

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Minimum Scaffold Diameter

(NCT00856856)
Timeframe: 3 years

Intervention	mm (Mean)
Absorb BVS	2.89

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Minimum Stent Area

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	5.96

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Minimum Stent Diameter

(NCT00856856)
Timeframe: 1 year

Intervention	mm (Mean)
Absorb BVS	2.74

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Myocardial Infarction

"Myocardial Infarction (MI):~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT00856856)
Timeframe: 1 year

Intervention	percentage of participants (Number)
ABSORB Stent	3.0

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Myocardial Infarction

Intervention	percentage of participants (Number)
ABSORB Stent	3.0

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Myocardial Infarction

Intervention	percentage of participants (Number)
ABSORB Stent	3.0

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Myocardial Infarction

Intervention	percentage of participants (Number)
ABSORB Stent	3.0

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Myocardial Infarction

Intervention	percentage of participants (Number)
ABSORB Stent	3.0

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Myocardial Infarction

"Myocardial Infarction (MI):~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of Creatine kinase (CK) levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT00856856)
Timeframe: 30 days

Intervention	percentage of participants (Number)
ABSORB Stent	2.0

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Number of Struts in Side Branch

(NCT00856856)
Timeframe: 1 year

Intervention	Number of struts (Mean)
Absorb BVS	0.1

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Number of Struts in Side Branch

(NCT00856856)
Timeframe: 2 years

Intervention	Number of struts (Mean)
Absorb BVS	0.2

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Number of Struts in Side Branch

(NCT00856856)
Timeframe: 3 years

Intervention	Number of struts (Mean)
Absorb BVS	0.2

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Number of Struts in Side Branch

(NCT00856856)
Timeframe: 5 years

Intervention	Number of struts (Mean)
Absorb BVS	0.0

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Number of Struts Per BVS

(NCT00856856)
Timeframe: 1 year

Intervention	Number of Struts (Mean)
Absorb BVS	162.1

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Number of Struts Per BVS

(NCT00856856)
Timeframe: 2 years

Intervention	Number of Struts (Mean)
Absorb BVS	160.9

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Number of Struts Per BVS

(NCT00856856)
Timeframe: 3 years

Intervention	Number of Struts (Mean)
Absorb BVS	145.2

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Number of Struts Per BVS

(NCT00856856)
Timeframe: 5 years

Intervention	Number of Struts (Mean)
Absorb BVS	7.1

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Percent (%) Lumen Area Stenosis

(NCT00856856)
Timeframe: 1 year

Intervention	Percentage of Lumen Area Stenosis (Mean)
Absorb BVS	28.70

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Percent (%) Lumen Area Stenosis

(NCT00856856)
Timeframe: 2 years

Intervention	Percentage of Lumen Area Stenosis (Mean)
Absorb BVS	28.75

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Percent (%) Lumen Area Stenosis

(NCT00856856)
Timeframe: 3 years

Intervention	Percentage of Lumen Area Stenosis (Mean)
Absorb BVS	28.01

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Percent (%) Lumen Area Stenosis

(NCT00856856)
Timeframe: 5 years

Intervention	Percentage of Lumen Area Stenosis (Mean)
Absorb BVS	34.32

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Persisting Dissection

Dissection at follow-up that was present post-procedure. (NCT00856856)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Persisting Dissection

Dissection at follow-up that was present post-procedure. (NCT00856856)
Timeframe: 180 days

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Persisting Dissection

Dissection at follow-up that was present post-procedure. (NCT00856856)
Timeframe: 2 years

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Persisting Dissection

Dissection at follow-up that was present post-procedure. (NCT00856856)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Persisting Dissection

Dissection at follow-up that was present post-procedure. (NCT00856856)
Timeframe: 5 years

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Persisting Incomplete Apposition

"Persisting incomplete apposition is defined as incomplete apposition at follow-up that was present post-procedure.~Incomplete Apposition: Failure of the scaffold to completely appose to the vessel wall after placement is defined as one or more scaffold strut separated from the vessel wall with evidence of blood speckles behind the strut in the ultrasound image." (NCT00856856)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Absorb BVS	3.5

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Persisting Incomplete Apposition

Intervention	Percentage of participants (Number)
Absorb BVS	2.3

[back to top]

Persisting Incomplete Apposition

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Persisting Incomplete Apposition

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 1 Year

Proximal Late Loss: proximal MLD post-procedure - proximal MLD at follow-up (proximal defined as within 5 mm of healthy tissue proximal to scaffold placement). (NCT00856856)
Timeframe: 1 year

Intervention	Millimeter (Mean)
Absorb BVS	0.12

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Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 180 Days

Proximal Late Loss: proximal MLD post-procedure - proximal MLD at follow-up (proximal defined as within 5 mm of healthy tissue proximal to scaffold placement). (NCT00856856)
Timeframe: 180 days

Intervention	Millimeter (Mean)
Absorb BVS	0.07

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Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 2 Years

Proximal Late Loss: proximal MLD post-procedure - proximal MLD at follow-up (proximal defined as within 5 mm of healthy tissue proximal to scaffold placement). (NCT00856856)
Timeframe: 2 years

Intervention	Millimeter (Mean)
Absorb BVS	0.12

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Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 3 Years

Proximal Late Loss: proximal MLD post-procedure - proximal MLD at follow-up (proximal defined as within 5 mm of healthy tissue proximal to scaffold placement). (NCT00856856)
Timeframe: 3 years

Intervention	Millimeter (Mean)
Absorb BVS	0.14

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Proximal Late Loss: Proximal MLD Post-procedure - Proximal MLD at 5 Years

Proximal Late Loss: proximal MLD post-procedure - proximal MLD at follow-up (proximal defined as within 5 mm of healthy tissue proximal to scaffold placement). (NCT00856856)
Timeframe: 5 years

Intervention	Millimeter (Mean)
Absorb BVS	0.14

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Scaffold Thrombosis

"Scaffold thrombosis will be categorized as acute (≤ 1day), subacute (>1day ≤ 30 days) and late (>30 days) and will be defined as any of the following:~Clinical presentation of acute coronary syndrome with angiographic evidence of scaffold thrombosis (angiographic appearance of thrombus within or adjacent to a previously treated target lesion)~In the absence of angiography, any unexplained death, or acute MI (ST segment elevation or new Q-wave)* in the distribution of the target lesion within 30 days *(Non-specific ST /T changes and cardiac enzyme elevations do not suffice)~Any thromboses that occur less than 30 days after the index procedure will not be counted as restenosis." (NCT00856856)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Absorb BVS	0

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Scaffold Thrombosis

Intervention	percentage of participants (Number)
Absorb BVS	0

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Scaffold Thrombosis

Intervention	percentage of participants (Number)
Absorb BVS	0

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Scaffold Thrombosis

Intervention	percentage of participants (Number)
ABSORB Stent	0

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Scaffold Thrombosis

Intervention	percentage of participants (Number)
Absorb BVS	0

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Scaffold Thrombosis

Intervention	percentage of participants (Number)
Absorb BVS	0

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Scaffold Volume

(NCT00856856)
Timeframe: 2 years

Intervention	mm^3 (Mean)
Absorb BVS	145.78

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Scaffold Volume

(NCT00856856)
Timeframe: 3 years

Intervention	mm^3 (Mean)
Absorb BVS	145.07

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Stent Volume

(NCT00856856)
Timeframe: 1 year

Intervention	mm^3 (Mean)
Absorb BVS	132.90

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Strut Volume

(NCT00856856)
Timeframe: 1 year

Intervention	mm^3 (Mean)
Absorb BVS	3.02

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Strut Volume

(NCT00856856)
Timeframe: 2 years

Intervention	mm^3 (Mean)
Absorb BVS	2.61

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Strut Volume

(NCT00856856)
Timeframe: 3 years

Intervention	mm^3 (Mean)
Absorb BVS	3.28

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Thrombus

(NCT00856856)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Thrombus

(NCT00856856)
Timeframe: 180 days

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Thrombus

(NCT00856856)
Timeframe: 2 years

Intervention	Percentage of participants (Number)
Absorb BVS	2.6

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Thrombus

(NCT00856856)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
Absorb BVS	2.08

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Thrombus

(NCT00856856)
Timeframe: 5 years

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Tissue Coverage Area BVS (Neointimal Area)

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	1.38

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Tissue Coverage Area BVS (Neointimal Area)

(NCT00856856)
Timeframe: 2 years

Intervention	mm^2 (Mean)
Absorb BVS	1.99

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Tissue Coverage Area BVS (Neointimal Area)

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	2.25

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Tissue Coverage Area Classical

(NCT00856856)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Absorb BVS	1.54

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Tissue Coverage Area Classical

(NCT00856856)
Timeframe: 2 years

Intervention	mm^2 (Mean)
Absorb BVS	2.13

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Tissue Coverage Area Classical

(NCT00856856)
Timeframe: 3 years

Intervention	mm^2 (Mean)
Absorb BVS	2.44

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Tissue Coverage Obstruction Volume BVS

(NCT00856856)
Timeframe: 1 year

Intervention	Percent of Tissue Coverage Obstruction (Mean)
Absorb BVS	19.40

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Tissue Coverage Obstruction Volume BVS

(NCT00856856)
Timeframe: 2 years

Intervention	Percent of Tissue Coverage Obstruction (Mean)
Absorb BVS	25.22

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Tissue Coverage Obstruction Volume BVS

(NCT00856856)
Timeframe: 3 years

Intervention	Percent of Tissue Coverage Obstruction (Mean)
Absorb BVS	27.01

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Ischemia Driven Target Lesion Revascularization (ID-TLR)

Intervention	percentage of participants (Number)
Absorb BVS	6.0

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Tissue Coverage Obstruction Volume Classical

(NCT00856856)
Timeframe: 2 years

Intervention	Percent of Tissue Coverage Obstruction (Mean)
Absorb BVS	27.10

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Tissue Coverage Obstruction Volume Classical

(NCT00856856)
Timeframe: 3 years

Intervention	Percent of Tissue Coverage Obstruction (Mean)
Absorb BVS	29.36

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Tissue Coverage Volume BVS

(NCT00856856)
Timeframe: 1 year

Intervention	mm^3 (Mean)
Absorb BVS	24.40

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Tissue Coverage Volume BVS

(NCT00856856)
Timeframe: 2 years

Intervention	mm^3 (Mean)
Absorb BVS	35.51

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Tissue Coverage Volume BVS

(NCT00856856)
Timeframe: 3 years

Intervention	mm^3 (Mean)
Absorb BVS	38.47

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Tissue Coverage Volume Classical

(NCT00856856)
Timeframe: 1 year

Intervention	mm^3 (Mean)
Absorb BVS	27.27

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Tissue Coverage Volume Classical

(NCT00856856)
Timeframe: 2 years

Intervention	mm^3 (Mean)
Absorb BVS	38.12

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Tissue Coverage Volume Classical

(NCT00856856)
Timeframe: 3 years

Intervention	mm^3 (Mean)
Absorb BVS	41.76

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Volume Obstruction (VO)

Defined as scaffold intimal hyperplasia and calculated as 100*(Scaffold Volume - Lumen Volume)/Scaffold Volume by IVUS. (NCT00856856)
Timeframe: 1 year

Intervention	percent of scaffold volume (Mean)
Absorb BVS	1.47

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Volume Obstruction (VO)

Defined as scaffold intimal hyperplasia and calculated as 100*(Scaffold Volume - Lumen Volume)/Scaffold Volume by IVUS. (NCT00856856)
Timeframe: 180 days

Intervention	percent of scaffold volume (Mean)
Absorb BVS	1.22

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Volume Obstruction (VO)

Defined as scaffold intimal hyperplasia and calculated as 100*(Scaffold Volume - Lumen Volume)/Scaffold Volume by IVUS. (NCT00856856)
Timeframe: 2 year

Intervention	percent of scaffold volume (Mean)
Absorb BVS	3.33

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Volume Obstruction (VO)

Defined as scaffold intimal hyperplasia and calculated as 100*(Scaffold Volume - Lumen Volume)/Scaffold Volume by IVUS. (NCT00856856)
Timeframe: 3 year

Intervention	percent of scaffold volume (Mean)
Absorb BVS	4.19

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Vasomotion Analysis: In-scaffold Mean Luminal Diameter

Vasomotion function was assessed in reaction to nitrate administration. (NCT00856856)
Timeframe: 5 years

Intervention	Millimeter (Mean)
	Pre-Nitro	Post-Nitro
Absorb BVS	2.49	2.56

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Cardiac Death

Intervention	percentage of participants (Number)
ABSORB Stent	0

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Clinical Device Success (Per Lesion)

Successful delivery and deployment of the Clinical Investigation scaffold at the intended target lesion and successful withdrawal of the scaffold delivery system with attainment of final residual stenosis of less than 50% of the target lesion by QCA (by visual estimation if QCA unavailable). Standard pre-dilation catheters and post-dilatation catheters (if applicable) may be used. Bailout patients will be included as device success only if the above criteria for clinical device are met. (NCT00856856)
Timeframe: On day 0 (the day of procedure)

Intervention	percentage of lesions (Number)
Absorb BVS	100.0

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Clinical Procedure Success (Per Patient)

Successful delivery and deployment of the Clinical Investigation scaffold at the intended target lesion and successful withdrawal of the scaffold delivery system with attainment of final residual stenosis of less than 50% of the target lesion by QCA (by visual estimation if QCA unavailable) and/or using any adjunctive device without the occurrence of ischemia-driven major adverse cardiac event (MACE) during the hospital stay with a maximum of first seven days post index procedure. (NCT00856856)
Timeframe: On day 0 (the day of procedure)

Intervention	percentage of participants (Number)
ABSORB Stent	98.0

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Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 1 Year

Distal Late Loss: distal MLD post-procedure - distal MLD at follow-up (distal defined as within 5 mm of healthy tissue distal to scaffold placement). (NCT00856856)
Timeframe: 1 year

Intervention	Millimeter (Mean)
Absorb BVS	0.07

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Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 180 Days

Distal Late Loss: distal MLD post-procedure - distal MLD at follow-up (distal defined as within 5 mm of healthy tissue distal to scaffold placement). (NCT00856856)
Timeframe: 180 days

Intervention	Millimeter (Mean)
Absorb BVS	0.07

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Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 2 Years

Distal Late Loss: distal MLD post-procedure - distal MLD at follow-up (distal defined as within 5 mm of healthy tissue distal to scaffold placement). (NCT00856856)
Timeframe: 2 years

Intervention	Millimeter (Mean)
Absorb BVS	0.04

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Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 3 Years

Distal Late Loss: distal MLD post-procedure - distal MLD at follow-up (distal defined as within 5 mm of healthy tissue distal to scaffold placement). (NCT00856856)
Timeframe: 3 years

Intervention	Millimeter (Mean)
Absorb BVS	0.08

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Distal Late Loss: Distal MLD Post-procedure - Distal MLD at 5 Years

Distal Late Loss: distal MLD post-procedure - distal MLD at follow-up (distal defined as within 5 mm of healthy tissue distal to scaffold placement). (NCT00856856)
Timeframe: 5 years

Intervention	Millimeter (Mean)
Absorb BVS	0.11

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Hierarchical Major Adverse Cardiac Event (MACE)

Major adverse cardiac events (MACE) is defined as the composite of cardiac death, all myocardial infarction,and clinically indicated target lesion revascularization (CI-TLR). (NCT00856856)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Absorb BVS	6.9

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Hierarchical Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
Absorb BVS	5.0

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Hierarchical Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
Absorb BVS	9.0

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Hierarchical Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
Absorb BVS	5.0

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Hierarchical Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
Absorb BVS	10.0

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Hierarchical Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
Absorb BVS	2.0

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Hierarchical Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
Absorb BVS	10.1

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Hierarchical Major Adverse Cardiac Event (MACE)

Intervention	percentage of participants (Number)
Absorb BVS	11.0

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Hierarchical Target Vessel Failure (TVF)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT00856856)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Absorb BVS	6.9

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Hierarchical Target Vessel Failure (TVF)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT00856856)
Timeframe: 180 days

Intervention	Percentage of participants (Number)
ABSORB Stent	5.0

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Hierarchical Target Vessel Failure (TVF)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT00856856)
Timeframe: 2 years

Intervention	percentage of participants (Number)
Absorb BVS	11.0

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Hierarchical Target Vessel Failure (TVF)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT00856856)
Timeframe: 270 days

Intervention	Percentage of participants (Number)
Absorb Stent	5.0

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Hierarchical Target Vessel Failure (TVF)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT00856856)
Timeframe: 3 years

Intervention	percentage of participants (Number)
Absorb BVS	13.0

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Hierarchical Target Vessel Failure (TVF)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT00856856)
Timeframe: 30 days

Intervention	percentage of participants (Number)
Absorb BVS	2.0

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Hierarchical Target Vessel Failure (TVF)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT00856856)
Timeframe: 4 years

Intervention	percentage of participants (Number)
Absorb BVS	13.1

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Hierarchical Target Vessel Failure (TVF)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT00856856)
Timeframe: 5 years

Intervention	percentage of participants (Number)
Absorb BVS	14.0

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In-scaffold Angiographic Binary Restenosis (ABR)

Percent of patients with a followup percent diameter stenosis of >=50% per QCA. (NCT00856856)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Absorb BVS	3.5

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In-scaffold Angiographic Binary Restenosis (ABR)

Percent of patients with a followup percent diameter stenosis of >=50% per QCA. (NCT00856856)
Timeframe: 180 days

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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In-scaffold Angiographic Binary Restenosis (ABR)

Percent of patients with a followup percent diameter stenosis of >=50% per QCA. (NCT00856856)
Timeframe: 2 years

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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In-scaffold Angiographic Binary Restenosis (ABR)

Percent of patients with a followup percent diameter stenosis of >=50% per QCA. (NCT00856856)
Timeframe: 3 years

Intervention	Percentage of participants (Number)
Absorb BVS	7.8

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In-scaffold Angiographic Binary Restenosis (ABR)

Percent of patients with a followup percent diameter stenosis of >=50% per QCA. (NCT00856856)
Timeframe: 5 years

Intervention	Percentage of participants (Number)
Absorb BVS	7.8

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In-scaffold Late Loss (LL): In-scaffold MLD Post-procedure - In-scaffold MLD at 2 Years

In-scaffold Late Loss: in-scaffold MLD post-procedure - in-scaffold MLD at follow-up. (NCT00856856)
Timeframe: 2 years

Intervention	Millimeter (Mean)
Absorb BVS	0.27

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In-scaffold Late Loss (LL): In-scaffold MLD Post-procedure - In-scaffold MLD at 3 Years

In-scaffold Late Loss: in-scaffold MLD post-procedure - in-scaffold MLD at follow-up. (NCT00856856)
Timeframe: 3 years

Intervention	Millimeter (Mean)
Absorb BVS	0.29

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In-scaffold Late Loss (LL): In-scaffold MLD Post-procedure - In-scaffold MLD at 5 Years

In-scaffold Late Loss: in-scaffold MLD post-procedure - in-scaffold MLD at follow-up. (NCT00856856)
Timeframe: 5 years

Intervention	Millimeter (Mean)
Absorb BVS	0.26

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In-scaffold Late Loss: In-scaffold MLD Post-procedure - In-scaffold MLD at 1 Year

In-scaffold Late Loss: in-scaffold MLD post-procedure - in-scaffold MLD at follow-up (NCT00856856)
Timeframe: 1 year

Intervention	Millimeter (Mean)
Absorb BVS	0.27

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In-scaffold Late Loss: In-scaffold MLD Post-procedure - In-scaffold MLD at 180 Days

In-scaffold Late Loss: in-scaffold MLD post-procedure - in-scaffold MLD at follow-up. (NCT00856856)
Timeframe: 180 days

Intervention	Millimeter (Mean)
Absorb BVS	0.19

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Tissue Coverage Obstruction Volume Classical

(NCT00856856)
Timeframe: 1 year

Intervention	Percent of Tissue Coverage Obstruction (Mean)
Absorb BVS	21.61

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% of Acutely Covered Struts

(NCT00856856)
Timeframe: 2 years

Intervention	Percent of Covered Struts (Mean)
Absorb BVS	98.07

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% of Acutely Covered Struts

(NCT00856856)
Timeframe: 3 years

Intervention	Percent of Covered Struts (Mean)
Absorb BVS	97.90

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% of Covered Struts (150 µm)

(NCT00856856)
Timeframe: 1 year

Intervention	Percent of Covered Struts (Mean)
Absorb BVS	96.86

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% of Uncovered Struts (150 µm)

(NCT00856856)
Timeframe: 1 year

Intervention	Percent of Uncovered Struts (Mean)
Absorb BVS	3.14

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% of Uncovered Struts (150 µm)

(NCT00856856)
Timeframe: 2 years

Intervention	Percent of Uncovered Struts (Mean)
Absorb BVS	1.93

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% of Uncovered Struts (150 µm)

(NCT00856856)
Timeframe: 3 years

Intervention	Percent of Uncovered Struts (Mean)
Absorb BVS	2.10

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Aneurysm

An abnormal expansion or protrusion of a coronary blood vessel resulting from a disease or weakening of the vessel's wall (all three layers) that exceeds the RVD of the vessel by 1.5 times. (NCT00856856)
Timeframe: 1 year

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Aneurysm

Intervention	Percentage of participants (Number)
Absorb BVS	2.4

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Aneurysm

Intervention	Percentage of participants (Number)
Absorb BVS	2.6

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Aneurysm

Intervention	Percentage of participants (Number)
Absorb BVS	2.08

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Aneurysm

Intervention	Percentage of participants (Number)
Absorb BVS	0.0

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Cardiac Death

Intervention	percentage of participants (Number)
ABSORB Stent	0

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Cardiac Death

Intervention	percentage of participants (Number)
ABSORB Stent	0

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Cardiac Death

Intervention	percentage of participants (Number)
ABSORB Stent	0

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Cardiac Death

Intervention	percentage of participants (Number)
ABSORB Stent	0

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Cardiac Death

Intervention	percentage of participants (Number)
ABSORB Stent	0

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In-scaffold Percent Diameter Stenosis (%DS)

Percent Diameter Stenosis is defined as the value calculated as 100 * (1 - MLD/RVD) using the mean values from two orthogonal views (when possible) by QCA. (NCT00856856)
Timeframe: 1 year

Intervention	percentage of diameter stenosis (Mean)
Absorb BVS	21.35

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In-scaffold Percent Diameter Stenosis (%DS)

Percent Diameter Stenosis is defined as the value calculated as 100 * (1 - MLD/RVD) using the mean values from two orthogonal views (when possible) by QCA. (NCT00856856)
Timeframe: 180 days

Intervention	percentage of diameter stenosis (Mean)
Absorb BVS	19.21

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Change in Visual Acuity From Baseline to Week 4 in Patients Treated With Everolimus

Best corrected visual acuity (BCVA) was assessed on both eyes. BCVA measurements were taken in sitting position using Early Treatment Diabetic Retinopathy Study (ETDRs)-like visual acuity testing charts at an initial testing distance specific to test charts. BCVA is measured from the number of letters the patient can read on the eye chart. (NCT00857259)
Timeframe: Baseline and week 4

Intervention	Letters (Mean)
	Baseline	4 Weeks	Change in baseline
Everolimus 5 mg	46	43	-3
Everolimus 5 mg and Ranibizumab 0.5 mg	55.3	63.2	4.4
Ranibizumab 0.5 mg	67.0	69.0	2.0

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Change in Central Retinal Thickness From Baseline to Week 4, as Measured by Optical Coherence Tomography (OCT)

Central retinal thickness was assessed by Optical coherence tomography (OCT). The primary thickness endpoint was the mean thickness of the foveal field of the macula map produced by the analysis of the sequence of six radial scans. Foveal field thickness was the average thickness of a circular field with a diameter of 1 mm. OCT images were analyzed by a central reading center. (NCT00857259)
Timeframe: Baseline and 4 weeks

Intervention	µm (Mean)
	Baseline	Week 4	Change from Baseline
Everolimus 5 mg and Ranibizumab 0.5 mg	244.3	217.6	-41.0
Oral Everolimus 5 mg	454.8	492.2	37.3
Ranibizumab 0.5 mg	306.0	308.0	2.0

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Occurrence of Treatment Failures From Month 6 to 9 and Month 9 to 18

Treatment failure was defined as composite endpoint of biopsy proven acute rejection of ISHLT 1990 grade ≥ 3A resp. ISHLT 2004 grade ≥ 2R, acute rejection episodes associated with hemodynamic compromise, graft loss / re-transplant, death, loss to follow up (at least one condition must be present). If participant had an occurrence in each period it was counted for each period. (NCT00862979)
Timeframe: Month 6 to Month 9; Month 9 to Month 18

Intervention	Occurences (Number)
	Month 6 to Month 9 Treatment failure - all reasons	Month 9 to Month 18 Treatment failure-all reasons
CNI-free-regimen	4	15
CNI-regimen	1	3

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Calculated Glomerular Filtration Rate (cGFR) According to Cockcroft-Gault at Month 12 and 18

Calculated Glomerular Filtration Rate (cGFR) according to Cockcroft-Gault at Month 12 and 18. For men: GFR=(140-Age) x Body weight (kg) / 72 x Serum Creatinine (mg/dl) For women: GFR=0.85 (140 -Age) x Body weight(kg)/ 72 x Serum Creatinine (mg/dl) (NCT00862979)
Timeframe: Month 12 and 18

Intervention	mL/min (Mean)
	Month 12	Month 18
CNI-free-regimen	69.8	66.9
CNI-regimen	54.2	54.2

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Serum Creatinine at Month 6, 8, 9, 10 12 and 18

Serum Creatinine is an indicator of renal function measured in the blood (NCT00862979)
Timeframe: Month 6, 8, 9, 10 12 and 18

Intervention	μmol/L (Mean)
	Month 6	Month 8	Month 9	Month 10	Month 12	Month 18
CNI-free-regimen	1.49	1.27	1.24	1.20	1.22	1.27
CNI-regimen	1.53	1.44	1.58	1.53	1.53	1.50

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Reciprocal Creatinine Slope Between Month 6 and Month 18

Reciprocal Creatinine Slope is an indication of renal function over time with a higher slope value indicating an improvement in renal function. (NCT00862979)
Timeframe: Between Month 6 and Month 18

Intervention	1/(μmol/L)/(hour) (Mean)
CNI-regimen	0.045
CNI-free-regimen	0.403

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Calculated Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula at Month 18

Calculated Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula at Month 18 cGFR (in mL/min/1.73 m2) = 186.3*(C-1.154)*(A-0.203)*G*R where C = the serum concentration of creatinine (mg/dL), A = age (years), G = 0.742 when gender is female, otherwise G = 1, R = 1.21 when race is black, otherwise R = 1. (NCT00862979)
Timeframe: Month 18

Intervention	mL/min (Mean)
CNI-regimen	54.2
CNI-free-regimen	66.9

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Occurrence of Major Cardiac Events (MACE) From Month 6 to 18

Major cardiac events (MACE) was defined as one of the following: any death, myocardial infarction, coronary artery bypass grafting (NCT00862979)
Timeframe: Month 6 to Month 18

Intervention	Occurences (Number)
	Myocardial infarction	Death
CNI-free-regimen	0	1
CNI-regimen	1	0

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Overall Response Rate (ORR)

Overall response rate (ORR) is the percentage of patients with a best overall response of complete response (CR) or partial response (PR) according to RECIST 1.0. Per RECIST criteria 1.0, CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters. (NCT00863655)
Timeframe: up to 21 months

Intervention	Percentage of participants (Number)
Everolimus + Exemestane	9.5
Placebo + Exemestane	0.4

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Estradiol Plasma Concentrations

Compare estradiol concentrations from baseline to week 4 in both treatment arms. (NCT00863655)
Timeframe: Baseline, Week 4

Intervention	pg/mL (Mean)
	Baseline (n: = 41, 14)	Week 4 (n: 38, 15)
Everolimus + Exemestane	5.62	3.50
Placebo + Exemestane	4.09	5.17

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Clinical Benefit Rate (CBR)

CBR is defined as the percentage of patients with best overall response of either complete response (CR), a partial response (PR) or stable disease (SD) >= 24 weeks, according to RECIST 1.0. Per RECIST criteria 1.0, CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters; SD = Neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for PD; PD = At least a 20% increase in the sum of the longest diameter of all measured target lesions, taking as reference the smallest sum of longest diameter of all target lesions recorded at or after baseline. (NCT00863655)
Timeframe: up to 21 months

Intervention	Percentage of participants (Number)
Everolimus + Exemestane	33.4
Placebo + Exemestane	18.0

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Duration of Response (Among Participants With Best Overall Response of CR or PR) Estimated Per Kaplan-Meier

Duration of response of CR or PR based on investigator applies only to patients whose best overall response was CR or PR (RECIST 1.0). The start date was the date of first documented response (CR or PR) and the end date and censoring is defined the same as that for time to progression. Per RECIST criteria 1.0, CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters. (NCT00863655)
Timeframe: 21 months

Intervention	Months (Median)
Everolimus + Exemestane	8.21
Placebo + Exemestane	NA

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Overall Survival (OS) by Number of Deaths

Overall survival, the key secondary endpoint in this study, is defined as the time from date of randomization to the date of death due to any cause. If a patient is not known to have died, survival was censored at the date of last contact. (NCT00863655)
Timeframe: up to 53 months

Intervention	Participants (Number)
Everolimus + Exemestane	267
Placebo + Exemestane	143

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Progression-free Survival (PFS) Based on Local Radiology Review of Tumor Assessments.

Progression-free survival, the primary endpoint in this study, is defined as the time from the date of randomization to the date of first documented radiological progression or death due to any cause. Disease progression was based on the tumor assessment by the local radiologist or investigator using RECIST 1.0 criteria. If a patient did not progress or known to have died at the date of the analysis cut-off or start of another antineoplastic therapy, the PFS date was censored to the date of last adequate tumor assessment prior to cut-off date or start of antineoplastic therapy. For patients with lytic or mixed (lytic+sclerotic) bone lesions, the following is considered progression: appearance of ≥1 new lytic lesions in bone; the appearance of ≥ new lesions outside of bone and unequivocal progression of existing bone lesions. (NCT00863655)
Timeframe: date of randomization to the date of first documented tumor progression or death from any cause, whichever occurs first, reported between day of first patient randomized up to about 19 months

Intervention	months (Median)
Everolimus + Exemestane	6.93
Placebo + Exemestane	2.83

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Overall Survival (OS) by Median

Overall survival, the key secondary endpoint in this study, is defined as the time from date of randomization to the date of death due to any cause. (NCT00863655)
Timeframe: up to 53 months

Intervention	Months (Median)
Everolimus + Exemestane	30.98
Placebo + Exemestane	26.55

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Proportion of Patients With no Deterioration of Eastern Cooperative Oncology Group Performance Status (ECOG PS) Using Kaplan-Meier

The ECOG PS (Eastern Cooperative Oncology Group Performance Scale) is a standard criteria for measuring how treatment of cancer impacts level of functioning in terms of the ability to care for oneself, daily activity, & physical ability (walking, working, etc.). Scale score ranges:0 to 5, 5 being the worst. Scale index: 0: Fully active, able to carry on all pre-disease performance without restriction. 1: Restricted in physically strenuous activity but ambulatory & able to carry out work of a light or sedentary nature. 2: Ambulatory & capable of all self-care but unable to carry out any work activities. Up & about more than 50% of waking hours. 3: Capable of only limited self-care, confined to bed or chair more than 50% of waking hours. 4 - Completely disabled. Cannot carry on any self-care. Totally confined to bed or chair. 5 - Dead. A deterioration of ECOG is an increase of 1 of the ECOG PS without improvement back to initial level at a subsequent time of measurement. (NCT00863655)
Timeframe: 2, 4, 6, 9 months

Intervention	Proportion of patients (Number)
	2 Months	4 Months	6 Months	9 Months
Everolimus + Exemestane	0.84	0.74	0.64	0.57
Placebo + Exemestane	0.87	0.80	0.67	0.47

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Proportion of Patients With Having no Overall Response Based on Investigator Assessment

overall response = complete response (CR) + partial response (PR) per RECIST 1.0 Time to overall response (CR or PR) based on investigator is the time between date of randomization/start of treatment until first documented response (CR or PR). This analysis included all patients/responders. Patients who did not achieve a confirmed PR or CR were censored at last adequate tumor assessment date when they did not progress. Per RECIST criteria 1.0, CR: Disappearance of all target lesions; PR: At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters. (NCT00863655)
Timeframe: 2, 4, 6, 9 months

Intervention	Proportion of patients (Number)
	2 months	4 months	6 months	9 months
Everolimus + Exemestane	0.96	0.93	0.92	0.90
Placebo + Exemestane	1.00	1.00	1.00	1.00

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Patient-reported Outcomes (PROs): Time to Deterioration of PRO Scores Using Kaplan Meier - EORTC QLQ-C30

"The QLQ-C30 is composed of both multi-item scales and single-item measures. These include 5 functional scales, 3 symptom scales, a global health status - QoL scale, and 6 single items. Each of the multi-item scales includes a different set of items - no item occurs in more than 1 scale. All of the scales measures range in score from 0 to 100. A high scale score = higher response level. Thus a high score for a functional scale represents a healthy level of function, a high score for the global health status / QoL represents a high quality of life but a high score for a symptom scale / item represents a high level of symptomatology / problems. The principle for scoring these scales: 1.) Estimate the average of the items that contribute to the scale = raw score. 2.) Linear transformation to standardize the raw score, so that scores range from 0 to 100; a higher score represents a higher (better) level of functioning, or a higher (worse) level of symptoms." (NCT00863655)
Timeframe: Up to 21 months

Intervention	Months (Median)
	Deterioration global health status score ≥ 5%	Deterioration in PF domain score of ≥ 5%	Deterioration in EF domain score of ≥ 5%	Deterioration in SF domain score of ≥ 5%
Everolimus + Exemestane	4.53	4.83	6.93	8.34
Placebo + Exemestane	4.40	4.37	6.93	7.03

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Exemestane Concentrations at Week 4

Characterize the PK of exemestane in combination with or without everolimus using Cmin and C2h at week 4 in a small group of patients. (NCT00863655)
Timeframe: predose, 2 hours post-dose

Intervention	ng/mL (Mean)
	Pre-dose (Cmin) (n: 34, n: 22)	2 hours post-dose (C2h) (n: 39, n: 22)
Everolimus + Exemestane	0.63	23.16
Placebo + Exemestane	0.43	13.30

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Everolimus Concentrations at Week 4

Characterize the pharmacokinetics (PK) of everolimus in combination with exemestane using Cmin (pre-dose) and C2h (post-dose) at week 4 in a small group of patients. (NCT00863655)
Timeframe: pre-dose, 2 hours post-dose

Intervention	ng/mL (Mean)
	Pre-dose (Cmin) (n:22)	2 hours post-dose (C2h) (n:24)
Everolimus + Exemestane	16.04	46.50

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Progression-free Survival

Progression-free survival is defined as the duration of time from start of treatment to time of documentation of progression or death (NCT00869999)
Timeframe: 2 years

Intervention	months (Median)
Everolimus/Rituximab	2.9

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Duration of Overall Response

Duration of overall response is measured from the time measurement criteria are met for complete response or partial response until the first date that recurrent or progressive disease is objectively documented. (NCT00869999)
Timeframe: 2 years

Intervention	months (Median)
Everolimus/Rituximab	8.1

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Overall Response Rate

Complete response plus partial response after 6 cycles. Response rate will be evaluated by using the modified Cheson criteria for lymphoma response. Complete response requires all of the following: 1) PET positive prior to therapy: mass of any size permitted if PET negative. Variable FDG-avid or PET negative prior to therapy: regression to normal size on CT (/= 1.5 cm before therapy) 2) Spleen (if enlarged before therapy) must have regressed in size and must not be palpable, 3) If bone marrow is known to be involved, repeat biopsy documents clearance. Partial response requires 1) >/= 50% decrease in SPD, 2) No new sites of disease or increase in the size of other nodes, liver or spleen, 3) Splenic and hepatic nodules must regress by at least 50% in SPD (NCT00869999)
Timeframe: Assessed at the conclusion of cycle 2, cycle 4 and cycle 6

Intervention	percentage of participants (Number)
Everolimus/Rituximab	38

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Clinical Benefit Rate (CBR) Equal to or Greater Than 24 Weeks - Full Population

CBR is defined as the percentage of participants whose best overall response is either complete response (CR), a partial response (PR) or stable disease (SD) lasting for at least 24 weeks, according to RECIST. This was assessed in the full patient population. Complete response is achieved when all lesions evaluated at Baseline are absent at subsequent visit. (NCT00876395)
Timeframe: up to about 23 months

Intervention	Percentage of participants (Number)
Everolimus + Paclitaxel + Trastuzumab	75.8
Placebo + Paclitaxel + Trastuzumab	81.2

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Clinical Benefit Rate (CBR) Equal to or Greater Than 24 Weeks - HR-negative Population

CBR is defined as the percentage of participants whose best overall response is either complete response (CR), a partial response (PR) or stable disease (SD) lasting for at least 24 weeks, according to RECIST. This was assessed in a subset of patients with Hormone Receptor Negative disease. Complete response is achieved when all lesions evaluated at Baseline are absent at subsequent visit. (NCT00876395)
Timeframe: up to about 23 months

Intervention	Percentage of participants (Number)
Everolimus + Paclitaxel + Trastuzumab	78.8
Placebo + Paclitaxel + Trastuzumab	79.6

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Overall Response Rate (ORR) - HR-negative Population

ORR is defined as the percentage of participants whose best overall response is either complete response (CR) or partial response (PR) according to RECIST. This was assessed in a subset of patients with Hormone Receptor Negative disease. Complete response is achieved when all lesions evaluated at Baseline are absent at subsequent visit. (NCT00876395)
Timeframe: up to about 23 months

Intervention	Percentage of participants (Number)
Everolimus + Paclitaxel + Trastuzumab	73.1
Placebo + Paclitaxel + Trastuzumab	70.9

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Overall Survival (OS) - Full Population

OS is defined as the time from date of randomization to the date of death due to any cause. For patients with documented progression, survival follow up was performed either by telephone or clinic visit at least every 3 months. Additional survival updates were requested prior to interim or final analysis or prior to providing data to the health authorities. This was assessed in the full patient population. (NCT00876395)
Timeframe: up to about 76 months

Intervention	Months (Median)
Everolimus + Paclitaxel + Trastuzumab	48.56
Placebo + Paclitaxel + Trastuzumab	49.97

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Time to Overall Response Based on Investigator - HR-negative Population

Time to overall response defined as the time between date of randomization until first documented response Complete reseponse (CR) or partial response (PR) ), according to RECIST. This was assessed in the full patient population and in a subset of patients with Hormone Receptor Negative disease. Complete response is achieved when all lesions evaluated at Baseline are absent at subsequent visit. (NCT00876395)
Timeframe: up to about 23 months

Intervention	months (Median)
Everolimus + Paclitaxel + Trastuzumab	1.94
Placebo + Paclitaxel + Trastuzumab	1.97

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Time to Overall Response Based on Investigator - Full Population

Intervention	months (Median)
Everolimus + Paclitaxel + Trastuzumab	2.10
Placebo + Paclitaxel + Trastuzumab	2.00

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Everolimus Blood Level Concentrations at Steady States for Everolimus

Blood levels at steady states for everolimus 10 mg/day and 5 mg/day. Only valid samples are included. Some patients had dose reduction to 5 mg daily dose therefore the everolimus blood concentration for them have been summarized separately. Cycle = 28 days (NCT00876395)
Timeframe: predose, 2 hours post-dose at Cycle 2/Day 1, Cycle 2/Day 15, Cycle 2/ Day 22

Intervention	ng/mL (Mean)
	Pre-dose (Cmin) @ C2D1	2 hrs post administration (C2h) @ C2D1	Pre-dose (Cmin) @ C2D15	2 hrs post administration (C2h) @ C2D15	Pre-dose (Cmin) @ C2D22	2 hrs post administration (C2h) @ C2D22
Everolimus 10 mg/Day	14.380	44.485	13.206	43.494	13.432	43.947
Everolimus 5 mg/Day	7.959	23.449	5.473	20.329	7.494	22.192

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Overall Response (OR) - Full Population

OR applies only to patients whose best OR was CR or PR. Start date = date of first documented response (CR or PR) and end date = date of documented response (CR or PR) and end date = date of event defined as the first documented progression or death due to underlying cause. Complete response is achieved when all lesions evaluated at Baseline are absent at subsequent visit. (NCT00876395)
Timeframe: up to about 23 months

Intervention	Percentage of participants (Number)
	Complete Response (CR)	Partial Response (PR)
Everolimus + Paclitaxel + Trastuzumab	5.6	61.5
Placebo + Paclitaxel + Trastuzumab	5.9	63.2

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Overall Response (OR) - HR-negative Population

OR applies only to patients whose best OR was CR or PR. Start date = date of first documented response (CR or PR) and end date = date of documented response (CR or PR) and end date = date of event defined as the first documented progression or death due to underlying cause. This was assessed in the HR-negative patient population. Complete response is achieved when all lesions evaluated at Baseline are absent at subsequent visit. (NCT00876395)
Timeframe: up to about 23 months

Intervention	Percentage of participants (Number)
	Complete Response (CR)	Partial Response (PR)
Everolimus + Paclitaxel + Trastuzumab	7.7	65.4
Placebo + Paclitaxel + Trastuzumab	2.9	68.0

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Paclitaxel Plasma Concentrations

Blood levels at steady states for everolimus/placebo (NCT00876395)
Timeframe: Cycle 2/Day 15 (Pre-infusion and end of infusion)

Intervention	ng/mL (Mean)
	Pre-infusion (Cmin) @ C2D15	End of infusion (Cmax) @ C2D15
Everolimus	1.424	5159.338
Everolimus Placebo	0	4296.697

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Time to Deterioration of Eastern Cooperative Oncology Group Performance Status (ECOG-PS) Score - HR-negative Population

Time to definitive deterioration of the ECOG PS by one category of the score from baseline will be performed. Baseline is the last available assessment on or before randomization date. A deterioration is considered definitive if no improvements in the ECOG PS status is observed at a subsequent time of measurement during the treatment period following the time point where the deterioration is observed. (NCT00876395)
Timeframe: up to about 56 months

Intervention	months (Median)
Everolimus + Paclitaxel + Trastuzumab	NA
Placebo + Paclitaxel + Trastuzumab	NA

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Time to Deterioration of Eastern Cooperative Oncology Group Performance Status (ECOG-PS) Score - Full Population

Intervention	months (Median)
Everolimus + Paclitaxel + Trastuzumab	39.20
Placebo + Paclitaxel + Trastuzumab	NA

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Progression-free Survival (PFS) Per Investigators' Assessment Based on Local Radiology Review - Full Population

PFS is defined as the time from the date of randomization to the date of first documented tumor progression or death from any cause, whichever occurs first. This was assessed in the full patient population. (NCT00876395)
Timeframe: date of randomization to the date of first documented tumor progression or death from any cause, whichever occurs first, reported between day of first patient randomized up to about 56 months

Intervention	months (Median)
Everolimus + Paclitaxel + Trastuzumab	14.95
Placebo + Paclitaxel + Trastuzumab	14.49

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Trastuzumab Serum Concentrations

Blood levels at steady states for everolimus/placebo (NCT00876395)
Timeframe: Cycle 4/Day 1 (Pre-infusion and end of infusion)

Intervention	microgram/ml (Mean)
	Pre-infusion (Cmin) @ C4D1	End of infusion (Cmax) @ C4D1
Everolimus + Trastuzumab	26.606	64.296
Everolimus Placebo	29.180	67.643

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Overall Response Rate (ORR) - Full Population

ORR is defined as the percentage of participants whose best overall response is either complete response (CR) or partial response (PR) according to RECIST. This was assessed in the full patient population. Complete response is achieved when all lesions evaluated at Baseline are absent at subsequent visit. (NCT00876395)
Timeframe: up to about 23 months

Intervention	Percentage of participants (Number)
Everolimus + Paclitaxel + Trastuzumab	67.1
Placebo + Paclitaxel + Trastuzumab	69.0

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Progression-free Survival (PFS) Per Investigators' Assessment Based on Local Radiology Review - (Hormone Receptor (HR)-Negative Population

PFS is defined as the time from the date of randomization to the date of first documented tumor progression or death from any cause, whichever occurs first. This was assessed in the HR-negative patient population. (NCT00876395)
Timeframe: date of randomization to the date of first documented tumor progression or death from any cause, whichever occurs first, reported between day of first patient randomized up to about 56 months

Intervention	Months (Median)
Everolimus + Paclitaxel + Trastuzumab	20.27
Placebo + Paclitaxel + Trastuzumab	13.08

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Overall Survival (OS) - HR-negative Population

OS is defined as the time from date of randomization to the date of death due to any cause. For patients with documented progression, survival follow up was performed either by telephone or clinic visit at least every 3 months. Additional survival updates were requested prior to interim or final analysis or prior to providing data to the health authorities. This was assessed in the HR-negative patient population. (NCT00876395)
Timeframe: up to about 76 months

Intervention	Months (Median)
Everolimus + Paclitaxel + Trastuzumab	56.97
Placebo + Paclitaxel + Trastuzumab	41.63

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Patient Reported Outcome (PRO): Time to Definitive Deterioration of European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire 30 (EORTC QLQ-C30) Scores

The EORTC QLQ-C30 global health status/quality of life sub-scale (QL) was pre-specified as the primary domain of interest, followed by physical functioning (PF), social functioning (SF) and emotional functioning (EF).The EORTC QLQ-C30 questionnaire, along with a module specific for gastric cancer patients (EORTC QLQ-STO22), was used to evaluate PRO. The QLQ-C30 has five function scales (physical, role, cognitive, emotional and social), three symptom scales (fatigue, pain and nausea/vomiting) and a global health status/quality of life scale. In addition, there are questions that assess specific symptoms. The QLQ-STO22 consists of 22 questions that make up five multi-item scales (dysphagia, pain, reflux, eating and anxiety) and four single-item scales (dry mouth, tasting, body image and hair loss). (NCT00879333)
Timeframe: 2.5 years

Intervention	Months (Median)
	In QL score by at least 5 % compared to baseline	In PF score by at least 5 % compared to baseline	In SF score by at least 5 % compared to baseline	In EF score by at least 5 % compared to baseline
Everolimus 10mg/Daily	1.51	1.35	1.87	1.84
Placebo	1.45	1.15	1.87	1.71

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Overall Response Rate (ORR)

ORR was defined as the proportion of patients with measurable disease in whom best overall response (OR) was either complete response (CR) or partial response (PR) according to RECIST criteria. (NCT00879333)
Timeframe: 2.5 years

Intervention	Participants (Number)
	Measurable Disease	Complete Response (CR)	Partial Response (PR)	Overall Response Rate (ORR)
Everolimus 10mg/Daily	379	1	16	17
Placebo	191	0	4	4

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Progression Free Survival (PFS)

Progression free survival was defined as the time from the date of randomization to the date of the first documented disease progression or death due to any cause, where progression was based on Investigator assessment of baseline and post-baseline scans according to RECIST. Progression free survival was censored if no PFS event was observed before the first to occur out of (i) the cut-off date, or (ii) the date when a further anticancer therapy was started. The censoring date was the date of the last adequate tumor assessment before either of these two events occurred. If a PFS event was observed after two or more missing or non-evaluable tumor assessments, then the date of progression was censored at the date of the last adequate tumor assessment; for a PFS event observed after a single missing or non-evaluable tumor assessment, the actual date of disease progression was used. Anslsis was done using Kaplan-Meier estimates method. (NCT00879333)
Timeframe: 2.5 years

Intervention	Months (Median)
Everolimus 10mg/Daily	1.68
Placebo	1.41

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Overall Survival (OS)

The primary objective of this study was to compare OS between everolimus + best supportive care (BSC) and placebo + BSC. OS, was defined as the time from date of randomization to the date of death due to any cause. If at the analysis cut-off date a patient was not known to have died, survival was censored at the date of the last contact. OS was analyzed using the Kaplan Meier estimates method. (NCT00879333)
Timeframe: 2.5 years

Intervention	Months (Median)
Everolimus 10mg/Daily	5.39
Placebo	4.34

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Time to Definitive Deterioration of Eastern Cooperative Oncology Group Performance Status (ECOG PS) Score

The ECOG PS scale was used to classify patients according to their functional impairment, with scores ranging from 0 (fully active) to 5 (dead). An analysis of the time to definitive deterioration of the ECOG PS by one category of the score from baseline was performed. Definitive deterioration was defined as a definitive increase by one category from baseline in ECOG PS, with no later improvements observed during the course of the study. A single measure reporting an increase in ECOG PS is sufficient to consider it as a definitive worsening only if it was the last one available for the patient. Kaplan-Meier method was used to estimate the distribution function of time to definitive worsening. (NCT00879333)
Timeframe: 2.5 years

Intervention	Months (Median)
Everolimus 10mg/Daily	2.30
Placebo	2.23

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Everolimus Steady State Concentraions at Predose (Cmin) and Cmax at Week 5

Cmin is the minimum (trough) steady-state drug concentration in the blood during multiple dosing and Cmax is the maximum (peak) blood drug concentration after dose administration. Cmax is estimated as the maximum of C1h and C2H. C1h is 1 hour post-dose blood concentration and C2h is 2 hour post-dose blood concentration. Only valid pre-dose (Cmin), C1h, and C2h everolimus samples were included in the analysis. Valid pre-dose samples were confirmed blood samples collected at steady-state, collected immediately prior to dosing on the same study day, and collected at approximately 24 ± 4 hours after the previous dose and with no vomiting within the first 4 hours following the last dose. Valid C1h and C2h samples were confirmed blood samples collected at steady-state and within ± 1 hour window and with no vomiting within the first 4 hours following the current and previous dose. (NCT00879333)
Timeframe: Week 5

Intervention	ng/mL (Mean)
	Pre-dose (Cmin) (n: 201,18)	Cmax (n: 218,16)
Everolimus 10mg/Daily	16.143	72.775
Everolimus 5 mg/Day	10.498	37.269

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Everolimus Steady State Concentraions at Predose (Cmin) and Cmax by Region Asia vs. Rest of the World (ROW) at Week 5

Intervention	ng/mL (Mean)
	Asia: Pre-dose (n:127, 11)	Asia: Cmax (n:132, 10)	Rest of the World: Pre-dose (n:74, 7)	Rest of the World: Cmax (n:86, 6)
Everolimus 10mg/Daily	16.804	73.568	15.009	71.558
Everolimus 5mg/Day	9.921	34.580	11.406	41.750

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Progression-free Survival

The time from randomization until disease progression, death, or date of last contact. Endpoints are progression or death. Patients who are not observed with an endpoint are censored. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) as an 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. (NCT00886691)
Timeframe: Duration of time from start of treatment to time of progression, approximately 4 years and 6 months.

Intervention	months (Median)
Everolimus (RAD001) Plus Bevacizumab	5.9
Placebo Plus Bevacizumab	4.5

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The Proportion of Patients With Measurable Disease Who Have Objective Tumor Responses by Treatment.

Complete and Partial Tumor Response by RECIST 1.0 (NCT00886691)
Timeframe: Up to approximately 4 years and 6 months

Intervention	percentage of participants responding (Number)
Everolimus (RAD001) Plus Bevacizumab	22.2
Placebo Plus Bevacizumab	12.1

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Percentage of Participants With at Least One Cancer Antigen 125 (CA-125) Response

Response as evaluated by CA-125 levels.A CA 125 test measures the amount of the protein CA 125 (cancer antigen 125) in blood.CA 125 is a tumor marker recommended for clinical use in the diagnosis and management of ovarian cancer. CA-125 responses were assessed with Rustin criteria. Initial values had to be 2x ULN (upper limit of normal) within 2 weeks of starting therapy to be considered evaluable.Patient were evaluated by using best overall response while receiving study therapy. (NCT00886691)
Timeframe: Prior to each cycle of treatment. Then follow-up every three months for 2 years , then every 6 months for 3 years. Duration was approximately 4 years and 6 months.

Intervention	percentage of participants (Number)
Everolimus (RAD001) Plus Bevacizumab	27.3
Placebo Plus Bevacizumab	15.4

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Characterize and Compare Progression-free Survival and Overall Survival in Patients With Measurable Disease (RECIST Criteria) and Patients With Detectable (Non-measurable) Disease

Progression-free survival and overall survival broken down by measurable disease status (NCT00886691)
Timeframe: Continued until disease progression, assessed up to approximately 4 years and 6 months

Intervention	Months (Median)
PFS (Progression Free Survival) in Non-measurable Patients	3.94
PFS (Progression Free Survival) in Measurable Patients	5.91
OS (Overall Survival) in Non-measurable Patients	11.10
OS (Overall Survival) in Measurable Patients	16.92

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Incidence of Adverse Events as Assessed by Common Terminology Criteria for Adverse Events Version 4.0 (CTCAE v4.0)

Number of participants with a grade of 3 or higher during the treatment period. (NCT00886691)
Timeframe: All Adverse Events (AEs) and Serious Adverse Events (SAEs) occurring during treatment and up to 30 days after stopping the study treatment, approximately 4 years and 6 months.

Intervention	Participants (Count of Participants)
Everolimus (RAD001) Plus Bevacizumab	43
Placebo Plus Bevacizumab	20

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Time to Definitive Deterioration of the Global Health Status/QoL Scores of the EORTC QLQ-C30 by First-Line Drug

The European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) contains 30 items. These include a global health status/QoL scale, five functional scales, three symptom scales, and six single items.The standardized score for the PF, fatigue subscales and global health status ranges from 0 to 100, with a higher score representing a high level of functioning/high level of symptom/high quality of life. Definitive deterioration by at least 10% was defined as a decrease in score by at least 10% compared to baseline, with no later increase above this threshold observed during the first line of treatment. A single measure reporting a decrease of at least 10% was considered definitive only if it was the last one available for the participant. (NCT00903175)
Timeframe: <=14 days prior to the first dose of study medication, on day 1, day 28 of every cycle, at the end of treatment visit, at the 28 day FUP visit and monthly thereafter for up to 3 months or until initiation of another anticancer therapy up to 35 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	7.92
Sunitinib 1L/Everolimus 2L	12.25

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Overall Response Rate (ORR) - First -Line (1-L)

ORR was defined as the number of participants with best overall response (BOR) of complete response (CR) or partial response (PR) and was based on investigator assessment of radiology data per RECIST. Participants with best overall response of 'Unknown' were treated as non-responders in the calculation of the ORR. Confirmed CR = at least two determinations of CR at least 4 weeks apart before progression. Confirmed PR = at least two determinations of PR or better at least 4 weeks apart before progression. CR required a disappearance of all target and non-target lesions. PR required at least a 30% decrease in the sum of the longest diameters of all target lesions, taking as a reference the baseline sum of the longest diameters. Radiological assessments : every 12 weeks until disease progression, the start of another antineoplastic therapy or for any other reason. (NCT00903175)
Timeframe: based on radiological assessments every 3 months until disease progression, start of another antineoplastic therapy or for any other reason up to 35 months

Intervention	percentage of participants (Number)
	Complete Response (CR)	Partial Response (PR)	Overall Response Rate (CR + PR)
Everolimus 1L/Sunitinib 2L	1	18	19
Sunitinib 1L/Everolimus 2L	3	59	62

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Time to Definitive Deterioration of the Physical Functioning Scale of the EORTC QLQ-C30 - by First and Second-Line Drugs Combined

The European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) contains 30 items. These include a global health status/QoL scale, five functional scales, three symptom scales, and six single items.The standardized score for the PF, fatigue subscales and global health status ranges from 0 to 100, with a higher score representing a high level of functioning/high level of symptom/high quality of life. Definitive deterioration by at least 10% was defined as a decrease in score by at least 10% compared to baseline, with no later increase above this threshold observed during the first line or second line treatment. A single measure reporting a decrease of at least 10% was considered definitive only if it was the last one available for the participant. (NCT00903175)
Timeframe: <=14 days prior to the first dose of study medication, on day 1, day 28 of every cycle, at the end of treatment visit, at the 28 day FUP visit and monthly thereafter for up to 3 months or until initiation of another anticancer therapy up to 35 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	12.25
Sunitinib 1L/Everolimus 2L	14.03

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Time to Definitive Deterioration of the Global Health Status/QoL Scores of the EORTC QLQ-C30 by First and Second-Line Drugs Combined

The European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) contains 30 items. These include a global health status/QoL scale, five functional scales, three symptom scales, and six single items. The standardized score for the PF, fatigue subscales and global health status ranges from 0 to 100, with a higher score representing a high level of functioning/high level of symptom/high quality of life. Definitive deterioration by at least 10% was defined as a decrease in score by at least 10% compared to baseline, with no later increase above this threshold observed during the first line or second line treatment. A single measure reporting a decrease of at least 10% was considered definitive only if it was the last one available for the participant. (NCT00903175)
Timeframe: <=14 days prior to the first dose of study medication, on day 1, day 28 of every cycle, at the end of treatment visit, at the 28 day FUP visit and monthly thereafter for up to 3 months or until initiation of another anticancer therapy up to 35 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	10.84
Sunitinib 1L/Everolimus 2L	12.71

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Time to Definitive Deterioration of the FKSI-DRS Risk Score by at Least 3 Score Units by First-line Drug

The Functional Assessment of Cancer Therapy - Kidney Symptom Index, Disease Related Symptoms (FKSI-DRS) is a set of items to assess symptoms experienced by patients with advanced kidney cancer. These symptoms include fatigue, pain, weight loss, dyspnea, cough, fever and hematuria. Each item is scored on a 5-point scale (0 = not at all; 4 = very much). The FKSI-DRS total score ranges from 0 (most severe symptoms) to 36 (no symptoms). Definitive deterioration was defined as a decrease by at least 3 units compared to baseline, with no later increase above this threshold observed during the 1-L of treatment. A single measure reporting a decrease of at least 3 units was considered definitive only if it was the last one available for the patient. (NCT00903175)
Timeframe: <=14 days prior to the first dose of study medication, on day 1, day 28 of every cycle, at the end of treatment visit, at the 28 day FUP visit and monthly thereafter for up to 3 months or until initiation of another anticancer therapy up to 35 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	12.65
Sunitinib 1L/Everolimus 2L	16.66

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Time to Definitive Deterioration of the FKSI-DRS Risk Score by at Least 3 Score Units by First and Second-line Drugs Combined

The Functional Assessment of Cancer Therapy - Kidney Symptom Index, Disease Related Symptoms (FKSI-DRS) is a set of items to assess symptoms experienced by patients with advanced kidney cancer. These symptoms include fatigue, pain, weight loss, dyspnea, cough, fever and hematuria. Each item is scored on a 5-point scale (0 = not at all; 4 = very much). The FKSI-DRS total score ranges from 0 (most severe symptoms) to 36 (no symptoms). Definitive deterioration was defined as a decrease by at least 3 units compared to baseline, with no later increase above this threshold observed during the 1-L or 2-L treatment. A single measure reporting a decrease of at least 3 units was considered definitive only if it was the last one available for the patient. (NCT00903175)
Timeframe: <=14 days prior to the first dose of study medication, on day 1, day 28 of every cycle, at the end of treatment visit, at the 28 day FUP visit and monthly thereafter for up to 3 months or until initiation of another anticancer therapy up to 35 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	14.23
Sunitinib 1L/Everolimus 2L	15.97

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Time to Definitive Deterioration of the Fatigue Scale of the EORTC QLQ-C30 by First-Line Drug

The European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) contains 30 items. These include a global health status/QoL scale, five functional scales, three symptom scales, and six single items.The standardized score for the PF, fatigue subscales and global health status ranges from 0 to 100, with a higher score representing a high level of functioning/high level of symptom/high quality of life. Definitive deterioration by at least 10% was defined as a decrease in score by at least 10% compared to baseline, with no later increase above this threshold observed during the first line of treatment. A single measure reporting a decrease of at least 10% was considered definitive only if it was the last one available for the participant. (NCT00903175)
Timeframe: <=14 days prior to the first dose of study medication, on day 1, day 28 of every cycle, at the end of treatment visit, at the 28 day FUP visit and monthly thereafter for up to 3 months or until initiation of another anticancer therapy up to 35 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	9.20
Sunitinib 1L/Everolimus 2L	11.37

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Time to Definitive Deterioration of the Fatigue Scale of the EORTC QLQ-C30 by First and Second-Line Drugs Combined

The European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) contains 30 items. These include a global health status/QoL scale, five functional scales, three symptom scales, and six single items. The standardized score for the PF, fatigue subscales and global health status ranges from 0 to 100, with a higher score representing a high level of functioning/high level of symptom/high quality of life. Definitive deterioration by at least 10% was defined as a decrease in score by at least 10% compared to baseline, with no later increase above this threshold observed during the first line or second line treatment. A single measure reporting a decrease of at least 10% was considered definitive only if it was the last one available for the participant. (NCT00903175)
Timeframe: <=14 days prior to the first dose of study medication, on day 1, day 28 of every cycle, at the end of treatment visit, at the 28 day FUP visit and monthly thereafter for up to 3 months or until initiation of another anticancer therapy up to 35 months

Intervention	Months (Mean)
Everolimus 1L/Sunitinib 2L	11.56
Sunitinib 1L/Everolimus 2L	13.34

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Progression-free Survival Combined (PFS-C)

PFS-C (1L and 2L study drugs combined) was a composite endpoint which combined both lines of study treatment. It was defined as the time from the date of randomization to the first of the following: date of death due to any cause, or date of the first radiologically documented progression disease during or after the second-line treatment period for patients with a radiologically documented progression disease in the first-line treatment period and who had crossed-over to second-line treatment no more than 6 weeks after progression. (NCT00903175)
Timeframe: based on radiological assessments every 3 months until disease progression, start of another antineoplastic therapy or for any other reason up to about 56 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	21.68
Sunitinib 1L/Everolimus 2L	22.18

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Progression Free Survival First-Line (PFS 1-L)

PFS_1L based on investigator assessment of radiology data by RECIST 1.0, was defined as the time from the date of randomization to the date of the first documented disease progression or death due to any cause during or after first-line treatment with everolimus or sunitinib. 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. (NCT00903175)
Timeframe: based on radiological assessments every 3 months until disease progression, start of another antineoplastic therapy or for any other reason up to 35 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	7.85
Sunitinib 1L/Everolimus 2L	10.71

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Overall Survival (OS)

Overall survival was defined as the time from date of randomization to date of death due to any cause. The analysis of OS included all deaths in the FAS regardless of when they were observed. (NCT00903175)
Timeframe: Every 2 months from randomization up to 3 years after last patient randomized

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	22.41
Sunitinib 1L/Everolimus 2L	29.47

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Duration of Response (DoR) - First-Line (1-L)

Duration of overall response (CR or PR) applies only to patients whose Best Overall Response (BOR) was Complete Response (CR) or Partial Response (PR) during the first-line treatment period. The start date was the date of first documented response (CR or PR) during the first-line treatment and the end date was the date of the event defined as the first documented progression or death due to underlying cancer during or after the same treatment line. (NCT00903175)
Timeframe: based on radiological assessments every 3 months until disease progression, start of another antineoplastic therapy or for any other reason up to 35 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	13.37
Sunitinib 1L/Everolimus 2L	17.25

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Time to Definitive Deterioration of the Physical Functioning (PF) Scale of the EORTC QLQ-C30 - by First-Line (1L) Drug

The European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) contains 30 items. These include a global health status/QoL scale, five functional scales, three symptom scales, and six single items. The standardized score for the PF, fatigue subscales and global health status ranges from 0 to 100, with a higher score representing a high level of functioning/high level of symptom/high quality of life. Definitive deterioration by at least 10% was defined as a decrease in score by at least 10% compared to baseline, with no later increase above this threshold observed during the first line of treatment. A single measure reporting a decrease of at least 10% was considered definitive only if it was the last one available for the participant. (NCT00903175)
Timeframe: <=14 days prior to the first dose of study medication, on day 1, day 28 of every cycle, at the end of treatment visit, at the 28 day FUP visit and monthly thereafter for up to 3 months or until initiation of another anticancer therapy up to 35 months

Intervention	Months (Median)
Everolimus 1L/Sunitinib 2L	13.47
Sunitinib 1L/Everolimus 2L	14.03

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Progression-free Survival (PFS) Until First Progression

Median PFS will be calculated based on time to first progression or death. (NCT00912340)
Timeframe: Every 3 to 4 weeks after study start, until progression or death, assessed up to 5 years

Intervention	months (Median)
Trastuzumab	2.0
Everolimus	5.7

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Progression-free Survival (PFS) in Patients Who Crossed Over

Median PFS will be calculated based on time to first progression or death. (NCT00912340)
Timeframe: Every 3 to 4 weeks after study start, until progression or death, assessed up to 5 years

Intervention	months (Median)
Trastuzumab	6.3
Everolimus	3.1

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Number of Patients With Treatment-related Adverse Events (AEs) as a Measure of Safety and Tolerability

Assessments will be made based on the analysis of reported incidence of treatment-emergent AEs (NCT00915603)
Timeframe: every 4 weeks until intolerable toxicity occurs

Intervention	participants (Number)
	Neutropenia	Febrile neutropenia	Anemia	Thrombocytopenia	Fatigue	Mucositis/stomatitis	Neuropathy	Diarrhea	Rash	Nausea/vomiting	Epistaxis	Arthralgia/myalgia	Alopecia	Anorexia/weight loss	Proteinuria	Dysgeusia	Headache	Hypertension	Dyspnea	Hypercholesterolemia
Paclitaxel/Bevacizumab/Everolimus	27	2	23	12	38	35	32	30	25	26	20	19	19	18	17	11	11	10	10	9
Paclitaxel/Bevacizumab/Placebo	26	2	8	8	29	18	31	17	13	19	15	10	27	13	10	8	7	10	9	3

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Duration of Response (DOR)

Defined as time between date of objective response and date of response to disease progression or death, as defined by RECIST v1.1 criteria. Objective response is defined as either complete response [CR] or partial response [PR]. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00915603)
Timeframe: every 8 weeks until treatment discontinuation, expected average 6 months

Intervention	months (Median)
Paclitaxel/Bevacizumab/Everolimus	7.8
Paclitaxel/Bevacizumab/Placebo	6.0

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Overall Response Rate (ORR)

The number of patients with observed complete response [CR] or partial response [PR]. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00915603)
Timeframe: every 8 weeks until treatment discontinuation, expected average of 18 months

Intervention	participants (Number)
Paclitaxel/Bevacizumab/Everolimus	35
Paclitaxel/Bevacizumab/Placebo	32

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Overall Survival (OS)

Assessed from Day 1 of study drug administration to date of death due to any cause. (NCT00915603)
Timeframe: every 8 weeks until treatment discontinuation, expected average 6 months

Intervention	months (Median)
Paclitaxel/Bevacizumab/Everolimus	17.5
Paclitaxel/Bevacizumab/Placebo	19.6

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Progression-Free Survival (PFS)

Progression-free survival will be measured from Day 1 of study drug administration to disease progression defined by Response Evaluation Criteria in Solid Tumors Criteria (RECIST v1.1) as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00915603)
Timeframe: every 8 weeks until progressive disease, expected average of 18 months

Intervention	months (Median)
Paclitaxel/Bevacizumab/Everolimus	9.1
Paclitaxel/Bevacizumab/Placebo	7.1

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Number of Phase I Participants With Dose-Limiting Toxicity Events (Phase I)

The Maximum Tolerated Dose (MTD) is defined as the dose level below the lowest dose that induces dose-limiting toxicity (DLT) in at least one-third of patients graded according to NCI Common Terminology Criteria for Adverse Events (CTCAE) version 3.0. Dose-limiting toxicities include non-hematologic events graded 3 or higher and deemed at least possibly related to treatment. A total of 6 patients treated at the MTD will be sufficient to identify common toxicities at the MTD. The number of patients reporting a dose-limiting event are reported. (NCT00918333)
Timeframe: 4 weeks

Intervention	Participants (Count of Participants)
Phase I (Panobinostat + Everolimus)	0

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Overall Response Rate (Phase II)

For myeloma, a complete response(CR, defined as Negative immunofixation(IFE) of the serum and urine, < 5% plasma cells in bone marrow(BM), Disappearance of plasmacytomas), stringent CR(sCR, defined as CR plus Normal serum FLC ratio, Absence of clonal cells in BM), very good partial response(VGPR, defined as PR plus Serum and urine M-component detectable by IFE but not on electrophoresis), partial response(PR, defined as a ≥ 50% reduction of serum M-protein and/or reduction in 24-h urinary M-protein by ≥ 90% or to <200 mg per 24 h), or minor response(MR, defined as ≥25% but < 49% reduction of serum M-protein and reduction in 24h urine M-protein by 50-89%) noted as the objective status. For lymphoma, a CR(defined as no evidence of measurable disease), or PR(defined as regression of measurable disease and no new sites of disease) noted as the objective status. Percentage of successes will be estimated by 100 times the number of successes divided by the total number of evaluable patients. (NCT00918333)
Timeframe: Up to 12 courses

Intervention	percentage of patients (Number)
Phase II (Lymphoma Patients Receiving 20 mg LBL589)	39
Phase II (Myeloma Patients Receiving 20 mg LBH589)	7
Phase II (Lymphoma Patients Receiving 30/40 mg LBH589)	20
Phase II (Myeloma Patients Receiving 30/40 mg LBH589)	0

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Duration of Response (Phase II)

Duration of response is defined as the time from the date at which the objective status is first noted to be (for myeloma) a complete response (CR, defined as Negative immunofixation(IFE) of the serum and urine, < 5% plasma cells in bone marrow(BM), Disappearance of plasmacytomas), stringent CR(sCR, defined as CR plus Normal serum FLC ratio, Absence of clonal cells in BM), very good partial response(VGPR, defined as PR plus Serum and urine M-component detectable by IFE but not on electrophoresis), partial response(PR, defined as a ≥ 50% reduction of serum M-protein and/or reduction in 24-h urinary M-protein by ≥ 90% or to <200 mg per 24 h) or minor response(MR, defined as ≥25% but < 49% reduction of serum M-protein and reduction in 24h urine M-protein by 50-89%); (for lymphoma) a CR(defined as no evidence of measurable disease), or PR(defined as regression of measurable disease and no new sites of disease) noted as the objective status. Estimated using the method of Kaplan-Meier. (NCT00918333)
Timeframe: The time from the date at which the patient's objective status is first noted to be a CR, sCR, VGPR, PR, or minor response to the earliest date progression is documented, assessed up to 2 years post-treatment

Intervention	months (Median)
Phase II (Lymphoma Patients Receiving 20 mg LBL589)	9.1
Phase II (Myeloma Patients Receiving 20 mg LBH589)	NA
Phase II (Lymphoma Patients Receiving 30/40 mg LBH589)	12.9

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Progression-free Survival (Phase II)

Progression-free survival time is defined as the time from registration to progression or death due to any cause. Progression is defined for myeloma as Any one or more of the following: Increase of 25% from lowest value in, Serum M-component (absolute increase must be ≥ 0.5 g/dl), Serum M-component increase ≥ 1 g/dl, if lowest M component was ≥ 5 g/dl,Urine M-component (absolute increase must be ≥ 200 mg/24 h), Bone marrow plasma cell percentage (absolute % must be ≥10%) Or any one or more of the following felt related to the underlying clonal plasma cell proliferative disorder: Development of new soft tissue plasmacytomas or bone lesions, Hypercalcemia (≥11.5 mg/dl) Decrease in hemoglobin of ≥2 g/dl, Serum creatinine level ≥2 mg/dl. Progression is defined for lymphoma as any new lesion or increase by ≥50% of previously involved sites from nadir. The median and 95% confidence intervals are estimated using the method of Kaplan-Meier. (NCT00918333)
Timeframe: Time from registration to progression or death due to any cause, assessed up to 2 years post-treatment

Intervention	months (Median)
Phase II (Lymphoma Patients Receiving 20 mg LBL589)	3.7
Phase II (Myeloma Patients Receiving 20 mg LBH589)	2.3
Phase II (Lymphoma Patients Receiving 30/40 mg LBH589)	4.2
Phase II (Myeloma Patients Receiving 30/40 mg LBH589)	4.3

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Overall Survival Time (Phase II)

Overall survival time is defined as the time from registration to death due to any cause. The median and 95% confidence intervals will be estimated using the method of Kaplan-Meier. (NCT00918333)
Timeframe: Time from registration to death due to any cause, assessed up to 2 years post-treatment

Intervention	months (Median)
Phase II (Lymphoma Patients Receiving 20 mg LBL589)	17.1
Phase II (Myeloma Patients Receiving 20 mg LBH589)	16.6
Phase II (Lymphoma Patients Receiving 30/40 mg LBH589)	35.4
Phase II (Myeloma Patients Receiving 30/40 mg LBH589)	21.7

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Number of Patients With Pathological Complete Response

Pathological complete response is defined as no residual tumor on histopathological analysis of both breast and axillary contents. (NCT00930930)
Timeframe: at time of surgery, week 15-18

Intervention	participants (Number)
Cisplatin and Paclitaxel + RAD001	34
Cisplatin and Paclitaxel + Placebo	17

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Clinical Tumor Response to Neoadjuvant Therapy as Measured by Ultrasound Immediately Before Surgery

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 (NCT00930930)
Timeframe: After treatment, week 12-15

Intervention	participants (Number)
	Complete Response	Partial Response	Stable Disease	Progressive Disease	Not Evaluable
Cisplatin and Paclitaxel + Placebo	23	19	5	0	1
Cisplatin and Paclitaxel + RAD001	48	27	18	2	1

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Number of Patients With Each Worst-grade Toxicity Response

Tables represent the number of patients with their worst-grade toxicity at each of five grades (grade 1, least severe to grade 5, most severe) following NCI Common Toxicity Criteria. Not all participants necessarily have an adverse event, thus not everyone will be accounted for in worst-grade toxicities. Likewise, one participant can potentially have more than one event in various grades 1-5 which accounts for the difference in number of patients analyzed and total number in the worst-grade toxicity tables. (NCT00930930)
Timeframe: week 12

Intervention	participants (Number)
	Number of patients with worst-grade toxicity 1	Number of patients with worst-grade toxicity 2	Number of patients with worst-grade toxicity 3	Number of patients with worst-grade toxicity 4	Number of patients with worst-grade toxicity 5
Cisplatin and Paclitaxel + Placebo	5	28	9	1	0
Cisplatin and Paclitaxel + RAD001	9	40	39	3	0

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Number of Patients That Underwent Breast Conservation Surgery

Defined as patients that did not undergo complete removal of a cancerous breast (mastectomy). (NCT00930930)
Timeframe: at the time of surgery, week 15-18

Intervention	participants (Number)
Cisplatin and Paclitaxel + RAD001	38
Cisplatin and Paclitaxel + Placebo	19

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To Determine the Maximum Tolerated Dose (MTD) of RAD001 in Combination of Weekly Abraxane and Determine the Phase II Dose of RAD001.

(NCT00934895)
Timeframe: 5 yrs

Intervention	mg (Number)
All Participants	5

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Progression-free Survival

Progression-free survival time is defined as the time from registration to progression or death due to any cause. The distribution of progression-free survival will be estimated using the method of Kaplan-Meier (NCT00935792)
Timeframe: up to 5 years

Intervention	Months (Median)
All Evaluable Patients	4.9

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Clinical Response (Complete or Partial Remission)

CR requires all of the following for a period of at least 2months:Absence of lymphadenopathy.No hepatomegaly or splenomegaly.Absence of constitutional symptoms.• Neutrophils>1500/ul•Platelets>100,000/ul • Hemoglobin >11.0gm/dl• Peripheral blood lymphocytes <4000/uLBonemarrow. normocellular with<30%of nucleated cells being lymphocytes.PR requires two for 2+months.≥50%decrease in peripheral blood lymphocyte count from the pretreatment baseline value.≥ 50%reduction in the sum of the products of the maximal perpendicular diameters of the largest measured node or nodal masses in the right and left cervical, axillary, and inguinal lymph node regions.≥ 50%reduction in size of liver and/or spleen noting the maximal distance below the respective costal margins of palpable hepatosplenomegaly during rest.Neutrophils>1500/ul or50%improvement over baseline. Platelets>100,000/ul or50%increase over baseline. Hemoglobin>11.0 gm/dl or50%increase over baseline without transfusions (NCT00935792)
Timeframe: After 2 courses of treatment

Intervention	participants (Number)
	Complete Response	Partial Response
Phase 1, Dose Level 1	0	3
Phase 1, Dose Level 2	1	1
Phase 2, Dose Level 1	0	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 (NCT00935792)
Timeframe: up to 5 years

Intervention	Months (Median)
All Evaluable Patients	29.5

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Time to Subsequent Therapy

(NCT00935792)
Timeframe: up to 5 years

Intervention	Months (Median)
All Evaluable Patients	13.9

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Duration of Response

Duration of response is defined for all evaluable patients who have achieved a clinical response as the date at which the patient's objective status is first noted to be a Complete Response or Partial Response to the earliest date progression is documented. The distribution of duration of response will be estimated using the method of Kaplan-Meier (NCT00935792)
Timeframe: up to 5 years

Intervention	Months (Median)
All Evaluable Patients	4.6

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Test the Safety and Tolerability of the Combination of Everolimus and Alemtuzumab.

The number and severity of all adverse events will be tabulated and summarized in this patient population. The grade 3+ adverse events will also be described and summarized in a similar fashion. This will provide an indication of the level of tolerance for this treatment combination in this patient group. Below is the number of patients that experienced a grade 3+ Adverse event that was at least possibly related to Treatment. (NCT00935792)
Timeframe: Up to 12 months past final treatment

Intervention	participants (Number)
All Evaluable Patients	16

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Number of Participants With Dose-Limiting Toxicities

"The maximum tolerated dose is the dose level below the lowest dose that induces dose-limiting toxicity in at least one-third of patients. A total of 6 patients treated at the MTD will be sufficient to identify common toxicities at the MTD. Dose-limiting toxicity will be defined as an adverse event attributed (definitely, probably, or possibly) to the study treatment and meeting the following criteria.~Hematologic: ANC ≤ 0.3 x 109/L or platelet count < 10 x 109/L Other nonhematologic: ≥grade 3 as per NCI Common Terminology Criteria for Adverse Events v3.0 except for fatigue, hyperlipidemia, and hyperglycemia." (NCT00935792)
Timeframe: 1 Month

Intervention	participants with DLTs (Number)
Phase 1, Dose Level 1	1
Phase 1, Dose Level 2	2

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Duration of Response

Duration of response was defined for all evaluable participants who have achieved an objective response as the date at which the participant's objective status is first noted to be either CR or PR to the date progression is documented. (NCT00936702)
Timeframe: Up to 3 years

Intervention	months (Median)
Treatment (Carboplatin, Paclitaxel, and Everolimus)	5.8

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Overall Survival

Overall survival was defined as the time from study enrollment to the time of death from any cause or last follow-up. (NCT00936702)
Timeframe: Time from registration to death or last follow-up (up to 3 years)

Intervention	months (Median)
Treatment (Carboplatin, Paclitaxel, and Everolimus)	10.1

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Percentage of Participants With Confirmed Tumor Responses

"Confirmed tumor response was defined to be either a complete response (CR) or partial response (PR) noted as the objective status on 2 consecutive evaluations at least 4 weeks apart.~Response was defined using Response Evaluation Criteria In Solid Tumors (RECIST) criteria:~Complete Response (CR): disappearance of all target lesions;~Partial Response (PR) 30% decrease in sum of longest diameter of target lesions;" (NCT00936702)
Timeframe: First 6 Cycles of treatment (an average of 6 months)

Intervention	percentage of participants (Number)
Treatment (Carboplatin, Paclitaxel, and Everolimus)	36

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Progression-free Survival

The progression-free survival (PFS) was defined as the time from date of registration to the documentation of disease progression or death as a result of any cause, whichever comes first. (NCT00936702)
Timeframe: Time from registration to the disease progression or death (up to 3 years)

Intervention	months (Median)
Treatment (Carboplatin, Paclitaxel, and Everolimus)	4.1

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Time to Treatment Failure

Time to treatment failure was defined to be the time from the date of registration to the date at which the participant is removed from treatment due to progression, adverse events, or refusal. (NCT00936702)
Timeframe: Up to 3 years

Intervention	months (Median)
Treatment (Carboplatin, Paclitaxel, and Everolimus)	3.1

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Median Overall Survival

Overall Survival (OS) is defined as the time from randomization (or registration) to death due to any cause, or censored at date last known alive. (NCT00936858)
Timeframe: Every 2 months for first 24 months, then every 3 months from >24 to 60 months; up to 5 years post study registration.

Intervention	months (Median)
Arm A	32.7

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Median Progression Free Survival

Progression free survival (PFS) is defined as the time from start of treatment to disease progression or death from any cause as estimated by Kaplan Meier methods. Progression is measured using RECIST 1.1 criteria, defined as at least a 20% increase in size in target lesion and/or unequivocal progression of non-target lesions and/or appearance of new lesions. Patients who have not progressed and are alive are censored at the date the patient is known to be progression-free. (NCT00936858)
Timeframe: Every 2 months for first 24 months, then every 3 months from >24 to 60 months; up to 48 months.

Intervention	months (Median)
Arm A	12.5

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Objective Response Rate

"The objective response rate is the proportion of participants achieving complete response (CR) or partial response (PR) on treatment based on Response Evaluation Criteria In Solid Tumors Criteria (RECIST 1.1) criteria.~PR or better is achieved if the following are true:~Target Lesions:~-At least a 30% 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.~Non-target Lesions:~No progression. No appearance new lesions or unequivocal progression of existing non-target lesions. Unequivocal progression should not normally trump target lesion status. It must be representative of overall disease status change, not a single lesion increase.~Bone Lesions:~->50% increase in lesions.~-No new lesions." (NCT00936858)
Timeframe: Every 2 months for first 24 months, then every 3 months from >24 to 60 months; up to 48 months.

Intervention	percentage of participants (Number)
Arm A	6

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Mean Change in Quality of Life [Medullary Thyroid Cancer Population Only]

"The M. D. Anderson Symptom Inventory (MDASI) questionnaire was used to assess quality of life. Questions 1 to 19 were scored. Each of the 19 questions have a response range of 0 - 10, where 0 represents not present and 10 represents as bad as you can imagine. The 19 responses are averaged together to create a mean score, with a lower score indicating a better quality of life. All questionnaire mean scores at each timepoint are averaged together to give a mean score at that timepoint (baseline and week 8) The mean change in quality of life is calculated by subtracting the baseline mean score from the week 8 mean score." (NCT00936858)
Timeframe: Measured at baseline and then again at cycle 8 (8 months).

Intervention	mean change in score on the MDASI scale (Mean)
Arm A	-0.0621

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12-Week Progression-Free Survival (PFS)

Tumor assessments performed by Computed Tomography (CT) scan or Magnetic Resonance Imaging (MRI) after 4 weeks, 12 weeks, then every 8 weeks thereafter. Participants who received at least one dose of RAD001+erlotinib and who die before 12 weeks, counted as having progressive disease. Response Evaluation Criteria in Solid Tumors (RECIST) defined as Complete Response (CR): Disappearance of all target lesions; Partial Response (PR): >30% decrease in sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. Progression-free survival defined as stable disease or better. Progressive Disease (PD): >20% increase in sum of LD of target lesions, taking as reference smallest sum LD recorded since treatment started or 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 smallest sum LD since treatment started. (NCT00942734)
Timeframe: 12 weeks

Intervention	Percentage of Participants (Number)
RAD001 + Erlotinib	48.57

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Part 1: Number of Participants Who Experienced One or More Adverse Events (AEs)

An AE is any unfavorable and unintended sign, symptom, or disease temporally associated with the use of study drug, whether or not considered related to this study drug. AEs may include the onset of new illness and the exacerbation of pre-existing conditions. (NCT00954512)
Timeframe: Up to ~30 days after the final dose of robatumumab (Up to ~14 months)

Intervention	Participants (Number)
Regimen A: FOLFIRI (± Cetuximab) + Robatumumab	2
Regimen B: Carboplatin + Paclitaxel + Robatumumab	3
Regimen D: Trastuzumab + Robatumumab	2
Regimen E: mTor Inhibitor (Everolimus) + Robatumumab	4
Regimen F: Gemcitabine (± Erlotinib) + Robatumumab	4

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Part 2: Number of Participants With Each Type of Response Evaluation Criteria in Solid Tumors (RECIST)-Determined Overall Best Response

Overall best response was determined by RECIST criteria. Types of overall response could be: Complete Response (CR), Partial Response (PR), Stable Disease (SD), Progressive Disease (PD), Not Assessable (NA) or Incomplete Response/Stable Disease (IR/SD). (NCT00954512)
Timeframe: Up to ~30 days after the final dose of robatumumab (Up to ~14 months)

,,,,

Intervention	Participants (Number)
	Complete Response (CR)	Partial Response (PR)	Stable Disease (SD)	Progressive Disease (PD)	Not Assessable (NA)	Incomplete Response/Stable Disease (IR/SD)
Regimen A: FOLFIRI (± Cetuximab) + Robatumumab	0	0	0	2	0	0
Regimen B: Carboplatin + Paclitaxel + Robatumumab	0	0	2	1	0	0
Regimen D: Trastuzumab + Robatumumab	0	0	1	1	0	0
Regimen E: mTor Inhibitor (Everolimus) + Robatumumab	0	0	2	1	0	0
Regimen F: Gemcitabine (± Erlotinib) + Robatumumab	0	0	1	1	0	0

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Number of Participants Who Experienced Adverse Events, Serious Adverse Events and Death

Participants with adverse events (serious plus non-serious), serious adverse events and death were reported. (NCT00956293)
Timeframe: Months 6, 12, 24, 36, 48 and 60

Intervention	Participants (Number)
	Adverse events (serious and non-serious)	Serious adverse events	Deaths
Control Group	21	11	0
Everolimus Group	50	28	0

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Change in Renal Function (Creatinine Slope)

X(slope)=(1/value of creatinine). (NCT00965094)
Timeframe: 3 months, 5 months, 7 months, 9 months

Intervention	mg/dl per month (Mean)
	(ITT) Baseline 2: Month 3 N=15, 15	(ITT) Month 3 (1st week) N=15, 4	(ITT) Month 3 (2nd week) N=15, 4	(ITT) Month 3 (3rd week) N=13, 2	(ITT) Month 3 (4th week) N=12, 0*	(ITT) Month 5 N=14, 15	(ITT) Month 7 N=14, 14	(ITT) Month 9 N=11, 15	(PP) Baseline 2: Month 3 N=11, 15	(PP) Month 3 (first week) N=11, 4	(PP) Month 3 (second week) N=11, 4	(PP) Month 3 (third week) N=10, 2	(PP) Month 3 (fourth week) N=9, 0*	(PP) Month 5 N=11, 15	(PP) Month 7 N=11, 14	(PP) Month 9 N=11, 15
Everolimus	0.7	0.7	0.8	0.7	0.8	0.8	0.7	0.8	0.7	0.7	0.8	0.7	0.8	0.8	0.8	0.8
Reference Therapy	0.7	0.8	0.9	0.9	NA	0.7	0.7	0.8	0.7	0.8	0.9	0.9	NA	0.7	0.7	0.8

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Participants Who Had Occurrence of Biopsy Proven Acute Rejection, Graft Loss or Death.

Biopsy-proven acute rejection was defined as a biopsy gradeed IA, IB, IIA, IIB, or III. The allograft was presumed to be lost if the patient started dialysis and was not able to subsequently be removed from dialysis. If the patient underwent a graft nephrectomy, then the day of nephrectomy was the day of graft loss. (NCT00965094)
Timeframe: 9 months

Intervention	Participants (Number)
	No	Yes
Everolimus	14	1
Reference Therapy	14	1

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Participants Who Had Occurrence of Treatment Failure.

Treatment failure was defined as a composite endpoint of biopsy-proven acute rejection, graft loss, death, loss to follow up, discontinuation due to lack of efficacy or toxicity or conversion to another regimen. (NCT00965094)
Timeframe: 9 months

Intervention	Participants (Number)
	No	Yes
Everolimus	10	5
Reference Therapy	14	1

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Assessment of GFR by the Cockcroft-Gault Method (LOCF)

the GFR was also calculated using the Cockcroft-Gault method (Cockcroft and Gault 1976) and the Modification of Diet in Renal Disease (MDRD) method (Levey et al., 1999, Rodrigo et al., 2003; Pierrat et al., 2003).Cockcroft-Gault formula For men: GFR= (140-Age)X Body Weight[kg]/72X Serum Creatinine[mg/dl] For women: GFR= 0,85x(140-Age) x Body Weight[kg]/72x Serum Creatinine [mg/dl] The Last Observation Carried Forward (LOCF) imputation technique was used for this analysis. (NCT00965094)
Timeframe: 9 months

Intervention	mL/min (Mean)
Everolimus	72.6
Reference Therapy	72.7

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Renal Function Assessed as Glomerula Filtration Rate (GFR) - Nankivell Method - 9 Months After Renal Transplantation (LOCF)

The glomerular filtration rate (GFR) is the best clinical estimate of renal function in health and disease, and correlates well with the clinical severity of renal function disturbances. The GFR, calculated according to the Nankivell formula, was used as the primary outcome measure in this study. This equation has been validated in renal transplant patients against the true GFR measured by a radionuclide method and has been confirmed as a very accurate method to calculate the GFR in this specific population (Gaspari et al., 2004)GFR = 6.7 / Scr + BW / 4 - Surea / 2-100 / (height)² + C Scr = serum creatinine concentration expressed in mmol/L. BW = body weight in kg, Surea = serum urea in mmol/L and Height is expressed in meters.The Last Observation Carried Forward (LOCF) imputation technique was used for this analysis. (NCT00965094)
Timeframe: 9 months

Intervention	mL/min/1.73m^2 (Mean)
Everolimus	15.0
Reference Therapy	16.6

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Maximum Tolerated Dose (MTD) of Everolimus With Panobinostat

MTD of the novel combination of Everolimus + Panobinostat (LBH589) in a phase-I study in participants with relapsed lymphoma (Hodgkin and non-Hodgkin) where MTD is defined as the highest dose at which no more than 1 in 6 of the participants in the cohort experiences one or more dose limiting toxicities (DLTs) in the first 28 day treatment cycle. Thirty patients were enrolled onto four dose levels: Everolimus (mg, orally) 5, 5, 10, 10 daily or Panobinostat (mg, orally) 10, 20, 20, 30 three times per week. The MTD was established without the use of colony stimulating factor in cycle 1. (NCT00967044)
Timeframe: 28 day treatment cycle

Intervention	mg, orally (Number)
	Everolimus (daily)	Panobinostat (three times weekly)
Panobinostat + Everolimus	10	20

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Overall Response Rate (OR) Where OR = CR + CRp + CRi

Number of participants out of total treated who experienced a complete response response according to RECIST criteria either (CR + CRp) CR Without Platelet Recovery. Response (CR + CRp) defined as Complete remission (CR): Disappearance of all clinical and/or radiologic evidence of disease. Neutrophil count > 1.0 x10^9/L, platelet count > 100 x10^9/L, and blasts < 5% in a normocellular or hypercellular marrow. Complete remission without platelet recovery (CRp): Peripheral blood and marrow parameters as for CR, but with platelet count > 20 x 10^9/L and < 100 x 10^9/L in the absence of platelet transfusions. CR with incomplete blood count recovery (CRi): Same as CR but platelets ≤ 100,000/mcl and/or neutrophils ≤ 1,000/mcl. (NCT00968253)
Timeframe: 8 courses of treatment, up to 24 weeks

Intervention	percentage of participants (Number)
Phase I: RAD001 5 mg + Combination Chemo	33
Phase I: RAD001 10 mg + Combination Chemo	33
Phase II: MTD RAD001 + Combination Chemo	33

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Participant Responses by Daily Dose Level Assignment (RAD001 5 mg, 10 mg and MTD 5 mg)

Response defined as Complete remission (CR): Disappearance of all clinical and/or radiologic evidence of disease. Neutrophil count > 1.0 x10^9/L, platelet count > 100 x10^9/L, and blasts < 5% in a normocellular or hypercellular marrow. Complete remission without platelet recovery (CRp): Peripheral blood and marrow parameters as for CR, but with platelet count > 20 x 10^9/L and < 100 x 10^9/L in the absence of platelet transfusions. CR with incomplete blood count recovery (CRi): Same as CR but platelets ≤ 100,000/mcl and/or neutrophils ≤ 1,000/mcl. Partial remission (PR): Peripheral blood count recovery as for CR, with decrease in marrow blasts by > 50% from pretreatment values with no more than 25% leukemia/lymphoma cells in the marrow. Nonresponder, Other: All other responses will be considered failures. (NCT00968253)
Timeframe: Up to 20 cycles of study drugs (21 day cycles) or till disease progression

Intervention	participants (Number)
	Complete Remission	Complete Remission without platelet recovery	CR with incomplete blood count recovery	Partial Remission	Nonresponder
Phase I: RAD001 10 mg + Combination Chemo	2	0	1	1	5
Phase I: RAD001 5 mg + Combination Chemo	1	0	0	1	1
Phase II: MTD RAD001 + Combination Chemo	3	1	0	0	8

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Maximum Tolerated Dose [MTD] Determination by Number of Participants With Dose Limiting Toxicity (DLT)

"The Maximum tolerated dose (MTD) was the highest dose level at which fewer than 2 of 6 patients developed a dose limiting toxicity (DLT) in the first two cycles of therapy. A 3 by 3 design was used for dose escalation in the phase I portion of the study.~A dose-limiting toxic effect (DLT) was defined as a clinically significant adverse event or abnormal laboratory value directly attributable to everolimus and assessed as unrelated to disease progression, intercurrent illness, or concomitant medications, occurring during the first or second cycle of therapy, that met any of the following criteria: CTCAE version 3.0 grade 3 increased AST or ALT for 7 days, CTCAE grade 4 increased AST or ALT of any duration, or any other clinically significant CTCAE grade 3 or 4 toxic effect. Electrolyte abnormalities (changes in glucose, chemistries, liver enzymes, pancreatic enzymes) correctable by optimal therapy and without clinical impact were not considered DLTs." (NCT00968253)
Timeframe: Following first two dose cycles (21 days/each), up to 42 days

Intervention	Participants (Count of Participants)
Phase I: RAD001 5 mg + Combination Chemo	0
Phase I: RAD001 10 mg + Combination Chemo	1

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Progression-free Survival (PFS), in the Treatment of Patients With Refractory Meningioma.

Progression-free survival (PFS) is defined as the time from randomization until objective tumor progression (PD) or death. Progression is defined per MacDonald criteria for response as ≥25% increase in size of enhancing tumor or any new tumor on MRI scan, neurologically worse, and steroids stable or increased. (NCT00972335)
Timeframe: 18 months

Intervention	months (Median)
Combination Therapy	22

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To Evaluate the Toxicity of Bevacizumab/Everolimus in Patients With Recurrent Meningioma.

(NCT00972335)
Timeframe: 18 months

Intervention	participants (Number)
	Thrombocytopenia	Anemia	Leukopenia	Neutropenia	Hypercholesterolemia	Mucositis	Fatigue	Proteinuria	Hypertriglyceridemia	Rash/desquamation	Diarrhea	Hypertension	Edema-limb	Vomiting	Anorexia	Nausea	Hyperglycemia	Pain - oral cavity	Epistaxis	Headache	Arthralgia
Combination Therapy	9	6	2	2	9	9	8	6	6	6	6	5	5	4	4	4	3	3	3	3	3

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Time to Next Therapy With Single Agent RAD001 Therapy in Previously Untreated WM

(NCT00976248)
Timeframe: End of follow-up, an average of 18 months

Intervention	Months (Median)
RAD001	15

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Overall Response Rate of RAD001 in Patients With Previously Untreated WM

"Overall Response = Complete Response + Near Complete Response + Very Good Partial Response + Partial Response + Minor Response Complete Response: resolution of all symptoms, normalization of serum IgM levels with complete disappearance of IgM paraprotein by immunofixation, and resolution of any adenopathy or splenomegaly. A near CR (nCR) is defined as fulfilling all CR criteria in the presence of positive immunofixation test for an IgM paraprotein.~Very Good Partial Response: > 90% reduction in serum IgM levels. Partial Response: > 50% reduction in serum IgM levels. Minor Response: 25-49% reduction in serum IgM levels Progressive Disease: greater than 25% increase in serum IgM level occurs from the lowest attained response value or progression of clinically significant disease related symptom(s).~Stable Disease: < 25% change in serum IgM levels, in the absence of new or increasing adenopathy or splenomegaly and/or other progressive signs or symptoms of WM" (NCT00976248)
Timeframe: End of Treatment, an average of 16 months

Intervention	participants (Number)
RAD001	22

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Time to Progression With Single Agent RAD001 Therapy in Previously Untreated WM.

Progression is defined as a 25% increase in serum IgM from the lowest attained response value or progression of clinically significant disease related symptoms. (NCT00976248)
Timeframe: End of Treatment, an average of 16 months

Intervention	Months (Median)
RAD001	21

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Confirmed Tumor Response Rate (Complete Response [CR] or Partial Response [PR]) According to Response Evaluation Criteria in Solid Tumors (RECIST) Criteria

Confirmed Tumor Response: A confirmed tumor response is defined to be a CR or PR (by the RECIST criteria) 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. A ninety percent confidence interval for the true proportion of confirmed tumor responses will be calculated assuming that the number of confirmed tumor responses follows a binomial distribution. (NCT00976573)
Timeframe: Up to 5 years

Intervention	percentage of patients (Number)
Arm A (Bevacizumab, Paclitaxel, and Carboplatin)	13
Arm B (Bevacizumab, Paclitaxel, Carboplatin, and Everolimus)	23

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Progression-free Survival

The primary endpoint is progression-free survival (PFS) defined as the time from randomization to documentation of disease progression or death without documentation of progression. The distribution of PFS times will be estimated using the Kaplan-Meier method. Progression is defined using the RECIST Criteria as at least a 20% increase in the sum of diameters of target lesions taking as reference the smallest sum of diameters recorded on study (this includes the baseline sum if that is the smallest on study) or the appearance of one or more new lesions. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm of target lesions, or the appearance of one or more new lesions, unequivocal progression of existing non-target lesions, although unequivocal progression should not normally trump target lesion status. It must be representative of overall disease status change, not a single lesion increase. (NCT00976573)
Timeframe: Time from randomization to documentation of disease progression or death without documentation of progression;Up to 5 years

Intervention	months (Median)
Arm A (Bevacizumab, Paclitaxel, and Carboplatin)	5.6
Arm B (Bevacizumab, Paclitaxel, Carboplatin, and Everolimus)	5.1

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Overall Survival Time

Overall survival time is defined as the time from registration to death due to any cause. The distribution of survival times will be estimated using the method of Kaplan-Meier. (NCT00976573)
Timeframe: up to 5 years

Intervention	months (Median)
Arm A (Bevacizumab, Paclitaxel, and Carboplatin)	14.5
Arm B (Bevacizumab, Paclitaxel, Carboplatin, and Everolimus)	10.8

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Toxicity

For this secondary endpoint, toxicity is defined as a grade 3 or higher adverse events that is classified as either possibly, probably, or definitely related to study treatment. The assignment of attribution to study treatment and grade (or degree of severity) of the adverse event are classified using the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. The percentage of participants reporting a grade 3 or higher toxicity is reported. For a list of all reported adverse events, please refer to the Adverse Events Section below. (NCT00976573)
Timeframe: Up to 5 years

Intervention	percentage of participants (Number)
	Neutropenia	Leukopenia	Fatigue
Arm A (Bevacizumab, Paclitaxel, and Carboplatin)	35	17	11
Arm B (Bevacizumab, Paclitaxel, Carboplatin, and Everolimus)	58	24	17

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Overall Response Rate

Overall Response Rate is the number of participants with a partial and complete response assessed by the Updated Cheson criteria for lymphoma. A complete response is complete disappearance of all detectable clinical and radiographic evidence of disease and disappearance of all disease-related symptoms if present before therapy and normalization of those biochemical abnormalities. If a subject has residual lesions on CT scan and the disease was fluorodeoxyglucose (FDG) avid pre-treatment, then that subject will be considered to be in a complete response. Partial response is a greater than or equal to 50% decrease in the sum of the products of the greatest diameters of 6 largest dominant nodes or nodal masses. No increase in size of nodes, liver or spleen and no new sites of disease (NCT00978432)
Timeframe: after 2 cycles of each study drug or after 2 cycles of doublet, up to 24 weeks

Intervention	participants (Number)
Arm 1a (RAD001 Followed by LBH589)	1
Arm 1b (LBH589 Followed by RAD001)	0
Doublet (Combination RAD001 and LBH589)	4

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Summary of Adverse Events (AEs)

Counts of adverse events or treatment-emergent adverse events (TEAE, defined as newly occurring or worsening after first dose) experienced by patients on study drug(s). National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE version 3.0) is used to assess severity. Relatedness to study drug is assessed by the investigator. (NCT00978432)
Timeframe: From the time of first dose of study drug until 4 weeks after participant has stopped study drug; up to 1 year

Intervention	events (Number)
	Blood and lymphatic AEs	Gastrointestinal AEs	General Disorder AEs	Investigation (Lab) AEs	Metabolism and Nutrition AEs	Musculoskeletal and Connective Tissue AEs	Nervous System AEs	Renal and Urinary AEs	Reproductive System AEs	Respiratory, thoracic and mediastinal AEs	Skin and Subcutaneous Tissue AEs	Vascular AEs
Arm 1a (RAD001 Followed by LBH589)	18	30	6	6	5	4	13	0	0	10	8	2
Arm 1b (LBH589 Followed by RAD001)	6	10	5	3	2	1	3	1	1	4	2	1
Doublet (Combination RAD001 and LBH589)	42	39	19	23	45	2	5	4	1	15	3	1

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Biomarker Correlations: Time to Progression

Potential correlations between time to progression and S6 protein and mTOR-related proteins in tumor tissue samples from these patients. (NCT00985192)
Timeframe: 30 months

Intervention	months (Median)
	p-S6 level 0-2	p-S6 level >2	p-mTOR level 0-2	p-mTOR level >2
Everolimus	1.75	3.4	1.8	2.6

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Efficacy in Terms of Progression Free Response

Progression-free survival (PFS), was defined as the time from the date of initial treatment to first objective documentation of disease progression, or death. Estimated using the Kaplan-Meier method. Complete response (CR) + partial response (PR) + stable disease (SD) were determined according to Response Evaluation Criteria In Solid Tumors (RECIST) criteria. Radiologic disease assessments were utilized. (NCT00985192)
Timeframe: evry 3 months in year 1, every 6 months after that

Intervention	months (Median)
Everolimus	1.8

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Overall Disease-control Rate in Patients With Previously Treated Unresectable or Metastatic Adenocarcinoma of the Upper Gastrointestinal Tract Treated With Everolimus.

Disease control rate (DCR), defined as complete response (CR) + partial response (PR) + stable disease (SD) according to Response Evaluation Criteria In Solid Tumors (RECIST) criteria. (NCT00985192)
Timeframe: Radiologic disease assessment was performed every 8 weeks (14 days = 1 cycle) treatment discontinuation.

Intervention	percent subjects with disease control (Number)
Everolimus	40

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Overall Survival

Overall Survival (OS), defined as the time from date of initial treatment to date of death. Survival function was estimated using the Kaplan-Meier method. (NCT00985192)
Timeframe: 2.5 year

Intervention	months (Median)
Everolimus	3.4

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Biomarker Correlations: Progression Free Survival

Potential correlations between progression free survival and S6 protein and mTOR-related proteins in tumor tissue samples from these patients. (NCT00985192)
Timeframe: 30 months

Intervention	months (Median)
	p-S6 level 0-2	p-S6 level >2	p-mTOR level 0-2	p-mTOR level >2
Everolimus	1.8	3.5	1.8	2.6

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Observed Biomarkers

Potential correlations between clinical outcome and biomarkers of interest, including S6 protein overexpression and/or other mTOR-related proteins in tumor tissue samples from these patients. (NCT00985192)
Timeframe: 30 months

Intervention	number of tissue blocks (Number)
	Tumor Grade 0, p-S6	Tumor Grade 1+, p-S6	Tumor Grade 2+, p-S6	Tumor Grade 3+, p-S6	Tumor Grade 4+, p-S6	Tumor Grade 0, p-mTOR	Tumor Grade 1+, p-mTOR	Tumor Grade 2+, p-mTOR	Tumor Grade 3+, p-mTOR	Tumor Grade 4+, p-mTOR
Everolimus	4	15	8	9	3	0	8	22	9	0

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Vinorelbine Blood Concentrations by Leading Dose and Time Point

Pre-infusion (Cmin) and end of infusion (C2h) vinorelbine PK blood samples were collected at Cycle 2 Day 1. Only valid vinorelbine PK blood samples collected at steady state were used in the analyses. (NCT01007942)
Timeframe: Cycle 2, Day 1

Intervention	ng/ml (Mean)
	Pre-infusion - dose (Cmin) (n: 76, 64)	End of infusion (Cmax) (n: 58, 49)
Everolimus	11.085	867.147
Everolimus Placebo	0.061	1068.51

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Trastuzumab Blood Concentrations by Leading Dose and Time Point

Pre-infusion (Cmin) and end of infusion (C2h) trastuzumab PK blood samples were collected at Cycle 3 Day 1. Only valid trastuzumab PK blood samples collected at steady state were used in the analyses. (NCT01007942)
Timeframe: Cycle 3, Day 1

Intervention	ng/ml (Mean)
	Pre-infusion - dose (Cmin) (n: 73, 57)	End of infusion (Cmax) (n: 75, 59)
Everolimus	23.351	64.279
Everolimus Placebo	24.526	60.576

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Progressive-free Survival (PFS) Per Investigator Assessment

PFS was defined as the time from the date of randomization to the date of first radiologically documented tumor progression or death from any cause, whichever occurs first. PFS primary analysis performed when 415 events were reached. 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. (NCT01007942)
Timeframe: Every 6 weeks until disease progression or death which ever occurred first up to about 41 months

Intervention	months (Median)
Everolimus + Vinorelbine + Trastuzumab	7.00
Placebo + Vinorelbine + Trastuzumab	5.78

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Overall Survival (OS)

OS was defined as the time from date of randomization to the date of death from any cause. Final OS was conducted when 388 deaths occurred. (NCT01007942)
Timeframe: Every 3 months until death up to 41 months

Intervention	months (Median)
Everolimus + Vinorelbine + Trastuzumab	23.46
Placebo + Vinorelbine + Trastuzumab	24.08

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Overall Response Rate (ORR)

ORR was defined as the percentage of participants whose best overall response was either complete response (CR) or partial response (PR) according to RECIST version 1.0. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT01007942)
Timeframe: Every 6 weeks until disease progression or death which ever occurred first up to about 41 months

Intervention	Percentage of participants (Number)
Everolimus + Vinorelbine + Trastuzumab	40.8
Placebo + Vinorelbine + Trastuzumab	37.2

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Median Time to Deterioration of the ECOG Performance Status Score

Time to deterioration of ECOG performance status score was summarized at time of assessment. ECOG (Eastern Cooperative Oncology Group)performance scale is a standard criteria for measuring how treatment of cancer impacts their level of functioning in terms of their ability to care for themselves, daily activity, & physical ability (walking, working, etc.). Scale score ranges from 0 to 5, 5 being the worst. ECOG scale index: 0 - Fully active, able to carry on all pre-disease performance without restriction. 1 - Restricted in physically strenuous activity but ambulatory & able to carry out work of a light or sedentary nature, e.g., light housework, office work. 2 - Ambulatory & capable of all self-care but unable to carry out any work activities. Up & about more than 50% of waking hours. 3 - Capable of only limited self-care, confined to bed or chair more than 50% of waking hours. 4 - Completely disabled. Cannot carry on any self-care. Totally confined to bed or chair. 5 - Dead (NCT01007942)
Timeframe: baseline, until disease progression or death up to about 41 months

Intervention	months (Median)
Everolimus + Vinorelbine + Trastuzumab	32.66
Placebo + Vinorelbine + Trastuzumab	21.55

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Clinical Benefit Rate (CBR)

CBR was defined as the percentage of participants whose best overall response, according to RECIST, was either complete response (CR), a partial response (PR) or stable disease (SD) lasting for at least 24 weeks. 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; SD = Neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for PD; PD = At least a 20% increase in the sum of the longest diameter of all measured target lesions, taking as reference the smallest sum of longest diameter of all target lesions recorded at or after baseline. (NCT01007942)
Timeframe: Every 6 weeks until disease progression or death which ever occurred first up to about 41 months

Intervention	Percentage of participants (Number)
Everolimus + Vinorelbine + Trastuzumab	59.2
Placebo + Vinorelbine + Trastuzumab	53.3

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Everolimus Blood Concentrations by Leading Dose and Time Point

Pre-dose (Cmin) and 2 hours post-dose (C2h) everolimus PK blood samples were collected at Cycle 2 Day 1. Only valid everolimus PK blood samples collected at steady state were used in the analyses. (NCT01007942)
Timeframe: Cycle 2, Day 1

Intervention	ng/ml (Mean)
	Pre-dose (Cmin) (n: 7, 32)	2 hours post administration (C2h) (n:10, 43)
Everolimus	5.652	22.005
Everolimus 2.5 mg	2.928	13.035

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PRO: Time to Deterioration in Global Health Status/QoL Domain Score of the European Organization for the Research and Treatment of Cancer (EORTC)-Core Quality of Life Questionnaire (QLQ-C30) (by at Least 10%)

PRO = patient reported outcomes; Time to deterioration (≥ 10% worsening from baseline), in the global health status of EORTC QLQ-C30 scale was done in the 3 functional scales (emotional, physical, & social functioning [EF, PF, & SF]). It contains 30 items & is composed of multi-item scales & single-item measures. These include 5 functional scales (physical, role, emotional, social & cognitive functioning), 3 symptom scales (fatigue, pain, nausea, & vomiting), a global health status/QoL scale, and 6 single items (dyspnea, diarrhea, constipation, anorexia, insomnia & financial impact). Each of the multi-item scale includes a different set of items - no item occurs in more than 1 scale. Each item in the EORTC QLQ-C30 has 4 response categories (1=Not at all, 2= A little, 3= Quite a bit, 4= Very much) with the higher number representing a worse outcome. The global health domain score of the QLQ-C30 questionnaire was pre-specified as the primary QoL domain of interest & disclosed here. (NCT01007942)
Timeframe: Baseline, until disease progression or death up to about 41 months

Intervention	months (Median)
	Deterioration - global QoL domain by at least 10%	Deterioration in the PF domain by at least 10%	Deterioration in the EF domain by at least 10%	Deterioration in the SF domain by at least 10%
Everolimus + Vinorelbine + Trastuzumab	8.31	11.96	15.18	11.33
Placebo + Vinorelbine + Trastuzumab	7.29	12.48	12.45	13.11

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Progression Free Survival (PFS) of RAD001 in Combination With Weekly Cetuximab and Cisplatin.

Median number of months for which participants are free of progression after initiating treatment with RAD001 in combination with weekly cetuximab and cisplatin. (NCT01009346)
Timeframe: 2 years

Intervention	months (Median)
Study Arm (RAD001)	2.8

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Maximum Tolerated Dose (MTD) of RAD001 in Combination With Cetuximab and Cisplatin.

MTD will be defined as a) the dose of RAD001 producing DLT in 0-1 out of 6 patients, or b) the dose level below the dose which produced DLT in <2 out of 6 patients, or c) the dose of 10mg po qd with less than 33% rate of DLT (NCT01009346)
Timeframe: 6 months

Intervention	mg (Number)
Study Arm (RAD001, Cetuximab, Cisplatin or Carboplatin)	10

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Overall Survival (OS)

Overall survival (OS) is defined as the time from randomization until death from any cause. (NCT01014351)
Timeframe: 18 months

Intervention	Months (Median)
Paclitaxel/Carboplatin/Everolimus	10.12

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Objective Response Rate (ORR)

Objective Response Rate (ORR) is defined as the Percentage of Patients Who Experience an Objective Benefit From Treatment. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by MRI or CT: 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. (NCT01014351)
Timeframe: 18 months

Intervention	percentage of patients (Number)
Paclitaxel/Carboplatin/Everolimus	17

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Progression-free Survival (PFS)

Progression-free survival (PFS) is defined as the time from randomization until objective tumor progression (PD) or death. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT01014351)
Timeframe: 18 months

Intervention	Months (Median)
Paclitaxel/Carboplatin/Everolimus	4.04

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Absolute and Percent Frequencies of Patients With LDL ≥ 100 mg/mL at 1, 3 and 6 Months, by Treatment Group

LDL = low density lipoprotein (NCT01017029)
Timeframe: 6 months

Intervention	participants (Number)
	Month 1	Month 3	Month 6
Delayed Introduction of Everolimus	38	37	36
Immediate Introduction of Everolimus	41	37	34

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Participants With at Least One Occurrence of Safety Composite Endpoint After 6 Months by Treatment Group

Comparison of 6-month cumulative incidence of safety composite endpoint (wound healing delay) related to initial transplant surgery, pleural/pericardial effusions and occurrence of acute renal insufficiency, defined as estimated glomerular filtration rate (eGFR) ≤ 30 mL/min/1.73 m2, between delayed everolimus arm and immediate everolimus arm (NCT01017029)
Timeframe: 6 months

Intervention	participants (Number)
Immediate Introduction of Everolimus	40
Delayed Introduction of Everolimus	30

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Participants With at Least One Occurrence of Composite Treatment Failure Events

Comparison of 6-months cumulative incidence of composite treatment failure events (BPAR ≥ 2R, rejection with hemodynamic compromise, graft loss, or death) between delayed everolimus arm and immediate everolimus arm (NCT01017029)
Timeframe: 6 months

Intervention	participants (Number)
Immediate Introduction of Everolimus	33
Delayed Introduction of Everolimus	26

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Hazard Cox's Model Analysis of Pericardial/Pleural Effusions

Pericardial effusions: any pericardial effusion defined as at least moderate (i.e. measuring at least 2.0 cm in diastole, in the point of largest distance between the pericardial leaflets), with or without signs of hemodynamic compromise, or leading to drainage or to prolonged hospitalization. Pleural effusions: need for surgical drainage tubes for longer than 7 days after surgery and subsequent pleural effusions leading to drainage. CI = confidence interval, HR = hazard ratio, MDRD = Modification of Diet in Renal Disease (NCT01017029)
Timeframe: 6 months

Intervention	participants (Number)
Immediate Introduction of Everolimus	30
Delayed Introduction of Everolimus	18

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Partcipants With at Least One Occurrence of Each Safety Composite Endpoint Event After 6 Months by Treatment Group

(NCT01017029)
Timeframe: 6 months

Intervention	participants (Number)
	Wound healing complication	Pleural effusion	Pericardial effusion	eGFR ≤ 30 mL/min/1.73 m2
Delayed Introduction of Everolimus	8	1	18	8
Immediate Introduction of Everolimus	10	1	30	7

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Participants With CMV Infection and CMV Syndrome/Disease After 6 Months by Treatment Group

CMV infection is defined as pp65 antigenemia or DNAemia (NCT01017029)
Timeframe: 6 months

Intervention	participants (Number)
	CMV infections	CMV syndrome/disease
Delayed Introduction of Everolimus	63	6
Immediate Introduction of Everolimus	46	3

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Overall Response Rate (ORR) Based on the Assessments by Investigator

ORR: % of patients whose overall disease response was a complete response (CR) or a partial response (PR) in 8 cycles CR: Complete normalization of all index nodal & extranodal lesions: Radiological regression to normal size of all lymph nodes & nodal masses & complete disappearance of all lesions PR: At least a 50% decrease in the SPD of all index nodal & extranodal lesions FDG-avid or PET positive prior to therapy: one or more PET positive at previously involved site.At least a 50% increase in the SPD of all index nodal & extranodal lesions, taking as reference the smallest sum of the product of the diameters of all index lesions recorded at or after baseline . Lesions PET positive if FDG-avid lymphoma or PET positive prior to therapy. Unknown (UNK): Progression not documented & one or more of the index lesions not assessed or assessed using a different method than baseline at the time of radiologic evaluation. Each cycle was 28 days. (NCT01022996)
Timeframe: at screening and every threee months beginning at cycle 3 until end of treatment due to progression of disease, unacceptable toxicity, death or discontinuation from the study for any other reason

Intervention	percentage of participants (Number)
	Complete response (CR)	Partial response (PR)	Response of CR or PR
RAD001	8.8	36.8	45.6

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Disease Control Rate (DCR)

The disease control rate was defined as the percentage of patients with a best overall response of CR, PR or stable disease (SD). (NCT01022996)
Timeframe: Every three months beginning at Cycle 3 until end of treatment due to progression of disease, unacceptable toxicity, death or discontinuation from the study for any other reason

Intervention	Percentage of participants (Number)
RAD001	80.7

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Duration of Disease Control

The duration of overall response (CR/PR) was applied only to patients whose best overall response was CR or PR. Duration of overall response was calculated from the date of the first documented response of CR or PR to the date of first documented disease progression or death due to any cause or start of a new antineoplastic therapy. (NCT01022996)
Timeframe: Every three months beginning at Cycle 3 until end of treatment due to progression of disease, unacceptable toxicity, death or discontinuation from the study for any other reason

Intervention	Days (Mean)
RAD001	321.9

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Progression Free Survival (PFS) by Kaplan-Meier Estimate

Progression-free survival (PFS) was defined as the time from the first date of treatment to the date of first documented disease progression or death due to any cause or start of a new antineoplastic therapy. An event for PFS was defined as a documented disease progression or death due to any cause or start of a new antineoplastic therapy, whichever occurred first. Cycle = 28 days. (NCT01022996)
Timeframe: Every three months beginning at Cycle 3 until end of treatment due to progression of disease, unacceptable toxicity, death or discontinuation from the study for any other reason

Intervention	Days (Median)
RAD001	8.0

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Time to Overall Response (TTR) Per Kaplan-Meier Estimate

Time to overall response was defined as the time from the first date of treatment to the date of first documented response of CR or PR. Time to overall response is applied to patients whose best overall response is CR or PR. Patients who drop-out or did not have a response (CR or PR) will be treated as censored at the date of last adequate tumor assessment. (NCT01022996)
Timeframe: Every three months beginning at Cycle 3 until end of treatment due to progression of disease, unacceptable toxicity, death or discontinuation from the study for any other reason

Intervention	Days (Median)
RAD001	NA

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Duration of Overall Response (DoR)

The duration of overall response was calculated from the date of first documented response (CR or PR) to the date of first documented disease progression or death due to any cause or start of a new antineoplastic therapy. This only applies to patients whose best overall response is CR or PR. (NCT01022996)
Timeframe: Every three months beginning at Cycle 3 until end of treatment due to progression of disease, unacceptable toxicity, death or discontinuation from the study for any other reason

Intervention	Days (Mean)
RAD001	350.8

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Treatment Failure Rate

Occurrence or not of treatment failure in each patient. Treatment failure was defined as a composite endpoint of biopsy-proven acute rejection (a biopsy graded IA, IB, IIA, IIB or III according to Banff '97 grading with 2007 update), graft loss, death or lost to follow-up occurring after randomization (V5) and within M12 (V9). (NCT01023815)
Timeframe: Between randomization (Month 3) and Month 12

Intervention	Participants (Number)
Group A - Once-a-day Regimen	3
Group B - Steroid Withdrawal Group	10
Group C - Standard Twice-a-day Group	2

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Number of Participants With Graft and Patient Survival After Randomization

"Graft Survival, calculated from the date of transplantation to the date of irreversible graft failure signified by return to long-term retransplantation or the date of the last follow-up during the period when the transplant was still functioning or to the date of death.~Patient survival, calculated from the date of transplantation to the date of death or the date of the last follow-up." (NCT01023815)
Timeframe: Month 3 to Month 12

Intervention	Participants (Number)
Group B - Steroid Withdrawal Group	68
Group C - Standard Twice-a-day Group	71

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Changes in the Estimated Glomerular Filtration Rate (eGFR) Between Randomization (Month 3) and Month 12

eGFR by Nankivell, in terms of descriptive statistics and change vs randomization visit - to compare the changes in the estimated GFR (Nankivell) between randomization and Month 12 in the steroid withdrawal group (Group B) to the change observed in the standard twice-a-day group (Group C), for non-inferiority (NCT01023815)
Timeframe: Month 3 to Month 12

Intervention	mL/min (Mean)
Group B - Steroid Withdrawal Group	-1.7
Group C - Standard Twice-a-day Group	2.5

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Biopsy Proven Acute Rejection (BPAR) Rate Between Randomization and Month 12

"Occurrence of BPAR (after randomization) between arm B (steroid withdrawal group) and arm c (standard twice-a-day group).~BPAR was defined as a biopsy graded IA, IB, IIA, IIB, or III according to Banff 1997 grading with 2007 update." (NCT01023815)
Timeframe: Month 3 to Month 12

Intervention	Participants (Number)
Group B - Steroid Withdrawal Group	9
Group C - Standard Twice-a-day Group	2

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Change in Serum Creatinine

Serum creatinine (a blood measurement) is an important indicator of renal health because it is an easily-measured by-product of muscle metabolism. Measuring serum creatinine is a simple test and it is the most commonly used indicator of renal function. (NCT01023815)
Timeframe: M3, M12

Intervention	mg/dL (Mean)
	Serum Creatinine @ month 3	Serum Creatinine @ month 12
Group B - Steroid Withdrawal Group	1.4	1.5
Group C - Standard Twice-a-day Group	1.4	1.4

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Change in Estimated Creatine Clearance

At each visit, estimated creatinine clearance was measured in the local laboratory to analyze the evolution of the renal function. The following indirect measures of renal function were computed: estimated creatinine clearance according to Cockcroft and Gault formula and MDRD formula. (NCT01023815)
Timeframe: M3, M12

Intervention	mL/min (Mean)
	Using Cockcroft and Gault model @ month 3	Using Cockcroft and Gault model @ month 12	Using MDRD-4 formular @ month 3	Using MDRD-4 formular @ month 12
Group B - Steroid Withdrawal Group	64.8	62.3	57.9	53.6
Group C - Standard Twice-a-day Group	63.0	66.9	58.8	61.8

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To Determine the Rate of Clinical Benefit (i.e. Rate of Complete or Partial Response Plus Stable Disease) at 16 Weeks for Patients With Malignant Mesothelioma Treated With Everolimus as Second or Third Line Therapy.

Intervention	participants (Number)
	Stable Disease	Progression of Disease
Patients Getting Everolimus	4	2

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Number of Participants With Incidence of Proteinuria Events

Number of participants with Incidence of proteinuria events indicating chronic kidney disease (NCT01025817)
Timeframe: Baseline and 12 Months

Intervention	Participants (Number)
	Baseline: Proteinuria (>=300 mg/g)	Month 12, Day 316-450: Proteinuria (>=300 mg/g)
Everolimus and Low Dose Tacrolimus	243	36
Mycophenolate Mofetil and Standard Dose Tacrolimus	250	35

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Number of Participants With Incidence Rates of BKV Viremia, BKV Viruria, or BKV Nephropathy

Participants with Incidence of BKV (viremia, viruria, or nephropathy). BKV is Polyomavirus type BK. (NCT01025817)
Timeframe: 12 Months

Intervention	Participants (Number)
	Lab evidence of BKV Viremia	Lab evidence of BKV Viruria	BKV Disease (Nephropathy)
Everolimus and Low Dose Tacrolimus	19	19	5
Mycophenolate Mofetil and Standard Dose Tacrolimus	27	15	5

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Number of Participants With Incidence of Adverse Events, Serious Adverse Events, and Tacrolimus-associated Adverse Events

Incidence of adverse events, serious adverse events, and tacrolimus-associated adverse events by System Organ Class (NCT01025817)
Timeframe: 12 Months

Intervention	Participants (Number)
	Any system organ class	Metabolism and nutrition disorders	Gastrointestinal disorders	Injury, poisoning and procedural complications	General disorders &administration site conditions	Infections and infestations	Investigations	Renal and urinary disorders	Vascular disorders	Blood and lymphatic system disorders	Nervous system disorders	Respiratory, thoracic and mediastinal disorders	Musculoskeletal and connective tissue disorders	Skin and subcutaneous tissue disorders	Psychiatric disorders	Reproductive system and breast disorders	Cardiac disorders	Eye disorders	Immune system disorders	Endocrine disorders	Neoplasms benign,malignant,other incl cysts/polyps	Ear and labyrinth disorders	Hepatobiliary disorders	Surgical and medical procedures	Congenital, familial and genetic disorders	Social circumstances
Everolimus and Low Dose Tacrolimus	303	266	233	223	199	184	150	141	131	130	125	122	110	109	96	56	51	26	13	12	10	7	6	2	0	0
Mycophenolate Mofetil and Standard Dose Tacrolimus	302	263	247	202	177	196	143	160	121	163	150	134	114	108	106	40	47	36	11	8	15	11	3	0	6	1

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Number of Participants With Incidence of CMV (Viremia, Syndrome and Disease)

Participants with incidence of CMV (viremia, syndrome and disease). CMV is cytomegalovirus. (NCT01025817)
Timeframe: 12 Months

Intervention	Participants (Number)
	CMV syndrome event	Lab evidence of CMV Viremia	CMV Disease
Everolimus and Low Dose Tacrolimus	9	7	2
Mycophenolate Mofetil and Standard Dose Tacrolimus	13	10	8

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Estimated Glomerular Filtration Rate (eGFR)

Renal function was assessed by estimated Glomerular Filtration Rate (eGFR) using the Modification of Diet in Renal Disease (MDRD) formula. MDRD formula: GFR [mL/min/1.73m˄2] = 186.3*(C˄-1.154)*(A˄-0.203)*G*R. DEFINITIONS: C = serum concentration of creatinine [mg/dL]; A = age [years]; G = 0.742 when gender is female, otherwise G = 1; R = 1.21 when race is black, otherwise R = 1 (NCT01025817)
Timeframe: 12 Months

Intervention	mL/min/1.73m˄2 (Mean)
Everolimus and Low Dose Tacrolimus	63.14
Mycophenolate Mofetil and Standard Dose Tacrolimus	63.06

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Number of Participants With Incidence of Composite Efficacy Failure

Efficacy failure rate used the composite endpoint of: (1) treated biopsy-proven acute rejection (BPAR)*, (2) graft loss**, (3) participant death or(4) loss to follow-up. *A treated BPAR was defined as a biopsy graded IA, IB, IIA, IIB, or III and which was treated with anti-rejection therapy. **Graft loss is defined as when the allograft was presumed lost on the day the participant started dialysis and was not able to subsequently be removed from dialysis. (NCT01025817)
Timeframe: 12 Months

Intervention	Participants (Number)
	Composite Endpoint	Treated Biopsy-proven Acute rejection (BPAR)	Graft Loss	Death	Loss to follow up
Everolimus and Low Dose Tacrolimus	76	59	4	6	9
Mycophenolate Mofetil and Standard Dose Tacrolimus	62	34	12	5	17

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Number of Participants With Incidence of New Onset of Diabetes Mellitus

Incidence of new onset diabetes mellitus defined as non-diabetic patients before transplantation, who are receiving glucose lowering treatment for more than 30 days post-transplant, or with a random plasma glucose ≥200 mg dL (11.1 mmol/L) with 2 fasting plasma glucose values ≥126 mg/dL (7 mmol/L) (NCT01025817)
Timeframe: 12 Months

Intervention	Participants (Number)
	Any New Onset Diabetes	randomGlucose≥200mg/dL w/2 fastingGlucose≥126mg/dL	Concomitant Diabetes medicine for 30 days or more
Everolimus and Low Dose Tacrolimus	25	15	13
Mycophenolate Mofetil and Standard Dose Tacrolimus	22	12	14

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Total Number of Participants Experienced a Response (Complete Response+Partial Response+Stable Disease)

The number participants who experienced Complete Response+Partial Response+Stable Disease per Response Evaluation Criteria in Solid Tumors (RECIST v1.1). (NCT01031381)
Timeframe: Within 4 weeks (28 days) of study treatment initiation (baseline)

Intervention	participants (Number)
RAD001 + Bevacizumab	4

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Progression-free Survival (PFS) at 6-months

The percentage of participants who were alive with the disease (cancer) at 6 months after treatment, but whose disease had not worsened/progressed per Response Evaluation Criteria in Solid Tumors (RECIST v1.1). (NCT01031381)
Timeframe: Up to 36 months (data collection period for the cohort); Up to 6 months for participant

Intervention	percentage of participants (Number)
RAD001 + Bevacizumab	28

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Patients With Overall Response

Per Response Evaluation Criteria in Solid Tumor (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 (NCT01031446)
Timeframe: every 12 weeks

Intervention	participants (Number)
	Complete Response	Partial Response	Progressive Disease	Stable Disease
RAD001 and Cisplatin and Paclitaxel	1	12	11	27

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Maximum Feasible Dose in Milligrams Per Meter Squared of Body Surface Area (mg/m2) of Cisplatin and Paclitaxel for Women With Metastatic Breast Cancer

The recommended dose for the Phase II trial will be the most prevalent dose delivered per week in Phase I that allows for safe and feasible administration of the medications.The maximum tolerated dose (MTD) is defined as the dose preceding that at which 2 or more of 3 patients experience dose-limiting toxicity (DLT) during the initial cycle of therapy. DLTs include Common Toxicity Criteria (CTC) Grade 4 neutropenia (absolute neutrophil count [ANC] < 0.5 x 10 9/L for > 5 days), febrile neutropenia (ANC < 1.0 x 10 0/L with fever > 38.5 degrees Centigrade) or documented infection associated with Grade 3-4 neutropenia, CTC Grade 4 thrombocytopenia < 25 x 10 9/L or CTC Grade 3 < 50-25 x 10 9/L thrombocytopenia with bleeding, and Grade 3-4 non-hematologic toxicity despite symptomatic therapy. (NCT01031446)
Timeframe: at 8 weeks

Intervention	mg/m2 (Number)
	Cisplatin	Paclitaxel
RAD001 and Cisplatin and Paclitazel	25	80

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Time to Progression in Patients With Metastatic Basal-like Breast Cancer.

Median duration in months from on-study to disease progression in patients with metastatic basal-like breast cancer. All patients with basal-like breast cancer are negative for estrogen, progesterone, and human epidermal growth factor (HER2) receptors. (NCT01031446)
Timeframe: Up to 64 weeks

Intervention	months (Median)
RAD001 and Cisplatin and Paclitaxel	4.0

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Time to Progression

Duration in months from date on-study to date patient exhibited progressive disease (NCT01031446)
Timeframe: Up to 64 weeks

Intervention	months (Median)
RAD001 and Cisplatin and Paclitaxel	4.0

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Patients With Progression-free Survival

Patients who had not experienced disease progression and who were alive at 6 months after study entry (NCT01031446)
Timeframe: at 6 months

Intervention	participants (Number)
RAD001 and Cisplatin and Paclitaxel	21

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Maximum Feasible Dose in mg of RAD001 (Everolimus)for Women With Metastatic Breast Cancer

The recommended dose for the Phase II trial will be the most prevalent dose delivered per day in Phase I that allows for safe and feasible administration the medication. The MTD is defined as the dose preceding that at which 2 or more of 3 patients experience dose-limiting toxicity (DLT) during the initial cycle of therapy. DLTs include Common Toxicity Criteria (CTC) Grade 4 neutropenia (absolute neutrophil count [ANC] < 0.5 x 10 9/L for > 5 days), febrile neutropenia (ANC < 1.0 x 10 0/L with fever > 38.5 degrees Centigrade) or documented infection associated with Grade 3-4 neutropenia, CTC Grade 4 thrombocytopenia < 25 x 10 9/L or CTC Grade 3 < 50-25 x 10 9/L thrombocytopenia with bleeding, and Grade 3-4 non-hematologic toxicity despite symptomatic therapy (NCT01031446)
Timeframe: at 8 weeks

Intervention	mg (Number)
RAD001 and Cisplatin and Paclitaxel	5

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Exploratory Objective: Correlation of PFS With Biomarkers

Exploratory analysis of serum biomarkers were undertaken to generate a potential signature for response. The correlation with 6 month progression free survival P value for four plasma biomarkers is reported. (NCT01034631)
Timeframe: 6 months

Intervention	Correlation with PFS P Value (Number)
	Serum Amyloid P-Component (SAP)	Sex Hormone-Binding Globulin (SHBG)	Matrix Metalloproteinase-9 (MMP-9)	Stem Cell Factor (SCF)
Phase II Participants With Sufficient Correlative Samples	0.0184	0.0063	0.0421	0.0291

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Phase II: Response Rate With Combination Therapy Compared to Everolimus Alone

Objective response is defined as a confirmed CR or PR per RECIST criteria. Complete Response (CR): Disappearance of all target lesions. Partial Response (PR): At least a 30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD. Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. 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. (NCT01034631)
Timeframe: 12 months

Intervention	Participants (Count of Participants)
Combination Arm A: Everolimus + BNC105P	1
Sequential Arm B:Everolimus Followed by BNC105P Monotherapy	1

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Phase I: Toxicities of BNC105P in Combination With Everolimus.

Determine the toxicities of BNC105P in combination with everolimus. Drug-related treatment emergent adverse events by CTCAE grade 2 or greater are reported (NCT01034631)
Timeframe: Until disease progression or unacceptable toxicity, up to 24 cycles or 24 months

Intervention	participants (Number)
	AST-SGOT Grade 2	Cough Grade 2	Dyspepsia Grade 2	Hemoglobin Grade 2	Hemoglobin Grade 3	Hypomagnesia Grade 2	Low Platelets Grade 2	Weight Loss Grade 2	Fatigue Grade 2	Left ventricular systolic dysfunction Grade 2	Mucositis (oral) Grade 2	Nail Infection Grade 2	Diaphoresis Grade 2	Pericardial effusion Grade 3	Pleural effusion Grade 2
Phase I Participants	1	1	1	4	1	1	1	1	2	1	2	1	1	1	1

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Phase II: Adverse Events of Everolimus and BNC105P When Administered as a Combination or Sequential Regimen.

Determine adverse events of everolimus and BNC105P when administered as a combination or sequential regimen. Total number of serious and non-serious adverse events for Arm A and Arm B are summarized. Complete adverse event information is supplied in the Adverse Events reporting section. (NCT01034631)
Timeframe: 12 months

Intervention	number of adverse events (Number)
	Non-Serious Adverse Events	Serious Adverse Events
Combination Arm A: Everolimus + BNC105P	1419	39
Sequential Arm B:Everolimus Followed by BNC105P Monotherapy	1654	50

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Phase I: Response Rate of BNC105P in Combination With Everolimus.

Number of objective responses per RECIST criteria. Complete Response (CR): Disappearance of all target lesions. Partial Response (PR): At least a 30% decrease in the sum of the LD of target lesions, taking as reference the baseline sum LD. Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. 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. (NCT01034631)
Timeframe: Until disease progression or unacceptable toxicity, up to 24 cycles or 24 months

Intervention	Participants (Count of Participants)
	CR	PR	SD	PD	Unknown
Phase I Participants	0	0	8	4	3

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Geometric Mean Half-life of BNC105 and BNC105P in Combination With Everolimus.

Determine the PK Profile for BN105P in combination with everolimus by calculating the geometric mean half-life of BNC105P (NCT01034631)
Timeframe: 12 months

Intervention	hours (Geometric Mean)
	Half-life of BNC105	Half-life of BNC105P
Phase I Participants	.32	.08

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Phase I: Maximum Tolerated Dose of BNC105P in Combination With Everolimus.

Phase I (NCT01034631)
Timeframe: Until disease progression or unacceptable toxicity, up to 24 cycles or 24 months

Intervention	mg/m^2 (Number)
Phase I Participants	16

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Phase II: 6-month Progression Free Survival (PFS) With the Addition of BNC105P to Everolimus.

Improvement in 6-month PFS with the addition of BNC105P to everolimus. Progression is defined using RECIST criteria as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions (NCT01034631)
Timeframe: 6 months

Intervention	probability of 6MPFS (Number)
Combination Arm A: Everolimus + BNC105P	.3382
Sequential Arm B:Everolimus Followed by BNC105P Monotherapy	.3030

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Phase II: Overall Survival

Determine overall survival probability, up to a maximum of 5 years from registration for protocol therapy. (NCT01034631)
Timeframe: 60 months

Intervention	probability of OS at 60 months. (Number)
Combination Arm A: Everolimus + BNC105P	.15
Sequential Arm B:Everolimus Followed by BNC105P Monotherapy	.21

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Phase II: Progression Free Survival (PFS) With BNC105P Alone in Patients After Progressing on Everolimus.

Median time to progression for arm P participants who crossed over to BNC105P monotherapy after progression. Progression is defined per RECIST criteria as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions (NCT01034631)
Timeframe: 12 months

Intervention	months (Median)
Arm B Participants Who Crossed Over to BNC105P Monotherapy	1.8

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Time to Tumor Progression (TTP)

TTP was defined as the time from the date of randomization to the date of the first documented radiologic confirmation of disease progression. Since the study did not meet the primary objective, TTP was not formally tested. (NCT01035229)
Timeframe: Until all patients have disease progression or leave study due to intolerable adverse events- Estimate of 1 year for each patient

Intervention	Months (Median)
Everolimus + Best Supportive Care (BSC)	2.96
Placebo + Best Supportive Care	2.60

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Time to Definitive Deterioration of EORTC QLQ-C30 Scores

The primary quality of life endpoint was the time to definitive 5% deterioration from baseline in the global health status/quality of life scale of the EORTC QLQ-C30 questionnaire. Definitive deterioration by at least 5% is defined as a decrease in score by at least 5% compared to baseline, with no later observed increase above this threshold. The EORTC quality of life questionnaire (QLQ) is an integrated system for assessing the healthrelated quality of life (QoL) of cancer patients participating in international clinical trials. All of the scales and single-item measures range in score from 0 to 100. A high scale score represents a higher response level. Thus a high score for a functional scale represents a high / healthy level of functioning, a high score for the global health status / QoL represents a high QoL, but a high score for a symptom scale / item represents a high level of symptomatology / problems. (NCT01035229)
Timeframe: Until all patients have disease progression or leave study due to intolerable adverse events - Estimate of 1 year for each patient.

Intervention	Months (Median)
Everolimus + Best Supportive Care (BSC)	2.86
Placebo + Best Supportive Care	3.45

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Time to Definitive Deterioration of ECOG Performance Score (PS) Score

Change in Eastern Cooperative Oncology Group (ECOG) were assessed by time to definitive performance status deterioration by at least one category on the ECOG scale. Deterioration was considered definitive if no improvement in the ECOG PS was observed at a subsequent measurement. ECOG PS: 0=Fully active, able to carry on all pre-disease performance without restriction, 1=Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature, e.g., light house work, office work; 2=Ambulatory and capable of all selfcare but unable to carry out any work activities. Up and about more than 50% of waking hours; 3=Capable of only limited selfcare, confined to bed or chair more than 50% of waking hours; 4=Completely disabled. Cannot carry on any selfcare. Totally confined to bed or chair; 5=Dead (NCT01035229)
Timeframe: Until all patients have disease progression or leave study due to intolerable adverse events- Estimate of 1 year for each patient.

Intervention	Months (Median)
Everolimus + Best Supportive Care (BSC)	4.27
Placebo + Best Supportive Care	4.47

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Pharmacokinetics Assessments - Cmin

Cmin is the pre-dose blood concentration at steady-state (ng/mL). Pre-dose (Cmin) blood samples were collected from all patients in both arms at Visit 3. Steady-state for the Cmin sample was defined as continuous administration of the same dose in the last 4 days prior to the collection of the Cmin sample. Steady-state for the 5 mg every other day regimen was defined as the state when the 5 mg dose was taken 2 days and 4 days before sampling. PK samples were only drawn at visit 3, and only analyzed for patients receiving everolimus at steady state (if patients had received the dose the previous 4 days). In addition summary statistics were only done for each everolimus dose when 3 samples were available. Only valid pre-dose (Cmin) everolimus samples were included in the analysis. (NCT01035229)
Timeframe: Until all patients have disease progression or leave study due to intolerable adverse events - Estimate of 1 year for each patient.

Intervention	ng/mL (Mean)
Everolimus 7.5mg + Best Supportive Care (BSC)	16.141
Everolimus 5mg + Best Supportive Care (BSC)	9.318

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Pharmacokinetics Assessments - Cmax

Cmax is the maximum (peak) blood drug concentration after dose administration (ng/mL) calculated as the maximum of C1h and C2h. C1h was 1 hour post-dose blood concentration (ng/mL) and C2h was 2 hour post-dose blood concentration (ng/mL). C1h and C2h post-dose samples were collected from all patients in both arms at Visit 3. Steady-state for the C1h and C2h samples was defined as continuous administration of the same dose in the previous 4 days and the day on which the C1h and C2h samples were collected. Steady-state for the 5 mg every other day regimen was defined as the state when the 5 mg dose was taken 2 days and 4 days before sampling. PK samples were only drawn at visit 3, and only analyzed for patients receiving everolimus at steady state (if patients had received the dose the previous 4 days). In addition summary statistics were only done for each everolimus dose when 3 samples were available. Only valid C1h and C2h everolimus samples were included in the analysis. (NCT01035229)
Timeframe: Until all patients have disease progression or leave study due to intolerable adverse events- Estimate of 1 year for each patient.

Intervention	ng/mL (Mean)
Everolimus 7.5mg + Best Supportive Care (BSC)	47.881
Everolimus 5mg + Best Supportive Care (BSC)	31.592

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Percentage of Participants With Disease Control Rate (DCR)

DCR is defined as the proportion of participants with a best objective response (BOR) of complete response (CR) or partial response (PR) or stable disease (SD) according to RECIST. The BOR was the best response recorded from the start of the treatment until disease progression. CR is disappearance of all target lesions; PR is at least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters; SD is neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for PD. PD is at least a 20% increase in the sum of the longest diameter of all measured target lesions, taking as reference the smallest sum of longest diameter of all target lesions recorded at or after baseline. (NCT01035229)
Timeframe: Until all patients have disease progression or leave study due to intolerable adverse events- Estimate of 1 year for each patient

Intervention	Percentage of Participants (Number)
Everolimus + Best Supportive Care (BSC)	56.1
Placebo + Best Supportive Care	45.1

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Overall Survival (OS)

OS was defined as the time from the date of randomization to the date of death from any cause. The comparison of OS between the 2 arms was done using a stratified log-rank test at one-sided 2.5% level of significance. (NCT01035229)
Timeframe: When 454 OS events were observed

Intervention	Months (Median)
Everolimus + Best Supportive Care (BSC)	7.56
Placebo + Best Supportive Care	7.33

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Evaluate Safety of the Combination at a Daily Dosing of 2.5mg RAD001, 5 mg RAD001 or 10 mg RAD001 (Phase 1 Part)

Number of patients who experienced a Dose Limiting Toxicity (DLT). DLT will be assessed in the first 28 days of dosing. Patients need to get dosed with 2 rounds/sessions of all chemotherapy agents in the first 28 days in order to be evaluable for DLT assessment. The primary endpoint is safety as summarized by dose limiting toxicity (DLT). (NCT01047293)
Timeframe: December 2011

Intervention	participants (Number)
ARM 1 RAD001 5 mg QOD	0
ARM 2 5mg RAD001 QD	1
ARM 3 10mg RAD001 QD	1

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Progression Free Survival at Six Months

(NCT01047293)
Timeframe: 6 months

Intervention	percentage of participants (Number)
All Patients	87

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PSA Response Rate

PSA response rate with response defined as => a 30% reduction in PSA (NCT01051570)
Timeframe: Day 1 of each cycle (every 21 days), through study completion, an average of 6 months

Intervention	percentage of participants (Number)
Carboplatin, RAD 001 & Prednisone	15

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Association of PSA Response Rate With Correlative Markers (Phospho mTOR, pAKT, and p70S6)

PSA response defined as a decrease of 30% or more will be tabled against mTOR, pAKT, and p70S6 (1+, 2+, 3+ vs ND) (NCT01051570)
Timeframe: Archival tissue will be collected if available. Optional biopsies pre-treatment and 24 hours after first everolimus and carboplatin dose

Intervention	participants (Number)
	pAKT(ND) vs Responder	mTOR(ND) vs Responder	p70S6(ND) vs Responder
Carboplatin, RAD 001 & Prednisone	1	0	1

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Overall Survival

Overall Survival as measured by the Kaplan-Meier method (NCT01051570)
Timeframe: After treatment, participants will be contacted every 3 months up to 4 years

Intervention	months (Median)
Carboplatin, RAD 001 & Prednisone	12.5

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Pharmacokinetics: Observed Carboplatin AUC Was Estimated Based on the Concentration in the 2.75-h Sample.

Using a limited sampling model (i.e., AUC = 0.52 × C2.75h + 0.92) (Sorensen et al., 1993), observed carboplatin AUC was estimated based on the concentration in the 2.75-h sample. (NCT01051570)
Timeframe: Samples were collected Cycle 2, Day 1

Intervention	mg/ml*min (Mean)
Carboplatin, RAD 001 & Prednisone	5.8

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Time to Progression (TTP)

Progression defined as at least a 20% increase in the sum of the longest diameter (LD) of target lesions taking as references the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT01051570)
Timeframe: Up to 63 days while on treatment, then up 90 days thereafter. From date of registration to date of progressive disease.

Intervention	months (Median)
Carboplatin, RAD 001 & Prednisone	2.5

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Number of Participants With Toxicity as Measured by NCI CTCAE v3.0 Criteria

Number of Participants with Grade 3/4 Toxicity as measured by NCI CTCAE v3.0 criteria (NCT01051570)
Timeframe: Day 1 of each cycle (every 21 days), through study completion, an average of 6 months

Intervention	Participants (Count of Participants)
	Anemia	Thrombocytopenia	Lymphopenia	Leukopenia	Infection without neutropenia	Hypophosphatemia	Neutropenia	Dehydration	Hyperglycemia	Hyponatremia	Pulmonary embolism	Fatigue	Hypercholesterolemia	Rash	AST	Hypomagnesemia	Hypokalemia
Carboplatin, RAD 001 & Prednisone	10	9	6	4	4	4	3	3	3	3	2	2	1	1	1	1	1

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Overall Survival (OS)

(NCT01051791)
Timeframe: Up to 60 months

Intervention	months (Median)
Everolimus 10 mg Daily	4.5

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Progression Free Survival (PFS)

(NCT01051791)
Timeframe: Up to 60 months

Intervention	months (Median)
Everolimus 10 mg Daily	1.5

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Objective Response Rate (ORR)

The number of patients with recurrent/refractory SCCHN (head and neck squamous cell carcinoma) treated with single-agent everolimus that, experience a Complete Response (CR) + number of patients that experience a Partial Response (PR ) / total evaluable patients. (NCT01051791)
Timeframe: Up to 60 months

Intervention	percentage of participants (Number)
Everolimus 10 mg Daily	0

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Clinical Benefit Rate (CBR)

The number of patients with recurrent/refractory SCCHN (head and neck squamous cell carcinoma) treated with single-agent everolimus that, experience a Complete Response (CR) + number of patients that experience a Partial Response (PR ) + number of patients that experience Stable Disease (SD) / total evaluable patients. (NCT01051791)
Timeframe: Up to 60 months

Intervention	percentage of participants (Number)
Everolimus 10 mg Daily	28

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Response

(NCT01057277)
Timeframe: 1 year

Intervention	participants (Number)
RAD001(Afinitor)	NA

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Overall Survival (OS) [Phase II]

OS based on the Kaplan-Meier method is defined as the time from study entry to death or date last known alive. (NCT01058655)
Timeframe: Long-term follow-up for survival was not specified per protocol. Participants were followed for up to 20 months on this study.

Intervention	months (Median)
Phase II: Everolimus 10 mg + Tivozanib 1 mg [Evaluable]	5.6

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Everolimus Maximum Tolerated Dose (MTD) [Phase I]

The everolimus MTD in combination with tivozanib is determined by the number of patients who experience a dose limiting toxicity (DLT). See subsequent primary outcome measure for the DLT definition. The MTD is defined as the highest dose at which fewer than one-third of patients experience a DLT. If no DLTs are observed, the MTD is not reached. (NCT01058655)
Timeframe: Patients were assessed continuously for toxicity while on study. The observation period for MTD evaluation was the first 28 days (cycle 1) of treatment.

Intervention	mg daily for 4 weeks of a 4 week cycle (Number)
Phase I: Evaluable	10

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Dose Limiting Toxicity (DLT) [Phase I]

A DLT was defined as a treatment-related (attribution possible, probable, definite) adverse event that meets any of the following criteria: Grade 3 (G3) or higher non-hematologic toxicity (excluding, nausea, vomiting, diarrhea, alopecia, hypertension, hypercholesterolemia, or hypertriglyceridemia); G3 diarrhea, nausea or vomiting lasting > 48 hours or leading to hospitalization, despite aggressive anti-diarrheal or anti-emetic medications; G4 diarrhea, despite aggressive anti-diarrheal medications; G4 vomiting, despite aggressive anti-emetic medications; G3 hypertension, for which blood pressure cannot be reduced to <150/100 with anti-hypertensive therapies; G4 hypertension or severe hypertension, as defined by systolic blood pressure >180 mmHg or diastolic blood pressure > 110 mmHg; G4 hypercholesterolemia or hypertriglyceridemia lasting > 7 days, despite appropriate use of anti-hyperlipidemic medications; G4 hematologic toxicity lasting for >5 days, including leukopenia, neutropen (NCT01058655)
Timeframe: Patients were assessed continuously for toxicity while on study. The observation period for DLT evaluation was the first 28 days (cycle 1) of treatment.

Intervention	Participants with DLT (Number)
Phase I Cohort 1: Everolimus 5 mg + Tivozanib 1 mg	0
Phase I Cohort 2: Everolimus 10 mg + Tivozanib 1 mg	0
Phase I Cohort 3: Everolimus 10 mg + Tivozanib 1.5 mg	2

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Disease Control Rate (DCR) [Phase II]

Disease Control Rate is defined as the percentage of patients who achieve confirmed stable disease (SD) or better on treatment based on RECIST 1.0 criteria. Per RECIST 1.0 for target lesions, complete response (CR) is disappearance of all target lesions and partial response (PR) is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. Progressive disease (PD) is at least a 20% increase in sum LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started. SD is neither PR nor PD. For non-target lesions, PD is the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. (NCT01058655)
Timeframe: Disease was assessed every 2 cycles on treatment. Median treatment duration on this study cohort was 2 months (range 1-16).

Intervention	percentage of participants (Number)
Phase II: Everolimus 10 mg + Tivozanib 1 mg [Evaluable]	50

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Tivozanib Maximum Tolerated Dose (MTD) [Phase I]

The tivozanib MTD in combination with everolimus is determined by the number of patients who experience a dose limiting toxicity (DLT). See subsequent primary outcome measure for the DLT definition. The MTD is defined as the highest dose at which fewer than one-third of patients experience a DLT. If no DLTs are observed, the MTD is not reached. (NCT01058655)
Timeframe: Patients were assessed continuously for toxicity while on study. The observation period for MTD evaluation was the first 28 days (cycle 1) of treatment.

Intervention	mg daily for 3 weeks of a 4 week cycle (Number)
Phase I: Evaluable	1.0

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Progression-Free Survival (PFS) [Phase II]

PFS based on the Kaplan-Meier method is defined as the time from study entry to the earliest documentation of disease progression (PD) or death. Participants alive without evidence of PD were censored at the earliest date of last disease assessment. Per RECIST 1.0 criteria: progressive disease (PD) is at least a 20% increase in the sum of longest diameter (LD) of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. PD for the evaluation of non-target lesions is the appearance of one or more new lesions and/or unequivocal progression of non-target lesions. (NCT01058655)
Timeframe: Disease was assessed radiographically to document clinical progression every 2 cycles on treatment. Participants were followed for up to 16 months since study entry.

Intervention	months (Median)
Phase II: Everolimus 10 mg + Tivozanib 1 mg [Evaluable]	3.0

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Change From Baseline in Forced Vital Capacity (FVC)

All spirometry evaluation followed recommendations of the Standardization of Lung Function Testing. All spirometry maneuvers were performed in sitting position whilst wearing nose clips. At least three acceptable maneuvers were performed for each time point, and results met within-test and between-test criteria for acceptability. The highest value was obtained of FVC from any of the three maneuvers that met acceptability criteria. Change from baseline in FVC was compared between everolimus and historical placebo data from multicenter trial of sirolimus in LAM. (MILES NCT00414648) due to absence of placebo group in this current study on a rare lung disease. These two studies had different study designs, so the change from baseline to 6 months (26 weeks) in MILES study was estimated from the publicly reported rate of change per month to provide a meaningful comparison. This historical control be can be viewed on the Novartis Clinical Trial Results website. (NCT01059318)
Timeframe: Baseline, 26 weeks

Intervention	mL (Mean)
Everolimus	10

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Change From Baseline in Forced Expiratory Volume in 1 Second (FEV1)

"All spirometry evaluation followed the recommendations of the Standardization of Lung Function Testing. All spirometry maneuvers were performed in the sitting position whilst wearing nose clips. At least three acceptable maneuvers were performed for each time point, and the results met within-test and between-test criteria for acceptability. The highest value was obtained of FEV1 from any of the three maneuvers that met acceptability criteria.~Change from baseline in FEV1 was compared between everolimus and historical placebo data from the MILES study (NCT00414648) due to the absence of a placebo group in this current study on a rare lung disease. These two studies had different study designs, so the change from baseline to 6 months (26 weeks) in MILES study was estimated from the publicly reported rate of change per month in order to provide a meaningful comparison. This historical control can be viewed on the Novartis Clinical Trial Results website." (NCT01059318)
Timeframe: Baseline, 26 weeks

Intervention	mL (Mean)
Everolimus	114

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Change From Baseline in Extended Pulmonary Function Testing

Extended pulmonary function testing such as Total Lung Capacity (TLC), Thoracic Gas Volume (TGV), Residual Volume (RV) were measured using a body plethysmograph (NCT01059318)
Timeframe: Baseline, 26 weeks

Intervention	Liters (L) (Mean)
	TLC	TGV	RV
Everolimus	0.199	0.267	0.169

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Change From Baseline in 6-minute Walk Test Score to Measure Exercise Capacity

A standardized 6-minute walk test (6MWT) was performed in accordance with the guidelines of the American Thoracic Society 2002. The test was done about the same time of day to avoid diurnal variation in an environment that had an adequate temperature to avoid additional burden to the patient due to heat or cold air. The distance walked in six minutes (6MWD) was recorded. (NCT01059318)
Timeframe: Baseline, 26 weeks

Intervention	meters (m) (Mean)
Everolimus	46.9

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Change From Baseline in Carbon Monoxide Diffusing Capacity (DLCO)

Carbon Monoxide Diffusing Capacity (DLCO) one of the extended pulmonary function testing which was also measured using a body plethysmograph. (NCT01059318)
Timeframe: Baseline, 26 weeks

Intervention	ml/min/mmHg (Mean)
Everolimus	-0.782

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Mean Trough (C0,ss) and Peak (C2,ss) Drug Concentration at Steady State

Venous blood samples (2 mL) for pharmacokinetic evaluation were collected pre dose and 2 hours post dose at preselected visits. (NCT01059318)
Timeframe: pre-dose and at 2 hour post dose at week 26

Intervention	ng/mL (Mean)
	Trough (C0, ss)	Peak (C2, ss)
Everolimus 10 mg/Day	11.0	45.7
Everolimus 2.5 mg/Day	3.1	12.1
Everolimus 5 mg/Day	5.8	22.6

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Change From Baseline in Vascular Endothelial Growth Factor-D (VEGF-D) Concentrations

Blood samples (1 mL) for determination of VEGF-D were collected from a forearm vein (direct venipuncture or from an indwelling cannula) and 2 aliquots of serum were collected. VEGF-D levels were determined from only 1 of the 2 serum aliquots, with the second acting as a back-up. A serum VEGF-D >800 pg/mL level supports a diagnosis of Lymphangioleiomyomatosis (LAM) (NCT01059318)
Timeframe: Baseline, 26 weeks

Intervention	pg/mL (Mean)
Everolimus 2.5 mg/Day	-464.3
Everolimus 5 mg/Day	-1113.2
Everolimus 10 mg/Day	-1771.7

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Change From Baseline in Oxygen Saturation

Oxygen saturation means the amount of oxygen in blood stream. Oxygen saturation was measured by using a Pulse Oximeter. (NCT01059318)
Timeframe: Baseline, 26 weeks

Intervention	percentage of oxygen (Mean)
Everolimus	0.8

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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.

Intervention	percentage of patients (Number)
	Grade 1	Grade 2	Grade 3	Grade 4	Grade 5
Ph II: RT + TMZ	0	0	3	3	2
Ph II: RT + TMZ + RAD001	0	3	5	0	1

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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.

Intervention	Participants (Count of Participants)
Ph I: RT + TMZ + RAD001 2.5 mg/Day	2
Ph I: RT + TMZ + RAD001 5 mg/Day	2
Ph I: RT + TMZ + RAD001 10 mg/Day	2

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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.

Intervention	months (Median)
Ph II: RT + TMZ	21.2
Ph II: RT + TMZ + RAD001	16.5

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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.

Intervention	months (Median)
Ph II: RT + TMZ	10.2
Ph II: RT + TMZ + RAD001	8.2

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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.

