niacinamide has been researched along with Neoplasms in 374 studies
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.
Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
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"This phase I trial evaluated the combination of the marine-derived cyclodepsipeptide plitidepsin (trade name Aplidin) with sorafenib or gemcitabine in advanced cancer and lymphoma patients." | 9.24 | Phase I dose-escalation study of plitidepsin in combination with sorafenib or gemcitabine in patients with refractory solid tumors or lymphomas. ( Alfaro, V; Aspeslagh, S; Bahleda, R; Extremera, S; Fudio, S; Gyan, E; Hollebecque, A; Salles, G; Soria, JC; Soto-Matos, A; Stein, M, 2017) |
"To determine the dose-limiting toxicities (DLT), maximum tolerated dose (MTD), pharmacokinetics, and pharmacodynamics of sorafenib in children with refractory extracranial solid tumors and evaluate the tolerability of the solid tumor MTD in children with refractory leukemias." | 9.16 | A phase I trial and pharmacokinetic study of sorafenib in children with refractory solid tumors or leukemias: a Children's Oncology Group Phase I Consortium report. ( Adamson, PC; Balis, FM; Baruchel, S; Blaney, SM; Burke, M; Fox, E; Glade Bender, J; Ingle, AM; Kim, A; Stempak, D; Weigel, B; Widemann, BC, 2012) |
"Hypertension is one of the major side effects of sorafenib, and reported incidences vary substantially among clinical trials." | 8.90 | Incidence and risk of sorafenib-induced hypertension: a systematic review and meta-analysis. ( Chen, J; Guo, H; Li, S; Li, Y; Liang, X; Meng, H; Shi, B; Zhang, D; Zhu, Y, 2014) |
"Sorafenib, a multi-kinase inhibitor, has been reported to be associated with hypertension (HTN)." | 8.89 | Risk of hypertension in cancer patients treated with sorafenib: an updated systematic review and meta-analysis. ( Funakoshi, T; Galsky, MD; Latif, A, 2013) |
" Eligible studies were prospective clinical trials of patients with cancer assigned single-drug sorafenib at 400 mg twice daily with data on hypertension available." | 8.84 | Incidence and risk of hypertension with sorafenib in patients with cancer: a systematic review and meta-analysis. ( Chen, JJ; Kudelka, A; Lu, J; Wu, S; Zhu, X, 2008) |
"Several case reports suggest sorafenib exposure and sorafenib-induced hyperbilirubinemia may be related to a (TA)(5/6/7) repeat polymorphism in UGT1A1*28 (UGT, uridine glucuronosyl transferase)." | 7.78 | Sorafenib is an inhibitor of UGT1A1 but is metabolized by UGT1A9: implications of genetic variants on pharmacokinetics and hyperbilirubinemia. ( Dahut, W; English, BC; Federspiel, J; Figg, WD; Gardner, ER; Giaccone, G; Jain, L; Kim, A; Kirkland, CT; Kohn, E; Kummar, S; Peer, CJ; Richardson, ED; Sissung, TM; Troutman, SM; Venzon, D; Widemann, B; Woo, S; Yarchoan, R, 2012) |
"Hypertension (HT) and hand-foot skin reactions (HFSR) may be related to the activity of bevacizumab and sorafenib." | 7.76 | Hypertension and hand-foot skin reactions related to VEGFR2 genotype and improved clinical outcome following bevacizumab and sorafenib. ( Baum, CE; Dahut, WL; Danesi, R; English, BC; Figg, WD; Giaccone, G; Jain, L; Kohn, EC; Kummar, S; Liewehr, D; Price, DK; Sissung, TM; Venitz, J; Venzon, D; Yarchoan, R, 2010) |
" However, adverse effects common to the tyrosine kinase inhibitor class occur at a noticeably higher rate with sorafenib use in thyroid cancer patients." | 6.53 | Toxic Effects of Sorafenib in Patients With Differentiated Thyroid Carcinoma Compared With Other Cancers. ( Jaffry, A; Jean, GW; Khan, SA; Mani, RM, 2016) |
"Blood pressure elevation is likely a pharmacodynamic marker of VEGF signaling pathway (VSP) inhibition and could be useful for optimizing safe and effective VSP inhibitor dosing." | 5.35 | Rapid development of hypertension by sorafenib: toxicity or target? ( Atkins, MB; Humphreys, BD, 2009) |
"Acetaldehyde formation was determined by GC-FID analysis in the head space of incubation mixtures." | 5.31 | Rat ventral prostate xanthine oxidase bioactivation of ethanol to acetaldehyde and 1-hydroxyethyl free radicals: analysis of its potential role in heavy alcohol drinking tumor-promoting effects. ( Castro, GD; Castro, JA; Costantini, MH; Delgado de Layño, AM, 2001) |
"This phase I trial evaluated the combination of the marine-derived cyclodepsipeptide plitidepsin (trade name Aplidin) with sorafenib or gemcitabine in advanced cancer and lymphoma patients." | 5.24 | Phase I dose-escalation study of plitidepsin in combination with sorafenib or gemcitabine in patients with refractory solid tumors or lymphomas. ( Alfaro, V; Aspeslagh, S; Bahleda, R; Extremera, S; Fudio, S; Gyan, E; Hollebecque, A; Salles, G; Soria, JC; Soto-Matos, A; Stein, M, 2017) |
"To determine the dose-limiting toxicities (DLT), maximum tolerated dose (MTD), pharmacokinetics, and pharmacodynamics of sorafenib in children with refractory extracranial solid tumors and evaluate the tolerability of the solid tumor MTD in children with refractory leukemias." | 5.16 | A phase I trial and pharmacokinetic study of sorafenib in children with refractory solid tumors or leukemias: a Children's Oncology Group Phase I Consortium report. ( Adamson, PC; Balis, FM; Baruchel, S; Blaney, SM; Burke, M; Fox, E; Glade Bender, J; Ingle, AM; Kim, A; Stempak, D; Weigel, B; Widemann, BC, 2012) |
"Hypertension is one of the major side effects of sorafenib, and reported incidences vary substantially among clinical trials." | 4.90 | Incidence and risk of sorafenib-induced hypertension: a systematic review and meta-analysis. ( Chen, J; Guo, H; Li, S; Li, Y; Liang, X; Meng, H; Shi, B; Zhang, D; Zhu, Y, 2014) |
"Sorafenib, a multi-kinase inhibitor, has been reported to be associated with hypertension (HTN)." | 4.89 | Risk of hypertension in cancer patients treated with sorafenib: an updated systematic review and meta-analysis. ( Funakoshi, T; Galsky, MD; Latif, A, 2013) |
" The most widely employed activator is resveratrol, a small polyphenol that improves insulin sensitivity and vascular function, boosts endurance, inhibits tumor formation, and ameliorates the early mortality associated with obesity in mice." | 4.86 | Biochemical effects of SIRT1 activators. ( Baur, JA, 2010) |
" Sunitinib and sorafenib are multitargeted TKIs that have been demonstrated to induce hypothyroidism and thyroid dysfunction." | 4.85 | Hypothyroidism related to tyrosine kinase inhibitors: an emerging toxic effect of targeted therapy. ( Barnabei, A; Corsello, SM; Gasparini, G; Longo, R; Torino, F, 2009) |
" Eligible studies were prospective clinical trials of patients with cancer assigned single-drug sorafenib at 400 mg twice daily with data on hypertension available." | 4.84 | Incidence and risk of hypertension with sorafenib in patients with cancer: a systematic review and meta-analysis. ( Chen, JJ; Kudelka, A; Lu, J; Wu, S; Zhu, X, 2008) |
"Ferroptosis is a recently identified form of regulated necrosis that can be experimentally induced in cancer cells with the chemical inducer erastin." | 3.80 | Sorafenib induces ferroptosis in human cancer cell lines originating from different solid tumors. ( Baert, M; Chauffert, B; Diouf, M; Galmiche, A; Godin, C; Lachaier, E; Louandre, C; Saidak, Z, 2014) |
"Several case reports suggest sorafenib exposure and sorafenib-induced hyperbilirubinemia may be related to a (TA)(5/6/7) repeat polymorphism in UGT1A1*28 (UGT, uridine glucuronosyl transferase)." | 3.78 | Sorafenib is an inhibitor of UGT1A1 but is metabolized by UGT1A9: implications of genetic variants on pharmacokinetics and hyperbilirubinemia. ( Dahut, W; English, BC; Federspiel, J; Figg, WD; Gardner, ER; Giaccone, G; Jain, L; Kim, A; Kirkland, CT; Kohn, E; Kummar, S; Peer, CJ; Richardson, ED; Sissung, TM; Troutman, SM; Venzon, D; Widemann, B; Woo, S; Yarchoan, R, 2012) |
"Hypertension (HT) and hand-foot skin reactions (HFSR) may be related to the activity of bevacizumab and sorafenib." | 3.76 | Hypertension and hand-foot skin reactions related to VEGFR2 genotype and improved clinical outcome following bevacizumab and sorafenib. ( Baum, CE; Dahut, WL; Danesi, R; English, BC; Figg, WD; Giaccone, G; Jain, L; Kohn, EC; Kummar, S; Liewehr, D; Price, DK; Sissung, TM; Venitz, J; Venzon, D; Yarchoan, R, 2010) |
"Hypertension is a mechanism-based toxicity of sorafenib and other cancer therapeutics that inhibit the vascular endothelial growth factor (VEGF) signaling pathway." | 3.75 | Ambulatory monitoring detects sorafenib-induced blood pressure elevations on the first day of treatment. ( Black, HR; Elliott, WJ; Karrison, T; Kasza, KE; Maitland, ML; Moshier, K; Ratain, MJ; Sit, L; Stadler, WM; Undevia, SD, 2009) |
"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." | 3.30 | 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) |
"Riluzole was given at 100 mg PO BID in combination with sorafenib, beginning at 200 mg PO daily and escalating in 200 mg increments per level in 28-day cycles." | 3.30 | A phase I trial of riluzole and sorafenib in patients with advanced solid tumors: CTEP #8850. ( Aisner, J; Cerchio, R; Chan, N; Chen, S; Ganesan, S; Goodin, S; Gounder, M; Li, J; Lin, H; Malhotra, J; Marinaro, C; Mehnert, JM; Portal, DE; Shih, W; Silk, AW; Spencer, KR; Stein, MN, 2023) |
"Nicotinamide metabolism is important in carcinogenesis." | 3.01 | Nicotinamide N-methyl transferase and cancer-associated thrombosis: insights to prevention and management. ( Ardakany, MR; Ebrahimi, S; Jabbari, P; Rezaei, N, 2023) |
"Four dosing schedules of pimasertib (once daily [qd], 5 days on, 2 days off; qd, 15 days on, 6 days off; continuous qd; continuous twice daily [bid]) were evaluated in patients with advanced solid tumors." | 3.01 | Selective Oral MEK1/2 Inhibitor Pimasertib: A Phase I Trial in Patients with Advanced Solid Tumors. ( Aftimos, P; Awada, A; Delord, JP; Dinulescu, M; Faivre, S; Gomez-Roca, C; Houédé, N; Italiano, A; Kefford, R; Kruse, V; Lebbé, C; Leijen, S; Lesimple, T; Massimini, G; Pages, C; Raymond, E; Rottey, S; Schellens, JHM; Scheuler, A, 2021) |
"Treatment-related adverse events included fatigue and nausea in the monotherapy arm (13% for each), hypothyroidism (30%) in the ramucirumab arm, diarrhea (54%) in the abemaciclib arm, and nausea (25%) in the merestinib arm." | 3.01 | Safety and Clinical Activity of a New Anti-PD-L1 Antibody as Monotherapy or Combined with Targeted Therapy in Advanced Solid Tumors: The PACT Phase Ia/Ib Trial. ( Bang, YJ; Bendell, J; Carlsen, M; Chow, KH; Chung, HC; de Miguel, MJ; Gandhi, L; Italiano, A; Lin, CC; Patnaik, A; Schmidt, S; Su, WC; Szpurka, AM; Vangerow, B; Xu, X; Yap, TA; Yu, D; Zhao, Y, 2021) |
" No significant drug-drug interactions were observed." | 2.90 | A phase I study of the HDM2 antagonist SAR405838 combined with the MEK inhibitor pimasertib in patients with advanced solid tumours. ( de Jonge, M; de Weger, VA; Demers, B; Deutsch, E; Goodstal, S; Hsu, K; Langenberg, MHG; Lolkema, M; Macé, S; Schellens, JHM; Thomas, K; Tuffal, G; Varga, A, 2019) |
"Sorafenib was administered days 1-28 and radiotherapy (30Gy in 10 fractions) was delivered days 8-12 and 15-19." | 2.84 | Phase I dose escalation study of concurrent palliative radiation therapy with sorafenib in three anatomical cohorts (Thorax, Abdomen, Pelvis): The TAP study. ( Brade, A; Chung, C; Dawson, L; Longo, J; Milosevic, M; Murray, L; Oza, A; Wan, J; Wang, L, 2017) |
"About 26 patients with solid tumors were treated in four different dosing schedules." | 2.84 | 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) |
" The maximum tolerated dose (MTD) and recommended phase 2 dose (RP2D) of pimasertib in combination with temsirolimus, safety and pharmacokinetics (PK) were investigated." | 2.84 | Phase I trial of MEK 1/2 inhibitor pimasertib combined with mTOR inhibitor temsirolimus in patients with advanced solid tumors. ( Fu, S; Guo, W; Janku, F; Kurzrock, R; Mita, A; Mita, M; Naing, A; Natale, R; Piha-Paul, SA; Zhao, C, 2017) |
" Plasma levels of refametinib, refametinib metabolite M17, and sorafenib were measured for pharmacokinetic assessments." | 2.82 | A Phase I Study of the Safety, Pharmacokinetics, and Pharmacodynamics of Combination Therapy with Refametinib plus Sorafenib in Patients with Advanced Cancer. ( Adjei, AA; Becerra, CH; Braiteh, F; Clendeninn, NJ; El-Khoueiry, A; Garbo, L; Gunawan, S; Hezel, AF; Iverson, C; Krissel, H; Leffingwell, DP; Manhard, KJ; Miner, JN; Rajagopalan, P; Richards, DA; Shen, Z; Sherman, M; Stephenson, JJ; Wilson, DM; Yeh, LT, 2016) |
"Sorafenib was administered twice daily and topotecan once daily on days 1-5 and 8-12 of each 28-day course." | 2.82 | Pediatric phase I trial of oral sorafenib and topotecan in refractory or recurrent pediatric solid malignancies. ( Caracciolo, J; Gill, J; Goldberg, J; Hale, GA; Isakoff, MS; Juan, TH; Lee, JK; Lush, RM; Manning, K; Mascarenhas, L; Neuger, AM; Reed, DR; Sandler, E; Smith, T; Sullivan, DM, 2016) |
" Because dosing delays and modifications were associated with the MTD, the recommended phase II dose was declared to be pemetrexed 500 mg/m2 every 14 days with oral sorafenib 400 mg given twice daily on days 1-5." | 2.82 | Phase I study of pemetrexed with sorafenib in advanced solid tumors. ( Booth, L; Bose, P; Dent, P; Geyer, CE; Gordon, S; Kmieciak, M; Massey, HD; McGuire, WP; Moran, RG; Poklepovic, A; Quigley, M; Roberts, JD; Shafer, DA; Shrader, E; Strickler, K; Tombes, MB; Wan, W, 2016) |
"Pimasertib showed a favourable pharmacokinetic profile with high absolute bioavailability and a unique metabolic pathway (conjugation with phosphoethanolamine)." | 2.82 | Pimasertib, a selective oral MEK1/2 inhibitor: absolute bioavailability, mass balance, elimination route, and metabolite profile in cancer patients. ( Johne, A; Massimini, G; Scheible, H; Udvaros, I; von Richter, O, 2016) |
"This phase I study evaluated the safety, tolerability, maximum tolerated dose (MTD), and recommended phase II dose (RP2D) of tivantinib combined with sorafenib in patients with advanced solid tumors." | 2.80 | Phase 1 trial of tivantinib in combination with sorafenib in adult patients with advanced solid tumors. ( Adjei, AA; Chai, F; Dy, GK; Goff, L; Lamar, M; Ma, WW; Martell, R; Means-Powell, JA; Puzanov, I; Saif, MW; Santoro, A; Savage, RE; Schwartz, B; Simonelli, M; Sosman, J; Zucali, P, 2015) |
"Patients with advanced solid tumors refractory to standard therapy were eligible." | 2.80 | Dual antiangiogenic inhibition: a phase I dose escalation and expansion trial targeting VEGF-A and VEGFR in patients with advanced solid tumors. ( Falchook, GS; Fu, S; Hong, DS; Huang, M; Janku, F; Jiang, Y; Kurzrock, R; Lin, Q; Naing, A; Parkhurst, K; Piha-Paul, SA; Tsimberidou, AM; Wheler, JJ; Zinner, R, 2015) |
"Entinostat was given orally once every 2 weeks, starting at a dose of 4 mg and escalating to 6 and 10 mg every 2 weeks." | 2.80 | A phase I study of the histone deacetylase (HDAC) inhibitor entinostat, in combination with sorafenib in patients with advanced solid tumors. ( Adjei, AA; Brady, W; DePaolo, D; Ding, Y; Dy, GK; Fetterly, G; Ma, WW; Ngamphaiboon, N; Reungwetwattana, T; Zhao, Y, 2015) |
" 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." | 2.80 | 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) |
"Lenalidomide and sorafenib was well tolerated and associated with disease stabilization for ≥6 months in patients with melanoma, adenoid cystic carcinoma, and ovarian adenocarcinoma." | 2.79 | Phase I clinical trial of lenalidomide in combination with sorafenib in patients with advanced cancer. ( Bedikian, AY; Falchook, G; Fu, S; Ganesan, P; Hong, DS; Janku, F; Kies, M; Kurzrock, R; Laday, S; Naing, A; Piha-Paul, S; Tsimberidou, AM; Wheler, J; Wolff, RA, 2014) |
"Patients with advanced metastatic solid tumors ineligible for or progressing on standard-of-care therapies with no history of cholecystitis or biliary disease were randomized 2:1:1 to receive motesanib 125 mg once daily (Arm A); 75 mg twice daily (BID), 14-days-on/7-days-off (Arm B); or 75 mg BID, 5-days-on/2-days-off (Arm C)." | 2.78 | The effect of different dosing regimens of motesanib on the gallbladder: a randomized phase 1b study in patients with advanced solid tumors. ( Belman, ND; Boccia, RV; Hei, YJ; Hsu, CP; Hurwitz, HI; Lipton, L; McCoy, S; Price, TJ; Rosen, LS; Stephenson, JJ; Tebbutt, NC; Wirth, LJ, 2013) |
"Sorafenib is an oral multikinase inhibitor with antiangiogenic and antitumor activity." | 2.78 | Alternative formulations of sorafenib for use in children. ( Baker, SD; Cai, X; Chen, Z; Christensen, R; Inaba, H; Li, L; Navid, F; Regel, J, 2013) |
"One patient with renal cell cancer had a partial response and 5 patients attained stable disease." | 2.78 | Phase 1 study of sorafenib in combination with bortezomib in patients with advanced malignancies. ( Adjei, AA; Bible, KC; Croghan, G; Erlichman, C; Jett, J; Kaufmann, SH; Kumar, SK; Markovic, SN; Marks, R; Molina, J; Moynihan, T; Qin, R; Quevedo, F; Richardson, R; Tan, A, 2013) |
"Sorafenib dose was escalated from 90 to 110 mg/m(2) twice daily with fixed doses of bevacizumab at 5 mg/kg every 3 weeks and cyclophosphamide at 50 mg/m(2) daily." | 2.78 | Phase I and clinical pharmacology study of bevacizumab, sorafenib, and low-dose cyclophosphamide in children and young adults with refractory/recurrent solid tumors. ( Baker, SD; Billups, CA; Davidoff, AM; Fofana, D; Furman, WL; Hu, S; Leung, W; McCarville, MB; McGregor, LM; Navid, F; Panetta, JC; Reddick, WE; Santana, VM; Spunt, SL; Stewart, CF; Turner, D; Wu, J, 2013) |
" Cohort C explored an alternate schedule of 7-day on/7-day off flat dose capecitabine 1,000 mg BID with continuous dosing of sorafenib 400 mg BID." | 2.77 | A drug interaction study evaluating the pharmacokinetics and toxicity of sorafenib in combination with capecitabine. ( Bendell, JC; Burris, HA; Greco, FA; Hainsworth, JD; Infante, JR; Jones, SF; Lane, CM; Spigel, DR; Yardley, DA, 2012) |
" This study investigated the safety, pharmacokinetics, and preliminary efficacy of sorafenib in combination with gemcitabine and cisplatin." | 2.77 | Phase IB study of sorafenib in combination with gemcitabine and cisplatin in patients with refractory solid tumors. ( Brendel, E; Kornacker, M; Kummer, G; Schultheis, B; Strumberg, D; Xia, C; Zeth, M, 2012) |
"Sorafenib is an oral tyrosine kinase inhibitor approved for the treatment of advanced renal cell carcinoma and hepatocellular carcinoma." | 2.77 | Saturable absorption of sorafenib in patients with solid tumors: a population model. ( Abbas, H; Billemont, B; Blanchet, B; Coriat, R; Dauphin, A; Goldwasser, F; Harcouet, L; Hornecker, M; Mir, O; Ropert, S; Sassi, H; Taieb, F; Tod, M, 2012) |
"Sorafenib is an orally administered multikinase inhibitor that exhibits antiangiogenic and antitumor activity." | 2.77 | Plasma protein binding of sorafenib, a multi kinase inhibitor: in vitro and in cancer patients. ( Pratz, KW; Rudek, MA; Smith, BD; Villarroel, MC; Wright, JJ; Xu, L, 2012) |
"Sorafenib plus 5-FU/LCV was generally well tolerated with encouraging antitumor activity and no clinically relevant drug-drug interactions in patients with advanced solid tumors." | 2.77 | Phase I trial of sorafenib in combination with 5-fluorouracil/leucovorin in advanced solid tumors. ( Atsmon, J; Brendel, E; Bulocinic, S; Figer, A; Geva, R; Nalbandyan, K; Shacham-Shmueli, E; Shpigel, S, 2012) |
"Most common adverse events (AEs) (grade 3-5) included neutropenia (89%), leucopaenia (81%), hand-foot skin reaction (30%) and fatigue (30%)." | 2.77 | Phase I trial to investigate the safety, pharmacokinetics and efficacy of sorafenib combined with docetaxel in patients with advanced refractory solid tumours. ( Awada, A; Bartholomeus, S; Brendel, E; Christensen, O; de Valeriola, D; Delaunoit, T; Gil, T; Hendlisz, A; Lathia, CD; Lebrun, F; Piccart-Gebhart, M; Radtke, M, 2012) |
" Treatment-emergent adverse events were generally mild and included fatigue, nausea, vomiting, and chills." | 2.77 | Safety and pharmacokinetics of ganitumab (AMG 479) combined with sorafenib, panitumumab, erlotinib, or gemcitabine in patients with advanced solid tumors. ( Chan, E; Deng, H; Friberg, G; Gilbert, J; Hwang, YC; Mahalingam, D; McCaffery, I; Michael, SA; Mita, AC; Mita, MM; Mulay, M; Puzanov, I; Rosen, LS; Sarantopoulos, J; Shubhakar, P; Zhu, M, 2012) |
"Fifty-three patients with advanced cancer received oral sorafenib 400 mg bid in continuous 28-day cycles in this open-label study." | 2.76 | A phase I open-label study evaluating the cardiovascular safety of sorafenib in patients with advanced cancer. ( Appleman, LJ; Cihon, F; Mazzu, A; Mita, AC; Shapiro, GI; Sundaresan, PR; Tolcher, AW, 2011) |
"Sorafenib 400 mg was administered twice daily continuously starting at day 2 of cycle 1." | 2.76 | Pharmacokinetic results of a phase I trial of sorafenib in combination with dacarbazine in patients with advanced solid tumors. ( Armand, JP; Brendel, E; Lathia, C; Ludwig, M; Robert, C; Ropert, S; Soria, JC, 2011) |
" Most frequent drug-related adverse events were hand-foot skin reaction (HFSR, 89%), diarrhea (71%), and fatigue (69%)." | 2.76 | Safety and pharmacokinetics of sorafenib combined with capecitabine in patients with advanced solid tumors: results of a phase 1 trial. ( Awada, A; Besse-Hammer, T; Brendel, E; Delesen, H; Gil, T; Hendlisz, A; Joosten, MC; Lathia, CD; Loembé, BA; Piccart-Ghebart, M; Van Hamme, J; Whenham, N, 2011) |
"Sirolimus can be safely combined with sorafenib or sunitinib." | 2.76 | Two drug interaction studies of sirolimus in combination with sorafenib or sunitinib in patients with advanced malignancies. ( Cohen, EE; Fleming, GF; Gangadhar, TC; Geary, D; House, LK; Janisch, L; Kocherginsky, M; Maitland, ML; Ramirez, J; Ratain, MJ; Undevia, SD; Wu, K, 2011) |
" Frequently occurring motesanib-related adverse events included diarrhea (n = 19), nausea (n = 18), vomiting (n = 13), and fatigue (n = 12), which were mostly of worst grade < 3." | 2.76 | Safety and pharmacokinetics of motesanib in combination with gemcitabine and erlotinib for the treatment of solid tumors: a phase 1b study. ( Adewoye, AH; Desai, J; Johnson, J; Kotasek, D; McCoy, S; Price, T; Siu, LL; Sun, YN; Tebbutt, N; Welch, S, 2011) |
"Sorafenib was administered alone for a 1-week run-in period, and then both drugs were given together continuously." | 2.75 | Phase I combination of sorafenib and erlotinib therapy in solid tumors: safety, pharmacokinetic, and pharmacodynamic evaluation from an expansion cohort. ( Bandarchi-Chamkhaleh, B; Chen, EX; Do, T; Duran, I; Le Tourneau, C; MacLean, M; Mak, TW; Metser, U; Nayyar, R; Pham, NA; Quintela-Fandino, M; Siu, LL; Tsao, M; Tusche, MW; Wang, L; Wright, JJ, 2010) |
"This phase Ib study evaluated the safety, pharmacokinetics, pharmacodynamics, and antitumor activity of AMG 102, a fully human monoclonal antibody against hepatocyte growth factor/scatter factor (HGF/SF), in combination with bevacizumab or motesanib in patients with advanced solid tumors." | 2.75 | A phase Ib study of AMG 102 in combination with bevacizumab or motesanib in patients with advanced solid tumors. ( Anderson, A; Beaupre, DM; Deng, H; Leitch, IM; Oliner, KS; Park, DJ; Rosen, PJ; Shubhakar, P; Sweeney, CJ; Yee, LK; Zhu, M, 2010) |
" The most frequently reported adverse events were elevated transaminases, hypophosphatemia, fatigue, anorexia, diarrhoea, nausea, rash and palmar-plantar erythrodysaesthesia." | 2.75 | A phase I dose-escalation study to evaluate safety and tolerability of sorafenib combined with sirolimus in patients with advanced solid cancer. ( Burger, DM; Desar, IM; Timmer-Bonte, JN; van der Graaf, WT; van Herpen, CM, 2010) |
"Sorafenib was administered as a 400-mg dose on day 1 for PK, and continuous daily dosing started on day 8." | 2.74 | Phase I and pharmacokinetic study of sorafenib in patients with hepatic or renal dysfunction: CALGB 60301. ( Abou-Alfa, G; Dees, EC; Desai, A; Edelman, MJ; Fakih, MG; Frank, RC; Hohl, RJ; Hollis, DR; Hwang, J; Kennedy, EB; Lewis, LD; Millard, F; Miller, AA; Murry, DJ; Owzar, K; Ratain, MJ; Villalona-Calero, MA, 2009) |
" Patients were randomized to receive a single oral dose of ketoconazole 400 mg either on day 8 (Sequence 1; n = 7) or day 15 (Sequence 2; n = 7), while pharmacokinetic samples were collected." | 2.73 | Effect of coadministration of ketoconazole, a strong CYP3A4 inhibitor, on pharmacokinetics and tolerability of motesanib diphosphate (AMG 706) in patients with advanced solid tumors. ( Chen, L; Heath, EI; Ingram, M; Lorusso, P; Malburg, L; McGreivy, J; Melara, R; Pilat, MJ; Sun, YN; Wiezorek, J; Yan, L, 2008) |
" Adverse events included hypertension, hand-foot syndrome, diarrhea, transaminitis, and fatigue." | 2.73 | Combination targeted therapy with sorafenib and bevacizumab results in enhanced toxicity and antitumor activity. ( Annunziata, CM; Azad, NS; Cao, L; Chen, HX; Chow, C; Figg, WD; Jain, L; Kohn, EC; Kotz, HL; Kwitkowski, VE; McNally, D; Minasian, L; Posadas, EM; Premkumar, A; Sarosy, G; Steinberg, SM; Wright, JJ, 2008) |
" Sixteen patients (62%) experienced motesanib-related adverse events, most commonly lethargy (n=6), diarrhoea (n=4), fatigue (n=3), headache (n=3), and nausea (n=3)." | 2.73 | Safety and pharmacokinetics of motesanib in combination with gemcitabine for the treatment of patients with solid tumours. ( Lipton, L; McCoy, S; McGreivy, J; Price, TJ; Rosenthal, MA; Sun, YN, 2008) |
"In an extended phase, colorectal cancer (CRC) patients received fixed-dose irinotecan 140 mg and sorafenib 400 mg bid (cohort 4)." | 2.73 | Results from an in vitro and a clinical/pharmacological phase I study with the combination irinotecan and sorafenib. ( Baas, F; Brendel, E; Christensen, O; Gmehling, D; Mross, K; Radtke, M; Steinbild, S; Unger, C; Voliotis, D, 2007) |
" The most frequent adverse events were fatigue (55%), diarrhea (51%), nausea (44%), and hypertension (42%)." | 2.73 | Safety, pharmacokinetics, and efficacy of AMG 706, an oral multikinase inhibitor, in patients with advanced solid tumors. ( Bass, MB; Benjamin, R; Chang, DD; Herbst, RS; Koutsoukos, A; Kurzrock, R; Mulay, M; Ng, C; Polverino, A; Purdom, M; Rosen, LS; Silverman, J; Sun, YN; Van Vugt, A; Wiezorek, JS; Xu, RY, 2007) |
"Sorafenib was administered alone for a 1-week run-in period, and then both drugs were given together continuously, with every 28 days considered as a cycle." | 2.73 | Phase I targeted combination trial of sorafenib and erlotinib in patients with advanced solid tumors. ( Chen, EX; Dancey, J; Duan, L; Duran, I; Hirte, H; Hotté, SJ; Lathia, C; MacLean, M; Pond, GR; Siu, LL; Turner, S; Walsh, S; Wright, JJ, 2007) |
"Sorafenib is a novel oral multikinase inhibitor that targets Raf serine/threonine and receptor tyrosine kinases, and inhibits tumor cell proliferation and angiogenesis." | 2.73 | Phase I and pharmacokinetic study of sorafenib, an oral multikinase inhibitor, in Japanese patients with advanced refractory solid tumors. ( Araki, K; Ebi, H; Kawada, K; Kim, YI; Kitagawa, K; Minami, H; Mukai, H; Nakajima, H; Nakajima, K; Tahara, M, 2008) |
"We previously reported a flow cytometry technique to monitor pharmacodynamic effects of the raf kinase inhibitor BAY 43-9006 based on the ability of phorbol ester (PMA) to phosphorylate extracellular-regulated kinase (ERK) in peripheral blood (Chow et al." | 2.72 | Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells. ( Chow, S; Hedley, D; Tong, FK, 2006) |
" Sorafenib demonstrated single-agent activity in Phase I studies, and was tolerated and inhibited tumor growth in combination with doxorubicin in preclinical studies." | 2.72 | Results of a Phase I trial of sorafenib (BAY 43-9006) in combination with doxorubicin in patients with refractory solid tumors. ( Brendel, E; Christensen, O; Flashar, C; Grubert, M; Henning, BF; Hilger, RA; Kupsch, P; Ludwig, M; Passarge, K; Richly, H; Scheulen, ME; Schwartz, B; Seeber, S; Strumberg, D; Voigtmann, R, 2006) |
" The most frequently reported adverse events over multiple cycles were gastrointestinal (75%), dermatologic (71%), constitutional (68%), pain (64%), or hepatic (61%) related." | 2.71 | Phase I safety and pharmacokinetics of BAY 43-9006 administered for 21 days on/7 days off in patients with advanced, refractory solid tumours. ( Awada, A; Bartholomeus, S; Brendel, E; de Valeriola, D; Gil, T; Haase, CG; Hendlisz, A; Mano, M; Piccart, M; Schwartz, B; Strumberg, D, 2005) |
" BAY 43-9006 was well tolerated, with mild to moderate toxicities; only six patients discontinued study therapy due to adverse events." | 2.71 | Phase I study to determine the safety and pharmacokinetics of the novel Raf kinase and VEGFR inhibitor BAY 43-9006, administered for 28 days on/7 days off in patients with advanced, refractory solid tumors. ( Cihon, F; Hirte, HW; Hotte, SJ; Lathia, C; Moore, M; Oza, A; Petrenciuc, O; Schwartz, B; Siu, L, 2005) |
" This phase I, open-label, nonrandomized, noncontrolled, single-arm, dose escalation study was done to determine the maximum tolerated dose (MTD), safety profile, pharmacokinetic variables, effect on biomarkers, and tumor response with BAY 43-9006 in 19 patients with advanced, refractory solid tumors." | 2.71 | Safety and pharmacokinetics of the dual action Raf kinase and vascular endothelial growth factor receptor inhibitor, BAY 43-9006, in patients with advanced, refractory solid tumors. ( Clark, JW; Eder, JP; Lathia, C; Lenz, HJ; Ryan, D, 2005) |
"Ten patients with advanced cancers were studied." | 2.68 | Human tumor blood flow is enhanced by nicotinamide and carbogen breathing. ( Chaplin, DJ; Hill, SA; Hoskin, PJ; Powell, ME; Saunders, MI, 1997) |
" Despite being orally bioavailable in cancer patients, pimasertib undergoes faster clearance with a short elimination half-life." | 2.58 | Pharmacology of Pimasertib, A Selective MEK1/2 Inhibitor. ( Srinivas, NR, 2018) |
"Sorafenib is a multikinase-tyrosine kinase inhibitor commonly used in a variety of cancers." | 2.55 | Risk of serious adverse events and fatal adverse events with sorafenib in patients with solid cancer: a meta-analysis of phase 3 randomized controlled trials†. ( Ando, M; Ando, Y; Gyawali, B; Honda, K; Shimokata, T, 2017) |
"The old-fashioned anticancer approaches, aiming at arresting cancer cell proliferation interfering with non-specific targets (e." | 2.55 | Kinase Inhibitors in Multitargeted Cancer Therapy. ( Bonsignore, R; Gentile, C; Lauria, A; Martorana, A, 2017) |
"Failure in cancer drug development exacts heavy burdens on patients and research systems." | 2.55 | Inefficiencies and Patient Burdens in the Development of the Targeted Cancer Drug Sorafenib: A Systematic Review. ( Carlisle, B; Fergusson, D; Hachem, Y; Kimmelman, J; Mattina, J, 2017) |
" However, adverse effects common to the tyrosine kinase inhibitor class occur at a noticeably higher rate with sorafenib use in thyroid cancer patients." | 2.53 | Toxic Effects of Sorafenib in Patients With Differentiated Thyroid Carcinoma Compared With Other Cancers. ( Jaffry, A; Jean, GW; Khan, SA; Mani, RM, 2016) |
" We detected a moderate dose-response in one clinically approved indication, hepatocellular carcinoma, but not in another approved malignancy, renal cell carcinoma, or when data were pooled across all malignancies tested." | 2.53 | Design and Reporting of Targeted Anticancer Preclinical Studies: A Meta-Analysis of Animal Studies Investigating Sorafenib Antitumor Efficacy. ( Fergusson, D; Henderson, VC; Kimmelman, J; MacKinnon, N; Mattina, J, 2016) |
" The development of in vivo tools to study OATP1A/1B functions has greatly advanced our mechanistic understanding of their functional role in drug pharmacokinetics, and their implications for therapeutic efficacy and toxic side effects of anticancer and other drug treatments." | 2.53 | The impact of Organic Anion-Transporting Polypeptides (OATPs) on disposition and toxicity of antitumor drugs: Insights from knockout and humanized mice. ( Durmus, S; Schinkel, AH; van Hoppe, S, 2016) |
"Sorafenib treatment results in long-term efficacy and low incidence of life-threatening toxicities." | 2.52 | The adverse effects of sorafenib in patients with advanced cancers. ( Gao, ZH; Li, Y; Qu, XJ, 2015) |
"Sorafenib is a relatively new multi-kinase inhibitor used to treat a wide range of cancers." | 2.52 | Risk of treatment-related mortality with sorafenib in cancer patients: a meta-analysis of 20 randomly controlled trials : Risk of sorafenib-associated death. ( Cheng, X; Cheng, Y; Kuang, Y; Pan, X; Yang, X, 2015) |
"Diarrhea was the most common GI event." | 2.50 | Risk of gastrointestinal events with sorafenib, sunitinib and pazopanib in patients with solid tumors: a systematic review and meta-analysis of clinical trials. ( Berardi, R; Burattini, L; Cascinu, S; Conti, A; De Giorgi, U; Iacovelli, R; Muzzonigro, G; Pantano, F; Santini, D; Santoni, M, 2014) |
"Sorafenib is a multi-tyrosine kinase inhibitor (TKI)." | 2.50 | Drug safety evaluation of sorafenib for treatment of solid tumors: consequences for the risk assessment and management of cancer patients. ( Alexandre, J; Blanchet, B; Boissier, E; Boudou-Rouquette, P; Cessot, A; Coriat, R; Durand, JP; Giroux, J; Goldwasser, F; Huillard, O; Thomas-Schoemann, A; Vidal, M, 2014) |
"Sorafenib was approved by the FDA in fast track for advanced renal cell cancer and hepatocellular cancer and shows good clinical activity in thyroid cancer." | 2.50 | Sorafenib: targeting multiple tyrosine kinases in cancer. ( Hasskarl, J, 2014) |
"Recently, cancer therapies have been supplemented by vascular endothelial growth factor (VEGF) inhibitors as anti-angiogenic agents." | 2.50 | Clinicopathological spectrum of kidney diseases in cancer patients treated with vascular endothelial growth factor inhibitors: a report of 5 cases and review of literature. ( Chandran, CB; Flombaum, CD; Glezerman, IG; Salvatore, SP; Seshan, SV; Usui, J, 2014) |
"Reducing cancer-treatment toxicity was a largely ignored research agenda, which is now emerging as an active area of investigation." | 2.49 | Body composition in chemotherapy: the promising role of CT scans. ( Prado, CM, 2013) |
"Variability in body composition of cancer patients may be a source of disparities in the metabolism of cytotoxic agents." | 2.49 | Assessment of nutritional status in cancer--the relationship between body composition and pharmacokinetics. ( Baracos, VE; Maia, YL; Ormsbee, M; Prado, CM; Sawyer, MB, 2013) |
"Sorafenib and sunitinib have been approved for the treatment of renal, hepatocellular, gastrointestinal and pancreatic neuoendocrine carcinomas." | 2.49 | Inhibition of RET activated pathways: novel strategies for therapeutic intervention in human cancers. ( Bottai, G; Santarpia, L, 2013) |
"Sorafenib is an oral multikinase inhibitor that acts by inhibiting tumor growth and disrupting tumor microvasculature through antiproliferative, anti-angiogenic and proapoptotic effects." | 2.48 | Molecular targeted therapies for cancer: sorafenib mono-therapy and its combination with other therapies (review). ( Ibrahim, N; Walsh, WR; Yang, JL; Yu, Y, 2012) |
"Resistance of cancer cells to chemotherapy and/or radiotherapy is a major challenge to current anticancer treatment." | 2.48 | Using NF-κB as a molecular target for theranostics in radiation oncology research. ( Chiang, IT; Hsu, FT; Hwang, JJ; Liu, YC, 2012) |
" On the other hand, the optimal combination and dosage of these drugs, selection of the apropriate biomarker and better understanding of the conflicting role of PDGFR and FGFR signaling in angiogenesis remain future challenges." | 2.48 | [Possibilities for inhibiting tumor-induced angiogenesis: results with multi-target tyrosine kinase inhibitors]. ( Döme, B; Török, S, 2012) |
" 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." | 2.48 | Evidence for therapeutic drug monitoring of targeted anticancer therapies. ( Balakrishnar, B; Clements, A; Gao, B; Gurney, H; Wong, M; Yeap, S, 2012) |
"During the last years novel anticancer treatments targeting specific molecules or genes involved in cancer development are being developed to improve outcome and reduce side-effects." | 2.48 | Polymorphisms to predict outcome to the tyrosine kinase inhibitors gefitinib, erlotinib, sorafenib and sunitinib. ( Erdem, L; Giovannetti, E; Honeywell, R; Leon, LG; Peters, GJ, 2012) |
"Most of the new anticancer treatments currently in developmental stage are based on targeted therapies, acting against numerous tumor cell abnormalities, like growth factors et their receptors, cell proliferation-inducing factors, molecules involved in DNA repair, cell death inducers, tumor invasion and angiogenesis." | 2.47 | [Indications and current development of new targeted therapies in pediatric oncology]. ( Geoerger, B; Leblond, P, 2011) |
"While loss of FBW7 sensitizes cancer cells to certain drugs, FBW7-/- cells are more resistant to other types of chemotherapies." | 2.47 | The two faces of FBW7 in cancer drug resistance. ( Fukushima, H; Gao, D; Inuzuka, H; Lau, AW; Liu, P; Wan, L; Wang, Z; Wei, W, 2011) |
"Targeted therapies against cancer have become more and more important." | 2.46 | Compounds in clinical Phase III and beyond. ( Bayer, M; Berdel, WE; Kessler, T; Liersch, R; Mesters, RM; Schwöppe, C, 2010) |
"Sorafenib was approved by the FDA in fast track for advanced renal cell cancer and hepatocellular cancer and shows good clinical activity in thyroid cancer." | 2.46 | Sorafenib. ( Hasskarl, J, 2010) |
" Strict monitoring of treatment-related adverse effects must be conducted in order to allow the early detection of cardiovascular toxicities and their prompt medication." | 2.46 | Cardiovascular safety of VEGF-targeting therapies: current evidence and handling strategies. ( Brandes, AA; Franceschi, E; Girardi, F, 2010) |
"Tumor tissue is composed of both cancer cells and stromal cells recruited from normal tissue." | 2.46 | Tumor-stromal cell interactions and opportunities for therapeutic intervention. ( Udagawa, T; Wood, M, 2010) |
"Targeted therapies are widely used in cancer because of their effectiveness, even in tumours that are resistant to conventional chemotherapy such as kidney or hepatocellular carcinomas." | 2.45 | [Targeted therapies and their indications in solid neoplasias]. ( Dreyer, C; Faivre, S; Raymond, E, 2009) |
"Increasing use of targeted anticancer agents that inhibit tyrosine kinase signaling (monoclonal antibodies or tyrosine kinase inhibitors) has dramatically improved the survival of patients with malignancies." | 2.45 | Cardiac dysfunction induced by novel targeted anticancer therapy: an emerging issue. ( Chen, MH, 2009) |
"Future potential uses of bevacizumab in cancer therapy will be discussed." | 2.45 | The role of antiangiogenesis therapy: bevacizumab and beyond. ( Cortés-Funes, H, 2009) |
"Sorafenib is an oral multikinase inhibitor that has been proven effective as a single-agent therapy in renal cell carcinoma, and there is a strong rationale for investigating its use in combination with other agents." | 2.44 | Selected combination therapy with sorafenib: a review of clinical data and perspectives in advanced solid tumors. ( Awada, A; D'Hondt, V; Dal Lago, L, 2008) |
"Sorafenib is an oral multikinase inhibitor that inhibits Raf serine/threonine kinases and receptor tyrosine kinases involved in tumor growth and angiogenesis." | 2.44 | Safety, pharmacokinetics, and preliminary antitumor activity of sorafenib: a review of four phase I trials in patients with advanced refractory solid tumors. ( Awada, A; Clark, JW; Eder, JP; Hendlisz, A; Hirte, HW; Lenz, HJ; Moore, MJ; Richly, H; Schwartz, B; Strumberg, D, 2007) |
"Clinical trials showing longer survival when chemotherapy is combined with antiangiogenic agents (AAs) have led to growing interest in designing combined modality protocols that exploit abnormalities in tumor vasculature." | 2.44 | Design of clinical trials of radiation combined with antiangiogenic therapy. ( Senan, S; Smit, EF, 2007) |
"Approved for the treatment of advanced renal cell carcinoma by the US FDA and other regulatory agencies, sorafenib is an agent with multiple targets that may also prove beneficial in other malignancies." | 2.44 | Sorafenib: delivering a targeted drug to the right targets. ( Flaherty, KT, 2007) |
"Advances in understanding the role of vascular endothelial growth factor (VEGF) in normal physiology are giving insight into the basis of adverse effects attributed to the use of VEGF inhibitors in clinical oncology." | 2.44 | Mechanisms of adverse effects of anti-VEGF therapy for cancer. ( Kamba, T; McDonald, DM, 2007) |
"Angiogenesis does not initiate malignancy but promotes tumor progression and metastasis." | 2.44 | [Oral drugs inhibiting the VEGF pathway]. ( Armand, JP; Mir, O; Ropert, S, 2007) |
"Molecularly targeted anticancer therapies are now available that have been rationally designed to interact with specific proteins associated with tumour development or progression." | 2.44 | New developments in multitargeted therapy for patients with solid tumours. ( Faivre, S; Le Tourneau, C; Raymond, E, 2008) |
"Sorafenib (Nexavar) is an oral multi-kinase inhibitor that inhibits Raf serine/threonine kinases and receptor tyrosine kinases involved in tumor growth and angiogenesis." | 2.44 | Safety and anti-tumor activity of sorafenib (Nexavar) in combination with other anti-cancer agents: a review of clinical trials. ( Awada, A; Takimoto, CH, 2008) |
" The most common Grade 3/4 adverse events experienced on thalidomide monotherapy were venous thrombosis (3." | 2.44 | Systematic review to establish the safety profiles for direct and indirect inhibitors of p38 Mitogen-activated protein kinases for treatment of cancer. A systematic review of the literature. ( Claflin, JE; Crean, S; Lahn, M; Linz, H; Noel, JK; Ranganathan, G, 2008) |
"Here, we review recent findings that cancer cell sensitivity to TRAIL is greatly increased when the Bcl-2 family protein Mcl-1 is down-regulated by the Raf/vascular endothelial growth factor kinase inhibitor sorafenib, a Food and Drug Administration-approved cancer drug." | 2.44 | Mcl-1: a gateway to TRAIL sensitization. ( El-Deiry, WS; Kim, SH; Ricci, MS, 2008) |
"Sorafenib (BAY 43-9006) is a novel oral bis-aryl urea compound originally developed as an inhibitor to RAF kinase for its anti-proliferative property." | 2.43 | Sorafenib (BAY 43-9006): review of clinical development. ( Chen, EX; Ng, R, 2006) |
"Sorafenib was well tolerated at the RDP, and induced sustained disease stabilization, particularly in patients with skin toxicity/diarrhoea." | 2.43 | Pooled safety analysis of BAY 43-9006 (sorafenib) monotherapy in patients with advanced solid tumours: Is rash associated with treatment outcome? ( Awada, A; Brueckner, A; Christensen, O; Clark, JW; Hirte, H; Hofstra, E; Piccart, P; Schwartz, B; Seeber, S; Strumberg, D; Voliotis, D, 2006) |
"Cachexia is a debilitating wasting syndrome and highly prevalent comorbidity in cancer patients." | 1.91 | NAD ( Beltrà, M; Corrà, S; Fornelli, C; Hsu, MY; Hulmi, JJ; Kivelä, R; Moletta, L; Penna, F; Pirinen, E; Pöllänen, N; Porporato, PE; Sandri, M; Sartori, R; Tonttila, K; Viscomi, C; Zampieri, S, 2023) |
"Multiple solid cancers distantly increase expression of Nnmt and its product 1-methylnicotinamide (MNAM) in the liver." | 1.72 | Remote solid cancers rewire hepatic nitrogen metabolism via host nicotinamide-N-methyltransferase. ( Bamba, T; Enya, S; Hamanishi, J; Harata, A; Hojo, H; Izumi, Y; Kashio, S; Kawamoto, H; Kawaoka, S; Konishi, R; Mandai, M; Miura, M; Mizuno, R; Nakao, M; Suzuki, Y; Takahashi, M; Yoda, M, 2022) |
"The metabolic challenges present in tumors attenuate the metabolic fitness and antitumor activity of tumor-infiltrating T lymphocytes (TILs)." | 1.56 | Disturbed mitochondrial dynamics in CD8 ( Bock, C; Chao, T; Cheng, WC; Coukos, G; Franco, F; Gao, M; Genolet, R; Ho, PC; Imrichova, H; Jandus, C; Jiang, YF; Liu, PS; Locasale, JW; Rincon-Restrepo, M; Tang, L; Vannini, N; Wang, H; Xiao, Z; Yu, YR; Zippelius, A, 2020) |
"Treatment with capecitabine did not significantly increase the mean antioxidant concentration." | 1.48 | Influence of Sorafenib, Sunitinib and Capecitabine on the Antioxidant Status of the Skin. ( Fuss, H; Jung, S; Lademann, J, 2018) |
"In our study, a wide variety of tumors underwent comprehensive genomic profiling for hundreds of known cancer genes using the FoundationOne™ or FoundationOne Heme™ comprehensive genomic profiling assays." | 1.43 | The distribution of BRAF gene fusions in solid tumors and response to targeted therapy. ( Ali, SM; Chmielecki, J; Chudnovsky, J; Elvin, JA; Gay, L; Gray, A; Johnson, A; Lipson, D; Miller, VA; Nakamura, BN; Roels, S; Ross, JS; Stephens, PJ; Vergilio, JA; Wang, K; Wong, MK; Yelensky, R, 2016) |
" The dosage was temporarily reduced in only two patients, and oral steroids were added in four." | 1.43 | Widespread morbilliform rash due to sorafenib or vemurafenib treatment for advanced cancer; experience of a tertiary dermato-oncology clinic. ( Amitay-Laish, I; Didkovsky, E; Hendler, D; Hodak, E; Lotem, M; Merims, S; Ollech, A; Popovtzer, A; Stemmer, SM, 2016) |
"Thirty-six patients with advanced cancer underwent molecular profiling with NGS with the intent of clinical application of available matched targeted agents." | 1.43 | Pilot Study of a Next-Generation Sequencing-Based Targeted Anticancer Therapy in Refractory Solid Tumors at a Korean Institution. ( Kim, HR; Kim, JH; Kim, S; Kwack, K; Lee, MG; Lim, SM; Moon, YW; Park, HS, 2016) |
" The structural difference between sorafenib and t-CUPM significantly reduces inhibitory spectrum of kinases by this analogue, and pharmacokinetic characterization demonstrates a 20-fold better oral bioavailability of t-CUPM than sorafenib in mice." | 1.42 | Biological evaluation of a novel sorafenib analogue, t-CUPM. ( Hammock, BD; Hwang, SH; Liu, JY; Morisseau, C; Wecksler, AT; Weiss, RH; Wettersten, HI; Wu, J, 2015) |
"Treatment with small molecule tyrosine kinase inhibitors (TKIs) has improved survival in many cancers, yet has been associated with an increased risk of adverse events." | 1.42 | Cardiovascular toxicity of multi-tyrosine kinase inhibitors in advanced solid tumors: a population-based observational study. ( Amir, E; Ethier, JL; Krzyzanowska, MK; Ocana, A; Seruga, B; Srikanthan, A, 2015) |
"Effective choice of anticancer drugs is important problem of modern medicine." | 1.42 | Combinatorial high-throughput experimental and bioinformatic approach identifies molecular pathways linked with the sensitivity to anticancer target drugs. ( Aliper, A; Borisov, N; Buzdin, A; Kholodenko, R; Malakhova, G; Roumiantsev, S; Shepelin, D; Suntsova, M; Vasilov, R; Venkova, L; Zhavoronkov, A, 2015) |
" Population pharmacokinetic (POPPK) modeling of motesanib and M4, an active metabolite, was performed to assess sources of variability in cancer patients." | 1.42 | Population pharmacokinetic modeling of motesanib and its active metabolite, M4, in cancer patients. ( Gosselin, NH; Hsu, CP; Lu, JF; Mouksassi, MS, 2015) |
"Sorafenib (SRF) is a multi-kinase inhibitor that has been shown to have antitumor activity against several types of cancers, but the effect of SRF on EBV-transformed B cells is unknown." | 1.40 | ROS-mediated JNK/p38-MAPK activation regulates Bax translocation in Sorafenib-induced apoptosis of EBV-transformed B cells. ( Choi, Y; Hur, DY; Kim, D; Kim, YS; Lee, HK; Park, GB, 2014) |
"Loss-of-function mutations in the Werner syndrome gene are associated with the premature onset of age-related diseases." | 1.40 | Downregulation of the Werner syndrome protein induces a metabolic shift that compromises redox homeostasis and limits proliferation of cancer cells. ( Cadenas, E; Chen, LY; Comai, L; Iglesias-Pedraz, JM; Li, B; Reddy, S; Yin, F, 2014) |
"In an application to data from hepatocellular carcinoma patients, the coupled stepwise approach is seen to facilitate joint interpretation of the different cause-specific Cox models." | 1.40 | Coupled variable selection for regression modeling of complex treatment patterns in a clinical cancer registry. ( Binder, H; Elsäßer, A; Schmidtmann, I; Weinmann, A, 2014) |
"As a result, NNMT-expressing cancer cells have an altered epigenetic state that includes hypomethylated histones and other cancer-related proteins combined with heightened expression of protumorigenic gene products." | 1.39 | NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink. ( Cravatt, BF; Ulanovskaya, OA; Zuhl, AM, 2013) |
"Treatment with sorafenib led to an increased keratinocyte proliferation and a tendency toward increased mitogen-activated protein kinase (MAPK) pathway activation in normal skin." | 1.38 | Skin tumors induced by sorafenib; paradoxic RAS-RAF pathway activation and oncogenic mutations of HRAS, TP53, and TGFBR1. ( André, J; Arnault, JP; Boussemart, L; Druillennec, S; Dumaz, N; Eggermont, AM; Escudier, B; Eychène, A; Hollville, E; Kamsu-Kom, N; Lacroix, L; Larcher, M; Malka, D; Mateus, C; Robert, C; Sarasin, A; Soria, JC; Spatz, A; Tomasic, G; Vagner, S; Wechsler, J, 2012) |
" Furthermore, the RAIN-Droplet model has facilitated the discovery of a novel pro-angiogenic capacity for sorafenib, which may impact the clinical application and dosing regimen of that drug." | 1.38 | RAIN-Droplet: a novel 3D in vitro angiogenesis model. ( Dong, Z; Nör, JE; Zeitlin, BD, 2012) |
"Sorafenib displays major interpatient pharmacokinetic variability." | 1.38 | Variability of sorafenib toxicity and exposure over time: a pharmacokinetic/pharmacodynamic analysis. ( Billemont, B; Blanchet, B; Boudou-Rouquette, P; Cabanes, L; Coriat, R; Franck, N; Goldwasser, F; Mir, O; Ropert, S; Tod, M, 2012) |
" Taken together, the data suggest that premexetred and sorafenib act synergistically to enhance tumor killing via the promotion of a toxic form of autophagy that leads to activation of the intrinsic apoptosis pathway, and predict that combination treatment represents a future therapeutic option in the treatment of solid tumors." | 1.37 | Sorafenib enhances pemetrexed cytotoxicity through an autophagy-dependent mechanism in cancer cells. ( Bareford, MD; Burow, ME; Cruickshanks, N; Dent, P; Eulitt, P; Fisher, PB; Grant, S; Hamed, HA; Hubbard, N; Moran, RG; Nephew, KP; Park, MA; Tang, Y; Tye, G; Yacoub, A, 2011) |
" Taken together, the data suggest that premexetred and sorafenib act synergistically to enhance tumor killing via the promotion of a toxic form of autophagy that leads to activation of the intrinsic apoptosis pathway, and predict that combination treatment represents a future therapeutic option in the treatment of solid tumors." | 1.37 | Sorafenib enhances pemetrexed cytotoxicity through an autophagy-dependent mechanism in cancer cells. ( Bareford, MD; Burow, ME; Cruickshanks, N; Dent, P; Fisher, PB; Grant, S; Hamed, HA; Moran, RG; Nephew, KP; Tang, Y, 2011) |
"Patients with advanced cancer including breast cancer, hepatocellular cancer and urothelial cancer frequently receive a chemotherapy regimen containing doxorubicin." | 1.36 | Sensitivity of doxorubicin-resistant cells to sorafenib: possible role for inhibition of eukaryotic initiation factor-2alpha phosphorylation. ( Eto, M; Itsumi, M; Naito, S; Shiota, M; Tada, Y; Takeuchi, A; Tatsugami, K; Uchiumi, T; Yokomizo, A, 2010) |
"Sorafenib is an inhibitor of multiple kinases (e." | 1.36 | Initial testing (stage 1) of the multi-targeted kinase inhibitor sorafenib by the pediatric preclinical testing program. ( Carol, H; Gorlick, R; Houghton, PJ; Kang, MH; Keir, ST; Kolb, EA; Lock, R; Maris, JM; Morton, CL; Reynolds, CP; Smith, MA; Watkins, A, 2010) |
"Sorafenib is a targeted drug specifically engineered to inhibit Raf serine/threonine kinases, which are part of the reticular activating system (RAS) oncogene pathway." | 1.35 | Cutaneous drug eruptions induced by sorafenib: a case series. ( Kung, EF; Maddox, JS; Petronic-Rosic, V; Sethi, A, 2008) |
"The primary objective of Phase II cancer trials is to evaluate the potential efficacy of a new regimen in terms of its antitumor activity in a given type of cancer." | 1.35 | Selecting promising treatments in randomized Phase II cancer trials with an active control. ( Cheung, YK, 2009) |
"The treatment of some cancer patients has shifted from traditional, non-specific cytotoxic chemotherapy to chronic treatment with molecular targeted therapies." | 1.35 | Therapeutic Drug Monitoring of the new targeted anticancer agents imatinib, nilotinib, dasatinib, sunitinib, sorafenib and lapatinib by LC tandem mass spectrometry. ( Decosterd, LA; Duchosal, MA; Haouala, A; Leyvraz, S; Montemurro, M; Ris, HB; Rochat, B; Widmer, N; Zaman, K; Zanolari, B, 2009) |
"Testing agents in cancers with multiple disease subtypes, in which the activity of a new treatment may vary between subtypes, presents statistical and logistical challenges." | 1.35 | Multiple Histology Phase II Trials. ( Crowley, J; Leblanc, M; Rankin, C, 2009) |
"Blood pressure elevation is likely a pharmacodynamic marker of VEGF signaling pathway (VSP) inhibition and could be useful for optimizing safe and effective VSP inhibitor dosing." | 1.35 | Rapid development of hypertension by sorafenib: toxicity or target? ( Atkins, MB; Humphreys, BD, 2009) |
" Once daily oral dosing of BAY 43-9006 demonstrated broad-spectrum antitumor activity in colon, breast, and non-small-cell lung cancer xenograft models." | 1.32 | BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. ( Adnane, L; Auclair, D; Bollag, G; Cao, Y; Carter, C; Chen, C; Eveleigh, D; Gawlak, S; Gedrich, R; Liu, L; Lynch, M; McHugh, M; McNabola, A; Post, LE; Riedl, B; Rong, H; Rowley, B; Shujath, J; Tang, L; Taylor, I; Trail, PA; Vincent, P; Voznesensky, A; Wilhelm, SM; Wilkie, D; Zhang, X, 2004) |
"Acetaldehyde formation was determined by GC-FID analysis in the head space of incubation mixtures." | 1.31 | Rat ventral prostate xanthine oxidase bioactivation of ethanol to acetaldehyde and 1-hydroxyethyl free radicals: analysis of its potential role in heavy alcohol drinking tumor-promoting effects. ( Castro, GD; Castro, JA; Costantini, MH; Delgado de Layño, AM, 2001) |
" Neither the peak concentration nor the area under the concentration/time curve (AUC) of nicotinamide, nor the main metabolites of nicotinamide appeared to correlate with the incidence of toxicity." | 1.29 | Nicotinamide pharmacokinetics in normal volunteers and patients undergoing palliative radiotherapy. ( Dennis, MF; Hodgkiss, RJ; Hoskin, PJ; Rojas, A; Saunders, MI; Stratford, MR, 1996) |
"Theophylline and MELPH were also found to act synergistically on the induction of SCEs." | 1.27 | Synergistic induction of sister-chromatid exchanges in lymphocytes from normal subjects and from patients under cytostatic therapy by inhibitors of poly(ADP-ribose)polymerase and antitumour agents. ( Dozi-Vassiliades, J; Hatzitheodoridou, P; Kourakis, A; Mourelatos, D; Tsiouris, J, 1985) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 26 (6.95) | 18.7374 |
1990's | 20 (5.35) | 18.2507 |
2000's | 111 (29.68) | 29.6817 |
2010's | 189 (50.53) | 24.3611 |
2020's | 28 (7.49) | 2.80 |
Authors | Studies |
---|---|
Abdelghany, L | 2 |
Zhang, X | 2 |
Kawabata, T | 1 |
Goto, S | 1 |
El-Mahdy, N | 1 |
Jingu, K | 2 |
Li, TS | 2 |
Gasparrini, M | 1 |
Audrito, V | 1 |
Wang, W | 1 |
Yang, C | 1 |
Wang, T | 1 |
Deng, H | 3 |
ElMokh, O | 1 |
Matsumoto, S | 1 |
Biniecka, P | 1 |
Bellotti, A | 1 |
Schaeuble, K | 1 |
Piacente, F | 1 |
Gallart-Ayala, H | 1 |
Ivanisevic, J | 1 |
Stamenkovic, I | 1 |
Nencioni, A | 3 |
Nahimana, A | 2 |
Duchosal, MA | 2 |
Mizuno, R | 1 |
Hojo, H | 1 |
Takahashi, M | 1 |
Kashio, S | 1 |
Enya, S | 1 |
Nakao, M | 1 |
Konishi, R | 1 |
Yoda, M | 1 |
Harata, A | 1 |
Hamanishi, J | 1 |
Kawamoto, H | 1 |
Mandai, M | 1 |
Suzuki, Y | 1 |
Miura, M | 1 |
Bamba, T | 1 |
Izumi, Y | 1 |
Kawaoka, S | 1 |
Hofer, SJ | 1 |
Kroemer, G | 2 |
Kepp, O | 1 |
Sun, D | 1 |
Dong, G | 2 |
Wu, Y | 1 |
Du, L | 1 |
Li, M | 1 |
Sheng, C | 1 |
Almeida, KH | 1 |
Avalos-Irving, L | 1 |
Berardinelli, S | 1 |
Chauvin, K | 1 |
Yanez, S | 1 |
Puszkiel, A | 1 |
You, B | 3 |
Payen, L | 1 |
Lopez, J | 1 |
Guitton, J | 3 |
Rousset, P | 1 |
Fontaine, J | 1 |
Péron, J | 2 |
Maillet, D | 2 |
Tartas, S | 1 |
Bonnin, N | 1 |
Trillet-Lenoir, V | 1 |
Colomban, O | 2 |
Augu-Denechere, D | 1 |
Freyer, G | 3 |
Tod, M | 8 |
Beltrà, M | 1 |
Pöllänen, N | 1 |
Fornelli, C | 1 |
Tonttila, K | 1 |
Hsu, MY | 1 |
Zampieri, S | 1 |
Moletta, L | 1 |
Corrà, S | 1 |
Porporato, PE | 1 |
Kivelä, R | 1 |
Viscomi, C | 1 |
Sandri, M | 1 |
Hulmi, JJ | 1 |
Sartori, R | 1 |
Pirinen, E | 1 |
Penna, F | 1 |
Spencer, KR | 1 |
Portal, DE | 1 |
Aisner, J | 1 |
Stein, MN | 1 |
Malhotra, J | 1 |
Shih, W | 1 |
Chan, N | 1 |
Silk, AW | 1 |
Ganesan, S | 1 |
Goodin, S | 1 |
Gounder, M | 1 |
Lin, H | 2 |
Li, J | 2 |
Cerchio, R | 1 |
Marinaro, C | 1 |
Chen, S | 1 |
Mehnert, JM | 1 |
Jabbari, P | 1 |
Ardakany, MR | 1 |
Ebrahimi, S | 1 |
Rezaei, N | 1 |
Xu, Y | 1 |
Sekiya, R | 1 |
Yan, C | 1 |
Megarity, CF | 1 |
Timson, DJ | 1 |
Yamazaki, K | 1 |
Doi, T | 1 |
Ikeda, M | 1 |
Okusaka, T | 1 |
Schueler, A | 1 |
Watanabe, M | 1 |
Ohtsu, A | 1 |
Song, SB | 1 |
Park, JS | 1 |
Chung, GJ | 1 |
Lee, IH | 1 |
Hwang, ES | 1 |
Witkowska-Patena, E | 1 |
Budzyńska, A | 1 |
Giżewska, A | 1 |
Dziuk, M | 1 |
Walęcka-Mazur, A | 1 |
Nikas, IP | 1 |