Intervention	percentage of participants (Number)
	Concurrent treatment: Grade 1	Concurrent treatment: Grade 2	Concurrent treatment: Grade 3	Concurrent treatment: Grade 4	Concurrent treatment: Grade 5	Post-RT treatment: Grade 1	Post-RT treatment: Grade 2	Post-RT treatment: Grade 3	Post-RT treatment: Grade 4	Post-RT treatment: Grade 5
Ph I: RT + TMZ + RAD001 10 mg/Day	12.5	0.0	87.5	0.0	0.0	0.0	100.0	0.0	0.0	0.0
Ph I: RT + TMZ + RAD001 2.5 mg/Day	0.0	0.0	50.0	50.0	0.0	0.0	0.0	71.4	14.3	14.3
Ph I: RT + TMZ + RAD001 5 mg/Day	11.1	33.3	44.4	11.1	0.0	0.0	42.9	28.6	0.0	0.0

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Number of Participants With Disease Progression

(NCT01068249)
Timeframe: from study entry (1st treatment) to date of tumor progression, date of death, or, for patients alive without tumor progression, date of last follow-up, up to 2 years

Intervention	Participants (Count of Participants)
RAD001 + Letrozole	31

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Number of Participants With Objective Response Rate

Objective response or stable disease rate monitored as patients accrue and are evaluated following the example of Thall and Simon. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT01068249)
Timeframe: at 8 weeks of treatment, then every 12 weeks, up to 2 years

Intervention	Participants (Count of Participants)
	Complete Response (CR)	Partial Response (PR)
RAD001 + Letrozole	9	2

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Number of Participants With Adverse Events (All Grades)

Toxicity was assessed using the National Cancer Institute Common Terminology Criteria for Adverse Events (version 3.0). (NCT01068249)
Timeframe: Adverse events were reported from first dose of study treatment until end of study treatment plus 30 days post treatment

Intervention	Participants (Count of Participants)
RAD001 + Letrozole	28

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Median Overall Survival (OS)

OS is defined as the interval from first dose of study treatment to the date of death, irrespective of the cause of death; subjects still alive will be censored at the date of the last contact (NCT01068249)
Timeframe: from (1st treatment) to death or, for living patients, date of last contact, up to 24.4 months

Intervention	months (Median)
RAD001 + Letrozole	14

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Median Progression Free Survival (PFS)

PFS is the time from first dose of study treatment until the first date of either objective disease progression or death due to any cause. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as a 30% 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. Median PFS was estimated using the Kaplan-Meier method. (NCT01068249)
Timeframe: from study entry (1st treatment) to date of tumor progression, date of death, or, for patients alive without tumor progression, date of last follow-up, assessed up to 2 years

Intervention	months (Median)
RAD001 + Letrozole	3

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Reduction in Seizure Frequency

The primary efficacy endpoint was the percentage of participants demonstrating a 50% or greater reduction in seizure frequency at the end of the maintenance phase (weeks 13-16) compared to baseline (weeks 1-4) (NCT01070316)
Timeframe: Baseline (Weeks 1-4), Week 16

Intervention	percentage (Number)
Everolimus	60

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Number of Participants Continuing Study Medication Over Time

(NCT01070316)
Timeframe: Individual subjects will be assessed every 6 months for up to 48 months; aggregate analysis will take place at end of study

Intervention	participants (Number)
	16 weeks	Entered Extension Phase (4 months)	6 months	12 months	18 months	24 months	30 months	36 months	42 months	48 months
Everolimus	20	18	18	17	16	16	16	15	14	14

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Number of Patients Reporting Dose-Limiting Toxicity (DLT) (Phase I)

The number of dose-limiting toxic events (DLT) for this combination of drug treatment will determine the Maximum Tolerated Dose (MTD) in subsequent phases of this study. The following events were defined as a DLT: a grade 4+ Neutropenia or platelet count decrease, a grade 4 infection, or any grade 3+ non-hematologic event as assessed using Common Terminology Criteria for Adverse Events (CTCAE) CTEP Version 4.0. Here, the number of patients reporting a DLT are reported (NCT01075321)
Timeframe: After one 28 day cycle

Intervention	Participants (Count of Participants)
Phase I: Dose Level -1	1
Phase I: Dose Level 0	2
Phase I: Dose Level 1	3
Phase II: Dose Level 0	0

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Duration of Response for All Eligible Patients

Duration of response is defined for all evaluable patients who have achieved an objective response as the date at which the patient's earliest objective status is first noted to be either a CR or PR to the earliest date progression is documented. (NCT01075321)
Timeframe: Up to 5 years

Intervention	months (Median)
All Patients (Everolimus and Lenalidomide)	14.7

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Overall Survival for All Eligible Patients

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. (NCT01075321)
Timeframe: Up to 5 years

Intervention	months (Median)
All Patients (Everolimus and Lenalidomide)	20.3

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Time to Treatment Failure for All Eligible Patients

Time to treatment failure is defined to be the time from registration to the date at which the patient is removed from treatment due to progression, adverse events, or refusal. The distribution of time to treatment failure will be estimated using the method of Kaplan-Meier. (NCT01075321)
Timeframe: Up to 5 years

Intervention	months (Median)
All Patients (Everolimus and Lenalidomide)	4.7

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Progression-Free Survival For All Eligible Patients

Progression-free survival time is defined as the time from registration to the earliest date of documentation of disease progression. The distribution of progression-free survival time will be estimated using the method of Kaplan-Meier. (NCT01075321)
Timeframe: Up to 5 years

Intervention	months (Median)
All Patients (Everolimus and Lenalidomide)	5.3

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Change in Interstitial Fibrosis/Tabular Atrophy (IF/TA) Grade

Difference (M12 - M3) in IF/TA grade. IF/TA grade was assessed during centralized reading according to the Banff 2005/2007 classification comprising grade I (<25%), grade II (25-50%) and grade III (>50% of lesions). (NCT01079143)
Timeframe: M3 and M12 post transplantation

,,,

Intervention	Number of Participants (Number)
	Difference in IF/TA grade -1	Difference in IF/TA grade 0	Difference in IF/TA grade 1	Difference in IF/TA grade 2	Difference in IF/TA grade 3
Certican EMT-	1	21	18	3	NA
Certican EMT+	5	9	7	3	2
Neoral EMT-	2	33	13	5	NA
Neoral EMT+	7	9	11	5	0

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Number of Participants With Progression of Renal Graft Fibrosis (Primary Comparison - ITT Population

"Progression of Interstitial Fibrosis/Tabular Atrophy (IF/TA) is the percentage (%) of participants with an increase >= 1 in IF/TA grade according to Banff (2005 - 2007)according to Epithelial-mesenchymal transition (EMT) profile and by treatment groups.~Grade I (the better): mild interstitial fibrosis and tubular atrophy (<25% of cortical area) Grade II : moderate interstitial fibrosis and tubular atrophy (26-50% of cortical area) Grade III (the worse) : severe interstitial fibrosis and tubular atrophy (>50% of cortical area)" (NCT01079143)
Timeframe: Month 3 (M3) and Month 12 (M12) post transplantation

Intervention	Participants (Number)
	Participants with an IF/TA grade <= II at M3	Participants with Fibrosis progression, M3 to M12
Certican EMT+	26	12
Neoral EMT+	31	16

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Number of Participants With Progression of Renal Fibrosis Using Numerical Quantification

Comparisons according to epithelial-mesenchymal transition (EMT) profile and immunosuppressive treatment (NCT01079143)
Timeframe: M3 to M12 post transplantation

,,,

Intervention	Participants (Number)
	Fibrosis Progression - No (n=24, 42, 31, 53)	Fibrosis progression - Yes (n=24, 42,31,43)	Fibrosis progression - Missing (n=24, 42, 31, 53)
Certican EMT-	30	12	1
Certican EMT+	18	6	2
Neoral EMT-	42	11	0
Neoral EMT+	19	12	0

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Number of Participants With Epithelial-mesenchymal Transition (EMT) Status

Incidence and severity of EMT status. EMT status was determined centrally using the graft biopsy taken at 3 months. The result was quickly obtained (within 7 to 15 days) and sent to the company in charge of randomization in order to allocate each patient to a treatment group and to provide the investigator with this information without confirming EMT status. (NCT01079143)
Timeframe: M3 and M12 post transplantation

,,,

Intervention	Participants (Number)
	EMT Status at M3-Negative (n=26,43,32,53)	EMT Status at M3- Positive (n=26,43,32,53)	EMT Status at M3 - Not done (n=26,43,32,53)	EMT Status at M12- Negative (n=25,41,32,53)	EMT Status at M12- Positive (n=25,41,32,53)	EMT Status at M12- Not done (n=25,41,32,53)
Certican EMT-	43	0	0	24	17	0
Certican EMT+	0	26	0	8	17	0
Neoral EMT-	53	0	0	36	17	0
Neoral EMT+	0	32	0	9	23	0

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Number of Participants With Epithelial-mesenchymal Transition (EMT) Score

"Incidence and severity of EMT score. The intensity of EMT markers expression present and detectable in the renal graft at an early stage following transplantation is known as EMT score.~EMT score 0 (the best): <1 EMT score 1 (the better): 1-10% of tubular atrophy EMT score 2: 10-25% of tubular atrophy EMT score 3: 25-50% of tubular atrophy EMT score 4 (the worst): >50% of tubular atrophy" (NCT01079143)
Timeframe: M3 and M12 post transplantation

,,,

Intervention	participants (Number)
	EMT Score 0 at M3 (n= 26,43,32, 53)	EMT Score 1 at M3 (n= 26,43,32, 53)	EMT Score 2 at M3 (n= 26,43,32, 53)	EMT Score 3 at M3 (n= 26,43,32, 53)	EMT Score 4 at M3 (n= 26,43,32, 53)	EMT Score 0 at M12 (n= 25,41,32, 53)	EMT Score 1 at M12 (n= 25,41,32, 53)	EMT Score 2 at M12 (n= 25,41,32, 53)	EMT Score 3 at M12 (n= 25,41,32, 53)	EMT Score 4 at M12 (n= 25,41,32, 53)	EMT Missing Score at M12 (n= 25,41,32, 53)
Certican EMT-	26	17	0	0	0	13	11	11	4	2	2
Certican EMT+	0	0	17	9	0	1	7	10	4	3	1
Neoral EMT-	28	25	0	0	0	19	17	12	4	1	0
Neoral EMT+	0	0	20	8	4	0	9	10	9	4	0

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Interstitial Fibrosis/Tabular Atrophy (IF/TA)

Incidence and severity of IF/TA according to 2005/2007 Banff classification system grades (grades l to lll). IF/TA grade was assessed during centralized reading according to the Banff 2005/2007 classification comprising grade I (<25%), grade II (25-50%) and grade III (>50% of lesions). (NCT01079143)
Timeframe: M3 and M12 post transplantation

,,,

Intervention	Number of participants (Number)
	Interstitial Fibrosis/Tubular Atrophy (IF/TA)	IF/TA grade at M3 at grade 1	IFTA grade at M3 at grade II	IF/TA grade at M3 at grade III	IF/TA grade at M12 at grade 0	IT/TA grade at M12 at grade I	IF/TA grade at M12 at grade II	IF/TA grade at M12 at grade III
Certican EMT-	38	5	0	0	20	18	5	0
Certican EMT+	13	11	2	0	9	8	6	3
Neoral EMT-	44	9	0	0	31	15	6	1
Neoral EMT+	13	17	1	1	7	15	9	1

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Incidence (Number) of BPAR

A biopsy proven acute rejection (BPAR) is defined as a biopsy graded IA, IB, IIA, IIB or III as per 2005/2007 Banff histological classification system. (NCT01079143)
Timeframe: M6 and M12 post transplantation

,,,

Intervention	Number of participants (Number)
	M6 - No	M6 - Yes	M12 - No	M12 - Yes
Certican EMT-	52	8	43	17
Certican EMT+	33	3	29	7
Neoral EMT-	59	0	56	3
Neoral EMT+	39	0	37	2

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Change in EMT Score

"Change (M12 - M3) in EMT Score. Progression in EMT score is defined as an increase by >=1 of EMT score from M3 to M12.~EMT score 0 (the best): <1 EMT score 1 (the better) : 1-10% of tubular atrophy EMT score 2 : 10-25% of tubular atrophy EMT score 3 : 25-50% of tubular atrophy EMT score 4 (the worst): >50% of tubular atrophy" (NCT01079143)
Timeframe: M3 and M12 post transplantation

Intervention	scores on a scale (Mean)
Certican EMT+	-0.3
Certican EMT-	0.9
Neoral EMT+	-0.3
Neoral EMT-	0.6

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Incidence (Number) of Subclinical Rejections and Borderline Lesions

"Incidence of subclinical rejections and borderline lesions with regards to histological evidence of rejection with clinical findings.~Subclinical rejections: rejection without clinical symptoms which is diagnosed by chance when a graft biopsy is performed.~Clinically suspected BPAR: rejection suspected because of the presence of clinical symptoms (fever, pain, increase of creatinine) and then confirmed by the graft biopsy.~Borderline lesions: suspicious for acute T-cell mediated rejection. This category is used when no intimal arteritis is present, but there are foci of tubulitis with minor interstitial infiltration or interstitial infiltration with mild tubulitis." (NCT01079143)
Timeframe: M3

Intervention	Participants (Number)
	Subclinical rejections-No (n=68, 84)	Subclinical rejections- Yes (n=68, 84)	Subclinical rejections- missing (n=68, 84)	Clinically suspected BPAR - No (N=68, 84)	Clinically suspected BPAR - Yes (N=68, 84)	Clinically suspected BPAR - Missing (N=68, 84)	Borderline lesions - No (n=68,84)	Borderline lesions - Yes (n=68,84)	Borderline lesions - Missing (n=68,84)
Certican	67	1	1	68	0	1	62	6	1
Neoral	84	0	1	84	0	1	71	13	1

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Change in Urine Protein/Creatinine Ratio (Without Imputation)

One of the factors associated with EMT progression between M3 and M12 according to univariate analysis (ITT biopsies M3 & M12). (NCT01079143)
Timeframe: Month 3 (baseline), Month 12

Intervention	mg/mmol (Mean)
Certican EMT+	44.4
Certican EMT-	3.5
Neoral EMT+	16.0
Neoral EMT-	29.8

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Change From Baseline (M3) in Estimated Glomerular Filtration Rate (eGFR)

"eGFR was calculated according to the abbreviated Modification of Diet in Renal Disease (MDRD) Formula and creatinine clearance according to the Cockcroft-Gault formula (mL/min/1.73m²).~LOCF = Last observation carried forward" (NCT01079143)
Timeframe: M3 (baseline) to M12 post transplantation

Intervention	mL/min/1.73m^2 (Least Squares Mean)
	without imputation	imputation by LOCF(96, 97)
Certican	6.99	5.96
Neoral	2.54	2.15

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Change in Estimated Glomerular Filtration Rate (eGFR) at M12 From Baseline (M3) - ANCOVA Model

The average patient renal function was evaluated on the basis of eGFR was calculated according to the abbreviated MDRD formula and creatinine clearance according to the Cockcroft-Gault formula (mL/min/1.73m²). (NCT01079143)
Timeframe: Baseline (M3), M12

,,,

Intervention	mL/min/1.73m² (Mean)
	without imputation	imputation by LOCF (36, 60, 39, 58)
Certican EMT-	5.6	27.3
Certican EMT+	8.6	-11.9
Neoral EMT-	3.8	-4.9
Neoral EMT+	1.5	5.1

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Incidence (Number) of Participants With Graft Losses

If a participant underwent a graft nephrectomy, then the day of nephrectomy was considered as the day of graft loss. (NCT01079143)
Timeframe: M6 and M12 post transplantation

,,,

Intervention	Participants (Number)
	M6 - No	M6 - Yes	M12 - No	M12 - Yes
Certican EMT-	60	0	56	4
Certican EMT+	36	0	35	1
Neoral EMT-	59	0	59	0
Neoral EMT+	39	0	38	1

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Type of Biopsy Proven Acute Rejection (BPAR)

"A biopsy proven acute rejection (BPAR) is defined as a biopsy graded IA, IB, IIA, IIB or III as per 2005/2007 Banff histological classification system.~Biopsy graded IA: Significant interstitial infiltration (> 25% of parenchyma) and foci of moderate tubulitis (> 4 mononuclear cells/tubular cross section or group of 10 tubular cells).~Biopsy grade IB: Significant interstitial infiltration (> 25% of parenchyma) and foci of severe tubulitis (> 10 mononuclear cells/tubular cross section or group of 10 tubular cells).~Biopsy grade IIA: Mild to moderate intimal arteritis. Biopsy graded IIB: Severe intimal arteritis comprising > 25% of the lumenal area.~Biopsy graded III: Transmural (full vessel wall thickness) arteritis and/or arterial fibrinoid change and necrosis of medial smooth muscle cells (with accompanying lymphocytic inflammation)." (NCT01079143)
Timeframe: M6 and M12 post transplantation

,,,

Intervention	Participants (Number)
	Cellular AR - No	Cellular AR - Yes
Certican EMT-	46	14
Certican EMT+	30	6
Neoral EMT-	58	1
Neoral EMT+	38	1

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Treatment Failures

A treatment failure is defined as biopsy proven acute rejection (BPAR), a graft loss, a death or a loss to follow up. It was assessed between randomization and 6 and 12 months post-transplantation. (NCT01079143)
Timeframe: M6 and M12 post transplantation

,,,

Intervention	Number of Participants (Number)
	M6: Treatment Failure- No	M6: Treatment Failure- Yes	M12: Treatment Failure- No	M12: Treatment Failure- Yes	M6: BPAR - No	M6: BPAR -Yes	M12: BPAR - No	M12: BPAR - Yes	M6: Graft Loss - No	M6: Graft Loss - Yes	M12: Graft Loss - No	M12: Graft Loss - Yes	M6: Death - No	M6: Death - Yes	M12: Death - No	M12: Death - Yes	M6: Loss to follow-up - No	M6: Loss to follow-up - Yes	M12: Loss to follow-up - No	M12: Loss to follow-up - Yes
Certican EMT-	52	8	42	18	52	8	43	17	60	0	56	4	60	0	60	0	60	0	59	1
Certican EMT+	33	3	29	7	33	3	29	7	36	0	35	1	36	0	36	0	36	0	36	0
Neoral EMT-	59	0	56	3	59	0	56	3	59	0	59	0	59	0	59	0	59	0	59	0
Neoral EMT+	39	0	36	3	39	0	37	2	39	0	38	1	39	0	39	0	39	0	39	0

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Change in Percentage of Interstitial Fibrosis (IF) by Numerical Quantification

Percentage of IF measured by numerical quantification. The IF percentage was transposed in grade according to the following rule: grade 0 for an IF % ≤5%, grade I for an IF % ranging from >5% to < 25%, grade II for an IF % ranging from 25 to 50%, grade III for an IF % >50%. Interstitial graft fibrosis has been identified as the primary cause of graft loss following death with a functional graft [3-5]. (NCT01079143)
Timeframe: M3 and M12 post transplantation

,,,

Intervention	Percentage of IF (Mean)
	Percentage of IF at M3 (n=26,43,32,53)	Percentage of IF at M12 (n=24,42,32,53)	Change in Percentage of IF (n=24,42,32,53)
Certican EMT-	15.9	20.9	4.9
Certican EMT+	22.8	27.6	5.1
Neoral EMT-	17.8	20.4	2.7
Neoral EMT+	23.4	27.4	3.9

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Severity of BPAR

,,,

Intervention	Participants (Number)
	M6: Banff type Grade IA	M6: Banff type Grade IB	M6: Banff type Grade IIA	M6: Banff type Grade IIB	M6: Banff type Grade III	M12: Banff type Grade IA	M12: Banff type Grade IB	M12: Banff type Grade IIA	M12: Banff type Grade IIB	M12: Banff type Grade III
Certican EMT-	2	4	0	1	0	7	5	1	1	0
Certican EMT+	0	0	1	0	0	2	2	1	0	0
Neoral EMT-	0	0	0	0	0	0	0	1	0	0
Neoral EMT+	0	0	0	0	0	1	0	0	0	0

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Risk Factors of IF/TA Progression

"Composite factors regarding fibrosis progression at 12 months using a logistic regression model; the parameters initially considered concerned the demographic characteristics of both recipient and donor, transplantation characteristics, hypertension, diabetes, study treatments, immunosuppression, EMT, IF/TA, function at M3, the onset of acute rejection, the presence of anti-donor antibodies at M12, infections and BK virus viremia.~Arteriolar hyaline thickening is thickening of the walls of arterioles by the deposition of homogeneous pink hyaline material.~BPAR is biopsy proven acute rejection. TEM progression is the increase ≥ 1 of TEM score between Month 3 and Month 12" (NCT01079143)
Timeframe: M12 post transplantation

Intervention	Participants (Number)
	Donor Sex - Male	Donor Sex - Female	Donor Age - <=50 years	Donor Age - >50 years	Expanded Criteria donor: NO	Expanded Criteria Donor: Yes	Delayed graft function: No	Delayed graft function: Yes	CC at M3 <50 mL/min/1.73m^2	CC at M3 >=50 mL/min/1.73m^2 (n=67, 85)	Mesangial matrix increase at M3 - 0 (n=64, 85)	Mesangial matrix (mm) increase at M3: 1 (n=64, 85)	Mesangial matrix increase at M3: 2 (n=64, 85)	Interstitial fibrosis (ci) at M3: 0 (n=66, 85)	Interstitial fibrosis (ci) at M3: 1 (n=66, 85)	Interstitial fibrosis (ci) at M3: 2 (n=66, 85)	Arteriolar hyaline thickening (ah) at M3: 0	Arteriolar hyaline thickening (ah) at M3: 1	Arteriolar hyaline thickening (ah) at M3: 2	Arteriolar hyaline thickening (ah) at M3: 3	BPAR - No	BPAR - Yes	TEM Progression fron M3-M12: No (n=67, 83)	TEM Progression fron M3-M12: Yes (n=67, 83)	TEM Progression fron M3-M12: Missing (n=67, 83)
No- No Fibrosis Progression	48	38	48	38	63	23	76	10	35	50	84	1	0	55	27	3	56	21	8	1	79	7	57	26	3
Yes- Fibrosis Progression	45	22	28	39	40	27	52	15	40	27	59	2	3	52	14	0	36	15	10	6	55	12	26	41	0

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Plasma Concentration of Lenalidomide

(NCT01088048)
Timeframe: Predose, 1.5 hours postdose at Week 1 and predose at Week 5

Intervention	ng/mL (Mean)
	Pre-dose (Week 1)	1.5 hr post-dose (Week 1)	Pre-dose (Week 5)
Lenalidomide (Cohort 7a, 7b, 7c)	NA	51.6	NA

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Plasma Concentration of Everolimus

(NCT01088048)
Timeframe: Predose, 1.5 hours postdose at Weeks 0 and 4

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	1.5 hr post-dose (Week 0)	Pre-dose (Week 4)	1.5 hr post-dose (Week 4)
Everolimus (Cohort 5a)	NA	93.0	3.0	56.3

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Plasma Concentration of Bendamustine

(NCT01088048)
Timeframe: Predose, 0.25, 0.5, 0.75, 1.0, 1.25, 1.5, 2.0, 3.0, 4.0, 5.0, 6.0 hours postdose at Week 0

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	0.25 hr post-dose (Week 0)	0.5 hr post-dose (Week 0)	0.75 hr post-dose (Week 0)	1.0 hr post-dose (Week 0)	1.25 hr post-dose (Week 0)	1.5 hr post-dose (Week 0)	2.0 hr post-dose (Week 0)	3.0 hr post-dose (Week 0)	4.0 hr post-dose (Week 0)	5.0 hr post-dose (Week 0)	6.0 hr post-dose (Week 0)
Bendamustine (Cohorts 1b, 2b, 3a, 3b, 3f, 3g, 4b, 5c)	NA	3484.1	4694.7	3433.2	2847.2	1916.4	1211.2	514.0	463.4	78.5	15.3	4.4

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Toxicity of Administration of IDELA

Percentage of participants experiencing toxicities of administration of IDELA were measured according to the Common Terminology Criteria for Adverse Events v4.02 (NCT01088048)
Timeframe: First dose date up to 5 years

Intervention	percentage of participants (Number)
Idelalisib + Rituximab	100.0
Idelalisib + Bendamustine	100.0
Idelalisib + Everolimus	100.0
Idelalisib + Bortezomib	83.33
Idelalisib + Rituximab + Bendamustine	100.0
Idelalisib + Ofatumumab	100.0
Idelalisib + Fludarabine	100.0
Idelalisib + Chlorambucil	100.0
Idelalisib + Rituximab + Chlorambucil	100.0
Idelalisib + Rituximab + Lenalidomide	100.0

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Time to Response

Time to response (TTR) was defined as the interval from the start of study drug to the first documentation of CR or PR. (NCT01088048)
Timeframe: Up to 5 years

Intervention	months (Median)
Idelalisib + Rituximab	1.9
Idelalisib + Bendamustine	1.9
Idelalisib + Everolimus	1.9
Idelalisib + Bortezomib	1.9
Idelalisib + Rituximab + Bendamustine	1.9
Idelalisib + Ofatumumab	1.9
Idelalisib + Fludarabine	1.9
Idelalisib + Chlorambucil	1.9
Idelalisib + Rituximab + Chlorambucil	1.9
Idelalisib + Rituximab + Lenalidomide	3.0

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Progression-free Survival

"Progression free survival (PFS) was defined as the interval from the start of study drug to the earlier of the first documentation of disease progression or death from any cause.~The response definitions were based on the following standard criteria established for each indication:~CLL: International Workshop on chronic lymphocytic leukemia (IWCLL), 2008~iNHL & MCL: Cheson, 2007" (NCT01088048)
Timeframe: Up to 5 years

Intervention	months (Median)
Idelalisib + Rituximab	NA
Idelalisib + Bendamustine	NA
Idelalisib + Everolimus	4.3
Idelalisib + Bortezomib	8.1
Idelalisib + Rituximab + Bendamustine	NA
Idelalisib + Ofatumumab	NA
Idelalisib + Fludarabine	NA
Idelalisib + Chlorambucil	NA
Idelalisib + Rituximab + Chlorambucil	NA
Idelalisib + Rituximab + Lenalidomide	NA

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Overall Survival

Overall Survival (OS) was defined as the interval from the start of study drug to death from any cause. (NCT01088048)
Timeframe: Up to 5 years

Intervention	months (Median)
Idelalisib + Rituximab	NA
Idelalisib + Bendamustine	NA
Idelalisib + Everolimus	NA
Idelalisib + Bortezomib	NA
Idelalisib + Rituximab + Bendamustine	NA
Idelalisib + Ofatumumab	NA
Idelalisib + Fludarabine	NA
Idelalisib + Chlorambucil	NA
Idelalisib + Rituximab + Chlorambucil	NA
Idelalisib + Rituximab + Lenalidomide	NA

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Overall Response Rate

"Overall Response Rate (ORR) was defined as the percentage of participants achieving a complete response (CR) or partial response (PR).~The response definitions were based on the following standard criteria established for each indication:~CLL: International Workshop on chronic lymphocytic leukemia (IWCLL),2008~iNHL & MCL: Cheson, 2007" (NCT01088048)
Timeframe: Up to 5 years

Intervention	percentage of participants (Number)
Idelalisib + Rituximab	78.4
Idelalisib + Bendamustine	84.3
Idelalisib + Everolimus	44.4
Idelalisib + Bortezomib	61.1
Idelalisib + Rituximab + Bendamustine	81.8
Idelalisib + Ofatumumab	71.4
Idelalisib + Fludarabine	91.7
Idelalisib + Chlorambucil	66.7
Idelalisib + Rituximab + Chlorambucil	93.3
Idelalisib + Rituximab + Lenalidomide	71.4

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Duration of Response

Duration of response (DOR) was defined as the interval from the first documentation of CR or PR to the earlier of the first documentation of disease progression or death from any cause. (NCT01088048)
Timeframe: Up to 5 years

Intervention	months (Median)
Idelalisib + Rituximab	NA
Idelalisib + Bendamustine	NA
Idelalisib + Everolimus	5.6
Idelalisib + Bortezomib	9.3
Idelalisib + Rituximab + Bendamustine	NA
Idelalisib + Ofatumumab	NA
Idelalisib + Fludarabine	NA
Idelalisib + Chlorambucil	NA
Idelalisib + Rituximab + Chlorambucil	NA
Idelalisib + Rituximab + Lenalidomide	NA

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Duration of Exposure to IDELA

Duration of exposure to IDELA was summarized using descriptive statistics. (NCT01088048)
Timeframe: First dose date up to 12 months

Intervention	months (Mean)
Idelalisib + Rituximab	8.1
Idelalisib + Bendamustine	7.6
Idelalisib + Everolimus	4.2
Idelalisib + Bortezomib	5.1
Idelalisib + Rituximab + Bendamustine	8.0
Idelalisib + Ofatumumab	8.3
Idelalisib + Fludarabine	8.9
Idelalisib + Chlorambucil	8.8
Idelalisib + Rituximab + Chlorambucil	8.7
Idelalisib + Rituximab + Lenalidomide	7.7

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Plasma Concentration of IDELA (Cohort 6)

(NCT01088048)
Timeframe: Predose, 1.5 hours postdose at Weeks 0, 4, 12 and 24

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	1.5 hr post-dose (Week 0)	Pre-dose (Week 4)	1.5 hr post-dose (Week 4)	Pre-dose (Week 12)	1.5 hr post-dose (Week 12)	Pre-dose (Week 24)	1.5 hr post-dose (Week 24)
Idelalisib 150 mg (Cohort 6)	0.0	1930.7	530.8	1869.8	677.9	1733.0	346.8	1710.7

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Plasma Concentration of IDELA (Cohort 7)

(NCT01088048)
Timeframe: Predose, 1.5 hours postdose at Weeks 0, 5 and 13

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	1.5 hr post-dose (Week 0)	Pre-dose (Week 5)	1.5 hr post-dose (Week 5)	Pre-dose (Week 13)	1.5 hr post-dose (Week 13)
Idelalisib 150 mg (Cohort 7)	NA	1603.1	20.7	1621.3	354.8	592.7

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Sub-study: Plasma Concentration of IDELA (Cohorts 1-4)

(NCT01088048)
Timeframe: pre dose and 0.5, 1, 1.5, 2.0, 3.0, 4.0, and 6.0 hours post dose

Intervention	ng/mL (Mean)
	Pre-dose	0.5 hr post-dose	1.0 hr post-dose	1.5 hr post-dose	2.0 hr post-dose	3.0 hr post-dose	4.0 hr post-dose	6.0 hr post-dose
Idelalisib 100 mg (Cohort 1a, 1b)	1.5	437.6	1022.4	1264.7	1282.7	1001.0	788.4	523.7
Idelalisib 150 mg (Cohorts 2a, 2b, 3a, 3c, 3d, 3e, 3f, 3g, 4a, 4b)	0.0	1222.1	1723.1	1599.2	1646.2	1238.5	879.8	489.3

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Plasma Concentration of IDELA (Cohort 4)

(NCT01088048)
Timeframe: Predose at Week 0; predose, 0.5, 1.0, 1.5, 2.0, 3.0, 4.0, 6.0 hours postdose at Week 4; predose, 1.5 hours postdose at Week 12; and predose, 1.5 hours postdose at Week 24

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	Pre-dose (Week 4)	0.5 hr post-dose (Week 4)	1.0 hr post-dose (Week 4)	1.5 hr post-dose (Week 4)	2.0 hr post-dose (Week 4)	3.0 hr post-dose (Week 4)	4.0 hr post-dose (Week 4)	6.0 hr post-dose (Week 4)	Pre-dose (Week 12)	1.5 hr post-dose (Week 12)	Pre-dose (Week 24)	1.5 hr post-dose (Week 24)
Idelalisib 150 mg (Cohort 4)	0.0	0.0	1119.5	994.5	1758.2	737.0	605.0	547.0	524.0	401.9	2018.2	752.5	2251.1

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Plasma Concentration of IDELA (Cohort 1, Cohorts 2 and 3, Cohort 5)

(NCT01088048)
Timeframe: Predose, 0.5, 1.0, 1.5, 2.0, 3.0, 4.0, 6.0 hours postdose at Week 0; predose, 1.5 hours postdose at Weeks 4, 12, and 24

Intervention	ng/mL (Mean)
	Pre-dose (Week 0)	0.5 hr post-dose (Week 0)	1.0 hr post-dose (Week 0)	1.5 hr post-dose (Week 0)	2.0 hr post-dose (Week 0)	3.0 hr post-dose (Week 0)	4.0 hr post-dose (Week 0)	6.0 hr post-dose (Week 0)	Pre-dose (Week 4)	1.5 hr post-dose (Week 4)	Pre-dose (Week 12)	1.5 hr post-dose (Week 12)	Pre-dose (Week 24)	1.5 hr post-dose (Week 24)
Idelalisib 100 mg (Cohort 1)	0.4	437.6	1022.4	1434.0	1282.7	1001.0	788.4	523.7	416.5	1297.2	361.9	1309.5	369.9	1061.6
Idelalisib 150 mg (Cohort 5)	0.0	1380.0	1600.0	1564.7	1400.0	1170.0	795.0	517.0	408.0	1877.9	433.9	1426.8	549.1	885.6
Idelalisib 150 mg (Cohorts 2 and 3)	68.8	1231.4	1789.3	2017.3	1732.8	1296.1	910.0	486.0	364.1	1808.1	351.4	1883.0	419.7	1840.1

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Percentage of Participants With Stable Disease (SD)

Percentage of participants with stable disease during treatment is defined as stable disease [SD] by RECIST 1.1 criteria as calculated in each treatment arm. Stable Disease (SD) is defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study. (NCT01108445)
Timeframe: Baseline to 36 months

Intervention	percentage of participants (Number)
RAD001	59.6
Sunitinib	64.7

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Percentage of Participants With Adverse Events

To assess toxicities associated with everolimus or sunitinib using NCI CTC version 4.0 criteria (NCT01108445)
Timeframe: 24 months

Intervention	percentage of participants (Number)
RAD001	63.2
Sunitinib	80.4

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Overall Response Rate

Defined as complete response [CR] and partial response [PR] by RECIST 1.1 criteria in each treatment arm.Overall Response Rate (ORR) = CR + PR. Complete Response (CR) is disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm. Partial Response (PR) is at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. (NCT01108445)
Timeframe: 24 months

Intervention	percentage of participants (Number)
RAD001	8.8
Sunitinib	17.6

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Median OS

To compare the median OS in each treatment arm. (NCT01108445)
Timeframe: Up to 40 months

Intervention	months (Median)
RAD001	13.2
Sunitinib	31.5

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12 Week Clinical Benefit Rate as Percentage

Rate of complete or partial response or stable disease by the RECIST 1.1 criteria lasting ≥ 12 weeks prior to progression. Benefit rate is defined as complete response [CR] and partial response [PR] and stable disease [SD] by RECIST 1.1 criteria in each treatment arm. Benefit rate = CR + PR + SD. Complete Response (CR) is disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm. Partial Response (PR) is 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 PD, taking as reference the smallest sum diameters while on study. (NCT01108445)
Timeframe: Baseline to 36 months

Intervention	percentage of particpants (Number)
RAD001	24.6
Sunitinib	41.2

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Median Duration of Response (CR, PR, and SD)

To compare the median duration of response (CR, PR, and SD) in each treatment arm. According to RECIST 1.1, Complete Response (CR) is disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm. Partial Response (PR) is 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 PD, taking as reference the smallest sum diameters while on study. (NCT01108445)
Timeframe: 24 months

Intervention	months (Median)
RAD001	3.9
Sunitinib	8.3

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Change in Quality-of-life

To compare change in quality-of-life, as measured by the FACT-KSI scale at baseline and end of treatment per subject in each treatment arm. Functional Assessment of Cancer Therapy Kidney Symptom Index. FKSI is a questionnaire for FACT-Kidney Symptom Index used to assess QoL/participant-reported outcomes for participants diagnosed with renal cell cancer. The FKSI contained 15 questions each ranging from 0 (not at all) to 4 (very much) so that FKSI ranged between 0-60 where higher scores reflects better functioning and fewer symptoms. (NCT01108445)
Timeframe: baseline, up to 40 months

Intervention	units on a scale (Mean)
RAD001	-6.6
Sunitinib	-6.4

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Change in Quality-of-life

To compare change in quality-of-life, as measured by the FACT-KSI scale at baseline and cycle 6 day1 per subject in each treatment arm. Functional Assessment of Cancer Therapy Kidney Symptom Index. FKSI is a questionnaire for FACT-Kidney Symptom Index used to assess QoL/participant-reported outcomes for participants diagnosed with renal cell cancer. The FKSI contained 15 questions each ranging from 0 (not at all) to 4 (very much) so that FKSI ranged between 0-60 where higher scores reflects better functioning and fewer symptoms. (NCT01108445)
Timeframe: baseline, cycle 6 day 1

Intervention	units on a scale (Mean)
RAD001	-4.4
Sunitinib	-2.1

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Progression Free Survival Rates

6-, 12-, and 24-month rates of PFS in each arm will be compared for each treatment arm. Progressive disease is defined as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. 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). (NCT01108445)
Timeframe: 6, 12 and 24 months

Intervention	percentage of participants (Number)
	6 Months	12 Months	24 Months
RAD001	40.3	17.0	9.3
Sunitinib	55.0	37.7	22.8

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PFS Expressed in Months

Progression-free survival (PFS) expressed in months as compared to an historic control (interferon-treated clear cell RCC control arm from the sunitinib phase III study). Progressive disease is defined as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. 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). (NCT01108445)
Timeframe: 24 months

Intervention	Months (Median)
RAD001	5.6
Sunitinib	8.3

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Best Tumor Shrinkage as a Percentile in Each Arm

To compare the best tumor shrinkage as a percentile in each treatment arm. The percentile change at each follow up visit is calculated by measuring the percentage change in the Sum of lesion measurement from baseline. The best tumor shrinkage is lowest percentile change. A decrease is indicated by a negative percentage. (NCT01108445)
Timeframe: 24 months

Intervention	percentile decrease (Median)
RAD001	-2.1
Sunitinib	-10.7

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Time-to-new Metastatic Disease in Each Treatment Arm

To compare the time-to-new metastatic disease in each treatment arm, defined from the date of first study agent administration to the onset of a new evaluable site of disease, excluding the primary site and all sites documented at baseline (NCT01108445)
Timeframe: 36 months

Intervention	months (Median)
RAD001	19.4
Sunitinib	36

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Anti-tumor Activity as Measured by Median Progression Free Survival Time

The primary objective will be to compare the anti-tumor activity of everolimus and sunitinib in subjects with mRCC with non-clear cell pathology, as measured by progression-free survival (PFS) following treatment initiation according to RECIST 1.1 criteria. Progressive disease is defined as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. 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). (NCT01108445)
Timeframe: 24 Months

Intervention	Months (Median)
RAD001	5.6
Sunitinib	8.3

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Overall Survival Rates

To compare overall survival (OS) rates at 6, 12, 24, and 36 months and over time in each treatment arm. (NCT01108445)
Timeframe: 6, 12, 24, 36 months

Intervention	percentage probability (Number)
	6 months	12 months	24 months	36 months
RAD001	83.5	57.7	40.8	35.7
Sunitinib	85.4	74.7	51.3	46.2

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Change in Quality-of-life

To compare change in quality-of-life, as measured by the FACT-KSI scale at baseline and cycle 3 day 1 per subject in each treatment arm. Functional Assessment of Cancer Therapy Kidney Symptom Index. FKSI is a questionnaire for FACT-Kidney Symptom Index used to assess QoL/participant-reported outcomes for participants diagnosed with renal cell cancer. The FKSI contained 15 questions each ranging from 0 (not at all) to 4 (very much) so that FKSI ranged between 0-60 where higher scores reflects better functioning and fewer symptoms. (NCT01108445)
Timeframe: baseline, cycle 3 day 1

Intervention	units on a scale (Mean)
RAD001	-3.5
Sunitinib	-0.9

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Site of Progression: Distant

Number of patients with distant progression (NCT01111058)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Everolimus (RAD001)	2
Placebo	2

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Site of Progression: Local-regional

Number of patients with local-regional progression (NCT01111058)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Everolimus (RAD001)	2
Placebo	5

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Site of Progression: Unknown

Number of patients with unknown site of progression (NCT01111058)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Everolimus (RAD001)	1
Placebo	1

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2 Year Progression Free Survival Rate

Time to disease progression or death from any cause--2 year rate (NCT01111058)
Timeframe: 2 years

Intervention	percentage of patients (Number)
Everolimus (RAD001)	56.1
Placebo	55.9

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Number of Participants With Toxicity

Adverse event rate, any type, any grade regardless of attribution (NCT01111058)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Everolimus (RAD001)	25
Placebo	16

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Estimated Glomerular Filtration Rate (eGFR)

Assessment of renal function by comparing change from randomization to Month 12 in eGFR (MDRD4) between treatment arms (Full analysis set). Renal function was assessed by estimated Glomerular Filtration Rate (eGFR) using the Modification of Diet in Renal Disease (MDRD) formula. MDRD formula: GFR [mL/min/1.73m˄2] = 186.3*(C˄-1.154)*(A˄-0.203)*G*R. DEFINITIONS: C = serum concentration of creatinine [mg/dL]; A = age [years]; G = 0.742 when gender is female, otherwise G = 1; R = 1.21 when race is black, otherwise R = 1 (NCT01114529)
Timeframe: Month 12

Intervention	mL/min/1.73m^2 (Mean)
Everolimus	64.1
Standard CNI (Tac)	61.5
Standard CNI (CsA)	58.4

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Incidence of Composite Efficacy Endpoint for Each Arm at Month 12 and Month 24

Efficacy failure rate used the composite endpoint of: (1) treated biopsy-proven acute rejection (BPAR)*, (2) graft loss**, or (3) death . *A treated BPAR was defined as a biopsy graded IA, IB, IIA, IIB, or III and which was treated with anti-rejection therapy. **Graft loss is defined as when the allograft was presumed lost on the day the participant started dialysis and was not able to subsequently be removed from dialysis or re-transplanted. (NCT01114529)
Timeframe: at 12 months and month 24 post-transplantation

Intervention	Number of incidence (Number)
	Month 12	Month 24
Everolimus	21	27
Standard CNI (CsA)	8	8
Standard CNI (Tac)	4	8

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Comparison of Incidence Rates of Efficacy Endpoints Between Treatment Arms (Full Analysis Set - 24 Month Analysis)

(treated BPAR ≥ IB, graft loss or death)A comparison of the incidence rates for the individual components of the composite efficacy endpoint between treatment arms (NCT01114529)
Timeframe: at 24 months post-transplantation

Intervention	Number of incidence (Number)
	Composite failure: tBPAR>=IB, graft loss, death	Composite tBPAR>=IB, graft loss, death, loss f/u	Composite of graft loss or Death	tBPAR>=IB	Graft loss	Death	Suspected Acute rejection	Subclinical Acute rejection	Acute rejection (AR)	Treated Acute rejection (tAR)	biopsy proven acute rejection (BPAR)	treated biopsy proven acute rejection (tBPAR)	tBPAR=IA	tBPAR=IB	tBPAR=IIA	tBPAR=IIB	tBPAR=III	Antibody tBPAR	Antibody mediated rejection (AMR)
Everolimus	27	35	10	18	4	8	61	0	52	40	37	32	16	14	3	2	0	2	16
Standard CNI (CsA)	8	15	4	5	2	4	19	0	15	14	13	13	8	5	1	0	0	1	3
Standard CNI (Tac)	8	14	6	3	2	5	27	0	14	9	8	7	3	3	0	0	0	1	4

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Change in Left Ventricular Mass Index (LVMi) From Randomization to Month 12 and Month 24

Evolution of left ventricular mass and hypertrophy were evaluated by left ventricular mass index (LVMi) assessed by echocardiography. LVMi is derived using a standard formula from dimensional measurements on the echocardiogram. Analysis of covariance was applied with treatment, center (as a random effect), and donor type as factors and LVMi at Randomization as covariate. (NCT01114529)
Timeframe: Randomization, Month 12 and Month 24

Intervention	g/m^2.7 (Mean)
	Randomization	Month 12	Month 24
Everolimus	50.30	49.95	46.66
Standard CNI (CsA)	51.13	50.96	47.91
Standard CNI (Tac)	51.08	48.98	45.63

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Percentage of Participants Achieving Complete Response (CR) or Partial Response (PR) [Response Rate (RR)]

Response was determined using Response Evaluation Criteria In Solid Tumors (RECIST v1.1) criteria. CR was defined as the disappearance of all target and non-target lesions and any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 millimeters (mm) and normalization of tumor marker level of non-target lesions; PR was defined as at least a 30% decrease in sum of longest diameter of target lesions. (NCT01115803)
Timeframe: Baseline to disease progression or death or up to 6 cycles of 28 days

Intervention	percentage of participants (Number)
Arm A - 50 mg LY2584702 QD + 150 mg Erlotinib QD	0
Arm A - 50 mg LY2584702 (BID) + 150 mg Erlotinib QD	0
Arm A - 100 mg LY2584702 BID + 150 mg Erlotinib QD	0
Arm A - 75 mg LY2584702 BID + 150 mg Erlotinib QD	0
Arm B - 50 mg LY2584702 QD + 10 mg Everolimus QD	0
Arm B - 100 mg LY2584702 QD + 10 mg Everolimus QD	0
Arm B - 50 mg LY2584702 BID + 10 mg Everolimus QD	0

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Number of Participants With Complete Response (CR), Partial Response (PR) or Stable Disease (SD) [Best Overall Response (BOR) (CR+PR+SD)]

BOR was determined using Response Evaluation Criteria In Solid Tumors (RECIST v1.1) criteria. CR was defined as the disappearance of all target and non-target lesions and any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 millimeters (mm) and normalization of tumor marker level of non-target lesions; PR was defined as at least a 30% decrease in sum of longest diameter (LD) of target lesions; Progressive Disease (PD) was defined as at least 20% increase in sum of LD of target lesions and minimum 5 mm increase over nadir. SD was defined as small changes that did not meet above criteria. (NCT01115803)
Timeframe: Baseline up to 112 Days

Intervention	Participants (Count of Participants)
Arm A - 50 mg LY2584702 QD + 150 mg Erlotinib QD	1
Arm A - 50 mg LY2584702 BID + 150 mg Erlotinib QD	1
Arm A - 100 mg LY2584702 BID + 150 mg Erlotinib QD	1
Arm A - 75 mg LY2584702 BID + 150 mg Erlotinib QD	1
Arm B - 50 mg LY2584702 QD + 10 mg Everolimus QD	0
Arm B - 100 mg LY2584702 QD + 10 mg Everolimus QD	2
Arm B - 50 mg LY2584702 BID + 10 mg Everolimus QD	2

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Number of Participants Who Died Due to Progressive Disease Within 30 Days of Study Drug Discontinuation

(NCT01115803)
Timeframe: Within 30 days of study drug discontinuation

Intervention	Participants (Count of Participants)
Arm A - 50 mg LY2584702 QD + 150 mg Erlotinib QD	0
Arm A - 50 mg LY2584702 BID + 150 mg Erlotinib QD	0
Arm A - 100 mg LY2584702 BID + 150 mg Erlotinib QD	0
Arm A - 75 mg LY2584702 BID + 150 mg Erlotinib QD	0
Arm B - 50 mg LY2584702 QD + 10 mg Everolimus QD	1
Arm B - 100 mg LY2584702 QD + 10 mg Everolimus QD	0
Arm B - 50 mg LY2584702 BID + 10 mg Everolimus QD	0

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Pharmacokinetics, Maximum Observed Plasma Concentration (Cmax) of LY2584702

(NCT01115803)
Timeframe: Cycle 1 Day 1 (C1 D1): predose, 0.5, 1, 2, 3, 5, 8 hours postdose and Cycle 1 Day 8 (C1 D8): predose, 0.5, 1, 2, 3, 5, and 8 hours postdose of 28-day cycle

,,,,,,

Intervention	nanograms per milliliter (ng/mL) (Geometric Mean)
	C1 D1, single dose	C1 D8, steady state
Arm A - 100 mg LY2584702 BID + 150 mg Erlotinib QD	2421.64	2709.61
Arm A - 50 mg LY2584702 BID + 150 mg Erlotinib QD	999.54	1636.71
Arm A - 50 mg LY2584702 QD + 150 mg Erlotinib QD	918.24	1125.46
Arm A - 75 mg LY2584702 BID + 150 mg Erlotinib QD	1768.59	1967.04
Arm B - 100 mg LY2584702 QD + 10 mg Everolimus QD	2286.22	2260.71
Arm B - 50 mg LY2584702 BID + 10 mg Everolimus QD	1569.24	2109.62
Arm B - 50 mg LY2584702 QD + 10 mg Everolimus QD	1192.46	1169.95

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Pharmacokinetics, Area Under the Concentration Time Curve (AUC)

AUC from time 0 to 8 hours (AUC0-8) and AUC from time 0 to infinity (AUC0-∞). (NCT01115803)
Timeframe: Cycle 1 Days 1 (C1 D1) and Cycle 1 Day 8 (C1 D8) of 28-day cycle

,,,,,,

Intervention	nanogramshours per milliliter (ngh/mL) (Geometric Mean)
	AUC0-8, D1, single dose	AUC0-8, D8, steady state	AUC0-∞, D1, single dose
Arm A - 100 mg LY2584702 BID + 150 mg Erlotinib QD	8610.54	15225.08	20813.83
Arm A - 50 mg LY2584702 BID + 150 mg Erlotinib QD	4308.98	7948.43	7627.50
Arm A - 50 mg LY2584702 QD + 150 mg Erlotinib QD	4436.60	5395.96	8699.54
Arm A - 75 mg LY2584702 BID + 150 mg Erlotinib QD	8091.93	13959.74	16254.07
Arm B - 100 mg LY2584702 QD + 10 mg Everolimus QD	11410.18	11327.33	22343.07
Arm B - 50 mg LY2584702 BID + 10 mg Everolimus QD	6097.44	10527.68	8764.13
Arm B - 50 mg LY2584702 QD + 10 mg Everolimus QD	5699.856	5460.80	11386.03

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Clinically Significant Effects (Number of Participants With Adverse Events)

Clinically significant events were defined as serious adverse events (SAEs) and other non-SAEs regardless of causality. A summary of serious and other non SAEs regardless of causality is located in the Reported Adverse Event module. (NCT01115803)
Timeframe: Baseline up to 7 months

,,,,,,

Intervention	Participants (Count of Participants)
	SAEs	Non-SAEs
Arm A - 100 mg LY2584702 BID + 150 mg Erlotinib QD	2	3
Arm A - 50 mg LY2584702 BID + 150 mg Erlotinib QD	2	5
Arm A - 50 mg LY2584702 QD + 150 mg Erlotinib QD	1	4
Arm A - 75 mg LY2584702 BID + 150 mg Erlotinib QD	3	5
Arm B - 100 mg LY2584702 QD + 10 mg Everolimus QD	2	3
Arm B - 50 mg LY2584702 BID + 10 mg Everolimus QD	2	6
Arm B - 50 mg LY2584702 QD + 10 mg Everolimus QD	2	3

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Recommended Dose for Phase 2 Studies

The recommended dose for the Phase 2 (Dose Confirmation Phase) study was determined by safety assessment. Doses were escalated following the assessment for toxicity based on Common Terminology Criteria for Adverse Events (CTCAE v4.0). Any adverse events (AE) that were possibly related to LY2584702 were considered toxicities. The Phase 2 dose of LY2584702 was not determined due to unacceptable toxicities of LY2584702 in combination with erlotinib or everolimus in Phase 1 of the study. (NCT01115803)
Timeframe: Baseline up to 6 cycles of 28 days

Intervention	milligrams (mg) (Number)
LY2584702 + Erlotinib	NA
LY2584702+Everolimus	NA

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PTEN Mutation Rate [Phase II]

The PTEN mutation rate is the percentage of patients with PTEN mutation identified in pre-therapy and post-therapy bone marrow samples per established methods. (NCT01125293)
Timeframe: Samples were collected pre-therapy before the beginning therapy (baseline) and post-therapy after finishing the 6th treatment cycle (168 days).

Intervention	percentage of participants (Number)
	MYD88/L265P mutation	CXCR4/C1013G mutation
Phase II	80	5

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Very-good-partial-response-or-better Rate [Phase II]

"Very-good-partial-response-or-better rate is the percentage of participants with complete response (CR) or very good partial response (VGPR) on to the combination of everolimus/bortezomib/rituximab. The combination regimen was received for up to 6 cycles.~CR:~Absence of serum monoclonal IgM protein by immunofixation~Normal serum IgM level~Complete resolution of extramedullary disease, i.e., lymphadenopathy and splenomegaly if present at baseline~Morphologically normal bone marrow aspirate and trephine biopsy~VGPR:~Monoclonal IgM protein is detectable ≥90% reduction in serum IgM level from baseline*~Complete resolution of extramedullary disease, i.e." (NCT01125293)
Timeframe: Up to 6 cycles (Day 168)

Intervention	percentage of participants (Number)
Phase II	4.3

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Treatment-Emergent Sensory Neuropathy Rate [Phase I]

Percentage of participants experiencing Grade 1 - Grade 3 treatment-emergent peripheral (sensory) neuropathy events based on CTCAEv3 as reported on case report forms for phase I participants. (NCT01125293)
Timeframe: Adverse events were assessed each cycle (ever 28 days) for 6 cycles then every 3 months on maintenance. Duration of therapy for the Phase I study up to 41 months.

Intervention	percentage of participants (Number)
Phase I Stage A Level 1	33
Phase I Stage A Level 2	33
Phase I Stage B Level 1	100
Phase I Stage B Level 2	67
Phase I Dose Expansion	50
Phase II	48

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Phase II Duration of Response (DoR)

"The DoR is defined as the elapsed time from date when the measurement criteria are first met for a complete or partial response (whichever status is recorded first) until the date of first observation of objective disease progression. Analysis of DoR will be as follows:~For responding patients who die without objective PD (including death from study disease), DoR will be censored at the date of the last objective progression-free disease assessment.~For responding patients not known to have died as of the data cut-off date and who do not have objective PD, DoR will be censored at the date of the last objective progression-free disease assessment.~For responding patients who receive subsequent systemic anticancer therapy (after discontinuation from the study chemotherapy) prior to objectively determined disease progression, DoR will be censored at the date of the last objective progression-free disease assessment prior to post discontinuation therapy." (NCT01125293)
Timeframe: Patients were assessed for disease every cycle while on treatment (168 days) and every three months while on maintenance therapy. In long-term follow-up, disease was monitored every 3 months. Study cohort median (range) follow-up was 15 (1 - 23) months.

Intervention	months (Median)
Phase II	14

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Phase II Overall Response Rate

"Overall response rate is percentage of participants with complete (CR), very good partial (VGPR), partial (PR), or minimal response (MR) as best response during treatment.~CR:~No serum monoclonal IgM protein by immunofixation~Normal IgM level~Complete resolution of extramedullary disease, i.e., lymphadenopathy and splenomegaly if present at baseline~Morphologically normal bone marrow aspirate and trephine biopsy~VGPR:~Monoclonal IgM protein is detectable ≥90% reduction in IgM level from baseline~Complete resolution of extramedullary disease, i.e., lymphadenopathy/splenomegaly if present at baseline~No new signs/symptoms of active disease~PR:~Monoclonal IgM protein is detectable ≥50% but <90% reduction in IgM level from baseline~Reduction in extramedullary disease~No new signs/symptoms of active disease~MR:~Monoclonal IgM protein is detectable ≥25% but <50% reduction in IgM level from baseline~No new signs/symptoms of active disease" (NCT01125293)
Timeframe: Up to 6 cycles (Day 168)

Intervention	percentage of participants (Number)
Phase II	87

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2 Year Progression-free-survival [Phase II]

2-year progression free survival (PFS) is the probability of participants alive and progression free at 2 years from study entry estimated using Kaplan-Meier methods. PFS is defined as the time from enrollment to progressive disease (PD) or death. PD is defined as ≥25% increase in serum IgM level from lowest nadir and/or progression in clinical features attributable the disease. Patients alive without PD and not reporting use of non-protocol therapy prior to PD are censored at date of last objective progression-free disease assessment. Patients reporting use of non-protocol therapy prior to PD are censored at date of last objective progression-free disease assessment date prior to post-discontinuation therapy. (NCT01125293)
Timeframe: Patients were assessed for disease every cycle while on treatment (168 days) and every three months while on maintenance therapy. In long-term follow-up, disease was monitored every 3 months. Study cohort median (range) follow-up was 15 (1 - 23) months.

Intervention	percent probability of PFS (Number)
Phase II	28

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2-year Time-to-progression Probability (TTP) [Phase II]

2-year TTP probability is based on Kaplan-Meier methods. TTP is defined as time from enrollment to the date of progressive disease (PD). PD is defined as ≥25% increase in serum IgM level from lowest nadir and/or progression in clinical features attributable the disease. Patients without PD and not reporting use of non-protocol therapy prior to PD are censored at date of last objective progression-free disease assessment. Patients reporting use of non-protocol therapy prior to PD are censored at date of last objective progression-free disease assessment date prior to post-discontinuation therapy. (NCT01125293)
Timeframe: Patients were assessed for disease every cycle while on treatment (168 days) and every three months while on maintenance therapy. In long-term follow-up, disease was monitored every 3 months. Study cohort median (range) follow-up was 15 (1 - 23) months.

Intervention	percent probability of progression (Number)
Phase II	28

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Everolimus Dose Limiting Toxicity (DLT) [Phase I]

"The following qualify as dose limiting toxicities:~Grade 3 or greater non-hematologic toxicity, considered by the investigator to be related to study drugs.~Grade 4 hematologic toxicity defined as: thrombocytopenia with platelets <10,000 µ/L on more than one occasion despite transfusion support; grade 4 neutropenia occurring for more than 7 days and/or resulting in neutropenic fever with elevated temperature (defined as > 101 degrees F). Lymphopenia, a recognized side effect of bortezomib, is not considered a DLT.~Inability to receive Day 1 dose for Cycle 2 due to toxicity" (NCT01125293)
Timeframe: Assessed within the first cycle (28 days) of the study.

Intervention	participants (Number)
Phase I Stage A Level 1	0
Phase I Stage A Level 2	0
Phase I Stage B Level 1	0
Phase I Stage B Level 2	0

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Everolimus Maximum Tolerated Dose (MTD) Stage A [Phase I]

The MTD of Everolimus/Rituximab combination is determined by the number of patients who have dose limiting toxicity (DLT). See DLT primary outcome measure for definition. MTD is defined as the highest dose where <1/3 participants experience a DLT. If no DLT's are observed on Level 1, 3 subjects will be enrolled in the Level 2. If >1/3 subjects in a cohort have DLT, that dose will not be considered safe, with no escalation (MTD exceeded). If 1/3 subjects experience DLT, the cohort will be expanded to 6 subjects. If <2 subjects with a DLT among the expanded cohort of 6 evaluable subjects a cohort of 3 subjects will be enrolled in the next higher dose level. If 2 or more subjects with a DLT among the expanded cohort of 6 subjects, that dose level will not be considered safe, no escalation (MTD exceeded). If no DLT's are observed, then the MTD is not reached. The MTD was not reached with 0/3 participants experiencing a DLT in the highest dose level. Higher doses were not planned/tested. (NCT01125293)
Timeframe: Assessed within the first cycle (28 days) of the study.

Intervention	mg (Number)
Phase I Stage A Level 1 and 2	10

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Everolimus Maximum Tolerated Dose (MTD) Stage B [Phase I]

The MTD of Everolimus/Bortezomib/Rituximab combination is determined by the number of patients who have dose limiting toxicity (DLT). See DLT primary outcome measure for definition. MTD is defined as the highest dose where <1/3 participants experience a DLT. If no DLT's are observed on Level 1, 3 subjects will be enrolled in the Level 2. If >1/3 subjects in a cohort have DLT, that dose will not be considered safe, with no escalation (MTD exceeded). If 1/3 subjects experience DLT, the cohort will be expanded to 6 subjects. If <2 subjects with a DLT among the expanded cohort of 6 evaluable subjects a cohort of 3 subjects will be enrolled in the next higher dose level. If 2 or more subjects with a DLT among the expanded cohort of 6 subjects, that dose level will not be considered safe, no escalation (MTD exceeded).If no DLT's observed, then the MTD is not reached. The MTD was not reached with 0/3 participants experiencing a DLT in the highest level. Higher doses were not planned/tested. (NCT01125293)
Timeframe: Assessed within the first cycle (28 days) of the study.

Intervention	mg (Number)
Phase I Stage B Level 1 & 2 and Dose Expansion	10

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Median Progression-free Survival Time

Progression-free survival time is defined as the time from first day of treatment to the first date of disease progression or death as a result of any cause. Progression was assessed every 2 cycles of treatment (6 weeks) by CT, CT/PET, or MRI. Progression is defined using RECIST 1.0, 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. (NCT01127763)
Timeframe: up to 1 year

Intervention	months (Median)
RAD001+Carboplatin	3

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Toxicity Profile-Non Hematological

Reported as percentage of patients who experienced grade 3 and higher non-hematological AEs related to the study drugs. (NCT01127763)
Timeframe: treatment period (up to 1 year) plus 30 days off treatment

Intervention	percentage of patients (Number)
	Nausea	Vomiting	Dehydration	Mucositis	Hypersensitivity
RAD001+Carboplatin (All Patients)	4	4	4	4	4

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Toxicity Profile-Hematological

Reported as percentage of patients who experienced grade 3 and higher hematological adverse events (AEs) related to the study drugs. (NCT01127763)
Timeframe: treatment period (up to 1 year) plus 30 days off treatment

Intervention	percentage of patients (Number)
	Anemia	Thrombocytopenia	Leukopenia	Neutropenia
RAD001+Carboplatin (All Patients)	4	28	4	12
RAD001+Carboplatin (AUC 4)	5	11	0	5
RAD001+Carboplatin (AUC 6 and 5)	0	71	14	29

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Clinical Benefit Rate (Complete Response, Partial Response, and Stable Disease That Lasts More Than 6 Months)

Clinical benefit rate is defined as the number of patients with complete response (CR), partial response (PR), or stable disease (SD) that lasts at least 6 months. Response was assessed every 2 cycles of treatment (6 weeks) by computed tomography (CT), CT/positron emission tomography (PET), or magnetic resonance imaging (MRI). Overall response evaluation is based on Response Evaluation Criteria In Solid Tumors 1.0 (RECIST 1.0). Per RECIST 1.0 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; Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. (NCT01127763)
Timeframe: up to 1 year

Intervention	percentage of patients (Number)
RAD001+Carboplatin	36

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Tumor Responses

Change in tumor size (sum of longest diameters of target lesions) after two cycles of induction therapy, expressed as log of ratio of post-treatment to baseline measure. (NCT01133678)
Timeframe: Baseline and 2 months

Intervention	dimensionless (log ratio) (Mean)
Everolimus	-0.609
Placebo	-0.796

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Summary of Plasma Concentrations of Lenvatinib for Sparse Pharmacokinetic (PK) Sampling for Phase 1b and Phase 2

Blood samples were collected during the Randomization Phase. Most participants had 6 samples taken over 3 cycles of treatment (sparse sampling - 2 samples taken per cycle, one at predose and one at 2 to 8 hours postdose). Plasma concentrations of lenvatinib were measured and concentration data were summarized. The summary statistics at time points with one or more below the limit of quantitation (BLQ) values were calculated by assigning zero for each BLQ value. (NCT01136733)
Timeframe: Cycle 1 (Day 1), Cycle 2 (Day 1), Cycle 3 (Day 1)

Intervention	ng/mL (Geometric Mean)
Cycle 1, Day 1 (0 Hours)	5.6
Cycle 1, Day 1 (2-8 Hours)	197
Cycle 2, Day 1 (0 Hours)	66.9
Cycle 2, Day 1 (2-8 Hours)	237
Cycle 3, Day 1 (0 Hours)	37.0
Cycle 3, Day 1 (2-8 Hours)	180

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Maximum Concentration of Everolimus (Cmax) in Blood When Administered Alone or in Combination With Lenvatinib

Cmax for everolimus was defined as the maximum observed concentration of everolimus in blood following administration of study treatment on Cycle 1 Day 15 and was obtained directly from the measured blood concentration-time curves. (NCT01136733)
Timeframe: Phase 2: Cycle 1 Day 15

Intervention	ng/mL (Mean)
Phase 2: 18 mg Lenvatinib + 5 mg Everolimus	38
Phase 2: 10 mg Everolimus	54

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Phase 2: Objective Response Rate (ORR)

The ORR was defined as the percentage of participants who had the best overall response (BOR) of complete response (CR) or partial response (PR) as determined by the investigator, using RECIST 1.1 in the evaluation of MRI or CT scans of targeted lesions. Tumor assessments were performed every 8 weeks (or sooner if there was evidence of progressive disease). The BOR was defined as the best response recorded from the start of the study treatment until discontinuation from the study. CR was defined as disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) had to have reduction in short axis to less than 10 mm. PR was defined as at least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. ORR = CR + PR was calculated with exact 95% CIs using the method of Clopper and Pearson. (NCT01136733)
Timeframe: Randomization (Cycle 1 Day 1) until first evidence of disease progression, assessed up to the data cutoff date (13 Jun 2014), or up to approximately 2 years and 3 months

Intervention	Percentage of participants (Number)
Phase 2 (Arm A): 18 mg Lenvatinib Plus 5 mg Everolimus	43.1
Phase 2 (Arm B): 24 mg Lenvatinib	26.9
Phase 2 (Arm C): 10 mg Everolimus	6.0

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Phase 2: Overall Survival (OS)

OS was defined as the time (in months) from the date of randomization until date of death from any cause. Median survival time was calculated using K-M estimate for each treatment arm and presented with 2-sided 95% CIs. Participants who were lost to follow-up or alive at the data cutoff date (10 Dec 2014) were censored at the date the participants were last known to be alive. (NCT01136733)
Timeframe: Randomization (Cycle 1 Day 1) until date of death from any cause, assessed up to the data cutoff date (10 Dec 2014), up to approximately 2 years and 9 months

Intervention	Months (Median)
Phase 2 (Arm A): 18 mg Lenvatinib Plus 5 mg Everolimus	25.5
Phase 2 (Arm B): 24 mg Lenvatinib	19.1
Phase 2 (Arm C): 10 mg Everolimus	15.4

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Phase 1b: Number of Participants With Dose-limiting Toxicity (DLT)

A DLT was defined as either a treatment-related failure to administer greater than or equal to (>=) 75% of the planned dosage of lenvatinib/everolimus or a specific National Cancer Institute Common Toxicity Criteria (NCI CTC) >= Grade 3 (severe or medically significant but not immediately life-threatening; hospitalization or prolongation of hospitalization indicated; disabling; limiting self-care daily living activities) hematologic or nonhematologic toxicities considered to be possibly related to lenvatinib and/or everolimus therapy assessed during the first treatment cycle of each dose level. Higher grade indicates more severe toxicity. (NCT01136733)
Timeframe: First dose of study drug (Cycle 1 Day 1) to end of first 4 weeks of therapy (Cycle 1)

Intervention	Participants (Number)
	Grade 3 abdominal pain	Grade 2 fatigue with Grade 1 GI reflux & anorexia	Grade 3 nausea	Grade 2 stomatitis
Phase 1b (Cohort 1): 12 mg Lenvatinib Plus 5 mg Everolimus	1	0	0	0
Phase 1b (Cohort 2): 18 mg Lenvatinib Plus 5 mg Everolimus	0	1	0	0
Phase 1b (Cohort 3): 24 mg Lenvatinib Plus 5 mg Everolimus	0	0	1	1

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Area Under the Blood Concentration-Time Curve From 0 to 24 Hours for Everolimus When Administered Alone or in Combination With Lenvatinib

Between 9 and 12 participants in each of the 3 treatment arms participated in an optional substudy where instead of the sparse sampling, 9 samples were to be taken over 1 single 24-hour period (i.e., intensive sampling) for full PK profiling. Blood samples were analyzed for study drug using standardized methods. PK parameters for everolimus were derived from everolimus concentration data using non-compartmental methods. Data were compared via descriptive statistics between single agent and combination therapy. (NCT01136733)
Timeframe: Phase 2: Cycle 1 Day 15 immediately predose, and 30 minutes, 1, 2, 3, 4, 8, 12 (optional), and 24 hours postdose (predose on Day 16)

Intervention	ng·hr/mL (Mean)
Phase 2: 18 mg Lenvatinib + 5 mg Everolimus	378
Phase 2: 10 mg Everolimus	463

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Phase 1b: Maximum Tolerated Dose (MTD) and Recommended Phase 2 (RP2) Dose

The highest dose level resulting in 0 or 1 DLT in 6 participants was to be considered the MTD of Phase 1b. Once the MTD was established, the participant cohort was expanded to a minimum of 10 participants. The MTD was confirmed by assessing DLTs during Cycle 1 and intolerable toxicities (i.e., not manageable with dose interruption and/or reduction) during Cycle 2 of therapy. Once the dose of lenvatinib/everolimus combination to be used in the succeeding Phase 2 part of the study was established, enrollment into Phase 2 was started. The RP2 dose was the same as the confirmed MTD and was used for the Phase 2 Treatment Arm A of this study. (NCT01136733)
Timeframe: First dose of study drug (Cycle 1 Day 1) to end of Cycle 2 (1 cycle = 28 days/4 weeks)

Intervention	mg/day (Number)
Phase 1b: Dose Escalation and MTD Expansion Cohorts	18.0

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Area Under the Plasma Concentration-Time Curve From 0 to 24 Hours (AUC(0-24)) for Lenvatinib When Administered Alone or in Combination With Everolimus

Between 9 and 12 participants in each of the 3 treatment arms participated in an optional substudy where instead of the sparse sampling, 9 samples were to be taken over 1 single 24-hour period (i.e., intensive sampling) for full PK profiling. Blood samples were analyzed for study drug using standardized methods. PK parameters for lenvatinib were derived from lenvatinib concentration data using non-compartmental methods. Data were compared via descriptive statistics between single agent and combination therapy. (NCT01136733)
Timeframe: Phase 2: Cycle 1 Day 15 immediately predose, and 30 minutes, 1, 2, 3, 4, 8, 12 (optional), and 24 hours postdose (predose on Day 16)

Intervention	ng·hr/mL (Mean)
Phase 2: 18 mg Lenvatinib + 5 mg Everolimus	3185
Phase 2: 24 mg Lenvatinib	5252

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Phase 2: Progression-Free Survival (PFS)

PFS was defined as the time (in months) from the date of first dose of study drug to the first documentation of disease progression or death, whichever occurred first. Kaplan-Meier (K-M) estimates were used to estimate median PFS, presented with 2-sided 95% confidence intervals (CIs). Tumor assessments were performed every 8 weeks (or sooner if there was evidence of progressive disease using computed tomography (CT) or magnetic resonance imaging (MRI) and scan acquisition techniques (including use or nonuse of intravenous (IV) contrast). Tumor response was determined at the site by the investigator and radiologist using Response Evaluation Criteria In Solid Tumors (RECIST) 1.1 in the evaluation of the tumor assessment scans. The date of objective disease progression was defined as the earliest date of radiological disease progression. Participants removed from therapy due to clinical progression with no radiologic confirmation were censored at their last radiologic assessment date. (NCT01136733)
Timeframe: Date of randomization into Phase 2 (Cycle 1 Day 1) to the date of first documentation of disease progression or death (whichever occurred first), assessed up to data cutoff date (13 Jun 2014), up to approximately 2 years and 3 months

Intervention	Months (Median)
Phase 2 (Arm A): 18 mg Lenvatinib Plus 5 mg Everolimus	14.6
Phase 2 (Arm B): 24 mg Lenvatinib	7.4
Phase 2 (Arm C): 10 mg Everolimus	5.5

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Summary of Blood Concentrations of Everolimus for Sparse PK Sampling for Phase 1b and Phase 2

Blood samples were collected during the Randomization Phase. Most participants had 6 samples taken over 3 cycles of treatment (sparse sampling - 2 samples taken per cycle, one at predose and one at 2 to 8 hours postdose). Whole blood concentrations of everolimus were measured and concentration data were summarized. The summary statistics at time points with one or more BLQ values were calculated by assigning zero for each BLQ value. (NCT01136733)
Timeframe: Cycle 1 (Day 1), Cycle 2 (Day 1), Cycle 3 (Day 1)

Intervention	ng/mL (Geometric Mean)
Cycle 1, Day 1 (0 Hours)	0.0
Cycle 1, Day 1 (2-8 Hours)	19.4
Cycle 2, Day 1 (0 Hours)	10.0
Cycle 2, Day 1 (2-8 Hours)	24.3
Cycle 3, Day 1 (0 Hours)	6.8
Cycle 3, Day 1 (2-8 Hours)	26.4

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Clinical Benefit Rate (CBR)

The CBR was defined as the percentage of participants who had BOR of CR, PR, or durable SD (duration of SD was greater than or equal to 23 weeks) and was based on investigator review data using RECIST 1.1. The BOR was defined as the best response recorded from the start of study treatment until discontinuation from the study. There was no requirement for confirmatory measurement of PR or CR to deem either one the BOR. The 95% CI was constructed using the method of Clopper and Pearson. CBR = CR + PR + SD greater than or equal to 23 weeks. (NCT01136733)
Timeframe: Baseline (Randomization) to first evidence of disease progression, assessed up to the data cutoff date (13 Jun 2014), or up to approximately 2 years and 3 months

Intervention	Percentage of participants (Number)
Phase 2 (Arm A): 18 mg Lenvatinib Plus 5 mg Everolimus	68.6
Phase 2 (Arm B): 24 mg Lenvatinib	65.4
Phase 2 (Arm C): 10 mg Everolimus	42.0

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Disease Control Rate (DCR)

The DCR was defined as the percentage of participants who had a BOR of CR or PR or SD (minimum duration from randomization to SD greater than or equal to 7 weeks). Assessments were performed every 8 weeks and were based on investigator review data using RECIST 1.1. The 95% CI was constructed using the method of Clopper and Pearson. DCR = CR + PR + SD greater than or equal to 7 weeks. (NCT01136733)
Timeframe: Baseline (Randomization) to first evidence of disease progression, assessed up to the data cutoff date (13 Jun 2014), or up to approximately 2 years and 3 months

Intervention	Percentage of participants (Number)
Phase 2 (Arm A): 18 mg Lenvatinib Plus 5 mg Everolimus	84.3
Phase 2 (Arm B): 24 mg Lenvatinib	78.8
Phase 2 (Arm C): 10 mg Everolimus	68.0

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Time to Cmax (Tmax) for Everolimus When Administered Alone or in Combination With Lenvatinib

Tmax for everolimus was the amount of time taken after administration of study treatment on Cycle 1 Day 15 to reach the maximum concentration (Cmax) of everolimus in blood. (NCT01136733)
Timeframe: Phase 2: Cycle 1 Day 15

Intervention	Hours (Median)
Phase 2: 18 mg Lenvatinib + 5 mg Everolimus	1.0
Phase 2: 10 mg Everolimus	1.0

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Durable Stable Disease (SD) Rate

The durable SD rate was defined as the percentage of participants whose BOR was SD and the duration of SD was greater than or equal to 23 weeks. The durable SD was based on investigator review data using RECIST 1.1. The 95% CI was constructed using the method of Clopper and Pearson. (NCT01136733)
Timeframe: Baseline (Randomization) to first evidence of disease progression, assessed up to the data cutoff date (13 Jun 2014), or up to approximately 2 years and 3 months

Intervention	Percentage of participants (Number)
Phase 2 (Arm A): 18 mg Lenvatinib Plus 5 mg Everolimus	25.5
Phase 2 (Arm B): 24 mg Lenvatinib	38.5
Phase 2 (Arm C): 10 mg Everolimus	36.0

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Maximum Concentration (Cmax) of Lenvatinib in Plasma When Administered Alone or in Combination With Everolimus

Cmax for lenvatinib was defined as the maximum observed concentration of lenvatinib in plasma following administration of study treatment on Cycle 1 Day 15 and was obtained directly from the measured plasma concentration-time curves. (NCT01136733)
Timeframe: Phase 2: Cycle 1 Day 15

Intervention	ng/mL (Mean)
Phase 2: 18 mg Lenvatinib + 5 mg Everolimus	327
Phase 2: 24 mg Lenvatinib	403

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Time to Cmax (Tmax) for Lenvatinib When Administered Alone or in Combination With Everolimus

Tmax for lenvatinib was the amount of time taken after administration of study treatment on Cycle 1 Day 15 to reach maximum concentration (Cmax) of lenvatinib in plasma. (NCT01136733)
Timeframe: Phase 2: Cycle 1 Day 15

Intervention	Hours (Median)
Phase 2: 18 mg Lenvatinib + 5 mg Everolimus	2.0
Phase 2: 24 mg Lenvatinib	4.0

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Effect of RAD001 on Pharmacokinetics AUC(0-inf) of JI-101

Determine the mean percent change that RAD001 has on the peak concentration as determined by calculating the AUC (0-inf) of JI101 in the presence and absence of RAD001 (NCT01149434)
Timeframe: pre-dose and at 0.5, 1, 2, 4, 6, 8, 10, and 24 hours after dosing (Cycle 1 Day 8 for RAD001 + JI101 and Cycle 1 Day 15 for JI-101 alone

Intervention	percentage change (Mean)
Pharmacokinetic Arm Phase 1	95.3

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Progression Free-Survival in the Ovarian Cancer Cohort

progression-free survival at 2 months. We define progression as using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), to detect 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. (NCT01149434)
Timeframe: 2 months

Intervention	percentage of participants (Number)
Pharmacodynamic Arm Phase 2	71.4

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Safety and Tolerability of JI-101

Number of patients experiencing a grade 2 or higher Adverse Event related to JI101 (NCT01149434)
Timeframe: 2 years

Intervention	Participants (Number)
Pharmacokinetic Arm Phase 1	4
Pharmacodynamic Arm Phase 2	12

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Effect of JI 101 on Pharmacokinetics Area Under Curve (AUC) (0-inf) of RAD001

Determine the mean percent change that JI-101 has on the peak concentration as determined by calculating the AUC (0-inf) of RAD001 in the presence and absence of JI-101 (NCT01149434)
Timeframe: pre-dose and at 0.5, 1, 2, 4, 6, 8, 10, and 24 hours after dosing (Cycle 1 Day 1 for RAD001 alone and Cycle 1 Day 8 for RAD001 + JI-101

Intervention	percentage change (Mean)
Pharmacokinetic Arm	165.6

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Tumor Response in the Ovarian Cancer Cohort

Response Rate determined by the sum of patients achieving complete or partial response to JI-101 as defined by Response Evaluation Criteria in Solid Tumors (NCT01149434)
Timeframe: 2 years

Intervention	Participants (Number)
Pharmacodynamic Arm Phase 2	0

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Tumor Response

Response Rate determined by the sum of patients achieving complete or partial response to JI-101 as defined by Response Evaluation Criteria in Solid Tumors. 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 (NCT01149434)
Timeframe: 2 years

Intervention	participants (Number)
Pharmacokinetic Arm Phase 1	0

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Incidence Rate of Composite Efficacy Failure Defined as Treated Biopsy Proven Acute Rejection (tBPAR ), Graft Loss or Death

The number of participants who experienced composite efficacy failure was analyzed. Composite efficacy failure was defined as treated biopsy proven acute rejection (tBPAR), graft loss, or death. A BPAR was defined as an acute rejection confirmed by biopsy with a Rejection Activity Index (RAI) score ≥ 3. tBPAR was defined as a BPAR which was treated with anti-rejection therapy. The RAI is used to score liver biopsies with acute rejection and is composed of 3 categories (portal inflammation, bile duct inflammation damage, and venous endothelial inflammation) each scored on a scale of 0 (absent) to 3 (severe) by a trained pathologist. The total RAI score = the sum of the scores of the 3 categories and ranges from 0 to 9, with a higher score indicating greater rejection. The graft was presumed to be lost on the day the patient was newly listed for a liver graft, received a graft re-transplant, or died. (NCT01150097)
Timeframe: from months 24 to 36

Intervention	Participants (Number)
Everolimus + Reduced Tacrolimus	2
Tacrolimus Elimination	1
Tacrolimus Control	3

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Incidence Rate of Composite Efficacy Failure Defined as Graft Loss or Death

The number of participants who experienced graft loss or death was analyzed. The graft was presumed to be lost on the day the patient was newly listed for a liver graft, received a graft re-transplant, or died. (NCT01150097)
Timeframe: from months 36 - 48

Intervention	Participants (Number)
Everolimus + Reduced Tacrolimus	0
Tacrolimus Elimination	0

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Change in Renal Function

Intervention	mL/min/1.73m^2 (Mean)
Everolimus + Reduced Tacrolimus	-0.9
Tacrolimus Elimination	2.5
Tacrolimus Control	-3.3

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Incidence Rate of Composite Efficacy Failure Defined as Graft Loss or Death

Intervention	Participants (Number)
Everolimus + Reduced Tacrolimus	2
Tacrolimus Elimination	0
Tacrolimus Control	1

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Incidence Rate of tBPAR

The number of participants who had a tBPAR was analyzed. tBPAR was defined as a BPAR which was treated with anti-rejection therapy. The RAI is used to score liver biopsies with acute rejection and is composed of 3 categories (portal inflammation, bile duct inflammation damage, and venous endothelial inflammation) each scored on a scale of 0 (absent) to 3 (severe) by a trained pathologist. The total RAI score = the sum of the scores of the 3 categories and ranges from 0 to 9, with a higher score indicating greater rejection. (NCT01150097)
Timeframe: from months 24 - 36

Intervention	Participants (Number)
Everolimus + Reduced Tacrolimus	0
Tacrolimus Elimination	1
Tacrolimus Control	2

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Incidence Rate of Composite Efficacy Failure Defined as Treated Biopsy Proven Acute Rejection (tBPAR ), Graft Loss or Death

Intervention	Participants (Number)
Everolimus + Reduced Tacrolimus	1
Tacrolimus Elimination	0

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Progression-Free Survival (PFS)

Progression-free survival (PFS) is defined as the time between Day 1 Cycle 1 and date of first documented recurrence or death. Patients who do not exhibit progression while on trial will be censored at their last known assessment. Progression is defined per RECIST criteria as either 1) at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest (nadir) sum since the treatment started, or the appearance of one or more new lesions. Requires not only 20% increase, but absolute increase of a minimum of 5 mm over sum. OR 2) Appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. (NCT01154335)
Timeframe: 18 Months

Intervention	months (Mean)
Dose Level 1	2.8
Dose Level 2	3.6
Dose Level 2a	1.6

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Response Rate

Response rate (RR) will be estimated as the proportion of patients exhibiting complete response or partial response out of all evaluable cases. Complete Response is defined per RECIST as disappearance of all target/non-target lesions and normalization of tumor markers. Partial Response is defined per RECIST as At least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD. (NCT01154335)
Timeframe: 18 months

Intervention	Participants (Count of Participants)
Dose Level 1	0
Dose Level 2	0
Dose Level 2a	0

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To Determine the Maximum Tolerated Dose (MTD) of the Combination of OSI-906 and Everolimus for the Treatment of Patients With Refractory Metastatic Colorectal Cancer.

The MTD of the drug combination will be determined as the highest dose at which ≤1 of 6 subjects experiences a Grade 3 or Grade 4 DLT according to National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) v4.0 (NCT01154335)
Timeframe: 18 Months

Intervention	milligrams (Number)
	OSI-906 BID Dose	Everolimus QD Dose
All Patients	50	5

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Overall Survival (OS)

Overall survival (OS) is defined as the time between Day 1 Cycle 1 to the date of death from any cause. Those remaining alive will be censored at their last known assessment or follow-up. (NCT01154335)
Timeframe: 18 months

Intervention	weeks (Mean)
Dose Level 1	5.1
Dose Level 2	5.1
Dose Level 2a	3.3

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Common Terminology Criteria for Adverse Events (CTCAE) Events

Number of participants experiencing serious CTCAE events in the study. (NCT01158651)
Timeframe: approximately 48 weeks

Intervention	participants (Number)
RAD001 (Everolimus) Active Therapy	23

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RAD001 Response Rate Based on 2D MRI Change From Baseline

Outcome is 2D MRI target tumor volume compared to baseline volume. Success criteria is volume less than 80% of baseline. (NCT01158651)
Timeframe: Approximately 48 weeks

Intervention	participants (Number)
RAD001 (Everolimus) Active Therapy	15

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Change From Baseline in Cardiovascular Biomarkers, C-reactive Protein (CRP)

Blood samples were collected to analyze CRP. A negative change from baseline indicates improvement. (NCT01169701)
Timeframe: Baseline, month 6, month 24

Intervention	mg/dl (Mean)
	Month 6 (n=27,30)	Month 24 (n=24,24)
Everolimus	0.326	-0.040
Tacrolimus	0.512	0.100

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Percentage of Participants With Biopsy-proven Acute Rejection (BPAR), Graft Loss, Death and Lost to Follow up

The incidence of BPAR, graft loss, death and lost to follow-up events was calculated using relative frequency. (NCT01169701)
Timeframe: Month 24

Intervention	Percentage of participants (Number)
	BPAR	Graft loss	Deaths	Lost to follow-up
Everolimus	0.00	0.00	0.00	0.00
Tacrolimus	0.00	0.00	0.00	3.13

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Change From Baseline in the Cardiovascular Biomarker, Type 1 Procollagen Amino-terminal-propeptide (PINP)

Blood samples were collected to analyze PCR. A negative change from baseline indicates improvement. (NCT01169701)
Timeframe: Baseline, month 6, month 24

Intervention	ug/l (Mean)
	Month 6 (n=27,30)	Month 24 (n=24,24)
Everolimus	-33.36	-28.17
Tacrolimus	-13.82	-13.65

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Renal Function as Measured by Estimated Glomerular Filtration Rate (eGFR)

Estimated GFR was caluclated using the modification of diet in renal disease (MDRD) formula. (NCT01169701)
Timeframe: Month 6, month 12, month 24

Intervention	mL/min/1.73m^2 (Mean)
	Month 6 (n=33,29)	Month 12 (n=32,28)	Month 24 (n=31,26)
Everolimus	63.781	61.225	60.779
Tacrolimus	55.648	57.757	57.727

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Renal Function Measured by Serum Creatinine

Serum samples were collected to analyze serum creatinine. (NCT01169701)
Timeframe: Month 6, month 12, month 24

Intervention	mg/dl (Mean)
	Month 6 (n=33,29)	Month 12 (n=32,28)	Month 24 (n= 31,26)
Everolimus	1.234	1.256	1.260
Tacrolimus	1.232	1.231	1.217

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Change From Baseline in the Cardiovascular Biomarker, N-terminal Pro-brain Natriuretic Peptide Fraction (NT-proBNP)

Blood samples were collected to analyze NT-proBNP. A negative change from baseline indicates improvement. (NCT01169701)
Timeframe: Baseline, month 6, month 24

Intervention	pg/mL (Mean)
	Month 6 (n=27,30)	Month 24 (n=24,24)
Everolimus	-79.10	-193.3
Tacrolimus	21.604	-80.20

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Change From Baseline in the Cardiovascular Biomarker, Glycosylated Hemoglobin (HbA1c)

Blood samples were collected to analyze HbA1c. A negative change from baseline indicates improvement. (NCT01169701)
Timeframe: Baseline, month 6, month 24

Intervention	Percentage of HbA1c (Mean)
	Month 6 (n=20,22)	Month12 (n=22,20)
Everolimus	0.159	0.185
Tacrolimus	0.015	0.045

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Change From Baseline in Cardiovascular Biomarkers: Troponin I and Collagen Type 1 C-telopeptide (ICTP)

Blood samples were collected to analyze Troponin I and collagen type 1 C-telopeptide (ICTP). A negative change from baseline indicates improvement. (NCT01169701)
Timeframe: Baseline, month 6, month 24

Intervention	ng/ml (Mean)
	Troponin 1, Month 6 (n=27,30)	Troponin 1, Month 24 (n=24,24)	ICTP, Month 6 (n=27,30)	ICTP, Month 24 (n=24,24)
Everolimus	-0.006	-0.007	-0.195	-0.125
Tacrolimus	0.000	0.003	0.049	-0.035

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Change From Baseline in the Cardiovascular Biomarker, Myeloperoxidase (MPO)

Blood samples were collected to analyze MPO. A negative change from baseline indicates improvement. (NCT01169701)
Timeframe: Baseline, month 6, month 24

Intervention	U/mL (Mean)
	Month 6 (n=27,30)	Month 24 (n=24,24)
Everolimus	-0.093	-0.642
Tacrolimus	0.433	-0.329

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Renal Function as Measured by Creatinine Clearance

Creatinine clearance was calculated using the Cockroft-Gault formula. (NCT01169701)
Timeframe: Month 6, month 12, month 24

Intervention	mg/min (Mean)
	Month 6 (n=29,25)	Month 12 (n=28,25)	Month 24 (n=28,24)
Everolimus	76.618	73.363	72.910
Tacrolimus	64.841	65.037	66.933

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Pulse Wave Velocity (PWV)

Utilizing the SphygmoCor Device, ECG leads placed at the carotid and femoral arteries provided the measure of the pulse wave at that particular arterial location. The distance between the two vascular beds divided by the pulse wave time shift provided a measure of the pulse wave velocity. (NCT01169701)
Timeframe: Month 6, month 24

Intervention	m/sec (Mean)
	Month 6 (n=31,30)	Month 24 (n=28,25)
Everolimus	7.40	7.06
Tacrolimus	7.01	7.58

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Change From Baseline in Left Ventricular Mass Index (LVMI)

Left ventricular hypertrophy grade was assessed by echocardiogram where the left ventricular mass index was calculated. The presence of LVM was defined as > 49.2 g/m^2.7 in men and >46.7 g/m^2.7 in women. A negative change from baseline indicates improvement. (NCT01169701)
Timeframe: Baseline, Month 24

Intervention	g/m^2.7 (Mean)
Tacrolimus	-6.071
Everolimus	-4.008

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Percentage of Participants With Major Cardiovascular Events (MACE)

The percentage of participants who experienced MACE were reported. MACE included acute myocardial infarction, insertion or replacement of implantable defibrillator, peripheral vascular disorders, congestive heart failure, coronary artery bypass, other events, percutaneous coronary intervention and stroke. (NCT01169701)
Timeframe: Month 24

Intervention	Percentage of participants (Number)
Tacrolimus	0.00
Everolimus	0.00

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Change From Baseline in Mean 24 Hour Systolic and Diastolic Blood Pressure

Blood pressure was measured using ambulatory blood pressure monitoring (ABPM). A negative change from baseline indicates improvement. (NCT01169701)
Timeframe: Baseline, Month 6, month 12, month 24

Intervention	mmHg (Mean)
	Month 6 (n=31,29)	Month 12 (n=28,24)	Month 24 (n=29,24)
Everolimus	3.2	2.7	2.0
Tacrolimus	-0.6	2.1	2.2

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Grade 4 Treatment-Related Toxicity Rate [Dose Finding]

Grade 4 treatment-related toxicity rate is the percentage of participants experiencing at least one treatment-related grade 4 adverse event (AE) with treatment attribution of possibly, probably or definite based on NCI Common Toxicity Criteria for Adverse Events version 4 (CTCAEv4) as reported on case report forms. (NCT01184326)
Timeframe: Participants were assessed for adverse events on days 1 and 15 for cycles 1-2 and every cycle thereafter; Treatment duration was up to 6 cycles in the Dose Level 0 cohort and 14 cycles in the Dose Level -1 cohort (1 cycle=28 days).

Intervention	percentage of participants (Number)
Dose Level 0: Everolimus 5mg + Pazopanib 600 mg [Dose Finding]	33.3
Dose Level -1: Everolimus 5mg + Pazopanib 400 mg [Dose Finding	0.0

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Dose Limiting Toxicity (DLT) [Phase I Dose Finding]

A DLT was defined as an adverse event (a) with treatment attribution of possible, probable, or definite, and (b) occurs during cycle 1, and (c) meets any of the following criteria: Grade 3 or 4 non-hematologic toxicity excluding: nausea/vomiting controlled with antiemetics, Grade 3 hypertension that resolves to ≤150/90 within 7 days with supportive care, and Grade 3 asymptomatic, clinically insignificant laboratory abnormalities (LDH, alkaline phosphatase due to bone metastases, and asymptomatic hypophosphatemia). Hematologic toxicity: Grade 4 thrombocytopenia, Grade 3 thrombocytopenia with bleeding, Grade 4 neutropenia which persists for >7 days, Grade 4 neutropenia associated with fever >38.5C; Hematologic toxicity excluded lymphopenia or anemia of any grade. Missing more than 5 days of planned doses for drug-related intolerable grade 2 toxicity;Toxicity related to therapy severe enough to require a dose-reduction. (NCT01184326)
Timeframe: Participants were assessed for adverse events on days 1 and 15 for cycles 1-2 and every cycle thereafter; The observation period for DLT evaluation was the first 28 days of treatment.

Intervention	Participants (Count of Participants)
Dose Level 0: Everolimus 5mg + Pazopanib 600 mg	2
Dose Level -1: Everolimus 5mg + Pazopanib 400 mg	0

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Objective Response Rate [Expansion]

The objective response rate (ORR) was defined as the percentage of participants achieving complete response (CR) or partial response (PR) based on RECIST 1.1 criteria on treatment. Per RECIST 1.1 for target lesions: CR is complete disappearance of all target lesions and PR is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. PR or better overall response assumes at a minimum incomplete response/stable disease (SD) for the evaluation of non-target lesions and absence of new lesions. (NCT01184326)
Timeframe: TDisease was evaluated radiologically at baseline and every 8 weeks on treatment; Treatment duration was up to 6 cycles in the Dose Level 0 cohort, 14 cycles in the Dose Level -1 cohort and 10 cycles in the expansion cohort (1 cycle=28 days).

Intervention	percentage of participants (Number)
All Phase I Dose Expansion Participants	21.4

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Median Progression-Free Survival [Expansion]

Progression-free survival based on the Kaplan-Meier method is defined as the duration of time from study entry to documented disease progression (PD) or death. Participants alive without PD are censored at date of last disease assessment. Per RECIST 1.1 for target lesions: PD is at least a 20% increase in sum longest diameter (LD), taking as reference the smallest sum on study with at least 5 mm absolute increase or the appearance of one or more new lesions. For non-target lesions, PD is appearance of one or more new lesions or unequivocal progression of existing non-target lesions. (NCT01184326)
Timeframe: Disease was evaluated radiologically at baseline and every 8 weeks on treatment; PFS follow-up was up to 9.2 months in the expansion cohort.

Intervention	months (Median)
All Phase I Dose Expansion Participants	2.9

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Mean Duration of Response [Expansion]

Duration of response was calculated as the time from achieving complete response (CR) or partial response (PR) based on RECIST 1.1 criteria on treatment until disease progression. Per RECIST 1.1 for target lesions: CR is complete disappearance of all target lesions and PR is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. PR or better overall response assumes at a minimum incomplete response/stable disease (SD) for the evaluation of non-target lesions and absence of new lesions. For target lesions: PD is at least a 20% increase in sum longest diameter (LD), taking as reference the smallest sum on study with at least 5 mm absolute increase or the appearance of one or more new lesions. For non-target lesions, PD is appearance of one or more new lesions or unequivocal progression of existing non-target lesions. (NCT01184326)
Timeframe: Disease was evaluated radiologically at baseline and every 8 weeks on treatment; PFS follow-up was up to 9.2 months in the expansion cohort.

Intervention	months (Mean)
All Phase I Dose Expansion Participants	4.9

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Grade 4 Treatment-Related Toxicity Rate [Expansion]

Grade 4 treatment-related toxicity rate is the percentage of participants experiencing at least one treatment-related grade 4 adverse event (AE) with treatment attribution of possibly, probably or definite based on NCI Common Toxicity Criteria for Adverse Events version 4 (CTCAEv4) as reported on case report forms. (NCT01184326)
Timeframe: Participants were assessed for adverse events on days 1 and 15 for cycles 1-2 and every cycle thereafter; Treatment duration was up to 10 cycles in the expansion cohort (1 cycle=28 days).

Intervention	percentage of participants (Number)
All Phase I Dose Expansion Participants	7.1

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Maximum Tolerated Dose (MTD) [Phase I Dose Finding]

The MTD of Pazopanib in combination with Everolimus 5 mg PO QD was determined by the number of patients who experience a dose limiting toxicity (DLT). See subsequent primary outcome measure for the DLT definition. The MTD is defined as the highest dose at which fewer than one-third of patients experience a DLT. If no DLTs are observed, the MTD is not reached. (NCT01184326)
Timeframe: Participants were assessed for adverse events on days 1 and 15 for cycles 1-2 and every cycle thereafter; The observation period for MTD evaluation was the first 28 days of treatment.

Intervention	mg (Number)
All Phase I Dose Finding Participants	400

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Progression Free Survival (PFS) for First Line Medication

The amount of time after the first line medication begins until the cancer gets worse progresses. Progression is measured by an increase in measures tumors of at least 20 %, or overall increase in all the tumors, or the presence of new tumors. (NCT01185366)
Timeframe: 7 months

Intervention	months (Median)
Everolimus	4.1
Sunitinib	6.1

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Number of Participants Who Experienced Either a Grade 3 or 4 Adverse Event

Side effects, also called adverse events, that were related to either drug were documented and graded for severity according to the Common Terminology Criteria for Adverse Events (CTCAE) version 3. Grades increases in severity from 1 - 5. Grade one is a mild change which only requires monitoring. Grade 2 is a moderate change and may require some medication. Grade 3 is severe and requires hospitalization. Grade 4 is life threatening. Grade 5 is death. (NCT01185366)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Everolimus	18
Sunitinib	27

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Number of Participants With Best Overall Response for First Line Medication

The best overall response for each participant was determined by using the Response Evaluation Criteria for Solid Tumors (RECIST). The responses are Complete Response (CR), Partial Response (PR), Stable Disease (SD), and Progression Disease (PD). CR is the disappearance of the cancer everywhere in the participant. PR is at least a 30 % reduction in the measured tumors from baseline. SD is no discernible change in the presence of cancer. Progressive disease is an increase of at least 20% of the measured cancer from the cancer's smallest measure. (NCT01185366)
Timeframe: 7 months

Intervention	Participants (Count of Participants)
	Complete Response	Partial Response	Stable Disease	Progressive Disease
Everolimus	0	1	26	8
Sunitinib	0	3	21	9

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Overall Survival of the First Line Therapy

The amount of time each participant is alive from the start of the first line therapy. (NCT01185366)
Timeframe: 17 months

Intervention	months (Median)
Everolimus	14.9
Sunitinib	16.2

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Progression Free Survival (PFS) for Crossover Medication

The amount of time after the crossover medication begins until the cancer gets worse progresses. Progression is measured by an increase in measures tumors of at least 20 %, or overall increase in all the tumors, or the presence of new tumors. (NCT01185366)
Timeframe: 4 months

Intervention	months (Median)
Everolimus	1.8
Sunitinib	1.8

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Toxicities, Graded According to the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.0

The number of patients reporting grade 3 or higher adverse events as graded by the NCI's Common Toxicity Criteria (CTCAE) Version 4 are reported here. A complete list of all reported adverse events is reported in the Adverse Events section of this report. (NCT01198158)
Timeframe: Up to 30 days after completion of study treatment

Intervention	Participants (Count of Participants)
	Grade 3 Adverse event	Grade 4 Adverse event
Arm I (Everolimus)	21	1
Arm II (Everolimus With Bevacizumab)	20	3

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Progression-free Survival (PFS)

Progression free survival (PFS) is defined as the time from the date of randomization to the date of disease progression or death resulting from any cause, whichever comes first. Progression is defined according to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. The median and 95% confidence intervals are estimated using the Kaplan-Meier estimator. (NCT01198158)
Timeframe: The time from randomization to disease progression or death from any cause, assessed up to 5.5 years

Intervention	months (Median)
Arm I (Everolimus)	7.2
Arm II (Everolimus With Bevacizumab)	6.9

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Objective Response Rate (CR + PR)

The response rate (percentage) is the percent of patients whose best response was Complete Response (CR) or Partial Response (PR) as defined by RECIST 1.1 criteria. Percentage of successes will be estimated by 100 times the number of successes divided by the total number of evaluable patients. (NCT01198158)
Timeframe: Up to 5.5 years

Intervention	percentage of participants (Number)
Arm I (Everolimus)	17.1
Arm II (Everolimus With Bevacizumab)	16.7

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Overall Survival (OS)

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. (NCT01198158)
Timeframe: The time from date of randomization to date of death due to any cause, assessed up to 5.5 years

Intervention	months (Median)
Arm I (Everolimus)	27.5
Arm II (Everolimus With Bevacizumab)	21.8

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Disease Control Rate (Stable Disease [SD] + Partial Response [PR] + Complete Response [CR]);

The disease control rate was based on the data as per local radiological review following the RECIST criteria. The disease control rate is defined as the proportion of patients with CR, PR, or SD and was summarized in terms of percentage with 95% exact Clopper-Pearson CIs (NCT01206764)
Timeframe: Approximately 4 years

Intervention	Percentage of Participants (Number)
RAD001	74.6

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PFS (Progression-Free Survival)

the time from the date of the start of RAD001 treatment to the date of the first documented disease progression or death due to any cause (NCT01206764)
Timeframe: Approximately 4 years

Intervention	Weeks (Median)
RAD001	27.71

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Overall Survival

Overall survival is defined as the time from date of start of treatment to date of death due to any cause. If a patient is not known to have died, survival will be censored at the date of last contact. (NCT01206764)
Timeframe: Approximately 4 years

Intervention	Weeks (Median)
RAD001	NA

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Objective Response Rate (ORR; Where ORR = CR + PR)

The overall tumor response was based on the data as per local radiological review, following RECIST criteria. The ORR is defined as the proportion of patients with CR or PR and was summarized in terms of percentage with 95% exact Clopper-Pearson CIs (NCT01206764)
Timeframe: Approximately 4 years

Intervention	Percentage of participants (Number)
RAD001	17

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Duration of Response (DOR)

The DOR analysis applied only to patients whose overall response was CR or PR and was defined as the time from onset of response (CR/PR) to progression or death from any cause (NCT01206764)
Timeframe: Approximately 4 years

Intervention	Weeks (Median)
RAD001	169

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Number of Adverse Events as a Measure of Safety and Tolerability

To determine the safety of everolimus and everolimus plus paclitaxel in this patient population. A summary with the count of events per grade is provided. (NCT01215136)
Timeframe: 5 months

Intervention	Number of Events (Number)
	Grade 1 Adverse Events	Grade 2 Adverse Events	Grade 3 Adverse Events	Grade 4 Adverse Events	Grade 5 Adverse Events
Cohort 1	10	9	4	0	0
Cohort 2	116	75	39	1	3

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Response Rate of Single-Agent Everolimus and Everolimus + Paclitaxel

To evaluate clinical benefit rate (complete response, partial response, and stable disease) at 4 months from initiation of treatment. (NCT01215136)
Timeframe: 4 months

Intervention	percentage of participants (Number)
Cohort 1	14.3
Cohort 2	37.9

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Progression Free Survival

To determine median progression free survival per RECIST 1.1, per cohort. (NCT01215136)
Timeframe: 4 months

Intervention	months (Median)
Cohort 1	2.3327
Cohort 2	5.8480

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Overall Survival

To determine median overall survival at 1-year from the initiation of treatment. (NCT01215136)
Timeframe: 12 months

Intervention	months (Median)
Cohort 1	4.5010
Cohort 2	10.8747

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Progression Free Survival

Progression Free Survival (PFS) was defined as the time from study entry until disease progression or death, whichever occurs first. The median PFS was estimated using the Kaplan-Meier method. Progression was assessed per RECIST criteria, and defined as at least a 20% increase in the sum of the longest diameters of target lesions (and an absolute increase of at least 0.5 cm) or the appearance of new lesions. (NCT01229943)
Timeframe: From study entry to the date of documented progression or death from any cause, up to 3 years

Intervention	months (Median)
Arm I (Octreotide Acetate and Everolimus)	14.0
Arm II (Octreotide Acetate, Everolimus, and Bevacizumab)	16.7

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Overall Survival (OS)

Overall survival (OS) is defined as the time from study entry to death from any cause. The median OS was estimated using the Kaplan-Meier method. (NCT01229943)
Timeframe: From registration to time of death, assessed up to 3 years

Intervention	months (Median)
Arm I (Octreotide Acetate and Everolimus)	35.0
Arm II (Octreotide Acetate, Everolimus, and Bevacizumab)	36.7

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Overall Response Rate

The proportion of patients who respond (completely or partially) to each combination regimen will be estimated. Response was defined using Response Evaluation Criteria In Solid Tumors (RECIST) criteria: Complete Response (CR): disappearance of all target lesions; Partial Response (PR) 30% decrease in sum of longest diameter of target lesions. (NCT01229943)
Timeframe: Up to 3 years

Intervention	percentage of participants (Number)
Arm I (Octreotide Acetate and Everolimus)	12
Arm II (Octreotide Acetate, Everolimus, and Bevacizumab)	31

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Progression-free Survival

Estimated using the product-limit method of Kaplan and Meier. From the date treatment started until the date of first documented progression or date of death from any cause, whichever came first. 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. (NCT01231399)
Timeframe: up to 5 years

Intervention	Months (Median)
Dose Level 1 - 2.5 mg Everolimus Daily	14.5

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Overall Survival

Estimated using the product-limit method of Kaplan and Meier. From the date treatment started until the date of death from any cause. (NCT01231399)
Timeframe: Up to 5 years.

Intervention	Months (Median)
Dose Level 1 - 2.5 mg Everolimus Daily	20.3

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Number of Subject With Overall Response

Intervention	participants (Number)
Dose Level 1 - 2.5 mg Everolimus Daily	5

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Maximum Tolerated Dose (MTD) of Everolimus

The highest dose tested in which fewer than 33% of patients experience an attributable DLT to the study drug, when at least 6 patients are treated at that dose and are evaluable for toxicity. Toxicities will be assessed using Common Terminology Criteria for Adverse Events (CTCAE) v4.0. (NCT01231399)
Timeframe: Course 1 (first 28 days)

Intervention	mg (Number)
Dose Level 1 - 2.5 mg Everolimus	2.5

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Disease Control Rate (DCR)

Disease Control Rate (DCR) was defined as the proportion of patients whose best overall response was either: Complete Response (CR), Partial Response (PR) or Stable Disease (SD). Disease Control Rate was calculated only for patients with measurable disease at baseline and was summarized using descriptive statistics. (NCT01231659)
Timeframe: From the date of randomization until the date of the first documented disease progression or date of death from any cause whichever came first, assessed for approximately 66 months

Intervention	Percentage of Participants (Number)
Everolimus + Letrozole	85.7

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Median Time to Overall Survival (OS)

Overall Survival (OS) was defined as the time from the date of study entry to date of death due to any cause. If a death had not observed by the date of analysis, then OS was censored at the date of last contact. Distribution of OS was estimated using the Kaplan Meier method. The median OS along with 95% CI was presented. (NCT01231659)
Timeframe: From Date of randomization up to approximately 66 months

Intervention	Months (Median)
Everolimus + Letrozole	22.3

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Median Time to Progression-Free Survival (PFS)

Progression Free Survival (PFS) was defined as the time from the date of study entry to the date of first documented tumor progression or death from any cause, whichever occurred first. If a patient did not have an event, PFS was censored at the last date of tumor assessment. For patients with measurable disease at baseline, progression was determined according to the RECIST 1.0 criteria. Only descriptive analysis done. (NCT01231659)
Timeframe: Date of randomization to the date of first documented tumor progression or death from any cause, whichever occurs first, reported between day of first patient randomized up to 66 months

Intervention	Months (Median)
Everolimus + Letrozole	9.0

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Percentage of Participants With Overall Response Rate (ORR)

Overall Response Rate (ORR) was defined as the proportion of patients whose best overall response was either complete response (CR) or partial response (PR) according to RECIST 1.0 for target lesions and assessed by CT: Complete Response (CR), disappearance of all target lesions for a period of at least one month; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (ORR) = CR + PR. Only descriptive statistics. (NCT01231659)
Timeframe: From the date of randomization until the date of the first documented disease progression or date of death from any cause whichever came first, assessed for approximately 15 months

Intervention	Percentage of Participants (Number)
Everolimus + Letrozole	37.2

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All Collected Deaths

"On treatment deaths were collected from FPFT up to 28 days after study drug discontinuation, for a maximum duration of 2002 days (treatment duration ranged from 1 to 1974 days).~Deaths post treatment survival follow up were collected after the on- treatment period, up to approximately 2092 days. Patients who didn't die during the on-treatment period and had not stopped study participation at the time of data cut-off (end of study) were censored." (NCT01231659)
Timeframe: up to 2002 days (on-treatment), up to approximately 2092 days (study duration)

Intervention	Participants (Count of Participants)
	On-treatment deaths	Post-treatment deaths	All deaths
Everolimus + Letrozole	2	50	52

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Long-term Safety and Tolerability

The assessment of safety was based mainly on the frequency of AEs and on the number of laboratory values that fell outside of pre-determined ranges. Other safety data (e.g. ECG, vital signs) were considered as appropriate. Only descriptive analysis done. (NCT01231659)
Timeframe: From Date of first dose up to approximately 66 months

Intervention	Participants (Number)
	AEs - All	AEs - Grade 3	AEs - Grade 4
Everolimus + Letrozole	72	39	7

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Median Overall Survival (OS) in Months

Overall survival reported in months as time interval between the date of treatment and the date of death or last follow-up. (NCT01239342)
Timeframe: Time interval between the date of treatment and the date of death or last follow-up, assessed up to 5 years

Intervention	Months (Median)
MK2206	23.5
Everolimus	15.7

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Summary of Selected Toxicities Grade 3 or Greater Toxicity Based on the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.0

Adverse Events (AEs) list of reported events with associated intervention agent in a uniform presentation of events. The method of Thall, Simon and Estey (1995, 1996) was used to collect study participants' safety data summarized by treatment arm, category, severity and relevance. Comprehensive listing of AEs collected on study can be found in Adverse Event section separated by severity, Serious and Other AEs and represented by treatment arm, organ system-category within defined severity. (NCT01239342)
Timeframe: Up to 5 years

Intervention	Toxicities (Number)
	Hyperglycemia	Hypertriglyceridemia	Hyperuricemia	Lymphocyte count decreased	Mucositis oral	Rash maculo-papular	Pruritus	Proteinuria	Pancreatitis	Lipase increased	Generalized muscle weakness	Dyspnea	Dehydration
Everolimus	1	1	0	1	0	0	0	0	0	0	0	0	0
MK2206	7	1	2	2	1	8	1	1	1	1	1	1	2

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Median Progression Free Survival (PFS) in Months

PFS defined as Time interval between date of treatment and date of disease progression, date of death or last follow-up date, whichever occurs first. Progression 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 nontarget lesion, or the appearance of new lesions. (NCT01239342)
Timeframe: Time interval between date of treatment and date of disease progression, date of death or last follow-up date, whichever occurs first, assessed up to 5 years

Intervention	Months (Median)
MK2206	3.68
Everolimus	5.98

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Overall Response Rate (ORR) Defined as Complete Response (CR) + Partial Response (PR)

Response for CR + PR defined by RECIST version 1.1. Repeat radiologic studies to evaluate disease progression or response (in accordance with restaging of disease) every 8 weeks. Complete Response (CR): Disappearance all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm. Partial Response (PR): >30% decrease in sum diameters of target lesions, reference baseline sum diameters. Progressive Disease (PD): >20% increase in sum diameters of target lesions, reference smallest sum on study (includes baseline sum if is smallest on study). In addition to relative increase of 20%, sum must demonstrate absolute increase >5 mm. (Note: appearance 1/+ new lesions considered progressions). Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, reference smallest sum diameters. (NCT01239342)
Timeframe: Up to 5 years

Intervention	percentage of participants (Number)
MK2206	14.3
Everolimus	0

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Evaluation of Renal Function

Evaluation of renal function (serum creatinine) 90 days after transplant and 365 days after transplant. (NCT01239472)
Timeframe: 90 days after transplant and 365 days after transplant

Intervention	mg/dL (Median)
	Cr 90days	Cr 365days
Everolimus	1.3	1.4
Tacrolimus	1.6	1.4

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Cytokines Evaluation

Cd106(VCAM-1) , IP-10/CXCL10, MIG/CXCL9, MCP-1/CCL2, IL-1, RANTES, IL-8, IL12p70, TNF, IL-10, IL-6, IL-1, VEGF, FGF, CD54(ICAM-1) were analysed in urine 90 days after transplant (before randomization), and 365 days after transplant. Material were conserved at -80 Celsius, and analysed by ELISA at same time. Data was shown in MFI units (NCT01239472)
Timeframe: Urine and biopsy data are collected 90 days and 365 days after transplant.

Intervention	MFI (Median)
	IP10 90days	IP10 365days	MCP1 90days	MCP1 365days	MIG 90days	MIG 365days	RANTES 90days	RANTES 365days	IL8 90days	IL8 365days	IL12 90days	IL12 365days	TNF 90days	TNF 365days	IL10 90days	IL10 365 days	IL6 90days	IL6 365days	IL1 90days	IL1 365days	VEGF 90days	VEGF 365days	FGF 90days	FGF 365days	CD106 90days	CD106 365days	CD54 90days	CD54 365days
Everolimus	893	147	4119	1375	433	580	145	155	624	435	124	124	146	157	164	182	349	262	215	228	70	45	43	29	28564	19614	1293	1664
Tacrolimus	380	763	2349	1306	396	287	148	144	495	641	116	124	136	153	155	179	282	281	212	228	82	84	39	30	43222	18324	1512	696

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Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)

Dual Anti-platelet Therapy (DAPT) is Aspirin & Clopidogrel/Ticlopidine/Other. (NCT01249027)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Observational	934

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Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)

Dual Anti-platelet Therapy (DAPT) is Aspirin & Clopidogrel/Ticlopidine/Other. (NCT01249027)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Observational	879

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Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)

Dual Anti-platelet Therapy (DAPT) is Aspirin & Clopidogrel/Ticlopidine/Other. (NCT01249027)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Observational	800

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Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)

Dual Anti-platelet Therapy (DAPT) is Aspirin and Clopidogrel/Ticlopidine/Other. (NCT01249027)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Observational	2231

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Number of Participants Compliance With Dual Anti-platelet Therapy (DAPT)

Dual Anti-platelet Therapy (DAPT) is Aspirin and Clopidogrel/Ticlopidine/Other. (NCT01249027)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Observational	1085

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Number of Participants Experiencing Death

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery).~- Non-cardiac death is defined as a death not due to cardiac causes (as defined above)." (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	75

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Number of Participants Experiencing Death

Intervention	Participants (Count of Participants)
Observational	98

[back to top]

Number of Participants Experiencing Death

Intervention	Participants (Count of Participants)
Observational	34

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Number of Participants Experiencing Death

Intervention	Participants (Count of Participants)
Observational	64

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Number of Participants With All Target Lesion Revascularization

Target Lesion Revascularization (TLR) is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. The target lesion is defined as the treated segment from 5 mm proximal to the scaffold and to 5 mm distal to the test scaffold. (NCT01249027)
Timeframe: 0 to 1502 days

Intervention	Participants (Count of Participants)
Observational	30

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Number of Participants With All Target Lesion Revascularization

Intervention	Participants (Count of Participants)
Observational	33

[back to top]

Number of Participants With All Target Lesion Revascularization

Intervention	Participants (Count of Participants)
Observational	21

[back to top]

Number of Participants With All Target Lesions Revascularization

Intervention	Participants (Count of Participants)
Observational	25

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Number of Participants With All Target Lesions Revascularization

Intervention	Participants (Count of Participants)
Observational	12

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Number of Participants With All Target Vessel Revascularization

Target Vessel Revascularization (TVR) is defined as any repeat percutaneous intervention or surgical bypass of any segment of the target vessel. The target vessel is defined as the entire major coronary vessel proximal and distal to the target lesion. (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	42

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Number of Participants With All Target Vessel Revascularization

Intervention	Participants (Count of Participants)
Observational	53

[back to top]

Number of Participants With All Target Vessel Revascularization

Intervention	Participants (Count of Participants)
Observational	60

[back to top]

Number of Participants With All Target Vessel Revascularization

Intervention	Participants (Count of Participants)
Observational	20

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Number of Participants With All Target Vessel Revascularization

Intervention	Participants (Count of Participants)
Observational	36

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Number of Participants With Any MI

"Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	23

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Number of Participants With Any MI

Intervention	Participants (Count of Participants)
Observational	28

[back to top]

Number of Participants With Any MI

Intervention	Participants (Count of Participants)
Observational	31

[back to top]

Number of Participants With Any MI

Intervention	Participants (Count of Participants)
Observational	20

[back to top]

Number of Participants With Any MI

Intervention	Participants (Count of Participants)
Observational	13

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Number of Participants With Composite Rate of All Death and Any MI

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI Development of new, pathological Q wave on the ECG.~Non-Q wave MI Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	92

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Number of Participants With Composite Rate of All Death and Any MI

Intervention	Participants (Count of Participants)
Observational	120

[back to top]

Number of Participants With Composite Rate of All Death and Any MI

Intervention	Participants (Count of Participants)
Observational	137

[back to top]

Number of Participants With Composite Rate of All Death and Any MI

Intervention	Participants (Count of Participants)
Observational	46

[back to top]

Number of Participants With Composite Rate of All Death and Any MI

Intervention	Participants (Count of Participants)
Observational	80

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Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	191

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Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 1502 days

Intervention	Participants (Count of Participants)
Observational	235

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Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 1867 days

Intervention	Participants (Count of Participants)
Observational	271

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Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 407 days

Intervention	Participants (Count of Participants)
Observational	90

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Number of Participants With Composite Rate of All Death, Any MI, and Any Repeat Revascularization

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 772 days

Intervention	Participants (Count of Participants)
Observational	154

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Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)

"Cardiac Death:Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery).~Target lesion revascularization is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion." (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	71

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Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)

Intervention	Participants (Count of Participants)
Observational	87

[back to top]

Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)

Intervention	Participants (Count of Participants)
Observational	95

[back to top]

Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)

Intervention	Participants (Count of Participants)
Observational	35

[back to top]

Number of Participants With Composite Rate of Cardiac Death, MI Attributed to the Target Vessel (TV-MI), and All Target Lesion Revascularization (TLR)

Intervention	Participants (Count of Participants)
Observational	62

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Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery).~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	63

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Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery).~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 1502 days

Intervention	Participants (Count of Participants)
Observational	76

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Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery).~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 1867 days

Intervention	Participants (Count of Participants)
Observational	84

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Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery).~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 407 days

Intervention	Participants (Count of Participants)
Observational	33

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Number of Participants With Incidence of the Composite Rate of Cardiac Death and Any Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery).~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01249027)
Timeframe: 0 to 772 days

Intervention	Participants (Count of Participants)
Observational	55

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Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))

"Ischemia-Driven Target Vessel Failure (TVF) is the composite endpoint comprised of~Cardiac death,~Myocardial infarction (Q wave and Non-Q wave),~Ischemia-driven target lesion revascularization by Coronary artery bypass grafting (CABG) or Percutaneous coronary intervention (PCI),~Ischemia-driven target vessel revascularization by CABG or PCI." (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	100

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Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))

Intervention	Participants (Count of Participants)
Observational	123

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Number of Participants Experiencing Death

Intervention	Participants (Count of Participants)
Observational	113

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Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))

Intervention	Participants (Count of Participants)
Observational	50

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Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))

Intervention	Participants (Count of Participants)
Observational	86

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Number of Participants With Major Bleeding Complications (According to GUSTO Classification)

"Bleeding complications will be defined according to the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) classification of severe, moderate, and mild bleeding events:~Severe or life-threatening: Either intracranial hemorrhage or bleeding that causes hemodynamic compromise and requires intervention Moderate: Bleeding that requires blood transfusion but does not result in hemodynamic compromise Mild: Bleeding that does not meet criteria for either moderate or severe bleeding" (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	26

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Number of Participants With Major Bleeding Complications (According to GUSTO Classification)

Intervention	Participants (Count of Participants)
Observational	31

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Number of Participants With Major Bleeding Complications (According to GUSTO Classification)

Intervention	Participants (Count of Participants)
Observational	18

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Number of Participants With Major Bleeding Complications (According to GUSTO Classification)

Intervention	Participants (Count of Participants)
Observational	18

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Number of Participants With Major Bleeding Complications (According to GUSTO Classification)

"Bleeding complications will be defined according to the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) classification of severe, moderate, and mild bleeding events:~Severe or life-threatening: Either intracranial hemorrhage or bleeding that causes hemodynamic compromise and requires intervention.~Moderate: Bleeding that requires blood transfusion but does not result in hemodynamic compromise.~Mild: Bleeding that does not meet criteria for either moderate or severe bleeding." (NCT01249027)
Timeframe: 0 to 407 days

Intervention	Participants (Count of Participants)
Observational	14

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Number of Participants With Revascularization

"Revascularization:~Target Lesion Revascularization (TLR) is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. The target lesion is defined as the treated segment from 5 mm proximal to the scaffold and to 5 mm distal to the test scaffold.~Target Vessel Revascularization (TVR) is defined as any repeat percutaneous intervention or surgical bypass of any segment of the target vessel. The target vessel is defined as the entire major coronary vessel proximal and distal to the target lesion.~Non Target Lesion Revascularization (Non-TLR) is any revascularization in the target vessel for a lesion other than the target lesion.~Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel." (NCT01249027)
Timeframe: 0 to 407 days

Intervention	Participants (Count of Participants)
Observational	49

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Number of Participants With Revascularization

"Revascularization:~Target Lesion Revascularization (TLR) is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. The target lesion is defined as the treated segment from 5 mm proximal to the scaffold and to 5 mm distal to the test scaffold.~Target Vessel Revascularization (TVR) is defined as any repeat percutaneous intervention or surgical bypass of any segment of the target vessel. The target vessel is defined as the entire major coronary vessel proximal and distal to the target lesion.~Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel." (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	111

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Number of Participants With Revascularization

"Revascularization:~Target Lesion Revascularization (TLR) is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. The target lesion is defined as the treated segment from 5 mm proximal to the scaffold and to 5 mm distal to the test scaffold.~Target Vessel Revascularization (TVR) is defined as any repeat percutaneous intervention or surgical bypass of any segment of the target vessel. The target vessel is defined as the entire major coronary vessel proximal and distal to the target lesion.~Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel." (NCT01249027)
Timeframe: 0 to 1502 days

Intervention	Participants (Count of Participants)
Observational	132

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Number of Participants With Revascularization

"Revascularization:~Target Lesion Revascularization (TLR) is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. The target lesion is defined as the treated segment from 5 mm proximal to the scaffold and to 5 mm distal to the test scaffold.~Target Vessel Revascularization (TVR) is defined as any repeat percutaneous intervention or surgical bypass of any segment of the target vessel. The target vessel is defined as the entire major coronary vessel proximal and distal to the target lesion.~Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel." (NCT01249027)
Timeframe: 0 to 1867 days

Intervention	Participants (Count of Participants)
Observational	154

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Number of Participants With Revascularization

"Revascularization:~Target Lesion Revascularization (TLR) is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. The target lesion is defined as the treated segment from 5 mm proximal to the scaffold and to 5 mm distal to the test scaffold.~Target Vessel Revascularization (TVR) is defined as any repeat percutaneous intervention or surgical bypass of any segment of the target vessel. The target vessel is defined as the entire major coronary vessel proximal and distal to the target lesion.~Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel." (NCT01249027)
Timeframe: 0 to 772 days

Intervention	Participants (Count of Participants)
Observational	83

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Number of Participants With Target Lesion Failure (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01249027)
Timeframe: 0 to 1137 days

Intervention	Participants (Count of Participants)
Observational	69

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Number of Participants With Target Lesion Failure (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01249027)
Timeframe: 0 to 1502 days

Intervention	Participants (Count of Participants)
Observational	85

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Number of Participants With Target Lesion Failure (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01249027)
Timeframe: 0 to 1867 days

Intervention	Participants (Count of Participants)
Observational	93

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Number of Participants With Target Lesion Failure (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01249027)
Timeframe: 0 to 772 days

Intervention	Participants (Count of Participants)
Observational	60

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Number of Participants With Target Lesion Failure (TLF) (Composite Rate of Cardiac Death, TV-MI and Ischemia-driven TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01249027)
Timeframe: 0 to 407 days

Intervention	Participants (Count of Participants)
Observational	35

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Number of Participants With Stent Thrombosis

"Definite Stent Thrombosis (ST) occurred by either angiographic/pathologic confirmation of ST.~Angiographic confirmation:The presence of a thrombus that originates in the stent/in the segment 5mm proximal/distal to the stent&presence of at least 1 of the following criteria within 48hours:~Acute onset of ischemic symptoms at rest~New ischemic ECG changes~Typical rise&fall in cardiac biomarkers~Nonocclusive &occlusive thrombus~Pathological confirmation:Evidence of recent thrombus within the stent determined at autopsy/via examination of tissue retrieved following thrombectomy.~Probable ST may occur due to:~Unexplained death within first 30 days~Irrespective of the time after the index procedure,any MI that is related to documented acute ischemia in the territory of the implanted stent without angiographic confirmation of ST&in the absence of any other obvious cause." (NCT01249027)
Timeframe: 0 to 1867 days

Intervention	Participants (Count of Participants)
	Definite	Definite & Probable
Observational	5	10

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Number of Participants With Ischemia-driven Target Vessel Failure (ID-TVF) (Composite Rate of Cardiac Death, All MI and Target Vessel Revascularization (TVR))

Intervention	Participants (Count of Participants)
Observational	136

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Number of Participants With Stable Disease (SD)

For patients with metastatic uveal melanoma treated with RAD001 and pasireotide LAR. (NCT01252251)
Timeframe: at 16 weeks

Intervention	Participants (Count of Participants)
RAD001 and Pasireotide LAR	7

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Median Progression Free Survival(PFS)

(NCT01252251)
Timeframe: Up to 3 years

Intervention	weeks (Median)
RAD001 and Pasireotide LAR	16

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Median Overall Survival (OS)

(NCT01252251)
Timeframe: Up to 3 years

Intervention	months (Median)
RAD001 and Pasireotide LAR	11

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Survival of Patients Treated

With Everolimus in combination with intravesical gemcitabine. Overall survival following start of therapy will be estimated using Kaplan-Meier methods. (NCT01259063)
Timeframe: 1 year

Intervention	% of pts with CR who relapsed in a year (Number)
Pts Who Failed or Relapsed After Intravesical BCG	21

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Complete Response (CR) Rate

Complete Response (CR) is defined as no evidence of disease (by cytology and cystoscopy). Partial Response is defined as negative cystoscopy and positive cytology. Progression is defined as the development of invasion or metastasis. If the participant develops a recurrence, they will be considered having failed treatment. Participants will also be considered having failed treatment if there is no response to treatment after two cycles. (NCT01259063)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
	Complete Response	Partial Response	Did not achieve CR or PR
Pts Who Failed or Relapsed After Intravesical BCG	17	8	8

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Phase I - Dose-limiting Toxicity (DLT)

Everolimus (mg) given in conjunction with intravesical gemcitabine (NCT01259063)
Timeframe: 8 weeks

Intervention	DLT (Number)
Pts Who Failed or Relapsed After Intravesical BCG	0

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Phase II - Patients Who Are Free of Disease at 1 Year

following start of therapy. (NCT01259063)
Timeframe: 1 year

Intervention	percentage of pts disease free at 1 year (Number)
Pts Who Failed or Relapsed After Intravesical BCG	21

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Phase I - Maximum Tolerated Dose (MTD)

of Everolimus given in conjunction with intravesical gemcitabine (NCT01259063)
Timeframe: 8 weeks

Intervention	mg daily of everolimus (Number)
Pts Who Failed or Relapsed After Intravesical BCG	10

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Number of Rejections Leading to Hemodynamic Compromise

Number of all rejections were recorded through the duration of the study with the intent to identify rejections leading to hemodynamic compromise. (NCT01266148)
Timeframe: 52 weeks

Intervention	rejections (Number)
	Total rejection	Treated rejection	Rejections with hemodynamic compromise
Control	128	17	0
Everolimus	185	43	0

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Measured Glomerular Filtration Rate (mGFR), 12 Months After Heart Transplantation

Measured Glomerular Filtration Rate (mGFR) describes the flow rate of filtered fluid through the kidney. GFR is equal to the clearance rate when any solute is freely filtered and is neither reabsorbed nor secreted by the kidneys. The rate therefore measured is the quantity of the substance in the urine that originated from a calculable volume of blood. Participants' urine was used for this assessment at week 52 after heart transplant. (NCT01266148)
Timeframe: Week 52

Intervention	mGFR ml/min (Mean)
Everolimus	79.8
Control	61.5

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Average Level of Protenuria at Week 52

Proteinuria is measured as the ratio of albumin/creatinine mg/mmol. Measurements were taken from participants urine samples. (NCT01266148)
Timeframe: 52 weeks

Intervention	mg/mmol (Mean)
Everolimus	7.2
Control	1.2

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Change in Quality of Life - Euro Quality of Life 5D (EQ-5D)

Change in Quality of Life was assessed via the EQ-5D questionnaire which consists of: EQ-5D-5L descriptive system and EQ Visual Analogue scale (EQ VAS). The EQ-5D-5L comprises 5 dimensions (mobility, self-care, usual activities, pain/discomfort, anxiety/depression). Each dimension has 5 levels (no problems, slight problems, moderate problems, severe problems, and extreme problems). The patient indicates his/her health state by checking the most appropriate statement. This decision results in a 1-digit number expressing the level selected for that dimension. The digits for 5 dimensions are combined in a 5-digit number describing the respondent's health state. The possible score is 1 to 5 where a lower number indicates improvement. The EQ VAS records the patient's self-rated health on a 20 cm vertical, visual analogue scale with endpoints labelled 'the best health you can imagine' and 'the worst health you can imagine'. The score is 0 to 100 where a higher score represents improvement. (NCT01266148)
Timeframe: Pre transplant and 52 weeks

Intervention	Units on a scale (Mean)
	EQ-5D-5L pre- transplant (n=45,49)	EQ-5D-5L at week 52 (n=41,44)	EQ VAS pre- transplant (n=41,48)	EQ VAS at week 52 (n=41,42)
Control	0.5069	0.8367	38.9	79.4
Everolimus	0.5750	0.8329	46.0	80.0

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Change in Calculated Glomerular Filtration Rate From Pre-transplantation to Week 52

Change in calculated glomerular filtration rate from pre-transplantation to week 52 was calculated according to the Modification of Diet in Renal Disease (MDRD) method. Measurements were taken prior to transplant (day 1), between weeks 7 to 11 and end week 52. (NCT01266148)
Timeframe: Day 1, weeks 7 to 11(baseline) and of week 52

Intervention	mGFR mL/min (Mean)
	Day 1 (n= 43, 47)	Weeks 7 to 11 (n= 46, 49)	Week 52 (n= 42, 53)
Control	-12.6	-6.8	-8.0
Everolimus	-13.0	7.4	27.8

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Progression of Chronic Allograft Vasculopathy (CAV) Based on Maximal Intimal Thickness (MIT) From Baseline to Week 52

The progression of chronic allograft vasculopathy (CAV) was assessed by intravascular ultrasound (IVUS) examinations and measured Maximal Intimal Thickness (MIT)(in mm). A major coronary epicardial artery (preferentially the left-anterior descending coronary artery) was imaged, and the MIT parameters were recorded at baseline and at week 52. (NCT01266148)
Timeframe: Baseline and week 52

Intervention	mm (Mean)
	Baseline (Week 7)	Week 52
Control	0.56	0.65
Everolimus	0.52	0.55

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Progression of Chronic Allograft Vasculopathy (CAV) Based on Incidence of Chronic Allograft Vasculopathy (CAV) From Baseline to Week 52

the progression of chronic allograft vasculopathy (CAV) assessed by intravascular ultrasound (IVUS) examinations, measured the incidence of CAV (in percent of patients) at baseline and at week 52. Incidence of CAV represents percent of patients having a MIT (maximal intima thickness) > 0.5 mm. (NCT01266148)
Timeframe: Baseline and week 52

Intervention	Percentage of patients (Number)
	No CAV at baseline (week 7)	CAV at baseline (week 7)	No CAV at week 52	CAV at week 52
Control	47.9	52.1	35.4	64.6
Everolimus	43.5	56.5	50	50

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Occurrence of Treatment Failures up to 12 Months After Transplant

Treatment failure was defined as the number of participants who died or lost their graft at any timepoint througout the duration of the study. (NCT01266148)
Timeframe: 52 weeks

Intervention	participants (Number)
	Treatment failure (death)	Graff loss	Total treatment failures (graft loss + death
Control	3	0	3
Everolimus	2	0	2

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Calculated Glomerular Filtration Rate From Pre-Transplantation to Week 52

Calculated Glomerular Filtration Rate from pre-transplantation to week 52 was calculated according to the Modification of Diet in Renal Disease (MDRD) method. Measurements were taken prior to transplant (day 1), between weeks 7 to 11 and end of week 52. (NCT01266148)
Timeframe: Day 1, weeks 7 to 11 and of week 52

Intervention	mGFR mL/min (Mean)
	Day 1 (n= 46, 48)	Weeks 7 to 11 (n=50, 51)	Week 52 (n= 45, 55)
Control	66.1	69.6	69.3
Everolimus	65.4	84.9	104.5

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Lipid Profile at 12 Months

Total Cholesterol, LDL-Chol, HDL-Chol and TG at week 52. Measurements were taken via participants blood samples. (NCT01266148)
Timeframe: 52 weeks

Intervention	mmol/L (Mean)
	Total cholesterol	LDL-C	HDL-C
Control	5.1	2.8	1.6
Everolimus	5.3	2.9	1.6

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Change in Quality of Life Assessed by SF-36 (Minnesota Living With Heart Failure Questionnaire ([MLHF)]) From Pre-transplant to Week 52 of Treatment

Change in Quality of Life was assessed via the SF-36 (Minnesota Living with Heart Failure questionnaire ([MLHF)]) before transplant surgery and at week 52 of treatment. The SF-36 is a validated, self-administered questionnaire. The questionnaire, which includes 36 questions measures 8 dimensions of health: physical function, role-physical, bodily pain, general health, vitality, social function, role-emotional, and mental health. Scores can be summarized in 2 summary components assessing physical and mental health. Items in each dimension are coded, aggregated, summed, and transformed into a scale ranging from 0 (worse health) to 100 (best health). (NCT01266148)
Timeframe: Pre transplant and 52 weeks

Intervention	Units on a scale (Mean)
	Physical Health pre- transplant	Physical Health at week 52	Mental Health pre- transplant	Mental Health at week 52
Control	32.9	48.8	38.7	53.9
Everolimus	30.8	48.8	46.2	51.5

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Number of Participants With Progression-free Survival

"Time from starting treatment until disease progression as defined using Response Evaluation CriteriaIn 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, or death." (NCT01270321)
Timeframe: Through study completion, an average of 1 year

Intervention	Participants (Count of Participants)
Arm A (Everolimus Alone)	17
Arm B (Pasireotide Alone)	9
Arm C (Everolimus + Pasireotide)	11

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Number of Participants With Response Per Responsive Evaluation Criteria in Solid Tumors Criteria (RECIST v1.0)

"Number of participants with 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." (NCT01270321)
Timeframe: Through study completion, an average of 1 year

Intervention	Participants (Count of Participants)
Arm A (Everolimus Alone)	17
Arm B (Pasireotide Alone)	9
Arm C (Everolimus + Pasireotide)	11

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All Collected Deaths

On treatment deaths were collected from FPFT up to 28 days after study drug discontinuation, for a maximum duration of 35.52 months (treatment duration ranged from 0.36 to to 35.52 months for the phase I part) and a maximum duration of 21.88 months (treatment duration of 0.16 to 21.88 months for the phase II part). Deaths post treatment survival follow up were collected after the on treatment period, up to 70 months. (NCT01275222)
Timeframe: approx. 35.52 months, approx. 70 months

,,,,,

Intervention	Participants (Number)
	Total Deaths	Deaths on-treatment
Phase l: RAD001 2.5mg/Day + Glivec 600mg/Day	8	3
Phase l: RAD001 2.5mg/Day + Glivec 800mg/Day	3	2
Phase l: RAD001 20mg/Week	12	2
Phase l: RAD001 5mg/Day + Glivec 600mg/Day	3	0
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day	9	3
Phase ll: Stratum ll (Post Second-line Therapy)	22	6

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4-Month Progression-free Survival (PFS) Rate - Phase II

Assessed clinical efficacy of the combination regimen in this patient population per Progression-free survival (PFS). Progression-free survival (PFS) was the time from date of start of treatment to the date of first documented progression or death due to any cause. Per protocol (PP) population includes patients with no known overall lesion response during 4 months +/- 2 weeks, or who later had response of CR/PR/stable disease (SD). PP population excludes patients with no known response during 4 months + / -2 weeks and no subsequent CR/PR/SD. (NCT01275222)
Timeframe: about 4 months

Intervention	Percentage of participants (Number)
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day	17.4
Phase ll: Stratum ll (Post Second-line Therapy)	37.1

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Best Overall Response (BOR) as Assessed by Overall Response (Complete Response (CR) & Partial Response (PR)) - Phase I & II

Assessed clinical efficacy of the combination regimen in this patient population per BOR by Overall response (CR + PR). Complete response: Disappearance of all target lesions; Partial response: ≥ 30% decrease in the sum of the longest diameter of target lesions compared to baseline (and not ≥20% increase compared to smallest sum). (NCT01275222)
Timeframe: 6 - 8 weeks

Intervention	Percentage of Participants (Number)
Phase l: RAD001 20mg/Week	0
Phase l: RAD001 2.5mg/Day + Glivec 600mg/Day	1
Phase l: RAD001 5mg/Day + Glivec 600mg/Day	0
Phase l: RAD001 2.5mg/Day + Glivec 800mg/Day	0.0
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day	0
Phase ll: Stratum ll (Post Second-line Therapy)	1

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Number of Participants With Adverse Events (AEs): Phase I & II

Assessed safety and tolerability of the combination administration of RAD001 and imatinib when given to patients with imatinib-refractory gastro-intestinal stromal tumors (GIST) by number of participants with adverse events. (NCT01275222)
Timeframe: 4 - 8 weeks

Intervention	Participants (Number)
Phase l: RAD001 20mg/Week	13
Phase l: RAD001 2.5mg/Day + Glivec 600mg/Day	13
Phase l: RAD001 5mg/Day + Glivec 600mg/Day	5
Phase l: RAD001 2.5mg/Day + Glivec 800mg/Day	11
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day	27
Phase ll: Stratum ll (Post Second-line Therapy)	47

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Overall Survival (OS) - Phase I & II

Assessed clinical efficacy of the combination regimen in this patient population per Overall Survival (OS). Overall survival was defined as the time from date of start of treatment to date of death due to any cause. For patients still receiving study medication at the time of the analysis, survival was censored at the date of last examination. If a patient was not known to have died but was no longer continuing with study medication, survival was censored at the date of last contact. (NCT01275222)
Timeframe: about 60 months

Intervention	months (Median)
Phase l: RAD001 20mg/Week	9.4
Phase l: RAD001 5mg/Day + Glivec 600mg/Day	10.9
Phase l: RAD001 2.5mg/Day + Glivec 600mg/Day	18.7
Phase l: RAD001 2.5mg/Day + Glivec 800mg/Day	NA
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day	14.9
Phase ll: Stratum ll (Post Second-line Therapy)	10.7

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Progression-free Survival (PFS) - Phase II

"Assessed clinical efficacy of the combination regimen in this patient population per Progression-free survival (PFS). Progression-free survival (PFS) was the time from date of start of treatment to the date of first documented progression or death due to any cause. If a patient had not progressed or died, progression-free survival was censored at the time of last adequate tumor assessment.~According to the study protocol no tumor assessments were performed after discontinuation of treatment with study drug. Therefore, for all patients who discontinued treatment without a documented progression but died thereafter, death was considered as PFS event only if it occurred within the regular safety follow-up of 28 days after discontinuation. Otherwise, the PFS time was censored at the last adequate tumor assessment." (NCT01275222)
Timeframe: about 60 months

Intervention	months (Median)
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day	1.9
Phase ll: Stratum ll (Post Second-line Therapy)	3.5

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Trough Concentrations for RAD001 and for Imatinib - Phase II

Assessed the pharmacokinetics (PK) of the combination administration of RAD001 and imatinib in this patient population. (NCT01275222)
Timeframe: Part II Daily regimen: Baseline, Days 8, 15 and thereafter approximately every two months starting at month 3 whenever possible

Intervention	ng/mL (Median)
	Week 2: RAD001	Week 3: RAD001	Week 9: RAD001	Month 4: RAD001	Baseline: Imatinib	Week 2: Imatinib	Week 3: Imatinib	Week 9: Imatinib	Month 4: Imatinib	Month 6: Imatinib	Month 8: Imatinib	Month 12: Imatinib
Phase ll: Stratum ll (Post Second-line Therapy)	12.100	12.750	10.950	7.840	501.50	540.00	718.00	899.0	446.00	2040.00	575.00	324.00

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Trough Concentrations for RAD001 and for Imatinib - Phase II

Intervention	ng/mL (Median)
	Week 2: RAD001	Week 3: RAD001	Baseline: Imatinib	Week 2: Imatinib	Week 3: Imatinib	Month 4: Imatinib	Month 6: Imatinib
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day	24.300	19.900	472.00	626.50	572.00	333.00	181.00

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Renal Function Assessed by Creatinine Clearance

Renal function was assessed by measuring serum creatinine and by computing creatinine clearance using the formula of Cockcroft-Gault. (NCT01276457)
Timeframe: Month 12, Month 18, and Month 24

Intervention	mL/min (Mean)
	Month 12 (n=111, 111)	Month 18 (n=108, 108)	Month 24 (n=106, 110)
Standard Everolimus Blood Target + Low Dose Cyclosporine	62.50	62.80	63.76
Upper Everolimus Blood Target + Very Low Dose Cyclosporine	61.26	60.90	61.92

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Number of Participants Who Died, Number of Participants Who Lost Their Graft, and Number of Participants Who Died or Lost Their Graft

A participant lost his graft if he/she started dialysis and was not able to subsequently be removed from dialysis or underwent graft nephrectomy. (NCT01276457)
Timeframe: Baseline to end of study (Month 24)

Intervention	Participants (Number)
	Died	Lost graft	Died or lost graft
Standard Everolimus Blood Target + Low Dose Cyclosporine	3	15	18
Upper Everolimus Blood Target + Very Low Dose Cyclosporine	2	6	8

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Number of Participants With Adverse Events (AE), Serious Adverse Events (SAE) or Deaths

Safety was assessed using reports of adverse events of all participants in this study. Serious adverse events are those events that resulted in death, were life threatening, required inpatient hospitalization or prolongation of existing hospitalization, resulted in persistent or significant disability/incapacity, or was a congenital anomaly/birth defect. (NCT01276457)
Timeframe: Baseline to end of study (Month 24)

Intervention	Partcipants (Number)
	AEs	Infection	Clinically significant AEs	SAEs	Died
Standard Everolimus Blood Target + Low Dose Cyclosporine	143	101	53	90	3
Upper Everolimus Blood Target + Very Low Dose Cyclosporine	142	95	58	85	2

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Number of Participants With Biopsy-proven Acute Rejection

A graft core biopsy was performed on all suspected acute rejection episodes within 48 hours. Biopsies were read by the local pathologist according to the 1997 Banff criteria. A biopsy-proven acute rejection was be defined as a biopsy graded IA, IB, IIA, IIB, or III. (NCT01276457)
Timeframe: Baseline to end of study (Month 24)

Intervention	Participants (Number)
Upper Everolimus Blood Target + Very Low Dose Cyclosporine	21
Standard Everolimus Blood Target + Low Dose Cyclosporine	21

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Response Rate (CR + PR) Assessed by RECIST 1.1 (Phase II)

(NCT01281865)
Timeframe: At 8 weeks

Intervention	participants (Number)
	Progression of Disease	Stable Disease
Arm 1-Treatment (Everolimus and Imatinib Mesylate)	4	5
Arm 2-Treatment (Everolimus and Imatinib Mesylate)	1	0

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Progression-free Survival (PFS)

Objective tumor responses were assessed every 2 cycles of chemotherapy with computed tomography or positron emission tomography/ computed tomography scans in accordance with Response Evaluation Criteria In Solid Tumors (RECIST) criteria. (NCT01283334)
Timeframe: The time of PFS was calculated as the time from study enrollment to the disease progression date, death date, or last contact, whichever came first, up to 25 months

Intervention	months (Median)
Carboplatin, Cetuximab and Everolimus	8.15

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To Measure the Safety and Clinical Effectiveness of the Combination of Carboplatin, Cetuximab and RAD001 in Patients With Advanced (Recurrent or Metastatic) Head and Neck Cancer

This phase 1 clinical trial used a standard 3 + 3 design. Four dose levels of everolimus were planned to be evaluated, and the standard 3 + 3 design with dose de-escalation was used in the trial. Namely, 3 patients were assigned to starting dose level 1. If no dose-limiting toxicity (DLT) was observed, the trial proceeded to the next dose level, and another cohort of 3 patients was enrolled. If at least 2 of the 3 patients experienced at least 1 DLT, then the dose level decreased; otherwise, if only 1 patient experienced DLT, then 3 more patients were enrolled at the same dose level. If none of the 3 additional patients experienced DLT, the dose was escalated; otherwise, the dose level decreased. Dose reduction continued until a dose level was reached at which 6 patients had been treated and at most 1 DLT was observed. (NCT01283334)
Timeframe: Within the first 21 days of therapy

Intervention	participants (Number)
Everolimus Dose Level 1 DLT	2
Everolimus Dose Level -1 DLT	1

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Evaluation of the Efficacy of RAD001 on Neurocognition in Patients With TSC Compared With Placebo.

"Baseline and 6 month Timepoint scores are reported for the following primary outcome measures:~Peabody Picture Vocabulary Test 4 (PPVT-4; Receptive Language Measure). Scores reported as (mean, SD). Range=40-160, higher scores are better.~Expressive Vocabulary Test 2 (EVT-2; Expressive Language Measure). Scores reported as (mean, SD). Range=40-160, higher scores are better.~Wide Range Assessment of Memory and Learning 2 (WRAML2; Measure of Verbal Memory and Attention ). Scores reported as (mean, SD). Range=1-19, higher scores are better.~Vineland Adaptive Behavior Scales-II (VABS-II; Measure of Adaptive Behavior). Scores reported as (mean, SD). Range = 40-160, higher scores are better.~Purdue Pegboard Test (Measure of Fine Motor Speed and Coordination). Scores reported as (mean, SD). Range = 40-160, higher scores are better." (NCT01289912)
Timeframe: 6 months

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Intervention	units on a scale (Mean)
	PPVT4 (Receptive Language)	EVT2 (Expressive Language)	WRAML2 Verbal Learning	WRAML2 Verbal Recall	VABS2 Adaptive Behavior Composite	VABS2 Communication	VABS2 Socialization	VABS2 Daily Living Skills	VABS2 Motor Skills	Pegboard, Dominant Hand	Pegboard, Non-Dominant Hand
Placebo - 6 Months	88.54	89.15	8.46	8.23	79.00	81.77	80.38	81.69	92.69	89.83	92.15
Placebo - Baseline	86.00	85.47	8.00	7.07	78.79	81.27	79.07	78.80	89.87	101.33	105.27
RAD001 - 6 Months	82.5	82.55	7.85	8.08	74.72	76.79	76.86	76.41	87.79	97.25	112.78
RAD001 - Baseline	81.06	90.00	7.14	7.52	72.06	73.68	74.10	74.68	78.83	103.06	119.30

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Evaluation of the Safety of RAD001 on Neurocognition in Patients With TSC Compared With Placebo in Patients With TSC.

Evaluation of the safety of RAD001 compared with placebo in patients with TSC focusing on NCI CTCAE Grade 3 and 4 adverse events, serious adverse events, and Grade 3 and 4 laboratory toxicities. (NCT01289912)
Timeframe: 6 months

Intervention	Adverse Events (Number)
RAD001	325
Placebo	147

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Comparison of Autism Spectrum Disorders Features Between Patients Taking RAD001 vs. Placebo

Scores for the Baseline and 6 Month Timepoints are reported. The secondary outcome measure was the Social Responsiveness Scale (SRS). Standard scores are reported with a mean of 100 and standard deviation of 15. The range is 40-160 with higher scores indicating a better outcome. (NCT01289912)
Timeframe: 6 months

,,,

Intervention	units on a scale (SRS) (Mean)
	SRS Social Responsiveness (range 40(worse) -160)	SRS Social Awareness	SRS Social Cognition	SRS Social Communication	SRS Social Motivation	SRS Autism Mannerisms
Placebo - 6 Months	80.62	67.38	81.15	76.85	72.77	79.77
Placebo - Baseline	77.14	67.40	76.43	74.36	69.80	76.71
RAD001 - 6 Months	75.69	64.86	76.17	71.69	67.24	78.66
RAD001 - Baseline	76.43	62.90	75.70	72.23	69.60	80.03

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Comparison of Behavioral Problems Between Patients Taking RAD001 vs Placebo

"Scores for Baseline and 6 Month Timepoints are reported for the following secondary outcome measures:~Behavior Rating Inventory of Executive Function (BRIEF) (Measure of executive functions) T-scores are reported, with a mean of 50 and a standard deviation of 10. The range is 30-100 with higher scores indicating a worse outcome.~Behavioral Assessment System for Children (BASC) (Measure of emotional and behavioral problems) T-scores are reported (mean of 50, SD of 10). The range is 30-100 with higher scores indicating a worse outcome. Conversely, on the Adaptive Skills subscale of the BASC, lower scores indicate a poorer outcome.~Strengths and Difficulties Questionnaire (SDQ). Includes questions related to emotional symptoms, conduct problems, inattention/hyperactivity, peer relationship problems and prosocial behavior. Responses to these items are summed to comprise a Total Difficulties Score, which ranges from 0-40, with lower scores indicating a better outcome" (NCT01289912)
Timeframe: 6 months

,,,

Intervention	units on a scale (Mean)
	BRIEF Global Executive Composite	BRIEF Behavioral Regulation Index	BRIEF Metacognition Index	BASC2 Behavioral Symptoms Index	BASC2 Externalizing Problems	BASC2 Internalizing Problems	BASC2 Adaptive Skills	SDQ Total Difficulties Scale
Placebo - 6 Months	62.25	60.83	61.83	57.54	52.62	56.00	42.08	14.42
Placebo - Baseline	70.50	70.93	68.07	62.29	57.36	58.43	38.79	16.00
RAD001 - 6 Months	64.68	62.57	64.57	55.41	52.34	51.45	40.00	13.20
RAD001 - Baseline	69.48	66.53	68.93	58.97	53.24	51.55	36.72	15.46

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Evaluation of the Efficacy of RAD001 on Neurocognition (Cambridge Neuropsychological Test Automated Battery) in Patients With TSC Compared With Placebo.

"Scores are reported for baseline and 6 month timepoints on the Cambridge Neuropsychological Test Automated Battery (CANTAB) subscales below. For all subscales, scores are reported as the mean difference between the study subjects and a normative population matched for age, gender and IQ (e.g., subject subscale score - mean of matched normative group = reported score). Higher scores represent a better outcome.~Spatial Span (SSP) (spatial memory span) Range: -3 to 3~Spatial Working Memory (working memory) Range: -3 to 3~Pattern Recognition Memory (PRM) (visual pattern recognition memory) Range: -3 to 3~Spatial Recognition Memory (SRM) (spatial recognition memory) Range: -4 to 4~Rapid Visual Information Processing (RVIP) (sustained attention) Range: -4 to 4~Stockings of Cambridge (SOC) (spatial planning) Range: -4 to 4~Intra-Extra Dimensional Set Shift (IDED) (cognitive flexibility) Range: -5 to 5~Reaction Time (processing speed) Range: -5 to 5" (NCT01289912)
Timeframe: 6 months

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Intervention	units on a scale (Mean)
	CANTAB Pattern Recognition Memory	CANTAB Spatial Recognition Memory	CANTAB Spatial Span	CANTAB Spatial Working Memory	CANTAB Reaction Time	CANTAB Rapid Visual Processing	CANTAB Stockings of Cambridge	CANTAB IDED
Placebo - 6 Months	-.91	-2.62	-1.29	-.73	-.88	-.97	-.58	-1.05
Placebo - Baseline	-1.48	-2.33	-1.32	-.66	-2.24	-.96	-1.38	-1.02
RAD001 - 6 Months	-1.09	-2.19	-1.32	-.27	-2.91	-1.2	-1.84	-2.24
RAD001 - Baseline	-1.23	-2.24	-1.02	-.67	-1.15	-1.41	-1.89	-1.48

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Comparison of Academic Skills Between Patients Taking RAD001 vs. Placebo

Scores are reported for Baseline and 6 Month Timepoints. The secondary outcome measure was the Wide Range Achievement Test 4 (WRAT4), which was used to assess academic skills. The Reading and Math subtests were used. Standard scores are reported which have a mean of 100 and a standard deviation of 15 (range=40-160 where higher is better). (NCT01289912)
Timeframe: 6 months

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Intervention	units on a scale (Mean)
	Word Reading (WRAT 4)	Math Computation (WRAT 4)
Placebo - 6 Months	91.15	77.31
Placebo - Baseline	86.80	76.00
RAD001 - 6 Months	84.45	73.81
RAD001 - Baseline	84.28	74.60

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Extracranial Response

"Extracranial response was measured using RECIST 1.1 criteria and defined as the number of subjects achieving CR or PR.~Complete Response (CR) - Disappearance of all target and nontarget 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 longest diameter AND an absolute decrease of at least 5mm in at least one target lesion.~Stable Disease (SD) - neither sufficient shrinkage to qualify for partial response nor sufficient increase to qualify for progressive disease, taking as reference the smallest sum of the longest diameter since the treatment started.~Progressive Disease (PD) - at least a 20% increase in the sum LD of target lesions, taking as reference the smallest sum of the longest diameter recorded since the treatment started AND an absolute increase in size of at least 5 mm in at least one target lesion OR the appearance of one or more new lesions of at least 6 mm in size." (NCT01305941)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Everolimus +Vinorelbine + Trastuzumab	5

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Time to Intracranial Progression.