Paschou, SA | 1 |
Ryu, HS | 1 |
Buqué, A | 1 |
Bloy, N | 1 |
Galluzzi, L | 1 |
Hamity, MV | 1 |
White, SR | 1 |
Blum, C | 1 |
Gibson-Corley, KN | 1 |
Hammond, DL | 1 |
Jones, JK | 1 |
Thompson, EM | 1 |
Yu, YR | 1 |
Imrichova, H | 1 |
Wang, H | 2 |
Chao, T | 1 |
Xiao, Z | 1 |
Gao, M | 1 |
Rincon-Restrepo, M | 1 |
Franco, F | 1 |
Genolet, R | 1 |
Cheng, WC | 1 |
Jandus, C | 1 |
Coukos, G | 1 |
Jiang, YF | 1 |
Locasale, JW | 1 |
Zippelius, A | 1 |
Liu, PS | 1 |
Tang, L | 2 |
Bock, C | 1 |
Vannini, N | 1 |
Ho, PC | 1 |
Delord, JP | 1 |
Italiano, A | 2 |
Awada, A | 9 |
Aftimos, P | 1 |
Houédé, N | 1 |
Lebbé, C | 1 |
Pages, C | 1 |
Lesimple, T | 1 |
Dinulescu, M | 1 |
Schellens, JHM | 2 |
Leijen, S | 1 |
Rottey, S | 1 |
Kruse, V | 1 |
Kefford, R | 1 |
Faivre, S | 3 |
Gomez-Roca, C | 1 |
Scheuler, A | 1 |
Massimini, G | 2 |
Raymond, E | 3 |
Patnaik, A | 4 |
Yap, TA | 1 |
Chung, HC | 1 |
de Miguel, MJ | 1 |
Bang, YJ | 1 |
Lin, CC | 1 |
Su, WC | 1 |
Chow, KH | 1 |
Szpurka, AM | 1 |
Yu, D | 2 |
Zhao, Y | 2 |
Carlsen, M | 1 |
Schmidt, S | 1 |
Vangerow, B | 1 |
Gandhi, L | 2 |
Xu, X | 1 |
Bendell, J | 1 |
Roberti, A | 1 |
Fernández, AF | 1 |
Fraga, MF | 1 |
Zhong, Y | 1 |
Yang, S | 1 |
Cui, J | 2 |
Wang, J | 1 |
Li, L | 4 |
Chen, Y | 2 |
Chen, J | 3 |
Feng, P | 1 |
Huang, S | 1 |
Li, H | 1 |
Han, Y | 1 |
Tang, G | 1 |
Hu, K | 1 |
Hayat, F | 1 |
Sonavane, M | 1 |
Makarov, MV | 1 |
Trammell, SAJ | 1 |
McPherson, P | 1 |
Gassman, NR | 1 |
Migaud, ME | 1 |
Mattiello, L | 1 |
Pucci, G | 1 |
Marchetti, F | 1 |
Diederich, M | 1 |
Gonfloni, S | 1 |
Gao, Y | 1 |
Martin, NI | 1 |
van Haren, MJ | 1 |
Ghanem, MS | 1 |
Monacelli, F | 1 |
Novak Kujundžić, R | 1 |
Prpić, M | 1 |
Đaković, N | 1 |
Dabelić, N | 1 |
Tomljanović, M | 1 |
Mojzeš, A | 1 |
Fröbe, A | 1 |
Trošelj, KG | 1 |
Chu, YY | 2 |
Cheng, HJ | 1 |
Tian, ZH | 1 |
Zhao, JC | 1 |
Li, G | 2 |
Sun, CJ | 1 |
Li, WB | 1 |
Gong, L | 1 |
Giacomini, MM | 1 |
Giacomini, C | 1 |
Maitland, ML | 7 |
Altman, RB | 1 |
Klein, TE | 1 |
Murray, L | 1 |
Longo, J | 1 |
Wan, J | 2 |
Chung, C | 1 |
Wang, L | 3 |
Dawson, L | 1 |
Milosevic, M | 1 |
Oza, A | 2 |
Brade, A | 1 |
Garrido, A | 1 |
Djouder, N | 1 |
Covell, DG | 1 |
Bruner, JK | 1 |
Ma, HS | 1 |
Qin, ACR | 1 |
Rudek, MA | 3 |
Jones, RJ | 1 |
Levis, MJ | 1 |
Pratz, KW | 2 |
Pratilas, CA | 1 |
Small, D | 1 |
Schloss, J | 1 |
Colosimo, M | 1 |
Hori, Y | 1 |
Ito, K | 1 |
Hamamichi, S | 1 |
Ozawa, Y | 1 |
Matsui, J | 1 |
Umeda, IO | 1 |
Fujii, H | 1 |
Srinivas, NR | 1 |
Zhang, C | 1 |
Chi, H | 1 |
Meng, Z | 1 |
Tharmalingham, H | 1 |
Hoskin, P | 1 |
Fuss, H | 1 |
Lademann, J | 1 |
Jung, S | 1 |
Schram, AM | 1 |
Mita, MM | 2 |
Damstrup, L | 1 |
Campana, F | 1 |
Hidalgo, M | 1 |
Grande, E | 1 |
Hyman, DM | 1 |
Heist, RS | 1 |
de Weger, VA | 1 |
de Jonge, M | 2 |
Langenberg, MHG | 1 |
Lolkema, M | 1 |
Varga, A | 1 |
Demers, B | 1 |
Thomas, K | 1 |
Hsu, K | 1 |
Tuffal, G | 1 |
Goodstal, S | 1 |
Macé, S | 1 |
Deutsch, E | 1 |
Ulanovskaya, OA | 1 |
Zuhl, AM | 1 |
Cravatt, BF | 1 |
Poot, AJ | 1 |
van der Wildt, B | 1 |
Stigter-van Walsum, M | 1 |
Rongen, M | 1 |
Schuit, RC | 1 |
Hendrikse, NH | 1 |
Eriksson, J | 1 |
van Dongen, GA | 1 |
Windhorst, AD | 1 |
Montecucco, F | 1 |
Cea, M | 1 |
Bauer, I | 1 |
Soncini, D | 1 |
Caffa, I | 1 |
Lasigliè, D | 1 |
Uccelli, A | 1 |
Bruzzone, S | 1 |
Funakoshi, T | 1 |
Latif, A | 1 |
Galsky, MD | 1 |
Rosen, LS | 4 |
Lipton, L | 2 |
Price, TJ | 2 |
Belman, ND | 1 |
Boccia, RV | 1 |
Hurwitz, HI | 1 |
Stephenson, JJ | 2 |
Wirth, LJ | 1 |
McCoy, S | 3 |
Hei, YJ | 1 |
Hsu, CP | 2 |
Tebbutt, NC | 1 |
Ganesan, P | 1 |
Piha-Paul, S | 1 |
Naing, A | 4 |
Falchook, G | 1 |
Wheler, J | 1 |
Fu, S | 3 |
Hong, DS | 4 |
Kurzrock, R | 6 |
Janku, F | 3 |
Laday, S | 1 |
Bedikian, AY | 1 |
Kies, M | 1 |
Wolff, RA | 1 |
Tsimberidou, AM | 2 |
Navid, F | 2 |
Christensen, R | 1 |
Inaba, H | 1 |
Chen, Z | 1 |
Cai, X | 1 |
Regel, J | 1 |
Baker, SD | 3 |
Prado, CM | 2 |
Kumar, SK | 1 |
Jett, J | 1 |
Marks, R | 1 |
Richardson, R | 1 |
Quevedo, F | 1 |
Moynihan, T | 1 |
Croghan, G | 1 |
Markovic, SN | 1 |
Bible, KC | 1 |
Qin, R | 1 |
Tan, A | 1 |
Molina, J | 1 |
Kaufmann, SH | 1 |
Erlichman, C | 1 |
Adjei, AA | 4 |
Bhatta, SS | 1 |
Wroblewski, KE | 1 |
Agarwal, KL | 1 |
Sit, L | 2 |
Cohen, EE | 3 |
Seiwert, TY | 1 |
Karrison, T | 2 |
Bakris, GL | 2 |
Ratain, MJ | 5 |
Vokes, EE | 1 |
Maia, YL | 1 |
Ormsbee, M | 1 |
Sawyer, MB | 1 |
Baracos, VE | 1 |
Hatzivassiliou, G | 1 |
Haling, JR | 1 |
Chen, H | 1 |
Song, K | 1 |
Price, S | 1 |
Heald, R | 1 |
Hewitt, JF | 1 |
Zak, M | 1 |
Peck, A | 1 |
Orr, C | 1 |
Merchant, M | 1 |
Hoeflich, KP | 1 |
Chan, J | 1 |
Luoh, SM | 1 |
Anderson, DJ | 1 |
Ludlam, MJ | 1 |
Wiesmann, C | 1 |
Ultsch, M | 1 |
Friedman, LS | 1 |
Malek, S | 1 |
Belvin, M | 1 |
Mieszawska, AJ | 1 |
Kim, Y | 1 |
Gianella, A | 1 |
van Rooy, I | 1 |
Priem, B | 1 |
Labarre, MP | 1 |
Ozcan, C | 1 |
Cormode, DP | 1 |
Petrov, A | 1 |
Langer, R | 1 |
Farokhzad, OC | 1 |
Fayad, ZA | 1 |
Mulder, WJ | 1 |
Lazar, V | 1 |
Lassau, N | 1 |
Meurice, G | 1 |
Loriot, Y | 1 |
Peña, C | 1 |
Massard, C | 1 |
Robert, C | 6 |
Robert, T | 1 |
Le Berre, MA | 1 |
de Baere, T | 1 |
Dessen, P | 1 |
Soria, JC | 5 |
Armand, JP | 4 |
Abdulghani, J | 1 |
Allen, JE | 1 |
Dicker, DT | 1 |
Liu, YY | 1 |
Goldenberg, D | 1 |
Smith, CD | 1 |
Humphreys, R | 1 |
El-Deiry, WS | 2 |
Santoni, M | 1 |
Conti, A | 1 |
De Giorgi, U | 1 |
Iacovelli, R | 1 |
Pantano, F | 1 |
Burattini, L | 1 |
Muzzonigro, G | 1 |
Berardi, R | 2 |
Santini, D | 1 |
Cascinu, S | 2 |
Wang, CF | 2 |
Mäkilä, EM | 2 |
Kaasalainen, MH | 1 |
Liu, D | 1 |
Sarparanta, MP | 2 |
Airaksinen, AJ | 2 |
Salonen, JJ | 2 |
Hirvonen, JT | 2 |
Santos, HA | 2 |
Escudero-Ortiz, V | 1 |
Pérez-Ruixo, JJ | 1 |
Valenzuela, B | 1 |
Thomeas, V | 2 |
Chow, S | 2 |
Gutierrez, JO | 1 |
Karovic, S | 2 |
Wroblewski, K | 1 |
Kistner-Griffin, E | 1 |
Karrison, TG | 2 |
Zhang, XJ | 1 |
Zhang, TY | 1 |
Yu, FF | 1 |
Wei, X | 1 |
Li, YS | 1 |
Xu, F | 1 |
Wei, LX | 1 |
He, J | 1 |
Park, GB | 1 |
Choi, Y | 1 |
Kim, YS | 1 |
Lee, HK | 1 |
Kim, D | 1 |
Hur, DY | 1 |
Liu, Y | 1 |
Feng, L | 1 |
Liu, T | 1 |
Zhang, L | 2 |
Yao, Y | 1 |
Zhang, N | 1 |
Liu, X | 1 |
Yu, C | 1 |
Li, W | 2 |
Li, Y | 2 |
Li, S | 1 |
Zhu, Y | 1 |
Liang, X | 1 |
Meng, H | 1 |
Zhang, D | 1 |
Guo, H | 1 |
Shi, B | 1 |
Wen, Y | 1 |
Levine, MR | 1 |
House, LK | 2 |
Wu, K | 2 |
Wright, JJ | 8 |
Fleming, GF | 2 |
Abdel-Rahman, O | 2 |
Fouad, M | 2 |
Toffalorio, F | 1 |
Spitaleri, G | 1 |
Catania, C | 1 |
Dal Zotto, L | 1 |
Noberasco, C | 1 |
Delmonte, A | 1 |
Santarpia, M | 1 |
Vecchio, F | 1 |
Brunelli, V | 1 |
Rampinelli, C | 1 |
Barberis, M | 1 |
Fumagalli, C | 1 |
Zucchetti, M | 1 |
Zangarini, M | 1 |
Diena, T | 1 |
Danesi, R | 2 |
de Braud, F | 1 |
De Pas, T | 1 |
Koldenhof, JJ | 1 |
Witteveen, PO | 1 |
de Vos, R | 1 |
Walraven, M | 1 |
Tillier, CN | 1 |
Verheul, HM | 1 |
Teunissen, SC | 1 |
Huillard, O | 2 |
Boissier, E | 1 |
Blanchet, B | 9 |
Thomas-Schoemann, A | 4 |
Cessot, A | 2 |
Boudou-Rouquette, P | 5 |
Durand, JP | 4 |
Coriat, R | 7 |
Giroux, J | 3 |
Alexandre, J | 2 |
Vidal, M | 3 |
Goldwasser, F | 10 |
Hasskarl, J | 2 |
Li, B | 2 |
Iglesias-Pedraz, JM | 1 |
Chen, LY | 1 |
Yin, F | 1 |
Cadenas, E | 1 |
Reddy, S | 1 |
Comai, L | 1 |
Kruzliak, P | 1 |
Hu, J | 1 |
Jing, H | 1 |
Sounni, NE | 1 |
Cimino, J | 1 |
Blacher, S | 1 |
Primac, I | 1 |
Truong, A | 1 |
Mazzucchelli, G | 1 |
Paye, A | 1 |
Calligaris, D | 1 |
Debois, D | 1 |
De Tullio, P | 1 |
Mari, B | 1 |
De Pauw, E | 1 |
Noel, A | 1 |
Usui, J | 1 |
Glezerman, IG | 1 |
Salvatore, SP | 1 |
Chandran, CB | 1 |
Flombaum, CD | 1 |
Seshan, SV | 1 |
Grimes, J | 1 |
Celler, A | 1 |
Puzanov, I | 3 |
Sosman, J | 1 |
Santoro, A | 2 |
Saif, MW | 1 |
Goff, L | 1 |
Dy, GK | 2 |
Zucali, P | 1 |
Means-Powell, JA | 1 |
Ma, WW | 2 |
Simonelli, M | 2 |
Martell, R | 1 |
Chai, F | 1 |
Lamar, M | 1 |
Savage, RE | 1 |
Schwartz, B | 9 |
Schmidtmann, I | 1 |
Elsäßer, A | 1 |
Weinmann, A | 1 |
Binder, H | 1 |
Falchook, GS | 1 |
Wheler, JJ | 2 |
Piha-Paul, SA | 2 |
Zinner, R | 1 |
Jiang, Y | 1 |
Huang, M | 1 |
Lin, Q | 1 |
Parkhurst, K | 1 |
Lachaier, E | 1 |
Louandre, C | 1 |
Godin, C | 1 |
Saidak, Z | 1 |
Baert, M | 1 |
Diouf, M | 1 |
Chauffert, B | 1 |
Galmiche, A | 1 |
Ngamphaiboon, N | 1 |
Reungwetwattana, T | 1 |
DePaolo, D | 1 |
Ding, Y | 1 |
Brady, W | 1 |
Fetterly, G | 1 |
Wecksler, AT | 1 |
Hwang, SH | 1 |
Liu, JY | 1 |
Wettersten, HI | 1 |
Morisseau, C | 1 |
Wu, J | 2 |
Weiss, RH | 1 |
Hammock, BD | 1 |
Gao, ZH | 1 |
Qu, XJ | 1 |
Mulay, M | 3 |
Rasmussen, E | 1 |
Wu, BM | 1 |
Bass, MB | 3 |
Zhong, ZD | 1 |
Friberg, G | 2 |
Hyvönen, ML | 1 |
Laakkonen, PM | 1 |
Tavallai, M | 2 |
Hamed, HA | 3 |
Roberts, JL | 3 |
Cruickshanks, N | 3 |
Chuckalovcak, J | 1 |
Poklepovic, A | 2 |
Booth, L | 3 |
Dent, P | 6 |
Tlemsani, C | 1 |
Arrondeau, J | 1 |
Srikanthan, A | 1 |
Ethier, JL | 1 |
Ocana, A | 1 |
Seruga, B | 1 |
Krzyzanowska, MK | 1 |
Amir, E | 1 |
Nourbakhsh, A | 1 |
Fidanza, A | 1 |
Cruz-Luna, T | 1 |
Smith, E | 1 |
Siembida, P | 1 |
Plamondon, P | 1 |
Cycon, KA | 1 |
Doern, CD | 1 |
El-Madani, M | 2 |
Hénin, E | 1 |
Lefort, T | 2 |
Cassier, P | 2 |
Valette, PJ | 2 |
Rodriguez-Lafrasse, C | 2 |
Berger, F | 1 |
Lachuer, J | 1 |
Slimane, K | 1 |
Barrois, C | 2 |
Rzymski, T | 1 |
Mikula, M | 1 |
Wiklik, K | 1 |
Brzózka, K | 1 |
Pollom, EL | 1 |
Deng, L | 1 |
Pai, RK | 1 |
Brown, JM | 3 |
Giaccia, A | 1 |
Loo, BW | 1 |
Shultz, DB | 1 |
Le, QT | 1 |
Koong, AC | 1 |
Chang, DT | 1 |
An, H | 1 |
Stoops, SL | 1 |
Deane, NG | 1 |
Zhu, J | 1 |
Zi, J | 1 |
Weaver, C | 1 |
Waterson, AG | 1 |
Zijlstra, A | 1 |
Lindsley, CW | 1 |
Beauchamp, RD | 1 |
Shin, H | 1 |
Gulbekyan, G | 1 |
Pustovalova, O | 1 |
Nikolsky, Y | 1 |
Hope, A | 1 |
Bessarabova, M | 1 |
Schu, M | 1 |
Kolpakova-Hart, E | 1 |
Merberg, D | 1 |
Dorner, A | 1 |
Trepicchio, WL | 1 |
Yang, X | 1 |
Pan, X | 1 |
Cheng, X | 1 |
Cheng, Y | 1 |
Kuang, Y | 1 |
Togashi, Y | 1 |
Nishio, K | 1 |
Miyanaga, A | 1 |
Gemma, A | 1 |
Ross, JS | 1 |
Wang, K | 1 |
Chmielecki, J | 1 |
Gay, L | 1 |
Johnson, A | 1 |
Chudnovsky, J | 1 |
Yelensky, R | 1 |
Lipson, D | 1 |
Ali, SM | 1 |
Elvin, JA | 1 |
Vergilio, JA | 1 |
Roels, S | 1 |
Miller, VA | 1 |
Nakamura, BN | 1 |
Gray, A | 1 |
Wong, MK | 1 |
Stephens, PJ | 1 |
Venkova, L | 1 |
Aliper, A | 1 |
Suntsova, M | 1 |
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GOLDIN, A | 1 |
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CIOTTI, MM | 1 |
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QUAGLIARIELLO, E | 2 |
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Kumar Mitra, A | 1 |
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Piccart, M | 2 |
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Gravell, A | 2 |
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Le Cesne, A | 1 |
Pautier, P | 1 |
Lhomme, C | 1 |
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Le Chevalier, T | 1 |
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Petrenciuc, O | 2 |
Clark, JW | 3 |
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Lenz, HJ | 2 |
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Takimoto, CH | 2 |
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Moore, MJ | 2 |
Hirte, H | 2 |
Piccart, P | 1 |
Hofstra, E | 1 |
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Veronese, ML | 1 |
Mosenkis, A | 1 |
Gallagher, M | 1 |
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Townsend, RR | 1 |
O'Dwyer, PJ | 1 |
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Hedley, D | 1 |
Henning, BF | 1 |
Passarge, K | 1 |
Flashar, C | 1 |
Voigtmann, R | 1 |
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Caraglia, M | 1 |
Tassone, P | 1 |
Marra, M | 1 |
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Tagliaferri, P | 1 |
Rodriguez-Viciana, P | 1 |
Tetsu, O | 1 |
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Okada, J | 1 |
Rauen, K | 1 |
McCormick, F | 1 |
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Kelley, SL | 1 |
Schreck, R | 1 |
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Curtiss, FR | 1 |
Lowinger, T | 1 |
Dumas, J | 1 |
Smith, RA | 1 |
Simantov, R | 1 |
Kelley, S | 1 |
Burton, A | 1 |
Gmehling, D | 1 |
Unger, C | 1 |
Arslan, MA | 1 |
Kutuk, O | 1 |
Basaga, H | 1 |
Hoogsteen, IJ | 1 |
Marres, HA | 1 |
van der Kogel, AJ | 1 |
Kaanders, JH | 1 |
Force, T | 1 |
Krause, DS | 1 |
Van Etten, RA | 1 |
Eichhorn, ME | 1 |
Kleespies, A | 1 |
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Jauch, KW | 1 |
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Van Vugt, A | 1 |
Purdom, M | 1 |
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Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
A Multicenter, Open Label, Phase I Trial of the MEK Inhibitor MSC1936369B Given Orally to Subjects With Solid Tumours[NCT00982865] | Phase 1 | 182 participants (Actual) | Interventional | 2007-12-31 | Completed | ||
A Phase 1a/1b Study of a Novel Anti-PD-L1 Checkpoint Antibody (LY3300054) Administered Alone or in Combination With Other Agents in Advanced Refractory Solid Tumors (Phase 1a/1b Anti-PD-L1 Combinations in Tumors-PACT)[NCT02791334] | Phase 1 | 215 participants (Anticipated) | Interventional | 2016-06-29 | Active, not recruiting | ||
A Phase 1 Study of Combination Therapy With SAR405838 and Pimasertib in Patients With Advanced Cancer[NCT01985191] | Phase 1 | 26 participants (Actual) | Interventional | 2013-11-30 | Completed | ||
An Open-Label, Randomized, Phase 1b Study Evaluating the Effect of Different Doses of AMG 706 on the Gallbladder in Subjects With Advanced Solid Tumors[NCT00448786] | Phase 1 | 49 participants (Actual) | Interventional | 2007-02-28 | Completed | ||
A Phase I Study of Lenalidomide in Combination With Bevacizumab, Sorafenib, Temsirolimus, or 5-fluorouracil, Leucovorin, Oxaliplatin (FOLFOX) in Patients With Advanced Cancers[NCT01183663] | Phase 1 | 180 participants (Actual) | Interventional | 2010-08-31 | Completed | ||
A Phase I Study of the Raf Kinase/VEGFR Inhibitor BAY 43-9006 in Combination With the Proteasome Inhibitor PS-341 in Patients With Advanced Malignancies[NCT00303797] | Phase 1 | 50 participants (Actual) | Interventional | 2005-12-31 | Completed | ||
A Phase 1/2 Study of the Combination of RDEA119 and Sorafenib in Patients With Advanced Cancer[NCT00785226] | Phase 1/Phase 2 | 62 participants (Actual) | Interventional | 2008-11-30 | Completed | ||
A Phase I, Open-Label, Single Center Trial to Investigate the Mass Balance, Metabolite Profile and Oral Bioavailability of Pimasertib in Cancer Patients With Locally Advanced or Metastatic Solid Tumors[NCT01713036] | Phase 1 | 6 participants (Actual) | Interventional | 2012-11-30 | 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 | ||
Phase I Dose Escalation Trial of MEK1/2 Inhibitor MSC1936369B Combined With Temsirolimus in Subjects With Advanced Solid Tumors[NCT01378377] | Phase 1 | 33 participants (Actual) | Interventional | 2011-05-27 | Terminated (stopped due to The trial was stopped due to the toxicities observed with the combination of pimasertib and temsirolimus.) | ||
Bevacizumab in Patients With Metastatic Renal Cell Carcinoma or Others Advanced Solid Tumors[NCT01202032] | Phase 1 | 36 participants (Anticipated) | Interventional | 2010-07-31 | Completed | ||
A Randomized, Open-label, Multi-center Phase II Study to Compare Bevacizumab Plus Sorafenib Versus Sorafenib for the Third-line Treatment of Patients With Metastatic Renal Cell Carcinoma[NCT02330783] | Phase 2 | 106 participants (Anticipated) | Interventional | 2014-12-31 | Recruiting | ||
An Open Label, Pilot Study Evaluating the Effect of Topical Sildenafil as Pre-Treatment for Hand-Foot Skin Reaction[NCT03229512] | Early Phase 1 | 2 participants (Actual) | Interventional | 2017-04-11 | Completed | ||
The Effect of Urea Cream on Sorafenib-associated Hand-Foot Skin Reaction in Patients With Korean Hepatocellular Carcinoma Patients: Multicenter, Prospective Randomized Double-Blind Controlled Study[NCT03212625] | Phase 4 | 288 participants (Actual) | Interventional | 2016-01-28 | Completed | ||
A Phase I Study of BAY 43-9006 (Sorafenib) in Combination With OSI-774 (Erlotinib; Tarceva) in Advanced Solid Tumors[NCT00126620] | Phase 1 | 17 participants (Actual) | Interventional | 2005-09-30 | Completed | ||
Effect of BAY 43-9006 (Sorafenib) on Cardiovascular Safety Parameters in Cancer Patients[NCT00259129] | Phase 1 | 53 participants (Actual) | Interventional | 2005-08-31 | Completed | ||
A Phase II Study of BAY 43-9006 (Sorafenib) in Metastatic, Androgen-Independent Prostate Cancer[NCT00090545] | Phase 2 | 46 participants (Actual) | Interventional | 2004-09-01 | Completed | ||
A Phase 1b, Open-label, Dose-finding Study of AMG 706 in Combination With Gemcitabine and Erlotinib to Treat Subjects With Solid Tumors[NCT01235416] | Phase 1 | 57 participants (Actual) | Interventional | 2005-09-30 | Completed | ||
Single Agent Sorafenib in Advanced Solid Tumors: Phase II Evaluation of Dose Re-Escalation Following a Dose Reduction (IST000375)[NCT00810394] | Phase 2 | 50 participants (Actual) | Interventional | 2008-12-31 | Completed | ||
Phase I and Pharmacokinetics Study of Lapatinib in Combination With Sorafenib in Patients With Advanced Refractory Solid Tumors[NCT00984425] | Phase 1 | 30 participants (Actual) | Interventional | 2009-09-30 | Completed | ||
Mechanism of Sorafenib Resistance in Patients With Advanced Hepatocellular Carcinoma[NCT02733809] | Phase 4 | 40 participants (Anticipated) | Interventional | 2014-01-31 | Recruiting | ||
Accelerated Growth of Synchronous Colorectal Liver Metastases: Effects of Neo-adjuvant Therapy[NCT00659022] | Phase 2 | 60 participants (Anticipated) | Interventional | 2008-07-31 | Recruiting | ||
A Phase II Trial of the Effect of Perindopril on HFSR Incidence and Severity in Patients Receiving Regorafenib With Refractory Metastatic Colorectal Carcinoma (mCRC)[NCT02651415] | Phase 2 | 12 participants (Actual) | Interventional | 2016-08-31 | Completed | ||
Histological Characterization and Differentiation of Rash From Other EGFR Inhibitors[NCT00709878] | 32 participants (Actual) | Observational | 2008-04-30 | Completed | |||
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 | ||
Angiogenesis Inhibitors and Hypertension: Clinical Aspects[NCT00511511] | 80 participants (Anticipated) | Observational | 2007-08-31 | Completed | |||
A Study of the Pharmacodynamic Effects of Anti-Vascular Endothelial Growth[NCT00698659] | 0 participants | Observational | 2007-08-31 | Terminated | |||
A Pilot, Pharmacodynamic Correlate Trial of Sirolimus in Combination With Chemotherapy (Idarubicin, Cytarabine) for the Treatment of Newly Diagnosed Acute Myelogenous Leukemia[NCT01822015] | Early Phase 1 | 55 participants (Actual) | Interventional | 2013-03-15 | Completed | ||
A Phase II Study of Azacitidine and Sirolimus for the Treatment of High Risk Myelodysplastic Syndrome or Acute Myeloid Leukemia Refractory to or Not Eligible for Intensive Chemotherapy[NCT01869114] | Phase 2 | 57 participants (Actual) | Interventional | 2013-07-08 | Active, not recruiting | ||
Personalized Cancer Therapy for Patients With Metastatic Medullary Thyroid or Metastatic Colon Cancer[NCT02363647] | 10 participants (Actual) | Interventional | 2015-01-31 | Terminated (stopped due to No Current Funding) | |||
A Phase 1, First in Human, Open-Label, Dose Finding Study Evaluating the Safety and Pharmacokinetics of AMG 706 in Subjects With Advanced Solid Tumors[NCT00093873] | Phase 1 | 71 participants (Actual) | Interventional | 2003-07-31 | Completed | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
DLT was defined as any of following toxicities at any dose level according to using National Cancer Institute Common Terminology Criteria for Adverse Events (AEs) v3.0(CTCAE), probably or possibly related to trial medication by investigator or sponsor: a)Any Grade 3 or more non-haematological toxicity excluding: (i)Grade 3 asymptomatic increase in liver function tests (Aspartate Aminotransferase, Alanine transaminase, Alkaline Phosphatase reversible within 7 days for subjects without liver involvement, or grade 4 for subjects with liver involvement; (ii)Grade 3 vomiting if it is encountered despite adequate and optimal therapy (e.g. serotonin [5HT3] antagonists and corticosteroids); (iii)Grade 3 diarrhoea if it is encountered despite adequate and optimal anti diarrhoea therapy; b)Grade 4 neutropenia of >5 days duration or febrile neutropenia lasting for more than 1 day; c)Grade 4 thrombocytopenia >1 day or grade 3 with bleeding; d)Any treatment delay >2 weeks due to drug-related AEs. (NCT00982865)
Timeframe: Day 1 up to Day 21 of Cycle 1
Intervention | Subjects (Number) |
---|---|
MSC1936369B Regimen 1 | 2 |
MSC1936369B Regimen 2 (Without Food Effect + With Food Effect) | 6 |
MSC1936369B Regimen 3 Once Daily (QD) | 0 |
MSC1936369B Regimen 3 Twice Daily | 6 |
(NCT00982865)
Timeframe: Baseline up to 253 weeks
Intervention | Subjects (Number) |
---|---|
MSC1936369B Regimen 1 | 10 |
MSC1936369B Regimen 2 (Without Food Effect + With Food Effect) | 14 |
MSC1936369B Regimen 3 Once Daily (QD) | 2 |
MSC1936369B Regimen 3 Twice Daily | 2 |
Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by λz. As AUCextra was >20% of AUC0-inf, t1/2 derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 1.5mg, 2.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Hours (h) (Geometric Mean) | |
---|---|---|
C1D1 | C1D12 | |
MSC1936369B 28 mg | 4.781 | 6.750 |
MSC1936369B 3.5 mg | 3.346 | 4.985 |
MSC1936369B 68 mg | 5.335 | 6.926 |
Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by λz. As AUCextra was >20% of AUC0-inf, t1/2 derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 1.5mg, 2.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Hours (h) (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D12 | C3D1 | |
MSC1936369B 120 mg | 5.247 | 3.964 | 3.038 |
MSC1936369B 14 mg | 4.599 | 3.236 | 2.811 |
MSC1936369B 45 mg | 5.389 | 4.688 | 2.931 |
MSC1936369B 7 mg | 3.405 | 9.249 | 2.959 |
MSC1936369B 94 mg | 5.351 | 5.672 | 2.842 |
Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by λz. Summarized data over Day 1 and Day 2 was reported. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, 12 and 24 hours post-dose on Cycle 1 Day 1 and Day 2
Intervention | Hour (h) (Geometric Mean) | |
---|---|---|
Fasted | Fed | |
MSC1936369B 150 mg | 4.452 | 6.123 |
MSC1936369B 90 mg | 4.898 | 4.534 |
Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by λz. As AUCextra was >20% of AUC0-inf, t1/2 derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 2mg, 3.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Hours (h) (Geometric Mean) | |
---|---|---|
C1D1 | C1D15 | |
MSC1936369B 7 mg | 2.594 | 2.335 |
MSC1936369B 14 mg | 5.119 | 4.443 |
MSC1936369B 28 mg | 5.115 | 6.646 |
MSC1936369B 45 mg | 4.187 | 5.277 |
Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by λz. As AUCextra was >20% of AUC0-inf, t1/2 derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 2mg, 3.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Hours (h) (Geometric Mean) | |
---|---|---|
C1D15 | C3D1 | |
MSC1936369B 5 mg | 2.941 | 2.732 |
Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by λz. As AUCextra was >20% of AUC0-inf, t1/2 derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 2mg, 3.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Hours (h) (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 120 mg | 5.057 | 4.851 | 2.863 |
MSC1936369B 150 mg | 4.904 | 5.479 | 2.418 |
MSC1936369B 195 mg | 5.641 | 6.016 | 2.628 |
MSC1936369B 68 mg | 3.305 | 6.441 | 3.477 |
MSC1936369B 255 mg | 4.313 | 4.847 | 2.260 |
MSC1936369B 94 mg | 4.826 | 5.193 | 2.853 |
Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by λz. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Hour (h) (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 60 mg | 4.236 | 5.259 | 1.780 |
MSC1936369B 90 mg | 4.097 | 5.599 | 2.680 |
Terminal half-life is the time measured for the concentration to decrease by one half. Terminal half-life calculated by natural log 2 divided by λz. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, and 10 h post-dose on Cycle 1 Day 1 and Day 15; pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 h post dose on Cycle 3 Day 1
Intervention | Hour (h) (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 45 mg | 2.050 | 2.890 | 3.144 |
MSC1936369B 60 mg | 2.509 | 3.265 | 2.636 |
MSC1936369B 75 mg | 2.814 | 3.210 | 3.260 |
Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. Apparent volume of distribution during the terminal phase, calculated as Vz = Dose/AUC0-inf multiplied by λz. Summarized data over Day 1 and Day 2 was reported. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, 12 and 24 hours post-dose on Cycle 1 Day 1 and Day 2
Intervention | Liter (Geometric Mean) | |
---|---|---|
Fasted | Fed | |
MSC1936369B 150 mg | 288.1 | 235.2 |
MSC1936369B 90 mg | 402.4 | 393.6 |
Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. Apparent volume of distribution during the terminal phase, calculated as Vz = Dose/AUC0-inf multiplied by λz. As AUCextra was >20% of AUC0-inf, Vz/F derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 2mg, 3.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Liter (Geometric Mean) | |
---|---|---|
C1D1 | C1D15 | |
MSC1936369B 14 mg | 473.32 | 555.9 |
MSC1936369B 28 mg | 319.40 | 432.5 |
MSC1936369B 45 mg | 331.36 | 378.0 |
MSC1936369B 7 mg | 339.58 | 454.6 |
Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. Apparent volume of distribution during the terminal phase, calculated as Vz = Dose/AUC0-inf multiplied by λz. As AUCextra was >20% of AUC0-inf, Vz/F derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 2mg, 3.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Liter (Geometric Mean) | |
---|---|---|
C1D15 | C3D1 | |
MSC1936369B 5 mg | 252.7 | 352.10 |
Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. Apparent volume of distribution during the terminal phase, calculated as Vz = Dose/AUC0-inf multiplied by λz. As AUCextra was >20% of AUC0-inf, Vz/F derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 2mg, 3.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Liter (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 120 mg | 361.12 | 646.9 | 201.39 |
MSC1936369B 150 mg | 463.92 | 642.1 | 212.92 |
MSC1936369B 195 mg | 440.55 | 464.2 | 274.24 |
MSC1936369B 255 mg | 377.28 | 295.1 | 144.24 |
MSC1936369B 68 mg | 366.00 | 406.6 | 206.07 |
MSC1936369B 94 mg | 428.99 | 385.6 | 244.16 |
Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. Apparent volume of distribution during the terminal phase, calculated as Vz = Dose/AUC0-inf multiplied by λz (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Liter (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 60 mg | 292.61 | 366.5 | 137.0 |
MSC1936369B 90 mg | 336.38 | 507.7 | 292.5 |
Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. Apparent volume of distribution during the terminal phase, calculated as Vz = Dose/AUC0-inf multiplied by λz (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, and 10 h post-dose on Cycle 1 Day 1 and Day 15; pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 h post dose on Cycle 3 Day 1
Intervention | Liter (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 45 mg | 339.51 | 297.9 | 571.8 |
MSC1936369B 60 mg | 292.59 | 315.0 | 392.9 |
MSC1936369B 75 mg | 340.43 | 437.6 | 362.6 |
Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. Apparent volume of distribution during the terminal phase, calculated as Vz = Dose/AUC0-inf multiplied by λz. As AUCextra was >20% of AUC0-inf, Vz/F derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 1.5mg, 2.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Liter (Geometric Mean) | |
---|---|---|
C1D1 | C1D12 | |
MSC1936369B 28 mg | 336.32 | 365.1 |
MSC1936369B 3.5 mg | 640.60 | 507.8 |
MSC1936369B 68 mg | 307.90 | 357.8 |
Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. Apparent volume of distribution during the terminal phase, calculated as Vz = Dose/AUC0-inf multiplied by λz. As AUCextra was >20% of AUC0-inf, Vz/F derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 1.5mg, 2.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Liter (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D12 | C3D1 | |
MSC1936369B 120 mg | 361.99 | 351.4 | 316.63 |
MSC1936369B 14 mg | 396.76 | 291.9 | 422.04 |
MSC1936369B 45 mg | 378.56 | 333.9 | 348.19 |
MSC1936369B 7 mg | 561.27 | 594.5 | 928.91 |
MSC1936369B 94 mg | 389.49 | 416.3 | 438.91 |
AUCextra was defined as a percentage of AUC0-inf obtained by extrapolation: %AUCextra = (1- [AUC0-t / AUC0-inf])*100. %AUCextra was reported in terms of percentage of AUC0-inf. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Percentage of AUC 0-∞ (Geometric Mean) | |