"Time to intracranial progression after administration of everolimus in combination with trastuzumab and vinorelbine as defined via modified RECIST criteria.~Progressive Disease (PD) - at least a 20% increase in the sum LD of target lesions, taking as reference the smallest sum of the longest diameter recorded since the treatment started AND an absolute increase in size of at least 5 mm in at least one target lesion OR the appearance of one or more new lesions of at least 6 mm in size." (NCT01305941)
Timeframe: 3 years

Intervention	months (Median)
Everolimus +Vinorelbine + Trastuzumab	3.93

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Toxicity

"Grade 3 or higher toxicities of interest are reported. Toxicity was assessed according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) v4.~The NCI CTCAE is a descriptive terminology which can be utilized for Adverse Event (AE) reporting. A grading (severity) scale is provided for each AE term. Grade 1 Mild; asymptomatic or mild symptoms; clinical or diagnostic observations only; intervention not indicated. Grade 2 Moderate; minimal, local or noninvasive intervention indicated; limiting age-appropriate instrumental Activities of Daily Living (ADL). Grade 3 Severe or medically significant but not immediately life-threatening; hospitalization or prolongation of hospitalization indicated; disabling; limiting self care ADL. Grade 4 Life-threatening consequences; urgent intervention indicated. Grade 5 Death related to AE." (NCT01305941)
Timeframe: 24 weeks

Intervention	Participants (Count of Participants)
	Alkaline phosphatase increased	Anemia	Anorexia	Asparate Aminotransferase Increased	Diarrhea	Febrile Neutropenia	Hyperkalemia	Lymphocyte Count Decreased	Mucositis Oral	Neutrophil Count Decreased	Pneumonitis	Sepsis	White Blood Cell Decreased
Everolimus +Vinorelbine + Trastuzumab	1	5	1	2	1	2	1	3	5	13	1	3	11

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Overall Survival

Overall survival (OS) after administration of everolimus in combination with trastuzumab and vinorelbine (NCT01305941)
Timeframe: 3 years

Intervention	years (Median)
Everolimus +Vinorelbine + Trastuzumab	1.01

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Intracranial Response Rate- MacDonald Criteria

"Intracranial tumor lesions were evaluated via gadolinium-enhanced brain MRI using the MacDonald criteria. Measurable disease is defined as at least 1 measurable brain lesion accurately measured in at least 2 dimensions (longest diameter) as ≥5.0 mm. Tumor size is the product of the 2 longest bi-dimensional lines.~Complete Response (CR)- Disappearance of all tumor on consecutive CT or MRI scans at least 1 month apart, off steroids for treatment of neurological symptoms, and neurologically stable or improved.~Partial Response (PR)- ≥50% reduction in size of tumor on consecutive CT or MRI scans at least 1 month part, steroids stable or reduced, and neurologically stable or improved.~Progressive Disease (PD)- ≥25% increase in size of tumor or any new tumor on CT or MRI scans, or neurologically worse, and steroids stable or increased due to neurologic symptoms.~Stable Disease (SD)- all other situations Overall Response Rate (ORR) is the sum of partial responses (PRs) and CRs." (NCT01305941)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Everolimus +Vinorelbine + Trastuzumab	1

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Functional Assessment of Cancer Therapy- Brain (FACT-Br) Change From Baseline to Assess Impact of Everolimus in Combination With Trastuzumab and Vinorelbine on Quality of Life

The FACT-Br is a 23-question self-report questionnaire subscale administered with the Functional Assessment of Cancer Therapy- General (FACT-G) which contains concerns relevant to patients with brain tumors . 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 times the number of questions in the domain, with 0 indicating worst and the highest possible value indicating best outcome. Total scores on the FACT-Br subscale range from 0 to 92 with lower scores indicating declining quality of life. The change from baseline is the difference in scores between the baseline and 9 week assessments. (NCT01305941)
Timeframe: 9 weeks

Intervention	units on a scale (Median)
Everolimus +Vinorelbine + Trastuzumab	-1.0

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Intracranial Objective Response Rate- Modified RECIST Criteria

"response will be evaluated via gadolinium-enhanced brain MRI using modified RECIST criteria.~Complete Response (CR) - Disappearance of all target and nontarget 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 longest diameter AND an absolute decrease of at least 5mm in at least one target lesion.~Stable Disease (SD) - neither sufficient shrinkage to qualify for partial response nor sufficient increase to qualify for progressive disease, taking as reference the smallest sum of the longest diameter since the treatment started.~Progressive Disease (PD) - at least a 20% increase in the sum LD of target lesions, taking as reference the smallest sum of the longest diameter recorded since the treatment started AND an absolute increase in size of at least 5 mm in at least one target lesion OR the appearance of one or more new lesions of at least 6 mm in size." (NCT01305941)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
	Complete Response	Partial Response	Stable Disease	Progressive Disease
Everolimus +Vinorelbine + Trastuzumab	0	1	17	8

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Functional Assessment Cancer Therapy- Breast (FACT-B) From Baseline to 9 Weeks of Treatment to Assess Impact of Everolimus in Combination With Trastuzumab and Vinorelbine on Quality of Life

The FACT-B is a 10-question self-report questionnaire subscale administered with the Functional Assessment of Cancer Therapy- General (FACT-G) which contains concerns relevant to patients with breast cancer. 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 times the number of questions in the domain, with 0 indicating worst and the highest possible value indicating best outcome. Total scores on the FACT-B subscale range from 0 to 40 with lower scores indicating declining quality of life. The change from baseline is the difference in scores between the baseline and 9 week assessments. (NCT01305941)
Timeframe: 9 weeks

Intervention	units on a scale (Median)
Everolimus +Vinorelbine + Trastuzumab	1.0

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Extracranial Time to Progression

"To evaluate the extracranial time to progression as determined by RECIST 1.1 criteria after administration of everolimus in combination with trastuzumab and vinorelbine.~Progressive Disease (PD) - at least a 20% increase in the sum LD of target lesions, taking as reference the smallest sum of the longest diameter recorded since the treatment started AND an absolute increase in size of at least 5 mm in at least one target lesion OR the appearance of one or more new lesions of at least 6 mm in size." (NCT01305941)
Timeframe: 3 years

Intervention	months (Median)
Everolimus +Vinorelbine + Trastuzumab	4.01

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Number of Participants Without New Bone Lesions After 12 Weeks of Treatment

(NCT01313559)
Timeframe: After 12 weeks of treatment

Intervention	participants (Number)
Cohort A (Pasireotide)	0
Cohort B (Pasireotide and Everolimus)	0

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Number of Participants With > 50% Decline From Baseline PSA Level

(NCT01313559)
Timeframe: After 12 weeks of treatment

Intervention	participants (Number)
Cohort A (Pasireotide)	2
Cohort B (Pasireotide and Everolimus)	0

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Number of Participants With Progression Free Survival (PFS) Based on RECIST 1.1 Criteria

Progression free survival (PFS) based on primary outcome criteria for disease progression. Patients without radiographic disease progression who permanently discontinue the study drugs will be censored (NCT01313559)
Timeframe: Assessed up to 30 days after completion of study treatment

Intervention	participants (Number)
Cohort A (Pasireotide)	0
Cohort B (Pasireotide and Everolimus)	0

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Number of Participants Alive and Progression Free After 12 Weeks of Treatment

Progression of disease is defined as disease progression by RECIST 1.1 criteria on CT scan (X-ray computed tomography), or appearance of > 2 new bone lesions on bone scan, or prostate-specific antigen (PSA) progression by Prostate Cancer Clinical Trials Working Group (PCWG2) criteria or death from any cause. (NCT01313559)
Timeframe: 12 weeks after treatment

Intervention	participants (Number)
Cohort A (Pasireotide)	0
Cohort B (Pasireotide and Everolimus)	0

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Percentage of Participants Progression-free

Tumors were assessed according to Response Evaluation Criteria in Solid tumors (RECIST) to determine progression-free status. Complete response (CR) is disappearance of all lesions (i.e. all evidence of disease, not just the target lesions) determined by 2 observations not less than 4 weeks apart; Partial response (PR) is > 30% decrease in the sum of longest diameters of target lesions compared to baseline, with response or stable disease observed in non-target lesions, and no new lesions; Stable disease (SD) is neither sufficient shrinkage to qualify for response or sufficient increase to qualify for progressive disease in target lesions, with response or stable disease observed in non-target lesions, and no new lesions; and Progressive disease (PD is: > 20% increase in the sum of longest diameters of target lesions compared to smallest sum longest diameter recorded. In addition, the sum must also demonstrate an absolute increase of at least 5mm. (NCT01317615)
Timeframe: 6 months

Intervention	Percentage of participants (Number)
RAD001 Plus Paclitaxel/Carboplatin	8.2

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Overall Survival (OS)

OS was defined as the time from date of start of treatment to date of death due to any cause. (NCT01317615)
Timeframe: 12 months

Intervention	Days (Median)
RAD001 Plus Paclitaxel/Carboplatin	298

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Percentage of Participants With Disease Control Rate (DCR)

DCR was defined as is the percentage of participants with a best overall response of CR or PR or SD. Complete response (CR) is disappearance of all lesions (i.e. all evidence of disease, not just the target lesions) determined by 2 observations not less than 4 weeks apart; Partial response (PR) is > 30% decrease in the sum of longest diameters of target lesions compared to baseline, with response or stable disease observed in non-target lesions, and no new lesions; Stable disease (SD) is neither sufficient shrinkage to qualify for response or sufficient increase to qualify for progressive disease in target lesions, with response or stable disease observed in non-target lesions, and no new lesions; and Progressive disease (PD is: > 20% increase in the sum of longest diameters of target lesions compared to smallest sum longest diameter recorded. In addition, the sum must also demonstrate an absolute increase of at least 5mm. (NCT01317615)
Timeframe: 3 months

Intervention	Percentage of participants (Number)
RAD001 Plus Paclitaxel/Carboplatin	73.5

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Progression Free Survival (PFS)

PFS was defined as the time from the date of start of treatment to date of event defined as the first documented progression or death due to any cause. (NCT01317615)
Timeframe: 6 months

Intervention	Days (Median)
RAD001 Plus Paclitaxel/Carboplatin	132

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Percentage of Participants With Overall Response Rate (ORR)

ORR was defined as is the proportion of participants with a best overall response of CR or PR. CR is disappearance of all lesions (i.e. all evidence of disease, not just the target lesions) determined by 2 observations not less than 4 weeks apart; Partial response. PR is > 30% decrease in the sum of longest diameters of target lesions compared to baseline, with response or stable disease observed in non-target lesions, and no new lesions. (NCT01317615)
Timeframe: 3 months

Intervention	Percentage of participants (Number)
RAD001 Plus Paclitaxel/Carboplatin	44.9

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Percentage of Participants Progression-free

Tumors were assessed according to Response Evaluation Criteria in Solid tumors (RECIST) to determine progression-free status. Complete response (CR): disappearance of all lesions (i.e. all evidence of disease, not just the target lesions) determined by 2 observations not less than 4 weeks apart; Partial response (PR): > 30% decrease in the sum of longest diameters of target lesions compared to baseline, with response or stable disease observed in non-target lesions, and no new lesions; Stable disease (SD): neither sufficient shrinkage to qualify for response or sufficient increase to qualify for progressive disease in target lesions, with response or stable disease observed in non-target lesions, and no new lesions; Progressive disease (PD): > 20% increase in the sum of longest diameters of target lesions compared to smallest sum longest diameter recorded. In addition, the sum must also demonstrate an absolute increase of at least 5mm. (NCT01317615)
Timeframe: 3 months

Intervention	Percentage of participants (Number)
RAD001 Plus Paclitaxel/Carboplatin	49.0

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Any Bleeding

(NCT01347554)
Timeframe: Two year

Intervention	participants (Number)
Xience V Stent Group	7
Endeavor Resolute Group	11

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Device-oriented Composite Outcome

defined as a composite of all-cause mortality, any MI (includes non-target vessel territory) and repeat revascularization (includes all target and non-target vessel) (NCT01347554)
Timeframe: Two years

Intervention	participants (Number)
Xience V Stent Group	20
Endeavor Resolute Group	24

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Device-oriented Composite Outcome

defined as a composite of cardiac death, Myocardial infarction not clearly attributable to a nontarget vessel and target lesion revascularization (NCT01347554)
Timeframe: Two year

Intervention	participants (Number)
Xience V Stent Group	12
Endeavor Resolute Group	13

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Stent Thrombosis

Definite and probable stent thrombosis (NCT01347554)
Timeframe: Two years

Intervention	participants (Number)
Xience V Stent Group	0
Endeavor Resolute Group	7

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Number of Patients With Objective Radiographic Responses Based on Volumetric MRI Measurements (In Stratum 2 Only)

"Response was assessed at the time that a follow up volumetric MRI scan is performed (after course 6 and then every 6 months and at the end of treatment).~Complete response (CR): complete resolution of all measurable or palpable PN for ≥ 28days and no appearance of new lesions.~Partial response (PR): A ≥ 20% reduction in the sum of the volume of all index PN lesions for ≥ 28days.~Stable disease (SD): A < 20% increase and < 20% decrease in the sum of the volume of all index PN lesions for ≥ 28days." (NCT01365468)
Timeframe: Screening, after course #6, then every 6 months and end of treatment(1 course=28days)

Intervention	Patients (Number)
	Complete Response	Partial Response	Stable Disease
Stratum 2	0	0	5

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Number of Patients With Adverse Events Assessed by Common Toxicity Criteria for Adverse Events (CTCAE) V.04

Adverse events were assessed according to the NCI Common Toxicity Criteria for Adverse Events (CTCAE) version 4.0. If CTCAE grading does not exist for an adverse event, the severity of mild, moderate, severe, and life-threatening, corresponding to grades 1 - 4 respectively, were used. CTCAE grade 5 (death) was not used in this study. (NCT01365468)
Timeframe: From the time ICF was signed until 28 days after End of Treatment (up to a maximum of 25 months)

Intervention	Patients (Number)
	At least one Grade 1 AE	At least one Grade 2 AE	At least one Grade 3 AE	At least one Grade 4 AE
Stratum 1	4	4	1	1
Stratum 2	5	5	0	0

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Time to Disease Progression (TTP) Based on Change in Volumetric MRI Measurements in Children and Adults (In Stratum I Only)

This endpoint was planned to be analyzed for only Stratum 1 patients. Progression of disease defined as a ≥ 20% increase in the volume (by volumetric MRI) of at least one of the index plexiform neurofibromas (PN) compared to the pretreatment volume measured prior to the start of the current treatment phase. (NCT01365468)
Timeframe: Screening, after course #6, #12, #18, #24, End of Treatment(1 course=28days)

Intervention	Days (Median)
Stratum 1	NA

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Overall Survival (OS) Using Kaplan Meier Method

Overall survival was defined as the time from date of randomization/start of treatment to date of death due to any cause. If a patient is not known to have died, survival was to be censored at the date of last contact. (NCT01374451)
Timeframe: Once 80 PFS events had occurred

Intervention	Percentage of participants (Number)
	6 months	12 months	18 months	24 months
Everolimus	93.7	86.1	75.5	71.0
Paseriotide LAR + Everolimus	93.5	85.5	81.4	77.0

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Progression-free Survival (PFS) Per Local Radiological Review

PFS per RECIST 1.0. (Response Evaluation Criteria in Solid Tumors). PFS was defined as the time from the date of randomization to the date of the first radiologically documented disease progression or death due to any cause. (NCT01374451)
Timeframe: Once 80 PFS events had occurred aproximately after 24 months

Intervention	months (Median)
Paseriotide LAR + Everolimus	16.82
Everolimus	16.59

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Summary of Pharmacokinetics (PK) for Everolimus for AUClast

(NCT01374451)
Timeframe: Cycle 2 Day 1

Intervention	ng*hr/mL (Mean)
Paseriotide LAR + Everolimus	511
Everolimus	378

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Summary of Pharmacokinetics (PK) for Everolimus for CL/F

(NCT01374451)
Timeframe: Cycle 2 Day 1

Intervention	L/hr (Mean)
Paseriotide LAR + Everolimus	20.0
Everolimus	29.0

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Summary of Pharmacokinetics (PK) for Everolimus for Cmax and Cmin

(NCT01374451)
Timeframe: Cycle 2 Day 1

Intervention	ng/mL (Mean)
	Cmax	Cmin
Everolimus	60.2	7.67
Paseriotide LAR + Everolimus	58.7	14.7

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Summary of Pharmacokinetics (PK) for Everolimus for Tmax

(NCT01374451)
Timeframe: Cycle 2 Day 1

Intervention	hr (Median)
Paseriotide LAR + Everolimus	1.00
Everolimus	0.500

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Safety and Tolerability Profile of Everolimus Alone or in Combination With Pasireotide LAR

Consisted of monitoring and recording the rate, type, severity, and causal relationship of adverse events (AEs) and serious AEs (SAEs) to treatment. The safety analysis was based mainly on the frequency of AEs or SAEs and on the number of laboratory values that fell outside of pre-determined range. (NCT01374451)
Timeframe: Once 80 PFS events had occurred

Intervention	Participants (Number)
	Deaths	Serious Adverse Events	Adverse Events
Everolimus	10	49	81
Paseriotide LAR + Everolimus	7	41	78

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Summary of Pasireotide Concentrations Following Intramuscular Injection of Pasireotide LAR 60mg

(NCT01374451)
Timeframe: Cycle 1 Day 21, Cycle 2 Day 29

Intervention	ng/mL (Mean)
	Cycle 1 Day 21 (n:69)	Cycle 2 Day 29 (n: 64)
Paseriotide LAR + Everolimus	21.6	19.9

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Objective Response Rate (ORR) as Per Radiology Review

"Objective response was determined by the local radiologist according to the RECIST Version 1.0. ORR is the percentage of patients with a best overall response of complete response (CR) or partial response (PR). This is also referred to as Overall response rate.~CR: Disappearance of all nontarget lesions. PR: At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the smallest sum of the longest diameter of all target lesions recorded at or after baseline." (NCT01374451)
Timeframe: Once 80 PFS events had occurred

Intervention	Percentage of participants (Number)
Paseriotide LAR + Everolimus	20.3
Everolimus	6.2

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Disease Control Rate (DCR) as Per Radiology Review

Disease control rate is the percentage of patients with a best overall response of CR or PR or stable disease (SD) determined by the local radiologist according to the Response Evaluation Criteria In Solid Tumors Criteria (RECIST) Version 1.0. CR: Disappearance of all nontarget lesions. PR: At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the smallest sum of the longest diameter of all target lesions recorded at or after baseline. SD: Neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for progressive disease (PD). PD: Any progression ≤ 18 weeks after randomization (and not qualifying for CR, PR or stable disease SD. (NCT01374451)
Timeframe: Once 80 PFS events had occurred

Intervention	Percentage of participants (Number)
Paseriotide LAR + Everolimus	77.2
Everolimus	82.7

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Number of Participants With Adverse Events

Number of participants with adverse events as a measure of safety and tolerability (NCT01376310)
Timeframe: Until 30 days after the last dose of study treatment. Subjects may have continued to receive study treatment until disease progression, death, unacceptable toxicity or until locally commercially available. The maximum duration of exposure was 76 months.

Intervention	Participants (Count of Participants)
	Adverse Events	Treatment-Related Adverse Events	Serious Adverse Events	Treatment-Related Serious Adverse Events
Cohort A (GSK1120212 < 24 Weeks)	119	101	26	8
Cohort B (GSK1120212 >= 24 Weeks)	30	26	13	4

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Time to Progression (TTP) Based on the Modified RECIST Criteria

"Time to Progression (TTP) defined as the time from the date of randomization to the date of first documented radiological confirmation of disease progression based on modified RECIST criteria. Progressive Disease: >20% increase in sum of the longest diameters (SLD) of viable target lesion (arterial phase enhancement)" (NCT01379521)
Timeframe: 3, 6, 12, 18 and 24 months

Intervention	months (Median)
Everolimus + TACE	6.3
Placebo + TACE	6.4

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Percentage of Participants With a Decrease in the Sum of the of Longest Diameters (SLD) of Target Lesions From Baseline to 30 Months

Percentage of participants with a decrease in the sum of the of longest diameters (SLD) of target lesions from Baseline to 30 months (NCT01379521)
Timeframe: baseline, 30 months

Intervention	Percentage of participants (Number)
Everolimus + TACE	93.8
Placebo + TACE	88.0

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Overall Survival (OS)

Overall survival was defined as the time from date of randomization to date of death due to any cause. If death had not occurred at the date of the analysis cut-off then OS was censored at the date of the last contact. (NCT01379521)
Timeframe: 6, 12, 18, 24, 30 months

Intervention	months (Median)
Everolimus + TACE	29.9
Placebo + TACE	21.7

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Participants Evaluated for Toxicity

Toxicity will be assessed using Common Terminology Criteria for Adverse Events (CTCAE) v4.0 (Gompertz 1825),. Toxicities will be summarized by type and grade using frequencies and rates. (NCT01399918)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Everolimus and Bevacizumab	55

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Secondary Endpoint Will be the Overall Response Rate (ORR)

per the international criteria defined by the Response Evaluation Criteria in Solid Tumors Committee (NCT01399918)
Timeframe: 1 year

Intervention	percent of participants with ORR (Number)
Everolimus and Bevacizumab	35

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To Evaluate the Efficacy of Combining Everolimus and Bevacizumab in Patients With Advanced RCC of Non-clear Cell Histology

the percent of patients alive and progression-free after 6 months of therapy. (NCT01399918)
Timeframe: 6 months

Intervention	percent of participants (Number)
Everolimus and Bevacizumab	78

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Incidence of Bacterial, Viral, and Fungal Infections at Month 12

Incidence of bacterial, viral, and fungal infections at Month 12 (NCT01404325)
Timeframe: Month 12

Intervention	incidences (Number)
	Bacterial infections	Viral infections	Fungal infections
Centre Specific Triple IS Regimen	4	20	0
Quadruple Low Level IS Regimen	3	14	3

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Incidence of Acute Rejection Episodes at Month 6 and Month 12

"Incidence of acute rejection episodes at Month 6 and Month 12. This table counts multiple occurrences of rejection in the same patient as different incidents. Every incident is associated with both an A and a B classification.~Classification A: Acute Rejection Grade 0 - none, Grade 1-minimal, Grade 2- mild, Grade 3-moderate, Grade 4-Severe; Classification B: Airway Inflammation-Grade 0-none, Grade 1R-low grade, Grade 2R-high grade, Grade X-ungradeable" (NCT01404325)
Timeframe: Month 6, Month 12

Intervention	incidences (Number)
	Up to 6 months: Classification A	Up to 6 months: Classification B	6 to 12 months: Classification A	6 to 12 months: Classification B
Centre Specific Triple IS Regimen	13	13	9	9
Quadruple Low Level IS Regimen	11	11	10	10

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High-Density Lipoprotein (HDL)Cholesterol Levels at Month 1, 3, 6, 9, 12

HDL Cholesterol levels at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	mmol/L (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	-0.1	-0.0	-0.0	-0.0	-0.0
Quadruple Low Level IS Regimen	0.1	0.1	0.1	0.0	0.0

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Exercise Capacity 6-Minute Walk Test(6MWT) at Month 6 and Month 12

Exercise capacity (6MWT) at Month 6 and Month 12 Measured by the Borg Scale. THE BORG SCALE 0 is Nothing at all, 0.5 is Very, very slight (just noticeable); 1 is Very slight, 2 is Slight (light); 3 is Moderate; 4 is Somewhat severe; 5 is Severe (heavy), 7 is Very severe, 10 is Very, very severe (maximal)The higher the Borg score implies increased shortness of breath and/or increased fatigue. (NCT01404325)
Timeframe: Month 6, Month 12

Intervention	Scores on a scale (Mean)
	Month 6-Borg score - Before start of test	Month 6-Borg score - At end of test	Month 12-Borg score - Before start of test	Month 12-Borg score - At end of test
Centre Specific Triple IS Regimen	0.39	1.64	0.42	2.06
Quadruple Low Level IS Regimen	0.47	1.75	0.38	2.08

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Calculated Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula at Month 1, 3, 6, 9, 12

Calculated Glomerular Filtration Rate (cGFR) Using Modification of Diet in Renal Disease (MDRD) Formula at Month 1, 3, 6, 9, 12 cGFR (in mL/min/1.73 m2) = 186.3*(C-1.154)*(A-0.203)*G*R where C = the serum concentration of creatinine (mg/dL), A = age (years), G = 0.742 when gender is female, otherwise G = 1, R = 1.21 when race is black, otherwise R = 1. (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	mL/min (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	65.8	63.3	62.3	61.7	60.5
Quadruple Low Level IS Regimen	72.0	68.7	67.6	67.4	67.0

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Calculated Glomerular Filtration Rate (cGFR) According to Cystatin C-based Hoek's Formula at Month 1, 3, 6, 9, 12

Calculated Glomerular Filtration Rate (cGFR) according to Cystatin C-based Hoek's formula at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	mL/min (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	61.8	60.3	58.7	57.7	57.5
Quadruple Low Level IS Regimen	68.5	65.7	63.0	61.8	60.8

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Calculated Glomerular Filtration Rate (cGFR) According to Chronic Kidney Disease Epidemiology Collaboration (CKD EPI) at Month 1, 3, 6, 9, 12

Calculated Glomerular Filtration Rate (cGFR) according to Chronic Kidney Disease Epidemiology Collaboration (CKD EPI) at Month 1, 3, 6, 9 and 12. The CKD-EPI equation, expressed as a single equation, is GFR = 141 × min(Scr/κ, 1)α × max(Scr/κ, 1)^-1.209 × 0.993Age × 1.018 (if female) × 1.159 (if black), where Scr is serum creatinine, κ is 0.7 for females and 0.9 for males, α is -0.329 for females and -0.411 for males, min indicates the minimum of Scr/ĸ or 1, and max indicates the maximum of Scr/κ or 1 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	mL/min (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	67.1	64.3	63.1	62.3	61.2
Quadruple Low Level IS Regimen	73.5	70.4	69.2	69.0	68.3

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Adherence to Target Ranges of Tacrolimus at Month 1, 3, 6, 9, 12

Adherence to target ranges of Tacrolimus at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	participant adherence (Number)
	Month 1 Below Target Range	Month 1 Within Target Range	Month 1 Above Target Range	Month 3 Below Target Range	Month 3 Within Target Range	Month 3 Above Target Range	Month 6 Below Target Range	Month 6 Within Target Range	Month 6 Above Target Range	Month 9 Below Target Range	Month 9 Within Target Range	Month 9 Above Target Range	Month 12 Below Target Range	Month 12 Within Target Range	Month 12 Above Target Range
Centre Specific Triple IS Regimen	0	45	0	0	47	0	1	45	0	0	46	0	0	47	0
Quadruple Low Level IS Regimen	3	24	17	3	23	18	5	23	12	2	18	18	3	23	15

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Adherence to Target Ranges of Everolimus at Month 1, 3, 6, 9, 12

Adherence to target ranges of everolimus at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	participant adherence (Number)
	Month 1 Below Target Range	Month 1 Within Target Range	Month 1 Above Target Range	Month 3 Below Target Range	Month 3 Within Target Range	Month 3 Above Target Range	Month 6 Below Target Range	Month 6 Within Target Range	Month 6 Above Target Range	Month 9 Below Target Range	Month 9 Within Target Range	Month 9 Above Target Range	Month 12 Below Target Range	Month 12 Within Target Range	Month 12 Above Target Range
Quadruple Low Level IS Regimen	10	42	14	5	41	15	7	39	12	5	34	13	3	38	9

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Adherence to Target Ranges of Cyclosporine A (CsA) at Month 1, 3, 6, 9, 12

Adherence to target ranges of Cyclosporine A (CsA) at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	participant adherence (Number)
	Month 1 Below Target Range	Month 1 Within Target Range	Month 1 Above Target Range	Month 3 Below Target Range	Month 3 Within Target Range	Month 3 Above Target Range	Month 6 Below Target Range	Month 6 Within Target Range	Month 6 Above Target Range	Month 9 Below Target Range	Month 9 Within Target Range	Month 9 Above Target Range	Month 12 Below Target Range	Month 12 Within Target Range	Month 12 Above Target Range
Centre Specific Triple IS Regimen	8	8	0	4	10	0	6	8	0	4	9	0	3	10	0
Quadruple Low Level IS Regimen	0	18	3	0	18	2	0	18	2	0	16	1	0	16	5

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Calculated Glomerular Filtration Rate (cGFR) According to Chronic Kidney Disease Epidemiology Collaboration (CKD EPI) at 12 Months

Calculated Glomerular Filtration Rate (cGFR) according to Chronic Kidney Disease Epidemiology Collaboration (CKD EPI) at 12 months The CKD-EPI equation, expressed as a single equation, is GFR = 141 × min(Scr/κ, 1)α × max(Scr/κ, 1)^-1.209 × 0.993Age × 1.018 (if female) × 1.159 (if black), where Scr is serum creatinine, κ is 0.7 for females and 0.9 for males, α is -0.329 for females and -0.411 for males, min indicates the minimum of Scr/ĸ or 1, and max indicates the maximum of Scr/κ or 1 (NCT01404325)
Timeframe: Month 12

Intervention	mL/min (Least Squares Mean)
Quadruple Low Level IS Regimen	64.5
Centre Specific Triple IS Regimen	54.6

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Calculated Glomerular Filtration Rate (cGFR) According to Cockcroft-Gault at Month 1, 3, 6, 9, 12

Calculated Glomerular Filtration Rate (cGFR) according to Cockcroft-Gault at Month 1, 3, 6, 9, 12 For men: GFR=(140-Age) x Body weight (kg) / 72 x Serum Creatinine (mg/dl) For women: GFR=0.85 (140 -Age) x Body weight(kg)/ 72 x Serum Creatinine (mg/dl) (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	mL/min (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	72.1	70.1	69.1	69.0	68.4
Quadruple Low Level IS Regimen	78.6	76.1	76.2	76.2	76.2

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Trough Levels of Everolimus at Month 1, 3, 6, 9, 12

Trough levels of everolimus at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	ng/mL (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Quadruple Low Level IS Regimen	4.2	4.4	4.1	4.5	4.3

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Trough Levels of Tacrolimus at Month 1, 3, 6, 9, 12

Trough levels of Tacrolimus at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	ng/mL (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	10.44	10.53	10.09	10.67	9.66
Quadruple Low Level IS Regimen	5.07	5.18	4.70	5.78	5.19

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Incidence of Patients Experiencing a Decline in GFR of < 10, 10-15, 15-20, 20-25 and > 25 mL/Min From Baseline to Month 6 and 12.

Incidence of patients experiencing a decline in GFR of < 10, 10-15, 15-20, 20-25 and > 25 mL/min from Baseline to Month 6 and 12calculated by the CKD-EPI method. Participants are counted in each decline level observed for that participant; this means participants may be counted in more than 1 decline level. (NCT01404325)
Timeframe: Baseline, Month 6, Month 12

Intervention	incidences (Number)
	Up to Month 6: < 10 mL/min	Up to Month 6: 10 - < 15 mL/min	Up to Month 6: 15 - < 20 mL/min	Up to Month 6: 20 - < 25 mL/min	Up to Month 6: > 25 mL/min	Up to Month 12: < 10 mL/min	Up to Month 12: 10 - < 15 mL/min	Up to Month 12: 15 - < 20 mL/min	Up to Month 12: 20 - < 25 mL/min	Up to Month 12: > 25 mL/min
Centre Specific Triple IS Regimen	44	18	11	7	7	53	27	18	9	9
Quadruple Low Level IS Regimen	28	9	6	2	3	36	10	8	8	7

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Trough Levels of Cyclosporine A (CsA) at Month 1, 3, 6, 9, 12

Trough levels of Cyclosporine A (CsA) at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	ng/mL (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	106	109	103	107	108
Quadruple Low Level IS Regimen	61	59.65	58.50	57.59	69.33

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Triglyceride Levels at Month 1, 3, 6, 9, 12

Triglyceride levels at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	mmol/L (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	2.0	2.1	2.0	2.0	2.1
Quadruple Low Level IS Regimen	2.6	2.7	2.6	2.7	2.7

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Total Cholesterol Levels at Month 1, 3, 6, 9, 12

Total Cholesterol levels at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	mmol/L (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	-0.2	-0.1	-0.2	-0.1	-0.1
Quadruple Low Level IS Regimen	0.8	1.0	1.1	1.1	0.8

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Quality of Life (QoL, SF36) at Month 6 and Month 12

Quality of Life (QoL, SF36) at Month 6 and Month 12 Scores can range from a minimum of 0 (maximum disability) to a maximum of 100 (no disability). (NCT01404325)
Timeframe: Month 6, Month 12

Intervention	scores on a scale (Mean)
	Month 6: Physical component summary score	Month 6: Mental component summary score	Month 6: Physical functioning	Month 6: Role-Physical	Month 6: Bodily pain	Month 6: General health perception	Month 6: Vitality	Month 6:Social functioning	Month 6: Role-Emotional	Month 6: Mental health	Month 12: Physical component summary score	Month 12: Mental component summary score	Month 12: Physical functioning	Month 12: Role-Physical	Month 12: Bodily Pain	Month 12: General health perception	Month 12: Vitality	Month 12: Social functioning	Month 12: Role-Emotional	Month 12: Mental health
Centre Specific Triple IS Regimen	48.9	52.6	84.1	77.1	81.3	70.6	70.0	88.9	84.8	81.0	47.7	53.8	82.5	78.0	80.1	65.8	69.9	90.5	86.2	81.8
Quadruple Low Level IS Regimen	46.9	51.5	78.8	71.1	76.4	65.4	67.4	84.1	84.7	78.5	47.2	49.7	77.4	68.3	76.8	66.7	65.7	82.3	79.4	75.4

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Incidence of Treated Arterial Hypertension up to Month 12

Incidence of treated of arterial hypertension up to Month 12 (NCT01404325)
Timeframe: up to Month 12

Intervention	incidences (Number)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	1	1	1	1	1
Quadruple Low Level IS Regimen	2	2	2	3	4

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Incidence of Renal Replacement Therapy at Month 6 and Month 12

Incidence of renal replacement therapy at Month 6 and Month 12: There were no incidences in either group where renal replacement therapy was required (NCT01404325)
Timeframe: Month 6, Month 12

Intervention	incidences (Number)
	up to Month 6	up to Month 12
Centre Specific Triple IS Regimen	0	0
Quadruple Low Level IS Regimen	0	0

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Incidence of Graft Loss/Re-transplantation at Month 6 and Month 12

Incidence of graft loss/re-transplantation at Month 6 and Month 12 (NCT01404325)
Timeframe: Month 6, Month 12

Intervention	incidences (Number)
	Month 6	Month 12
Centre Specific Triple IS Regimen	0	1
Quadruple Low Level IS Regimen	0	1

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Low-Density Lipoprotein (LDL)Cholesterol Levels at Month 1, 3, 6, 9, 12

LDL Cholesterol levels at Month 1, 3, 6, 9, 12 (NCT01404325)
Timeframe: Month 1, 3, 6, 9, 12

Intervention	mmol/L (Mean)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	0.0	-0.0	-0.0	0.1	0.1
Quadruple Low Level IS Regimen	0.4	0.6	0.7	0.8	0.5

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Incidence of Diabetes Mellitus up to Month 12

Incidence of Diabetes Mellitus up to Month 12 (NCT01404325)
Timeframe: up to Month 12

Intervention	incidences (Number)
	Month 1	Month 3	Month 6	Month 9	Month 12
Centre Specific Triple IS Regimen	0	0	1	1	1
Quadruple Low Level IS Regimen	0	0	0	1	1

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Incidence of Death at Month 6 and Month 12

Incidence of death at Month 6 and Month 12 (NCT01404325)
Timeframe: Month 6, Month 12

Intervention	incidences (Number)
	Month 6	Month 12
Centre Specific Triple IS Regimen	0	1
Quadruple Low Level IS Regimen	0	3

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Incidence of Bronchiolitis Obliterans Syndrome (BOS) at Month 6 and Month 12

Incidence of Bronchiolitis obliterans syndrome (BOS) at Month 6 and Month 12 BOS 0 is FEV1 > 90% of baseline and FEF25-75% > 75% of baseline; BOS 0-p is FEV1 81-90% of baseline and/or FEF25-75% ≤ 75% of baseline; BOS 1 is FEV1 66-80% of baseline; BOS 2 is FEV1 51-65% of baseline; BOS 3 is FEV1 ≤ 50% of baseline (NCT01404325)
Timeframe: Month 6, Month 12

Intervention	incidences (Number)
	Month 6 - Total (all grades)	Month 6 - BOS 0	Month 6 - BOS 0p	Month 6 - BOS 1	Month 6 - BOS 2	Month 6 - BOS 3	Month 6 - BOS (>/=1)	Month 12 - Total (all grades)	Month 12 - BOS 0	Month 12 - BOS 0p	Month 12 - BOS 1	Month 12 - BOS 2	Month 12 - BOS 3	Month 12 - BOS (>/=1)
Centre Specific Triple IS Regimen	61	40	14	5	0	2	7	61	38	14	5	1	3	9
Quadruple Low Level IS Regimen	66	36	26	3	1	0	4	66	35	26	3	1	1	5

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Change From Baseline in Serum Creatinine - ITT

Blood samples were collected to assess serum creatinine measurements. A negative change from baseline indicates improvement. (NCT01410448)
Timeframe: baseline, 3 months

Intervention	mg/dL (Mean)
Immediate Everolimus (IE)	-4.79
Delayed Everolimus (DE)	-5.13

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Change From Baseline in Serum Creatinine - Modified ITT

Blood samples were collected to assess serum creatinine measurements. A negative change from baseline indicates improvement. (NCT01410448)
Timeframe: baseline, 12 months

Intervention	mg/dL (Mean)
Immediate Everolimus (IE)	-4.96
Delayed Everolimus (DE)	-5.22

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Percentage of Participants With Proteinuria

Incidence of proteinuria (>1,000 mg/day in urine collected in 24 hours or > 1.0 if measured on the urine protein/creatinine concentration ratio in a spot urine sample) was assessed. (NCT01410448)
Timeframe: 3 months

Intervention	Percentage of participants (Number)
	Yes	No	Missing
Delayed Everolimus (DE)	4.21	68.42	27.37
Immediate Everolimus (IE)	4.15	68.91	26.94

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Percentage of Participants Who Experienced Treatment Failure - Worst-case Scenario

The percentage of participants who experienced treatment failure was assessed. Treatment failure was defined as the occurrence of at least one failure event among death, graft loss or biopsy-proven acute rejection (BPAR). In the worst-case scenario, treatment failure was identified in one of the following cases: occurrence of at least one treatment failure event or study discontinuation due to any reason. (NCT01410448)
Timeframe: 3 months

Intervention	Percentage of participants (Number)
Immediate Everolimus (IE)	11.40
Delayed Everolimus (DE)	21.05

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Percentage of Participants With a New Onset of Diabetes

The percentage of participants with a new onset of diabetes was assessed. (NCT01410448)
Timeframe: 12 months

Intervention	Percentage of participants (Number)
Immediate Everolimus (IE)	3.14
Delayed Everolimus (DE)	4.05

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Percentage of Participants With a New Onset of Malignancy

The percentage of participants with a new onset of malignancy was assessed. (NCT01410448)
Timeframe: 12 months

Intervention	Percentage of participants (Number)
Immediate Everolimus (IE)	0
Delayed Everolimus (DE)	0.68

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Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) (Calculated With Modified Diet in Renal Disease (MDRD)-4 Formula - ITT

Renal function was assessed by measuring serum creatinine and serum urea and by calculating creatinine clearance using the MDRD-4 formula. eGFR = 186.3*(serum creatinine [mg/dL])^-1.154 * (age at screening) -0.203 * (0.742 if female) * (1.21 if African American). A positive change from baseline indicates improvement. (NCT01410448)
Timeframe: baseline, 3 Months

Intervention	mL/min (Mean)
Immediate Everolimus (IE)	38.64
Delayed Everolimus (DE)	39.13

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Percentage of Participants With Acute Rejection (AR)

AR was defined as an episode of increased serum creatinine >30% that was clinically diagnosed as an acute rejection but was not biopsy proven. (NCT01410448)
Timeframe: 12 months

Intervention	Percentage of participants (Number)
Immediate Everolimus (IE)	12.44
Delayed Everolimus (DE)	10.53

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Participant/Graft Survival Rate: Percentage of Participants With Failure Events of Death or Graft Loss - Worst-case Scenario

The percentage of participants who experienced death or graft loss was assessed. In the worst-case scenario, failure, i.e. participants death or graft loss, was identified in one of the following cases: occurrence of at least one failure event or study discontinuation due to any reason. (NCT01410448)
Timeframe: 3 months

Intervention	Percentage of participants (Number)
Immediate Everolimus (IE)	6.74
Delayed Everolimus (DE)	18.42

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Percentage of Participants Without Wound Healing Complications - Worst-case Scenario

The percentage of participants without wound healing complications was assessed. Wound healing complications consisted of lymphorrhea, fluid collections, wound dehiscence, wound infections and incisional hernia. In the worst-case scenario, failure, i.e. at least one healing complication occurrence, was identified in one of the following cases: wound complication occurrence, missing information about wound complication occurrence or study discontinuation due to any reason for participants who did not complete the 12 month follow-up visit. (NCT01410448)
Timeframe: 12 months

Intervention	Percentage of participants (Number)
Immediate Everolimus (IE)	65.80
Delayed Everolimus (DE)	59.47

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Duration of DGF

The duration of DGF was defined as the elapsed time from first to last day of post-transplant dialysis. (NCT01410448)
Timeframe: 3 months

Intervention	Days (Median)
Immediate Everolimus (IE)	8.50
Delayed Everolimus (DE)	5.50

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Patient Survival Rate: Percentage of Deaths - Worst-case Scenario

The percentage of deaths was assessed. In the worst-case scenario, failure, i.e. death, was identified in one of the following cases: participant's death or study discontinuation due to any reason. (NCT01410448)
Timeframe: 3 Months, 12 months

Intervention	Percentage of participants (Number)
Immediate Everolimus (IE)	6.22
Delayed Everolimus (DE)	18.42

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Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) (Calculated With Modified Diet in Renal Disease (MDRD)-4 Formula - Modified ITT

Intervention	mL/min (Mean)
Immediate Everolimus (IE)	41.26
Delayed Everolimus (DE)	41.56

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Percentage of Participants Without Wound Healing Complications - Worst-case Scenario

The percentage of participants without wound healing complications was assessed. Wound healing complications consisted of lymphorrhea, fluid collections, wound dehiscence, wound infections and incisional hernia. In the worst-case scenario, failure, i.e. at least one healing complication occurrence, was identified in one of the following cases: wound complication occurrence, missing information about wound complication occurrence, or study discontinuation due to any reason. (NCT01410448)
Timeframe: 3 months

Intervention	Percentage of participants (Number)
Immediate Everolimus (IE)	68.39
Delayed Everolimus (DE)	61.58

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Graft Survival Rate: Percentage of Participants With Graft Loss - Worst-case Scenario

The percentage of participants who experienced graft loss was assessed. In the worst-case scenario, failure, i.e. graft loss, was identified in one of the following cases: occurrence of graft loss or discontinuation due to any reason. (NCT01410448)
Timeframe: 3 months, 12 months

Intervention	Percentage of participants (Number)
	3 months	12 months
Delayed Everolimus (DE)	18.42	19.47
Immediate Everolimus (IE)	6.74	7.25

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Percentage of Participants With BPAR - Worst-case Scenario

A biopsy-proven acute rejection was defined as a biopsy graded IA, IB, IIA, IIB or III. In the worst-case scenario, failure, i.e. BPAR, was identified in one of the following cases: occurrence of BPAR or study discontinuation due to any reason. (NCT01410448)
Timeframe: 3 Months, 12 months

Intervention	Percentage of participants (Number)
	3 monts	12 months
Delayed Everolimus (DE)	21.05	24.74
Immediate Everolimus (IE)	11.40	15.54

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Percentage of Participants With Delayed Graft Function (DGF) -

DGF was defined as the need for dialysis in the first week after transplant, excluding Renal Replacement Therapy within the first 24 hours after transplantation. (NCT01410448)
Timeframe: 3 Months

Intervention	Percentage of participants (Number)
Immediate Everolimus (IE)	23.83
Delayed Everolimus (DE)	31.58

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Audiologic Response

"Defined as improvement in speech discrimination score (SDS), defined as an improvement in the score above the 95% critical difference threshold, compared to baseline audiogram at initiation of treatment. Audiologic worsening: decrease in SDS score below the 95% critical difference threshold, compared to baseline audiogram at initiation of treatment.~Patients with vestibular schwannomas will receive baseline audiograms within 28 days before enrollments and subsequent audiograms at the time of each MRI." (NCT01419639)
Timeframe: 1 Year

Intervention	participants (Number)
RAD001	0

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Change in Tumor Size From Baseline

(NCT01419639)
Timeframe: 1 Year

Intervention	% of change in tumor size from baseline (Median)
RAD001	5.72

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Radiographic Response

To estimate the objective response rates to RAD001 in patients with NF2-related tumors including cranial nerve schwannomas, meningiomas and ependymomas. Radiographic response for study purposes = greater than or equal to 15% reduction in tumor volume in any of the target tumors (partial response). Complete disappearance of any of the target tumors = complete response. MRI of the brain and spine will be performed every 3 months. If an objective response (15% reduction in tumor volume compared to baseline) is observed in any target tumor or stable disease, drug will be continued. (NCT01419639)
Timeframe: 1 Year

Intervention	participants (Number)
RAD001	0

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
Absorb BVS™	57
XIENCE™	34

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
Absorb BVS™	1
XIENCE™	0

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Number of Participants With All Revascularization

Revascularization: Target Lesion Revascularization (TLR) is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. The target lesion is defined as the treated segment from 5 mm proximal to the scaffold and to 5 mm distal to the test scaffold. Target Vessel Revascularization (TVR) is defined as any repeat percutaneous intervention or surgical bypass of any segment of the target vessel. The target vessel is defined as the entire major coronary vessel proximal and distal to the target lesion. Non Target Lesion Revascularization (Non-TLR) is any revascularization in the target vessel for a lesion other than the target lesion. Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel. (NCT01425281)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Absorb BVS™	59
XIENCE™	34

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Number of Participants With DMR (All Death, All MI, All Revascularization)

DMR is the composite of All Death, All MI, All Revascularization (NCT01425281)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Absorb BVS™	76
XIENCE™	40

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Number of Participants With DMR (All Death, All MI, All Revascularization)

DMR is the composite of All Death, All MI, All Revascularization (NCT01425281)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Absorb BVS™	80
XIENCE™	41

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Number of Participants With DMR (All Death, All MI, All Revascularization)

DMR is the composite of All Death, All MI, All Revascularization (NCT01425281)
Timeframe: In-hospital (≤ 7 days of post index procedure)

Intervention	Participants (Count of Participants)
Absorb BVS™	13
XIENCE™	2

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Number of Participants With DMR (All Death, All MI, All Revascularization)

DMR is the composite of All Death, All MI, All Revascularization. (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	24
XIENCE™	15

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Number of Participants With DMR (All Death, All MI, All Revascularization)

DMR is the composite of All Death, All MI, All Revascularization. (NCT01425281)
Timeframe: 180 days

Intervention	Participants (Count of Participants)
Absorb BVS™	19
XIENCE™	9

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Number of Participants With DMR (All Death, All MI, All Revascularization)

DMR is the composite of All Death, All MI, All Revascularization. (NCT01425281)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Absorb BVS™	38
XIENCE™	21

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Number of Participants With DMR (All Death, All MI, All Revascularization)

DMR is the composite of All Death, All MI, All Revascularization. (NCT01425281)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Absorb BVS™	68
XIENCE™	39

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Number of Participants With DMR (All Death, All MI, All Revascularization)

DMR is the composite of All Death, All MI, All Revascularization. (NCT01425281)
Timeframe: 30 days

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	4

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Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)

Major adverse cardiac events (MACE) is defined as the composite of cardiac death, all myocardial infarction, and ischemic driven target lesion revascularization (ID-TLR). (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	17
XIENCE™	5

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Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	3

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Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)

Intervention	Participants (Count of Participants)
Absorb BVS™	25
XIENCE™	7

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Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)

Intervention	Participants (Count of Participants)
Absorb BVS™	38
XIENCE™	11

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Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	2

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Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)

Intervention	Participants (Count of Participants)
Absorb BVS™	40
XIENCE™	12

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Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)

Intervention	Participants (Count of Participants)
Absorb BVS™	41
XIENCE™	13

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Number of Participants With Major Adverse Cardiac Events (MACE) (Cardiac Death, All MI, ID-TLR)

Intervention	Participants (Count of Participants)
Absorb BVS™	13
XIENCE™	2

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Number of Participants With Non Target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel. (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	6
XIENCE™	6

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Number of Participants With Non Target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel. (NCT01425281)
Timeframe: 180 days

Intervention	Participants (Count of Participants)
Absorb BVS™	4
XIENCE™	3

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Number of Participants With Non Target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel. (NCT01425281)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Absorb BVS™	22
XIENCE™	19

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Number of Participants With Non Target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel. (NCT01425281)
Timeframe: 30 days

Intervention	Participants (Count of Participants)
Absorb BVS™	1
XIENCE™	0

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Number of Participants With Non Target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel. (NCT01425281)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Absorb BVS™	29
XIENCE™	20

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Number of Participants With Non Target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel. (NCT01425281)
Timeframe: In-hospital (≤ 7 days of post index procedure)

Intervention	Participants (Count of Participants)
Absorb BVS™	0
XIENCE™	0

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Number of Participants With Non-Target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR) is any revascularization in a vessel other than the target vessel. (NCT01425281)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Absorb BVS™	30
XIENCE™	20

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Number of Participants With Procedural Success

Achievement of final in-scaffold/stent residual stenosis of less than 50% by QCA with successful delivery and deployment of at least one study scaffold/stent at the intended target lesion and successful withdrawal of the delivery system for all target lesions without the occurrence of cardiac death, target vessel MI or repeat TLR during the hospital stay. (NCT01425281)
Timeframe: From the start of index procedure to end of index procedure

Intervention	Participants (Count of Participants)
Absorb BVS™	322
XIENCE™	164

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Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, Target Vessel Myocardial Infarction (TV-MI), ID-TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01425281)
Timeframe: 30 days

Intervention	Participants (Count of Participants)
Absorb BVS™	13
XIENCE™	2

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Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	16
XIENCE™	5

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Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01425281)
Timeframe: 180 days

Intervention	Participants (Count of Participants)
Absorb BVS™	13
XIENCE™	3

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Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01425281)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Absorb BVS™	23
XIENCE™	5

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Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01425281)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Absorb BVS™	34
XIENCE™	8

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Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01425281)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Absorb BVS™	37
XIENCE™	9

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Number of Participants With Target Lesion Failure (TLF) (Cardiac Death, TV-MI, ID-TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01425281)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Absorb BVS™	38
XIENCE™	9

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Number of Participants With Target Lesion Failure (TLF) (Cardiac Death,(Target Vessel Myocardial Infarction(TV-MI), ID-TLR)

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT01425281)
Timeframe: In-hospital (≤ 7 days of post index procedure)

Intervention	Participants (Count of Participants)
Absorb BVS™	12
XIENCE™	2

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Number of Participants With Target Lesion Revascularization (TLR)

"Target Lesion Revascularization is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. All TLR should be classified prospectively as clinically indicated (CI) or not clinically indicated by the investigator prior to repeat angiography. An independent angiographic core laboratory should verify that the severity of percent diameter stenosis meets requirements for clinical indication and will overrule in cases where investigator reports are not in agreement.~The target lesion is defined as the treated segment from 5 mm proximal to the stent and to 5 mm distal to the scaffold/stent." (NCT01425281)
Timeframe: 30 days

Intervention	Participants (Count of Participants)
Absorb BVS™	2
XIENCE™	0

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Number of Participants With Target Lesion Revascularization (TLR)

Intervention	Participants (Count of Participants)
Absorb BVS™	1
XIENCE™	0

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Number of Participants With Target Lesion Revascularization (TLR)

"Target Lesion Revascularization is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. All TLR should be classified prospectively as clinically indicated [CI] or not clinically indicated by the investigator prior to repeat angiography. An independent angiographic core laboratory should verify that the severity of percent diameter stenosis meets requirements for clinical indication and will overrule in cases where investigator reports are not in agreement.~The target lesion is defined as the treated segment from 5 mm proximal to the stent and to 5 mm distal to the scaffold/stent." (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	4
XIENCE™	3

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Number of Participants With Target Lesion Revascularization (TLR)

"Target Lesion Revascularization is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. All TLR should be classified prospectively as clinically indicated [CI] or not clinically indicated by the investigator prior to repeat angiography. An independent angiographic core laboratory should verify that the severity of percent diameter stenosis meets requirements for clinical indication and will overrule in cases where investigator reports are not in agreement.~The target lesion is defined as the treated segment from 5 mm proximal to the stent and to 5 mm distal to the scaffold/stent." (NCT01425281)
Timeframe: 180 days

Intervention	Participants (Count of Participants)
Absorb BVS™	2
XIENCE™	1

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Number of Participants With Target Lesion Revascularization (TLR)

"Target Lesion Revascularization is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. All TLR should be classified prospectively as clinically indicated [CI] or not clinically indicated by the investigator prior to repeat angiography. An independent angiographic core laboratory should verify that the severity of percent diameter stenosis meets requirements for clinical indication and will overrule in cases where investigator reports are not in agreement.~The target lesion is defined as the treated segment from 5 mm proximal to the stent and to 5 mm distal to the scaffold/stent." (NCT01425281)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Absorb BVS™	9
XIENCE™	3

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Number of Participants With Target Lesion Revascularization (TLR)

"Target Lesion Revascularization is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. All TLR should be classified prospectively as clinically indicated [CI] or not clinically indicated by the investigator prior to repeat angiography. An independent angiographic core laboratory should verify that the severity of percent diameter stenosis meets requirements for clinical indication and will overrule in cases where investigator reports are not in agreement.~The target lesion is defined as the treated segment from 5 mm proximal to the stent and to 5 mm distal to the scaffold/stent." (NCT01425281)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Absorb BVS™	24
XIENCE™	8

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Number of Participants With Target Lesion Revascularization (TLR)

"Target Lesion Revascularization is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. All TLR should be classified prospectively as clinically indicated [CI] or not clinically indicated by the investigator prior to repeat angiography. An independent angiographic core laboratory should verify that the severity of percent diameter stenosis meets requirements for clinical indication and will overrule in cases where investigator reports are not in agreement.~The target lesion is defined as the treated segment from 5 mm proximal to the stent and to 5 mm distal to the scaffold/stent." (NCT01425281)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Absorb BVS™	27
XIENCE™	8

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Number of Participants With Target Lesion Revascularization (TLR)

"Target Lesion Revascularization is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. All TLR should be classified prospectively as clinically indicated [CI] or not clinically indicated by the investigator prior to repeat angiography. An independent angiographic core laboratory should verify that the severity of percent diameter stenosis meets requirements for clinical indication and will overrule in cases where investigator reports are not in agreement.~The target lesion is defined as the treated segment from 5 mm proximal to the stent and to 5 mm distal to the scaffold/stent." (NCT01425281)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Absorb BVS™	28
XIENCE™	8

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Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR) (NCT01425281)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Absorb BVS™	45
XIENCE™	21

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Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR) (NCT01425281)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Absorb BVS™	47
XIENCE™	22

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Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	18
XIENCE™	8

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Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT01425281)
Timeframe: 180 days

Intervention	Participants (Count of Participants)
Absorb BVS™	15
XIENCE™	5

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Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT01425281)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Absorb BVS™	28
XIENCE™	11

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Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT01425281)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Absorb BVS™	41
XIENCE™	20

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Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT01425281)
Timeframe: 30 days

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	3

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Number of Participants With Target Vessel Failure (TVF) (Cardiac Death, All MI, ID-TVR)

Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or Ischemic-Driven Target Vessel Revascularization (ID-TVR). (NCT01425281)
Timeframe: In-hospital (≤ 7 days of post index procedure)

Intervention	Participants (Count of Participants)
Absorb BVS™	13
XIENCE™	2

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Number of Participants With Target Vessel Revascularization (TVR)

Target Vessel Revascularization is defined as any repeat percutaneous intervention or surgical bypass of any segment of the target vessel. The target vessel is defined as the entire major coronary vessel proximal and distal to the target lesion which includes upstream and downstream branches and the target lesion itself. (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	8
XIENCE™	8

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Number of Participants With Target Vessel Revascularization (TVR)

Intervention	Participants (Count of Participants)
Absorb BVS™	4
XIENCE™	4

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Number of Participants With Target Vessel Revascularization (TVR)

Intervention	Participants (Count of Participants)
Absorb BVS™	15
XIENCE™	9

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Number of Participants With Target Vessel Revascularization (TVR)

Intervention	Participants (Count of Participants)
Absorb BVS™	33
XIENCE™	19

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Number of Participants With Target Vessel Revascularization (TVR)

Intervention	Participants (Count of Participants)
Absorb BVS™	2
XIENCE™	2

[back to top]

Number of Participants With Target Vessel Revascularization (TVR)

Intervention	Participants (Count of Participants)
Absorb BVS™	38
XIENCE™	19

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Number of Participants With Target Vessel Revascularization (TVR)

Intervention	Participants (Count of Participants)
Absorb BVS™	41
XIENCE™	19

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Number of Participants With Target Vessel Revascularization (TVR)

Intervention	Participants (Count of Participants)
Absorb BVS™	1
XIENCE™	0

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Number of Participants With Acute Stent/Scaffold Thrombosis

"Scaffold/Stent thrombosis should be reported as a cumulative value at the different time points.~Timings:~Acute:0-24 hours;Subacute:>24 hours-30 days;Late:30 days-1 year;Very late:>1 year.~Definite stent thrombosis occurred by either angiographic/pathologic confirmation.~Angiographic confirmation:The presence of a thrombus that originates in the stent or in the segment 5 mm proximal or distal to the stent&presence of at least 1 of the following criteria within a 48-hour time window~-Acute onset of ischemic symptoms at rest;New ischemic ECG changes;Typical rise&fall in cardiac biomarkers;Nonocclusive/Occlusive thrombus~Pathological confirmation:Evidence of recent thrombus.~Probable stent thrombosis may occur after intracoronary stenting due to:~Unexplained death within first 30 days~Any MI that is related to documented acute ischemia in the territory of the implanted stent without angiographic confirmation of stent thrombosis&in the absence of any other obvious cause." (NCT01425281)
Timeframe: <=1 day

Intervention	Participants (Count of Participants)
	Definite	Probable
Absorb BVS™	1	0
XIENCE™	0	0

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Number of Participants With Acute/Subacute Stent/Scaffold Thrombosis

Intervention	Participants (Count of Participants)
	Definite	Probable
Absorb BVS™	2	0
XIENCE™	0	0

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Number of Participants With Cumulative Stent/Scaffold Thrombosis

Intervention	Participants (Count of Participants)
	Definite	Probable
Absorb BVS™	8	1
XIENCE™	0	0

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Number of Participants With Late Stent/Scaffold Thrombosis

Intervention	Participants (Count of Participants)
	Definite	Probable
Absorb BVS™	0	1
XIENCE™	0	0

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Number of Participants With Subacute Stent/Scaffold Thrombosis

Intervention	Participants (Count of Participants)
	Definite	Probable
Absorb BVS™	1	0
XIENCE™	0	0

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Number of Participants With Very Late Stent/Scaffold Thrombosis

Intervention	Participants (Count of Participants)
	Definite	Probable
Absorb BVS™	6	0
XIENCE™	0	0

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Number of Participants With Non Target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR)is any revascularization in a vessel other than the target vessel. (NCT01425281)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Absorb BVS™	10
XIENCE™	11

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Absolute Difference (3 Years Post Nitrate- 3 Years Pre Nitrate) In-Scaffold Mean Lumen Diameter (MLD)

In-scaffold:Within the margins of the scaffold. (NCT01425281)
Timeframe: 3 years

Intervention	mm (Mean)
Absorb BVS™	0.05
XIENCE™	0.06

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Absolute Difference (3 Years Post-nitrate - Post Procedure Post-nitrate) In-Scaffold Minimum Lumen Diameter

In-scaffold:Within the margins of the scaffold. (NCT01425281)
Timeframe: 3 years

Intervention	mm (Mean)
Absorb BVS™	-0.37
XIENCE™	-0.25

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Device Success

Successful delivery and deployment of the first study scaffold/stent the intended target lesion and successful withdrawal of the delivery system with attainment of final in-scaffold/stent residual stenosis of less than 50% by quantitative coronary angiography (QCA). (NCT01425281)
Timeframe: From the start of index procedure to end of index procedure

Intervention	Percentage of lesions (Number)
Absorb BVS™	99.5
XIENCE™	100

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Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)

"All deaths are considered cardiac unless an unequivocal non-cardiac cause can be established. Specifically, any unexpected death even in subjects with coexisting potentially fatal non-cardiac disease (e.g. cancer, infection) should be classified as cardiac.~• Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~• Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~• Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma." (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	0
XIENCE™	1

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Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)

Intervention	Participants (Count of Participants)
Absorb BVS™	0
XIENCE™	1

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Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)

Intervention	Participants (Count of Participants)
Absorb BVS™	4
XIENCE™	1

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Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)

Intervention	Participants (Count of Participants)
Absorb BVS™	8
XIENCE™	6

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Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)

Intervention	Participants (Count of Participants)
Absorb BVS™	0
XIENCE™	0

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Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)

"All deaths are considered cardiac unless an unequivocal non-cardiac cause can be established. Specifically, any unexpected death even in subjects with coexisting potentially fatal non-cardiac disease (e.g. cancer, infection) should be classified as cardiac.~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma." (NCT01425281)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Absorb BVS™	11
XIENCE™	7

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Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)

"All deaths are considered cardiac unless an unequivocal non-cardiac cause can be established. Specifically, any unexpected death even in subjects with coexisting potentially fatal non-cardiac disease (e.g. cancer, infection) should be classified as cardiac.~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma." (NCT01425281)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Absorb BVS™	13
XIENCE™	7

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Number of Participants Experiencing All Death (Cardiac, Vascular, Non-Cardiovascular)

"All deaths are considered cardiac unless an unequivocal non-cardiac cause can be established. Specifically, any unexpected death even in subjects with coexisting potentially fatal non-cardiac disease (e.g. cancer, infection) should be classified as cardiac.~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma." (NCT01425281)
Timeframe: In-hospital (≤ 7 days of post index procedure)

Intervention	Participants (Count of Participants)
Absorb BVS™	0
XIENCE™	0

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Number of Participants Experiencing All Death/All MI

"All deaths includes~• Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~• Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~• Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI Development of new, pathological Q wave on the ECG.~Non-Q wave MI Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 180 days

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	3

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Number of Participants Experiencing All Death/All MI

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	2

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Number of Participants Experiencing All Death/All MI

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), un witnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma. Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Absorb BVS™	35
XIENCE™	12

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Number of Participants Experiencing All Death/All MI

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), un witnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Absorb BVS™	22
XIENCE™	5

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Number of Participants Experiencing All Death/All MI

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), un witnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Absorb BVS™	33
XIENCE™	11

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Number of Participants Experiencing All Death/All MI

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma. Myocardial Infarction (MI)~Q wave MI Development of new, pathological Q wave on the ECG.~Non-Q wave MI Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 5 years

Intervention	Participants (Count of Participants)
Absorb BVS™	37
XIENCE™	13

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Number of Participants Experiencing All Death/All MI

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI) Q wave MI Development of new, pathological Q wave on the ECG. Non-Q wave MI Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: In-hospital (≤ 7 days of post index procedure)

Intervention	Participants (Count of Participants)
Absorb BVS™	13
XIENCE™	2

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Number of Participants Experiencing All Death/All MI

"All deaths includes~Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	15
XIENCE™	3

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Number of Participants Experiencing Cardiac Death/All MI

"Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), un witnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Myocardial Infarction (MI) Q wave MI: Development of new, pathological Q wave on the ECG. Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Absorb BVS™	29
XIENCE™	9

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Number of Participants Experiencing Cardiac Death/All MI

Intervention	Participants (Count of Participants)
Absorb BVS™	29
XIENCE™	10

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Number of Participants Experiencing Cardiac Death/All MI

Intervention	Participants (Count of Participants)
Absorb BVS™	13
XIENCE™	2

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Number of Participants Experiencing Cardiac Death/All MI

"Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), un witnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Absorb BVS™	15
XIENCE™	2

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Number of Participants Experiencing Cardiac Death/All MI

"Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), un witnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 180 days

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	2

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Number of Participants Experiencing Cardiac Death/All MI

"Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), un witnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Absorb BVS™	20
XIENCE™	4

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Number of Participants Experiencing Cardiac Death/All MI

"Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), un witnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 3 years

Intervention	Participants (Count of Participants)
Absorb BVS™	28
XIENCE™	8

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Number of Participants Experiencing Cardiac Death/All MI

"Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), un witnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 30 days

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	2

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Number of Participants With All Myocardial Infarction (Per Protocol Definition)

Intervention	Participants (Count of Participants)
Absorb BVS™	15
XIENCE™	2

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Number of Participants With All Myocardial Infarction (Per Protocol Definition)

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	2

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Number of Participants With All Myocardial Infarction (Per Protocol Definition)

Intervention	Participants (Count of Participants)
Absorb BVS™	19
XIENCE™	4

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Number of Participants With All Myocardial Infarction (Per Protocol Definition)

Intervention	Participants (Count of Participants)
Absorb BVS™	27
XIENCE™	5

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Number of Participants With All Myocardial Infarction (Per Protocol Definition)

"Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of Creatine kinase (CK) levels to ≥ two times the upper limit of normal (ULN) with elevated Creatine kinase-MB (CK-MB) in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 30 days

Intervention	Participants (Count of Participants)
Absorb BVS™	14
XIENCE™	2

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Number of Participants With All Myocardial Infarction (Per Protocol Definition)

Intervention	Participants (Count of Participants)
Absorb BVS™	13
XIENCE™	2

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Number of Participants With All Myocardial Infarction (Per Protocol Definition)

"Myocardial Infarction (MI)~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01425281)
Timeframe: 4 years

Intervention	Participants (Count of Participants)
Absorb BVS™	27
XIENCE™	5

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Number of Participants With All Myocardial Infarction (Per Protocol Definition)

Intervention	Participants (Count of Participants)
Absorb BVS™	27
XIENCE™	6

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
Absorb BVS™	12
XIENCE™	12

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
Absorb BVS™	7
XIENCE™	6

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
Absorb BVS™	22
XIENCE™	18

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
Absorb BVS™	49
XIENCE™	33

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
Absorb BVS™	2
XIENCE™	2

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Maximum Tolerated Dose of Sorafenib for Participants With Recurrent Malignant Gliomas

Maximum tolerated dose of sorafenib for participants with recurrent malignant gliomas. MTD is defined as the dose at which fewer than one-third of participants experience a dose limiting toxicity (DLT) to one of the study drugs. A DLT is any grade 3 thrombocytopenia, grade 4 anemia, grade 4 neutropenia, or febrile neutropenia of any grade. Any non-hematologic grade 3 or grade 4 toxicity, excluding alopecia and/or hand/foot reaction. Failure to recover from toxicities (to grade 1 or less) to be eligible for re-treatment with sorafenib within 14 days of the last dose of sorafenib. (NCT01434602)
Timeframe: First 28 days of treatment only (cycle 1)

Intervention	mg (Number)
All Participants	400

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Median Amount of Time a Participant Survives After Therapy for Participants With Recurrent Malignant Glioma (Group A, Group B, and Group C) Treated With Everolimus and Sorafenib Measured From the Time of Study Enrollment

Median amount of time a participant survives after therapy for participants with recurrent malignant glioma (Group A, Group B, and Group C) treated with everolimus and sorafenib measured from the time of study enrollment. (NCT01434602)
Timeframe: From the time of study enrollment up to 1.5 years

Intervention	Months (Median)
Phase 2 Group A Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	7.75
Phase 2 Group B Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	4.77
Phase 2 Group C Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	11.97

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Median Amount of Time Participants Survives Without Disease Progression for Groups A, B, and C Treated With Everolimus and Sorafenib

Median amount of time participants survives without disease progression for Groups A, B, and C treated with everolimus and sorafenib. Progression was measured by brain magnetic resonance imaging (MRI) tumor measurements. Progression is defined as >25% increase in the sum of products of perpendicular diameters of enhancing lesions (over baseline if no decrease) on stable or increasing dose of corticosteroids; and/or significant increase in T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) non-enhancing lesion on stable or increasing doses of corticosteroids compared to baseline scan or best response following initiation or therapy, not due to co-morbid events (radiation therapy, demyelination, ischemic injury, infection, seizures, postoperative changes, or other treatment effects). Any new lesion. (NCT01434602)
Timeframe: Up to 6 months

Intervention	Months (Median)
Phase 2 Group A Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	1.92
Phase 2 Group B Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	1.17
Phase 2 Group C Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	1.87

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Number of Participants With a Dose-limiting Toxicity (DLT)

A DLT is any grade 3 thrombocytopenia, grade 4 anemia, grade 4 neutropenia, or febrile neutropenia of any grade. Any non-hematologic grade 3 or grade 4 toxicity, excluding alopecia and/or hand/foot reaction. Failure to recover from toxicities (to grade 1 or less) to be eligible for re-treatment with sorafenib and everolimus within 14 days of the last dose of sorafenib and everolimus. (NCT01434602)
Timeframe: First 28 days of treatment only (cycle 1)

Intervention	Participants (Count of Participants)
Phase I Dose Level I Sorafenib 400mg Twice Daily + Everolimus 5mg Daily	3
Phase I Dose Level -1 Sorafenib 400mg Twice Daily, 7 Days on, 7 Off + Everolimus 5mg Daily	1

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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. (NCT01434602)
Timeframe: Date treatment consent signed to date off study, approximately 21 months and 18 days, 30 months and twelve days, 83 months and 8 days, and 84 months and 26 days for each group respectively.

Intervention	Participants (Count of Participants)
Phase I Dose Level I Sorafenib 400mg Twice Daily + Everolimus 5mg Daily	6
Phase I Dose Level -1 Sorafenib 400mg Twice Daily, 7 Days on, 7 Off + Everolimus 5mg Daily	7
Phase 2 Group A Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	12
Phase 2 Group B Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	38
Phase 2 Group C Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	20

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Percentage of Participants Who Survived Without Disease Progression at 3 Months After Treatment for Glioblastoma Participants With Prior Bevacizumab Exposure

Percentage of participants who survived without disease progression at 3 months after treatment for glioblastoma participants with prior bevacizumab exposure. Progression was measured by brain magnetic resonance imaging (MRI) tumor measurements. Progression is defined as >25% increase in the sum of products of perpendicular diameters of enhancing lesions (over baseline if no decrease) on stable or increasing dose of corticosteroids; and/or significant increase in T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) non-enhancing lesion on stable or increasing doses of corticosteroids compared to baseline scan or best response following initiation or therapy, not due to co-morbid events (radiation therapy, demyelination, ischemic injury, infection, seizures, postoperative changes, or other treatment effects). Any new lesion. (NCT01434602)
Timeframe: 3 months

Intervention	Percentage of participants (Number)
Phase 2 Group B Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	12.9

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Rate of Participants Symptom Interference With Function

To evaluate the occurrence of symptoms and correlate to disease progression and tolerance to treatment using the MD Anderson Symptom Inventory-Brain Tumor Module (MDASI-BT) self-reporting tool. The MDASI-BT consists of 23 symptoms rated on an 11-point scale (0 - did not interfere, to 10 - interfered completely) to indicate the symptoms that interfere with a participant's life in the last 24 hours. We calculated the mean symptom interference at the time of clinical evaluation. (NCT01434602)
Timeframe: Completed at baseline, before a brain or spine magnetic resonance imaging (MRI)/clinical evaluation, and at cycle 1-2, cycle 4, cycle 6, cycle 8, cycle 10 and cycle 12 (each cycle is 28 days)

Intervention	score on a scale (Mean)
	Baseline	Cycle 1	Cycle 2
Phase I Dose Level I Sorafenib 400mg Twice Daily + Everolimus 5mg Daily	5.0	4.2	5.0

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Percentage of Participants Who Survived Without Disease Progression at 6 Months After Treatment for Anaplastic Glioma (AG) Participants With no Prior Bevacizumab Exposure

Percentage of participants who survived without disease progression at 6 months after treatment for anaplastic glioma (AG) participants with no prior bevacizumab exposure. Progression was measured by brain magnetic resonance imaging (MRI) tumor measurements. Progression is defined as >25% increase in the sum of products of perpendicular diameters of enhancing lesions (over baseline if no decrease) on stable or increasing dose of corticosteroids; and/or significant increase in T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) non-enhancing lesion on stable or increasing doses of corticosteroids compared to baseline scan or best response following initiation or therapy, not due to co-morbid events (radiation therapy, demyelination, ischemic injury, infection, seizures, postoperative changes, or other treatment effects). Any new lesion. (NCT01434602)
Timeframe: 6 months

Intervention	Percentage of participants (Number)
Phase 2 Group C Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	26.7

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Percentage of Participants Who Survived Without Disease Progression at 6 Months After Treatment for Glioblastoma Participants With no Prior Bevacizumab Exposure

Percentage of participants who survived without disease progression at 6 months after treatment for glioblastoma participants with no prior bevacizumab exposure. Progression was measured by brain magnetic resonance imaging (MRI) tumor measurements. Progression is defined as >25% increase in the sum of products of perpendicular diameters of enhancing lesions (over baseline if no decrease) on stable or increasing dose of corticosteroids; and/or significant increase in T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) non-enhancing lesion on stable or increasing doses of corticosteroids compared to baseline scan or best response following initiation or therapy, not due to co-morbid events (radiation therapy, demyelination, ischemic injury, infection, seizures, postoperative changes, or other treatment effects). Any new lesion. (NCT01434602)
Timeframe: 6 months

Intervention	Percentage of participants (Number)
Phase 2 Group A Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	8.33

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Objective Response for Participants With Recurrent Malignant Gliomas (Group A, Group B, and Group C) Treated With Everolimus and Sorafenib

Objective response for participants with recurrent malignant gliomas treated with everolimus and sorafenib was assessed by brain magnetic resonance imaging (MRI) tumor measurements. Complete Response is complete disappearance of all CE measurable and evaluable disease. Partial Response is greater than or equal to 50% decrease under baseline in the sum of products of perpendicular diameters of the two largest CE measurable lesions, sustained for at least 4 weeks. Progressive Disease >25% increase in the sum of products of perpendicular diameters of enhancing lesions (over baseline if no decrease) on stable or increasing dose of corticosteroids, significant increase in T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) non-enhancing lesion on stable or increasing doses of corticosteroids compared to baseline scan or best response following initiation or therapy, not due to co-morbid events, or any new lesion. Stable Disease does not qualify for CR, PR, or progression. (NCT01434602)
Timeframe: After 1 cycle of treatment, or those who exhibit objective progression prior the end of cycle 1 (one cycle = 28 days).

Intervention	Participants (Count of Participants)
	Complete Response	Partial Response	Progressive Disease	Stable Disease	Not Evaluable
Phase 2 Group A Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on 7 Off + Everolimus 5mg Daily	0	0	4	8	0
Phase 2 Group B Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	0	0	17	16	7
Phase 2 Group C Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	0	2	7	10	2

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Rate of Participants Symptom Severity

To evaluate the occurrence of symptoms and correlate to disease progression and tolerance to treatment using the MD Anderson Symptom Inventory-Brain Tumor Module (MDASI-BT) self-reporting tool. The MDASI-BT consists of 23 symptoms rated on an 11-point scale (0 - not present, to 10 - as bad as you can imagine) to indicate the presence and severity of the symptom. We calculated the mean core symptom severity at the time of clinical evaluation. (NCT01434602)
Timeframe: Completed at baseline, before a brain or spine magnetic resonance imaging (MRI)/clinical evaluation, and at cycle 1-2, cycle 4, cycle 6, cycle 8, cycle 10 and cycle 12 (each cycle is 28 days)

Intervention	score on a scale (Mean)
	Baseline	Cycle 1	Cycle 2	Cycle 4	Cycle 6	Cycle 8	Cycle 10	Cycle 12
Phase 2 Group C Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	1.3	1.8	1.5	1.8	1.4	1.8	1.5	1.4

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Rate of Participants Symptom Severity

To evaluate the occurrence of symptoms and correlate to disease progression and tolerance to treatment using the MD Anderson Symptom Inventory-Brain Tumor Module (MDASI-BT) self-reporting tool. The MDASI-BT consists of 23 symptoms rated on an 11-point scale (0 - not present, to 10 - as bad as you can imagine) to indicate the presence and severity of the symptom. We calculated the mean core symptom severity at the time of clinical evaluation. (NCT01434602)
Timeframe: Completed at baseline, before a brain or spine magnetic resonance imaging (MRI)/clinical evaluation, and at cycle 1-2, cycle 4, cycle 6, cycle 8, cycle 10 and cycle 12 (each cycle is 28 days)

Intervention	score on a scale (Mean)
	Baseline	Cycle 1	Cycle 2	Cycle 4
Phase 1 Dose Level -1 Sorafenib 400mg Twice Daily 7 Days On, & Days Off + Everolimus Daily	1.3	1.6	1.9	0.4
Phase 2 Group A Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on 7 Off + Everolimus 5mg Daily	1.5	2.2	2.3	1.3
Phase 2 Group B Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	2.0	2.5	3.4	3.5

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Rate of Participants Symptom Severity

To evaluate the occurrence of symptoms and correlate to disease progression and tolerance to treatment using the MD Anderson Symptom Inventory-Brain Tumor Module (MDASI-BT) self-reporting tool. The MDASI-BT consists of 23 symptoms rated on an 11-point scale (0 - not present, to 10 - as bad as you can imagine) to indicate the presence and severity of the symptom. We calculated the mean core symptom severity at the time of clinical evaluation. (NCT01434602)
Timeframe: Completed at baseline, before a brain or spine magnetic resonance imaging (MRI)/clinical evaluation, and at cycle 1-2, cycle 4, cycle 6, cycle 8, cycle 10 and cycle 12 (each cycle is 28 days)

Intervention	score on a scale (Mean)
	Baseline	Cycle 1	Cycle 2
Phase 1 Dose LEvel 1 Sorafenib 400mg Twice Daily + Everolimus 5mg Daily	3.9	3.8	3.5

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Rate of Participants Symptom Interference With Function

Intervention	score on a scale (Mean)
	Baseline	Cycle 1	Cycle 2	Cycle 4	Cycle 6	Cycle 8	Cycle 10	Cycle 12
Phase 2 Group C Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	2.1	2.5	1.8	3.3	2.0	2.4	1.6	1.2

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Rate of Participants Symptom Interference With Function

Intervention	score on a scale (Mean)
	Baseline	Cycle 1	Cycle 2	Cycle 4
Phase 2 Group A Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on 7 Off + Everolimus 5mg Daily	2.3	3.3	4.3	2.8
Phase 2 Group B Dose Level -1 Sorafenib 400mg Twice Daily 7 Days on, 7 Off + Everolimus 5mg Daily	3.4	4.1	6.4	4.2
Phase I Dose Level -1 Sorafenib 400mg Twice Daily, 7 Days on, 7 Off + Everolimus 5mg Daily	1.5	2.3	2.8	0.3

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Maximum Tolerated Dose of Everolimus for Participants With Recurrent Malignant Gliomas

Maximum tolerated dose of everolimus for participants with recurrent malignant gliomas. MTD is defined as the dose at which fewer than one-third of participants experience a dose limiting toxicity (DLT) to one of the study drugs. A DLT is any grade 3 thrombocytopenia, grade 4 anemia, grade 4 neutropenia, or febrile neutropenia of any grade. Any non-hematologic grade 3 or grade 4 toxicity, excluding alopecia and/or hand/foot reaction. Failure to recover from toxicities (to grade 1 or less) to be eligible for re-treatment with everolimus within 14 days of the last dose of everolimus. (NCT01434602)
Timeframe: First 28 days of treatment only (cycle 1)

Intervention	mg (Number)
All Participants	5

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Number of Individuals Experiencing Toxicity

Safety determinations are based on the rate of drug-related adverse events (AEs) reported based upon the toxicity as measured by the NCI Common Terminology Criteria for Adverse Events version 4.0 (CTCAE v4.0). (NCT01488487)
Timeframe: 3.5 years

Intervention	participants (Number)
	Dose Limiting Toxicities (DLT)	Any adverse event
Everolimus + Pasireotide	1	24

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Objective Response Rate (ORR)

"ORR is the rate of complete responses (CRs) + partial responses (PRs) as determined by RECIST (v1.1) and modified HCC RECIST criteria. Responses defined as follows:~CR: disappearance of all clinical/radiological evidence of tumor including any intratumoral arterial enhancement in all target lesions.~Partial Response (PR): at least a 30% decrease in the sum of diameters of viable (contrast enhancement in the arterial phase) target lesions, referencing the baseline sum.~Stable Disease (SD): any cases that do not qualify for either partial response or progressive disease.~Progressive Disease (PD): an increase of at least 20% in the sum of the diameters of viable target lesions, referencing the nadir sum, and/or the appearance of one or more new lesions. A new hepatic nodule signals PD when the longest diameter is at least 10 mm and the nodule shows the typical vascular pattern of HCC on dynamic imaging or if at least 1-cm interval growth is seen in subsequent scans." (NCT01488487)
Timeframe: 3.5 years

Intervention	percentage of participants (Number)
	Radiographic response (CR or PR)	Stable disease
Everolimus + Pasireotide	0	45.5

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Time to Progression (TTP)

Time to progression is defined as the time from study enrollment until radiological progression in a previously embolized lobe, development of new lesions in an untreated lobe, or evidence of extrahepatic progression (based on modified Hepatocellular Carcinoma (HCC) Response Evaluation Criteria In Solid Tumors (RECIST) criteria). Patients will be followed until death. Patients that die of causes unrelated to the study drug without evidence of progression will be censored. (NCT01488487)
Timeframe: 3.5 years

Intervention	months (Median)
Everolimus + Pasireotide	3.5

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Overall Survival (OS)

Overall survival is defined as the time from study enrollment until death. (NCT01488487)
Timeframe: 3.5 years

Intervention	months (Median)
Everolimus + Pasireotide	6.7

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Duration of Response (DoR)

DoR was defined as the time from the first occurrence of PR or CR (as per local radiological review) until the date of the first documented disease progression or death due to underlying cancer. (NCT01491672)
Timeframe: 20 months

Intervention	months (Median)
Prior Sunitinib	10.8
Other Prior Vascular Endothelial Growth Factor (VEGF)	7.4
Prior Cytokines	9.2
All Participants	9.2

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Clinical Benefit Rate (CBR)

CBR was defined as the proportion of patients with best overall response of complete response (CR) or partial response (PR) or stable disease based on the local radiological data according to the RECIST 1.0 criteria. (NCT01491672)
Timeframe: 20 months

Intervention	Participants (Number)
Prior Sunitinib	41
Other Prior Vascular Endothelial Growth Factor (VEGF)	48
Prior Cytokines	11
All Participants	100

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Duration of PFS for Each First-line Treatment Cohort

Duration of PFS during second-line treatment was defined as the time from the date of enrollment to the date of the first documented disease progression or death due to any cause. Participants' assessment was based on the local radiological data according to the RECIST 1.0 Criteria. (NCT01491672)
Timeframe: 20 months

Intervention	months (Median)
Prior Sunitinib	5.6
Other Prior Vascular Endothelial Growth Factor (VEGF)	7.8
Prior Cytokines	12.9

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Progression-free Survival (PFS) - All Participants

PFS during second-line treatment was defined as the time from the date of enrollment to the date of the first documented disease progression or death due to any cause. The primary analysis of PFS was based on a local radiology review of CT scans and MRI collected until the participant experienced disease progression according to Response Evaluation Criteria in Solid Tumors (RECIST) 1.0. (NCT01491672)
Timeframe: 20 months

Intervention	months (Median)
All Participants	7.4

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Overall Survival (OS)

OS was defined as the time from date of enrollment to date of death due to any cause. (NCT01491672)
Timeframe: 28 months

Intervention	months (Median)
Prior Sunitinib	23.8
Other Prior Vascular Endothelial Growth Factor (VEGF)	17.2
Prior Cytokines	NA
All Participants	23.8

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Objective Response Rate (ORR)

ORR was defined as the proportion of participants with best overall response of CR or PR based on the local radiological data according to the RECIST 1.0 Criteria (NCT01491672)
Timeframe: 20 months

Intervention	Participants (Number)
Prior Sunitinib	4
Other Prior Vascular Endothelial Growth Factor (VEGF)	3
Prior Cytokines	3
All Participants	10

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Clinical Benefit Rate of Patients Treated With the Combination of Letrozole and Lapatinib and Then After Progression, Treated With Everolimus, Letrozole and Lapatinib.

"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; Progression, 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; Stable Disease (SD), neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for disease progression.~Clinical benefit rate is defined as complete response+partial response+ stable disease. All participants will be treated with the combination of letrozole and lapatinib. Once the participant progresses on this regimen, the participant will be treated with everolimus, letrozole and lapatinib until they progress." (NCT01499160)
Timeframe: From date of study entry until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 24 months

Intervention	Participants (Count of Participants)
Letrozole in Combination With Lapatinib Followed by Everolimus	6

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PROGRESSION FREE SURVIVAL TUMOR ASSESSMENT

Patients treated with the combination of Letrozole and Lapatinib will provide tumor biopsy sample (NCT01499160)
Timeframe: From date of study entry until 4 weeks after removal from study or until death (whichever occurs first) up to 24 months.

Intervention	Participants (Count of Participants)
Letrozole in Combination With Lapatinib Followed by Everolimus	6

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Myocardial Infarction (MI) Related to the Target Vessel

New Q-waves in ≥2 leads lasting ≥0.04 sec with creatine kinase (CK) MB or troponin >normal; if no new Q-waves total CK levels >3× normal (peri-percutaneous coronary intervention [PCI]) or >2× normal (spontaneous) with elevated CK-MB or troponin >3× normal (peri-PCI) or >2× normal (spontaneous) plus at least one of the following: ECG changes indicating new ischemia (new ST-T changes, left bundle branch block), imaging evidence of new loss of viable myocardium, or new regional wall motion abnormality. Similar for MI diagnosis post coronary artery bypass graft with CK-MB or troponin >5× normal (NCT01510327)
Timeframe: 6 months

Intervention	percentage of participants (Number)
PROMUS Element	0.0

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Maximum Observed Everolimus Blood Concentration (Cmax)

Venous blood draw up to 24 hours prior to implantation of the first study stent (predose time point) and at 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours after completion of implantation of the last study stent (NCT01510327)
Timeframe: Predose <24 hours; post dose at 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours

Intervention	ng/mL (Mean)
Everolimus Dose of 95.4 µg	0.71
Everolimus Dose of 102.4 µg	0.67
Everolimus Dose of 138.6 µg	0.91

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Definite + Probable Stent Thrombosis Rate Based on Academic Research Consortium (ARC) Definition

DEFINITE ST: acute coronary syndrome and angiographic or pathologic evidence of stent thrombosis; PROBABLE ST: unexplained death within 30 days or target-vessel infarction without angiographic information ARC ST is reported as a cumulative value at different time points and within the different separate time points. Time 0 is the time point after the guide catheter has been removed. Acute ST: 0-24 hours after stent implantation; Subacute ST: >24 hours to 30 days post; late ST: >30 days to 1 year post; Very late ST: >1 year post; NOTE: Acute/subacute can be replaced by early ST (0-30 days). (NCT01510327)
Timeframe: >30 days-1 year

Intervention	percentage of participants (Number)
PROMUS Element	0.0

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Definite + Probable Stent Thrombosis Rate Based on Academic Research Consortium (ARC) Definition

Intervention	percentage of participants (Number)
PROMUS Element	0.0

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Definite + Probable Stent Thrombosis (ST) Rate Based on Academic Research Consortium (ARC) Definition

Intervention	percentage of participants (Number)
PROMUS Element	0.0

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Area Under the Concentration Versus Time Curve (AUC 0-t) Everolimus

Venous blood draw up to 24 hours prior to implantation of the first study stent (predose time point) and at 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours after completion of implantation of the last study stent; t is the last time at which concentration can be quantified (NCT01510327)
Timeframe: Predose <24 hours; post dose at 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours

Intervention	ng*hr/mL (Mean)
Everolimus Dose of 95.4 µg	7.27
Everolimus Dose of 102.4 µg	6.45
Everolimus Dose of 138.6 µg	10.87

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Area Under the Concentration Versus Time Curve (AUC 0-infinity) Everolimus

Venous blood draw up to 24 hours prior to implantation of the first study stent (predose time point), 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours after implantation of the last study stent. (NCT01510327)
Timeframe: Predose <24 hours; post dose at 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours

Intervention	ng*hr/mL (Mean)
Everolimus Dose of 95.4 µg	19.26
Everolimus Dose of 102.4 µg	12.95
Everolimus Dose of 138.6 µg	60.74

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Area Under the Concentration Versus Time Curve (AUC 0-24), Everolimus

Intervention	ng*hr/mL (Mean)
Everolimus Dose of 95.4 µg	6.83
Everolimus Dose of 102.4 µg	6.14
Everolimus Dose of 138.6 µg	9.51

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All Death

Number of participants no longer alive (NCT01510327)
Timeframe: 6 months

Intervention	percentage of participants who died (Number)
PROMUS Element	0.0

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Time of Occurrence of Maximum Everolimus Concentration (Tmax)

Intervention	hours (Mean)
Everolimus Dose of 95.4 µg	0.47
Everolimus Dose of 102.4 µg	0.62
Everolimus Dose of 138.6 µg	0.52

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Total Blood Clearance - Everolimus (CL)

Venous blood draw up to 24 hours prior to implantation of the first study stent (predose time point), 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours after completion of implantation of the last study stent. (NCT01510327)
Timeframe: Predose <24 hours; post dose at 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours

Intervention	L/h (Mean)
Everolimus Dose of 95.4 µg	6445
Everolimus Dose of 102.4 µg	8044
Everolimus Dose of 138.6 µg	2511

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Terminal Phase Half-life (t1/2) Everolimus

Venous blood draw up to 24 hours prior to implantation of the first study stent (predose time point), at 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours after completion of implantation of the last study stent. (NCT01510327)
Timeframe: Predose <24 hours; post dose at 30 minutes, 1, 2, 4, 6, 12, 24, 48, and 72 hours

Intervention	Hours (Mean)
Everolimus Dose of 95.4 µg	34.19
Everolimus Dose of 102.4 µg	22.83
Everolimus Dose of 138.6 µg	136.06

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Target Vessel Revascularization (TVR)

TVR is any ischemia-driven repeat percutaneous intervention to improve blood flow, or bypass surgery of not previously existing lesions with diameter stenosis ≥50% by quantitative coronary angiography in the target vessel, including the target lesion. (NCT01510327)
Timeframe: 6 months

Intervention	percentage of participants (Number)
PROMUS Element	0.0

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Target Lesion Revascularization (TLR)

TLR is any ischemia-driven repeat percutaneous intervention to improve blood flow of the successfully treated target lesion or bypass surgery of the target vessel with a graft distally to the successfully treated target lesion. (NCT01510327)
Timeframe: 6 months

Intervention	percentage of participants (Number)
PROMUS Element	0.0

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Overall Survival (OS) of Patients Treated With Everolimus After Failure of First-line Sunitinib or Pazopanib Therapy up to 48 Months

Overall survival (OS) was defined as the time from date of start of treatment to date of death due to any cause. If a patient was not known to have died, survival will be censored at the date of last contact. (NCT01514448)
Timeframe: 48 months

Intervention	months (Median)
1st Line SUN	14.8
1st Line PAZ	20.4

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Percentage of Patients With Overall Response Rate (ORR) Treated With Everolimus After Failure of First-line Sunitinib or Pazopanib Therapy at Month 6

Overall response rate (ORR) is the Percentage of patients with a best overall response of complete response (CR) or partial response (PR) by month 6. ORR was assessed according to RECIST 1.1 criteria. Partial response (PR) required at least a 30% decrease in the sum of the longest diameters of all target lesions, taking as reference the baseline sum of the longest diameters. Complete response (CR) required a disappearance of all target and non-target lesions. (NCT01514448)
Timeframe: Month 6

Intervention	percentage of participants (Number)
1st Line SUN	0.0
1st Line PAZ	0.0

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Percentage of Progression-free Patients by Month 6

Percentage of progression-free patients by month 6 after starting everolimus treatment. For the purpose of the binomial design of the study, a patient being 'progression-free' will be defined as a patient without disease progression by month 6 whereas a subject with progressive disease by month 6 will not be counted as 'progression-free'. The primary variable was derived from radiologic tumor assessments according to Response Evaluation Criteria in Solid Tumors (RECIST 1.1.) Disease progression was either 1) a 20% increase in the sum of the longest diameter of all target lesions, taking as reference the smallest sum of the longest diameters of all target lesions recorded at or after baseline (minimum absolute increase 5 mm in sum) or 2) the appearance of a new lesion or 3) the unequivocal progression of non-target lesions overall. (NCT01514448)
Timeframe: Month 6

Intervention	Percentage of participants (Number)
1st Line SUN	8.3
1st Line PAZ	46.2

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Progression-Free Survival (PFS) as the Time Interval Between First Intake of Everolimus and First Documented Disease Progression or Death Due to Any Cause at 24 Months

Progression-free survival (PFS) is the time from date of start of treatment to the date of event defined as the first documented progression or death due to any cause. If a patient did not have an event, progression-free survival was censored at the date of last adequate tumor assessment (NCT01514448)
Timeframe: 24 months

Intervention	months (Median)
1st Line SUN	2.8
1st Line PAZ	8.0

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Time to Definitive Deterioration in Functional Assessment of Cancer Therapy - General (FACT-G) Questionnaire Total Score

"FACT-G is a self-assessed health-related quality of life questionnaire. The questionnaire is comprised of 27 questions examining physical, social/family, emotional, and functional well-being. Participants responded to the items on a five-point scale, ranging from 0: Not at all to 4: Very much. The total score ranges from 0 to 108, with higher scores indicating a better patient-reported outcome/quality of life.~Definitive deterioration is defined as a decrease in the total score by at least 7 points compared to baseline with no further improvement.~Death was considered as worsening of the FACT-G total score if it occurred close to the last available assessment, where close was defined as twice the planned period between two assessments. Patients without definitive worsening prior to analysis cut-off or prior to start of another anticancer therapy were censored at the date of their last assessment." (NCT01524783)
Timeframe: From randomization to definitive deterioration of FACT-G total score, assessed up to approximately 3 years

Intervention	Months (Median)
Everolimus + BSC	13.01
Placebo + BSC	9.23

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Overall Survival (OS)

OS is defined as the time from the date of randomization to date of death due to any cause. If a death had not been observed by the date of analysis cut-off, then OS was censored at the date of last contact. All participants randomized to placebo arm who crossed over to everolimus were censored. (NCT01524783)
Timeframe: From date of randomization to date of death, assessed up to approximately 8 years

Intervention	Months (Median)
Everolimus + BSC	43.1
Placebo + BSC	41.76

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Disease Control Rate (DCR) Based on Modified RECIST 1.0 and as Per Central Radiology Assessment

"DCR is defined as the proportion of subjects with best overall response of CR or PR or stable disease based on modified RECIST 1.0 and as per central radiology assessment.~CR: disappearance of all target lesions. PR: At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters.~Stable disease: Neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for progression." (NCT01524783)
Timeframe: From randomization until end of treatment, assessed up to approximately 2.5 years

Intervention	Percentage of participants (Number)
Everolimus + BSC	82.4
Placebo + BSC	64.9

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Pharmacokinetics (PK): Predose Concentration (Cmin) of Everolimus at Day 29

A pre-dose blood sample at day 29 was collected to determine the exposure of everolimus at the steady-state pre-dose concentration (Cmin). Cmin is provided for participants randomized to everolimus+BSC who received 10mg of everolimus daily and also for participants randomized to everolimus+BSC who received 5mg of everolimus daily which was required for a number of participants in the study experiencing adverse events requiring dose modifications (NCT01524783)
Timeframe: Pre-dose at Day 29.

Intervention	nanogram/milliliter (ng/mL) (Mean)
	10mg daily dose	5mg daily dose
Everolimus + BSC	16.382	4.700

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Overall Response Rate (ORR) as Per Modified RECIST 1.0 According to Central Evaluation

"ORR is defined as the proportion of patients with best overall response (BOR) of complete response (CR) or partial response (PR), according to central evaluation and as per modified RECIST 1.0.~CR: disappearance of all target lesions. PR: At least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters." (NCT01524783)
Timeframe: From randomization until end of treatment, assessed up to approximately 2.5 years

Intervention	Percentage of participants (Number)
Everolimus + BSC	2.0
Placebo + BSC	1.0

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Time to Definitive Deterioration in World Health Organization (WHO) Performance Status (PS) Change

"WHO PS is a scale rated from 0 (fully active) to 5 (death) by a healthcare professional to assess the overall status of a patient: a lower score represents a higher ability to perform daily tasks. Deterioration is defined as an increase of at least one point compared to baseline. Deterioration is considered definitive if no improvements in the WHO PS status is observed at a subsequent time of measurement during the treatment period following the time point where the deterioration is observed. Death was considered as worsening of the WHO PS if it occurred close to the last available assessment, where close was defined as twice the planned period between two assessments. Patients without definitive worsening prior to analysis cut-off or prior to start of another anticancer therapy were censored at the date of their last assessment." (NCT01524783)
Timeframe: From randomization to definitive deterioration of WHO performance status, assessed up to approximately 3 years

Intervention	Months (Median)
Everolimus + BSC	24.08
Placebo + BSC	24.15

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Probability of Participants Remaining Event-Free in Progression-Free Survival (PFS) Based on Central Radiology Assessment

"PFS is defined as the time from randomization to the date of the first documented tumor progression or death from any cause, whichever comes first.~Progression was defined using modified RECIST 1.0 and as per central radiology assessment as at least a 20% increase in the sum of diameter of all measured target lesions, taking as reference the smallest sum of diameter of all target lesions recorded at or after baseline. Progression was assessed by cat scan (CT) and/or magnetic resonance imaging (MRI).~For participants who had not progressed or died at the analysis cut-off date, PFS was censored at the date of the last adequate tumor evaluation date. An adequate tumour assessment is a tumour assessment with an overall response other than unknown.~The percentage event-free probability estimate is the estimated probability that a patient will remain event-free in PFS up to the specified time point." (NCT01524783)
Timeframe: From date of randomization to progression or death, whichever comes first, assessed up to 27 months

Intervention	Percent event-free probability in PFS (Number)
	2 months	4 months	6 months	8 months	10 months	12 months	15 months	18 months	21 months	24 months	27 months
Everolimus + BSC	90.1	81.2	72.1	62.4	51.7	44.4	40.1	31.8	27.6	22.0	NA
Placebo + BSC	74.6	49.1	40.1	35.8	31.3	28.1	26.4	24.4	17.4	17.4	17.4

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Change From Baseline in Neuron Specific Enolase (NSE) Levels

NSE is a potential biomarker for tumor response. Blood samples were collected for assessment of NSE levels. Change from Baseline at a particular visit was calculated as the NSE level at that visit minus Baseline. (NCT01524783)
Timeframe: From baseline (every 4 weeks) up to Week 116

Intervention	microgram/liter (ug/L) (Mean)
	Week 4	Week 8	Week 12	Week 16	Week 20	Week 24	Week 28	Week 32	Week 36	Week 40	Week 44	Week 48	Week 52	Week 56	Week 60	Week 64	Week 68	Week 72	Week 76	Week 80	Week 84	Week 88	Week 92	Week 96	Week 100	Week 104	Week 108	Week 112	Week 116
Everolimus + BSC	0.1	0.3	-0.3	2.0	0.8	1.7	1.1	1.5	2.0	1.2	0.8	2.0	1.5	3.6	2.4	4.4	1.1	1.6	1.7	2.9	8.0	2.2	4.0	4.3	1.8	2.9	5.5	2.8	10.6
Placebo + BSC	-2.2	-4.2	15.5	4.1	5.3	6.7	0.4	3.1	2.0	1.2	1.2	0.6	0.7	0.9	0.1	0.9	1.9	0.7	0.6	0.7	0.1	0.6	0.1	0.0	-0.2	-1.7	-0.5	-3.2	0.2

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Change From Baseline in Chromogranin A (CgA) Levels

CgA is a potential biomarker for tumor response. Blood samples were collected for assessment of CgA levels. Change from Baseline at a particular visit was calculated as the CgA level at that visit minus Baseline. (NCT01524783)
Timeframe: From baseline (every 4 weeks) up to 116 weeks

Intervention	microgram/liter (ug/L) (Mean)
	Week 4	Week 8	Week 12	Week 16	Week 20	Week 24	Week 28	Week 32	Week 36	Week 40	Week 44	Week 48	Week 52	Week 56	Week 60	Week 64	Week 68	Week 72	Week 76	Week 80	Week 84	Week 88	Week 92	Week 96	Week 100	Week 104	Week 108	Week 112	Week 116
Everolimus + BSC	434.8	162.3	396.7	263.5	162.1	253.2	587.2	508.5	94.7	511.4	552.8	1326.2	1196.2	1920.6	1722.0	3811.0	1413.3	239.5	3256.5	5421.0	4379.9	571.2	765.5	984.6	935.3	1466.4	2245.8	2817.0	2951.8
Placebo + BSC	1154.3	2697.6	1176.0	1450.4	3640.1	1783.9	1350.3	2000.7	180.9	207.6	140.6	129.0	124.2	134.9	120.9	141.6	222.6	233.7	210.9	286.3	175.4	-9.4	63.7	146.5	-12.7	-21.7	215.9	514.5	99.6

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All Collected Deaths

"Deaths on-treatment were collected from first dose of study treatment until end of study treatment plus 30 days post treatment, up to maximum duration of approximately 8 years.~Total Deaths were collected from first dose of study treatment until end of post-treatment survival follow, up to maximum duration of approximately 8 years." (NCT01524783)
Timeframe: On-treatment deaths: up to approximately 8 years. All deaths: up to approximately 8 years

,,,

Intervention	Participants (Number)
	On-treatment deaths	Total deaths
Everolimus + BSC (Throughout the Study)	10	126
Everolimus +BSC (Crossover)	0	1
Everolimus+BSC (All)	10	127
Placebo + BSC (Blinded Period)	5	57

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Incidence of Biopsy Proven Antibody Mediated Rejection.

To evaluate the proportion of patients with the following efficacy events: biopsy proven antibody mediated rejection/Steroid resistant BPAR and BPAR treated with T cell depleting therapy. (NCT01544491)
Timeframe: at 12 and 36 months post-transplantation

Intervention	Participants (Count of Participants)
	patients with BPAR at 12 months	BPAR Steroid resistant,12 months	BPAR, T Cell depleting therapy 12 months	patients with BPAR at 36 months	BPAR Steroid resistant,36 months	BPAR, T Cell depleting therapy 36 months
EVR+rTAC	7	1	1	6	1	2
MMF+sTAC	8	0	1	12	2	1

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Number of Participants Having Reached the Composite Efficacy Endpoint of Biopsy-proven Acute Rejection

To estimate the rate of the composite efficacy endpoint of biopsy-proven acute rejection (BPAR), graft loss or death at 12 months post transplantation in primary paediatric kidney transplant recipients converted at 4-6 weeks post-transplantation from MMF + standard TAC regimen and steroids, to everolimus + reduced dose TAC regimen and steroid withdrawal at 6 months, versus continuation of MMF + standard TAC regimen and steroids. (NCT01544491)
Timeframe: 12 months, 36 months

Intervention	Participants (Count of Participants)
	12 months	36 months
EVR+rTAC	5	5
MMF+sTAC	3	5

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To Evaluate Renal Function, Assessed by Glomerular Filtration Rate (eGFR) and Estimated by the Schwartz Formula (Extended), at Month 12

To evaluate renal function assessed by Glomerular Filtration Rate (eGFR) estimated by the Schwartz Formula (extended) (Schwartz, 2009). Results given as change from randomization (NCT01544491)
Timeframe: 12 months post-transplantation

Intervention	mL/min/1.73m2 (Mean)
EVR+rTAC	4.6
MMF+sTAC	-0.0

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Chronic Allograft Nephropathy / Interstitial Fibrosis and Tubular Atrophy

To evaluate the proportion of patients with chronic allograft nephropathy (interstitial fibrosis and tubular atrophy, IF/TA) by histopathology and its progression.The term chronic allograft nephropathy was used inappropriately in the protocol and therefore, replaced by interstitial fibrosis and tubular atrophy (NCT01544491)
Timeframe: at 12 and 36 months post-transplantation.

Intervention	Participants (Count of Participants)
	12 months	36 months
EVR+rTAC	3	11
MMF+sTAC	3	7

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Composite Efficacy Endpoint

To evaluate the proportion of patients with the following efficacy events: Biopsy Proven Acute Rejection (BPAR), graft loss or death. The efficacy events will be descriptively summarized by treatment group. (NCT01544491)
Timeframe: at 12 and 36 months post-transplantation

Intervention	Participants (Count of Participants)
	month 12 composite efficacy endpoint	graft loss 12 months	death 12 months	acute rejection 12 months	treated acute rejection 12 months	Biopsy proven acute rejection 12 months	treated Biopsy proven acute rejection 12 months	month 36 composite efficacy endpoint	graft loss 36 months	death 36 months	acute rejection 36 months	Biopsy proven acute rejection 36 months	treated Biopsy proven acute rejection 36 months
EVR+rTAC	5	0	0	5	5	5	5	5	1	0	5	5	5
MMF+sTAC	3	0	0	4	4	3	3	5	2	0	7	5	5

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Evaluation of Evolution of Renal Allograft Function Over Time

results given as eGFR values by time interval (NCT01544491)
Timeframe: baseline, 6 months, 12 months , 24 months, 36 months

Intervention	ml/min/1.73m2 (Mean)
	baseline	month 6	month 12	month 24	month 36
EVR+rTAC	14.2	76.6	76.9	72.9	68.2
MMF+sTAC	13.1	68.3	67.8	68.6	69.6

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Growth/Development : Weight, Height, BMI : Change From Baseline

Evaluation of the potential effects upon the bone growth. The Z-score is a statistical tool which helps to assess data (here child growth parameters) relative to a reference or standard population. The Z-score describes the distance and direction of an observation away from the population median (or mean, however, here the median was used). A negative Z-score shows that data are lower than the median of the standard population, a positive Z-score shows that data are higher than the median of the standard population, and a Z-score of zero shows that the data are equal to the median of the standard population. The more the Z-score is distant from 0, the more expressed is for example underweight or overweight. (NCT01544491)
Timeframe: month 12 , month 36 post transplantation.

Intervention	z score (Mean)
	Height month 12	Height month 36	Weight month 12	Weight month 36	BMI month 12	BMI month 36
EVR+rTAC	0.37	0.72	0.30	0.61	0.00	0.02
MMF+sTAC	0.20	0.39	0.42	0.82	0.24	0.47

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To Evaluate Renal Function, Assessed by Glomerular Filtration Rate (eGFR) and Estimated by the Schwartz Formula (Abbreviated), at Month 12 and 36

To evaluate renal function assessed by Glomerular Filtration Rate (eGFR) estimated by the Schwartz Formula (abbreviated) (Schwartz, 2009). (NCT01544491)
Timeframe: 12 months and 36 months post-transplantation

Intervention	mL/min/1.73m2 (Mean)
	12 months	36 months
EVR+rTAC	76.7	68.1
MMF+sTAC	71.7	67.3

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To Evaluate the Severity of BPAR (Acute T-cell Mediated Rejection Only) (Banff 2009)

"T-cell mediated rejection severity :~Type IA - Significant interstitial infiltration (> 25% of parenchyma) and foci of moderate tubulitis (> 4 mononuclear cells/tubular cross section or group of 10 tubular cells).~Type IB - Significant interstitial infiltration (> 25% of parenchyma) and foci of severe tubulitis (> 10 mononuclear cells/tubular cross section or group of 10 tubular cells).~Type IIA - Mild to moderate intimal arteritis Type IIB - Severe intimal arteritis comprising > 25% of the lumenal area Type III - Transmural (full vessel wall thickness) arteritis and/or arterial fibrinoid change and necrosis of medial smooth muscle cells (with accompanying lymphocytic inflammation)" (NCT01544491)
Timeframe: month 12, month 36

Intervention	Participants (Count of Participants)
	month 12 grade IA	month 12 grade IB	month 12 grade IIA	month 12 grade IIB	month 12 grade III	month 36 grade IA	month 36 grade IB	month 36 grade IIA	month 36 grade IIB	month 36 grade III
EVR+rTAC	3	1	0	0	0	3	2	0	0	0
MMF+sTAC	1	0	2	0	0	1	0	1	1	1

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To Evaluate the Time to Event of BPAR

Time to incidence of Event, given in terms of number of participants with an Event according to time interval up to 36 months (NCT01544491)
Timeframe: 36 months

Intervention	Participants (Count of Participants)
	day 1-7	day 8-14	day 15-28	day 29-56	day 57-84	day 85-150	day 151- 240	day 241-330	day 331- 510	day 511-690	day 691-870	day 871-1050	after day 1050
EVR+rTAC	0	0	1	0	0	2	0	1	0	1	0	0	0
MMF+sTAC	0	0	0	0	0	2	0	2	1	0	0	0	0

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Proteinuria (Urinary Protein/Creatinine Ratio)

The urinary protein/creatinine ratio will be descriptively summarized by treatment group at each visit. The incidence rate of patients with proteinuria will be categorized in <0.2 g/mg/mg, 0.2<2.0 mg/mg and ≥ 2.0 mg/mg and summarized by treatment groups at each visit. (NCT01544491)
Timeframe: at 12 and 36 months post-transplantation

Intervention	Participants (Count of Participants)
	Baseline < 200mg/g	Baseline 200 - < 2000 mg/g	Baseline >= 2000 mg/g	Month 12 < 200mg/g	Month 12 200 - < 2000 mg/g	Month 12 >= 2000 mg/g	Month 36 < 200mg/g	Month 36 200 - < 2000 mg/g	Month 36 >= 2000 mg/g
EVR+rTAC	1	12	14	19	13	0	23	10	1
MMF+sTAC	2	12	15	28	11	0	23	11	0

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Overall Survival From the Start (OSS) of Study Treatment

Time from first pazopanib dose until death due to any cause in patients who received at least one dose of pazopanib followed by everolimus (NCT01545817)
Timeframe: Throughout the study, up to 4 years

Intervention	Months (Median)
Pazopanib	35.7

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Overall Survival of Everolimus (OSE)

Time from first everolimus dose until death due to any cause (NCT01545817)
Timeframe: Throughout the study period, up to 4 years

Intervention	months (Median)
Everolimus	15.6

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Progression Free Survival (PFS) Rates

PFS rates 3 and 6 months after date of first dose of second-line everolimus treatment. (NCT01545817)
Timeframe: 3 months, 6 months

Intervention	Survival probability (Number)
	3 months	6 months
All Patients	0.737	0.355

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Objective Response Rate (ORR) for the Pazopanib Treatment Period Using RECIST

"Percentage of patients with Complete or Partial Response at any time following the start of first-line pazopanib treatment.~RECIST Complete Response is defined to be a disappearance of all target lesion(s). RECIST Partial Response is defined to be at least a 30% decrease in the sum of the target lesion LDs." (NCT01545817)
Timeframe: Throughout the study period, up to 4 years

Intervention	Percentages of participants (Number)
	Complete response	Partial response
All Patients	6.8	39.2

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Objective Response Rate (ORR) for the Everolimus Treatment Period Using RECIST

"Percentage of patients with Complete or Partial Response at any time following the start of second-line everolimus treatment as per RECIST.~RECIST Complete Response is defined to be a disappearance of all target lesion(s). RECIST Partial Response is defined to be at least a 30% decrease in the sum of the target lesion LDs." (NCT01545817)
Timeframe: Throughout the study, up to 4 years

Intervention	Percentages of Participants (Number)
	Complete response	Partial response
All Patients	0.0	7.9

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Progression Free Survival (PFS) for the Everolimus Treatment Period Using RECIST

"Time between the date of first everolimus dose and date of disease progression or death (whichever comes first) in patients treated initially with pazopanib.~Disease progression is measured by RECIST (Response Evaluation Criteria in Solid Tumors), which is at least a 20% increase in the sum of the target lesion longest diameters (LDs)." (NCT01545817)
Timeframe: Throughout the study period, up to 4 years

Intervention	months (Median)
Everolimus	5.1

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PFS for the Pazopanib Treatment Period Using RECIST

Time from first pazopanib dose until disease progression or death from any cause (whichever occurred earlier), provided this occurred prior to the start of everolimus and within 6 months of last dose of pazopanib (NCT01545817)
Timeframe: Throughout the study period, up to 4 years

Intervention	Months (Number)
Pazopanib	11.0

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Incidence of HCV Related Fibrosis

Incidence of hepatitis C virus (HCV) related fibrosis assessed as treatment emergent adverse events of special interest (NCT01551212)
Timeframe: 12 months

Intervention	Participants (Count of Participants)
Everolimus/Tacrolimus	1
Tacrolimus	0

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Estimated GFR - PP Set

This was a sensitivity analysis for the primary outcome measure based on the per-protocol set of patients. (NCT01551212)
Timeframe: month 12

Intervention	mL/min (Mean)
Everolimus/Tacrolimus	74.83
Tacrolimus	70.65

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Estimated Glomerular Filtration Rate (GFR)

The estmated GFR was calculated using MDRD-4 formula (Modification of Diet in Renal Disease Study Group). (NCT01551212)
Timeframe: month 12

Intervention	mL/min (Mean)
Everolimus/Tacrolimus	73.46
Tacrolimus	71.95

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Incidence of de Novo HCC Malignancies

Incidence of de novo Hepatocellular Carcinoma (HCC) malignancies assessed as treatment emergent adverse events of special interest (NCT01551212)
Timeframe: 12 months

Intervention	Participants (Count of Participants)
Everolimus/Tacrolimus	0
Tacrolimus	2

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Number of Participants With HCV

Number of Participants with HCV (hepatitis C virus) assessed as treatment emergent adverse events of special interest (NCT01551212)
Timeframe: 12 months

Intervention	Participants (Count of Participants)
Everolimus/Tacrolimus	6
Tacrolimus	12

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Percentage of Participants With Treated Biopsy Proven Acute Rejection (BPAR), Graft Loss or Death

Percentage of Participants with Treated Biopsy Proven Acute Rejection (BPAR), Graft Loss or Death at Month 12 (NCT01551212)
Timeframe: 12 months

Intervention	Percent of Patients (Number)
Everolimus/Tacrolimus	9.5
Tacrolimus	7.9

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Biochemical Response Rate (BRR) for 5HIAA Levels

The percentages are the biochemical response rates i.e. percentage of patients showing normalization i.e. return to within normal ranges, or a decrease of >= 50% from baseline of 5HIAA concentrations. (NCT01563354)
Timeframe: Baseline up Week 52

Intervention	percentage of participants (Number)
	Week 12	Week 24	Week 36	Week 48	Week 52
Everolimus	11.1	11.1	11.1	0	0
Pasireotide LAR	20.0	5.0	5.0	5.0	5.0
Pasireotide LAR and Everolimus Combination	10.0	20.0	5.0	5.0	10.0

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Duration of Biochemical Response (DBR), by Treatment (Full Analysis Set)

Time from the first documentation of biochemical response to the first documentation of biochemical progression or to death due to any cause, whichever occurred first. Biochemical progression is defined as an increase of serum CgA levels ≥ 25% compared to baseline. (NCT01563354)
Timeframe: Baseline up to Month 18

Intervention	months (Median)
Pasireotide LAR	14.75
Everolimus	2.00
Pasireotide LAR and Everolimus Combination	8.38

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Summary of Duration of Response (Months)

Date of first objective tumor response to date of tumor progression or death due to any cause. (NCT01563354)
Timeframe: Every 3 months up to Year 1

Intervention	months (Number)
	25th percentile	Median	75th percentile
Everolimus	NA	NA	NA
Pasireotide LAR	NA	NA	NA
Pasireotide LAR and Everolimus Combination	NA	NA	NA

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Percentage of Participants Progression-free at 9 Months Based on Response Evaluation Criteria In Solid Tumors v1.1 (RECIST v1.1)

"Patients with Complete Response (CR), Partial Response (PR), or Stable Disease (SD) at Month 9 were to be considered as progression-free based on RECIST v1.1. Patients with missing tumor assessment, or with overall lesion response unknown at Month 9 were considered as non progression-free, unless any of the following assessments at Week 48 or Week 52 indicate CR, PR, or SD, in which case the patient was to be considered as progression-free at Month 9. Patients discontinuing the study for any reason prior to the 9 month assessment were to be considered as non progression-free." (NCT01563354)
Timeframe: Baseline up to 9 months

Intervention	percentage of participants (Number)
	Complete response	Partial response	Stable disease	Progression-free (PF) at Month 9
Everolimus	0	2.4	31.0	33.3
Pasireotide LAR	0	2.4	34.1	39.0
Pasireotide LAR and Everolimus Combination	0	2.4	48.8	58.5

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12-month Disease Control Rate (DCR) and Objective Response Rate (ORR)

Objective response rate (ORR) was defined as the percentage of patients showing a best overall response (BOR) of CR or PR during the core study according to RECIST v1.1 criteria. The best overall response is interpreted as the best response recorded from the start of the treatment until disease progression/recurrence, death from any cause or until the patient withdraws consent, whichever is earliest. DCR was was defined as the percentage of participants with a best overall response of complete response, partial response or stable disease during 12 months of treatment according to RECIST v1.1. (NCT01563354)
Timeframe: Baseline up to Month 12

Intervention	percentage of participants (Number)
	Objective response (CR+PR)	Disease control rate (CR+PR+SD)	Complete response (CR)	Partial response (PR)	Stable disease	Progressive disease	Unknown	Not assessed	Discontinued before month 12
Everolimus	2.4	73.8	0	2.4	71.4	4.8	4.8	16.7	64.3
Pasireotide LAR	2.4	80.5	0	2.4	78.0	14.6	2.4	2.4	68.3
Pasireotide LAR and Everolimus Combination	4.9	78.0	0	4.9	73.2	7.3	0	14.6	63.4

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Summary of Progression-free Survival (PFS) Based on RECIST v1.1

Time from first study drug administration to objective tumor progression or death from any cause according to RECIST v1.1 (NCT01563354)
Timeframe: Baseline, every 3 months up to 69 months

Intervention	months (Median)
Pasireotide LAR	8.51
Everolimus	12.48
Pasireotide LAR and Everolimus Combination	16.53

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Biochemical Response Rate (BRR) for Chromogranin A (CgA) Levels

Percentage of patients showing normalization or a decrease of ≥ 30% of serum CgA concentrations compared to baseline. (NCT01563354)
Timeframe: Baseline up to Week 52

Intervention	percentage of participants (Number)
	Week 12	Week 24	Week 36	Week 48	Week 52
Everolimus	7.4	7.4	3.7	0	0
Pasireotide LAR	20.6	8.8	8.8	8.8	5.9
Pasireotide LAR and Everolimus Combination	17.1	20.0	11.4	11.4	5.7

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Kaplan-Meier Estimates of Progression-free Survival (PFS)

Percent (%) event-free probability estimate is the estimated probability that a patient will remain event-free up to the specified time point. Percent event-free probability estimates are obtained from the Kaplan-Meier survival estimates. Events are time from first study drug administration to objective tumor progression or death from any cause according to RECIST v1.1. (NCT01563354)
Timeframe: Baseline, every 3 months up to 69 months

Intervention	event free probability estimates (Number)
	3 months	6 months	9 months	12 months	15 months	18 months	21 months	24 months	27 months	30 months	33 months	36 months	39 months	42 months	45 months	48 months	51 months	54 months	57 months	60 months	63 months	66 months	69 months
Everolimus	91.2	63.5	56.9	50.2	46.8	38.6	29.4	19.6	19.6	9.8	9.8	9.8	9.8	9.8	9.8	9.8	NA	NA	NA	NA	NA	NA	NA
Pasireotide LAR	83.6	68.2	49.6	39.9	32.6	21.8	14.5	14.5	14.5	10.9	10.9	10.9	10.9	10.9	10.9	10.9	10.9	10.9	10.9	10.9	10.9	NA	NA
Pasireotide LAR and Everolimus Combination	88.6	85.5	79.2	55.5	51.2	42.7	38.0	28.5	28.5	19.0	19.0	14.2	14.2	14.2	14.2	14.2	14.2	14.2	7.1	7.1	7.1	7.1	7.1

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Summary of Time to Response (Months)

Time from start of treatment to the first observed objective tumor response (partial response or complete response) observed according to RECIST v1.1. (NCT01563354)
Timeframe: Every 3 months up to Year 1

Intervention	months (Number)
	25th percentile	Median	75th percentile
Everolimus	NA	NA	NA
Pasireotide LAR	NA	NA	NA
Pasireotide LAR and Everolimus Combination	NA	NA	NA

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Kaplan-Meier Event-free Probability Estimate for Biochemical Progression-free Survival Based on CgA Levels

Percent (%) Event-free probability estimate is the estimated probability that a patient will remain event-free up to the specified time point. Percent event-free probability estimates are obtained from the Kaplan-Meier survival estimates. Events are biochemical progressions, i.e., an increase of CgA levels >= 25% compared to baseline or deaths due to any cause. (NCT01563354)
Timeframe: Baseline, every 3 months up to Month 24

Intervention	event free probability estimates (Number)
	3 months	6 months	9 months	12 months	15 months	18 months	21 months	24 months
Everolimus	35.4	17.7	11.0	7.4	NA	NA	NA	NA
Pasireotide LAR	43.1	29.5	18.5	18.5	18.5	13.8	13.8	NA
Pasireotide LAR and Everolimus Combination	77.1	44.5	29.7	26.4	18.1	18.1	18.1	18.1

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Kaplan-Meier Event-free Probability Estimate Based on CgA Levels

Kaplan Meier estimates are for Duration of biochemical response (DBR) outcome measure. Events are biochemical progressions i.e. an increase of CgA levels >= 25% compared to baseline or deaths due to any cause. Percent (%) Event-free probability estimate is the estimated probability that a patient will remain event-free up to the specified time point. (NCT01563354)
Timeframe: Baseline, every 3 months up to Month 18

Intervention	event free probability estimates (Number)
	3 months	6 months	9 months	12 months	15 months	18 months
Everolimus	37.5	NA	NA	NA	NA	NA
Pasireotide LAR	75.0	56.3	56.3	56.3	37.5	37.5
Pasireotide LAR and Everolimus Combination	77.8	77.8	44.4	44.4	44.4	44.4

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Summary of Biochemical Progression-free Survival Based on CgA Levels by Treatment

Intervention	months (Median)
Pasireotide LAR	2.89
Everolimus	2.86
Pasireotide LAR and Everolimus Combination	5.62

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Number of Participants With an Adverse Event.

Number of participants with an adverse event. Please refer to the adverse event reporting for more detail. (NCT01582009)
Timeframe: The time from registration up to 3 years

Intervention	Participants (Count of Participants)
Arm I: Oral Panobinostat and Oral Everolimus	26

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Number of Participants With Clinical Response

Number of participants with clinical response. Response will be evaluated in this study using the new international criteria proposed by the Response Evaluation Criteria in Solid Tumors ver 1.0 Committee [JNCI 92(3):205-216, 2000]. Changes in only the largest diameter (unidimensional measurement) of the tumor lesions are used in the RECIST ver. 1.0 criteria. (NCT01582009)
Timeframe: The time from registration up to 3 years

Intervention	Participants (Count of Participants)
Arm I: Oral Panobinostat and Oral Everolimus	0

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Progression-free Survival (PFS)

6 month PFS survival rate. Calculated as the total number of failures (deaths or progression) divided by the total follow-up or exposure time of patients on study. Assessed using Kaplan Meier and Proportional Hazards. (NCT01582009)
Timeframe: The time from registration to documentation of disease progression up to 3 years

Intervention	percentage of participants (Number)
Arm I: Oral Panobinostat and Oral Everolimus	28

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Median Progression Free Survival

Median progression free survival. Assessed using Kaplan Meier and Proportional Hazards. (NCT01582009)
Timeframe: The time from registration up to 3 years

Intervention	months (Median)
Arm I: Oral Panobinostat and Oral Everolimus	5.3

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6-month Overall Survival Rate

6-month overall survival rate (NCT01582009)
Timeframe: The time from registration up to 3 years

Intervention	percentage of participants (Number)
Arm I: Oral Panobinostat and Oral Everolimus	96

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Mean EORTC QLQ-G.I. NET21 Score (Core)

The EORTC QLQ-G.I. NET21 contains 21 questions and has three defined multi-item symptom scales (endocrine - 3 questions, gastrointestinal - 5 questions, and treatment related side effects - 3 questions), two single item symptoms (bone/muscle pain and concern about weight loss), two psychosocial scales (social function - 3 questions and disease-related worries - 3 questions) and two other single items (sexuality and communication). For each of the 9 domains, final scores are transformed such that they range from 0-100, where higher scores indicate worsening. (NCT01595009)
Timeframe: Baseline, weeks 4, 8, 20, 32, 44, and end of treatment (EOT) up to week 82

Intervention	units on a scale (Mean)
	Endocrine, Baseline	Endocrine, week 4	Endocrine, week 8	Endocrine, week 20	Endocrine, week 32	Endocrine, week 44	Endocrine, EOT up to week 82	G.I., Baseline	G.I., week 4	G.I., week 8	G.I., week 20	G.I., week 32	G.I., week 44	G.I., EOT up to week 82	Treatment, baseline	Treatment, week 4	Treatment, week 8	Treatment, week 20	Treatment, week 32	Treatment, week 44	Treatment, EOT up to week 82	Social function, Baseline	Social function, week 4	Social function, week 8	Social function, week 20	Social function, week 32	Social function, week 44	Social function, EOT up to week 82	Disease-related worries, Baseline	Disease-related worries, week 4	Disease-related worries, week 8	Disease-related worries, week 20	Disease-related worries, week 32	Disease-related worries, week 44	Disease-related worries, EOT up to week 82	Muscle/bone pain, Baseline	Muscle/bone pain, week 4	Muscle/bone pain, week 8	Muscle/bone pain, week 20	Muscle/bone pain, week 32	Muscle/bone pain, week 44	Muscle/bone pain, EOT up to week 82	Sexual function, Baseline	Sexual function, week 4	Sexual function, week 8	Sexual function, week 20	Sexual function, week 32	Sexual function, EOT up to week 82	Communication function, Baseline	Communication function, week 4	Communication function, week 8	Communication function, week 20	Communication function, week 32	Communication function, week 44	Communication function, EOT up to week 82	Body image, Baseline	Body image, week 4	Body image, week 8	Body image, week 20	Body image, week 32	Body image, week 44	Body image, EOT up to week 82
pNET (Core)	12.99	13.21	13.47	12.50	16.67	0.00	9.49	23.69	23.02	22.34	25.63	25.00	0.00	25.85	9.26	17.72	16.18	28.70	27.78	16.67	22.06	39.56	36.52	38.35	40.28	38.89	33.33	38.89	43.10	39.20	40.56	37.50	38.89	33.33	42.89	26.67	24.07	31.18	41.67	50.00	33.33	34.13	35.46	21.05	28.79	33.33	11.11	25.81	7.58	8.18	12.22	14.29	8.33	0.00	12.70	15.90	15.09	21.51	16.67	0.00	0.00	23.02

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Change in EORTC QLQ-G.I. NET21 Score at the End of Treatment From Baseline (Baseline = First Day of Treatment in the Extension) (E1)

The EORTC QLQ-G.I. NET21 contains 21 questions and has three defined multi-item symptom scales (endocrine - 3 questions, gastrointestinal - 5 questions, and treatment related side effects - 3 questions), two single item symptoms (bone/muscle pain and concern about weight loss), two psychosocial scales (social function - 3 questions, disease-related worries - 3 questions) and two other single items (sexuality and communication). For each of the 9 domains, final scores are transformed such that they range from 0-100, where higher scores indicate worsening outcomes. A positive change from baseline indicates worsening. (NCT01595009)
Timeframe: baseline, every 12 weeks and up to 4 years

Intervention	units on a scale (Mean)
	Social function	Disease-related worries	Sexual function	Communicative functioning	Endocrine scale	G.I. scale	Treatment scale	Muscle/bone pain symptom	Body image
GI NET	7.41	-0.93	50.00	11.11	5.56	14.44	5.56	33.33	0.00

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Number and Percentage of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs) and Deaths During the Extension Phase (E1)

The number of participants with AEs, SAEs and deaths were assessed. (NCT01595009)
Timeframe: from the first day of treatment in the extension up to 4 years

Intervention	Participants (Count of Participants)
	AEs	SAEs	Deaths
GI NET	11	4	1
Lung NET (E1)	4	1	0

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Investigator-assessed Best Overall Response During the Extension Phase (E1)

Best overall response was determined from the sequence of investigator overall lesions responses according to Response Evaluation Criteria in Solid Tumors (RECIST). Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR; Progression, 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. (NCT01595009)
Timeframe: from the start of treatment, every 12 weeks for the first year and then every 6 months up to 4 years

Intervention	Participants (Count of Participants)
	Complete response	Partial response	Stable disease	Progressive disease	Unknown
GI NET	0	1	7	3	0
Lung NET (E1)	0	0	2	2	0

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Number and Percentage of Participants With Ratings of 'no Problem, 'Some Problem' and 'Extreme Problem' in the EuroQol Five Dimensions Questionnaire (EQ-5D) (Core)

"The EQ-5D is divided into two distinct sections. The first section includes one item addressing each of five dimensions (mobility, self-care, usual activity, pain/discomfort, and anxiety/depression). Patients rate each of these items from no problem, some problem, or extreme problem. A composite health index is then defined by combining the levels for each dimension. The second section of the questionnaire measures self-rated (global) health status utilizing a vertically oriented visual analogue scale where 100 represents the best possible health state and 0 represents the worst possible health state. Respondents are asked to rate their current health by placing a mark along this continuum. The scores from each section are then transformed into a single health utility score. Overall scores range from 0 to 1 with lower scores representing a higher level of dysfunction." (NCT01595009)
Timeframe: Baseline, weeks 4, 8, 20, 32, 44, and end of treatment (EOT) up to week 82

Intervention	Participants (Count of Participants)
	Baseline, Mobility, No problem	Baseline, Mobility, Some problem	Baseline, Mobility, Extreme problem	Baseline, Self-care, No problem	Baseline, Self-care, Some problem	Baseline, Usual activities, No problem	Baseline, Usual activities, Some problem	Baseline, Usual actvities, Extreme problem	Baseline, Pain/Discomfort, No problem	Baseline, Pain/discomfort, Some problem	Baseline, Pain/discomfort, Extreme problem	Baseline, Anxiety/depression, No problem	Baseline, Anxiety/depression, Some problem	Baseline, Anxiety/depression, Extreme problem	Week 4, Mobility, No problem	Week 4, Mobility, Some problem	Week 4, Mobility, Extreme problem	Week 4, Self-care, No problem	Week 4, Self-care, Some problem	Week 4, Self-care, Extreme problem	Week 4, Usual activities, No problem	Week 4, Usual activities, Some problem	Week 4, Usual activities, Extreme problem	Week 4, Pain/discomfort, No problem	Week 4, Pain/discomfort, Some problem	Week 4, Pain/discomfort, Extreme problem	Week 4, Anxiety/depression, No problem	Week 4, Anxiety depression, Some problem	Week 4, Anxiety/depression, Extreme problem	Week 8, Mobility, No problem	Week 8, Mobility, Some problem	Week 8, Mobility, Extreme problem	Week 8, Self-care, No problem	Week 8, Self-care, Some problem	Week 8, Self-care, Extreme problem	Week 8, Usual activities, No problem	Week 8, Usual activities, Some problem	Week 8, Usual activties, Extreme problem	Week 8, Pain/discomfort, No problem	Week 8, Pain/discomfort, Some problem	Week 8, Pain/discomfort, Extreme problem	Week 8, Anxiety/depression, No problem	Week 8, Anxiety/depression, Some problem	Week 8, Anxiety/depression, Extreme problem	Week 20, Mobility, No problem	Week 20, Mobility, Some problem	Week 20, Mobility, Extreme problem	Week 20, Self-care, No problem	Week 20, Self-care, Some problem	Week 20, Usual activities, No problem	Week 20 Usual activities, Some problem	Week 20, Usual activities, Extreme problem	Week 20, Pain/discomfort, No problem	Week 20, Pain/discomfort, Some problem	Week 20, Pain/discomfort, Extreme problem	Week 20, Anxiety/depression, No problem	Week 20, Anxiety/depression, Some problem	Week 20, Anxiety/depression, Extreme problem	Week 32, Mobility, No problem	Week 32, Mobility, Some problem	Week 32, Mobility, Extreme problem	Week 32, Self-care, No problem	Week 32, Self-care, Some problem	Week 32, Self-care, Extreme problem	Week 32, Usual activities, No problem	Week 32, Usual activities, Some problem	Week 32, Usual activities, Extreme problem	Week 32, Pain/discomfort, No problem	Week 32, Pain/discomfort, Some problem	Week 32, Pain/discomfort, Extreme problem	Week 32, Anxiety/depression, No problem	Week 32, Anxiety/depression, Some problem	Week 32, Anxiety/depression, Extreme problem	Week 44, Mobility, No problem	Week 44, Mobility, Some problem	Week 44, Mobility, Extreme problem	Week 44, Self-care, No problem	Week 44, Self-care, Some problem	Week 44, Usual activities, No problem	Week 44, usual activities, Some problem	Week 44, Pain/discomfort, No problem	Week 44, Pain/discomfort, Some problem	Week 44, Anxiry/depression, No problem	Week 44, Anxiety/depression, Some problem	Week 44, Anxiety/depression, Extreme problem	EOT up to Week 82, Mobility, No problem	EOT up to Week 82, Mobility, Some problem	EOT up to Week 82, Mobility, Extreme problem	EOT up to Week 82, Self-care, No problem	EOT up to Week 82, Self-care, Some problem	EOT up to Week 82, Self-care, Extreme problem	EOT up toWeek 82, Usual activities, No problem	EOT up to Week 82, Usual activities, Some problem	EOT up to Week 82, Usual activities, Extreme prob.	EOT up to Week 82, Pain/discomfort, No problem	EOT up to Week 82, Pain/discomfort, Some problem	EOT up to Week 82, Pain/discomfort, Extreme prob.	EOT up to Week 82, Anxiety/depression, No problem	EOT up to Week 82, Anxiety/depression, Some prob.	EOT up toWeek 82, Anxiety/depression, Extreme prob
Non-pNET (Core)	76	35	1	102	10	60	46	6	40	66	7	53	54	6	66	37	1	86	16	2	55	42	7	30	64	8	57	43	3	45	37	3	70	15	1	40	41	5	25	52	10	38	41	8	37	17	1	49	6	30	22	2	19	34	2	27	23	5	25	12	2	32	3	2	22	14	3	10	27	2	20	14	5	9	4	1	12	2	6	7	6	8	7	6	1	42	31	4	56	19	1	29	36	11	18	48	11	31	40	6

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Number and Percentage of Participants With Ratings of 'no Problem, 'Some Problem' and 'Extreme Problem' in the EuroQol Five Dimensions Questionnaire (EQ-5D) (Core)

Intervention	Participants (Count of Participants)
	Baseline, Mobility, No problem	Baseline, Mobility, Some problem	Baseline, Mobility, Extreme problem	Baseline, Self-care, No problem	Baseline, Self-care, Some problem	Baseline, Self-care, Extreme problem	Baseline, Usual activities, No problem	Baseline, Usual activities, Some problem	Baseline, Usual actvities, Extreme problem	Baseline, Pain/Discomfort, No problem	Baseline, Pain/discomfort, Some problem	Baseline, Pain/discomfort, Extreme problem	Baseline, Anxiety/depression, No problem	Baseline, Anxiety/depression, Some problem	Baseline, Anxiety/depression, Extreme problem	Week 4, Mobility, No problem	Week 4, Mobility, Some problem	Week 4, Mobility, Extreme problem	Week 4, Self-care, No problem	Week 4, Self-care, Some problem	Week 4, Self-care, Extreme problem	Week 4, Usual activities, No problem	Week 4, Usual activities, Some problem	Week 4, Usual activities, Extreme problem	Week 4, Pain/discomfort, No problem	Week 4, Pain/discomfort, Some problem	Week 4, Pain/discomfort, Extreme problem	Week 4, Anxiety/depression, No problem	Week 4, Anxiety depression, Some problem	Week 4, Anxiety/depression, Extreme problem	Week 8, Mobility, No problem	Week 8, Mobility, Some problem	Week 8, Mobility, Extreme problem	Week 8, Self-care, No problem	Week 8, Self-care, Some problem	Week 8, Self-care, Extreme problem	Week 8, Usual activities, No problem	Week 8, Usual activities, Some problem	Week 8, Usual activties, Extreme problem	Week 8, Pain/discomfort, No problem	Week 8, Pain/discomfort, Some problem	Week 8, Pain/discomfort, Extreme problem	Week 8, Anxiety/depression, No problem	Week 8, Anxiety/depression, Some problem	Week 8, Anxiety/depression, Extreme problem	Week 20, Mobility, No problem	Week 20, Mobility, Some problem	Week 20, Self-care, No problem	Week 20, Self-care, Some problem	Week 20, Usual activities, No problem	Week 20 Usual activities, Some problem	Week 20, Usual activities, Extreme problem	Week 20, Pain/discomfort, No problem	Week 20, Pain/discomfort, Some problem	Week 20, Pain/discomfort, Extreme problem	Week 20, Anxiety/depression, No problem	Week 20, Anxiety/depression, Some problem	Week 20, Anxiety/depression, Extreme problem	Week 32, Mobility, No problem	Week 32, Mobility, Some problem	Week 32, Self-care, No problem	Week 32, Usual activities, No problem	Week 32, Usual activities, Some problem	Week 32, Pain/discomfort, No problem	Week 32, Pain/discomfort, Some problem	Week 32, Anxiety/depression, No problem	Week 32, Anxiety/depression, Some problem	Week 44, Mobility, No problem	Week 44, Mobility, Some problem	Week 44, Self-care, No problem	Week 44, usual activities, Some problem	Week 44, Pain/discomfort, Some problem	Week 44, Anxiry/depression, No problem	Week 44, Anxiety/depression, Some problem	EOT up to Week 82, Mobility, No problem	EOT up to Week 82, Mobility, Some problem	EOT up to Week 82, Mobility, Extreme problem	EOT up to Week 82, Self-care, No problem	EOT up to Week 82, Self-care, Some problem	EOT up to Week 82, Self-care, Extreme problem	EOT up toWeek 82, Usual activities, No problem	EOT up to Week 82, Usual activities, Some problem	EOT up to Week 82, Usual activities, Extreme prob.	EOT up to Week 82, Pain/discomfort, No problem	EOT up to Week 82, Pain/discomfort, Some problem	EOT up to Week 82, Pain/discomfort, Extreme prob.	EOT up to Week 82, Anxiety/depression, No problem	EOT up to Week 82, Anxiety/depression, Some prob.	EOT up toWeek 82, Anxiety/depression, Extreme prob
pNET (Core)	84	31	2	100	15	2	71	43	4	59	52	6	65	47	5	72	27	2	89	10	3	66	31	4	39	58	3	54	46	1	48	24	2	61	7	6	46	23	4	34	32	7	43	30	1	26	3	25	4	18	10	1	12	16	1	16	12	1	3	2	5	4	1	1	4	4	1	2	1	3	3	3	1	2	59	23	4	69	12	2	54	24	5	43	36	5	48	33	3

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Change in EORTC QLQ-G.I. NET21 Score at the End of Treatment From Baseline (Baseline = First Day of Treatment in the Extension) (E1)

The EORTC QLQ-G.I. NET21 contains 21 questions and has three defined multi-item symptom scales (endocrine - 3 questions, gastrointestinal - 5 questions, and treatment related side effects - 3 questions), two single item symptoms (bone/muscle pain and concern about weight loss), two psychosocial scales (social function - 3 questions, disease-related worries - 3 questions) and two other single items (sexuality and communication). For each of the 9 domains, final scores are transformed such that they range from 0-100, where higher scores indicate worsening outcomes. A positive change from baseline indicates worsening. (NCT01595009)
Timeframe: baseline, every 12 weeks and up to 4 years

Intervention	units on a scale (Mean)
	Social function	Disease-related worries	Communicative functioning	Endocrine scale	G.I. scale	Treatment scale	Body image
Lung NET (E1)	11.11	44.44	0.00	11.11	0.00	-16.67	0.00

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Investigator-assessed Progression Free Survival (PFS) (E1)

PFS was defined as the time from the date of the start of therapy in the extension study to the date of the first radiologically documented disease progression or death due to any cause. If a participant had not progressed or died at the analysis cut-off date or when he/she received any further anti-neoplastic therapy, PFS was censored at the time of the last adequate tumor evaluation before the cut-off date or the anti-neoplastic therapy start date. (NCT01595009)
Timeframe: from first date of treatment in the extension up to 4 years

Intervention	Days (Median)
Lung NET (E1)	159
GI NET (E1)	655

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Investigator-assessed Progression Free Survival (PFS) (Core)

PFS was defined as the time from the date of the first dose to the date of the first radiologically documented disease progression or death due to any cause. If a participant had not progressed or died at the study end date or when he/she received any further anti-neoplastic therapy, PFS was censored at the time of the last tumor assessment before the end of study date. Progression was 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. (NCT01595009)
Timeframe: from the day of first treatment up to 19 months

Intervention	Months (Median)
pNET (Core)	7.62
Non-pNET (Core)	10.78

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Change in European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30 (EORTC QLQ-C30) Score at the End of Treatment From Baseline (Baseline = First Day of Treatment in the Extension) (E1)

"The EORTC QLQ-C30 contains 30 questions assessed by the participant. There are 9 multiple-item scales: 5 scales that assess aspects of functioning (physical, role, cognitive, emotional, and social); 3 symptom scales (Fatigue, Pain, and Nausea and Vomiting); and a global health status and QOL scale. There are 5 single-item measures assessing additional symptoms (i.e., dyspnea, loss of appetite, insomnia, constipation, and diarrhea) and a single item concerning perceived financial impact of the disease. All but two questions have 4-point scales ranging from Not at all to Very much. The two questions concerning global health status and QOL have 7 point scales with ratings ranging from Very poor to Excellent. For each of the 14 domains, changes are calculated as value at later time point minus value at baseline, and final scores are transformed such that they range from 0-100, where higher scores indicate better outcomes. A positive change from baseline indicates improvement." (NCT01595009)
Timeframe: baseline, every 12 weeks and up to 4 years

Intervention	score on a scale (Mean)
	Global health status/QoL	Functional scale: Physical functioning	Functional scale: Role functioning	Functional scale: Emotional functioning	Functional scale: Cognitive functioning	Functional scale: Social functioning	Symptom scale: Fatigue	Symptom scale: Nausea and vomiting	Symptom scale: Pain	Symptom scale: Dyspnea	Symptom scale: Insomnia	Symptom scale: Appetite loss	Symptom scale: Constipation	Symptom scale: Diarrhea	Symptom scale: Financial difficulties
GI NET	-0.00	0.00	5.56	-1.85	-16.67	-8.33	-3.70	0.00	16.67	-5.56	11.11	0.00	5.56	-16.67	16.67
Lung NET (E1)	0.00	6.67	-16.67	-25.00	-66.67	0.00	0.00	0.00	0.00	0.00	33.33	0.00	0.00	0.00	-33.33

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Mean European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30 (EORTC QLQ-C30) Score (Core)

"The EORTC QLQ-C30 contains 30 questions assessed by the participant. There are 9 multiple-item scales: 5 scales that assess aspects of functioning (physical, role functioning, cognitive, emotional, and social); 3 symptom scales (Fatigue, Pain, and Nausea and Vomiting); and a global health status/Quality of Life (QOL) scale. There are 5 single-item measures assessing additional symptoms (i.e., dyspnea, loss of appetite, insomnia, constipation, and diarrhea) and a single item concerning perceived financial impact of the disease. All but two questions have 4-point scales ranging from Not at all to Very much. The two questions concerning global health status/ QOL have 7 point scales with ratings ranging from Very poor to Excellent. For each of the 14 domains, final scores are transformed such that they range from 0-100, where higher scores indicate improvement." (NCT01595009)
Timeframe: Baseline, weeks 4, 8, 20, 32, 44, and end of treatment (EOT) up to week 82

Intervention	units on a scale (Mean)
	Global health status/QOL, Baseline	Global health status/QOL, Week 4	Global health status/QOL, Week 8	Global health status/QOL,Week 20	Global health status/QOL, Week 32	Global health status/QOL, Week 44	Global health status/QOL, EOT up to Week 82	Physical functioning, Baseline	Physical functioning, week 4	Physical functioning, week 8	Physical functioning, week 20	Physical functioning, week 32	Physical functioning, week 44	Physical functioning, EOT up to week 82	Role functioning, Baseline	Role functioning, week 4	Role functioning, week 8	Role functioning, week 20	Role functioning, week 32	Role functioning, week 44	Role functioning, EOT up to week 82	Emotional functioning, Baseline	Emotional functioning, week 4	Emotional functioning, week 8	Emotional functioning, week 20	Emotional functioning, week 32	Emotional functioning, week 44	Emotional functioning, EOT up to week 82	Cognitive functioning, Baseline	Cognitive functioning, week 4	Cognitive functioning, week 8	Cognitive functioning, week 20	Cognitive functioning, week 32	Cognitive functioning, week 44	Cognitive functioning, EOT up to week 82	Social functioning, Baseline	Social functioning, week 4	Social functioning, week 8	Social functioning, week 20	Social functioning, week 32	Social functioning, week 44	Social functioning, EOT up to week 82	Fatigue, baseline	Fatigue, week 4	Fatigue, week 8	Fatigue, week 20	Fatigue, week 32	Fatigue, week 44	Fatigue, EOT up to week 82	Nausea and vomiting, Baseline	Nausea and vomiting, week 4	Nausea and vomiting, week 8	Nausea and vomiting, week 20	Nausea and vomiting, week 32	Nausea and vomiting, week 44	Nausea and vomiting, EOT up to week 82	Pain, Baseline	Pain, week 4	Pain, week 8	Pain, week 20	Pain, week 32	Pain, week 44	Pain, EOT up to week 82	Dyspnea, Baseline	Dyspnea, week 4	Dyspnea, week 8	Dyspnea, week 20	Dyspnea, week 32	Dyspnea, week 44	Dyspnea, EOT up to week 82	Insomnia, Baseline	Insomnia, week 4	Insomnia, week 8	Insomnia, week 24	Insomnia, week 32	Insomnia, week 48	Insomnia, EOT up o week 82	Appetite loss, Baseline	Appetitie loss, week 4	Appetitie loss, week 8	Appetitie loss, week 24	Appetitie loss, week 36	Appetitie loss, week 44	Appetitie loss, EOT up to week 82	Constipation, Baseline	Constipation, week 4	Constipation, week 8	Constipation, week 20	Constipation, week 32	Constipation, week 44	Constipation, EOT up to week 82	Diarrhea, Baseline	Diarrhea, week 4	Diarrhea, week 8	Diarrhea, week 20	Diarrhea, week 32	Diarrhea, week 44	Diarrhea, EOT up to week 82	Financial difficulties, Baseline	Financial difficulties, week 4	Financial difficulties, week 8	Financial difficulties, week 20	Financial difficulties, week 32	Financial difficulties, week 44	Financial difficulties, EOT up to week 82
Non-pNET (Core)	60.53	58.91	56.59	59.65	56.20	57.74	48.86	72.97	68.62	67.48	73.71	71.62	76.19	60.94	67.27	62.25	58.14	58.33	55.26	66.67	49.13	67.20	66.69	64.02	63.16	61.11	65.67	57.63	80.61	78.80	76.33	78.65	75.21	84.52	73.46	67.42	67.80	65.31	66.07	66.24	72.62	52.89	42.39	43.58	48.86	44.44	48.72	38.89	56.49	9.46	7.43	10.34	6.14	5.98	4.76	15.80	31.21	30.88	37.55	33.33	34.62	26.19	43.90	24.32	26.14	29.12	28.07	35.90	21.43	33.77	28.18	32.36	29.02	35.09	33.33	28.57	34.63	18.62	21.90	25.67	20.47	23.93	26.19	33.77	13.21	11.33	7.58	8.77	4.27	2.38	10.39	36.67	38.19	42.42	31.58	40.17	40.48	39.04	16.52	16.67	16.86	19.88	21.37	19.05	27.63
pNET (Core)	64.93	63.15	59.72	63.10	50.0	61.11	61.40	79.89	77.02	76.22	79.77	68.00	68.89	75.70	75.28	72.49	71.83	79.76	66.67	61.11	67.84	74.79	76.31	73.38	76.19	81.67	75.00	74.61	84.17	86.11	81.94	83.93	86.67	94.44	81.35	75.56	78.71	75.69	73.21	60.00	66.67	75.10	31.30	35.22	36.91	34.29	42.22	37.04	38.83	11.25	10.52	9.59	8.05	6.67	11.11	9.69	21.57	25.91	25.23	27.98	43.33	38.89	27.33	16.11	17.80	21.00	11.49	13.33	22.22	25.19	24.72	27.78	32.88	24.14	26.67	22.22	32.17	20.56	25.16	24.66	18.39	20.00	11.11	24.14	13.06	11.00	10.50	6.90	0.00	0.00	12.79	19.89	20.92	27.40	16.67	13.33	22.22	25.97	18.77	16.67	19.44	21.43	40.00	22.22	21.71

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Mean EQ-5D Visual Analogue Scale (VAS) Score (Core)

Intervention	units on a scale (Mean)
	Baseline	Week 4	Week 8	Week 20	Week 32	Week 44	EOT up to Week 82
Non-pNET (Core)	63.9	63.8	61.2	64.6	62.0	68.6	55.3
pNET (Core)	68.8	69.3	64.6	67.4	42.6	66.7	66.5

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Mean EORTC QLQ-G.I. NET21 Score (Core)

Intervention	units on a scale (Mean)
	Endocrine, Baseline	Endocrine, week 4	Endocrine, week 8	Endocrine, week 20	Endocrine, week 32	Endocrine, week 44	Endocrine, EOT up to week 82	G.I., Baseline	G.I., week 4	G.I., week 8	G.I., week 20	G.I., week 32	G.I., week 44	G.I., EOT up to week 82	Treatment, baseline	Treatment, week 4	Treatment, week 8	Treatment, week 20	Treatment, week 32	Treatment, week 44	Treatment, EOT up to week 82	Social function, Baseline	Social function, week 4	Social function, week 8	Social function, week 20	Social function, week 32	Social function, week 44	Social function, EOT up to week 82	Disease-related worries, Baseline	Disease-related worries, week 4	Disease-related worries, week 8	Disease-related worries, week 20	Disease-related worries, week 32	Disease-related worries, week 44	Disease-related worries, EOT up to week 82	Muscle/bone pain, Baseline	Muscle/bone pain, week 4	Muscle/bone pain, week 8	Muscle/bone pain, week 20	Muscle/bone pain, week 32	Muscle/bone pain, week 44	Muscle/bone pain, EOT up to week 82	Sexual function, Baseline	Sexual function, week 4	Sexual function, week 8	Sexual function, week 20	Sexual function, week 32	Sexual function, week 44	Sexual function, EOT up to week 82	Communication function, Baseline	Communication function, week 4	Communication function, week 8	Communication function, week 20	Communication function, week 32	Communication function, week 44	Communication function, EOT up to week 82	Body image, Baseline	Body image, week 4	Body image, week 8	Body image, week 20	Body image, week 32	Body image, week 44	Body image, EOT up to week 82
Non-pNET (Core)	23.52	17.85	16.79	15.87	13.74	7.14	15.20	26.19	23.39	27.53	22.31	26.84	20.95	30.48	18.44	22.22	20.27	19.74	24.49	18.18	24.81	47.42	45.28	46.49	42.66	48.54	40.08	54.22	53.94	46.33	47.32	46.83	53.51	44.05	55.04	29.66	33.00	33.33	34.52	40.35	26.19	40.89	39.32	40.89	43.92	38.10	29.17	47.62	48.94	9.88	6.46	9.69	10.30	7.89	4.76	12.61	22.43	22.79	26.10	30.30	28.83	30.95	34.70

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Number and Percentage of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs) and Deaths (Core)

The number of participants with AEs, SAEs and deaths were assessed. (NCT01595009)
Timeframe: from the day of first treatment up to 19 months

Intervention	Participants (Count of Participants)
	Adverse events	Serious adverse events	Deaths
Non-pNET (Core)	109	59	10
pNET (Core)	90	25	5

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Change in EuroQol Five Dimensions Questionnaire (EQ-5D) Score at the End of Treatment From Baseline (Baseline = First Day of Treatment in the Extension) (E1)

The EQ-5D contains 2 sections:1st section has 1 item addressing each of 5 dimensions (mobility, self-care, usual activity, pain/discomfort, anxiety/depression). Each dimension has 3 levels: no problems, some problems, extreme problems, 1-3, respectively. A health state is defined by combining 1 level from each dimension. 243 health states are possible. Each state is referred to in a 5 digit code. E.g., state 11111 indicates no problems on any dimension, while state 11223 indicates no problems with mobility and self-care, some problems with performing usual activities, moderate pain or discomfort and extreme anxiety or depression. The 2nd section measures self-rated health status using a visual analogue scale (VAS) where 100 represents best possible health and 0 represents worst possible health. Patients are asked to rate their current health by placing a mark on the VAS. Scores from each section are then transformed into an overall score of 0 or 1, with 0= higher level of dysfunction. (NCT01595009)
Timeframe: baseline, every 12 weeks and up to 4 years

Intervention	units on a scale (Mean)
	Composite health index	Self-rated health status
GI NET	-8.58	-4.17
Lung NET (E1)	7.26	-10.00

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Investigator-assessed Best Overall Response (Core)

Intervention	Participants (Count of Participants)
	Partial response (PR)	Stable disease (SD)	Progressive disease (PD)	Unknown	Objective response rate (complete response or PR)
Non-pNET (Core)	1	84	8	27	1
pNET (Core)	2	74	9	41	2

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Estimated Glomerular Filtration Rate (eGFR) at Day 8 and Week 24

(MDRDa formula) with imputation by last observation carried forward (LOCF) (NCT01596062)
Timeframe: Day 8, Week 24

Intervention	mL/min/1.73m^2 (Mean)
	Day 8	Week 24 (n= 3, 6, 6)
Simulect 40mg + Neoral + Myfortic + Steroids	35.0	31.9
Simulect 80mg + Certican + Myfortic + Steroids	49.9	54.4
Simulect 80mg + Neoral + Myfortic + Steroids	53.8	55.7

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AUC of Basiliximab Binding to CD25 Receptors From Day 0 to Day 84

Mean AUC was calculated only for patients who received two Simulect injections. (NCT01596062)
Timeframe: Day 84 (Week 12) post-transplantation

Intervention	Weeks * Percentage of T cells (Mean)
Simulect 40mg + Neoral + Myfortic + Steroids	7.0
Simulect 80mg + Neoral + Myfortic + Steroids	9.9
Simulect 80mg + Certican + Myfortic + Steroids	8.4

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Area Under the Curve (AUC) of CD25 Saturation by Basiliximab From Day 0 to Day 84

CD25 saturation is the percentage of T cells expressing CD25. Mean AUC of CD25 was calculated only for patients who received two Simulect® injections. (NCT01596062)
Timeframe: Day 84 (Week 12) after transplantation

Intervention	Weeks * Percentage of saturated CD25 (Mean)
Simulect 40mg + Neoral + Myfortic + Steroids	8.4
Simulect 80mg + Neoral + Myfortic + Steroids	11.1
Simulect 80mg + Certican + Myfortic + Steroids	9.7

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Saturation Rate of CD25 Antigen Saturation by Basiliximab

CD25 saturation is the percentage of T cells expressing CD25 (NCT01596062)
Timeframe: Day 0, Day 1, Day 4, Day 6, Day 14, Day 21, Day 28, Day 42, Day 56 and Day 84 (Week 12) post-transplantation

Intervention	percentage of T cells (Mean)
	Day 0 (before injection)	Day 0 (2 hours after injection)	Day 1	Day 4 (before injection); (n= 3, 6, 6)	Day 4 (2 hours after injection): (n= 3, 6, 5)	Day 6: (n= 3, 6, 6)	Day 14: (n= 3, 6, 6)	Day 21: (n= 3, 6, 6)	Day 28: (n= 3, 6, 6)	Day 42: (n= 3, 6, 5)	Day 56: (n= 3, 6, 5)	Day 84 (Week 12): (n= 3, 6, 5)
Simulect 40mg + Neoral + Myfortic + Steroids	0.0	93.7	95.7	100.0	96.7	98.7	98.3	100.0	95.3	78.3	65.0	0.0
Simulect 80mg + Certican + Myfortic + Steroids	0.0	94.7	99.0	93.7	84.8	94.0	97.3	92.5	92.7	99.2	94.2	14.2
Simulect 80mg + Neoral + Myfortic + Steroids	0.0	96.7	97.7	96.2	96.3	100.0	96.7	94.5	100.0	100.0	93.3	67.5

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Percentage of Participants With Biopsy Proven Acute Rejection (BPAR) According to Type and Severity

Antibody mediated acute rejection: C4d deposition, presence of circulating antidonor antibody, morphologic evidence of acute tissue injury such as acute tubular necrosis-like minimal inflammation or capillary and/or glomerular inflammation and/or thromboses or arterial inflammation. Cellular acute rejection: acute T-cell mediated rejection Type IA: Significant interstitial infiltration (> 25% of parenchyma) and foci of moderate tubulitis (> 4 mononuclear cells/tubular cross section or group of 10 tubular cells) Type IB: Significant interstitial infiltration (> 25% of parenchyma) and foci of severe tubulitis (> 10 mononuclear cells/tubular cross section or group of 10 tubular cells) Type IIA: Mild to moderate intimal arteritis. Type IIB: Severe intimal arteritis comprising > 25% of the lumenal area. Type III: Transmural (full vessel wall thickness) arteritis and/or arterial fibrinoid change and necrosis of medial smooth muscle cells (with accompanying lymphocytic inflammation). (NCT01596062)
Timeframe: Day 84 (Week 12), Week 24 post-transplantation

Intervention	Percentage of participants (Number)
	Day 84 (Week 12): Antibody mediated AR - No	Day 84 (Week 12): Antibody mediated AR - Yes	Day 84 (Week 12): Cellular AR - No	Day 84 (Week 12): Cellular AR - Yes	Day 84 (Week 12): Banff type lA	Day 84 (Week 12): Banff type lB	Day 84 (Week 12): Banff type llA	Day 84 (Week 12): Banff type llB	Day 84 (Week 12): Banff type lll (C AR)	Week 24: Antibody mediated AR - No	Week 24: Antibody mediated AR - Yes	Week 24: Cellular AR - No	Week 24: Cellular AR - Yes	Week 24: Banff type lA	Week 24: Banff type lB	Week 24: Banff type llA	Week 24: Banff type llB	Week 24: Banff type lll
Simulect 40mg + Neoral + Myfortic + Steroids	66.7	33.3	100.0	0.0	0.0	0.0	0.0	0.0	0.0	66.7	33.3	100.0	0.0	0.0	0.0	0.0	0.0	0.0
Simulect 80mg + Certican + Myfortic + Steroids	85.7	14.3	57.1	42.9	14.3	14.3	0.0	14.3	0.0	85.7	14.3	57.1	42.9	0.0	28.6	0.0	14.3	0.0
Simulect 80mg + Neoral + Myfortic + Steroids	100.0	0.0	83.3	16.7	0.0	16.7	0.0	0.0	0.0	100.0	0.0	83.3	16.7	0.0	16.7	0.0	0.0	0.0