---|---|---|
C1D1 | C1D12 | |
MSC1936369B 1.5 mg | 42.23 | 33.84 |
MSC1936369B 68 mg | 4.08 | 6.56 |
AUCextra was defined as a percentage of AUC0-inf obtained by extrapolation: %AUCextra = (1- [AUC0-t / AUC0-inf])*100. %AUCextra was reported in terms of percentage of AUC0-inf. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Percentage of AUC 0-∞ (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D12 | C3D1 | |
MSC1936369B 1 mg | 81.33 | 50.60 | 55.15 |
MSC1936369B 120 mg | 5.28 | 2.97 | 26.05 |
MSC1936369B 14 mg | 5.31 | 7.83 | 15.84 |
MSC1936369B 2.5 mg | 43.45 | 40.60 | 55.79 |
MSC1936369B 28 mg | 5.39 | 6.57 | 28.06 |
MSC1936369B 3.5 mg | 26.80 | 21.27 | 32.85 |
MSC1936369B 45 mg | 3.52 | 8.17 | 27.67 |
MSC1936369B 7 mg | 13.08 | 19.82 | 21.27 |
MSC1936369B 94 mg | 4.09 | 7.94 | 16.54 |
AUCextra was defined as a percentage of AUC0-inf obtained by extrapolation: AUCextra = (1- [AUC0-t / AUC0-inf])*100. AUCextra was reported in terms of percentage of AUC0-inf. Summarized data over Day 1 and Day 2 was reported. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, 12 and 24 hours post-dose on Cycle 1 Day 1 and Day 2
Intervention | Percentage of AUC 0-∞ (Geometric Mean) | |
---|---|---|
Fasted | Fed | |
MSC1936369B 150 mg | 1.74 | 9.96 |
MSC1936369B 90 mg | 2.54 | 2.21 |
AUCextra was defined as a percentage of AUC0-inf obtained by extrapolation: %AUCextra = (1- [AUC0-t / AUC0-inf])*100. %AUCextra was reported in terms of percentage of AUC0-inf. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Percentage of AUC 0-∞ (Geometric Mean) |
---|---|
C1D15 | |
MSC1936369B 1 mg | 40.86 |
AUCextra was defined as a percentage of AUC0-inf obtained by extrapolation: %AUCextra = (1- [AUC0-t / AUC0-inf])*100. %AUCextra was reported in terms of percentage of AUC0-inf. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Percentage of AUC 0-∞ (Geometric Mean) | |
---|---|---|
C1D1 | C1D15 | |
MSC1936369B 45 mg | 1.46 | 2.96 |
MSC1936369B 14 mg | 12.17 | 12.45 |
AUCextra was defined as a percentage of AUC0-inf obtained by extrapolation: %AUCextra = (1- [AUC0-t / AUC0-inf])*100. %AUCextra was reported in terms of percentage of AUC0-inf. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Percentage of AUC 0-∞ (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 120 mg | 2.94 | 5.82 | 16.22 |
MSC1936369B 150 mg | 2.64 | 4.82 | 17.54 |
MSC1936369B 195 mg | 4.36 | 5.77 | 23.45 |
MSC1936369B 2 mg | 55.78 | 33.34 | 33.93 |
MSC1936369B 255 mg | 3.57 | 5.22 | 11.15 |
MSC1936369B 28 mg | 3.29 | 6.89 | 26.32 |
MSC1936369B 3.5 mg | 31.63 | 35.29 | 33.77 |
MSC1936369B 5 mg | 27.25 | 21.93 | 17.27 |
MSC1936369B 68 mg | 2.66 | 5.00 | 15.35 |
MSC1936369B 7 mg | 15.10 | 19.45 | 20.68 |
MSC1936369B 94 mg | 2.60 | 3.40 | 18.02 |
AUCextra was defined as a percentage of AUC0-inf obtained by extrapolation: AUCextra = (1- [AUC0-t / AUC0-inf])*100. AUCextra was reported in terms of percentage of AUC0-inf. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | percentage of AUC 0-∞ (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 60 mg | 1.88 | 7.95 | 9.11 |
MSC1936369B 90 mg | 2.11 | 4.28 | 17.56 |
AUCextra was defined as a percentage of AUC0-inf obtained by extrapolation: AUCextra = (1- [AUC0-t / AUC0-inf])*100. AUCextra was reported in terms of percentage of AUC0-inf. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, and 10 h post-dose on Cycle 1 Day 1 and Day 15; pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 h post dose on Cycle 3 Day 1
Intervention | Percentage of AUC 0-∞ (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 45 mg | 16.82 | 11.78 | 30.63 |
MSC1936369B 60 mg | 7.70 | 14.14 | 16.43 |
MSC1936369B 75 mg | 10.90 | 19.19 | 21.34 |
AUC0-inf was calculated by combining AUC0-t and AUCextra. AUC extra represents an extrapolated value obtained by Clast/ λz, where Clast is the calculated plasma concentration at the last sampling time point at which the measured plasma concentration is at or above the Lower Limit of quantification (LLQ) and λz is the apparent terminal rate constant determined by log-linear regression analysis of the measured plasma concentrations of the terminal log-linear phase. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | |
---|---|---|
C1D1 | C1D12 | |
MSC1936369B 1.5 mg | 6.2 | 9.4 |
MSC1936369B 68 mg | 1699.7 | 2108.2 |
AUC0-inf was calculated by combining AUC0-t and AUCextra. AUC extra represents an extrapolated value obtained by Clast/ λz, where Clast is the calculated plasma concentration at the last sampling time point at which the measured plasma concentration is at or above the Lower Limit of quantification (LLQ) and λz is the apparent terminal rate constant determined by log-linear regression analysis of the measured plasma concentrations of the terminal log-linear phase. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D12 | C3D1 | |
MSC1936369B 1 mg | 136.2 | 38.3 | 15.4 |
MSC1936369B 120 mg | 2773.5 | 2022.8 | 3477.6 |
MSC1936369B 14 mg | 234.1 | 206.3 | 134.5 |
MSC1936369B 2.5 mg | 55.5 | 43.8 | 47.6 |
MSC1936369B 28 mg | 574.2 | 805.6 | 489.8 |
MSC1936369B 3.5 mg | 31.4 | 47.5 | 34.4 |
MSC1936369B 45 mg | 924.2 | 960.7 | 1072.1 |
MSC1936369B 7 mg | 61.3 | 105.6 | 55.5 |
MSC1936369B 94 mg | 1836.4 | 2257.6 | 1056.0 |
AUC0-inf was calculated by combining AUC0-t and AUCextra. AUC extra represents an extrapolated value obtained by Clast/ λz, where Clast is the calculated plasma concentration at the last sampling time point at which the measured plasma concentration is at or above the Lower Limit of quantification (LLQ) and λz is the apparent terminal rate constant determined by log-linear regression analysis of the measured plasma concentrations of the terminal log-linear phase. Summarized data over Day 1 and Day 2 was reported. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, 12 and 24 hours post-dose on Cycle 1 Day 1 and Day 2
Intervention | hour*ng/mL (Geometric Mean) | |
---|---|---|
Fasted | Fed | |
MSC1936369B 150 mg | 3344.3 | 5633.8 |
MSC1936369B 90 mg | 1580.6 | 1495.7 |
AUC0-inf was calculated by combining AUC0-t and AUCextra. AUC extra represents an extrapolated value obtained by Clast/ λz, where Clast is the calculated plasma concentration at the last sampling time point at which the measured plasma concentration was at or above the Lower Limit of quantification (LLQ) and λz is the apparent terminal rate constant determined by log-linear regression analysis of the measured plasma concentrations of the terminal log-linear phase. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) |
---|---|
C1D15 | |
MSC1936369B 1 mg | 15.7 |
AUC0-inf was calculated by combining AUC0-t and AUCextra. AUC extra represents an extrapolated value obtained by Clast/ λz, where Clast is the calculated plasma concentration at the last sampling time point at which the measured plasma concentration was at or above the Lower Limit of quantification (LLQ) and λz is the apparent terminal rate constant determined by log-linear regression analysis of the measured plasma concentrations of the terminal log-linear phase. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | |
---|---|---|
C1D1 | C1D15 | |
MSC1936369B 45 mg | 820.4 | 933.9 |
MSC1936369B 14 mg | 218.4 | 172.2 |
AUC0-inf was calculated by combining AUC0-t and AUCextra. AUC extra represents an extrapolated value obtained by Clast/ λz, where Clast is the calculated plasma concentration at the last sampling time point at which the measured plasma concentration was at or above the Lower Limit of quantification (LLQ) and λz is the apparent terminal rate constant determined by log-linear regression analysis of the measured plasma concentrations of the terminal log-linear phase. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 120 mg | 2424.2 | 2129.0 | 2461.3 |
MSC1936369B 195 mg | 3602.2 | 3900.8 | 3452.9 |
MSC1936369B 2 mg | 23.4 | 33.3 | 15.4 |
MSC1936369B 255 mg | 4300.3 | 6232.1 | 5651.1 |
MSC1936369B 28 mg | 646.9 | 669.1 | 415.6 |
MSC1936369B 3.5 mg | 23.6 | 21.9 | 41.2 |
MSC1936369B 150 mg | 2287.8 | 2029.9 | 2796.2 |
MSC1936369B 5 mg | 59.1 | 102.0 | 49.5 |
MSC1936369B 68 mg | 885.8 | 1665.2 | 1655.1 |
MSC1936369B 7 mg | 90.3 | 89.7 | 58.1 |
MSC1936369B 94 mg | 1525.6 | 1893.2 | 1584.8 |
AUC0-inf was calculated by combining AUC0-t and AUCextra. AUC extra represents an extrapolated value obtained by Clast/ λz, where Clast is the calculated plasma concentration at the last sampling time point at which the measured plasma concentration is at or above the Lower Limit of quantification (LLQ) and λz is the apparent terminal rate constant determined by log-linear regression analysis of the measured plasma concentrations of the terminal log-linear phase. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 60 mg | 1253.1 | 1753.9 | 1597.0 |
MSC1936369B 90 mg | 1581.4 | 1517.1 | 1400.3 |
AUC0-inf was calculated by combining AUC0-t and AUCextra. AUC extra represents an extrapolated value obtained by Clast/ λz, where Clast is the calculated plasma concentration at the last sampling time point at which the measured plasma concentration is at or above the Lower Limit of quantification (LLQ) and λz is the apparent terminal rate constant determined by log-linear regression analysis of the measured plasma concentrations of the terminal log-linear phase. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, and 10 h post-dose on Cycle 1 Day 1 and Day 15; pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 h post dose on Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 45 mg | 527.6 | 674.1 | 696.0 |
MSC1936369B 60 mg | 742.3 | 1004.2 | 700.8 |
MSC1936369B 75 mg | 939.9 | 978.4 | 1285.7 |
Area under the plasma concentration vs time curve from time zero to the last sampling time t at which the concentration was at or above the lower limit of quantification (LLQ). AUC0-t was to be calculated according to the mixed log-linear trapezoidal rule. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | |
---|---|---|
C1D1 | C1D15 | |
MSC1936369B 14 mg | 188.4 | 161.5 |
MSC1936369B 45 mg | 808.0 | 906.3 |
Area under the plasma concentration vs time curve from time zero to the last sampling time t at which the concentration was at or above the lower limit of quantification (LLQ). AUC0-t was to be calculated according to the mixed log-linear trapezoidal rule. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 1 mg | 1.9 | 4.3 | 0.5 |
MSC1936369B 120 mg | 2287.0 | 1862.3 | 2053.6 |
MSC1936369B 150 mg | 2216.5 | 2086.6 | 2171.2 |
MSC1936369B 195 mg | 3415.6 | 3436.8 | 2484.5 |
MSC1936369B 2 mg | 8.2 | 22.2 | 10.2 |
MSC1936369B 255 mg | 4041.3 | 5765.9 | 4906.3 |
MSC1936369B 28 mg | 625.7 | 621.2 | 306.2 |
MSC1936369B 3.5 mg | 6.7 | 13.8 | 26.2 |
MSC1936369B 5 mg | 67.9 | 79.3 | 40.5 |
MSC1936369B 68 mg | 861.1 | 1553.9 | 1394.7 |
MSC1936369B 7 mg | 74.4 | 67.8 | 46.1 |
MSC1936369B 94 mg | 1484.6 | 1826.2 | 1299.3 |
Area under the plasma concentration vs time curve from time zero to the last sampling time t at which the concentration was at or above the lower limit of quantification (LLQ). AUC0-t was to be calculated according to the mixed log-linear trapezoidal rule. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | hour*nanogram per milliliter (h*ng/mL) (Geometric Mean) | |
---|---|---|
C1D1 | C1D12 | |
MSC1936369B 68 mg | 1624.8 | 1900.3 |
Area under the plasma concentration vs time curve from time zero to the last sampling time t at which the concentration was at or above the lower limit of quantification (LLQ). AUC0-t was to be calculated according to the mixed log-linear trapezoidal rule. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | hour*nanogram per milliliter (h*ng/mL) (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D12 | C3D1 | |
MSC1936369B 1.5 mg | 5.2 | 6.0 | 2.7 |
MSC1936369B 120 mg | 2292.4 | 1682.4 | 2064.1 |
MSC1936369B 14 mg | 213.9 | 182.0 | 113.2 |
MSC1936369B 2.5 mg | 18.5 | 26.0 | 21.0 |
MSC1936369B 28 mg | 531.3 | 691.9 | 334.9 |
MSC1936369B 3.5 mg | 22.7 | 35.9 | 23.0 |
MSC1936369B 45 mg | 889.0 | 880.0 | 666.3 |
MSC1936369B 1 mg | 4.6 | 7.0 | 6.9 |
MSC1936369B 7 mg | 52.7 | 83.6 | 45.2 |
MSC1936369B 94 mg | 1748.1 | 1991.4 | 876.7 |
Area under the plasma concentration vs time curve from time zero to the last sampling time t at which the concentration was at or above the lower limit of quantification (LLQ). AUC0-t was to be calculated according to the mixed log-linear trapezoidal rule. Summarized data over Day 1 and Day 2 was reported. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, 12 and 24 hours post-dose on Cycle 1 Day 1 and Day 2
Intervention | hour*ng/mL (Geometric Mean) | |
---|---|---|
Fasted | Fed | |
MSC1936369B 150 mg | 3286 | 5072.9 |
MSC1936369B 90 mg | 1509.6 | 1458.3 |
Area under the plasma concentration vs time curve from time zero to the last sampling time t at which the concentration was at or above the lower limit of quantification (LLQ). AUC0-t was to be calculated according to the mixed log-linear trapezoidal rule. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 60 mg | 1229.3 | 1532.4 | 1392.3 |
MSC1936369B 90 mg | 1544.9 | 1428.8 | 1122.5 |
Area under the plasma concentration vs time curve from time zero to the last sampling time t at which the concentration was at or above the lower limit of quantification (LLQ). AUC0-t was to be calculated according to the mixed log-linear trapezoidal rule. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, and 10 h post-dose on Cycle 1 Day 1 and Day 15; pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 h post dose on Cycle 3 Day 1
Intervention | hour*ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 45 mg | 407.2 | 589.3 | 450.0 |
MSC1936369B 60 mg | 681.4 | 838.8 | 577.0 |
MSC1936369B 75 mg | 791.1 | 710.3 | 1005.0 |
Pharmacokinetic (PK) parameter Cmax was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours (h) post-dose on Cycle 1(C1) Day 1 (D1), Cycle 1 Day 12 (D12) and Cycle 3 (C3) Day 1
Intervention | nanogram per milliliter (ng/mL) (Geometric Mean) | |
---|---|---|
C1D1 | C1D12 | |
MSC1936369B 68 mg | 357.39 | 413.58 |
Pharmacokinetic (PK) parameter Cmax was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours (h) post-dose on Cycle 1(C1) Day 1 (D1), Cycle 1 Day 12 (D12) and Cycle 3 (C3) Day 1
Intervention | nanogram per milliliter (ng/mL) (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D12 | C3D1 | |
MSC1936369B 1 mg | 2.02 | 2.92 | 2.00 |
MSC1936369B 1.5 mg | 3.20 | 2.69 | 2.90 |
MSC1936369B 120 mg | 428.85 | 425.26 | 652.70 |
MSC1936369B 14 mg | 62.32 | 54.47 | 51.30 |
MSC1936369B 2.5 mg | 4.21 | 6.29 | 5.60 |
MSC1936369B 28 mg | 126.21 | 150.67 | 84.70 |
MSC1936369B 3.5 mg | 6.69 | 9.75 | 8.06 |
MSC1936369B 45 mg | 212.96 | 175.94 | 167.75 |
MSC1936369B 7 mg | 12.60 | 21.93 | 10.90 |
MSC1936369B 94 mg | 325.99 | 602.12 | 282.44 |
Cmax was obtained directly from the concentration versus time curve. Summarized data over Day 1 and Day 2 was reported. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, 12 and 24 hours post-dose on Cycle 1 Day 1 and Day 2
Intervention | ng/mL (Geometric Mean) | |
---|---|---|
Fasted | Fed | |
MSC1936369B 150 mg | 1158.00 | 370.70 |
MSC1936369B 90 mg | 321.14 | 305.94 |
Cmax was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | ng/mL (Geometric Mean) | |
---|---|---|
C1D1 | C1D15 | |
MSC1936369B 14 mg | 39.19 | 34.87 |
MSC1936369B 45 mg | 321.85 | 286.88 |
Cmax was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 120 mg | 605.11 | 492.81 | 568.49 |
MSC1936369B 150 mg | 539.02 | 450.29 | 795.86 |
MSC1936369B 195 mg | 680.87 | 629.85 | 773.14 |
MSC1936369B 2 mg | 2.87 | 7.77 | 4.30 |
MSC1936369B 255 mg | 990.92 | 1535.60 | 2344.91 |
MSC1936369B 28 mg | 187.98 | 131.71 | 96.60 |
MSC1936369B 3.5 mg | 4.55 | 4.21 | 6.56 |
MSC1936369B 1 mg | 1.65 | 2.28 | 1.25 |
MSC1936369B 5 mg | 17.26 | 18.78 | 14.81 |
MSC1936369B 68 mg | 306.63 | 539.17 | 710.94 |
MSC1936369B 7 mg | 30.90 | 18.47 | 16.10 |
MSC1936369B 94 mg | 373.59 | 432.46 | 532.80 |
Cmax was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 60 mg | 241.27 | 316.08 | 473.27 |
MSC1936369B 90 mg | 402.77 | 324.80 | 376.62 |
Cmax was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, and 10 h post-dose on Cycle 1 Day 1 and Day 15; pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 h post dose on Cycle 3 Day 1
Intervention | ng/mL (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 45 mg | 132.57 | 178.09 | 139.60 |
MSC1936369B 60 mg | 206.46 | 231.12 | 157.46 |
MSC1936369B 75 mg | 263.08 | 190.42 | 329.28 |
Number of subjects with clinical benefit (CR, PR, or SD) and PD according to Response Evaluation Criteria in Solid Tumors (RECIST Version 1.0) was reported. CR: defined as disappearance of all target and all non-target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm. PR: defined as at least a 30% decrease in sum of longest diameter of target lesions, taking as reference the baseline sum of longest diameter. PD:defined as at least a 20% increase in sum of longest diameter of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study) or unequivocal progression of existing non-target lesions. SD: defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum of longest diameter while on study. (NCT00982865)
Timeframe: Baseline until disease progression (assessed up to end of treatment [253 weeks])
Intervention | Subjects (Number) | |||
---|---|---|---|---|
CR | PR | SD | PD | |
MSC1936369B Regimen 1 | 0 | 0 | 19 | 20 |
MSC1936369B Regimen 2 and Regimen 2 Food Effect | 0 | 4 | 34 | 33 |
MSC1936369B Regimen 3 Once Daily (QD) | 0 | 2 | 9 | 4 |
MSC1936369B Regimen 3 Twice Daily | 1 | 6 | 14 | 12 |
Any clinically significant changes in laboratory evaluations and vital signs were recorded as treatment emergent adverse events. The clinical laboratory parameters that were assessed included: Hematological parameters, Blood chemistry parameters, Urinalysis and the vital signs that were assessed included: Blood pressure, Heart rate, Temperature and Weight. SAF analysis was used. (NCT00982865)
Timeframe: Baseline up to 253 weeks
Intervention | Subjects (Number) | |||||||||||||||||||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Haemoglobin decreased | Anaemia | Lymphopenia | Thrombocytopenia | Platelet count decreased | Neutropenia | Leukopenia | Pancytopenia | Hyponatraemia | Hypokalaemia | Hyperkalaemia | Hypocalcaemia | Hypercalcaemia | Hypomagnesaemia | Hypophosphataemia | Hepatic enzyme increased | Hepatic function abnormal | Alanine aminotransferase increased | Aspartate aminotransferase increased | Blood alkaline phosphatase increased | Hyperbilirubinaemia | Blood lactate dehydrogenase increased | Blood creatine phosphokinase increased | Blood creatinine increased | Blood 25-hydroxycholecalciferol decreased | Vitamin D decreased | Blood parathyroid hormone increased | Hyperglycaemia | C-reactive protein increased | Proteinuria | Hyperthyroidism | Hypoalbuminaemia | Weight increased | Weight decreased | Hyperthermia | Hypertension | Hypotension | Heart rate increased | Tachycardia | Blood potassium increased | |
MSC1936369B Regimen 1 | 1 | 10 | 3 | 3 | 0 | 0 | 0 | 0 | 0 | 4 | 1 | 2 | 0 | 2 | 0 | 0 | 0 | 0 | 1 | 1 | 1 | 1 | 1 | 0 | 1 | 0 | 1 | 0 | 0 | 0 | 0 | 3 | 0 | 6 | 1 | 7 | 3 | 1 | 3 | 1 |
MSC1936369B Regimen 2 (Without Food Effect + With Food Effect) | 2 | 23 | 7 | 6 | 1 | 4 | 0 | 0 | 1 | 10 | 0 | 7 | 3 | 3 | 2 | 1 | 1 | 1 | 1 | 0 | 1 | 0 | 2 | 1 | 1 | 1 | 1 | 1 | 1 | 0 | 0 | 4 | 3 | 8 | 5 | 5 | 1 | 0 | 0 | 0 |
MSC1936369B Regimen 3 Once Daily (QD) | 0 | 3 | 0 | 2 | 0 | 0 | 1 | 0 | 0 | 2 | 0 | 0 | 0 | 2 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 0 | 0 | 0 | 4 | 0 | 1 | 2 | 0 | 2 | 0 |
MSC1936369B Regimen 3 Twice Daily | 0 | 3 | 0 | 1 | 0 | 1 | 0 | 1 | 1 | 2 | 0 | 1 | 0 | 0 | 0 | 0 | 0 | 2 | 2 | 1 | 0 | 1 | 5 | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 1 | 2 | 3 | 2 | 1 | 4 | 0 | 0 | 0 | 0 |
AE was defined as any untoward medical occurrence which does not necessarily have a causal relationship with this the study drug. An AE was defined as any unfavourable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of study drug, whether or not considered related to the study drug. A serious AE 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. Treatment-emergent are events between first dose of study drug and up to 253 weeks. TEAEs include both Serious TEAEs and non-serious TEAEs. (NCT00982865)
Timeframe: Baseline up to 253 weeks
Intervention | Subjects (Number) | ||
---|---|---|---|
TEAEs | Serious TEAEs | TEAEs leading to discontinuation | |
MSC1936369B Regimen 1 | 47 | 23 | 13 |
MSC1936369B Regimen 2 (Without Food Effect + With Food Effect) | 82 | 45 | 22 |
MSC1936369B Regimen 3 Once Daily (QD) | 15 | 8 | 2 |
MSC1936369B Regimen 3 Twice Daily | 34 | 21 | 6 |
(NCT00982865)
Timeframe: Pre-dose on C1D1, C1D2, C1D5, C1D8; 2, 4, 8 h post-dose on C1D1; pre-dose, 2, 8, 24 h post-dose on C1D12-15; pre-dose, 2, 4 h post-dose on C1D3
Intervention | fold change (Mean) | |||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
C1D1, Pre-dose (pERK) | C1D1, 2 h post-dose (pERK) | C1D1, 8 h post-dose (pERK) | C1D2, Pre-dose (pERK) | C1D8, Pre-dose (pERK) | C1D12-15, Pre-dose (pERK) | C1D12-15, 2 h Post-dose (pERK) | C1D12-15, 8 h Post-dose (pERK) | C1D12-15, 24 h Post-dose (pERK) | C1D1, Pre-dose (Tot ERK) | C1D1, 2 h post-dose (Tot ERK) | C1D1, 8 h post-dose (Tot ERK) | C1D2, Pre-dose (Tot ERK) | C1D8, Pre-dose (Tot ERK) | C1D12-15, Pre-dose (Tot ERK) | C1D12-15, 2 h Post-dose (Tot ERK) | C1D12-15, 8 h Post-dose (Tot ERK) | C1D12-15, 24 h Post-dose (Tot ERK) | |
MSC1936369B Regimen 3 Once Daily | 4.121 | 1.178 | 1.878 | 3.081 | 2.541 | 3.241 | 1.471 | 1.902 | 2.598 | 1.02 | 1.078 | 1.078 | 1.013 | 0.944 | 1.333 | 1.335 | 1.044 | 1.048 |
MSC1936369B Regimen 3 Twice Daily | 3.629 | 1.249 | 1.821 | 2.069 | 2.235 | 2.16 | 1.315 | 1.98 | 2.043 | 1.086 | 1.079 | 1.098 | 1.108 | 1.049 | 1.047 | 1.059 | 1.026 | 1.068 |
(NCT00982865)
Timeframe: Pre-dose on C1D1, C1D2, C1D5, C1D8; 2, 4, 8 h post-dose on C1D1; pre-dose, 2, 8, 24 h post-dose on C1D12-15; pre-dose, 2, 4 h post-dose on C1D3
Intervention | fold change (Mean) | |||||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
C1D1, Pre-dose (pERK) | C1D1, 2 h post-dose (pERK) | C1D1, 4 h post-dose (pERK) | C1D1, 8 h post-dose (pERK) | C1D2, Pre-dose (pERK) | C1D8, Pre-dose (pERK) | C1D12-15, Pre-dose (pERK) | C1D12-15, 2 h Post-dose (pERK) | C1D12-15, 8 h Post-dose (pERK) | C1D12-15, 24 h Post-dose (pERK) | C3D1, Pre-dose (pERK) | C3D1, 2 h Post-dose (pERK) | C3D1, 4 h Post-dose (pERK) | C1D1, Pre-dose (Tot ERK) | C1D1, 2 h post-dose (Tot ERK) | C1D1, 4 h post-dose (Tot ERK) | C1D1, 8 h post-dose (Tot ERK) | C1D2, Pre-dose (Tot ERK) | C1D8, Pre-dose (Tot ERK) | C1D12-15, Pre-dose (Tot ERK) | C1D12-15, 2 h Post-dose (Tot ERK) | C1D12-15, 8 h Post-dose (Tot ERK) | C1D12-15, 24 h Post-dose (Tot ERK) | C3D1, Pre-dose (Tot ERK) | C3D1, 2 h Post-dose (Tot ERK) | C3D1, 4 h Post-dose (Tot ERK) | |
MSC1936369B Regimen 2 (Without Food Effect + With Food Effect) | 3.937 | 1.305 | 3.422 | 1.454 | 2.411 | 2.868 | 3.265 | 1.293 | 1.653 | 2.476 | 3.716 | 1.288 | 2.688 | 1.075 | 1.069 | 1.012 | 1.095 | 1.13 | 1.108 | 1.118 | 1.125 | 1.041 | 1.045 | 1.138 | 1.251 | 1.052 |
(NCT00982865)
Timeframe: Pre-dose on C1D1, C1D2, C1D5, C1D8; 2, 4, 8 h post-dose on C1D1; pre-dose, 2, 8, 24 h post-dose on C1D12-15; pre-dose, 2, 4 h post-dose on C1D3
Intervention | fold change (Mean) | |||||||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
C1D1, Pre-dose (pERK) | C1D1, 2 h post-dose (pERK) | C1D1, 4 h post-dose (pERK) | C1D1, 8 h post-dose (pERK) | C1D2, Pre-dose (pERK) | C1D5, Pre-dose (pERK) | C1D8, Pre-dose (pERK) | C1D12-15, Pre-dose (pERK) | C1D12-15, 2 h Post-dose (pERK) | C1D12-15, 8 h Post-dose (pERK) | C1D12-15, 24 h Post-dose (pERK) | C3D1, Pre-dose (pERK) | C3D1, 2 h Post-dose (pERK) | C3D1, 4 h Post-dose (pERK) | C1D1, Pre-dose (Tot ERK) | C1D1, 2 h post-dose (Tot ERK) | C1D1, 4 h post-dose (Tot ERK) | C1D1, 8 h post-dose (Tot ERK) | C1D2, Pre-dose (Tot ERK) | C1D5, Pre-dose (Tot ERK) | C1D8, Pre-dose (Tot ERK) | C1D12-15, Pre-dose (Tot ERK) | C1D12-15, 2 h Post-dose (Tot ERK) | C1D12-15, 8 h Post-dose (Tot ERK) | C1D12-15, 24 h Post-dose (Tot ERK) | C3D1, Pre-dose (Tot ERK) | C3D1, 2 h Post-dose (Tot ERK) | C3D1, 4 h Post-dose (Tot ERK) | |
MSC1936369B Regimen 1 | 4.524 | 1.235 | 3.828 | 1.454 | 2.853 | 2.722 | 4.48 | 3.257 | 1.252 | 1.514 | 2.768 | 5.179 | 1.795 | 3.106 | 1.1 | 1.063 | 1.059 | 1.058 | 1.075 | 1.163 | 1.233 | 1.223 | 1.04 | 0.994 | 1.047 | 1.074 | 1.087 | 0.674 |
Time to reach the maximum plasma concentration (Tmax) was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Hours (h) (Median) | |
---|---|---|
C1D1 | C1D12 | |
MSC1936369B 68 mg | 1.000 | 1.000 |
Time to reach the maximum plasma concentration (Tmax) was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Hours (h) (Median) | ||
---|---|---|---|
C1D1 | C1D12 | C3D1 | |
MSC1936369B 1 mg | 1.500 | 1.633 | 1.52 |
MSC1936369B 1.5 mg | 0.750 | 0.533 | 0.500 |
MSC1936369B 120 mg | 1.017 | 1.083 | 2.000 |
MSC1936369B 14 mg | 1.000 | 1.500 | 1.500 |
MSC1936369B 2.5 mg | 1.500 | 1.000 | 1.52 |
MSC1936369B 28 mg | 1.500 | 1.000 | 1.000 |
MSC1936369B 3.5 mg | 1.500 | 1.000 | 1.000 |
MSC1936369B 45 mg | 1.017 | 2.000 | 1.508 |
MSC1936369B 7 mg | 1.500 | 1.017 | 1.517 |
MSC1936369B 94 mg | 1.483 | 1.500 | 1.767 |
Time to reach the maximum plasma concentration (Tmax) was obtained directly from the concentration versus time curve. Summarized data over Day 1 and Day 2 was reported. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, 12 and 24 hours post-dose on Cycle 1 Day 1 and Day 2
Intervention | Hours (h) (Median) | |
---|---|---|
Fasted | Fed | |
MSC1936369B 150 mg | 1.000 | 6.000 |
MSC1936369B 90 mg | 1.600 | 2.033 |
Time to reach the maximum plasma concentration (Tmax) was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Hours (h) (Median) | |
---|---|---|
C1D1 | C1D15 | |
MSC1936369B 14 mg | 1.500 | 1.500 |
MSC1936369B 45 mg | 0.500 | 1.500 |
Time to reach the maximum plasma concentration (Tmax) was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Hours (h) (Median) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 1 mg | 1.500 | 1.500 | 1.250 |
MSC1936369B 120 mg | 1.250 | 2.000 | 1.042 |
MSC1936369B 150 mg | 1.500 | 1.517 | 1.333 |
MSC1936369B 195 mg | 1.250 | 1.250 | 1.000 |
MSC1936369B 2 mg | 1.017 | 0.967 | 2.000 |
MSC1936369B 255 mg | 2.000 | 1.458 | 1.000 |
MSC1936369B 28 mg | 1.000 | 1.017 | 1.50 |
MSC1936369B 3.5 mg | 1.500 | 2.000 | 1.258 |
MSC1936369B 5 mg | 1.000 | 0.667 | 1.000 |
MSC1936369B 68 mg | 1.000 | 1.250 | 0.500 |
MSC1936369B 7 mg | 0.533 | 1.008 | 2.500 |
MSC1936369B 94 mg | 1.500 | 1.500 | 2.000 |
Time to reach the maximum plasma concentration (Tmax) was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Hours (h) (Median) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 60 mg | 1.033 | 2.500 | 2.000 |
MSC1936369B 90 mg | 1.500 | 1.492 | 1.000 |
Time to reach the maximum plasma concentration (Tmax) was obtained directly from the concentration versus time curve. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, and 10 h post-dose on Cycle 1 Day 1 and Day 15; pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 h post dose on Cycle 3 Day 1
Intervention | Hours (h) (Median) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 45 mg | 1.500 | 1.500 | 1.467 |
MSC1936369B 60 mg | 1.000 | 1.500 | 1.183 |
MSC1936369B 75 mg | 0.667 | 1.500 | 1.467 |
Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Apparent body clearance of the drug from plasma, CL= Dose/AUC0-inf. As AUCextra was >20% of AUC0-inf, CL/f derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 1.5mg, 2.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Liter per hour (Geometric Mean) | |
---|---|---|
C1D1 | C1D12 | |
MSC1936369B 28 mg | 48.76 | 37.49 |
MSC1936369B 3.5 mg | 132.69 | 70.60 |
MSC1936369B 68 mg | 40.01 | 35.80 |
Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Apparent body clearance of the drug from plasma, CL= Dose/AUC0-inf. As AUCextra was >20% of AUC0-inf, CL/f derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 1.5mg, 2.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 12 and Cycle 3 Day 1
Intervention | Liter per hour (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D12 | C3D1 | |
MSC1936369B 120 mg | 47.82 | 61.44 | 72.25 |
MSC1936369B 14 mg | 59.80 | 62.53 | 104.07 |
MSC1936369B 45 mg | 48.69 | 49.37 | 82.35 |
MSC1936369B 7 mg | 114.26 | 44.55 | 217.56 |
MSC1936369B 94 mg | 50.45 | 50.88 | 107.06 |
Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Apparent body clearance of the drug from plasma, CL= Dose/AUC0-inf. Summarized data over Day 1 and Day 2 was reported. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, 12 and 24 hours post-dose on Cycle 1 Day 1 and Day 2
Intervention | Liter per hour (Geometric Mean) | |
---|---|---|
Fasted | Fed | |
MSC1936369B 150 mg | 44.85 | 26.62 |
MSC1936369B 90 mg | 56.94 | 60.17 |
Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Apparent body clearance of the drug from plasma, CL= Dose/AUC0-inf. As AUCextra was >20% of AUC0-inf, CL/f derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 2mg, 3.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Liter per hour (Geometric Mean) | |
---|---|---|
C1D1 | C1D15 | |
MSC1936369B 14 mg | 64.09 | 86.72 |
MSC1936369B 28 mg | 43.28 | 45.10 |
MSC1936369B 45 mg | 54.85 | 49.65 |
MSC1936369B 7 mg | 90.76 | 134.9 |
Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Apparent body clearance of the drug from plasma, CL= Dose/AUC0-inf. As AUCextra was >20% of AUC0-inf, CL/f derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 2mg, 3.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Liter per hour (Geometric Mean) | |
---|---|---|
C1D15 | C3D1 | |
MSC1936369B 5 mg | 59.55 | 89.34 |
Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Apparent body clearance of the drug from plasma, CL= Dose/AUC0-inf. As AUCextra was >20% of AUC0-inf, CL/f derived from λz was regarded as implausible & not calculated for arms MSC1936369B 1mg, 2mg, 3.5 mg. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Liter per hour (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 120 mg | 49.50 | 92.42 | 48.76 |
MSC1936369B 150 mg | 65.57 | 81.22 | 61.04 |
MSC1936369B 195 mg | 54.13 | 53.49 | 72.33 |
MSC1936369B 255 mg | 60.63 | 42.20 | 44.23 |
MSC1936369B 68 mg | 76.77 | 43.76 | 41.08 |
MSC1936369B 94 mg | 61.61 | 51.47 | 59.31 |
Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Apparent body clearance of the drug from plasma, CL= Dose/AUC0-inf. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 and 24 hours post-dose on Cycle 1 Day 1, Cycle 1 Day 15 and Cycle 3 Day 1
Intervention | Liter per hour (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 60 mg | 47.88 | 48.31 | 53.36 |
MSC1936369B 90 mg | 56.91 | 62.85 | 75.63 |
Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. Apparent body clearance of the drug from plasma, CL= Dose/AUC0-inf. (NCT00982865)
Timeframe: Pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8, and 10 h post-dose on Cycle 1 Day 1 and Day 15; pre-dose, 0.5, 1, 1.5, 2, 2.5, 4, 6, 8 h post dose on Cycle 3 Day 1
Intervention | Liter per hour (Geometric Mean) | ||
---|---|---|---|
C1D1 | C1D15 | C3D1 | |
MSC1936369B 45 mg | 114.82 | 71.44 | 126.1 |
MSC1936369B 60 mg | 80.83 | 66.89 | 103.3 |
MSC1936369B 75 mg | 83.86 | 94.48 | 77.09 |
λz of total [14C] radioactivity was determined from the terminal slope of the log-transformed plasma concentration curve using linear regression on terminal data points of the curve. (NCT01713036)
Timeframe: Pre dose, 0.5, 0.75, 1.0, 1.5, 2.0, 2.5, 4.0, 6.0, 8.0, 10.0, 12.0, 24.0, 48.0, 72.0, 96.0 and 168.0 hours post [14C]-labeled pimasertib dose on Day 8
Intervention | per hour (Geometric Mean) |
---|---|
Pimasertib | 0.04084 |
(NCT01713036)
Timeframe: Pre dose, 0.5, 0.75, 1.0, 1.5, 2.0, 2.5, 4.0, 6.0, 8.0, 10.0, 12.0, 24.0, 48.0, 72.0, 96.0 and 168.0 hours post [14C]-labeled pimasertib dose on Day 8
Intervention | hour (Median) |
---|---|
Pimasertib | 14.41 |
Volume of distribution was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired plasma concentration of a drug. Apparent volume of distribution after oral dose (Vz/f) was influenced by the fraction absorbed. Vz/f of total radioactivity during the terminal phase was calculated by dividing the dose with the product of area under the plasma concentration time curve and apparent terminal rate constant (dose/AUC0inf*λz). (NCT01713036)
Timeframe: Pre dose, 0.5, 0.75, 1.0, 1.5, 2.0, 2.5, 4.0, 6.0, 8.0, 10.0, 12.0, 24.0, 48.0, 72.0, 96.0 and 168.0 hours post [14C]-labeled pimasertib dose on Day 8
Intervention | Liter (Geometric Mean) |
---|---|
Pimasertib | 253.5 |
(NCT01713036)
Timeframe: Pre-dose, 0.5, 1, 1.5, 3, 5, 7, 9, 11, 15, 23, and 47 hours post [14C] intravenous pimasertib dose on Day 1
Intervention | hour*picogram equivalent/milliliter (Geometric Mean) |
---|---|
Pimasertib | 37.4 |
(NCT01713036)
Timeframe: Pre-dose, 0.5, 0.75, 1, 1.5, 2, 2.5, 4, 6, 8, 10, 12, 16, 24, and 48 hours post unlabeled pimasertib dose on Day 1
Intervention | hour*nanogram/milliliter (Geometric Mean) |
---|---|
Pimasertib | 957.4 |
Area under the plasma concentration time curve from time zero to the last sampling time at which the concentration is at or above the lower limit of quantification was calculated by using mixed log linear trapezoidal rule. Unit of assessment was hour*nanogram equivalent per milliliter (hr*ng eq/mL). (NCT01713036)
Timeframe: Pre dose, 0.5, 0.75, 1.0, 1.5, 2.0, 2.5, 4.0, 6.0, 8.0, 10.0, 12.0, 24.0, 48.0, 72.0, 96.0 and 168.0 hours post [14C]-labeled pimasertib dose on Day 8
Intervention | hr*ng eq/mL (Geometric Mean) |
---|---|
Pimasertib | 5318 |
(NCT01713036)
Timeframe: Pre-dose, 0.5, 1, 1.5, 3, 5, 7, 9, 11, 15, 23, and 47 hours post [14C] intravenous pimasertib dose on Day 1
Intervention | hour*picogram equivalent/milliliter (Geometric Mean) |
---|---|
Pimasertib | 36.0 |
(NCT01713036)
Timeframe: Pre-dose, 0.5, 0.75, 1, 1.5, 2, 2.5, 4, 6, 8, 10, 12, 16, 24, and 48 hours post unlabeled pimasertib dose on Day 1
Intervention | hour*nanogram/milliliter (Geometric Mean) |
---|---|
Pimasertib | 937.2 |
Area under the concentration time curve (AUC) from time zero to infinity (AUC0-inf) was calculated from AUC0-t + AUCextra, where AUCextra = Clast calc/λz. Clast calc was the calculated plasma concentration at the last sampling time point at which plasma concentration was at or above the lower limit of quantification was measured and λz represents apparent terminal elimination rate constant. (NCT01713036)
Timeframe: Pre dose, 0.5, 0.75, 1.0, 1.5, 2.0, 2.5, 4.0, 6.0, 8.0, 10.0, 12.0, 24.0, 48.0, 72.0, 96.0 and 168.0 hours post [14C]-labeled pimasertib dose on Day 8
Intervention | hr*ng eq/mL (Geometric Mean) |
---|---|
Pimasertib | 5711 |
(NCT01713036)
Timeframe: 1.5 hour post [14C]-labeled pimasertib dose on Day 8
Intervention | Ratio (Mean) |
---|---|
Pimasertib | 0.687 |
Fraction of unbound drug (fu) is defined as the ratio of unbound drug concentration to the total drug concentration multiplied by 100. (NCT01713036)
Timeframe: 1.5 hour post [14C]-labeled pimasertib dose on Day 8
Intervention | percentage of unbound drug (Mean) |
---|---|
Pimasertib | 6.702 |
(NCT01713036)
Timeframe: Pre-dose, 0.5, 1, 1.5, 3, 5, 7, 9, 11, 15, 23, and 47 hours post [14C] intravenous pimasertib dose on Day 1
Intervention | picogram equivalent per milliliter (Geometric Mean) |
---|---|
Pimasertib | 12.67 |
Unit of assessment was nanogram equivalent per milliliter (ng eq/mL). (NCT01713036)
Timeframe: Pre dose, 0.5, 0.75, 1.0, 1.5, 2.0, 2.5, 4.0, 6.0, 8.0, 10.0, 12.0, 24.0, 48.0, 72.0, 96.0 and 168.0 hours post [14C]-labeled pimasertib dose on Day 8
Intervention | ng eq/mL (Geometric Mean) |
---|---|
Pimasertib | 774.1 |
(NCT01713036)
Timeframe: Pre-dose 0.5, 0.75, 1, 1.5, 2, 2.5, 4, 6, 8, 10, 12, 16, 24, and 48 hours post unlabeled pimasertib dose on Day 1
Intervention | ng/mL (Geometric Mean) |
---|---|
Pimasertib | 265 |
Oral bioavailability (F) was calculated using the formula=AUC0-inf oral/dose oral) / (AUC0-inf iv/dose iv) * 100%, where AUC0-inf is the area under the concentration time curve (AUC) from time zero to infinity. (NCT01713036)
Timeframe: Pre-dose, 0.5, 0.75, 1, 1.5, 2, 2.5, 4, 6, 8, 10, 12, 16, 24, and 48 hours post unlabeled pimasertib dose on Day 1; Pre-dose, 0.5, 1, 1.5, 3, 5, 7, 9, 11, 15, 23, and 47 hours post [14C] labeled pimasertib dose on Day 1
Intervention | percentage bioavailability (Number) |
---|---|
Pimasertib | 73 |
The volume of distribution of the central or plasma compartment (Vc) was calculated using the formula=Dose/C0 (NCT01713036)
Timeframe: Pre-dose, 0.5, 1, 1.5, 3, 5, 7, 9, 11, 15, 23, and 47 hours post intravenous [14C] pimasertib dose on Day 1
Intervention | Liter (Geometric Mean) |
---|---|
Pimasertib | 83.668 |
(NCT01713036)
Timeframe: Pre dose, 0.5, 0.75, 1.0, 1.5, 2.0, 2.5, 4.0, 6.0, 8.0, 10.0, 12.0, 24.0, 48.0, 72.0, 96.0 and 168.0 hours post [14C]-labeled pimasertib dose on Day 8
Intervention | hour (Median) |
---|---|
Pimasertib | 1.5 |
Clearance of a drug was a measure of the rate at which a drug is metabolized or eliminated by normal biological processes. CL/f was influenced by the fraction absorbed. Apparent body clearance of total radioactivity from plasma was calculated by dividing the dose with area under the plasma concentration time curve from zero to infinity (Dose/AUC0inf). (NCT01713036)
Timeframe: Pre dose, 0.5, 0.75, 1.0, 1.5, 2.0, 2.5, 4.0, 6.0, 8.0, 10.0, 12.0, 24.0, 48.0, 72.0, 96.0 and 168.0 hours post [14C]-labeled pimasertib dose on Day 8
Intervention | liter per hour (Geometric Mean) |
---|---|
Pimasertib | 10.35 |
The λz of M445 and M554 was determined from the terminal slope of the log-transformed plasma concentration curve using linear regression on terminal data points of the curve. (NCT01713036)
Timeframe: Predose, 1.0, 2.0, 4.0, 10 and 24 hour post [14C]-labeled pimasertib dose on Day 8
Intervention | per hour (Geometric Mean) | |
---|---|---|
M445 | M554 | |
Pimasertib | 0.2542 | 0.07021 |
Apparent terminal elimination rate constant (λz) was determined from the terminal slope of the log-transformed plasma concentration curve using linear regression on terminal data points of the curve. (NCT01713036)
Timeframe: Pre-dose, 0.5, 0.75, 1, 1.5, 2, 2.5, 4, 6, 8, 10, 12, 16, 24, and 48 hours post unlabeled pimasertib dose on Day 1; Pre-dose, 0.5, 1, 1.5, 3, 5, 7, 9, 11, 15, 23, and 47 hours post intravenous [14C] labeled pimasertib dose on Day 1
Intervention | per hour (Geometric Mean) | |
---|---|---|
Unlabeled pimasertib | Intravenous [14C] pimasertib | |
Pimasertib | 0.1096 | 0.1994 |
(NCT01713036)
Timeframe: Predose, 1.0, 2.0, 4.0, 10 and 24 hour post [14C]-labeled pimasertib dose on Day 8
Intervention | hour (Median) | |
---|---|---|
M445 | M554 | |
Pimasertib | 2.653 | 10.81 |
The apparent volume of distribution during the terminal phase following oral administration (Vz/f) and the apparent volume of distribution during the terminal phase following intravenous administration was calculated by using the formula=Dose/( AUC0-inf* λz). (NCT01713036)
Timeframe: Pre-dose, 0.5, 0.75, 1, 1.5, 2, 2.5, 4, 6, 8, 10, 12, 16, 24, and 48 hours post unlabeled pimasertib dose on Day 1; Pre-dose, 0.5, 1, 1.5, 3, 5, 7, 9, 11, 15, 23, and 47 hours post [14C] labeled pimasertib dose on Day 1
Intervention | Liter (Geometric Mean) | |
---|---|---|
Unlabeled pimasertib | Intravenous [14C] pimasertib | |
Pimasertib | 571.77 | 229.35 |
AUC from time 0 to infinity (AUC0-inf), was calculated from AUC0-t + AUCextra, where AUCextra = Clast calc/lambda z (λz). Clast calc was the calculated plasma concentration at the last sampling time point at which plasma concentration was at or above the lower limit of quantification was measured and λz represents apparent terminal elimination rate constant. (NCT01713036)
Timeframe: Predose, 1.0, 2.0, 4.0, 10 and 24 hour post [14C]-labeled pimasertib dose on Day 8
Intervention | hr*ng eq/mL (Geometric Mean) | |
---|---|---|
M445 | M554 | |
Pimasertib | 1134.72 | 3135.61 |
Area under the plasma concentration-time curve from time zero to the last sampling time (AUC0-t) at which the concentration is at or above the lower limit of quantification. (NCT01713036)
Timeframe: Predose, 1.0, 2.0, 4.0, 10 and 24 hour post [14C]-labeled pimasertib dose on Day 8
Intervention | hr*ng eq/mL (Geometric Mean) | |
---|---|---|
M445 | M554 | |
Pimasertib | 976.39 | 1410.30 |
Recovery of total [14C]-radioactivity was determined in excreta, i.e., urine and feces at each sampling period subsequent to oral administration of [14C]-pimasertib on Day 8. Cumulative recovery of total [14C]-radioactivity in terms of percentage of dose recovered in urine and feces and total percentage of dose recovered was reported for the outcome measure. (NCT01713036)
Timeframe: Urine: 0-4, 4-8, 8-12, 12-24, 24-48, 48-72, and 72-96 hours post [14C]-labeled pimasertib dose on Day 8; Feces: 0-12, 12-24, 24-48, 48-72, 72-96, 96-120, 120-144, and 144-168 hours post [14C]-labeled pimasertib dose on Day 8
Intervention | percentage of dose recovered (Geometric Mean) | ||
---|---|---|---|
Urine | Feces | Total | |
Pimasertib | 52.8 | 30.7 | 85.1 |
Maximum observed plasma concentration (Cmax) for the metabolites M445 and M554 was calculated. (NCT01713036)
Timeframe: Predose, 1.0, 2.0, 4.0, 10 and 24 hour post [14C]-labeled pimasertib dose on Day 8
Intervention | Nanogram equivalent per milliliter (Geometric Mean) | |
---|---|---|
M445 | M554 | |
Pimasertib | 300.93 | 174.64 |
Identification and profiling of the metabolites was done. The total number of metabolites and the number of metabolites identified as major were reported. (NCT01713036)
Timeframe: Pre-dose 1.0, 2.0, 4.0, 10 and 24 hours post [14C]-labeled Pimasertib dose on Day 8
Intervention | metabolites (Number) | |
---|---|---|
Overall | Major | |
Pimasertib | 14 | 2 |
An AE was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. An SAE was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. Treatment-emergent are events between first dose of study drug administration until 30+/-2 days after the last dose of study drug administration that were absent before treatment or that worsened relative to pre treatment state. (NCT01713036)
Timeframe: Part A and B: From the first dose of study drug administration until 30+/-2 days after the last dose of study drug administration, assessed up to 18 months
Intervention | subjects (Number) | |||
---|---|---|---|---|
TEAEs | Serious TEAEs | TEAEs leading to death | TEAEs leading to discontinuation | |
Pimasertib | 6 | 2 | 1 | 3 |
Anti tumor activity defined as CR, PR, or stable disease and PD based on the investigator tumor evaluations performed every 2 cycles in accordance with Response Evaluation Criteria In Solid Tumors (RECIST) v1.1. CR =Disappearance of all target lesions except lymph nodes (LN); LN must have a decrease in the short axis to less than (<)10 millimeter (mm); PR = 30% decrease in sum of diameters of target lesions taking as reference the baseline sum diameters; Progressed Disease (PD) = 20% increase in sum of diameters of target lesions; the appearance of >=1 new lesions; SD= Neither shrinkage to qualify for PR nor increase to qualify for PD taking the smallest sum diameters on study as reference. For non-target lesions a CR = Disappearance of all non-target lesions and all LN must be non-pathological in size <10 mm; Non-CR/Non PD: persistence of one or more non-target lesions; PD = unequivocal progression of existing non-target lesions or appearance of new ones. (NCT01713036)
Timeframe: From the screening every 2 cycles until end of the treatment, assessed up to 18 months
Intervention | subjects (Number) | ||||
---|---|---|---|---|---|
Stable disease | Progressive disease | Confirmed Response | Partial Response | Non evaluable | |
Pimasertib | 3 | 1 | 0 | 0 | 1 |
(NCT01713036)
Timeframe: Pre-dose 1.0, 2.0, 4.0, 10 and 24 hours post [14C]-labeled Pimasertib dose on Day 8
Intervention | nanogram equivalent per milliliter (Mean) | |||||
---|---|---|---|---|---|---|
Predose | Hour 1 | Hour 2.0 | Hour 4.0 | Hour 10.0 | Hour 24.0 | |
Pimasertib | 0.0 | 695.2 | 691.2 | 379.3 | 165.6 | 46.62 |
Plasma concentration of the Pimasertib metabolite M445 and M554 were presented for the outcome measure. (NCT01713036)
Timeframe: Predose, 1.0, 2.0, 4.0, 10 and 24 hour post [14C]-labeled pimasertib dose on Day 8
Intervention | Nanogram equivalent per milliliter (Mean) | |||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|
M445 (Predose)(n=6) | M445 (Hour 1.0)(n=6) | M445 (Hour 2.0)(n=6) | M445 (Hour 4.0)(n=6) | M445 (Hour 10.0)(n=5) | M445 (Hour 24.0)(n=3) | M554(Predose)(n=6) | M554(Hour 1.0)(n=6) | M554 (Hour 2.0)(n=6) | M554 (Hour 4.0)(n=6) | M554 (Hour 10.0) (n=5) | M554 (Hour 24.0) (n=3) | |
Pimasertib | 0.0 | 285.2 | 262.2 | 85.05 | 28.58 | 0.0 | 0.0 | 87.53 | 167.6 | 169.1 | 108.8 | 51.33 |
Time to reach maximum plasma concentration (Tmax) for the metabolites M445 and M554 was calculated. (NCT01713036)
Timeframe: Predose, 1.0, 2.0, 4.0, 10 and 24 hour post [14C]-labeled pimasertib dose on Day 8
Intervention | hour (Median) | |
---|---|---|
M445 | M554 | |
Pimasertib | 1.5 | 4 |
(NCT01713036)
Timeframe: Pre-dose 0.5, 0.75, 1, 1.5, 2, 2.5, 4, 6, 8, 10, 12, 16, 24, and 48 hours post unlabeled pimasertib dose on Day 1; Pre-dose, 0.5, 1, 1.5, 3, 5, 7, 9, 11, 15, 23, and 47 hours post intravenous [14C] labeled pimasertib dose on Day 1
Intervention | hours (Median) | |
---|---|---|
Unlabeled pimasertib | [14C] intravenous pimasertib | |
Pimasertib | 0.75 | 0.5 |
The total body clearance of drug from plasma following oral administration (Cl/f) and the total body clearance of drug from plasma following intravenous administration was calculated by dividing the Dose with area under the plasma concentration time curve from time zero to infinity (AUC0 inf)=Dose/AUC0- inf. (NCT01713036)
Timeframe: Pre-dose, 0.5, 0.75, 1, 1.5, 2, 2.5, 4, 6, 8, 10, 12, 16, 24, and 48 hours post unlabeled pimasertib dose on Day 1; Pre-dose, 0.5, 1, 1.5, 3, 5, 7, 9, 11, 15, 23, and 47 hours post intravenous [14C] labeled pimasertib dose on Day 1
Intervention | liter per hour (Geometric Mean) | |
---|---|---|
Unlabeled pimasertib | Intravenous [14C] pimasertib | |
Pimasertib | 62.67 | 45.73 |
DLT was defined as any of the following toxicities graded as per National Cancer Institute (NCI) common terminology criteria for adverse events (NCI CTCAE v4.0) encountered within cycle 1 of treatment at any dose level and judged not to be related to the underlying disease or concomitant medications. A treatment emergent adverse event (TEAE) of potential clinical significance such that further dose escalation would expose subjects to unacceptable risk; any Grade >=3 non-hematological toxicity except Grade 3 asymptomatic increases in liver function tests, diarrhea, nausea or vomiting with duration <= 48 hours and alopecia; Grade 4 neutropenia of >5 days duration or febrile neutropenia of >1 day duration; Grade 3 thrombocytopenia with bleeding or Grade 4 thrombocytopenia; any treatment interruption >2 weeks due to adverse events; any severe, impairing daily functions or life-threatening, complication or abnormality not defined in NCI-CTCAE that is attributable to the therapy. (NCT01378377)
Timeframe: Up to 21 Days (within Cycle 1)
Intervention | subjects (Number) |
---|---|
Pimasertib 45 mg+Temsirolimus 12.5 mg | 0 |
Pimasertib 45 mg+Temsirolimus 25 mg | 7 |
Pimasertib 75 mg+Temsirolimus 25 mg | 2 |
An AE was defined as any new untoward medical occurrences/worsening of pre-existing medical condition, whether or not related to study drug. The TEAEs were those events that occur between first dose of trial treatment and up to 30 days after last dose of the trial treatment that were absent before treatment or that worsened relative to pretreatment state. (NCT01378377)
Timeframe: From the start of the trial treatment until data cut-off date (23 February 2012)
Intervention | subjects (Number) |
---|---|
Pimasertib 45 mg+Temsirolimus 12.5 mg | 4 |
Pimasertib 45 mg+Temsirolimus 25 mg | 23 |
Pimasertib 75 mg+Temsirolimus 25 mg | 6 |
Clearance (CL) of a drug was a measure of the rate at which a drug was metabolized or eliminated by normal biological processes. The CL obtained after oral dose (CL/F) was influenced by the fraction of the dose absorbed (bioavailability). Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | liter/hour (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 64.31 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 53.6 |
Clearance (CL) of a drug was a measure of the rate at which a drug was metabolized or eliminated by normal biological processes. The CL obtained after oral dose (CL/F) was influenced by the fraction of the dose absorbed (bioavailability). Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | liter/hour (Median) | |
---|---|---|
DDI: Day 1 | DDI: Day 9 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 81.25 | 71.99 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 54.36 | 55.9 |
The t1/2 was defined as the time required for the plasma concentration of drug to decrease 50% in the final stage of its elimination. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 7.746 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 5.712 |
The t1/2 was defined as the time required for the plasma concentration of drug to decrease 50% in the final stage of its elimination. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour (Median) | |
---|---|---|
DDI: Day 1 | DDI: Day 9 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 5.915 | 6.08 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 5.886 | 5.896 |
The t1/2 was defined as the time required for the plasma concentration of drug to decrease 50% in the final stage of its elimination. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 29.08 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 10.42 |
The t1/2 was defined as the time required for the plasma concentration of drug to decrease 50% in the final stage of its elimination. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour (Median) | |
---|---|---|
DDI: Day 9 | DDI: Day 16 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 25.57 | 20.62 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 13.2 | 19.14 |
Volume of distribution (Vz) was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired serum concentration of a drug. The Vz after oral dose (Vz/F) was influenced by the fraction absorbed. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | liter (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 760.6 |
Pimasertib 75 mg+Temsirolimus (TEM) 25 mg (Non-DDI) | 416.5 |
Volume of distribution (Vz) was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired serum concentration of a drug. The Vz after oral dose (Vz/F) was influenced by the fraction absorbed. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | liter (Median) | |
---|---|---|
DDI: Day 1 | DDI: Day 9 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 691.3 | 517.6 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 536.5 | 519.5 |
The AUC(0-inf) was estimated by determining the total area under the curve of the concentration versus time curve extrapolated to infinity. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour*nanogram/milliliter (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 4026 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 2194 |
The AUC(0-inf) was estimated by determining the total area under the curve of the concentration versus time curve extrapolated to infinity. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour*nanogram/milliliter (Median) | |
---|---|---|
DDI: Day 9 | DDI: Day 16 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 2452 | 2006 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 2130 | 2743 |
The AUCtau was defined as the area under the concentration curve divided by the dosing interval. AUC(0-inf) was estimated by determining the total area under the curve of the concentration versus time curve extrapolated to infinity. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1 for AUCtau; DDI cohorts: Day 1 of Cycle 1 AUC0-inf
Intervention | hour*nanogram/milliliter (Median) |
---|---|
Non-DDI: AUCtau: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 706 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 1402 |
The AUCtau was defined as the area under the concentration curve divided by the dosing interval. AUC(0-inf) was estimated by determining the total area under the curve of the concentration versus time curve extrapolated to infinity. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1 for AUCtau; DDI cohorts: Day 1 of Cycle 1 AUC0-inf
Intervention | hour*nanogram/milliliter (Median) | |
---|---|---|
DDI: AUCtau: Day 9 | DDI: AUC0-inf: Day 1 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 628 | 573.2 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 805 | 828.6 |
Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: Drug-drug interaction (DDI) cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | nanogram/milliliter (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 197.6 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 308.1 |
Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: Drug-drug interaction (DDI) cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | nanogram/milliliter (Median) | |
---|---|---|
DDI: Day 1 | DDI: Day 9 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 185.2 | 131 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 193.5 | 192.1 |
Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 8
Intervention | nanogram/milliliter (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 489.9 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 480.9 |
Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 8
Intervention | nanogram/milliliter (Median) | |
---|---|---|
DDI: Day 9 | DDI: Day 16 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 457.5 | 281.1 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 505.3 | 511.8 |
Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 1.5 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 0.5833 |
Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 1 and 9 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour (Median) | |
---|---|---|
DDI: Day 1 | DDI: Day 9 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 1 | 2.3 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 1.5 | 1.133 |
Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 0.5 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 0.55 |
Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | hour (Median) | |
---|---|---|
DDI: Day 9 | DDI: Day 16 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 0.7417 | 0.9333 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 0.5667 | 0.5 |
The clearance of a drug was a measure of the rate at which a drug was metabolized or eliminated by normal biological processes. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | liter/hour (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 6.284 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 11.39 |
The clearance of a drug was a measure of the rate at which a drug was metabolized or eliminated by normal biological processes. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | liter/hour (Median) | |
---|---|---|
DDI: Day 9 | DDI: Day 16 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 5.378 | 7.528 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 11.73 | 9.292 |
The Vz was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired serum concentration of a drug. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | liter (Median) |
---|---|
Non-DDI: Day 8 | |
Pimasertib 45 mg+Temsirolimus 25 mg (Non-DDI) | 309.7 |
Pimasertib 75 mg+Temsirolimus 25 mg (Non-DDI) | 172.9 |
The Vz was defined as the theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired serum concentration of a drug. Pharmacokinetic parameters were reported based on DDI and non-DDI cohorts as per plan. (NCT01378377)
Timeframe: DDI cohorts: Days 9 and 16 of Cycle 1; Non-DDI cohorts: Day 8 of Cycle 1
Intervention | liter (Median) | |
---|---|---|
DDI: Day 9 | DDI: Day 16 | |
Pimasertib 45 mg+Temsirolimus 12.5 mg (DDI) | 152 | 189.5 |
Pimasertib 45 mg+Temsirolimus 25 mg (DDI) | 244.5 | 233 |
Geometric mean exposure for sorafenib. (NCT00090545)
Timeframe: 0, 0.25, 0.50, 1, 2, 4, 6, 8, 12, and 24 hours post-dose
Intervention | mg/L.h (Geometric Mean) |
---|---|
First Stage - Disease Progression | 9.76 |
Second Stage - Increased Accrual | 18.63 |
Plasma concentration-time profile for sorafenib. (NCT00090545)
Timeframe: 0, 0.25, 0.50, 1, 2, 4, 6, 8, 12, AND 24 hours post dose
Intervention | mg/L (Mean) |
---|---|
First Stage - Disease Progression | 1.28 |
Second Stage - Increased Accrual | 2.57 |
Time from treatment start date until date of death or date last known alive. (NCT00090545)
Timeframe: Time from treatment start date until date of death or date last known alive, approximately 18.3 months.