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Percentage of Participants With of Biopsy Proven Acute Rejection (BPAR)

BPAR is one of the components of treatment failure. One assessment of efficacy was BPAR. Renal graft biopsies were performed and the renal tissue was examined to determine if there was acute rejection of the renal transplant. (NCT01596062)
Timeframe: Day 84 (Week 12), Week 24 post-transplantation

Intervention	Percentage of participants (Number)
	Day 84 (Week 12): No	Day 84 (Week 12):Yes	Week 24: No	Week 24:Yes
Simulect 40mg + Neoral + Myfortic + Steroids	66.7	33.3	66.7	33.3
Simulect 80mg + Certican + Myfortic + Steroids	42.9	57.1	42.9	57.1
Simulect 80mg + Neoral + Myfortic + Steroids	83.3	16.7	83.3	16.7

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Percentage of T-cells That Bind Basiliximab to CD25 Receptors

This is the percentage of T cells binding basiliximab at all timepoints. (NCT01596062)
Timeframe: Day 0, Day 1, Day 4, Day 6, Day 14, Day 21, Day 28, Day 42, Day 56 and Day 84 (Week 12) post-transplantation

Intervention	Percentage of T cells (Mean)
	Day 0 (before injection)	Day 0 (2 hours after injection)	Day 1 (n= 3, 5, 7)	Day 4 (before injection): (n= 3, 6, 6)	Day 4 (2 hours after injection): (n= 3, 5, 5)	Day 6: (n= 3, 6, 6)	Day 14: (n= 3, 6, 6)	Day 21: (n= 3, 6, 6)	Day 28: (n= 3, 6, 6)	Day 42: (n= 3, 6, 5)	Day 56: (n= 3, 6, 5)	Day 84 (Week 12): (n= 3, 6, 5)
Simulect 40mg + Neoral + Myfortic + Steroids	0.0	95.3	70.0	100.0	100.0	91.7	100.0	89.0	76.3	47.3	53.0	6.7
Simulect 80mg + Certican + Myfortic + Steroids	4.7	81.6	91.4	53.0	81.2	98.3	93.8	85.8	82.7	78.8	75.2	15.8
Simulect 80mg + Neoral + Myfortic + Steroids	0.0	96.2	64.8	59.0	83.4	99.0	89.0	87.7	91.0	84.0	88.8	57.7

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Proportion of CD3+, CD4+, CD8+, CD19+ and CD56+ T Cells

Cell counts of various subpopulations of T, B and NK lymphocytes (CD3, CD4, CD8, CD19 and CD56) (flow cytometry). (NCT01596062)
Timeframe: Day 0, Day 6, Day 42, Day 84 (Week 12)

Intervention	10^9 cells/L (Mean)
	CD3 cells count at Day 0 (before injection)	CD3 cells count at Day 6: (n= 3, 6, 6)	CD3 cells count at Day 42: (n= 3, 6, 5)	CD3 cells count at Day 84 (Week 12): (n= 3, 6, 6)	CD4 cells count at Day 0 (before injection)	CD4 cells count at Day 6: (n= 3, 6, 6)	CD4 cells count at Day 42: (n= 3, 6, 5)	CD4 cells count at Day 84 (Week 12): (n= 3, 6, 6)	CD8 cells count at Day 0 (before injection)	CD8 cells count at Day 6: (n= 3, 6, 6)	CD8 cells count at Day 42: (n= 3, 6, 5)	CD8 cells count at Day 84 (Week 12): (n= 3, 6, 6)	CD19 cells count at Day 0 (before injection)	CD19 cells count at Day 6: (n=3, 6, 6)	CD19 cells count at Day 42: (n= 3, 6, 5)	CD19 cells count at Day 84 (Week 12): (n= 3, 6, 6)	CD56 cells count at Day 0 (before injection)	CD56 cells count at Day 6: (n= 3, 6, 6)	CD56 cells count at Day 42: (n= 3, 6, 5)	CD56 cells count at Day 84 (Week 12): (n= 3, 6, 6)
Simulect 40mg + Neoral + Myfortic + Steroids	0.5	0.6	0.5	0.8	0.4	0.5	0.3	0.6	0.1	0.2	0.1	0.2	0.1	0.1	0.1	0.2	0.1	0.1	0.1	0.1
Simulect 80mg + Certican + Myfortic + Steroids	0.7	0.9	1.1	1.1	0.5	0.6	0.8	0.7	0.2	0.2	0.4	0.3	0.1	0.2	0.2	0.1	0.2	0.2	0.2	0.1
Simulect 80mg + Neoral + Myfortic + Steroids	0.9	1.1	1.2	1.2	0.6	0.7	0.8	0.8	0.3	0.3	0.3	0.3	0.1	0.2	0.2	0.1	0.2	0.1	0.2	0.1

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Percentage of Participants With of Treatment Failures

Treatment failure was defined either as a BPAR, a graft loss, a death or a loss to follow-up. An extended treatment failure was also defined including treated borderline lesions, BPAR, graft loss, death or loss to follow-up. Treated borderline lesions were considered as acute rejection by investigators and DMC experts. (NCT01596062)
Timeframe: Day 84 (Week 12), Week 24

Intervention	Percentage of participants (Number)
	Day84 (Week 12): BPAR and/or borderline lesions-No	Day84 (Week 12):BPAR and/or borderline lesions-Yes	Day 84 (Week 12): Graft loss - No	Day 84 (Week 12): Graft loss - Yes	Day 84 (Week 12): Death - No	Day 84 (Week 12): Death - Yes	Day 84 (Week 12): Loss to follow-up - No	Day 84 (Week 12): Loss to follow-up - Yes	Week 24: BPAR or borderline lesions - No	Week 24: Graft loss - No	Week 24: Death - No	Week 24: Loss to follow-up - No	Week 24: Loss to follow-up - Yes	Week 24: BPAR or borderline lesions - Yes	Week 24: Graft loss - Yes	Week 24: Death - Yes
Simulect 40mg + Neoral + Myfortic + Steroids	66.7	33.3	66.7	33.3	100.0	0.0	100.0	0.0	66.7	66.7	100.0	100.0	0.0	33.3	33.3	0.0
Simulect 80mg + Certican + Myfortic + Steroids	14.3	85.7	100.0	0.0	100.0	0.0	100.0	0.0	14.3	100.0	100.0	100.0	0.0	85.7	0.0	0.0
Simulect 80mg + Neoral + Myfortic + Steroids	66.7	33.3	100.0	0.0	100.0	0.0	100.0	0.0	66.7	100.0	100.0	100.0	0.0	33.3	0.0	0.0

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Growth Development - Height at Baseline and Month 24

"Individual growth measurements were compared with the gender and age-specific growth percentiles in the CDC growth charts for the US population. Each value observed is thus represented by the (approximated) percentage of subjects with a lower value in the reference population. Changes were calculated on this scale and thus express the change in growth measurements relative to the percentiles in the CDC growth charts.~Patients were classified into growth percentile categories (<=5, >5-25, >25-50, >50-75, >75-95 and >95% percentile)." (NCT01598987)
Timeframe: Baseline, Month 24

,,,,,,

Intervention	Percentages (Number)
	Decrease	No Change	Increase >3 to 5%	Increase >5 to 10%	Increase >10%
<=5% Percentile	0.0	50.0	33.3	0.0	16.7
>25% - 50% Percentile	33.3	0.0	0.0	33.3	33.3
>5% - 25% Percentile	12.5	12.5	12.5	0.0	62.5
>50% - 75% Percentile	0.0	0.0	0.0	0.0	100.0
>75% - 95% Percentile	0.0	50.0	50.0	0.0	0.0
>95% Percentile	0.0	100.0	0.0	0.0	0.0
Total	9.00	27.3	18.2	4.5	40.9

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Growth Development - Height at Baseline and Month 12

,,,,,,

Intervention	Percentages (Number)
	Decrease	No Change	Increase >3 to 5%	Increase >5 to 10%	Increase >10%
<=5% Percentile	0.0	68.8	12.5	0.0	18.8
>25% - 50% Percentile	16.7	33.3	0.0	16.7	33.3
>5% - 25% Percentile	26.7	20.0	6.7	20.0	26.7
>50% - 75% Percentile	14.3	28.6	0.0	14.3	42.9
>75% - 95% Percentile	25.0	50.0	25.0	0.0	0.0
>95% Percentile	0.0	100.0	0.0	0.0	0.0
Total	14.0	44.0	8.0	10.0	24.0

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Change From Baseline in Estimated Glomerular Filtration Rate - Month 12

Evolution of renal function assessed by estimated Glomerular Filtration Rate (eGFR) calculated by the Chronic Kidney Disease in Children (CKiD) Schwartz formula (Schwartz 2009), expressed in mean change in eGFR of CKiD between start of study (baseline assessment) and Month 12. (NCT01598987)
Timeframe: Baseline, Month 12

Intervention	mL/min/1.73m^2 (Mean)
Everolimus Based Regimen	6.2

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Change From Baseline in Estimated Glomerular Filtration Rate - Month 24

Intervention	mL/min/1.73m2 (Mean)
Everolimus Based Regimen	4.5

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Kaplan-Meier Estimates for Failure Rates of Efficacy Endpoints

"The proportion of patients with composite efficacy failure (treated biopsy proven acute rejection[tBPAR], graft loss [GL] , death [D]) before/at Month 12 and Month 24, estimated with Kaplan-Meier (KM) methods and the proportion of patients who experienced any of the components of composite efficacy failure (tBPAR, GL, D) before/at Month 12 and Month 24, separately for each component.~AR: acute rejection; BPAR: biopsy proven acute rejection. Rate = Kaplan-Meier estimate for failure in %; CI = confidence interval for failure rate." (NCT01598987)
Timeframe: At 12-month and 24-month after start of study drug

Intervention	Percentages (Number)
	Month 12: tBPAR,GL,or D	Month 12: tBPAR,GL,D,or loss to follow-up	Month 12: Treated BPAR	Month 12: Graft loss	Month 12: Death	Month 12: Graft loss or death	Month 12: BPAR	Month 12: Treated AR	Month 24: tBPAR,GL,or D	Month 24: tBPAR,GL,D,or loss to follow-up	Month 24: Treated BPAR	Month 24: Graft Loss	Month 24: Death	Month 24: Graft loss or death	Month 24: BPAR	Month 24: Treated AR
Everolimus Based Regimen	1.9	1.9	1.9	0.0	0.0	0.0	3.7	3.6	5.9	9.7	5.9	0.0	0.0	0.0	11.9	7.7

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Growth Development - Weight at Baseline and Month 24

,,,,,

Intervention	Percentages (Number)
	Decrease	No Change	Increase >3 to 5%	Increase >5 to 10%	Increase >10%
<=5% Percentile	0.0	50.0	16.7	16.7	16.7
>25% - 50% Percentile	100.0	0.0	0.0	0.0	0.0
>5% - 25% Percentile	40.0	0	0	20.0	40.0
>50% - 75% Percentile	12.5	25.0	12.5	12.5	37.5
>95% Percentile	0.0	100.0	0.0	0.0	0.0
Total	22.7	27.3	9.1	13.6	27.3

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Growth Development - Weight at Baseline and Month 12

,,,,,,

Intervention	Percentages (Number)
	Decrease	No Change	Increase >3 to 5%	Increase >5 to 10%	Increase >10%
<=5% Percentile	0.0	33.3	0.0	26.7	40.0
>25% - 50% Percentile	42.9	0.0	0.0	0.0	57.1
>5% - 25% Percentile	20.0	20.0	0.0	0.0	60.0
>50% - 75% Percentile	72.7	18.2	0.0	9.1	0.0
>75% - 95% Percentile	16.7	33.3	16.7	0.0	33.3
>95% Percentile	0.0	100.0	0.0	0.0	0.0
Total	28.0	24.0	2.0	10.0	36.0

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Evidence of Reduction of BK Viruria and/or Clearance of BK Viremia

composite outcome of a 50% or greater reduction in BKV urine levels and/or complete clearance of BKV viremia by 3 months after randomization (NCT01624948)
Timeframe: 3 months post-randomization

Intervention	participants (Number)
Everolimus+Tacrolimus/Prednisone	11
Standard of Care: 50% Reduction of MPA	8

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Proteinuria

(NCT01624948)
Timeframe: 3 months post-randomization

Intervention	g/g creatinine (Mean)
Everolimus+Tacrolimus/Prednisone	0.16
Standard of Care: 50% Reduction of MPA	0.23

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p70S6 Kinase Phosphorylation

(NCT01624948)
Timeframe: 3 months post-randomization

Intervention	Mean Fluorescence Intensity (Median)
Reached Primary Endpoint	5002
Failed to Reach Primary Endpoint	4353

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Cholesterol

(NCT01624948)
Timeframe: 3 months post-randomization

Intervention	mg/dL (Mean)
Everolimus+Tacrolimus/Prednisone	212
Standard of Care: 50% Reduction of MPA	170

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Evaluation for the Development of BK Virus Nephropathy or Doubling of BK Viremia Levels

A doubling of BK viremia levels or the development of BKV nephropathy in subjects enrolled in the experimental study arm will prompt a conversion to standard care therapy. We will closely monitor BKV levels in the urine and blood and assess renal function monthly, as per our usual standard of care. Based on BKV results as well as renal function, as assessed by serum Cr, biopsies may be done for cause. Patients will have a final visit at month 4 to monitor for adverse events. (NCT01624948)
Timeframe: 3 months post-randomization

Intervention	participants (Number)
Everolimus+Tacrolimus/Prednisone	2
Standard of Care: 50% Reduction of MPA	2

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Median Between the Calculated Mean Residual Expression of NFAT-regulated Genes

"Measurement of the expression of three NFAT-regulated genes IL-2, interferon gamma, and GM-CSF, to predict a rejection episode.~The residual gene expression after Tacrolimus intake was calculated as T1.5/T0*100, where T0 is the adjusted number of transcripts at Tacrolimus pre-dose level and T1.5 is the number of transcripts 1.5 hours after drug intake. For all three genes the residual expression was averaged and presented as MRE of NFAT-regulated genes." (NCT01624948)
Timeframe: 3 months post-randomization

Intervention	percent residual expression (Median)
Rejection	46.35
No Rejection	29.12

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Change From Baseline (Randomization) in Serum Creatinine

"Change in serum creatinine concentrations from baseline (randomization) to week 24 post-randomization was one of the efficacy assessments of renal function.~Baseline was Day 28 visit." (NCT01625377)
Timeframe: Baseline, Week 24

Intervention	µmol/L (Mean)
Tacrolimus	7.2
Everolimus (RAD001)	-1.3

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Number of Patients With Treated or Not Treated Biopsy Proven Acute Rejection (BPAR)

Biopsy proven acute rejection was defined as a clinically suspected acute rejection confirmed by biopsy. (NCT01625377)
Timeframe: at 12 week and 24 week

Intervention	Patients (Number)
	Week 12, Treated BPAR	Week 12, Not treated BPAR	Week 24, Treated BPAR	Week 24, Not Treated BPAR
Everolimus (RAD001)	2	0	8	1
Tacrolimus	2	0	2	0

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Change From Baseline (Randomization) in Creatinine Clearance Estimated Using the Adjusted Cockcroft-Gault Formula

Creatinine clearance by the Cockcroft-Gault formula is computed in mL/min/1.73m^2 from the creatinine clearance in mL/min by multiplying it by 1.73 and dividing it by the body surface area Baseline was Day 28 visit. (NCT01625377)
Timeframe: Baseline, Week 24

Intervention	mL/min/1.73m^2 (Mean)
Tacrolimus	-9.0
Everolimus (RAD001)	0.7

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Change From Baseline (Randomization) in Glomerular Filtration Rate Estimated by CKD-EPI Formula

"GFR estimated by using the Chronic kidney disease- epidemiology (CKD-EPI) formula:~eGFR (mL/min/1.73m^2) = 141 * min(C/K,1)^ α * max(C/K,1)^-1.209 * 0.993^A * 1.1018 (if male) * 1.159 (if black) where C = serum creatinine (in mg/dL) ; A = Age (in years); K = 0.7 for women and 0.9 for men; α = -0.329 for women and -0.411 for men. Baseline was Day 28 visit." (NCT01625377)
Timeframe: Baseline, Week 24

Intervention	mL/min/1.73m^2 (Mean)
Tacrolimus	-6.9
Everolimus (RAD001)	2.4

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Change From Baseline (Randomization) in Renal Function

"Change in renal function was measured by change in glomerular filtration rate (GFR). GFR calculated using the abbreviated modification of diet in renal disease (aMDRD) formula.~GFR in mL/min/1.73m^2 for men of non-black ethnicity: 186 * [C/88]^-1.154 * [A]^-0.023*G*R ; C = serum creatinine (in μmol/L); A = Age (in years). G = 0.742 when the patient is a women; Otherwise G=1 R= 1.21 when the patient was of black ethnicity; Otherwise R = 1 Baseline was Day 28 visit." (NCT01625377)
Timeframe: Baseline, Week 24

Intervention	mL/min/1.73m^2 (Least Squares Mean)
Tacrolimus	-13.29
Everolimus (RAD001)	1.05

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Change From Baseline (Randomization) in Urine Protein/Creatinine Ratio

Change in urine protein/creatinine ratio from baseline (randomization) to week 24 post-randomization was one of the efficacy assessments of renal function. Baseline was Day 28 visit. (NCT01625377)
Timeframe: Baseline, week 24

Intervention	mg/mmol (Mean)
Tacrolimus	-2.3
Everolimus (RAD001)	21.9

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Change From Baseline (Randomization) in Glomerular Filtration Rate Estimated by Abbreviated Modification of Diet in Renal Disease (MDRD) Formula

"Change in glomerular filtration rate was calculated using the MDRD abbreviated formula.~GFR in mL/min/1.73m^2 for men of non-black ethnicity: 186 * [C/88]^-1.154 * [A]^-0.023*G*R ; C = serum creatinine (in μmol/L); A = Age (in years). G = 0.742 when the patient is a women; Otherwise G=1 R= 1.21 when the patient was of black ethnicity; Otherwise R = 1 Baseline was Day 28 visit." (NCT01625377)
Timeframe: Baseline, Week 24

Intervention	mL/min/1.73m^2 (Mean)
Tacrolimus	-11.8
Everolimus (RAD001)	0.1

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Number of Patients in Different Stages of Chronic Kidney Diseases According to the K/DOQI Classification System

"Kidney disease outcomes quality initiative (K/DOQI) classification is based on glomerular filtration rate (GFR), abbreviated MDRD formula (mL/min/1.73m^2) :~Stage 1 : GFR >= 90; Stage 2 = GFR was between 60-89; Stage 3 = GFR was between 30-59 ; Stage 4 = GFR was between 15-29; Stage 5 = GFR was < 15 (or dialysis)" (NCT01625377)
Timeframe: At Week 24

Intervention	Patients (Number)
	Stage 1	Stage 2	Stage 3	Stage 4	Stage 5
Everolimus (RAD001)	41	29	4	0	0
Tacrolimus	24	34	28	0	0

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Number of Patients Reported With Different Categories of Severity of BPAR According to Banff Classification

"Biopsy proven acute rejection was defined as a clinically suspected acute rejection confirmed by biopsy.~The severity of BPAR was categorized as :~Mild (Banff grade I, RAI = 4 and 5) Moderate (Banff grade II, RAI = 6 and 7) Severe (Banff grade III, RAI = 8 and 9) Banff Rejection Activity Index (RAI) comprises 3 components scored from 0 to 3: venous endothelial inflammation; bile duct inflammation damage; and portal inflammation; the scores are combined to an overall score (the RAI) ranging from 0 to 9. An overall score of 0-3 is considered indeterminate, score of 4-5 is mild acute, score of 6-7 is moderate acute , and score of 8-9 is severe acute. Only the episode with the highest total RAI score for each participant was counted." (NCT01625377)
Timeframe: at 12 week and 24 week

Intervention	Patients (Number)
	Week 12: Mild	Week 12: Moderate	Week 12: Severe	Week 24: Mild	Week 24: Moderate	Week 24: Sever
Everolimus (RAD001)	1	1	0	5	3	0
Tacrolimus	1	1	0	1	1	0

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Number of Patients With Any Adverse Events, Serious Adverse Events, Death and Premature Discontinuation

Baseline was Day 28 visit. This endpoint reports patients with total adverse events (any), serious adverse events, death and premature discontinuation. (NCT01625377)
Timeframe: Baseline to 24 weeks

Intervention	Patients (Number)
	Any Adverse events	Serious Adverse events	Death	At least one AE led to premature discontinuation
Everolimus (RAD001)	81	42	2	18
Tacrolimus	85	28	1	4

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Number of Patients With Death or Graft Loss

The graft was presumed to be lost on the day the patient was registered again on the waiting list, or the day he/she received a new graft. (NCT01625377)
Timeframe: at week 24

Intervention	Patients (Number)
	Graft Loss	Death
Everolimus (RAD001)	0	1
Tacrolimus	1	1

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Number of Patients With Treated or Untreated BPAR With RAI Score Greater Than 3

"Biopsy proven acute rejection (BPAR) was defined as a clinically suspected acute rejection confirmed by biopsy. The Banff Rejection Activity Index (RAI) comprises 3 components scored from 0 to 3: venous endothelial inflammation; bile duct inflammation damage; and portal inflammation; the scores are combined to an overall score (the RAI) ranging from 0 to 9. An overall score of 0-3 is considered indeterminate, score of 4-5 is mild acute, score of 6-7 is moderate acute , and score of 8-9 is severe acute. Only the episode with the highest total RAI score for each participant was counted.~The patients with treated or untreated BPAR having RAI score > 3 were reported in this end point." (NCT01625377)
Timeframe: At 24 weeks

Intervention	Patients (Number)
	Not Treated BPAR: RAI score >3	Not Treated BPAR: Missing RAI score	Treated BPAR: RAI score >3
Everolimus (RAD001)	0	1	8
Tacrolimus	0	0	2

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Number of Patients With Treatment Failures

"Incidence of treatment failures, assessed with composite criterion including treated biopsy proven acute rejection (tBPAR) with a rejection activity index (RAI) according to Banff classification >3, graft loss or death at 6 months.~Biopsy proven acute rejection (BPAR) was defined as a clinically suspected acute rejection confirmed by biopsy. The Banff Rejection Activity Index (RAI) comprises 3 components scored from 0 to 3: venous endothelial inflammation; bile duct inflammation damage; and portal inflammation; the scores are combined to an overall score (the RAI) ranging from 0 to 9. An overall score of 0-3 is considered indeterminate, score of 4-5 is mild acute, score of 6-7 is moderate acute , and score of 8-9 is severe acute. Only the episode with the highest total RAI score for each participant was counted.~The graft was presumed to be lost on the day the patient was registered again on the waiting list, or the day he/she received a new graft." (NCT01625377)
Timeframe: At week 12 and week 24

Intervention	Patients (Number)
	week 12, Treatment failures - NO	week 12, Treatment failures - YES	week 24, Treatment failures - NO	week 24, Treatment failures - YES
Everolimus (RAD001)	88	2	81	9
Tacrolimus	91	2	89	4

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Overall Survival (OS)

Overall survival (OS) was defined as the time from study enrollment to death from any cause. Data on vital status were collected after study completion through May 1, 2018 and were used in the determination of OS. (NCT01627067)
Timeframe: From the registration until disease progression, death, unacceptable toxicity, or withdraw of study consent, whichever occurred first assessed up to 67 months

Intervention	months (Median)
Everolimus + Exemestane + Metformin	28.8

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Progression-Free Survival (PFS)

The primary end point of this study was progression-free survival (PFS), defined as the time from study enrollment to disease progression or death from any cause, whichever occurred first. Data for PFS were censored at the time of a patient's removal from study. All other analyses were post-hoc and should be regarded as such. (NCT01627067)
Timeframe: From the registration until disease progression, death, unacceptable toxicity, or withdraw of study consent, whichever occurred first assessed up to 67 months

Intervention	months (Median)
Everolimus + Exemestane + Metformin	6.3

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Compare Overall Survival (OS) Between the Number of Obese and Overweight Participants

Overall survival (OS) was defined as the time from study enrollment to death from any cause. Data on vital status were collected after study completion through May 1, 2018 and were used in the determination of OS. Compare OS between obese participants ( n=11; BMI >/=25 kg/m2) and overweight participants (n=11; BMI NCT01627067)
Timeframe: From the registration until disease progression, death, unacceptable toxicity, or withdraw of study consent, whichever occurred first assessed up to 67 months

Intervention	Participants (Count of Participants)
	Obese participants	Overweight participants
Compare OS Between Obese Patient and Overweight Participants	11	11

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Compare Progression Free Survival (PFS) Between the Number of Obese and Overweight Participants

The primary end point of this study was progression-free survival (PFS), defined as the time from study enrollment to disease progression or death from any cause, whichever occurred first. Data for PFS were censored at the time of a participants removal from study. Compare PFS between overweight patients (n=11; BMI /=25 kg/m2) on univariable cox regression analysis. (NCT01627067)
Timeframe: From the registration until disease progression, death, unacceptable toxicity, or withdraw of study consent, whichever occurred first assessed up to 67 months

Intervention	Participants (Count of Participants)
	Obese participants	Overweight participants
Compare PFS Between Obese and Overweight Participants	11	11

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Number of Participants With Response

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. The clinical benefit rate (CBR) was defined as the proportion of patients with a best overall response of CR, PR or SD (non-CR/non-PD for patients without measurable disease) lasting at least 24 weeks. For patients with a best overall response of CR or PR, the duration of response (DOR) was defined as the time from first documentation of CR or PR to the time of disease progression. Data on the DOR and PFS were censored at the time of a patient's removal from the study. For patients with a best overall response of SD (non-CR/non-PD for patients without measurable disease),the duration of SD (non-CR/non-PD for patients without measurable disease) was defined as the time from study enrollment to the time of disease progression. (NCT01627067)
Timeframe: From the registration until disease progression, death, unacceptable toxicity, or withdraw of study consent, whichever occurred first assessed up to 67 months

Intervention	Participants (Count of Participants)
	Complete Response	Partial response	Stable Disease lasting >=24 wks	Stable Disease lasting <24 wks	Progressive disease	Overall response (CR+PR)	Clinical benefit (CR+PR+SD >/= 24 wks
Everolimus + Exemestane + Metformin	0	5	7	5	5	5	12

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Progression Free Survival (PFS)

PFS is defined as the time from the date of randomization until the date of the first radiologically documented disease progression or death due to any cause. PFS is based on local investigator assessment. Patients will be followed up for the duration of the study and for an expected average of every 12 weeks after randomization. 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 all target lesions, or unequivocal progression of non-target lesions, or the appearance of new lesions. (NCT01628913)
Timeframe: up to approx. 18 months

Intervention	Months (Median)
BEZ235	8.2
Everolimus	10.8

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Efficacy of Treatment

Determine the efficacy of everolimus in the treatment of CTCL as overall response rate (ORR) (NCT01637090)
Timeframe: 12 months after beginning treatment

Intervention	()
All Patients on Study	0

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Progression-free Survival

Determine progression-free survival of CTCL patients treated with everolimus (NCT01637090)
Timeframe: two years after discontinuing study treatment

Intervention	()
All Patients on Study	0

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Effect of mTOR on Tumors

Determine mTOR (mammilian target of rapamycin) pathway activation and number of regulatory T cells (Tregs) in pre-treated tumor tissue and evaluate changes following treatment (NCT01637090)
Timeframe: one year

Intervention	()
All Patients on Study	0

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Time to Response

Determine time to response (TTR)/duration of objective response (DOR) (NCT01637090)
Timeframe: three months

Intervention	()
All Patients on Study	0

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Number of Participants With Adverse Events as a Measure of Safety and Tolerability

Determine the adverse event profile and tolerability of everolimus in patients with CTCL (NCT01637090)
Timeframe: Up to one year

Intervention	participants (Number)
All Patients on Study	3

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Median PFS

Kaplan-Meier PFS will be measured from the date that study therapy is initiated until the date of first evidence of radiographic disease progression, global clinical deterioration as determined by study investigators, or death. (NCT01642186)
Timeframe: 2 years

Intervention	months (Median)
Arm A Everolimus	2.6
Arm B Letrozole Plus Leuprolide	2.7
Arm C Combination Everolimus, Letrozole and Leuprolide	2.4

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Number of Participants With One or More Adverse Events/Toxicity

Adverse events/toxicity will be monitored and recorded using the CTCAE version 4.0 and summarized descriptively. (NCT01642186)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm A Everolimus	9
Arm B Letrozole Plus Leuprolide	9
Arm C Combination Everolimus, Letrozole and Leuprolide	10

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Number of Participants With Tissue Biomarkers Collected

Associations between baseline tissue biomarkers and PFS6 will be assessed using Fisher's exact test for categorical biomarkers, trend tests for ordinal biomarkers and Wilcoxon rank-sum test for continuous biomarkers. For patients undergoing surgery, changes in tissue biomarkers from baseline to surgery will be summarized descriptively in an exploratory fashion. (NCT01642186)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm A Everolimus	9
Arm B Letrozole Plus Leuprolide	9
Arm C Combination Everolimus, Letrozole and Leuprolide	10

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Percentage of Participants With Stable Disease

Objective responses will be reported using RECIST guidelines (version 1.1). Objective response will be estimated using binomial proportions and exact 95% CIs will be provided. Stable Disease is defined as neither sufficient shrinkage (compared to baseline) to qualify for Partial Reponse nor sufficient increase (taking as reference the smallest sum diameters while on study) to qualify for Progressive Disease. (NCT01642186)
Timeframe: 2 years

Intervention	Percentage of pts with stable disease (Number)
Arm A Everolimus	55
Arm B Letrozole Plus Leuprolide	37
Arm C Combination Everolimus, Letrozole and Leuprolide	11

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Median Overall Survival (OS)

Kaplan-Meier OS will be measured from the date that study therapy was commenced until the date of death. (NCT01642186)
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 100 months

Intervention	months (Median)
Arm A Everolimus	12.5
Arm B Letrozole Plus Leuprolide	14.0
Arm C Combination Everolimus, Letrozole and Leuprolide	10.6

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Change in T Cell & B Cell Generation

Evaluate the change in regulatory T cell generation and review the relationship of the newly generated T cells with their function in the two maintenance immunosuppressive regimens at baseline, 3 and 12 months post-transplant. (NCT01653847)
Timeframe: Baseline, 3 months, and 12 months post-transplant

Intervention	Mean % of Treg cells in peripheral blood (Mean)
	Baseline	3 Months	12 Months
Group 1: Tacrolimus With MMF.	1.05	0.8	0.81
Group 2: Tacrolimus With Everolimus	0.93	1.12	1.18

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Renal Allograft Survival

The number of subjects with renal allograft survival. (NCT01653847)
Timeframe: 12 months post-transplant

Intervention	Participants (Count of Participants)
Group 1: Tacrolimus With MMF.	20
Group 2: Tacrolimus With Everolimus	20

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Patient Survival

The number of patients who were alive at 2 years post transplant (NCT01653847)
Timeframe: baseline - 24 months post transplant

Intervention	Participants (Count of Participants)
Group 1: Tacrolimus With MMF.	20
Group 2: Tacrolimus With Everolimus	20

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Acute Rejection

Number of subjects who experience acute rejection of the renal allograft. (NCT01653847)
Timeframe: 12 months post transplant

Intervention	Participants (Count of Participants)
Group 1: Tacrolimus With MMF.	4
Group 2: Tacrolimus With Everolimus	0

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Change in Glomerular Filtration Rate (GFR)

Evaluate the change in graft function (as measured by GFR) at 12 months post-transplant from baseline. (NCT01653847)
Timeframe: 3 months, 6 months, and 12 months post-transplant

Intervention	ml/minutes per 1.73 meters^2 (Mean)
	3 months	6 months	12 months
Group 1: Tacrolimus With MMF.	63	64	65
Group 2: Tacrolimus With Everolimus	66	64	72

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Vascular Endothelial Growth Factor (VEGF) and Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) Levels at Baseline and Pre-Cycles 3 and 5

To assess changes in Vascular Endothelial Growth Factor (VEGF) and Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) Levels in peripheral blood specimens during treatment. (NCT01661283)
Timeframe: Baseline, Pre-Cycle 3, Pre-Cycle 5

Intervention	pg/mL (Median)
	VEGF- Baseline	VEGF- Pre Cycle 3	VEGF- Pre Cycle 5	VEGFR2- Baseline	VEGFR2 Pre Cycle 3	VEGFR2 Pre Cycle 5
Treatment	103.58	184.24	192.49	1363.76	911.89	863.85

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Clinical Benefit Rate (Complete Response, Partial Response, and Stable Disease at ≥ 4 Months Using World Health Organization (WHO) Criteria) of Everolimus in Combination With Bevacizumab

"Evaluate if the combination of the mTOR inhibitor everolimus combined with the angiogenesis inhibitor bevacizumab would result in a modest clinical benefit rate, which included confirmed partial and complete responses and disease stability for four or more treatment cycles based on WHO Response Criteria. Per WHO for target lesions: Complete Response (CR): Disappearance of all known disease, determined by two consecutive observations not less than 4 weeks apart.~Partial Response (PR): A > 50% decrease in the total tumor load of the lesions that have been measured to determine the effect of therapy not less than four weeks apart. The observations must be consecutive. Stable Disease (SD): A 50% decrease in total tumor area cannot be established nor has a 25% increase in the size of one or more measurable lesions been demonstrated." (NCT01661283)
Timeframe: Assessed at Baseline and prior to Cycle 3, 5, 7, 9, etc., for up to 2 years. 1 cycle =28 days

Intervention	Participants (Count of Participants)
Treatment	3

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Number of Participants With Response Stratified by Individuals With Sporadic or NF1 Associated MPNST

To explore differences in the response rate to everolimus in combination with bevacizumab in individuals with sporadic and NF1 associated MPNST. Responses include confirmed partial and complete responses and disease stability for four or more treatment cycles based on WHO Response Criteria. Per WHO for target lesions: Complete Response (CR): Disappearance of all known disease, determined by two consecutive observations not less than 4 weeks apart. Partial Response (PR): A > 50% decrease in the total tumor load of the lesions that have been measured to determine the effect of therapy not less than four weeks apart. The observations must be consecutive. Stable Disease (SD): A 50% decrease in total tumor area cannot be established nor has a 25% increase in the size of one or more measurable lesions been demonstrated. (NCT01661283)
Timeframe: Assessed at Baseline and prior to Cycle 3, 5, 7, 9, etc., for up to 2 years. 1 cycle =28 days

Intervention	Participants (Count of Participants)
	NF1 associated MPNST	Sporadic MPNST
Treatment	2	1

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Safety as Assessed by Avoidance of Grade 3-4 Adverse Events

Number of participants who did not experience at least one grade 3-4 adverse event by CTCAE 4.0. (NCT01665768)
Timeframe: Up to 3 years

Intervention	Participants (Count of Participants)
Everolimus and Rituximab	1

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Event Free Survival (EFS)

Percentage of participants alive without disease progression. As defined by Cheson criteria, disease progression is a new lesion or >= 50% increase in the size of previously identified sites of disease. EFS was estimated using Kaplan-Meier survival analysis. (NCT01665768)
Timeframe: 2.5 years

Intervention	percentage of participants (Number)
Everolimus and Rituximab	58

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Number of Participants With Abnormal Hematology and Serum Chemistry Laboratory Parameters by Worse CTC Grade - SI Units

Common Terminology Criteria (CTC) version 4.0 in International System of Units (SI); Gr 3=Severe, Gr 4= Potentially Life-threatening or disabling. Hematology parameters=Hemoglobin (Gr 3: < 8.0 g/dL), Platelet Count (Gr 3: 25.0 -< 50.0*10^9 c/L; Gr 4: < 25.0*10^9 c/L), Leukocyte Count (Gr 3: 1.0 -< 2.0*10^3 c/µL; Gr4: < 1.0*10^3 c/µL), Absolute Lymphocyte Count (Gr 3: 0.2 -< 0.5*10^3 c/µL; Gr 4: < 0.2*10^3 c/µL), Absolute Neutrophil Count (Gr 3: 0.5 - < 1.0*10^3 c/µL; Gr 4: < 0.5*10^3 c/µL). Liver Function parameters=Alkaline Phosphatase (Gr 3: > 5.0 - 20.0 U/L * ULN; Gr 4: > 20.0 U/L * ULN), AST (Gr 3: > 5.0 - 20.0 U/L * ULN; Gr 4: > 20.0 U/L * ULN), ALT (Gr 3: > 5.0 - 20.0 U/L * ULN; Gr 4: > 20.0 U/L * ULN), tBIL (Gr 3: > 3.0 - 10.0 mg/dL * ULN; Gr 4: > 10.0 mg/dL * ULN). Renal parameter=Creatinine (Grade: Gr3: > 3.0 - 6.0 mg/dL *ULN; Gr4: > 6.0 mg/dL *ULN). Cells per microliter (c/µL). Cells per Liter (c/L). Grams per deciliter (g/dL). Milligrams per deciliter (mg/dL). (NCT01668784)
Timeframe: Day 1 to 30 days post study completion (approximately 106 months)

Intervention	Participants (Count of Participants)
	Hemoglobin, Grade 3	Platelet Count, Grade 3	Platelet Count, Grade 4	Leukocytes, Grade 3	Leukocytes, Grade 4	Lymphocytes (absolute), Grade 3	Lymphocytes (absolute), Grade 4	Absolute Neutrophil Count, Grade 3	Absolute Neutrophil Count, Grade 4	Alkaline Phosphatase, Grade 3	Aspartate Aminotransferase, Grade 3	Aspartate Aminotransferase, Grade 4	Alanine Aminotransferase, Grade 3	Alanine Aminotransferase, Grade 4	Bilirubin Total, Grade 3	Creatinine, Grade 3	Creatinine, Grade 4	Hypercalcemia, Grade 3	Hypercalcemia, Grade 4	Hypocalcemia, Grade 3	Hypocalcemia, Grade 4	Hyperkalemia, Grade 3	Hyperkalemia, Grade 4	Hypokalemia, Grade 3	Hypermagnesmia, Grade 3	Hypomagnesmia, Grade 3	Hyponatremia, Grade 3	Hyponatremia, Grade 4
Everolimus	61	6	1	1	0	43	6	2	1	3	6	0	3	0	2	5	1	1	1	4	0	7	0	3	0	0	22	1
Nivolumab	33	1	0	0	1	28	3	0	0	11	9	2	12	1	3	5	3	7	4	2	1	11	3	5	3	1	26	1

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Number of Participants Meeting Marked Laboratory Abnormality Criteria in Specific Liver and Thyroid Tests

Aspartate aminotransferase, AST. Alanine aminotransaminase, ALT. Total bilirubin, tBIL. Thyroid stimulating hormone, TSH. Upper limit of normal (ULN). Units per Liter (U/L). Results reported in International System of Units (SI). (NCT01668784)
Timeframe: Day 1 to 30 days post study completion (approximately 106 months)

Intervention	Participants (Count of Participants)
	ALT or AST > 3.0*ULN	ALT or AST > 5.0*ULN	ALT or AST > 10.0*ULN	ALT or AST > 20.0*ULN	Total Bilirubin > 2.0*ULN	ALT or AST>3.0*ULN, tBIL>2.0 ULN, 1day	ALT or AST>3.0*ULN, tBIL>2.0 ULN,30day	TSH > ULN	TSH < LLN
Everolimus	15	7	1	0	2	0	1	78	60
Nivolumab	32	20	9	2	6	3	4	159	60

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Overall Survival (OS) at Primary Endpoint

Overall Survival (OS) was defined as the time from randomization to the date of death. Participants that had not died were censored at last known date alive. Median OS time was calculated using Kaplan-Meier Estimates. Interim analysis for the Primary Endpoint occurred after 398 deaths (70% of the total OS events needed for final analysis). At that time the data monitoring committee noted that the pre-specified boundary for OS (nominal significance level p < 0.0148) was crossed while no new safety signals that would affect continuation of the study were found. The study was stopped early by the Sponsor, Bristol-Myers Squibb (BMS) and the interim analysis became the final analysis. As a result, participants in the everolimus groups could be assessed for a crossover to nivolumab treatment if they met all inclusion criteria. (NCT01668784)
Timeframe: Randomization until 398 deaths, up to May 2015 (approximately 30 months)

Intervention	months (Median)
Nivolumab	25.00
Everolimus	19.55

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Investigator-assessed Objective Response Rate (ORR)

ORR is defined as Percentage of participants with a best response of complete response (CR) or partial response (PR) divided by number of randomized participants. CR=Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 10 mm.; PR=At least a 30% decrease in the sum of diameters of target lesions, the baseline sum diameters used as reference. Tumor assessments began at 8 weeks following randomization and continued every 8 weeks for the first year, then every 12 weeks thereafter until disease progression or death. CIs used Clopper and Pearson. (NCT01668784)
Timeframe: from randomization up to disease progression or death (approximately up to 105 Months)

Intervention	percentage of participants (Number)
Nivolumab	25.9
Everolimus	6.1

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Extended Collection to Post Hoc Overall Survival (OS)

"Overall Survival (OS) was defined as the time from randomization to the date of death. Participants that had not died were censored at last known date alive. Median OS time was calculated using Kaplan-Meier Estimates. Interim analysis for the Primary Endpoint occurred after 398 deaths (70% of the total OS events needed for final analysis). At that time the data monitoring committee noted that the pre-specified boundary for OS (nominal significance level p < 0.0148) was crossed while no new safety signals that would affect continuation of the study were found. The study was stopped early by the Sponsor, Bristol-Myers Squibb (BMS) and the interim analysis became the final analysis. As a result, participants in the everolimus groups could be assessed for a crossover to nivolumab treatment if they met all inclusion criteria.~This outcome measure represents an updated version of the primary endpoint to include additional data collection that has occurred after the primary completion date. (NCT01668784)
Timeframe: from randomization up to disease progression or death (approximately up to 105 months)

Intervention	Months (Median)
Nivolumab	25.82
Everolimus	19.55

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Investigator-assessed Duration of Objective Response

Duration of objective response is defined as the time from study start date to response, CR or partial response, PR) to the date of the first documented tumor progression as determined by the investigator (per RECIST 1.1 criteria or clinical) or death due to any cause, whichever occurred first. For participants who neither progress nor die, the duration of objective response were censored at the same time they were censored for the primary definition. CR=Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 10 mm.; PR=At least a 30% decrease in the sum of diameters of target lesions, the baseline sum diameters used as reference. Based on Kaplan-Meier Estimates. (NCT01668784)
Timeframe: From randomization to date of disease progression or death or censoring if no progression or death occurred (approximately 105 months)

Intervention	months (Median)
Nivolumab	13.11
Everolimus	10.18

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Number of Participants With Serious Adverse Events, Death, Discontinuation Due to Adverse Events

Adverse event (AE) defined: any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that may not have a causal relationship with treatment. Serious adverse event (SAE) defined: a medical event that at any dose results in death, persistent or significant disability/incapacity, or drug dependency/abuse; is life-threatening, an important medical event, or a congenital anomaly/birth defect; or requires or prolongs hospitalization. (NCT01668784)
Timeframe: Day of first dose to 30 days post study completion (approximately 106 months)

Intervention	Participants (Count of Participants)
	Deaths	SAEs	Drug related SAEs	Drug related AEs	Discontinued due to Drug-related AEs	Discontinued due to AEs	Adverse Events
Everolimus	342	177	55	353	51	82	387
Nivolumab	324	211	51	327	40	85	398

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Investigator-assessed Time of Progression-free Survival (PFS)

PFS=time from randomization to date of first documented tumor progression as determined by investigator (per RECIST 1.1 criteria or clinical) or death due to any cause, whichever occurred first. Participants who die without a reported prior progression and without subsequent anti-cancer therapy were considered to have progressed on the date of their death. Participants who did not progress or die were censored on the date of their last evaluable tumor assessment. Participants who did not have any on-study tumor assessments and did not die were censored on the date they were randomized. Participants who received any subsequent anti-cancer therapy without a prior reported progression were censored at the last evaluable tumor assessment prior to or on initiation date of the subsequent anti-cancer therapy. Progressive disease: >=20% increase in sum of target lesion diameters and sum must show absolute increase of >=5mm; smallest sum on study as reference. Based on Kaplan-Meier Estimates. (NCT01668784)
Timeframe: from randomization up to disease progression or death (approximately up to 105 Months)

Intervention	months (Median)
Nivolumab	4.21
Everolimus	4.50

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Percentage of Participants With Disease-related Symptom Progression (DRSP)

Disease-related symptom progression rate (DRSPR)=a decrease of two points in the Functional Assessment of Cancer Therapy-Kidney Symptom Index - Disease Related Symptoms (FKSI-DRS) questionnaire relative to the participant's baseline FKSI-DRS score with no later increase above this threshold observed during the course of the study. The 9 items of the FKSI-DRS were summarized into a symptom scale ranging in score from 0 to 36, with 0 being the worst possible score and 36 being the best possible score. A single measure reporting a decrease of at least 2 units was considered disease-related symptom progression only if it was the last one available for the participant. In order to consider a questionnaire received as valid, over 50% of the items were to be completed. Calculated by the Clopper-Pearson method for each treatment group. (NCT01668784)
Timeframe: from randomization up to disease progression or death (approximately up to 105 Months)

Intervention	percentage of participants (Number)
	Disease-related Symptom Progression Rate (DRSPR)	DRSPR Including Death and Investigator Progression
Everolimus	54.6	99.4
Nivolumab	44.6	95.5

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Overall Survival (OS) by Programmed Death-Ligand 1 (PD-L1) Expression Level

Quantifiable PD-L1 expression=percent of tumor cell membrane staining in a minimum of 100 evaluable tumor cells per Dako PD-L1 IHC assay. If the PD-L1 staining could not be quantified it was classified as: indeterminate=tumor cell membrane staining hampered for reasons attributed to biology of tumor biopsy specimen and not due to improper sample preparation or handling; not evaluable=tumor biopsy specimen was not optimally collected or prepared. Not evaluable determined from H&E process before the tumor biopsy specimen was sent for evaluation or from H&E process during PD-L1 evaluation; baseline PD-L1 expression=if more than one tumor biopsy specimen was available, the most recently collected specimen with a quantifiable result. If all specimens for a given participant are either indeterminate or not evaluable, then the PD-L1 expression was considered indeterminate as long as at least one specimen is indeterminate. Otherwise, PD-L1 expression was considered not evaluable. (NCT01668784)
Timeframe: Randomization to date of death or date of last contact for patients without documentation of death, up to May 2015 (approximately 30 months)

Intervention	months (Median)
	Participant PD-L1 expression >=1%	Participant PD-L1 expression <1%
Everolimus	4.17	4.67
Nivolumab	5.36	3.94

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Investigator-assessed Time to Objective Response

Time to objective response is defined as the time from randomization to first response (complete response, CR or partial response, PR). CR=Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 10 mm.; PR=At least a 30% decrease in the sum of diameters of target lesions, the baseline sum diameters used as reference. (NCT01668784)
Timeframe: Randomization to date of first response (approximately 105 months)

Intervention	months (Median)
Nivolumab	3.55
Everolimus	3.71

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Distant Recurrence-Free Survival (DRFS)

Time from date of registration to date of invasive distant disease recurrence, second invasive primary cancer (breast or not) or death due to any cause. Patients last known to be alive who have not experienced distant recurrence, or second primary cancer are censored at their last contact date. The results were presented as 5-year DRFS estimate. (NCT01674140)
Timeframe: 5 years after last accrual

Intervention	percentage of participants (Number)
Placebo	75.7
Everolimus	76.9

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Invasive Disease-Free Survival (IDFS)

Time from date of registration to date of first invasive recurrence (local, regional or distant), second invasive primary cancer (breast or not), or death due to any cause. Patients last known to be alive who have not experienced recurrence or second primary cancer are censored at their last contact date. The results were presented as 5-year IDFS estimate. (NCT01674140)
Timeframe: Up to 5 years post registration

Intervention	percentage of participants (Number)
Placebo	74.4
Everolimus	74.9

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Overall Survival (OS)

Time from date of registration to date of death due to any cause. Patients last known to be alive are censored at their last contact date. The results were presented as 5-year OS estimate. (NCT01674140)
Timeframe: 5 years after last accrual

Intervention	percentage of participants (Number)
Placebo	85.8
Everolimus	88.1

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Toxicity Based on Common Terminology Criteria for Adverse Events (CTCAE) Version 4.0, Assessed up to 10 Years.

Toxicity based on Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. Only adverse events that are possibly, probably, or definitely related to study drug are reported. (NCT01674140)
Timeframe: Every 6 weeks while on protocol therapy. Adverse events (AEs) that occurred during follow up after protocol treatment were reported as late AEs, for every 6 months for the first 2 years and then yearly until 10 years after registration.

Intervention	Participants (Number)
	Abdominal pain	Alanine aminotransferase increased	Allergic reaction	Anemia	Anxiety	Appendicitis	Appendicitis perforated	Arthralgia	Ascites	Aspartate aminotransferase increased	Back pain	Bone pain	Breast infection	Cardiac arrest	Cholecystitis	Cholesterol high	Colitis	Cough	Dehydration	Depression	Diarrhea	Dizziness	Dyspnea	Edema face	Edema limbs	Eye disorders - Other, specify	Eye infection	Fatigue	Fever	Gallbladder infection	Gallbladder perforation	Gastrointestinal disorders - Other, specify	General disorders and admin site conditions - Other	Generalized muscle weakness	Headache	Heart failure	Hip fracture	Hot flashes	Hyperglycemia	Hyperhidrosis	Hyperkalemia	Hypertension	Hypertriglyceridemia	Hypokalemia	Hyponatremia	Hypophosphatemia	Hypoxia	Immune system disorders - Other, specify	Infections and infestations - Other, specify	Infusion related reaction	Insomnia	Investigations - Other, specify	Irregular menstruation	Joint infection	Kidney infection	Left ventricular systolic dysfunction	Lipase increased	Lung infection	Lymphedema	Lymphocyte count decreased	Menorrhagia	Mucositis oral	Muscle weakness lower limb	Muscle weakness upper limb	Musculoskeletal and connective tiss disorder - Other	Myalgia	Nasal congestion	Nausea	Neck pain	Nervous system disorders - Other, specify	Neuralgia	Neutrophil count decreased	Obesity	Otitis media	Pain	Pain in extremity	Papulopustular rash	Paroxysmal atrial tachycardia	Periorbital edema	Peripheral sensory neuropathy	Platelet count decreased	Pleural effusion	Pneumonitis	Portal vein thrombosis	Postoperative hemorrhage	Productive cough	Pruritus	Psychiatric disorders - Other, specify	Pulmonary edema	Radiation recall reaction (dermatologic)	Rash acneiform	Rash maculo-papular	Rash pustular	Respiratory failure	Sepsis	Seroma	Skin and subcutaneous tissue disorders - Other	Skin infection	Skin ulceration	Soft tissue infection	Sore throat	Suicidal ideation	Suicide attempt	Thromboembolic event	Tooth infection	Upper respiratory infection	Urinary tract infection	Vascular access complication	Vomiting	Weight gain	Weight loss	White blood cell decreased	Wound complication	Wound dehiscence	Wound infection
Everolimus	7	4	2	10	0	1	2	5	1	6	0	1	6	0	1	9	1	2	3	2	13	2	7	1	1	1	1	23	1	1	1	2	1	1	4	4	1	0	33	2	1	15	35	5	2	1	2	1	5	1	3	1	1	1	2	2	0	6	1	36	0	60	1	0	1	2	1	2	1	0	1	22	0	1	0	0	1	0	2	2	4	2	7	1	1	1	2	0	1	2	1	4	2	0	7	1	3	8	2	2	1	1	1	5	1	1	2	1	1	0	2	20	5	4	6
Placebo	1	1	0	0	1	2	0	1	0	1	1	0	1	1	0	0	1	0	0	0	3	0	2	0	0	0	0	6	0	0	0	0	0	0	1	0	0	2	1	0	0	6	4	0	0	0	0	0	4	0	0	0	1	0	0	0	1	2	0	5	1	2	0	1	0	0	0	0	1	1	0	3	1	0	1	1	0	1	0	1	1	0	1	0	0	0	1	1	0	0	0	0	0	1	0	0	0	3	0	0	0	0	0	3	0	0	1	0	1	2	0	2	0	1	0

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Incidence of Chronic Allograft Nephropathy (CAI) at 12 Months Post-transplant

Incidence of (biopsy-proven) chronic allograft nephropathy (CAI) [interstitial fibrosis and tubular atrophy, using standard Banff criteria] at 12 months post-transplant. (NCT01680861)
Timeframe: 1 year

Intervention	participants (Number)
Tacrolimus/Everolimus	3
Tacrolimus/EC-MPS	3

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BPAR (Biopsy-proven Acute Rejection) Incidence During the First 12 Months Post-transplant

BPAR (biopsy-proven acute rejection) incidence during the first 12 months post-transplant. Grading is determined using standard Banff criteria. (NCT01680861)
Timeframe: 1 year

Intervention	participants (Number)
Tacrolimus/Everolimus	1
Tacrolimus/EC-MPS	3

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Discontinuance of Any Study Medication (Tacrolimus, Everolimus, or EC-MPS)

(NCT01680861)
Timeframe: during the first 12 months post-transplant

Intervention	participants (Number)
Tacrolimus/Everolimus	0
Tacrolimus/EC-MPS	1

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eGFR (Calculated Glomerular Filtration Rate), i.e., Renal Function, at 1 Month Post-transplant.

using the abbreviated MDRD formula. (NCT01680861)
Timeframe: at 1 month post-transplant

Intervention	ml/min per 1.73 m2 (Mean)
Tacrolimus/Everolimus	82.1
Tacrolimus/EC-MPS	62.1

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eGFR (Renal Function) at 6 Months Post-transplant

using the abbreviated MDRD formula. (NCT01680861)
Timeframe: at 6 months post-transplant

Intervention	ml/min per 1.73 m2 (Mean)
Tacrolimus/Everolimus	66.7
Tacrolimus/EC-MPS	63.7

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eGFR (Renal Function) at Month 3 Post-transplant

Renal function as determined by the estimated glomerular filtration rate (eGFR) at 3 months post-transplant, using the abbreviated MDRD formula. (NCT01680861)
Timeframe: at 3 months post-transplant

Intervention	ml/min per 1.73 m^2 (Mean)
Tacrolimus/Everolimus	75.7
Tacrolimus/EC-MPS	65.6

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Graft Loss (Return to Permanent Dialysis or Death)

(NCT01680861)
Timeframe: during the first 12 months post-transplant

Intervention	participants (Number)
Tacrolimus/Everolimus	0
Tacrolimus/EC-MPS	0

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First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Overall Health at the End of the First Stomatitis Episode

"The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The second item asked the participant to rate their overall health from 0 (worst possible) to 10 (perfect health). The overall health OSDQ score are presented as the shift from Day 1 of first stomatitis episode value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first stomatitis value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment.~Only participants who were randomized in the stomatitis sub-study were included in this analysis." (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	Dexamethasone: From 2 (Day 1) to 5 (end of first stomatitis)	Dexamethasone: From 4 (Day 1) to 3 (end of first stomatitis)	Dexamethasone: From 5 (Day 1) to 5 (end of first stomatitis)	Dexamethasone: From 5 (Day 1) to 6 (end of first stomatitis)	Dexamethasone: From 5 (Day 1) to 7 (end of first stomatitis)	Dexamethasone: From 6 (Day 1) to 5 (end of first stomatitis)	Dexamethasone: From 6 (Day 1) to 7 (end of first stomatitis)	Dexamethasone: From 7 (Day 1) to 3 (end of first stomatitis)	Dexamethasone: From 8 (Day 1) to 8 (end of first stomatitis)	Dexamethasone: From 8 (Day 1) to 9 (end of first stomatitis)	Dexamethasone: From 9 (Day 1) to 9 (end of first stomatitis)	SoC: From 0 (Day 1) to 5 (end of first stomatitis)	SoC: From 4 (Day 1) to 3 (end of first stomatitis)	SoC: From 4 (Day 1) to 8 (end of first stomatitis)	SoC: From 5 (Day 1) to 5 (end of first stomatitis)	SoC: From 6 (Day 1) to 7 (end of first stomatitis)	SoC: From 7 (Day 1) to 3 (end of first stomatitis)	SoC: From 8 (Day 1) to 9 (end of first stomatitis)	SoC: From 8 (Day 1) to 10 (end of first stomatitis)	SoC: From 9 (Day 1) to 4 (end of first stomatitis)	SoC: From 9 (Day 1) to 9 (end of first stomatitis)	SoC: From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First-line Treatment)	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	2	2

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First-line Treatment: Progression-free Survival (PFS)

PFS in the first line setting is defined as the time from the date of enrollment to the date of first documented progression based on local radiology review or death due to any cause. If a participant did not progress or was not known to have died at the date of the analysis cut-off or start of another antineoplastic therapy, the PFS date was censored to the date of last adequate tumor assessment prior to cut-off date or start of antineoplastic therapy. The median PFS was estimated and presented along with 95% confidence intervals. The primary analysis of PFS for first line was performed 12 months after the last patient's recruitment. (NCT01698918)
Timeframe: From the date of enrollment to the date of first documented progression or deaths, assessed up to approximately 2.8 years

Intervention	Months (Median)
Everolimus+Letrozole (First-line Treatment)	NA

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First-line Treatment: Overall Response Rate (ORR)

"ORR in first line setting is defined as the percentage of participants while on first-line treatment with best overall response of complete response (CR) or partial response (PR) according to RECIST version 1.0 based on local review. Confidence intervals were calculated based on the Exact Clopper-Pearson method.~ORR while on first-line treatment was assessed up to 24 months after the last patient's recruitment.~CR: disappearance of all target lesions PR: at least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters." (NCT01698918)
Timeframe: From the date of enrollment until discontinuation of first-line treatment, assessed up to approximately 3.8 years

Intervention	Percentage of participants (Number)
Everolimus+Letrozole (First Line Treatment)	45.0

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First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Mouth and Throat Soreness Limiting Swallowing, Drinking, Eating, Talking and Sleeping at the End of the First Stomatitis Episode

"The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The fourth item asked the participant to rate how much their mouth and throat soreness limited them in 1) swallowing, 2) drinking, 3) eating, 4) talking and 5) sleeping. For each activity, mouth and throat soreness scores ranged from 0 (not limited) to 4 (unable to do). Scores are presented as the shift from Day 1 of first stomatitis stomatitis value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first episode value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment.~Only participants who were randomized in the stomatitis sub-study were included in this analysis." (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	Swallowing (dexamethasone): From 0 (Day 1) to 0 (end of first stomatitis)	Swallowing (dexamethasone): From 1 (Day 1) to 0 (end of first stomatitis)	Swallowing (dexamethasone): From 1 (Day 1) to 1 (end of first stomatitis)	Swallowing (dexamethasone): From 2 (Day 1) to 0 (end of first stomatitis)	Swallowing (dexamethasone): From 2 (Day 1) to 2 (end of first stomatitis)	Swallowing (SoC): From 0 (Day 1) to 0 (end of first stomatitis)	Swallowing (SoC): From 1 (Day 1) to 2 (end of first stomatitis)	Swallowing (SoC): From 2 (Day 1) to 0 (end of first stomatitis)	Swallowing (SoC): From 2 (Day 1) to 1 (end of first stomatitis)	Swallowing (SoC): From 3 (Day 1) to 0 (end of first stomatitis)	Swallowing (SoC): From 3 (Day 1) to 1 (end of first stomatitis)	Swallowing (SoC): From missing value (Day 1) to missing value (end of first stomatitis)	Drinking (dexamethasone): From 0 (Day 1) to 0 (end of first stomatitis)	Drinking (dexamethasone): From 1 (Day 1) to 0 (end of first stomatitis)	Drinking (dexamethasone): From 1 (Day 1) to 1 (end of first stomatitis)	Drinking (dexamethasone): From 2 (Day 1) to 0 (end of first stomatitis)	Drinking (dexamethasone): From 2 (Day 1) to 2 (end of first stomatitis)	Drinking (SoC): From 0 (Day 1) to 0 (end of first stomatitis)	Drinking (SoC): From 0 (Day 1) to 1 (end of first stomatitis)	Drinking (SoC): From 2 (Day 1) to 0 (end of first stomatitis)	Drinking (SoC): From 2 (Day 1) to 1 (end of first stomatitis)	Drinking (SoC): From 3 (Day 1) to 0 (end of first stomatitis)	Drinking (SoC): From 3 (Day 1) to 1 (end of first stomatitis)	Drinking (SoC): From missing value (Day 1) to missing value (end of first stomatitis)	Eating (dexamethasone): From 0 (Day 1) to 0 (end of first stomatitis)	Eating (dexamethasone): From 1 (Day 1) to 0 (end of first stomatitis)	Eating (dexamethasone): From 1 (Day 1) to 1 (end of first stomatitis)	Eating (dexamethasone): From 2 (Day 1) to 0 (end of first stomatitis)	Eating (dexamethasone): From 2 (Day 1) to 1 (end of first stomatitis)	Eating (dexamethasone): From 2 (Day 1) to 2 (end of first stomatitis)	Eating (dexamethasone): From 3 (Day 1) to 1 (end of first stomatitis)	Eating (SoC): From 1 (Day 1) to 0 (end of first stomatitis)	Eating (SoC): From 1 (Day 1) to 1 (end of first stomatitis)	Eating (SoC): From 2 (Day 1) to 0 (end of first stomatitis)	Eating (SoC): From 3 (Day 1) to 0 (end of first stomatitis)	Eating (SoC): From 3 (Day 1) to 1 (end of first stomatitis)	Eating (SoC): From 3 (Day 1) to 2 (end of first stomatitis)	Eating (SoC): From 4 (Day 1) to 1 (end of first stomatitis)	Eating (SoC): From missing value (Day 1) to missing value (end of first stomatitis)	Talking (dexamethasone): From 0 (Day 1) to 0 (end of first stomatitis)	Talking (dexamethasone): From 1 (Day 1) to 0 (end of first stomatitis)	Talking (dexamethasone): From 2 (Day 1) to 0 (end of first stomatitis)	Talking (dexamethasone): From 2 (Day 1) to 1 (end of first stomatitis)	Talking (dexamethasone): From 2 (Day 1) to 2 (end of first stomatitis)	Talking (SoC): From 0 (Day 1) to 0 (end of first stomatitis)	Talking (SoC): From 0 (Day 1) to 1 (end of first stomatitis)	Talking (SoC): From 1 (Day 1) to 0 (end of first stomatitis)	Talking (SoC): From 2 (Day 1) to 0 (end of first stomatitis)	Talking (SoC): From 2 (Day 1) to 1 (end of first stomatitis)	Talking (SoC): From 3 (Day 1) to 0 (end of first stomatitis)	Talking (SoC): From 3 (Day 1) to 2 (end of first stomatitis)	Talking (SoC): From missing value (Day 1) to missing value (end of first stomatitis)	Sleeping (dexamethasone): From 0 (Day 1) to 0 (end of first stomatitis)	Sleeping (dexamethasone): From 1 (Day 1) to 0 (end of first stomatitis)	Sleeping (dexamethasone): From 2 (Day 1) to 0 (end of stomatitis)	Sleeping (dexamethasone): From 2 (Day 1) to 1 (end of first stomatitis)	Sleeping (dexamethasone): From 2 (Day 1) to 2 (end of first stomatitis)	Sleeping (SoC): From 0 (Day 1) to 0 (end of first stomatitis)	Sleeping (SoC): From 0 (Day 1) to 2 (end of first stomatitis)	Sleeping (SoC): From 1 (Day 1) to 1 (end of first stomatitis)	Sleeping (SoC): From 2 (Day 1) to 0 (end of first stomatitis)	Sleeping (SoC): From 3 (Day 1) to 0 (end of first stomatitis)	Sleeping (SoC): From 3 (Day 1) to 1 (end of first stomatitis)	Sleeping (SoC): From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First-line Treatment)	6	2	1	1	1	5	1	1	2	1	1	2	6	2	1	1	1	3	2	3	1	1	1	2	3	1	2	1	2	1	1	2	1	1	1	2	3	1	2	6	1	2	1	1	5	1	1	1	1	1	1	2	7	1	1	1	1	5	1	1	2	1	1	2

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First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Mouth Pain Severity Affecting Daily Activities at the End of the First Stomatitis Episode

"The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The sixth item asked the participant to rate their mouth pain severity affecting daily activities score from 0 (no effect on daily activities) to 10 (completely prevented from doing daily activities). The mouth pain severity affecting daily activities OSDQ scores are presented as the shift from Day 1 of first stomatitis episode value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first stomatitis value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment.~Only participants who were randomized in the stomatitis sub-study were included in this analysis." (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	Dexamethasone: From 0 (Day 1) to 0 (end of first stomatitis)	Dexamethasone: From 1 (Day 1) to 0 (end of first stomatitis)	Dexamethasone: From 2 (Day 1) to 0 (end of first stomatitis)	Dexamethasone: From 3 (Day 1) to 2 (end of first stomatitis)	Dexamethasone: From 5 (Day 1) to 3 (end of first stomatitis)	Dexamethasone: From 6 (Day 1) to 1 (end of first stomatitis)	SoC: From 0 (Day 1) to 0 (end of first stomatitis)	SoC: From 1 (Day 1) to 4 (end of first stomatitis)	SoC: From 2 (Day 1) to 2 (end of first stomatitis)	SoC: From 3 (Day 1) to 0 (end of first stomatitis)	SoC: From 3 (Day 1) to 1 (end of first stomatitis)	SoC: From 5 (Day 1) to 2 (end of first stomatitis)	SoC: From 5 (Day 1) to 5 (end of first stomatitis)	SoC: From 9 (Day 1) to 0 (end of first stomatitis)	SoC: From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First-line Treatment)	5	1	2	1	1	1	4	1	1	1	1	1	1	1	2

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First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Mouth Pain Severity at the End of the First Stomatitis Episode

"The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The fifth item asked the participant to rate their mouth pain severity from 0 (no pain) to 10 (unbearable pain). The mouth pain severity OSDQ scores are presented as the shift from Day 1 of first stomatitis episode value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first stomatitis value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment.~Only participants who were randomized in the stomatitis sub-study were included in this analysis." (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	Dexamethasone: From 0 (Day 1) to 0 (end of first stomatitis)	Dexamethasone: From 1 (Day 1) to 2 (end of first stomatitis)	Dexamethasone: From 2 (Day 1) to 0 (end of first stomatitis)	Dexamethasone: From 3 (Day 1) to 0 (end of first stomatitis)	Dexamethasone: From 3 (Day 1) to 1 (end of first stomatitis)	Dexamethasone: From 3 (Day 1) to 2 (end of first stomatitis)	Dexamethasone: From 5 (Day 1) to 2 (end of first stomatitis)	Dexamethasone: From 5 (Day 1) to 3 (end of first stomatitis)	Dexamethasone: From 7 (Day 1) to 1 (end of first stomatitis)	SoC: From 1 (Day 1) to 0 (end of first stomatitis)	SoC: From 1 (Day 1) to 1 (end of first stomatitis)	SoC: From 4 (Day 1) to 1 (end of first stomatitis)	SoC: From 5 (Day 1) to 5 (end of first stomatitis)	SoC: From 7 (Day 1) to 0 (end of first stomatitis)	SoC: From 8 (Day 1) to 2 (end of first stomatitis)	SoC: From 8 (Day 1) to 4 (end of first stomatitis)	SoC: From 8 (Day 1) to 6 (end of first stomatitis)	SoC: From 9 (Day 1) to 0 (end of first stomatitis)	SoC: From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First-line Treatment)	1	1	2	2	1	1	1	1	1	1	1	2	1	1	1	2	1	1	2

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First-line Treatment: Duration of First Stomatitis Based on OSDQ

The duration of the first stomatitis episode was calculated using the start and end date recorded in the OSDQ. The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis. The first item of the questionnaire asked the participants the date when they experienced the first symptoms of stomatitis. Start date of the first occurrence of stomatitis is defined as the first date ever recorded for this item in the questionnaire. Stop date of the first stomatitis episode is defined as the last date the OSDQ was completed for this episode. Participants were censored if they died before resolution of stomatitis, received a new anticancer therapy, discontinued the study treatment with no resolution of the stomatitis or the stomatitis event was still on-going at the cut-off. PROs were assessed up to 24 months after last patient's recruitment. (NCT01698918)
Timeframe: From start date of first stomatitis episode in first line until its resolution, assessed up to 3.8 years

Intervention	Weeks (Median)
Everolimus+Letrozole (First-line Treatment)	12.3

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First-line Treatment (Stomatitis Sub-study): Duration of First Stomatitis Based on OSDQ

The duration of the first stomatitis was calculated using the start and end date reported in the OSDQ. The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis. The first item asked the participants the date when they experienced the first symptoms of stomatitis. Start date of the first stomatitis is defined as the first date ever recorded for this item in the questionnaire. Stop date of the first stomatitis is defined as the last date the OSDQ was completed for this episode. Participants were censored if they died before resolution of stomatitis, received a new anticancer therapy, discontinued the study treatment with no resolution of the stomatitis or the stomatitis was still on-going at the cut-off. PROs were assessed up to 24 months after last patient's recruitment. Only participants who were randomized in the stomatitis sub-study were included in this analysis. (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Weeks (Median)
	Dexamethasone	Standard of Care
Everolimus+Letrozole (First-line Treatment)	NA	13.7

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First-line Treatment (Stomatitis Sub-study): Number of Participants With Shift of Response in OSDQ Score on Mouth and Throat Soreness at the End of the First Stomatitis Episode

"The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The third item asked the participant to rate their mouth and throat soreness from 0 (no soreness) to 4 (extreme soreness). The mouth and throat soreness OSDQ scores are presented as the shift from Day 1 of first stomatitis episode value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first stomatitis value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment.~Only participants who were randomized in the stomatitis sub-study were included in this analysis." (NCT01698918)
Timeframe: From start date of stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	Dexamethasone: From 0 (Day 1) to 0 (end of first stomatitis)	Dexamethasone: From 1 (Day 1) to 0 (end of first stomatitis)	Dexamethasone: From 1 (Day 1) to 1 (end of first stomatitis)	Dexamethasone: From 2 (Day 1) to 0 (end of first stomatitis)	Dexamethasone: From 2 (Day 1) to 1 (end of first stomatitis)	Dexamethasone: From 3 (Day 1) to 1 (end of first stomatitis)	SoC: From 1 (Day 1) to 0 (end of first stomatitis)	SoC: From 1 (Day 1) to 1 (end of first stomatitis)	SoC: From 2 (Day 1) to 1 (end of first stomatitis)	SoC: From 3 (Day 1) to 0 (end of first stomatitis)	SoC: From 3 (Day 1) to 1 (end of first stomatitis	SoC: From 3 (Day 1) to 2 (end of first stomatitis	SoC: From 4 (Day 1) to 1 (end of first stomatitis	SoC: From 4 (Day 1) to 2 (end of first stomatitis	SoC: From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First-line Treatment)	1	3	2	1	3	1	1	1	1	2	1	3	1	1	2

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First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Mouth and Throat Soreness Limiting Swallowing, Drinking, Eating, Talking and Sleeping at the End of the First Stomatitis Episode

The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The fourth item asked the participant to rate how much their mouth and throat soreness limited them in 1) swallowing, 2) drinking, 3) eating, 4) talking and 5) sleeping. For each activity, mouth and throat soreness scores ranged from 0 (not limited) to 4 (unable to do). Scores are presented as the shift from Day 1 of first stomatitis episode value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first stomatitis value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment. (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	Swallowing: From 0 (Day 1) to 0 (end of first stomatitis)	Swallowing: From 0 (Day 1) to 1 (end of first stomatitis)	Swallowing: From 0 (Day 1) to 2 (end of first stomatitis)	Swallowing: From 1 (Day 1) to 0 (end of first stomatitis)	Swallowing: From 1 (Day 1) to 1 (end of first stomatitis)	Swallowing: From 1 (Day 1) to 2 (end of first stomatitis)	Swallowing: From 1 (Day 1) to 3 (end of first stomatitis)	Swallowing: From 2 (Day 1) to 0 (end of first stomatitis)	Swallowing: From 2 (Day 1) to 1 (end of first stomatitis)	Swallowing: From 2 (Day 1) to 2 (end of first stomatitis)	Swallowing: From 3 (Day 1) to 0 (end of first stomatitis)	Swallowing: From 3 (Day 1) to 1 (end of first stomatitis)	Swallowing: From 3 (Day 1) to 3 (end of first stomatitis)	Swallowing: From missing value (Day 1) to missing value (end of first stomatitis)	Drinking: From 0 (Day 1) to 0 (end of first stomatitis)	Drinking: From 0 (Day 1) to 1 (end of first stomatitis)	Drinking: From 0 (Day 1) to 2 (end of first stomatitis)	Drinking: From 1 (Day 1) to 0 (end of first stomatitis)	Drinking: From 1 (Day 1) to 1 (end of first stomatitis)	Drinking: From 1 (Day 1) to 2 (end of first stomatitis)	Drinking: From 2 (Day 1) to 0 (end of first stomatitis)	Drinking: From 2 (Day 1) to 1 (end of first stomatitis)	Drinking: From 2 (Day 1) to 2 (end of first stomatitis)	Drinking: From 2 (Day 1) to 3 (end of first stomatitis)	Drinking: From 3 (Day 1) to 0 (end of first stomatitis)	Drinking: From 3 (Day 1) to 1 (end of first stomatitis)	Drinking: From 3 (Day 1) to 3 (end of first stomatitis)	Drinking: From missing value (Day 1) to missing value (end of first stomatitis)	Eating: From 0 (Day 1) to 0 (end of first stomatitis)	Eating: From 0 (Day 1) to 1 (end of first stomatitis)	Eating: From 0 (Day 1) to 2 (end of first stomatitis)	Eating: From 1 (Day 1) to 0 (end of first stomatitis)	Eating: From 1 (Day 1) to 1 (end of first stomatitis)	Eating: From 1 (Day 1) to 2 (end of first stomatitis)	Eating: From 2 (Day 1) to 0 (end of first stomatitis)	Eating: From 2 (Day 1) to 1 (end of first stomatitis)	Eating: From 2 (Day 1) to 2 (end of first stomatitis)	Eating: From 2 (Day 1) to 3 (end of first stomatitis)	Eating: From 3 (Day 1) to 0 (end of first stomatitis)	Eating: From 3 (Day 1) to 1 (end of first stomatitis)	Eating: From 3 (Day 1) to 2 (end of first stomatitis)	Eating: From 3 (Day 1) to 3 (end of first stomatitis)	Eating: From 4 (Day 1) to 1 (end of first stomatitis)	Eating: From missing value (Day 1) to missing value (end of first stomatitis)	Talking: From 0 (Day 1) to 0 (end of first stomatitis)	Talking: From 0 (Day 1) to 1 (end of first stomatitis)	Talking: From 1 (Day 1) to 0 (end of first stomatitis)	Talking: From 1 (Day 1) to 1 (end of first stomatitis)	Talking: From 2 (Day 1) to 0 (end of first stomatitis)	Talking: From 2 (Day 1) to 1 (end of first stomatitis)	Talking: From 2 (Day 1) to 2 (end of first stomatitis)	Talking: From 2 (Day 1) to 3 (end of first stomatitis)	Talking: From 3 (Day 1) to 0 (end of first stomatitis)	Talking: From 3 (Day 1) to 2 (end of first stomatitis)	Talking: From 3 (Day 1) to 3 (end of first stomatitis)	Talking: From missing value (Day 1) to missing value (end of first stomatitis)	Sleeping: From 0 (Day 1) to 0 (end of first stomatitis)	Sleeping: From 0 (Day 1) to 1 (end of first stomatitis)	Sleeping: From 0 (Day 1) to 2 (end of first stomatitis)	Sleeping: From 1 (Day 1) to 0 (end of first stomatitis)	Sleeping: From 1 (Day 1) to 1 (end of first stomatitis)	Sleeping: From 1 (Day 1) to 2 (end of first stomatitis)	Sleeping: From 2 (Day 1) to 0 (end of first stomatitis)	Sleeping: From 2 (Day 1) to 1 (end of first stomatitis)	Sleeping: From 2 (Day 1) to 2 (end of first stomatitis)	Sleeping: From 3 (Day 1) to 0 (end of first stomatitis)	Sleeping: From 3 (Day 1) to 1 (end of first stomatitis)	Sleeping: From 3 (Day 1) to 2 (end of first stomatitis)	Sleeping: From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First Line Treatment)	40	3	1	7	6	3	1	6	4	2	8	2	2	7	48	4	1	10	5	1	4	3	3	2	6	1	1	9	17	2	1	14	11	2	8	3	4	2	7	6	3	4	1	7	45	5	12	2	5	2	3	1	4	1	3	9	48	4	1	8	2	2	4	3	6	1	1	1	11

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First-line Treatment: Clinical Benefit Rate (CBR)

"CBR in first line is defined as the percentage of participants while on first-line treatment with best overall response of CR, PR or stable disease (SD) with a duration of 24 weeks or longer, according to RECIST version 1.0 based on local review. Confidence intervals (CI) were calculated based on the Exact Clopper-Pearson method.~CBR while on first-line treatment was assessed up to 24 months after the last patient's recruitment.~CR: disappearance of all target lesions PR: at least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters.~SD: Neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for progressive disease" (NCT01698918)
Timeframe: From the date of enrollment until first-line treatment discontinuation, assessed up to approximately 3.8 years

Intervention	Percentage of participants (Number)
Everolimus+Letrozole (First-line Treatment)	74.3

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All Collected Deaths

"On-treatment deaths in first line were collected from first dose of first-line treatment until the date of last administration of the first-line study treatment plus 28 days for participants not entering second-line or the minimum between the date of last administration of the first-line study treatment plus 28 days and the date of first administration of second-line study treatment minus one day for participants entering second line, up to 7.3 years. On-treatment deaths in second line were collected from first dose of second-line treatment to 28 days after the last administration of second-line treatment, up to 5.4 years.~Post-treatment survival follow-up deaths were collected from day 29 after last dose of study treatment to end of study, up to 7.3 years.~All deaths refer to the sum of on-treatment deaths and post-treatment deaths." (NCT01698918)
Timeframe: On-treatment deaths in first line: Up to 7.3 years. On-treatment deaths in second line: Up to 5.4 years. Post-treatment and all deaths: Up to 7.3 years

Intervention	Participants (Number)
	On -treatment deaths in first line	On-treatment deaths in second line	Post-treatment survival follow-up deaths	All deaths
Everolimus + Letrozole/Exemestane (First-line and Second-line Treatment)	11	2	49	62

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Second-line Treatment: Progression-free Survival (PFS)

"PFS in the second line setting is defined as the time interval between the start of the second-line treatment and documented disease progression based on local radiology review or death due to any cause reported during or after second-line treatment period. If a participant did not progress or was not known to have died at the date of the analysis cut-off or start of another antineoplastic therapy, the PFS date was censored to the date of last adequate tumor assessment prior to cut-off date or start of antineoplastic therapy. The median PFS was estimated and presented along with 95% confidence intervals.~PFS while on second-line treatment was assessed up to 24 months after the last patient's recruitment." (NCT01698918)
Timeframe: From the start of the second-line treatment until the date of first documented progression or death, assessed up to approximately 2.4 years

Intervention	Months (Median)
Everolimus+Exemestane (Second Line Treatment)	3.7

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First-line Treatment (Stomatitis Sub-study): Time to First Stomatitis Episode as Assessed by the OSDQ

"The time to first occurrence of stomatitis based on OSDQ is defined as time from first study treatment administration in the first line to start date of the first stomatitis episode recorded in the OSDQ. The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The first item asked the participants when they experienced the first symptoms of stomatitis. Start date of the first occurrence of stomatitis is defined as the first date ever recorded for this item in the questionnaire. PROs were assessed up to 24 months after last patient's recruitment.~Only participants who were randomized in the stomatitis sub-study were included in this analysis." (NCT01698918)
Timeframe: From first study treatment administration in the first line until first stomatitis episode, assessed up to approximately 3.8 years

Intervention	Weeks (Median)
	Dexamethasone	Standard of care
Everolimus+ Letrozole (First-line Treatment)	1.4	2.3

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First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Mouth and Throat Soreness at the End of the First Stomatitis Episode

The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The third item asked the participant to rate their mouth and throat soreness from 0 (no soreness) to 4 (extreme soreness). The mouth and throat soreness OSDQ scores are presented as the shift from Day 1 of first stomatitis episode value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first stomatitis value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment. (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	From 0 (Day 1) to 0 (end of first stomatitis)	From 1 (Day 1) to 0 (end of first stomatitis)	From 1 (Day 1) to 1 (end of first stomatitis)	From 1 (Day 1) to 2 (end of first stomatitis)	From 2 (Day 1) to 0 (end of first stomatitis)	From 2 (Day 1) to 1 (end of first stomatitis)	From 2 (Day 1) to 2 (end of first stomatitis)	From 2 (Day 1) to 3 (end of first stomatitis)	From 3 (Day 1) to 0 (end of first stomatitis)	From 3 (Day 1) to 1 (end of first stomatitis)	From 3 (Day 1) to 2 (end of first stomatitis)	From 3 (Day 1) to 3 (end of first stomatitis)	From 3 (Day 1) to 4 (end of first stomatitis)	From 4 (Day 1) to 1 (end of first stomatitis)	From 4 (Day 1) to 2 (end of first stomatitis)	From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First-line Treatment)	3	22	12	3	13	7	4	1	9	4	5	1	1	2	1	4

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First-line Treatment: Time to First Stomatitis Episode as Assessed by the Oral Stomatitis Daily Questionnaire (OSDQ)

The time to first occurrence of stomatitis based on OSDQ is defined as time from first-line treatment administration to start date of the stomatitis episode recorded in the OSDQ in the first line. The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The first item asked the participants when they experienced the first symptoms of stomatitis. Start date of the first occurrence of stomatitis is defined as the first date ever recorded for this item in the questionnaire. Patient reported outcomes (PROs) were assessed up to 24 months after last patient's recruitment. (NCT01698918)
Timeframe: From first-line treatment administration until first stomatitis episode in the first line, assessed up to approximately 3.8 years

Intervention	Weeks (Median)
Everolimus+Letrozole (First-line Treatment)	1.7

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First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Mouth Pain Severity Affecting Daily Activities at the End of the First Stomatitis Episode

The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The sixth item asked the participant to rate their mouth pain severity affecting daily activities score from 0 (no effect on daily activities) to 10 (completely prevented from doing daily activities). The mouth pain severity affecting daily activities OSDQ scores are presented as the shift from Day 1 of first stomatitis episode value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first stomatitis value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment. (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	From 0 (Day 1) to 0 (end of first stomatitis)	From 0 (Day 1) to 1 (end of first stomatitis)	From 0 (Day 1) to 5 (end of first stomatitis)	From 1 (Day 1) to 0 (end of first stomatitis)	From 1 (Day 1) to 1 (end of first stomatitis)	From 1 (Day 1) to 4 (end of first stomatitis)	From 2 (Day 1) to 0 (end of first stomatitis)	From 2 (Day 1) to 1 (end of first stomatitis)	From 2 (Day 1) to 2 (end of first stomatitis)	From 2 (Day 1) to 3 (end of first stomatitis)	From 2 (Day 1) to 4 (end of first stomatitis)	From 3 (Day 1) to 0 (end of first stomatitis)	From 3 (Day 1) to 1 (end of first stomatitis)	From 3 (Day 1) to 2 (end of first stomatitis)	From 3 (Day 1) to 3 (end of first stomatitis)	From 3 (Day 1) to 4 (end of first stomatitis)	From 4 (Day 1) to 0 (end of first stomatitis)	From 5 (Day 1) to 0 (end of first stomatitis)	From 5 (Day 1) to 1 (end of first stomatitis)	From 5 (Day 1) to 2 (end of first stomatitis)	From 5 (Day 1) to 3 (end of first stomatitis)	From 5 (Day 1) to 5 (end of first stomatitis)	From 5 (Day 1) to 6 (end of first stomatitis)	From 6 (Day 1) to 1 (end of first stomatitis)	From 6 (Day 1) to 5 (end of first stomatitis)	From 6 (Day 1) to 8 (end of first stomatitis)	From 7 (Day 1) to 0 (end of first stomatitis)	From 8 (Day 1) to 0 (end of first stomatitis)	From 8 (Day 1) to 8 (end of first stomatitis)	From 8 (Day 1) to 10 (end of first stomatitis)	From 9 (Day 1) to 0 (end of first stomatitis)	From 9 (Day 1) to 8 (end of first stomatitis)	From 10 (Day 1) to 10 (end of first stomatitis)	From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First-line Treatment)	33	1	1	7	4	2	6	1	3	1	1	3	3	1	1	1	2	2	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	4

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First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Mouth Pain Severity at the End of the First Stomatitis Episode

The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily until the resolution of the stomatitis episode. The fifth item asked the participant to rate their mouth pain severity from 0 (no pain) to 10 (unbearable pain). The mouth pain severity OSDQ scores are presented as the shift from Day 1 of first stomatitis episode value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first stomatitis value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment. (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	From 0 (Day 1) to 0 (end of first stomatitis)	From 1 (Day 1) to 0 (end of first stomatitis)	From 1 (Day 1) to 1 (end of first stomatitis)	From 1 (Day 1) to 2 (end of first stomatitis)	From 1 (Day 1) to 3 (end of first stomatitis)	From 1 (Day 1) to 5 (end of first stomatitis)	From 2 (Day 1) to 0 (end of first stomatitis)	From 2 (Day 1) to 3 (end of first stomatitis)	From 3 (Day 1) to 0 (end of first stomatitis)	From 3 (Day 1) to 1 (end of first stomatitis)	From 3 (Day 1) to 2 (end of first stomatitis)	From 3 (Day 1) to 3 (end of first stomatitis)	From 3 (Day 1) to 4 (end of first stomatitis)	From 4 (Day 1) to 0 (end of first stomatitis)	From 4 (Day 1) to 1 (end of first stomatitis)	From 4 (Day 1) to 4 (end of first stomatitis)	From 4 (Day 1) to 5 (end of first stomatitis)	From 5 (Day 1) to 0 (end of first stomatitis)	From 5 (Day 1) to 1 (end of first stomatitis)	From 5 (Day 1) to 2 (end of first stomatitis)	From 5 (Day 1) to 3 (end of first stomatitis)	From 5 (Day 1) to 4 (end of first stomatitis)	From 5 (Day 1) to 5 (end of first stomatitis)	From 5 (Day 1) to 6 (end of first stomatitis)	From 5 (Day 1) to 7 (end of first stomatitis)	From 5 (Day 1) to 10 (end of first stomatitis)	From 6 (Day 1) to 0 (end of first stomatitis)	From 6 (Day 1) to 1 (end of first stomatitis)	From 6 (Day 1) to 2 (end of first stomatitis)	From 6 (Day 1) to 5 (end of first stomatitis)	From 6 (Day 1) to 6 (end of first stomatitis)	From 6 (Day 1) to 8 (end of first stomatitis)	From 7 (Day 1) to 0 (end of first stomatitis)	From 7 (Day 1) to 1 (end of first stomatitis)	From 7 (Day 1) to 2 (end of first stomatitis)	From 7 (Day 1) to 7 (end of first stomatitis)	From 8 (Day 1) to 0 (end of first stomatitis)	From 8 (Day 1) to 2 (end of first stomatitis)	From 8 (Day 1) to 4 (end of first stomatitis)	From 8 (Day 1) to 5 (end of first stomatitis)	From 8 (Day 1) to 6 (end of first stomatitis)	From 8 (Day 1) to 9 (end of first stomatitis)	From 9 (Day 1) to 0 (end of first stomatitis)	From 9 (Day 1) to 9 (end of first stomatitis)	From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First-line Treatment)	5	10	6	1	1	1	6	1	7	1	2	1	2	4	2	1	1	3	1	1	1	1	1	1	1	1	2	1	1	1	1	1	2	2	1	1	3	1	2	1	1	1	2	1	4

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Second-line Treatment: Overall Response Rate (ORR)

"ORR in second line is defined as the percentage of participants receiving second-line study treatment with best overall response of complete response (CR) or partial response (PR) according to RECIST version 1.0 based on local review. Confidence intervals (CI) were calculated based on the Exact Clopper-Pearson method.~ORR while on second-line treatment was assessed up to 24 months after the last patient's recruitment.~CR: disappearance of all target lesions PR: at least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters" (NCT01698918)
Timeframe: From the start of the second-line treatment up to approximately 2.4 years

Intervention	Percentage of participants (Number)
Everolimus+Exemestane (Second-line Treatment)	6.0

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First-line Treatment: Number of Participants With Shift of Response in OSDQ Score on Overall Health at the End of the First Stomatitis Episode

The OSDQ is a patient self-administered 6-item questionnaire with a 24-hour recall period. Participants completed the questionnaire daily up to the resolution of the stomatitis episode. The second item asked the participant to rate their overall health from 0 (worst possible) to 10 (perfect health). The overall health OSDQ scores are presented as the shift from Day 1 of first stomatitis episode value to the value at the end of the first episode of stomatitis. Day 1 is defined as the first OSDQ questionnaire recorded. End of first stomatitis value is defined as the last OSDQ questionnaire of the first episode of stomatitis. PROs were assessed up to 24 months after last patient's recruitment. (NCT01698918)
Timeframe: From start date of first stomatitis episode until its resolution, assessed up to 3.8 years

Intervention	Participants (Count of Participants)
	From 0 (Day 1) to 0 (end of first stomatitis)	From 0 (Day 1) to 1 (end of first stomatitis)	From 0 (Day 1) to 5 (end of first stomatitis)	From 1 (Day 1) to 1 (end of first stomatitis)	From 1 (Day 1) to 2 (end of first stomatitis)	From 2 (Day 1) to 5 (end of first stomatitis)	From 2 (Day 1) to 8 (end of first stomatitis)	From 3 (Day 1) to 0 (end of first stomatitis)	From 3 (Day 1) to 3 (end of first stomatitis)	From 3 (Day 1) to 5 (end of first stomatitis)	From 3 (Day 1) to 10 (end of first stomatitis)	From 4 (Day 1) to 3 (end of first stomatitis)	From 4 (Day 1) to 5 (end of first stomatitis)	From 4 (Day 1) to 7 (end of first stomatitis)	From 4 (Day 1) to 8 (end of first stomatitis)	From 5 (Day 1) to 0 (end of first stomatitis)	From 5 (Day 1) to 3 (end of first stomatitis)	From 5 (Day 1) to 4 (end of first stomatitis)	From 5 (Day 1) to 5 (end of first stomatitis)	From 5 (Day 1) to 6 (end of first stomatitis)	From 5 (Day 1) to 7 (end of first stomatitis)	From 5 (Day 1) to 9 (end of first stomatitis)	From 5 (Day 1) to 10 (end of first stomatitis)	From 6 (Day 1) to 5 (end of first stomatitis)	From 6 (Day 1) to 6 (end of first stomatitis)	From 6 (Day 1) to 7 (end of first stomatitis)	From 6 (Day 1) to 9 (end of first stomatitis)	From 7 (Day 1) to 3 (end of first stomatitis)	From 7 (Day 1) to 4 (end of first stomatitis)	From 7 (Day 1) to 5 (end of first stomatitis)	From 7 (Day 1) to 7 (end of first stomatitis)	From 7 (Day 1) to 9 (end of first stomatitis)	From 8 (Day 1) to 1 (end of first stomatitis)	From 8 (Day 1) to 7 (end of first stomatitis)	From 8 (Day 1) to 8 (end of first stomatitis)	From 8 (Day 1) to 9 (end of first stomatitis)	From 8 (Day 1) to 10 (end of first stomatitis)	From 9 (Day 1) to 0 (end of first stomatitis)	From 9 (Day 1) to 4 (end of first stomatitis)	From 9 (Day 1) to 8 (end of first stomatitis)	From 9 (Day 1) to 9 (end of first stomatitis)	From 10 (Day 1) to 3 (end of first stomatitis)	From 10 (Day 1) to 9 (end of first stomatitis)	From missing value (Day 1) to missing value (end of first stomatitis)
Everolimus+Letrozole (First-line Treatment)	2	1	1	1	1	1	2	1	3	2	2	2	1	1	2	1	3	1	7	4	3	1	2	2	3	2	2	2	1	1	3	1	1	1	4	5	2	1	2	1	8	1	1	3

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Second-line Treatment: Clinical Benefit Rate (CBR)

"CBR in second line is defined as the percentage of participants receiving second-line study treatment with best overall response of CR, PR or stable disease (SD) with a duration of 24 weeks or longer, according to RECIST version 1.0 based on local review. Confidence intervals (CI) were calculated based on the Exact Clopper-Pearson method.~CBR while on second-line treatment was assessed up to 24 months after the last patient's recruitment.~CR: disappearance of all target lesions PR: at least a 30% decrease in the sum of the longest diameter of all target lesions, taking as reference the baseline sum of the longest diameters.~SD: Neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for progressive disease" (NCT01698918)
Timeframe: From the start of the second-line treatment up to approximately 2.4 years

Intervention	Percentage of participants (Number)
Everolimus+Exemestane (Second-line Treatment)	28.0

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Number of Participants With Clinical Benfit During Extension Phase

Number of participants with clinical benefit as judged by the investigator during the extension phase. The extension phase for up to 3 years for participants who were continuing to benefit from study treatment following the end of the core study phase (24 months after last patient's recruitment) was added in the amendment 5 (dated 14-Feb-2017). Results are presented by line of treatment (NCT01698918)
Timeframe: From the end of core phase (upon approval of amendment 5) up to approximately 3 years

Intervention	Participants (Count of Participants)
	Extension Week 1	Extension Week 12	Extension Week 24	Extension Week 36	Extension Week 48	Extension Week 60	Extension Week 72	Extension Week 84	Extension Week 96	Extension Week 108	Extension Week 120	Extension Week 132	Extension Week 144	Extension End of treatment
Everolimus+Exemestane (Second-line Treatment)	6	5	4	3	3	3	3	3	3	3	2	1	1	1
Everolimus+Letrozole (First-line Treatment)	34	30	28	23	20	18	16	13	12	12	11	10	8	11

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Overall Survival (OS)

"OS following first-line treatment with everolimus + letrozole is defined as the time from the date of receiving first line study treatment to date of death due to any cause (including first-line and second-line treatment periods). If a participant was not known to have died, survival was censored at the date of last contact.~OS following first-line treatment was assessed up to 24 months after last patient's recruitment." (NCT01698918)
Timeframe: From the date of enrollment to date of death, assessed up to approximately 3.8 years

Intervention	Months (Median)
Everolimus+Letrozole/Exemestane (First-line Treatment and Second-line Treatment)	NA

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Seizure Free Rates by Time Window

Percentage of seizure-free participants for each 12-week time window. (NCT01713946)
Timeframe: Weeks 18, 30, 42, 54, 66, 78, 90 & 102

Intervention	Percentage of seizure-free participants (Number)
	Week 18	Week 30	Week 42	Week 54	Week 66	Week 78	Week 90	Week 102
Everolimus Long Term Evaluation (LTE)	3.98	6.87	8.44	8.70	10.99	13.49	14.86	15.18

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Long Term Evaluation: Relationship Between Seizure Frequency and Time-normalized Everolimus Concentration at Trough (Cmin,TN) - Repeated Measures Analysis

A repeated measures analysis considering fixed 2-week intervals and including the level of exposure (time-normalized Cmin values), the time on-treatment and the seizure frequency at baseline quantified the estimated percentage change over 2 weeks in seizure frequency associated with a double exposure to everolimus, 15 days more on treatment and half the seizure frequency at baseline. A positive percentage change means a reduction in seizure frequency whereas a negative percentage change means an increase in seizure frequency. (NCT01713946)
Timeframe: During everolimus treatment from start of everolimus up to the end of the extension phase, an average of 1.7 year

Intervention	% change over 2-wk in seizures freq. (Mean)
	By doubling the time-normalized Cmin (log scale)	By reporting half the seizure freq. at baseline	By adding 12 weeks on treatmen
Everolimus Long Term Evaluation (LTE)	8.93	48.82	6.42

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Core Phase: Median Percentage Change From Baseline in Seizure Frequency by Time Normalized Minimum Concentration

Percentage change from baseline in average weekly seizure frequency during the maintenance period of the Core phase is calculated as follow: (SFcfb) = 100 × (SFB - SFM) ÷ SFB where SFB is the average weekly seizure frequency in the Baseline phase and SFM is the average weekly seizure frequency in the maintenance period of the Core phase. A positive percentage change from baseline (SFcfb) means a reduction in seizure frequency whereas a negative percentage change from baseline (SFcfb) means an increase in seizure frequency. (NCT01713946)
Timeframe: Baseline (8-week period before randomization), Week 7 to 18 (12-week maintenance period of the core phase)

Intervention	Percentage change (Median)
<3 ng/mL	20.55
3-7 ng/mL	35.56
>7-<9 ng/mL	39.72
9-15 ng/mL	47.69
>15 ng/mL	61.56

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Core Phase: Food & Drug Administration (FDA): Percentage Change From Baseline in Partial Onset-seizure Frequency

"Comparison of median percent change from baseline in weekly seizure frequency in the everolimus low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm during maintenance period of the core phase. Percentage change from baseline in average weekly seizure frequency during the maintenance period of the Core phase (SFcfb) = 100 × (SFB - SFM) ÷ SFB where:~SFB is the average weekly seizure frequency in the Baseline phase SFM is the average weekly seizure frequency in the maintenance period of the Core phase A positive percentage change from baseline (SFcfb) means a reduction in seizure frequency whereas a negative percentage change from baseline (SFcfb) means an increase in seizure frequency." (NCT01713946)
Timeframe: Baseline (8-week period before randomization), Week 7 to 18 (12-week maintenance period of the core phase)

Intervention	Percentage change from baseline (Median)
Everolimus LT Target of 3 to 7 ng/mL	29.29
Everolimus HT Target of 9 to 15 ng/mL	39.55
Placebo	14.86

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Core Phase: Percentage of Patients With at Least a 25% Reduction in Seizure Frequency

Comparison of percentage of patients with at least ≥ 25% reduction in seizure frequency in the everolimus low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm during maintenance period of the core phase. At least 25% reduction from baseline in partial-onset seizure frequency during maintenance period of the core phase. (NCT01713946)
Timeframe: Baseline (8-week period before randomization), Week 7 to 18 (12-week maintenance period of the core phase)

Intervention	Percentage of participants (Number)
Everolimus LT Target of 3 to 7 ng/mL	52.1
Everolimus HT Target of 9 to 15 ng/mL	70.0
Placebo	37.8

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Core Phase: Impact of Everolimus on Anti-epileptic Drugs (AEDs) Concentrations

Impact of everolimus on AED concentrations at trough. Pre-dose plasma samples to measure AED concentrations were measured at at Visits 1 (Screening), 2 (Baseline), 3, and 5. Effects of everolimus on the exposure of antiepileptic drugs was assessed by comparing the anti-epileptic drug concentrations at Visits 1 and 2 (AEDs alone) and at Visits 3 and 5 (AEDs plus everolimus). (NCT01713946)
Timeframe: Baseline, Weeks 1 & 3

Intervention	ng/mL (Geometric Mean)
Valporic Acid	0.962
Carbamazepine	1.108
Clobazam	1.093
N-desmethylclobazam	1.071
Topiramate	0.983
TRI477	1.086
TRI476	1.194
Clonazepam	1.065
Zonisamide	1.028
Phenobarbital	0.957
Phenytoin	1.020

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Percentage of Seizure-free Patients During the Maintenance Period of the Core Phase

Comparison of seizure freedom (100% reduction in seizure frequency) in the everolimus low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm during maintenance period of the core phase. Seizure free means a 100% reduction from baseline in partial-onset seizure frequency during maintenance period of the core phase. (NCT01713946)
Timeframe: Baseline (8-week period before randomization), Week 7 to 18 (12-week maintenance period of the core phase)

Intervention	Percentage of seizure-free participants (Number)
Everolimus LT Target of 3 to 7 ng/mL	5.1
Everolimus HT Target of 9 to 15 ng/mL	3.8
Placebo	0.8

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Core Phase: Change From Baseline in the Overall Vineland-II Adaptive Behavior Composite (ABC) Score

Comparison of adaptive functioning using the VABS-II composite score in the everolimus low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm. The Vineland II assesses an individual's development of personal independence & social responsibility. The questionnaire contains 433 items which assess 15 subdomains organized into the five domains of Communication, Daily Living Skills, Socialization, Motor Skills and Maladaptive Behavior. The overall Adaptive Behavior Composite (ABC) score is obtained by summing the standard scores of the first four domain scores for patients aged less than 7 years, or the first 3 domain scores for patients aged 7 or older (the Maladaptive Behavior domain is optional). The ABC standard score ranges from 20 to 160 with a mean of 100 and a standard deviation of 15. Higher scores correspond to improved adaptive level. Note that 2 questionnaires with ABC scores<20 (data issues) were included in this analysis. (NCT01713946)
Timeframe: Baseline, 18 weeks

Intervention	scores on a scale (Median)
	Baseline	End of Core Phase	Change from Baseline
Everolimus HT Target of 9 to 15 ng/mL	56.50	55.00	0.00
Everolimus LT Target of 3 to 7 ng/mL	58.00	54.00	-1.00
Placebo	55.00	55.00	0.00

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Long Term Evaluation: Incidence of Suicide Attempt, Suicidal Ideation or Behavior During Core Phase Per Columbia Suicide Severity Rating Scale (C-SSRS) Outcomes

The C-SSRS was completed at each visit. The table below presents the number of patients who reported at least one completed suicide, one suicide attempt, one preparatory action toward imminent suicidal behavior, one suicidal ideation and one self-injurious behavior without suicidal intent at any time point after starting everolimus. (NCT01713946)
Timeframe: During everolimus treatment from start of everolimus up to permanent discontinuation of everolimus, an average of 2.3 years

Intervention	Participants (Number)
	Completed suicide	Suicidal attempt	Prep. actions toward imminent suicidal behavior	Suicidal ideation	Self-injurious behavior without suicide intent
Everolimus Long Term Evaluation (LTE)	0	1	2	7	1

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Core Phase: Response Rate in Seizure Frequency by Time Normalized Minimum Concentration

Comparison of response rate in seizure frequency for 5 categories of time-normalized minimum concentration (Cmin, TN) (< 3 ng/mL; 3-7 ng/mL; >7-<9 ng/mL; 9-15 ng/mL; >15 ng/mL). Response rate is the percentage of patients with ≥ 50% reduction from baseline in average weekly partial-onset seizure frequency during the maintenance period of the Core phase. (NCT01713946)
Timeframe: Baseline (8-week period before randomization), Week 7 to 18 (12-week maintenance period of the core phase)

Intervention	Percentage of responders (Median)
<3 ng/mL	14.3
3-7 ng/mL	29.9
>7-<9 ng/mL	44.2
9-15 ng/mL	50.0
>15 ng/mL	50.0

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Core Phase: European Medicine Agency (EMA): Seizure Frequency Response Rate

Comparison of response rates in the everolimus low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm. Response means at least a 50% reduction from baseline in partial-onset seizure frequency during the maintenance period of the core phase. (NCT01713946)
Timeframe: Baseline (8-week period before randomization), Week 7 to 18 (12-week maintenance period of the core phase)

Intervention	Percentage of responders (Number)
Everolimus LT Target of 3 to 7 ng/mL	28.2
Everolimus HT Target of 9 to 15 ng/mL	40.0
Placebo	15.1

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Core Phase: Changes From Baseline in Number of Seizure-free Days

Comparison of seizure-free days relative to baseline in the everolimus low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm during maintenance period of the core phase (NCT01713946)
Timeframe: Baseline (8-week period before randomization), Week 7 to 18 (12-week maintenance period of the core phase)

Intervention	Number of seizure-free days -per 28 days (Median)
Everolimus LT Target of 3 to 7 ng/mL	2.00
Everolimus HT Target of 9 to 15 ng/mL	4.01
Placebo	0.47

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Core Phase: Change From Baseline in the QOLIE-31-P Overall Quality-of-life Score for Patients Aged >=18 Years

Comparison of quality of life (from 3 age specific questionnaires) in the everolimus low-trough treatment arm (3-7 ng/mL), hightrough treatment arm (9-15 ng/mL) and placebo arm at the end of the core phase. The Quality of Life in Epilepsy Inventory-31-Problems (QOLIE-31-P) is a survey of health-related quality of life for adults with epilepsy. The QOLIE-31-P is completed by the patient. It contains 39 items, of which a total of 30 are used to make up 7 different subscales. Scores range from 0-100, with higher scores indicating a greater level of functioning and QoL. The overall quality of life score is obtained by summing a linear combination of the 7 subscale scores, where each subscale is multiplied by a relative weight that is obtained from the patient's answer to 7 items of this questionnaire. (NCT01713946)
Timeframe: Baseline, Week 18

Intervention	scores on a scale (Median)
	Baseline	End of Core Phase	Change from Baseline
Everolimus HT Target of 9 to 15 ng/mL	43.2	37.1	0.4
Everolimus LT Target of 3 to 7 ng/mL	39.5	48.6	-0.5
Placebo	43.6	54.8	5.3

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Long Term Evaluation: Effect of Everolimus Over Time in the Overall Wechsler Nonverbal Composite Score

The brief version of the WNV consists of a 2-subtest battery: only Matrices and Recognition subtests for patients under 8, and Matrices and Spatial Span subtests for patients aged 8 to 21. Based on the raw scores obtained from the subtests, standardized z-scores were calculated for each subtest using the following formula: Zscore = (X - b)/Sb where X is the raw score of the subtest, b and Sb represent the mean and standard deviation respectively of the subtest score recorded at baseline for the study population. The composite WNV score was computed by summing up the Z-scores of the 3 subtests of the WNV (i.e. matrices, recognition, and coding for patients aged <8 years and matrices, spatial span, and coding for patients aged 8 to 21 years). The composite WNV score has no range (NCT01713946)
Timeframe: Baseline, Weeks 18, 42, 66 and 90

Intervention	scores on a scale (Median)
	Baseline	Week 18	Week 42	Week 66	Week 90
Everolimus Long Term Evaluation (LTE)	-0.53	-0.44	-0.36	0.13	-0.06

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Long Term Evaluation: Effect of Everolimus Over Time in the Overall Vineland-II Adaptive Behavior Composite (ABC) Score

Intervention	scores on a scale (Median)
	Baseline	Week 18	Week 42	Week 66	Week 90
Everolimus Long Term Evaluation (LTE)	56.00	53.50	55.50	57.00	49.50

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Core Phase: Probability That a Patient Remains On-treatment up to a Specified Time Point

"Comparison of time to treatment discontinuation in the everolimus low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm during the core phase. Treatment duration is defined as the time from randomization until the date of permanent study treatment discontinuation (for any reason) at any time during the Core phase.~The percentage event-free probability estimate is the estimated probability that a patient will remain on-treatment up to a specified time point (Week 6, 12, 18)" (NCT01713946)
Timeframe: Week 6, Week 12, Week 18

Intervention	Percentage event-free prob. estimates (Number)
	Week 6	Week 12	Week 18
Everolimus HT Target of 9 to 15 ng/mL	96.2	95.4	71.5
Everolimus LT Target of 3 to 7 ng/mL	97.4	95.7	70.1
Placebo	99.2	97.5	75.6

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Core Phase: Incidence of Suicide Attempt, Suicidal Ideation or Behavior During Core Phase Per Columbia Suicide Severity Rating Scale (C-SSRS) Outcomes

"Comparison of suicidality using the C-SSRS in the everolimus low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm. The Columbia-Suicide Severity Rating Scale (C-SSRS) is a questionnaire used for suicide assessment developed by multiple institutions, including Columbia University, with NIMH support. The scale is evidence-supported and is part of a national and international public health initiative involving the assessment of suicidality. There are different scoring systems depending on the population. The important elements to note are that the higher the scores on the individual items and the more yes items, the higher the suicide risk." (NCT01713946)
Timeframe: Baseline, Week 18

Intervention	Participants (Number)
	Completed suicide	Suicide attempt	Prep actions toward imminent suicidal behavior	Suicidal ideation	Self-injurious behavior without suicide intent
Everolimus HT Target of 9 to 15 ng/mL	0	0	0	1	0
Everolimus LT Target of 3 to 7 ng/mL	0	1	2	3	0
Placebo	0	0	0	0	0

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Core Phase: Distribution of Reduction From Baseline in Seizure Frequency

Comparison of percentage of patients in six categories of seizure reduction from baseline (≤ -25% (exacerbation); > -25% to < 25% (no change); ≥ 25% to < 50%; ≥ 50% to < 75%; ≥ 75% to < 100%; 100% (seizure-freedom)) in the everolimus low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm during maintenance period of the core phase (NCT01713946)
Timeframe: Baseline (8-week period before randomization), Week 7 to 18 (12-week maintenance period of the core phase)

Intervention	Percentage of participants (Number)
	100% (seizure free)	≥ 75 to <100 (75% responder)	≥ 50 to <75 (50% responder)	≥ 25 to <50 (25% responder)	>-25 to <25 (No change)	≤ -25 (Exacerbation)	Missing (missing)
Everolimus HT Target of 9 to 15 ng/mL	3.8	15.4	20.8	30.0	18.5	11.5	0.0
Everolimus LT Target of 3 to 7 ng/mL	5.1	6.0	17.1	23.9	35.0	12.8	0.0
Placebo	0.8	5.0	9.2	22.7	41.2	20.2	0.8

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Core Phase: Change From Baseline in the QOLIE-AD-48 Overall Quality-of-life Score for Patients >=11 to 18 Years

Comparison of quality of life (from 3 age specific questionnaires) in the everolimus low-trough treatment arm (3-7 ng/mL), hightrough treatment arm (9-15 ng/mL) and placebo arm at the end of the core phase. The Quality of Life in Epilepsy Inventory for Adolescents-48 (QOLIE-AD-48) is a survey of health-related quality of life for adolescents 11 to 18 years of age with epilepsy. The QOLIE-AD-48 is completed by the patient. It contains 48 items which assess 8 subscales. Scores range from 0-100, with higher scores corresponding to improved QoL. The overall quality of life score is obtained by summing a linear combination of the 8 subscale scores, where each subscale is multiplied by a relative weight that is provided in the original publication. (NCT01713946)
Timeframe: Baseline, Week 18

Intervention	scores on a scale (Median)
	Baseline	End of Core Phase	Change from Baseline
Everolimus HT Target of 9 to 15 ng/mL	58.8	60.7	5.8
Everolimus LT Target of 3 to 7 ng/mL	56.1	58.5	4.7
Placebo	59.6	65.4	7.2

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Core Phase: Change From Baseline in Wechsler Nonverbal Composite Score

Intervention	scores on a scale (Median)
	Baseline	End of Core Phase	Change from Baseline
Everolimus HT Target of 9 to 15 ng/mL	-0.69	-0.89	0.00
Everolimus LT Target of 3 to 7 ng/mL	-0.48	-0.04	0.00
Placebo	-1.11	-0.51	0.00

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Long Term Evaluation: Percentage Change From Start of Everolimus in Seizure Frequency by Time Window

"Percentage change from start of everolimus in average weekly seizure frequency (SFcfe) = 100 × (SFe - SFtw) ÷ SFe where:~SFe is the average weekly seizure frequency in the 8-week period before start of everolimus SFtw is the average weekly seizure frequency in a 12-week time window A positive percentage change from start of everolimus (SFcfe) means a reduction in seizure frequency whereas a negative percentage change from start of everolimus (SFcfe) means an increase in seizure frequency." (NCT01713946)
Timeframe: Baseline (8-week period before start of everolimus), Week 7 to 18, Week 19 to 30, and 12 weeks thereafter up to Week 102

Intervention	Percent change (Median)
	Week 18	Week 30	Week 42	Week 54	Week 66	Week 78	Week 90	Week 102
Everolimus Long Term Evaluation (LTE)	31.65	35.74	42.86	46.05	49.07	51.69	57.33	59.69

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Core Phase: Change From Baseline in the QOLCE Overall Quality-of-life Score for Patients <11 Years

Comparison of quality of life in the everolimus (from 3 age specific questionnaires) low-trough treatment arm (3-7 ng/mL), high-trough treatment arm (9-15 ng/mL) and placebo arm at the end of the core phase. The Quality of Life Childhood Epilepsy (QOLCE) questionnaire, used for patients < 11 years at baseline, was completed by the patient's parent or caregiver. It consists of 16 subscales (13 multi-item scales and 3 single item scales) and one overall quality-of-life score. Scores range from 0-100, with higher scores corresponding to improved QoL. The Overall Quality of Life Score is computed by adding each subscale score for each individual and then dividing by 16. (NCT01713946)
Timeframe: Baseline, Week 18

Intervention	scores on a scale (Median)
	Baseline	End of Core Phase	Change from Baseline
Everolimus HT Target of 9 to 15 ng/mL	56.5	59.5	0.0
Everolimus LT Target of 3 to 7 ng/mL	52.3	53.6	0.2
Placebo	55.3	57.2	1.0

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Percentage of Participants With Progression Free Survival at 6 Months

Response was be determined by bi-dimensional diameters. RECIST criteria will be collected and used for secondary evaluation. Patients will have brain MRI scans with and without gadolinium performed prior to therapy, after every second course in the first year, after every third course in the second year, and at the End of Study visit (if not done within prior 3 months). Spine MRIs should be performed prior to therapy and at the same time points as standard brain MRIs if clinically indicated. (NCT01734512)
Timeframe: Up to 6 months

Intervention	percentage (Number)
Everolimus	67

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Overall Survival (OS) Events (Number of Deaths) - FAS

Overall survival (OS) is defined as the time from date of start of treatment to date of death due to any cause. If a patient is not known to have died, survival will be censored at the date of last contact. Time to median OS was not estimable. (NCT01743560)
Timeframe: Start of treatment to the date of death up to approximately 48 weeks

Intervention	Number of events (Number)
	Deaths	Number of censored observations
Everolimus and Exemestane	8	41

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Overall Survival (OS) - % Event-free Probability Estimate - FAS

Overall survival (OS) is defined as the time from date of start of treatment to date of death due to any cause. If a patient is not known to have died, survival will be censored at the date of last contact. (NCT01743560)
Timeframe: Start of treatment to the date of death up to approximately 48 weeks

Intervention	Percentage of participants (Number)
	Event free at 12 weeks	Event free at 24 weeks	Event free at 36 weeks	Event free at 48 weeks
Everolimus and Exemestane	93.3	83.9	74.2	74.2

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Change From Baseline EORTC Quality of Life Questionnaire of Cancer Patients QLQ-C30 at Each Time Point

The QLQ-C30 is composed of multi-item scales and single-item measures including 5 functional scales, 3 symptom scales, a global health status-QoL scale, and 6 single items. Each of the multi-item scales includes a different set of items - no item occurs in more than 1 scale. High scale score=higher response level; a high score for a functional scale=a healthy level of function, high score for the global health status/QoL=high quality of life but a high score for a symptom scale / item=high level of symptomatology/problems. The principle for scoring these scales: 1.) Estimate the average of the items that contribute to the scale = raw score. 2.) Linear transformation to standardize the raw score, so that scores range from 0 to 100. Results should be interpreted with caution as the numbers of patients with available data over time were limited, and because of high variances as evidenced by large standard deviations (NCT01743560)
Timeframe: Baseline 12,24,36,48 weeks

,,,

Intervention	scores (Mean)
	Global health status/QoL	Physical functioning	Role functioning	Emotional functioning	Cognitive functioning	Social functioning	Fatigue	Nausea/ vomiting	Pain	Dyspnea	Insomnia	Appetite loss	Constipation	Diarrhea	Financial problems
Week 12	-9.0	-5.1	-4.5	2.6	-8.6	-9.9	8.6	-1.2	1.2	18.5	3.7	30.9	4.9	4.9	-1.2
Week 24	-3.6	-1.0	3.1	-3.1	-5.2	-9.4	9.5	2.9	3.9	8.3	2.0	23.5	11.8	8.3	-10.4
Week 36	1.9	4.9	8.3	7.5	1.3	3.8	0.9	-3.8	-1.3	2.6	0	12.8	10.3	-5.1	-10.3
Week 48	-8.3	-10.8	-12.3	0.6	-3.7	-14.7	7.3	-2.4	0.6	10.7	-3.6	16.7	8.3	7.4	-2.6

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Progression-free Survival (PFS) - % Event-free Probability Estimate - FAS

Progression-free survival (PFS) is the time from date of start of treatment to the date of event defined as the first documented progression or death due to any cause. If a patient has not had an event, progression-free survival is censored at the date of last adequate tumor assessment. Tumor assessment and response was evaluated according to RECIST v1.1Response was assessed by local radiology review. The PFS was analyzed using the Kaplan Meier method. (NCT01743560)
Timeframe: Start of treatment to the date of event defined as first documented progression due to any cause up to approximately 48 weeks

Intervention	Percentage of participants (Number)
	Event free at 12 weeks	Event free at 24 weeks	Event free at 36 weeks	Event free at 48 weeks
Everolimus and Exemestane	67.9	49.1	28.9	18.4

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Progression-free Survival (PFS) Events as Per Investigators - FAS

Progression-free survival (PFS) is the time from date of start of treatment to the date of event defined as the first documented progression or death due to any cause. If a patient has not had an event, progression-free survival is censored at the date of last adequate tumor assessment. Tumor assessment and response was evaluated according to RECIST v1.1Response was assessed by local radiology review. (NCT01743560)
Timeframe: Start of treatment to the date of event defined as first documented progression due to any cause up to approximately 48 weeks

Intervention	Number of events (Number)
	Deaths	Progression of disease	Number of censored observations
Everolimus and Exemestane	8	25	16

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Change From Baseline in EuroQoL 5-dimension Visual Analogue Scores - FAS

EuroQoL Quality of Life Scale (EQ-5D) is a standardized instrument to assess health state values. The EQ-5D essentially consists of 2 pages: the EQ-5D descriptive system and the EQ visual analogue scale (VAS). For the visual analogue scale, participants draw a line from a box to the point on the thermometer-like scale corresponding to their health state, 0-100 (100 = Best health state). Weights are used to score the responses to the 5 domains, with scores ranging from 0 to 1 (where a score of 1 represents a perfect state). Scores for the visual analogue scale reflect the position where participant's line crosses the thermometer-like scale. Results should be interpreted with caution as the numbers of patients with available data over time were limited, and because of high variances as evidenced by large standard deviations (NCT01743560)
Timeframe: Baseline 12,24,36,48 weeks

Intervention	units on a scale (Mean)
Week 12	-7.9
Week 24	-6.1
Week 36	-6.3
Week 48	-11.6

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Overall Response Rate of Everolimus and Exemestane Treatment in Postmenopausal Women With Hormone Receptor Positive Locally Advanced or Metastatic Breast Cancer

The Overall Response Rate (ORR) was defined as the proportion of patients with a best OR of confirmed CR or PR by week 48. Treatment success is defined as: The best Overall Response (OR) for each patient is determined from the sequence of investigator overall lesion responses according to Response Evaluation Criteria in Solid Tumors (RECIST 1.1.). To be assigned a best OR of Complete Responese (CR) at least two determinations of CR at least 4 weeks apart before progression are required. To be assigned a best OR of Partial Response (PR) at least two determinations of PR or better at least 4 weeks apart before progression (and not qualifying for a CR) are required. (NCT01743560)
Timeframe: At 48 weeks

Intervention	Percentage of participants (Number)
Everolimus and Exemestane	14.3

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Progression-free Survival (PFS) by Median Time in Weeks as Per Investigators - FAS

Progression-free survival (PFS) is the time from date of start of treatment to the date of event defined as the first documented progression or death due to any cause. If a patient has not had an event, progression-free survival is censored at the date of last adequate tumor assessment. Tumor assessment and response was evaluated according to RECIST v1.1Response was assessed by local radiology review. (NCT01743560)
Timeframe: Start of treatment to the date of event defined as first documented progression due to any cause up to approximately 48 weeks

Intervention	weeks (Median)
Everolimus and Exemestane	23.6

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Percentage of Patient Responses in EuroQoL 5-dimension Questionnaire - FAS

EuroQoL Quality of Life Scale (EQ-5D) is a standardized instrument to assess health state values is a standardized instrument to assess health state values. The EQ-5D essentially consists of 2 pages: the EQ-5D descriptive system and the EQ visual analogue scale (VAS). The EQ-5D descriptive system is comprised of the following 5 dimensions: mobility, self-care, usual activities, pain/discomfort, and anxiety/depression. Each dimension has 5 levels: no problems, slight problems, moderate problems, severe problems and extreme problems. Percentage of participants' responses were presented by visits. Results should be interpreted with caution as the numbers of patients with available data over time were limited. (NCT01743560)
Timeframe: Baseline 12,24,36,48 weeks

,,,,

Intervention	Percentage of participants (Number)
	Mobility-no problem	Mobility-slight problem	Mobility-moderate problem	Mobility-severe problem	Mobility-unable to walk	Self-care - no problem	Self-care - slight problem	Self-care - moderate problem	Self-care -severe problem	Self-care - unable	Usual activities - no problems	Usual activities - slight problems	Usual activities - moderate problems	Usual activities - severe problems	Usual activities -unable to do	Pain/discomfort - none	Pain/discomfort - slight	Pain/discomfort - moderate	Pain/discomfort - severe	Pain/discomfort - extreme	Anxiety/depression - none	Anxiety/depression - slight	Anxiety/depression - moderate	Anxiety/depression - severe	Anxiety/depression - extreme
Day 1	38.8	18.4	32.7	6.1	0	69.4	18.4	6.1	2.0	0	30.6	22.4	28.6	10.2	4.1	20.4	30.6	40.8	4.1	0	44.9	34.7	16.3	0	0
Week 12	20.4	14.3	20.4	2.0	0	44.9	4.1	8.2	0	0	14.3	16.3	22.4	4.1	0	14.3	16.3	22.4	4.1	0	22.4	22.4	12.2	0	0
Week 24	18.4	10.2	8.2	0	0	34.7	0	2.0	0	0	22.4	2.0	12.2	0	0	10.2	18.4	8.2	0	0	18.4	12.2	6.1	0	0
Week 36	14.3	8.2	2.0	2.0	0	24.5	0	2.0	0	0	14.3	8.2	2.0	2.0	0	12.2	8.2	6.1	0	0	16.3	10.2	0	0	0
Week 48	16.3	16.3	14.3	6.1	4.1	40.8	10.2	4.1	2.0	0	18.4	14.3	12.2	6.1	6.1	18.4	20.4	14.3	4.1	0	22.4	20.4	8.2	6.1	0

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Best Overall Response of Everolimus and Exemestane Treatment in Postmenopausal Women With Hormone Receptor Positive Locally Advanced or Metastatic Breast Cancer

The best Overall Response (OR) for each patient is determined from the sequence of investigator overall lesion responses according to Response Evaluation Criteria in Solid Tumors (RECIST 1.1.). To be assigned a best OR of Complete Responese (CR) at least two determinations of CR at least 4 weeks apart before progression are required. To be assigned a best OR of Partial Response (PR) at least two determinations of PR or better at least 4 weeks apart before progression (and not qualifying for a CR) are required.The Overall Response Rate (ORR) was defined as the proportion of patients with a best OR of confirmed CR or PR by week 48. (NCT01743560)
Timeframe: At 48 weeks

Intervention	participants (Number)
	Patients with measurable disease at baseline	Patients with non-measurable disease at baseline	Best at WK 48 - Complete Response (CR)	Best at WK 48 - Partial Response (PR)	Best at WK 48 - Stable Disease (SD)	Best at WK 48 - Progressive Disease (PD)	Unknown	Missing
Everolimus and Exemestane	39	10	0	7	18	15	1	8

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Mean Change in Treatment Satisfaction Questionnaire for Medication (TSQM) Between Week 3 and 12

TSQM was used to measure the Patients' self-reported satisfaction or dissatisfaction with the study treatment. The differences in mean scale scores between weeks 3 and 12 comparing treatment satisfaction in the different treatment arms: everolimus + exemestane combination therapy versus everolimus monotherapy, and everolimus + exemestane combination therapy versus capecitabine monotherapy. The TSQM version 1.4 domain scores range from 0 to 100 with higher scores representing a higher satisfaction on that domain. (NCT01783444)
Timeframe: Week 3, Week 12

Intervention	Unit on a scale (Mean)
	Side-effects	Effectiveness	Convenience	Global satisfaction
Capecitabine 1250 mg/m2	-2.6	1.2	0.5	2.3
Everolimus 10 mg	-9.1	1.2	1.0	1.8
Everolimus 10 mg + Exemestane 25 mg	-4.8	-2.2	-0.6	-1.0

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Time to Eastern Cooperative Oncology Group (ECOG) Performance Deterioration

The Eastern Cooperative Oncology Group (ECOG) Performance Status is a scale used to assess physical health of subjects,ranging from 0 (most active) to 5 (least active). Definitive deterioration is defined as no improvement in the ECOG status following observation of the deterioration. (NCT01783444)
Timeframe: Baseline, every 6 weeks up to about 43 months

Intervention	Weeks (Median)
Everolimus 10 mg + Exemestane 25 mg	72.57
Everolimus 10 mg	126.57
Capecitabine 1250 mg/m2	120.00

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Time to 10% Definitive Deterioration in the Global Health Status / Quality of Life

The global health status/QoL scale score of the QLQ-C30 is identified as the primary PRO variable of interest. Physical Functioning (PF), Emotional Functioning (EF) and Social Functioning (SF) scale scores of the QLQ-C30. The time to definitive 10% deterioration is the number of days between the date of randomization and the date of the assessment at which definitive deterioration is seen. Definitive 10% (5-point) deterioration is defined as a decrease in score by at least 10% (5-points) compared to baseline, with no later increase above this threshold observed during the course of the study. (NCT01783444)
Timeframe: Baseline, every 6 weeks up to about 43 months

Intervention	Weeks (Median)
Everolimus 10 mg + Exemestane 25 mg	30.86
Everolimus 10 mg	23.86
Capecitabine 1250 mg/m2	61.29

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Progression Free Survival (PFS) - Everolimus Plus Exemestane Versus Capecitabine Alone

Progression Free Survival (PFS) is defined as the time from date of randomization to the date of first radiologically documented progression or death due to any cause. If a patient did not have an event, PFS was censored at the date of the last adequate tumor assessment. PFS was compared between the everolimus + exemestane combination therapy with the everolimus monotherapy. (NCT01783444)
Timeframe: Date of randomization to the date of first documented tumor progression or death from any cause, whichever occurs first, reported between day of first patient randomized up to 39 months

Intervention	Months (Median)
Everolimus 10 mg + Exemestane 25 mg	8.41
Capecitabine 1250 mg/m2	9.59

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Progression Free Survival (PFS) - Everolimus Plus Exemestane Versus Everolimus Alone

Intervention	Months (Median)
Everolimus 10 mg + Exemestane 25 mg	8.41
Everolimus 10 mg	6.77

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Clinical Benefit Rate (CBR)

Clinical Benefit Rate (CBR) is defined as the proportion of participants with a best overall response of complete response (CR) or partial response (PR) or stable disease (SD) or Non-CR/non-PD lasting more than 24 weeks based on local investigator's assessment according to RECIST 1.1. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR, Stable disease (SD), neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for PD; CBR = CR+PR+SD. Only descriptive statistics. (NCT01783444)
Timeframe: From the date of randomization until the date of the first documented disease progression or date of death from any cause whichever came first, assessed for approximately 43 months

Intervention	Percentage of Participants (Number)
Everolimus 10 mg + Exemestane 25 mg	59
Everolimus 10 mg	43
Capecitabine 1250 mg/m2	53

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Overall Response Rate (ORR)

Overall Response Rate (ORR) as the proportion of patients whose best overall response is either complete response (CR) or partial response (PR) according to RECIST 1.1 This was assessed in the full patient population. Complete response is achieved when all lesions evaluated at baseline are absent at subsequent visit. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. Only descriptive statistics. (NCT01783444)
Timeframe: From the date of randomization until the date of the first documented disease progression or date of death from any cause whichever came first, assessed for approximately 43 months

Intervention	Percentage of Participants (Number)
Everolimus 10 mg + Exemestane 25 mg	21
Everolimus 10 mg	12
Capecitabine 1250 mg/m2	23

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All Collected Deaths

"On treatment deaths were collected from FPFT up to 30 days after study drug discontinuation, for a maximum duration of 224 weeks (treatment duration ranged from 1.3 to 220.0 weeks).~Deaths post treatment survival follow up were collected after the on- treatment period, up to approximately 5 years. Patients who didn't die during the on-treatment period and had not stopped study participation at the time of data cut-off (end of study) were censored." (NCT01783444)
Timeframe: up to 224 weeks (on-treatment), up to approximately 5 years (study duration)

Intervention	Participants (Count of Participants)
	On-treatment deaths	Post-treatment deaths	All deaths
Capecitabine 1250 mg/m2	2	57	59
Everolimus 10 mg	5	55	60
Everolimus 10 mg + Exemestane 25 mg	9	62	71

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Overall Survival (OS)

Overall Survival (OS) is defined as the time from date of randomization to date of death due to any cause. If a patient was not known to have died by the date of analysis cut-off, OS was censored at the date of last known date patient alive. (NCT01783444)
Timeframe: Every 3 months following end of treatment visit, assessed for approximately 54 months

Intervention	Months (Median)
Everolimus 10 mg + Exemestane 25 mg	23.06
Everolimus 10 mg	29.27
Capecitabine 1250 mg/m2	25.56

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Disease Stabilization Rate - Phase II

"Disease stabilization rate is defined as the proportion of patients achieving a best overall response of complete response, partial response, or stable disease.~Complete Response (CR): Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~Partial Response (PR): At least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters.~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. Persistence of one or more non-target lesion(s) and/or maintenance of tumor marker level above the normal limits." (NCT01784861)
Timeframe: Through completion of treatment (estimated to be 12 months)

Intervention	Participants (Count of Participants)
Phase II: X-82 + Everolimus	1

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Progression Free Survival (PFS) - Phase II

"PFS is defined as the duration of time from start of treatment to time of progression or death, whichever occurs first.~Progressive Disease (PD): 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. Appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions. Unequivocal progression should not normally trump target lesion status. It must be representative of overall disease status change, not a single lesion increase." (NCT01784861)
Timeframe: Up to 3 years

Intervention	days (Median)
Phase II: X-82 + Everolimus	183

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Recommended Phase II Dose of X-82

(NCT01784861)
Timeframe: Completion of 1st cycle for all patients in Phase I portion of study (completed in approximately 20 months)

Intervention	mg (Number)
Phase I All Dose Levels: X-82 + Everolimus	300

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Number of Participants With Toxicity - Phase II

Toxicity will be graded by NCI Common Terminology Criteria for Adverse Events (CTCAE version 4.0) (NCT01784861)
Timeframe: Through 30 days after completion of treatment (estimated to be 13 months)

Intervention	Participants (Count of Participants)
	Diarrhea	Mucositis oral	Nausea	Vomiting	Chest pain	Edema limbs	Hematoma	Mouth sores	Creatinine increased	Platelet count decreased	Hip pain	Leg cramps	Dizziness	Headache	Allergic rhinitis	Rash acneiform	Rash maculo-papular	Hypertension
Phase II: X-82 + Everolimus	2	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1	1

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Overall Toxicities - Phase I

-Toxicities will be graded by the NCI Common Terminology Criteria for Adverse Events (CTCAE version 4.0) (NCT01784861)
Timeframe: 30 days after completion of treatment (estimated to be 13 months)

,,,,

Intervention	Participants (Count of Participants)
	Anemia	Hearing impaired	Peripheral vision/depth perception impairment	Abdominal distension	Abdominal pain	Colonic fistula	Constipation	Diarrhea	Dry mouth	Dyspepsia	Flatulence	Hemorrhoids	Intra-abdominal hemorrhage	Loss of taste	Mucositis oral	Nausea	Rectal fissure	Stomach pain	Taste changes	Vomiting	Chills	Edema face	Edema limbs	Fatigue	Fever	Pain	Cold sores	Elevated lactate dehydrogenase total	Oral thrush	Peritoneal infection	Sinusitis	Upper respiratory infection	Urinary tract infection	Bruising	Slow wound healing	Alkaline phosphatase increased	Blood bilirubin increased	Creatinine increased	Neutrophil count decreased	Platelet count decreased	Weight loss	Anorexia	Dehydration	Hypernatremia	Hypertriglyceridemia	Hypophosphatemia	Arthralgia	Back pain	Flank pain	Myalgia	Pain to extremity	Aphasia	Dizziness	Dysgeusia	Headache	Tremor	Trigeminal nerve disorder	Anxiety	Confusion	Depression	Insomnia	Libido decreased	Mood swings	Hematuria	Urinary frequency	Testicular pain	Cough	Dyspnea	Epistaxis	Hiccups	Hypoxia	Nasal congestion	Sore throat	Alopecia	Hair color changes	Pruritis	Rash acneiform	Rash maculo-papular	Skin hypopigmentation	Skin thinning	Hot flashes	Hypertension	Dysphagia	Hypovolemia	Intraperitoneal bleeding	Night sweats	Thromboembolic event	Lung infection	Pancreas infection	Sepsis	Diabetic ketoacidosis	Stroke	Pleural effusion	Mesenteric ischemia
Phase I Dose Level 0: X-82 + Everolimus	0	1	0	0	1	0	0	2	0	0	0	0	0	0	2	1	0	0	0	1	0	0	0	1	0	0	0	0	0	0	0	1	1	0	0	0	0	0	0	0	1	1	1	0	0	0	0	0	0	0	0	1	1	0	1	0	0	0	0	0	1	0	0	0	0	0	0	1	0	1	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	1	0	0	0	0	0	1	0	0
Phase I Dose Level 1: X-82 + Everolimus	1	0	1	1	0	0	1	2	0	1	0	0	1	0	2	1	0	0	0	1	1	0	1	2	1	0	0	0	2	1	1	0	0	0	0	0	0	0	0	0	0	1	0	0	0	0	0	1	1	0	0	0	1	0	0	0	0	0	1	0	0	0	0	0	0	0	0	1	0	0	1	0	0	0	0	0	0	1	1	0	0	0	0	1	1	0	1	0	0	1	1	0	0	1
Phase I Dose Level 2: X-82 + Everolimus	0	0	0	0	1	0	1	2	0	0	1	0	0	0	2	1	0	1	1	1	1	0	2	3	0	2	1	0	0	0	0	0	0	0	0	0	0	0	2	0	1	3	0	0	0	0	1	1	1	0	0	0	0	0	0	1	1	1	0	1	0	0	0	1	0	0	2	1	1	0	0	0	1	1	1	0	0	2	1	0	0	1	0	0	0	0	0	0	0	0	0	0	0	0
Phase I Dose Level 3: X-82 + Everolimus	1	0	0	0	5	1	1	3	2	0	1	1	0	1	4	3	1	0	0	2	3	4	3	5	2	0	0	0	0	0	2	0	0	2	1	1	1	1	3	4	1	3	0	0	2	1	0	2	1	1	2	0	2	2	3	0	0	0	1	1	3	1	1	0	2	1	2	1	3	0	0	1	0	0	0	2	1	2	0	1	0	1	0	0	0	0	1	0	0	0	0	0	1	0
Phase I Dose Level 4: X-82 + Everolimus	0	0	0	0	2	0	0	2	0	0	0	0	1	0	2	1	0	0	0	1	0	0	1	2	0	1	0	1	0	0	0	0	0	0	0	0	0	1	0	0	0	3	2	1	1	0	1	0	0	0	0	0	1	1	1	0	0	0	0	0	1	0	0	0	0	0	1	1	0	0	0	0	0	0	0	0	1	1	0	0	1	0	1	0	0	0	0	1	1	0	0	0	0	0

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Number of Participants With Dose Limiting Toxicities - Phase I

Tolerability of X-82 in combination with everolimus will be determined by NCI Common Terminology Criteria for Adverse Events (CTCAE version 4.0) (NCT01784861)
Timeframe: Completion of 1st cycle for all patients in Phase I portion of study (completed in approximately 20 months)

Intervention	Participants (Count of Participants)
Phase I Dose Level 0: X-82 + Everolimus	0
Phase I Dose Level 1: X-82 + Everolimus	0
Phase I Dose Level 2: X-82 + Everolimus	0
Phase I Dose Level 3: X-82 + Everolimus	1
Phase I Dose Level 4: X-82 + Everolimus	0

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Objective Response Rate (Complete Response + Partial Response) - Phase II

"Complete Response (CR): Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~Partial Response (PR): At least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters." (NCT01784861)
Timeframe: Through completion of treatment (estimated to be 12 months)

Intervention	Participants (Count of Participants)
Phase II: X-82 + Everolimus	0

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Overall Survival - Phase II

Start of the treatment until death. (NCT01784861)
Timeframe: Up to 3 years

Intervention	days (Median)
Phase II: X-82 + Everolimus	115

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Percentage of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)

Any sign or symptom that occurs during the study treatment plus the 30 days post treatment. All SAEs were captured in safety database from enrollment. Safety data collection was changed in the protocol amendment released in March 2016: AEs and SAEs were captured in the clinical database from protocol amendment release (18 March 2016). Hence, SAEs from both safety database and clinical database are summarized separately. (NCT01789281)
Timeframe: SAEs collected in safety database from enrollment to end of treatment (EOT) plus 30 days, up to approximately 7.2 years. AEs/SAEs collected in clinical database from protocol amendment date 18 March 2016 to EOT plus 30 days, up to approximately 4.5 years

Intervention	Participants (Count of Participants)
	SAEs (Safety database)	Treatment-related SAEs (Safety database)	AEs (Clinical Database)	Tretament-related AEs (Clinical Database)	SAEs (Clinical Database)	Treatment-related SAEs (Clinical Database)
Everolimus	6	1	7	4	2	0
Everolimus+Sandostatin LAR	9	4	7	4	4	2

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Percentage of Patients With Clinical Benefit

Percentage of patients with clinical benefit as judged by the investigator. Investigator attestation of continued clinical benefit was collected in clinical database after protocol amendment (release date 18 March 2016). Clinical benefit assessment before protocol amendment was done retrospectively. (NCT01789281)
Timeframe: After 3 months from enrollment, every 3 months, until end of treatment, assessed up to 7.2 years

Intervention	Participants (Count of Participants)
	At 3 months	At 6 months	At 9 months	At 12 months	At 15 months	At 18 months	At 21 months	At 24 months	At 27 months	At 30 months	At 33 months	At 36 months	At 39 months	At 42 months	At 45 months	At 48 months	At 51 months	At 54 months	At 57 months	At 60 months	At 63 months	At 66 months	At 69 months	At 72 months	At 75 months	At 78 months	At 81 months	At 84 months
Everolimus	9	8	8	8	8	8	8	6	5	3	2	1	1	1	1	1	1	0	0	0	0	0	0	0	0	0	0	0
Everolimus+Sandostatin LAR	7	7	7	7	7	7	7	7	7	7	7	7	7	6	6	6	6	6	5	5	4	4	3	3	3	2	1	0

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Clinical Benefit Rate

Clinical benefit rate is defined as number of patients with objective response (complete response or partial response) or stable disease for at least 24 weeks divided by number of patients randomized in each arm. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI and/or CT: Partial Response (PR) is defined as >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD) is defined as neither sufficient shrinkage to qualify for a Partial Response nor sufficient increase to qualify for Progression of Disease; Complete Response (CR) is defined as disappearance of all target lesions. (NCT01797120)
Timeframe: Every 3 months until progression or up to 3 years

Intervention	proportion of patients (Number)
Fulvestrant & Everolimus	0.636
Fulvestrant & Placebo	0.415

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Objective Response Rate

Objective response rate is defined as number of patients with complete or partial response (by Physical Exam, CT or MRI) divided by number of patients randomized in each arm (NCT01797120)
Timeframe: Every 3 months until progression or up to 3 years

Intervention	proportion of patients (Number)
Fulvestrant & Everolimus	0.182
Fulvestrant & Placebo	0.123

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Overall Survival

Overall survival will be characterized using Kaplan-Meier plots and other descriptive metrics. (NCT01797120)
Timeframe: Every 3 months until progression or up to 3 years

Intervention	months (Median)
Fulvestrant & Everolimus	28.3
Fulvestrant & Placebo	31.4

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Progression-free Survival

Progression-free survival documented by Physical Exam, CT Scan or MRI in post-menopausal patients with hormone-receptor positive metastatic breast cancer that is resistant to aromatase inhibitor therapy treated with fulvestrant and everolimus compared to fulvestrant alone from randomization to documented disease progression or death. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT01797120)
Timeframe: Every 3 months until progression or up to 3 years

Intervention	months (Median)
Fulvestrant & Everolimus	10.3
Fulvestrant & Placebo	5.1

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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

,,,,,,,,,,,,

Intervention	Participants (Count of Participants)
	Complete Response	Partial Response
TAC1 -> TAC4	0	0
TAC2	0	0
TAC2 -> TAC1	0	0
TAC2 -> TAC3	0	0
TAC3	0	1
TAC3 -> TAC1	0	0
TAC3 -> TAC1 -> TAC4	0	0
TAC3 -> TAC4	0	0
TAC4	0	0
TAC4 -> TAC1	0	0
TAC4 -> TAC2	0	0
TAC4 -> TAC3	0	0
Treatment Assignment Code 1 (TAC1)	0	0

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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

Intervention	proportion of participants (Number)
Treatment Assignment Code 1 (TAC1)	0.23
TAC1 -> TAC4	0.00
TAC2	0.22
TAC2 -> TAC1	0.00
TAC2 -> TAC3	1.00
TAC3	0.41
TAC3 -> TAC1	0.50
TAC3 -> TAC1 -> TAC4	0.00
TAC3 -> TAC4	0.00
TAC4	0.13
TAC4 -> TAC1	0.29
TAC4 -> TAC2	0.00
TAC4 -> TAC3	0.00

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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.

Intervention	Participants (Count of Participants)
Treatment Assignment Code 1 (TAC1)	13
TAC1 -> TAC4	1
TAC2	9
TAC2 -> TAC1	1
TAC2 -> TAC3	1
TAC3	22
TAC3 -> TAC1	2
TAC3 -> TAC1 -> TAC4	1
TAC3 -> TAC4	2
TAC4	15
TAC4 -> TAC1	7
TAC4 -> TAC2	1
TAC4 -> TAC3	2
Participants Enrolled But Not Treated	2

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Percent of Participants With Delayed Graft Function by Day

Delayed graft function (DGF) was defined as the need for dialysis within the first 7 days post-transplantation, excluding the first post-transplantation day. (NCT01843348)
Timeframe: Post transplant up to day 7

Intervention	Percent of participants (Number)
	day 1 (8,7,4)	day 2 (2,2,2)	day 3 (5,1,2)	day 4 (4,2,4)	day 5 (4,5,3)	day 6 (1,1,2)	day 7 (2,4,0)	>7 days (9,16,21)
CycA+Certican	10.5	5.3	5.3	10.5	7.9	5.3	0.0	55.3
TAC+Certican	18.4	5.3	2.6	5.3	13.2	2.6	10.5	42.1
TAC+MPA	22.9	5.7	14.3	11.4	11.4	2.9	5.7	25.7

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Glomular Filtration Rate (GFR) mL/Min Via Cockcroft- Gault Method at Month 12 Post Transplant

Cockcroft-Gault formula: For men: GFR= ((140-age) × body weight in kg)∕(72 x serum creatinine in mg∕dl)For women: GFR= (0.85×(140-age) × body weight in kg)∕(72 x serum creatinine in mg/dl), ), last observation carried forward (LOCF) was used for imputation of missing values, ANCOVA model (NCT01843348)
Timeframe: Month 12 post transplant

Intervention	mL/min per 1.73m² (Least Squares Mean)
TAC+MPA	60.26
TAC+Certican	52.25
CycA+Certican	51.30

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Glomular Filtration Rate (GFR) Via Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) Method at Month 12 Post Transplant

Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) method = GFR=141 x min(Scr/κ, 1)α x max(Scr/κ, 1)1.209 x 0.993Age x 1.018 [if female] x 1.159 [if black] where Scr is serum creatinine, κ is 0.7 for females and 0.9 for males, α is 0.329 for females and 0.411 for males, min indicates the minimum of Scr/κ or 1, and max indicates the maximum of Scr/κ or 1. last observation carried forward (LOCF) was used for imputation of missing values, ANCOVA model (NCT01843348)
Timeframe: Month 12 post transplant

Intervention	mL/min per 1.73m² (Least Squares Mean)
TAC+MPA	51.62
TAC+Certican	44.42
CycA+Certican	42.44

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Glomular Filtration Rate (GFR) Via Modification of Diet in Renal Disease (MDRD) Method at Month 12 Post Transplant

Modification of Diet in Renal Disease (MDRD) = For men: GFR = 170 x (serum creatinine -0,999) x (age-0,176) x (urea nitrogen -0,17) x (albumin0,318) For women: GFR = 170 x (serum creatinine -0,999) x (age-0,176) x (urea nitrogen -0,17) x albumin0,318) x 0.762 with urea nitrogen = urea / 2.144. last observation carried forward (LOCF) was used for imputation of missing values, ANCOVA model (NCT01843348)
Timeframe: Month 12 post transplant

Intervention	mL/min per 1.73m² (Least Squares Mean)
TAC+MPA	53.24
TAC+Certican	45.72
CycA+Certican	43.47

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Duration of Wound Healing

A wound will be considered healed if all the suture material and staples are removed and the wound is intact. Number of participants is based on all patients of the respective treatment group in the safety set, excluding patients with no answer (unknown). (NCT01843348)
Timeframe: Post transplant until individual reporting

Intervention	days (Mean)
TAC+MPA	42.4
TAC+Certican	54.1
CycA+Certican	85.3

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Glomular Filtration Rate (GFR) mL/Min Via Nankivell Method at Month 12 - Standard Regimen vs Certican Regimens

"To demonstrate non-inferiority in renal function assessed by glomerular filtration rate (Nankivell formula) in at least one of the Certican® treatment regimens compared to the standard regimen group at month 12 post-transplantation in renal transplant patients. Nankivell formula:~GFR = 6.7/Scr + BW/4 - Surea/2 - 100/(height)² + C where Scr is the serum creatinine concentration expressed in mmol/L, BW the body weight in kg, Surea the serum urea in mmol/L, height in m, and the constant C is 35 for male and 25 for female patients. The eGFR is expressed in mL/min per 1.73m². If a patient was on dialysis at the time of urea or creatinine assessment, the eGFR was set to 0. Analysis set = per protocol set" (NCT01843348)
Timeframe: One year post transplant

Intervention	mL/min per 1.73m² (Mean)
	Month 1 - Day 1 to 60 (146,111,78)	Month 3 - Day 61 to 136 (143,108,79)	Month 6 - Day 137 to 228 (142,108,76)	Month 9 - Day 229 to 319 (140,106,77)	Month12 - Day 320 to 450 (147,111, 80)
CycA+Certican	59.47	62.22	63.17	62.89	61.51
TAC+Certican	60.54	61.21	62.76	64.68	63.34
TAC+MPA	62.62	66.36	68.05	69.47	70.41

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Percent of Participants With Delayed Graft Function and Slow Graft Function

Delayed graft function (DGF) was defined as the need for dialysis within the first 7 days post-transplantation, excluding the first post-transplantation day. Slow graft function (SGF) was defined as a serum creatinine >3.0 mg/dL at Day 5 post-transplantation. Full analysis set (NCT01843348)
Timeframe: Post transplant to month 12

Intervention	Percent of participants (Number)
	Delayed graft function (197,187,172)	Slow graft function (195,187,171)
CycA+Certican	22.1	49.7
TAC+Certican	20.3	48.7
TAC+MPA	17.8	46.2

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Percent of Participants With Viral Infections

Viral infections for BKV Virus Humane Polyomavirus 1 and Cytomegalovirus (NCT01843348)
Timeframe: Post transplant to month 12

Intervention	Percent of participants (Number)
	Viral infections - CMVMissing	Viral infections - CMVAsymptomatic	Viral infections - CMVMild	Viral infections - CMVModerate	Viral infections - CMVSevere	Viral infections - BKVAsymptomatic	Viral infections - BKVMild	Viral infections - BKVModerate	Viral infections - BKVSevere
CycA+Certican	1.0	1.0	1.0	1.0	0.0	5.0	3.0	1.0	0
TAC+Certican	0.0	1.0	2.0	1.0	0.0	8.0	7.0	2.0	0
TAC+MPA	1.0	7.0	5.0	6.0	1.0	10.0	5.0	7.0	0

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Percent of Participants With Wound Healing Complications During Study

Information collected to report wound healing process which included percentage of participants with complications, fluid collections detected and occurrence of lymphoceles (NCT01843348)
Timeframe: Post transplant until individual reporting

Intervention	Percent of participants (Number)
	Wound healing complication	Fluids detected	Occurrence of lymphoceles
CycA+Certican	22.2	27.8	21.8
TAC+Certican	19.1	26.8	18.2
TAC+MPA	14.3	18.7	11.8

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Percentage of Participants With Composite Treatment Failure Endpoints - Difference Between Groups at Month 12

Combined endpoint included: biopsy proven acute rejection (BPAR) defined as a rejection which was acute and proven by biopsy, graft loss (GL) defined as: allograft was presumed to be lost on the day the patient starts dialysis and not able to be removed from dialysis or death. Patients who prematurely discontinued the study: if the patient did not suffer from an event before discontinuation and reason was not related to efficacy, the patient was assessed as having had no event, otherwise the patient was assessed as having had an event. Full analysis set (FAS) (NCT01843348)
Timeframe: Month 12 post transplant

,,,,

Intervention	Percentage of participants (Number)
	BPAR or graft loss or death	BPAR, graft loss, death, or loss of follow-up
CycA+Certican	24.6	32.7
CycA+Certican -Tac+MPA - Difference Between Groups	14.9	17.1
TAC+Certican	13.0	22.6
Tac+Certican - Tac+MPA - Difference Between Groups	3.2	7.0
TAC+MPA	9.8	15.6

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Percentage of Participants With Treatment Failure Endpoints at Month 12

Treatment failure endpoints: biopsy proven acute rejection (BPAR) defined as a rejection which was acute and proven by biopsy, graft loss (GL) defined as: allograft was presumed to be lost on the day the patient starts dialysis and not able to be removed from dialysis or death. Patients who prematurely discontinued the study: if the patient did not suffer from an event before discontinuation and reason was not related to efficacy, the patient was assessed as having had no event, otherwise the patient was assessed as having had an event. Full analysis set (FAS) (NCT01843348)
Timeframe: Month 12 post transplant

Intervention	Percentage of participants (Number)
	Biopsy proven acute rejection (BPAR)	Treated BPAR (tBPAR)	Graft loss	Death
CycA+Certican	24.6	23.6	9.0	6.5
TAC+Certican	12.0	11.5	6.3	6.3
TAC+MPA	9.3	8.8	5.4	4.9

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Objective Response Rate (ORR)

Objective Response Rate (ORR) is the number of participants with a best response of complete response (CR) or partial response (PR) divided by number of randomized participants. ORR was assessed by the Independent Radiology Committee (IRC) per RECIST 1.1 which was confirmed by a subsequent visit >= 28 days later, and was analyzed in the Intent to Treat (ITT) population at the time of the primary analysis of Progression Free Survival (PFS). The data cutoff date was 22 May 2015. (NCT01865747)
Timeframe: ORR was assessed at 8 weeks post-randomization, every 8 weeks for 12 months, and every 12 weeks until date of disease progression or death, up to May 2015 (approximately 21 months)

Intervention	percentage of participants (Number)
Cabozantinib (XL184)	17
Everolimus (Afinitor)	3

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Overall Survival (OS)

Overall Survival (OS) is defined as the time from randomization to the date of death. Participants that had not died were censored at last known date alive. Median OS was calculated using Kaplan-Meier estimates. Interim analyses for OS occurred after 320 deaths (78% of the total OS events needed for final analysis). (NCT01865747)
Timeframe: OS was measured from the time of randomization until 320 deaths, approximately 28 months

Intervention	months (Number)
Cabozantinib (XL184)	21.4
Everolimus (Afinitor)	16.5

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Progression-free Survival (PFS)

The primary analysis of PFS is the time from randomization to date of first documented tumor progression as determined by investigator (per RECIST 1.1 criteria) or death due to any cause, whichever occurred first. A Kaplan-Meier analysis was performed to estimate the median duration. (NCT01865747)
Timeframe: PFS is measured from the date of randomization until the date of first documented disease progression or date of death from any cause as determined by the Independent Radiology Committee (IRC) per RECIST 1.1, assessed for up to 17 months.