Intervention | Months (Median) |
---|---|
First Stage - Disease Progression | 18 |
Second Stage - Increased Accrual | 18.3 |
Here is the number of participants with adverse events. For the detailed list of adverse events, see the adverse event module. (NCT00090545)
Timeframe: Date treatment consent signed to date off study, approximately 49 months.
Intervention | Participants (Count of Participants) |
---|---|
First Stage - Disease Progression | 22 |
Second Stage - Increased Accrual | 23 |
Determine whether BAY 43-9006 when used to treat metastatic prostate cancer is associated with having 50% of Patients Progression Free at 4 Months by clinical, radiographic, and prostatic specific antigen (PSA)criteria. (NCT00090545)
Timeframe: 4 months
Intervention | months (Median) |
---|---|
First Stage - Disease Progression | 1.83 |
Second Stage - Increased Accrual | 3.7 |
Time to maximum concentration for sorafenib. (NCT00090545)
Timeframe: 0, 0.25, 0.50, 1, 2, 4, 6, 8, 12, and 24 hours post-dose
Intervention | hours (Median) |
---|---|
First Stage - Disease Progression | 0.68 |
Second Stage - Increased Accrual | 8 |
Overall response was evaluated by the RECIST. Complete Response (CR) is the disappearance of all target lesions. Partial Response (PR) is at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters. Progressive Disease (PD) is at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. Stable Disease (SD) is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study. (NCT00090545)
Timeframe: Every 2 cycles (1 cycle = 28 days)
Intervention | Participants (Count of Participants) | |||
---|---|---|---|---|
Complete Response | Partial Response | Progressive Disease | Stable Disease | |
First Stage - Disease Progression | 0 | 0 | 8 | 0 |
Second Stage - Increased Accrual | 0 | 1 | 13 | 10 |
Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST) 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). (NCT00810394)
Timeframe: At least 3 months
Intervention | Participants (Count of Participants) |
---|---|
Sorafenib | 0 |
Overall percentage of patients tolerating a dose escalation to 600 mg twice daily for 28 days plus the percentage tolerating a re-escalation to 400 mg twice daily in Cycle 3. (NCT00810394)
Timeframe: At least 3 months
Intervention | Participants (Count of Participants) |
---|---|
Sorafenib | 11 |
Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST), 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. (NCT00810394)
Timeframe: Up to 2 years
Intervention | months (Median) |
---|---|
Sorafenib | 4.7 |
Median time course for participants to develop worst grade 3 HFSR toxicity is defined as the time (days) from start date of study drug to date of first documented grade 3 HFSR toxicity and will be calculated only for patients who had a HFSR toxicity grade 3. (NCT02651415)
Timeframe: p to Safety Follow-Up Visit (30 days +/- 7 days after permanently stopping study treatment)
Intervention | days (Median) |
---|---|
Single Arm Trial | 12 |
Median time (in months) to PFS. PFS is defined as the time from start date of study drugs to the date of first documented disease progression (radiological or clinical) or death due to any cause, if death occurs before progression is documented. PFS will be evaluated based on RECIST v1.1 criteria, 20% progression or any new lesion. (NCT02651415)
Timeframe: From start date of study drugs to the date of first documented disease progression or death due to any cause.
Intervention | Months (Median) |
---|---|
Single Arm Trial | 2.60 |
"The trial will measure the toxicities of HFSR in participants receiving both perindopril and regorafenib using the CTCAE v4.03 criteria.~The toxicity of HFSR will be expressed based on the number of participants in the study (N=10) who are experiencing HFSR of all grades." (NCT02651415)
Timeframe: Up to Safety Follow-Up Visit (30 days +/- 7 days after permanently stopping study treatment)
Intervention | Participants (Count of Participants) |
---|---|
Single Arm Trial | 7 |
The number of participants that experienced an HFSR of grade 3 or above as assessed by CTCAE v4.03 criteria when treated with a combination of regorafenib and perindopril. (NCT02651415)
Timeframe: Up to Safety Follow-Up Visit (30 days +/- 7 days after permanently stopping study treatment)
Intervention | Participants (Count of Participants) |
---|---|
Single Arm Trial | 5 |
All grades of adverse events (including HFSR) will be evaluated using CTCAE v4.03, at baseline and at D1 of each cycle while they are on the study drug and during the 30-day follow-up period (Post therapy). (NCT02651415)
Timeframe: At baseline and at D1 of each cycle while on the study drug and during the 30-day follow-up period
Intervention | participants (Number) |
---|---|
Single Arm Trial | 10 |
All grades of hypertension will be evaluated using CTCAE v4.03, weekly for the first six weeks while they are on the study drug, then every second week and during the 30-day follow-up period (Post therapy). (NCT02651415)
Timeframe: Weekly for the first six weeks while on the study drug, then every second week and during the 30-day follow-up period
Intervention | Participants (Count of Participants) |
---|---|
Single Arm Trial | 6 |
(NCT00709878)
Timeframe: 6 months
Intervention | Total number of cases (Number) | ||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Ulceration | Parakeratosis | Acanthosis | Epidermal atrophy | Epidermal dysmaturation | Epidermal dyskeratosis | Epidermal neutrophilc infiltrate | Epidermal monocytic infiltrate | Epidermal eosinophilic infiltrate | Dermal neutrophilic infiltrate | Dermal monocytic infiltrate | Dermal eosinophilic infiltrate | Follicular concretions | Follicular neutrophilic pustule | Dysmorphic follicle | Follicular dyskeratosis | Follicular neurtrophilic infiltrate | Follicular monocytic infiltrate | Follicular eosinophilic infiltrate | Eccrine dyskeratosis | Eccrine necrosis | Eccrine infiltrate | Sebaceous infiltrate | |
Patients Treated With Cetuximab (C) | 1 | 2 | 1 | 5 | 3 | 3 | 1 | 0 | 0 | 0 | 4 | 2 | 5 | 4 | 2 | 3 | 5 | 2 | 1 | 1 | 2 | 0 | 1 |
Patients Treated With Erlotinib (E) | 2 | 0 | 0 | 4 | 0 | 0 | 1 | 0 | 1 | 4 | 4 | 0 | 3 | 6 | 4 | 1 | 7 | 2 | 1 | 0 | 1 | 0 | 3 |
Patients Treated With Lapatinib (L) | 1 | 1 | 1 | 7 | 2 | 3 | 1 | 0 | 0 | 2 | 1 | 2 | 3 | 3 | 4 | 4 | 5 | 2 | 2 | 0 | 0 | 0 | 0 |
Patients Treated With Panitumumab (P) | 0 | 1 | 0 | 2 | 1 | 0 | 0 | 2 | 0 | 2 | 4 | 0 | 2 | 3 | 2 | 1 | 3 | 2 | 1 | 0 | 0 | 0 | 1 |
141 reviews available for niacinamide and Neoplasms
Article | Year |
---|---|
NAMPT: A critical driver and therapeutic target for cancer.
Topics: Animals; Cytokines; Mammals; NAD; Neoplasms; Niacinamide; Nicotinamide Phosphoribosyltransferase | 2022 |
Complex roles of nicotinamide N-methyltransferase in cancer progression.
Topics: Humans; Neoplasms; Niacinamide; Nicotinamide N-Methyltransferase | 2022 |
Nicotinamide N-methyl transferase and cancer-associated thrombosis: insights to prevention and management.
Topics: Antineoplastic Agents; Carcinogenesis; Humans; Neoplasms; Niacinamide; Nicotinamide N-Methyltransfer | 2023 |
Diverse therapeutic efficacies and more diverse mechanisms of nicotinamide.
Topics: Animals; Cell Survival; Fibrosis; Humans; Inflammation; Mitochondria; Neoplasms; Niacinamide; Skin D | 2019 |
The Role of Nicotinamide in Cancer Chemoprevention and Therapy.
Topics: Clinical Trials, Phase III as Topic; Humans; NAD; Neoplasm Proteins; Neoplasms; Niacinamide; Poly (A | 2020 |
Possible mechanisms of cancer prevention by nicotinamide.
Topics: Dietary Supplements; Humans; Neoplasms; Niacinamide; Randomized Controlled Trials as Topic | 2021 |
Allosteric Inhibition of ABL Kinases: Therapeutic Potential in Cancer.
Topics: Allosteric Regulation; Animals; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Clinical | 2020 |
Nicotinamide N-methyltransferase: At the crossroads between cellular metabolism and epigenetic regulation.
Topics: Adipose Tissue; Animals; Epigenesis, Genetic; Humans; Insulin Resistance; Liver; NAD; Neoplasms; Nia | 2021 |
Nicotinamide N-methyl transferase (NNMT): An emerging therapeutic target.
Topics: Enzyme Inhibitors; Humans; Metabolic Diseases; Neoplasms; Neurodegenerative Diseases; Niacinamide; N | 2021 |
Advances in NAD-Lowering Agents for Cancer Treatment.
Topics: Animals; Antineoplastic Agents; Biosynthetic Pathways; Cell Death; Cell Line, Tumor; Cell Survival; | 2021 |
Nicotinamide N-Methyltransferase in Acquisition of Stem Cell Properties and Therapy Resistance in Cancer.
Topics: Humans; Methylation; NAD; Neoplasm Proteins; Neoplasms; Neoplastic Stem Cells; Niacinamide; Nicotina | 2021 |
PharmGKB summary: sorafenib pathways.
Topics: Animals; Antineoplastic Agents; Clinical Trials as Topic; Gene Regulatory Networks; Humans; Neoplasm | 2017 |
NAD
Topics: Aging; Humans; Incidence; Life Expectancy; Longevity; NAD; Neoplasms; Niacinamide; Nicotinamide Mono | 2017 |
B Vitamin Complex and Chemotherapy-Induced Peripheral Neuropathy.
Topics: Animals; Humans; Neoplasms; Niacinamide; Organoplatinum Compounds; Oxaliplatin; Peripheral Nervous S | 2017 |
Pharmacology of Pimasertib, A Selective MEK1/2 Inhibitor.
Topics: Humans; MAP Kinase Kinase 1; MAP Kinase Kinase 2; Neoplasms; Niacinamide; Protein Kinase Inhibitors | 2018 |
Clinical trials targeting hypoxia.
Topics: Animals; Cell Hypoxia; Female; Humans; Male; Misonidazole; Neoplasms; Niacinamide; Oxygen Consumptio | 2019 |
Nicotinamide phosphoribosyltransferase (NAMPT) inhibitors as therapeutics: rationales, controversies, clinical experience.
Topics: Animals; Enzyme Inhibitors; Humans; Inflammation; Neoplasms; Niacinamide; Nicotinamide Phosphoribosy | 2013 |
Risk of hypertension in cancer patients treated with sorafenib: an updated systematic review and meta-analysis.
Topics: Antineoplastic Agents; Blood Pressure; Chi-Square Distribution; Drug Administration Schedule; Humans | 2013 |
Body composition in chemotherapy: the promising role of CT scans.
Topics: Anthracyclines; Body Composition; Body Weight; Chemotherapy, Adjuvant; Drug Therapy; Drug-Related Si | 2013 |
Assessment of nutritional status in cancer--the relationship between body composition and pharmacokinetics.
Topics: Antineoplastic Agents; Body Composition; Body Mass Index; Capecitabine; Deoxycytidine; Fluorouracil; | 2013 |
Risk of gastrointestinal events with sorafenib, sunitinib and pazopanib in patients with solid tumors: a systematic review and meta-analysis of clinical trials.
Topics: Adverse Drug Reaction Reporting Systems; Carcinoma, Renal Cell; Clinical Trials as Topic; Diarrhea; | 2014 |
Risk of treatment-related mortality with sorafenib in patients with cancer.
Topics: Antineoplastic Agents; Clinical Trials as Topic; Drug-Related Side Effects and Adverse Reactions; Hu | 2014 |
Incidence and risk of sorafenib-induced hypertension: a systematic review and meta-analysis.
Topics: Aged; Antineoplastic Agents; Carcinoma, Renal Cell; Drug Therapy; Humans; Hypertension; Incidence; K | 2014 |
Risk of mucocutaneous toxicities in patients with solid tumors treated with sorafenib: an updated systematic review and meta-analysis.
Topics: Alopecia; Antineoplastic Agents; Clinical Trials, Phase II as Topic; Clinical Trials, Phase III as T | 2014 |
Drug safety evaluation of sorafenib for treatment of solid tumors: consequences for the risk assessment and management of cancer patients.
Topics: Antineoplastic Agents; Case Management; Drug Interactions; Humans; Neoplasms; Niacinamide; Phenylure | 2014 |
Sorafenib: targeting multiple tyrosine kinases in cancer.
Topics: Animals; Antineoplastic Agents; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Protein Kinase | 2014 |
Sirtuin inhibitors as anticancer agents.
Topics: Animals; Antineoplastic Agents; Benzamides; Enzyme Inhibitors; Humans; Naphthols; Neoplasms; Niacina | 2014 |
Clinicopathological spectrum of kidney diseases in cancer patients treated with vascular endothelial growth factor inhibitors: a report of 5 cases and review of literature.
Topics: Acute Kidney Injury; Aged; Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineoplasti | 2014 |
Risk of cardiovascular toxicities in patients with solid tumors treated with sorafenib: an updated systematic review and meta-analysis.
Topics: Antineoplastic Agents; Cardiotoxicity; Cardiovascular Diseases; Clinical Trials, Phase II as Topic; | 2014 |
The adverse effects of sorafenib in patients with advanced cancers.
Topics: Antineoplastic Agents; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Protein Kinase Inhibito | 2015 |
Effect of glucuronidation on transport and tissue accumulation of tyrosine kinase inhibitors: consequences for the clinical management of sorafenib and regorafenib.
Topics: Animals; Antineoplastic Agents; Biological Transport; Glucuronides; Glucuronosyltransferase; Humans; | 2015 |
CDK8 kinase--An emerging target in targeted cancer therapy.
Topics: Cyclin-Dependent Kinase 8; Gene Expression Regulation, Neoplastic; Humans; Molecular Structure; Neop | 2015 |
Gastrointestinal Toxicities With Combined Antiangiogenic and Stereotactic Body Radiation Therapy.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Bevacizumab; Combined Modality Therapy; | 2015 |
Risk of treatment-related mortality with sorafenib in cancer patients: a meta-analysis of 20 randomly controlled trials : Risk of sorafenib-associated death.
Topics: Antineoplastic Agents; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Protein Kinase Inhibito | 2015 |
[Kinase inhibitors and their resistance].
Topics: Antibodies, Monoclonal, Humanized; Benzamides; Biomarkers, Tumor; Crizotinib; Drug Discovery; Drug R | 2015 |
[Anti-angiogenesis and molecular targeted therapies].
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Pro | 2015 |
Targeting the RAS pathway by mitogen-activated protein kinase inhibitors.
Topics: Animals; Azetidines; Benzamides; Benzimidazoles; Diphenylamine; Genes, ras; GTP Phosphohydrolases; H | 2015 |
Toxic Effects of Sorafenib in Patients With Differentiated Thyroid Carcinoma Compared With Other Cancers.
Topics: Antineoplastic Agents; Carcinoma; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Sorafenib; T | 2016 |
Antiangiogenic therapy in oncology: current status and future directions.
Topics: Angiogenesis Inhibitors; Angiopoietin-1; Biomarkers, Tumor; Disease-Free Survival; Drug Resistance, | 2016 |
Telomerase inhibitors: a patent review (2010-2015).
Topics: Animals; Antineoplastic Agents; Drug Design; Enzyme Inhibitors; Humans; Indoles; Inflammation; Neopl | 2016 |
Design and Reporting of Targeted Anticancer Preclinical Studies: A Meta-Analysis of Animal Studies Investigating Sorafenib Antitumor Efficacy.
Topics: Animals; Antineoplastic Agents; Disease Models, Animal; Neoplasms; Niacinamide; Phenylurea Compounds | 2016 |
The impact of Organic Anion-Transporting Polypeptides (OATPs) on disposition and toxicity of antitumor drugs: Insights from knockout and humanized mice.
Topics: Animals; Antineoplastic Agents; Camptothecin; Doxorubicin; Drug Interactions; Gene Expression; Hepat | 2016 |
Risk of serious adverse events and fatal adverse events with sorafenib in patients with solid cancer: a meta-analysis of phase 3 randomized controlled trials†.
Topics: Antineoplastic Agents; Clinical Trials, Phase III as Topic; Humans; Neoplasms; Niacinamide; Phenylur | 2017 |
Toxicity of concurrent stereotactic radiotherapy and targeted therapy or immunotherapy: A systematic review.
Topics: Antineoplastic Combined Chemotherapy Protocols; Bevacizumab; Cetuximab; CTLA-4 Antigen; Humans; Immu | 2017 |
Kinase Inhibitors in Multitargeted Cancer Therapy.
Topics: Anilides; Crizotinib; Humans; Imatinib Mesylate; Imidazoles; Indoles; Neoplasms; Niacinamide; Phenyl | 2017 |
Inefficiencies and Patient Burdens in the Development of the Targeted Cancer Drug Sorafenib: A Systematic Review.
Topics: Antineoplastic Agents; Clinical Trials as Topic; Confidence Intervals; Humans; Molecular Targeted Th | 2017 |
[Oncology 2008].
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Antineoplastic Com | 2008 |
Biomarkers of angiogenesis for the development of antiangiogenic therapies in oncology: tools or decorations?
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonate | 2008 |
Sorafenib (BAY 43-9006): review of clinical development.
Topics: Antineoplastic Agents; Benzenesulfonates; Drug Design; Drug Therapy, Combination; Humans; Neoplasms; | 2006 |
Selected combination therapy with sorafenib: a review of clinical data and perspectives in advanced solid tumors.
Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Humans; Ne | 2008 |
Evolving strategies for the management of hand-foot skin reaction associated with the multitargeted kinase inhibitors sorafenib and sunitinib.
Topics: Benzenesulfonates; Foot Dermatoses; Hand Dermatoses; Humans; Indoles; Neoplasms; Niacinamide; Phenyl | 2008 |
Evolving strategies for the management of hand-foot skin reaction associated with the multitargeted kinase inhibitors sorafenib and sunitinib.
Topics: Benzenesulfonates; Foot Dermatoses; Hand Dermatoses; Humans; Indoles; Neoplasms; Niacinamide; Phenyl | 2008 |
Evolving strategies for the management of hand-foot skin reaction associated with the multitargeted kinase inhibitors sorafenib and sunitinib.
Topics: Benzenesulfonates; Foot Dermatoses; Hand Dermatoses; Humans; Indoles; Neoplasms; Niacinamide; Phenyl | 2008 |
Evolving strategies for the management of hand-foot skin reaction associated with the multitargeted kinase inhibitors sorafenib and sunitinib.
Topics: Benzenesulfonates; Foot Dermatoses; Hand Dermatoses; Humans; Indoles; Neoplasms; Niacinamide; Phenyl | 2008 |
Dermatologic symptoms associated with the multikinase inhibitor sorafenib.
Topics: Antineoplastic Agents; Benzenesulfonates; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Prot | 2009 |
[Targeted therapies and their indications in solid neoplasias].
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic C | 2009 |
Hypothyroidism related to tyrosine kinase inhibitors: an emerging toxic effect of targeted therapy.
Topics: Antineoplastic Agents; Benzenesulfonates; Drug Therapy, Combination; Humans; Hypothyroidism; Indoles | 2009 |
Cardiovascular toxicities: clues to optimal administration of vascular endothelial growth factor signaling pathway inhibitors.
Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineo | 2009 |
Cardiac dysfunction induced by novel targeted anticancer therapy: an emerging issue.
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Benzenesulfonates; | 2009 |
Renal toxicity of targeted therapies.
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonates; Bevacizumab; Clinical | 2009 |
Angiogenesis regulated by VEGF and its receptors and its clinical application.
Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineo | 2009 |
The role of antiangiogenesis therapy: bevacizumab and beyond.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A | 2009 |
An overview of small-molecule inhibitors of VEGFR signaling.
Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Benzenesulfonates; Cadherins; Clinical Tria | 2009 |
NAD(+) -dependent histone deacetylases (sirtuins) as novel therapeutic targets.
Topics: Animals; Epigenesis, Genetic; HIV Infections; Humans; Inhibitory Concentration 50; Models, Chemical; | 2010 |
It takes two to tango: combinations of conventional cytotoxics with compounds targeting the vascular endothelial growth factor-vascular endothelial growth factor receptor pathway in patients with solid malignancies.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic C | 2010 |
Biochemical effects of SIRT1 activators.
Topics: Animals; Cardiotonic Agents; Energy Metabolism; Enzyme Activation; Heterocyclic Compounds, 4 or More | 2010 |
[Bemusement and strategy on the efficacy of clinical application of targeted anticancer drugs].
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antimetabolites, | 2009 |
Compounds in clinical Phase III and beyond.
Topics: Angiogenesis Inhibitors; Axitinib; Benzenesulfonates; Clinical Trials, Phase III as Topic; Endostati | 2010 |
Sorafenib.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Renal Cell; Clinical Trials as Topic; | 2010 |
Vascular endothelial growth factor targeted therapy in the perioperative setting: implications for patient care.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A | 2010 |
Telomerase inhibitors for the treatment of brain tumors and the potential of intranasal delivery.
Topics: Administration, Intranasal; Animals; Blood-Brain Barrier; Brain Neoplasms; Enzyme Inhibitors; Humans | 2010 |
The hand-foot-syndrome associated with medical tumor therapy - classification and management.
Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Dermatolog | 2010 |
[Anti-angiogenic drugs].
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonate | 2010 |
Cardiovascular safety of VEGF-targeting therapies: current evidence and handling strategies.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A | 2010 |
[Cutaneous side effects of the multikinase inhibitors sorafenib and sunitinib].
Topics: Antineoplastic Agents; Benzenesulfonates; Drug Delivery Systems; Drug Eruptions; Humans; Indoles; Ne | 2010 |
Tumor-stromal cell interactions and opportunities for therapeutic intervention.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A | 2010 |
Inherited hepatocellular carcinoma.
Topics: Algorithms; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Hepatocellular; Catheter Ablation; | 2010 |
In pursuit of new anti-angiogenic therapies for cancer treatment.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A | 2011 |
Meta-analysis of dermatological toxicities associated with sorafenib.
Topics: Antineoplastic Agents; Benzenesulfonates; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Prot | 2011 |
[Indications and current development of new targeted therapies in pediatric oncology].
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Benzamides; Benzen | 2011 |
Targeted-therapy and imaging response: a new paradigm for clinical evaluation?
Topics: Antineoplastic Agents; Benzamides; Benzenesulfonates; Clinical Trials as Topic; Diagnostic Imaging; | 2011 |
[Targeting the RAS signalling pathway in cancer].
Topics: Antineoplastic Agents; Benzenesulfonates; Colorectal Neoplasms; ErbB Receptors; Extracellular Signal | 2011 |
The two faces of FBW7 in cancer drug resistance.
Topics: Amyloid Precursor Protein Secretases; Apoptosis; Benzenesulfonates; Biphenyl Compounds; Cell Cycle P | 2011 |
Anti-angiogenic therapy: concept to clinic.
Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal, Humanized; Benzenesulfonates; Bevacizumab; | 2012 |
Immunology in the clinic review series; focus on cancer: tumour-associated macrophages: undisputed stars of the inflammatory tumour microenvironment.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzenesulfonates; Chemotaxis; C | 2012 |
Meta-analysis of randomized controlled trials for the incidence and risk of treatment-related mortality in patients with cancer treated with vascular endothelial growth factor tyrosine kinase inhibitors.
Topics: Antineoplastic Agents; Benzenesulfonates; Humans; Indazoles; Indoles; Neoplasms; Niacinamide; Phenyl | 2012 |
Molecular targeted therapies for cancer: sorafenib mono-therapy and its combination with other therapies (review).
Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; C | 2012 |
Using NF-κB as a molecular target for theranostics in radiation oncology research.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Combined Modality Therapy; Drug Resistance, Neopl | 2012 |
[Possibilities for inhibiting tumor-induced angiogenesis: results with multi-target tyrosine kinase inhibitors].
Topics: Angiogenesis Inhibitors; Animals; Axitinib; Benzenesulfonates; Humans; Imidazoles; Indazoles; Indole | 2012 |
Combining antiangiogenics to overcome resistance: rationale and clinical experience.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Pro | 2012 |
Evidence for therapeutic drug monitoring of targeted anticancer therapies.
Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antibodies, Monoclonal, Murine-D | 2012 |
Hypothyroidism during treatment with tyrosine kinase inhibitors.
Topics: Carcinoma, Renal Cell; Dose-Response Relationship, Drug; Gastrointestinal Neoplasms; Humans; Indoles | 2012 |
Inhibition of RET activated pathways: novel strategies for therapeutic intervention in human cancers.
Topics: Animals; Antineoplastic Agents; Drug Design; Humans; Indoles; Molecular Targeted Therapy; Neoplasms; | 2013 |
Polymorphisms to predict outcome to the tyrosine kinase inhibitors gefitinib, erlotinib, sorafenib and sunitinib.
Topics: Animals; Antineoplastic Agents; ATP Binding Cassette Transporter, Subfamily G, Member 2; ATP-Binding | 2012 |
[Nintedanib (BIBF 1120) in the treatment of solid cancers: an overview of biological and clinical aspects].
Topics: Animals; Antineoplastic Agents; Axitinib; Benzenesulfonates; Carcinoma, Hepatocellular; Clinical Tri | 2012 |
[Advances in the study of structural modifications of multi-target anticancer drug sorafenib].
Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Humans; Molecular Structure; Neoplasms; Neovascula | 2012 |
The importance of tumor metabolism in cancer prognosis and therapy; pre-clinical studies on rodent tumors with agents that improve tumor oxygenation.
Topics: Animals; Blood Glucose; Carbon Dioxide; Humans; Lactic Acid; Magnetic Resonance Imaging; Neoplasms; | 2002 |
BAY 43-9006: early clinical data in patients with advanced solid malignancies.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase I as Topic; Humans; Neopla | 2002 |
BAY 43-9006: preclinical data.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Cell Division; Disease Progression; Humans; Mice; | 2002 |
Targeting intracellular signal transduction. A new paradigm for a brave new world of molecularly targeted therapeutics.