Intervention	months (Number)
Cabozantinib (XL184)	7.4
Everolimus (Afinitor)	3.8

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Composite Efficacy Failure of Treated Biopsy in Everolimus With Reduced Tacrolimus Group Compared to Standard Tacrolimus in Patients From Japan Only

"Rate of composite efficacy failure of treated biopsy in everolimus with reduced tacrolimus group compared to standard tacrolimus from randomization in core study up to 36 months in the extension study.~Composite endpoint = treated BPAR, graft loss or death. AR = Acute rejection; tAR = treated AR; BPR = biopsy proven rejection; BPAR = biopsy proven acute rejection; tBPAR = treated BPAR" (NCT01888432)
Timeframe: randomization, 36 months post transplantion

Intervention	Participants (Number)
	Composite endpoint	On-treatment composite endpoint	Graft loss/death	tBPAR	Graft loss	Death	AR	tAR	BPR	BPAR
EVR+Reduced TAC	2	1	1	2	0	1	3	2	6	3
TAC Control	1	0	1	0	1	0	2	0	3	2

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Number of Participants With Composite of tBPAR, Graft Loss, and Death

Compare between the treatment group EVR with rTAC vs standard TAC: incidence of a composite of tBPAR, graft loss, death (NCT01888432)
Timeframe: Month 24 post transplantation

Intervention	Participants (Count of Participants)
	tBPAR/graft loss/death	On-treatment tBPAR/graft loss/death
EVR+Reduced TAC	12	7
TAC Control	11	9

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Number of Participants With Time to Recurrence of HCC in Subjects With a Diagnosis of HCC at the Time of Liver Transplantation

Patients transplanted for HCC or with HCC diagnosed at time of transplantation were monitored for HCC recurrence according to local practice. For example routine laboratory monitoring/tests, tumor markers, hepatic ultrasound, computed tomography scans (CAT, CT) or MRI (especially Fe-MRI) on a regular basis per local practice. (NCT01888432)
Timeframe: Month 12 and Month 24

Intervention	Participants (Count of Participants)
	HCC recurrence (n/M) - month 12	HCC recurrence (n/M) - month 24
EVR+Reduced TAC	0	1
TAC Control	5	6

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Compare Renal Function Over Time Assessed by the Change by eGFR, Post-randomization

Change in renal function from randomization to month 24 assessed by the change in estimated GFR (MDRD-4). Rate of change of renal function. (NCT01888432)
Timeframe: From randomziation to month 24

Intervention	mL/min/1.73 m2 (Least Squares Mean)
EVR+Reduced TAC	-11.01
TAC Control	-14.26

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Renal Function by Estimated Glomerular Filtration Rate (eGFR) From Randomization

Renal function (change in estimated glomerular filtration rate (eGFR)) from randomization to Month 12 post transplantation with everolimus (EVR) in combination with reduced tacrolimus (rTAC) compared to standard exposure tacrolimus (TAC) in living donor liver transplant recipients. (NCT01888432)
Timeframe: From randomization to month 12

Intervention	mL/min/1.73 m^2 (Least Squares Mean)
EVR+Reduced TAC	-7.94
TAC Control	-12.09

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Number of Subjects Experiencing Adverse Events/Infections by SOC

(NCT01888432)
Timeframe: Month 24

Intervention	Participants (Count of Participants)
	Any AE/infection	Blood and lymphatic system disorders	Cardiac disorders	Congenital, familial and genetic disorders	Ear and labyrinth disorders	Endocrine disorders	Eye disorders	Gastrointestinal disorders	General disorders&admin site conditions	Hepatobiliary disorders	Immune system disorders	Infections and infestations	Injury, poisoning&proced. complications	Investigations	Metabolism and nutrition disorders	Musculoskeletal and connective tissue disorders	Neoplasms benign, malig&unspecified (cysts&polyps)	Nervous system disorders	Product issues#	Psychiatric disorders	Renal and urinary disorders	Reproductive system&breast dis.	Respiratory, thoracic&mediastinal dis.	Skin&subcutaneous tissue disorders	Vascular disorders
EVR+Reduced TAC	140	44	15	1	2	1	17	98	48	44	8	84	36	61	87	30	10	38	1	33	46	9	34	39	38
TAC Control	136	32	12	2	5	2	15	74	42	40	11	70	28	68	60	43	17	44	1	26	36	12	39	44	30

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Number of Participants With Composite Efficacy Failure of Treated Biopsy Proven Acute Rejection, Graft Loss or Death in Everolimus With Reduced Tacrolimus Group Compared to Standard Tacrolimus

Rate of composite efficacy failure of treated biopsy proven acute rejection (tBPAR ≥ RAI score 3), graft loss (GL) or death (D) in everolimus with reduced tacrolimus group compared to standard tacrolimus at 12 months (NCT01888432)
Timeframe: 12 months post transplantation

Intervention	Participants (Count of Participants)
EVR+Reduced TAC	7
TAC Control	8

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Compare Incidence of tAR

Compare between the treatment group EVR with rTAC vs standard TAC: incidence of treated acute rejection (tAR). (NCT01888432)
Timeframe: Month 12 and Month 24 post transplantation

Intervention	Participants (Count of Participants)
	Month 12	Month 24
EVR+Reduced TAC	5	7
TAC Control	6	7

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Renal Function by Estimated Glomerular Filtration Rate (All Extension Patients)

Renal function (change in estimated glomerular filtration rate (eGFR)) from randomization to Month 36 post transplantation with everolimus (EVR) in combination with reduced tacrolimus (rTAC) compared to standard exposure tacrolimus (TAC) in living donor liver transplant recipients in Japan (NCT01888432)
Timeframe: randomization, at 36 months post transplantation

Intervention	mL/min/1.73m2 (Least Squares Mean)
EVR+Reduced TAC	-26.88
TAC Control	-16.87

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Compare Incidence of a Composite of Death or Graft Loss

Compare between the treatment group EVR with rTAC vs standard TAC: Incidence of a composite of death or graft loss (NCT01888432)
Timeframe: Month 12 and Month 24 post transplantation

Intervention	Participants (Count of Participants)
	Month 12	Month 24
EVR+Reduced TAC	4	8
TAC Control	3	5

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Compare Incidence of AR

Compare between the treatment group EVR with rTAC vs standard TAC: incidence of acute rejection (AR) (NCT01888432)
Timeframe: Month 12 and Month 24 post transplantation

Intervention	Participants (Count of Participants)
	Month 12	Month 24
EVR+Reduced TAC	9	12
TAC Control	8	9

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Compare Incidence of BPAR

Compare between the treatment group EVR with rTAC vs standard TAC: incidence of a composite of biopsy proven acute rejection (BPAR) (NCT01888432)
Timeframe: Month 12 and Month 24 post transplantation

Intervention	Participants (Count of Participants)
	Month 12	Month 24
EVR+Reduced TAC	7	8
TAC Control	6	7

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Compare Incidence of Death

Compare between the treatment group EVR with rTAC vs standard TAC: incidence of death (NCT01888432)
Timeframe: Month 12 and Month 24 post transplantation

Intervention	Participants (Count of Participants)
	Month 12	Month 24	Month 24 (on-treatment death)
EVR+Reduced TAC	4	8	4
TAC Control	3	4	3

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Compare Incidence of Graft Loss

Compare between the treatment group EVR with rTAC vs standard TAC: incidence of graft loss (NCT01888432)
Timeframe: Month 12 and Month 24 post transplantation

Intervention	Participants (Count of Participants)
	Month 12	month 24	month 24 (on-treatment graft loss)
EVR+Reduced TAC	0	0	0
TAC Control	0	1	0

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Compare Incidence of Notable Safety Events (SAEs, Infections and Serious Infections Leading to Premature Discontinuation)

Notable events include death, Serious AE/infection,, and AE/infection leading to discontinuation of study medication. (NCT01888432)
Timeframe: Month 24

Intervention	Participants (Count of Participants)
	Any notable events	Death	Serious AE/Infection	AE/Infection lead. to premature disc of study med
EVR+Reduced TAC	86	8	83	21
TAC Control	82	4	78	18

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Compare Incidence of tBPAR

Compare between the treatment group EVR with rTAC vs standard TAC: Incidence of tBPAR (NCT01888432)
Timeframe: Month 12 and Month 24 post transplantation

Intervention	Participants (Count of Participants)
	tBPAR - month 12	tBPAR - month 24	On-treatment tBPAR - month 24
EVR+Reduced TAC	3	4	3
TAC Control	5	6	6

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Number of All Death (Cardiac, Vascular, and Non-cardiovascular)

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.) This study as no primary or secondary endpoints, all endpoints are of equal weight.~- Non-cardiac death is defined as a death not due to cardiac causes (as defined above).~This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: 0 through 1885 Days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	91

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Number of All Deaths, Myocardial Infarction, Any Repetitive Revascularization Composite Endpoints

"All deaths include Cardiac death, Cardiovascular death and Non-cardiovascular death.~Myocardial Infarction (MI):~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of Creatine kinase (CK) levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves.~This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: 0 through 1885 Days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	330

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Number of Participants With All Target Vessel Revascularization (TVR)

"Target Vessel Revascularization is defined as any repeat percutaneous intervention or surgical bypass of any segment of the target vessel. The target vessel is defined as the entire major coronary vessel proximal and distal to the target lesion which includes upstream and downstream branches and the target lesion itself.~This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: 0 through 1885 Days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	26

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Number of Participants With All TLR

This study has no primary or secondary endpoints, all endpoints are of equal weight. (NCT01894152)
Timeframe: ≤ 7 days after index procedure (Hospitalization)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	1

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Number of Participants With All TLR

This study has no primary or secondary endpoints, all endpoints are of equal weight. (NCT01894152)
Timeframe: 0 to 1885 days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	58

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Number of Participants With ID-TVR (TLR and TVR, Non-target Lesion)

"This study has no primary or secondary endpoints, all endpoints are of equal weight.~Revascularization includes TLR, TVR, non-target lesion, and non TVR." (NCT01894152)
Timeframe: 0 to 1885 days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	59

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Number of Participants With Cardiac Death and All Myocardial Infarction (MI) (Q-wave and Non-Q Wave) Composite Endpoint

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded.~(This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality, cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.)~Myocardial Infarction (MI):~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of Creatine kinase (CK) levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves.~This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: ≤ 7 days after index procedure (Hospitalization)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	7

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Number of Participants With All TVR (TLR and TVR, Non-target Lesion)

"This study has no primary or secondary endpoints, all endpoints are of equal weight.~All TVR (TLR and TVR, non-target lesion)" (NCT01894152)
Timeframe: ≤ 7 days after index procedure (Hospitalization)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	1

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Number of Participants With ID-TVR (TLR and TVR, Non-target Lesion)

"This study has no primary or secondary endpoints, all endpoints are of equal weight.~Revascularization includes TLR, TVR, non-target lesion, and non TVR." (NCT01894152)
Timeframe: ≤ 7 days after index procedure (Hospitalization)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	1

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Number of Participants With Target Lesion Failure (TLF)

"Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR).~This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: ≤ 7 days after index procedure (Hospitalization)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	5

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Number of Participants With Sub-acute Stent Thrombosis

"This study has no primary or secondary endpoints, all endpoints are of equal weight.~Scaffold/Stent thrombosis should be reported as a cumulative value at the different time points and with the different separate time points. Time 0 is defined as the time point after the guiding catheter has been removed and the subject left the catheterization lab.~Timings:~Acute scaffold/stent thrombosis : 0 - 24 hours post stent implantation Subacute scaffold/stent thrombosis: >24 hours - 30 days post stent implantation Late scaffold/stent thrombosis: 30 days - 1 year post stent implantation Extremely late scaffold/stent thrombosis: >1 year post stent implantation" (NCT01894152)
Timeframe: > 1 day to 30 days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	2

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Number of Participants With ID-TVR, Non-target Lesion

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	0

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Number of Participants With ID-TVR, Non-target Lesion

"This study has no primary or secondary endpoints, all endpoints are of equal weight.~Revascularization includes TLR, TVR, non-target lesion, and non TVR." (NCT01894152)
Timeframe: 0 to 1885 days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	22

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Number of Participants With Late Stent Thrombosis

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	1

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Number of Participants With Overall Stent Thrombosis

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	3

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Number of All Death (Cardiac, Vascular, and Non-cardiovascular)

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.) This study as no primary or secondary endpoints, all endpoints are of equal weight.~- Non-cardiac death is defined as a death not due to cardiac causes (as defined above).~This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: ≤ 7 days after index procedure (Hospitalization)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	3

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Number of Participants With Early Stent Thrombosis

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	2

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Number of All Deaths, Myocardial Infarction, Any Repetitive Revascularization Composite Endpoints

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	8

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Number of Participants With All TVR (TLR and TVR, Non-target Lesion)

"This study has no primary or secondary endpoints, all endpoints are of equal weight.~All TVR (TLR and TVR, non-target lesion)" (NCT01894152)
Timeframe: 0 to 1885 days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	84

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Number of Participants With Target Lesion Failure (TLF)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	100

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Number of Participants With Very Late Stent Thrombosis

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	0

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Number of Participants With Acute Stent Thrombosis

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	0

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Number of Participants With Target Vessel Failure (ID-TVF) (Cardiac Death, All Myocardial Infarctions and Ischemia-driven Target Vessel Revascularization)

"Target Vessel Failure (TVF) is the composite of Cardiac Death, Myocardial infarction (MI) or ischemia-driven Target Vessel Revascularization (ID-TVR).~This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: ≤ 7 days after index procedure (Hospitalization)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	7

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Number of Participants With Target Vessel ARC MI

"This study has no primary or secondary endpoints, all endpoints are of equal weight.~Myocardial Infarction (MI):~Q wave MI: Development of new, pathological Q wave on the ECG. Non-Q wave MI: Elevation of Creatine kinase (CK) levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT01894152)
Timeframe: 0 to 1885 days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	23

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Number of Participants With Target Vessel ARC MI

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	2

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Number of Participants With Composite Rate of All Deaths and Myocardial Infarctions (MI)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	8

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Number of Participants With ID-TLR

"This study has no primary or secondary endpoints, all endpoints are of equal weight.~Revascularization includes TLR, TVR, non-target lesion, and non TVR." (NCT01894152)
Timeframe: 0 to 1885 days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	37

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Number of Participants With ID-TLR

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	1

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Number of Participants With Target Vessel Failure (ID-TVF) (Cardiac Death, All Myocardial Infarctions and Ischemia-driven Target Vessel Revascularization)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	180

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Number of Participants With Cardiogenic Death, Target Vessel Blood Flow Myocardial Infarction, Target Lesion Revascularization Composite Endpoint

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded.~(This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality, cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.)~Myocardial Infarction (MI): Patient diagnosed with myocardial infarction, but its relation with target vessel not clear, therefore considered target vessel myocardial infarction.~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of Creatine kinase (CK) levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves.~This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: ≤ 7 days after index procedure (Hospitalization)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	5

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Number of Participants With Cardiogenic Death, Target Vessel Blood Flow Myocardial Infarction, Target Lesion Revascularization Composite Endpoint

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded.~(This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality, cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.) Myocardial Infarction (MI): Patient diagnosed with myocardial infarction, but its relation with target vessel not clear, therefore considered target vessel myocardial infarction.~Q wave MI: Development of new, pathological Q wave on the ECG.~Non-Q wave MI: Elevation of Creatine kinase (CK) levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves.~This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: 0 through 1885 Days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	120

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Number of Participants With Composite Rate of All Deaths and Myocardial Infarctions (MI)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	156

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Number of Participants With All Target Vessel Revascularization (TVR)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	0

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Number of Participants With All Revascularization (Target Lesion, Target Vessel, and Non-target Vessel) (PCI and Coronary Artery Bypass Graft [CABG])

"This study has no primary or secondary endpoints, all endpoints are of equal weight.~All Revascularization includes Coronary artery bypass grafting and Percutaneous coronary intervention" (NCT01894152)
Timeframe: 0 through 1885 Days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	223

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Number of Participants With All Revascularization (Target Lesion, Target Vessel, and Non-target Vessel) (PCI and Coronary Artery Bypass Graft [CABG])

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	1

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Number of Participants With All Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)

"Myocardial Infarction (MI)~Q wave MI Development of new, pathological Q wave on the ECG~Non-Q wave MI Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves This study has no primary or secondary endpoints, all endpoints are of equal weight." (NCT01894152)
Timeframe: 0 through 1885 Days

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	75

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Number of Participants With All Myocardial Infarction (MI) (Including Q-wave and Non-Q-wave)

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	6

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Number of Participants With Cardiac Death and All Myocardial Infarction (MI) (Q-wave and Non-Q Wave) Composite Endpoint

Intervention	Participants (Count of Participants)
XIENCE PRIME Everolimus Eluting Coronary Stent System (EECSS)	114

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The Number of Polyoma BK Viremia Patients

Patients will be monitored at regular interval for the development of Polyomavirus Viremia. (NCT01911546)
Timeframe: 12 months

Intervention	Participants (Count of Participants)
Everolimus + Low-dose Tacrolimus	5

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The Number of CMV Viremia

The number of patients with CMV viremia (NCT01911546)
Timeframe: 12 Months

Intervention	Participants (Count of Participants)
Everolimus + Low-dose Tacrolimus	0

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Incidence of Cell Mediated Rejection (CMR)

Patients will be monitored for any episodes of CMR. (NCT01911546)
Timeframe: 6 months

Intervention	Participants (Count of Participants)
Everolimus + Low-dose Tacrolimus	2

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Incidence of Antibody Mediated Rejection (ABMR)

Protocol biopsies were obtained at T0 and 6 months post transplant. (NCT01911546)
Timeframe: 6 months

Intervention	Participants (Count of Participants)
Everolimus + Low-dose Tacrolimus	2

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Frequency of Seizures Assessed by Total Number of Seizures

Parents will be asked to document the frequency of their child's seizures using a manual or electronic (seizuretracker.com) seizure diary. The total number of seizures at baseline for all participants. (NCT01929642)
Timeframe: at baseline

Intervention	seizures (Number)
Everolimus or Sirolimus	0

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Feasibility Measurements of Parental Stress

"Measurements of stress will be administered. Specifically, we will use the Parental Stress Index. Quantifying stress, as well as compliance with the study protocol, will allow investigators to objectively assess the feasibility of a larger clinical trial of sirolimus in patients with TSC.~Parental stress index maximum score: 180 Parental stress index minimum score: 36 higher raw scores indicate higher levels of stress." (NCT01929642)
Timeframe: Change from baseline to EOT visit 12 week 53

Intervention	units on a scale (Mean)
Everolimus or Sirolimus	111

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Cognitive Function as Assessed by the Capute Scale

"Score range maximum: 100 Score range minimum: 0~High values represent a high cognitive function Below 70 is abnormal. 70-100 is the normal range." (NCT01929642)
Timeframe: 1 year

Intervention	score on a scale (Mean)
Everolimus or Sirolimus	15

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Caregiver Burden

"The Caregiver Burden Scale is a standard set of questions which will be used to measure the non-medical impact of TSC on caregivers and how it affects the feasibility of study completion.~The Caregiver's Burden Scale (CBS) is a 22-item scale that assess subjectively experienced burden by caregiver's to chronically disabled persons. maximum scores: 88 & Minumum scores: 22~High values represent a worse outcome" (NCT01929642)
Timeframe: Change from baseline to EOT visit 12 week 53

Intervention	units on a scale (Mean)
Everolimus or Sirolimus	61

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Number of Participants With Compliance to the Treatment Protocol.

One outcome measurement of feasibility will include family/patient compliance with the treatment protocol, which will be assessed and documented at every study visit and telephone follow-up call, by the physician and/or study team member. This was calculated by calculating dividing the total number of study visits and study assessments completed by the total number of study visits and study assessments indicated by the treatment protocol. (NCT01929642)
Timeframe: Change from baseline to EOT visit 12 week 53

Intervention	percentage of completed visits/measures (Number)
	Participant 002	Participant 003	Participant 001
Everolimus or Sirolimus	100	58	58

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Total Number of Aggressions or Self-injuries

This is the total number of aggressions or self-injuries for all participants. (NCT01929642)
Timeframe: 1 year

Intervention	Number of aggressions or self-injuries (Number)
Everolimus or Sirolimus	82

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Repetitive Behavior

"Repetitive behavior will be assessed using the Repetitive Behavior Scale - revised, a questionnaire to characterize several domains of repetitive behavior including ritualistic behavior, stereotypic behavior, self-injurious behavior, compulsive behavior, and restricted interests.~There are 36 items on the scale. Behaviors are rated on a 4-point scale: 0-Behavior does not occur, 1-Behavior occurs and is a mild problem, 2-Behavior occurs and is a moderate problem, 3-Behavior occurs and is a severe problem.~Maximum score: 108 & minimum score: 0 A high score represents the worse outcome" (NCT01929642)
Timeframe: 1 year

Intervention	score on a scale (Mean)
Everolimus or Sirolimus	69

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Tumor Response

"Evaluate tumor response using RECIST criteria after 12 weeks of treatment at definitive surgery.~Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR., or similar definition that is accurate and appropriate." (NCT01931163)
Timeframe: tumor response at 12 weeks after treatment

Intervention	Participants (Count of Participants)
Everolimus Plus Cisplatin	22

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Leukopenia

The number of patients with leukopenia as indicated by white blood cell count less than 1.0, absolute neutrophil count less than 500 or the need for exogenous granulocyte stimulating factor administration (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	1

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Infection Requiring Hospitalization

The number of patients with serious infections as defined by need for hospitalization (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	11

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Impaired Glucose Tolerance

The number of patients with impaired glucose tolerance as indicated by fasting blood glucose levels, Hemoglobin A1C (HgbA1C) levels and the need for hypoglycemic medications (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	14

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Graft Survival

Graft survival is defined as the percentage of kidney transplants still functioning at 2 years post baseline visit . One patient died of natural causes at 12 months with a functioning graft. (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	49

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Gastrointestinal Complaints

The number of patients with gastrointestinal complaints as indicated by abdominal pain, nausea, vomiting or diarrhea not accounted for by a specific episode of illness such as gastroenteritis (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	22

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Development of Donor Specific Antibody

The number of patients with incidence of development of donor specific antibody (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	2

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Cytomegalovirus

The number of patients with Incidence of cytomegalovirus infection as defined by need for hospitalization (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	0

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BK Nephropathy

The number of patients with BK nephropathy as defined by biopsy. Note that biopsies were not required as part of the study but were only done as part of the patient's standard of care if rejection was suspected (i.e. if the serum creatinine increased by 25% and was not associated with elevated tacrolimus levels or clinical signs of dehydration/illness to account for elevated creatinine) (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	0

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BK Infection

The number of patients with BK infection as defined by blood titers requiring reduction in immunosuppressive dose (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	7

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Biopsy Proven Acute Rejection

The percentage of patients with a treated biopsy-proven acute rejection (a co-primary endpoint) within the 2 year study time period (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	1

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Cardiovascular Complications

The number of patients with cardiovascular complications as indicated by conditions such as dysrhythmias, coronary artery disease requiring intervention or myocardial infarction (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	1

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Lipid Levels

The number of patients with hyperlipidemia as defined by the development of new onset hyperlipidemia in the baseline negative patients and the number of baseline positive patients who required starting a new lipid-lowering medication or an increase in dose of their lipid-lowering medication over the course of the study (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
	Baseline negative patients with new onset hyperlipidemia	Baseline positive patients started on new lipid-lowering medication or needing increase in dose
Arm 1 Everolimus/Reduced Dose Tacrolimus	7	19

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Thrombocytopenia

The number of patients with thrombocytopenia as defined by platelet count less than 50 (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	0

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Renal Function

"Renal function in patients will be assessed using glomerular filtration rate (GFR) as measured by the Modified Diet Renal Disease (MDRD) estimation.~Glomerular filtration is the process by which the kidneys filter the blood, removing excess wastes and fluids. Glomerular filtration rate (GFR) is a calculation that determines how well the blood is filtered by the kidneys, which is one way to measure remaining kidney function. GFR is also used to find the stage of chronic kidney disease. Glomerular filtration rate is usually calculated using a mathematical formula that compares a person's size, age, sex, and race to serum creatinine levels. The higher the GFR number, the better the kidney function; the lower the GFR number, the worse the kidney function. A GFR of 60 or higher is in the normal range. A GFR below 60 may mean kidney disease. A GFR of 15 or lower may mean kidney failure." (NCT01935128)
Timeframe: 2 years

Intervention	mL/min/1.73 m2 (Mean)
Arm 1 Everolimus/Reduced Dose Tacrolimus	65.70

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Proteinuria

The number of patients with proteinuria as defined by spot urine protein to creatinine ratio greater than 1.0 (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	7

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Pneumonitis

The number of patients with pneumonitis as demonstrated by lung inflammation symptoms such as shortness of breath and/or cough requiring clinical intervention and management (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	3

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Patient Survival

Patient survival is defined as the percentage of patients still surviving at 2 years post baseline visit (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	49

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Neurotoxicity

The number of patients with neurotoxicity as evidenced by incidence of new onset seizure activity or tremors (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	1

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Mouth Ulcers

The number of patients with stomatitis/aphthous ulcer (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	14

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Malignancies

The number of patients developing malignancies including post-transplant lymphoproliferative disorders (NCT01935128)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Arm 1 Everolimus/Reduced Dose Tacrolimus	2

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Recipient and Donor Genotyping for Selected Variants of CYP3A5, ABCB1 (MDR1), and CYP4A Genes

A blood sample was obtained from recipients and donors to measure gene polymorphism effects on metabolism of calcineurin inhibitor and everolimus. The polymorphisms are represented as the number of SNP occurrences for the CYP3A5, ABCB1 (MDR1) gene, and CYP4A4*22 genes. (NCT01936519)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
	Recipient Genotypes : rs776746 (CYP3A5 gene)	Recipient Genotypes : rs1045642 (ABCB1 gene)	Recipient Genotypes : rs1128503 (ABCB1 gene)	Recipient Genotypes : rs2032582 (ABCB1 gene)	Recipient Genotypes : rs35599367 (CYP4A4*22 gene)	Donor Genotypes : rs776746 (CYP3A5 gene)	Donor Genotypes : rs1045642 (ABCB1 gene)	Donor Genotypes : rs1128503 (ABCB1 gene)	Donor Genotypes : rs2032582 (ABCB1 gene)	Donor Genotypes : rs35599367 (Cyp4A4*22)
Calcineurin Inhibitor and Mycophenolic Acid	11	6	7	1	1	3	1	0	0	0
Everolimus and Mycophenolic Acid	11	6	8	0	1	0	5	0	0	1

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Renal Function as Measured by 24 Hour Urine Creatinine Clearance

Renal Function was assessed by 24 hr urine collection creatinine clearance measured (mL/min). 24 Hr urine collection was assessed at baseline, 6 months, 1 year, and 2 years post transplant. (NCT01936519)
Timeframe: 6 months, 1 year, and 2 years

Intervention	mL/min (Mean)
	24hr Urine Creatinine Clearance at 6 months	24hr Urine Creatinine Clearance at 1 year	24hr Urine Creatinine Clearance at 2 years
Calcineurin Inhibitor With Mycophenolic Acid	68.09	68.09	61.54
Everolimus With Mycophenolic Acid	70.75	86.8	90.63

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Renal Function as Measured by Cockcroft Gault Creatinine Clearance

The Cockcroft-Gault formula for estimating creatinine clearance was determined at 6 months, 1 year, and 2 years post transplant (NCT01936519)
Timeframe: 6 months, 1 year, and 2 years

Intervention	mL/min/1.73m2 (Mean)
	Cockcroft Gault Creatinine Clearance at 6 months	Cockcroft Gault Creatinine Clearance at 1 year	Cockcroft Gault Creatinine Clearance at 2 years
Calcineurin Inhibitor and Mycophenolic Acid	79.84	86.84	80.85
Everolimus and Mycophenolic Acid	100.17	113.47	108.16

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Renal Function as Measured by Iothalamate Clearance

Iothalamate Clearance was assessed at 6 months, 1 year, and 2 years post transplant. (NCT01936519)
Timeframe: 6 months, 1 year, and 2 years

Intervention	mL/min/1.73m2 (Mean)
	Iothalamate Clearance at 6 months	Iothalamate Clearance at 1 year	Iothalamate Clearance at 2 years
Calcineurin Inhibitor and Mycophenolic Acid	67.99	66.65	57.19
Everolimus and Mycophenolic Acid	74.23	104.01	79.41

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Renal Function as Measured by Modification of Diet in Renal Disease (MDRD) Estimated Glomerular Filtration Rate (eGFR)

Modification of Diet in Renal Disease (MDRD) estimated Glomerular Filtration Rate (eGFR) was assessed at 6 months, 1 year, and 2 years post transplant. (NCT01936519)
Timeframe: 6 months, 1 year, and 2 years

Intervention	mL/min/1.73 m2 (Mean)
	MDRD eGFR at 6 months	MDRD eGFR at 1 year	MDRD eGFR at 2 years
Calcineurin Inhibitor and Mycophenolic Acid	62.18	60.63	53.29
Everolimus and Mycophenolic Acid	81.27	88.01	87.37

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Renal Function as Measured by Serum Creatinine Level

Serum creatinine levels were assessed at 6 months, 1 year, and 2 years post transplant (NCT01936519)
Timeframe: 6 months, 1 year, and 2 years

Intervention	mg/dL (Mean)
	Serum Creatinine at 6 months	Serum Creatinine at 1 year	Serum Creatinine at 2 years
Calcineurin Inhibitor and Mycophenolic Acid	1.29	1.29	1.51
Everolimus and Mycophenolic Acid	1.02	0.95	0.95

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Number of Participants With Composite Endpoint of Graft Survival (Non-death Censored) and Biopsy Proven Acute Rejection at 1 Year

"The primary objective of this pilot study will be to determine equivalency of Zortress® as compared to Rapamune® when used in our de novo immunosuppression regimen following renal transplantation. The primary endpoint will be a composite endpoint of graft survival (non-death censored) and biopsy proven acute rejection at 1 year. The primary outcome of immunosuppressive protection would be studied in our Thymoglobulin and rapid steroid discontinuation protocol, with half-dose Neoral as described above." (NCT01976390)
Timeframe: 1 Year

Intervention	Participants (Count of Participants)
	graft survival (non-death censored) at 1 year	biopsy proven acute rejection at 1 year
Rapamune (Sirolimus)	19	19
Zortress (Everolimus)	40	38

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Number of Pariticipants With Adverse Events as a Measure of Safety and Tolerability

Any sign or symptom that occurs during the study treatment plus the 30 days post treatment. (NCT02017860)
Timeframe: Adverse events were collected from first dose of study treatment until end of study treatment plus 30 days post treatment, up to maximum duration of approximately 5 years.

Intervention	Count of Participants (Number)
	Participants who had at least one Adverse Event	Participants with Grade 3/4 Adverse Event
Everolimus	4	2

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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

Intervention	percentage of participants (Number)
Arm 1: Everolimus	25
Arm 2: Everolimus and Temozolomide	NA
Arm 3: Everolimus (1p/19q Co-deletion Present)	50

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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

Intervention	percentage of participants (Number)
Arm 1: Everolimus	31
Arm 2: Everolimus and Temozolomide	NA

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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

Intervention	percentage of participants (Number)
Arm 3: Everolimus (1p/19q Co-deletion Present)	55.5

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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

Intervention	percentage of participants (Number)
Arm 1: Everolimus	NA
Arm 2: Everolimus and Temozolomide	NA
Arm 3: Everolimus (1p/19q Co-deletion Present)	NA

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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

Intervention	months (Median)
Arm 1: Everolimus	25.8
Arm 2: Everolimus and Temozolomide	NA
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

Intervention	percentage of participants (Number)
Arm 1: Everolimus	0
Arm 2: Everolimus and Temozolomide	NA
Arm 3: Everolimus (1p/19q Co-deletion Present)	11

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Overall Survival (OS)

OS is defined as time from randomization to death from any cause. Patients who are still alive are censored at the last date of known alive. (NCT02031536)
Timeframe: assessed every 3 months if < 2 years from study entry, and every 6 months up to 5 years from study entry or death, whichever occurred first

Intervention	years (Median)
Arm A (Everolimus)	2.05

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Disease Free Survival (DFS)

DFS is defined as time from randomization to disease recurrence or death, whichever occurred first. Patients who are still alive are censored at the last date of known free of recurrence. (NCT02031536)
Timeframe: assessed every 12 weeks while on treatment and then every 3 months if < 2 years from study entry; every 6 months up to 5 years from study entry or recurrence, whichever occurred first

Intervention	years (Median)
Arm A (Everolimus)	1.3

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Safety of Simvastatin in the Treatment of LAM-S and LAM-TS Patients

Safety is a primary outcome measure which will be assessed by any major changes or deterioration in patient health. (NCT02061397)
Timeframe: 5 months

Intervention	participants (Number)
Single Simvastatin Treatment Arm	0

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Percent Predicted FEV1

Lung function will be measured by FEV1: forced expiratory volume in 1s mean and calculated as % predicted +_ SD (standard deviation). (NCT02061397)
Timeframe: 5 months

Intervention	percent predicted FEV1 (Mean)
Single Simvastatin Treatment Arm	-2.9

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Time to Resolution of Stomatitis From Grade 2 or Greater to Grade 1 or Less

The number of days to achieve resolution of stomatitis from grade 2 or greater to grade 1 or less was assessed. Grade 1 = minimal symptoms, normal diet; grade 2 = symptomatic, but able to swallow a modified diet; grade 3 = symptomatic and unable to aliment or hydrate orally; and grade 4 = symptoms associated with life-threatening consequences. (NCT02069093)
Timeframe: 56 days

Intervention	Days (Median)
Dexamethasone Based Mouthwash	NA

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Blood Concentration of Everolimus and Exemestane

Blood samples were collected and analyzed. (NCT02069093)
Timeframe: 28 days (pre-dose)

Intervention	ng/mL (Geometric Mean)
	Everolimus (n=42)	Exemestane (n=48)
Dexamethasone Based Mouthwash	12.047	0.657

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Dose Intensity of Everolimus and Exemestane

The dose intensity was calculated as the cumulative dose of everolimus or exemestane divided by the length of time on treatment during the first 56 days of treatment. (NCT02069093)
Timeframe: 56 days

Intervention	mg/day (Median)
	Everolimus	Exemestane
Dexamethasone Based Mouthwash	10.0	25.0

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Number of Participants With All Grades of Stomatitis

The number of participants with all grades of stomatitis was defined as the number of participants who had stomatitis grade 1 or higher. Grade 1 = minimal symptoms, normal diet; grade 2 = symptomatic, but able to swallow a modified diet; grade 3 = symptomatic and unable to aliment or hydrate orally; and grade 4 = symptoms associated with life-threatening consequences. (NCT02069093)
Timeframe: 56 days

Intervention	Participants (Number)
	Stomatitis all grade	Not evaluable
Dexamethasone Based Mouthwash	18	1

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Number of Participants With Stomatitis Grade ≥ 2

The incidence of grade ≥ 2 stomatitis was reported. Grade 1 = minimal symptoms, normal diet; grade 2 = symptomatic, but able to swallow a modified diet; grade 3 = symptomatic and unable to aliment or hydrate orally; and grade 4 = symptoms associated with life-threatening consequences. (NCT02069093)
Timeframe: 56 days

Intervention	Participants (Number)
	Stomatitis grade >=2: Yes	Stomatitis grade >=2: No	Stomatitis grade >=2: Not evaluable
Dexamethasone Based Mouthwash	2	83	1

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Median Number of Mouthwashes Per Day

The median number of mouthwashes per day was assessed. (NCT02069093)
Timeframe: 56 days

Intervention	Number of mouthwashes (Median)
Dexamethasone Based Mouthwash	3.95

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Percentage of Healthy Tissue Coverage That Was Greater Than 40 Micrometers

The secondary efficacy endpoint is mechanistic Optical coherence tomography (OCT) healthy level of intimal tissue coverage, determined by the OCT core laboratory at 1 year for subjects in Cohorts A and B. This reports the percentage of healthy tissue coverage that was great than 40 micrometers. (NCT02073565)
Timeframe: 1 year

Intervention	Healthy Tissue Strut Coverage (>40 µm) % (Mean)
Combo	91.27
Everolimus Eluting Stent (EES)	74.82

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Number of Patients Exhibiting Human Antimurine Antibody (HAMA) Reaction

Serum will be assessed for HAMA development at index, 30 days, and 12 months in Cohort B subjects. Human antimurine antibody plasma assessment will be with blood draws performed during index procedure, 30 day follow-up visit, and 1 year catheterizations. (NCT02073565)
Timeframe: Day of device implantation, 30 days, 12 months

Intervention	Participants (Count of Participants)
	Baseline HAMA Responders	30 day HAMA Responders	1 Year HAMA Responders
Combo	0	0	0
Everolimus Eluting Stent (EES)	0	0	0

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Number of Participants With Target Vessel Failure (TVF)

The primary clinical endpoint of Target Vessel Failure (TVF), defined as cardiac death, target-vessel myocardial infarction (MI), or ischemia-driven Target Vessel Revascularization(TVR) by percutaneous or surgical methods, at 1 year. (NCT02073565)
Timeframe: 1 year follow-up

Intervention	Participants (Count of Participants)
Combo	20
Everolimus Eluting Stent (EES)	12

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Number of Patients With Clinically and Functionally Ischemia-Driven Target Lesion Revascularization (TLR)

Clinically and functionally ischemia-driven target lesion revascularization (TLR), including use of target-vessel Fractional Flow Reserve (FFR), analyzed dichotomously using the Fractional Flow Reserve (FFR) vs. Angiography in Multivessel Evaluation (FAME) study criteria of 0.8 during a 2 minute infusion of adenosine or adenosine triphosphate.34 Abnormal FFR-driven interventions at 1 year will be included in the evaluation of ischemia-driven TLR. (NCT02073565)
Timeframe: 1 year

Intervention	Participants (Count of Participants)
Combo	12
Everolimus Eluting Stent (EES)	8

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Adverse Drug Reactions

Measure and compare the incidence of significant immunosuppressant-related adverse drug reactions for each group. (NCT02096107)
Timeframe: 2 year

Intervention	Participants (Count of Participants)
Low Intensity Tacrolimus	11
Standard of Care	6

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Percentage of Participants Discontinuing or Modifying Immunosuppressant Use

Measure and compare the rates of immunosuppressant discontinuation and modification for each group. (NCT02096107)
Timeframe: 2 year

Intervention	percentage of participants (Number)
Low Intensity Tacrolimus	37
Standard of Care	20

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Kidney Allograft Survival

Compare the patient and graft survival rates at one-year post-transplant in each group. (NCT02096107)
Timeframe: 1 year

Intervention	percentage of patients graft survival (Number)
Low Intensity Tacrolimus	100
Standard of Care	100

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Infection

Compare the rates of post-transplant infections, including CMV, BK, and admissions to the hospital for infectious causes in each group. (NCT02096107)
Timeframe: 2 year

Intervention	percentage of subjects with infection (Number)
Low Intensity Tacrolimus	17
Standard of Care	30

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Renal Function Measured by Estimated Glomerular Filtration Rate (eGFR)

Measure and compare the estimated GFR (using the 4-variable modified MDRD equation) in patients converted to everolimus, low intensity tacrolimus and prednisone versus the standard of care tacrolimus, mycophenolate and prednisone regimen, both at one year and two years post-transplant. (NCT02096107)
Timeframe: 1 year

Intervention	mL/min/1.73 m^2 (Mean)
Low Intensity Tacrolimus	59
Standard of Care	56

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Kidney Allograft Fibrosis Assessment

"Measure and compare the change in interstitial fibrosis (morphometric analysis of trichrome stained slides) at one-year post-transplant in patients converted to everolimus, low intensity tacrolimus and prednisone versus the standard of care tacrolimus, mycophenolate and prednisone regimen.~The scale is a percentage of the tissue that demonstrates fibrosis. The scale range is 0 to 100%. The higher the percentage, the worse the fibrosis and the poorer the prognosis. A lower score (percentage) is therefore better." (NCT02096107)
Timeframe: 1 year

Intervention	% of fibrosis (Mean)
	Baseline	End of Follow-up
Low Intensity Tacrolimus	22.9	22.9
Standard of Care	20.8	27.8

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In Stent: Mean Thickness of Strut Coverage at Follow up

Mean thickness of strut coverage at follow up (In-Stent safety endpoint). Struts have been considered as covered when tissue overlying the struts is >0 μm by optical coherence tomography (OCT) (NCT02098876)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Resolute Integrity DES	0.118
Xience Xpedition DES	0.096

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In Stent Mean Cross-sectional Area of Neo-intimal Tissue Coverage

Cross-sectional area in neointimal hyperplasia by Optical Coherence Tomography (OCT) at 1 year following stent placement (NCT02098876)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Resolute Integrity DES	1.381
Xience Xpedition DES	0.949

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Stent Edge -Change in Plaque Area (Efficacy Endpoint) at 5 mm Proximal and Distal to Stent.

Change in plaque area at the stent edges will be calculated from the change in plaque area in the 5 mm proximal and distal segments by intravascular ultrasound (IVUS); calculated as follow-up values minus baseline values (NCT02098876)
Timeframe: 1 year

Intervention	mm^2 (Mean)
Resolute Integrity DES	-0.8
Xience Xpedition DES	-0.5

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In Stent: Plaque Prolapse Post-PCI (In-Stent Mechanistic Endpoint)

Plaque will be identified by Optical Coherence Tomography (OCT)- In-Stent: Plaque prolapse post-PCI (In-Stent mechanistic endpoint) (NCT02098876)
Timeframe: Immediately after stent implantation

Intervention	mm^2 (Mean)
Resolute Integrity DES	0.12
Xience Xpedition DES	0.13

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Stent Edge: Percent Area With Low Wall Shear Stress (WSS) at Stent Edges Post-PCI (Mechanistic Endpoint)

The % area of low wall shear stress in the 5 mm proximal and distal segments immediately after stent implantation will be measured by intravascular ultrasound (IVUS). (NCT02098876)
Timeframe: Immediately after stent implantation

Intervention	percentage of area (Mean)
Resolute Integrity DES	0.6
Xience Xpedition DES	0.64

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In-Stent: Degree of Vascular Straightening Post-percutaneous Coronary Intervention (PCI) (In-Stent Mechanistic Endpoint)

post PCI angulation by Angio: In-Stent: Degree of vascular straightening post-percutaneous coronary intervention (PCI) (In-Stent mechanistic endpoint) (NCT02098876)
Timeframe: Immediately after stent implantation

Intervention	Degree (Mean)
Resolute Integrity DES	40
Xience Xpedition DES	36

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In-Stent: Percent Area of Low Wall Shear Stress (WSS)-(In-Stent Mechanistic Endpoint)

The % area of low wall shear stress immediately after stent implantation will be measured by Optical Coherence Tomography (OCT) (NCT02098876)
Timeframe: Immediately after stent implantation

Intervention	percentage of area (Mean)
Resolute Integrity DES	0.9
Xience Xpedition DES	0.9

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Stent Edge: Degree of Vascular Straightening Post-percutaneous Coronary Intervention (PCI) at the Stent Edges (Stent Edge Mechanistic Endpoint)

Degree of vascular straightening post-percutaneous coronary intervention (PCI) at the stent edges (Stent Edge mechanistic endpoint) will be measured post PCI angulation by Angio (NCT02098876)
Timeframe: Immediately after stent implantation

Intervention	Degrees (Mean)
Resolute Integrity DES	22
Xience Xpedition DES	21

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Renal Function Assessed by Estimated Glomerular Filtartion Rate (eGFR)

"Renal function was assessed by eGFR using the MDRD-4 formula at 12 months after transplant:~eGFR = 186.3 * (serum creatinine)-1.154 * age-0.203 * (0.742 for women) * (1.21 if African American) where serum creatinine was in mg/dL and age in years." (NCT02115113)
Timeframe: At 12 months post-transplant

Intervention	mL/min/1.73m^2 (Least Squares Mean)
Group A (Tacrolimus Elimination Arm)	85.50
Group B (Tacrolimus Minimization Arm)	80.26

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Percentage of Participants With Treated Biopsy Proven Acute Rejection (tBPAR) Acute Rejection (AR), Graft Loss (GL) or Death (D)

Participants were assessed for tBPAR, AR, GL or death. For all suspected rejection episodes, regardless of initiation of anti-rejection treatment, a liver biopsy was to be performed preferably within 24 hours, latest within 48 hours whenever clinically possible. A treated biopsy proven acute rejection was considered an episode of acute rejection when demonstrated by local pathology reading with a rejection activity index of at least 3 or greater of acute rejection index and when treated with anti-rejection therapy. The allograft was considered lost on the day the subject was re-transplanted or died due to liver failure. (NCT02115113)
Timeframe: At 12 and 18 months post-transplant

Intervention	Participants (Count of Participants)
	tBPAR, 12 months	AR, 12 months	GL, 12 months	Death, 12 months	tBPAR, 18 months	AR, 18 months	GL, 18 months	Death, 18 months
Group A (Tacrolimus Elimination Arm)	2	2	0	1	2	2	0	1
Group B (Tacrolimus Minimization Arm)	1	1	0	0	1	1	0	1

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Change From Baseline (Randomization) in Serum Creatinine at 12 Months Post-transplant

Blood samples were collected to assess serum creatinine. (NCT02115113)
Timeframe: baseline, 12 months post-transplant

Intervention	mg/dL (Least Squares Mean)
Group A (Tacrolimus Elimination Arm)	-0.11
Group B (Tacrolimus Minimization Arm)	-0.05

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Number of Subjects With Disease Progression Using the Response Evaluation Criteria in Solid Tumors (RECIST) Version 1.1 (Phase IB)

Progression determined using response evaluation criteria in solid tumors (RECIST) version 1.1 or showed clinical progression. RECIST criteria for progression includes: 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 (including the baseline scan if that is the smallest), and at least a 5mm increase or the appearance of new lesions. Rates and associated 95% confidence limits will be estimated. (NCT02120469)
Timeframe: Up to 2 years

Intervention	Participants (Count of Participants)
Dose Level B1	10
Dose Level A1	8
Dose Level A2	3

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Number of Participants With Grade 3 or Higher Toxicities (Phase IB)

Will be graded according to the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. Rates and associated 95% exact Clopper and Pearson binomial confidence limits will be estimated for grade 3 or higher toxicities attributed to eribulin mesylate or everolimus. (NCT02120469)
Timeframe: On treatment, 21 days per cycle up to 2 years

Intervention	Participants (Count of Participants)
Dose Level B1	8
Dose Level A1	5
Dose Level A2	3

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Number of Participants Experiencing a Dose Limiting Toxicity (DLT) (Phase I) and the Recommended Phase IB Dose (RP2D)

DLT defined as an adverse event (AE) or abnormal laboratory value as at least possibly related to the study medication and meets any of the criteria per NCI CTCAE v4.0. (NCT02120469)
Timeframe: First cycle on treatment, up to 21 days

Intervention	Participants (Count of Participants)
Dose Level B1	4
Dose Level A1	4
Dose Level A2	2

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Median Progression Free Survival (Phase IB)

Kaplan Meier methods will be used to estimate the median and 95% confidence limits over all dose levels per protocol plan. (NCT02120469)
Timeframe: Form the date treatment begins until the first date on which recurrence, progression, or death due to any cause, assessed up to 2 years

Intervention	months (Median)
Treatment (Everolimus, Eribulin Mesylate)	2.6

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Median Overall Survival (Phase IB)

Kaplan Meier methods will be used to estimate the median and 95% confidence limits across all dose levels per protocol plan. (NCT02120469)
Timeframe: From start of treatment to death due to any cause, assessed up to 2 years

Intervention	months (Median)
Treatment (Everolimus, Eribulin Mesylate)	8.3

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Absolute Values of Blood Pressure: Mean

Absolute (mean and median) values for SBP and DBP at 3, 6, 12 and 24 months posttransplant; (NCT02137239)
Timeframe: Up to 24 Months

Intervention	mmHg (Mean)
	Diastolic Month 3	Systolic Month 3	Diastolic Month 6	Systolic Month 6	Diastolic Month 12	Systolic Month 12	Diastolic Month 24	Systolic Month 24
Treatment A	78.7	134.2	77.4	128.1	78.7	131.0	78.1	130.9
Treatment B	77.7	131.0	79.4	133.0	80.1	131.0	78.5	131.7

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Absolute Calculated Glomerular Filtration Rate (cGFR): Mean

Absolute (mean and median) cGFR values at 3, 6, 12 and 24 months post-transplant, as determined from the 4-variable Modification of Diet in Renal Disease (MDRD) formula (NCT02137239)
Timeframe: Up 24 Months post-transplant

Intervention	mL/min/1.73 m^2 (Mean)
	At 3 Months	At 6 Months	At 12 Months	At 24 Months
Treatment A	69.2	66.0	66.2	71.8
Treatment B	62.2	63.9	62.0	68.7

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Time to Clinically-suspected Biopsy-proven Acute Rejection (CSBPAR).

Time to Clinically suspected biopsy proven acute rejection (NCT02137239)
Timeframe: Up to 24 Months

Intervention	Months (Mean)
Treatment A	NA
Treatment B	NA

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Percentage of Participants With Serious Adverse Events (SAEs)

Percentage of participants with SAEs up to 24 months post-transplant (NCT02137239)
Timeframe: Up to 24 months Post-Transplant

Intervention	Percentage of participants with SAEs (Number)
Treatment A	52.0
Treatment B	60.6

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Percentage of Participants With Adverse Events (AEs)

Percentage of participants with AEs up to 24 months post-transplant (NCT02137239)
Timeframe: Up to 24 months Post-Transplant

Intervention	Percentage of participants with AEs (Number)
Treatment A	100.0
Treatment B	97.0

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Percentage of Particpants With Laboratory Test Abnormalities (LTAs)

Percentage of participants with laboratory tests with marked laboratory abnormalities (NCT02137239)
Timeframe: At 24 Months

Intervention	Percentage of participants (Number)
	Hemoglobin (Low)	Leukocytes (low)	Lymphocyte (Absolute) (low)	Neutrophils (Absolute) (low)	Aspartate Aminotransferase (High)	Creatinine (High)	Inorganic Phosphorus (low)	Potassium (high)	Sodium (low)	Albumin (low)	Glucose (high)	Triglycerides (high)	Uric Acid (high)
Treatment A	12.0	0	84.0	0	4.0	16.0	24.0	4.0	4.0	0	8.0	12.0	8.0
Treatment B	6.1	3.0	69.7	3.0	0	3.0	12.1	0	0	3.0	12.1	0	0

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Urine Protein Creatinine Ratio (UPr/Cr)

Urine protein to creatinine ratio (UPr/Cr) at 3, 6, 12 and 24 months post-transplant. (NCT02137239)
Timeframe: Up 24 Months post-transplant

Intervention	mg Protein/mg Creatinine (Mean)
	At 3 Months	At 6 Months	At 12 Months	At 24 Months
Treatment A	0.3146	0.3896	0.2835	0.3940
Treatment B	0.1412	0.1461	0.1849	0.1685

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Treatment Differences in Therapeutic Modalities

Treatment Received for Biopsy Proven Acute Rejection (Banff Grade IA or Higher), or Humoral (Antibody Mediated) Rejection Treatment regimen: Categorical analysis of CSBPAR episodes by treatment received. (NCT02137239)
Timeframe: at 6, 12 and 24 Months

Intervention	Percentage of participants with CSBPARs (Number)
	Corticosteroids (6 months)	Lymphocyte depleting agent (6 months)	Plasmapheresis (6 months)	IVIG (6 months)	Rituximab (6 months)	Corticosteroids (12 months)	Lymphocyte depleting agent (12 months)	Plasmapheresis (12 months)	IVIG (12 months)	Rituximab (12 months)	Corticosteroids (24 months)	Lymphocyte depleting agent (24 months)	Plasmapheresis (24 months)	IVIG (24 months)	Rituximab (24 months)
Treatment A	7.7	0	0	0	0	15.4	3.8	0	0	0	19.2	3.8	0	0	0
Treatment B	9.4	6.3	0	3.1	0	12.5	6.3	0	3.1	0	12.5	6.3	0	3.1	0

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Time to Event: Graft Loss and Death

The Number of days to participant Graft Loss and death for any reason (NCT02137239)
Timeframe: Up to 728 Days

Intervention	Days (Number)
	Graft Loss
Treatment A	107
Treatment B	2

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Percentage of Participants With New Onset Diabetes After Transplant

Percentage of participants with New Onset Diabetes After Transplantation (NODAT) at 6, 12, and 24 months post-transplant. (NCT02137239)
Timeframe: up to 24 months

Intervention	Percentage of participants (Number)
	Up to 6 Months	Up to 12 Months	Up to 24 Months
Treatment A	11.5	11.5	15.4
Treatment B	6.3	6.3	12.5

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Percentage of Participants With Events of Special Interest (ESIs)

"Percentage of participants which have one of the following events of special interest:~Serious Infections Post-Transplant Lymphoproliferative Disorder (PTLD) Progressive multifocal leukoencephalopathy (PML) Malignancies (Other than PTLD) including non-melanoma skin carcinomas (Malignancies) Tuberculosis Infections Central Nervous System (CNS) Infections Viral Infections Infusion Related reactions within 24 hours since belatacept infusion" (NCT02137239)
Timeframe: Up to 24 Months

Intervention	Percentage of participants with ESIs (Number)
	Serious Infections	PTLD	PML	Malignancies	TB	CNS Infections	Viral Infections	Infusion Related Reactions
Treatment A	16	4.0	0	4.0	0	0	0	1
Treatment B	15.2	3.0	0	3.0	0	0	0	0

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Percentage of Participants With Donor Specific Anti-HLA Antibodies (DSA)

Percentage of participants with, and titers of pre-existing (pre-transplant) DSA on Day 1 (pre-transplant, pre-dose), and at Months 12 and 24 posttransplant (NCT02137239)
Timeframe: Up to 24 Months

Intervention	Percentage of Participants (Number)
	Baseline Class 1 DSA	Baseline Class 2 DSA	Baseline Both Class 1 and 2 DSA	12 Month Class 1 DSA	12 Month Class 2 DSA	12 Month Both Class 1 and 2 DSA	24 Month Class 1 DSA	24 Month Class 2 DSA	24 Month Both Class 1 and 2 DSA
Treatment A	10	0	0	8.00	0	0	8.00	0	0
Treatment B	0	0	0	0	3.03	0	3.03	3.03	0

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Percentage of Participants With De Novo Donor Specific Anti-HLA Antibodies (DSA)

Characterization of any de novo DSA detected by IgM and IgG subclasses, and by the presence or absence of complement fixing properties. (NCT02137239)
Timeframe: Up to 24 Months

Intervention	Percentage (Number)
	Baseline Class 1 DSA	Baseline Class 2 DSA	Baseline Both Class 1 and 2 DSA	De Novo 12 Month Class 1 DSA	De Novo 12 Month Class 2 DSA	De Novo 12 Month Both Class 1 and 2 DSA	De Novo 24 Month Class 1 DSA	De Novo 24 Month Class 2 DSA	De Novo 24 Month Both Class 1 and 2 DSA
Treatment A	10	0	0	0	0	0	0	0	0
Treatment B	0	0	0	0	0	0	3.45	0	0

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Percentage of Participants With BANFF Grade by Severity Grades. BANFF Type (Grade) for Acute/Active Rejection

"Treatment differences in the severity grades to treat all episodes of CSBPAR at 6, 12, and 24 months post-transplant.~Type 1A - Cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of moderate tubulitis (>4 mononuclear cells/Tubular cross section or group of 10 Tubular cell). Type 1B - Cases with significant interstitial infiltration (>25% of parenchyma affected) and foci of moderate tubulitis (>10 mononuclear cells/Tubular cross section or group of 10 Tubular cell).Type 2A - Cases with mild to moderate intimal arteritis.Type 2B - Cases with severe intimal arteritis comprising >25% of the luminal area. Type 3 - Cases with transmural arteritis and/or arterial fibrinoid change and necrosis of medial smooth muscle cells (v3 with accompanying lymphocytic inflammation)" (NCT02137239)
Timeframe: At 6, 12 and 24 Months

Intervention	Percentage of Participants (Number)
	6 Months: Mild Acute (1A)	6 Months: Mild Acute (1B)	6 Months: Moderate Acute (2A)	6 Months: Moderate Acute (2B)	6 Months: Severe Acute	12 Months: Mild Acute (1A)	12 Months: Mild Acute (1B)	12 Months: Moderate Acute (2A)	12 Months: Moderate Acute (2B)	12 Months: Severe Acute	24 Months: Mild Acute (1A)	24 Months: Mild Acute (1B)	24 Months: Moderate Acute (2A)	24 Months: Moderate Acute (2B)	24 Months: Severe Acute
Treatment A	3.8	0	7.7	0	0	7.7	0	7.7	0	0	11.5	0	7.7	0	0
Treatment B	0	3.1	6.3	0	0	3.1	3.1	6.3	0	0	3.1	3.1	6.3	0	0

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Percentage of Clinically-suspected Biopsy-proven Acute Rejection (CSBPAR) at 6 Months

Number of Participants with Clinically-suspected biopsy-proven acute rejection (CSBPAR) at 6 Months (NCT02137239)
Timeframe: 6 Months

Intervention	Percentage of participants (Number)
Treatment A	7.7
Treatment B	9.4

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Number of Participants Who Survive With a Functioning Graft

Number of all participants who survive with a functioning graft at 6, 12 and 24 months post transplant (NCT02137239)
Timeframe: At 6, 12 and 24 months

Intervention	Participants (Count of Participants)
	At 6 Months	At 12 Months	At 24 Months
Treatment A	25	25	25
Treatment B	31	31	31

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Number of Participants Who Experience Graft Loss Post Transplant

Number of all participants who experience graft loss at 6, 12 and 24 months post transplant (NCT02137239)
Timeframe: At 6, 12 and 24 months

Intervention	Participants (Count of Participants)
	At 6 Months	At 12 Months	At 24 Months
Treatment A	1	1	1
Treatment B	1	1	1

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Number of Participants Deaths Post Transplant

Number of participant deaths at 6, 12 and 24 months post transplant (NCT02137239)
Timeframe: up to 24 months

Intervention	Participants (Count of Participants)
	At 6 Months	At 12 Months	At 24 Months
Treatment A	0	0	0
Treatment B	0	0	0

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Median Calculated Glomerular Filtration Rate (cGFR)

Median cGFR values at 3, 6, 12 and 24 months post-transplant, as determined from the 4-variable Modification of Diet in Renal Disease (MDRD) formula (NCT02137239)
Timeframe: Up 24 Months post-transplant

Intervention	mL/min/1.73 m^2 (Median)
	At 3 Months	At 6 Months	At 12 Months	At 24 Months
Treatment A	64.0	64.0	66.0	73.5
Treatment B	62.0	67.0	62.5	68.0

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Mean Changes From Baseline Values of Lipid Values

"Mean changes from baseline values in the following:~Serum total cholesterol (TC) Serum high density lipoprotein (HDL) cholesterol Serum low density lipoprotein (LDL) cholesterol Serum triglycerides (TG)" (NCT02137239)
Timeframe: at months 12 and 24

Intervention	mg/dL (Mean)
	TC Month 12	TC Month 24	HDL Month 12	HDL Month 24	LDL Month 12	LDL Month 24	TG Month 12	TG Month 24
Treatment A	25.7	26.6	5.4	6.2	25.7	17.4	3.3	106.8
Treatment B	-2.8	10.0	1.9	4.8	10.8	15.7	-86.1	-13.6

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Mean Changes From Baseline Values for Blood Pressure

Mean changes from baseline values for SBP and DBP at 6, 12 and 24 months post-transplant (NCT02137239)
Timeframe: Up to 24 Months

Intervention	mmHg (Mean)
	Diastolic Month 6	Systolic Month 6	Diastolic Month 12	Systolic Month 12	Diastolic Month 24	Systolic Month 24
Treatment A	1.0	-4.0	2.3	-1.1	0.9	-2.3
Treatment B	4.8	-0.7	5.4	-3.2	2.1	-4.2

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Mean Change From Month 3 in cGFR

The mean change from Month 3 cGFR at 3, 6, 12 and 24 months post-transplant (NCT02137239)
Timeframe: Up 24 Months post-transplant

Intervention	mL/min/1.73 m^2 (Mean)
	At 3 Months	At 6 Months	At 12 Months	At 24 Months
Treatment A	0	-3.2	-3.1	3.1
Treatment B	0	2.8	1.4	6.3

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Mean and Mean Change From Baseline in Whole Blood HbA1c

Mean whole blood HbA1C concentrations, and mean changes from baseline values at Months 6, 12 and 24 months post-transplant. (NCT02137239)
Timeframe: Up to 24 months

Intervention	mg/dL (Mean)
	Mean Value at 6 months	Change from baseline at 6 months	Mean Value at 12 months	Change from baseline at 12 months	Mean Value at 24 months	Change from baseline at 24 months
Treatment A	6.11	0.34	6.18	0.47	6.24	0.66
Treatment B	6.13	0.48	6.21	0.32	6.29	0.41

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Mean and Mean Change From Baseline in Blood Glucose

Mean fasting blood glucose levels, and mean changes from baseline values at Months 6, 12 and 24 months post- transplant (NCT02137239)
Timeframe: Up to 24 months

Intervention	mg/dL (Mean)
	Mean Value at 6 months	Change from baseline at 6 months	Mean Value at 12 months	Change from baseline at 12 months	Mean Value at 24 months	Change from baseline at 24 months
Treatment A	107.2	4.9	101.1	-1.3	127.5	22.3
Treatment B	107.2	4.8	127.5	20.6	111.8	15.0

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Clinically-suspected Biopsy-proven Acute Rejection (CSBPAR) at 6, 12 and 24 Months

"Clinically-suspected biopsy-proven acute rejection (CSBPAR) at 6, 12 and 24 Months~Change in the incidence of CSBPAR at 6, 12 and 24 months post transplant, in the belatacept + EVL(Treatment A) as compared to TAC + MMF (Treatment B)." (NCT02137239)
Timeframe: Up to 24 Months

Intervention	Percentage of CSBPAR (Number)
	CSBPAR at 6 Months	CSBPAR at 12 months	CSBPAR at 24 Months
Treatment A	7.7	11.5	15.4
Treatment B	9.4	12.5	12.5

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Absolute Values of Fasting Lipid Values: Median

"Absolute (mean and median) values at 3, 6, 12 and 24 months post-transplant for the following:~Serum total cholesterol (TC) Serum high density lipoprotein (HDL) cholesterol Serum low density lipoprotein (LDL) cholesterol Serum triglycerides (TG)" (NCT02137239)
Timeframe: Up to 24 Months

Intervention	mg/dL (Median)
	TC Month 3	TC Month 6	TC Month 12	TC Month 24	HDL Month 3	HDL Month 6	HDL Month 12	HDL Month 24	LDL Month 3	LDL Month 6	LDL Month 12	LDL Month 24	TG Month 3	TG Month 6	TG Month 12	TG Month 24
Treatment A	167.0	187.0	184.0	193.0	45.0	45.5	50.0	49.0	89.0	99.5	104.0	103.5	147.0	157.5	154.0	159.0
Treatment B	173.0	178.0	171.5	166.0	49.0	49.0	47.0	49.0	95.0	100.0	91.5	86.0	128.0	126.0	130.0	114.0

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Absolute Values of Fasting Lipid Values: Mean

Intervention	mg/dL (Mean)
	TC Month 3	TC Month 6	TC Month 12	TC Month 24	HDL Month 3	HDL Month 6	HDL Month 12	HDL Month 24	LDL Month 3	LDL Month 6	LDL Month 12	LDL Month 24	TG Month 3	TG Month 6	TG Month 12	TG Month 24
Treatment A	181.2	197.7	189.0	193.2	50.6	46.4	49.4	50.1	96.9	115.2	107.5	97.9	171.6	180.0	162.4	263.4
Treatment B	174.4	175	169.9	168.2	50.4	53.9	49.6	51.3	96.5	93.7	88.0	91.5	137.8	138.3	161.3	145.0

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Absolute Values of Blood Pressure: Median

Absolute (mean and median) values for SBP and DBP at 3, 6, 12 and 24 months posttransplant; (NCT02137239)
Timeframe: Up to 24 Months

Intervention	mmHg (Median)
	Diastolic Month 3	Systolic Month 3	Diastolic Month 6	Systolic Month 6	Diastolic Month 12	Systolic Month 12	Diastolic Month 24	Systolic Month 24
Treatment A	78.5	135.5	75.5	127.0	77.0	130.0	78.0	130.0
Treatment B	80.0	131.0	80.0	131.0	81.0	126.0	79.0	130.0

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Progression-free Survival (Fulvestrant Versus Fulvestrant + Everolimus + Anastrozole)

From date of registration to date of first documentation of progression or death due to any cause. Participants last known to be alive without report of progression are censored at date of last contact. (NCT02137837)
Timeframe: up to 5 years

Intervention	months (Median)
Arm 1: Fulvestrant + Everolimus Placebo + Anastrozole Placebo	14.0
Arm 3: Fulvestrant + Everolimus + Anastrozole	9.9

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Progression Free Survival (Fulvestrant + Everolimus vs Fulvestrant + Everolimus + Anastrozole)

Intervention	months (Median)
Arm 2: Fulvestrant + Everolimus + Anastrozole Placebo	11.3
Arm 3: Fulvestrant + Everolimus + Anastrozole	9.90

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Overall Survival

From date of registration to date of death due to any cause. Participants last known to be alive without report of progression are censored at date of last contact. (NCT02137837)
Timeframe: up to 5 years

Intervention	months (Median)
Arm 1: Fulvestrant + Everolimus Placebo + Anastrozole Placebo	46.8
Arm 2: Fulvestrant + Everolimus + Anastrozole Placebo	56.6
Arm 3: Fulvestrant + Everolimus + Anastrozole	33.6

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Molecular Determinants of Response in Circulating Tumor Cells: CTC-ETI

CTC-Endocrine Therapy Index (CTC-ETI) on the CellSearch® platform. Based on enumeration of CTC/7.5 mL of whole blood, with >= 5 being elevated. (Due to limited samples collected, full analysis was not able to be performed as planned, so outcome measure reported here is number with elevated Day 1 CTC.) (NCT02137837)
Timeframe: Day 1, Day 29, time of progression (Day 29 to be collected only if Day 1 CTC was elevated.)

Intervention	Participants (Count of Participants)
Arm 1: Fulvestrant + Everolimus Placebo + Anastrozole Placebo	1
Arm 2: Fulvestrant + Everolimus + Anastrozole Placebo	1
Arm 3: Fulvestrant + Everolimus + Anastrozole	0

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Clinical Benefit Rate

Proportion of participants who have confirmed and unconfirmed partial response, complete response or stable disease. (NCT02137837)
Timeframe: assessed every 12 weeks, up to 5 years

Intervention	percentage of participants (Number)
Arm 1: Fulvestrant + Everolimus Placebo + Anastrozole Placebo	69
Arm 2: Fulvestrant + Everolimus + Anastrozole Placebo	83
Arm 3: Fulvestrant + Everolimus + Anastrozole	67

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Number of Patients With Gr 3 Through 5 Adverse Events That Are Related to Study Drugs

Adverse Events (AEs) are reported by CTCAE Version 4.0. Only adverse events that are possibly, probably or definitely related to study drug are reported. (NCT02137837)
Timeframe: Duration of treatment and follow up until death or 5 years post registration

Intervention	Participants (Number)
	Abdominal pain	Anorexia	Aspartate aminotransferase increased	Dehydration	Diarrhea	Fatigue	Flu like symptoms	Generalized muscle weakness	Hyperglycemia	Hypertension	Hypocalcemia	Hypokalemia	Hyponatremia	Hypophosphatemia	Hypotension	Localized edema	Lymphocyte count decreased	Mucositis oral	Neutrophil count decreased	Rash maculo-papular	Resp, thoracic and mediastinal disorders - Other	Sore throat	Thromboembolic event	Vomiting	White blood cell decreased
Arm 1: Fulvestrant + Everolimus Placebo + Anastrozole Placebo	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0
Arm 2: Fulvestrant + Everolimus + Anastrozole Placebo	1	1	1	2	1	2	1	1	1	2	1	2	1	1	0	1	1	0	2	0	1	0	0	1	1
Arm 3: Fulvestrant + Everolimus + Anastrozole	0	1	0	1	0	0	0	0	0	2	0	1	0	0	1	0	0	1	0	1	0	1	1	0	0

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Response Rate

Proportion of participants who have confirmed or unconfirmed partial or complete response to therapy (NCT02137837)
Timeframe: assessed every 12 weeks, up to 5 years

Intervention	percentage of participants (Number)
Arm 1: Fulvestrant + Everolimus Placebo + Anastrozole Placebo	22
Arm 2: Fulvestrant + Everolimus + Anastrozole Placebo	60
Arm 3: Fulvestrant + Everolimus + Anastrozole	44

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Progression-Free Survival (Fulvestrant vs Fulvestrant + Everolimus )

From date of registration to date of first documentation of progression or death due to any cause. Participants last known to be alive are censored at date of last contact. (NCT02137837)
Timeframe: up to 5 years

Intervention	months (Median)
Arm 1: Fulvestrant + Everolimus Placebo + Anastrozole Placebo	14.0
Arm 2: Fulvestrant + Everolimus + Anastrozole Placebo	11.3

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Progression Free Survival

Progression Free Survival (PFS) was defined as the time from randomization to the first of either disease progression or death from any cause. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT02143726)
Timeframe: 4 years and 4 months

Intervention	Months (Median)
Arm 1 (Sorafenib)	9.4
Arm 2 (Sorafenib and Everolimus)	24.7

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Overall Survival

(NCT02143726)
Timeframe: 5 years

Intervention	Months (Median)
Arm 1 (Sorafenib)	NA
Arm 2 (Sorafenib and Everolimus)	40.1

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Confirmed Response Rate

A patient will be classified as a confirmed response per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT02143726)
Timeframe: 4 years 4 months

Intervention	Proportion of participants (Number)
Arm 1 (Sorafenib)	0.188
Arm 2 (Sorafenib and Everolimus)	0.235

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Number of Participants With Grade 3 or Higher Adverse Events

The maximum grade for each type of adverse event will be summarized using CTCAE version 4.0. The frequency and percentage of grade 3+ adverse events will be compared between the 2 treatment arms. (NCT02143726)
Timeframe: 4 years 3 months

Intervention	Participants (Count of Participants)
Arm 1 (Sorafenib)	10
Arm 2 (Sorafenib and Everolimus)	12

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Percent of Participants With Grade 3 or Higher Infectious Adverse Event(s)

"The severity of infectious adverse events (AEs) was classified into grades as follows:~Grade 1 = asymptomatic; clinical or diagnostic observation only; intervention with oral antibiotic, antifungal, or antiviral agent only; no invasive intervention required~Grade 2 = symptomatic; intervention with intravenous antibiotic, antifungal, or antiviral agent; invasive intervention may be required~Grade 3 = any infection associated with hemodynamic compromise requiring pressors; any infection necessitating intensive care unit level of care; any infection necessitating operative intervention; any infection involving the central nervous system; any infection with a positive fungal blood culture; any proven or probable aspergillus infection; any tissue invasive fungal infection; any pneumocystis jiroveci infection~Grade 4 = life-threatening infection~Grade 5 = death resulting from infection" (NCT02188719)
Timeframe: Transplantation to 40 Weeks Post Transplantation

Intervention	Percent of Participants (Number)
Cohort 1	0
Cohort 2	11.1

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Percent of Participants With Adverse Events (AEs) Attributable to the Donor Alloantigen Reactive Tregs (darTregs) Infusion

"AEs classified by the site investigator/clinician as possibly or definitely related to the study treatment, the Donor Alloantigen Reactive Tregs (darTregs) infusion. These AEs include:~infusion reaction~Grade 3 or higher cytokine release syndrome (Reference: National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 4.0 (4/28/2009) grading criteria~malignant cellular transformation." (NCT02188719)
Timeframe: Transplantation to 40 Weeks Post Transplantation

Intervention	Percent of Participants (Number)
Cohort 2	0

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Percent of Participants With Grade 2 or Higher Hematologic Adverse Events (AEs) of Anemia, Neutropenia, and/or Thrombocytopenia

"The severity of adverse events (AEs) was classified into grades using the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 4.0 (4/28/2009):~Grade 1 = mild AE~Grade 2 = moderate AE~Grade 3 = severe and undesirable AE~Grade 4 = life-threatening or disabling AE~Grade 5 = death" (NCT02188719)
Timeframe: Transplantation to 40 Weeks Post Transplantation

Intervention	Percent of Participants (Number)
	Anemia	Neutropenia	Thrombocytopenia
Cohort 1	66.7	16.7	16.7
Cohort 2	22.2	0	0

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Percent of Participants With Biopsy-Proven Acute and/or Chronic Rejection

"Biopsy-proven acute rejection graded as Mild, Moderate or Severe, per 1997 Banff classification. Chronic Rejection graded using Banff 2000 classification.~References: 1.) Banff Schema for Grading Liver Allograft Rejection: An International Consensus Document developed by an international panel of experts in liver transplantation pathology, hepatology, and surgery (Hepatology 1997; 25(3): 658-663). 2.) Update of the International Banff Schema for Liver Allograft Rejection: Working Recommendations for the Histopathologic Staging and Reporting of Chronic Rejection (Hepatology 2000; 31(3): 792-799)." (NCT02188719)
Timeframe: Transplantation to 40 Weeks Post Transplantation

Intervention	Percent of Participants (Number)
	Mild Acute Rejection	Moderate Acute Rejection	Severe Acute Rejection	Chronic Rejection
Cohort 1	0	0	0	0
Cohort 2	11.1	0	0	0

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Percent of Participants With Grade 3 or Higher Wound Complication(s) Adverse Event(s)

"The severity of adverse events (AEs) was classified into grades using the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 4.0 (4/28/2009):~Grade 3 wound complications are defined as Hernia without evidence of strangulation; fascial disruption/dehiscence; primary wound closure or revision by operative intervention indicated~Grade 4 complications are defined as Hernia with evidence of strangulation; major reconstruction flap, grafting, resection, or amputation indicated" (NCT02188719)
Timeframe: Transplantation to 40 Weeks Post Transplantation

Intervention	Percent of Participants (Number)
Cohort 1	0
Cohort 2	0

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Progression-free Survival

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT02201212)
Timeframe: Baseline, Up to 2 Years

Intervention	months (Median)
Everolimus	2.0

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Duration of Response

Duration of Response Rate (NCT02201212)
Timeframe: Baseline, Every 8 weeks, 2 Years

Intervention	months (Median)
Everolimus	12.7

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Toxicity Rate

CTCAE v4.0 Toxicity Rate Grade 3 or higher (NCT02201212)
Timeframe: 2 Years

Intervention	Participants (Count of Participants)
Everolimus	3

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Objective Response Rate

"RECIST 1.1 criteria for Objective Response:~Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by 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" (NCT02201212)
Timeframe: Baseline, Every 8 weeks, 2 Years

Intervention	Participants (Count of Participants)
Everolimus	2

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Overall Survival

Overall Survival Rate (NCT02201212)
Timeframe: 4 Years

Intervention	months (Median)
Everolimus	7.27

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Median Survival

Survival is defined as the duration alive from study entry until death. (NCT02228681)
Timeframe: Following treatment discontinuation, patients are followed quarterly for 2 years, semi-annually for 3 more years, annually thereafter.

Intervention	Months (Median)
Everolimus and Letrozole	NA
Tamoxifen and Medroxyprogesterone Acetate	16.6

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Frequency of Response

"A confirmed complete or partial response as defined by RECIST 1.1 was considered a response. Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR" (NCT02228681)
Timeframe: From date of randomization until the date of first documented progression or date of death , up to 3 years.

Intervention	Number of participants (Number)
Everolimus and Letrozole	9
Tamoxifen and Medroxyprogesterone Acetate	8

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Frequency and Severity of CTCAE (Common Toxicity Criteria for Adverse Events) Version 4

Maximum grade of physician assessed adverse events graded and categorized using Common Toxicity Criteria for Adverse Events (CTCAE) version 4 (NCT02228681)
Timeframe: Assessed throughout the treatment period and for 30 days after discontinuation of treatment. Treatment continues until progression of disease.

Intervention	Participants (Count of Participants)
	Grade 1	Grade 2	Grade 3	Grade 4	Grade 5
Everolimus and Letrozole	2	6	27	2	0
Tamoxifen and Medroxyprogesterone Acetate	2	14	17	2	1

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Median Progression-free Survival

Progression-free Survival is defined as the duration alive from study entry until progression is documented, or death; whichever comes sooner. Progressive disease is defined as at least a 5 mm absolute increase and a 20% relative increase in the sum of measurable target lesions' longest dimensions relative to the smallest sum at baseline or on study or the appearance of new lesions or unequivocal progression of existing non-target lesions. (NCT02228681)
Timeframe: Tumor measurements were done at 8 and 16 weeks after initiating treatment and then every 12 weeks and compared with baseline measurements prior to treatment. Measurements are continued until disease progression is documented or death.

Intervention	months (Median)
Everolimus and Letrozole	6.4
Tamoxifen and Medroxyprogesterone Acetate	3.7

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PEPI Score

To obtain the PEPI score, risk points for relapse-free survival (RFS) are assigned depending on the hazard ratio (HR) from the multivariable analysis. The total PEPI score assigned to each patient is the sum of the risk points derived from the pT stage, pN stage, Ki67 level, and estrogen receptor status of the surgical specimen. A HR in the range of 1 to 2 receives one risk point; a HR in the 2 to 2.5 range, two risk points; a HR greater than 2.5, three risk points. The total risk point score for each patient is the sum of all the risk points accumulated from the four factors in the model, ranges from 0 (best possible outcome) to 12 (worst possible outcome). (NCT02236572)
Timeframe: up to 26 weeks

Intervention	units on a scale (Median)
Aromatase Inhibitor Plus Everolimus	3

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Participant Ability to Tolerate Study Treatment With Minimal Side Effects

Adverse events (using CTCAE (4.0)) that begin or worsen after informed consent were recorded. Adverse events are itemized in the adverse events module (in terms of total events and total participants experiencing events). Presented are the total number of participants that experience adverse events. For clarification, counts of participants that experienced serious adverse events and counts of participants that experienced 'other' (not serious) adverse events are presented separately. (NCT02236572)
Timeframe: Up to 26 weeks

Intervention	Participants (Count of Participants)
	Participants with Serious Adverse Events	Participants with Other (Not Including Serious) Adverse Events
Aromatase Inhibitor Plus Everolimus	5	17

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Symptomatic Skeletal Event-free Survival (SSE-FS)

Time from date of randomization to occurrence of one of the following, whichever happened earlier: 1) an on study SSE, which was defined as the use of external beam radiotherapy (EBRT) to relieve skeletal symptoms, the occurrence of new symptomatic pathological bone fractures (vertebral or nonvertebral), the occurrence of spinal cord compression, a tumor related orthopedic surgical intervention; or 2) death from any cause. Per Protocol Amendment 10, following primary analysis completion, further assessments were focused on safety, and only limited efficacy data including SSE and survival were collected and not designed to support reconsideration of the primary analysis efficacy conclusions. Accordingly, no formal statistical analyses were performed for primary and secondary efficacy outcomes in the final analysis. All primary and secondary efficacy outcome measures presented in this document came from the primary completion analysis. (NCT02258451)
Timeframe: Up to 55 months

Intervention	Months (Median)
Radium-223 + EXE/EVE	21.1
Placebo + EXE/EVE	19.9

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Number of Participants With Hematological Toxicities: Worst Grade Under Treatment (From First Dosing Till Primary Analysis)

(NCT02258451)
Timeframe: From first dosing till primary analysis cutoff date, up to 55 months

Intervention	Participants (Count of Participants)
	Anemia72094292					Anemia72094293	Leukocytosis72094292	Leukocytosis72094293	Hemoglobin increased72094292	Hemoglobin increased72094293	Lymphocyte count decreased72094292	Lymphocyte count decreased72094293	Lymphocyte count increased72094293	Lymphocyte count increased72094292	Neutrophil count decreased72094293	Neutrophil count decreased72094292	Platelet count decreased72094293	Platelet count decreased72094292	White blood cell decreased72094293	White blood cell decreased72094292
	Normal	Grade 1	Grade 2	Grade 3	Grade 4
Radium-223 + EXE/EVE	61
Placebo + EXE/EVE	57
Radium-223 + EXE/EVE	43
Placebo + EXE/EVE	55
Radium-223 + EXE/EVE	21
Placebo + EXE/EVE	11
Radium-223 + EXE/EVE	14
Placebo + EXE/EVE	14
Radium-223 + EXE/EVE	139
Placebo + EXE/EVE	137
Radium-223 + EXE/EVE	0
Radium-223 + EXE/EVE	1
Radium-223 + EXE/EVE	138
Radium-223 + EXE/EVE	20
Placebo + EXE/EVE	33
Radium-223 + EXE/EVE	63
Placebo + EXE/EVE	45
Placebo + EXE/EVE	24
Radium-223 + EXE/EVE	11
Placebo + EXE/EVE	35
Placebo + EXE/EVE	0
Radium-223 + EXE/EVE	2
Placebo + EXE/EVE	2
Radium-223 + EXE/EVE	137
Placebo + EXE/EVE	135
Radium-223 + EXE/EVE	24
Placebo + EXE/EVE	29
Radium-223 + EXE/EVE	47
Placebo + EXE/EVE	28
Radium-223 + EXE/EVE	19
Radium-223 + EXE/EVE	49
Placebo + EXE/EVE	78
Radium-223 + EXE/EVE	60
Placebo + EXE/EVE	61
Radium-223 + EXE/EVE	7
Radium-223 + EXE/EVE	64
Placebo + EXE/EVE	74
Radium-223 + EXE/EVE	37
Placebo + EXE/EVE	47
Radium-223 + EXE/EVE	59
Placebo + EXE/EVE	36
Radium-223 + EXE/EVE	17
Placebo + EXE/EVE	3
Placebo + EXE/EVE	1
Radium-223 + EXE/EVE	25
Placebo + EXE/EVE	50

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Number of Participants With Hematological Toxicities: Worst Grade Under Treatment

(NCT02258451)
Timeframe: From first dosing up to 30 days after the last administration of study treatments, up to 72.6 months

Intervention	Participants (Count of Participants)
	Anemia72094292					Anemia72094293	Leukocytosis72094293	Leukocytosis72094292	Hemoglobin increased72094292	Hemoglobin increased72094293	Lymphocyte count decreased72094293	Lymphocyte count decreased72094292	Lymphocyte count increased72094293	Lymphocyte count increased72094292	Neutrophil count decreased72094293	Neutrophil count decreased72094292	Platelet count decreased72094293	Platelet count decreased72094292	White blood cell decreased72094293	White blood cell decreased72094292
	Grade 3	Normal	Grade 1	Grade 2	Grade 4
Radium-223 + EXE/EVE	61
Placebo + EXE/EVE	57
Radium-223 + EXE/EVE	43
Placebo + EXE/EVE	55
Radium-223 + EXE/EVE	21
Placebo + EXE/EVE	11
Radium-223 + EXE/EVE	14
Placebo + EXE/EVE	14
Radium-223 + EXE/EVE	139
Placebo + EXE/EVE	0
Radium-223 + EXE/EVE	138
Placebo + EXE/EVE	137
Radium-223 + EXE/EVE	20
Placebo + EXE/EVE	33
Radium-223 + EXE/EVE	63
Placebo + EXE/EVE	45
Placebo + EXE/EVE	24
Radium-223 + EXE/EVE	2
Radium-223 + EXE/EVE	11
Placebo + EXE/EVE	35
Placebo + EXE/EVE	2
Radium-223 + EXE/EVE	137
Placebo + EXE/EVE	135
Radium-223 + EXE/EVE	23
Placebo + EXE/EVE	30
Radium-223 + EXE/EVE	48
Placebo + EXE/EVE	28
Radium-223 + EXE/EVE	19
Radium-223 + EXE/EVE	0
Radium-223 + EXE/EVE	49
Placebo + EXE/EVE	77
Radium-223 + EXE/EVE	60
Placebo + EXE/EVE	60
Radium-223 + EXE/EVE	7
Radium-223 + EXE/EVE	64
Placebo + EXE/EVE	74
Radium-223 + EXE/EVE	37
Placebo + EXE/EVE	48
Radium-223 + EXE/EVE	59
Placebo + EXE/EVE	37
Radium-223 + EXE/EVE	17
Placebo + EXE/EVE	3
Radium-223 + EXE/EVE	1
Placebo + EXE/EVE	1
Radium-223 + EXE/EVE	25

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Number of Participants With Treatment-emergent Adverse Events (TEAEs) (From First Dosing Till Primary Analysis)

An AE was any untoward medical occurrence (i.e. any unfavorable and unintended sign [including abnormal laboratory findings], symptom or disease) in a patient or clinical investigation participant after providing written informed consent for participation in the study. AEs were considered to be treatment-emergent if they started or worsened after first application of study intervention up to 30 days after end of treatment with study intervention. A serious adverse event (SAE) was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening; persistent or significant disability/incapacity; congenital anomaly; another medical important serious event as judged by the investigator and an occurrence of any additional malignancies, including acute myelocytic leukemia or hematological conditions. (NCT02258451)
Timeframe: From first dosing till primary analysis cutoff date, up to 55 months

Intervention	Participants (Count of Participants)
	Any TEAE	Serious TEAE	Radium-223/Placebo-related TEAEs	Exemestane-related TEAEs	Everolimus-related TEAEs
Placebo + EXE/EVE	136	53	50	64	125
Radium-223 + EXE/EVE	139	57	73	75	130

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Radiological Progression-free Survival (rPFS)

Time from the date of randomization to the date of confirmed radiological progression in either soft tissue, viscera or bone, or death (if death occurs before progression). Progression is defined using the modified RECIST 1.1 criteria (the modification refers to bone lesions assessment). Progression is defined as a 20% increase in the sum of the longest diameter of target lesions, or an unequivocal increase in non-target lesions, or the appearance of new lesions. All bone lesions are considered non-measurable and new bone lesions identified by bone scan should be confirmed by further imaging (CT/MRI). If a new bone lesion or unequivocal increase in size of bone lesions is only visible on a CT/MRI and not visible on a technetium-99m bone scan, progression should be declared without further confirmation. (NCT02258451)
Timeframe: Up to 55 months

Intervention	Months (Median)
Radium-223 + EXE/EVE	7.9
Placebo + EXE/EVE	6.7

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Number of Participants With Post-treatment Chemotherapy Related Adverse Events (From First Dosing Till Primary Analysis)

(NCT02258451)
Timeframe: From post-treatment till primary analysis cutoff date, up to 55 months

Intervention	Participants (Count of Participants)
	All system organ classes_Any_Grade 3	All system organ classes_Any_Grade 4	Blood and lymphatic system disorders_Any_Grade 3	Blood and lymphatic system disorders_Febrile neutropenia_Grade 3	Investigations_Any_Grade 4	Investigations_Neutrophil count decreased_Grade 4
Placebo + EXE/EVE	0	0	0	0	0	0
Radium-223 + EXE/EVE	1	1	1	1	1	1

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Number of Participants With Post-treatment Chemotherapy Related Adverse Events

According to protocol amendment 10, all participants who completed the EOT visit will be transferred to a separate extended safety follow-up study for their remaining follow-up. Thus, no further post-treatment data were collected after protocol amendment 10. (NCT02258451)
Timeframe: From post-treatment till end of study, up to 45.8 months

Intervention	Participants (Count of Participants)
	All system organ classes_Any_Grade 3	All system organ classes_Any_Grade 4	Blood and lymphatic system disorders_Any_Grade 3	Blood and lymphatic system disorders_Febrile neutropenia_Grade 3	Investigations_Any_Grade 4	Investigations_Neutrophil count decreased_Grade 4
Placebo + EXE/EVE	0	0	0	0	0	0
Radium-223 + EXE/EVE	1	1	1	1	1	1

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Number of Participants With New Primary Malignancies

(NCT02258451)
Timeframe: From first dosing till end of study, up to 72.6 months

Intervention	Participants (Count of Participants)
Radium-223 + EXE/EVE	1
Placebo + EXE/EVE	0

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Number of Participants With New Primary Malignancies During Study Treatment Till Primary Analysis

(NCT02258451)
Timeframe: From first dosing till primary analysis cutoff date, up to 55 months

Intervention	Participants (Count of Participants)
Radium-223 + EXE/EVE	1
Placebo + EXE/EVE	0

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Time to Cytotoxic Chemotherapy

Time from the date of randomization to the date of the first cytotoxic chemotherapy (NCT02258451)
Timeframe: Up to 55 months

Intervention	Months (Median)
Radium-223 + EXE/EVE	13.7
Placebo + EXE/EVE	11.6

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Time to Opiate Use for Cancer Pain

Interval from the date of randomization to the date of opiate use (NCT02258451)
Timeframe: Up to 55 months

Intervention	Months (Median)
Radium-223 + EXE/EVE	21.4
Placebo + EXE/EVE	18.4

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Overall Survival

The time from the date of randomization to the date of death due to any cause. Per Protocol Amendment 10, following primary analysis completion, further assessments were focused on safety, and only limited efficacy data including SSE and survival were collected and not designed to support reconsideration of the primary analysis efficacy conclusions. Accordingly, no formal statistical analyses were performed for primary and secondary efficacy outcomes in the final analysis. All primary and secondary efficacy outcome measures presented in this document came from the primary completion analysis. (NCT02258451)
Timeframe: Up to 55 months

Intervention	Months (Median)
Radium-223 + EXE/EVE	25.0
Placebo + EXE/EVE	26.4

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Percentage of Participants With Pain Improvement

In the percentage of participants with confirmed pain improvement. Confirmed pain improvement is defined a 2-point decrease or more in BPI-SF WPS from baseline over 2 consecutive measurements conducted at least 4 weeks apart, without an increase in pain management (IPM). An IPM is defined as the initiation of any opioid in participants not taking opioids at baseline, the initiation of a strong opioid in participants taking a weak opioid at baseline, or the initiation of an additional strong opioid in participants taking a strong opioid at baseline. (NCT02258451)
Timeframe: Up to 55 months

Intervention	percentage of participants (Number)
Radium-223 + EXE/EVE	38.5
Placebo + EXE/EVE	34.4

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

Intervention	Participants (Count of Participants)
	Any TEAE	Serious TEAE	Radium-223/Placebo-related TEAEs	Exemestane-related TEAEs	Everolimus-related TEAEs
Placebo + EXE/EVE	136	55	50	64	125
Radium-223 + EXE/EVE	139	57	73	75	130

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Time to Pain Progression

"Time from randomization to the first date a participant experienced pain progression based on WPS. Pain progression was defined as an increase of 2 or more points in the BPI-SF Worst pain in 24 hours score from baseline observed at 2 consecutive evaluations ≥4 weeks apart or an increase in pain management (IPM) with respect to baseline, whichever occurred first. An IPM is defined as the initiation of any opioid in participants not taking opioids at baseline, the initiation of a strong opioid in participants taking a weak opioid at baseline, or the initiation of an additional strong opioid in participants taking a strong opioid at baseline." (NCT02258451)
Timeframe: Up to 55 months

Intervention	Months (Median)
Radium-223 + EXE/EVE	7.6
Placebo + EXE/EVE	5.7

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Mean of Number of Tumor Assessment Visits - Based on Targeted Therapy Group and Other Treatments Group at Inclusion

(NCT02264665)
Timeframe: During 2 years of prospective follow-up

Intervention	Visits (Mean)
Targeted Therapy at Inclusion	5.8
Other Treatments at Inclusion	5.5

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Number of Participants With Adverse Events Leading to Death - Based on Treatment Received At-least Once During the Study

An AE was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. Adverse events leading to death are reported in this outcome measure. Participants in this outcome measure were grouped according to type of treatment received at least once during study irrespective of treatment they initiated or were receiving at time of inclusion. (NCT02264665)
Timeframe: During 2 years of prospective follow-up

Intervention	Participants (Count of Participants)
Everolimus During Study	3
Sunitinib During Study	2
Chemotherapy During Study	11
Somatostatin Analogues During Study at Inclusion	12
Metabolic Radiotherapy During Study	2
Other Than Study Treatments During Study	1

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OS Rate at 2 Years- Based on Targeted Therapy Group and Other Treatments Group at Inclusion

OS was the percentage of participants who were alive at 2 years of prospective follow-up. OS was defined as the time (in months) from the date of start of treatment (of the treatment line ongoing at the time of inclusion in the study) to the date of death due to any cause. Participants with no event or lost to follow-up or alive at the end of the study were censored at their last follow-up date (last follow-up date or last news). Analysis was performed using Kaplan-Meier method. (NCT02264665)
Timeframe: At 2 years of prospective follow-up

Intervention	Percentage of participants (Number)
Targeted Therapy at Inclusion	63.9
Other Treatments at Inclusion	71.7

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Number of Participants Who Had a Change in Their Treatment - Based on Targeted Therapy Group and Other Treatments Group at Inclusion

In this outcome measure, number of participants with a change in treatment compared to treatment at inclusion is reported. (NCT02264665)
Timeframe: During 2 years of prospective follow-up

Intervention	Participants (Count of Participants)
Targeted Therapy at Inclusion	44
Other Treatments at Inclusion	68

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Overall Survival (OS) Rate at 2 Years - Based on Type of Treatment at Inclusion

Intervention	Percentage of participants (Number)
Everolimus (Targeted Therapy) at Inclusion	60.2
Sunitinib (Targeted Therapy) at Inclusion	68.4
Chemotherapy (Other Treatment) at Inclusion	69.6
Somatostatin Analogues (Other Treatment) at Inclusion	79.7
Metabolic Radiotherapy (Other Treatment) at Inclusion	NA

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PFS at 2 Years Assessed by Investigator Per RECIST v1.1 - Based on Targeted Therapy Group and Other Treatments Group at Inclusion

PFS was defined as time (in months) from date of start of treatment (the treatment line ongoing at the time of inclusion in the study) to first documentation of PD or date of death due to any cause, when receiving the main treatment at the time of inclusion. RECIST v1.1, PD: at least a 20% increase in sum of diameters of target lesions, taking as reference smallest sum on study treatment (this included baseline sum if that is smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. Unequivocal progression of existing non-target lesions. Appearance of 1 or more new target or non-target lesions. If a participant did not have an event, data censoring was done at the last recorded time to PD or the last tumor assessment, last disease assessment. Analysis was performed using Kaplan-Meier method. (NCT02264665)
Timeframe: At 2 years of prospective follow-up

Intervention	Percentage of participants (Number)
Targeted Therapy at Inclusion	19.9
Other Treatments at Inclusion	29.0

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Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs), Treatment Related AEs, SAEs and SAEs With Common Terminology Criteria For Adverse Events (CTCAE) 3, 4 and 5, v4.0-Based on Treatment Received At-least Once During Study

AE: any untoward medical occurrence in participant who received study drug without regard to possibility of causal relationship. SAE: any AE, regardless of dose, that: led to death; was life-threatening; required hospitalization or prolonged hospitalization; led to persistent or significant incapacity or led to congenital anomaly or birth defect. Treatment-related AE was any untoward medical occurrence attributed to study drug in participant who received study drug. Relatedness to treatment was assessed by investigator. Per CTCAE 4.0, Grade 3 (Severe) events=unacceptable or intolerable events, significantly interrupting usual daily activity, require systemic drug therapy/other treatment. Grade 4=Life-threatening events Grade 5 (Death) events=death related to an AE. Participants in this outcome measure were grouped according to type of treatment received at least once during study irrespective of treatment they initiated or were receiving at time of inclusion. (NCT02264665)
Timeframe: During 2 years of prospective follow-up

,,,,,

Intervention	Participants (Count of Participants)
	AE	Treatment Related AE	SAE	Treatment Related SAE	At least one grade 3 AE	At least one grade 3 SAE	At least one AE of grade 4 or higher
Chemotherapy During Study	63	48	26	5	18	12	18
Everolimus During Study	43	31	21	6	21	14	6
Metabolic Radiotherapy During Study	6	2	3	1	1	0	2
Other Than Study Treatments During Study	8	0	3	0	3	0	1
Somatostatin Analogues During Study	48	13	24	1	14	12	16
Sunitinib During Study	32	24	9	2	11	6	2

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Number of Participants With Adverse Events Leading to Discontinuation of Treatment - Based on Treatment Received At-least Once During the Study

An AE was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. Participants in this outcome measure were grouped according to type of treatment received at least once during study irrespective of treatment they initiated or were receiving at time of inclusion. (NCT02264665)
Timeframe: During 2 years of prospective follow-up

,,,,,

Intervention	Participants (Count of Participants)
	Temporary discontinuation of treatment	Permanent discontinuation of treatment
Chemotherapy During Study	11	12
Everolimus During Study	15	14
Metabolic Radiotherapy During Study	0	0
Other Than Study Treatment During Study	1	1
Somatostatin Analogues During Study at Inclusion	8	12
Sunitinib During Study	9	10

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Number of Participants With Different Types of Investigation Used for Tumor Assessment - Based on Targeted Therapy Group and Other Treatments Group at Inclusion

The different types of investigations were performed for assessment of tumor regardless of treatment received. Investigations performed were Computed Tomography (CT) scan, Magnetic Resonance Imaging (MRI), Positron Emission Tomography (PET) scan, Octreoscan, Ultrasound. All the investigations were used at least once during the study for all treatments. (NCT02264665)
Timeframe: During 2 years of prospective follow-up

Intervention	Participants (Count of Participants)
	CT Scan	MRI	PET Scan	Octreoscan	Ultrasound	Imaging (CT scan and/or MRI)
Other Treatments at Inclusion	65	45	15	15	4	74
Targeted Therapy at Inclusion	48	28	11	13	6	52

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Number of Participants With Types of Main Lines of Treatment Received During the Follow-up - Based on Targeted Therapy Group and Other Treatments Group at Inclusion

The types of main lines of treatment included 1st line, 2nd line, 3rd line, 4th line, 5th line, 6th line, 7th line and 8th line. (NCT02264665)
Timeframe: During 2 years of prospective follow-up

Intervention	Participants (Count of Participants)
	1st line	2nd line	3rd line	4th line	5th line	6th line	7th line	8th line
Other Treatments at Inclusion	38	43	30	26	15	2	1	0
Targeted Therapy at Inclusion	8	27	25	28	15	7	4	2

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Number of Main Lines of Treatment Received During the Study - Based on Targeted Therapy Group and Other Treatments Group at Inclusion

The number of main lines of treatment received during the study treatment are reported in this outcome measure. (NCT02264665)
Timeframe: During 2 years of prospective follow-up

Intervention	Treatment lines (Mean)
Targeted Therapy at Inclusion	3.7
Other Treatments at Inclusion	2.8

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Number of Combined Main Lines of Treatments Received - Based on Targeted Therapy Group and Other Treatments Group at Inclusion

The number of lines of combined main treatment administered during the study were assessed. (NCT02264665)
Timeframe: During 2 years of prospective follow-up

Intervention	Treatment lines (Mean)
Targeted Therapy at Inclusion	3.9
Other Treatments at Inclusion	2.9

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Progression-Free Survival (PFS) at 2 Years Assessed by Investigator Per Response Evaluation Criteria in Solid Tumors (RECIST) Version (v) 1.1 - Based on Type of Treatment at Inclusion

PFS was defined as time (in months) from date of start of treatment (the treatment line ongoing at the time of inclusion in the study) to first documentation of disease progression (PD) or date of death due to any cause, when receiving the main treatment at the time of inclusion. RECIST v1.1, PD: at least a 20% increase in sum of diameters of target lesions, taking as reference smallest sum on study treatment (this included baseline sum if that is smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 millimeters (mm). Unequivocal progression of existing non-target lesions. Appearance of 1 or more new target or non-target lesions. If a participant did not have an event, data censoring was done at the last recorded time to PD or the last tumor assessment, last disease assessment. Analysis was performed using Kaplan-Meier method. (NCT02264665)
Timeframe: At 2 years of prospective follow-up

Intervention	Percentage of participants (Number)
Everolimus (Targeted Therapy) at Inclusion	26.5
Sunitinib (Targeted Therapy) at Inclusion	19.3
Chemotherapy (Other Treatment) at Inclusion	36.5
Somatostatin Analogues (Other Treatment) at Inclusion	38.6
Metabolic Radiotherapy (Other Treatment) at Inclusion	NA

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Progression Free Survival (PFS)

"PFS will be estimated using the method of Kaplan-Meier. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), Disease progression in evaluable patients will be defined as one or more of the following:~Any new disease and/or clear progression of evaluable disease; OR 2 fold elevation in CA-125 from its lowest level (either initial level or nadir, whichever is lowest, since study enrollment) combined with CA-125 elevation confirmed by re-assay at any time." (NCT02283658)
Timeframe: Time from registration to the first of either disease progression or death from any cause, assessed up to 2 years

Intervention	Months (Median)
Treatment (Everolimus and Letrozole)	3.9

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Percentage of Participants With CA-125 Response

CA-125 response: The key secondary endpoint of the study will be a CA-125 response, defined as a 50% or greater reduction in baseline CA-125. The null hypothesis will be set at CA-125 response rate of 8.3%, based on the response of single agent letrozole, as reported by Bowman et al (7). The treatment of letrozole and everolimus will be considered promising, based on CA-125, if the observed CA-125 response rate is 30% or more. (NCT02283658)
Timeframe: Up to 2 years

Intervention	percentage of patients (Number)
Treatment (Everolimus and Letrozole)	21

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Percentage of Patients Alive and Progression Free Survival at 12 Weeks

"The percentage of PFS12 successes will be estimated by the number of successes divided by the total number of evaluable patients. Ninety-five percent confidence intervals for the true success proportion will be calculated according to the exact binomial method. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), Disease progression in evaluable patients will be defined as one or more of the following:~Any new disease and/or clear progression of evaluable disease; OR~2 fold elevation in CA-125 from its lowest level (either initial level or nadir, whichever is lowest, since study enrollment) combined with CA-125 elevation confirmed by re-assay at any time." (NCT02283658)
Timeframe: 12 weeks

Intervention	percentage of patients (Number)
Treatment (Everolimus and Letrozole)	47

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Confirmed Response Rate, Estimated Using RECIST 1.1 Criteria

"A confirmed tumor response is defined to be either a complete response or partial response noted as the objective status on 2 consecutive evaluations at least 4 weeks apart. A complete response (CR) in evaluable patients will be defined as:~Disappearance of any sign of (evaluable) disease, AND~Normalization of CA-125; if CA-125 normalizes, it should be confirmed at any time.~A partial response (PR) in evaluable patients will be defined as:~Decrement in CA-125 by >50%, and~Improvement in any additional evaluable disease (if present) as assessed by the enrolling physician." (NCT02283658)
Timeframe: Up to 24 weeks

Intervention	percentage of patients (Number)
Treatment (Everolimus and Letrozole)	16

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Overall Suravival(OS)

OS will be estimated using the method of Kaplan-Meier. (NCT02283658)
Timeframe: Time from registration to death from any cause, assessed up to 2 years

Intervention	Months (Median)
Treatment (Everolimus and Letrozole)	13

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Number of Participants Experiencing Adverse Events

The number of patients with adverse events.The maximum grade for each type of adverse event (AE) will be recorded for each patient, and frequency tables will be reviewed to determine AE patterns. These tables are reported in the adverse events section of this report. (NCT02283658)
Timeframe: Up to 30 days post-treatment

Intervention	Participants (Count of Participants)
Treatment (Everolimus and Letrozole)	19

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Median Time From First Occurrence of CR or PR to Disease Progression or Death Also Called Duration of Response (DOR)

Only those patients who achieved Complete Response or Partial Response will be included in the summaries of DOR. DOR is defined as time from first date of response of CR or PR to disease progression or death as defined by RECIST v1.1 criteria. Participants who are alive and free from disease progression will be censored at the date of last tumor assessment. Patients who receive non-protocol therapy (subsequent therapy) prior to incurring an event will be censored at the date of last tumor assessment prior to the start of subsequent therapy. A CR is the complete disappearance of all target lesions. A PR is a decrease of 30% or more of the diameter(s) of all target lesions from the baseline sum of diameters. (NCT02291913)
Timeframe: every 8 weeks until discontinuation, up to 20 months

Intervention	months (Median)
Everolimus	8.8

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Median Progression Free Survival (PFS)

PFS is defined as the time from Day 1 of study drug administration to disease progression as defined by RECIST (Response Evaluation Criteria in Solid Tumors) version 1.1 criteria, or death on study. Participants who are alive and free from disease progression will be censored at the date of last radiologic tumor assessment. Participants who receive non-protocol therapy (subsequent therapy) prior to incurring an event will be censored at the date of last tumor assessment prior to the start of subsequent therapy. Participants who do not have a post-baseline tumor assessment will be censored at the date of first treatment (Day 1). (NCT02291913)
Timeframe: up to 3 years

Intervention	months (Median)
Everolimus	7.2

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Number of Patients With Adverse Events (AEs) as a Measure of Safety and Tolerability

Assessments were made through analysis of the reported incidence of treatment-emergent AEs. All participants who received at least one dose of protocol treatment were followed for safety. Adverse events were collected from day of first dose to 30 days after last protocol treatment and graded according to National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.03. (NCT02291913)
Timeframe: Up to 20 months

Intervention	Participants (Count of Participants)
Everolimus	48

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Number of Patients With an Objective Response (CR or PR) Also Called the Overall Response Rate (ORR).

Defined as the number of patients with objective evidence of complete or partial response (CR or PR) using RECIST version 1.1. A CR is the complete disappearance of all target lesions. A PR is a decrease of 30% or more of the diameter(s) of all target lesions from the baseline sum of diameters. (NCT02291913)
Timeframe: every 8 weeks until discontinuation, up to 20 months

Intervention	Participants (Count of Participants)
Everolimus	2

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Number of Participants With CR, PR, or 6 Months of SD Also Called Clinical Benefit Rate (CBR)

The proportion of patients with Complete Response (CR) or Partial Response (PR) or 6 months or more of Stable Disease (SD). A CR is the complete disappearance of all target lesions. A PR is a decrease of 30% or more of the diameter(s) of all target lesions from the baseline sum of diameters. SD is not meeting the criteria for PR or a 20% increase in target lesions called Progressive Disease (PD). (NCT02291913)
Timeframe: Up to 20 months

Intervention	Participants (Count of Participants)
Everolimus	12

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Median Overall Survival (OS)

Defined as the time from date of first study treatment to date of death due to any cause. Patients who are alive will be censored at the date of last known date alive. (NCT02291913)
Timeframe: up to 3 years from first treatment

Intervention	months (Median)
Everolimus	26.7

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Overall Survival

Overall survival is defined as the time from treatment start date until date of death or date last known alive following therapy. (NCT02315625)
Timeframe: Up to approximately 4 years

Intervention	Months (Median)
Sunitinib First, Everolimus Second	25.5
Everolimus First, Sunitinib Second	10.7

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Number of Participants With Serious and Non-Serious Adverse Events

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. (NCT02315625)
Timeframe: Date treatment consent signed to date off study approximately 49 months and 9 days.

Intervention	Participants (Count of Participants)
Sunitinib	15
Everolimus	11

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Number of Participants With an Overall Response

Overall response was assessed by the Response Evaluation Criteria in Solid Tumors (RECIST) is defined as Complete Response (CR), Partial Response (PR), and Stable Disease (SD). Complete Response is disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm. Partial Response is at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum of diameters. Stable Disease is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for Progressive Disease (PD) (e.g. appearance of one or more new lesions), taking as reference the smallest sum of diameters while on study. (NCT02315625)
Timeframe: Every 3 months until disease progression, up to 12 months

Intervention	Participants (Count of Participants)
Sunitinib First, Everolimus Second	1
Everolimus First, Sunitinib Second	0

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Median Survival Time (MST)

MST is the amount of time a subject survives after therapy. (NCT02315625)
Timeframe: Death, an average of 12 months follow up

Intervention	Months (Median)
Sunitinib First, Everolimus Second	9.5
Everolimus First, Sunitinib Second	5.5

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Median Amount of Time Subject Survives Without Disease Progression After Treatment

Median amount of time subject survives without disease progression after treatment. Progression was assessed by the Response Evaluation Criteria in Solid Tumors (RECIST) and is 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. The appearance of one or more new lesions is also considered progressions. (NCT02315625)
Timeframe: Up to approximately 2 years

Intervention	months (Median)
Sunitinib First, Everolimus Second	7
Everolimus First, Sunitinib Second	18

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3D Photographic Measurement of Surface Volume of Cutaneous Neurofibroma Lesion

Photographs of selected lesions to measure surface volume. (NCT02332902)
Timeframe: 6 months

Intervention	mm^3 (Mean)
	Baseline	6 months
Intervention	32.54	33.93

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Number of Participants With Grade 3-4 Adverse Events

Determination if orally administered Afinitor is safe in patients a indicated by lack of Grade 3-4 adverse events during the trial period. (NCT02332902)
Timeframe: 6 months

Intervention	Participants (Count of Participants)
Intervention	0

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Mutations Associated With Therapeutic Response

-To correlate mutations in the mTOR pathway with therapeutic response with everolimus (NCT02352844)
Timeframe: Completion of treatment (estimated average of 6 months)

Intervention	Participants (Count of Participants)
	STK11 c.375-2del	STK11 c.375-8C>G
Arm 1 (Everolimus)	1	1

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Response Rate (RR)

The primary endpoint will be to describe the response rate using RECIST 1.1. Response rate will be defined as complete response (disappearance of all target lesion) plus partial response (a least a 30% decrease in the sum of diameters of target lesions). (NCT02352844)
Timeframe: Completion of treatment (estimated average of 6 months)

Intervention	Participants (Count of Participants)
Arm 1 (Everolimus)	1

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Genetic Changes Associated With Disease Progression

-To investigate the genetic changes associated with disease progression following treatment with everolimus. (NCT02352844)
Timeframe: Completion of treatment (estimated average of 6 months)

Intervention	Participants (Count of Participants)
	NF1 p.E8*	STK11 p.E199*	NF1 p.Y489C	STK11 exon 1 E33X	STK11 L282fs*5	NF1 c.7190C>T	NF1 c.7253C>T
Arm 1 (Everolimus)	1	1	1	1	1	1	1

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Number of Lesions With Lesion Success

Defined as attainment of < 30% residual stenosis of the target lesion using any percutaneous method. (NCT02389946)
Timeframe: Hospital Discharge (6-24 hours post-index procedure)

Intervention	Lesions (Count of Units)
Orsiro Sirolimus Coronary Stent System	1102
Xience Everolimus Coronary Stent System	579

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Number of Participants With Procedure Success

Defined as attainment of < 30% residual stenosis of the target lesion using the assigned study stent only without occurrence of in-hospital major adverse cardiac events (MACE; composite of all-cause death, Q-wave or non-Q-wave MI, and any clinically-driven TLR). (NCT02389946)
Timeframe: Hospital Discharge (6-24 hours post-index procedure)

Intervention	Participants (Count of Participants)
Orsiro Sirolimus Coronary Stent System	827
Xience Everolimus Coronary Stent System	401

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Number of Participants With TLF and Individual TLF Components

TLF events are defined as cardiac death, target vessel Q-wave or non-Q-wave MI, or any clinically-driven TLR. The number of participants with any TLF event is provided, as well as number of participants with each of the individual components. (NCT02389946)
Timeframe: Hospital Discharge (6-24 hours post-index procedure), 1, 6, 12 months, 2, 3, 4 and 5 years

Intervention	Participants (Count of Participants)
	6-24 hours post-index TLF Total	6-24 hours post-index TLF Component: Cardiac Death	6-24 hours post-index TLF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	6-24 hours post-index TLF Component: Clinically-driven TLR	1-month TLF Total	1-month TLF Component: Cardiac Death	1-month TLF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	1-month TLF Component: Clinically-driven TLR	6-month TLF Total	6-month TLF Component: Cardiac Death	6-month TLF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	6-month TLF Component: Clinically-driven TLR	12-month TLF Total	12-month TLF Component: Cardiac Death	12-month TLF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	12-month TLF Component: Clinically-driven TLR	2-year TLF Total	2-year TLF Component: Cardiac Death	2-year TLF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	2-year TLF Component: Clinically-driven TLR	3-year TLF Total	3-year TLF Component: Cardiac Death	3-year TLF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	3-year TLF Component: Clinically-driven TLR	4-year TLF Total	4-year TLF Component: Cardiac Death	4-year TLF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	4-year TLF Component: Clinically-driven TLR	5-year TLF Total	5-year TLF Component: Cardiac Death	5-year TLF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	5-year TLF Component: Clinically-driven TLR
Orsiro Sirolimus Coronary Stent System	35	1	34	2	37	1	36	4	47	1	38	13	52	1	39	17	64	5	45	21	72	9	46	27	91	17	49	38	104	21	56	48
Xience Everolimus Coronary Stent System	31	1	29	2	32	1	30	3	39	2	34	8	41	3	35	10	48	2	39	19	56	5	41	25	60	5	44	28	66	8	45	32

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Percentage of Participants With Target Lesion Failure (TLF) at 12 Months Post-Index Procedure by Bayesian Estimation

TLF is defined as all cardiac death, target vessel Q-wave or non-Q-wave myocardial infarction (MI), or clinically driven target lesion revascularization (TLR). (NCT02389946)
Timeframe: 12-Months

Intervention	Percentage of participants (Mean)
Orsiro Sirolimus Coronary Stent System	6.32
Xience Everolimus Coronary Stent System	8.90

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Number of Participants With MACE and Individual MACE Components

MACE events are defined as all-cause death, Q-wave or non-Q-wave MI, or any clinically-driven TLR. The number of participants with any MACE event is provided, as well as number of participants with each of the individual components. (NCT02389946)
Timeframe: Hospital Discharge (6-24 hours post-index procedure), 1, 6, 12 months, 2, 3, 4 and 5 years

Intervention	Participants (Count of Participants)
	6-24 hours post-index MACE Total	6-24 hours post-index MACE Component: Death	6-24 hours post-index MACE Component: Protocol defined Q-Wave or non-Q-wave MI	6-24 hours post-index MACE Component: Clinically-driven TLR	1-month MACE Total	1-month MACE Component: Death	1-month MACE Component: Protocol defined Q-Wave or non-Q-wave MI	1-month MACE Component: Clinically-driven TLR	6-month MACE Total	6-month MACE Component: Death	6-month MACE Component: Protocol-defined Q-Wave or non-Q-wave MI	6-month MACE Component: Clinically-driven TLR	12-month MACE Total	12-month MACE Component: Death	12-month MACE Component: Protocol-defined Q-Wave or non-Q-wave MI	12-month MACE Component: Clinically-driven TLR	2-year MACE Total	2-year MACE Component: Death	2-year MACE Component: Protocol-defined Q-Wave or non-Q-wave MI	2-year MACE Component: Clinically-driven TLR	3-year MACE Total	3-year MACE Component: Death	3-year MACE Component: Protocol-defined Q-Wave or non-Q-wave MI	3-year MACE Component: Clinically-driven TLR	4-year MACE Total	4-year MACE Component: Death	4-year MACE Component: Protocol-defined Q-Wave or non-Q-wave MI	4-year MACE Component: Clinically-driven TLR	5-year MACE Total	5-year MACE Component: Death	5-year MACE Component: Protocol-defined Q-Wave or non-Q-wave MI	5-year MACE Clinically-driven TLR
Orsiro Sirolimus Coronary Stent System	35	1	34	2	39	1	38	4	53	6	40	13	59	7	41	17	85	16	56	21	102	27	60	27	133	45	66	38	155	56	76	48
Xience Everolimus Coronary Stent System	31	1	30	2	32	1	31	3	42	4	36	8	44	6	37	10	56	9	42	19	73	17	49	25	81	22	52	28	92	27	58	32

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Number of Participants With Myocardial Infarction

(NCT02389946)
Timeframe: Hospital Discharge (6-24 hours post-index procedure), 1, 6, 12 months, 2, 3, 4 and 5 years

Intervention	Participants (Count of Participants)
	6-24 hours post-index procedure	1-month post-index procedure	6-month	12-month	2-year	3-year	4-year	5-year
Orsiro Sirolimus Coronary Stent System	34	38	40	41	56	60	66	76
Xience Everolimus Coronary Stent System	30	31	36	37	42	49	52	58

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Number of Participants With Myocardial Infarction or Cardiac Death

(NCT02389946)
Timeframe: Hospital Discharge (6-24 hours post-index procedure), 1, 6, 12 months, 2, 3, 4 and 5 years

Intervention	Participants (Count of Participants)
	Hospital Discharge (6-24 hours post-index procedure)	1-month	6-month	12-month	2-year	3-year	4-year	5-year
Orsiro Sirolimus Coronary Stent System	35	39	41	42	61	68	82	94
Xience Everolimus Coronary Stent System	30	31	37	39	43	51	54	61

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Number of Participants With Stent Thrombosis

Stent thrombosis according to the Academic Research Consortium criteria. (NCT02389946)
Timeframe: 24 hours, 30 days, 1 year, and 5 years post-index procedure

Intervention	Participants (Count of Participants)
	Possible ARC Stent Thrombosis Total	Possible ARC Stent Thrombosis Acute (<=24 hours)	Possible ARC Stent Thrombosis Sub-acute (>24 hours and <=30 days)	Possible ARC Stent Thrombosis Late (>30 days and <=1 year)	Possible ARC Stent Thrombosis Very Late (>1 year)	Definite/Probable ARC Stent Thrombosis Total	Definite/Probable ARC Stent Thrombosis Acute (<=24 hours)	Definite/Probable ARC Stent Thrombosis Sub-acute (>24 hours and <=30 days)	Definite/Probable ARC Stent Thrombosis Late (>30 days and <=1 year)	Definite/Probable ARC Stent Thrombosis Very Late (>1 year)
Orsiro Sirolimus Coronary Stent System	11	0	0	0	11	5	1	2	1	1
Xience Everolimus Coronary Stent System	6	0	0	1	5	7	0	1	2	4

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Number of Participants With Target Vessel Failure (TVF) and Individual TVF Components

TVF events are defined as cardiac death, target vessel Q-wave or non-Q-wave MI, or any clinically-driven TVR. The number of participants with any TVF event is provided, as well as number of participants with each of the individual components. (NCT02389946)
Timeframe: Hospital Discharge (6-24 hours post-index procedure), 1, 6, 12 months, 2, 3, 4 and 5 years

Intervention	Participants (Count of Participants)
	6-24 hours post-index TVF Total	6-24 hours post-index TVF Component: Cardiac Death	6-24 hours post-index TVF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	6-24 hours post-index TVF Component: Clinically-driven TVR	1-month TVF Total	1-month TVF Component: Cardiac Death	1-month TVF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	1-month TVF Component: Clinically-driven TVR	6-month TVF Total	6-month TVF Component: Cardiac Death	6-month TVF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	6-month TVF Component: Clinically-driven TVR	12-month TVF Total	12-month TVF Component: Cardiac Death	12-month TVF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	12-month TVF Component: Clinically-driven TVR	2-year TVF Total	2-year TVF Component: Cardiac Death	2-year TVF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	2-year TVF Component: Clinically-driven TVR	3-year TVF Total	3-year TVF Component: Cardiac Death	3-year TVF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	3-year TVF Component: Clinically-driven TVR	4-year TVF Total	4-year TVF Component: Cardiac Death	4-year TVF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	4-year TVF Component: Clinically-driven TVR	5-year TVF Total	5-year TVF Component: Cardiac Death	5-year TVF Component: Protocol-defined Target Vessel Q-wave or non-Q-Wave MI	5-year TVF Component: Clinically-driven TVR
Orsiro Sirolimus Coronary Stent System	35	1	34	2	38	1	36	5	51	1	38	18	60	1	39	27	74	5	45	37	84	9	46	45	110	17	49	63	127	21	56	78
Xience Everolimus Coronary Stent System	31	1	29	2	32	1	30	4	40	2	34	10	45	3	35	15	56	2	39	30	68	5	41	40	74	5	44	46	81	8	45	51

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Number of Lesions With Device Success

Defined as attainment of < 30% residual stenosis of the target lesion using the assigned study stent only. (NCT02389946)
Timeframe: Hospital Discharge (6-24 hours post-index procedure)

Intervention	Lesions (Number)
Orsiro Sirolimus Coronary Stent System	1082
Xience Everolimus Coronary Stent System	566

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Plasma HIV RNA

Plasma HIV RNA was quantified in a highly sensitive single-copy assay (SCA) using repetitive sampling in the Panther system (Hologic) at the Blood Systems Research Institute. Up to 18 replicates were tested for each sample in order to determine plasma RNA levels as low as 0.18 copies/mL. (NCT02429869)
Timeframe: Baseline, Month 2, Month 6, Month 12 (6 months post discontinuation of everolimus)

Intervention	nucleic acid copies per million cells (Median)
	Baseline	Month 2	Month 6	Month 12
Everolimus	0.291	0.584	1.042	0.941

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Cell-associated Total HIV RNA

Peripheral blood mononuclear cells were isolated from whole blood using the Ficoll density gradient technique. Peripheral blood CD4 T cells were enriched by negative selection using antibody-coupled magnetic beads (Stem Cell Technologies) prior to simultaneous RNA and DNA isolation using cell-sparing protocols (AllPrep, Qiagen). Bulk CD4+ T cell or PBMC-associated HIV DNA and unspliced RNA were quantified using real-time PCR methods.The primer and probe sequences targeted conserved regions to enable quantification of a broad range of HIV subtypes. Values were normalized to DNA quantification of a human housekeeping gene (CCR5) in order to determine nucleic acid copies per million CD4+ T cell or PBMC as described. In addition to traditional quantitative PCR, a novel single-cell-in-droplet (scd)PCR method was used to quantify the absolute number or frequency of individual purified CD4+ T cells that express unspliced HIV RNA. (NCT02429869)
Timeframe: Baseline, Month 2, Month 6, Month 12 (6 months post discontinuation of everolimus)

Intervention	nucleic acid copies per million cells (Median)
	Baseline HIV RNA CD4+	Month 2 HIV RNA CD4+	Month 6 HIV RNA CD4+	Month 12 HIV RNA CD4+
Everolimus	423	310	702	354

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Cell-associated HIV DNA

Intervention	nucleic acid copies per million cells (Median)
	Baseline	Month 2	Month 6	Month 12
Everolimus	35	43	81	16

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Blood Total VEGF Levels (Not Only VEGF-D)

(NCT02451696)
Timeframe: 28 days

Intervention	pg/ml (Mean)
Treated Subjects	56.5
Reference Subjects	50.85

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mTOR Brain Tissue-S6 Phosphate by Western Blot

(NCT02451696)
Timeframe: 28 days

Intervention	normalized val-protein relative to actin (Mean)
Treated Subjects	0.49
Reference Subjects	0.81

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Number of Patients With Adverse Events

.Adverse event monitoring should be continued for at least 30 days (or 5 half-lives, whichever is longer) following the last dose of study treatment (NCT02451696)
Timeframe: 6 weeks

Intervention	Participants (Count of Participants)
Treated Subjects	0
Reference Subjects	0

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HMGB1 Expression in Brain Tissue

HMGB1 expression is measured through label-free quantification (LFQ). LFQ is a method in mass spectroscopy that determines the relative amount of proteins in biological samples. The unit of measure is LFQ intensity; a higher LFQ intensity indicates greater HMGB1 expression. (NCT02451696)
Timeframe: 28 days

Intervention	LFQ intensity (Mean)
Treated Subjects	14.85
Reference Subjects	15.06

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Blood Everolimus Levels

mTOR signaling in blood (NCT02451696)
Timeframe: 28 days

Intervention	ng/ml (Mean)
Treated Subjects	12.35
Reference Subjects	2

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Objective Response Rate (ORR)

ORR was defined as the percentage of participants who achieved BOR of CR or PR. ORR was assessed using RECIST 1.1. (NCT02454478)
Timeframe: From first dose of study drug until PD, development of unacceptable toxicity, participant requests to discontinue, withdrawal of consent or study termination (up to approximately 23 months)

Intervention	percentage of participants (Number)
Lenvatinib 18 mg + Everolimus 5 mg	71.4

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Tss,Max: Time to Reach the Maximum Plasma Concentration (Cmax) at Steady State for Levatinib and Everolimus

(NCT02454478)
Timeframe: Cycle 1 Day 15 predose and at 1, 2, 4 ,8, and 24 hours postdose (Cycle length=28 days)

Intervention	hour (Median)
	Lenvatinib: Cycle 1 Day 15	Everolimus: Cycle 1 Day 15
Lenvatinib 18 mg + Everolimus 5 mg	3.77	0.97

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

(NCT02454478)
Timeframe: Baseline up to 30 days after the last dose of study drug (up to approximately 21.5 months)

Intervention	participants (Number)
	TEAE	SAE
Lenvatinib 18 mg + Everolimus 5 mg	7	3

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Number of Participants With the Minimum Percent Change From Baseline in the Sum of Diameters of Target Lesions

(NCT02454478)
Timeframe: Baseline up to first tumor assessment at which diameter of target lesions were available (up to approximately 23 months)

Intervention	participants (Number)
	Less than or equal to (<=) -30%	Greater than (>) -30% to less than (<) 20%	Greater than or equal to (>=) 20%
Lenvatinib 18 mg + Everolimus 5 mg	5	1	1

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Disease Control Rate (DCR)

DCR was defined as the percentage of participants who achieved BOR of CR, PR, or SD. DCR was assessed based on RECIST 1.1. (NCT02454478)
Timeframe: From first dose of study drug until PD, development of unacceptable toxicity, participant requests to discontinue, withdrawal of consent or study termination (up to approximately 23 months)

Intervention	percentage of participants (Number)
Lenvatinib 18 mg + Everolimus 5 mg	85.7

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Number of Participants With Best Overall Response (BOR)

BOR included complete response (CR), partial response (PR), stable disease (SD), and PD (progressive disease). BOR was assessed using Response Evaluation Criteria in Solid Tumor (RECIST) 1.1 (NCT02454478)
Timeframe: From first dose of study drug until PD, development of unacceptable toxicity, participant requests to discontinue, withdrawal of consent or study termination (up to approximately 23 months)

Intervention	participants (Number)
	CR	PR	SD	PD
Lenvatinib 18 mg + Everolimus 5 mg	0	5	1	1

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Css,Max: Maximum Observed Plasma Concentration at Steady State for Levatinib and Everolimus

(NCT02454478)
Timeframe: Cycle 1 Day 15 predose and at 1, 2, 4 ,8, and 24 hours postdose (Cycle length=28 days)

Intervention	ng/mL (Mean)
	Lenvatinib: Cycle 1 Day 15	Everolimus: Cycle 1 Day 15
Lenvatinib 18 mg + Everolimus 5 mg	257	41.5

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Cmax: Maximum Observed Plasma Concentration for Levatinib and Everolimus

(NCT02454478)
Timeframe: Cycle 1 Day 1 predose and at 1, 2, 4 ,8, and 24 hours postdose (Cycle length=28 days)

Intervention	nanogram per milliliter (ng/mL) (Mean)
	Lenvatinib: Cycle 1 Day 1	Everolimus: Cycle 1 Day 1
Lenvatinib 18 mg + Everolimus 5 mg	289	39.1

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Tmax: Time to Reach the Maximum Plasma Concentration (Cmax) for Levatinib and Everolimus

(NCT02454478)
Timeframe: Cycle 1 Day 1 predose and at 1, 2, 4 ,8, and 24 hours postdose (Cycle length=28 days)

Intervention	hour (Median)
	Lenvatinib: Cycle 1 Day 1	Everolimus: Cycle 1 Day 1
Lenvatinib 18 mg + Everolimus 5 mg	3.87	0.92

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Number of Participants Who Experienced Any Dose Limiting Toxicity (DLT)

DLT was defined as toxicity related to the combination therapy and was graded according to Common Terminology Criteria for Adverse Events version 4.03 (CTCAE v4.03). (NCT02454478)
Timeframe: From first dose of study drug up to Cycle 1 Day 28 (Cycle length=28 days)

Intervention	participants (Number)
Lenvatinib 18 mg + Everolimus 5 mg	0

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AUC 0-t: Area Under the Concentration-time Curve From Zero (Pre-dose) to Time of Last Quantifiable Concentration for Levatinib and Everolimus

(NCT02454478)
Timeframe: Cycle 1 Day 1 and Cycle 1 Day 15 predose and at 1, 2, 4 ,8, and 24 hours postdose (Cycle length=28 days)

Intervention	hour * nanogram per milliliter (h*ng/mL) (Mean)
	Lenvatinib: Cycle 1 Day 1	Everolimus: Cycle 1 Day 1	Lenvatinib: Cycle 1 Day 15	Everolimus: Cycle 1 Day 15
Lenvatinib 18 mg + Everolimus 5 mg	2770	211	3220	401

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Count of Participants With Non-serious Adverse Events Assessed by the Common Terminology Criteria in Adverse Events (CTCAE v4.0)

Here is the count of participants with 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. (NCT02504892)
Timeframe: Date treatment consent signed to date off study, approximately 8 months and 28 days.

Intervention	Participants (Count of Participants)
Birt-Hogg-Dube Syndrome	3

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Progression-free Survival (PFS)

Progression-free survival is defined as the time interval from start of treatment to documented evidence of disease progression. Progression is at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes baseline sum if that is the smallest on study). The sum must also demonstrate an absolute increase of at least 5mm. Note: the appearance of one or more new lesions is also progression. Progressive disease was assessed by the Response Evaluation in Solid Tumors (RECIST) criteria v1.1. (NCT02504892)
Timeframe: median follow-up time: 9 months

Intervention	Months (Median)
Birt-Hogg-Dube Syndrome	NA

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Overall Response Rate With Everolimus Treatment.

Overall best response is defined as the best response recorded from the start of the treatment until disease progression/recurrence (taking as reference for progressive disease the smallest measurements recorded since the treatment started). Response was assessed by the Response Evaluation in Solid Tumors (RECIST) criteria v1.1. Progressive disease is at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes baseline sum if that is the smallest on study). The sum must also demonstrate an absolute increase of at least 5mm. Note: the appearance of one or more new lesions is also progression. Complete response is disappearance of all target lesions. Partial response is at least a 30% decrease in the sum of the diameters of target lesions. Stable disease is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum of diameters while on study. (NCT02504892)
Timeframe: End of treatment: every 12 weeks up to 1 year

Intervention	Participants (Count of Participants)
	Complete Response	Partial Response	Stable Disease	Progressive Disease
Birt-Hogg-Dube Syndrome	0	0	3	0

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Overall Survival (OS)

Overall Survival is defined as the time between the first day of treatment to the day of death. (NCT02504892)
Timeframe: From the first day of treatment to the day of death, up to 1 year

Intervention	Months (Median)
Birt-Hogg-Dube Syndrome	NA

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	59

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	73

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	78

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	85

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	88

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Number of Participants With All Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	34

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Number of Participants With Myocardial Infarction

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	2

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Number of Participants With Myocardial Infarction

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	3

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Number of Participants With Cardiac Death or MI

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.) Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT02513719)
Timeframe: 0 to 1 year

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	5

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Number of Participants With Cardiac Death or MI

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.)~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT02513719)
Timeframe: 0 to 2 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	6

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Number of Participants With Cardiac Death or MI

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.)~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT02513719)
Timeframe: 0 to 3 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	8

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Number of Participants With Cardiac Death or MI

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.)~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT02513719)
Timeframe: 0 to 4 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	8

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Number of Participants With Cardiac Death or MI

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.)~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT02513719)
Timeframe: 0 to 5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	12

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Number of Participants With Cardiac Death or MI

"Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery.)~Myocardial Infarction (MI) - Q wave MI: Development of new, pathological Q wave on the ECG.~-Non-Q wave MI: Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves." (NCT02513719)
Timeframe: 0 to 8 months

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	5

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Number of Participants With Cardiac Death or Target Vessel MI

Cardiac death is defined as any death in which a cardiac cause cannot be excluded. (This includes but is not limited to acute myocardial infarction, cardiac perforation/pericardial tamponade, arrhythmia or conduction abnormality,cerebrovascular accident within 30 days of the procedure or cerebrovascular accident suspected of being related to the procedure, death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery). (NCT02513719)
Timeframe: 0 to 2 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	4

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Number of Participants With Cardiac Death or Target Vessel MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	6

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Number of Participants With Cardiac Death or Target Vessel MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	6

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Number of Participants With Cardiac Death or Target Vessel MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	9

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Number of Participants With Target Vessel Failure

Target vessel failure includes cardiac death, MI and ischemia driven TLR; ischemia driven TVR, non TLR; ischemia driven TVR (TLR or TVR, nonTLR). (NCT02513719)
Timeframe: 0 to 1 year

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	22

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Number of Participants With Myocardial Infarction

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	2

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Number of Participants With Major Adverse Cardiac Events (MACE)

Major adverse cardiac events (MACE) is defined as the composite of cardiac death, all myocardial infarction, and Clinically indicated target lesion revascularization (CI-TLR). (NCT02513719)
Timeframe: 0 to 8 months

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	9

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Number of Participants With Major Adverse Cardiac Events (MACE)

Major adverse cardiac events (MACE) is defined as the composite of cardiac death, all myocardial infarction, and clinically indicated target lesion revascularization (CI-TLR). (NCT02513719)
Timeframe: 0 to 5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	28

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Number of Participants With Major Adverse Cardiac Events (MACE)

Major adverse cardiac events (MACE) is defined as the composite of cardiac death, all myocardial infarction, and clinically indicated target lesion revascularization (CI-TLR). (NCT02513719)
Timeframe: 0 to 4 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	23

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Number of Participants With Major Adverse Cardiac Events (MACE)

Major adverse cardiac events (MACE) is defined as the composite of cardiac death, all myocardial infarction, and clinically indicated target lesion revascularization (CI-TLR). (NCT02513719)
Timeframe: 0 to 3 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	23

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Number of Participants With Major Adverse Cardiac Events (MACE)

Major adverse cardiac events (MACE) is defined as the composite of cardiac death, all myocardial infarction, and clinically indicated target lesion revascularization (CI-TLR). (NCT02513719)
Timeframe: 0 to 2 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	18

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Number of Participants With Major Adverse Cardiac Events (MACE)

Major adverse cardiac events (MACE) is defined as the composite of cardiac death, all myocardial infarction, and clinically indicated target lesion revascularization (CI-TLR). (NCT02513719)
Timeframe: 0 to 1 year

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	12

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Number of Participants With Hemorrhage

"Bleeding complications will be defined according to the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) classification of severe, moderate, and mild bleeding events.~Severe or life-threatening:~Either intracranial hemorrhage or bleeding that causes hemodynamic compromise and requires intervention~Moderate:~Bleeding that requires blood transfusion but does not result in hemodynamic compromise~Mild:~Bleeding that does not meet criteria for either moderate or severe bleeding" (NCT02513719)
Timeframe: 0 to 8 months

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	0

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Number of Participants With Hemorrhage

"Bleeding complications will be defined according to the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) classification of severe, moderate, and mild bleeding events.~Severe or life-threatening:~Either intracranial hemorrhage or bleeding that causes hemodynamic compromise and requires intervention~Moderate:~Bleeding that requires blood transfusion but does not result in hemodynamic compromise~Mild:~Bleeding that does not meet criteria for either moderate or severe bleeding" (NCT02513719)
Timeframe: 0 to 2 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	2

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Number of Participants With Hemorrhage

"Bleeding complications will be defined according to the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) classification of severe, moderate, and mild bleeding events.~Severe or life-threatening:~Either intracranial hemorrhage or bleeding that causes hemodynamic compromise and requires intervention~Moderate:~Bleeding that requires blood transfusion but does not result in hemodynamic compromise~Mild:~Bleeding that does not meet criteria for either moderate or severe bleeding" (NCT02513719)
Timeframe: 0 to 1 year

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	1

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Number of Participants With Hemorrhage

"Bleeding complications will be defined according to the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) classification of severe, moderate, and mild bleeding events.~Severe or life-threatening: Either intracranial hemorrhage or bleeding that causes hemodynamic compromise and requires intervention; Moderate: Bleeding that requires blood transfusion but does not result in hemodynamic compromise; Mild: Bleeding that does not meet criteria for either moderate or severe bleeding." (NCT02513719)
Timeframe: 0 to 5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	4

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Number of Participants With Hemorrhage

"Bleeding complications will be defined according to the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) classification of severe, moderate, and mild bleeding events.~Severe or life-threatening: Either intracranial hemorrhage or bleeding that causes hemodynamic compromise and requires intervention; Moderate: Bleeding that requires blood transfusion but does not result in hemodynamic compromise; Mild: Bleeding that does not meet criteria for either moderate or severe bleeding." (NCT02513719)
Timeframe: 0 to 4 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	4

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Number of Participants With Hemorrhage

"Bleeding complications will be defined according to the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) classification of severe, moderate, and mild bleeding events.~Severe or life-threatening: Either intracranial hemorrhage or bleeding that causes hemodynamic compromise and requires intervention; Moderate: Bleeding that requires blood transfusion but does not result in hemodynamic compromise; Mild: Bleeding that does not meet criteria for either moderate or severe bleeding." (NCT02513719)
Timeframe: 0 to 3 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	4

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Number of Participants With Death or MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	6

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Number of Participants With Death or MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	9

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Number of Participants With Death or MI

"All deaths includes Cardiac death: Any death due to proximate cardiac cause (e.g. MI, low-output failure, fatal arrhythmia), unwitnessed death and death of unknown cause, all procedure related deaths including those related to concomitant treatment.~Vascular death: Death due to non-coronary vascular causes such as cerebrovascular disease, pulmonary embolism, ruptured aortic aneurysm, dissecting aneurysm, or other vascular cause.~Non-cardiovascular death: Any death not covered by the above definitions such as death caused by infection, malignancy, sepsis, pulmonary causes, accident, suicide or trauma.~Myocardial Infarction (MI) Q wave MI Development of new, pathological Q wave on the ECG. Non-Q wave MI Elevation of CK levels to ≥ two times the upper limit of normal (ULN) with elevated CK-MB in the absence of new pathological Q waves" (NCT02513719)
Timeframe: 0 to 5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	33

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Number of Participants With Death or MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	27

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Number of Participants With Death or MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	22

[back to top]

Number of Participants With Death or MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	14

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Number of Participants With Cardiac Death or Target-Vessel MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	4

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Net Gain: In-stent, In-segment

Difference between acute gain and late loss. (NCT02513719)
Timeframe: Post-Procedure (on day 0)

Intervention	Millimeter (Mean)
	Stent	Segment
XIENCE PRIME SV Everolimus Eluting Coronary Stent	1.31	1.08

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Late Loss(LL): In-stent,In-segment,Proximal, and Distal

Proximal and distal late loss was calculated by [post-procedure minimum lumen diameter (MLD)] - [MLD at 8 months]. (NCT02513719)
Timeframe: 8 months

Intervention	Millimeter (Mean)
	Stent	Proximal	Distal	Segment
XIENCE PRIME SV Everolimus Eluting Coronary Stent	0.23	0.13	-0.03	0.09

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Acute Gain: In-stent,In-segment

The acute gain was defined as the difference between post- and preprocedural minimal lumen diameter (MLD). (NCT02513719)
Timeframe: Pre procedure to post procedure (on day 0)

Intervention	Millimeter (Mean)
	Stent	Segment
XIENCE PRIME SV Everolimus Eluting Coronary Stent	1.56	1.16

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Success Rate: XIENCE PRIME Implant Success by Patient

"The stent lengths used were 8 mm, 12 mm, and 15 mm,18 mm, 23 mm, and 28 mm and the stent diameter was 2.25 mm.~Implant success is assessed as per physicians decision, but means that the stent could be implanted at the intended location." (NCT02513719)
Timeframe: < or = 1 day

Intervention	participants (Number)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	100

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Success Rate: Percentage of Lesions With Procedural Success

Achievement of final in-scaffold/stent residual stenosis of less than 50% by QCA with successful delivery and deployment of at least one study scaffold/stent at the intended target lesion and successful withdrawal of the delivery system for all target lesions without the occurrence of cardiac death, target vessel MI or repeat TLR during the hospital stay (less than or equal to 7 days). (NCT02513719)
Timeframe: < or = 1 day

Intervention	Percentage of lesions (Number)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	100

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Success Rate: Percentage of Devices With Implant Success

"The stent lengths used were 8 mm, 12 mm, and 15 mm,18 mm, 23 mm, and 28 mm and the stent diameter was 2.25mm.~Successful delivery and deployment of the first study scaffold/stent the intended target lesion and successful withdrawal of the delivery system with attainment of final in-scaffold/stent residual stenosis of less than 50% by quantitative coronary angiography (QCA)." (NCT02513719)
Timeframe: < or = 1 day

Intervention	percentage of devices (Number)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	100

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Percent Diameter Stenosis (%DS)

The value calculated as 100 * (1- minimum lumen diameter/reference vessel diameter) (MLD/RVD) using the mean values from two orthogonal views (when possible) by quantitative coronary angiography (QCA). (NCT02513719)
Timeframe: Pre-procedure

Intervention	Percent Diameter stenosis (Mean)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	73.62

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Percent Diameter Stenosis (%DS)

Intervention	Percent Diameter stenosis (Mean)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	26.03

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Percent Diameter Stenosis (%DS)

Intervention	Percent Diameter stenosis (Mean)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	28.31

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Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)

The number of patient with Ischemia-driven Target vessel revascularization (TLR or TVR, non-TLR) (NCT02513719)
Timeframe: 0 to 2 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	42

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Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)

Target vessel revascularization (TLR or TVR, non-TLR) includes ischemia driven TVR (TLR or TVR, non-TLR) or non-ischemia driven TVR (TLR or TVR, non-TLR) (NCT02513719)
Timeframe: 0-5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	51

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Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)

Target vessel revascularization (TLR or TVR, non-TLR) includes ischemia driven TVR (TLR or TVR, non-TLR) or non-ischemia driven TVR (TLR or TVR, non-TLR) (NCT02513719)
Timeframe: 0-4 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	47

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Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)

Target vessel revascularization (TLR or TVR, non-TLR) includes ischemia driven TVR (TLR or TVR, non-TLR) or non-ischemia driven TVR (TLR or TVR, non-TLR) (NCT02513719)
Timeframe: 0-3 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	45

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Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)

Target vessel revascularization (TLR or TVR, non-TLR) includes ischemia driven TVR (TLR or TVR, non-TLR) or non-ischemia driven TVR (TLR or TVR, non-TLR) (NCT02513719)
Timeframe: 0 to 8 months

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	21

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Number of Participants With Target Vessel Revascularization (TLR or TVR, Non-TLR)

Target vessel revascularization (TLR or TVR, non-TLR) includes ischemia driven TVR (TLR or TVR, non-TLR) or non-ischemia driven TVR (TLR or TVR, non-TLR) (NCT02513719)
Timeframe: 0 to 1 year

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	34

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Number of Participants With Target Vessel Failure

Target vessel failure includes cardiac death, MI, ischemia driven TLR, ischemia driven TVR, non TLR and ischemia driven TVR (TLR or TVR, nonTLR). (NCT02513719)
Timeframe: 0 to 8 months

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	16

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Number of Participants With Target Vessel Failure

Target vessel failure includes cardiac death, MI and ischemia driven TLR; ischemia driven TVR, non TLR; ischemia driven TVR (TLR or TVR, nonTLR). (NCT02513719)
Timeframe: 0 to 5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	45

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Number of Participants With Target Vessel Failure

Target vessel failure includes cardiac death, MI and ischemia driven TLR; ischemia driven TVR, non TLR; ischemia driven TVR (TLR or TVR, nonTLR). (NCT02513719)
Timeframe: 0 to 4 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	39

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Number of Participants With Target Vessel Failure

Target vessel failure includes cardiac death, MI and ischemia driven TLR; ischemia driven TVR, non TLR; ischemia driven TVR (TLR or TVR, nonTLR). (NCT02513719)
Timeframe: 0 to 3 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	35

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Number of Participants With Target Vessel Failure

Target vessel failure includes cardiac death, MI and ischemia driven TLR; ischemia driven TVR, non TLR; ischemia driven TVR (TLR or TVR, nonTLR). (NCT02513719)
Timeframe: 0 to 2 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	30

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Number of Participants With Target Lesion Revascularization

Target lesion revascularization is defined as any repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion. Target lesion revascularization (TLR) includes ischemia driven TLR and non-ischemia driven TLR (NCT02513719)
Timeframe: 0-5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	27

[back to top]

Number of Participants With Target Lesion Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	26

[back to top]

Number of Participants With Target Lesion Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	25

[back to top]

Number of Participants With Target Lesion Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	9

[back to top]

Number of Participants With Target Lesion Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	22

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Number of Participants With Target Lesion Revascularization

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	16

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Number of Participants With Target Lesion Failure

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT02513719)
Timeframe: 0 to 8 months

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	8

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Number of Participants With Cardiac Death or Target Vessel-MI

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	5

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Number of Participants With Target Lesion Failure

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT02513719)
Timeframe: 0 to 5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	25

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Number of Participants With Target Lesion Failure

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT02513719)
Timeframe: 0 to 4 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	21

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Number of Participants With Target Lesion Failure

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT02513719)
Timeframe: 0 to 3 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	21

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Number of Participants With Target Lesion Failure

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT02513719)
Timeframe: 0 to 2 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	16

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Number of Participants With Target Lesion Failure

Target Lesion Failure is composite of Cardiac death/ Target Vessel Myocardial Infarction (TV-MI)/ Ischemic-Driven Target Lesion Revascularization (ID-TLR). (NCT02513719)
Timeframe: 0 to 1 year

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	11

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Number of Participants With Stent Thrombosis: Very Late

"Stent/Scaffold Thrombosis (per ARC): Stent/Scaffold Thrombosis should be reported as a cumulative value over time and at various individual time points. Time 0 is defined as the time point after the guiding catheter has been removed and the subject left the catheterization lab.~Timings:~Very late stent thrombosis : >1 year after stent implantation." (NCT02513719)
Timeframe: >1 year post stent implantation

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	0

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Number of Death

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	7

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Number of Death

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	11

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Number of Death

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	20

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Number of Death

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	25

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Number of Death

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	30

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Number of Death

Death includes cardiac death, non-cardiac death and non-coronary death. (NCT02513719)
Timeframe: 0 to 8 months

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	4

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Number of Participants With All Death/All MI/All Revascularization

(NCT02513719)
Timeframe: 0 to 1 year

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	66

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Number of Participants With All Death/All MI/All Revascularization

(NCT02513719)
Timeframe: 0 to 2 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	84

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Number of Participants With All Death/All MI/All Revascularization

(NCT02513719)
Timeframe: 0 to 3 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	96

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Number of Participants With All Death/All MI/All Revascularization

(NCT02513719)
Timeframe: 0 to 4 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	106

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Number of Participants With All Death/All MI/All Revascularization

(NCT02513719)
Timeframe: 0 to 5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	111

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Number of Participants With Stent Thrombosis: Subacute

"Stent/Scaffold Thrombosis (per ARC): Stent/Scaffold Thrombosis should be reported as a cumulative value over time and at various individual time points. Time 0 is defined as the time point after the guiding catheter has been removed and the subject left the catheterization lab.~Timings:~Subacute stent thrombosis : >24 hours to 30 days after stent implantation" (NCT02513719)
Timeframe: >24 hours to 30 days post stent implantation

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	0

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Number of Participants With Stent Thrombosis: Late

"Stent/Scaffold Thrombosis (per ARC): Stent/Scaffold Thrombosis should be reported as a cumulative value over time and at various individual time points. Time 0 is defined as the time point after the guiding catheter has been removed and the subject left the catheterization lab.~Timings:~Late stent thrombosis : >30 days to 1 year after stent implantation" (NCT02513719)
Timeframe: 30 days to 1 year post stent implantation

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	1

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Number of Participants With Stent Thrombosis: Acute

"Stent/Scaffold Thrombosis (per ARC): Stent/Scaffold Thrombosis should be reported as a cumulative value over time and at various individual time points. Time 0 is defined as the time point after the guiding catheter has been removed and the subject left the catheterization lab.~Timing:~Acute stent thrombosis: 0 to 24 hours after stent implantation" (NCT02513719)
Timeframe: 0-24 hours post stent implantation

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	1

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Number of Participants With Non-target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR) is any revascularization in a vessel other than the target vessel. (NCT02513719)
Timeframe: 0 to 8 months

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	16

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Number of Participants With Non-target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR) is any revascularization in a vessel other than the target vessel. (NCT02513719)
Timeframe: 0 to 5 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	58

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Number of Participants With Non-target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR) is any revascularization in a vessel other than the target vessel. (NCT02513719)
Timeframe: 0 to 4 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	55

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Number of Participants With Non-target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR) is any revascularization in a vessel other than the target vessel. (NCT02513719)
Timeframe: 0 to 3 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	45

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Number of Participants With Non-target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR) is any revascularization in a vessel other than the target vessel. (NCT02513719)
Timeframe: 0 to 2 years

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	42

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Number of Participants With Non-target Vessel Revascularization (Non-TVR)

Non Target Vessel Revascularization (Non-TVR) is any revascularization in a vessel other than the target vessel. (NCT02513719)
Timeframe: 0 to 1 year

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	32

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Number of Participants With Myocardial Infarction

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	5

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Number of Participants With Myocardial Infarction

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	4

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Number of Participants With Myocardial Infarction

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	4

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Number of Participants With All Death/All MI/All Revascularization

(NCT02513719)
Timeframe: 0 to 8 months

Intervention	Participants (Count of Participants)
XIENCE PRIME SV Everolimus Eluting Coronary Stent	38

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Number of Participants Who Experienced Dose-limiting Toxicities

Evaluate the number of participants who had a dose limiting toxicity with the combination of letrozole with everolimus and TRC105 per treatment arm (NCT02520063)
Timeframe: 4 weeks

Intervention	participants (Number)
Phase I Cohort 1	1
Phase I Cohort 2	0

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Number of Patients With Tumor Volume Reduction Greater Than 25%

Measuring the efficacy and tolerability of everolimus by measuring the number of patients with tumor volume reduction greater than 25% in sporadic AMLs as measured by DCE MRI (NCT02539459)
Timeframe: 12 months

Intervention	Participants (Count of Participants)
Treatment (Everolimus)	5

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Safety and Tolerability of Everolimus in Patients With Sporadic AML

Number of participants with treatment-related adverse events requiring dose reduction or study withdrawal as assessed by Common Toxicity Criteria for Adverse Effects (CTCAE v4.0) (NCT02539459)
Timeframe: 12 months

Intervention	Participants (Count of Participants)
Treatment (Everolimus)	10

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Number of Participants Who Progressed

"The PFS is defined as the time elapsed between treatment initiation and tumor progression or death from any cause, with censoring of patients who are lost to follow-up. Progression is defined using the Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1): At least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20, the sum must also demonstrate an absolute increase of at least 5 mm. (Note: the appearance of one or more new lesions is also considered progression)." (NCT02560012)
Timeframe: From date of enrollment until the date of first documented progression, date of death from any cause, or date that the study was stopped, whichever came first, an average of 16 months

Intervention	Participants (Count of Participants)
Personalized Therapy	0

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Phase 1b: Terminal Elimination Rate Constant (λz) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4

Actual collection times relative to ibrutinib administration were used for the calculation of pharmacokinetic parameters of ibrutinib and PCI-45227. For actual predose collection times that were < 0, these values were set equal to 0. Predose concentrations were applied as 24 hour concentrations in order to calculate steady-state (Cycle 2 Day 1) pharmacokinetic parameters for ibrutinib and PCI-45227. The λz is the apparent elimination rate constant obtained by linear regression of three or more log-transformed data points in the terminal phase (not including Cmax). (NCT02599324)
Timeframe: Cycle 2 Day 1: predose, 1 h ± 15 min, 2 h ± 15 min, 4 h ± 15 min, 6 h ± 15 min postdose

,,,,,

Intervention	1/h (Mean)
	Ibrutininb	PCI-45227
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	0.125	0.0870
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	0.101	0.137
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	0.195	0.149
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	0.135	0.118
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	NA	0.0897
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	0.132	0.0942

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Phase 1b: Area Under the Concentration-Time Curve to Last Observed Time Point (AUClast) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4

Actual collection times relative to ibrutinib administration were used for the calculation of pharmacokinetic parameters of ibrutinib and PCI-45227. For actual predose collection times that were < 0, these values were set equal to 0. Predose concentrations were applied as 24 hour concentrations in order to calculate steady-state (Cycle 2 Day 1) pharmacokinetic parameters for ibrutinib and PCI-45227. The AUClast was calculated by the linear trapezoidal method. (NCT02599324)
Timeframe: Cycle 2 Day 1: predose, 1 h ± 15 min, 2 h ± 15 min, 4 h ± 15 min, 6 h ± 15 min postdose

,,,,,,

Intervention	ng∙h/mL (Mean)
	Ibrutininb	PCI-45227
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	1316	548
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	2568	1810
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	1180	859
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	3227	2380
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	1107	1165
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	847	1527
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	2647	2178

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Phase 1b: Apparent Total Clearance at Steady-State (CLss/F) for Ibrutinib in Cohorts 1 to 4

Actual collection times relative to ibrutinib administration were used for the calculation of pharmacokinetic parameters of ibrutinib and PCI-45227. For actual predose collection times that were < 0, these values were set equal to 0. Predose concentrations were applied as 24 hour concentrations in order to calculate steady-state (Cycle 2 Day 1) pharmacokinetic parameters for ibrutinib and PCI-45227. Apparent total CLss/F (Cycle 2 Day 1) was calculated as dose/AUC0-24h. (NCT02599324)
Timeframe: Cycle 2 Day 1: predose, 1 h ± 15 min, 2 h ± 15 min, 4 h ± 15 min, 6 h ± 15 min postdose

Intervention	L/h (Mean)
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	1103
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	622
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	994
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	1067
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	1102
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	645
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	595

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Phase 1b: Terminal Elimination Rate Constant (λz) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4

Intervention	1/h (Mean)
	Ibrutininb
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	NA

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Phase 1b: Terminal Elimination Half-Life (t1/2term) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4

Actual collection times relative to ibrutinib administration were used for the calculation of pharmacokinetic parameters of ibrutinib and PCI-45227. For actual predose collection times that were < 0, these values were set equal to 0. Predose concentrations were applied as 24 hour concentrations in order to calculate steady-state (Cycle 2 Day 1) pharmacokinetic parameters for ibrutinib and PCI-45227. The apparent t1/2term was calculated by ln(2)/λz, where λz is the apparent elimination rate constant obtained by linear regression of three or more log-transformed data points in the terminal phase (not including Cmax). (NCT02599324)
Timeframe: Cycle 2 Day 1: predose, 1 h ± 15 min, 2 h ± 15 min, 4 h ± 15 min, 6 h ± 15 min postdose

,,,,,,

Intervention	hours (Mean)
	Ibrutininb	PCI-45227
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	NA	NA
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	6.28	8.00
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	7.24	5.08
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	4.31	6.79
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	5.54	6.48
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	NA	8.10
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	5.52	8.02

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Phase 1b: Observed Maximum Concentration (Cmax) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4

Actual collection times relative to ibrutinib administration were used for the calculation of pharmacokinetic parameters of ibrutinib and PCI-45227. For actual predose collection times that were < 0, these values were set equal to 0. Predose concentrations were applied as 24 hour concentrations in order to calculate steady-state (Cycle 2 Day 1) pharmacokinetic parameters for ibrutinib and PCI-45227. The Cmax was noted as observed. (NCT02599324)
Timeframe: Cycle 2 Day 1: predose, 1 h ± 15 min, 2 h ± 15 min, 4 h ± 15 min, 6 h ± 15 min postdose

,,,,,,

Intervention	ng/mL (Mean)
	Ibrutininb	PCI-45227
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	172	51.2
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	351	147
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	260	127
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	424	198
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	164	106
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	172	154
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	371	177

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Phase 1b: Disease Control Rate (DCR) in Cohorts 1 to 6

DCR is is defined as the percentage of participants who have a best response of PR, CR, or stable disease (SD) to therapy in accordance with RECIST 1.1 criteria. CR: The disappearance of all target and non-target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 10 mm. Normalization of tumor marker level, if relevant. All lymph nodes must be non-pathological in size (< 10 mm short axis). PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD since the treatment started (baseline or after). For SD, tthere was no need for confirmation by a subsequent imaging assessment. (NCT02599324)
Timeframe: Maximum time on study (Phase 1b only) for Cohort 1 was 37.4 months; for Cohort 2 was 44.7 months; for Cohort 3 was 41.9 months; for Cohort 4 was 34.2 months; for Cohort 5 was 17.3 months; for Cohort 6 was 20.1 months.

Intervention	percentage of participants (Number)
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	66.7
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	71.4
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	75.0
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	50.0
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	77.8
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	75.0
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	80.0
Cohort 5 (UC): Ibrutinib 840 mg	37.5
Cohort 6 (UC): Ibrutinib 560 mg + Pembrolizumab	76.9

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Phase 1b: Number of Participants With Dose-Limiting Toxicities (DLTs) in Cohorts 1 to 6

A DLT was defined as any Grade 3 (severe) or higher non-hematologic or Grade 4 (life-threatening) hematologic adverse event (AE) occurring during the DLT observation period that was considered to be at least possibly related to the study treatment (ibrutinib or drug combination). (NCT02599324)
Timeframe: 21 days after the initiation of therapy at the start of Cycle 1

Intervention	Participants (Count of Participants)
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	0
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	1
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	0
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	0
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	2
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	0
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	0
Cohort 5 (UC): Ibrutinib 840 mg	0
Cohort 6 (UC): Ibrutinib 560 mg + Pembrolizumab	0

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Phase 1b: ORR in Cohorts 1 to 6

ORR is defined as the percentage of participants who have a best response of partial response (PR) or complete response (CR) to therapy in accordance with RECIST 1.1 criteria. CR: The disappearance of all target and non-target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 10 mm. Normalization of tumor marker level, if relevant. All lymph nodes must be non-pathological in size (< 10 mm short axis). PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. (NCT02599324)
Timeframe: Maximum time on study (Phase 1b only) for Cohort 1 was 37.4 months; for Cohort 2 was 44.7 months; for Cohort 3 was 41.9 months; for Cohort 4 was 34.2 months; for Cohort 5 was 17.3 months; for Cohort 6 was 20.1 months.

Intervention	percentage of participants (Number)
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	0
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	0
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	50.0
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	20.0
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	11.1
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	12.5
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	0
Cohort 5 (UC): Ibrutinib 840 mg	12.5
Cohort 6 (UC): Ibrutinib 560 mg + Pembrolizumab	38.5

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Phase 1b/2 RP2D: DCR in Cohorts 1 to 6

DCR is is defined as the percentage of participants who have a best response of PR, CR, or SD to therapy in accordance with RECIST 1.1 criteria. CR: The disappearance of all target and non-target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 10 mm. Normalization of tumor marker level, if relevant. All lymph nodes must be non-pathological in size (< 10 mm short axis). PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD since the treatment started (baseline or after). For SD, tthere was no need for confirmation by a subsequent imaging assessment. (NCT02599324)
Timeframe: Maximum time on study (Phase 1b/2 RP2D) for Cohort 1 was 37.4 months; for Cohort 2 was 44.7 months; for Cohort 3 was 41.9 months; for Cohort 4 was 23.5 months; for Cohort 5 was 17.3 months; for Cohort 6 was 20.1 months. (Reverse Kaplan-Meier estimates)

Intervention	percentage of participants (Number)
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	80.6
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	66.7
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	74.4
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	83.0
Cohort 5 (UC): Ibrutinib 840 mg	48.3
Cohort 6 (UC): Ibrutinib 560 mg + Pembrolizumab	71.4

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Phase 1b/2 RP2D: Duration of Response (DOR) in Cohorts 1 to 6

"DOR is defined for confirmed responders (PR or better) as time from the date of initial response (PR or better) to the date of first documentation of PD (according to RECIST 1.1) or death, whichever occurs first, regardless of use of subsequent anti-cancer treatment. Confirmed responders without documentation of PD or death or with unknown status at the data extraction were censored at the last adequate post-baseline disease assessment showing no evidence of PD. PD was defined as at least a 20% increase in the size of target lesions with an absolute increase of at least 5 mm, unequivocal progression of existing non-target lesions, or the appearance of one or more new lesions.~Per protocol, participants in Phase 1b receiving the Phase 2 RP2D and participants in Phase 2 RP2D were analyzed together." (NCT02599324)
Timeframe: Maximum time on study (Phase 1b/2 RP2D) for Cohort 1 was 37.4 months; for Cohort 2 was 44.7 months; for Cohort 3 was 41.9 months; for Cohort 4 was 23.5 months; for Cohort 5 was 17.3 months; for Cohort 6 was 20.1 months. (Reverse Kaplan-Meier estimates)

Intervention	months (Median)
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	3.1
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	4.4
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	5.5
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	11.1
Cohort 5 (UC): Ibrutinib 840 mg	3.5
Cohort 6 (UC): Ibrutinib 560 mg + Pembrolizumab	NA

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Phase 1b/2 RP2D: ORR in Cohorts 1 and 2

ORR is defined as the percentage of participants who have a best response to therapy of PR or CR in accordance with RECIST 1.1 criteria. CR: The disappearance of all target and non-target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 10 mm. Normalization of tumor marker level, if relevant. All lymph nodes must be non-pathological in size (< 10 mm short axis). PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. (NCT02599324)
Timeframe: Maximum time on study for Cohort 1 (Phase 1b/2 RP2D) was 37.4 months; for Cohort 2 (Phase 1b/2 RP2D) was 44.7 months. (Reverse Kaplan-Meier estimates)

Intervention	percentage of participants (Number)
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	2.8
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	26.3

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Phase 1b/2 RP2D: Overall Response Rate (ORR) as Assessed by Investigator in Cohorts 3 to 6

ORR is defined as the percentage of participants who have a best response of partial response (PR) or complete response (CR) to therapy in accordance with RECIST 1.1 criteria. CR: The disappearance of all target and non-target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to < 10 mm. Normalization of tumor marker level, if relevant. All lymph nodes must be non-pathological in size (< 10 mm short axis). PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. (NCT02599324)
Timeframe: Maximum time on study (Phase 1b/2 RP2D) for Cohort 3 was 41.9 months; for Cohort 4 was 23.5 months; for Cohort 5 was 17.3 months; for Cohort 6 was 20.1 months.

Intervention	percentage of participants (Number)
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	17.9
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	14.9
Cohort 5 (UC): Ibrutinib 840 mg	6.9
Cohort 6 (UC): Ibrutinib 560 mg + Pembrolizumab	35.7

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Phase 1b/2 RP2D: Overall Survival (OS) in Cohorts 1 to 6

OS is defined as the time from the date of first dose of study treatment to the date of death from any cause. Subjects who were not known to have died at the data extraction will be censored at date last known alive. (NCT02599324)
Timeframe: Maximum time on study (Phase 1b/2 RP2D) for Cohort 1 was 37.4 months; for Cohort 2 was 44.7 months; for Cohort 3 was 41.9 months; for Cohort 4 was 23.5 months; for Cohort 5 was 17.3 months; for Cohort 6 was 20.1 months. (Reverse Kaplan-Meier estimates)

Intervention	months (Median)
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	21.0
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	8.2
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	7.3
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	15.0
Cohort 5 (UC): Ibrutinib 840 mg	8.2
Cohort 6 (UC): Ibrutinib 560 mg + Pembrolizumab	15.7

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Phase 1b/2 RP2D: PFS in Cohorts 3 to 6

PFS is defined as the time from the date of first dose of study treatment to the date of first documentation of PD or date of death from any cause, whichever occurs first, regardless of the use of subsequent anti-cancer treatment. PD was defined in accordance with RECIST 1.1 criteria. (NCT02599324)
Timeframe: Maximum time on study (Phase 1b/2 RP2D) for Cohort 3 was 41.9 months; for Cohort 4 was 23.5 months; for Cohort 5 was 17.3 months; for Cohort 6 was 20.1 months. (Reverse Kaplan-Meier estimates)

Intervention	months (Median)
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	4.0
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	5.4
Cohort 5 (UC): Ibrutinib 840 mg	1.6
Cohort 6 (UC): Ibrutinib 560 mg + Pembrolizumab	2.9

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Phase 1b/2 RP2D: Progression-Free Survival (PFS) as Assessed by Investigator in Cohorts 1 and 2

PFS is defined as the time from the date of first dose of study treatment to the date of first documentation of progressive disease (PD) or date of death from any cause, whichever occurs first, regardless of the use of subsequent anti-cancer treatment. PD was defined in accordance with Response Evaluation Criteria In Solid Tumors (RECIST) criteria version 1.1. PD: At least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study), and an absolute increase of ≥ 5 mm, or unequivocal progression of existing non-target lesions or the appearance of new lesions. (NCT02599324)
Timeframe: Maximum time on study for Cohort 1 (Phase 1b/2 RP2D) was 37.4 months; for Cohort 2 (Phase 1b/2 RP2D) was 44.7 months.

Intervention	months (Median)
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	5.6
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	4.1

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Phase 1b: Area Under the Concentration-Time Curve From Time 0 to Hour 24 (AUC0-24h) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4

Actual collection times relative to ibrutinib administration were used for the calculation of pharmacokinetic parameters of ibrutinib and PCI-45227. For actual predose collection times that were < 0, these values were set equal to 0. Predose concentrations were applied as 24 hour concentrations in order to calculate steady-state (Cycle 2 Day 1) pharmacokinetic parameters for ibrutinib and PCI-45227. The AUC0-24h was calculated by the linear trapezoidal method. (NCT02599324)
Timeframe: Cycle 2 Day 1: predose, 1 h ± 15 min, 2 h ± 15 min, 4 h ± 15 min, 6 h ± 15 min postdose

,,,,,,

Intervention	ng∙h/mL (Mean)
	Ibrutininb	PCI-45227
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	1467	646
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	2568	1810
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	2194	1146
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	3503	2604
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	1253	1254
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	980	1527
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	2807	2178

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Phase 1b: Time of Last Observed Concentration (Tlast) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4

Actual collection times relative to ibrutinib administration were used for the calculation of pharmacokinetic parameters of ibrutinib and PCI-45227. For actual predose collection times that were < 0, these values were set equal to 0. Predose concentrations were applied as 24 hour concentrations in order to calculate steady-state (Cycle 2 Day 1) pharmacokinetic parameters for ibrutinib and PCI-45227. The tlast was noted as observed. (NCT02599324)
Timeframe: Cycle 2 Day 1: predose, 1 h ± 15 min, 2 h ± 15 min, 4 h ± 15 min, 6 h ± 15 min postdose

,,,,,,

Intervention	hours (Median)
	Ibrutininb	PCI-45227
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	15.0	15.0
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	24.0	24.0
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	24.0	24.0
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	24.0	24.0
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	24.0	24.0
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	24.0	24.0
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	24.0	24.0

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Phase 1b: Time to Cmax (Tmax) for Ibrutinib and Its Metabolite PCI-45227 in Cohorts 1 to 4

Actual collection times relative to ibrutinib administration were used for the calculation of pharmacokinetic parameters of ibrutinib and PCI-45227. For actual predose collection times that were < 0, these values were set equal to 0. Predose concentrations were applied as 24 hour concentrations in order to calculate steady-state (Cycle 2 Day 1) pharmacokinetic parameters for ibrutinib and PCI-45227. The tmax was noted as observed. (NCT02599324)
Timeframe: Cycle 2 Day 1: predose, 1 h ± 15 min, 2 h ± 15 min, 4 h ± 15 min, 6 h ± 15 min postdose

,,,,,,

Intervention	hours (Median)
	Ibrutininb	PCI-45227
Cohort 1 (RCC): Ibrutinib 560 mg + Everolimus	3.01	3.03
Cohort 1 (RCC): Ibrutinib 840 mg + Everolimus	2.00	3.93
Cohort 2 (UC): Ibrutinib 560 mg + Paclitaxel	3.71	4.00
Cohort 2 (UC): Ibrutinib 840 mg + Paclitaxel	4.00	4.00
Cohort 3 (GA): Ibrutinib 560 mg + Docetaxel	3.89	4.00
Cohort 4 (CRC): Ibrutinib 560 mg + Cetuximab	2.89	2.99
Cohort 4 (CRC): Ibrutinib 840 mg + Cetuximab	2.03	4.00

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Number of Participants With Treatment-Emergent Adverse Events (TEAEs)

An AE was defined as any untoward medical occurrence in participants administered a pharmaceutical product; the untoward medical occurrence does not necessarily have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of a medicinal (investigational) product whether or not it is related to the medicinal product. TEAE was defined as the event that occur after administration of the first dose of study drug and through 30 days after the last dose of study drug. (NCT02724020)
Timeframe: From first dose of study drug through 30 days after the last dose of study drug (approximately up to 31 months)

Intervention	Participants (Count of Participants)
Arm A: Single-agent Everolimus 10 mg QD	32
Arm B: Single-agent MLN0128 30 mg QW	30
Arm C: Combination of MLN0128 4 mg QD + MLN1117 200 mg QD	31

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Objective Response Rate (ORR)

ORR was defined as the percentage of participants among response evaluable analysis set who achieve a best overall response of complete response (CR) or partial response (PR) based on investigators assessment of response following RECIST 1.1. CR was defined as disappearance of all target lesions, non-target lesions, no new lesions, and normalization of tumor marker level. PR was defined as at least a 30% decrease in the sum of diameters of target lesions, no progression in non-target lesion, and no new lesions. (NCT02724020)
Timeframe: From first dose of study drug to disease progression or death (up to 51 months)

Intervention	percentage of participants (Number)
Arm A: Single-agent Everolimus 10 mg QD	15.6
Arm B: Single-agent MLN0128 30 mg QW	0
Arm C: Combination of MLN0128 4 mg QD + MLN1117 200 mg QD	6.5

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Overall Survival (OS)

Overall survival in months was defined as the time from the date of randomization to the date of death. (NCT02724020)
Timeframe: From first dose of study drug through 30 days after the last dose of study drug (up to 51 months)

Intervention	months (Median)
Arm A: Single-agent Everolimus 10 mg QD	22.4
Arm B: Single-agent MLN0128 30 mg QW	16.2
Arm C: Combination of MLN0128 4 mg QD + MLN1117 200 mg QD	18.1

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Progression-Free Survival (PFS)

PFS was defined as the time from the date of randomization to the date of first documentation of progressive disease (PD) or death due to any cause, whichever occurs first. Per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 criteria. PD was defined as at least a 20% increase in the sum of the longest diameter (LD) of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT02724020)
Timeframe: From first dose of study drug up to disease progression or death, assessed up to 43 months

Intervention	months (Median)
Arm A: Single-agent Everolimus 10 mg QD	3.8
Arm B: Single-agent MLN0128 30 mg QW	3.6
Arm C: Combination of MLN0128 4 mg QD + MLN1117 200 mg QD	3.1

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Time-to-progression (TTP)

TTP in months is defined as the time from the date of randomization to the date of first documentation of progression. Per RECIST v1.1, PD was defined as at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT02724020)
Timeframe: From first dose of study drug up to disease progression or death (up to 51 months)

Intervention	months (Median)
Arm A: Single-agent Everolimus 10 mg QD	3.8
Arm B: Single-agent MLN0128 30 mg QW	3.5
Arm C: Combination of MLN0128 4 mg QD + MLN1117 200 mg QD	3.7

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Clinical Benefit Rate (CBR)

CBR is defined as the percentage of participants who achieve a best response of CR, PR or stable disease (SD) of any duration. CR was defined as disappearance of all target lesions, non-target lesions, no new lesions, and normalization of tumor marker level. PR was defined as at least a 30% decrease in the sum of diameters of target lesions, no progression in non-target lesion, and no new lesions. SD was defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. (NCT02724020)
Timeframe: From first dose of study drug up to disease progression or death (up to 51 months)

Intervention	percentage of participants (Number)
Arm A: Single-agent Everolimus 10 mg QD	62.5
Arm B: Single-agent MLN0128 30 mg QW	50.0
Arm C: Combination of MLN0128 4 mg QD + MLN1117 200 mg QD	54.8

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CBR With SD Duration of at Least 16 Weeks

CBR with SD duration of at least 4 months (CBR-16) was defined as the percentage of participants who achieve CR or PR of any duration or have SD with duration of at least 16 weeks. CR was defined as disappearance of all target lesions, non-target lesions, no new lesions, and normalization of tumor marker level. PR was defined as at least a 30% decrease in the sum of diameters of target lesions, no progression in non-target lesion, and no new lesions. SD was defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. (NCT02724020)
Timeframe: Up to Week 16

Intervention	percentage of participants (Number)
Arm A: Single-agent Everolimus 10 mg QD	40.6
Arm B: Single-agent MLN0128 30 mg QW	25.0
Arm C: Combination of MLN0128 4 mg QD + MLN1117 200 mg QD	29.0

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Duration of Overall Response (DOR) by Group - Phase II

Patients whose best response is complete response (CR) or partial response (PR). The start date is the date of first documented response (CR or PR) and the end date is the date of first documented progression or death due to underlying cancer. (NCT02732119)
Timeframe: Baseline up to approximately 16 months

Intervention	months (Median)
Group 1	14.6
Group 2	6.4

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Participants With Dose Limiting Toxicities by Preferred Term in Cycle 1 (28 Days) - in Phase I

A dose-limiting toxicity (DLT) is defined as an adverse event or abnormal laboratory value assessed as having a reasonably possible relationship to the study medication(s) and is unrelated to disease, disease progression, inter-current illness, or concomitant medications that occurs within the first 28 days of treatment (cycle 1) and meets any of the criteria defined in the protocol. National Cancer Institute Common Terminology Criteria for Adverse events (NCI CTCAE) version 4.03 will be used for all grading. (NCT02732119)
Timeframe: Baseline up to 28 days

Intervention	Participants (Count of Participants)
	Febrile neutropenia Grade 3	Neutropenia Grade 4	Thrombocytopenia Grade 4	Cardiac tamponade Grade 4	Diarrhea Grade 3	Hyperglycemia Grade 4
Cohort A	1	0	0	1	1	0
Cohort B	1	1	1	0	0	0
Cohort C	0	0	0	0	0	1

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Everolimus Pharmacokinetic Plasma Concentrations by Cohort - Phase I

Plasma concentrations; below limit of quantitation values set to zero (NCT02732119)
Timeframe: Cycle 1,2: Day 1 and 15 - pre-dose, 2 and 4 hour post dose, Cycle 3 , Day 1 - pre-dose

Intervention	ng/mL (Median)
	Cycle 1, Day 15 Pre-dose	Cycle 1, Day 15 2 H, post dose	Cycle 1, Day 15 4 H, post dose	Cycle 2, Day 1 Pre-dose	Cycle 2, Day 15 Pre-dose	Cycle 2, Day 15 2 H post-dose	Cycle 2, Day 15 4 H post-dose	Cycle 3, Day 1 4 H pre-dose
Cohort A	7.82	15.2	17.7	6.47	5.89	21.8	13.7	4.7
Cohort B	8.31	17	16.2	6.22	4.26	14.5	9.13	6.97
Cohort C	8.28	36.2	21.5	7.76	7.17	22.1	26.9	6.33

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Everolimus Pharmacokinetic Plasma Concentrations - Phase II

Plasma concentrations; below limit of quantitation values set to zero (NCT02732119)
Timeframe: Cycle 1,2: Day 1 and 15 - pre-dose, 2 and 4 hour post dose, Cycle 3 , Day 1 - pre-dose

Intervention	ng/mL (Median)
	Cycle 1, Day 15 pre dose	Cycle 1, Day 15 2 H post-dose	Cycle 1, Day 15 4 H post-dose	Cycle 2 Day 1 pre-dose	Cycle 2, Day 15 pre-dose	Cycle 2, Day 15 2 H post-dose	Cycle 2, Day 15 4 H post-dose	Cycle 3, Day 1 pre-dose
Group 1	214	644	583	199	245	652	642	193
Group 2	132	372	323	125	170	442	406	198

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Clinical Benefit Rate as Per Central Review by Group- Phase II

"Clinical Benefit Rate (CBR) is defined as the percentage of participants with a complete response (CR) or partial response (PR) or with stable disease (SD) as per Response Evaluation Criteria in Solid Tumors (RECIST) V1.1 or Non-Complete Response or Non-Progressive Disease (NCRNPD) during first 24 weeks of first dose. CR=disappearance of all non-nodal target lesions, PR=at least a 30% decrease in the sum of diameter of all target lesions, SD=neither sufficient shrinkage to qualify for PR or CR nor an increase in lesions which would qualify for progressive disease (PD), PD=at least a 20% increase in the sum of diameter of all target lesions.~The hypothesis was to be rejected if the lower limit of the 95% Confidence Interval for Clinical Benefit Rate (CBR) was greater than 10%." (NCT02732119)
Timeframe: From baseline up to 24 weeks

Intervention	percentage of participants (Number)
	Overall response rate (CR+PR):	CBR - CR+PR+SD (NCRNPD) by 24 weeks	Disease control rate (CR+PR+SD(NCRNPD)
Group 1	6.5	65.2	65.2
Group 2	9.4	59.4	59.4

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Clinical Benefit Rate as Per Central Review by Dose Cohort - Phase I

Clinical Benefit Rate (CBR) is defined as the percentage of patients with a complete response (CR) or partial response (PR) or with stable disease (SD) at 24 weeks as per Response Evaluation Criteria in Solid Tumors (RECIST) V1.1 or Non-Complete Response Non-Progressive Disease (NCRNPD) up to Week 24 and at Week 24. (NCT02732119)
Timeframe: Baseline up to 24 weeks and at week 24

Intervention	percentage of participants (Number)
	Overall response rate (CR+PR):	CBR - CR+PR+SD (NCRNPD) by 24 weeks	CBR - CR+PR+SD (NCRNPD) at 24 weeks	Disease control rate (CR+PR+SD(NCRNPD)
Cohort B	10.0	80.0	0.0	80.0
Cohort C	28.6	100.0	28.6	100

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Clinical Benefit Rate as Per Central Review by Dose Cohort - Phase I

Intervention	percentage of participants (Number)
	CBR - CR+PR+SD (NCRNPD) by 24 weeks	CBR - CR+PR+SD (NCRNPD) at 24 weeks	Disease control rate (CR+PR+SD(NCRNPD)
Cohort A	62.5	0	62.5

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Best Overall Responses (BOR) Summary Table as Per Central Review by Group - Phase II

Complete response (CR) or partial response (PR), or stable disease (SD) at 24 weeks as per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 or Non-CR Non-PD (NCRNPD) at Week 24. (NCT02732119)
Timeframe: Baseline up to 24 weeks and at 24 weeks

Intervention	Participants (Count of Participants)
	Participants with measurable disease at baseline	Participants with non-measurable disease at baseline	Complete response (CR)	Partial Response (PR)	Stable disease (SD)	Progressive disease (PD)	NCRNPD - Non-complete response non-progressive disease	Unknown
Group 1	35	11	0	3	17	14	10	2
Group 2	21	11	0	3	6	12	10	1

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Time to Definitive Deterioration of ECOG Performance Status in One Category of the Score by Group - Phase II

Time to definitive deterioration of ECOG performance status in one category of score is defined as the time from the date of randomization to the date of event, which is defined as at least one score lower than the baseline. (NCT02732119)
Timeframe: Baseline up to approximately 8 months

Intervention	median (Number)
Group 1	NA
Group 2	12.0

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Summary of Progression-free Survival (PFS) (Months), as Per Central Review by Group - Phase II

Progression is defined as <= 12 weeks after randomization/ start of treatment (and not qualifying for CR, PR or SD). (NCT02732119)
Timeframe: Baseline up to approximately 32 months

Intervention	months (Median)
Group 1	8.0
Group 2	4.7

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Overall Survival (OS) by Group - Phase II

Overall survival is the time from date of first treatment to the date of death due to any cause. If a patient is not known to have died, survival will be censored at the last date of contact. (NCT02732119)
Timeframe: Baseline up to approximately 32 months

Intervention	months (Median)
Group 1	27.4
Group 2	NA

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Best Overall Responses (BOR) Summary Table as Per Central Review by Cohort - Phase I

Complete response (CR) or partial response (PR), or stable disease (SD)as per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 or Non-CR Non-PD (NCRNPD) (NCT02732119)
Timeframe: From baseline up to 24 weeks

Intervention	Participants (Count of Participants)
	Participants with measurable disease at baseline	Participants with non-measurable disease at baseline	Complete response (CR)	Partial Response (PR)	Stable disease (SD)	Progressive disease (PD)	NCRNPD - Non-complete response non-progressive disease	Unknown
Cohort A	5	3	0	0	3	3	2	0
Cohort B	7	3	0	1	6	0	1	2
Cohort C	4	3	0	2	2	0	3	0

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Amount of Treg Cells Observed in Peripheral Blood in Patients With and Without Rejection

flow cytometry immunophenotyping and gene expression microassays to assess amount of Treg cells and mRNA in peripheral blood in patients with and without rejection (after Tacc withdrwal) (NCT02736227)
Timeframe: Six months post transplantation

Intervention	percentage of CD4 positive cell (Mean)
Graft Rejection After Tacrolimus Was Discontinued (REJ)	10
No Graft Rejection After Tacrolimus Weaning (Non REJ)	5

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Progression-free Survival (PFS) by Independent Imaging Review (IIR)

PFS assessed by IIR was defined as the time from the date of randomization to the date of the first documentation of progressive disease (PD) or death (whichever occurred first) using Response Evaluation Criteria in Solid Tumors (RECIST 1.1). PD was defined as at least a 20 percent (%) increase or 5 millimeter (mm) increase in the sum of diameters of target lesions (taking as reference the smallest sum on study) recorded since the treatment started or the appearance of 1 or more new lesions. PFS was analyzed using Kaplan-Meier method. (NCT02811861)
Timeframe: From the date of randomization to the date of the first documentation of PD or date of death, whichever occurred first or up to data cutoff date 28 Aug 2020 (up to approximately 46 months)

Intervention	months (Median)
Lenvatinib 18 mg Plus Everolimus 5 mg	14.7
Lenvatinib 20 mg Plus Pembrolizumab 200 mg	23.9
Sunitinib 50 mg	9.2

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Measured Glomerular Filtration Rate (mGFR)

Renal function as assessed by measured Glomerular Filtration Rate (mGFR) (Cr-EDTA or iohexol clearance). Baseline Visit 1 and Patient 4252 excluded from the intent treat analysis set. (NCT02864706)
Timeframe: at the 5-7 year follow-up visit

Intervention	mL/min/1.73m2 (Least Squares Mean)
Everolimus	74.7
Control	62.4

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Progression of Cardiac Allograft Vasculopathy (CAV) Recorded by Intravascular Ultrasound (IVUS)

"Cardiac Allograft Vasculopathy (CAV) was defined as mean maximal intimal thickness (MIT)~≥0.5 mm, measured for the entire matched pullback recording by intravascular ultrasound (IVUS). The incidence of CAV at 5-7 years was compared between groups using the Cochran-Mantel-Haenszel test with stratification according to baseline distribution of CAV incidence." (NCT02864706)
Timeframe: within 5-7 years

Intervention	mm (Mean)
Everolimus	0.13
Control	0.23

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Change From Baseline in Visual Analog Scale (VAS)

"Change in visual analog scale (VAS) from baseline to the 5 to 7 Year follow up visit.~0 is no pain; and 10 is the worst possible pain" (NCT02864706)
Timeframe: baseline, at the 5-7 year visit

Intervention	mm (Mean)
Everolimus	35.6
Control	34.0

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Change From Baseline in the Euro Quality of Life 5D

"Change from baseline in Euro Quality of Life-5D from 3 Year Follow-Up to 5 to 7 Year Follow-Up Baseline Visit 1 (ITT Set)~Euro Quality of Life 5D (EQ-5D): is a descriptive system of healthrelated quality of life states consisting of five dimensions (mobility, self-care, usual activities, pain/discomfort and anxiety/depression) each of which can be assessed as one of three levels of severity (no problems/some or moderate problems/extreme problems). A Visual Analogue Scale (VAS)-scale is also included in the EQ-5D questionnaire.~The EQ-5D index is calculated based on the United Kingdom Time Trade-Off (TTO) N3 value set which converts the five dimensions scores into a single measure with a possible range from -0.163 (worst possible health state) to +1 (perfect health). A positive change from baseline indicates an improvement in Quality of Life." (NCT02864706)
Timeframe: Baseline, 5-7 year visit

Intervention	scores on the scale (Mean)
Everolimus	0.2323
Control	0.2982

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Number of Participants With Beck Depression Inventory (BDI)

Beck Depression Inventory (BDI) Score has the following categories of depression. Normal, Mild, Moderate Severe and Missing. (NCT02864706)
Timeframe: at the 5-7 year visit

Intervention	Participants (Count of Participants)
	Normal	Mild	Moderate	Severe	Missing
Control	13	4	5	0	5
Everolimus	15	6	2	1	3

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Quality of Life by SF-36 Change From Pre-transplantation to 5-7 Year Follow-up

This Quality of life Short Form Survey with 36 items (Minnesota Living with Heart Failure Questionnaire)was administered to patients pre-transplantation and after transplantation at the 5-7 year visit. This data represents the change. The survey consist of scores on a scale. Each form is scaled from 0 t 100. 0 = maximum disability and 100 equals no disability. (NCT02864706)
Timeframe: at the 5-7 year visit

Intervention	scores on a scale (Mean)
	Physical Health Summary	Mental Health Summary	Physical Functioning	Role Physical	Bodily Pain	General Health	Vitality	Social Functioning	Role Emotional	Mental Health
Control	13.2	15.3	40.8	55.1	7.2	23.4	28.9	43.9	42.8	14.4
Everolimus	16.8	10.4	36.7	50.2	10.3	25.7	30.0	39.9	23.8	8.6

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Percent of Participants With Incidence of Coronary Allograft Vasculopathy (CAV)

Intervention	percent of participants (Number)
Everolimus	53
Control	74

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Myocardial Structure and Function

Myocardial structure and function by echocardiography assessment measured by ventricular end systolic diameter. (NCT02864706)
Timeframe: within 5-7 years

Intervention	cm (Mean)
	LVESD (left ventricular end systolic diameter)	LVEDD (left ventricular end diastolic diameter)
Control	3.1	4.9
Everolimus	3.1	4.7

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Duration of Response (DOR) [Phase 2a]

Response will be assessed among participants eligible for the phase IIa part of the study who received at least one dose of the study drugs at the MTD/RP2D and have measurable disease at screening. DOR defined based on the duration of stable disease. (NCT02871791)
Timeframe: Disease evaluations were performed every 8 weeks (within 24 weeks of initiation of study treatment) or every 12 weeks (greater than 24 weeks of initiation of study treatment). Treatment duration has a median of 111 days and maximum of 681 days.

Intervention	months (Median)
Palbociclib, Everolimus, Exemestane	4.24

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Median Progression Free Survival (PFS) [Phase 2a]

Progression-free survival based on the Kaplan-Meier method is defined as the duration of time from study entry to documented disease progression (PD) or death. Per RECIST 1.1 criteria: progressive disease (PD) is at least a 20% increase in the sum of longest diameter (LD) of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. PD for the evaluation of non-target lesions is the appearance of one or more new lesions and/or unequivocal progression of non-target lesions. (NCT02871791)
Timeframe: Disease is evaluated and followed-up every 8 weeks, with median of 20.04 months and maximum of 35.64 months.

Intervention	months (Median)
Palbociclib, Everolimus, Exemestane	3.8

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Overall Response Rate (ORR) [Phase 2a]

The objective response rate (ORR) was defined as the proportion of participants achieving complete response (CR) or partial response (PR) based on RECIST 1.1 criteria on treatment. (NCT02871791)
Timeframe: Disease evaluations were performed every 8 weeks (within 24 weeks of initiation of study treatment) or every 12 weeks (greater than 24 weeks of initiation of study treatment). Treatment duration has a median of 111 days and maximum of 681 days.

Intervention	Participants (Count of Participants)
Palbociclib, Everolimus, Exemestane	0

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Clinical Benefit Rate (CBR) [Phase 2a]

CBR is defined as the proportion of participants achieving complete response, partial response or stable disease for more than 6 months (CR+PR+SD ≥ 24 weeks) taking as reference the smallest measurements recorded since the treatment started, including the baseline measurements. (NCT02871791)
Timeframe: Disease evaluations were performed every 8 weeks (within 24 weeks of initiation of study treatment) or every 12 weeks (greater than 24 weeks of initiation of study treatment). Treatment duration has a median of 111 days and maximum of 681 days.

Intervention	Participants (Count of Participants)
Palbociclib, Everolimus, Exemestane	6

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Disease Control Rate (DCR) [Phase 2a]

The DCR defined as the proportion of patient that has CR+PR+SD>=12 weeks. Response will be assessed among participants eligible for the phase IIa part of the study who received at least one dose of the study drugs at the MTD/RP2D and have measurable disease at screening. (NCT02871791)
Timeframe: Disease evaluations were performed every 8 weeks (within 24 weeks of initiation of study treatment) or every 12 weeks (greater than 24 weeks of initiation of study treatment). Treatment duration has a median of 111 days and maximum of 681 days.

Intervention	proportion of patients (Number)
Palbociclib, Everolimus, Exemestane	0.563

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Overall Survival (OS)

OS was defined as the time from the date of the first dose of study drug until the date of death from any cause. OS was analyzed using Kaplan Meier method. In the absence of death before data cutoff, participants were censored either at the date last known to be alive or the date of data cutoff, whichever came earlier. Participants were followed for survival every 12 weeks after the end of treatment visit. If a clinic visit was not feasible, follow-up information was obtained via telephone or email. (NCT02915783)
Timeframe: From the date of the first dose of study drug until the date of death from any cause (up to approximately 4 years 8 months)

Intervention	months (Median)
Lenvatinib 18 mg/Day + Everolimus 5 mg/Day	16.33

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Objective Response Rate (ORR)

ORR was assessed by the investigator based on Response Evaluation Criteria in Solid Tumors (RECIST) version (v) 1.1. ORR was defined as the percentage of participants with confirmed best overall response (BOR) of complete response (CR) or partial response (PR). CR was defined as the disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis to less than (<) 10 millimeters (mm). PR was defined as at least a 30 percent (%) decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. (NCT02915783)
Timeframe: From the date of the first dose of study drug to the date of the first documentation of disease progression or death, whichever occurred first (up to approximately 3 years 9 months)

Intervention	percentage of participants (Number)
Lenvatinib 18 mg/Day + Everolimus 5 mg/Day	25.8

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Progression-free Survival (PFS)

PFS was assessed by investigator per RECIST v1.1, defined as time from date of first dose of study drug to date of first documentation of progressive disease (PD) or death whichever occurred first. PD: greater than or equal to (>=) 20% increase in sum of diameters of target lesions, reference-smallest sum recorded in study (sum at baseline if that was smallest). Sum of diameters must have absolute increase of >=5 mm. Appearance of >=1 new lesions also considered PD. PFS was analyzed using Kaplan Meier method. PFS was censored on date of last adequate radiologic assessment prior to new anticancer therapy, more than one missed visits, treatment discontinuation, and cutoff date when no PD or death occurred before any of these (on first dose of study treatment if no adequate post baseline tumor assessment was available), per publication by Food and Drug Administration (FDA) 'Guidance for Industry Clinical Trial Endpoints for the Approval of Cancer Drugs and Biologics (2007). (NCT02915783)
Timeframe: From the date of the first dose of study drug to the date of the first documentation of disease progression or death, whichever occurred first (up to approximately 3 years 9 months)

Intervention	months (Median)
Lenvatinib 18 mg/Day + Everolimus 5 mg/Day	13.11

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Percent of Participants Experiencing Acute Allograft Rejection

Estimate the composite of treatment failure rate, defined as acute allograft rejection with a Banff grade 1A or higher, graft loss, or death at six months post-conversion, in patients converted to a once-daily immunosuppressant regimen of Envarsus®, everolimus, and prednisone versus patients converted to a twice-daily regimen of Envarsus®, MMF, and prednisone. (NCT02954198)
Timeframe: Baseline to 6 months post conversion

Intervention	Participants (Count of Participants)
Control: Envarsus + MMF	0
Intervention: Envarsus + Everoliumus	0

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Subject Specific Change on Medication Side Effect Scale

Examine subject specific change on a validated Medication Side Effect Scale at the time of the conversion versus six months post-conversion, compared between the two arms. Side effect burden scale is from 0 to 180. A lower score is less side effect burden, a higher score is more side effect burden. (NCT02954198)
Timeframe: Baseline to 6 months post conversion

Intervention	units on a scale (Mean)
	Baseline	6 month post-conversion
Control: Envarsus + MMF	71	93
Intervention: Envarsus + Everoliumus	37	38

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Self-reported Medication Adherence From Baseline to 6 Months.

Percent of subjects reporting high medication adherence at baseline compared to 6 months post-conversion, using the Morisky Medication Adherence scale (MMAS). The MMAS rates medication adherence on a scale of 0 to 8. 0 is high adherence, 1-2 is medium adherence, and greater than or equal to 3 is low adherence. (NCT02954198)
Timeframe: 6 months post conversion

Intervention	% of participants (Number)
	Baseline	6 months post-conversion
Control: Envarsus + MMF	80	59
Intervention: Envarsus + Everoliumus	45	47

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Percent of Participants Who Experienced Kidney Transplant Graft Loss

Measure and compare time-to-event analysis between the two arms graft loss (time to event analysis) (NCT02954198)
Timeframe: Baseline to 6 months post conversion

Intervention	Participants (Count of Participants)
Control: Envarsus + MMF	0
Intervention: Envarsus + Everoliumus	0

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Percentage of Participants With a ≥ 50% Reduction in Daily Corticosteroid Dose

All corticosteroid dosages prescribed to the participant and all dose changes during the study were to be recorded for assessment of participants with a ≥ 50% reduction in daily corticosteroid dose. (NCT03112603)
Timeframe: from Day 15 up to Day 182

Intervention	percentage of participants (Number)
	Day 15 to ≤ Day 28	Day 29 to ≤ Day 42	Day 43 to ≤ Day 56	Day 57 to ≤ Day 70	Day 71 to ≤ Day 84	Day 85 to ≤ Day 98	Day 99 to ≤ Day 112	Day 113 to ≤ Day 126	Day 127 to ≤ Day 140	Day 141 to ≤ Day 154	Day 155 to ≤ Day 168	Day 169 to ≤ Day 182
Best Available Therapy	13.2	33.1	41.1	47.9	51.4	54.0	60.4	66.2	68.3	68.3	71.6	88.8
Ruxolitinib	12.7	35.0	48.4	58.7	62.3	69.5	71.2	73.2	72.8	70.0	74.6	81.9

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t1/2 of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"t1/2 was defined as the apparent terminal phase disposition half-life of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Intervention	hours (Geometric Mean)
	Day 1	Day 15
Ruxolitinib	2.40	2.32

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Tmax of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"tmax was defined as the time to reach the maximum plasma concentration of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Intervention	hours (Median)
	Day 1	Day 15
Ruxolitinib	0.833	1.00

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Vz/F of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"Vz/F was defined as the apparent oral dose volume of distribution of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Intervention	Liters (Geometric Mean)
	Day 1	Day 15
Ruxolitinib	54.0	50.9

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Rate of Failure-free Survival (FFS)

Composite time to event endpoint incorporating the following FFS events: (i) relapse or recurrence of underlying disease or death due to underlying disease, (ii) nonrelapse mortality, or (iii) addition or initiation of another systemic therapy for cGvHD. (NCT03112603)
Timeframe: Baseline to when the last participant reached Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Intervention	months (Median)
Ruxolitinib	NA
Best Available Therapy	5.7

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CL/F of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"CL/F was defined as the oral dose clearance of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Intervention	Liters/hour (Geometric Mean)
	Day 1	Day 15
Ruxolitinib	15.6	15.2

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Cmax of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"Cmax was defined as the maximum observed plasma concentration of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Intervention	nanograms per milliliter (ng/mL) (Geometric Mean)
	Day 1	Day 15
Ruxolitinib	167	215

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Change From Baseline in Functional Assessment of Cancer Therapy - Bone Marrow Transplantation (FACT-BMT)

"Change from Baseline was calculated as the post-Baseline value minus the Baseline value. The FACT-BMT is a 50-item self-report questionnaire that measures the effect of a therapy on domains including physical, functional, social/family, and emotional well-being, together with additional concerns relevant for bone marrow transplantation participants. The questions were based on a 5-point Likert scale, where 0 corresponds to not at all and 4 corresponds to very much. The higher the final score, the better the quality of life. The FACT-BMT total score ranges from 0 to 148." (NCT03112603)
Timeframe: Baseline; up to Cycle 39 Day 1 (each cycle was comprised of 4 weeks)

Intervention	scores on a scale (Mean)
	Cycle 2 Day 1	Cycle 3 Day 1	Cycle 4 Day 1	Cycle 5 Day 1	Cycle 6 Day 1	Cycle 7 Day 1	Cycle 9 Day 1	Cycle 12 Day 1	Cycle 15 Day 1	Cycle 18 Day 1	Cycle 21 Day 1	Cycle 24 Day 1	Cycle 27 Day 1	Cycle 30 Day 1	Cycle 33 Day 1	Cycle 36 Day 1	Cycle 39 Day 1
Best Available Therapy	-0.22	-1.82	-1.05	-0.23	2.41	0.85	1.20	3.74	7.58	8.19	3.68	7.84	5.10	5.75	5.67	4.77	6.64
Ruxolitinib	2.32	0.62	1.98	1.25	2.91	4.14	5.32	7.26	5.07	4.10	5.24	5.90	6.23	7.53	5.17	8.72	8.65

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Change From Baseline in EQ-5D-5L

The EQ-5D-5L is a descriptive classification consisting of five dimensions of health: mobility, self-care, usual activities, anxiety/depression, and pain/discomfort. The five-level version (no problems, slight problems, moderate problems, severe problems, and extreme problems) uses a 5-point Likert scale, with 1 being no problems and 5 being extreme problems. (NCT03112603)
Timeframe: Baseline; up to Cycle 39 Day 1 (each cycle was comprised of 4 weeks)

Intervention	scores on a scale (Mean)
	Cycle 2 Day 1	Cycle 3 Day 1	Cycle 4 Day 1	Cycle 5 Day 1	Cycle 6 Day 1	Cycle 7 Day 1	Cycle 9 Day 1	Cycle 12 Day 1	Cycle 15 Day 1	Cycle 18 Day 1	Cycle 21 Day 1	Cycle 24 Day 1	Cycle 27 Day 1	Cycle 30 Day 1	Cycle 33 Day 1	Cycle 36 Day 1	Cycle 39 Day 1
Best Available Therapy	-0.01	-0.04	-0.01	-0.03	0.01	-0.00	-0.02	0.02	0.03	0.02	-0.00	0.01	0.03	0.01	0.05	0.04	0.01
Ruxolitinib	0.03	0.03	0.04	0.02	0.05	0.07	0.07	0.07	0.07	0.07	0.08	0.07	0.06	0.05	0.00	0.06	0.06

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AUClast of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"AUClast was defined as the area under the concentration-time curve up to the last measurable concentration of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Intervention	ng*hour/mL (Geometric Mean)
	Day 1	Day 15
Ruxolitinib	636	945

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Best Overall Response (BOR) at Cycle 7 Day 1

BOR was defined as the percentage of participants who achieved an overall response (CR+PR) based on cGvHD disease assessments (National Institutes of Health Consensus Criteria) without the requirement of additional systemic therapies for an earlier progression, mixed response, or non-response at any time point (up to Cycle 7 Day 1 or the start of additional systemic therapy for cGvHD). Scoring of response was relative to the organ score at the time of randomization. CR: complete resolution of all signs and symptoms of cGVHD in all evaluable organs without the initiation or addition of new systemic therapy. PR: improvement in at least one organ (e.g., improvement of 1 or more points on a 4- to 7-point scale, or an improvement of 2 or more points on a 10- to 12-point scale) without progression in other organs or sites, initiation, or addition of new systemic therapies. This analysis was based on the primary cutoff date (May 2020). (NCT03112603)
Timeframe: up to Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Intervention	percentage of participants (Number)
Ruxolitinib	76.4
Best Available Therapy	60.4

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BOR During Cross-over Treatment With Ruxolitinib

BOR was defined as the percentage of participants who achieved an overall response (CR+PR) based on cGvHD disease assessments (National Institutes of Health Consensus Criteria) without the requirement of additional systemic therapies for an earlier progression, mixed response, or non-response at any time point (up to Cycle 7 Day 1 or the start of additional systemic therapy for cGvHD). Scoring of response was relative to the organ score at the time of randomization. CR: complete resolution of all signs and symptoms of cGVHD in all evaluable organs without the initiation or addition of new systemic therapy. PR: improvement in at least one organ (e.g., improvement of 1 or more points on a 4- to 7-point scale, or an improvement of 2 or more points on a 10- to 12-point scale) without progression in other organs or sites, initiation, or addition of new systemic therapies. (NCT03112603)
Timeframe: from Crossover Cycle 1 Day 1 to any time point up to and including Crossover Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Intervention	percentage of participants (Number)
Ruxolitinib Cross-Over Period	81.4

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Duration of Response Through Study Completion

DOR was defined as the time from first response until cGvHD progression, death, or the date of change/addition of systemic therapies for cGvHD and as assessed for responders only. Response was based on cGvHD disease assessments (National Institutes of Health consensus criteria). Duration of response was evaluated in participants who achieved a CR or PR at or before Cycle 7 Day 1. The analysis included a larger number of participants than the number of participants who achieved CR or PR at Cycle 7 Day 1 (82 ruxolitinib and 42 BAT) because the analysis took into account not only those participants who achieved CR or PR at Cycle 7 Day 1, but also participants who achieved CR or PR before Cycle 7 Day 1 but who may have lost their response at Cycle 7 Day 1. For this reason, the number of participants in this analysis does not align with the best overall response (BOR) at Cycle 7 Day 1. This analysis was based on the cutoff date upon study completion (December 2022). (NCT03112603)
Timeframe: from first response to LPLV (approximately 5 years)

Intervention	Months (Median)
Ruxolitinib	NA
Best Available Therapy	6.4

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Efficacy of Ruxolitinib Versus Investigator's Choice Best Available Therapy (BAT) in Participants With Moderate or Severe Steroid Refractory Chronic Graft Versus Host Disease (SR-cGvHD) Assessed by Overall Response Rate (ORR) at the Cycle 7 Day 1 Visit

ORR was defined as the percentage of participants in each arm demonstrating a complete response (CR) or partial response (PR) based on chronic GvHD (cGvHD) disease assessments (National Institutes of Health Consensus Criteria) without the requirement of additional systemic therapies for an earlier progression, mixed response, or non-response. Scoring of response was relative to the organ score at the time of randomization. CR: complete resolution of all signs and symptoms of cGVHD in all evaluable organs without the initiation or addition of new systemic therapy. PR: improvement in at least one organ (e.g., improvement of 1 or more points on a 4- to 7-point scale, or an improvement of 2 or more points on a 10- to 12-point scale) without progression in other organs or sites, initiation, or addition of new systemic therapies. (NCT03112603)
Timeframe: Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Intervention	percentage of participants (Number)
Ruxolitinib	49.7
Best Available Therapy	25.6

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Number of Participants With Any Treatment-emergent Adverse Event (TEAE)

Adverse events were defined as the appearance of (or worsening of any pre-existing) undesirable signs, symptoms, or medical conditions that occurred after the participant's signed informed consent was obtained. Abnormal laboratory values or test results occurring after informed consent constituted adverse events only if they induced clinical signs or symptoms, were considered clinically significant, required therapy (e.g., hematologic abnormality that required transfusion or hematological stem cell support), or required changes in study medication(s). TEAEs were defined as those AEs that started or worsened during the on-treatment period (either randomized or cross-over period). (NCT03112603)
Timeframe: from Baseline to LPLV (approximately 5 years)

Intervention	Participants (Count of Participants)
Ruxolitinib	165
Best Available Therapy	148
Ruxolitinib Cross-Over Period	70

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AUCinf of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"AUCinf was defined as the area under the concentration-time curve from time 0 to infinity. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Intervention	ng*hour/mL (Geometric Mean)
	Day 1
Ruxolitinib	642

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Utilization of Medical Resources

The percentage of participants with at least one submission to healthcare encounter was assessed. (NCT03112603)
Timeframe: from Baseline to LPLV (approximately 5 years)

Intervention	percentage of participants (Number)
Ruxolitinib	57.0
Best Available Therapy	65.8

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Rate of Participants With Clinically Relevant Improvement of the Modified Lee cGvHD Symptom Scale Score

"To assess improvement of symptoms based on the total symptom score (TSS); a responder was defined as having achieved a clinically relevant reduction from Baseline of the TSS. The scale consists of 30 items in 7 subscales (skin, eye, mouth, lung, nutrition, energy, and psychological). Participants reported their level of symptom bother over the previous month on a 5-point likert scale: not at all, slightly, moderately, quite a bit, or extremely. Subscale scores and the summary score range from 0 to 100, with a higher score indicating worse symptoms." (NCT03112603)
Timeframe: Baseline; Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Intervention	percentage of participants (Number)
Ruxolitinib	24.2
Best Available Therapy	11.0

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ORR at the End of Cycle 3

ORR was defined as the percentage of participants in each arm demonstrating a CR or PR based on cGvHD disease assessments (National Institutes of Health Consensus Criteria) without the requirement of additional systemic therapies for an earlier progression, mixed response, or non-response. Scoring of response was relative to the organ score at the time of randomization. CR: complete resolution of all signs and symptoms of cGVHD in all evaluable organs without the initiation or addition of new systemic therapy. PR: improvement in at least one organ (e.g., improvement of 1 or more points on a 4- to 7-point scale, or an improvement of 2 or more points on a 10- to 12-point scale) without progression in other organs or sites, initiation, or addition of new systemic therapies. (NCT03112603)
Timeframe: Cycle 4 Day 1 (each cycle was comprised of 4 weeks)

Intervention	percentage of participants (Number)
Ruxolitinib	54.5
Best Available Therapy	31.1

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Rate of FFS at Study Completion

Composite time to event endpoint incorporating the following FFS events: (i) relapse or recurrence of underlying disease or death due to underlying disease, (ii) nonrelapse mortality, or (iii) addition or initiation of another systemic therapy for cGvHD. (NCT03112603)
Timeframe: From Baseline to Last Participant Last Visit (LPLV) (approximately 5 years)

Intervention	months (Median)
Ruxolitinib	38.4
Best Available Therapy	5.7

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Overall Survival (OS)

Overall survival was defined as the time from the date of randomization to the date of death due to any cause. (NCT03112603)
Timeframe: from the date of randomization to the date of death due to any cause up to LPLV (approximately 5 years)

Intervention	months (Median)
Ruxolitinib	NA
Best Available Therapy	NA

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Cumulative Incidence of Malignancy Relapse/Recurrence (MR)

Defined as the cumulative incidence rate from competing risk analysis of MR from the date of randomization to hematologic malignancy relapse/recurrence. (NCT03112603)
Timeframe: Months 3, 6, 12, 18, 24, 30, and 36

Intervention	percentage of participants (Number)
	0 to < 3 months	3 to < 6 months	6 to < 12 months	12 to < 18 months	18 to < 24 months	24 to <30 months	30 to <36 months
Best Available Therapy	1.31	2.65	6.08	6.08	6.08	6.78	7.50
Ruxolitinib	1.92	3.22	5.18	7.82	8.48	8.48	8.48

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Cumulative Incidence of Non-relapse Mortality (NRM)

Defined as the cumulative incidence rate from competing risk analysis for NRM from the date of randomization to the date of death not preceded by underlying disease relapse/recurrence. (NCT03112603)
Timeframe: Months 3, 6, 12, 18, 24, 30, and 36

Intervention	percentage of participants (Number)
	Month 3	Month 6	Month 12	Month 18	Month 24	Month 30	Month 36
Best Available Therapy	4.44	6.43	15.12	16.48	19.22	19.22	22.0
Ruxolitinib	5.45	9.13	15.30	15.93	17.83	17.83	17.83

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Percentage of Participants Successfully Tapered Off of All Corticosteroids

All corticosteroid dosages prescribed to the participant and all dose changes during the study were to be recorded for assessment of participants who successfully tapered off of all corticosteroids. Participants who completely tapered off corticosteroids refer to those who permanently discontinued steroids as per the dose administration panel and who did not restart steroids in the same interval. Participants who were tapered off and continued follow-up were also counted as being tapered off with 0 dose in subsequent intervals until they discontinued from the main treatment period or restarted steroid treatment. (NCT03112603)
Timeframe: up to Day 179

Intervention	percentage of participants (Number)
	Day 1 to ≤ Day 28	Day 29 to ≤ Day 56	Day 57 to ≤ Day 84	Day 85 to ≤ Day 112	Day 113 to ≤ Day 140	Day 141 to ≤ Day 168	Day 169 to ≤ Day 179
Best Available Therapy	2.6	5.4	8.5	10.3	12.4	16.8	15.9
Ruxolitinib	2.5	9.6	14.0	16.3	19.7	24.2	24.1

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Overall Survival (OS)

Overall survival is defined as the time from randomization to the date of death from any cause. Participants with no documentation of death on-study were censored at the date at which they were last known to be alive. (NCT03163667)
Timeframe: As of the data cutoff date of 30 Sep 2020; maximum duration of follow-up for OS was 30.4 months.

Intervention	months (Median)
Placebo + Everolimus	9.72
CB-839 + Everolimus	14.37

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Progression Free Survival (PFS)

"PFS was defined as the time from randomization to the date of documented disease progression (assessed by Investigator per Response Evaluation Criteria in Solid Tumors [RECIST] v1.1) within 2 scheduled scan intervals following previous evaluable radiologic tumor assessment or death for any cause, whichever occurred first. Participants with no documentation of disease progression or death on-study were censored at the date of last available tumor assessment.~Progressive Disease (PD) per RECIST 1.1: At least a 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum on study. In addition, the sum must also demonstrate an absolute increase of at least 5 mm." (NCT03163667)
Timeframe: As of the primary data cutoff date of 26 Apr 2019; maximum duration of follow-up for PFS was 11.2 months.

Intervention	months (Median)
Placebo + Everolimus	1.91
CB-839 + Everolimus	3.81

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Health-Related Quality of Life (HRQoL) Assessed by Functional Assessment of Cancer Therapy Kidney Syndrome Index-Disease-Related Symptoms (FKSI-DRS) Scores

The FKSI-DRS consisted of 9 items that experts and participants had indicated are important targets for the treatment of advanced kidney cancer, and that clinical experts had indicated are primarily disease-related, as opposed to treatment-related. Symptoms assessed on the FKSI-DRS included lack of energy, fatigue, weight loss, pain, bone pain, shortness of breath, cough, fever, or hematuria. Each item was scored on a 5-point Likert-type scale (0 = not at all; 4 = very much) where total score ranged from 0 (worst) to 36 (best), where higher scores correspond to better outcomes. (NCT03173560)
Timeframe: At baseline (prior to first dose of study drug), on Day 1 of each subsequent cycle (cycle length =28 days), and at the Off-treatment visit (up to 29 months)

Intervention	score on a scale (Mean)
	Baseline	Cycle 2 Day 1	Cycle 3 Day 1	Cycle 4 Day 1	Cycle 5 Day 1	Cycle 6 Day 1	Cycle 7 Day 1	Cycle 8 Day 1	Cycle 9 Day 1	Cycle 10 Day 1	Cycle 11 Day 1	Cycle 12 Day 1	Cycle 13 Day 1	Cycle 14 Day 1	Cycle 15 Day 1	Cycle 16 Day 1	Cycle 17 Day 1	Cycle 18 Day 1	Cycle 19 Day 1	Cycle 20 Day 1	Cycle 21 Day 1	Cycle 22 Day 1	Cycle 23 Day 1	Cycle 24 Day 1	Cycle 25 Day 1	Cycle 26 Day 1	Cycle 27 Day 1	Cycle 28 Day 1	Cycle 29 Day 1	Cycle 30 Day 1	Off-treatment Visit
Lenvatinib 18 mg + Everolimus 5 mg	29	28.31	28.80	29.11	29.14	29.46	29.58	29.85	29.84	30.70	30.09	30.75	30.93	31.06	30.52	30.91	31.52	31.41	30.82	30.69	32	30.59	30.29	31.58	31.69	29.82	32.86	33.67	33.40	36	27.86

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Health-Related Quality of Life (HRQoL) Assessed by Functional Assessment of Cancer Therapy Kidney Syndrome Index-Disease-Related Symptoms (FKSI-DRS) Scores

Intervention	score on a scale (Mean)
	Baseline	Cycle 2 Day 1	Cycle 3 Day 1	Cycle 4 Day 1	Cycle 5 Day 1	Cycle 6 Day 1	Cycle 7 Day 1	Cycle 8 Day 1	Cycle 9 Day 1	Cycle 10 Day 1	Cycle 11 Day 1	Cycle 12 Day 1	Cycle 13 Day 1	Cycle 14 Day 1	Cycle 15 Day 1	Cycle 16 Day 1	Cycle 17 Day 1	Cycle 18 Day 1	Cycle 19 Day 1	Cycle 20 Day 1	Cycle 21 Day 1	Cycle 22 Day 1	Cycle 23 Day 1	Cycle 24 Day 1	Cycle 25 Day 1	Cycle 26 Day 1	Cycle 27 Day 1	Cycle 28 Day 1	Cycle 29 Day 1	Cycle 30 Day 1	Cycle 31 Day 1	Off-treatment Visit
Lenvatinib 14 mg + Everolimus 5 mg	29.69	28.43	28.26	27.97	28	28.63	28.31	28.36	28.58	29.10	29.56	29.34	29.26	29.81	30.09	29.93	29.36	29.81	28.48	28.77	29.35	30.32	30.53	29.47	27.92	28.75	29.83	30.50	29.50	30.75	31	27.42

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HRQoL Assessed by European Organization for the Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-C30 Scores

The EORT QLQ-C30 consisted of 30 questions comprising 9 multiple-item scales and 6 single items. Multiple-item scales of QLQ-C30 consisted of 5 functional scales (physical, role, emotional, cognitive, and social) and 3 symptom scales (fatigue, nausea and vomiting, pain) and a global health status/QOL score. Six single-item scales of QLQ-C30 involved dyspnea, insomnia, appetite loss, constipation, diarrhea and financial difficulties. First 28 questions used a 4-point scale (1 = Not at all to 4 = Very much); and last 2 questions used a 7-point scale (1 = Very poor to 7 = Excellent). Scores for all scales range from 0 to 100. For the overall HRQoL and functioning scales, a higher score was correlated with better HRQoL, whereas a higher score for symptom scales represented worse HRQoL. (NCT03173560)
Timeframe: At baseline (prior to first dose of study drug), on Day 1 of each subsequent cycle (cycle length =28 days), and at the Off-treatment visit (up to 29 months)

Intervention	score on a scale (Mean)
	Global Health Status/QoL Score; Baseline	Global Health Status/QoL Score; Cycle 2 Day 1	Global Health Status/QoL Score; Cycle 3 Day 1	Global Health Status/QoL Score; Cycle 4 Day 1	Global Health Status/QoL Score; Cycle 5 Day 1	Global Health Status/QoL Score; Cycle 6 Day 1	Global Health Status/QoL Score; Cycle 7 Day 1	Global Health Status/QoL Score; Cycle 8 Day 1	Global Health Status/QoL Score; Cycle 9 Day 1	Global Health Status/QoL Score; Cycle 10 Day 1	Global Health Status/QoL Score; Cycle 11 Day 1	Global Health Status/QoL Score; Cycle 12 Day 1	Global Health Status/QoL Score; Cycle 13 Day 1	Global Health Status/QoL Score; Cycle 14 Day 1	Global Health Status/QoL Score; Cycle 15 Day 1	Global Health Status/QoL Score; Cycle 16 Day 1	Global Health Status/QoL Score; Cycle 17 Day 1	Global Health Status/QoL Score; Cycle 18 Day 1	Global Health Status/QoL Score; Cycle 19 Day 1	Global Health Status/QoL Score; Cycle 20 Day 1	Global Health Status/QoL Score; Cycle 21 Day 1	Global Health Status/QoL Score; Cycle 22 Day 1	Global Health Status/QoL Score; Cycle 23 Day 1	Global Health Status/QoL Score; Cycle 24 Day 1	Global Health Status/QoL Score; Cycle 25 Day 1	Global Health Status/QoL Score; Cycle 26 Day 1	Global Health Status/QoL Score; Cycle 27 Day 1	Global Health Status/QoL Score; Cycle 28 Day 1	Global Health Status/QoL Score; Cycle 29 Day 1	Global Health Status/QoL Score; Cycle 30 Day 1	Global Health Status/QoL Score; Off-treatment Visit	Physical Functioning Score; Baseline	Physical Functioning Score; Cycle 2 Day 1	Physical Functioning Score; Cycle 3 Day 1	Physical Functioning Score; Cycle 4 Day 1	Physical Functioning Score; Cycle 5 Day 1	Physical Functioning Score; Cycle 6 Day 1	Physical Functioning Score; Cycle 7 Day 1	Physical Functioning Score; Cycle 8 Day 1	Physical Functioning Score; Cycle 9 Day 1	Physical Functioning Score; Cycle 10 Day 1	Physical Functioning Score; Cycle 11 Day 1	Physical Functioning Score; Cycle 12 Day 1	Physical Functioning Score; Cycle 13 Day 1	Physical Functioning Score; Cycle 14 Day 1	Physical Functioning Score; Cycle 15 Day 1	Physical Functioning Score; Cycle 16 Day 1	Physical Functioning Score; Cycle 17 Day 1	Physical Functioning Score; Cycle 18 Day 1	Physical Functioning Score; Cycle 19 Day 1	Physical Functioning Score; Cycle 20 Day 1	Physical Functioning Score; Cycle 21 Day 1	Physical Functioning Score; Cycle 22 Day 1	Physical Functioning Score; Cycle 23 Day 1	Physical Functioning Score; Cycle 24 Day 1	Physical Functioning Score; Cycle 25 Day 1	Physical Functioning Score; Cycle 26 Day 1	Physical Functioning Score; Cycle 27 Day 1	Physical Functioning Score; Cycle 28 Day 1	Physical Functioning Score; Cycle 29 Day 1	Physical Functioning Score; Cycle 30 Day 1	Physical Functioning Score; Off-treatment Visit	Role Functioning Score; Baseline	Role Functioning Score; Cycle 2 Day 1	Role Functioning Score; Cycle 3 Day 1	Role Functioning Score; Cycle 4 Day 1	Role Functioning Score; Cycle 5 Day 1	Role Functioning Score; Cycle 6 Day 1	Role Functioning Score; Cycle 7 Day 1	Role Functioning Score; Cycle 8 Day 1	Role Functioning Score; Cycle 9 Day 1	Role Functioning Score; Cycle 10 Day 1	Role Functioning Score; Cycle 11 Day 1	Role Functioning Score; Cycle 12 Day 1	Role Functioning Score; Cycle 13 Day 1	Role Functioning Score; Cycle 14 Day 1	Role Functioning Score; Cycle 15 Day 1	Role Functioning Score; Cycle 16 Day 1	Role Functioning Score; Cycle 17 Day 1	Role Functioning Score; Cycle 18 Day 1	Role Functioning Score; Cycle 19 Day 1	Role Functioning Score; Cycle 20 Day 1	Role Functioning Score; Cycle 21 Day 1	Role Functioning Score; Cycle 22 Day 1	Role Functioning Score; Cycle 23 Day 1	Role Functioning Score; Cycle 24 Day 1	Role Functioning Score; Cycle 25 Day 1	Role Functioning Score; Cycle 26 Day 1	Role Functioning Score; Cycle 27 Day 1	Role Functioning Score; Cycle 28 Day 1	Role Functioning Score; Cycle 29 Day 1	Role Functioning Score; Cycle 30 Day 1	Role Functioning Score; Off-treatment Visit	Emotional Functioning Score; Baseline	Emotional Functioning Score; Cycle 2 Day 1	Emotional Functioning Score; Cycle 3 Day 1	Emotional Functioning Score; Cycle 4 Day 1	Emotional Functioning Score; Cycle 5 Day 1	Emotional Functioning Score; Cycle 6 Day 1	Emotional Functioning Score; Cycle 7 Day 1	Emotional Functioning Score; Cycle 8 Day 1	Emotional Functioning Score; Cycle 9 Day 1	Emotional Functioning Score; Cycle 10 Day 1	Emotional Functioning Score; Cycle 11 Day 1	Emotional Functioning Score; Cycle 12 Day 1	Emotional Functioning Score; Cycle 13 Day 1	Emotional Functioning Score; Cycle 14 Day 1	Emotional Functioning Score; Cycle 15 Day 1	Emotional Functioning Score; Cycle 16 Day 1	Emotional Functioning Score; Cycle 17 Day 1	Emotional Functioning Score; Cycle 18 Day 1	Emotional Functioning Score; Cycle 19 Day 1	Emotional Functioning Score; Cycle 20 Day 1	Emotional Functioning Score; Cycle 21 Day 1	Emotional Functioning Score; Cycle 22 Day 1	Emotional Functioning Score; Cycle 23 Day 1	Emotional Functioning Score; Cycle 24 Day 1	Emotional Functioning Score; Cycle 25 Day 1	Emotional Functioning Score; Cycle 26 Day 1	Emotional Functioning Score; Cycle 27 Day 1	Emotional Functioning Score; Cycle 28 Day 1	Emotional Functioning Score; Cycle 29 Day 1	Emotional Functioning Score; Cycle 30 Day 1	Emotional Functioning Score; Off-treatment Visit	Cognitive Functioning Score; Baseline	Cognitive Functioning Score; Cycle 2 Day 1	Cognitive Functioning Score; Cycle 3 Day 1	Cognitive Functioning Score; Cycle 4 Day 1	Cognitive Functioning Score; Cycle 5 Day 1	Cognitive Functioning Score; Cycle 6 Day 1	Cognitive Functioning Score; Cycle 7 Day 1	Cognitive Functioning Score; Cycle 8 Day 1	Cognitive Functioning Score; Cycle 9 Day 1	Cognitive Functioning Score; Cycle 10 Day 1	Cognitive Functioning Score; Cycle 11 Day 1	Cognitive Functioning Score; Cycle 12 Day 1	Cognitive Functioning Score; Cycle 13 Day 1	Cognitive Functioning Score; Cycle 14 Day 1	Cognitive Functioning Score; Cycle 15 Day 1	Cognitive Functioning Score; Cycle 16 Day 1	Cognitive Functioning Score; Cycle 17 Day 1	Cognitive Functioning Score; Cycle 18 Day 1	Cognitive Functioning Score; Cycle 19 Day 1	Cognitive Functioning Score; Cycle 20 Day 1	Cognitive Functioning Score; Cycle 21 Day 1	Cognitive Functioning Score; Cycle 22 Day 1	Cognitive Functioning Score; Cycle 23 Day 1	Cognitive Functioning Score; Cycle 24 Day 1	Cognitive Functioning Score; Cycle 25 Day 1	Cognitive Functioning Score; Cycle 26 Day 1	Cognitive Functioning Score; Cycle 27 Day 1	Cognitive Functioning Score; Cycle 28 Day 1	Cognitive Functioning Score; Cycle 29 Day 1	Cognitive Functioning Score; Cycle 30 Day 1	Cognitive Functioning Score; Off-treatment Visit	Social Functioning Score; Baseline	Social Functioning Score; Cycle 2 Day 1	Social Functioning Score; Cycle 3 Day 1	Social Functioning Score; Cycle 4 Day 1	Social Functioning Score; Cycle 5 Day 1	Social Functioning Score; Cycle 6 Day 1	Social Functioning Score; Cycle 7 Day 1	Social Functioning Score; Cycle 8 Day 1	Social Functioning Score; Cycle 9 Day 1	Social Functioning Score; Cycle 10 Day 1	Social Functioning Score; Cycle 11 Day 1	Social Functioning Score; Cycle 12 Day 1	Social Functioning Score; Cycle 13 Day 1	Social Functioning Score; Cycle 14 Day 1	Social Functioning Score; Cycle 15 Day 1	Social Functioning Score; Cycle 16 Day 1	Social Functioning Score; Cycle 17 Day 1	Social Functioning Score; Cycle 18 Day 1	Social Functioning Score; Cycle 19 Day 1	Social Functioning Score; Cycle 20 Day 1	Social Functioning Score; Cycle 21 Day 1	Social Functioning Score; Cycle 22 Day 1	Social Functioning Score; Cycle 23 Day 1	Social Functioning Score; Cycle 24 Day 1	Social Functioning Score; Cycle 25 Day 1	Social Functioning Score; Cycle 26 Day 1	Social Functioning Score; Cycle 27 Day 1	Social Functioning Score; Cycle 28 Day 1	Social Functioning Score; Cycle 29 Day 1	Social Functioning Score; Cycle 30 Day 1	Social Functioning Score; Off-treatment Visit	Fatigue Score; Baseline	Fatigue Score; Cycle 2 Day 1	Fatigue Score; Cycle 3 Day 1	Fatigue Score; Cycle 4 Day 1	Fatigue Score; Cycle 5 Day 1	Fatigue Score; Cycle 6 Day 1	Fatigue Score; Cycle 7 Day 1	Fatigue Score; Cycle 8 Day 1	Fatigue Score; Cycle 9 Day 1	Fatigue Score; Cycle 10 Day 1	Fatigue Score; Cycle 11 Day 1	Fatigue Score; Cycle 12 Day 1	Fatigue Score; Cycle 13 Day 1	Fatigue Score; Cycle 14 Day 1	Fatigue Score; Cycle 15 Day 1	Fatigue Score; Cycle 16 Day 1	Fatigue Score; Cycle 17 Day 1	Fatigue Score; Cycle 18 Day 1	Fatigue Score; Cycle 19 Day 1	Fatigue Score; Cycle 20 Day 1	Fatigue Score; Cycle 21 Day 1	Fatigue Score; Cycle 22 Day 1	Fatigue Score; Cycle 23 Day 1	Fatigue Score; Cycle 24 Day 1	Fatigue Score; Cycle 25 Day 1	Fatigue Score; Cycle 26 Day 1	Fatigue Score; Cycle 27 Day 1	Fatigue Score; Cycle 28 Day 1	Fatigue Score; Cycle 29 Day 1	Fatigue Score; Cycle 30 Day 1	Fatigue Score; Off-treatment Visit	Nausea and Vomiting Score; Baseline	Nausea and Vomiting Score; Cycle 2 Day 1	Nausea and Vomiting Score; Cycle 3 Day 1	Nausea and Vomiting Score; Cycle 4 Day 1	Nausea and Vomiting Score; Cycle 5 Day 1	Nausea and Vomiting Score; Cycle 6 Day 1	Nausea and Vomiting Score; Cycle 7 Day 1	Nausea and Vomiting Score; Cycle 8 Day 1	Nausea and Vomiting Score; Cycle 9 Day 1	Nausea and Vomiting Score; Cycle 10 Day 1	Nausea and Vomiting Score; Cycle 11 Day 1	Nausea and Vomiting Score; Cycle 12 Day 1	Nausea and Vomiting Score; Cycle 13 Day 1	Nausea and Vomiting Score; Cycle 14 Day 1	Nausea and Vomiting Score; Cycle 15 Day 1	Nausea and Vomiting Score; Cycle 16 Day 1	Nausea and Vomiting Score; Cycle 17 Day 1	Nausea and Vomiting Score; Cycle 18 Day 1	Nausea and Vomiting Score; Cycle 19 Day 1	Nausea and Vomiting Score; Cycle 20 Day 1	Nausea and Vomiting Score; Cycle 21 Day 1	Nausea and Vomiting Score; Cycle 22 Day 1	Nausea and Vomiting Score; Cycle 23 Day 1	Nausea and Vomiting Score; Cycle 24 Day 1	Nausea and Vomiting Score; Cycle 25 Day 1	Nausea and Vomiting Score; Cycle 26 Day 1	Nausea and Vomiting Score; Cycle 27 Day 1	Nausea and Vomiting Score; Cycle 28 Day 1	Nausea and Vomiting Score; Cycle 29 Day 1	Nausea and Vomiting Score; Cycle 30 Day 1	Nausea and Vomiting Score; Off-treatment Visit	Pain Score; Baseline	Pain Score; Cycle 2 Day 1	Pain Score; Cycle 3 Day 1	Pain Score; Cycle 4 Day 1	Pain Score; Cycle 5 Day 1	Pain Score; Cycle 6 Day 1	Pain Score; Cycle 7 Day 1	Pain Score; Cycle 8 Day 1	Pain Score; Cycle 9 Day 1	Pain Score; Cycle 10 Day 1	Pain Score; Cycle 11 Day 1	Pain Score; Cycle 12 Day 1	Pain Score; Cycle 13 Day 1	Pain Score; Cycle 14 Day 1	Pain Score; Cycle 15 Day 1	Pain Score; Cycle 16 Day 1	Pain Score; Cycle 17 Day 1	Pain Score; Cycle 18 Day 1	Pain Score; Cycle 19 Day 1	Pain Score; Cycle 20 Day 1	Pain Score; Cycle 21 Day 1	Pain Score; Cycle 22 Day 1	Pain Score; Cycle 23 Day 1	Pain Score; Cycle 24 Day 1	Pain Score; Cycle 25 Day 1	Pain Score; Cycle 26 Day 1	Pain Score; Cycle 27 Day 1	Pain Score; Cycle 28 Day 1	Pain Score; Cycle 29 Day 1	Pain Score; Cycle 30 Day 1	Pain Score; Off-treatment Visit	Dyspnea Score; Baseline	Dyspnea Score; Cycle 2 Day 1	Dyspnea Score; Cycle 3 Day 1	Dyspnea Score; Cycle 4 Day 1	Dyspnea Score; Cycle 5 Day 1	Dyspnea Score; Cycle 6 Day 1	Dyspnea Score; Cycle 7 Day 1	Dyspnea Score; Cycle 8 Day 1	Dyspnea Score; Cycle 9 Day 1	Dyspnea Score; Cycle 10 Day 1	Dyspnea Score; Cycle 11 Day 1	Dyspnea Score; Cycle 12 Day 1	Dyspnea Score; Cycle 13 Day 1	Dyspnea Score; Cycle 14 Day 1	Dyspnea Score; Cycle 15 Day 1	Dyspnea Score; Cycle 16 Day 1	Dyspnea Score; Cycle 17 Day 1	Dyspnea Score; Cycle 18 Day 1	Dyspnea Score; Cycle 19 Day 1	Dyspnea Score; Cycle 20 Day 1	Dyspnea Score; Cycle 21 Day 1	Dyspnea Score; Cycle 22 Day 1	Dyspnea Score; Cycle 23 Day 1	Dyspnea Score; Cycle 24 Day 1	Dyspnea Score; Cycle 25 Day 1	Dyspnea Score; Cycle 26 Day 1	Dyspnea Score; Cycle 27 Day 1	Dyspnea Score; Cycle 28 Day 1	Dyspnea Score; Cycle 29 Day 1	Dyspnea Score; Cycle 30 Day 1	Dyspnea Score; Off-treatment Visit	Insomnia Score; Baseline	Insomnia Score; Cycle 2 Day 1	Insomnia Score; Cycle 3 Day 1	Insomnia Score; Cycle 4 Day 1	Insomnia Score; Cycle 5 Day 1	Insomnia Score; Cycle 6 Day 1	Insomnia Score; Cycle 7 Day 1	Insomnia Score; Cycle 8 Day 1	Insomnia Score; Cycle 9 Day 1	Insomnia Score; Cycle 10 Day 1	Insomnia Score; Cycle 11 Day 1	Insomnia Score; Cycle 12 Day 1	Insomnia Score; Cycle 13 Day 1	Insomnia Score; Cycle 14 Day 1	Insomnia Score; Cycle 15 Day 1	Insomnia Score; Cycle 16 Day 1	Insomnia Score; Cycle 17 Day 1	Insomnia Score; Cycle 18 Day 1	Insomnia Score; Cycle 19 Day 1	Insomnia Score; Cycle 20 Day 1	Insomnia Score; Cycle 21 Day 1	Insomnia Score; Cycle 22 Day 1	Insomnia Score; Cycle 23 Day 1	Insomnia Score; Cycle 24 Day 1	Insomnia Score; Cycle 25 Day 1	Insomnia Score; Cycle 26 Day 1	Insomnia Score; Cycle 27 Day 1	Insomnia Score; Cycle 28 Day 1	Insomnia Score; Cycle 29 Day 1	Insomnia Score; Cycle 30 Day 1	Insomnia Score; Off-treatment Visit	Appetite Loss Score; Baseline	Appetite Loss Score; Cycle 2 Day 1	Appetite Loss Score; Cycle 3 Day 1	Appetite Loss Score; Cycle 4 Day 1	Appetite Loss Score; Cycle 5 Day 1	Appetite Loss Score; Cycle 6 Day 1	Appetite Loss Score; Cycle 7 Day 1	Appetite Loss Score; Cycle 8 Day 1	Appetite Loss Score; Cycle 9 Day 1	Appetite Loss Score; Cycle 10 Day 1	Appetite Loss Score; Cycle 11 Day 1	Appetite Loss Score; Cycle 12 Day 1	Appetite Loss Score; Cycle 13 Day 1	Appetite Loss Score; Cycle 14 Day 1	Appetite Loss Score; Cycle 15 Day 1	Appetite Loss Score; Cycle 16 Day 1	Appetite Loss Score; Cycle 17 Day 1	Appetite Loss Score; Cycle 18 Day 1	Appetite Loss Score; Cycle 19 Day 1	Appetite Loss Score; Cycle 20 Day 1	Appetite Loss Score; Cycle 21 Day 1	Appetite Loss Score; Cycle 22 Day 1	Appetite Loss Score; Cycle 23 Day 1	Appetite Loss Score; Cycle 24 Day 1	Appetite Loss Score; Cycle 25 Day 1	Appetite Loss Score; Cycle 26 Day 1	Appetite Loss Score; Cycle 27 Day 1	Appetite Loss Score; Cycle 28 Day 1	Appetite Loss Score; Cycle 29 Day 1	Appetite Loss Score; Cycle 30 Day 1	Appetite Loss Score; Off-treatment Visit	Constipation Score; Baseline	Constipation Score; Cycle 2 Day 1	Constipation Score; Cycle 3 Day 1	Constipation Score; Cycle 4 Day 1	Constipation Score; Cycle 5 Day 1	Constipation Score; Cycle 6 Day 1	Constipation Score; Cycle 7 Day 1	Constipation Score; Cycle 8 Day 1	Constipation Score; Cycle 9 Day 1	Constipation Score; Cycle 10 Day 1	Constipation Score; Cycle 11 Day 1	Constipation Score; Cycle 12 Day 1	Constipation Score; Cycle 13 Day 1	Constipation Score; Cycle 14 Day 1	Constipation Score; Cycle 15 Day 1	Constipation Score; Cycle 16 Day 1	Constipation Score; Cycle 17 Day 1	Constipation Score; Cycle 18 Day 1	Constipation Score; Cycle 19 Day 1	Constipation Score; Cycle 20 Day 1	Constipation Score; Cycle 21 Day 1	Constipation Score; Cycle 22 Day 1	Constipation Score; Cycle 23 Day 1	Constipation Score; Cycle 24 Day 1	Constipation Score; Cycle 25 Day 1	Constipation Score; Cycle 26 Day 1	Constipation Score; Cycle 27 Day 1	Constipation Score; Cycle 28 Day 1	Constipation Score; Cycle 29 Day 1	Constipation Score; Cycle 30 Day 1	Constipation Score; Off-treatment Visit	Diarrhea Score; Baseline	Diarrhea Score; Cycle 2 Day 1	Diarrhea Score; Cycle 3 Day 1	Diarrhea Score; Cycle 4 Day 1	Diarrhea Score; Cycle 5 Day 1	Diarrhea Score; Cycle 6 Day 1	Diarrhea Score; Cycle 7 Day 1	Diarrhea Score; Cycle 8 Day 1	Diarrhea Score; Cycle 9 Day 1	Diarrhea Score; Cycle 10 Day 1	Diarrhea Score; Cycle 11 Day 1	Diarrhea Score; Cycle 12 Day 1	Diarrhea Score; Cycle 13 Day 1	Diarrhea Score; Cycle 14 Day 1	Diarrhea Score; Cycle 15 Day 1	Diarrhea Score; Cycle 16 Day 1	Diarrhea Score; Cycle 17 Day 1	Diarrhea Score; Cycle 18 Day 1	Diarrhea Score; Cycle 19 Day 1	Diarrhea Score; Cycle 20 Day 1	Diarrhea Score; Cycle 21 Day 1	Diarrhea Score; Cycle 22 Day 1	Diarrhea Score; Cycle 23 Day 1	Diarrhea Score; Cycle 24 Day 1	Diarrhea Score; Cycle 25 Day 1	Diarrhea Score; Cycle 26 Day 1	Diarrhea Score; Cycle 27 Day 1	Diarrhea Score; Cycle 28 Day 1	Diarrhea Score; Cycle 29 Day 1	Diarrhea Score; Cycle 30 Day 1	Diarrhea Score; Off-treatment Visit	Financial Difficulties Score; Baseline	Financial Difficulties Score; Cycle 2 Day 1	Financial Difficulties Score; Cycle 3 Day 1	Financial Difficulties Score; Cycle 4 Day 1	Financial Difficulties Score; Cycle 5 Day 1	Financial Difficulties Score; Cycle 6 Day 1	Financial Difficulties Score; Cycle 7 Day 1	Financial Difficulties Score; Cycle 8 Day 1	Financial Difficulties Score; Cycle 9 Day 1	Financial Difficulties Score; Cycle 10 Day 1	Financial Difficulties Score; Cycle 11 Day 1	Financial Difficulties Score; Cycle 12 Day 1	Financial Difficulties Score; Cycle 13 Day 1	Financial Difficulties Score; Cycle 14 Day 1	Financial Difficulties Score; Cycle 15 Day 1	Financial Difficulties Score; Cycle 16 Day 1	Financial Difficulties Score; Cycle 17 Day 1	Financial Difficulties Score; Cycle 18 Day 1	Financial Difficulties Score; Cycle 19 Day 1	Financial Difficulties Score; Cycle 20 Day 1	Financial Difficulties Score; Cycle 21 Day 1	Financial Difficulties Score; Cycle 22 Day 1	Financial Difficulties Score; Cycle 23 Day 1	Financial Difficulties Score; Cycle 24 Day 1	Financial Difficulties Score; Cycle 25 Day 1	Financial Difficulties Score; Cycle 26 Day 1	Financial Difficulties Score; Cycle 27 Day 1	Financial Difficulties Score; Cycle 28 Day 1	Financial Difficulties Score; Cycle 29 Day 1	Financial Difficulties Score; Cycle 30 Day 1	Financial Difficulties Score; Off-treatment Visit
Lenvatinib 18 mg + Everolimus 5 mg	63.58	60.93	61.85	62.62	63.76	63.73	62.54	62.11	63.77	66.44	65.86	66.94	68.94	70.35	66.83	64.54	67.71	68.38	66.67	66.40	71.13	66.05	66.67	65.79	69.79	60.90	71.43	77.78	75	66.67	56.05	76.60	75.38	76.15	75.40	77.85	77.76	78.41	79.11	80.60	81.20	81.13	83.01	80.24	82.39	80.92	81.74	82.33	81.52	81.57	82.80	84.29	82.72	81.39	83.86	84.17	71.79	85.71	90	86.67	100	70.41	75.72	69.33	72.18	73.60	72.44	73.75	73.97	75.60	75.91	76.89	79.11	80.91	80	81.13	74.84	79.08	83.75	82.35	77.45	79.57	81.55	77.78	79.86	83.33	82.29	69.23	90.48	97.22	96.67	100	63.51	80.06	82.06	82.90	84.19	84.52	84.38	84.29	84.88	85.96	87.84	87.15	86.67	87.27	87.50	87.25	87.41	87.08	86.76	84.80	86.56	88.99	89.20	87.15	87.28	90.63	85.26	95.24	100	100	100	73.87	89.51	88.85	87.47	90.32	87.43	87.68	87.94	88.49	87.68	90.44	88.89	88.61	89.70	87.18	83.99	89.36	89.58	90.20	89.22	91.94	88.10	90.12	88.19	92.11	98.96	92.31	95.24	100	100	100	80.41	78.29	77.15	77.19	77.33	79.63	78.71	77.30	79.04	78.62	85.14	85.19	83.89	83.94	83.97	81.37	80.80	80.42	82.84	80.88	81.72	82.14	82.10	83.33	84.21	84.38	76.92	95.24	100	100	100	66.89	31.76	36.74	36.62	32.68	35.17	33.19	30.79	30.81	30.80	27.11	27.46	23.48	25.05	25.58	28.98	25.53	25	24.84	27.45	27.24	23.02	26.75	29.17	26.90	25.69	37.61	20.63	16.67	15.56	11.11	38.89	6.28	9.56	9.74	12.17	11.42	10.14	8.57	10.14	9.96	7.78	8.69	6.99	6.97	7.55	8.82	9.22	5	9.31	7.35	10.22	7.74	8.64	6.25	7.89	2.08	14.10	16.67	8.33	0	0	6.76	23.77	27.04	25	22.87	22.97	22.50	23.65	23.20	21.01	19.33	18.06	18.55	18.48	16.04	17.65	18.44	17.50	16.67	19.61	19.35	17.86	22.84	18.06	14.91	15.63	21.79	11.90	2.78	6.67	0	27.70	22.22	19.56	19.72	17.52	15.75	18.89	15.87	14.09	14.49	11.56	15.02	12.90	10.91	10.69	12.42	9.93	10	10.78	9.80	11.83	7.14	12.35	11.11	12.28	8.33	15.38	14.29	16.67	20	0	21.62	22.84	19.91	23	20.19	22.05	17.50	20	19.59	16.67	18.22	17.37	13.98	13.33	11.95	16	14.89	13.33	11.76	13.73	12.90	10.71	6.17	11.11	12.28	12.50	20.51	9.52	11.11	13.33	0	28.83	18.31	27.56	29.81	30.90	30.67	26.11	26.98	25.00	25.36	22.22	22.07	18.82	17.28	17.61	24.18	22.70	22.50	22.22	20.59	21.51	15.48	17.28	20.83	15.79	18.75	23.08	9.52	11.11	0	0	25.23	12.55	11.11	10.80	9.80	9.87	8.47	7.44	7.22	9.42	8.00	7.98	9.68	9.09	7.69	9.33	9.93	5.00	7.84	9.80	8.60	7.14	7.41	11.11	8.77	18.75	15.38	0	0	0	0	12.61	6.79	17.66	27.19	29.41	29.33	26.89	31.75	31.27	28.62	29.33	26.85	22.78	23.03	24.36	30.07	23.40	29.17	25.49	21.57	22.58	21.43	24.69	22.22	19.30	18.75	17.95	33.33	22.22	20.00	0	12.16	20.37	15.01	18.20	16.42	18.78	17.80	15.87	17.53	16.67	17.35	16.20	16.11	19.14	17.31	19.61	17.02	19.17	19.61	20.59	20.43	20.24	20.99	23.61	19.30	16.67	20.51	0	0	0	0	25.11

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HRQoL Assessed by European Quality of Life (EuroQol) Five-Dimensional, 3-Level (EQ-5D-3L) Index Score and Visual Analogue Scale (VAS)

"The EQ-5D-3L is a health profile questionnaire assessing quality of life along 5 dimensions. Participants rate 5 dimensions of health (mobility, self-care, usual activities, pain/discomfort, and anxiety/depression) by choosing from 3 answering options (1=no problems; 2=some problems; 3=extreme problems). The summed score ranges from 5-15 with 5 corresponding to no problems and 15 corresponding to severe problems in the 5 dimensions. The EQ-5D index was calculated by applying preference-based weights (tariffs) to the scores of the five health state dimensions. Index values can range from -1 to 1, with 0 representing a health state equivalent to death and 1 representing perfect health. EQ-5D-3L also included an EQ visual analogue scale (VAS) that ranges between 100 (best imaginable health) and 0 (worst imaginable health). Decrease from baseline in EQ-5D-3L signifies improvement. Total index EQ-5D-3L summary score was weighted with a range of -0.594 (worst) to 1.0 (best)." (NCT03173560)
Timeframe: At baseline (prior to first dose of study drug), on Day 1 of each subsequent cycle (cycle length =28 days), and at the Off-treatment visit (up to 29 months)

Intervention	score on a scale (Mean)
	EQ-5D Index Score; Baseline	EQ-5D Index Score; Cycle 2 Day 1	EQ-5D Index Score; Cycle 3 Day 1	EQ-5D Index Score; Cycle 4 Day 1	EQ-5D Index Score; Cycle 5 Day 1	EQ-5D Index Score; Cycle 6 Day 1	EQ-5D Index Score; Cycle 7 Day 1	EQ-5D Index Score; Cycle 8 Day 1	EQ-5D Index Score; Cycle 9 Day 1	EQ-5D Index Score; Cycle 10 Day 1	EQ-5D Index Score; Cycle 11 Day 1	EQ-5D Index Score; Cycle 12 Day 1	EQ-5D Index Score; Cycle 13 Day 1	EQ-5D Index Score; Cycle 14 Day 1	EQ-5D Index Score; Cycle 15 Day 1	EQ-5D Index Score; Cycle 16 Day 1	EQ-5D Index Score; Cycle 17 Day 1	EQ-5D Index Score; Cycle 18 Day 1	EQ-5D Index Score; Cycle 19 Day 1	EQ-5D Index Score; Cycle 20 Day 1	EQ-5D Index Score; Cycle 21 Day 1	EQ-5D Index Score; Cycle 22 Day 1	EQ-5D Index Score; Cycle 23 Day 1	EQ-5D Index Score; Cycle 24 Day 1	EQ-5D Index Score; Cycle 25 Day 1	EQ-5D Index Score; Cycle 26 Day 1	EQ-5D Index Score; Cycle 27 Day 1	EQ-5D Index Score; Cycle 28 Day 1	EQ-5D Index Score; Cycle 29 Day 1	EQ-5D Index Score; Cycle 30 Day 1	EQ-5D Index Score; Off-treatment Visit	EQ-VAS Score; Baseline	EQ-VAS Score; Cycle 2 Day 1	EQ-VAS Score; Cycle 3 Day 1	EQ-VAS Score; Cycle 4 Day 1	EQ-VAS Score; Cycle 5 Day 1	EQ-VAS Score; Cycle 6 Day 1	EQ-VAS Score; Cycle 7 Day 1	EQ-VAS Score; Cycle 8 Day 1	EQ-VAS Score; Cycle 9 Day 1	EQ-VAS Score; Cycle 10 Day 1	EQ-VAS Score; Cycle 11 Day 1	EQ-VAS Score; Cycle 12 Day 1	EQ-VAS Score; Cycle 13 Day 1	EQ-VAS Score; Cycle 14 Day 1	EQ-VAS Score; Cycle 15 Day 1	EQ-VAS Score; Cycle 16 Day 1	EQ-VAS Score; Cycle 17 Day 1	EQ-VAS Score; Cycle 18 Day 1	EQ-VAS Score; Cycle 19 Day 1	EQ-VAS Score; Cycle 20 Day 1	EQ-VAS Score; Cycle 21 Day 1	EQ-VAS Score; Cycle 22 Day 1	EQ-VAS Score; Cycle 23 Day 1	EQ-VAS Score; Cycle 24 Day 1	EQ-VAS Score; Cycle 25 Day 1	EQ-VAS Score; Cycle 26 Day 1	EQ-VAS Score; Cycle 27 Day 1	EQ-VAS Score; Cycle 28 Day 1	EQ-VAS Score; Cycle 29 Day 1	EQ-VAS Score; Cycle 30 Day 1	EQ-VAS Score; Off-treatment Visit
Lenvatinib 18 mg + Everolimus 5 mg	0.78	0.76	0.78	0.78	0.78	0.77	0.78	0.80	0.79	0.81	0.82	0.83	0.82	0.83	0.81	0.81	0.83	0.84	0.79	0.82	0.83	0.85	0.82	0.84	0.83	0.73	0.93	0.97	0.96	1	0.68	70.01	69.52	70.71	69.66	70.30	71.73	70.39	70.40	69.92	73.18	73.21	74.46	74.35	74.40	72.58	72.80	73.80	73.71	71.76	72.07	76.46	74.44	73.67	71.21	72.81	65.23	77.43	77.50	74	50	62.66

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Overall Survival (OS)

OS was defined as the time from the date of randomization until the date of death from any cause. In the absence of confirmation of death, participants will be censored either at the date that the participant was last known to be alive or the date of data cutoff for the primary analysis, whichever comes earlier. Median OS was to be calculated using Kaplan-Meier estimate and presented with 2-sided 95% confidence interval. (NCT03173560)
Timeframe: From the date of randomization until the date of death from any cause, or up to date of data cut off for the primary analysis (up to 29 months)

Intervention	months (Median)
Lenvatinib 14 mg + Everolimus 5 mg	27.0
Lenvatinib 18 mg + Everolimus 5 mg	NA

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Number of Participants With TEAEs and Serious TEAEs

TEAEs were defined as those adverse events (AEs) that occurred (or worsened, if present at Baseline) after the first dose of study drug through 28 days after the last dose of study drug. An AE was defined as any untoward medical occurrence in a participants or clinical investigation participant administered an investigational product. An AE does not necessarily have a causal relationship with medicinal product. A serious adverse event (SAE) was defined as any AE if it resulted in death or life-threatening AE or required inpatient hospitalization or prolongation of existing hospitalization or resulted in persistent or significant incapacity or substantial disruption of the ability to conduct normal life functions or was a congenital anomaly/birth defect. (NCT03173560)
Timeframe: From date of first dose of study drug up to 28 days after last dose of study drug, or date of data cut off for the primary analysis (up to 29 months)

Intervention	Participants (Count of Participants)
	Participants With TEAEs	Participants With Serious TEAEs
Lenvatinib 14 mg + Everolimus 5 mg	173	85
Lenvatinib 18 mg + Everolimus 5 mg	167	82

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HRQoL Assessed by European Organization for the Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-C30 Scores

Intervention	score on a scale (Mean)
	Global Health Status/QoL Score; Baseline	Global Health Status/QoL Score; Cycle 2 Day 1	Global Health Status/QoL Score; Cycle 3 Day 1	Global Health Status/QoL Score; Cycle 4 Day 1	Global Health Status/QoL Score; Cycle 5 Day 1	Global Health Status/QoL Score; Cycle 6 Day 1	Global Health Status/QoL Score; Cycle 7 Day 1	Global Health Status/QoL Score; Cycle 8 Day 1	Global Health Status/QoL Score; Cycle 9 Day 1	Global Health Status/QoL Score; Cycle 10 Day 1	Global Health Status/QoL Score; Cycle 11 Day 1	Global Health Status/QoL Score; Cycle 12 Day 1	Global Health Status/QoL Score; Cycle 13 Day 1	Global Health Status/QoL Score; Cycle 14 Day 1	Global Health Status/QoL Score; Cycle 15 Day 1	Global Health Status/QoL Score; Cycle 16 Day 1	Global Health Status/QoL Score; Cycle 17 Day 1	Global Health Status/QoL Score; Cycle 18 Day 1	Global Health Status/QoL Score; Cycle 19 Day 1	Global Health Status/QoL Score; Cycle 20 Day 1	Global Health Status/QoL Score; Cycle 21 Day 1	Global Health Status/QoL Score; Cycle 22 Day 1	Global Health Status/QoL Score; Cycle 23 Day 1	Global Health Status/QoL Score; Cycle 24 Day 1	Global Health Status/QoL Score; Cycle 25 Day 1	Global Health Status/QoL Score; Cycle 26 Day 1	Global Health Status/QoL Score; Cycle 27 Day 1	Global Health Status/QoL Score; Cycle 28 Day 1	Global Health Status/QoL Score; Cycle 29 Day 1	Global Health Status/QoL Score; Cycle 30 Day 1	Global Health Status/QoL Score; Cycle 31 Day 1	Global Health Status/QoL Score; Off-treatment Visit	Physical Functioning Score; Baseline	Physical Functioning Score; Cycle 2 Day 1	Physical Functioning Score; Cycle 3 Day 1	Physical Functioning Score; Cycle 4 Day 1	Physical Functioning Score; Cycle 5 Day 1	Physical Functioning Score; Cycle 6 Day 1	Physical Functioning Score; Cycle 7 Day 1	Physical Functioning Score; Cycle 8 Day 1	Physical Functioning Score; Cycle 9 Day 1	Physical Functioning Score; Cycle 10 Day 1	Physical Functioning Score; Cycle 11 Day 1	Physical Functioning Score; Cycle 12 Day 1	Physical Functioning Score; Cycle 13 Day 1	Physical Functioning Score; Cycle 14 Day 1	Physical Functioning Score; Cycle 15 Day 1	Physical Functioning Score; Cycle 16 Day 1	Physical Functioning Score; Cycle 17 Day 1	Physical Functioning Score; Cycle 18 Day 1	Physical Functioning Score; Cycle 19 Day 1	Physical Functioning Score; Cycle 20 Day 1	Physical Functioning Score; Cycle 21 Day 1	Physical Functioning Score; Cycle 22 Day 1	Physical Functioning Score; Cycle 23 Day 1	Physical Functioning Score; Cycle 24 Day 1	Physical Functioning Score; Cycle 25 Day 1	Physical Functioning Score; Cycle 26 Day 1	Physical Functioning Score; Cycle 27 Day 1	Physical Functioning Score; Cycle 28 Day 1	Physical Functioning Score; Cycle 29 Day 1	Physical Functioning Score; Cycle 30 Day 1	Physical Functioning Score; Cycle 31 Day 1	Physical Functioning Score; Off-treatment Visit	Role Functioning Score; Baseline	Role Functioning Score; Cycle 2 Day 1	Role Functioning Score; Cycle 3 Day 1	Role Functioning Score; Cycle 4 Day 1	Role Functioning Score; Cycle 5 Day 1	Role Functioning Score; Cycle 6 Day 1	Role Functioning Score; Cycle 7 Day 1	Role Functioning Score; Cycle 8 Day 1	Role Functioning Score; Cycle 9 Day 1	Role Functioning Score; Cycle 10 Day 1	Role Functioning Score; Cycle 11 Day 1	Role Functioning Score; Cycle 12 Day 1	Role Functioning Score; Cycle 13 Day 1	Role Functioning Score; Cycle 14 Day 1	Role Functioning Score; Cycle 15 Day 1	Role Functioning Score; Cycle 16 Day 1	Role Functioning Score; Cycle 17 Day 1	Role Functioning Score; Cycle 18 Day 1	Role Functioning Score; Cycle 19 Day 1	Role Functioning Score; Cycle 20 Day 1	Role Functioning Score; Cycle 21 Day 1	Role Functioning Score; Cycle 22 Day 1	Role Functioning Score; Cycle 23 Day 1	Role Functioning Score; Cycle 24 Day 1	Role Functioning Score; Cycle 25 Day 1	Role Functioning Score; Cycle 26 Day 1	Role Functioning Score; Cycle 27 Day 1	Role Functioning Score; Cycle 28 Day 1	Role Functioning Score; Cycle 29 Day 1	Role Functioning Score; Cycle 30 Day 1	Role Functioning Score; Cycle 31 Day 1	Role Functioning Score; Off-treatment Visit	Emotional Functioning Score; Baseline	Emotional Functioning Score; Cycle 2 Day 1	Emotional Functioning Score; Cycle 3 Day 1	Emotional Functioning Score; Cycle 4 Day 1	Emotional Functioning Score; Cycle 5 Day 1	Emotional Functioning Score; Cycle 6 Day 1	Emotional Functioning Score; Cycle 7 Day 1	Emotional Functioning Score; Cycle 8 Day 1	Emotional Functioning Score; Cycle 9 Day 1	Emotional Functioning Score; Cycle 10 Day 1	Emotional Functioning Score; Cycle 11 Day 1	Emotional Functioning Score; Cycle 12 Day 1	Emotional Functioning Score; Cycle 13 Day 1	Emotional Functioning Score; Cycle 14 Day 1	Emotional Functioning Score; Cycle 15 Day 1	Emotional Functioning Score; Cycle 16 Day 1	Emotional Functioning Score; Cycle 17 Day 1	Emotional Functioning Score; Cycle 18 Day 1	Emotional Functioning Score; Cycle 19 Day 1	Emotional Functioning Score; Cycle 20 Day 1	Emotional Functioning Score; Cycle 21 Day 1	Emotional Functioning Score; Cycle 22 Day 1	Emotional Functioning Score; Cycle 23 Day 1	Emotional Functioning Score; Cycle 24 Day 1	Emotional Functioning Score; Cycle 25 Day 1	Emotional Functioning Score; Cycle 26 Day 1	Emotional Functioning Score; Cycle 27 Day 1	Emotional Functioning Score; Cycle 28 Day 1	Emotional Functioning Score; Cycle 29 Day 1	Emotional Functioning Score; Cycle 30 Day 1	Emotional Functioning Score; Cycle 31 Day 1	Emotional Functioning Score; Off-treatment Visit	Cognitive Functioning Score; Baseline	Cognitive Functioning Score; Cycle 2 Day 1	Cognitive Functioning Score; Cycle 3 Day 1	Cognitive Functioning Score; Cycle 4 Day 1	Cognitive Functioning Score; Cycle 5 Day 1	Cognitive Functioning Score; Cycle 6 Day 1	Cognitive Functioning Score; Cycle 7 Day 1	Cognitive Functioning Score; Cycle 8 Day 1	Cognitive Functioning Score; Cycle 9 Day 1	Cognitive Functioning Score; Cycle 10 Day 1	Cognitive Functioning Score; Cycle 11 Day 1	Cognitive Functioning Score; Cycle 12 Day 1	Cognitive Functioning Score; Cycle 13 Day 1	Cognitive Functioning Score; Cycle 14 Day 1	Cognitive Functioning Score; Cycle 15 Day 1	Cognitive Functioning Score; Cycle 16 Day 1	Cognitive Functioning Score; Cycle 17 Day 1	Cognitive Functioning Score; Cycle 18 Day 1	Cognitive Functioning Score; Cycle 19 Day 1	Cognitive Functioning Score; Cycle 20 Day 1	Cognitive Functioning Score; Cycle 21 Day 1	Cognitive Functioning Score; Cycle 22 Day 1	Cognitive Functioning Score; Cycle 23 Day 1	Cognitive Functioning Score; Cycle 24 Day 1	Cognitive Functioning Score; Cycle 25 Day 1	Cognitive Functioning Score; Cycle 26 Day 1	Cognitive Functioning Score; Cycle 27 Day 1	Cognitive Functioning Score; Cycle 28 Day 1	Cognitive Functioning Score; Cycle 29 Day 1	Cognitive Functioning Score; Cycle 30 Day 1	Cognitive Functioning Score; Cycle 31 Day 1	Cognitive Functioning Score; Off-treatment Visit	Social Functioning Score; Baseline	Social Functioning Score; Cycle 2 Day 1	Social Functioning Score; Cycle 3 Day 1	Social Functioning Score; Cycle 4 Day 1	Social Functioning Score; Cycle 5 Day 1	Social Functioning Score; Cycle 6 Day 1	Social Functioning Score; Cycle 7 Day 1	Social Functioning Score; Cycle 8 Day 1	Social Functioning Score; Cycle 9 Day 1	Social Functioning Score; Cycle 10 Day 1	Social Functioning Score; Cycle 11 Day 1	Social Functioning Score; Cycle 12 Day 1	Social Functioning Score; Cycle 13 Day 1	Social Functioning Score; Cycle 14 Day 1	Social Functioning Score; Cycle 15 Day 1	Social Functioning Score; Cycle 16 Day 1	Social Functioning Score; Cycle 17 Day 1	Social Functioning Score; Cycle 18 Day 1	Social Functioning Score; Cycle 19 Day 1	Social Functioning Score; Cycle 20 Day 1	Social Functioning Score; Cycle 21 Day 1	Social Functioning Score; Cycle 22 Day 1	Social Functioning Score; Cycle 23 Day 1	Social Functioning Score; Cycle 24 Day 1	Social Functioning Score; Cycle 25 Day 1	Social Functioning Score; Cycle 26 Day 1	Social Functioning Score; Cycle 27 Day 1	Social Functioning Score; Cycle 28 Day 1	Social Functioning Score; Cycle 29 Day 1	Social Functioning Score; Cycle 30 Day 1	Social Functioning Score; Cycle 31 Day 1	Social Functioning Score; Off-treatment Visit	Fatigue Score; Baseline	Fatigue Score; Cycle 2 Day 1	Fatigue Score; Cycle 3 Day 1	Fatigue Score; Cycle 4 Day 1	Fatigue Score; Cycle 5 Day 1	Fatigue Score; Cycle 6 Day 1	Fatigue Score; Cycle 7 Day 1	Fatigue Score; Cycle 8 Day 1	Fatigue Score; Cycle 9 Day 1	Fatigue Score; Cycle 10 Day 1	Fatigue Score; Cycle 11 Day 1	Fatigue Score; Cycle 12 Day 1	Fatigue Score; Cycle 13 Day 1	Fatigue Score; Cycle 14 Day 1	Fatigue Score; Cycle 15 Day 1	Fatigue Score; Cycle 16 Day 1	Fatigue Score; Cycle 17 Day 1	Fatigue Score; Cycle 18 Day 1	Fatigue Score; Cycle 19 Day 1	Fatigue Score; Cycle 20 Day 1	Fatigue Score; Cycle 21 Day 1	Fatigue Score; Cycle 22 Day 1	Fatigue Score; Cycle 23 Day 1	Fatigue Score; Cycle 24 Day 1	Fatigue Score; Cycle 25 Day 1	Fatigue Score; Cycle 26 Day 1	Fatigue Score; Cycle 27 Day 1	Fatigue Score; Cycle 28 Day 1	Fatigue Score; Cycle 29 Day 1	Fatigue Score; Cycle 30 Day 1	Fatigue Score; Cycle 31 Day 1	Fatigue Score; Off-treatment Visit	Nausea and Vomiting Score; Baseline	Nausea and Vomiting Score; Cycle 2 Day 1	Nausea and Vomiting Score; Cycle 3 Day 1	Nausea and Vomiting Score; Cycle 4 Day 1	Nausea and Vomiting Score; Cycle 5 Day 1	Nausea and Vomiting Score; Cycle 6 Day 1	Nausea and Vomiting Score; Cycle 7 Day 1	Nausea and Vomiting Score; Cycle 8 Day 1	Nausea and Vomiting Score; Cycle 9 Day 1	Nausea and Vomiting Score; Cycle 10 Day 1	Nausea and Vomiting Score; Cycle 11 Day 1	Nausea and Vomiting Score; Cycle 12 Day 1	Nausea and Vomiting Score; Cycle 13 Day 1	Nausea and Vomiting Score; Cycle 14 Day 1	Nausea and Vomiting Score; Cycle 15 Day 1	Nausea and Vomiting Score; Cycle 16 Day 1	Nausea and Vomiting Score; Cycle 17 Day 1	Nausea and Vomiting Score; Cycle 18 Day 1	Nausea and Vomiting Score; Cycle 19 Day 1	Nausea and Vomiting Score; Cycle 20 Day 1	Nausea and Vomiting Score; Cycle 21 Day 1	Nausea and Vomiting Score; Cycle 22 Day 1	Nausea and Vomiting Score; Cycle 23 Day 1	Nausea and Vomiting Score; Cycle 24 Day 1	Nausea and Vomiting Score; Cycle 25 Day 1	Nausea and Vomiting Score; Cycle 26 Day 1	Nausea and Vomiting Score; Cycle 27 Day 1	Nausea and Vomiting Score; Cycle 28 Day 1	Nausea and Vomiting Score; Cycle 29 Day 1	Nausea and Vomiting Score; Cycle 30 Day 1	Nausea and Vomiting Score; Cycle 31 Day 1	Nausea and Vomiting Score; Off-treatment Visit	Pain Score; Baseline	Pain Score; Cycle 2 Day 1	Pain Score; Cycle 3 Day 1	Pain Score; Cycle 4 Day 1	Pain Score; Cycle 5 Day 1	Pain Score; Cycle 6 Day 1	Pain Score; Cycle 7 Day 1	Pain Score; Cycle 8 Day 1	Pain Score; Cycle 9 Day 1	Pain Score; Cycle 10 Day 1	Pain Score; Cycle 11 Day 1	Pain Score; Cycle 12 Day 1	Pain Score; Cycle 13 Day 1	Pain Score; Cycle 14 Day 1	Pain Score; Cycle 15 Day 1	Pain Score; Cycle 16 Day 1	Pain Score; Cycle 17 Day 1	Pain Score; Cycle 18 Day 1	Pain Score; Cycle 19 Day 1	Pain Score; Cycle 20 Day 1	Pain Score; Cycle 21 Day 1	Pain Score; Cycle 22 Day 1	Pain Score; Cycle 23 Day 1	Pain Score; Cycle 24 Day 1	Pain Score; Cycle 25 Day 1	Pain Score; Cycle 26 Day 1	Pain Score; Cycle 27 Day 1	Pain Score; Cycle 28 Day 1	Pain Score; Cycle 29 Day 1	Pain Score; Cycle 30 Day 1	Pain Score; Cycle 31 Day 1	Pain Score; Off-treatment Visit	Dyspnea Score; Baseline	Dyspnea Score; Cycle 2 Day 1	Dyspnea Score; Cycle 3 Day 1	Dyspnea Score; Cycle 4 Day 1	Dyspnea Score; Cycle 5 Day 1	Dyspnea Score; Cycle 6 Day 1	Dyspnea Score; Cycle 7 Day 1	Dyspnea Score; Cycle 8 Day 1	Dyspnea Score; Cycle 9 Day 1	Dyspnea Score; Cycle 10 Day 1	Dyspnea Score; Cycle 11 Day 1	Dyspnea Score; Cycle 12 Day 1	Dyspnea Score; Cycle 13 Day 1	Dyspnea Score; Cycle 14 Day 1	Dyspnea Score; Cycle 15 Day 1	Dyspnea Score; Cycle 16 Day 1	Dyspnea Score; Cycle 17 Day 1	Dyspnea Score; Cycle 18 Day 1	Dyspnea Score; Cycle 19 Day 1	Dyspnea Score; Cycle 20 Day 1	Dyspnea Score; Cycle 21 Day 1	Dyspnea Score; Cycle 22 Day 1	Dyspnea Score; Cycle 23 Day 1	Dyspnea Score; Cycle 24 Day 1	Dyspnea Score; Cycle 25 Day 1	Dyspnea Score; Cycle 26 Day 1	Dyspnea Score; Cycle 27 Day 1	Dyspnea Score; Cycle 28 Day 1	Dyspnea Score; Cycle 29 Day 1	Dyspnea Score; Cycle 30 Day 1	Dyspnea Score; Cycle 31 Day 1	Dyspnea Score; Off-treatment Visit	Insomnia Score; Baseline	Insomnia Score; Cycle 2 Day 1	Insomnia Score; Cycle 3 Day 1	Insomnia Score; Cycle 4 Day 1	Insomnia Score; Cycle 5 Day 1	Insomnia Score; Cycle 6 Day 1	Insomnia Score; Cycle 7 Day 1	Insomnia Score; Cycle 8 Day 1	Insomnia Score; Cycle 9 Day 1	Insomnia Score; Cycle 10 Day 1	Insomnia Score; Cycle 11 Day 1	Insomnia Score; Cycle 12 Day 1	Insomnia Score; Cycle 13 Day 1	Insomnia Score; Cycle 14 Day 1	Insomnia Score; Cycle 15 Day 1	Insomnia Score; Cycle 16 Day 1	Insomnia Score; Cycle 17 Day 1	Insomnia Score; Cycle 18 Day 1	Insomnia Score; Cycle 19 Day 1	Insomnia Score; Cycle 20 Day 1	Insomnia Score; Cycle 21 Day 1	Insomnia Score; Cycle 22 Day 1	Insomnia Score; Cycle 23 Day 1	Insomnia Score; Cycle 24 Day 1	Insomnia Score; Cycle 25 Day 1	Insomnia Score; Cycle 26 Day 1	Insomnia Score; Cycle 27 Day 1	Insomnia Score; Cycle 28 Day 1	Insomnia Score; Cycle 29 Day 1	Insomnia Score; Cycle 30 Day 1	Insomnia Score; Cycle 31 Day 1	Insomnia Score; Off-treatment Visit	Appetite Loss Score; Baseline	Appetite Loss Score; Cycle 2 Day 1	Appetite Loss Score; Cycle 3 Day 1	Appetite Loss Score; Cycle 4 Day 1	Appetite Loss Score; Cycle 5 Day 1	Appetite Loss Score; Cycle 6 Day 1	Appetite Loss Score; Cycle 7 Day 1	Appetite Loss Score; Cycle 8 Day 1	Appetite Loss Score; Cycle 9 Day 1	Appetite Loss Score; Cycle 10 Day 1	Appetite Loss Score; Cycle 11 Day 1	Appetite Loss Score; Cycle 12 Day 1	Appetite Loss Score; Cycle 13 Day 1	Appetite Loss Score; Cycle 14 Day 1	Appetite Loss Score; Cycle 15 Day 1	Appetite Loss Score; Cycle 16 Day 1	Appetite Loss Score; Cycle 17 Day 1	Appetite Loss Score; Cycle 18 Day 1	Appetite Loss Score; Cycle 19 Day 1	Appetite Loss Score; Cycle 20 Day 1	Appetite Loss Score; Cycle 21 Day 1	Appetite Loss Score; Cycle 22 Day 1	Appetite Loss Score; Cycle 23 Day 1	Appetite Loss Score; Cycle 24 Day 1	Appetite Loss Score; Cycle 25 Day 1	Appetite Loss Score; Cycle 26 Day 1	Appetite Loss Score; Cycle 27 Day 1	Appetite Loss Score; Cycle 28 Day 1	Appetite Loss Score; Cycle 29 Day 1	Appetite Loss Score; Cycle 30 Day 1	Appetite Loss Score; Cycle 31 Day 1	Appetite Loss Score; Off-treatment Visit	Constipation Score; Baseline	Constipation Score; Cycle 2 Day 1	Constipation Score; Cycle 3 Day 1	Constipation Score; Cycle 4 Day 1	Constipation Score; Cycle 5 Day 1	Constipation Score; Cycle 6 Day 1	Constipation Score; Cycle 7 Day 1	Constipation Score; Cycle 8 Day 1	Constipation Score; Cycle 9 Day 1	Constipation Score; Cycle 10 Day 1	Constipation Score; Cycle 11 Day 1	Constipation Score; Cycle 12 Day 1	Constipation Score; Cycle 13 Day 1	Constipation Score; Cycle 14 Day 1	Constipation Score; Cycle 15 Day 1	Constipation Score; Cycle 16 Day 1	Constipation Score; Cycle 17 Day 1	Constipation Score; Cycle 18 Day 1	Constipation Score; Cycle 19 Day 1	Constipation Score; Cycle 20 Day 1	Constipation Score; Cycle 21 Day 1	Constipation Score; Cycle 22 Day 1	Constipation Score; Cycle 23 Day 1	Constipation Score; Cycle 24 Day 1	Constipation Score; Cycle 25 Day 1	Constipation Score; Cycle 26 Day 1	Constipation Score; Cycle 27 Day 1	Constipation Score; Cycle 28 Day 1	Constipation Score; Cycle 29 Day 1	Constipation Score; Cycle 30 Day 1	Constipation Score; Cycle 31 Day 1	Constipation Score; Off-treatment Visit	Diarrhea Score; Baseline	Diarrhea Score; Cycle 2 Day 1	Diarrhea Score; Cycle 3 Day 1	Diarrhea Score; Cycle 4 Day 1	Diarrhea Score; Cycle 5 Day 1	Diarrhea Score; Cycle 6 Day 1	Diarrhea Score; Cycle 7 Day 1	Diarrhea Score; Cycle 8 Day 1	Diarrhea Score; Cycle 9 Day 1	Diarrhea Score; Cycle 10 Day 1	Diarrhea Score; Cycle 11 Day 1	Diarrhea Score; Cycle 12 Day 1	Diarrhea Score; Cycle 13 Day 1	Diarrhea Score; Cycle 14 Day 1	Diarrhea Score; Cycle 15 Day 1	Diarrhea Score; Cycle 16 Day 1	Diarrhea Score; Cycle 17 Day 1	Diarrhea Score; Cycle 18 Day 1	Diarrhea Score; Cycle 19 Day 1	Diarrhea Score; Cycle 20 Day 1	Diarrhea Score; Cycle 21 Day 1	Diarrhea Score; Cycle 22 Day 1	Diarrhea Score; Cycle 23 Day 1	Diarrhea Score; Cycle 24 Day 1	Diarrhea Score; Cycle 25 Day 1	Diarrhea Score; Cycle 26 Day 1	Diarrhea Score; Cycle 27 Day 1	Diarrhea Score; Cycle 28 Day 1	Diarrhea Score; Cycle 29 Day 1	Diarrhea Score; Cycle 30 Day 1	Diarrhea Score; Cycle 31 Day 1	Diarrhea Score; Off-treatment Visit	Financial Difficulties Score; Baseline	Financial Difficulties Score; Cycle 2 Day 1	Financial Difficulties Score; Cycle 3 Day 1	Financial Difficulties Score; Cycle 4 Day 1	Financial Difficulties Score; Cycle 5 Day 1	Financial Difficulties Score; Cycle 6 Day 1	Financial Difficulties Score; Cycle 7 Day 1	Financial Difficulties Score; Cycle 8 Day 1	Financial Difficulties Score; Cycle 9 Day 1	Financial Difficulties Score; Cycle 10 Day 1	Financial Difficulties Score; Cycle 11 Day 1	Financial Difficulties Score; Cycle 12 Day 1	Financial Difficulties Score; Cycle 13 Day 1	Financial Difficulties Score; Cycle 14 Day 1	Financial Difficulties Score; Cycle 15 Day 1	Financial Difficulties Score; Cycle 16 Day 1	Financial Difficulties Score; Cycle 17 Day 1	Financial Difficulties Score; Cycle 18 Day 1	Financial Difficulties Score; Cycle 19 Day 1	Financial Difficulties Score; Cycle 20 Day 1	Financial Difficulties Score; Cycle 21 Day 1	Financial Difficulties Score; Cycle 22 Day 1	Financial Difficulties Score; Cycle 23 Day 1	Financial Difficulties Score; Cycle 24 Day 1	Financial Difficulties Score; Cycle 25 Day 1	Financial Difficulties Score; Cycle 26 Day 1	Financial Difficulties Score; Cycle 27 Day 1	Financial Difficulties Score; Cycle 28 Day 1	Financial Difficulties Score; Cycle 29 Day 1	Financial Difficulties Score; Cycle 30 Day 1	Financial Difficulties Score; Cycle 31 Day 1	Financial Difficulties Score; Off-treatment Visit
Lenvatinib 14 mg + Everolimus 5 mg	63.35	58.60	56.43	58.71	59.38	58.75	58.72	58.68	58.97	63.13	60.87	57.81	59.39	61.56	62.98	61.59	60.88	59.68	58.33	58.95	57.05	62.72	60	64.44	58.33	59.38	59.72	58.33	56.25	54.17	33.33	51.04	76.36	73.54	72.74	70.90	72.80	72.17	73.02	72.77	74.54	75.06	73.72	75.52	74.55	75.78	75.45	73.46	71.85	75.48	76.67	73.09	74.62	80.35	79.56	77.33	72.78	76.67	76.67	78.33	78.33	76.67	80	64.50	73.78	68.25	67	66.67	67.32	68.16	66.51	68.20	67.58	68.52	69.57	70.51	69.64	71.09	72.73	70.33	65.74	67.74	67.28	70.37	69.23	75.44	73.33	78.89	77.78	75	77.78	79.17	75	87.50	66.67	60.97	79.35	79.41	78.47	78.26	75.85	80.60	77.18	79.08	78.75	80.04	82.25	81.51	79.32	81.35	80.30	81.50	79.63	81.90	81.17	80.25	81.73	85.09	86.67	88.89	83.33	77.08	80.56	75	75	75	66.67	69.62	87.91	87.15	84.45	83.58	83.99	84.71	82.40	81.97	83.70	85.39	84.06	85.42	83.93	85.71	84.85	83.74	82.87	83.87	80.25	82.10	81.41	88.60	83.33	84.44	84.72	89.58	83.33	91.67	91.67	87.50	83.33	75.21	77.29	73.46	72.04	71.43	71.78	70.80	71.70	70.24	72.16	72.43	73.91	76.56	72.92	72.79	72.73	73.17	70.37	76.88	74.07	75.31	73.72	79.82	82.22	83.33	87.50	83.33	80.56	83.33	79.17	70.83	100	64.58	31.32	39.21	40.09	40.21	37.54	38.80	38.06	36.14	35.90	34.57	32.37	32.82	35.52	30.84	28.03	33.33	33.33	34.05	37.04	34.57	34.19	26.32	26.67	28.15	33.33	26.39	27.78	22.22	22.22	25	33.33	43.47	7.60	11.50	14.86	15.80	12.07	12.74	12.46	13.10	12.27	15.02	11.11	12.82	12.20	14.97	14.02	11.38	14.35	10.75	16.67	16.67	12.82	7.02	5.56	6.67	13.89	4.17	5.56	12.50	16.67	8.33	16.67	13.33	23.39	26.79	27.63	26.67	29.04	26.29	28.04	27.38	27.11	26.95	27.29	26.41	24.40	22.11	24.24	29.67	27.78	25.27	31.48	29.63	26.92	23.68	21.11	22.22	27.78	27.08	25	25	25	25	33.33	28.33	21.18	18.90	20.63	19.90	19.16	16.67	19.37	19.24	15.93	17.92	18.63	13.54	13.69	15.65	15.15	16.26	15.74	16.13	15.38	23.46	15.38	17.54	13.33	20	22.22	16.67	11.11	16.67	25	16.67	33.33	24.68	23.08	26.11	30.39	26.57	23.02	24.86	25.08	26.46	25.56	24.58	24.02	23.44	21.43	18.06	18.94	20.33	17.59	27.96	24.69	25.93	23.08	21.05	26.67	24.44	16.67	16.67	22.22	25	25	25	33.33	32.05	15.79	26.79	31.97	32.09	30.47	30.35	29.28	29.25	29.30	27.57	24.15	22.05	23.21	19.73	17.42	23.58	20.37	19.35	19.75	23.46	23.08	17.54	17.78	13.33	19.44	29.17	16.67	8.33	16.67	8.33	0	29.58	15.98	10.40	9.52	11.11	12.24	8.47	11.01	9.62	6.23	6.58	6.76	5.64	3.64	5.44	5.43	5.98	11.11	7.53	9.88	8.64	8.97	7.02	6.67	4.44	5.56	8.33	16.67	25.00	25.00	16.67	33.33	13.33	6.43	22.29	32.21	35.59	28.61	31.96	33.64	29.55	34.43	29.22	28.02	28.49	26.19	26.53	29.55	20.33	21.30	21.51	23.46	19.75	20.51	17.54	15.56	11.11	19.44	25.00	33.33	16.67	8.33	16.67	33.33	18.33	21.76	21.08	23.13	22.90	22.93	25.00	30.16	25.43	25.56	22.50	26.26	24.87	23.03	20.83	21.71	21.67	23.81	17.20	18.52	16.05	19.23	24.56	17.78	17.78	16.67	20.83	16.67	25.00	25.00	25.00	0	31.65

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Objective Response Rate (ORR)

ORR was defined as the percentage of participants with a BOR of CR or PR at the at the end of treatment based on investigator assessment according to RECIST v1.1. CR: defined as the disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis to <10 mm. PR: defined as at least a 30 % decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. To be considered a BOR, all responses had to be confirmed no less than 4 weeks after the initial assessment of response. (NCT03173560)
Timeframe: From date of randomization up to first documentation of PD or date of death, whichever occurred first or up to the date of data cut off for the primary analysis (up to 29 months)

Intervention	percentage of participants (Number)
Lenvatinib 14 mg + Everolimus 5 mg	34.6
Lenvatinib 18 mg + Everolimus 5 mg	40.6

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HRQoL Assessed by European Quality of Life (EuroQol) Five-Dimensional, 3-Level (EQ-5D-3L) Index Score and Visual Analogue Scale (VAS)

Intervention	score on a scale (Mean)
	EQ-5D Index Score; Baseline	EQ-5D Index Score; Cycle 2 Day 1	EQ-5D Index Score; Cycle 3 Day 1	EQ-5D Index Score; Cycle 4 Day 1	EQ-5D Index Score; Cycle 5 Day 1	EQ-5D Index Score; Cycle 6 Day 1	EQ-5D Index Score; Cycle 7 Day 1	EQ-5D Index Score; Cycle 8 Day 1	EQ-5D Index Score; Cycle 9 Day 1	EQ-5D Index Score; Cycle 10 Day 1	EQ-5D Index Score; Cycle 11 Day 1	EQ-5D Index Score; Cycle 12 Day 1	EQ-5D Index Score; Cycle 13 Day 1	EQ-5D Index Score; Cycle 14 Day 1	EQ-5D Index Score; Cycle 15 Day 1	EQ-5D Index Score; Cycle 16 Day 1	EQ-5D Index Score; Cycle 17 Day 1	EQ-5D Index Score; Cycle 18 Day 1	EQ-5D Index Score; Cycle 19 Day 1	EQ-5D Index Score; Cycle 20 Day 1	EQ-5D Index Score; Cycle 21 Day 1	EQ-5D Index Score; Cycle 22 Day 1	EQ-5D Index Score; Cycle 23 Day 1	EQ-5D Index Score; Cycle 24 Day 1	EQ-5D Index Score; Cycle 25 Day 1	EQ-5D Index Score; Cycle 26 Day 1	EQ-5D Index Score; Cycle 27 Day 1	EQ-5D Index Score; Cycle 28 Day 1	EQ-5D Index Score; Cycle 29 Day 1	EQ-5D Index Score; Cycle 30 Day 1	EQ-5D Index Score; Cycle 31 Day 1	EQ-5D Index Score; Off-treatment Visit	EQ-VAS Score; Baseline	EQ-VAS Score; Cycle 2 Day 1	EQ-VAS Score; Cycle 3 Day 1	EQ-VAS Score; Cycle 4 Day 1	EQ-VAS Score; Cycle 5 Day 1	EQ-VAS Score; Cycle 6 Day 1	EQ-VAS Score; Cycle 7 Day 1	EQ-VAS Score; Cycle 8 Day 1	EQ-VAS Score; Cycle 9 Day 1	EQ-VAS Score; Cycle 10 Day 1	EQ-VAS Score; Cycle 11 Day 1	EQ-VAS Score; Cycle 12 Day 1	EQ-VAS Score; Cycle 13 Day 1	EQ-VAS Score; Cycle 14 Day 1	EQ-VAS Score; Cycle 15 Day 1	EQ-VAS Score; Cycle 16 Day 1	EQ-VAS Score; Cycle 17 Day 1	EQ-VAS Score; Cycle 18 Day 1	EQ-VAS Score; Cycle 19 Day 1	EQ-VAS Score; Cycle 20 Day 1	EQ-VAS Score; Cycle 21 Day 1	EQ-VAS Score; Cycle 22 Day 1	EQ-VAS Score; Cycle 23 Day 1	EQ-VAS Score; Cycle 24 Day 1	EQ-VAS Score; Cycle 25 Day 1	EQ-VAS Score; Cycle 26 Day 1	EQ-VAS Score; Cycle 27 Day 1	EQ-VAS Score; Cycle 28 Day 1	EQ-VAS Score; Cycle 29 Day 1	EQ-VAS Score; Cycle 30 Day 1	EQ-VAS Score; Cycle 31 Day 1	EQ-VAS Score; Off-treatment Visit
Lenvatinib 14 mg + Everolimus 5 mg	0.76	0.76	0.73	0.73	0.73	0.73	0.71	0.75	0.73	0.76	0.77	0.77	0.76	0.77	0.76	0.73	0.73	0.76	0.69	0.70	0.73	0.74	0.74	0.75	0.70	0.72	0.77	0.73	0.74	0.61	0.87	0.61	68.57	66.05	66.22	65.69	65.86	65.53	65.74	64.16	65.51	66.92	67.74	66.46	65.64	66.41	67.05	66.54	65.78	64.70	62.15	62.70	62.12	65.21	67.73	65.27	60.58	64.13	61.83	54.25	52.75	51.75	35	58.48

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Objective Response Rate at Week 24 (ORR24W)

ORR24W was defined as the percentage of participants with a best overall response (BOR) of complete response (CR) or partial response (PR) at the Week 24 (after randomization) time point, during treatment or within 28 days after the last dose date but on or prior to the start of new anticancer therapy based on investigator assessment according to Response Evaluation Criteria In Solid Tumors (RECIST) version 1.1. CR: defined as the disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis to less than (<) 10 millimeters (mm). PR: defined as at least a 30 percent (%) decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. To be considered a BOR, all responses had to be confirmed no less than 4 weeks after the initial assessment of response. (NCT03173560)
Timeframe: At Week 24

Intervention	percentage of participants (Number)
Lenvatinib 14 mg + Everolimus 5 mg	32.1
Lenvatinib 18 mg + Everolimus 5 mg	34.8

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Percentage of Participants With Intolerable Grade 2 or Any Grade >=Grade 3 TEAEs Within 24 Weeks

TEAE was defined as an adverse event (AE) with an onset that had occurred after receiving study drug. A severity grade was defined by the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 4.03. As per NCI-CTCAE, Grade 1 scales as Mild; Grade 2 scales as Moderate; Grade 3 scales as severe or medically significant but not immediately life threatening; Grade 4 scales as life-threatening consequences; and Grade 5 scales as death related to AE. (NCT03173560)
Timeframe: Up to Week 24

Intervention	percentage of participants (Number)
Lenvatinib 14 mg + Everolimus 5 mg	82.8
Lenvatinib 18 mg + Everolimus 5 mg	79.6

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Percentage of Participants Who Discontinued Treatment Due to Toxicity

Percentage of participants who discontinued treatment due to toxicity, defined as the percentage of participants who discontinued study treatment due to TEAEs. Toxicity (except hypertension and non-infectious pneumonitis) was assessed according to NCI-CTCAE v4.03. (NCT03173560)
Timeframe: From date of first dose of study drug up to 28 days after last dose of study drug, or date of data cut off for the primary analysis (up to 29 months)

Intervention	percentage of participants (Number)
Lenvatinib 14 mg + Everolimus 5 mg	15.7
Lenvatinib 18 mg + Everolimus 5 mg	17.5

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Progression-free Survival (PFS)

PFS was defined as the time from the date of randomization to the date of the first documentation of PD by investigator assessment or date of death, whichever occurred first according to RECIST v1.1. PD: at least 20% increase (including an absolute increase of at least 5 millimeter [mm]) in the sum of diameter (SOD) of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. Median PFS was analyzed using the Kaplan-Meier product-limit estimates for each treatment group and presented with 2-sided 95% confidence interval (CI). (NCT03173560)
Timeframe: From the date of randomization to the date of the first documentation of PD or date of death, whichever occurred first or up to date of data cutoff for the primary analysis (up to 29 months)

Intervention	months (Median)
Lenvatinib 14 mg + Everolimus 5 mg	11.1
Lenvatinib 18 mg + Everolimus 5 mg	14.7

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Progression-free Survival After Next Line of Therapy (PFS2)

PFS2, defined as the time from randomization to the date of PD after next line of therapy or death from any cause, whichever occurred first based on investigator assessment according to RECIST v1.1. PD: at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. Median PFS2 was analyzed using the Kaplan-Meier product-limit estimates for each treatment group and presented with 2-sided 95% CI. (NCT03173560)
Timeframe: From the time of randomization to the date of PD after next line of therapy or death from any cause or the date of data cutoff for the primary analysis, whichever occurs first (up to 29 months)

Intervention	months (Median)
Lenvatinib 14 mg + Everolimus 5 mg	18.2
Lenvatinib 18 mg + Everolimus 5 mg	19.5

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Time to Treatment Failure Due to Toxicity

Time to treatment failure due to toxicity was defined as the time from the date of randomization to the date that a participant discontinued study treatment due to TEAEs. Toxicity (except hypertension and non-infectious pneumonitis) was assessed according to CTCAE v4.03. (NCT03173560)
Timeframe: From the date of randomization to the date of discontinuation of study treatment due to TEAEs, or date of data cut off for the primary analysis (up to 29 months)

Intervention	months (Median)
Lenvatinib 14 mg + Everolimus 5 mg	3.15
Lenvatinib 18 mg + Everolimus 5 mg	5.70

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Percentage of Participants Response Rates (Best Overall and Overall)

The best overall response for each patient is determined from the sequence of investigator overall lesion responses according to RECIST 1.1: Complete Response (CR)=disappearance of target lesions, Partial Response (PR) was >=30% decrease in sum of diameter of lesions, Progressive Disease (PD) was >=20% decrease in sum of diameter of lesions, Stable Disease (SD) does not qualify for PR, CR or PD, Unknown=not documented or assessed. To be assigned a best overall response of CR at least two determinations of CR at least 4 weeks apart before progression are required. To be assigned a best overall response of PR at least two determinations of PR or better at least 4 weeks apart before progression (and not qualifying for a CR) are required. The Overall response rate (ORR) is the percentage of patients with a best overall response of confirmed complete (CR) or partial (PR) response. The 95% confidence intervals (CI) were computed using the Clopper-Pearson method (NCT03176238)
Timeframe: Baseline up to approximately 43 weeks for Asian countires and 32 weeks for Non-Asian countries

Intervention	Percentage of participants (Number)
	Complete response (CR)	Partial response (PR)	Stable disease (SD)	Progressive disease (PD)	Unknown (UNK)	Overall response rate (ORR: CR+PR)
Asian Everolimus + Exemestane	1.5	20.1	51.3	18.1	9.0	21.6
Non-Asian Everolimus + Exemestane	0.00	8.3	63.9	19.4	8.3	8.3
Total	1.3	18.3	53.2	18.3	8.9	19.6

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Summary of Number of Participants With Treatment Emergent Adverse Events (TEAE) - All Grades

Adverse events (AEs), serious adverse events (SAEs), changes from baseline in vital signs and laboratory results (hematology, blood chemistry, lipid profile) qualifying and reported as AEs. Although a patient might had two or more adverse events the patient is only counted once in a category. The same patient might appear in different categories. AESI: Adverse events of special interest. (NCT03176238)
Timeframe: Baseline up to approximately 43 weeks for Asian countires and 32 weeks for Non-Asian countries including a 30 day post treatment follow up period

Intervention	Participants (Count of Participants)
	no TEAE	at least 1 TEAE	at least 1 drug-related TEAE	at least 1 serious TEAE (STEAE)	STEAE leading to death	Non-fatal STEAE	at least 1 drug-related STEAE	at least 1 drug-related STEAE - death	at least 1 drug-related non-fatal STEAE	TEAE leading to permanent tx discontinuation	1 TE AESI
Asian Everolimus + Exemestane	4	195	185	59	6	53	28	2	26	25	172
Non-Asian Everolimus + Exemestane	0	36	33	16	4	12	8	1	7	11	34
Total	4	231	218	75	10	65	36	3	33	36	206

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Percent of Participants Event-free Probability Estimates of Deterioration of Eastern Cooperative Oncology Group (ECOG) Performance Status

Time to deterioration of ECOG performance status, from baseline will be assessed using the ECOG Performance Status Scale (Oken, 1982). Time to deterioration is the time from date of start of treatment to the date of the event defined as deterioration. Deterioration is defined as an increase in performance status from 0 to 2 or greater, an increase in performance status from 1-2 to 3 or greater, or death due to any cause. Event-free probability estimate is the estimated probability that a patient will remain event-free up to the specified time point. Event-free probability estimates were are obtained from the Kaplan-Meier survival estimates. (NCT03176238)
Timeframe: Baseline up to approximately 50 weeks

Intervention	percent of participants (Number)
	Week 0 n=199,36,235	Week 20 n=134,18,152	Week 50 n=58,7,65
Asian Everolimus + Exemestane	100.0	95.0	90.6
Non-Asian Everolimus + Exemestane	100.0	79.8	70.4
Total	100.00	92.7	87.6

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Percentage of Participants Clinical Benefit Rate

Clinical benefit rate: Patients with best overall response rate of CR (any duration), PR (any duration) and SD with duration of 24 weeks or longer according to RECIST 1.1 criteria: Complete Response (CR)=disappearance of target lesions, Partial Response (PR) was >=30% decrease in sum of diameter of lesions, Progressive Disease (PD) was >=20% decrease in sum of diameter of lesions, Stable Disease (SD) does not qualify for PR, CR or PD, Unknown=not documented or assessed. Best overall response of CR = at least two determinations of CR at least 4 weeks apart before progression are required. Best overall response of PR = at least two determinations of PR or better at least 4 weeks apart before progression (and not qualifying for a CR) are required. The Overall response rate (ORR) is the percentage of patients with a best overall response of confirmed complete (CR) or partial (PR) response. The 95% confidence intervals (CI) were computed using the Clopper-Pearson method. (NCT03176238)
Timeframe: Baseline up to approximately 43 weeks for Asian countires and 32 weeks for Non-Asian countries

Intervention	Percentage of participants (Number)
Asian Everolimus + Exemestane	48.2
Non-Asian Everolimus + Exemestane	30.6
Total	45.5

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Progression Free Survival (PFS)

"PFS is time from date of start of treatment to date of disease progression or death due to any cause, whichever occurs first.~b Percentiles with 95% CIs are calculated from PROC LIFETEST output using method of Brookmeyer and Crowley (1982)" (NCT03176238)
Timeframe: Baseline up to approximately 43 weeks for Asian countires and 40 weeks for Non-Asian countries

Intervention	weeks (Median)
Asian Everolimus and Exemestane	40.6
Non-Asian Everolimus + Exemestane	37.0
Total	40.6

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Phase 2: Objective Response Rate (ORR)

ORR was defined as the percentage of participants with BOR of CR or PR based on investigator assessment according to RECIST version 1.1 for non-HGG cohorts and RANO for HGG cohort. CR was defined as disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 mm. PR was defined as at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. (NCT03245151)
Timeframe: From the date of the first dose of study drug to the date of first documentation of disease progression or death, which ever occurred first (up to 6.5 months)

Intervention	percentage of participants (Number)
Phase 2: Cohort 1, Ewing Sarcoma	0.0
Phase 2: Cohort 2, Rhabdomyosarcoma	10.0
Phase 2: Cohort 3, HGG	0.0

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Phase 2: Number of Participants With Any Treatment-emergent Serious Adverse Event (TESAE)

A TESAE was any untoward medical occurrence that at any dose: resulted in death; life threatening condition; required inpatient hospitalization or prolongation of existing hospitalization; resulted in persistent or significant disability/incapacity; was a congenital anomaly/birth defect or was medically important due to other reasons than the above mentioned criteria. An adverse event was defined as any untoward medical occurrence in a participant administered an investigational product. (NCT03245151)
Timeframe: From date of first dose up to 28 days after the last dose of study treatment (up to 7.5 months)

Intervention	Participants (Count of Participants)
Phase 2: Cohort 1, Ewing Sarcoma	6
Phase 2: Cohort 2, Rhabdomyosarcoma	8
Phase 2: Cohort 3, HGG	8

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Phase 2: Number of Participants With Any Treatment-emergent Adverse Event (TEAE)

A TEAE was defined as an adverse event that emerged during treatment, having been absent at pretreatment or reemerged during treatment, having been present at pretreatment but stopped before treatment, or worsened in severity during treatment relative to the pretreatment state, when the adverse event is continuous. An adverse event was defined as any untoward medical occurrence in a participant administered an investigational product. (NCT03245151)
Timeframe: From date of first dose up to 28 days after the last dose of study treatment (up to 7.5 months)

Intervention	Participants (Count of Participants)
Phase 2: Cohort 1, Ewing Sarcoma	10
Phase 2: Cohort 2, Rhabdomyosarcoma	19
Phase 2: Cohort 3, HGG	11

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Phase 1: Disease Control Rate (DCR)

DCR was defined as percentage of participants with a confirmed CR, PR, or stable disease (SD) (SD duration >=7 weeks since the first dose of study treatment) divided by number of participants in analysis set. DCR was assessed by an investigator based on RECIST v1.1 for non-HGG participants or RANO for HGG participants. CR: disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 mm. PR: at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD. PD: at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. (NCT03245151)
Timeframe: From first dose of study drug until PD or death, whichever occurred first (up to 16.5 months)

Intervention	percentage of participants (Number)
Phase 1: Lenvatinib 8 mg/m^2 + Everolimus 3 mg/m^2	20.0
Phase 1: Lenvatinib 11 mg/m^2 + Everolimus 3 mg/m^2	50.0

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Phase 2: Duration of Response (DOR)

DOR was defined as the time (in months) from the date of first observation of confirmed response (PR or CR) to the date of the first observation of progression based on the investigator's assessment utilizing RECIST 1.1 for non-HGG cohorts and RANO for HGG cohort, or date of death, whatever the cause. CR: disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 mm. PR: at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. PD was defined as at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. (NCT03245151)
Timeframe: From date of the first observation of CR or PR until the date of first observation of progression or date of death (up to 6.5 months)

Intervention	months (Median)
Phase 2: Cohort 2, Rhabdomyosarcoma	2.4

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Phase 2: Disease Control Rate (DCR)

DCR was defined as percentage of participants with confirmed CR, PR, or SD (SD duration greater than or equal to [>=] 7 weeks since first dose of study treatment) divided by number of participants in analysis set. DCR was assessed by investigator based on RECIST v1.1 for non-HGG cohorts or RANO for HGG cohort. CR: disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 mm. PR: at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD. PD: at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. (NCT03245151)
Timeframe: From first dose of study drug until PD or death, whichever occurred first (up to 6.5 months)

Intervention	percentage of participants (Number)
Phase 2: Cohort 1, Ewing Sarcoma	40.0
Phase 2: Cohort 2, Rhabdomyosarcoma	40.0
Phase 2: Cohort 3, HGG	30.0

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Phase 2: Clinical Benefit Rate (CBR)

CBR was defined as percentage of participants who had BOR of CR, PR, or durable SD (SD duration >=23 weeks since the first dose of study treatment) divided by number of participants in analysis set. CBR was assessed by an investigator based on RECIST v1.1 for non-HGG cohorts or RANO for HGG cohort. CR: disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 mm. PR: at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD. PD: at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. (NCT03245151)
Timeframe: From first dose of study drug until PD or death, whichever occurred first (up to 6.5 months)

Intervention	percentage of participants (Number)
Phase 2: Cohort 1, Ewing Sarcoma	20.0
Phase 2: Cohort 2, Rhabdomyosarcoma	10.0
Phase 2: Cohort 3, HGG	0.0

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Phase 1: Recommended Phase 2 Dose (RP2D) of Lenvatinib in Combination With Everolimus

The RP2D of lenvatinib in combination with everolimus was determined by Dose Escalation Committee (DEC) based on safety (including DLTs), pharmacokinetic and clinical data. DLT was graded according to CTCAE v4.03. (NCT03245151)
Timeframe: Cycle 1 (Each cycle was of 28 days)

Intervention	mg/m^2 (Number)
Phase 1: Lenvatinib + Everolimus (All Participants)	11

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Phase 1: Objective Response Rate (ORR)

Intervention	percentage of participants (Number)
Phase 1: Lenvatinib 8 mg/m^2 + Everolimus 3 mg/m^2	0.0
Phase 1: Lenvatinib 11 mg/m^2 + Everolimus 3 mg/m^2	0.0

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Phase 1: Number of Participants With Any Treatment-emergent Serious Adverse Event (TESAE)

Intervention	Participants (Count of Participants)
Phase 1: Lenvatinib 8 mg/m^2 + Everolimus 3 mg/m^2	2
Phase 1: Lenvatinib 11 mg/m^2 + Everolimus 3 mg/m^2	12

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Phase 1: Number of Participants With Any Treatment-emergent Adverse Event (TEAE)

Intervention	Participants (Count of Participants)
Phase 1: Lenvatinib 8 mg/m^2 + Everolimus 3 mg/m^2	5
Phase 1: Lenvatinib 11 mg/m^2 + Everolimus 3 mg/m^2	18

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Phase 1: Maximum Tolerated Dose (MTD) of Lenvatinib in Combination With Everolimus

MTD was defined as the highest dose level at which no more than 1/6 participants experienced a dose limiting toxicity (DLTs), with the next higher dose having at least 0 of 3 or 1 of 6 participants experiencing DLTs. DLT was graded according to common terminology criteria for adverse events (CTCAE) version 4.03. (NCT03245151)
Timeframe: Cycle 1 (Each cycle was of 28 days)

Intervention	milligram per square meter (mg/m^2) (Number)
Phase 1: Lenvatinib + Everolimus (All Participants)	11

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Phase 1: Clinical Benefit Rate (CBR)

CBR was defined as percentage of participants who had BOR of CR, PR, or durable SD (SD duration >=23 weeks since the first dose of study treatment) divided by number of participants in analysis set. CBR was assessed by an investigator based on RECIST v1.1 for non-HGG participants or RANO for HGG participants. CR: disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis <10 mm. PR: at least a 30% decrease in the SOD of target lesions, taking as reference the baseline sum diameters. SD: neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest SOD. PD: at least 20% increase (including an absolute increase of at least 5 mm) in the SOD of target lesions, taking as reference the smallest sum and/or unequivocal progression of existing non-target lesions and/or appearance of 1 or more new lesions. (NCT03245151)
Timeframe: From first dose of study drug until PD or death, whichever occurred first (up to 16.5 months)

Intervention	percentage of participants (Number)
Phase 1: Lenvatinib 8 mg/m^2 + Everolimus 3 mg/m^2	20.0
Phase 1: Lenvatinib 11 mg/m^2 + Everolimus 3 mg/m^2	22.2

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Phase 1: Trough Concentrations (Ctrough) of Everolimus When Administered in Combination With Lenvatinib

Trough concentrations of everolimus was quantified using validated liquid LC-MS/MS methods. (NCT03245151)
Timeframe: Cycle 1 Days 1, 2, 15 and 22: Pre-dose (Cycle length=28 days)

Intervention	ng/mL (Mean)
	Cycle 1 Day 1: Pre-dose	Cycle 1 Day 2: Pre-dose	Cycle 1 Day 15: Pre-dose	Cycle 1 Day 22: Pre-dose
Phase 1: Lenvatinib 11 mg/m^2 + Everolimus 3 mg/m^2	0.0	2.2	5.1	4.2
Phase 1: Lenvatinib 8 mg/m^2 + Everolimus 3 mg/m^2	0.0	2.1	3.2	2.8

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Phase 1: Time to Reach Maximum Plasma Concentration (Cmax) of Lenvatinib (Tmax)

Tmax of lenvatinib was quantified using validated liquid LC-MS/MS methods. (NCT03245151)
Timeframe: Cycle 1 Days 1 and 15: 0-8 hours post-dose (Cycle length=28 days)

Intervention	hours (Median)
	Cycle 1 Day 1	Cycle 1 Day 15
Phase 1: Lenvatinib 11 mg/m^2 + Everolimus 3 mg/m^2	2.890	2.950
Phase 1: Lenvatinib 8 mg/m^2 + Everolimus 3 mg/m^2	3.000	3.950

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Phase 1: Maximum Plasma Concentration of Lenvatinib (Cmax)

Cmax of lenvatinib was quantified using validated liquid LC-MS/MS methods. (NCT03245151)
Timeframe: Cycle 1 Days 1 and 15: 0-8 hours post-dose (Cycle length=28 days)

Intervention	nanogram per milliliter (ng/mL) (Mean)
	Cycle 1 Day 1	Cycle 1 Day 15
Phase 1: Lenvatinib 11 mg/m^2 + Everolimus 3 mg/m^2	404.13	447.62
Phase 1: Lenvatinib 8 mg/m^2 + Everolimus 3 mg/m^2	240.20	314.20

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Phase 1: Area Under the Plasma Concentration-time Curve From Time Zero to Time of Last Quantifiable Concentration of Lenvatinib (AUC[0-t Hours])

AUC0-t of lenvatinib was quantified using validated liquid chromatography tandem mass spectrometry (LC-MS/MS) methods. (NCT03245151)
Timeframe: Cycle 1 Days 1 and 15: 0-8 hours post-dose (Cycle length=28 days)

Intervention	nanogramhour per milliliter (nghr/mL) (Mean)
	Cycle 1 Day 1	Cycle 1 Day 15
Phase 1: Lenvatinib 11 mg/m^2 + Everolimus 3 mg/m^2	3281.1	2139.8
Phase 1: Lenvatinib 8 mg/m^2 + Everolimus 3 mg/m^2	2338.0	1328.0

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Phase 2: Objective Response Rate (ORR) at Week 16

ORR at Week 16 was defined as the percentage of participants with a best overall response (BOR) of complete response (CR) or partial response (PR) at Week 16 based on investigator assessment according to response evaluation criteria in solid tumors (RECIST) version 1.1 for non-HGG cohorts and response assessment in neuro-oncology (RANO) for HGG cohort. CR was defined as disappearance of all target and non-target lesions (non-lymph nodes). All pathological lymph nodes (whether target or non-target) must have a reduction in their short axis less than (<) 10 millimeter (mm). PR was defined as at least a 30 percent (%) decrease in the sum of diameter (SOD) of target lesions, taking as reference the baseline sum diameters. (NCT03245151)
Timeframe: Week 16

Intervention	percentage of participants (Number)
Phase 2: Cohort 1, Ewing Sarcoma	0.0
Phase 2: Cohort 2, Rhabdomyosarcoma	10.0
Phase 2: Cohort 3, HGG	0

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Progression-free Survival in Participants With Newly Diagnosed High-grade Glioma (HGG)

Percentage of participants without progression, defined as 25% increase in the size of the tumor or appearance of new lesions. (NCT03352427)
Timeframe: 12 months

Intervention	percentage of participants (Number)
Dasatinib+Everolimus	0

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Progression-free Survival in Participants With Newly Diagnosed Diffuse Intrinsic Pontine Glioma (DIPG)

Percentage of participants without progression, defined as 25% increase in the size of the tumor or appearance of new lesions. (NCT03352427)
Timeframe: 8 months

Intervention	percentage of participants (Number)
Dasatinib+Everolimus	0

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Overall Survival

Percentage of patients alive at one year. (NCT03352427)
Timeframe: 1 year

Intervention	percentage of participants (Number)
Dasatinib+Everolimus	0

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Overall Response Rate (OR) (Partial Response or Better) in Participants With Refractory or Recurrent Glioma

The overall response assessment will take into account response in both target and non-target lesions, as well as the appearance of new lesions. Partial Response (PR) will be defined as ≥50% decrease in size of tumor in comparison to baseline measurements. Complete Response (CR) will be defined as the disappearance of all abnormal signal. This includes return to normal size of the brain stem for brain stem lesions. Reported as percentage of participants with partial or better response at 56 days. (NCT03352427)
Timeframe: 56 Days

Intervention	percentage of participants (Number)
Dasatinib+Everolimus	0

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Overall Survival

Percentage of participants alive at 2 years. (NCT03352427)
Timeframe: up to 17 months

Intervention	percentage of participants (Number)
Dasatinib+Everolimus	0

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Ribociclib Half-Life as Obtained From the Phase 1 Study

Ribociclib plasma concentration-time data obtained from patients received Phase I defined treatment will be modeled using compartmental approaches to estimate the half-life (hrs) for each dose level on days 1 and 17 of course 1. Patients who were enrolled in the Surgical stratum but subsequently received Phase I defined treatment with PK data available will also be included in the analysis population. 5 patients from surgical stratum received dose level 1 treatment. (NCT03387020)
Timeframe: Pre-dose, 1, 2, 4, 8, 24, 32 (day 1 course 1 only), & 48 (day 1 course 1 only) hours after dose on days 1 and 17 of course 1.

Intervention	hours (Median)
Dose Level 1, Day 1 of Course 1	11.7
Dose Level 1, Day 17 of Course 1	8.9
Dose Level 2, Day 1 of Course 1	8.5
Dose Level 2, Day 17 of Course 1	7.5

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Maximum Tolerated Dose of Ribociclib and Everolimus

Defined as the highest dose level at which six patients have been treated with at most one patient experiencing a dose limiting toxicity (DLT) and the next higher dose level has been determined to be too toxic. Will be estimated using a Rolling-6 phase I design. Only patients who are evaluable for DLT will be consider for estimating of Maximum Tolerated Dose. Patient who were enrolled under Surgical cohort but received sufficient study defined treatment would also be evaluable for DLT. (NCT03387020)
Timeframe: 4 weeks

Intervention	mg/m^2/day (Number)
	Ribociclib	Everolumus
DLT Evaluable Set	120	1.2

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Average Tumor and Plasma Concentrations of Ribociclib for the Surgical Study

Average tumor Ribociclib concentrations will be compared to plasma concentrations. The mean tumor-to-plasma ratio of Ribociclib at the time of surgery will be described. (NCT03387020)
Timeframe: Surgical study: Prior to starting ribociclib (day -7 or -10), prior to ribociclib dose on days -5 & -2, day 0, and at the time of surgery

Intervention	ratio (Median)
Surgical	14.6

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Everolimus Half Life as Obtained From the Phase 1 Study

Everolimus plasma concentration-time data obtained from patients received Phase I defined treatment will be modeled using compartmental approaches to estimate the half-life (hrs) for each dose level on day 17 of course 1 and day 1 of course 2. Patients who were enrolled in the Surgical stratum but subsequently received Phase I defined treatment with PK data available will also be included in the analysis population. 5 patients from surgical stratum received dose level 1 treatment. (NCT03387020)
Timeframe: Pre-dose, 0.5 (course 2 only), 1, 1.5 (course 2 only), 2, 4, 6 (course 2 only), 8, & 24 hours after dose on day 17 of course 1, and day 1 of course 2

Intervention	hours (Median)
Dose Level 1, Day 17 of Course 1	13.5
Dose Level 1, Day 1 of Course 2	14.5
Dose Level 2, Day 17 of Course 1	11.2
Dose Level 2, Day 1 of Course 2	11.5

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Objective Responses (Complete Response + Partial Response)

Number of patients with sustained objective responses will be reported by stratum and dose. Objective response refers to at least 50% reduction in 2 dimensional measurements of the tumor. In order to count towards this objective, any response needs to be sustained for at least 8 weeks. (NCT03387020)
Timeframe: Up to 2 years

Intervention	Participants (Count of Participants)
Phase I, Dose Level 1	0
Phase I, Dose Level 2	0
Surgical	0

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Percent Change in ki67 Between Archival and Post-treatment Tissue

For the surgical study, Ki67 will be evaluated in paired pre-treatment tumor (diagnostic) and post-treatment tumor (recurrent) tissue in consenting patients to assess percent change. The percent of Ki67 in tumor tissues will be measured and the result is presented as the percent of Ki67 in post-treatment tumor minus the percent of Ki67 measured in pre-treatment tumor. (NCT03387020)
Timeframe: Up to 2 years

Intervention	Change of Percentage of Ki67 in Tumor (Median)
Surgical	-20

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Everolimus AUC (Area Under the Plasma Concentration Versus Time Curve) as Obtained From the Phase I Study

Everolimus plasma concentration-time data obtained from patients who received Phase I defined treatment will be modeled using compartmental approaches to estimate the AUC (hr*nM) for each dose level on day 17 of course 1 and day 1 of course 2. Patients who were enrolled in the Surgical stratum but subsequently received Phase I defined treatment with PK data available will also be included in the analysis population. 5 patients from surgical stratum received dose level 1 treatment. (NCT03387020)
Timeframe: Pre-dose, 0.5 (course 2 only), 1, 1.5 (course 2 only), 2, 4, 6 (course 2 only), 8, 24 hours after dose on day 17 of course 1, and day 1 of course 2.

Intervention	hr*nM (Median)
Dose Level 1, Day 17 of Course 1	201
Dose Level 1, Day 1 of Course 2	80.1
Dose Level 2, Day 17 of Course 1	147.5
Dose Level 2, Day 1 of Course 2	59

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Ribociclib AUC (Area Under the Plasma Concentration Versus Time Curve) as Obtained From the Patients Who Received Phase I Defined Treatment

Ribociclib plasma concentration-time data obtained from patients who received Phase I defined treatment will be modeled using compartmental approaches to estimate the AUC (hr*μM) for each dose level on days 1 and 17 of course 1. Patients who were enrolled in the Surgical stratum but subsequently received Phase I defined treatment with PK data available will also be included in the analysis population. 5 patients from surgical stratum received dose level 1 treatment. (NCT03387020)
Timeframe: Pre-dose, 1, 2, 4, 8, 24, 32 (day 1 course 1 only), & 48 (day 1 course 1 only) hours after dose on days 1 and 17 of course 1.

Intervention	hr*uM (Median)
Dose Level 1, Day 1 of Course 1	3.96
Dose Level 1, Day 17 of Course 1	10.3
Dose Level 2, Day 1 of Course 1	12.0
Dose Level 2, Day 17 of Course 1	10.15

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Incidence of Cytomegalovirus Infection or Disease

Incidence of CMV infection/disease in three study groups (SRL, EVR anda MPS). (NCT03468478)
Timeframe: 12 months follow up

Intervention	Participants (Count of Participants)
Sirolimus +Tacrolimus	9
Everolimus +Tacrolimus	7
Mycophenolate +Tacrolimus	39

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Percentage of Participants With Best Overall Response (BOR) Status of Angiomyolipoma (AML) Response During Maximum Treatment Duration of 48 Weeks

"BOR status is the best status recorded from start of treatment until disease progression. AML response status: reduction in AML volume of at least 50% relative to screening AML. In addition, AML response have to satisfy: no new AML ≥ 1 cm in longest diameter are identified, neither kidney increases in volume by more than 20% from nadir (where nadir is the lowest kidney volume at the screening), the participant does not have any angiomyolipoma-related bleeding of grade equal or over 2 (as defined by NCI CTCAE, version 4.03).~Up to five of the largest measurable lesions (≥ 1 cm in longest diameter) in each kidney were measured at screening via Magnetic Resonance Imaging/Computed tomography (MRI/CT) and were defined as screening AML. The sum of the volumes of these individual lesions was defined as AML volume and it was measured at each assessment during the trial. Increases in the AML volume were evidence of worsening AML, decreases were evidence of clinical response." (NCT03525834)
Timeframe: Baseline, 48 weeks

Intervention	Participants (Count of Participants)
Everolimus	28

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Percentage of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)

Percentage of participants with AEs and SAEs including significant changes from baseline in vital signs, electrocardiograms and laboratory parameters (laboratory assessments included hematology, biochemistry, coagulation and urinalysis) qualifying and reported as AEs. The percentage of participants in each category is reported in the table. (NCT03525834)
Timeframe: From the start of treatment to 30 days after end of treatment, assessed up to maximum duration of 52 weeks

Intervention	Participants (Count of Participants)
	AEs	Treatment-related AEs	SAEs	Treatment-related SAEs
Everolimus	40	39	6	2

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Percentage of Participants With Best Overall Response Status of Angiomyolipoma (AML) Progression During Maximum Treatment Duration of 48 Weeks

"AML progression status is defined as one or more of the following: an increase from nadir of 25% or more in AML volume to a value greater than screening AML (where nadir is the lowest AML volume obtained for the participant previously in the trial), the appearance of a new AML ≥ 1.0 cm in longest diameter, an increase from nadir of 20% or more in the volume of either kidney to a value greater than screening (where nadir is the lowest kidney volume obtained for the participant previously in the trial), angiomyolipoma-related bleeding grade ≥2 (as defined by NCI CTCAE, version 4.03).~Up to five of the largest measurable lesions (≥ 1 cm in longest diameter) in each kidney were measured at screening via Magnetic Resonance Imaging/Computed tomography (MRI/CT) and were defined as screening AML. The sum of the volumes of these individual lesions was defined as AML volume and it was measured at each assessment during the trial. Increases in the AML volume were evidence of worsening AML." (NCT03525834)
Timeframe: Baseline, 48 weeks

Intervention	Participants (Count of Participants)
Everolimus	1

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Percentage of Participants With Severe Renal Impairment

"Renal impairment is defined as calculated Creatinine Clearance (CrCl) < 30 mL/min. CrCl was measured at baseline and at four other time points; only the baseline and the worst post-baseline value for every participant were counted (lowest value for CrCl).~Creatinine clearance was estimated using the Cockcroft-Gault formula:~creatinine clearance (mL/minute) = urine creatinine concentration (mL/dL) x volume of urine (mL/24 hour) / plasma creatinine concentration (mg/dL) x 1440 minute/24 hour" (NCT03525834)
Timeframe: Baseline, 48 weeks

Intervention	Participants (Count of Participants)
	Baseline	Post-baseline, 48 weeks
Everolimus	0	1

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Percentage of Participants With NCI CTCA Grade 3/4 Serum Creatinine

NCI CTCAE grade 3/4 serum creatinine is defined as > 3.0 x upper limits of normal (ULN). Serum creatinine was measured at baseline and at four other time points; only the worst post-baseline value for every participant was counted (highest value for serum creatinine). (NCT03525834)
Timeframe: Baseline, 48 weeks

Intervention	Participants (Count of Participants)
	Baseline	Post-baseline, 48 weeks
Everolimus	0	0

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Duration of Disease Control (DC)

"Duration of disease control (DC), defined as the time from randomisation until the earliest of disease progression (according to Response Evaluation Criteria In Solid Tumors (RECIST, version 1.1) in combination with modified MD Anderson Criteria (for bone lesion assessment) or death from any cause, among patients with DC. Duration of DC was assessed by independent reviewers.~The duration of DC was calculated as followed:~For patients with disease progression or death:~Duration of DC [days] = date of outcome - date of randomisation + 1~For patients without disease progression or death:~Duration of DC (censored) [days] = date of outcome - date of randomisation + 1" (NCT03659136)
Timeframe: From randomisation until the earliest of progressive disease or death from any cause, up to 892 days.

Intervention	Months (Median)
1000 mg Xentuzumab + 10 mg Everolimus + 25 mg Exemestane	14.6
Placebo + 10 mg Everolimus + 25 mg Exemestane	18.4

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Overall Survival (OS)

"Overall survival (OS) defined as the time from randomisation until death from any cause. For patients with 'event' as an outcome for OS:~OS[days] = date of outcome - date of randomisation + 1.~For patients with 'censored' as an outcome for OS:~OS (censored)[days] = date of outcome - date of randomisation + 1." (NCT03659136)
Timeframe: From randomisation until death from any cause, up to 995 days.

Intervention	Months (Median)
1000 mg Xentuzumab + 10 mg Everolimus + 25 mg Exemestane	NA
Placebo + 10 mg Everolimus + 25 mg Exemestane	NA

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Progression Free Survival (PFS)

Progression-free survival (PFS) defined as the time from randomisation until progressive disease (PD) according to Response Evaluation Criteria In Solid Tumors (RECIST, version 1.1) in combination with modified MD Anderson Criteria (for bone lesion assessment), based on blinded independent assessment or death from any cause, whichever occurred earlier. As per RECIST, PD is defined as at least a 20% increase in the sum of diameters of target lesions, unequivocal progression of non-target lesions or the appearance of new lesions. (NCT03659136)
Timeframe: From randomisation until the earliest of disease progression, death or the time point of primary PFS analysis, up to 892 days.