Topics: Adult; Animals; Antineoplastic Agents; Benzamides; Benzenesulfonates; Child; Clinical Trials as Topi | 2002 |
BAY-43-9006 Bayer/Onyx.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Clinical Trials as Topic; Drugs, Investigational; | 2003 |
Raf pathway inhibitors in oncology.
Topics: Animals; Benzenesulfonates; Enzyme Inhibitors; Humans; MAP Kinase Signaling System; Neoplasms; Niaci | 2003 |
High interstitial fluid pressure - an obstacle in cancer therapy.
Topics: Alprostadil; Animals; Antineoplastic Agents; Biological Transport; Bradykinin; Extracellular Fluid; | 2004 |
Raf kinase inhibitors in oncology.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Clinical Trials as Topic; Drug Delivery Systems; | 2005 |
Recent progress in targeting the Raf/MEK/ERK pathway with inhibitors in cancer drug discovery.
Topics: Animals; Benzamides; Benzenesulfonates; Clinical Trials as Topic; Diphenylamine; Extracellular Signa | 2005 |
Cutaneous side-effects of kinase inhibitors and blocking antibodies.
Topics: Antibodies, Blocking; Antineoplastic Agents; Benzamides; Benzenesulfonates; ErbB Receptors; Hair Dis | 2005 |
Cutaneous side-effects of kinase inhibitors and blocking antibodies.
Topics: Antibodies, Blocking; Antineoplastic Agents; Benzamides; Benzenesulfonates; ErbB Receptors; Hair Dis | 2005 |
Cutaneous side-effects of kinase inhibitors and blocking antibodies.
Topics: Antibodies, Blocking; Antineoplastic Agents; Benzamides; Benzenesulfonates; ErbB Receptors; Hair Dis | 2005 |
Cutaneous side-effects of kinase inhibitors and blocking antibodies.
Topics: Antibodies, Blocking; Antineoplastic Agents; Benzamides; Benzenesulfonates; ErbB Receptors; Hair Dis | 2005 |
Raf: a strategic target for therapeutic development against cancer.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Down-Regulation; Drug Delivery Systems; Humans; M | 2005 |
Update on angiogenesis inhibitors.
Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzene | 2005 |
Regulation of c-Raf-1: therapeutic implications.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase I as Topic; Clinical Trial | 2003 |
Pooled safety analysis of BAY 43-9006 (sorafenib) monotherapy in patients with advanced solid tumours: Is rash associated with treatment outcome?
Topics: Administration, Oral; Adolescent; Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Clinical Tr | 2006 |
Targeting Raf-kinase: molecular rationales and translational issues.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Humans; Neoplasms; Niacinamide; Phenylurea Compou | 2006 |
Cancer targets in the Ras pathway.
Topics: Antineoplastic Agents; Benzenesulfonates; Drug Design; Female; Genes, ras; Humans; Male; Models, Bio | 2005 |
Role of Raf kinase in cancer: therapeutic potential of targeting the Raf/MEK/ERK signal transduction pathway.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Renal Cell; Cell Transformation, Neopl | 2006 |
Raf kinases: oncogenesis and drug discovery.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Clinical Trials as Topic; Disease Models, Animal; | 2006 |
Discovery and development of sorafenib: a multikinase inhibitor for treating cancer.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Carcinoma, Renal Cell; Clinical Trials as Topic; | 2006 |
Protein kinases as drug targets in cancer.
Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzamides; Benzenesulfonates; G | 2006 |
The hypoxic tumour microenvironment, patient selection and hypoxia-modifying treatments.
Topics: Anemia; Biomarkers, Tumor; Carbon Dioxide; Cell Hypoxia; Humans; Hyperbaric Oxygenation; Neoplasms; | 2007 |
Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition.
Topics: Adaptor Proteins, Signal Transducing; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Ben | 2007 |
Angiogenesis in cancer: molecular mechanisms, clinical impact.
Topics: Angiogenesis Inhibitors; Angiogenic Proteins; Benzenesulfonates; Carcinoma, Squamous Cell; Humans; I | 2007 |
Safety, pharmacokinetics, and preliminary antitumor activity of sorafenib: a review of four phase I trials in patients with advanced refractory solid tumors.
Topics: Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase I as Topic; Humans; Neoplasm Metast | 2007 |
Design of clinical trials of radiation combined with antiangiogenic therapy.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonate | 2007 |
Sorafenib: delivering a targeted drug to the right targets.
Topics: Antineoplastic Agents; Benzenesulfonates; Carcinoma, Hepatocellular; Carcinoma, Renal Cell; Clinical | 2007 |
Mechanisms of adverse effects of anti-VEGF therapy for cancer.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic A | 2007 |
Multitarget tyrosine kinase inhibition: [and the winner is...].
Topics: Antineoplastic Agents; Clinical Trials, Phase I as Topic; Humans; Indoles; Neoplasms; Niacinamide; O | 2007 |
B-Raf kinase inhibitors for cancer treatment.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Enzyme Inhibitors; Humans; Imidazoles; Neoplasms; | 2007 |
[Oral drugs inhibiting the VEGF pathway].
Topics: Administration, Oral; Angiogenesis Inhibitors; Animals; Asthenia; Axitinib; Benzenesulfonates; Human | 2007 |
Playing only one instrument may be not enough: limitations and future of the antiangiogenic treatment of cancer.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antineoplastic Agents; Benzenesulfonates; Carcinoma | 2007 |
New developments in multitargeted therapy for patients with solid tumours.
Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Benzenesulfonates | 2008 |
Safety and anti-tumor activity of sorafenib (Nexavar) in combination with other anti-cancer agents: a review of clinical trials.
Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; C | 2008 |
Systematic review to establish the safety profiles for direct and indirect inhibitors of p38 Mitogen-activated protein kinases for treatment of cancer. A systematic review of the literature.
Topics: Antineoplastic Agents; Benzenesulfonates; Humans; Neoplasms; Niacinamide; p38 Mitogen-Activated Prot | 2008 |
Risk of hand-foot skin reaction with sorafenib: a systematic review and meta-analysis.
Topics: Antineoplastic Agents; Benzenesulfonates; Carcinoma, Renal Cell; Disease Progression; Drug Eruptions | 2008 |
Incidence and risk of hypertension with sorafenib in patients with cancer: a systematic review and meta-analysis.
Topics: Angiogenesis Inhibitors; Antineoplastic Agents; Benzenesulfonates; Humans; Hypertension; Incidence; | 2008 |
From single- to multi-target drugs in cancer therapy: when aspecificity becomes an advantage.
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Antineoplastic Com | 2008 |
Mcl-1: a gateway to TRAIL sensitization.
Topics: Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Down-Regulation; Drug Resistance, | 2008 |
Physiology aspects of pyridine nucleotide regulation in mammals.
Topics: Adrenal Cortex Hormones; Animals; Female; Glyceraldehyde-3-Phosphate Dehydrogenases; Humans; Hyperth | 1980 |
Nicotinamide and other benzamide analogs as agents for overcoming hypoxic cell radiation resistance in tumours. A review.
Topics: Animals; Benzamides; Cell Hypoxia; Combined Modality Therapy; Humans; Neoplasms; Niacinamide; Radiat | 1995 |
Clinical results of hypoxic cell radiosensitisation from hyperbaric oxygen to accelerated radiotherapy, carbogen and nicotinamide.
Topics: Blood Transfusion; Carbon Dioxide; Cell Hypoxia; Humans; Hyperbaric Oxygenation; Neoplasms; Niacinam | 1996 |
ARCON--current status: summary of a workshop on preclinical and clinical studies.
Topics: Animals; Carbon Dioxide; Cell Division; Cell Hypoxia; Head and Neck Neoplasms; Humans; Neoplasm Recu | 1997 |
[Vitamins and apoptosis--induction of apoptosis in human cancer cells by nicotinic acid-related compounds].
Topics: Apoptosis; Caspase Inhibitors; HeLa Cells; HL-60 Cells; Humans; K562 Cells; Neoplasms; Niacinamide; | 1999 |
Improvement of tumor oxygenation by mild hyperthermia.
Topics: Animals; Carbon Dioxide; Cell Hypoxia; Combined Modality Therapy; Dogs; Humans; Hyperthermia, Induce | 2001 |
Hypoxia as a target for combined modality treatments.
Topics: Antineoplastic Combined Chemotherapy Protocols; Carbon Dioxide; Cell Hypoxia; Combined Modality Ther | 2002 |
Nicotinamide and the hypoxia problem.
Topics: Humans; Hypoxia; Neoplasms; Niacinamide; Radiation Injuries; Radiation Tolerance | 1991 |
Today's carcinochemotherapy: some of its achievements, failures and prospects.
Topics: Alkylating Agents; Antibiotics, Antineoplastic; Antibody-Producing Cells; Antimetabolites; Antineopl | 1970 |
Some developments in the use of radiophosphorus.
Topics: Amplifiers, Electronic; Androgens; Animals; Breast Neoplasms; DNA; Electrons; Estrogens; Eye Neoplas | 1972 |
72 trials available for niacinamide and Neoplasms
Article | Year |
---|---|
A PK-PD model linking biomarker dynamics to progression-free survival in patients treated with everolimus and sorafenib combination therapy, EVESOR phase I trial.
Topics: Biomarkers; Everolimus; Humans; Neoplasms; Niacinamide; Phenylurea Compounds; Progression-Free Survi | 2023 |
A phase I trial of riluzole and sorafenib in patients with advanced solid tumors: CTEP #8850.
Topics: Antineoplastic Combined Chemotherapy Protocols; Humans; Maximum Tolerated Dose; Neoplasms; Niacinami | 2023 |
Phase I trial of pimasertib monotherapy in Japanese patients with solid tumors and those with hepatocellular carcinoma.
Topics: Adult; Aged; Carcinoma, Hepatocellular; Dose-Response Relationship, Drug; Female; Humans; Japan; Liv | 2019 |
Selective Oral MEK1/2 Inhibitor Pimasertib: A Phase I Trial in Patients with Advanced Solid Tumors.
Topics: Adult; Aged; Aged, 80 and over; Female; Humans; Male; Middle Aged; Neoplasms; Niacinamide; Protein K | 2021 |
Safety and Clinical Activity of a New Anti-PD-L1 Antibody as Monotherapy or Combined with Targeted Therapy in Advanced Solid Tumors: The PACT Phase Ia/Ib Trial.
Topics: Adult; Aged; Aged, 80 and over; Aminopyridines; Antibodies, Monoclonal; Antibodies, Monoclonal, Huma | 2021 |
Phase I dose escalation study of concurrent palliative radiation therapy with sorafenib in three anatomical cohorts (Thorax, Abdomen, Pelvis): The TAP study.
Topics: Adult; Aged; Aged, 80 and over; Chemoradiotherapy; Cohort Studies; Dose-Response Relationship, Drug; | 2017 |
A phase Ib dose-escalation and expansion study of the oral MEK inhibitor pimasertib and PI3K/MTOR inhibitor voxtalisib in patients with advanced solid tumours.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Female; Humans; Male; Middle Aged; Mito | 2018 |
A phase I study of the HDM2 antagonist SAR405838 combined with the MEK inhibitor pimasertib in patients with advanced solid tumours.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Dose-Response Relationship, Drug; Femal | 2019 |
The effect of different dosing regimens of motesanib on the gallbladder: a randomized phase 1b study in patients with advanced solid tumors.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Female; Gallbladder; Humans; Indoles; Male; M | 2013 |
Phase I clinical trial of lenalidomide in combination with sorafenib in patients with advanced cancer.
Topics: Adult; Aged; Angiogenesis Inhibitors; Antineoplastic Combined Chemotherapy Protocols; Disease-Free S | 2014 |
Alternative formulations of sorafenib for use in children.
Topics: Administration, Oral; Adolescent; Adult; Antineoplastic Agents; Child; Child, Preschool; Female; Hum | 2013 |
Phase 1 study of sorafenib in combination with bortezomib in patients with advanced malignancies.
Topics: Adult; Aged; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Boronic Acids; B | 2013 |
Sorafenib plus dacarbazine in solid tumors: a phase I study with dynamic contrast-enhanced ultrasonography and genomic analysis of sequential tumor biopsy samples.
Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Biopsy; Dacarbazine; Female; Gene Expression R | 2014 |
Technical considerations in the development of circulating peptides as pharmacodynamic biomarkers for angiogenesis inhibitors.
Topics: Adult; Aged; Angiogenesis Inhibitors; Angiopoietin-2; Biomarkers; Exercise; Female; Humans; Male; Mi | 2014 |
Sorafenib dose escalation is not uniformly associated with blood pressure elevations in normotensive patients with advanced malignancies.
Topics: Adult; Aged; Blood Pressure; Dose-Response Relationship, Drug; Female; Humans; Male; Middle Aged; Ne | 2014 |
Phase ib of sorafenib in combination with everolimus in patients with advanced solid tumors, selected on the basis of molecular targets.
Topics: Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Everolimus; Extracellular Sig | 2014 |
Phase 1 trial of tivantinib in combination with sorafenib in adult patients with advanced solid tumors.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Cytochrome P-450 CYP | 2015 |
Dual antiangiogenic inhibition: a phase I dose escalation and expansion trial targeting VEGF-A and VEGFR in patients with advanced solid tumors.
Topics: Adult; Aged; Aged, 80 and over; Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Antineop | 2015 |
A phase I study of the histone deacetylase (HDAC) inhibitor entinostat, in combination with sorafenib in patients with advanced solid tumors.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzamide | 2015 |
A phase 1b, open-label study of trebananib plus bevacizumab or motesanib in patients with solid tumours.
Topics: Adult; Aged; Aged, 80 and over; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemother | 2014 |
Multiparameter Phase I trials: a tool for model-based development of targeted agent combinations--example of EVESOR trial.
Topics: Angiogenesis Inhibitors; Antineoplastic Combined Chemotherapy Protocols; Biopsy; Everolimus; Humans; | 2015 |
A Phase I Study of the Safety, Pharmacokinetics, and Pharmacodynamics of Combination Therapy with Refametinib plus Sorafenib in Patients with Advanced Cancer.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Combined Modality Thera | 2016 |
Pediatric phase I trial of oral sorafenib and topotecan in refractory or recurrent pediatric solid malignancies.
Topics: Administration, Oral; Adolescent; Antineoplastic Agents; Child; Drug Administration Schedule; Drug M | 2016 |
Phase I study of pemetrexed with sorafenib in advanced solid tumors.
Topics: Adult; Aged; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Biomarkers, Tumo | 2016 |
Pimasertib, a selective oral MEK1/2 inhibitor: absolute bioavailability, mass balance, elimination route, and metabolite profile in cancer patients.
Topics: Administration, Oral; Antineoplastic Agents; Biological Availability; Carbon Radioisotopes; Ethanola | 2016 |
Metabolism of the MEK1/2 Inhibitor Pimasertib Involves a Novel Conjugation with Phosphoethanolamine in Patients with Solid Tumors.
Topics: Adolescent; Adult; Aged; Biotransformation; Ethanolamines; Humans; Male; MAP Kinase Kinase 1; MAP Ki | 2017 |
Phase I dose-escalation study of plitidepsin in combination with sorafenib or gemcitabine in patients with refractory solid tumors or lymphomas.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols | 2017 |
EVESOR, a model-based, multiparameter, Phase I trial to optimize the benefit/toxicity ratio of everolimus and sorafenib.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Drug Administration Schedule; Everolimu | 2017 |
Phase I trial of MEK 1/2 inhibitor pimasertib combined with mTOR inhibitor temsirolimus in patients with advanced solid tumors.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Female; Humans; Male | 2017 |
Effect of coadministration of ketoconazole, a strong CYP3A4 inhibitor, on pharmacokinetics and tolerability of motesanib diphosphate (AMG 706) in patients with advanced solid tumors.
Topics: Aged; Cross-Over Studies; Cytochrome P-450 CYP3A; Cytochrome P-450 CYP3A Inhibitors; Drug Administra | 2008 |
Combination targeted therapy with sorafenib and bevacizumab results in enhanced toxicity and antitumor activity.
Topics: Administration, Oral; Adult; Aged; Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Mono | 2008 |
Combination targeted therapy with sorafenib and bevacizumab results in enhanced toxicity and antitumor activity.
Topics: Administration, Oral; Adult; Aged; Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Mono | 2008 |
Combination targeted therapy with sorafenib and bevacizumab results in enhanced toxicity and antitumor activity.
Topics: Administration, Oral; Adult; Aged; Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Mono | 2008 |
Combination targeted therapy with sorafenib and bevacizumab results in enhanced toxicity and antitumor activity.
Topics: Administration, Oral; Adult; Aged; Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Mono | 2008 |
Safety and pharmacokinetics of motesanib in combination with gemcitabine for the treatment of patients with solid tumours.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Deoxycytidine; Drug Administration Sche | 2008 |
Phase I and pharmacokinetic study of sorafenib in patients with hepatic or renal dysfunction: CALGB 60301.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Benzenesulfonates; Fema | 2009 |
Phase I trial of a combination of the multikinase inhibitor sorafenib and the farnesyltransferase inhibitor tipifarnib in advanced malignancies.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Benzenes | 2009 |
Phase 1 study of the investigational, oral angiogenesis inhibitor motesanib in Japanese patients with advanced solid tumors.
Topics: Adult; Aged; Angiogenesis Inhibitors; Antineoplastic Agents; Dose-Response Relationship, Drug; Femal | 2010 |
Phase I combination of sorafenib and erlotinib therapy in solid tumors: safety, pharmacokinetic, and pharmacodynamic evaluation from an expansion cohort.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Area Under Curve; Benzenesulfonates; Bi | 2010 |
A phase Ib study of AMG 102 in combination with bevacizumab or motesanib in patients with advanced solid tumors.
Topics: Adult; Aged; Aged, 80 and over; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineopl | 2010 |
A phase I open-label study evaluating the cardiovascular safety of sorafenib in patients with advanced cancer.
Topics: Aged; Antineoplastic Agents; Area Under Curve; Benzenesulfonates; Blood Pressure; Electrocardiograph | 2011 |
Pharmacokinetic results of a phase I trial of sorafenib in combination with dacarbazine in patients with advanced solid tumors.
Topics: Aminoimidazole Carboxamide; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Dacar | 2011 |
A phase I dose-escalation study to evaluate safety and tolerability of sorafenib combined with sirolimus in patients with advanced solid cancer.
Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Female; Humans; Male; Maxi | 2010 |
Safety and pharmacokinetics of sorafenib combined with capecitabine in patients with advanced solid tumors: results of a phase 1 trial.
Topics: Adult; Aged; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Area Under Curve | 2011 |
Two drug interaction studies of sirolimus in combination with sorafenib or sunitinib in patients with advanced malignancies.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Area Under Curve; Benzenesulfonates; Dr | 2011 |
A drug interaction study evaluating the pharmacokinetics and toxicity of sorafenib in combination with capecitabine.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Area Under Curve; Be | 2012 |
Phase IB study of sorafenib in combination with gemcitabine and cisplatin in patients with refractory solid tumors.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Area Under Curve; Benzenesulfonates; Ci | 2012 |
Safety and pharmacokinetics of motesanib in combination with gemcitabine and erlotinib for the treatment of solid tumors: a phase 1b study.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Area Under Curve; Cohort Studies; Deoxy | 2011 |
Saturable absorption of sorafenib in patients with solid tumors: a population model.
Topics: Absorption; Administration, Oral; Adult; Aged; Aged, 80 and over; Biological Availability; Dose-Resp | 2012 |
Feasibility study of intra-patient sorafenib dose-escalation or re-escalation in patients with previously treated advanced solid tumors.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Cohort Studies; Dose-Response Relationship, D | 2012 |
Plasma protein binding of sorafenib, a multi kinase inhibitor: in vitro and in cancer patients.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Blood Proteins; Female; Humans; Male; Middle | 2012 |
Paclitaxel in combination with sorafenib and bevacizumab in patients with locally advanced or metastatic solid tumors.
Topics: Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates | 2012 |
Phase I trial of sorafenib in combination with 5-fluorouracil/leucovorin in advanced solid tumors.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antineoplasti | 2012 |
Phase I trial to investigate the safety, pharmacokinetics and efficacy of sorafenib combined with docetaxel in patients with advanced refractory solid tumours.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Cohort Studies; Dise | 2012 |
Safety and pharmacokinetics of ganitumab (AMG 479) combined with sorafenib, panitumumab, erlotinib, or gemcitabine in patients with advanced solid tumors.
Topics: Adult; Aged; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chem | 2012 |
A phase I trial and pharmacokinetic study of sorafenib in children with refractory solid tumors or leukemias: a Children's Oncology Group Phase I Consortium report.
Topics: Adolescent; Antineoplastic Agents; Child; Child, Preschool; Female; Humans; Leukemia; Male; Neoplasm | 2012 |
The effect of hand-foot skin reaction associated with the multikinase inhibitors sorafenib and sunitinib on health-related quality of life.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Female; Hand-Foot Syndrome; Humans; Indoles; | 2012 |
Phase I and clinical pharmacology study of bevacizumab, sorafenib, and low-dose cyclophosphamide in children and young adults with refractory/recurrent solid tumors.
Topics: Adolescent; Adult; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Protocols | 2013 |
Phase I pharmacokinetic and pharmacodynamic study of lapatinib in combination with sorafenib in patients with advanced refractory solid tumors.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Disease Progression; Dose-Response Rela | 2013 |
Results of phase I pharmacokinetic and pharmacodynamic studies of the Raf kinase inhibitor BAY 43-9006 in patients with solid tumors.
Topics: Benzenesulfonates; Dose-Response Relationship, Drug; Drug Administration Schedule; Enzyme Inhibitors | 2002 |
A phase I clinical and pharmacokinetic study of the Raf kinase inhibitor (RKI) BAY 43-9006 administered in combination with doxorubicin in patients with solid tumors.
Topics: Administration, Oral; Antineoplastic Combined Chemotherapy Protocols; Area Under Curve; Aspartate Am | 2003 |
Drug-drug interaction pharmacokinetic study with the Raf kinase inhibitor (RKI) BAY 43-9006 administered in combination with irinotecan (CPT-11) in patients with solid tumors.
Topics: Administration, Oral; Antineoplastic Agents, Phytogenic; Benzenesulfonates; Camptothecin; Dose-Respo | 2003 |
Correlation of ERK-phosphorylation and toxicities in patients treated with the Raf kinase inhibitor BAY 43-9006.
Topics: Adult; Area Under Curve; Benzenesulfonates; Diarrhea; Drug Administration Schedule; Exanthema; Human | 2004 |
Phase I safety and pharmacokinetics of BAY 43-9006 administered for 21 days on/7 days off in patients with advanced, refractory solid tumours.
Topics: Adult; Aged; Benzenesulfonates; Carcinoma, Renal Cell; Drug Administration Schedule; Female; Humans; | 2005 |
Phase I study to determine the safety and pharmacokinetics of the novel Raf kinase and VEGFR inhibitor BAY 43-9006, administered for 28 days on/7 days off in patients with advanced, refractory solid tumors.
Topics: Administration, Oral; Adult; Aged; Benzenesulfonates; Drug Administration Schedule; Enzyme Inhibitor | 2005 |
Safety and pharmacokinetics of the dual action Raf kinase and vascular endothelial growth factor receptor inhibitor, BAY 43-9006, in patients with advanced, refractory solid tumors.
Topics: Adult; Aged; Antineoplastic Agents; Area Under Curve; Benzenesulfonates; Biomarkers, Tumor; Biopsy; | 2005 |
Phase I trial of sorafenib and gemcitabine in advanced solid tumors with an expanded cohort in advanced pancreatic cancer.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; D | 2006 |
Mechanisms of hypertension associated with BAY 43-9006.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Benzenesulfonates; Drug Administration Schedul | 2006 |
Mechanisms of hypertension associated with BAY 43-9006.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Benzenesulfonates; Drug Administration Schedul | 2006 |
Mechanisms of hypertension associated with BAY 43-9006.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Benzenesulfonates; Drug Administration Schedul | 2006 |
Mechanisms of hypertension associated with BAY 43-9006.
Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Benzenesulfonates; Drug Administration Schedul | 2006 |
Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells.
Topics: Aged; Aged, 80 and over; Antigens, CD; Antigens, CD34; Antigens, Differentiation, Myelomonocytic; Be | 2006 |
Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells.
Topics: Aged; Aged, 80 and over; Antigens, CD; Antigens, CD34; Antigens, Differentiation, Myelomonocytic; Be | 2006 |
Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells.
Topics: Aged; Aged, 80 and over; Antigens, CD; Antigens, CD34; Antigens, Differentiation, Myelomonocytic; Be | 2006 |
Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells.
Topics: Aged; Aged, 80 and over; Antigens, CD; Antigens, CD34; Antigens, Differentiation, Myelomonocytic; Be | 2006 |
Results of a Phase I trial of sorafenib (BAY 43-9006) in combination with doxorubicin in patients with refractory solid tumors.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Dose-Response Relati | 2006 |
Results from an in vitro and a clinical/pharmacological phase I study with the combination irinotecan and sorafenib.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Camptothecin; Cohort | 2007 |
Safety, pharmacokinetics, and efficacy of AMG 706, an oral multikinase inhibitor, in patients with advanced solid tumors.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Area Under Curve; Female; Humans; Hypertensio | 2007 |
Phase I targeted combination trial of sorafenib and erlotinib in patients with advanced solid tumors.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; ErbB Receptors; Erlo | 2007 |
Phase I and pharmacokinetic study of sorafenib, an oral multikinase inhibitor, in Japanese patients with advanced refractory solid tumors.
Topics: Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Extracellular Signal-Regulated MAP Kinases; F | 2008 |
Human tumor blood flow is enhanced by nicotinamide and carbogen breathing.
Topics: Administration, Inhalation; Administration, Oral; Carbon Dioxide; Female; Humans; Laser-Doppler Flow | 1997 |
161 other studies available for niacinamide and Neoplasms
Article | Year |
---|---|
Nicaraven prevents the fast growth of inflamed tumors by an anti-inflammatory mechanism.
Topics: Animals; Anti-Inflammatory Agents; Biomarkers, Tumor; Cytokines; Humans; Inflammation; Macrophages; | 2021 |
Gut microbiota severely hampers the efficacy of NAD-lowering therapy in leukemia.
Topics: Cell Line, Tumor; Cytokines; Gastrointestinal Microbiome; Humans; Leukemia; NAD; Neoplasms; Niacinam | 2022 |
Remote solid cancers rewire hepatic nitrogen metabolism via host nicotinamide-N-methyltransferase.
Topics: Animals; Liver; Mice; Neoplasms; Niacinamide; Nicotinamide N-Methyltransferase; Nitrogen; Uracil; Ur | 2022 |
Autophagy-inducing nutritional interventions in experimental and clinical oncology.
Topics: Autophagy; Carcinogenesis; Humans; Medical Oncology; Methionine; Micronutrients; Neoplasms; Niacinam | 2022 |
Fluorescent and theranostic probes for imaging nicotinamide phosphoribosyl transferase (NAMPT).
Topics: Cell Proliferation; Cytokines; Humans; Neoplasms; Niacinamide; Nicotinamide Phosphoribosyltransferas | 2023 |
Novel carbon skeletons activate human NicotinAMide Phosphoribosyl Transferase (NAMPT) enzyme in biochemical assay.
Topics: Cytokines; Humans; NAD; Neoplasms; Niacinamide; Nicotinamide Phosphoribosyltransferase; Sirtuins | 2023 |
NAD
Topics: Animals; Cachexia; Humans; Mice; Muscle, Skeletal; NAD; Neoplasms; Niacin; Niacinamide | 2023 |
Nicaraven Exerts a Limited Effect on Radiation-Induced Inhibition of Tumor Growth in a Subcutaneous Murine Tumor Model.
Topics: Animals; Antioxidants; Mice; Neoplasms; Niacinamide; Radiation Injuries | 2023 |
Cancer-associated variants of human NQO1: impacts on inhibitor binding and cooperativity.
Topics: Dicumarol; Enzyme Stability; Humans; Kinetics; NAD(P)H Dehydrogenase (Quinone); Neoplasms; Niacinami | 2019 |
Ordered subset expectation maximisation vs Bayesian penalised likelihood reconstruction algorithm in 18F-PSMA-1007 PET/CT.
Topics: Aged; Algorithms; Bayes Theorem; Fluorine Radioisotopes; Humans; Likelihood Functions; Middle Aged; | 2020 |
Nicotinamide riboside relieves paclitaxel-induced peripheral neuropathy and enhances suppression of tumor growth in tumor-bearing rats.
Topics: Animals; Female; Neoplasms; Niacinamide; Paclitaxel; Peripheral Nervous System Diseases; Pyridinium | 2020 |
Disturbed mitochondrial dynamics in CD8
Topics: Biomarkers; CD8-Positive T-Lymphocytes; Epigenesis, Genetic; Epigenomics; Humans; Lymphocyte Count; | 2020 |
Novel
Topics: Alzheimer Disease; Animals; Bipolar Disorder; Blood-Brain Barrier; Brain; Cell Line, Tumor; Diabetes | 2021 |
The Biochemical Pathways of Nicotinamide-Derived Pyridones.
Topics: Autophagy; Cell Line, Tumor; HEK293 Cells; Humans; NAD; Neoplasms; Niacinamide; Pyridones | 2021 |
Asciminib Mitigates DNA Damage Stress Signaling Induced by Cyclophosphamide in the Ovary.
Topics: Animals; Antineoplastic Agents, Alkylating; Apoptosis; Cyclophosphamide; Disease Models, Animal; DNA | 2021 |
Rational drug design of indazole-based diarylurea derivatives as anticancer agents.
Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Proliferation; Computer-Aided Design; Drug Design; Dru | 2017 |
A data mining approach for identifying pathway-gene biomarkers for predicting clinical outcome: A case study of erlotinib and sorafenib.
Topics: Antineoplastic Agents; Biomarkers, Pharmacological; Biomarkers, Tumor; Cluster Analysis; Data Mining | 2017 |
Adaptation to TKI Treatment Reactivates ERK Signaling in Tyrosine Kinase-Driven Leukemias and Other Malignancies.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Cell Line, Tumor; Cell Prolifer | 2017 |
Functional Characterization of VEGF- and FGF-induced Tumor Blood Vessel Models in Human Cancer Xenografts.
Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Cell Survival; Deoxycytidine; Dose-Response Relati | 2017 |
Synergistic anticancer effects of bufalin and sorafenib by regulating apoptosis associated proteins.
Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Bufanolides; Cell Line, Tumor; Cell Proliferation | 2018 |
Influence of Sorafenib, Sunitinib and Capecitabine on the Antioxidant Status of the Skin.
Topics: Administration, Oral; Aged; Aged, 80 and over; Antioxidants; Capecitabine; Carotenoids; Female; Hand | 2018 |
NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink.
Topics: Epigenesis, Genetic; Humans; Methionine; Methylation; Models, Genetic; Neoplasms; Niacinamide; Nicot | 2013 |
[¹¹C]Sorafenib: radiosynthesis and preclinical evaluation in tumor-bearing mice of a new TKI-PET tracer.
Topics: Animals; Carbon Radioisotopes; Cell Line, Tumor; Cell Transformation, Neoplastic; Male; Mice; Neopla | 2013 |
Effects of vascular endothelial growth factor signaling inhibition on human erythropoiesis.
Topics: Axitinib; Blood Pressure; Clinical Trials as Topic; Combined Modality Therapy; Erythrocyte Count; Er | 2013 |
Mechanism of MEK inhibition determines efficacy in mutant KRAS- versus BRAF-driven cancers.
Topics: Allosteric Regulation; Azetidines; Cell Survival; Clinical Trials as Topic; Crystallography, X-Ray; | 2013 |
Synthesis of polymer-lipid nanoparticles for image-guided delivery of dual modality therapy.
Topics: Angiogenesis Inhibitors; Animals; Antibiotics, Antineoplastic; Doxorubicin; Drug Delivery Systems; F | 2013 |
Sorafenib sensitizes solid tumors to Apo2L/TRAIL and Apo2L/TRAIL receptor agonist antibodies by the Jak2-Stat3-Mcl1 axis.
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Apoptosis; Blotting, Western; Cell Line, | 2013 |
Copper-free azide-alkyne cycloaddition of targeting peptides to porous silicon nanoparticles for intracellular drug uptake.
Topics: Alkynes; Antineoplastic Agents; Azides; Cell Line, Tumor; Cell Proliferation; Click Chemistry; Cyclo | 2014 |
Development and validation of an HPLC-UV method for sorafenib quantification in human plasma and application to patients with cancer in routine clinical practice.