Intervention	Months (Median)
1000 mg Xentuzumab + 10 mg Everolimus + 25 mg Exemestane	12.7
Placebo + 10 mg Everolimus + 25 mg Exemestane	11.0

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Time to Pain Progression or Intensification of Pain Palliation

"Time to pain progression or intensification of pain palliation was defined as the time from randomisation until the earliest of:~2 point increase from baseline in the Brief Pain Inventory - Short Form (BPI-SF), Item 3 (worst pain), without a decrease (of ≥1 point) from baseline analgesics use (via the 8-point Analgesic Quantification Algorithm [AQA]), or~2 point increase from baseline in the AQA, or Death." (NCT03659136)
Timeframe: From randomisation until the earliest of pain progression, intensification of pain palliation, death or the time point of progression free survival analysis, up to 843 days.

Intervention	Months (Median)
1000 mg Xentuzumab + 10 mg Everolimus + 25 mg Exemestane	5.6
Placebo + 10 mg Everolimus + 25 mg Exemestane	3.0

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Number of Participants With Objective Response (OR)

Number of participants with objective response (OR) by independent assessment. OR is defined as a best overall response of complete response (CR) or partial response (PR). Best overall response is defined according to RECIST v1.1 in combination with modified MD Anderson Criteria (for bone lesion assessment) and will consider all tumor assessments from randomisation until the earliest of PD, start of subsequent anti-cancer therapy, loss to follow-up, withdrawal of consent or death. To be aligned with the primary endpoint derivation, tumor assessments after two or more consecutively misses assessments were not considered. (NCT03659136)
Timeframe: From randomisation until end of treatment, up to 892 days.

Intervention	Participants (Count of Participants)
1000 mg Xentuzumab + 10 mg Everolimus + 25 mg Exemestane	6
Placebo + 10 mg Everolimus + 25 mg Exemestane	5

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Number of Patients With Disease Control (DC)

Disease control (DC) was defined as a best overall response (BOR) of either complete response (CR), partial response (PR), stable disease (SD) or Non-CR/No-PD. SD and Non-CR/Non-PR must have been observed up until at least week 24 tumor assessment. BOR was defined according to RECIST v1.1 in combination with modified MD Anderson Criteria (for bone lesion assessment) based on all evaluable tumor assessments from randomisation until the earliest of PD, start of subsequent anti-cancer therapy, loss to follow-up, withdrawal of consent or death. To be aligned with the primary endpoint derivation, tumor assessments after two or more consecutively misses assessments were not considered. DC was assessed by independent reviewers. (NCT03659136)
Timeframe: From randomisation until the earliest of progressive disease or death from any cause, up to 892 days.

Intervention	Participants (Count of Participants)
1000 mg Xentuzumab + 10 mg Everolimus + 25 mg Exemestane	29
Placebo + 10 mg Everolimus + 25 mg Exemestane	25

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Severity of Mouth Pain Scores by Ethnicity

Average Area Under the Curve per assessment (aAUCpa) of mouth pain scores as measured by NAMPS will be computed for each patient to summarize the sequence of numerical analogue mouth pain scores over the eight week study period. Scores are reported on a 0-100 scale, where 100 = better outcome QOL (i.e. less pain). The aAUCpa is the average of each AUC between each sequential assessment from treatment-initiation to the end of the treatment at 8 weeks post-treatment-initiation and will be compared between the two treatment arms. (NCT03839940)
Timeframe: Up to 8 weeks

Intervention	scores on scale * days (Mean)
	Not Hispanic or Latino	Other
Group I (Dexamethasone)	12.1	0.0
Group II (Placebo)	4.9	0.0

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Severity of Mouth Pain Scores by Sex

Intervention	scores on scale * days (Mean)
	Female	Male
Group I (Dexamethasone)	11.4	11.0
Group II (Placebo)	2.7	18.8

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Incidence Rate of the mTOR Inhibitor-associated Stomatitis (mIAS)-Related Pain Based on Daily Self-reports Via the Numerical Analogue Scale by Ethnicity.

"NIH-required analysis. The numerical analogue mouth pain score (NAMPS) is a single item measured on a 0 to 10 scale, with 0 corresponding to No pain and 10 corresponding to Pain as bad as it can be. Will compare the incidence rate of any mouth pain (i.e., any score greater than 0) as assessed by the NAMPS between the prevention versus early treatment approaches using a Chi-square test." (NCT03839940)
Timeframe: Up to 8 weeks

Intervention	Participants (Count of Participants)
	Not Hispanic or Latino72443917		Not Hispanic or Latino72443916	Other72443917	Other72443916
	No Pain	Pain
Group I (Dexamethasone)	6
Group II (Placebo)	7
Group I (Dexamethasone)	9
Group II (Placebo)	9
Group I (Dexamethasone)	1
Group II (Placebo)	1
Group I (Dexamethasone)	0
Group II (Placebo)	0

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Incidence Rate of the mTOR Inhibitor-associated Stomatitis (mIAS)-Related Pain Based on Daily Self-reports Via the Numerical Analogue Scale by Race

Intervention	Participants (Count of Participants)
	Black or African American72443916		Black or African American72443917	White72443916	White72443917
	No Pain	Pain
Group I (Dexamethasone)	1
Group II (Placebo)	0
Group I (Dexamethasone)	3
Group II (Placebo)	1
Group I (Dexamethasone)	6
Group II (Placebo)	8

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Incidence Rate of the mTOR Inhibitor-associated Stomatitis (mIAS)-Related Pain Based on Daily Self-reports Via the Numerical Analogue Scale by Sex

Intervention	Participants (Count of Participants)
	Female72443916		Female72443917	Male72443916	Male72443917
	No Pain	Pain
Group I (Dexamethasone)	5
Group II (Placebo)	8
Group I (Dexamethasone)	7
Group II (Placebo)	7
Group I (Dexamethasone)	2
Group II (Placebo)	0
Group II (Placebo)	2

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Severity of Mouth Pain Scores

Intervention	scores on scale * days (Mean)
Group I (Dexamethasone)	11.3
Group II (Placebo)	4.6

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Severity of Mouth Pain Scores by Race

Intervention	scores on scale * days (Mean)
	Black or African American	White
Group I (Dexamethasone)	9.3	12.0
Group II (Placebo)	7.9	4.4

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Incidence of Acute Rejection

Biopsy-proven according to Banff 2017 criteria (NCT04177095)
Timeframe: Through study completion, 1 year

Intervention	Participants (Count of Participants)
Belatacept Treated Patients	0

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Incidence of de Novo Donor Specific Antibodies

Screened for using Luminex platform (NCT04177095)
Timeframe: At 12 months

Intervention	Participants (Count of Participants)
Belatacept Treated Patients	0

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Rate of New-onset Proteinuria

Defined as g/g creatinine, measured on random urine sample (NCT04177095)
Timeframe: At 12 months

Intervention	Participants (Count of Participants)
Belatacept Treated Patients	1

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Survival

Overall and death-censored graft survival (NCT04177095)
Timeframe: At 12 months

Intervention	Participants (Count of Participants)
Belatacept Treated Patients	12

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Incidence of Acute Rejection

Biopsy-proven according to Banff 2017 criteria (NCT04177095)
Timeframe: Enrollment through 12 months

Intervention	Participants (Count of Participants)
Belatacept Treated Patients	0

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Increase in eGFR

Calculated using CKD-EPI formula (NCT04177095)
Timeframe: From baseline to 12 months

Intervention	Participants (Count of Participants)
Belatacept Treated Patients	6

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Substance	Relationship Strength	Studies	Trials	Classes	Roles
phosphoserine Phosphoserine: The phosphoric acid ester of serine.	2.21	1	0	non-proteinogenic alpha-amino acid; O-phosphoamino acid; serine derivative	human metabolite
gamma-aminobutyric acid gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.. gamma-aminobutyric acid : A gamma-amino acid that is butanoic acid with the amino substituent located at C-4.	2	1	0	amino acid zwitterion; gamma-amino acid; monocarboxylic acid	human metabolite; neurotransmitter; Saccharomyces cerevisiae metabolite; signalling molecule
adenine [no description available]	5.68	9	0	6-aminopurines; purine nucleobase	Daphnia magna metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
beta-alanine [no description available]	2.03	1	0	amino acid zwitterion; beta-amino acid	agonist; fundamental metabolite; human metabolite; inhibitor; neurotransmitter
benzyl alcohol Benzyl Alcohol: A colorless liquid with a sharp burning taste and slight odor. It is used as a local anesthetic and to reduce pain associated with LIDOCAINE injection. Also, it is used in the manufacture of other benzyl compounds, as a pharmaceutic aid, and in perfumery and flavoring.. hydroxytoluene : Any member of the class of toluenes carrying one or more hydroxy substituents.. benzyl alcohol : An aromatic alcohol that consists of benzene bearing a single hydroxymethyl substituent.. aromatic alcohol : Any alcohol in which the alcoholic hydroxy group is attached to a carbon which is itself bonded to an aromatic ring.. aromatic primary alcohol : Any primary alcohol in which the alcoholic hydroxy group is attached to a carbon which is itself bonded to an aromatic ring.	2.05	1	0	benzyl alcohols	antioxidant; fragrance; metabolite; solvent
betaine glycine betaine : The amino acid betaine derived from glycine.	3.66	2	0	amino-acid betaine; glycine derivative	fundamental metabolite
bromide Bromides: Salts of hydrobromic acid, HBr, with the bromine atom in the 1- oxidation state. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)	3.51	1	0	halide anion; monoatomic bromine
carbamates [no description available]	2.61	2	0	amino-acid anion
carbon monoxide Carbon Monoxide: Carbon monoxide (CO). A poisonous colorless, odorless, tasteless gas. It combines with hemoglobin to form carboxyhemoglobin, which has no oxygen carrying capacity. The resultant oxygen deprivation causes headache, dizziness, decreased pulse and respiratory rates, unconsciousness, and death. (From Merck Index, 11th ed). carbon monoxide : A one-carbon compound in which the carbon is joined only to a single oxygen. It is a colourless, odourless, tasteless, toxic gas.	7.1	1	0	carbon oxide; gas molecular entity; one-carbon compound	biomarker; EC 1.9.3.1 (cytochrome c oxidase) inhibitor; human metabolite; ligand; metabolite; mitochondrial respiratory-chain inhibitor; mouse metabolite; neurotoxin; neurotransmitter; P450 inhibitor; probe; signalling molecule; vasodilator agent
carnitine [no description available]	2.21	1	0	amino-acid betaine	human metabolite; mouse metabolite
choline [no description available]	2.17	1	0	cholines	allergen; Daphnia magna metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; neurotransmitter; nutrient; plant metabolite; Saccharomyces cerevisiae metabolite
bupropion Bupropion: A propiophenone-derived antidepressant and antismoking agent that inhibits the uptake of DOPAMINE.. bupropion : An aromatic ketone that is propiophenone carrying a tert-butylamino group at position 2 and a chloro substituent at position 3 on the phenyl ring.	3.23	1	0	aromatic ketone; monochlorobenzenes; secondary amino compound	antidepressant; environmental contaminant; xenobiotic
aminocaproic acid Aminocaproic Acid: An antifibrinolytic agent that acts by inhibiting plasminogen activators which have fibrinolytic properties.. 6-aminohexanoic acid : An epsilon-amino acid comprising hexanoic acid carrying an amino substituent at position C-6. Used to control postoperative bleeding, and to treat overdose effects of the thrombolytic agents streptokinase and tissue plasminogen activator.	3.23	1	0	amino acid zwitterion; epsilon-amino acid; omega-amino fatty acid	antifibrinolytic drug; hematologic agent; metabolite
creatine [no description available]	2.44	2	0	glycine derivative; guanidines; zwitterion	geroprotector; human metabolite; mouse metabolite; neuroprotective agent; nutraceutical
lactic acid Lactic Acid: A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed). 2-hydroxypropanoic acid : A 2-hydroxy monocarboxylic acid that is propanoic acid in which one of the alpha-hydrogens is replaced by a hydroxy group.	10.41	20	2	2-hydroxy monocarboxylic acid	algal 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.	2.95	1	0	sulfoxide; volatile organic compound	alkylating agent; antidote; Escherichia coli metabolite; geroprotector; MRI contrast agent; non-narcotic analgesic; polar aprotic solvent; radical scavenger
gamma-butyrobetaine 4-(trimethylammonio)butanoate : An amino-acid betaine gamma-aminobutyric acid zwitterion in which all of the hydrogens attached to the nitrogen are replaced by methyl groups.	2.21	1	0	amino-acid betaine	Escherichia coli metabolite; human metabolite
glycine [no description available]	2.58	2	0	alpha-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.	2.13	1	0	alditol; triol	algal metabolite; detergent; Escherichia coli metabolite; geroprotector; human metabolite; mouse metabolite; osmolyte; Saccharomyces cerevisiae metabolite; solvent
iodine Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically.. diiodine : Molecule comprising two covalently bonded iodine atoms with overall zero charge..	2.06	1	0	diatomic iodine	nutrient
kynurenine Kynurenine: A metabolite of the essential amino acid tryptophan metabolized via the tryptophan-kynurenine pathway.. kynurenine : A ketone that is alanine in which one of the methyl hydrogens is substituted by a 2-aminobenzoyl group.	2.21	1	0	aromatic ketone; non-proteinogenic alpha-amino acid; substituted aniline	human metabolite
methanol Methanol: A colorless, flammable liquid used in the manufacture of FORMALDEHYDE and ACETIC ACID, in chemical synthesis, antifreeze, and as a solvent. Ingestion of methanol is toxic and may cause blindness.. primary alcohol : A primary alcohol is a compound in which a hydroxy group, -OH, is attached to a saturated carbon atom which has either three hydrogen atoms attached to it or only one other carbon atom and two hydrogen atoms attached to it.. methanol : The primary alcohol that is the simplest aliphatic alcohol, comprising a methyl and an alcohol group.	2.41	1	0	alkyl alcohol; one-carbon compound; primary alcohol; volatile organic compound	amphiprotic solvent; Escherichia coli metabolite; fuel; human metabolite; mouse metabolite; Mycoplasma genitalium metabolite
melatonin [no description available]	2.08	1	0	acetamides; 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.	2.05	1	0	metal 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.	17.88	136	24	pyridine alkaloid; pyridinecarboxamide; vitamin B3	anti-inflammatory agent; antioxidant; cofactor; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; EC 3.5.1.98 (histone deacetylase) inhibitor; Escherichia coli metabolite; geroprotector; human urinary metabolite; metabolite; mouse metabolite; neuroprotective agent; Saccharomyces cerevisiae metabolite; Sir2 inhibitor
niacin Niacin: A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.. vitamin B3 : Any member of a group of vitamers that belong to the chemical structural class called pyridines that exhibit biological activity against vitamin B3 deficiency. Vitamin B3 deficiency causes a condition known as pellagra whose symptoms include depression, dermatitis and diarrhea. The vitamers include nicotinic acid and nicotinamide (and their ionized and salt forms).. nicotinic acid : A pyridinemonocarboxylic acid that is pyridine in which the hydrogen at position 3 is replaced by a carboxy group.	3.23	1	0	pyridine 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
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.	2	1	0	C4-dicarboxylic acid; oxo dicarboxylic acid	geroprotector; 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.	3.17	5	0	phosphocholines	allergen; 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.	3.61	2	0	monocarboxylic acid amide; N-acylammonia; pyrazines	antitubercular agent; prodrug
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).	3.23	1	0	hydroxymethylpyridine; methylpyridines; monohydroxypyridine; vitamin B6	cofactor; Escherichia coli metabolite; human metabolite; mouse metabolite; 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.	3.23	1	0	primary alcohol; vitamin B1	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
trimethyloxamine trimethyloxamine: used in manufacture of quaternary ammonium cpds; insect attractant; warming agent for gas; oxidant; structure. trimethylamine N-oxide : A tertiary amine oxide resulting from the oxidation of the amino group of trimethylamine.	2.48	2	0	tertiary amine oxide	Escherichia coli metabolite; metabolite; osmolyte
urea pseudourea: clinical use; structure. isourea : A carboximidic acid that is the imidic acid tautomer of urea, H2NC(=NH)OH, and its hydrocarbyl derivatives.	2.1	1	0	isourea; monocarboxylic acid amide; one-carbon compound	Daphnia magna metabolite; Escherichia coli metabolite; fertilizer; flour treatment agent; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
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.	2.08	1	0	monochlorobenzenes; N-arylpiperazine	drug metabolite; environmental contaminant; serotonergic agonist; xenobiotic
phenytoin [no description available]	4.22	2	0	imidazolidine-2,4-dione	anticonvulsant; drug allergen; sodium channel blocker; teratogenic agent
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.	2.08	1	0	acridines; 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.	3.23	1	0	aromatic 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.	3.61	2	0	acetamides; phenols	antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; cyclooxygenase 3 inhibitor; environmental contaminant; ferroptosis inducer; geroprotector; hepatotoxic agent; human blood serum metabolite; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic
acetazolamide Acetazolamide: One of the CARBONIC ANHYDRASE INHIBITORS that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337)	3.91	3	0	monocarboxylic acid amide; sulfonamide; thiadiazoles	anticonvulsant; diuretic; EC 4.2.1.1 (carbonic anhydrase) inhibitor
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.	3.23	1	0	acetohydroxamic 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	3.23	1	0	alpha-amino acid ester
albendazole [no description available]	3.61	2	0	aryl sulfide; benzimidazoles; benzimidazolylcarbamate fungicide; carbamate ester	anthelminthic drug; microtubule-destabilising agent; tubulin modulator
albuterol Albuterol: A short-acting beta-2 adrenergic agonist that is primarily used as a bronchodilator agent to treat ASTHMA. Albuterol is prepared as a racemic mixture of R(-) and S(+) stereoisomers. The stereospecific preparation of R(-) isomer of albuterol is referred to as levalbuterol.. albuterol : A member of the class of phenylethanolamines that is 4-(2-amino-1-hydroxyethyl)-2-(hydroxymethyl)phenol having a tert-butyl group attached to the nirogen atom. It acts as a beta-adrenergic agonist used in the treatment of asthma and chronic obstructive pulmonary disease (COPD).	3.61	2	0	phenols; 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.	3.23	1	0	1,1-bis(phosphonic acid); primary amino compound	bone density conservation agent; EC 2.5.1.1 (dimethylallyltranstransferase) inhibitor
alfuzosin alfuzosin: structure given in first source	3.23	1	0	monocarboxylic 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.	3.23	1	0	imidazoles; 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.	3.23	1	0	organochlorine 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.	2.08	1	0	secondary 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.	3.23	1	0	triamino-1,3,5-triazine
amantadine amant: an antiviral compound consisting of an adamantane derivative chemically linked to a water-solube polyanioic matrix; structure in first source	3.23	1	0	adamantanes; 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.	3.23	1	0	quaternary ammonium ion	EC 3.1.1.8 (cholinesterase) inhibitor
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.	3.61	2	0	acetamides; 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.	3.23	1	0	diamine; 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.	2.08	1	0	dicarboximide; piperidones; substituted aniline	adrenergic agent; anticonvulsant; antineoplastic agent; EC 1.14.14.14 (aromatase) 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.	3.23	1	0	N-acylglycine	Daphnia magna metabolite
theophylline [no description available]	3.61	2	0	dimethylxanthine	adenosine receptor antagonist; anti-asthmatic drug; anti-inflammatory agent; bronchodilator agent; drug metabolite; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; fungal metabolite; human blood serum metabolite; immunomodulator; muscle relaxant; vasodilator agent
amiodarone Amiodarone: An antianginal and class III antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting POTASSIUM CHANNELS and VOLTAGE-GATED SODIUM CHANNELS. There is a resulting decrease in heart rate and in vascular resistance.. amiodarone : A member of the class of 1-benzofurans that is 1-benzofuran substituted by a butyl group at position 2 and a 4-[2-(diethylamino)ethoxy]-3,5-diiodobenzoyl group at position 3. It is a cardiovascular drug used for the treatment of cardiac dysrhythmias.	3.87	3	0	1-benzofurans; aromatic ketone; organoiodine compound; tertiary amino compound	cardiovascular drug
dan 2163 [no description available]	2.08	1	0	aromatic 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.	3.61	2	0	carbotricyclic 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.	2.08	1	0	monocarboxylic 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.	4.34	5	0	dihydropyridine; ethyl ester; methyl ester; monochlorobenzenes; primary amino compound	antihypertensive agent; calcium channel blocker; vasodilator agent
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.	3.61	2	0	dibenzooxazepine	adrenergic uptake inhibitor; antidepressant; dopaminergic antagonist; geroprotector; serotonin uptake inhibitor
amsacrine Amsacrine: An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.. amsacrine : A sulfonamide that is N-phenylmethanesulfonamide substituted by a methoxy group at position 3 and an acridin-9-ylamino group at position 4. It exhibits antineoplastic activity.	2.08	1	0	acridines; aromatic ether; sulfonamide	antineoplastic agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
anastrozole [no description available]	9.93	14	3	nitrile; triazoles	antineoplastic agent; EC 1.14.14.14 (aromatase) inhibitor
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.	2.08	1	0	anthracenes	antipsoriatic
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.	2.08	1	0	pyrazolone	antipyretic; 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.	20.09	50	27	benzoic 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.	2.08	1	0	benzimidazoles; piperidines	anti-allergic agent; anticoronaviral agent; H1-receptor antagonist
atenolol Atenolol: A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.. atenolol : An ethanolamine compound having a (4-carbamoylmethylphenoxy)methyl group at the 1-position and an N-isopropyl substituent.	3.61	2	0	ethanolamines; monocarboxylic acid amide; propanolamine	anti-arrhythmia drug; antihypertensive agent; beta-adrenergic antagonist; environmental contaminant; sympatholytic agent; xenobiotic
azathioprine Azathioprine: An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed). azathioprine : A thiopurine that is 6-mercaptopurine in which the mercapto hydrogen is replaced by a 1-methyl-4-nitroimidazol-5-yl group. It is a prodrug for mercaptopurine and is used as an immunosuppressant, prescribed for the treatment of inflammatory conditions and after organ transplantation and also for treatment of Crohn's didease and MS.	15.47	63	20	aryl sulfide; C-nitro compound; imidazoles; thiopurine	antimetabolite; antineoplastic agent; carcinogenic agent; DNA synthesis inhibitor; hepatotoxic agent; immunosuppressive agent; prodrug
baclofen [no description available]	3.61	2	0	amino acid zwitterion; gamma-amino acid; monocarboxylic acid; monochlorobenzenes; primary amino compound	central nervous system depressant; GABA agonist; muscle relaxant
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.	3.23	1	0	indazoles; 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.	3.23	1	0	benzothiadiazine; sulfonamide	antihypertensive agent; diuretic
benzbromarone Benzbromarone: Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout.. benzbromarone : 1-Benzofuran substituted at C-2 and C-3 by an ethyl group and a 3,5-dibromo-4-hydroxybenzoyl group respectively. An inhibitor of CYP2C9, it is used as an anti-gout medication.	3.61	2	0	1-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.	2.08	1	0	benzoate ester; substituted aniline	allergen; antipruritic drug; sensitiser; topical anaesthetic
betaxolol [no description available]	3.23	1	0	propanolamine	antihypertensive 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.	3.23	1	0	carbamate ester; quaternary ammonium ion	muscarinic agonist
bicalutamide bicalutamide: approved for treatment of advanced prostate cancer. N-[4-cyano-3-(trifluoromethyl)phenyl]-3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanamide : A member of the class of (trifluoromethyl)benzenes that is 4-amino-2-(trifluoromethyl)benzonitrile in which one of the amino hydrogens is substituted by a 3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanoyl group.. bicalutamide : A racemate comprising of equal amounts of (R)-bicalutamide and (S)-bicalutamide. It is an oral non-steroidal antiandrogen used in the treatment of prostate cancer and hirsutism.	12.78	6	2	(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.	2.08	1	0	biphenyls; 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.	3.23	1	0	piperidines; 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)	3.61	2	0	diarylmethane
bisindolylmaleimide iv [no description available]	2.41	1	0	indoles; maleimides
bisoprolol Bisoprolol: A cardioselective beta-1 adrenergic blocker. It is effective in the management of HYPERTENSION and ANGINA PECTORIS.	3.23	1	0	secondary alcohol; secondary amine	anti-arrhythmia drug; antihypertensive agent; beta-adrenergic antagonist; sympatholytic agent
bromopride bromopride: RN given refers to parent cpd; structure	2.08	1	0	benzamides
bronopol [no description available]	2.08	1	0	nitro compound
bumetanide [no description available]	3.61	2	0	amino acid; benzoic acids; sulfonamide	diuretic; EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor
buspirone Buspirone: An anxiolytic agent and serotonin receptor agonist belonging to the azaspirodecanedione class of compounds. Its structure is unrelated to those of the BENZODIAZAPINES, but it has an efficacy comparable to DIAZEPAM.. buspirone : An azaspiro compound that is 8-azaspiro[4.5]decane-7,9-dione substituted at the nitrogen atom by a 4-(piperazin-1-yl)butyl group which in turn is substituted by a pyrimidin-2-yl group at the N(4) position.	3.23	1	0	azaspiro compound; N-alkylpiperazine; N-arylpiperazine; organic heteropolycyclic compound; piperidones; pyrimidines	anxiolytic drug; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; sedative; serotonergic agonist
busulfan [no description available]	3.91	3	0	methanesulfonate ester	alkylating agent; antineoplastic agent; carcinogenic agent; insect sterilant; teratogenic agent
secbutabarbital secbutabarbital: Butabarbital (a synonym for Secbutabarbital) should be distinguished from Butobarbital	3.23	1	0	barbiturates
caffeine [no description available]	3.61	2	0	purine 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.	5.95	7	1	aromatic ether; nitrile; polyether; tertiary amino compound
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.	3.23	1	0	benzimidazolecarboxylic acid; biphenylyltetrazole	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
carbamazepine Carbamazepine: A dibenzazepine that acts as a sodium channel blocker. It is used as an anticonvulsant for the treatment of grand mal and psychomotor or focal SEIZURES. It may also be used in the management of BIPOLAR DISORDER, and has analgesic properties.. carbamazepine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine carrying a carbamoyl substituent at the azepine nitrogen, used as an anticonvulsant.	4.45	3	0	dibenzoazepine; 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.	3.23	1	0	monochlorobenzenes; 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.	3.23	1	0	carbamate ester	muscle 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.	2.08	1	0	N-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.	2.08	1	0	carbazoles; organochlorine compound	EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-steroidal anti-inflammatory drug; photosensitizing agent
carvedilol [no description available]	3.61	2	0	carbazoles; secondary alcohol; secondary amino compound	alpha-adrenergic antagonist; antihypertensive agent; beta-adrenergic antagonist; cardiovascular drug; vasodilator agent
celecoxib [no description available]	3.61	2	0	organofluorine compound; pyrazoles; sulfonamide; toluenes	cyclooxygenase 2 inhibitor; geroprotector; non-narcotic analgesic; non-steroidal anti-inflammatory drug
cetirizine Cetirizine: A potent second-generation histamine H1 antagonist that is effective in the treatment of allergic rhinitis, chronic urticaria, and pollen-induced asthma. Unlike many traditional antihistamines, it does not cause drowsiness or anticholinergic side effects.. cetirizine : A member of the class of piperazines that is piperazine in which the hydrogens attached to nitrogen are replaced by a (4-chlorophenyl)(phenyl)methyl and a 2-(carboxymethoxy)ethyl group respectively.	3.23	1	0	ether; monocarboxylic acid; monochlorobenzenes; piperazines	anti-allergic agent; environmental contaminant; H1-receptor antagonist; xenobiotic
chetomin chetomin: C31H30N6O6S4, similar to epipolythiodioxopiperazines. chetomin : An organic heteropentacyclic compound of the class of epipolythiodioxopiperazine. Isolated from Chaetomium globosum and Farrowia seminuda, it exhibits immunosuppressive activity.	2.21	1	0	indoles; organic disulfide; organic heteropentacyclic compound	Chaetomium metabolite; immunosuppressive agent
chlorambucil Chlorambucil: A nitrogen mustard alkylating agent used as antineoplastic for chronic lymphocytic leukemia, Hodgkin's disease, and others. Although it is less toxic than most other nitrogen mustards, it has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (Merck Index, 11th ed). chlorambucil : A monocarboxylic acid that is butanoic acid substituted at position 4 by a 4-[bis(2-chloroethyl)amino]phenyl group. A chemotherapy drug that can be used in combination with the antibody obinutuzumab for the treatment of chronic lymphocytic leukemia.	3.91	3	0	aromatic 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	3.23	1	0	diarylmethane
chlordiazepoxide Chlordiazepoxide: An anxiolytic benzodiazepine derivative with anticonvulsant, sedative, and amnesic properties. It has also been used in the symptomatic treatment of alcohol withdrawal.. chlordiazepoxide : A benzodiazepine that is 3H-1,4-benzodiazepine 4-oxide substituted by a chloro group at position 7, a phenyl group at position 5 and a methylamino group at position 2.	3.61	2	0	benzodiazepine
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.	3.23	1	0	1,3-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.	4.99	11	0	aminoquinoline; 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.	3.23	1	0	benzothiadiazine	antihypertensive agent; diuretic
chlorpheniramine Chlorpheniramine: A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than PROMETHAZINE.. chlorphenamine : A tertiary amino compound that is propylamine which is substituted at position 3 by a pyridin-2-yl group and a p-chlorophenyl group and in which the hydrogens attached to the nitrogen are replaced by methyl groups. A histamine H1 antagonist, it is used to relieve the symptoms of hay fever, rhinitis, urticaria, and asthma.	3.61	2	0	monochlorobenzenes; pyridines; tertiary amino compound	anti-allergic agent; antidepressant; antipruritic drug; H1-receptor antagonist; histamine antagonist; serotonin uptake inhibitor
chlorpromazine Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking DOPAMINE RECEPTORS. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup.. chlorpromazine : A substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropanamine moiety.	3.94	3	0	organochlorine compound; phenothiazines; tertiary amine	anticoronaviral agent; antiemetic; dopaminergic antagonist; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; phenothiazine antipsychotic drug
chlorpropamide Chlorpropamide: A sulfonylurea hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277). chlorpropamide : An N-sulfonylurea that is urea in which a hydrogen attached to one of the nitrogens is substituted by 4-chlorobenzenesulfonyl group and a hydrogen attached to the other nitrogen is substituted by propyl group. Chlorpropamide is a hypoglycaemic agent used in the treatment of type 2 (non-insulin-dependent) diabetes mellitus not responding to dietary modification.	3.61	2	0	monochlorobenzenes; N-sulfonylurea	hypoglycemic agent; insulin secretagogue
chlorthalidone Chlorthalidone: A benzenesulfonamide-phthalimidine that tautomerizes to a BENZOPHENONES form. It is considered a thiazide-like diuretic.	3.61	2	0	isoindoles; monochlorobenzenes; sulfonamide
chlorzoxazone Chlorzoxazone: A centrally acting central muscle relaxant with sedative properties. It is claimed to inhibit muscle spasm by exerting an effect primarily at the level of the spinal cord and subcortical areas of the brain. (From Martindale, The Extra Pharmacopoea, 30th ed, p1202). chlorzoxazone : A member of the class of 1,3-benzoxazoles that is 1,3-benzoxazol-2-ol in which the hydrogen atom at position 5 is substituted by chlorine. A centrally acting muscle relaxant with sedative properties, it is used for the symptomatic treatment of painful muscle spasm.	3.61	2	0	1,3-benzoxazoles; heteroaryl hydroxy compound; organochlorine compound	muscle relaxant; sedative
cifenline [no description available]	2.08	1	0	diarylmethane
ciclopirox [no description available]	2.08	1	0	cyclic 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.	2.08	1	0	aromatic ether; thiazolidinone	antineoplastic agent; insulin-sensitizing drug
cilostazol [no description available]	9.1	4	0	lactam; tetrazoles	anticoagulant; bronchodilator agent; EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor; fibrin modulating drug; neuroprotective agent; platelet aggregation inhibitor; vasodilator agent
cimetidine Cimetidine: A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.. cimetidine : A member of the class of guanidines that consists of guanidine carrying a methyl substituent at position 1, a cyano group at position 2 and a 2-{[(5-methyl-1H-imidazol-4-yl)methyl]sulfanyl}ethyl group at position 3. It is a H2-receptor antagonist that inhibits the production of acid in stomach.	3.61	2	0	aliphatic sulfide; guanidines; imidazoles; nitrile	adjuvant; analgesic; anti-ulcer drug; H2-receptor antagonist; P450 inhibitor
ciprofibrate [no description available]	2.08	1	0	cyclopropanes; monocarboxylic acid; organochlorine compound	antilipemic drug
ciprofloxacin Ciprofloxacin: A broad-spectrum antimicrobial carboxyfluoroquinoline.. ciprofloxacin : A quinolone that is quinolin-4(1H)-one bearing cyclopropyl, carboxylic acid, fluoro and piperazin-1-yl substituents at positions 1, 3, 6 and 7, respectively.	3.61	2	0	aminoquinoline; 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
citalopram Citalopram: A furancarbonitrile that is one of the serotonin uptake inhibitors used as an antidepressant. The drug is also effective in reducing ethanol uptake in alcoholics and is used in depressed patients who also suffer from TARDIVE DYSKINESIA in preference to tricyclic antidepressants, which aggravate dyskinesia.. citalopram : A racemate comprising equimolar amounts of (R)-citalopram and its enantiomer, escitalopram. It is used as an antidepressant, although only escitalopram is active.. 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile : A nitrile that is 1,3-dihydro-2-benzofuran-5-carbonitrile in which one of the hydrogens at position 1 is replaced by a p-fluorophenyl group, while the other is replaced by a 3-(dimethylamino)propyl group.	3.91	3	0	2-benzofurans; cyclic ether; nitrile; organofluorine compound; tertiary amino compound
cl 387785 CL 387785: structure in first source. N-{4-[(3-bromophenyl)amino]quinazolin-6-yl}but-2-ynamide : A member of the class of quinazolines that is 4,6-diaminoquinazoine in which the one of the hydrogens attached to the amino group at position 4 has been replaced by a m-bromophenyl group while one of the hydrogens attached to the amino group at position 6 has been replaced by a but-2-ynoyl group.	2.07	1	0	bromobenzenes; quinazolines; secondary carboxamide; ynamide	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; epidermal growth factor receptor antagonist
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.	2.08	1	0	monohydroxyquinoline; 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.	4.51	3	0	1,4-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.	2.08	1	0	monochlorobenzenes; phenazines	dye; leprostatic drug; non-steroidal anti-inflammatory drug
clofibrate angiokapsul: contains clofibrate & insoitolnicotinate	3.61	2	0	aromatic ether; ethyl ester; monochlorobenzenes	anticholesteremic drug; antilipemic drug; geroprotector; PPARalpha agonist
clomiphene [no description available]	3.61	2	0	tertiary amine	estrogen antagonist; estrogen receptor modulator
clomipramine Clomipramine: A tricyclic antidepressant similar to IMIPRAMINE that selectively inhibits the uptake of serotonin in the brain. It is readily absorbed from the gastrointestinal tract and demethylated in the liver to form its primary active metabolite, desmethylclomipramine.. clomipramine : A dibenzoazepine that is 10,11-dihydro-5H-dibenzo[b,f]azepine which is substituted by chlorine at position 3 and in which the hydrogen attached to the nitrogen is replaced by a 3-(dimethylamino)propyl group. One of the more sedating tricyclic antidepressants, it is used as the hydrochloride salt for the treatment of depression as well as obsessive-compulsive disorder and phobias.	3.61	2	0	dibenzoazepine	anticoronaviral 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.	4.22	2	0	1,4-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.	3.23	1	0	clonidine; imidazoline
4-chloro-N-(2,6-dimethyl-1-piperidinyl)-3-sulfamoylbenzamide [no description available]	2.08	1	0	sulfonamide
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.	3.23	1	0	1,4-benzodiazepinone	anticonvulsant; anxiolytic drug; GABA modulator; prodrug
clotrimazole [no description available]	8.66	2	0	conazole antifungal drug; imidazole antifungal drug; imidazoles; monochlorobenzenes	antiinfective agent; environmental contaminant; xenobiotic
4-cresol 4-cresol: RN given refers to parent cpd. p-cresol : A cresol that consists of toluene substituted by a hydroxy group at position 4. It is a metabolite of aromatic amino acid metabolism produced by intestinal microflora in humans and animals.	2.21	1	0	cresol	Escherichia coli metabolite; human metabolite; uremic toxin
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.	3.23	1	0	carbotricyclic compound	antidepressant; 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.	3.23	1	0	organic 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.	3.23	1	0	piperidines; tertiary amine	anti-allergic agent; antipruritic drug; gastrointestinal drug; H1-receptor antagonist; serotonergic antagonist
dapsone [no description available]	3.61	2	0	substituted aniline; sulfone	anti-inflammatory drug; antiinfective agent; antimalarial; leprostatic drug
deferoxamine Deferoxamine: Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the mesylate form.. desferrioxamine B : An acyclic desferrioxamine that is butanedioic acid in which one of the carboxy groups undergoes formal condensation with the primary amino group of N-(5-aminopentyl)-N-hydroxyacetamide and the second carboxy group undergoes formal condensation with the hydroxyamino group of N(1)-(5-aminopentyl)-N(1)-hydroxy-N(4)-[5-(hydroxyamino)pentyl]butanediamide. It is a siderophore native to Streptomyces pilosus biosynthesised by the DesABCD enzyme cluster as a high affinity Fe(III) chelator.	3.23	1	0	acyclic desferrioxamine	bacterial metabolite; ferroptosis inhibitor; iron chelator; siderophore
desipramine Desipramine: A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.. desipramine : A dibenzoazepine consisting of 10,11-dihydro-5H-dibenzo[b,f]azepine substituted on nitrogen with a 3-(methylamino)propyl group.	3.61	2	0	dibenzoazepine; secondary amino compound	adrenergic uptake inhibitor; alpha-adrenergic antagonist; antidepressant; cholinergic antagonist; drug allergen; EC 3.1.4.12 (sphingomyelin phosphodiesterase) inhibitor; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; H1-receptor antagonist; serotonin uptake inhibitor
amphetamine Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.. 1-phenylpropan-2-amine : A primary amine that is isopropylamine in which a hydrogen attached to one of the methyl groups has been replaced by a phenyl group.. amphetamine : A racemate comprising equimolar amounts of (R)-amphetamine (also known as levamphetamine or levoamphetamine) and (S)-amphetamine (also known as dexamfetamine or dextroamphetamine.	3.23	1	0	primary amine
diazepam Diazepam: A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.. diazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a methyl group at position 1 and a phenyl group at position 5.	3.91	3	0	1,4-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.	4.11	4	0	benzothiadiazine; 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.	3.23	1	0	amino 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
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.	3.23	1	0	dichlorobenzene; 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.	3.23	1	0	carboxylic ester; tertiary amine	antispasmodic drug; muscarinic antagonist; parasympatholytic
pentetic acid Pentetic Acid: An iron chelating agent with properties like EDETIC ACID. DTPA has also been used as a chelator for other metals, such as plutonium.	3.23	1	0	pentacarboxylic acid	copper chelator
diflunisal Diflunisal: A salicylate derivative and anti-inflammatory analgesic with actions and side effects similar to those of ASPIRIN.. diflunisal : An organofluorine compound comprising salicylic acid having a 2,4-difluorophenyl group at the 5-position.	3.23	1	0	monohydroxybenzoic 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.	3.23	1	0	dithiol; 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.	3.59	2	0	ether; tertiary amino compound	anti-allergic agent; antidyskinesia agent; antiemetic; antiparkinson drug; antipruritic drug; antitussive; H1-receptor antagonist; local anaesthetic; muscarinic antagonist; oneirogen; sedative
dipyridamole Dipyridamole: A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752). dipyridamole : A pyrimidopyrimidine that is 2,2',2'',2'''-(pyrimido[5,4-d]pyrimidine-2,6-diyldinitrilo)tetraethanol substituted by piperidin-1-yl groups at positions 4 and 8 respectively. A vasodilator agent, it inhibits the formation of blood clots.	3.61	2	0	piperidines; pyrimidopyrimidine; tertiary amino compound; tetrol	adenosine phosphodiesterase inhibitor; EC 3.5.4.4 (adenosine deaminase) inhibitor; platelet aggregation inhibitor; vasodilator agent
disopyramide Disopyramide: A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine. It also possesses some anticholinergic and local anesthetic properties.. disopyramide : A monocarboxylic acid amide that is butanamide substituted by a diisopropylamino group at position 4, a phenyl group at position 2 and a pyridin-2-yl group at position 2. It is used as a anti-arrhythmia drug.	3.61	2	0	monocarboxylic acid amide; pyridines; tertiary amino compound	anti-arrhythmia drug
disulfiram [no description available]	3.61	2	0	organic 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.	5.56	8	0	branched-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
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.	2.08	1	0	benzimidazoles; 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.	3.61	2	0	aromatic 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.	3.23	1	0	morpholines; 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.	3.23	1	0	aromatic amine; benzodioxine; monocarboxylic acid amide; N-acylpiperazine; N-arylpiperazine; quinazolines	alpha-adrenergic antagonist; antihyperplasia drug; antihypertensive agent; antineoplastic agent; vasodilator agent
doxepin Doxepin: A dibenzoxepin tricyclic compound. It displays a range of pharmacological actions including maintaining adrenergic innervation. Its mechanism of action is not fully understood, but it appears to block reuptake of monoaminergic neurotransmitters into presynaptic terminals. It also possesses anticholinergic activity and modulates antagonism of histamine H(1)- and H(2)-receptors.. doxepin : A dibenzooxepine that is 6,11-dihydrodibenzo[b,e]oxepine substituted by a 3-(dimethylamino)propylidene group at position 11. It is used as an antidepressant drug.	3.61	2	0	dibenzooxepine; 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.	3.23	1	0	pyridines; 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.	3.23	1	0	aromatic 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.	3.23	1	0	oxopurine; propane-1,2-diols	bronchodilator agent; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; muscle relaxant; vasodilator agent
ebastine [no description available]	2.08	1	0	organic molecular entity
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.	3.23	1	0	phenols; quaternary ammonium ion	antidote; diagnostic agent; EC 3.1.1.8 (cholinesterase) inhibitor
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.	2.08	1	0	1,8-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.	2.15	1	0
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.	3.23	1	0	triazoles; 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.	3.91	3	0	aromatic 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.	5.04	4	0	dicarboximide; 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.	3.23	1	0	imidazolidine-2,4-dione	anticonvulsant
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.	3.23	1	0	1,1-bis(phosphonic acid)	antineoplastic agent; bone density conservation agent; chelator
etodolac Etodolac: A non-steroidal anti-inflammatory agent and cyclooxygenase-2 (COX-2) inhibitor with potent analgesic and anti-arthritic properties. It has been shown to be effective in the treatment of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; ANKYLOSING SPONDYLITIS; and in the alleviation of postoperative pain (PAIN, POSTOPERATIVE).. etodolac : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is substituted by a 1,8-diethyl-1,3,4,9-tetrahydropyrano[3,4-b]indol-1-yl moiety. A preferential inhibitor of cyclo-oxygenase 2 and non-steroidal anti-inflammatory, it is used for the treatment of rheumatoid arthritis and osteoarthritis, and for the alleviation of postoperative pain. Administered as the racemate, only the (S)-enantiomer is active.	3.23	1	0	monocarboxylic acid; organic heterotricyclic compound	antipyretic; cyclooxygenase 2 inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
brl 42810 [no description available]	3.61	2	0	2-aminopurines; acetate ester	antiviral drug; prodrug
felbamate Felbamate: A PEGylated phenylcarbamate derivative that acts as an antagonist of NMDA RECEPTORS. It is used as an anticonvulsant, primarily for the treatment of SEIZURES in severe refractory EPILEPSY.. felbamate : The bis(carbamate ester) of 2-phenylpropane-1,3-diol. An anticonvulsant, it is used in the treatment of epilepsy.	4.89	3	0	carbamate ester	anticonvulsant; 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.	2.08	1	0	biphenyls; 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.	3.61	2	0	dichlorobenzene; 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.	5.01	3	0	(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	3.61	2	0	aromatic 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.	3.23	1	0	benzazepine	alpha-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.	3.23	1	0	monocarboxylic acid	antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; drug allergen; non-narcotic analgesic; non-steroidal anti-inflammatory drug
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.	3.23	1	0	piperidines; tertiary amine	anti-allergic agent; H1-receptor antagonist
fipexide fipexide: regulates dopaminergic systems at macromolecular level	3.23	1	0	benzodioxoles
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.	3.23	1	0	carboxylic ester; flavones; piperidines; tertiary amino compound	antispasmodic drug; muscarinic antagonist; parasympatholytic
flecainide Flecainide: A potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial ARRHYTHMIAS and TACHYCARDIAS.. flecainide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 2,5-bis(2,2,2-trifluoroethoxy)benzoic acid with the primary amino group of piperidin-2-ylmethylamine. An antiarrhythmic agent used (in the form of its acetate salt) to prevent and treat tachyarrhythmia (abnormal fast rhythm of the heart).	3.23	1	0	aromatic 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.	2.08	1	0	difluorobenzene; 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.	9.11	4	0	conazole antifungal drug; difluorobenzene; tertiary alcohol; triazole antifungal drug	environmental contaminant; P450 inhibitor; xenobiotic
flucytosine Flucytosine: A fluorinated cytosine analog that is used as an antifungal agent.. flucytosine : An organofluorine compound that is cytosine that is substituted at position 5 by a fluorine. A prodrug for the antifungal 5-fluorouracil, it is used for the treatment of systemic fungal infections.	3.61	2	0	aminopyrimidine; nucleoside analogue; organofluorine compound; pyrimidine antifungal drug; pyrimidone	prodrug
fluphenazine [no description available]	3.23	1	0	N-alkylpiperazine; organofluorine compound; phenothiazines	anticoronaviral agent; dopaminergic antagonist; phenothiazine antipsychotic drug
flumazenil Flumazenil: A potent benzodiazepine receptor antagonist. Since it reverses the sedative and other actions of benzodiazepines, it has been suggested as an antidote to benzodiazepine overdoses.. flumazenil : An organic heterotricyclic compound that is 5,6-dihydro-4H-imidazo[1,5-a][1,4]benzodiazepine which is substituted at positions 3, 5, 6, and 8 by ethoxycarbonyl, methyl, oxo, and fluoro groups, respectively. It is used as an antidote to benzodiazepine overdose.	3.61	2	0	ethyl ester; imidazobenzodiazepine; organofluorine compound	antidote to benzodiazepine poisoning; GABA antagonist
fluorescite fluorescein (acid form) : A xanthene dye that is highly fluorescent and commonly used as a fluorescent tracer.	3.61	2	0	benzoic 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.	13.16	36	16	nucleobase analogue; organofluorine compound	antimetabolite; antineoplastic agent; environmental contaminant; immunosuppressive agent; radiosensitizing agent; xenobiotic
fluoxetine Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.. fluoxetine : A racemate comprising equimolar amounts of (R)- and (S)-fluoxetine. A selective serotonin reuptake inhibitor (SSRI), it is used (generally as the hydrochloride salt) for the treatment of depression (and the depressive phase of bipolar disorder), bullimia nervosa, and obsessive-compulsive disorder.. N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]propan-1-amine : An aromatic ether consisting of 4-trifluoromethylphenol in which the hydrogen of the phenolic hydroxy group is replaced by a 3-(methylamino)-1-phenylpropyl group.	3.61	2	0	(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.	3.23	1	0	1,4-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.	3.23	1	0	fluorobiphenyl; monocarboxylic acid	antipyretic; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
flutamide Flutamide: An antiandrogen with about the same potency as cyproterone in rodent and canine species.	3.61	2	0	(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.	3.23	1	0	pyrazoles	antidote; 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.	4.13	2	0	carboxylic acid; one-carbon compound; phosphonic acids	antiviral drug; geroprotector; HIV-1 reverse transcriptase inhibitor; sodium-dependent Pi-transporter inhibitor
furosemide Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.. furosemide : A chlorobenzoic acid that is 4-chlorobenzoic acid substituted by a (furan-2-ylmethyl)amino and a sulfamoyl group at position 2 and 5 respectively. It is a diuretic used in the treatment of congestive heart failure.	3.61	2	0	chlorobenzoic 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.	4.22	2	0	gamma-amino acid	anticonvulsant; calcium channel blocker; environmental contaminant; xenobiotic
gemfibrozil [no description available]	3.61	2	0	aromatic ether	antilipemic 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.	3.23	1	0	aminoquinoline; 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.	2.08	1	0	N-sulfonylurea	hypoglycemic agent; insulin secretagogue; radical scavenger
glimepiride glimepiride: structure given in first source	3.61	2	0	sulfonamide
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.	3.61	2	0	aromatic amide; monocarboxylic acid amide; N-sulfonylurea; pyrazines	EC 2.7.1.33 (pantothenate kinase) inhibitor; hypoglycemic agent; insulin secretagogue
glyburide Glyburide: An antidiabetic sulfonylurea derivative with actions like those of chlorpropamide. glyburide : An N-sulfonylurea that is acetohexamide in which the acetyl group is replaced by a 2-(5-chloro-2-methoxybenzamido)ethyl group.	3.61	2	0	monochlorobenzenes; 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]	3.23	1	0	benzenes
granisetron [no description available]	3.23	1	0	aromatic amide; indazoles
guaifenesin Guaifenesin: An expectorant that also has some muscle relaxing action. It is used in many cough preparations.	3.23	1	0	methoxybenzenes
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.	3.23	1	0	azocanes; guanidines	adrenergic antagonist; antihypertensive agent; sympatholytic agent
guanfacine Guanfacine: A centrally acting antihypertensive agent with specificity towards ADRENERGIC ALPHA-2 RECEPTORS.	3.61	2	0	acetamides
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.	3.23	1	0	carboxamidine; 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.	2.21	1	0	isoquinolines; 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.	2.58	2	0	isoquinolines; N-sulfonyldiazepane	antihypertensive agent; calcium channel blocker; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; geroprotector; neuroprotective agent; nootropic agent; vasodilator agent
haloperidol Haloperidol: A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279). haloperidol : A compound composed of a central piperidine structure with hydroxy and p-chlorophenyl substituents at position 4 and an N-linked p-fluorobutyrophenone moiety.	3.61	2	0	aromatic ketone; hydroxypiperidine; monochlorobenzenes; organofluorine compound; tertiary alcohol	antidyskinesia agent; antiemetic; dopaminergic antagonist; first generation antipsychotic; serotonergic antagonist
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.	3.51	1	0	phosphocholines; phospholipid	anti-inflammatory agent; anticoronaviral agent; antifungal agent; antineoplastic agent; antiprotozoal drug; apoptosis inducer; immunomodulator; protein kinase inhibitor
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.	3.23	1	0	azaarene; hydrazines; ortho-fused heteroarene; phthalazines	antihypertensive agent; vasodilator agent
hydrochlorothiazide Hydrochlorothiazide: A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.. hydrochlorothiazide : A benzothiadiazine that is 3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide substituted by a chloro group at position 6 and a sulfonamide at 7. It is diuretic used for the treatment of hypertension and congestive heart failure.	3.61	2	0	benzothiadiazine; 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.	3.61	2	0	benzothiadiazine; 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.	12.71	5	2	aminoquinoline; organochlorine compound; primary alcohol; secondary amino compound; tertiary amino compound	anticoronaviral agent; antimalarial; antirheumatic drug; dermatologic drug
hydroxyurea [no description available]	3.61	2	0	one-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.	3.23	1	0	hydroxyether; monochlorobenzenes; N-alkylpiperazine	anticoronaviral agent; antipruritic drug; anxiolytic drug; dermatologic drug; H1-receptor antagonist
ibuprofen Midol: combination of cinnamedrine, phenacetin, aspirin & caffeine	3.23	1	0	monocarboxylic acid	antipyretic; 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.	3.23	1	0	primary amine
lidocaine Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.. lidocaine : The monocarboxylic acid amide resulting from the formal condensation of N,N-diethylglycine with 2,6-dimethylaniline.	3.61	2	0	benzenes; monocarboxylic acid amide; tertiary amino compound	anti-arrhythmia drug; drug allergen; environmental contaminant; local anaesthetic; xenobiotic
ifosfamide [no description available]	7.44	4	2	ifosfamides	alkylating agent; antineoplastic agent; environmental contaminant; immunosuppressive agent; xenobiotic
imipramine Imipramine: The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group.. imipramine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine substituted by a 3-(dimethylamino)propyl group at the nitrogen atom.	3.61	2	0	dibenzoazepine	adrenergic uptake inhibitor; antidepressant; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
amrinone Amrinone: A positive inotropic cardiotonic (CARDIOTONIC AGENTS) with vasodilator properties, phosphodiesterase 3 inhibitory activity, and the ability to stimulate calcium ion influx into the cardiac cell.. amrinone : A 3,4'-bipyridine substituted at positions 5 and 6 by an amino group and a keto function respectively. A pyridine phosphodiesterase 3 inhibitor, it is a drug that may improve the prognosis in patients with congestive heart failure.	3.61	2	0	bipyridines	EC 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.	3.61	2	0	indoles; organochlorine compound; sulfonamide	antihypertensive agent; diuretic
indomethacin Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits CYCLOOXYGENASE, which is necessary for the formation of PROSTAGLANDINS and other AUTACOIDS. It also inhibits the motility of POLYMORPHONUCLEAR LEUKOCYTES.. indometacin : A member of the class of indole-3-acetic acids that is indole-3-acetic acid in which the indole ring is substituted at positions 1, 2 and 5 by p-chlorobenzoyl, methyl, and methoxy groups, respectively. A non-steroidal anti-inflammatory drug, it is used in the treatment of musculoskeletal and joint disorders including osteoarthritis, rheumatoid arthritis, gout, bursitis and tendinitis.	3.61	2	0	aromatic 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.	2.78	3	0	benzenedicarboxamide; 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.	2.07	1	0	dicarboxylic acid diamide; organoiodine compound	environmental contaminant; nephrotoxic agent; radioopaque medium; xenobiotic
ioversol [no description available]	3.23	1	0	amidobenzoic acid
iproniazid [no description available]	3.61	2	0	carbohydrazide; pyridines
avapro Irbesartan: A spiro compound, biphenyl and tetrazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION, and in the treatment of kidney disease.. irbesartan : A biphenylyltetrazole that is an angiotensin II receptor antagonist used mainly for the treatment of hypertension.	3.9	3	0	azaspiro 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)	3.23	1	0	benzenes
isoniazid Hydra: A genus of freshwater polyps in the family Hydridae, order Hydroida, class HYDROZOA. They are of special interest because of their complex organization and because their adult organization corresponds roughly to the gastrula of higher animals.. hydrazide : Compounds derived from oxoacids RkE(=O)l(OH)m (l =/= 0) by replacing -OH by -NRNR2 (R groups are commonly H). (IUPAC).	3.61	2	0	carbohydrazide	antitubercular agent; drug allergen
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.	3.23	1	0	catechols; 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.	3.23	1	0	alkylbenzene
isradipine Isradipine: A potent antagonist of CALCIUM CHANNELS that is highly selective for VASCULAR SMOOTH MUSCLE. It is effective in the treatment of chronic stable angina pectoris, hypertension, and congestive cardiac failure.	3.61	2	0	benzoxadiazole; dihydropyridine; isopropyl ester; methyl ester
itraconazole [no description available]	3.61	2	0	piperazines
4-(4'-hydroxyphenyl)-amino-6,7-dimethoxyquinazoline WHI P131: a quinazoline derivative, inhibitor of glioblastoma cell adhesion and migration	2.15	1	0
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).	3.51	1	0	indolobenzazepine; 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.	3.61	2	0	cyclohexanones; 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.	2.08	1	0	aromatic 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.	10.68	5	1	dichlorobenzene; dioxolane; ether; imidazoles; N-acylpiperazine; N-arylpiperazine
ketoprofen Ketoprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.. ketoprofen : An oxo monocarboxylic acid that consists of propionic acid substituted by a 3-benzoylphenyl group at position 2.	3.23	1	0	benzophenones; 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.	3.23	1	0	amino acid; aromatic ketone; monocarboxylic acid; pyrrolizines; racemate	analgesic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
labetalol Labetalol: A salicylamide derivative that is a non-cardioselective blocker of BETA-ADRENERGIC RECEPTORS and ALPHA-1 ADRENERGIC RECEPTORS.. labetalol : A diastereoisomeric mixture of approximately equal amounts of all four possible stereoisomers ((R,S)-labetolol, (S,R)-labetolol, (S,S)-labetalol and (R,R)-labetalol). It is an adrenergic antagonist used to treat high blood pressure.. 2-hydroxy-5-{1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl}benzamide : A member of the class of benzamides that is benzamide substituted by a hydroxy group at position 2 and by a 1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl group at position 5.	3.23	1	0	benzamides; benzenes; phenols; primary carboxamide; salicylamides; secondary alcohol; secondary amino compound
lamotrigine [no description available]	5.04	4	0	1,2,4-triazines; dichlorobenzene; primary arylamine	anticonvulsant; antidepressant; antimanic drug; calcium channel blocker; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; environmental contaminant; excitatory amino acid antagonist; geroprotector; non-narcotic analgesic; xenobiotic
lansoprazole Lansoprazole: A 2,2,2-trifluoroethoxypyridyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS. Lansoprazole is a racemic mixture of (R)- and (S)-isomers.	3.61	2	0	benzimidazoles; pyridines; sulfoxide	anti-ulcer drug; EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor
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.	4.76	8	0	(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]	14.62	47	16	nitrile; 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.	2.08	1	0	aromatic 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.	3.23	1	0	fluoroquinolone antibiotic; N-arylpiperazine; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone	antimicrobial agent; antitubercular agent; photosensitizing agent
lomustine [no description available]	3.61	2	0	N-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.	3.23	1	0	monocarboxylic 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.	3.61	2	0	benzocycloheptapyridine; 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.	3.23	1	0	benzodiazepine
losartan Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.. losartan : A biphenylyltetrazole where a 1,1'-biphenyl group is attached at the 5-position and has an additional trisubstituted imidazol-1-ylmethyl group at the 4'-position	3.59	2	0	biphenylyltetrazole; imidazoles	angiotensin receptor antagonist; anti-arrhythmia drug; antihypertensive agent; endothelin receptor antagonist
loxapine Loxapine: An antipsychotic agent used in SCHIZOPHRENIA.	3.23	1	0	dibenzooxazepine	antipsychotic 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	4.04	13	0	chromones; morpholines; organochlorine compound	autophagy inhibitor; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; geroprotector
maprotiline Maprotiline: A bridged-ring tetracyclic antidepressant that is both mechanistically and functionally similar to the tricyclic antidepressants, including side effects associated with its use.	3.61	2	0	anthracenes
mebendazole Mebendazole: A benzimidazole that acts by interfering with CARBOHYDRATE METABOLISM and inhibiting polymerization of MICROTUBULES.. mebendazole : A carbamate ester that is methyl 1H-benzimidazol-2-ylcarbamate substituted by a benzoyl group at position 5.	3.61	2	0	aromatic 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.	3.23	1	0	primary aliphatic amine
mechlorethamine nitrogen mustard : Compounds having two beta-haloalkyl groups bound to a nitrogen atom, as in (X-CH2-CH2)2NR.	3.23	1	0	nitrogen 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.	3.23	1	0	diarylmethane
meclofenamic acid Meclofenamic Acid: A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.. meclofenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 2,6-dichloro-3-methylphenyl group. A non-steroidal anti-inflammatory drug, it is used as the sodium salt for the treatment of dysmenorrhoea (painful periods), osteoarthritis and rheumatoid arthritis.	3.23	1	0	aminobenzoic 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
mefenamic acid Mefenamic Acid: A non-steroidal anti-inflammatory agent with analgesic, anti-inflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase.. mefenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 2,3-dimethylphenyl group. Although classed as a non-steroidal anti-inflammatory drug, its anti-inflammatory properties are considered to be minor. It is used to relieve mild to moderate pain, including headaches, dental pain, osteoarthritis and rheumatoid arthritis.	3.61	2	0	aminobenzoic acid; secondary amino compound	analgesic; antipyretic; antirheumatic drug; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; environmental contaminant; non-steroidal anti-inflammatory drug; xenobiotic
memantine [no description available]	3.23	1	0	adamantanes; 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.	2.17	1	0	1,4-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	3.23	1	0	diarylmethane
meperidine Meperidine: A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration.. pethidine : A piperidinecarboxylate ester that is piperidine which is substituted by a methyl group at position 1 and by phenyl and ethoxycarbonyl groups at position 4. It is an analgesic which is used for the treatment of moderate to severe pain, including postoperative pain and labour pain.	3.23	1	0	ethyl 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.	3.23	1	0	imidazolidine-2,4-dione	anticonvulsant
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.	3.23	1	0	piperidinecarboxamide	drug allergen; local anaesthetic
meprobamate Meprobamate: A carbamate with hypnotic, sedative, and some muscle relaxant properties, although in therapeutic doses reduction of anxiety rather than a direct effect may be responsible for muscle relaxation. Meprobamate has been reported to have anticonvulsant actions against petit mal seizures, but not against grand mal seizures (which may be exacerbated). It is used in the treatment of ANXIETY DISORDERS, and also for the short-term management of INSOMNIA but has largely been superseded by the BENZODIAZEPINES. (From Martindale, The Extra Pharmacopoeia, 30th ed, p603)	3.23	1	0	organic 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.	3.23	1	0	amino 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.	3.23	1	0	phenothiazines; 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.	3.23	1	0	aralkylamino 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.	10.17	26	3	guanidines	environmental 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.	3.23	1	0	benzenes; diarylmethane; ketone; tertiary amino compound
methazolamide Methazolamide: A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.	3.23	1	0	sulfonamide; 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.	3.23	1	0	aromatic ether; carbamate ester; secondary alcohol
methoxsalen Methoxsalen: A naturally occurring furocoumarin compound found in several species of plants, including Psoralea corylifolia. It is a photoactive substance that forms DNA ADDUCTS in the presence of ultraviolet A irradiation.. methoxsalen : A member of the class of psoralens that is 7H-furo[3,2-g]chromen-7-one in which the 9 position is substituted by a methoxy group. It is a constituent of the fruits of Ammi majus. Like other psoralens, trioxsalen causes photosensitization of the skin. It is administered topically or orally in conjunction with UV-A for phototherapy treatment of vitiligo and severe psoriasis.	3.23	1	0	aromatic ether; psoralens	antineoplastic agent; cross-linking reagent; dermatologic drug; photosensitizing agent; plant metabolite
methyclothiazide Methyclothiazide: A thiazide diuretic with properties similar to those of HYDROCHLOROTHIAZIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p825)	3.23	1	0	benzothiadiazine
methylphenidate Methylphenidate: A central nervous system stimulant used most commonly in the treatment of ATTENTION DEFICIT DISORDER in children and for NARCOLEPSY. Its mechanisms appear to be similar to those of DEXTROAMPHETAMINE. The d-isomer of this drug is referred to as DEXMETHYLPHENIDATE HYDROCHLORIDE.. methylphenidate : A racemate comprising equimolar amounts of the two threo isomers of methyl phenyl(piperidin-2-yl)acetate. A central stimulant and indirect-acting sympathomimetic, is used (generally as the hydrochloride salt) in the treatment of hyperactivity disorders in children and for the treatment of narcolepsy.. methyl phenyl(piperidin-2-yl)acetate : A amino acid ester that is methyl phenylacetate in which one of the hydrogens alpha to the carbonyl group is replaced by a piperidin-2-yl group.	3.23	1	0	beta-amino acid ester; methyl ester; piperidines
metoclopramide Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic.. metoclopramide : A member of the class of benzamides resulting from the formal condensation of 4-amino-5-chloro-2-methoxybenzoic acid with the primary amino group of N,N-diethylethane-1,2-diamine.	3.61	2	0	benzamides; 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.	3.23	1	0	organochlorine compound; quinazolines; sulfonamide	antihypertensive agent; diuretic; ion transport inhibitor
metoprolol Metoprolol: A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.. metoprolol : A propanolamine that is 1-(propan-2-ylamino)propan-2-ol substituted by a 4-(2-methoxyethyl)phenoxy group at position 1.	3.88	3	0	aromatic 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.	3.61	2	0	C-nitro compound; imidazoles; primary alcohol	antiamoebic agent; antibacterial drug; antimicrobial agent; antiparasitic agent; antitrichomonal drug; environmental contaminant; prodrug; radiosensitizing agent; xenobiotic
metyrapone Metyrapone: An inhibitor of the enzyme STEROID 11-BETA-MONOOXYGENASE. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of CUSHING SYNDROME.. metyrapone : An aromatic ketone that is 3,3-dimethylbutan-2-one in which the methyl groups at positions 1 and 4 are replaced by pyridin-3-yl groups. A steroid 11beta-monooxygenase (EC 1.14.15.4) inhibitor, it is used in the diagnosis of adrenal insufficiency.	3.23	1	0	aromatic ketone	antimetabolite; 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.	3.61	2	0	aromatic ether; primary amino compound	anti-arrhythmia drug
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.	10.27	3	1	imidazobenzodiazepine; 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.	3.23	1	0	amino acid amide; aromatic ether; secondary alcohol	alpha-adrenergic agonist; prodrug; sympathomimetic agent; vasoconstrictor agent
milrinone [no description available]	3.23	1	0	bipyridines; nitrile; pyridone	cardiotonic drug; EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor; platelet aggregation inhibitor; vasodilator agent
minoxidil Minoxidil: A potent direct-acting peripheral vasodilator (VASODILATOR AGENTS) that reduces peripheral resistance and produces a fall in BLOOD PRESSURE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p371). minoxidil : A pyrimidine N-oxide that is pyrimidine-2,4-diamine 3-oxide substituted by a piperidin-1-yl group at position 6.	3.61	2	0	dialkylarylamine; tertiary amino compound
mirtazapine Mirtazapine: A piperazinoazepine tetracyclic compound that enhances the release of NOREPINEPHRINE and SEROTONIN through blockage of presynaptic ALPHA-2 ADRENERGIC RECEPTORS. It also blocks both 5-HT2 and 5-HT3 serotonin receptors and is a potent HISTAMINE H1 RECEPTOR antagonist. It is used for the treatment of depression, and may also be useful for the treatment of anxiety disorders.	3.61	2	0	benzazepine; 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.	4.24	2	0	diarylmethane
mitoxantrone Mitoxantrone: An anthracenedione-derived antineoplastic agent.. mitoxantrone : A dihydroxyanthraquinone that is 1,4-dihydroxy-9,10-anthraquinone which is substituted by 6-hydroxy-1,4-diazahexyl groups at positions 5 and 8.	4.4	3	0	dihydroxyanthraquinone	analgesic; 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.	2.08	1	0	benzamides; 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.	3.23	1	0	monocarboxylic 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)	3.23	1	0	monoterpenoid
entinostat [no description available]	4.41	3	0	benzamides; carbamate ester; primary amino compound; pyridines; substituted aniline	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor
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.	2.08	1	0	acetamides; benzamides	anti-arrhythmia drug
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.	3.23	1	0	methoxynaphthalene; methyl ketone	cyclooxygenase 2 inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug; prodrug
nadolol [no description available]	3.61	2	0	tetralins
nalidixic acid [no description available]	3.61	2	0	1,8-naphthyridine derivative; monocarboxylic acid; quinolone antibiotic	antibacterial drug; antimicrobial agent; DNA synthesis inhibitor
naratriptan naratriptan: structure given in first source	3.23	1	0	heteroarylpiperidine; sulfonamide; tryptamines	serotonergic agonist; vasoconstrictor agent
nefazodone nefazodone: may be useful as an opiate adjunct	3.61	2	0	aromatic 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.	2.08	1	0	benzoxazocine; 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.	2.08	1	0	quaternary ammonium ion	antidote to curare poisoning; EC 3.1.1.7 (acetylcholinesterase) inhibitor
nevirapine Nevirapine: A potent, non-nucleoside reverse transcriptase inhibitor used in combination with nucleoside analogues for treatment of HIV INFECTIONS and AIDS.. nevirapine : A dipyridodiazepine that is 5,11-dihydro-6H-dipyrido[3,2-b:2',3'-e][1,4]diazepine which is substituted by methyl, oxo, and cyclopropyl groups at positions 4, 6, and 11, respectively. A non-nucleoside reverse transcriptase inhibitor with activity against HIV-1, it is used in combination with other antiretrovirals for the treatment of HIV infection.	3.61	2	0	cyclopropanes; dipyridodiazepine	antiviral drug; HIV-1 reverse transcriptase inhibitor
nialamide Nialamide: An MAO inhibitor that is used as an antidepressive agent.	3.23	1	0	organonitrogen compound; organooxygen compound
nicardipine Nicardipine: A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.. nicardipine : A racemate comprising equimolar amounts of (R)- and (S)-nicardipine. It is a calcium channel blocker which is used to treat hypertension.. 2-[benzyl(methyl)amino]ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine substituted by a methyl, {2-[benzyl(methyl)amino]ethoxy}carbonyl, 3-nitrophenyl, methoxycarbonyl and methyl groups at positions 2, 3, 4, 5 and 6, respectively.	3.61	2	0	benzenes; C-nitro compound; diester; dihydropyridine; methyl ester; tertiary amino compound
nifedipine Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.	5.29	3	1	C-nitro compound; dihydropyridine; methyl ester	calcium channel blocker; human metabolite; tocolytic agent; vasodilator agent
nilutamide [no description available]	3.23	1	0	(trifluoromethyl)benzenes; C-nitro compound; imidazolidinone	androgen antagonist; antineoplastic agent
nimesulide nimesulide: structure. nimesulide : An aromatic ether having phenyl and 2-methylsulfonamido-5-nitrophenyl as the two aryl groups.	3.61	2	0	aromatic ether; C-nitro compound; sulfonamide	cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
nimodipine Nimodipine: A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.. nimodipine : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a (2-methoxyethoxy)carbonyl group at position 3, a m-nitrophenyl group at position 4, and an isopropoxycarbonyl group at position 5. An L-type calcium channel blocker, it acts particularly on cerebral circulation, and is used both orally and intravenously for the prevention and treatment of subarachnoid hemorrhage from ruptured intracranial aneurysm.	3.61	2	0	2-methoxyethyl ester; C-nitro compound; dicarboxylic acids and O-substituted derivatives; diester; dihydropyridine; isopropyl ester	antihypertensive agent; calcium channel blocker; cardiovascular drug; vasodilator agent
nisoldipine Nisoldipine: A dihydropyridine calcium channel antagonist that acts as a potent arterial vasodilator and antihypertensive agent. It is also effective in patients with cardiac failure and angina.. nisoldipine : A racemate consisting of equimolar amounts of (R)- and (S)-nisoldipine. A calcium channel blocker, it is used in the treatment of hypertension and angina pectoris.. methyl 2-methylpropyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a methoxycarbonyl group at position 3, an o-nitrophenyl group at position 4, and an isobutoxycarbonyl group at position 5. The racemate, a calcium channel blocker, is used in the treatment of hypertension and angina pectoris.	3.61	2	0	C-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).	2.08	1	0	1,4-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.	2.08	1	0	C-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.	11.28	5	2	nitroglycerol	explosive; muscle relaxant; nitric oxide donor; prodrug; tocolytic agent; vasodilator agent; xenobiotic
nizatidine [no description available]	3.23	1	0	1,3-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.	3.23	1	0	isoquinolines	dopamine uptake inhibitor
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.	3.61	2	0	fluoroquinolone antibiotic; N-arylpiperazine; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone	antibacterial drug; DNA synthesis inhibitor; environmental contaminant; xenobiotic
nortriptyline Nortriptyline: A metabolite of AMITRIPTYLINE that is also used as an antidepressive agent. Nortriptyline is used in major depression, dysthymia, and atypical depressions.. nortriptyline : An organic tricyclic compound that is 10,11-dihydro-5H-dibenzo[a,d][7]annulene substituted by a 3-(methylamino)propylidene group at position 5. It is an active metabolite of amitriptyline.	3.61	2	0	organic tricyclic compound; secondary amine	adrenergic uptake inhibitor; analgesic; antidepressant; antineoplastic agent; apoptosis inducer; drug metabolite
ofloxacin Ofloxacin: A synthetic fluoroquinolone antibacterial agent that inhibits the supercoiling activity of bacterial DNA GYRASE, halting DNA REPLICATION.. 9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid : An oxazinoquinoline that is 2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinolin-7-one substituted by methyl, carboxy, fluoro, and 4-methylpiperazin-1-yl groups at positions 3, 6, 9, and 10, respectively.. ofloxacin : A racemate comprising equimolar amounts of levofloxacin and dextrofloxacin. It is a synthetic fluoroquinolone antibacterial agent which inhibits the supercoiling activity of bacterial DNA gyrase, halting DNA replication.	3.61	2	0	3-oxo monocarboxylic acid; N-arylpiperazine; N-methylpiperazine; organofluorine compound; oxazinoquinoline
olomoucine olomoucine: inhibits protein P34CDC2. olomoucine : A 9H-purine that is substituted by a (2-hydroxyethyl)nitrilo, benzylnitrilo and a methyl group at positions 2,6 and 9, respectively. It is a cyclin-dependent kinase inhibitor.	2.41	1	0	2,6-diaminopurines; ethanolamines	EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
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.	3.61	2	0	aromatic 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.	3.61	2	0	carbazoles
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.	3.23	1	0	ether; 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.	2.49	2	0	1,3,5-triazines; monocarboxylic acid
oxaprozin Oxaprozin: An oxazole-propionic acid derivative, cyclooxygenase inhibitor, and non-steroidal anti-inflammatory drug that is used in the treatment of pain and inflammation associated with of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; and ARTHRITIS, JUVENILE.. oxaprozin : A monocarboxylic acid that is a propionic acid derivative having a 4,5-diphenyl-1,3-oxazol-2-yl substituent at position 3. It is non-steroidal anti-inflammatory drug commonly used to relieve the pain and inflammatory responses associated with osteoarthritis and rheumatoid arthritis.	3.61	2	0	1,3-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.	3.23	1	0	1,4-benzodiazepinone; organochlorine compound	anxiolytic drug; environmental contaminant; 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.	3.94	3	0	acetylenic compound; carboxylic ester; racemate; tertiary alcohol; tertiary amino compound	antispasmodic drug; calcium channel blocker; local anaesthetic; muscarinic antagonist; muscle relaxant; parasympatholytic
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.	3.23	1	0	aminobenzoic acid; phenols	antitubercular agent
pamidronate [no description available]	3.23	1	0	phosphonoacetic 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.	3.23	1	0	aromatic ether; benzimidazoles; organofluorine compound; pyridines; sulfoxide	anti-ulcer drug; EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor; environmental contaminant; xenobiotic
papaverine Papaverine: An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels.. papaverine : A benzylisoquinoline alkaloid that is isoquinoline substituted by methoxy groups at positions 6 and 7 and a 3,4-dimethoxybenzyl group at position 1. It has been isolated from Papaver somniferum.	3.61	2	0	benzylisoquinoline alkaloid; dimethoxybenzene; isoquinolines	antispasmodic drug; vasodilator agent
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'.	2.1	1	0	aromatic 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.	3.61	2	0	1,3-oxazoles	central 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.	3.61	2	0	aromatic 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.	3.23	1	0	barbiturates	GABAA receptor agonist
pentoxifylline [no description available]	3.61	2	0	oxopurine
perhexiline Perhexiline: 2-(2,2-Dicyclohexylethyl)piperidine. Coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis.	3.23	1	0	piperidines	cardiovascular drug
perphenazine Perphenazine: An antipsychotic phenothiazine derivative with actions and uses similar to those of CHLORPROMAZINE.. perphenazine : A phenothiazine derivative in which the phenothiazine tricycle carries a chloro substituent at the 2-position and a 3-[4-(2-hydroxyethyl)piperazin-1-yl]propyl group at N-10.	3.61	2	0	N-(2-hydroxyethyl)piperazine; N-alkylpiperazine; organochlorine compound; phenothiazines	antiemetic; dopaminergic antagonist; phenothiazine antipsychotic drug
phenacetin Saridon: contains phenacetin, caffeine, propyphenazone & pyrithyldione	2.08	1	0	acetamides; 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.	9.74	4	0	barbiturates	anticonvulsant; drug allergen; excitatory amino acid antagonist; sedative
phenoxybenzamine Phenoxybenzamine: An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.	3.23	1	0	aromatic 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.	3.23	1	0	primary amine	adrenergic 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.	3.23	1	0	monocarboxylic acid	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor; prodrug
pindolol Pindolol: A moderately lipophilic beta blocker (ADRENERGIC BETA-ANTAGONISTS). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638). pindolol : A member of the class of indols which is the 2-hydroxy-3-(isopropylamino)propyl ether derivative of 1H-indol-4-ol.	3.61	2	0	indoles; 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.	4.25	5	0	aromatic 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
piracetam Piracetam: A compound suggested to be both a nootropic and a neuroprotective agent.	2.08	1	0	organonitrogen compound; organooxygen compound
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.	2.08	1	0	N-arylpiperazine
polythiazide [no description available]	3.23	1	0	benzothiadiazine
duodote duodote: consists of atropine and pralidoxime chloride; for treating those exposed to organophosphorus-containing nerve agents	3.23	1	0	pyridinium ion	antidote to organophosphate poisoning; antidote to sarin poisoning; cholinergic drug; cholinesterase reactivator
ono 1078 pranlukast: SRS-A antagonist; leukotriene D4 receptor antagonist	2.08	1	0	chromones
pyranoprofen pyranoprofen: RN given refers to unlabled parent cpd; structure given in first source	2.08	1	0	pyridochromene
praziquantel azinox: Russian drug	3.61	2	0	isoquinolines
prazosin Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.. prazosin : A member of the class of piperazines that is piperazine substituted by a furan-2-ylcarbonyl group and a 4-amino-6,7-dimethoxyquinazolin-2-yl group at positions 1 and 4 respectively.	3.61	2	0	aromatic ether; furans; monocarboxylic acid amide; piperazines; quinazolines	alpha-adrenergic antagonist; antihypertensive agent; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
primaquine Primaquine: An aminoquinoline that is given by mouth to produce a radical cure and prevent relapse of vivax and ovale malarias following treatment with a blood schizontocide. It has also been used to prevent transmission of falciparum malaria by those returning to areas where there is a potential for re-introduction of malaria. Adverse effects include anemias and GI disturbances. (From Martindale, The Extra Pharmacopeia, 30th ed, p404). primaquine : An N-substituted diamine that is pentane-1,4-diamine substituted by a 6-methoxyquinolin-8-yl group at the N(4) position. It is a drug used in the treatment of malaria and Pneumocystis pneumonia.	3.61	2	0	aminoquinoline; aromatic ether; N-substituted diamine	antimalarial
primidone Primidone: A barbiturate derivative that acts as a GABA modulator and anti-epileptic agent. It is partly metabolized to PHENOBARBITAL in the body and owes some of its actions to this metabolite.. primidone : A pyrimidone that is dihydropyrimidine-4,6(1H,5H)-dione substituted by an ethyl and a phenyl group at position 5. It is used as an anticonvulsant for treatment of various types of seizures.	3.61	2	0	pyrimidone	anticonvulsant; environmental contaminant; xenobiotic
probenecid Probenecid: The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.. probenecid : A sulfonamide in which the nitrogen of 4-sulfamoylbenzoic acid is substituted with two propyl groups.	3.88	3	0	benzoic acids; sulfonamide	uricosuric drug
procainamide Procainamide: A class Ia antiarrhythmic drug that is structurally-related to PROCAINE.. procainamide : A benzamide that is 4-aminobenzamide substituted on the amide N by a 2-(diethylamino)ethyl group. It is a pharmaceutical antiarrhythmic agent used for the medical treatment of cardiac arrhythmias.	3.61	2	0	benzamides	anti-arrhythmia drug; platelet aggregation inhibitor; sodium channel blocker
procarbazine Procarbazine: An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease.. procarbazine : A benzamide obtained by formal condensation of the carboxy group of 4-[(2-methylhydrazino)methyl]benzoic acid with the amino group of isopropylamine. An antineoplastic chemotherapy drug used for treatment of Hodgkin's lymphoma. Metabolism yields azo-procarbazine and hydrogen peroxide, which results in the breaking of DNA strands.	3.23	1	0	benzamides; hydrazines	antineoplastic agent
prochlorperazine Prochlorperazine: A phenothiazine antipsychotic used principally in the treatment of NAUSEA; VOMITING; and VERTIGO. It is more likely than CHLORPROMAZINE to cause EXTRAPYRAMIDAL DISORDERS. (From Martindale, The Extra Pharmacopoeia, 30th ed, p612). prochlorperazine : A member of the class of phenothiazines that is 10H-phenothiazine having a chloro substituent at the 2-position and a 3-(4-methylpiperazin-1-yl)propyl group at the N-10 position.	3.61	2	0	N-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.	3.61	2	0	pyrrolidines; tertiary alcohol	antidyskinesia agent; antiparkinson drug; muscarinic antagonist
promethazine Promethazine: A phenothiazine derivative with histamine H1-blocking, antimuscarinic, and sedative properties. It is used as an antiallergic, in pruritus, for motion sickness and sedation, and also in animals.. promethazine : A tertiary amine that is a substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropan-2-amine moiety.	3.61	2	0	phenothiazines; tertiary amine	anti-allergic agent; anticoronaviral agent; antiemetic; antipruritic drug; H1-receptor antagonist; local anaesthetic; sedative
propachlor propachlor: structure. propachlor : An anilide that consists of 2-chloroacetanilide bearing an N-isopropyl substituent.	7.07	1	0	anilide; monocarboxylic acid amide; organochlorine compound	environmental contaminant; herbicide; xenobiotic
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.	3.61	2	0	aromatic 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.	3.23	1	0	xanthenes
propofol Propofol: An intravenous anesthetic agent which has the advantage of a very rapid onset after infusion or bolus injection plus a very short recovery period of a couple of minutes. (From Smith and Reynard, Textbook of Pharmacology, 1992, 1st ed, p206). Propofol has been used as ANTICONVULSANTS and ANTIEMETICS.. propofol : A phenol resulting from the formal substitution of the hydrogen at the 2 position of 1,3-diisopropylbenzene by a hydroxy group.	3.63	2	0	phenols	anticonvulsant; 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.	4.07	4	0	naphthalenes; propanolamine; secondary amine	anti-arrhythmia drug; antihypertensive agent; anxiolytic drug; beta-adrenergic antagonist; environmental contaminant; human blood serum metabolite; vasodilator agent; xenobiotic
protriptyline Protriptyline: Tricyclic antidepressant similar in action and side effects to IMIPRAMINE. It may produce excitation.	3.23	1	0	carbotricyclic compound	antidepressant
pyridostigmine [no description available]	3.23	1	0	pyridinium ion
pyrimethamine Maloprim: contains above 2 cpds	3.23	1	0	aminopyrimidine; monochlorobenzenes	antimalarial; antiprotozoal drug; EC 1.5.1.3 (dihydrofolate reductase) inhibitor
sch 16134 quazepam: structure given in first source	3.23	1	0	benzodiazepine
quetiapine [no description available]	3.23	1	0	dibenzothiazepine; 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.	3.23	1	0	benzimidazoles; 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.	3.23	1	0	1-benzothiophenes; aromatic ketone; N-oxyethylpiperidine; phenols	bone density conservation agent; estrogen antagonist; estrogen receptor modulator
ranitidine [no description available]	2.08	1	0	aralkylamine
riluzole Riluzole: A glutamate antagonist (RECEPTORS, GLUTAMATE) used as an anticonvulsant (ANTICONVULSANTS) and to prolong the survival of patients with AMYOTROPHIC LATERAL SCLEROSIS.	3.61	2	0	benzothiazoles
rimantadine Rimantadine: An RNA synthesis inhibitor that is used as an antiviral agent in the prophylaxis and treatment of influenza.	3.23	1	0	alkylamine
risperidone Risperidone: A selective blocker of DOPAMINE D2 RECEPTORS and SEROTONIN 5-HT2 RECEPTORS that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of SCHIZOPHRENIA.. risperidone : A member of the class of pyridopyrimidines that is 2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one carrying an additional 2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl group at position 2.	3.61	2	0	1,2-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	3.23	1	0	tryptamines	anti-inflammatory drug; serotonergic agonist; vasoconstrictor agent
rofecoxib [no description available]	2.08	1	0	butenolide; sulfone	analgesic; cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
ropinirole [no description available]	3.23	1	0	indolones; tertiary amine	antidyskinesia agent; antiparkinson drug; central nervous system drug; dopamine agonist
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.	3.23	1	0	benzoate 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
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.	3.23	1	0	barbiturates	anaesthesia adjuvant; GABA modulator; sedative
sibutramine sibutramine: serotonin and norepinephrine transporter inhibitor; Meridia is tradename for sibutramine hydrochloride	3.23	1	0	organochlorine compound; tertiary amino compound	anti-obesity agent; serotonin uptake inhibitor
sulfadiazine Sulfadiazine: One of the short-acting SULFONAMIDES used in combination with PYRIMETHAMINE to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections.. sulfadiazine : A sulfonamide consisting of pyrimidine with a 4-aminobenzenesulfonamido group at the 2-position.. diazine : The parent structure of the diazines.	3.61	2	0	pyrimidines; substituted aniline; sulfonamide antibiotic; sulfonamide	antiinfective agent; antimicrobial agent; antiprotozoal drug; coccidiostat; drug allergen; EC 1.1.1.153 [sepiapterin reductase (L-erythro-7,8-dihydrobiopterin forming)] inhibitor; EC 2.5.1.15 (dihydropteroate synthase) inhibitor; environmental contaminant; xenobiotic
risedronic acid Risedronic Acid: A pyridine and diphosphonic acid derivative that acts as a CALCIUM CHANNEL BLOCKER and inhibits BONE RESORPTION.	3.23	1	0	pyridines
sotalol Sotalol: An adrenergic beta-antagonist that is used in the treatment of life-threatening arrhythmias.. sotalol : A sulfonamide that is N-phenylmethanesulfonamide in which the phenyl group is substituted at position 4 by a 1-hydroxy-2-(isopropylamino)ethyl group. It has both beta-adrenoreceptor blocking (Vaughan Williams Class II) and cardiac action potential duration prolongation (Vaughan Williams Class III) antiarrhythmic properties. It is used (usually as the hydrochloride salt) for the management of ventricular and supraventricular arrhythmias.	3.61	2	0	ethanolamines; secondary alcohol; secondary amino compound; sulfonamide	anti-arrhythmia drug; beta-adrenergic antagonist; environmental contaminant; xenobiotic
imatinib [no description available]	4.67	4	0	aromatic 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).	12.33	6	2	dicarboxylic 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.	3.23	1	0	quaternary ammonium ion; succinate ester	drug allergen; muscle relaxant; neuromuscular agent
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.	3.23	1	0	sulfonamide 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.	2.08	1	0	isoxazoles; 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
sulfanitran [no description available]	2.08	1	0	sulfonamide
sulfasalazine Sulfasalazine: A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907). sulfasalazine : An azobenzene consisting of diphenyldiazene having a carboxy substituent at the 4-position, a hydroxy substituent at the 3-position and a 2-pyridylaminosulphonyl substituent at the 4'-position.	3.61	2	0
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.	3.23	1	0	1,3-thiazoles; substituted aniline; sulfonamide antibiotic; sulfonamide	antiinfective agent; drug allergen; EC 2.5.1.15 (dihydropteroate synthase) inhibitor; environmental contaminant; xenobiotic
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.	2.08	1	0	isoxazoles; sulfonamide antibiotic; sulfonamide	antibacterial drug; drug allergen
sulforaphane sulforaphane: from Cardaria draba L.. sulforaphane : An isothiocyanate having a 4-(methylsulfinyl)butyl group attached to the nitrogen.	2.89	3	0	isothiocyanate; 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]	3.23	1	0	alkylbenzene
sumatriptan Sumatriptan: A serotonin agonist that acts selectively at 5HT1 receptors. It is used in the treatment of MIGRAINE DISORDERS.. sumatriptan : A sulfonamide that consists of N,N-dimethyltryptamine bearing an additional (N-methylsulfamoyl)methyl substituent at position 5. Selective agonist for a vascular 5-HT1 receptor subtype (probably a member of the 5-HT1D family). Used (in the form of its succinate salt) for the acute treatment of migraine with or without aura in adults.	3.61	2	0	sulfonamide; tryptamines	serotonergic agonist; vasoconstrictor agent
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.	2.08	1	0	N-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.	2.08	1	0	acetylenic compound; ethyl ester; pyridines; retinoid; thiochromane	keratolytic drug; prodrug; teratogenic agent
tegafur [no description available]	2.49	2	0	organohalogen compound; pyrimidines
temazepam Temazepam: A benzodiazepine that acts as a GAMMA-AMINOBUTYRIC ACID modulator and anti-anxiety agent.	3.23	1	0	benzodiazepine
temozolomide [no description available]	13.54	30	9	imidazotetrazine; monocarboxylic acid amide; triazene derivative	alkylating agent; antineoplastic agent; prodrug
terazosin Terazosin: induces decreased blood pressure; used in the treatment of benign prostatic hyperplasia	3.61	2	0	furans; piperazines; primary amino compound; quinazolines	alpha-adrenergic antagonist; antihypertensive agent; antineoplastic agent
terbutaline Terbutaline: A selective beta-2 adrenergic agonist used as a bronchodilator and tocolytic.. terbutaline : A member of the class of phenylethanolamines that is catechol substituted at position 5 by a 2-(tert-butylamino)-1-hydroxyethyl group.	3.61	2	0	phenylethanolamines; 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.	2.08	1	0	diarylmethane
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.	9.79	12	2	phthalimides; piperidones
thiabendazole Tresaderm: dermatologic soln containing dexamethasone, thiabendazole & neomycin sulfate	3.23	1	0	1,3-thiazoles; benzimidazole fungicide; benzimidazoles	antifungal agrochemical; antinematodal drug
thioridazine Thioridazine: A phenothiazine antipsychotic used in the management of PHYCOSES, including SCHIZOPHRENIA.. thioridazine : A phenothiazine derivative having a methylsulfanyl subsitituent at the 2-position and a (1-methylpiperidin-2-yl)ethyl] group at the N-10 position.	3.23	1	0	phenothiazines; 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).	3.61	2	0	aziridines
tiapride [no description available]	2.08	1	0	benzamides
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.	14.38	43	19	monochlorobenzenes; 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.	2.08	1	0	aromatic 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.	3.61	2	0	imidazoles	antiamoebic agent; antibacterial drug; antiparasitic agent; antiprotozoal drug
tiopronin Tiopronin: Sulfhydryl acylated derivative of GLYCINE.	3.23	1	0	N-acyl-amino acid
tizanidine tizanidine: RN given refers to parent cpd; structure. tizanidine : 2,1,3-Benzothiadiazole substituted at C-4 by a Delta(1)-imidazolin-2-ylamino group and at C-4 by a chloro group. It is an agonist at alpha2-adrenergic receptor sites.	3.61	2	0	benzothiadiazole; 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)	2.08	1	0	pyridinecarboxamide
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.	3.23	1	0	N-sulfonylurea	hypoglycemic agent; potassium channel blocker
tolbutamide Tolbutamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). tolbutamide : An N-sulfonylurea that consists of 1-butylurea having a tosyl group attached at the 3-position.	3.61	2	0	N-sulfonylurea	human 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.	3.23	1	0	aromatic ketone; monocarboxylic acid; pyrroles	EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-steroidal anti-inflammatory drug
tolnaftate [no description available]	2.08	1	0	monothiocarbamic ester	antifungal drug
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.	3.23	1	0	aromatic ether; tertiary alcohol; tertiary amino compound
tranexamic acid Tranexamic Acid: Antifibrinolytic hemostatic used in severe hemorrhage.	3.23	1	0	amino acid
trazodone Trazodone: A serotonin uptake inhibitor that is used as an antidepressive agent. It has been shown to be effective in patients with major depressive disorders and other subsets of depressive disorders. It is generally more useful in depressive disorders associated with insomnia and anxiety. This drug does not aggravate psychotic symptoms in patients with schizophrenia or schizoaffective disorders. (From AMA Drug Evaluations Annual, 1994, p309). trazodone : An N-arylpiperazine in which one nitrogen is substituted by a 3-chlorophenyl group, while the other is substituted by a 3-(3-oxo[1,2,4]triazolo[4,3-a]pyridin-2(3H)-yl)propyl group.	3.61	2	0	monochlorobenzenes; N-alkylpiperazine; N-arylpiperazine; triazolopyridine	adrenergic antagonist; antidepressant; anxiolytic drug; H1-receptor antagonist; sedative; serotonin uptake inhibitor
triamterene Triamterene: A pteridinetriamine compound that inhibits SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS.. triamterene : Pteridine substituted at positions 2, 4 and 7 with amino groups and at position 6 with a phenyl group. A sodium channel blocker, it is used as a diuretic in the treatment of hypertension and oedema.	3.61	2	0	pteridines	diuretic; 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.	3.23	1	0	triazolobenzodiazepine	sedative
trifluoperazine [no description available]	3.23	1	0	N-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
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.	3.23	1	0	amine
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.	3.23	1	0	oxazolidinone	anticonvulsant; 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.	3.23	1	0	benzamides; tertiary amino compound	antiemetic
trimethoprim Trimethoprim: A pyrimidine inhibitor of dihydrofolate reductase, it is an antibacterial related to PYRIMETHAMINE. It is potentiated by SULFONAMIDES and the TRIMETHOPRIM, SULFAMETHOXAZOLE DRUG COMBINATION is the form most often used. It is sometimes used alone as an antimalarial. TRIMETHOPRIM RESISTANCE has been reported.. trimethoprim : An aminopyrimidine antibiotic whose structure consists of pyrimidine 2,4-diamine and 1,2,3-trimethoxybenzene moieties linked by a methylene bridge.	3.61	2	0	aminopyrimidine; 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.	3.23	1	0
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.	3.23	1	0	dibenzoazepine; tertiary amino compound	antidepressant; environmental contaminant; xenobiotic
troglitazone Troglitazone: A chroman and thiazolidinedione derivative that acts as a PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS (PPAR) agonist. It was formerly used in the treatment of TYPE 2 DIABETES MELLITUS, but has been withdrawn due to hepatotoxicity.	3.61	2	0	chromanes; 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
thenoyltrifluoroacetone Thenoyltrifluoroacetone: Chelating agent and inhibitor of cellular respiration.	2.08	1	0
tyramine [no description available]	3.23	1	0	monoamine molecular messenger; primary amino compound; tyramines	EC 3.1.1.8 (cholinesterase) inhibitor; Escherichia coli metabolite; human metabolite; mouse metabolite; neurotransmitter
tyrphostin a9 [no description available]	2.41	1	0	alkylbenzene	geroprotector
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.	3.23	1	0	aminopyridine; 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.	2.08	1	0	undecenoic acid	antifungal drug; plant metabolite
urapidil [no description available]	2.08	1	0	piperazines
venlafaxine venlafaxine : A tertiary amino compound that is N,N-dimethylethanamine substituted at position 1 by a 1-hydroxycyclohexyl and 4-methoxyphenyl group.	3.61	2	0	cyclohexanols; monomethoxybenzene; tertiary alcohol; tertiary amino compound	adrenergic uptake inhibitor; analgesic; antidepressant; dopamine uptake inhibitor; environmental contaminant; serotonin uptake inhibitor; xenobiotic
vigabatrin [no description available]	5.85	6	0	gamma-amino acid	anticonvulsant; EC 2.6.1.19 (4-aminobutyrate--2-oxoglutarate transaminase) inhibitor
pirinixic acid pirinixic acid: structure	2.08	1	0	aryl sulfide; organochlorine compound; pyrimidines
ici 204,219 zafirlukast: a leukotriene D4 receptor antagonist	3.61	2	0	carbamate 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.	3.61	2	0	nitrile; pyrazolopyrimidine	anticonvulsant; anxiolytic drug; central nervous system depressant; sedative
zolpidem Zolpidem: An imidazopyridine derivative and short-acting GABA-A receptor agonist that is used for the treatment of INSOMNIA.. zolpidem : An imidazo[1,2-a]pyridine compound having a 4-tolyl group at the 2-position, an N,N-dimethylcarbamoylmethyl group at the 3-position and a methyl substituent at the 6-position.	3.23	1	0	imidazopyridine	central nervous system depressant; GABA agonist; sedative
zonisamide Zonisamide: A benzisoxazole and sulfonamide derivative that acts as a CALCIUM CHANNEL blocker. It is used primarily as an adjunctive antiepileptic agent for the treatment of PARTIAL SEIZURES, with or without secondary generalization.. zonisamide : A 1,2-benzoxazole compound having a sulfamoylmethyl substituent at the 3-position.	5.04	4	0	1,2-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.	2.08	1	0	monochloropyridine; pyrrolopyrazine	central nervous system depressant; sedative
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.	3.23	1	0	corticosteroid 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.	10.91	2	1	mitomycin	alkylating agent; antineoplastic agent
prednisolone Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.. prednisolone : A glucocorticoid that is prednisone in which the oxo group at position 11 has been reduced to the corresponding beta-hydroxy group. It is a drug metabolite of prednisone.	11.67	35	13	11beta-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.	3.8	1	1	16alpha-hydroxy steroid; 17beta-hydroxy steroid; 3-hydroxy steroid	estrogen; human metabolite; human xenobiotic metabolite; mouse metabolite
reserpine Reserpine: An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.. reserpine : An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria.	3.61	2	0	alkaloid 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
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.	3.23	1	0	imidazoles; phenols; substituted aniline; tertiary amino compound	alpha-adrenergic antagonist; vasodilator agent
sorbitol D-glucitol : The D-enantiomer of glucitol (also known as D-sorbitol).	3.23	1	0	glucitol	cathartic; Escherichia coli metabolite; food humectant; human metabolite; laxative; metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite; sweetening agent
hydroxyproline Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ASCORBIC ACID can result in impaired hydroxyproline formation.. hydroxyproline : A proline derivative that is proline substituted by at least one hydroxy group.	3.33	6	0	4-hydroxyproline; L-alpha-amino acid zwitterion	human metabolite; mouse metabolite; plant metabolite
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.	3.71	2	0	2-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.	3.23	1	0	1-phenylpropan-2-amine	adrenergic agent; adrenergic uptake inhibitor; dopamine uptake inhibitor; dopaminergic agent; neurotoxin; sympathomimetic agent
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.	3.97	3	0	3-oxo-Delta(4) steroid; oxaspiro compound; steroid lactone; thioester	aldosterone antagonist; antihypertensive agent; diuretic; environmental contaminant; xenobiotic
aldosterone [no description available]	3.59	1	1	11beta-hydroxy steroid; 18-oxo steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(4) steroid; C21-steroid hormone; mineralocorticoid; primary alpha-hydroxy ketone; steroid aldehyde	human metabolite; mouse metabolite
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.	3.61	2	0	non-proteinogenic alpha-amino acid; penicillamine	antirheumatic drug; chelator; copper chelator; drug allergen
cysteine [no description available]	3.23	1	0	cysteine 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.	13.75	35	21	11-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.	5.1	2	1	17-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.	3.23	1	0	17beta-hydroxy steroid; 3-oxo steroid; anabolic androgenic steroid; oxa-steroid	anabolic agent; androgen
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.	3.23	1	0	penicillin allergen; penicillin	antibacterial drug; drug allergen; epitope
pilocarpine Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.. (+)-pilocarpine : The (+)-enantiomer of pilocarpine.	3.23	1	0	pilocarpine	antiglaucoma 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.	3.23	1	0	2-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.	2.08	1	0	chlorocarbon; chloromethanes	hepatotoxic agent; refrigerant
alanine Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases IMMUNITY, and provides energy for muscle tissue, BRAIN, and the CENTRAL NERVOUS SYSTEM.. alanine : An alpha-amino acid that consists of propionic acid bearing an amino substituent at position 2.	2.41	1	0	alanine zwitterion; alanine; L-alpha-amino acid; proteinogenic amino acid; pyruvate family amino acid	EC 4.3.1.15 (diaminopropionate ammonia-lyase) inhibitor; fundamental metabolite
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.	2.58	2	0	L-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.	3.61	2	0	C-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.	2	1	0	aspartate 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.	6.79	6	1	amino 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
vincristine [no description available]	3.23	1	0	acetate ester; formamides; methyl ester; organic heteropentacyclic compound; organic heterotetracyclic compound; tertiary alcohol; tertiary amino compound; vinca alkaloid	antineoplastic agent; drug; microtubule-destabilising agent; plant metabolite; tubulin modulator
physostigmine Physostigmine: A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.	3.23	1	0	carbamate ester; indole alkaloid	antidote to curare poisoning; EC 3.1.1.8 (cholinesterase) inhibitor; miotic
ethinyl estradiol Ethinyl Estradiol: A semisynthetic alkylated ESTRADIOL with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally, and is often used as the estrogenic component in ORAL CONTRACEPTIVES.. 17alpha-ethynylestradiol : A 3-hydroxy steroid that is estradiol substituted by a ethynyl group at position 17. It is a xenoestrogen synthesized from estradiol and has been shown to exhibit high estrogenic potency on oral administration.	2.51	2	0	17-hydroxy steroid; 3-hydroxy steroid; terminal acetylenic compound	xenoestrogen
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.	2.08	1	0	bisbenzylisoquinoline alkaloid	drug 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.	3.61	2	0	aporphine alkaloid	alpha-adrenergic drug; antidyskinesia agent; antiparkinson drug; dopamine agonist; emetic; serotonergic drug
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.	3.23	1	0	17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; enone	anabolic agent; androgen; antineoplastic agent
tetrabenazine 9,10-dimethoxy-3-isobutyl-1,3,4,6,7,11b-hexahydro-2H-pyrido[2,1-a]isoquinolin-2-one : A benzoquinolizine that is 1,2,3,4,4a,9,10,10a-octahydrophenanthrene in which the carbon at position 10a is replaced by a nitrogen and which is substituted by an isobutyl group at position 2, an oxo group at position 3, and methoxy groups at positions 6 and 7.	3.23	1	0	benzoquinolizine; 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.	2.13	1	0	adenosine 5'-phosphate; purine ribonucleoside 5'-diphosphate	fundamental metabolite; human metabolite
kanamycin a Kanamycin: Antibiotic complex produced by Streptomyces kanamyceticus from Japanese soil. Comprises 3 components: kanamycin A, the major component, and kanamycins B and C, the minor components.. kanamycin : Kanamycin is a naturally occurring antibiotic complex from Streptomyces kanamyceticus that consists of several components: kanamycin A, the major component (also usually designated as kanamycin), and kanamycins B, C, D and X the minor components.	3.61	2	0	kanamycins	bacterial 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.	2.03	1	0	pyrimidine 2'-deoxyribonucleoside	antimetabolite; antineoplastic agent
carbostyril Quinolones: A group of derivatives of naphthyridine carboxylic acid, quinoline carboxylic acid, or NALIDIXIC ACID.. quinolin-2(1H)-one : A quinolone that is 1,2-dihydroquinoline substituted by an oxo group at position 2.	7.27	9	2	monohydroxyquinoline; quinolone	bacterial xenobiotic metabolite
levodopa Levodopa: The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.. L-dopa : An optically active form of dopa having L-configuration. Used to treat the stiffness, tremors, spasms, and poor muscle control of Parkinson's disease	2.08	1	0	amino 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.	3.23	1	0	ethylenediamine derivative; polyamino carboxylic acid; tetracarboxylic acid	anticoagulant; antidote; chelator; copper chelator; geroprotector
cysteamine Cysteamine: A mercaptoethylamine compound that is endogenously derived from the COENZYME A degradative pathway. The fact that cysteamine is readily transported into LYSOSOMES where it reacts with CYSTINE to form cysteine-cysteamine disulfide and CYSTEINE has led to its use in CYSTINE DEPLETING AGENTS for the treatment of CYSTINOSIS.. cysteamine : An amine that consists of an ethane skeleton substituted with a thiol group at C-1 and an amino group at C-2.	3.68	2	0	amine; thiol	geroprotector; human metabolite; mouse metabolite; radiation protective agent
acetylcholine chloride acetylcholine chloride : The chloride salt of acetylcholine, and a parasympatomimetic drug.	3.23	1	0	quaternary 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.	3.23	1	0	phenothiazines
adenosine monophosphate Adenosine Monophosphate: Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position.	2.9	2	0	adenosine 5'-phosphate; purine ribonucleoside 5'-monophosphate	adenosine A1 receptor agonist; cofactor; EC 3.1.3.1 (alkaline phosphatase) inhibitor; EC 3.1.3.11 (fructose-bisphosphatase) inhibitor; fundamental metabolite; micronutrient; nutraceutical
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.	3.23	1	0	penicillin 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.	2.25	1	0	organic chloride salt	acid-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
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.	3.23	1	0	calcium salt	chelator
methionine Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.. methionine : A sulfur-containing amino acid that is butyric acid bearing an amino substituent at position 2 and a methylthio substituent at position 4.	3.63	2	0	aspartate family amino acid; L-alpha-amino acid; methionine zwitterion; methionine; proteinogenic amino acid	antidote to paracetamol poisoning; human metabolite; micronutrient; mouse metabolite; nutraceutical
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.	9.16	4	0	alkaloid; colchicine	anti-inflammatory agent; gout suppressant; mutagen
mebanazine mebanazine: RN given refers to parent cpd without isomeric designation; structure	3.23	1	0	benzenes
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.	3.23	1	0	penicillin	antibacterial agent; antibacterial drug
triamcinolone diacetate triamcinolone diacetate: lysyl oxidase antagonist; Polcortolon may also refers to triamcinolone	2.08	1	0	corticosteroid hormone
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).	3.23	1	0	4-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)	3.23	1	0	aromatic ketone
ampicillin Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic.. ampicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-phenylacetamido group.	3.23	1	0	beta-lactam antibiotic; penicillin allergen; penicillin	antibacterial drug
mannitol [no description available]	3.54	2	0	mannitol	allergen; 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]	13.92	8	3	beta-D-arabinoside; monosaccharide derivative; pyrimidine nucleoside	antimetabolite; antineoplastic agent; antiviral agent; immunosuppressive agent
medroxyprogesterone acetate [no description available]	2.08	1	0	20-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.	2.17	1	0	L-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.	2.13	1	0	amino 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
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.	2.21	1	0	erythrose 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.	3.63	2	0	arginine; glutamine family amino acid; L-alpha-amino acid; proteinogenic amino acid	biomarker; Escherichia coli metabolite; micronutrient; mouse metabolite; nutraceutical
methylene chloride Methylene Chloride: A chlorinated hydrocarbon that has been used as an inhalation anesthetic and acts as a narcotic in high concentrations. Its primary use is as a solvent in manufacturing and food technology.. dichloromethane : A member of the class of chloromethanes that is methane in which two of the hydrogens have been replaced by chlorine. A dense, non-flammible colourless liquid at room temperature (b.p. 40degreeC, d = 1.33) which is immiscible with water, it is widely used as a solvent, a paint stripper, and for the removal of caffeine from coffee and tea.	2.1	1	0	chloromethanes; volatile organic compound	carcinogenic agent; polar aprotic solvent; refrigerant
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.	3.23	1	0	fluoroalkane; 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.	2.08	1	0	11beta-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.	3.23	1	0	11beta-hydroxy steroid; 17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; anabolic androgenic steroid; fluorinated steroid	anabolic agent; antineoplastic agent
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	3.23	1	0	organic molecular entity
tromethamine Tromethamine: An organic amine proton acceptor. It is used in the synthesis of surface-active agents and pharmaceuticals; as an emulsifying agent for cosmetic creams and lotions, mineral oil and paraffin wax emulsions, as a biological buffer, and used as an alkalizer. (From Merck, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p1424)	3.23	1	0	primary amino compound; triol	buffer
methylprednisolone Methylprednisolone: A PREDNISOLONE derivative with similar anti-inflammatory action.. 6alpha-methylprednisolone : The 6alpha-stereoisomer of 6-methylprednisolone.	7.82	20	3	6-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.	2.08	1	0	organic heteropentacyclic compound; rotenones	antineoplastic agent; metabolite; mitochondrial NADH:ubiquinone reductase inhibitor; phytogenic insecticide; piscicide; toxin
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.	3.23	1	0	organobromine compound; pyridines	anti-allergic agent; H1-receptor antagonist
penicillin v Penicillin V: A broad-spectrum penicillin antibiotic used orally in the treatment of mild to moderate infections by susceptible gram-positive organisms.. phenoxymethylpenicillin : A penicillin compound having a 6beta-(phenoxyacetyl)amino side-chain.	3.23	1	0	penicillin 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.	3.23	1	0	glucitol derivative; nitrate ester	nitric oxide donor; vasodilator agent
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.	3.23	1	0	phenylethanolamines; 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.	3.23	1	0	aromatic ketone; tertiary amine	appetite depressant
quinoxalines quinoxaline : A naphthyridine in which the nitrogens are at positions 1 and 4.	2.03	1	0	mancude organic heterobicyclic parent; naphthyridine; ortho-fused heteroarene
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.	2.04	1	0	carbonyl compound
dilactide dilactide: structure given in first source	4.41	1	1	dioxanes
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.	3.23	1	0	benzoate ester; secondary amino compound; substituted aniline	anaesthetic; antitussive
pyrroles 1H-pyrrole : A tautomer of pyrrole that has the double bonds at positions 2 and 4.. pyrrole : A five-membered monocyclic heteroarene comprising one NH and four CH units which forms the parent compound of the pyrrole group of compounds. Its five-membered ring structure has three tautomers. A 'closed class'.. azole : Any monocyclic heteroarene consisting of a five-membered ring containing nitrogen. Azoles can also contain one or more other non-carbon atoms, such as nitrogen, sulfur or oxygen.	19.4	220	25	pyrrole; secondary amine
thiophenes Thiophenes: A monocyclic heteroarene furan in which the oxygen atom is replaced by a sulfur.. thiophenes : Compounds containing at least one thiophene ring.	8.71	8	3	mancude organic heteromonocyclic parent; monocyclic heteroarene; thiophenes; volatile organic compound	non-polar solvent
methylergonovine Methylergonovine: A homolog of ERGONOVINE containing one more CH2 group. (Merck Index, 11th ed)	3.23	1	0	ergoline alkaloid
phenformin Phenformin: A biguanide hypoglycemic agent with actions and uses similar to those of METFORMIN. Although it is generally considered to be associated with an unacceptably high incidence of lactic acidosis, often fatal, it is still available in some countries. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). phenformin : A member of the class of biguanides that is biguanide in which one of the terminal nitrogen atoms is substituted by a 2-phenylethyl group. It was used as an anti-diabetic drug but was later withdrawn from the market due to potential risk of lactic acidosis.	2.52	2	0	biguanides	antineoplastic agent; geroprotector; hypoglycemic agent
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.	2.13	1	0	anthrapyrazole; aromatic ketone; cyclic ketone	antineoplastic agent; c-Jun N-terminal kinase inhibitor; geroprotector
cinchophen cinchophen: was heading 1963-94; ACIPHENOCHINOLIUM was see CHINOPHEN 1978-94; use QUINOLINES to search CINCHOPHEN 1966-94	3.23	1	0	quinolines
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.	3.23	1	0	penicillin allergen; penicillin	antibacterial drug
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.	3.23	1	0	acetylenic compound; barbiturates	drug allergen; intravenous anaesthetic
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.	16.45	79	17	azaarene; mancude organic heterobicyclic parent; ortho-fused heteroarene; quinazolines
indazoles Indazoles: A group of heterocyclic aromatic organic compounds consisting of the fusion of BENZENE and PYRAZOLES.	16.51	87	13	indazole
benzoxazoles 1,3-benzoxazole : A benzoxazole in which the benzene ring is fused to a 1,3-oxazole ring across positions 4 and 5.. benzoxazole : Compounds based on a fused 1,2- or 1,3-oxazole and benzene bicyclic ring skeleton.	3.23	5	0	1,3-benzoxazoles; mancude organic heterobicyclic parent
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.	2.78	3	0	isoxazoles; mancude organic heteromonocyclic parent; monocyclic heteroarene
thiazoles [no description available]	8.75	18	1	1,3-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.	10.21	17	3	diazine; pyrazines	Daphnia magna metabolite
nitroblue tetrazolium Nitroblue Tetrazolium: Colorless to yellow dye that is reducible to blue or black formazan crystals by certain cells; formerly used to distinguish between nonbacterial and bacterial diseases, the latter causing neutrophils to reduce the dye; used to confirm diagnosis of chronic granulomatous disease.	2.05	1	0	organic cation
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.	3.23	1	0	phenethylamine alkaloid; phenylethanolamines	bacterial metabolite; environmental contaminant; nasal decongestant; plant metabolite; sympathomimetic agent; vasoconstrictor agent; xenobiotic
hydrazine diamine : Any polyamine that contains two amino groups.	2.13	1	0	azane; hydrazines	EC 4.3.1.10 (serine-sulfate ammonia-lyase) inhibitor
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.	2.75	3	0	pyrrolizidine alkaloid
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.	3.61	2	0	mixture	bronchodilator 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.	3.91	3	0	N-glycosyl-1,3,5-triazine; nucleoside analogue	antineoplastic agent
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.	3.61	2	0	benzazepine 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.	3.23	1	0	steroid 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.	2.08	1	0	aminoimidazole; monocarboxylic acid amide	mouse metabolite
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.	2.08	1	0	hydrochloride	antineoplastic agent
betamethasone Betamethasone: A glucocorticoid given orally, parenterally, by local injection, by inhalation, or applied topically in the management of various disorders in which corticosteroids are indicated. Its lack of mineralocorticoid properties makes betamethasone particularly suitable for treating cerebral edema and congenital adrenal hyperplasia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p724)	2.08	1	0	11beta-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
2-aminopurine 2-Aminopurine: A purine that is an isomer of ADENINE (6-aminopurine).. aminopurine : Any purine having at least one amino substituent.. 2-aminopurine : The parent compound of the 2-aminopurines, comprising a purine core carrying an amino substituent at the 2-position.	2.13	1	0	2-aminopurines; nucleobase analogue	antimetabolite
fluorobenzenes Fluorobenzenes: Derivatives of BENZENE that contain FLUORINE.. monofluorobenzene : The simplest member of the class of monofluorobenzenes that is benzene carrying a single fluoro substituent.. fluorobenzenes : Any fluoroarene that is a benzene or a substituted benzene carrying at least one fluoro group.	4.4	1	1	monofluorobenzenes	NMR chemical shift reference compound
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.	3.23	1	0	1-benzyl-3-(dimethylamino)-2-methyl-1-phenylpropyl propanoate	mu-opioid receptor agonist; opioid analgesic
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.	3.23	1	0	bile acid; C24-steroid; dihydroxy-5beta-cholanic acid	human metabolite; mouse metabolite
rhein [no description available]	7.41	1	0	dihydroxyanthraquinone
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.	2.08	1	0	isoquinoline alkaloid; pyridoisoquinoline	antiamoebic agent; anticoronaviral agent; antiinfective agent; antimalarial; antineoplastic agent; antiprotozoal drug; antiviral agent; autophagy inhibitor; emetic; expectorant; plant metabolite; protein synthesis inhibitor
kainic acid Kainic Acid: (2S-(2 alpha,3 beta,4 beta))-2-Carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid. Ascaricide obtained from the red alga Digenea simplex. It is a potent excitatory amino acid agonist at some types of excitatory amino acid receptors and has been used to discriminate among receptor types. Like many excitatory amino acid agonists it can cause neurotoxicity and has been used experimentally for that purpose.	7.61	2	0	dicarboxylic acid; L-proline derivative; non-proteinogenic L-alpha-amino acid; pyrrolidinecarboxylic acid	antinematodal drug; excitatory amino acid agonist
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.	3.23	1	0	4-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.	10.75	24	2
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.	3.23	1	0	ergot alkaloid; semisynthetic derivative	dopamine agonist; non-narcotic analgesic; serotonergic agonist; sympatholytic agent; vasoconstrictor agent
medroxyprogesterone [no description available]	3.68	2	0	17alpha-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	3.61	2	0	diarylmethane
methamphetamine Methamphetamine: A central nervous system stimulant and sympathomimetic with actions and uses similar to DEXTROAMPHETAMINE. The smokable form is a drug of abuse and is referred to as crank, crystal, crystal meth, ice, and speed.. methamphetamine : A member of the class of amphetamines in which the amino group of (S)-amphetamine carries a methyl substituent.	3.23	1	0	amphetamines; secondary amine	central nervous system stimulant; environmental contaminant; neurotoxin; psychotropic drug; xenobiotic
levocarnitine (R)-carnitine : The (R)-enantiomer of carnitine.	3.23	1	0	carnitine	antilipemic drug; nootropic agent; nutraceutical; Saccharomyces cerevisiae metabolite; water-soluble vitamin (role)
malondialdehyde Malondialdehyde: The dialdehyde of malonic acid.. malonaldehyde : A dialdehyde that is propane substituted by two oxo groups at the terminal carbon atoms respectively. A biomarker of oxidative damage to lipids caused by smoking, it exists in vivo mainly in the enol form.	2.13	1	0	dialdehyde	biomarker
sulfanilylurea sulfanilylurea: antimicrobial agent; structure	3.23	1	0	benzenes; sulfonamide
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.	2.08	1	0	isothiocyanate	insecticide
lactulose [no description available]	3.23	1	0	glycosylfructose	gastrointestinal drug; laxative
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.	2.52	2	0	aromatic 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
megestrol acetate [no description available]	3.61	2	0	20-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]	3.23	1	0
acetylcysteine N-acetyl-L-cysteine : An N-acetyl-L-amino acid that is the N-acetylated derivative of the natural amino acid L-cysteine.	3.58	2	0	acetylcysteine; L-cysteine derivative; N-acetyl-L-amino acid	antidote to paracetamol poisoning; antiinfective agent; antioxidant; antiviral drug; ferroptosis inhibitor; geroprotector; human metabolite; mucolytic; radical scavenger; vulnerary
erythromycin 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.	10.24	3	1	cyclic ketone; erythromycin
hydroxychloroquine sulfate [no description available]	2.08	1	0
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.	2.05	1	0	N-nitrosoureas	alkylating 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.	3.61	2	0	17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; terminal acetylenic compound	contraceptive drug; female contraceptive drug; progestin; synthetic oral contraceptive
vinblastine [no description available]	2.11	1	0
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.	3.23	1	0	ethyl ester; nitrile; piperidinecarboxylate ester; tertiary amine	antidiarrhoeal drug
deoxycytidine [no description available]	12.13	30	11	pyrimidine 2'-deoxyribonucleoside	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
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.	2.08	1	0	hydrochloride	antitubercular 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.	3.23	1	0	ethanolamines; ethylenediamine derivative	antitubercular agent; environmental contaminant; xenobiotic
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.	2.81	3	0
antimycin a [no description available]	2.08	1	0	benzamides; 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.	3.23	1	0	glycopeptide	antibacterial 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.	3.23	1	0	alpha-tocopherol	algal metabolite; antiatherogenic agent; anticoagulant; antioxidant; antiviral agent; EC 2.7.11.13 (protein kinase C) inhibitor; immunomodulator; micronutrient; nutraceutical; plant metabolite
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.	2.08	1	0	aliphatic 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.	3.23	1	0	monocarboxylic acid	EC 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	2.08	1	0	aromatic ketone
metaxalone [no description available]	3.23	1	0	aromatic 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.	3.23	1	0	cyclic acetal; cyclic hemiketal; cyclic ketone; pyranobenzodioxin; secondary alcohol; secondary amino compound	antibacterial drug; antimicrobial agent; bacterial metabolite
dronabinol Dronabinol: A psychoactive compound extracted from the resin of Cannabis sativa (marihuana, hashish). The isomer delta-9-tetrahydrocannabinol (THC) is considered the most active form, producing characteristic mood and perceptual changes associated with this compound.. Delta(9)-tetrahydrocannabinol : A diterpenoid that is 6a,7,8,10a-tetrahydro-6H-benzo[c]chromene substituted at position 1 by a hydroxy group, positions 6, 6 and 9 by methyl groups and at position 3 by a pentyl group. The principal psychoactive constituent of the cannabis plant, it is used for treatment of anorexia associated with AIDS as well as nausea and vomiting associated with cancer chemotherapy.	3.23	1	0	benzochromene; 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.	3.23	1	0	aromatic 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.	3.23	1	0	benzimidazoles; heteroarylpiperidine; organofluorine compound	antidyskinesia agent; dopaminergic antagonist; first generation antipsychotic; H1-receptor antagonist; serotonergic antagonist
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.	3.23	1	0	brompheniramine	anti-allergic agent; H1-receptor antagonist
sulfur hexafluoride Sulfur Hexafluoride: Sulfur hexafluoride. An inert gas used mainly as a test gas in respiratory physiology. Other uses include its injection in vitreoretinal surgery to restore the vitreous chamber and as a tracer in monitoring the dispersion and deposition of air pollutants.. sulfur hexafluoride : A sulfur coordination entity consisting of six fluorine atoms attached to a central sulfur atom. It is the most potent greenhouse gas currently known, with a global warming potential of 23,900 times that of CO2 over a 100 year period (SF6 has an estimated lifetime in the atmosphere of between 800 and 3,000 years).	2.94	1	0	sulfur coordination entity	greenhouse gas; NMR chemical shift reference compound; ultrasound contrast agent
stavudine Stavudine: A dideoxynucleoside analog that inhibits reverse transcriptase and has in vitro activity against HIV.. stavudine : A nucleoside analogue obtained by formal dehydration across positions 2 and 3 of thymidine. An inhibitor of HIV-1 reverse transcriptase	3.61	2	0	dihydrofuran; nucleoside analogue; organic molecular entity	antimetabolite; antiviral agent; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
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.	3.61	2	0	dichlorobenzene; 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.	2.11	1	0	fluorescein isothiocyanate
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.	3.23	1	0	17alpha-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.	2.25	1	0	2-phenylcyclopropan-1-amine
streptomycin [no description available]	3.23	1	0	antibiotic antifungal drug; antibiotic fungicide; streptomycins	antibacterial drug; antifungal agrochemical; antimicrobial agent; antimicrobial drug; bacterial metabolite; protein synthesis inhibitor
butylhydroxybutylnitrosamine Butylhydroxybutylnitrosamine: A substituted carcinogenic nitrosamine.. N-butyl-N-(4-hydroxybutyl)nitrosamine : A nitrosamine that has butyl and 4-hydroxybutyl substituents. In mice, it causes high-grade, invasive cancers in the urinary bladder, but not in any other tissues.	2.08	1	0	nitrosamine; primary alcohol	carcinogenic agent
cladribine [no description available]	3.9	3	0	organochlorine compound; purine 2'-deoxyribonucleoside	antineoplastic agent; immunosuppressive agent
carbenicillin Carbenicillin: Broad-spectrum semisynthetic penicillin derivative used parenterally. It is susceptible to gastric juice and penicillinase and may damage platelet function.. carbenicillin : A penicillin antibiotic having a 6beta-2-carboxy-2-phenylacetamido side-chain.	3.23	1	0	penicillin allergen; penicillin	antibacterial drug
metocurine metocurine: from Chinese herb Cyclea hainanensis Mrr	2.08	1	0	isoquinolines
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.	2.25	1	0	penicillin allergen; penicillin	antibacterial drug
clomacran clomacran: RN given refers to parent cpd; structure	3.23	1	0	acridines
vidarabine adenine arabinoside : A purine nucleoside in which adenine is attached to arabinofuranose via a beta-N(9)-glycosidic bond.	3.86	3	0	beta-D-arabinoside; purine nucleoside	antineoplastic agent; bacterial metabolite; nucleoside antibiotic
methenamine hippurate methenamine hippurate: both parts of molecule contribute to its antibacterial action	3.23	1	0	N-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.	3.23	1	0	azobenzenes; dicarboxylic acid	non-steroidal anti-inflammatory drug; prodrug
n-methylaspartate N-Methylaspartate: An amino acid that, as the D-isomer, is the defining agonist for the NMDA receptor subtype of glutamate receptors (RECEPTORS, NMDA).. N-methyl-D-aspartic acid : An aspartic acid derivative having an N-methyl substituent and D-configuration.	2.11	1	0	amino dicarboxylic acid; D-alpha-amino acid; D-aspartic acid derivative; secondary amino compound	neurotransmitter agent
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.	2.08	1	0	organic sodium salt	antineoplastic agent; bone density conservation agent; chelator
lutetium Lutetium: An element of the rare earth family of metals. It has the atomic symbol Lu, atomic number 71, and atomic weight 175.	8.89	2	1	d-block element atom; lanthanoid atom
platinum Platinum: A heavy, soft, whitish metal, resembling tin, with atomic number 78, atomic weight 195.084, symbol Pt. It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as alutiae.	11.74	37	16	elemental platinum; nickel group element atom; platinum group metal atom
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.	11.38	28	18	titanium group element atom
chromium Chromium: A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens.. chromium ion : An chromium atom having a net electric charge.. chromium atom : A chromium group element atom that has atomic number 24.	12.61	35	11	chromium group element atom; metal allergen	micronutrient
europium Europium: An element of the rare earth family of metals. It has the atomic symbol Eu, atomic number 63, and atomic weight 152. Europium is used in the form of its salts as coatings for cathode ray tubes and in the form of its organic derivatives as shift reagents in NMR spectroscopy.	2.1	1	0	f-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.	2.8	3	0	copper group element atom; elemental gold
zirconium Zirconium: A rather rare metallic element with atomic number 40, atomic weight 91.224, and symbol Zr.	2.49	2	0	titanium 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.	2.08	1	0	pyrimidine 2',3'-dideoxyribonucleoside	antimetabolite; antiviral drug; HIV-1 reverse transcriptase inhibitor
mercuric chloride Mercuric Chloride: Mercury chloride (HgCl2). A highly toxic compound that volatizes slightly at ordinary temperature and appreciably at 100 degrees C. It is corrosive to mucous membranes and used as a topical antiseptic and disinfectant.. mercury dichloride : A mercury coordination entity made up of linear triatomic molecules in which a mercury atom is bonded to two chlorines. Water-soluble, it is highly toxic. Once used in a wide variety of applications, including preserving wood and anatomical specimens, embalming and disinfecting, as an intensifier in photography, as a mordant for rabbit and beaver furs, and freeing gold from lead, its use has markedly declined as less toxic alternatives have been developed.	1.99	1	0	mercury coordination entity	sensitiser
camptothecin NSC 100880: carboxylate (opened lactone) form of camptothecin; RN refers to (S)-isomer; structure given in first source	7.86	12	2	delta-lactone; pyranoindolizinoquinoline; quinoline alkaloid; tertiary alcohol	antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor; genotoxin; plant metabolite
zinc sulfate Zinc Sulfate: A compound given in the treatment of conditions associated with zinc deficiency such as acrodermatitis enteropathica. Externally, zinc sulfate is used as an astringent in lotions and eye drops. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995). zinc sulfate : A metal sulfate compound having zinc(2+) as the counterion.	2.51	2	0	metal sulfate; zinc molecular entity	fertilizer
sodium thiosulfate sodium thiosulfate: do not confuse synonym sodium hyposulfite with sodium hyposulfite, synonym for di-Na salt of dithionous acid. sodium thiosulfate : An inorganic sodium salt composed of sodium and thiosulfate ions in a 2:1 ratio.	3.23	1	0	inorganic sodium salt	antidote to cyanide poisoning; antifungal drug; nephroprotective agent
deuterium Deuterium: The stable isotope of hydrogen. It has one neutron and one proton in the nucleus.	2.98	4	0	dihydrogen
mafenide acetate [no description available]	2.08	1	0	carboxylic acid
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.	3.13	4	0	titanium oxides	food colouring
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;	2.08	1	0	anthraquinone
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.	3.23	1	0	selegiline; terminal acetylenic compound	geroprotector
selegiline hydrochloride, (r)-isomer [no description available]	2.08	1	0	hydrochloride; 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.	3.27	1	0	6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazole	antinematodal 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.	3.23	1	0	monochlorobenzenes; N-alkylpyrrolidine	anti-allergic agent; antipruritic drug; H1-receptor antagonist; muscarinic antagonist
thiamphenicol [no description available]	2.08	1	0	monocarboxylic acid amide; sulfone	antimicrobial agent; immunosuppressive agent
pancuronium bromide pancuronium bromide : A bromide salt consisting of two bromide ions and one pancuronium dication.	2.08	1	0	bromide salt	cholinergic antagonist; muscle relaxant; nicotinic 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.	3.23	1	0	beta-lactam antibiotic allergen; cephalosporin; semisynthetic derivative	antibacterial drug
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.	2.08	1	0	C-nitro compound; imidazoles; organochlorine compound; secondary alcohol	antiamoebic agent; antibacterial drug; antiinfective agent; antiprotozoal drug; antitrichomonal drug; epitope
danazol Danazol: A synthetic steroid with antigonadotropic and anti-estrogenic activities that acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. Danazol has been used in the treatment of endometriosis and some benign breast disorders.	3.61	2	0	17beta-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	3.23	1	0
laxagetten 4,4'-diacetoxydiphenylpyridylemethane [no description available]	3.23	1	0
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.	5.91	2	1	aminoglycoside antibiotic; anthracycline; p-quinones; tetracenequinones	antineoplastic agent; bacterial metabolite
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.	3.61	2	0	nucleoside analogue; organofluorine compound; purine arabinonucleoside monophosphate	antimetabolite; antineoplastic agent; antiviral agent; DNA synthesis inhibitor; immunosuppressive agent; prodrug
alclofenac alclofenac: was heading 1975-94 (was see under PHENYLACETATES 1975-90); use PHENYLACETATES to search ALCLOFENAC 1975-94; an anti-inflammatory agent used in the treatment of rheumatoid arthritis; acts also as an analgesic and an antipyretic. alclofenac : An aromatic ether in which the ether oxygen links an allyl group to the 4-position of (3-chlorophenyl)acetic acid.A non-steroidal anti-inflammatory drug, it was withdrawn from the UK market in 1979 due to concerns with its association with vasculitis and rash.	3.23	1	0	aromatic ether; monocarboxylic acid; monochlorobenzenes	drug allergen; non-narcotic analgesic; non-steroidal anti-inflammatory drug
bromocriptine Bromocriptine: A semisynthetic ergotamine alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion.	3.23	1	0	indole alkaloid	antidyskinesia agent; antiparkinson drug; dopamine agonist; hormone antagonist
phenyl acetate phenyl acetate: The ester formed between phenol and acetic acid. Don't confuse with phenylacetic acid derivatives listed under PHENYLACETATES.. phenyl acetate : An acetate ester obtained by the formal condensation of phenol with acetic acid.	2.6	1	0	benzenes; phenyl acetates
cetylpyridinium chloride anhydrous tserigel: according to first source contains polyvinylbutyral & cetylpyridinium chloride; UD only lists cetylpyridinium chloride as constituent. cetylpyridinium chloride : A pyridinium salt that has N-hexadecylpyridinium as the cation and chloride as the anion. It has antiseptic properties and is used in solutions or lozenges for the treatment of minor infections of the mouth and throat.	2.15	1	0	chloride salt; organic chloride salt	antiseptic drug; surfactant
oxyphenisatin [no description available]	3.23	1	0	indoles
fludrocortisone Fludrocortisone: A synthetic mineralocorticoid with anti-inflammatory activity.	3.66	2	0	11beta-hydroxy steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(4) steroid; C21-steroid; fluorinated steroid; mineralocorticoid	adrenergic agent; anti-inflammatory drug
ursodeoxycholic acid Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.. ursodeoxycholic acid : A bile acid found in the bile of bears (Ursidae) as a conjugate with taurine. Used therapeutically, it prevents the synthesis and absorption of cholesterol and can lead to the dissolution of gallstones.. ursodeoxycholate : A bile acid anion that is the conjugate base of ursodeoxycholic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.	3.23	1	0	bile acid; C24-steroid; dihydroxy-5beta-cholanic acid	human metabolite; mouse metabolite
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.	2.08	1	0	C-nitro compound; imidazoles; monocarboxylic acid amide	antiprotozoal drug
4-methoxyamphetamine 4-methoxyamphetamine: para-methoxy derivative to amphetamine with hallucinogenic properties; minor descriptor (75-86); on line & INDEX MEDICUS search AMPHETAMINES (75-86); RN given refers to parent compound without isomeric designation	10.77	16	8
transferrin Transferrin: An iron-binding beta1-globulin that is synthesized in the LIVER and secreted into the blood. It plays a central role in the transport of IRON throughout the circulation. A variety of transferrin isoforms exist in humans, including some that are considered markers for specific disease states.	2.03	1	0
glutamic acid Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.. glutamic acid : An alpha-amino acid that is glutaric acid bearing a single amino substituent at position 2.	2.48	2	0	glutamic 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	3.23	1	0	chlorphenamine
alovudine [no description available]	2.77	3	0	pyrimidine 2',3'-dideoxyribonucleoside
clometacin clometacin: structure	3.23	1	0	N-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.	3.23	1	0	beta-lactam antibiotic allergen; cephalosporin; tetrazoles; thiadiazoles	antibacterial drug
amoxicillin Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to AMPICILLIN except that its resistance to gastric acid permits higher serum levels with oral administration.. amoxicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-(4-hydroxyphenyl)acetamido group.	3.61	2	0	penicillin 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.	3.61	2	0	timolol	anti-arrhythmia drug; antiglaucoma drug; antihypertensive agent; beta-adrenergic antagonist
indoramin Indoramin: An alpha-1 adrenergic antagonist that is commonly used as an antihypertensive agent.	2.08	1	0	tryptamines
benthiocarb Saturn: The sixth planet in order from the sun. It is one of the five outer planets of the solar system. Its twelve natural satellites include Phoebe and Titan.	3.48	1	1	monochlorobenzenes; monothiocarbamic ester
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.	4.45	3	0	cyclic 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.	3.61	2	0	catechols; hydrazines; monocarboxylic acid	antiparkinson drug; dopaminergic agent; EC 4.1.1.28 (aromatic-L-amino-acid decarboxylase) inhibitor
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.	3.23	1	0	carbamate 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.	3.23	1	0	amino acid; carbocyclic fatty acid; carbotricyclic compound; secondary amino compound	antidepressant; dopamine uptake inhibitor
zidovudine Zidovudine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.. zidovudine : A pyrimidine 2',3'-dideoxyribonucleoside compound having a 3'-azido substituent and thymine as the nucleobase.	3.61	2	0	azide; 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)	2.08	1	0	organic molecular entity
pirprofen pirprofen: anti-inflammatory agent used in therapy of rheumatoid arthritis; prostaglandin synthetase inhibitor; more potent than indomethacin; structure	3.23	1	0	pyrroline
tobramycin Tobramycin: An aminoglycoside, broad-spectrum antibiotic produced by Streptomyces tenebrarius. It is effective against gram-negative bacteria, especially the PSEUDOMONAS species. It is a 10% component of the antibiotic complex, NEBRAMYCIN, produced by the same species.. tobramycin : A amino cyclitol glycoside that is kanamycin B lacking the 3-hydroxy substituent from the 2,6-diaminoglucose ring.	2.08	1	0	amino cyclitol glycoside	antibacterial 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).	22.25	294	112	taxane diterpenoid; tetracyclic diterpenoid	antineoplastic agent; human metabolite; metabolite; microtubule-stabilising agent
etoposide [no description available]	9.4	12	2	beta-D-glucoside; furonaphthodioxole; organic heterotetracyclic compound	antineoplastic agent; DNA synthesis inhibitor
dobutamine Dobutamine: A catecholamine derivative with specificity for BETA-1 ADRENERGIC RECEPTORS. It is commonly used as a cardiotonic agent after CARDIAC SURGERY and during DOBUTAMINE STRESS ECHOCARDIOGRAPHY.. dobutamine : A catecholamine that is 4-(3-aminobutyl)phenol in which one of the hydrogens attached to the nitrogen is substituted by a 2-(3,4-dihydroxyphenyl)ethyl group. A beta1-adrenergic receptor agonist that has cardiac stimulant action without evoking vasoconstriction or tachycardia, it is used as the hydrochloride to increase the contractility of the heart in the management of acute heart failure.	3.23	1	0	catecholamine; secondary amine	beta-adrenergic agonist; cardiotonic drug; sympathomimetic agent
penbutolol Penbutolol: A nonselective beta-blocker used as an antihypertensive and an antianginal agent.	3.23	1	0	ethanolamines
ribavirin Rebetron: Rebetron is tradename	4.28	5	0	1-ribosyltriazole; aromatic amide; monocarboxylic acid amide; primary carboxamide	anticoronaviral agent; antiinfective agent; antimetabolite; antiviral agent; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
amikacin Amikacin: A broad-spectrum antibiotic derived from KANAMYCIN. It is reno- and oto-toxic like the other aminoglycoside antibiotics.. amikacin : An amino cyclitol glycoside that is kanamycin A acylated at the N-1 position by a 4-amino-2-hydroxybutyryl group.	3.61	2	0	alpha-D-glucoside; amino cyclitol glycoside; aminoglycoside; carboxamide	antibacterial drug; antimicrobial agent; nephrotoxin
cephradine Cephradine: A semi-synthetic cephalosporin antibiotic.. cephradine : A first-generation cephalosporin antibiotic with a methyl substituent at position 3, and a (2R)-2-amino-2-cyclohexa-1,4-dien-1-ylacetamido substituent at position 7, of the cephem skeleton.	3.23	1	0	beta-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.	3.23	1	0	aromatic ether; aromatic ketone; dichlorobenzene; monocarboxylic acid; thiophenes	antihypertensive agent; hepatotoxic agent; loop diuretic
methyldopa Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.. alpha-methyl-L-dopa : A derivative of L-tyrosine having a methyl group at the alpha-position and an additional hydroxy group at the 3-position on the phenyl ring.	3.23	1	0	L-tyrosine derivative; non-proteinogenic L-alpha-amino acid	alpha-adrenergic agonist; antihypertensive agent; hapten; peripheral nervous system drug; sympatholytic agent
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.	8.89	3	0	5-[2-(dimethylamino)ethyl]-2-(4-methoxyphenyl)-4-oxo-2,3,4,5-tetrahydro-1,5-benzothiazepin-3-yl acetate	antihypertensive agent; calcium channel blocker; vasodilator agent
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.	3.17	1	0	dichlorobenzene; 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.	2.08	1	0	organic 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.	3.23	1	0	acetate ester; androstane; quaternary ammonium ion	drug allergen; muscle relaxant; neuromuscular agent; nicotinic antagonist
benoxaprofen benoxaprofen: RN given refers to parent cpd; structure. benoxaprofen : A monocarboxylic acid that is propionic acid substituted at position 2 by a 2-(4-chlorophenyl)-1,3-benzoxazol-5-yl group. It was used as a non-steroidal anti-inflammatory drug until 1982 when it was withdrawn from the market due to adverse side-effects including liver necrosis, photosensitivity, and carcinogenicity in animals.	3.23	1	0	1,3-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
exifone [no description available]	3.23	1	0	benzophenones
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.	7.13	1	0	pyridone	antipyretic; 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.	3.23	1	0	[2,8-bis(trifluoromethyl)quinolin-4-yl]-(2-piperidyl)methanol	antimalarial
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	3.61	2	0	benzamides; 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.	3.23	1	0	anilide; ether; piperidines; thiophenes	anaesthesia adjuvant; intravenous anaesthetic; mu-opioid receptor agonist; opioid analgesic
acarbose [no description available]	3.61	2	0	tetrasaccharide derivative	EC 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.	3.23	1	0	aminopyridine; N-sulfonylurea; secondary amino compound	antihypertensive agent; loop diuretic
epirubicin Epirubicin: An anthracycline which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA.	9.82	7	5	aminoglycoside; 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
lorcainide [no description available]	2.08	1	0	acetamides
idarubicin Idarubicin: An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA.	3.23	1	0	anthracycline antibiotic; deoxy hexoside; monosaccharide derivative
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.	3.23	1	0	penicillin 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.	8.65	2	0	aromatic ether; benzodioxoles; organofluorine compound; piperidines	antidepressant; anxiolytic drug; hepatotoxic agent; P450 inhibitor; serotonin uptake inhibitor
triciribine phosphate [no description available]	2.15	1	0
captopril Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.. captopril : A L-proline derivative in which L-proline is substituted on nitrogen with a (2S)-2-methyl-3-sulfanylpropanoyl group. It is used as an anti-hypertensive ACE inhibitor drug.	3.9	3	0	alkanethiol; 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.	3.23	1	0	cephalosporin	antibacterial drug
staurosporine [no description available]	2.08	1	0	indolocarbazole 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.	2.08	1	0	one-carbon compound; organic sodium salt	antiviral drug
atracurium Atracurium: A non-depolarizing neuromuscular blocking agent with short duration of action. Its lack of significant cardiovascular effects and its lack of dependence on good kidney function for elimination provide clinical advantage over alternate non-depolarizing neuromuscular blocking agents.. atracurium : A diester compound consisting of pentane-1,5-diol with both hydroxyls bearing 3-[1-(3,4-dimethoxybenzyl)-6,7-dimethoxy-2-methyl-3,4-dihydroisoquinolinium-2(1H)-yl]propanoyl groups.	3.23	1	0	diester; quaternary ammonium ion	muscle relaxant; nicotinic antagonist
atracurium besylate atracurium besylate : The bisbenzenesulfonate salt of atracurium.	2.08	1	0	organosulfonate salt; quaternary ammonium salt	muscle relaxant; nicotinic antagonist
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.	2.08	1	0	nitrate ester; pyridinecarboxamide	potassium channel opener; vasodilator agent
pergolide Pergolide: A long-acting dopamine agonist which has been used to treat PARKINSON DISEASE and HYPERPROLACTINEMIA but withdrawn from some markets due to potential for HEART VALVE DISEASES.. pergolide : A diamine that is ergoline in which the beta-hydrogen at position 8 is replaced by a (methylthio)methyl group and the hydrogen attached to the piperidine nitrogen (position 6) is replaced by a propyl group. A dopamine D2 receptor agonist which also has D1 and D2 agonist properties, it is used as the mesylate salt in the management of Parkinson's disease, although it was withdrawn from the U.S. and Canadian markets in 2007 due to an increased risk of cardiac valve dysfunction.	3.23	1	0	diamine; 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.	2.08	1	0	methanesulfonate salt	antiparkinson 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.	3.61	2	0	cephalosporin	antibacterial drug
talniflumate talniflumate: an anti-inflammatory molecule for the treatment of cystic fibrosis, chronic obstructive pulmonary disease and asthma	2.08	1	0	benzofurans
fenoldopam mesylate [no description available]	2.08	1	0	benzazepine
fialuridine [no description available]	3.23	1	0
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.	3.61	2	0	cephalosporin	antibacterial 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.	2.08	1	0	fluoroquinolone antibiotic; monocarboxylic acid; N-alkylpiperazine; N-arylpiperazine; quinolone antibiotic; quinolone	antibacterial drug; antiinfective agent; DNA synthesis inhibitor
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.	3.23	1	0	monocarboxylic 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.	3.23	1	0	piperidines; tertiary amino compound	anti-HIV agent; EC 2.4.1.80 (ceramide glucosyltransferase) inhibitor
haloperidol decanoate [no description available]	3.23	1	0	organic molecular entity
cefotetan Cefotetan: A semisynthetic cephamycin antibiotic that is administered intravenously or intramuscularly. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative microorganisms.. cefotetan : A semi-synthetic second-generation cephamycin antibiotic with [(1-methyl-1H-tetrazol-5-yl)sulfanyl]methyl, methoxy and {[4-(2-amino-1-carboxy-2-oxoethylidene)-1,3-dithietan-2-yl]carbonyl}amino groups at the 3, 7alpha, and 7beta positions, respectively, of the cephem skeleton. It is resistant to a wide range of beta-lactamases and is active against a broad spectrum of aerobic and anaerobic Gram-positive and Gram-negative microorganisms.	3.61	2	0
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).	9.3	5	0	delta-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	2.08	1	0	aminopyridine
tolrestat tolrestat: RN & structure given in first source	3.23	1	0	naphthalenes	EC 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.	2.08	1	0	aromatic ketone
stepronin [no description available]	2.08	1	0	N-acyl-amino acid
piritrexim piritrexim: RN given refers to parent cpd; structure given in first source	3.14	1	0
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.	6.9	6	2	delta-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.	2.08	1	0	benzodioxine; 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.	2.08	1	0	dimethoxybenzene
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.	3.23	1	0
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.	6.12	3	1	3-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.	4.31	5	0	N-acylurea	antineoplastic agent; antiparkinson drug; dopamine agonist
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.	2.08	1	0	hydrochloride	adrenergic uptake inhibitor; antidepressant
atomoxetine atomoxetine : A secondary amino compound having methyl and 3-(2-methylphenoxy)-3-phenylpropan-1-yl substituents.	3.23	1	0	aromatic ether; secondary amino compound; toluenes	adrenergic uptake inhibitor; antidepressant; environmental contaminant; xenobiotic
quinapril Quinapril: A tetrahydroisoquinoline derivative and ANGIOTENSIN CONVERTING ENZYME inhibitor that is used in the treatment of HYPERTENSION and HEART FAILURE.. quinapril : A member of the class of isoquinolines that is (3S)-2-L-alanyl-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid in which the alpha-amino group of the alanyl residue has been substituted by a 1-ethoxycarbonyl-4-phenylbutan-2-yl group (the all-S isomer). A prodrug for quinaprilat (by hydrolysis of the ethyl ester to the corresponding carboxylic acid), it is used as an angiotensin-converting enzyme inhibitor (ACE inhibitor) used (generally as the hydrochloride salt) for the treatment of hypertension and congestive heart failure.	3.89	3	0	dicarboxylic acid monoester; ethyl ester; isoquinolines; tertiary carboxamide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; prodrug
alpidem [no description available]	3.23	1	0	imidazoles
mifepristone Mifepristone: A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.	3.61	2	0	3-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.	8.58	2	0	aromatic 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
gusperimus gusperimus: synthesized by chemical modification of spergualin; in combination with cyclosporin A prevents diabetes in predisposed NOD mice; structure given in first source; RN given refers to (-)-isomer trihydrochloride	2.42	2	0	N-acyl-amino acid
fosphenytoin fosphenytoin: structure given in first & second source	3.23	1	0	imidazolidine-2,4-dione
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.	2.08	1	0	naphthoic 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.	3.23	1	0	aromatic 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.	3.61	2	0	3-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.	3.9	3	0	imidazoquinoline	antineoplastic agent; interferon inducer
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.	3.23	1	0	aromatic ether; ethanolamines; methyl ester; secondary alcohol; secondary amino compound
sertindole sertindole : A phenylindole that is 1H-indole which is substituted on the nitrogen by a p-chlorophenyl group, at position 5 by chlorine, and at position 3 by a piperidin-4-yl group, which is itself substituted on the nitrogen by a 2-(2-oxoimidazolidin-1-yl)ethyl group.	2.08	1	0	heteroarylpiperidine; 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.	2.08	1	0	adamantanes; 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.	3.23	1	0	6-aminopurines; ether; phosphonic acids	antiviral drug; DNA synthesis inhibitor; drug metabolite; HIV-1 reverse transcriptase inhibitor; nephrotoxic agent
aromasil [no description available]	18.55	118	43	17-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]	2.08	1	0	fluoroquinolone antibiotic; N-arylpiperazine; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone
zileuton [no description available]	3.61	2	0	1-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.	14.68	50	22	methyl ester; monochlorobenzenes; thienopyridine	anticoagulant; P2Y12 receptor antagonist; platelet aggregation inhibitor
cidofovir anhydrous Cidofovir: An acyclic nucleoside phosphonate that acts as a competitive inhibitor of viral DNA polymerases. It is used in the treatment of RETINITIS caused by CYTOMEGALOVIRUS INFECTIONS and may also be useful for treating HERPESVIRUS INFECTIONS.. cidofovir anhydrous : Cytosine substituted at the 1 position by a 3-hydroxy-2-(phosphonomethoxy)propyl group (S configuration). A nucleoside analogue, it is an injectable antiviral used for the treatment of cytomegalovirus (CMV) retinitis in AIDS patients.	3.61	2	0	phosphonic 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.	4.22	2	0	beta-amino acid; piperidinemonocarboxylic acid; tertiary amino compound; thiophenes	anticonvulsant; GABA reuptake inhibitor
topotecan Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.. topotecan : A pyranoindolizinoquinoline used as an antineoplastic agent. It is a derivative of camptothecin and works by binding to the topoisomerase I-DNA complex and preventing religation of these 328 single strand breaks.	11.02	4	1	pyranoindolizinoquinoline	antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor
bromfenac bromfenac: bromfenac sodium is the active cpd; structure in first source. bromfenac : Amfenac in which the the hydrogen at the 4 position of the benzoyl group is substituted by bromine. It is used for the management of ocular pain and treatment of postoperative inflammation in patients who have undergone cataract extraction. It was withdrawn from the US market in 1998, following concerns over off-label abuse and hepatic failure.	3.61	2	0	aromatic amino acid; benzophenones; organobromine compound; substituted aniline	non-narcotic analgesic; non-steroidal anti-inflammatory drug
gemcitabine hydrochloride [no description available]	2.08	1	0	hydrochloride; 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.	10.36	21	4	organofluorine compound; pyrimidine 2'-deoxyribonucleoside	antimetabolite; antineoplastic agent; antiviral drug; DNA synthesis inhibitor; EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor; environmental contaminant; immunosuppressive agent; photosensitizing agent; prodrug; radiosensitizing agent; xenobiotic
ibutilide ibutilide: RN & structure in first source; RN refers to the fumarate salt	3.23	1	0	benzenes; 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.	3.61	2	0	aromatic 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.	3.23	1	0	alpha-amino acid ester; anilide; monocarboxylic acid amide; piperidinecarboxylate ester	intravenous anaesthetic; mu-opioid receptor agonist; opioid analgesic; sedative
atorvastatin calcium anhydrous [no description available]	2.08	1	0	organic calcium salt
atorvastatin [no description available]	11.95	4	2	aromatic amide; dihydroxy monocarboxylic acid; monofluorobenzenes; pyrroles; statin (synthetic)	environmental contaminant; xenobiotic
lamivudine [no description available]	3.61	2	0	monothioacetal; 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.	2.08	1	0	duloxetine hydrochloride	antidepressant
duloxetine [no description available]	3.23	1	0	duloxetine
irinotecan [no description available]	9.21	13	3	carbamate ester; delta-lactone; N-acylpiperidine; pyranoindolizinoquinoline; ring assembly; tertiary alcohol; tertiary amino compound	antineoplastic agent; apoptosis inducer; EC 5.99.1.2 (DNA topoisomerase) inhibitor; prodrug
valsartan Valsartan: A tetrazole derivative and ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to treat HYPERTENSION.. valsartan : A monocarboxylic acid amide consisting of L-valine in which the amino hydrogens have been replaced by a pentanoyl and a [2'-(1H-tetrazol-5-yl)biphenyl]-4-yl]methyl group. It exhibits antihypertensive activity.	3.61	2	0	biphenylyltetrazole; 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.	3.23	1	0
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.	3.23	1	0	1,2-benzisothiazole; indolones; organochlorine compound; piperazines	antipsychotic agent; dopaminergic antagonist; histamine antagonist; muscarinic antagonist; psychotropic drug; serotonergic antagonist
zolmitriptan zolmitriptan: an antimigraine compound; a serotonin (5HT)-1D receptor agonist. zolmitriptan : A member of the class of tryptamines that is N,N-dimethyltryptamine in which the hydrogen at position 5 of the indole ring has been replaced by a [(4S)-2-oxo-1,3-oxazolidin-4-yl]methyl group. A serotonin 5-HT1 B and D receptor agonist, it is used for the treatment of migraine.	3.61	2	0	oxazolidinone; 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.	3.35	1	0	organoiodine 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.	2.08	1	0	6-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.	3.61	2	0	monothioacetal; nucleoside analogue; organofluorine compound; pyrimidone	antiviral drug; HIV-1 reverse transcriptase inhibitor
tasosartan tasosartan: angiotensin II antagonist; structure given in first source	3.23	1	0	biphenyls
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	3.23	1	0	organochlorine 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.	3.23	1	0	L-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.	12.34	24	12	carbamate 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	3.23	1	0	adenosines; purines D-ribonucleoside	analgesic; anti-arrhythmia drug; fundamental metabolite; human metabolite; vasodilator agent
paroxetine hydrochloride paroxetine hydrochloride : The hydrochloride salt of paroxetine. It is an antidepressant drug.	2.08	1	0	hydrochloride	antidepressant; anxiolytic drug; hepatotoxic agent; P450 inhibitor; serotonin uptake inhibitor
bupropion hydrochloride [no description available]	2.08	1	0	aromatic ketone
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.	2.08	1	0	hydrochloride	adrenergic antagonist; antidepressant; H1-receptor antagonist; sedative; serotonin uptake inhibitor
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.	3.23	1	0
cefprozil [no description available]	3.23	1	0	cephalosporin; semisynthetic derivative	antibacterial drug
doxazosin mesylate Cardura: Trade name in United States.	2.08	1	0	methanesulfonate salt	geroprotector
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.	3.61	2	0	acetylenic 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.	3.61	2	0	aryl sulfide; benzamides; organic heterobicyclic compound; phenols; secondary alcohol; tertiary amino compound	antineoplastic agent; HIV protease inhibitor
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.	2.08	1	0	2-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.	2.08	1	0	hydrochloride; 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.	3.23	1	0	aromatic ketone; chlorobenzophenone; monocarboxylic acid	drug metabolite; marine xenobiotic 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.	2.77	3	0	organic bromide salt	colorimetric reagent; dye
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.	3.87	3	0	azacycloalkane; 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]	3.61	2	0	carbamate 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.	3.6	2	0	acetamides; amino acid ester; cyclohexenecarboxylate ester; primary amino compound	antiviral drug; EC 3.2.1.18 (exo-alpha-sialidase) inhibitor; environmental contaminant; prodrug; xenobiotic
n-acetylaspartic acid N-acetyl-L-aspartic acid : An N-acyl-L-aspartic acid in which the acyl group is specified as acetyl.	2	1	0	N-acetyl-L-amino acid; N-acyl-L-aspartic acid	antioxidant; human metabolite; mouse metabolite; nutraceutical; rat metabolite
aica ribonucleotide AICA ribonucleotide: purine precursor that has antineoplastic activity. AICA ribonucleotide : A 1-(phosphoribosyl)imidazolecarboxamide that is acadesine in which the hydroxy group at the 5' position has been converted to its monophosphate derivative.	2.08	1	0	1-(phosphoribosyl)imidazolecarboxamide; aminoimidazole	cardiovascular drug; Escherichia coli metabolite; human metabolite; mouse metabolite; plant metabolite; Saccharomyces cerevisiae metabolite
ticlopidine hydrochloride [no description available]	2.08	1	0	hydrochloride
proadifen hydrochloride [no description available]	2.25	1	0
epirubicin hydrochloride [no description available]	2.08	1	0
glutathione disulfide Glutathione Disulfide: A GLUTATHIONE dimer formed by a disulfide bond between the cysteine sulfhydryl side chains during the course of being oxidized.	2.08	1	0	glutathione derivative; organic disulfide	Escherichia coli metabolite; mouse metabolite
histamine phosphate histamine phosphate : A phosphate salt that is the diphosphate salt of histamine.	3.23	1	0	phosphate salt	histamine agonist
cephalosporin c cephalosporin C: RN given refers to parent cpd; structure in Merck, 9th ed, #1937. cephalosporin C : A cephalosporin antibiotic carrying a 3-acetoxymethyl substituent and a 6-oxo-N(6)-L-lysino group at position 7.	2.07	1	0	cephalosporin	fungal metabolite
tilbroquinol [no description available]	3.23	1	0	organohalogen compound; quinolines
bendamustine [no description available]	3.23	1	0	benzimidazoles
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.	3.23	1	0	organic heterotricyclic compound; pyridines	cyclooxygenase 1 inhibitor; hepatotoxic agent; non-narcotic analgesic; non-steroidal anti-inflammatory drug; platelet aggregation inhibitor; prodrug
milnacipran Milnacipran: A cyclopropanecarboxamide serotonin and norepinephrine reuptake inhibitor (SNRI) that is used in the treatment of FIBROMYALGIA.	2.05	1	0	acetamides
ebrotidine ebrotidine: an H2-receptor antagonist and gastric mucosa protector	3.23	1	0	sulfonamide
pazufloxacin [no description available]	2.08	1	0	quinolines
repaglinide [no description available]	3.61	2	0	piperidines
telmisartan Telmisartan: A biphenyl compound and benzimidazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION.. telmisartan : A member of the class of benzimidazoles used widely in the treatment of hypertension.	3.61	2	0	benzimidazoles; biphenyls; carboxybiphenyl	angiotensin receptor antagonist; antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; environmental contaminant; xenobiotic
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.	18.92	42	11	1,2,3-triazole
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.	2.08	1	0
fluorodeoxyglucose f18 Fluorodeoxyglucose F18: The compound is given by intravenous injection to do POSITRON-EMISSION TOMOGRAPHY for the assessment of cerebral and myocardial glucose metabolism in various physiological or pathological states including stroke and myocardial ischemia. It is also employed for the detection of malignant tumors including those of the brain, liver, and thyroid gland. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1162)	9.68	19	9	2-deoxy-2-((18)F)fluoro-D-glucose; 2-deoxy-2-fluoro-aldehydo-D-glucose
sertraline Sertraline: A selective serotonin uptake inhibitor that is used in the treatment of depression.. sertraline : A member of the class of tetralins that is tetralin which is substituted at positions 1 and 4 by a methylamino and a 3,4-dichlorophenyl group, respectively (the S,S diastereoisomer). A selective serotonin-reuptake inhibitor (SSRI), it is administered orally as the hydrochloride salt as an antidepressant for the treatment of depression, obsessive-compulsive disorder, panic disorder and post-traumatic stress disorder.	3.23	1	0	dichlorobenzene; secondary amino compound; tetralins	antidepressant; serotonin uptake inhibitor
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.	7.99	13	2	1,1-bis(phosphonic acid); imidazoles	bone density conservation agent
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.	2.08	1	0	organic peroxide; sesquiterpene lactone	antimalarial; plant metabolite
brinzolamide brinzolamide: an antiglaucoma agent	2.08	1	0	sulfonamide; thienothiazine	antiglaucoma drug; EC 4.2.1.1 (carbonic anhydrase) inhibitor
drospirenone drospirenone: a progestational compound with antimineralocorticoid and antiandrogenic activity; structure given in first source	2.08	1	0	3-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.	2.08	1	0	artemisinin derivative; cyclic acetal; organic peroxide; semisynthetic derivative; sesquiterpenoid	antimalarial
5-fluoropyrimidine [no description available]	3.47	1	1
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.	3.23	1	0	acetamides; organosulfonic acid	environmental contaminant; neurotransmitter agent; xenobiotic
isaxonine isaxonine: promotes nerve growth	3.23	1	0	aminopyrimidine
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.	3.23	1	0	chromanes; diol; organofluorine compound; secondary alcohol; secondary amino compound
uk 68798 [no description available]	3.61	2	0	aromatic ether; sulfonamide; tertiary amino compound	anti-arrhythmia drug; potassium channel blocker
hp 873 iloperidone: an atypical, negative symptom antipsychotic agent. iloperidone : A member of the class of piperidines that is the 4-acetyl-2-methoxyphenyl ether of 3-(piperidin-1-yl)propan-1-ol which is substituted at position 4 of the piperidine ring by a 6-fluoro-1,2-benzoxazol-3-yl group. A member of the group of second generation antipsychotics (also known as an atypical antipsychotics), it is used for the treatment of schizophrenia.	3.61	2	0	1,2-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.	3.23	1	0	razoxane	antineoplastic 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.	2.17	1	0	nordihydroguaiaretic acid	antineoplastic agent; hypoglycemic agent; lipoxygenase inhibitor; metabolite
loxapine succinate [no description available]	2.08	1	0	succinate salt	geroprotector
fenoxypropazine [no description available]	3.23	1	0	aromatic 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.	4.83	9	0	conazole antifungal drug; difluorobenzene; pyrimidines; tertiary alcohol; triazole antifungal drug	P450 inhibitor
betamipron [no description available]	2.08	1	0	organonitrogen compound; organooxygen compound
uroxatral [no description available]	2.08	1	0	hydrochloride
aceclofenac [no description available]	3.61	2	0	amino acid; carboxylic ester; dichlorobenzene; monocarboxylic acid; secondary amino compound	EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
nitrefazole [no description available]	3.23	1	0	imidazoles
thiocolchicoside [no description available]	2.08	1	0	glycoside
picropodophyllin picropodophyllin: isolated from American May apple (Podophyllum); inhibits IGF-I autophosphorylation without interfering with tyrosine kinase activity. picropodophyllotoxin : An organic heterotetracyclic compound that has a furonaphthodioxole skeleton bearing 3,4,5-trimethoxyphenyl and hydroxy substituents.	2.15	1	0	furonaphthodioxole; lignan; organic heterotetracyclic compound	antineoplastic agent; insulin-like growth factor receptor 1 antagonist; plant metabolite; tyrosine kinase inhibitor
bes 2-[bis(2-hydroxyethyl)amino]ethanesulfonic acid : A Good's buffer substance, pKa = 7.15 at 20 degreeC.	4.95	2	2	1,1-diunsubstituted alkanesulfonate; amino sulfonic acid; BES
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.	3.61	2	0	carbapenems
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.	3.23	1	0	hydroxy-1,2-naphthoquinone
bendamustine hydrochloride [no description available]	7.38	7	2
rivastigmine [no description available]	3.23	1	0	carbamate ester; tertiary amino compound	cholinergic drug; EC 3.1.1.8 (cholinesterase) inhibitor; neuroprotective agent
frovatriptan [no description available]	3.23	1	0	carbazoles
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.	3.23	1	0	indoles; N-alkylpyrrolidine; sulfone	non-steroidal anti-inflammatory drug; serotonergic agonist; vasoconstrictor agent
rosiglitazone [no description available]	3.61	2	0	aminopyridine; thiazolidinediones	EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor; ferroptosis inhibitor; insulin-sensitizing drug
tamiflu [no description available]	2.08	1	0	phosphate salt
bexarotene [no description available]	3.61	2	0	benzoic acids; naphthalenes; retinoid	antineoplastic agent
s20098 [no description available]	2.08	1	0	acetamides
flunisolide flunisolide: flunisolide HFA is a formulation of flunisolide using hydrofluoroalkane (HFA) as propellant in place of chlorofluorocarbon (CFC) ones	2.08	1	0	11beta-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
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.	2.08	1	0	organoammonium salt	analgesic; 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.	8.9	3	0	macrolide antibiotic	antibacterial 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.	2.08	1	0	3-(1-methylpyrrolidin-2-yl)pyridine	anxiolytic drug; biomarker; immunomodulator; mitogen; neurotoxin; nicotinic acetylcholine receptor agonist; peripheral nervous system drug; phytogenic insecticide; plant metabolite; psychotropic drug; teratogenic agent; xenobiotic
moexipril [no description available]	3.23	1	0	peptide
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.	7.05	1	0	amino acid zwitterion; homocysteine; serine family amino acid	fundamental metabolite; mouse metabolite
gliquidone gliquidone: structure; RN given refers to parent cpd	2.08	1	0	isoquinolines
mci 9038 [no description available]	3.23	1	0	peptide
lopinavir [no description available]	2.54	2	0	amphetamines; dicarboxylic acid diamide	anticoronaviral agent; antiviral drug; HIV protease inhibitor
norcantharidin norcantharidin: structure given in first source; RN given refers to cpds without isomeric designation	7.41	1	0	furofuran
titanium nitride (tin) titanium nitride: RN given refers to unspecified MF	3.5	1	1
pyrimidine dimers Pyrimidine Dimers: Dimers found in DNA chains damaged by ULTRAVIOLET RAYS. They consist of two adjacent PYRIMIDINE NUCLEOTIDES, usually THYMINE nucleotides, in which the pyrimidine residues are covalently joined by a cyclobutane ring. These dimers block DNA REPLICATION.	2.46	2	0
combretastatin combretastatin: cytotoxic principle from South African tree COMBRETUM caffrum; structure given in first source; acts at COLCHICINE site of TUBULIN	2.13	1	0
moxifloxacin hydrochloride moxifloxacin hydrochloride : A hydrochloride comprising equimolar amounts of moxifloxacin and hydrogen chloride.	2.08	1	0	hydrochloride	antibacterial drug
cobalt Cobalt: A trace element that is a component of vitamin B12. It has the atomic symbol Co, atomic number 27, and atomic weight 58.93. It is used in nuclear weapons, alloys, and pigments. Deficiency in animals leads to anemia; its excess in humans can lead to erythrocytosis.. cobalt(1+) : A monovalent inorganic cation obtained from cobalt.. cobalt atom : A cobalt group element atom that has atomic number 27.	7.94	12	1	cobalt group element atom; metal allergen	micronutrient
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.	12.91	39	5	17beta-hydroxy steroid; 3-hydroxy steroid; organofluorine compound; sulfoxide	antineoplastic agent; estrogen antagonist; estrogen receptor antagonist
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.	3.58	2	0
mizoribine [no description available]	9.13	4	0	imidazoles	anticoronaviral agent
sr141716 [no description available]	2.08	1	0	amidopiperidine; carbohydrazide; dichlorobenzene; monochlorobenzenes; pyrazoles	anti-obesity agent; appetite depressant; CB1 receptor antagonist
bosentan anhydrous Bosentan: A sulfonamide and pyrimidine derivative that acts as a dual endothelin receptor antagonist used to manage PULMONARY HYPERTENSION and SYSTEMIC SCLEROSIS.	3.61	2	0	primary 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.	2.1	1	0	diterpene 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
racecadotril racecadotril: parenterally active enkephalinase inhibitor	2.08	1	0	N-acyl-amino acid
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	3.23	1	0	alpha-amino acid ester; dicarboxylic acid monoester; ethyl ester; organic heterobicyclic compound	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
1-hydroxymethylmidazolam 1-hydroxymethylmidazolam: metabolite of midazolam. 1-hydroxymidazolam : An imidazobenzodiazepine that is midazolam in which one of the hydrogens of the methyl group is substituted by a hydroxy group. It is the major metabolite of the anesthetic, midazolam.	3.47	1	1	aromatic primary alcohol; imidazobenzodiazepine; monofluorobenzenes; organochlorine compound	drug metabolite; human blood serum metabolite; human urinary metabolite
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).	7.43	15	1	hydrochloride	immunosuppressive 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.	2.07	1	0	aminodiol; primary amino compound	antineoplastic agent; CB1 receptor antagonist; immunosuppressive agent; prodrug; sphingosine-1-phosphate receptor agonist
asiaticoside [no description available]	2.25	1	0
ecteinascidin 743 [no description available]	3.86	3	0	acetate 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.	2.52	2	0
tadalafil [no description available]	3.61	2	0	benzodioxoles; pyrazinopyridoindole	EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor; vasodilator agent
paliperidone 3-{2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl}-9-hydroxy-2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one : A member of the class of pyridopyrimidines that is 9-hydroxy-2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one carrying an additional 2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl group at position 2.. paliperidone : A racemate comprising equimolar amounts of (R)- and (S)-paliperidone. Paliperidone is the primary active metabolite of the older antipsychotic risperidone and is used for treatment of schizophrenia.	3.23	1	0	1,2-benzoxazoles; heteroarylpiperidine; organofluorine compound; pyridopyrimidine; secondary alcohol
nitisinone [no description available]	3.23	1	0	(trifluoromethyl)benzenes; C-nitro compound; cyclohexanones; mesotrione	EC 1.13.11.27 (4-hydroxyphenylpyruvate dioxygenase) inhibitor
plavix [no description available]	2.08	1	0	azaheterocycle sulfate salt; organoammonium sulfate salt	anticoagulant; P2Y12 receptor antagonist; platelet aggregation inhibitor
asiatic acid [no description available]	2.25	1	0	monocarboxylic acid; pentacyclic triterpenoid; triol	angiogenesis modulating agent; metabolite
clofarabine [no description available]	3.61	2	0	adenosines; organofluorine compound	antimetabolite; antineoplastic agent
pramipexole Pramipexole: A benzothiazole derivative and dopamine agonist with antioxidant properties that is used in the treatment of PARKINSON DISEASE and RESTLESS LEGS SYNDROME.. pramipexole : A member of the class of benzothiazoles that is 4,5,6,7-tetrahydro-1,3-benzothiazole in which the hydrogens at the 2 and 6-pro-S-positions are substituted by amino and propylamino groups, respectively.	3.61	2	0	benzothiazoles; diamine	antidyskinesia agent; antiparkinson drug; dopamine agonist; radical scavenger
valdecoxib [no description available]	3.61	2	0	isoxazoles; sulfonamide	antipyretic; antirheumatic drug; cyclooxygenase 2 inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug
1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid 1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid: structure given in first source. DOTA : An azamacrocyle in which four nitrogen atoms at positions 1, 4, 7 and 10 of a twelve-membered ring are each substituted with a carboxymethyl group.	2.41	1	0	azamacrocycle	chelator; copper chelator
san 58035 [no description available]	2.45	2	0
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.	15.43	25	3	methanesulfonate salt	anticoronaviral 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.	3.23	1	0	indoles; sulfonamide; tertiary amine	non-steroidal anti-inflammatory drug; serotonergic agonist; vasoconstrictor agent
mk 0663 [no description available]	2.08	1	0	bipyridines; organochlorine compound; sulfone	cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
gefitinib [no description available]	11.4	27	4	aromatic ether; monochlorobenzenes; monofluorobenzenes; morpholines; quinazolines; secondary amino compound; tertiary amino compound	antineoplastic agent; epidermal growth factor receptor antagonist
4-carboxyfluorescein [no description available]	2.15	1	0	monocarboxylic acid	fluorochrome
vadimezan vadimezan : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by a 5,6-dimethyl-9-oxoxanthen-4-yl group.	2.5	2	0	monocarboxylic acid; xanthones	antineoplastic agent
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.	3.61	2	0	benzocycloheptapyridine	anti-allergic agent; cholinergic antagonist; drug metabolite; H1-receptor antagonist
1,4,7-triazacyclononane-n,n',n''-triacetic acid 1,4,7-triazacyclononane-N,N',N''-triacetic acid: structure given in first source	2.08	1	0
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.	3.23	1	0	cyclohexanols; phenols; tertiary amino compound	antidepressant; drug metabolite; marine xenobiotic metabolite
lestaurtinib [no description available]	2.63	2	0	indolocarbazole
methotrexate [no description available]	10.64	5	1	dicarboxylic acid; monocarboxylic acid amide; pteridines	abortifacient; antimetabolite; antineoplastic agent; antirheumatic drug; dermatologic drug; DNA synthesis inhibitor; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; immunosuppressive agent
tamsulosin [no description available]	3.23	1	0	5-(2-{[2-(2-ethoxyphenoxy)ethyl]amino}propyl)-2-methoxybenzenesulfonamide	alpha-adrenergic antagonist; antineoplastic agent
rufinamide rufinamide: for treatment of Lennox-Gastaut syndrome; structure in first source	3.59	2	0	aromatic amide; heteroarene
sulbactam [no description available]	2.08	1	0	penicillanic acids
olmesartan medoxomil Olmesartan Medoxomil: An ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to manage HYPERTENSION.	3.61	2	0	biphenyls
dexpanthenol dexpanthenol: The alcohol of pantothenic acid	3.23	1	0	amino 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.	3.23	1	0	sulfonamide	prodrug
abiraterone [no description available]	2.08	1	0	3beta-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.	3.87	3	0	1,3-thiazolemonocarboxylic acid; aromatic ether; nitrile	EC 1.17.3.2 (xanthine oxidase) inhibitor
pomalidomide 3-aminophthalimidoglutarimide: structure in first source	10.85	3	1	aromatic amine; dicarboximide; isoindoles; piperidones	angiogenesis inhibitor; antineoplastic agent; immunomodulator
proline Proline: A non-essential amino acid that is synthesized from GLUTAMIC ACID. It is an essential component of COLLAGEN and is important for proper functioning of joints and tendons.. proline : An alpha-amino acid that is pyrrolidine bearing a carboxy substituent at position 2.	2.07	1	0	amino acid zwitterion; glutamine family amino acid; L-alpha-amino acid; proline; proteinogenic amino acid	algal metabolite; compatible osmolytes; Escherichia coli metabolite; micronutrient; mouse metabolite; nutraceutical; Saccharomyces cerevisiae metabolite
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.	3.23	1	0	1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile	antidepressant; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
lexapro Lexapro: Trade name of escitalopram, the active S-enantiomer of the racemic citalopram.	2.08	1	0
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.	3.59	2	0	N-acyl-L-glutamic acid; pteridines; terminal acetylenic compound	antimetabolite; antineoplastic agent; EC 1.5.1.3 (dihydrofolate reductase) inhibitor
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.	10.77	21	6	secondary alpha-hydroxy ketone; tetracyclic diterpenoid	antimalarial; antineoplastic agent; photosensitizing agent
perifosine [no description available]	3.02	4	0	ammonium betaine; phospholipid	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
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).	3.23	1	0	carbohydrazide	antiviral 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.	9.68	3	0	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	antineoplastic agent; EC 2.5.1.58 (protein farnesyltransferase) inhibitor
levofloxacin Levofloxacin: The L-isomer of Ofloxacin.. levofloxacin : An optically active form of ofloxacin having (S)-configuration; an inhibitor of bacterial topoisomerase IV and DNA gyrase.	3.61	2	0	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; 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).	3.61	2	0	azetidines; 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.	3.23	1	0	carbapenemcarboxylic acid; pyrrolidinecarboxamide	antibacterial drug
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.	3.61	2	0	amino acid; monocarboxylic acid; organochlorine compound; organofluorine compound; secondary amino compound	cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
conivaptan conivaptan : The amide resulting from the formal condensation of 4-[(biphenyl-2-ylcarbonyl)amino]benzoic acid with the benzazepine nitrogen of 2-methyl-1,4,5,6-tetrahydroimidazo[4,5-d][1]benzazepine. It is an antagonist for two of the three types of arginine vasopressin (AVP) receptors, V1a and V2. It is used as its hydrochloride salt for the treatment of hyponatraemia (low blood sodium levels) caused by syndrome of inappropriate antidiuretic hormone (SIADH).	3.23	1	0	benzazepine	aquaretic; vasopressin receptor antagonist
vatalanib [no description available]	6.35	7	2	monochlorobenzenes; phthalazines; pyridines; secondary amino compound	angiogenesis inhibitor; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; vascular endothelial growth factor receptor antagonist
moxifloxacin Moxifloxacin: A fluoroquinolone that acts as an inhibitor of DNA TOPOISOMERASE II and is used as a broad-spectrum antibacterial agent.. moxifloxacin : A quinolone that consists of 4-oxo-1,4-dihydroquinoline-3-carboxylic acid bearing a cyclopropyl substituent at position 1, a fluoro substitiuent at position 6, a (4aS,7aS)-octahydro-6H-pyrrolo[3,4-b]pyridin-6-yl group at position 7 and a methoxy substituent at position 8. A member of the fluoroquinolone class of antibacterial agents.	3.23	1	0	aromatic ether; cyclopropanes; fluoroquinolone antibiotic; pyrrolidinopiperidine; quinolinemonocarboxylic acid; quinolone antibiotic; quinolone	antibacterial drug
pralnacasan pralnacasan: NSAID, ICE inhibitor & metastasis inhibitor; RN & structure in first source	3.23	1	0
clevidipine clevidipine: a calcium channel blocker and antihypertensive agent; structure in first source	3.23	1	0	dihydropyridine
ruboxistaurin ruboxistaurin: inhibits protein kinase C beta; structure in first source	2.15	1	0
solifenacin [no description available]	3.23	1	0	isoquinolines
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.	3.23	1	0	methyl phenyl(piperidin-2-yl)acetate	adrenergic agent
xamoterol Xamoterol: A phenoxypropanolamine derivative that is a selective beta-1-adrenergic agonist.	2.08	1	0	morpholines
naproxen Naproxen: An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout.. naproxen : A methoxynaphthalene that is 2-methoxynaphthalene substituted by a carboxy ethyl group at position 6. Naproxen is a non-steroidal anti-inflammatory drug commonly used for the reduction of pain, fever, inflammation and stiffness caused by conditions such as osteoarthritis, kidney stones, rheumatoid arthritis, psoriatic arthritis, gout, ankylosing spondylitis, menstrual cramps, tendinitis, bursitis, and for the treatment of primary dysmenorrhea. It works by inhibiting both the COX-1 and COX-2 enzymes.	3.61	2	0	methoxynaphthalene; monocarboxylic acid	antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; drug allergen; environmental contaminant; gout suppressant; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic
canertinib [no description available]	2.63	2	0	monochlorobenzenes; morpholines; organofluorine compound; quinazolines	antineoplastic agent; tyrosine kinase inhibitor
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.	3.23	1	0	(trifluoromethyl)benzenes; naphthalenes; secondary amino compound	calcimimetic; P450 inhibitor
lubiprostone [no description available]	3.23	1	0
olmesartan olmesartan: an active metabolite of CS 866	3.51	1	1	biphenylyltetrazole	angiotensin receptor antagonist; antihypertensive agent
telbivudine [no description available]	3.61	2	0	pyrimidine 2'-deoxyribonucleoside	antiviral drug; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
tipifarnib [no description available]	3.35	1	0	imidazoles; monochlorobenzenes; primary amino compound; quinolone	antineoplastic agent; apoptosis inducer; EC 2.5.1.58 (protein farnesyltransferase) inhibitor
cyc 202 seliciclib : 2,6-Diaminopurine carrying benzylamino, (2R)-1-hydroxybutan-2-yl and isopropyl substituents at C-6, C-2-N and N-9 respectively. It is an experimental drug candidate in the family of pharmacological cyclin-dependent kinase (CDK) inhibitors.	2.63	2	0	2,6-diaminopurines	antiviral drug; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
platycodin d platycodin D: triterpenoid saponin from a root of Platycodon grandiflorum; RN refers to (2beta,3beta,16alpha)-isomer; structure given in first source	2.15	1	0	triterpenoid saponin	metabolite
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.	3.23	1	0	amino 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.	3.23	1	0	antibiotic antifungal drug; azamacrocycle; echinocandin; heterodetic cyclic peptide; semisynthetic derivative
aminopterin Aminopterin: A folic acid derivative used as a rodenticide that has been shown to be teratogenic.	2.05	1	0	dicarboxylic acid	EC 1.5.1.3 (dihydrofolate reductase) inhibitor; mutagen
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.	3.23	1	0	corticosteroid 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.	3.57	2	0
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).	9.37	4	1	amino acid zwitterion; angiotensin II	human metabolite
fiduxosin fiduxosin: fiduxosin (ABT-980) is the (3aR,9bR)-isomer; structure in first source	3.23	1	0
atropine tropan-3alpha-yl 3-hydroxy-2-phenylpropanoate : A tropane alkaloid that is (1R,5)-8-methyl-8-azabicyclo[3.2.1]octane substituted by a (3-hydroxy-2-phenylpropanoyl)oxy group at position 3.	3.61	2	0
sb 203580 [no description available]	3.92	2	0	imidazoles; 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
sb 216763 [no description available]	2.08	1	0	indoles; maleimides
enzastaurin [no description available]	5.48	4	1	indoles; maleimides
erlotinib [no description available]	3.98	3	0	aromatic ether; quinazolines; secondary amino compound; terminal acetylenic compound	antineoplastic agent; epidermal growth factor receptor antagonist; protein kinase inhibitor
erlotinib hydrochloride [no description available]	13.01	34	8	hydrochloride; terminal acetylenic compound	antineoplastic agent; protein kinase inhibitor
5-carboxyfluorescein diacetate acetoxymethyl ester 5-carboxyfluorescein diacetate acetoxymethyl ester: is an indirect measure of cell membrane integrity-are noninvasive and can be monitored conveniently directly in multiwell plates	2.15	1	0
etravirine [no description available]	3.23	1	0	aminopyrimidine; aromatic ether; dinitrile; organobromine compound	antiviral agent; HIV-1 reverse transcriptase inhibitor
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.	3.23	1	0	1-benzofurans; aromatic ether; aromatic ketone; sulfonamide; tertiary amino compound	anti-arrhythmia drug; environmental contaminant; xenobiotic
ramelteon ramelteon: melatonin MT1/MT2 receptor agonist	3.61	2	0	indanes
lapatinib [no description available]	11.18	24	1	furans; 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.	3.23	1	0	carbamate 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.	3.61	2	0	benzoic acids; monocarboxylic acid; phenols; triazoles	iron chelator
bms204352 BMS204352: a calcium-sensitive opener of maxi-K potassium channels; structure in first source	2.08	1	0
tbc-11251 sitaxsentan: endothelin A receptor antagonist; structure in first source	3.61	2	0	benzodioxoles
tolvaptan [no description available]	4.61	4	0	benzazepine; benzenedicarboxamide	aquaretic; vasopressin receptor antagonist
sorafenib [no description available]	18.57	157	25	(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
alagebrium alagebrium: an advanced glycation endproducts (AGE) cross-link breaker	7.15	1	0
lenalidomide [no description available]	10.84	13	4	aromatic amine; dicarboximide; isoindoles; piperidones	angiogenesis inhibitor; antineoplastic agent; immunomodulator
regadenoson [no description available]	3.23	1	0	purine 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.	5.61	6	0	N-acyl-amino acid
vincaleukoblastine [no description available]	3.61	2	0	acetate 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
vincristine sulfate [no description available]	2.08	1	0	organic sulfate salt	antineoplastic agent; geroprotector
benzofurans Benzofurans: Compounds that contain a BENZENE ring fused to a furan ring.	5.91	2	2
benzarone benzarone: antihemorrhagic agent; structure	3.23	1	0	1-benzofurans
estramustine Estramustine: A nitrogen mustard linked to estradiol, usually as phosphate; used to treat prostatic neoplasms; also has radiation protective properties.. estramustine : A carbamate ester obtained by the formal condensation of the hydroxy group of 17beta-estradiol with the carboxy group of bis(2-chloroethyl)carbamic acid.	3.23	1	0	17beta-hydroxy steroid; carbamate ester; organochlorine compound	alkylating agent; antineoplastic agent; radiation protective agent
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.	3.35	1	0	alkaloid ester; enol ether; organic heteropentacyclic compound; tertiary alcohol	anticoronaviral agent; antineoplastic agent; apoptosis inducer; protein synthesis inhibitor
wortmannin [no description available]	3.92	3	0	acetate 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
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.	3.93	3	0
bortezomib [no description available]	11.25	24	4	amino 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.	9.18	4	0	1,3-thiazoles; carbamate ester; carboxamide; L-valine derivative; ureas	antiviral drug; environmental contaminant; HIV protease inhibitor; xenobiotic
dihydropyridines Dihydropyridines: Pyridine moieties which are partially saturated by the addition of two hydrogen atoms in any position.	2.21	1	0
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.	2.47	2	0
carboplatin [no description available]	12.26	22	10
fibrin Fibrin: A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.	3.24	5	0	peptide
bradykinin [no description available]	2.1	1	0	oligopeptide	human blood serum metabolite; vasodilator agent
elastin [no description available]	7.59	2	0	oligopeptide
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.	2.17	1	0	3,5-dihydroxy-3-methylpentanoic acid
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.	3.23	1	0	heterodetic cyclic peptide; peptide hormone	oxytocic; vasodilator agent
s-adenosyl-3-methylthiopropylamine S-adenosyl-3-methylthiopropylamine: decarboxylated S-adenosylmethionine	2.15	1	0	adenosines; sulfonium compound	Escherichia coli metabolite; human urinary metabolite; mouse metabolite; rat metabolite
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.	7.1	1	0	11alpha-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
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.	3.61	2	0	coformycins	antimetabolite; antineoplastic agent; Aspergillus metabolite; bacterial metabolite; EC 3.5.4.4 (adenosine deaminase) inhibitor
quinidine Quinidine: An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.. quinidine : A cinchona alkaloid consisting of cinchonine with the hydrogen at the 6-position of the quinoline ring substituted by methoxy.	3.61	2	0	cinchona alkaloid	alpha-adrenergic antagonist; anti-arrhythmia drug; antimalarial; drug allergen; EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor; EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor; muscarinic antagonist; P450 inhibitor; potassium channel blocker; sodium channel blocker
meropenem Meropenem: A thienamycin derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of bacterial infections, including infections in immunocompromised patients.. meropenem : A carbapenemcarboxylic acid in which the azetidine and pyrroline rings carry 1-hydroxymethyl and in which the azetidine and pyrroline rings carry 1-hydroxymethyl and 5-(dimethylcarbamoyl)pyrrolidin-3-ylthio substituents respectively.	3.61	2	0	alpha,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.	3.23	1	0	1-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.	3.23	1	0	beta-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.	2.08	1	0	cardenolide glycoside	EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor
saquinavir Saquinavir: An HIV protease inhibitor which acts as an analog of an HIV protease cleavage site. It is a highly specific inhibitor of HIV-1 and HIV-2 proteases, and also inhibits CYTOCHROME P-450 CYP3A.. saquinavir : An aspartic acid derivative obtained by formal condensation of the primary amino group of (2S,3R)-4-[(3S,4aS,8aS)-3-(tert-butylcarbamoyl)octahydroisoquinolin-2(1H)-yl]-3-hydroxy-1-phenylbutan-2-ylamine with the carboxy group of N(2)(-quinolin-2-ylcarbonyl)-L-asparagine. An inhibitor of HIV-1 protease.	3.61	2	0	L-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.	3.23	1	0	acetate ester; steroid ester	cholinergic antagonist; muscle relaxant; nicotinic antagonist
abacavir abacavir: a carbocyclic nucleoside with potent selective anti-HIV activity. abacavir : A 2,6-diaminopurine that is (1S)-cyclopent-2-en-1-ylmethanol in which the pro-R hydrogen at the 4-position is substituted by a 2-amino-6-(cyclopropylamino)-9H-purin-9-yl group. A nucleoside analogue reverse transcriptase inhibitor (NRTI) with antiretroviral activity against HIV, it is used (particularly as the sulfate) with other antiretrovirals in combination therapy of HIV infection.	3.23	1	0	2,6-diaminopurines	antiviral drug; drug allergen; HIV-1 reverse transcriptase inhibitor
perindopril erbumine [no description available]	2.08	1	0	addition compound	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
miglitol [no description available]	3.61	2	0	piperidines
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.	3.23	1	0	L-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.	2.08	1	0	organic bromide salt; quaternary ammonium salt	muscle relaxant; neuromuscular agent
linezolid [no description available]	3.61	2	0	acetamides; morpholines; organofluorine compound; oxazolidinone	antibacterial drug; protein synthesis inhibitor
ginsenoside rf ginsenoside Rf: from ginseng. ginsenoside Rf : A ginsenoside found in Panax ginseng and Panax japonicus var. major 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 beta-D-glucopyranosyl-(1->2)-beta-D-glucopyranoside, and in which a double bond has been introduced at the 24-25 position.	3.51	1	0	12beta-hydroxy steroid; 20-hydroxy steroid; 3beta-hydroxy-4,4-dimethylsteroid; 3beta-hydroxy steroid; beta-D-glucoside; disaccharide derivative; ginsenoside; tetracyclic triterpenoid	antineoplastic agent; apoptosis inducer; plant metabolite
genipin [no description available]	7.15	1	0	iridoid monoterpenoid	anti-inflammatory agent; antioxidant; apoptosis inhibitor; cross-linking reagent; hepatotoxic agent; uncoupling protein inhibitor
cyclopamine [no description available]	3.21	1	0	piperidines	glioma-associated oncogene inhibitor
clindamycin phosphate [no description available]	3.23	1	0
pemirolast potassium salt [no description available]	2.08	1	0
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.	3.61	2	0	3-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]	3.23	1	0	tertiary amine	antispasmodic drug; muscarinic antagonist; muscle relaxant
ao 128 AO 128: alpha-glucosidase inhibitor; structure given in first source	2.08	1	0	organic 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.	2.08	1	0	11beta-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.	3.23	1	0	1-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.	2.08	1	0	11beta-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
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.	4.45	6	0	retinoic 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
resveratrol trans-resveratrol : A resveratrol in which the double bond has E configuration.	2.59	2	0	resveratrol	antioxidant; 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).	3.23	1	0	retinol; vitamin A	human metabolite; mouse metabolite; plant metabolite
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.	2.11	1	0	octadec-9-enoic acid	antioxidant; 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.	20.54	309	59	macrolide lactam	bacterial metabolite; immunosuppressive agent
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).	3.23	1	0	dihydroxy monocarboxylic acid; monofluorobenzenes; pyrimidines; statin (synthetic); sulfonamide	anti-inflammatory agent; antilipemic drug; cardioprotective agent; CETP inhibitor; environmental contaminant; xenobiotic
cocaine Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.. cocaine : A tropane alkaloid obtained from leaves of the South American shrub Erythroxylon coca.	2.63	2	0	benzoate 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
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.	19.93	229	68	2-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.	2.08	1	0	alpha,beta-unsaturated carboxylic ester; epoxide; monocarboxylic acid; oxanes; secondary alcohol; triol	antibacterial drug; bacterial metabolite; protein synthesis inhibitor
clindamycin Clindamycin: An antibacterial agent that is a semisynthetic analog of LINCOMYCIN.. clindamycin : A carbohydrate-containing antibiotic that is the semisynthetic derivative of lincomycin, a natural antibiotic.	3.23	1	0
fosfomycin Fosfomycin: An antibiotic produced by Streptomyces fradiae.. fosfomycin : A phosphonic acid having an (R,S)-1,2-epoxypropyl group attached to phosphorus.	3.23	1	0	epoxide; 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.	4.42	3	0	macrolide antibiotic	antibacterial drug; environmental contaminant; xenobiotic
pd 166326 PD 166326: a pyrido(2,3-d)pyrimidine src tyrosine kinase inhibitor	2.41	1	0
epothilone b [no description available]	2.76	3	0	epothilone; epoxide	antineoplastic agent; apoptosis inducer; microtubule-stabilising agent
y 27632 Y 27632: RN given for di-HCl salt; inhibits Rho-associated protein kinase; inhibits calcium sensitization to affect smooth muscle relaxation; structure in first source. Y-27632 : A monocarboxylic acid amide that is trans-[(1R)-1-aminoethyl]cyclohexanecarboxamide in which one of the nitrogens of the aminocarbony group is substituted by a pyridine nucleus. It has been shown to exhibit inhibitory activity against Rho-associated protein kinase (ROCK) enzyme.	2.21	1	0	aromatic amide
octreotide [no description available]	3.23	1	0
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).	4.25	5	0	epothilone; epoxide	antineoplastic agent; metabolite; microtubule-stabilising agent; tubulin modulator
eptifibatide [no description available]	3.23	1	0	homodetic cyclic peptide; macrocycle; organic disulfide	anticoagulant; platelet aggregation inhibitor
afimoxifene afimoxifene : A tertiary amino compound that is tamoxifen in which the phenyl group which is in a Z- relationship to the ethyl substituent is hydroxylated at the para- position. It is the active metabolite of tamoxifen.	2.75	3	0	phenols; tertiary amino compound	antineoplastic agent; estrogen receptor antagonist; metabolite
decitabine [no description available]	4.13	4	0	2'-deoxyribonucleoside
teniposide [no description available]	3.61	2	0	aromatic 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).	2.15	1	0
valrubicin [no description available]	2.08	1	0	anthracycline; trifluoroacetamide
purvalanol a 6-((3-chloro)anilino)-2-(isopropyl-2-hydroxyethylamino)-9-isopropylpurine: purvalanol A is the (1R)-isomer;	2.41	1	0	purvalanol
dactinomycin Dactinomycin: A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)	3.23	1	0	actinomycin	mutagen
melphalan Melphalan: An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.. melphalan : A phenylalanine derivative comprising L-phenylalanine having [bis(2-chloroethyl)amino group at the 4-position on the phenyl ring.	3.91	3	0	L-phenylalanine derivative; nitrogen mustard; non-proteinogenic L-alpha-amino acid; organochlorine compound	alkylating agent; antineoplastic agent; carcinogenic agent; drug allergen; immunosuppressive agent
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.	2.47	2	0	amino 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.	3.23	1	0	nucleoside analogue; phosphonic acids	antiviral drug; drug metabolite; HIV-1 reverse transcriptase inhibitor
posaconazole [no description available]	3.87	3	0	aromatic ether; conazole antifungal drug; N-arylpiperazine; organofluorine compound; oxolanes; triazole antifungal drug; triazoles	trypanocidal drug
gw 257406x maribavir: has antiviral activity against human cytomegalovirus	2.1	1	0
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.	2.08	1	0	C-nitro compound; delta-lactone; pyranoindolizinoquinoline; semisynthetic derivative; tertiary alcohol	antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor; prodrug
terameprocol [no description available]	7.17	1	0	lignan
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.	3.57	2	0	antibiotic antifungal drug; echinocandin	antiinfective agent
riboflavin vitamin B2 : Any member of a group of vitamers that belong to the chemical structural class called flavins that exhibit biological activity against vitamin B2 deficiency. Symptoms associated with vitamin B2 deficiency include glossitis, seborrhea, angular stomaitis, cheilosis and photophobia. The vitamers include riboflavin and its phosphate derivatives (and includes their salt, ionised and hydrate forms).	3.23	1	0	flavin; 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.	3.23	1	0	one-carbon compound; organic sodium salt	antacid; food anticaking agent
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.	3.23	1	0	arsenic oxide	antineoplastic agent; insecticide
1,3-bis(3,5-dichlorophenyl)urea 1,3-bis(3,5-dichlorophenyl)urea: COH - City of Hope; has antineoplastic activity	2.6	1	0
sr 90107 fondaparinux sodium : An organic sodium salt, being the decasodium salt of fondaparinux.	3.23	1	0
meglumine iodipamide [no description available]	3.23	1	0	organoammonium salt	radioopaque medium
stilbenes Stilbenes: Organic compounds that contain 1,2-diphenylethylene as a functional group.. trans-stilbene : The trans-isomer of stilbene.	2.15	1	0	stilbene
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.	3.23	1	0	peptide hormone; tripeptide	human metabolite
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.	6.91	6	1	olefinic 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.	3.61	2	0	vasopressin	cardiovascular drug; hematologic agent; mitogen
s 1033 [no description available]	5.85	11	0	(trifluoromethyl)benzenes; imidazoles; pyridines; pyrimidines; secondary amino compound; secondary carboxamide	anticoronaviral agent; antineoplastic agent; tyrosine kinase inhibitor
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.	2.08	1	0	17beta-hydroxy steroid; 3-hydroxy steroid; androstanoid; epoxy steroid; nitrile	abortifacient; antineoplastic agent; EC 1.1.1.210 [3beta(or 20alpha)-hydroxysteroid dehydrogenase] inhibitor
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.	2.08	1	0	acetate salt	antineoplastic 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.	9.63	2	2	oligopeptide	anti-estrogen; antineoplastic agent; gonadotropin releasing hormone agonist
fludarabine [no description available]	3.86	3	0	purine nucleoside
propylthiouracil Propylthiouracil: A thiourea antithyroid agent. Propythiouracil inhibits the synthesis of thyroxine and inhibits the peripheral conversion of throxine to tri-iodothyronine. It is used in the treatment of hyperthyroidism. (From Martindale, The Extra Pharmacopeoia, 30th ed, p534). 6-propyl-2-thiouracil : A pyrimidinethione consisting of uracil in which the 2-oxo group is substituted by a thio group and the hydrogen at position 6 is substituted by a propyl group.	3.61	2	0	pyrimidinethione	antidote to paracetamol poisoning; antimetabolite; antioxidant; antithyroid drug; carcinogenic agent; EC 1.14.13.39 (nitric oxide synthase) inhibitor; hormone antagonist
etomidate Etomidate: Imidazole derivative anesthetic and hypnotic with little effect on blood gases, ventilation, or the cardiovascular system. It has been proposed as an induction anesthetic.. etomidate : The ethyl ester of 1-[(1R)-1-phenylethyl]-1H-imidazole-5-carboxylic acid. It is an intravenous general anaesthetic with no analgesic activity.	3.23	1	0	ethyl 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.	3.61	2	0	aryl thiol; purines; thiocarbonyl compound	anticoronaviral agent; antimetabolite; antineoplastic agent
3,3',4,5'-tetrahydroxystilbene 3,3',4,5'-tetrahydroxystilbene: demethyl derivative of isorhapontigenin; structure in first source; a Syk kinase inhibitor; found in heartwood of FABACEAE; inhibitor of photosynthesis in spinach chloroplasts; may be inhibitor of plant growth; RN given refers to (E)-isomer. piceatannol : A stilbenol that is trans-stilbene in which one of the phenyl groups is substituted by hydroxy groups at positions 3 and 4, while the other phenyl group is substituted by hydroxy groups at positions 3 and 5.	2.6	1	0	catechols; polyphenol; resorcinols; stilbenol	antineoplastic agent; apoptosis inducer; geroprotector; hypoglycemic agent; plant metabolite; protein kinase inhibitor; tyrosine kinase inhibitor
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).	2.08	1	0	sulpiride	antidepressant; 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'.	3.23	1	0	1,4,5,6-tetrahydropyrimidines; carboxamidine; thiophenes	antinematodal drug
4-(4-(4-chloro-phenyl)thiazol-2-ylamino)phenol [no description available]	2.41	1	0	substituted aniline
thiothixene [no description available]	3.23	1	0	N-methylpiperazine	anticoronaviral 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.	3.61	2	0	zopiclone	central 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.	9.48	6	0	aromatic 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.	3.23	1	0	diarylmethane
5-(4-ethylbenzylidene)-2-thioxothiazolidin-4-one [no description available]	2.11	1	0
methimazole Methimazole: A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. This is done by interfering with the oxidation of iodide ion and iodotyrosyl groups through inhibition of the peroxidase enzyme.. methimazole : A member of the class of imidazoles that it imidazole-2-thione in which a methyl group replaces the hydrogen which is attached to a nitrogen.	3.61	2	0	1,3-dihydroimidazole-2-thiones	antithyroid 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.	2.08	1	0	diarylmethane; 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.	3.61	2	0	monocarboxylic 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
terbinafine [no description available]	3.23	1	0	acetylenic 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.	2.08	1	0	monocarboxylic acid; thiazolidines	EC 1.1.1.21 (aldehyde reductase) inhibitor
drotaverin drotaverin: Hungarian drug; RN given refers to parent cpd; structure	2.08	1	0	isoquinolines
xl147 [no description available]	2.15	1	0	aromatic amine; benzothiadiazole; quinoxaline derivative; sulfonamide	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
thioguanine anhydrous Thioguanine: An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.. tioguanine : A 2-aminopurine that is the 6-thiono derivative of 2-amino-1,9-dihydro-6H-purine. Incorporates into DNA and inhibits synthesis. Used in the treatment of leukaemia.	3.23	1	0	2-aminopurines	anticoronaviral agent; antimetabolite; antineoplastic 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.	3.23	1	0	dicarboxylic acid; dithiol; sulfur-containing carboxylic acid	chelator
digoxin Digoxin: A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666). digoxin : A cardenolide glycoside that is digitoxin beta-hydroxylated at C-12. A cardiac glycoside extracted from the foxglove plant, Digitalis lanata, it is used to control ventricular rate in atrial fibrillation and in the management of congestive heart failure with atrial fibrillation, but the margin between toxic and therapeutic doses is small.	3.58	2	0	cardenolide glycoside; steroid saponin	anti-arrhythmia drug; cardiotonic drug; EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor; epitope
streptozocin [no description available]	3.23	1	0
tamoxifen [no description available]	11.19	33	3	stilbenoid; 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
nadp [no description available]	2.77	3	0
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.	3.23	1	0	pyridines; thiocarboxamide	antilipemic drug; antitubercular agent; fatty acid synthesis inhibitor; leprostatic drug; prodrug
cancidas [no description available]	3.23	1	0
ace-011 ACE-011: a dimeric fusion protein consisting of the extracellular domain of the human ActRIIA linked to the Fc portion of human IgG1 and may be an effective therapy in a variety of diseases involving bone loss	3.19	1	0
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.	2.08	1	0	11alpha-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.	3.23	1	0	carbohydrate-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.	2.08	1	0	cyclodepsipeptide; macrocycle	antimicrobial agent; antiviral agent; bacterial metabolite; potassium ionophore
ranitidine Ranitidine: A non-imidazole blocker of those histamine receptors that mediate gastric secretion (H2 receptors). It is used to treat gastrointestinal ulcers.. ranitidine : A member of the class of furans used to treat peptic ulcer disease (PUD) and gastroesophageal reflux disease.	3.23	1	0	C-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	3.23	1	0
hmr 3647 [no description available]	3.61	2	0
latoconazole latoconazole: RN refers to cpd without isomeric designation; latoconazole is (E)-isomer; structure given in first source	2.08	1	0	conazole antifungal drug; imidazole antifungal drug
maraviroc [no description available]	3.61	2	0	tropane alkaloid
toremifene citrate [no description available]	2.08	1	0	stilbenoid	anticoronaviral 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.	4.22	4	0	aromatic 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	3.5	7	0	aryl sulfide; dinitrile; enamine; substituted aniline	antineoplastic agent; antioxidant; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; osteogenesis regulator; vasoconstrictor agent
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).	3.61	2	0	beta-D-arabinoside; monosaccharide derivative; purine nucleoside	antineoplastic agent; DNA synthesis inhibitor; prodrug
bms 387032 N-(5-(((5-(1,1-dimethylethyl)-2-oxazolyl)methyl)thio)-2-thiazolyl)-4-piperidinecarboxamide: a CDK2 inhibitor with antineoplastic activity; structure in first source. N-(5-{[(5-tert-butyl-1,3-oxazol-2-yl)methyl]sulfanyl}-1,3-thiazol-2-yl)piperidine-4-carboxamide : A secondary carboxamide resulting from the formal condensation of the carboxy group of piperidine-4-carboxylic acid with the amino group of 5-{[(5-tert-butyl-1,3-oxazol-2-yl)methyl]sulfanyl}-1,3-thiazol-2-amine. It is an ATP-competitive inhibitor of CDK2, CDK7 and CDK9 kinases and exhibits anti-cancer properties.	2.15	1	0	1,3-oxazoles; 1,3-thiazoles; organic sulfide; piperidinecarboxamide; secondary carboxamide	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
cobaltous chloride cobaltous chloride: RN given refers to unlabeled cpd; RN in Chemline for cobalt trichloride: 10241-04-0; RN for 60-labeled cpd: 14543-09-0; RN for 57-labeled cpd: 164113-89-1; RN for 58-labeled cpd: 29377-09-1; structure. cobalt dichloride : A cobalt salt in which the cobalt metal is in the +2 oxidation state and the counter-anion is chloride. It is used as an indicator for water in desiccants.	2.13	1	0	cobalt salt; inorganic chloride	allergen; calcium channel blocker; sensitiser; two-colour indicator
nitrogen dioxide Nitrogen Dioxide: Nitrogen oxide (NO2). A highly poisonous gas. Exposure produces inflammation of lungs that may only cause slight pain or pass unnoticed, but resulting edema several days later may cause death. (From Merck, 11th ed) It is a major atmospheric pollutant that is able to absorb UV light that does not reach the earth's surface.	2.41	1	0	nitrogen oxide
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.	3.23	1	0	amino disaccharide; glycosylgalactose derivative; iduronic acids; oligosaccharide sulfate
dolasetron [no description available]	3.23	1	0	indolyl carboxylic acid
gestodene Gestodene: synthetic steroid with progestational activity; RN given refers to (17alpha)-isomer	2.08	1	0	steroid	estrogen
orlistat Orlistat: A lactone derivative of LEUCINE that acts as a pancreatic lipase inhibitor to limit the absorption of dietary fat; it is used in the management of obesity.. orlistat : A carboxylic ester resulting from the formal condensation of the carboxy group of N-formyl-L-leucine with the hydroxy group of (3S,4S)-3-hexyl-4-[(2S)-2-hydroxytridecyl]oxetan-2-one. A pancreatic lipase inhibitor, it is used as an anti-obesity drug.	3.61	2	0	beta-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
quinine [no description available]	3.61	2	0	cinchona alkaloid	antimalarial; muscle relaxant; non-narcotic analgesic
e 7010 E 7010: inhibits tubulin polymerization; structure given in first source	2.25	1	0	sulfonamide
sf 2370 SF 2370: indolocarbazole isolated from Actinomadura sp. SF-2370; structure given in first source. K-252a : A organic heterooctacyclic compound that is a potent inhibitor of protein kinase C and is isolated from Nocardiopsis sp K-252a	2.15	1	0	bridged compound; gamma-lactam; methyl ester; organic heterooctacyclic compound	antimicrobial agent; bacterial metabolite; EC 2.7.11.13 (protein kinase C) inhibitor; tropomyosin-related kinase B receptor antagonist
cystine [no description available]	2.25	1	0
fospropofol [no description available]	3.23	1	0	alkylbenzene
tandutinib [no description available]	2.15	1	0	aromatic ether; N-arylpiperazine; N-carbamoylpiperazine; phenylureas; piperidines; quinazolines; tertiary amino compound	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
freedom Freedom: The rights of individuals to act and make decisions without external constraints.	2.6	1	0
azilect [no description available]	2.08	1	0
rasagiline [no description available]	3.23	1	0	indanes; secondary amine; terminal acetylenic compound	EC 1.4.3.4 (monoamine oxidase) inhibitor; neuroprotective agent
dasatinib N-(2-chloro-6-methylphenyl)-2-((6-(4-(2-hydroxyethyl)piperazin-1-yl)-2-methylpyrimidin-4-yl)amino)-1,3-thiazole-5-carboxamide: a dasatinib prodrug; structure in first source. dasatinib (anhydrous) : An aminopyrimidine that is 2-methylpyrimidine which is substituted at position 4 by the primary amino group of 2-amino-1,3-thiazole-5-carboxylic acid and at position 6 by a 4-(2-hydroxyethyl)piperazin-1-yl group, and in which the carboxylic acid group has been formally condensed with 2-chloro-6-methylaniline to afford the corresponding amide. A multi-targeted kinase inhibitor, it is used, particularly as the monohydrate, for the treatment of chronic, accelerated, or myeloid or lymphoid blast phase chronic myeloid leukemia. Note that the name 'dasatinib' is used to refer to the monohydrate (USAN) as well as to anhydrous dasatinib (INN).	8.1	20	0	1,3-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
ha 1100 HA 1100: intracellular calcium antagonist	2.15	1	0
7-epi-hydroxystaurosporine [no description available]	2.15	1	0
zd 6474 CH 331: structure in first source	8.04	9	3	aromatic ether; organobromine compound; organofluorine compound; piperidines; quinazolines; secondary amine	antineoplastic agent; tyrosine kinase inhibitor
ML162 ML162 : A monochlorobenzene that is benzene substituted by (chloroacetyl){2-oxo-2-[(2-phenylethyl)amino]-1-(thiophen-2-yl)ethyl}amino, chloro and methoxy groups at positions 1, 3 and 4, respectively. It is a covalent inhibitor of glutathione peroxidase 4 (GPX4) that induces ferroptosis in cells.	2.25	1	0	monochlorobenzenes; monomethoxybenzene; organochlorine compound; secondary carboxamide; tertiary carboxamide; thiophenes	EC 1.11.1.9 (glutathione peroxidase) inhibitor; ferroptosis inducer
naphthoquinones Naphthoquinones: Naphthalene rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups.	2.52	2	0
sitagliptin sitagliptin : A triazolopyrazine that exhibits hypoglycemic activity.	3.61	2	0	triazolopyrazine; trifluorobenzene	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; environmental contaminant; hypoglycemic agent; serine proteinase inhibitor; xenobiotic
rhodamine 123 Rhodamine 123: A fluorescent probe with low toxicity which is a potent substrate for ATP BINDING CASSETTE TRANSPORTER, SUBFAMILY B, MEMBER 1 and the bacterial multidrug efflux transporter. It is used to assess mitochondrial bioenergetics in living cells and to measure the efflux activity of ATP BINDING CASSETTE TRANSPORTER, SUBFAMILY B, MEMBER 1 in both normal and malignant cells. (Leukemia 1997;11(7):1124-30). rhodamine 123(1+) : A cationic fluorescent dye derived from 9-phenylxanthene.	2.21	1	0	organic cation; xanthene dye	fluorochrome
tolcapone Tolcapone: A benzophenone and nitrophenol compound that acts as an inhibitor of CATECHOL O-METHYLTRANSFERASE, an enzyme involved in the metabolism of DOPAMINE and LEVODOPA. It is used in the treatment of PARKINSON DISEASE in patients for whom levodopa is ineffective or contraindicated.. tolcapone : Benzophenone substituted on one of the phenyl rings at C-3 and C-4 by hydroxy groups and at C-5 by a nitro group, and on the other phenyl ring by a methyl group at C-4. It is an inhibitor of catechol O-methyltransferase.	3.61	2	0	2-nitrophenols; benzophenones; catechols	antiparkinson drug; EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
alsterpaullone alsterpaullone: structure in first source. alsterpaullone : An organic heterotetracyclic compound that is 1,3-dihydro-2H-1-benzazepin-2-one which shares its 4-5 bond with the 3-2 bond of 5-nitro-1H-indole.	3.92	2	0	C-nitro compound; caprolactams; organic heterotetracyclic compound	anti-HIV-1 agent; antineoplastic agent; apoptosis inducer; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor; EC 2.7.11.26 (tau-protein kinase) inhibitor
imd 0354 N-(3,5-bis(trifluoromethyl)phenyl)-5-chloro-2-hydroxybenzamide: a cardioprotective agent that inhibits IkappaB kinase beta (IKKbeta); structure in first source	2.15	1	0	benzamides
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.	7.43	15	1	sphing-4-enine	human metabolite; mouse metabolite
quercetin [no description available]	7.52	2	0	7-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
calcitriol dihydroxy-vitamin D3: as a major in vitro metabolite of 1alpha,25-dihydroxyvitamin D3, produced in primary cultures of neonatal human keratinocytes	3.87	3	0	D3 vitamins; hydroxycalciol; triol	antineoplastic agent; antipsoriatic; bone density conservation agent; calcium channel agonist; calcium channel modulator; hormone; human metabolite; immunomodulator; metabolite; mouse metabolite; nutraceutical
alprostadil [no description available]	2.08	1	0	prostaglandins E	anticoagulant; 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.	6.24	3	1	hydroxy seco-steroid; seco-ergostane; vitamin D	bone density conservation agent; nutraceutical; plant metabolite; rodenticide
genistein [no description available]	2.41	1	0	7-hydroxyisoflavones	antineoplastic 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.	4.06	3	0	antibiotic antifungal drug; macrolide antibiotic; polyene antibiotic	antiamoebic agent; antiprotozoal drug; bacterial metabolite
pulmicort Budesonide: A glucocorticoid used in the management of ASTHMA, the treatment of various skin disorders, and allergic RHINITIS.. budesonide : A glucocorticoid steroid having a highly oxygenated pregna-1,4-diene structure. It is used mainly in the treatment of asthma and non-infectious rhinitis and for treatment and prevention of nasal polyposis.	3.61	2	0	11beta-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.	3.61	2	0
eprosartan eprosartan: angiotensin II receptor antagonist. eprosartan : A member of the class of imidazoles and thiophenes that is an angiotensin II receptor antagonist used for the treatment of high blood pressure.	3.61	2	0	dicarboxylic acid; imidazoles; thiophenes	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
montelukast montelukast: a leukotriene D4 receptor antagonist	3.23	1	0	aliphatic 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.	3.23	1	0	isoquinolines
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.	2.08	1	0	maleate salt	anti-allergic agent
dexchlorpheniramine maleate [no description available]	2.08	1	0	organic molecular entity
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.	3.23	1	0
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.	3.61	2	0	carboxylic ester; ether; gamma-lactone; phenols; tertiary amino compound	anticoronaviral agent; EC 1.1.1.205 (IMP dehydrogenase) inhibitor; immunosuppressive agent; prodrug
entacapone entacapone: structure given in first source. entacapone : A monocarboxylic acid amide that is N,N-diethylprop-2-enamide in which the hydrogen at position 2 is substituted by a cyano group and the hydrogen at the 3E position is substituted by a 3,4-dihydroxy-5-nitrophenyl group.	3.61	2	0	2-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]	3.23	1	0	hydroxy seco-steroid; seco-cholestane	antiparathyroid drug
maytansine Maytansine: An ansa macrolide isolated from the MAYTENUS genus of East African shrubs.. maytansine : An organic heterotetracyclic compound and 19-membered macrocyclic lactam antibiotic originally isolated from the Ethiopian shrub Maytenus serrata but also found in other Maytenus species. It exhibits cytotoxicity against many tumour cell lines.	5.57	5	0	alpha-amino acid ester; carbamate ester; epoxide; maytansinoid; organic heterotetracyclic compound; organochlorine compound	antimicrobial agent; antimitotic; antineoplastic agent; plant metabolite; tubulin modulator
rottlerin rottlerin: an angiogenesis inhibitor; an inhibitor of protein kinase Cdelta (PKCdelta) and calmodulin kinase III; RN refers to (E)-isomer; do not confuse this chalcone with an anthraquinone that is also called rottlerin (RN 481-72-1);. rottlerin : A chromenol that is 2,2-dimethyl-2H-chromene substituted by hydroxy groups at positions 5 and 7, a 3-acetyl-2,4,6-trihydroxy-5-methylbenzyl group at position 6 and a (1E)-3-oxo-1-phenylprop-1-en-3-yl group at position 8. A potassium channel opener, it is isolated from Mallotus philippensis.	2.41	1	0	aromatic ketone; benzenetriol; chromenol; enone; methyl ketone	anti-allergic agent; antihypertensive agent; antineoplastic agent; apoptosis inducer; K-ATP channel agonist; metabolite
l 660,711 [no description available]	2.08	1	0	quinolines
l 683590 immunomycin: from Streptomyces hygroscopicus; structure given in first source	2.46	2	0	ether; lactol; macrolide; secondary alcohol	antifungal agent; bacterial metabolite; immunosuppressive agent
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.	2.08	1	0	(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.	2.51	2	0	amidobenzoic 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.	3.23	1	0	cephalosporin; dicarboxylic acid	antibacterial drug
imipenem [no description available]	2.08	1	0	carbapenems
etretinate retinoid : Oxygenated derivatives of 3,7-dimethyl-1-(2,6,6-trimethylcyclohex-1-enyl)nona-1,3,5,7-tetraene and derivatives thereof.	2.08	1	0	enoate 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.	3.61	2	0	retinoic acid	antineoplastic agent; keratolytic drug; teratogenic agent
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.	2.08	1	0	organoammonium salt	anti-asthmatic drug; H1-receptor antagonist
epoprostenol [no description available]	3.23	1	0	prostaglandins I	mouse metabolite
indocyanine green [no description available]	3.23	1	0	1,1-diunsubstituted alkanesulfonate; benzoindole; cyanine dye
dinoprost tromethamine [no description available]	2.08	1	0	organic molecular entity
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.	3.23	1	0	N-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.	3.23	1	0	cyclopropanes; dihydroxy monocarboxylic acid; monofluorobenzenes; quinolines; statin (synthetic)	antioxidant
rosuvastatin calcium S 4522: structure in first source	2.08	1	0	N-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.	2.08	1	0	allylamine antifungal drug; hydrochloride	EC 1.14.13.132 (squalene monooxygenase) inhibitor; P450 inhibitor
ethamolin monoethanolamine oleate: used for treatment of pyogenic granuloma	3.23	1	0	long-chain fatty acid
alatrofloxacin mesylate [no description available]	3.23	1	0
codeine [no description available]	3.23	1	0	morphinane 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	4.4	3	0	homodetic cyclic peptide	anti-asthmatic drug; anticoronaviral agent; antifungal agent; antirheumatic drug; carcinogenic agent; dermatologic drug; EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor; geroprotector; immunosuppressive agent; metabolite
natamycin [no description available]	2.08	1	0	antibiotic antifungal drug; dicarboxylic acid monoester; epoxide; macrolide antibiotic; monosaccharide derivative; polyene antibiotic	antifungal agrochemical; antimicrobial food preservative; apoptosis inducer; bacterial metabolite; ophthalmology drug
acitretin Acitretin: An oral retinoid effective in the treatment of psoriasis. It is the major metabolite of ETRETINATE with the advantage of a much shorter half-life when compared with etretinate.. acitretin : A retinoid that consists of 3,7-dimethylnona-2,4,6,8-tetraenoic acid having a 4-methoxy-2,3,6-trimethylphenyl group attached at position 9.	3.61	2	0	acitretin; alpha,beta-unsaturated monocarboxylic acid; retinoid	keratolytic drug
estropipate estropipate: used therapeutically in menopausal patients	3.23	1	0	piperazinium 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.	3.23	1	0	morphinane 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.	5.22	5	0	pyrrolidin-2-ones	anticonvulsant; 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.	3.23	1	0	carbacephem; zwitterion	antibacterial drug; antimicrobial agent
nabilone nabilone: cannabinol deriv; RN given refers to cpd without isomeric designation; structure	3.23	1	0
nalmefene nalmefene: RN given refers to 5-alpha isomer	2.08	1	0	morphinane alkaloid
naloxone Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.. naloxone : A synthetic morphinane alkaloid that is morphinone in which the enone double bond has been reduced to a single bond, the hydrogen at position 14 has been replaced by a hydroxy group, and the methyl group attached to the nitrogen has been replaced by an allyl group. A specific opioid antagonist, it is used (commonly as its hydrochloride salt) to reverse the effects of opioids, both following their use of opioids during surgery and in cases of known or suspected opioid overdose.	3.61	2	0	morphinane 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.	3.23	1	0	organic 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)	3.23	1	0	morphinane 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.	3.23	1	0	phylloquinones; 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.	31.15	3,267	875	antibiotic 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.	5.04	4	0	cyclic 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.	3.23	1	0
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.	2.63	2	0	dihydroxyflavone; hydroxypiperidine; monochlorobenzenes; tertiary amino compound	antineoplastic agent; antirheumatic drug; apoptosis inducer; EC 2.7.11.22 (cyclin-dependent kinase) 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.	3.23	1	0	morphinane 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]	2.08	1	0
acipimox acipimox: lipolysis inhibitor	2.08	1	0	pyrazinecarboxylic acid
atosiban [no description available]	2.08	1	0	oligopeptide
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.	3.23	1	0	amphetamines; 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.	2.08	1	0	monocarboxylic acid amide	antiglaucoma drug; antihypertensive agent
clobetasol Clobetasol: A derivative of PREDNISOLONE with high glucocorticoid activity and low mineralocorticoid activity. Absorbed through the skin faster than FLUOCINONIDE, it is used topically in treatment of PSORIASIS but may cause marked adrenocortical suppression.. clobetasol : A 3-oxo-Delta(1),Delta(4)-steroid that is 16beta-methylpregna-1,4-diene-3,20-dione bearing hydroxy groups at the 11beta and 17alpha positions, fluorine at position 9, and a chlorine substituent at position 21. It is used as its 17alpha-propionate ester to treat various skin disorders, including exzema and psoriasis.	7.81	3	0	11beta-hydroxy steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 3-oxo-Delta(1),Delta(4)-steroid; chlorinated steroid; fluorinated steroid; glucocorticoid; tertiary alpha-hydroxy ketone	anti-inflammatory drug; SMO receptor agonist
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.	3.23	1	0	heterodetic cyclic peptide	diagnostic agent; renal agent; vasopressin receptor agonist
dexmedetomidine [no description available]	3.23	1	0	medetomidine	alpha-adrenergic agonist; analgesic; non-narcotic analgesic; sedative
goserelin Goserelin: A synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE. Goserelin is used in treatments of malignant NEOPLASMS of the prostate, uterine fibromas, and metastatic breast cancer.	3.64	2	0	organic molecular entity
lacidipine [no description available]	2.21	1	0	cinnamate ester; tert-butyl ester
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.	2.08	1	0	isopropyl ester; prostaglandins Falpha; triol	antiglaucoma drug; antihypertensive agent; EC 4.2.1.1 (carbonic anhydrase) inhibitor; prodrug
lysophosphatidylcholines lysophosphatidylcholine : An acylglycerophosphocholine resulting from partial hydrolysis of a phosphatidylcholine, which removes one of the fatty acyl groups. The structure is depicted in the image where R1 = acyl, R2 = H or where R1 = H, R2 = acyl.	7.15	1	0	1-O-acyl-sn-glycero-3-phosphocholine
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.	3.23	1	0	organic heteropentacyclic compound	mu-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.	3.61	2	0	phenylalanine derivative
vinorelbine [no description available]	3.23	1	0	acetate ester; methyl ester; organic heteropentacyclic compound; organic heterotetracyclic compound; ring assembly; vinca alkaloid	antineoplastic agent; photosensitizing agent
3-[6-[4-(trifluoromethoxy)anilino]-4-pyrimidinyl]benzamide [no description available]	2.41	1	0	pyrimidines
silodosin silodosin: an alpha(1a)-adrenoceptor-selective antagonist; structure given in first source	3.59	2	0	indolecarboxamide
licochalcone a licochalcone A: has both anti-inflammatory and antineoplastic activities; structure given in first source; isolated from root of Glycyrrhiza inflata; RN given refers to (E)-isomer	2.25	1	0	chalcones
fluvoxamine Fluvoxamine: A selective serotonin reuptake inhibitor that is used in the treatment of DEPRESSION and a variety of ANXIETY DISORDERS.. fluvoxamine : An oxime O-ether that is benzene substituted by a (1E)-N-(2-aminoethoxy)-5-methoxypentanimidoyl group at position 1 and a trifluoromethyl group at position 4. It is a selective serotonin reuptake inhibitor that is used for the treatment of obsessive-compulsive disorder.	3.23	1	0	(trifluoromethyl)benzenes; 5-methoxyvalerophenone O-(2-aminoethyl)oxime	antidepressant; anxiolytic drug; serotonin uptake inhibitor
bosutinib 4-((2,4-dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methyl-1-piperazinyl)propoxy)-3-quinolinecarbonitrile: a Src kinase inhibitor; structure in first source	2.63	2	0	aminoquinoline; aromatic ether; dichlorobenzene; N-methylpiperazine; nitrile; tertiary amino compound	antineoplastic agent; tyrosine kinase inhibitor
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.	2.15	1	0
su 11248 [no description available]	20.28	253	29	monocarboxylic 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]	10.9	27	2	aminopyridine; aromatic ketone; cyclopentanes; piperidines; pyridopyrimidine; secondary amino compound; tertiary amino compound	antineoplastic agent; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
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.	2.08	1	0	nitrile; 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.	3.61	2	0	dihydroxy monocarboxylic acid; indoles; organofluorine compound
molsidomine [no description available]	2.08	1	0	ethyl ester; morpholines; oxadiazole; zwitterion	antioxidant; apoptosis inhibitor; cardioprotective agent; nitric oxide donor; vasodilator agent
levorphanol Levorphanol: A narcotic analgesic that may be habit-forming. It is nearly as effective orally as by injection.	3.23	1	0	morphinane alkaloid
arsenic Arsenic: A shiny gray element with atomic symbol As, atomic number 33, and atomic weight 75. It occurs throughout the universe, mostly in the form of metallic arsenides. Most forms are toxic. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), arsenic and certain arsenic compounds have been listed as known carcinogens. (From Merck Index, 11th ed)	2.51	2	0	metalloid atom; pnictogen	micronutrient
naltrexone Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.. naltrexone : An organic heteropentacyclic compound that is naloxone substituted in which the allyl group attached to the nitrogen is replaced by a cyclopropylmethyl group. A mu-opioid receptor antagonist, it is used to treat alcohol dependence.	3.23	1	0	cyclopropanes; morphinane-like compound; organic heteropentacyclic compound	antidote to opioid poisoning; central nervous system depressant; environmental contaminant; mu-opioid receptor antagonist; xenobiotic
dextromethorphan Dextromethorphan: Methyl analog of DEXTRORPHAN that shows high affinity binding to several regions of the brain, including the medullary cough center. This compound is an NMDA receptor antagonist (RECEPTORS, N-METHYL-D-ASPARTATE) and acts as a non-competitive channel blocker. It is one of the widely used ANTITUSSIVES, and is also used to study the involvement of glutamate receptors in neurotoxicity.. dextromethorphan : A 6-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthrene in which the sterocenters at positions 4a, 10 and 10a have S-configuration. It is a prodrug of dextrorphan and used as an antitussive drug for suppressing cough.	3.23	1	0	6-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthrene	antitussive; 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.	3.61	2	0	morphinane alkaloid	antitussive; kappa-opioid receptor agonist; mu-opioid receptor agonist; opioid analgesic
cefixime [no description available]	3.61	2	0	cephalosporin	antibacterial 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.	3.89	3	0	dipeptide	EC 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.	3.23	1	0	benzazepine; 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.	3.87	3	0	azabicycloalkane; 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.	3.23	1	0
indinavir sulfate Indinavir: A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.	3.61	2	0	dicarboxylic acid diamide; N-(2-hydroxyethyl)piperazine; piperazinecarboxamide	HIV protease inhibitor
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)	3.23	1	0	styrenes
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.	2.08	1	0	maleate salt	antihypertensive 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).	3.23	1	0	dicarboxylic acid monoester; dipeptide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; geroprotector; prodrug
trientine hydrochloride [no description available]	3.23	1	0
n-methylscopolamine bromide scopolamine methobromide : A quaternary ammonium salt resulting from the reaction of the amino group of scopolamine with methyl bromide.	3.23	1	0
bleomycin [no description available]	3.23	1	0	bleomycin	antineoplastic agent; metabolite
phosphorus Phosphorus: A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.	2.17	1	0	monoatomic phosphorus; nonmetal atom; pnictogen	macronutrient
enalaprilat anhydrous Enalaprilat: The active metabolite of ENALAPRIL and one of the potent, intravenously administered, ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. It is an effective agent for the treatment of essential hypertension and has beneficial hemodynamic effects in heart failure. The drug produces renal vasodilation with an increase in sodium excretion.. enalaprilat dihydrate : The dihydrate form of enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor that is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is administered by intravenous injection.. enalaprilat (anhydrous) : Enalapril in which the ethyl ester group has been hydrolysed to the corresponding carboxylic acid. Enalaprilat is an angiotensin-converting enzyme (ACE) inhibitor and is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is given by intravenous injection, usually as the dihydrate.	3.61	2	0	dicarboxylic acid; dipeptide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) 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.	3.23	1	0	amidoxime; 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]	3.23	1	0	3-(carbamoyloxymethyl)cephalosporin; furans; oxime O-ether	drug allergen
ceftriaxone [no description available]	3.23	1	0	1,2,4-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.	3.23	1	0	cephalosporin; oxime O-ether	antibacterial drug
pafuramidine pafuramidine: a prodrug of furamidine	3.23	1	0
ceftazidime [no description available]	3.23	1	0	cephalosporin; 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.	3.61	2	0	dicarboxylic acid monoester; dipeptide; ethyl ester; organic heterobicyclic compound; secondary amino compound; tertiary carboxamide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; prodrug
pregabalin Pregabalin: A gamma-aminobutyric acid (GABA) derivative that functions as a CALCIUM CHANNEL BLOCKER and is used as an ANTICONVULSANT as well as an ANTI-ANXIETY AGENT. It is also used as an ANALGESIC in the treatment of NEUROPATHIC PAIN and FIBROMYALGIA.. pregabalin : A gamma-amino acid that is gamma-aminobutyric acid (GABA) carrying an isobutyl substitutent at the beta-position (the S-enantiomer). Binds with high affinity to the alpha2-delta site (an auxiliary subunit of voltage-gated calcium channels) in central nervous system tissues.	4.45	3	0	gamma-amino acid	anticonvulsant; calcium channel blocker
alvimopan anhydrous alvimopan: mu opioid receptor antagonist; intended to treat constipation in patients taking opiates for pain	3.61	2	0	peptide
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.	3.23	1	0	monocarboxylic acid amide; monomethoxybenzene	antihypertensive agent
vx680 [no description available]	2.15	1	0	N-arylpiperazine
famotidine [no description available]	3.61	2	0	1,3-thiazoles; guanidines; sulfonamide	anti-ulcer drug; H2-receptor antagonist; P450 inhibitor
cefotaxime Cefotaxime: Semisynthetic broad-spectrum cephalosporin.. cefotaxime : A cephalosporin compound having acetoxymethyl and [2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups.	3.23	1	0	1,3-thiazoles; cephalosporin; oxime O-ether	antibacterial drug; drug allergen
aztreonam [no description available]	3.23	1	0	beta-lactam antibiotic allergen; monobactam	antibacterial drug; drug allergen; EC 2.4.1.129 (peptidoglycan glycosyltransferase) inhibitor
viroxime [no description available]	2.41	1	0
cci 15641 [no description available]	2.08	1	0	cephalosporin
22,23-dihydroavermectin b(1)a 22,23-dihydroavermectin B(1)a: C48H74O14; major component of IVERMECTIN; MW 875.093; structure given in first source. 22,23-dihydroavermectin B1a : A macrocyclic lactone that is avermectin B1a in which the double bond present in the spirocyclic ring system has been reduced to a single bond. It is the major component of ivermectin.	3.51	1	0	macrocyclic lactone; spiroketal
cefpodoxime [no description available]	3.23	1	0	carboxylic 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.	3.23	1	0	azabicycloalkane; delta-lactam; organic heterotricyclic compound	antiemetic; serotonergic antagonist
(3S,5S,6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid Fluvastatin: An indole-heptanoic acid derivative that inhibits HMG COA REDUCTASE and is used to treat HYPERCHOLESTEROLEMIA. In contrast to other statins, it does not appear to interact with other drugs that inhibit CYP3A4.. (3S,5S,6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid : A (6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid diastereoisomer in which both chiral centres have S configuration.. fluvastatin : A racemate comprising equimolar amounts of (3R,5S)- and (3S,5R)-fluvastatin. An HMG-CoA reductase inhibitor, it is used (often as the corresponding sodium salt) to reduce triglycerides and LDL-cholesterol, and increase HDL-chloesterol, in the treatment of hyperlipidaemia.	5.46	5	1	(6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid
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.	2.08	1	0	fumarate salt	antiviral drug; HIV-1 reverse transcriptase inhibitor; prodrug
cyc 116 4-methyl-5-(2-(4-morpholinophenylamino)pyrimidin-4-yl)thiazol-2-amine: an aurora kinase inhibitor; structure in first source	2.15	1	0
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.	2.08	1	0	brompheniramine maleate	anti-allergic agent; H1-receptor antagonist
rifaximin [no description available]	3.61	2	0	acetate ester; cyclic ketal; lactam; macrocycle; organic heterohexacyclic compound; rifamycins; semisynthetic derivative	antimicrobial agent; gastrointestinal drug; orphan drug
mycophenolic acid glucuronide [no description available]	3.46	1	1
ixabepilone [no description available]	4.37	3	0	1,3-thiazoles; beta-hydroxy ketone; epoxide; lactam; macrocycle	antineoplastic agent; microtubule-destabilising agent
ekb 569 EKB 569: an EGF receptor kinase inhibitor	2.15	1	0	aminoquinoline; monocarboxylic acid amide; monochlorobenzenes; nitrile	protein kinase inhibitor
axitinib [no description available]	14.24	58	4	aryl sulfide; benzamides; indazoles; pyridines	antineoplastic agent; tyrosine kinase inhibitor; vascular endothelial growth factor receptor antagonist
cgp-56697 Artemether, Lumefantrine Drug Combination: Drug combination of artemether and lumefantrine that is used to treat PLASMODIUM FALCIPARUM MALARIA.	2.05	1	0
glucuronyl glucosamine glycan sulfate [no description available]	2.11	1	0
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.	2.08	1	0	carboxylic acid; carboxylic ester; cephalosporin	antibacterial drug; prodrug
ceftizoxime [no description available]	3.23	1	0	cephalosporin	antibacterial drug
1-methyl-d-lysergic acid butanolamide [no description available]	3.23	1	0	ergot alkaloid; monocarboxylic acid amide	serotonergic antagonist; sympatholytic agent; vasoconstrictor agent
beta-escin [no description available]	2.15	1	0
fluphenazine [no description available]	2.08	1	0
nitrofurantoin Nitrofurantoin: A urinary anti-infective agent effective against most gram-positive and gram-negative organisms. Although sulfonamides and antibiotics are usually the agents of choice for urinary tract infections, nitrofurantoin is widely used for prophylaxis and long-term suppression.. nitrofurantoin : An imidazolidine-2,4-dione that is hydantoin substituted at position 1 by a [(5-nitro-2-furyl)methylene]amino group. An antibiotic that damages bacterial DNA.	3.61	2	0	imidazolidine-2,4-dione; nitrofuran antibiotic; organonitrogen heterocyclic antibiotic; organooxygen heterocyclic antibiotic	antibacterial drug; antiinfective agent; hepatotoxic agent
sb 334867-a 1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea: selective OX1 receptor antagonist	2.1	1	0	naphthyridine derivative
6 beta-hydroxycortisol 6 beta-hydroxycortisol: RN given refers to the (6beta,11beta)-isomer; see also record for 6 alpha-hydrocortisol. 6beta-hydroxycortisol : A C21-steroid that is cortisol bearing an additional hydroxy substituent at the 6beta-position. In humans, it is produced as a metabolite of cortisol by cytochrome p450-3A4 (CYP3A4, an important enzyme involved in the metabolism of a variety of exogenous and endogenous compounds) and can be used to detect moderate and potent CYP3A4 inhibition in vivo.	3.39	1	1	11beta-hydroxy steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(4) steroid; 6beta-hydroxy steroid; C21-steroid; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone	human metabolite; mammalian metabolite; probe
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.	2.49	2	0	diamine; ergoline alkaloid; indole alkaloid fundamental parent; indole alkaloid; organic heterotetracyclic compound
dantrolene [no description available]	3.23	1	0
roxithromycin (E)-roxithromycin : A major geometrical isomer of roxithromycin.	2.08	1	0	roxithromycin	environmental contaminant; xenobiotic
cefdinir [no description available]	3.61	2	0	cephalosporin; ketoxime	antibacterial drug
etonogestrel [no description available]	3.23	1	0	17beta-hydroxy steroid; 3-oxo-Delta(4) steroid; terminal acetylenic compound	contraceptive drug; female contraceptive drug; progestin
bisoprolol, fumarate (1:1) salt [no description available]	2.08	1	0
artesunate artesunic acid: RN given for (3R-(3alpha,5abeta,6beta,8abeta,9alpha,10alpha,12beta,(2aR*))-isomer; succinic ester of artemether	2.08	1	0	artemisinin derivative; cyclic acetal; dicarboxylic acid monoester; hemisuccinate; semisynthetic derivative; sesquiterpenoid	antimalarial; antineoplastic agent; ferroptosis inducer
etoposide phosphate [no description available]	2.08	1	0	furonaphthodioxole
ciclesonide ciclesonide: nasal spray approved for seasonal and perennial allergic rhinitis	2.08	1	0	organic molecular entity
perfosfamide [no description available]	2.15	1	0
temsirolimus [no description available]	5.16	5	0	macrolide 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.	3.61	2	0	(trifluoromethyl)benzenes; aza-steroid; delta-lactam	antihyperplasia drug; EC 1.3.1.22 [3-oxo-5alpha-steroid 4-dehydrogenase (NADP(+))] inhibitor
tekturna [no description available]	2.08	1	0	fumarate salt	antihypertensive agent
pd 184352 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide: inhibits MAP kinase kinase; structure in first source	2.61	2	0	aminobenzoic acid
voclosporin voclosporin: semi-synthetic cyclosporine A analog & calcineurin inhibitor; FDA approved use to treat lupus nephritis.	3.15	1	0	homodetic cyclic peptide
lu 208075 ambrisentan: an ET(A) receptor antagonist and antihypertensive agent; studied for use in pulmonary arterial hypertension	3.23	1	0	diarylmethane
bibx 1382bs BIBX 1382BS: an ErbB receptor kinase inhibitor; no further information available 4/2001	3.71	2	0	substituted aniline
vildagliptin [no description available]	2.08	1	0	amino acid amide
fesoterodine fesoterodine: a muscarinic antagonist for treatment of overactive bladder	3.59	2	0	diarylmethane
belinostat [no description available]	2.21	1	0	hydroxamic acid; olefinic compound; sulfonamide	antineoplastic agent; EC 3.5.1.98 (histone deacetylase) inhibitor
on 01910 ON 01910: a Plk1 inhibitor with antineoplastic activity; structure in first source. N-[2-methoxy-5-({[2-(2,4,6-trimethoxyphenyl)ethenyl]sulfonyl}methyl)phenyl]glycine : A glycine derivative that is glycine in which one of the hydrogens of the amino group is substituted by a 2-methoxy-5-({[2-(2,4,6-trimethoxyphenyl)ethenyl]sulfonyl}methyl)phenyl group.. rigosertib : An N-[2-methoxy-5-({[2-(2,4,6-trimethoxyphenyl)ethenyl]sulfonyl}methyl)phenyl]glycine in which the double bond has E-configuration. It is a non-ATP-competitive inhibitor of PLK1 with an IC50 of 9 nM and exhibits anti-cancer properties.	2.15	1	0	N-[2-methoxy-5-({[2-(2,4,6-trimethoxyphenyl)ethenyl]sulfonyl}methyl)phenyl]glycine	antineoplastic agent; apoptosis inducer; EC 2.7.11.21 (polo kinase) inhibitor; microtubule-destabilising agent
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.	7.2	9	4	cinnamamides; hydroxamic acid; methylindole; secondary amino compound	angiogenesis modulating agent; antineoplastic agent; EC 3.5.1.98 (histone deacetylase) inhibitor
staurosporine staurosporinium : Conjugate acid of staurosporine.	3.13	1	0	ammonium ion derivative
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.	7.15	1	0	penicillanic acids
phosphocreatine Phosphocreatine: An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996). phosphagen : Any of a group of guanidine or amidine phosphates that function as storage depots for high-energy phosphate in muscle with the purpose of regenerating ATP from ADP during muscular contraction.. N-phosphocreatine : A phosphoamino acid consisting of creatine having a phospho group attached at the primary nitrogen of the guanidino group.	2.41	2	0	phosphagen; phosphoamino acid	human metabolite; mouse metabolite
taxane taxane: produced by Taxomyces andreanae	7.11	1	0	diterpene; terpenoid fundamental parent
sgd 301-76 [no description available]	2.08	1	0	conazole antifungal drug; imidazole antifungal drug; organic nitrate salt	antiinfective agent
fluvoxamine maleate [no description available]	2.08	1	0	(trifluoromethyl)benzenes
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.	2.08	1	0
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.	3.23	1	0	1,8-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.	3.61	2	0	benzimidazoles; sulfoxide
gemifloxacin mesylate gemifloxacin mesylate : The mesylate salt of gemifloxacin.	2.08	1	0	methanesulfonate salt	antimicrobial agent; topoisomerase IV inhibitor
fosinopril [no description available]	3.23	1	0
vacuolin-1 vacuolin-1: inhibits Ca2-dependent lysosomal exocytosis	2.41	1	0
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.	3.23	1	0	2-[(diphenylmethyl)sulfinyl]acetamide	central nervous system stimulant; eugeroic
av 412 [no description available]	2.15	1	0
telatinib [no description available]	2.15	1	0
y-39983 Y-39983: SNJ-1656 is an ophthalmic solution of Y-39983; ROCK (rho kinase) inhibitor, promotes regeneration of crushed axons of retinal ganglion cells; structure in first source	2.15	1	0	pyrrolopyridine
cp 547632 3-(4-bromo-2,6-difluorobenzyloxy)-5-(3-(4-pyrrolidin-1-ylbutyl)ureido)isothiazole-4-carboxylic acid amide: inhibits vascular endothelial growth factor receptor-2 tyrosine kinase; structure in first source	2.15	1	0
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.	15.46	48	15	aromatic 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).	3.07	4	0	difluorobenzene; 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
midostaurin midostaurin : An organic heterooctacyclic compound that is the N-benzoyl derivative of staurosporine.	3.9	3	0	benzamides; gamma-lactam; indolocarbazole; organic heterooctacyclic compound	antineoplastic agent; EC 2.7.11.13 (protein kinase C) 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.	3.23	1	0	oligopeptide
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.	3.59	2	0	alkylbenzene
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.	2.15	1	0	acetate ester; delta-lactone; organic heterotetracyclic compound; tertiary amino compound	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
upamostat [no description available]	3.47	1	1
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.	3.23	1	0	organic molecular entity
novolimus novolimus: belongs to the family of macrocyclic lactones with immunosuppressive and anti-proliferative properties	3.43	6	0
ripasudil [no description available]	2.59	2	0	isoquinolines
mocetinostat mocetinostat: undergoing phase II clinical trials for treatment of cancer. mocetinostat : A benzamide obtained by formal condensation of the carboxy group of 4-({[4-(pyridin-3-yl)pyrimidin-2-yl]amino}methyl)benzoic acid with one of the amino groups of benzene-1,2-diamine. It is an orally active and isotype-selective HDAC inhibitor which exhibits antitumour activity (IC50 = 0.15, 0.29, 1.66 and 0.59 muM for HDAC1, HDAC2, HDAC3 and HDAC11).	2.13	1	0	aminopyrimidine; benzamides; pyridines; secondary amino compound; secondary carboxamide; substituted aniline	antineoplastic agent; apoptosis inducer; autophagy inducer; cardioprotective agent; EC 3.5.1.98 (histone deacetylase) inhibitor; hepatotoxic agent
osi 930 OSI 930: inhibits both receptor tyrosine kinase Kit and kinase insert domain receptor; structure in first source	2.15	1	0	aromatic amide
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.	3.23	1	0	carboxylic acid; cephalosporin	antibacterial drug
scio-469 SCIO-469: a small-molecule p38 mitogen-activated protein (MAP) kinase inhibitor for potential oral therapy for inflammatory disorders; in phase lib clinical trials for rheumatoid arthritis 4/2004. talmapimod : An indolecarboxamide obtained by formal condensation of the carboxy group of 6-chloro-3-[(dimethylamino)(oxo)acetyl]-1-methylindole-5-carboxylic acid with the secondary amino group of (2S,5R)-1-[(4-fluorophenyl)methyl]-2,5-dimethylpiperazine. It is a potent inhibitor of MAPK and exhibits anti-cancer properties.	2.15	1	0	aromatic amide; aromatic ketone; chloroindole; dicarboxylic acid diamide; indolecarboxamide; monofluorobenzenes; N-acylpiperazine; N-alkylpiperazine	antineoplastic agent; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
ticagrelor Ticagrelor: An adenosine triphosphate analogue and reversible P2Y12 PURINORECEPTOR antagonist that inhibits ADP-mediated PLATELET AGGREGATION. It is used for the prevention of THROMBOEMBOLISM by patients with ACUTE CORONARY SYNDROME or a history of MYOCARDIAL INFARCTION.. ticagrelor : A triazolopyrimidine that is an adenosine isostere; the cyclopentane ring is similar to ribose and the nitrogen-rich [1,2,3]triazolo[4,5-d]pyrimidine moiety resembles the nucleobase adenine. A platelet aggregation inhibitor which is used for prevention of thromboembolic events in patients with acute coronary syndrome.	4.28	2	1	aryl sulfide; hydroxyether; organofluorine compound; secondary amino compound; triazolopyrimidines	P2Y12 receptor antagonist; platelet aggregation inhibitor
cp 724714 2-methoxy-N-(3-(4-((3-methyl-4-((6-methyl-3-pyridinyl)oxy)phenyl)amino)-6-quinazolinyl)-2-propenyl)acetamide: CP-724714 is the ((2E)-isomer, 1:1.5 succinate); structure in first source	2.15	1	0	2-methoxy-N-[3-[4-[3-methyl-4-[(6-methyl-3-pyridinyl)oxy]anilino]-6-quinazolinyl]prop-2-enyl]acetamide	antineoplastic agent; apoptosis inducer; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; hepatotoxic agent
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.	7.57	2	0	aromatic 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	20.62	205	77	lactam; macrolide
pi103 PI103: pyridofuropyrimidine antineoplastic; a potent inhibitor of class I phosphatidylinositide 3-kinases (PI3K); structure in first soruce	2.13	1	0	aromatic amine; morpholines; organic heterotricyclic compound; phenols; tertiary amino compound	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor
hmn-214 (E)-4-(2-(2-(N-acetyl-N-(4-methoxybenzenesulfonyl)amino)stilbazole)) 1-oxide: an antineoplastic agent; structure in first source	2.15	1	0
tivozanib N-(2-chloro-4-((6,7-dimethoxy-4-quinolyl)oxy)phenyl)-N'-(5-methyl-3-isoxazolyl)urea: KNR-951 is the HCl, monohydrate salt; an antineoplastic agent; structure in first source	15.02	9	1	aromatic ether
hki 272 [no description available]	4.97	6	0	nitrile; quinolines	antineoplastic agent; tyrosine kinase inhibitor
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.	5.34	6	0	N-acylpiperidine; nitrile; pyrrolopyrimidine; tertiary amino compound	antirheumatic drug; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
cediranib [no description available]	4.39	3	0	aromatic ether
tae226 TAE226: an adhesion kinase inhibitor, offers an attractive therapeutic approach in ovarian carcinoma; structure in first source	2.05	1	0	morpholines
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]	3.74	3	0	organonitrogen 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.	11.59	17	6	homodetic cyclic peptide; peptide hormone	antineoplastic agent
chir 99021 Chir 99021: structure in first source. CHIR 99021 : A member of the class of aminopyrimidines that is 2-aminopyrimidine substituted at positions N2, 5 and 6 by (5-cyanopyridin-2-yl)ethyl, 4-methylimidazol-2-yl and 2,4-dichlorophenyl groups respectively.	2.15	1	0	aminopyridine; aminopyrimidine; cyanopyridine; diamine; dichlorobenzene; imidazoles; secondary amino compound	EC 2.7.11.26 (tau-protein kinase) inhibitor
osu 03012 OSU 03012: a PDK-1 inhibitor; structure in first source	2.41	1	0	antibiotic antifungal drug; aromatic amide; glycine derivative; organofluorine compound; phenanthrenes; pyrazoles	antineoplastic agent; apoptosis inducer; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
masitinib [no description available]	2.15	1	0	1,3-thiazoles; benzamides; N-alkylpiperazine; pyridines	antineoplastic agent; antirheumatic drug; tyrosine kinase inhibitor
bx795 BX795: structure in first source	2.41	1	0	ureas
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.	2.15	1	0	aromatic 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.	15.81	66	11	aminopyrimidine; indazoles; sulfonamide	angiogenesis modulating agent; antineoplastic agent; tyrosine kinase inhibitor; vascular endothelial growth factor receptor antagonist
sepantronium sepantronium: a survivin suppressant with antineoplastic activity. sepantronium : An organic cation that is 1-(2-methoxyethyl)-2-methyl-1H-naphtho[2,3-d]imidazole-4,9-dione in which the nitrogen at position 3 of the napthoimidazole moiety has been alkylated by a pyrazin-2-ylmethyl group.	2.52	2	0	organic cation
azd 6244 AZD 6244: a MEK inhibitor	3.5	7	0	benzimidazoles; bromobenzenes; hydroxamic acid ester; monochlorobenzenes; organofluorine compound; secondary amino compound	anticoronaviral agent; antineoplastic agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
su 14813 5-((5-fluoro-2-oxo-1,2-dihydro-3H-indol-3-ylidene)methyl)-N-(2-hydroxy-3-morpholin-4-ylpropyl)-2,4-dimethyl-1H-pyrrole-3-carboxamide: has both antineoplastic and antiangiogenic activities; structure in first source	2.15	1	0
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.	10.02	12	6
a 443654 A 443654: an Akt kinase inhibitor; structure in first source	2.41	1	0	indoles
apilimod [no description available]	3.92	2	0
besifloxacin [no description available]	2.05	1	0	quinolines
bibw 2992 [no description available]	5.02	6	0	aromatic ether; enamide; furans; monochlorobenzenes; organofluorine compound; quinazolines; secondary carboxamide; tertiary amino compound	antineoplastic agent; tyrosine kinase inhibitor
pik 75 PIK 75: structure in first source	2.41	1	0
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.	2.87	3	0	benzimidazoles; bromobenzenes; hydroxamic acid ester; monofluorobenzenes; secondary amino compound	antineoplastic agent; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
sotrastaurin sotrastaurin: a potent protein kinase C-selective inhibitor; structure in first source. sotrastaurin : A member of the class of maleimides that is maleimide which is substituted at position 3 by an indol-3-yl group and at position 4 by a quinazolin-4-yl group, which in turn is substituted at position 2 by a 4-methylpiperazin-1-yl group. It is a potent and selective inhibitor of protein kinase C and has been investigated as an immunosuppresant in renal transplant patients.	8.76	12	2	indoles; maleimides; N-alkylpiperazine; N-arylpiperazine; quinazolines	anticoronaviral agent; EC 2.7.11.13 (protein kinase C) inhibitor; immunosuppressive agent
aee 788 AEE 788: structure in first source	4.96	8	1	6-{4-[(4-ethylpiperazin-1-yl)methyl]phenyl}-N-(1-phenylethyl)-7H-pyrrolo[2,3-d]pyrimidin-4-amine	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; epidermal growth factor receptor antagonist; trypanocidal drug
saracatinib [no description available]	4.06	3	0	aromatic ether; benzodioxoles; diether; N-methylpiperazine; organochlorine compound; oxanes; quinazolines; secondary amino compound	anticoronaviral agent; antineoplastic agent; apoptosis inducer; autophagy inducer; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor; radiosensitizing agent
vx 702 VX 702: a p38 MAP kinase inhibitor	2.15	1	0	phenylpyridine
crenolanib [no description available]	2.15	1	0	aminopiperidine; aromatic ether; benzimidazoles; oxetanes; quinolines; tertiary amino compound	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
tg100-115 3,3'-(2,4-diaminopteridine-6,7-diyl)diphenol: for treatment of ischemia reperfusion injury; structure in first source	2.15	1	0	pteridines
cc 401 CC 401: an anthrapyrazolone	2.15	1	0	pyrazoles; ring assembly
bms 599626 [no description available]	2.15	1	0
exel-7647 tesevatinib : A member of the class of quinazolines that is quinazoline substituted by (3,4-dichloro-2-fluorophenyl)amino, methoxy, and [(3aR,5r,6aS)-2-methyloctahydrocyclopenta[c]pyrrol-5-yl]methoxy groups at positions 4, 6 and 7, respectively. It is a multi-target tyrosine kinase inhibitor of EGFR, ErbB2, KDR, Flt4 and EphB4 and exhibits anti-cancer properties.	2.15	1	0
volasertib BI 6727: a polo-like kinase inhibitor with broad antitumor activity; structure in first source	2.15	1	0
amg 009 AMG 009: an anti-inflammatory agent; structure in first source	2.08	1	0
oxadiazoles Oxadiazoles: Compounds containing five-membered heteroaromatic rings containing two carbons, two nitrogens, and one oxygen atom which exist in various regioisomeric forms.	2.52	2	0
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.	3.15	1	0	acetate ester; methyl ester; organic heteropentacyclic compound; organic heterotetracyclic compound; semisynthetic derivative; vinca alkaloid	antineoplastic agent
cyclosporine metabolite m17 cyclosporin A metabolite M17 : A cyclosporin A derivative that is cyclosporin A in which residue 1 [(2S,3R,4R,6E)-3-hydroxy-4-methyl-2-(methylamino)oct-6-enoic acid] has undergone allylic oxidation to give the corresponding primary allylic alcohol. It specifically inhibits growth of renal cells in culture.	2	1	0	cyclosporin A derivative; primary allylic alcohol	drug metabolite
cefotaxime sodium [no description available]	2.08	1	0	organic sodium salt
baci-im [no description available]	3.23	1	0	homodetic cyclic peptide; polypeptide; zwitterion	antibacterial agent; antimicrobial agent
ds-5272 [no description available]	2.25	1	0
azd 7762 [no description available]	2.15	1	0	aromatic amide; thiophenes
regorafenib [no description available]	4.42	5	0	(trifluoromethyl)benzenes; aromatic ether; monochlorobenzenes; monofluorobenzenes; phenylureas; pyridinecarboxamide	antineoplastic agent; hepatotoxic agent; tyrosine kinase inhibitor
3beta-hydroxy-17-(1h-benzimidazole-1-yl)androsta-5,16-diene 3-hydroxy-17-(1H-benzimidazole-1-yl)androsta-5,16-diene: has antineoplastic activity; structure in first source	2.05	1	0	3-hydroxy steroid	androgen
6-[[5-fluoro-2-(3,4,5-trimethoxyanilino)-4-pyrimidinyl]amino]-2,2-dimethyl-4H-pyrido[3,2-b][1,4]oxazin-3-one [no description available]	2.15	1	0	methoxybenzenes; substituted aniline
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.	7.41	1	0	aromatic ether; diether; monochlorobenzenes; N-acylpiperazine; N-alkylpiperazine; quinazolines; tertiary carboxamide	antineoplastic agent; ferroptosis inducer; voltage-dependent anion channel inhibitor
brivanib [no description available]	2.15	1	0	aromatic ether; diether; fluoroindole; pyrrolotriazine; secondary alcohol	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; drug metabolite; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; fibroblast growth factor receptor antagonist
bms 477118 [no description available]	3.23	1	0	adamantanes; azabicycloalkane; monocarboxylic acid amide; nitrile; tertiary alcohol	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; hypoglycemic agent
auy 954 AUY 954: an S1P(1) receptor agonist; structure in first source	2.03	1	0
mp470 [no description available]	2.15	1	0	N-arylpiperazine
rgb 286638 [no description available]	2.15	1	0
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.	3.23	1	0	nystatins
np 031112 tideglusib: an NSAID and neuroprotective agent. tideglusib : A member of the class of thiadiazolidines that is 1,2,4-thiadiazolidine-3,5-dione which is substituted by a naphthalen-1-yl group at position 2 and by a benzyl group at position 4. It is a non-ATP competitive inhibitor of glycogen synthase kinase 3beta (GSK3beta) and has neuroprotective effects. Currently under clinical investigation for the treatment of Alzheimer's disease and progressive supranuclear palsy.	3.73	2	0	benzenes; naphthalenes; thiadiazolidine	anti-inflammatory agent; apoptosis inducer; EC 2.7.11.26 (tau-protein kinase) inhibitor; neuroprotective agent
at 7519 4-(2,6-dichlorobenzamido)-N-(piperidin-4-yl)-pyrazole-3-carboxamide : A member of the class of pryrazoles that is 4-amino-1H-pyrazole-3-carboxylic acid in which the primary amino group has been acylated by a 2,6-dichlorobenzoyl group and in which the carboxylic acid has been converted into a carboxamide by formal condensation with the primary amino group of 4-aminopiperidine.	2.15	1	0	dichlorobenzene; piperidines; pyrazoles; secondary carboxamide	antineoplastic agent; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
bms-690514 [no description available]	2.15	1	0
er-086526 eribulin: a halichondrin B derivative that suppresses microtubule growth and acts as an antimitotic agent; structure in first source. eribulin : A fully synthetic macrocyclic ketone analogue of marine sponge natural products. Inhibits growth phase of microtubules via tubulin-based antimitotic mechanism, which leads to G2/M cell-cycle block, disruption of mitotic spindles, and, ultimately, apoptotic cell death after prolonged mitotic blockage	3.95	2	1	cyclic ketal; cyclic ketone; macrocycle; polycyclic ether; polyether; primary amino compound	antineoplastic agent; microtubule-destabilising agent
bi 2536 [no description available]	2.63	2	0
inno-406 [no description available]	2.15	1	0	biaryl
kw 2449 KW 2449: has both multikinase inhibitory activity and antineoplastic activity; structure in first source	2.15	1	0
danusertib [no description available]	2.57	2	0	piperazines
nvp-aew541 [no description available]	3.32	6	0
abt 869 [no description available]	2.15	1	0	aromatic amine; indazoles; phenylureas	angiogenesis inhibitor; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
azd 8931 sapitinib : A member of the class of quinazolines that is 4-amino-7-methoxyquinazoline in which the amino group has been substituted by a 3-chloro-2-fluorophenyl group and in which position 6 of the quinoline ring has been substituted by a {1-[2-(methylamino)-2-oxoethyl]piperidin-4-yl}oxy group. Sapitinib is a dual tyrosine kinase inhibitor (TKI) of epithelial growth factor receptors (EGFR) HER2 and HER3.	2.15	1	0	aromatic ether; monochlorobenzenes; monofluorobenzenes; piperidines; quinazolines; secondary amino compound; tertiary amino compound	EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; epidermal growth factor receptor antagonist
arq 197 [no description available]	3.65	2	0	indoles
azd 1152 AZD-1152 : A member of the of quinazolines that is 4-aminoquinazolin-7-ol in which the amino group at position 4 has been substituted by a 5-[2-(3-fluoroanilino)-2-oxoethyl]-1H-pyrazol-3-yl group, while the hydroxy group at position 7 has been converted into the corresponding 3-[ethyl(2-hydroxyethyl)aminopropyl ether.	2.15	1	0	anilide; monoalkyl phosphate; monofluorobenzenes; pyrazoles; quinazolines; secondary amino compound; secondary carboxamide; tertiary amino compound	antineoplastic agent; Aurora kinase inhibitor; prodrug
pf 00299804 dacomitinib: a pan-ERBB inhibitor. dacomitinib : A member of the class of quinazolines that is 7-methoxyquinazoline-4,6-diamine in which the amino group at position 4 is substituted by a 3-chloro-4-fluorophenyl group and the amino group at position 6 is substituted by an (E)-4-(piperidin-1-yl)but-2-enoyl group.	2.15	1	0	enamide; monochlorobenzenes; monofluorobenzenes; piperidines; quinazolines; secondary amino compound; secondary carboxamide; tertiary amino compound	antineoplastic agent; epidermal growth factor receptor antagonist
ridaforolimus [no description available]	10.94	31	0	macrolide lactam
ch 4987655 [no description available]	2.15	1	0
6-(5-((cyclopropylamino)carbonyl)-3-fluoro-2-methylphenyl)-n-(2,2-dimethylprpyl)-3-pyridinecarboxamide [no description available]	2.15	1	0	phenylpyridine
carfilzomib [no description available]	4.42	3	0	epoxide; morpholines; tetrapeptide	antineoplastic agent; proteasome inhibitor
apremilast [no description available]	7.6	1	0	aromatic ether; N-acetylarylamine; phthalimides; sulfone	non-steroidal anti-inflammatory drug; phosphodiesterase IV inhibitor
cc-930 [no description available]	2.15	1	0
tak 285 N-(2-(4-((3-chloro-4-(3-(trifluoromethyl)phenoxy)phenyl)amino)-5H-pyrrolo(3,2-d)pyrimidin-5-yl)ethyl)-3-hydroxy-3-methylbutanamide: also inhibits HER2; structure in first source	2.15	1	0
milnacipran [no description available]	3.23	1	0	acetamides
idelalisib idelalisib: an antineoplastic agent and p110delta inhibitor; structure in first source. idelalisib : A member of the class of quinazolines that is 5-fluoro-3-phenylquinazolin-4-one in which the hydrogen at position 2 is replaced by a (1S)-1-(3H-purin-6-ylamino)propyl group. used for for the treatment of refractory indolent non-Hodgkin's lymphoma and relapsed chronic lymphocytic leukemia.	4.58	2	0	aromatic amine; organofluorine compound; purines; quinazolines; secondary amino compound	antineoplastic agent; apoptosis inducer; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
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)	8.36	5	0	3-[1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(piperidin-4-yl)pyrazol-4-yl]pyridin-2-amine	antineoplastic agent; biomarker; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
osi 906 [no description available]	2.15	1	0	cyclobutanes; quinolines
cgp 57380 CGP 57380: inhibits the mitogen-activated protein kinase-interacting kinase Mnk1	2.84	3	0	pyrazolopyrimidine
chir-265 [no description available]	2.78	3	0	aromatic ether
motesanib [no description available]	2.15	1	0	pyridinecarboxamide
fostamatinib fostamatinib: a spleen tyrosine kinase (Syk) inhibitor, metabolized to R406	2.15	1	0
trametinib [no description available]	11.74	10	2	acetamides; 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
mln8054 [no description available]	2.15	1	0	benzazepine
pf-562,271 [no description available]	2.15	1	0	indoles
pha 767491 PHA 767491: a Cdc7 inhibitor; structure in first source	2.41	1	0	pyrrolopyridine
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.	2.76	3	0
jnj-26483327 JNJ-26483327: an orally active macrocyclic tyrosine kinase inhibitor for treatment of patients with advanced solid tumours; in Phase I trial, 9/2010	3.62	2	0
ly2603618 [no description available]	2.15	1	0	ureas
veliparib [no description available]	5.06	2	1	benzimidazoles	EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
scopolamine hydrobromide [no description available]	3.23	1	0
tg100801 [no description available]	2.15	1	0
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.	14.75	45	4	imidazoquinoline; nitrile; quinolines; ring assembly; ureas	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor
bgt226 BGT226 free base : An imidazoquinoline that is 3-methyl-2-oxo-2,3-dihydro-1H-imidazo[4,5-c]quinoline substituted at position 1 by a 3-trifluoromethyl-4-(piperazin-1-yl)phenyl group and at position 8 by a 6-methoxypyridin-3-yl group. A dual PI3K/mTOR inhibitor.. BGT226 : The maleate salt of 8-(6-methoxypyridin-3-yl)-3-methyl-1-[4-(piperazin-1-yl)-3-(trifluoromethyl)phenyl]-1,3-dihydro-2H-imidazo[4,5-c]quinolin-2-one. A dual PI3K/mTOR inhibitor.	2.15	1	0	aromatic ether; imidazoquinoline; N-arylpiperazine; organofluorine compound; pyridines	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor
palomid 529 [no description available]	2.1	1	0
thienopyridine thienopyridine: patients were treated with thienopyridine after percutaneous coronary intervention; Antiplatelet Agents. thienopyridine : Any organic heterobicyclic compound whose skeleton results from the formal ortho-fusion of any bond of a pyridine with any bond of a thiophene.	4.43	1	1
rabeprazole sodium [no description available]	2.08	1	0	organic sodium salt
icatibant icatibant: a potent bradykinin (B2) receptor antagonist; WIN 65365 is an L-Tic(7) stereoisomer. icatibant : A ten-membered synthetic oligopeptide consisting of D-Arg, Arg, Pro, Hyp, Gly, Thi, Ser, D-Tic, Oic, and Arg residues joined in sequrence. A bradykinin receptor antagonist used as its acetate salt for the treatment of acute attacks of hereditary angioedema in adult patients.	2.1	1	0
jaw [no description available]	7.21	1	0	indolecarboxamide
3-(4-chlorophenyl)-adamantane-1-carboxylic acid (pyridin-4-ylmethyl)amide [no description available]	2.41	1	0	organochlorine compound
nad NAD(1-) : An anionic form of nicotinamide adenine dinucleotide arising from deprotonation of the two OH groups of the diphosphate moiety.	2.02	1	0	organophosphate oxoanion	cofactor; human metabolite; hydrogen acceptor; Saccharomyces cerevisiae metabolite
mdv 3100 [no description available]	2.13	1	0	(trifluoromethyl)benzenes; benzamides; imidazolidinone; monofluorobenzenes; nitrile; thiocarbonyl compound	androgen antagonist; antineoplastic agent
gsk 461364 GSK 461364: an antineoplastic agent that inhibits polo-like kinase 1	2.15	1	0	(trifluoromethyl)benzenes
azd 1152-hqpa AZD2811: has antineoplastic activity; structure in first source	2.15	1	0	anilide; monofluorobenzenes; primary alcohol; pyrazoles; quinazolines; secondary amino compound; secondary carboxamide; tertiary amino compound	antineoplastic agent; Aurora kinase inhibitor
enmd 2076 ENMD 2076: an antiangiogenic agent with aurora kinase inhibitory and antineoplastic activities	2.15	1	0
e 7050 [no description available]	2.15	1	0	aromatic ether
2-amino-8-ethyl-4-methyl-6-(1H-pyrazol-5-yl)-7-pyrido[2,3-d]pyrimidinone [no description available]	2.15	1	0	pyrazolopyridine
tak-901 [no description available]	2.15	1	0
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.	3.61	2	0	polypeptide	anticoagulant; EC 3.4.21.5 (thrombin) inhibitor
somatostatin [no description available]	2.08	1	0	heterodetic cyclic peptide; peptide hormone
atrial natriuretic factor Atrial Natriuretic Factor: A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.	2.96	1	0	polypeptide
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.	3.23	1	0
ganirelix [no description available]	3.23	1	0	polypeptide
gastrins Gastrins: A family of gastrointestinal peptide hormones that excite the secretion of GASTRIC JUICE. They may also occur in the central nervous system where they are presumed to be neurotransmitters.	3.53	1	1
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.	8.53	1	1	peptide hormone
teriparatide [no description available]	3.23	1	0	polypeptide
salmon calcitonin [no description available]	3.23	1	0	heterodetic cyclic peptide; peptide hormone; polypeptide	bone density conservation agent; metabolite
oligonucleotides [no description available]	3.55	2	0
ly-146032 [no description available]	3.61	2	0	heterodetic cyclic peptide; lipopeptide antibiotic; lipopeptide; macrocycle; macrolide	antibacterial drug; bacterial metabolite; calcium-dependent antibiotics
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	3.59	2	0	polypeptide
c-peptide C-Peptide: The middle segment of proinsulin that is between the N-terminal B-chain and the C-terminal A-chain. It is a pancreatic peptide of about 31 residues, depending on the species. Upon proteolytic cleavage of proinsulin, equimolar INSULIN and C-peptide are released. C-peptide immunoassay has been used to assess pancreatic beta cell function in diabetic patients with circulating insulin antibodies or exogenous insulin. Half-life of C-peptide is 30 min, almost 8 times that of insulin.	2.13	1	0
exenatide [no description available]	3.23	1	0
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.	2.08	1	0
endothelin-1 Endothelin-1: A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)	2.07	1	0
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.	2.15	1	0	aromatic 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	12.65	16	1	aminopyridine; aminopyrimidine; morpholines; organofluorine compound	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
azd 1480 [no description available]	2.52	2	0
famitinib famitinib: structure in first source	2.13	1	0
azd8330 [no description available]	2.63	2	0	pyridinecarboxamide
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	2.15	1	0
ro5126766 RO5126766: a dual MEK/RAF kinase inhibitor. CH5126766 : A member of the class of coumarins that is 4-methyl-7-[(pyrimidin-2-yl)oxy]coumarin carrying an additional [2-[(methylaminosulfonyl)amino]-3-fluoropyridin-4-yl]methyl substituent at position 3.	3.73	2	0	aryloxypyrimidine; coumarins; organofluorine compound; pyridines; sulfamides	antineoplastic agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
fedratinib fedratinib: a selective small-molecule inhibitor of JAK2	2.63	2	0	sulfonamide
gsk690693 [no description available]	2.52	2	0	1,2,5-oxadiazole; acetylenic compound; aromatic amine; aromatic ether; imidazopyridine; piperidines; primary amino compound; tertiary alcohol	antineoplastic agent; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
cnf 2024 [no description available]	2.25	1	0	2-aminopurines; aromatic ether; organochlorine compound; pyridines	antineoplastic agent; Hsp90 inhibitor
ku 0063794 Ku 0063794: an mTOR inhibitor; structure in first source	3.27	5	0	benzyl 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	3.96	3	0
azd5438 [no description available]	2.15	1	0	sulfonamide
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.	2.08	1	0	organic sodium salt; statin (semi-synthetic)	anticholesteremic drug
alendronate sodium [no description available]	2.08	1	0
sphingosine kinase [no description available]	7.54	2	0
pf 04217903 [no description available]	2.15	1	0	quinolines
gdc 0941 pictrelisib : A sulfonamide composed of indazole, morpholine, and methylsulfonyl-substituted piperazine rings bound to a thienopyrimidine ring.	4	3	0	indazoles; morpholines; piperazines; sulfonamide; thienopyrimidine	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
sl 80.0750 [no description available]	2.08	1	0
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.	3.51	1	1
chitosan [no description available]	7.17	1	0
icotinib [no description available]	2.15	1	0
ph 797804 PH 797804: an NSAID; structure in first source. PH 797804 : A member of the class of benzamides obtained by formal condensation of the carboxy group of 3-{3-bromo-4-[(2,4-difluorobenzyl)oxy]-6-methyl-2-oxopyridin-1-yl}-4-methylbenzoic acid with the amino group of methylamine.	2.15	1	0	aromatic ether; benzamides; organobromine compound; organofluorine compound; pyridone	anti-inflammatory agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
umirolimus umirolimus: sirolimus derivative from a biodegradable polylactic acid polymer; possesses enhanced anti-inflammatory and antiproliferative activity with an improved pharmacokinetic profile; structure in first source	15.74	59	25	lactam; macrolide
kx-01 [no description available]	2.15	1	0
mesna Mesna: A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from ANTINEOPLASTIC AGENTS, such as IFOSFAMIDE or CYCLOPHOSPHAMIDE.	3.61	2	0	organosulfonic acid
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.	2.08	1	0	potassium salt	antibacterial 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.	3.23	1	0	lactate salt; organic sodium salt	food acidity regulator; food preservative
piperacillin sodium [no description available]	2.08	1	0	organic sodium salt
sodium iothalamate [no description available]	3.23	1	0
oxacillin sodium [no description available]	2.08	1	0	organic 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.	2.08	1	0	organic sodium salt
azlocillin sodium [no description available]	2.08	1	0	organic sodium salt
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.	3.14	1	0
olaparib [no description available]	3.98	3	0	cyclopropanes; monofluorobenzenes; N-acylpiperazine; phthalazines	antineoplastic agent; apoptosis inducer; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
mk 5108 [no description available]	2.15	1	0	aromatic ether
cx 4945 [no description available]	3.73	2	0
cudc 101 7-(4-(3-ethynylphenylamino)-7-methoxyquinazolin-6-yloxy)-N-hydroxyheptanamide: a histone deacetylase inhibitor; structure in first source	2.15	1	0
s-adenosylmethionine (R)-S-adenosyl-L-methionine : An S-adenosyl-L-methionine that has R-configuration.. S-adenosyl-L-methionine zwitterion : A zwitterionic tautomer of S-adenosyl-L-methionine arising from shift of the proton from the carboxy group to the amino group.. (R)-S-adenosyl-L-methionine zwitterion : An S-adenosyl-L-methionine zwitterion that has R-configuration; major species at pH 7.3.. (S)-S-adenosyl-L-methionine zwitterion : An S-adenosyl-L-methionine zwitterion that has S-configuration; major species at pH 7.3.. S-adenosyl-L-methionine : A sulfonium compound that is the S-adenosyl derivative of L-methionine. It is an intermediate in the metabolic pathway of methionine.	2.15	1	0	organic cation; sulfonium compound	coenzyme; cofactor; human metabolite; micronutrient; Mycoplasma genitalium metabolite; nutraceutical; Saccharomyces cerevisiae metabolite
arry-614 pexmetinib: inhibits both p38 mitogen-activated protein kinase and Tie2 protein	2.15	1	0
tak 593 TAK 593: structure in first source	2.15	1	0
mln 8237 MLN 8237: an aurora kinase A inhibitor	2.15	1	0	benzazepine
lde225 sonidegib: specific Smoothened/Smo antagonist. sonidegib : A member of the classo of biphenyls that is the amide obtained by formal condensation of the carboxy group of 2-methyl-4'-(trifluoromethoxy)[1,1'-biphenyl]-3-carboxylic acid with the amino group of 6-(2,6-dimethylmorpholin-4-yl)pyridin-3-amine. Used (as its phosphate salt) for treatment of locally advanced basal cell carcinoma.	2.1	1	0	aminopyridine; aromatic ether; benzamides; biphenyls; morpholines; organofluorine compound; tertiary amino compound	antineoplastic agent; Hedgehog signaling pathway inhibitor; SMO receptor antagonist
gdc 0449 HhAntag691: inhibits the hedgehog pathway and ABC transporters; has antineoplastic activity	3.64	2	0	benzamides; monochlorobenzenes; pyridines; sulfone	antineoplastic agent; Hedgehog signaling pathway inhibitor; SMO receptor antagonist; teratogenic agent
sgx 523 [no description available]	2.15	1	0	aryl sulfide; biaryl; pyrazoles; quinolines; triazolopyridazine	c-Met tyrosine kinase inhibitor; nephrotoxic agent
bms 754807 BMS 754807: an IGR-1R kinase inhibitor; structure in first source	2.15	1	0	pyrazoles; pyridines; pyrrolidines; pyrrolotriazine	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
gdc-0068 ipatasertib: an Akt kinase inhibitor; structure in first source	2.31	1	0	N-arylpiperazine
bms 777607 N-(4-(2-amino-3-chloropyridin-4-yloxy)-3-fluorophenyl)-4-ethoxy-1-(4-fluorophenyl)-2-oxo-1,2-dihydropyridine-3-carboxamide: a Met kinase inhibitor; structure in first source	2.15	1	0	aromatic amide
sgi 1776 SGI 1776: a Pim kinase inhibitor; structure in first source	2.15	1	0	imidazoles
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.	5.7	9	0	acrylamides; aromatic amine; aromatic ether; N-acylpiperidine; pyrazolopyrimidine; tertiary carboxamide	antineoplastic agent; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
ponatinib [no description available]	2.15	1	0	(trifluoromethyl)benzenes; acetylenic compound; benzamides; imidazopyridazine; N-methylpiperazine	antineoplastic agent; tyrosine kinase inhibitor
amg 900 N-(4-((3-(2-amino-4-pyrimidinyl)-2-pyridinyl)oxy)phenyl)-4-(4-methyl-2-thienyl)-1-phthalazinamine: a pan-aurora kinase inhibitor; structure in first source	2.15	1	0
mk-1775 adavosertib: a Wee1 kinase inhibitor; structure in first source	4	2	1	piperazines
AMG-208 [no description available]	2.15	1	0	aromatic ether; quinolines; triazolopyridazine	antineoplastic agent; c-Met tyrosine kinase inhibitor
sch772984 [no description available]	2.17	1	0	biaryl; indazoles; N-acylpiperazine; N-alkylpyrrolidine; N-arylpiperazine; pyridines; pyrimidines; pyrrolidinecarboxamide; secondary carboxamide; tertiary amino compound; tertiary carboxamide	analgesic; antineoplastic agent; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
quizartinib [no description available]	2.63	2	0	benzoimidazothiazole; isoxazoles; morpholines; phenylureas	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; necroptosis inhibitor
at13148 [no description available]	2.15	1	0
tak 733 [no description available]	2.15	1	0
mk 2206 MK 2206: a protein kinase inhibitor and antineoplastic agent	5.66	16	1	organic heterotricyclic compound	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
navitoclax [no description available]	2.17	1	0	aryl sulfide; monochlorobenzenes; morpholines; N-sulfonylcarboxamide; organofluorine compound; piperazines; secondary amino compound; sulfone; tertiary amino compound	antineoplastic agent; apoptosis inducer; B-cell lymphoma 2 inhibitor
sns 314 SNS 314: an aurora kinase inhibitor; structure in first source	2.15	1	0	ureas
lucitanib E-3810: a multi-kinase inhibitor with antineoplastic activity; structure in first source. E-3810 : A hydrochloride salt obtained by reaction of 6-({7-[(1-aminocyclopropyl)methoxy]-6-methoxyquinolin-4-yl}oxy)-N-methyl-1-naphthamide with one equivalent of hydrochloric acid. E-3810 is a dual VEGFR and FGFR inhibitor. E-3810 free base : A naphthalenecarboxamide obtained from formal condensation of the carboxy group of aminocyclopropyl)methoxy]-6-methoxyquinolin-4-yl}oxy)-1-naphthoic acid with methylamine.	2.15	1	0	aromatic ether; cyclopropanes; naphthalenecarboxamide; primary amino compound; quinolines	antineoplastic agent; fibroblast growth factor receptor antagonist; vascular endothelial growth factor receptor antagonist
pf-04691502 [no description available]	2.15	1	0
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.	2.63	2	0	aminopyrimidine; 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
cardiovascular agents Cardiovascular Agents: Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.	23.93	507	175
dcc-2036 rebastinib: an inhibitor of Tie2 tyrosine kinase receptor and antineoplastic agent	2.15	1	0	organofluorine compound; phenylureas; pyrazoles; pyridinecarboxamide; quinolines	tyrosine kinase inhibitor
trelstar Triptorelin Pamoate: A potent synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE with D-tryptophan substitution at residue 6.	2.25	1	0
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.	3.23	1	0	oligopeptide	antineoplastic 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.	16.55	53	22	aromatic ether; dicarboxylic acid diamide; organofluorine compound; quinolines	antineoplastic agent; tyrosine kinase inhibitor
defactinib [no description available]	2.53	2	0
ly2584702 [no description available]	9.83	2	1
incb-018424 [no description available]	4.2	4	0	nitrile; pyrazoles; pyrrolopyrimidine	antineoplastic agent; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
poziotinib HM781-36B: antitumor irreversible Pan-HER inhibitor for treatment of gastric cancer	2.15	1	0	acrylamides; aromatic ether; dichlorobenzene; diether; monofluorobenzenes; N-acylpiperidine; quinazolines; secondary amino compound; substituted aniline	antineoplastic agent; apoptosis inducer; epidermal growth factor receptor antagonist
asp3026 ASP3026: an anaplastic lymphoma receptor tyrosine kinase inhibitor; structure in first source. ASP-3026 : A member of the class of diamino-1,3,5-triazines that is 1,3,5-triazine-2,4-diamine in which the amino groups at positions 2 and 4 are respectively carrying 2-methoxy-4-[4-(4-methylpiperazin-1-yl)piperidin-1-yl]phenyl and 2-(propan-2-ylsulfonyl)phenyl substituents. It is a potent inhibitor of anaplastic lymphoma kinase (ALK), Ack and ROS1 activity (IC50 values are 3.5, 5.8 and 8.9 nM respectively) and exhibits anti-cancer properties.	2.15	1	0	aromatic amine; diamino-1,3,5-triazine; monomethoxybenzene; N-methylpiperazine; piperidines; secondary amino compound; sulfone	antimalarial; antineoplastic agent; apoptosis inducer; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; EC 6.1.1.6 (lysine--tRNA ligase) 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.	2.15	1	0	benzamides; 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
pexidartinib pexidartinib: inhibits both CSF1R and c-kit receptor tyrosine kinase; structure in first source. pexidartinib : A pyrrolopyridine that is 5-chloro-1H-pyrrolo[2,3-b]pyridine which is substituted by a [6-({[6-(trifluoromethyl)pyridin-3-yl]methyl}amino)pyridin-3-yl]methyl group at position 3. It is a potent multi-targeted receptor tyrosine kinase inhibitor of CSF-1R, KIT, and FLT3 (IC50 of 20 nM, 10 nM and 160 nM, respectively). Approved by the FDA for the treatment of adult patients with symptomatic tenosynovial giant cell tumor (TGCT).	2.15	1	0	aminopyridine; organochlorine compound; organofluorine compound; pyrrolopyridine; secondary amino compound	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
bms-790052 daclatasvir: an HCV NS5A inhibitor. daclatasvir : A member of the class of biphenyls that is a potent inhibitor of nonstructural protein 5A and is used (as its hydrochloride salt) for treatment of hepatitis C.	2.17	1	0	biphenyls; carbamate ester; carboxamide; imidazoles; valine derivative	antiviral drug; nonstructural protein 5A inhibitor
TAK-580 MLN 2480: brain-penetrant RAF dimer antagonist. TAK-580 : A 1,3-thiazolecarboxamide that is 2-[(1R)-1-aminoethyl]-1,3-thiazole-5-carboxylic acid in which the carboxy group undergoes formal condensation with the amino group of 5-chloro-4-(trifluoromethyl)pyridin-2-amine and in which the amino group undergoes formal condensation with the carboxy group of 6-amino-5-chloropyrimidine-4-carboxylic acid. It is a pan-RAF kinase inhibitor which is currently in clinical development for the treatment of radiographically recurrent or progressive low-grade glioma in children and young adults.	2.15	1	0	1,3-thiazolecarboxamide; aminopyrimidine; chloropyridine; organofluorine compound; pyrimidinecarboxamide; secondary carboxamide	antineoplastic agent; apoptosis inducer; B-Raf inhibitor
gsk 2126458 omipalisib: inhibitor of mTOR protein. omipalisib : A member of the class of quinolines that is quinoline which is substituted by pyridazin-4-yl and 5-[(2,4-difluorobenzene-1-sulfonyl)amino]-6-methoxypyridin-3-yl groups at positions 4 and 6, respectively. It is a highly potent inhibitor of PI3K and mTOR developed by GlaxoSmithKline and was previously in human phase 1 clinical trials for the treatment of idiopathic pulmonary fibrosis and solid tumors.	3.96	3	0	aromatic ether; difluorobenzene; pyridazines; pyridines; quinolines; sulfonamide	anticoronaviral agent; antineoplastic agent; autophagy inducer; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor; radiosensitizing agent
emd1214063 tepotinib: MET inhibitor	2.15	1	0
fit-039 FIT-039: CDK9 inhibitor; structure in first source	2.41	1	0
pf 3758309 PF 3758309: a PAK4 p21-activated kinase inhibitor; structure in first source	2.15	1	0	organic heterobicyclic compound; organonitrogen heterocyclic compound; organosulfur heterocyclic compound
gdc 0980 [no description available]	2.15	1	0
cx 5461 CX 5461: structure in first source	2.13	1	0	diazepine; naphthyridine derivative; organic heterotetracyclic compound; pyrazines; secondary carboxamide	antineoplastic agent; apoptosis inducer; EC 2.7.7.6 (RNA polymerase) inhibitor
azd2014 vistusertib: potent and selective dual mTORC1 and mTORC2 inhibitor; structure in first source	11.3	9	1
(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	4.85	9	0	benzyl alcohols; morpholines; pyridopyrimidine; tertiary amino compound	antineoplastic agent; apoptosis inducer; mTOR inhibitor
plx4032 [no description available]	7.14	9	1	aromatic 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	2.15	1	0	aromatic ether
arry-334543 ARRY-334543: an antagonist of ATP-binding cassette subfamily G member 2 (ABCG2); structure in first source	2.15	1	0
kin-193 [no description available]	2.15	1	0	pyridopyrimidine
mk 2461 [no description available]	2.15	1	0
bay 869766 [no description available]	2.63	2	0
as 703026 [no description available]	2.15	1	0	pyridinecarboxamide
elafin Elafin: A secretory proteinase inhibitory protein that was initially purified from human SKIN. It is found in a variety mucosal secretions and is present at high levels in SPUTUM. Elafin may play a role in the innate immunity (IMMUNITY, INNATE) response of the LUNG.	5.51	4	1
baricitinib [no description available]	4.06	3	0	azetidines; nitrile; pyrazoles; pyrrolopyrimidine; sulfonamide	anti-inflammatory agent; antirheumatic drug; antiviral agent; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor; immunosuppressive agent
piperidines Piperidines: A family of hexahydropyridines.	10.3	18	3
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.	4.14	4	0
dabrafenib [no description available]	3.97	3	0	1,3-thiazoles; aminopyrimidine; organofluorine compound; sulfonamide	anticoronaviral agent; antineoplastic agent; B-Raf inhibitor
pki 587 gedatolisib: inhibits both phosphatidylinositol 3-kinase and mTOR; structure in first source	2.55	2	0
4-(cyclopropylamino)-2-((4-(4-(ethylsulfonyl)piperazin-1-yl)phenyl)amino)pyrimidine-5-carboxamide 4-(cyclopropylamino)-2-((4-(4-(ethylsulfonyl)piperazin-1-yl)phenyl)amino)pyrimidine-5-carboxamide: a protein kinase inhibitor; structure in first source	2.41	1	0
grazoprevir grazoprevir: has antiviral activity; component of Zepatier. grazoprevir : An azamacrocyclic compound that is a hepatitis C protease inhibitor used in combination with elbasvir (under the brand name Zepatier) for treatment of chronic HCV genotypes 1 or 4 infection in adults.	3.19	1	0	aromatic ether; azamacrocycle; carbamate ester; cyclopropanes; lactam; N-sulfonylcarboxamide; quinoxaline derivative	antiviral drug; hepatitis C protease inhibitor; hepatoprotective agent
n-(3-fluoro-4-((1-methyl-6-(1h-pyrazol-4-yl)-1h-indazol-5 yl)oxy)phenyl)-1-(4-fluorophenyl)-6-methyl-2-oxo-1,2-dihydropyridine-3-carboxamide merestinib: in phase I clinical trials (2013); structure in first source	2.15	1	0
ribociclib ribociclib: inhibits both CDK4 and CDK6	7.5	7	1
abt-450 paritaprevir: inhibits HCV NS3 protease. paritaprevir : An azamacrocycle which is used which is in combination with dasabuvir sodium hydrate, ombitasvir and ritonavir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	2.41	1	0
letermovir letermovir: has antiviral activity; structure in first source	7.6	1	0
mk-8033 1-(3-(1-methyl-1H-pyrazol-4-yl)-5-oxo-5H-benzo(4,5)cyclohepta(1,2-b)pyridin-7-yl)-N-(pyridin-2-ylmethyl)methanesulfonamide: inhibits both Ron and c-Met kinases; structure in first source	2.15	1	0
sofosbuvir Sofosbuvir: A uridine monophosphate analog inhibitor of HEPATITIS C VIRUS (HCV) polymerase NS5B that is used as an ANTIVIRAL AGENT in the treatment of CHRONIC HEPATITIS C.. sofosbuvir : A nucleotide conjugate that is used in combination with ledipasvir (under the trade name Harvoni) for the treatment of chronic hepatitis C genotype 1 infection.	2.17	1	0	isopropyl ester; L-alanyl ester; nucleotide conjugate; organofluorine compound; phosphoramidate ester	antiviral drug; hepatitis C protease inhibitor; prodrug
5-(4-amino-1-propan-2-yl-3-pyrazolo[3,4-d]pyrimidinyl)-1,3-benzoxazol-2-amine sapanisertib: an mTOR inhibitor	3.25	5	0	benzoxazole
exenatide Exenatide: A synthetic form of exendin-4, a 39-amino acid peptide isolated from the venom of the Gila monster lizard (Heloderma suspectum). Exenatide increases CYCLIC AMP levels in pancreatic acinar cells and acts as a GLUCAGON-LIKE PEPTIDE-1 RECEPTOR (GLP-1) agonist and incretin mimetic, enhancing insulin secretion in response to increased glucose levels; it also suppresses inappropriate glucagon secretion and slows gastric emptying. It is used an anti-diabetic and anti-obesity agent.	7.13	1	0
pha 793887 [no description available]	2.15	1	0	piperidinecarboxamide
ly2784544 [no description available]	2.41	1	0	pyridazines
sb 1518 [no description available]	2.63	2	0
abemaciclib [no description available]	11.14	8	0
mk-8776 [no description available]	2.15	1	0
afuresertib [no description available]	2.15	1	0	amphetamines
arry-371797 ARRY-371797: a p38 MAP kinase inhibitor	3.51	1	0
gsk 1070916 GSK 1070916: an antineoplastic agent with aurora B/C kinase inhibitory activity	2.15	1	0	pyrazoles; ring assembly
jnj38877605 [no description available]	2.52	2	0	quinolines
dinaciclib [no description available]	4.06	3	0	pyrazolopyrimidine
gilteritinib gilteritinib: an FLT3/AXL protein tyrosine kinase inhibitor. gilteritinib : A member of the class of pyrazines that is pyrazine-2-carboxamide which is substituted by {3-methoxy-4-[4-(4-methylpiperazin-1-yl)piperidin-1-yl]phenyl}nitrilo, (oxan-4-yl)nitrilo and ethyl groups at positions 3,5 and 6, respectively. It is a potent inhibitor of FLT3 and AXL tyrosine kinase receptors (IC50 = 0.29 nM and 0.73 nM, respectively). Approved by the FDA for the treatment of acute myeloid leukemia in patients who have a FLT3 gene mutation.	4.06	3	0	aromatic amine; monomethoxybenzene; N-methylpiperazine; oxanes; piperidines; primary carboxamide; pyrazines; secondary amino compound	antineoplastic agent; apoptosis inducer; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
alectinib [no description available]	2.15	1	0	aromatic ketone; morpholines; nitrile; organic heterotetracyclic compound; piperidines	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
glpg0634 [no description available]	2.63	2	0
abt-199 venetoclax: A BCL-2 inhibitor with antineoplastic activity that is used in the treatment of CHRONIC LYMPHOCYTIC LEUKEMIA associated with chromosome 17p deletion; structure in first source.. venetoclax : A member of the class of pyrrolopyridines that is a potent inhibitor of the antiapoptotic protein B-cell lymphoma 2. It is used for treamtment of chronic lymphocytic leukemia with 17p deletion.	2.94	3	0	aromatic ether; C-nitro compound; monochlorobenzenes; N-alkylpiperazine; N-arylpiperazine; N-sulfonylcarboxamide; oxanes; pyrrolopyridine	antineoplastic agent; apoptosis inducer; B-cell lymphoma 2 inhibitor
ipi-145 [no description available]	2.17	1	0	isoquinolines
delgocitinib delgocitinib: a Janus kinase inhibitor. delgocitinib : A pyrrolopyrimidine that is 7H-pyrrolo[2,3-d]pyrimidine substituted by a (3S,4R)-1-(cyanoacetyl)-3-methyl-1,6-diazaspiro[3.4]octan-6-yl group at position 4. It is a pan-Janus kinase (JAK) inhibitor and is approved for treatment of atopic dermatitis (AD) in Japan.	2.41	1	0	azaspiro compound; N-acylazetidine; nitrile; pyrrolopyrimidine; tertiary amino compound; tertiary carboxamide	anti-inflammatory drug; antipsoriatic; antiseborrheic; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
encorafenib encorafenib: a BRAF inhibitor	2.59	2	0
bms-911543 N,N-dicyclopropyl-4-((1,5-dimethyl-1H-pyrazol-3-yl)amino)-6-ethyl-1-methyl-1,6-dihydroimidazo(4,5-d)pyrrolo(2,3b)pyridine-7-carboxamide: has antineoplastic activity; structure in first source	2.15	1	0
gsk2141795 GSK2141795: an Akt inhibitor with antineoplastic activity; structure in first source	2.15	1	0
pf-4708671 [no description available]	2.25	1	0
azd8186 [no description available]	2.15	1	0
nvp-cgm097 NVP-CGM097: an MDM2 and HDM2 inhibitor; structure in first source	2.13	1	0
incb039110 INCB039110: a JAK1 inhibitor; structure in first source	2.41	1	0
ascorbic acid Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.. L-ascorbic acid : The L-enantiomer of ascorbic acid and conjugate acid of L-ascorbate.. L-ascorbate : The L-enantiomer of ascorbate and conjugate base of L-ascorbic acid, arising from selective deprotonation of the 3-hydroxy group. Required for a range of essential metabolic reactions in all animals and plants.. vitamin C : Any member of a group of vitamers that belong to the chemical structural class called butenolides that exhibit biological activity against vitamin C deficiency in animals. The vitamers include L-ascorbic acid and its salt, ionized and oxidized forms.	3.65	2	0	ascorbic acid; vitamin C	coenzyme; cofactor; flour treatment agent; food antioxidant; food colour retention agent; geroprotector; plant metabolite; skin lightening agent
raltegravir [no description available]	3.23	1	0	1,2,4-oxadiazole; dicarboxylic acid amide; hydroxypyrimidine; monofluorobenzenes; pyrimidone; secondary carboxamide	antiviral drug; HIV-1 integrase inhibitor
tetracycline Tetracycline: A naphthacene antibiotic that inhibits AMINO ACYL TRNA binding during protein synthesis.. tetracycline : A broad-spectrum polyketide antibiotic produced by the Streptomyces genus of actinobacteria.	3.61	2	0
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.	3.23	1	0
minocycline Minocycline: A TETRACYCLINE analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant STAPHYLOCOCCUS infections.. minocycline : A tetracycline analogue having a dimethylamino group at position 7 and lacking the methyl and hydroxy groups at position 5.	3.23	1	0
piroxicam [no description available]	3.61	2	0	benzothiazine; 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	2.08	1	0	aromatic amide
mobic Meloxicam: A benzothiazine and thiazole derivative that acts as a NSAID and cyclooxygenase-2 (COX-2) inhibitor. It is used in the treatment of RHEUMATOID ARTHRITIS; OSTEOARTHRITIS; and ANKYLOSING SPONDYLITIS.. meloxicam : A benzothiazine that is piroxicam in which the pyridin-2-yl group is replaced by a 5-methyl-1,3-thiazol-2-yl group. A non-steroidal anti-inflammatory drug and selective inhibitor of COX-2, it is used particularly for the management of rheumatoid arthritis.	3.61	2	0	1,3-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.	2.08	1	0	heteroaryl 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.	2.08	1	0	benzothiazine; 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.	3.23	1	0	benzenes; hydroxycoumarin; methyl ketone
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.	3.23	1	0
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.	3.23	1	0	sulfonamide	antiviral drug; HIV protease inhibitor
minocycline hydrochloride [no description available]	2.08	1	0
tigecycline [no description available]	3.61	2	0
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.	2.08	1	0	heteroaryl 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	2.07	1	0
abt-333 dasabuvir: an antiviral agent. dasabuvir : A member of the class of pyrimidone, which is (as the monohydrate of its sodium salt) in combination with ombitasvir, paritaprevir and ritonavir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	2.41	1	0	aromatic ether; naphthalenes; pyrimidone; sulfonamide	antiviral drug; nonnucleoside hepatitis C virus polymerase inhibitor
byl719 [no description available]	7.84	10	1	proline derivative
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.	2.54	2	0
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.	6.28	10	1
cep-32496 agerafenib: inhibitor of RAF family kinases; structure in first source	2.15	1	0
rociletinib rociletinib: inhibits epidermal growth factor receptor tyrosine kinase activity; structure in first source	2.15	1	0
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.	2.15	1	0	aminopyrimidine; aromatic ether; organochlorine compound; piperidines; secondary amino compound; sulfone	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
kpt-251 KPT-251: a selective inhibitor of nuclear export; structure in first source	2.13	1	0
cc214-2 CC214-2: an mTOR kinase inhibitor; structure in first source	3.51	1	0
cc-223 [no description available]	2.57	2	0
azd1208 [no description available]	2.15	1	0
vx-509 [no description available]	2.15	1	0
vx-970 berzosertib: an ATR kinase inhibitor	2.41	1	0	sulfonamide
debio 1347 CH5183284: a fibroblast growth factor receptor antagonist; structure in first source	2.15	1	0
ledipasvir ledipasvir : A benzimidazole derivative that is used in combination with sofosbuvir (under the trade name Harvoni) for the treatment of chronic hepatitis C genotype 1 infection.	2.17	1	0	azaspiro compound; benzimidazole; bridged compound; carbamate ester; carboxamide; fluorenes; imidazoles; L-valine derivative; N-acylpyrrolidine; organofluorine compound	antiviral drug; hepatitis C protease inhibitor
volitinib [no description available]	2.15	1	0
selinexor selinexor: inhibits karyopherin XPO1	2.13	1	0
kpt-276 KPT-276: a selective inhibitor of nuclear export; inhibits both the XPO1 gene and the CRM1 protein	2.13	1	0
osimertinib osimertinib: an EGFR tyrosine kinase inhibitor. osimertinib : A member of the class of aminopyrimidines that is 4-(1-methylindol-3-yl)pyrimidin-2-amine in which one of the amino hydrogens is replaced by a 2-methoxy-4-[2-(dimethylamino)ethyl](methyl)amino-5-acrylamidophenyl group. Used (as the mesylate salt) for treatment of EGFR T790M mutation positive non-small cell lung cancer.	3.73	2	0	acrylamides; aminopyrimidine; biaryl; indoles; monomethoxybenzene; secondary amino compound; secondary carboxamide; substituted aniline; tertiary amino compound	antineoplastic agent; epidermal growth factor receptor antagonist
cb-839 [no description available]	2.31	1	0
as 1842856 5-amino-7-(cyclohexylamino)-1-ethyl-6-fluoro-4-oxo-1,4-dihydroquinoline-3-carboxylic acid: inhibits Foxo1 transactivation; inhibits mRNA levels of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase; structure in first source. AS1842856 : A quinolone that is 4-quinolone substituted at positions 1, 3, 5, 6 and 7 by ethyl, carboxy, amino, fluorine, and cyclohexylamino groups, respectively. It can directly bind to and block the transcription activity of the active forkhead box protein O1 (Foxo1), but not the Ser256-phosphorylated form. It induces cell death and growth arrest in Burkitt lymphoma cell lines at low concentrations.	2.1	1	0	organofluorine compound; primary amino compound; quinolinemonocarboxylic acid; quinolone; secondary amino compound; tertiary amino compound	anti-obesity agent; antineoplastic agent; apoptosis inducer; autophagy inhibitor; forkhead box protein O1 inhibitor; hypoglycemic agent
sar405 SAR405: a Vps34 inhibitor with antineoplastic activity; structure in first source	2.1	1	0
imetelstat [no description available]	3.13	1	0
glutaminase [no description available]	10.5	4	1
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.	13.74	12	3
onc201 TIC10 compound: a TRAIL-dependent antitumor agent; structure in first source	7.17	1	0
fertinex [no description available]	3.23	1	0
ldc4297 LDC4297: a CDK7 inhibitor with antineoplastic activity; structure in first source. LDC4297 : A pyrazolotriazine that is pyrazolo[1,5-a][1,3,5]triazine substituted by a piperidin-3-yloxy group, [2-(1H-pyrazol-1-yl)benzyl]nitrilo group and an isopropyl group at positions 2, 4 and 8 respectively. It is a potent and selective CDK7 inhibitor and exhibits antiviral activity.	2.41	1	0	aromatic ether; piperidines; pyrazoles; pyrazolotriazine; secondary amino compound	antineoplastic agent; antiviral agent; apoptosis inducer; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone: an interleukin-1beta converting enzyme (ICE)-like protease inhibitor	2.48	2	0
nephrin nephrin: gene nephrin is mutated in congenital nephrotic syndrome; amino acid sequence in first source; GenBank F19541; RefSeq NM_019459 (mouse), NM_004646 (human), NM_022628 (rat)	2.55	2	0
s 8932 [no description available]	2.41	1	0	aromatic amine; C-nucleoside; carboxylic ester; nitrile; phosphoramidate ester; pyrrolotriazine	anticoronaviral agent; antiviral drug; prodrug
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).	21.6	375	115
triciribine triciribine: structure. triciribine : A nucleoside analogue in which the nucleobase portion is a 1,4,5,6,8-pentaazaacenaphthylene ring system substituted with an amino group at position 3, and a methyl group at position 5 and is bound to the beta-D-ribofuranosyl moiety by an N(1)-glycosidic linkage.	2.03	1	0
gallium ga 68 dotatate gallium Ga 68 dotatate: A radioactive diagnostic agent used for POSITRON EMISSION TOMOGRAPHY (PET) imaging of SOMATOSTATIN RECEPTOR positive neuroendocrine tumors and malignant abdominal paraganglioma.	2.17	1	0
thromboplastin Thromboplastin: Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.	2.43	2	0
lutetium lu 177 dotatate 177Lu-DOTA-octreotate: an somatostatin receptor agonist	5.37	6	0
exudates Malaysia: A parliamentary democracy with a constitutional monarch in southeast Asia, consisting of 11 states (West Malaysia) on the Malay Peninsula and two states (East Malaysia) on the island of BORNEO. It is also called the Federation of Malaysia. Its capital is Kuala Lumpur. Before 1963 it was the Union of Malaya. It reorganized in 1948 as the Federation of Malaya, becoming independent from British Malaya in 1957 and becoming Malaysia in 1963 as a federation of Malaya, Sabah, Sarawak, and Singapore (which seceded in 1965). The form Malay- probably derives from the Tamil malay, mountain, with reference to its geography. (From Webster's New Geographical Dictionary, 1988, p715 & Room, Brewer's Dictionary of Names, 1992, p329)	2.25	1	0
at 9283 [no description available]	2.63	2	0
otssp167 OTS167: inhibitor of maternal embryonic leucine zipper kinase (MELK) with potential antineoplastic activity	2.15	1	0
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.	3.61	2	0	2-aminopurines; oxopurine; primary alcohol; secondary alcohol	antiviral drug; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
chir 258 [no description available]	2.15	1	0
acyclovir Acyclovir: A GUANOSINE analog that acts as an antimetabolite. Viruses are especially susceptible. Used especially against herpes.. acyclovir : An oxopurine that is guanine substituted by a (2-hydroxyethoxy)methyl substituent at position 9. Used in the treatment of viral infections.	3.93	3	0	2-aminopurines; oxopurine	antimetabolite; antiviral drug
osi 027 OSI 027: inhibits both mTORC1 and mTORC2; structure in first source	3.23	5	0
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.	6.99	4	4	5-formyltetrahydrofolic acid	antineoplastic agent; metabolite
deoxyguanosine [no description available]	2.49	2	0	purine 2'-deoxyribonucleoside; purines 2'-deoxy-D-ribonucleoside	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
guanine [no description available]	4.92	4	2	2-aminopurines; oxopurine; purine nucleobase	algal metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
folic acid folcysteine: used to promote fertility in chickens. vitamin B9 : Any B-vitamin that exhibits biological activity against vitamin B9 deficiency. Vitamin B9 refers to the many forms of folic acid and its derivatives, including tetrahydrofolic acid (the active form), methyltetrahydrofolate (the primary form found in blood), methenyltetrahydrofolate, folinic acid amongst others. They are present in abundance in green leafy vegetables, citrus fruits, and animal products. Lack of vitamin B9 leads to anemia, a condition in which the body cannot produce sufficient number of red blood cells. Symptoms of vitamin B9 deficiency include fatigue, muscle weakness, and pale skin.	10.57	4	0	folic acids; N-acyl-amino acid	human metabolite; mouse metabolite; nutrient
3-methyladenine N3-methyladenine: structure in first source	2.5	2	0
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)	11.16	5	1	cyclic ketal; hydrazone; N-iminopiperazine; N-methylpiperazine; rifamycins; semisynthetic derivative; zwitterion	angiogenesis inhibitor; antiamoebic agent; antineoplastic agent; antitubercular agent; DNA synthesis inhibitor; EC 2.7.7.6 (RNA polymerase) inhibitor; Escherichia coli metabolite; geroprotector; leprostatic drug; neuroprotective agent; pregnane X receptor agonist; protein synthesis inhibitor
clozapine Clozapine: A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent.. clozapine : A benzodiazepine that is 5H-dibenzo[b,e][1,4]diazepine substituted by a chloro group at position 8 and a 4-methylpiperazin-1-yl group at position 11. It is a second generation antipsychotic used in the treatment of psychiatric disorders like schizophrenia.	3.61	2	0	benzodiazepine; 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.	13.05	26	8	dacarbazine
didanosine Didanosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. Didanosine is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase; ddI is then metabolized to dideoxyadenosine triphosphate, its putative active metabolite.. didanosine : A purine 2',3'-dideoxyribonucleoside that is inosine in which the hydroxy groups at both the 2' and the 3' positions on the sugar moiety have been replaced by hydrogen. An antiviral drug, it is used as a medication to treat HIV/AIDS.	3.61	2	0	purine 2',3'-dideoxyribonucleoside	antimetabolite; antiviral drug; EC 2.4.2.1 (purine-nucleoside phosphorylase) inhibitor; geroprotector; HIV-1 reverse transcriptase inhibitor
ganciclovir [no description available]	6.48	7	1	2-aminopurines; oxopurine	antiinfective agent; antiviral drug
valtrex [no description available]	2.08	1	0	organic 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.	3.23	1	0	L-valyl ester	antiviral 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.	3.23	1	0	piperazines; pyrazolopyrimidine; sulfonamide	EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor; vasodilator agent
olanzapine Olanzapine: A benzodiazepine derivative that binds SEROTONIN RECEPTORS; MUSCARINIC RECEPTORS; HISTAMINE H1 RECEPTORS; ADRENERGIC ALPHA-1 RECEPTORS; and DOPAMINE RECEPTORS. It is an antipsychotic agent used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER; and MAJOR DEPRESSIVE DISORDER; it may also reduce nausea and vomiting in patients undergoing chemotherapy.. olanzapine : A benzodiazepine that is 10H-thieno[2,3-b][1,5]benzodiazepine substituted by a methyl group at position 2 and a 4-methylpiperazin-1-yl group at position 4.	3.61	2	0	benzodiazepine; N-arylpiperazine; N-methylpiperazine	antiemetic; dopaminergic antagonist; histamine antagonist; muscarinic antagonist; second generation antipsychotic; serotonergic antagonist; serotonin uptake inhibitor
raltitrexed [no description available]	2.08	1	0	N-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.	3.23	1	0	imidazotriazine; N-alkylpiperazine; N-sulfonylpiperazine	EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; vasodilator agent
allopurinol Allopurinol: A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.. allopurinol : A bicyclic structure comprising a pyrazole ring fused to a hydroxy-substituted pyrimidine ring.	3.61	2	0	nucleobase analogue; organic heterobicyclic compound	antimetabolite; EC 1.17.3.2 (xanthine oxidase) inhibitor; gout suppressant; radical scavenger
2,2'-(hydroxynitrosohydrazono)bis-ethanamine 2,2'-(hydroxynitrosohydrazono)bis-ethanamine: a nitric oxide (NO) generating compound. 1,1-bis(2-aminoethyl)-2-hydroxy-3-oxotriazane : A nitroso compound that is triazane in which the the nitrogen at position 1 is substituted by two 2-aminoethyl groups, that at position 2 is substituted by a hydroxy group, and that at position 3 is substituted by an oxo group.	2.21	1	0
citrovorum factor [no description available]	3.61	2	0	tetrahydrofolic acid
leucovorin 5-formyltetrahydrofolic acid : A formyltetrahydrofolic acid in which the formyl group is located at position 5.	3.23	1	0	formyltetrahydrofolic acid	Escherichia coli metabolite; mouse metabolite
rifapentine rifapentine: cyclopentyl derivative of rifampicin	4.4	3	0	N-alkylpiperazine; N-iminopiperazine; rifamycins	antitubercular agent; leprostatic drug
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.	3.23	1	0	imidazoquinazoline	anticoagulant; antifibrinolytic drug; cardiovascular drug; platelet aggregation inhibitor
forodesine forodesine: structure in first source	3.46	1	1	dihydroxypyrrolidine; pyrrolopyrimidine
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	3.23	1	0	carboxamidine; 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).	11.88	6	2	N-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
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.	2.79	3	0	citrate salt	EC 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.	4.62	4	0	L-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.	3.61	2	0	(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.	3.23	1	0	(trifluoromethyl)benzenes; cyclic acetal; morpholines; phosphoramide; triazoles	antiemetic; neurokinin-1 receptor antagonist; prodrug
tegaserod maleate [no description available]	2.08	1	0	maleate salt	serotonergic agonist
rifabutin [no description available]	4.4	3	0
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.	2.49	2	0	(trifluoromethyl)benzenes; thiopyranopyrimidine	tankyrase inhibitor
ag-879 AG-879: structure given in first source	2.41	1	0
hesperadin [no description available]	2.41	1	0
nintedanib nintedanib : A member of the class of oxindoles that is a kinase inhibitor used (in the form of its ethylsulfonate salt) for the treatment of idiopathic pulmonary fibrosis and cancer.	2.15	1	0
3'-hydroxy-5'-(4-isobutylpiperazinyl)benzoxazinorifamycin KRM 1648: structure in first source	3.19	1	0	phenoxazine
8-hydroxy-2'-deoxyguanosine 8-Hydroxy-2'-Deoxyguanosine: Common oxidized form of deoxyguanosine in which C-8 position of guanine base has a carbonyl group.. 8-hydroxy-2'-deoxyguanosine : Guanosine substituted at the purine 8-position by a hydroxy group. It is used as a biomarker of oxidative DNA damage.	2.49	2	0	guanosines	biomarker
levomefolate calcium levomefolate calcium: an ingredient in Contraceptives, Oral, Combined. levomefolate calcium : An organic calcium salt of (6S)-5-methyltetrahydrofolic acid.	3.23	1	0	organic calcium salt	antidepressant
bay 80-6946 copanlisib: an antineoplastic agent with PI3K inhibitory activity; structure in first source. copanlisib : An imidazoquinazoline that is 2,3-dihydroimidazo[1,2-c]quinazoline substituted by (2-aminopyrimidine-5-carbonyl)amino, methoxy, and 3-(morpholin-4-yl)propoxy groups at positions 5, 7 and 8, respectively. It is a intravenous pan-class I PI3K inhibitor used for the treatment of relapsed follicular lymphoma in patients who have received at least 2 prior systemic therapies.	4.58	2	0
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.	9.61	7	0	aromatic amine; biaryl; hydroxyindoles; phenols; primary amino compound; pyrazolopyrimidine	antineoplastic agent; mTOR inhibitor
nms-e973 NMS-E973: structure in first source	2.25	1	0
sotorasib sotorasib: a KRAS(G12C) inhibitor. sotorasib : A pyridopyrimidine that is pyrido[2,3-d]pyrimidin-2(1H)-one substituted by 4-methyl-2-(propan-2-yl)pyridin-3-yl, (2S)-2-methyl-4-(prop-2-enoyl)piperazin-1-yl, fluoro and 2-fluoro-6-hydroxyphenyl groups at positions 1, 4, 6 and 7, respectively. It is approved for the treatment of patients with non-small cell lung cancer having KRAS(G12C) mutations.	7.41	1	0	acrylamides; methylpyridines; monofluorobenzenes; N-acylpiperazine; phenols; pyridopyrimidine; tertiary amino compound; tertiary carboxamide	antineoplastic agent
concanavalin a Concanavalin A: A MANNOSE/GLUCOSE binding lectin isolated from the jack bean (Canavalia ensiformis). It is a potent mitogen used to stimulate cell proliferation in lymphocytes, primarily T-lymphocyte, cultures.	2	1	0
pyrimidinones Pyrimidinones: Heterocyclic compounds known as 2-pyrimidones (or 2-hydroxypyrimidines) and 4-pyrimidones (or 4-hydroxypyrimidines) with the general formula C4H4N2O.	7.06	10	3

everolimus

Cross-References

Synonyms (82)

Research Excerpts

Overview

Effects

Actions

Treatment

Toxicity

Pharmacokinetics

Compound-Compound Interactions

Bioavailability

Dosage Studied

Roles (5)

Drug Classes (6)

Protein Targets (317)

Potency Measurements

Inhibition Measurements

Activation Measurements

Biological Processes (2590)

Molecular Functions (534)

Ceullar Components (410)

Bioassays (391)

Research

Studies (5,432)

Market Indicators

Research Demand Index: 82.19

Study Types

Clinical Trials (895)

Trial Overview

Trial Outcomes

Overall Objective Response

Clinical Benefit Rate

Number of Participants With Objective Response Plus Stable Disease Rate (CR + PR + SD)

Overall Objective Response

Progression Free Survival (PFS)

Calculated Creatinine Clearance at 6 Month and 12 Month

Number of Participants With Biopsy-proven Acute Rejection (BPAR) Episodes, Graft Loss, Death or Loss to Follow-up

Renal Function Measured by Calculated Glomerular Filtration Rate (GFR Calculated According to the Nankivell Formula)

Serum Creatinine at Month 6 and 12

Number of Participants With Any Wound Healing Disorder During the 12-month Treatment Period

Number of Participants Considered in Failure for the Primary Failure Endpoint at 6 Months Post-transplantation.

Number of Participants Considered in Failure for the Primary Failure Endpoint at 3 Months

Number of Participants Considered in Failure for the Primary Failure Endpoint at 12 Months Post-transplantation.

Number of Participants Who Underwent Any Dialysis Within the 12-month Treatment Period

Duration of Dialysis

Number of Participants With Occurrence of Treatment Failures

Number of Participants With Occurrence of Biopsy Proven Acute Rejection (BPAR), Graft Loss or Death

Number of Participants Who Experienced an Adverse Event or Serious Adverse Event

Changes in Cardiovascular Risk From Month 4.5 to Final Assessment at Month 12

Renal Function (Nankivell Formula) at Month 12 Post Transplantation.

Number of Participants With Safety Parameters

Change in mGFR by Baseline Calculated Creatinine Clearance (Cockcroft-Gault Formula)

Renal Function Assessed by Measured GFR (mGFR)

Target Vessel Failure (TVF)

% Volume Obstruction (% VO)

Acute Success: Clinical Device

Acute Success: Clinical Procedure

Distal Late Loss

In-segment % Angiographic Binary Restenosis (% ABR) Rate

In-segment % Diameter Stenosis (% DS)

In-stent % Angiographic Binary Restenosis (% ABR) Rate

In-stent % Diameter Stenosis (% DS)

In-stent Late Loss

Ischemia Driven Major Adverse Cardiac Event (MACE)

Ischemia Driven Major Adverse Cardiac Event (MACE)

Ischemia Driven Major Adverse Cardiac Event (MACE)

Ischemia Driven Major Adverse Cardiac Event (MACE)

Ischemia Driven Major Adverse Cardiac Event (MACE)

Ischemia Driven Major Adverse Cardiac Event (MACE)

Ischemia Driven Target Lesion Revascularization (ID-TLR)

Ischemia Driven Target Lesion Revascularization (ID-TLR)

Ischemia Driven Major Adverse Cardiac Event(MACE)

Ischemia Driven Target Lesion Revascularization (ID-TLR)

Ischemia Driven Target Lesion Revascularization (ID-TLR)

Ischemia Driven Target Lesion Revascularization (ID-TLR)

Ischemia Driven Target Lesion Revascularization (ID-TLR)

Ischemia Driven Target Lesion Revascularization (ID-TLR)

Ischemia Driven Target Lesion Revascularization (ID-TLR)

Ischemia Driven Target Vessel Revascularization (ID-TVR)