Topics: Antineoplastic Agents; Area Under Curve; Calibration; Chromatography, High Pressure Liquid; Dose-Res | 2014 |
ROS-mediated JNK/p38-MAPK activation regulates Bax translocation in Sorafenib-induced apoptosis of EBV-transformed B cells.
Topics: Apoptosis; B-Lymphocytes; bcl-2-Associated X Protein; Herpesvirus 4, Human; Humans; MAP Kinase Signa | 2014 |
Multifunctional pH-sensitive polymeric nanoparticles for theranostics evaluated experimentally in cancer.
Topics: Animals; Antineoplastic Agents; Apoptosis; Contrast Media; Drug Carriers; Hep G2 Cells; Histidine; H | 2014 |
ABT-263 enhances sorafenib-induced apoptosis associated with Akt activity and the expression of Bax and p21((CIP1/WAF1)) in human cancer cells.
Topics: Aniline Compounds; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; bcl-2-Associa | 2014 |
Symptoms from treatment with sunitinib or sorafenib: a multicenter explorative cohort study to explore the influence of patient-reported outcomes on therapy decisions.
Topics: Adult; Aged; Aged, 80 and over; Angiogenesis Inhibitors; Cohort Studies; Decision Making; Female; Hu | 2014 |
Downregulation of the Werner syndrome protein induces a metabolic shift that compromises redox homeostasis and limits proliferation of cancer cells.
Topics: Animals; Antioxidants; Cell Line, Tumor; Cell Proliferation; Cell Respiration; Cellular Senescence; | 2014 |
VEGF pathway inhibitors-induced hypertension: next step in therapy.
Topics: Antineoplastic Agents; Humans; Hypertension; Neoplasms; Niacinamide; Phenylurea Compounds | 2014 |
Blocking lipid synthesis overcomes tumor regrowth and metastasis after antiangiogenic therapy withdrawal.
Topics: Angiogenesis Inhibitors; Animals; Cell Line, Tumor; Disease Progression; Fatty Acid Synthases; Homeo | 2014 |
Comparison of internal dose estimates obtained using organ-level, voxel S value, and Monte Carlo techniques.
Topics: Algorithms; Computer Simulation; Female; Humans; Iodine Radioisotopes; Kidney; Liver; Lutetium; Male | 2014 |
Coupled variable selection for regression modeling of complex treatment patterns in a clinical cancer registry.
Topics: Aged; Antineoplastic Agents; Carcinoma, Hepatocellular; Confounding Factors, Epidemiologic; Data Int | 2014 |
Sorafenib induces ferroptosis in human cancer cell lines originating from different solid tumors.
Topics: Apoptosis; Biomarkers, Tumor; Blotting, Western; Cell Proliferation; Humans; L-Lactate Dehydrogenase | 2014 |
Biological evaluation of a novel sorafenib analogue, t-CUPM.
Topics: Administration, Oral; Animals; Animals, Outbred Strains; Antineoplastic Agents; Apoptosis; Biologica | 2015 |
Multifunctional porous silicon nanoparticles for cancer theranostics.
Topics: Angiogenesis Inhibitors; Animals; Cell Line, Tumor; Humans; Male; Mice, Nude; Nanoparticles; Neoplas | 2015 |
Nexavar/Stivarga and viagra interact to kill tumor cells.
Topics: Apoptosis; Cell Proliferation; Cyclic Nucleotide Phosphodiesterases, Type 5; Drug Synergism; Gene Ex | 2015 |
Cardiovascular toxicity of multi-tyrosine kinase inhibitors in advanced solid tumors: a population-based observational study.
Topics: Adult; Aged, 80 and over; Canada; Cardiovascular Diseases; Female; Humans; Indoles; Male; Middle Age | 2015 |
GRP78/Dna K Is a Target for Nexavar/Stivarga/Votrient in the Treatment of Human Malignancies, Viral Infections and Bacterial Diseases.
Topics: Animals; Bacterial Infections; Cell Line, Tumor; Endoplasmic Reticulum Chaperone BiP; Escherichia co | 2015 |
Small molecule/ML327 mediated transcriptional de-repression of E-cadherin and inhibition of epithelial-to-mesenchymal transition.
Topics: Animals; Cadherins; Cell Line, Tumor; Chick Embryo; Colorectal Neoplasms; Epithelial-Mesenchymal Tra | 2015 |
Development of a Drug-Response Modeling Framework to Identify Cell Line Derived Translational Biomarkers That Can Predict Treatment Outcome to Erlotinib or Sorafenib.
Topics: Antineoplastic Agents; Biomarkers, Pharmacological; Cell Line, Tumor; Clinical Trials, Phase II as T | 2015 |
The distribution of BRAF gene fusions in solid tumors and response to targeted therapy.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Child; Child, Preschool; Female; | 2016 |
Combinatorial high-throughput experimental and bioinformatic approach identifies molecular pathways linked with the sensitivity to anticancer target drugs.
Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Survival; Computational Biology; Gene Expression Profi | 2015 |
Inhibition of FOXP3/NFAT Interaction Enhances T Cell Function after TCR Stimulation.
Topics: Animals; Antineoplastic Agents; CD40 Ligand; Cell Proliferation; CTLA-4 Antigen; Female; Forkhead Tr | 2015 |
Target prices for mass production of tyrosine kinase inhibitors for global cancer treatment.
Topics: Antineoplastic Agents; Commerce; Drug Industry; Erlotinib Hydrochloride; Global Health; Humans; Imat | 2016 |
Widespread morbilliform rash due to sorafenib or vemurafenib treatment for advanced cancer; experience of a tertiary dermato-oncology clinic.
Topics: Aged; Antineoplastic Agents; Drug Eruptions; Exanthema; Female; Humans; Indoles; Male; Middle Aged; | 2016 |
In vitro and in vivo evaluation of drug-eluting microspheres designed for transarterial chemoembolization therapy.
Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Cell Survival; Cisplatin; Drug Delivery Systems; D | 2016 |
Pilot Study of a Next-Generation Sequencing-Based Targeted Anticancer Therapy in Refractory Solid Tumors at a Korean Institution.
Topics: Adult; Afatinib; Aged; Antineoplastic Agents; Asian People; Class I Phosphatidylinositol 3-Kinases; | 2016 |
Multicentric survey on dose reduction/interruption of cancer drug therapy in 12.472 patients: indicators of suspected adverse reactions.
Topics: Antineoplastic Agents; Capecitabine; Docetaxel; Drug Administration Schedule; Humans; Neoplasms; Nia | 2016 |
Population pharmacokinetic modeling of motesanib and its active metabolite, M4, in cancer patients.
Topics: Administration, Oral; Adult; Aged; Angiogenesis Inhibitors; Asian People; Biotransformation; Clinica | 2015 |
Patient-specific blood pressure correction technique for arterial stiffness: evaluation in a cohort on anti-angiogenic medication.
Topics: Adult; Aged; Algorithms; Angiogenesis Inhibitors; Blood Pressure; Carotid Arteries; Cohort Studies; | 2017 |
Exploration of 2-((Pyridin-4-ylmethyl)amino)nicotinamide Derivatives as Potent Reversal Agents against P-Glycoprotein-Mediated Multidrug Resistance.
Topics: Antibiotics, Antineoplastic; ATP Binding Cassette Transporter, Subfamily B, Member 1; Cytochrome P-4 | 2017 |
Challenges and pitfalls of combining targeted agents in phase I studies.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic C | 2008 |
Vorinostat and sorafenib synergistically kill tumor cells via FLIP suppression and CD95 activation.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Benzenesulfonates; CASP8 and FADD-Like Ap | 2008 |
Tyrosine kinase inhibitors: can promising new therapy associated with cardiac toxicity strengthen the concept of teamwork?
Topics: Antineoplastic Agents; Benzenesulfonates; Cardiovascular Diseases; Humans; Indoles; Neoplasms; Niaci | 2008 |
Comparison of the effects of the kinase inhibitors imatinib, sorafenib, and transforming growth factor-beta receptor inhibitor on extravasation of nanoparticles from neovasculature.
Topics: Animals; Benzamides; Benzenesulfonates; Cell Line, Tumor; Extravasation of Diagnostic and Therapeuti | 2009 |
Cutaneous drug eruptions induced by sorafenib: a case series.
Topics: Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Drug Eruptions; Erythema; Female; Humans; Mid | 2008 |
Blood flow and Vd (water): both biomarkers required for interpreting the effects of vascular targeting agents on tumor and normal tissue.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Biomarkers, Tumor; Carbon Dioxide; Female; Hu | 2009 |
Validation of an HPLC-UV method for sorafenib determination in human plasma and application to cancer patients in routine clinical practice.
Topics: Aged; Angiogenesis Inhibitors; Antineoplastic Agents; Benzenesulfonates; Calibration; Chromatography | 2009 |
Selecting promising treatments in randomized Phase II cancer trials with an active control.
Topics: Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Clinical Trials, Phase II as Topi | 2009 |
VEGF inhibition and metastasis: possible implications for antiangiogenic therapy.
Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzene | 2009 |
Therapeutic Drug Monitoring of the new targeted anticancer agents imatinib, nilotinib, dasatinib, sunitinib, sorafenib and lapatinib by LC tandem mass spectrometry.
Topics: Antineoplastic Agents; Benzamides; Benzenesulfonates; Chromatography, Liquid; Dasatinib; Drug Monito | 2009 |
How well do angiogenesis inhibitors work? Biomarkers of response prove elusive.
Topics: Angiogenesis Inhibitors; Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzene | 2009 |
Multiple Histology Phase II Trials.
Topics: Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase II as Topic; Computer Simulation; H | 2009 |
Array of cutaneous adverse effects associated with sorafenib.
Topics: Benzenesulfonates; Biopsy, Needle; Cohort Studies; Dose-Response Relationship, Drug; Drug Administra | 2009 |
Statins potentiate cytostatic/cytotoxic activity of sorafenib but not sunitinib against tumor cell lines in vitro.
Topics: Animals; Apoptosis; Benzenesulfonates; Blotting, Western; Cell Cycle; Cell Line, Tumor; Cell Surviva | 2010 |
A computational approach to compare microvessel distributions in tumors following antiangiogenic treatments.
Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Benzenesulfonates; Cell Line, Tumor; Comput | 2009 |
Ambulatory monitoring detects sorafenib-induced blood pressure elevations on the first day of treatment.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Benzenesulfonates; Blood Pressure; Blood Pres | 2009 |
Rapid development of hypertension by sorafenib: toxicity or target?
Topics: Angiogenesis Inhibitors; Animals; Benzenesulfonates; Blood Pressure; Drug Delivery Systems; Drug Dos | 2009 |
Tyrosine kinase inhibitor-induced macrocytosis.
Topics: Anemia, Macrocytic; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Benzenesulfonates; E | 2009 |
Risk of bleeding not increased by sorafenib or sunitinib.
Topics: Antineoplastic Agents; Benzenesulfonates; Hemorrhage; Humans; Indoles; Neoplasms; Niacinamide; Pheny | 2010 |
[Correction of metabolic disturbances in cancer patients in the early postanesthesia period].
Topics: Adult; Aged; Anesthesia, General; Dose-Response Relationship, Drug; Drug Combinations; Female; Flavi | 2010 |
Pneumatosis intestinalis associated with treatment of cancer patients with the vascular growth factor receptor tyrosine kinase inhibitors sorafenib and sunitinib.
Topics: Adult; Benzenesulfonates; Disease Progression; Fatal Outcome; Female; Humans; Indoles; Male; Middle | 2011 |
Sensitivity of doxorubicin-resistant cells to sorafenib: possible role for inhibition of eukaryotic initiation factor-2alpha phosphorylation.
Topics: Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Cell Proliferation; Cell Survival | 2010 |
Hypertension and hand-foot skin reactions related to VEGFR2 genotype and improved clinical outcome following bevacizumab and sorafenib.
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Combined Chemotherapy Prot | 2010 |
Initial testing (stage 1) of the multi-targeted kinase inhibitor sorafenib by the pediatric preclinical testing program.
Topics: Animals; Benzenesulfonates; Cell Line, Tumor; Child; Female; Humans; Mice; Mice, Inbred BALB C; Mice | 2010 |
Effect of the tyrosine kinase inhibitors (sunitinib, sorafenib, dasatinib, and imatinib) on blood glucose levels in diabetic and nondiabetic patients in general clinical practice.
Topics: Aged; Antineoplastic Agents; Benzamides; Benzenesulfonates; Blood Glucose; Dasatinib; Diabetes Melli | 2011 |
Spiny follicular hyperkeratosis eruption: a new cutaneous adverse effect of sorafenib.
Topics: Adult; Aged; Aged, 80 and over; Angiogenesis Inhibitors; Benzenesulfonates; Drug Eruptions; Female; | 2010 |
Sorafenib and its tosylate salt: a multikinase inhibitor for treating cancer.
Topics: Antineoplastic Agents; Benzenesulfonates; Crystallography, X-Ray; Enzyme Inhibitors; Humans; Hydroge | 2011 |
An approach to meta-analysis of dose-finding studies.
Topics: Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase I as Topic; Computer S | 2011 |
Design, synthesis and evaluation of novel rhodanine-containing sorafenib analogs as potential antitumor agents.
Topics: Antineoplastic Agents; Benzenesulfonates; Cell Line, Tumor; Cell Proliferation; HT29 Cells; Humans; | 2011 |
Sorafenib enhances the antitumor effects of chemoradiation treatment by downregulating ERCC-1 and XRCC-1 DNA repair proteins.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Cell Line, Tumor; Cell Movement; Cell Proliferati | 2011 |
Sorafenib enhances pemetrexed cytotoxicity through an autophagy-dependent mechanism in cancer cells.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Autophagy; Benzenesulfonates; Cell Line, Tu | 2011 |
99mTc-HYNIC-spermine for imaging polyamine transport system-positive tumours: preclinical evaluation.
Topics: Animals; Biological Transport; Carrier Proteins; Cell Line, Tumor; Drug Stability; Female; Humans; H | 2011 |
Functional and clinical evidence of the influence of sorafenib binding to albumin on sorafenib disposition in adult cancer patients.
Topics: Adult; Antineoplastic Agents; Benzenesulfonates; Bilirubin; Female; Humans; Male; Neoplasms; Niacina | 2011 |
Preparation of the albumin nanoparticle system loaded with both paclitaxel and sorafenib and its evaluation in vitro and in vivo.
Topics: Animals; Antineoplastic Agents; Benzenesulfonates; Cattle; Cell Line, Tumor; Drug Carriers; Female; | 2011 |
[Antioxidant protection as a component of anesthetic management cancer patients].
Topics: Adaptation, Physiological; Aged; Anesthetics, Combined; Antioxidants; Balanced Anesthesia; Drug Comb | 2011 |
[Adverse effects of new oncologic therapies].
Topics: Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Antineoplastic Com | 2011 |
Sorafenib enhances pemetrexed cytotoxicity through an autophagy-dependent mechanism in cancer cells.
Topics: Animals; Antineoplastic Agents; Autophagy; Benzenesulfonates; Cell Line, Tumor; Dose-Response Relati | 2011 |
New imidazo[2,1-b]thiazole derivatives: synthesis, in vitro anticancer evaluation, and in silico studies.
Topics: Antineoplastic Agents; Benzenesulfonates; Cell Line, Tumor; Cell Proliferation; Drug Screening Assay | 2011 |
Skin tumors induced by sorafenib; paradoxic RAS-RAF pathway activation and oncogenic mutations of HRAS, TP53, and TGFBR1.
Topics: Adult; Aged; Antineoplastic Agents; Benzenesulfonates; Biomarkers, Tumor; Blotting, Western; Carcino | 2012 |
Sorafenib is an inhibitor of UGT1A1 but is metabolized by UGT1A9: implications of genetic variants on pharmacokinetics and hyperbilirubinemia.
Topics: Aged; Antineoplastic Agents; Area Under Curve; Benzenesulfonates; Bilirubin; Clinical Trials as Topi | 2012 |
A novel approach to manage skin toxicity caused by therapeutic agents targeting epidermal growth factor receptor.
Topics: Antineoplastic Agents; Camellia sinensis; Drug Therapy, Combination; ErbB Receptors; Humans; Neoplas | 2012 |
RAIN-Droplet: a novel 3D in vitro angiogenesis model.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Benzenesulfonates; Bevacizumab; Cells, C | 2012 |
Variability of sorafenib toxicity and exposure over time: a pharmacokinetic/pharmacodynamic analysis.
Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Area Under Curve; Benzenesulfonates; Chromato | 2012 |
Early sorafenib-induced toxicity is associated with drug exposure and UGTIA9 genetic polymorphism in patients with solid tumors: a preliminary study.
Topics: Aged; Antineoplastic Agents; Area Under Curve; Diarrhea; Female; Genotype; Glucuronosyltransferase; | 2012 |
The important roles of RET, VEGFR2 and the RAF/MEK/ERK pathway in cancer treatment with sorafenib.
Topics: Antineoplastic Agents; Blotting, Western; Cell Culture Techniques; Cell Line, Tumor; Cell Proliferat | 2012 |
No end in sight for telomerase-targeted cancer drugs.
Topics: Antineoplastic Agents; Clinical Trials as Topic; Humans; Indoles; Molecular Targeted Therapy; Neopla | 2013 |
Contribution of OATP1B1 and OATP1B3 to the disposition of sorafenib and sorafenib-glucuronide.
Topics: Animals; Antineoplastic Agents; Glucuronic Acid; HEK293 Cells; Humans; Liver-Specific Organic Anion | 2013 |
Taking cancer-drug toxicity to heart.
Topics: Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Bevacizumab; Doxorubicin; Heart Failure; H | 2013 |
Nicotinamide-containing sunscreens for use in Australasian countries and cancer-provoking conditions.
Topics: Australasia; DNA Repair; Models, Theoretical; Neoplasms; Niacinamide; Sunscreening Agents | 2003 |
Nicotinamide content of some normal and malignant tissues; the apparent absence of niacin in epidermis.
Topics: Epidermis; Neoplasms; Niacin; Niacinamide; Nicotinic Acids | 1952 |
Significance of enzymatically catalyzed exchange reactions in chemotherapy.
Topics: Animals; Coenzymes; Liver; Mice; Neoplasms; Niacin; Niacinamide; Nicotinic Acids; Pyridines; Tryptop | 1954 |
[Methylated nicotinamide in the liver in neoplasms in rats].
Topics: Animals; Liver; Neoplasms; Niacin; Niacinamide; Nicotinic Acids; Rats | 1955 |
Tryptophan-nicotinic acid metabolism in patients with tumours of the bladder. Changes in the excretory products after treatment with nicotinamide and vitamin B6.
Topics: Humans; Neoplasms; Niacin; Niacinamide; Nicotinic Acids; Tryptophan; Urinary Bladder Neoplasms; Vita | 1961 |
[Studies on the metabolic conversion of tryptophan into nicotinic acid in individuals with tumors of the bladder. Modifications in the urinary excretory picture after the administration of nicotinamide and vitamin B6].
Topics: Humans; Neoplasms; Niacin; Niacinamide; Nicotinic Acids; Tryptophan; Urinary Bladder Neoplasms; Vita | 1960 |
[On the influence of carcinostatic agents on the DPN metabolism of tumors. I. Incorporation of C-14-ribose and C-14-nicotinamide into the DPN of ascites cells].
Topics: Antineoplastic Agents; Ascites; Coenzymes; NAD; Neoplasms; Niacin; Niacinamide; Nicotinic Acids; Rib | 1960 |
Inhibiting effect of nicotinamide and diphosphopyridine nucleotide on the methylcholanthrene sarcoma in rats.
Topics: Animals; Coenzymes; Methylcholanthrene; NAD; Neoplasms; Niacin; Niacinamide; Nicotinic Acids; Rats; | 1961 |
Substrate specificity and inhibition of nicotinamide mononucleotideadenylyl transferase of liver nuclei: possible mechanism of effect of 6-mercaptopurine on tumour growth.
Topics: Cell Nucleus; Liver; Mercaptopurine; Neoplasms; Niacin; Niacinamide; Substrate Specificity; Transfer | 1961 |
[Evaluation of nicotinic acid and nicotinamide for the biosynthesis of DPN in ascites tumor cells].
Topics: Ascites; Coenzymes; NAD; Neoplasms; Niacin; Niacinamide; Nicotinic Acids | 1961 |
Uptake of nicotinic acid-C-14 and nicotinamide-C-14 by ascites cells in vitro.
Topics: Ascites; In Vitro Techniques; NAD; Neoplasms; Neoplasms, Experimental; Niacin; Niacinamide; Nicotini | 1963 |
6-AMINONICOTINAMIDE AND THE RADIOSENSITIVITY OF HUMAN LIVER CELLS IN CULTURE.
Topics: 6-Aminonicotinamide; Animals; Carcinoma, Ehrlich Tumor; Chromosomes; Fetus; Liver; Mice; Neoplasms; | 1963 |
CONCENTRATIONS AND RATES OF SYNTHESIS OF NICOTINAMIDE-ADENINE-DINUCLEODIDE PHOSPHATE IN PRECANCEROUS LIVERS AND HEPATOMAS INDUCED BY AZO-DYE FEEDING.
Topics: Adenine; Carcinogens; Carcinoma, Hepatocellular; Liver; Liver Neoplasms; NADP; Neoplasms; Neoplasms, | 1964 |
[THE PROTECTIVE EFFECT OF NICOTINAMIDE ON RADIATION-INDUCED INJURY OF DNA SYNTHESIS AS A CELL POPULATION PROBLEM].
Topics: Animals; Carbohydrate Metabolism; Carcinoma, Ehrlich Tumor; DNA; DNA, Neoplasm; NAD; Neoplasm Protei | 1964 |
THE EFFECT OF CIGARETTE SMOKING ON BLADDER CARCINOGENS IN MAN.
Topics: Amino Acids; Carcinogens; Humans; Male; Metabolism; Neoplasms; Niacin; Niacinamide; Nicotiana; Smoki | 1965 |
[INVESTIGATION ON THE DECREASE IN CONCENTRATION OF NAD IN LYMPHOSARCOMA ASCITES CELLS FOLLOWING X-IRRADIATION].
Topics: Ascites; Chromatography; Lymphoma; Lymphoma, Non-Hodgkin; Metabolism; NAD; Neoplasms; Neoplasms, Exp | 1965 |
STIMULATION OF DPN TURNOVER IN ASCITES TUMOR CELLS BY LOW X-RAY DOSES.
Topics: Animals; Ascites; Carcinoma; Carcinoma, Ehrlich Tumor; DNA; DNA, Neoplasm; Metabolism; N-Glycosyl Hy | 1965 |
Influence of nicotic acid and nicotinamide on diphosphopyridine nucleotide (DPN) Synthesis in ascites tumor cells.
Topics: Animals; Ascites; Carcinoma, Ehrlich Tumor; Coenzymes; NAD; Neoplasms; Niacin; Niacinamide; Nicotini | 1961 |
In vivo determination of tumor oxygenation during growth and in response to carbogen breathing using 15C5-loaded alginate capsules as fluorine-19 magnetic resonance imaging oxygen sensors.
Topics: Alginates; Animals; Carbon Dioxide; Cell Hypoxia; Crown Ethers; Fluorine; Glucuronic Acid; Hexuronic | 2004 |
BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis.
Topics: Administration, Oral; Animals; Benzenesulfonates; Cell Line, Tumor; Disease Progression; Female; Hum | 2004 |
BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis.
Topics: Administration, Oral; Animals; Benzenesulfonates; Cell Line, Tumor; Disease Progression; Female; Hum | 2004 |
BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis.
Topics: Administration, Oral; Animals; Benzenesulfonates; Cell Line, Tumor; Disease Progression; Female; Hum | 2004 |
BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis.
Topics: Administration, Oral; Animals; Benzenesulfonates; Cell Line, Tumor; Disease Progression; Female; Hum | 2004 |
In vivo modulation of signaling factors involved in cell survival.
Topics: Animals; Blotting, Western; Cell Line, Tumor; Cell Survival; Curcumin; Cytosol; Extracellular Signal | 2004 |
Cancer. Encouraging results for second-generation antiangiogenesis drugs.
Topics: Angiogenesis Inhibitors; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Benzenesulfonate | 2005 |
Clinical trials referral resource. Current clinical trials of BAY 43-9006, Part 1.
Topics: Angiogenesis Inhibitors; Benzenesulfonates; Clinical Trials as Topic; Humans; Neoplasms; Niacinamide | 2005 |
Clinical trials referral resource.
Topics: Antineoplastic Agents; Benzenesulfonates; Clinical Trials as Topic; Humans; Neoplasms; Niacinamide; | 2005 |
Drug approval triggers debate on future direction for cancer treatments.
Topics: Antineoplastic Agents; Benzenesulfonates; Drug Approval; Drug Design; Enzyme Inhibitors; Neoplasms; | 2006 |
Pharmacy benefit spending on oral chemotherapy drugs.
Topics: Administration, Oral; Ambulatory Care; Antineoplastic Agents; Benzamides; Benzenesulfonates; Capecit | 2006 |
Speeding up cancer-drug development.
Topics: Benzenesulfonates; Carcinoma, Hepatocellular; Carcinoma, Renal Cell; Clinical Trials, Phase II as To | 2006 |
A tale of two drugs.
Topics: Adenine Nucleotides; Antineoplastic Agents; Arabinonucleosides; Benzenesulfonates; Clofarabine; Drug | 2006 |
A novel oral indoline-sulfonamide agent, N-[1-(4-methoxybenzenesulfonyl)-2,3-dihydro-1H-indol-7-yl]-isonicotinamide (J30), exhibits potent activity against human cancer cells in vitro and in vivo through the disruption of microtubule.
Topics: Administration, Oral; Animals; Antineoplastic Agents; Apoptosis; Binding Sites; Caspases; Cell Cycle | 2007 |
American Society of Clinical Oncology--43rd annual meeting. Translating research into practice.
Topics: Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Benzenesu | 2007 |
ASCO 2007: plenary top 5.
Topics: Antineoplastic Agents; Benzenesulfonates; Carcinoma, Hepatocellular; Carcinoma, Renal Cell; Carcinom | 2007 |
Examining heterogeneity in phase II trial designs may improve success in phase III.
Topics: Antineoplastic Agents; Benzenesulfonates; Clinical Trials, Phase II as Topic; Clinical Trials, Phase | 2008 |
Quantifying hypertension in patients with cancer treated with sorafenib.
Topics: Antineoplastic Agents; Benzenesulfonates; Humans; Hypertension; Neoplasms; Niacinamide; Phenylurea C | 2008 |
Carbogen breathing with nicotinamide improves the oxygen status of tumours in patients.
Topics: Adult; Aged; Aged, 80 and over; Carbon Dioxide; Female; Humans; Male; Middle Aged; Neoplasms; Niacin | 1995 |
ARCON.
Topics: Animals; Carbon Dioxide; Humans; Neoplasms; Niacinamide; Oxygen; Radiation-Sensitizing Agents; Radio | 1994 |
Blood flow modification by nicotinamide and metoclopramide in mouse tumours growing in different sites.
Topics: Animals; Cardiac Output; Colonic Neoplasms; Male; Mammary Neoplasms, Experimental; Metoclopramide; M | 1993 |
Nicotinamide pharmacokinetics in patients.
Topics: Administration, Oral; Combined Modality Therapy; Humans; Hyperthermia, Induced; Neoplasms; Niacinami | 1995 |
Nicotinamide pharmacokinetics in normal volunteers and patients undergoing palliative radiotherapy.
Topics: Administration, Oral; Female; Half-Life; Humans; Incidence; Male; Neoplasms; Niacinamide; Palliative | 1996 |
Nicotinamide and pentoxifylline increase human leucocyte filterability: a possible mechanism for reduction of acute hypoxia.
Topics: Cell Hypoxia; Dose-Response Relationship, Drug; Filtration; Humans; Leukocytes; Neoplasms; Niacinami | 1996 |
The potential for improving radiotherapy outcome by improving the oxygen supply to solid tumours.
Topics: Animals; Carbon Dioxide; Cell Hypoxia; Cells, Cultured; Humans; Mice; Neoplasms; Neoplasms, Experime | 1996 |
ARCON.
Topics: Animals; Carbon Dioxide; Cell Hypoxia; Humans; Mice; Neoplasms; Neoplasms, Experimental; Niacinamide | 1996 |
Comments on hyperbaric oxygen and carbogen/nicotinamide with fractionated radiation.
Topics: Carbon Dioxide; Humans; Hyperbaric Oxygenation; Hypoxia; Models, Biological; Neoplasms; Niacinamide; | 1997 |
Impact of nicotinamide on human tumour hypoxic fraction measured using the comet assay.
Topics: Administration, Oral; Biopsy, Needle; Cell Hypoxia; DNA Damage; DNA, Neoplasm; Dose Fractionation, R | 1997 |
Rat ventral prostate xanthine oxidase bioactivation of ethanol to acetaldehyde and 1-hydroxyethyl free radicals: analysis of its potential role in heavy alcohol drinking tumor-promoting effects.
Topics: Acetaldehyde; Alcohol Drinking; Allopurinol; Animals; Antimetabolites; Caffeine; Carcinogens; Chroma | 2001 |
Negative control of p53 by Sir2alpha promotes cell survival under stress.
Topics: Animals; Apoptosis; Blotting, Western; Cell Death; Cell Line; Cell Survival; DNA Damage; DNA, Comple | 2001 |
The modification of human tumour blood flow using pentoxifylline, nicotinamide and carbogen.
Topics: Administration, Inhalation; Administration, Oral; Adult; Aged; Carbon Dioxide; Female; Humans; Laser | 2002 |
ARCON: accelerated radiotherapy with carbogen and nicotinamide.
Topics: Carbon Dioxide; Cell Hypoxia; Humans; Neoplasms; Niacinamide; Oxygen Consumption; Radiation Toleranc | 1992 |
Carbogen and nicotinamide: expectations too high? (response to J. Martin Brown)
Topics: Animals; Carbon Dioxide; Humans; Mice; Neoplasms; Neoplasms, Experimental; Niacinamide; Oxygen; Radi | 1992 |
Extrapolations from laboratory and preclinical studies for the use of carbogen and nicotinamide in radiotherapy.
Topics: Animals; Carbon Dioxide; Humans; Mice; Neoplasms; Neoplasms, Experimental; Niacinamide; Oxygen; Radi | 1992 |
Carbogen and nicotinamide: expectations too high?
Topics: Animals; Carbon Dioxide; Humans; Mice; Neoplasms; Neoplasms, Experimental; Niacinamide; Oxygen; Radi | 1992 |
Synthesis of 5-beta-D-ribofuranosylnicotinamide and its N-methyl derivative. The isosteric and isoelectronic analogues of nicotinamide nucleoside.
Topics: NAD; Neoplasms; Niacinamide; Ribonucleosides | 1987 |
Synergistic induction of sister-chromatid exchanges in lymphocytes from normal subjects and from patients under cytostatic therapy by inhibitors of poly(ADP-ribose)polymerase and antitumour agents.
Topics: Antineoplastic Agents; DNA Repair; Drug Synergism; Humans; In Vitro Techniques; Lymphocytes; NAD+ Nu | 1985 |
[The effect of oxygen on the status of blood gases in oncological patients receiving radiation therapy].
Topics: Blood Gas Analysis; Carbon Dioxide; Humans; Hypoxia; Neoplasms; Niacinamide; Oxygen; Oxygen Consumpt | 1968 |
Early effects of nicotinamide, 2,4-dichloro-phenoxy acetic acid & actinomycin-D on the synthesis of nicotinamide amidohydrolase in rumex acetosa tumour tissue.
Topics: Acetates; Amidohydrolases; Dactinomycin; Enzyme Induction; Neoplasms; Niacinamide; Phenols; Plant Di | 1971 |
Excretion of 5-hydroxyindole acetic acid and n1-methylnicotinamide in advanced cancer patients.
Topics: Aged; Humans; Hydroxyindoleacetic Acid; Middle Aged; Neoplasms; Niacinamide; Tryptophan | 1973 |
From protozoa to bacteria and viruses. Fifty years with microbes (André Lwoff).
Topics: Bibliographies as Topic; Ciliophora; Crustacea; Eukaryota; Eye; Fever; France; Growth Substances; He | 1971 |